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Confused with gamete sorting problem
A man has the genotype AaBbCc, in other words he is heterozygous in three uncoupled loci on three different chromosomes. A, B and C are the dominant alleles while a, b and c are the recessive alleles.
1. How many gametes can he form?
The answer is 8 and I can see how you derive that by just manually writing each and every one down but what is the mathematical method to derive this? I tried permutations but none I came up with worked.
2. He has a child with a woman of the same genotype (AaBbCc) how many different genotypes can the offspring have?
Here the answer is 27. I'm not sure how they came to this conclusion either?
3. What is the probability that the offspring has the genotype AaBbCc?
This is about the time I start flipping tables because it seems to me that it's 1 out of 27. There are 27 different genotypes and this is ONE of them?!
But the answer is 1/8 as there's a 50% chance of Aa, Bb and Cc when mixing apparently so it becomes 1/2*1/2*1/2. Why isn't it just 1 of the possible genotypes?

Since there are 2 alleles of each gene and 3 different genes, 2EE3 = 8? Let's test this by making a table, for 1 gene there are two different kinds of gametes, so 2EE1 = 2, for 2 genes there are 4 different kinds of gametes (AB, Ab, aB, ab) so 2EE2 = 4, and you already did the calculation yourself for 3 genes, and 2EE3 =  8.

Why don't you try working it out yourself for 4 genes and see if you come up with 16 different kinds of gametes?

Two words: Punnett Square. In this case for a trihybrid cross:

That is a Bernoulli coin-flipping probability. If you are flipping a true coin three times in a row, how often will you get three heads in a row? 1/8? All the events are independent, right? what about the Punnett square? Does it give the same result somehow?

Here is the answer worked out for you.


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X-recessive disorder pedigree confusing me

This is a pedigree of a family in which bleeder disease, an x-recessive disease, is present. I am asked which marker, A or B, the disease is linked to.
I've asked about this type of problem before: X-recessive disorders and genetic markers
The solution there was the fact that the families were unrelated so the disease being linked with a marker in one family did not correspond to the disease being linked to the same marker in another family.
The answer to this problem is "A". However this is ONE family and there are males in this family with the A marker on their only X-chromosomes who are unaffected and women with two A markers who are also unaffected. How would you explain that? They have the marker for the disease on both alleles but not the disease?

Look at my answer in this post http://biology.stackexchange.com/questions/30885/understanding-recombination-scoring-in-family-pedigrees/30887#30887. That should answer why some males can carry the A marker and not get the disease.

So I:1 is a recombinant and the sick allele is the A allele from the mom?

Your account should be closed for asking several homework questions every single day.

Remember: A and B are genetic markers that might be linked to the disease gene. Neither A nor B are actually the hemophilia disease mutation (or gene), A or B are proxies, or substitutes for the mutation in the disease gene.
Since it is an X-linked recessive, it is only the Mother's two X chromosomes that are candidates.  You can completely ignore the Father's copy of X that also happens to carry the A marker.
In the F1 generation every male who received the copy of the Mother's X marked with A died, and every male who received her X marked with B survived. Therefore her X marked with A is linked to the mutation.
Those other AA females are either heterozygotes, or outsiders who married into the family. The outsiders do not carry the mutation.
Perhaps your confusion is due in part to the fact that some key facts are not explicit in the pedigree diagram from your instructor's course materials? Try drawing the various genotypes out like this:

source: Stack Exchange

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Why do surface mole tunnels follow directly below the electric fenceline
I have electric fencing enclosing five acres, and moles always seem to tunnel in a straight line just under the electric fence - are they following a force field? Can that be?

Interesting, they do not follow under the non-charged fences. Now to work out a way to tap this energy-field following and turn it into a death trap! There must be an electrical engineer who can figure out a 'better trap' in this situation. My place has hundreds of destructive moles and I would love to get rid of them all!

Rumor has it that some moles, such as the star nosed mole, have electroreceptors in their nose.

In 1993, Gould and colleagues proposed that the star-like proboscis had electroreceptors and that the mole was therefore able to sense the electrical field of its prey[24] prior to mechanical inspection by its appendages. Through behavioral experiments, they demonstrated that moles preferred an artificial worm with the simulated electrical field of a live earthworm to an identical arrangement without the electrical field.

They may thus be sensing the electrical field of the fence, and interpreting it as a nearby tasty worm.

This seems to suggest an experiment. Put up more fences, some hooked up to electricity, some without, to act as controls. See if the fences with power attract more moles than fences without. If possible, adjust the voltage to each fence to see if stronger electric fields attract more moles. I know your standard fence charger doesn't let you adjust the voltage easily though, so it might take some effort to do that.

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How do carrier RNAs increase yield in sequencing experiments?
I would like to know how carrier RNAs increase yield in RNA/DNA sequencing experiments. Is their main function in the precipitation steps of each protocol (i.e. small quantities are difficult to precipitate and the carrier RNAs add material), or do they have a role at other stages in the process as well?

What kind of sequencing methods and which step in the method are you talking about? In many cases, carrier is added to visualize precipitates and/or get efficient precipitation.

If you are adding phenol-chloroform extracted tRNA then that is a carrier for the precipitation steps. Some people use linear acrylamide for the same purpose.

Thank you for the information, but this does not answer my question. Are carrier RNAs used at other steps in preparation for sequencing?

I've used glycogen for this too.


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A free book/resource for learning genetics?
I took an undergrad class in genetics. I felt it was not too intensive and I do not feel prepared for grad school (if I can manage to get in.)
Does anyone know of a preferably free resource for learning genetics?
I know the field is very large, but I would like to be competent in the field, considering I also want to learn more about genomics as well. And I figure one must first have a fundamental understanding of either computer science or biology to be successful in genomics, both of which I lack.

MIT Open CourseWare?

"Not expensive" I understand, "free" doesn't make much sense: you can afford to attend a grad school, but not to buy a book? Really? Maybe that's really the case, but the odds are quite low.

@Lohoris        I said that I was thinking of grad school, if it was possible. Sometimes they give people "free rides" I heard if they are competent enough and desired enough. I doubt I fit into that category.

Doesn't matter: even if you hadn't to pay for the school at all, you would still have other expenses just to live. And if you can cover those, then you most likely can afford to buy a non-expensive book too.

@Lohoris           I guess your right, I just always like saving money though. I figure I would buy a book when I became a bit more competent.

@Lohoris: Different countries, different "grad schools". Here I am, doing my PhD and being paid (not a huge amount, but well enough to survive for sure) for teaching and working on research projects. This is how it can work in Germany. There is also stipends and whatnot.

As you said, the question is pretty broad. Genetics is a big gigantic field and it is quite hard to know what you are exactly looking for. If you could refine into one of the subfields (molecular genetics, population genetics, phylogenetics, etc..) it would be much easier to give you better advice. As you talk about both biology and bioinformatics, it might be worth to specify whether you are looking for learning more in fundamental genetics or learning more in the methodologies to analyse genetic data.
Principles of Genetics
You may want in an introductory class in genetics. Here is a course on MIT Open CourseWare, but it may be too easy for you.
Bioinformatics
You may want to take a bioinformatics course. There are so many bioinformatics course online that there is a wikipedia page to list them (there).
Side skills
Programming
You may just want to learn to code in R, Python, Perl or Shell script (to cite few examples). You'll find tons of beginner tutorial online.
Statistics
Or you might want to learn more about statistics. KhanAcademy has a very good (but very introductory) statistics class.

Great answer. Would add Perl in the side skills as it is massively used in genomics because very powerful for treating text-based data. Also understanding Linux and its command-line interface is a must-know.

@cagliari2005 Thanks! I edited the answer. One might want to add C++ eventually. I would have not thought about Perl as I personally don't use it.

I work at the Wellcome Trust Sanger Institute, one of the world's largest genomics centres. We do maintain a website for the public wanting to learn about genomics, but it might be a bit basic for you: YourGenome.org
You can get into this field without going through grad school:

learn at least one programming language (Python is probably the key one today; perl was everything 10 years ago but not much new is starting in that language now)
try getting involved in open source bioinformatics projects, such as the Global Alliance
apply for a support role in a genomics centre, such as working as a programmer within a research group, or in their IT support groups.  Genomics is a field you can learn on the job.

To give a background, I have also taken a intro level genomics course and enjoyed it. The coding was just a taste( "hello world" and the like) but my coding needs alot of more work. I was a comp sci major, but flunked out because my coding and understanding of proofs was not good enough. In the genomics course, I did a gene annotation project under the Genomics Education Partnership (http://gep.wustl.edu/curriculum/student_work) similar to the ones on that page. Is that relevant experience in genomics?

The Coursera Introduction to Genetics and Evolution is an excellent MOOC.
If I remember correctly it contains links chapters in the online version of Griffiths et al (i.e. deep links to this: http://www.ncbi.nlm.nih.gov/books/NBK21766/ )
There is also Introduction to Biology - The Secret of Life from EdX, it is not just genetics, it covers a lot of molecular biology and biochem too, but it is by far the best course of it's type I've ever taken, and I'd say you could jump in on the genetics and skip the biochem if that is your preference. The simulation "experiments" (e.g. breeding fruit flies) are superb.
If you want to get in to bioinformatics and you don't have strong programming skills then take a look at Algorithms, Biology, and Programming for Beginners. The same people also offer more advanced courses on Coursera too, if you have more programming experience. The course is language agnostic, but Python is really the main language in the field so I'd strongly suggest you do any dev work in that.


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Can plants live forever?
I know that some plants die for old age like a
lettuce. But there are trees like Baobabs or larger Ficus in the tropics of whom we don't know their age. And trees like spruce reaching 9950 years old, which die for environmental factors and not by age.
However, E.g. when we multiply vegetatively an olive or cacao tree, we use a fragment or clone from a unique individual passing the same genetic information, again and again.
Then, can these plants live forever?

See also: http://biology.stackexchange.com/questions/2055/do-trees-age-on-a-microscopic-level/ and http://biology.stackexchange.com/questions/7010/is-there-any-kind-of-immortality-in-plants?rq=1

The answers to these questions often boil down to "what do you mean by live forever?".
You've included vegetative cloning, so I infer that counts as one living organism for your purposes. In that case, the answer is absolutely.
Pando is at least 10 thousand years old and only getting larger. The Cavendish banana is about 150 years old, but produces at least 70 million tons of bananas yearly.
See here for other giant clones. Of particular interest is King's Lomatia, represented as a species by a single, sterile, individual. Fossilized triploid leaves are too old for carbon dating(at least 45 thousand years old), so it's essentially unknown how old it is.
I would be comfortable declaring Pando immortal, since it's way too big to be eaten, too resilient to burn down, and has already survived the middle and end(at least!) of an ice age. That just leaves (ha) disease and basically nothing else as possible threats.

Pando is actually thought to be ~80,000 years old.

Forever no. For thousands of years yes. And not only plants, other organisms have what is called biological immortality. Look here for some examples https://en.m.wikipedia.org/wiki/List_of_long-living_organisms


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How do we know that ammonites are a kind of cephalopod rather than another type of mollusc?
On a recent fossil hunting trip, I found a small fossil that an expert identified for me as an ammonite beak. He told me such fossils are not uncommon, but are not normally found with their parent shell due to the decay of the soft tissues holding the beak in place.
I know that under some unusual conditions, (i.e. the Burgess Shale) the soft tissues of animals can be preserved. And a quick google search reveals that there are rare belemnite fossils with their tentacles in place.
However I can find no reference to any ammonite fossils, nor any of the orthocone clades, with soft part preservation.
Shells of similar shape and structure are not unknown in other groups of mollusic (i.e gastropods). So: what characteristics of the shell make taxonomists sure that ammonites and orthocones are cephalopods rather than some other kind of mollusc?

Probably the presence of chambered shells with siphuncles, like present-day nautiloids.

I can find no reference to any ammonite fossils, nor any of the orthocone clades, with soft part preservation.
Soft–part preservation in heteromorph ammonites from the Cenomanian–Turonian Boundary Event (OAE 2) in north–west Germany
Soft-tissue preservation in the Middle Jurassic ammonite Cadoceras from Central Russia
And references therein for the handful of other ammonite soft part preservations

It really is mostly the siphuncle as @augurar mentioned. The siphuncle is present in modern ammonites, cuttlefish, and Spirula(a deep-sea squid with an internal chambered shell). It links shelled cephalopods neatly with other cephalopods(both extant and extinct) and distinguishes them from other shelled things like snails.

I am proud that I can answer your very, very good question!
You are right that the soft tissue of ammonites is very, very rare. But along with beaks (I believe you meant aptychi) you can find something with similar function called radula, which is (at least for devonian ammonoids) both in morphology and in number of elements identical to recent coleoids! Ammonites belong to ammonoids and this puts them closer to Coleoids than to Nautiloids. Nautiloids have very, very similar external shell, but with siphuncle going differently and many other details - one would expect them to be closely related.
It is now well known fact that ammonites are ammonoids. And that both ammonoids and coleoids evolved from bactrites.
For more info see:
Kröger, B., Vinther, J. & Fuchs, D. (2011): Cephalopod origin and evolution: A congruent picture emerging from fossils, development and molecules. ― Bioessays, 33, 602–613.

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Why is Benzylpenicillin better in Bacterial Meningitis than Amoxicillin?
Both are beta lactams.
However, benzylpenicillin, which is also called penicillin G i.e. narrow group antibiotic.
I have now in both the following as a mechanism of action

Binds to PBP in bacterial cell wall, causing deficit in the cell wall and causing cell death.

where I would like to differentiate clearly benzylpenicillin from amocillin.
How is benzylpenicillin better in bacterial meningitis than amoxicillin?

As the term meningitis is pretty broad, you should probably narrow this down to bacterial meningitis. There I would say the antibiotic is used to which the bacteria are sensitive.

@Chris I narrowed it. Specificity of course, but this is a general question. If you have those drugs, give their indications. I see bacterial meningitis in benzylpenicillin as indication, but not in amoxicillin. However, googling shows that amoxicillin has induced some meningitis but I do not know if it has been used in bacterial-meningitis.

Can you share your source that penicillin G is better than amoxicillin? You also stated in your initial revision that you have read about amoxicillin induced meningitis; that amoxicillin can induce aseptic meningitis seems like penicillin G has an advantage. http://m.cid.oxfordjournals.org/content/46/4/642.1.full

@canadiane No, this is a class note. Yes, it may be related to the fact that amoxicillin can even induce meningitis, probably because the increased resistance of the drug (wider spectrum than penicillin G but more resistance also). Good link! Make it an answer with a small summary, please.

Amoxicillin is just penicillin with a hydroxyl group off the ring and an extra amine group..

Their mechanisms of action are the same. Their ability to cross the blood-brain barrier are the same. They can both cause seizures.
Both are used to treat to meningitis. The selection of one over the other would be based on the sensitivity of the infecting organism, and the ability to cross the blood-brain barrier in inflamed meninges.
There are better drugs to treat meningitis.
Penetration of Drugs through the Blood-Cerebrospinal Fluid/Blood-Brain Barrier for Treatment of Central Nervous System Infections

Excellent idea to explain this by structure! Do both work in the similar analogue in Syphilis? Similarly, I think better drugs for that.

benzylpenicillin is actively transported into the brain via the oat‐3 transporters.  Amox is only poorly diffuses through the blood brain barrier. https://onlinelibrary.wiley.com/doi/full/10.1111/j.1471-4159.2009.06451.x


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How does amiodarone act as an alpha and beta blocker?
Amiodarone is potassium channel blocker but also voltage-gated Na+ channel blocker according to Pubchem. However, upon reading my notes I discovered

Amiodarone blocks potassium channels and block alpha and beta channels.

I think it must be alpha and beta receptors here, instead of channel. Pubchem proposes that there may beta-blocker-like properties in amiodarone.
However, its alpha-like properties are obscure to me as I cannot find any sources. How is amiodarone working as alpha and beta blocker?

Are your notes a good source of reliable information?

hello again masi, my interstitial fluid & pharmacology friend... yes, the adrenergic receptors work via 2nd messenger not as ion channels... also as I understand it a lot of the class III antiarrhythmics have properties of all the other classes and class II are beta-blocker... so this is confirmation of your source... like you I also have no information about alpha blockade as this is irrelevant to it's effects as an antiarrhythmic... my source is my memory from med school, even less reliable than your notes....

Amiodarone inhibits sodium, potassium and calcium currents. Its major antiarrhythmic properties are thought to be related to prolongation of the
action potential duration. Amiodarone also exerts an antiadrenergic
effect by non competitively inhibiting alpha- and beta-receptors (Ghuran & Camm, 2000).
Alpha blockers relax certain muscles and help small blood vessels remain open by antagonizing norepinephrine's tightening effects on the muscles in the walls of smaller arteries and veins, which improves blood flow and lowers blood pressure (Mayo Clinic). Beta blockers decrease the effects of epinephrine (adrenaline), reducing heart rate and reducing its force, thereby reducing blood pressure. Beta blockers also help blood vessels open up to improve blood flow (Mayo Clinic).
Alpha-adrenergic receptors and Beta-adrenergic receptors are G-protein coupled receptors (Wallukat, 2002). Hence, they do not form channels and your notes are incorrect. The ion currents are mediated by channels, though.
References
- Ghuran & Camm, J Clin Basic Cardiol (2000); 3: 206
- Wallukat, Herz (2002); 27(7): 683-90


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Can carnivores survive on a (processed) vegetarian diet? Why or why not?
There are many differences in for example the digestive system between carnivores, herbivores and omnivores.
It seems that in certain kinds of species adaptability with respect to diet is possible. What I have heard is that it is impossible for carnivores to survive on a non-meat diet.
Therefore I wanted to ask: Is it really impossible for a carnivore to survive on a vegetarian diet, even when the fruits/vegetables/plants are processed? I could see how their digestive tract would not allow for them to survive on grass, but what about certain kinds of nuts, mushrooms, or even processed plant based foods?
If it is impossible to survive on these diets, why?(With respect to either causes in their digestive system or substantial differences between meats and any type of vegetarian food.

I think this is too broad - "carnivores" is a large and loose group of species that range from obligate to facultative carnivores, and the answer to your question is likely to depend on exactly what species your are talking about.

Thank you very much for this specification. I am talking about species which are categorized under obligate carnivores.

This would be a great question here: http://area51.stackexchange.com/proposals/94068/veganism-vegetarianism

With arbitrarily broad meaning of "processed", yes. If absolutely nothing else, elemental purification and inorganic synthesis of something chemically resembling meat in nutrition is possible. Prohibitively expensive and stupid, yes, but possible. So then the question becomes exactly how much processing you need to do. Without clear bounds on that question and inadequate research on the metabolism of obligate carnivores, nothing closer than a broad stab at an answer makes sense. That said, here's a broad stab.
For instance, you'd probably need to synthesize vitamin D3, carnosine, DHA, and a handful of other things from plant extract, which is possible but difficult. Carnivores often have carnosine synthases, for instance. Cats have two distinct carnosine synthases. In terms of dietary sufficiency, that may or may not be enough. To be sure, you'd have to break it down to amino acids and build it back up again, essentially. Obligate carnivores are likely to have a number of other metabolic needs that aren't met with, for instance, pulverized soybeans. You're going to need at least one vat for fermenting raw amino acids into carnosine, and probably another for vitamin D3. Seawater microalgae contain lots of DHA, so that is probably something to look into. You could oversupplement alpha-linolenic acid instead of supplementing DHA, which might or might not work. There's not a lot of study into carnivore metabolism, so prepare to make some discoveries the hard way. Genetic studies can only take you so far, so don't try this on your favorite pet first.
In short: yes, you can raise carnivores on a diet made from plants and plant material. Rhetorical you, as in it is possible. It's probably not something you can do at home, even if you're wealthy.
(I'm assuming "feeding the vegetable matter to chickens" falls outside the domain of "processed" but it would be much easier than large-scale amino acid purification and fermentation.)

I would rephrase this to be "No, not without synthesizing certain essential nutrients not found in plants".  Otherwise you might as well say that you could also feed carnivores on a diet of "processed" air, water, and dirt.

Thank you very much for your answer. As I understood it is normal that carnosine is synthesized within animals by a natural process involving beta-alanine and histidine. (In humans the enzymes, which carnivores may lack, will decompose the carnosine into beta-alanine and histidine when taken into the mouth in that form).

Vitamin D3, in humans is not taken in as such. It is mostly vitamin D activated by the kidney and the liver. Where hydroxyl groups are added to activate it. One of the groups is the carbon 25 through the liver and the other  carbon 1. This leads to the most active form of vitamin D= 1 25-dihydroxyvitamin d3. Is it for carnivores, like humans, the case that this vitamin must be processed in their own bodies to be useful? If so, would they need meat, unlike humans, to get enough of this vitamin?
(It seems that mushrooms that have been exposed to ultraviolet b light contain high lvls vitamine d.

Calvo MS, Garthoff LH, Feeney MJ, et al. "Light exposed mushrooms: From development to market of naturally enhanced plant sources of vitamin D." Proceedings of the 5th International Congress on Vegetarian Nutrition. Loma Linda, CA; March, 2008.

As for DHA (And EPA) That seems like a workable idea! (That is if their digestive system would allow to process it) (Which I would not know why it wouldn't)

To supplement vitamin D you might not need to mess around with mushrooms. Carnivores do still have vitamin D synthesis machinery(at least dogs do) but they're too hairy to get all their vitamin D that way. Just shave your dog every so often? That might work.

Of course it is possible for a carnivore to live with a vegetarian diet. Technically you could come up with a complete meal out of vegetables and make a carnivore pup live with it. Dogs and cats are good example of it. They can learn to eat vegi-processed food and as far the nutrients needed are present they will grow and live well. To make them eat raw vegetables is more difficult.
As correctly asked by the commenters, here some links where you can find some info about:
Vitamin D3 in plants (many thinks that only meat/fish contains it)
Carnosine also can be synthesise by the body, here the main references
DHA that is contained in several veg food
Vitamin B12 from cyanobacteria

I agree with you, but you should back up your answer with sources

I'm not sure this answer is factually accurate. For example: dogs and cats differ in their ability to synthesize taurine, an otherwise essential amino acid. Synthetic taurine is cheap, but it's not possible to feed a cat "a complete meal out of vegetables" without adding certain nutrients.

Nope, the answer is wrong when it stays this general. We cannot synthesize certain important vitamins (B12 for example) and there is not plant source for it.

Ok, as soon I have time I will add some references. All the essential stuff can be found in some plant even if it could be hart to found them in the supermarket. Vit B12  for example can be synthesized very easily an thus supplemented. I am quite sure that it exists some plant, mushroom or bacteria rich in B12. Again, tomorrow I will post the sources.

Thank you very much for your answer Alec. Dogs are considered omnivorous, while cats are considered strict carnivores. Does your answer mean that cats could survive without meat? Once again thank you for your answer.

@Chris, vitamin B12 is present in lots of vegetables, here a small list of them http://www.healthaliciousness.com/articles/foods-high-in-riboflavin-vitamin-B2.php

@St.Clair Bij I think that cat can live without meat, yes. I don't think they can survive just eating salad, but I am sure that a vegetarian only meal can be prepared to support all the nutrition needs of a cat. Algae, plants, veg, beans, mushrooms, fruits (milk and egg - that should be considered vegetarian as well) the sources of nutrients on this planet are countless.

@Resonating: taurine is not an amino acid. It does not even have a carboxylate group. It is an amino alkyl sulphonic acid

@alec_djinn I am talking about B12, not B2, as you linked. If you look on the relevant list, you will see that all the B12 there is derived from animals (meat, milk, eggs...).

To conclude, here an overview of vitamin D3 in plants (many thinks that only meat/fish contains it) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3651966/   Carnosine also can be synthesise by the body, here the main references http://www.genome.jp/dbget-bin/www_bget?enzyme+6.3.2.11  Finally DHA is contained in several veg food http://www.livestrong.com/article/291208-vegetarian-sources-of-dha-epa/     With this I hope to have answered all the doubts about my post. If not please let's continue the discussion...

@Chris.. sorry for the confusion.. here the right link. http://www.ncbi.nlm.nih.gov/pubmed/20108213

Beautiful Alec, I appreciate the research and the answer!

@Chris Vitamin B12 is not synthesized by animals at all. It is synthesized by bacteria in the guts of herbivores. Vitamin B12 supplements you find on the market are also synthesized by bacteria. http://en.wikipedia.org/wiki/Vitamin_B12#Sources

@CactusWoman I know. Still, there is source for us from plants.

@WYSIWYG Wow. You're right. I don't know why I thought that. I'll leave my comment as a warning to others.


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Do plants with non-green leaves have chlorophyll and photosynthesis?
Is it even possible that plants with non-green leaves have chlorophyll, and do such non-green leaved plants carry out photosynthesis?

Yes, it is possible, but not necessarily the case.
Non-green leaves with chlorophyl: There are leaves that don't appear green, but do have chlorophyl and therefore can conduct photosynthesis. (See, for instance, refraction effects in white caladiums or the link in the answer by Resonating).
Non-green leaves without chlorophyl: There are leaves that don't appear green because they have no chlorophyl, and so do not conduct photosynthesis. (See, for instance, parasitic plants like the Oronbanche linked by Cactuswoman or this Monotropa)

They do have chlorophyll, at least in general. There are a couple very rare exceptions, but if it can stand up on its own, it contains chlorophyll. The green is just washed out by a very bright red pigment.

All photosynthesis reaction does need chlorophyll,even in cyanobacteria and algae the difference is the type of chlorophyll ( which depends on available wavelength of light and energy efficiency ) fully parasite plants on the other hand doesn't contain chlorophyll and this force them to live as parasites ( keep in mind that we do have half parasitic plants too,which their problem is lack of roots,they do photosynthesis just like other plants ) plants with non-green leafs does contain chlorophyll in some cases even more than green plants ( in my own experience berberis which is a red to alizarin crimson violet shade has more chlorophyll than a greek lettuce) the other pigments are working as helping energy harvesters in photosynthetic reactions, light/shade controllers or simply a survival strategic materials in answer to climate changes,habitat problems and environmental stresses

Parasitic plants such as Orobanche lack chlorophyll and cannot photosynthesize. They obtain all of their energy from paratising another organism.


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What is the scientific name of this plant?
I found this one on a hill here in Palestine. It's about 20 cm in height. Note that it does exist in this regions, but scantily.

The plant is of Lamiaceae family and its common name is Shell Flower or Bells of Ireland.
Its "scientific" aka latin name is Moluccella laevis.


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What kind of beetle is this?
I live in Denmark, Europe and I found this insect wandering around in my garden the other day. It's some kind of beetle, but I don't know what kind it is or the species. The beetle could also fly and had red wings beneath its armor.
Help would be much appreciated. Thank you.

If you were in the U.S., I'd guess it was a Firefly.

@RBarryYoung "I live in Denmark, Europe", which isn't in the US.

As @Ilan wrote, this is a Cantharidae but most probably Cantharis fusca, which is very common species in northern Europe. Cantharis rustica is similar but has reddish femurs and the black spot is more centered on the pronotum. It is not C. lecontei, which is a North American species.
If you go looking at flowers of Anthriscus sylvestris for an hour or two, you will most likely see at least Cantharis fusca, Cantharis rustica and Cantharis obscura - they are all very common in Scandinavia during early spring/summer. The larvae of all these species live on the ground/in plant litter as predators.
Cantharis fusca

Cantharis rustica         .................... Cantharis obscura

Just wondering, does the term "femur" also apply to insect anatomy?

@MarchHo Yes, although of course they are not homologous to vertebrate limbs.  The first segment of an insect's leg is called the femur, the next the tibia, and so on.  (Gotta call them something I guess.)

@MarchHo As augurar wrote; yes its called femur, which is defined as the first long segement of an insect's leg, between the trochanter and the tibia.

Interesting to hear. Im a physiotherapist and we use femur and tibia too. Thats cool its the same terminology in insects.

@fileunderwater. Thank you for the added info and pics.

The beetle resembles Soldier beetle, especially Cantharis lecontei
Soldier Beetles (Cantharidae) » Cantharinae » Cantharini » Cantharis

Wow. That is exactly the one. Thank you very much.

@Lanka you are always welcome %)

Can i ask you how in the world you knew that? It says that the beetle was found in the US. Im amazed that we have the little guy also here in Denmark. So cool:)

@Lanke You should like Nabokov first - he was a great entomologist, I am a little one %))

Well i think you have an outstanding knowledge of the animal realm. Im very pleased to have gotten knowledge about "my" bug. And im happy to have found this Biology SE.

The genus is correct but not the species - Cantharis is large and found on many continents.

interesting that in Russia this one is called "A fireman beetle" - жук-пожарник - for it reportedly likes to put eggs into warm ashes if he can find some

@Arioch. Thats and special behavior. Maybe its because the eggs like warm climate to hatch?


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How much heat can a human sustain?
For how long can a human sustain a temperature of 180 degrees Fahrenheit (82oC) without damage in a confined place?
For instance, suppose a person is sitting in a steam-filled room, without external air flow (but with enough oxygen) - how long could one resist the heat before permanent physical damage would occur?

Short answer
Water of 180 oF (82 oC) causes immediate scalding (thermal burn wounds).
Background
The severity of a scald injury depends on the temperature to which the skin is exposed, and for how long. Residential water heaters warm up tap water typically to 120 oF (48 oC). At this temperature, the skin of adults requires an average of five minutes of exposure for a full thickness burn to occur. When the temperature of a hot liquid is increased to 140 oF (60 oC)) it takes only five seconds or less for a serious burn to occur. Coffee, tea, hot chocolate and other hot beverages are usually served at 160 to 180 oF (71 - 82 oC), resulting in almost instantaneous burns that will require surgery (American Burn Association).
How these numbers apply to steam I am not sure, but I think they will be comparable, given that steam is essentially made up of a dense mass of water droplets. Further, the amount of steam obviously matters. Consider these numbers: The temperature in a sauna typically ranges from 160-200 oF (71 - 93 oC) with a low level of humidity (ranging from 5 - 30%). Steam rooms provide moist heat from a water-filled generator pumping steam into the enclosed room. The temperature in a steam room typically ranges from 110-114 degrees Fahrenheit (43 - 46 oC) with a humidity level of 100%.
There is anecdotal evidence of the Russia-born Ivan Ivanitz Chabert (1792-1859), who supposedly entered an iron oven in Paris with a few trays of meat, and stayed there unscathed for 5 minutes at a temperature of 380 degrees F (193 oC). When he re-emerged from the oven the meat was cooked, while the only noticeable effect on him were profuse sweating and a dramatic increase in heart rate (from 98 to 168 bpm).
This experiment shows the remarkable capacity of the human body to reduce overheating by means of evaporative cooling (sweating). However, the effects of steam are far more devastating to the human body than dry heat. Not only does it carry much more energy than hot air, it also prevents perspiration by saturating the air with water vapor.
References
- American Burn Association Educator's Guide

AFAIK the main difference in steam's behavior comes from "latent heat", in which the energy absorbed by the liquid as it changes into gas is released when it changes back into a liquid. But that'll only happen above 100 deg C -> http://scienceline.ucsb.edu/getkey.php?key=1322

Depends highly on the amount of steam in the room. Most if the heat energy does not come from the air, but from the steam that is condensing on your skin. I can tell from my own experience that I regularly spend 20-30 minutes in 80c sauna while pouring more water to the stove every few minutes without getting too uncomfortable (as long as I have water to drink). 100c sauna maybe 10-20 minutes and 120 c sauna 5-10 minutes. If you don't throw any water, you can stay in much longer. It is also worth to mention that people normally are NOT used to this kind of temperatures and will feel uncomfortable much earlier if they are not used to the heat.
I can take an example from the last Finnish Sauna Championships: a Russian guy died and a finnish guy burned 70% of his skin after spending only 6 minutes in 110c sauna. However, a few years back the same guy lasted for 16 minutes in the same 110c temperature without burns. Again, the difference was made by the humidity. In the final, half liters of water was poured every 30 seconds. Half liter per 30 seconds in a small sauna means the air is constantly over saturated with water and it is constantly condensing on the skin without a moment of relief.
Around 50 people die annually in the sauna in Finland. Most of them are either very old (70+), very drunk or/and have an existing disease. Normally you cannot get burns in the sauna as long as you are hydrated enough to sweat and your body is not completely messed up by alcohol. If you pass out in the sauna, your body does not function properly with managing the heat stress. Dehydration in people under the influence of alcohol heightens the risk of hypotension which impairs skin blood circulation.
Here one article claims A 30-minute stay in a sauna with a temperature of 80 degrees C increases rectal temperature by about 0.9 degrees C in adults. If the rise stays constant, a fatal level of hyperthermia (about 5 c increase in body temperature) is reached in around 2.5 hours. This estimation is probably based on a relatively dry sauna.


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Explanation of protocol in DNA extraction experiment
In the Materials and Methods section of this paper on DNA extraction and analysis from hair I do not understand some parts of their protocol methods. In particular:

"The digested hair solution was then extracted twice with two volumes of phenol saturated by Tris-EDTA (TE) buffer (Sigma), and once with two volumes of chloroform. "

How do the volumes of phenol and chloroform come into play? I know they are used for an organic-solvent extraction, but what was the actual procedure used, i.e., the steps for adding each chemical?
Another question I had was on the buffer they used:

"0.01 M Tris-HCL(ph8), 0.005 M EDTA, 0.1 M NaC1, 0.039 M DTT, 2% SDS"

That whole combination would be the "Tris buffer" then yes? And the proteinase K would then be added to some of this buffer to digest the hair?

http://www.bionut.ki.se/groups/mer/doku.php?id=mouse_tail_dna_extraction You might want to check this protocol for phenol/chloroform extraction. It is tricky to say which is Tris buffer, but to digest hair, proteinase K would be added into buffer containing Tris, EDTA, NaCl, SDS and DTT. However, I feel 2% SDS is a bit too high. Check the protocol again.

The DNA solution has a fixed volume (e.g., 0.1 mL). To a suitable test tube is added 0.2 mL of buffer-saturated phenol. After closing the test tube the mixture is mixed well, typically using a vortex mixer, but possibly by careful, repeated inversion. The aqueous phase and the organic phase are barely miscible. The tube is centrifuged to speed up the equilibration, and concentrate the denatured protein at the interface. After centrifugation the aqueous layer is carefully removed to a fresh test tube.
That is one organic extraction. This is repeated with a fresh aliquot of buffer-saturated phenol (another 0.2 mL). Then the aqueous phase is decanted again and extracted with 0.2 mL of CHCl3.
According to the recipe you provided, the buffer-saturated phenol was purchased from a vendor (Sigma-Aldrich Chemicals, of St. Louis, Missouri, USA), so you can look up the ingredients and composition on their online catalogue (no doubt).
The buffer recipe you provided is the proteinase K digestion buffer. It is typically performed at an elevated temperature.
This protocol is designed to isolate DNA from the nuclei of hair cells. Fully half of the contents of a eukaryotic nucleus are chromosomal proteins, by mass, so the proteinase K digestion step not only breaks open the hair cells, but also helps to remove all of the unwanted, contaminating cellular and nuclear proteins.

How does the cholorform come into play though?

Chloroform is also an organic reagent. It forms a dense immiscible layer and helps to remove any residual phenol from the aqueous phase, and also should clean up the last traces of denatured protein.  You should consider obtaining a biochemistry laboratory manual that explains these basic techniques.

Would you have any suggestions for a biochem lab manual?

@RoSiv Sambrook & Maniatis Molecular Cloning is a good start.


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Mating types in fungi (and somatogamy)
I would have some related questions about the mating types of fungi.

Does a single spore generate a mycelium possessing only one mating type? If it does not in general, do Ascomycota and Basidiomycota possess only one mating type per individual mycelium?
Are homothallism and heterothallism properties of the individual mycelium or of the species? The definitions that I find in my book and on line confuse me. I understand that homothallism is the property of a mycelium (possessing only one mating type or can it possess many mating types in a similar way to hermaphrodite animals? cfr. question 1) that can mate with itself (if it can possess many mating types and it can mate with itself only by using gametes of different mating types, is it still homothallic?) and heterothallism is the property of a mycelium that is not homothallic, but I am not sure I understand, because I read of homothallic and heterothallic species too: is a homothallic species a species where at least some individual is homothallic, where all individuals are homothallic or something else?
I am sure that mating type is a property characterising at least gametes, but is it a property of indiviual cells too? As an example, I know that it is necessary, among many species of fungi, for two gametes to belong to two different mating types in order to produce a zygote. Some fungi, as it is the rule among Basidiomycota, reproduce by somatogamy, i.e. the nuclei generating the zygote are from somatic cells, other than gametes. In such cases, are there species where it is necessary for the somatic cells of a homothallic mycelium to belong to a different type than the type with which they are undergoing plasmogamy? Thank you very much for any answer!

Background:
Most fungi can reproduce sexually and asexually, and some even parasexually. Fungal reproduction is complicated! For one high-level review, see here.
Idiomorphs are alternative versions of the mating type locus on homologous chromosomes that are completely dissimilar and encode unrelated proteins.
Heterothallic - also called outbreeding: male and female reproductive structures are in different individuals. Partners have opposite mating-types with compatible MAT idiomorphs
Homothallic - also called inbreeding: male and female reproductive structures in the same individual. Partners have the same mating type but both MAT idiomorphs are present in the same genome and used in mating-type switching.
Heterothallic species are said to be homogenic incompatible (incompatibility due to the same allele), heterogenic incompatibility (incompatibility due to different alleles) occurs when the offspring of a heterothallic cross between different strainss shows negative heterosis. There are forms of heterogenic incompatibility that appear to act only in the sexual phase. For more discussion of these ideas see here.
Note that mating type and sex are not the same as sex is determined by mating structure and mating type may have no effect on sexual structure only on the nucleic content.
Answers:
1. I am not certain, but my understanding is that a haploid spore will generate a haploid mycelium of the same mating type. Note that things can get more complicated because you can have bifactorial incompatible mating types (e.g. two unlinked mating loci).
2. Homothallism and heterothallism are properties of the species (or at least they are treated as such). Nonetheless, there are some species for which thallic state is variable, mediated by genomic alterations.
3.  I am not entirely sure I understand the question here. In Basidiomycota (Club Fungi) Mycelia of + or - mating type will fuse to form a dikaryotic (two nuclei) mycelium for the majority of the life cycle. Only under unfavorable conditions will karyogamy (the fusing of the haploid nuclei) occur to form diploid hyphae and fruiting bodies where meiosis will take place to create haploid spores with mating types which will generate the new mycelia. Part of what makes the lifecycle here difficult is remembering that diploid somatic cells will have both mating types. (Life Cycle)


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Isogametes and oogametes
I have found the following definitions of different types of gametes:

isogametes: gametes looking and behaving the same;
heterogametes: gametes different in size or in behaviour;
oogametes: gametes different in size and behaviour.

I have some doubts about the exact meaning of behaviour in such definitions. I know that there exist species where gametes of the same mating type can originate a zygote, for ex. in some fungi.
Do differing heterogametes and oogametes always belong to different mating types?
Thank you very much for any clarification!

Where are these definitions from?  Wiktionary defines a heterogamete as "Either of a pair of conjugating gametes that differ in structure or behaviour".

@augurar Thank you for the comment! They are from an Italian language text. It may happen that scientific language usage is different in different countries: edited OP to fit Wiktionary's definition

What do you mean with "Do differing eterogametes and oogametes always belong to different mating types?"? That different individual gametes always belong to different mating types, or that different types of oogametes (e.g. egg and sperm) always belong to different mating types?

@fileunderwater I mean "Do the different types of oogametes (or heterogametes) necessarily belong to different mating types (ex.: + and -) (or can they be produced by the same mating type)?". I'm basically looking for definitions as rigourous and precise as possible. Thank you for the comment!

@Self-teachingworker excellent question. Me too have this question; in-addition I want to know; if such 2 type of isogamy exists (you mentioned some fungus) (type-1: any gamete can fuse with any other gamete, i.e. there is not existence of 2 sex; and type-2: all gametes looks exactly same and shows exactly same movements or activity etc, but they are of 2 types... male and female... inside, so that one sort of gamete doesn't fuse with same sort). I'm not talking about physiological anisogamy.

Allow me to start off with a nice picture showing the differences - note female gametes are on the left while male gametes are on the right in my examples:

Isogametes
For a gamete to be considered an isogamete the other gamete that it meets up with to produce is exactly the same in both size, structure and movement. [2] It is literally trying to find itself. The "male" and "female" are literally no different and it is impossible to tell which is which.
When you look at the picture the two gametes are exactly the same in every way except that they are facing each other in this picture.

The next two are forms of anisogamy:

(source: ulsfmovie.org)
Heterogametes
These gametes differ in at least one of the following:

size
structure
sex

Although it can also be a combination of these three things. [3] As you can see here the female can be structurally the same as the male. (Bottom and top examples of the second picture). From my understanding (although someone can come and prove me wrong) Oogametes are a specific from of heterogamous.
Oogametes
Oogametes differ in size, sex AND function. Females are stationary while males move. [4] Females are also much larger than males. (For instance in humans the cell that divides to make sperm divides equally while the cell that divides in the female divides to make one egg and three polar bodies.)

Very kind answer! What does "sex" mean in the "heterogametes" definition? Does it mean "mating type"? I've read that isogametes undergoing fusion must belong to different mating type at least in some species (ex.: in some strains of Chlamydomonas): must any two (including iso-, hetero- and oo-) gametes undergoing fusion belong to different mating types in all organisms? I've got some doubts because, for ex., of homothallic fungi ( http://biology.stackexchange.com/questions/35057/mating-types-in-fungi-and-somatogamy?rq=1 )... I heartily thank you again!

Male vs female. Like sperm vs egg @Self-teachingDavide

OK: I assume you mean male = motile, female = stationary. Thank you!!!

Yes, exactly @Self-TeachingDavide

The second picture shows nothing and when clicked, redirects to a dead link.


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How to grow fibroblast colonies from single cells?
I need to establish a cell line starting from single cells seeded on a 96 wells plate by a FACS sorter. The cells I am using are human fibroblasts RPE-1 cultured in F12 medium supplemented with 10% FBS and antibiotics. After having seeded 5x96 cells (one cell per well in 5 plates) I have obtained only 4 colonies. Does anyone know any good (preferably personally tested) protocol to efficiently grow fibroblast colonies from single cells?

Why do you sort the cells when you use a cell line? Additionally: What kind of colonies do you want? 2D, 3D?

I have engineered the cells using the CRISPR/Cas system and I sort the transfected one (GFP expressing vector). However, since only 1% of the transfected will have the right modification and since my final goal is to obtain a new cell line, I need to grow colonies out of single cells (2D, 3D doesn't matter), and then screen them to find the one carrying the correct modification.

This should be relatively straight forward. Sort the cells into single wells so all descendants are clones of the sorted cell and let them grow until they are dense enough to be transferred into a bigger plate (probably 48 or 24 well). Continue this process until you can go into big cell culture flasks or plates and make sure that you freeze away a number of aliquots as a backup if something goes wrong. Expand the cells further until you have enough cells to do an analysis.
Keratinocytes need some time to get highly proliferative (around a week or so) and if you don't grow them on a layer of feeder cells, usually also need a special conditioned medium. See the references below (if you have trouble accessing the papers, let me know).
What often also helps is the use of conditioned media. I know this from other cells in the skin which often don't like to grow (at least not as primary cells) unless you use conditioned media. For this, take of the media from the same sort of cells (here it would be keratinocytes) before it is completely used (typically yellow if the media contains pH indicators), centrifuge it to remove any cell debris and then mix it with fresh media to let your cells grow. You might need to experiment a bit with the mixing ratio between the "used" and the fresh media, but 50%:50% is usually a good starting point.
References:

Isolation and cultivation of human keratinocytes  from skin or
plucked hair for the generation of  induced pluripotent stem cells
Culture techniques for human keratinocytes
Improvement of human keratinocyte isolation and culture using
thermolysin

I did that but I got only 4 cells (out of almost 500) to grow into colonies and it took 3 weeks! Fibroblasts don't like to grow alone (at least this is what I am experiencing) so I was looking for suggestions about the protocol to use to make them grow well even if isolated.. I tried to seed different amount of cells but less than 1000 cells per well nothing grows. I will look to the links you posted.

What media and what kind of plates do you use?

F12 medium supplemented with 10% FBS and antibiotics. Very standard 96 wells plates for cell cultures. The cells grow perfectly if I seed them in large number but a single cell will not grow. I think I need to tweak the medium, maybe use 50% conditioned medium... But before rushing in tens of tests I wanted to ask if someone have a nice running protocol to accomplish the task.

That's what I would suggest as well, the use of conditioned medium. We rarely do keratinocytes, more melanocytes and melanoma and they often don't like to grow if there are not enough cells.

This is just to let all of you know that I am trying your suggestions. As soon I will have the results I will sign the correct answer.

Conditioned medium worked very well! in few days I can see colonies growing from single cells!

Although I have not yet done, in general, cells are happier in a conditioning medium. Grow the original cells in 10cm dishes and save the medium and use it to grow single colonies. You might want to mix used and fresh medium (1:1 ratio).
Growth factors are another option. Insulin is sometimes used, but it also depends on cells.
Coating the surface of well with extracellular matrix such as collagen could be effective.
If your cells are normal human fibroblast, cells get senescent, stopping growing. You might want to use immortalized cells like hTERT RPE-1, although you should be careful because immortalization could cause characteristic changes.

Thank you for the suggestion, I am indeed using hTERT RPE-1, I will try growing them in 1:1 conditioned medium and see..


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How do cold conditions help organ transplants?
Body organs are kept cold in-between explanting them from the donor and implanting them in the new host. How do these cold conditions help organs to stay viable while they haven't fresh blood, energy and oxygen supply?

I edited the wording slightly. If you aren't happy with these changes feel free to roll back.

No worries, +1, nice question

By lowering down the metabolism of these organs. Since metabolism is lowered the requirement for oxygen and energy goes down.

Thanks, its true but I am looking for a more informative answer like SolarLinux's answer.

This paper actually goes into the whole history of organ transplants.
In short it seems to have the following effects:

preservation - usually with a specific solution to help.
slows down extracorporeal ischaemic damage
slows down hypoxic damage
slows down the metabolism (energy consumption) and thus the need for oxygen that blood provides.

Remember that the cooling doesn't allow the organ to live indefinitely, and may only work for a few short hours depending on the organ.
I highly recommend reading the paper if you'd like to know more about organ transplant. They went into great detail about the past and present and the abstract also says they discuss new techniques about to be don't in clinical trials.

This site is so useful and its participants are great. Thank You

Of course, glad I could help. I was quite impressed by the paper myself @MySky


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Does Acromegaly cause actual expansion of the zygomatic(cheek) bone
Acromegaly is a disorder in adults involving excess growth hormone production. Since epiphyseal fusion has already taken place in most bones of adults , this does not cause an increase in stature. Certain features of the face such as the jaw may be changed due the fact that the flat bones, such as the maxilla do not undergo epiphyseal fusion and may enlarge.
Several reports describe a prominent zygomatic arch due to arcomegaly, such as this. As I understand ,the zygomatic bone cannot enlarge due to its being fused in adults.
Can acromegaly cause an actual enlargement of the underlying zygomatic bone ?


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Better population models than the logistic equation
For modelling the population of a single species in a region, the logistic equation is used
$$ \frac{dN}{dt} =kN\Big(1-\frac{N}{K}\Big) $$
where $N$ is the number of organisms, $K$ is the carrying capacity, and $k$ is a constant.
However, for most real primary consumers, in the absence of predation, the population usually deviates from the standard sigmoidal curve in two ways

The population typically overshoots the carrying capacity before decaying again to the carrying capacity
The population usually oscillates around the carrying capacity, rather then remaining constant

Are there any better mathematical models for describing growth mediated by density dependent factors of primary consumers in the absence of predation?

You should explain what exactly do you mean by better

I agree with @WYSIWYG - this is opinion-based at the moment. Are you asking for models that can accomodate for your points 1 and 2? What other types of models have you looked at?

I don't see how using the world "better" is opinion based. The point of models is to accurately simulate real systems. By "better" I mean more accurate at producing the experimentally observed population versus time graphs, which display the points I mentioned above.

The thing is that many types of models can produce the type of dynamics that you describe. Whether they are suitable for a particular species depends on the biology of this species though, and you haven't included any information about the organism you want to model (prey/predator? generation length? discrete or continuous reproduction? etc etc). And whether something is "better" is rather opinion based, while "What types of models can accomodate for points 1 and 2 in the absence of predation, and describe a population with discrete reproductive events?" can be answered more easily .

I think "better" is pretty well defined in the question, and the edits presumably address the above concerns. Voted to reopen.

The accepted answer does not deal with the question as I understand it, which is whether continuous time models can display non monotonous behaviours (overshoots and oscillations being two examples). Note that one can give a pretty clear and complete answer to this question. OP: How comes?

I'm not explicitly interested in only continuous time models, but with any model than can accurately simulate an ecosystem. And in some ways, for organisms that have a well defined seasonal mating cycle, a discrete time model makes more sense.

All the more reason to make this explicit in your question from the start, don't you think? At the moment, said question only mentions continuous time models. (Unrelated: Please use @.)

It is not complicated to make your own model of population growth
You can make a model with any kind of function, it is not super hard. It just happen that logistic growth offer quite a good match to observations. You can have exponential growth, linear growth, quadratic growth, ...
However, there are more possible behaviours behind those models than what you think!
The behaviour that you describe is totally possible with a discrete time logistic model. In short, consider the recursion equation $n_{t+1} = f(n_t)$. Consider also $\hat n$ as being an equilibrium of your system (typically n=0 or n=k, where k is the carrying capacity). In other words, $\hat n$ satisfies the equation $\hat n = f(\hat n)$. And finally consider the statistics $\lambda$ which is equal to the derivative of $f(n)$ over $n$ evaluated at the equilibrium $\hat n$. If $\lambda < 0$, then you have oscillatory behaviour (and therefore overshoot) at the vicinity of the equilibrium $\hat n$. Using the correct parameters, the logistics equation gives you a lambda smaller than 0 (typically between $-1 > \lambda > 0$), and therefore you can have the oscillatory behaviour you describe.
If you have any trouble to make these basic analyses of those models, I strongly recommend that book.


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How many dinosaur genes are in a chicken genome?
I read recently that we can "work back" to a dinosaur by selectively turning off certain genes in chickens, and we were able to create a chicken with a snout instead of a beak.
How many dinosaur genes are still hanging around in a chicken genome? I understand there is a lot of overlap for vertebrates, but shouldn't these genes have shuffled out over time?
Otherwise, couldn't we work back to worm or even earlier life forms? Is the whole history of a creature's evolution contained in its genome?
Edit This was a news story about a month ago. Here's excerpts from the BBC's write-up: "Chicken grows face of dinosaur: A chicken embryo with a dinosaur-like snout instead of a beak has been developed by scientists"

To understand how one changed into another, a team has been tampering
  with the molecular processes that make up a beak in chickens.
By doing so, they have managed to create a chicken embryo with a
  dinosaur-like snout and palate, similar to that of small feathered
  dinosaurs like Velociraptor. The results are published in the journal
  Evolution.

Link to Evolution paper included.
Also this piece from about a year ago: "Paleontologist Jack Horner is hard at work trying to turn a chicken into a dinosaur"

In 2009, the world’s most famous paleontologist made a bold claim. In
  “How to Build a Dinosaur,” Jack Horner proposed re-creating a small
  dinosaur by reactivating ancient DNA found in its descendants,
  chickens.
The toothy snout is already here. At his lab at Harvard Medical
  School, Matthew Harris has made chicken embryos that express ancient
  genes for the growth of conical, crocodile-like teeth.

What were you reading?

Related: attempting to give a chicken a tail: http://www.evodevojournal.com/content/5/1/25

@canadianer I edited the question to include an article about a paper in Evolution, and also an earlier article about a project by Jack Horner.

The must-see Jack Horner's TED talk about the "chickenosaurus" https://www.ted.com/talks/jack_horner_building_a_dinosaur_from_a_chicken?language=en

Chicken is a dinosaur..It is a theropod (same group as T.rex )

@WYSIWYG: Wrong.  If chickens are dinosaurs, then mammals are reptiles, and all of them are fish.  As to having common genes, humans share about 50% of their genes with cabbages :-)

@jamesqf You are wrong. Please read the wiki page on theropods. Reptile is not a clade (monophyletic group). Like humans are primates, chicken are theropod dinosaurs.

Be careful when reading media as they tend to exaggerate. That Abzhanov paper is interesting; it will be better when it's published and the figures released. He does a lot of evo-devo work surrounding beak development. What they did in this paper was to inhibit in chick embryos two signalling pathways (which are actually conserved amongst all animals, not just birds and reptiles) so that their expression domain more closely matched that of extant reptiles (which lack medial activation, as opposed birds). They found that doing so results in premaxillary and palatine bones which resemble ancestral archosaurs. While incredibly interesting, this is a far cry from creating living chickens with dinosaur snouts.
To somewhat answer your question, chickens do not contain all of the genes that dinosaurs once had. They will have both gained and lost information. There will be much conservation in the same way that there is conservation between all organisms. For example, the Wnt pathway studied in this paper is conserved across all animals, from chickens to humans to placazoans to, presumably, dinosaurs. It's impossible to say how much has changed since we do not have any whole dinosaur genomes, but it's also important to note that it's not only which genes an organism has but also when and where they are expressed and how they interact.

What does evo-devo mean?

@user151841 evolutionary developmental biology


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Do I not have any alleles from my mom's mom & my dad's dad?
So, I have an XX, & I got an X from my mom, & an X from my dad. My dad would have gotten his only X from his mother, & my mother could have gotten the X I got from her father or mother. That would mean I did not get either X gene from either my mom's mom or dad, or my dad's dad - does that mean that I have "less" of their genetics in me? Say I got my mom's dad's X, would that mean I have less of my mom's mom's genetic traits?

Speaking of your DNA in general, you have alleles from all four of your grandparents.  The 22 pairs of autosomes (non-sex chromosomes) can receive DNA from all four with random mixing.  On a few chromosome pairs you may be missing alleles from one of your grandparents due to the randomness, but on average you will have about a quarter of your autosomes from each of them.
The X (and Y, for males) chromosomes are special, though.  The X you inherit from your mother will have alleles from both your maternal grandparents.  The X that you, as a female, get from your father has no alleles from his father, so that grandfather's X alleles are always missing from your genome.
Because of the random mixing, you will have slightly varying amounts of DNA from each of your grandparents: it won't be exactly 25% for each of them.  Because of the special X inheritance, your paternal grandfather will on average contribute slightly less than the other three grandparents.  (Because of another quirk, mitochondrial inheritance, your maternal grandmother will contribute on average a very small amount more than the other three grandparents.)

Regarding your second paragraph, you should consider recombination between the pseudoautosomal regions of the X and Y chromosome.

Nice summary. Sex chromosome inheritance is interesting, for instance that paternal grandmothers are on average more closely related to their granddaughters than their grandsons: Fox et al. 2009. Grandma plays favourites: X-chromosome relatedness and sex-specific childhood mortality. Proc. Roy. Soc. B


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The ermine's colour and geographical range
Ermines turn white during the winter, with only the tip of the tail remaining black. However, in the southern regions of the ermine's range it clearly doesn't get so white. Encyclopedia of Life says that:

However, in the Netherlands, the animals are often only partially white.

Ermine's range is clearly much more southern than the Netherlands:

Wikimedia, stoat range
So I was wondering where does the border go, north of which the ermines are completely white and south of which they remain more brown? I understand it necessarily is not a clear cut line, mountains have impact and subspecies may differ, but I would assume someone must have mapped this. Or is it just weather related, will a southern ermine turn white if the winter is really cold?
I'm just asking this out of curiosity, but the question is rather relevant. Ermine pelt has a long history as an important trade item, and the most valued pelts must have originated on the white side of this line.

The color change of Mustela erminea (more commonly known as ermine/stoat/short-tailed weasel) is both temperature-dependent and photoperiodic (depending on the length of the day). Bissonette 1943 and King and Moody 2012 show that the molting of the ermine happens as a result of the change in daylight lengths.  The King and Moody paper addresses the temperature dependence, using stoats (ermines) in New Zealand as an example:

In temperate countries such as New Zealand, stoats frequently fail to complete the full change to white. Such animals are not necessarily all caught in the process of moulting. If ambient temperature fell below the threshold for whitening of the lower part of the body but not the rest, new hair would grow white on the tail and flanks and brown on the head and back.

This is a chemical effect of lower temperature (King and Moody):

Experimental work has established that production of brown hair depends on melanocyte-stimulating hormone (MSH); in cold climates in autumn the synthesis of MSH by the pituitary is inhibited.

They don't provide a specific temperature at which the white color change does or doesn't occur, but I suspect that in nature it'd be very difficult to create a map since temperature is not constant year-to-year. There would most likely be an intermediate zone of partially white animals (both in terms of a mixture of brown and white animals, and a single animal that is not fully white).


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Why pick just a single bacterial transformed colony
So after bacteria have been transformed to perhaps grow up a plasmid of interest, why pick only a single bacterial colony from a selective plate for further expansion?
I understand that this is to ensure that you are only working with a single genetic makeup because each separate colony is derived from only a single bacterium. What I can't rationalize is that if I am trying to expand and isolate a plasmid of interest, all colony expansions on a selective antibiotic plate should contain my plasmid. So is it really necessary to take only a single colony, because all colonies I pick should  be useful to me.

If you want to do multiple preps, then by all means pick multiple colonies, but keep them separate. The point of picking a single colony is that it's (theoretically) a single clone, so you're sure that your starting material isn't contaminated with another sequence.

Right, when I make a plasmid, I typically grab 24 colonies because my centrifuge can hold 24 tubes. Keep them all separate and labeled. There have been times when only 1 of the 24 had what I wanted.

Why risk a heterogeneous culture? Pragmatic workflow is always best.

This is a matter of pragmatism in the culture process.
Taking 100 colonies instead of 1 increases the inoculation volume by a factor of 100, which then saves you perhaps 2 hours of bacterial growth time before your culture reaches the OD you want.
However, mutations and loss of plasmid in culture, while unlikely, are possible, especially if the bacteria were not cloning strains with their recombinases knocked out. In such a case, you would risk the downstream experiments being contaminated with mutants, be that protein expression, retroviral plasmid production, or something else.
Worse still, the mixture of bacteria containing mutants is less likely to be detected, since had you picked a single mutant colony, there would be absolutely no result, but a contaminated culture would produce a low but still positive result. Therefore, you may end up wasting many days or weeks troubleshooting your downstream experiments.
Therefore, picking single colonies is simply a matter of "better safe than sorry".

While all colonies on a selective media SHOULD contain a resistance gene, that's a long way from them containing the plasmid you want. A typical cloning experiment will insert a gene of interest into a empty vector backbone to make an intact plasmid. The backbone usually contains some antibiotic resistance gene. If your gene of interest is not correctly inserted, but the empty vector religates on itself, it will make a viable colony without your gene.
Additionally, I have seen mutations happen even when an insert is correctly inserted, and if you're doing blunt end ligation, there is always a risk of getting your insert in backwards or ligating two vectors together.

And that all make sense but let's say for instance that we are growing up a plasmid from a stock solution which has already been sequenced and the resistance gene and the gene of interest are both on a single plasmid. Now is it relatively safe to just pick any number of colonies and assume that they would all have the gene of interest?

You can easily test this. Resuspend a few scrapings of your frozen stock in a small volume of media and plate serial dilutions on both plates with drug and plates without drug. Let the same culture grow in a shaker for 90 min (with drug) and do the same two sets of serial dilutions. If the frozen stock is pure the counts will be the same plus/minus drug. Likewise after growing in liquid. If you grow the liquid long enough the drug will get used up and you may start to see cells that lack a plasmid start to accumulate.

@TheNightman You will get your plasmid but it is not relatively safe. If the downstream analysis/experiments are complex then you want to make sure you start with the best material you can. You might extract plasmids with mutations if pooling colonies together and this could be very problematic for subsequent experiments. Sometimes very little details make an experiment succeed or fail.


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Why do negative ions flow into a cell in an inhibitory synapse, even though a neuron has a negative resting potential?
In my spare time I have been reading an introductory Psychology textbook and this question came to my mind after reading about action potentials.  I have no previous knowledge in chemistry so if I do need some sort of other knowledge I would appreciate if I could be told what I need to learn in order to understand the physiology of the nervous system better. So Why do negative ions come into a cell during an inhibitory synapse even though a neuron has a negative charged resting potential?
I understand this question might be extremely vague and impossible to answer without previous knowledge of the physiology of the nervous system. Any help would be greatly appreciated.

Welcome to chemistry.SE! I reckon this is perfectly on-topic here, but is there a reason you didn't ask this on Biology.SE? A better understanding of the workings of nervous system could lead to better answers.

Oh sorry about that.  I wasn't aware about a biology section.  I literally just found out about this website so i'm extremely nooby.

Welcome to Biology! I see that @Jonsca rightfully migrated your interesting question to us. I have made some slight edits to your question, feel free to roll back if it is not to your liking.

Short answer
Negative ions can flow against the electrical gradient into the cell, provided their concentration gradient across the cell membrane is large enough.
Background
When an ion channel opens, the resultant ion flow is dependent on two things; the membrane potential (which is indeed negative at rest) and the concentration gradient of the ion.
Consider the activation of a GABAA receptor. GABA is the principial inhibitory neurotransmitter in the nervous system. GABA opens the associated Cl- channel on GABAA receptors.
Using the Nernst equation one can approximate the membrane potential (Veq) at which an ion is in equilibrium. It mainly depends on the concentration of the ion X outside and inside the cell ([X]o and [X]i, respectively).[Cl]o is approximately 103 mM, and [Cl]i 4 mM. Hence, there exists a large concentration gradient with lots of it outside the cell.

Nernst equation. Source: Physiology Web
In a neuron, the Nernst potential of Cl- is around -71 mV. Hence, given that the resting membrane potential is approximately -70 mV for a typical neuron, no Cl- flux will occur when Cl- channels open, because the resting membrane potential is equal to the equilibrium potential of Cl-. However, when a neuron is depolarized by stimulatory neurotransmitters (e.g., glutamate), the membrane potential may be reduced to, say, -60 mV. This is still more negative than the action potential threshold (about -55 mV), but very close to it. So without any inhibition the neuron would be close to firing a spike. However, when GABA is released presynaptically, opening of the Cl- channels coupled to GABAA receptors will result in Cl- influx, because the membrane potential is higher (more positive) than the equilibrium potential of Cl-. In effect, Cl- will enter the cell until its equilibrium potential is reached, re-polarizing the neuron back to -70 mV and hence inhibiting it.

Wow thank you so much for your detailed answer!

@user16831 - my pleasure! I hope my answer did not get too technical. I see you are just getting comfortable in this area of science. Also, considering you are new - you can vote on any answers you receive by using the up/down vote buttons. You may accept an answer by clicking the check mark. However, you don't have to user the voting system. It's up to you :)

I had to read it a few times but I like details haha :)

I can't add any detail to AliceD's answer, but I can put it in different terms, and perhaps that could be helpful to you.
Yes, Cl- ions are negatively charged, and the neuron is very often negatively charged. Given only those two facts, yes, you would think Cl- would not enter the neuron. But there is another key fact: diffusion.
The Cl- ions feel the force of electrical repulsion, but since they are at body temperature they also feel the force of slamming into each other at very high speeds and bouncing every which way. This "slamming force" tends to spread them out, and that is otherwise known as diffusion. Since there are many more of them outside the neuron than inside (due to active pumping them to that imbalanced state), the force of diffusion tends to drive them inside the neuron--at least as long as it's not too negative in there! If it is too negative, then no, the force of diffusion is not enough to push the Cl- ions into the neuron, and in fact they may leave the neuron.
What I've written here is, I think, (essentially) equivalent to AliceD's fine answer.

Afaik, chloride ions are not actively pumped out of the cell.

@AliceD http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3282916/ as an example.


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Are there medical treatments that were so effective they were never subjected to a randomized control trial?
I'm thinking of things like antibiotics for meningitis or tuberculosis, or thiamine for Wernicke-Korsakoff syndrome. In those cases the magnitude of the treatment effect might have been so great that it would have been unethical to assign subjects to a placebo group. However, I couldn't find any sources to attest that randomized control trials were never done in relation to those treatments.
I'm referring to treatments trialled in a time and place in which randomized control trials were an option.

there were no clinical trials in olden days

In Japan, the government approved some chinese medicine without clinical trials, even if the system to approve drugs has been already established for a decade by referring to the system by western countries. The medicine is still covered by insurance.

Most surgical medical treatments fall into this category.  For example, patients with acute appendicitis who do not receive an appendectomy will die from peritonitis.  Also, it is difficult to obtain ethics approval for an RCT where you open up a person and then sew them back up  simply as a sham treatment.

Often new treatments are compared against best available treatment rather than placebo to alleviate ethical issues.

In recent years, clinical trials are all necessary. You have to have the randomised control To make sure it isn't a placebo effect. If and only if the drug seems to be super effective will they cut the randomised control short and give the real drug to everyone.
Sadly, while it may seem unethical, there was a cancer treatment that two cousins got into. The normal treatment guaranteed death, while the new drug actually had people practically bouncing off their death beds. One got the placebo - in this case normal treatment since it's unethical to not at least give standard care - and the other got the drug. The drug worked so well, the doctors tried to push to cut the trial short but they wouldn't and the one on the normal treatment died.
This drug was PLX4032.
blogspot uproar
clinical trial information
NYTimes article
So to my knowledge about clinical trials, no trial has been able to skip that stage. It's actually Called Phase III testing of the drug, followed by Phase IV which is administration to the public. It can, however, be shortened if it is promising enough.


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Does inhaling glue (glue sniffing) reduce appetite?
I have heard from many homeless people that they sniff glue just to reduce appetite, as it comes cheap and is more affordable than actual food.
Is this true, and if yes, why? This is totally opposite to the effects of marijuana where people feel hungry.

GLUE SNIFFING : Involves inhaling the fumes from domestic and
  industrial products (glue etc.).

I think the reason why they sniff glue is the same as why they sniff petrol; they seek an escape route out of their misery and boredom. Being cheap intoxicants they suffice their demands. It has little, if anything to do with reducing appetite if you ask me.

@AliceD yes, agreed ! But I have told by many that it reduces their apetite

I have tried that enough number of times to say that it doesn't reduce appetite. It gives hallucinations though.

I searched for credible material and you seem to be right!

Short answer
Various inhalants, most notably organic solvents including those used in paint and glue suppress appetite.
Background
From the Division of Alcohol and Drug Abuse I learned the following:

Initial effects [of various inhalants] include nausea [...], and a loss of appetite.

And the Humanitarian Irin News reports the following on Nepali street youths:

The adhesive glue contains toluene, [an] intoxicating hydrocarbon [...]. The solvent [...] causes hallucinations as well as dampening hunger pangs [...].

Indeed, acute exposure to organic solvents has been associated with a loss of appetite (Gregerson, 1998), and chronic exposure to toluene in the industrial workforce has also been linked to appetite suppression (Kishi et al., 1993).
References
- Gregerson, Am J Industr Med (1998); 14(6): 681–701
- Kishi et al., Environmental Res (1993); 62(2): 303–13

This may not be absolute. For example not everyone would feel nausea (in fact one may have the feeling of being lively) or loss of appetite. Only thing that I can say surely about glue sniffing is that it irritates the mucosa.

@WYSIWYG - I added scholarly references including a meta study. The anecdotal material cited supports this view. Your experience against the literature :)

I can bring all my friends and accomplices in the crime for testimony :P There may be chronic effects but not in the sense that OP is asking.

@WYSIWYG - I double checked my references and I conclude the effects of sniffing have obscured your memory :) The Gregerson study specifically mentions acute effects on appetite, which is confirmed by OP, the news report and the Drug Abuse website.

Or perhaps I am quite voracious inherently :D


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Can I leave BL21(DE3) cells in room temperature?
I am preparing competent cells, and I finished inoculating a single colony in SOB. It has been incubating at 37 degrees Celsius for almost 16 hours since, and it's getting very late where I live. I wanted to do the large-scale inoculation a few (at least 7) hours from now instead of right away, but I do not want the cells to start dying. Can I take the cells out of the incubator and leave the cells in room temperature? I'm hesitant about this because even at room temperature, wouldn't cells still be growing, making it possible for cells to die as well? What extra steps, if any, should I take before using the cells?

Don't do this. User fresh cells thoughout the process, everything else can affect your transformation efficiency in the end.

What would you suggest?

I always did the preculture (picking a single colony from the plate) overnight (12-16 hrs typically) and then started the main culture from which I harvest the cells for the competent cells the next morning. Here you need to carefully check the OD anyways to not overgrow the cells.

I meant to do that, but I end up having to do the preculture in the morning (long story), so now I feel like I should either start harvesting or (as someone suggested to me) leave it in room temperature.

I would use a fresh overnight culture then. A colleague tested this a while ago and the cells which are stored for a while give less efficient transformation rates.

What kind of inoculation? What is the final purpose? It may not be a problem at all. Ask someone in your lab to take the cells out and keep them in 4⁰C

If you leave the cells at R/T what are you worried might happen?  This strain is a lambda lysogen that produces bacteriophage T7 RNA polymerase (correct?). Therefore it stands to reason that you wish to express some foreign gene product under the control of the T7 promoter, so we are talking about a transformation where you already have the plasmid in hand and are just changing hosts.  So you don't need the competent cells to have a transformation efficiency greater than 1EE8 per ug--1EE6 per ug would be more than enough. Leaving them out at R/T might be okay, or it might ruin them.

I have not transformed the cells yet. I was told to follow a protocol to make the cells competent before transformaton. In a few hours I will be cleaning the cells and planning to perform transformation. Also, wouldn't putting the cells in 4 degrees Celsius form ice and cause damage to the cells upon thawing?

4 C° is fridge temperature, above the freezing point of water. Are you thinking of 4F° or perhaps -4C°?

Yes, I know it is fridge temperature, which is why I was worried that it could freeze and damage the cells upon thawing. The overnight cells ended up alright, although their growth curve lagged a bit, but overall it was OK. Thank you all for your inputs.

Pure water freezes at 0C, but the buffer that render the cells competent for DNA transformation contains divalent cations (usually Ca++). These ions will cause freezing point depression (like sprinkling rock salt on an icy sidewalk). So I would not expect the bacterial cells to freeze until the temperature was well below 0C. You also need to take into account that the bacterial cells contain lots of ions (all of the proteins, for example) and is about 150 mM in total (various physiological ions). Finally, if your recipe includes glycerol that also depresses the freezing point further.


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What dragonfly is this?
I photographed a dragonfly but can't really identify the species using http://www.libellen.tv/. Are there any other resources I could use?
The pictures were taken in early June, around 11:00 next to a lake at 1700 meters above sea level. The pictures were taken in the Alps in Austria.

This does nothing to answer the question, but I'd like to formally register my jealousy of your ability to wander through the Alps in late spring taking pictures of dragonflies.

This is Libellula quadrimaculata, which is a common and very widespread species (North America, Europe, Asia at least). This is based on the relatively wide and flat abdomen (hard to judge due to the angle though), which suggests Libellula, brown/golden colour and a brownish wingbase. The main problem I have with the pictures (which makes my suggestion more uncertain) is that it is really hard to see the wingspots in your pictures, due to sun glare. Libellula quadrimaculata is one of the few European species that has four wing-spots (hence the english name Four-spotted chaser), which is why the wing-spots are important to see. However, I think I see hints of wing-spots at the middle of the wing (greyish patches on the top picture), which suggests four spots on each wing pair.
Edit
The distinctive four spots vary greatly in size among individuals and though small they are clearly present. The yellowish tint in the wings and the hairy thorax are also distinctive. The shining wings suggest this individual just emerged (from its larval stadium).  Colors may be less distinctive in these young individuals.
There are no similair species.

(picture from wikipedia)
More pictures of the species can be found here

I would consider myself an expert on European dragonflies and can verify this is libellula quadrimaculata.


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Is hunger pushing cognitive ability in humans?
We have a lot of those questions here that base on personal anecdotes and I try to avoid asking any of those. Still, after skipping breakfast and an extremely effective work day so far I started wondering.
I have always felt, that for most cognitive tasks I perform best before breakfast. Of course some of it is sure related to being very awake and supposedly having a biorhythm that favours working in the morning, but I have always related this to not having eaten and also surprisingly not feeling hungry at all until basically deciding to eat "because I really should eat something" around noon.
So today I decided to find out, if this phenomenon is more widely known or just anecdotal for me. Of course there is a lot of information on how digestion makes you feel tired and you should not expect to be very productive directly after eating. That was not what I am looking for.
Finally I found this 2006 NY Times article about "Empty-Stomach Intelligence", where it is stated that at least for mice being "mildly starving" seems to increase cognitive ability based on the hormone ghrelin targeting not only the hippothalamus, but also the hippocampus.
I then tried finding a relevant publication and was only lead to this one, describing the original study about ghrelin influencing food intake, but seemingly not the "sidetrack" of it influencing cognitive abilities during starving.
Now I am lost. Is there any newer publication about this phenomenon that I completely missed, possibly even in relation to how humans can perform cognitive tasks while being mildly starved?

my guess is following: today people have much more food and food has much more nutritious value than in previous times. So average body is generally running in parasympathetic mode, digesting and resting. That takes attention from CNS, including brain functioning. Mild fasting releases that external pressure. I'd suggest search for link between daily glucose level and brain ability/performance

Still it is curious for me because it is so counterintuitive. Most people I know if they have to work hard on a cognitive level they tend to snack nuts, chocolate, anything they are used to to keep their attention up. And this does boost your attention for a short while. The mild fasting on the other hand seems to be a more long-term approach (long-term being around 6 hours).

This question is more suitable for cognitive sciences and I vote to close therefore. I bet it will be well received there.

I'm voting to close this question as off-topic because it is a well targeted question for Cognitive Sciences. +1 for the nice question :)

I think it has a biological answer. I vaguely remember reading somewhere that either leptin or ghrelin (or both) have an effect on cognitive performance. Orexins also regulate wakefulness, so they may be part of it as well, as more wakefulness tends to produce better attention, and lots of cognitive ability depends on focused attention.

@rumtscho I was kind of looking for that biological answer, especially any additional explanation to the ghrelin theory from the newspaper article. I am not at all into cognitive science, so saw this as a biological (endocrinology) question.

@skymningen Moderate hunger can serve as an activating factor for the body to increase its alertness and thus, as a side effect, can mildly push cognitive ability. Another factor which can make you percieve hunger as a more sober state of mind is that endorphines are released in response to satisfaction of hunger. Endorphines are known to be able to cause unconditioned happiness which reduces the need in any activity, even make one sleepy, thus seemingly decreasing cognitive abilities of the person.


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What's the difference between blood value units 'mE/l', 'mU/l', 'mIU/l' and 'mEq/l'?
Wikipedia suggests 'mE/l' is the dutch or german translation (using 'eenheid'/'einheit' for 'unit') for 'mU/l', which can also be written as 'mIU/l'.
The article mentions The IU should not be confused with the enzyme unit, also known as the International unit of enzyme activity and abbreviated as U.. Is it safe to assume that in case of the unit 'mU/l' one never means the enzyme unit? I figure this is because the enzyme unit specifies a rate of conversion, which is not a blood value and would be meaningless to specify 'per liter'.
I have also encountered 'mEq/l', of which I am pretty sure it is different from 'mU/l', going by the wikipedia article.

did you read wiki article? there seems to be definitions on how units converted in mg. equivalents are essentially moles multiplied by charge of chemical. please read those pages and then articulate exact questions here

I was looking for confirmation that 'mE/l', 'mU/l' and 'mIU/l' are the same, but all different from 'mEq/l'. 'Is there a difference' is a yes/no question, which seems less appropriate to ask on stackexchange than a 'what's the difference' question. Since it's hard to google these units and they are easily confused I hope to establish a single reference here.


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How Scientists sequence, assemble and annotate plant genomes?
I previously read this question and this paper and learned good things about this topic. my current question is that scientists use which tools, algorithms, soft wares... to sequence, assemble and annotate plant genomes?
For each genome project do they develop new tools and algorithms or there are some tools that are useful for (almost) all genome projects?
Are there any comprehensive site, book or paper that have plant genome sequencing and annotation protocols?

Given the C-value paradox (where there may be massive amounts of non-coding DNA, much of it often repetitive), and the fact that polyploidy seems more frequent in the plant kingdom than in animals, (e.g., bananas, wheat), I can imagine some challenges at the assembly step, but I am not aware of a specific tool or approach that is only used by plant genome projects. DNA is DNA for every kingdom, and eukaryotic genes are eukaryotic genes, regardless of species, right? Software and algorithms don't care where the DNA comes from.

But I think algorithms will consider long repeats in plant genomes

Let's try and answer all three parts of your question.
Sequencing
The general method is the same. Sequencing is just sequencing. But as for every single sequencing, there are factors to consider and protocols to be selected.
One important thing is, that you might want comparably long reads to cope with the repeats and the general large size of plant genomes. To get long reads, you need long input DNA sequences. Therefor you would want to follow a suitable protocol for high molecular weight plant DNA. That might be hard, because plant DNA can be difficult to extract based on the plant and tissue you have, as most easily put you have to "crack open" the cell wall in the very beginning.
After that, it is general sequencing. Although, as I already said you might opt for long reads (PacBio) and/or good coverage. If that is not at all feasible, you might choose to do targeted sequencing and only capture the whole exome (or only the genes you are interested in) to reduce both cost and analysis complexity.
Assembly
Now you have probably accumulated a lot of sequence and also potentially long sequence. There are multiple tools you could use for assembly and generally you can use the same for plants that you might want to use for example for a human genome assembly. One example that works well on large plant genomes is MaSuRCA, another is Allpaths-LG. There are some assemblers designed to cope with long repeats, but quite often you just assemble and then try figuring out the repeat regions later, for example by improving a shotgun read assembly with long reads from another technique.
Annotation
This one definitely has specific tools for plant genomes. Well, large genomes. The main thing in annotation is finding potential genes and comparing them to databases to annotate them with function. Plants do splice and plants can have long introns, even ones including long repeats.
One gene prediction software example that works on plants is Augustus, but for some model organisms there are even organism-specific pipelines and tools for this task. And of course, on the database part you would choose to rely on a plant specific database (if you do not use NCBI-NR anyway). Those can also be species or genus specific like the ones you find on the TAIR (Arapidopsis) project.
TLDR:
It's in fact complicated. On one hand, there is a need of specific tools and databases, on the other you might go well with standard tools, but would have to adapt parameters, do additional pre- or post-processing steps and so on.

Thank you. very use full answer. I have a question: in annotation part, if I have a set of assembled sequences, how can I compare (align?) all them with databases like NCBI or TAIR to find possible matches? Are there automatic ways or I'll code or do that manually?

There is a variety of alignment tools, the most used and most widely known is BLAST. There is a web server at http://blast.ncbi.nlm.nih.gov/Blast.cgi but for complete plant assemblies or even all proteins found in one plant you would have to install and run it locally. In case you are not aligning pre-predicted protein sequences but want to align against RNA or protein databases, you would need a spliced aligner.