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What is the cause of dry cough?
I first thought this question in the case of

the cause of dry throat after 3-day recovery of dry cough?

but then I realised that the cause of dry cough can be a general thing.
Assume the person had three days recovery of dry cough under Montelukast and codeine (tablet).
He visited gym with little cardiotraining just after the catarrhal inflammation ended (no yellow mucose from throat during mornings anymore.
Just after the training, he felt dry throat after very weak coughs (no codeine medication when doing sport).
I am not sure if the dry throat is caused by

atrophy of the membranes in the throat
or dry cough by Acute respiratory viral infection (possibly through reflex arch; cannot be sure this because no codeine medication).

Let's assume that the dry throat is caused by dry cough (although weak) because virus particle can pass easily the scarring of the mucose membrane in the throat.
I think the atrophy of the membranes in the throat are NOT felt as dry.
Dry cough of the infection is felt shortly as dry.
The sympaticus activity clears the mucose membrane from the throat which alleviated the pain and also irritated the scarring.
Acute virus infection stimulates serous inflammation (as described here) which in the scarred tissue is felt once again as catarrhal inflammation.
So I think the cause of dry cough is catarrhal inflammation.
The localisation of the inflammation is essential to determine the type of inflammation, I think.
What is the cause of dry cough?

Cough-variant asthma is a common cause for a non-productive dry cough.  Asthma is not a single condition involving bronchospasm and with associated wheezing - there is a variant that is primarily or only coughing.
There are different inciting factors that bring on symptoms cough-variant asthma.  Most commonly they are exercise-induced, cold-induced, allergy-induced, or quite commonly it happens following a viral respiratory infection (post-viral-URI).  Symptoms can be acute (exercise or cold) lasting minutes, or chronic lasting days-weeks or even indefinitely.
The pathophysiology for each is different.  The latter 2 are inflammatory processes, as you mentioned, each a little different (hypersensitivity versus residual infectious inflammation).  I am a little uncertain about the mechanisms you described, and I am not sure the correct thing to focus on is scarring.  I would focus primarily on the inflammation.  Inflamed mucous membranes are extremely sensitive, reacting to even dry or cold air.
Using a long-term steroid inhaler is a preferred method of handling chronic cough-variant asthma, as it reduces airway inflammation.
There can be other causes of cough such as postnasal drip, chronic rhinitis, sinusitis, or gastroesophageal reflux disease (GERD or heartburn).

How do you differentiate between chronic rhinitis and cough-variant asthma? I think the latter can be a complication of the former. There is no cause such as atrophy of mucose of throat in your list. Assume you use Flixotide. Without washing your mouth after the inhaler, the steroids can cause bleeding from throat. So I think the mucose membrane of throat is vulnerable to atrophy too.

Cough variant asthma has few to no nasal symptoms; chronic rhinitis can have a cough component.  As for atrophy, good point.  I am not certain about that, but it sounds solid.  Inhalers are things like what's listed here: http://www.webmd.com/asthma/guide/asthma-control-with-anti-inflammatory-drugs  (these arebrand names like QVar, not chemical/generic names like beclamethasone btw - look them up.)

UpToDate and AccessMedicine are great resources for human physio/pathophys if you are connected with a university.  If your univ doesn't have it, UTD is IMHO worth its weight in gold for mechanism of action/pathology, differential diagnoses, treatment, and prognoses. Medscape is also excellent too, which is probably cheaper.  WebMD is not supported by a university and is supported by ads; its reliability for accuracy and unbiased info is questionable.

I should add that UTD and Medscape are what many many medical professionals (from med students to residents to practicing physicians, as well as PA and NP and probably RN students as well) use for a source of peer-reviewed best-practice guidelines in addition to journals and digests from one's field (like AAFP etc).


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What do nerves have to do with feeling nervous?
I was thinking about how when people say: "Nerve cells don't regenerate" (which is, apparently, not true at least for some kinds of nerves) and "You're making me nervous" they might not refer to the same "nerves".
What makes a person "feel nervous"? Does it have anything to do with nervous system?
Bonus question: How did people come up with the thought that nerve cells don't regenerate?

As buzrw's first comment states, most nervousness is primarily a sympathetic nervous system response.
There are also neurotransmitter imbalances involved with anxiety, especially in anxiety disorders.  The NT are dopamine, serotonin, and norepinephrine.
I want to clarify buzrw's comment on nerve cell regeneration, as I am unsure if he is stating it's proven to exist or to not exist.  "Primary neurons are not readily mitotic..." makes me think it's the latter.
Neuroregeneration is proven. Mayo Clinic has good information here and this is a well-phrased simplified answer here.
It is more commonly seen in peripheral nervous system, as the central nervous system has limited capabilities to regenerate.  Mostly it is regrowth of severed axons of  cells, and differs between different nerve cell types.  There are other types of regeneration as well.  They involve many physiological processes we're only starting to understand, such as the role of neuroligin.  Without getting too technical, there is a lot that can be done to help stimulate and guide the regrowth of some neural damage, but there are still chasms in our knowledge in the fields of neurology and psychiatry.

Yes, it's a response caused by a division of the autonomic nervous system, called the sympathetic autonomic nervous system.
Regarding nerve cell regeneration, it's not a thought it's proven. Primary neurons are not readily mitotic.

Could you explain a bit more what is the difference between these nerve cells and primary neurons?

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Genome Project Focusing on gene ADRB2?
I am not sure which project database to use UCSC or Ensembl for my asthma study about ADRB2 gene (Arg/Arg-16 genotype).
I am using the original Human Genome Project database at the moment.
However, I think Ensembl may be better suited for me.
Which genome database is good for Asthma research for Single Nucleotide Polymorphism (SNP variations)?
I am looking for something which has existing visualisation tools or one where you can easily write one yourself.

I don't understand what you're asking. Ensembl has subsections that let you look at a single genomes. The fact that the database has other genomes is irrelevant.  What are you calling the "original Human Genome Project"? Do you mean UCSC? What kind of data do you want to visualize?

I think it can be UCSC that was first out. Tools that give overview of the database and let me then focus on some sample.

There is actually no difference between the databases, as they use the same datasets. Only the way you can display and look at the data is different. I like Ensembl more, but this is a flavour. And I got a pretty good introduction to it.

@Masi, all of them do that, that's the point og a genome browser. Can you please edit your question and narrow it down? I still don't know what you need that neither the UCSC nor Ensembl offer you. The only way to choose between them is personal choice or specific tools provided but since you don't explain what you want to do, it's hard to help.

@terdon Thank you for feedback! I pickup the gene Arg/Arg-16 which I am browsing in infantile asthma.

I ask again, please clarify. Arg/Arg16 is not a gene, its a genotype; I think the gene you mean is ADRB2. You still have not told us what is missing from the tools you are using. You have not explained what exactly you want to visualize nor what exactly you are looking at. I am beginning to guess you are after SNP variations but I'm not sure. You mention vertebrates, does that mean you want to do a comparative analysis of some sort? Please [edit] and be more specific.

Thank you for helpful comments! I focused the question even more. Just ADRB2 and SNP.

So you are looking for a way to find mapped SNPs in the ADRB2 gene?

Yes. You are right.

If you are looking for variations in a gene, there are a few databases you an consult.
You can of course use the usual genome browsers, search for your gene and then select the variations listed. For ADRB2 this looks like this on Ensembl. If you plan to retrieve and compare data from different genomes/genes, I really recommend learning how to use Biomart, as this is a very powerful tool.
Then you can use specific databases or search engines, which only target SNP's. Examples would be: DBSnp and SPSmart (which queries different databases).

Very clear and excellent answer! Thank you for mentioning those tools! I am in the beginning of reviewing and learning them. :)

You're welcome. BTW: If you have the chance of participating in one of the Ensembl courses, do it. It is definitely worth the time.

I will do it when my studies go to Clinics phase.

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"Gold standard" for CNV detection methods?
Is there a generally accepted "gold standard" for testing the performance of CNV detection methods?  I'm interested both in learning about existing datasets that may serve as gold standards for CNV detection, as well in methods for producing such datasets in the first place.
(In case it matters, I'm primarily interested in the evaluation of CNV detection methods in laboratory mice.)
Thanks!

MLPA (multiplex-ligation dependent probe amplification). www.mlpa.com


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How do cats shed their fur?
Dogs shed their fur twice a year, so I assume this is the same with cats.
What is the mechanism whereby the change in temperature (assuming this is what causes the shedding) leads to the falling off of fur? Is it the same mechanism as balding?

Basic reasons as to why cats shed fur can be found in this link and this link.
An elaborate understanding of shedding in animals including cats can be obtained from this link. Hope that helps.

It would be extra helpful if you could summarize the content of the links in your response. :)

I would suggest that he read and get the info he needs and put in any queries later on. I prefer guiding rather than making it too easy

I would agree if it were only for OP. But what about all the other people who come to Bio.SE to get an answer to this question? For the health of this community, I think having a tiny bit more detail would be a good thing.


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How do download a list of the gene length of all genes?
I would like to get the gene length information of all the human genes. Is there a quick way to get this information? Thank you!

Which genome are you looking for?

The Ensembl 2005 data is here: http://www.zoology.ubc.ca/~whitlock/ABD/teaching/datasets/04/datasets04.html

Some basic information like length can be obtained in the GTF file (you can get the latest ENCODE GTF from the UCSC genome browser).
Other information are also available and obtainable from the UCSC genome browser → table browser. Select the group and tracks that you want from the corresponding dropdown boxes. You can export the data as a text file or forward it to the galaxy interface for analysis.
If you are familiar with some programming then you can pull out the lengths (it is not explicitly given in the output or in the GTF). Also, the gene length may be different from the mRNA length because of the presence of introns in the former. The third field in the GTF file denotes the feature (gene, transcript, exon, etc); you can parse the GTF for picking up only desired features, lets say the mRNAs.
The fourth and fifth fields denote start and end positions respectively; all you have to do is end - start to obtain the length.
A small scriptlet such as this would work in linux/cygwin terminal (I wont go in detail because this is not the scope of this forum):
awk -F "\t" '$3=="transcript"{print $9, $5-$4}' file.gtf > output.txt

The $9 refers to the ninth field which holds information about that feature including the gene name, gene id etc.
The first link that I mentioned also shows some basic methods of extracting information from GTF.

I'd use Ensembl's BioMart.  It's not connecting for me right this second, but it should have that information.
http://www.ensembl.org/index.html


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Why only able to close one eyelid? Genetic reason?
Eye-dominance is a critical thing with bows: right-eye-dominant is recommended to do the aiming on the right eye here otherwise inaccuracy. This made me think whether all people are even able to do this. I have seen people who can only close one eye or two eyes at the same time but not two eyes separately. What is the factor determining this? Is this determined by genes, learning or by something else? Is it possible that the other side of the eye muscles are missing because they have not been needed for the survival? I discussed missing muscles with my medical friends and they mentioned that there are muscles that some people do miss such as in hands because they are not essential for survival. I don't know whether certain muscles in face could be missing with some people or is this just learning thing?

Without having any scientific knowledge on the matter, I imagine it might simply be a matter of having learned it or not. I remember I had to practice for quite some time as a child before managing to reliably close each eyelid separately.


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If not intelligent design, what is an alternative scientific theory to evolution?
In the popular culture, Intelligent Design is often portrayed as trying to be an alternate theory to evolution.  However, as the following question points out, it is not scientific, and so cannot be an alternative theory.
What is the viability of Intelligent Design as a supplement to chemical abiogenesis and Darwinian Evolution?
But, this also puts evolution in a tight spot.  Science progresses by competing theories.  Yet, there is no competing theory to evolution as a whole, only variations within the theory (e.g. Neo-Darwinism vs Punctuated Equilibrium).  So, if there are no scientific alternatives to evolution, does that make it unscientific as well?  If there are no proposed alternatives, how do we know evolution got it right?  And finally, what would a non-ID alternative to evolution look like?
Full disclosure: I am quite interested in ID, and do believe it is scientific and testable, but that is not what I am addressing with this question.
UPDATE: For those downvoting this question, how do you suggest I improve it?  Is it not a valid question?
To use an evolutionary analogy, without a diversity of theories our understanding of where we came from will not evolve and remain fit.  Shouldn't evolutionary theory apply to evolutionary theory itself?

I am quite interested in ID, and do believe it is scientific and testable : How do you propose to test it ?

That's material for another question.  Does it interest you?

No. It doesn't interest me- I think it is a deliberate neo-creationist approach. With a premise that is based on religious belief, no test can be unbiased.
Why downvote: Evolution is an active field of research. You should read about it (not necessarily too deeply) and understand its principles before proposing a new theory or to test the validity of a theory that lacks a scientific premise.

Shouldn't evolutionary theory apply to evolutionary theory itself?: Hmm.. That's what research is :)

There have been alternatives, but they're all silly and ridiculous and were quickly debunked.

Too long for a comment: You have a misconception about scientific theories: They are not competing what is wrong or right. They are set up, tested, corrected if necessary or discarded if they can not be proven. Science (or more Scientists) has no problem with rejecting a theory when no other is available. There are always things which can not be explained with the current knowledge, but this is the way this process works. And scientists have no problems admitting this.
BTW: It is not theoretical because it is called a theory. Darwin's theory has been proven quite a number of times and works pretty well - but it has its limitations because of findings he couldn't know of, but this doesn't make it wrong. It is a bit like Newton's theory of gravity and Einstein's general theory of relativity. The first cannot explain certain phenomena that the later can, which doesn't make Newton wrong.
The other thing is, that ID is in fact no scientific theory. A theory makes a prediction, has some foundation on earlier work and can be falsified/proven. It will be corrected if it has minor loopholes and discarded if completely incorrect (For example, see Lamarck's theory of evolution, that was once discarded but is being revisited in the light of the recently discovered phenomenon of transgenerational epigenetic inheritance).
ID is built just on beliefs and is nothing but a refined form of creationism; it doesn't make predictions and can not be falsified or tested (because it is just a belief). This makes it completely unscientific.

Well, if we don't have any alternatives, how do we know we have the right theory?  For example, see Popper: http://en.wikipedia.org/wiki/Conjectures_and_Refutations  All other fields of science would be nowhere without being put up against alternative theories and refuting them.

Again, you have a misconception that hypotheses need to be tested in a competitive fashion. There were alternatives to Darwin's evolution, see Lamarckism. The reason evolution has lasted so long, and was promoted from hypothesis to theory, is because it works extraordinarily well in many circumstances. For the aspects that Darwin could not have known about (e.g., epigenetics), the theory has been improved, or "upgraded", to account for the current body of evidence.

Darwinism and Lamarckism are both different evolutionary mechanisms.

Additionally, even in the case you mention it is debatable that Darwinism has completely won out over Lamarckism.  For example, see the Baldwin effect.

@yters. there is no war between Darwinists and Lamarckists and there are no fanatic groups that support either of these so called factions. Darwin's theory fits in almost all situations. The neo-Lamarckists are just evoking the term Lamarckism to generate some melodrama. Lamarck himself was not aware of transgenerational epigenetic inheritance. Darwin's theory was more complete than Lamarck's, when they were published. What we, as scientists, are trying to proceed towards is a more comprehensive and complete evolutionary theory- that will explain everything. ID is just a hindrance to this.

@yters A theory is not proven right but competition. It is proven more right when the theory is able to make prediction that matches reality. If the prediction of the theory does not match reality, the theory is wrong, it is either revised or discarded. It does not matter if there is competition. If two theories failed to predict reality, both theories are wrong and we have a situation where no known theory works.  There are no competitors to evolution theory, because nobody is able to create a theory that can encompass all known facts and make better predictions,

@yters there's no alternative to gravity therefore gravity isn't scientific by your logic.

@Praearcturus before the theory of gravity Aristotle claimed everything sought its rightful location in the universe.  Newton's theory worked better.

@yters okey then
https://en.wikipedia.org/wiki/Alternatives_to_evolution_by_natural_selection

@Praearcturus great, that's exactly what I am asking, what are the alternatives.  Your page and a bit of description about how they are alternative theories to evolution would be an acceptable answer to this question.

I try to avoid getting involved in these debates, but I feel the need to point out that if you are going to debate these issues you must make sure that you use terms correctly. Here is the first paragraph from the WP entry for Evolution:

Evolution is the change in the inherited characteristics of biological populations over successive generations. Evolutionary processes give rise to diversity at every level of biological organisation, including species, individual organisms and molecules such as DNA and proteins.

None of this is theoretical - it is observable. In my opinion the term Theory of Evolution is so broad as to be meaningless.

This is a good comment but I think when someone shows up and their first act is to set up a soap box they may not be in receiving mode. +1


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Is infrared photosynthesis possible?
The post-apocalyptic science fiction novel Dark Universe by Daniel F. Galouye has some plants living inside bunkers that use infrared light for photosynthesis. There are speculations that extraterrestrial plants might use the same trick on planets orbiting red dwarfs and that their leaves would be totally black. Would this type of photosynthesis be possible and are there any plants on low-light environments from Earth that might do this already?

There is an algea that uses IR:
The newfound pigment, dubbed chlorophyll f, absorbs light most efficiently at a wavelength around 706 nanometers, just beyond the red end of the visible spectrum, researchers report online August 19 in Science. This unique absorbance appears to occur thanks to a chemical decoration known as a formyl group on the chlorophyll’s carbon number two. That chemical tweak probably allows the algaelike organism that makes chlorophyll f to conduct photosynthesis while living beneath other photosynthesizers that capture all the other usable light. https://www.wired.com/2010/08/infrared-chlorophyl/
Infra red can't directly disassociate CO2, it's too low in energy, so that it represents a relatively inefficient and complex chemical pathway for photosynthesis compared to conventional. Research shows that multiple IR photons can be converted to other photons using photon up-conversion, and then used for photosynthesis http://www.sciencedirect.com/science/article/pii/S0360319912001838
here is the most clear summary of why IR is absorbed as heat by water, visible light is gentle and goes through water and excites electrons to do chemical reactions, and UV is too energetic. https://www.reddit.com/r/askscience/comments/14jsms/can_plants_perform_photosynthesis_using_non/

I would hardly ever say never where biology is concerned.  In this case that utilizing red rather than blue light for a plant would require many of the basic assumptions of photosynthesis in terrestrial plants to be revised, but since we're talking about another planet, that might not really be an issue.
If we are asking only about how we could change our plants to work with IR light, I'd say that might take a few hundred million years of selection and it's harder to imagine.
Firstly photosynthesis in another planet doesn't have to fix carbon or produce oxygen - both of these chemical processes utilize the relatively greater energy produced in blue and red light photosynthesis we see in plants here.
Secondly using IR would have its particular questions associated with it.  In this case the energy quanta are very small and in fact in the same range as chemical bond vibrational energies.  Such energy might be hard to capture with any efficiency since simple heat would tend to compete with the photon, so this would work better if the entire system were at a relatively low temperature.
The leaves could be black or they could be completely clear by the way.

"utilizing red rather than blue light for a plant would require many of the basic assumptions of photosynthesis" Both answers to Are two colors (red + blue) necessary for LED grow lights, or would either color be sufficient? indicate that it's primarily red light that's useful in photosynthesis and blue light for phototropism. Yes blue light can excite chlorophyl as well, but all you need is circa 680 nm to make it work. That's already almost infrared if we used 700 nm as the boundary.

Several other answers provide actual examples where wavelengths longer than 700 nm are already in use by life on Earth for photosynthesis, so I think this needs some rewriting to align with actual facts. I noticed that you don't draw from any supporting sources for these assertions.

Photosynthetic bacteria can use infrared light down to 1050 nm (Blastochloris) for photosynthesis.
Oxygenic photosynthesis seems to have limit at about 750 nm.
I think there are organisms that can use longer wavelengths for both oxygenic and anoxygenic photosynthesis.  It is just they have not been looked for in the right way.
Here are some papers of mine.
92).    RITCHIE, R.J., LARKUM, A.W.D. and RIBAS, A. (2017) Could Photosynthesis function on Proxima Centauri b? International Journal of Astrobiology 0(0): 1 –30 doi: 10.1017/S1473550417000167.
93).    LARKUM, A.W.D., RITCHIE, R.J., and RAVEN, J.A. (2018). REVIEW: Living off the Sun: chlorophylls, bacteriochlorophylls and rhodopsins. Photosynthetica 56: 11–43, DOI: 10.1007/s11099-018-0792-x

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What are the factors that control the speed of propagation of neuronal signals?
If we consider an analogy between a wire and a neuron there may be some resemblance between the factors controlling the data flow rate. For example the increased width of wire leads to decreased resistance etc; similarly increasing or decreasing the thickness of myelin sheath may have an effect on the conductivity or data transfer between neurons.
Are there additional factors that can control the speed of nervous conduction?

Are you interesting in processing speed (could be measured via reaction time for example) or in speed of signal transfer?

I think both are related to each other?arn't they.I mean one effects the other.My interest is in processing speed and yes/obviously it could be measured with reaction time but i was was interested what make's this speed at the cellular level

In this case look at synaptic delay. In my best knowledge it's the most time consuming factor of nervous conduction

Unfortunately, we cannot consider an analogy between a neuron and a wire; they are altogether different. Do you want to ask about the processing power of the brain, or speed of signal along a neuron? I suggest you pick one, and revise your question accordingly - unlike in electronics, these are quite separate concerns.

Well you are right i am interested in processing power of brain and i thought speed signal along a neuron will be involved in that matter.I think its to late for me to revise.

The diameter of axons also makes a difference, the thicker the axon, the faster the rate of action potential conduction. This is seen in invertebrates, such as squid. Squid have giant axons (up to 2mm in diameter), which exhibit rapid conduction rates. See Wikipedia 'squid giant axon', in which it says up to 1mm, but I have measured 2mm myself. These are not found in mammals.
Original research on squid giant axon  was by Cole & Curtis (The Journal of general physiology, 1939). For more recent research see Hartline & Colman (Curr Biol. 2007 Jan 9;17(1):R29-35.).
Work by Hodgkin, Huxley and Katz (The Journal of physiology, 1952,  116(4): 424–448) using squid giant axons lead to the elucidation of the mechanism of action potential conduction and a Nobel prize. Academic summary here: http://jp.physoc.org/content/538/1/2.full
Wikipedia: see the Goldman equation (Goldman shared the Nobel Prize with Hodgkins and Katz). This is more frequently known as the Goldman-Hodgkin-Katz  equation in UK publications.

The myelin sheath of a neuron affects conduction of action potentials.
Things to read through at wikipedia for example are the Nodes of Ranvier, the saltatory conduction and the Schwann cells.
There might be other features changing nervous conduction, but those are the ones I remember from my study times.

The question already includes the case of myelination.

It included also the words "may have". I just pointed out that this assumption is true. And the question only mentioned thickness, not gaps.


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How is the growth of benign tumors suppressed?
A benign tumor  has an outer layer of cancerous cells beyond which are regular cells (I Think).  The Tumor must have some kind of boundary layer like a wall where somehow the cancerous cells can't affect any more normal cells outside the wall. A Benign Tumor I think can be inactive for many months; it might never grow anymore. Might it be that the cancer cells at this Benign Tumor Wall are inhibited from affecting any more cells? Could there be an Apoptosis shut-off inhibitor or a cell-death pathway shutting-off inhibitor in this case?

Immune system fights cancer ...

Are inhibitors part of the immune system?

There are some cells...I think NK cells..search NK cells on wikipedia

The primary difference between a benign tumor and a malignant tumor is that the former cannot metastasize; therefore they remain within the tissue boundaries.They grow slowly and are are not very de-differentiated thereby retaining some of the tissue organization.
Another point to be considered is that benign tumors do not cause vascularization (formation of blood vessels in the tumor tissue; triggered by secretion of VEGF), which also limits its growth.

I think the first part of your answer is more a definition than a mechanism. In addition, I thought benign tumors were bound within a certain structure that prevented them from growing out of control and from metastasis (I am definitely not an expert!) Perhaps a reference would be in place in your answer?

@ChrisStronks Yes it is a definition only. I cannot find a reference for the wall preventing its overgrowth. Metastasis happens because of a cellular differentiation event (such as EMT). It is not a wall that restricts the escape of the rogue cell. I need to add references, I am looking for a proper one.

Does a benign tumor have some chemical or gene expression that blocks the secretion of VEGF?

Is a benign tumour unable to metastasize because it can not cause vascularization (and then maybe there is no oncogenesis)?. Also does the apoptosis mechanisms in a benign tumour still 'work'?

This is not entirely correct. A benign tumor is not cancer, for example, a skin tag. A malignant tumor is cancer, for example, astrocytoma. The distinction is not the ability to metastasize, though this does tend to be a characteristic of malignant (cancerous) tumors and not of benign (non cancerous) tumors. There are exceptions that can help clarify this. For example, most malignant CNS tumors do not metastasize. See Chapter 7 of Robbins and Cotran for these definitions. Malignant means cancer. Period.

@DeNovo Yes you are right about CNS tumours. I don't have a great expertise in classification of cancers. It would be great if you can add an answer.


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What is the difference between transformation and transfection?
What is the difference between transformation and transfection? How do both of these methods work?

If you are interested in the history of molecular biology this is an interesting question.
Basically transformation came to be used to describe experiments in which the phenotype of an organism was changed by the uptake of DNA, and because of the way this developed in  bacterial systems this DNA was usually a plasmid. Then it became possible to use purified phage DNA to infect cells, whereupon the 'transformed' cells produced phage particles - for obvious reasons this was called transfection.
When efforts turned to getting the same techniques working with cultured animal cells many of the vectors were based on viral genomes (e.g. SV40) and these workers referred to this as transfection. At this point the distinction between the two terms became meaningless, and usage tends to be for historical reasons. Interestingly in molecular manipulations of yeast, where there are no viruses, the transfection word is rarely used.

To add on with how the words are currently used, bacteria undergo transformation, while introducing plasmids to cell lines is called transfection (often incorrectly, since most people don't use live virus for infection, but use cationic lipids instead).

@ leonardo, but I have met many scientists who work wth animal cells who refer to introducing plasmids into bacteria as transfection

Alan, it just proves how confused the two terms have become. The proper term in that case is transformation -- naked uptake of DNA, just as it would be for liposome-mediated "transfection"

@leonardo: well, in case of animal cells electroporation is also called transfection (or new words such as nucleofection). We routinely use the term transfection for animal cells but retain the use of transformation for bacteria. The usage, as Alan said, is purely due to historical reasons

As far as I know (and I haven't found no evidence against it) this is mostly a semantic difference. Both processes describe the addition of genetic material into cells using various techniques.
Transformation is here mostly used for bacterial work (transforming plasmids for example), while transfection is almost exclusively used for eukaryotic cells. The reason may be, that the term transformation is used in eukaryotic cells as well to describe the progresion of cells into cancer cells.
The techniques are not very different and there are a lot of them. Transfections often use transfection agents, which form pores in the cell membrane through which the DNA can enter the cell. This can also be done by using a short electropulse. A lot of transformations are done using "chemically treated" cells, where the cells are brought into a state in which they take up DNA which adheres to their outside.
The Wikipedia articles on Transfection and Transformation gives you more details on the methods.


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To measure frequencies of eosinophils and neutrophils in airways
I am reading this paragraph about RS killed-vaccine in Encyclopedia of Virology, Third Edition (2008), vol. 3, pp. 70-77

What is this data called by which you can say that the frequencies of eosinophils and neutrophils increased within airways?
I think sample is first taken from throat and cultivated on some general culture (blood agar).
Then, specimen is looked under microscope.
Similarly done for the sample after vaccine.
Then, visual comparison with identifying visually eosinophils and neutrophils.
Is the conclusion made based on culturing, microscopy and visual sampling by eye?
Mass spectrometry
I am not sure anymore if this technique is useful at all.
Mass spectrometry can give different intensities and masses.
If so, the intensity of the corresponding peaks should be greater after the vaccine.
Can this kind of conclusion be made based on mass spectrometry?
Interesting would be to know the exact spectrum of eosinophils and neutrophils after the vaccine. I think they do not increase proportionally.
The one increases more than the other.

Protein mass spec in the 1960s? In this time Sanger did the first protein sequencing, so I highly doubt that it happened with it. From which paper comes this information or has your textbook linked some reference for that? I would say these are either biopsies which are subsequently stained or swabs that where tested. This is from the "Desk Encyclopedia of General Virology" right?

@Chris Today. Can you make such a test with mass spectrometry? I think yes, but the problem can be the amount of the substance from the cultivated specimen.

I think there are ways, yes.

The original tests where done with blood and then:

An eosinophillc index was calculated by multiplying the percentage of
  eosinophiles found in the routine white blood count by the total white
  blood count. An index of greater than 250 was considered positive.

See table 8 in this paper: "Field evaluation of a respiratory syncytial virus vaccine and a trivalent parainfluenza virus vaccine in a pediatric population." So they measure the eosinophils in the periphery not in the airways.
This article used histologic techniques: "Respiratory syncytial virus disease in infants despite prior administration of antigenic inactivated vaccine." Both articles are from 1969.
Newer studies used micropical techniques and FACS analysis, but these experiments were done with mice: "Respiratory synctial virus infection in BALB/c mice previously immunized with formalin-inactivated virus induces enhanced pulmonary inflammatory response with a predominant Th2-like cytokine pattern."

Thank you for your clear meta-analysis and excellent sources! I asked this question because I am interested in separating differently energetic (number of vacuoles inside and their size) eosinophils and neutrophils from one another in video. In all those publications, we have two stages: 1) initial and 2) shortly after the vaccination. I am interested in what is happening between and after these two stages among granulocytes. Some method which enables me to take samples continuously. I think histology and microscopy of each stage is necessary. Then processing pictures and making t-f plane.


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Coalescent theory - independence of coalescent times
Let $T_i$ be the time to coalesce from $n(t)=i+1$ to $n(t)=i$, where $n(t)$ is the number of sites that have not coalesced yet. In the below example the maximum $n(0)=6$.

As I understand it, many mathematical developments in coalescent theory depends on the fact that the random variables $T_i$ are independent (but not identically distributed). In other words...
$$f_{T_n, T_{n-1}, …. T_3, T_2}(t_n, t_{n-1},….,t_3, t_2) = \prod_{i=2}^n f_{T_i}(t_i)$$
What are the assumptions for this equation to hold true? Below are some suggestions

No selection
Selection is not varying through time
Stable population size
Random mating
Both sexes have the same genetic background
Both sexes have the same variance in fitness
...

source

[Remi, you always make me read up things with your questions. At least half an hour is gone in this. But it's good :)].. As per wikipedia article on coalescent theory, population is also assumed to be very large for continuous approximation of coalescence time (exponential dist).

@WYSIWYG ha ha I'm glad, I can help you seeking for more knowledge with my questions. I may try to write a longer background for my following questions, so to spare some time to the readers.

@WYSIWYG Remi.b I like the reading for your questions, some have even prompted me to buy new books!

As long as members of a generation "randomly choose" their ancestor in the previous generation the law of independent probability (your equation) will hold.
Any study of coalescent theory begins with the Wright-Fisher model. The assumptions are:

finite diploid population of constant size N,
non-overlapping generations (simultaneous reproduction),
random mating,
no mutation, selection, or migration.

These assumptions are consistent with independent non-identically distributed waiting times. An example of an assumption under which independence no longer holds:
Individual B's random choice in generation 2 of ancestor A in generation 1 reduces the probability that individual C in generation 2 will choose A. In other words, the likelihood that A will give its genes to the next generation falls off with each new recipient. Then the independence no longer holds.
See, e.g., Deonier, Computational Genome Analysis (2005, Springer) at pp. 392 ff.
J. Wakely's paper Coalescent Theory: An Introduction (Systematic Biology, 58:1, Feb. 2009) may be one of the best overviews of this immense topic available. He mentions Kingman's 1982 mathematical proof (which I haven't gone through) of the coalescent process (Stochastic Processes and their Applications 13 (1982)--available as a free download from ScienceDirect).

+1 Good guy @daniel! You're answering to many of my questions. I am actually reading (a bit slowly because I have quite a lot of things to do beside this reading) John Wakeley's book, Coalescent Theory, an Introduction. I was expecting that the only assumptions for the independency of $T_i$ were those of the underlying Wright-Fisher or Moran model. I wasn't sure though. Thank you

@Remi.b: It is good for me to work through some of these questions, which are interesting and thoughtful. I too am busy or I would work on more of them! Thanks.

Your link to the Wakely paper is broke. Could you please write out the full reference so that it can be searched even if the link is broke? Thank you.

@Hans: Thank you I will get to this soon. Appreciate the heads-up.


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What species is this mammal?
I saw a mammal that looked like a large squirrel. I haven't seen anything quite like it. Can you help me identify it?

Squirrel-like, "hunched over" posture.
It was too large to be an eastern squirrel—approximately 2.5 feet, from nose to tail.
It had a fluffy tail like an eastern squirrel, not short and rat-like like a ferret.
Black face with white nose, body was chestnut-brown.
I saw this on the ground, not in a tree.
I saw it in a pine forest in east-central Alabama.
At one point, it sat up on its hind legs.

It sounds pretty much like a fox squirrel (or better: as masked face fox squirrel which are found in Alabama).
They look like this (taken from this website):

There seems to be quite some variation in terms of fur color, some animals are more greyish:

Taken from here, this website also contains some additional information.


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translation of scientific names
I am trying to determine the "translated" meanings (not seeking the common names) of different insects, (presently some bees and wasps).  Does anyone know of a printed or internet resource that defines the various names. I have one for plants, but not for animals.  Knowing the (English) meaning of the Latin / Greek/ etc. is often very informative -- IF I can find it.
I can give more specifics if you want.
Thanks.
Glen B
Olympia WA, USA

All you need to do is use a Latin/English and/or Greek/English dictionary. This is not really related to biology but linguistics.

This question appears to be off-topic because it is about nomenclature and the meanings of words in dead languages, not biology.

what OP meant by latin and greek names is the binomial nomenclature (which for historical reasons is in latin and greek)

Glen, sometimes there are many species that have same colloquial name. For e.g. frog includes hundreds of species. If you require high level of detail, you may need to look for more comprehensive lists.
There are zoology dictionaries such as this. I think it should serve your purpose.

There are multiple resources that are in use as far as I can see from a quick google search. You would find the Integrated Taxonomic Information System (ITIS) quite useful. It includes details on scientific papers published about a specific species.


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Can someone suggest me good opencourseware links for learning computational biology basics?
My internet is slow and I have only 1GB data usage allowed for this month. And I want to make maximum out of it for learning some basics of computational biology.
Which are the best online course (freely available lectures) suggestions for me?

coursera has some good courses!

MIT-OCW also has decent video lectures.. Bulk download the videos and watch them on your player..

ok let me see. But internet is expensive for me still. :(

http://ocw.mit.edu/courses/health-sciences-and-technology/hst-508-genomics-and-computational-biology-fall-2002/audio-lectures/
Download all the slides if you want good resources.

OK let me see those.


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"selective pressure" or "selection pressure"?
Editing a manuscript of mine, a co-author changes "selection pressure" to "selective pressure". Are those two terms interchangeable? Or are there subtle differences that I'm not aware of?
The sentence under consideration: "In contrast, gene expression changes during development and tissue formation are under high selection/selective pressure."
FWIW, "selection pressure" is a bit more popular in the literature.

I had a colleague that was against the use of "pressure" altogether - I can't fully remember his argument but it was a long the lines of just saying selection is correct grammatically, and selection is not a type of pressure. I feel he is fighting a losing battle though because its becoming more common. You might get a better justified response on the English language SE.

Selective/selection is being used as an adjective to qualify 'pressure'. My gut feeling is that is better to avoid using a noun (selection) as an adjective, so selective is to be preferred.

From a grammar standpoint I would think that "selection pressure" is a compound noun. But I was looking for a biological answer, if one is more appropriate than the other.

Could you possibly give the sentence it is in?

@GriffinEvo: done

I'd say "subject to strong selection"

Selective sounds better to me, though I cannot think of a reason why. I expect that a reader will get the same meaning from either choice.

As far as online references are concerned, they should be equivalent (as "selective" becomes "making a selection"). The important difference in my understanding is that speaking in terms of biology, "selection" triggers associations with evolutionary terminology, whereas "selective" doesn't. Thus, as far as I am concerned, "selective pressure" could be referring to some machine that has a method of applying pressure to one thing but not another, whereas "selection pressure" immediately makes me think of factors benefitting the proliferation of one thing over another. Hence I would personally prefer "selection pressure".
Given the ambiguity, you probably won't be able to make all readers happy with either of the two. Thus, it might be best just to use a different phrasing as suggested e.g. by rg255 ("subject to selection").

... if you do say "subject to strong selection" does this make me a co-author??? @michaelkuhn ;)

I think second author at least! :P

let me think about it :)


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Getting goosebumps at will
I can get goosebumps at will, regardless of the environment. Its mostly visible on my arms, and I can feel it on my head. It requires some level of concentration to achieve this.
My questions are : what biological mechanisms are involved in doing this ? Is it common ? Is it useful ?

It is a vestigial reflex: http://en.wikipedia.org/wiki/Goose_bumps

Interesting!  I haven't seen anyone able to do this deliberately.
Goose bumps are caused by the tiny muscles at the base of hair follicles contracting, and the hair stands up.  The skin around it puckers.  It's mediated by the sympathetic nervous system (the "fight-or-flight" aspect of the system).  This is how animals' fur stands up when afraid or upset (think of a scared cat).
It's called the pilomotor reflex.  It also helps them keep warm (fur insulates) - so it happens when we're cold too.  But since we have so few hairs, it's not very useful to us. It's more of a vestigial reflex than anything.
It happens for other reasons too.  See the wikipedia article, it's a good place to start.  For more info, look at this article or a medical textbook.
If you can do it at will, you likely are in tune fairly well with your sympathetic nervous system.  That's excellent.  You may be able to make minor alterations in your pulse and blood pressure through breathing regulation - check out the concept of biofeedback.  It is a way to help manage stress, keep yourself calm in terrible situations, manage anxiety or panic disorders, anger management.....
Being able to use physical self-awareness to affect physiological changes takes practice to develop as a skill.  You've got a great start!


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Draw simplified phylogenetic tree for kids
I need to draw simple, phylogenetic tree for kids lecture.
I am looking for an online tool where I can enter organisms (e.g., human, wasp, fungus) and get figure of a phylogenetic tree. Tree should be based on how close those organisms are (I don't need genome alignments).
Similar figure producing tool would be perfect.

Just download an existing diagram.. To make a tree you would need to put in reference sequences.

Have a look at this Website. It might be helpful.

@WYSIWYG where can I do so?

You can find images of trees by google search.. but if you want to make a tree yourself you would need some reference sequence. Entire genome is not used for that but some sequences such as 18s rRNA are frequently used. Doing an alignment is inevitable, but the algorithms (such as clustalW) do it under the hood.

you can use http://itol.embl.de to get trees based on the NCBI taxonomy, but you'd have to use a graphic program to make them prettier

As per your requirements I will suggest:
http://www.onezoom.org/

I don't know what background you have given the kids or what level, but here's something we do in a non-majors freshman level biology course that could easily be adjusted. First, to get them thinking about trees and relationships, give them a simple family genealogy (use only 1 parent for simplicity). I use my family tree going back to my grandmother. With cousins, aunts, and siblings, they begin to understand how to interpret family trees. You can substitute the family names with organism names to make it a basic phylogenetic tree.
We teach tree construction simply. We give students a list of six species (fake birds) with DNA sequences that are only 20 nucleotides long. Students have to calculate the number of base pair differences between each pair of sequences which, in our case, range from 2-10 nucleotides.
They then use the pairwise differences to construct their tree, with the understanding that fewer nucleotide differences between organisms means they are more closely related.
You can do this type of activity over a couple of days (depending on time). Then, you can begin to show them trees that become gradually more complex. Because the kids will have constructed a tree and now how it is constructed, they will have a much easier time interpreting larger trees.


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What are the functions of disulphide bonds?
What are the functions of disulphide bonds between amino acids in proteins or peptides?

Disulfide bonds form between different amino acids of a protein chain and the help to stabilize and maintain a distinct three dimensional form. In principle this looks like this (pipcture from the Wikipedia page on Disulfide bonds):

Disulphide bonds (or bridges) can also hold different subunits of larger protein complexes together, one example for this would be antibodies. Here the light and the heavy chains are connected by disulfide bonds, they also play a role for maintaining the structure of the single protein chains (image from here):

Disulphide bonds occur in proteins, not amino acids, although they involve a covalent bond between two amino acids (both cysteine).
The received wisdom is that disulphides are used as extra stabilisation of the structure of proteins which are secreted, or which have an extracellular domain. It's important to get hold of the idea that they do not occur in the cytoplasm, but are only formed in proteins which pass through the secretory pathway: they are formed in the endoplasmic reticulum (ER), and there are resident ER proteins (protein disulphide isomerases) whose function is to assist in their formation.
Classical examples of disulphide-bonded proteins are insulin (where the A and B chains are linked by disulphides) and immunoglobulin G where each Ig domain has an intradomain disulphide, and where the heavy chains are linked by disulphides. There are, of course, many others.
Cells also contain the tripeptide glutathione which includes a cysteine residue. the ratio of oxidised (disulphide bonded dimers) to reduced (monomers) glutathione helps to set the redox state of the cytoplasm and the lumen of the endoplasmic reticulum.


text:
Why is brown fat brown?
I read in Tortora and Derrickson Anatomy and Physiology that :

Another type, called brown adipose tissue obtains its darker color
  from a very rich blood supply , along with numerous pigmented
  mitochondria that participate in aerobic cellular respiration.

From Wikipedia :

...brown adipocytes contain numerous smaller droplets and a much
  higher number of (iron-containing) mitochondria, which make it brown.

The conclusion seems to be that there should be some iron containing pigment in the mitochondria of  BAT which (along with a rich blood supply) gives brown colour to the BAT.
What is the brown pigment present in the mitochondria of BAT ? Is it the uncoupler protein - thermogenin ?

You quote it yourself: The adipocytes contain higher numbers of mitchondria (which contain iron) and this makes the cells look brown. See red blood cells for example. The high iron content makes the color in both cases.

@Chris But what is the iron doing in mitochondria? Cofactor to some enzyme present in excessive amounts ?

There are different functions: Mitochondria store iron, then it is part of enzymes in the form of iron-sulphur complexes and is also important in the heme synthesis. See this paper if you want to got into the details.

Brown fat is so-called because it contains a large number of mitochondria, certainly greater than its white fat counterpart. The reason for the excess in mitochondria is to participate in thermogenesis (incidentally, brown fat is also called thermogenic adipose tissue). Nearly all mammals have brown fat (excluding pigs), especially those that hibernate. Brown fat require larger numbers of mitochondria in order for the fat to be used in beta oxidation (which is carried out directly by mitochondria), and subsequently produces heat via the electron transport chain. This also requires greater access to oxygen from the blood, and as a result, greater capillary density also darkens the appearance of the gross tissue. Mitochondria themselves are dark because of the iron content; vitamins B2, B6 and B12; as well as the pigmented flavins (FADx).

I just wanted to add that newborns have more brown fat than adults because this allows them to generate more heat. It is very important for newborns to generate more heat because their volume/surface ratio is smaller than that of adults, and so, their energy exchange would be unbalanced, if not for this brown fat that supplies the "offset".


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Can someone who is color blind recover color vision by surgical means?
I am currently studying color blindness, and there is no medicine that can help it. Is it possible nonetheless for someone who is color blind to have their eyes restored to normal color vision by replacing the patient's eyes with donor eyes? Please explain any answer. Thanks!

No this is not currently possible as eye replacement surgery is not possible.
Colour blindness is either congenital genetic, such as your X linked forms, or due to a degenerative condition such as retinitis pigmentosa. It can also be acquired through retinal damage or brain injury such as stroke effecting specific areas of the visual cortex.
One of the major problems in restoring colour vision would be that the brain itself may not have the required structure to interpret the signals. The visual cortex is 'patterned' as we develop beginning inside the womb and continuing as a baby. During this process neurological connections in the visual cortex are stimulated so that we develop the necessary networks to interpret the signals from our eyes. If we lack the input of our eyes the brain conducts something called neural pruning where the unused neural connections are destroyed never to be regrown. Therefore if you lack visual stimulus for colour you prune these connections. If we were to somehow replace this colour stimulus later our brains would not be able to interpret it. In a somewhat similar circumstance to this it has been found with individuals who are born with congenital cataracts. If they have their cataracts fixed later in life having spent their childhood blind, despite being able to 'see' they cannot interpret the images they receive.
In individuals who loose there colour due to degenration of the retina, if we were able to repair the retina, through stem cell or transplant therapy then perhaps colour vision would return.
An individual who lost colour vision due to brain injury cannot have their colour vision returned as we cannot repair such injuries.

I agree with this answer but I'm not so sure people whose vision was restored would not be able to use the some of the information. Such a hypothetical treatment would be very similar to deaf people getting cochlear implants. The chance of success with these decreases with every increase in year but it's not zero at any age: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518393/

@mimat I guess it depends a lot on the time in which sensory loss happened. If it happened during early development, neural pruning would be more advanced than if it happened during adulthood.

Most forms of color blindness are caused by defects in the eyes, not the brain.  Usually the receptors in they eye that are supposed to be sensitive to one fraction of the visible spectrum don't work properly.  So yes, replacing the whole eye (I don't know if that's possible now) would in theory fix those forms of color blindness, thought it's likely that the brain would be confused getting a new kind of signal that it had never received before.


text:
Is life in a supercritical fluid possible?
Someone claimed that the dinosaurs could only live because back then athmospheric density was around 650 kg/m³, providing some buyoncy, this claim is checked on Skeptics SE. The claim itself is beside the point now. A simple calculation shows us that an atmsphere with this density would be supercritical in underwise normal conditions, the pressure would be increased by a factor of roughly 520. See my answer to the skeptics question for a bit more explanation. I would say that a supercritical air atmosphere rules out life for several reasons:

The high effusity of the fluid may mean that cell membranes don't work
Proteins fold differently under high pressure, requiring specific adaptions
If the partial pressure of oxygen is increased proportionally, the atmosphere is highly toxic
If the partial pressure of oxygen remains at current levels, it is a trace gas and reactions relying on oxygen may run into kinetic problems (There may be a sweet spot between the last two issues)

Anyway, those are just my hunches, I never heard of experiments about life in supercritical fluids and I'm no biologist so my hunches may be totally wrong. My question is: Can we rule out life in supercritical fluids; if not can we rule out air breathing, multi cellular animal life?
Or has any life been shown to thrive in a supercritical fluid?
To stress again, the part with buoyant dinosaurs was given for background (and amusement), I'm only asking here to check my hunch that suprecriticality rules out life.


text:
Could light/occasional smoking strengthen the lungs?
Here's my thought process, correct me where I'm wrong.  It seems the human body has thresholds.
Examples: You lift too much weight, and the muscles and tendons risk serious injury, but otherwise they tend to rebuild stronger to handle more weight.  Too much sun can lead to sunburn or worse, but moderate UVB exposure can lead to melanogenesis and increase protection to UV damage.
Do the lungs behave in a similar manner where a small amount of smoking might actually strengthen your lungs before reaching the threshold where you're causing severe damage?  My guess is the answer is "probably/somewhat" but that there haven't been any studies since it'd be difficult to analyze and quantify, but maybe somebody has an answer based on theory.

From your examples only the first is really true. Exercise leads to better physical abilities (within some boundaries).
Sunlight on the other hand is always potentially dangerous, depending on the dose. But the damages accumulate over the years which finally lead to the so called senile lentigos (others call them aging spots) occuring in sun exposed skin from the age of 50.
And the same is true for cigarette smoke. Here you expose yourself to a nasty cocktail of potentially harmful to cancerogenous substances (tar, polycyclic aromatic hydrocarbons, benzene, nicotine and much more). These do potential harm to your lungs depending on the dose (meaning how many cigarettes you smoke a day), but there is nothing like a harmless amount. Your lungs will eventually recover from this (tar takes the longest to be removed), but it is definitely not good.

Out of the womb, a person might be extremely prone to sunburn, but wouldn't 15 years of moderate exposure increase the overexposure threshold?  Maybe my usage of the word "strengthen" is inappropriate, I mean more along the lines of increasing the threshold until damage.  From my admittedly limited perspective, the human body seems to increase it's ability to withstand when exposed to harm, so long as the harmful factors are not prolonged and recovery time is allowed.

Sun exposure is difficult, since we need it to some degree to produce vitamin D. Nevertheless it can be pretty harmful, even in "small doses". The other problem are the harmful factors itself. There are a lot of things where the body can adapt and recover, like for drinking alcohol (which is also cytotoxic). For other substances which are cancerogenous this is not true. There every hit can be the fatal one which develops into a malignancy. Of course the dose plays a role here, too. But this is the reason why I can't consider smoking harmless.


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Needing help in order to infer the statistical hypothesis tests performed in an old paper
I am in great need of help in order to infer the statistical hypothesis tests performed in an old paper. However I need to make some reasonable guesses only from the abstract of the paper since the original text is in chinese which i can not understand (after extensive search i was also unable to find the original text even in chinese)
The title of the paper is:
“Detection of sister chromatic exchange in workers exposed to coal tar pitch and to coke oven volatiles"
The abstract of the paper (which was published in 1998 is the following):
In order to know the changes of genetic toxicological effects on workers occupationally exposed to polycyclic aromatic hydrocarbons (PAHs), sister chromatic exchange(SCE) was detected by the methods of peripheral lymphocyte culture in 23 workers exposed to coal tar pitch (CTP) and in 19 workers exposed to coke oven volatiles (COV) and 12 normal controls. The results suggested that the SCE in occupational workers was significantly higher than that in controls (11.31 vs 6.37, P < 0.001). The SCE in workers exposed to CTP and to COV was higher than that of control (10.27 and 12.58 vs 6.37) respectively. In workers exposed to CTP and COV, there were no differences of SCE for smokers and nonsmokers (P > 0.05). It is indicated that CTP and COV caused strong genetic toxicity and injury to chromosome.
In your opinion how do you think that the above reasarch was organized
For example: a) What types of statistical hypothesis testing was performed by the reasearchers b) What kind of data was collected and used for each statistical hypothesis test c) What methods were employed for the each hypothesis test ?

What does the methods section of the paper say? Which paper is this exactly?

The name of the paper is "Detection of sister chromatic exchange in workers exposed to coal tar pitch and to coke oven volatiles"... I have searched the text but only the abstract is available in pubmed (although i log in using my university acccount). Also the original text is supposed to be written in chinese.

This is a bit hard to say because the original paper in chinese.

Well at least I need your opinions... they would be rather helpfull... What do you think are the most possiblescenarios...

I will write about it a bit later today. Right now my time is a bit scarce.

Someone else can probably elaborate on how "peripheral lymphocyte culture" works, but this is what the statistical results suggest to me:

The results suggested that the SCE in occupational workers was significantly higher than that in controls (11.31 vs 6.37, P < 0.001).

This is a two-sample t-test. Occupational workers were pooled into one group and the mean value of SCE for those workers (11.31) was compared to controls (6.37). The null hypothesis is that the means are not different. They reject the null hypothesis. It would be nice if they included the standard errors for the means, so that you would have a sense for the amount of variation within the groups.

The SCE in workers exposed to CTP and to COV was higher than that of control (10.27 and 12.58 vs 6.37) respectively.

This is likely an ANOVA with three groups (CTP, COV, and control). This test is kind of redundant with the first test, since the appropriate post-hoc test will tell you that CTP and COV are both significantly higher than control. But since they report only one P-value, then this is probably the overall F-test for the ANOVA. So all they can say with this test is "at least one group is different." You don't know if, for example, CTP and COV are different from one another. It's not clear from the text that they did a posthoc test (Tukey's HSD, for example), but I doubt it.

In workers exposed to CTP and COV, there were no differences of SCE for smokers and nonsmokers (P > 0.05).

Considering only the occupational groups, the sample is divided into smokers and non-smokers. There was no significant difference in mean SCE between the groups. This is a two-sample t-test like the first one. The null hypothesis is that the means are not different. They fail to reject the null hypothesis.
It's also possible (but impossible to determine from the abstract alone) that they did a single, larger multiple regression. Properly coded, they would be able to, at once, test for occupational vs. control, CTP vs. COV vs. control, and smoker vs. non-smoker. It would be pretty dicey with such a small sample, so they probably didn't take that approach.
Why do we perform t-tests?
The null hypothesis of a two-sample t-test is that the means of two groups are not different from one another.
How do we know that our data follows a normal distribution? Shouldn't we perform tests in order to decide whether our data follows normal distribution and is of equal variance?
Assumptions of t-tests include normal distributions within groups and equal variance between groups. These should be checked prior to carrying out the test. We can assume that the authors did these tests, but they are very rarely reported.
In case the criteria needed to perform a t-test are not fulfilled should we choose a non parametric equivalent?
Non-parametric alternatives should be considered when the assumptions are not met. That being said, t-tests are pretty robust to violations of these assumptions.
Also the anova mentioned in the answer above is an N-way anova?
ANOVA in general is a test of equality among N groups. So you could think of a t-test as just a special kind of ANOVA on two groups (indeed, they are numerically equal).

Peripheral lymphocyte culture means they draw blood samples from the persons and isolate lymphocytes from it which they put into cell culture to grow them for later analysis. The peripheral means that these are lymphocytes which are in the periphery, compared to those who are in lymphoid tissues (like spleen or lymph nodes) or in the bone marrow. For deciding which statistical test to use, I found the trre image in this thread useful.

@kmm Thank you for your answer, it is really usefull but i have the following questions: Why do we perfrom ttests? How do we know that our data follows  a normal distribution ? Shouldn't we perform tests in order to decide whether our data follows normal distribution and is of equal variance ? In case the criteria needed to perform ttest are not fullfilled should we choose a non parametric equivalent ? Also the anova mentioned in the answer above is an N-way anova ??

@obelix This site isn't really set up or intended for extensive discussion. I've added answers to your questions above. This is really information that is covered in any introductory statistics textbook. There is a free, very good textbook at https://sites.google.com/site/ncstats/


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MAPK signalling pathway initial conditions
I would like to know the initial conditions and locations of the chemical reagents in the MAPK cascasde.
I'm going to plug this information into a reaction diffusion simulation.
From reading various papers I have gleaned the following:
[MKKK]total = 100nm; [MKK]total = 300nm; [MAPK]total = 300nm

MKKK]total = [MKKK] + [MKKK-P]
[MKK]total = [MKK] + [MKK-P] + [MKK-PP]
[MAPK]total = [MAPK] + [MAPK-P] + [MAPK-PP]

Ras-GTP seems to have an initial concentration of 30 nM and seems to start at the nucleus.

ppMAPK seems to have an initial concentration of 0.

I can't figure out where the rest of the reagents start and what thier concentrations are. People always seem to miss this out from their work...
Thanks

This is probably because it is not important for most people. I did work in this field and it was interesting that proof that the signal came down the cascade (and via which) but not how the concentration were.

@Chris what do you advise doing? Should I make the other reagents equally distributed throughout the system? Should I just make up concentrations?


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How can stem cells be counted in body?
In the study of supercentenarian woman here, it was found that all her blood cells are formed from only two stem cells (ancestor stem cells).
How scientists can distinguish cell ancestors?
Aren't all genes of one body identical?
If there are somatic mutations, which are increasing while lifetime, then how they could know, that there are more ancestor stem cells in childhood? Shouldn't it be less mutations and cell lines less distinguishable?
May be stem cells only can be counted in oldness.
Then how is it possible to know, that there are 20000 of stem cells at birth?


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Is it firmly established, that mutations are sufficient for cancer?
It is evident for scientists, that all cancer cells have some mutated genes. Say mutations in general.
But this evidence means necessary condition.
But what about sufficient conditions?
Is it possible, that mutations are necessary but insufficient for cancer?
I.e. may be other factors exist, which are probably more important?

About what other factors are you thinking?

Does not matter, but I can imagine some.

Can you tell me the ones you have in mind?

For example, I speculate, that immune tolerance is controlled by suppressor cells, that are antigen specific. I.e. for each tissue, which is not causing immune response, there is a specific suppressor population. If extra suppressors appear, then immune system become tolerant for cancer. If mutation occurs after that, then cancer develops. Contrary: if kill specific suppressor population, cancer will regress.

@Chris, so what can you say?

Acquiring mutations (more than one) are the necessary (and sufficient) steps on the way to cancer. The current opinion is that cells need "multiple hits" to fully transform into a cancer cell. It is also called the Knudson hypothesis, the original paper is here.
For example melanocytes (the pigment cells in the body) which acquire the activating BRAF V600E mutation (which is an important step in getting a melanoma cell, this mutation is found in about 70% of all melanoma) is not enough to transform the cell. Other mutations are necessary to do this.
Among the things important for cells to become malignant are to escape the apoptosis mechanisms of the cells and also the immune system. Both are linked to the mutation, inactivation or epigenetic silencing of genes, so I would say genes are the key to cancer.
For further readings these two articles should be interesting:

Are oncogenes sufficient to cause human cancer?
Significance of multiple mutations in cancer

I was thinking of this, and have more questions...

See next question pls http://biology.stackexchange.com/questions/17208/why-cancer-mutations-do-accumulate-sequentially


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Is process, opposite for growth, known for mammals?
Every animal born small, then grow larger and larger.
The same is true for parts of the animal bodies.
Is there any cases, when body or part of the body diminishes in size and mass, while staying healthy?

Do any example of structure existing in insect's larvaes but not in adults would answer your question? What about the thin skin that human baby have between their fingers and get lost later?

In humans at least (I'm not sure about other mammals), the thymus grown until puberty and then shrinks gradually, a process called involution. I'm not sure if this meets your criteria. The thymus remains "healthy," but it's function greatly diminishes over time.

Not a mammal, but the paradoxical frog (Pseudis paradoxa) starts life as a small tadpole that grows into a large tadpole and ends up as a much smaller frog. There are bound to be other examples of this phenomenon, but this is the one that immediately sprang to mind.


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What species is this worm?
I was at the park lying on the grass and its the third time I have seen them, I used to think they were parasites when I was like 7. It is the very small brown worm on the green leaf. It moves by squiggling. It comes in different colors but same size.
http://postimg.org/image/ea3x2nw95/
http://postimg.org/image/zfawh9pr1/

Location, time of year, and description of the habitat/vegitation are going to help.

Location: local park in Miami. Also found in trees as one spontaneously fell on my finger and squiggled on it mildly fast when I was 7, in Honduras. Time of year is both summertime/late spring. Lots of leaves

"Brown string" and "on the green leaf" are of little help for me at least: where is it?

to be honest, I cant find it.. edit the picture on paint and add a red circle around the worm.

And please use the add image button. Do not use third party sites. This one actually is blocked in my lab for some reason (Not your fault actually. My sysadmin needs to be boiled in hot oil. Nonetheless it is better to use the approved image uploader)

For me it looks like an inchworms which are the larvae of geometer moth or Geometridae.
By your picture it is almost impossible to see of which type it is.
I took picture of one in Switzerland (but likely not the same as yours).

Full resolution here: https://flic.kr/p/utFsiU

Is this what you mean?

It's pretty hard to tell from this photo, and I'm no entemologist, but to me, it looks like it may be a wireworm, a larvae of a click beetle. This is a diverse group, so I think it would be pretty difficult to give a specific identification. (More images)

It was attached to the edge of the leaf. It's not on a leaf.


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Why cancer mutations do accumulate sequentially?
According to Knudson hypothesis, cancer mutations accumulate in order. Statistics says, that cancer probability increases as sixth order of age, which may mean six consequential steps to cancer.
But, mutations are random in nature. There is no apparent cause, why mutations ABCDEF can't occur in reverse order, i.e. FEDCBA and any other possible orders.
If unordered, any number of required mutations should cause flat age dependency.
Hence, something is ordering these mutations, i.e. making mutation B impossible until A occurs and so on.
What is it?
UPDATE
Cancer incidence dependency on age:

The graph is not linear, which means that mutations are not independent.
UPDATE 2
Let's regard some cancer, which requires 6 mutations. It's incidence distribution should be like shown above.
Now suppose we knew the distribution of all precancer stages, i.e. the distribution of people with 1, 2, 3 and so on mutations. These distributions should look similar to final distribution

Now let's regard only one (first) mutation.
Why is it's incidence age dependent?
Mutations are random. They should not depend on age. If they do depend on age, then they are not random. If "they" are not random, then "they" are not mutations.
Or, in other words, the cause of progression is not a mutation itself.
Isn't it true?

if this is true - and it might not be - i'd say its possible that mutations out of order are simply not viable and disappear from the cell population. cancer is a fault in cell division so it could be the case that most oncogene mutations are selectively removed.

I can't imagine how malignant mutations can be viable by one but not viable in sequence (and, finally, fatal if 6).

there are cellular mechanisms to kill badly behaving cells.  i tend to agree with you - i doubt the sequence is a rigorous set that must be followed exactly in some order.

This is a very broad topic that deserves an entire book. I would like to add to the given answers that not all the mutations occur sequentially.
This is the case of chromothripsis and similar massive reshuffling events that occur in around 2-5% of all cancers.

The sequence of mutations is important. Some mutations may allow other mutations to be not deleterious to the cell. For example, p53 loss will help oncogenic RAS mutations. The latter mutations will otherwise cause senescence response. Also, epigenetic changes, like p16 inactivation, can be a precursor that may allow oncogenic mutations to be selected. Thus the order of mutations is highly important, and non-genetic events preceding this order is also important. Wonder if there is literature on rate of mutations as a cell ages. Because if mutation rate increases, then that could also explain t

TL;DR:

A sixth order probability curve of cancer does not mean six steps. The order of the curve has nothing to do with the number or sequence of mutations.
Causes why ABCD could be more likely than DABC exist and have been extensively studied
Repair and control ("defence") mechanisms are what does the 'ordering' of steps by selecting for mutations which can circumvent them

The sigmoidal shape of the curve thus reflects the slow accumulation of "defence"-damaging mutations, which increase their own probability and thus the slope of the curve. I don't know if the slight decrease in slope towards the end reflects a real limit to the incidence of cancers, or if it's an issue related to the data, its availability or the way it is gathered (but has no basis in substance i.e. there isn't actually a limit).
To elaborate:
There are many biological factors which play into helping you understand the problem you are wondering about, and the fact that different cancers work differently does not make it easier. I would highly recommend that you check out Hallmarks of Cancer, the Wikipedia article also cites the interesting original publication. Basically, certain principles underly all cancers, but different cancers have different tendencies to develop certain hallmarks in a particular order.
Randomness of mutations:
Mutations are not random. The nature of DNA sequences affects their susceptibility to DNA lesions, i.e. damage caused by chemical processes such as a nucleotide losing its base, dimerisation of thymidine, single or double strand breaks and so on. Lesions occur all the time, so there are mechanisms in place to fix all types of DNA lesions. Occasionally however, the circumstances will permit e.g. two lesions to coincide or the repair process itself to make an error, which then leads to a permanent change of the DNA sequence that cannot be fixed anymore because the original sequence has been lost. This is a mutation, and mutations are also not random because the nature of DNA sequences affects the chancefor them to incur lesions that cannot be repaired.
Hence, one reason why certain mutations occur more frequently than others is because they are actually more likely to occur. But this isn't the main reason.
Cell self-control
There are higher levels of control than DNA repair. Various mechanisms in the cell exist to detect malfunctioning proteins (due to mutations in their gene) and degrade them - though sometimes malfunctioning proteins can still escape these mechanisms. Even in this case, there is an additional safety layer created by various mechanisms which lead a cell to kill itself (apoptosis). These are triggered for example if excessive DNA damage is detected, or if the cell-internal signals for and against proliferation are conflicting.
Sequential accumulation of mutations
The result of repair and control mechanisms (which I will now call "defence mechanisms") is on the one hand that we are far more resistant to mutations than we would be without them. On the other hand however, they create selection for mutations which are not affected by them.
This is where multi-hit models of cancer come from. A "first hit", "enabling mutation" or whatever you want to call it would be a mutation which itself is not affected by defence mechanisms - and simultaneously impairs the defence against other mutation(s). The "second hit", "initiating mutation",... would be a mutation which causes cancerous cell behaviour, but would be eliminated by a defence mechanism without the first hit.
This means that mutations do not always occur in the same sequence but rather, they occur in all sequences and sequences other than those that we find in cancer cells are eliminated.
Note that not all cancers have several mutations or a sequence. For example, chronic myeloid leukaemia (CML, a blood cancer) in the vast majority of cases is caused by a translocation from chromosome 19 to chromosome 22 which results in the famous Philadelphia chromosome and produces the BCR-ABL fusion gene. This single mutation is sufficient to cause CML.
Age-dependency of mutations:
Mutations can affect all parts of a cell's machinery, including the lesion repair mechanisms. This means that throughout its life time, a cell can (and will) accumulate mutations which increase the likelihood of further mutations. Mature cells usually have short life spans and mutations to their DNA repair machinery die with them relatively soon (days or weeks). However, pluripotent stem cells (PSC) in the tissues are just as likely to develop these mutations as mature cells - and PSCs are the ones which renew the tissue throughout life by differentiating into mature cells.
Thus, a mutation in a PSC remains for life, and the longer you live, the higher the chance that one mutation will affect the chance for gaining further mutations. This is why for all cancer types, the risk to develop them increases with age (though there are a few which are most likely at young age!)

Mutations occur indeed randomly. Most of them are either repaired or the cells go either into senescence or apoptosis and will cause no harm. Some mutations are harmless while others are among the ones which can cause cancer.
These genes, which are often mutated in cancers are called oncogenes and they are either mutated (permanently activated or inactivated) or misregulated (up- or downregulated, amplified etc.) in many cancers. These are preferrably genes which are involved in the regulation of cell cycle (which is usually halted if cells acquire mutations, something that the cell has to overcome), growth, division, differentiation and also apoptosis (genes which are regulating apoptosis are very often affected).
These mutation doesn't have to occur in a certain order, they need to overcome some "threshold" to transform the cell. During this whole process the tanforming cell has to escape the checks of the body which eliminates these cells.

Sorry, didn't understand. How threshold makes power dependence on age? If we observe 6th power, then we need 6 thresholds.

I am a bit unsure about six necessary mutations. This is something he analysed for retinoblastoma cells and it may not be true for other cancer types. The idea that you need more than one mutation on the other hand is widely accepted as far as I know.

But any graph of any cancer incidence is not linear. While any number of required random mutations would give flat graph. For example, if we require 3 mutations with probabilities of P1, P2 and P3 respectively, then graph will be P(t) = P1P2P3 = const. I.e. the probability that required 3 mutations occur simultaneously. To have curved plot, we need that mutations be not independent.

The question here is how you see the term dependent. Are they dependent in a way that they need to occur in a certain order? Not to my knowledge. Are they dependent that they happen in a number of oncogenes? This is something I would answer with yes. This and this links should be interesting.

ok I agree, that mutations should not appear in one sequence, but they should appear by one. Why? See my update 2 pls

I think this is a semantic misunderstanding. Her link says that incidence accumulates as the sixth power of age (i.e., a 6th order polynomial describes the relationship). This has nothing to do with the number of mutations, much less the order. It is a misunderstanding of the idea of sixth power.

Maybe your question is essentially semantic.
You have I think misinterpreted the phrase "sixth order." A sixth order* polynomial is one of the form $p = k_6 x^6 + k_5x^5+k_4x^4+k_3x^3+k_2x^2+k_1x +k_0.$ The $k_i$ are constants.
The graph caption in the first link in your post [Nordling] says that cancer mortality increases as the sixth power of age. You refer to this mathematical modeling idea in your question. This has nothing to do with the number of mutations or the order in which they occur. It simply means the trend can be modeled with a sixth degree polynomial.
In the case of your graph something like $y = k\cdot x^6 + 2000$ for an appropriate value of k gives an idea.

Knudson's hypothesis, also known as the "multiple hit hypothesis," says nothing about the order in which mutations occur.
Edit: The word 'random' as applied to mutations (and almost everything else), while still in use, may be incorrect and I removed it from this answer.
*The reference in the linked article uses the term "power." The term "order" in this context is a slight abuse of language. The correct term would be "degree," as in, a "sixth degree polynomial." Order is related to the highest degree of a set of polynomials spanning a vector space, not the topic here.

That's what I think, too. Thanks for pointing it out so clearly.

The ordering is due to how the most dangerous mutations knock out tumor-suppressing genes.
Assuming that mutations are random and uniformly distributed, most random bad mutations will be caught and prompt DNA repair or apoptosis. The best way for a mutation to avoid being caught is to disable DNA repair or tumor-suppressing genes. An obvious no-brainer example would be a nonsense mutation in TP53. After that, further mutations will quickly follow and bad mutations that would have previously been caught are now allowed to slip through.
The 2nd other prominent source of cancerous mutations are malfunctions in cell growth/migration signaling, although the most dangerous forms of these also require tumor-suppressing genes to be disabled first.


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Study case of the inheritance system of Oenothera
I've been told some interesting facts about oenothera. Apparently in this species some lineages have been through some translocations and in results to these translocations and in consequence, some chromosomes are inherited exclusively through the female function while some other chromosomes are inherited only through the male function.
Can you please provide a summary description of how things work in this species concerning the meiosis, the haplo-diplontic life cycle and the recombination?

I would recommend looking at this paper, and in particular the section "A SHORT INTRODUCTION TO OENOTHERA GENETICS":

The genetics of Oenothera is a genetics of entire haploid genomes (Renner complexes), which inherit as single units and are entitled with names such as hjohansen, Galbicans, or Gflavens (for terminology, see materials and methods). All loci of a Renner complex are in linkage disequilibrium.

Figure 1 from that paper shows what that looks like in meiosis, in terms of its impact on chromosome pairing- basically chromosome pairing forms rings of chromosomes linked by translocations.

Figure 1.
Additionally, it appears that plastid inheritance is biparental to some extent. These also contain pollen-lethal factors related to autosomes, such that cytonuclear incompatibilities kill pollen recombinants between a Renner complex and plastids (eggs are unaffected, Figure 2, 3):

Consequently, the F1 generation is identical to the parental generation without segregation of traits, since chromosomes separate as a set without intermixing.

The set of plastids ("plastome") will then break down in the F2 such that assortment can happen.

Selfing of appropriate flowers ensures that only plastome I is inherited to the next generation. However, in F2 the nuclear genome splits into the progenies CC-I and AC-I...

Since the ring of 14 chromosomes should inhibit free segregation of individual chromosomes and practically homologous recombination between haploid genomes in the hybrid AC, the coding potential of the A and C genomes is not mixed and a seemingly unchanged, homozygous CC genotype, now associated with plastome I, occurs in F2.

Figure 2.

Figure 3.
So it's rather complex. Hopefully that sheds some light on it, but it's understandable if it's still confusing!


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Detecting food fraud
There's undoubtedly more than one way to do this, but if a DIY biologist were to attempt to detect food fraud (e.g. as done by students from Stanford University and Trinity School, Manhattan with respect to fish samples from markets and sushi restaurants), then what would be the minimum steps and equipment?
(I know barely anything about molecular genetics, but have been reading about DremelFuge, OpenPCR, and Blue Transilluminator, and wondered whether they - or things like them - might get such an investigator some of the way towards the goal above; and what else would be required.)

In principle this can be done at home. How familiar are you with PCR?

@Chris, I understand in outline what PCR is supposed to do, but not in detail; nor have I ever performed PCR myself.

I have described the general process below, but I don't think detailed protocols belong on this site. (But perhaps it would be OK to write them in tag-wikis?). Even with very detailed protocols, there is often quite a bit of expected knowledge that is not mentioned, though. The best solution is perhaps to get some hands-on training with someone knowledgable. That said, neither PCR nor gel electrophoresis is particularly difficult, so you might be able to do it without instruction, but expect quite a bit of blundering in the start!

There are several ways you could go about identifying species through DNA. If you want to do everything yourself, the simplest option in terms of equipment needed consists of evaluating fragment lengths observed during gel electrophoresis after amplifying specific DNA sequences using PCR.
If you are content with some outsourcing, you can also send DNA samples to a commercial company for sequence analysis.
A compromise between these options in terms of information obtained, is to do study Restriction Fragment Length Polymorphism (RFLP) by amplifying DNA fragments and using restriction enzymes to cut the fragments, before analyzing the fragmentation pattern using gel electrophoresis. To perform RFLP analysis, you would need to obtain restriction enzymes in addition to the chemicals mentioned below, and they can be a bit pricey.
The minimum equipment would consist of a PCR machine, one or more pipettes with matching pipette tips, a gel electrophoresis tray with power supply and a transilluminator (preferably blue-light/non-UV). A centrifuge is not strictly necessary, but can be useful for processing/filtering your DNA source.
Some chemicals will also be needed: Polymerase and dNTPs for the PCR reaction (or a pre-made "master mix" containing both), electrophoresis-grade agarose and running buffer for the electrophoresis, along with a DNA dye specific to the type of transilluminator (Usually UV or blue light). For a blue-light transilluminator, GelGreen is a suitable DNA dye. You will also want to use a "loading dye" to mix in your DNA sample before applying it to the electrophoresis gel. This can either be purchased or prepared yourself by mixing sugar and food coloring in water.
You need some form of heating to dissolve the agarose - a microwave oven is convenient for this, but take care to avoid over-heating, glass explosions or flash boiling. It is convenient but not strictly necessary to have some lab glassware. Preferably use a screw-top bottle to mix your agarose solution. Always leave the top off when heating bottles.
Photographic equipment can be also useful for documenting results of gel electrophoresis.
Finally, you will need single-stranded DNA oligomers (primers) specific to the DNA regions you want to amplify. DNA primers can be bought from a number of companies, but it varies how easy it is for non-affiliated individuals to order and make payments. Macrogen has been my choice: They both deliver DNA primers and perform DNA sequencing.
You may be interested in the following thread on the DIY Bio e-mail group: https://groups.google.com/forum/#!topic/diybio/cPzfEuiZH58
I have collected some of the primer sequences mentioned in the thread on a page on OpenWetware: http://openwetware.org/wiki/User:Jarle_Pahr/Meat

Thanks :) Maybe I just haven't read enough, but is there a DIY protocol that would allow the detection of material from a completely unexpected species? My current understanding is that one needs a PCR primer (or perhaps restriction enzyme) appropriate to each species one wishes to test for: e.g. the only way to detect, say, tuna fish in dodgy "beef" bolognese would be to use a primer suitable for amplifying tuna DNA fragments, but this would not detect haddock present in the same sample. Is there a DIY protocol that would detect the haddock without specifically testing for it?

This can in principle be done at least partly with DIY methods, by using PCR followed by gel electrophoresis. The DremelFuge, OpenPCR, and Blue Transilluminator would be the primary tools, along with pipettes, test tubes, autoclave (or equivalent), etc.
For a clear video demonstration of using PCR to amplify DNA from various samples, as well as a PDF containing the details of the protocol used, see www.dnabarcoding101.org. That procedure would be followed by using gel electrophoresis on a small portion of the amplified product, to check that the product appears to be of adequate quality for sequencing. If so, then the remaining portion of the product can be sent to a lab for sequencing.
Alternatively, by using a suitable primer for each species one wishes to test for, one could check for the presence of that species using PCR and gel electrophoresis alone.


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Trauma, blood loss and thirst
Back story.
Watched an episode of Arctic Air, (season three episode six), where they are practicing and hoping to become a licensed search and rescue airline.
Anyhow; two hikers gets attacked by a grizzly bear and whilst one get killed the other manages to throw himself off a cliff and ending up with his leg pinched under a rock. He also has big lacerations on his chest from the grizzly. Finally he manages to send a distress signal.
Though not licensed a team travels out to asses the situation. As they find the wounded climber they start to help. First they clean the lacerations by pouring alcohol over them, and then lay some bandages on top. After a while the injured man complains he is thirsty, and they give him water.

TLDR;/Question If I recall correctly one should not give water to a trauma patient. They can have internal bleeding and/or, as in this case big external wounds which likely has caused quite some blood loss.
Liquid will, IIRC, cause some bad effect on the re-production on blood, and might also affect existing blood.
Am I correct in this? If so; what happens and why should one not give liquid to the patient?
Guess there could be some situations where liquid is proper. E.g. patient has been laying in exposure to sun for N hours and dehydration might also cause ill effects... ? (Kidneys, blood-pressure, plasma?) But that might be a negative in any case if one suspect internal bleeding?

If you are satisfied with the answer, please do close the question by selecting it as the answer.

After some general research there are specifically 3 arguments that I came across that people give for supporting this particular theory.
1) somebody seriously injured might be given an anesthesia shot by the doctor or whoever that treats him first up for relief from the pain and distress. This would lead to relaxation of the stomach muscles and the contents of your stomach can travel up to your throat and into your lungs which would be fatal. Read about pulmonary aspiration.
2) the second case is if there is an injury to the gut or the GI tract, then providing water would be counter productive. A layman might not be able to assess the level of injury to someone just by sight.
3) the third is that giving water would increase blood pressure and (sometimes) apparently dilute the scars. This could also lead to chances where sutured wounds might reopen.
There are no real guidelines as to how much water can be given to an injured person. Depends on the situation or how much time he has been bleeding for and the kind of environment that he is subjected to like you pointed out. Some medics have recommended sucking on citrus fruits to prevent dehydration. Also, swabbing the patient all over the body with a cold compress can provide some relief and delay dehydration.
Guidelines for bleeding victims are here.

Thanks. I do not recall where I have it from, but believe it was some first aid course. IIRC the tutor also mentioned some ill effects by giving water but do not recall the reasoning behind it. Believe he also mentioned vomiting -> bad if e.g. neck injury. Your answer gives good pointers. I dug up this discussion, but they seem to be somewhat conflicting in their explanations. http://www.nairaland.com/1460146/dont-drink-water-bleeding-injury . Guess the peristalsis mentioned by Lagusta might have been what the tutor mentioned.

It's the first one.  A trauma patient will likely need an anaesthetic at some point so the aim is to keep them nil by mouth to avoid the risk of airway compromise caused by vomiting.  If they are desperate for water, the advice is small sips or being given an ice chip to suck