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Does every wave length of UV kill bacteria?
Will every wave length of UV work for killing bacteria? So will UV A, UV B and UV C all work? Or will only the shortest of the three, UV C, work? Also, will the average UV lamp help against bacterial growth (if it is shone on an object for 3-5 minutes for example)? What about a longer period: a bacterial colony in a petri dish under an average household UV lamp for a day? Would the growth be reduced noticeably? Or would the change be too small to notice when using the average UV lamp? Does the type of UV also matter for this (A/B/C)?

Can you tell us where you want to use UV as an antibacterial measure?

I'm planning on using it on two places: on my hands, and on a bacterial colony in a petri dish with nutrients.

The CDC's disinfection guidelines lists UV radiation between 328 and 210nm as effective for disinfection, with a maximum of bactericidal activity occurring between 240-280nm. At this wavelength DNA damage (Thymine dimers) is induced with a high rate.
Due to practical reasons UV light is mostly used to disinfect water, if used in rooms there is some effectiveness against microorganisms in the air and some on surfaces, but on one hand the effectiveness is reduced  by square with the distance from the UV source and on the other hand you need completely empty surfaces where nothing casts shadows. The other problems are plastic materials which may get damaged by repeated UV exposure.
Have a look at this reference (only available via Google Books): "Principles and practices of disinfection, preservation and sterilization." and this subchapter.

I'm planning on using it both directly on my hands, with the lamp being quite close to my hands (we're talking about a distance of centimeters here). I'm also planning on shining the lamp on a bacterial colony in a petri dish with nutrients, again with quite a small distance (decimeters, this time).

Be very careful with your hands. This will cause sunburns in a very short time (depending on the source this might happen in minutes).

Would 3-5 minutes be harmful? Because that's how long I'm planning on exposing my own skin. The fear of getting sunburns would, however, be quite a strong reason not to.

With the UV sources that I know from the lab this is definitely enough to get a strong sunburn. But why do you want to expose your skin like this?

I would like to know whether the UV light would be able to kill the bacteria on my hands and disinfect them.

No, mo likely not. Or not completely as your hands are not a flat surface. There will be shadows and areas of low exposure. Plus the risk of sunburns (which can also occur in the eye when you look to long into the lightsource with unprotected eyes. Chemical disinfection works better. Even better is wearing gloves and disinfect them.

Forget the sunburns. The UV kills the bacteria because it is applied at wavelengths and for time periods which cause lots of DNA damage. If you do this to your hands regularly, you're practically inviting melanoma.

@RumiP. It will cause immediate damage to your skin and this is important to keep in mind. This can lead (in the longer perspective) to the development of skin cancer (can also be other forms like squamous cell carcinoma or basal cell carcinoma).


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Definition of "structural underdominance"?
In Stathos and Fishman (2014), the authors refer to the concept of structural underdominance. The first time they mention it is in the first paragraph of the second page (left column) and the term is followed by some kind of definition in parenthesis. It is written:

Furthermore, artifical doubling of chromosomes in sterile plant hybrids can sometimes restore normal meiosis and fertility (Stebbins 1950), a pattern diagnostic of structural underdominance (heterozygote inferiority).

In addition to how they use the term "Structural underdominance" in this paper, the above definition is confusing to me.
Is structural underdominance a specific type of underdominance (heterozygote disadvantage)? Is it the evolutionary process by which a population is lead to diminish the average underdominance along their loci? Is it a predisposition of the genetic architecture to display underdominance when a chromosomal rearrangement occurs? In short the question is:
What is the definition of "structural underdominance"?

I understand heterozygote inferiority (also underdominance or heterozygote disadvantage) as the opposite of heterozygote advantage, that is, lower fitness of the heterozygous genotype than either homozygote (as reference, see Hedrick, 2009, p. 119). I haven't seen the term structural underdominance before. However, heterozygote disadvantage can sometimes be seen in species/subspecies hybrids and also chromosomal heterozygotes (see Hedrick, 2009, p 140), and this might be what the term structural underdominance is describing (structural as in chromosomal). This can then lead to unbalanced gametes with low viability, which means low fitness compared to homozygotes. The quote you have included also talks about plant hybrids, which makes this explanation likely, and it also makes sense since they mention artifical doubling as a solution. If I have understood the process correctly, chromosomal doubling should lead to better pairing of chromosomes and lower risk of unbalanced chromosome translocations.
Also note that Hedrick labels heterozygote disadvantage as an unstable equilibrium (p. 140ff), but I haven't looked more closely at the dynamics behind this.

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How and why did mammals go back to the oceans?
If I understand evolutionary biology correctly, mammals first evolved on land as small, rodent-like creatures, in a time when reptiles were dominant on land. Eventually, they diversified into the species we know today. Some of these species, however, are aquatic - whales and dolphins readily spring to mind. Why did the ancestors of whales and dolphins leave the land to go to the oceans? How did they evolve from their original form to their superficially ichthyoid appearance today?

I'll focus on whales and dolphins (cetaceans) as you mention them by name and they are representative for other marine mammals such as seals or manatees. The evolution of cetaceans was one of the fascinating evolutionary mysteries. Clearly, they were mammals, but which mammals were their closest relatives? Clues to solve this mystery began to appear in the 1980s and 1990s.
During the 1980s and into the 1990s, paleontologists discovered several fossils that were clearly land-based mammals but shared many skeletal features with cetaceans. These fossils, including Pakicetus [(Gingerich et al. 1983)] and Rodhocetus (Gingerich et al. 1994), shared skeletal features that are unique to whales and to the Artiodactyla, commonly known as the even-toed mammals. Artiodactyls includes deer, sheep, pigs, bison, and hippopotamuses. Artiodactyls and the fossil whales share a unique skeletal feature of the ankle called an astrogalus, shown in the picture below. The astragalus is a "double pulley" structure that contributes to the ankle joint. This picture is taken from an excellent summary of whale evolution, provided by the Understanding Evolution site hosted by University of California at Berkeley. The astragalus is not present in other mammals.

The fossil whales and modern cetaceans also share unique features of the skull around the area of the ear, called a tympanic bulla. Although all mammals have bullae (plural of bulla), the bullae of cetaceans and the whale fossils is unique compared to other mammals. For more on the bulla, see this Talk Origins page. More on fossil whales can be found at the Berkeley Comparative Museum of Paleontology. The many fossils that have been found are transitional forms that link artiodactyls and modern cetaceans.

Source
Around the same time as the fossil discoveries, genetic analysis added additional evidence supporting a relationship between the artiodactyls and cetaceans (Milinkovitch et al. 1993). Although early genetic analytical techniques were not as robust as they are today, many genetic studies have since supported and refined the conclusions of Milinkovitch et al. Current evidence shows that the closest living relative of cetaceans are the hippos (see, for example Price et al. 2005 and Agnarsson and May-Collado 2008). The relationships are shown below in this figure from the Agnarsson and May-Collado paper. The dark lines are the artiodactyls and cetaceans, formally called the Cetartiodactyla.

The question remains: why? The most likely explanation is that cetaceans evolved to exploit an unfilled ecological niche or adapted to new niches that formed as a result of plate tectonics or other types of environmental changes that occurred 50-55 million years ago. The niche describes all of the living and non-living resources needed by an organism to survive. Although land-based mammals were increasing in diversity, few or none were present in the oceans. The basic hypothesis is that the early whale-like artiodactyls, like Indohyus and Pakicetus were land-based (terrestrial) mammals that spent most of their time near the water's edge. Over time, they adapted to the niches in the ocean. Fossils like Ambulcetus and Rodhocetus showed clear evidence of swimming ability, with flattened tails and the enlarged rear feet. In addition, the nostrils shifted from the front of the face to the top of the head, which we recognize as the blowhole.
The shift to the aquatic habitat allowed these species to exploit resources that were not available to land-based mammals, thereby reducing competition for the resources. Reduced competition allows more individuals to survive and reproduce.
Similar scenarios are very likely for other marine mammals, such as seals or manatees. They evolved to take advantage of ecological niches that were not filled by other organisms. This basic concept, evolving to fill available niches, is a common outcome of the evolutionary process.
The of adaptation of cetaceans and other mammals to the oceans may be similar to that of the hippopotamus. Hippos spend most of their time in the water, and they show many adaptations that allow them to live in the aquatic environment.  The eyes and nostrils of the hippo are high on the head, which allows them to remain almost entirely submerged but still see and smell, as shown below.

(Hippo photo by Johannes Lunberg, Flickr Creative Commons.)
Hippos feed underwaters, they are heavy enough to walk on the bottom of the river, and the mate and give birth underwater. The young can suckle underwater. Clearly, hippos seem to be another mammal that is "returning to water." Similar types of processes must have occurred in cetaceans for them to adapt to the marine habitat.

Citations
Agnarsson, I. and L.J. May-Collado. 2008. The phylogeny of Cetartiodactyla: The importance of dense taxon sampling, missing data, and the remarkable promise of cytochrome b to provide reliable species-level phylogenies. Molecular Phylogenetics and Evolution 48: 964-985.
Gingerich, P.D. et al. 1983. Origin of whales in epicontinental remnant seas: New evidence from the early Eocene of Pakistan. Science 220: 403-406.
Gingerich, P.D. et al. 1994. New whale from the Eocene of Pakistan and the origin of cetacean swimming. Nature 368: 844-847.
Milinkovitch, M.C. et al. 1993. Revised phylogeny of whales suggested by mitochondrial ribosomal DNA sequences. Nature 361: 346-348.
Price, S.A. 2005. A complete phylogeny of the whales, dolphins and even-toed hoofed mammals (Cetartiodactyla). Biological Reviews 80: 445-473.

+1 - Exactly. Because the seas were there, full of food. It's a great example of how evolution works.

Nice write up!  I can see how a deep wader like a hippo might have started getting fins and going further out into the water, much the way manatees and sea lions seem to be doing.  The phylogenetic tree really helps.

@shigeta Thanks for reminding me about the hippos. I meant to include them in my answer. It was late though and I got sleepy, so went to bed instead. :)

While "filling niches" always sounds nice, it must mean that the niche is there, i.e. that no other already existing species is living there. Given that water based animals are probably more likely to adapt to niches in water I think there must be another advantage that mammals had over those that tried to filled the niece from water. Maybe something with changing water levels(tide)?

@PlasmaHH You're correct that the cetaceans could have adapted to a newly forming niche. It is also possible that the niche was there and empty. For example, the plesiosaurs and ichthyosaurs may have filled the niches. Their extinction would have left the niches empty. It is not safe to say that existing aquatic organisms were more likely to fill those niches, given the nature of the evolutionary process. Besides, the niches were filled first by reptiles.

@PlasmaHH Also remember that this did not happen all in one great leap.  Something land dwelling evolved to be slightly more aquatic, and that animal more aquatic still, and so on until we had fully aquatic whales.  Though this is very very much not what happened, it's easy enough to imagine something raccoon-like evolving into something otter-like, and seal-like, and whale-like in turn.  Each step in the chain provides a benefit to the species, but the niche that the last species filled never had to exist for the first.

@MikeTaylor Thanks for the answer; this is pretty in-depth and definitely answers my question.

Sorry for arriving so late to this discussion - a very illuminating write-up, @Mike Taylor, nevertheless. On the subject of why mammals were better suited to exploit the niche than piscine and reptilian competitors, I’d guess that warm-bloodedness gave them an advantage.

How did they evolve from their original form to their superficially ichthyoid appearance today?

This is an example of convergent evolution. Fish appear as they do (streamlined body shape, wide tail, fins, etc.) since these are adaptations to the underwater environment they're living and evolving in. These features are only "ichthyoid" or "fishy" because the fish 'got there first'. Instead, we can think of such features as "ocean-favourable".
Reptiles evolved on land, and hence have a generally different appearance from fish, but those which went back into the oceans to become the ichthyosaurs adapted again to live in that environment. Since they faced similar problems as fish (drag from the water, the need to maneuver in 3D, etc.), natural selection would favour the same "ocean-favourable" features as the fish (but not exclusively; for example, turtles have a rather different appearance, which is "ocean-favourable" but not as "fishy").
When mammals ventured into the oceans, they also faced these same problems and the same selection pressures, so they also gained a more "ocean-favourable" appearance.

Great answer. The idea of convergent evolution makes a lot of sense, and it's a pretty cool mechanism.

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Do couples having children later in life act as an evolutionary mechanism?
Ok, this may be just wild nonsense and I have to warn that my knowledge on the subject is limited.
I was reading about how in some countries people choose to have children later in life. After that this question came to my mind?
If human couples chose to have children later in life, lets say 40s 50s - disregarding keeping an younger self gamete preserved - wouldn't this result in the people less resistant to the effect of aging being unable to reproduce,  creating a more longevous generation? thus enabling future generations to reproduce even later lenghtening the average lifespan of humans?
ps: After reading this sounded a little too eugenic, by no means I'm trying to make this an legitimate theory or suggest an experiment, it's just a doubt - maybe good for some science fiction story...

Could you clarify your third paragraph? I think I know what you are asking but I'm not positive.

Are you suggesting that women store eggs while young to use post menopause? Becuase that would probably select for women who make eggs that handle IVF well, rather than for longer life.

Are you asking if there is a selective pressure to reproduce later in life?

@Jonathan Can you give us your opinion about the discussion in the comments below Mike Taylor's answer?

@MikeTaylor I'm not sure on how to clarify? I was wondering if the choice of reproducing later in life, allowing only those who were "fitter" at older ages to have children, would result on people that aged "better" and would make these people live longer...
I know that many aspects have to be taken out of the picture, like drugs, gamete preservation , the whole humanity having children later. It's just a wild hypothesis .

@GoodGravy no, i didn't even thought of this, it's more like a question on "what if everybody chose to have  children later"

@user137  no, my question is more on the lines of "what if only the women that had their menopause later in life reproduced"

Many factors have to be considered.  First, although more women are delaying pregnancy until after the age of 35, the overall percentage of women doing so remains very small, as shown by this figure from this New York Times article. Only about 9% of pregnancies in the United States (for 2008) were in women over the age of 35. Most pregnancies still occur in younger women. I suspect this is especially true when considered globally.

Getting pregnant later in life is more difficult, is more likely to result in miscarriage, and is more likely to result in some types of birth defects. The issues are discussed by the Mayo Clinic, WebMD, and summarized by Parenting Magazine. On average, individuals with birth defects are themselves less likely to reproduce (Skjaerven 1999).
For natural selection to favor a particular trait (such as later pregnancy), the individuals with the trait must have higher relative fitness, meaning they produce more offspring on average compared to other individuals. However, relatively few women have late-age pregnancies, more of the offspring are likely to have birth defects, and those offspring are themselves less likely to reproduce. In other words, on average, late-age pregnancies would have reduced fitness compared to individuals that get pregnant at earlier ages.
Most importantly, though, the decision to wait until later in life is a conscious choice, not a genetic trait. Natural selection can only work on genetic variation associated with particular traits. If the choice for delayed pregnancy has no genetic basis, then it is invisible to natural selection, and so cannot evolve.

Citation
Skjaerven, R. et al. 1999. A population-based study of survival and childbearing among female subjects with birth defects and the risk of recurrence in their children. The New England Journal of Medicine 340: 1057-1062.

The OP may have thought (and he would have been right) that if we delay reproduction, then deleterious alleles acting late in life will be purged yielding to a longer lifespan. This post is probably of interest to the OP.

@Remi.b Yes, if all or most individuals delayed reproduction but I do not think that is likely to happen. Most individuals reproduce early so the late-acting deleterious alleles would remain in the population, sensu the mutation accumulation hypothesis in GriffinEvo's answer in the post you link to. There would also have to be selection to remove the other deleterious effects of late-age pregnancies that potentially reduce fitness independent of life span.

The OP is asking "If human couples chose to have children later in life[..]". He therefore does not ask whether it is likely that individuals suddenly change their habit and start to reproduce later in life, he is asking how will senescence evolve if we assume that individuals reproduce later in life. I agree that the 3rd paragraph is kinda unclear.

@Remi.b I suspect you are correct that it may be a more theoretical question. I can delete or change my answer pending clarification from the OP.

Supposing I understood the question correctly, don't delete it anyway, it is always good to have some insights about the validity of the assumption

@Remi.b Fair enough! :)

I should have clarified this , but I didn't mean to say everyone is having child later - in Brazil teenage pregnacy is going through the roof - I meant more as a "what if this happened" question...
And please don't delete this, it's related to the question and great material

You will appreciate reading this post and have a look to the wikipedia article on the evolution of aging. I make below a quick summary and apply it to your question but I think it is worth looking at the other post on aging.
In short: Theory of aging
Imagine a deleterious (=negative) allele (=variant of a gene) that is expressed throughout the lifetime. This allele (by definition of a deleterious allele) will decrease the reproductive success of the carrier. Now consider another allele who is expressed only late in life, maybe after the first reproduction but before the second reproduction. This allele will decrease the reproductive success of the carrier but by a lower magnitude that did the allele that was acting throughout the lifetime so that it is more likely for this second allele to rise in frequency in the population to the point of becoming fixed (=reaching a frequency of 100%). In other words, natural selection is less strong on alleles acting late in life.  i.e. deleterious alleles acting late in life are more likely to get fixed resulting in the expression of many disease late in life. In the worst case, we can talk about alleles that are expressed after the time of the last reproduction. These alleles are not at all selected against (I make abstraction of kin selection here). Therefore, we should not be able to live long after the age of reproduction. non-reproductive grandmothers is kind of an exception and is explained by kin selection but I don't want to go into these details. Also, today's medicine explain why we live so long even after the last reproduction. For example articulation related disease that we experience at older age is often caused by this kind of alleles that are expressed only late in life. You can also consider alleles that are beneficial early in life but detrimental at the end of the life. THeir probability of fixation is even greater and these alleles have already been observed in nature. For more info about the evolution of aging, have a look to this post.
What happen if human decide to delay their reproduction age
So, what happen if suddenly all humans decide to reproduce later. Well, this will increase the selection against alleles that are expressed late in life and in the long run this will increase human lifespan (or at least it will increase the time during which humans are healthy). So yes, your hypothesis is right. However, as a sidenote, medicine may mess things up in the story!
Is it plausible that humans will start delaying their reproduction age?
For consideration of whether it is likely that the human population decide to delay their reproduction age, see @MikeTaylor's answer.


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Which C. elegans would be appropriate for general study?
Would wild type N2 be best or Dyp-11? I know they're different, but I just want to observe the worms to see life stages, movement, etc. Dyp-11 seems like it would be easy to see but N2 is the wild type so I need help making an appropriate decision.

What do you want to see? Just the worms?

What question do you want to answer? The "appropriate" decision will depend on what exactly you want to investigate. What conclusions will you want to draw from your research?

Yes, all I want to see is the worms themselves.

I suspect that that dpy-11-mutants (that's what you likely meant) are not very representative neither from the morphological nor from the behavioral points of view, because they have anomalies in body shape (dumpy appearance) and male tail morphology (see in WormBase and in Ko and Chow).
For a general purpose the wild-type should be best.


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How does the human body use energy?
As far as I know the glucose gets processed from carbs and fats and as a result carbon dioxide, water and "energy" are released. The carbon dioxide and water are expelled by the body, and then energy is used by the muscles. But how exactly is it used? What happens to this "energy" and what is it exactly?

Our body does not produce carbon monoxide. It does produce carbon dioxide.

Indeed, there is still one carbon monoxide in your post.

@ddiez :))))))))

You can break down the energy expenditure of the human body in terms of the different organs which use it up: this is done in this biochemistry book for instance, http://www.ncbi.nlm.nih.gov/books/NBK22436/
You can also look at the detailed expenditure of each cell: although the amounts will vary according to cell type (neuron vs. muscle cell, say!), the "budget items" are the same. See this thread: Breakdown of energy expenditure at the level of a single cell

Thanks! So the "energy" is actually ATP, which is then used for different chemical processes? Is there any pattern that's common to all these processes, such as periodicity for example?

Not all energy goes into ATP or GTP cycles, but these are the common way of having ready-to-use energy for molecular processes, e.g. molecular motors (in muscles but also other cells, to exert forces or to carry loads around e.g.). Heat is being produced without producing ATP/GTP, e.g.

I'm not sure what you mean by "pattern".


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Is there any way the food industry can benefit from biofilms?
I realize all of the disadvantages, but I am wondering if the food industry can actually benefit from the formation of biofilms.

"In the production of some fermented foods, biofilms are an essential element for optimum production. During the production of vinegar, acetic acid bacteria are allowed to grow on wood chips. The biofilm that is formed helps make the conversion of substrate to acid more efficient." - http://www.foodsafetymagazine.com/magazine-archive1/februarymarch-2005/beating-back-biofilms-in-food-processing/

inf3rno's comment provides a great example, in the production of vinegar (Food Safety Magazine):

In the production of some fermented foods, biofilms are an essential element for optimum production. During the production of vinegar, acetic acid bacteria are allowed to grow on wood chips. The biofilm that is formed helps make the conversion of substrate to acid more efficient.

This paper, Biofilms in the Food Environment (Czaczyk & Myszka, 2014) also provides examples of biofilm use in industrial food production (on page 75, 14th page in the linked PDF):

Bioreactors
  with biofilms (biofilms represent a natural form of cell immobilization) are used to obtain acetic acid, citric acid, ethanol, and polysaccharides.

You can also check out Chapter 7 of this book of the same name, Biofilms in the Food Environment, for more information, if you're interested. It's not available for free online but you may be able to find it in a library.


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What does it mean to have different "metabolism"?
We hear talk of different body types, and that it is more difficult for certain people to lose weight than others. On the other hand, when my physician recommends that I lose weight, they say that it is really just as simple as "calories in, calories out". How can we reconcile these two?
Perhaps the "calories out" portion is different for different people? I.e. some people burn more calories than others do, doing the same activities, but their hunger level does not compensate for this?
Apologies if this is off-topic

There are differences in metabolism, and the "calories in" part is the one which differs more than the "calories out" part.
People do lose different amount of calories for the same action, but for mostly mechanical reasons. If a 50 kg person walks up a mountain at 3 km/h, and a 100 kg person walks up the same mountain at the same speed, the 100 kg person will expend more energy, because they did more work. And then there are slight differences in how we do our movement - some people's gait is more efficient than others', and uses less energy. But this is not really interesting for the explanation of having it easy/hard to lose weight.
The point is that the amount of food we intake is determined by our hunger, and our hunger is determined by hormones. Then, the amount of fat we store is also determined by hormones. If your body "thinks" you should be putting on weight, and you go on a calorie-reduced diet, it won't just start complementing the missing energy from the fat stored in your adipose tissue. Rather, it will continue diverting some of your food intake to make more fat storage, all the while rationing the energy available for other activities: making you feel tired so you don't move much, shutting down some luxurious, energy-hungry processes in the brain, mostly the ones associated with higher mental functioning, and making you feel hungry and cold so you will be more motivated to seek out food and eat. The hormones which regulate these processes are many, most of them are poorly understood, some are probably not yet discovered (orexin, one of the main hunger regulating compounds, was only discovered sometime in the last 5 years I think), and we really don't have a complete picture of everything that is involved. It is a complex mesh of finely balanced homeostatic systems which interact with each other and the environment.
The people who say that it is as simple as "calories in, calories out" are right. They are right in the sense that, if you just observe a human being and measure their energy household, you will be able to document the amounts of energy consumed, expended and stored, and the energy consumed will equal the energy consumed plus the energy stored.
But to derive from this that we are talking about a passive overflow system and, if we reduce intake, storage is also reduced, is a big leap of faith and has been proven wrong again and again. Living systems are actively reacting to any influences from outside, by mechanisms much more intricate than simple mechanic rules. Mechanics tells us that if I push you, you will fall over; experience tells us that if I push you, you will brace yourself so you don't fall over, and then try to stop me from pushing you by using words, force, or whatever else you have at your disposal. Our physiological systems are the same way. They like the situation they have chosen to be in as much as you like standing upright. If somebody comes from outside and tries to forcibly change their status quo, they do whatever they can to 1) resist and retain the status quo, and 2) stop the outside force if possible.
As for the difference in metabolism: the hormone systems of different people are differently "tuned". For example, eating pure glucose causes insulin production to spike, and excess insulin causes glucose to be removed from the bloodstream, plus a handful of other effects. But the size of the insulin spike is different in different people. Also, the extent to which cells react to elevated insulin is different. When the reaction becomes dangerously weak at even high insulin levels, we say that it's a pathological variation, and call it "metabolic syndrome". If goes really towards zero, it's called diabetes type two. And this is an example about just one of the hormones connected to metabolism and the distribution and use of energy in the body.
On a simpler level, there is no difference in metabolism where physical energy calculation is concerned. Expending one molecule of ATP will let the same number of Na+ ions to move the same distance along a nerve dendrite, across humans. But this level is not really interesting when it comes to gaining or losing weight.

Some people burn more calories than others, in the default mode.
Just sitting in a chair, I warm the seat much more than some other members of my family.  That heat has to come from somewhere.
That's a different metabolism.
But, that's not something you can order and install.  It's not a pill.  Your doctor is right to focus on what you can control, and that's intake - along with your activity level; or outgo.  (But most people are unwilling to actually do the work to change their activity level to a higher one, which is why doctors don't even try anymore - patients just lie, and then doctors have to try to catch them at it, and nobody's got time for that).
What you eat may also impact the number of calories that stick.  Not everything you eat gets digested, some passes through.  And digestion itself burns calories.  Things that are harder to digest take more energy, and leave less surplus behind.
Easy things are... easier to digest and get all the calories from.
In addition, thinner people lose weight easier.  Not fair, right?  That's life.
It may have something to do with your microfauna, but that's not well studied.  And, we're not even sure if you can permanently change those populations.

http://www.mayoclinic.org/healthy-living/weight-loss/in-depth/metabolism/art-20046508

The warming of the seat is anecdotal speculation.

So you're arguing that heat happens magically, and doesn't require caloric input? Do tell us more, I can't wait to hear about it.

And why should thinner people loose weight easier?

If I had a handy cite, I'd give it to you.  Yeah, yeah, Abraham Lincoln said don't believe everything you read on the internutz

You say "Not well studied" - It is important to cite some material that is studied in your answer.

http://www.nytimes.com/2013/09/06/health/gut-bacteria-from-thin-humans-can-slim-mice-down.html?pagewanted=1&nl=todaysheadlines&emc=edit_th_20130906&_r=2&pagewanted=all&

And what are 'those populations'?

Populations of microfauna

It is more of a comment as it stands. Earn 9 more reputation and you can comment anywhere.

Thanks for the upvote, to help me comment - oh wait.

The warming of the seat is anecdotal speculation. And why should thinner people loose weight easier? You say "Not well studied" - It is important to cite some material that is studied in your answer. And what are 'those populations'? This answer may need some work. It is more of a comment as it stands. Earn 9 more reputation and you can comment anywhere.


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Is body energy production and consumption cyclical?
If we look into how energy is produced by the humans, it always involves some kind of periodicity: fuel combustion rotates engines, water rotates turbines, nuclear chain reactions heat up water, which rotates turbines, dynamo machines, etc.
So that means that with a few exceptions humans produce most energy (electricity) using rotation or some kind of cyclical rotative movement (as it proved to be the most efficient way of doing that).
Now what if we look at the human body? It is producing the energy from the food that we consume, converting carbs and proteins into glucose, which is then broken down into carbon dioxide, water and ATP. This ATP is then used in chemical reactions that are needed to contract the muscles or to send impulses within the brain.
The question is: Does anybody know – are those chemical reactions also cyclical in their nature? And if not, what's the common dynamical property (pattern) that can be observed in them all, if any?
Thank you and sorry for the long intro, but I thought it's important you know where I come from.

Do you mean a literal cyclical motion i.e a rotation? http://www.youtube.com/watch?v=PjdPTY1wHdQ ATP synthase rotates and takes advantage of a membrane potential to change its conformation. Would you like an expansion on this answer, or have I misunderstood your question?

the enzyme that produces ATP in fact, rotates like a little chemical motor.  not sure if this really answers your question... https://www.youtube.com/watch?v=zOSyGTYCRFw


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What is this tissue?
Does anybody recognize this picture and can tell me what organ it came from?

just in case this is homework.. http://meta.biology.stackexchange.com/questions/266/homework-policy-for-faq

This is not homework. I am creating a software system which will be used in biologic research. This is one of the pictures I might be using in the design, possibly as some sort of background. I am genuinely curious what the pretty daisy-like cells (or multi-cell structures?) are :) and also want to know more about it so I can search for similar images.

ok - just wanted to check (this is the sort of thing that gets posted a lot from students looking for a quick answer). It's a nice image, good luck

See Wheater's Functional Histology p. 283 Fig. 14.29e

Update 3: Credit should go to @Cornelius and @DMSever for initially identifying the tissue correctly. I incorporated D M Sever's answer into mine (Update 2,below) because his answer is being down voted for brevity, but he is a recognized authority in the field. I'll remove his answer from mine if his answer ends up being retained.
I showed this question to my histological colleague. He suggested that the tissue is most likely a submucosal gland from either the duodenum (Brunner's glands) or the esophagus. My colleague also said that your image is quite similar to submucosal glands in the large intestine but the presence of smooth muscle surrounding the glands eliminates the large intestine.
Update 1: My histological colleague forwarded your question to one of his histological colleagues. He too said Brunner's gland.
Update 2: My histological colleague forwarded your question to his most trusted histological colleague. He said colon, specifically the transverse sections through Crypts of Lieberkuhn. He then signed on as @DMSever and posted a brief but authoritative answer. He's a veteran of histological affairs.
Here's a photo of Brunner's glands in the duodenum, taken from here.

Here's a photo of the esophageal submucosal glands, taken from here.

I know it is your colleague who delivered the final identification, but you are the one who went to the trouble to ask two other people on my behalf, so I give you the accepted answer. I hope your colleague doesn't mind.

I'm not really sure, but it seems like a cross section of intestinal villi / intestinal glands from the large intestine.
Here are some images:

Jubal Harshaw. Large intestine villi cross sectioned showing goblet cells_100X_CS0187 on ShutterStock
Jubal Harshaw. Large intestine villi shown in both longitudinal section and cross section on ShutterStock
Garry DeLong. Light micrograph of large intestine villi in cross section, showing goblet cells (Magnification x400) on Getty Images
Hill, M.A. (2014) Embryology Gastrointestinal Tract - Colon Histology. Retrieved September 24, 2014, from https://php.med.unsw.edu.au/embryology/index.php?title=Gastrointestinal_Tract_-_Colon_Histology

And this is one image from the last link:

Crypts of Lieberkühn - (intestinal gland, intestinal crypt) [...] Transverse

It is from the Colon - transverse sections through crypts of Lieberkuhn seen there.
For references see:
Wheater's Functional Histology p. 283 Fig. 14.29e
UNSW Embryology.

Welcome to Biology.SE. DS said you mentioned a particular text. Would you mind editing your answer to include that reference? Answers on Biology.SE are considered stronger answers with references. Not everyone here will know of your expertise in the field.

Can you please expand your answer with some references? Actually it is more a comment.

I think the special "warning" should be removed now. This answer basically contains the same information as the top voted answer minus links to images, and names the specific structure seen in the picture.


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What is the biological reason for a burst appendix being potentially lethal?
Given that the appendix does not seem to be used by the human body, what is the biological reason that it is potentially lethal when this organ bursts?
Also, what would cause the 'burst'?

Necessary conditions
In order for the process culminating in appendiceal rupture to begin, there must first be proximal obstruction of the lumen (the inside cavity of the appendix) that prevents normal communication with the bowel.

Obstruction is most commonly caused by a fecalith, which results from accumulation and inspissation of fecal matter around vegetable fibers.
  The bowel wall inside the (now closed) appendix continues to secrete muscous, and bacteria continue to multiply, producing the distention that is often perceived as nausea, vomiting, and poorly localized abdominal pain.1

The process leading to rupture
As the pressure in the appendix increases, venous pressure is exceeded. This means blood can no longer exit the venules of the appendix normally. In the presence of ongoing arterial flow, this leads to vascular engorgement, worsening the distention and increasing pressure further. The inflammatory process spreads from the lumen (inside) of the appendix to the serosa (outside) and then to the parietal peritoneum (lining of the abdominal cavity). This last step is what causes the characteristic shift in pain from poorly localized visceral pain to focal right lower quadrant pain.
As distention worsens, arterial pressure is eventually exceeded, and the most poorly vascularized areas of the appendix (generally just beyond the point of obstruction on the antimesenteric border) infarct first. Dead tissue has very little structural integrity, and once infarction happens perforation is likely to follow quickly.
Why this is (sometimes) lethal
There are several possible mechanisms, more than one of which is probably operative in most cases.
The three I have listed below all converge on the same final common pathway: In the absence of adequate systemic blood pressure (shock), the heart is not able to pump normally and will eventually deteriorate into a non-perfusing rhythm (a.k.a death).

Bacteria in the peritoneal cavity:
As in bowel perforation of any cause (e.g. perforated peptic ulcer, perforated diverticulum, traumatic perforation), bacteria in the peritoneal cavity (the “free space” outside the bowel within the abdomen) triggers an intense inflammatory reaction and fluid sequestration. Fluid pulled from the circulation into the peritoneal space causes hypotension and (hypovolemic) shock.
Infarcted bowel: Dead tissue connected to the body is never a good situation. Intracellular contents are released into the bloodstream – electrolyte release can cause hyperkalemia and other electrolyte imbalances; reactive oxygen species can lead to hypotension and (distributive) shock.
Sepsis: Bacteria (generally gram negative rods from among normal gut flora – most commonly Escherichia coli or Bacteroides fragilis)
may enter the bloodstream due to compromised vessels during the process of infarction and rupture. Lipopolysaccharides in the cell wall of gram-negative bacterial organisms lead to activation of monocytes and macrophages. This results in increased levels of interleukin-1 and tumor necrosis factor and eventually of IL-6 and IL-8. These cause widespread endothelial injury leading to diffuse alveolar damage in the lungs and activation of the coagulation system leading to disseminated intravascular coagulation. These cytokines also lead to systemic vasodilation and (distributive, septic) shock.

References

1. Silen W. Chapter 300. Acute Appendicitis and Peritonitis. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. eds. Harrison's Principles of Internal Medicine, 18e. New York, NY: McGraw-Hill; 2012.

2. Kemp WL, Burns DK, Brown TG. Chapter 8. Hemodynamics. Pathology: The Big Picture. New York, NY: McGraw-Hill; 2008.

3. Charles Brunicardi, F. Acute Appendicitis. Schwartz's Manual of Surgery; 2006.

The appendix doesn't burst by itself. It just lives there quietly, not causing problems.
But if it gets infected, it gets full of bacteria, their waste (frequently toxic), and whatever liquids your body exuded into it to fight the infection. It is also connected to your digestive tract, which contains half-digested food.
When the appendix swells due to the infection, the pressure can build up enough that it bursts - unlike, say, the bladder, which also can be infected, and also has a baglike shape, but it also has a way to get emptied, which reduces the pressure. It is like having a boil filled with pus, you know how the skin on them gets thin and can burst. But this boil is inside of you, not on the outside.
And once it's burst, all this pus goes into your bloodstream, full of bacteria and toxins. If this is not treated, you get sepsis and die.
This is the biological mechanism for dying from burst appendix.If by reason you are asking why we have  a useless organ which can kill us -  nobody knows for sure, but our best guess is that evolution just hasn't gotten around to get rid of it. It served a function once, and has been getting smaller and smaller since then, but the genes which cause it to appear haven't yet been bred out of humanity.
As pointed out in the comment, it is not a useless organ (turns out my biology teacher in highschool was wrong). It has a function, and just like any other organ, it is useful while healthy and can kill you if it gets a disease.

The appendix is not useless. See: http://biology.stackexchange.com/questions/1502/is-the-appendix-a-vestigial-structure-in-all-vertebrates

@kmm thank you for pointing that out, I didn't know it's a myth. It's so widespread, I'm pretty sure I learned it at school.


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Why is Psoriasis treated with Cortisone, when stress (which releases Cortisol) is known to aggravate the condition?
It is well known that stress isn't good for psoriasis , yet why do we treat the illness with Cortisone, a compound very similar to cortisol (and "has a similar name, genesis, and function", according to wikipedia) whilst cortisol is released in the body in stress situations?

For treatment reasons cortisol is named Hydrocortisone (probably to avoid problems with the similar names) and this is often only referenced to as cortisone (although this is not correct). Cortisol (Hydrocortisone) is the active form, while cortison is not. See here for some more details.
Glucocorticoids (like Cortisol or Prednisolone) suppress acute inflammation and also have immuno modulative (downregulate) or suppressive function. Since the immune system causes the problems in Psoriasis it is downregulated to control the outcome of the disease.
First it sounds counterintuitive to use Glucocorticoids for the treatment of psoriasis as this hormone is released during stress (in this case to mobilize energy resources). However, there is a study which looked precisely at the cortisol levels in psoriasis patients and also recorded their stress levels.
What they found was interesting: First they could correlate the peaks in the stress levels with a psoriasis attack about four weeks later. Then they found that the Cortisol levels of the patients where significantly lower in stres situations than for healthy control persons. Additionally they found that patients which had permenant high stress levels also showed significantly lower permanent Cortisol levels. So here the stress seems to negatively influence the cortisol levels which then prepares the way for psoriasis attacks. Using high levels of topically administered Cortisol seems to reverse this effect.
You can find the study here:

How stress gets under the skin: cortisol and stress reactivity in
psoriasis.

so if hydrocortisone is released in the body in periods of stress, the suppressing effect on psoriasis would increase. But why does stress worsen psoriasis?

@user2606722 I expanded my answer.

thank you very much! It was exactly the answer I was looking for!


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Need to make a library of mammalian coding sequences
I want to clone ~100 different coding sequences from human or mouse into an expression vector to analyze phenotypes in tissue culture. I can do all of the steps, but I'm not sure what I should use as the template for my reactions. Ideally, I would purchase a pool of full length cDNAs from a bunch of organs, and amplify from that. Less ideally, I can generate cDNAs myself, from multiple organs and pool them. Does anyone have suggestions on a template source?

If you plan to take one isoform for each one of the genes, then I see no point in amplifying them pools of tissues.

The goal is to do a miniscreen for proteins of annotated with a specific function (there are about 100 genes). The idea is to automate the task as much as possible, without spending too much time choosing isoforms or fusion points.  I just don't have experience doing this, so I'm not sure if such libraries exist, or if I essentially need to start from scratch from cDNAs and gene specific primers. I figures that by pooling cDNAs I would most likely amplify the most abundant isoform.

Verify where these transcripts are generally present (this should not be difficult for common organisms)
If they are all expressed in a certain tissue use cDNA from that tissue
If not then pool the cDNAs from different tissues such that all genes can be amplified
cDNA libraries (including whole organism) are also available and you may obtain them from the nearest repository (I guess NCBI also provides).

Some other things you can do:

Ask the primer synthesis company to provide primer sets it in a
96well format.
DNA synthesis is also a decent option (it takes something like $0.5
per base pair), but that can be expensive if your cDNAs are huge.


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Thermochemistry of gabapentin
So I am taking a new class at my institution called Theoretic Nuclear Thermochemical Pharmacology, (I know big name, it's an elective from a real pioneering fronteirsman in our department :P) and I am curious about the metabolism of gabapentin and how this might relate to thermochemistry?  I am curious how this drug metabolizes in the liver and how it neurochemically alters the brain such that it reduces mania in patients that are bipolar and may also have mood disorders.  Any kind of relevant literature would be appreciated, something to guide me in the right direction.  I mean I understand liver metabolism and what it does but its relation to mania and how it's thermochemical still boggles me.

@ChrisStronks Isn't this a commonly accepted term? Anyhow, I think in some cases entropy dominates rather than heat.

Also, the way you phrased your question is too open ended, and it's hard to answer. You should rewrite it so that it has one clear answer.

@Superbest - thanks for the link. Having read this weblink, and re-reading the question I think I would have phrased the question as "I am wondering (1) what the drug metabolism is of gabapentin in the liver; (2) whether these catabolic liver reaction(s) are exothermic or endothermic; (3) how gabapentin or its metabolites reduce mania in bipolar patients (i.e., gabapentin's pharmacodynamics); and (4) how the thermochemistry of liver-catabolism of gabapentin relates to its manialytic properties" I think the question's scope is too broad, as it mixes basic toxicology and neuropharmacology.


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recolonize earth desert with plants : which plants first?
if willing to recolonize earth desert , let's say sahara or any dehydrated and sterile land, without intensive human intervention, what would be the first plants / algae / fungi /bacteria to grow ?
what could be the strategy to slowly bring back biodiversity and trigger new water cycles ?

I think this is far too broad since you cover recolonization (for humans?), restoring biodiversity (from where/what?) and water cycles. Ask several smaller questions instead, preferably including your own ideas and preliminary research to answer them.

this question is answerable, but it just needs a longer answer...

This is a big idea that's gaining momentum in many people's minds across the world.  This is a brief and probably inadequate survey and hopefully other answers / comments will fill out a better picture.
Most of the plans to reclaim arid regions are not completely hands off.  It seems that the current thinking is that if we waited for microbes and lichen to reclaim arid soil, it would take too long.  Most of them focus on trees.
Trees are fantastic because they can grow in climates that have minimal water once they are established.  They can claim moisture from the air, remove pollution from the air, reduce the ground temperature, sequester carbon, prevent erosion, and make the environment more accommodating to other plants.
Some estimates are that to curb the expansion of deserts worldwide, 30 billion trees should be planted every year for the next decade.
The tree one plants varies depending on the place and application, but the selection of the plant is more than just a climatic choice.  Trees are grown in nurseries when their needs for water are most intensive, and then need to be cared for until they are established enough to survive on their own.
The Green Belt project was the focus of the 2004 Nobel Peace Prize.  Its success in rolling back desertification was because of its understanding of the causes of desertification in many cases as a social effect.*  People harvest the trees, graze the land dry, burn grassland etc.  Green Belt created networks of local people and incentivized them to grow trees, selecting trees which had agricultural and economic value so that they would help the local economy.
The Great Green Wall project is a successor to this idea.  Attempting to contain the Sahara desert's spread across the continent of Africa.   Their plan is to have a different organization in each country, including automation of sorts to collect water from the air and rain for more continuous support of young trees.

there are arguments that ultimately the animal ecosystem needs to be involved.

i suppose a strategy would be :
-find among xerophyte plant ( http://en.wikipedia.org/wiki/Xerophyte ).
-selecting plants that needs the less water, grow fast and expand on surface, and produce the maximum biomass.
-the soil produced by the pioneer plants would allow other plants to grow.
-these last plants would be selected for their better ability to condensate water and cool the atmosphere down and humidify it, and for producing more biomass that would allow a third pool of plants to grow


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Can Mono-Cell or other organism self-replicate?
I have a question regarding how organism replicate them self to create an other organism,
We know that in animal reign, we need a male and female that will generate a new being.
what I want to know is if there is a micro organism that can create another one without a partner of the same kind? and in that case how this organism can do that?
hope my question was clear!
Thanks!

The short answer is yes, there are single-celled organisms that can reproduce without another "partner". Probably the most famous example is that of bacteria.
What you're talking about is known as asexual reproduction. In bacteria, the process is known as binary fission, where one bacterium (known as the parent cell) divides into two organisms (known as daughter cells). These two cells will be genetically identical (barring any mutations) to the parent cell, because there has been no combination (for lack of a better term) of DNA, as there is in sexual reproduction.
The process works the same way it does in cells in multicellular organisms, such as humans: DNA "unwinds" (again due to lack of a better term) in the center of the cell, complementary bases are added to each of the now-separate strands (adenine with thymine, guanine with cytosine), the other parts of the cell are duplicated, and, gradually, the bacterium splits in two. The process can be very quick, compared to the nine months humans spend in the womb.
Asexual reproduction is not unique to single-celled organisms, though. While it is prevalent (and easy) in bacteria, some multicellular organisms reproduce asexually. Some plants are capable or this via self-pollination, and there have been some reports (albeit rather dubious) of certain "common" animals reproducing asexually.
There are advantages and disadvantages to asexual reproduction. One advantage is obvious: no mate necessary. As long as an organism has enough energy and nutrients to reproduce, it can. Also, the process is quick, and easy. There are some disadvantages, though. The big one is that there is no recombination from multiple DNA sources - that is, the resulting organism will have exactly (again, barring mutations) the same genes as its parent - for better or for worse. If an asexually-reproducing organism has a defect that still allows it to reproduce, chances are, its offspring will have that defect.
Some sources:
http://plato.acadiau.ca/courses/biol/Microbiology/Replication.htm
http://www.yourarticlelibrary.com/biology/asexual-reproduction-in-animals-characteristics-occurrence-and-types/11727/
http://www.mpipks-dresden.mpg.de/~mbsffe09/talks/Krug.pdf
http://www.britannica.com/EBchecked/topic/498542/reproduction

I disagree with your statement that asexual reproduction is known as binary fission in bacteria. Some bacteria reproduce by budding and some eukaryotes and archaea reproduce by binary fission.

@canadianer Are you saying that binary fission is not unique to bacteria, that it is not the only method used by bacteria to reproduce asexually (which I knew but did not put in), or that it is not correct terminology?

Ok, does it happened in nature that the resulting organism have different DNA then the parents?

If there is one parent, and there are no mutations, then the offspring will have the same DNA as the parent. If there are multiple parents with different DNA, then the organism will have different DNA than the parents.


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What are the ways to test for protein in the canine urine?
I know that one way is to use the reagent sticks and the refractometer, but this is inaccurate. Is protein distinguishable when using a microscope? Is it time sensitive(i.e. have to test it right away)?

After some research, I could primarily find two tests for testing the protein content in dog urine.
1) The Urinalysis dipstick test (reference) which has a chance of giving false positive results (reference). Here is the link to a lab test done using the dipstick method and the results that the researchers got.

A sample Dipstick (reference)
2) The second test would be the benzethonium chloride test (reference).

This test precipitates the protein and increases the turbidity of the
  sample. The turbidity is proportional to the protein concentration.
  This technique is very sensitive and can yield accurate results in
  samples with very low protein concentrations (< 20 mg/dL).

A lab study done using this procedure to precipitate protein (reference).

The urine sample is best read within 30 minutes of collection
  otherwise certain factors (like crystals, bacteria and cells) may
  alter their composition (dissolve or multiply) over time. If you
  collect a urine sample at home, please drop it off at your veterinary
  clinic as soon as possible (reference).

Reasons for excess protein if present in the urine of your pet is listed in this article.

Sorry to bother again, did you find out by chance whether the upc ratio test is time sensitive or not?

@shooting-squirrel Since the quality of the sample is what could be affected after the aforesaid time period. I believe that the quality of any urine related test after that time period could be skewed.

@shooting-squirrel I just found an article which said that if sufficiently refrigerated, the sample should be alright for maybe even 24 hours. Don't worry about it if you handed over the sample to the lab.


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Hormones and body mass
I was wondering how some animals (bulls, elephants etc.) become so large by only eating grass or plant based material and why some humans can build large amounts of muscle and mass without a proper diet.
1. How do both get their essential amino acids in order to build muscle and mass?
2. Can hormones independently build muscle and mass regardless of the food or amount of calories ingested?

All life has amino acids. That bulls and elephants are alive suggests that they can obtain any amino acids that they can't synthesise from their diet.

hormones are only signals - how the organism responds to hormones is tuned by evolution in each organism.

The amino acids to build muscle and lean mass come from essential amino acids that must be consumed via diet that contains these, which most plants do not.

Could more hormones then possibly send a signal to extract more nutritious material from food in order to build more mass?


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Meta-analysis of fruits in blocking Cytochrome family
My professor says that some drugs cannot be used with grapefruit.
I am trying to search a list of cytochromes and their effect to block members in the cytochrome family. Some in Cyt P450.
What is the main meta-analysis of fruits in blocking cytochrome family?

While I haven't found a list which is restricted to fruits, I found this page: P450 Drug interaction table. They list quite a number of substances which inhibit different isoforms of the P450 protein and also give the original references.
This list gives a large number of herbals which inhibit different P450 isoenzymes. The disadvantage is that they do not give further references so if you want to have a closer look you will probably have to spend some time with Pubmed.

Thank you! The table includes the grapefruit juice as moderate inhibitor that was emphasized by my lecturer. I did not see any other significant food there.

The second list contains a number of latin names of different plants. If you translate them into the normally used ones (Wikipedia is helpful here) you can see if there are other fruits among them.

I asked my old Latin teacher how to learn the latin names of different fruit. I think there is some logic behind the fruit names.

Add the complete latin name into the search field of the Wikipedia to get the normally used name. Works pretty well.

Any possibility of doing it for those all at once? Doing list search?


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What is hTAP?? Please help
Could not find a single article regarding this. What is hTAP? Tap is Transfer associated protein, that I know, but what is hTAP??(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)

From which context do you have this?

I recommend that you put some more effort into your questions, they're mostly lacking context and are often rather easy to google.

I did search for hTAP, did not find any useful information

You definitely need to add some context - what sentence(s) did you see it in, and where? A Web Of Science search for hTAP in the TITLE field points to "Human thyrotropin-releasing hormone-associated peptide" but that doesn't appear to be relevant. It isn't unusual for acronyms like this to have several meanings.

I'm voting to close this question as off-topic because the question lacks any effort whatsoever.

hTAP refers to human TAP protein (reference). And how do you know that TAP refers to Transfer Associated Protein? I believe it stands for Transporter Associated with Antigen Processing (reference). Your facts are wrong which is why your question couldn't be answered.

http://www.springer.com/biomed/immunology/book/978-1-4939-1114-1
this book has TAp written as transfer associated protein

@user3237995 I don't know about the book because I don't have it but that article definitely mentions TAP as Transporter Associated with Antigen Processing in the abbreviation section. So why did you link me to it?


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Data Bias in protein-protein interactions data
Databases like STRING have so many predicted as well as experimental interactions data for many organisms.However there is a bias in the data which they have?.

a)The first is gene co-occurrence  which is more like a circular argument.
b)And the second one is that all interactions that are predicted computationally are tested for experimental interactions.This leads to a bias in the interaction data available for organisms in STRING.

How do we overcome this data bias while using STRING interaction data for analysis purpose?

a)Avoiding evidence channels of gene co-occurrence is one way.Is there any other way other than this?
b)How to statistically say that the bias is not governing the data or any way to test statistical significance of the data bias?

I'm one of the STRING maintainers, so I hope I can clear things up a bit.
Gene co-occurrence: genomic context methods are very useful for bacterial genomes, but not so much for eukaryotes. However, they are actually the most unbiased data we have, since there's no human influence (beyond selecting species for sequencing).
Benchmarking: Interactions predicted from text-mining etc. are benchmarked against the KEGG database. However, this doesn't necessarily lead to biases, as this benchmarking is basically a calibration step.
Actual biases: For eukaryotes, most interaction data comes from the experimental, database and text-mining channel. All of these are biased in various ways: e.g. there are study biases (disease genes will get more attention) and technical biases (some proteins are hard to work with)
As we don't know the actual set of protein-protein interactions, we can probably not test for biases in the data.

Could you please answer this question http://biology.stackexchange.com/questions/25914/string-id-allelic-differences-and-splice-variants


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Encephalitozoon cuniculi
Can anyone advise me a literature supporting the claim that Encephalitozoon cuniculi is an aerobic organism? I have seen papers saying otherwise, but also I was told that this is not quite true.


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Defining dominance and selection in these formulae
This paper uses two equations to explain the different conditions under which sexually antagonistic genetic variance is maintained in a population, while allowing for unequal dominance, for autosomally linked loci:
$h_f / 1-h_m + h_fs_f   <$ $ $ $   s_m/s_f   <  1-h_f/h_m(1-s_f)$
And X-chromosome linked (X-linked) loci:
$2 h_f / 1+h_f s_f < $ $ $ $ s_m/s_f < $ $ $ $2(1-h_f)/1-h_f s_f$
where $s_m$ and $s_f$ are the selection coffecients against the less fit homozygote (or hemizygote) in males and females respectively where the most fit genotype has a relative fitness of 1. Similarly $h_m$ and $h_f$ represent the dominance of the less fit allele in males and females, and $h_m$ is not applicable in the X-linked equation because there is no dominance (due to hemizygosity it can only be homozygote).
I'm having a little trouble understanding how $s$ and $h$ are defined here.
For $s$, is it the fitness of the deleterious homozygote or the difference in relative fitness between the two homozygotes? Such that either $s$ = the relative fitness of the homozygote, or, $s$ = 1 - relative fitness of deleterious homozygote, where one represents the fitness of the fittest homozygote thus giving the fitness differential.
For $h$, is the dominance defined as the fitness difference between the less-fit homozygote and the heterozygote, or the most-fit homozygote and the heterozygote? Or is it the deviation from the average fitness of the two homozygotes?
Going from the graph (see below for values of fitnesses), what are the values of $s_m$, $s_f$, $h_m$, and $h_f$ where the dashed line is Females and solid line is Males. I see possible values of either $s_m$ = 0.2 or 0.8 (fittest genotype - fitness of weakest), likewise $s_f$ is either 0.3 or 0.7, $h_m$ is either 0.1 (deviation from most-fit genotype), 0.7 (deviation from least-fit) , or 0.3 (deviation from average) and $h_f$ is either 0.3, 0.4, or 0.05.

The values here are, as fitnesses for genotypes A1A1, A1A2, and A2A2, for males, 1.0, 0.9, 0.2, and for females 0.3, 0.7, 1.0.

Fry (2010) borrowed his variables from Kidwell et al. (1977).  Kidwell defines the fitness of each genotype as,
$w_{m1}$, $w_{f1}$ = male and female fitness of the A$_1$A$_1$ genotype.
$w_{m2}$, $w_{f2}$ = male and female fitness of the A$_1$A$_2$ genotype.
$w_{m3}$, $w_{f3}$ = male and female fitness of the A$_2$A$_2$ genotype.
Kidwell then establishes the following parameters for each fitness variable for opposing additive selection,
$w_{m1} = w_{f3} = 1$,
$w_{m2} = 1-.5s_m$,
$w_{f2} = 1-.5s_f$,
$w_{m3} = 1-s_m$, and
$w_{f1} = 1-s_f$.
Therefore,
$s_m = 1-w_{m3}$, and
$s_f = 1-w_{f1}$.
$s_m$ and $s_f$ are the relative fitness differences between the two homozygous genotypes of each gender. The heterozygotes are assumed to have half of that differential. This is what Fry refers to on page 2 (page 1511 of the publication):

In Kidwell et al.’s notation ... the most fit genotype in a given sex has a relative fitness of 1, and $s_m$ and $s_f$ are the selection coefficients against the less-fit homozygote (or hemizygote) in males and females, respectively.

For opposing selection with arbitrary dominance, Kidwell parameterizes the heterozygous fitness components as
$w_{m2} = 1-h_ms_m$, and
$w_{f2} = 1-h_fs_f$.
Notice that $h$ is modifying the fitness difference $s$ in the heterozygotes. This is due to incomplete dominance of one allele over the other. If both alleles in a heterozygote contribute equally to the phenotype, then $h = 0.5$, and you have the additive fitness described above ($w = 1-.5s$).
If one allele is incompletely dominant over the other, the selective difference $s$ will be modified by some amount, $h$. If A$_1$ is only slightly dominant over A$_2$, (say, $h=0.6$), the effect on $w$ won't be much different than if $h=0.5$. Both alleles will affect fitness but the more dominant allele will have a slightly greater affect on fitness than the other allele. If one allele is much more dominant, then $h$ becomes larger and the more dominant allele contributes more to the overall fitness than the other allele.
Finally, if $h=1$ then one allele is completely dominant so the other allele will not contribute at all to fitness. When $h=1$, the equations reduce to $w = 1 - s$ (for the respective genders), remembering that $h$ is based on the dominance of the allele with maximum fitness in the other gender.
Consider a female. Her maximum fitness is the A$_2$A$_2$ genotype.  If A$_1$ is completely dominant over A$_2$, then a heterozygous female would have fitness equal to the A$_1$A$_1$ genotype which, for females is defined as $w = 1-s_f$. On the other hand, if A$_1$ is not completely dominant over A$_2$, then the heterozygote will have some reduction in fitness but not as much as for complete dominance.
To answer your final question about your figure, given the following values for A$_1$A$_1$, A$_1$A$_2$, and $_2$A$_2$, respectively:
$w_m = 1, 0.9, 0.2$, and
$w_f = 0.3, 0.7, 1$, then
$s_m = 1 - 0.2 = 0.8$, and
$s_f = 1 - 0.7 = 0.7$.
For the heterozygosity effect ($h$), given that
$w = 1 - hs$, then
$h = \frac{1-w}{s}$, therefore
$h_{m2} = \frac{1 - 0.9}{0.8} = 0.125$.
A$_1$ is nearly completely dominant over A$_2$ in males, so the presence of A$_2$ is the male is not reducing his fitness by very much. For females,
$h_{f2} = \frac{1-0.7}{0.7} = 0.429$.
The presence of the dominant A$_1$ allele in females has stronger heterozygous effect so her fitness is reduced more, compared to heterozygous males.
Citations
Fry, J.D. 2010. The genomic location of sexually antagonistic variation: some cautionary comments. Evolution 64: 1510-1516.
Kidwell, J.F. et al. 1977. Regions of stable equilibria for models of differential selection in the two sexes under random mating. Genetics 85: 171-183.

Hi @MikeTaylor Thanks for the answer, I've just edited a couple of the annotations which I think were incorrect, could you check the edit history to proof them for me please

also should "Therefore,
sm=1−wm1, and
sf=1−wf3." read as "Therefore,
sm=1−wm 3 , and
sf=1−wf 1 ."

@GriffinEvo Thanks for your careful proofing. I also added a bit more to answer your question about your figure.

Thanks again, I had gotten myself tangled - I knew how to define a selection coefficient but got spiralled out by self doubt when reading the paper and getting tangled in the math of it all! It's all cleared up for me now (and I've managed to recreate fry's results, using dummy data in R I have managed to duplicate figure 3a and 3b)


text:
force required to do damage to child's leg/feet in collision
I'm currently working on a toy robot for a student project. Part of this robot is the fact that it will be moving around quite fast. As such hitting the child can and most likely will happen. As such we are obviously worried about safety. So what type of forces can a child safely withstand? The robot will most likely not be very tall (45 cm) and be shaped like the top half of a sphere, as such most collisions will happen with the shins or the feet.
I do hope this is in the correct  stack exchange and that this isn't supposed to go into a different stack exchange.

This question appears to be off-topic because it is about not in the scope of biology SE, not likely to be answerable given the current information, not likely to be answerable at all (I doubt any one has been able to get funding to study how much force a child's legs can take before they break...) & there's too many variables. You should be considering other options first such as how to make the robot not damage a child, like padding, shape, or not having it hit the child at all!

You should also take in account that it is a toy. Even if a collision does not damage the child, it might still scare it. Which is reason enough to avoid collisions.

I know that I have to use padding but the main question is: how much padding? In order to find out I would like to know a maximum safe force so that I can calculate how much padding to add. I will of course add in AI that avoids targets but this can never be assumed to work(it only has to go wrong once).


text:
What keeps the resting potential of neurons constant at -70 mV?
I know the sodium-potassium pump pumps out 3 Na+ ions and pumps in 2 K+ ions per reaction so the negative charge in the axon increases. However, once the voltage (difference of charge inside and outside of the neuron) gets down to -70 mV, this stops going further below. Why?
I know that this is because of other transport proteins and the presence of anions and cations in the axon, but what are those proteins and ions precisely? There are always negatively charged proteins inside a cell, including a neuron, so I assume there must be a strong force which keeps the voltage from going down.
By the way, is the opening and closing of an ion channel triggered by the voltage of the neuron or the concentration of the ion?

Take a look at the wiki article for Resting Potential: http://en.wikipedia.org/wiki/Resting_potential. Essentially, you form a balance between the electrical force pushing ions through the channels and the force caused by an imbalance in chemical concentration in ions across the membrane.

What about the mitochondrial inner membrane potential of neurons? Does this even have to be more negative for mitochondria to work?

Potassium tends to leak out of the cell via "Potassium leak channel" - These are passive potassium channels that do not require ATP or energy. Potassium flows along the concentration gradient - from inside to outside.

The neuronal cell membrane is quite permeable to K+. Because the Na+,K+-ATPase pumps K+ inside of the cell, K+ tends to diffuse outward again, thereby taking positive charge outside the cell and making it negative inside (see Further Reading 1). This outward flow of K+ stops at a certain point, because the driving force of K+ diffusion out of the cell along with its concentration gradient, equals the charge gradient, which becomes more and more negative inside the cell as more K+ diffuses out (see Further Reading 2). Hence an equilibrium is reached which is close to the resting membrane potential of -70 mV. Other ions such as Cl- are also relatively permeable and affect the resting membrane potential (see Further Reading 1). Ions such as Na+ and Ca2+ are typically highly impermeable and do not substantially affect the resting potential.
As to your second sub-question:voltage-gated channels are gated through voltage differences (Purves et al., 2001), not ion concentration differences.
Further Readings
1. If the average resting potential of a neuron is -70 mV, why is there such a high ratio of K+ ions inside relative to out?
2. Why do negative ions flow into a cell in an inhibitory synapse, even though a neuron has a negative resting potential?
Reference
- Purves et al., Neuroscience (2001). 2nd ed. Sunderland (MA): Sinauer Associates


text:
Question about *Cryptosporidium hominis*
Cryptosporidium muris infects mostly rodents and it is usually found in gastric gladns. Cryptosporidium parvum infects humans and certain animals and it is found in the terminal ileum and colon.
There is also Cryptosporidium hominis that infects only humans. My question is

where exactly in the human gastrointestinal tract it resides?

This page seems to indicate that it adheres to the epithelium of different internal organs. They write:

The sporozoites are released and parasitize epithelial cells (b, c) of the gastrointestinal tract or other tissues such as the respiratory tract.

Here is the figure from that page:

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


text:
How long does a mosquito take to land on a host, bite, and fly off?
How long does a mosquito take to land on a host, start its bite, end its bite and then fly off?
And what about different species?
I am most interested in human hosts.
References to web sites or books would be appreciated.
I cannot find this even after extensive trawling of Google.

That's an interesting question and not easy to answer. I haven't found data for humans but from experiments with mice. They analysed how the mosquito actually bites, probes for the blood vessels (not all bites are successful) and finally sucks bloods. In their research  they observed feeding times between 150 and 329 seconds, depending on the size of the blood vessel. The mean feeding time was 240 seconds. It also depends on the age of the mosquito, older mosquitos suck longer. To this comes the time for probing (mean time 142 seconds) and the time before the mosquito starts probing after it landed (mean time 6.5 seconds). This totals to about 389 seconds (or roughly 6.5 minutes) total time after landing. This data can be found in table 1 of reference 2.
This is pretty interesting, they also show videos of the mosquito probing the skin for a blood vessel. You can find a pretty nice summary in the first reference and the original paper in the second:

Here’s What Happens Inside You When a Mosquito Bites
Visualizing Non Infectious and Infectious Anopheles gambiae Blood
Feedings in Naive and Saliva-Immunized Mice.

Table 1 from reference 2 above has additional data on the time to start of probing (mean time to start 6.5 seconds), probing duration (mean time 142 seconds) which I presume are before the feeding time (mean time about 240 seconds). The mosquitoes involved were Anopheles gambiae. It must be noted that this was in a controlled laboratory environment on mice, not humans, but the data is still a very good start.

You are right. So this adds to the 240 seconds, coming in total to about 389 seconds. I know that this is in a laboratory environment but I haven't found any other serious data on this topic.

Nice finds Chris +1

Nice answer +1. Having worked with mosquitoes during my undergrad, I can tell that it very much depend on the activity on the host though. A mosquito coming to bite you the night while you're partying with your friends outside might often just land and go away too afraid that we sensed its presence. But if you're sleeping (and if you're not moving during your sleep), then the mosquito may take longer. I haven't read the paper but those estimates seem to correspond to static hosts.

Btw, I've been told that bites when they have to hurry up hurt more than bites when they had time to suck, make sure to be completely fed and leave when they finished. But that might be a urban legend, I don't know.

Gillett studied the feeding behavior of Aedes africanus and Aedes aegypti, the abstract says that

They showed that while the period between salivary injection and the
  onset of irritation was the same in both species (ca. 3 min)

It seems to me that the abstract does not say whether the hosts were humans or not. Unfortunately I am not able to get the full paper.
GILLETT, J. D. Natural selection and feeding speed in a blood-sucking insect. Proceedings of the Royal Society of London B: Biological Sciences, 1967, 167.1008: 316-329.

This does not address the question


text:
What is Colloidal biology and does it have any scientific background?
There is the following bulletin published for the History of Chemistry Vol. 32: 105-118 in 2007:
“MOLECULAR” VERSUS “COLLOIDAL”: CONTROVERSIES IN BIOLOGY AND BIOCHEMISTRY, 1900–1940*
written by PhD habilitation research professor Ute Deichmann at the Leo Baeck Institute (LBI) in London and leader of the History of the Biological and Chemical Sciences Research Group at the Instritute for Genetics, University of Cologne.
Therefore, the question is: What is Colloidal biology, what are the basic differences between molecular biology and does it have any background in modern scientific community?

The WP page on colloids http://en.wikipedia.org/wiki/Colloid#In_biology has a useful jumping off point (see subheading "In biology"). There is a discussion in the book "A History of Molecular Biology" my Michel Morange.

There are two antipodes: The molecular (or makromolecular) biology, which has the concept of large macromolecules which fulfill one task. This can for example be an enzyme which breaks down its subtrate. The properties and the structure of all molecules of the enzyme are the same and the factor determining the function of the enzyme.
The coloidal biology assumes that the function is granted by adding small amounts of an enzyme to water to form a colloid, which thenchanges the properties of the water in the way that it does break down the subtrate. Life was also explained as the sum of the functions of the colloids building the body.
This theory came up in a time when macromolecules and their functions where not very well understood. The better understanding of macromolecules rendered this theory irrelevant. This is also neatly sumarized in the conclusions section of the article you cite.


text:
Can diseases be transmitted wirelessly?
According to the recent research about Electromagnetic Signals from Bacterial DNA (A. Widom, J. Swain, Y. N. Srivastava, S. Sivasubramanian) it seems there is a possibility of a "wireless" version of intercellular communication which was found in bacterial communities.
The paper's abstract reports:

Chemical reactions can be induced at a distance due to the propagation
  of electromagnetic signals during intermediate chemical stages.
  Although is is well known at optical frequencies, e.g. photosynthetic
  reactions, electromagnetic signals hold true for muck lower
  frequencies. In E. coli bacteria such electromagnetic signals can be
  generated by electric transitions between energy levels describing
  electrons moving around DNA loops.

The authors further note:

There has been considerable interest in bacterial communities wherein
  a bacterium is connected to neighboring bacteria by means of narrow
  nanowires[5-7]. It is believed that the purpose of the nanowires is to
  allow for intercellular electronic communications. More advanced on
  the evolutionary scale are the more modern bacterial communities which
  are wireless. The electromagnetic signals sent from a bacterium to
  neighboring bacteria can be due to relatively low frequency electron
  level transitions within DNA.

Conclusions says:

Although biochemical reactions are often described in terms of
  molecular contacts, electromagnetic signals can often be employed to
  allow chemical reaction control at a distance.
...
The wireless broadcasts can in principle be of both the AM and FM
  variety due to the magnetic flux periodicity in electron energy
  spectra in bacterial DNA orbital motions. AM signals can arise from
  the Bohr transition frequencies between different electronic energy
  orbitals about the DNA loops.

Wired article Bacteria on the Radio: DNA Could Act as Antenna comments:

Theoretical physicists have proposed an explanation for how bacteria
  might transmit electromagnetic signals: Chromosomes could act like
  antennae, with electrons traveling gene circuits to produce
  species-specific wavelengths.
In Widom’s arXiv paper, he and other physicists calculate that as
  electrons flowed through loops of DNA in E. coli and Mycoplasma pirum,
  the species tested by Montagnier, they should generate wavelengths
  similar to what was recorded.
“Different species have different lengths of DNA” in their
  chromosomes, he said. “These lengths probably determine frequency.”
“This could be a wireless version,” said Widom. “Bacteria that set up
  nanowires are, on an evolutionary scale, fairly old. It’s occurred to
  me that more modern bacteria may use wireless.”

It seems that the concept of electromagnetic signal transmission in bacteria is not new and such an idea originates with Nobel Laureate virologist Luc Montagnier (2009), who detected electromagnetic signals after wrapping inductor coils around flasks of water, hooked up to an amplifier, which contained E. coli and Mycoplasma pirum. The frequency of the signals measured was about 1kHz.
That kind of communication could also explain the phenomenon of quorum sensing mechanism, where bacteria communicate with one another to establish the population density of micro-organisms of their own kind within their proximal environment.
Based on above, the question is, is there any possibility that the diseases can be transmitted wirelessly? Are there any further research around this topic?

While some of this concept indeed exists (bacterial nanowires), the rest is utter nonsense. Calling this publication paper is also an exaggeration, as this has been published on arxiv which does not provide peer review. Diseases are only transmitted by real microbes (bacteria, viruses etc.). The naming of Luc Montagnier makes this completely cheesy as this man hasn't made any real science for years and only done pseudoscience.

Even if DNA can create an electromagnetic signal around 1KHz that doesn't imply communication. Molecules can absorb or emit electromagnetic radiation at several frequencies, but no one claims this is communication. If the signal is real, it's probably just an intrinsic property of DNA, and putting a solution of pure DNA in water would probably produce the same signal. If someone comes back and demonstrates that bacteria grown while exposed to a strong 1KHz signal show different properties than a non exposed control, then I'd be more interested.


text:
How can I text-mine full-text articles from PubMed?
I want to do a text mining study using full-text versions of articles I find on PubMed. My intended search protocol will be roughly as follows:

Search PubMed using a gene name (and any alternate names) as the query, all matching papers are subjected to Step 2; my understanding is that this will return articles that mention the gene in their abstract
Search full-text for any and all matches from a list of keywords; assign each paper a score based on the number of matching keywords; any papers that match have to be read by a human but the most relevant papers will have a higher score and get read first

The two-step search needs to be repeated many times with different genes in Step1 so an automated approach is probably worth the time it will take to develop.
I know enough about programming that I could write a script to do Step2 if I had the paper as a plain-text document (I program in Perl but I also know a little Python) but I have no idea how I could automate the process of searching for papers, downloading them, converting them to plain-text documents that my program could work on.
I considered posting this in StackOverflow but have opted for this site because I have not ruled out the possibility that this can be done without doing my programming.
UPDATE: I have found one tool that might be very useful for exactly this problem. Unfortunately, I am not in a position to ask for a free trial so I cannot evaluate it. Even if it is an appropriate tool, I will most likely not be able to use it for my study.

Thats interesting. Would be interesting so see if there is a ready solution for it.

Do you mean all papers indexed in PubMed, or only those in PubMedCentral that have free full text available.

All papers, @MadScientist

Note that bulk-downloading papers without permission may violate the terms of use of the repositories or journals where they are hosted.  Journals could revoke your subscription (or your institution's) or threaten legal action.

@NateEldredge, thanks for pointing that out. Do you think I could get around that problem by setting up my pipeline to download then analyze each paper before downloading the next one?

I doubt it.  They would probably look for an excessive total number of downloads in a month; a short delay between downloads wouldn't help.  Worst case scenario: http://en.wikipedia.org/wiki/Aaron_Swartz

I'm voting to close this question as off-topic because this is a question about mining and sifting data not Biology.

I appreciate your point about this question being off-topic. My rationale for posting it here is because of the possibility of finding PubMed-specific solutions; something that could be helpful to biologists with limited computer skills.

Below is a Python script that might help you to get started  (apologies if it fails the Pythonic test - it works!). It uses the Entrez part of the Biopython library. The script sets up a query, in this case yeast AND Saccharomyces against the pmc database. Also note that this script uses the 2 step process that NCBI likes you to use - the first part of the fetchByQuery function gets a set of results then the second part uses those results to actually obtain the data.
The output is an xml file which you get to parse with your favourite tools. In your case you will need to get out the text sections and do your token analysis. If you use Python for that I recommend the Natural Language Toolkit (NLTK).
In your case you could just set up search terms as a Python list and loop through writing each dataset to a file named from the search term.
from Bio import Entrez

import urllib
import urllib2
import sys

def fetchByQuery(query,days):
    Entrez.email = "xxx" # you must give NCBI an email address
    searchHandle=Entrez.esearch(db="pmc", reldate=days, term=query, usehistory="y")
    searchResults=Entrez.read(searchHandle)
    searchHandle.close()
    webEnv=searchResults["WebEnv"]
    queryKey=searchResults["QueryKey"]
    batchSize=10
    try:
        fetchHandle = Entrez.efetch(db="pmc", retmax=100, retmode="xml", webenv=webEnv, query_key=queryKey)
        data=fetchHandle.read()
        fetchHandle.close()
        return data
    except:
        return None

days=100 #looking for papers in the last 100 days
termList=["yeast","Saccharomyces"]

query=" AND ".join(termList)
xml_data=fetchByQuery(query,days)
if xml_data==None:
    print 80*"*"+"\n"
    print "This search returned no hits"

else:
    f=open("pmcXml.txt" ,"w")
    f.write(xml_data)
    f.close()

I think it's possible with Entrez Direct
You'd start with something like:
esearch -db pubmed -query "atp6"

And then pipe that to maybe efetch -format ?? and then continue with gnu coreutils. It might be that only abstracts are available as text, in this case, you'd have to extract e.g. pubmed ids and then come up with a way to batch fetch those somehow..


text:
How do I prepare a solution? (Calculation)
I have to make 100mL of 400mM NaOH. How do I go about calculating what I need to prepare this?

This is relatively easy. First: Look up the molecular weight of sodium hydroxide: Wikipedia gives a molar weight of 39.997 grams/mole (lets round this to 40 g/mole thats easier to calculate and the error in this is marginal).
So when you dissolve 40 g of it in 1 l of water, you have a 1000 mM (or 1 M) solution. Since you only want to have a 400 mM solution, you need to multiply the final concentration with the molar weight to get the amount of NaOH for one litre:
40 g/mole * 0.4 mole/l = 16 g of NaOH per litre. Since you only need 100 ml, you only need 1/10th of the NaOH (1.6 g).
So to prepare 100 ml of a 400 mM NaOH solution you dissolve 1.6 g of NaOH in 80ml of water and fill up to 100ml in a appropriate messuring cylinder.

Thank you. I have struggled with these types of problems since we were first introduced to them. For future reference, I would do a similar technique if say I needed a different amount of solute?

This is usually the easiest way. Calculate the amount for 1l (since this is usually the basis) and the take the fraction for the actually needed amount. With the calculation above you could easily calculate this for 250ml or also 600ml.


text:
What is the most critical step of plasmid purification?
During the process of plasmid purification and quantification, which step is the most critical to the success of the process?

What scale are we talking about? Because Giga preps are different from mini preps.

It's for a mini prep.

Dear friend, there are many ways to extract plasmid. Which ones are you talking about?

There are a few critical steps (which sounds horrible if written together, but the method per se is robust and usually without problems):

Resuspension of the pellet: Make sure it is really resuspended and not floating around as a big blob. If it is not resuspended properly your yields will go down dramatically.
NaOH/SDS-Lysis: Don't lyse for too long as you may end up with low quality DNA. This denatures the plasmid and makes it often useless for subsequent enzymatic reactions.
Mixing: Don't mix too harsh once you lyse the cells, otherwise you may break up genomic DNA of the bacteria which subsequently stays in solution and is not precipitated during neutralization.
Neutralization: Make sure you mix good here (by inverting the tubes 4-6 times) but not too harsh. It is critical to neutralize the whole lysate, otherwise proteins may stay in solution.
Drying: Overdrying of pellets can cause problems when you try to dissolve them again.

Just to add some details, don't lyse for more than 5 minutes, have the neutralization buffer ready to go so after you get your last sample lysed and mixed immediately add neutralization buffer to the first samples. When mixing, it's only ok to vortex the cell pellet prior to lysis, after adding lysis buffer, ONLY MIX BY INVERTING THE TUBE. Vortexing after this point can shear DNA. If you overdry the pellets, you can resuspend them by leaving them in the TE buffer for several minutes at 37C. And don't do too many samples to handle them all, with practice you can do 24 samples without trouble.

Thanks for this additions. More than 24 is usually not possible, since this is the limit for most benchtop centrifuges. Some even take up only 18 tubes.

So, in summary, all of the steps are critical.

@AlanBoyd You can loose yield in all of them. I wouldn't say one is much more complicated than others.

@Chris I agree, I was trying to stress to the OP that the whole process should be carried out carefully, which is what you said.  Remembering to add antibiotic to the cultures is also critical!


text:
PDB file SEQRES have different data?
In PDB file, SEQRES represent the aminoacids but some pdb file present the "GLC" and some other.
for example
SEQRES   1 A   26  GLC GLC GLC GLC GLC GLC GLC GLC GLC GLC GLC GLC GLC
SEQRES   2 A   26  GLC GLC GLC GLC GLC GLC GLC GLC GLC GLC GLC GLC GLC
SEQRES   1 B   26  GLC GLC GLC GLC GLC GLC GLC GLC GLC GLC GLC GLC GLC
SEQRES   2 B   26  GLC GLC GLC GLC GLC GLC GLC GLC GLC GLC GLC GLC GLC

In that PDB ID: 1C58
What are this and What are represent the SEQRES?

The pdb file that you mention is entitled:

V-Amylose at atomic resolution: X-ray structure of a cycloamylose with 26 glucose residues (cyclomaltohexaicosaose).

So, it isn't a protein at all, it is a circular oligosaccharide consisting of 26 glucose (GLC) residues. I imagine that the usual fields in the pdb file have been fudged to accommodate this.

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