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Can we use differential equations for population that is discrete?
Population dynamics is often modeled using ODE. For example one common model is logistic growth model:
$$\frac{dx}{dt} = k.x.\left(1-\frac{x}{C}\right)$$
where x is population size, k is rate constant for growth, C is carrying capacity.
But population is a discrete variable. It is not continuous. It always takes whole numbers. You can have a population of 3000 fish, but not 3001.2 fish.
Then how can one use population as a dependent variable in a differential equation?
Integration of the ODE, given above, will give me a function to calculate size of population, x(t), at time t, when size of the population at t = 0, was x0. We can specify a whole number for x0. Here, x(t) can be a real number with fraction, but a population size is always a whole number.
How does one tackle this anomaly?

You can make the continuous approximation when the population size is large. As mentioned by arboviral, there are algorithms that allow you to perform stochastic simulations with discrete variables. However, these are computationally much more intensive than integration of ODEs. Moreover, analytical solutions for the master-equations (time evolution of probabilities) are very difficult to calculate. Therefore, whenever possible, people go for ODE-based continuous models.
These models would give incorrect representation of the dynamics for small populations and fail to explain phenomena such as extinction. However, they can explain the dynamics of large populations fairly well. So the choice of the modelling approach depends on the questions you want to ask and the complexity/computational cost of the model.

+1 To cite a famous example of continuous approximations, there are the diffusion equation approach to markov models such as those used by Kimura.

@Remi.b yes. And diffusion equations are also used for migration models.

Isn't this the basis of calculcus, that you can approximate things by computing the limits of smaller and smaller divisions?  And aren't many differential equations applied to things like fluid flows that are fundamentally discrete (being made of atoms), but can be approximated very closely by assuming they're continuous?

I'd hardly call myself an expert on this topic by any stretch of the imagination, but you can actually come up with good approximations based on ODE-based models by rounding off to the nearest whole number (assuming that your populations are sufficiently large). The key word is "approximation" - it's not actually all that big of a deal to have to round your number when you realize that 3001.2 is just an approximation to begin with. You're not predicting that there will be exactly 3001.2 fish, you're predicting that there'll be approximately that many. In fact, predicting that there will be 3001.2 fish when there were actually 3000 a superb approximation: that's an error of only approximately 0.0003% once when you round down to 3001.
The important thing to keep in mind about mathematical models is that answers tend to be less "cut-and-dry" than you may be used to from other fields of mathematics. Most people think mathematics is all about having one correct way to come to "the" correct answer, but that mentality doesn't really apply to mathematical models. Try to think of models more in terms of "better vs. worse" as opposed to "right vs. wrong."
The other factor, of course, is that it can be difficult (or impossible) to know the exact value of all of the variables. For example, I was recently working on a mathematical model of urban pigeon populations. As shown in this question, it's not all that easy to get accurate population data on pigeons, and it's certainly extremely difficult to know what the exact carrying capacity is for a given area. (Quick - what's London's total carrying capacity for pigeons?)
This doesn't apply to this particular differential equation, but there are plenty of cases (both in differential equations in particular and in mathematical modeling in general) where it's either impractical or impossible to come up with an exact numerical solution. (You can often use various approximation techniques like Euler's Method, for example, to come up with good approximations; you can also use graphical techniques like direction fields to get a sense of general trends). This kind of a situation actually comes up a lot in practical cases that we'd like to be able to come up with a good model.
TL;DR Your model's an approximation to begin with, so I wouldn't worry too much about having to round.

Yes, you can. For example, the Gillespie algorithm (Gillespie-Doob algorithm) generates a statistically correct trajectory of a discrete population from a system of differential equations. This is computationally more intensive than treating a discrete population size as continuous, so is only normally used for relatively small populations.


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Practical utility of genes responsible for the biosynthesis of a useful compound in a plant
Assuming a woody plant naturally has a valuable compound, say a kind of sterol. During an RNA-seq analysis, almost all genes involved in the biosynthesis pathway of this sterol were identified in the plant. I was wondering what are the benefits of this finding? If this study was done in a bacterium or fungus instead of a plant, the importance of this finding is clearer, at least for me, since these simple organisms can be the factory of valuable compounds by genetic engineering technology. But, what about a woody plant which cannot be engineered and grown in bulk?

In most-cases these secondary-metabolites have some-or-some ecological importance. Such as a bitter taste, a pungent smell etc. to repel certain species of herbivore animals (including insects)

Somtimes steroidal-compounds and phytoestrogens (they are not steroidal but similar activity), disrupt insect's (caterpillar's) molding cycle and kill them.

Indeed the compound synthesis come from in-born error-of metabolism, they get selective advantages while evolution.

They are no-more called "waste-products". Now they are called as the group of compound used for defense and communication.

If you are telling about commercial or human-purpose, then yes there are importances. Sometimes after sacrificing many big trees a little amount of compounds found. So sometimes the compound/ medicine is made using tissue culture... quite like bacteria culture. The genetic/ molecular pathways targeted. Sometimes to synthesize a complex bio-compound in a chemistry-lab, biological pathways are studied.

Taxol is a big example. It is found in the gymnosperm Taxus brevifolia

"which cannot be engineered and grown in bulk"... "cannot" does not mean "could not". This is beauty of science. You can't find a way doesn't mean there is no way. When there was no computer, it was a sci-fi. say the "password" of sesame in arabian nights. But now it is truth. Now we anyone don't know proper cure of cancer but that doesn't prove we could not be able to discover the path

Thank you very much for all your comment, Always Confused!

You essentially gave the answer in your question. By identifying the biosynthetic pathway(s) required to create the compound in the plant, its natural host, those genes can then be cloned and transferred into an expression system like bacteria, yeast, or other plant cells like Arabidopsis thaliana to generate larger quantities of the compound of interest than would be possible from harvesting and processing the original plant itself.

Thank you, that's right. However, I'm looking for other benefits of such finding. In fact, this plant has the highest amount of this kind of sterol amongst nut. How can this information be useful, especially in practical science? Please share me any suggestions if you have.

@Mary your original question did not include this information. Please edit your post and add these additional details. I answered the question as it was posed. For what purpose are you seeking this information? If it is for a class or other educational purposes, please read our homework policy. Briefly, you are required to show your previous research and thinking on the matter, not just pose a question and expect it to be answered in full.

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Meaning of "Antibody is 50% w/w pure of interfering proteins"
From Google Patents, "Preparing antibodies from cho cell cultures for conjugation":

An isolated antibody or ADC is typically at least 50% w/w pure of interfering proteins and other contaminants arising from its production or purification but does not exclude the possibility that the monoclonal antibody is combined with an excess of pharmaceutical acceptable carrier(s) or other vehicle intended to facilitate its use. Sometimes monoclonal antibodies or ADCs are at least 60%, 70%, 80%, 90%, 95 or 99% w/w pure of interfering proteins and contaminants from production or purification.

Does it mean that even after purification the antibody solution may have an amount of impurities totaling to up to 50% of the antibody itself, in terms of weight? That the total weight of impurities may reach 50% of the antibody weight?
Maybe "an isolated antibody" is an antibody just after it has been produced? But the mention of "purification" confuses me. Why then such a high impurity content?

Patents are not the best source for reliable information, and obviously are not that readable. In this case they mean that of the purified product (usually that what comes of a protein A column I think), at least 50% of the weight is antibody. Or less (silly patents).
Commercial purification of antibodies (and proteins in general) is usually not that thorough. Most of the times what you'll get is just culture supernatant with cells removed, maybe some ammonium sulfate precipitation fraction or if it's thermostable just the proteins that are left after the production-solution is heated.

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Role of calcium chloride during competent cell preparation
I am aware of the fact that $CaCl_2$ settles down on the cell wall making it less negative may be by forming bond with Teichoic acid. Also due to the positive charge it attracts DNA (DNA is negatively charged due to phosphate group). But is there anything else the $CaCl_2$ does? Also if its the work of $CaCl_2$ why we are adding $MgCl_2$ first in the standard protocol of the making competent cell preparation chemically?

Even after so many years, nobody really knows what CaCl₂ does.

@WYSIWYG That's really true. Exact mechanism is not really known. Everybody hypothesis that this may be the reason. But what exactly happen maybe few people knows.

Please run a spelling check before posting a question. Whatever your first language, you can set it to English. We expect posters to be "comeptent" enough to do that.

Although we do not have any conclusive proof about how $CaCl_2$ works, the suggested mechanism is much similar to what you have suggested. When $CaCl_2$ dissociates in aqeous solution, $Ca^{2+}$ ions bind to the phosphate groups in DNA as well as the inner core of lipopolysaccharides in cell membrane (Dagert et al, 1979), neutralizing them. After this, heat shock allows uptake of this DNA into the host (how heat shock works is also not known; it is suggested that increased temperature creates pores in cell membrane, see this answer). For visual representation, see this diagram (from here):

Regarding $MgCl_2$, the role of $Mg^{2+}$ is not completely understood either. However, $Mg^{2+}$ is known to promote cell growth (Hanahan et al, 1983). It might be because $Mg^{2+}$ is an important factor required for functioning of ribosomes (Nierhaus et al, 2014). Anyhow, its role in increasing competence seems to be lesser than that of $Ca^{2+}$.
P.S.: during the experiment, $Mn^{2+}$, $Rb^+$ and $K^+$ also work effectively along with $Ca^{2+}$ (Hanahan et al, 1983).
References:

Dagert, M.; Ehrlich, S. (1979). "Prolonged incubation in calcium chloride improves the competence of Escherichia coli cells". Gene. 6 (1): 23–28. doi:10.1016/0378-1119(79)90082-9. PMID 383576
Douglas Hanahan, Studies on transformation of Escherichia coli with plasmids, Journal of Molecular Biology, Volume 166, Issue 4, 1983, Pages 557-580, ISSN 0022-2836, http://dx.doi.org/10.1016/S0022-2836(83)80284-8.
Nierhaus K.H. $Mg^{2+}$, $K^+$, and the ribosome J. Bacteriol.  2014 196 3817-3819


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Please help to identify this insect
It is approx 1.5 inch (3 cm to 4.5 cm) long

The insect's back and wings.

Insect from its forward side
Just few hours ago (around night 10 to 10.30 pm local time), this insect entered into our home, flying in high-speed and hitting to wall, objects, and to us. To keep it calm we turned the room-light off. Then it became steady on my father's shirt even after the light again turned on, and it was a beautiful moth-like insect. After taking photo it gently freed out of the room.
Here in India, it is rainy season (after summer).

P.S. I've very very little-experience in practical-zoology, however after few hours google search it seems to match with those moths tagged as "hawk-moths", and another notable feature when it was flying it looked like a hummingbird or a small bird, that was written in the description of some "hawk-moths" in different sites. Initially we're taking time to decide whether it is an insect or a bird.

What part of India are you in?

@MattDMo West Bengal. Kolkata.

It looks like http://static.inaturalist.org/photos/330773/medium.jpg?1444601918 http://rainforest-australia.com/Hawk%20Moth%20w.jpg,  ; http://www.whatsthatbug.com/wp-content/uploads/2010/11/vine_hawkmoth_hawaii_gini.jpg, http://farm3.staticflickr.com/2655/4241673563_da597de6fa.jpg, and https://farm9.staticflickr.com/8349/8223004042_a23ffc8029.jpg. etc.

If I able to identify it by someone, I'll upload it here. Thanks.

Related one, from same country : http://biology.stackexchange.com/questions/50432/a-new-species-of-small-bird

As MattDMo suggested, this is a hawk moth.  Given your location and season, this is why I thought it was either the Impatiens hawkmoth (Theretra oldenlandiae) or the  White-edged hunter hawkmoth (Theretra lycetus).  And finally, why I now think it is the Brown-Banded Hunter (Theretra silhetensis).
Brown-Banded Hunter Hawkmoth
The Theretra silhetensis exhibits a solid white line along the upperside of its abdomen, and more of a faded banding pattern on the forethat corresponds with your picture.  These moths are also common in India.

It is differs from T. oldenlandiae in being very much paler in color
and with white line down center of abdomen.

When it comes down to it, that solid single white line is the biggest indicator it is a T. silhetensis over a T. oldenlandiae or T. lycetus.

While my final answer is the brown-banded hunter hawkmoth, below are the original two species I suspected it was and why.  I've included them below simply for reference / alternative comparisons.
Impatiens Hawkmoth
Theretra oldenlandiae was my original instinct, since it is a more common in your area and the banding/stripe pattern matches to a T.

But, upon closer inspection, there are two things that don't quite align:

Your Specimen exhibits pink suffusion, especially on the back edge of the fore wing.
Your specimen has a single dorsal line, not two.

For these two reasons I think it is not the Impatiens Hawkmoth and thought it was more likely the...
White-edged hunter hawkmoth
Theretra lycetus is not as common on the T. oldenlandiae for your location, but the pink suffusion supports this idea.  See below for a picture:

This still doesn't explain the double vs. single white stripe along the upper abdomen.  Which is why I know believe it is the...

As an aside, this could be an example of polymorphism vs. identifying characters. Welcome to the world of taxonomic lumpers and splitters...

I agree with your eventual answer, but do you think you could put your final answer a bit nearer the top? :)

Fair enough...Now edited to save reading time.

Thanks. Also I don't  know, how-frequent posting of identification question is considered as OK, (i.e. is there any limit on it) in this SE community, however I posted this-one because this-insect was very surprising to us... it looked like a tiny bird when it was flying.

First-one (Theretra silhetensis) shows excellent matching

No problem at all.  I think as long as you do not spam posts you should be in the clear (although I'm not the final say in the matter).  As for confusing a moth for a bird, you aren't the first one! This moth in the same Sphingidae family was posted just last week!  And thank you to your post!  Very clear picture of the moth with a good explanation

This is almost certainly a Hawkmoth in the family Sphingidae, possibly (I am in no way, shape, or form an entomologist) an example of Therectra alecto, known as the Levant Hawkmoth:

This page gave me the clue, and the link to the page above. Like I said, I'm not an entomologist :)

probably this one you're telling about http://www.whatsthatbug.com/wp-content/uploads/2015/10/hawkmoth_india_arjun-300x290.jpg. However our-one contains very bold  long mark on back. However like our-one, yours also contain the black dot on 2 wings.

Almost positive it's the Impatiens hawkmoth, (Theretra oldenlandiae), which is common in India.  Site for reference

@DGruenewald I think you're right. Go ahead and write up an answer.


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Pathophysiology of babinski sign in spinal cord injury?
How can we differentiate between upper motor and lower motor neuron lesions on the basis of babinski's sign ?

Could you add some more background to the question? I.e., what is babinski's sign?

shouldnt people (to whom the question is intended to be answered by) know it ?

The SE network, including Bio, is not just for your answer only, it is built for the community at large. Supplying background information aids that purpose.

Short answer : If the Babinski sign is positive in adults, it indicates an upper motor neuron lesion.
Long answer :
The plantar reflex is an interesting reflex since it has two physiological responses. One in kids 1-2 years of age and another in the rest. It is one of the primitive reflexes that are present in infants but are cortically inhibited later in life.
The primitive response to the plantar reflex is extension of the hallux and fanning out of the toes. Once the kid is around 1-2 yrs of age, the corticospinal tracts are fully myelinated and this primitive reflex is inhibited leading to the flexion of the hallux.
Extension of the hallux is regarded as a positive Babinski sign while flexion is sometimes called negative babinski.
So in an adult, due to cortical inhibition of the primitive reflex, the plantar reflex should yield flexion of the hallux. But if it pathologically shows a babinski positive, it indicates the absence of cortical inhibition - an upper motor neuron lesion. This might be a serious neurological issue and you'd want to do a CT brain, CSF study or an MRI spine to localise the lesion.
On the other hand a negative babinski in kids who should be showing the primitive reflex, may be showing signs of spasticity. This should direct us towards progressive neurological disorders like cerebral palsy.


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Making sense out of the visual representation of transcription
Most people are familiar with the following diagram. Some genomic DNA with a promoter region, exons and introns. This is transcribed into RNA that is then translated into a polypeptide.

When we look closer at the strand that is being transcribed we can distinguish between the two as the sense and anti-sense strands.

So the transcription factors and RNA polymerase bind and begins transcribing mRNA in the 5' to 3' direction and thus reading the anti-sense strand in the 3' to 5' direction and have the same sequence as the sense DNA strand, substituting U for T in the mRNA.

My question would be, shouldn't the exons be numbered in the reverse order as shown in the first picture I provided. So instead of Promoter -> Exon1 -> Intron -> Exon 2, should it be, Promoter -> Exon N -> Intron -> Exon N-1?
Also, in bioinformatic sites are the gene sequences listed in the sense or anti-sense strand? I have noticed in some bioinformatic tools, to determine what polypeptide will result from a DNA sequence, one must input the sense strand in 5'to 3' orientation and not the anti-sense strand.

All visual representations and nearly all coordinate systems are based on the sense strand. The polymerase machinery has no clue about what is sense and what is antisense, because each is the antisense of the other.
For visual representation this makes much more sense and relays more information as it removes the extra complicated layer of information. And, in most cases the gene structures are declared in the order of the reference genome which is always the positive or sense strand.
Next coming to the bioinformatics part, most of your databases such as UCSC, Ensemble and NCBI maintain gene coordinates on the reference genome, But, there's a catch, when reporting the information through a bed file,
Negative stranded genes are reported as chromosome stop start by NCBI (last I used it was a one a half years ago), UCSC will provide the chromosome start stop and both will report the strandedness, UCSC expects that you the bioinformatician will create the reverse complement when you find the strand information, while NCBI expects that your program will fail a sanity check because stop - start will come as negative, implying that you cannot make a mistake while parsing NCBI bed files. Furthermore, UCSC indexes are maintained as 0 based, while NCBI is maintained as 1 based.
I would urge you to validate this information
But why not just keep a negative strand as well? while keeping the gene coordinates and elements for the antisense in the format you just mentioned.
Because speaking from a Computational point of view it just makes more sense, this system would consume more storage (please remember the entire system was formulated before storage became as cheap as it is today) it would consume more memory during tasks (exactly double of what it is consuming today). So it's just better to have a positive strand reference genome and all genes and elements based on that.
Just an example of how alignment of sequencing reads works,

You align your read to the reference genome
Aligns? If yes it has mapped to the positive strand
No? Reverse complement the read and align back
Aligns? If yes it has mapped to the negative strand
No? Possibly an erroneous read or other artefacts.

GTF/GFF3 has the start stop order along with strand orientation. I think this has become more or less a standard format for annotations for all repositories.

Gene sequences are annotated in the sense strand. So, these diagrams are correct.

In the top diagram, the ATG start is on the left, and the stop codon is on the right.  Exon one is the left most exon.  That's all correctly illustrated.
If you look up a transcript sequence in, say, ensembl, it will be the same way, the start sequence will be in the beginning, the stop codon at the end.  That's the convention.


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Glycolysis - ATP production
In glycolysis, 2 ATP molecules are produced from each triose phosphate molecule (to give a total of 4 ATP produced; 2 net produced as 2 were initially used up in the reaction).
I don't understand how this would be the case, as each triose phosphate only has one phosphate group available to form ATP from ADP, meaning that one ATP is produced per triose phosphate. I know this cannot be the case as this would mean a 0 net production of ATP defeating the purpose of glycolysis, but i can't get my head around why.
out of curiosity, would the other remaining two phosphates that are required come from other sources, i.e. 2 phosphates + the 2 phosphates already from the two trios phosphate molecules to give us the 4 ATP molecules (2 net ATP)
Many thanks in advance.

Possible duplicate of Where do the four ADPs come from in the second stage of glycolysis?

@VanceLAlbaugh — I agree that the two questions are related and would be better as one, but the other question wants to know where the ADPs that accept the phosphate come from, whereas this asks about where the phosphates that are not from ATP come from. That is not covered in the other question or its accepted answer.

The other two phosphates come from inorganic phosphate* in solution (Pi — in my diagram below) at the glyceraldehyde phosphate dehydrogenase stage. (Two, of course, because there are two molecules of triose.)

This is covered in Berg et al. Section 16.1.5.
*The term inorganic phosphate is used because there are various different anions in solution derived from phosphoric acid, depending on the pH. At physiological pH the predominant species is the double-negativly charged, monohydrogen phosphate.

Though David has already answered as I wished to write one for this question here's my answer$-$
You say that

In glycolysis, 2 ATP molecules are produced from each triose phosphate molecule ... I don't understand how this would be the case, as each triose phosphate only has one phosphate group

but you are wrong here as each triose phosphate is destined to undergo phosphorylation before they are dephosphorylated to yield 2 ATPs each.
Here are the reactions:
You can see that out of the two trioses Glyceraldehyde-3-phosphate is phosphorylated into a compound (1,3-bisphosphoglycerate) that has two phosphoryl groups. Similarly Dihydroxy acetone phosphate the other triose is first converted into glyceraldehyde-3-phosphate by an isomerisation reaction catalysed by triosephosphate isomerase. This glyceraldehyde-3-PO$_4$ formed undergoes phosphorylation to form a two phosphoryl group containing compound.

would the other remaining two phosphates that are required come from other sources..?

Yes the Phosphate group added to Glyceraldehyde-3-PO$_4$ is derived from orthophosphate (HPO43−).

Probably just loose writing. I imagine what the OP meant was something like "In the second stage of glycolysis, after one hexose is converted to two triose molecules in the aldolase reaction, each of these produce 2 ATPs". And his concern seemed to be that the aldolase reaction produced  triose monophosphates (from the previous di-phosphorylated hexose) so where did the other phosphate come from? He was looking for more ATP input and failed to notice the orthophosphate.

@David Probably.

@David I have seen people using the term OP quite often here. What does it stand for? Is it Owner of Post?

— I believe it stands for Original Poster, but don't quote me on that. Certainly it refers to the person who posted the question. I really shouldn't use it because Poster takes no time to write, and acronyms like this present a barrier to new users. They imply that there is an in-group who know these things. That is why I have always kicked students hard who write dissertations full of lab abbreviations. After that I guess I'll have to refer to the poster in future.

@A.P Does this answer clear your doubts? Let me know if I could help.


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How to protect my mounted insect specimens from ... insects?
I have a modest collection of insect specimens that I caught, prepared, mounted, and dried myself. I'm entirely an amateur collector, so my procedure may be causing me this trouble now, but here's how I preserved them.

Killed in the freezer
Placed in a sealed container on a dry platform, with a 50% isopropyl alcohol solution under it. This lets the specimen thaw and remain moist, while the alcohol prevents rotting.
Kept in container for two to three days.
Stretched over foam and held in place with paper and pins.
Kept on stretching board for three weeks.
Placed in a consumer grade display box.
Stored in a dark, dry closet.

It's been a while since I worked on this hobby, but I do like to pull the collection out from time to time and admire it. Today, I was surprised and disappointed to find that some of my best specimens have been turned to dust by a small caterpillar type bug. There are live bugs in my display case, eating my bugs!
I've had these for years without issue, and now I find this. What can I do about it? How can I keep this from happening again? Should my preservation procedure include some other step? How are they even surviving? There's no moisture in there at all!
I'd rather not put something toxic in my display case, as I like to take them out and examine them without the glass in the way. I don't want to be exposed to toxic things every time I look at them. I hope there's some effective, cheap, and safe thing I can do. I've become rather proud of my collection, but it's disheartening to have worms eating them before they've even eaten me.
Here's some pictures of the devastation:

That stain on the right used to be a specimen.

The big pile of dust there on the left used to be a praying mantis. I don't even know what the pile on the right use to be.

This beetle's entire insides have been eaten.

This horsefly looks like it was mounted a hundred years ago.

Apparently moths and butterflies don't taste very good.

The culprit! This little guy and his pals are responsible. You can see exoskeleton sheddings all throughout the other pictures.

I was hoping for a specimen or preservation or specimen-preservation tag. Perhaps it's worth creating.

Sad to see! I don't have any help with your question, but I can say that your culprit is a dermestid beetle, maybe museum beetle or one of it's relatives. This page http://bughunter.tamu.edu/preservation/preservationconsider/ suggests putting your box in the freezer to kill any remaining living pests...

The same thing happened to me. I actually get the little guys out of the beetles by putting them in the extreme heat. I put my collection outside in the summer heat and the beetles start to crawl out of my specimens. Then I kill them and refreeze my insects that I saw them crawl out of. It only takes about 10 minutes till they start to exit. Your butterflies will be chewed up too. I use a clear piece of plastic over my collection to act like a green house. Now I periodically put it outside on sunny days just to check

Related: What kind of insect can this be?..., Can anyone help confirm this tiny insect larvae?,
Bug Identification: Is this small tubular, black bug a bed bug?, Varied Carpet Beetle Larvae, What is the name of the critter depicted..., What small insect is this?, What bug is this...

I put a few mothballs in my collection boxes changing them every month and I occasionally put them in the freezer for a day or two.

I ran into the same issue when collecting bees in a hot, humid environment.  As arboviralstated, freezing is a great way to help with the infection but keep in mind:

It may not kill all of your pests
It will not keep your specimen from future pests
It may damage your samples

From the USDA website, you could pretty cheaply use paradichlorobenzene or naphthalene:

Two of the most widely used fumigants are paradichlorobenzene (PDB)
  and naphthalene, both of which are obtainable in balls or flakes.
  Never mix PDB with naphthalene as they react chemically and produce a
  liquid that may damage the collection. It should be noted, that most
  major collections are now moving away from the use of solid fumigants
  because of health concerns and in some jurisdictions, it is now
  against regulations to use some fumigants.

That being said, I used a combination of freezing and then naphthalene (moth balls).  It's cheap and anecdotally pretty effective for my purposes.  I also didn't access my collection frequently once established, so the health concerns were less of a worry for me.
Definitely worth mentioning that there has been talk that using naphthalene  or PDB may damage DNA and hurt DNA extractions on down the road, but this is demonstrably false.  That being said, keep in mind these chemicals still pose some heath effects - especially with prolonged or occupational exposure - such as poisoning and carcinogenic risk.

As @picapica says, these look like beetles of the genus Anthrena: museum beetles, furniture carpet beetles or something similar. I'd lean towards furniture carpet beetle (Anthrena flavipes) myself, but this isn't a species ID question.
Your best bet would be to use an insecticide. However, pages 18-19 of Story (1998) "Approaches to pest management in museums" list 15 non-chemical ways to deal with these beetles. Based on this source, I suggest you:

physically remove as much of the infestation as you can, then
freeze the whole collection (again, as first suggested in the comment by @picapica).

Dermestid beetles like Anthrena are relatively heat-tolerant and the other control methods are more based around reducing the chance of an infestation in the first place. To be effective, freezing may need to be as low as -30°C (generally domestic freezers will only maintain temperatures from −23 to −18°C) and sustained for up to three days.
Once you've got rid of this infestation, some of the other suggestions to avoid reinfestation may be useful, such as sealing or screening possible routes of entry in the cases to stop beetles getting back in.
Nice collection, by the way!

Yup, definitely looks like carpet beetle (likely Anthrenus sp)  larvae

Adding to the allready fine answers, I would suggest to use some camphor. Camphor is relatively inexpensive. I could buy it at the local pharmacy, but depending on your location, it might or might not be available there.
I successfully used camphor to get rid of Dermestids. However, it is much more effective to prevent infestation than to get rid of one.
However, if you use it, you might not want to store your collection in a part of a building where people spend prolonged times. Also, you definitely want to put your collection in a near-airtight container. Camphor  evaporates quickly, and an airtight container is important to keep the atmosphere more or less saturated. Glass, of course, is best. Plastic might permeable, and even get brtittle, depending on the specific material. Sidenote: Professional and (very expensive cabinets) use hardwood boxes with a glass cover cemented in the lid, which have the additional advantage of making it difficult for dermestids to get in.
You should apply it using a watch glass, and not let it come into direct contact with both your collections and the material the specimens are pinned on.

Use borates, like for wood treatment. It's not a repellent like moth balls but it will kill them and not be smelly and it has low toxicity.
Borates are also used in taxidermy, especially for controlling dermestid beetles, however salty crusts can develop so, you might have to play around with the concentration- so that you don't use too much.
Also, peppermint and citronella are fine repellents. There are repellent satchets on the market, but you could probably save your money and just get a dram of peppermint oil or (pure) citronella oil (soak a piece of wood- like cedar).
Also, DEET is good repellent. But these repellents won't last as long as moth balls.

Another addition.
If you like to avoid chemicals, I recommend using vacuum bags that are meant to store clothes in, which you can easily buy. They are like big zipper bags that close airtight and keep away the pests. This is an alternative to very expensive airtight boxes.
To get rid of beetle larvae that are in your collection, you need to kill them. For me, it always sufficed to freeze at -18, but this might not always work. My home freezer is quite small, so I would re-pin the insects to a smaller box, clean up the 'main box' very thoroughly (also removing bottom plate!!!), and after 3 days of freezing put the insects back. Check your collection at least once a year.
I have old museum boxes with lids that do not close so well anymore. Since I use vacuum bags I (5 years now) had no beetle infestation so far.
"Apparently moths and butterflies don't taste very good."
Well, you were lucky. These beetles love moths and butterflies the most!

Great idea. I'm headed to Walmart right now ;)

I preserve all my bugs in resin. It is an absolute ton of work, and not always guaranteed to turn out, but I have successfully done over 150 bugs.

So you mean your specimens are left encapsulated in a clear plastic like material? Do you not find it difficult to inspect them afterward because of refraction?

refraction really isn’t a problem, but I usually only polish the front or top of my pieces, so if further inspection is needed underneath, I would have to sand and polish the back. I will never have to worry about mold, parasites, breakage, discoloration, or deterioration. I did my first piece 17 years ago, and it is still in perfect condition

I don’t see any way to post pics in these replies, but you are welcome to check out my work on Facebook. Enchanting creations by Sonja. Message me with any questions you have.

Nice work on your Facebook page. Even if there is some aesthetic degradation, a resin preservation is undoubtedly more durable and lasting. I'll surely experiment with this in the future.

I like your collection!  I am sorry about the beetle tragedy.
I recommend that in addition to killing the ones you have in the collection (freezing) that you put your collection in a beetle proof container to save what is left. That is not practical for a mounted water buffalo but I am sure you can find a Tupperware-type container that can house your collection and prevent beetle entry.
Also: check the rest of that closet.  Those beetles came from somewhere.  Carpet beetles ate tracks in one of my nice coats a few years back.  You might have a colony in the closet.  Remove the stuff, shake it out and spray the floor with roach spray.

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


text:
Does some form of self organizing map exist in the brain?
Self organizing maps (SOM's) are an extremely interesting and powerful tool in the field of artificial neural networks. My question is: Does something similar exist in the brain? Or are these systems completely "man made"?
Also, if there are such things in the brain, how do they work?

These are great questions.  The SOM was absolutely biologically inspired.  Sure, there are many examples.
Examples of self-organizing topographical feature maps in the human brain include the the sensory homunculus, retinotopic maps, and the entorhinal cortex.  There are even maps such as these in the midbrain auditory nucleus of the barn owl as well as the auditory cortex of the mustache bat.
As to how they work and organize in nature, that is still an active area of research, and it seems like there are no experimental conclusions that suggest the existence of  universal rules for self-organization of sensory maps in the brain.  As far as I know, however, Kohonen's theory that these maps organize via a combination of lateral inhibition and Hebbian learning has not yet been displaced by a more modern idea.


text:
How does residual chlorine in tap water work?
As I understand it, residual chlorine levels in tap water are below 1mg/l in the UK. Most chlorine based cleaning products suggest at least 1% solution to be effective (quite a long way off 0.5mg/l by my maths).
Given that chlorine has a very slight disadvantage to health (albeit a tiny one), if 0.5mg/l is not enough to kill harmful bacteria, why is it there at all? If it is enough to kill bacteria, how does it do it when cleaning products require what seems to be several thousand times greater concentrations to do the same job?

Actually, I think that to qualify this statment, you should use about a 3.33% solution of household (5%) bleach for disinfecting. So that's actually, 0.15% sodium hypochlorite solution.
Also, time and pH are factors. A 0.15% bleach solution will kill many bacteria within 5 minutes. But after a few days, a more dilute solution will also have killed many bacteria.
Also, given that household bleach has a pH of around 11, a 1% solution will have a pH of about 9. The optimal pH is about 6, where all of the -OCl is converted to HOCl which is roughly 80x more effective as a germicide.
So, I realize that 0.5mg/L is still about 3000 times less than 1.5g/L (= 0.15%), and that's the real question. The real answer is that the place where the bleach is added (in a municipal supply) is at the filter, where bacteria collect. Once the old filter has been bleached the fresh water supply is allowed to resume which flushes the bleach along (at tolerable levels). Also, they often use other oxidizing agent which are synergistic with HOCl, so that they can reduce their cost and improve the function.

Great, thanks. Just a couple of things 1. Are you saying that residual chlorine is really just a by-product of the main cleaning process and it's not deliberately put in at all? 2. Is the time/dilution effect roughly equivalent. i.e would tap water have the same disinfection effect as a bleach solution after 3000x5=15,000 minutes (10-11 days)?

@Isaacson it's not so simple. With antibiotics there's a threshold or minimum inhibitory concentraton. But there are many different kinds of bacteria, each with their own MIC. But at the filter, they are not using 0.15% bleach. They can use much less and wait a few hours. I don't suppose that 0.5mg/L Would be germicidal, but that's really just an average. sometimes it's higher or lower. I avoid using tap water for growing bacteria, because it does make a little difference though.

I've marked the answer because I think it's the best I'm going to get, but still a little confused. You say "I don't suppose 0.5mg/l would be germicidal", this pretty much still leaves open the question of what's it there for then? If it does not kill germs, why don't the water companies just remove all the chlorine before piping the water out, is it that the "little difference" you mention is enough to justify it from a public health perspective?

Well, bleach isn't that bad for you. It's kind of like oxidized salt. Compared with the amount of salt we need and actually ingest, there's no way it is making any difference, health-wise. Every thing can kill you, if you have too much... too much water and you destroy your kidneys or simply drown. Too much air, too much light, too much heat, too much anything will kill. But we need all these things (in the right amount). Chlorine is an oxidizer. It breaks down into common salt.

@Isaacson it's at 0.5mg/L after the water has resumed. In the filter area I'm sure it's probably way higher, like around 0.001% bleach which reacts with germs and turns into salt. They will use just enough to kill the germs probably within 24 hours. Then they resume water flow through the filter and the residual chlorine gets diluted. Now I'm not very familiar with municipal supplies. They are all built and operated a little differently. I'm just saying this is one probable scenario.

From the Drinking Water Inspectorate's own leaflet on Chlorine "the trace of chlorine is there only to preserve the high quality of the water as it passes through the miles of pipes used to convey water to homes and workplaces". So the question remains, how does it achieve this at doses too low to be germicidal? What is this 'quality' that it is 'preserving'?

If someone could explain this to me we'd have the answer. From the WHO recommendations for drinking water safety it says under residual chlorine that to achieve a log2 reduction in bacteria you need "Ct99 = 0.04–0.08 min·mg/l; 5 °C; pH 6-7)" By my understanding at 0.5mg/l you would need less than 1 tenth of a minute contact (0.5 x 0.1 = 0.05). That can't be right, it would make tap water an effective disinfectant within minutes, can anyone explain why?

As WHO says in that report, Bacillus, Clostridium, Mycobacterium and Nocardia can be resistant to chlorine disinfection. Different bacteria have different MICs. Also, a reduction never reaches zero unless you have a digital world... luckily, cells are digital so you can achieve complete sterility. But suppose you have 10^6 bacteria per ml. Using WHO's numbers, with e. coli, 0.04mg/min L^-1 for the hypoclorous acid (pH 7) or 0.92mg/min L^-1 for the hypochlorite ion (pH 8.5). Which means 0.5 at low pH will probably kill 99% of E. coli in a minute. So after 3 minutes you should have 1 cfu left.

Please see page 46 the report from WHO.


text:
Availability of a database containing the proteins of Vibrio cholerae and their corresponding gene sequences
I wanted a list of all the proteins (amino acid sequences) and their corresponding gene sequences of Vibrio cholerae. I tried to search in patric, but the number of amino acid sequences and gene sequences do not match, as they have provided the whole genome. I need to know if there is a database where all the proteins of Vibrio cholerae and their corresponding gene sequences can be obtained in a single file or in a couple of files. Copy pasting 4000-5000 genome and protein sequences individually from the internet seems cumbersome to me.

You want to go to PATRIC > Data > Download Tool.
From the Taxonomy tree, find Vibrio cholerae, choose Type of annotation as either PATRIC/RefSeq or both, choose the type of file you want (gbk or faa) and download from there.

have tried that. the number of gene and protein sequences do not match

Did you get the genes from PATRIC or NCBI? If the number of genes do not match the genes would be more. Considering that you have non-coding sequences, rRNA and tRNA genes and also hypothetical and predicted sequences.

i got it from patric.


text:
SRAP marker sequences
I am looking into SRAP markers and I have realized I am not sure if I need a reverse complement of the sequence given in the article or they are "ready to use" primers?

Can you add sources or links to your markers and explain what you are planning to do so that users can provide you with more accurate answers?

Which article are you talking about?


text:
Do males ever produce the offspring?
Are there any non-asexual species in which the male of the species produces the offspring?
If so, why are they considered male and not female?

Yes the males of a group of bony fish Syngnathidae can bear offsprings or as you say produce offsprings. This group includes Seahorses and Pipefishes. In some species the male have either a brood pouch attached to the trunk or its tail while in others the egg is attached to the trunk or tail laid by the female.The fertilisation takes place in the pouch or in water before implantation.
Here are some pictures :
1.Male seahorse with brood pouch and a slender female without a brood pouch

2.Male seahorse giving birth to a baby seahorse

3.Male Syngnathus sp.(pipe fish) with the brood pouch

Inset image C shows eggs in pouch of pregnant male and Inset E shows Embryos in the pouch of pregnant male. (Images taken from researchgate.net and peaubleue.org)
Now coming to your question

why are they considered male and not female?

Though the males here bear the baby but the baby results from fertilisation of a sperm produced by the male (the same seahorse that is destined to bear the baby) and an ovum produced by the female (the other seahorse without a brood pouch).
The sperm / male gamete producing individual is a male and a ovum/female gamete producing individual is a female. The provision of being able to bear a child does not change the sex.
Note: Seahorse is an oviviviparous organism i.e they are organisms in which the fertilised eggs develop inside the parent's body until they are ready to hatch.
P.S. Brood pouch is a cavity outside the body of these fishes in which the eggs develop and hatch.
Source: Wikipedia

Good answer +1. Might be worth also going a tiny bit further in the definition of male vs female and define sperm vs ovum. Males produce small gametes while female produce large gametes. You might also want to say a word about species like yeast that have mating types and not gender as there are no difference in gamete size.

@Remi.b Thank you. I'm glad that you liked it. Its my third answer in this community. I was thinking about doing some research on the sex determination of seahorse/ fish in general and then adding it to the answer.

I stumbled upon two images of Syngnathus sp. and have merged it into one and added to my answer.

Thanks @SanjuktaGhosh; Great answer that perfectly combines knowledge and the pictures that transport the fascination that drives/drove (at least many of) us into biology. Looking forward to your additions. +1 anyways.

Parental care by the male parent is off course relatively common, especially in birds and mammals. Cases were the male actually does most of the 'breeding' are relatively rare. I think @Sanjuktaghosh gave a beautiful example, but there are a few more:

Mouthbreeders keep there offspring in the mouth for considerable amounts of time. In most mouthbreeders, the female takes the eggs, but Darwin's Frog is a notable example were the male does.
Biparental mouthbrooding occurs where both parents take some of the eggs. This is found in some fish species.
A different example is the Emperors penguin, where the female lays a single egg, which is incubated by the male while the female returns to the sea to feed. To keep it warm, he puts this egg on top off its feet, folding his belly over it. A picture of dad with the egg can be found here
A final example, with thanks to Sanjuktaghosh, is the Northern jacana

Like your Emperor penguin link to dailymail. Parenting by the male parent is also observed in a polyandrous bird Northern Jacana.


text:
do cancer cells respond to EM fields?
Do cancer cells respond to electromagnetic fields? If so, can someone please provide reliable information as to how they behave in such fields? Do you suppose the growth rate to be affected in any way ?

I guess you are talking about low energetic EM fields, right? Do you have any special treatment in mind?

Can you be more specific about what kind(s) of cancer you are interested in? Cancer is not one thing at the cellular level. Cancers come in all types.

@Chris, if cancer cells are basically due to uncontrolled growth, we can try to control them using different frequencies and intensities of EM fields. After all, neural signals are electromagnetic in nature. If those EM signals can control the body and its growth, maybe we can use some to inhibit growth as well.

@kmm, suppose i take a lump of gastric cancer cells and expose them to EM fields(variable or constant). Will any significant effect be observed?

Most likely not. There is an approved therapy for brain tumors called tumor therapy fields, but there is little (if any) proof, that this works. Additionally, neural signals are a little bit more complicated than just being a field.


text:
What nutrients are best suited for growing E.Coli
I am looking to grow E.Coli (In a nutrient agar dish) to be used in an E.Coli lawn and was wondering what specific nutrients should be used to ensure the E.Coli grows optimally? Any answers or links to relative resources are greatly appreciated!

Do you have any reasons to not use standard LB agar plates?

Welcome to Biology.SE! Please consider taking the tour. You might also want to add some more information to your question showing what research you've already done yourself.
Specifically regarding your question, it's not my area but I suspect this will help: http://www.exptec.com/Bacterial%20E.coli%20Growth%20Media.htm

If you don't have any specific reason to use something else, LB is your best bet. It's cheap and it works well.

Optimal is a funny thing; it depends upon what you want. The purpose of the bacteria, is probably the most important aspect when considering the nutrients. There are many recipes capable of growing E. coli. What does optimal or best mean to you and why? Is selectivity or differentiation a factor? How important is cost? Are you aiming for industrial level production or just testing. Do you have a bioreactor? Or are you looking for something low tech... maybe from food-mart?
For what it's worth, you might find minimal salts media and solid state fermentation interesting.
Different strains like different nutrients, of course. So, phenotypical tests are sometimes helpful when figuring what an undescribed strain likes (and doesn't like).
That being said... I can offer a little insight here.
"+" for growth/utilization;  "-" for weak or no growth/utilization:
                 E. coli    E. coli inactive**  E. coli 0157:H7

Pectin                 -            -                   -
Dextrin                ++           ++                  -
Sucrose                -            -                   +++
Glycerol               +++          +++                 +++
Stachyose              -            -                   -
D-Fructose             ++           ++                  ++
D-Maltose              +            ++                  ++
D-Raffinose            +            -                   +++
α-D-Glucose            +            +                   +
α-D-Lactose            +            -                   ++
D-Trehalose            ++           +++                 +++
D-Galactose            ++           +++                 +++
L-Fucose               +++          +++                 +++
L-Rhamnose             +++          -                   ++
D-Sorbitol             +++          +                   -
D-Mannitol             +            ++                  ++
Methyl Pyruvate        +++          +++                 +++
Tween 40               -            -                   -

Gelatin                -            -                   -
L-Alanine              +++          +++                 +++
L-Arginine             +            -                   -
L-Histidine            -            -                   -
D-Serine               +++          +++                 -
L-Serine               +++          +++                 +++
D-Aspartic Acid        -            -                   -
L-Aspartic Acid        +++          +++                 +++

D-Glucoronic Acid      +++          +++                 +++

Citric Acid            -            -                   -
L-Malic Acid           +++          +++                 +++
Acetic Acid            +++          +++                 +++
Acetoacetic Acid       +            +                   -
L-Lactic Acid          +            -                   -
Mucic Acid             ++           -                   +++
D-Malic Acid           +            +++                 +++
Propionic Acid         ++           ++                  +++
Formic Acid            +            -                   +

D-Salicin              -            -                   -
Lithium Cloride        +++          ++                  ++
Na Butyrate            +++          +++                 +++
pH 5                   +++          +++                 +++
8% NaCl                ++           +                   -
D-Serine (high)        ++           +                   -
Potassium Tellurate    +            +                   +++
Na Bromate            +/-           -                   ++

E. coli inactive** is lactose-negative, non-motile- often misidentified as Shigella

As suggested by Chris, classical LB medium should be fine. There is a reason why it has been used for the last 65 years. Some people supplement it with extra sucrose or sodium chloride, but I think these are mere customs rather than experimentally-proven improvement.
If you want to re-create LB from pure components, read about minimal media. They are a mixture of glucose, ammonium salts, microelements and vitamins. A rather long list that I won't post here can be found at http://structuralbiology.uchc.edu/protocols/pdfs/nmr_sample_preparation.pdf


text:
Role of dam methylase in bacteria
In bacteria, an enzyme called dam methylase (Deoxyadenosine methylase)  methylates adenines (A) in the sequence GATC in the new strand formed after replication.
What role does this methylation play?
I read that it has something to do with proofreading. If this is so, then how?

The dam methylase has three different functions:

Correction replication errors, since the new DNA molecule
is only hemimethylated (the old strand is methylated, the newly
synthesized is not). Since the proof-reading only takes place on the
new strand, errors introduced during replication can be corrected.
Regulation of replication: The ori of the chromosome is methylated to ensure that is only replicated once.
Regulation of transcription: Methylation of GATC sequences promote the transcription of genes.

For further details see the references.
References:

The great GATC: DNA methylation in E. coli
The dam and dcm strains of Escherichia coli--a review.
Dam methylation: coordinating cellular processes.


text:
Can telomere length maintenance be an answer to increased life span of human beings?
Telomere shortening may prevent the development of cancer in human aged cells by limiting the number of cell divisions. However, shortening of telomeres impairs immune function and thus might also increase susceptibility to cancer.Hence if length of telomere is kept constant, wouldn't it lead to development of cancerous cells rather than increase of life span?

Possible duplicate of Is each generation getting older?


text:
How much Cardiomyocyte Move in Relation to its Neurons?
I am trying to estimate how much cardiomyocyte and its things (mitochondria) move in relation to neurons

Movement of neurons (1)
Movement of cardiomyocytes
Movement of cardiomyocytes' mitochondrias (2)
...
Movement of stem cells - I think we can ignore this one

Motivation: some imaging projects have focused on the neurons etc ECG/... because they move relatively little in comparison to cardiomyocytes and their organelles; my interest is in the electromuscular view and I would like to understand how the movement of cardiomyocytes and their mitochondrias could be adjusted/calibrated in the time-frequency (t-f) data (spectrogram/...) of cardiomyocytes
Pseudocode
Simplistic view about including the effect of cytoarchitecture of organelles on the dynamics/movements based on statistics and probabilistic approaches
function getMitochondriaDynamics2D(signal2D, edges, Cytoarchitecture):
signal2D=$1;
edgesN=size($2,2);
organelles=[neurons, cardiomyocyte_minus_mitochondia, mitochondria, ...]; % given
organelles.cytoarchitecture = $3; % probabilistic values in Statistics
organelles.dynamics = zeros(1,edgesN-1); % preallocation

% Limit dynamics by cytoarchitectural restrictions
for organelle in organelles
    % include here systemic effects on organelles but Ignored here
    % etc Age, Smoking, ...

    % Let's loop local changes
    for edge in organelles.dynamics
        organelle.dynamics(edge) = organelle.dynamics(edge) .* ...
            organelle.cytoarchitecture(edge);
    end
end

return signal2D .*organelle(mitochondria).dynamics;

end

%% TODO here
function analysisMitochondriaDynamics2D(dynamics2D)
    ...
end

To find those probabilistic values

Embryology but I am weak here
databases and/or publications - which?

Biochemistry
I do not understand how much this should be considered here, but it could help to get any model

Atrial cardiomyocyte calcium signalling
mobility of the delayed-rectifer K+ channel Kv2.1 (3)

Useful keywoards

cardiomyocyte adult mobility

Hypothesis and Math/Physics/Bio
Hypothetical View of t-f data (2D) in cardiomyocytes: regular points separated by steady-gel-like areas - - seems to artifact of the movement
Physics about characterizing such areas:

... [ which mathematical methods ] ...

Sources
There are much studies in Embryology about cardiomyocytes and their movement, but I cannot understand their relation in the topic

Piquereau, Mitochondrial dynamics in the adult cardiomyocytes: which roles for a highly specialized cell?, 2013
How to measure Na/K channel activation at the membrane level?
Localization and mobility of the delayed-rectifer K+ channel Kv2.1 in adult cardiomyocytes.
Mitochondrial dynamics in the adult cardiomyocytes: which roles for a highly specialized cell?
PubMed with cardiomyocyte+"patch clamp", about measuring plated cells which are from hearts freshly minced in collagenase / EDTA. See PMIDs 27364017, 27076034, 26142302, 26241168, 26378152, ... [NickSandor]

Useful keywords

adult cardiomyocyte
possibly: Atrial cardiomyocyte calcium signalling
Mitochondrial dynamics
cytoarchitecture restrictions dynamics


text:
how does a dna probe work in DNA fingerprinting?
It says in my textbook ' after hybridisation with VNTR probe,  the autoradiogram gives many bands of different sizes '.  I tried looking on the net and it said there that probe is ' a radioactively labeled ssdna which binds to complementary dna '
My question is,  how do we know that if the DNA we are testing does contain complementary sequences?

You should look up VNTR. Take a look at the wiki page and it will tell you that VNTRs are Variable Number Tandem Repeats, the length of which varies between individuals, making these irreplaceable in DNA fingerprinting and such.
The trick is, all individuals will have it, but the pattern will be different, so you probe such regions which are formed as a stretch of k-mers. And you already know that they will be complementary, because we all carry them.

If you know what genome you are looking at, and your probes are validated for that species, then your sample will have that sequence.


text:
Is casein hydrolysate the same thing as casamino acids?
Probably a dumb question, but these seem identical. If a protocol calls for one, can I use the other instead?

Roughly, yes they are similar, but there are processing differences- the real difference is filtering. A product containing simply casein hydrosylate will only be roughly filtered with lots of peptides (like body builder products). Whereas casamino acids should be primarily clean/free amino acids (like nutrients for bacteria).
The actual manufacturing methods will be proprietary for the manufacturer... but you can trust that they are basically doing whatever works best to obtain the individual amino acids and/or whatever is cheapest for obtaining a useable product.
I have used bodybuiling and several other grades of casein products for growing bacteria. I have found that although various products may get the job done there are some serious drawbacks to casein products not intended for growing bacteria.
Differences include clarity of media, cleaning of glassware/fermenter/bioreactor, sudzing of aerated media, and the microorganism. Some microorganisms won't grow very well, and generally, those that can may still not grow quite as well or as fast... so that extra 10% or 20% cfus may be important (or maybe not since the price for quality may be 10 times higher).
The quality-features vs price must be weighed by the grower. Personally, I sometimes autoclave a cheap casein product in one (easy to clean) vessel then rag-filter it into another (then autoclave it again) for growing bacteria... but that's because I have about a thousand pounds of rough casein hydrosylate, and only a kg or so of casamino acids (for particular studies). This method does not eliminate all of the problems but it does reduce some of them.


text:
Comparing the amount of domestic animals and wild animals?
From some material, I read about the ammonia (NH3) emission from animal waste.
I found that the emission from domestic animals are greater than wild animals.
Then, I can't help wondering the amount of wild animals and domestic animals(cow, pig, chicken, etc). Which has the greater amount on Earth? And how to estimate the amount approximately?

You may find this interesting: https://xkcd.com/1338/

Can you please link and cite your source? That would definitely help.

The comparing of NH3 emission was from a textbook named Atmospheric Science by Hobbs.Link

And how to estimate the amount approximately?

You cannot. Most of the earth is water, and fauna diversity is highest in water. We are still tagging and tracking the movement and reproduction cycles of animals, and that is a never ending task. I say we cannot reach an accurate approximation because of how these projects work. They are targeted towards the monitoring of specific species. Next, different countries have different approaches towards conservation of the same species, and above all this many countries choose not to report numbers. The example which comes to mind is the Red panda. As many animals come inside the radar of active conservation efforts, even more remain outside it.
In fact, some time ago I read a compelling article about why the WWF should change their logo to a Red panda (or known as the lesser panda) rather than the giant panda, the argument being that awareness about the giant panda is very high while red pandas are still misunderstood as pandas. Unfortunately I cannot find that article now, but you can visit the red panda network to find out more.

Which has the greater amount on Earth?

Second, what do you consider as a wild animal? are insects included? are gutter rats included? Is the infestation of wild boars near the now defunct Fukushima plant included? If yes then they outnumber domesticated animals by a long shot. I would dare to say that cities are habitats more for members belonging to Animalia but not belonging to Homo.


text:
Why is Leptospirosis so difficult to catch?
I was on a small mammals training course and the professor was warning of the dangers of Leptospirosis. Apparently 5-40% of Rats have it and an unknown proportion of other animals. The warning sheet they handed out listed farmers, gardeners, etc as 'at risk' groups. I looked it up on the NHS website out of interest but it said there were only about 25 cases a year in the UK, even of the mild form.
I understand that it dies when it's dried out, but still, in notoriously rainy Britain, I can't seem to make sense of the numbers. There are at least half a million farmers in our country, probably a similar amount of gardeners, at least several thousand homeless and poverty stricken who must live in very close proximity to the huge urban Rat population, not to mention the potential for rodents to get into domestic water tanks. In rainy weather everything can stay wet for days. Also, if I remember rightly, an Olympic athlete recently died from it, so it obviously doesn't require a weak physiology to get in.
So, the question is, given what seems to me to be a massive prevalence (40% of all Rats), vast contact opportunities (all land workers during spells of wet weather), and seemingly a tough little organism (can kill an Olympic athlete), why is it so rare (25 cases in 70,000,000 people)?

Leptospira, the bacteria is largely found in the urine. So the urine from the rat has to get into cuts or wounds of a human. That seems rather unlikely. For such a thing to happen, you need ample rains, improper sewage and lots of rats. So apart from occupational groups, the disease also has an epidemic nature. During heavy rains in Mumbai, rodent infested sewers overflow and there's sudden spike in leptospirosis cases. I don't know the nos. but my micro txt calls it the most widespread zoonosis. Spells of wet weather aren't enough, there needs to be water logging combined with contamination.

Yes, Leptospirosis is, of course, a major problem in tropical areas, but as far as I know, there has never been an epidemic in Britain, yet we have some floods as well as all the other things I listed in my question. What puzzles me is there seems to be nothing in the bacterium's characteristics or mode of transmission that would account for the lack of epidemic in Britain. A little further reading I've done since asking the question seems to even imply that it can survive in moist soil http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds95e-eng.php, we shouldn't even need a rainy season.

An epidemiologist must be able to answer this question but id like to point out that the presence of bacteria doesn't necessarily lead to infection. Something as ubiquitous as Clostridium tetani in the soil doesn't cause tetanus in everyone (even in pre-vaccination era).

That's true, but the mode of transmission with C.tetani is what prevents it from reaching epidemic scales, it requires a relatively deep wound. What I seem to be missing is the equivalent characteristic of Leptospires which prevents Leptospirosis from reaching epidemic proportions in Britain.

Both deep and superficial wounds can cause tetanus. In recent times superficial wounds have become the main mode infection, more than deep wounds. This may be because deeper wounds receive more attention. I know this is off-track but still...

No, not at all off-track, I see what you're saying, it may indicate that other pathogens share whatever it is that Leptospires have which make them more difficult to catch than their prevalence in the environment would at first suggest. Do you happen to know if Tetanus has a mild form? One theory I considered with Leptospirosis, is because it has a mild form, it is under-recorded and in fact thousands of people are catching it without even noticing (this would then tally with the prevalence). Of course this just moves the question to why the severe form is so rare.

Any inputs? @theforestecologist

Based on some climate informatics, however, using our examples of Mumbai and I'm going to use London here: It's always warmer in Mumbai, closer to an average of 30C compared to ~20C in London. And when it rains in Mumbai, it rains: 60-70mm rain average in London compared to 600mm or greater during the months it actually does rain in Mumbai. I'd also consider healthcare standard. There are many things in play that need considering.

Yes, I've read that the disease is more of a problem in Tropical areas, but I've not read anything to indicate why. As I said in my post, it is not killed by cold weather (certainly not 10-20C anyway) and it can already survive for many weeks in just damp mud, it doesn't need any rain at all let alone 600mm. What I'm really after is why, from a physiological point of view, the bacterium is so much worse off in temperate zones.

Let me simplify the question. Rodents getting into the cold water tank is a problem described by various plumbing books as "quite common". People, wash, bathe, brush teeth and occasionally drink this water. The incidence of Leptospirosis from unknown sources in the UK is fewer than ten (eliminating foreign travel, water-sports and occupational exposure). So the question is, how do we get from a "quite common" situation which provides direct water-bourne exposure to rodents, in a country of 70,000,000, to fewer than ten (if any) cases of Leptospirosis caused by this type of exposure?

I see no-one has been able to answer this, but just in case anyone is considering the question, I've just found an interesting set of data from the national archives on reported zoonosis in the UK. It records the ages, and often causes, of all reported cases of Leptospirosis. Using age as a proxy for domestic sources (a domestic source would affect all ages equally) it would seem, as far as records go back, that no-one has ever contracted Leptospirosis this way, so I'm looking to explain not just a low chance, but no chance at all.


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How much does an experiment on monkeys cost?
Including legal fees, the paperwork, the housing, the food etc. (provided there is already a lab with biomedical lab equipment and space for the housing) for let's say the final testing phase of a novel drug over a duration of 3-5 months. what are the monthly and per monkey costs (for the questions sake let us say we have 10)? And how would the costs compare to a similiar study on mice?
I'm just curious because I could not find any figures on the internet.
EDIT: Provided I would get the get legal approvement,
EDIT2: and it is based in the US.
EDIT3: in California.

Welcome to biology SE! This particular question has many answers based on the location of your study, Institutional costs, legal costs which differ between countries, Insitutional costs also take into account the fees paid to the technical staff. If you provide your country/location it would help the people here provide a better answer.

As far as my two cents go. I met a PI at a conference who had to get some brain surgeries done on mice and he said that he was looking at approximately 30K $ per monkey. He worked in the US.

I'm voting to close this question as off-topic because its about managing experiments, not science

@KoustavPal per month?

@rg255 could you tell me where such a question would be better situated?

sorry he mentioned it for monkeys. That was the cost he would incur per monkey from housing, feeding until the completion of a single experiment on a single monkey. Nope, now that I remember correctly I think it was more like 5K for the facility and 25K for the surgery

@rg255 don't you think this question would fall within this site as per the on topic guide http://biology.stackexchange.com/help/on-topic. I would consider it to be in the third category, "questions about techniques in a biological or biochemical laboratory"

Questions on interdisciplinary subjects like bioinformatics are also welcome, as long as they focus on the biological part of the subject. - I would say financial management of experiments does not focus on biology

@rg255 playing devil's advocate somewhat, but this isn't interdisciplinary, it's 100% biology. I'd say it falls under "questions about techniques in a biological or biochemical laboratory", which doesn't actually require "focus on the biological part of the study" (the way the on-topic page is worded). Personally, I also think it's an interesting and useful question, and I can't think of another SE that would be able to cover it better.

@rg255 but you should also consider the fact that only an Investigator or a scientist who has written a grant for experimenting on monkeys can provide a reasonable answer to this.

I would not consider this off-topic but  the cost of the experiment will very much depend on the kind of experiment, the country of residence (local laws and taxes) and the kind of monkey as well. Therefore the question is broad. @daveid you should talk to someone near you for better understanding. BTW, check this out.

Also there's no attempt to work out the costs for themselves (lack of effort so "homework") and is very broad - the cost will vary greatly with the type of experiment

@rg255 I would say this is specific enough - I know some scientists who do animal experiments (not on primates and not in the US, otherwise I could attempt an answer) and generally all you need for a grant application costing is the number (and type) of animals, the experiment duration and the containment level (if the work requires it). And to be honest this is an area where there is so little public information it would be difficult for the OP to get any information themselves.

I contacted http://www.understandinganimalresearch.org.uk/ and they've offered to send me some information about this next week.

@arboviral +1 above and beyond!

I attended a seminar yesterday by Prof. Martin Hofmann-Apitius which described literature/data mining to generate the knowledge of a subsystem (+ bel) correlated against the funding invested into that subsystem. You can use this to find which parts of a system are over-funded (and exhaustive) or underfunded and incomplete, and this can potentially guide you to a more efficient answer. Although I see the point of this question, a much more apt question is "How much does a result cost when studying disease/system X?" I now see those questions will be much more answerable in a few years time!


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epiphyte mats in tropical forests
I read in an ecology text book ("Ecology: Concepts and Applications" (7th edition) by Manuel Molles) that trees in tropical forests can be sustained despite the poor soil is because they extract nutrients from epiphyte mats. Trees send roots from trunks and branches to get nutrients from epiphyte mats that are located high up in the canopy. I would like to visualize these roots. Are there any pictures available (conveniently in the Internet) showing these roots?
Or are these roots usually located beneath epiphyte mats (e.g., very short) and cannot be seen unless we remove epiphyte mats?

Good question +1. In general it is good to link the book and cite it directly rather than reporting indirectly what they said.

The textbook is "Ecology: Concepts and Applications" (7th edition) by Manuel Molles (ISBN-10: 0077837282) (ISBN-13: 978-0077837280).

What other specific-informations are given about them? any scientific name/ genus/ family? any geographic location? any particular forest?

The book says this finding was made by Dr. Nalini Nadlarni. If I were to look at Nadlarni’s publications, there should be some information. If I cut-and-paste a paragraph from the book, “Nadlarni’s research showed that in both temperate and tropical rain forests, trees access these nutrient stores by sending out roots from their trunks and branches high above the ground. These roots grow into the epiphyte mats and extract nutrients from them. As a consequence of this research, we now know that to understand the nutrient economy of rainforests the ecologist must venture into treetops.”

Adventitious roots into epiphyte mats aren't all that uncommon, and aren't restricted to the tropics. They can occur in old growth forests in the pacific northwest (my neck of the woods). A well-developed bryophyte mat in a single upper canopy tree can store up to six metric tons of water, plus all the mineral nutrients from atmospheric deposition. For the tree, it's a huge advantage to be able to tap into that epiphyte mat rather than rely on bringing up water from their subterranean roots. As far as visualizing it goes, yes, you would have to remove the mat to see them, but they look very similar to subterranean roots. Not sure if this is helpful, but I like to think of it like this: when a new meristem is formed, it's basically undifferentiated, and if there's sufficient water and mineral nutrition it can develop into a root (or a shoot if it's getting sunlight). The tree doesn't care if that's below ground or in the canopy.

Any examples could you provide?

Examples of trees that do this: bigleaf maple (Acer macrophylla), red alder (Alnus rubra) in the PNW, and a wide variety in the tropics: Metrosideros collina, Cheirodendron trigynum, Ocotea spp, Xylosma spp, etc, etc. See Nadkarni's work for a more thorough treatment.

So you should include them in your answer; and if possible, some verifiable source. That's the  OP(original post) looking for. (to write in italics, give 1 star mark at start and 1 star mark at end of italic phrase). Thanks for your Great effort.

Welcome to Biology SE. You could visit the tour-page for basic informations, the help-page, and for formatting  tasks in command prompt, visit this help sub-page Thanks :)

I never heard of it. Tropical forest soils may be poor, but the litter over the soil is where most nutrients are recycled and become available to trees. That's why without forest = without litter = without fertility = desert. At least in the Amazon.
Some researchers who studied the Amazonian soils are Harald Sioli and Philip Fearnside. You may find some of their old studies available on-line. If they ask some payment, try sci-hub.cc.


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why thymectomy doesn't lead to humoral immunity deficiency?
thymus is a place where T cells educate. in all textbooks it says if you remove thymus you will have cellular immunity deficiency. so in that case you should also be humoral immunity  deficient,then why it is only the cellular immunity which is ruined?

It depends on what age the thymus is removed. There are studies that suggest after a certain age, a thymectomy has no significant effect on the human T cell compartment.

A similar question from me. Though not happy with the answer. http://biology.stackexchange.com/questions/44103/does-atrophy-of-the-thymus-not-effect-t-cell-selection-and-tolerance


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Is the technology "identitas v1 forensics chip" related to microarray technology?
Available resource but difficult for me to make scence
Relation about crime scene and identitas v1 forensics chip
Is the technology "identitas v1 forensics chip" related to microarray technology?
if true ,as I know, different combination of genes are expressed in different parts of our body which means a certain tissue only makes particular types of mRNA.
Then my question raised: How can a CSI crew reconstruct a person's virtual appearance (for example skin color, face structure) by a piece of microarray with limited tissue (for example cells from saliva) and mRNA?
I mean saliva cells don't make pigment of our body, so how can the eye color or skin color be presumed, for example?
Otherwise, what is the technique "identitas v1 forensics chip "which allow us  to detect several phenotype  simultaneously?
According to the information I Know,"identitas v1 forensics chip" it contains hundreds of thousands of short sequences of DNA that binds to SNPs,where the DNA from the crime scene binds to this chip can allow software to reconstruct the appearance of the person of interest.
the chip is the first to provide data on all these traits simultaneously. Other devices can determine at most two at a time – usually eye and hair colour.

It'recommended to include information in your question rather than just providing the links - could you add some information about this chip to the body of your question?

Sure! I will try to describe it as best as I could.

Interesting question. The answer lies encoded in our DNA. If you take eye color for example, the genes important here are well known. The most important are OCA2, HERC2, SLC24A4 and TYR.
These are involved in different parts of the pigmentation process, any mutations in these genes lead to changes in pigmentation. Since also the variants, which lead to a altered pigmentation are known, you only need to analyze some cells containing genomic DNA from your suspect to check for these mutations (or SNP, single nucleotide polymorphisms).
The same is true for hair and skin color. So if you identify one or several mutations in the MC1R gene, you can be pretty sure, that your suspect is red haired, has pretty light skin and a high chance for green eyes.
This technique doesn't need to know the exact expression of a certain gene, but needs information on the cause for a phenotype (like skin, hair or eye color) and the causative gene.
The "Identitas v1 forensics chip" is a microarray chip, unfortunately, the company website is not really a source for information. You can find some in the New Scientist article you linked. This is basically a microarray (or chip) where all the forensically interesting and known SNPs about how a person looks like are analyzed.
It gives basic information (or at least a chance) how a persons looks like, what CSI does in the series is usually widely exagerated.

Thanks a lot! But I feel sorry for my incomplete and unclear description to my question. I still wonder  if  "identitas v1 forensics chip" have any connection with microarray and how they work? if true ,how can the SNPs be detected when they don't express?


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Growth of Axons
Does anybody know a paper in which the growth of axons, i. e. their length in dependence of time was measured? I did some literature mining myself, but couldn' t find any results.
I'm looking for a graph that shows the length of an axon in dependence of time.

Can you add where and what you searched for? It will help others know what to avoid in duplicating your efforts.

There are many papers on that topic. Please clarify what exactly do you want and what have you already looked for. Also, please add a [tag:reference-request] tag addressing all the necessary requirements mentioned in its tag-wiki.

I've looked already for the topic "growth of an axon", but I couldn't find the results I wanted.

http://www.google.com/search?q=axon+growth+dynamics


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What is the difficulty with cloning and genetic engineering in humans?
I asked this question many years ago and was told by my molecular biology professor that humans were (simply) more complicated than goats.
So, I didn't get a straight answer, but supposing he told the truth, what's the problem? Or are people really more complex than goats, from an engineering or genetic standpoint?

A molecular biology professor said "humans were (simply) more complicated than goats". Did (s)he really say that?! I know little about cloning but it sounds wrong to me. The main difference is likely to be a difference of ethics, not biology.

@Remi.b It's the truth. So, I also asked a related question on the philosophy SE: What is the ethical reason for avoiding genetic engineering in humans? Please chime in if you can shed light on that!

Please state your question clearly without reference to the title so it can be considered independently. We are not interested in your personal history, only what you are asking and what effort you have made to find an answer.

The question you are asking is an ethical problem rather than a biological one. This particular nature article highlights the problem I am speaking about.
In brief, children afflicted with SCID were subjected to what at the time was termed as a pioneering retroviral treatment. The idea being you replace the defective gene with the real one, in case of the quoted study, of 11 patients, 9 were cured and one of these babies developed leukemia due to the treatment. This was one of the first trials and it showed how these treatments can go awry.
Fast forward to today, last year you may have heard, something called the three parent babies garnered a lot of attention. This is basically mitochondrial donation, where a third-party provides mitochondria for IVFs for reasons where parents opting for IVFs may not be able to undergo successful IVFs due to mitochondrial mutations. This posed and still poses a serious ethical question, because what you are doing is mixing heritable DNA between lineages, please note that most geneticists will never cross this line, i.e. editing the genome such that the offspring carries the edited genome. Almost always the modified individuals are sterile (I know of no GMO crop which is not sterile)
But not to say, we have done nothing in terms of genetic engineering.
Scientists for the same reason (A human life is more important than any animal's) are wary of editing the human genome directly, so we now we also have something called siRNA treatment is just one example. And this is a list of siRNA based drugs which were in various stages of clinical trials in 2013. I know of a few which entered trial since then.
Lastly, this is just the tip of the iceberg, there's a whole lot which could be said on this topic, but it boils down to the same ethical problems.
Just so you know, since 2001, we have a lot of newer genome editing tools, such as TALENs and CRISPR-Cas. But remember, they still have the same problem as retroviruses from 2001, the issue about off-targets.
What if your tool targets a region which it isn't supposed to target?
Will another child develop a condition due to the treatment?
To avoid such an issue, we need to understand much better how the genome works, and sadly still we don't know enough. I cannot quote the study here because I have no idea where it is published, but at a recent conference I heard a talk from a lady about how retroviral integration works. The idea being, if retroviruses don't need specific integration sites, they should integrate at the first genomic region they encounter, that is not the case. I will not go into more detail. But I hope you have some food for thought.
UPDATE ON Genetic Engineering at a preconception stage

This is a link to the Nature article on Venter's minimal cell. There also exists an artificial Yeast genome page. The point I am trying to make is, we are really at the basic stages even now.
I will outline to you the behemoth scale problem we are facing.
2002: The first human genome draft is published. All the media is rife with stories about how we are going to unlock the secret to life.
Since then, DNA methylation and histone modifications have come to the foray as regulators of genome functionality.
We knew that DNA was transcribed into RNA and translated into protein. Noncoding RNAs came to the foray and messed up everything.
We thought that DNA functionality was governed by DNA methylation and Histone modifications, come 2009, we saw the first major article on Chromatin architecture. We understood that the genome has switches called Enhancers and promoters which regulated when and for how long RNA is transcribed. But sometimes these switches were so far away, we did not know how they switched on their target genes.
The problem can be summarized as this, making an artificial bacteria is easier than a human. In humans you have multiple layers of regulation, there's the DNA, where one part is silent (heterochromatin) and one part is active (Euchromatin), DNA methylation and histone modifications affect how genes are expressed, these modifications allow opening of the DNA so that genes can be expressed, The DNA is further compartmentalised (architecture) so that switches only affect nearby genes in 3D space. Non-coding RNAs act as messenger in such areas relaying proteins to their target DNA regions. So the cell is a mess!
Not to say that goat biology is simpler, just that a goat's life is cheaper than a human's. So we wouldn't feel a thing while "euthanising" goats for the advancement of mankind.

I had not heard about 3 parent babies... but I must be psychic or something because I was just thinking about it earlier today! Cool articles. But I would say that retroviral techniques are not really relevant with respect to what I mean. I understand the faulty tech- especially with multicellular organisms. I really meant engineering at preconception-stage.

Ahh...that needs a more detailed explanation.

Well, I think you did a good job pointing out the faults with the current progress with respect to later stages. But I would love it if you could add details regarding the technical problems at the single cell stage. Are there design or technical hurdles which make engineering more difficult for humans than other animals?

Well, I do feel bad for an animal that suffers. But + for calling my teacher a rotten liar (ha!)... but seriously he was a decent person.

There's a separate Stack Exchange for ethics, go there if you want to argue about that.
The first problem is how little is known about the functions of every gene. To properly roll out gene mods for humans, you have to know all the interactions of the original genes and their products and have an accurate computer model that predicts problems and other effects of the upgraded versions
Another problem: re-use of parts of the genome. In particular, some genes are used for several purposes, which means you could upgrade something and completely break something that would seem unrelated. It's similar to manually editing a compressed file's dictionary - changing 1 bit/base of compressed file content changes several in the output.
Then there's the problem of unexpected edits. What happens if your gene-editing framework misses and modifies something it shouldn't?
Assuming you ever get it working at a cost that people (or at least the military) will pay, you now have to figure out how to deliver the gene mods. Invasive or non-invasive? Retrovirus? Biocompatible DNA-producing chip? Update framework? Ability to roll back a bad update?
Cloning is even harder because you have to replicate the proper development conditions and there are all sorts of "gotchas" such as imprinting.
In short, humans might need to undergo an initial adaptation stage where these "gotchas" are gradually edited out and a synthetic programmable DNA editing and updating organ gets added - as a prerequisite for further upgrade.
With all of these difficulties, it's entirely possible that the best path to "Human 2.0" might be upgrade through machine parts maintained by microscale robots.


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Longevity Experiments
I realize this is a bit of a long shot, but sometime this year I was reading a paper about experiments that I believe were performed in Drosophila (may have been planaria) where breeding was delayed until late adulthood through separation of the sexes. After a number of generations there was significant lifespan increase.
Anybody come across this that can point me to it?

Planaria are hermaphrodites.

Look into Michael Rose's work at UC Irvine. No sure if this is what you were thinking of.


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Can neurons divide if somehow centrioles are introduced in nerve cells?
I am a biology student, so i know that centrioles are required for cell division, and i also know that nerve cells lack centrioles.
My question is that if somehow compatible  centrioles were introduced to the nerve cells, would their division be possible?

Welcome to Biology SE! I think it would be helpful for people to know your understanding of mitosis and meiosis. Since you say you are a biology student, how much of cell division have you studied?

Please read about cell division and what happens there first and then rephrase your question. Adding centrioles alone wouldn't certainly be enough.

Induced Pluripotent Cells
https://en.wikipedia.org/wiki/Induced_pluripotent_stem_cell?wprov=sfla1
You should probably look into this. This introduces what is called iPSCs, which are stem cells derived from adult cells.
What it is is that  they use signals that are found in embryonic cells, and the adult cells revert from their differentiated form into cells that can become virtually anything.