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Why have plants evolved to photosynthesize glucose instead of another molecular compound?
I think this question can be broken down into two sub-questions:

Why do plants produce $C_6H_{12}O_6$ as opposed to another molecule following the formula of $C_nH_{2n}O_n$? Why not $C_8H_{16}O_8$, $C_4H_{8}O_4$, or any other of the many possible variations? Does it likely have something to do with stability or some other property that glucose has that many other variations on the formula do not?
Why have they evolved to produce a molecule following the formula $C_nH_{2n}O_n$ at all? In short...why carbohydrates as opposed to another family of compounds?

My assumption is these are questions that have been researched extensively in biology and evolutionary biology and have at least tentative answers.
I'm looking for either your best hypothesis or a currently popular hypothesis within the relevant scientific disciplines. I understand there is likely no "definitive" answer, but probably at best pretty good hypotheses.

Evolution had already worked out how to break down glucose for energy...why reinvent the wheel?

I hope you get an interesting answer, but be aware that while "why" questions are easy to ask they are very difficult if not impossible to answer. Maybe there were multiple metabolisms and the glucose based one was better. Maybe glucose based metabolism happened to occur first and now we are stuck with it because it is too central to change.  Assume you came up with a reasonable hypothesis — how would you test it?

@tyersome Perhaps you couldn't test it. I've amended the post to ask for "your best hypothesis or a currently popular hypothesis within the relevant scientific disciplines." I understand there is no "definitive" answer to this and I hope this addition to my question makes that clear.

This is a brief answer (for me) to point out that:
Your question is not really concerned with photosynthesis but is actually about the choice of the carbon constituents of living cells.
First you talk about photosynthesis as if it is a single process, however it is two separable processes:

The Light Reactions convert solar energy into chemical energy (in the form of ATP and NAD(P)H).
The Dark Reactions use the chemical energy to reduce carbon dioxide and elaborate it to more complex molecules.

Photosynthesis is so elaborate chemically that it clearly was not the first process by which living organisms managed to convert environmental energy into a usable form. So the question becomes:

Q. Why is chemical energy trapped by living organisms used to make
  compounds such as glucose 6-P?

and giving what may at first sight seem to be a frivolous answer

A. Because glucose 6-P and its precursors and metabolites were suitable molecules for building the structural components of cells, that had arisen early in evolution.

So the question becomes:

Q. Why did the structural components, energy storage, genetic information
  etc. of cells evolve to employ the particular molecules that we find
  today, most of which can be formed from glucose metabolites?

And that is a very broad question about a very speculative area of chemical evolution, which cannot be summarized here.
In general one would imagine that the answer is related to the carbon components available in the environment and the possibilities of chemical transformations. However the trap is that one ends up arguing that things are the way they are because that was best. Which is all very well until one discovers dirty little secrets such as the fact that archaea evolved different chemical constituents for their cell membranes.
Footnote
My first degree was in chemistry. Since becoming a biochemist/molecular biologist I have almost never talked in terms of overall chemical formulae of molecules in the manner of the question. It has seldom been a useful way to approach biochemical reactions or intermediates. What has been more important is to look at their structures and ask how they lend themselves to their functions or interconversions.


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Why is the GULO pseudo gene expressed in humans?
The GULO pseudo gene is being expressed in humans according to Genecards.
Why is this still taking place after tens of millions of years since then gene lost the capacity to encode for a functional enzyme?

I suggest thinking about this from a different direction — something like: "What selection pressure is there for loss of expression of the GULO pseudogene?"
When thinking about that question note that the expression level is very low (less than 1 transcript in a million in the tissue with the highest level of expression.
In general, evolution is messy and I think your null hypothesis should be that this as a vestigial trait.
In other words, unless you can show that there is a significant cost for the low level of expression seen from this pseudogene there is nothing to explain.

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In the context of heterotrophic theory of abiogenesis, what is an organism that eats other organisms called?
In the heterotrophic theory for the origin of life, we imagine a primordial soup that is rich in organic compounds and the first organisms emerge eating those compounds. Since these organic compounds are external to this early organism, this early organism is a heterotroph. But it is not like any current heterotroph since it doesn't eat other organisms or their byproducts. Is there a special name for this 'type-0' heterotroph?
At some point, some organisms emerge that eat other organisms (i.e. eat those 'type-0' heterotrophs that are already around). These new organisms are more like the standard heterotrophs of today. Is there a special name for this 'type-1' heterotroph?
I am looking for the terminology that distinguishes the heterotroph that eats only organic compounds that are non-organisms in the primordial soup ('type-0')  versus the heterotroph that eats other organisms ('type-1').
Normally, I could call the 'type-0' a primary heterotroph and the 'type-1' a secondary heterotroph. But we usually think of primary heterotrophs as things that eat autotrophs and at the start of the heterotropic theory, there are no autotrophs to eat. The primordial soup of the environment itself is the 'producer'.
If there is no standard name, would it be strange to call the 'type-0' heterotrophs as 'nullary heterotrophs' and the organisms that eat other organisms as 'non-nullary heterotrophs'?

@Artem, it's been a while! Good to see you back on Biology.SE.
I doubt that any rigorous terminology exist to describe these "type-0 heterotrophs" living on "non-organismic" organic compounds.
You might be assuming that early organic matters can naturally be categorized as being fundamentally alive vs fundamentally non-living. It is more a question of philosophy of the definition of life than anything else but, to my experience, most authors who wrote about the definition of life tend to consider early life as a spectrum from "definitely not living" to "definitely a living thing". The existence of this spectrum questions the need for the terminology you are looking for.

Actually it can, but most authors just wants to grant a safe passage for themselves just in case some later experimental evidence shows their hypothesis as being wrong by assuming there is no such thing as a clear distinction between life and non-life. The fact is that such a distinction CAN, in reality, be made if you have a sufficiently advanced understanding of what Life is vs. what it's not, but since we don't have enough evidence for it people just like to assume such a distinction is impossible in both principle and reality.

I just wish to add that the core of the problem is the fact we don't have a complete theory addressing the Life/non-Life border cases and this is why we don't have either proper terminology to address the distinction between a living and non-living entities, nor do we know is the distinction between living and non-living matter a spectrum or clear cut point. The reason too many researchers like to, as I said before, assume it's a spectrum is because that's the risk-aversion scenario for many of them and in such way they can save face if their hypothesis turn out to be incorrect.

If you are a researcher in the field and you know there is a high chance of being incorrect you would prefer to use blurry terms and "a spectrum" vs a clear-cut line because you put less of your reputation in stake if proven wrong, won't you? But that's secondary, to an extent-anthropomorphic feature which doesn't equate with physical reality. And that reality is that the chances of Life being clearly defined and of being a spectrum of characteristics are just about equal. However, that's too much for most people to stick their necks out and claim they can pinpoint it, that's why you will

find most people talking about spectra instead of a number of clearly definable traits to distinguish a living organism from non-living entities. And that's something you will very rarely find mentioned in the papers themselves, this is why I felt like I needed to elucidate the point in the comment section. So you may now appearances can be deceiving and there is the possibility people would just prefer to talk this way in order not to make claims they can't prove, even if said claims can turn out to be reality.

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Jungle blindness?
Can people who live in green scenic areas like a jungle be more exposed to green light causing them to not be able to perceive green light as well as someone who may live in a desert void of color? Similar to snow blindness can strong color also blind a person to a spectrum of light but over a longer period of time?

Photokeratitis (snow blindness) is essentially a sunburn of the eye — it is caused by UV damage to the cornea.
Green wavelengths (no matter how vivid they might seem) don't have the same energy as UV wavelengths and are thus cannot cause the same kind of damage. (Which is not to say that you couldn't be blinded by a green laser, but that isn't a "natural" phenomenon.)
In addition, the amount of UV reflected from plants is typically very low:

Generally, 85–95% of the UV-B radiation is absorbed by the leaf1.

This suggests that any sort of jungle blindness one might experience is highly unlikely to be related to what happens in photokeratitis — especially since any given photon will likely have been transmitted through and/or reflected by one or more leaves in any dense plant community.
I can't rule out some sort of psychological effect, but I have seen no evidence of that either in the literature or anecdotally.
Reference:
1: Suchar, V. A., & Robberecht, R. (2015). Integration and scaling of UV‐B radiation effects on plants: from DNA to leaf. Ecology and evolution, 5(13), 2544-2555.


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Finger Millet ( a.k.a Ragi millet ) for house sparrow
I have a sparrow feeder at home, and im wondering whether Finger Millets are good for the little sparrow's tummy .. ? Looking for advice , thanks !

I'm no expert, but several things come immediately to mind.   First, as you know, small birds like to eat millet, which must seem like fast-food to them.   However, sparrows are ordinarily urban creatures these days, and while they might have forgotten how nice millet is to eat, they'll probably enjoy it too, in sensible quantities.   You might even want to experiment with various seeds to determine just how much; bearing in mind that just because a creature loves a particular food does not mean that it is not also harmful to them.   (Consider the case of sunflower seeds and cancer in white cockatoos; and pizzas in humans).
It's hard to imagine a creature as tough and versatile as a sparrow having any difficulty with such food though.  Don't worry.


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Species specific White Blood Cells (WBC) composition
In our ongoing immunology undergrad course I learnt that neutrophil primarily fights off bacterial infection and lymphocyte is produced in response to viral infection. I also learnt that neutrophil count in humans is about 70 % in human WBCs while in horse lymphocytes account for 68% of WBC. It is supposed to make humans more immune to bacterial infection and similarly horses better adapted to fight off viral infections. However I cannot find out any relevant material as to what could be the reason that such biased WBC cell component composition has evolved in different species. Please help me find out relevant material on this.

World Boxing Council? Please do not use abbreviations in titles and define them the first time you use them.

Sorry about that.


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Chirality of anti-bodies
Do anti-bodies in the blood stream present chirality?
I am interested in this question from a mathematical and physical point of view. A person allowed to travel through a fourth spatial dimension is able to come back in this world as her mirror image. The heart will be on the right side now etc.
If the anti-bodies are chiral dependent they won't recognize the old viruses, so the person will die soon.

If you have a question about the chirality of proteins please do some research before asking here, as all posters are expected to do. If you are still unclear after your research, explain why, but please do not dilute it with fictional anecdotes about people returning from a fourth dimension. It is not necessary.

@dimachaerus - please discontinue the harassment of other users. Thanks.

@user1136 - answers in comments are not encouraged. Comments are reserved for inquiries to OP in terms of clarification of the post. If you think you know an answer, either write up as a full-blown answer (including sources), or refrain from commenting at all. Given your interesting comments, I suggest turning i into an answers. Just add some sources and expand on the key issues. I've deleted the comment. If you need the comment for further processing, and you can't retrieve it, just ping me here. Thanks.

"so the person will die soon" except, perhaps, that the pathogens can't act on the reverse-chirality of the person.  On the other hand, the person will probably not find any nutrients that they can digest, as sugars, proteins, etc are chiral, and so will starve.

Antibodies are proteins and proteins are made up of L-amino acids, which have at least 1 chiral centre. Therefore proteins contain chiral centres. So yes antibodies have chirality.

@dimachaerus If the part of the virus/bacteria that the antibody recognizes is not chiral then it doesn't matter. However most likely it will be chiral then yes it probably wont be recognized anymore.

Welcome to the site. Could you add resources to your answer, and expand a little bit on the key issues? One-liners aren't encouraged. +1 for the answer though, it seems to make a lot of sense.


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Why are human feces riskier than urine with regard to spreading diseases?
I came across a Wikipedia article titled "Urine diversion". It explains different ways, including using special diversionary toilets, and treating the collection of human feces and urine separately as opposed to just flushing everything down the toilet, maybe something most people in well developed countries are used to. These sentences caught my attention:

Separate treatment of the two types of waste is justified since urine is nearly sterile and low in pathogens, provided an individual is healthy.[3] This means that urine can be readily utilized as a fertilizer or discharged with less risk to community.[4]
Human feces, on the other hand are high in pathogens, including up to 120 viruses and need to be treated well before it can be safely used in agriculture.
Urine diversion - principle (Wikipedia article)

So urine is nearly sterile and low in pathogens, however it qualifies that statement with the condition that the person producing that urine is healthy. I assume when they compare this to feces they do so with all other things being equal (ie., provided an individual is healthy).
It claims that there may be up to 120 viruses in feces, as opposed to urine which it characterizes as being relatively low risk. I assume that feces are riskier in transmission of diseases because it naturally contains more pathogens, but it doesn't explain what these viruses or pathogens are. I was wondering if someone could elaborate on the risks of feces over urine, and also, notwithstanding that it says that urine is relatively low-risk, what health issues can be caused by reusing urine.

I like your question, but it seems a bit unfocused — I've made a suggested edit to the title that I hope better reflects the core of what you were asking.  If you approve of that change, I suggest editing the body to focus on that particular question.  I would then separate out the other question (about risks) into a new question.

@tyersome Thanks for the suggested edit. I edited the title and made the question about 50 words shorter. Hopefully it's more focused and clearer. Feel free to make any improvements/edits.

You're welcome — that is much better!

Many gut microbes are pathobionts or opportunistic pathogens — these organisms can be part of the normal gut flora (microbiome) of healthy individuals, but under the right (for them) circumstances (e.g.s: when introduced into the bloodstream by a cut, or due to immunosuppression) they can cause disease.1,2
As for urine, there are many fewer microbes present (>400 species and 109 to 1011 bacteria/g of contents in the large intestine vs. <100 species and on the order of 105 bacteria per mL of urine).3-5  Note, however, it is still far from sterile!5-7
You might also find the following of interest:
https://www.who.int/water_sanitation_health/dwq/iwachap5.pdf

References:
1: Hornef, M. (2015). Pathogens, commensal symbionts, and pathobionts: discovery and functional effects on the host. ILAR journal, 56(2), 159-162.

2: Price, L. B., Hungate, B. A., Koch, B. J., Davis, G. S., & Liu, C. M. (2017). Colonizing opportunistic pathogens (COPs): the beasts in all of us. PLoS pathogens, 13(8), e1006369.

3: Davis, C. P. (1996). Normal flora. In Medical Microbiology. 4th edition. University of Texas Medical Branch at Galveston.

4: Barnett, B. J., & Stephens, D. S. (1997). Urinary tract infection: an overview. The American journal of the medical sciences, 314(4), 245-249.

5: Lewis, D. A., Brown, R., Williams, J., White, P., Jacobson, S. K., Marchesi, J., & Drake, M. J. (2013). The human urinary microbiome; bacterial DNA in voided urine of asymptomatic adults. Frontiers in cellular and infection microbiology, 3, 41.

6: Hilt, E. E., McKinley, K., Pearce, M. M., Rosenfeld, A. B., Zilliox, M. J., Mueller, E. R., ... & Schreckenberger, P. C. (2014). Urine is not sterile: use of enhanced urine culture techniques to detect resident bacterial flora in the adult female bladder. Journal of clinical microbiology, 52(3), 871-876.

7: Whiteside, S. A., Razvi, H., Dave, S., Reid, G., & Burton, J. P. (2015). The microbiome of the urinary tract—a role beyond infection. Nature Reviews Urology, 12(2), 81.

It's not sterile, but it has far fewer microorganisms than nearly any other bodily fluid.

Urine is contaminated with skin bacteria and possibly something excreted from your blood. A very tiny fraction of urine is microbial.
Feces is basically a solid mass of undigested food, gut bacteria, and their byproducts. Many gut bacteria in particular have evolved in the conditions the human body produces so many can survive well in human tissue. about 30% of the solid weight of feces is bacteria or bacterial byproducts.
All things being equal, feces contains orders of magnitude more bacteria than urine by unit mass.

The kidney is essentially a filter which extracts dissolved waste products & water from the blood.  It basically allows only molecular-sized things to pass, otherwise it would continually leak blood cells.
The digestive tract OTOH is basically a tube.  Stuff gets mashed up at one end and ejected at the other.  Even fairly large objects can pass through unaltered.  So any bacteria that enter the tract can (if they can survive stomach acids &c) pass through the tract.  Moreover, many find the intestines a warm & comfortable place to live and reproduce.  Once the population has grown, some of it will be ejected with each bowel movement.  While most of the bacteria are harmless or even beneficial (see "gut microbiome" for more info), some, like some varieties of E. coli or the cholera bacterium, can cause serious illness.

Thanks, this addresses my query about the difference between feces and urine. I was just wondering, since you said that E. Coli or the cholera bacterium can be found in stool, does this mean that the person who passed the stool is infected with these bacteria? If that's the case, are we still talking about a "healthy individual"?

I can only speak to what I am familiar with, but I would assume that the large majority of those viruses are bacteriophages. These bacteriophages, or "phages" for short, are viruses that infect bacteria. I should mention that these phages are not human pathogens though. When we go out into the field to discover novel phages, we often go to wastewater treatment facilities to get a sample of raw sewage. These samples contain billions of phages, and after some treatment, you can use the sample and a stock culture of bacteria to propagate that phage. The pathogens are also most likely opportunistic pathogens, like staphylococcus epidermidis. These are bacteria that are a component of the normal human microbiome but may become pathogens in the right circumstances. You could also find clostridium bacteria in human feces and salmonella among many others. Also, if you are infected with an infectious agent, bodily fluids and stool will be a easy place to find them.


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What is this hairy, striped orange-black caterpillar?
There are so many these hairy, striped orange-black caterpillars in my backyard.

What are these caterpillars? Are these dangerous?

Welcome to Biology.SE! For identification questions please: 1) upload an appropriately sized image (free tools for image resizing exist — e.g. https://picresize.com/), 2) include the location (e.g. country and region — the more specific the better), and 3) include habitat information (e.g. type of plant community and species the caterpillar was found on). ——— The location and habitat can be essential clues for identification and links are discouraged since 1) if they can break they render this post and any answers worthless, and 2) they can be used to link to malicious websites.  Thanks!

Resembles Lophocampa maculata but with orange and black striping reversed (and similar in pattern to Platyprepia virginalis but without the abundant white setae). Also, L. maculata appears to be confined to more northern regions of North America* based on the range information I've seen.  I've seen images of your exact specimen from Costa Rica here.

It's a woolly bear caterpillar which will later grow to become Isabella tiger moth.

Are you sure, it's the same? The color scheme is reversed in the picture..

OP's specimen is possibly Erebidae like the woolly bear, but the woolly bear (Pyrrharctia isabella) doesn't live as far south as I assume the OP's image was taken. Also, as the previous comment pointed out, just look at the color difference between your guess and the OP's picture to realize it is likely incorrect. Please be more careful when answering [tag:species-identification] questions on this site. Also, your answers should provide greater detail and reputable sources to support your claim. See our [help] for advice for writing good answers. Thanks!


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Changes of permeability and driving force during voltage clamp
An action potential can be understood in terms of voltage changes, and these are fundamentally a function of relative permeability changes, mostly for Sodium and Potassium ions. If for instance the relative permeability of a cell strongly changes in favor of Sodium, the membrane potential approaches the equilibrium potential of this ion, leading to the depolarization of the membrane.
I understand that voltage clamp methods allow us to assess these permeability changes by "clamping" the membrane potential, and equivalently keeping the driving force constant:
$I = g * (V_m - E_{eq})$
with $V_m - E_{eq}$ being the driving force.
Related to that, I have two questions:
(1) Say we are approaching the Na+ equilibrium during an action potential peak, being closer to the Na+-equilibrium means a smaller driving force, hence the ion flux is an interaction driving force x permeability. Hence why the strong emphasis on permeability if the driving force is as relevant?
(2) When we clamp the voltage, say below the Na+ equilibrium at -20mV, we will have a constant influx of Na+. While I understand that this influx consists of only few ions entering the cell, doesn't clamping over a longer period of time change the concentration because the pumps can not keep up with the constant influx of cations, adding up over time?

Relative ion permeabilities determine the equilibrium for a given configuration of ion channels. You can easily understand what is about to happen to the voltage of a cell if you know the permeabilities: if the equilibrium voltage is more positive than the present voltage, then the voltage will increase over time. The rate at which it increases depends on the membrane time constant, which depends on the capacitance of the cell (which is based mostly on membrane area, and stays relatively constant) and the resistance; the resistance is, again, based on permeability.
So permeabilities tell you A) Where you are going, and B) How fast you are going there. This is all relevant if you are living in "voltage land": you can actually ignore currents completely and just think in terms of voltage. This is the situation in 'current clamp' recording and for the most part I would say is the easier way to understand the 'big picture' for a neuron.
If, however, you want to think about currents themselves, then you typically clamp the voltage. Clamping the voltage also keeps the driving force constant (at least over the time scales on which voltage-clamp experiments make sense). In that case, you are right, you can't ignore driving force, however, in that case you are usually setting the driving force (by setting the voltage), and measuring the current. "Driving force" is then only necessary to figure out the permeability.
If you voltage clamp a cell at a depolarized potential for a long time (minutes), eventually yes the ion concentrations will change. Voltage-gated sodium channels tend to inactivate pretty quickly, so you actually won't get much sodium current when you voltage clamp at -20 mV for a long time, at least not in the soma, but you might get more current out in the distal processes that are not clamped well and other ions like calcium. Cells do not hold up well under long-term voltage clamp, however. I believe the main culprit is calcium toxicity, though it might vary by cell type and other particulars of the recording configuration. You can also kill a cell by just disrupting the membrane and making it more leaky: the concentrations change faster than the pumps can keep up with and you get excitotoxic cell death.
I usually recommend Purves' Neuroscience as a basic textbook, and the Methods in Enzymology volume on Ion Channels edited by Rudy and Iverson for patch clamp techniques and related practical wisdom.

Right, that makes sense. So when we do not clamp, driving force is relevant for explaining currents - do I understand that correctly?

@Pugl What do you mean by "when we do not clamp"?

During the action potential, that was what the original post was referring to (I understand that driving force is constant during voltage clamp).

@Pugl It kind of matters what exactly you are trying to look at. If you are recording in current clamp mode with 0 current, then you are just measuring voltage. You don't have enough information because you don't know the instantaneous resistance. But if you were creating a simulation of an action potential, and you are setting the conductances, then yes you could use the driving force to calculate the current in the equation you mentioned.


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How accurate are Illumina microarray chips for genotyping?
What is the error rate for these machines in genotyping (like for 23&me)? What is the chance of a false positive or false negative?

23andme uses DNA microarrays ("chips") to perform genotyping. These methods only assay a set of previously known single nucleotide variants, so the probability of missing some specific variant (false negative) is high if that variant is not specifically assayed. It is not quite 100% as frequently known variants missing from the chip are closely associated with a variant that is on the chip, so you can sometimes impute missing data.
Sequencing-based methods will in theory pick up unanticipated variants, but they have their own foibles.
Generally both methods are quite good at single nucleotide variants (SNVs) but are bad to only ok at other kinds of variants. See for example (this paper (chosen somewhat at random, there are many similar papers) to see what the state of the art is for sequencing-based non-SNV calls.
Getting back to chips, these themselves depend somewhat on what version of the genotyping chip is used. For specific information on different versions of 23andme chips, I recommend this blog. For tech specs on the most recent Illumina chip used by 23andme, you can see their product sheet, and specifically Table 5. Their data claims that call rate among targeted variants is >99%, and among those the reproducibility is >99.9%. However things can be reproducibly wrong, so that's not exactly false positive that you requested.
Though it's somewhat old, this paper will give you a sense of both technologies in terms of variant ascertainment, claiming 89% sensitivity and 99.6% specificity (for European genotypes only) for either low coverage sequencing or a then-current chip.
To learn more about how these stats work for chips, specifically for false positives, this video may help.
Hope that helps.

Thank you for the thoughtful response. Am I correct in saying that since what they refer to as the "call rate" is >99.5%, that out of 650,000 SNPs 32,500 are erroneous?! That seems ridiculously high especially if those SNPs are for disease variant alleles

Hi Joe, I am understanding "call rate" to mean the rate at which the chip provides enough information for the chip-reading software to be confident enough to give a genotype in the first place. To state it differently, <0.5% of the SNP data will be missing. So not a false positive, but maybe a false negative. Also, SNPs are usually present in triplicate/quadruplicate on a chip, so there is backup for failures. For serious disease though, a chip is not a great detection tool for this reason, I believe chips are generally not used medically (?). Mostly for research cause they're quite cheap.


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Why can early embryos survive freezing?
According to this
Blastocyst & Embryo Freezing in IVF

Embryos can be frozen at the pronuclear stage (one cell), or at any stage after that up to and including the blastocyst stage (5-7 days after fertilization).

Given that freezing normally destroys mammalian cells1 why can early stage embryos survive being frozen?
Reference:
1: Shier, W. T. (1988). Studies on the mechanisms of mammalian cell killing by a freeze-thaw cycle: conditions that prevent cell killing using nucleated freezing. Cryobiology, 25(2), 110-120.

I think you might find this answer to a somewhat related question of interest:
https://biology.stackexchange.com/questions/43077/could-a-single-cell-be-brought-to-life/43092#43092 ——— Since freezing usually kills tissues unless they are specially treated, I think a better question would be why early embryos can survive freezing! Based on this, I've suggested edits to your question.

The reason why cells (and tissues) die during freezing is that ice crystals rupture the cell membranes1,2, so to me it seems the question is actually why early embryos can survive this process.
The answer depends on the technique used, but it comes down to size.  Small tissues (or cells) have a large surface area to volume ratio.
In techniques that use cryoprotectants (compounds that suppress ice crystal formation), the small size allows efficient replacement of water by cryoprotectant prior to freezing (and the reverse after thawing) so that the cells don't have time to die1,2.
In flash freezing (vitrification), the small size allows the entire tissue to be frozen instantaneously, which also suppresses ice crystal formation1,2.
This Scientific American article is very relevant as well.

References:
 1: Konc, J., Kanyó, K., Kriston, R., Somoskői, B., & Cseh, S. (2014). Cryopreservation of embryos and oocytes in human assisted reproduction. BioMed research international, 2014.

2: Loutradi, K. E., Kolibianakis, E. M., Venetis, C. A., Papanikolaou, E. G., Pados, G., Bontis, I., & Tarlatzis, B. C. (2008). Cryopreservation of human embryos by vitrification or slow freezing: a systematic review and meta-analysis. Fertility and sterility, 90(1), 186-193.


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What Ultimately Controls DNA Transcription?
Transcription of DNA and further splicing of mRNA is regulated by various transcription factors, small nuclear RNAs and so on; similarly such related mechanisms as transposition of transposons.
All such factors and mechanisms, including those linked to inter-cellular signalling mediated by peptides and various so-called epigenetic enzymatic processes, require and are dependent upon transcription itself, in the first place of DNA codons.
What mechanism then is supposed ultimately to control the expression, eventually as peptides translated from mRNA, of information encoded in DNA; if it is not peptides thus encoded? That is, since transcription depends on transcription factors which themselves require transcription requiring further transcription factors, does this mean that in the entirety of its function, DNA controls itself?
How then can DNA and its transcription be conceived as a such a self-controlling function?

Transcription of DNA is ultimately controlled by "various transcription factors, small nuclear RNAs and so on" in the cell.
The molecules which make up the "various transcription factors", etc. are already present in the cell when a new transcription begins.  As you note, most all of these molecules are themselves dependent on the transcription of DNA, but also of the availability of component molecules (e.g. nucleotides, amino acids) and of processing mechanisms such as ribosomes.
So, a new instance of transcription requires a working cellular environment, and that environment was created and maintained as directed by DNA molecules at an earlier time.  Usually those DNA molecules were exactly the same as the ones from which the transcription is proceeding. Occasionally, those DNA molecules would have been physically different, but adequately compatible, such as the source chromosomes which were copied during mitosis to create the current DNA molecule.


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What are the uses of Helical Wheel Projections in Structural Biology?
I have seen helical wheel projections used to illustrate amphipathic helices in proteins.  Are there any other uses for these models?

Welcome to Biology.SE! The first part of your question is opinion based (what does often mean) and thus is not appropriate for this site — in addition it is not clear how knowing the frequency of this type of diagram is helpful. The second part of your question seems more appropriate for bioinformatics.stackexchange.com since it is a technical rather than biological question. ——— Please take the time to check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask. Thanks!

I agree with @tyersome — it’s a better fit for SE Bionformatics, especially if you ask more precise questions eg for a program that will generate them.

Apologies. I have edited the question.

Helical wheel projections can be useful anytime you have a protein or peptide with one or more α-helical regions. They allow you to see whether any "property" is present along one side of a peptide. This can be useful in recognizing potential protein-protein interacting motifs such as leucine zippers.
The wikipedia article on "Helical wheels" also looks like a good place to start learning more about this.

Sounds like the questions is asking for uses besides this one.


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Relationship between membrane current and voltage in neurons
Depolarization of neurons leads currents of different magnitudes flow in or out of the cell, and the Sodium and Potassium currents can be separately plotted (Purves):

Caption: Relationship between current amplitude and membrane potential,
taken from experiments such as the one shown in Figure 3.2. Whereas the late outward
current increases steeply with increasing depolarization, the early inward current
first increases in magnitude, but then decreases and reverses to outward current
at about +55 mV (the sodium equilibrium potential). (After Hodgkin et al.,
1952.)
Here we see the dependency of the currents (early: Sodium, late: Potassium) on membrane potential.
What I was wondering was this: It looks like the dependency of the Sodium current on the membrane potential is very non-linear.
However, experiments which assess the amplitude of injected current on excitatory postsynaptic potentials (EPSP) state that the amplitude of EPSPs are proportional to the injected current. How is this consistent with the non-linear current/permeability changes of Sodium? Is the Sodium current linearly dependent on voltage (and vice versa) before the action potential threshold is reached?

I don't have Purves in front of me, can you add the caption there? And careful with the axes: the x-axis is voltage, not time, so saying "a dependency on time would have the "early" function shifted to the left" does not make sense.

I have added the caption. Yes exactly, here the x-axis is voltage. If it would be time, as the name says, the early function would be left-shifted wrt to the late function. I removed that comment now though.

This is a bit of a strange way to plot out these data, I think Figure 3.2 is easier to understand, but basically these are data plotted from early voltage-clamp experiments trying to walk you through how the Hodgkin-Huxley model was developed.
They step the voltage to a particular point and look at the current. There are two phases to this current: an early transient and a later plateau.

The shape of the "early" component ultimately results from the multiplication of two functions: the gating curve of the voltage-gated sodium channels and the reversal potential for sodium around 50 mV. If the voltage gated channels were simply open all the time, you would just have a straight line through +50mV, it would follow the right-side shape of the curve. The left-side of the curve is due to more channels opening as you depolarize more.
For the late component, which comes from voltage-gated potassium channels, all of the dependence is on voltage, because the plateau is at a point where all the potassium channels are open. You will also notice, however, that the slope changes a bit in time: it's steeper at the higher voltages, because the potassium channels open more quickly (and also sodium channels inactivate; the combination of the two would make it hard to separate them here).
Your picture is a bit different from these traces plotted in time: figure 3.3 is showing the peak of each component as a function of the voltage step. I think it would be better to present 3.3 as a series of data points rather than a smooth curve to make this more obvious.
Note that the actual numbers here are a bit different than one would see in a mammalian cell, because these original experiments used the squid giant axon which has some differences in voltage dependence, gating, and ion concentrations.
The reason sodium and potassium can be seen separately in these voltage clamp experiments is because:
A) Sodium channels open really fast early on, and then inactivate
B) Therefore, in the long term the potassium current dominates the sodium current.
If you blocked the potassium current and VG sodium channels didn't inactivate, the "early" part would look like a mirror image of the "late" part of the voltage-clamp traces. As-is, the early component is mostly sodium but also includes some voltage-gated potassium current as well that cancels it out and makes it appear smaller than it would otherwise be.
If you look at the late curve in your original figure, it's mostly straight from the point that all the K channels are open. For the late component, the K permeability is at max by -30mV so after that it's all linear from driving force. The little curve at the bottom up to about -30mV is the range at which not all the K channels are open, otherwise it would be a completely straight line, and it would reverse at the K reversal potential instead of asymptoting around zero. But it's not exactly zero because there is also some leak which is mostly potassium, and that does reverse around the K reversal.

Many thanks for the answer - I think I understand these points, also that in my plot we have max(current) for each point on the x-axis (mV). But my question is this: (1) If I understand correctly, the non-linearity of Na+ follows from the non-linear permeability changes and the time-dependent inactivation of Na+, correct? (2) Does this then also mean that K+ permeability is constant over mV (hence the somewhat linear function in the plot I have used)? But in particular: (3) If Na+ permeability changes are non-linear, how can EPSPs be a linear function of injected current amplitude?

@Pugl I don't follow what you are asking about EPSPs and injected current. EPSPs are caused by activating ligand-gated ion channels. In that case, the amplitude corresponds to how many ligand-gated channels are bound and opened (aka, the permeability). If you open enough of them to also open voltage-gated sodium channels, then you get a nonlinear response, including possibly an action potential if the EPSP is large enough to reach threshold. One could also inject current to mimic an EPSP, and you'd have the same result. However these experiments are in voltage clamp, not IC.

@Pugl I'd also add that the difference between sodium and potassium here is largely because sodium channels inactivate and because the potassium current dominates the sodium current at a long time. If you blocked the potassium current and VG sodium channels didn't inactivate, the "early" part would look like a mirror image of the "late" part of the voltage-clamp traces. As-is, the early component is mostly sodium but also includes some voltage-gated potassium current as well that cancels it out.

Ok that is important to understand, thanks for the addition: Hence the non-linear part in the functions is time-dependent inactivation of Na+ channels. The only thing that still confuses me is this: I often read that higher mV also means more K+ channels are open (and not only that they open more quickly). Would this in contrast not mean that the mv/mA plot would be non-linear (as permeability is the proportionality constant in Ohm's law, and we would have different slopes for different mV)?

(2/2) ...or, I guess the linearity is a result of the permeability x driving force interaction?

@Pugl Both inactivation and activation, yes. If you look at the late curve in your original figure, it's mostly straight from the point that all the K channels are open. The little curve at the bottom up to about -30mV is the range at which not all the K channels are open, otherwise it would be a completely straight line, and it would reverse at the K reversal potential instead of asymptoting around zero. But it's not exactly zero because there is also some leak which is mostly potassium, and that does reverse around the K reversal.

Yes permeability x driving force. For the late component, the K permeability is at max by -30mV so after that it's all linear from driving force.


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Predatory insect - what kind?
I've seen several of these insects near my house in southeast Michigan this summer, including the one seen here feeding on a green bottle fly. What are they?

Probably Efferia or Promachus but I can't know for sure without knowing the size. How big was it?

@Praearcturus IIRC 2-3cm, but not positive. Feels like forever ago :)

That looks like a type of "robber fly" — compare with this image:

BugGuide is a great resource for identification of insects, spiders and their ilk.

Definitely correct! Thanks

You're welcome, glad I could help!


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What is the purpose of getting a rabies vaccine after exposure?
After exposure to the virus, it is already inside you and your immune system will start to recognize it. Is the vaccine then just a way to kickstart this process so the body can fight off the infection sooner? Is it just a way to introduce much more antigen to the system than would be present only a few hours post exposure from actual virus replication? Or is the boost coming from adjuvants?

Rabies virus enters the body, typically from a bite, and then enters nerves which it follows up to the brain. An immune response to a first exposure of a pathogen generally takes many days, perhaps weeks, to develop to the point where it's protective. This is often even slower when the pathogen is in nerves, which are relatively sheltered from the immune system, and when there's only a small amount of virus present.
After rabies exposure, people are given two treatments: They're given  rabies immune globulin, which contains pre-formed antibodies against rabies, and they're also given the vaccine.
The rabies immune globulin is the most important of these. It provides immediate protection, beginning within minutes of injection. If the virus has not yet entered the nerve cell (which often takes quite a while) then this globulin will bind to and inactivate all, or almost all, of the virus.
Giving the vaccine as well is an added precaution. It will give a faster, probably much faster, response than would the natural virus. There may be only a few rabies viruses present -- it only takes one! -- and of course the natural virus is doing everything in its power to avoid making a strong immune response, whereas the vaccine is the opposite. It has large amounts of antigen, and it's optimized for making a strong immune response. (Rabies vaccine post-exposure is boosted on days 3, 7, and 14 after the first dose. That's an extremely aggressive vaccination procedure that you don't see with any routine treatments.) The vaccine might drive a protective immune response within a few days, while the natural virus might take a month, or never.
If the rabies immune globulin doesn't catch all the virus, or if it temporarily blocks it but then some escapes -- then the vaccine-induced immune response might protect them.

CDC page on post-exposure vaccination
CDC page on post-exposure globulin


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How long it takes medium size dog's corpse being decomposed?
I am not a Biology student or expert. Moved the post from Pets SE.
Around a month ago, my 12 years old dog passed away. And I buried her in our front yard (mostly soil, 1 meter depth, wrapped in some cloth fabric material). The thing is I have a plan to sell my house, but don't have nerve to move away if my dog's corpse have not completely decomposed. There is a hard feeling to leave her like that, you know, the family bond stuff. So it will be relieving if her body are completely decomposed when that happen.
Background I live in Yogyakarta, Indonesia, which has tropical climate. But from the past few month, we have pretty unusual cold temperature during night until around 9 am, because of Australian Cold Monsoon. I mention this in case it has logical factor of how decomposition works.

Maybe Medical Sciences Stack Exchange is more suitable. Vets can answer this question there.

That's a very warm climate, about 25'C year average, which causes very rapid decompostion. 1m deep is about the same temperature, according to graphs. The limiting factor for you will be the air in the soil. wet compact clay can be very low on oxygen, and sand has the highest oxygen. to be on the safe side, you can also ask the new owner if you can come back in 2 years to collect the bones and cover the garden, and give him some extra flowers. My guess is that there can still be some non-bone material there for 2-3 years, hairs for 3-4 years. recall your dog, he is in the sky, dont be guilty.

@com.prehensible “He is in the sky”? Read the question. The poster said the animal is rotting in the ground.


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Understanding the "Waterfall Illusion"
Motion after-effect illusions, such as the waterfall illusion, refer to illusions where fixating a screen which shows stimuli moving in a particular direction  elicits the perception of motion in the opposed direction when subsequently looking at a static image.
Here is an example: Video Motion After-Effect
The explanation is typically that adaptation effects lead to a saturation of the firing rates of neurons encoding the viewed motion direction.
So far so good - but why do we then perceive afterwards motion in the opposite direction, and not in any other direction where no adaptation has happened?

This is a more detailed answer about conceptual mechanisms from the same author as AliceD is citing:
The first row represents the sensors (for instance photoreceptors) while the second row
represents higher order responses (for instance of MT neurons). The latter's response is their resting level response plus the difference of the corresponding channel minus the opponent channel's response (so yes, the assumption is that there is an opponent mechanism). As you can see, there is no response beyond baseline before adaptation
as the difference between the sensor's responses is zero. During adaptation, when subjects are seeing an upward motion, the corresponding response is higher, too.

Now after adaptation, the opposed system shows an above baseline response as now the up sensors display some form of adaptation, hence shifting the response difference of the sensors in the favour of the opponent motion direction:

I am not familiar with the underlying biophysical mechanisms, this model possibly suggests, however, decreased feedforward inhibition after adaptation.
Mather, the motion aftereffect: a modern perspective

The motion after-effect (MAE) is believed to be primarily due to adaptation of direction sensitive cells in the middle temporal area (MT) (Fig. 1.). The directional cells in this area of the cortex are selectively sensitive to motion in one direction. Hence, looking at a waterfall will selectively cause adaptation in those cells tuned to the direction of the waterfall. When one looks away, the MT cells responsive to opposite directions will become dominant, as their counterparts are momentarily shut down and one will see the waterfall running in opposite direction.
Adaptation thus apparently weakens the opponent input to the adapted MT cells, enabling an enhanced response to motion balanced stimuli. However, the possibility of adaptation occurring in MT neurons themselves cannot be ruled out (Mather et al., 2008).
The MT area is one of the principal visual cortical areas devoted to motion sensing and hence a likely culprit for MAE. However, fMRI studies have indicated that a lot more visual areas in the brain may be involved, either directly, or indirectly, including V1, V2, V3, VP, V3A, V4, and also MT (Mather et al., 2008).

Fig. 1. Two visual streams dominate vision: the dorsal 'where" pathway (containing the direction-sensitive MT area), and the ventral 'what' pathway. source: InTech Open
Reference
- Mather et al., Trends Cog Sci (2008); 12(12): 481-7

Ok thanks, but my question is not so much about the where (I am somewhat aware of MT and the dorsal stream, and that the size of the adapted area allows us to infer if it is a upstream inferred property or happens in MT itself), but why it is exactly the 180 degree opposite direction which then becomes perceptually salient, and not say the direction which is 32 degrees different. I am not sure if your answer addresses my question

@user234 the MT cells are sensitive to specific directions, per the answer, so yeah, I'm covering the Q pretty heads on I guess

Ok but then I just don't get it from your answer, and would like to understand better: I get that the cells are selective, ie tuned, for a particular motion direction. But when firing rate to this motion direction is attenuated, why is it exactly the opponent direction which becomes perceptually salient? What's the mechanism? Like there must be some opponency mechanism for directions different by 180 degrees I guess?


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Consider gene is countable, can anyone give a concrete example of "a gene"?
gene is a countable noun but people always say genes, so what is A gene?
for instance, Each chromosome contains many genes, so, which part of the chromosome of Escherichia coli could be A gene?

Welcome to Biology.SE! It is expected that you will demonstrate that you have done research on your own before asking questions here — for example you could start with this: https://ghr.nlm.nih.gov/primer/basics/gene ——— Please also take the time to check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask. Thanks!

There are about 20,000 genes in the human genome. Here are the first 5 genes (following alphabetical order) on chromosome 1:

AADACL3: Arylacetamide deacetylase-like 3
AADACL4: Arylacetamide deacetylase-like 4
ACADM: acyl-Coenzyme A dehydrogenase, C-4 to C-12 straight chain
ACTL8: Actin-like 8
ADGRL2 (1p31.1): adhesion G protein-coupled receptor L2


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DNA and Genes, which consists of which? It seems that the hot answer on quora is different to the nih post
This quora's answer has got 8.3k views and 20 Upvoters.
"Genes are a part of the DNA."
per nih, "Genes are made up of DNA, which is telling the truth."
in my understanding, the quora version indicate that

DNA consists of Genes, and DNA is bigger than a gene, in the context of same living thing, such as a specific escherichia coli.

while the nih version indicate that

Genes consists of DNA, and a gene is bigger than DNA, in the context of same living thing, such as a specific escherichia coli.

did I misunderstand somewhere?

What difference does "part of" and "made of" makes in your mind? How does it change your conception of what DNA and genes are and aren't?

@Remi.b Which one is bigger in your mind, in the context of same species, such as escherichia coli?

Bigger between what and what? The expression "made of" cannot be said to be bigger/smaller than the expression "part of". I don't understand your comment.

Oh did you mean "is DNA bigger than a gene?". The question has bad semantic but anyway... yes DNA is bigger than a gene. DNA is a massive molecule. Specific locations on this molecule cde for proteins. These sequences are called genes.

@Remi.b thanks for your reminder, I've updated the post.

I don't find the text you quote on the linked page. Also, can you add a more informative title for your question?

As @kmm points out,  the quote you include doesn't actually appear in the NIH article you link to. You may want to go back to that article and re-read it. Were you reading a Google Translate version of it by any chance?

DNA is a large molecule which is particular interest relies in the succession of nucleotide that composes it. The genetic information is contained in the succession of nucleotides (I will ignore epigenetics here for simplicity). A given position of any length on the DNA molecule is called a locus.
A gene is typically defined as a protein coding sequence. In other words, a gene is a locus. A gene is not so much a structural element that makes the DNA, it is rather a functional element.

Thanks for your answer. Take this example, AADACL3 on chromosome 1, thanks again for that question, is a gene. in the meanwhile, is it also a DNA? it seem to be not, "DNA basically contains two copies of 23 chromosomes each" from that quora post.


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In a Chromosome, 2 nm is the length of what?
this figure comes from the nature

2 nm at the top right hand corner is the length of what?

DNA is a long, thread-like molecule. 2nm is the approximate width of the DNA molecule.


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Which chemokines are being produced by melanocytes?
I am looking into Vitiligo it's an autoimmune disease that results in apoptosis of melanocytes due to misfolded protein accumulation.
It also dramatically increases breast cancer rates (600 times) within one to five years from the first symptoms of Vitiligo. One function of melanocytes is to produce chemokines however I was unable to find any info on which ones.
Which chemokines are being produced by melanocytes?


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Diffussion coefficient of blood
What it the diffusion coefficient of blood in, e.g. water?
It is needed for microchannel length calculations
I have found a bit different nubmers: 0.94 and 1.66 microns^2/ms, but not sure

Welcome to Biology.SE! Please add references to your question (i.e. where you obtained those numbers). Also, please clarify whether you are asking about human blood. If so, can you specify what population(s) of humans this blood is from. There wont be a single number since blood viscosity (which will affect diffusion) can vary significantly both within and between populations — e.g. people living at high altitudes typically show increased blood viscosity.  You may find this article interesting: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4162413/


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How hard would it be to create a protein "by chance"?
I just read an article about David Gelernter, who was arguing against Darwin's theory of Natural Selection. He said one particular thing which stood out to me:
"...how hard it would be to create just one new protein by chance — the odds are so astronomical that there are fewer atoms in the entire universe in comparison: “The odds bury you. It can’t be done.”
I'm wondering how one could back up this idea. My back of the envelope (not being a biologist...) would go something like this:
Protiens are made of amino acids. Amino acids are essentially made up of four things, C, H, O, and N. In order to "make" amino acids, I just gotta give these things the right energy so they can strip some electrons and hook up to each other. If want to make all amino acids with say 20 molecules, I get four choices for each of twenty things, or $4^{20}\sim 10^{12}$ possible amino acids. Wikipedia tells me "most proteins are built from up to 20 different amino acids", so how many proteins are there made up to 20 amino acids?
$$(10^{12})^{20}\sim 10^{240}$$
So ignoring overcounting and how stupid this estimate is, that's a big number. And indeed, that's bigger then the number of atoms in the universe (like $10^{80}$ by some estimates).
Can someone confirm that's how he arrived at that estimate?
NOTE: Careful, I am not trying to get into an argument about Darwin - I only want to know how people who use this argument, make this argument.

It's a ridiculous statement, so you'd have to ask him how he arrived at it.

Sounded like an argument he was referring to though, right? It's true, if this is just him I'm asking a pointless question.

@cduston It's a bit like if you told someone that you walked to work, and they started telling you about how impossible it is to teleport from home to work. It kind of doesn't matter how they got their numbers about how improbable teleportation of an intact human being is, once they've refused to accept that you accomplished this by walking, the details of their alternative explanation don't really matter.

I don't wish to appear to be answering this question in a comment, and I have the feeling that it has been asked before, but if it hasn't anyone is welcome to expand on the following thoughts. 1. This is a common statistical fallacy. You have to ask what false assumptions are being made. What does creating a protein by chance actually mean? 2. The evidence says that it is possible to create a catalytic active molecule by 'chance' by the aptamer selection experiments. Lots of them. Just like there are lots of polyclonal antibodies against the same epitope. So how ever clever the arguments...

@David: I agree with everything you've said, but it wouldn't count as an answer because it doesn't address what assumptions he's using. I'm essentially assuming that "picking" means "combining", but of course there's a lot of missing chemistry there. Can you add more reasonable mechanics and still get the same argument?

@Cell: I asked here because I want to see if this argument can be made with some biology and chemistry principles. If so, it would give the argument more weight. For example, if I ran a simulation for 13.7 Gyr and didn't randomly produce any amino acids, the argument would be somewhat more valid. I'm asking if there is anything to be found of that nature in these arguments.

@cduston It's probably better to explore the abiogenesis tag to look at ways that people have studied creation of biologically-relevant molecules before biology, rather than starting from a nonsense argument.

David is right, this question (more generally) has been asked before  on skeptics https://skeptics.stackexchange.com/questions/32283/are-the-outcomes-of-evolution-too-improbable-to-have-occurred-in-the-earths-lif/32286#32286

I'm not trying to answer the question: I'm saying that this is a conjouring trick. You are so busy following this calculation that you don't question its relevence to biology, even though from your experience you know that it is a trick. You have been tricked into accepting a deliberately vague false premise of the sort that evolution requires the chance formation from scratch of one specific 100-amino acid protein. We all enjoy being tricked by a good conjourer, but we don't go away believing in magic, do we?

Why would a protein have to form on its own? proteins in life are constructed by nucleic acids,  we already know RNA can occur by chance.

In the original column for The Claremont Review of Books, David Gelertner does not suggest starting from atoms, but from amino acids. This changes the calculation slightly:

The total count of possible 150-link chains, where each link is chosen separately from 20 amino acids, is 20^150. In other words, many. 20^150 roughly equals 10^195, and there are only 10^80 atoms in the universe.

In any case, these kinds of estimates are purely theoretical and are not hugely useful. We do not know how early proteins evolved, but they did not have to just assemble from scratch.

As mentioned in the comments, this kind of argument for creationism (or 'Intelligent Design') is like a card trick - you start by dazzling with vast numbers, and use them to conceal the logical sleight of hand.
The premise of his argument is simple - there are a vast number of possible sequences, only a small fraction of those can fold into functional proteins, and there have not been enough mutations to make up the difference.
There is this strange argument:

But what does generating new forms of life entail? Many biologists agree that generating a new shape of protein is the essence of it

I'm not sure who these 'many biologists' are, but the relationship between novel folds and new species is not clear to me, at least.
Anyway, the second part of his argument relies on the work by Douglas Axe on estimating the fraction of functional folds (see this paper for example). Although he describes him a bit oddly ("Axe is a distinguished biologist with five-star breeding") it's reasonable to make this kind of estimate.

He estimated that, of all 150-link amino acid sequences, 1 in 10^74 will be capable of folding into a stable protein. To say that your chances are 1 in 10^74 is no different, in practice, from saying that they are zero. It’s not surprising that your chances of hitting a stable protein that performs some useful function, and might therefore play a part in evolution, are even smaller. Axe puts them at 1 in 10^77.

So here is the very small number to contrast with the very large one of the first step. Now for the 'bridge' - the large number of attempts that would be necessary to make a very rare event (a folded, functional protein) possible.

Suppose, then, that every bacterium that has ever lived contributes one mutation before its demise to the history of life. This is a generous assumption; most bacteria pass on their genetic information unchanged, unmutated. Mutations are the exception. In any case, there have evidently been, in the whole history of life, around 10^40 bacteria—yielding around 1040 mutations under Axe’s assumptions.

So the argument - roughly - is that 10^-77 * 10^40 is still very small. That is, mutations are not frequent enough to overcome the extreme rarity of functional sequences.
The sleight of hand, I think, is to confuse abiogenesis and mutation. When talking about the entire 'landscape' of possible sequences we are talking about abiogenesis - randomly picking 150 amino acids (say) from an alphabet of 20. When talking about bacteria we are obviously talking about mutation.
We really have no idea how the first primordial proteins formed, or what their properties were. They could have used a smaller set of amino acids (although this does not change the numbers much), or could have assembled from multiple smaller peptides, or even been partially folded.
On the other hand, mutation of existing proteins necessarily happens on sequences that can already fold. Moving to a sequence that is a neighbour in fold space is very different to picking a completely new point in that space.
So really, the numbers do not tell us anything because they relate to separate questions.

But what have the number of atoms in the universe to do with anything? It implies that every possible protein would need to be made to get one that did the trick and that’s what evolution assumes and that’s impossible. You’re looking where the conman wants you to look, and not noticing what he’s doing with the cards.

This is the answer - if we can get a citation for the quote I'll mark it as such.

@David: again, I explicitly asked to not look at the cards. I wanted to know if the calculation involved anything except for a basic understanding of chemistry and probability, and apparently that is all. It's also enough for us to know how much worth to assign to it.

When talking about abiogenesis it's also worth to mention that modern life uses 20 (actually 21-22) aminoacids - we don't know how many it were initially but it's pretty clear that starting number of amino acids was smaller (i.e. more common & simple aa's like glycine and alanine have more triplet codons). This can change the number of possible combinations by several orders of magnitude

@Nicolai - That's what I meant by "restricted set of amino acids", I'll make that clearer. However it doesn't make much difference to the numbers - 5^150 is roughly 7*10^104 which is still a huge number. As David says, combinatorial arguments like this are a bit of a distraction.


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What is the Definition of Homologous Chromosomes? length, gene position are the same or similar?
what is the Definition of Homologous Chromosomes?
this post says

Homologous chromosomes are chromosome pairs (one from each parent)
  that are similar in length, gene position, and centromere
  location.

and then

The position of the genes on each homologous chromosome is the same.

are length, gene position of a pair of chromosomes the same or similar?
if exactly the same (I guess not), job well done.
if just similar, What is the Definition of similar? 99% same?
in the case of a pair of human Chromosome 1, what is the exact number of base pairs that are the same?

Before posting to this site you should research your question. Although you have cited one source, there are better places to look. You need to understand the (molecular) biological concepts rather than make the mistake of physical scientists in thinking things are defined by numerical cutoffs. Wikipedia can be a good source, and here gives a good basic explanation, which is fleshed out in the section on meiosis in Alberts et al. on NCBI bookshelf — an excellent resource.

Unfortunately despite the impression given by the many poor explanations available (including the one you quoted), homologous is not a synonym for similar.
Homology is defined as the existence of shared ancestry1,2.  Thus, structures being homologous simply means they had a common ancestor — i.e. homology is a relationship not a property of an individual structure.
The "definition" you quote is actually a description of what you typically see when comparing two homologous chromosomes within a species. High levels of sequence similarity suggest homology, but are not sufficient to prove it.  (To test that requires building phylogenetic trees.)
(One classic example of this is the superficial similarity between dolphins and sharks, which is an example of convergence not homology.  Another is the homology between bird and bat wings — they are not homologous as wings, though they are homologous as tetrapod forelimbs.)
Consequently, for two chromosomes to be homologous they must have descended from a (potentially much earlier) chromosome that has been duplicated possibly for many generations (the ancestral chromosome might even have existed in a now extinct ancestral species).
So, if an inversion happens within a chromosome (and changes the ordering of the genetic loci) that chromosome is still homologous to the parental type chromosome that didn't undergo inversion.
ETA: Note that chromosomes don't need to be in the same cell (or even the same species) to be homologous and chromosomes can be homologous even if the cell they are in is not diploid.  For example, the human chromosome 1 is homologous to the chimpanzee chromosome 1.

Similarity is a measurement of "distance" between sequences, but while very similar sequences are likely to be homologous there is no magical value of similarity that proves (or disproves) homology.

Individual humans are about 99.9% identical (depends on how you measure this) at the nucleotide level, so that will also be true for chromosome 1.

Finally, the UC Berkeley Museum of Paleontology also has useful resources for understanding evolution including some material on homology — e.g.:
https://evolution.berkeley.edu/evolibrary/article/lines_04

References:
1: Brigandt, Ingo, "Essay: Homology". Embryo Project Encyclopedia (2011-11-23). ISSN: 1940-5030 http://embryo.asu.edu/handle/10776/1754.

2: Mindell, D. P., & Meyer, A. (2001). Homology evolving. Trends in Ecology & Evolution, 16(8), 434-440.

Sorry to be a wet blanket after all your work, but it seems to me this is not answering the (very naive) question which is about diploidy — at least the first quotation — the poster perhaps confusing it with the use of homology in relation to similar genes or gene regions (but seldom chromosomes) between species

The first link the poster gives has a classic picture of a pair of human chromosomes and refers to one being maternal and one paternal. It doesn’t say anything about diploidy, but that is what that reflects (isn’t it) and was a choice of words to try to explain what I thought was your misinterpretation. The term “homologous chromosomes” was (I imagine) used years before the term “homologous” was used in comparing the sequences of genes from different organisms. PS Criticize my arguments, say if you think I am violating the code of conduct, but please do not make general personal observations.

@David: My apologies, that was not intended as a personal attack. I will delete the offending comment and be more careful in the future to keep my focus on content. ——— I still don't see why you think the OP is asking about diploidy.  The concept of homologous chromosomes are most commonly introduced during discussions of meiosis (which in my experience will always be presented in a diploid context for lower level students). Consequently it seems natural to discuss the concept of homologous chromosomes in a diploid. However, I will edit my answer to emphasize this distinction.


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Is this a bedbug? (with picture)
I had some potentially infested clothing (and shoes) in a bathtub, and just after I bagged them to wash, I spotted this little fellow running away.  I put it in a plastic food container and snapped a photo as close up as my phone could get:

Is this a bed bug?  Its length is about 3 mm, so presumably it would be a nymph if so.  Compared to pictures on the Web, it certainly looks similar.  However, it seems too thin (even for a nymph), and the antennas don't have that outward crook that all of the pictures (even of nymphs) seem to have.  Also, at the time that I took the picture, it could not have fed on blood in the previous 12 hours.  So hopefully it's not a bed bug at all; but maybe there's nothing else that it could be, and the pictures give the wrong impression of what's possible.  Can anyone tell?
This is not a StackExchange that I'm used to, so if this is an inappropriate question, then I apologize, and I'd appreciate any suggestions of where to ask instead.
ETA:  This is in the Midwest/Great Plains region of the USA.
ETA:  Having seen more pictures, the thinner (or really, longer) form seems to be after they have fed.  But as I said, this could not have fed within 12 hours at least (when the clothes it might have been in were removed, plus the people had no apparent bites).  And that doesn't explain the relatively straight antennas.  But it does seem closer now.
ETA:  The picture doesn't seem to match any of the false IDs of bed bugs on this site, nor the related insects at bugguide.net.  (And it compares to the actual bed bugs with the slight differences that I noted already.)

Welcome to Biology.SE!  This appears to be a frequently asked question — have you looked at the related questions e.g.: https://biology.stackexchange.com/questions/56200/insect-identification-is-this-a-bedbug?rq=1?  Also, bugguide.net is probably a better place for this sort of question.

Hi @tyersome and thanks for your reply.  Yes, I did look at related questions, including that one, and I've added a paragraph at the end about why they didn't solve this.  And I did look at bugguide.net (also mentioned in my new last paragraph), but I didn't realize before that they have their own identification service, so I'm going to try that now too.

Not a bedbug. They are laterally expanded, not narrow like this one. I can't tell for sure from the picture, but I would guess that it is either a collembolan or a thrips. You could narrow your image search to these two groups. (Collembola, Thysanoptera).

Thanks, @KarlKjer!  Someone on bugguide.net also suggested a springtail, and it does look rather like the one at https://bugguide.net/node/view/90808


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What are these two nerves running parallel to the spine called?
I was looking for a human body nervous system, and often times i found a picture like the one below, where there are two nerves running parallel to the spinal column. I searched for it, but nothing came up.

Can anyone tell me what are the names to these two nerve column parallel to the spine and what are their functions?

From this closeup image, you can see there is more than one nerve on each side that is parallel to the spine.

Source: imgur.com
First, they are the right and left sympathetic trunk that run from the base of the skull to the coccyx.

Image source: Earthslab.com
Additionally, they could be the right and left long thoracic nerve, which innervate the serratus anterior muscles in the chest wall. In your image they appear like running along the spine, but in reality they run vertically and laterally in the chest wall.

Source: Semantic Scholar


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What are these little creatures on the fish?
I'm not a fisherman, but I just caught a cod fish (my first one) and found a lot of strange little creatures all over the fish:

What are those? Are they harmful to the fish, or to the human?
Edit: it's caught on Faroe Islands

For identification questions please: 1) upload an image, and 2) include the location (e.g. country and region — the more specific the better). ——— The location can be an essential clue for identification and links are discouraged since 1) if they break they render this post and any answers worthless, and 2) they can be used to link to malicious websites. Thanks!

Though it's hard to say exactly what you're talking about based on the image, that cod appears to have several sea lice on it:
https://en.wikipedia.org/wiki/Sea_louse
Sea lice are common parasites of fish.


text:
What separates humans from other animals?
It is clear that humans are distinguished from the other species on Earth, but what specific features are the cause? Other animals like chimpanzees have been shown to have consciousness and some self-awareness, dolphins likewise have a form of structured communication. What features of human biology (physical and/or mental) are unique to the human race as far as we know?
I would also appreciate any books or articles on these aspects of human biology if possible.
Thanks in advance!

"It is clear that humans are distinguished" - clear in what way? There are lots of species that are much more unusual compared to their relatives than humans are to theirs.

In the sense that we have subordinated the natural world to our control to a degree unmatched by any other animal. I’m asking what the biological preconditions of this are.

Humans are distunguished from other species by humans, due to chauvinism.

Unmatched by any other animal? There are only some 7 billion humans. There are 10,000 trillion ants. In our own bodies, there are as many bacterial cells as actual human cells.

To an extent I’m sure, but it isn’t purely that we ascribe exceptional qualities to humans simply because we are humans. No other animal species can manipulate its environment for specific ends in the same way humans can, which is what enabled us to develop our modern society. We must have some unique biological features that allow us to do this.

https://en.wikipedia.org/wiki/Lateral_prefrontal_cortex

When we take other similar species (or sub-species) into account, like neanderthals, we see that the difference is in the level of some capabilities like problem solving and memory.
And because of the level of these capabilities, modern humans can be distinguished as an animal which isn't bounded to a specific habitat on Earth.
If one looks to the animal species that live today and want to "distinguish" human, then she/he can think that there's a massive difference between human's and other amimals' communication and problem solving capabilities. But, rather than a difference, we need to look this as a kind of gap which isn't actually exist.
So, if needed, we can distinguish modern humans as a species from others on the basis of the results of their capabilities, not on the basis of the biological properties that cause these results.
Of course, this kind of questioning (trying to distinguish human) doesn't affect biological classification and identification of species at all, but it can affect people's general attitude and opinion on this issue.

Welcome to Biology.SE! Your answer reads like an opinion rather than being based on facts.  What evidence can you supply for differences in problem solving and memory between Neanderthals and modern humans?  Answers are much more likely to receive a favorable response if they include supporting references.  ——— You may wish to consult the help pages for additional advice on how to provide effective answers: biology.stackexchange.com/help/how-to-answer. Thanks!

I mentioned Neanderthals just to bring to attention that modern humans/humans aren't "unique" in any way when we take all the species/sub-species that lived on Earth into account.


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Does food lose some of its mass in form of energy during metabolism?
I had an argument with someone.
I argued that when a cat eats 1 kg of food, the sum of subsequent output (poo + pee + sweat + change of body mass) must be equal to 1 kg.
My opponent argued that the output will be less than 1 kg because a part of food is converted into energy.
Please rule.

Welcome to Biology.SE! It is expected that you will demonstrate that you have done research on your own before asking questions here — for example you could start with this: https://wtamu.edu/~cbaird/sq/2013/10/21/why-is-mass-conserved-in-chemical-reactions/ ——— Please take the time to check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask. Thanks!

Possible duplicate: https://biology.stackexchange.com/questions/73288/when-you-lose-weight-how-does-the-mass-exit-your-body

Possible duplicate of When you lose weight, how does the mass exit your body?

So your opponent is claiming that your cat is a nuclear reactor?  One thing you're neglecting here is that a portion of the mass of the food will leave as CO2.

This is NOT a duplicate of When you lose weight, how does the mass exit your body? because that question explicitly says 'And please, don't suggest that it was "converted to energy"' and the answer avoids that aspect, while the present question explicitly asks about conversion into energy.  The answers are different from the point of view of a biologist or chemist versus that of a physicist.

During metabolism, the energy is released from the chemical bonds, while the atoms and their atomic mass and therefore the mass of everything what a cat eats and excretes remains the same.

@Jan - technically spoken you are incorrect

Physics answer that is a bit silly
If you want to be real technical about physics, mass and energy are the same thing, so any chemical bond that has some energy and is broken results in a change of mass (mgkrebb's estimated in a comment the final mass would be 999.999999814 g, if you started with 1 kg of protein, also known to a very precise biologist as 1.000 kg).
This is sort of a "technically correct" answer that is totally silly from the standpoint of biology, but if your opponent wants to stand by it as "technically correct" based on physics, so be it. We are talking about changes in mass that are not measurable by modern science to sufficient precision, these are only theoretical ideas based on relationships between mass and energy that can be measured on a much larger scale.
Biology answer
Since this is Biology.SE, the biology answer is that mass is conserved in chemical reactions. If you greatly simplify the metabolism of, say, glucose, to the equation:
C6H12O6 + 6 O2 --> 6 CO2 + 6 H2O
you find that the net result is that the hydrogen and oxygen atoms become water, and the carbon atoms become part of carbon dioxide (yes I am simplifying where the actual atoms end up in the biochemical reactions, just talking in terms of net changes here). Other food molecules are processed similarly, and will produce some combination of water/carbon dioxide/nitrogenous wastes. If your cat eats 1 kg of food, that 1 kg of food will become 1 kg of something else out to many many decimal places: waste solids (including anything not digested at all) and liquids, exhaled carbon dioxide, lost skin/hair, etc.
Physics answer if you just want to win the argument
If you want to still win the argument with the physics-based answer that relies on mass-energy equivalence and ignores the fact that from the perspective of biology they are best understood as different concepts, then it's just as fair to go the other way and treat the lost energy as mass, in which case you'd consider the heat lost by the cat's metabolism as mass and include that tiny tiny tiny fraction in the 1 kg and call it a day.

Though part of that 1 kg of food is indigestable bits that just get passed through.

@jamesqf That would be included in the waste solids.

I wouldn't characterize the most precise accepted scientific description as "a bit silly", but the resulting mass deficit is at present immeasurable. If you feed the cat 1 kg of protein and it was entirely metabolized, it would release about 4000 kcal of energy, equivalent to 1.862e-7 g of mass. This means the products from the 1000 grams of food would not conserve all their mass, but instead have a mass of "only" 999.999999814 grams.

@mgkrebbs From a biological perspective, measures out to 10-12 significant digits are, in fact, silly. Just as silly as using relativity when a physical system is within the bounds of Newtonian mechanics. There are too many sources of variation and error to give measurements of that precision any meaning. It doesn't make the physics wrong or not precise, of course, but chemists and biologists don't worry about those differences. Neither do physicists in most contexts.

@BryanKrause, I agree that there is no practical importance to the mass change since it is immeasurable, and therefore it should be dismissed for thinking about most problems since it adds useless detail when considering how most things work. For arguments and wagering, however, the immeasurable details do matter.

Love this answer +1

@mgkrebbs Fair enough. I'll add your number to my answer if you don't mind because I do think it's useful.

@BryanKrause, that'd be fine.

Your opponent is correct. Some mass transforms to energy; the amount is negligible.  One good  source
If you and your friend decide to do an experiment in a controlled environment and measure the masses with a scientific scale with the highest precision available today, you will see that the total mass at the beginning of the experiment and the total mass at the end are same. Because, the scale isn't precise enough to measure very very small amounts of mass.
But, this won't mean that your opponent is wrong. Because, in terms of physical laws, there will be a very small amount of change in the total mass which is the source of the energy that will be released in metabolism in various kinds like heat.
This physics.stackexchange thread can be helpful to understand the physical nature of the event..

We are looking for more extensive answers explaining the topic. You just quote someone making an assertion without any evidence behind it. What is needed to support your argument is a calculation showing how much mass is converted into energy in a specific chemical reaction. Can you provide this?

No I can't provide a calculation and this would be unnecessary as it isn't the question.

Hardin, I am trying to help you understand how this site works. @Bryan Krause has supplied just such an answer. Please read the Help on Answering Questions.

Edited my answer. Hope this helps.


text:
Non-coding DNA as a protection to deleterious mutations
We know that most part of our genome (at least 75 percent) is non-coding DNA. Can it be a way to protect the organism from mutations in important genes, such as the ones which control cellular cycle, as a mutations is much more likely to occur on these parts of the genome?
I've never been told if it could have such a function, and I thought about recently and wasn't able to find a clear answer.
So thanks in advance

You seem to be under the impression that there are a set number mutations per cell, which is not true.  The number of mutations is roughly proportional to the number of bases  — this is because mutations typically happen as a result of errors during DNA replication .1  Consequently, more DNA will not protect the coding portions of the genome from mutation.
The reason why mutations appear to be suppressed in coding regions is due to selection.2

References:
1: Lodish, H., Berk, A., Zipursky, S. L., Matsudaira, P., Baltimore, D., & Darnell, J. (2000). Molecular cell biology 4th edition. National Center for Biotechnology Information, Bookshelf.

2: Griffiths, A.J.F., Gelbart, W.M., Miller, J.H. and Lewontin, R.C. (1990) The Molecular Basis of Mutation. In: Modern Genetic Analysis. W.H. Freeman and Company, New York.


text:
Lysozyme amino acid sequence: N-terminal extension
I looked up the amino acid sequence of lysozyme here: http://www.biology-pages.info/L/Lysozyme.html
Then I crossed referenced that with the lysozyme sequence on UniProt: https://www.uniprot.org/uniprot/B8YK79
My question is why does the sequence on UniProt start with eighteen other amino acids before getting to the start of the sequence described in the first source?
The sequence on UniProt starts with "MRSLLILVLCFLPLAALG".  I know the M comes from the start codon in the gene for the protein, but where does the rest of this come from?

If you scroll down through the uniprot entry you will come to a section with the heading PTM/Processing.
From this you can see that the first 18 amino acids are a signal peptide.
You can learn more about signal peptides from any good introductory textbook covering cell-biology — alternatively Khan Academy is a good source for learning the basics.


text:
What is that? Dry brown fungus? See photo please

It has appeared two days in a row on my balcony, at exactly the same place. There's nothing near that can give me a hint of what it is. The birds can access the place easily. It's an inch in size, it's dry. In the photography you can see a eyelash and some hair, because has been taken after sweeping.
The place is Jerez de la Frontera (Cadiz, Spain).
What it could be? I'm curious and I would like to know why it appears.

Welcome to Biology.SE! For identification questions please: 1) include the location (e.g. country and region — the more specific the better), and 2) include habitat information (e.g.s: what types of plants grow nearby and whether you are near water). ——— The location and habitat can be essential clues for identification. Thanks!

Looks like bits of insulation. Are birds making a nest above where this appears?

No, birds aren't making a nest above.


text:
Is it possible to detect whether an organism has been gene edited (by humans)?
Is it possible to detect whether an organism has been gene edited? For example, if someone gene-edits a human embryo (e.g., as He Jiankui did last year), can one later detect whether the human has been gene-edited?

This is largely going to depend on what is changed. Gene editing can cover a wide range of things.

If you had access to the DNA of the organism's parent(s) then you could make an inference about whether the child's genome is consistent with being edited, assuming that the edit was done early enough in the embryo's existence for the edit to be present in all/most of its cells. If the organism is a chimera/mosaic, then it may be possible to detect the edit by comparing different tissues within the organism, and identifying differences which do not look like 'natural' somatic mutations.  However, I don't think we have a good handle yet on what the natural range of somatic mutations looks like, so it might be difficult to assess whether any difference found were of an engineered origin.

I think you're last point is very important - depending on the type of change introduced (and the technique used) it could look like a single point mutation or other minor changes that are indistinguishable from natural chance events.