text:
Why cooked food considered nutritious if proteins decompose at much lower temperatures?
Food is cooked/baked at temperatures that are significantly higher than what's considered normal for proteins/amino acids (40°C). Why is it, then, that such food is still considered nutritious after cooking? (meat, cheesecake, lentils, quinoa, mushrooms, etc.)

Where are you getting the 40°C temperature from? Denaturation of most proteins happens at higher temperatures than that. And what do you mean by decompose?

@MadScientist, maybe it's just bad memory. Can you share a source that gives some numbers?

Cooking is just a form of digestion.

What is digestion?

Digestion is the process of breaking down big molecules into smaller molecules. When you cook food you break down big molecules into its small components.

Why do we digest food?

Think about a long sequence of DNA for example. You eat corn and you have in your body a long sequence of corn DNA. What can you do with that long molecule....well, nothing. You need to break this long molecule down in order to be able to assimilate the constitutive nutrients. With those nutrients, you can now make up your own DNA. In other words, we need to break the big Lego castle that is food to get the building blocks in order to rebuild a spaceship. Digestion refer to the first process (breaking up the Lego castle). We refer to the part of the metabolism who breaks things down as catabolism and we refer to the part of metabolism that build things up as anabolism. Note that catabolism + anabolism = metabolism.

Why do we cook then instead of digesting by ourself

Digestion takes much energy and require the organism to have the right organs and to have the right matter (enzymes and stuff). We can save up energy (and the other stuff) by digesting the food outside our body. One could say that humans, (just like spiders for example) are performing external digestion.

Why cooked food considered nutritious

Cooked food don't have more nutrients than raw food. It is actually likely that in the process of cooking you would lose some nutrients going in the water that you throw away typically.
The big difference is that nutrients in cooked food are easy to assimilate which might end up being more healthy depending on the specific food source. Cooking may also destroy potentially toxic products.
Note that in response to the cooking behaviour, human gut has evolved to be shorter than it was in our ancestor.

then why are we advised to consume most vegetables raw?

@Sparkler according to this article, it's actually healthier to cook a lot of veggies. It actually breaks things down within the vegetables that our bodies might not be able to do.


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How do female hormones cause blood to clot?
On most female-hormone supplements you get a warning that is something like this:

The use of a combination hormonal contraceptives (CHC), like NuvaRing, is associated with increased risks of several serious side effects, including blood clots, stroke, or heart attack. (Nuvaring)

The use of a CHC, like NuvaRing, is associated with increased risks of several serious side effects, including blood clots, stroke, or heart attack.
It also goes onto state that smoking can increase these risks.

What makes these hormones so dangerous (prone to clotting)?
If a person is naturally high in these hormones are they at a higher risk of blood clots?
Why/How does smoking affect the hormones - or is the increase risk just due to the natural risk of smoking?

These combination contraceptives contain two substances: Estrogen and progestin (a synthetic progesterone). Both are used together to overcome the negative effects of single substance drugs as acne or sickness.
The risk for blood clots has been known for quite a while (see reference 1 and 2) and is generally caused by raised levels of clotting factors (especially VII and X), increased plasma fibrinogen, increased platelet aggregation in the blood and reduced activity of antithrombin III (which inhibits coagulation). This can happen as well in pregnancy when the factors are naturally elevated (that's the way these contraceptives simulate pregnancy to the body). The paper shows this nicely for two of the factors of the blood coagulation cascade (factor VII and X):

This risk is relatively rare, it affects only about 1-5 in 10.000 women, but is still not negligible. The risk is much higher in persons with defects in the blood coagulation cascade. Compared to this, pregnant women have a risk for blood clots of 5-20 per 10.000 women (for details see here).
Blood coagulation is really fine tuned to ensure proper function when necessary but no blood clotting when not. Basically activating and deactivating hold a balance, as depicted in figure 1 from reference 3:

Smoking now disturbs this balance by inhibiting fibrinolysis and promoting the accumulation of fibrin and pushes it more to the site of coagulation. What causes the problem here is the elevation of clotting factors in combination with the disturbance of the balance between activation and inhibition of clotting. See reference 3 for the details.
This effect seems to be limited to high concentration single estrogen and estrogen/progestin combination preparations, while there seems to be no such effect in progestin single preparations (although data is limited here). There is also a significant difference in the type of estrogen used. See references 4 and 5 for more details.
The mechanism of how this works is relatively straightforward. The estrogen binds to the estrogen receptor on the cell surface and forms a receptor-ligand complex. This leads to signalling inside the cells which finally results in changed gene expression. Additionally the complex can be internalized by the cell. Inside the cell this complex can bind to the so-called "hormone response element" and also regulate the expression of genes. This is explained in detail for Factor XII in reference 6 (and works like this for other parts as well). See the image for illustration (from reference 7):

References:

Relation between oral contraceptive hormones and blood clotting
Use of combined oral contraceptives and risk of venous
thromboembolism: nested case-control studies using the QResearch and
CPRD databases
Hemostatic effects of smoking and oral contraceptive use
Coagulation effects of oral contraception.
Lower Risk of Cardiovascular Events in Postmenopausal Women Taking
Oral Estradiol Compared With Oral Conjugated Equine Estrogens
Molecular basis of estrogen regulation of Hageman factor XII gene
expression.
Estrogen synthesis and signaling pathways during aging: from
periphery to brain

This particular product contains estradiol. Are these findings true for only progesterone or are they applicable for estradiol as well?

The info on estrogen signaling is great. Can you emphasize on the pathways that would lead to regulation of hemostasis.

@WYSIWYG I am not exactly sure which information you are looking for.

The relationship between estrogen signaling and blood clotting

I am not sure, if this has been researched in all detail, at least I haven't found a paper right now. I will have a look into it.

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Why is polysome loading affected by double stranded structure?
Why polysomes are not able to load properly onto a transcript if a transcript has a double-stranded structure in it?

You mean to say a single ribosome is loaded but multiple ribosomes are not loading? Do you have any data on this or you just heard it somewhere? Usually secondary structures are resolved by elongation factors (4A). In general secondary structures will impede ribosome movement. You should add more details in your question.

I was reading the following article "C. elegans and H. sapiens mRNAs with edited 3′ UTRs are present on polysomes". According to it, polysomes are not able to load properly on to the transcript if two inverted alu repeats make a double stranded structure within a transcript.

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Does learning increase the number of neurons in the brain?
I am attempting to understand neurogenesis related to learning. Does learning increase the number of neurons in the human brain? What would be some good scientific publications to read?

So in other words the number of connections between neurons is just changed? Where could I find some good references for that?

We should probably wait for @AliceD to answer, since he knows the field better.

@WYSIWYG: I am not so sure that it doesn't, and I think it actually does lead to new cells.

@AliceD Not in most cases esp. in adults. There is some neurogenesis in the dentate gyrus which may perhaps be regulated by some hippocampal activity (there is a paper which says that). Another point of view is that neurogenesis might lead to amnesia (this was in science some months back). Anyways I just gave a casual comment- I take it back :)

@user16406 It does happen but in most cases learning basically adds/strengthens the synapses.

Not necessary. Neurons are very complex and dynamic. They can be regulated both pre-synaptically and post-synaptically. I think you should read about neural plasticity. It will give you more insight on how the neurons might be able to "learn" without the need to form new projections to adjacent neurons.
Edit: Perhaps you want an answer specific for the role of neurogenesis in learning, but I still think that reading about neural plasticity will give you a good answer for your question.

0I thought we had something that prevented new neurons from forming and that learning was a change in synapsis. (However, you shouldn't take my word for it. @AliceD

@SolarLunix - Check my answer. There is definitely neurogenesis. also see http://biology.stackexchange.com/questions/25880/can-brain-cells-move/25889#25889

Short answer
Training increases white and gray matter densities in the brain. This may reflect increases in neuronal cell counts especially in the hippocampus. In the cortex, however, such observed changes are probably more reflective of other processes, such as synaptogenesis.
Background
Gray matter is generally viewed as being the neuronal cell bodies, while white matter corresponds to myelinated fiber tracts. Changes in both can be reflective of changes in cellular content, but changes in gray matter are generally more directly related to changes in cell numbers, which you are after.
A striking example of the effects of learning on the brain is observed in subjects that start to learn to juggle. These people have been shown to have increased gray matter density in the occipito-parietal regions (the visual motion areas). These changes are apparent after as little as 7 days of training. Such experience-dependent changes are also observed in white matter. Occipito-parietal regions are involved in visuo-motor coordination, reaching and grasping. There have been a host of other studies that showed similar changes in the brain. For example, taxi drivers were shown to have increased hippocampal volumes.
There is good evidence for adult neurogenesis occurring with learning in the hippocampus. Adult neurogenesis also produces thousands of new granule cells in the dentate gyrus every month, but this is a relatively small increase in total number of hippocampal neurons. Furthermore, although there have been reports of neurogenesis in the mammalian adult neocortex, this is controversial.
Thus, neurogenesis is likely a minor factor in MRI changes, particularly those found outside the hippocampus.
Instead, other factors such as increase in glial cell numbers, synaptogenesis, changes in dendritic structures, axonal sprouting and re-routing and even vascular changes may underly the observed changes in imaging studies.
Note: there is a host of imaging studies available on effects of learning on structural changes in the brain. The referenced review article cites many.
Reference
- Zatorre et al., Nature Neurosci (2012); 15: 528–36

The no. of neurons only increase during development.
As, a person grows, the no. of neurons is constant or decreases (degradation due to injury or other brain diseases). The no. never increases.

Learning anything (say, a phone no.) requires repeated thinking. The thinking can be continuous in the brain or re-induced by revision. Therefore, learning anything STRENGTHENS the connections; not increase in neuron no.
I can't help you with any Scientific Paper. The image was taken from a Textbook.

Without proper references such a strong statement is unfounded. -1

The figure is from Campbell Biology

The number of neurons does not only increase during development.


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Defining Resistance and Sensitivity Thresholds for IC50
I have a dataset containing IC50 data for each of my cell lines and up to 80 drugs. Basically for each drug I want to be able to define an IC50 threshold where if a cell line has an IC50 above that threshold it is resistant, and if it is below that threshold it is sensitive.
I'm trying to think of the best way of doing this: I was thinking of taking the median for each drug as the threshold but I realize that's quite crude. Are there any more robust statistical techniques I could use to define such a threshold for each drug?
Thanks!

You might want to see the distribution of IC50s. If the majority do not obtain resistance, the histogram may show a normal distribution. Then you would know where less than 5% or 1% of population distribute.
If you have a few cell lines know as resistant against the chemical, you could use them to decide threshold.
PS
Each drug has different effective dosage. You can not draw the same threshold for different drugs. If you have lots of cell lines, you could apply the strategy I mentioned above for a single drug.

IC50 has an exact definition, that is half-maximal inhibitory concentration. To get this you need to make a series of dilutions of each of your drugs and test your cell lines in each concentration and assess how they grow (eg measure Optical density, colony size, cell count or whatever applies to your cells and setup). Then you can set up a inhibition curve that is a function of the concentration. This most likely looks like a sigmoid curve and the inflection point gives you the IC50 value.
An example image form the wikipedia page of IC50 (recommended to read):

So in your case, you already have IC50 values (for wild types I assume), and you need to assess your (probably mutant ?) cell lines to see if they are sensitive or resistant. Standard lab practice recommends using wild-type controls and at least 3 parallel controls. You can compare the average growth of WTs to your cell line at the IC50 concentration you already got in your dataset, and calculate standard deviation, and 95% confidence interval. With some simplification if the 95%CI of your cell line is greater than the wt 95%CI it is most likely that your cell line is resistant to that drug, on the other hand if its lower then that cell line is sensitive to the drug in question.


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Mutation That Loses Stop Codon
Someone asked this in my class and my instructor wasn't sure in her answer, doesn't anyone know what happens in protein synthesis if a mutation causes mRNA to not possess a stop codon? Would the protein eventually stop? Would it keep coding into the poly-A chain and insert a bunch of phenylalanine?

No, this will not happen. mRNAs are inspected in the nucleus before they are exported into the cytoplasm (at least in eukaryotes), where transcription and translation don't happen at the same place. This ensures that no mRNAs without stop codons or premature stop codons are exported. This phenomenon is called
"mRNA surveillance". mRNAs that do not pass this quality check, are degraded. See the Wiki reference for some basic information and the references below for more.
References:

Process or perish: quality control in mRNA biogenesis.
The exosome and RNA quality control in the nucleus
A faux 3′-UTR promotes aberrant termination and triggers
nonsense-mediated mRNA decay

you can add a note on non-stop mediated decay mechanism

@WYSIWYG You mean how the RNA is removed? I can do that later.

Technically, NMD takes place in the eukaryotic cytoplasm, because that is where the ribosomes are translating mRNAs containing "early" termination codons.  The situation the OP describes, where the wild-type stop codon is mutated to a codon recognized by a charged tRNA will just result in a slightly longer protein with an extra tag on the C-terminus.  A normal 3'-UTR will contain additional stop codons in all frames--on a random basis. This (the extra a.a., residues) also occurs in cells expressing a suppressor tRNA, the activated a.a. will get inserted instead, and the protein will be longer.

@mdperry I am not talking about NMD (nonsense mediated decay). There is another mechanism called nonstop decay. Yes I agree that the protein will be longer in that case. This is detected and the faulty products are cleared off.

Downvote. It obviously does happen, see the answer below.

Yes you are correct. These mRNAs, that lack stop codon will cause translation to continue into the poly-A tail (it will result in addition of lysines not phenylalanine). Since no stop codon is present, the ribosome remains attached to the mRNA. Under these circumstances, a pathway known as non-stop decay is activated.
An important protein in this pathway — Ski7 detects a stalled ribosome and initiates the decay process for both the peptide and the mRNA. The poly-lysine tail of the peptide has been shown to fasten the peptide decay process.

In prokaryotes too, the non-stop mutations cause the ribosome to run through the stop codon and to eventually stall. However, there are no poly-A tails and ribsosome recovery pathway is different from that of eukaryotes. An RNA called tmRNA (a hybrid of tRNA and mRNA) binds to the the A-site using its tRNA-like domain. Then the translation proceeds through the mRNA domain of tmRNA (this is called trans-translation) which causes an addition of a peptide tag (that acts like a degradation signal) to the stalled polypeptide and finally leads to ribosome release when the stop codon is reached.

References:
Non-stop decay:
            Klauer and van Hoof. Degradation of mRNAs that lack a stop codon: A decade of nonstop progress. Wiley Interdiscip Rev RNA. 2012 Sep-Oct; 3(5): 649–660.
tmRNA:              Jannsen and Hayes. The tmRNA ribosome rescue system. Adv Protein Chem Struct Biol. 2012; 86: 151–191.

This is the best answer I think since some mRNA obviously escapes nuclear surveillance (or these pathways wouldn't exist) and the question specifically asks what happens during protein synthesis. Perhaps it's also worth mentioning tmRNA, since we eukaryotes aren't the only organisms out there (it's also an ingenious mechanism of simultaneously targeting the aberrant protein for degradation whilst rescuing the stalled ribosome).

@canadianer thanks for pointing that out. Added :)

In fact, it is rare that stop codon mutation causes translation of polyA sequence in mammalian cells because you will find another in-frame stop codon downstream. And some stop codon mutations still producing the protein stably(1).
However, as WYSIWYG mentions, in the absence of alternative in-frame stop codon, mRNAs would be degraded. It is also called none-stop decay(2). I am not sure that this phrase gets popularity though.


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Is lumosity.com based on science?
I always see these Lumosity ads on TV, and I personally feel they are just trying to "sell me something". I did some layman's research (wikipedia) and read that "Studies of Lumosity's effectiveness have shown mixed results".
Does anyone with knowledge on the topic of learning know if the "brain games" they post are simply games? I guess the proper question would be:
Can games like the ones Lumosity offers increase cognitive ability?

This question on Cognitive Science SE has a couple good answers about this topic: http://cogsci.stackexchange.com/questions/1705/how-valid-is-lumositys-brain-performance-index-and-what-normative-information-i

Most advertisements are trying to "sell you something", namely, the product being advertised.

I'm voting to close this question as off-topic because the purpose of SE Biology is not to make judgement on television programmes or advertisments. This is not therefore a question about biology that allows an objective answer.

Zickefoose et al. did a study, and showed that while you might improve while playing the game, it called into question if you actually improved outside of just getting better at the game.
Redick et al. also reported that when they did a double blind study in brain games like Luminosity that you improved in the games, but they didn't see any transfer from game to every-day life.
Also see my previous answer on the topic: Cognitive Science Forum

I figured as much, although only based on personal opinion more than actual data. Thanks

wow, that's even harsher than I was expecting :O (expected it to at least have some effect, though less than most other/better forms of studying/training/etc.)

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System biology and evolution: Book-recommendations
I have relatively good knowledge in evolutionary biology and in population genetics. I am getting more and more interested in the evolution of ...

genetic developmental processes
gene interactions
gene expression
plasticity
intrinsic or cellular noise
mutational robustness

It seems that i am getting increasingly interested in a field that is in between population genetics and system biology. I know very little about system biology.
Can you please give me some recommendations for books (and other readings such as reviews) that talk about the evolution of those processes that are usually studied by system biologists? I am much more interested in a book that presents concepts and methods than a book listing empirical observations. Also, I am not interested in medicine but in biology.

Systems Biology seems so new that I would expect that most books on that topic would probably be collections of articles from symposia. Given your detailed list the first author that springs to mind is Stuart A. Kaufmann (there might be another 'f' in his name).  I recently saw someone here cite his 1993 book 'On the Origins of Order' he is a real theoretical biologist, like Francis Crick. He was affiliated with bothe the Penn Medical School and the Santa Fe Institute think tank.

I am afraid there is no single book that will cover these topics. The Introduction to Systems Biology by Uri Alon does not talk much about evolution of gene networks; it is mostly about network motifs and their dynamic behaviour. You can have a look at Barabasi's works for evolution of gene regulatory networks (This book-chapter is not really about GRN but may be useful as it talks about fitness of network nodes).

@mdperry I cited that book recently. (There is an extra 'f' and one less 'n' ;P ). It is good, though I haven't proceeded beyond fist few chapters.

I haven't read it, but this book looks interesting to me: Evolutionary Systems Biology

@falsum yes it looks like a very good fit and it is very recent. The book is expensive though but I just discovered I have access to an online version through my University. Quite convenient. Thnks

Here there are a couple that I own:
The "classic" from Uri Alon touches many of the topics you mention. It is easy to read and goes relatively deep into the methods. There seems to be a new edition (if you search it in Amazon it will pop up), but it was planned for last year's April and then delayed so no so clear when will be actually published. For the original one: Amazon link
Title: An Introduction to Systems Biology: Design Principles of Biological Circuits
Year: 2006
Author: Uri Alon
Publisher: Chapman & Hall/CRC Mathematical and Computational Biology

The other book is this textbook "Systems biology" by  Edda Klipp and others. I attended a talk by Edda Klipp two years ago and she seems to be doing interesting things. This book is more general, covering, somewhat superficially, many topics. It can be good to get a general idea on the field. Amazon link.
Title: Systems Biology Paperback
Year: 2009
Author: Edda Klipp, Wolfram Liebermeister, Christoph Wierling, Axel Kowald, Hans Lehrach, Ralf Herwig
Publisher: Wiley-Blackwell

There are many others (see Amazon results here). Maybe other members can comment on some of the other titles.

Sounds like Alon's book would be a good fit. Thnks for this great recommendation. +1 I'll wait to see if I get other opinion and then I'll probably go for Alon's book.

Sure, wait for other opinion. There are many books and not sure I got the best ones! I would also like to know about other good books.


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If one endures the same form pain over a long period of time, would the pain begin to lose intensity?
Metaphorically thinking, if one endured the pain of constant burning for decades, would the pain slowly lose its strength?

It depends on the kind of pain. A literal hot thing being applied at 200F or more? A 120F thing hot enough to be uncomfortable but not enough to cause tissue damage? A chemical irritant?

@Resonating Craig is probably thinking of long-term pain, such as back pain from a slipped disk or an old injury.

Under the assumption that the temperature experienced is not high enough to simply burn the nerves responsible for the pain (which would lead to insensible regions), yes and it would due to what is called receptor desensitization. In the case of burning pain the receptor involved is called the transient-receptor potential channel V1 (TRPV1). It is the same receptor involve in the oral burning sensation of spiciness.
Now two scenarios are possible given your question, namely a constant stimulus over a long period and "oscillating" stimuli (i.e. a repetition of stimuli followed by non-stimulated periods).
Constant stimulus
I provided a similar answer to this question: What features cause mechano sensory adaptation?. This is the scenario where you keep the painful stimulus constant over a period of time. Here desensitization, i.e. reduction in pain feeling, is due to a direct receptor desensitization. This happens because the receptor is internalized (also called receptor-mediated endocytosis) into the cell after being activated and it takes some times for the receptor to reach the cell membrane again meaning if the stimulus remains constant, pretty much no receptors will be left on the cell membrane.  After decades long term desensitization will occur and is slightly different in it's mechanism compared to standard desensitization as described hereafter.
"Oscillating" stimuli
In the case you are talking about a chronic pain interrupted by periods of non stimulation then long term desensitization will occur. In this scenario, the concentration of receptors will be reduced semi-permanently (i.e. reduced expression of the receptor) in the receptor cells reducing the pain signal. This is what happens with spiciness sensation. People eating regularly very spicy will physiologically be less sensitive to spices as they have less receptors sensing the spices provoking a reduced burning sensation.

Just as a footnote, very long chronic pain will also change the brain wiring of the pain signal but as I don't know enough about neurobiology I will leave that appart.

@AliceD Nocireceptors are molecular receptors not neurons, at least when you talk to a molecular physiologist. Receptor internalization occurs and is the primary way cells become desensitized. I will add references when I have some time but for the time being I worked and published several papers linked to taste perception and receptor-based signaling.

I'm looking forward seeing these references. Interesting stuff. Ping me after edits and happy to remove the -1. I thought pain was mediated by nerve endings - https://en.wikipedia.org/wiki/Nociceptor

@AliceD This is perfectly true but the nerve ending have molecular receptors on them (for noxious heat pain, namely TPRV1), this is what I called a nocireceptor, I guess we have a scale issue :). I modified my answer to include the concept of Receptor-mediated endocytosis, i.e. internalization. By the way you should post an answer on the brain adaptation to pain as you know way more than I do on this subject.

Yes, you are right. Thanks for clarifying. I removed the -1 and after adding  a reference I'm happy to upvote.

Short answer
Chronic pain may be very persistent and even worsen over time, but it will depend on the underlying pathology. If the pathology disappears over time, so may the pain.
Background
There are roughly two kinds of pain:

Acute pain is pain that lasts for a short time and occurs following surgery or trauma or other condition. It acts as a warning to the body to seek help.
Chronic pain is pain that lasts beyond the time expected for healing healing following surgery or trauma or other condition. It can also exist without a clear reason at all.

A large body of basic research indicates that chronic pain is associated with neuroplastic changes in the nervous system at peripheral, spinal cord and brain levels. Thus chronic pain is shown to have a distinct pathology that often worsens over time, and constitutes a serious separate disease entity.
However, if the underlying pathology disappears, the pain may lessen. However, based on the cited paper, I do not think chronic pain gets less severe over time due to neural adaptation.
Excerpt from the linked article upon request:

These and other changes may contribute to the development of alterations in central [spinal] neuronal responsiveness, which share features of wind-up and long-term potentiation and are collectively known as “central sensitization.” [...] These alterations in cell responsiveness may be evidenced by a number of symptoms and signs, including spontaneous pain [...]. This [...] has been demonstrated in patients who have chronic pain associated with whiplash injury and fibromyalgia and suggests that the presence of pain [...] is associated with increased sensitivity of spinal neurons.

Reference
- Siddall & Cousins, Anesth Analg (2004); 99: 510-520.

Perhaps desensitization occurs, but at the perceptual level it may not be noticeable I guess.


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How is it possible for only one in five children to have brown eyes when their parents both have brown eyes?
I have observed that parents having brown eyes had three female offspring with blue eyes, one son with green eyes, while only the youngest daughter had brown eyes.
How can they produce so many blue-eyed offspring?

You directly observed it, why are you asking if it's possible? Also, you should rephrase your question to remove all personal aspects.

Eye colour is more complex than one colour being dominant over the other. At least 10 genes and the relationship between those genes account for many factors including hue and saturation.

I would recommend to "father" to perform genetic testings in question does he related to these children at all.

""My mother," answered Telemakhos, "tells me I am son to Odysseus, but it is a wise child that knows his own father." - Homer, ca 1000 BCE.

My father's father had blue eyes.  My mother has blue-green eyes.  Between the two of them they produced four brown-eyed daughters, all with strong family resemblances.  Probability is only meaningful with a much larger sample set.

Possible...yes of course! The answer could stop there but I guess you want to ask how likely it is.
Here is a chart of probability of a given kid to have eyes of a certain color given the parents eyes color. (Note that the second column contain probabilites and not odds contrary to what the figure is stating).

The probability that $k$ kids out of $n$ have eyes of a color which appears with probability $p$ is given by the probability mass function of the binomial distribution $\binom{n}{k} p^k (1-p)^{n-k}$
Knowing that both parents have brown eyes (even for your oldest sister):

The probability that exactly one out of 5 offsprings have brown eyes (and the others have eyes of another color) is about 0.015 (3 out of 200).
The probability that exactly 3 offsprings have blue eyes (and the others have eyes of another color) is about 0.0021 (2 out of 1000)

You might want to calculate the probability of having $k$ or more kids that have eyes of a given color (a p.value) is obtained by summing probabilities. For example, the probability that 3 or more kids (out of 5) have blue eyes is  $\binom{5}{3} 0.0625^3 (1-0.0625)^{5-3} + \binom{5}{4} 0.0625^4 (1-0.0625)^{5-4} + \binom{5}{5}  0.0625^5  (1-0.0625)^{5-5} ≈ 0.0022$
Learn more about Stats
You'll probably want to learn a bit about statistics if some things are unclear. You might want to make sure you understand the concept of p.value and its interest and make sure you understand what a binomial distribution is. You may also want to understand the concept of multiple testing to avoid falling in simple pitfalls.

Where is that image from?

Hum... I quickly took something from google image. I already saw this kind of image several time and assumed it was trustful. Does it seems wrong to you? There are several images of the kind all showing more or less the same probabilities

@Remi.b Although I agree that they are important concepts I fail to see what does p.value and multiple testing have to do with your answer? As far as I know you are not performing null distribution hypothesis testing, just computing probabilities. (I see the relation for the binomial distribution though).

@Remi.b I'm not saying it's wrong, l just think you should cite your source both for fairness and so people (such as myself) can read more about how the probabilities were derived.

@canadianer ou are right. I'll add a reference if I can find one.

@ddiez multiple testing: Because one can calculate p.value about anything and will be very shocked as soon as (s)he find something that is unlikely to happen. Typically if the OP starts calculating the probability to have 3 or more kids with blue eyes and the probability to have 1 or less kids with brown eyes or the probability etc... p.value: I disagree. I calculated a p.value. I performed a binomial test (exact test) and got a p.value by calculating the probability of something or anything judged more extreme to happen.

@Remi.b p.value is not the same as probability (https://en.wikipedia.org/wiki/P-value). Well, it is a probability but the p.value is defined in the context of hypothesis testing where you test whether you reject or not the null hypothesis. The p.value defines the probability of being wrong when rejecting the null. In that context multiple testing is necessary when performing more than one test.

A p.value is the probability of a given event or any event more extreme to happen given that Ho is true. This is what I calculated. A binomial test is a statistical test (based on hypothesis testing just like any statistical test) and what I calculated is indeed a p.value. Just pick a significance level (0.05 for example) to make your test. If the OP calculate those pvalues for the number of eyes of any color in each family, (s)he will be performing 3 tests (as there are 3 possible colors) and therefore there is an issue of multiple testing. Btw, awesome website @ddiez!

I do not think we agree here :-) Maybe we should discuss this in more length in chat, but I have limited time to visit the site unfortunately! At any rate, your recommendation in the answer is an important one and so from that point of view I have no complaints.

Flashbacks to maths with the binomial expansion... :P

After thinking about it for a while I have arrived to a slightly but important different view on this problem. I will try to explain the statistics behind it to the best of my knowledge. I will use the eyes’ color probabilities in @Remi.b’s response, but of course those may not be accurate and the results can change accordingly.
The problem is to determine how likely is to have 3 children with blue eyes, 1 with green eyes and 1 with brown eyes when the parents both have brown eyes. I will assume each child is independently born (e.g. there are not identical twins). We can use the analogy of a bag with balls from which we draw 5 balls independently.
Imagine you have several bags with $n=100$ balls each. The balls can be brown (M), blue (B) and green (G). Depending on the bag, you will have different proportion of balls. For example, in the bag labelled MM (for brown:brown), there are 75 M balls, 19 G balls and 6 B balls (rounding the probabilities in @Remi.b's answer). The bag labelled GB does not have any M balls (0), and has 50 G and 50 B balls. And so on. This gives us for each bag the probabilities defined in @Remi.b’s response.
Although there are many bags in our particular case we only care about the MM bag, so we should only consider those probabilities. Imagine now you pick five balls at random from this (the MM) bag. What is the probability that you will get $m=1$, $g=3$ and $b=1$ (with m, g and b representing the number of M, G and B balls respectively)? Because there are three types of balls (or categories) this is described by the multinomial distribution (and not the binomial, which describes events involving two categories, like the flip of a coin). The multinomial probability mass function is defined in this problem as:
$$ Pr(M=m,G=g,B=b) = \frac{n!}{m!g!b!} p_M^{m} p_G^{g} p_B^b
$$
Where $P_i$ are the probabilities described above, n is the total number of childs, and m, g, and b are the number of childs with M, G and B eye color respectively. Therefore, for our family we have the following computation:
$$
Pr(M=1,G=1,B=3) = \frac{5!}{1!1!3!}(0.75)^1(0.1875)^1(0.0625)^3 = 0.000686643
$$
The probability (~0.07%) looks very low, but it is basically about 7 out of 10,000 families with parents having both brown eyes and 5 children. Given the large human population it is difficult but not impossible.
Personally, I knew a family where the parents had both brown eyes and the two children had blue eyes. Always wondered about it but this is the first time I actually tried to think about the probabilities! In this case the probability would be 0.00390625 (~0.4%).
BTW, you can easily compute the same in R with the following code:
> dmultinom(c(1,1,3), 5, c(.75, .1875, .0625))
[1] 0.0006866455
> dmultinom(c(0,0,2), 2, c(.75, .1875, .0625))
[1] 0.00390625


text:
Can kit foxes and red foxes produce offspring?
Can a kit fox (Vulpes macrotis) and a red fox (Vulpes vulpes) together produce offspring?
Would such a hybrid be fertile?

Red foxes will kill kit foxes in the wild, so presumably this would be a pretty big barrier to producing offspring.

I realize that it does not occur in the wild, but I was interested in whether they were genetically compatible enough.

Yes, a red fox and a kit fox could produce hybrid offspring, but it would be sterile.
Sterile red fox / arctic fox (V. lagopus) hybrids have been bred for the fur trade for decades (source).
Arctic foxes are quite closely related to kit foxes, and both species are equally distantly related to red foxes, so since one can produce hybrids then the other should be able to as well. Here's a screenshot from onezoom.org showing their relation. (Arctic fox = Vulpes lagopus)

Red fox / kit fox hybrids have not been observed in the wild, and kit foxes are not widely kept in captivity except in zoos, so I am not aware of any record of such hybrids. It would likely take intentional effort on the part of a fox breeder to produce them.


text:
Immortality Gene? Really?
I read somewhere in the internet and wondered if human genes have deactivated immortality genes locked somewhere in the DNA strand. Is this statement true? What does it mean for human lifespan?

"I read somewhere in the internet" -- please link to the specific claim, because this clearly doesn't have a shred of truth to it.  It will help those answering explain why it's not true.

The original article i was referring is unavailable but here is one claim.It could be a conspiracy theory, but one could never be sure with genetic engineering. http://www.livescience.com/6967-hang-25-year-wait-immortality.html

Honestly, I understand you are asking this question in earnest, but everything in that interview screams that that person is a crackpot.  Ten years into his research and I've never heard anything, so he's behind schedule!

I remember De Grey, he gave a TED talk 10 years ago http://www.ted.com/talks/aubrey_de_grey_says_we_can_avoid_aging?language=en. I don't recall him talking about specifically a gene for immortality but I guess this is the telomerase gene and in this case well it's very simplistic to say it's locked somewhere... If I remember well overexpressing this gene allowed to reconstruct the chromosome telomeres and a study in mice showed they would live longer. The problem is that telomerase only will not make any organisms immortal...

I looked up the subject of the interview you linked at livescience.com on PubMed, and looked back to about 2010 before giving up. There are 121 citations in that search, and nearly all of them are in Rejuvenation Research, a journal that he just happens to be the editor of. All of the references I looked up were quite obviously editorials, so it looks like this guy is just playing at being a scientist. Maybe he's good at synthesizing current research, but he sure isn't contributing anything original.

-1: You should add more information. At this moment it is difficult to predict what internet source you are talking about and therefore its authenticity cannot be verified. In general you should put in some effort before asking a question.

In tissue culture and cell engineering fields, the word "immortal" is often used to express something else instead of human or animal life spun. When you take cells from human tissues and grow them in test tubes--although flasks or dishes are used in reality--, cells stop growing after long term culture. They say it is cellular senescence. Several genes actually regulate this cellular senescence, and inactivation of these genes causes infinite cell proliferation. This is immortalization of cells. Then, cells in a human bodies are immortalized, do they get immortal? Probably, not. Cellular senescence partially explains senescence of bodies, but these two are different things. In human bodies, cellular immortalizaion occasionally occur. It is tumor pathologically.

I think you read about the telomerase: https://en.wikipedia.org/wiki/Telomerase
The chromosomes while duplicating, they loose some of the DNA segments from their ends, from the telomer. This is believed to have a direct effect on senescence.
The telomerase reproduces the end DNA strip of the chromosomes. This enzyme is found in active form in stem cells and in white blood cells.
The DNA sequence coding this enzyme is found in every cell, but in an inactivated form. Probably the article you are referring to, was talking about the telomerase, because it can be activated in almost every cell in our body. But this can lead to uncontrolled growth of the cells, and when this happens we talk about cancer.
More information at: https://en.wikipedia.org/wiki/Telomere#Structure.2C_function_and_evolutionary_biology

The article probably had a scrap of truth to it. Ageing is not plastic and longevity can be altered in a variety of ways. Although caloric restriction seems to affect longevity the most, there are also longevity genes from a range of cellular processes that have been identified in yeast and mice, indicating that ageing is a whole system process. But none of those genes are "immortality genes". Finding and testing their effects in humans is difficult.
Here is a video on the background on ageing.
Related answer that you might find interesting.


text:
How does the structure of the pancreatic acinar cell relates to its function?
So the pancreatic acinar cell synthesizes, stores and secretes digestive enzyme precursors called zymogens e.g. pepsinogen.
The structure of the acinar cell shows that there is an apical and basal side. The basal half of the cell is almost entirely filled with rough endoplasmic reticulum which can be shown with pyronin stain showing up pink due to the rRNA of ribosomes. The nucleus is also on the basal side which explains why rER is there too, since the nuclear envelop is connected with the ER membrane. Zymogen granules are on the apical region. Any thoughts as to why there is this polarity in cell?

The secretion pushes the cell organelles to the basal part.
(although the fat cells have no polarity, their organelles have been pushed to one side of the cell:

Comparing to adipose cells, the acinar cells secrete their specific proteins on one specific end of the cell, this is why in contrast with fat cells they have well defined polarity.


text:
Why is the administration of exogenous Anti-D not harmful to the foetus?
Haemolytic disease of the newborn can result from Rhesus incompatibility in utero.  In this disease an Rh- mother becomes exposed to the antigens of an Rh+ foetus by fetomaternal haemorrhage causing her to mount an immune response against the D antigen.  In her second pregnancy, repeat exposure to the D antigen activates memory cells causing a large production of IgG Anti-D antibodies that cross the placenta adhering to foetal red blood cells, which are then destroyed.
To prevent this, Rh- mothers are normally given exogenous Anti-D at 28 and 34 weeks gestation or after any sensitising event.  The aim of this treatment as I understand it is to 'mop up' any D antigen in the maternal bloodstream, covering it in exogenous antigen so the mother's immune system does not mount its own response.
I had previously assumed that these exogenous antibodies would be IgM to avoid them crossing the placenta, however looking at the summaries of product characteristics for some of the common preparations I see that "at least 95%" of protein content other than albumin is IgG.  I then wondered if the exogenous antibodies had a much reduced half life, however the half life is "about 3-4 weeks."
Why does the exogenous IgG not cause haemolytic disease of the newborn in the exact same way that endogenous IgG would in a previously exposed woman who had not had prophylaxis?  Is it dose-dependent or am I missing something entirely?

I've had a difficult time getting anything definitive to support my answer to your specific question of safety, however, I thought I'd go out on a limb and give you my understanding. A recent review of what is known about this can be found at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2809506/
I think you are on the right track with your 'dose-dependence' hypothesis. This is exactly what the makers of RhoGAM suggest, saying that the amount of antibody administered at 28 weeks into the pregnancy is sufficient to block any Rh antigen on Red Blood Cells that escape into the mother's blood, but insufficient to cross the placenta and be a problem. At this time the child will be large enough that any RhoGAM that does cross the placenta will not kill enough Red Blood Cells to harm the child.
Mom gets another dose of antibody after the delivery in order to ensure thorough coverage of antigen that results from mixing of blood at that time, however this dose is not a problem as the baby has already left the mother.
By the way, the rationale for the antenatal dose is that post-partum administration alone failed to prevent sero-conversion in almost 2% of Rh- women, putatively due to transplacental hemorrhaging.

That's an excellent article, thank you.  I had wondered if they used primarily IgG2 to reduce placental transmission but this is not the case (the article indicating IgG1 and IgG3).  If a 125 unit dose can neutralise only 1.25 ml of D+ve blood and not all of it crosses the placenta then this is likely to be an insignificant dose to cause harm.  I assume this could cause harm with a greater number of repeated doses after sensitising events but I think this is sufficient evidence to say that it is indeed a dose dependent phenomenon.  Thanks!

I think this just isn't really the kind of thing that can be explored in a dose escalation trial (at least not in humans) and it would be meaningless to try to extrapolate from any other species.

From the most up-to-date article I can find on the D-GAM treatment, IgG1 is primarily used, followed by IgG2. To be precise:
64.3% IgG1, 29.0% IgG2, 6.2% IgG3, 0.5% IgG4

Another treatment for this is Rhophylac. In this case, we have: 84.1% IgG1, 7.6% IgG2, 9.1% IgG3, 1.0% IgG4

Where you say "insufficient to cross the placenta and be a problem" - the review paper you link to actually makes this clearer. It explains that some of it can cross the placenta, but not enough to endanger the newborn.

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


text:
Why do some bad traits evolve, and good ones don't?
If a trait would be advantageous to an organism then why hasn't it evolved yet?
Conversely, if a trait is not advantageous or mildly disadvantageous, why does it exist?
In other words why does evolution not make the organism more "perfect"?

This is a general question that would be applicable for any kind of trait. Please keep the answers precise and scientific.
Read this meta post for more information: Questions asking for evolutionary reasons

A classical article on the subject: The spandrels of san marco and the panglossian paradigm

Technically, i found that to be a very muddled, vague question, 1/ with no examples to illustrate an example trait. 2/ deducting that evolution follows a retrograde course by encourageing negative traits. 3/ why is it making an animal NOT more perfect... is too vague a concept to talk about and it caps off the previous vague statements with a nonsensical culmination which would have greatly benifited from trait examples, more perfect/less perfect examples, and statements which generalize trait selection which is not generally true.

there are no bad traits that are not related to another good one. please give some examples.

The answers to this question are very good and I think it useful as a portmanteau reference for closing questions related to it. But I have always been put off by the title. Most questions are from people playing God, asking why such and such a thing they think advantageous has not evolved. The evolution of bad traits (sickle cell anaemia etc.) is a quite separate question that can have a much clearer and more objective answer. Could we do something about this?

During the process of selection, individuals having disadvantageous traits are weeded out. If the selection pressure isn't strong enough then mildly disadvantageous traits will continue to persist in the population.
So the reasons for why a trait is not evolved even though it may be advantageous to the organism, are:

There is no strong pressure against the individuals not having that trait. In other words lack of the trait is not strongly disadvantageous.
The trait might have a tradeoff which essentially makes no change to the overall fitness.
Not enough time has elapsed for an advantageous mutation to get fixed. This doesn't mean that the mutation had not happened yet. It means that the situation that rendered the mutation advantageous had arisen quite recently. Consider the example of a mutation that confers resistance against a disease. The mutation wouldn't be advantageous if there was no disease. When a population encounters the disease for the first time, then the mutation would gain advantage but it will take some time to establish itself in the population.
The rate for that specific mutation is low and therefore it has not yet happened. Mutation rates are not uniform across the genome and certain regions acquire mutations faster than the others. Irrespective of that, if the overall mutation rate is low then it would take a lot of time for a mutation to arise and until then its effects cannot be seen.
The specific trait is too genetically distant: it cannot be the result of a mutation in a single generation. It might, conceivably, develop after successive generations, each mutating farther, but if the intervening mutations are at too much of a disadvantage, they will not survive to reproduce and allow a new generation to mutate further away from the original population.
The disadvantage from not having the trait normally arises only after the reproductive stage of the individual's lifecycle is mostly over.  This is a special case of "no strong pressure", because evolution selects genes, not the organism. In other words the beneficial mutation does not alter the reproductive fitness.
Koinophillia resulted in the trait being unattractive to females. Since most mutations are detrimental females don't want to mate with anyone with an obvious mutation, since there is a high chance it will be harmful to their child.  Thus females instinctually find any obvious physical difference unattractive, even if it would have been beneficial.  This tends to limit the rate or ability for physical differences to appear in a large & stable mating community.

Evolution is not a directed process and it does not actively try to look for an optimum. The fitness of an individual does not have any meaning in the absence of the selection pressure.

If you have a relevant addition then please feel free to edit this answer.

Here it is implyed that NOT having the trait is a drawback ie that there is a selection pressure against not having the trait.
So I think the true answer is that keeping diversity or even traits that are drawbacks is an advantage : if there is a pandemy of malaria, having drepanocytose will be an advantage. Moreover having the whole population stuck in the same local fitness maxima is not good for exploration of potential greater maxima

@agemO It is implied here that there is no strong selection pressure against not having a trait. Therefore the trait does not establish itself. The case of malarial resistance that you mention would be an example of tradeoff: sickle cell disease being a tradeoff for malarial resistance.

Ok I think I underestimated the "strong" part in what you wrote.
For the tradeoff part, I think even without an already existing tradeoff, keeping diversity is usefull for parameters exploration or to adapt to a future environemental change

I think it's important to point out that in order for many useful adaptations to evolve, they need to start evolving in a way that is either not important to the species survival or differently important to it's survival.  This relates to the 'genetic distance' you mentioned.  For example, it's not like one animal sprouted some wings and then because it could fly, had lots of offspring.  Evolution of low-impact features is not a strange phenomenon but rather it is a crucial part the process.

How beneficial a trait is is also strongly affected by its environment and environments change constantly. Since it has no foresight natural selection is always playing catch up with the environment.

There's always the most obvious: Evolution is chance.
Some traits allow an individual to have a higher chance to produce offspring. That doesn't mean individuals with that trait have more offspring, not even on average unless the law of large numbers applies. A randomly mutated perfect squirrel could appear, and since it's only one, it gets run over by a car before it can reproduce and all perfect traits are lost.
Then there is a chance that a trait is beneficial for the individual, but doesn't have a significant effect on its chance of having offspring. For example, take human eyesight. People with really poor eyesight have a disadvantage. But most people have good enough eyesight until they are too old to have kids, so it doesn't matter to evolution if they fall off a cliff afterwards. It may even be advantageous if kids don't have to spend resources to care for their parents.
And a very nice effect is a swarm effect where you look at entire swarms, for example of fish. Take a swarm or community that reproduces primarily within itself, where for some reason only traits that are beneficial for the individual can get inherited. As soon as the swarm gets into competition with a superior swarm - where traits that benefited the swarm got inherited - the entirety of the former swarm may die.
There's also the effect of society. If during one decade a society thinks people with green hair are not attractive partners - even though it's better for camouflage - it sucks to have green hair during that decade. This doesn't only apply to humans. I remember reading that among some bird species the singing evolves and which songs are "hip"/attractive depends on social factors as well as genes. Just imagine what would have happened if a small number of humans would have started to grow bat wings that made them fully capable of flight, during the time of the Spanish Inquisition - rather than spreading the new gene they would have burned on a stake.
Let's not forget about the really cool effect of frequency dependent selection where a trait is only beneficial if not too many other individuals have it. These traits can be beneficial for an individual, or a species, or both, but only if not too many individuals carry the trait. A community of humans can benefit from super smart people who have limited control of their bodies and emotions, but if all humans in the community are like that the community has a problem.
Last but not least, there's the change in external conditions. If conditions change, many species will simply go extinct (e.g. Ice Age). Imagine all viruses disappear. If there are no viruses, a trait that makes the immune system more efficient against bacteria and cancer at the expense of having no defense against viruses, is clearly a beneficial trade. Then viruses come back and every species that adapted the "no defense against viruses" trait goes extinct from a viral infection. This can make it beneficial to not adapt new traits too quickly.
In summary: By accepting that evolution is a random process where individuals with more advantageous traits are simply somewhat more likely to have more offspring, and where entire communities or subspecies are slightly more likely to go extinct if the traits are less beneficial for the community, you get all of the above effects and many more. Keep in mind that individuals with advantageous traits are in no way guaranteed to have more offspring, and communities can be wiped out or flourish due to all kinds of incidents that completely ignore how advantageous or disadvantageous their traits are.

I didn't expect that analogy.

@armani Nobody expects the Spanish Inquisition!

"There's always the most obvious: Evolution is chance."
Not necessarily so.
Predictable Evolution Trumps Randomness of Mutations
http://www.scientificamerican.com/article/predictable-evolution-trumps-randomness-of-mutations/

@MakotoKato Evolution is a (flawed) optimization algorithm based on chance. Es an effect, in some cases the predictability of some changes happening can be very high, especially with bacteria in a controlled environment, where you have a massive number of individuals combined with a massive number of generations. It's why we can predict more bacteria will become resistant to more antibiotics over time.

Because evolution is an effect, not a cause.  That is, there's no "God of Evolution" out there deciding that this or that trait would be beneficial to a species, and deciding to add it.  Evolution just works* on whatever random variations happen to come along.
*And as others have pointed out, it works statistically, not deterministically.

@WYSIWYG: I think this post does add something that has been missed, which is a succinct reason why traits aren't evolved on demand.  The other answers, while correct, are long-winded enough to IMHO lose some people.

I actually like this answer. This kind of question makes the most sense in a mental model which silently assumes intelligent design of organisms, even if the asker believes in evolution and is unaware of the inconsistency of his knowledge structure. All the other answers explain the points in which evolution behaves unlike intelligent design, but this one also notes which core assumption is responsible for the misunderstanding.

Below are the reasons I can think of. The list is not exhaustive and there are some conceptual overlaps.

The trait seems advantageous but it is not, maybe due to its effect on another component of fitness (trade-off). It sounds to me to be the most likely explanation whenever you are wondering why a given species does not carry a given trait. In other words, the fitness landscape matter.
The trait is not that easy to build it requires a series of mutations that are either neutral, quasi-neutral or deleterious.
The mutation just hasn't happened yet (lag load).
the mutant variant had appeared several times but got extinct because of genetic drift even though it was beneficial (assuming no fitness valley to cross).
Putting the two previous points together, if only one mutation (one SNP) is needed to build this trait and if the trait is beneficial but quasi-neutral, then the expected time before fixation to occur is around $10^9$ generations. Here is why. Let $N$ be the population size and $\mu$ be the mutation rate. In a diploid population (but the end result is the same for the haploids), there are $2n\mu$ appearing at this locus each generation. As the mutation is quasi-neutral, its probability of fixation (calculated from Wright-Fisher equations or Moran birth-death process, or from Kimura's diffusion equation) is $\frac{1}{2}N$. Therefore the rate at which fixation occur is $2N\mu \frac{1}{2N} = \mu$. $\mu$ for an SNP in a species that has a large genome is around  $10^{-9}$. The probability that fixation occurs in $t$ generations is given by the exponential distribution with parameter $\mu$ ad the expected value of this exponential distribution is $\frac{1}{10^{-9}} = 10^9$ generations. If there is one generation per year, that takes a lot of time! Of course, those calculations are a good approximation when the trait of interest is quasi-neutral. If the positive selection is very very strong on this trait to the point that we can completely neglect drift, then the expected time for the mutant to occur is $\frac{1}{2N\mu}$, which is $10^5$ for a population size of $N = 10000$ which is still quite a lot. In the meantime, the environment or the genetic background may change so that the trait is not advantageous anymore. The above calculations assumed that the trait appeared with only one mutation and that only one SNP can cause the trait to exist. One can be more general by summing exponential distribution (for multiple mutation scenarios) and increasing the mutation rate (for mutations at different loci can make the trait exist).
the mutant variant had appeared several times but got extinct because of drift because the Ne in the genomic region is very low due to the act that there are many loci under selection in the surroundings (background selection).
the trait is beneficial and occur sometime but either stay at low frequency or even regularly disappear due to a migration of individuals coming from an environment where this trait is strongly deleterious (dispersal load).
Be careful to understand what evolution does and therefore to understand what advantageous mean. Taking kin selection/group selection/lineage selection apart to make things easier, an advantageous allele is the one who increases the fitness of its carrier. The effect of a given allele depends on the environment and on the genetic background in which it exists. A beneficial allele does not necessarily increase survival or increase the probability of the population to not get extinct. Think about sexual selection typically.

Evolution occurs by a change in gene frequencies, with gene frequencies potentially affected by four mechanisms (mutation, migration, drift, and selection).

The answer to the question Why does the seemingly advantageous trait X not evolve? could be:

The mutations for a trait have never occurred within a population, or such genes have never migrated into the population
The mutation(s) to cause such a trait may have once been present in a population but migration and/or drift and/or selection has since removed them from the population
Selection has removed the mutations causing the seemingly advantageous trait because the same (or tightly linked) genes have other deleterious effects by pleiotropy

Similarly, the answer to the question Why does the seemingly disadvantageous trait X evolve? could be any of the following:

Alternative genes have never been introduced to the population by mutation or migration
Mutation, drift, and migration have allowed the gene to fix over other more advantageous genes
Selection has spread the mutations causing the seemingly disadvantageous trait because the same (or tightly linked) genes have other beneficial effects by pleiotropy

Note also that the trait may seem (dis)advantageous in the current adaptive landscape, but selection exhibits temporal variation
Read here on why and how genetic variation is required for evolution/adaptation to occur
Read here for more about the process of adaptation
Read here for more on genetic variation
Read here for more on rapid evolution
Read here for more on the relationship between multivariate selection and adaptation
A detrimental phenotypic character may have no genetic variance, so it may be impossible for selection to stop such occurring; many diseases have considerable environmental inducers (e.g. selection can't work against emphysema developed as a result of smoking, but it can work against genes that increase the tendency of developing emphysema).

All the previous answers are very good. However, I feel a point was missed (or maybe I didn't read deeply enough).
I will highlight the concept of fitness landscapes. This is how it looks:

The peaks represent the fitness of the species for a particular allele frequency. In the multipeak scenario, there are valleys which represent, obviously, reduced fitness. The concept of evolution being a chance event translates to "local peaks are favored over the global peak". As a result, a species may reach a high fitness level even though a higher peak exists (assume the highest peak is the perfect organism you speak of). Once it has climbed a peak, to change to the other peak it has to go through a valley i.e reduced fitness to improve. If nature was a benevolent entity then it could have been a grand transition. However, less fitness makes species susceptible to die off and hence they mostly don't make the transition making the perfect organism statistically less likely.
I also attach a link a .gif to show species heading to a certain peak. Notice the fact that no one likes to stay in the valley and rapidly swarms to the peak.

Richard Dawkins devoted an entire chapter of The Extended Phenotype to this question, Constraints on Perfection (the third chapter in the edition I have to hand); he listed six (not including those he critiqued as perhaps not being such strong constraints as others have suggested). The whole thing is worth a read, but for brevity, I'll state the six he had in mind here:

Time lags (a given adaptation may arrive in the future)
Historical constraints (the new system has to modify the old rather than starting from scratch)
Available genetic variation (for example, this may explain why many non-functional body parts shrink instead of disappearing)
Constraints of costs and materials (big brains, for example, are so expensive we're very unusual in having a net use for them)
Imperfections at one level due to selection at another level (Dawkins had previously spent a whole book, The Selfish Gene, arguing - among other things - that what's good for the gene may not be good for the individual)
Mistakes due to environmental unpredictability or 'malevolence' (an organism is built to be well-suited to average and dangerous conditions in their environment, and cannot quickly update its structure for every possible contingency)

Let's break this down to cover your two questions individually
Question 1 If a trait would be advantageous to an organism then why hasn't it evolved yet?
This one is really easy, natural selection, as well as other forms of selection, can only work with the variation that arises through mutation. Mutation is a random process evolution has no control about what variation will arise it can only select from those that do. Successful mutations tend to be small changes (small changes are less likely to disrupt a complex process like an organism) because of this organisms can get stuck with disadvantageous setups because evolution cannot go back to drawing board, it cannot go through a disadvantageous change to get an advantageous one.
My classic example is human back problems, a spine is a horrible thing to use to support weight upright but a spine was all evolution had to work with, it was the best option of what was available and being upright was a bigger advantage than the problems with a spine were a disadvantage. Designing a whole new system would be better but the chances of the hundreds of thousands of mutations need to "start over from scratch"  are so astronomically unlikely we will never see it. Evolution can only select for the best out of what is available and mutation can only make small changes to what is available.
Another example is the Laryngeal nerve in giraffes which is a 14ft nerve that literally only goes a few inches, but since the nerve evolved when a straight line from the brain to the tongue left the heart in front of it (fish), as terrestrial vertebrates developed necks and moved the heart into the chest the nerve is stuck running down around the heart before returning to the head, a ~14ft detour. having the nerve is a bigger advantage than the detour is a disadvantage, and a mutation redirecting the nerve would be a large complex mutation thus is unlikely to ever occur. A historical legacy like this is responsible for a lot of bad adaptations that stick around, changing them is just too difficult to happen by random mutation.
Question 2 Conversely, if a trait is not advantageous or mildly disadvantageous, why does it exist?
there are a few components to this no trait is advantageous in an of itself, it is advantageous in a particular organism and environment. Sharks beautifully adapted masters of the ocean, drop one in the Sahara and it is doomed. what is good in one environment is often a disadvantage in another. Combine this with the fact that organisms move(or spread) and the fact that environments change and it is easy to see how organisms can end with a mildly disadvantageous adaptation. Adaptations for hunting from the ice was an advantage for polar bears when ice was plentiful now that the ice is disappearing it is not so advantageous. but the ice is disappearing faster than evolution can change the polar bears.
Often the changes in environment are changes in the other organisms around them, being extremely fast is actually a horrible adaptation for gazelle in many ways, it makes them fragile, it makes them small and weaker than other ungulates, it spends calories to grow muscles that could be used to produce larger offspring or taller bodies, etc, but in an environment with cheetah not being fast is a worse disadvantage. In this way, evolution is often about taking the least bad out of a set of bad "choices". And of course, the faster the gazelle get the faster the cheetah get until they are too specialized to live any other way. This push to specialization is very common however specialized organisms are the least able to handle change, they are too specialized to do anything different. So if say a new predator shows up that can force fragile cheetah away from their kills (humans) the cheetah are screwed, they could suffer a huge die off (Africa) or go extinct (North America). Evolution cannot make you good in every direction, you cannot be both a good swimmer and a good climber and a good digger.
Another aspect is cost vs benefit, a trait does not occur in isolation, a body is a complex thing, the same mutation that makes some humans  resistant to cholera also makes them more susceptible to cystic fibrosis, this will be an net advantage when cholera is a big threat and a net disadvantage when cholera is rare. they key term here is net there is no condition when it is purely an advantage or disadvantage. Basically, all traits fall into this cost-benefit comparison. No trait is an advantage in every situation, every change has a cost, even if it is just calories that could be spent elsewhere.  We know of no traits that are purely a disadvantage that persists but there are many many (if not all of them) such tradeoff traits, a disadvantage for an advantage.
Another example is sexual selection, some traits help you to find or attract mates but are detrimental to your survival, but reproduction is a bigger advantage in evolution than survival. Evolution simply cannot favour genes if they never make it into the next generation consistently. So you end with peacock tails that get the males killed but are the only way to find mates. A male without the huge tail will not mate and the male offspring of a female without the desire for big tails will suffer the same problem (because the female keeps ending up with unattractive male offspring) so it is basically impossible for peacocks males to stop growing huge tails and it is unlikely peacock females will stop preferring bigger and bigger tails. Thus even though it is very detrimental to peacock survival the trait sticks around because it is an advantage in reproduction.


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Deciding a reasonable threshold for copy number variation in a CNV (SNP array) TCGA dataset
Is there a methodology to select a reasonable threshold for copy number variation in a CNV (SNP array) TCGA dataset, to define when there is a significative alteration?
Can I download CNV data for normal samples and take the 95th percentile of distribution? Are there better methods?
Update
This is the percentiles plot of the two distribution (Tumor vs Normal) of values, for the same technology (SNP array) and the same genome (hg19).
The tumor distribution has slightly more extreme values, though it is not enough in my opinion. For this reason I think I should not use a percentile score (the 5th and the 95th percentile of the normal samples distribution, for instance) to define the thresholds to call CNV alterations in the tumor samples.

Your suggested approach of comparing to the baseline distribution on a point-by-point basis isn't bad, although it's going to be susceptible to small false positives from noise. You'd probably want to only use events that span a certain minimum number of consecutive observations.
You might also want to look into circular binary segmentation, as described here: http://www.ncbi.nlm.nih.gov/pubmed/15475419.

I have updated my question, could you please give a look at it and let me know what do you think?

Hmm, okay, I think I see. No, you don't want to compare the intensity of the tumor at any one position against the 5-95% distribution of the normal across the whole array. You want to compare the intensity of the tumor at one position against the normal at that position. This will normalize for sequence-specific binding differences.

There are many methods for the analysis of CNV. If you are an R user I would recommend you to take a look at the Bioconductor package list, in particular the section for copy number variation. Currently it contains 50 packages!


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is left brachiochephalic vein and left pulmonary artery is same?
I am reading about ligamentum arteriosum which connects the left pulmonary artery and descending aorta. But I am seeing that if any figure shows left brachiochephalic vein it does not show left pulmonary artery (and vice versa). Are they both the same?

Veins are not the same as arteries. A non-capillary blood vessel is either one or the other, not both.

Please include references for those figures or add those figures to your question. Plus, as MattDMo said, veins cannot be simultaneously labelled as arteries. I guess the figures are intended to show veins and arteries separately (and not in the same picture). In any case that cannot be verified unless you show us the figures.

They are structurally and functionally distinct. The left brachiocephalic vein joins the superior vena cava which returns deoxygenated blood to the right side of the heart. Deoxygenated blood is pumped OUT of the right heart and travels to the left lung via the left pulmonary artery.
The two don't always appear in the same image because many anatomical images remove structures that aren't the area of focus for clarity. However a quick google image search reveals several pictures that illustrate the distinct positions of both.

No, they are not the same.  The left brachiocephalic vein receives de-oxygenated blood from the left subclavian vein (draining the left arm) and the left internal jugular vein (draining the brain and parts of the face).  The brachiocephalic vein then joins with the superior vena cava which flows into the right atrium.
The left pulmonary artery carries the deoxygenated blood that has just passed through the right atrium and ventricle, through the pulmonary trunk to the left lung for oxygenation.
In the foetal circulation, the ductus arteroisus (before it closes into the ligamentum arteriosum) allows blood to bypass the lungs, which are not oxygenated in the uterus!
Please see this diagram (which shows the foetal circulation including PDA for you).  The left brachiocephalic vein is circled in yellow, whilst the left pulmonary artery is circled in green.

Image from public domain edition of Gray's.


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Why is wind cold for humans?
Coming out of the pool the other day, I felt very cold because I was wet and the wind picked up. My idea is that a "cold" feeling should be associated with low temperatures, but it's indeed wrong.
Why do we perceive wind at a farely normal temperature as cold?

Evaporation of water..

So why would it be worse if I'm wet?

@SolarLunix I got what you mean, but still it is not clear how a bigger evaporated mass of water should cause my body temperature to fall or give me the perception of this happening

Is your question why does wind feel cold or why do we feel cold when we're wet?

I'm voting to close this question as off-topic because it is about physics

You don't just feel colder, you ARE colder, or at least your skin is.  It's not just a human thing: hygroscopes & wet bulb thermometers use the same phenomenon to measure humidity & dew point, evaporative coolers use it to cool homes, refrigerators & air conditioners use it with other refrigerants than water...

Whatever this question inclosed for, I just wish to raise attention that this should not be closed because it is physics. It is psychophysics and sensory systems deal with physical stimuli.

@AliceD: But it's not about sensory systems, really.  That is, the perception of cold is not some sort of illusion: the temperature receptors in the skin are accurately reporting a lower temperature due to increased evaporation.  A thermometer on the skin would report the same thing.

@jamesqf - exactly my point. That is why it should not be closed, as this question is exactly borderline Biology. If one asks what the wavelengths are recognized by the retinal photoreceptors, it is also not closed because it is physics.

@AliceD: True enough, and I wasn't suggesting it be closed.  It's just that there are really two separate questions implied here: 1) How do we sense temperature? and 2) Why does evaporation cause cooling?  Now if the OP wants to know the answer to #2, that's a physics question.  But if s/he's more interested in how temperature is perceived, that's a biology question.  (Just as explaining how photoreceptors work gets us into chemistry.)

the question is based on a false premise (that the air temperature alone determines the temperature experienced) see also: http://meta.biology.stackexchange.com/questions/3111/not-all-questions-featuring-something-biological-are-biology-questions?cb=1 your question could easily be reformated as "why does something cool down more quickly when wetted or blown on?" which is a physics question

One important point that you might not be considering is the heat of vaporization.
You may be aware that while it normally takes 4.18 J (1 calorie) of heat to raise 1 gram of water 1 °C, it takes around 2250 J of heat to raise 1 g of water from liquid at 99.5 °C to gas at 100.5 °C, due to the energy needed to go from a liquid to a gas. - What you may not know is that the enthalpy of vaporization isn't limited to vaporization at the boiling point. Any conversion of water to water vapor requires heat of vaporization, though exactly how much is temperature dependant.
So when water evaporates, it cools things much more than one might expect from the "average" energy (or even statistically above average energy) a water molecule may have in the liquid state - several hundred times more. All this is driven by the entropic benefits of having water molecules in the gaseous state rather than the liquid state.
Wind makes the process more efficient because it removes the water-vapor laden air, unbalancing the equilibrium of the process in favor of further evaporation. More water makes it more efficient (to a point), because there's more water to evaporate and the rate of evaporation increases, increasing the removal of heat.
This is not just a physiological perception effect - one can actually measure the temperature drop when water evaporates. Evaporative coolers make use of this effect, and traditional wet-bulb hygrometers (psychrometers) use exactly this effect to measure the humidity -- in some cases you can get a temperature differential of 20 °C or more between a dry bulb thermometer and a wet bulb thermometer.
There is a small perceptual effect in that the evaporative cooling is happening on your skin, where a large number of temperature receptors are located. Therefore, your skin (and temperature receptors) feel a cooling effect even if your core temperature doesn't change detectably. Local cooling produces a larger temperature change than might be expected if you calculated for a whole-body heat change.

This is what I wanted. Love it! Thank you very much!

"takes around 2250 J of heat to raise 1 g of water from liquid at 99.5 °C to gas at 100.5 °C" wow! very new to me.

This phenomena has nothing to do with any different kinds of receptors.
When we are wet, we have lots of water on our surface. The evaporation of water causes cooling.
Blowing wind tends to make evaporation faster. So, even if wind blows at normal temperature, we feel cold. If we are not wet, there is some water on our body surface. This water is low in quantity as compared  to when we are wet. So, we feel less cooling this time.
Also, water has high specific heat i.e. it doesen't change temperature very easily. So,even on a warm day, we don't feel the heat if we are soaked.

It is not clear to me as why water evaporation should cause cooling. Could you please explain this point more thoroughly? Thank you.

The surface molecules can escape out only if they have energy high enough. So, if they leave the surface, some energy is lost. this loss causes cooling.

Change in Energy = Change in Mass * Specific Heat * Change in Temperature. In this case, the energy is high in comparison to mass. So loss of 1 molecule can't compensate the loss of energy so there is slight change in temperature. Effective movement of lots of water molecules result in cooling

At normal conditions, there are equal no. of water molecules leaving and arriving at the surface. So, no change in temp. at normal conditions.

The equation that you cite is an experimental law valid in macroscopic systems which have fixed mass, mixing these results with microscopic analysis often leads to discrepancies. Of course one high energy molecule is lost, but it is also one that required more energy for its temperature to be maintained.

As other answers and comments have stated the reason that you feel cooler when the wind is blowing (wind chill factor often gets talked about on the news) is because evaporation is speed up by the wind. The reason that this evaporation causes cooling (explained in more detail here) is because when water evaporates, that water takes its energy with it. That energy loss to you is in the form of heat, thus making you feel colder.
However, there is a little bit more to it than that. If you look on How stuff works - windchill factor they go onto to talk about how the process of convection is what makes you feel cooler. What's happening is you're actually warming the air around your body up, and as the wind blows it's wisking that nice warm air away from your body replacing it with much colder air. The faster the wind blows, the faster your warm air is taken away from your body. When the wind blows fast the molecules around you move away from you faster so you have less time to heat them.
How Stuff Works says this about convection:

Convection - Convection is a property of liquids and gases. It occurs
  because when a liquid or gas gets hot, it tends to rise above the rest
  of the body of liquid or gas. So, if you have a hot bowl of soup on
  the table, it heats a layer of air surrounding the bowl. That layer
  then rises because it is hotter than the surrounding air. Cold air
  fills in the space left by the rising hot air. This new cold air then
  heats up and rises, and the cycle repeats. It is possible to speed up
  convection -- that is why you blow on hot soup to cool it down. If it
  weren't for convection your soup would stay hot a lot longer, because
  it turns out that air is a pretty poor heat conductor.

So while evaporation plays a minor roll, it's most likely because you're no longer able to heat up the air around you as efficiently when the wind blows all that nice warm air away.

The distribution of the speed of the molecules is Maxwellian, and the variance should not be very significant, meaning that the molecule speed should not vary consistently from the average speed. At least, not enough to modify the average temperature by many degrees. Am I wrong?

The thing is that it won't modify the average temperature very significantly, but it will make it feel slightly colder. It's really about perception. We may not see a significant change in actual temperature, but we can feel the small difference. (Like some of us are freezing at 71F but feel perfect at 72F - that one degree F difference (which is only a fraction of a degree C) makes a huge difference in how we feel). @bharb

I wouldn't call the sensation of being hit by a strong wind a feeling of slight change in temperature. It can be quite drastic, depending on the speed of the wind.

@bharb I've changed my answer.


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Which process is right to describe V(D)J recombination? RAG-1 and RSS recurring process
I'm studying V(D)J recombination. I think I have two incompatible books about explantaion of the process. Which is right?

In Molecular Biology of the Cell 5th Ed., firstly RAG (-1?) combines to RSSs of V and J genes independently. After that, a hairpin loop is formated by paring random(?) RAGs.
In Janeway's Immunobiology 8th Ed., RAG complex (RAG-1 and RAG-2) has two sites for RSSs from the beginning. And in the figure, V gene is firstly recruited for a site. J gene combines to the RAG complex after V gene.

It would be helpful if you could provide an actual excerpt from the text instead of a garbled summation. It's honestly hard to tell what your interpretation even is with some of the grammatical errors and use of incorrect terms to describe interactions.

The question is whether components of the RAG complex bind the RSS of V and J segments independently and then come together to form the complete complex or whether the RAG complex assembles completely on one one RSS and then binds the second.

Excerpt from Cellular and Molecular Immunology, 8th ED, p.181-182. Don't up-vote me, i just thought this text offers a good, up-to-date explanation.

The Mechanism of V(D)J Recombination
Rearrangement of Ig and TCR genes represents a special kind of non-homologous DNA recombination
  event, mediated by the coordinated activities of several
  enzymes, some of which are found only in developing
  lymphocytes, whereas others are ubiquitous DNA double-stranded break repair (DSBR) enzymes.Although
  the mechanism of V(D)J recombination is fairly well
  understood and will be described here, how exactly
  specific loci are made accessible to the machinery
  involved in recombination remains to be determined.
  It is likely that the accessibility of the Ig and TCR loci to
  the enzymes that mediate recombination is regulated
  in developing B and T cells by several mechanisms,
  including epigenetic alterations in chromatin structure
  and DNA as discussed earlier, and basal transcriptional
  activity in the gene loci.
  The process of V(D)J recombination can be divided
  into four distinct events that flow sequentially from one
  to the next (Fig. 8-10):
1. Synapsis: Portions of the chromosome on which the
  antigen receptor gene is located are made accessible
  to the recombination machinery. Two selected coding segments and their adjacent RSSs are brought
  together by a chromosomal looping event and held
  in position for subsequent cleavage, processing, and
  joining.
2. Cleavage: Double-stranded breaks are enzymatically generated at RSS-coding sequence junctions
  by machinery that is lymphoid specific. Two proteins encoded by lymphoid-specific genes, called
  recombination-activating gene 1and recombination-activating gene 2(RAG1and RAG2), form
  a  complex, containing two molecules of each protein,
  that plays an essential role in V(D)J recombination.
  The Rag-1/Rag-2complex is also known as the V(D)J
  recombinase.The Rag-1 protein, in a manner similar to a restriction endonuclease, recognizes the DNA
  sequence at the junction between a heptamer and a
  coding segment and cleaves it, but it is enzymatically
  active only when complexed with the Rag-2 protein.
  The Rag-2 protein may help link the Rag-1/Rag-2 tetramer to other proteins, including accessibility factors that bring these proteins to specific open receptor
  gene loci at specific times and at defined stages of lymphocyte development. Rag-1 and Rag-2 contribute to
  holding together gene segments during the process of
  chromosomal folding or synapsis. Rag-1 then makes
  a nick (on one DNA strand) between the coding end
  and the heptamer. The released 3′OH of the coding
  end then attacks a phosphodiester bond on the other
  DNA strand, forming a covalent hairpin. The signal
  end (including the heptamer and the rest of the RSS)
  does not form a hairpin and is generated as a blunt
  double-stranded DNA terminus that undergoes no
  further processing. This double-stranded break results
  in a closed hairpin of one coding segment being held
  in apposition to the closed hairpin of the other coding end and two blunt recombination signal ends being placed next to each other. Rag-1 and Rag-2, apart
  from generating the double-stranded breaks, also hold
  the hairpin ends and the blunt ends together before
  the modification of the coding ends and the process of
  ligation.
RAGgenes are lymphoid specific and are expressed
  only in developing B and T cells. Rag proteins are
  expressed mainly in the G0and G1
  stages of the cell
  cycle and are inactivated in proliferating cells. It is
  thought that limiting DNA cleavage and recombination
  to the G
  0 and G1
  stages minimizes the risk of generating inappropriate DNA breaks during DNA replication or during mitosis. Mice without functional Rag1
  or Rag2genes (Ragknockout mice) fail to develop B or
  T lymphocytes, and Rag-1 or Rag-2 deficiency is also
  a rare cause of SCID, in which patients also lack all
  lymphocytes.
3. Hairpin opening and end-processing: The broken
  coding ends are modified by the addition or removal
  of bases, and thus greater diversity is generated. After the formation of double-stranded breaks, hairpins must be resolved (opened up) at the coding
  junctions, and bases may be added to or removed
  from the coding ends to ensure even greater diversification. Artemisis an endonuclease that opens
  up the hairpins at the coding ends. In the absence
  of Artemis, hairpins cannot be opened, and mature
  T and B cells cannot be generated. Mutations in
  ARTEMIS are a rare cause of SCID, similar to patients with RAG1or RAG2mutations. (see Chapter
  21). A lymphoid-specific enzyme, called terminal
  deoxynucleotidyl transferase (TdT), adds bases to
  broken DNA ends and will be discussed later in the
  chapter in the context of junctional diversity.
4. Joining: The broken coding ends as well as the signal ends are brought together and ligated by a double-stranded break repair process found in all cells
  that is called nonhomologous end joining. A number
  of ubiquitous factors participate in nonhomologous
  end joining. Ku70 and Ku80 are DNA end-binding
  proteins that bind to the breaks and recruit the catalytic subunit of DNA-dependent protein kinase
  (DNA-PK), a double-stranded DNA repair enzyme.
  This enzyme is defective in mice carrying the severe
  combined immunodeficiency (scid)mutation, and mutations in the gene encoding this enzyme have also
  been discovered in human SCID patients (see Chapter
  21). Like Rag-deficient mice, scidmice fail to produce
  mature lymphocytes. DNA-PK also phosphorylates
  and activates Artemis, which, as mentioned before, is
  involved in end processing. Ligation of the processed
  broken ends is mediated by DNA ligase IV and XRCC4,
  the latter being a non-catalytic but essential subunit of
  the ligase.

Figure 8-10, Cellular and Molecular Immunology, 8e, p182.

If you downvote you should include an explanation.

Upvoted to bring balance to the force. Also all RSSes are not identical in the TCR/BCR genes. The RSS structure is a conserved heptamer followed by either a 12 or 23bp unconserved spacer, followed by a conserved nonamer. An RSS (12) and RSS (23) recombine much more efficiently than two (12) or two (23) sites. The direction and location of the (12) vs (23) sites facilitates the desired juxtaposition of a V site with a D/J site.


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What causes head hair to be different than body and face hair?
If you feel your head hair, it typically feels a lot softer and is easier to manage (comb, brush, fix) than a lot of other hair on your body - specifically I'm thinking about beard hair and pubic hair, which typically are a lot coarser than the hair on your head.
Why are these hairs thicker?
What causes them to grow differently than the hair on our head?

Have a look at this post.

I have previously looked at that post @WYSIWYG, but I don't understand what makes the hair coarse on the body but fine on the head.

Is it so?? I don't think that is true.

Well, pull out a piece of hair from your head, and pull out a pubic or beard hair and compare them, the beard and pubic hair are thicker. Also, if you look at hair closely under a microscope, scientists can tell if it is a "head hair" or a "body hair" @WYSIWYG

Yes, of course body hair is different from head hair based on texture and thickness but I just said that the former may not be necessarily "coarser". It also varies from person to person.

What kind of answer are you looking for? Hair coverings are affected by follicle structure,and eyelashes and eyebrows and so on are also different. An evolutionary reason why these hairs would be different is one thing, and a complete description of all the weird follicles on your body is another.

A little of both, but more the description of the follicle. Although why it got there in evolution would be interesting to know, too. @Resonating