text:
Why is extracellular measurement of action potentials so different from intracellular?
I had read in a paper that present a low noise amplifier the following:
"...This level of input signal is larger than both typical action potentials (<500μV) and local field potentials (<5 mV). If a larger input signal is expected, the amplifier’s supply voltage can be increased at the expense of higher power consumption.We verified that our neural amplifier works in a real recording environment by using it to record action potentials in the robust nucleus of the arcopallium (RA) of the anesthesized zebra finch. Data were taken with a carbon fiber electrode (Kation Scientific, Inc.) electrode that had an impedance of approximately 800kHz at 1 KHz. A long extracellular trace and a short extracellular trace recorded from our amplifier (normalized by its gain) are shown in Figure 2. They were found to be identical to that recorded by a commercial neural amplifier (A-M Systems, Model 1800)."
Link:

http://www.rle.mit.edu/acbs/pdfpublications/journal_papers/woradorn_tbcas_neural_amp.pdf

Please, can someone help me to understand how we can measure an action potential as shown in figure 2? We know that action potential amplitude is approximately 70mV as shown in figure 1 but figure 2 shows that is approximately 70μV.Is this possible?
Figure 1

Figure 2

I'm going to mostly duplicate my answer to another question Neural signals amplitude since it's exactly the same as this one, but it has no upvotes so I can't vote as duplicate. Once I get an upvote either place I'll vote to close the other.
In the first figure, those voltages refer to the difference between the inside and outside of the cell (i.e., -70mV means the cell is 70mV more negative than the outside).
You can't possibly measure that potential difference from outside of a cell. When you do extracellular recording, like in the second figure, you are measuring spatial differences in ion concentrations that occur due to ions flowing in and out of cells. For example, when a cell fires an action potential, lots of positive ions flow into the cell; this makes the area just around the cell slightly more negative than an area further away. The magnitude of this potential as measured depends greatly on your recording configuration, the type of signal you are recording (i.e., population activity or just a single cell; synaptic currents versus action potentials), how close your electrode is to the signal you are recording, and where your ground is (or position of both of your electrodes if you are doing a bipolar recording).
Also, in this second recording, either the voltage is reversed (i.e., the electrode near the cell is taken as ground), or it is actually measuring return currents in the dendrites of the cell; otherwise, the action potential would be in the opposite polarity (downward first, then upward) compared to inside the cell.
Although it varies, in most cases the signals you record extracellularly are on the order of microvolts to a couple of volts.
Lastly, in the quote you reference, the line before it was:

The total harmonic distortion (THD) of our amplifier stays
  below 1% for input signals smaller than 7.3 mV peak-to-peak.

That article is describing an amplifier system for recording extracellularly (potentially for a brain-machine interface). They are saying that one type of distorting noise is not a problem in their amplifier at the input voltages you would expect in an extracellular recording of spikes or local field potentials, which indeed would usually be less than 5 mV. This amplifier would not be suitable for recording intracellularly.

Thank you so much mr Bryan Krause for your response. Sorry for my comment but I would to understand one point.You refer that "That article is describing an amplifier system for recording extracellularly "and also "This amplifier would not be suitable for recording intracellularly."Can you help me to understand the difference when amplifier records intracellularly compared with extracellularly ?What changes in neural signals that record? Maybe the difference is the place of implant in brain?Is any of the recording methods better? Thank you in advance.

Read about whole-cell patch clamp (though there are a couple other methods for recording intracellularly). Intracellular recordings are necessary to measure the magnitude of inputs to individual cells. Extracellular recordings can measure outputs from single or multiple cells, and/or field potentials that approximate inputs to populations of cells. It isn't fair to say one is better than the other: they are different, for different purposes.

For long-term recordings (over weeks and months), only extracellular recordings are currently technologically feasible.

Thank you so much, Mr Bryan Krause. I search for this answer for days!


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Is an adaptation against impact of fall a factor in babies' bones' structure?
Obviously, babies' bones need to be flexible to get through the pelvic bone. But is that the only reason? Could it be that as babies aren't able to maintain stability, they need bones less prone to damage?

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text:
How does natural selection affects seasonal polyphenism in animals?
How does natural selection affects seasonal polyphenism in animals?
In this Wikipedia article there is a following statement:

Since these animals in widely separated groups have evolved
separately, the similarity of coloration is due to convergent
evolution, on the presumption that natural selection favours a
particular coloration in a particular environment.

By looking at e.g. snowshoe rabbits, how can it be that natural selection "favors" a particular coloration during winter and summer? Is not the environment causes coloration without any "benefit" for these animals? How can it be proved, that these animals change their coloration because it is useful for them?

Thanks, the article focuses on social aspects only, but I will read it anyway. I'm more interested in ecological impact on coloration, though. And yes, I'm looking for the articles providing evidence. I.e. I want to see natural selection in action.

I think that the textbook case of Peppered moths is a good example of how an environment can influence coloration and of evolution in action. It is not seasonal change but the principle is similar. https://en.wikipedia.org/wiki/Peppered_moth_evolution

[H]ow can it be that natural selection "favors" a particular coloration during winter and summer?

Camouflage for example. In regions, where it snows some animals would take advantage to have a fur colour that match the substrate in which they live and they may therefore be selected for having a white fur in winter and a non-white fur in summer.
Consider for example Lepus lepus in summer

vs in winter

How can it be proved, that these animals change their coloration because it is useful for them?

There are a whole lot of possible experimental design.
Considering seasonal coat colour in response to predation, a simple and obvious approach would be to experimentally dye the individuals and see how their survival varies depending on the colour they have been dyed.
Sometimes, you may have a sister clade that is non-plastic which it might be of interest to test against (depending on the exact question at play).

I'm more interested in ecological impact on coloration [..] I'm looking for the articles providing evidence

Cases of local adaptation (such as Hoesktra 2006 for example) or other evidence of natural selection on coat colour such as differential selection among lineages are probably way more common. But if you are specifically interested in seasonal variation then, here are a few papers I could find with a quick google scholar search showing selection on seasonal variation for fur colour.

Zimova 2013 and Zimova et al. 2016 in snowshoe hares (which is listed in the wikipedia article)
Turner 1961 in pastry larvae
Maybe Ornborg et al. 2002 on blue tits

Thank you for the quick response. I'd agree coloration is due camouflage, but it is hard for me to believe in that without evidence. Also, in summer they are more visible, but they are also visible in winter, though little more less. As to the testing method you proposed, I think it would be a good way to test natural selection in action. By the way, could this coloration happen without natural selection?

Ok, is there a specific species for which you are looking for an original paper? (I picked Lepus lepus quite randomly, I do not mean that there is evidence for this specific species).

Any of the species from that list in the Wiki article I've provided would be interesting for me.

Please see edit in my answer.

@user35970 I think the issue is not about whether you can see the animal in its summer camo in the summer, especially in pictures of that animal (presumably selected by the photographer when you can see the animal..). The issue is that if it wore its winter coat in summer, it would stand out white against a non-white background; if it wore its summer coat in winter, it would stand out against a white background. It's certainly fine to have some skepticism, but being harder to see seems like it carries a pretty obvious benefit for any species, prey or predator.

@Remi.b Thanks, this is what I was looking for. Still the information present in those articles is not convincing enough to be sure that the camouflage is due natural selection, the difference in numbers of survival rates are too small, the testing methods are not good enough. There could be also a lot more factors influencing the decreasing/increasing of animal survival probability, not just their coloration and background.

What I've realized though, is that it is very difficult to test natural selection - is it really that acquired characteristics benefits the animal or it is simply a coincidence that these characteristics promotes better survival and thus it only seems to us that it brings a significant benefit for the animal.

@BryanKrause Yes, that is logical assumption, but in initial stages of acquiring characteristics there is seems no natural selection, if it is so, then natural selection cannot be a driving and creative force of evolution (as per Darwin, Modern synthesis), it is simply that species with certain characteristics tend to survive and reproduce and these characteristics are "stabilized" in time.

@user35970 Sounds like you are being extremely opinion-based. You are selecting a specific trait (fur colour seasonal variation) and ask for evidence that it is adaptive, you read the paper and (whether or not your have much knowledge in data analysis but it does not sounds like you do reading your comments) you conclude that the paper is not good enough. There are tens of thousands of evidence out there (see for example the Hoekstra paper; I'm about to publish one more myself), it is not so hard to give an evidence that a trait is beneficial over another one.

Also, calling selection a creative force sounds like you you would take advantage of having a look at an intro course to evolutionary biology such as Understanding Evolution by UC Berkeley for example

@user35970: Differences in survival rates don't have to be large to have an effect, when they act over many thousands of generations.  A practical way to test this would be to e.g. find a closely-related species (or even the same species) that lives in an area with little or no winter snow cover, and observe whether the same color changes occur, and their timing.  Or (if you have sufficient time and funding, move color-changing species to a different location, and observe whether the change becomes less common over time.

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Dominance and recessive relationship of alleles
You can find easily in textbooks that definitions for dominant and recessive alleles as follows:
Dominant allele: produces working protein and shows its effects in hybrid state.
Recessive allele: produces defective protein and remains suppressed in hybrid state.
But I have these confusion:

Defectiveness or benefit is relative thing.
There are many genetic diseases which are caused by dominant genes, for example short toe fingers. The protein related to it is also defective.

Another definition includes dominant as wild type most circulated while recessive as mutant allele. But even this seems to be unsatisfactory as every mutation cannot be recessive or defective.
Then, finally, what determines dominance of an allele over others?

These definitions are wrong. Can you please directly quote a definition from a specific textbook(s) (so that we can boo the author if the textbook is indeed wrong). While the recessive allele is probably more often associated with the production of a non-working protein, it is definitely not how the term recessive is defined.

Yeah, these are bad definitions.  A better one would be "Two alleles are in a classic dominant/recessive relationship if the heterozygous phenotype is the same as the homozygous dominant phenotype, and different from the homozyogus recessive phenotype"

Possible duplicate of Is protein production doubled if you have homozygous dominant genes as opposed to heterozygous genes?

Phenotype determines dominance. The "rules" you state are just general possibilities that are most likely; they are not correct definitions. "dominant as wild type most circulated" is just completely totally false.
It's common to have mutations that cause loss of function. These often end up as recessive alleles, because the second copy still makes a functional protein. It's not about the allele being suppressed necessarily, and doesn't have anything to do with benefit or not, it's just that the other copy is able to do the job, so you don't see much effect. Because there are often feedback mechanisms for gene expression, having 1 less copy in the genome often means much less than a 50% reduction in protein.
It's also common to have mutations that cause negative gain-of-function: these are often dominant, because you only need one copy for that negative effect to be observed.
However, as you point out, these aren't always the case. You could have an allele where loss of a single copy causes a deleterious phenotype. Sometimes these might more appropriately be considered "incomplete dominance."
I think it's important to note that these terms are really labels based on phenotypes, they are not biological realities. An allele could be thought to be completely dominant, but under further study actually demonstrates a form of incomplete dominance or co-dominance.
The Wikipedia page on dominance has some better definitions for you.


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Has the gestation (pregnancy) period for humans always been 9 months?
At this point in our evolutionary progress, the expected human gestation period is (roughly) nine months long. My question is, has this duration of time always been the same for homo sapiens? Or, are pregnancies getting longer/shorter?

My attempts so far: upon searching online, I was only able to find a single reddit thread, of which didn't provide much of anything. And then, on Wiki's page for gestation it provides a link that should contain content on the "evolution of gestation related features for mammals", however, the link revealed itself to just be a page that outlines all mammalian evolutionary developments, and I'm not able to find the forementioned gestation specific information within it.

First off, I am not one of the close voters. 1 vote is because pob (the answer to your question is probably unknown, but that's not really a good reason to vote to close I guess), the other because of homework (it indeed shows no prior research effort - you could do a Google search first, show your findings here and then decide to still ask the question yes or no).

Yes, I think evolution didn't have much effect on the gestation period.

@Charles Unfortunately, "homework" here is defined as doing background work on your own to try and answer the question. Even if you can't, to be able to say "this is what I have found and where I found it" is important to know the scope of possible answers. See meta for much discussion of the longstanding problem with the "homework" close.

@kmm I've updated my post to address this concern. Thanks :)

If pregnancy durations are different from the recent past, it wouldn't be at all clear whether this was due to evolution or other factors. There is also so much variation in what a "normal" pregnancy duration is in modern humans that this question couldn't be answered. The references to developing "more complex bodies with time" and efficiency at offspring development suggest this question is going way beyond the scope that it initially intended to.

@BryanKrause I've edited my post to exclude this idea of becoming more or less "complex", as well as refocus my description of human gestation duration to be the (roughly) "expected" length [of time], instead of "typical", since I suppose typical references actual occurrences (of which, as you said, can significantly vary), instead of the ideal.

human gestation period
According to the link gestation period doesn't vary much between great apes.
I don't see any signs that human are becoming "more complex". In fact human babies are uniquely underdeveloped compared with other mammals (large brain size, upright posture)

The article you link to seems to suggest that the gestation period is mostly dependent upon the size of the creature. So, if humans were to drastically increase/decrease in size, then perhaps gestation periods would also change?

But for the blue whale it is only 11 months.


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Why cooking make foods , e.g rice, vegetable etc, soft?
My initial guess was it is due to absorption of water during cooking (role of heat is probably to accelerate this process). So to verify this I have left uncooked rice  in water for two days but so far it hasn't softened noticably. May be for sufficient absorption of water for softening I have to leave it longer. Or may be my initial hypothesis is wrong altogether.

It is a nice question, but it probably better suited for cooking.SE. So I am voting to close this one here.

Heat is definitely involved in speeding up the water absorption. In general, every 10 degrees C roughly doubles the reaction rate, so a reaction in 100°C water would be expected to run about 256 times faster than in 20°C water. It's not a perfect estimate, but it's probably good enough for cooking. I suspect that the exterior of your cold rice will turn mushy before the interior is soft though.

@another'Homosapien' chemistry might be even better.

Short answer Hydrolysis
Cooking shortens many molecules, particularly carbohydrates and proteins although almost anything long is affected. By heating them in a aqueous environment (many foods supply their own water) we are inducing billions of hydrolysis reactions. This chops up long polymers into shorter ones.For proteins heat also causes them to unwind which makes them easier to digest.  In effect we are outsourcing a major portion of the digestion. This is why cooking is believed to have evolved as a behavior in the first place – it greatly increases the nutrient availability of the food by putting it in a much more easily digested state. Without heat the number of hydrolysis reactions is negligible, although a few things like extreme PH or infusion of enzymes can be substituted for heat.
For most edible molecules shortening them also makes them softer (most macronutrients are polymers, after all) which is an additional benefit. This is also why there is a balance in cooking, cook too long or at too high a temprature and you start to get lots of other kinds of reactions that produce new indigestible molecules. Cook too short or too low a temp and you get few hydrolysis reactions and it essentially does nothing. Hydrolysis is one of the reasons cooking will also dry out foods, since water is being used up in hydrolysis.

The main reason to cook food is to break the cell wall. All plant cells have a cell wall, which is hard and tough. By cooking it you break the cell wall and your food will be softer and easier to digest.
For your rice example, of course the grain will need to absorb water to soften. By cooking it you break the cell wall, which is still intact in your uncooked rice in water. The cell wall here prevents the uncooked rice grain to absorb as much water as cooked grains (in which the cell wall was broken).

Then why do we cook meat?

Cooking meat is wise to do, because you kill bacteria with the heat. Also the heat will break tough filaments such as collagen, which makes it easier for us to digest.

Cooking meat also causes the proteins to unwind, making them much easier to digest meaning you end up absorbing a lot more of it, the estimates are between a 75-100% more calories for the same piece of meat.


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Why is the pressure pulse bigger after exercise?
Right after exercise, is the amplitude of the pulse smaller or bigger than resting period? And why is that ?

I would guess that pulse pressure increases after exercise. As I understand it,

Systolic pressure is simply resistance against the pressure wave of the ejected blood. Since the stroke volume is increased in exercise to deliver more blood, systolic pressure will be definitely be increased.
During diastole, the major resistance to flow is due to peripheral resistance (major arteries now assist flow by releasing stored energy), and this is reduced in exercise due to vasodilation. Although there is more flow, since the resistance is markedly reduced, diastolic pressure may drop.

Hence, pulse pressure should increase.

It'd be important to note that during exercise, there is systemic vasoconstriction but vasodilation in the vessels to the muscles. This sums up to a net vasodilation (due to the enormous bulk of musculature), resulting in a fall in net peripheral resistance and hence, the diastolic pressure.


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Abnormal Spider Behavior?
A year or so ago, a spider that may have been a recluse, wolf or hobo (or anything visually similar), crawled up onto my bed. We locked eyes for a moment, and then it charged at me.
I don't recall whether I killed it or captured and released it, but it is definitely the most aggressive spider I've ever encountered. In fact, I've never known any spider to proactively attack (large mammals such as myself).
Is this a normal or even precedented behavior (in common species of spider in the U.S.)? Is there any specific reason that a spider might behave this way?

No, spiders do not charge at people or mammals to attack them. They can sometimes bite a mammal if the mammal is pinching one of its legs.
Spiders often run towards shadows. For many spiders, their eyes are merely light censors and darkness is a familiar safe spot for them. Many people misinterpret a spider's sprint towards them as some kind of 'charge' while it is usually an attempt to run to safety and not an act of aggression.
The spider family that you speculate on could be reduced if you include geography as the Hobo spider and brown recluse do not really share much distribution region. Wolf spiders can be found throughout North America, though.

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What is this tiny jumping cocoon?
I found this little jumpy cocoon thingie clinking approximately once every 4-5 seconds inside a metal lid. It's been jumping inside there for about a day since I first found it like that. It has a tiny flat mark on one of its sides which suggests that's how it initially stuck itself to something, and then got unstuck. What is this thing?
Here's a short web vid of it: https://giant.gfycat.com/IcyHarmfulCentipede.webm
And here's a static pic:

Update:
It stopped jumping around after about 1.5 days since I found it, and we decided to carefully cut it open with a paper knife. Inside was a white grub with a tiny orange dot on one of its ends, all foldy like a bendy part of a cocktail straw. It was still at first, but we sprayed it with water and put it on a leaf. It started moving around slowly, and looked like it was soaking up water. When we checked up on it later, it had disappeared and probably crawled away somewhere. Unfortunately, I didn't take any pictures of that, so it could have been anything.

excellent video!  I look forward to learning the answer.

@Will I posted an update.

Where in the world are you?

This was found in Russia, near Moscow.


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Can methionine peptidase liberate selenomethionine?
Can methionine peptidase liberate selenomethionine from proteins? I'd be happy to know if any can that are active in humans, but am also especially curious about METAP2.

methionine peptidase is not specific enough. There are many different enzymes (from different organisms) belonging to that "family". Which one are you interested in?

I'd be happy to know if any can that are active in humans, but am also especially curious about METAP2.

Are you aware that METAP2 cleaves only N-term Met, and only followed by a subset of the standard amino acids?


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What is the biggest structure in nature for structural coloration?
I'm interested in the actual sizes behind structural coloration: I find it fascinating and I think it may have a couple very nice applications.
The problem is I couldn't find anything but vague references about the actual structures' dimensions. Like, the thickness of the walls, their diameter, the height...
I'm sorry about the tags but I couldn't find anything fitting. Is this, like the wrong stackexchange section?
Edit: For what I mean by structural coloration please refer to https://en.wikipedia.org/wiki/Structural_coloration.

Structural coloration[a] is the production of colour by microscopically structured surfaces fine enough to interfere with visible light, sometimes in combination with pigments. For example, peacock tail feathers are pigmented brown, but their microscopic structure makes them also reflect blue, turquoise, and green light, and they are often iridescent.

You should define what you mean by "structural coloration", because with just the information in the question you could be talking about house paint. .


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Estimated cost for diy biohacking
How much would it cost (more precise the better) if i wish to start a diy bio lab in my own house. Assuming that all I want is a functional set and to create maybe simple things like glowing bacteria/glowing fish/deadly virus（jk)

are you talking about just combining premade store bought genes or or do you need to be able to discover new ones.

@John probably making my own? Since I dont think i know where i can acquire new genes

you can buy them in catalogues, I have actually done the glowing bacteria combination a dozen times with high school students.

Respectfully, I don't think this post is related to biology. This question could be answered 100% without ever mentioning a single biology concept. VTC.

@charles, true but it is a question I doubt anyone but a biological scientist could answer. However it might be better placed in world building.

@John Hmm.. I think that anyone who has access to eBay or Amazon could just search "DIY biohacking kit" and find a great deal of results, though they might not have an idea of what they're looking at.

@John You're not wrong, but I think that would place it better on a chat forum than on here.

I don't understand the down votes; this question has a clear answer that seems to show the question is reasonable. It may not be "fancy biology" but this appears to be a real thing.

" ... you can get started for around $500 or less with a little improvisation and patience." -- How to Set Up Your Own DIY Bio Lab
The $500 is pretty minimal and you won't get much done with that -- they mention other equipment (like a PCR machine) -- and you'd need to be extremely handy to be able to build all the equipment by hand.  More likely you're looking at thousands or several thousands of dollars.
Several sites give guidance:

A How-To For DIYbio Lab Equipment
Genome at Home: Biohackers Build Their Own Labs

Getting reagents may not be easy; I don't know how readily companies sell to individuals.
Don't forget that some experiments may require approval by animal care committees etc, unless you want to be arrested for animal abuse.
You might look into biohacker collectives, which are shared spaces where multiple "hackers" can use common equipment.

I was certain these would all turn out to be joke links, but wow this is a thing! Are  PRC reagents for example controlled substances, or once you have a machine, can you just order them from Amazon? (err, I mean Aldrich)

PCR reagents aren't controlled (as far as I know) -- there's nothing toxic about them -- but the companies that carry them aren't used to dealing with individuals, so you might have a hard time ordering them.


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Why are spiders afraid of flies caught in their web?
I recently noticed a fly got caught in a spider web in my house. The fly was very energetic and, even though caught, continued to flap it's one wing (which I think might have been partially free) with hyper-speed.
Initially I thought it was just trying to get free from the web but then I noticed that when the tiny spider (it was smaller than the fly) approached it to, presumably, try to inject its venom the fly started to again energetically flap it's wing and it scared the spider off.
I was wondering - why did the spider got scared? I know animals do not perceive threats quite like us and even a big lioness might give way to a tiny mongoose if the mongoose threatens with a fight (I'm guessing both because unnecessary fighting expends precious energy and any wound can be bad with no hospitals around) but still as far as I know the fly can't harm the spider in any way even if it is free and much less when it is bound and while it would be smarter for the spider to just sit and patiently wait for the fly to drop out of exhaustion he is also risking it getting free, eventually.
So why are spiders scared of flies caught in their web?

from https://www.researchgate.net/figure/234696071_fig5_Figure-1-Differences-in-attack-strategies-upon-safe-and-dangerous-prey-in-orb-web

The linked article is pretty cool.  Bottom line: predators need to be careful.  If they get hurt they cant hunt and they starve.  Spiders have different strategies depending on perceived dangerousness of a prey item.  The linked article, for example, categorizes dipterans (flies) as nondangerous to spiders but orthopterans (crickets) as dangerous.  How are crickets dangerous?
For your spider I can think of 1 of 3 things.
1: Fly is dangerous to spider in a way not obvious to you.  Maybe it is poisonous, or can bite, or has sharp spines on the leg.
2:  Fly is perceived by spider as similar to dangerous prey.  I have watched spiders address wasps in their webs and the spiders are careful.   If there are flies that mimic the appearance of wasps / bees to get respect, why not one that behaves in the web like a wasp to get respect?  A cool idea and testable too.
3:  What you see is the danger.  A big fly thrashing around might be enough to damage the spider.  A spider not desperate for food might not want to risk getting hit.  Spiders are not that durable.  That makes sense to me.


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Why do soil bacteria produce nitrous oxide as a result of anhydrous ammonia fertilizer application?
The NPR article and 4 minute audio news item Can Anyone, Even Walmart, Stem The Heat-Trapping Flood Of Nitrogen On Farms? discusses unexpected contributions of greenhouse gasses from the manufacture of consumer goods. One example is bread, or agricultural products in general, and part of this is the anhydrous ammonia used in fertilizer.
Carbon dioxide seems to be a bi-product of the manufacture, but nitrous oxide a more potent greenhouse gas is produced by bacteria in the soil as a result of application of ammonia.

Manufacturing nitrogen fertilizer is energy-intensive, burning lots of fossil fuels and releasing carbon dioxide. What's just as damaging, and perhaps even more so, is what happens when it's spread on a field. Bacteria feed on it and release a super-powerful greenhouse gas called nitrous oxide.
These bacteria are naturally present in the soil, says Philip Robertson, a researcher at Michigan State University, "but once they get exposed to nitrogen fertilizer, they really light up" and pump out nitrous oxide.

Question: Is it common for most soil bacteria to make significant quantities of nitrous oxide after ammonia is added, or is there only a small subset of bacteria present in soil that might do this? Also, what is the metabolic pathway in this case? Is this a waste product from "eating" ammonia, or something more complicated/subtle?

below: Anhydrous ammonia tanks in a newly planted wheat field. Walmart has promised big cuts in emissions of greenhouse gases. To meet that goal, though, the giant retailer may have to persuade farmers to use less fertilizer. It won't be easy. TheBusman/Getty Images. From here.

This is just a step in the nitrogen cycle, called nitrification. It's performed by chemoautotrophic prokaryotes that obtain energy oxidising ammonia to NO. So, answering your questions: 1. no, only very specific species do that. 2. It is a waste product for that given species, but NO will be subsequently metabolised by other species.

@GerardoFurtado I see, but my question is about nitrous oxide N${}_2$O and not nitric oxide NO.

Thanks, but I'm a bit busy now and here at BioSE if you don't write a thesis with 5 chapters, references and acknowledgements you get some downvotes. Just wait some time and someone else will write a proper answer.

@GerardoFurtado I understand what you mean - thanks! Also I've just changed my comment above - sorry about that.

My bad, in my mind I read "nitric oxide". Mmm, if you're talking about N2O things are more complex, because it is produced both in nitrification and in denitrification: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5016788/. See this: "The emission of N2O is the result of multiple biological pathways, such as nitrification (autotrophic and heterotrophic), denitrification, dissimilatory nitrate reduction to ammonium (DNRA), nitrifer denitrification, and non-biological chemodenitrification".

@GerardoFurtado after a quick skim of the discussion and conclusion sections, I can see that this is in no way going to be an easy question to answer. Yikes! :-)

Addressing the first part of your question:

Is it common for most soil bacteria to make significant quantities of
  nitrous oxide after ammonia is added, or is there only a small subset
  of bacteria present in soil that might do this?

No, not all soil bacteria can oxidize ammonia. According to wiki:

The oxidation of ammonia into nitrite is performed by two groups of
  organisms, ammonia-oxidizing bacteria (AOB) and ammonia-oxidizing
  archaea (AOA).

The role of archaea in the soil nitrogen cycle is not well-known yet, although it could be greater than that of bacteria. On the other hand, the role and metabolism of AOB are more or less studied.
The process of ammonia-oxidizing is also called nitrification and AOB sometimes referred as nitrifying bacteria. The most known bacteria genera from this group are Methylomonas, Nitrosococcus, Nitrosomonas and Nitrosospira. I think the most studied species is Nitrosomonas europaea Winogradsky 1892.
For reference see: Arp DJ, Sayavedra-Soto LA, Hommes NG. Molecular biology and biochemistry of ammonia oxidation by Nitrosomonas europaea. Arch. Microbiol. 178 (2002) 250-5.
The second part of the question:

What is the metabolic pathway in this case?

Although, the metabolic pathways vary in different genera, let's look at ammonia metabolism in N. europea.
In the simplest case, it is a two-step process.
According to KEGG:
Step 1. The enzyme ammonia monooxygenase converts ammonia to hydroxylamine. The enzyme contains copper, iron and possibly zinc. It requires two electrons, which are derived indirectly from the quinone pool via a membrane-bound donor. The reaction is:
NH3 + a reduced acceptor + O2 = NH2OH + an acceptor + H2O

Step 2. The enzyme hydroxylamine dehydrogenase converts hydroxylamine to nitrite. This reaction requires specialized cytochrome as an acceptor of electrons. The reaction is:
NH2OH + H2O + 4 ferricytochrome c = NO2 + 4 ferrocytochrome c + 5 H+

While nitrite is the main product, the enzyme from N. europaea can produce nitric oxide as well. Therefore Step 2 can produce nitric oxide (NO). In this case, additional mechanisms of converting NO to NO2 are involved.
Further destiny of released nitrite can be different. In one process it could be oxidized by different microorganisms (bacteria, archaea) to nitrate (NO3) which could be consumed by plants or washed out to deeper horizons with water. In another case, nitrite, nitric oxide and nitrate could be involved in process of denitrification. During this process, a group of denitrifying organisms (bacteria, archaea and fungi) consume nitrogenous compounds and reduce them to nitrogen (N2), which can escape to the atmosphere. This process can occur through different metabolic pathways mainly with aid of reductases like nitric oxide reductase. One of the possible intermediate product of such pathways is a nitrous oxide (NO2). If N2O escapes from cells we can observe a resale of nitrous oxide from soil.
Let's return to your first question, and particularly to the part where you ask about significant amounts of nitrous oxide.
First of all, nitrification is a natural process and is a part of the nitrogen cycle. Some organisms fixate nitrogen and convert it to ammonia, some oxidize ammonia to nitrous compounds and some of them reduce it back to nitrogen. It occurs everywhere virtually in all terrestrial and water biocenoses. In a healthy ecosystem, the inflow of nitrogen is theoretically equal to the outflow (with temporal deposition in trophic chains). In such natural conditions, the release of nitrous oxide should be neglectable.
The situation changes significantly when we add an ammonia to soil artificially as a fertilizer. The main problem is that we break an equilibrium between nitrogen fixation, nitrification and denitrification. The second big problem is that an ammonia is toxic for most organisms, so we can alter microbiome. In such case, we can expect an excess of products of nitrification and improper denitrification with exaggerated levels of released nitrous oxide. The actual proportions vary significantly depending on both biotic and abiotic conditions, therefore it is difficult to predict real levels of nitrous oxide released without in situ examination.
P.S. sorry for possible bad writing.

Very interesting and informative answer! I will take a closer look in the morning, thank you!

Well that was quite a long morning! Nonetheless thank you very much for your answer! Just fyi I've asked a related question in Earth Science SE: How can agricultural ammonia lead to PM2.5 production in the atmosphere?

if I give you a can of anhydrous ammonia, and I drop in a match, it will blow up, yielding nitrous oxides.
it is an exothermic energy releasing reaction.
bacteria figured this out, and use this same chemical reaction, albeit with more steps, to derive their own energy, and therefore drive their own matabolism.
like the way a marshmallow (sugar) will burn, our bodies have figured out how to burn sugar without heat and yield ATP, certain bacteria do the same, but with ammonia. the nitrous oxides are then converted into nitrites by other bacteria, and finally to nitrate by yet other bacteria. And finally, some of the nitrates go into the plants, while others, get turned back into nitrogen, like when bitrate in gunpowder explodes (cool!)
this is called "nitrification" as some people in the comments have said.
google the nitrogen cycle if you havent already. it is very fascinating.

Can you be a little more specific than "bacterial have figured this out"? Are you suggesting that they have very recently evolved to do this after the application of anhydrous ammonia became common, or is there enough naturally occurring anhydrous ammonia in the environment that this pathway exists already? Can you also re-read the question (the part explicitly labeled Question:) and address it specifically? Thanks!

as soon as the ammonia hits the dirt, it stops being anhydrous. also, bacteria have always known how to do this

OK that's very helpful! Would you consider addressing the question as asked: Question: Is it common for most soil bacteria to make significant quantities of nitrous oxide after ammonia is added, or is there only a small subset of bacteria present in soil that might do this? Also, what is the metabolic pathway in this case? Is this a waste product from "eating" ammonia, or something more complicated/subtle?


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How do marine mammals stay hydrated?
This is a question that has always bothered me. A quick internet search yields "metabolic processes" as the reason for how marine mammals obtain water, but what are those processes and why don't land mammals have them? In other words, what are the specific differences between marine and non-marine mammals in how they stay hydrated?

@Charles correct me if I'm wrong, but isn't marine biology (and the word marine) referring directly to the ocean and therefore salt water?

Upon searching google, there are dozens of results that directly answer this. For example, here. However, it seems that you're asking two separate questions in your post, those being: 1) "How do marine mammals stay hydrated?" and, 2) "Why don't land mammals have those [metabolic processes] too?". I would suggest focusing on just one.

"For most whales and dolphins, however, we simply do not know how they get their water, because it is difficult to observe these animals." That is a troubling line :( The article seemed to conclude that some marine mammals have more efficient kidneys?

"... marine mammals that feed on fish consume food with a salt content similar to that of their own blood, thereby avoiding the problem entirely. Indeed, a study of California sea lions showed that, on a diet of fish, these animals can live without drinking fresh water at all. Some species of seals and sea lions apparently do drink seawater at least occasionally, as do common dolphins and sea otters, but the practice is very rare in some other species."


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How are neural pathways discovered?
I have seen the spinal cord and it's a white, soft, slippery cylinder that has a small diameter (about 25-30 milimeters). It absolutely doesn't have a macroscopocally reticular texture that would allow us to track down individual pathways. Same goes for the brain, it's also not macroscopically reticular and yet we know a lot of connections inside the brain.
So what's the technique used to discover these neural pathways and the information about in which parts of the pathway are synapses located?
Example of what we know is here under the "Major neural pathways" title.

Check this out.

There are are few ways this can be done.
One important example, is case of Phineas Cage who's accident lead to severe brain damage. This changed his behavior, which allowed scientist to connect physiology with behavior. Namely, left frontal lobe damage caused change in personality, without significant change in other important behaviors such as memory.
Same way we can look on naturally occurred brain damage via modern imaging techniques (X-ray, CT, MRI, fMRI) and connect those to behavioral abnormalities.
We can also learn about neural substrate of behavior by experimenting in the lab: by looking at effects of tissue damage. Basically, you ask "what happens if we damage this part of the brain". This way we can figure out parts of brain that regulate different parts of sleep by dissecting animal's brain stem in different regions.
Another option is to "look" at brain while it functions and detect important active regions. Here you can use any number of techniques: fMRI, EEG, direct electrode probing of brain regions, or in animals optical calcium imaging. Point is that in these experiments you ask (or make) your subjects to perform behavior X and see how and where that behavior activates neurons.

You are answering a rather different question than what the OP asked. For example how is any of this related to how we discovered the corticospinal tract, which is in the link of major pathways that the OP provided? I think the OP is looking for information on the anatomical methods used and not so much on links between anatomy and behavior.


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Shell in garden snail
I was wondering that how does shell of garden snail "grows " with growth of snail.
Small snail possess shell as its size but as it grows shell grows. How do they enlarge cavity inside shell?

The snails enlarge the shell by adding material at the lip.  The addition of material is sometimes noncontinuous and shows up as rings, sort of like tree rings.  You can see the growth rings in this photo.

I found the photo here http://ediblesouthflorida.ediblecommunities.com/things-do/snails-slugs-millipedes-oh-my
As the shell spirals outward the diameter of the added rings gets larger and larger.  It has to get larger if it is to spiral - addition of the same sized rings would make a donut-like torus.


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How is the first Triceratops born?
To clarify at first, I have very little knowledge in biology and paleontology so there might be very obvious things I overlook.
According to the evolution theory, there must be a graduate evolution process over millions of years such that the skull and the horns of the Triceratops gradually appear over time. However why there is no fossil record of such "intermediate" form between Triceratops and earlier dinosaurs? I mean there must be some intermediate dinosaurs that has a short skull that almost looks like a small mountain on the neck and very short horns. However based on my internet search I can't find any information that confirms existence of such intermediate dinosaurs.
I just want to know is there any such evidence of graduate evolution among paleontologists or the evolution of dinosaurs is still much based on speculation (without firm evidence)?

Note btw that it is a standard layman misrepresentation of evolutionary processes to think that evolution must necessarily be very slow. This is not necessarily true.

@Remi.b Are you referring to some kind of 'evolution in bursts'? I feel I heard about it, not sure where!

@HarryWeasley I started to answer your comment and realized it would deserve its own post. So, I opened a post asking your question (and directly answered it) here.

Very related: Where are the evolutionary “inbetweeners”?.

Yes, there are many early examples of ceratopsians before Triceratops. The oldest clear member of the lineage is Liaoceratops: "the oldest ceratopsian ever found ... was about the size of a large dog. It had a blunt beak and a dainty neck frill. ... Liaoceratops was a puny forebear of the feisty Triceratops. Size, horns and spectacular frills came later in ceratopsian evolution."  Here's a reconstruction:

Protoceratops is very well known, and is a pretty obvious intermediate between famous ceratopsians like Triceratops and early ones like Liaceratops:

This cladogram shows a number of steps in ceratopsian evolution (right side of the diagram):

Note the steps it describes: Starting with early forms that have a vaguely frill-like structure, we see added: Rostral bone with "horns" that are barely visible; Frill, with jugal "horns"; Enlarged frill and skull; Postorbital horns; Nasal horn.

Thank you so much. This is exactly what I am looking for.

A quick look a the sheer variety of ceratopsians is helpful. Even right at the top of the tree there is a lot of variation. https://66.media.tumblr.com/35e87e230a6c1589aef6c474d90ed9c3/tumblr_na7av0v1Gv1srcpvio1_1280.jpg

As in any 'species' of animals, Triceratops in the ceratopsian family came about through natural selection as changes that benefited some members were passed on to the next generation. Today, we can see how a species can change by just looking at all of the dog breeds that have developed in just a few hundred years through selective breeding. All domestic dogs are descended from primitive dogs over 10,000 years ago. Today, there are over 350 recognized dog breeds and probably well over 100 'new' breeds that have not gained recognized status. You can see how over hundreds of thousands of years that 'natural selection' would create variations within a species. This does not create a 'new' animal, just a variation within the species. A dog is a dog, a ceratopsian was a ceratopsian and a human is a human regardless of the differences between individuals. https://pediaa.com/difference-between-natural-selection-and-evolution/

Welcome to Biology.SE. This looks like it could become a good answer, but answers are much more likely to receive a favorable response if they include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and thus not appropriate here. An example of how to format references. In addition, it is best to focus on unanswered or poorly answered questions. ——— Please take the [tour] and consult the [help] pages for additional advice on [answer] and [ask] effectively on this site.

If you are looking to a more recent evolution of Triceratops you can follow the cladogram to the subfamily Chasmosaurinae and then to the tribe Triceratopsini. You'll find there Eotriceratops, which looks very much like a bigger Triceratops and might has been his direct ancestor, as it lived 68 MYA.
The rest of your question is more philosophical than informative and echos "the chicken and the egg" paradox, or "when exactly an animal evolves into a distinct species?"


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What is measured by electroencephalograms and local field potentials?
In the Scholarpedia article on local field potentials (2013), I read:

The current view is that EEG and LFPs are generated by synchronized
  synaptic currents arising on cortical neurons, possibly through the
  formation of dipoles (Niedermeyer and Lopes da Silva, 1998; Nunez and
  Srinivasan, 2005).

There are three things I do not understand:

What does "on neurons" mean? Why not "in" or "around neurons"?
I assume that what is measured is the electric potential in an electric field that is generated by charges (the ions). So only the changes of the measured potential are due to currents, the potential itself (at any given point in time) is only due to the distribution of charges. Is that view correct? Independent of the nature of the charges.
What exactly are the above mentioned dipoles? Of which are they formed and what is their size? (At least, the article says "possibly generated through the formation of dipoles".)

Does all this sum up to the picture that it is all and only about the ions that pass through the ligand-gated channels at a synapse and the electric field and potential generated by them, the contribution of all other charges being cancelled and filtered out?

[I give this as a sketchy answer being aware that it might be nonsense. So feel free to downvote in this case. I should have mentioned - thanks to Bryan for having remembered me - that this answer has been inspired by Buzsáki/Anastassiou/Koch's article on The origin of extracellular fields and currents and just tries to sketch the mental image this article evoked in me.]
I assume that what is actually measured by an EEG electrode is an effective dipole moment in the upper cortical layers underneath the electrode (which decays with $1/r^2$). The way this dipole moment is created by "brain currents" is the matter of this answer.
There seem to be some premises under which a measurable EEG signal (= a dipole) can be detected:

The presynaptic action potentials must arrive highly synchronized. (Additive superposition.).
The apic dendrites of the pyramidal neurons that give rise to the dipole must be vertically oriented (pointing to the skull, resp. the electrode). (Orientation of the dipole.)
The sodium potassium pumps trying to restore the rest potential are unevenly distributed, i.e. mainly located at the soma. (Breaking the symmetry.)

This is the situation for the neuron (gray) at rest:

The dipole then forms as follows in three steps:
Step 1: An presynaptic action potential releases neurotransmitters that open ligand-gated ion channels causing sodium ions to enter the neuron.

Step 2: The extra sodium ions wander quickly to the soma. This happens passively, i.e. driven by repulsion and diffusion. At the end of step 2, all ions inside the neuron are distributed approximately evenly (i.e. not giving rise to an inner dipole).

Step 3: At the soma sodium ions are pumped out of the neuron. During this step equidistribution of ions is maintained inside the neuron (still no dipole inside the neuron).

In the extracellular medium, we now have an observable dipole.
Summary: What is measured by an EEG are not directly "brain currents" but an effective dipole moment that results from three different currents on different time scales:

Ions passing the membrane of apic dendrites into the neuron. (Slow.)
A net flow of ions wandering from dendrite to soma (driven by repulsion and diffusion). (Fast.)
Ions leaving the soma, e.g. by sodium pottasium pumps. (Slow.)

I'll come and post a more researched answer; this one is mostly not nonsense, but I think you can do better if you rely on actual published work rather than conjecture. :) http://www.nature.com/nrn/journal/v13/n6/full/nrn3241.html is a good paper. Great question, though.

I read this paper, and my answer was inspired by it. I just tried to sketch my understanding, i.e. my mental picture it evoked.

Isn't it something like a miraculous accident, that the apic dendrites are arranged vertically in the topmost layers of the cortex? Otherwise we wouldn't be able to record EEGs?

And without EEGs we would know much less about the workings of our brains. Compare this to the miraculous accident of fine-tuned natural constants that guarantee a stable universe giving rise to the evolution of brains: https://en.wikipedia.org/wiki/Fine-tuned_Universe

@Bryan: I am looking forward to your answer!

1) Is on neurons because here neurons are considered as population, in this case the cortical neurons.
2) Yes this point of view is correct since the electric potential is generate by charges present outside and inside of the cell. Is the movement of this charge that could generate the electric field.
3)According to wikipedia

An electric dipole is a separation of positive and negative charges.
  The simplest example of this is a pair of electric charges of equal
  magnitude but opposite sign, separated by some (usually small) distance

In this case the cortical neurons have some zone where they are positive charges and other zone where they are negatively charged give to them the propriety to be considered as dipole.
The ability to generate a potential by neurons is due by the ions that pass through the channel that could be voltage-gate (open when a specific potential is reach) or ligand-gate (active in presence of a ligand). Depending on the concentration of a specific ions found inside and outside of neurons, this ion can exit or enter the cell if the correct channel is open.
Hope this could help you.

I guess it is not the movement of the charges that generates the electric field but a) their mere presence and distribution or b) that generates the dynamics of the field.

@HansStricker yes is the distribution of the charges that determine the electric field in this case the membrane potential. The fact that after a signal the charge will be able to enter or exit from the cell, generate the potential.

Thanks for the answer, but to be honest: it didn't really help clarifying things. (E.g. I didn't ask what a dipole is, but what it is formed of.)

Even though this image is to depict the neuronal origins of the fMRI hemodynamic response, doesn't it also depict quite well the neural origins of the EEG response:

from Scott Huettel, Neuroimaging the Aging Mind, p. 14


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Has a walrus ever been filmed catching a seal under water?
Walruses have been long thought to be grazing feeders, scooping up clams from the sea floor. However, when walruses bodies have been examined by scientists, frequently the remains of seals are found in their stomachs. This has led to the speculation that walruses hunt seals, however, apparently this behavior has not been observed because it would take place under water, if it occurred. The Wikipedia merely says that the "importance of seals in the walrus diet is under debate". Has anyone ever filmed a walrus hunting, catching and eating a seal under water?

If you can attach a camera to the head of a giant walrus, it's perhaps the best way to film it. You can send the filming suggestion to the bbc or to sir-dave's office which is well connected with nature cinamatographers. Strangely, I only found this: https://edition.cnn.com/2018/12/07/americas/seals-eels-nostril-hawaii-intl-scli/index.html


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Which organism can point us to the evolution of sight?
I'm trying to identify the basic biological mechanisms for sight.
Could you help me with identifying any organism that has the most basic ability to see objects?
Most importantly, creatures like dogs, cats, insects are able to not just see light, but are also able to identify objects and other living beings. I feel that an organism could be classified as "being able to see" if it can identify objects and movement and use its "visual sensory organ" to help it move around, locate food, identify species of animals, differentiate between living and non-living and escape predators if any.
Even if an organism can see just black and white or the most basic perception of sight, it would qualify for what I'm searching for. Is there any such known organism that has such a basic visual perception and has the way its eye+brain perceives images, been studied?
I'm not referring to the kind of "photosensitivity" that plants have. Detecting the presence and direction of light is not sufficient.

Could the downvoter please explain why this is a bad question?

Here is my explanation why someone would downvote such a question: having taught evolution for more than 20 years, I'm always annoyed by "less evolved" (or least) and "more evolved". That simply doesn't make any sense in evolution. It's a medieval concept, a scala naturae, persisting in the 21st century. That being said, this question has no answer because it's based on a wrong (or nonexistent) assumption. If that's the reasoning behind the downvote we'll probably never know.

"less evolved" does not mean anything. Instead you can ask "What was the first lineage to evolve the ability to detect electromagnetic waves?"

It doesn't make sense for an organism to be "less evolved" because every organism has been equally subjected to billions of years of evolution.

Which is the least evolved organism that can see?

The term less evolved does not mean anything. Instead one can ask

Which lineage was the first to evolve the ability to see?

And by "see" of course, I mean detect electromagnetic waves. Seeing does not imply color vision and does not imply accurate vision.
It will be hard to tell really which lineage came up with vision first. But I am sure you'll be interested to know that some cyanobacteria are able to detect electromagnetic waves (reviewed in Nilsson and Colley 2016).

Thanks Remi. You've linked to an excellent article. They conclude that "Both photoreception and vision thus have multiple origins", and "The ‘simplest’ organisms with real eyes are warnowiid dinoflagellates".

I remember from Zoology lessons (on University) that flatworms (Platyhelminthes) already can detect light. I am not sure if this is the least evolved organism though. Do you mean animal or really organism. Plants and algae are also organisms in which light is very import for them to detect.

Thanks. I do not just mean the ability to sense if light is present or not. I'm asking about the capability to see objects/beings and interpret them as objects/beings.

Alright, with your definition flatworms are not the ones you are looking for. See here about their eyes, they detect light dark only. Your question becomes a bit more difficult when added "brain" and "perception of images", because what do you consider a brain? Do molluscs have a brain? Do they perceive images? How do we know??

That's why I asked "has that visual perception and the way its eye+brain perceives images been studied?". btw, I'm not the downvoter.

I don't know why someone down votes your question, some people do this without any reason or explanation. I will try to neutralize with up vote, but don't know how long it will stronghold.

@Nav see objects/beings and interpret them as objects/beings is rather undefined. A bacteria that can sense light and react to it can be argued to being able to interpret the presence of objects.


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What kind of flying insect is this?
What kind of flying insect is this? It kinda resembles a dragonfly but it had what looked like a stinger on the end of it's tail. It was found in Franklin, Ohio.

Better provide some visuals, else it will be very difficult to identify.

The OP did add an image, however, they didn't add the reference. I suggested an edit that does reveal the image of the dragonfly.

... it kinda resembles a dragonfly ...

That's because it is a dragonfly! This is a female Tramea onusta, most commonly known as a "Red Saddlebag", which comes from the red coloration found at the lower regions of the dragonfly's hindwings.

... it had what looked like a stinger on the end of it's tail.

That's exactly correct! Female dragonflies have what look to be a stinger, however, they're used for laying eggs instead (and not as a weapon). (source, p.5)


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Why there is no blood in a bird's egg?
Egg consists of some albumin and yellow colored yolk.
But it is a living organism with red colored blood, it should contain red blood.
so why can't we find the blood in the egg (specifically bird's egg)?

Simple: You don't see it, because there is no blood in eggs.

@user60306 seriously, at least show some research effort and instead of calling the egg white 'transparent gel', use its proper term (albumen).

It is not a living organism. It is a live cell. There is a vast difference.

You do not see blood because you are looking at unfertilized eggs.  These are the chicken eggs that one gets from the supermarket.  The hens are bred to lay these even with no rooster.  No chick will ever grow from these eggs.
If you have a fertilized egg that is about to hatch and open it, you will find a chick.  Inside the chick there is blood, should you wish to check.
If you have a fertilized egg that will hatch eventually and open it, you will find signs of the developing chick.

If the egg has been laid very recently you may see only what looks like a tiny spot of blood.  Occasionally you will find this in a farm egg.  That is what will become the chick.  Depicted is a day 4 egg.


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What is the advantage of the inverted image on the retina?
Recently, I learned that the image of the world which we see actually reaches the retina inverted.
This is due to the fact that the retina lies behind the focus of our eyes.
I have two questions:

When the retina lies behind the focus and the lens in our eyes has a spherical shape, shouldn't left and right also be interchanged?
What is the advantage of this? Why does the retina lie behind the focus and not in front of it?
Or doesn’t it matter since our brain is not a real screen and it’s only a question of the correct interpretation of the electic signals?

The reason lies in the physics of lenses. There is no advantage for us.

As is said, i totally understand the reason (i.e. the physics going on). But i only read that up and down interchange and not that left and right do the same which makes for me no sense.

I am not sure what you mean with:"the retina lies behind the focus of our eyes", but normal eyes (or those corrected with glasses) have the focus point on the retina. Convex lenses project images inverted (up-side-down, and left-becomes-right). This is how lenses work, a law of nature. We as organisms can either use it and correct it in our brain or develop something better (which is in evolution not always possible). So there is not an advantage above normal projection, because normal projection is never developed in the course of evolution.

If the focus is exactly on the retina, then how should the brain know where the light originally came from. I mean if the light is not separated in space, all information is gone and you left with a bright point.

Right and left also get inverted. A spherical retina ensures that every point of the retina is at equal distance to the pupil to ensure no distortion. In healthy eyes, the focus point should be on the retina. If any of this is unclear to you, then you really should have consider your question on Physics.SE but not on Biology.SE. Our brain inverses the image received in the retina. Assuming it takes a tiny bit of energy to do so, then this inversion really does not come at an advantage. It is just a basic fact of physics, any living creature with an eye has to deal with.

I'm voting to close this question as off-topic because the question is about basic physical optics and not biology.

@b.nota According to my opinion, convex lenses do not automatically invert pictures. The law of nature says 'If the lens is biconvex or plano-convex, a collimated beam of light passing through the lens converges to a spot (a focus) behind the lens'. So all light beams intersect in the focal point and split again (now interchanged) behind the focal point. So therefore i wanted to know if it is an advantage that you have the retina behind the focal point for maybe a better focusing.

@Max W Maybe you should just take a lens (magnifying glass) and see what happens with the projection. This is indeed more a question for Physics and not Biology. I am still puzzled with your "behind focus point" theory, where did you get that "opinion"? The whole reason for wearing glasses is to get the focus on the right place, which is the retina.

@Remi.b I asked the question here in Biology.SE because i am no expert considering the human eye and what advantages it might have to have the retina behind the focal point. The phiscis are far too simple to see any advantage if condsider only a lense and its focus point. I thought something more goes on here that only biologists might know.

@Remi.b I came to that opinion simply by thinking. And it can not work if the focal point lies exactly on the retina. How do you split the information apart if every lightbeam meets in one single point?

@MaxW That isn't what in focus means. Focus is about taking all the light originating from the same point and putting it in the same place on the surface of the retina. Not putting all of the light from everywhere in the same place. The only way to do this is with inversion.  "according to your opinion" doesn't change physics.

Don't confuse the focal point of a lens with the pinhole effect of the eye. The latter inverts the image. I have seen diagrams that also confuse these concepts.

"not that left and right do the same which makes for me no sense." Double check your physics.

There may be no advantage of the inverted image on the retina. But there is an advantage with the lens that refractes the image inverted.
Our eye lens is of convex in nature. Now lets see what is the advantage of convex lens being our eye lens.

Source : http://www.ivyroses.com/HumanBody/Eye/concave-and-convex-lenses.php
The light from the object, when reaches the convex lens it gets refracted and gets "converged" and is a "real image" and also "diminished" but the problem is it makes the light inverted.
Now let us see what happens if our eye lens is a concave lens.

Source : http://www.ivyroses.com/HumanBody/Eye/concave-and-convex-lenses.php
In this case, when the light from the object from a distance reaches the lens, the lens "diverges" the light, also it "enlarges" the image, but it produces an "erect" image but the major problem is that the image is "virtual".
We know how evolution works, it selects more advantageous option generally.
Case - 1: If the lens is convex, the only problem the eye has to handle is that the image is inverted.
Case - 2: But if the lens is concave, it should converge the diverged light, it should diminish it and it should also make it real.
If we take both cases into consideration, case - 1 seems to be easily handled, that's why we have inverted image falling in the retina. There maybe no other specific advantage associated with it.

I totally understand that the lens should be convex, this is not my question. You could simply place the retina a bit in front of the focal point and the picture would not be flipped. So, does this little extra space of moving the retina away from the lens give any optical advantage?

Say me the exact point where the retina should be placed so that convex lens gives an erect image, at f or between between f and 2f or where exactly? I have been taught that you get  an inverted image where ever you place the screen. Refer - http://physics.tutorvista.com/light/convex-lens.html . Only when the object is at 0cm to 25cm, you will get an erect image but that will damage the lens.

@MaxW That's not at all how it works. Whether in front or behind the focal plane, the image will not be in focus; it will be blurry. The pictures in the answer here are showing light from one origin, one object, not light from different objects. It is flipped as soon as it goes through the lens.


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Replicator dynamics giving probabilities greater than 1?
I have a linear replicator equation and I want to simulate its dynamics to find the resting point and hopefully the Nash equilibrium.
I defined strategies' payoff as  $ \vec f = C*\vec p+ \vec b$, where $C$ is a community matrix similar to the one in Lotka volterra models, $p$ is the vector of probabilities for each strategy and b is a vector of constants. From what I understand, this is very similar to the replicator dynamics for a linear model, except that I'm adding a constant.
However, when I iterate over $\vec p_{t+1} =  \vec p_t+ \vec p_t (\vec f- \sum\vec f \vec p_t) $,   $\vec p_{t+1}$ frequently gets values greater than one or smaller than zero, which from my understanding is not suppose to happen.
An example to show the issue:
$C = \begin{pmatrix} -1 && -1.1 && 0 \\ 1 && -1.0 && -1.1 \\ 0 && 1 && 0 \end{pmatrix}; \space \vec b= \begin{pmatrix} 0.7 \\ 0 \\ 0 \end{pmatrix}; \vec p_0 = \begin{pmatrix} 0.8 \\ 0.9 \\ 0.25 \end{pmatrix} $
In this situation,  the second element of $\vec p_1 $ equals 1.448550!
What could be causing this error? Am I calculating  the replicator dynamics wrong? Does adding a constant to fitness "breaks" the replicator dynamics? Is my understanding wrong and replicator dynamics can go above 1 or below 0?

Can you please describe the meaning behind your equation because it does not really look like Lotka-Volterra equations? Lotka-Volterra equations are explained in this post.

Sorry, I mean that payoff of a strategy depends on the frequency of use of these strategies. This is represented by the matrix C. In the example, the -1 on the top left indicates that the more strategy 1 is used, the smaller is it's payoff. Likewise the more strategy 2 is used the smaller is the payoff of strategy 1 by a factor of -1.1. however irrespective of strategies distribution in the population there is a baseline payoff b for every strategy.

It is hard to tell what you are trying to compute. It is not obvious to me looking at the equation that $\arrow p$ must contain probabilities. Also, it is a bit weird that you are adding a baseline at every generation. Of course, the baseline fitness / probability (or whatever is represented of $\arrow p$) will very quickly become greater than 1.

$ \vec p$ is supposed to represent the proportion of time exercising a behavior (eg feeding). Every individual, ie every row of C and every element of in p, is supposed to have a value going from 0 to 1, representing how much of the time it spends doing said behavior. but the benefit of foraging more or less depends on how much other individuals are doing. Thus I want to know if there is any equilibrium point where all individuals stick with a certain proportion of time feeding. Hope it helps, and thanks for the time invested

If I'm to provide an answer to this, I first need to know: How did you obtain the values for the $C$ matrix? How did you come up with the definition of $f$? What purpose does the $b$ vector serve? And lastly, in your recurrence relation (definition of $p_{t+1}$), regarding the summand expression, are you multiplying the $f$ vector with the $p$ vector?  I tried looking at your mathjax but it still wasn't clear from where you didn't bracket anything. Also, at first glance, shouldn't it be $p_{t+1} = p_{t} * p_{t}(...)$? i.e., multiplication between the two terms, and not addition?

This is happening because the fitness for your first strategy can be negative. In the case of the discrete replicator dynamics, the fitness cannot be negative. Otherwise, you can leave the simplex. Note that the continuous replicator dynamics doesn't have this restriction (the fitness can be negative).


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Did the eclipse make the leaves fall?
I live in Pittsburgh PA, the eclipse on Monday August 21 was only about 80% coverage here.  It was notably darker, but less dark then an overcast day. The night of August 21, had a low temp of about 70F.  On my daily walk the following day (Aug 22) there was notable amount of fallen leaves from the trees along my daily walk (mostly maple), by this morning (Wednesday Aug 23) the leaf fall has increased such that the grounds crews are out cleaning the leaves.
Did the eclipse make the leaves fall?

I think the photo period has to change for longer than a few hours to cause leaves to drop. I would imagine cold could kill tender growth much faster.

What said by ebrohman is correct. In fact there are two factor that led to leaves falling when fall approaching: photoperiod and the circadian rhythm (24 hours) of the plant.
In the circadian rhythm is possible observe oscillation in proteins expression. Some of the proteins that regulate leaves abscission (aka falling) have an oscillations in their expression and present a pic of the expression in the late afternoon. Moreover to be active this protein need to be on "a dark" condition because the light will lead to proteins degradation.
For exemple
Imagine that in summer there is a long day condition with sunlight present from 7am until 20am (photoperiod) and that the proteins that lead to leaves abscission is expressed by the plant around 6pm (circadian rhythm). Due the presence of the sunlight the proteins will be degrade.
When the hour of sunlight decrease (with fall approaching) the proteins is day by day less degraded and this could led to the plant to prepare itself for the winter, also with the leaves abscission.
If you are interested to know more about the argument I can suggest you an interesting review write by Pin and Nilsson (2012)
Cold
Is possible that a decrease in the temperature lead to a leaves falling. However I think that temperature has to decrease significantly over more day to allow any changes in plants structure.
I hope that my answer could help, if you do not understand something let me know. I will try to explain it in a different way.


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Difference between Trophic and Tactic movements
What is the difference between Trophic (eg. Chemotrophic) and Tactic (eg. Chemotactic) movements?
In Bryophytes, Anthrezoids are attracted towards Archegonia. This is Chemotactic movement. In Spermatophytes, Pollen tube moves towards Ovule. This is due to Chemotrophic movement.
This is was taught in our school today. But to me, in both cases the male part is attracted to female part using certain chemicles. So what is the difference between them? Broadly speaking, what is the difference between Tactic and Trophic movements?

I think that you got a bit confused about terminology. In fact Chemotrophic is an organism that obtain energy by organic or inorganic molecules.
In your case I think that you want to know the difference between Chemotropism and Chemotaxis.
Chemotropism

Chemo-tropism is the growth of organisms (or parts of an organism, including individual cells) such as bacteria and plants, navigated by chemical stimulus from outside of the organism or organisms part [...]
An example of chemo-tropic movement can be seen during the growth of the pollen tube, where growth is always towards the ovules.

Chemotaxis

Chemotaxis (from chemo- + taxis) is the movement of an organism in response to a chemical stimulus.Somatic cells, bacteria, and other single-cell or multicellular organisms direct their movements according to certain chemicals in their environment. This is important for bacteria to find food (e.g., glucose) by swimming toward the highest concentration of food molecules, or to flee from poisons (e.g., phenol). In multicellular organisms, chemotaxis is critical to early development (e.g., movement of sperm towards the egg during fertilization) and subsequent phases of development (e.g., migration of neurons or lymphocytes) as well as in normal function.

Hence, to sum up (Chemo)taxis is the physical movement of a cell (or an organism) in response to a (chemical) stimulus, as done by the Antherozoids that are attracted towards Archegonia.  However (Chemo)tropism is the growth on organism toward a (chemical) signal, like done by Spermatophytes where pollen tube moves (so it growths) towards the Ovule.
Hope this explanation help you to clarify.


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Which ICs can I use to amplify electrical signals from plants?
I wanted to record variation potential and action potential generated in plants due to some stimulus. So which are the ICs that I can use for the amplifying the signals and what kind of experimental setup would be best. I was thinking of using Ag/AgCl microelectrodes with 0.1M KCl solution for measuring the electrical impulses in tomato plants.


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Non competitive inhibitors and Uncompetitive
Non competitive inhibitors affects the function of enzymes and slows the rate of reaction. Can I say the same for uncompetitive inhibitors ? Because Vmax decreases and it takes longer to form products .
However when I plot the graph both gradients needs to be the same ? So I'm a little confuse here to whether for uncompetitive inhibitors, it does affect the function of enzymes and slow down the rate of reaction .

I am not really sure to understand completely your question, but both non competitive and uncompetitive inhibitors affect the rate (Vmax) of the reaction by decrease it. In fact in both case, the enzyme (E) takes longer to transform the substrates (S) in to products (or to release it).
To better allow you understand I put below two mechanism of action for uncompetitive inhibition and non competitive inhibition.
Uncompetitive inhibition

Uncompetitive inhibition is unique in that the inhibitor binds to the enzyme-substrate complex. This could imply that the binding site for the inhibitor is accessible only after the enzyme has bound to its substrate. This reduction in the effective concentration of the E-S complex increases the enzyme's apparent affinity for the substrate through Le Chatelier's principle (Km is lowered) and decreases the maximum enzyme activity (Vmax), as it takes longer for the substrate or product to leave the active site.

Non competitive inhibition

Non-competitive inhibition models a system where the inhibitor and the substrate may both be bound to the enzyme at any given time. When both the substrate and the inhibitor are bound, the enzyme-substrate-inhibitor complex cannot form product and can only be converted back to the enzyme-substrate complex or the enzyme-inhibitor complex [...]
This type of inhibition reduces the maximum rate of a chemical reaction without changing the apparent binding affinity of the catalyst for the substrate.

Hope this could help.


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What does (-;-) after a gene mean?
I'm using Promethease to examine genome data originally downloaded from 23andMe. Some genes I notice do not show allele information (eg. (G;G), (C;G)) and instead seem to be blank (-;-) like in the screenshot I provided. Can someone please tell me what this means? Thanks in advance.

I suggest you to take the tutorial you can found from here
Before the $(-;-)$ there is the specific location of the gene in the DNA. Between the brackets you have your specific genotypes at the location marked before. So, whatever is inside the brackets is referred to a single nucleotide polymorphism (SNP) found in your gene. If there is nothing, as the case of the screenshot that you provided, is possible that they are not able to determine the SNP (so the SNP is not found and this information is missing).

Thanks for your answer. Yes, I'll look at the tutorial.

@OGLdude You are welcome, if you think that my answer is good, mark the question as answered by accepting the answer ;)


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How much variation in mutation rate in there in the human genome?
In humans, the average mutation rate is estimated to be around $2.5 \cdot 10^{-8}$ (Nachman and Crowell, 2000). Of course this mutation varies from sequence to sequence.
Can you please give some ideas of how much variation in mutation rate there is in the human genome?
There are many ways to express such variation. One could give the lowest and highest mutation rate or shows a mutation rate map over either the whole genome or a randomly chosen sequence.

Cool question. Unfortunately, I don't have a complete answer; the best I can do is summarize some literature. I'd be happy to look more if you want to discuss though. Also, sorry the answer is a little scattered and I apologize if you were already aware of all this!
One thing I will suggest though is that this is hard to do for the human genome in isolation; hence why much of the literature draws on other animals as well.
In any case, the literature on this topic is quite expansive, so I am afraid this is merely the tip of the iceberg. Hopefully it's helpful though.

Firstly, I know of two genomic mutation rate maps that might interest you (as you suggest in your question). One in Genome-wide patterns and properties of de novo mutations in humans by Francioli et al, looking at de novo mutations in humans (obviously more concerned with germline mutations), and another in Mutational heterogeneity in cancer and the search for new cancer genes by Lawrence et al, which (unsurprisingly) is concerned with somatic mutation rates and the resulting oncogenics.
A great review, although not entirely human-specific, is Variation in the mutation rate across mammalian genomes by Hodgkinson and Eyre-Walker. They note that:

Small-scale effects: G & C mutate more than A & T, CG dinucleotides are highly correlated to higher mutation in non-coding DNA, and there appear to be hyper-mutable sites (conserved across species) that are susceptible to SNPs. These effects vary across the genome as well. Indeed, certain regions of mitochondrial DNA also have highly variable mutation rates. Oddly, GC-rich islands may be less mutable (for certain mutation types), and may affect nearby nucleotides, particularly methylated ones.
Transciption sites: somatic tissue has lower mutation rates of transcribed areas than non-transcribed ones. In germ tissue, there is an interesting effect for certain types of mutations increasing as one moves away from the transcription start site, but not others.
Other mutations: indel mutations tend to co-occur with point mutations
Mutation rates are spatially correlated at multiple scales.
Chromosomes: for humans, it seems the Y chromosome is the most mutable, followed by the X, and then the autosomes. There is also a difference in the mutation rate between autosomes, but it appears this is overshadowed by the intra-autosomal mutation rates.

Not explicitly noted by the paper, but intutive and sometimes implied, is the lower mutation rate in coding and regulatory regions (e.g. enhancers, promoters,...).
Another paper is Evolution of Local Mutation Rate and Its Determinants by Terekhanova et al. They note local mutation rates in primates (obviously including humans) are highly correlated across the genome. This correlation weakens as evolutionary distance grows (e.g. humans to mice). They also look at the influence of several genomic features on local mutation rates.
Not in humans, but Evidence of non-random mutation rates suggests an evolutionary risk management strategy by Martincorena et al look at mutation rates across E. Coli genomes, finding enormous variability, particularly lower rates in highly expressed genes.
Since we have not yet seen chromatin structure pop up much, I'd like to point out the cool paper The effects of chromatin organization on variation in mutation rates in the genome by Makova and Hardison. Therein, they find that mutations of different types are affected differently by open vs closed chromatin states; roughly, closed chromatin encourages base substitutions, whereas indels occur more often in areas with open chromatin.
Finally, some of the difficulties in assessing mutation variability are explained by Eyre-Walker and Eyre-Walker, in How Much of the Variation in the Mutation Rate Along the Human Genome Can Be Explained?

Some related work
For mutation rates in germ-line cells specifically, see:

Properties and rates of germline mutations in humans by Campbell and Eichler
Determinants of Mutation Rate Variation in the Human Germline by Segurel et al
Variation in genome-wide mutation rates within and between
human families by Conrad et al

which describe some patterns in mutation variability across the genome, but are often more concerned with inter-individual factors.
Also here are two early papers using comparative genomics to look at mutation rates:

Mutation rates in mammalian genomes by Kumar and Subramanian
Deterministic Mutation Rate Variation in the
Human Genome by Smith et al

which focus on inter-species comparison, but also discuss compositional differences (e.g. GC richness).


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The source of ABA for inducing stomatal closure in the detached leaves?
As you may know, when leaves detached from the whole plant close their stomata to maintain water and prevent wilting. Could you please let me know what is the mechanism of stomatal closure in the detached leaves? if it is induced by ABA, what is the source of ABA under these conditions?
Please provide me the corresponding links for your answers as I couldn't find an appropriate answer for the question.
Thanks

I think that ABA could be one of the player involved on the stomatal closure in detached leaves. In fact originally it was think that ABA is the main player on abscisic leaf but this in correct only for a small number of plants. Moreover ABA is produce in terminal buds to slow down the plants growth and prepare it for the winter (it is also produce in response to water depravation by roots). So probably ABA could also migrate in leaves and provoke the stomata closure.
This is what wikipedia suggest by looking on Abscisic acid.

ABA was originally believed to be involved in abscission. This is now known to be the case only in a small number of plants. ABA-mediated signaling also plays an important part in plant responses to environmental stress and plant pathogens [...].
Abscisic acid owes its names to its role in the abscission of plant leaves. In preparation for winter, ABA is produced in terminal buds.This slows plant growth and directs leaf primordia to develop scales to protect the dormant buds during the cold season. ABA also inhibits the division of cells in the vascular cambium, adjusting to cold conditions in the winter by suspending primary and secondary growth.

By digging more on internet I found that abscission (the shedding hence the dropping of the plant leaves) occurs after the senescence of the leaf. In fact, before the leaf falling, the plant draws resources out of leaves and degraded the chlorophyll. This will cause also the change of colour (the leaves are green thanks to the presence of chlorophylls).
Finally I think that the stomata closure is also due by the darkness and the senescence. In fact the open or close state of stomata is mediate by guard cell and their state (swollen guard cell stomata is open, shrunken guard cell stomata is closed. Those state are influenced by Temperature, Darkness, Photoperiod, pH and also ABA. Hence when the plant start to take out nutriments from leaves, on leaves there will be a rise on pH and a diminution on water contents that will provoke the closure of stomata. Those two image could maybe help 3.

Hope my answer will help.


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Where does the extra blood in arterial circulation when exercising come from?
When exercising more blood is in our arterial circulation.
Where did this blood come from and how did it get there ?

http://health.howstuffworks.com/wellness/diet-fitness/exercise/sports-physiology8.htm

Please do some googling before asking here.

Contraction of muscles presses on the veins and increases venous pressure, which increases blood return to the heart and therefore increases cardiac output via the Frank-Starling mechanism.
Importantly, the total volume of blood in the body does not change by this mechanism, though the amount in the arteries can increase because there is less blood in the veins.
That part of the story is just a minor contributor, though. The more substantial circulatory adaptations to exercise involve the flow rate to muscles. More blood gets to the muscles because heart rate increases, vessels in the active muscles dilate, and vessels in the gut constrict. None of these mechanisms change the amount of blood in circulation, they only change the flow rate in the muscles.

The splanchnic circulation serves as a reservoir for blood.  The splanchnic circulation consists of visceral and digestive organs.  Blood can be mobilized from these organs out to the muscles in time of need.
from http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1943356

I think of this as blood's regular job, helping move nutrients around, dropping them off in the liver.  Peacetime work.  When it is time to mobilize, blood moves out of these organs and into the periphery where the muscles can get it.
same source

The Splanchnic Blood Reservoir Normovolemic healthy male adults have a
  blood volume of approximately 70 ml/kg body weight. Splanchnic organs
  constitute 10% of the body weight, but they contain 25% of the total
  blood volume. 1,6 Nearly two thirds of the splanchnic blood (i.e.  , >
  800 ml) can be autotransfused into the systemic circulation within
  seconds (table 2). The liver and intestines each provide between 300
  and 400 ml of the blood; the spleen only contributes approximately 100
  ml, but the hematocrit of this blood often approaches 75%. Therefore,
  the splanchnic vasculature serves as an important blood reservoir for
  the circulatory system.

Other animals can mobilize more from their splanchnic beds.  Humans do mobilize blood from the spleen but dogs have contractile spleens that can actually squeeze blood out into the circulation when the muscles need it.

I sure don't understand the down vote.  Isn't this a good answer for the bio stack?

Not the down voter. Asking for reasons for down votes is unlikely to get you any answers for two reasons: 1) people are reluctant to give explanations for them and 2) even worse, when someone (like me) comes along and explains why it might have happened, they get blamed for the down vote and nasty comments ensue. Two reasons are enough, but there are more.


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How does selection affect allele frequency?
Question
People who are carriers for Blooms Syndrome have developed a selective
advantage. How would this affect the allele frequency of the disease allele?
My thoughts
Natural selection will occur, only the carrier is selected and the affected will be selected against, leading to an imbalance of the Hardy-Weinburg equilibrium.

At Biology.stackexchange we expect that people show some effort to find an answer by themselves, otherwise questions are considered off-topic and will be closed. The same happens to homework/assigment questions with no effort to solve them. So, what have you found out?

i found a few different things. Natural selection will occur, only the carrier is selected and the affected will be selected against. Leading to an imbalance of the hardy-weinburg equilibrium. - sorry, it is my first time asking qns and even coming to this page so i dont really know the 'rules' of this website.

Welcome to Biology.SE! I edited your post (title, tag and I added your comment onto it), to make it on-topic. Feel free to roll back if you don't like the edit.

This is slightly tangential, but I question one of the premises for your question ("People who are carriers for Blooms Syndrome have developed a selective advantage"). On Wikipedia https://en.wikipedia.org/wiki/Bloom_syndrome and briefly on Pubmed, I don't see any such evidence. Or was this meant to be a hypothetical for the purpose of understanding population genetics?

Question

People who are carriers for Blooms Syndrome have developed a selective advantage. How would this affect the allele frequency of the disease allele?

Your answer

Natural selection will occur [..]

This is correct. Anytime you have a fitness differential among different genotypes, selection will affect allele frequencies.

[..] [l]eading to an imbalance of the hardy-weinburg equilibrium.

Hard-Weinberg equilibrium describes the relationships between allele frequencies and genotype frequencies. Selection can sure affect this relationship at some stage of life but it will not affect this relationship just after fecundation.
In any case, the question does not seem to expect you to talk about that. The question is asking about allele frequency only.
If you want to understand Hardy-Weinberg, you should definitely have a look at Solving Hardy Weinberg problems.
What I would answer
Not assuming any extra knowledge, the only simple, logic answer is to say that the frequency of the allele coding for the Blooms Syndrome will likely increase in frequency in the population, eventually reaching fixation. This increase in allele frequency would yield to an increase in the frequency of carriers of Blooms Syndrome.
Of course, if there is heterozygote advantage (aka. overdominance for fitness), then in an infinite population, the allele should never fully reach fixation.
If we were to know more about the genetics of the Blooms Syndrom or the specific selection advantage (and eventually many other things one may want to consider) one could formulate a more quantitative answer.

Won't reach fixation if homozygote Bloom syndrome genotype is deleterious (as seems to be true) and only carriers have a fitness advantage (cf. sickle-cell allele)

Is there heterozygote advantage (a.k.a overdominance for fitness) in the locus causing variation for Blooms syndrom? I edited the answer adding a "if there is overdominance" type of paragraph. Thanks

Original question might need to be closed with "unclear what you're asking". If OP is referring to Bloom syndrome https://en.wikipedia.org/wiki/Bloom_syndrome , it seems pretty clear that being homozygous for the variant allele is deleterious. Thus I was guessing that the question was a hypothetical "suppose there was overdominance at this locus, what would happen"?


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Distribution of sodium–potassium pumps
How are sodium–potassium pumps distributed over the membrane of a neuron? Where are the most, where are the fewest? Or does this dependent on the type of neuron?
Are there known and understandable correlations between the local densities of  sodium–potassium pumps and other membrane molecules (like ligand-gated or voltage-gated ion channels)?