genetics - What does phasing mean?

This refers to haplotype phase (aka gametic phase). This essentially means knowing which allele belongs to which copy of the chromosome, or alternatively, which alleles appear together on the same chromosome.

In short-read sequencing, for example, it is difficult to resolve the haplotype of two heterozygous SNPs if they have not been covered by the same read. If you observe A/a and B/b, you do not know whether you have AB + ab or aB + Ab. So you would say you do not know the phasing.

See the Wikipedia links for more information.

neuroscience - Systems identification in small neural network

For very small systems like the worm c.elegans it must be possible to record from all neurons at the same time, at least optically.

While it is true that whole organism optical recording is technically possible in C. elegans, I'm not aware of any published work where all neurons were identified and recorded from simultaneously and then combined with connectivity data in a systematic way.

I should note, that this isn't limited to C. elegans. Florian Engert's lab has published whole-organism recordings from zebrafish as well. At the moment, though, there are still technical challenges to work out before we get the input-output relationships you desire on a whole organism level. First off, the recordings aren't truly simultaneous, in the sense that it still takes time to build up 3D images from z-stacks. Second, the image processing to label neurons is not yet robust. And finally, the most popular optical indicators are based on calcium levels and thus provide only a proxy for membrane potential and furthermore they have limitations in time resolution, range and accuracy.

The field, however, is progressing rapidly and I suspect that these challenges will be overcome in the next few years.

What are the best databases to ask such questions?

There are no database yet for C. elegans neural activity, likely because the number of groups publishing optical recordings in C. elegans is still fairly small. But as more labs pick up the technique, I think the value of a database will become more obvious to the community and the OpenWorm project is providing some well-needed leadership in this area.

Finally, I should point out that in the end we may find that neural activity and connectivity provide only one part of the story. It is likely that in C. elegans neuromodulators and other "unwired" connections between neurons could play very important roles as well.

senescence - Do crocodiles age?

Well, this needs to be broken down into two parts. Do Crocodilians age (undergo senescence), and are Crocodilians immortal (will only die of external causes)?

Are Crocodilians immortal?
- No. They appear to live about as long as humans before they die.

Measuring crocodile age is unreliable, although several techniques are used to derive a reasonable guess. The most common method is to measure lamellar growth rings in bones and teeth—each ring corresponds to a change in growth rate which typically occurs once a year between dry and wet seasons. Bearing these inaccuracies in mind, the oldest crocodilians appear to be the largest species. C. porosus is estimated to live around 70 years on average, with limited evidence of some individuals exceeding 100 years. One of the oldest crocodiles recorded died in a zoo in Russia. A male freshwater crocodile at the Australia Zoo is estimated to be 130 years old. He was rescued from the wild by Bob Irwin and Steve Irwin after being shot twice by hunters. As a result of the shootings, this crocodile (known affectionately as "Mr. Freshy") has lost his right eye.

Do Crocodilians undergo senescence (show signs of aging)? Well, if this study from "Gerontology" written by Patnaik BK in 1994 is to believed... Maybe not.

Evidences and mechanisms of rapid or negligible senescence in reptiles are still fragmentary and unclear... neither the increase in mortality rate and accumulation of lipofuscin nor the reproductive senility have been shown conclusively in ageing reptile populations.

So, while Crocodiles and Alligators (both Crocodilians) definitely have a finite lifespan, because they just continue to grow it's hard to tell how long they have left until the day they die.

biochemistry - Can jellyfish improve Black Sea environment?

According to this study, cited by many popular science magazines, jellyfish and other, smaller animals can contribute to the vertical ocean stir as much as currents do.

Black Sea chemistry and biodiversity is highly coupled with the lack of vertical currents, present in oceans or bigger seas. (Some ) effects are limited salinity in the top layers - and many ocean fish species cannot live in black sea - and limited space for life (under 50 meters there is no oxygen)

Can the jellyfish population (which is exploding now) change the stratification of water layers enough that the highly saline waters from bottom go up, and oxygen goes down, allowing a completely new ecosystem here?

If yes, what are the outcomes of such prospects? Besides the potentially catastrophic release of hydrogen sulphide form the bottom, can it be an improvement for the biodiversity here?

zoology - Why would the Camargue horses have a white coat while the foal have a dark coat?

Our own hair will also turn gray (indeed, yours seems to be on its way, if you don't mind me saying so) but there need not be an advantage to that; if it doesn't affect our ability to have successful children it probably doesn't matter much to evolution or selection. When it comes to animals that interact with humans, though, many traits are selected for, even those without an advantage, in fact often we select for disadvantageous traits (if they were advantageous, we might not need to select for them in the first place).

As this 2008 paper from Nature Genetics goes into, the "graying with age [phenotype] is an autosomal dominant trait" overwhelmingly caused by "a 4.6-kb duplication in intron 6 of STX17 (syntaxin-17) that constitutes a cis-acting regulatory mutation". To answer your question, though:

The Gray horse provides a notable example of how humans have cherry-picked mutations with favorable phenotypic effects in domestic animals... The prestige of riding a white horse has thus led to selection of the Gray-causing mutation by humans; this mutation is by far the most common cause of white color in horse.

This phenotype is actually often detrimental, as white/gray horses can have eye problems and higher rates of skin cancer; Camargue's are particularly susceptible to melanomas, present in around 70% of horses by age 15. There does seem to be some benefit, though, as the second paper I linked suggests these horses are subject to fewer fly attacks.

EDIT: I seem to have been unclear and you seem to have misunderstood my answer. Let me break it down:

That is an example of why something negative or pointless might persist, as would a dominant inheritance pattern that is fixed in a population: negative traits that are only weakly deleterious have a non-negligible chance of fixation. Asking what the advantage is is somewhat of a moot question because every single Camargue horse has the trait; asking what caused a seemingly-negative phenotype to become fixed is a good question, but likely an unanswerable one as it occurred long ago.

As a side note, how long a breed has been in an area does not simply imply breed purity. Here's a quote from the International Museum of the Horse:

Through the centuries many armies have passed by the Camargue, including the Greeks, Romans and Arabs. The horses brought with these armies influenced the Camargue over time. It has even been suggested that the Camargue has had some influence on the early breeds in Spain as armies took them back home.

mammals - How compatible are mammalian digestive systems?

I think this would depend entirely on the diet of the host and donor mammal.

Assuming they are of similar size and diet, I don't see any reason why this wouldn't work. The gut tends to absorb more or less everything in the food.

If the diet of the two mammals differed significantly, I could see some problems with eating the correct foods. Herbivores with the significantly shorter carnivore gut would have trouble killing and eating things without carnivore teeth/claws/what have you, and the plants would not provide enough nutrition on their own. Rabbits, for instance, have a two-pass digestive system, so in order to use a rabbit gut the mammal would have to eat their own feces regularly. (Rabbits have digestive bacteria in their colon, but grass has to travel to the colon and then back 'upstream' to the absorptive part of the gut. So this is achieved by going around again.)

biochemistry - Chemical structure prediction

I'd like to do chemical structure prediction using a known molecule formulas. I'm familiar with de novo protein structure prediction, but are there any programs which will go from formula to structure with optimal geometry of random small chemicals (say 30 atoms)? I found http://cccbdb.nist.gov/mdlmol1.asp but it selects mol files from a limited database. I need a command line UNIX program which computes mols from formulas.

---

Concise structural formulas popular during past ages are unable to describe every type of chemical structure like morphine. I found no software that supports csf (Smiles and inchi are popular but are encoded and not human readable). When the bonds of the structure are known geometric minimization (DG-AMMOS) orients the structure to a stable native like direction.
http://www.mti.univ-paris-diderot.fr/fr/downloads.html

skin - Why Do Healing Wounds Feel Warmer To The Touch?

I fell over on my bicycle trying to avoid running over a rattlesnake, and ended up badly skinning my knee. It immediately began to bleed, but soon clotted.

It has been 2 days now and it has formed a thin scab and is healing well as far as I can tell. I was chilly from the air conditioning, and I noticed the wounded knee was much warmer than the healthy knee. It was very warm, while the other was rather cold to the touch.

I read here about skin healing, and thought, maybe it is because the blood rushed there to clot the wound. But, the wound is already clotted and sealed and the worst is over. So my question is:

• Why is my wound and the area around it so much warmer days after the injury?

structural biology - Isotropy of sarcomere bands in skeletal muscle cells

As seen under a polarization microscope, the A-Band in skeletal muscle fibres is so named because it is anisotropic in its refractive index which is a characteristic of orderly crystalline structure. On the other hand, the I-Band is so named because of its isotropic nature, as far as its refractive index is considered, which is characteristic of Amorphous substances or substances which lack long-range order. Both are filamentous (as opposed to globular) in the sarcomere (Actin is present as F-Actin).

But then why this difference in the characteristics of refractive index,
which is indicative of order (i.e crystalline or amorphous?) in their
molecular structure?

Moreover, is the H-Band anisotropic?

If not, then the anisotropy of the remaining part of A-Band must be a consequence of the relative arrangement of Actin and Myosin which are independently isotropic, and hence cannot give a possible isotropic arrangement.

If yes, then that indicates that the myosin filaments are anisotropic in themselves and actin filaments are isotropic. But, in the region of their overlapping (A-Band minus H-Band), the overlap is between an anisotropic (myosin) and an isotropic (actin) component which shouldn't be anisotropic because the randomness of actin filaments (i.e. its isotropicity) should make the entire configuration isotropic?

I am sorry if I am wrong in my understanding of isotropic and anisotropic characteristics, or if my question sounds too "physics-related", but this has been bothering me for quite some while now.

Here is a directly related question I asked on physics.se. It partly solves the problem of possible arrangement of isotropic elements to generate anisotropy.

biochemistry - How to prevent protein precipitation?

Alas, the great problems with protein formulation. I assume that the labeling chemistry forces you to use the 8.5 pH. (I don't think this is necessarily true since succinimidyl chemistry does work at pH=7.2 and the NHS ester is fairly unstable above pH=8.6)

We usually tackle this problem entirely by brute force ie. testing multiple buffer condition with different bases and different salt concentrations. First attempt would be to try out all of the Good's Buffers notablely HEPES, TRIS, MOPS, Tricine, Maybe you should look at both zwitterionic buffers and non-zwitterionic buffers. In your case, the succinimidyl is vunerable to primary amines so avoid things like Tris/Glycine.

The second thing to test would be various salt concentrations. Since you're already dumping in Sodium Bicarb, NaCl should be great. Unfortunately, this is where things get tricky since it is hard to know if your protein precipitates at low salt or high. A test from 20 mM, 50 mM, 100 mM, 150 mM, 200 mM, 500 mM should cover most of the interesting regimes.

Alternatively the sudden change in the ionic environment around your protein may be causing it to precipitate. You probably should dialyze or purified your protein in PBS to allow it to refold appropriately.

human genetics - What is a Mitochondrial Eve and Y-chromosomal Adam

When talking about a maternal unbroken linage and a paternal unbroken linage, is the meaning that Mitochondrial Eve had a linage of only women reaching every person today, and the same with Y-chromosomal Adam and men?

Kind of, yes. The concept behind Mitochondrial Eve and Y-Chromosomal Adam has to due with cell replication and basic genetics.

The Mitochondria ("Power Generators" of the cell) are directly inherited from mother to daughter cell. That is, new cells do not start with 0 and are forced to make them de novo. Some Mitochondria are replicated before division and some are 'given' to the daughter cell to start with.

Because of the unique way that Mitochondria are inherited, when it comes to creating new humans it means that only the Mother's Mitochondria are given to any children she gives birth to regardless of the sex of the child. So I, being male, have my Mother's Mitochondria - which the same as my Grandmother's - and the same as my Great-Grandmother's - etc. etc. etc. until you can trace that line back to "Mitochondrial Evel" whose Mitochondria are the origin for all humans on the planet and are inherited Maternally.

In that sense it is an unbroken lineage of genetic information as inherited from mothers, though not exclusive to women.

"Y-Chromosomal Adam" is a similar concept - Women do not have a "Y"-Chromosome, so every Y-Chromosome men have today had to originate from somewhere. It's trickier to do than tracing Mitochondrial DNA because while Mitochondria are inherited exclusively from mother to child, there could have been multiple Fathers to Mitochondrial Eve's children and other similar complications that muck things up.

How is the specific "identity" or time period of those persons is known, assuming that researchers didn't check the Mitochondrial DNA or Y-chromosome of every single living human being today?

For "Y-Chromosome Adam" it's still more or less in the data-gathering phase as far as I was last aware. It's not as concrete as "Mitochondrial Eve", which has a very solid body of work supporting her.

The "identity" is known because the more in common a person's genes have with the genes of another, the more closely they are related. The researchers took a lot of genes from very divergent populations, and compared them. The researchers were then able to tell which portions were common among all of the Mitochondrial DNA, which had changed the most, and which had changed the least from each other. Using that data, you can construct a rough image of what the originator (or LCA - Last Common Ancestor) had for their own genetic makeup.

You can construe a time period because portions of your DNA (either Mitochondrial or Nuclear) acquire/tolerate mutations at an expected rate - say 1 mutation every 1.5 Million Years. So as long as you have a rough idea of what your LCA's genes looked like (see above), then a modern day sample with 5 mutations is 7.5 M.Y. away from the LCA.

how can they know for sure that there aren't some tribes in the Amazons, which have a direct female linage to Mitochondrial Eve's sister?

They didn't when they started testing. That's part of the fun of the project.

The "Out of Africa Hypothesis" rose in prominence partially due to the findings of the research. It basically posits that the ancestors of humans evolved once in Africa, and then spread from Africa to the rest of the world. Because the Mitochondrial Eve research concludes that "Eve" was around before we spread throughout the rest of the world, it implies that every ancestor already had Eve's legacy when they started migrating into Europe, Asia, the Philippines, etc. Thus every human on Earth, no matter where they are today, shares traits with Mitochondrial Eve.

For the Amazonian tribes, they would have inherited it from their ancestors in North America, which were ancestors of tribes in Asia who crossed an ice bridge into North America, and the tribes in Asia came out of Africa.

zoology - How do animals/plants change for each season?

There are various parameters that describe change of seasons such as day length, temperature, humidity. But it can be assumed that most of these parameters ultimately depend on one parameter- day length.

The response of plants towards the length of day/night cycle is called photoperiodism (which dictates spring flowering).

This article explains the effect of a gene called CONSTANS(CO) on spring flowering. CO is post transcriptionally regulated by cryptochromes and phyochromes.

The circadian rhythm in CO mRNA abundance was proposed to represent a photoperiod response rhythm, in which exposure to light coincides with CO expression only under LDs (Long Day) and thereby triggers flowering.

......

We propose that early in the day phyB promotes the degradation of CO whereas in the evening cryptochromes and phyA antagonize this degradation and stabilize CO protein,

However, my knowledge of plant molecular biology is not that great and I would advise that you refer the mentioned article and the cross references cited in that.

human biology - How does the body measure dehydration?

From Wikipedia entry on thirst:

In the mammalian brain, the posterior surface of the hypothalamus
forms the front wall of the third ventricle (a cerebrospinal
fluid-filled cavity) and clusters of cells (osmoreceptors) on this
surface, notably in the organum vasculosum of the lamina terminalis
(OVLT) and subfornical organ (SFO), signal this cellular dehydration
to other parts of the brain, and thirst is experienced. Destruction of
this part of the hypothalamus in humans and other animals results in
partial or total loss of desire to drink even with extremely high salt
concentration in the extracellular fluids.1

The entry on osmoreceptor says in part:

When the osmotic pressure of blood changes (i.e. it is more or less
dilute), water diffusion into and out of the osmoreceptor cells
changes. That is, they expand when the blood plasma is more dilute and
contract with higher concentration.

It also describes how the kidney measures chlorine anion flow through some nephrons, which triggers a cascade of messenger molecules resulting in increased blood levels of the hormone angiotensin, which also results in thirst messages originating in the hypothalamus.

1Derek A. Denton (8 June 2006). The primordial emotions: the dawning of consciousness. Oxford University Press. pp. 118–19. ISBN 978-0-19-920314-7.

2Walter F., PhD. Boron (2005). Medical Physiology: A Cellular And Molecular Approach. Elsevier/Saunders. ISBN 1-4160-2328-3. Page 872

endocrinology - Steroid Hormone Signalling

Note: Since my area of expertise is with peptide hormones, I will offer a partial answer.

Steroid hormones are carried through the circulation by binding to globular proteins. When these hormones are released from binding proteins, the classical route of action is by free diffusion through the cell membrane. This diffusion is due to their aromatic structure. You rightly point out that the classical receptors of these hormones are found in the cytoplasm or nucleus. For example, estrogen signalling as a classic signalling template which has genomic (DNA) and non-genomic (protein) targets to exert its effects.

Non-canonical signalling can occur through at least one G-protein coupled receptor (GPCR). Unlike most GPCR's which are localized to the cell membrane, GPR30 appears to be localized to the endoplasmic reticulum, which means steroid signalling still occurs through canonical means and also this newer pathway.

Then again, there are also steroid effects that modulate ion channels, for example GABA receptors. These are not specific receptors where only a steroid hormone can have an effect, yet they can activate or inhibit the effects (along with other drugs).

microbiology - Where would Saccharomyces cerevisiae be found in highest concentrations in environment?

Here is a link to an interesting article which reports a survey of wild isolates of Saccharomyces cerevisiae in China.

Wang, Qi-Ming, et al. (2012) Surprisingly diverged populations of Saccharomyces cerevisiae in natural environments remote from human activity. Mol Ecol 21: 5404-5417

A relevant quotation from the article:

In addition to grapes and oak tree (Quercus spp.) bark, S. cerevisiae was successfully iso-lated from a variety of damaged fruit collected in orchards or markets in different provinces of China; from the bark of different deciduous trees; forest soil and rotten wood collected in primeval, original secondary and planted forests located in different regions covering temperate, subtropical and tropical climate zones from northern to southern China. Unexpectedly, the success rate of S. cerevisiae isolation from fruit samples (6.5%) was lower than that from tree bark (16.5%), soil (10.8%) and rotten wood (9.2%) samples. S. cerevisiae was more frequently isolated from forest soil samples (success rate 13.7%) than from orchard soil samples (success rate 9.1%). Among the fruits giving positive S. cerevisiae isolation, grape samples showed the lowest success rate.

Table S2 in the supplemental information records isolates as follows:

climatic zone    sites   isolates
__________________________________
tropical           5       20
subtropical        2       14
temperate          13      51

Superficially, from this it looks as if there would probably be little difference between New York state (humid, continental) and Florida (humid, subtropical).

gene regulation - How does the enzyme Dicer function in the RISC complex?

Dicer is an endo-ribonuclease belonging to the RNAse-III class. Dicer is not a part of the RISC. It however helps in the formation of RISC by cleaving dsRNA or the stem of hairpin RNA on two ends which liberates a small dsRNA product. Then one of the strands is loaded into the RISC.

There are several reviews on this topic and there is a video as well which you can find on youtube.

human biology - When was the purpose of bone marrow discovered?

I'm currently reading William Cheselden's book Osteographia or The Anatomy of the Bones, which was published in 1733 (for the pretty pictures, naturally; not up to date anatomy). When he addresses the topic of bone marrow, he says,

Every cylindrical bone has a large middle cavity, which contains an oily marrow, and a great number of lesser cells towards their extremities, which contain a bloody marrow. [...] The bloody marrow is also found in all spongy cells of the bones. [...] The use of the first kind of marrow I imagine is to soften, and render less brittle, the harder fibres of bones near which it is seated; and that the other marrow is of the same use to the less compact fibres, which the more oily marrow might have made to soft; and that for this reason, there is less of the oily marrow, and more of the bloody in young bones than in old ones.

Which strikes me as completely incorrect -- though correct me if I'm wrong. So, when was the purpose of marrow in hematopoiesis discovered, and by whom?

ecoli - Can Escherichia coli survive on glucose and water alone?

Yes, but no. In other words, this quote is not probably not true in the ways you'd think. Bacteria can survive on practically nothing for long periods of time, but whether you call that life is subjective.

Nitrogen is necessary for all the co-enzymes and proteins to sustain life. In order to get energy, if E coli. needs to metabolize nitrogen to waste at all, all the bacteria would eventually all die out. The same feat for human beings would be to add a little sugar into sewage and surviving on it. Nobody would die right away, but its hard to call that living maybe.

Unless a medium is exchanged, E coli in a laboratory culture will start a massive die off. When the E coli culture becomes terminal in this way, a portion of the bacteria go into stationary phases where the bacteria can survive for very long times - for months or possibly years. So some of the bacteria would survive, but they would be dormant. You might not call this survival, but tens of thousands of bacteria are still alive and can generate colonies if transferred to fresh media.

Laboratory cultures and media are of course artificial conditions which don't reflect the environment which bacteria are adapted. In their life cycle, they typically have other sorts of behavior and experience low nutrient conditions often enough. Bacteria are also different in that a 99.99% die off can be considered a typical event in some cases.

ethology - Tool use by animals: research history

I was under impression that data about quite a lot different species using different tools is a fairly modern phenomenon, i.e., all of the research is fairly recent.

Around 50 years ago it was widely believed, by scientists too, that it was only apes that are able to use tools. I was recently told that it's basically nonsense and scientists have been studying different tool-using animals since the beginning of the 20th century or earlier.

Where could I get more info on research done in this area? I'd be especially thankful for those done in USSR, since it used to be my country and my knowledge on everything was basically limited by the Iron Curtain. However, I am also interested in research done worldwide as well.

genetics - Which X-Y chromosomes have the developmental genes for mammals?

First, while half the chromosomes come from each of the two parents, these two sets of chromosomes are not termed X and Y (they would usually be called maternal and paternal). The terms X and Y refer to potential members of just one pair of the 23 pairs (in humans) of chromosomes, and X chromosomes can come from either the mother or the father. The presence or absence of a Y chromosome determines sex in mammals.

The Y chromosome contains one gene, SRY, which determines sex, and almost no nother genes. SRY simply switches on the "make a male" program in the cells.

Essentially all other genes, including any toolbox genes, come from both parents, one copy from each. (An exception, in males, are those genes on the X chromosome, which in males are present in only one copy and which came from the mother. Another exception is mitochondrial genes.)

entomology - Is it possible for parasitic wasp to alter the behaviour of it's host after emerging from it?

In the study by Whitfield 1990 (1) I found the information that the parasitic wasp from family Ichneumonidae have interesting symbiotic viruses called polydnaviruses. This virus stay as provirus in the wasps genome and is transmitted vertically between subsequent generations of parasitoid. It does not harm the wasp and it is transmitted to the wasps hosts (usually caterpillar). The virus does not replicate in the caterpillar, but alter it's physiology: supress immune response and metamorphosis and increases the amount of nutrients in caterpillars hemolymph.

Still, I have not found any references about this kind of virus altering the behaviour of the caterpillar after the emergence of wasps larvae.

[1] Whitfield, J. B. (1990). Parasitoids, Polydnaviruses and Endosymbiosis. Parasitology Today, 6(12), 381-384. (free PDF)

cardiology - What would life expectancy be in the western world in the absence of Ischemic heart disease?

This paper from 1991 is intervention-based, so it reports the effects of behavior modification on lifespan in people who turned 35 in 1990. The authors report the gains for each individual behavior and then say:

Eliminating coronary heart disease mortality is estimated to extend the average life expectancy of a 35-year-old man by 3.1 years and a 35-year-old woman by 3.3 years

Which they feel is a modest increase but I rather disagree. This report estimates the that reduction in death due to heart disease of over 50% between 1950 and 1995 gained around 3.5 years, although most of that is probably due to better medical treatments. This 2004 study used 1998 data from the UK and estimated that:

The average gain in life expectancy from the elimination of cardiovascular disease risk as a cause of death was 4.0 years for all the 35 year-old men in the sample (n = 24), and 1.8 years for all the 35 year-old women in the sample (n = 32).

Although I would note the low sample size. I didn't expect to find much, so I was surprised to find these... and with similar results! One big issue is that a lot of the more recent research has focused on smoking, weight/BMI, and blood pressure reduction, rather than all IHD/CHD/CAD; I found tons of those. As a side note, simply reducing TV watching to less than two hours a day can lead to a gain of almost 1.5 years.

What is Luc Montagnier's research on electromagnetic signals from DNA about?

I think that ymar poses an excellent set of questions that should be discussed on these forums. It brings back memories (sic) of the memory of water controversy.

I'll quote from Andy Coghlan's excellent article published in New Scientist in 2011

Draw your own conclusions. (The emphases are mine).

... So what have
Montagnier and his team actually found? Full details of the
experiments are not yet available, but the basic set-up is as follows.

Two adjacent but physically separate test tubes were placed within a
copper coil and subjected to a very weak extremely low frequency
electromagnetic field of 7 hertz. The apparatus was isolated from
Earth's natural magnetic field to stop it interfering with the
experiment. One tube contained a fragment of DNA around 100 bases
long; the second tube contained pure water.

After 16 to 18 hours, both
samples were independently subjected to the polymerase chain reaction
(PCR), a method routinely used to amplify traces of DNA by using
enzymes to make many copies of the original material.

The gene
fragment was apparently recovered from both tubes, even though one
should have contained just water (see diagram).

DNA was only recovered
if the original solution of DNA - whose concentration has not been
revealed - had been subjected to several dilution cycles before being
placed in the magnetic field. In each cycle it was diluted 10-fold,
and "ghost" DNA was only recovered after between seven and 12
dilutions of the original. It was not found at the ultra-high
dilutions used in homeopathy.

Physicists in Montagnier's team suggest
that DNA emits low-frequency electromagnetic waves which imprint the
structure of the molecule onto the water.

This structure, they claim,
is preserved and amplified through quantum coherence effects, and
because it mimics the shape of the original DNA, the enzymes in the
PCR process mistake it for DNA itself, and somehow use it as a
template to make DNA matching that which "sent" the signal

I always knew there was something suspect about genetics! Stick to biochemistry, that's what I say :-)