text:
Why don’t different organisms have nucleic acid genomes containing different bases and sugar?
All organisms contain genetic material. Be it DNA or RNA, both of them have a fixed pentose group (deoxyribose and ribose). Also they contain the same types of nitrogenous bases, Adenine, Thymine(or Uracil), Guanine, Cytosine.
What makes ribose and these notrogenous bases so good that among all the molecules in our pre-historic chemical pool, these selective compounds made our genetic material.
Why don't different organisms have different bases/sugars? I understand that we all have a common evolutionary ancestor so the the genetic material will be similar. But mutation is possible, so why is that there are no nucleic acids found naturally that are made of different bases or sugars? Just for example, if we had a hexose like glucose for the sugar instead of pentose..

I've rewritten your title. to eliminate the misleading "predetermined" which is not the right word. I think it reflects your question.

'Why' questions are usually hard in biology and are interesting to think about but rarely useful to ask. :)

@AlexDeLarge is right. They are generally end up as matters of opinion, which strictly makes them off topic. It is more useful to ask something more specific like "Has anyone built artificial polynucleotides with a hexose instead of a pentose, and if so how did its properties differ from DNA and RNA?" That can be answered, but asking about every possible base or sugar cannot.

common-ancestry and common 'language' of molecular information (common 'meaning' or usage)

maybe the usage not changed with time. But modified base found in certain viruses like 5-hydroxymethylcytosine found in certain bacteriophage. Several modified base found in tRNA.

Everyone is giving you a hard time for this question. But it's a great question! Good for you for asking it.
The answer is that we really don't know why nucleic acids are composed of ribose, as opposed to any other sugars. We don't even know why life on earth only uses L-ribose instead of D-ribose. Or if instead of being carbon-based, we don't know if extraterrestrial life could be silicon-based.
Similarly, two D and L forms of amino acids also exist. (Right handed vs left handed mirror-image molecules that otherwise act the same.) Organisms on earth only use the L-form! We have no idea why. If a meteorite landed on earth that contained D-amino acids, that would really throw scientists for a loop.
(*this link might be of interest to you: https://en.wikipedia.org/wiki/Murchison_meteorite#Organic_compounds)
I'm going to give you a word of advice, and I really hope you get to read this. You are an "out of the box" thinker and the average people will get stumped when you ask questions like this. Ignore them.
If everyone asked grey, imaginative questions instead of following the black-and-white rules they learned, society wouldn't function. But individuals like you help advance society. We need both types of people equally. You happen to be in the latter category. People in the first category will have a difficult time with the questions you ask. Accept and respect them, but continue on and keep asking your questions anyway.
Eventually, you will find people who think like you do. I suggest finding others interested in astrobiology, which is a growing field and that needs people like you in it. Maybe biochemistry or evolutionary physiology too.

People are not giving a "hard time" but correcting a wrong understanding of basic concepts. This is also not "out of the box thinking". At the moment most of your answer is opinion based - please work on this.

This is not an answer to the question. And it's wrong to say that organisms on earth use L-carbohydrates; in fact they mostly use D-carbohydrates. Further, most meteorites contain both D and L-molecules. The selectivity in handedness is, as far as we know, a property of life on earth. Regarding your comments on the open mindedness. It is good to ask questions all the time, but it is better to ask questions that are based on solid science and reasoning. In that sense, pointing to misconceptions is not 'giving a hard time' but helping others to learn.

You are incorrect in your assertion that:

…there are NO nucleic acids found naturally that are made of different bases or sugars

Different bases are found in the anti-codon loop of transfer RNA, in the cap of eukaryotic messenger RNA and in ribosomal RNA, which also contains modified sugars.
You might say that this is pedantic or not to the point, as these variants do not occur in the genetic material. However at least it demonstrates that Nature has ‘played’ with this and decided only to use these fancy Lego bricks for special projects.
I dislike questions of the sort you pose, because any answer tends to be of the form “The structure we have is favoured because it can do this, this and this, which nothing else can do as well.” And, of course, we really don’t know that nothing else can do it — we just assume so because things are the way they are.
With that disclaimer, one might suggest that Mother Nature has shown a willingness to improve on things by moving from RNA genomes to ‘better’ DNA genomes with a different sugar and one different base. (My own explanation of why this is ‘better’ can be found in  answer to Why deoxyribose for DNA and ribose for RNA?.) So although we can’t be sure that another system would not work as well, the fact Mother Nature has stuck with DNA suggests that she has found nothing that works sufficiently better to move to that. (In academic circles this circular argument is expressed in terms of evolutionary advantage.)

David, it is strange that you (as far as I know you) are using personification and anthropomorphism to explain a phenomenon.

@WYSIWYG — It would be anthropomorphism if I wrote about enzymes or bacteria wanting or trying to do something. It was meant as metaphoric humour — oh beware humour in an international context or where you can't see the other's face! You could say it skirts on vitalism or deism — I changed my original 'Nature' to 'Mother Nature' to go with my Lego brick analogy. I wanted to be brief so as not to get sucked into tortuous arguments about the evolution of molecules where one has to discuss enzymes/ribozymes, different genetic codes etc. Perhaps I should have confined myself to a comment.

It sounds like you are confused about how Darwinian evolution "works".  For example, as we survey the current life forms in this biosphere there is absolutely no evidence that these species (or their molecules, which you refer to) are optimized in any way, shape, or form.  All we can state with any certainty is that at some time in the past, during one, or more, selective events, all the species that used ribose, deoxyribose, and the five common bases (A, C, G, T, and U) for their genetic material, survived to reproduce, and contribute progeny to the next generation.
If that putative selective event was different, then perhaps all the pentose-based species would have died off, and we would all have hexose-based genetic material.
We don't know how many different genetic material recipes were tried out before this one "won".
Evolution can only work on, or select, or select against, the current batch of organisms.  It is not an optimization algorithm, it is a filter that lets variants through.
It may well be that our genetic material, for example, replicates faster than the other candidates. That could be a selective advantage, but it doesn't have to be.
So what are you really asking here (since your original question contains incorrect assumptions)?

A small extra note on your question: you are wrongly using the term 'mutation'. Mutation is a process that can work on genes (or chromosomes). As the definition of mutation states:
"The changing of the structure of a gene, resulting in a variant form which may be transmitted to subsequent generations, caused by the alteration of single base units in DNA, or the deletion, insertion, or rearrangement of larger sections of genes or chromosomes."
So mutation works on genes (and their order, sequence, ...), with genes as the 'smallest unit'. It does not work on the molecular structure of genes. If changes in the molecular structure of the pyrimidines/purines are made, these are chemical reactions resulting in other molecules. Which is a completely different proces than 'mutation'.

We all have a common ancestor.  It had a set of genetic mechanisms that worked, and was overall better at surviving than whatever else was available at the time.
Its advantage may have been its DNA/RNA, or it may have been something else and the DNA/RNA just came along for the ride.
At this point you have a planet full of of moderately successful organisms that are all genetically related.  If any completely new organisms appeared, they would be out-competed before they got off the ground.
Now, you can imagine an organism getting a mutation changing the way the genetic code is read. What happens then?  That organism would be unable to read its own genome, and it would die.
What would be needed for a successful switch of code? Let say that we want to use Neoadenine instead of Adenine.
First, the cell needs to produce Neoadenine instead of Adenine.
Second, it needs to produce transfer-RNA that correctly transcribes codons containing Neoadenine.
Third, it needs to change all the existing genes to the new code.
Not only this, but it needs to do all this while not being eaten by its unmutated cousins.
So far, this has happened only once, when either DNA became RNA or the other way around.
The odds of it happening again are small, outside a laboratory dish.


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Method to estimate age of a variant from genotype data
I will obtain array genotype data from approximately 60 related individuals who all share a rare pathogenic variant, which is at such a high frequency in the enlarged family due to a founder effect.
Is there any software that I can use to estimate the "age" of this founder effect i.e. how long ago there was a "most recent common ancestor", basing on the haplotypes observed from genotype data?

Welcome to Biology.SE. Coalescent theory is what you need. Take a look at this list of available software.

You will need genome-wide data to make a good estimate of the time to founder effect. If you only genotyped individuals for the single locus explaining variance for the disease, you won't be able to estimate much. What kind of data do you have exactly?

ABC to the Jensen style might be useful but it won't be as easy as feeding your raw data to a software.

I am not sure on the exact array version on which samples have been genotyped, but it will be genome-wide (I guess it'll be Illumina Omni Express, approx 700k SNPs). Thanks for the suggestions, please let me know if you happen to find some other software....I am also looking in the literature but there seems not to be anything particularly user-friendly to do this...

source: Stack Exchange

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How to convert PDB file of Amino Acids to rotamer tuples list of all AAs instances
Either by Python command, or via specific application (like Chimera) publicly available. Please provide example or link to one of.
I have to detect AA location within MAP (density) 3D matrix. And to verify with PDB format (which models same 3D structure). Each AA may have different rotamer (aka 3 angles usually used to describe AA exact position related to carbon C_alpha atom (the atom which AA side chain exits from). To justify inaccuracies - I need to show that (among other reasons) - inaccuracy is caused since not all possible rotamers existed in my training set (I use machine learning classification to decide what AA is it, and where it stands within cryo- EM scan).

sounds like a very specific question - you may want to give a little more detail to help others follow what you are asking - just my thougts

I clarified upon request, thanks for suggestion to improve chances for proper and and exact answers.

As far as I am aware, Python commands are instructions you write on the command line to run individual lines of Python code. I presume it is a Python program you are after, but why do you specify this one language?

I am student at Computer Science department, and this post is about bioinformatic workshop I must proceed through. Teaching stuff guidelines require to implement in Python. Python is interpreter language where you can write single command. And you can build as well huge projects with many files - which call each other.

Python has dozens of packages specified for various uses. And this versatility is as well a challenge to find "the niche" where programmer needs to spread his code. So I ask here what are commands or packages. Or other external programs of on-line web sites which provide conversion from PDB file format to list of all AA rotamers instances.

I'm voting to close this question as off-topic because this site only accepts bioinformatics questions relating to the underlying biology of the computations, not how to do the computations themselves. If you have tried some code and need help, you may visit [so], but they will not give package recommendations or write your code for you - you must show effort. You might also want to visit a bioinformatics forum such as Biostars for suggestions.

I don't know whether it was you who down-voted my answer, but let me try to clarify before this is closed. The rotamer is one of three conformations of the side-chain dihedral angle chi1. If you use a program such as dhedral it will give you a table of dihedral angles, including ch1 (except for gly). It would seem trivial to then check within defined ranges to determine whether chi1 corresponds to trans gauche+ or guache–. To repeat, Dunbrack is one of the people who has worked in this area (http://dunbrack.fccc.edu/bbdep2010/) and may be able to help you.

I’m not sure if it is what you are after, but I have used Roland Dunbrack's dihedral perl script to get dihedral angles, the header of which is:
 RL_Dunbrack@fccc.edu

 usage
 dihedral.pl filename [chain]

 dihedral.pl pdb2hla.ent
     will print out all dihedrals from file pdb2hla.ent
 dihedral.pl pdb2hla.ent A
     will print out dihedrals only from chain A

I don’t know if it’s on his website as I got it from him personally. If not, or even if it’s not what you need, email him — he is likely to be able to help you.

I downvoted this for several reasons. First, the question is off-topic. From How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here. Next, the OP is specifically asking for a Python script, and you (sort of) gave them a Perl script. Python != Perl, most certainly. Finally, you didn't provide the actual script! You listed the header (which is useless), and basically said "Go find it yourself" even though you have it in your possession.

First @MattDMo, you've every right to vote down my answer (and suggest the closure of the question). I had thought the downvote might have been from the poster. In my defence, I couldn't make the script I had freely available as I had obtained it directly from Dunbrack when I needed a replacement or update for a previous program of his (for Silicon Graphics or something). It doesn't have a free distribution licence, so it would have been discourtious and illegal for me to distribute it to third parties. As for giving the header, that was a quick way to indicate what the program did.

The OP couldn't have downvoted, because they only have 1 rep. You need 125 rep to downvote. I understand why you can't distribute the program, perhaps my wording could have been a bit better. Overall, it just seems to me that you might have been better off just not answering, or leaving a comment suggesting the OP get in touch with Dr Dunbrack, since the answer itself isn't terribly helpful. Just my 2 cents, no hard feelings :)

@MattDMo — Fair enough. No hard feelings.

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Do the mother's genes determine the sons' (heredity) intelligence more than the father's?
It is a general belief that a person's intelligence is determined by both nature and nurture.
I can find a study by Turner 1996 ( in fact, this is the motivation of this question), which makes the claim that since several genes which determine intelligence appear to be located on the X chromosome, the one men inherit from their mothers, and since a man only has one X chromosome inherited from his mother, so that's why mom's intelligence is very important to her sons, even more so than the father's!
Thus, my question is, do the mother's genes determine the sons' inherited intelligence more than the father's, as claimed by the above paper? In other words, a man inherits less intelligence from his father than from his mother? Note that I don't discount the possibility that the father could have helped to raise his son's intelligence by actively nurturing him in the correct way, just that as far as the "intellect genes" ( if there are such things) are concerned, the father plays less role than the mom.
A similar question is asked at Skeptic.SE, but it is geared more towards the contribution of mom's genes against all factors that account for son's intelligence, nurture and nature. My question is focused exclusively on the contribution of mom's genes vs. dad's.
Any new research on this front?

You might want to take a look on the wikipedia site for x-linked recessive inheritance. The article by Turner mentions that out of 325 known recessively inherited genes associated with mental retardation, 17 are positioned on the x-chromosome. In case you are a male and have one of these seventeen recessive genes on your x-chromosome causing you in some way to be less intelligent, you must have inherited that gene from your mother. In those cases it is more like you inherit "stupidity" genes from your mother, who might be an unaffected carrier of the stupidity gene due to the fact that she has two X-chromosomes and the gene causing mental retardation is only present in one of those x-chromosomes.
There might of course also be recessive genes on the X-chromosome causing males, who has only one X-chromosome, to be smarter but genes that are not causing disease might not be so interesting to investigate from a medical point of view.
According to wikipedia there are 499 x-linked genes and the total number of "vaguely defined traits" are 983.
I would say that yes, as a man you inherit more genes from your mother than from you father affecting your intelligence due to the fact that some genes on your x-chromosome affect your intelligence. Whatever the 499 x-linked genes do, you could say that traits affected by those genes to a greater extent are determined by your mothers genes than by your fathers, if you are a male.
Technically you would of course also have to take the genes on the y-chromosome, which are much fewer, into account.

If we approximate that the human male genome has a total of 20000 protein coding genes, the x-chromosome has 800 protein coding genes and the y-chromosome has 60 protein coding genes a male gets on average (19940/(19940+19200))*100 = approximately 50.945 percent of his protein coding genes from his mother. Now for a highly polygenic trait depending on genes homogenously distributed on all chromosomes one would naively expect that 50.945 percent of the genes contributing to that trait is inherited from his mother.

Intelligence is a highly polygenic trait and genetic variants affecting intelligence appear to be (very roughly) uniformly distributed over all chromosomes. If intelligence is inherited more from the mother than the father, the actual effect of this difference appears to be negligible. (This is also evident from simple studies that test mother-child and father-child correlations, and they find no difference)

Do genes/genetic variants on the y-chromosome contribute as must to the total variation of intelligence in males as the genes/genetic variants on the x-chromosome even though the y-chromosome is much shorter? You inherit genes you do not inherit "intelligence".

No, since the y-chromosome is much smaller, it is expected to contribute less to the variance. But what I'm saying is that the of the total genome, the X-chromosome is only a small fraction of it. Hence, if mothers contribute more to the inheritance of intelligence, then this bigger contribution is at most negligibly larger. We have simple studies that check the correlation of intelligence (or height, or other highly polygenic traits) of father-child and mother-child, and no difference tends to be found. Hence, there can be at most a small difference in contribution.

In Lee et al, 2018 they look at genome association of educational attainment (which is highly correlated genetically with intelligence). In the Manhattan plot you can see a rough "genetic architecture" of the trait in question, and one can see that it is widely distributed over the entire genome. They also analyze the contribution of the X-chromosome.

@Eff, you would like to expand on your comment and make it into an answer?

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Is it one queen bee per hive or per colony?
I've come across lots of information on the lifecycle of bees, but I cannot find the answer to my question.
If a beekeeper had, say 6 hives, would there be six queens (one per hive) or one (for the whole colony)? Maybe they would be considered six separate colonies, I'm not sure, but that would be a different question.

Every beehive contains one colony, and every colony has one queen. (Of course there are exceptions, like if a queen dies or is about to be replaced, but I don't think that's what you're asking.)
A swarm is a specific thing, when the queen and part of a colony has taken off from the original colony to form a new one.
I think Wikipedia works well if you need more information on beekeeping terminology:
https://en.wikipedia.org/wiki/Beehive
https://en.wikipedia.org/wiki/Swarming_(honey_bee)
Edit: To clarify, I only have experience of keeping European honey bees (Apis mellifera).

I think this is species specific no? I have some memory of some species having multiple queens per beehive, but could well be wrong - it could be some species of ants or wasps!

@rg255 I don't know! I'm only familiar with keeping Apis mellifera. Hmm... Maybe someone else will show up and let us know.

@rg255 I found this: "in the Brazilian stingless bee Schwarziana quadripunctata, a single nest may have multiple queens or even dwarf queens, ready to replace a dominant queen in a case of sudden death."  But they aren't honey bees. Might still be other species that do weird things, though. https://en.wikipedia.org/wiki/Queen_bee

In honeybees, there is usually one queen per hive / colony. The original queen will leave with the swarm and leave numerous queen cells behind. Mostly one new virgin queen will hatch and kill the others or some of the worker bees kill the others by not letting them hatch or starving them, or breaking open the queen cells. However not infrequently there may be smaller cast swarms that leave a strong colony, each with one or sometimes numerous virgin queens.
If a establishes mated mature queen is damaged, I'll or running out of sperm, the workers will make one or more new queens. These will have to be mated and it is well known that the old and new queen can co- exist peacefully for a period in the hive.
We do not yet understand many factors influencing this.
Reference: The Buzz About Bees by Prof Jurgen Tautz ( original text in German ) Springer books 2nd den 2009 ISBN 978-3-540-78727-3

That's interesting about the old and new queen co-existing peacefully. There must be some sort of chemical signal given off by the old queen so the workers or new queen don't kill her.


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Could trees be engineered to produce rainfall-nucleators?
Scientists are using genetic engineering to make trees produce more terpenes. Is it possible to genetically engineer trees to produce more hygroscopic volatile organic compounds? These trees could be used in drought areas to create more rain.

Welcome to Biology.SE! Don't forget to take the tour. Could you add a source for your terpenes claim? It would also help to give examples of hygroscopic volative organic compounds, although it's not essential.

I can't recall any hygroscopic volatile compound. Hygroscopic molecules  carry-out electrostatic attraction (polar or ionic whatever) with each-other, so they are in most cases not volatile.

Your question is just too broad (also opinion based). Please add details and avoid asking open ended questions.

I think it is 2 question : 1. could we genetically engineer trees to produce any compound?  (that is a broad question) and 2. hygroscopic materials sometimes used to produce artificial rainfall, so is there any volatile (organic-volatile preferable) compound that is also hygroscopic? (which is a pure chemistry question).

probably this question is inspired from any such artificial rainfall article like https://en.wikipedia.org/wiki/Cloud_seeding#Methodology


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Why denatured proteins can't fold back in their native form
I was wondering why a denatured protein isn't able to fold back into it's native form again.
Because a polypeptide before it's folded has a enthalphy and entropy drive to do so. What does the denaturation process do whith this favouring force to fold into the native structure.
In my opinion I can't see the differences between the unfolded protein (direct after translation) and the denaturated protein.

Some denatured proteins can refold into their native state, although at varying rates. The classic (if slightly dubious) Anfinsen experiment demonstrated that. (see e.g. http://sandwalk.blogspot.co.uk/2007/02/anfinsen-experiment-in-protein-folding.html)

In short: the unfolded state is a high-energy state of the protein, which will move towards lower-energy states. Some of these states are the folded protein, while others states are denatured protein (forming "wrong" interactions with itself or other proteins). Energy barriers between these states keep the protein in the denatured state even though the folded state might me more favorable.
Or in other words: it's trapped in the denatured state because of kinetics, even though thermodynamics would favor the folded state.
A nice figure to illustrate this: http://www.ghrnet.org/index.php/jbmbr/article/viewFile/1027/1397/6798
If you go into a little bit more detail, you will find that a lot of proteins (especially larger ones) are usually folded by chaperones. These helper proteins will bind to the emerging protein chain to prevent it from aggregating. In a sense they guide the protein to a folded state. In a similar way, chaperones can help proteins overcome the energy bariers that normally prevent it from going from an aggregated state to a folded state.
This review in Science  is very complete, but also contains some nice figures that give you an idea of what happens:
http://science.sciencemag.org/content/353/6294/aac4354.long /
If you're a pirate: http://science.sciencemag.org.sci-hub.bz/content/353/6294/aac4354.long

You have not explained how the 'energy landscape' differs between the newly synthesized protein (which folds) and the denatured protein (which may or may not fold).

Any discussion about protein folding also needs to include chaperones, without which many newly-synthesized proteins would not be able to fold (or re-fold after some sort of conformational "damage").

There would be only one energy landscape for the protein. Denatured protein in my answer is specifically aggregated denatured protein, as I assume this is what OP is talking about. A perfectly lonely heat-denatured protein would fold just as easily as a freshly synthesized one, but usually this is not the case that's discussed when talking about denatured proteins.

@MattDMo: I think most proteins fold just fine without chaperones. In bacteria chaperones are all called heat-shock proteins, so to me it seems they're only required under stress. Do you have any sources showing that these chaperones are folding a large proportion of all proteins all the time?

@VonBeche I'll find you some references in a minute. Yes, many chaperones are called HSPs because that is the context in which they were discovered, but further research has shown their indispensability in the "normal" cellular context (at least in mammalian cells, which I am most familiar with).

Might explain the difference. I work with bacteria, and I see a lot of heterologous proteins being expressed just fine without their own chaperones. I'll just believe you when you say it's much more common in mammalian cells.

@VonBeche here are some references. Some may be paywalled, I apologize if that's the case and you can't get access. If you really want to read one, just let me know and I'll get a PDF for you on Monday. http://www.ncbi.nlm.nih.gov/pubmed/18432918, http://www.ncbi.nlm.nih.gov/pubmed/27365453, https://en.wikipedia.org/wiki/Chaperone_(protein), http://www.ncbi.nlm.nih.gov/pubmed/27134861, http://www.ncbi.nlm.nih.gov/pubmed/26973652, etc.

@MattDMo: I skimmed the Science review a bit, and it looks really really good. Turns out it's mostly "it depends", and for small (bacterial) proteins chaperones are not required, but I'll add a bit to my answer.

Thanyou for the information! @MattDMo


text:
How ants handle the huge "data" from multiple pheromone trails?
We know that every single ant produces pheromones to communicate and inform others. When there are millions of ants, how do they handle that many signals without getting confused?

Why expect every signal to be different? Many would be redundant or boosting, along a trail leading to much food or in the presence of predators, for example. Then there's likely a priority system that would let "colony in danger" signals block out everything else.


text:
Is Thyroxine a hormone?
I have read the phrase 'T3 is three to four times more potent than T4' several times both in books and websites. But isn't T4 a prohormone of T3? Why do then these sources talk about its potency as a hormone(I suppose)?

does T4 have no signaling activity of its own?

@AlwaysConfused I didn't find any. But since you pointed out I'll do some research.

If it show some signal-inducing activity (i.e. received by a receptor), then it could be considered as a hormone. Then we can also tell T4 is a hormone which is converted into another hormone T3.

It is necessary to distinguish between classical and non-classical actions of thyroid hormones.
Classical action involves nuclear THR (or TR) receptors (TR alpha1, TR beta1, TR beta2). They are activated by T3, 3,5-T2, TRIAC and 3,5-DIAC, and blocked by rT3 and rTRIAC. T4 and TETRAC hardly have an effect on nuclear thyroid hormone receptors, but they are converted in the periphery and in target tissues by deiodinases to T3 and 3,5-T2, and TRIAC and 3,5-DIAC, respectively. From the classical perspective, T4 and TETRAC are therefore prohormones and not hormones in the narrower sense.
Non-classical action denotes binding of thyroid hormones to integrin receptors on the cell membrane. The resulting non-genomic actions may be directly mediated by T4 and TETRAC and don't require deiodination. From the non-classical perspective T4 and TETRAC are hormones sensu stricto.

Figure from Hoermann et al. 2015 (CC BY license)
References

Hoermann R, Midgley JE, Larisch R, Dietrich JW. Homeostatic Control of the
Thyroid-Pituitary Axis: Perspectives for Diagnosis and Treatment. Front
Endocrinol (Lausanne). 2015 Nov 20;6:177. doi: 10.3389/fendo.2015.00177.
eCollection 2015. Review. PMID 26635726
Davis PJ, Goglia F, Leonard JL. Nongenomic actions of thyroid hormone. Nat Rev Endocrinol. 2016 Feb;12(2):111-21. doi: 10.1038/nrendo.2015.205. PMID 26668118.

What do Classical action and Non-classical action mean? I haven't encountered these terms before.

Well, this distinction is a rather new concept. Of course, it wouldn't have made sense before the discovery of non-classical pathways. See the projects page of the THYROID TRANS ACT program for a short overview or paper [2] for a more detailled reference.

THYROID TRANS ACT Projects: http://www.thyroidtransact.de/projects/

Moeller LC, Broecker-Preuss M. Transcriptional regulation by nonclassical action of thyroid hormone. Thyroid Res. 2011 Aug 3;4 Suppl 1:S6. doi: 10.1186/1756-6614-4-S1-S6. PMID 21835053; PMCID PMC3155112 https://www.ncbi.nlm.nih.gov/pubmed/21835053/.

Both T3 and T4 are functional in human body...T3 being only more potent. Both of them fulfill the features of being a hormone, in fact both of them serve the same function in human body. Yes, T4 produces T3 in the peripheral circulation, so you can say it is a pro-hormone of T3, but that dosen't remove it from the hormones. Another example is Angiotensin I which is a pro-hormone (besides itself being a hormone) of Angiotensin II. There are so many other examples.
Following are the references for my answer -
Ganong W F, Review of Medical Physiology, 25th edition, 2016, page- 341
http://press.endocrine.org/doi/abs/10.1210/jcem-36-6-1050?journalCode=jcem
https://www.labome.org/grant/r21/hd/is/thyroxine/is-thyroxine-more-than-a-prohormone--8448119.html
http://thirdworld.nl/l-thyroxine-acts-as-a-hormone-as-well-as-a-prohormone-at-the-cell-membrane

We like people to provide references for scientific assertions. They may well be correct but how can we tell if you don't give the information to check them.

Both T3 and T4 are hormones produced by thyroid. The difference between the two is the presence of 3 reps. 4 iodine atoms.
Hormones usually work only on specific cells, by interactions to specific receptors. These receptors may be found on cellular membrane, intracellular, on nuclear membrane or even inside the nucleus.
So, to answer your question, T3 is more potent with reference to T4 hormone for the fact that only T3 can enter the nucleus of the cell. Therefore T4 must be reduced to T3 to generate a nuclear answer.
Lang, Schmidt, Heckman, "Physiologie des Menschen", 31.Auflage

I don’t know, but I suspect that T4 was characterized first and fulfils the classic definition of a hormone being secreted by a gland and carried in the blood to its target.
Potency is the measure of some biological or biochemical assay of the effect of these agents in the target tissue, so that you can talk about potency regardless of other attributes of a molecule.
Even when it was established later (I presume) that T4 is converted to T3 in the target tissue, and T3 is very active, the possibility would have existed that this conversion might only be partial (there will presumably always be some T4 present there) and the question arises whether both of these molecules have biological activity and function. The results of measurements of ‘potency’ are part of the argument or consideration as to whether T4 is just a precursor or also an agent in its own right.
I think the thing to bear in mind is although you might read nice clear-cut statements in text books and the like, the observations on which they are based are often not so clear-cut, so authors are being both prudent and scientific in presenting the data to the reader.
Finally, there is the question of semantics. Even if T4 is completely converted to T3 in the target tissue, you could still say that it is a hormone because it is secreted by an endocrine gland, passes in the blood to a target tissue where it has an effect. The fact that its effect requires it to be modified in the tissue doesn’t invalidate its description as a molecule that has an effect on a target tissue. So on that basis you can justify calling it a hormone (as well as a prohormone). I also suspect there may be historical reasons for retaining the description.


text:
Collecting virgin fruit flies
Suppose that you place P generation wild type males and mutant virgin females in a vial and allow them to mate. You leave this vial undisturbed in the incubator for 12 days. Could you collect F1 flies for your inter se cross out of this vial? Why or why not?

What do you think? If you don't attempt to answer or provide adequate evidence that you have tried researching your question, it will be closed as "homework" (although maybe not technically your homework, it signifies putting in adequate self-effort).

I am really confused about this question and I am not trying to get help for homework... I feel like the answer would be that you can't collect flies from this vial since the mutant females wouldn't be virgin anyone and they could have mated already.

The answer depends which species (melanogaster, simulans, yakuba etc.), strain/population (e.g. Canton S, DGRP), mutant line (e.g. eb, CiD), food substance, larval density, and incubator settings (temperature, humidity etc.).
The rough answer is no, but if you clear the already hatched flies from the vial in the morning (~1 hour before lights on) and collect flies within a few of hours they should be virgin. Day 12 will likely be too late to collect many as most will have hatched at 25 degrees, at 18 degrees this may slow development but you should be certain that it will not affect your experiment, and report it properly in the methods. You could also collect and store them for a few days in single sex vials (all males or all females), then check the food that you store them in for larvae before using them, this helps to ensure virgins are actually virgins. If you find lots of eggs or even a single little larvae then throw the vial away. This also allows the females to mature properly, allowing them to eat some yeast and they will be more willing to mate when needed.
An experienced fly handler should be able to sort consistently enough to have just a few back up vials. If it is a beginner then make many vials with few flies in, this reduces the damage if a male slips through, it's much nicer to throw away a vial of 10 females than a vial of 100!
(Answer based on >7 years practical experience with D. simulans and D. melanogaster, collecting tens to hundreds of thousands of virgin flies in that time).


text:
What do blue cone cells add to visual function?
First of all, I saw this other question in the SE sites with a good answer, but I didn't find an explanation about the blue cones specifically.
So most human beings have 3 types of cones (cells specialized in color sensing : blue, green and red).
While it may seem obvious that the red and green-sensing cones are an evolutionary advantage (given our natural environment and how we ate for millenia), for instance to locate fruits and differentiate ripeness, I can't find a clear advantage in having the blue cones. Blue doesn't seem to relate to anything like food, predators, sexuality. Am I missing an obvious utility ?
Let's try to imagine what happens if we remove blue cones :

The sky would look gray. I don't see a survival issue there.
We wouldn't be able to make a difference between yellow and white (white = green + red in this case). Is it a big deal ?

I have the reflex to think "if a character is widespread, there must be a good reason". It seems I should rather say "there must be an explanation".
So I'm trying to think differently, and here are other possible approaches to address this question :

I read that dogs have only blue & yellow cones. Maybe our ancestors had only two cone types, including blue, then a third type appeared and blue stayed just because it wasn't a problem to keep it ?
What we call visible spectrum is in fact the only part of the spectrum that can go through air and water (in the eye) without being absorbed (link). Blue cones would be there just because "hey there's something to see" ?
For a long time we had only fires to look at, at night. No TV or screen with Q&A sites to consult. Is it possible that some of our ancestors stared for too long a hot fire, losing green and red cones ? Those with blue cones were not totally blind and managed to reproduce ! (this one is... almost a joke)

Sadly these approaches don't really convince me.
ADDITION : here is a visual example to see what happens if we remove blue information from an image (original image taken here). The image without any blue (middle) is confusing because it makes you think we could see yellow (while yellow wouldn't be different from white). That's why I added the image on the right, containing only information from red and green channels (the blue channel is replaced by min(Red,Green)). I think it illustrates well that blue isn't important, at least for vegetables and fruits !

Just a quick correction: this and other Stack Exchange sites are not "forums". Instead, they are question and answer sites. Please take the [tour] to learn more. There is actually quite a significant difference.

I used "forums" as a generic word, I'm not confusing the two systems. I didn't know it was better to avoid this word here, thanks. Or... are you talking about how I wrote my question, too "forum-way" ?

Water is blue (though only in some cases). I would love to find blue water from a distance.

@AnubhavGoel That's an interesting idea ! As you say, water only appears blue in some cases but that may be enough to be a convincing explanation. This image illustrates a case where it's easier to see a lake if we see the blue tint in the middle of green trees.

So you solved your own question!!! Just change it into a nice answer☺

The sky is also blue. I could imagine (but this is pure speculation) that, for tree-living species, blue can help to distinguish the background sky from foliage and branches etc., which would be useful for climbing and jumping. Ground-dwelling animals, on the other hand, don't need to distinguish the sky from other objects.

@StephanMatthiesen I don't find any clear advantage in seeing the sky as blue instead of grey in a green environment : it seems we can distinguish it anyway. That's what lead to my question in the first place. So far the only circumstances I can think of that require distinguishing blue specifically are seeing a river in a grey environment or seeing blue veins (note that veins appear blue only due to the absorption characteristics and depth of skin).

@GhislainBugnicourt Not sure I understand that. What is "grey" with two colours? Wouldn't the blue sky stimulate the green cones more than the red, so it would appear greenish rather than "grey"? The blueberries in your transformed images are much closer to the green vegetables.

Short answer
Primate color vision started off with photosensitive cells detecting medium to long wavelengths (M/L cones detecting greens and reds) and short wavelengths (S cones most sensitive to blue). By neurophysiologically weighing their relative contributions the full spectrum (red, orange, yellow, green, blue and indigo) can be detected by dichromats. Addition of a slightly different M/L cone and generating separate M and L cones increases the resolution of color vision in the medium and long wavelengths, which is thought to enhance color discrimination useful for foraging fruits. Indeed, blue in itself is not needed for this task. However, missing the blue cones would eliminate a large proportion of the visual spectrum.
Background
Evolutionary spoken, primate vision started off with dichromatic vision. These early dichromats had retinas with one type of cone sensitive to medium-to-long wavelengths (M/L cones) and one type sensitive to short wavelengths (S cones) (Jacobs, 1996). This organization determines the dynamic range of color vision, i.e., to see colors from short wavelengths (greens and blues) to long wavelengths (red and yellows). Weighing their relative contributions by neural networks in the retina allows the intermediate wavelengths to be resolved.
Later in evolution, some diurnal species had a gene duplication on their X chromosome, generating a M/L duplicate gene (Jacobs, 2009). Small mutations in these genes eventually paved the way for two closely related M/L opsins, namely one a little more sensitive to longer wavelengths (L opsin) and one to slightly shorter wavelengths (M opsin). The dynamic range of color vision still depends heavily on the S opsin in the blue cones, as the M and L opsins have absorbance spectra much closer to each other (Fig. 1). The benefit of two opsins with nearly identical absorbance spectra is a higher color discrimination ability (higher color resolution) in the medium to long wavelengths. High discriminating power in the red-yellow-green part of the spectrum is thought to be beneficial for diurnal fruit foraging primate species (Jacobs, 1996). Note that cones need a lot of photons to operate; nocturnal primates are typically dichromats and they will not benefit anyway from another M/L cone.
For fruit foraging alone, the L and M cones do a pretty good job, as your example shows. However, there is more to the eye than food alone. Eliminating the blue cones would substantially narrow down the dynamic range of color vision. Further, evolution started off with S and L/M cones and added another M/L cone to that existing system. Evolution didn't start off with a blind ape and the goal to generate the perfect fruit forager; no it started off with a dichromat and over time improved its ability to seek food during daylight.

Fig. 1. Absorbance spectra of the different opsins. source: Kevin MD
References
- Jacobs, PNAS (1996); 93: 577-81
- Jacobs, Philos Trans R Soc Lond B Biol Sci (2009); 364(1531): 2957–67

Very informative, thanks ! I'm still intrigued about the fact that dichromatic primates had blue S cones and not something around cyan-green : what objects of the environment did they need to distinguish at such low wavelengths ? So far the only lead I have is water as proposed by Anubhav Goel in comments above.

Very interesting. I've been wondering/speculating if blue helps tree-living species to distinguish the background sky from branches and foliage, which would make climbing and jumping easier and safer. The Jacobs papers are a bit vague on possible adaptive value, mostly discuss fruit although they mention other uses (like distinguishing skin colouration), and so far I haven't seen the sky mentioned. Do you know or have an opinion about that?


text:
Larger Ant in trail
Today I left a spoon on my sink that accidentally still had some honey in it, and a while later I had a huge line of ants trailing in to get it. Before doing anything about it, I observed the ants' behavior and noticed there were two larger sized ants walking along, and they seemed to have some sort of a hunchback.
I killed one of them (sorry any lovers, but they were invading my kitchen) and noticed a whole bunch of ants swarmed around it's body immediately. I later, sprayed some venom to kill the ants off, and now that I come over later, I see more ants have swarmed aground the larger dead Ant, even over the poison.
My questions are, are these queen ants? If so, how come there were two, and just trailing along to get food like the others? I live in Portugal, of it helps any.
Thank you very much.
Rest in peace, ants...

Can you please post a picture?

Unfortunately it's gone now. I should've done that...

I'm sorry to say so, but I suppose you are not very familiar with ants?
I can't be completely sure since you have no picture, but the way you describe it, very possibly these 2 larger ants were 'soldiers'.
Most ant colonies exist of 3 different types of ants. They are all sisters from each other, and daughters of 1 queen. A queen stays in the colony and her sole purpose is to lay eggs. She does this continuously (while she is fed by worker ants) and thus never leaves the nest. She stays there until she dies. The worker ants are 'workers', gathering food, expanding and repairing the nest when needed, taking care of the eggs and larvae. They are small and probably the type of ants you think of when someone is generally talking about ants.
The last class of ants are the 'soldiers'. Their task is to protect the colony agains intruders (an other ant colony, termites, other insects or animals,...). They differ in size from the worker ants (differences can be small or very big, depending on the ant species). Soldiers are bigger than the worker ants, and have bigger mandibles (used to "bite" intruders) and thus bigger 'cheek muscles' to operate these mandibles. Possibly this is what you described as the 'hunchback'.
Furthermore, ants use chemical signals to communicate with each other. They can lay a 'track' of these chemicals, for example, to show the way to a food source to other worker ants, which can then follow the track and help to bring the food back to the nest. Often the worker ants (gathering food) are accompanied by several soldier ants, to protect them from other insects (or animals,...). These soldier ants also use chemicals to communicate. When attacked, they can release an alarm chemical that attracts other (soldier) ants, to come help them fight an intruder.
Most possibly, by using the poison you killed some ants, which results in the automatic release of the 'alarm signals', attracting even more ants...
I hope this answers your question.

I wouldn't say I'm not familiar, I'd say I'm not knowledgable xD
Your answer was very interesting though. But I can say that the hunchback was an actual hunchback, not a larger head. I looked at photos of queen ants, and it seemed very similar to the larger back a queen has after loosing it's wings. Is there any situation where a multiple-queen hive would send out 2 queens?
Again, thank you very much.

Not the queen.  Once she has made her wedding flight and hatches a few eggs, she is never out and about again, unless the nest moves.
Some ants enslave other species of ants.  This is what the "hunchbacks" sound like.

This could be correct, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

There are also worker ants assigned as morticians, so to speak. When you kill off a group of ants, they come out to gather the dead for a burial of sorts. This may explain the appearance of the new ants gathering around the dead.

Welcome to Biology.SE! This could be correct, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


text:
Laurus Nobilis parasite identification
In north Italy were I live I have two plants of laurus at the two sides of a garden. One of them has some sort of parasite on its leaves.

Someone know something about it? Leaves are covered with something like an oil.

Looks like some sort of scale insect. You should add where you're located, that might be helpful.

As @picapica has pointed out, I presume these are scale insects, the first instar of Japanese wax scale, Ceroplastes japonicus.
Laurus sp. is a host of this hemiptera in Italy.
Here is an image showing the second instar from Italy:

These are the adult females :


text:
What is the smallest pressure differential that humans can detect?
While cooking dinner under an extractor on its lowest setting, I noticed that none of the steam (referenced by the amount of fogging on a nearby window, compared to the absence of the fan, was effectively zero) was going anywhere else but through it.
However, placing my hand under the hood, I couldn't feel a difference in pressure. This is most likely due to two things: my hand smoothly transitioned from "normal" atmospheric pressure to the "adjusted" pressure near the hood, and the hood area is quite wide, so that extraction is done over the significant area not covered by my hand and hence less pressure applied.
But it got me thinking, and a literature check revealed nothing helpful so far, as to what is the smallest pressure differential detectable by the skin of the human body?
I would prefer to exclude anything related to hearing, as this is a well-researched area but tells us nothing about the other 99.9% of what is directly exposed to atmospheric pressure changes. Answers that cover particular parts of the body beyond skin and ears (for example, the eyes) are appreciated but only additional.

Short answer
The sensitivity to pressure differences highly depends on the study setup used. A paper resembling the conditions in your kitchen experiment concludes that the just noticeable difference ranges from 19 to 35 kPa.
Background
The smallest difference that can be perceived between two stimulus levels is called the just noticeable difference, or JND. The issue with determining pressure difference JNDs is that it may be dependent on many things. To name a few important factors are the place on the body and the type of stimulus used. The fingertips and tongue are among the most sensitive parts of the body, while the back is way less sensitive to mechanical stimulation. The type of stimulus may also dramatically affect the findings, because vibratory stimuli are sensed by other types of mechanoreceptors than static pressure stimuli.
Having said that, I found a paper describing an experiment that resembled your kitchen experiment pretty well . The authors used air puffs applied to the fingertips. They used an apparatus where the nozzle could be adjusted to accommodate different aperture sizes. The authors tested 10 normal, right handed controls and used a standard 2 alternative forced choice (2AFC) task applied as a method of constant stimuli. Personally I would have adopted an adaptive 2AFC task, but both methods are valid. The authors conclude that

Subject-averaged pressure JND values ranged from 19.4 – 24.7 kPa, with no statistical differences observed between aperture sizes.

Reference
- 33rd Bianchi et al., Annual International Conference of the IEEE EMBS Boston, Massachusetts USA, August 30 - September 3, 2011

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


text:
Do organs or any structure in the human body shrink/shorten if it's function is no longer useful?

Charles Darwin was one of the first scientists to theorize on the function of the appendix, which in his day had been identified only in humans and other great apes. He hypothesized that the distant ancestors of these animals survived on a diet of leaves, and so they required a large cecum, a portion of the gut that houses bacteria that can break down stubborn plant tissue. Later, he speculated, these ancestors shifted to a largely fruit-based diet that was easier to digest. A large cecum was no longer necessary, and it began to shrink...Darwin thought the appendix, which juts off of the cecum, is one of its former folds that shriveled up as the cecum shrank. Consequently, he thought it carried no function.

I recently read a source which states the above. It made me wonder that if there is some other organ/part in our body which may shrink as further evolution progresses and it's use diminishes, just like our appendix. I'd like to know if this 'theory of shrinking' applies to any organ that may become useless.

If you read the Wikipedia article on the appendix, you'll see that the hypothesis of vestigiality is simply incorrect. It is quite important in maintaining the balance of flora in the gut, and also plays an important role in immunity. Remember, Darwin lived 150 years ago, and not everything he proposed was correct. Even Einstein was wrong on occasion.

Reading your title you seem to be talking about development, while the post is about evolution. You should check the definitions of these two terms if they are unclear to you.

If you were interested about development (but I doubt you are), muscles and bones would be good examples.

You should link to the original article you are quoting.

@MattDMo I've read this article thrice but nowhere does it state for sure that the appendix DOES HAVE THIS FUNCTION ONLY and without it our body will suffer complications. Not just Wikipedia, but almost every site uses the phrase '...may have this function' or 'may house good bacteria...' far too much. And Huffington Post still states it's function to be 'in much debate'.

You're using the Huffington Post for scientific information??? Could you maybe try journal articles from the past few years instead?

And you're actually trusting Wikipedia on this??

It's not just Huffington Post it's practically every alternate web result that states this.

First of all, our appendix isn't 'useless'. Their is a high concentration of lymph nodes (higher than anywhere else in your gut), so it might not be needed for digestion anymore, but it's function somewhat shifted to a more immunological role.
Secondly, yes there are other organs/body parts that shrink over time. In evolutionary time, look at our tailbone. In monkeys it's still a full tail, in apes it's almost nothing, and in humans it's still present in the skeleton, but not visible on the 'outside' anymore. Probably in a few (hundred/thousand/..) years it will be completely reduced until it is no longer present in the human skeleton (because since we don't have a tail anymore, it doesn't have any function anymore).
Over a much shorter timescale it is also possible. For example the thymus expands in puberty, and afterwards it shrinks until it is almost completely gone.

The thymus does not shrink because of vestigiality or lack of use. It is simply part of the development of the immune system, that T cell maturation and development moves from it elsewhere, like the lymph nodes, spleen, and bone marrow. You already repeated what I said much earlier about the appendix. Finally, the coccyx is certainly not without function. It serves as an attachment site for ligaments, muscles, and tendons, and is an insertion point for muscles in the pelvic floor. It is also important for stabilization when you're sitting.


text:
Why do basil leaves turn black?
I notice that when I buy basil it is fresh and green in the store, but when I take it home it wilts and turns black within 24 hours.
Why does it do this?

That seems pretty fast to me. How is it stored in the store and how do you store it at home? Specifically, is it frozen at any point or bashed around during transport at all?

collected green leaves sometimes turned black. Maybe it is the same process like cut apple turns black.

I've seen some fig latexes often turn red or black.


text:
Is there any reason an arbitrary DNA sequence such as 5'-ACACACACAC-3' would not exist in nature?
I am making a DNA model for my class, and I looked up some examples and they all have different sequences of bases. If I choose an arbitrary sequence like:
5'-ACACACACAC-3'
3'-TGTGTGTGTG-5'

or
5'-ATATATATAT-3'
3'-TATATATATA-5'

Is there any reason it would not exist in nature?

What do you mean by left and right? Or the order of bonds changing? Have you consulted a basic book of biochemistry or molecular biology or looked at the DNA entry for Wikipedia. I have voted close this question as unclear. You need to put more effort into understanding DNA before making models.

How do you know I've put no effort into understanding DNA? I've researched this question for a clear answer but have found nothing, which is why I asked here. Stop acting as if an unclear question is an "inconvenience" to the forum as two others kindly answered it. You can't just close a question because it is unclear - a simple edit will fix it. P.S: I don't own a biochemistry or molecular biology book.

This is not a forum, but a question and answer site that has certain rules about questions to maintain its usefulness and standards. You can read them here: http://biology.stackexchange.com/help/how-to-ask. Questions should demonstrate effort — yours does not. The fact that you do not own a biochemistry book is no justification and suggests you are in the wrong place — there are many online resources on DNA. One of the use of the comment facility is to ask for clarification and improvements in the question. This I did and you have not responded.

You appear to be building a model of a double-stranded DNA 10-mer but are afraid that the sequence of bases you intend to use might be disallowed by some biological or chemical principle of which you are unaware, as your knowledge in these areas is minimal. I have edited your question to this effect. It is such a broad and basic question that I believe the it should be closed: there is no reason any random DNA sequence would not be found in some genome. However, the repetitive sequence proposed may mislead your audience into thinking this is a necessary feature of DNA. I would chose another.

There is no reason. Look up PDB search for your sequence and its likely its already been identified somewhere. What cant be done yet is, take and arbitrary sequence, and say with any certainty what its is for.. that we cant do. Best is comparison against what is already known from any homology

The proposed sequences are so short, it's almost certain they exist in nature.

You must first understand a few things:

What are proteins made of
What is DNA made of
What is the relationship between DNA and proteins

From DNA to proteins
DNA is transcribed into RNA which is then translated into protein. The protein, then has some effect (e.g. could be an enzymatic effect) such as affecting the level of sugar in the cell, digesting some lipids or affecting the expression of other genes.
More information on Khan Academy > Central Dogma
What is DNA made of?
DNA (or at least the genetic code) is made 4 different molecules which are called nucleotides. We abbreviate their names by the letters A,T,C and G.
What are proteins made of?
Proteins are made of amino-acids. There are ~20 different amino acids.
Genetic code
For the interest of your question it is now essential to understand how does the succession of nucleotides A,T,C,G in the DNA is reflected in the protein. This is called the genetic code.
We call a series of three nucleotides, a codon. AAT is a codon for example. Each codon (except special codons) correspond to a specific amino acid. This correspondance is called the genetic code. Here is the universal genetic code (where the T has been replaced by U because RNA contains U instead of T)

Consider for example the codon UAU and AUU (where only the order changes) The first one codes for the amino acid Tyr while the other codes for Ile. So yes, the order matters.
Information theory
Globally speaking, for any information the order of a sequence is of fundamental importance! More information on Khan Academy > Information Theory.

So, because the order of the bonds differs every time, I could theoretically make a DNA model like this, and it would be correct? AT CG AT CG AT CG AT CG AT CG

Please delete the reference to the central dogma. You do not need to give a name to the principal you state and it is not Crick's Central Dogma, which is basically that the information in DNA can go to protein but not in the other direction. I document this in detail in answer to http://biology.stackexchange.com/questions/49201/crick-s-central-dogma-counter-cases/49210#49210

@David I agree it is not worth using this term after all. I was tempted to use it as a consequence of the link to a Khan Academy video that is called central dogma. Is it better now?

You're still using the term "Centra Dogma"...

@Deadfult what does that sequence actually mean? Is it 5'-ATCGATCGATCGATCGATCG-3'? That's fine, as long as you include the antiparallel 5'-CGATCGATCGATCGATCGAT-3' as the paired strand.

DNA has a polarity that is based on the numbering of the carbon atoms in the deoxyribose molecules in the sugar phosphate backbones of the two complementary strands.
So, for example, the 3'-OH of one base's sugar is attached, via a phosphate, to the 5'-OH of the sugar on the adjacent base in the strand.
Therefore, we say, that one end of a single-stranded piece of DNA has a 5'-end, and at the other end a 3'-end.
Go no further until you understand this concept and can draw a picture of this.
In Watson and Crick's model for double-stranded DNA the two complementary strands are anti-parallel. In other words, if you imagine the double helix like a ladder, then one of the legs of the ladder is oriented in the 5' --> 3' direction, while the other, complementary strand is oriented in the 3' --> 5' direction.
When we describe a DNA sequence, by convention we read the sequence strands in the 5'--> 3' direction.
So now you should be able to state your query more succinctly.

Yes they do matter. Imagine reading just one side of the DNA strand. This is how the code is actually read, so the order would change that side's reading.

ACAAGATGCCATTG

is different than

ACAAGATGCCATTC

Notice the different last base making the message different. This can affect transcoding to proteins.
Just like the change of one letter can change the meaning of the english word "petty" to be "patty". The same is true for any encoded message.

Alright, so let's say I made my model like this then:
AT
CG
AT
CG
AT
CG
AT
CG
AT
CG
Theoretically, this would be correct right?

Correct for what? I have no idea what you are asking

Base-sequence on a strand will NOT matter until you are telling about a specific gene or motif.
However, when you make 2 strands, you have to STRICTLY  maintain the BASE-PAIR RULE.
p.s. Be sure the 2 strands will never touch each other; they'll maintain a same parallel-distance throughout their lengths; and both helix will have the same-direction of coiling (right-handed screw type, for  Watson-Crick model and B-DNA).


text:
What is a normal healthy amount of Titratable acid in a person's blood?
A person's normal pH for arterial blood is 7.41 and venous blood is 7.36.
But I am curious to what is a normal amount of Titratable Acid in someone's blood?

As you say yourself blood is kept in a slightly basic range (and this is tightly controlled). Why do you think there should be free acid present here?

There are proton pumps involved with pH regulation, right?

@GabrielFair yes, what's your point? Just because there is a proton pump doesn't mean there's free hydronium ion (or any other type of acid ion) in circulation. In fact, in vivo it's exactly the opposite.

Isn't titratable acidity expressed as percent lactic acid? Isn't there lactic acid in the blood?


text:
Identification of a segmented black insect in France

Found in the Lot department of southern France.

I have no idea what it is. Do you have any more information? Like did it move? How? Did it have any features not visible in the photos? I think I see some sort of pincers in one end, did it have legs?

was it walking?

Tag add suggest zoology. Entomology means insect (not all arthropods) , so if it is Not an insect then Zoology  could be a broader term to include it.

Are you sure this is an insect. Did it have 6 legs? (Comment originally fro @Kasper)

I think I've seen a similar thing in another stackexchange "species-identification" post, and it was a larvae of some dipteran, but I cannot find something like that in
http://www.dep.wv.gov/wwe/getinvolved/sos/documents/benthic/midatlinverts/diptera.pdf

I think this is some sort of soldier fly larva (family Stratiomyidae). That would explain lack of legs. There are thousands of species world wide, with both aquatic and terrestrial larvae, so it might be possible to narrow it down a bit more.
Image from bugguide.net for comparison:

Thanks to @bli for reminding me of dipteran larvae!


text:
How do legs of tiny insects/spiders like mosquito/Opiliones work?
I think I understand how legs of humans work. We have bones to which muscles are attached. Muscles can only contract / relax. By the combination of many different muscles we can make complex movements:

Image source: https://commons.wikimedia.org/wiki/File:1015_Types_of_Contraction_new.jpg
However, I have no idea how this works for insects / spiders. On the one hand, I'm not sure where the muscles should be attached to due to the exoskeleton. On the other hand, I have difficulties imagining that the same system works for legs which are this tiny:

Image source: https://commons.wikimedia.org/wiki/File:Spider-IMG_1630.jpg

insects too have muscles

Probably the OP is asking is there any muscles at terminal, stick-like fragments and their joints.

Moskito... did you mean 'mosQUito'?

@AlwaysConfused Yes, thank you. I fixed the spelling.

Arthropods use basically the same system to operate their legs. Yes their legs are tiny, but so are their muscles.(Is it so hard to imagine everything is downscaled? Their digestive system is also much smaller, but they don't need to eat the same amount as we do either...)
In general it's just a kind of smaller-sized mechanism that is based on the same principles: use a muscle to create tension over a joint, and so move the appendages. The big difference is off course that in mammals the muscles work against an internal skeleton, and in arthropods the muscles attach to the inner surface of an external skeleton.

I try to save daddy-long-legs spiders that can't climb out of my bathtub. I do so by grabbing one of their legs. Sometimes the legs detaches. If I squeeze the end of the leg that was attached to the body of the spider, the leg extends. How does this work?

Well the subject of how insects move their limbs is a bit more complicated than suggested by Kasper.
Insects do have flexors and extensors muscles to move their legs. But there are other options too.
Spider legs work by hydraulic fluid. The spider has flexor.. but extension is done by pumping hemolymph into the leg.
Also it has been discovered that certain movements of insect legs is due to the chitin skeleton flexing and join structure. ie energy is stored in the chitin, and the structure of the joint cause the legs to return to the rest position.
https://www.sciencedaily.com/releases/2013/07/130718130524.htm


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Identifying whether amino acids are hydrophobic or hydrophillic
How do you figure out whether an amino acid is hydrophobic or hydrophilic? (other than memorization) I know that it has something to do with the R groups of the amino acids, and that polar molecules are hydrophilic, while nonpolar molecules are hydrophobic, but that's about it. Please give a simple answer, I don't need too much information other than an easy way to tell.

This question isn't about biology but about learning it, so no doubt it will be closed very soon. However the general answer is that you need to learn chemistry in order to know other than by memorisation. Like it or not, biochemistry/structural biology/molecular biology involves basic chemical knowledge. Without that you are going to have to memorize things without understanding them. I would start learning chemistry  as soon as possible.

Checkout: "What is the difference between polar and charged amino acids?" on Biology StackExchange

@mdperry if you're going to reference a different question, please include a link.

Does the side chain contain any Nitrogen (N), Oxygen (O), or Sulfur (S) atoms?  If it does, then chances are high that this particular R-group is polar (although it may not be charged).
The converse is also true, if the R-group lacks any of those three atoms then chances are high that the side chain is polar.  There are exceptions; Methionine has a Sulfur, but is quite hydrophobic (non-polar).  Tryptophan has a nitrogen but is non-polar.

...and lysine and arginine can be considered both hydrophobic and hydrophilic, as can tyrosine (the latter being particularly important in certain enzyme mechanisms). Encouraging this sort of rote learning of dangerous half-truths is anti-science. The only decent advice is to learn some very basic chemistry, for which there must be dozens of reasonable on-line sources.

I know this isn't how you are "supposed" to do it, but it isn't easy to memorize all 20 amino acids, and this helps a lot with identifying whether they are hydrophobic or hydrophilic. I'll just have to remember that methionine and tryptophan are hydrophobic.

@Anonymous you need to learn basic chemistry first. Going along with what david said, it's not just a matter of memorizing the 20 AAs and saying "W is hydrophobic, S is hydrophilic". You need to be able to understand why, and how some can be classified as both, depending on context.

@MattDMo I'm studying campbell biology right now, didn't see anything that would help with learning that

@Anonymous Thank you for selecting my anti-scientific "dangerous half-truths" as the answer to your question; I am very glad that you found it helpful.  I realized I did not provide you with a reference of any sort, so here is a biochemistry textbook of mine: https://www.pearsonhighered.com/program/Moran-Principles-of-Biochemistry-5th-Edition/PGM264296.html.  I fear I am growing old and may not be up-to-date on the newest methods for learning these chemical principles.  We did indeed memorize all 20 a.a. structures as biochemistry undergraduates in the 1970s (in our Organic chemistry course).

@mdperry Your answer helped a lot with my question, and that's what an answer is supposed to do. Btw, studying biology really hasn't really changed much besides extra information to know


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Have there been any measurements on the genomic differences between cancer cell DNA and healthy cell DNA?
I'm loooking for simple stats like the average number of base pair differences to normal cells, average diversity between different cancer cells, etc.

Check out dcc.icgc.org, a data portal dealing with what you describe.

Yes, there are two genome projects, which aim to identify the critical mutations (and by looking for them, they discover all the mutations in a given cancer) by sequencing DNA from the cancer cells and healthy cells from the same patient.
These are "The Cancer Genome Atlas" (TCGA) and "The Cancer Genome Project (TCGP)". Both project publish their complete data and ways to browse them. The data from the TCGP can be found in the "Catalogue of somatic mutations in cancer" (COSMIC), the data from the TCGA on their project site.


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"Imperviate" is it a word what can be substituted?
Sentence:
The aquaporins allow water to pass through the membrane and imperviate any solute molecules from diffusing across.
I'm looking for a word that pretty much is the opposite of perviate or to occlude.
http://www.etymonline.com/index.php?term=impervious

Since this question is not about biology but language, it is off-topic here. I will move it to english language and learning.

It was already moved there how it came back? http://english.stackexchange.com/questions/347911/imperviate-is-it-a-word-what-can-be-substituted


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Why are different mesenchymal stem cells used for articular, auricular, septal nasal and costal chondrocytes?

Why do stem cell researchers use the mesenchymal stem cells shown in the table above for these specific types of chrondrocytes? Can you only use bone marrow to make articular cartilage, or are there other types of cartilage that can be made using bone marrow, if so which other types of cartilage?

Who is "they"? Why are certain cells in the body of different lineages than other, somewhat similar cells? Because that's how the body evolved. "Why" questions about evolution are rarely informative or helpful.

@MattDMo: I was referring to stem cell researchers. For example: Can you only use bone marrow to make articular cartilage, or are there other types of cartilage that can be made using bone marrow, if so which other types of cartilage?

OK, I see. Thanks for clarifying. You might want to add the ideas of your entire comment to the question so everyone understands.


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Is there variability in genetic combination from the same sperm and egg combination
Given a single sperm and a single egg, is there more than one resulting DNA combination they can form given the same human process of combining that genetic material. That is if I have the  DNA off an egg sequenced and the DNA off a sperm sequenced, can I programmatically determine the DNA of the child formed by that egg and sperm?

This is a very-excellent as-well fundamental question

If there are possibilities of variation... practically impossible to test. However if clones of a single egg and clones of single-sperm, could be prepared, that would be comparable to what you're searching-for; but when told "exactly 1 egg and 1 sperm", there you get  only 1 scope to fuse them so you have no way to test other possibilities. In Louis Carroll's term,  "Nothing is impossible; but some things are impassible".

@AlwaysConfused, I'm approaching this from the point of view of calculating a genome from the supplied materials. I listened to a ted talk where a process could - accurately - predict a persons face from only their DNA and my immediate thought was "Could you do the same thing prior to conception".

Assuming we know the haplotype of the ovule and the haplotype of the spermatozoid, then the genotype of the future egg is perfectly deterministic. This is true to the extend that none of the following rare events occur:

mitochondria could be inherited from the father as well
mutations in the broad sense (see here for definitions) may occur outside an event of mitosis or meiosis
The egg might pick up random sequence floating in the environment

Of course epigenetics elements might vary but this is another discussion.

There will be any number of combinations that can result during recombination and chromosome separation no?

Recombination and segregation occurs during meiosis, that is before the formation of the gametes (spermatozoid and ovule). Once we take we consider the haplotype of a specific spermatozoid and the haplotype of a specific ovule, the genotype of the egg is deterministic (except above listed rare events).


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Which insect is this?
I just found what i think is an insect on floor of my balcony. From what i know, it is a Praying mantis. I want to keep it as a pet but for that i want to its exact species.

If it helps:
 Location: Bangalore, India
Temperature : $23^{\circ}$ C

Could someone help me identify it pleas.

I presume it is an Indian bark Mantis , Humbertiella ceylonica.

This mantis can be kept at between 21 and 28 degrees comfortably and does not need a drop in temperature at night.

References: bugzuk.com and Google


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What could I call such nucleic-acid-Sequence? A sort of palindromic sequence? is there any term called mirror repeat?
5'... ATGCC|CCGTA ...3'
3'... TACGG|GGCAT ...5'
or say
5'... AAGT|TGAA ...3'
3'... TTCA|ACTT ...5'
or in generalised way; on each strand;
ABCDEF|FEDCBA
Is there any terminology for such-sort of repeat? A sort of palindromic sequence? A sort of inverted repeat? or mirror-repeat?  Does they really exist in nature?
(I could not yet found any helpful answer in web, including wikipedia.)
UPDATE
I asked this question because the term "palindromic sequence" is not like the situation in OP but "palindromic sequence"  is like this:
5'... ATGCTTTC|GAAAGCAT ...3'
3'... TACGAAAG|CTTTCGTA ...5'
or  in general;
5'... A B C D E F | M N P Q R S ...3'
3'... S R Q P N M | F E D C B A ...5'
Where on single-strand there is no symmetry when read (3'---> 5') and (5' ---> 3').
BUT I'm not telling like that. i'm telling about a situation where a reflection-symmetry present in each single strand when read (3'---> 5') or (5' ---> 3').
like
5'... A B C D E F | F E D C B A ...3'
3'... S R Q P N M | M N P Q R S ...5'
From no angle it is a palindromic-sequence because the symmetry is not between 2 opposite strand.
This question came to my mind when for first- time I'd taught about palindromic sequence. I was unable to "literally" match it with verbal palindromes like "AND MADAM DNA" . Rather it was looking to me like
I EAT CAKE
EKAC TAE I
So I thought, if really there exist any sequence literally like "AND MADAM DNA"... whatever if there is any terminology for it or not.

One other Q/A site mentions about a term "mirror repeat", with exact same  situation as OP,  but gave no reference and further biological importance.

http://www.answers.com/Q/Mirror_repeats_in_DNA

Latest revision of Wikipedia also mentions a term mirror repeat and everted repeat, but no further explanation and hyperlink is given.
Another result from google search.

    URL: https://s3.amazonaws.com/classconnection/27/flashcards/2952027/jpg/mirror_repeat-14FB21C6EBF540D2120.jpg

I found some links in web, but some are  about other-topics based on DNA-symmetries, and some (those giving a direct  definition or  terminology) contain too-little information and no reference, like this:  http://www.answers.com/Q/Mirror_repeats_in_DNA

I'm wondering so-many websites used the term "mirror repeat" exactly in same meaning as I asked !!!! but none reaches to origin of the term. https://quizlet.com/11685525/chapter-8-slides-flash-cards/ , https://o.quizlet.com/o4SEbpAdTIwyIgNv6uLjMA_m.jpg fig 8-18 , https://www.studyblue.com/notes/note/n/nucleotides-and-nucleic-acids/deck/15240912,  (not readily accessible) https://s3.amazonaws.com/classconnection/27/flashcards/2952027/jpg/mirror_repeat-14FB21C6EBF540D2120.jpg (google image search result)

Another  from google search: http://slideplayer.com/slide/5171943/  .   Page 54/65.  URL:   http://images.slideplayer.com/16/5171943/slides/slide_54.jpg

The last attached image (from google image results) helped me  proceed a further lot because there are lot of articles in web about "Hoogsteen structure". Here is one.http://ase.tufts.edu/biology/labs/mirkin/documents/1995AnnRevBio-Mirkin.pdf

"a related arrangement is mirror repeat, in which the inverted repeat sequence is non palindromic. These sequences play important roles by showing or blocking protein synthesis by the ribosome- a process called transcription attenuation (see chapter 18)-or forming recognition sites for restriction enzymes" https://books.google.co.in/books?id=HmUdBQAAQBAJ&lpg=PA191&ots=TKF0OiYsAa&dq=biological%20significance%20of%20hoogsteen%20structure%20mirror%20repeat&pg=PA191#v=onepage&q=biological%20significance%20of%20hoogsteen%20structure%20mirror%20repeat&f=false

I think the situation you showed should be called mirror-everted repeats: to my knowledge they occur very rarely, and I only found references in this and this articles, even though no graphic explanation is provided.

No? I did not find them same.

please see my update

Sorry about that, just updated my answer.

Don't worry patterns are always tricky and almost whole of  biology is about patterns.

@ Roberto The links you gave wasn't helpful because first one (http://www.microbiologyresearch.org/error/authentication;jsessionid=1f6fbsnhjmcl.x-sgm-live-03) shows page doesn't exist, and second one (http://www.sciencedirect.com/science/article/pii/S0923250899001163?np=y) tells to buy (right-now which is not being possible, sad for that) and its preview contains no diagram, so you could provide some diagram etc. from these articles, I'll be grateful

No. the second article is not free-access.

I've let you know the second article is Not free access.

@ Roberto Preste Since the portion of your answer before the update isn't correct, if you kindly modify that-portion; I'll accept this answer.

The term:

‘reverse tandem repeat’

has been used by a few authors, but the Google search engine retrieves only 28 instances, of which no more than 20 are unique.
There are about three times as many hits for:

‘reverse tandem duplication’

which would be a more precise term in the current instance.

To whoever made the original entry. Answers in SE Biology should be written as answers not rhetorical questions, and supported by evidence or argument. That is why I edited this answer, discovering a more common term courtesy of Google's autocomplete.

As an example of biological symmetry, with my tongue in my cheek, I would call this a mirage.
My reason is that from a structural point of view a sequence of the type you present:
5'... ATGCC|CCGTA ...3'
3'... TACGG|GGCAT ...5'

does not have mirror-image symmetry. This lack of symmetry is because of the asymmetric nature of the phosphodiester bond. The 5' and 3' in your diagram clearly illustrate this fact (3' is not the reflection of 5' either typographically or structurally) If you don’t follow this, draw out each phosphodiester bond in the sequence halves. The base order in the second half may mirror that in the first half, but the directionality of the phosphodiester bonds is the same.
This is not just pedantry but explains why (or is consistent with) such structures appear to have no importance in biology and hence no name. (One only gives names to things one needs to refer to.) One would not expect such structures to occur frequently as they can not be generated by duplication (inverted or not). Those that do occur by chance lack symmetry and would be no more likely to bind proteins than any other sequence (symmetrical DNA structures apparently lending themselves to protein-recognition).
I imagine one could describe such structures in a mathematical sense and give them a name, but if that is your question it should be migrated to a different SE.

No not exact in mathematical sense... but rather was finding biological occurrence.  I can't confirmedly say there is no biological importance... one i've read about such a sequence in certain biochemistry text... but then I was in hurry situations... I forgot to note-down that . Later-on I could not recall where I've read that.  I yet think this question is properly about biology.

Thanks yes it is not about mirror-image of stereochemistry. It is just about genetic sequence.

If anyone don't know about a thing, how they can start conclude like "it has no importance", or "off-topic" or such. I agree I don't know that is why I am doing a question. But when a professional user doesn't know about a thing yet hurry to decide an action... it really wonders me. (wrote for every moderator, not any specific one)

@AlwaysConfused — You asked "Does they really exist in nature?" so a comment on their biological importance was a valid reply. It was not a suggestion that your question was unimportant. I had tried to answer your question from a biological perspective, but felt it possible that you were still interested in the logical aspects. In the latter case I felt it more likely that mathematicians or people interested in language would be more likely to be able to answer your question. Migrating it to another SE group is not rejecting it, just helping you find the appropriate audience.

Its ok but google search showing me, many source telling about such sequences, and even with same terminology (though none of them directs to proper source). Even another user posted an answer. Then a statement "such structures appear to have no importance in biology and hence no name. " was quite surprising. I wished  to keep the question in biology, but if you still think some-other site like maths or chemistry could give better answer, let me know.


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How long does it take for dopamine to reach normal levels after a significant drop?
The building block sequence for is: Phenylalanine << Tyrosine << L-Dopa << Dopamine. It’s produced in only a few, very specific regions: Substantia Nigra and the Ventral Tegmental Area. Although, on average does this take minutes, hours, days, weeks? And does releasing it between synapses or something else for normal activity affect the time?
Ultimately, I am trying to find a graph of the average anergia level after sex. Or similarly, dopamine levels after orgasm. Most of the research I have come across is about disorders or is too general. Also, there are informal articles and graphs of dopamine levels, but they very widely and are not sourced.

dupe from same user. http://biology.stackexchange.com/questions/51445/how-is-dopamine-produced-in-the-brain You know you can edit previous questions right? You should look at the comments, expand your answer and ask questions if you don't know what to do.

That's the whole point of SE way of doing things. You get new information and you expand the same question not create another one a bit more in detail. Or would you like someone to just answer vaguely to the other question and more in detail to this one? You should improve the previous questions instead of re-writing the same question it just gets confusing otherwise not to say completely redundant.

200 milliseconds as the half life of dopamine provides no meaningful (to me at least) connection to the question at hand. The Study of dopamine turnover uses a very obfuscated argot to laymen. Is there significance to this study in relation to the question? As for the question itself, is it too complicated to answer to a non-chemist?

Nice that you put everything together, that was my only point.

I transformed the chat into an answer...

I can see a couple of problems in the question:
First problem, you assume that anergia (not sure that's how you call being tired) after sex is caused by dopamine depletion, I'm not sure this is the case or that lack of dopamine has been related to anergia at all. We know from Parkinson patients that Dopamine is related with action initiation (http://www.nature.com/nature/journal/v466/n7305/abs/nature09263.html) not necessarily with lack of energy or motivation.
Second problem, depletion (the term you originally used) means no more dopamine is system, either because you block it somehow (antagonist), you block its receptors (receptor antagonist) or you block one of the precusors involved in synthesizing it eventually depleting your reserves. "Significant drop" needs to be quantified.
Dopamine (DA) synthesis is an ongoing process, and DA is an essential neurotransmitter / neuromodulator in the brain just like Serotonin (more on that later). This means that it probably has different roles. One phasic referring to its neurotransmitter properties and one tonic referring to its global levels in the brain and how it modulates ongoing synaptic activity.
Normal activity does not deplete DA, and yes, no matter how crazy you think you are, sex is considered normal activity. You can obviously have variations of basal levels of DA depending on your activity but they are way removed from the depletion criteria.
Furthermore, the brain is very parsimonious in its synthesis efforts, it has specialized molecules that recover neurotransmitters that where unused from the synaptic cleft, these molecules are appropriately called reuptakers.
Now to attempt to answer your question considering the problems:
I don't know about DA but I do have some experience with serotonin depletion.
Serotonin (5-hydroxytryptamine, 5-HT) is synthesized from tryptophan that you cannot produce endogenously. Lucky for us that tryptophan is in almost every food we eat which means that there is no lack of it.
You can, in experimental conditions, ask people to drink a glass of a very disgusting liquid that will bind to your tryptophan preventing it from being used in new 5-HT synthesis. It takes approximately 4-6 hours for it to work (e.g. http://web.stanford.edu/~knutson/ans/bjork99.pdf methods section), which means that in 5 hours you used up all your reserves of 5-HT. This meansthat your "refilling" process would be about the same time  in order to get to pre-depletion levels (you might be able to be in a functional regime before that if you ignore the reserves part).
So from this 5-HT example I would say that unless something is very different in the case of DA to recover from depletion it would have to be in the hours time frame.
Another way of looking at it can be looking at the half-life of the molecule which gives you an idea of how much time it lives. This can be used to calculate how much production there has to be to maintain a level of X. The turnover is the amount of time that it takes to, well, turn over, so replace DA in the system that should be in the same order of magnitude as coming back from a depletion experiment.

I may have been trying to be pretentious before by having "depletion." I was about to put this question on Cog Psych SE.  (It should not be asked on Cog Psych SE, correct?)

I wouldn't in its current form, but maybe people there can have some insight, you are not convinced with my answer?

Assuming sex reduces tonic levels of dopamine, you want to know how long it takes to go back up? I would say, as stated in the answer, that if it would take hours to go to basal levels after depletion it could take minutes to recover from a small dip because of sex. or do you have a specific question in mind?


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The meaning of the "Score" in ScanProsite
I'm doing some research about a proteïne which is sequenced, however Í'm not able to find any information about the score which ProSite scan shows after finding an possible domain profile.

I have read the prosite help, however there isn't anything which explains what the score means.

The score provides an indication of well a specific profile (which is a weight matrix) matches the profile for the domain. Section II.B. Profiles development explains this in further detail.
A paper that outlines the development of PROSITE notes that they primarily use a cut-off of 8.5 and explains the score thus;

the raw scores in PROSITE profiles are converted into so-called ‘log10
  per residue E-values’, allowing the computation of the number of
  expected matches with equal or higher score in a database of a given
  size. For instance a match with a normalised score of 9.0 or higher is
  expected to occur about once in a database of one billion residues.

Why isn't it just an E-value just like in BLAST? I read your references but I can't get it clear. Do you know how it's calculated? @Michael_A

The paper that I linked to outlines how the E-values are calculated and it also provides an explanation for why they used this approach.


text:
Apical meristem regrowth?
When the shoot apical meristem is cut out/removed, it induces lateral growth. I'm wondering if this means that that stem will never grow vertically again. Is there a way to stop lateral growth after the apical meristem is removed? Is there a way to grow that meristem back again?
Thank you

If you again cut all the apical buds of lateral branches, the same would induced on the lateral branches.

Keeping the plant alive, one way to maintain the "apical-dominance" of a certain branch, could be adding auxin (a group of plant hormone) artificially.  (the same function was served by shoot apex). But since you rejected the apical-meristem, the axis will no-more grow tall. However, an way could be there; grafting an apex on the cutaway top.

what plant? Different plants will give you very different answers here


text:
How can fennec foxes eat scorpions?
I just watched a video of a small desert fox (fennec) that toys and eats a scorpion. Although I am unsure of the exact type of scorpion, it is apparently quite able to sting. Another online instance of the same video states that the scorpion is Androctonus Australis. Not only is this breed severely venomous and claiming, as its name suggests, human lives every year, but it is also well armoured. You can hear it when the fennec chews on it...
Fennec Fox eats Scorpion
So, my question, which might be stupid: how can this fox take the scorpion in its snout again and again? I notice that it lets the scorpion go many times. Is it able to avoid being stung? Is it extremely resistant to venoms? I read in the Wikipedia article, that it eats insects, but was unable to find out more!
I was able to find some information about hedgehogs and snake venom, but nothing similar about canines. In the case of hedgehogs, a partial immunity is apparently due to a protein called erinacin in its muscles.
After a user kindly corrected my spelling, I found some comments beneath YouTube videos, claiming it was nearly immune to scorpion venom. Sadly without additional information.

Very carefully.  First remove the stinger, the rest is relatively easy.  In your video, you see the fox quickly bite at the stinger, then back off.  Over and over until the scorpion's abdomen was loose as a rag, unable to launch the stinger at 3:08 minutes.  3:32 - you can see the stinger is almost off.  3:40 - stinger gone, she can now eat it more calmly.

I have to admit it's hard for me to see if she gets stung. But even with these techniques, they must get stung every once in a while, right?


text:
Special bacteria in infants
This question is similar to a previous question, but is not the same.
I was told, you are born with a bacteria in your digestive track that are made by the body. Can a body in development create it's own bacteria from nothing? Also said by the teacher the first time you take an antibiotic it is gone forever?  Can a body in development create it own bacteria from stem cells? Is there such a bacteria, can it be cultured and re-introduced into the body?

No, no human (or any other eukaryote lineage) are able to "create bacteria". The story you were told is wrong.
However and interestingly, female parasitoid wasps seem to "create viruses" (Herniou et al. 2013). The viruses are part of the wasp genome (lysogenic phase) and detach (lytic phase) in the ovaries only. The viruses, then infect the caterpillar in which the mother lay its eggs. The viruses ensure to reduce the immune system of the caterpillar in order to protect the wasp egg (and later larvae) and ensure its development to adulthood.

Whoever told you this story is wrong. Bacteria are prokaryotic single celled organisms, humans are eukaroytic multicellular organisms. These are so different, that it is impossible to convert one into the other.
When babies are born, their digestive tract is sterile (see reference 1 for details and a huge amount of additional references). However, it is colonized by different species of bacteria in a matter of hours, depending on the delivery and also the feeding methods.
References:

Newborn baby digestive tract
Postnatal Development of Intestinal Microflora as Influenced by
Infant Nutrition
Why is initial bacterial colonization of the intestine important to
the infant’s and child’s health?

Pasteur and Redi disproved spontaneous generation a century ago.  So no, babies are not magically making bacteria in their guts.