text:
How do animals lose heat?
I remember being told as a child that dogs stick their tongue out to stay cool, because they can't sweat like us. This made sense to me.
But only a couple of days ago I suddenly thought: What about all the other animals?! I mean, I don't see a cat or a horse putting their tongues out, and yet I don't see them sweating either. How do they lose heat? How do different kinds of animals lose heat?

There are a number of ways, which are briefly summarized here. I also recommend reading this nice Scitable article on thermoregulation. It is not too technical. Felines do pant when they get hot. Horses do sweat. Jackrabbits can enlarge the blood vessels in their large ears to eliminate excess heat. Bird use a process called gular flapping, which is similar to panting of dogs and cats.  Animals can move into shaded areas.  The possible mechanisms are many.


text:
RNA-Seq library construction challenges: the biases of RNA fragmentation vs cDNA fragmentation
I recently watched a presentation on RNA-seq that covered some of the choices one can make along the way, and I didn't fully understand one of the choices in particular.  Near the beginning of the process, you can choose a fragmentation method (e.g. RNA: nebulization, hydrolysis; cDNA: sonication, Dnase I treatment). Each fragmentation method is biased in its own way, and the goals of the study may influence the choice of method.
I didn't fully understand the reasons for the characteristic biases (how do they happen?), and when to choose one method versus the other (which methods work best for which goals?).  Put another way, what are the mechanistic explanations for the characteristic biases that result from each method, and what is the significance as far as downstream processing and associated challenges?
Edit:
The heart of this question is about fully understanding the particular choice of when and how to fragment.  The reason I have not accepted an answer, yet, is that the answers provided so far address the mechanism part of the question, but not the ultimate reasons for choosing one versus the other.

The biases depend on fragmentation methods. DNA is usually fragmented physical shearing. (nebulization/sonication). The overrepresentation is because of the ends being more stable (easy to break a stick from the middle). There are other kinds of fragmentation methods (thermal-catalytic) and there the biases are different (modern kits claim that they have very less bias)

Bias can happen at other levels too- reverse transcription, priming, amplification etc

Good question, a lot of this is still being figured out. Here's what's known so far:
Fragmentation methods based on restriction enzymes aren't random.
Reverse-transcription performed with poly dT-oligomers, which bind to the 3' poly-A tails, is strongly biased towards 3’ end of transcripts.
Reverse-transcription with random hexamers results in an under-representation of 3’ ends. This is from the reduced number of priming positions at which the reverse transcriptase enzyme can start cDNA synthesis.

messenger RNA has a poli A tail at its 5´ end. thus when the poly-dT hybridize the mRNA in the reverse transcription the cDNA will carry this poly-dT at its 3`end. Thus, as reverse transcription will always start at the 3´ and of the mRNA its is more likely that this region is better rev. transcribed. Bigger the mRNA is bigger will be this concern.
About the bias related to RNA fragmentation I don't know, I can make the guess that both ends are more lost due to the fragmentation itself
watch this video from life technologies
http://www.youtube.com/watch?v=0MJIbrS4fbQ

source: Stack Exchange

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

sort: votes


text:
Cross-integration of puma subspecies populations
A major concern of conservationists  in south Florida is the population of native Pumas, the Florida Panther.
Until recently, it was thought that the Pumas were a genetically distinct subspecies, but some genetic studies have shown that they may not be, and so their subspecies status is disputed.
If the population of Pumas in Florida is genetically distinct from other populations in North America, is there any precedent for using a distinct subspecies to bolster populations of an endangered subspecies?
If the population of Pumas in Florida is not genetically distinct from other populations in North America, would there be any behavioral issues (hunting, etc.) in animals brought from other biomes to south Florida, either as adults or offspring of transplanted adults?

The study you are referring to is probably a study by Culver et al. (2000). They performed a genetic analysis of 315 individuals of the American Puma (Puma concolor), also known as the cougar. Their thorough analysis (especially for the late 1990s) showed that the Florida panther and the western North American pumas were the same subspecies, Puma concolor couguar (note the proper spelling of the subpecies). All individuals north of Nicaragua are this subspecies. From Nicaragua south into South America, they recognized five additional subspecies of American Puma.  The distribution of the subspecies, as well as the sample locations, are shown in the figure below, taken from Culver et al. (2000).

Notice in the figure above that the American Puma used to occupy most of North America but now is restricted to the the region west of the Rocky Mountains, except for the isolated Florida population. Because the genetics of the Florida Panther and the western American Puma are effectively the same, individuals from the western US can be introduced into southern Florida. This idea was first proposed (to my knowledge) by Hedrick (1995) as a conservation measure by introducing genetic variation and reduce the effects of inbreeding. In that same year, eight female pumas were transferred to Florida from Texas, which had the population of panthers closest to Florida. Introducing pumas from outside of Florida has pros and cons, reviewed by Pimm et al. (2005), from both a short-term conservation perspective as well as long-term evolutionary perspectives.
Several years after the Texas pumas were introduced, Johnson et al. (2010) performed a genetic analysis of the Florida population. They showed that the Texas females were indeed reproducing in Florida. The release of Texas panthers did introduce more genetic variation into the Florida population and reduce the effects of inbreeding. The net effect was that more Florida panthers were surviving. The downside is that habitat loss continues and the effective population size is still very small. That means that inbreeding is still very much an issue.
The studies to date have focused on genetic integration and overall recovery due to the introduction of genetic variation but I did not find any studies that reported any behavioral changes since the 1995 introduction. Given that it was only 8 females, I would not expect any significantly different behaviors to be introduced into the Florida population.
Introducing more genetic variation from Texas (and perhaps populations farther west) may be helpful but ultimately preservation of habitat and improving ability of individuals to move among available habitat fragments via corridors is necessary to protect the species long term.
Citations
Culver, M. et al. 2000. Genetic ancestry of the American Puma (Puma concolor). Journal of Heredity 91: 186-197. (open access)
Hedrick, P.W. 1995. Gene flow and genetic restoration: The Florida panther as a case study. Journal of Conservation Biology 9: 996-1007.
Johnson, W.E. et al. 2010. Genetic restoration of the Florida Panther. Science 329: 1641-1645.
Pimm, S.L. et al. 2005. The genetic rescue of the Florida panther. Animal Conservatation 9: 115-122. This issue of Animal Conservation has a few articles dedicated to the Florida Panther.

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


text:
Vitamins located closely under the peel?
I came across an old saying (I would even call it a myth) that vitamins are concentrated under (or close under) the peel of apples or potatoes and
other fruit. This implies that they are more healthier when not pealed. My question is: Is this true? And does it make sense to concentrate important
substances there, where they might get lost when the peel is damaged?

There are some vitamins in the peel of some fruits/vegetables. The color of many fruits and vegetables is the result of high carotene concentration in the peel. $\beta$-carotene is converted by the human body into retinal, which is a form of vitamin A [1].
Another example is vitamin C. Guava and citrus category fruits contain high amounts of ascorbic acid in their peel and orange's peel contains greater amounts of vitamin C than its juice [2].
There are also other compounds in fruits peel like B vitamins and minerals [2].

This implies that they are more healthier when not pealed.

In most situations, yes. The peel can absorb insecticide sprays and can also contain high amounts of fibers which can cause indigestion [2]. The peel can contain allergens [3].

And does it make sense to concentrate important substances there, where they might get lost when the peel is damaged?

Yes. For example carotene plays a role in photosynthesis [1]. Fibers improve mechanical properties of the peel, thus protecting the fruit.

References:

Wikipedia contributors, "Carotene," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Carotene&oldid=625015773 (accessed September 14, 2014).
Umesh Rudrappa, www.nutrition-and-you.com. Fruit peel nutrition facts
Wikipedia contributors, "Peel (fruit)," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Peel_(fruit)&oldid=624708837 (accessed September 14, 2014).


text:
Did spiders respond to light for building webs before artificial light was invented?
I have noticed that during summer, beautiful spider colonies grow wherever a strong light is:

I'm wonder whether spiders evolved to seek naturally lighted areas where they build nests (before artificial lights) or if they always had the ability to seek places full of juicy insects - and in cities this ability just leads them to lights.

Here's a null hypothesis based on perception bias: perhaps spiders build their webs all over, but they're a lot easier for us humans to see when they're built next to lights. Consider, for instance, the days when the dew and light is just right and suddenly the forest seems to be full of spider webs – they were there all along, but just harder to perceive. I'm not saying your observation is wrong, necessarily, just offering a null to compare your observations against.

Well, the webs are here when it's day too - still the concentration is around lights. You can see the lights being all dirty because of them.

New Answer, following discussion in comments below.
Spiders are capable of choosing habitats based on the specific requirements of the species (reviewed by Riechert and Gillepsie 1986). Spiders move within and among suitable habitat for a number of reasons, including damage to existing webs, and life history changes that require new habitat types. They point out that spiders are probably choosing the proper habitat based on various cues from the habitat. How the spiders respond to the cues would have been shaped by natural selection. The specific cues used will vary among the different species of spiders but may include wind speed and direction, thermal regime (which affects dehydation foraging time), odor cues, density of competing spiders, and more. The many options are reviewed by Riechert and Gillepsie, which is freely available and not too filled with technical jargon.
Many species of spiders do select their habitat based on prey availability. Gillespie (1987)  lists a number of references. She also studied the long-jawed orb weaving spider, which lives along streams and rivers.  She found that this spider tends to build nests in open areas near water, which prevented dehydration, but the exact site chosen was determined by prey availability. Enders (1973) studied a different orb-weaving species. He found that the juveniles were most often in densely vegetation areas but that the adults were in more open areas at the edges of woods. He suggested that web site selection of adults is driven by light.
Heiling (1999) performed an interesting study on a nocturnal orb-web spider. The spider lives near the water so it will sometimes build its orb webs on the bridges crossing the water. She found that more spiders build their webs near the lights on one particular bridge compared to unlit parts of the bridge that were otherwise built the same. She found that there was more insect activity around the lighted area (no surprise there) and that the spiders that built near the lights caught more of those insects compared to the spiders that built away from the lights.
Perhaps the most interesting result is when she studied the behavior of these spiders in the lab. Spiders that were born and raised in the lab preferentially went to the artificial light source. These had never before been exposed to the artificial lights. She argued that the light-seeking ability of the orb-web spiders she studied is genetic.
These studies suggest that light may have functioned as a visual cue for web location long before humans lit up the night sky with house and street lights, at least for spiders that build webs in open areas. Spiders may identify open areas by light cues (lighter vs darker), perhaps along with other cues such as air movement and humidity. Lighter areas would presumably be more open and thus favorable to large numbers of flying insects. Natural selection would favor spiders that responded to light for web construction. Artificial lights may present a very strong visual cue that attracts spiders, as well as insects.
However, other cues such as olfactory cues (mentioned by Riechert and Gillepsie 1986) may attract spiders. If insect prey are found in high abundance in open areas or near artificial lights, then you would expect higher concentrations of chemical odors emitted by the insects, thus drawing more spiders.
Clearly, more studies similar to that of Heiling (1999) but across a broader range of web-building spiders are necessary to determine whether many web-building spiders are responding to light and if the response is genetically determined.
Citations
Enders, F. 1973. Selection of habitat by the spider Argiope aurantia Lucas (Araneidae). American Midland Naturalist 90: 47-55.
Gillepsie, R.G. 1987. The mechanism of habitat selection in the long-jawed orb-weaving spider Tetragnatha elongata (Araneae, Tetragnathidae). Journal of Arachnology 15: 81-90.
Heiling, A.M. 1999. Why do noctural orb-web spiders (Araneidae) search for light? Behavioral and Ecological Sociobiology 46: 43-49.
Riechert, S.E. and R.G. Gillespie. 1986. Habitat choice and utilization in web-building spiders. In: Spiders: Webs, Behavior, and Evolution (W.A. Shear, ed). Stanford University Press, California, USA.
Legacy answer
Spiders evolved long before street lights were invented. The oldest known spider fossil dates back to between 374-380 million years ago (Coddington and Levi 1991.  Street lighting of any type only goes back a few centuries. So, spiders were spinning webs long before humans evolved, and before we humans began lighting our streets and homes at night.
The spiders are simply taking advantage of the situation. The lights draw insects, the food for the spiders. Webs constructed near light sources may catch more insects than webs constructed away from lights.  Could this affect the current or future evolution of spiders? Perhaps. The spiders that build webs near the lights may get more food, which allows them to obtain more energy, and potentially produce more offspring. This would increase their fitness relative to spiders that do not build webs near lights, which could lead to evolutionary change occurring over the next several thousands of years. However, it may be that so many insects flying around the web end up damaging the web much more often than the spiders away from the lights, so the spiders near the light expend much more energy maintaining the web and removing insects they don't eat.  This is one extremely hypothetical example (of many; see comments) to illustrate the point. We can't actually predict what evolutionary changes might occur, or even if they will occur.
Some of the hypotheses stated in the comments below could be tested to determine whether natural selection is possibly occurring on spider species that build near lights, or if the observation is simply observation bias as noted by @Oreotrephes.

Do you think we can assume no bias in our observation (the potential bias is: we see the webs that are held in the lights much better than the others)?

Assuming no bias, do you think that 1) spiders construct their webs where there is a source of heat because they have evolved in order to construct their webs in these places (as warm temperature attract insects) (you seemed to say no but I am not sure) 2) spiders construct their webs all over but those that are poorly located die 3) spiders construct their webs all over but when they starve they move 4) spiders observe spots of high insect concentration before constructing their web. All of these explanations would explain why there are more webs in the light.

@Remi.b I made no assumptions. I took the question solely at face value. You and Oreotrephes are correct about the potential for visual bias. My hypothetical example was based on spiders building near lights because insects are attracted to light. Your hypotheses are testable but I'm skeptical about whether spiders can scout out spots of high concentration in advance of web building. It's also possible some spider species are themselves attracted to light but benefit from the insect concentration.

Oh my... I didn't ask why spiders build webs near lights! It's damn obvious. I was only curious if they can find a place where flyer insects appear or if their instincts have changed to seek lights automatically - because they're definitely going to attract flying insects.

@TomášZato I misunderstood. Evolution is mentioned in the question and question title. It's still not clear to me what you mean by changed. Do you mean changed due to natural selection?  Changed since when? I wasn't trying to answer why* spiders build near lights. That was just a hypothetical example. I can tell from you question that you understand spiders are feeding on insects. I think we had a miscommunication. :) Perhaps you could edit and clarify your question?

Yeah, I think it's a problem for me to write this question properly in english. I'll try to clarify with another comment and after that I'll take my time rethinking the question. I was asking, whether spiders evolved (due to the natural selection) to seek lights where they build nests or if they always (that means before artificial lights) had the ability to seek places full of juicy insects - and in cities this ability just leads them to ligts. I know, it's almost no difference, but it interests me and I don't know how to find the answer myself.

@TomášZato OK, I think I understand your question. I'll begin working on a new answer.

@TomášZato I've updated my answer to hopefully match the question you were actually asking. I also edited your question somewhat, using part of what you wrote in a comment above. If you don't like my edit or want to use your own changes, you can still edit your question and undo my changes.


text:
Which process is needed to complete male reproductive development?
In order to properly complete male reproductive development:
A. primordial germ cells must begin Meiosis I in utero.
B. Sertoli cells must produce testosterone.
C. Dihydrotestosterone must masculinize Wolffian duct derivatives
D. the paramesonephric ducts must degenerate
E. the metanephros must form the genital epithelium

My attempt:  I think the answer is C because testosterone turns into DHT which then masculinzing the wolffian duct.  Other people I am studying with claim the answer is D (which is true) except that I dont think the loss of the paramesonephric duct is needed to complete male repro development.

Regarding option C:
Although it is correct that testosterone is converted into DHT, it is the former, not the latter, which is responsible for differentiation of the mesonephric (a.k.a. Wolffian) ducts:

Between 8 and 12 weeks, the initial secretion of testosterone stimulates mesonephric ducts to transform into a system of organs—the epididymis, vas deferens, and seminal vesicle—that connect the testes with the urethra.*

DHT (dihydrotestosterone) is produced in the Leydig cells by the 5α-Reductase enzyme. It is required for induction of the external male genitalia (urethra, penis, and scrotum) and prostate from the embryonic ureteral groove, and for testicular descent into scrotum.
Regarding option D:
Sertoli cells secrete Anti Müllerian Hormone (AMH), which causes degeneration of the müllerian (a.k.a. paramesonephric) ducts between weeks 8 and 10.  It is normal to speak about degeneration of the müllerian ducts as a defining aspect of male embryology, and thus I believe answer D is correct. Your point is taken, however:

Nevertheless, small müllerian duct remnants can be detected in the adult male, including a small cap of tissue associated with the testis, called the appendix testis, and an expansion of the prostatic urethra, called the prostatic utricle.*

*Larsen's Human Embryology , Fourth Edition. Chapter 15: Development of the Urogenital System. pp 479-541.
Copyright © 2009 by Churchill Livingstone, an imprint of Elsevier Inc.


text:
Why do baby mammals tend to play?
Why do babies of any mammal tend to play ? From humans to small dog pups, cubs of a lion, baby bears, etc.
*I am not sure if the tag I chose is correct or not. Please correct me if I'm wrong.

Because it is a way to try things and learn.

Play has been described for some birds. See also here.

If you find the book Sociobiology, by E.O. Wilson, it writes an entire section on the subject. It seems to be a preparation for adult life, simulating behaviors necessary for an adult (e.g. fight, hunt, etc). Though I don't know why it would have evolved more in mammals...

Related: Why does a housecat (or other predator) play with it's food before killing and eating it? Does it make the food taste better?


text:
Kinesiology Tape Benefits
Recently, kinesiology tape has become popular, especially in CrossFit. I have also noted its' use in the NFL, and I want to say Tennis as well.
What beneficial effects does this tape offer our bodies (muscles, joints)?  Is there any definitive proof of its' benefits? Can there be negative effects? I don't foresee any, but if it does something to your body, I could see a possibility of prolonged use causing some kind of alternate effects.

This is in the discussion for quite a while. I have found no scientific studies which back the claims of kinesio tape. A review article (from which the quote below is taken) found no clinically important results which support the claims of the tape. The results about range-of-motion were inconsistant and it is not clear if the changes found were beneficial or not. They state:

KT had some substantial effects on muscle activity, but it was unclear
  whether these changes were beneficial or harmful. In conclusion, there
  was little quality evidence to support the use of KT over other types
  of elastic taping in the management or prevention of sports injuries.
  KT may have a small beneficial role in improving strength, range of
  motion in certain injured cohorts and force sense error compared with
  other tapes, but further studies are needed to confirm these findings.

The study can be found here (links to the PDF):

Kinesio Taping in Treatment and Prevention of Sports Injuries

Other (also critical) studies are these:

A systematic review of the effectiveness of kinesio taping for
musculoskeletal injury.
The clinical effects of Kinesio® Tex taping: A systematic review.

The problem with these studies is that they are obviously not rigorous enough to make clear statements if KT is beneficial or not. Or (and this is also very possible) that the effect which is claimed to be there does not exist. Besides this, a placebo effect exists very well, since there is an intervention and also something present on the athlete.
There is now a new study avalaible which is blinded and placebo-controlled. This study finds no benefits for Kinesio Tape above a placebo. The study can be found here, there is also a summary available here.

In response to your answer, I have added one more piece to my question. Please see my edit. Your citation confuses me a little bit, and perhaps my confusion isn't directed towards you, but towards authors of that piece. How is it unclear if changes were beneficial or harmful?

@OverMind I have expanded my answer.

This may be opinionated - but do you think more quality tests will come in the near future? I am wondering if its' placebo effect has instilled itself into athletes because it's "new" and some big-named athletes have worn it in public. I would love to see some truly definitive evidence of its' effects and not same half-ass claim that "it can provide benefits and has been related to alleviating swelling.." blah blah.

I am not sure. Personally I am sceptical, since effects should clearly show up in a properly done study. I haven't looked up all the studies in the reviews but a few and these looked ok.

I'm a skeptic as well, and agree 100% with your gut feeling. Thanks for answering.


text:
Question about microaerophilic parasite tolerance for oxygen
Does anyone know what is the maximal concentration of oxygen that can be tolerated by the parasite Giardia intestinalis?

Short answer: 50-60 µM O2 is ok; 80 µM is toxic.
Giardia lamblia (aka intestinalis) is a microaerophilic intestinal parasite.
According to:

Lloyd et al. (2000) The microaerophilic flagellate Giardia intestinalis: oxygen and its reaction products collapse membrane potential and cause cytotoxicity. Microbiology 146: 3109 - 3118

Giardia colonises the upper intestine, and the oxygen concentration there has been measured at 60 µM. At oxygen concentrations up to 50 µM the organism can scavenge oxygen; above 80 µM oxygen inhibits the oxygen-scavenging process. In this paper the authors used 10% air (equivalent to 25 µM oxygen) to characterise  oxygen toxicity.
The source of oxygen sensitivity was investigated by:

Li and Wang (2006) A likely molecular basis of the susceptibility of Giardia lamblia towards oxygen Molecular Microbiology 59: 202 - 211

These authors propose that the enzyme DT-diaphorase, previously suggested as a component of the oxygen detoxification system promotes the formation of reactive oxygen species which lead to death. Thus they found that overproduction increased sensitivity to oxygen, whereas a knock-down decreased sensitivity. This work does not, however, use controlled microaerophilic conditions.


text:
How many water molecules will be generated when single nucleotides are used to make this RNA: 5’-UUAACCGUCAG-3’?
Based on what we learned on condensation reactions, how many water molecules will be generated when single nucleotides are used to make this RNA: 5’-UUAACCGUCAG-3’
I had an online biology quiz with this question, and I thought it would be one molecule for each nucleotide, for 11 total. The answer I have been given is 10. I feel like I am missing something obvious.

I just wanted to point out that the net generation of water is 0 since, for every condensation reaction of two nucleotides by RNA polymerase, there is a subsequent hydrolysis of pyrophosphate by pyrophosphatase.

To amplify what @canadianer wrote seven years ago, RNA is made from nucleotide triphosphates condensing with the 3'OH end of a nascent chain to give pyrophosphate. No water is generated. So the correct answer is 0, regardless of the fate of the pyrophosphate. I notice that a Google search for images of the reaction features one from Researchgate showing a NMP reacting to give water. This is a RNA ligase reaction. Only NTPs or NDPs participate in RNA synthesis. The nonsense generated by problem questions to students!

It's one for every phosphodiester bond formed. 11 nucleotides, but only 10 bonds needed to join them into an oligonucleotide:
1  2  3  4  5  6  7  8  9  10 11
N--N--N--N--N--N--N--N--N--N--N
 1  2  3  4  5  6  7  8  9  10


text:
Manufacturing of Bio Molecules
Can we Manufacture bio molecules say e.g. the simplest Sugar, C12,H22,O11 the way we do with any other mechanical component. So, we know all about the Structure and arrangement of Atoms in Sugar - so do the design send the commands to the manufacturing machine which will use C,H and O elements and put them in them specified order !
If it's not doable today, what's the reason? -
1. Our lack of understanding of the Structure of Sugar atoms  or
2. The specialized method which will put nascent atoms into the configuration of Sugar. Are people anywhere in the world trying to work this way? Please give references.

If that is meant to be sucrose, that isn't the simplest sugar. Technically I think it would be glyceraldehyde (C3) which makes the task a little easier. If you want a cyclic molecule maybe ribose, C5.

This is more about chemistry than biology (synthetic chemistry to be exact) and should be moved to Chem.SE in my opinion.

I agree with Armatus on that one, I'm afraid. You'll have better luck on the chemistry site.

this question needs more detail - its not going to make more sense to chemists. what is it we don't know about molecules like sugars?

Dear Shigeta, my question simply means that, do we know enough to create molecules like Sugar from scratch. I am not talking about synthesizing. Or is it that we know all the details, but it is not possible because of technological limitations (it may or may not be practical, I am not bothered). I am talking about possibilities and am keen to know the limits!

There are literally millions of biomolecules.  Some of them we know the structures and chemical properties of others we know nothing about.   I'm going to focus on sugars.  It would be too broad a question probably even to list all biomolecules, much less describe how their chemical synthesis would be performed.
The good news is that industrial manufacturing of biomolecules is done for thousands of compounds and even available.  Certainly chemical synthesis of sugars is possible and even available but is very expensive and often produces side products compared to fermentation processes or extraction from plants say.
Sugars, for instance glucose are very similar, but if you look at this structure you will see that the four OH (alcohol) groups could point up or down.  Any manufacture of glucose would have to get each one of these bonds exactly right.  This is D-glucose, which is commonly available as extracted with water from sugar beets and sugar cane.  I can buy 10 pounds of it at the store for less than $10.

Compare with L-glucose, which is synthesized by a chemist.  Its available (though not really recommended for human consumption because its got impurities and doesn't necessarily pass FDA definitions of purity to be a food) at the cost of $87 per gram.
So the answer is probably best put like this: who would pay \$87,000 for a bag of sugar when they could pay $10?  Cases where one would have to pay a company to produce a biomolecule, its going to cost...

Great answer, but my impression was that the question was about some sort of nanosynthesis.

why not write it up Alan?  there seem to be more than one way to read the question...

I don't have an answer to my reading of the question.

@AlanBoyd reword and make a new post

Thanks friends for your inputs. As Alan Boyd has mentioned, my question has to do with the methods available to manufacture. I am aware that synthesis is cheaper, but I want to know, if there is a system/machine which takes various aspects of the design of complex molecules (the knowledge gained through structural an functional studies) as input and gives the desired molecule as output. The machine has nano scale control to fix things at the right place and uses elements as the manufacturing material. Also, please give references to such work.

nano scale is not enough of a description in itself to answer this question, i still interpret the nano scale manipulation would still be a small scale of synthetic, enzymatic or fermentation methods.  we have no demonstrated way of making most biomolecules... there are practically an infinite number of them.  do you have a reference?

In short, no, molecules aren't synthesised that way. This is because the common atoms that in biomolecules (C, O, H, N, P) don't occur as individual atoms in nature and it would be extremely difficult (and unnecessary) to keep them in a single-atom state ready for assembly into a molecule in some way.
However, chemists are able to synthesise almost any kind of biomolecule desired by performing different routine reactions in a targeted fashion. The efficiency of production and the purity of the product obtained can vary extremely, but in principle any biomolecule up to a reasonable size could be synthesised chemically that way - as long as the desired product is itself chemically stable.
While theoretically, the repertoire of reactions you can do that way might be limited, there is no machine that does them routinely according to a program you put in, because there are too many variables that need to be adjusted depending on the current aim of synthesis and much more flexibility is needed than such a machine could provide.
I'm waiting for a reply from my chemistry friend on a few examples of those reactions.

authors: مهدي محمد الصباري


text:
Question about flavodiiron protein
I came across an article about flavodiiron proteins that are responsible for reducing ${\rm O}_2$ to ${\rm H}_2{\rm O}$ thereby protecting the anaerobic prokaryotes and some eukaryotes from oxidative stress. However, I am confused about the structure of that protein and its relation to heme proteins. Is this a heme protein?
The article I am reading is:

Di Matteo et al., The O2-scavenging flavodiiron protein in the human parasite Giardia intestinalis. J Biol Chem. 2008 Feb 15;283(7):4061-8. Epub 2007 Dec 12.

No flavodiiron proteins are not haem proteins. See here for a simple depiction. Basically there is a flavin, and there are two iron atoms which go through a FeII/FeIII cycle during catalytic activity. These iron atoms are not held in  haem, but rather via carboxylate ligands.

No, Hemes are not proteins. They are porphyrins (large organic molecules) which are composed of four pyrrolic groups linked together. In the middle the coordinate the iron atom which is responsible for the activity. The combination of heme and iron is called a prosthetic group or co-factor. They are bound by the protein.

The image shows the Heme B from the Wikipedia.

Right, thank you. However I meant heme proteins in the sense of http://en.wikipedia.org/wiki/Hemeprotein
In other words, is flavodiiron protein a heme protein?


text:
Plotting metabolic networks?
I need to draw a map of the core metabolism of E.coli. Associated with each reaction in the map I have a number that indicates the flux through this reaction. I want the map to reflect these fluxes through the color of each reaction in the map.
I have tried using tools like Mathematica and Cytoscape, but it is very hard to get a nice layout of the metabolic network. I have seen maps of E.coli metabolism which look very nice on paper. What I need is a map like these, but where I can define the colors of the reactions.
For example, see the image below for an example. Forget about the yellow bounding boxes delimiting compartments. I can spare those.

Can you provide a link or two to the type of metabolic map design / layout you prefer?

@MikeTaylor Added a picture to the question.

Have you looked into papers from systems biology groups which publish these networks reconstructions? They should state there what software was used.

@Chris I haven't found any. There are some tools available, for example, http://www.metdraw.com/. But when I upload my E.coli SBML model, the plot layout is a disaster. There used to be a web IPython notebook that one could use for some prebuilt models, where you just had to input the reaction fluxes. But now it's gone: http://nbviewer.ipython.org/github/opencobra/cobrapy/blob/master/documentation_builder/visbio.ipynb

There is a package called igraph in R but I am not sure that will be very convenient. If you don't get a satisfying answer here you may want to try asking on stackOverflow.

I echo @Remi.b and asking on StackOverflow.

Afaik. there is no good automated layout for graphs. I tried everything (even d3 force layout) with much smaller graphs (not in biology topic) and nothing worked... I am afraid you have to do it manually. I usually order the nodes manually with yed and after that it can draw the links automatically.

I would check out the intelligent diagram drawing software, like Graphviz which can really assist in making good layouts (requires some computer and maybe programming affinity) which can be made beautiful later with Photoshop or like. Or Yed, which could work for more manual style of work. And, if you are capable of writing computer programs, then tools like https://processing.org/ are a nice choice. All in all what you need is on the border of diagramms and infographics, so it's not just diagramming. And of course you must understand what you draw and what is the hierarchy in the diagram.

This is an old question, but Escher is a web app that has been developed that now enables the drawing of these maps using a web tool. Further customization (like reaction colors) could be manually manipulated in the downloadable SVG file.
From the main page linked above, you can load in the E. coli core model and look at (and manipulate) the map:

Escher is described in this publication in PLOS Computational Biology.

A very useful contribution to SE Biology. The fact that the question is old is irrelevant, as you have realized. I imagine there will be others like me that were unaware of this.

@David if you are interested in exploring further, Escher now has add-ons for simulating and visualizing model output overlaid on the map using Escher-FBA described in a very recent publication. You can knock out reactions, change reaction bounds, and all sorts of things (simulates using glpk on the front-end).

I'm not sure if they will be useful for your application, but you should look into software used to visualize ecological networks (and maybe also software used for drawing electrical charts). The type of data used there is very similar to what you want to plot, with nodes and links along with metadata for links on e.g. rates or connection strenghts.
I can point you to mangal by ecologist Tim Poisot (blogpost on mangal here), SBGN (Systems Biology Graphical Notation), and there is also the R-package diagram. However, I haven't used them much so I cannot say how useful they will be.

The basic problem is one of prior knowledge. The information you have about E. coli metabolism is in the form of a simple network, i.e. a list of nodes and the edges (along with their weights) that connect them. From this information alone it's impossible to know, for example, that the reactions in the TCA cycle should be plotted as a perfect circle (that's the circle in the middle of your example graph).
The only source for that information that's likely to be compatible with all of the metabolite/reaction names in your SBML file is the BiGG database. You can download maps that contain, among other things, x-y coordinates for all of the nodes in a metabolic network so that when you plot them they're not arranged in a big sloppy mess. You can then use a tool like COBRA to make the actual plots (look up the documentation for readCbMap and drawFlux).
Even this won't be as pretty as you'd like. The best answer, unfortunately, is a piece of software called Simpheny, which is commercial software that costs about a zillion dollars and is not freely available.

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


text:
Could this Francobelgian comic book woman really have these 4 diseases at the same time?
I'm doing an archive binge of a paper comic "The Kiekeboes". One of the characters is an elderly woman currently at the doctor, and she says the has the following illnesses:

Erythema Exsudativum Multiforme;
Necrobiosis Lipoïdica;
Phlegmasia Alba Dolens;
and Metropathia Haemorrhagica.

now, I googled these, and these are apparently real diseases (which actually makes sense, since she said she found them in her medical dictionary), namely 3 skin diseases and 1 menstruation problem. However, I find it hard to believe an elderly woman could have 3 different skin diseases and a menstrual disorder at the same time, especially since she already stopped menstruating.
Is it possible for a patient to have all 4 of these illnesses at the same time? Or do the causes interfere with each other too much for that? I don't want to know how to cure it, I just wonder how much they're talking out of their anuses.

Image I just took with my camera:

Kiekeboe 21: the Piri-Piri Pills, Page 17, strip 30. Author: Merho. Publisher: J.Hoste NV (currently part of Standaard Uitgeverij). Picture taken by Nate Kerkhofs on 16 september 2014.
It is in Dutch, but the names of the illenesses are clearly readable (since they're Latin anyway).
The doctor asks "what are you here for, madame? a cold, reumathism, headache?" right before this. The woman answers "no, doctor, I'm struggling with ... and also ... not to mention ... and a really annoying .... The doctor then replies "but madame, where did you get all those illnesses?" the woman replies "in my medical encyclopaedia!".

I hope this question isn't too off-topic. I understand that Medical questions are somewhat iffy, but since this isn't about a personal situation, I assume it's on-topic?

This is fine for the site.  The disease process is definitely a part of the biology.  We're more concerned about people asking for personal treatment advice than anything.

Erythema multiforme (minor) can and does occur in a lot of people; while it is usually self-limited, it can recur, especially when the trigger is an unsuspected food.[1] How common is it? It is very common.
Necrobiosis Lipoidica is not uncommon in diabetics, less common but still found in non-diabetics. It can occur at any age, including the eighth decade. It also shows a sex predilection, being 3 times more common in women than in men.[2] How common is it? It is not rare.
Phlegmasia Alba and Cerulea Dolens[3] is serious and associated with deep vein thrombosis, which is an acute event. It is not uncommon, but it's not chronic. (More than 600,000 cases of venous thromboembolism are estimated to occur each year in the United States, all of which can lead to Phlegmasia Alba and Cerulea Dolens. How common is it? Luckily, not very. If the author is referring to garden-variety thrombophlebitis, though, that's a chronic problem, and not uncommon in the elderly. Thrombophlebitis is chronic and common enough.
I'm not going to address Metropathia Haemorrhagica, because, as you have noted, it's found in menstruating women.
Diseases generally don't really interfere with each other; some diseases can't co-exist (you can't have hyperthyroidism and hypothyroidism at the same time, for example, or have an active pituitary gland tumor and empty sella syndrome at the same time), but diseases don't interfere with each other exactly. Some diseases have common underlying foundations, so can occur co-morbidly, for example collagen vascular diseases can manifest with skin, joint, and lung findings, which might not be diagnosed as several manifestations of one disorder if it's not obvious. A better example might be diabetes, where similar underlying pathologies cause, say, heart disease, skin disease, eye-problems and kidney disease together.
Whatever, the likelihood of a little old lady having all four of your diseases are nil. The first three all the time (assuming not garden variety thrombophlebitis) - nil. Once, not impossible once, but not chronically. Of the first two - not far fetched. The first - common as dirt (comes and goes, though.)
I hope this helped.
[1] Erythema Multiforme on Medscape
[2] Necrobiosis Lipoidica on Medscape
[3] Phlegmasia Alba and Cerulea Dolens on Medscape

@anongoodnurse Insulting other users is not acceptable, and I expect that this won't happen again. @caseyr547 It is not your job to enforce any laws here, I'm removing the entire conversation, the tone was inappropriate.

@caseyr547 I don't care what you report to anyone, I don't see any malpractice here, but I'm neither a laywer nor a US citizen anyway. This doesn't belong in the comments here, but on meta.

@MadScientist - I did take it to meta.

All these are possible side effects of oral estrogen progesterone pills used in perimenopausal or postmenopausal in Hormonal Replacement Therapy(HRT) by a diabetic female.
Irregular bleeding and endometrial carcinoma are known adverse effects of HRT.
Hence, Metropathia Haemorrhagica is quite possible.
Any drug given is usually liable to produce signs of allergy and hypersensitivity, especially in women (more prone to immune disorders).So, the skin disorders, Erythema multiforme is quite possible, if the women suffers from diabetes mellitus type 2, Necrobiosis Lipoidica is quite possible and could ve worsen by Erythema multiforme.
HRT and venous thrombosis
This article from NCBI tells how HRT increase risk of deep venous thrombosis by 2 to 5 fold compared to those not taking.
So, Plegmasia Alba is quite possible.

So, the Answer is HRT in postmenopausal Diabetic female, quite common these days, especially countries trying to copy west.


text:
How are drug metabolism and detection related?
If someone is taking treatment for a psychiatric disorder (e.g. diazepine), then would traces of the metabolized drug be detectable in their sweat or saliva?
Any links to resources regarding this, or any help is greatly appreciated!

Short answer: Yes.
Diazepine is a ring-structure that forms the basis for the class of drugs called benzodiazepines. This class includes long acting and short acting agents. If you're actually talking about diazepam, it's one of the long acting agents, which means the half-life of the metabolite in your body (and it's detection) is long.
The National Highway Traffic Safety Administration has good reasons to want to collect samples of various drugs non-invasively, and, indeed, they're headed toward saliva for screening. A neat little item called a Drugwipe can pick up traces of diazepam from not only saliva and sweat, but from surfaces people have touched.*
The real kicker, though, is hair, from any part of your body. Drug use(including diazepam) can be  detected in hair for months after (even single) use, and many employers are now going for hair sample testing to screen for drug use.
*Saliva and Sweat Testing With Drugwipe®.


text:
What's the longest transcript known?
What's the longest functional transcript known?  I'm wondering about RNA length post splicing, so not including introns.

You are looking for the longest, processed mRNA transcript. In which species? Human?

I was wondering if anyone knew of any beyond the human set.  We might have found one today in the Databases....

Top 10 long processed transcripts in humans (with multiple isoforms), from gencode 19 annotations:
Transcript    Length(bases)
------------------------
TTN-018        108861     <-- Titin
TTN-019        103988
TTN-002        101206
KCNQ1OT1-001    91666
TTN-201         82413
TTN-202         82212
TTN-003         81838
MUC16-001       43732
TSIX-001        37026
MCC-009         29616

Ignoring isoforms (only longest isoforms shown)
Transcript    Length(bases)
------------------------
TTN-018         108861
KCNQ1OT1-001     91666
MUC16-001        43732
TSIX-001         37026
MCC-009          29616
TRAPPC9-015      29514
SYNE1-001        27602
GRIN2B-001       27204
OBSCN-011        26811
NEB-204          26020

Titin clearly is the longest transcript in humans
However this is the list of longest genes:
Gene           Length(Kb)
-------------------------
CNTNAP2        2304.64
LSAMP          2186.93
DLG2           2169.35
DMD            2092.29
PTPRD          2084.57
MACROD2        2057.83
CSMD1          2056.87
EYS            1987.24
LRP1B          1900.28
PCDH15         1806.76
CTNNA3         1783.65
ROBO2          1740.82
RBFOX1         1691.87
NRXN3          1619.64
DAB1           1548.83
RP11-420N3.2   1536.21
PDE4D          1513.42
FHIT           1502.09
AGBL4          1491.06
CCSER1         1474.33

Top 5 in Zebrafish (Zv9.75); longest isoforms:
ttna-203             93727   <-- Titin
ttnb-202             82632
si:dkey-16p6.1-001   67263
syne2b-201           31867
si:dkey-30j22.1-001  29269

Top 5 in Drosophila (FlyBase r6.02); longest isoforms:
dp-RQ           71300   <-- Dumpy
sls-RP          56448   <-- Titin
Muc14A-RA       48719
Msp300-RG       43105
Ank2-RU         42107

Top 5 in C.elegans (WormBase WS220); longest isoforms:
W06H8.8g        55623   <-- Titin
K07E12.1a.2     39257   <-- dig-1
ZK973.6         25608
C09D1.1b        24198
C41A3.1         23457

Top 5 in Arabidopsis (TAIR 10.23):
AT1G67120.1     16272   <-- Midasin homolog
AT3G02260.1     15451   <-- Calossin-like protein
AT5G28263.1     15194
AT1G43060.1     14622
AT5G30269.1     14590

Top 5 in yeast (SGD):
YLR106C         14733   <-- Midasin
Q0045           12884   <-- Subunit I of cytochrome c oxidase
YKR054C         12279
YHR099W         11235
YDR457W          9807

It seems that Titin is on the top of the list in many species. Interesting.

I think a good candidate is the human titin gene. The gene itself has 363 exons, depending on the isoform it has between 27.000 and 34.000 residues. This makes up a processed mRNA length of up to 100kb for the full length isoform. See either the Wikipedia article or the one linked below for more details:

The complete gene sequence of titin, expression of an unusual
approximately 700-kDa titin isoform, and its interaction with
obscurin identify a novel Z-line to I-band linking system

If you are looking for the longest primary transcript, then the human dystrophin gene should be your favorite. It has a length of about 2.4 Megabases for the primary transcript, the processed transcript has only a length of about 14kb. It takes about 16 hours to transcribe and co-transcriptionally splice the sequence. See here for more details:

The human dystrophin gene requires 16 hours to be transcribed and is
cotranscriptionally spliced.

why does it transcribe 2.4 million bases and cut it down to 14,000? Seems like a waste of time and energy, not to mention the potential for mutations, which if muscular dystrophy is any clue, would be deadly.

alternative splicing is a wierd thing to be sure. biology is not rational but then human science has not yet produced a living cell from first principles...

Cases like this make me wonder why alternative splicing would be worth it. If you divide 2.4 million bases by 14000 bases you get 171.4. Seems like you could just make multiple copies of dystrophin to cover all the isoforms and still save space, and only need to transcribe the copy you want. Evolution should have gotten an engineering degree.

I don't have a reference for this, but I was told by a professor once that a long developmental gene is Drosophila takes longer to transcribe than the length of the cell cycle during initial development so that is not actually expressed until the cell cycle lengthens later in development. That's perhaps one answer (if uncommon) to the question of why some genes are so long.


text:
MHC restricted peptide
What is an MHC restricted peptide?
I got this definition from wikipaedia, but cannot exactly extract what the phrase MHC restricted peptide means.

MHC-restricted antigen recognition, or MHC restriction, refers to the fact that a given T cell will recognize a peptide antigen only when it is bound to a host body's own MHC molecule. Normally, as T cells are stimulated only in the presence of self-MHC molecules, antigen is recognized only as peptides bound to self-MHC molecules.

I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful.

First of all MHC stands for major histocompatibility complex. There are two types of MHC.
MHC type one is present on all of our cells with a nucleus. The purpose of these protein complexes is called antigen presentation. T-cells cannot recognize free antigens on their own, it has to be presented to them in the proper way. This is what these proteins do. In every cell there are lots and lots of proteins, that get digested to small polypeptides (short aminoacid sequences) by proteases during the natural recycling process. The cell takes a small portion of these polypeptides and presents them on its surface through MHC I complexes, that the immune system can read. This is like the cell saying to the immune syytem that "hey I got these proteins in me". Now if the cell is infected (by a virus most likely) then the "attacker's" proteins get digested and presented as well and its like saying " hey I'm infected and the attacker has these proteins".
MHC II serves similar function but it is only present on professional antigen presenting cells (APCs). These complexes present peptides derived from proteins consumed and digested through phagocytosis or receptor mediated endocytosis. It's like saying "hey we got a larger attacker and it has these proteins"
So, long story short T-cells cannot recognise antigens on their own it needs to be presented to them on MHC complexes and then and only then can they be activated.
Edit: A list of useful articles in the topic of antigen processing / presentation for further details:
January 14, 1998 14:59 Annual Reviews AR052-12
Annu. Rev. Immunol. 1998. 16:323–58
MECHANISMS OF MHC CLASS I–RESTRICTED ANTIGEN
PROCESSING Eric Pamer and Peter Cresswell
Cell, Vol. 76, 287-299, January 28, 1994.
MHC-Dependent Antigen Processing and Peptide Presentation: Providing
Ligands for T Lymphocyte Activation
Terry Y Nakagawa, Alexaiider Y Kudensky
The role of lysosomal proteinases in MHC class Il-mediated antigen processing
and presentation
This one may require subscription.
and the wiki page :)

I would also like to add an analogy to poka.nandor's answer that I used to explain my girlfriend (who studies law lol) MHC restriction. Imagine you have a plate and a sandwich. When the sandwich is not on the plate you do not know that it is a sandwich. When someone puts the sandwich on the plate you suddenly realise it is a sandwich. Basicly T-cells require the context of the MHC to recognise peptides.


text:
Does unequal dominance mean the X-chromosome should be a coldspot for antagonistic variation?
Sexually antagonistic genetic variation, in a simple model, will persist if the benefit to one sex is (near) equal to the cost in the other, otherwise the polymorphism will be selected out of the population.
[Rice's theory][1] suggests that sexually antagonistic genetic variance should be over-represented on the X-chromosome, because males are hemizygous (thus express male beneficial alleles more often than females) and females have the X-chromosome 2/3rds of the time (thus female benefit does not need to equal male cost for persistence). This model expands the range of conditions under which SA variation can persist.
[Fry argues here][2] that unequal dominance means the conditions under which sexually antagonistic variation can be maintained in the autosomes. Because of dominance the mean population fitness is increased under conditions of polymorphism (cost of a new allele to one sex < the benefit to the other). This model also expands the range of conditions under which SA variation can persist.
I think Fry concludes that the X-chromosome should therefore be expected to, not only not be a hotspot, but to be a coldspot (a dearth of SA variation on the X).
Conceptually, why does the hypothesis of unequal dominance make the autosomes more permissive to genetic variation than the X-chromosome? (Therefore making the X- a coldspot for SA variation). This is what his abstract says, it seems to suggest that...

"..such polymorphisms are expected to be more common on the
  X-chromosome... here I show that there are plausible assumptions under
  which the reverse is expected to be true."


text:
What is MHC haplotype?
What is MHC haplotype? I did check out the wiki article, but did not understand.

(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

When you are asking these kinds of questions, please ask about specific things. Just saying "I did not understand" is far too broad. Google is your friend when trying to understand difficult words or concepts - there are many more resources on the internet than just Wikipedia.

I have an answer for this question, similar to but expanded upon the answer already provided. @user3237995 asked a basic biological question: What is a haplotype?. Why can we not provide this basic biological understanding? There are not many answers. A haplotype is a haplotype? It's not a question about the complexities of MHC. It is asking what is a haplotype. It is a simple answer. Aren't we here to help people understand biology?

@Mike Taylor Thanks a lot for your support, I hope you provide me with our answer so that I can read it and understand

A haplotype is commonly defined as

...a group of genes within an organism that was inherited together from a single parent. -- Nature Scitable

This definition of haplotype applies whether it is just a few genes or all of the genes on an entire chromosome$^1$. In the case of the major histocompatibility complex, it is a group of more than 200 genes on chromosome 6 (Janeway et al. 2001). The set of alleles$^1$ inherited together from one parent form the MHC haplotype. Thus, one offspring will inherit two different MHC haplotypes, one from each parent. The different haplotypes with so many genes helps keep genetic variation in the overall complex, which improves the immune response ability of the organism.
The term is derived from haploid, which means half of the normal set of chromosomes. Humans for example are diploid, meaning it has two copies of each chromosome, one inherited from the mother (maternal) and one inherited from the father (paternal). So, when you inherit just one half of the crhomosome pair, you are inheriting a haplotype.
For general reference, it's important to note that haplotype was not always used to reference a group of two or more genes inherited together. It was commonly used to as a term to represent a sequence of nucleotides together on the same chromosome, even if only part of a single gene. For example, Bowen et al. (1995) used mitochondrial haplotypes to study the migration of loggerhead turtles across the Pacific Ocean. They used 350 nucleotides of the mitochondrial control region. The control region is over 1000 nucleotides in size but Bowen and colleagues only used 350 nucleotides from part of the control region.  This use was very common in the 1990s and early 2000s before it became easier and less expensive to sequence entire genomes, or at least many genes.
Citaton
Bowen, B.W. et al. 1995. Trans-Pacific migrations of the loggerhead turtle (*Caretta caretta) demonstrated with mitochondrial DNA markers. Proceedings of the National Academy of Sciences USA 92: 3731-3734.
Janeway, Jr., C.A. et al. 2001. Immunobiology, 5th edition. Garland Science, New York.
Footnote

More accurately, it would be the set of alleles at each gene locus (gene location) inherited together. The same genes are inherited from either parent, but the alleles (variations of the gene) may be different between the two parents.

As stated in wiki
"The major histocompatibility complex (MHC) is a set of cell surface molecules encoded by a large gene family in all vertebrates which controls a major part of the immune system. MHC molecules mediate interactions of leukocytes, also called white blood cells (WBCs), which are immune cells, with other leukocytes or with body cells. MHC determines compatibility of donors for organ transplant as well as one's susceptibility to an autoimmune disease via crossreacting immunization. In humans, MHC is also called human leukocyte antigen (HLA)."
Basically, MHC control immune system and it work based on principle lock and key. MHC has specific cell surface that can bind to foreign materials that have compatible binding site and recognise it as pathogen or harmful compound.

functionality of MHC is understood, but what is the word haplotype ??

@user3237995 http://en.wikipedia.org/wiki/Haplotype

@user3237995 in my simple understanding, it is as follows: we have pairs of chromosomes in our genotype. The haplotype is represented by the set you get when you take one chromosome from each pair (either maternal or paternal). The genes on those chromosomes are used to build proteins (like MHC's). Therefore, an MHC haplotype would be the set of either paternal or maternal (but not both) genes used to build MHC's in an individual.


text:
Difference between sequential and conformational epitope
Is the difference only in its structure? Like conformational epitope has 3D structure while sequential has a linear structure?(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

Yes, the difference is "only" in the 3D structure. This makes some differences when proteins change their shape; antibodies which recognize conformational epitopes are usually not well suited for lab work, as proteins are often denatured here.
The different epitopes are also called linear epitopes (for the sequential) and discontinous epitope (for the conformational). Schematically this look like this:

Nice diagram. Where did you get it from ?

From a book: Immunology for Medical Students.


text:
Affinity isolated peptide
What is affinity isolated peptides??(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

A peptide or protein can be purified by affinity chromatography. The principle is that the peptide has some substrate to which it will bind, retarding its progress through the column compared to the rest of the peptide population. A couple of typical examples are:

Using a His6 tag put on recombinant molecules, IIRC it binds to Ni2+ trapped in the chromatographic resin and is eluted with a chelator like EDTA.
Immunoaffinity chromatography, where you have a population of antibodies on the chromatographic resin which are specific to the protein that you want to purify (or alternatively having the immunogen bound to the resin so that you can purify the antibodies against it)

Mighty Wikipedia has a link about affinity chromatography here.

so its basically purification or extraction of peptide from a mixture using affinity chromatography...

Affinity isolated peptides/proteins are an output/product of affinity chromatography.


text:
What is the "Spandrels" debate about?
In a former question, as a side question, I asked a clarification about the "Spandrels" paper. Being not a biologist, it was the first time I encoutered it.
Subsequently I tried to collect some information, because I read that the paper is debated and deemed "wrong" by at least a part of the community.
Despite my efforts I have not fully grasped what the issue is:

is the incorrect reference to the architectural element? (i.e., the paper is wrong because it uses a not fully agreeable comparison)
are some (or all) the claims in it wrong? if yes, are there any suggested reading to understand why?

I ask specifically because the first reference I encountered points to Dawkins, and I would like to understand if this paper is a mere pawn in the big "gradualists versus punctuationists" debate or if it has merits on his own.

While spandrels might not have been a suitable metaphor, that doesn't change the primary argument made by Gould and Lewontin. I'll write up an answer later this afternoon.

Short version
The paper has nothing to do with punctuated equilibrum vs. gradualism (see also here), which was published a few years earlier. This debate is much different (but equally important, I think).
The authors of the Spandrels paper criticized evolutionary biologists of taking a very narrow view of the evolutionary process. They claiming (wrongly) that evolutionary biologists believed that every single trait on an organism was an adaptation that resulted from natural selection. The trait would not be present unless it was an adaptation. The authors claimed (rightly) that traits could not be considered independently. Instead, the traits had to be considered in light of the evolutionary history and developmental biology of the organism. To your specific questions:

The architectural metaphor was wrong. Does it make their entire argument wrong? No. They did not understand architecture. That does not mean they did not understand evolutionary biology.
Are some of their claims wrong? I think yes and no, but the full answer requires more nuance than can really be given here so read the long answer below if interested. I don't know of a single reference that supports/rebuts the Spandrels paper but consider Why Evolution is True by Jerry Coyne, The Greatest Show in Earth by Richard Dawkins, and Endless Forms Most Beautiful by Sean Carroll. None of these address directly the charges lodged by the Spandrels paper but they do show how evolutionary biology is integrative of many ideas instead of isolating each trait without considering the biology of the entire organism. (I have no commerical interest in any of these books. I simply support the ideas presented.)

Long version from my perspective.
In 1979, Stephen J. Gould and Richard C. Lewontin (hereafter, G&L) published a paper, "The Spandrels of San Marco and the Panglossian Paradigm: A Critique of the Adaptationist Programme", in the Proceedings of the Royal Society of London, Series B.  The title of the paper mixes two metaphors. The first is the character Dr. Pangloss from Voltaire's "Candide." Dr. Pangloss is a bit of an optimist, who says,

It is demonstrable ... that things cannot be otherwise than as they are; for as all things have been created for some end, they must necessarily be created for the best end. Observe, for instance, the nose is formed for spectacles, therefore we wear spectacles. The legs are visibly designed for stockings, accordingly we wear stockings. ... [A]nd they, who assert that everything is right, do not express themselves correctly; they should say that everything is best." - Dr. Pangloss

Dr. Pangloss is saying that everything has a purpose, and each thing is designed specifically for that purpose. G&L extend this metaphor to evolutionary biologists.  G&L claim that evolutionary biologists (at least to the time of their publication) tended to make claims similar to Dr. Pangloss: every trait that could be found on an organism results from natural selection and adaptation.  G&L write,

An adaptationist programme has dominated evolutionary thought in England and the United States during the past forty years. It is based on faith in the power of natural selection as an optimizing agent. It proceeds by breaking an organism into unitary "traits" and proposing an adaptive story for each considered separately. - G&L

Hence, the Panglossian paradigm. Every trait has an adaptive purpose and is necessarily the "best" that it can be. G&L then argue that evolutionary biologists of the time failed to consider the entire organism when assigning adaptive value to each trait separately.

We criticize this approach and attempt to reassert a competing notion ... that organisms must be analyzed as integrated wholes, with bauplane so constrained by phyletic heritage, pathways of development, and general architecture that the constraints themselves become more interesting and more important in delimiting pathways of change than the selective force that may mediate change when it occurs. - G&L

G&L are saying that the many organismal traits are functions of evolutionary history, developmental pathways, and other structural contraints.  G&L argue that most evolutionary biologists of the time did not consider the entire organism when ascribing adaptive value to any one trait. In G&L Panglossian metaphoric terms, evolutionary biologists had decided that the adaptive value of the nose was to support glasses, but they had failed to consider that the nose may have evolved for other reasons (e.g., smell) and that the supportive value of the nose was an evolutionar by-product instead of an evolutionary cause.
This brings us to the second metaphor, the architectural spandrels. Spandrels are triangular spaces that form when two arches meet, or when an arch meets a rectangle.  According to G&L, spandrels are a necessary by-product of the architectural joining of the two shapes. The spandrel itself serves no purpose. In evolutionary terms, spandrels have no adaptive significance that resulted from natural selection. Instead, they are an evolutionary by-product that resulted from selection on other traits (arches and rectangles).
While the architectural metaphor apparently fails, their primary argument does not change.  Traits cannot be considered individually. Traits of an organisms must be evaluated as one part of the entire organism, together with it's developmental biology and its evolutionary history.
Here are two examples to represent their argument, written for a general audience. The first example is based on the human hand.  Our hand has five fingers. Each finger except the thumb has three bones (called phalanges), which you can see easily when you curl your finger. The thumb has only two phalanges. What is the adaptive value of having four fingers with three bones each, and a thumb with two bones? You might say that such a structure imparts excellent manual dexterity, from grasping to manipulating objects. But, would we not have that same dexterity if we had four fingers, or six? Why does the thumb have only two bones and not three? How could that be adaptive? These specific traits may not be the direct result of natural selection.
The structure of our hand is explained by our evolutionary history. Our primate ancestors had five fingers. So did our earliest mammalian ancestors, as did our earliest reptilian ancestors. However, some of the earliest amphibian ancestors, such as Acanthostega, had more than five digits (toes, fingers). Somewhere in early amphibian evolutionary history, our ancestral lineage converged on five digits, and most descendant vertebrates retain that five digit pattern. Even those vertebrates today without five digits usually display five digits during development, such as the ostrich (scroll down to image of blue-stained bones). If we assigned an adaptive purpose to the  human hand independently of its evolutionary history, we might very well be wrong.  Science doesn't like wrong.
Think about the five toes of your foot. Each toe has three bones except for the big toe, which has two bones. Manual dexterity? No. Evolutionary history? Yes.
The second example is the groove in your upper lip below your nose. This groove is called the philtrum. Can you think of an adaptive function for the philtrum? You might think that it helps to direct odors towards our nostrils, or hypothesize some other adaptive purpose. However, it appears that the philtrum is a by-product of the development of our embryonic face (YouTube video). The trait of our philtrum may not have adaptive significance. It is a by-product our face formation when the two sides meet in the middle.
G&L's publication produced quite an uproar. It's easy to find criticisms of the paper. Some have criticized the architectural metaphor. A bad metaphor does not necessarily make a bad scientific argument. Others have criticized the scientific rigor of their arugments. This blog entry, associated with the respected ecology journal Oikos, dislikes the paper and identifies several problems. The Oikos blog also links to several other sites that either support or dislike the G&L article. Most evolutionary biologists disliked the claim that they did not see the "whole organism."
Rightfully so, I think. I do not know of one evolutionary biologist (myself included) that has ever considered a particular trait without considering the broader evolutionary history of an organism. Indeed, considerable effort is spent by evolutionary biologists to determine how the evolutionary history of an organism influences its trait. The same applies for evolutionary developmental biology and other biological processes. For example, Martin et al. (1993) related evolutionary rate to body size, metabolic rate, and generation time of various animals, a very integrative (not isolating) approach.
To be fair, I think the G&L paper needs to be considered in the context of its time. Remember that i was published in 1979. Reread the first G&L quote above. They say, "during the past forty years."  The G&L paper was published in 1979. Forty years before this paper was published was during the "modern evolutionary synthesis." Without going into details (ask another question on Biology.SE!) the modern evolutionary synthesis provided the genetic mechanism (and so much more) that explaiend how Darwin's concept of natural selection could actually work. Once the relationship between Mendelian genetic inheritance and natural selection was proposed, many evolutionary biologists tested this connection. It is not surprising to me that G&L perceived this strong "bias" towards a selectionist (Panglossian) paradigm because many biologists of the time were trying to understand how Mendelian genetics contributed to natural selection.
At the time of the modern synthesis, the structure of DNA was not yet known.  The structure was finally realized by Watson and Crick (and Franklin!) in 1953, only 26 years before G&L's paper. Today we think nothing about the DNA structure but molecular genetics has advanced so much since G&L's publication that we have a much greater understanding of evolution and natural selection at the genetic level. Today, you can't study the evolution of a trait without considering its underlying genetic architecture.
In my opinion, one of the most, and perhaps the most, important development in the field of evolutionary biology is the field of evolutionary developmental biology (evo-devo). This field did not really mature as a discipline until about 2000, when the Proceedings of the National Academy of Sciences in the US devoted an entire issue to the topic. Developmental biology was a discpline that G&L had argued was important to consider. I'd bet that even they had no idea how important the evo-devo discipline would become to understanding evolutionary change. Still, recognition of the relationship between evolution and development was recognized as long ago as the mid-1800s by Ernst Haeckel. Evolutionary biologists were not necessarily considering traits in isolation from evolutionary history or developmental biology.
In the end, G&L used broad brush strokes to paint evolutionary biologists into a small canvas, claiming that biologists had a narrow evolutionary viewpoint. The evolutionary biologists responded (then and now) that their perspective was wide, even when focused on a particular trait.
The G&L paper continues to prompt considerable debate, which I think is the value of their paper. Every young graduate student should be required to read the paper. Even jaded scientists need a refreshing jolt to an established way of thinking. Our thought processes will alway benefit when we are reminded that evolutionary biology is a broad discipline that must embrace many other disciplines to arrive at a full understanding of the history of life on Earth.

may I point out that at the This [blog entry] seems to be missing a link?

@Federico Fixed.


text:
Is it possible to calculate the energy required to speak a word?
I was discussing with a colleague whether speaking would require more energy than communicating via instant message (GTalk, etc..).
If this is possible, then I'm particularly interested in whether certain sounds may consume more energy that others, and consequently could one language be more efficient than another.

It may be more useful to consider the total amount of sound required to convey information. It has always seemed to me that Italian is particularly profligate. Example chosen at random: bread maker (English, 3 syllables); macchina per il pane (Italian, 7 syllables). But, of course, this isn't really a biology question.

https://www.popsci.com/ask-us-anything-how-much-exercise-do-we-get-talking/

For animals to check the amount of energy used for a certain behavior you can use a RESPIROMETER. It basically calculates the oxygen consumption.
In your case you could calculate for writing a sentence vs speaking the same sentence.
Regarding your second question:
At least in birds more than the type of sound (the frequency modulation) what matters for energy consumption is the amplitude --> how loud is your sound.

adding to this answer; hence you would feel more tired if you'd been shouting the whole day-

It could be theoratically possible if you fitted a glucose sensor to a person's body and asked that person to do nothing other than talk, for say a period of 1 minute. Then, when he/she talks, the amount of glucose metabolized during that time period could be measured, and subsequently, the no. of calories required for speech. Of course, the amount of calories required for breathing and even doing nothing (sitting, which consumes 75 calories of energy per hour) must be deducted.

Sitting consumes more than negligible amounts of energy. In fact, sleep consumes energy.

Most of the energy consumed by the body is required to keep the body temperature stable, and keep the brain alive. Even physical activity (if not extreme) doesn't come close to it.

I don't think measuring glucose would be sensitive enough.


text:
Exclusive microtubule minus-end labeling
Like the title explains I am looking for a way to exclusively label microtubule minus end in vivo. Looking through the literature I could not find any techniques yet. Do you have an idea?

γ-Tubulin is specifically localized to the minus end of microtubules. GFP labeled γ-Tubulin can be used to label the minus ends in-vivo and without the requirement of staining. Fan et al have developed a phage display antibody specific to α-Tubulin that can be used to visualize minus ends. See the figure below.

The image is an electron-micrograph but it is certainly possible to do a fluorescent microscopy after IHC staining.


text:
What is the difference between regular blood, a woman's and a virgin's menstrual blood?
There are many stories that blood contains the life-force energy and specifically menstrual (period) blood has always been a feature of many rituals and some ancient Sumerian tablets mentioned that menstrual blood was the 'gold of the gods'.
So it is true that the menstrual blood is highly oxygenated, the purest of all blood and it carries the decoded DNA?
Or what differences are known to modern science between regular blood, a woman's period blood and virgin's period blood?

I think dead tissue in menstrual blood is a waste matter that should be excreted.

The "purest of all blood" is fresh out of the bone marrow, i.e. in your circulatory system.
Menstrual blood is a combination of blood, some mucous, and dead endometrial tissue.

The endometrium consists of a single layer of columnar epithelium resting on the stroma, a layer of connective tissue that varies in thickness according to hormonal influences. Simple tubular uterine glands reach from the endometrial surface through to the base of the stroma, which also carries a rich blood supply of spiral arteries... Proliferation is induced by estrogen (follicular phase of menstrual cycle), and later changes in this layer are engendered by progesterone from the corpus luteum (luteal phase). It is adapted to provide an optimum environment for the implantation and growth of the embryo. In the absence of progesterone, the arteries supplying blood to the functional layer constrict, so that cells in that layer become ischaemic and die, leading to menstruation.

So, menstrual "blood" is a combination of sloughed off stromal and glandular tissue, broken down vascular cells and blood, and, no, it is not highly oxygenated (it's kind of darker than normal blood. It doesn't carry any "decoded DNA". It's basically a waste product at this point, dead, dying and no longer functional tissue.
Virgin's flow is just as dead as non-virgin's flow. Cultures obtained at hysterectomy indicate that the endometrial cavity is normally sterile. The major difference between a virgin and a non-virgin is that the possibility of infection of endometrial tissue exists in non-virgins.
Of course myths will arise around menstrual flow. After all, when it was alive, it was the medium for implantation of a blastocyst. But they are just myths.
Endometrium Histology
Infections as a Cause of Infertility


text:
What is the difference between clinical and non-clinical depression, and is there a term for different severity of the bipolar disorder?
I was looking for a term which describes a bipolar disorder of lesser severity.
I know from experience from someone I know well, what a very severe case of the bipolar disorder looks like, when an otherwise very intelligent and very sane person can become completely unstable in both directions, and requires medication to basically survive it.
I'm searching for a term which has indeed the symptoms of the bipolar disorder, but is not as severe as to require medication to basically survive the mood swings. I'm not talking about being just sad for something or craving attention. I'm talking about the very real symptoms of mania, followed by depression, just not as severe to be fatally dangerous without medical intervention. A severity which I would describe of being able to cope with by learning about it and a good degree of self-control, exercise, and good eating habits.
I thought the term was clinical versus non-clinical depression, but a search of the Internet made me doubt it. They talked about it as if the clinical was a case where there is a "disorder of the brain" and the non-clinical was "just sad because of a sad event", so either were those forums wrong (I guess so, because of their apparent unprofessional writing style, and they never seemed to know about bipolar, they thought manic depression was just about being very very sad), or there is another term which best answers my question.

I found a serious-looking article which uses the term "nonclinical", but in the context of borderline and not bipolar> http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772134/

vsv - bipolar and borderline are different (mostly unrelated) disorders, but the notion of "non-clinical" is widely used. I updated my answer to include this. (Sorry, I had mis-read it as "subclinical" the first time around.)

I think the main question here is:

Is there a term…which describes a bipolar disorder of lesser severity[?]

Yes. There are a couple ways to think about this, but you’re clearly accustomed to differentiating the manic and depressive phases of bipolar disorder, so I’ll start with that.
There is mania (excerpted from DSM 5*):

A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased goal-directed activity or energy, lasting at least 1 week and present most of the day, nearly every day...
B. During the period of mood disturbance and increased energy or activity, three (or more) of the following symptoms (four if the mood is only irritable) are present to a significant degree and represent a noticeable change from usual behavior:

Inflated self-esteem or grandiosity.
Decreased need for sleep
More talkative than usual or pressure to keep talking.
Flight of ideas or subjective experience that thoughts are racing.
Distractibility
Increase in goal-directed activity
Excessive involvement in activities that have a high potential for painful consequences

C. The mood disturbance is sufficiently severe to cause marked impairment in social or occupational functioning....

And there is hypomania:

A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 4 consecutive days and present most of the day, nearly every day. ….
B. [This criteria is the same as for mania.]
  ....
  E. The episode is not severe enough to cause marked impairment in social or occupational functioning or to necessitate hospitalization.

I have bolded the main differences between the two definitions. You can see that hypomania is the term for the less severe form of the manic phase of bipolar depression.
Neither mania nor hypomania is likely to occur in the absence of depressive symptoms, however. Thus, there are two basic phenotypes of bipolar disorder (summarized from DSM 5*):
Bipolar I disorder: Patient experiences mania; depressive periods may not qualify as Major Depressive Disorder.
Bipolar II disorder: Major Depressive episodes are required; manic phase may be hypomanic. (This is classically considered a less severe syndrome, but this notion has been challenged in recent years.)
And finally, one more term for you:
Cyclothymic disorder: patient experiences both hypomanic and depressive periods without ever fulfilling the criteria for an episode of mania, hypomania, or major depression.
(Your other question you seem to already know the answer to, but since it's in the title.....  Nonclinical depression refers to something on the spectrum of normal (i.e. not pathological), such as situational mood disturbance. A related concept, subclinical depression is a loose term to describe depressive symptoms that don't meet criteria for Major Depressive Disorder..)

*American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing.

I appreciate your effort put into this answer, it made most of the terms a bit more clear. Just so I know I understood it correctly, even though there are a lot of differences between them besides severity, if we tried to arrange them from the most severe to the least severe, we would end up with Bipolar I, Bipolar II, hypomania, cyclothymia, subclinical, non-clinical?

@vsz - I'm glad it was helpful. Mania/hypomania are phases of bipolar d/o, so conceptually it doesn't work to make a hierarchy this way. Bipolar I includes full-blown mania +/- MDD; bipolar II includes hypomania but full-blown MDD; cyclothymia includes only the milder forms of both. Subclinical and non-clinical are not strict DSM terms and can be applied to any disorder. For bipolar, "subclinical" is basically the same as cyclothymia, and there isn't really "non-clinical" bipolar d/o. Hope that's clearer.

(Sorry, MDD = Major Depressive Disorder)

Nonclinical depression is a popular term for the natural reactions to the external factors, such as loss, seasonal changes, emotional stress
http://www.depressionfree.com/non-clinical.html
while the major types of clinical depression are as follows:
Major Depressive Disorder
Major depression is a severe mental disorder that deeply affects an individual’s way of life and characterized by the inability to enjoy life fully and be satisfied.
Dysthymia
Dysthymia is a type of chronic mild depression.
Bipolar Disorder
Bipolar disorder, also known as manic depression, is characterized by constant mood changes.
Cyclothymic Disorder
Cyclothymic disorder is often described as a milder form of bipolar disorder.
Seasonal Affective Disorder
Severe mood change according to the season. Aka SAD
Melancholia
Antenatal And Postnatal Depression

can you add some links to each of those terms (preferably from a non commercial web site)?


text:
How closely related are two parasites Giardia intestinalis and Trichomonas vaginalis?
How closely related (from the evolutional point of view) are parasites Giardia intestinalis and Trichomonas vaginalis? Giardia genome is about 12 Mb and its major cellular proceses are rather simple. The genome of Trichomonas is approximately 160 Mb. What about its cellular processes, is it also a 'minimalist'?

Basically, Giarda is a an Excavates while Trichomonas is a Cercozoa meaning a Rhizaria (Chromealveolates in the broad sense as noticed by @har-wradim in the comments (now deleted) because Cercozoa are neither Chromista nor alveolata). Because the very basis of the tree of eukaryotes is still unresolved (eukaryotes), the most recent common ancestor of these two species is just an old eukaryote! In other words, these two species are not more closely related than are related a cat and a chestnut tree!
The links yield to Tolweb.org which shows you the phylogenetic tree and allows you to explore the relationships between organisms. Have a look to eukaryote tree especially to see the positions of the Rhizaria and Cercozoa.

One more point: While Giardia and Trichomonas both lack mitochondria, the former has mitosomes and the latter has hydrogenosomes. Mitosome has the most reduced functionality

Be careful though that Tolweb is not always very up-to-date.


text:
Why aren't introns found on the ends of pre-RNA?
We recently learned in genetics class that exons always cap the ends of nascent RNA. I have been trying to figure out the reason why introns can't instead be found on the ends instead of exons. The end introns would still have their 5' and 3' splice sites, and assuming the splicing machinery functions correctly, these introns would be removed. The only thing I could imagine occurring is inappropriate nucleophilic attack of the end 3' hydroxy group at the end 5' phosphate leading to a single circular RNA. However, in a normal situation where exons are at the ends, if introns in an RNA are  all removed simultaneously than it is possible that the free 3' hydroxy group of say intron 2 could attack the 5' end of another intron leading to inappropriate cleavage of the intervening exon so having exons at the ends does not solve that problem. I don't think my explanation is correct, any ideas?

You should revise splicing mechanisms. Splicing requires that the intron be flanked by exons. There can be nucleolytic clipping of the ends- as in case of tRNAs, but they are not generally referred to as introns (though one technically can).

I was unclear..I was asking why introns are not found before the 1st exon and after the last.

There are untranslated regions of mRNA flanking the exons, even after splicing. These are creatively called the 5' and 3' untranslated regions. These regions help regulate translation and mRNA stability. I've never heard of it, but maybe there are cases where RNA gets cut out from between an exon and an untranslated region.

Neither pre-mRNA or mature mRNA begin with exons, they begin with the 5'UTR. Are you asking why the sequence after the 5'UTR is always an exon? Or are you asking why there can't be introns before the 5'UTR?

@user137 (and Armatus) UTRs are exons, some of them even contain introns and are spliced just like coding exons.

@terdon So the definition of exon is the RNA that isn't removed, rather than RNA that becomes translated into protein?

@user137 exactly. Being an exon has nothing whatsoever to do with being a coding exon. You even have transcripts that don't code for protein at all but that contain introns regardless.

RNA splicing refers to a certain kind of RNA processing mechanism which leads to the excision and exclusion of some regions of the primary transcript. You should note that this is not the only method by which such a thing can happen; Endo-ribonucleases can clip the ends of the transcript and this happens in the case of tRNA-processing. But as "splicing" happens it is essential that the excised region be in the interior of the transcript. See the figure.

RNA splicing begins with assembly of helper proteins at the intron/exon borders. These splicing factors act as beacons to guide small nuclear ribo proteins to form a splicing machine, called the spliceosome. These animation is showing this happening in real time.
see>
http://education-portal.com/academy/lesson/rna-splicing-of-introns-exons-and-other-forms-of-rna-processing.html#lesson
http://www.youtube.com/watch?v=FVuAwBGw_pQ
http://www.sumanasinc.com/webcontent/animations/content/mRNAsplicing.html


text:
Are there any drawbacks to having a fixed-Köhler microscope?
I am considering to buy the Zeiss Primo star microscope. There are two variants: one with so called "Full Köhler" illumination and one with "Fixed-Köhler" illumination. Are there any drawbacks to having it fixed? When I would not want to have Köhler illumination?

IMHO: there's hardly any reason why you should't use Köhler illumination. It's the method of choice to achieve bright and even illumination, in the entire FOV, permitting max. resolution. In a well designed system.
Köhler has only one drawback: often it turns out to be impossible to achieve even illumination at low power in the entire FOV. Usually, but not aways, the manufacturer has made provisions to achieve propper illumination at low power at the condenser level.
Allow me to add that I'm not a fan of the Primostar stand, which is a microscope build on order for Zeiss, probably by Meji.
Compared to the older Black, grey and white Zeiss Standard stands, it's a toy...

I wonder where that -1 came from


text:
Linkage disequilibrium D sign
Linkage disequilibrium D equals
$D=x_{11}−p1⋅q1$
where:
Haplotype        Frequency
$A_{1}B_{1}          = x_{11}$
$A_{1}B_{2}          = x_{12}$
$A_{2}B_{1}          = x_{21}$
$A_{2}B_{2}          = x_{22}$
and
Allele    Frequency
$A_{1}=p_{1}=    x_{11}+x_{12}$
$A_{2}       = p_{2}=x_{21}+x_{22}$
$B_{1}       = q_{1}=x_{11}+x_{21}$
$B_{2}       = q_{2}=x_{12}+x_{22}$
Shouldn't:
1) $D = x_{11}-p_{1}q_{1}$ or $x_{11} = p_{1}q_{1}+D $
2) $**D=  x_{12}-p_{1}q_{2}$ or $x_{12} = p_{1}q_{2}+D**$
3) $**D=  x_{21}-p_{2}q_{1}$ or $x_{21} = p_{2}q_{1}+D**$
4) $D=  x_{22}-p_{2}q_{2}$ or $x_{22} = p_{2}q_{2}+D$
Why do all the papers show:
1) $x_{11}=p_{1}q_{1}+D$
2) $**x_{12}=p_{1}q_{2}-D**$
3) $**x_{21}=p_{2}q_{1}-D**$
4) $x_{22}=p_{2}q_{2}+D$
ex: http://en.wikipedia.org/wiki/Linkage_disequilibrium
Question:
why for the relationship between the haplotype frequencies and allele frequencies and D is there a difference in sign. In other words by the formula shouldn't it always be +D rather than -D?

Your question would be more appreciable if you'd use MathJax. For example "x12=p1q2-D" becomes "$X_{12}=p_1q_1-D$" by writing "X_{12}=p_1q_1-D" between dollar signs. More info about MathJax here


text:
Is intron removal coordinated?
Are the introns present in a nascent rna molecule removed simultaneously or are they removed in some sort of sequential fashion or is removal completely random?

There are two different ways to interpret this question:

Does the spliceosome splice all introns of an mRNA simultaneously or sequentially?

Can a spliced mRNA be re-spliced?

How does a spliceosome proceed along the mRNA?
According to this review:

splicing generally proceeds in a 5′ to 3′ direction, although neighboring introns are not always excised in this order, nor are all introns completely removed during synthesis (36).

Splicing tends to happen immediately following transcription of introns, so it is to some extent necessarily sequential (same review):

Time course measurements by RT-PCR of multiple pre-RNA species synthesized after reversing 3 hours of DRB inhibition have shown that intron excision occurs within 5 – 10 minutes of synthesis of the downstream neighboring exon, irrespective of the length of the intron, the length of the gene or whether the intron is excised by the major or minor spliceosome (42).

Thus, it is not physically possible in many cases to splice all the introns of a RNA simultaneously, because splicing begins before pre-mRNA synthesis is even complete.
Re-splicing mature/spliced mRNA
There are a few different mechanisms by which RNA can be spliced at more than one point. For example, ribozyme splicing occurs in a spliceosome-independent fashion, so an mRNA with a ribozyme in it and also non-ribozyme introns will necessarily have multiple rounds of splicing.
There is additionally so-called recursive splicing of very long genes/introns. This is when a spliced intron must be handled in multiple rounds due to its length/complexity; it's a bit involved so I won't go into it here.


text:
How can I download a gene sequence from GenBank (NCBI)?
Could you tell me the steps to find and download a gene sequence from GeneBank?
I would appreciate your help.

I think you can very easily find the steps for this with a little research.

Go to the NCBI website, fill the search field with relevant information in the upper part of page, select "nucleotide" from the drop-down menu just to the left of the search field and click search. You will get a list of items, by clicking "FASTA" link below any of them will bring you the corresponding sequence.
Depending on your interest, you can choose other databases from that menu, and some of them are interlinked. For example you can do the search by selecting "gene" instead of "nucleotide" and when displaying a selected gene info, you can see the links that lead to nucleotide database for getting the sequence.