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Why myelin sheat does not cover the whole axon?
Is there an optimal lenght for myelin sheats to be effective and lead potential across the nerve cell? This has always bugged me.

The nodes of Ranvier (the gaps between myelin sheath segments) speed up the action potential because the electric current can jump from node to node (or gap to gap). If the myelin covered the entire axon, the signal wouldn't have the gaps to speed up the signal. As for optimal length, the gap is 1μm long, but can be longer, on the order of millimeters depending on the type of cell. The length of the myelin doesn't matter so much as the length of the nodes of Ranvier because they are where the Na+/K+ channels are found so the ion exchange can occur. This is how an action potetial can occur, so the myelin not covering the entire axon is crucial for the ability of neurons to propagate a signal.

Yeah I wanted to know if there was an optimal lenght for myelin coverage. I was thinking that probably with a too long myelin cover the jump of potential couldnt occur. Is that right?

Yes, so longer myelin as in a longer distance between nodes, would likely affect the efficiency of the current jumping from node to node .

Can you link me to some original research paper or review about this particular topic? I couldnt be able to find anything about. Probably I'm using the wrong keywords.

http://jnnp.bmj.com/content/40/8/769.short
This paper talks about it! :)


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How exactly does a prion cause disease?
During my study of the immune system,  I came across 2 very contrasting explanation as to how prions work.
Firstly, scientific American pointed out this:
link here:

"A major breakthrough occurred when researchers discovered that the infectious agent consists primarily of a protein found in the membranes of normal cells, but in this case the protein has an altered shape, or conformation. Some scientists hypothesized that the distorted protein could bind to other proteins of the same type and induce them to change their conformation as well, producing a chain reaction that propagates the disease and generates new infectious material. Since then, the gene for this protein has been successfully cloned, and studies using transgenic mice have bolstered the prion hypothesis. The evidence in support of the hypothesis is now very strong, though not incontrovertible

However based on this website

The guess was that they infected cells by causing normal prions to become misshapen, too. That theory, though, has been proven false, though it is still commonly believed. (See Sanctuary: Bad Bad Prions from Discover, dated 9 January of this year for an example of the ongoing belief.) The first serious attack on the prion-as-infectious-agent theory was reported in Medical Hypotheses in 1997. The article makes the case that prions trigger an autoimmune response.(1) As becomes clear the more one looks into the issue, this makes sense and fits the facts as known.

The problem right now is that my campbell 11th edition textbook, which is the newest edition and just recently revised also points to the same explanation as the first source.
Which source is correct in showing the method in which prions cause diseases?

i don't see any contradiction between the two quotations.
The first quotation describes the formation and expansion of prions. Note that many proteins have a potential to misfold into the so-called prions. Prions are misfolded proteins, which in their original, natural conformation have their specific biological functions or their function is unknown (which does not mean they don't have any).
The second quotation speculates about the disease caused by the prions rather than the formation of the prions. By the way, what is "a normal prion"? Prion is an abnormal state of a protein.

I agree with commenter Martin Klvana, but there are a couple things going on here I wanted to touch on:

I think that your second quote is making an error in saying that if prions cause immune responses that means they aren't "infectious" in the sense of propagating misfolding of homologous proteins. The standard understanding is that prions work biochemically by refolding prionogenic proteins to make more infection prion particles (see e.g. wikipedia), similar to your source 1 and your textbook. It's completely possible that these newly infectious prion particles lead to immune reactions in additional to the "infecting" particle. The key here is to separate the biochemical phenomenon (propagated misfolding of proteins) from the medical phenomenon (disease, immunological response).
To more directly answer the question: as far as I can tell from scanning a couple of articles (here, here), immune responses are not a prominent part of the best-known prion diseases, but I'm not an expert and could be wrong. I was unable to easily locate the 1997 Medical Hypotheses paper referenced by your source 2.
I haven't looked deeply into this, but that website appears to be run by an advocacy group and the "read full article" link is broken. So... I would put less stock in that source. Advocacy groups are fine and all but I don't think that their blog posts are good sources of biomedical science information.

Hope that helps.

it becomes really obvious the advocacy group articles is not written by a scientist as they talk about prions lacking a "life imperative" that viruses supposedly have. This lack of a metaphysical force is supposed to explain why it can't be an infectious agent instead it displays a lack of basic biological knowledge.

source: Stack Exchange

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

sort: votes


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MOPS Media Recipe Protocol - Well Defined
I am trying to find a clear protocol for making MOPS media. However, when looking online, I am finding that this media is loosely defined and I can not find a good protocol. (I have been looking for a couple of hours now)
In addition, there seems to be something called 'MOPS buffer'. What is the difference between the two?
Additionally, if someone could direct me to a good protocol for this media I would appreciate it.

This seems to depend strongly on what you want to do with the bacteria.  What do you want to do with you bacteria? Mops is one of the buffer substances used in bioscientific reasearch. Dissolved in water and brought to the right pH it makes MOPS Buffer.

I am doing a metagenomic anaylsis on soil, thus there are probably multiple bacterial types. It is suppose to be used for a general culturing media.

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


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Do single nucleotides spontaneously bind to ss DNA?
Do single nucleotides spontaneously bind to ss DNA? AT. GC. I realize the rhibisome is usually needed for making a strand, but what about randomly hbonded base pairs? Does this occur?

note that a binding might be thermally unstable; e.g.: assume 1-2 nucleotides in various approximations for annealing temperature of oligo-nucleotides such as https://jeltsch.org/annealing_temperature and note that annealing temperature would be very low, and potentially at a temperature where water is frozen

“I realize the rhibisome is usually needed for making a strand”. If this is indicative of your knowledge I suggest you do some homework by reading a book on molecular biology before asking questions of this type. An introductory section on basic chemistry would also not come amiss.

Potentially, transiently. There’s an entropic penalty for a single nucleotide to bind a DNA strand which would not be offset by any enthalpic gain (if there is any). I’ve no idea where that equilibrium lies, but it’s probably far away from base pairing.

I am no expert on the topic, but single stranded DNA is commonly found during DNA replication, when DNA helicase splits apart the DNA strands so that the DNA can be replicated. When this occurs, the two DNA strands naturally have a high affinity for each other, bearing complementary base pair sequences, and another molecule must be present in order to prevent the two DNA strands from re-binding. These are single-stranded binding proteins, and they bind to ssDNA to prevent re-binding from occurring. As this prevents the DNA from binding to the antiparallel strand, I would imagine it has a role in preventing single DNA nucleotides from binding to the DNA strand as well.

Please reference your response!


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Identify little green long legged bug

Discovered attempting to hide on bathroom sink handle at night, though bathroom light had been left on.
Barely reacted to attempts to capture it at all. No flying. No jumping. Just really slow crawling.
Found Eastern US. 2017/11/18

Please update question time of year it was found. If you have a better picture, please upload that, too.

looks like the nymph of some species of Hemipteran. Hold on...

The photo is not high quality, but the shape and size of the insect definitely point towards it being the nymph of some species of assassin bug (order hemiptera, family Reduviidae).
See this as an example:

Specifically, your specimen looks similar to one found in a home in Virginia.
The genus is likely Zelus, and based on it's greenish hue, I'd say it's an individual of the eastern US's most common species of Zelus, Zelus luridus (Pale Green Assassin Bug).

 Source: Christine Hanrahan

Nymphs are solid green, wingless, and with narrow bodies

The most reliable feature to distinguish this species from others is the pair of spines on the rear corners of the pronotum. These spines are long on the lighter colored individuals and shorter on ones that are darker. It can also be distinguished by dark bands on the distal ends of the femurs, but these can often be too light to be easily seen. [Source].


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Reason for name "Motile sperm domain-containing protein 2" if it has nothing to do with sperm
I am interested in a gene with the name "motile sperm domain-containing protein 2".
The entry for the human gene in uniprot suggests that it does not have any relation to sperm or spermatogenesis.
If this is so, why does the name make reference to sperm?

Please read the Tour as a new user to this site and especially how to ask good questions. Then, do some research yourself. Have you looked up the original papers on this protein or any reviews. They may be able to clarify a question of terminology. If you have to post, give a reference to the gene (Uniprot number and link) and tell us what organism it is in. Otherwise your question is unlikely to receive responses and is likely to be closed as off-topic.

Hi, I have checked many references and no chance!

Organism? Reference? Please read comments carefully before replying.

Hi David and thank you for your helps. There is not any organism or references that I can mention and there is no difference that this gene is expressing in which organism! we have a sequence of nucleotides that its annotation is refering to "motile sperm ...", So it is not important that this gene is expressing where in the animal kingdom. about the reference, it is not important to mention (I have mentioned one). many annotation database share same names, uniprot, trembl, NCBI. please attention that my question is this"why we use sperm in a gene name that is not working in sperm?"thats all.

Also asked on biostars

But eventually you are someone else did provide a link and I edited your question to indicate the species and take into account the content of the link. @DevonRyan has provided you with an answer. I suggest you accept it.

@FarbodEmami Note that you don't have to accept an answer if you don't believe it adequately answers your question (or if you believe the way in which it answers the question is unsatisfactory).

As you can tell from the gene name, it contains a domain (a "major sperm protein domain)") that happens to have "sperm" in its name. That doesn't mean that the protein itself have anything to do with sperm. There are a lot of examples of gene names like this, where they're named after some random domain they contain until later their names are changed. MSOPD2 has only had a known function for a few months.
As an aside, if you actually work on this gene then one would hope that you would have taken the whopping 5 minutes required to figure this out in pubmed.

Downvoted for the belittling snark of the "aside". If you think this question is too simple to be worth a Q&A on this StackExchange, then don't write an answer - downvote or vote-to-close and move on.


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How can some residues in the active site of enzymes be protonated with a pKa < 7?
It is reported in many papers, that some residues in the active site of enzymes need to be protonated to get functional enzyme, where these residues have a low pKa (for let us say 5).
How can that happen in the physiological conditions (with pH=~7.4)?
It is mentioned that a raise in the pKa value is happening during the catalytic activity to get that protonation state. But how is that happening?
Here is a publication where this protonation and pKa raising is described.
https://www.ncbi.nlm.nih.gov/pubmed/7306491

This conclusion is confirmed by the result that a group with a pK value of 6.7 must be protonated for the binding of methotrexate. It is proposed that the binding involves the formation with N-5 of dihydrofolate or N-1 of methotrexate of a hydrogen bond which has considerable ionic character and which lies within a hydrophobic environment. Further, it is suggested that the same hydrogen acts as an auxiliary catalyst which facilitates hydride transfer from NADPH to dihydrofolate for its conversion to tetrahydrofolate. Evidence to support this suggestion comes from the finding that the V profile is similar to the V/K profile except that the pK of the group which must be protonated for maximum enzyme activity is shifted upward by about 2 pH units. Such an increase in a pK value is consistent with the formation of a hydrogen ionic bond in the ternary enzyme-NADPH-dihydrofolate complex. The results of inactivation experiments with trinitrobenzenesulfonate appear to indicate that a lysine residue is necessary to maintain the enzyme in its active conformation.

Generally speaking, even though physiological pH is generally ~7.4, this is not necessarily the pH inside the enzyme active site. The enzyme's catalytic machinery may experience a completely different pH for one of two reasons: 1) because the enzyme is located in a place where the pH is simply not 7.4, and 2) The enzyme's amino acid composition shifts either the pH in the active site or the pKa of the active site residues relative to the surrounding environment such that the effective local pH in the catalytic site is lower or higher than 7.4.
For example, there are places in humans, such as the stomach or around muscle cells during anaerobic respiration where the pH is actually acidic relative to the standard physiological pH of 7.4, due to the presence of HCl or lactic acid respectively. Additionally, certain subcellular organelles, such as lysosomes, also are relatively acidic, since they are a site for breaking down proteins into amino acids.
However, the case presented in this paper seems to be an example of the second situation, where an enzyme that is in a pH neutral environment relies on one or more protonated amino acids to perform catalysis. This is relatively common. Basically, the enzyme's active site has an amino acid composition that when folded correctly, alters the local pH around the catalytic residues to favor catalysis. For example, in the enzyme acetylcholinesterase, the active site serine is rendered nucleophilic by being positioned next to a glutamate and a histidine, in an arrangement referred to as a catalytic triad. The glutamate is an acidic residue, and its close proximity to the histidine means that it will stabilize the protonated form of the histidine. Energetically, this makes protonation of the histidine very favorable. This causes the histidine to take a proton from the active site serine. Now that serine's oxygen is deprotonated, it can act as a strong nucleophile. After the serine forms a covalent interaction with the substrate, the histidine will facilitate a similar nucleophilic attack by a water molecule, regenerating the enzyme and completing the catalytic cycle.
Something similar is seen with the beta-lactamase TEM-1. In this case, TEM-1 uses a lysine (pKa ~11) instead of histidine (pKa ~6), so multiple acidic residues are in the active site to facilitate the deprotonation of the lysine during the catalytic cycle. In effect, the amino acid composition of the active site allows for the shuffling of protons needed for catalysis.
So to summarize, while physiological pH is widely regarded to be 7.4, an enzyme's catalytic machinery may experience a very different pH through either the cellular/physiological localization, or through the amino acid composition of the active site. In the latter case, the presence of acidic or basic residues can alter the protonation state of other acidic or basic residues, meaning the effective pKa of these residues or the effective pH around them is higher or lower than 7.4.

Additionally, many enzymes use metal cofactors that facilitate proton transfer reactions by altering pKa of active site groups. For example, DNA polymerase beta binds two Mg2+ ions, one of which alters pKa of the 3'-OH group of the 3'-terminal nucleotide, which makes the proton transfer to an active site aspartate residue or to the bulk water thermodynamically (much more) feasible.

It seems incorrect to say that the enzymes are altering the pH of their active sites. Rather they are altering the pKa of the active site residues. I would also add that pKa is a measure of equilibrium and thus even if, for example, the pKa of a moiety is below the pH, this does not mean it is completely deprotonated.

Martin - Thanks, I totally forgot to mention that; it is an important point.

Canadianer - Thanks! Your second point is important and I didn't to mention it. Concerning your first point, while I agree that it is generally more useful to think about residue pKa rather than pH of the active site changing, and that this is probably the more important factor, I would think (I may be wrong)  that both are changing. If a pocket in a protein has many acidic or basic residues, the solvent in the pocket will likely have more or less hydrogen ions per unit volume than the solvent outside the pocket. Since pH is a measure of [H+], this would differ between the two environments.


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Question on the concept of mitochondrial Eve
My question is about the very definition of this common ancestor.
Why shouldn't be the mother of mitocondrial Eve the real Eva m (and so on to grand grand ...mother)? All I know on the subject comes from Wikipedia. My question comes from the idea that mitochondrial DNA is passed from mother to daughter. I do not see where to stop back in time.
Please consider that here I am not asking for details or controversies. Just the significance of mitochondrial Eve.

I don't really understand your question. What do you call Eva m exactly? The MRCA of all of today's mitochondria in humans? What do you call real Eva m?

It is mitochondrial Eve,  not Eva and is sometimes abbreviated mt-Eve or mt-MRCA (see the wiki article)

As the Wikipedia article says:

In human genetics, the Mitochondrial Eve (also mt-Eve, mt-MRCA) is the matrilineal most recent common ancestor (MRCA) of all currently living humans

Note the use of the words "most recent".  The mother and grandmother of the actual Mitochondrial Eve were living before Mitochondrial Eve, and thus are less recent than she is.

Thanks. I somehow skip that. I am amazed by this. How it comes that we are not from 2, 3 , n ... maternal lines ? I just discovered it yesterday and makes me wonder.


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Help me identify these two ants
I recently found these two winged ants near a colony. There were 5, but 3 flew away.
Location: Nassau/The Bahamas. November 19, 2017.
Are they queens? And What species?

The square head and the distance between the abdomen and the thorax lead to Myrmecinae, probably Pheidole, Pheidologeton/Carrebara or some granivorous species.


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Units of parameters in epidemiological model
The simplest malaria model is given by $$\frac{dI}{dt} = \frac{\alpha \beta I}{\alpha I + r} (1-I) - \mu I$$
where $\mu$ is the death rate of humans, $\alpha$ is the transmission rate from humans to mosquitoes, $\beta$ is the transmission rate from infected mosquitoes to susceptible humans, and $r$ is the natural death rate of mosquitoes.
Assuming the units are given in $d^{-1}$, or per day, we can assume $r$ to be rather large, given that it isn't part of a larger product (and thus isn't a proportion). We can thus assume $r$ to be anywhere from a few dozen to a few hundred, depending on the size of the population. Recall that this is the amount of mosquitoes killed per day.
$\alpha$ is the transmission rate from humans to mosquitoes, and does appear to be a proportion, so $0 < \alpha < 1$. Thus, $\alpha$ is the probability a mosquito not carrying malaria bites a human $\textit{with}$ malaria. Assuming nothing more than 15% of a population of humans has malaria, and that 95% of a mosquito population do not carry malaria, this is $0.15*0.95 = \alpha = 0.143,$ or a 14% probability.
$\beta$ is also a proportion, and is the transmission rate from infected mosquitoes to susceptible humans. Rather, $\beta$ is the probability an infected mosquito will bite a human. Assuming a generous mosquito population (a few thousand at the least), we assume that about 5% carry malaria and (based on our previous assumptions) they have a 85% chance of biting a susceptible human (given that 15% are already infected). So $\beta = 0.05*0.85 = 0.0425$.
$\mu$ is given as the death rate of humans. Neglecting deaths by reasons other than malaria itself, we assume this value to be about $0.3\%$, given 627,000 deaths in 2012 out out of an estimated 207 million cases that year.
Is this analysis correct? If not, where can I find values for the above parameters? Are there any case studies where I can calculate the above values?
Thank you in advance.

To use more accurate figures, currently only ~3% of the world's population has malaria, and, roughly 20% of mosquitos that are able to carry malaria actually live long enough to potentially [have and] spread the disease.


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Why are newly grown leaves red?
After a period of heavy rain, several trees in my garden will put out an impressive burst of new leaves, with an incredible vibrant red colour, almost the colour of port wine. The new leaves will then slowly turn green.
I understand that the leaves turn green once they start producing chloroplasts and chlorophyll, but what is responsible for this initial red colour that is so very vibrant? And what biological role does it play?

It is anthocyanins that are produced to protect the developing photosystems (chlorophylls) from being damaged by sunlight.
As you have noted, it dissipates as the photosystems become adapted to the ambient light levels. Were you able to shade your trees for several weeks, you would likely also see their leaves turn red right after you removed the shade (easily done with trees in pots). Again, it is anthocyanin positioned in the leaf in a layer above the chloroplasts, but it will not be as vibrantly red because of the green chloroplasts below.

Cool, thanks! So do these anthocyanins function in a similar fashion to melanin in humans and fungi, absorbing UV light?

Yes, @GrumpyMammoth, I believe so. Melanin notably dissipates the energy from UV light whereas it is primarily blue light with anthocyanin in leaves such as we are talking about. It is noteworthy trivia that anthocyanin is a pH indicator.


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Meiosis and combinations of chromosomes
I was pondering about the genetics of siblings. It occured to me that a pair of biological brother and sister (not brothers or sisters) could inherit completely distinct sets of chromosomes from their parents, the mathematical probability being $\frac{1}{2^{46}}$.
This calculation is based on the assumption that each pair of chromosomes, upon meiosis, get separated independently of other pairs. Do you think I’m right about that? Has anyone looked into this matter? Could it be that a chromosome prefers to be accompanied by a specific chromosome (in a pair other than its own) during meiosis?
Edit: I only have a high school level understanding on this matter and I just realized that my speculation directly contradicts Mendel’s law of segregation. But as pointed out in the comment on the answer, some wiggly interaction might interfere with the assortment with some peculiar genes, although it doesn’t mean that some chromosomes are more fond of each other. Close the case.

It would be right if there were no recombination (see also crossing over) and no new mutations. However, there are crossover and there are mutations and hence the calculation is wrong.
Segregation
You have solved this problem yourself. You assumed that chromosomes segregate perfectly independently which is a rather sound assumption. The probability is $\frac{1}{2^{46}}$
Recombination
Assuming a genome-wide recombination rate of 22.8 (Wang et al. 2012) and assuming that the number of recombination is Poisson distributed, then the probability of no recombination is $e^{-22.8} ≈ 1.25\cdot 10^{-10}$.
Multiply this number by $\frac{1}{2^{46}}$ and you get about $1.8 \cdot 10^{-24}$. I would note however, that the assumption that the number of crossover is Poisson distributed might not hold (even if it is how it is typically modelled)
Mutation
Now assuming a genome-wide mutation rate of 45 (Rhabari et al. 2016), and assuming that the number of mutations is Poisson distributed, then the probability of no mutation to happen is $e^{-45} ≈ 2.9 \cdot 10^{-20}$.
Hence the probability becomes $\frac{1}{2^{46}} \cdot e^{-22.8} \cdot e^{-45} ≈ 10^{-44}$.
Note that we assumed that the number of mutations and the number of crossovers are independent which is definitely wrong. If we were to know the correlation, we could make better estimates. This would bring our estimate to some higher probability.

Whoa, I never knew that recombinations are so likely. And I believe you’re talking about recombinations between pairs and nonpairs of chromosomes, which does make my assumption false. Now let me elaborate: apart from recombinations and mutations, could there be any tendency of certain chromosomes from the same parent or whatever ‘like’ each other, going hand in hand in meiosis? Maybe it’s a silly question.

I think chromosomes segregate completely independently but I am not sure. Also, you might want to read about meiotic drive.

That looks like exactly what I was looking for!


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Mathematical model for malaria
The simplest malaria model is as follows:
$$\frac{dI}{dt} = \frac{\alpha \beta I}{\alpha I + r} (1-I) - \mu I$$
where $r$ is the natural death rate of mosquitoes, $\mu$ is the death rate of humans, $\beta$ is the transmission rate from infected mosquitoes to susceptible humans, and $\alpha$ is the transmission rate from humans to mosquitoes. However, for $I \ge 1$, $dI/dt$ is negative. Wouldn't that imply that the infected class is always shrinking from the start? How does this make sense?

What is I? Overall infections?

Yes, $dI/dt$ is the rate of change of the infected population.

Where did the model come from? I'm thinking hard trying to figure this out, maybe a bit more background could help.

Martcheva, Introduction to Mathematical Epidemiology.

I am afraid you may have to read your textbook more closely. The question on page 29 states that this equation models the proportion of infected humans. If $I$  $≥1$ that would mean that there are more people are infected than there are people in total - e.g. 3/2 of people are infected - this clearly doesn't make sense.
Thus $1≥I$ when using this model.

Ah, thank you very much for clarifying. You've spared me much frustration!


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Identification of Unknown Insects found in landfill (spider like)
Could someone help me to identify the following spider-like insects? They are very small, so I used a macro lens to capture them. I have tried to capture them as clearly as possible.
They are about 2-3mm long with a black hairy head/belly.

They were collected from a closed section of Tseung Kwan O Landfill and Clear Water Bay Country Park of Hong Kong. This area is revegetated so the ecology is much like an area which contains many kind of trees.

Spiders for sure (4 pairs of legs, two body parts), but very hard to tell from their condition and the quality of the photos.


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Why are insects unafraid when you tap at them from the other side of glass?
In the summer months we frequently try and kill mosquitos in our home. They are tremendously skittish and get airborne pretty quickly as you approach them. However, if they land on a piece of glass (a window for example) they don't seem at all bothered at you approaching from the other side and tapping the glass where they have landed.
Is this some strange physiology of insects (or at least mosquitos) that they cannot look down? Is it that their eyes function differently to our eyes and cannot see through the glass? For sure, their brains cannot be  developed enough to understand the safety afforded by the glass.

Since insect brains do not contain enough neurons for higher level emotions such as fear, much of their behavior is programmed and reflexive. When you approach them, they have evolved to fly away. Glass, on the other hand is not something they evolved to "understand". They likely are not programmed to see something approaching them from below their legs as they are sitting securely on a hard substrate as a threat. They can look down. They just don't "get" glass.


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Gene density percentage
What do we mean when we say that: Haemophilus influenza genome is 85% genic.
How do we measure gene density in percentage, especially for the above-mentioned case?

It means that 85% of its genome is coded for proteins (ORFs). The other 15% not, so these can be regulatory elements, repeats, or other.
You can measure that by measuring the total length of all ORFs, and compare it with the total length of the genome.


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tissue-specific expression of homolog genes
Two or more genes are homolog if thay have similar sequences. homolog sequences between species are called orthologs (caused by speciation events) and homolog sequences in an species are called paralogs (caused by duplication events).
I would like to know what is expression pattern of paralogs or orthologs in an specific tissue. Are paralog (or ortholog) genes have same expression in a tissue or they express different?
I hope my question is clear, but if it has mistakes I appreciate your corrections.

The evolution of new genes is frequently associated with gene duplication. The paralogous genes are then free to evolve on their own into new functions over time. Sometimes (usually) the paralog will end up with a frame shift, or stop codon that inactivates it. But your question is lacking the element of time. At the instant of gene duplication, each copy is identical. However, one copy may lack the control elements (usually upstream), and not be transcribed. Or one copy may eventually evolve a new, tissue specific function. But whether the copy is inactivated, or evolves a new function, or remains active is not the same for every instance. It depends on how each copy changes under the influences of mutation and selection.

Nice answer. can you please introduce me some articles talking about this topic?

I just Googled:    "gene duplication" paralog function.     and got a lot of informative hits.


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"Secondary refractory period" of class 1 neurons?
In Izhikevich's Dynamical Systems in Neuroscience, p. 199, one learns about a class of neurons that can be forced to fire with maximal frequency:

Injecting a constant current of appropriate size (here: 320pA) a neuron of this class can be forced to fire with maximal frequency. The frequency is determined by the refractory period of the ion channels producing the action potential.
What the picture does not show is what happens beyond the half-of-a-second that is recorded and displayed: Will the neuron continue to fire with maximal frequency forever, as long as the input current is applied? I guess eventually it gets exhausted and must pause or lower its frequency.
My questions:

General: For which injected currents can the neuron continue to fire with the corresponding frequency forever? Beyond which current $I_{critical}$ does it have to make a pause or lower the frequency?
Qualitative: Beyond $I_{critical}$, does it make a pause or does it lower its frequency? Or both?
Quantitative: If it makes a pause, when and how long is it? (This could be called its "secondary refractory period".) If it lowers its frequency, when does it start (to lower its frequency) and by which rate?

Your picture shows tonic firing, not bursting; tonic firing is sort of the opposite of bursting. Try a Google Images search for "neuron burst firing" or something similar.

Burst firing is due to intrinsic properties of some neurons that cause them to fire >1 action potentials in a group. Maximal tonic firing is just the maximum firing rate of a cell given a constant depolarizing current.

Bursting!=maximally firing - those are not the same things. Have you tried a google image search for "neuron burst firing" to see how that is clearly different from the activity you show here?

Let us continue this discussion in chat.

I removed any mentions of "bursting".

@BryanKrause: I asked a more mathematically oriented question at Mathematics SE. If you want to take a look...

I think you've already picked up on this from your realization that E is not a depleting resource but rather one that is regenerated: as long as that regeneration rate is greater than the loss rate, there will be no change in the capability to fire. Hopefully that helps answer some of your questions here.

@BryanKrause: It does (help).


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What is the proper naming of Aminoacyl-tRNAs?
I want to refer to an aminoacyl-tRNA with the anticodon 3'-UAC-5' that is charged with methionine. What is the proper name for this molecule?

I don't work with tRNA, but the convention I was taught for such a tRNA was $Met-tRNA^{Met}$. I don't know of any standard nomenclature incorporating the anticodon, which is not to say that there isn't any.

@canadianer —There is, but it is only adequate to a point, and the particular example raises one type of complication. I'll post in detail tomorrow if no one else has.

@David, I would be very much interested in your explanation.

OK. A bit obsessive, but many years ago I was responsible for a chapter on protein synthesis in a text book. The lack of a standard nomenclature (unless I have missed something) reflects both the smaller number of people working on RNA, rather than DNA, today, and the large number of tRNA genes in eukaryotes.

Minimal Answer
If all you want to do is exactly what you have specified, on the basis of a 2013 paper on the human tRNAs identified in the 1000 genes project, the format would seem to be:

Met-tRNAMet(CAU)
or
methionyl-tRNAMet(CAU)

Notice that the anticodon is written in the 5ʹ→3ʹ direction, as in the paper, and that Met is capitalized, as recommended in this IUPAC publication of 1970 (sic).
I do have reservations about this as I have been unable to find tRNA nomenclature recommendations (not even in RNA journals), and the paper concerns genes (although a different nomenclature is used there — transfer RNA-Met (CAT) 1-1 etc.). Furthermore, my recommendation to use CAU, rather than CAT (used in the quoted paper) is only based on my experience of scientists who work on tRNA, rather than their genes would use (although it can be justified in a broader context: see below).
A variation on this is to be found in a 2017 paper:
$\mathrm{Met\text{-}tRNA^{Met}{}_{CAU}}$
So I suspect there is no ‘official’ nomenclature.
Problems in giving a more comprehensive answer
The answer above is adequate in certain circumstances, e.g. in differentiating in a paper or a lecture between two species (e.g. with different anticodons, although this does not occur with methionine). The problems occur when you wish to distinguish one tRNA from all other tRNAs present in a cell or encoded in a genome. I list some potential ambiguities:

Initiating v. elongating Met-tRNAs (in the case cited)
Anticodons containing modified bases
Distinct tRNAs with the same amino acid specificity and the same anticodon
Cytoplasmic v. mitochondrial tRNAs in eukaryotes
tRNAs from different species

Possible solutions
Different Met-tRNAs
This is often most important as both initiating and elongating Met-tRNAs have the same anticodon but are structurally and functionally distinct. Differentiation is generally done by way of a subscript: originally ‘f’ or ‘m’, respectively, but for eukaryotes now generally ‘i’ or no subscript:
$\mathrm{Met\text{-}tRNA^{met}_f} \quad or \quad \mathrm{Met\text{-}tRNA^{met}_m}$
$\mathrm{Met\text{-}tRNA^{met}_i} \quad or \quad \mathrm{Met\text{-}tRNA^{met}}$
Anticodons containing modified bases
It was observed early on that the anticodons of tRNA contained modified bases — e.g. inosine, which had particular patterns of ‘wobble’ codon recognition (see my answer to another SE question). Therefore, in many cases it would be important to specifiy these — which is why I recommend using U, rather than T, e.g.

Tyr-tRNATyr(GΨA)

tRNAs with same anticodon
Gene duplication often results in tRNAs with the same specificity and the same anticodon. In some cases the sequences are identical, so there is no way of distinguishing them, but in other cases mutations will occur that do not change the function. To distinguish such species with a single base (here at position 40) the 1000 genomes paper uses the following style:

(G40) tRNAArg(GCA)
or
(C40) tRNAArg(GCA)

At the genetic level arbitrary numbering is used for human tRNAs, e.g.

transfer RNA-Met (CAT) 1-1
transfer RNA-Met (CAT) 1-2

whereas in Drosophila a variant of this style is used, e.g.

transfer RNA:Methionine-CAT 1-1
transfer RNA:Methionine-CAT 1-2

Cytoplasmic v. mitochondrial tRNAs
It is important to remember that the mitochondria of eukaryotes contain their own set of tRNAs, and to distinguish these if necessary by a preceeding ‘mitochondrial’. In Drosophila the symbol would be ‘mt:tRNA:Met-CAT’, and the name ‘mitochondrial transfer RNA:Methionine-CAT’.
Species
Obviously, one can specify the species by a preceeding adjective. I mention this to point out that set of tRNAs is different for different species.

Good answer. I typeset your Word equations with LaTeX and changed methionine-tRNA to methionyl-tRNA based on the recommendations of the 1970 IUPAC publication.

@canadianer — Thanks. One becomes so concerned with the difficult things that one doesn't notice mistakes in the simple ones.

@David, This is great. I do not work with RNA except when I teach my biology students about transcription and translation. I want them to have a consistent naming system when I tell them about different tRNA molecules with their respective amino acid attached.

I think for the initiator, it is at least quite common to say tRNA(superscript)fMet in bacteria, rolling the indication into the AA part. It seems to be the same situation for tRNA^(iMet) in eukaryotes, at least within the nomenclature of GtRNAdb.

@MingyeWang — Thank you for this. The genomic tRNA database you mention did not exist when I wrote my original answer, but it is easy to see why they adopted this style: database storage of text with both subscript and superscript at the same level is more difficult (for users as well as programers) than a single superscript. For academic publications and textbooks I personally would advocate the more traditional form as it does not indicate that the methionine is actually formylated (which it may not be in some bacteria), and iMet is chemical nonsense. But there is no standard.


text:
Why do floaters in the human eye appear to have a squiggly-line, tubular shape?
If you intentionally try not to tune out visual floaters in the eye, you can see them very clearly and they seem to have a squiggly line shape but with a volumous tubular look. Why is this?
They almost look like some kind of microbe as seen through a microscope, but that seems like a naive guess, and I'm curious to know the scientific explanation of why these entities look the way they do.

Eye floaters are usually small flecks of collagen floating inside of your eye (the same substance that is present in the extra-cellular matrix) and as you age they can clump together and cast shadows on your retina.
They may look like microbes to you because the clumping gives the appearance of a thread-like or rod shape, commonly associated with microbes. The light falling on the eye will enhance this by making them look transparent and somewhat like microbes. But rest assured they aren't, because if they are, then you certainly have superhuman eyes!


text:
At what level of relation does inbreeding become dangerous?
Inbreeding within first cousins appears to have an established history of dangers, and anything closer than that relationship also.
However, how distantly related do two individuals have to be for the risks of inbreeding to be in line with having a child with an unrelated person?
Are second cousin children more likely to have children with defects? 3rd cousins? 4th?

Are you talking about interbreeding or inbreeding? You are using both words. I would assume you're talking about humans, right?

@Remi.b yes I am talking about humans

And I'm talking about inbreeding

Possible duplicate of Is marriage with half-cousin's daughter more risky than marriage with others?

Any level of inbreeding increases the risk of genetic disorders, but one single instance is not dangerous. The issue appears when inbreeding becomes the norm and goes on and on and on. Even two siblings could have a child with only a small increase in the percentage of having a genetic disorder. Now, after 50 generations of doing that, it becomes really bad...


text:
Is there any biological evidence that is not suggestive of or seems to disprove evolution?
Often, in science, when we have evidence that doesn't fit our paradigm, we bend it until the paradigm collapses.
Although there is plenty of decent evidence for evolution, is there anything that does not fit the evolutionary paradigm? Is there any biological evidence that is not suggestive of or seems to disprove evolution? Or is everything merely hunky-dorey?

all evolution or just some? Human evolution has not been fully outlined yet. We know the process, but we don't have a clear A to B to C if that's what you mean. If you mean evolution as a whole then no. Evolution deniers from my experience tend to disapprove of carbon dating, stating that carbon dating is wrong and hence all calculations done with it are wrong. However, even most Christians nowadays don't support spontaneous creation, but rather believe the ancient Hebrew word "yom" means a period of time not a 24 hour day.

I'm not sure whether a one-word answer is allowed, but "No" would seem perfectly adequate.

@Charlie Is carbon dating even relevant to evolution? C-14 has a half-life of about 5000 years, and going back too many half lives reduces the accuracy. If we assume a 10 half-life limit for reliable measurements, that's still only 50,000 years, which is almost meaningless on an evolutionary time scale.

Evolution is a broad field of knowledge. There are definitely a few elements of our current theory of evolution that does not perfectly match observations. However, those concern small details and might not of much interest to you. Here are a few examples

We don't know the relative importance of background selection and selective sweep at explaining genome-wide variation in genetic diversity.
We don't really have much of an idea what fraction of speciation happen in sympatry.
We don't understand well how recombination rate evolves to differ in different genders.
We don't really understand what are the limits and/or costs of phenotypic plasticity that makes phenotypic plasticity less frequent that we would otherwise expect.
We don't really understand the patterns of genetic diversity on sexual chromosomes at the intersection with the pseudo-autosomal region (PAR).
We don't fully understand how much expansion load (a type of mutation load caused by the sampling of individuals at the expansion edge of a population) there is in human population.
We don't really know whether the mitochondrion (and other double membranes organelles) was first a endo-parasite or a endo-symbiont.

If you are asking whether there are evidences suggesting that evolution is not happening or that humans and chimpanzee do not actually share a common ancestor but were created independently, then no, there is no such evidence.
You should have a look at the related post Is Evolution a fact?

Please clarify your question. Evolution per se is an observation, not a theory. We see it literally every day (I am a virologist and my organisms literally evolve on that time scale). It is impossible to argue rationally that evolution doesn't occur; it's like denying that when I spill my coffee the mess falls downward. Even pre-Darwin scientists universally accepted that evolution occurred. Even "Creation Scientists" (who are not scientists, but religious fundamentalists) can't deny that evolution occurs. Evolution is a fact, not a theory.
Are you asking if the theory of evolution through natural selection (which is what most people think "the theory of evolution" is, and what religious people call "Darwinism") explains everything? No, of course not. It's a theory that is over 150 years old, and it hasn't been the sole theory underlying evolution for over 50 years. Other theories, including sexual selection, neutral drift, and nearly-neutral drift, were proposed in order to account for many aspects of observed evolution that natural selection doesn't account for.
If there were other aspects of observed evolution that weren't accounted for by one or more of these underlying theories, then further theories would be proposed. Evolutionary theory is pragmatic, not dogmatic.
At the moment, there are no observations I'm aware of that can't be accounted for by the present combination of theories.

I agree with Remi.b that there are some things we don't yet fully understand. However, Darwin got it right. A theory is an explanation of observations. It is laid out to be disproven. Evolution, as a theory, has stood 158 years of attack without being disproven. It predicted Mendelian genetics, and molecular biology. Sexual selection seems to be outside natural selection, which is why Darwin considered it a special kind of selection. The "theory" is as strong as science can ever support. "Facts" and "proofs" are for math. But if we had any proof that evolution did not fit our observations, the theory would be falsified.

Please do not fall into the common mistake of confusing theory and hypothesis. What you describe is a hypothesis, a theory is backed by solid  evidence and can be used to describe experiments. See here for more details.

I am fully aware of the difference. Evolution is among the most highly supported theories that is fully supported by experimental evidence.

Evolution is not a theory, it is a very fitting name for an ongoing process. There is no need for an experiment to prove evolution (viz. my answer).


text:
Meaning of term ‘rapidly labeled RNA’
I encountered the term, “rapidly labeled RNA”, in the article: Rapidly labeled HeLa cell nuclear RNA. I. Identification by zone sedimentation of a heterogeneous fraction separate from ribosomal precursor RNA. (1966).
I would appreciate it if someone could explain to me what it means or implies.

Explanatory answer
Rapidly-labelled RNA was the RNA labelled by radioactive precursor during a short period (the pulse), terminated by swamping the system with an excess of non-radioactive precursor (the chase). This is known as a pulse–chase, and is described in the methods section of the paper cited in the question and reiterated by @SeRe as an answer. Such a pulse–chase preferentially labels RNA species that have short turnover times (i.e. half-lives of the same order of the pulse), and was thus regarded as a way of studying messenger RNA.
This strategy and its interpretation was an extrapolation from what was known about mRNA in the regulation of bacterial gene expression, but the descriptive term ‘rapidly-labelled RNA’ was used rather than ‘mRNA’ because there was no direct evidence to support such an assignment in nucleated mammalian cells. Indeed, there were major problems because the rapidly-labelled RNA in the nucleus was of a different size to the RNA that subsequently appeared in the cytoplasm, and, indeed, there was no simple precursor–product relationship between the two. In retrospect this is not surprising given what we now know about the splicing of eukaryotic mRNAs and the fact that most of them have much longer half-lives than bacterial mRNAs. However, at the time there was a school of thought that interpreted these results as evidence against the idea of mRNA in eukaryotes, and one of the purposes of the paper cited was to demonstrate that some of the rapidly-labelled RNA that appeared in the cytoplasm had properties consistent with mRNA.
The historic context
It may be necessary to explain to younger scientists that this work was done before DNA cloning, before RNA sequencing (never mind DNA sequencing), before the discovery of polyadenylation of eukaryotic mRNAs (the ‘handle’ for purifying them), in short, at a time when no specific mRNA had yet been identified or isolated (see, e.g., the Wikipedia article on The History of RNA Biology). As documented in Mathew Cobb’s excellent article ‘Who discovered mRNA?’, mRNA wasn’t really discovered but was an idea to account for the rapid response of the lac system (observed in genetic experiments) in terms of a previous unexplained labelled RNA with a DNA-like base composition observed associated with more abundant stable RNA (ribosomes) when bacteriophage infected E. coli. Subsequent work, presented in papers by Brenner et al. and Gros et al. in the same issue of Nature in 1961, in effect documented this RNA more precisely in phage-infected cells and showed that it differed from ribosomal RNA. The importance of the work of Mathhaei and Nirenberg in establishing cell-free systems for translating polyU and subsequently other artificial polynucleotides cannot be underestimated. However, it is important to recognize that the genetic code was not deciphered using genuine mRNA.
It was natural to assume the mRNA model extended to eukaryotic cells, but at that time there was no convenient system with an abundant mRNA like that of bacteriophage and so the presumed differentiating characteristic of short half-life was used, as seen in a plethora of papers on ‘rapidly-labelled RNA’. Many of these were opportunistic, claiming to document anticipated hormonal or other effects on eukaryotic gene expression. Consequently the demonstration that much of the rapidly-labelled RNA in the nucleus never reached the cytoplasmic ribosomal location had the effect of discrediting not only these papers, but the very idea that mRNA existed in eukaryotes. This may seem rather absurd today, but the foremost ‘eukaryotic mRNA denier’ (as he might be termed in contemporary parlance) was the eminent Oxford Professor of Pathology, Henry Harris FRS, who developed man–mouse heterokaryons and set out his ideas in a published monograph entitled ‘Nucleus and Cytoplasm’ (a copy of which I once possessed). So it is relevant that Warner et al. (1966) refer specifically to Harris in the discussion section of their paper, which describes work that addresses the issues Harris had raised.
If there is a moral to this story (and it is always easier to draw morals after the event) it is perhaps that Harris was happy to confusticate lack of proof with disproof in an area that was peripheral to his main concerns, and that the groups in New York — and Jonathan Warner, especially, having previously described polysomes in Alexander Rich’s lab — were prepared to accept the fact that the situation was more complicated than originally thought, but were not prepared to throw out the baby with the bath water.

They performed an experiment where they treated cells with [3H]-uridine (tritium-labeled uridine) for a short period of time (5 min). Afterwards, they added non-labeled uridine, cytidine, and thymidine in excess. So in principle, rapidly labeled RNA is radioactively labeled RNA after a short period of time.

But you haven't explained why. What was interesting about RNA that was labelled under these conditions? Why would the poster be reading a 50 year old paper about it?

But he never asked why. He wanted an explanation for the term rapidly labeled RNA. And obviously, my explanation was sufficient for him as he accepted the answer.

If your answer was only to reiterate what the poster could have read in the methods section, then you shouldn't have answered the question on that basis and the implication that the answer would have been of no general interest for biology. There is a greater general interest implicit in the question and which is a valid, but more comprehensive and comprehensible answer to the question "could you please explain it (what rapidly-labelled RNA is) to me?" If you know, please include it in your answer, if not, I will answer it myself.


text:
Where are action potentials initially created?
Is the axon hillock still the place where one thinks and talks of that action potentials are initially created? (I've heard this place moved into the direction of the axon initial segment.)
If one doesn't want to commit oneself whether it's the axon hillock or the initial segment where action potentials are initially created – because it's somewhere inbetween or at both of them, or it depends on the type of neuron, or we don't know, or we don't care:

How does one talk about that place unequivocally?

Is there an abstract (non-anatomical) terminus technicus for "the place where action potentials are initially created"?

Action potentials are initiated where there is a high density of voltage-gated $Na^+$ channels and that may vary from cell to cell, as you guessed. For an illustrative example see the figure below, reproduced with permission from Kole et al. (2008).

Density of voltage-gated $Na^+$ channels and $Na^+$ influx along the axon of a cortical pyramidal neuron.
Reproduced with permission © Nature Publishing Group
As you can see, in this cell type voltage-gated $Na^+$ channels, labelled in green in the left-most image, are predominantly expressed away from the axon hillock. We can also observe that the expression of voltage-gated $Na^+$ channels correlates with the degree of $Na^+$ influx in a monotonic relationship (right-most panel).
In smaller cells action potential initiation can happen closer to the axon hillock and in cells of some invertebrates even in multiple locations (Kole and Stuart 2012). What may be the advantage of using the axon initial segment (AIS) as the sole site of initiation of action potentials (APs)? Here is a direct quote from Kole and Stuart (2012):

[The AIS] has a small local
  capacitance ($C$) and therefore requires less inward current ($I$),
  that is, a smaller number of $Na^+$ channels per unit area, to
  generate APs compared to larger structures, such as the soma
  or proximal dendrites. Hence, the AIS is also an energetically
  favorable site for AP initiation. Furthermore, the small capacitance
  of the AIS favors rapid changes in membrane potential,
  as occurs during the upstroke of the AP ($dV/dt = I/C$). Finally, it
  is worth noting that having a single site of AP generation provides
  neurons a single locus where inhibition can gate AP initiation. [...] Initiation of APs
  further from the soma, taking advantage of the electrical isolation
  of this region, is a strategy used in some neurons to increase their
  capacity to discriminate the arrival time of different synaptic
  inputs.

References
M. H. P. Kole et al., Action potential generation requires a high sodium channel density in the axon initial segment. Nat. Neurosci. 11, 178–186 (2008). doi: 10.1038/nn2040
M. H. P. Kole, G. J. Stuart, Signal Processing in the Axon Initial Segment. Neuron. 73, 235–247 (2012). doi: 10.1016/j.neuron.2012.01.007

So wouldn't something like "spike-generating density" be a perfect name, analoguous to postsynaptic density

I only addressed what I think is the essence of your question, i.e. where are action potentials generated, and avoided the linguistic aspect. Usually, terms are established by use in the literature when there is a purpose for them and it's not my place to create new terms in this forum. Suffice it to say that the phrase predominantly used is "action potential initiation site" or a variant thereof.

That's what I wanted to know! I didn't want to invent a new term, when there is already an established one.

By help of the term you gave me, I immediately found this article:  https://www.ncbi.nlm.nih.gov/m/pubmed/8786434/

... and this one about multiple AP initiating sites: https://www.ncbi.nlm.nih.gov/m/pubmed/11535672/?i=2&from=/8786434/related

In the meanwhile I also found the phrase "trigger zone".


text:
Why is liquefactive necrosis only seen in brain?
Liquefactive necrosis is a type of necrosis uniquely observed in brain. This occurs due to breakdown of cellular proteins by the action of hydrolytic enzymes.
In other parts of the body, usually a different form-coagulative necrosis is seen.
What makes the brain so unique that this form of necrosis is only limited to brain?

According to Wikipedia citing this article, liquefactive necrosis is not restricted to brain only. NCBI books describes, how liquefactive necrosis is induced. Seems to be dependent on neutrophils. They also claim that coagulative necrosis occurs in every organ except the brain. But I just made a quick search. I hope I could help you anyway.

Liquefactive necrosis is indeed only seen in the brain in the absence of infection, but it is also seen in the case of some bacterial infections.  The reason is that liquefactive necrosis is, as you said, caused by the release of digestive enzymes and constituents of neutrophils.  Bacteria will, under some circumstances, release those enzymes, causing the cells to be devoured.
The fact that liquefactive necrosis is seen in the brain in the absence of bacterial infection is in part due to the fact that neurons have a higher lysosomal content, leading to a higher tendency toward autolysis, and in part due to a high concentration of neutrophils which swarm into an affected area.

Sources:

What happens after brain tissue dies?, PathologyStudent.com, 2012
Liquefecative necrosis, Medigoo.com, 2016
Necrosis, Cell (Liquefactive, Coagulative, Caseous, Fat, Fibrinoid, and Gangrenous), Rotimi Adigun1; Steve S. Bhimj, 2017


text:
Is burnt THC still psychoactive?
Asking from a more practical angle. If one smokes a joint - does the THC in the embers contribute to getting high - or is it only the THC released by the heat of the smoke in the not-burning section which contributes?
(same question for CBDs - I assume the answer will be equivalent)

The THC molecule needs to be intact to be functional in the brain, so the vaporized THC from your 'joint' will contribute to being high. If the THC molecule burns (disintegrates, I don't know at which temperature this happens), you'll get probably some extra tar which does not contribute.
So all THC molecules that are vaporized by the heat of the burning tip, in or next to the ember, will be functional.

who voted down and why? can you maybe provide a source/study?

Don't mind the down voters, there are always some frustrated people around. I don't think there is scientific literature about how THC vaporizes from a cigarette. Most THC studies were done by injecting mice and rats (with too high doses). How THC is released from a burning cigarette is also not really a biological question, but is physics.

at the end of the day the question boils down to whether the heat of the embers destroys or significantly changes the THC molecule - that should be answerable.

Vaporizing THC under lower (not burning) temperatures give the same psychoactive effect. Vaporizers (sort of electric cigarettes) are very popular today, which do not burn but evaporate the THC from herb. I think you are better of talking to someone in a 'smartshop' instead of finding a scientific publication about this subject.

yes - of course - I know that - my question refers specifically to the THC burning in the ember. not about whether vaping works.

But don't you think THC is already vaporized before it can really burn? I mean in a forest fire for example, when a tree burns, the water will vaporize before it disintegrates into H2 and O2.

that's basically what I would like to figure out. first I would like to know whether THC can be active if burnt - then the conclusion would logically follow and a joint is just a convection vaporizer using smoke.


text:
Is there a chemical that can be used to subdue ants only temporarily without permanent harm?
I would like to know as I want to contribute to a biodiversity project that wants to create a database with ant feature measurements. I'm not sure if I like the idea of killing ants however (even though it's just a single ant with limited ability to suffer, I know) so I'm looking for a way to immobilize ants long enough to take some detailed measurements but without having to kill them or harm them permanently.
Related question: how could I clean the ant so that it's not marked with the chemical used in the perception of other ants?
I know that for the database they may require keeping the specimen (and therefore killing it) in the name of science so that it can be checked by others but I'm more concerned with the question whether in principle these measurements could be taken without permanently harming the ant and how this could be done in practice.
Thank you for your help!

You can try insect anaesthetics: https://peerj.com/preprints/2571.pdf scientists like to take ants home for the microscope and collecting.

Thanks, that article is pretty solid. Wish it were published so there would be more people looking into it.

CO2 is often used for temporary knockouts of insects. I've used it myself for fruit flies (Drosophila melanogaster), and it's quite straightforward and very effective to hit them with it until they're asleep. However, this was in a rather expensive lab that had CO2 on tap - not a particularly accessible method to the average person.
What I'd recommend instead is to chill the ants. Simply capture them and put them in the fridge for a while. Read this wiki article and go to the part about "quiesence" for more. Quote: "quiescence acts like an anesthetic". It's short term, non-harmful and fully reversible. Also much more accessible to someone who isn't working in a big expensive lab. I assume that the ants will stay still long enough for your measurements - if not: put them back in the fridge for a bit. And better yet, there's no chemicals used, so no need to clean the ant and there's no cost to you.

Thanks! I will try quiescence first I think and if that doesn't work well enough I'll see how hard it is to get an affordable and portable CO2 applier. Found this tip so far: http://www.instructables.com/id/Rapid-Insect-Anesthesia/


text:
What are this designs which I found on curry leaves?
Curry leaves is the plant name where I found designs, but what are the designs present on the leaf?
Location: Argentina

some leaf-mining insect larvae would be the cause. Sometimes such species are specialists (i.e., only attack one narrow range of taxa), while other times the species might be more of a generalist.


text:
Protein molar mass from Uniprot ID?
I have a long list of uniprot IDs. How can I get the mass of the "canonical" isoform for each? Ideally from some Python library.

You don't need any external library, it's enough to query Uniprot and extract the data you want from the response.
Here an example in Python 3:
from urllib.request import urlopen

id = "P42212"
data = urlopen("http://www.uniprot.org/uniprot/" + id + ".txt").read().decode()
result = data.split('SQ   ')[-1] #here all the info you need
mw = int(result.split(';')[1].strip().split()[0]) #extract the molecular weigth
print(mw)

If you want to batch query a lot of sequences then I suggest to sleep(0.5) after each query to avoid problems with their server.
Update
As correctly pointed out by @Jerven (see comment below), you can query the mass directly.
In this case, the code is the following:
from urllib.request import urlopen

id = "P42212"
data = urlopen("http://www.uniprot.org/uniprot/?query=id:{}&format=tab&columns=id,mass".format(id)).read().decode()
result = data.split('\n')[1].replace(',','')
mw = int(result.split('\t')[-1])
print(mw)

I don't have Python 3 available, so I can't try this as it is. I am not sure how to translate into Python 2...

It should be the same, except the import from urllib import urlopen maybe also .decode() can be removed. Of course, print without parentheses. I can't try now. Let me know.

You can use the column/tab/csv download to avoid needing to fetch the whole TXT file. Also do keep in mind that these are predicted masses and are not suitable for e.g. MS work as is. e.g. http://www.uniprot.org/uniprot/?sort=&desc=&compress=no&query=&fil=&limit=10&force=no&preview=true&format=tab&columns=id,mass

@Jerven I am not sure how to interpret that table. I agree that it would be nicer to have a smaller text to download, but the masses reported on the link you posted are not related to the whole protein. Can you make an example of how to get the protein mass for ID P42212 using "column/tab/csv download" ?

@alec_djinn just add id:P42212 to the query field i.e. http://www.uniprot.org/uniprot/?query=id:P42212&format=tab&columns=id,mass see our help pages for more details http://www.uniprot.org/help/programmatic_access


text:
Are there cases when genus name is equal to the name of a higher taxon?
Are there any cases when the name of a genus equal to the name of a higher taxon: family, order, class, etc. in botany and zoology?

I doubt so.... Familiy names typically end in -cae or -dae while genus names typically end in -us/ -um/-a and others but not in -dae/-cae.

I answer for botany: no.
The International Code of Nomenclature for algae, fungi, and plants has strict requirements on names:
Article 16.1 has:

The name of a taxon above the rank of family is treated as a noun in the plural and is written with an initial capital letter. (...)

Article 18.1 has:

The name of a family is a plural adjective used as a noun; it is formed from the genitive singular of a name of an included genus by replacing the genitive singular inflection (Latin -ae, -i, -us, -is; transcribed Greek -ou, -os, -es, -as, or -ous, and its equivalent -eos) with the termination -aceae (but see Art. 18.5)

And article 20.1 has instead:

The name of a genus is a noun in the nominative singular, or a word treated as such, and is written with an initial capital letter.

On later article it is explained how to latinize names, with simpler rules (compared to Latin).  So genus are singular and higher rank are plural.
Additionally, for botanical nomenclature, an name for ranks between family and phylum rank is made usually by concatenating a genus name with some suffixes (which are rank specific, see article 16.3, 18.1). So reading a name, one could derive also the rank.  Just few families still have a old name, but still ending with 'ae' (e.g. Compositae, Cruciferae, etc., Art 18.5).  Now (just since 2011-2012 version) there are more exceptions in code, but for historical reasons and for names outside plants in stricter term.
Note: Some old names are automatically corrected with new rules (see e.g. 18.4), so we should have not equal names.

And what about zoological nomenclature?

Previously there were an other answer, mainly for zoological nomenclature.  I think it is potentially possible: zoology is also more complex: much more diverse and sectoral. I expect that on botany, if not you, one of your colleagues, will remember some high taxa name.

The purpose of nomenclature is to distinguish groups of entities that are worth distinguishing.
Giving the same name to different groups of entities would be absurd. It sometimes happens by mistake, but when such an absurdity is detected by the scientific community, the newly proposed name must be changed to be validly published (and recognized by the scientific community).

Does that mean that in the verified (or validated, or checked) taxonomy there are no any duplicating names of higher taxa?

None. And, needless to say, it applies to (and across) all the three domains of life (Bacteria, Archaea, and Eukarya).

Same name on different codex are allowed (discouraged, but it is possible and name remain valid. so it is difficult to change the name again [priority]). "Recommendation 54A.1: Authors naming new taxa under this Code should, as far as is practicable, avoid using such names as already exist for zoological and bacteriological taxa.". IIRC there are few cases with the same genus name across code (but different organism).

If you take all the taxons into consideration, yes, it can sort of happen - particularly on the genus/species level. The confusion is generally avoided since species are usually referred to by genus and species, using the name twice, whereas the genus is simply referred to by the genus name.
For example, the genus Vulpes includes all true foxes. (Wikapedia)
The genus Vulpes includes multiple species, such as the arctic fox (Vulpes lagopus), the swift fox (Vulpes velox), etc.   One of the most widely distributed species of fox, however, is called the Vulpes vulpes, also known as the red fox.
As Remi.b said in his comment, this is very unlikely to happen in higher taxons, since there are general rules that are followed in their naming, and it changes from level to level.

Hmm, why the downvote, I wonder.  I won't bite if you drop a comment... :)

But do you know any exception when a genus name equal to the name of a higher taxon?

Ah, I see what you mean.  Sorry, I was misreading the question, my bad. I'm not aware of any, but I'll dig around a bit.

Your answer is confusing the term species with the specific epithet. As the species name is a binomen, i.e. composed of two words, it cannot possibly be confused with a genus name.


text:
What are these lines that connect into cells called?
I just recently watched a very interesting video that showed cell division under a microscope. In the video, you can see cells that have either one, two or more lines connected to them. What are these called?
Source: https://youtu.be/rgLJrvoX_qo

It's not clear to me to which lines you are referring to.

I added a photo and I apologize for the confusion. You can see multiple strands going off from each cell in photo.

I think it's likely they are filopodia; however, without knowing more background on the image and what cells we are looking at and under what conditions I'd leave that as just a hesitant guess.

@Bryan Krause I believe you are correct and thank you so much. I am reading into what exactly this Filopodia is and what it does. Thanks for sharing something new with me I love to learn. I don't know how to upvote but just wanted to say thank you.


text:
Dilute DNA plasmids with distilled water
I just extracted the DNA plasmid from E.Coli and dilute them in EB buffer. However, I've just figured out that the next step, which is electroporation, required that the DNA plasmid be diluted in Distilled H2O. Can anybody help me to know how to transfer the DNA plasmid from EB buffer to Distilled H2O?
To be clear, the EB buffer I used is from Qiagen. It contains 10mM Tris-Cl, pH 8.5.
https://www.qiagen.com/sg/resources/faq?id=d8ef773f-6a37-4993-908b-8bbc7bc5c8d6&lang=en

EB buffer is just Tris isn't it? I don't think that would interfere with electroporation. If you must change, you could precipitate or dialyse.

Please define EB buffer. In general avoid lab slang. I have edited your question to do so regarding distilled water, but I have no idea what EB buffer is and if it is not defined will vote to close your question as unclear.

Buffer EB is simply 10mM Tris buffer, ph 8.5. I think you are worried about the ions present in your electroporation. There are two things to consider:

What is the concentration of your DNA and how much do you need for the electroporation?
In which final volume is the electroporation taking place?

In my experience, usually you add a very small amount of DNA (a few microliters) to 100, 250 or 400µl (depending on the cuvettes used) final volume. Here a tiny amount of Tris does not interfere or cause a short circuit.


text:
Which method of seed dispersal is the most common among the seed plants?
The five most common methods of seed dispersal in the plant kingdom are:

wind (anemochory): tumbleweeds, dandelions, maples
animals:(epizoochory) externally - burs / (endozoochory) internally - fruits
water (hydrochory): aquatic-water lily/terrestrial-mangrove trees
gravity (barochory): apples, coconuts
ballistic (ballochory): impatiens, geraniums

source: https://en.wikipedia.org/wiki/Seed_dispersal
As far as which one of these five is the most common, this site says that animal dispersal is more common than wind but nothing in relation to the other methods listed above.  Each method likely is most common in it's most well suited niche, but which one is the most common (in the widest range of species) overall?

Clarification: When you say most common, do you mean: 1. Common to the widest range of species or 2. Common to the greatest number of individual plants? Say hypothetically you could have a billion different species with only ten individual plants each present, or you could have ten different species each with a billion individual plants.

Widest range of species.  Good catch.

This paper from Herrera (1989) investigates the role of endozoochory in Angiosperm diversification, and it has a table that can help answering your question, since it deals with all seed plant families:

As you can see, among Gymnosperms there is no question: endozoochory is the most common mechanism of dispersal.
Unfortunately, things are a bit more complicated among Angiosperms. Exclusive endozoochory is not the most common mechanism (27.1% versus 72.9%). However, if we take into account that the plants that perform endozoochory are actually the sum of the first and second ("mixed") columns, the total is 50.9, which is more than 50%. Of course, there is a mathematical possibility that another method, together with the "mixed" column, also surpass 50%.
Finally, it's worth mentioning that the authors are calculating the frequencies of endozoochory only. If one adds epizoochory to that number (zoochory = epizoochory + endozoochory), the frequency of zoochory is even higher.

Source: Herrera, C. (1989). Seed Dispersal by Animals: A Role in Angiosperm Diversification?. The American Naturalist, 133(3), pp.309-322.

As per the question though, I'd have to ask: in these families, how many genera and species do they have? As the question is looking for the most common technique between species, not families

I was foreseeing this question. It's very ease to determine how many species those families contain (295000 for the 277 Angiosperm families and 1000 for the 14 Gimnosperm families). However, the authors don't define to what families those percentages are related. Also, I doubt OP will find a nice and finished statistic for species: the best they can find is a description for each family, and then computing the number of species from there.... that is, a lot of work.

Well, frankly, that is frustrating on the part of the authors! Any ideas on where to look for a more definitive answer? This really isn't my area of biology, but dang it, now I'm curious, and I want to find out!


text:
Limit on the Number of Facial Phenotype
Individuals of each species all have unique facial structure variations (shape of nose, position of chin etc) from humans to birds and fish etc. We humans don't seem to be reaching mathematical limit of uniqueness easily (maybe till the end of the world) considering huge variation and all possible combinations that define our facial structure/traits. However some animal populations are way more larger than humans and each year they reproduce in large amounts.  Considering their huge populations, is it possible for some species to reach their mathematical limit of having unique facial structure variations therefore start repeating the same facial structures?  For example can individuals of some fish species (sardines, sea breams etc) be already sharing exact same facial structure/geometry as a result of reaching all posible facial structure  variation limit?

Why do you think this facial uniqueness is the case?  It would seem to be easily disproved by observing a population, say blonde Hollywood starlets, and noticing that most of them are pretty much indistinguishable.

Are you talking about uniqueness to the exact atom? Or maybe this is too extreme. If it is, then you need to clearly define how similar two faces need to be to be considered the same. The question for the moment is unclear.

Okay, theoretically possible, but only in theory.  Practically, it's totally impossible.  Let's start by defining why it would theoretically be possible.
Theoretically, there are only so many possible arrangements of proteins in the face, which would represent a limited number of possible facial appearances.  However, as you probably guessed, there are zillions of proteins being expressed in each body organ, such as an eye.  So just from the perspective of the number of different possibilities, it would be impossible.
One might think that since the facial features are controlled by genetic variation, eventually these features will begin to repeat themselves, but such is not the case, for two reasons:

There are way to many genes - and alleles - that control facial features.  We're talking thousands if not millions.  When you raise that number of alleles to each others' powers, you start to see the impossibility of repeating the exact same combination, especially since every new generation is introducing new alleles from a new blood line.

Genetic code is not the only thing that changes how you look.  A whole branch of genetics, epigenetics, is devoted to the changes of gene expression unrelated to DNA sequence.  The expression can be changed by environmental factors, even as early as when the embryo is forming the placenta.  This is why identical twins (who have identical DNA) do not actually look exactly the same, or even have identical fingerprints.

Bottom line, totally impossible.

Sources:

Face shape is in the genes, PLOS, 2016
Epigenetics, Wikapedia, 2017
Why do identical twins have physical differences?, Anonymous, 2005
Introduction to epigenetics, University of Leicester, 2013
How many Proteins exist in human body?, Innovateus, 2013

You seem to assume that all of the facial variation is due to genetics. The only environmental variance you accept is via epigenetics and use twin fingerprints as example. Most traits do not have a heritability greater than 0.3. See this post if you don't know much about quantitative genetics and the definition of heritability.

I am downvoting because the post invites the reader to think that only genetics matter and that the question can be boiled down to genetic diversity.

Thank you @Remi.b, I appreciate your frankness.  I will definitely give that post a read.


text:
Do adult mosquitoes have color preferences?
Do adult mosquitoes get particularly attracted or repelled by any colour, or darkness or light? If so, what are they?

"Mosquito" is a quite broad term, since it englobes several Genera and more than 3500 species. But, at least for some Genera, there are indeed colour preferences.
For instance, Aedes seems to have colour preferences. Have a look at this table from Gjullin (1947), from a research in which the effect of different coloured clothing on the biting rate was investigated:

As you can see, black is the new black for Aedes mosquitoes. At least in the shirt of their victims.
Also, in his paper from 1903, Alpheus Packard describes an interesting experience, this time with Anopheles:

Color-preference in the Mosquito
In continuation of their researches on the structure and biology of Anopheles maculipennis, the commonest British mosquito and one known to convey malaria, Dr. Nuttall and Mr. A. E. Shipley observed some interesting facts on the preference this species exhibits for different colors and for different shades of color. The experiments were conducted as follows : In a spacious  photographic studio a large muslin tent was set up with one end against the glass window through which the sunlight poured. At the bottom of the tent were some large pans for the Anopheles to breed in, and these were from time to time renewed.
The mosquitoes were fed on bananas, which, it may be noted, must be kept fairly fresh, otherwise dates or figs are preferable. On one side of the tent seventeen boxes without lids were piled one upon the other, the order being changed each day so as to eliminate any preference due to position or exposure to light. Each box was lined with a cloth having a slightly rough surface — not a shiny or smooth one — to which a mosquito could easily cling. The experiment consisted in counting the number of mosquitoes found in each box on seventeen different days.
The results obtained are striking. During the seventeen days on which the count was made, 108 mosquitoes were found in the navy-blue box, 90 in the dark-red box, 81 in a reddish-brown box, 59 in the scarlet box, and 49 in the black box. There was at this point a sharp drop to 31 in a slate-gray box and 24 in an olive-green box. Violet, leaf-green, and full-blue boxes had respectively 18, 17 and 14. Pearl-gray had 9, pale green 4, light-blue 2, ochre and white 2 each, orange I, and pale yellow about the color of khaki none at all.
It is thus evident that color has a marked power of attracting this species of
   mosquito, and that the color which is by far the most attractive is navy-blue. In both services and equally amongst civilians this is a very common, perhaps the commonest, color for male attire. The experiments just quoted show that it is at least equally popular with malaria-carrying mosquitoes. Light colors were avoided, especially those with a tinge of yellow. Khaki-colored garments would seem to have other advantages besides that of invisibility on a light soil.

Sources:

C. M. Gjullin; Effect of Clothing Color on the Rate of Attack of Aëdes Mosquitoes, Journal of Economic Entomology, Volume 40, Issue 3, 1 June 1947, Pages 326–327.
Packard, A. S. “Color-Preference in Insects.” Journal of the New York Entomological Society, vol. 11, no. 3, 1903, pp. 132–137. JSTOR, JSTOR, www.jstor.org/stable/25003044.

I might be misreading this, but isn't that the effect of different coloured clothing on mosquito presence rather than bite rate?

@DavidMulder Yes: the author is counting how many mosquitoes are landing on the subject. I kept "biting rate" on my answer because, according to the author, "the purpose of the present investigation was to determine what effect different coloured clothing would have on the bitting rate".

Night-time mosquitoes sense IR, UV and CO2 and aromatics as well as colors.  Mosquitos can smell blood through the skin too. https://www.asianscientist.com/2015/10/in-the-lab/mosquitoes-detect-veins/
Black converts the most sunlight to infra red, and white does the least.
2009 Significantly more Anopheles quadrimaculatus females were aspirated from resting boxes fitted with red and IR LEDs than from those with blue or green LEDs, or from the unlit control https://www.ncbi.nlm.nih.gov/pubmed/19852218
Here's a earler conflicting study which is less rigorous, it suggests that different mosquitos prefer different night-light colors. https://www.biodiversitylibrary.org/content/part/JAMCA/JAMCA_V14_N2_P186-195.pdf
Section analysis of the mosquito eye conducted by Kay et al. revealed its sensitivity to ultraviolet (UV) rays. Shimoda et al. used LED light sources with low energy consumption and specific wavelengths to pest control7. Field and laboratory investigations into mosquito response to artificial light have shown, that blue and green light is often more attractive than that in the yellow-orange and red regions of the visible spectrum. https://www.nature.com/articles/srep40074 strobe/fast on and off of the lights caused 2.5 times more mosquitos to be trapped.
http://www.cell.com/current-biology/abstract/S0960-9822(15)00740-X

Short answer
Mozzie preference to colors depends heavily on the species under investigation, as well as the specific preference test used.
Background
Mosquito color preference has been investigated mostly by investigating their preference of oviposition (the process of laying eggs).
When given the choice between black and white containers, Toxorhynchites r. rutilus oviposit preferably in black containers, but about
21% of the females laid at least some eggs in white containers, even in the presence of a black one. 26% used a white container only if a black one was not available (Hilburn et al., 1993)
Aedes Triseriatus females also showed a preference for dark sites for oviposition (Wilton, 1968).
Light-trapping has also been used by putting LEDS in traps and see how many mozzies are caught. Here, shorter wavelengths are associated with higher preference (red < green < blue) in Coquillettidia perturbans, but Culex nigripalpus,  Culex tarsalis, Culex quinquefosciatus and Anopheles sierrenis show no preference whatsoever. Anopheles stephensi however, is highly attracted to UV, but blues, greens, and yellows were less attractive as a clear light bulb (Burkett, 1998.
References
- Burkett et al., JAMCA, l4(2): 195-9
- Hilburn et al, Mosquito News (1983); 43(3): 302-6
- Wilton, J Med Entomol (1968); 5(2): 189–94


text:
What processes regulate the sex of offspring?
It is known that some species are more likely to born male than female (and some maybe vice versa). I understand that it is due to evolutionary perspective (average number of adult males is close to that of females), I want to know about how it is regulated.
What I thought is that spermatozoa are made by half as Y and half as X chromosome. Then mitosis and meiosis and the probability that one of them will die is equal for both types. So, somewhere I feel lost.
Also, can it be regulated by female body or not? According to this paper claiming that hormone levels in women affect the likelyhood to born son. Possibly it is just because they choose males that are more likely to have more Y spermatozoa than X, but if it is some chemical mechanism to regulate that I'd like to know.
I'm not asking only about humans, mechanisms can be similar in almost all mammals. I'm not asking about other species: I know some are regulated by temperature, etc. This question is only about mammals.

I think you are only asking about mammals. Males and females are not universally defined by chromosomes, or genitalia. They are defined by the size of their gametes. Female gametes are larger than male gametes. Some fish switch from males to females as they grow larger. The sex of some reptiles are determines by temperature. So are you asking ONLY about mammals?

You need to specify an organism. The process differs widely throughout the animal kingdom.

@David I guess mechanisms are similar throughout all mammals.

Probably. But birds, fish and fruit flies...

@David I tagged this question with mammals, not fish, birds or fruit flies.

Tags are for indexing. Anything central should be in the question.

No, all mammals are not alike.  Monotremes have very complex sex chromosomes, not much at all like that of other mammals.

@swbarnes2, but is their sex regulated in different way, not like of other mammals (which one present in spermatozoa)?

I don't really understand the question. The only question mark in your question is in the question Also, can it be regulated by female body or not? which, obviously does not stand by itself. Can you please try to rephrase and clarify your question.

@Remi.b, in fact, maybe I should have changed it to "Wgat processes in women regulate the sex of offspring?" Although since I have asked this question I have read that male and spermatozoa are somehow different and that vaginal acidness can affect the sex of offspring. Yet, I am not sure since that was not scientific article.

What processes regulate the sex of offspring?

The processes rulating the sex of offspring may occur in both males and females and be direct or indirect.

What I thought is that spermatozoa are made by half as Y and half as X chromosome. Then mitosis and meiosis and the probability that one of them will die is equal for both types. So, somewhere I feel lost.

This may not be entirely true. The phenomenon called "Meiotic drive" may change the ratio from 1:1. Meiotic Drive occurs through selfish genes. See "Selfish-gene theory" for more info.

Also, can it be regulated by female body or not?
if it is some chemical mechanism to regulate that I'd like to know.

Possibly, there is such in mammals. There is a bunch of mechanisms called "Cryptic female choice". Some of them are chemical. Although, the article is about birds, it can be the case similar mechanism is present in mammals.
Given that higher androgen level exposure in mothers affect make their offspring more male-typical in playing behavior we might consider that in general makes offsrpings more masculine. This would be a good reason for female organisms with higher androgen levels to favor sperm with Y chromosome present.

Possibly it is just because they choose males that are more likely to have more Y spermatozoa than X

Yes, this is possible. But considering cryptic female choice we may say the same for males. Some of them may seek those females who are more likely to get pregnant with particular sex spermatozoon.

Answering by my own since only now I occasionally came across with "Cryptic female choice" article.

In theory spermatozoa are indeed produced in a 50:50 X:Y ratio. However, there are factors which can change the ratio, such as hormone-disrupting agents or even food.
Best known factor in the female body is timing. There are different theories of which The Shettles method is the most well known I think. In this theory they think that boy sperm are faster than girl sperm, but don't live longer. So to have sex around the date of ovulation highers the chance of getting a boy (their sperm is faster), but for a girl sex should be planned a few days before ovulation (they live longer). It is all theory, of course, so there are no guaranties.

Interesting information.  Official / credible sources would radically improve this answer, though.

I have changed the link for Shettles method to wiki, where there are more links to NEJM papers, the results are conflicting though between both NEJM studies, so credible sources are not always 100% waterproof. I speak of a theory therefore, this is stuff I had in high school Biology class when I was still a kid.

If you had linked to the wiki references directly yourself, it would be easier to see that they are very old references, and that the most recent ones do not support the Shettles method.

@swbarnes2 Please link to more recent ones, to support your comment.

Okay, I can link to what you indirectly referenced... https://www.ncbi.nlm.nih.gov/pubmed/11191075 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1440662/

Both can play a factor across mammalia.In humans it is difficult to study effectively (we can't lock people and cages and mate them in controlled patterns, nor will most parents volunteer to hormone injections for their fetus)  So we have less data on humans than for other species.
In other mammals we have had more luck and a variety of mechanisms exist, often several competing mechanisms withing the same species even.  Not surprising if you think about out what gender the males genes "wants" and what ratio the females genes want will not always coincide. In rats for instance the R2D2 gene (I shit you not) prevents female offspring by preferentially differentiating germ cells so only those that carry it become sperm. The gene sits on the Y chromosome so it is selfishly passing itself on at the cost of often wiping out populations becasue they have no females. this is the most extreme mechanism know but it illustrates the sheer variety that exist.
dominance and stress are often good predictive factors, while known mechanisms include Hormones driven differential implantation, differential ova production, differential spermatozoa formation, and differential sperm survival. More mechanisms almost certainly exist but the search for them is relatively new so it is not surprising most studies will list them as potential influences.
Many mechanisms actually makes sense evolutionarily speaking, since there are several competing factors preferring one sex or the other as far as the parents genes are concerned. For instance if the ratios get too far away from the normal ratios it creates a n increasingly strong advantage to produce offspring of the sex in the minority. Another factor is parenting style of the species, in more or less monogamous species the sex has little impact while if you are a species that has harems females are sure thing with low pay off (numbers of offspring) while males are high risk high reward, low chance of reproduce but those that do have LOTS of offspring. Even things like for genes on the Y chromosome every female is a failure is a factor. You mist also consider that chromosome profile is not the only controlling factor, sex phenotypes that do not match their genotype is surprisingly common in mammalian.
Source


text:
How is Na concentration re-established after action potential
I understand that the repolarization is because some K+ chanels are opened with the action potential. But whats happens with the sodium chemical gradient that is needed for a new action potential? Are there further Na-K pumps in the axon membrane?

Na+/K+ pumps are extremely ubiquitous. I recall reading that 1/3rd of an average cell's energy budget goes to maintaining that gradient, with neurons bringing this up to 2/3rds.

Yes, there are Na-K pumps all over.
However, it is important to recognize that ion concentrations change very little during action potentials. The change in membrane potential is due to changes in ion conductances, very few ions actually flow. It is still necessary to maintain concentration gradients over many many action potentials, but the change in concentrations during the course of a single action potential is negligible.

Probably too late to ask but I'd love an explanation for the downvote.

No not too late. Just a lack of sources. Also the fact it's a four liner makes it a bit of a content less answer. Ping me once updated. Happy to upvote.

Heck, the question is quite poor too. Poor question, mediocre answer. I'll remove the downvote.

@AliceD If you want to merge it with https://biology.stackexchange.com/questions/57064/why-is-it-possible-to-calculate-the-equilibrium-potential-of-an-ion-using-the-ne that could be done, I like my answer better there anyways. Might need to make a new canonical answer and question to fit all those types of questions though, because there are a variety of questions people ask that deserve basically exactly the same response.


text:
Dark and bright sides in fluorescence microscopy images?
I have used Phalloidin to label F-actin in ethanol fixed cells ( I know formaldehyde might have been a better choice for fixation). I am new to new to this and I am experiencing that one part of image is bright while other portion is dark (please see attached image). I have already checked that its not due to the lever which we use to shift from bino mode to image mode (eye to camera mode). i have captured images previously and they looked perfect.I dont know what's wrong? Does anyone know what might be the problem?
As I said, I am new to this so it might be a very stupid question but I preferred to ask.
Thanks in advance!
Best,
Ankur

My fluorescence microscopy is rather rusty, but it looks like you have a light gradient from left to right (as opposed to a fixed line).  Is it possible that you have a light focusing adjustment that's out of wack?

Also, the background (at least on my screen) appears to follow that gradient, suggesting to me that it's not an issue with the staining, but rather with a light source direction.

@rotaredom explanation is the most likely, i.e. that the light source is not properly aligned. You can test that by, for example, imaging another specimen that you know has worked before. Alternatively, you may want to double-check that the slide is truly parallel to the objective, although everything looks reasonably in focus to me.