text:
Complementary DNA synthesis
Does the reverse transcriptase enzyme recognize thymine to synthesize the complementary strand of cDNA?

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

One reason we do it as @theforestecologist suggests is that it avoids us repeating stuff at you that you already know or have already looked up.


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How does taxonomy work? The case of the Avian Dinosaurs
I recently discovered that the class Aves (or Birds) has been renamed Avian Dinosaurs. My question is when this taxonomic denomination achieved the consensus of the scientific community and through witch process, this change was made.

Freudian slip there. Witchcraft is a reasonable explanation.

There was a taxonomic revolution brought about by cladistics https://en.wikipedia.org/wiki/Cladistics. Willi Hennig wrote about it in 1950, but he was an East German, and his work did not gain traction in the West until it was translated into English in the late 1960s. Then it took a while to become consensus. Since then, all taxonomy is based on phylogenetic relationships. So for 100 years, we talked about "Reptiles" and knew what they were. Under phylogenetic taxonomy however, once we understood that birds were descended from theropod dinosaurs, nomenclatural rules require that birds ARE dinosaurs. This makes sense, because a Robin is more closely related to a Tyrannosaurus than a Tyrannosaurus is to an Iguanodon. Technically, taxonomy changes with the publication of phylogenies that make formal nomenclatural changes. Once a peer-reviewed paper is published, the names change. But sometimes phylogeny papers are sloppy, or wrong. So for something as major as Avian Dinosaurs, it would generally take more than just one sloppy paper to change consensus. Scientists now consider birds to be Dinosaurs. The public will continue thinking of Dinosaurs without birds. This is a difference between common names and scientific names. Birds are a subgroup of Dinosauria. Consensus depends on whether you are a scientist or not. Scientists now are at a consensus that Birds are derived from theropod dinosaurs, and therefore, ARE dinosaurs. The consensus of the public will lag behind.

Some other interesting phylogenies that render old names obsolete: Crustacea is paraphyletic. Crustaceans and Insects now form a group, Pancrustacea. Snakes are closely related to varanid lizards (are part of Lizards), so snakes ARE lizards, and both are in the group Squamata. Call them both squamates. There is no "Kingdom Protista", as protists are wildly polyphyletic.

The tree picture is only (mostly) accurate at the scale of at/above ~1million year separations and within plants or within animals+fungi, OR when considering an individual gene. Closely related species can interbreed (i.e. sapians + neanderthals), and if you try to put animals and plants into the same tree you run into endosymbiosis. Finally, bacteria swap genes so much the tree is significantly not-a-tree.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


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Chromosome size without heterochromatin
Im doing different analysis of the human chromosomes and diffent loci, however when using different databases, the heterochromatin structures are not part of the human genomes. I know that heterochromatin is a more dense structure within the DNA and stained differently and are not part of the different reference genomes.
However all the information regarding the human chromosome sizes, I can find all includes the heterochromatin regions.
So i would like to know, is there anywhere i can find the length of the human chromosomes without the heterochromatin structures?
Thanks for your time and help.

There are a couple of caveats that need to be addressed before answering this question:

We don't know all of the regions in the human genome that can be heterochromatic. In some cases large chunks of heterochromatin are simply missing from the genome assembly. For a somewhat outdated but still informative review of the topic see here.
Which regions are heterochromatic differs from cell to cell. For example, I would recommend reading about the differences between constitutive and facultative heterochromatin at wikipedia.
Heterochromatic regions of the genome are very important biologically and not taking them into account could be a mistake, though it depends on your motivations.

The human genome project initially estimated that 92% of their original genome build is euchromatic, 2.85 Gbp total. However that original genome build has been substantially updated. That estimate is close enough for many purposes, probably. But we've learned a lot about genome structure and biology since that time.
We do have a lot of data that is highly correlated with what we think of as heterochromatin. The UCSC human genome browser has a lot of information about chromatin modifications (I would look at the ENCODE analysis section here). In principle you can make educated guesses about regions of heterochromatin based on chromatin modifications. This will be somewhat noisy, and you will have to make decisions about which cell types are relevant, as they will have somewhat different regions.
For more information about which chromatin modifications might be relevant, you might start looking here. You will likely need to analyze some data yourself to find a more precise answer.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Does the Rayleigh formula apply to electron microscopes or only light microscopes?
I am asked to determine the resolving power of both a TEM (transmission electron microscope) and a SEM (scanning electron microscope) and given the Rayleigh formula below.
$$Resolution=\frac{0.61\lambda}{N.A.}$$
Where $\lambda=0.0039$nm since the wavelength of an electron is $0.039$ angstroms and $1Å=0.1$nm.
I am also told that the N.A. the numerical aperture for the TEM is $0.01$
So, $$Resolution=\frac{0.61(0.0039nm)}{0.01}=0.24nm$$
For the SEM I am not given the N.A. but I am told that the resolution is $10$nm
My problem is if I use the Rayleigh formula  $$Resolution=\frac{0.61\lambda}{N.A.}=10nm$$ I get $$N.A.=0.0002379$$ Which would imply that the aperture for the SEM is greater than that of TEM since N.A for TEM is $0.01$ and SEM is $0.00023$ $$0.01>0.00023$$.
My problem is that I'm told the greater the aperture (smaller value of aperture) the greater the resolution but as you can see from the equations above this doesn't seem to make sense, The only explanation I can think of is that the Rayleigh formula does not apply to electron microscopes. Any advice would be greatly appreciated thank you.

This is more than likely better asked in physics SE, however since you contextualized it biologically somewhat I will answer it here.
You are correct in your concern. The Rayleigh Criterion and the associated calculations(Rayleigh Scattering) are talking about the minimum separation of 2 light sources to resolve a given object. From this we are able to derive nice metrics like resolution and so forth. As you say, this describes the resolving of light wrt to the diffraction limit.
In order to calculate the resolving power of an SEM or TEM you need to do a different set of calculations.
First, the theoretical limit of EM microscope resolution is given by the De Broglie Wavelength of the accelerated electrons. However, as with the calculations for the Rayleigh Criterion, there are other factors to consider. For a full walkthrough see this. You take Abbe's equation for resolution in a perfect optical system, and take account of the other factors at play(optics for example).

The resolution of an SEM is not set by the electron wavelength, but rather by the size of the electron beam that is scanned over the sample. Imagine you had a flashlight scanning over a patch of ground, and were recording the reflected light intensity, without using any lenses, to reconstruct the surface features -- your resolution would be roughly the spot size, and not the Rayleigh limit. It's important to keep in mind that the Rayleigh limit is the best resolution one can have; it's easy to do worse!
A TEM, in contrast, does use lensing of electron beams, via magnetic fields.


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Bacterial Growth Formula
What are the units of $N$: the colonies of bacteria or the viable cell count?
This is in regards to the bacterial growth formula used during serial dilutions,
$$
N =N(0) e^{kt} \quad .
$$

Either; they're identical to the units of $N(0)$.  In $N =N(0) e^{kt}$,

$t$ has units of time (days, minutes, whatever you have chosen)
$k$ has units of (1/time) (inverse of $t$'s units)
$kt$ is thus unitless, as is $e^{kt}$
$N$ and $N(0)$ have the same units.

If $N$ is a number of something, like anything that is just a number, it is dimensionless and unitless, or with dimension and unit 1.
Note that in chemistry, the "amount" of a substance is not dimensionless but of dimension "amount of matter", with the mole as unit. It is however connected to the number (dimensionless and unitless) of elementary entities in this substance (whether they are atomes, molecules, etc.) through the Avogadro's constant ($N_A = 6,022 140 76 × 10^{23}$ mol$^{–1}$).
However, if your question is whether $N$ and $N(0)$ count the number of individual cells or the number of colonies, I think there is some confusion in your question as the number of colonies (after plating) is a proxi for quantifying the number of viable cells at the moment of plating. But you cannot apply the formula directly to the "number of colonies" since once plated this number will not increase exponentially but stay constant. So $N$ and $N(0)$ refer to the number of (viable) cells.


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How much Oxygen can the Human body carry?
Basically - the title: How much Oxygen does a human body carry at a single point?

What have I tried: A friend of mine has done some calculations and came up with the following numbers. Neither of us are biologists or have higher degrees in biology. His calculation went something like:

Our body absorbs about 0.033g of Oxygen when we inhale (source).

That's about 0.00103 moles of oxygen.
Through ATP reaction that's about 0.00515 moles of ATP

We have 270 millions of hemoglobin per red blood cell, and roughly 25 trillions of blood cells in our body (wiki), and each Hemoglobin molecule "carries" up to 4 oxygen molecules.
Thus, in total, our body's hemoglobin can carry about (2.5 * 10^13) * (270 * 10^6) * 4 = 1.437 grams of oxygen

How far is the 1.437g number have?
Related (but not the same question) question I found here: How much energy we get from oxygen?.
Note: this is specifically about oxygen we use in our respiratory system - and not the oxygen in the water :]

What do you mean by "carry"?  My first thought is a strong person carrying a large Dewar vessel full of liquid oxygen :-)

@jamesqf as in - "our blood carries oxygen through our body - how much oxygen does it carry at a given point?"

Don't forget that all of the water and many of the organic compounds in our bodies also contain oxygen...

Presumably you have your own reasons for asking this question, but you should not be surprised if nobody else is interested unless you explain why it is of interest.

@David I am interested in this because it is interesting and because we are trying to practice doing these calculations as non-biologists :]

Fair enough. This sort of thing is a minority interest, but you may find a physiologist on the list who does these types of calculations.

@David that is fair, this site and community does not owe me an answer and I am not entitled to anyone's help. I am just hoping that someone who also finds this interesting but has more technical competence than me takes a look and does the calculations better than me.


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Where to find a list of genes coding for protein in human
I have raw read counts extracted by htseq from STAR alignment
I have both data with both Ensembl IDs and gene symbols, but I need only a latest list of protein coding genes in human; I googled but I did not find
Any suggestion please?

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done (e.g., what search terms), what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Submit your ensembl IDs to biomart, and get the "gene biotype".  "protein-coding" is one of the options there.


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Species identification: 2.5mm (3/32" or 1.5/8") brownish ant in highrise apartment
Can anyone please identify this ant?
In case it helps, 3 attempts of using Ortho Ant Bgon Max gel and bait has not helped.  They 2 were administered 2 weeks apart.  Apparently, it's basically borax and sugar water.
A respondent at this DIY Stack Exchange page referred me to "Ant Identification Keys" section at this site.  It seems that it may be a 2-node Big-Headed Ant, but it's hard to be sure.
Photos:

Update:
Location: Ottawa, Ontario (Canada); latitude 45 degrees north. It's an urban centre, and my highrise is by a main city street, but also with a creek on one side. I first noticed the ants in the kitchen in July, at the height of our summer heat, or perhaps at the tail end of it. I'm rent a 1-bedroom apartment on the 9th floor, facing the creek side and the major street.
Of possible relevance: The neighbour on my kitchen side says that he has never seen an ant. My unit is quite clean, with the only exception that I generate so little garbage that I change it infrequently. I spray inside with alcohol several times a day so that I'm not ravishing the environment by changing bags frequently. Most of the content are fruit/veggy peels/cuttings (no meats/fats or starch), and mostly oranges, which ants apparently hate. I've recently sprayed and wiped down the garbage in order to not use it until I've solved my ant problem.
Since paying close attention, I notice the ants on the floor and upper cupboards, whereas I only saw them before when they crossed the counter. Back then, I thought the ants were attracted to water from a leak that I found under the kitchen sink, or the dampened particle board due to water seeping from the rim of the sink. The latter would suggest carpenter ants, which like sweet things, like the borax/sugar mix that my store-bought baits were apparently based on.  However, the 2.5mm size of my foraging ants are much smaller than the 6-25mm described by this local federal government site.  My ants' 3/32" is also much smaller than the 6/32"+ C. sayi carpenter ant described here.
The leak has been repaired for about 2 months, and I've taken care to wipe up around the sink. No apparent relief from the ants, and the bait is mostly untouched. I'm wondering if the ants may be coming from elsewhere.  Upon reflection, however, I do recall seeing what might bhe the calling card of carpenter ants for years -- fine wood chips under some of the bottom hinges of the cabinet and cupboard doors in the kitchen.  It literally took years for them to accumulate to the point of noticability.  Maybe carpenter ants been visiting for years, and only this summer decided to move in.

Hi. It seems your previous post was closed as homework because it showed little research effort on your part (see our homework policy to make sense of that). Two important parts of our policy require that the question not be trivial and that you demonstrate your own research effort. The question in your previous post was essentially is this an ant or a termite?. These two insects are quite different, and even a simple <1 min Google search would have demonstrated it was an ant and not a termite. As such, the community voted to close.

This new post is much improved. It's a much more focused post that provides much of the necessary info that [tag:species-identification] posts require, it asks a non-trivial question (ants are hard to ID to lower taxonomic levels!), and you've adequately demonstrated that you've done your own research and provided what seems like an educated guess. As such, I suspect this post will be much more positively received here. Good job, thanks for the effort, and I hope you get your answer!

According to the pest control expert, the ants are likely pharaoh ants.  It matches the description on the Wikipedia page in all respects:

Colour
Size
Pervasiveness in indoor environments throughout the world

He is treating the problem in my unit and a neighbour's unit using Maxforce Quantum.  It could take some time :( .
This is not conducive to a fitness regime of pushups, situps, leg lifts, and side planks (all on the ground, of course).  It doesn't help that my apartment largely has wall-to-wall carpeting coloured with a brown and white texture.  Spraying down the vicinity with vinegar is unlikely to help, as the ants have clearly demonstrated a lack of repulsion from vinegar droplets.


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Why are human mothers told to "push" out a baby?
I've always wondered why human mothers are instructed to "push" when giving birth.
Every other animal just gives birth of it's own accord. Albeit perhaps from a different position with the help of gravity. You don't have to tell a giraffe to push.
But for some reason humans feel like mothers can only give birth through conscious will power.
Surely, if the mother just let the body do it's natural thing, the baby would come out just the same.
What's more, I would expect that if the mother was consciously "pushing" using the wrong muscles this would hinder rather than help the birth. (Does a woman even have mental control over this?)
Also, what's the rush? As long as the umblical cord is still attached, should it matter how long the birth takes?
When did this idea of telling the mother to "push" first start, and is it common practice around the world?
Here is an article which questions this idea: https://curiosity.com/topics/should-we-stop-telling-women-to-push-during-labor-curiosity/

Also like telling the husband to go out and chop wood - keeps the attention where it is needed...

@Solar But I've read that no attention is needed. As animals can give birth even if unconscious. Actually I read that a hospital in Kent England, has recently stopped telling mothers to push and it actually has reduced stiches and such-like and that this only started in the 1920's as more mothers gave birth in hospitals.

Now you should update your question...

@arsak https://curiosity.com/topics/should-we-stop-telling-women-to-push-during-labor-curiosity/


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Is there any evidence that genes which are associated with physically adjacent structures are located near each other within the genome?
I am not sure if there are individual genes for, say, fingers and if so, would such genes be near the genes that affect hand growth? If not "near" in the Euclidean sense, could there be a different metric where genes for associated structures could be considered near?

There aren’t genes for fingers, and the answer to the question of whether genes for associated functions are physically associated in the genome depends on the organism. You need to research the genetics of limb development before asking this sort of specific question.

@David: can you suggest links or search terms? I of course did try to search but got only general results. If there is an organism which had this property, can you give me an example? I am not merely interested in limb development but general rules for how the genome is laid out.

I shouldn’t answer in comments, but if you were hoping there were rules — in anything other than bacteria — I’m afraid you will be disappointed. Try searching for operons and gene clusters.

https://en.m.wikipedia.org/wiki/Hox_gene#Colinearity

@canadianer — You really ought to answer rather than comment, as the example you give would appear to be the exception rather than the rule, which the poor computer scientist (for I imagine that is what the poster is) will get the wrong impression.

@David: pretty good guess except I am a comfortable (by no means wealthy) computer scientist.

@releseabe — Apologies for the "poor", but both on this list and in life I have repeatedly encountered numerical scientists interested in finding problems in biology to apply their skills to. Among the problems that arise are 1. Biology (even the molecular variety) doesn't genearlly follow clean rules, 2. The low-hanging fruit has already been picked, 3. Although biology is intellectually stupid (speaking as an ex-chemist) you need to learn some to understand the problems.(Others on the list will hate me for saying this.)


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Medical terminology for asymmetrically-shaped paired body parts?
Some people have different sized feet [source], a limb that is slightly longer than the contralateral (on other side of the body) limb [source], or other instances of paired body parts being different sizes.
These size differences in paired body parts on the same individual is referred to as hemihypertrophy (or hemihyperplasia).
However, what is the terminology used to describe variation of shape/form of paired contralateral body structures?

In other words, what is the general term for contralateral asymmetry?

For example, some women's breasts are asymmetrically shaped ("breast asymmetry"), and some people's fingers are different shapes (for example, unilateral brachydactyly type D).

 Source: Wikipedia
I assume a term other than "asymmetry" is used, but I have not come across any such generalized terminology.


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Why does mold grow on silicone caulk?
I notice mold likes to grow on silicone caulk. I find it odd since silicone is mostly inorganic and doesn't contain any nutrients for mold to grow on unlike soil and clothing. Can mold metabolize silicon?

Can you please post a picture?

The EPA has outlawed certain fungicides from time to time ; it takes time for manufacturers to develop new ones. I have caulk around some windows that has turned black with mold but a nearby window with different caulk is still white . The windows are about 10 years old . 25 year old original caulk is still white . (These are all exterior exposures). It depends on the mold inhibitors available at the time.

This product brochure seems to give a reasonable explanation:

The following conditions help to form mould on sealants:

High air humidity with little movement of air, eg: in bathrooms, showers, kitchens etc.
Warmth
Nutrients in the form of organic deposits. e.g. residues from body care materials
  such as soap, shower gel etc.

Since elastic silicone joints have low thermal conductivity they are the warmest part of a tiled surface and where mould thrives best, in combination with organic residues and moisture.


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Protein function and how it does not get affected with amino acid
How is it possible that a protein's function is not changed when an amino acid within it is replaced?

Good question. But it’s your homework, so you’re the one who is supposed to answer. Read the Tour and the Help on Homework questions.

The side chains of some amino acids are not reactive and therefore not involved in any covalent chemistry in enzyme active centers.
Isoleucine, an essential amino acid, is one of the three amino acids having branched hydrocarbon side chains. It is usually interchangeable with leucine and occasionally with valine in proteins.
Typical amino acids and their alternatives usually have similar physicochemical properties.
Amino acid replacement is a change from one amino acid to a different amino acid in a protein due to point mutation in the corresponding DNA sequence. It is caused by nonsynonymous missense mutation which changes the codon sequence to code for another amino acid instead of the original.
The effects of amino acid replacement may vary depending on how similar or dissimilar the replaced amino acids are, as well as on their position in the sequence or the structure.
References:
http://www.biology.arizona.edu/biochemistry/problem_sets/aa/Isoleusine.html
https://en.wikipedia.org/wiki/Amino_acid_replacement

Please do not answer obvious homework questions where the poster has made no attempt to answer himself.  That is against site policy and, in effect, you are helping the poster to cheat.

@david you seem to be on a mission when it comes to new users. I understand you have good intentions in mind but maybe your actions could be a double-edged sword which on one side cleans SE up but on the other side sterilizes if from new users. Is your subjective opinion that this is a homework post. I like the question so I answered. Did the question/answer set make SE a little bit richer place? You could have suggested to edit the question or something

— I do not normally respond to personal remarks: I just flag them to the moderators for deletion. However as you are a relatively new user, let me explain to you something about how SE works. It is regulated (for want of a better word) by its users, according to their status in the list. Elected moderators are the final adjudicators, and in this case I imagine one of them closed the question quickly. Users who have accumulated a certain number of points are asked to help by considering close votes, commenting to new users etc. That is what I was doing — my civic duty.

@David can be a bit cranky and blunt, and I do wish he would work on being more welcoming, but I think most of the time he's correct even if the message could be delivered differently. In this particular case, I think the question is a clear homework question, and unfortunately, people that ask a question like this are likely to just copy paste from your answer into the box on their quiz and not learn anything: that's why Biology.SE has a homework policy that differs from some other SE sites. Here's a good meta thread: https://biology.meta.stackexchange.com/questions/3377/homework-questions

@BryanKrause I understand and agree. However:) different biology enthusiasts are on different educational level. A layman or a teenager's question might come off as homework attempt. I realize that I won't change anyone's mind but since we are talking about it - Instead of making people feel unwelcome, how about answering all valid questions which don't contain "help, homework, urgent keywords" and then in the future close the obvious qeustions as duplicate. Having the obvious question/answer sets would bring a lot more search engine traffic and make this place bigger, richer.

@TardiGrade I think it's explained well in that meta thread, so I don't want to rehash it here, but tl;dr: because answering those questions does active harm. I consider it unethical to help people cheat, especially when the person they are cheating the most is themselves. We are happy to help people with their homework when they've demonstrated effort. If you want this policy to change you can make a case on Meta.


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What's it called when a male seahorse gets "inseminated"?
I am looking for the scientific term for the process where a male seahorse receives eggs from the female. For example, we usually say, "the male inseminates the female with sperm." What is the correct term to use for seahorses? Would you say "the female inseminates the male with eggs", or is another term more appropriate?

Short answer
I think that "egg deposition" by means of the female "ovipositor" seems the most commonly used terminology.
Background
A cursory Google search yielded quite a few alternatives, ordered here from the most fancy to the least:

...that are deposited directly into the brood pouch ... (Look et al., 2007)
...transferring their eggs directly into the male brood pouch... (Masonjones & Lewis, 1997)
...the female injects her eggs into the male’s pouch using her penis-like ovipositor
...once all the eggs are inserted

References
- Look et al., J Exp Biol (2007); 210: 432-7
- Masonjones & Lewis, Copeia 1996; (3): 634-40


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Human evolutionary innovation for rapidly restoring glycogen, and link to cardiovascular disease?
I'm a physicist, not a biologist, but I'm interested in human evolution and its link to the physiology of endurance sports. Circa August 2019, I read an article in the newspaper whose contents I'll summarize below from memory. I mentioned this to a colleague who teaches anatomy and physiology, and he said that it sounded not very credible. I told him I'd find the article and send him a link, but I wasn't able to find it again. I'm wondering if anyone can help me find the original scientific paper, or a popularization.
According to this account, humans have a mutation, not present in other primates, so that when we eat, our glycogen stores are replenished quite a bit faster -- maybe by a factor of 2 or something. Of course digestion is complicated, and the speed of digestion depends on the macronutrient and even on the subtype of that macronutrient (e.g., we probably process maltodextrin faster than whole-wheat bread), but for typical foods I think the idea was that a human would rebuild their liver and muscle glycogen reserves in a few hours, as oppose to twice that for other primates.
The article also said that this evolutionary innovation had a cost associated with it -- that it led to an increased susceptibility to certain types of cardiovascular disease, which our close relatives don't get as easily.

Be careful, increased cardiovascular disease in humans could just be due to our upright stance. that puts a lot more pressure on our cardiovascular system for our body mass.

@John, I don't think Ben Cromwell is asking about the biology but is requesting if the specific article can be found or if there is any evidence supporting that "narrative".

A 2017 review by Oldfors suggested to me that mutations in glycogenins might be involved, but I have been unable to find any subsequent reports to substantiate this, and nothing regarding differences between human and non-human primates.

Summary

We (Homo genus) used a lot more glycogen as we sweated while we foraged.
Our efficient metabolism allowed us to replete our glycogen stores with seemingly little trade-off.
Those same metabolic genes are associated with obesity risk
Obesity is a risk factor for heart disease

Sweat uses glycogen
...and lots of sweating was beneficial for our species survival
I think what you are indirectly asking about, as unlikely as it seems, is sweat production.
It is known that humans have a large number of eccrine sweat glands compared to other animals, for which glycogen is the primary energy substrate.
The ability to thermally vent via full-body eccrine sweat glands in this way, in conjunction with bipedalism, allowed foraging in the midday heat when predation is low.
This is limited to the genus Homo (Leiberman, 2015), although it is not clear exactly which mutations are responsible as far as I can tell.
Glycogen stores are more supported by their capillaries, and by extension have faster repletion, in primates in hotter drier climates and indeed in humans (Best & Kamilar, 2018).
Now at this point, you are thinking "Aha! More capillaries mean more pressure on the cardiovascular system and more disease".
I cannot find any evidence directly linking those two.
A note on glycogen production differences in our close relatives
The 1,4-alpha-glucan-branching enzyme indeed seems similar across close species.
So either we have relatively larger livers to cope with this, or some complex genetic mechanism produces more of the protein.
A quick BLAST alignment shows the identity of the 1,4-alpha-glucan-branching enzyme of chimpanzee species at >99% and E~0. The top results are shown below:

Entry   Organism    Organism ID Info            Status

Q04446  Homo sapiens (Human)    9606    E-value: 0.0;   Score: 3,814;   Ident.: 100.0%      reviewed
A0A2R9CB94  Pan paniscus (Pygmy chimpanzee) (Bonobo)    9597    E-value: 0.0;   Score: 3,803;   Ident.: 99.6%       unreviewed
H2QMY2  Pan troglodytes (Chimpanzee)    9598    E-value: 0.0;   Score: 3,803;   Ident.: 99.6%       unreviewed
G3SDH8  Gorilla gorilla gorilla (Western lowland gorilla)   9595    E-value: 0.0;   Score: 3,798;   Ident.: 99.4%       unreviewed
A0A096NQ25  Papio anubis (Olive baboon) 9555    E-value: 0.0;   Score: 3,729;   Ident.: 97.6%       unreviewed
A0A2K6ANP2  Macaca nemestrina (Pig-tailed macaque)  9545    E-value: 0.0;   Score: 3,723;   Ident.: 97.3%       unreviewed
A0A0D9R0S5  Chlorocebus sabaeus (Green monkey) (Cercopithecus sabaeus)  60711   E-value: 0.0;   Score: 3,718;   Ident.: 97.4%       unreviewed
A0A2K5W1V0  Macaca fascicularis (Crab-eating macaque) (Cynomolgus monkey)   9541    E-value: 0.0;   Score: 3,716;   Ident.: 97.2%       unreviewed
A0A2I3GDY3  Nomascus leucogenys (Northern white-cheeked gibbon) (Hylobates leucogenys)  61853   E-value: 0.0;   Score: 3,714;   Ident.: 97.2%       unreviewed
A0A2K5I4Z7  Colobus angolensis palliatus (Peters' Angolan colobus)  336983  E-value: 0.0;   Score: 3,713;   Ident.: 96.7%       unreviewed
A0A1D5R8L3  Macaca mulatta (Rhesus macaque) 9544    E-value: 0.0;   Score: 3,712;   Ident.: 97.2%       unreviewed
A0A2K6KT87  Rhinopithecus bieti (Black snub-nosed monkey) (Pygathrix bieti) 61621   E-value: 0.0;   Score: 3,705;   Ident.: 96.9%       unreviewed
A0A2K6PB45  Rhinopithecus roxellana (Golden snub-nosed monkey) (Pygathrix roxellana)    61622   E-value: 0.0;   Score: 3,699;   Ident.: 96.7%       unreviewed
A0A2R9CB98  Pan paniscus (Pygmy chimpanzee) (Bonobo)    9597    E-value: 0.0;   Score: 3,680;   Ident.: 99.0%       unreviewed
A0A2I3T5K0  Pan troglodytes (Chimpanzee)    9598    E-value: 0.0;   Score: 3,680;   Ident.: 99.0%       unreviewed
A0A2I2ZFX5  Gorilla gorilla gorilla (Western lowland gorilla)   9595    E-value: 0.0;   Score: 3,675;   Ident.: 98.8%       unreviewed
A0A2K5QWD9  Cebus capucinus imitator    1737458 E-value: 0.0;   Score: 3,665;   Ident.: 96.0%       unreviewed
A0A2K6SM68  Saimiri boliviensis boliviensis (Bolivian squirrel monkey)  39432   E-value: 0.0;   Score: 3,661;   Ident.: 95.9%       unreviewed
F7FDF1  Callithrix jacchus (White-tufted-ear marmoset)  9483    E-value: 0.0;   Score: 3,627;   Ident.: 96.0%       unreviewed
A0A2K6ANP4  Macaca nemestrina (Pig-tailed macaque)  9545    E-value: 0.0;   Score: 3,610;   Ident.: 95.3%       unreviewed
A0A2I3MXY4  Papio anubis (Olive baboon) 9555    E-value: 0.0;   Score: 3,607;   Ident.: 96.9%       unreviewed

Although this is only one protein of a multi-protein metabolic pathway, I think there must be something much more complex about how our glycogen is repleted to deal with the higher demand than simple differences in proteins.
Increase metabolism and disease
Humans have benefitted from a "thrifty genotype" when it comes to metabolism (Neel, 1999).
This, and the well-cited 1962 paper it is based on linking our faster metabolism to diabetes (Neel, 1962), may indeed be the paper you are looking for, but in my personal opinion, it is not very quantitative by today's standards and comes from the days before we had access to genomic data.
Although glycogen is only part of the story, it is generally accepted in the community that humans have an optimised metabolism. In terms of disease related to our metabolic evolution, GWAS showed that the genes that allow our increased metabolic activity is linked with obesity risk factors (Castillo et al., 2017).
To link that to your original question, obesity is linked with heart disease according to, well, everyone that has ever looked at it. Here is an NHS link to show it is a principal part of modern healthcare.
It may not be the exact answer you were expecting, so it will be fascinating if other papers corroborate this more directly.
Big brains need a faster metabolism
The scipop article you may have read could be from Science Daily, however this does not mention glycogen. This covers the Pontzer et al., 2016 paper which shows that we have a faster metabolism and this is linked with our brain size compared to our close primate relatives (another angle to the Leiberman 2015 paper discussed below).
The scipop article goes on to talk about research linking this to an increased risk of heart disease, not mentioned in the original Nature article.

One hell of an explanation, credible in many ways

This is interesting and well written, thanks. It's not the info I was looking for, but all cool stuff to know about, e.g., I hadn't known there was glycogen elsewhere than in muscles and the liver.

@BenCrowell Yes, I've been trying to dig around for the news article, but with no success... However, I hope the principles here show that fundamentally what you read about was probably correct and has scientific underpinning in the literature. The last piece of the puzzle; I can't find any straightforward metabolic data about repletion rates directly comparing primates.


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Cheap enzyme assay for a high school lab
At the moment, I'm designing an experiment for a high school lab with no financial resources. I need to assess the impact of a variety of factors on a specific enzyme's reaction with its respective substrate and determine the rate of reaction. Normally this would require some combination of an assay kit and a plate reader. Though cheaper versions of the former are within my budget, the latter is not.
What are the cheapest ways you can think of to:
1) Get access to enzymes and the substrate;
2) Make them react in a controlled manner;
and 3) Assess the rate of reaction from the resultant substance?

Do you have a specific enzyme and substrate in mind?

No specific enzyme or substrate in mind. The only condition is that it can't be amylase.

There is the classic potato starch/iodine/amylase experiment:
http://dailynexus.com/2016-08-31/chemistry-101-the-classic-potato-iodine-blueblack-experiment-finally-has-an-explanation/
From memory, when you add iodine to a small piece of potato, the potato starch reacts to produce a dark blue/black colour.  The amylase enzyme in human saliva can break down the starch and remove the colour, which is effected by spitting into the test tube.
You might need to try titrations to work out how to do number 3.

How specifically would I use titrations?

That's a good question.  Now I think about it, I don't know how you would be able to assess the rate of reaction. My thought was to try increasing amounts of saliva until some kind of threshold was reached, but I don't know if that helps at all.

Someone has already mentioned catalase and potatoes, but another way to do it would be to use hydrogen peroxide. The students could cut the potato up smaller to investigate the impact of surface area, heat/cool the mixture using a beaker with water in and a thermometer, and change the amount of potato used. So a few variations of conditions for a fairly low cost!
To measure rates, you can pop a bung attached to a tube and gas syringe onto the test tube when the potato is added, and record the volume of oxygen evolved within a given period of time, or the amount present at different time points (say, every thirty seconds). Lots of fun graph drawing for the students, and they can work out the initial rate of reaction etc! :)
If you're looking for a qualitative result, this experiment produces bubbles and foams up so you can go for which reaction produces the greatest height of bubbles in the tube. Perhaps the students could measure this height with a ruler to get quantative data?
I hope this is helpful!

In order to set up an enzyme assay that allows quantitative kinetic analysis three key requirements come to mind:

The assay should be sensitive
A plot of velocity versus enzyme concentration should be linear and through the origin at both high and low substrate concentrations.
The initial rate should be measured.

Spectrophotometric Assays
Spectrophotometry is a very versatile method for measuring changes in absorbance with time, and if an enzyme produces a product that differs in absorbance (at a given wavelength) from that of the substrate, this can be the basis of a very convenient assay: NAD(P)H absorbs at 340nm whereas NAD$^+$ does not, for example
Furthermore, if the extinction coefficient is known (6220 M$^{-1}$ cm$^{-1}$ for NADH), initial rates may be quantitatively expressed as micromoles of product formed/minute (rather than change in absorbance per min).
Things are even easier if the chromogen absorbs in the visible region.
The p-nitro-phenolate anion is yellow, for instance, and any enzyme that produces p-nitro-phenol from a colorless (or near colorless) substrate at relatively high pH may be assayed by monitoring the increase in absorbance at about 400nm.
A further advantage is that the extinction coefficient is high (Dawson quotes a figure of 18000 M$^{-1}$ cm$^{-1}$ for p-nitro-phenol at pH 8-9 and 400nm, making this assay method roughly three times more sensitive than NAD/NADH).

If spectrophotometry is the chosen method, a valid assay requires that The Beer-Lambert law be obeyed within the absorbance range of the experiment.

Possible Examples
Alkaline phosphatase may be assayed with p-nitrophenylphosphate as substrate, producing yellow p-nitro-phenol as product. Thus recording the  increase in absorbance at about 400nm with time is the basis of a valid, sensitive assay.
In addition, many proteases and esterases may be assayed with p-nitro-phenylacetate, where the action of the enzyme also produces p-nitro-phenol as product. This includes chymotrypsin.
Both p-nitro-phenylphosphate and p-nitro-phenylacetate these are relatively cheap.
Another possibility is mushroom tyrosinase, which may be assayed spectrophotometically by measuring the decrease in absorbance at  475nm due to the formation of DOPA-quinone from L-DOPA, and there is a very concise and detailed description available.
There are many other possibilities.
Smartphone 'Spectrophometer'
The problem with spectrophotometry is that equipment is expensive.  However, a number of authors, have shown that smartphones may be used as 'spectrophotometers' in the visible region.
A very simple and effective method has been described by Kuntzleman & Jacobson (2016), and Kuntzlman has posted an outstanding blog which includes a YouTube video that describes the method in detail.
To understand the method, we need to be aware that a colored solution absorbs light in the region of its complementary color. A solution appears red (to us humans) because green light is absorbed. A yellow-orange solution absorbs (mainly) blue light.  (Complementary color may be obtained by consulting a colorwheel)
The method uses a  smartphone camera, together with an App to give average red, green and blue (RGB) values for pixels found in a 'detection circle'.
Light reflected from a background complementary to the color of the solution of interest is passed through the solution and is detected by the camera by noting the decrease in either the R, G or B value.
Other than a smartphone, all that is needed is a cardboard box with holes cut to accommodate a cuvette or other vessel and a sheet of paper or cardboard colored in the complementary color, which is placed behind the cuvette (to reflect light of the appropriate wavelength through the solution).
In the video example, red light is detected by using a green background and recording the decrease in G value.   The Beer-Lambert law was then be used to convert G values to absorbance. (The video even includes a spreadsheet example showing how to do this).
It should be easy to adapt this method for use in enzyme assay. Use of a timer is all that is required to record changes in absorbance with time, thus allowing the initial rate to be estimated.
There is one caveat.  The App by Kuntzleman is colorometer and this does not seem to be available for iPhone 7 and higher.  However, it appears that the App is still functional on Android devices.
References

Use Your Smartphone as an "Absorption Spectrophotometer" [Tom Kuntzleman blog]
Kuntzleman,TS & Jacobson, EC (2016) Teaching Beer’s Law and Absorption Spectrophotometry with a Smart Phone: A Substantially Simplified Protocol J. Chem. Educ. 93, 1249-1252 [ACS Site]
Smartphone "Spectrophotometer" [YouTube]
Rodriquez, MO & Flurkey, WH.  (1992) Biochemistry Project To Study Mushroom Tyrosinase. Enzyme Localization, Isoenzymes, and Detergent Activation J. Chem. Educ. 69 767 [ACS Site]

So, using a the colorometer, how would I ascertain the hydrogen peroxide content of a given solution?

Catalase from blood. Prick your finger,  collect a small amount of blood. Add some hydrogen peroxide to the blood, it will foam as the catalase decomposes the hydrogen peroxide. Obviously there are biohazard considerations when dealing with human blood. Some plants, notable horseradish also contain peroxidase if you wish to avoid pinpricks.

NO. You can’t do this sort of thing anymore! Not in Britain at least. We used to have medical students do blood glucose on themselves after fasting. That was pre-HIV. Not now. Don’t go there.

So, what substrate would you recommend I use? Additionally, how would I assess the rate of reaction?

The substrate is the hydrogen peroxide, the enzyme is contained on blood, horseradish, and a number of microorganisms. You can assess the rate of reaction by observing the bubbles produced, or collecting the oxygen in an inverted jar filled with water. David: calm down. What happens when someone gets a bloody nose or scrapes their knee? Do we call a hazmat team and incinerate the waste? No, we throw them in the trash and move on. Certainly the teacher could prick their own finger to obtain less than 20uL of blood for the sake of an experiment.

In theory you could buy some blood from a local butchers' so it's not that bad of an idea. But you'd have to check with health and safety due to the risk of blood borne diseases and religious concerns. Surely if you can dissect kidneys in class, you can use a test tube of blood though


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How are new antigens recognised by the body?
I understand that non-self cells are engulfed by APCs, and are recognised by Helper T cells for the cell-mediated response to occur, but the Helper T cell must have the specific binding for such an interaction to occur surely? How are such new binding sites available in naive Helper T cells for the recognition of the antigen to occur?

Helper T cell (CD4+) with it's T cell receptors (TCRs) can only recognize an antigen when it is complexed with major histocompatibility complex (MHC class II) molecules on the surface of other cells. T cell receptor binds to the MHC-antigen complex.
This guy explains it very well https://youtu.be/TadJkUCJLHo
references:
https://www.sciencedirect.com/topics/neuroscience/mhc-class-ii


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What causes sodium channels to open?
What triggers the opening of sodium channels in a neuronal membrane? Is it acetylcholine that activates sodium channels in the postsynaptic membrane?
Are sodium channels like receptors that have to bind to something (like a protein or an ion) to open? If so, what is the substance that forces Na+ channels to open?

Sodium channels are primarily voltage-gated - these are the channels responsible for action potentials.
Many other receptors are ligand-gated, and these are typically the signal that causes the initial voltage change that opens the voltage-gated sodium channels; however, these channels are less selective cation channels and are permeable to ions like potassium as well as sodium. Still, their permeability to sodium is quite important and so they may also be thought of as sodium channels sometimes.
These include neurotransmitter gated channels like nicotinic acetylcholine receptors and AMPA (glutamate) receptors, and transient receptor potential channels like the TRPV1 receptor that is sensitive to painful heat and the chemical capsaicin which makes chili peppers "hot."

Thanks for the answer but I'm still confused. The Wikipedia link says that a change in the cell's membrane causes a change in the state of nearby Na+ channels and opens them. But I thought that a change in the membrane's electric potential (i.e. action potential?) is possible after the sodium channels have opened already and not before it. So, how can the cell's membrane potential change if no sodium ions have entered the cell yet? Do you see what I'm trying to say? I'm afraid that I'm not explaining myself well.

@stressedout Action potentials are driven by a positive feedback loop among voltage-gated sodium channels once a cell is depolarized enough. The initial depolarization is not an action potential and comes from someplace else, usually the ligand-gated channels I described. I recommend a basic textbook on neurobiology like Purves' "Neuroscience" or Kandel's "Principles of Neural Science" - both will explain this in detail.


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What pH ranges are used in industrial scale fermentation?
When reading

Hans-Peter Meyer, Wolfgang Minas, and Diego Schmidhalter (2017) Industrial-Scale Fermentation. Industrial Biotechnology: Products and Processes, First Edition. Edited by Christoph Wittmann and James C. Liao.
  © 2017 Wiley-VCH Verlag GmbH & Co. KGaA. Published 2017 by Wiley-VCH Verlag GmbH & Co. KGaA.

I came across the following passage describing industrial up-scaling of fermentation processes (in general):

1.3.1
Process Development – Scale-Up Starts at Laboratory Scale
Process scale-up should be considered early on while the biological expression
  system is still under development. Factors such as genetic stability for at least
  the number of generations needed for a scaled-up production, and the need and
  impact on the environment of selection markers, should be evaluated before
  process development is started. The use of antibiotics as selective markers in the
  production medium should be avoided. Throughout development of media and
  cultivation conditions, it is important that parameter settings remain realistic and
  scalable, always indicated with upper and lower limits reflecting the safe operating
  range (process design space), for example, pH 7 ± 0.3.

I am quite surprised about the narrow pH range specified (pH $7 \pm 0.3$). I assumed that the pH range would be much wider, similar to lab scale. Is this really common practice?

Fermentation pH will differ a great deal depending on the bacteria or fungi being used and the process. But it is not uncommon to have a relatively narrow range of pH as a target. Remember pH is the -log[H+] so the pH scale is not linear. Also some fermentation reaction involve very expensive pharmaceuticals or intermediates, a single fermentation batch may have a value in the hundreds of thousands of dollars so keeping +/- 0.3 range in pH is trivial.


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"Spontaneous Immortalization"
HaCaT keratinocytes are described as "spontaneously immortalized "(see paper below) due to aneuploidy or chromosomal alteration.
From the paper I get that this is a literal term, that the cells just continued growing (?) in vitro and never went into senescence without any "human-induced" transformation.
Is this a common procedure for cell immortalization or a rather rare example?
[http://jcb.rupress.org/content/106/3/761.long][1]

It depends how you define it. Many early cell lines (as well as some modern ones) were derived from tumors. Tumors are spontaneously immortalized cells which became immortalized in vivo. If you're asking how often researchers collect primary cells (non immortalized) and grow them with the hopes they will become immortal the answer is pretty much never.


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Do ringneck parrots reject eggs of other parrots in their nest / eggs touched by humans?
I've put up artificial parrot homes in my terrace. Parrots have been nesting there and have laid eggs in them.
Of late i have been observing a large gathering of crows and a few hawks perching in the nearby trees, like never before,  presumably due to the large number of artificial nests and feeders that i've put up for sparrows and parrots.
I observed that in one of the parrot nests, the mother/father haven't returned for almost a week now, and i'm worried for the eggs.
1) If i transport them secretly to another nest, will the host couple accept them ?
2) Can parrots sense if humans touch their eggs ? Will they reject them?


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How many plants or trees should one plant to take carbon dioxide from atmosphere?
I'm interested on computing things. I know that some biologists have done mathematical modelling. Has anyone took any calculations on the following?
How many trees or plants should one plant such that those plants takes more $CO_2$ from atmosphere than human uses in his or her life? Feel free to make reasonable assumptions.


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Are neurotransmitters part of the endocrine system?
I was speaking with a substitute teacher of mine, and we were discussing whether neurotransmitters are part of the endocrine system or not. My class just spent an entire semester on the topic of the endocrine and nervous systems. From my knowledge, they are not part of the same system, because they function very differently and they are not activated by the same triggers. Does anyone have any info on this subject? I am interested what the case is an why.

I think that the "neuroendocrine system" is a better way to think about hormones and their regulation. Without neurotransmitters, the brain could not inform many of  the body's glands that hormones need to be secreted, e.g. the pituitary gland's secretion of TSH, FSH, LH, oxytocin, etc. Separating them is fine for study, but in reality, they often work together.

I think the reason is because neurons don`t deliver their contents into the blood stream.

Short answer
Synaptic signaling can be seen as a type of paracrine signaling, and is hence not an example of an endocrine system.
Background
Khan Academy has a nice accessible overview on this confusing topic:
Paracrine signaling
Signalling between nearby cells that are near one another van occur through the release of chemical messengers that diffuse through the intercellular space. This relatively short-distance communication is called paracrine signaling. Notable paracrine signaling occurs during development, where growth-hormone gradients regulate the differentiation of the various tissues.
Synaptic signaling
A unique type of paracrine signaling occurs between neuronal cells, namely synaptic signaling.
Autocrine signaling
Autocrine signaling refers to cell signaling to itself. Like paracrine signaling, autocrine signaling is important during development, but also in tumor metastasis.
Endocrine signaling
Communication over longer distances often occurs through the circulatory system is called endocrine signaling. Often it occurs through the release of hormones into the bloodstream. Hormones are produced and released by specialized cells and target cells in distant parts of the body. Endocrine glands include the thyroid, hypothalamus, and the pituitary, among others. For example, the pituitary in the brain releases growth hormone that affects growth and other functions throughout the body.
Juxtracrine signaling
Cells can also interact via direct contact. For instance, gap junctions in animals and plasmodesmata in plants allow for a direct communication between cells by forming tiny channels, allowing small compounds and ions to cross the cell's membrane to a neighboring cell. It occurs for instance in the brain.

Neurotransmitters are secreted by the nerve cells and act directly on other nerve cells, muscle cells or glands (like adrenal medulla) via synapses, so they travel "short distance" (nanometers).
Endocrine glands secrete substances (mainly hormones) into the blood by which they travel "long distance" to the target organs.
Neurotransmitters are quick (seconds) and endocrine substances are slow messengers (minutes).
Norepinephrine (noradrenaline) acts both as a neurotransmitter (between the nerve cells) and hormone (secreted from the adrenal medulla into the blood). Several other substances, such as dopamine, can also act both as neurotransmitters and hormones, but they are still a part of two different systems - the quick one that acts via the nerves and the slow one that acts via the blood.
As mentioned in comments, nervous and endocrine system are connected, so one can merge two systems into a larger neuroendocrine system, a part of which is, for example, hypothalamic–pituitary–adrenal axis that enables stress response.


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Name for fluid that leaks out of phyllid (non-vascular) plants?
As Wikipedia says (https://en.wikipedia.org/wiki/Non-vascular_plant):

Consequently, phyllids are unable to control the rate of water loss from their tissues and are said to be poikilohydric.

And indeed, if you've touched these types of plants, they can feel wet and sometimes even slimy. Sometimes the liquid leaking out can look like dew drops, too.
Is there a proper term for this fluid? I thought sap at first, but it seems that term is reserved for vascular plants.

They often feel wet because they grow in damp environments, but you can absolutely dry a moss and re-hydrate it. Slimy texture might be external such as algae or it might be a product of the plant.

I don't know of a name for the external water, but the process of plant water loss is called "transpiration", the evaporation of water from the tissues of a plant.
Note that the phenomena you describe, slimy plants or "dew drops", are not due to transpiration, as transpiration doesn't leave liquid water on the leaves. The sliminess you describe sounds more like plant mucus (mucilage).
The dew drops could be just that, external water. It also sounds like a something called "guttation," a process in vascular plants where transpiration is decreased (such as at night) but water pressure in the roots is high, basically pushing the water out of the leaf. This water is, essentially, sap, since it comes from the plant xylem. The composition of guttation fluid is mainly glucose and some amino acids, which would give more of a sticky texture, while mucilage is composed of a mixture of highly branched carbohydrates and glycoproteins.
I'm not aware of guttation occurring in non-vascular plants, and it may be unlikely since they lack xylem and don't have many ways of slowing transpiration. However, guttation occurs in some mushrooms, so roots and xylem are not an absolute requirement.


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What does it mean to have square brackets around a genus name?
For example [Eubacterium] rectale

The NCBI Taxonomy staff places square brackets around the genus for some species (examples: [Bacillus] aminovorans, [Candida] auris) to indicate that they are misclassified*, meaning placed incorrectly in a higher taxonomic rank.
References:
https://support.nlm.nih.gov/knowledgebase/article/KA-03379/en-us


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chromosome 19 and recombination
Im doing a project with structural variation created by recombination within the human genome during spermatogenesis, where im especially examining intrachromatid homolog recombination.
I find that chromosome 19 is less prone to recombine and form strutural variation. I know that chromosome 19 has a high gene density and have a high amount of linked genes, so a low CentiMorgan unit. But some articles, states that chromosome 19 contains duplicated regions, which i would assume would be prone to recombine with intrachromatid recombination.
So my question is, from an evolutionary perspective, does anyone know any articles, which might describe why chr 19 is less likely to recombine. if chromosome 19 have a higher amount of life essential genes, or is it simply the high density between the repeats which affects the recombination (so sort of like heterchromatin structures).
I've looked and cannot find any results to support that chromosome 19 are "more different" when compared to other autosomes. As an example chromosome 1 has a higher CentiMorgan unit and are thus more likely to recombine, so "it" handles structural variations better, but it still contains important genes.
Thanks for your help.


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Is it true to say that the genome of trees includes or at least "encapsulates" the genome of mushrooms?
As a botany amateur, I know that mushrooms (which are of course studied in field of mycology and not botany) are dependent in trees or shrubs (and maybe also bushes) and that there are generally strong symbiotic relations between trees and mushrooms.
If mushrooms are strongly tree dependent and appear per tree species, is it true to say that the genome of trees includes the genome of mushrooms by some mechanism?

Are mushrooms in general symbiotic with trees - that is, does the tree derive some benefit - or are they parasitic?  Indeed, from casual observation it seems as though a good many mushrooms only live on dead trees...

No.
Evidence: If you go to the TreeGenes site and examine those tree genomes that have been sequenced you won’t find any fungal chromosome sequences. (And vice versa.)
Reason: Although trees and mushrooms may develop symbiotic relationships they are independently viable (at least the trees), and even two organisms that can only survive in a symbiotic relationship have separate nuclei with separate chromosomes. They are distinguishable, so they are distinguished.

Such a shame that the only sourced answer gets downvoted. +1

Hello David. Thank you for the answer. One thing I misunderstood when reading it is this: they are independently viable (at least the trees). Please consider further explaining this. Thanks anyway,

@JohnDoea — I mean that the trees can exist without the fungi. I do not know about the parasitic fungi, but imagine that they may also be able to do so, or at least evolved independently.

A symbiotic relationship is entirely unrelated to the genetic origins of the participating organisms. Symbiosis only requires that the organisms interact in a manner that benefits both parties. There is nothing that requires any genetic similarity between symbiotic organisms. You may happen to find that particular species of trees and mushrooms do indeed share parts of their genome, but whether or not they are symbiotic has no bearing on that.

The word genome gets tossed around a lot but it really is a technical term. The genome is the total heritable genetic information carried by a cell or organism. It is possible for one organism to incorporate the DNA of another into its genome, for example, extrachromosomal plasmid DNA found in E-coli, however in this case its not like the tree is incorporating the DNA of the mushroom into its cells. It's possible that depending on their evolutionary relation there is consensus between their genome in the form of homologous genes, but thats due to shared ancestry, not their symbiosis.

You are suggesting gene transfer horizontally from funghi to plants. Rephrase "encapsulate whole genomes" to "include some genes" and you would be correct:
Most plant–fungus horizontal gene transfer events are ancient and rare, but they may have provided important gene functions leading to wider substrate use and habitat spread for plants and fungi. Since these events are rare and ancient, they have been difficult to detect and remain relatively unknown. https://en.m.wikipedia.org/wiki/Plant%E2%80%93fungus_horizontal_gene_transfer?wprov=sfla1


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What is this 5"-across spider found in my bedroom in France?
As the subject-line says, what is s/he? I've removed more spiders than I remember over the years, but one that almost fills a pint-glass was approached with some trepidation!

N.B. Found last-week (late Summer), French Jura. Sent packing to the garden...

It looks like a type of Wolf spider https://en.wikipedia.org/wiki/Wolf_spider

We ask species ID answers to be accompanied by a confirming photograph and background details, e.g.  whether the location of the species matches the distribution profile of the species ID, if the size and color of the species match etc etc.

Not a wolf spider - looks more like a funnel weaver, related to the Giant house spiders. Perhaps Aterigena ligurica


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Source for 'EVERY living organism uses ATP as energy carrier', and can we make a synthetic one that doesn't?
I have read it repeatedly that 'all living organisms use ATP as an energy currency etc' and 'some use GTP in addition'. However I am yet to find a reliable resource, rather than just quora/reddit/researchgate posts, that states this.
Also, would it be possible to create a synthetic organism which does not use ATP? Or GTP? What might be the best energy currency to use then?

Well your request for a source is rather like asking who first reported that 2+2=4. Not quite, but that should give the idea to someone who has not studied biochemistry. I doubt that you will find a source, but the following from Jacques Monod — the Nobel laureate — is worth quoting:

“Anything found to be true of E. coli must also be true of elephants.”

In fact, this turns out not to be true for anything, but it is true of the role of ATP.
The better question, I think, is not what the source of such a quotation is, but what is the evidence for such an opinion. The evidence that has accumulated over the last 80 years or so is from examining the metabolic pathways present in different organisms, and, more recently, sequencing their genomes to identify the genes for various enzymes. What has been observed is a core of common pathways, involving a core mechanism of energy metabolism involving ATP. This is consistent with the idea that this arose early in evolution and was fixed in the last common ancestor of living things.
If you want a more recent source to the ideas above, I suggest another SE Biology question, Immortal genes common to all organisms, may provide a starting point.


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Effect of toxin-producing phytoplankton on zooplankton?
I've been searching for quite a while without really finding an answer to this question, so I decided to try it here.
Some phytoplankton species produce toxins as a defense strategy. But what exactly happens to the predator, e.g., to zooplankton?
I've read that they may have a decreased reproductivity. But is there a faster effect acting as a defense mechanism such as phytoplankton sensing zooplankton, then producing toxins and zooplankton sensing the toxins and avoiding the area or similar? Otherwise, it would be quite a long-time defense.. If anybody knows something about this, please answer and give me a reference.
Thanks a lot!


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Is the salt obtained from meat (as the primary diet) nutritionally sufficient?
This post is derived from that one, where someone says

if you meant salt as a nutrient such as carbs, protein and all, there is salt in the stuff one eats already.

The background is "Naked and Afraid", a Discovery Channel survival show, where a group of people survive for 21 or 40 days without any cloth or food.
They are not next to a shore. They are in amazon jungle or Solani River Basin in Africa.
The footage shows that the candidates got food by hunting but never got additional salt.
They are hunting in Africa. Don't they need additional salt? Is the amount of salt they got from animals like impala sufficient?

Hunter-gatherers rarely if ever added salt to their foods, and studies of salt-free Yanomamo Indians have shown these indigenous people to maintain low blood pressures that do not increase with aging (Oliver et al, 1975).

--The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic. European Journal of Clinical Nutrition (2002) 56, Suppl 1, S42–S52 (PDF link)
(The Yanomamo Indians were/are hunter-gatherers, but that doesn't necessarily mean their diet was mainly meat - plants and fruits are important components. However, meat is likely to be higher in salt than plants, so this just supports the general principle.)


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Why can't geese regurgitate food?
I saw this harrowing video on how barnacle goslings have to jump off very high cliffs because the parent's can't feed them. The death rate seems high. Why did natural selection come to favor jumping rather than the parents bringing food to the nest like most bird species?
From Wikipedia:

Like all geese, the goslings are not fed by the adults. Instead of
  bringing food to the newly hatched goslings, the goslings are brought
  to the ground. Unable to fly, the three-day-old goslings jump off the
  cliff and fall; their small size, feathery down, and very light weight
  helps to protect some of them from serious injury when they hit the
  rocks below, but many die from the impact.

This page mentions geese and sais they can regurgitate food: https://www.caspervanleeuwen.info/images/PDFs/Kleyheeg_and_Van_Leeuwen_2015_Aqua_Bot.pdf Geese prefer acorns and proper carbohydrate, and if there is not enough food and there's too far to fly, perhaps the geese and the chicks deplete themselves and don't consume enough to grow maximally. Those geese didn't find a good nest, they only need to be 10 meters high up the cliff?!

It means more food and faster growth; and higher chance of survival if they stay with the parents. It is explained for guillemots whose chicks (jumplings) jump off cliff also based on a study; thus it should be similar for barnacle geese. "Our measurements show that the male feeds the chick twice as much as both parents could if the chick remained in the colony," says Morten Frederiksen of Aarhus University in Denmark. Source: earthtouchnews


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During DNA foot-printing, what is the purpose of radioactively labeling only one end of the DNA fragment?
I read that during DNA foot-printing analysis, DNA is radioactively labeled on one end before being cleaved by DNase 1. I understand that it is labeled so in order to locate the fragment on a gel, but I don't understand why it is only labeled on one end? If the DNase cleaves it in two, wouldn't the other end be un-labeled and untraceable? Therefore kind of defeating the purpose of labeling it at all?

I assume you know the starting length of the labeled DNA. What can you can infer from that information? What would happen if you labeled both ends? ——— To understand this you probably need to draw some pictures ...

Preamble
Although there is a Wikipedia page with a general account of DNA footprinting, this perhaps does not put sufficient emphasis on the general strategy, making reference to the Maxam & Gilbert DNA sequencing method, with which contemporary students are not likely to be familiar. Elsewhere on SE Biology I have summarized the strategy of different DNA sequencing methods, so I shall use that as a starting point for this answer.
The Strategy of DNA Footprinting
In DNA sequencing there are two conceptual pieces of information one is trying to discover: the identity of a base, and the position at which it lies. A third point of importance is the practical technique one uses to realize a strategy. The method of DNA sequencing developed by Maxam & Gilbert used specific chemicals to fragment pieces of DNA:

The particular chemical used identified the base as the last one on one of the fragments produced.
The length of the fragment indicated the position with respect to one of the ends, which was used as a reference point.
End-labelling of one end of the original DNA allowed fragments containing the reference point to be visualized, distinguishing them from others that were unlabelled and hence generated elsewhere.

In DNA-footprinting we are not concerned with identifying the bases: the DNA has probably already been sequenced or we can do that separately. We are in interested in positional information, and we shall see that this also involves fragments — generated by the non-specific DNase — and their visualization, as in the method of Maxam & Gilbert.
This is explained in the figure below, my own modification of Coutney2008.jpg, in the Wikipedia article mentioned.

The frame on the extreme left addresses the question of labelling and visualization by showing the fragmentation of uniformed-labelled DNA by DNase. In this example the DNase cleaves at three points (arrows), generating four fragments of different sizes, A, B, C and D. If these fragments are separated and visualized by their radioactivity (by autoradiography) there is no way of knowing their position in relation to the reference point. So whatever our strategy is in relation to protein-binding (explained below) the positional information is not revealed. We cannot tell that fragment A contains the reference point.
Now let us turn to Frame 1, which is in effect the Maxam & Gilbert strategy without the base-identification. The DNA is labelled at one end and treated with DNase at a concentration that will generate a range of fragment sizes. The ones we are interested in are those that include the reference point, which is the end we have labelled. These fragments have been coloured pink. Other fragments (light blue) that do not include the reference point will be generated — including some of the same size as those of interest — but these will not interfere with our analysis as they are not labelled and will not be visualized after the fragments have been separated according to size on denaturing gels and subjected to autoradiography (see gel lane 1). (The unlabelled ‘light blue’ portions may have been fragmented further, but this has not been shown for clarity.)
The footprinting strategy is shown in Frame 2. The experiment of Frame 1 is repeated with the DNA-binding protein (bright blue oval) added. Now the region of DNA to which the protein binds will be protected from DNase. Thus, fragments terminating within this region will be missing and be absent from lane 2 of the gel. Hence the position at which the protein binds is specified as the distance of the missing fragments from the labelled reference point. (There are likely to be fragments of the same size as the missing ones in the mixture, but, to repeat, because of the end-labelling they will not be visualized.)


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Name/term for mechanisms by wich the relative size/number of cells of some tissue/organ are preserved
The cells of some organ or tissue are dividing and also dies (apoptosis). But this happens in somehow controlled manner so that the total size of the organ is approximately preserved or the total number of cells approximately stays the same. As far as I understand, this is somehow collective process, because cells in one side of the tissues should somehow coordinate the division/apoptosis processes with the cells of the far side. I have read in one book about cells, that such controlling mechanisms are purely undesrtood even today. Of course, such mechanisms work only approximately (or - to be more precise - they are more complex than just static preservation of the size/number), e.g. numberadipose cells can increase with time.
But anyway - my question is - what is the name/term for such controlling mechanisms and what are other important keywords/terms which I can use for searching more research papers about this theme?
I have specific interest in the control of those processes, e.g., with the aim to bound those processes for adipose cells and to encourage those processes for the muscle cell.
"cell cycle control" and Hippo-pathways mechanisms can be the answers, but I am still searching for the matter.

'Eutely' is the term used for organisms with a fixed number of somatic cells. I'm not aware of any term for sub-organismic structures.

Welcome to SE Biology. Answers here should be supported by some sort of external authority or verification so people can check if they are correct. I realize it is not difficult to look up the word you suggest, but it would be better if you could edit your answer to provide a link. The format is square brackets for the linked text and normal brackets for the link, with no spaces between (unlike my example to demonstrate): [Eutely] (https://simple.wikipedia.org/wiki/Eutely)

You are referring to organ “scaling” and “allometry”.

We're looking for long answers that provide some explanation and context. Don't just give a one-line answer; explain why your answer is right, ideally with citations. Answers that don't include explanations may be removed.

"what is the name/term for such controlling mechanisms and what are other important keywords/terms which I can use for searching more research papers about this theme?" The question asks for a search term. Judging an answer by length is like judging an airplane by weight.

I am not merely judging by length. The comment above is a standard statement for "insufficient explanation" that I just copy-pasted. Your answer could be better if you provided some explanation or references (or both).

Allometry is in my view a correct answer. I have no quarrel with that. I agree however that the answer is best expanded on a little bit. I don't think a good answer is one that is minimally sufficient, because they are not explanatory nor pedagogical. Scaling and allometry are not the same thing; it would be prudent to explain each, ideally with an example, or at least a link to a useful, practical page that works the explanation well. I also do not think that considering allometric relationships addresses the question completely; there is emphasis on the control aspect of organ size.


text:
Are there pre-synaptic alpha 2 receptors in the post-ganglionic synapses of the heart?
Are there pre-synaptic alpha 2 receptors in the post-ganglionic synapses of the heart?
I haven't found any sources that clearly state whether they do or not. I'm also not sure if they exist in most post-ganglionic synapses, or if they do in just specific ones. The reason I ask is wanting to understand the reflex tachycardia non-selective alpha blockers like phenoxybenzamine cause.
One of the side effects of phenoxybenzamine is reflex tachycardia, caused by, from my understanding, partly a reflex to the initially decreased blood pressure and due to the blocking of alpha 2 receptors, increasing nor-adrenaline release. Does this occur by :

Blocking alpha 2 receptors at other sites, causing increased blood levels of nor-adrenaline, which then cause increased heart rate.

OR

Blocking alpha 2 receptors in the heart, increasing local increase of nor-adrenaline?

The heart of course does have Alpha 2 pre synaptic receptors , the definition states that alpha 2 receptors are present on sympathetic postganglionic endings , so I don't see why heart should be an exception .
I will explain to you how reflex tachycardia occurs .
When you give non selective blockers , presynaptic Alpha 2 are blocked , therefore the pre synaptic neurons cannot sense NE amount in synaptic cleft , so they release large amounts of NE . BUT , post synaptic alpha1 is also blocked , so this large amount of NE cannot act BUT THE HEART DOES NOT HAVE alpha 1 it has BETA 1 receptors which are perfectly capable of being stimulated by this large amount of NE that is released , hence causing tachycardia.


text:
Looking for a good and complete Enzimology exercises book
I mean, I want to practice with challenging exercises and I want to know the theory behind them. So, I started reading:

Organic Chemistry: Yurkanis, P.
Enzyme kinetics: Bisswanger, H.
Biotechnology procedures and experiments Handbook: Harisha, S.
But just the first one has problems and not about enzymes at all.

So, I looking for a good (theoretic) and complete (challenging with exercises) book about enzymes.

I generally regard book recommendations off-topic. I cannot recommend a book but suggest you see if you can "look inside" Cornish-Bowden's Fundamentals of Enzyme Kinetics. He is well regarded, and there are some calculations in his book judging by the three pages of solutions to problems. Only three pages though.

So, why are off-topic?? The book you recommend me is very fine. It cover many of the topics in my syllabus. Just $55. Thanks man.

The reason it could be considered off-topic as an answer is that any recommendation is subjective opinion, and this is a question and answer site about biological problems. But glad my comment is of use.


text:
Why is facial symmetry of the opposite sex attractive?
Why do we give so much importance to the symmetry of face in the opposite sex? Why do we yearn to reproduce with a person with a beautiful face? How is it important for survival, if at all? Is there a biological explanation for this?

Who exactly is "we" here?  From my own experience & observation, I hardly think it is universal to regard the face as all that important in attractiveness.

Well it does seem like symmetric faces are more attractive (to both genders; Grammar and Thornil, 1994)

@Remi.b: I think you misunderstood what I was trying to say.  I'll accept that symmetric faces are more attractive than non-symmetric ones; what I'm questioning is the idea that the face, whether beautiful or not, is more than a minor factor in overall attractiveness.

@jamesqf What does it matter if its minor or major factor? My question was about the fact that it clearly has some importance in survival why else would people care about facial symmetry?

@user10093863: The problem is your assumption that "we yearn to reproduce with a person with a beautiful face", which at least from my observation isn't generally true.  I could cite any number of examples, from the feminist complaints about men not looking at their faces, to the cruel description of a fat woman as "but she has such a pretty face".

@jamesqf You clearly are living in a dreamworld or have never been to a normal school or college, let alone an outdoor setting like restaurant or a bar. If you genuinely believe that people don't give any importance to facial symmetry in the opposite sex, then I think you are living in the world of non-smelly farts and invisible poops.

@user10093863: At the risk of descending into crudity, are you living in a dreamworld where you've never heard the expression "just put a bag over her head"?  Do a thought experiment (or a real one if you can get funding :-)).  Take your bar or whatever, dress half the people in revealing clothing but have them wear masks, have the other half show their faces but wear something that completely conceals the body.  Now which half do you suppose is going to get the most interest from the opposite sex?

@jamesqf Wow that makes no sense. My question is regarding facial symmetry, it has nothing to do with the body.

@user10093863: No, you asked explicitly why "...we yearn to reproduce with a person with a beautiful face?"  The answer to that is that WE don't.  Now maybe some people do, because different people find different things attractive.  But if beautiful faces were a major factor in sexual attraction, Playboy could have been a success with nothing but head shots :-)

@jamesqf The reason you won't admit to the fact that you and I and everyone else is highly attracted to facial symmetry is because you want to live in a world where we are attracted based on important things like someone's intelligence rather than their looks, however, I hate to break this bubble for you but humans are still pretty primitive when it comes to attraction. Our brains have not evolved much for thousands of years and we used to be attracted to others based on their facial symmetry and physicality. So, what makes you think that it is any different nowadays?

@user10093863: You've entirely misunderstood what I've been trying to point out, which has nothing to do with whether I'd like intelligence to be sexually attractive.  (I don't think I've even mentioned intelligence AT ALL.)  It's that when it comes to sexual attraction, the face plays little part, at least for men.  (I think also for women, but I have limited data, not being one.)  To be crude (since nothing else seems to get through), most men look at tits, ass, legs, waist &c long before the face, and will pretty much ignore the face if the rest is attractive enough.

@jamesqf As I have mentioned before, you live in a dreamland. Producers hire pretty faces for lead roles because they know that more people are going to watch. Why do you think people want to watch pretty faces? Because it is soothing to the eye? No, because people are more attracted to pretty faces and find it hard not to look at them. What do you think this phenomenon is if not sexual attraction? Ever heard of the phrase 'sex sells'? If it was merely about 'tits, ass, legs, waist, etc' then wouldn't they hire based on physique rather than facial symmetry? Its so hard to get through you.

@user10093863: The first problem with your reasoning is that anyone movie/TV producers hire (for other than character rolls) is already several standard deviations out on the T&A bell curve.  You don't see them hiring the fat girls (or men) with pretty faces, do you?  The second problem is assuming that movies (other than porn, of course) are all about sexual attraction.  While I'm not a movie fan, people do seem to watch them for reasons other than sex. And if it seems hard to get through to me, it's because you insist on holding to an obviously false thesis :-)

Are you claiming that face symmetry is unimportant for gay people?

@swbarnes2 Are you virtue signalling here?

Why is it 'virtue' signaling' to acknowledge the existence of gay people?

Because biology.

Facial symmetry is currently believed the be a sign of developmental stability and good health and thus good genes.  More precisely a sign of genetic diversity in a potential partner.

Parasites, disease, or injury can cause asymmetries. The complexity of the face, and our visual sensitivity to facial features, makes us most sensitive to subtle symmetries and asymmetries in facial features.
Therefore facial symmetry is a sensitive and reliable indicator of health. Healthy mates are more likely to possess good genes to pass on for strong healthy offspring. Healthy mates are also likely to be more physically capable of producing and raising offspring.
Any individual who possesses a gene that causes attraction to symmetric partners is more likely to select such a mate. That individual is therefore likely to produce more offspring, and more likely to produce strong healthy offspring.
Therefore the gene for attraction to facial symmetry is more likely to survive and spread.

Welcome to Biology.SE! Your answer sounds reasonable, however, it is likely to receive a more favorable response if you include supporting references (primary literature is best). ——— Please also take the [tour] and then consult the help pages for additional advice [Answer] effectively on this site and then edit your answer accordingly. Thanks!


text:
During weight loss, do we inhale more oxygen?
During weight loss, triglycerides which are composed of carbon, hydrogen and oxygen, are broken down. During respiration, the inhaled $O_2$ is bonded to a carbon atom to form $CO_2$ which we exhale. However this process happens anyway, even one isn’t trying to lose weight. So that suggests to me that during weight loss people must inhale more oxygen, otherwise where are all those extra carbon atoms that we now have going?

Read about ketones.

First one needs to make it clear that oxidation of foodstuffs, either those in the diet or from deposited reserves, occurs in order to generate energy (ATP) for life’s processes — the most evident to the non-biochemist being to perform muscular work. So, as the poster correctly implies, this will occur in both fasting and non-fasting individuals, and the fairest comparison would be between the same individual performing the same amount of energy-requiring processes.
Let us consider this comparison in the simplest situation where the person “losing weight” is fasting, i.e. has no food intake (rather than being on some fancy diet). After his glycogen has been depleted, the fasting individual will be producing all the energy for his various needs by oxidizing triglycerides that had been deposited previously in his fat cells. The amount of oxygen he inhales (assuming this is strictly related to requirement — I’m not a physiologist, so I don't know) will be that required to oxidize the triglycerides to produce this required energy.
Now compare this to the same individual, not fasting. His energy needs have been assumed to be the same as in the fasting state, but he is generating this energy from his food intake. Making the unlikely assumption for comparison that this were all triglyceride, the amount of oxygen needed to oxidize this would be exactly the same as the fasting individual.
I think that deals with the fallacy in the question, perhaps caused by not reflecting on what the oxygen inhaled by the non-fasting individual is used for. Technically one should admit that if the simplistic assumptions do not hold, the strict equivalence would not either. Different foodstuffs (carbohydrates, fats, proteins) are in different oxidation states, so the amount of oxygen required to oxidize them in the fed individual would depend on diet. If the food intake of the fed individual were greater than his needs and he was depositing glycogen or fat, extra ATP would be required to do this, which would likely be generated by oxidative phosphorylation. No doubt one can think of other possibilities, but these were not the focus of the question.


text:
Why spider's web don't burn when electricity touches it?
I saw and spider on it's web at an electrical cable and thinked: If the web is made of proteins, why dont burn.
Sorry, the photo is dark because is night in Ecuador

Spider silk can conduct electricity. Some spiders use this material property of conductivity to capture prey. https://www.ncbi.nlm.nih.gov/pubmed/24323174
So I'm going on the assumption that both electrical lines spanning the web are bare and that they are live, i.e. carrying current. I will also assume that these lines are carrying the same current.
With electricity, it might help to think of the analogy of a waterfall. Water at the top of a waterfall has potential energy, which is converted to kinetic energy when it goes over the waterfall. The water accelerates towards the earth as it falls. There is a height or "gradient" between the top of the waterfall and its bottom, which allows water to accelerate from the top towards the bottom of the fall.
Electrons in electricity work in much the same way. Between two points along a conductor, you need a voltage gradient to establish an electric field, which moves electrons in a particular direction — just as the waterfall creates a gradient of high ground to low ground that enables water to flow.
If you have two wires (both conductors) running at the same voltage, and if you connect them with another conductor, like a spider's web, electrons will not run through the web because there is no voltage differential that creates an electric field that drives the flow of electrons between that connection. https://en.wikipedia.org/wiki/Electric_potential
Here, the web and spider are likely unhurt, because the two lines do not provide a voltage difference needed to have electrons move across the silk, like water would flow over a waterfall.
If the spider web was grounded — if its web were instead connected from one of the electrical wires to the earth — electricity would likely run through the web and, potentially, burn the web (and the spider). But from your photograph, it looks like the web is connected to both wires that ℗r assumption) are at the same voltage.
This is the same principle that allows electricians to work on maintaining electrical pylons without shutting down the power grid. https://en.wikipedia.org/wiki/Live-line_working
They work in such a way as to maintain the same voltage as the lines they are working on. If they were grounded — if they held a copper wire, say, that was plugged into the earth — or if there was anything conductive that the electrician was connected to that established a dangerous voltage gradient, and if they started working on live electrical lines, they would get fried. Same with the spider, if the web was grounded in a similar way.
Further, if the two wires were running at different voltages, then electricity could conduct through the spider web and cause some damage.
This answer relies on a lot of assumptions from the photograph. Feel free to clarify if those assumptions would change the parameters of the question and my answer.

I really doubt that this answer is correct.  If that's a single-phase line (typical of residential supply), there IS a voltage difference between the phase and neutral wires.  (Likewise if it's 2 wires of a 3 phase system.)  If the lines are live, and spider silk conducted electricity, there would be a sufficent current flow for the resistance to heat the silk, or any conductor, to its melting/vaporizing point.  All you'd get is a brief arc.   But in fact normal (dry) spider silk is a pretty good insulator.

These lines could perhaps be fence wiring to keep in animals, but I can't really tell and it isn't mentioned in the question. I would definitely suggest adding your answer, if you feel it is appropriate or my answer is incorrect.

Thanks Alex. Yes, your assumptions were correct, and the Live-line working assumption is very logic to me.


text:
Human femur maximum strength
In this video https://www.youtube.com/watch?v=os98s9kBlOI it is demonstrated that a moose leg bone can support until nearly 10 tonne before break. Is there any similar demonstration on human femurs? How much weight a human femur can support vertically before it is crushed?

that's not a whole bone just a section, there are similar test of other cortical bone. https://www.sciencedirect.com/science/article/pii/B9780128038024000111

It just uses a tiny cube (5mm x 5mm x 5mm) of cortical bone from a femur. Is there any tests that used whole human femurs?

I doubt it, there is not much scientific value to such an act and getting human bone for testing is not easy.

Do you think the midshaft section look stronger than it looks because of its structure (which is shorter with both ends flattened)? I think if it is a whole leg bone, it will break much faster.

That video isn't a scientific test, bone has aligned strength, putting a full femur with curves and rounded ends in a press with flat surfaces doesn't tell you anything useful. Bone is not subjected to force in that way in a living creature, that is why scientific test use small segments.

So that being said, a midshaft section with flattened ends look stronger (can support more load) than it seems because it is more stable compare to a whole leg bone. Isn't it?


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Do vitamin enriched foods preserve their value when exposed to higher temperatures?
At what temperatures do different kinds of vitamins are destroyed or lose their nutritional value?
Imagine you went to the store and bought vitamin enriched cacao powder. Then you made yourself a hot drink by pouring boiling water. How much in general(approximately) vitamins were destroyed by that heat.
"How to prepare/cook" usually doesn't have this kind of information. Thus any benefits of vitamins are lost(?).

There is already a lot of information on this topic (also for non-biochemists). Did you try googling "heat sensitivity of vitamins"?

@WYSIWYG yes, I have googled it. Bottom line every article or page that I have found just says - "yes vitamins lose their value when heated" (I am not very good at googling or finding this kind of data when it comes to biology). Not very informative, I understand that they lose their value. I wanted to know how serious those effects can be.

This question is not about biology in terms of SE Biology but domestic science, unless it is a personal medical question, which would be off-topic. It might fit Chemistry SE if it were not so broad/imprecise.

@David I see. I thought that since it's about vitamins and they have biochemical functions that occur in our bodies - it would be fit for biology. But since the question is more outside of terms of biology and closer to chemistry and reactions, I agree with you that it may better fit Chemistry. Although, it would be incorrect moving it after Jan's answer. Biology, chemistry and physics are tightly coupled together, so I guess it's not that big of an issue, is it?

I understand that the question is not of a nearly perfect quality. But due to my incompetence in this topic that is naturally what I could do.

Here's one estimation about how much vitamins or minerals can get lost due to various "food processing" (cooking, drying, freezing) methods:
According to NutritionData, cooking can result in a loss of vitamins:

Vitamin A: 25%
Vitamin C: 50 %
Vitamin B complex vitamins: 25-70%
Minerals: 25-70%; most important: potassium loss in cooking water. In this study with potatoes:

Leaching alone did not significantly reduce levels of potassium or
  other minerals in tubers. Boiling tuber cubes and shredded tubers
  decreased potassium levels by 50% and 75%, respectively.

According to USDA retention factors, the following vitamins are most affected by food processing:

Vitamin C
Vitamin B1, B6, B12 and folate

Vitamin and mineral loss is related to both the temperature and time of cooking.
Mineral loss can be prevented by cooking in vapour (steaming) instead of cooking in water.
According to this source, the following can be loses after heat treatment at 70 °C and (90 °C):

Vitamin A: 10% (30-40%)
Vitamin D: 15% (35%)
Vitamin B1: 15% (50%)
Folic acid: 5-20% (45%)
Vitamin C: 40% (85%)

But the minerals won't be truly lost if the cooking water is not thrown away.

@WYSIWYG,  most people throw away cooking water after boiling potatoes. Since potatoes are rich in potassium, a lot of it can be lost that way. If the water is consumed, of course no minerals are lost. I added one study about potatoes.