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No bands show up in gel electrophoresis, not even marker
I haven't seen any gel lanes in neither my PCR samples nor the marker itself when photographing them.  This is not my first time performing 1.2% agarose gel electrophoresis.
I see gel lanes when I take the gel out the apparatus, but when I go to photograph them:  nothing shows up.  I only let the samples "run" for 30-40 minutes (when I ran for an hour, the bands almost ran off the gel).
Tried using different markers:  no luck.
Re-added some more EtBr to better stain the gel:  no luck.
I am also keeping the lights off in the dark room, so I do not think I am exposing the film to light early on (errors still a possibility though).
What could I be doing wrong?  Am I taking the film out too early?

I don't understand the part of your question where you refer to film in a darkroom. If you are staining with EtBr then you must be using a UV lamp to visualise the bands. There is usually no question of "taking film out" since the gel is usually photographed with a digital system of some kind. Please explain exactly what you do with the stained gel.

Do you see the color from the loading dye migrating through the gel?

was the electrodes/ gel set on correct direction (polarity)?

also possible you took the film too late, so all bands and dye-front came out from gel

since you mentioned 30-40 minutes... I run my sample on agarose gel only for about 20 minutes at 100V, and can see good bands. try reducing the time.

What I can quickly think of is that you were running the gel incorrectly: instead of from - to + direction,  You ran it the other way around and your DNA went out of the gel. Another thing might be that the UV light was not turned on or is broken.

Here's my $0.02 at troubleshooting:

I see gel lanes when I take the gel out the apparatus,

Good, you're loading your gel correctly and the density is correct so the DNA sits at the bottom of the wells.

but when I go to photograph them: nothing shows up.

This points to a problem with image formation: not enough EtBr, not enough DNA, burnt out UV bulb, incorrect UV filter, or incorrect imaging station settings.

I only let the samples "run" for 30-40 minutes (when I ran for an hour, the bands almost ran off the gel).

You've run the electrophoresis in the correct direction and not long enough to run the bands completely out of the gel.

Tried using different markers: no luck.

Are you loading enough DNA with these markers?

Re-added some more EtBr to better stain the gel: no luck.

I suspect a problem with the gel documentation system.

I am also keeping the lights off in the dark room, so I do not think I am exposing the film to light early on (errors still a possibility though). Am I taking the film out too early?

I don't know what you're talking about here. EtBr is a fluorescent dye under UV illumination, and doesn't normally require photographic film. Some systems will capture an image of the gel using a "Polaroid" sort of camera, but that works because the gel was exposed to UV light and the incoming light was filtered accordingly. Most systems however use a gel documentation system with a transilluminating tray and digital camera system to take an image.
Some things to try:
1) Prepare two samples: a standard marker lane, and a DNA lane of known concentration (load up a lot of DNA, like 1-2 ug of plasmid to know that you can't miss the band).  Add 1 uL stock EtBr to each lane's sample, mix, then load on the gel. Run the gel using your usual parameters, keeping a eye on the migrating dye front the make sure you don't run the DNA off the gel. This will make sure that you have two good samples that should appear on the gel, and that they are plenty bright by having excess EtBr.
2) Image the gel. Things to double check here:

is the emission wavelength correct? EtBr requires short or medium wave UV illumination (250-300 nm), but some systems have long wave illumination as well. Long wave will not work.
is there filter setting correct? EtBr fluoresces with a red peak (595 nm max), and if a filter is in place to remove this band, you won't see anything either. Usually there is no filter, or an "EtBr/UV" filter option. Here's a technical document with an example of setting up for EtBr capture.
is the camera set with an appropriate shutter speed/exposure time? Try experimenting with 20 ms to 200 ms. On our system, 40 ms is ideal. Too short an exposure time means that you won't see anything.
is the camera iris set the maximally open? If the iris is closed too much, it restricts the incoming light for image formation and eiter no image or a weak image will form. This will also impact ideal exposure time (see above).
is the camera in focus and operational? Can you image an object like your gloved hand or the physical gel before getting the EtBr settings correct?

May your gene of interest will not be cloned perfectly that is the reason, make sure that first you have to run pcr well accourding to your sequece then run the gel

This is not an answer to the question, please edit it to avoid downvotes/deletion.


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Do's and Don't's of Undergraduate Research?
I was fortunate enough to get a position as a researcher for the Mayo Clinic's SURF Program this year.  My PI's lab focus is on the the immune system's role in CNS axonal and neuronal injury, specifically through the lens of how innate and adaptive immune effectors interact w/ infected neurons.
Although I do research under a professor at my college and I volunteered for a state university lab during the previous summer, this is my first REU/SURF opportunity, and I REALLY want to make a good impression.  Here are my questions:
What are the do's and don't's in terms of being a skilled and efficient researcher?
Since I am still an undergrad, I know that I will be a less useful asset to the lab than a grad student or post-doc, but what can I do as an undergrad to not burden my colleagues and PI?
Thank you all for your help!  Wishing you all the very best!

This question appears to be off-topic because it is more suitable for academia.

This is indeed off topic. However, what can you do? Learn. That's all that will be expected of you.

Ask plenty of questions and write everything down. If you do not write notes when someone is explaining something to you, it will be embarrassing to go back and ask them a second time to explain it again. Before you get to the lab I would locate/Ask for review articles related to the project. Realize that you will likely shadowing a senior person while you are there, adapt to their schedule. Don't spend your incubation times face booking. Use this time to build relationships with others in the lab and on your floor and try to absorb as much information about the way the world of science works. Speaking from personal experience the small things you learn there may be insignificant but may come to be important to you in the future. If you have your own project, realize that it will probably be a small one attached to a bigger project another lab member is working on. Thats a good thing, because your time there is not long enough to get into something complicated. A simple, clear, and focused question will be key to your success.
What you should take away from the experience is not necessarily something that will amount to publication, but the actually experience in the actual process of designing experiments, performing them, and analyzing data. Assuming you are doing this to help prepare you to go on to work on a graduate degree in your favorite area of biology then remember that this is here to help you get to the next level. Programs like this allow you to demonstrate that you understand what it takes to perform graduate-level work, and potentially become a successful scientist one day.

Another thing: Take advise from people which have more experience than you, but also question things (not everything though). The last thing is especially important to understand what you are doing.

source: Stack Exchange

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What is the evolutionary purpose of the topology of the human ear?
What is the evolutionary purpose of the topology of human ears? I understand why the ears may have a funnel-like shape but if the various "hills and valleys" do not amplify incoming sound, what purpose do they have?

Humans do not have the ability to move their outer ear in response to sound. Many animals can do that, and use it to determine the source of the sound waves. Thus, human outer ears are equipped with many "hills and valleys". It does not provide amplification (because the waves can lose their energy bouncing around the ridges), but rather gives the brain more information about the sources' location in space. The brain calculates that location by determining minute differences in the time it takes for the sound to reach sensory cells in the inner ear on both sides. The shape basically attenuates the raw information. That way you get different properties of the sound wave that enters your ear depending on the angle at which it fell on you outer ear.

Could you support your answer with references? Have the effects of different pinna morphologies been tested in humans?

Different ears are shaped differently. Does that mean the brain is aware of the topology of the ear and aware of how sound is affected by it?

Humans can localize the horizontal location of sound ("azimuth") using temporal cues (sound reaches the 'closer' ear first') and level (the head blocks some sound so it louder at the 'closer' eat) cues, depending on frequency.
For detecting the "height" or "elevation" of a sound, other cues are necessary. "Pinna cues" refer to a pattern of level distortions at different frequencies that, combined with predictable elements of natural sound (such as harmonics), allow the listener to determine elevation. The head also contributes, so these cues are grouped together as a "Head Related Transfer Function." Importantly, the two ears are never perfectly the same, so these cues can be differentiated from the azimuth cues I described earlier. One can measure these pinna cues by placing a microphone in the auditory canal.
The Wikipedia article on sound localization has some more information, as do several online course postings and textbooks, for example this one, or by searching for terms like "sound localization elevation pinna".

I'm guessing this is the same as spectral filtering for sound localisation?

Yes; "spectral cues," "head related transfer function," "pinna cues," - these are all related terms with varying levels of application/specificity but they effectively refer to the same thing.

One possible advantage is that's it's probably the best adapted to being able to hear a very low volume source of sound no matter which direction it's coming from. A horse ear on the other hand, is probably the best adapted to being able to hear an even lower volume source in only a very narrow range of directions. One reason for being able to hear well in any direction is to avoid predators. Maybe in our evolutionary history, we sometimes went into a jungle and there was a dinofelis lurking in it with silencers on its feet and we couldn't see it so we evolved ear the shape we did so that we could hear it from really far away if it started walking no matter which direction it was from us and prepare to fend it off with spears. Maybe we always had ears the shape we do then we just started evolving to have horse like ears so that we could keep moving our ears until we locate the dinofelis and then in response to that, the dinofelis evoled to stop walking a very short time after it starts when it's in the jungle so that we can't hear it from further away anymore so it became advantageous to hear as far as we can in any direction so we stopped further evolving horse like ears and that's why some people can move their ears a tiny bit. One reason for being able to hear such a low volume source in any direction is to catch prey. Deers probably evolved ears shaped the way they are so that they could keep turning them until they hear a prey animal and then keep their ears pointed towards it so that they can keep hearing it so that they can hunt it.

Evolution doesn't have a purpose. In that light, it's quite possible for an ear to be poorly adapted to hearing - which in fact it is compared to other species.
Stereo hearing (two ears, so you can better detect where the sound is coming from) is heritage from our ancestors, and I know for a fact it didn't evolve further in humans because there was no evolutionary pressure.
In any case, the topology isn't exclusive to our species and is heritage from our mammalian lineage. At some point in our lineage, the species/individuals who had this topology of the ear were able to gather sound waves better and that affected their survival so they passed on the trait to their offspring. Ear topology didn't evolve in humans.

Can you provide citations to support your assertions? What makes you certain that the ear in humans has not been subject to selection? I'm not suggesting that it has, but I would like to know if there is evidence to the contrary.

Just take a look at the ear(s) of any great ape. Clearly ear hasn't been changed much within our species and the development took part much earlier in our lineage.

But we don't know what the ear of the most recent common ancestor of humans and chimpanzees looked like.

No, we don't, because we don't know what the common ancestor is, when it lived, and what it looked like. No fossil has been found. We can only presume ears of this shape are a shared trait derived from the common ancestor, otherwise we'd be saying it evolved independently at least four times. That's next to impossible.

This answer is misleading and takes the conversation in an unnecessary direction - the question doesn't include an explicit misunderstanding of evolution. I don't believe the question needs to be read as "what are the unique adaptations for hearing in the human ear." I read the question as "Ears look funny. Is there any reason applicable to survival/fitness for ears to look the way they do?"

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what these suffixes mean,-coel,-blast,-cyst?
in the connective tissue (Bones) we have 3 types  osteoblast, osteocoel,osteocyst what are they and why they differ.

have you tried searching the net for the answer. Wikipedia might be able to answer this question.

-blast : A precursor/progenitor/immature cell..
-coel : A fluid filled cavity...
cyst : A clump of cells with a defined boundary...

@WYSIWYG - even if it's short, please post answers to questions as actual answers. Comments should just be used to clarify the question, not answer it. See this meta topic for a discussion regarding this issue. Thanks!

@MattDMo: thanks for clarification.. I'll take care.. Since this question is closed, i won't be able to convert this one

You can easily search this on the web.
Osteoblasts are the immature cells of bone which are responsible for the production and mineralization of bone matrix.
Osteocytes are the mature cells of bone found in open spaces in bone called lacunae. The functions of osteocytes includes maintenance of bone and  calcium homeostasis.
Osteoclasts are responsible for removal of bone.
Source : Tortora and Derrickson


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Are viruses self-propelled?
So obviously, viruses are nonliving. But when my teacher was teaching viruses in the video (we're doing "flip" learning this semester), the way he described it, it seemed like the viruses responded to their environment in that they moved around until they found a cell of the right type, and then they latched on and hijacked it.
I had always thought of it more like that they were just kind of floating around, carried by the host system (blood in animals for example), until they "bumped into" the right kind of cells and both sets of membrane proteins "docked". But my theory/idea doesn't really make sense because it doesn't account for how viruses would be able to infect bacteria.
But, the idea that viruses propel themselves doesn't make much sense either, because viruses are nonliving, and one of the characteristics of life that they do not meet is that living things acquire and use energy.
In summary my question is, how are viruses propelled? Do they move themselves, or are they moved by external forces?

All of your reasoning is correct - viruses are not motile (i.e. not self-propelled).
I don't understand why you think this would cause a difficulty in the case of bacteria.
Edit in response to comment @Remi.b
Some cursory research on estimating probabilities of collisions between particles engaged in random walks has revealed some very challenging maths. So I decided to simply look at some data.
Remarkably there is a fairly recent paper describing investigations of the kinetics of bacteriophage adsorption.

Moldovan, et al. (2007) On Kinetics of Phage Adsorption. Biophysical Journal 93:303–315

I didn't realise it was still possible to publish papers like this, but in fact it is very interesting. For our current purposes we only need to consider the data presented in Figure 3, which show that when E. coli cells at a density of 108 cells ml-1 are mixed with bacteriophage λ at a density of 5 x 104 particles ml-1, then 90% of the phage have attached to a bacterial cell within less than 10 min.
Just to relate this to a real life situation, it is estimated that sea water contains bacteria at a density of 106 cells ml-1 and phage at 5 x 107 particles ml-1.

The OP says "But my theory/idea doesn't really make sense because it doesn't account for how viruses would be able to infect bacteria". I think the OP's issue with the fact that viruses are not motile is that he/she doesn't get how they would manage to "find" bacteria (or host cells). One could maybe improve its answer by talking about probability of "finding a new host" and about the behavior (in short) of the virus when it enters in contact with a potential host bacteria.

What do you mean with "I didn't realise it was still possible to publish papers like this"?

It was a bit of a throwaway comment - it seems to me to hark back to the days of the phage group (Delbruck, Luria, Hershey et al), and it is particularly interesting that the authors are physicists (as was Delbruck). As I said, it is an interesting paper, and I certainly didn't mean any disrespect to the authors.

You are right, viruses are neither alive, nor are they moving by themselves. They are moved by passive movements (e.g. the bloodstream or movements of the air) until they meet their target cells. This can be either a cell in the human body (for flu viruses these are cells of the respiratory tract for example) or bacteria (for bacteriophages).
For bacteria both can happen, viruses floating around meet a bacteria they can infect or the other way that moving bacteria meet the virus.

The existing answers are correct. However, there is now one example of a self-propelled† virus.
Herpesviruses assimilate kinesin to produce motorized viral particles

Here, using herpes simplex virus type I and pseudorabies virus as model alphaherpesviruses, we show that a cellular kinesin motor is captured by virions in epithelial cells, carried between cells, and subsequently used in neurons to traffic to nuclei.

Essentially, herpesvirus has been shown to co-opt host-derived kinesin-1 to move from the centrosome to the nucleus along microtubules.
† It’s not self-propelled in the sense that it encodes its own factors to enable autonomous movement, though the described mechanism is more sophisticated than simple Brownian motion. If flagellar chemotaxis in bacteria is analogous to a boat on open water, then kinesin-propelled motion is like a train ride; you are constrained to the tracks.

There are a bunch of viruses that are transported on actin filaments and the like, but this is wild; taking the mechanism with you!! There is so much left to discover in biology.

Wild, indeed!

Viruses move by Brownian motion 1  The definition of temperature is there are an average of about 2 calories (little c) (= 8.3 J) per kelvin, mole, and degree of freedom.  2  Multiply that by 1 mole/6.02E23 molecules and you have the Boltzmann constant (1.4E-23 J/(K*DOF).   So the virus has three dimensions - three degrees of freedom - of physical translation at 300 K room temperature, to get, say, 900 times the Boltzmann constant or 1.2E-21 J of energy.
Which doesn't sound like much, but kinetic energy = 1/2 mass x velocity squared, so if the virus weighs, say, 100,000 daltons = 100,000/(6.02E23) grams, then you divide the joules by this (converting to kg) to get 0.2 m^2/s^2 - take the square root and you have about 0.6 m/s, or about 1.3 miles per hour.
So the virus ambles along at a walking pace (give or take - see the Boltzmann distribution), requiring NO ENERGY to do so.  The caveat is that it has no control over where it goes; this is heat energy.  You might say that the virus, like a stealthy flatus in a crowded room, is an agent of chaos (or at least entropy), on a mission to go forth and spread out.

The term self-propelled requires some finer qualification in the case of bacteriophages. Although bacteriophages are generally carried via Brownian motion, as described in the other answers, in some of them the attachment process exhibits autonomous propulsion. In particular, they may walk on the surface of a bacteria (see modeling video here) and they inject their genetic material with a syringe-like motion. In doing so they dispense the energy stored in the viral proteins during their synthesis and the phage assembly - in other words they remain nonliving entities, unable to acquire energy and convert it to useful work, their motion being a programmed one, like that of a released spring.

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Raising two legs together while lying on bed
Let's do some exercise(duh!)
Ok so lie on the bed. Lift your left leg. Put it down. Lift your right leg.Put it down. Easy?
Now lift your left leg and without putting it down, lift your right leg. Easy ? No.
Now try to lift both the legs together. Easy ? No.
My question : What is the anatomical reason ( arrangement of muscles around the bones etc.) which makes it difficult ?

I don't know if this is relevant, but with one leg down, we actually push against the bed while raising the other to increase the upward normal force and to shift the normal force toe-wards to maintain stability. This cannot be done if both legs are in air.

@SatwikPasani If your reasoning is correct, it would be interesting to know whether people with only one leg are able to raise their leg easily.

I suspect it is just physics. Each of your legs makes up about 1/6 of body mass, leaving about 2/3 of your mass superior to your hips.
Raising one leg requires action of the hip flexors (i.e., iliopsoas complex) but also activity in the anterior abdominal wall muscles (rectus abdominis, obliques) and back muscles to stabilize your abdomen. To raise the other leg simultaneously, you recruit the ipsilateral hip flexors. But, importantly, you probably have already maximally recruited most of your abdominal and back muscles.
Imagine the body as a lever system. With one leg raised, you have 1/6 of body mass balanced against 2/3. With both legs up, you have 1/3 vs. 2/3 and with potentially increased torque, because your legs are long (a force acting at a larger distance). The muscle forces to stabilize that must be larger, but the additional muscles are not there.
I can raise both legs with difficulty (admittedly, $n=1$).


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Systems Biology of triacylglycerol (TAG) synthesis in Jatropha
I need the genetic regulatory network of TAG synthesis (Kennedy pathway) of Jatropha plant??
Or is there any way to convert metabolic pathway into genetic regulatory network?

Please look up some literature. Look for transcription factor binding sites in the promoters of the genes involved in the pathway. If jatropha genome is not sequenced then look for homologs in the nearest species. it is not possible to obtain a gene regulatory network from a metabolic network.

Triacylglycerol synthesis in plants is probably highly conserved.  The metabolic pathway is here.
The Jatropha genome sequence is also available.
Given this some effort has been made to figure out how these genes are regulated.  This is a microarray study of Jatropha focusing on fatty acid and TAG biosynthesis.   This gives some idea of how TAG genes respond to one another, but of course will not find the promoter sequences or the transcription factors themselves.
Having spent a summer going over fatty acid synthesis, I can only say that there has been a lot of wet lab work done on these pathways which would probably be conserved in the Jatropha plant.  The literature would be quite extensive.  Integrating all of that is more like a paper for publication than an answer on stackexchange.  This sort of outlines the procedure... do you have a more focused question?
I'll outline one way of approaching this - there are an uncountable number of variants if you tweak it.  There are other ways to get this, most notably looking for defective mutants, the method which is still used in plants quite a bit.
Anyway here is a genome based approach:
1) Identify genes in the pathway of interest. choose 10 or so genes that you think constitute your network.  This is an editorial decision. Ultimately if you start looking at genes regulated by the same transcription factors as being included in your network, you will eventually take in the entire genome and the work will be impossible to accomplish.
2) find candidate promotor binding sites. look at the upstream promotor regions for all these genes.  you can look at how these are conserved between similar plants by examining the same gene promotor regions aligned against each other.  This doesn't work very well.
2b) Another way of finding these is to do a pull down experiment where transcription factors are bound to DNA and a DNAse digestion is done and remaining fragments identify the binding sites.  All this somewhat assumes that you kind of know which transcription factors are responsible for each gene. That is probably not the case here.
3) find the transcription factors important for the plant pathway.  this is not easy - one way is to try knock outs of the TF genes.  I imagine this plant has 4000 + of these genes.  around 1-2% may be involved.
So far these methods have been use for the ENCODE project as well as some bacterial genomes.  a plant is a new scenario which will have issues of its own.

Yes..I need the details of how to get the gentic regulatory network of TAG synthesis Pathway?? A step wise protocol please. How to get The regulatory gene network from geneome of Jatropha curcas.

do you mean transcription factor binding sites or also the mechanims of regulation? still sounds like you are looking for a few hundred pages or a review article.

I dont have much knowledge about systems biology and gene regulatory network. I have do the pathway modelling in two forms...frst for metabolic pathway and then for gene regultory network. I dnt know how to do it with gene regultory network?


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Can humans eat grass?
Can a human eat grass and digest it?
Could it be possible to use it as food just like other plants such as wheat or beans?

Note that many of our grains are grasses. We can't metabolize cellulose, but the seeds contain enough other materials -- especially after cooking or grinding to break down any cellulose barriers around them -- to be worth eating. That may not be what you intended to ask, though.

From a taxonomic point of view, wheat is a grass. So yes, we can eat it. Narrow down and clarify your question.

To elaborate on A random zoologist's answer, the problem is that the human digestive system does not contain any cellulase enzymes. Cellulases are a class of enzymes that break down cellulose, the chief structural component of plants.  You might be able to obtain a small amount of nutrition from grass or other cellulose-rich materials, but as the plant cell walls are made of cellulose, most of the plant material will be indigestible.

At the end of the linked article it is stated that cellulase is used to treat phytobezoars, which apparently are indigestible masses of cellulose stuck in the stomach. Could one take a supplement that renders the grass more digestible?

It would probably not be useful as a supplement, as the enzymes wouldn't last very long in the stomach. Fun fact: An alternative to cellulase for treating phytobezoars is coca-cola administred through the nose: http://www.medicine.virginia.edu/clinical/departments/medicine/divisions/digestive-health/nutrition-support-team/nutrition-articles/practicalgasto1.04.pdf

Could we cook the grass and break down the cell walls?

Not easily. To break the crystalline structure of cellulose by cooking requires a temperature of 320 C and 250 atmospheres of pressure: http://en.wikipedia.org/wiki/Cellulose#Structure_and_properties

Cellulases are generally slow, which is why mammals that have microbes that can break down cellulose also have very long transit/residence times in their guts. In the extreme case, ruminants (cows for example) have developed huge, multi-chambered guts to ensure that food stays in their digestive system long enough for the cellulases to act on a useful percentage of the food they ingest. So a human gut with cellulases is still not going to get useful amounts of nutrition out of ingested cellulose.

Also interesting and relevant: most animals that do digest grass actually host bacteria which produce cellulase, this is because the gene for producing cellulase hasn't evolved in animals, nor have many other genes for extracting maximal nutrition from plants. By farming bacteria in their guts (why cows have so many stomachs) they can get their nutrition by digesting the bacteria and the broken down plant matter.

Hi.well first of all you need to understand difference between plant and fruit.as jarlemag said grass n other green parts of plant contain Cellulases which wehuman cant digest.we dont have specific enzyme for that.also we dont bacteria that digest green plants.on the other hand fruit is nothing but a ovary of a plant containing the seed and nutrient which a seed need for development.although i said in my last we can digest some plants.

Potatoes and beans also contains cellulose (because it is found in any-plant's cell wall). However potatoes store high amount of starch and beans store high-level of proteins. We digest and absorb only that-portion

Wheat and other grasses are very significant sources for human nutrition.  Grass seeds are digestible; seeds have to digest themselves to sprout, with very little biochemical machinery.  Human civilization is founded on the ability to cultivate grass to eat.
It is due to pepsin that a cellulase supplement would not help to digest grass stems and leaves.  Pepsin is the enzyme in the stomach that breaks peptide bonds and from its perspective, cellulase is just another peptide chain (pepsin is so effective, the stomach has to prevent itself from being digested while at the same time maintaining enough pepsin to digest food — because pepsin digests pepsin).  Cellulose is a tough sugar polymer (as is chitin, which forms insect and fungus exoskeletons), so after all the cellulase was digested by pepsin only bacteria from the intestine could process the remaining cellulose.  What the bacteria convert it to might make one ill.
Humans can derive significant nutrition from bamboo shoots, which have less robust cellulose than in mature plants, and bamboo is a grass.  Pandas also cannot digest cellulose effectively, but that doesn't stop them from trying.  They might eventually develop a cellulase gene by sheer willpower and tenacity.

@jarlemag: inhaling sugar water could quickly become a very bad idea.  Encouraging microbes to colonize near the brain may result in them converting neurons into more microbes.  The Naegleria amoebae can be very aggressive.  In Pakistan and India it is somehow traditional to treat illness by putting water up one's nose; when it is not recognized how clean the water must be to do that safely, people die.

The soda is not inhaled. It's transferred directly to the stomach through a tube inserted through the nose: http://en.wikipedia.org/wiki/Gastric_lavage Anyway, it is a medical treatment and I'm no doctor - I'm sure there are proper protocols for it but I don't know anything more about it.

Also, though I do not know, it is likely that the soda is being used for its acidic properties. If so, diet soda would work just as well, and so it is as likely to be aspartame water that is being administered via a nasogastric tube (not inhaled) as it is to be sugar water.

Yes. Apparently some protocols use regular soda and some use diet soda.

Good point about the bamboo shoots.

Well, humans can eat grass, but it will not be digested. Cause to digest grass our body needs different kind of enzymes, which lack in humans so they can't digest grass directly although humans can eat grass, but not recommended.
Similarly our body has different enzymes to digest wheat and beans etc. Also remember rice, wheat and beans are fruit, not plant. Although we can digest some of the plant.

Aren't fruits parts of plants?

"Also remember rice, wheat and beans are fruit, not plant". what is meant by this ??

I think this is a beginners mistake. I think A random zoologist thinks fruits aren't parts of plants. This isn't true, I think.

I think he meant that the rice, wheat and beans that we eat are the fruits of the rice, wheat and bean plants, and thus have a different composition than the rest of the plant. The Wikipedia article on cereals says "A cereal is a grass, a member of the monocot family Poaceae, cultivated for the edible components of its grain (botanically, a type of fruit called a caryopsis)"

Even in times of famine, when people are literally dying from hunger, they do not eat grass - it is not digestible. But they eat cooked artiplex, which commonly grows by roadsides.


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Absorption rate of Infrequently eating animals?
Clearly, creatures such as us humans, after vastly increasing the entropy of our food, expel most of the mass that we consume.
Some creatures, however, do NOT get the opportunity to eat nearly as often, even though these creatures are if anything more competitive (and perhaps cannibalistic!) than we are - snakes come to mind here, as do spiders.
Such a lifestyle implies that growing large - or at least to adult form - quickly has a huge advantage evolutionary.
So the awkward question that arises is thus: do such animals have a higher "absorption rate", if you will, then humans and other frequent feeders?
In other words, do such animals maximize their diet by incorporating more of the mass of their food and expelling less of it, or is there some physics/chemistry which makes this difficult?
Thanks!

I'll take a stab at this.
What fraction of your food is absorbed and what fraction is expelled is a function of what kind and how much indigestible material there is in the food, and not related to how often the animal eats.
How often an animal eats is a function of its metabolic demands(how many calories it needs) and how many calories it can get in one meal. Reptiles, as ectotherms, have a lower metabolic demand than endotherms. In addition, snakes can swallow huge amounts(relative to body weight) of high-calorie food in one sitting. As a result, snakes eat infrequently. Pet snakes are fed weekly or biweekly, depending on a number of factors. A reticulated python can swallow and digest something up to its own body weight. Ten weeks of digestion gives 1.4% of its own body weight daily, even without fasting.
Elephants are a migratory large mammal and eat about 4% of their body weight each day, more or less. This takes about 12-18 hours to collect, according to these people.
Elephants eat high-fiber, low-calorie foods, and as a result about 20% of their food mass is turned directly into poop. They feed often, and don't absorb much. Hummingbirds eat constantly, consuming their own body weight in food each day, but poop almost not at all. Their feces contains the indigestible parts of their food, just as the elephant feces does. The different is that large parts of elephant diet is indigestible fiber, while a tiny part of the hummingbird diet is indigestible insect exoskeletons.
All creatures absorb as much nutrition from their food as they can, and expel the remainder. How much remainder there is depends on what kind of food they eat.
Growth rates versus digestion rates and mass intake is a totally different and much more complicated question. Generally speaking, the growth-limiting factor is DNA replication or an essential acid or mineral deficiency and not a raw mass problem.


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What is the quality rate of intrinsic autoregulation in the heart?
Autoregulation is the maintenance of constant blood flow to an organ in spite of fluctuations in Blood pressure.
It involves the relaxation of myocardium and contraction.
It is local.
I know that autoregulation is best done in the brain, well in kidneys and badly in skeletal muscle.
I am interested how it is in the heart.
I think it should be at least good.
Brain can be thought more important.
However, I am not sure.
How good is the autoregulation of the blood flow in the heart?

My conjecture: Intrinsic regulation is done in the heart the second best, after the brain.
This idea is based on the fact that the brain controls heart's some autonomic functions.
It is an open research question how the autonomic nervous system affects the intrinsic functions of the heart - and the reverse is true too.
To answer this question, we need to understand the autonomic regulation of the heart better i.e. the inner-physiology of the heart's electrical activity.


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Real time PCR parameter CT
When puting a real time PCR, parameter CT, which means threshold cycle, is used. What does it mean really? according to wikipedia "The number of cycles at which the fluorescence exceeds the threshold is called the threshold cycle (Ct)"
could anyone put it in conext?

Realtime PCR uses a fluorescent dye which binds to double-stranded DNA and thus allows to measure the growing amount of DNA by each cycle. The DNA added to the reaction also binds the fluorescent dye and makes some part of the fluorescent background. When the PCR reaction starts, it takes a while until enough DNA is synthesized to go over the background and to be able to reliable distinguish the signal from the noise. I think this becomes clearer, when you look at the image below (from the NIH):

The Ct is the point where the signal can be distinguished from the background when it enters the exponential grwoth phase. The no template control stays below this threshold.

and when you make the calibration curve does it really matter which range of dilutions you choose or does it have to be a logarithmic serie? besides, when you get your results for different CTs, which is the criteria when choosing the correct dilution?

If you know the concentration of your standard exactly, you could do only one reaction. However it is better to do at least a few dilutions to see if your dilutions are correct and to test if your standard is amplified linear (meaning 10x more standard gives an accordingly higher signal). I would always choose a dilution which is as close as possible to your gene of interest. I mostly avoided absolute quantifications if possible, since relative quantifications usually where sufficient for us.

what do you mean with " I would always choose a dilution which is as close as possible to your gene of interest."?

That I use the curve (when I make more than one) which is nearest to my sample of interest. This way you avoid to skew you calculation by non-linear amplifications.

and when i use the most diluted concentrations i often get fold changes really diverse when comparing to the more concentrated. Is there any criteria i could follow to discard those results?


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What kind of a microscope do I need to see cell organelles?
I would like to study cells and looking for a microscope that would allow me to see:

groups of cells
individual cell
cells organelles

I would like to target insects and mammal tissue.
I would be very grateful for info in magnification ranges that I need and maybe some popular models of microscopes.
Is there a difference between digital and non-digital microscopes for that purpose?

groups of cells

A normal light microscope. 4x-20x magnification

individual cell

Lo resolution: Light microscope with 40x magnification.
High resolution: Confocal microscope with 40-100x magnification.

cell organelles

Low resolution: Confocal microscope with >=60x magnification.
Note: some organelles are easier to visualize while others are difficult. With confocal you can manage to see almost all of them with low resolution i.e you will be able to detect their location and distribution but wont be able view their fine structure.
To view the structure of organelles you would definitely need an Electron Microscope.

Is there a difference between digital and non-digital microscopes for that purpose?

If you are not too much into the optics of it then I guess it wont matter. I prefer if it has an analog mode along with a digital mode. Image acquisition is anyways digital.
Popular models: Leica, Zeiss and Olympus are popular brands. You select the model as per your requirements.

Is 40x magnification enough to see if a bacteria is dead or alive?

@user46147 you cannot, that easily. Also depends on the type of bacteria. You would need some kind of stain/fluorescence marker to differentiate viable cells from dead cells.


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To characterise diameter of capillaries in organs
I know that there exist Continuous capillaries (skeletal muscle, adipose tissue, connective tissue, pulmonary circulation), Fenestrated capillaries (small intestine, renal glomerulus, exocrine glands), and Discontinuous capillaries (sinusoids; liver, spleen, bone marrow and hypophysis).
However, I am not sure how to characterise these.
The diameter of capillaries is different for each.
I have not managed to find any figure which present the relationship of diameter of these capillaries.
I have reviewed books Guyton, Pocock and Lange.
What are the diameters of capillaries in different organs?

This question is dependent on the specific patient at hand.
I think in the normal situation the diameter of the capillaries is about the same in each organ.
Better question would be: how does the diameter changes in relation to the venous and arterial ends of the capillaries?
Then, think about how big portion of the capillaries are in the venous end in the organ.
I cannot say that 50% of capillaries are on the venous end of the organ and 50% on the arterial side.
This is again an open research question.

authors: Иннокентий Жвац


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How to determine whether a newly discovered dinosaur is not a young one and not an entirely different species?
Every once in a while, there is an official announce that a new species has been discovered. For example, paleontologists have recently discovered a dinosaur they named Nanuqsaurus hoglundi, which really resembles Tyrannosaurus Rex, but in a smaller version. It also lived during the same era. Is there something that indicates it's a cousin of the T-Rex, and not Mr. Rex's son?
Other small dinosaurs include the Compsognathus, the Microraptor and others. Why were they classified as new species when they were discovered?
Considering evolution over a few million years, my guess is that some earlier species may have been smaller and evolved into more complex animals, bigger bodies, horns, frills, etc.

Diagnosing extinct species is even more difficult than extant taxa (see this question). Because systematists describing fossil species (usually) only have skeletons, they compare to other fossils. You are correct that diagnosing a species from only a skeleton can be tricky. What defines what you call a genus, a species, etc.? How morphologically dissimilar can two skeletons be before you call them different species? The running joke is that if you found fossils of a chihuahua skeleton and a great dane skeleton, you would certainly call them different species. But by modern biological species concepts, they are the same species. Then there are extant species that are essentially indistinguishable in terms of their skeletons, but do not interbreed, and so are probably different species.
Sometimes there is consensus, and sometimes there is not. This disagreement can lead to a description of a new species by one person being reclassified ("revised" is the term used) as another species. There are lots of examples of this among dinosaurs. Most famously, Brontosaurus was revised as actually being Apatosaurus. More recently, and relevant to your question, Nanotyrannus is thought by some to be a juvenile Tyrannosaurus rex.
So then how did Fiorillo and Tykowski, who described Nanuqsaurus hoglundi, decide that it was (1) not just a juvenile T. rex and (2) that it was a new species? Their rationale is laid out really well in their paper, primarily in the sections "Diagnosis" and "Description". You rightly picked out the two questions that paleontologists reading this paper would want to know.
Nanuqsaurus is not a juvenile:

The dorsomedial edge of the maxilla is marked by deep pockets separated by pronounced transverse ridges. These together formed a strong peg-in-socket articulation between the dorsal margin of the maxilla and the ventrolateral edge of the nasal. The same kind of deeply interlocking naso-maxillary contact is a well-documented character that is also present only in developmentally mature individuals of the derived tyrannosaurines Daspletosaurus torosus, Tarbosaurus bataar, and Tyrannosaurus rex 2, [6], [20], [21], [22]. The nasal-maxilla contact is either smoothly grooved or bears only weak scalloping in immature individuals and more basal tyrannosauroids 2, [6]. The presence of this feature in DMNH 21461 is evidence that the material also represents a developmentally mature individual.

What they are saying here is that maxilla (part of the front of the upper jaw) in Nanuqsaurus has a very characteristic relationship to the nasal bone in which they form a peg-and-socket joint. This relationship is found in tyrannosaurine dinosaurs like Tyrannosaurus, Daspletosaurus, and Tarbosaurus. But more importantly, it is only found in adult tyrannosaurines. So they conclude that Nanuqsaurus is an adult.
Nanuqsaurus is a distinct species from Tyrannosaurus and other tyrannosaurines

In all three hypotheses of phylogeny, Nanuqsaurus hoglundi was found to be a derived tyrannosaurine, the sister taxon to the Tarbosaurus + Tyrannosaurus clade (Figure 6). This node was supported by a single unambiguous character, the presence of a dorsoventrally tall, paired sagittal crest on the frontal. The age of Nanuqsaurus hoglundi (70-69Ma) is consistent with its place in the recovered hypothesis of tyrannosauroid phylogeny, positioned in time between the more basal Daspletosaurus torosus (Middle to Late Campanian) and the more derived Tyrannosaurus rex (latest Maastrichtian) among other North American tyrannosaurines.

The authors ran a phylogenetic analysis of characters coded for Nanuqsaurus and about 20 other taxa. Nanuqsaurus has enough shared characteristics to put to solidly among tyrannosaurine (near Tyrannosaurus, Daspletosaurus, and Tarbosaurus). But, importantly, it has a characteristic that none of these others have: "the presence of a dorsoventrally tall, paired sagittal crest on the frontal."
Based on its being an adult and having a character that is not found anywhere else among tyrannosaurines, Fiorillo and Tykowski name a new species. I'm simplifying what they did, but that's the general idea. To their credit, they acknowledge that there is not a lot distinguishing the new species and discuss in much more detail their rationale and the implications of their results.

Thanks a lot for your answer! Just a small detail... You seem to have linked the same article 2 times. Nanotyrannus should like to what website?

I fixed the Nanotyrannus link.


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Is it easier to burn a calorie of fat or a calorie of a carbohydrate?
Say someone eats 100 calories of chocolate vs. 100 calories of carrots. Something tells me that eating the chocolate will lead to you generating more fat. Will it? Is it harder to burn the calories that you consumed from the chocolate?

It isn't burning of the calorie you should consider as once digested different calories are stored in the same manner, it is actually the digestion itself.
Proteins are by far the most energy requiring foods to digest such that around 20% of the calories in proteins are used in extracting them. In comparison carbohydrates are much easier at around 5-10% whilst fats are even easier to digest.
But think of it in simple terms, chewing a vegetable and digesting it down and the relatively sheer quantity of mass you need to make it calorifically the same value as chocolate means that yes 100 calories isn't 100 calories.
All then in terms of real life application, our bodies respond to how much we eat. If we eat a large volume of low calorie food we will eat less calories in total. This also plays an important role.
Source: http://www.ncbi.nlm.nih.gov/pubmed/20613890

So when you eat carbs, you really only have to "burn off" 90-95% of it (because the act of digesting it does some of the work for you), whereas fat you have to burn close to 100% of it?

AndroidPenguin, if you dont mind let me add a one liner summary for your answer: Nothing is burnt inside the body; it is either fixed, spent or excreted.

@user6035 yes. Although so many other factors apply!


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How much solar energy required to produce enough food for a herbivore?
Just curious, how much solar energy can power an (herbivore) animal? Specifically, is it enough sunlight on Mercury (4 to 10 times brighter than on Earth) to "feed" a zebra? Will it be sufficient at 10x more effective photosynthesis? Notwithstanding lack of atmosphere, water being buried deep and other minor problems, of course :)

BMR is the amount of energy an animal uses just by being alive. BMR is proportional to the mammal's mass. More precisely, BMR is proportional to the mammal's mass to the power of 3/4. A 0.1 kg mammal has a BRM of 10 kcal/day. Using the aforementioned proportionality, a 600 kg mammal (average mass of a cow) will have a BMR of 6800 kcal/day.
This means that a cow would need about 6800 kcal of energy per 24 hours (1440 minutes) to survive.
The amount of solar energy reaching the earth’s atmosphere is 0.00194 kcal per square centimeter per minute. Since, according to you, there is 10 times the amount of sun in Mercury, there should be 0.0194 kcal per square centimeter per minute hitting Mercury.
0.0194 kcal per minute for 720 minutes (counting only day - since there is no sun during the night) equals 13.968 kcal per square centimeter per day. At this rate, the sun has to hit an area of 486 cm squared to harness enough energy for the cow.
In summary:

The average cow needs about 6800 kcal per day to survive (BMR)
On Mercury, the sun generates 13.968 kcal per square cm
Which means, the sun has to hit an area of 486 square cm

In one sentence:

In order to power a cow on Mercury, the sun has to hit an area of 486 cm for 720 minutes.

To learn more:

https://en.wikipedia.org/wiki/Kleiber%27s_law
http://www.ase.org/resources/measuring-number-calories-sunlight

According to wikipedia's [phoyosynthetic efficiency] (http://en.wikipedia.org/wiki/Photosynthetic_efficiency) a typical plant will convert about 1% of solar energy into chemical energy. But if our chlorofylled cow utilize sugar cane's 8%-efficient photosynthesis, then deal with overradiation, we get 6075 sq. cm area needed. Since day on Mercury is very long, we can require cow migration toward zenith, doubling energy production and eliminating 40% loss on photo-respiration. Finally, we got 1735 sq cm to light up. 40x43 cm, fine.

any thoughts on How much energy do small spiders expend when they are just waiting for their web to vibrate?

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


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How do viruses or bacteria survive outside the body long enough to spread?
Say I cough on my table, then someone else touches it and picks up something I've got... how is it that these things can live outside the body, how long can they manage it, and how long is generally 'safe' to consider something no longer carrying these germs?

depends on the species and its constitution... Can you be a little more precise..

It depends entirely on the environment the virus or bacterium is in and also the size of it.
Virus
With regards to viruses, the most important thing is typically whether or not the virus has an outer membrane or envelope.
Non-enveloped viruses such as rhinoviruses, noroviruses and adenoviruses can in fact survive for long periods outside the host (up to several days) whereas viruses with membranes such as HIV, influenza and the herpes viruses which do well in the host survive for shorter time periods.
Experiments with rhinoviruses and influenza viruses have shown potential survival times ranging from a few minutes to 48 hours or more.  They remain active longer on stainless steel, plastic and similar hard surfaces than on fabric and other soft surfaces.
This is because many enveloped viruses rely on the proteins on the surface of the membrane to attach to the host cell, this envelope is generally sensitive to degradation to sunlight and normal cleaning procedures.
Outbreaks associated with the non-enveloped viruses can continue for many months due to their relative stability in the environment, think of winter vomiting outbreaks, hand foot and mouth in animals as good examples of this phenomenon.
Bacteria
Because bacteria can undergo metabolism, synthesise proteins etc. for themselves, their life span is usually longer. If we split them into gram positive and gram negative its easier to discuss. Gram positive bacteria have a protein coat that prevents drying allowing them to survive longer. An example is the bacteria Staphylococcus aureus, which is responsible for toxic shock syndrome, food poisoning, and wound infections. With its protein coat it can withstand temperature and humidity extremes. The spore may survive for weeks on dry clothing using sloughed skin cells for food. The Bacillus anthracis, the anthrax bacteria, can also form spores and survive tens to hundreds of years. This is in comparison to gram negative which need humidity. An infamous example is Escherichia coli which survives typically only a few hours at best.

Viruses really take to heart the idea of "quantity, not quality." Like animals and plants, viruses and bacteria are a completely different ball game (even more so than animals and plants).
As you maybe know, you have bacteria floating around you in the air right now. Realistically, a single T4 bacteriophage (a type of virus) has a life cycle of about 20-30 minutes at 37 C°. However, in this time period, it often reproduces in a bacterium and creates tens if not hundreds more phage particles using the bacterium like a machine that was hacked to do its bidding.
The only way to prevent a virus from attacking is through vaccinations and other preemptive measures, as it is so difficult to prevent reproduction.
Bacteria are so different they, for all intents and purposes, cannot be approximated. For a rough approximation, somewhere from hours to weeks.

Virus particles (virions) are not alive. They are just a Genome Delivery Vehicle. They are essentially like landmines. However like different types of landmines different types of viruses can remain "active" for longer or shorter.
Those depend as explained above on the virion structure but also on Humidity and temperature, the fomite (surface) and the ammount of virions. Some viruses need up to 10k Virons to cause disease. The higher this "Particle to PFU ratio" is the lower the chance they can remain active outside the body for long. So if the Virus in question needs few particles, is not enveloped then this one can in theory live for quite a while outside, Norovirus for example is one of those.


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Publicly available genotype data?
I am a statistician and I'd like to test my new method on biological data. For this I am looking for genotype data for a number of individuals. That is, I am looking for something like this:

                    | Individual 1 | Individual 2 | Individual 3 | Individual 4 | ....
Chromosome 1 SNP 1  | AA           | BA           | AB           | BB           |
Chromosome 1 SNP 2  | AB           | AA           | AB           | BA           |
Chromosome 2 SNP 1  | BB           | AB           | BB           | AB           |
etc.

I don't really care about the species. Ideally I'd like to have data for complex and less complex genotypes (different number of chromosomes and number of SNP's).
Are there any publicly available data sets like this? I have been searching the internet, but I can't find any.

that's the stated purpose of the thousand genomes project.
the thousand genomes project has.. 1000 genomes.
its all downloadable.
http://www.1000genomes.org/

How about the allele frequency database?
http://alfred.med.yale.edu/alfred/index.asp
One of the main problems with SNP databases is that there are a lot of them so you can get lost quickly. This sight gives some overview on the available resources:
http://www.humgen.nl/SNP_databases.html
Hope this helps.

There is a vast amount of genotype data available at VectorBase's population biology browser, it is a database of insects which behave according to many mathematical assumptions - e.g. the non-overlapping discrete generations and homogeneous mating landscape.


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circularizing DNA molecules?
I have been reading about next-generation sequencing technologies that can sequence long reads. Even though the origin of my question is sequencing technologies, the question I am asking is about the basics of DNA biochemistry.
One of the issues in manipulating DNA samples seems to be the ability to circularize long linear DNA molecules into circular DNA molecules. What are the technical challenges of circularising DNA molecules longer than 50Kbp?

sorry i mistook 50kb as 50bp.. If you are referring to Moleculo then it still has to undergo the HiSeq type of sequencing. I guess splitting the genome just makes the assembly easier.. Can you indicate the references which quote the 50kbp limit.. Ilumina says it is 10kbp..

I am not sure if it is a limit of input or ease of protocol/assembly.. Because it is not impossible to clone 50-100kb in plasmids.. Is circularization an essential step?  Illumina doesn't explain the process in detail.

From Illumina LRS FAQ: "Long reads are generated by creating one or several libraries from an individual sample, depending on each sample type. To create a library, genomic DNA is first fragmented to approximately 10 kilobases (Kb). Next, these fragments are clonally amplified, sheared, and labeled with a unique index. The fragments are then sequenced using Illumina technology. The short sequence reads originating from each molecule are assembled separately into synthetic long reads using proprietary algorithms, resulting in a full sequence of each long fragment."

@WYSIWYG, I clarified my question. Although I want to know about DNA circularization because of my interest in next-generation sequencing, my question is not about next-gen.

For ligation of a linear molecule to occur, the two ends must come together at the active site of the DNA ligase. In a simple molecular cloning experiment the aim is usually to avoid recircularisation of a cut plasmid vector, and instead to get a new fragment of DNA inserted into the vector. However because the ends of the linearised circular plasmid are tethered together (by being ends of the same molecule) they are more likely to encounter each other than they are to encounter the end of an incoming fragment. This is usually overcome, in part, by increasing the relative concentration of the target fragment.
If you are aiming to recircularise a long fragment then the opposite effect will come into play: the ends of individual long molecules will be much more independent and so the end of another molecule will be likely to compete successfully for ligation. In theory this effect could be overcome by reducing the DNA concentration, but I assume that this is impractical for other reasons.

thanks for your answer, which is very clear and something that didn't occur to me before. I have a follow-up question in a new post.

http://biology.stackexchange.com/q/15737/658


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Evolution of Homo Erectus to Homo Sapiens
I just read an article on Wikipedia and noticed that some similarities between Homo Erectus and Homo Sapiens in the "Comparative table of Homo species". My question is;
Is it possible to say that some members of Homo Erectus species
have survived up to now and they are living in modern world as members
of Homo Sapiens?

It is not plausible that members of Homo erectus would survive and remain a separate species from Homo sapiens. For members of Homo erectus to survive implies that there wasn't significant interbreeding with Homo sapiens, which would require a significant population of Homo erectus.
There is some evidence that Homo erectus and other hominids interbred with Homo sapiens. So it is more likely that there may be some people with more genetic traits from Homo erectus than others. However, by significant interbreeding, there currently only exists a single species that may contain ancestors from multiple hominid species.

Not sure about H.erectus, but there is very strong evidence of interbreeding between H.neanderthalensis and H.sapiens as well as between the Denisovans and H.sapiens. It's likely that if the any of the Homo species overlapped (in time and space) and were similar enough to produce fertile offspring, there would have been interbreeding between them.

Recently read Why Does It Matter If Homo sapiens Had Sex With Neanderthals?. That is an interesting viewpoint about my question.


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If DNA has a half life of about 500 years, how can old seeds be planted?
According to this article, DNA has a half life of 512 years
Wikipedia claims that there are seeds planted as old as 31000 years
Doing the basic math $100 / (2^{30000/512})$ we get that only about
$2.2989191*10^{-16}%$ of the DNA would be left
So how do these plants still grow when replanted?

That half-life was for temperatures of 13.1ºC. In more ideal conditions, such as for temperature of −5 ºC or drier conditions, the half-life would be longer. The Wikpedia article in fact states that the seeds that were 31,000 years old were frozen under permafrost.
The original article estimates that the half-life at −5 ºC (for a 30 bp fragment of mtDNA from bone) would be 158,000 years. I'm not sure how well this data can be extrapolated to seeds.

For completeness, so flowing my math there would be 87.66% DNA reaming in the seed

The source paper for the article is this one: The half-life of DNA in bone: measuring decay kinetics in 158 dated fossils (available for free). The crux of their methodology is given in the abstract "By analysing mitochondrial DNA (mtDNA) from 158 radiocarbon-dated bones of the extinct New Zealand moa..."
So the article you linked is talking about DNA survival after cell death in fossilised bones. Seeds have not undergone cell death; they're still a small collection of living cells designed to survive in a state of near inactivity until the conditions are suitable for them to germinate. It's therefore not at all clear that we should expect the results from this experiment to generalise to seeds. Doubly so given that, as pointed out by Jonathan, the fossils were effectively held at around 13.1ºC whereas the seeds in the study you mention were found in the permafrost.
Finally, the seeds weren't viable on their own. It was only with significant intervention that scientists were able to get the embryos contained within the seeds to grow.

+1 for showing that the Materials and Methods section of an article is as important (if not more) than its Results section.

authors: Максим Караваев


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Examples of animals with different number of chromosomes that can interbreed?
When I was first started to write this question, I wanted to know how species evolve to have a different chromosomal arrangement, such as having two pairs of chromosomes instead of one? However, I think I have resolved my misunderstanding by reading:
http://scienceblogs.com/pharyngula/2008/04/21/basics-how-can-chromosome-numb/
My basic misunderstanding was that I thought animals with a different number of chromosomes couldn't reproduce, which appears to be wrong. My question is now, are there examples of animals that can interbreed that have a different number of chromosomes (particularly offspring that are not sterile)? Is there a species that is known to have a variation in the number of chromosomes (yet, somehow, hasn't yet resulted in complete speciation); or are there two species that can be interbred and result in fertile offspring?

Such examples are not that rare: multiple species are polymorphic for supernumerary (B-chromosomes), others are known to show intra-specific Robertsonian polymorphism (fusions of acrocentric/separation of metacentric chromosomes).
One very well studied example, which covers both intra- and inter-specific crossings, are isopod crustaceans from the Jaera albifrons complex. They show Robertsonian variation (and additionally sometimes B-chromosomes):

different species in the same location normally have different chromosomal numbers;
on the macrogeographical level at least some species show certain gradients in chromosomal numbers;
sometimes the same variation can be observed on the level of local populations.

Hybrids between species are viable and not sterile, but rare in nature. Fecundity of hybrids is lower than that of the parental species, and this seems to serve as an additional post-zygotic mechanism of species isolation.
Crossings between specimens of the same species with different numbers of chromosomes do occur in mixed populations and are also possible for parents coming from different extremities of the above mentioned chromosomal cline. In the case of mixed populations frequency of these hetezygotes is less than expected by Hardy-Weinberg. Such offspring is fertile, and its lowered frequency is associated with higher incidence of abnormal meiosis.
On the cytological level (normal) meiosis in a heterozygote individual is remarkable in showing trivalents instead of bivalents for the polymorphic chromosomes:

(a metaphase with a trivalent in the center and two bivalents) (from Staiger & Bocquet 1956)
In addition, in four out of five species of the complex chromosomal sex determination is of the following uncommon type: males are homogametic with sex chromosomes ZZ, while females are heterogametic with ZW1W2 chromosomes. So, females normally have in total an odd number of chromosomes and in their meiosis one observes a trivalent similar to the one shown above: the metacentric Z-chromosome conjugates with the two acrocentrix W-chromosomes.
Some references available on-line:

Lécher & Prunus 1971 (in French)
Solignac 1981 (English, on isolating mechanisms in general)
Lécher et al 1995 (a review in English)
Kappas et al 2013 (a review in English - see pages 23-26)

These are highly relevant to the question, but not accessible on the web:

Lécher 1967 (Cytogénétique de l'hybridation expérimentale et naturelle chez l'Isopode Jaera (albifrons) syei Bocquet)
Lécher 1967 (Polysomie autosomique chez l'Isopode Jaera albifrons syei Bocquet)
Staiger & Bocquet 1956 (Les chromosomes de la super-espèce Jaera marina (Fabr.) et de quelques autres Janiridae (Isopodes Asellotes))


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Omics integration questions
Let's say that I have a population of Mus musculus in the lab. I divide it in a control group and a test group. The test group is constantly subjected to a stress (example: elevated UV radiation). Both groups are allowed to reproduce for 20 generations.
I want to fully characterize and compare what changed in each offspring (control vs test group) by using omics. The objective is then to integrate all these information in a new database with the pathways that change and by what magnitude.

Should I use genomics or/and exomics or/and epigenomics?
If I do one of the above and proteomics, why could I need the transcriptomics for?
Would the metabolomics, which are mainly punctual measures, add any valuable information?

This is a purely didatic exercise.

Should I use genomics or/and exomics or/and epigenomics?

Depends on what you want to look at. Whole genome sequencing will give you all the mutations. If you are interested only in the coding part of the genome then you can go for exome sequencing. Though, exome sequencing will save your time and resources considerably, you may lose out a lot of relevant information from the non-coding and regulatory part of the genome.
Epigenomics is a very broad term. There are several aspects to it. You can go for the DNA methylome, Nucleosome positioning, or ChIP-Seq for Histone modification/variants.
I would suggest that if you can afford it then go for whole genome sequencing. Next choice would be exome sequencing. Once you have these data it might be relevant to add the third layer of DNA methylome.

If I do one of the above and proteomics, why could I need the transcriptomics for?

Transcriptomics is easier and better standardized than proteomics. There are also many good analysis tools.
There are several ncRNA, which has been shown to play important role in cellular homeostasis and gene regulation. You will miss out those.
You will save money. The reagents used for the transcriptomics experiments are the same as the ones used for the genomics experiments. Proteomics is a different domain altogether. You might need to look for collaborators.

Would the metabolomics, which are mainly punctual measures, add any valuable information?

Sure, they do add information. Whether of great value or not depends on the study that you are carrying out. For e.g if you are studying the role of stress in diabetes then doing a metabolomics study may be of great value.

Small note.. Do exome if you don't have money/resources for WGS.. else do WGS.


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How do Kangaroo mothers deliver the correct kind of milk to the correct joey?
Mother kangaroos are able to rear multiple joeys (young kangaroos) at different stages of development at the same time. According to Wikipedia, "the mother is able to produce two different kinds of milk simultaneously for the newborn and the older joey still in the pouch." What biological mechanisms are able to ensure that the correct joey gets the correct kind of milk? Do different teats produce different types of milk and somehow the joeys know which teat to suck from; or is each teat able to deliver both types of milk and the teat is able to tell from the mouth conformation (or something else) which type of milk to deliver?

i shouldnt wonder if the joeys prefer the taste of the milk that is best for them..

The younger Joey remains attached to the teat from which it receives its milk for the period of nine months until it leaves the pouch. So that would be teat from which milk suitable for the newborn is available (reference 1 and reference 2). The older Joeys also have an incredible sense of smell by which it can detect the teat from which it gets the milk it requires but it stands to reason that they cant get milk from the teat to which the younger joey is attached. (reference)


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Would expression of GroEL and GroES in erythrocytes be a potentially effective therapy for sickle cell disease?
Would expression of GroEL and GroES in erythrocytes be a potentially effective therapeutic strategy for sickle cell disease? Why or why not?

Apart from the answers from WYSIWYG I would add that the formation of filaments of Hb in sickle cells isn't really misfolding or misassembly, rather it is due to a new assembly pathway which results from the Glu>Val mutation. GroEL helps a protein to avoid kinetic traps en route to folding, filament formation is an extra process tacked on at the end of normal folding.

GroEL and GroES are multiprotein chaperonin complexes: Not so easy to ectopically express
Erythrocytes do not have nucleus: you cannot stably express anything in mature erythrocytes.
If your aim is to do a stable gene expression (which would require genomic integration), the better way is to do a gene therapy: culture haematopoetic stem cells, Correct the mutation by homologous recombination. Put the cells back into the bone marrow.


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Why can't ciliary muscles in the human eye relax like other muscles?
I had laser eye surgery a decade ago, but in recent years my eyesight has become significantly myopic. I consulted an ophthalmologist to see if this was eye strain because I work at computers a lot, or part of a natural degradation of the eye over time, or both. My ophthalmologist seems to believe that in my case I'm youngish enough that the natural degradation with age is minimal, and that it's mostly eye strain that is my problem. She believes I can get my eyesight back to roughly 90% of my post-surgery sight ability, if I can reduce eye strain. She gave me some eye drops to help with dryness, and recommended various ways to for me to help my eyes recuperate.
I decided to look into eye strain to learn more about what conditions cause it and what can alleviate it. What I learned is that the lens of the eye needs to be flatter to accommodate focusing on far objects, and rounded to focus on near objects. The way the lens becomes flat is by using spring-like connective tissue called choroids that pull it taught. Attached to these choroids are muscles called ciliary muscles that stretch the choroids out when they contract. This action causes the choroids to stop pulling on the lens, and the lens will retract into a more rounded shape. So, when the ciliary muscles are relaxed, you can see far. When the ciliary muscles are contracted, you can see close up. This diagram from the York University website was the clearest explanation I have come across:

Thus, the reason for my current inability to focus on far objects is that so much focusing on close objects, mainly computer monitors, is straining my eyes. In order to regain the ability to focus on far objects, I need to reduce strain and allow the muscles to relax. If they relax, the choroids can pull the eye to the flatter shape needed to see far.
However, I can't reconcile that model with how I understand the mechanics of the other muscles in my body. If I go to the gym and run or lift weights, or in any way expose my muscles to work, they respond by getting stronger without sacrificing the ability to stop contracting. The muscles in my body don't lose the ability to relax, no matter how much I train them. I have never heard of anyone who worked out too hard or too long such that their bicep would remain in a permanent state of contraction.
In fact, in my experience, after a hard workout, it's impossible to prevent my muscles from relaxing and resisting doing more work. When I do a bicep curl at the gym, and I do it to the point that I can't lift the weight anymore, my muscle gives up and I drop the weight. Similarly, if I've spent a long time looking at close up objects, shouldn't my ciliary muscles give up, allowing the choroids to take over, making clear far vision the unavoidable outcome?
The idea that my ciliary muscles need to relax in order to see far also seems to contradict my personal anecdotal experience. Sometimes I am able to see far away, but I can't hold it for more than a few seconds. If I try to maintain focus on far objects for too long, I get an uncomfortable feeling in my eyes that is hard to describe, but it's a form of pain that forces me to give up. My vision goes blurry, and I can only see close objects again. If my bicep worked the same way, it would be as if it hurt to let my arm hang straight down with a weight, and the only way to alleviate it would be to raise the weight, which makes no sense. I feel like the effort is in seeing far, and that when I'm tired, I can only see close up.
It's not that the case that I think that all medical research on the eye has it backwards, it must be that there is some aspect of this that I am not seeing (pun intended).
How can it be that the ciliary muscles, unlike other muscles, lose their ability to relax?
Why is it that my ciliary muscles don't become exhausted and allow the choroids to take over by default?

Regarding focusing on far away objects - perhaps that is unrelated to the distance? I imagine you would "stare" at the objects with intense concentration, rather than gazing casually, and would probably blink less and move your gaze direction less, fatiguing the retina.

To relax the eye muscles and prevent eyestrain, you can follow the 20-20-20 rule: every 20 minutes look at something at least 20 feet away for at least 20 seconds. That should work for problems that aren't pathological at least but I'm not an expert so take the advice with a grain of salt (the rule is a sound one but the later half of my answer is just my opinion).

First of all, I should correct some points that were misunderstood.
Don't change the question because this will lead to confusion.
"The way the lens becomes flat is by using spring-like connective tissue called choroids that pull it taught."
In classic ophthalmology you don't need to think about choroid in direct relation to accommodation: choroid is a sponge-like layer between the sclera and retina and in general it is consisted of blood vessels. The anterior part of the choroid continues anteriorly to became a ciliary body which in turn contains ciliary muscle - one circular muscle per eye. From the ciliary body/muscle spread zonules (zonule fibers) and they are fixed on the lens equator.
Physiology: contraction of ciliary muscle causes zonules to became loosen and "free" the lens to became more convex and move the focus anteriorly (not choroid contracts itself). If the ciliary muscle relaxes then zonules are tighten up and the lens consequently becomes more flat (less convex) moving the focus posteriorly. In other words you can say it in the terms of depth of focus - convex lens gives less depth, less convex gives more depth of focus.
Thus, the classical choroid layer does not perform any action (look at your choroid related link - there are almost nothing about accommodation).
"Permanent state of contraction" can be physiological (=normal) as well as abnormal one, and it is very common in some conditions (muscles spasms). One example is priapism, where corporal smooth muscle contraction causes permanent and dangerous penile erection which can be medical emergency (priapism is by far more complex, so take the explanation like a metaphor).
If we refer to "accommodation spasm" there is analogy to "muscle spasm" (and partially to priapism), but I should state we believe that spasm of ciliary muscle exists - since we don't see it directly. Probably (and take this sentence as speculation, since I cannot give you reference right now) the causes of this is not a muscle spasm itself, but the state of zonular fibers which cannot come back to their base state. I like the example with iron rod - if you will contract it fast and many times, at some point it can be "loosen" as well as fractured (and probably it does happens to zonules too). Probably (I say "probably" to underline the point we do not exactly know this), the "accommodation spasm" is partially misname and in future the investigations will clarify that.
Probably, you will learn some interesting facts from definition of "pseudoexfoliation" syndrome, but I do not explain it here because it is not related directly to the question. From wiki "has been known to cause a weakening of structures within the eye which help hold the eye's lens in place, called lens zonules"
Another example for analogy for continued "spasm" is the situation when one should care something heavy for a long distance without releasing the grasp - finally one can get not only spastic contraction but also severe ischemic damage to the fingers.
Considering your case, you should know about pathological (degenerative) myopia where the eye expands posteriorly and consequently the focus is before the retina which should be corrected by minus lenses. It is well known fact that myopic eyes have longer axial length then normal eyes. Probably, it is your case.
So, as you can see, the answer to your question is not a clear cut, but assumption. The ciliary muscle does can relax, but probably the problem is more complex then only ciliary muscle related issue.
PS The image you reposted is a little bitconfusing one and is not exact. This one is classical and gives better understanding of the anatomy -

I'm not a eye doctor but I do workout. I would like to say something about your metaphor or comparison from the ciliary muscle to the body muscles.
Let's look at a workout. In a workout, you strain the muscle then relax the muscle repeatedly until you exhaust the muscle.  Another part of the exercise is stretching. If you don't stretch, you will lose full range of motion. For instance, if I were to do a regiment of bicep curls for the first time, and I slept that night with my arm cocked, it would be a painful effort to straighten it the next day. If I don't stretch it my arm would stay in that position having limited motion. The muscle is relaxed but it's range has changed. Another example would be, when I was a teen, I did karate and could do the splits. Now-a-days I can not do the splits no matter how much my muscles are relaxed.
Looking at the computer all day isn't comparable to working out a muscle because you don't contract and relax repeatedly. You only contract.
Now let's look at the body muscles in a more relevant metaphor - Tension. Tension is an involuntary reaction. Because you hold the muscle in a contraction state for such a long time, it tends to want to stay contracted without you making the effort. A lot of people hold tension in their neck and shoulders and no matter how much pain it causes them, they can't relax it voluntarily.
Muscles have a mind of there own (muscle memory). To assume you have complete control over them is wishful thinking. I assume that the ciliary muscle is no different.

Can you please add some references to your answer?

There are a few more things that need to be considered to get a better understanding of the physiology.
The ciliary muscles are not skeletal muscles (voluntary muscles that you can control) but smooth muscles (involuntary muscles which are under the control of the autonomous nervous system, which is self regulated by the parts of brain not under the conscious control). This has several deep implications.

Smooth muscles do not hypertrophy - grow and become thick like skeletal muscles - They are more or less constant and their growth/strengthening is more related to hormones than regular contraction/relaxation exercises
Smooth muscles are supplied by autonomic nervous system - Parasympathetic system is the main supply. Recently evidence for sympathetic innervation of ciliary muscles has been found.

Generally, there is a balance between the sympathetic and parasympathetic, the balance being driven by the need brain perceives. An imbalance in these systems can cause accommodation problems

This point is speculation based on proved biological laws: Law of tension-stress: This states that if under constant tension, the biological systems grow.

Gradual traction on living tissues creates stress that can stimulate and maintain the regeneration and growth of certain tissues. Slow, steady tension of tissue causes them to become metabolically activated, resulting in an increase in their proliferative and biosynthetic functions. These processes are dependent upon two main factors:

The quantity and quality of blood supply to the tissue being mechanically stressed and
The stimulating effects of tensile forces acting along the lines of muscular contractions because collagen fibers are generally aligned parallel to the vector of tension-stress.
  source:http://jontristermd.com/for-physicians/the-tension-stress-effect-on-the-genesis-and-growth-of-tissue-2

This may cause changes in the choroid that may reduce the tension on the zonules causing a semi-permanent/permanent myopia.

Thank you for responding. I think there's some interesting and useful information here in your answer. However, you've used a lot of deeply technical terminology that makes it very hard to follow and understand. If you could rephrase your answer with a non expert audience in mind, I think it would be a lot more informative and helpful.

After reading various theories of how the ciliary muscle body works, I came across a convincing new theory by Dr Goldberg, one of reciprocal action. In other words, the lens is only under posterior (rear-inner side) tension when focusing on near objects, but anterior (front-outer side) tension when focusing on distant objects. In both cases the lens is under a form of zonular tension. The ciliary muscle moves forward (near focus) and backward (distant focus), actuating the zonular strings and circular apparatus accordingly. As I have witnessed how I sometimes have to force myself to focus in the distance, I am inclined to believe that relaxation of the ciliary body only leads to a medium focus, and while contraction, either forward and backward, for near and distant focussing respectively. In other words, the ciliary body would also contract slightly for a distant focus, but this contraction would be in opposite direction. There's a video illustrating Dr Goldberg's theory: https://www.youtube.com/watch?v=1yIpyitm6eE
I must add that there are theories saying that the zonular fibre gets stretched (permanently longer) when using too much near-vision, so that when ciliary muscle body relaxes, the lens is not held taut enough, causing it to be always convex (nearsighted).

The ciliary muscle is made of smooth muscle rather than skeletal muscle.  These two types of muscles have different mechanisms for contraction and relaxation.  Skeletal muscle is relaxed unless it is stimulated by a nerve.  Smooth muscle is able to lock itself into a contracted state through a chemical reaction (phosphorylation).  It then does the reverse chemical reaction (dephosphorylation) to relax.  This is important because smooth muscles do things like keep the urine in your bladder (urinary sphincter), and you don't want that muscle getting tired and giving up.

Can you add references or other credible sources to allow others to background read on your answer?


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enzymes that stabilize DNA loops
As a follow-up of a previous question, I would like to know what enzymes or protein complexes have been used to manipulate DNA samples into stabilizing DNA loops.
I have read that cohesin is one of such enzymes, but works as a transcription factor by binding specific DNA motifs.

My interest is in knowing what other enzymes will create DNA loops with no DNA motif biases from a DNA extraction.
This is a follow-up question to this one, as ultimately I would like to know if there could be any ways of optimizing the process of DNA circularization of very long stretches of human (or mammalian) double-stranded DNA, from several kilobases to megabases, by first creating stable DNA loops that leave two DNA ends close by for a more effective ligation process.
Any ideas?

With specific attention to more efficient ligation (e.g., after restriction enzyme digestion), there are commercial products on the market that use a modified topoisomerase to catalyze such a ligation.

I have read that cohesin is one of such enzymes, but works as a
  transcription factor by binding specific DNA motifs.

Cohesin binding is not motif dependent (like transcription factors) and is also dynamic. Though sequence may have a role it is, just as in the case of nucleosomes,  mostly the overall composition rather than a sequence based motif:
From this article:

Cohesin binding peaks correspond closely to peaks of high local AT
  composition, a base composition periodicity of ∼15 kb that is distinct
  from the ∼50 kb periodicity of base composition isochores, consistent
  with axis association of cohesins.

DNA-protein complexes can be crosslinked and subsequently the loops can be pulled down. However, this is tricky. You would need to cut the DNA at the loop ends in order to ligate them together. I don't know how to do that (Perhaps by using an antibody linked to an endonuclease).


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Why are low throughput methods more trustable for protein interaction?
I read that protein interactions found using high throughput methods are less trustable than those found using low throughput methods.
For example, searching for interaction of BRCA2 on BioGRID, I got this result.
So, we won't be sure about the interaction of BRCA2 with SIRT1 as it has been found with a high throughput method.
My question: Could you give me a very simple explanation of what is the meaning of high and low throughput techniques ? (I have a vague idea reading it on web but I am not satisfied with my understanding.) Why is high throughput not reliable in this case?
One reason I can think is that they involve mostly in vitro studies.

This article is a bad example, it has been retracted. See here.
But this doesn't matter for the methods.
This is usually done by so called "genome wide association studies". There you compare the regulation of your group of interest with a "normal" group to find genes which are differently expressed. This is something we did: We overexpressed a transcription factor in a cell line and compared it to the untransfected cell line, which doesn't have this factor. The comparision brings up differently expressed genes. This is either done with microarrays or today more like by ChIP-sequencing (let me know, if you want to know more, I can go into the details).
When you analyze such data, you first cut-off all data, which is below a certain threshold to be sure, that you reduce the number of false positives. A low threshold for the recognition of changes means that you are more likely to have false positive genes in your final list. This might happen due to changes in the cell or the conditions, secondary effects and so on. And you will also have signals, which appear statistically and which are false positive.
If you choose your threshold too high, you will reduce the number of false positives, but on the downside you will also generate false negatives, since you refuse genes which only have a relatively low change but are real. The balance between this is not always easy. As a rule of thumb usually everything which changes at least twofold in expression is used (unless you control better).
Even when filtered, the output of the experiment will still contain some false positives. Then you will also record some secondary effects, meaning that you gene of interest regulates a second, which regulates a third. Since both will come up in the analysis, it will look like that the third gene is regulated by the first (and not the second, as it would be correct). And these are the reasons why usually every intereaction between two genes (or better: Between a protein and a gene when talking about a transcription factor or two proteins) needs to be verified in the wet lab. And this is work, which can be pretty hard.


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Does the lung absorb organic food?
Imagine you swallow something up and not everything gets out of the windpipe (this is possible right?).
Would it be possible for the lung to handle with the rest implying that it is organic? Would it slowing absorb it?

I'd suspect that the bacteria in your lungs would end up with a feast, you'd end up with a major or minor lung infection and hopefully, once the food is gone, the bacteria will go back to their normal population levels and everything will be hunky-dory. Or you could die.

Not well - see aspiration pneumonia - small amounts of food would be dealt with without too much problem, simply being coughed up.  Lung tissue isn't designed to digest or absorb so I can't imagine it being anywhere near effective in this regard

It would also absorb inorganic food by the way, salt for example.

When we eat the architecture makes sure most if not all the food ends up in our foodpipe rather than our windpipe. This is aided by a structure called the epiglottis.
However frequently foods may be inhaled, for example if a drink is sucked through a straw more if it gets into the lungs compared to if we drink it. Occasionally we will inhale a peanut or something else which typically occurs due to abnormal relaxation or muscular problems in the structures involved. This may be due to a neurological disease (e.g. myasthenia gravis) or because simply drinking too much and inhaling peanuts or vomit (aspiration).
If the inhaled substance is small and lipid soluble e.g. alcohol, it can pass through the alveoli at the end of the lung to the rich blood supply. If it doesn't we rely on macrophages to digest the food. They aren't frequent enough to digest anything substantial. Bacteria however are great at munching this up and increase substantially in number. Typically your lowest airways are sterile but food can interfere with clearance mechanisms and provide a home. The part of the lung blocked (distal to the foreign object) can collapse and frequently does. In the long run this may cause bronchiectasis, where an infection recurrently affects the area due to permanent damage done during the initial event resulting in widened airways and an ongoing inflammatory response. The inflammatory response reveals even more receptors for bacteria to latch on to.


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Selection on linked loci in a diploid population
Let’s consider two linked loci $A$ and $B$ that are both bi-allelic. In consequence, we have four different possible haplotypes $A_1B_1$, $A_1B_2$, $A_2B_1$, $A_2B_2$, which frequencies are $X_1$, $X_2$, $X_3$, $X_4$ respectively. Let the linkage disequilibrium $D$ be defined as:
$$D=X_1X_4 - X_2X_3$$
The change in haplotype frequencies through time is given by:
$$\delta X_1 = \frac{X_1(w_1 - \bar w) - Drw_{14}}{\bar w}$$
$$\delta X_2 = \frac{X_2(w_2 - \bar w) - Drw_{14}}{\bar w}$$
$$\delta X_3 = \frac{X_3(w_3 - \bar w) - Drw_{14}}{\bar w}$$
$$\delta X_4 = \frac{X_4(w_4 - \bar w) - Drw_{14}}{\bar w}$$
, where

$r$ is the recombination rate between the loci $A$ and $B$
$\bar w$ is the mean fitness (sum of the fitnesses of each haplotype weighted by their relative frequencies)
$w_{14}$ is the fitness of the (diploid) individual that has the 1st and the 4th haplotypes
$w_i = X_1w_{i1} + X_2w_{i2} + X_3w_{i3} + X_4w_{i4}$

The change in allele frequency of locus $A$ is $x$ and $1-x$. The change of allele frequency of locus $B$ is $y$ and $1-y$. Those changes are given by the addition of haplotypes frequencies:
$$\delta x = \delta X_1 + \delta X_2$$
and
$$\delta y = \delta X_1 + \delta X_3$$
Question
I don’t fully understand these formulae! Could you please help me making sense of them. Especially of the presence of the expression $-Drw_{14}$.

source

These equations describe how the haplotype frequencies will change over time due to a combination of recombination and natural selection.
Before I proceed, I need to change your four $\delta X_i$ formulas above. Lewontin and Kojima (1960) writes the equations as:
$$\Delta X_i = \frac{X_i(w_i - \bar w) \pm Drw_{14}}{\bar w}$$
where the minus sign is used for $i = 1,4$ and the plus sign is used for $i=2,3$. (See also this chapter by Sergey Gavrilets.) Decreasing the frequency of a haplotype through recombination will necessarily increase the frequency of a different haplotype (adjusted by selection).
$D$ is the measure of linkage disequilibrium. It ranges from $-0.25$ to $0.25$ and indicates how much the haplotype frequencies deviate from an expectation of no linkage ($D=0$, the loci are independent).
First, assume no natural selection. That is, $w_i = 1$ and therefore ${\bar w} = 1$. When fitness is equal, the equations reduce down to
$$\Delta X_i = \pm Dr$$
Some recombination will occur between the linked loci proportional to the distance between them. In a large randomly mating population with no selection, $D$ will eventually decay to zero.  The larger the value of $r$, the quicker that decay will occur. Eventually, the haplotype frequencies will appear as if they are not linked. (See this figure.).
For example, assume that $A$ and $B$ are linked, with these four haplotype frequencies:
$$A_1B_1 = 0.5$$
$$A_1B_2 = 0.38$$
$$A_2B_1 = 0.05$$
$$A_2B_2 = 0.07$$
In the absence of natural selection and assuming that $r=0.1$, then $\Delta X_i = \pm 0.0016$, again with plus or minus depending on the value of $i$. This is the rate the frequencies will change each generation.  As $r$ decreases, the rate of decay decreases.
Differential fitness among the haplotypes will also affect the rate of decay. The fitness interactions among loci on the same chromosomes and between homologs can get rather complex depending heterozygote advantage, epistasis, etc. (see Lewontin 1964 for several fitness models).
The equation $w_i = X_1w_{i1} + X_2w_{i2} + X_3w_{i3} + X_4w_{i4}$ is the average fitness of the each haplotype in combination with all the other possible haplotypes. For example, for $w_1$, you're calculating the average fitness of four genotypes: $A_1B_1/A_1B_1$, $A_1B_1/A_1B_2$, $A_1B_1/A_2B_1$, and $A_1B_1/A_12B_2$.
I am uncertain why $w_{14}$ is used in the second term of the numerator. I thought it might be because that combination is heterozygous at both loci so recombination generates all four possible haplotypes. However, both Lewontin and Kojima (1960) and Lewontin (1964) use $w_{11}$. It may also be that a relative fitness component is necessary for comparison so the fitness of any one of the genotypes could be used there. I don't know.
Regrdless, as a simple example to illustrate the effects of selection, assume $r=0.1$, $\bar w = 0.5$, and $w_{14} = 1$ (heterozygote advantage, given maximum relative fitness). For $w_1 = 0.9$ then $\Delta X_1 = 0.397$. Selection strongly favors this haplotype in all genotypic combinations so it will increase in frequency.  For $w_1 = 0.3$ then $\Delta X_1 = -0.203$. The haplotype is selected against and decreases much more rapidly, relative to no selection at all.  The same idea would apply for the other haplotypes.
References
Lewontin, R.C. 1964. The interaction of selection and linkage. I. General considerations; heterotic models. Genetics 49: 49-67.
Lewontin, R.C. and K.-I. Kojima. 1960. The evolutionary dynamics of complex polymorphisms. Evolution 14: 458-472.