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How do I measure bacterial growth in agar dishes (either by cell mass or by cell count)?
I am doing an experiment in which I am growing S. mutans in agar dishes, and I am not sure how I would measure the growth of the S. mutans. I am also not sure if I would do this by measuring cell mass or by cell count. Any ideas?

please specify what exactly you starting with and what exactly you want to achieve

@aaaaaa he hasn't been here for over 2 years.

The most simple way is seeding the plates with a suspension of bacteria ensuring that you spread the solution properly. Then you can count the number of colonies, wich would be equal to the number of single cells.
If you want to mesure the growth speed, usually it's simpler to just measure the diameter of the colonies, always ensuring you inoculate the plates with the same amount of inoculum.
Lastly, it's even easier to estimate the growth if your culture is un liquid media and you measure the optic density with an spectophotometer.

I don't understand the effect of not "always ensuring you inoculate the plates with the same amount of inoculum."

If you inoculate a plate with 100bacteria/ml and a second plate with 1000bacteria/ml, the second one will have more colonies, even if the effect of the experiment would have the opposite effect.

Thank you so much. And thank you for clarifying that statement. I was about to ask the same question. Also, I understand the second part, but I am still confused on what you mean by "seeding the plates with a suspension of bacteria ensuring that you spread the solution properly. Then you can count the number of colonies, which would be equal to the number of single cells." I'm sorry if this is a silly question, it's just that I'm in 8th grade and pretty new to this. I am doing this for science fair, actually.

Imagine you have a liquid media with a concentration of 100 bacteria/ml and you inoculate a plate with 1 ml. In theory, every single cell will grow to form a colony, so you must have around 100 colonies. If you don't spread it properly, all 100 colonies will appear clustered, and you won't be able to identify single colonies. That's why you must spread the inoculum yo form an homogenous layer over the agar, normally using an inoculation loop.

"Then you can count the number of colonies, wich would be equal to the number of single cells." - it won't. It will be equal to the number of CFUs, not cells.

you will almost certainly want to perform serial dilutions of your suspension, and plate the serial dilutions using the spread plate method (or pour plate method). The dilutions will make it much easier to count the number of bacteria.
Generally, it is not recommended to count more than 250 colonies on a plate for reasons of accuracy (but I never count more than like 50, because that is the whole reason for doing serial dilutions). Here is a nice picture of what I am talking about. It includes a description of how to calculate the number of organisms in the original solution. They have chosen to count the number of bacteria on the fourth plate (1:10,000 dilution) in order to estimate the number of bacteria in the original inoculum. Hope this helps]1

By the way, the prototypical selective media for S.mutans is mitis-salivarius agar. You should check out this paper about growing S. mutans http://jcm.asm.org/content/4/1/95.full.pdf

Your answer makes me happy, because it provides a real microbiological technique used in labs. You would make it even better by clarifying the difference between CFU counts and cell counts. And it would be nice to add that the process must be replicated to estimate error.

Ehhh alright, well CFU stands for colony forming unit. Each one of those dots on the plate is a colony, and we are assuming that each colony is the result of a single cell from the original solution. So by counting the number of colonies on the plate we are also counting the number of single cells in the original solution that started the colonies on the plate, aka colony forming units(CFU). And sure, you could do this in dup or triplicate if you want and report the average of the counts, but this method is understood to be just an estimation, so choose the methodology that fits best for you.


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Does bright environment strain eyes more than dim?
I'm trying to figure out how to modify my working conditions so that I can program longer without harming my eyes. Because doing so experimentally hasn't given conclusive results so far, I decided to ask for studies in this area.
Does looking at a bright screen in a well lit room strain eyes more than looking at dark screen in a dark room for prolonged periods of time? Or is there a middle ground somewhere in-between that is most harmless? Or is it a combination of contrasting screen/background?
I'm not asking for medical advice here. I already went to several doctors and they gave me different, sometimes contradicting answers, so I'm just looking for research.

Personal taste seems to matter a lot here, but for me the simple solution is just not to have a bright computer screen.  White text on a black background is far easier on my eyes.

Here's a link from the Oklahoma State University's Environmental Health and Safety suggestions on office ergonomics.  It's got the following:

If the light in the work area is too bright or too dim, the human eye has to work extra hard to compensate for these harsh environmental factors. People may not even be aware that their eyes are under duress, but over time they may develop symptoms of eyestrain.
Solution: Use indirect, ambient lighting and an adjustable light source at the desk, where extra illumination is required.

Most sources seem to discuss the effect of too much brightness, although there's a good chance that's a function of the fact that we often need interior lighting.  Where there are suggestions, it's usually to achieve some level of parity, such as from here:

Adjust the brightness of the display so it's approximately the same as the brightness of your surrounding workstation. As a test, look at the white background of this Web page. If it looks like a light source, it's too bright. If it seems dull and gray, it may be too dark.

As a side note, I would recommend f.lux.  It's a piece of software that, outside of daylight hours, adjusts your screen's color.  I can barely look at another computer after dark anymore.

And what's the problem with eyestrain? Is it going to have any permanent effect like causing myopia and etc?

@Pacerier That's a separate question that you can ask if you like, but essentially no.  It's annoying and hurts and is inconvenient.  http://www.mayoclinic.org/diseases-conditions/eyestrain/basics/complications/con-20032649

I think the principle is "everything in moderation". Environment should be not very bright and not very dimmed. Also, the contrast should be moderate too, i.e. having bright screen in dark room is not good. Also, he type of work should not be very constant, i.e. you should sometimes change looking at the screen to looking in the window and similar.
Remember, that the light is required for stimulating the brain activity.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

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Do brain cells shrink during REM sleep or a lucid dream?
In this BBC news article a study shows that during sleep brain cells shrink to open up the gaps between neurons and allow fluid to wash the brain clean.  But do the cells shrink and undergo the whole procedure during REM sleep and lucid dreaming?

According to the research(M. Nedergaard and team) it only says it was tested when mice were asleep but there is no information about which stage of the sleep. It would be interesting to know which stage of sleep in future.

I have to add that the authors do not show any evidence for cell shrinkage. In fact, the word shrink is not mentioned even once in the article. Therefore the BBC article is not correct. To answer your question, all we know is that there is more fluid clearance; the authors do not show the mechanisms for this.

For those who have access, here's the full text.
Having read the paper, I can't give you a good answer.  This study was performed in mice, not humans, and "sleep" was achieved in a few ways.  Mice normally sleep most of the day, so it was easy to get mice sleeping normally.  They also induced "sleep" through anesthesia (incidentally, they saw these same results in anesthetized mice, which I think is quite interesting).  The state of "sleep" was confirmed mainly through the measurement of brain waves, in particular the delta wave.  Delta waves correlate to deep sleep, and that's what they measured.  Panels D and G from figure 1 (below) basically confirm just that - the mice were asleep - and that's all we know so far.  More exciting research to be done!

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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What is the physiological difference between snorting/swallowing cocaine
I know that mucosa inside the nose absorbs cocaine molecules when snorting cocaine, but what difference is there compared to swallowing?
Also more cocaine administration equals more cocaine molecules in the brain equals more inhibition of repute equals more serotonin–norepinephrine–dopamine in the synaptic clefts equals more work for receptors equals more intense effect, right?  What about the duration of a particular molecule which inhibits reuptake? How long this particular molecule stands there?

You can easily google for this question and find plenty of disreputable sources, but this is another case where Wikipedia does an okay job.  There are some misleading and erroneous sentences, but this one basically sums it up:

Compared to ingestion, the faster absorption of insufflated cocaine results in quicker attainment of maximum drug effects.

Mainly, take a look at this 1981 article.  The researchers gave participants cocaine, measured drug activity, and did then did a great review of the literature.  They found that, like plenty of other drugs, ingesting cocaine results in a slower but longer-lasting effect.
Your stomach is not an efficient route of absorption for things besides water, alcohol, and aspirin; besides, it's highly acidic.


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Why do I need a flu shot every year, while many other vaccinations last years or even a lifetime?
Is it a viral vs. bacterial thing?
Is there just more variety among types of flu than other diseases, so that this year's vaccines don't cover next year's flu?

The flu virus changes rapidly so that the current vaccine doesn't work against the new strains.
The way vaccines work is that they teach our immune system what to look out for. The vaccine contains bits of the virus but in a form that can't cause a proper infection, the body learns what to look for and next time before the virus can really get going the immune system kills it off first.
In the case of flu, every year it looks different enough that the targeting mechanisms of our body don't recognise it. Flu being a RNA virus frequently mutates until it is slightly different. This is called antigenic drift, the changing of the antigens or the parts our body recognises.
On top of that there's lots and lots of types of the influenza virus, that can not only infect humans but others which affect other animals. Occasionally the virus might combine with a random other strain making it completely new: an animal flu and human flu hybrid. These are the epidemics of swine or avian flu etc. This recombination is called antigenic shift.
So each year scientists predict which viruses will affect us this coming year and grow them ready for vaccines. Of course there's some of the old virus floating around looking for someone to infect, but those infected can't be infected by it again if the immune system is working.

Thank you! Looking based on your answer at the wikipedia page for RNA viruses I see that polio and measles are also RNA viruses. Why don't they mutate as quickly as the flu? Or is there just less biodiversity among those viruses than the flu?

HPV is a DNA virus that mutates at the same rate as our DNA. In comparison, there's the viruses you mentioned that mutate slowly and HIV another RNA virus that mutates so fast every couple of copies has a mutation. RNA itself is less stable, so RNA viruses mutate. However the real mutation rate is all about the error checking of the enzyme. HIV has no error checking basically and doesn't care. Increased mutations means more variability and immune escape but more non-functional virus particles. Too much or too little is a bad thing.

OK, I think I understand. The influenza virus does less error checking than some other RNA viruses and so it mutates faster. Is that right?

Yup! The scientific term for this is that the polymerases lack proofreading.

Would also add the influenza virus has strains that infect many animal species, ranging from humans, birds, pigs, horses, seals,
whales, camels. Should two influenza strains infect the same cell, they can swap parts of it genomes. This allows the influenza virus to very rapid change. Much higher than polio and measles which only inflect humans.

What you call influenza isn't a specific virus which is always the same, but a virus that has numerous different strains. Flu virus is constantly alive on this planet, and there are numerous different types, such as the ones which infect humans, the ones that infect birds, and occasionally a virus that mutates to infect humans although it shouldn't as it infects birds only.
Viruses evolve very quickly. The strain of flu virus which was rampant last year definitely won't be the one to look out for this year. What scientists are doing is a very difficult job - they're tracking the progress of different flu virus strains and trying to make an educated guess about the strain or strains which might spread the most during the flu season. And then they come up with a flu vaccine which is a mix that targets the several strains that were identified as being the biggest threat.
It's a hit or miss kind of thing, and it's quite possible that the scientists get it wrong, or not necessarily wrong, but something happens in the virus evolution process that renders this year's vaccine useless.
Also, it's possible to get a flu vaccine and still get flu - if you happen to come in contact with a strain that wasn't targeted by the vaccine. Viruses evolve very very quickly, so vaccine isn't failsafe, virus can evolve in some other person, you come in contact with the virus and get infected despite being vaccined against the original strain.

I hear you that viruses evolve very quickly. It's interesting that the combination of viruses we call "influenza" seems to change so much more quickly than polio and measles (see comments on @AndroidPenguin's answer above).


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How does smoking, an environmental factor, cause cancer, fundamentally a genetic disease?
If cancer is fundamentally a genetic disease, how might an environmental factor such as smoking cause cancer?

Cancer is fundamentally a disease of genetics(it involves genes and genetic damage), but it's not a genetic disease in the way you might be thinking (strictly heritable). You cannot inherit cancer the way you inherit Huntington's. You can inherit an increased risk of cancer, though. Once you are born your genes are not fixed in stone forever. They can be changed with carcinogens or other processes.

Because cigarette smoke contains many carcinogens.  Carcinogens can cause cancer by directly affecting the genome.  Wikipedia has a list of those present in cigarette smoke, which includes classics such as lead, benzene, and formaldehyde, not to mention radioactive polonium.

There are carcinogens in smoke but they've not been shown to be the cause of cancer in smokers.  Note that some smokers never develop cancer or heart disease; some have lived more than 100 years.
Just because something is classified as a carcinogen doesn't mean it causes cancer in everyone and doesn't mean a given exposure to a particular carcinogen has any effect at all.  All smoking does is increase one's risk of developing cancer.  That it increases risk is not a fact but the association between smoking and cancer is significant, statistically.  (This means it meets certain mathematical criteria and is, therefore, not mere opinion).
Chromosomal replication is not perfect and a healthy cell can replicate only a limited number of times.  Cancer is characterized (in part) by a loss of this control.    When DNA mutates in a way that results in the loss of this control an otherwise-healthy cell (now a mutation) results.  Smoking increases cell turnover and the increased turnover increases the likelihood this type of mutation will occur.
You can think of skin cancers in the same way.  This is the reason an exposure resulting in a color change (sunburn, tanning including that from a tanning booth) increases the risk of skin cancer.
Over a typical lifetime we develop a handful of cancerous tumors.  They're killed by our immune system.  Symptoms of malignant cancer develop when the immune system hasn't been effective.

The fact that not everyone who smokes develop cancer does not rule out that those carcinogens be (amongst) the causes of cancer in those people who do.

Just out of interest - how could it ever be shown that the carcinogens in cigarette smoke caused a specific case of cancer? My feeling is that this is impossible, and that the chain of potential causation from smoking>carcinogens>increased risk of lung cancer is as good as we can get.


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What is the origin of viruses? How could they get both living and non-living characteristics?
I read that viruses are called intermediate between living and non-living particles. Well, if so, then where did they originate from?  From living or non-living? If they originated from either living or non-living then how could they have both the characteristics of living and non-living?

Here is a somehow similar post that might interest you. But it does not answer the interesting question of their origin.


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Adenosine metabolism
Are adenosine or its catabolites increased in inflamed airways? How can I assess this? I am trying to use inhibitors for adenosine deaminase, xanthine oxidase, and purine nucleoside phosphorylase, but I don't have a protocol.

do you want to measure these compounds ?

I want to see if Adenosine/ its metabolites levels at different inflammation levels of severerity

This depends on whose air way and what you are doing to inflame it.  Are you using a mouse model and having them huff LPS?


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Bioinformatics tool for "pairwise alignment" of complementary sequences?
I'm currently working on some ribozyme binding, and I'm looking for a tool that will essentially analyze the regions of the degree of complementarity in two sequences in order to extrapolate efficiency of binding. After thinking about it, I'm essentially looking for "the opposite" of BLAST, in that BLAST looks for regions of similarity in sequences in the same orientation, while I'm looking for  regions of complementarity in sequence in the opposite orientation.
Does such a tool exist?
EDIT 1
To clarify, I'm looking for a tool that can detect the most optimal regions of complementarity in two sequences when both are aligned as such:

5' TCGAAUAACTCGTCUGAUGAGUCGCUGAAAUGCGACGAAACCGTTAACGGA 3'
3'   GTTTTACGCAAAGCAGCGTAAAGTCGCTGAGTAGTCACTTTAATGAC   5'

The opposite? You mean regions of low similarity or actually complementary? If the latter, just use translated blast flavors. If you post an example sequence to clarify, I should be able to give you a precise answer.

Sorry for the confusion: looking for regions of high complementarity. Will edit question in a moment.

I'm not sure this is what you need since the sequences you posted are not actually complementary as far as I can tell. However, exonerate is one of the most powerful tools out there and can do this as well. Using these sequences as examples:

>query
  TAGCTTATTGATGGGAGGAGAGTCCGTGCACATGACAGACCTTGGCTGTCCCAGACTGCAGGAAGCCCAGG
  >target
  CCTGGGCTTCCTGCAGTCTGGGACAGCCAAGTCTGTTATGTGCACGTACTCTCCTCCCCTCAATAAGCTA

And this command (should be run on a *nix system):
exonerate -m coding2coding -q qq.fa -t test.fa -s 0

I get this output:
C4 Alignment:
------------
         Query: query [revcomp]
        Target: target
         Model: genome2genome
     Raw score: 312
   Query range: 71 -> 0
  Target range: 0 -> 70

 71 :                                                          CCA       :  6
      CCTGGGCTTCCTGCAGTCTGGGACAGCCAAGGTCTGTCATGTGCACGGACTCTCCTCProTCAATA
      |||||||||||||||||||||||||||||| |||||| ||||||||| |||||||||||+||||||
      CCTGGGCTTCCTGCAGTCTGGGACAGCCAA-GTCTGTTATGTGCACGTACTCTCCTCProTCAATA
  1 :                                                          CCC       : 65

  5 : AGCTA :  1
      |||||
 66 : AGCTA : 70

vulgar: query 71 0 - target 0 70 + 312 M 30 30 G 1 0 M 26 26 C 3 3 M 11 11

C4 Alignment:
------------
         Query: query
        Target: target [revcomp]
         Model: genome2genome
     Raw score: 309
   Query range: 0 -> 71
  Target range: 70 -> 0

  1 :                      GTC                                           : 66
      TAGCTTATTGATGGGAGGAGAValCGTGCACATGACAGACCTTGGCTGTCCCAGACTGCAGGAAGC
      ||||||||||| |||||||||||+||||||||| ||||| ||||||||||||||||||||||||||
      TAGCTTATTGAGGGGAGGAGAValCGTGCACATAACAGA-CTTGGCTGTCCCAGACTGCAGGAAGC
 70 :                      GTA                                           :  6

 67 : CCAGG : 71
      |||||
  5 : CCAGG :  1

vulgar: query 0 71 + target 70 0 - 309 M 21 21 C 3 3 M 15 15 G 1 0 M 31 31

Basically it gives you two alignments, one reading the target 3->5 and the query 5->3 and one the other way around.
Alternatively, you could do a translated blast search, tBLASTx which will translate both target and query sequence and so, should find complementary regions.

Is that where you grabbed yours?  I just installed it and got different results.  Some of it is visual (AA names, 1 versus 0-based indexing) but the scores are pretty different.

@Amory I'm using the one from the Debian repos, v. 2.2.0. Yes, the page you linked to is the homepage, so I'm guessing you just got a newer version and they've changed the algorithm a bit. Perhaps a different scoring matrix. In any case, the score here is irrelevant since it will depend directly on the length of the sequence.

@terdon On second thought, would doing a regular pairwise alignment with the reverse-complement of only of the sequences yield the same result?

@LanceLafontaine probably but it will be slower and perhaps less accurate. If you are looking for possibly complementary sequences that can bind to each other I would use something like exonerate or blast rather than a sequence aligner.

@terdon: I dont understand why you suggested tblast. Translation has got no relation to complementarity.

@WYSIWYG I recommended tBLASTx. tBLASTx will translate input sequences in all 6 frames which includes the - strand which is the reverse complement of the + strand. Therefore, it can be used to find complementary sequences since the 5'->3' translation of the plus strand will be the 3'->5' translation of the - strand.

yes but same translational product can arise with different codons and therefore you wont be able to assess complementarity..

@WYSIWYG indeed, I am just very used to translated blast searches and it was the first thing I thought of because they will also show weaker complimentarity. Since most homonymous codons change only in the wobble position, you might be able to spot complimentarity more easily precisely because of the code's redundancy. In any case, exonerate was my first suggestion, and I agree that your simple nucleotide blast is probably better than translations.

Just run blast with only the Plus-Minus alignments. See this post in biostar; it is similar to what you are interested in. This is for the standalone version. I am not sure about how to do it in the online blast.
If you have just two sequences then you can use UNAfold for checking complementarity.

You could try using a tool to estimate the binding affinities of the two sequences, i.e. OligoCalc
http://www.basic.northwestern.edu/biotools/OligoCalc.html


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Does Blood Loss Shorten Telomeres?
If blood loss necessitates immediate cell division to replace lost cells, does the increase in cell division correlate to shortening of telomeres? Does it further cause the Hayflick Limit to be reached sooner? Does blood loss accelerate apoptosis?

One that down votes should make a comment to inform the OP what goes wrong with its question.

while it may be true that blood cells themselves come from HSC, there are more things in the blood than just those cells.
Research such as http://www.telegraph.co.uk/health/9615779/Transfusion-of-young-blood-could-delay-onset-of-diseases-like-Alzheimers.html is showing that indeed higher than normal blood loss over a long period of time may then cause more rapid-than-normal cell division and premature aging. Something interesting along these lines: fasting for a day every few days is shown to increase lifespan, might be related to simply slowing cell division... we don't know.

Nope, nope, and nope.  A cursory glance over any page on hematopoesis will reveal that blood cells are replenished from HSC, hematopoetic stem cells, which are self-renewing stem cells.  Telomerase is activated in stem cells.

So what you are saying is that blood cells have no limit on cell divisions; and the telomere shortening theory does not apply to them? To which cells does it apply?

@Angelo Blood stem cells have no limit.  Stem cells theoretically have an indefinite potential to divide.  They express telomerase and are not subject to the Hayflick limit in the same way as other cells.


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Standard letter for 5-methylcytosine
I'm working on a piece of software that computes melting temperatures for nucleic acid duplexes, and I'm about to add support for 5-methylcytosine as a nucleotide base.  At the moment, the bases accepted by the program are adenine, cytosine, guanine, thymine and uracil, with their standard letters A,C,G,T,U.  Is there a standard letter for 5-methylcytosine?  The only example I've found is this paper, which uses an italic C for 5mc, but I want a distinct letter.  The three candidates I've thought of are:

5 - for '5-methylcytosine'
M - for 'methyl'
B - Since methylation of U gives you T, which is one place earlier in the alphabet, so methylation of C gives B.

Well, don't use M or B, those are already taken (C or A, and not A, respectively).  You can see the full list here: http://www.dna.affrc.go.jp/misc/MPsrch/InfoIUPAC.html (The enWiki article on Nucleobases lists a few others but I would ignore those as 1. D is present in both and 2. they are rare and inapplicable)
5-methylcytosine isn't on there.  If you want to be pedantic about it, 5-methylcytosine is an epigenetic marker and as such is by definition not a genetic sequence; that remains simply a C and, genetically, the sequence is the same, despite the fact that it may indeed make a difference.
Most of the time people use m5C, so I'd go with 5 if I were you.  That certainly isn't used for anything else and if you must use a single character most anybody will know what you are talking about.

As Amory suggests the IUPAC "Recommendations on Organic & Biochemical Nomenclature, Symbols & Terminology etc." (http://www.chem.qmul.ac.uk/iupac/) are probably the best place to start. From a quick scan the obviously relevant documents would be:

"Abbreviations and Symbols for Nucleic Acids, Polynucleotides and their Constituents"
"Nomenclature for Incompletely Specified Bases in Nucleic Acid Sequences"

These provide the complete description of the commonly used IUPAC nucleic acid codes, including both the one letter and three letter variants.

Just to fully document the IUPAC advice on this, here is the relevant section from the Nomenclature for  Incompletely Specified Bases in Nucleic Acid Sequences as reproduced here in the link provided by @Hamish McWilliam.

5.2. Modified nucleotides
In a number of organisms DNA and RNA are modified at certain positions. For instance, the DNA of Escherichia coli is usually methylated on N-6 of the adenine residue in the sequence 5'-GATC-3' [23]. The present nomenclature does not allocate any specific symbol to these modified nucleotides for the following reasons. (1) The presence or absence of a given modification depends upon the location of the DNA. Sequences modified in one organism may not be modified in another. (2) Modification is usually statistical, in that only a proportion of possible sites for modification may actually be utilised in vivo. Modification of a nucleotide or base in a given polynucleotide is not a function of the sequence per se. Although it is recognised that stable RNA species (tRNA and rRNA) often carry a constant pattern of post-translational modification. the present nomenclature is not intended to overlap with or supplant existing systems. It would probably be impossible to devise a simple and logical system that avoided all conflict with previous usage. One should therefore recognise that such conflict is possible and take steps to prevent it from generating confusion, for example in relation to the symbols B, D and S, which have been recommended for 5-bromouridine, 5,6-dihydrouridine and thiouridine respectively [1], or W, which is sometimes used for wyosine.


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Are recessive, deleterious alleles less common on the X chromosome than the autosomes in humans?
As there is a potential for them to be more readily purged in hemizygous males (and in cell lineages in females with the deleterious-allele-bearing chromosome activated), I would expect the frequency of deleterious alleles to be lower on this chromosome than in autosomes. Is this information known?

Just to make sure I understand the question. When you say "Is this information known", you actually ask "Are empirical observations coherent with this hypothesis?"

Yes, that's at least in part what I mean. Thank you, @Remi.b. I imagine other hypotheses might also explain this empirical observation, if it indeed exists. I would also be interested to know whether this particular hypothesis has found stronger support than alternative hypotheses. But I would be most curious, as you say, about whether empirical data supports this prediction.

"Monosomy for the X chromosome in humans creates a genetic Achilles' heel for nature to deal with."
The article I quoted1 tackles this issue.  It's from the turn of the century, though, so quite old in sequencing/genetic terms, but the science is still sound as far as I can tell.  Here's the money quote:

Hence, the X chromosome appears to have a lower gene density and should yield fewer deleterious mutations per megabase of DNA.

In short, yes, you're correct.  There appears to be less overall information on the X-chromosome, deleterious or not, and selection is faster; the X chromosome is just flat-out less diverse.  This article goes into quite a bit more but says essentially the same thing: "On one hand, the greater effectiveness of selection on males due to the hemizygous expression of the X, which may be further reinforced by sexual selection, is expected to lower the mutation load for females at shared loci."  Here is a more recent article stating the same: "This finding [X-chromosomes with lower linkage disequalibrium] is consistent with more rapid selection against deleterious mutations when the X is monosomic in males, and to a lesser extent, under random inactivation (Lyonization) in females."
Finally, here is a piece written a few years back by a colleague of mine that goes into depth on the subject.  The second half deals with population differences (also fascinating), but the first part has a lot of good detail on what you want.


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Did animals evolve from plants?
Did animals evolve from plants? Did animals' ancestors have chloroplasts in their cells?

Why do you think that animals evolved from plants?

@Michael Kuhn because animals and fungi (uniconts) evolved from biconts. Biconts currently represented only by plants.

I see! The relation of the eukaryote ancestor to the unikont/bikont split is still debated. Here's one option supported by rare genomic changes: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2817406/figure/fig4/ where a chloroplast-less ancestor acquires a chloroplast on the way to plants

Based on your comments to the answers and above... it seems that your question is "Did the common ancestor of plants and animals have chloroplasts?" In my opinion, this is quite distinct from "Did animals evolve from plants?"

No. Animals form the kingdom Animalia (or Metazoa) which is distinct from the Plantae kingdom.
Both evolved independently from single-celled eukaryotes.
In fact, animals are more closely related to fungi than to plants.

Did those single-celled eukariotes have chloroplasts?

@Anixx No. Chloroplasts originally developed in green algae, after divergence from the single-celled common ancestor of plants and metazoa.

Which implies that multi-cellularity evolved independently at least twice, once in plants and once in animals (and possibly in fungi as well). Interesting.

@Keith Ha! Actually, “Multicellularity has evolved independently at least 46 times …”

@KonradRudolph: Wow. That could have some interesting implications for extraterrestrial life. Planets where life has developed but hasn't evolved beyond single-cell organisms might be less common than I would have assumed. (Unless there's something special about terrestrial single-celled organisms that makes the development of multi-cellularity unusually easy.)

@KeithThompson Indeed, it does have these implications: There are potential hard-to-cross thresholds to higher life forms, which prevents their abundance in the Universe (and may help explain the Fermi paradox), but evolution of multicellularity is not one of them.

@Konrad Rudolph What are these "potential hard-to-cross thresholds"? What are they called (or what should I google for)?

@user17915 Such a threshold is usually called a “Great Filter”. There’s a good overview of the argument on Wait but Why.


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What is the difference between "lineage restriction" and "differentiated" in terms of stem cell biology
Is there a subtle difference between these two concepts or are they basically the same thing? When I mean differentiated, I don't mean terminally differentiated.

lineage restricted stem cells are multipotent i.e they can give rise to only a few types of cells. Embryonic stem cell to hematopetic cell is also differentiation. Differentiation just means becoming into a specialized cell which can even be a lineage restricted multipotent stem cell.

So they are basically the same concept?

differentiation leads to lineage restriction

I agree with @WYSIWYG and add that I tend to see 'lineage restriction' usually as a function of assay conditions  (ie the precursor cell population could become X and Y but now the cell can only become X, so the cell is lineage restricted) whereas differentiation is a function of phenotype (i.e. looks more like maturing cell X than maturing cell Y).   But the concepts are clearly inter-related

When you look at the development of the embryo, at the beginning all cells are totipotent, meaning they can develop into any cell type of the body. This changes relatively fast by differentiation, which means that the totipotent cells develop into more specialized cell types, which then can not give rise to all cell types. So the different germ layers (meso, ecto- and endoderm) develop and from these all the cell types in our body. See the first figure for clarification (from here):

Lineage restriction means that you have a differentiated cell line, which can only further develop into cells of this line. So hematipoietic stem cells can only further develop into cells of the hematopietic line (lymphocytes, erythrocytes, basophiles and so on), like shown in the figure below (taken from here):


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Why can't sodium butyrate be delivered orally in humans and other mammals?
I think I know why -- bioavailability problems but since I have no firm evidence to support this theory I thought I would ask the biology stackexchange community for their input. I'd like some firm bioavailability data of sodium butyrate in mammals, preferably humans.

Unpleasant taste is in fact the primary reason. Phenylbutyrate is an alternative that has a comparatively milder odour and taste and is therefore used instead.
https://www.mayoclinic.org/drugs-supplements/sodium-phenylbutyrate-oral-route/description/drg-20066057

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How essential is vitamin B3 to the diet?
I know this might seem contradictory since by definition a vitamin is an essential part of the diet but I have read that nicotinamide, a form of vitamin B3, can be synthesised from L-tryptophan. Is it possible for a person to synthesise all their vitamin B3 requirements from one's dietary intake of L-tryptophan?

According to one study:

It was calculated that if the excretory percentage of niacin metabolites in the urine were 60%, of the tryptophan ingested, the conversion factor would be a value of 67, meaning that is 67 mg of tryptophan is equal to 1 mg of niacin.

However, the study has a pretty low power with only 10 participants and an indirect measure of niacin.
Is it possible that a person could get all of their niacin from tryptophan? Probably - you just need to eat enough tryptophan, which is also an Essential Amino Acid. The body may preferentially keep Tryptophan (which it does not store) until Niacin runs out (which also cannot be stored).


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How is temperature sensed?
Can anyone summarize the mechanism by which when an object of a given temperature is placed in contact with, say, the skin on a human fingertip, the average speed of the particles of the object is converted into nerve signals to the brain?
If you can answer that, how about the format of how the temperature is encoded in the nerve signals?

In the periphery (e.g. on our fingertips), our body senses external temperature through nerve terminals, expressing certain TRP channels. These are ion channels that are sensitive to temperature (note that TRP channels can be sensitive to several things, such as pH, light, and stretch) and allow entrance of cations in the cell when the temperature is higher or lower than a certain threshold.
Six TRP channels have been described as been involved in sensing different temperature ranges1,2:

TRPV1 is activated at >43 °C
TRPV2 at >52 °C
TRPV3 at ~> 34-38 °C
TRPV4 at ~> 27-35 °C
TRPM8 at ~< 25-28 °C
TRPA1 at ~< 17 °C

Not surprisingly, TRPV1 and TRPV2 are also involved in nociception (=pain perception).
The exact molecular mechanisms by which different temperatures open different TRP channels are unclear, although some biophysical models have been proposed.3
I am not sure of the exact "format" in which sensory fibers encode different temperature, but I would assume that the neuron would fire faster the more the temperature is distant from the specific threshold (hot or cold).

1 Thermosensation and pain. - J Neurobiol. 2004 Oct;61(1):3-12.
2 Sensing hot and cold with TRP channels. - Int J Hyperthermia. 2011;27(4):388-98.
3 - Thermal gating of TRP ion channels: food for thought? - Sci STKE. 2006 Mar 14;2006(326):pe12.

How are objects of temperatures in the middle of the 18-24 °C sensed?  Is it expected that further channels will be found?  I really enjoyed your answer - it's particularly interesting to me to have discovered, as a by-product of following your links, how the burning effect of chilli peppers is as a result of TRPV1.

@Rory: 18-24 is covered by TRPM8

Also, about the chillies: that is a very nice example of a "false sensation". Chillies don't really burn you, but as capsaicin is detected by the same receptors as high temperatures your brain cannot distinguish between the two.

What is the mechanism by which the cell allows entrance of cations at a certain temperature?

@user1997744 I'm not an expert on this topic, but an educated guess would be that the structure of the channel changes with temperature.
Aside from reference #3 in my answer, this review also seems to go in quite a detailed description (in the "Activation mechanisms" section there is a "Heat" subsection).

To complement on nico's answer (I don't have enough rep to comment), TRP channels seems to be also sensitive to increment or decrement of temperature as reported recently in a paper by Gallio et al1.
Probably that channels have incomplete adaptative behavior that make them sensitive both to increment and absolute temperature values.

[1] Gallio M, Ofstad TA, Macpherson LJ, Wang JW, Zuker CS (2011).  The coding of temperature in the Drosophila brain. Cell 144: 614-624.


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Current state of direct RNA sequencing
I had a colleague ask me recently whether mRNAs could be sequenced directly. I found this Nature paper[1] published by Helicos in 2009, in which they describe their developments in the area. It's been several years since this was published, and yet RNAseq and most other transcriptomic analysis is still done by first reverse transcribing RNA into complementary DNA.
What is the current state of RNA sequencing? Has Helicos failed to deliver on their technology? Have any other platforms risen to the challenge (or attempted to do so)? Or is the technology successfully in production and still simply overshadowed by the wide adoption of traditional cDNA-based sequencing methods?

Ozsolak F, Platt AR, Jones DR, Reifenberger JG, Sass LE, McInerney P, Thompson JF,  Bowers J, Jarosz M, Milos PM. 2009. Direct RNA sequencing. Nature, 461, 814-818, doi:10.1038/nature08390.

Helicos stopped shipping reagents around 2010-2011, as they couldn't compete with Illumina. For now it seems that reverse transcription -> Illumina-sequenced cDNA is so much cheaper than any other option, that's the method that is dominant.
Oxford Nanopore has discussed direct RNA profiling, but unfortunately their first product still hasn't shipped (for DNA or otherwise), and they haven't even released data, it may be a little while longer.

There was a paper that just came out about in situ RNA seq, but at the moment the limit of the sequence obtained is an underwhelming 4 bp. Still, its a cool technique and if it is advanced it could be useful in single cell RNA-seq, without the need of amplification or library prep
http://www.ncbi.nlm.nih.gov/pubmed/23852452


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What are the limiting factors for gene length and number of exons?
I recently downloaded gene annotations for Homo sapiens from Ensembl for some bioinformatic analysis. The vast majority of the gene annotations have 20 exons or less, although there are some that have as many as 250. I know enough about gene annotation to take these predictions with a grain of salt, but it got me thinking...what are the biologically relevant factors that might limit the length, exon number, etc of a gene? Is there any real possibility for a gene to have 50 exons? 100 exons? 250 exons? From a biological standpoint, where is the line drawn and why?

I got the compressed (gzip) GTF files directly from the FTP site with wget.

Agree with mbq - titan is the longest gene I know of and it has well over 100 exons. Titin and dystrophin are well characterized genetically and not predictions.  titin is the champion exoner with 363 exons.
Its only examples like this that can allow the gene predictors to run on as long as they do I think as the predictions are trimmed heuristically to resemble the known gene structures/lengths/junctions etc.


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How do you go from virus infection to disease?
I heard on the radio a few days ago1 a discussion on viruses and diseases (go figure why :)).
The guest was very precise in how the virus enters a cell, how its RNA merges with the cell's one and how it turns the cell into a "virus factory" (roughly speaking).
The question which was not accurately answered was "and so what? how does this makes someone actually sick?"
One of the points vaguely confirmed by the virologist (following a question from the journalist) was that the immune response of the body (notably the raised temperature) was what we perceived as the disease.
Since their time was short, there were no more deliberations on that interesting point.
My question: what happens that turns the "virus replication" activity into disease? I understand that the raised temperature is a direct effect of the immune system fighting these foreign bodies (the virus) but there are other effects such as headache, cough, etc.
Are all of these a consequence of the immune system fighting back? Or is the virus changing the way the cells function, and therefore they fail at their intended activity?

1 French radio France Culture, the guest was Olivier Schwartz, director of the Dept of Virus and Immunology of the Institut Pasteur, link to the podcast (in French, obviously)

This question is very general and seems more appropriate to SE Medical Sciences.

In viral infections, the disease (on the cell/tissue level) is mainly due to immune response that results in inflammation, for example, of the throat mucosal lining, which can trigger symptoms, such as dry cough.
Each symptom has its own trigger. For example, in flu:

The mucous membranes lining the nasal and sinus cavities can become
  inflamed when infected with the flu virus. This results in increased
  pressure around the eyes and face, which may lead to a magnified
  headache (National Headache Foundation).

and

The immune reaction to the viral infection and the interferon response
  are responsible for the viral syndrome that includes high fever,
  coryza, and body aches (StatPearls).

How viruses cause symptoms is a broad question - it depends on the virus and exact symptom, so just few more examples:

In viral pneumonia, immune response triggers inflammation in the lung alveoli, which can result in shortness of breath (StatPearls).
In AIDS, HIV virus destroys CD4 lymphycites and thus impairs cell-mediated immunity, which makes the infected person vulnerable for infections, so most symptoms are from those infections, for example, oral thrush due to overgrowth of Candida yeasts in the mouth (MerckManual).

Viruses usually do not cause disease or symptoms by merely changing the function of the cells, but by damaging them, so it's more about "injury" than just a changed function. The damage of the cells and the viruses themselves trigger inflammation and most of symptoms usually originate from it.

Thank you very much. Does that mean that the functions of the cell themselves are not degraded to the point of a malfunction? In other words, if a cell is supposed to work in a certain way and a virus comes in - the activity of the cell is not significantly impaired? (which could lead to something not being produced, or over produced, or something else being produced instead (beside the virus replica))

@WoJ, It's more about damage of the cell, which is worse than impaired function. I expanded my anser a bit.

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Where are the statistics for vaccine side effects?
My son told me that that during a discussion at school someone mentioned statistics about side effects of vaccines (I assume that the discussion was about standard vaccines in France). The numbers were completely off (1/100 "illness", 1/100 "death" - again, these numbers do not make sense).
I wanted to provide him facts to rationalize (quantify) the discussion but it is now an hour I am searching on French, Canadian and US official sites (as well as WHO) and I cannot find any statistics on side effects (from mild to mortal).
I understand that "side effects" and "vaccines" are general concepts but I want to start with anything to just show the error. Let's say that "side effect" is anything from "reasonably impacting" (so not an arm which hurts for 48 hours) to death, and "vaccines" is anything from the typical set a child will get.
Is there a place where such statistics are available?
Please note that I am not talking here about "vaccines cause autism" (there is plenty of information about that) or "vaccines are not useful" (plenty of comparative studies as well). I also understand that vaccination is a pro-vs-cons decision, I have a hard time finding the "cons" in the form of numbers.

(World Health Organisation, 2014. p. 2) shows the adverse effect (side-effect) rates for the MMR vaccine. For instance, fever  between the 7th to 12th day after vaccination occurs in 5 to 15% of vaccine recipients and rashes occur in 2-5% of vaccines, etc. Page 6 summarises the results in a table. As you point out, the adverse effects are variable in severity and dependent on the particular vaccine; an organisation like the WHO will take into account the risk and severity of these adverse effects before recommending the use of the vaccine. And as you point out, it is not believed by the scientific community at large that vaccines have links with autism.
References
World Health Organisation. (2014). Information sheet observed rate of vaccine reactions measles, mumps and rubella vaccines.

Thank you, this is an excellent stating point - particularly the page 6 you mention. I will translate it to French and make it available for discussion.

There are WHO information sheets on different vaccines here, and there are informative tables at the bottom of each technical report and studies cited throughout. The CDC has an extensive publications list on vaccine safety, and by accessing the "Specific Vaccines" tab at the CDC immunization safety office, you're directed to information on individual vaccines.

The CDC links for specific vaccines have products listed with links to FDA information pages. You can look through the drug package inserts for good information on adverse events.

@CKM: thank you. I have gone though the WHO site and found information about the kind of side effects but not the numbers. The specific sheets you point to in your second link are excellent - I just went though two of them and they give rates for mild effects (not for severe, but that's a start and I will dig further). I also saw the VAERS site mentioned elsewhere, but it is a technical reporting system, without statistics. Anyway - I have now plenty of information to prepare my son for the war for science :) Thanks again.

@CKM: thank you. I have gone though the WHO site and found information about the kind of side effects but not the numbers. The specific sheets you point to in your second link are excellent - I just went though two of them and they give rates for mild effects (not for severe, but that's a start and I will dig further). I also saw the VAERS site mentioned elsewhere, but it is a technical reporting system, without statistics. Anyway - I have now plenty of information to prepare my son for the war for science :) Thanks again.

@WoJ Well the statistics presented in the WHO technical documents are reported in tables as events per n doses, and so using MMR as an example, rash is reported as 5 per 100 doses or 0.05% for the measles vaccine.

Also consider that for relatively safe vaccines, serious adverse events such as grade III and IV may not have occurred or been linked to the vaccine administration, and so those weren't reported.


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What are these white spots on a dracena
I have a Dracaena Marginata which started to have some white spots. They turn out to be some kind of "mold"

which can be removed when swapping the leaf and then leaves some discolored spots

They usually appear when the leafs get yellow (because of it, or because I have forgotten to water for too long) and seem to be more present at the base of the leaf.
What is this?
And more importantly: is it a problem for the plant? (minor issue, though it is a gift from my children) or for me? (major issue, and death sentence for the plant)

I think  they are bugs for further info, I dont know much about plants.

I do not think so, they are completely immobile and look like some sort of mold when scrubbed

It is, as har-wradim suggested, scale. We had them on our Dracaena, I suggest you get a pesticide on them quickly, make sure to get all of the plant, they like to be around the base of the leaves near the trunk of the plant, and contemplate removing the worst affected leaves, we lost our plant because of it!

Looks like some kind of scale insect

These are plant pathogens commonly known as scale insect (Coccoidea). Among the genera mentioned to infect Dracaena marginata here and here the most likely candidate is Pinnaspis.
They are close relatives of aphids and psyllids (and more distantly -- also to true bugs). Cochineal is probably the most famous representative of the superfamily. Scale insects suck host's sap and can be quite dangerous to the plant. Adult females are immobile and the spreading is performed by nymphs and (when present) males.
As far as I know they are harmless to humans. When digested (products of) at least cochineal can cause allergic reaction in some persons.

Thank you - I will use some of the methods I found on the net to hopefully get rid it.


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Are there wounds which never completely heal?
I have a cut on a knuckle which occasionally opens (usually during winter), to disappear after some time (it is usually fine during the summer). This is going on for years now and yes, I will show this to my doctor (it is more a nuisance than anything else but there is the risk of infection).
Then during a recent discussion about the Vietnam War, the story of Phan Thi Kim Phuc was mentioned and I recall that I read years ago that she said (quoting from memory) that "[her] wounds still open, usually in summer".
I was wondering what is the mechanism of such wounds which heal, but not completely (to reopen after some time or on some conditions).
Her story is horrific and the extent of her wounds (and also the nature of the wound - inflicted by Napalm) make me think that there may have been some changes in the skin so deep that the consistency of the skin is not there anymore (wildly speculating).
In my absolutely minor case, however, there are no particular reasons for the wound to open - it is just closed and then, sometimes, decides to reopen to re-heal some time afterwards. Since this is otherwise healthy skin (it looks perfect when the cut is closed) I wonder if there are mechanical or chemical reasons for these behaviours?

Yes, there is a mechanistic (and an environmental) reason for the same lesion to occur and heal every year. You can alter this with some effort, though. Use a high quality moisturizer for your hands year-round, and wear gloves outside in the winter. If you adhere to this, your skin will not break open.  After a few of years of this, it will have really finished healing itself. This is much cheaper than moving to the tropics, where it would not occur (but other things will.)


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Is there a relationship between HDL-C and LDL-C?
For a gentle introduction to cholesterol and its functions, see a great answer on SE Biology
Whenever I read about how to deal with cholesterol level, the rule is to keep a low LDL fraction, ad a high HDL one.
How to achieve this usually falls into the categories of a healthy body (sport), a healthy diet and possibly medicamentation.
Since generally the advice is more or less the same for both goals (lowering one fraction and increasing the other one), I was wondering if there is a strong relationship between these fractions. In other words - is moving one in the right directions automatically drags the other one (also in the right direction)?
Anecdotally (and this is what triggered my question), I saw my LDL crash almost by 250% (not by chance but through a good diet, etc. - over a few months) and, surprisingly, the HDL go down by 30% as well.


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Garden plant in south of France
When visiting the south of France (around St Tropez) I had a plant in the garden which I initially mistook for mint but the aroma of the leaves (when rubbed) was distinctly different (I cannot put a name on it, it is sweet and remotely reminds of orange).
The plant has bare branches (it is a bush), and beside the leaves there are some round things which I took a picture of (sorry for my abysmal lacks in correct botanical words - these are the last two photos).
The photos are as of end of October.
The leaves are not smooth, they have some kind of tiny barbs which I can feel when rubbing the leave upwards (towards the petiole). The other way round (from the petiole) is smooth.
I cannot tell about the taste yet as my wife suggested that I wait for more information (just kidding).


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How difficult is it to adapt an existing vaccine to a virus variant?
There is (at least in France) an ongoing discussion about the Astra-Zeneca vaccine which is perceived as "outdated" because of the prevalence of new variants (the vaccine was designed based on the initial virus)(*).
How difficult is it to create a new vaccine that targets a new variant of the virus? (specifically adenovirus vector vaccines like the AstraZeneca one, but any general information is welcome as well)
My understanding is that the clinical trials are not needed anymore (in the same way as a flu vaccine is recreated each year without clinical trials because the difference is in the virus variants only) so is there a strictly biological, incompressible delay? (ability to target the new variant)?

My main question, related to biology, is above, the following alternative questions are OT for the site, but I am asking them in case they would be relevant:

Or is there a financial aspect? (too expensive to create a new vaccine)
Or is this because Astra-Zeneca believes that the current vaccine is OK, despite the backslash?

(*)

An example of the reluctance (in French): https://www.dna.fr/sante/2021/02/19/haguenau-la-moitie-des-50-64-ans-refuse-le-vaccin-astrazeneca.
In SA the AZ vaccine was stopped due to concerns about efficacity on the new variant, which influenced the French opinion as we also have SA variants in the wild (again, in French): https://www.midilibre.fr/2021/02/08/coronavirus-lafrique-du-sud-suspend-lutilisation-du-vaccin-dastrazeneca-juge-inefficace-sur-le-variant-9360903.php.

Please note I am not saying this is the case - I am just curious how hard it is to create a new vaccine for a variant.

Can you share some info regarding the fact that AstraZeneca vaccine is "outdated"?

@FabioMarroni: there is an ongoing discussion in the French news about the AZ vaccine (vs the others). This is the default vaccine for <65 yo patients and there is a reluctance of the population to use it because of reports about the fact they are not effective for the new strains. It may or may not be true (and is another interesting question), this triggered my main question (and the extra ones in the exact context of AZ).

@FabioMarroni (cont'd) An example of the reluctance (in French): https://www.dna.fr/sante/2021/02/19/haguenau-la-moitie-des-50-64-ans-refuse-le-vaccin-astrazeneca. In SA it was stopped as well, which influenced the French opinion as we also have SA variants in the wild (again, in French): https://www.midilibre.fr/2021/02/08/coronavirus-lafrique-du-sud-suspend-lutilisation-du-vaccin-dastrazeneca-juge-inefficace-sur-le-variant-9360903.php. Please note I am not saying this si the case - I am just curious how hard it is to create a new vaccine for a variant.

@FabioMarroni: I updated the question with the last part of my comment to indeed give some context (in French, unfortunately)

Are you asking about vaccines in general or specifically about adenovirus vector vaccines like the AstraZeneca vaccine? I can imagine that the steps to adapt to new mutations differ between different types of vaccines.

@Arsak: I am particularly interested in adenovirus vector vaccines like the AstraZeneca vaccine, but any general information is welcome - if relevant (= if there is a common trend between different kind of viruses)

This question seems to me to be off topic as it relates to industrial pharmacy, rather than a biological problem. And I don't think we need to know about the attitude of the French public. Pasteur must be turning in his grave.

@David: France was for context. If you feel that my question about a "strictly biological, incompressible delay" is indeed off-topic please vote to close. I was not completely sure myself that this would be in-topic but I do not think there is a better place (and I tried to keep it limited to biology)

I did vote to close. You might try SE Medical Sciences, but this sort of question is in the realm of Pharmaceutical Engineering, where even the most experienced people on this list are dependent on general articles in Nature and the like.


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What kind of hornet is this?
I live in France, in western suburbs of Paris. For a few days I have seen two of the insects below in my apartment. It is slightly smaller than a thumb, say 4cm (1.58") (sorry for not putting a ruler next to it but I was afraid it could chomp out my hand).

I tried to use this picture to differentiate the hornet:

(from left to right: bee, wasp, European hornet, Asian hornet).
It looks like this is the European hornet and I did not kill it (apparently they are useful, not sure about that) but would like to be ready with the flamethrower next time if needed. We are also actively encouraged to report Asian hornets.

You've identified it correctly; the size/markings/coloring are right for the European hornet worker female. They should not be in your house, though; I'd be concerned that there's a nest in the building and some of the hornets are confused as to how to get outdoors. If you can open the window for them, it might work, but move slowly. I really hate killing things, but if they were stuck in my house (and this used to happen with some regularity at one of my dwellings) I would use a rag or whatever was necessary to protect my humans from a confused hornet trying unsucessfully to get outside.

This is indeed a European Hornet (Vespa crabro) of the genus Vespa

The European hornet (Vespa crabro) is the largest eusocial wasp native to Europe. It is also the only true hornet (genus Vespa) found in North America, having been introduced to the United States and Canada from Europe as early as 1840.Vespines, such as V. crabro, are known for making intricate paper-like nests out of surrounding plant materials and other fibers. Unlike most other vespines, reproductive suppression involves worker policing instead of queen pheromone control, as was previously thought.
This species stings in response to being stepped on or grabbed, but generally avoids conflict. It is also defensive of its nest and can be aggressive around food sources. Care should be taken when they are found in these circumstances, as they may sting without warning. European hornets are largely carnivorous and hunt large insects such as beetles, wasps, large moths, dragonflies, and mantises. They also feed on fallen fruit and other sources of sugary food. Mutual predation between medium-sized hornets and the Asilidae (robber flies) is often reported. Source: https://wikipedia.org

Image ref: https://www.inaturalist.org/photos/18078852, Photo 18078852, (c) Jakob Fahr, some rights reserved (CC BY-NC), uploaded by Jakob Fahr


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Is this a local insect?
The monster below got into my house today (west of Paris, France). It is about 3 cm (1.2 inches) long.

I have no idea if this is a local insect that I would then let free, or some invasive species I will kill (we have from time to time alerts about invasive insect species (especially mosquitoes) that put in danger the local ones)

Incidentally it looks like it has a couple of parasitic mites on its legs

@bob1: ah, I thought that was dust (she spent sometime in the house)

I don't think those are parasitic mites - I think they are pseudoscorpions - maybe hitching a ride to new homes?

I have no expertise in (French) insects, but this looks like it might be a crane fly (family: Tipulidae) in the genus Ctenophora.  The larvae of these flies feed on decaying wood, so a lack of (partially) dead trees or other dead wood in your vicinity would suggest this is not correct.
The hunched-back with long legs are suggestive of the crane-fly family and the V-shaped groove on the back more-or-less connecting the wing-bases is (according to the wikipedia article) characteristic of this family.
In particular, this looks quite similar to many pictures online of the Cone-horn cranefly (Ctenophora pectinicornis), which is found in your area

Image by Margaret McLoughlin.
My understanding is that the simple antennae indicate that this is a female — males have feathery antennae.

Crane fly was my thought too. Looks like a case of mimicry with a wasp/bee as well.


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What do the signs +/+ +/- mean in this image?

I don't understand what this graph is supposed to explain, especially what the signs +/+ or -/- mean. I just know it characterises some rats.

Where did you find this graph? In a book? If yes, do they give their source? This would help a lot.

No it was just a copy in an handout given in class

Diploid organisms, such as we are, generally have two copies of each gene (excepting the sex chromosomes in males).  In order to display the genotype for each, geneticists use shorthand.  When referring to a gene, + means the wildtype, which is the "normal" version, and - means that the gene is missing, often a knockout.  So a typical individual's genome for a particular gene will be +/+, a hemizygote (one copy deleted) is +/-, and a complete knockout is -/-.
The image is talking about peroxisomes, claiming that they are required for life, specifically the gene Pex5.  You can look at the graph at see that compared to the wildtype (open circles), the -/- individuals (open squares) don't make it to a normal birth weight; their lifespan is less than three days.  The +/- hemizygotes (filled circles) match the +/+ wildtype, indicating that this locus displays haplosufficiency, which means that only one functioning copy is needed for a typical phenotype.


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What are uses of fossils?
What are the geological uses of fossils and how could it be utilised?
From The Institute for Creation Science:

Fossils are typically found in sedimentary rock, almost all of which were originally deposited as sediments by moving water. Subsequent processes hardened them into sedimentary rock, as overlying pressure squeezed the water out and the grains were cemented together. Often plants and animals were trapped, being buried in the sediments. As the sediments hardened into sedimentary rock, the dead things hardened into fossils.

This question appears to be off-topic because it is about geology.

What exactly to you mean by uses?

Utilized by whom? I use one as a paperweight.

That is a direct quote from a creation science website, a rather disreputable source.

@Amory did you read that article? It contains this wonderful gem of logic: "One more thing. These catastrophically deposited marine fossils, entombed as they are in regionally extensive sedimentary rock, are all found on the continents! There are hardly any marine fossils found in the deep ocean basins." So, fossils are found more often on the continents than in the deep ocean, and this has nothing to do with the fact that it's a wee bit more difficult to search the bottom of the ocean than to search my back yard! Ain't the bible grand?

Beautiful!  I think my favorite was "...these fossils were found as creationists did their research from a creationist/flood perspective. They found what evolutionist/uniformitarian seekers missed."  As if.

I want o lmfao because ...

Since you're talking about Geo, then the short answer to that would be:
To check how long such specie (animals or plants) existed on the planet (earth obviously)!
For example: You came to know about Dinosaurs using the Fossils and you made up their whole skeleton and then using your imagination you created the body.
Usage:
Keeping the above example in mind, fossils are used to know the period of extinction of the living being or the existance or both.
Fossils are sometimes used as Fossil fuel too, but that's in liquid form when they are decomposed anaerobically by the bacteria and all that info, please check the reference for this.
And what is the last paragraph about? Some information eh? I was not able to understand its usage and utility to the question! Sorry :)
Reference
https://en.wikipedia.org/wiki/Fossil_fuel (Fossil Fuel)


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Can retroviral delivery systems "overwrite" genes?
As the question states, what are the limits of retroviral genetic delivery systems?
Are they limited to adding additional gene sequences to a cell, or can they actually overwrite specified segments of DNA?
Or, more aptly described, can they remove one segment of DNA, and insert a new segment (whether the same or different length) in the spot where the old segment used to be?

To me "overwriting" seems to imply limited memory (e.g. based on using computer memory as a metaphor for DNA), while changes in DNA are due to deletion, insertion and single base mutations (substitutions). Chromosomal translocations are another case (as deletion->insertion).

Well, I am a programmer, so that is the first metaphor that comes to mind for me.  :)  . I'll reword and clarify a bit.

Retroviruses, such as HIV, have a genome that is composed of RNA.  Once inside the host cell, that RNA is reverse-transcribed into DNA; it is that DNA which is inserted into the host genome.  All retroviral genomes are integrated through insertion; there is never any replacement.
Some retroviruses do, however, disrupt normal gene function.  Mouse mammary tumor virus (MMTV) or Human T-lymphotropic viurs (HTLV) will often insert inside or near host genes termed "oncogenes," that, when disrupted, can lead to cancer formation.1,2  Viruses could cause up to 15% of cancers in humans.3  So, no actual genetic replacement, but there can definitely be genetic disruption and a deleterious functional change.
This ability, to insert new genes, has recently been touted as a new way to cure many diseases.  Here's the most recent case, where the researchers used a retroviral backbone to insert a functional gene into some children; i.e., genetic engineering (Side note: Every time you see an article saying how scientists used HIV to cure a disease or something, this is what they mean.  It's akin to calling dental X-rays "giant death lasers that fight cavities.").  With luck we will get better and better at it, but right now it's only successful in limited cases for very specific diseases; massive genetic engineering of humans is still far off (unless you count bone marrow transplants).

Nice answer, but a few references (especially for the removal function) would be great.

A friend is telling me about genetics research she has worked on regarding treating Huntington's disease, but that a true cure would be hard because it's genetic. So not being a geneticist, the first thing came to mind was well, use a retrovirus to deliver a cure. Would an RV be able to add code then which 'disrupts' the faulty genes, and add new code which does what the bad ones should've been doing?

@fileunderwater I added a few references, in particular a solid review.  It's not a particularly new concept so there's plenty out there.

@eidylon I tried to answer your question a bit, pointing to some research people are currently doing.  GE on that scale is still a long ways away but it's amazing the strides we're making right now.

Just to give a simpler example of what Amory has explained. Viruses can overwrite existing information, just not the way you would think if coming from the world of computers.
As already mentioned, viruses have the ability to insert their genetic information into the host's genome. They do this by essentially cutting the host DNA open and inserting themselves between the cuts. This insertion can disrupt a gene, thereby, in a sense, overwriting it.
To take a simple metaphor, consider the following sentence (a "gene"):

Hello, my name is Bob.

If I were to insert a new sequence of characters into that sentence, it's meaning would be lost:

Hellalkehfgawpif galsdhfblasud hyflaishbflaegfvlhD BFHDFLHFEiDBFKHDBfo, my name is Bob

While the original sentence is still there so it has not been overwritten in the strictest sense of the term, the information it contains has now been lost to the cell so the result is the same.


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Growth Hormone and diabetes
Growth hormone and insulin like growth factors are diabetogenic, so I assume that people with high growth hormone (say due to pituitary tumor) may be at high risk for diabetes.  Has any correlation been established between these two? I know that diabetes is a multifactorial disorder and so only a correlation may be established.

@leonardo I think this should not affect diabetes type 1 as dt1 is a mostly autoimmune disorder. So if some papers are available on this, I think, they would mostly be on type 2.

Yes:

That GH has an effect on glycaemic control is most evident from the abnormal glucose tolerance seen in acromegalics...

acromegaly is defined as abnormal growth of the hands, feet, and face, caused by overproduction of growth hormone by the pituitary gland.
Such an effect has been known for decades, which makes sense given how interrelated the axes are.  Although I think the best evidence is the fact that the side effects of growth hormone therapy says that Some patients have developed diabetes mellitus...


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Antibody production in secondary immune response
Can IgG antibodies be produced in the secondary immune response without the help of T cells?
Is the affinity of antibody for antigens higher during secondary immune response?

1)  The secondary response requires CD4+ T cells to activate memory B cells.  That first paper actually gives some evidence that some of the rapidity could arise because T cells and memory B cells are in very close proximity to each other in germinal centers.
2) Yes.  The affinity of antibodies increases during the initial infection, both through isotype switching and affinity maturation, producing far superior antibodies.  Upon reactivation, memory B cells can undergo further somatic hupermutation.


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Does mitosis include cytokinesis?
I found that some books include cytokinesis within mitosis, but some other books I have referred to include only the dividing of the nucleus as mitosis and do not include cytokinesis.
Can anyone help me out? Please include a source in your answer.

Cytokinesis is separate from mitosis.
What edition are you looking at?  To quote from the Fourth Edition:

The cell cycle culminates in the division of the cytoplasm by cytokinesis. In a typical cell, cytokinesis accompanies every mitosis, although some cells, such as Drosophila embryos (discussed later) and vertebrate osteoclasts (discussed in Chapter 22), undergo mitosis without cytokinesis and become multinucleate. Cytokinesis begins in anaphase and ends in telophase, reaching completion as the next interphase begins.

The mouse-over definition of cytokinesis there is:

Division of the cytoplasm of a plant or animal cell into two, as distinct from the division of its nucleus (which is mitosis)

Oh! I got confused between M phase and mitosis.


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Number of MHCs in neurons
I have read that neurons have proportionately less MHC molecules than other cells of the body. What is the advantage of this?

Antigen presentation by MHC will induce a cytotoxic response by the immune system, which is usually a good thing in the body since most cells can just divide and replicate again.  Neurons, however, are particularly ineffective at regenerating from such an attack, and are not easy to come by; they are also rather important!  Better not to risk it, eh?
That being said, neuronal expression of MHC is actually a pretty complex case, and this open-access article is a good start down the rabbit hole (see also here, here, and here if you have access).

What happens if a neuron is infected by bacterium, let's say which is definitely gonna kill it ? If it presents an antigen then also it will be lysed and if it doesn't then the bacteria will kill it.

Are the few MHC molecules there just so that the immune system is warned of the presence of bacteria ? Does that make any difference if few MHC presents the antigen or thousands present it ? Is there a threshold over which a cytotoxic response takes place ?

@biogirl Listeria monocytogenes does just that and can cause bacterial meningitis, which is highly lethal.  Neurons can respond to interferons and can upregulate MHC expression during infection; there's even some evidence that impairment of neuron function itself spurs that process (here and here).  T-cells can respond if presented with as few as 3 MHC-peptide complexes.

The brain also has resident immune cells, in particular microglia.

I might be wrong but I don't see any advantage of having lesser MHC. As you say T cells respond with as few as 3 MHC complexes. So then what is the point of having fewer MHC to protect it from cytotoxic response ; as you say in your answer ?

Just because they can doesn't mean doing so is particularly efficient.  Besides, T-cells aren't floating around through the brain like elsewhere.  Usually, it seems, MHC is not readily expressed unless induced by infection.


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Variation in MHC in humans
What evolutionary process lead to so much variation in MHC? What is the advantage of having such variation?

Here are two free articles that go into the subject very nicely, I think:

Major Histocompatibility Complex (MHC)
How pathogens drive genetic diversity: MHC, mechanisms and misunderstandings

The MHC loci are the single most important determinant of our immune system's response to foreign invaders and are absolutely necessary for discrimination between self and non-self.  Because of the massive diversity amongst those pathogens, no one single MHC allele will allow the best response.  For example, the delta-32 deletion that bears resistance to HIV also increases susceptibility to West Nile; if you're more likely to suffer from the latter, that is a fitness reduction that could be selected against.  Thus, more alleles will survive in the population as all can be advantageous.  This is called balancing selection.
Additionally, the microbial invaders mutate and evolve much, much faster than our genome does, so you want to have the greatest breadth of MHC present in the population and in an individual in order to maximize resistance to whatever may arise.  At a population level, it is also advantageous because it means that the entire populace won't succumb to a certain infection.  If everyone has similar alleles one virus could wipe everyone out; we observe something similar happen with our crops, for example, when grown in massive monocultures.  There is also a fair amount of evidence, mainly in humans and mice I believe, supporting a role for MHC in mate selection.  Individuals seem to find potential mates with different MHC alleles more attractive, presumably to maximize the fitness of their offspring.
MHC is an absolutely fascinating subject (I'm researching it at the moment!).


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Variations in Genome Sizes
Why is there wide variation in genome size amongst groups of protists, insects, amphibians and plants, but less variation within groups of mammals and reptiles?

You're asking about the C-value enigma, in particular this kind of diagram:1

The quick answer is that there is no "why" in evolution; things happen and if they're beneficial they tend to stick around more than the deleterious things.  The longer, (slightly) more satisfying answer is non-coding DNA.  Thanks to non-coding DNA the size of a genome doesn't even correlate to the number of genes.  The human genome, for example, has over 20,000 genes but is less than two percent protein-coding; the flower Utricularia gibba, however, has over 28,000 genes with about two orders of magnitude smaller of a genome, due to the fact that its genome is 97% protein-coding.  In short, there is no real meaning to be found in genome size variation due to non-coding portions, which while they are sometimes important regulators can often be just transposons (40% of our genome).  I will also point out that all of those groups you mention have species with significant polyploidy.

The are a number of other interesting ideas.  In the process of researching this, I stumbled upon the Animal Genome Size Database, which is an absolute gem of a treasure trove.  It's an unbelievable mine where I've spent a good half-hour just reading.  In particular, the statistics pages list interesting correlations for certain groups.  Mammalian genome size, for example, correlates:

Positively with red blood cell size, despite lack of nuclei
Negatively with metabolic rate
Not at all with developmental rate or longevity

For amphibians, however, there is:

Positive correlation with red blood cell and nucleus sizes in both frogs and salamanders
Negative correlation with developmental rate in many groups
Negative correlation with brain complexity in both frogs and salamanders
No strong relationship with metabolic rate in either frogs or salamanders
Some association with intensity and frequency of metamorphosis

If you have time, I highly recommend reading through T. Ryan Gregory's PhD thesis entitled The C-Value Enigma.  It's around 350 pages, but each chapter is in separate pdfs and is the most in-depth treatment I've seen, despite being about a decade old.  It's been moderately life-changing for me to read, some of the interpretations he presents challenged my thinking on the subject of genome evolution entirely.  Should genomes be treated as individuals, and what would that mean?  I digress.  Chapters 3, 4, 6, and 7 are what you'll want, in particular the last twenty or so pages of chapter 7.
Dr. Gregory now has a faculty position and his lab's research page is a little easier to read.  I love this image:

As genome size increases in eukaryotes, the percentage of the genome composed of genes (white circles) becomes smaller. Conversely, the percentage of the genome made up of transposable elements (black circles) increases with genome size.

It seems like the best way to look at genome size and find some meaning is within a specific group.  There are correlations, for example, that are present in frogs and salamanders, but not in either group alone.  Some of the groups are very unbalanced; in insects, only Orthoptera tend to have very large genomes.  Interestingly, a number of those groups also undergo some form of metamorphosis, but the correlations aren't what you might have expected:  insects that develop quickly and metamorphose have smaller genomes, but "[i]n a more general sense, small genome size seems linked to rapid diversification... Conversely, insects without metamorphosis may possess very large genomes..."


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Function of ER in reviewing mutated proteins
At least in the case of Cystic Fibrosis it happens that a mutant protein (which could actually function!) is held in the ER because the ER detects it as misfolded. Does this happen in every type of mutant protein?
If so, should I conclude that such genetic disorders are caused because of the total absence of a protein rather than because of a misfolded protein? If not, why would the ER or anything else in the cell allow some mutated proteins to do any job (Like in the case of Sickle cell anaemia, where an amino acid substitution happens)?
How do scientists conclude that a misfolded protein could have done a good enough job (Like in the case of cystic fibrosis)?

Membrane proteins have to go to the ER from where they are transported to the Golgi apparatus. Usually these proteins are translocated into the ER while translation is still going on. There are chaperones (such as calbindin) in ER which help in translocation and also catalyze initial steps of folding. ER is also involved in unfolded protein response. Unless the protein is properly folded it is not transported to Golgi. However, this process is regulated at many steps and I wont add a detailed explanation of the mechanism, in this answer.
To conclude ER is involved in this case because the protein considered is a membrane protein.

If we assume that the process which checks whether the protein is properly folded has nothing wrong, then is it safe to assume that all genetic disorders in proteins which are checked by the system happen because of the absence of those proteins (which will be held in ER) rather than because of a misfolded protein allowed to function ?

misfolded proteins can themselves be toxic to the cells and that is why their rapid folding or clearance is important. Sometimes the protein synthesis can overwhelm the folding ability of the cell which may cause the accumulation of the former. Plus, a mutated protein may simply be difficult to fold.
And, ER is not the only site for protein folding. Cytosolic proteins fold with the assistance of cytosolic chaperones (Hsps)


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Euthyrodism and goitre
I read in Tortora and Derrickson that goitre is associated with euthyrodism.
How is that possible?

I don't know the answer, but here is a fairly recent and highly-cited review that may be a good place to start: Krohn et al. (2005) Molecular pathogenesis of euthyroid and toxic multinodular goiter. Endocrine Reviews 26: 504-524

In this context, euthyroidism refers to the amount of hormone present.
What is a goiter:

The term “goiter” simply refers to the abnormal enlargement of the thyroid gland. It is important to know that the presence of a goiter does not necessarily mean that the thyroid gland is malfunctioning. A goiter can occur in a gland that is producing too much hormone (hyperthyroidism), too little hormone (hypothyroidism), or the correct amount of hormone (euthyroidism). A goiter indicates there is a condition present which is causing the thyroid to grow abnormally.

See also here and here for more of the same info.
ETA: According to this:

Chronic lymphocytic thyroiditis (CLT), also known as Hashimoto thyroiditis, is an autoimmune, inflammatory process that causes up to 55% to 65% of all euthyroid goitres...

Although, as the link I already gave above state, regular ol' iodine deficiency can still cause euthyroid goiter.

What condition can cause an increase in size of thyroid gland but still produce normal amount of thyroxine ? (I specifically want to know this.)


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Number of genes required to sustain life
Are there estimates of the minimum number of genes required to sustain life?
In what I mean by life here, I don't include viruses.

Interesting question, but you'll need to define needed as well. There are lists of essential genes, those whose loss is deleterious (at least in yeast). If you are looking for the theoretical minimum possible in an imaginary organism, that is a different matter.

Since RNA is the presumed precursor to DNA and might have sustained life before DNA evolved, do RNA counterparts count?

well.. i think if you exclude viruses then you should also exclude mycoplasma because both are obligate parasites.
So when you say minimal genome it is essential to define the conditions under which a genome has to function. The retroviral genome is sufficient to sustain life given a host. For free-living organisms the number of genes is obviously higher.

Depends on what kind of life you want!  The Database of Essential Genes lists genes essential for life for a number of species, although I would be wary of some of the numbers; bacterial results are probably more reliable but it lists 118 for humans and 2114 for mice.  There are a bunch of different numbers for different E. coli strains, with larger numbers being published earlier, go figure.
It of course varies by species.  In mid-August of this year, scientists reported the smallest genome yet: 112kb with only 137 protein-coding genes (predicted).  Crazy!  That doesn't mean it's the smallest number of genes though, just what we've found.  Some folks in 2006 predicted the smallest would be 113kb and 151 genes - pretty close close to the above, all in all.
For something a little more familiar and studied, though, Craig Venter has made synthetic biology his goal.  Part of trying to create life is knowing what the bare minimum is.  Working with Mycoplasma genitalium, he and his crew knocked out each gene and found that 381 were indeed essential.


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Can antibodies be formed against white blood cells after blood transfusion?
If antibodies are produced against other blood groups' red blood cells, why can't antibodies form against white blood cells, of any blood group? (even the same one, as MHC will be different in almost all individuals)

Antibodies and other immune responses do indeed occur against the donor's white blood cells. However, white blood cells are present in relatively tiny quantities (3-10 million WBCs per ml of blood vs 4-6 billion cells per ml).
Because the number of WBCs is so low, the immune reaction to them is also proportionally lower, with fever being a typical (and minor) complication of the reaction to WBCs. Some blood banks remove WBCs from blood to prevent these reactions.
For more information on the possible types of reactions to blood transfusions, see Wikipedia.
EDIT: Even in cases where the transfusion does not produce any symptoms, an immune reaction is most assuredly happening. In those cases, the immune system is simply killing off the foreign WBCs without any fuss.

Adding - very late to this - the most common symptom of a WBC incompatibility in a transfusion is a short-lived rash (looks like "heat rash") and low fever.
The HLA antigens are not very "antigenic" compared to the main blood group antigens, and the problem is mostly seen in people who have had multiple transfusions over a period of time.

Welcome and thanks for your answer. Could you add a reference to your answer?


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Do mitochondrial DNA have repair enzymes?
Mitochondria are considered endosymbionts originated from a prokaryote. So, do they have a DNA repair mechanism ?

Yes, mtDNA can be repaired by enzymes coded by nuclear genes.
http://www.ncbi.nlm.nih.gov/pubmed/22992591


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Transfer of antibodies from mother to fetus
My questions: When does fetus begins to acquire antibodies from mother? Does it continue throughout the pregnancy?
From Wikipedia: http://en.wikipedia.org/wiki/Passive_immunity

This occurs around the third month of gestation.

From Helena Curtis Biology :

During the last month of pregnancy , the baby usually begins to acquire antibodies from its mother,....

I believe that both these sources are reliable but they contradict when the transfer of antibodies starts.

only IgG-1, 3 & 4 cross the placenta. The transfer of antibodies would start as soon as umbilical vein develops.

@WYSIWYG Yup, those are the antibodies that are transfered but I am interested in when they are transfered.

as i recall, they are actually gathered by cells and actively transported across the placental barrier.  there is an Fc receptor.  a trained immunologist might be the best person to answer this question.

Both are technically correct.  Here's a review that goes into some detail about the process: IgG Placental Transfer in Healthy and Pathological Pregnancies.  It's worth a read if you're interested in the subject.  In particular, it cites a study of immunoglobulin transport which:

demonstrated a continuous rise in IgG levels in the fetal circulation between 17 and 41 weeks of gestation. Fetal IgG concentrations were only 5%–10% of the maternal levels at weeks 17–22 but reached 50% of the maternal concentrations at weeks 28–32. The majority of IgG is acquired by the fetus during the last 4 weeks of pregnancy, and fetal IgG concentrations usually exceed maternal ones by 20%–30% at full term.

So it begins a wee bit before week 17, so definitely within the second trimester, but it is only by the third that concentrations begin to be truly meaningful.  However, most of the antibody acquired, going above the maternal level, is done in the last month.


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What is the genomic position of HLA-B*1502 variation?
I've searched the position and SNP ID of HLA-B*1502 variation. However, I couldn't find that where this variant exactly located on genome or HLA-B gene.

HLA-B*1502 is not a SNP ID but rather, a name of an allele of HLA-B. This allele is made up of multiple mutations which can be found here.


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Why do Asian people have black hair and Northern people have golden hair?
I have got two questions.

Why do majority of Asian people have black hair?
Why do majority of people from the northern countries (Sweeden, Norway, Finland) have light (golden) hair?

Thanks for an answer.

Please put a bit more research effort into your question and please be aware of generalisations. Where is it written that all people from Asia or all people in Scandinavia have black or blonde hair respectively. Try to add some sources. I am fairly certain that you will find loads of people with dark hair colour in Scandinavia and that you will find people with blonde hair in Asia. Perhaps you need to go back to the drawing board and think a little longer about what you actually want to ask, e.g. how is hair colour determined, what genes are involved etc.

I am not questioning your own personal observation but I do question that you have seen all people living in Asia in order to make the claim that you make in your question. Also, may I please remind you that this is a scientific knowledge Q&A website. The purpose of this website is not to validate your personal opinions, claims or observations. If you do hold one of the aforementioned things please do back it up with data or legitimate source (published / peer-reviewed).

I'm voting to close this question as off-topic because it lacks primary research and appears to be based on completely unscientific presumption.

All people don't have those hair colors. All people from those Northern countries aren't blond, and there are blond people outside of Northern Europe; I don't know if you count Melanesians as "Asian", but they have blond people among them:
https://en.wikipedia.org/wiki/Melanesians#Incidence_of_blond_hair_in_Melanesia
Still; there are two, really three, different kinds of answers to this type of question.
1) Human populations differ through random drift and assortative mating: populations that are separated will develop different mutations over time that make them look different, and different populations may find different traits attractive (including traits that mark them as part of that population), which would work to amplify those differences even when the populations interact. There is no deep reason for those traits other than "that mutation happened to occur and spread through this population".
2) Certain traits are more or less useful in different environments, and thus will spread through natural selection. The issue here is that this is the kind of explanation people intuitively love (every difference must have a reason for its existence) but it's actually very hard to separate it from the first explanation.
3) Certain traits can be considered "human-default", as in the common ancestor of humans had it, most humans still have it, so the question of "why does a human population have this trait" is less relevant than "why do some human populations not have this trait".
So having said that, black hair seems like the clearly ancestral state, and so Asian populations probably have black hair for the same reason almost all human populations have black hair. And black hair seems common in great apes in general - Orang Utans are the only exception I can think of.
As for Northern Europeans, blond hair and white skin are actually one of those traits where it's hard to separate random variation from natural selection. It is quite likely there are advantages to being fair in high latitudes where there is little sunlight; you need less protection from the sun in the first place, and you need to be able to get enough vitamin D from sunlight on the other. However this applies much more obviously to skin than to hair. Blond hair is the result of very few mutations, which are thought to have appeared around 11,000 years ago. So it could be that those mutations happened to occur and to spread through those populations and not others and that's why they're blond and most other human populations (Melanesians excepted) are not. Or it could be that once those mutations happened they spread particularly well in those populations because it was adaptive in their environment. The question isn't scientifically settled.
https://en.wikipedia.org/wiki/Blond#Evolution_of_blond_hair


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Who was the first to talk about evolvability?
"Evolvability is the capacity of a system for adaptive evolution." (source) There are several other definitions though:

Who was the first person to use the word "evolvability"?
Who was the first to introduce the concept of evolvability? in which article?

More appropriate for ELU.se?  I'm not convinced either way.

You can probably trace he concept back to the dawn of mankind, it is such an obvious idea (not as it applies to life and evolution, just the idea of adaptive change). For example, you could even claim Heraclitus' Everything flows as an early example though adaptability is not implied.

My literature searches have turned up dead ends, so this is less of a full answer and more of some groundwork, but Google ngrams suggests somewhere around 1931 for the first usage, with meaningful usages beginning in earnest int he early 70s.  Their book previews from that era are sadly lacking; I can't find the usage of the ones from the 40s and 50s they do list sadly, but there are definitely some misnomers that show up in programming.  There's a 1973 work and one from 1977 that at least appear to be the correct usage, with the one from 1973 using it as a "new" concept.

Oxford English Dictionary has this as first occurrence: 1931   J. A. Thomson in W. Rose Outl. Mod. Knowl. 231   "We have already mentioned evolvability as one of the nine characteristics of organisms."