text:
Components of the concept of Developmental Noise?
Developmental noise is a concept that correspond to the amount of possible phenotypic variance of a given genotype in a given environment.
Intrinsic noise (aka Cellular noise) is a component of developmental noise and it refers to phenotypic variations caused by the stochasticity of biochemical processes.
My question is:
What are the other component(s) of developmental noise?

There are two good papers on this that I like a lot:
Noise in Gene Expression: Origins, Consequences, and Control
Cellular decision making and biological noise: from microbes to mammals.
I think they can tell you better than I can, but the major other source of noise is extrinsic noise. Extrinsic noise typically is taken to means two things (both of which are related):
1. Physical noise from the environment that affects biological processes (thermodynamic fluctuations, for example)
2. Intercellular heterogeneity caused by, for example, unequal division. This is also related to cells not being "well mixed" - essentially, molecules found inside of cells are not evenly distributed throughout it.
There may be other kinds of noise, but I think extrinsic is really the main one you should think about.

These papers sound interesting.

Another source of developmental noise is due to diffusion. Diffusive processes are stochastic and induce noise in morphogen gradients and results in the concentration as being "jagged". Recent results have directly measured the noise in morphogen gradients of the developing zebrafish.
In fact, when you think about the low copy numbers of transcription factors which are thought to be morphogens,there must be a massive amount of noise in gradients which the developing systems have to account for.


text:
Why is lead dangerous?
Lead is known to be bad for your health for a long time, but I can't find a explanation why is it so.
In school they teach that heavy metals are poisonous, and they are trapped inside our bodies. I can just assume that the liver can't process those elements. But I still don't understand why this happens.
And finally why is lead different from, let's say, gold that is also a very dense metal, but is safe.

Please read http://en.wikipedia.org/wiki/Lead_poisoning and update your question if you have additional specific concerns.

Lead acts as a poison in a variety ways relative to what tissue it is exposed to. For example, lead is able to pass through the blood-brain barrier where it can act act as Calcium homolog to interfere with neurotransmitter release. In the blood, Lead inhibits porphobilogen synthase, an enzyme required for heme synthesis.
Lead's toxicity mechanisms include:

Its ability bind sulfhydryl groups, common to many enzymes
Its ability displace metals in enzyme complexes
Its ability to act as a Calcium homolog

Lead's valence electron configuration is $\require{mhchem} \ce{[Xe] 4f^14 5d^10 6s^2 6p^2}$; which means it has two electrons in its valence shell. This pair of valence electrons contribute's to Lead's ability to act as a Calcium analog and to Lead's tendency to form compounds in which it has an oxidation state of +2. Many such compounds dissolve in lightly acidic solutions. This has created lead exposure hazards when acidic tap water was pumped through lead pipes and when fruit juices have been served from ceramic vessels with lead-containing glazes.
Lead Poisoning
Lead

The part about the elements and their electons is pure speculation. Can you please either correct it or take it out? Following your argumentation gold should be as reactive as other elements which only need one electron to reach noble gas configuration. Gold in fact is so unreactive that it is always found in its elementar form in nature.

source: Stack Exchange

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text:
Simulating Drug Entry in Protein and binding?
Is there any simulation protocol or paper which can simulate the dynamics of drug entry and  interaction with the target protein?

often there is no specific path of diffusion into the active site - it will tend to be a statistical ensemble of possible paths...

This is a tough topic, have a look at the following references and see, if they can help you:

Structural modelling and dynamics of proteins for insights into drug
interactions.
Ligand entry pathways in the ligand binding domain of PPARγ receptor
Pathway and mechanism of drug binding to G-protein-coupled receptors
Molecular Dynamic Simulation and Inhibitor Prediction of Cysteine
Synthase Structured Model as a Potential Drug Target for
Trichomoniasis

Absolutely, the two I've had the most success are working with a radiolabeled and a fluorescently labeled version of the drug. Many drugs autofluoresce as well and this can be easily tracked.
When it's labeled as mentioned above microscopy or a luminometer, spectrophomoter or a scintillation counter can evaluate fractions or whole cells, or purified binding substrates.

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text:
Hair loss in a nuclear submarine?
Biologically, how prevalent is hair loss on a nuclear submarine? How can prolonged exposure to radiation levels typically present on a nuclear sub affect a person, say over a year or even more?

http://nnsa.energy.gov/sites/default/files/nnsa/02-12-multiplefiles/NT-11-2%20FINAL.pdf

@canadianer Actually that is one of the links that I have mentioned in the answer I put up.

I did check your post to see if you had included it but apparently I missed it!

Nice question but wonder if better served In Physics stack?

The question is not clear. Can you improve it by providing more context and writing out what you are asking? Specifically, are you talking about nuclear submarines?

I knew a man in one of my chemistry classes who served on a nuclear submarine and worked with the reactor. He not only still had a full head of hair but told me that his radiation exposure tag picked up more radiation in a day on the beach than in 6 months next to the reactor. Obviously it's an anecdote, but I generally think people are too afraid of radiation.

Just read the pdf @canadianer linked, and it says average exposure per person per year is 0.022REM, wikipedia says people should be exposed to less than 100mREM per year, which is about 5 times more than what the naval personnel are exposed too. I may have missed something, I only spent 90 seconds to find these numbers.

If the question is related to exposure to radiation in a Nuclear submarine then the answer is valid for radiation exposure irrespective of the place.
As you are aware there are many effects of radiation. Some of them are.

Nausea and vomiting
Diarrhea
Skin burns (skin reddening)
Weakness
Lethargy and fatigue
Loss of appetite (anorexia)
Fainting
Dehydration
Inflammation of tissues (swelling, redness or tenderness)
Hemorrhages under the skin
Bleeding from your nose, gums or mouth
Anemia
Hair loss (usually from just the scalp)
Decrease in platelets (reference)

Of course there is no safe quantity of radiation that has been quantified (reference) and there are personal anecdotes by submarine officers about first hand problems they faced due to radiation (reference). However, since this is a career you chose, you can be happy that the amount of radiation that you would be exposed to has decreased over the years (reference). Since you are interested in the biological aspect of what happens in your body due to radiation, I quote

When cells -- and what lies within them -- get exposed to radiation,
  components of DNA and critical proteins within the cell get all jazzed
  up (ionized), meaning that the electrons with our atoms get kicked
  out, causing the DNA strands to break and the proteins to cramp up
  (denature).
Ionizing Radiation:

Leads to the production of free radicals
Breaks critical chemical bonds
Leads to changes in cellular structure within irradiated cells
Damages vital molecules, such as DNA, RNA, and other regulatory
  proteins

Because our cells are mostly water, this ionizing radiation breaking
  H$_2$0 down is harmful to free radicals (H$^+$ and OH$^-$). While cells are
  damaged by free radicals all the time, they normally repair
  themselves, keeping the body healthy. However, high doses of radiation
  can damage the cell's ability to repair itself, and then all hell
  breaks loose.
This shakes things up all over the body.
Let's do a head-to-toe walk-through to investigate how high doses of
  radiation can damage the human body.
BRAIN: Nerve cells (neurons) and brain blood vessels can die, leading to seizures.
EYES: Radiation exposure increases the risk of cataracts.
THYROID: When a nuclear reactor malfunctions, radioactive iodine (I-131) can be released into the atmosphere (this is one of the
  particles that hangs out in a "radioactive plume"). The thyroid is
  very sensitive to the effects of I-131 (in fact, I-131's affinity for
  the thyroid is used therapeutically to specifically attract radiation
  to the thyroid in order to treat thyroid cancer and overactive
  thyroid). When a healthy thyroid is exposed to I-131, it can lead to
  decreased thyroid function and, over time, thyroid cancer.
LUNGS: When you breathe in invisible nuclear fallout particles, it can lead to lung cancer down the road.
HEART: High doses of radiation can damage the cells in the blood vessels that feed the heart, reducing cardiac function.
GI TRACT: Sensitive cells in the intestinal lining can be damaged, leading to nausea, bloody vomiting, and bloody diarrhea.
REPRODUCTIVE ORGANS: Rapidly dividing cells (eggs and sperm) in the ovaries and testes can die, leading to sterility.
SKIN: Rapidly dividing skin cells can be damaged, leading to skin lesions and burn.
LYMPHATIC SYSTEM: Rapidly dividing lymphatic cells die and damaged bone marrow may have trouble replenishing these immune-boosting cells,
  increasing the risk of infection (reference).

Many jobs have occupational diseases connected with it so I would say don't worry about it too much, enjoy your job and keep your fingers off the firing mechanism.

Nice answer. While the effects of a given are arguably kinda unknown, it would still be interesting to have some measurements (in Bequerel/Curries, in Greys or even more useful in Sievert/rems) or radioactivity in submarine.

@Remi.b Don't recall finding any but could exist.


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VMD set molecule as top using script
I have 10 molecules in VMD main screen and I was wondering if there is a script command to change what molecule is the top.
For example, molecule ID 9 is the top. But I want to change the top to 1, without using mouse.
Thanks!

Welcome to Biology.SE, Daniel. VMD has a mailing list, which may also be able to provide an answer.

Great! Thank you very much for you help. I'm gonna ask there :)

VMD -> atomselect top ID


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What is the use of shampoo; is it for the hair or for the scalp?
Apologies for the confusing question; I did not know how to better ask it.
I was doing a search on wikipedia when I found this statement.
Wikipedia's entry on hair states;

"The hair that is visible is the hair shaft, which exhibits no
  biochemical activity and is considered "dead"."

With that being said, why does one use shampoo? Is it because of the scalp that requires nourishment and cleaning because skin is not of a "dead" nature? Or is it to maintain the silkiness and smoothness of hair? Because it seems really redundant to take care of and maintain something which is already "dead".

both..Depending on the shampoo components, it can help nourish and clean the scalp as well as maintain hair texture. It would be redundant to take care of your hair if it wasn't a part of personal cleanliness and grooming.

@thelastword so it's safe to say when one takes care of his/her hair; it's only for personal grooming and does not bring about any health benefit?

gair, maybe so because I can't find any positives of specifically cleaning your hair and not your scalp. But the scalp has to be clean to prevent or delay the onset of scalp acne, scalp bleeding and dandruff. You wouldn't be cleaning your scalp alone without your hair though.

I'm skeptical of any claim that shampoo "nourishes" your scalp…

@canadianer http://www.ncbi.nlm.nih.gov/pubmed/15303780 ; http://www.ncbi.nlm.nih.gov/pubmed/8245236 ; I would call these 2 trials as examples of scalp nourishment by different shampoos. Maybe not in the strict sense, but you still have to admit that they do help in scalp treatment.

I think maybe we have different definitions of nourishment.

Neither hair nor scalp, really. Watch the rpoerts of uncontacted tribes of the Amazon. They seem to still have scalps and hair. Modern Western shampoos are designed to remove the natural smell, provide mainly (food-like) unnatural, but socially desired smell, and boost volume. The trials you are listing are for people with health problems, and the intervention is not "nourishing". Getting rid of dandruff is not similar to eating.

We shampoo our hair because of sebum. In humans, sebaceous glands are most numerous on the face and scalp, with (on the scalp at least) several glands plus a hair follicle making up a pilosebaceous unit.
Each gland secretes sebum, initially a colorless and odorless fatty substance (plus dead cells) that spreads from the scalp outward over the hair, but that breaks down by bacteria producing strong odors.
Look at a person who has not washed their hair in a week and it will be easy to understand why we wash the "dead" stuff on our heads. It looks oily and it eventually smells bad as well.

So with this being said, the reason for shampooing is for the benefit of the scalp? Since the sebum control is essential to prevent hair that smells bad-

It's for your benefit. The scalp will be still alive and well, although with a socially unacceptable smell.

@NickSandor ohh I see- thank you for clearing it up

Poorly kept hair directly contribute poor scalp hygiene and may result in health conditions, like Polish plait.
Of course grooming plays an important role as well, and perhaps even dominant role in modern western culture. We can see it, for example, by the variation in frequency of washing hair - if in US it is customary to wash hair every day, in Europe it is considered that using shampoo once in three-four days is quite enough. Note that, if washed regularly at the same interval, the hair does not appear dirty, as it gets oily more slowly than if washed every day.

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What are the molecular mechanisms behind tachyphylaxis (downregulation of receptors in response to an agonist?)
Anyone know of a good source which explains this?  Or is this still an open question?  This wikipedia article describes some molecular biology behind morphine tolerance, but it sounds like its newer research, and isn't fully understood. http://en.wikipedia.org/wiki/Drug_tolerance
I would have thought that something like this would be very well understood.

There are many mechanisms of receptor down-regulation, including internalisation and degradation e.g for the epidermal growth factor receptor and uncoupling via post-translational modifcation e.g. for G protein-coupled receptors.
In the case of opioid receptors there is emerging evidence that down-regulation is achieved, at least in part, by post-transcriptional regulation by a microRNA. Presumably this could also accompanied by inactivation of existing receptors, but if the adaptation/desenitisation is long-term then normal receptor turnover may be sufficient.


text:
Does "Garbage Enzyme cleaner" contain cleaning enzymes?
There are many recipes which call for using fruit peel fermentation process to make a concentrated enzyme cleaner solution, some variations call to add bakers yeast. So the question arises that does this recipe really have those cleaning  enzymes and how are they generated?
This says that it may not have the cleaning enzymes, but maybe some other cleaning agents like vinegar or alcohol.
A discussion from two independent researchers on this topic give contrasting positions
Moreover if fruits  like Pineapple and papaya are used does it make the solution more potent?

The discussion you linked (here) shows that both researchers agree that 'garbage enzymes' are mostly acetic acid or vinegar, with a low pH(3-4). Fresh papayas contain papain, but roughly 2% of the enzyme self-digests per day in aqueous solution. Bromelain from pineapples is still active at acidic pH. Like most other proteases, it self-digests much more rapidly than papain. As a result, any digestive enzymes present when the mixture was made would destroy themselves by the time the mixture matured.
((Those among you quick at math will note that perhaps 1/5 of the papain activity would remain after ninety days. While true, there's evidence yeast cultures eat gluten for sustenance, and if they can digest gluten they'll digest papain. There's no reason to expect yeast to leave a delicious protein source unused.))
If the solution acquired proteases somehow, they would self-digest under the conditions the 'garbage enzyme' solution is stored at(room temperature, aqueous solution, nothing exotic like formaldehyde, months). The yeast itself by the time the fermentation is complete has died, destroyed by the acetic acid(or ethanol, depending) they created. Any digestive enzymes used by the yeast to dissolve proteins destroy themselves as the mixture matures and the yeast die off.
If the mixture starts with no digestive enzymes, there's no mechanism to get appreciable amounts active digestive enzymes. If the mixture does start with digestive enzymes(papaya or pineapple), either the yeast will eat them and then die or they will digest themselves and the yeast will eat the byproducts. Finally, the yeast will die.
It's a vinegar/alcohol blend, depending on how much oxygen is available during the fermentation, and it smells like whatever you put in it. If you used orange peels, it probably smells pretty okay. That's why it cleans.
If you are anxious to use real live proteases, there are powdered papaya/pineapple/etc powders you could reconstitute in water right before use. They are usually sold as meat tenderizer among other things. There are also blends of enzymes sold for pet urine deodorizing, and general purpose cleaning fluid with bacterial and enzymatic action. Formulating those at home is going to be fairly involved, but if you wanted an enzymatic cleaner you made yourself that's how to do it.

Just for the sake of curiosity how do we prevent self-digest happening by laundry detergents? E.g. in the stomach pepsinogen is activated by pH lower than 3 (HCl secretion), and it activates the other proteolytic enzymes after that.

I think you answered your own question with respect to stomach enzymes, but most laundry detergents are just detergents and have no proteolytic activity, as far as I'm aware. I will admit I'm not keeping tabs on laundry science advancements, however.

thanks , but what about the intra cellular enzymes of dead yeast?

What about them? Few people recommend a lambic beer or yogurt as a cleaning agent, even though both contain intracellular enzymes. The fraction of intracellular proteins that are digestive or proteolytic in nature is extremely small. If it's intracellular proteins from yeast that you're after, mix brewer's yeast with a little dish soap to destroy the cell membranes and enjoy the intracellular protein soup. No need to let them ferment for three months, and what you save on time you can spend on more yeast.

"but most laundry detergents are just detergents and have no proteolytic activity" - just the opposite. if you just want a detergent you can use soap, or horse chestnut (saponin), etc... proteolytic activity is important to clear stains like grass, blood, chocolate, etc...

The stain-fighting ability of laundry detergent is due to oxidizers unless you have 'bio' detergent(I don't, but you can buy them) with proteases, amylases, lipases to break down proteins, carbohydrates, and fats respectively. The pigments in grass stains for example(mostly chlorophyll) will not be attacked by proteases, because they're not proteins.

so how to actually measure enzymes in the output

also is it possible to multiply the enzymes?

@JeremyKemball Afaik most of the pigments are bound to proteins and are in cells organs. Proteases (and other enzymes) degrade cells and pigment-protein complexes, so the pigment will be easier to wash out. (Oxidizers do something similar.) Btw there can be pigment degrading enzymes in the detergents as well, e.g. chlorophyllase. This bio detergent term is not used in my country, I guess it is a marketing term, because my laundry detergent (and basicly all laundry detergents I can by in the shop) contains enzymes. (Next time please use @ if you want to answer my comment.)

@Bioguy We usually measure enzyme activity and not enzyme content. You need something you can measure and the enzyme can degrade, and you can measure the decreasing concentration of that thing.

@JeremyKemball It is possible to change the pH, salt content, temperature, etc... in order to prevent self-digestion. I guess most of the detergents use the same solution. So when the detergent is diluted in water and warmed up by the wash machine, then the enzymes become active... Btw. only proteases self-digest, so there can be amylases, lipases, etc... in these garbage enzyme cleaners.

There could indeed be those things, and pH changes are how the stomach(for example) avoids self-digesting. And there is certainly some amount of amylase/lipase/etc present. Nearly all living things have some amylase around at all times. 'Garbage enzyme' cleaners do not have a plausible source of large quantities of enzymes, and the very inconsistency of the conditions given means that even if under very specific circumstances you had a magical recipe that provided a lot of lipase or something, most garbage enzyme formulations will not have enough enzymes to actually achieve anything.

There is some evidence that garbage enzymes have significant enzyme activity, so they really work.

The decomposable waste thrown into the environment can be used to
  produce value added bio-product which in turn reduces the production
  of greenhouse gas. Garbage enzyme is one such value added product
  produced by fermentation of organic solid waste. In the present study
  enzyme activity and disinfectant potential of garbage enzyme was
  evaluated and its influence on reduction of total solids, suspended
  solids and pathogens in dairy waste activated sludge were studied. The
  result showed the garbage enzyme possesses protease, amylase and
  lipase activity and reduced 37.2% of total solids, 38.6% of suspended
  solids and 99% of pathogens in dairy waste activated sludge. This
  significant result may be helpful for researchers to compare the
  effectiveness of earth-friendly garbage enzyme treatment of industrial
  sludge with various physical and chemical pre-treatment methods to
  improve the bio gas production from the sludge digestion unit.

2014 - INVESTIGATION OF BIO CATALYTIC POTENTIAL OF GARBAGE ENZYME AND ITS INFLUENCE ON STABILIZATION OF INDUSTRIAL WASTE ACTIVATED SLUDGE
2011 - A Study of the Garbage Enzyme’s Effects in
Domestic Wastewater

This study was conducted to explore the feasibility of using Garbage
  Enzyme to treat sullage. The enzyme was prepared from fruits dregs,
  kitchen waste, molasses and water and capable of having reinforcing
  and cleaning function to work with nature. In this study, sullage was
  collected at open drainage at Arked Meranti, Arked Cengal and Kolej 9
  cafeteria?s and enzyme dosage determinations were done at laboratory
  scale. Sullage collected were analysed for BOD, COD, TSS and oil and
  grease. From the result obtained all samples treated using garbage
  enzyme prepared shows removal of BOD was 60% , COD and oil and grease
  almost 90%, then TSS was 80% after 7 days of treatment with different
  dosage of enzyme.

2010 - Garbage enzyme as an alternative method in treatment of sullage - pdf

To answer your questions:

So the question arises that does this recipe really have those
  cleaning enzymes and how are they generated?

Fruits, biological garbage etc... all contains cells, and those cells contain enzymes. By the fermentation process the cells are breaking down (lysis) and they release their enzymes.

Moreover if fruits like Pineapple and papaya are used does it make the
  solution more potent?

Pineapple and papaya contain proteases (e.g. bromelain). Enzymes are proteins, so these proteases can degrade them as well. (I think these proteases can be inhibited safely, but this would require a lot of research.) So I think it is not a good idea to ferment pineapple or papaya, because the result will be a significant loss of enzyme activity.


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Appropriate Buffer for electerophoresis of DNA & Protein TBE or TAE?
Which buffer is best for DNA Electrophoresis and which is best for Protein to be have a sharp bond?
Considering a higher electrical conductivity compared to TAE & TBE and the generation of less heat. If anyone has a particular formulation (add other materials to improve quality) which is obtained as a result of practical experience. I would be grateful if you send me that.

The standard for DNA agarose gel is TAE and for the protein, it depends on the size of the protein and the gel type used! Some times MOPS works best and sometimes Tris-acetate works best. It really depends on the gel used and also the protein and its size. You just have to experiment with them and see which works best for you! This document by Invitrogen might be of help (http://tools.lifetechnologies.com/Content/SFS/ProductNotes/F_050711_NuPage-TS-TL-MKT-HL.pdf). To prevent apparatus over heating, put them in a cold room. I can give you my TAE components if you wish!

@Bez please introduse why TAE stand a standard buffer for DNA (are it works for any size of that even in PFGE?).If you have a table for size of proteins and relative buffer that can complete your upper idea about proteins buffer difference please put complete of them in a answer form.

TAE is the standard DNA agarose gel buffer according to Sambrook et al., 1989 and is used by practically every scientist that I know of for running agarose gels for DNA. Please look at figure 2 for the best gel to use for your protein of interest (http://www.lifetechnologies.com/uk/en/home/life-science/protein-expression-and-analysis/protein-gel-electrophoresis/protein-gels/novex-nupage-sds-page-gels/nupage-sds-page-bis-tris-gel.html). Since the question is on hold I cannot add a new answer but as soon as it opens I will put my comments as a full response.

It would be great if this could be reopened so we can write proper answers and not have to use the comments for this.

The question which buffer for DNA is better is quite old. Both have their pros and cons and I list a few of them:

TBE is a better conductor and is thus less prone for overheating the
gel
Borate is a powerful enzyme inhibitor, so if you want to apply
enzymatic steps downstream, TAE is the better choice
TAE gives a better resolution for large fragments
TBE has a higher resolution for fragments <2kb so it is better here

Both buffers appeared in the 70s when the electrophoresis of nucleic acids was developed (in fact it was derived from protein electrophoresis)
and haven't been changed or optimized much since then, although there is a number of disadvantages:
First EDTA is not really necessary for DNA electrophoresis (it is for RNA, which is also the most likely reason it is still in there). Then
Tris is not the best buffering substance here. Besides being relative expensive it creates a temperature-current feedback loop,
meaning the higher the current gets, the higher the temperature will be. This leads to a higher gel temperature with all the
negative effects of it. For more details on this, have a look into reference 1.
There has been some research on this matter and there are some suggestions available for better running buffers (details are in references 2 and 3).
In short these are:

10mM sodium boric acid (Na2B4O7/Borax): separation of DNA fragments
from 100bp-5kbp
5mM lithium acetate (LiOOCCH3): separation of fragments longer than 3
kbp
1mM lithium boric acid (Li2B4O7): separation of small DNA fragments
and ssDNA

The borate in this buffers is still problematic in terms of a possible enzymatic inhibition, but this can be overcome with a simple ethanol
precipitation of the DNA (which of course also applies for use of TBE buffer).

History and principles of conductive media for standard DNA
electrophoresis.
Sodium boric acid: a Tris-free, cooler conductive medium for DNA
electrophoresis
Ultra-fast high-resolution agarose electrophoresis of DNA and RNA
using low-molarity conductive media

I have had good experience using a lithium boric acid buffer from Faster Better Media. I use it for RNA gels, but it's advertised for DNA gels. I don't think it can do protein, but I've never tried it. I'm not an electrician, but higher conductivity may be the opposite of what you want. The lithium boric acid buffer claims to have less conductivity than a tris based buffer, allowing you turn the voltage up much higher while producing less heat. The higher voltage pushes the DNA down the gel faster, and keeps the bands sharper. My RNA gels take 30 minutes to run, used to take 3 hours. Of course, those slow gels used a MOPS based buffer and formaldehyde to denature the RNA.

The funny thing is one of the founder of Faster Better Media wrote the articles I cited :-)

Grossly, it does not matter what buffer you use. It is the pH that matters.
For DNA electrophoresis EDTA is added in order to chelate divalent cations that serve as cofactors for nucleases. Tris is the base of the buffer and is used to set pH. Along with Tris one can use Boric acid, Acetic acid or phosphoric acid for adjusting the pH.
The buffering range can be obtained by the Henderson-Hasselbalch equation.
The choice of buffers depends on pH range, ease of preparation/storage and fine resolving properties and runtime properties such as heating etc (also mentioned by others).
MOPS is another buffering agent. I am not very sure why MOPS is used instead of Tris for RNA gels; perhaps the latter forms adducts with formaldehyde  by Mannich's reaction whereas MOPS cannot undergo that reaction. MOPS is also a Zwitter-ionic species and maintains neutral pH. RNA should not be kept in alkaline pH. At acidic pH, RNA will become neutral and will not move.
For protein electrophoresis things are a little different. Glycine-Chloride buffer is used because it allows stacking.

There are already many great answers to your question, however I thought I put my comments in form of an answer.
The standard for DNA agarose gel is TAE and for the protein, it depends on the size of the protein and the gel type used! Some times MOPS works best and sometimes Tris-acetate works best. It really depends on the gel used and also the protein and its size. You just have to experiment with them and see which works best for you! This document by Invitrogen might be of help. To prevent apparatus over heating, put them in a cold room. I can give you my TAE components if you wish!
TAE is the standard DNA agarose gel buffer according to Sambrook et al., 1989 and is used by practically every scientist that I know of for running agarose gels for DNA. Please look at figure 2 for the best gel to use for your protein of interest, which has been shown in form of a table.


text:
Do the eggs for larger litters come from the same meiosis events, or different ones?
There are some species of animals that give birth to more than one pup at a time. In these species, are the fertilized eggs all from one or a limited group of meiosis processes, or are they from different ones?
To illustrate the idea, take for example a case where some animal ends up with seven offspring in a litter. Do the original eggs come from different meiosis events?
Meiosis   Meiosis   Meiosis   Meiosis   Meiosis   Meiosis   Meiosis
   |         |         |         |         |         |         |
   V         V         V         V         V         V         V
   1         2         3         4         5         6         7

Or from a smaller set of events?
  Meiosis     Meiosis
 / |  | \     |  |  |
V  V  V  V    V  V  V
1  2  3  4    5  6  7

I am aware that, at least in mammals, that egg cells are actually produced long before they are used, and pooled for later use:
Meiosis  Meiosis  Meiosis
   \\\\    ||||    ////
    VVVV   VVVV   VVVV
    =====Egg Pool======
    |  |  |  |  |  |  |
    V  V  V  V  V  V  V
    1  2  3  4  5  6  7

I do not have any idea how this would work for other types of life though, like birds, reptiles, or fish. How does it work for those sorts of life?
I am mainly interested in this to understand how the mother's chromosomes are represented in the offspring. Are all of her chromosomes guaranteed to be represented in at least one offspring?

I'm not sure about the ubiquity of this but, in many animals, each primary oocyte that undergoes oogenesis only produces one mature egg. The other products of meiosis are polar bodies, which are not fertilised. These cells often degenerate but can sometimes play supportive roles in embryogenesis.

To answer your question, each mature egg is necessarily from a different meiosis event and so it is not guaranteed that all of the mother's chromosomes are represented in her offspring.

OK, thanks. This is exactly what I was looking for.

@canadianer why would all of mother's chromosomes not be represented in her offspring?

Do you mean to say all of the 2x chromosomes of a diploid species?

@CRags Each egg contains half of her chromosomes, independently assorted and recombined. It's unlikely in smaller numbers of offspring that every piece of every chromosome will have been passed on.

While your question asking about birds, reptiles and fish (oh my!) may be too broad, hopefully looking at frog oogenesis can show some differences in large offspring number v. small offspring number. Some frogs even give birth to live offspring (Iskandar et al. 2014).
Much of this explanation can be found in Developmental Biology, 6th edition by Gilbert SF.
In frogs, meiosis happens in stages (Developmental Biology):

This shows that different "cohorts" of oocytes form, develop, and are released, rather than a single group of mitotic events that are released gradually (as in humans). When the eggs have undergone vitellogenesis (yolk development), they are ready for fertilization.
As far as this question is concerned:

I am mainly interested in this to understand how the mother's chromosomes are represented in the offspring. Are all of her chromosomes guaranteed to be represented in at least one offspring?

If you're asking whether or not all of the mother's chromosomes will be represented in her total offspring, perhaps--with a large number of offspring (and a high ratio of fertilized eggs) the probability is very high.
No single offspring will contain all of its mother's chromosomes. Let's look at a diploid organism with two pairs of chromosomes: A and B. At the beginning of meiosis I, a cell will have one copy of both pairs:
A1 A2 B1 B2

Then comes synthesis, duplicating all chromosomes. Now we have two copies of each pair:
A1A1 A2A2 B1B1 B2B2

In prophase, chromosomes are condensed and the duplicated pairs connect in a process called synapsis:
A1A1-A2A2 B1B1-B2B2

In anaphase, the pairs are pulled apart so that each daughter cell has two copies of a single member of the pair:
daughter Y: A1A1 B2B2
daughter Z: A2A2 B1B1

Note that at this point it is not possible for either of the daughter cells to contain all of the mother's chromosomes.
With meiosis II, these copies are pulled apart, making four daughter cells:
daughter Y1: A1 B2
daughter Y2: A1 B2
daughter Z1: A2 B1
daughter Z2: A2 B1

These are now haploid, and await the male's sperm to make them diploid once more. Also note that daughters Y1/Y2 and Z1/Z2 are chromosomally identical (they can be different in practice with crossing over).
Here is a prettier representation of what I just described (Wikipedia):

The key is to remember that pairs of chromosomes and copies of chromosomes are different and to keep track of how they segregate during meiosis.
Edit: To address your clarification:

I am not talking about whether or not any of the daughter cells contains all of the mothers genetic material by itself, but rather whether every segment of genetic material is found in at least one offspring.

This is more of a probability question. If all oocytes mature, and are fertilized, the answer is clearly yes. However, not all oocytes are fertilized. Let's look at the same four daughter cells from my earlier example:
daughter Y1: A1 B2
daughter Y2: A1 B2
daughter Z1: A2 B1
daughter Z2: A2 B1

Let's say 2/4 (50%) are fertilized by the male frog. Going through all possible fertilizations, let's see how many combinations result in all of the mother's genetic material being passed down:
Y1, Y2 - No
Y1, Z1 - Yes
Y1, Z2 - Yes
Y2, Z1 - Yes
Y2, Z2 - Yes
Z1, Z2 - No

The answer to your question really depends on what proportion of oocytes make it to maturity, and what proportion of mature oocytes are fertilized. The probability of all the mother's genetic material being passed down increases with increasing fertilization ratio/egg number, so given the high number of offspring produced by many species of frog, I'd say that there is a good chance of all the mother's genetic material making it to the next generation, although it is not guaranteed.

I am not talking about whether or not any of the daughter cells contains all of the mothers genetic material by itself, but rather whether every segment of genetic material is found in at least one offspring.

@AJMansfield I addressed your clarification further in my recent edit


text:
brain activity responsible for imagination
Which part of brain is responsible for advance or unseen imagination
For example:ones brain can make a situation in mind which is impossible to happen ...which part of brain is hyper active?

Edit: Added two studies to better show how different types of imagination tasks use different parts of the brain.
Imagination is a complex process that can use many regions of the brain. Insights into how our brain imagines have been gained through a number of studies. There is not an "imagination" area of the brain. Instead, different areas, and often several at a time, may be used depending on the type of imagination. I'll highlight a few examples here.
Ogino et al. (2007) asked 10 male participants to imagine feeling pain while watching pictures suggesting either pain or fear. Both pain and fear tended to activate an area of the brain called the anterior cingulate cortex (ACC), which helps to regulate blood pressure and heart rate among other basic nervous functions. Imagining pain activated not only the ACC but also another four areas of the brain were especially active. In comparison, fear tended to activate the ACC and the hypothalamus, which regulates the "flight or fight" response. Both sides of the brain were activated at the same time.
Boly et al. (2007) studied 12 brain-injured patients who where not capable of communicating. They were not in a coma. They were asked to imaging tasks involving spatial skills or motor skills. The two most common areas of the brain that were activated were the supplementary motor area, which helps to control movement, and the dorsal premotor cortex, which may contribute to movement and spatial coordination. (Wikipedia information so interpret cautiously.)
A detailed study was recently provided in a study by Schlegel et al. 2013. (An alternate version is here; both versions are open access.) Summaries of their work written for the general public can be found in Popular Science and Science Daily.
The scientists identified what they called the "mental workspace" which is not a particular region of the brain but instead is several different regions of the brain (from both sides of the brain) interacting together.
The researchers asked the study participants (9 males and 6 females) to select from a set of abstract shapes to assemble a particular target shape.  The target shape (the one the participants had to create) was a 2x2 grid. Each abstract shape that to be selected would fit one of the grids. So, four abstract shapes had to be selected to assemble the target shape. They also tested the reverse: Given a target shape, could the participants identify the four abstract shapes needed to make the target shape.
During the task, the researchers used functional magnetic resonance imaging (fMRI) to monitor brain activity. After the analysis of the fMRI results, they identified 11 distinct regions of the brain were active during the task.  In nearly all cases, the regions were active in both sides of the brain. However, I noticed that one region, the medial frontal cortex, only appeared to be active in the left side of the brain. This region was identified as one important component of the mental workspace for certain tasks.
The researchers concluded that four of the 11 regions were most important. You can see the regions of the brain in any four of the links above (and the abstract shapes in all but the Science Daily article). They argue that the interaction among the four major and seven minor regions contribute to our process of imagination.
Each of the three studies I highlighted requires the participants to perform different types of imgination tasks. Each type of task showed that different regions of the brain were used. Each type of task also required that several areas of the brain were used simultaneously during the imagination process. Together, these results show that no single part of the brain is used for imagination. Instead, many different areas are used, depending on what the person is imagining.
Citations
Boly, M. et al. 2007. When thoughts become action: An fMRI paradigm to study volitional brain activity in non-communicative brain injured patients. NeuroImage 36: 979-992.
Ogino, Y. et al. 207. Inner experience of pain: Imagination of pain while viewing images showing painful events forms subjective pain representation in human brain. Cerebral Cortex 17: 1139-1146.
Schlegel et al. 2013.  Network structure and dynamics of the mental workspace.  Proceedings of the National Academy of Sciences USA 110: 16277-16282.


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Why do we use DNA sequencing methods such as shotgun?
I am learning about DNA cloning for the first time. What I understand is that, in order to clone DNA, we break-up the original gene into shreds. Then try to piece it back together.
Why exactly do we do this? Instead wouldn't it be better to clone one base at a time? Basically in pseudo code:
old_dna_strand = 'ACTCATGCGAGCGTCAGTAGTACGTACTG'
new_dna = ""
for base in old_dna_strand:
    new_dna+=base

That looks a lot more easier and a lot less prone to errors. Why do we have weird methods such as shotgun?
Thanks in advance. Let me know if i should clarify or update anything in this question.

This is a technique from the "old time" of genome sequencing. The underlying method for sequencing is the Sanger chain termination method which can have read lenghts between 100 and 1000 basepairs (depending on the instruments used). This means you have to break down longer DNA molecules, clone and subsequently sequence them. There are two methods possible.
The first is called chromosome (or primer) walking and starts with sequencing the first piece. The next piece of DNA (which is  and then uses a specific primer from the end of the sequence. The next (contigous) piece of the sequence is then sequenced using a primer which is complementary to the end of the first sequence read and so on. This technique doesn't require much assembling, but you need a lot of primers and it is relatively slow.
To overcome this problem the shotgun sequencing method was developed. Here the DNA is broken into different pieces (not all broken at the same place), cloned and sequenced with primers specific for the vector used for cloning. The leads to overlapping sequences which then have to be assembled into one sequence on the computer. This method allows the parallelization of the sequencing (you can prepare a lot of sequencing reactions at the same time and run them) which makes the process much faster and also avoids the need for sequence specific primers. The problems are to sequence repetitive sequences, as overlaps are not as clear here. To resolve this problems a first draft is made and then critical regions are resequenced using other techniques as primer walking. Have a look at the Wikipedia page about shotgun sequencing if you want to read more details.

wow! thanks for the quick reply. Makes more sense now.

Primer walking will always give the exact replica of the original DNA. Shotgun sequencing can have potential mix-ups though (since we randomly cut-up the DNA). Is this problematic in most situations?

It can be, especially for repeat sequences. Generally a rough draft is created by shotgunning and it is then finished by filling gaps with multiple techniques (including chromosome walking).

@canadianer Thanks for filling in here. I'll add this to the answer as well.


text:
Highest Pressure Human Body Can Survive In?
One design for underwater human inhabited environments is to have equal pressure between the surrounding water and the submerged habitat, thus allowing a section of the floor to be open to the water and removing the necessity for strong plating to protect it.  This requires the air pressure within the environment to be greater than atmospheric pressure so that it can withstand the pressure of both the atmosphere and the pressure from the overlying water.
So how much pressure can the human body survive in without need for special suits and breathing apparatuses (as this would place a limit on how deep you could build such an environment without special accommodation)?
Edit: So far i've found an article about a man trapped in a sunken boat who survived for days in an air pocket trapped in the bathroom 100 feet down.  He couldn't resurface without the use of a diving bell and gradual decompression; but this case provides a lower bound for how high the highest pressure can be.
Calculations:  14.7 psi (atm pressure) + 1200 inches*0.037 psi/in^3 = 60 psi for the underwater pocket (roughly 4 times atmospheric pressure).
http://news.nationalgeographic.com/news/2013/12/131204-nigerian-air-bubble-survival-shipwreck-viral-video-science/

Without breathing apparatuses, the pressure isn't the limiting factor for survival. The lack of oxygen is...

Plants might refresh the air or might not; but supposing you had a means to freshen the air, and using whatever composition of the gas would maximize the highest pressure at which humans could breathe.  Or if that is too difficult, just plug in condensed atmospheric air.

oh... athmospheric pressure. I though you would be completely submersed, somehow, sorry. In this scenario, you would actually fare pretty well, AFAICT.

http://en.wikipedia.org/wiki/Deep_diving

do you consider a diving bell a diving apparatus?

I was just going to ask "How deep a diving bell can a human breathe in?" and saw this Q. Hoping to find an answer here..

It's common for saturation divers to live under pressure for weeks if not months at a time beyond a pressure of 1000 feet of seawater, but typically not more than 1500 feet. I believe the limitations are more economical rather than physiological. 1000 FSW requires special mixed gas controls to prevent the narcotic effects of nitrogen that occuer under pressure. That's why helium is added. But then helium steals the diver's heat, so special warming systems are required. Decompressing after these long periods takes days.

According to Israel Ramirez on Quora, the practical maximum is about 70 atmospheres of pressure. Any higher than that and people won't be able to breathe.

The deepest recorded simulated dive is still the on-shore French Hydra 10 experiment at 701 msw (meters salt water); at a pressure of 71 atm. Since breathing a mixture containing helium is required at such depths (to avoid the extreme narcosis produced by nitrogen at such depths), the new problem helium causes is

High-pressure nervous syndrome (HPNS). HPNS, brought on by breathing helium under extreme pressure causes tremors, myoclonic jerking, somnolence, EEG changes, visual disturbance, nausea, dizziness, and decreased mental performance. Symptoms of HPNS are exacerbated by rapid compression, a feature common to ultra-deep "bounce" dives.

Actually that Wikipedia description is a bit misleading, the problem is caused by any gas mixture, not just helium, but other gasses like nitrogen or hydrogen have a narcotic effect that counteracts HPNS. HPNS sets in at about 120m:

The high pressure
  neurological syndrome (HPNS) begins to show signs at about 1.3 MPa (120 m) and its effects intensify at greater depths.
  HPNS starts with tremor at the distal extremities, nausea, or moderate psychomotor and cognitive disturbances. More severe
  consequences are proximal tremor, vomit, hyperreflexia, sleepiness, and psychomotor or cognitive compromise. Fasciculations
  and myoclonia may occur during severe HPNS. Extreme cases may show psychosis bouts, and focalized or generalized
  convulsive seizures. Electrophysiological studies during HPNS display an EEG characterized by reduction of high frequency
  activity (alpha and beta waves) and increased slow activity, modification of evoked potentials of various modalities (auditory,
  visual, somatosensory), reduced nerve conduction velocity and changes in latency. Studies using experimental animals have
  shown that these signs and symptoms are progressive and directly dependent on the pressure. HPNS features at neuronal and
  network levels are depression of synaptic transmission and paradoxical hyperexcitability.

The problem with extreme helim pressure was partially alleviated in the Hydra experiments by mixing/replacing some of it with hydrogen, in the so-called Hydreliox mixture.

For the Hydra VIII mission at 50 atmospheres of ambient pressure, the mixture used was 49% hydrogen, 50.2% helium, and 0.8% oxygen.

The French did this based on prior experiments which found that the narcotic effect of hydrogen reduces HPNS (or even completely eliminates it at lower depths):

A H2-He-O2 mixture with 54 to 56% hydrogen was studied with 6 subjects (professional divers) during 2 dives to 450 m. The 38-h compression was the same as that used with other types of breathing mixtures (He-O2 and He-N2-O2). The results obtained during compression and during the stay at 450 m in H2-He-O2 show that the EEG changes (increase of theta activities in the anterior regions of the skull, decrease of alpha activities) are similar to those found with other respiratory mixtures. On the other hand, the other symptoms of high pressure neurologic syndrome (HPNS) were clearly improved for the same depths. Thus, neurologic symptoms (tremor, dysmetria, myoclonia, drowsiness) are nonexistent, and the performances during psychometric tests remain similar to those of the surface. Hydrogen, with its narcotic potency, suppresses some symptoms of HPNS and seems to open new perspectives for deep diving.

Of course, having hydrogen (in such large proportion) and oxygen in a gas mixture poses dangers of fire, explosion etc. This is avoided by decreasing the oxygen concentration; alas this cannot be a one-step process (for diving):

The major problem with hydrogen-oxygen mixtures is the potential for explosion. Although the concentration of oxygen needed for combustion of oxygen-hydrogen mixes varies a bit with pressure, a general rule of thumb is that hydrogen-oxygen mixes above 5 %  O2 are at-risk.. So, to avoid nasty fires and explosions, hydrogen is only considered as a breathing gas component at pressures where a less-than 5% oxygen concentration in the breathing gas mix gives a partial pressure of oxygen great enough to sustain life. Perhaps the most common example of a hydrogen-fire related disaster is the destruction of the Hindenburg dirigible. [...]
In 1944 Arne Zetterstrom discovered a way to breach the transition between compressed air and Hydrox without risking explosion. The technique was to descend to 100 feet and switch to a 4% oxygen / 96 % nitrogen mixture. After breathing this mix for sufficient time to allow the oxygen concentration in the lungs to drop below the "explosion threshold," the diver switched to Hydrox and continued descent. On ascent, the diver again used the Nitrox (4% O2 / 96% N2) as a transition between Hydrox and air. Using this technique, he descended to 363 feet. At that depth, the alteration in voice characteristics, coupled with excitement, made communication impossible and additional dives used a telegraph key.  [...]
During the mid 1960's research into the use of hydrogen in breathing gases resumed with animals breathing Hydrox for up to 24 hours at 70 Ata. One interesting aspect of the animal research was the suggestion that hydrogen reduced the HPNS (high pressure nervous syndrome) often observed with helium based gas mixes on deep dives. Ultimately animals would be taken to 3500 feet on hydrox.
In 1983 COMEX, the French deep diving concern (perhaps more famous in the US as the company providing the submersible used in the recovery of artifacts from the Titanic) began a series of dives to investigate the narcotic potential of hydrogen. Divers including H.G. DeLauze, President of COMEX, descended in open sea to approximately 300 feet for five minutes. The divers could not perceive a difference between Hydox and Heliox at that depth.  Chamber dives to 300 m (984 ft) demonstrated that hydrogen possessed a narcotic effect different from nitrogen. Hydrogen narcosis (the "hydrogen effect") had a tendency to be more psychotropic, i.e. more like LSD, while nitrogen narcosis had an effect similar to alcohol. This deeper work suggested that Hydrox as a binary gas mix would not be too useful at depths below about 500 feet.

Based on that COMEX developed a protocol of switching from heliox to hydreliox at 250msw.
A more recent (1994) COMEX paper reported that at 500m (on hydreliox), manual dexterity was about 80% of the surface one, while the arithmetic ability decreased to 60%. So not dying and being able to function as on the surface, aren't the same thing.
Also these experiments are time consuming and costly. In Hydra VIII, the whole thing took one month, of which only 10 days or so were spent at maximum depth. And in case "something bad happens" interventions aren't easy in such settings.
A 1984 American experiment with trimix at 650m was aborted after one of the three subjects (despite negative previous neuropsychiatric screening, as well having substantial commercial diving experience and successfully taking part in the previous experiments of the series) developed hallucinations and then full blown mania at 625-650m.

The Atlantis IV dive was designed to test the ability of 5%
  N2 trimix breathing mixture (5% N2, 0.5 atmosphere
  oxygen, with the balance helium) to counteract the
  [high pressure nervous] syndrome without nitrogen narcosis. [...]
The dive began with an initial compression rate of
  30 m/hour to 300 m (1000 ft) sea water equivalent
  pressure. By day 3 of the dive, at about 470 m, subject
  C had developed significant insomnia. On day 4 (540
  m), this subject became stressed and complained of
  mild auditory illusions of music and visual distortions
  consisting of a “halo effect” around the chamber’s
  apparatus. On day 5 (625 m) of the dive, the subject’s
  irritability, insomnia, and agitation worsened. He was medicated with temazepam, 60 mg, and achieved
  substantial relief of these symptoms after 15 hours’
  sleep. However, with further compression to 650 m,
  subject C experienced a recrudescence of auditory and
  visual illusions and developed rapid speech, racing
  thoughts, shortened attention span, and difficulty in
  focusing on tasks. Ankle clonus, marked hyperreflexia,
  and myoclonic jerking were documented, and he complained of nausea and weakness. In contrast, the other
  two subjects performed normally in almost all respects.
  On day 9 (650 m), the subject stated he felt “paranoid”
  and that he felt like “I’m going insane.” He
  began to carry a mirror to look at himself to “remind
  myself that I’m not a raving maniac.” He stated that
  colors were enhanced and vivid and he could see
  “unusual” mosaic patterns on the metalwork within
  the chamber. He was unable to comply with instructions
  to enable cognitive function to be tested because
  of extreme agitation and distractibility.[...]
Early on day 9 (650 m), the decision was made to
  halt the dive, but decompression from 650 m is still
  experimental and could not be accelerated. Because the
  decompression process was expected to last as long as 30 days, it was necessary to consider medicating the
  subject more intensively. Since lithium had been shown
  to exacerbate symptoms of the high pressure nervous
  syndrome in animals and the effects of phenothiazines
  at such high pressures were virtually unknown,
  the decision was made to control the diver’s agitation
  with benzodiazepines. Accordingly, diazepam was used in doses up to 120 mg/day. This treatment only
  mildly sedated the subject and provided no real control
  of his behavior.
  The subject’s agitation persisted over the next 14
  days and was marked by decrements in his cognitive
  function and bursts of aggressive paranoia, grandiosity,
  and irritability. By day 24 of the dive (383 m), the
  subject’s irritable and aggressive behavior was becoming
  potentially dangerous and led to the decision to
  medicate with chlorpromazine, up to 300 mg/day.
  Within 48 hours of the beginning of chlorpromazine
  treatment there was dramatic improvement in the
  subject’s behavior. He became relatively calm and
  better organized. He denied having illusions or hallucinations. [...]
Ten days after exiting the chamber, the subject again
  exhibited signs of hypomania including hyperactivity,
  insomnia, and irritability. Lithium carbonate therapy
  lessened these symptoms and was continued prophylactically
  for 6 months. It was then discontinued
  without any recurrence of symptoms.


text:
What is the point of DNA sequencing?
This is a very very basic question. I've looked at methods such as chromosome sequencing and shotgun sequencing. Wikipedia says that:
DNA sequencing is the process of determining the precise order of nucleotides within a DNA molecule
For instance, with methods such as shotgun, we already have the original DNA. If we have access to the original DNA itself, don't we ALREADY know the sequence of nucleotides?
Why exactly do we need to 're-build' the DNA with methods such as shotgun and chromosome walking, when we already have the original DNA available? If we have the original DNA, don't we already have the original sequence of nucleotides?
It makes me think that these techniques for 'DNA sequencing' is sort-of pointless. But, obviously I am misunderstanding something.
Thanks in advance, any simple pointers would be great.

In some sense, this is like saying "what is the point of studying a cell, we already have the cell in our hands." We don't know anything about a cell by having a test tube full of them. This goes for DNA, proteins, RNA, etc. as well. You can purify DNA from an organism without knowing the nucleotides.

No, you don't. Having the DNA in your hand means that you have access to a macromolecule, not more.
Think of the DNA as a book (or a library). From holding the book in your hands, you don't know what the content is. You have to actively read the book to get this information.
Sequencing a piece of DNA is basically the same. Your readout is the sequence of the bases which is essential to understand (or do research on it) a certain piece of DNA. With this knowledge you can see where genes start and end, define introns and exons (for eukaroytes) and so on.

From a bioinformatics point of view: We are given a string of DNA characters (e.g. CTCGAT), then use shotgun to re-create the exact same string? I don't quite understand the point of that when we have the original string available.

@lostguy If you're given a DNA sequence, you obviously don't need to sequence it. But what if you're given a DNA molecule where the sequence is unknown? That is where sequencing is useful.

Oh okay, thanks a lot. that makes more sense. I am doing bioinformatics homework and this type of problem came up. I kept asking myself: "What's the point of this"? But now I see.
Out of curiosity, how are methods like shotgun used practically (if we don't have the original DNA string)? Do we physically randomly cut-up DNA? (Hmm, that doesn't seem realistic)

@lostguy Yes, that's exactly what occurs. DNA is physically sheared into random sized fragments, typically through sonication. Appropriately sized fragments are selected by gel electrophoresis and cloned into plasmids for amplification/sequencing. That's a very general overview, actual experimental protocols will differ and modern (next-gen) sequencing uses different methods.


text:
Why do I breathe out of BOTH nostrils?
After reading the question why do I only breathe out of one nostril I realized that breathing out of both isn't common. I have always breathed out of both, and when I get a stuffy nose, or a runny nose, it's on both sides. If only one side is stuffed, I'll just lay on my side a bit to even it out until I can breathe out of both again. I've always though that was totally normal! What does it mean that my autonomous nervous system is not alternating my breathing?

If you're concerned, talk to a doctor - we can't give you medical advice here. Speaking biologically though, as you can read on the page you linked, we don't really know whether the nasal cycle serves any purpose. The only explanation I've heard is to reduce desensitisation of the olfactory sensors from overstimulation (basically giving each side of the nose alternating breaks). Assuming that, the only effect of a genetic variant that doesn't have a nasal cycle would be a weaker sense of smell.

@Armatus The nasal cycle may also be an artifact of the way our autonomic nervous systems works in bilaterally symmetric animals. Another hypothesis is nasal defense. I included some links in my answer to the one-nostril question, if you're interested. :)

The odds are that you're noticing the equality of patent nostrils in the middle of a changeover, when both are equally patent. Also, the shape of your nose may be permitting the congested side to still be fairly patent. Your nose is doing what it's supposed to be doing (and everybody suffers bilateral congestion during colds, allergies, etc.) If it were not, you would be plagued by dry, painful and bleeding nares (um... are you?)


text:
How does temperature influence the rate of protein degradation?
For computer modeling purposes, I am looking for some referenced quantitative measurements of the effect(s) of temperature on biochemical reactions.
Question
In particular, my question is:
How does temperature influence the rate of protein degradation?
Reducing the scope of my question
My question might be too broad in the sense that there might have too much variance in how different proteins respond to temperature in order to draw in general tendency. If this is so, someone willing to answer may reduce the question to transcription factor, to General Transcription Factor (GTF) or even to TFIIA.

I am NOT looking for..
I am not looking for a theoretical explanation of how temperature influences this process (I have basic understanding of the importance of the activation energy as displayed on a Maxwell-Boltzman distribution and of the Michaelis-Menten equation).
I am looking for..
I am looking for a function that I can plug in my algorithms to incorporate the influence of various temperatures on the process I want to simulate. I want to simulate the average gene network from an average standard eukaryote. For other purpose, I chose parameter values coming from the yeast. A index such as the Q10 would be very useful as well.
Similar already-answered question
Similar questions have been asked and answered here and here

Temperature dependence of rate parameters can be obtained by Arrhenius Equation. $ \frac{k^∗_1}{k_1}=e^{ \left(-\frac{Ea}{R}\Big[\frac{1}{T^∗}−\frac{1}{T}\Big]\right)}$

Catalysed reaction also depend on the structural stability of the catalyst (for e.g. enzymes). Also it is important to know if a reaction is primarily enthalpy/entropy driven. These are more of general comments about dependence of any reaction on temperature.

Yes, I looked at a bunch of equation of the kind (Eyring and Van't Hoff) but it didn't really help me to infer any values for protein decay.

Are you looking at protein decay in eukaryotes? If so then you can see the effect of temperature of proteasome structure. Nonetheless, the rates of degradation for different proteins would be different. Can you state your precise problem because this is kind of very broad.

Thanks for your comments @WYSIWYG. I just need some general effect of temperature on protein decay. The proteins I will models are transcription factors. I am not interested in any single protein but I would like to have some appreciation, an order of magnitude of how globally speaking the temperature influences the rate of protein decay. I need that for simulation purpose, that is why I am not restricted to any protein but would need to know the influence of temperature on the average protein. Please let me know if my question is still too broad or too vague.

I want to simulate the evolution of genetic architecture when after a sudden change in temperature or in an environment that is temporally heterogenous in terms of the temperature.

It is broad in the sense that not all enzymes will be equally susceptible to temperature. You can assume that they are at their optimum. Perhaps you can model the loss of activity due to increased temperature (protein denaturation) as gamma/chi square or exponential function and the effect of low temperature using the chemical thermodynamic equations. But the point is that we don't know if they are at their optimum or not or how each of they may perform at different temperatures.

This comment applies to all the three related questions. Degradation might be the simplest because all you need to worry is about the activity of proteasome (the very basic degradation process not considering different ubiquitin ligases etc). In bacteria you may consider some 'x' protease instead of proteasome and assume saturation kinetics for degradation.

Let us continue this discussion in chat.

This is a general answer for all three of your related questions:

This one
How does Temperature influences the rate of protein turnover?
How is the rate of transcription influenced by temperature?

Since you said:

I want to simulate the evolution of genetic architecture when after a
  sudden change in temperature or in an environment that is temporally
  heterogeneous in terms of the temperature

You should see this paper. They have studied the dependence of growth rate on temperature. This was measured for different organisms (all poikilotherms).
See this figure:

Figure S1 from Dell et. al 2011. PNAS

The unimodal thermal response of radial growth rate of sac fungi (m/(colony*s)). Green and brown curves are OLS regressions to the Boltzmann-Arrhenius model (Eq. 1) for the subset of data that are the rise and fall components, respectively. These components were extracted by the algorithm described in the Materials and Methods. For
  this particular response, the rise was obtained by the algorithm
  through removal of the measurements at the 4 highest temperatures and
  the fall through removal of measurements at the 5 lowest temperatures.
  The blue curve is the best fit to the Johnson & Lewin model (SI
  Methods) (1). Values shown are estimated activation energies with 95%
  confidence intervals for the respective response components. Dotted
  vertical arrows are estimated temperatures for Topt –the temperature
  at which the trait value is optimal–calculated from the direct method
  (red) and Johnson & Lewin model (blue). See SI for more details. Data
  are from Fargues et al. (9)

As you can see, the curve is skewed. The left side of the curve from Topt follows the activation energy model (Arrhenius/Boltzmann). The right side, though they say in the figure legend also fits the model, it seems to me that the phenomenon is somewhat different. The steepness of the curve is perhaps because of denaturation of enzyme active site and therefore a loss of activity. For different enzymes the denaturation kinetics would vary.
I happened to stumble into the author of this paper and that is how I got to know of this work. He seemed to agree that the right half steepness might be because of enzyme denaturation.
Also have a look at this article which is about the temperature dependence of the activity of the proteasome of a thermophile (same principles apply for mesophiles).
Figure 2 of the article:

Normalized Cbz-Ala-Ala-Leu-pNA hydrolysis activity of (filled squares)
  purified native and (filled circles) 70°C heat-purified recombinant (α
  + β) Mj proteasome. To normalize recombinant activity to native activity a multiplier of 1.92 was used. Error bars for the native
  sample represent one standard deviation for triplicate assays.
  Measured temperature errors were ±2°C.

Bottomline (From my comments)
You can assume that the enzymes are at their optimum. You can model the loss of activity due to increased temperature (protein denaturation) as gamma/chi square or exponential function (or the fitted function on the denaturation kinetics) and the effect of low temperature using the chemical thermodynamic equations. But the point is that we don't know if they are at their optimum or not or how each of they may perform at different temperatures.

Nice! I very much appreciate your answer and how much you designed it to apply to my specific needs. Thank you!

Yes, the loss on the right side is because of too high temperatures. Actually the proteins denaturate by too low temperatures or too high pressures as well.


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Why is gastric lavage considered to be helpful only if a patient comes to a hospital within 1 hour of a toxic ingestion?
Why is gastric lavage considered to be helpful only if a patient comes to a hospital within 1 hour of a toxic ingestion? How severe would the effects be if a patient came to the hospital after the recommended 1 hour time frame?

Gastric lavage only washes out ("lavages") the stomach ("gastrium"). Gastric emptying time is generally ~60-120 min, probably on the lower end of that for ingested liquids. After that amount of time, most of the toxic substance will be beyond the level of the pyloric sphincter (i.e. in the duodenum) and not accessible to lavage.
The second question is not possible to answer without some information about what specific toxic ingestion you are interested in knowing about.

Gastric emptying, which used to be well-accepted and seems intuitively
  beneficial, should not be routinely done. It does not clearly reduce
  overall morbidity or mortality and has risks. Gastric emptying is
  considered if it can be done within 1 h of a life-threatening
  ingestion. However, many poisonings manifest too late, and whether a
  poisoning is life threatening is not always clear. Thus, gastric
  emptying is seldom indicated and, if a caustic substance has been
  ingested, is contraindicated (see Caustic Ingestion).
If gastric emptying is used, gastric lavage is the preferred method.
  Gastric lavage may cause complications such as epistaxis, aspiration,
  or, rarely, oropharyngeal or esophageal injury. Syrup of ipecac has
  unpredictable effects, often causes prolonged vomiting, and may not
  remove substantial amounts of poison from the stomach. Syrup of ipecac
  may be warranted if the ingested agent is highly toxic and transport
  time to the emergency department is unusually long, but this is
  uncommon in the US.

ref:http://www.merckmanuals.com/professional/injuries_poisoning/poisoning/general_principles_of_poisoning.html#v1118455

Agreed, but the OP's question was not, "is gastric lavage routinely appropriate?" but rather "why does it need to be done within one hour?". Also, this is formatted as a quotation. If it is, could you provide attribution information?


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Oxidation means inflamation?
All right, I was reading article on nutrition, that focussed on content analysis of pastry-like food product for kids. I have to say that I am not sure this article would pass the imaginary smell test, although it didn't raise any serious red flags, except one.
Among other things, this article said that oxidation means inflammation. It said this in connection with use of rapeseed oil in said product, saying rapeseed oil is less saturated and therefore more likely to oxidize. It then implied, that when this oxidation takes place in the human body, it leads to inflammation.
Now I am no biology, medicine, or nutrition specialist, but if something is still stuck in my head from high school biology, it is that inflammation is the physical manifestation of our immune system fighting off infection, no? Apart of some autoimmune reactions, I don't see how ingesting rapeseed oil could cause inflammation.
So my question is this: is it really possible to safely say: "oxidation = inflammation"? Or is it total nonsense? Or is there some theory that could support such claim and how reliable is this theory? Isn't it just one of those hypothesis disguised as theories?
Said article is in Czech, otherwise I would link it for you.

EDIT: Article link here, you can try it with Google translate :)

You should link the article anyway. You have an international audience for your question. :)

OK I edited in a link :) might be of help.

Inflammation is not only a response against infection. It can also be triggered by any alteration in homeostasis. For example, high-cholesterol diet causes and increase in LDL particles in the blood, which deposit in the blood vessel's walls, causing an inflammatory response that when it gets out of control leads to atherosclerosis. Oxidative stress is associated with inflammation but I would not say oxidation=inflammation.

Oxidation does not mean inflammation. But oxidation can be a cause of inflammation.
Oxidation processes are part of normal cell metabolism (mostly in mithocondria). They lead to reactive oxygen species ($O_2^-$, $H_2O_2$ and $OH-$) which can trigger inflammation via activation of some transcription factors:

NF-κB, AP-1, p53, HIF-1α, PPAR-γ, β-catenin/Wnt, and Nrf2 [1]

The metabolic processes also produce some  antioxidants to inactivate those reactive oxygen species. But the excess of oxidants leads to oxidative stress which seem to be linked with inflammation and even to cancer [1].

rapeseed oil is less saturated and therefore more likely to oxidize

Being "less saturated" I guess it would be better, as studies have found that saturated fatty acid promote inflammation [2], while unsaturated fats decrease the production of inflammatory cytokines and reactive oxygen species [3].

So my question is this: is it really possible to safely say: "oxidation = inflammation"?

NO. By definition, oxidation is a chemical reaction in which a molecule, atom or ion loses electrons [4]. On the other hand, inflammation is a very complex process, a biological response to harmful stimuli and requires cellular interaction [5].

References:

Reuter S, Gupta SC, Chaturvedi MM, Aggarwal BB. Oxidative stress, inflammation, and cancer: how are they linked? Free Radic. Biol. Med. 2010 Dec 1;49(11):1603-16. doi: 10.1016/j.freeradbiomed.2010.09.006. PubMed PMID: 20840865.
Saturated Fatty Acids and Inflammation: Who Pays the Toll?
Alan Chait and Francis Kim
Arterioscler Thromb Vasc Biol. 2010;30:692-693, doi:10.1161/ATVBAHA.110.203984
Supplement: n–3 Fatty Acids: Recommendations for Therapeutics and Prevention:
Philip C Calder
n−3 Polyunsaturated fatty acids, inflammation, and inflammatory diseases
Am J Clin Nutr June 2006 83: 6 S1505-1519S
Wikipedia contributors, "Redox," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Redox&oldid=621442954 (accessed September 13, 2014).
Wikipedia contributors, "Inflammation," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Inflammation&oldid=625272396 (accessed September 13, 2014).

Small addition: Oxidation can be cause as well as an effect of inflammation.


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Name of This Black and White Dove
I spotted this dove in a park. It was foraging among Rock Doves, Seagulls, Ibises and a few others.
It appears similar to Pied Rock Doves, but I am not certain if this is correct.

Any idea what the name of this dove is?

It's a pied version of the Rock Pigeon (Columbia livia), aka Rock Dove. According to the Cornell Lab of Ornithology, the pied variety of Rock Pigeon is one of any color that has splotches of white on the body. I think that fits your bird very well. It's not a different species, but just one of several color varieties of Rock Pigeon.
If you are not familiar with Cornell's site and enjoy birds, their All About Birds site is very nice.

Also called Piebald (Pied for short as mentioned above.) It's a pretty common mutation among different animals. Dogs, deer, and snakes such as the ball python exhibit this trait. So yeah, your bird is still a rock dove.

 the bird above is a pigeon, local breed of pigeon in African, just like any other pigeon, it has all features a pigeon has! It was got as a result of mating a brown male pigeon with a black white colored female pigeon, All local breeds from Africa!?

Welcome to Biology.SE. You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without that support, your answer is indistinguishable from opinion and thus is inappropriate for this site. ——— Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then delete or edit your answer accordingly.


text:
Help identify this awesome climbing plant with velcro like stem
I got this plant sprouting in my window box this spring. Starting from a single seed, it has grown into an impressive array of branching climbing vines, reaching 6 feet tall. The stem turned red as it matured. The most awesome feature of this plant is that the stem is covered in micro hooks that cling to everything. I've seen it cling to a paint on a metal gutter pipe I can think of these hooks as velcro or gecko feet.
Can someone help me identify this plant?

climbing vine
stem is covered in tiny hooks that are very clingy
grows to 6 feet tall
stem turns to red as it matures
segmented leaves
leaves grow to palm size
new leaves sprout from stem where old leaves were connected
 -

In what general region of what country is this plant? Do you know if it is native or if it cultivated? Also, check in with Gardening and Landscaping.SE as someone there may be able to help you.

I don't know its name, but kill it now! Some bird dropped it. This plant appeared in my yard five years ago and now it's choking everything. It is the most invasive weed I've ever seen.

If you found this plant in flowering condition, plz upload picture of its inflorescence and flowers in close up

I think this might be Japanese hops. Well, what I have in my yard is Japanese hops.

As I said, it's horrible.
Description and Biology:

Plant: herbaceous annual, twining, shallow-rooted vine that can climb to heights of ten or more feet with the help of rough-textured stems covered with short, sharp, downward pointing prickles that can be very irritating to the skin.

Leaves: leaves are rough-textured, paired, simple, palmate (like a hand) with typically 5-7 lobes; leaf margins are toothed.

Flowers, fruits and seeds: flowering occurs in July and August; male and female flowers are borne on separate plants; male flowers are very small, greenish yellow and occur in branched panicles; female flowers are in pale green, plump, drooping, cone-like structures with overlapping scales that become ‘hops’; hop scales and the seeds are covered with yellow glands; seeds are about 1/8 in. in diameter, roundish with a blunt tip, and light brown with darker specks; seeds mature through September.

Spreads: by seed which begins to germinate in early spring, but new plants may continue to emerge as the season progresses if sunlight and moisture are available; seeds are dispersed by animals (including people), machinery and floodwaters.

Look-alikes: native common hop (Humulus lupulus) looks very much like Japanese hop but it is usually 3-lobed or unlobed; native bur cucumber (Sicyos angulatus) lacks prickles, has tendrils, and the leaves have much less pronounced lobes.

Prevention and Control: Do not purchase, plant or transplant this species.

@Alex Stone - sorry it took me so long to edit with more info. Really, trust me, kill it before it sets seed (which it's doing right now.)

Thanks for the description. The plant never had a chance to flower and is mostly dead now. I will dispose of the rest of it.

The Velcro Vine, known variously as Cleavers, Goose Grass and Bedstraw is botanically known as Galium aparine. New spring growth can be juiced or eaten in salads or on sandwiches. It can be used to stimulate and decongest  the lymphatic system and as a diuretic to remove excess H2O.

Can you add sources and an identifying image of the species so people can background read on your answer?

That plant clearly is not galium aparine. Leaf morphology is completely different. Not sure what it is, but it grows as an invasive weed in my garden in Burlington, VT. Please DO NOT try to eat it.

This is not cleavers. Not by a long shot!


text:
Effect of extremely hard water on marine life?
When researching water quality standards, I found that a minimum and maximum was set for water hardness. Several sources also state that water can in fact be too hard. The question is how does hard water harm marine life? I understand that it is required to reduce the toxicity of Hydrogen ions and other trace metals, but cannot find anything concerning the effect of water that is too hard.

I don't have any direct adverse effects of extremely hard water but marine organisms have quiet specific ranges of hardness according to http://www.cichlid-forum.com/articles/hardness.php

Wiki Found relatively easily on wikipedia. Affects cystein residues in proteins, binds to DNA backbone, affects prostetic groups, etcetc.

You should define hardness in your question. There a few types of hardness defined. In general, increasing hardness is a result of increasing pH and vice versa; which means hardness (increasing from another reason) may also lead to a n increase in pH. marine water is not just a simple composition of salts... edit for dummies added.

Water hardness refers to the concentration of calcium and magnesium ions in fresh water. Has nothing to do with pH. In salt water, these ions are at much higher concentrations and thus water hardness makes no sense in salt water.

Hard water helps in direct and indirect ways.
Indirectly, hard water plays an important role in regulation of pH. Respiration and other physiological activities release substances into water that change the water pH and the ions that cause hardness act as buffers and help maintain pH.
Directly, they determine the ease with which osmoregulation occurs. The harder the water, the lesser the influx of water. So the fishes act like an open system and are influenced by the surrounding water.
There are very few fish who absolutely need soft water to survive.
Since your pH and hardness are pretty low, it allows you to raise multiple fish from South America. You could do tetras, dwarf cichlids and New World cichlids, Plecos as well.
Potentially discus and altum angelfish as well if you're up to the huge challenge.
However, livebearers will not tolerate this type of water. That goes the same for African cichlids.
Otherwise hard water is completely fine for marine life and other aquatic species.
Link
Link
Hope this information helped!
-Sartoaster

If you look at the Wiki text on Hard Water, Marine hard water is not mentioned once. That's because it's a term used mostly to qualify freshwater.
Sea water doesn't vary alot in the oceans, only in inland seas and near estuaries and glacial melt, it's called brackish water, brine, not soft seawater.
Sea water which undiluted is called salty, highly saline, high salinity, water, not Hard Seawater.
Marine life isn't affected by the stone type mineral content of the seawater as much as by the highly reactive salts, both sodium and chloride are very harmful to life compared to most stones a the less soluble mineral salts.
Seawater contains a lot more calcium generally than most river water, even though some river water can be completely saturated in calcium and have very high PH. Some fish can adapt to a wide range of soft water hardness, and some fish can adapt to very salty water, but most fish are specialists who don't live in wildly varying ecosystems, only in the sea and in constant softness freshwater.
Read some aquarium chemistry experiments. they are aquariumabulous and will give you a lot of knowledge about marine biogeochemistry. It's pretty interesting to look at any pond and river and plant and know what chemistry it has, what it needs, and the processes changing it, it's quite simple to learn too, just learn some basic experiments and guides on water and pedology organic and mineral reactions and biology.


text:
The evolutionary process in bird wings, especially with regard to winglets
In this answer on aviation.SE a comparison is made between the shapes of airplanes wings and the shapes of birds wings. It concludes with the following remark:

After all, no bird has winglets. Not a single one.

In addition to be a disputable assertion (the wing tips such as the eagle's could be considered akin to a "winglet" of the fanned type) this has stricken me as based on a quite wrong assumption of how evolution works.
I tried to make my point in the comments only to reach this point:

So you consider evolved wings as not mature. The winglet modification is just waiting to happen? Nature never tried it, in >100 million years of biological flight? Could be, yes. But is extremely unlikely. That settles it for me.

Am I correct in identifying this in a wrong interpretation of the evolutionary process?
As I understand the evolutionary process, the current bird wings are not necessarily perfect, are simply the version that so far has given the best advantage. The lack of "winglets" in birds cannot then be explained simply by assuming that they do not improve the wing, but it could also be that there has never been an evolutionary pressure to evolve them or that since birds flap their wings they would be detrimental instead of beneficial or whatever other reason.
Is my understanding of the evolutionary process correct? if not, where am I at fault?

As a small addendum, another user cited the "Spandrels" in comparison to the above debate, could someone explain what could have been the meaning of the comparison?

Planes have wing dimensions and velocity at least an order of magnitude greater than birds, so the physics is different. In order to make a like-for like comparison, the plane wing would have to be placed in a wind tunnel with a fluid of much higher kinematic viscosity than air, which would supress wingtip vortices considerably. For more info google Reynolds Number.

there is always a evolutionary need, there is competition for food, escaping from predators quicker etc. if its advantageous and there is any natural selection, theres a evolutionary need.

I looked up winglets so I had context for this answer. I'm interpreting winglets as the vertical tips at the end of airplane wings. If so, then you are correct. The spread primary feathers of soaring birds like eagles function as winglets (Tucker 1993). Airbus has a biomimicry web page devoted to some of the biological designs, including winglets, they incorporated into their airplane designs. Some studies suggest airplant winglets do increase efficiency (e.g., Hossain et al. 2011), but there is still some debate.
From the aviation.se answer:

Look at birds: They use two different wingtip designs. I guess we will both agree that those designs are mature after millions of years of evolution. And still there are two distinct wing tip shapes: One is the "fingered" wingtip with large, spread-out feathers, and one is the pointed tip you find from seagulls to albatrosses. Why is there not one, mature design?
This has to do with the environment they are used in. Seabirds fly in an unobstructed environment with steady winds and need to stay aloft for longer duration. All other birds have to cope with trees obstructing a straight flight path and gusts from hills, or those trees. They need to maneuver quickly and cope with gusty winds. This is helped by a reduced span and the possibility to fold the outer wing in or fan it out in an instance. Hence the fingered wingtip.

Although bird wings do tend to match his descriptions, he is not correct that these correspond entirely to ocean-going birds vs all other birds. Many inland birds have pointed wings, including swallows, nightjars, swifts, and falcons.  Some seagoing birds have winglets, such as pelicans and cormorants.  While wing type is shaped by natural selection in a given environment, it also reflects the evolutionary history of the birds.
There is not "one, mature design" because wings many different shapes and sizeshave evolved under varying selective pressures. For example, the long pointed wings of ocean-going albatrosses are excellent for gliding with little energy expenditure but they are lousy for taking flight or for landing. Other wings are shorter and broader, providing greater maneuverability in the woods. In this sense, there is no perfect wing. Each has evolved for different evolutionary reasons.
The main question
From the aviation.SE thread:

the fact that no random mutation has produced a winglet* in birds is in no way a demonstration that airplanes do not benefit from them, there is no logical relationship. [*even though the "fanned" design you refer, such as the eagle's, can be considered a form of optimum winglet] –  Federico

followed by this response:

So you consider evolved wings as not mature. The winglet modification is just waiting to happen? Nature never tried it, in >100 million years of biological flight? Could be, yes. But is extremely unlikely. That settles it for me...

Federico is correct. The basic wing type was set long ago as birds evolved from non-avian dinosaurs. Comparisons of modern bird wings with fossils suggest that the basic structure of bird wings has not changed very much since then. The current structure may be the best that has evolved by natural selection so far but that does not mean the wing cannot be improved further. As you noted, mutations could occur in existing genes that lead to further improvements of the structure and function of the wings. If those mutations never occur, then the improvements won't occur. This is one constraint of the evolutionary process (Hoffman 2014). Natural selection can only work with existing traits, using existing genes and genetic variation.
Another consideration is that wings for powered flight have evolved independently at least four times (birds, bats, insects, pterosaurs). Each time, a different type of wing evolved. Is one better than another? Bat wings have aerodynamic properties very different from birds but function very well for bats (Hedenstrom et al. 2009). Along the lines of your argument above, each wing type perhaps is (or was for pterosaurs) optimum given the environmental circumstances and evolutionary constraints. That doesn't mean they could not be improved.  If a wing evolves again in some organismal group in the distant evolutionary future, odds are very good that the structure will be different from those that have evolved so far. Perhaps that wing will be even more efficient than current wings.
Spandrels

Another user cited the "Spandrels" in comparison to the above debate, could someone explain what could have been the meaning of the comparison?

The use of "spandrels" in evolutionary biology stems back to a well-known paper by Stephen Jay Gould and Richard C. Lewontin called "The spandrels of San Marco and the Panglossian paradigm: a critique of the adaptionist programme", published in 1979 (Gould and Lewontin 1979). A spandrel is the space that forms between two adjacent arches or between an arch and a rectangular shape.  The spandrel emerges as a result of putting two arches next to each other and filling the space. It results from the joining of two arches. It was not specifically designed as part of the arch. Gould and Lewontin claim that evolutionary biologists are too quick to assign adaptive value to every trait on an organism, and argue that not every trait results directly from adaptation. Instead, they say, the trait may be a "spandrel" that emerged as a by-product of other traits. The "spandrel trait" has no adaptive value in and of itself.
The use of spandrels in the comments of the aviation discussion is not clear to me. Clearly, the person intended the evolutionary meaning, mentioning the paper by name. But I cannot tell at all the person's intent.
Edits: Incorporated comments by @Federico and @Andrew - thanks. I corrected horrendous typos and attempted to add clarity.
Citations
Hedenstrom, A. et al. 2009. Bird or bat: comparing airframe design and flight performance. Bioinspiration & Biomimetics 4 015001. doi:10.1088/1748-3182/4/1/015001
Hoffmann, A.A. 2014. Evolutionary limits and constraints. Pp. 247-252. In: The Princeton Guide to Evolution, Princeton University Press, USA.
Hossain et al. 2011. Drag analysis of an aircraft wing model with and without bird feather like winglet. International Journal of Mechanical, Aerospace, Industrial and Mechatronics Engineering 5: 30-35.
Tucker, V.A. 1993. Gliding birds: Reducion of induced drag by wing tip slots between the primary feathers. Journal of Experimental Biology 180: 285-310.

thanks for the answer. As for the efficiency of the winglets, it severely depends on the constraints and is debated. And turbulence is an unavoidable byproduct of lift generation, so I guess birds will neve fly "wake-free".

@Federico I certainly don't pretend to understand the intricacies of aerodynamics. :) It's interesting how geese have evolved flying in a V formation to take advantage of lift provided from individuals closer to the front of the formation.

I was not pretending you to, I simply pointed that out so that you can eventually review your answer to remove debatable points. I am aware of the formation flying of migrating birds, but the question/dabate was more focused on solitary ones. As for the "mature" remark, I guess it uses it in lieu of "whatever will happen, the shape won't change much" or "the current wing shape is the best possible one".

"...the long pointed wings of ocean-going albatrosses are excellent for gliding with little energy expenditure but they are lousy for taking flight".   ...and landing, apparently.

@Federico I've modified my answer in light of your (and other) comments. I've also tried to add clarity and remove redundancy.

One point you never mention is that birds are different to airplanes in how they are propelled. Airplane wings are completely fixed and don't flap. Would airplane-style winglets work on "flappy" wings? I suspect not.

@romkyns I agree that a fixed airplane winglet would not function well on a bird wing. It doesn't matter because birds achieve the same effect with the spread primary feathers at the wing tip. Besides, anything more than a stork with a jet engine is a scary prospect! :)

The logical assertion "winglets have not happened in a long time, therefore they are not advantageous" is incorrect.
It is possible for an advantageous trait not to evolve even when advantageous, if there is no "path" to it. The trait only occurs gradually, in small incremental steps. If intermediary steps are harmful, the trait will not occur, even if the end result would be beneficial.
(now, this does not say anything specific about winglets, just about the general argument)

One famous example of an "imperfection" that keeps existing despite a better solution being available can be seen here: https://www.youtube.com/watch?v=cO1a1Ek-HD0 (beware, video features dissection of a giraffe)
There is a nerve that connects the brain to the larinx. In fish, this nerve is somewhat short, but in the giraffe, it is enormous. The interesting thing is: the points this nerve connects are very near, even on the giraffe.
What happened was the the nerve passes below an artery. For fish, this is irrelevant. But, as larger mammals evolved, the nerve had to gradually grow to a bigger path. Evolution could not do the "reengeneering" to have a smaller nerve, because there was no immediately advantageous way to do it.

thanks, this is also the kind of review I was looking for.

It is also possible that airplane-style winglets hinder more than they help on wings that need to be flapped.

There are two possibilites with evolutionary processes: The development either never went into this direction or it brought no advantages. Besides this two possibilities the claims from the other forum are wrong. Birds (not all of them though) do have winglet-like structures. If you look at big birds, you can see feathers on the end of the wings looking like this:

These feather fulfill exactly the same purpose here. Some more information can be found here and also in the Wikipedia.

The Harun Yahya site is not the best site for reference. While his overview is correct, he has very strong creationist beliefs and very strong anti-evolutionary beliefs. He attributes to the design of bird wings to his god, not evolution.

Ups. Thanks for noticing. I will look up another one.

For the sake of openness, Chris, I did not intend to tell you what you should or should not include in your answer. That is up to you. I have strong opinions about including creationist ideas in evolutionary discussions though and that slipped through. I hope you accepted my comment in the positive spirit intended and not as a criticism.

@MikeTaylor Don't worry. I welcome critic to my answers and comments - I don't see this as something negative but as a chance to get answers better or learn something. And I don't like to include creationism in evolution either as it is simply unscientific. So yes, your comment was very welcome since this simply slipped through.