text:
Does the cell have a mechanism to determine DNA sequence from protein?
Something like a reverse genetic code.

No. Why would it need to?

@MattDMo - That's the answer. Post it as such.

For the same reason some bacteria introduce foreign, viral, DNA into their own genome.

@TMOTTM I'm not sure I understand your reasoning. Some bacteria integrate foreign DNA into their genomes as a means of testing defensive mechanisms and evolving in a rapidly changing environment. I still don't see any possible reason to "reverse translate" a protein, for the reasons Remi.b and I discuss below - the number of possible mRNA or DNA sequences per protein sequence is absolutely astronomical, and would do the organism no good at all, as it wouldn't be codon-optimized. I simply don't see a reason for doing it.

Sure, the number of possibilities are astronomical. The cell has various mechanisms to proof-read DNA, still, certain proteins get translated wrongly and are over-active --> for this protein, the proof-reading at DNA level fails.

"Reverse translation"
Translation is the process by which an mRNA is "translated" into a protein.
It is impossible to get the exact DNA sequence from the protein sequence because a large number different DNA strands could code for the exact same proteins. In other words, there is a loss of information in the translation process. See codon redundancy and I am not even talking about introns and UTR.
Now, it is theoretically possible to get one of the large number of possible DNA sequence from the protein sequence. I am not aware of any natural process that does this job.
"Reverse transcription"
Transcription is the process by which DNA is "transcribed" into a mRNA.
It is possible to get the DNA sequence from an mRNA. And it just so happen that such process does exist! A "reverse transcription" if you want. The enzyme that does this job is called reverse transcriptase. Reverse transcriptase is mainly found in retro-viruses but there are a number of non-retro viruses that have a reverse transcriptase.

"several different DNA strands could code for the exact same proteins." I think you're dramatically underestimating here. A polypeptide 400 AA long could conceivably correspond to exponential numbers of possible DNA sequences when you calculate the number of alternatives at each and every position. "Several" just doesn't cut it.

Ha ha, yes indeed. I replaced "several" by "a large number".

A Reverse Translatase, if it was discovered, would be the biggest discovery in biology (maybe in science generally?) in the last 30 years. We would LOVE to be able to treat proteins as strings of information in the same way as we do nucleotides.
But there are good theoretical reasons why it's unlikely. As already mentioned above - the RNA->protein map isn't unique, so the enzyme would only give you one possible mRNA for the protein. But there are bigger issues. DNA, and to a lesser extent RNAs, all have pretty similar physical properties regardless of sequence. proteins really, really don't. Any enzyme going from protein to RNA would have to be ridiculously complex and versatile (much more so than the already bewildering ribosome), to disassemble the almost infinite varieties of protein. Moreover proteins almost always get further modifications that aren't clearly encoded by their RNA sequence - they get chopped up, bonded to themselves, and have extra chemical groups, sometimes big ones, stuck on.The map from RNA->protein is really, really complicated. And this is kind of the point of proteins.
Going from DNA to RNA or backwards is like converting between the master copy of a blueprint, and the working copy used on a building site. It can be done almost perfectly. Going from protein to RNA is more like going from the building itself to the blueprint. The difficulty of the problem is of a completely different level.

I understand. But assume, the protein was first partially degraded.

What is involved  in making a specific antibody to a specific antigen? The immune system recognizes an unfamiliar epitope on a molecule and a dance of enzymatic activity begins where V and J gene segments are cleaved and spliced, d-nucleotidyl transferases may insert nucleotides in V and D segments, with as many possible choreography as there are possible antibody specificity. The master choreographer for all these possible scenarios must by necessity reside ultimately in our germ cell line. Ultimately, even if some predisposed somatic mutations take place, we must assume that this ability to respond to any antigen, even the myriad of synthetic antigens created in modern laboratories, is inherited. And therein lies the problem.
Back in 1976, I wrote the following to Dr. Marvin Fishman, one of the pioneers in Immune RNA research at St Jude Children Research Hospital:

It is hard to conceive how genes for antigens that had yet to come
  into existence would have been preserved through eons of evolution
  since there would be absolutely no natural selective pressure to
  insure their continuation in the germ line. One possible mechanism for
  the generation of antibody diversity is the formation of informational
  RNA in certain specialized cells in response to a given antigen and
  the distribution of this RNA to other cells involved in the immune
  response. Your work has shown the existence of I-RNA and its
  informational role. Its mechanism of formation is not yet known. It
  seems unlikely to me, for reasons stated above, that the macrophages
  responsible for making I-RNA carry this information in their genome.
  It would have been evolutionarily simpler to develop an enzyme system
  capable of making the appropriate I-RNA when it comes in contact with
  the Ag in question. This system would only have to provide information
  for the combining site of an immunoglobulin. Once this piece of RNA is
  made, it can be incorporated into the macrophage’s genome by the
  reverse transcriptase at the appropriate site and then the information
  for a whole specific immunoglobulin could be released through
  transcription. This hypothesis can be checked by adding an inhibitor
  of the reverse transcriptase along with the antigen. This should
  prevent release of I-RNA capable of coding for a whole Ab in a cell
  free system. Actinomycin-D would also inhibit the release by the
  macrophages of I-RNA...

What I was proposing to Dr. Fishman and all of my professors at the time was the existence of “Reverse Translatase”, an enzyme that could read the epitope site of a foreign protein and encode the proper nucleic acid sequence that would then become the template on which the amino acid chain that would constitute an anti-epitope could be assembled. At this point, let me provide a little background on Immune RNA.
It was found that a percentage of macrophages from peritoneal exudates, induced by injection of mineral oil into the peritoneal cavity of mice, incubated in vitro with antigens the donor animals never came in contact with, could process these antigens and elaborate specialized RNA that could transfer immunity. The first hints that macrophages played a crucial role in antibody production came in the late 50s when Fishman et al. showed that antibody production to a specific antigen could be initiated in vitro in lymph node fragments after their stimulation with cell free extract from macrophages that had been incubated with the antigen in question. It was shown that adding the antigen itself to these fragments initiated no response. Only the extract from the macrophage-antigen soup elicited a response. Furthermore, treating this extract with RNase before adding it to the lymph node fragments totally destroyed its capacity to stimulate antibody production in those fragments. Immune RNA was born. Later the standard experiments were conducted with spleen cell cultures mainly instead of lymph node fragments.
It seems to me that the most economical system that could have evolved is the capability to process antigens with a Reverse Translatase system of enzymes that would then transmit information that would be incorporated in the hypervariable or combining site of a specific antibody. This new RNA could then be inserted in the appropriate gene segment of B cells via Reverse Transcriptase that would henceforth become memory cells capable of a secondary immune response. It would be a much more efficient and more easily attainable way for nature to achieve specificity rather than the cleavage, splicing and recombination of gene segments in a predetermined choreography with a billion variations. A few experimental facts that were known in the 70s on the elaboration of I-RNA seem, if not confirm, to at least suggest such a hypothesis.

The addition of Actinomycin D, rifampicin or dimethylrifampicin inhibit the formation of I-RNA by these specialized macrophages indicating the need for RNA polymerase and Reverse Transcriptase activity for its formation. This is what one would expect if a new nucleic acid chain was formed by reverse translation and then had to be incorporated into the macrophage’s genome before a completed I-RNA could be transcribed.
And this is a most important point: the formation of RNA-antigen complexes that is found in those peritoneal exudates macrophages as a precursor to the completed I-RNA strands was not inhibited by either Actinomycin D or rifampin suggesting that the RNA formed in those complexes during the antigen processing phase was not transcribed but formed in another manner, perhaps by Reverse Translatase.
The ability of I-RNA to stimulate antibody production in spleen cell cultures is not inhibited by Actinomycin D nor rifampicin indicating clearly that there is no need for transcription of any gene for the antibody produced. The information for the whole antibody must be completely contained in the I-RNA.

So the evidence suggests that some antigens are first sequestered by a specialized sub-population of macrophages that process them by first forming RNA-antigen complexes. That RNA does not need to be transcribed from any gene region since its formation is not blocked by inhibitors of RNA polymerase, but is perhaps elaborated by a Reverse Translatase that probably makes up the major protein component of those complexes. The next step seems to be incorporation of that RNA into a gene region by reverse transcriptase and then transcription of the complete strand of I-RNA. This I-RNA is released and picked up by B lymphocytes that can then initiate an antibody response. Once this I-RNA is incorporated in the appropriate gene region of the B cells by reverse transcription, they become committed memory cells capable of a more rapid secondary immune response if stimulated again by the antigen.
Proof of the existence of such an enzyme would be in RNA-DNA hybridization studies. If one could extract the RNA from the RNA-protein complexes that seem crucial as a precursor to the formation of I-RNA in those specialized cells and show that it would only hybridize with DNA from V or D gene segments of committed memory B cells but not unsensitized B cells from the same donor, it would be a powerful argument for the existence of reverse translation. An assay for such an enzyme or enzyme system by demonstrating uptake of an appropriate tritiated nucleic acid could also be attempted. Its most likely source, if it exists, would be those RNA-protein complexes found in peritoneal exudates cells exposed to antigen.

Can you please format your answer by including paragraphs? At the moment this is very hard to read. Additionally please also add some references.


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In this illustration about CRISPR function, what do these objects mean (image provided)?
In the paper on CRISPRs, the following figure is shown:

I added the light-green boxes.
What do the red arrows and the line with a filled circle on the far left mean?
What does the arrow in the middle mean (also just infront of cas9)?
Is the purple square to be understood as the RNA section in the B plot (blue arrow)?
Taken from here.
The caption is (cited):

The type II-A system from S. pyogenes is shown as an example. (A) The
  cas gene operon with tracrRNA and the CRISPR array. (B) The natural
  pathway of antiviral defense involves association of Cas9 with the
  antirepeat-repeat RNA (tracrRNA:crRNA) duplexes, RNA co-processing by
  ribonuclease III, further trimming, R-loop formation, and target DNA
  cleavage. (C) Details of the natural DNA cleavage with the duplex
  tracrRNA:crRNA.

The arrow direction denote transcription direction and its location denotes the transcription start site. The circle is probably the transcription terminator (I cannot access this article at the moment, but this is what it should mean).
The purple boxes refer to the protospacers which are derived from foreign DNA. These elements help in recognizing and cleaving foreign DNA. These are transcribed as RNA which in turn guide the Cas complex to the target DNA. In a way, these protospacers provide some kind of immunological memory to the bacteria. See the below figure (From Nuñez et al. 2015 ):

"They are the protospacers": What exactly do you mean by "they"?

@TMOTTM the purple boxes.. I'll edit the answer

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Are gizzard muscles voluntary or involuntary?
I started raising chickens this year. They have amazing appetites, and I often wonder what eating is like for them. They have no teeth, so they don't chew their food as they eat it. They do seem to have some sense of taste, because they often bite off a bit of something and then spit it right back out. But the only equivalent of chewing for them occurs in their gizzard. Because the gizzard is pretty far down the digestive tract, I would assume that it's an involuntary muscle. But all chewing being unconscious for them also sounds kind of crazy.
I'm trying to discover the answer to this question on the internet and I'm surprised that the answer hasn't been easier to find. Does anyone here know? Do birds masticate unconsciously?

As a guess, I think it would be controled by smooth muscle tissue since wikipedia states that it is a "modified stomach". Therefore, since smooth muslce tissue is controled by the Automatic Nervous System, I would say they do not have conscious control. Although I have read that some birds swallow stones to aid in digestion. https://en.wikipedia.org/wiki/Gizzard  , https://en.wikipedia.org/wiki/Peristalsis , https://en.wikipedia.org/wiki/Enteric_nervous_system

I found the same in this book, published just over 100 years ago. The book appears to be the result of some pretty rigorous study, so I expect it is a reliable source.
On page 294, it refers to the gizzard as an involuntary sphincter, and again on page 302 it refers to the grinding of food in poultry as involuntary. In fact it says that because poultry grind all of their food, whether it needs it or not, they found that chickens digest whole grain corn more completely than if the grain is first cracked or ground. That is in contrast to other farm animals studied. I also find that odd, because I have noticed that my hens strongly prefer cracked corn. I've often seen them pick up and cast aside whole or mostly whole kernels. I guess digestive efficiency is not their top priority.

Involuntary. The gizzard, like our stomachs, works unconciously. However, chickens do choose to peck up stones to help along the process, whether that is by instinct or otherwise. (I raised chickens a long time but a proper reference is below)
This book on commercial poultry raising says involuntary

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Where would vegetarians/vegans get a substitute of hemo/myoglobin from?
As far as I understand, there is a difference in the iron absorbed from meat than from other sources like grains and vegetables.
If this is the case, is it possible that not ingesting the hemoglobin and myoglobin found in meat leads to some kind of deficiency in a protein or iron itself that creates some symptoms similar to anemia, like fatigue or headaches? Or, is the iron found in non-meat products just as viable as that found in meat-based products?

Your two questions seem unrelated. How is your question on whether non-consumption of myoglobin from meat cause anaemia related to iron content in vegetarian food? Plus, there are other iron containing proteins in the animal body and there are excellent plant-based sources of iron. Your question is not clear to me.

I can't take your comment seriously because if you had any knowledge on the subject, you would know your question doesn't make sense, you don't understand the subject well enough to understand what I asked.

The following informations is taken this source. It also lists some references. If this doesn't answer your question let me know in the comments.
Iron is found in food in two forms, heme and non-heme iron. Heme iron, which makes up 40 percent of the iron in meat, poultry, and fish, is well absorbed. Non-heme iron, 60 percent of the iron in animal tissue and all the iron in plants (fruits, vegetables, grains, nuts) is less well absorbed. Because vegan diets only contain non-heme iron, vegans should be especially aware of foods that are high in iron and techniques that can promote iron absorption. Recommendations for iron for vegetarians (including vegans) may be as much as 1.8 times higher than for non-vegetarians.
Some might expect that since the vegan diet contains a form of iron that is not that well absorbed, vegans might be prone to developing iron deficiency anemia. However, surveys of vegans have found that iron deficiency anemia is no more common among vegetarians than among the general population although vegans tend to have lower iron stores.
The reason for the satisfactory iron status of many vegans may be that commonly eaten foods are high in iron.For example, you would have to eat more than 1700 calories of sirloin steak to get the same amount of iron as found in 100 calories of spinach.
Another reason for the satisfactory iron status of vegans is that vegan diets are high in vitamin C. Vitamin C acts to markedly increase absorption of non-heme iron. Adding a vitamin C source to a meal increases non-heme iron absorption up to six-fold which makes the absorption of non-heme iron as good or better than that of heme iron.
Fortunately, many vegetables, such as broccoli and bok choy, which are high in iron, are also high in vitamin C so that the iron in these foods is very well absorbed. Commonly eaten combinations, such as beans and tomato sauce or stir-fried tofu and broccoli, also result in generous levels of iron absorption.

These numbers for spinach are based on an ancient typo, compare also the actual values i.e. on wikipedia. The actual difference between spinach & steak would only be around 1.7x

Okay, so the iron in non-heme sources is less absorbed, but enough of it can still be consumed to match exactly what one would absorb from a quantity of meat. So the source doesn't make a difference as long as a sufficient quantity is absorbed in the end?

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Why do our bodies maintain blood pressure but not the flow rate?
This might be a silly question but i'm not not clear
I'm always told that blood pressure is homeostatic parameter and can't not be changed but isn't what important is the flow rate to the organs? why not maintain flow rate
Doesn't having enough blood flow to the organ already satisfy our bodies to function properly or do pressure play any role? what happens if blood flow is constant but blood pressure drop below normal
there's some case when one have blood lost , pressure drop and our bodies respond by constricting artery and that results in decreased cardiac output.Isn't that worst? decrease cardiac output just to maintain blood pressure
Forgive my little understanding out this I know my thought is kind of logically wrong but please help me understand. thank you

A constant blood-flow would not be advantageous to organisms with a varying activity level. The blood supplies (mainly) oxygen to the tissues and the supply of course needs to match the requirements. Organisms rely on a number of mechanisms to ensure this match, one of these is to increase the blood-flow (heart-beat). But flow through a (blood) vessel relates directly to the pressure and inversely to the cross-sectional area of the vessel, so if the flow is increased, the organism must accept either a higher blood pressure or expand  the blood-vessels. Of course, it is in reality a compromise of both mechanisms.

Hi FrankS. Welcome to [biology.se]. Your answer is good but if you could expand a bit on the activity part, it would be great.

What I mean by "activity" is primarily muscle work. If you exercise the muscles work harder, which requires more energy and oxygen. Also for homeothermic organisms, producing more heat to keep warm in a cold environment means higher metabolism and thus higher oxygen consumption. Constantly keeping the blood/oxygen supply at a high level is not an economical solution in a competitive nature where food is scarce.

By regulating the pressure the body is regulating the flow rate. Pressure is the driving force for flow and as shown in this equation below (called the Hagen–Poiseuille equation) pressure drop and flow rate are related to each other for laminar flow in a cylindrical tube. So its impossible in your scenario to keep the flow rate constant but reduce pressure drop for the same size blood vessel.
{\displaystyle \Delta P={\frac {8\mu LQ}{\pi R^{4}}}}
You are right that flow rate is the key parameter because it's important to deliver adequate oxygen to all the tissues in the body or they'll die.

But if your pressure drop.flow rate drop yes but doesn’t further constrictinf the vessel with drop the flow rate even more as the flow is restricted because of more resstance? Why do our body constrict the blood vessel when pressure drop just to increase pressure but reduce flow rate?

I'm always told that blood pressure is homeostatic parameter and can't not be changed
Homeostatic doesn't mean it is constant. It means if it goes high or low it tries to revert back to equilibrium.If you check your blood pressure it doesn't show 120/80. What you call normal is the statistical average of all.
Other questions I do not know the answer.

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What are these insects
I am conducting research and these insects were found on my biological sample (sections of pig's femora placed in an artificial water setting).
My location: Mississauga, ON
What species of insects are these?

Please provide the following to receive an answer: Where are you? Where did you collect these specimens? What is your "biological sample"? What sizes are the specimens?

Were they alive or dead? Do you have photos showing the entire insect larvae (i.e. including not only its head/thorax, but also abdomen and posterior end)?

The small one was alive, but the larger one was dead as the samples were placed in a freezer.


text:
Is feeding birds only after a snowstorm helpful or harmful?
We had a very rare snowstorm here which left the ground covered in 8" of snow and trees covered in snow and ice. It'll likely all melt away in the coming days as we have sunny days and temps rise above freezing.
I noticed some birds poking around the snow on my back deck, so I cut up some raw untoasted walnuts and almonds into small pieces and and scattered them out on the deck and have seen a number of small birds stopping by to feed.
I travel away from home a lot and can't reliably keep a bird feeder stocked, so I'm wondering if this temporary food source is helpful or harmful to the birds since I'm not going to keep it up after the snow melts.
My concern about harm is about causing them to change their behavior and training them to keep looking for food on my deck after I stop feeding them in a few days. I'm assuming that the raw nuts I'm feeding them won't cause any harm even if it's not a well balanced diet, but I don't really have anything more suitable.
I don't know what type of birds they are, they are around 3" high, typical Pacific Northwest birds, I guess.

[pets.se] may be better place for your question. It should be on-topic here too. Can you please add some information on what kind of birds are these. That would be an important factor.

Pets stack exchange specifically excludes wild animals: not livestock, wildlife, and pests in and around your home.  I don't know what kind of birds they are, but I added some photos. Based on this  and this answer, Biology seemed to be an appropriate place to ask.

it's helpful if you give them healthy food which strengthens them, i.e. natural oily foods like seeds, veg oil and natural whole carbs. oil is the most energetically dense and digestible fattening form of food and in the antarctic a cold guy can eat an entire bar of butter without noticing it. birds like vegetable oils, peanuts, seeds. they had it a bit hard with h1n1 virus, it can help to mitigate the effects of man's destruction on them. it also artificially selects certain birds for favorable survival treatment in the cold spells.

@com.prehensible please don't answer in comments. If you think you know the answer then please post one with suitable references.

Feeding for a short period should be helpful, not harmful to the birds, particularly if it is during or following a cold storm.  (Ground feeding birds, such as the Junco or Towhee shown in your picture have particular difficulty after a storm covers the ground with snow.)  A concern people have with feeding is that feeding will create a dependency of the birds on the artificially supplied food.  The worst case of this would be expected to occur during fall migration, where an unusual supply of food might delay birds from migrating, which may be detrimental if they cannot survive the colder weather they may encounter because of the delay.  Other than that period, short term feeding should not be problematic since the birds will not develop a strong visiting habit over a short period.
Dependence on human feeding was studied by Brittingham and Temple in an article "Does Winter Bird Feeding Promote Dependency?".  This study evaluated chickadees in two areas, one which had supplemental food available for a year.  The next year, without food available for either area, showed no difference between the resident birds of the two areas.  Although they didn't test suddenly discontinuing food in midwinter, they do comment on that scenario:

We did not test what happens when feeders are removed unexpectedly from a site in the middle of winter, but we suspect that this would not be as detrimental as is typically thought. In winter, a natural food patch may disappear suddenly as a result of a winter snow or ice storm or the foraging activities of other flock members. As a result, chickadees apparently track a number of food patches at all times and sample a number of areas continuously no matter how abundant food is in any one patch. This strategy is necessary for surviving in an unpredictable and fluctuating environment. People consider bird feeders to be a very predictable food source, but in terms of evolutionary time, they have only been available for a very short time. For birds, they are probably no different than any other food patch.

Thank you, that's exactly the kind of information I was looking for. I was told by someone that I shouldn't have started feeding them since now they are hooked on using me as a food source and I need to keep it up all winter, but I feel more confident now that just feeding them while there's significant snow cover is better than not feeding them at all.

It does help them if they have proper feed:
quote:

studies have shown that birds making it through the winter in better physical condition see those benefits carry over into the nesting season.
  Bird feeding produces significantly earlier egg laying dates, larger clutches of eggs, higher chick weights and higher overall breeding success across a wide range of bird species2,6.

https://blog.nature.org/science/2015/01/05/winter-bird-feeding-good-or-bad-for-birds/

I clarified my question that my concern is more about feeding them only for the few days while the snow is on the ground, not general long-term feeding.


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Are stroma lamellum and grannum lamellum the same?
I have a picture in my textbook that is confusing me as to how they are different.I tried looking for some info on the internet, but could'nt get it clear.Please help me.

Could  anyone please help with this homework issue,now that schools are closed?

I will try to help. But, in the future, please post a picture of the confusing diagram to help us help you.
edit: now that I see your diagram, I'm not sure if this answer is helpful. Will re-consider and possibly edit this response. Thanks for including it!
Grana lamellae refer to the lamellae (membranes) in direct contact with photosynthetic stacks (grana), where the stroma lamellae are the ones that are connecting between individual stacks (see here). My understanding is that they are functionally and compositionally very similar, the only difference being the region of the lamellae in question (link to paper, sorry for JSTOR paywall). Check out the Wikipedia page for Chloroplasts for some more diagrams. Maybe one here will help this make more sense to you!

Is thylakoid membrane continuous with inner membrane ?


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What is the oval shaped bone in the heads of some fishes?

I had a dish of fish and found 2 oval shaped nearly 1cm long bones in its head.What help does it do to the fish? what is its name?
I have clicked the picture myself .

perhaps you can put an arrow on one of these pics so we know where it's from https://www.google.com/search?biw=1241&bih=646&tbm=isch&sxsrf=ACYBGNQoji81vb-xuKWibW4RhulDGDMTmw%3A1578738792915&sa=1&ei=aKQZXqy-N7KMlwSem5mQCw&q=Channa++skull&oq=Channa++skull&gs_l=img.3...8758.8758..8869...0.0..0.149.463.1j3......0....1..gws-wiz-img.......35i39.mfErXoy7XxM&ved=0ahUKEwisksenrPvmAhUyxoUKHZ5NBrIQ4dUDCAc&uact=5

Seems like otoliths. Put a more detailed image for better identification.

Thanks priyanka das

Haha, it's Priyanshu. I'm not cent percent sure if its otolith or not. Just in case you don't know what otoliths are, let me tell you we too have them. They are calcium carbonate granules present in our inner ear. They strike against the sensory hair cells present in there whenever our head moves, thus giving us a sense of movement and balance.

I am a professional fish biologist and those are otoliths; I have aged thousands of them. They are primarily used in maintaining equilibrium, hearing, and balance. The details of the shape of the otolith can vary between species but generally look very similar. They are located in the skull of the fish, usually at the back.
Here is an image of other otoliths:
Photo source: Examples of common fish otoliths found at archaeological sites in Florida. Images from the Florida Fish and Wildlife Conservation Commission http://www.flickr.com/photos/myfwc/sets/72157625872804969/
Otoliths are calcium based structures located within otolithic organs (the sacule, lagena, and utricle) and make up the inner ear of boney (teleost) fishes. They come in pairs and there are three of them: Sagittal (within the saccule), lapillali otoliths (within the utricle) and asterisci (within the lagena). They are made of calcium carbonate and are generally composed in two different crystalline formations, aragonite and vaterite; crystalline form and amount depend on the otolith and stress induce metabolic processes. Otoliths are formed as the fish grows. In periods of fast growth (warmer months) the otolith forms faster and in periods of slow growth (colder months) the otolith forms more slowly. Given the cyclical pattern of warm and cold months in the year, the otolith form annuli (growth rings); annuli can be used to age fish just like rings on a tree. Additionally, they are metabolically inert and cannot be reabsorbed as calcium reserves like other boney structures in the fish; thus, they are a permanent record of the fish's age. This permanent record can also be used to evaluate the life history (i.e., movement patterns) using trace element analysis.
Specifically, how do they work/help the fish? Within the sacule, lagena, and utricle the otoliths are suspended in endolymphatic fluid within their respective organs. The organs have hair-like sensors in them that detect vibration or movement of the otoliths within, triggering an associated nervous stimuli. The nervous stimuli are then interpreted as movement and orientation.
Here are some sources:
https://dfo-mpo.gc.ca/science/aah-saa/otoliths/info/introduction-eng.html
https://en.m.wikipedia.org/wiki/Otolith#Description
https://www.sciencedirect.com/topics/earth-and-planetary-sciences/otolith
https://www.daf.qld.gov.au/business-priorities/fisheries/monitoring-compliance/monitoring-reporting/commercial-fisheries/species-specific/estimated-fish-age
This book is also an excellent resource for a much more in-depth look:
https://fisheries.org/bookstore/all-titles/professional-and-trade/55078c/

Answers should be complete. It's great that you added the citations, but your post needs to indicate why it's correct without reading external links that may die or change. Either summarize these sources in your own words or find photo evidence, etc. Include this info directly in your answer so users can know why you're right without *needing" to click on your links. Citations are for support, not to send users elsewhere for answers. Also, indicating you're an expert is irrelevant -- convenient for having proper knowledge to cite, but not necessary here or adequate to use as "support"

I have edited the original post to provide example photos, additional detail, and more external information if the readers wish to explore further.

Excellent. Thanks for the added effort. +1


text:
What are the lower and upper hearing limits of the human ear?
I am looking for the loudness limits, expressed in decibels, for the human ear.
Google and Wikipedia is only giving me the frequency limit that the human ear can receive, but I cannot find mention about the decibel limits.
Related question on acoustic frequency: why-do-humans-hear-better-between-2khz-and-5khz

Decibel limit for what? The lowest discernible sound? That depends on frequency, age of listener, etc. The level at which damage occurs? What kind of damage? The level at which deafness occurs? How quickly are you talking about? Seconds? Minutes? Instantaneously? Basically, please [edit] your question (don't respond in the comments) and clarify what exactly you're looking for. Otherwise, this question may be closed as "Too Broad" or "Unclear What You're Asking".

i am not asking in frequency limit, i want answer in decibels, db.

I edited your question to improve its clarity

ok why you removed word decibel in the question.

I didn't, just in the title as loudness is pretty much by definition expressed in dB. Also - write @AliceD before you ask for clarification to ping me

sorry, thank you, for making my question more clear

Short answer
Hearing threshold is 0 dB SPL at 1 kHz, and pain threshold is around 125 dB SPL at that frequency.
Background
Loudness thresholds depend on acoustic frequency (pitch), as depicted in the following figure:

Loudness contours in human. Source: Stanford Uni
When expressed in dB sound pressure level (dB SPL) the threshold of pain is approximately 125 dB SPL. The lower bound peaks at a hearing threshold of about -5 dB SPL at 4 kHz (maximum sensitivity). Outside that frequency, hearing sensitivity declines (and threshold hence increases).
Note that dB SPL references to a sound pressure of 20 µPa = 2 × 10−5 Pa. This sound pressure corresponds to the hearing threshold at 1 kHz and is hence defined as 0 dB SPL. (Stanford Uni).

Further reading
Why do humans hear better between 2kHz and 5 kHz

but you haven't mentioned any number between this and this is the decibel limit for human ear.

I did, and it's in the graph. Now in the short answer as well.

@KlaytonThomas - since you are new here - if the answer is to your liking and sufficient please accept it by clicking the check button on the left and/or upvote it. If it is not what you were after, just let us know :)

authors: Олександр Савицький


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Unidentified Spider
Apologies for the rubbish quality of the image, but I found this spider while in the shower. I’m not exactly sure what species it is and wonder if someone can help me out.
I live in southeast Michigan, it was a relatively humid day and it is 1 degree Centigrade presently. It is 9:29 PM EST. I’d say the body of the spider is about a centimeter long. Any help is appreciated.

This is Cheiracanthium sp. with common name "Yellow Sac Spider." It is very common in North American homes, distinctly identifiable by having a homogenous colour that is almost an translucent yellow (sometimes yellow-green or yellow-brown) with no particular markings (no stripes or dots) aside from the cardiac mark (the dorsal line on its abdomen).
It often has black feet like in this photo and is sometimes alternately called a 'black footed sac spider.'
There are two species of this genus widespread across North America: C.mildei and C.inclusum which are difficult to separate from photos like this. It is generally understood that C.mildei is commonly found indoors while C.inclusum is commonly found outdoors.


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Is the General Cirrate Octopus Form the Basalmost Octopoda Morphology?
The reason I ask this is due to the distinctive internal mantle shells of cirrina, of which the incerrata have stylets that are a remnant of the cirrate shell. Along with this, both cirrate octopuses and Vampyroteuthis have a gladius (although with different morphologies) with fins upon their mantles, which incirrate octopuses lack.
Also, a relatively recent study presents a view that cirrate octopuses are actually paraphyletic, being an evolutionary grade rather than a monophyletic group. Can it be inferred then that the basalmost octopus form is then a pelagic form with a gladius that uses mantle fins as the primary form of locomotion, and the incirrate form normally associated with octopuses is a drastic deviation?


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Question regarding when it's a homoplasy in a phylogenetic tree
If you have 2 organisms that both come directly from the same common ancestor on a phylogenetic tree, and that common ancestor does not have trait "x", is it possible for both of its direct descendants to develop that trait "x" independently, and would that be an example of a homoplasy?

Can you draw what you are describing?

Phylogenetic tree vs first generation offspring
Please note that on a phylogenetic tree, the time scale is big enough so that the generation time is completely undistinguishable. Hence, questions of first generation offspring won't rise. Also, in practice when reconstructing a phylogenetic tree, our level of accuracy does not allow us to distinguish exactly at what generation did specific mutation occur.
Rephrasing your question
The term homoplasy is typically used in the context of phylogenetics. Also, most of the time the term homoplasy refer to phenotypic trait and not to genetic sequence but I will not go into these specific complications here. The term is also mainly used in intro textbook and not so much in the peer-reviewed literature. In all cases, one can define the concept of homoplasy as a shared trait that is caused by a mutation that is not identical by descent. In other words, if in two lineages/individuals that share the same trait, the trait is caused by the same mutation(s) (same, not only by its state but by descent), then the shared trait does not represent a homoplasy.
With this, I can rephrase your question as

If two siblings share a (heritable) trait that the direct parent does not have, are the traits identical by descent?

If two siblings share a (heritable) trait that the direct parent does not have, are the traits identical by descent?
Well.. it depends as to whether the mutations happened happened twice independently in the two different gametes or if the mutation happened once in the (germ line) lineage that gave rise to these gametes in the parent body.
The second is much more likely. Because, it is very unlikely for the same mutation to happen twice independently in two different gametes for the same individual and much more likely that the mutation happened once in a cell that gave rise to the two gametes, it is very much more likely that the shared trait among the two offsprings is caused by a mutation that is identical by descent. Hence, not a homoplasy.

editted I think I did a poor job of explaining my question and for that I apologize, let me rephrase it. I am trying to take a tree that is in a state of synapomorphy and turn it into a tree that is not. So can I create the condition of a homoplasy simply by moving the introduction of a trait to the branches that come off after the common ancestor instead of before the common ancestor?

did you see my most recent comment?

I did but did not quite understand it so I ignored it. If you could maybe make a drawing in the post, that might help.


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What neurons' projections comprise the olfactory nerve (Cranial Nerve 1)?
Recently, I have been learning about olfaction. To my surprise, I am having a heck of a time finding explicit information regarding which neurons' axons are comprising the olfactory nerve. I am aware that there are several cells types that are relevant in the olfactory bulb: mitral cells, olfactory sensory neurons, tufted cells, and many more. However, I have not been able to find any source that definitively states from which neuron type the projections that comprise the olfactory nerve arise from.
I keep seeing articles that seem to imply olfactory sensory neurons comprise the olfactory nerve, but this doesn't seem right to me. My understanding is that the projections that emanate from the olfactory bulb and terminate in the brain constitute the olfactory nerve. The only thing I can think of is that the "olfactory bulb" is actually being considered "part of the brain"...in which case, the olfactory sensory neurons are technically peripheral neurons.
If that is the case, what exactly are the olfactory bulbs? Are they part of the telencephalon? Are they an outgrowth similar to how the optic nerves are outgrowths of the telencephalon and therefore not "true nerves"?

Olfactory receptor neurons (ORNs) in the olfactory epithelium in the nasal cavity project to the olfactory bulb; this projection is Cranial Nerve 1 and it's more of a collection of fibers rather than a highly organized nerve.
Your surprise or confusion is probably based on this:

My understanding is that the projections that emanate from the olfactory bulb and terminate in the brain constitute the olfactory nerve

...which is false: the olfactory nerve is the step prior to the olfactory bulb. The olfactory bulb is part of the brain.
I'll add that I have seen poor diagrams of the brain that point to the olfactory bulb and label is as cranial nerve 1, which is false or at least misleading.

what exactly is the olfactory bulb, then? It's certainly not a cortical structure. Is it classified as a subcortical, telencephalic-derived structure?

It's part of the forebrain, specifically the telencephalon. It's of course not neocortical, but much of the telencephalon is not, for example it includes the basal ganglia.


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At What Rate Do Ions Leak Out of a Plasma Membrane Segment That Has No Ion Channels?
In reading about the purpose of myelin during action potential propagation, I came across a point of confusion.
From what I understand, one of the primary "benefits" of myelin is that it aids in increasing the transverse resistance of an axon...which, biologically, is equivalent to stating that it minimizes the extent to which ions move out of or into the cytoplasm of the axon.
However, I feel as though I have always been taught that "the plasma membrane is impermeable to charged particles" and am therefore confused as to what additional benefit is conferred on the axon by the myelin.
Consider the following two cases:
Case A) The action potential starts at the axon initial segment. The subsequent segment is myelinated. The action potential, through passive diffusion, makes its way down the myelinated section until it reaches the 1st node of ranvier, where the action potential is subsequently regenerated.
Case B) The action potential starts at the axon initial segment. The subsequent segment is unmyelinated but contains no ion channels (or pumps). The action potential, through passive diffusion, makes its way down this unmyelinated section that has no ion channels (the same distance as in Case A) until it reaches a dense collection of voltage gated sodium channels.
In case B, will the action potential be regenerated? Or has the passive diffusion event suffered from too much "leakage"? If so, is it really true that:
(the plasma membrane + myelin) transverse resistance >> (the plasma membrane) transverse resistance alone

I'm going to mostly skip over the title of your question and focus on the confusion in the body, because the question in the title is a bit of an XY problem. It doesn't make much biological sense to think about a membrane that is truly that resistive (that is, I am unaware of any example neuron, or even any other cell, that has that property).

If there were truly no channels of any sort, you could indeed consider the resistance to be very high, at least as high as one could measure in patch clamp. Additionally, what matters is not the resistance itself but the ratio of the transverse to axial resistance; relative to the axial resistance the transverse resistance is already very high.

From what I understand, one of the primary "benefits" of myelin is that it aids in increasing the transverse resistance of an axon

Your understanding is not completely correct. The insulating benefit of myelin (ignoring other organizational benefits) is not only related to the transverse resistance, but importantly to a decrease of the capacitance of the membrane (see Moore et al 1978 or Richardson et al 2000 for some example simulations; also any reasonable neuroscience textbook will explain this). You can test this yourself in a simulation environment like NEURON.
Myelin decreases capacitance by effectively increasing the distance between the 'plates' of the membrane capacitor (see this answer).
In order to charge a long length of membrane with channels on only at short segments, you would need enough charges to come in within that short segment to charge the entire length of axon, and the potential would decay with distance.
Myelin does also affect resistance, but that's mostly important because the membrane does not consist only of a phospholipid bilayer and there is non-zero leak. For example, there are channels under the lipid bilayer that establish a resting potential (Chiu & Ritchie, 1984).

Chiu, S. Y., & Ritchie, J. M. (1984). On the physiological role of internodal potassium channels and the security of conduction in myelinated nerve fibres. Proceedings of the Royal society of London. Series B. Biological sciences, 220(1221), 415-422.
Moore, J. W., Joyner, R. W., Brill, M. H., Waxman, S. D., & Najar-Joa, M. (1978). Simulations of conduction in uniform myelinated fibers. Relative sensitivity to changes in nodal and internodal parameters. Biophysical journal, 21(2), 147-160.
Richardson, A. G., McIntyre, C. C., & Grill, W. M. (2000). Modelling the effects of electric fields on nerve fibres: influence of the myelin sheath. Medical and Biological Engineering and Computing, 38(4), 438-446.

For clarification, are you saying that there are leak channels present in the plasma membrane that directly underlays the myelin sheath? My understanding was that the plasma membrane that lays just beneath the myelin sheath is effectively "barren" of any sort of channel or pump.

otherwise it seems like the only energetically favorable purpose of the myelin is the reduced capacitance that you mentioned...because, if I'm the neuron...why don't I just create patches of plasma membrane that have no pump or channels. In which case, I don't understand why people even mention the fact that "increased transverse resistance" is an advantage of the myelin's presence.

Yes. See the Chiu paper for example (they talk about VGK channels but any channel means resistance isn't zero). There are also more recent papers that show the myelin itself contains channels. Also it's possible some people don't quite understand what they are saying, but in general I would agree with a statement that the capacitance reduction is most important.


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What is the difference in the electrical excitability between a "large diameter soma" and a "large diameter axon"
There are two stereotyped statements that I have seen during my coursework regarding electric properties of neurons:

Large diameter axons propagate action potentials more quickly than small diameter axons
Large motor neurons are the last motor neurons to be recruited

Separately, I have always understood these statements through the following lens:
Explanation for 1. (for arguments sake, lets talk about unmyelinated neurons...so, for example, a C-fiber with a small diameter and a C-fiber with a slightly larger diameter). The reason the larger diameter neuron will propagate its action potential more quickly is because, in a given cross section of the axon, there are more voltage gated sodium channels present along the circumference. Consequently, the speed with which the incoming sodium signal is generated is quicker. I am aware of "reduced longitudinal resistance" for larger axons, but I am purposely ignoring this...please continue reading.
Explanation for 2. Idealizing the soma of a neuron as a sphere, we know that capacitance increases with increasing radius (related to the distribution of charge along a 'longer' circumference). Consequently, for a large soma, the amount of charge required in order to observe a change in potential difference across the membrane is MORE than it would be for a smaller soma.
When treated individually, both of these statements are intuitively "okay". However, when I think of these two statements together, confusion arises:
A. Shouldn't the increased total number of ion channels observed in the larger diameter axon also be observed in the larger soma?
B. Shouldn't the capacitance increase observed in the larger soma also be observed in the larger unmyelinated axon?
If both of these statements are equivalently applicable in both cases, why do the two statements "1" and "2" seem fundamentally different?
The only rationale I can think is the following: The % of surface area occupied by ion channels on the soma membrane is significantly less than the % of surface area occupied by ion channels on the axon membrane. Consequently, the axon can offset its increased capacitance by the gain in additional ion channels. However, the soma cannot offset its increased capacitance because the % of ion channels occupying its surface is below this "capacitance offset" value.
Edit:
I have provided two pictures to help clarify my question:

As you can see from the above two images, the values in the two tables are the exact same. Summarizing, the larger soma and larger myelinated segment of axon both exhibit:

Less Longitudinal Resistance
Greater Capacitance
Greater Surface Area Available for Ion Channels

I have previously asked two separate questions:
Here_1: Are large cell bodies of neurons harder to depolarize than small cell bodies of neurons?
and
Here_2: Why do larger diameter myelinated axons have greater conduction velocities than small diameter myelinated axons?
The conclusions from the two questions were that larger somas take longer to depolarize and larger axons transmit electric signal more quickly.
Even though both 'entities' exhibit shared electrical properties, it appears as though the outcome of having these electrical properties is fundamentally different. In one case, the membrane is taking longer to depolarize...but in another case, the membrane is depolarizing quickly!
What am I missing that results in my perception that electrical properties are somehow being differently applied to the soma of a neuron and the axon of a neuron?
(Note that this question involves the myelinated section of the neuron so there is no need to talk about nodes of ranvier or any sort of "active" electric process)

Can you cite where your assumptions are coming from? I think you are taking things to be rules that are not rules. Also: where is the stimulus coming from? why are you talking about receptors on axons? why are you applying motor neuron ideas to C-fibers?

The "receptor" was a typo. I have corrected some other typos accordingly. My assumptions are coming from my own intuitive understanding of physics and other general sources. C fibers were chosen because they are unmyelinated...I didn't want to involve myelin in this discussion...and why should the electrical phenomenon affecting motor neurons not be extendable to the electrical phenomenon affecting any other sort of neuron?

Because the "size principle" is an experimental finding with motor neurons. It is not a rule for all neurons. Please separate out your question a bit too, there is far too much here to unpack, and ask a single answerable question.

From what I recall, isn't the intuition behind the size principle the very concept that I mentioned? Namely, that larger cell bodies have larger capacitance and therefore their membranes take more positive charge in order to depolarize?

I really think you'll enjoy the NEURON program (neuron.yale.edu) that I've recommended to you before if you want to test out some of your thoughts. In any event, the size principle is an experimental finding, not a physics one. That doesn't mean physical properties of size don't have an influence, but it also doesn't mean size is the only factor.

Hmmm. So, besides the size principle observed in motor neurons, you’re saying that neurons with larger somas actually fire with LESS total input than with neurons that have smaller somas (i.e. large somas are more sensitive to input than neurons with smaller somas?)

I never said that.

Then I do not understand any of your preceding comments. Why do you take issue with me generalizing the intuition behind the size principle of motor neurons to all other neurons? It seems to me that larger somas should therefore require greater input (as compared to smaller somas) in order for the axon initial segment to be sufficiently depolarized such that it initiates the action potential.

What I said is that size is not the only determining factor, and you should not assume that a larger cell is activated at higher threshold if you aren't talking about a motor neuron: that principle counts for motor neurons only, others you have to approach on a case by case basis.

If it's helpful, i've broken down my question into two other questions: https://biology.stackexchange.com/questions/82885/why-do-larger-diameter-axons-have-greater-conduction-velocities-than-small-diame and https://biology.stackexchange.com/questions/82883/are-large-cell-bodies-of-neurons-harder-to-depolarize-than-small-cell-bodies-of
hopefully that should "clean up" the question a bit...and my confusion regarding some of the general principles I often hear regarding the electric properties of neurons with different morphology.

Closed as too broad to allow the other two questions to remain.

Does the soma fires action potentials?

Depends on your definition of soma (AIS included?)...but no, it does not.

I don't see any difference between your soma and your myelinated axon.Then, they are fundamentally a nonconductive compartment. So if for the same entity you get two different results, there's something you`re not considering.


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When are neuropeptides loaded into vesicles?
It is well known that small neurotransmitters like monoamines (dopamine, serotonin, etc), acetylcholine, glutamate, etc are loaded into vesicles at the axon terminal. Stated differently, synaptic vesicles,SVs (which are the name of the vesicle type that store small neurotransmitters), are made locally within the axon terminal, and then ultimately loaded with small neurotransmitters.
However, I cannot seem to find when larger molecules, like neuropeptides, are actually loaded into their vesicles. I know that neuropeptides are made in the soma, but I am unsure of when they are loaded into their vesicles.
Are neuropeptides loaded into their vesicles at the synapse?
" Small-molecule neurotransmitters are synthesized locally within the axon terminal" https://web.williams.edu/imput/synapse/pages/I.html
"As a rule, the synthesis of small-molecule neurotransmitters occurs within presynaptic terminals" https://www.ncbi.nlm.nih.gov/books/NBK11110/
"SVs are made locally at the terminals and are regenerated after exocytosis"  https://www.sciencedirect.com/science/article/pii/B9780080450469013929

Can you cite your sources? There are major errors in your question, almost all of the things you say you "know" are incorrect.

here are the citations. If the small molecules are synthesized locally within the axon terminal, they are clearly being stored in the vesicle within the axon terminal. This is the general dogma of vesicular packaging.

What about the rest of your statements? You've cited only the things are correct, you haven't corrected anything that is wrong.

I am unaware of any of my statements being wrong. Could you please enlighten me? I am not trying to promulgate false information. These are my understandings of concepts.

" Stated differently, vesicles are made in the soma, shipped down to the axon terminal (via motor proteins), and then ultimately loaded with small neurotransmitters." is wrong.

Thank you for catching that. I was unaware that synaptic vesicles were strictly produced from the recycling process at the axon terminal.

This paper is very interesting: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4194108/
and wonderfully highlights how motor proteins and endocytosis work together to create the SVs that are ultimately loaded with small neurotransmitters

Neuropeptides are packaged in the soma via the Golgi into dense core vesicles, similar to how other types of secreted proteins are packaged.
These vesicles are transported to axon terminals where they await release signals.

Sossin, W. S., Fisher, J. M., & Scheller, R. H. (1989). Cellular and molecular biology of neuropeptide processing and packaging. Neuron, 2(5), 1407-1417.
Wong, M. Y., Zhou, C., Shakiryanova, D., Lloyd, T. E., Deitcher, D. L., & Levitan, E. S. (2012). Neuropeptide delivery to synapses by long-range vesicle circulation and sporadic capture. Cell, 148(5), 1029-1038.

Do dense core vesicles also have all of the traditional synaptic transmembrane proteins in them like synaptotagmin and synaptobrevin? Or are those specifically unique to the "synaptic vesicles"

@S.Cramer At least some of them do. Some are not released by calcium so I'm not sure what machinery they have for membrane fusion.

Interesting. I ask because the one article that I mentioned in the comments above (about "synaptic vesicles") explains that the specific transmembrane synaptic proteins are only incorporated into the vesicle once the components have FIRST merged with the axon terminal. Then, via an endocytosis process, these transmembrane proteins are somehow selected to be included in the synaptic vesicle during its assembly. If you're saying that "at least some of them do", then clearly these transmembrane proteins are being incorporated in to the vesicle membrane in a very different manner. Cheers~

Can you point me to where in the article you see that?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4194108/
In figure 3, it looks as though the particular proteins that will be used for synaptic vesicles are first shipped to the synapse via a standard trafficking vesicle. Then, upon arriving at the axon terminal, this trafficking vesicle fuses with the axon terminal. Thereafter, an endocytotic process incorporates these "deposited" proteins into the synaptic vesicle. That's how I am interpreting the figure, at least.

Ah I see, well for the small molecule vesicles of course that is the case because they do not come pre-packaged and are recycling membrane from the synapse. It's possible that dense core vesicles undergo some merge with an endosome at some point, I'm not sure though, I'd have to research that separately. I just know that at some point some of them will contain synaptotagmin.


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Relationship between blood pressure time series and ventricular dynamics of the heart
The answer to this question is probably very straightforward, but I have actually had some difficulty finding an explicit answer online.
To what extent does the oscillatory pattern of arterial blood pressure (over small increments in time) mirror the oscillatory pattern of heart beat. For simplicity, imagine my heart beat signal is a binary signal where 0 means blood is not being ejected and 1 means blood is being ejected into circulation.
Said differently, if I detect a transient (where the interval of time is less than one second) increase in arterial pressure (e.g. a local peak), can I always accurately map that event to the "causal" contraction of the ventricles during blood ejection?
Similarly, can I use an arterial blood pressure time series to accurately recreate the binary signal of the heart beat? (Though, perhaps there will be a slight time shift due to the propagation speed of a pressure wave).
To provide another silly example: if my arterial pressure time series has 60 peaks (and corresponding "separating troughs"), can I confidently assert that the heart beat 60 times?

What happens when you take a pulse?

@BryanKrause ehhh. I was hoping for a legitimate paper. Taking a radial pulse is likely a grandfathered in practice that predates technology from the past 50+ years...I'm reluctant to claim something as canonical in the absence of quantitative evidence. I did not know if there was some paper that simultaneously measured time series of a ventricular valves open/close states and an arbitrary artery's vessel pressure. Certainly the radial pulse can be used as a proxy for heart beat (that's why it's a grandfathered in practice) but can it capture ectopic heart beats that eject very little blood?

Be careful not to ask an "XY" question. If you want to ask about ectopic heart beats then ask about that rather than the vague question you wrote here.


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Is it possible for human body to convert carbohydrates to protein?
Is it possible for human body to convert carbohydrates to protein to build muscle for example?
EDIT: I read in many articles that you should eat more than 1.5 gram protein for each 1 kg weight of your body to gain muscle, but I see some bodybuilders that I know they don't eat that much of protein but gain muscle and have muscular body. So it was interesting to me to ask this question here!

Welcome to Biology.SE. Your question could be interpreted a number of ways. In particular, it sounds like nutrition and bodybuilding question, but could be a biochemistry question. Could you edit your question to clarify what kind of answer you're looking for?

In short, no, because proteins contain nitrogen, and carbs do not.

@swbarnes2: So body can not add this nitrogen or combine carbs with something that can add this nitrogen to them and make protein?

Just to further clarify my comment, the answer depends a great deal on what you mean by "carbs" (glucose? bread?) and "is it possible"

@DeNovo: Thank you for remark. I want to know, if is it essential to eat 1.5 or 2 grams of protein(especially whey) to build extra muscles or it's just advertising tricks and a person with normal diet(without eating extra whey powders or eating 10 eggs per day) can make extra muscles if he just eats more food(I mean he just increases his normal diet whatever he was eating before, not only increasing protein)?

It sounds like you're looking for an answer that is more suited for fitness.SE. The biology stack would be more suited for this question if it was about biochemistry. I'd note that, re: the biochemistry question, in addition to @user1136's comment, a glucose load is associated with increased activity in protein anabolic pathways. This may be because of the insulin response.

@DeNovo: No I am not looking for workout advices! I asked here to see the scientific view of this, if is it possible or not!

Some amino acids can be synthesized from carbohydrates if nitrogen and any other necessary mineral elements are present. But some carbohydrates have to be ingested.

@Tak: Do you know those amino acids that can be synthesized from carbohydrates are enough to making new muscles or building new muscles need other type of amino acids that can't be reached by carbohydrates syntheses?

Essential amino acids cannot be synthesized from carbs, but non-essential amino acids can be synthesized. Intermediates from the citric acid cycle or pyruvate can be used to synthesize at least 11 kinds of non-essential amino acids. They will be incorporated into muscle, but you need all the essential amino acids available in order to produce complete proteins that will build muscle tissue. Proteins are made from the entire repertoire of amino acids, and I don't think there exist any (perhaps very, very few, none to my knowledge, *I've checked the literature) that are made from only non-essential acids.

PS. I'm sorry the question is on hold @user145959, there are poorly behaving regulars and/or mods here, and one that is blindly downvoting every post of mine. The question can humans convert carbohydrates to protein is a biology question, one asked very frequently in biochemistry classes; it is definitively not a homework question, the questioner has repeated that they are interested in a scientific verdict. It's clarified that you specifically want to know whether anabolism is taking place... And people are still voting to close the question. Come on guys, what are you doing?

@SPr re "Come on guys, what are you doing": I would encourage you to open a meta discussion. re: downvotes, I'd encourage you to not take downvotes personally, but consider them to be feedback about your answers. I don't think you have a serial downvoter. I downvoted this one, and haven't recently downvoted any other answers of yours. I downvoted because the OP isn't asking about biochemical carbohydrates, but nutritional "carbs", which usually include carbohydrates AND protein. That and the lack of references led to my downvote. I should have made a comment when downvoting.

@SPr on reflection, my downvote reasoning doesn't make a lot of sense. I'll remove it. I'm not going to upvote, though, since it doesn't have any references and doesn't seem to address the question, which is essentially "what should I eat in order to bulk up", not "what are the biochemical pathways from which glucose can contribute carbon to amino acid synthesis".


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List of heritability estimates in humans?
Many people on this site ask questions that directly or indirectly have to do with heritability in human.
Do you know a list of estimates of heritability of various traits in humans? Or could you try to create such list?
That might be great to have various kind of traits, personality traits, life-history traits, morphological traits, …
I am not necessarily asking for GWA studies that inform about what genes explain the observed variance (although that would be really great) but just some estimates of heritability and eventually information about the method used (parent-offspring regression, twins, ...) and which population was studied.

Do you think about a list of traits (for example hair color) and genes associated to it?

@Chris I did not expect something as accurate as the results of a GWAs. I was just thinking about a list of values of heritability for a list of traits. If one wants to add the way it's been measure, on which population and if it is a GWAs, give more info about what genes and how many genes explain the variance then it is really really cool but I will accept the answer even if it is not that perfect!

You may consider consulting the H2DB database. The database is quite new, so the number of heritability estimates is not very high at the moment (currently 225 estimates for human, 838 estimates in total), but it's a start. The database is described in a paper by Kaminuma et al.(2)


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Definitions of robustness and canalization
The concepts of robustness and canalization are fashionable today in the biology literature. However, I am not sure of their definitions and I am not sure either that all authors actually use the same definition.
I am therefore asking here for a the definitions of these terms or for a short review of the common definitions of robustness and canalization. How do different authors define these words? I am particularly interested in...

The differences between robustness and canalization (canalization seems to apply more in developmental biology than robustness who seems to be a more general concepts)
At what level do these concepts apply? To populations, to genotypes, to both, ..?
How does the concept of adaptation link to these definitions.
How does the concept of plasticity fits in opposition of the concepts of robustness and canalization?

As canalization is defined in your question (also in wikipedia) it means robustness.
Semantically it is possible to differentiate the two.
Robustness of a system refers to its sensitivity to perturbations. In other words small differences in parameters would not affect the steady state of the system (parameter changes in a physically plausible range would not lead to bifurcations).
By system I mean a set of entities connected to each other in a defined fashion. For example an ecosystem in which different species are connected to each other by interactions of the food chain. At steady state a system configuration (for instance- 10 foxes, 100 rabbits, 10000 grasses, 1000 honeybees etc) remains constant over time (that, however, doesn't mean it is static). Or in case of development a system may be the body defined by a set of certain phenotypes.
Canalization/channelization refers to mechanisms that make the system follow a certain trajectory. So if you see it mathematically canalization keeps the trajectory dictated by a  given set of eigenvectors. In case of development you may call mechanisms such as dosage compensation, functional compensation by isoforms, parallel metabolic flux channels etc as canalizing mechanisms.
So in contemporary usage we can call a system robust (a property of a system) whereas we should address mechanisms that help to preserve trajectories as canalizations. The final aim of canalization is to render robustness to the system but it is not the only mechanism that is responsible for robustness (for e.g. the steady state may just be independent of certain parameters).
Robustness is a property of the system and is dependent on how the different entities of the system are coupled and what their interaction parameters are (rates etc).
You should note that these are parlances that are adopted by different groups in the scientific community and may perhaps mean the same thing- this is merely my attempt to remove redundancy of terms by the means of semantics.
Now, plasticity is a different concept altogether. Plasticity is in a way opposite to robustness. This means that the qualitative nature of the system can change if certain parameters are tweaked. However, the system should still maintain its stability. In a stable system mild perturbations from steady state will result in system going back to that steady state - like a ball in a well. However, a system may inherently allow for multiple steady states (like switches), and depending on certain parameters the system can be in either of the states (but if pushed too far then the system can go to another stable steady state). This is called multistability.
NOTE: some people also use the term plastic to mean "responsive". The above definition may not be exhaustive or the most perfect.

THanks for your answer, it is already very informative although I am still a bit confused. When you say that robustness is a property of a system, do you mean it is a property of genotypes, populations, both, ..? Robustness is the property of a system to always produce the same phenotype while canalization is the mechanism of this system that yield to the production of always the same phenotype. hum... Did I get it right? What do you call trajectories when you say that canalization preserves trajectories? Thanks a lot for your help.

Are you aware of an article that directly compares the definitions of these two concepts?

No I haven't read an article which compares them.

There are several subconcepts within the concept of robustness. Several definitions exist for all of these concepts and I am just suggesting one variant of the possible definitions below.

Mutational robustness

Might be defined as a function of the mean and variance of the distribution of mutational effects.

Environmental robustness

Might be defined as the opposite of phenotypic plasticity. Here, plasticity is not only defined as adaptive plasticity. Plasticity is any phenotypic change induced by an environmental change. Environmental robustness might therefore eventually be defined as the inverse of the slope of the reaction norm.

Developmental robustness

Might be defined as the variance of phenotypes that a given genotype produces in a given environment.

From Gilbert and Epel (2009), page 384, Canalization is developmental robustness.
In Biology, those concepts almost always refers to genotypes. Rarely do they apply to populations or ecosystems and when they do the definitions are often quite different.


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The concepts of relatedness - Hamilton's rule and kin selection
Here is a quotation from this wikipedia page

The relatedness parameter (r) in Hamilton's rule was introduced in
  1922 by Sewall Wright as a coefficient of relationship that gives the
  probability that at a random locus, the alleles there will be
  identical by descent.[14] Subsequent authors, including Hamilton,
  sometimes reformulate this with a regression, which, unlike
  probabilities, can be negative.

Here is my question:

What are all the different definitions of relatedness in biology?

how do we calculate them?
what do they mean?

You should break this up into several questions - too many questions rolled into one at the moment, and single answers will probably not cover all of them.

@fileunderwater I updated the post. Thanks for your comment.

Is that really trying to imply that there are significantly different definitions?  It seems to me the intent was just to put it in terms of an equation with more useful numbers.  This terrifying paper from 1964 gives some of the follow-up works, in particular works from Cockerham in 1954 and a number of papers by Kempthorne, in particular this from 1955 and this from 1963.  There is also Malecot's method of coancestry from 1948. (WorldCat.org link)  The idea was mainly to look relatedness outside of the specific limitations present in Wright's work.  Some of the math in those are more accessible than others...


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Human population growth - where can I find the data?
Out of curiosity, I'd like play around with data of human global demography.
Where can I find data that describe the "per region (per continent for example) population size" versus time since the "Out-of-Africa Event" or earlier?
Here is for example the kind of graph I'd like to reproduce but if possible in a region per region basis.

I don't think that data is available.. For recent data you can look at census of different regions

National censuses are collected, published and disseminated primarily by each country's census or national statistical office (NSO) or its equivalent. Census data are published in each country's vernacular, and as appropriate, many offer English as well as other language versions.
Statistical offices of international agencies (e.g. United Nations, statistical organizations for member states like the ASEAN, Eurostat, and OECD), also publish statistical data including population figures. The most consistent data in terms of format and frequency, whether online or in print are usually generated from them.

The US Library of congress provides some interesting links here:
http://www.loc.gov/rr/business/census/intlcensus.html
Also Cornell provides a few resources also:
https://www.ciser.cornell.edu/ASPs/datasource.asp
If you still need some information, your best bet is to then contact social scientists and ask for their opinion.


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System biology and evolution: Book-recommendations
I have relatively good knowledge in evolutionary biology and in population genetics. I am getting more and more interested in the evolution of ...

genetic developmental processes
gene interactions
gene expression
plasticity
intrinsic or cellular noise
mutational robustness

It seems that i am getting increasingly interested in a field that is in between population genetics and system biology. I know very little about system biology.
Can you please give me some recommendations for books (and other readings such as reviews) that talk about the evolution of those processes that are usually studied by system biologists? I am much more interested in a book that presents concepts and methods than a book listing empirical observations. Also, I am not interested in medicine but in biology.

Systems Biology seems so new that I would expect that most books on that topic would probably be collections of articles from symposia. Given your detailed list the first author that springs to mind is Stuart A. Kaufmann (there might be another 'f' in his name).  I recently saw someone here cite his 1993 book 'On the Origins of Order' he is a real theoretical biologist, like Francis Crick. He was affiliated with bothe the Penn Medical School and the Santa Fe Institute think tank.

I am afraid there is no single book that will cover these topics. The Introduction to Systems Biology by Uri Alon does not talk much about evolution of gene networks; it is mostly about network motifs and their dynamic behaviour. You can have a look at Barabasi's works for evolution of gene regulatory networks (This book-chapter is not really about GRN but may be useful as it talks about fitness of network nodes).

@mdperry I cited that book recently. (There is an extra 'f' and one less 'n' ;P ). It is good, though I haven't proceeded beyond fist few chapters.

I haven't read it, but this book looks interesting to me: Evolutionary Systems Biology

@falsum yes it looks like a very good fit and it is very recent. The book is expensive though but I just discovered I have access to an online version through my University. Quite convenient. Thnks

Here there are a couple that I own:
The "classic" from Uri Alon touches many of the topics you mention. It is easy to read and goes relatively deep into the methods. There seems to be a new edition (if you search it in Amazon it will pop up), but it was planned for last year's April and then delayed so no so clear when will be actually published. For the original one: Amazon link
Title: An Introduction to Systems Biology: Design Principles of Biological Circuits
Year: 2006
Author: Uri Alon
Publisher: Chapman & Hall/CRC Mathematical and Computational Biology

The other book is this textbook "Systems biology" by  Edda Klipp and others. I attended a talk by Edda Klipp two years ago and she seems to be doing interesting things. This book is more general, covering, somewhat superficially, many topics. It can be good to get a general idea on the field. Amazon link.
Title: Systems Biology Paperback
Year: 2009
Author: Edda Klipp, Wolfram Liebermeister, Christoph Wierling, Axel Kowald, Hans Lehrach, Ralf Herwig
Publisher: Wiley-Blackwell

There are many others (see Amazon results here). Maybe other members can comment on some of the other titles.

Sounds like Alon's book would be a good fit. Thnks for this great recommendation. +1 I'll wait to see if I get other opinion and then I'll probably go for Alon's book.

Sure, wait for other opinion. There are many books and not sure I got the best ones! I would also like to know about other good books.


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Isopropanol precipitation of DNA - duration and magnitude of cold storage
DNA prep protocols often include a final precipitation step with alcohol, often isopropanol, where the DNA must be kept in the alcohol, at a low temperature such as -20C or -70C, often overnight.
What is the point of keeping it at low temperature? Is lower better? At what point do you see diminishing returns?
What about the time? Is overnight really necessary, or would, say, an hour suffice? Do lower temperatures result in quicker precipitation?

For the precipitation you use different reagents: First you add salt under slightly acidic conditions to make sure that the DNA precipitates in a less polar environment. This is achieved by adding alcoholes like ethanol or isopropanol.
It is commonly thought that a incubation at low temperatures enhances the results, but this is interestingly not true. There is a paper from the Bethesda Research Laboratories which is called "Ethanol Precipitation of DNA." which analyzes these relationships (temperature, time and alcohol concentration) in great detail, its definitely worth reading.
Figure 1-3 from this paper shows the influence for Ethanol (but I am pretty sure that this is not much different for isopropanol):

I would prefer ethanol precipitation to ispropanol whenever possible. Isopropanol co-precipates salts, so you have to wash a few times with 70% ethanol and it is less volatile than ethanol, so the drying step takes longer. Its also less effective cleaning organic compounds like phenol away and sometimes the pellets are harder to see.
On the other it can be useful when you have to deal with large volumes, since you only need 0,7 volumes of isopropanol compared with 2,5 volumes of ethanol.
Precipitations with Isopropanol are usually not incubated but centrifuged directly after mixing. Here is a protocol from my lab (which originally came from Qiagen, if I remember correct):

Adjust the salt concentration, for example, with sodium acetate (0.3
   M, pH 5.2, final concentration) or ammonium acetate (2.0–2.5 M,
   final concentration).
Add 0.6–0.7 volumes of room-temperature isopropanol to the DNA
       solution and mix well.
Centrifuge the sample immediately at 10,000–15,000 x g for 15–30 min
   at 4°C
Carefully decant the supernatant without disturbing the pellet.
Wash the DNA pellet by adding 1–10 ml (depending on the size of the
preparation) of room-temperature 70% ethanol. This removes
co-precipitated salt and replaces the isopropanol with the more
volatile ethanol, making the DNA easier to redissolve.
Centrifuge at 10,000–15,000 x g for 5–15 min at 4°C
Repeat the washing and centrifugation steps once more.
Carefully decant the supernatant without disturbing the pellet.
Air-dry the pellet for 5–20 min (depending on the size of the
pellet).
Redissolve the DNA in a suitable buffer.

It seems that overnight incubation is absolutely superfluous based on Fig.2 - or am I mistaken?

Thats how I read it and how we do it. I have never had any problems with short incubation times.

Why can you conclude that overnight incubations are superfluous when they only examined conditions up to 10 minutes? The 5-minute difference between incubating for 5 or 10 minutes seems pretty minor compared to the possibility of incubation for 15+ hours. In general, I'm not so sure I can rule out that temperature might also have a better effect if the samples were left for 15 hours as opposed to 10 minutes.

Because you should be able to see a difference between 0 (simply mixing) and 10 minutes. And its also my own experience with fits with this data.

@Chris I find your experience more credible than Fig. 2. What if the amount of precipitate over time looks like a Michaelis-Menten curve (http://dwb4.unl.edu/Chem/CHEM869K/CHEM869KLinks/www.curvefit.com/1952b0e0.gif change x-axis to time and y-axis to amount of precipitate)? Then a lot would rapidly precipitate out, but a significant fraction might take a long time to come out in a short time; you wouldn't necessarily see the difference between 5 min and 10 min, but you might notice a difference after 15 hr.

I agree that for most applications, Fig. 2 shows that waiting a short time gives reasonable yields. But without seeing the data point for 15 hours, you're extrapolating, I can imagine plausible scenarios where that extrapolation could be false, and if you care about getting as much of your sample as possible, I would want to see evidence that waiting 15 hrs doesn't improve yields before I take that out of my protocol. Your experience with this seems more credible to me, although have you done the experiment where you compare yields from just mixing the sample and leaving the sample overnight?

The freezing at -70C, how long do you recommend it ?

@AnuragMishra 20-30 Minutes, longer is not necessary.

Is it okay to use Sodium Chloride, instead of Sodium Acetate ?

That depends on the pH you are working at. If it is already slightly acidic, than NaCl is usually ok. If not, use sodium acetate to make sure that the DNA gets enough protons. This reduces the solubility. One thing: If you have a lot of questions, please ask a new question with it and not as in the comments below other questions.


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Ancestral states of sex determination system
Most (maybe all?) species that reproduce sexually have either genders (anisogamy) or mating types (isogamy). There exist today many different type of sexual determination system. There is a whole complicated continuum from species where the gender is exclusively determined genetically (genetic determination system, GSD) to those where the gender is determined by the environment (environment determination system, ESD).
Knowing that genders (and mating types) evolved several independently, what seem to be the ancestral states of sex determination system? Where the first sexually reproducing lineages GSD or ESD? Does it differ between lineages?

I saw a talk a couple of years back, many esd systems are strongly g*e. So there is a threshold of the environmental factor where all become one sex or the other. Then at intermediate environmental values you can develop males and females

Yes, as argued in Evolution of Sex Determination all liability factor (factor that define the sex relative to a threshold) follows a norm of reaction and therefore the concept of GSD makes sense only by defining the range of environmental condition where which the sex is only defined by the genes. But I think my question is still of interest even to the light of a more accurate definition of GSD and ESD.

Agreed. On another note,do you have that book? I nearly bought it this week -what do you think of it (assuming you do have it?)

No, I don't have it. I very often want to buy it but I stop right before doing so when I see its price! I read part of this book during my master degree, just before it got published for a class I attended at the University of Lausanne with Nicolas Perrin (one of the two authors) and I really appreciate it. It was for me a totally new subject and the book made a good job to introduce me into it. I also thought that the book makes a good job of providing both a good theoretical understanding and a rather impressive list of study cases separately into different paragraphs.

I bought the book, they printed the pages upside down...

@GriffinEvo Oh no! You got a defective copy. You can probably asked to be reimburse.


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What indices can we use to describe fitness landscapes?
We usually talk of smooth or rugged fitness landscape.

Are there any (standard) indices to measure the "structure" of fitness landscapes?

For example, one might consider the mean epistatic interactions (over all possible combination of loci)

This paper uses 4 metrics for discreet landscapes.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240586/
Deviation from additivity: How much your genes interact (normalized). Fitness in a purely additive landscape with three genes, for example, is F=f(x)+g(y)+h(z) where f,g, and h are each functions of one variable (the x,y, and z "genes"/coordinates). Deviation measures how far from additivity the fitness is. Higher is not always rougher but it is "trickier" since the effects of changing a gene depend on other genes.
Peak fraction: The % of points that are local peaks (discreet landscapes only), higher is rougher.
Tree component: The % of points that have at most one neighbor of higher fitness. Lower is rougher and indicates that there is a choice as to which direction to travel.
% monotonic paths: The fraction of paths (of all possible shortest paths from a given point to the peak) that don't go downhill. This calculation is averaged over all starting points in the landscape (excluding the peak). Lower is rougher.


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Conservation Genetics - Book recommendations
Can you please give me some advice for a book in (evolutionary) conservation genetics that offers an in-depth review of the mathematical formulations used in this field.
I read the book Evolutionary Conservation Biology (Ferrière and Dieckmann, 2009) and I really liked it. I'm seeking for another book of the same kind that goes further on the part A (Theory of Extinction) and especially on the concern of the importance of population structure and the genetic load. I am also interested in landscape genetics.

A comprehensive book on ecology????

@caseyrs547 as the subject remains fairly broad I hoped I could find a book rather than articles. Books are often more entertaining than articles. But you might be right. I'll wait to see if anyone suggest me something.

@WYSIWYG No, I am not looking at a book on ecology. I am interested in genetics extinction (population genetics based explanation for population extinction) and about how the environment shape the genome of populations. Not a book on this extremely broad field which is ecology.

This book "A primer of conservation genetics" would suit quite well I think. In particular chapter five deals with "Genetics and Extinction" and is preceded by a lot of population genetics based theory. A beginner might also combine it with "A primer of ecological genetics" (Hartl & Conner) but you seem to have enough Pop gen knowledge to not need it!
The landscape genetics is perhaps a bit lacking from this book though. Maybe a better and more comprehensive solution, but slightly more advanced, is this book which does feature some aspects of landscape genetics in chapter 15 along with good population genetics type coverage of extinction.

If you're interested in learning about the mathematics of population genetics, Population Genetics and Microevolutionary Theory by Alan Templeton is an absolutely amazing resource.
If you check out the index, here are entries under population structure:
assortative mating, admixture, linkage disequilibrium, coarse-grained spatial heterogeneity, gene flow, gene flow and population history, gene flow vs admixture, microevolution modeling, multiple inheritance modes, natural selection, adaptation, and fitness.
Heterozygosity and other mathematical descriptors are particularly relevant to conservation (the author has been involved in various conservation projects). Furthermore, there are various entries on viability.
Plus there's plenty of information in it about the effects of landscape on gene flow and other population structural features.


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Crusty eyes in the morning
Often, after waking up from a night's sleep hard, flaky, pale yellow crystals are deposited around the eyelids (which easily wash off with water).
What are these? Why are they yellow? What are they made of? Is their amount proportional to the length of sleep?

This is quite common. It is most likely dried rheum (also know by slang terms such as "sleep", "eye boogers", "eye crusties", etc.).
Rheum is the result of dried mucus, tears (and the salt and minerals therein), as well as dead blood and skin cells.
Essentially it is all the stuff that’s normally in your eye that eventually dries up making the contents more condensed giving it a light yellow color. When all that stuff is in your tears it is spread out enough that your tears are still mostly clear.


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What is meant by 73 hour birth
I was reading an article, when I read a sentence saying, His mother ... nearly died less than three years later during Mathers' 73-hour birth.
What does mean by 73-hour birth?

This isn't really a Biology question, it just means that Mathers took 73 hours to be born.  If you need further explanation, I'd suggest trying English Language Learners http://ell.stackexchange.com/

This question appears to be off-topic because it is about use of the English Language

I could find that topic related to Eminem's mother, Debbie Mathers-Briggs, who almost died delivering her first son(Eminem) at the end of a 73-hour labor or 73-hour birth. That "73 hour birth" means she was in labor(to undergo the efforts of childbirth) for "73 hours".

yah, anyone can find that article by reading Mathers :D and yes, thanks for the answer :)


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Why are dolphins so smart?
It seems that dolphins have (among?) the highest encephalization quotients found outside of humans, higher even than chimpanzees. By the "use it or lose it" principle this indicates that intelligence must be particularly valuable in their niche. Why is that? They are predatory and social, and both of those are associated with intelligence, but why are dolphins smarter than other predatory pack animals? For example, is there something about being an air-breathing organism living in water that makes having a high EQ particularly adaptive?

I would also like to point out that they are intelligent in the way we perceive "intelligent". It would be interesting to know what help, if any, they get by having " human type - intelligency"

Aren't bacteria and viruses just as intelligent as any master criminal ? Changing their appearance so often that they do not get caught !

It's less about the brain size, I think, more about the metabolic cost of brains. Brains are among the most costly organs to keep what it comes to oxygen demand. Air-breathing increases available oxygen for the body, hence mammals have larger brains that for example fish.
In diving animals the metabolic cost of brains is connected to the diving time (can't find the reference at the moment). Sperm whales shut down parts of their brains on long dives and do not have particularly active brains in general. Dolphins are mostly shallow diving animals. Maybe the selection favors higher brain metabolism potentially increasing the ability to catch prey and avoid predators? Pure speculation, though.

It might not fully answer your question…
Cost of having a heavy brain
Generally speaking, having a heavy organ is an important cost for flying animals, a medium cost for terrestrial animals and a low cost for marine animals. Loosely speaking, the principle "use it or lose it" does not apply with the same strength in all animals in regards to brain weight. If you create a regression between "intelligence" and "need of being intelligent"(supposing it means something!) in terrestrial mammals and add the dolphin on your graph, you might be surprised that the dolphin does not fit on the regression but it might only be due to the fact that they live in water which is much more dense than air so that it is less costly to carry a big brain. So, yes there might have something to do with "living in the water".
Indexes of intelligence
EQ does not mean intelligence! It is just an index. And we have to understand that people first were happy to think that humans are very smart because they have a big brain but they were terribly confused when they've learned that sperm whales brain weight 8kg! So they tried finding other indexes. EQ is one of them and we're quite happy to use it because it places humans at the first position. But it does not mean that this index is a good representation of intelligence. Some small birds with their tiny brain were shown to be have a spatial memory that is much more efficient that the one of humans for example.
Something else. When looking at these indexes one should not forget that size (or weight) does not equals efficiency. Let's make an analogy with computers. You can have a good software or a good hardware. Big brains are not necessarily very efficient!

Now, it is still true that dolphins are good at performing many tasks that we link to the concept of intelligence. Dolphins have complex social organization that is probably link with their intelligence. I would tend to think (just a guess) that there are many social factors involved into the evolution of their cognitive abilities. Because the social structure changes as cognitive abilities evolves, it seems to me quite hard to know what factors made that clever individuals were more fit than stupid ones at every moment during the evolution of dolphins. But I might overlook the complexity of the problem. And I honestly never learned any article concerning the role or the evolution of cognitive abilities in dolphins.