text:
Why do lions keep young preys and don't kill them right away?
I saw some (actually several) videos on Youtube of young lions and lionesses that after hunting baby preys keep them and even seem to play with them. The lions don't seem to want to hurt them but they don't seem to want to let them go either. Most of the video titles are "lions protecting baby ....", I don't believe that. On the comments people say "the lion is saving it for later". My guess is that the lion wants to give the baby animal for the younger lions. What destiny will the baby prey most probably have?

Possibly to help the cubs learn how to hunt.  Cheetah will do this but I'm not sure about lions.  A quick google search only came up with this one newspaper article, with photos, but I didn't see a source for the article.  http://www.dailymail.co.uk/news/article-3429745/Taught-kill-mummy-Lion-cub-shown-hunt-lioness-wounds-prey-lets-youngster-finish-off.html

@Kurt I think you're probably right but the Daily Mail is probably one of the least reliable newspapers in the English language so I'd be wary about using it as a source :)

@Jam - Yeah, that's why I didn't want to use it as an answer.  I'm hoping somebody can find a scientific source to back it up.


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How rapidly do human mitochondrial ribosomes turn over?
How rapidly do human mitochondrial ribosomes turn over?
The inside of the mitochondrion is a highly oxidizing environment that can damage RNA and DNA. How long do mitochondrial ribosomes last before needing to be replaced?

source: Stack Exchange

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text:
Can you please identify this beetle? (Rajasthan)

I thought that it was dangerous and kept it under a polythene at my home, in Rajasthan.
Is this insect harmful, rare or common? If the pic is not clear, I would like to mention that it is green, six-legged and its body is separated in two from the neck.

This looks more like a true bug than a beetle, and may be a member of superfamily Pentatomoidea; the photo isn't as clear as I would like.  If I'm right as to group, species range in habit from predator to agricultural pest (and North American members of similar appearance are closer to the latter).

I agree. Not a beetle, but a Pentatomidae.

Not harmful to people but some species in the family are agricultural pests. Common name is "stink bug", named for the defensive scent it gives off when threatened.

I also agree. Looks like some species of stink bug (also called a shield bug) in the Pentatomidae family. As Karl said, these are often agricultural pests. Other than a fowl odor when crushed, these insects pose no direct danger to you.

@Karl I think you can make an answer out of your comments. There will probably be no need to ID that organism down to the genus level.

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What does the nucleus look like in S phase of Meiosis?
I was watching an animation video about Meiosis and this is what the video shows (pics attached.)
It shows that before synthesis, each chromosome exists as single chromatid and then after replication, it has a sister chromatid. I am confused because germ cells are diploid, so shouldn't the S phase look like this?
It should start with 23 chromosomes (46 different DNA's) and then replicated to 46 chromosomes (92 different DNA) which then get assorted into 4 different cells?

In terms of chromosome number
During meiosis, the meiocyte is a diploid cell ( 46 chromosomes for human). So during the S-phase , the meiocyte would contain 46 chromosomes.
At the end of meiosis I, the divided meiocyte contains 23 chromosomes so it's called the reductional division
At the end of meiosis II each cell contains 23 chromosomes.
In terms of chromatid number and number of DNA molecules
Meiocyte in S phase contains 2 chromatid in each chromosome, so the number of DNA molecules is doubled (if you consider that each chromatid is composed of a pair of DNA strands like in Watson Crick Model, then each chromosome of S phase contains 4 strands... So 46×4 strands of DNA is present. Often each helix / duplex is considered one DNA molecule , so in that case you have 46×2 molecules. So you have to be careful with the terminology mentioned.
After meiosis I there are 23 chromosomes in each divided cell with 2 chromatids in each chromosome...So there are 23×2 DNA molecules.
After meiosis II there are 23 chromosomes with 1 chromatid...So they contain only 23 DNA molecules.

It states mitosis here but it is the same for meiosis at this stage. What you have drawn for the inside of the first cell is already 44 chromosomes.
Hope this helps

At the beginning, germ cells are diploid and as far as I know they are the cells that give rise to gametes which are haploid.
Here how it goes, the germ cell is containing 46 chromosomes and in S phase, these chromosomes replicate so that each chromosome will be made of 2 chromatids resulting in 92 chromatid.
In meiosis I, the germ cell divides and the 46 chromosomes divide as well giving two cells each containing 23 chromosomes and 46 chromatid.
The meiosis yet hasn’t finished. In meiosis II, each daughter cell containing 23 chromosomes will divide to two daughter cells. In this division, the chromatids in each chromosome will separate. In other words, the 46 chromatids in each cell will divide and each cell from the new daughter cells will be containing 23 chromatids. So now we have 4 haploid cells each one containing 23 CHROMATIDS ( a gamete ) all coming form one original diploid germ cell.
Those chromatids will then be referred to as chromosomes.

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What percent of e coli genes are necessary for survival?
I would like to know, in a typical e coli genome what percent of genes the organism could not survive without. That is, if all the other genes evolved except that one, the organism would not be viable.

There are a few groups worldwide working on a minimal genome; until they've managed to get a reference minimum, we won't know how much is necessary.

About 10% in rich media.
There are lots of papers that try to answer this question. The basic way you do it is you knock out one gene at a time, either in parallel experiments or (more common nowadays) in a pooled experiment, and figure out which knockouts survive and which don't.
The most recent study counts 358 essential genes (out of about 4000 genes in E. coli). http://mbio.asm.org/content/9/1/e02096-17.full . Figure 2 compares a few other papers.
The exact answer will depend on the exact conditions you grow the cells in (if you have fewer nutrients or other stressful conditions, more genes will be essential).


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Why do eyes change colour after death?
Why exactly do eyes turn black when we die? (Or even change colour at all).
The source of inspiration to this question is due to this video https://www.youtube.com/watch?v=6mNs_TcUyHc&t=627s (it's a cow's eye being dissected). The man explained how the cornea is crystal clear in an actual cow but since it's been preserved, the preservative has denatured the protein causing it to turn cloudy.
So why does our eye change colour when we die when no preservative is used?
I know this is a pretty gruesome question to ask but curiosity has the best of me haha.

Living tissues are not usually transparent. Obviously, the crystalline lens needs to be in order to let light go through. This is done by a fairly complicated system that requires active pumping of ions in and out. When that system stops, the lens becomes opaque resulting in that white cloudy appearance. This can happen in living animals (including humans) too, such as in cataract.

Please add references in your answer.


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How does it make sense to speak of heritability of qualitative traits?
As far as I understand, heritability is defined as "proportion of variation of a phenotypical trait due to genetic variation between individuals in a population".
I see the concept is being applied on quantitative that can be measured with numbers, can be compared (i.e., $\mathrm{A}$ is taller than $\mathrm{B}$ by $x$ units of height) and varies continuously to form a distribution (e.g IQ forms a Gaussian distribution).
heritability in the narrow sense ($h^2$) has a mathematical definition. For a given quantitative trait $x$ of a population that forms a distribution with certain average and certain variance $V_P$ then $$h^2 = \dfrac{V_G}{V_P}$$ where $V_G$ is the variance in population due to variance in genetics and $V_P=V_G +V_E$ where $V_E$ is variance in population due to enviromental variation (I ignored other terms in the definition of $V_P$).
IQ has mean of 100 with $h^2=0.8$. So for a person whose IQ is 105 (5 points above average), genetic contribution contributed to this $0.8*5=4$ points difference and the remaining 1 point difference is environment.
I also see how the concept can be applied on qualitative traits (by this I mean traits that don't satisfy the properties of quantitative traits) even in the absence of well-defined notion of variance $V_P$ because the trait doesn't form a distribution. For example in a population of flowers that can only be red or blue.This red/blue trait does not have a well-defined $V_P$. We can still meaningfully say that this trait has $h^2=1$ since any variation in the color (red vs blue) is due to genetic variation. We can also speak meaningfully and say a certain qualitative trait has $h^2=0$ meaning any variation in the trait is due to different environments.
On the other hand, I think qualitative traits can have either $h^2=0$ or $1$ but no value in between, since $V_P$ is not well-defined (and hence $V_G$ and $V_E$ as well are not well-defined) for them.
Consider sexual orientation for example. Based on some twin studies it was estimated that homosexuality has $h^2=0.5$. But what does that mean really? how does homosexuality vary to form a variance? A person is either homosexual or not(heterosexual, bisexual or asexual).
My question is how to apply this $h^2=0.5$ value of homosexuality in the same way I applied it above on IQ?
More generally how to meaningfully be able to interpret heritiability of other qualitative traits (mental disorders for example like schizphrenia with $h^2=0.8$) that has has no well-defined $V_P$ and whose $h^2$ value is not $1$ or $0$ but rather lies between them?

Can you give us reference for twin study on homosexuality, or even on IQ?

The concept of heritability is a concept coming from quantitative genetics. It only applies to quantitative traits. This does not mean that the trait must be continuous. Discrete traits (such as the number of eyes for example) are quantitative traits.
For boolean traits, it is common to set one outcome to 0 and the other to 1. Which outcome is set to which value does not matter as it won't affect the variance. To take your example of homosexuality, one would classify all individuals as homosexual or heterosexual and set homosexual to 0 and heterosexual to 1 (or vice-versa) and compute the heritability from there. Of course, categorising people as either heterosexual or homosexual completely misses the diversity of sexual orientation. The ability to put its tongue in the vertical position would be a better example of a boolean trait.
As far as I know, for non-boolean nominal traits, the concept of heritability is undefined.

I would imagine you could create dummy boolean variables for nominal traits, and analyze them as a boolean to get their heritability.

I think after some research I found the answer to the question. Measuring heritability of binary traits (e.g, diseases that do not conform to Mendelian rules like diabetes, mental disorders like schizophrenia and bipolar and etc) is based on the liability threshold model.
This theory assumes that every binary trait has underlying liability value that predisposes an individual for this trait. This liability varies continuously and forms a Gaussian distribution for a population. There's a threshold value of liability after which an individual becomes affected by this trait and it manifests itself (e.g, becomes schizophrenic). A person below the threshold value will be unaffected (e.g., does not have schizophrenia).
The theory posits that the source of variance $V_P$ of liability among the population is owing to genetic and environmental variances $V_G$ and $V_E$ respectively.
heritability as estimated by twin studies of monozygotic and dizygotic twins then estimates the heritability of the liability of a binary trait (e.g, homosexuality). In this case the formal definition of $h^2$ applies.

Using a threshold model based on a liability factor implies you having a liability factor and hence a quantitative trait.

Having a liability factor does not imply a quantitative trait. In fact, the threshold model is designed specifically to deal with binary traits. The underlying liability, i.e. the genetic + environmental risk, is Gaussian but the trait (e.g., having a heart attack or not, dying or not) is continuous. This is known to be the case for many diseases. A simple analogy is your risk of lung cancer increases continuously with every second you're smoking a cigarette, but the trait of having lung cancer or not is not quantitative. Binary can be considered continuous or categorical so it may semantics.


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Is it possible to induce protein activation via frequency-specific mechanical waves?
Would it be possible to induce shape changes in specific proteins by providing specific frequencies of mechanical waves in a thermostatically controlled environment such that those proteins may be activated without requiring regular ligand binding?

This should defentily be possible and most likely already exists in the form of touch or pain receptors.
In the case of mechanical nocireceptors, which sense pressure or other mechanical changes in the tissue to signal pain, it's quite likely that there are distinct channel proteins that can correspond to mechanical deformation/pressure/etc, but I couldn't find any specifically known protein.
Most touch receptors seem to be based on bigger structures made up by neurons, so I'm not sure if they have one specific protein that senses mechanical movement, but I also wouldn't exclude that option - especially since almost nothing is known about non-human/mammalian touch receptors.


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Are there mainstream views on the mandrill's coloration's being so unique?

According to the Wikipedia article:

Mandrills are noted as being exceptionally colourful for mammalian
  standards. Charles Darwin wrote in The Descent of Man that "no other
  member in the whole class of mammals is coloured in so extraordinary a
  manner as the adult male mandrill's".

So I know that in many species sexual dimorphism can act as a feature which is selected by sexual selection, I'm not surprised because there are other examples. But the male mandrill seems exceptional, especially according to what I've read, among mammals. Seems very curious to me, especially its face.
I was wondering if there are mainstream explanations for why the mandrill in particular should have such striking colours maybe more than any other mammals.

Mandrills are also extremely sexually dimorphic in terms of size (and fangs and muscularity, I believe). In fact, one of the most sexually dimorphic of all mammals. The extreme coloration and the sex differences in size both speak to a substantial degree of sexual selection.
Now as for the ultimate question, why mandrills have experienced so much sexual selection... I don't know.


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Help understanding cell replication animations
I often come across these animations about molecular biology showing for example how cell replication works, how virus infection works etc. Take this video as an example
https://www.youtube.com/watch?v=odRyv7V8LAE
HIV virus infects T helper cells using receptors on the cell surface which are cd4 molecule, it binds to the receptors using envelope protein. But the video shows you a little ball with some hooks that attaches to another little ball with other hooks.
I understand this is an useful abstraction, but could someone recommend a book or other materials to a novice like me who would like to understand how this really works? Question is probably too general but I am really interested in basics only. Hopefully someone could help
Thanks

When these animations are made by experts, they are actually not abstractions. Animations like this one [https://www.youtube.com/watch?v=X_tYrnv_o6A] actually don't show you an "idea" of how this looks but the actual shape of the individual molecules involved.
The reason we can now for many proteins draw pictures of how the molecule looks on the tiny scale that it is, is the field of structural biology. The scientists working in this field use techniques like X-ray crystallography, nuclear magnetic reconance spectroscopy and cryogenic electron microscopy to determine the structure of a protein at resolutions down to 2.7 Å (Angstrom, 1Å = 0.1nm). Once they manage to get a reliable picture of how a protein molecule looks, they publish their work and submit it to the world-wide protein data bank, which you can access freely using one of three websites: PDBe, PDBj and RCSB.
I tried searching for the proteins in your animation (CD4 and the HIV envelope protein gp120). Some structures do exist for them (e.g. http://www.ebi.ac.uk/pdbe/entry/pdb/2ny1) but they seem to contain only part of what's shown in the animation. Often certain parts of proteins can't be identified by structural biology for technical reasons, but we know they must be there based on the genetic information we have, and we can make some educated guesses about what those bits of the protein might look like. It seems in this animation, there was quite a bit of educated guessing involved.
A lot of biological science nowadays goes by the paradigm "seeing is believing". Many modern animations are reproduced from actual recordings where the process shown in the animation can be seen happening in reality. Cell divison for example is an intensively researched process that has been filmed using many different microscopic techniques and focussing on many different parts of the cell, figuring out what each protein or other molecule does during the process. Putting together knowledge from many different teams, you can generate a full picture of what everything is doing at the same time.
As far as reading recommendations go, any basic molecular biology textbook like Molecular Biology of the Cell by Alberts et al. (pick it up from a library), or lectures freely available online should allow you to gradually wrap your head around it.


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How harmful is aluminium?
I have been taught in school that aluminium is harmful for brain.
Thus sour meals should not be cooked in aluminium pots and it is unhealthy to add lemon juice to tea while there is teabag in the cup, as acid facilitates aluminium release.
The only safe limit for aluminium intake I know is FDA pediatric limit for parenteral sources (5 μg/kg bw/day). I know no research the limit is based on, but I have read an abstract of a paper claiming it was impossible to comply with the regulation in patients weighting less than 50 kg.
Nowadays aluminium ions are present in several vaccines, which are considered safe to be injected intramuscularly in infants despite despite being  nowhere near the FDA limit.
I'm quite confused how strict should I be in avoidance of aluminium intake (especially dietetary intake - which I expect to be far less effective than parenteral).
[EDIT]
It seems aluminium is also a component of some antacids which are used to treat heartburn.
Does it mean aluminium consumption is safe at general, or it is just considered to be less harmful than acid indigestion (there are some side effects  mentioned - but nothing about accumulation in the brain)?

@RonJohn I think iron is even more hamful then. ;)

Too true, but this wasn't a comparative question...  :)

Now I'm wondering if the discount was worthwhile on that depleted uranium skillet.

@jamesqf if God had wanted man to hit with aluminum bats, he wouldn't have invented trees!

well the thing to understand is that "toxicity"  is relative.Anything can be harmful if consumed in high quantities .

If cooked using aluminum pots ,the aluminium reacts with the aluminium creating aluminium salts ,which may be more harmful than the metal in elemental state, as it accumulates easily.

a bit of both and also, sorry for the typo .-. , been doing that all day

@pranavB23 it nicely fits the level of abstraction of other comments ;)

@pranavB23: Yes, for instance both water and oxygen are necessary for life, but too much of either will kill you.  E.g. https://www.webmd.com/fitness-exercise/features/water-intoxication#1

@jamesqf which reminds me about threat of dihydrogen monoxide ;)

Here is a link to the Public Health Statement for Aluminum produced by the Centers for Disease Control and Prevention (CDC) in the United States.  There is much more information on the web page but the following are some of the more pertinent points to your question.
Potential Health Effects
Workers

Workers who breathe large amounts of aluminum dusts can
  have lung problems, such as coughing or changes that show up in chest
  X-rays. The use of breathing masks and controls on the levels of dust
  in factories have largely eliminated this problem.
Some workers who breathe aluminum-containing dusts or aluminum fumes
  have decreased performance in some tests that measure functions of the
  nervous system.

Humans

Oral exposure to aluminum is usually not harmful. Some studies
  show that people exposed to high levels of aluminum may develop
  Alzheimer’s disease, but other studies have not found this to be true.
  We do not know for certain that aluminum causes Alzheimer’s disease.
Some people who have kidney disease store a lot of aluminum in their
  bodies. The kidney disease causes less aluminum to be removed from the
  body in the urine. Sometimes, these people developed bone or brain
  diseases that doctors think were caused by the excess aluminum.
Although aluminum-containing over the counter oral products are
  considered safe in healthy individuals at recommended doses, some
  adverse effects have been observed following long-term use in some
  individuals.

Some regulation and recommendations:

Drinking water

The EPA has recommended a Secondary Maximum Contaminant Level (SMCL)
  of 0.05–0.2 mg/L for aluminum in drinking water. The SMCL is not based
  on levels that will affect humans or animals. It is based on taste,
  smell, or color.

Consumer products

The FDA has determined that aluminum used as food additives and
  medicinals such as antacids are generally safe.
FDA set a limit for bottled water of 0.2 mg/L.

Workplace air

OSHA set a legal limit of 15 mg/m3 (total dust) and 5 mg/m3
  (respirable fraction) aluminum in dusts averaged over an 8 hour work
  day.

Yep, good catch.  I needed to remove the Inhalation at the beginning of the sentence.  I'll revise to avoid any further confusion.

Why is there one section titled "Workers" and another "Humans"?

@Phil each of these species obviously lives in a different environment, thus have a different aluminium exposure ;)

@Phil: Possibly because some of it is taken from information provided for industrial safety uses?  After all, the only people who are likely to be exposed to large amounts of aluminum dust are people who work in aluminum-related industries.  Note also that inhaling large amounts of any sort of dust is not a good idea, and is rather different from ingesting material in solution.

@jamesqf are the workers not human then?

@Phil: When have I suggested otherwise?

@jamesqf by defending the incredibly odd scenario where we have information under two headings: "Workers" and "Humans".  It's clear from the content "Workers" does not refer to bees (for instance), but human beings who happen to be working with the stuff.  Which makes "Humans" an odd heading for the next paragraph.  It implies the other paragraph isn't referring to humans (ie, the workers aren't human).  Perhaps "Workers" and "The general public" would be a better set of headings?  Just defending it as copy-paste means the author was sloppy and lazy.

@Phil: As I said, because the only people likely to have significant long-term exposure to aluminum dust are those who work in aluminum-related industries.  Whereas "humans" - the general public PLUS workers - is about equally likely to be exposed to dissolved aluminum-containing chemicals from cooking pots, antacids, and the like.

Just as a note: "some adverse effects [...] in some individuals" is extremely vague. It is unclear whether CDC refers to brain and bone disease observed in people with kidney disease, or to other adverse effects in otherwise healthy people.


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Can anyone identify what type of bug this is?
Can anyone identify what type of bug this is?

Hi, @Correo. Can you tell us where this bug was found please?

From a rummage around Google images for "black and red striped bugs", your insect looks a bit like:

Mylabris syriaca

Hycleus ornatus, although yours has different antennae.

The antennae do not match Hycleus, and it is definitely not Pyrrhocoris (Hemiptera). It does look like a blister beetle, as is Mylabris.

looks like Mylabris syriaca to me..

I'll take a wild guess and say that this is Mylabris quadripunctata


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Xylem in the centre of the root
I want to ask a question about xylem in the centre of the root.
I am reading a book about transport in plants, and it reads this regarding the root structure:

Roots are subjected to vertical stresses - they have to be able to resist being pulled out of the soil.  A central core of strong xylem tissue gives ideal resistance to being uprooted and at the same time gives economy of space.

I'm confused about this passage.
How does the centre of the root being xylem tissue exactly prevent the resistance to pulling forces upwards out of the soil?

(+1) because this doesn't make any sense to me - I can't see why having xylem further to the centre of the root would withstand vertical stretching forces

Roots also must resist compression, as root tips push out against soil particles.

Further, I think your diagram of root structure only applies to the young growth near the root tip, just as near the apical meristems above ground are xylem-phloem bundles separate by cambium. Between, the core of xylem (wood) covered by cambium, covered by phloem, covered by various epidermal tissues prevails in woody plants

The is something called the Pressure Stiffening Effect (turn on a coiled garden hose and watch it try and uncoil for instance), pressure in the fluid filled xylem stiffens the root, making it harder to pull out, Roots are rarely completely vertical or straight to pulling them from the soil generally involves them flexing, which the stiffening pressure resists. its the same reason an Inverted Y of steel can anchor in soil but an inverted Y of rope will not, the steel resists bending thus you have to displace all the soil above it to remove it.


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Ribosomes producing proteins, but need proteins to be produced?
So according to my textbook:

RNA is used to create ribosomal RNA (known as rRNA) which is then combined with proteins to form the ribomsomes necessary for protein synthesis.

I'm a bit confused with this statement, as ribosomes are needed to synthesise proteins, but in order to create ribosomes proteins are needed in the first place. How does this work, does the proteins needed for the creation of rRNA come from a different source? Or by synthesising proteins via ribosomes produce more proteins than required to create the ribosomes in the first place?
Also, where are the proteins synthesised? On cytoplasmic ribosomes, or on ribosomes bound to the RER?
Thanks!

Ribosomes are the only means we know by which cells produce proteins. Consequently, all proteins are made by a ribosome, including the proteins that then become part of a new ribosome. It's never a question of "more proteins than required" because there are different types of proteins and to make a ribosome, you need those specific types of proteins known as ribosomal proteins. The process of making ribosomes is known as ribosome biogenesis.
This raises the obvious question of where a cell gets its ribosomes from when it is "born". The answer is simple: from its parent. When a cell divides, each daughter cell is made of the components of the parent. The cytoplasm also gets divided, and each daughter cell receives mitochondria, ER, etc. from the parent cell. By the time those ribosomes break down, they will have produced new ribosomal proteins for new ribosomes already.
According to this review from 2017, it appears the ribosomal proteins made in the cytoplasm (so, cytoplasmic ribosomes) get shuttled into the nucleolus, where they get assembled with rRNA to make new ribosomes, which then get exported out of the nucleus into the cytoplasm.

To clarify on the original poster's question of "does the ribosome produce more proteins than is required": maybe it's not obvious to them that a ribosome is continuously producing proteins and will produce many proteins (not a fixed quantity) over its lifetime.


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In the Selfish Gene, the chapter about ESS, how do the doves spread their genes?
In his explanation of the Evolutionary Stable Strategy, in the Selfish Gene, Richard Dawkins repeats a couple of times, that a population of hawk-type males would make the ground for a dove-type individual to spreat his genes, because the dove always retreats against a hawk and if an average hawk loses every second match, than he'll be worse off than the dove that always retreats and stays unhurt.
My question is - how dose a male, that does not win a single contest for a mate and therefore doesn't get to mate at all, spreat his genes?
Does the ESS imply that there are ways to breed bypassing the contest?

I don't know enough about the model to really give an answer, but I guess that if a dove keeps trying he might eventually come across a mate who isn't being protected by a hawk. The dove's strategy isn't winning fights, but in finding opportunities where there won't be a fight.

Game theory
Your question is not as specific to biology as you may think. The hawk-dove game is a type of game in game theory, a field of mathematics. Game theory is used in biology, in economics, in psychology and many other disciplines.
The hawk-dove game is often called the chicken game. If a game is defined as a chicken game, then it has an equilibrium different from 0 or 1. Otherwise, it may not.
You need to fully specify the scenario of interest to figure our what type of game we're dealing with to know what type of game we're dealing with and what are the possible equilibriums.
For more information, have a look at the mathematical field of game theory.
You specific scenario
The scenario as written in your post is not fully discribed. In your question, you define the doves such as they have a fitness (or a payoff in game theory terms) of 0, whatever is the state of the population. For such case, of course, a frequency of doves of 1 cannot be an ESS. However, under such case, you are not dealing with a hawk-dove game. I suspect you misunderstood the game as defined by Dawkins (it is also possible that Dawkins did not fully define the game he's talking about).
In short...
In short, I can't say much else than just "read more about game theory". However, you might want to cite exactly Dawkins so that we can understand exactly how he describes the specific game at play and comment on the expected outcome.

A male that does not mate will not spread his genes. Females might, if they have the option to reproduce asexually. However, this is probably not the answer you are after though. What you need to do is to look at the assumptions behind the game theory model being used.
For instance, some of the assumptions in a basic ESS-analysis are usually:

that the population size is infinite.
that the game payoffs are fitness modifiers and do not determine absolute levels of fitness.

Point 1 means that the game payoffs refer to the average payoff of individuals in each type of encounter. Point 2 means that there is always a baseline level of fitness, so all strategies are able to reproduce. Sometimes, assumption 2 is reformulated in terms of asexual populations, which means that all individuals will be able to reproduce (so the hawk-dove game will strictly not the modelling access to mates).
Therefore, doves (which never escalate a contest) will be able to "spread their genes" (win the contest) 50% of the times when there is a dove-dove contest (here is a description of what appears to be the normal version of the hawk-dove game). A single dove that enters a population will also be able to reproduce, even though it will never win contests (based on assumption 2). Again, remember that the game payoffs are fitness modifiers and does not determine the absolute level of fitness.
This means that individuals that play the dove strategy will still be able to spread their genes to later generations, but this doesn't preclude that certain dove individuals never get the chance to reproduce. This also means that there isn't any need for "ways to breed bypassing the contest", since one of the assumptions is that all strategies can reproduce, and in this case all strategies also have a payout option where they sometimes win the contest (which is the case for the hawk-dove game).

You are adding assumptions that are not there.
You assume not winning equals not mating, it doesn't, if a dove meets a female by herself they mate. The example of elephant seals he uses shows this, some males fight others wait for unattended females.

Oh, didn't notice that..


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Does human behaviour that is caused by inheritance depend on the environment and lifestyle in general?
Different breeds of common domesticated animals such as horses and dogs clearly show different behaviour, instincts, social relationships and similar, due to their biological inheritance. Still they can easily mate with other breeds of the same species. This also applies to wild animals, for example the wolfs living in the rainforest on the Canadian west coast prey on fish (and are maybe expected, with time, to go through a similar transformation as the predecessor to dolphins, that where actually wolf like animals, did when they resettled to the oceans) while inland wolfs prey on moose and elk etc, which requires completely different hunting technique, tactics, pack size and so on.
Are there any similar examples for humans? I reckon that living in the jungle or in the desert or on Greenland should reward different behaviours/traits that influence behaviour. Also going from a hunter-gatherer society to an agricultural society should reward different behaviours, social skills and similar aspect of human life.
Are humans like other animals in this respect (any examples?) or are we unique (?) in the animal kingdom when it comes to the influence of genetics on our behaviour?
One reason I ask is that I got second hand (without sources) information claiming that the natives of Mexico has the highest prevalence, of any population measured, of genes that are known to be connected with/causing ADHD. Mexico was also one the last places on the planet where humankind settled.
The argument went something like this: "during prehistoric time individuals with ADHD tendencies tended to be more adventurous than their peers and therefore traveled further". If this is true, people in Mexico's behaviour should be slightly different from people in current Kenya and Tanzania (by many scientists claimed to the birthplace of humankind), at least if you measure ADHD related traits.

I feel that 99% of the time that someone asks "are human unique concerning ?", the answer is nope. There's nothing exceptional about humans in this respect.
Rephrasing your question
Your question can be rephrased

Is heritability sometimes different from 0 or 1 for humans too?

If you do not understand well why this is a good rephrasing of your question, then you should definitely have a look at this post.
Is heritability sometimes different from 0 or 1 for humans too?
Yes, humans are not exceptional in this regard. In humans, other animals, plants, fungi, bacteria, archeabacteria and for any other living things, any behaviour (and any phenotypic trait in fact) can have a heritability that differs from both 0 and 1, or in other words, there can be for any trait both genetic and environmental variance underlying phenotypic variance in the population.
In fact, very few traits that have a non-zero genetic variance has no environmental variance. Have a look at the post List of heritability estimates in humans? for a list of traits on which we measured heritability.
ADHD
The difficulty with a trait like ADHD is that the methodology to measure it vary a lot from one country to another or even from one practitioner to another. But yes, for ADHD too, there is both genetic and environmental variance underlying the observe phenotypic variance (Thapar et al., 2000).

FYI, @Remi.b, Chrome is flagging your website for not being secure.  I would screenshot it to you except there is no capacity to post a screenshot in a comment.

FYI, my assumption was that humans are not unique in this respect. However, it is a very sensitive subject because a logical next step would be that certain ethnicities ("races") might be better on organizing their lifes or societies which would lead to the conclusion that different outcomes between ethnicities or countries are "fair" and well motivated.

Different ethnicities might differ for genetic reasons as much as they may differ for environmental reasons. The environment in which an individual is born will depends upon the climate, the social environment, etc... Environmental factors such as the social environment or the amount of wealth is greatly affected by the past events of the society in which the individual  was born. There is nothing too sensitive about that. It becomes sensitive when you try to put a judgment of what is "good" or "bad" and when you try to make an a priori judgment of why the outcome is as it is.

For example, if you consider that the situation in Great Britain is bad because you don't like their food, then you might either not realize that food taste is very personal and you might put too a weird emphasis on food when judging the value of people.

As another example, if you consider that the current political situation in Syria is bad (which, so far the vast majority of people would happily agree with) and that you assume this bas situation is caused by the fact that they are genetically more violent, then you ignore the history of the region and the various international interest that is causing the current situation. That's were subject become sensitive. Anyway, I am definitely off-topic here!

As @Remi.b said (I upvoted, by the way), humans are rarely completely unique. The first law of behavioral genetics is that all behavioral traits show non-zero genetic influence (This is one of the most replicated findings in the field). More precisely, heritability estimates of behavioral traits are larger than zero, $h^2>0$ (but smaller than one, therefore environmental differences also contribute to the variance of the phenotype).
Population Differences
You say the following:

Different breeds of common domesticated animals such as horses and dogs clearly show different behaviour, instincts, social relationships and similar, due to their biological inheritance. Still they can easily mate with other breeds of the same species.

Then you question whether humans are different in this way. As you noted, it is a socially sensitive topic, but influential geneticist David Reich has very recently written an opinion piece on this sensitive topic (which I suggest you read in full, given your question).
For example, here is a quote by Reich:

While most people will agree that finding a genetic explanation for an elevated rate of disease is important, they often draw the line there. Finding genetic influences on a propensity for disease is one thing, they argue, but looking for such influences on behavior and cognition is another.
But whether we like it or not, that line has already been crossed. [...]

Regarding population differences:

And since all traits influenced by genetics are expected to differ across populations (because the frequencies of genetic variations are rarely exactly the same across populations), the genetic influences on behavior and cognition will differ across populations, too.

Attention deficit hyperactivity disorder
I have not looked into the genetics of ADHD. It is possible that native Mexicans have a higher rate of ADHD-increasing alleles -- I simply don't know. However, I would suggest you don't completely accept this claim without good sources from primary literature (Also the evolutionary "story" for this claim didn't sound too convincing, in my opinion. However, that may just be because you've been given a weak version of the argument). As with anything, the variance in ADHD is partially due to genetic differences.


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What kind of worm is this?
What kind of worm is this? I’ve seen them in my bathroom and kitchen which are both ceramic tile. This morning I walked in the kitchen and this one just so happened to be dead.

Welcome to Biology.SE. Where do you live (country/region/type of ecosystem)? What is the approximate size? Did you notice any behaviour of interest? How fast do they move? Any other info?

I'd say that isnt a worm but a nonvenomous blind snake specie named Indotyphlops braminus
(Indotyphlops braminus)  .(Brahminy Worm Snake )


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If we sequenced the genome of every species, would all phylogenies agree?
The Tree of Life is still up for debate. Most of this debate seems to be due to a lack of genomic information, but that deficiency is decreasing rapidly with advances in technology and sequencing power.
Hypothetically, if we knew the genome of every species, would we resolve all phylogenetic debates? If not, what would still be up for debate?

Horizontal gene transfer
Don't expect to have a tree! Horizontal gene transfer happens and therefore we would end up with a network, not a tree.
Gene trees
Different DNA sequences have different evolutionary histories. See, in particular, the question of incomplete lineage sorting. This means that one may compute a tree for a given DNA sequence that must disagree with the tree of another sequence. So, don't expect a perfect species tree where all sequences will agree on.
Note that the two points "Horizontal gene transfer" and "Gene trees" are highly related. So much so that they could fit together.
Not all individuals have been discovered
If by saying of every organism, you meant "of every organism that we encounter", then we still have the issue of organisms that we have never encountered. If you meant "absolutely every individual that exist", then this is a non-issue. It also matters as to whether you mean every individual of every species or just one individual per species.
Also, it is slightly unclear whether, in your hypothesis, we can sequence all dead individuals! Extinct lineages would still not be resolved if we cannot sequence them.
Massive mutational events
It is possible that very large mutational event could prevent us to see the exact relationship between individuals. But that would only interfere on an extremely fine scale phylogeny (intra-species level).
Methodology
If we really sample all the individuals, the detail of the methodology may not matter much. It will still need to be decided whether we want to consider AATC closer to AA.C or to AGTC (where . indicates a deletion). Again, this will likely only matter on a very fine scale (intra-species level).
Computational power
Of course, if we sequence every nucleotide that exists on earth, we would never have the computational power to even store the data. Not talking about actually processing it. We would not either have the computational power to process the sequencing (nor the necessary amount of products to allow for the sequencing to happen).
If you meant to fully sequence only one individual per species (and then again the arbitrary nature of the concept of species will complicate things up), then we might have the computational power (see @KonradRudolf's comment)

The concept of species can often be misleading. You might want to read the post How could humans have interbred with Neanderthals if we're a different species? for a discussion on the concept of species.

You could compress the data. Lots of it is similar; I'm sure that somebody would come up with a data compression algorithm that works better than the existing ones on groups of genomes.

“we would never have the computational power to even store the data.” — I’m not sure how you got there. Even uncompressed, genomic data isn’t that big. The human (haplotype) genome is a measly 3 GiB. Assuming this is representative (it’s actually rather on the high end!), and assuming estimates of 8.7 million distinct species, this would result ~26 PiB data. That’s peanuts. Modern sequencing efforts routinely produce as much data each month!

@KonradRudolph He was not talking about merely sequencing any (however defined) species but every distinct genome - which is basically every life form on earth. So at least a few billion times what you calculated.

@Nicolai Fair point but given the text of the actual question this is probably just an inaccuracy in the title (OP means “organism” = “species” rather than “organism” = “individual).

@KonradRudolph Yes, that's why I said if we sample every nucleotide that exist on earth. I edited this part to make it even clearer.

@Remi.b I think "sample" is the wrong term then because it means that you don't look at each one individually.

I am not sure I understand why sample is not a good term. I replaced "sample" by "sequence". If you have a better alternative, please feel free to edit the answer. Thanks

Assuming he meant every species, it's within range of a DVD jukebox.

@KonradRudolph Do we really produce ~26PB per month? You might want to try an answer to the question How much Open Access Data is there in genetics?

@Remi.b Not "we": Multiple individual institutes/companies each. Thanks for the link, I'll try to find some official statistics. Most of this is unfortunately neither Open Access nor public in any way.

@Nicolai Due to heavy redundancy in many species genomes (all those conserved regions especially), a "billion times" is really not all that much. You could quite easily store a large number of genomes in a radix tree or another highly compact data structure. SNPs and such do not need to be explicitly specified for each individual creature.

A quick (but not quite glib) answer (having worked in the field): Given identical sequences of DNA from well-known species with likely close relationships - in other words, comparing beetles with other beetles, rather than snakes or bananas - respected researchers almost never arrive at the same phylogenetic trees, especially with very large sequences of DNA, even if they are working with exactly the same DNA samples.
There are several reasons.

Researchers have differing opinions about the weight to give the likelihood of different possible mutations that could have resulted in the differences between the DNA sequences. This automatically results in different phylogenetic trees. This leads to:
There are innumerable paths that could lead to the differences in DNA sequences. This means that there is no way of knowing the actual path that in fact led to any given difference, much less all of them that make up even two different species. This then means that there are innumerable different phylogenetic trees describing the possible ancestry of even two relatively similar species. Computerized tree generating and sorting algorithms are used to make sense of the huge numbers involved, but they cannot and do not list all of the possible trees, as that cannot be done. The list is infinite in size. Instead, they stop generating trees once they reach a pre-set limit (by the researcher, based on heuristics) of likelihood, then sort the ones they have. It's not as random as it sounds, but there is a degree of guesswork in any phylogenetic tree. This could only be mitigated by knowing the DNA sequences of every single ancestor of every single organism so that we could see how the DNA changes at every base pair in each sequence in each generation. It is a little like asking for time travel, but the math is harder.
There is fundamental disagreement, from species to species, about which changes in DNA make for different species and which merely represent variation in a single species. In reality, there is approximately one mutation for every cell division (see this article on mutation rates in humans for a look at the scale of the problem1) across most known species, most of which are meaningless or are spontaneously removed via cell or (often, in the case of germ cells) organismal death. This is a real issue, discussed at length by systematic taxonomists.
Because the DNA of different species is actually different, it is not possible to achieve a one-to-one match of the DNA sequences between two species. Researchers make a best guess,  based on what they think is most likely (and gets more difficult the more species are used).
Statistical methods (which are required by the infinite size of the data sets, even with (relatively) small amounts of DNA and numbers of species) only tell the likelihood of a particular tree. They cannot predict the actual phylogeny. This can only be known if all (or at least most) of the ancestors of each of the representative organisms' DNA can be examined for the mutations that resulted in speciation.

In short (because this answer really was not, despite what I originally said), DNA sequences of every extant species would not be enough to resolve phylogeny. DNA sequences of every extant individual organism would not be enough. Only knowing the DNA sequences of every organism that has ever lived would be enough to resolve phylogeny completely.

No, but it would help. First, though, let's talk about limitations. The limitation you speak of is not rapidly disappearing. The barcode initiative (attempting to sequence a small fragment of mt DNA from every organism on Earth) has been going strong for almost 20 years now and is not even close to covering every species on Earth. Many species have only been encountered once, and have not been seen since their description. Most species remain undescribed. Then there is the issue of computing power. To analyze the data for 10 million species (one ballpark estimate for the number of species on Earth), or even 1.8 million (current number) would not be possible. In addition, phylogeneticists are an argumentative bunch. It is likely there would be debates over methodology. There would also likely be errors in the handling of the data. There would be contamination issues, and labelling errors.
However, as you said, your question was hypothetical. A carefully, error-free analysis, assuming complete coverage and perfect models, and assuming we had the computing power to do it would resolve most of the debate. It would still not resolve species with reticulate evolution or hard polytomies (groups that simultaneously split into more than two lineages). For that, you would need more than one individual to represent a species, and even with say 10 per species, it would be difficult.

Also the vast majority of species are extinct thus have no DNA left to sample.

"[T]hus" seems to be a bit rash. DNA can be preserved in and extracted from all sorts of media, e.g., amber. The amber doesn't care much whether the species embedded in it is extinct or not.

This question is a lot like asking "if we found every fossil there is, would we know everything about life in the past?" or "if we found every ancient manuscript that exists, would we know everything about history?". The answer for both of those is "no", because fossils and manuscripts are an inherently incomplete record. Not all organisms fossilize; not everything is written down; not all fossils or manuscripts survived until today, and those that did suffered various levels of decay; the longer it's been, the more they've decayed.
The same is true of the phylogenetic signal one can infer from genes. The reason we can infer ancestry from genes in the first place is that everyone gets their genes from their parents, and those genes are slightly modified each generation. This means that siblings have very similar genes, cousins have slightly less similar genes, and so on so forth until you have every living thing's family tree.
Except that several factors mess this up. Here are a few:

Everyone doesn't get their genes from their parents. Animals mostly do, but bacteria swap genes such that each gene can have its own family tree, independent of that of the bacteria it's in. This is extremely relevant to the origin of life in particular because it involved bacteria and archaea.
The "very similar, less similar, etc" ranking works if we have infinitely large genes, containing infinite information. If we don't, then at some point you get two individuals whose every base of DNA is different from one another, and from that point on they can't get more different, however distantly they're related. Also, with finite DNA you get mutations on top of mutations - you might have two distantly-related lineages that get the same mutation by chance, or an old mutation gets reversed, or a new mutation happens on top of an old one, looking like only one mutation. All of this can blur the "signal" of relatedness, and it's the reason phylogenetic trees are calculated using statistical methods and as much DNA information as is practical. We (most of us) have huge genomes, which is the reason we can make phylogenetic trees as good as the ones we do, but there are genomes small enough that they can have been completely shuffled since life began, and it's harder to build phylogenetic trees there. On the opposite end of the spectrum, organisms that are so closely related that there are few differences to work from can be hard to sort out too, simply because a single event like mutations overlapping or being reverted can have a bigger impact when it isn't drowned out by thousands of other differences.
The theory also relies on the mutations being random; every individual is different from their parent to a predictable extent because no factor makes some mutations more likely than others. This is the case for many parts of the genome, and that does make them pretty good for phylogenetics, but many other parts are selected for or against. Meaning some mutations are more likely to stick around because they're beneficial at some point, and others are more likely to get weeded out quickly because they're harmful. This is why, even in organisms with small genomes that could be entirely shuffled since life began, they aren't really entirely shuffled: the parts of the genome that are necessary for life stay the same. This can be good for examining deep phylogeny, because it means those sequences change a lot more slowly. It can also be bad, because now family relationships aren't the only reason they change: fitness also affects that and you can no longer be sure that two organisms have similar or different DNA because of their relatedness, or because they've adapted to the same or different functions. This depends on the DNA in question, whether the function can be done by many different DNA configurations or only one, but at the end of the day, it's another factor to muddle the relatedness signal. And while the slower rate of change in conserved sequences makes it possible to separate very deep phylogenies, by the same token it won't do so at a very high resolution, because there are fewer differences to work from.

So essentially, like fossils and manuscripts genomic information is an imperfect signal for building family trees, and it's a decaying one - the longer it's been, the more time there's been for the various factors that make it imperfect in the first place to work their magic. So to answer your question, having the genomic information for all species or organisms would help a lot with resolving the Tree of Life, and might even resolve all the current debates on it. But it might also not. Hard to know without actually resolving the debates. And even if it does, there would still probably be outstanding questions; the general outline of the picture would be clear but there would still be all kinds of details that weren't filled.


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Does a cell deprived of growth factors undergo apoptosis or G0 stasis?
I can't seem to find a decisive answer on this topic in any of my textbooks. If a cell is deprived of growth factors does it:

Activate apoptosis
Go into the G0 phase but keep living?

Thanks.


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Building microtubules
I have some questions regarding building microtubules:

Do alpha and beta monomers always exist as dimers when they are bonding to form tubulin?
When tubulin structure is destroyed, do alpha and beta monomers fall apart as dimers or monomers? and does it happen at the positive or negative end?

Microtubules polymerise from and depolymerise into alpha-beta-tubulin dimers.
Both happen on both ends, see this question: At which end does polymerization of microtubules occur?.

Thanks for your answer. Wouldn’t it be more favorable to connect monomers rather than dimers ? because then it wouldn’t matter how the dimers are oriented to get alpha on top of beta.

The orientation of each monomer would still need to be the same, regardless of the order in which the bonds are made, because none of the molecules involved are symmetric. I don't know though how it's better to have dimers around as building blocks rather than monomers.


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PCR a plasmid with self-complimentary regions?
I am trying to do a PCR using a plasmid as the template, pretty basic stuff. But the problem is that my forward primer just happens to bind to another location on the plasmid in the reverse orientation, in between the proper forward binding site and the reverse binding site. This isn't an example of non-specific binding, the sequences are perfect because the plasmid contains self-complimentary regions and my forward primer just happens to land right on it.
Here is a diagram:

Simply optimizing the melting point or magnesium concentrations probably won't help, because the sequences are the same. I'm doing this cloning to insert a reporter gene into the vector, and I need to place it very precisely, so I don't know if I can order a new set of primers, the insert needs to fit there.
The bad PCR product is about 500 bases shorter than the good product, but I only see the bad band on gel when I run a normal PCR. If I reduce the amount of forward primer and increase the reverse oligo, I can see the good band, but the bad band is still there and the total yield is much lower.
So my idea right now is to do an asymmetric PCR using the reverse primer only, then add forward primer to create the double-stranded DNA, then separate the good and bad bands using gel electrophoresis. But I don't have a clue how many cycles I should run each step, or how much forward primer to add, etc. Additionally, asymmetric PCR has low yield due to arithmetic amplification, but once I add the forward primers it can begin symmetric PCR and geometrically amplify both bands, but I think the shorter bad band wins out.
Does anyone here have experience with this sort of complex PCR, or suggestions to improve my yield?

What's the problem wtih using a lower percentage gel and running it for a long time on low voltage to separate the two bands and cut out only the longer one you want?

Can you amplify two separate regions that meet at a restriction site and reconnect them by ligation? Without knowing the exact sequences and purpose, I'm afraid it's hard to give clear recommendations, because the best way to approach this kind of thing tends to be highly specific.

@Armatus When doing the PCR using equal amounts of both primers, I did not see the desired 3000 base band, only the bad 2500 base band on gel. The ladder had bands at both 3000 and 2500, so I know the bands should have resolved if they were both present in the PCR sample. The shorter band must be winning out. I was able to see both bands when I used much more reverse primer than forward primer, but the bands were very faint.

@JackAidley I designed the cloning procedure around InFusion cloning, but that system can work with multiple fragments as long as they have a 15 base overlap. I can probably design a couple more oligos that bind on top of a restriction site. That will let me cut the plasmid and PCR the shorter pieces with overlapping ends in separate reactions, then mix all the parts together for the InFusion reaction. I'll let you know how it works, but it will take time to get the new oligos.

@user137: if you combine the fragments by PCR won't you encounter the exact same problem with your fusion (aka stitch) PCR?

@JackAidley I don't think so. If I find a good restriction site I can cut the plasmid at that site and create a new set of forward and reverse oligos that bind at the cut end. I can run 1 reaction using the blue primer from above and the new reverse primer, and the other reaction using the green primer and the new forward primer. The blue forward primer can still bind to the bad red site, but if the plasmid is cut between the red and blue sites it shouldn't amplify. I've done a similar thing using this same plasmid at a different site, where I had direct repeats around an EcoRV site.

@user137: That's not what I meant. You suggested combining the fragments at the end using an overlap; wouldn't your fwd/rev primers for the final product be your current ones?

How much longer would the forward primer have to anneal uniquely to the one locus?

@JackAidley The InFusion reaction doesn't use PCR to assemble the fragments. Each fragment is created by separate PCRs, but the assembly is carried out using proprietary enzymes that can attach fragments with a 15 base overlap. This manual might explain more than I can

@swbarnes2 At least 9 bases, but it's already 30 bases long. Of course a 39 or 40 base oligo isn't impossible.

@user137 great that should work then.

From experience, your present problem will not completely go away no matter what you do.  The idea for asymmetric PCR is not a bad idea. However, you will only get linear amplification of the desired product from the initial single primer, so you will not "see" any product even after 30-40 cycles.  This first single primer PCR might also cause downstream problems with amplification of undesired products made during the second PCR (junk products).
I agree with comment #1, but then neatly cut the "visible" "good" band out of the gel.  Suspend (crush) the agarose band in sterile TE buffer, and then use an aliquot of that as template for a secondary PCR (use equal primers - maybe 30 cycles).  This should provide more than enough "good" starting template.
Alternately, you could design a new forward primer that does not have a bad secondary location on your plasmid.


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Nonpancreatic digestion of tryglicerides
In an answer about coconut oil I can read

the digestion of coconut oil does not involve in the Pancreatic digestive enzyme system

In both primary and secondary school I have learned that fat needs to be processed by pancreatic lipase as tryglicerides can not be absorbed.
Are medium-chain tryglicerides an exception (they can be absorbed), are there other (nonpancreatic) lipases in human digestion system, or is the linked answer wrong?

There are two possibilities concerning the further metabolism of MCTs: the glycerides are absorbed and immediately transported through the portal vein to the liver whereupon they are oxidised to release energy.
Alternatively, dependent on the size of the MCT, ranging from hexanoic acid tails to dodecanoic acid tails, it may undergo the standard catalysis by pancreative lipase to form monoglycerides, diglycerides and free fatty acids.
More information regarding the physiological effects of middle-chain fatty acids may be available from: https://academic.oup.com/jn/article/132/3/329/4687297


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Why are my calculations for O2 requirements of daily metabolism so far off?
When I attempt to calculate the O2 necessary for a day of metabolism at rest (for an imaginary average human) and compare it with the expected O2 consumed per day my results differ by a factor of 3. I don't expect it to be 1 to 1, but a factor of 3 makes me think that I am missing a fundamental concept.
For our fictional human, I'm starting with the values for 1 MET. Specifically:

RMR (kcal / kg / hr) = 1
VO2 (mL / kg / min) = 3.5

I then define the weight of my human:

weight (kg) = 70
RMR (kcal / hr) = 70
VO2 (mL / min) = 245

And convert to more useful units:

RMR (kcal / day) = 70 * 24 = 1680
VO2 (L / day) = 245 * 60 * 24 / 1000 = 352.8

At this point, my understanding is that consuming 352.8 L of oxygen should produce somewhere in the ballpark of 1680 kcal at rest. My next assumption is going to be that aerobic respiration of glucose is accounting for all of the energy throughout this day of rest. I'm aware this isn't reality, but I wouldn't expect it to be 3x off. I'd guess that either this assumption is wrong or I'm misunderstanding something in the following math.
Let's start with some more constants regarding cellular respiration.

ATP creates 7.3 kcal / mol
An average of 30 ATP are generated per glucose (glycolysis, krebs, etc)
6 O2 are required to aerobically metabolize 1 glucose

Given the energy to ATP ratio, we can compute the ATP necessary per day. I should note that the result here is about twice as high as reference numbers I've seen so I am suspicious.

ATP (mol / day) = 1680 / 7.3 = 230.1369863
Glucose (mol / day ) = 230.1369863 / 30 = 7.671232877
O2 (mol / day) = 7.671232877 * 6 = 46.02739726

To convert the O2 requirements for our ATP from moles to liters, we use Avogadro's law at standard pressure (100 kPa) to conclude there are 22.712 liters per mole in a gas.

O2 (L / day) = 46.02739726 * 22.712 = 1045.374247

And finally, we can see that my calculation says that you need 1045.37 liters of oxygen to produce 1680 kcal of energy through aerobic respiration, but earlier I computed that you should only need 352.8 liters using 1 MET as my basis. There were assumptions made in there, but these results make me think that I am still misunderstanding a fundamental concept.

The math was correct, but there was a misunderstanding in what some of the numbers represent. The energy expenditures listed for RMR include resting dietary thermogenesis in addition to the actual ATP energy used for work. You can see that the same is done for reporting Calories in food (e.g. 4 per carb) at http://www.fao.org/docrep/006/Y5022E/y5022e04.htm
When this is taken into account, we use 686 kcal/mole of glucose to get similar oxygen numbers. This includes the energy for the ATP and the energy from heat.

In other words, RMR accounts for energy actually burned while ATP from metabolism accounts only for energy that can be made use of. The reference values arrive at 4 kcal/g glucose RMR and about 1.2 kcal/g glucose useful energy. This is an extremely interesting result tbh, surely somebody must have published about this inefficiency of metabolism..?

Yeah, there’s stuff out there about that efficiency and how it changes under certain conditions and for different pathways. I found it interesting that rmr and estimations for exercise and the like basically get made for the efficiency of a specific mix of fuels (e.g. carbs/fats). Thus they should be less accurate for calorie balancing if you have a keto diet or some other extreme. With all the other variables, it’s probably lost in the noise, but definately news to me.

Your 1680kcal/day estimate for a resting human of 70kg sounds about right.
Pages around the web agree to about 11000 L of air inhaled and 550 L of oxygen consumed from it per day. I'd guess that includes resting + activity, so the 350 L estimate for resting metabolism sounds roughly accurate.
At 7.3 kcal / mol ATP and 30 ATP / glucose, you arrive at 219 kcal / mol glucose.
Wikipedia lists -2880kJ/mol of glucose (https://en.wikipedia.org/wiki/Cellular_respiration). That's 688.3 kcal/mol glucose. Unfortunately, the page doesn't cite a source, but continuing your calculation from there: For 1680 kcal you then only need 2.44 mol of glucose per day, 14.64 mol of O2 and therefore 332.6 L of O2. So 688.3 kcal/mol glucose fits the expected O2 consumption roughly.
The molecular weight of glucose is 180.16 g/mol. For 219 kcal/mol, you would arrive at 1.22 kcal/g. Conversely, 688.3 kcal/mol gives you 3.82 kcal/g. Again, the latter value is definitely closer to nutritional information found for glucose from different generally accepted references (3.75-4kcal/g).
The only explanation I can offer for this is that the ATP generated from glucose metabolism accounts only for about 35% of the energy contained in the glucose - which implies that the remaining energy is wasted.

Both of those reference values appear to be completely correct: https://en.wikipedia.org/wiki/Adenosine_triphosphate#Chemical_properties

As Aidley mentions, those values seem widely accepted. The 36 ATP number you found is more of a theoretical upper limit that isn’t going to happen in practice. However, I do agree that if they were wrong, it might help :)

I updated my answer with some additional thinking )

Most sites list that the efficiency of ATP production is 38% with the rest of the energy lost as heat due to the total energy in the glucose against the usable ATP produced. This site also says it can be up to 50% in a cell, but I haven't seen that elsewhere: http://www.tiem.utk.edu/~gross/bioed/webmodules/ATPEfficiency.htm  All that said, I don't think any of that heat energy is usable by the body - you need to ATP to actually do the listed daily work of RMR.

I found another site listing intracellular conditions creating more energy per ATP (13 kcal/mole which is one higher than the prior site I listed). Running the math with 13, I get that 129 mol/day of ATP which is much closer to the reference numbers I have seen. For O2, I get 587 L/day which is much closer. I'm not sure if it's within range of error, though.  https://eng.umd.edu/~nsw/chbe482/energy.htm

It is also very suspicious that your math using all the glucose energy (100% atp efficiency) get so close to the expected result. It makes me wonder if there is actually just a misunderstanding on what initial RMR represents. My expectation is that it would be the actual atp energy actually used by the muscles and organs and not the lossy energy burned from the glucose, but maybe that is wrong? Yes I think so! So the missing piece here (regardless of ATP kcal) is that the RMR is including dietary thermogenesis (the extra heat energy).

This is also included in the nutritional values reported on food: http://www.fao.org/docrep/006/Y5022E/y5022e04.htm Thus, I think the numbers we see for Calories for RMR/BMR/exercise aren't the actual energy of the work performed but the energy that was there to start metabolizing. I'll post an answer with my misunderstanding. Thanks for the help!

So the conclusion is that our glucose metabolism is actually just that inefficient...

Yep. That said, Ive found a lot more info saying that in a living cell, you get far more atp out of the system due to the amount of other stuff (adp, etc) and ph and so on. Efficiency can go up to above 50% or somethin around there.


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Is this black locust?
This grows in Modiin, Israel. The leaves look like black locust (Pseudoacacia robinia) to me, but the branches are very knobby. Can anyone identify it?

Doesn't look like locust to me, but that's just a guess.  If it's a locust, the stems will probably have thorns on them.  Also, if mature enought it will have clusters of cream colored (or pink in one variety), fragrant, pea-shaped flowers in another month or so.

Although the photos are less than ideal, and I can't see any flowers or fruit, I can clearly see that the leaves are "evenly pinnate" and rounded distally (not pointed). The wood structure also looks bumpy.  Given Israel as the neighborhood, it is likely to be a carob tree (Ceratonia siliqua) which is native to the Mediterranean region.  This tree is sometimes mistakenly called a "locust" tree.  See Links below.
https://en.wikipedia.org/wiki/Ceratonia_siliqua
http://tree-species.blogspot.com/2008/04/carob-tree-ceratonia-siliqua.html


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Chunks of cells after trypsinization
Recently I've came across a problem after trypsinization of my stably transfected CHO-cells. When I add medium to rinse off the cells from the bottom of the flask, there are usually big chunks of cells, which I almost cannot resuspend properly... I also tried to increase the incubation time with trypsin, but it did not help much.
Does anyone have a solution for this? The trypsin I use is the same batch as usual and in the meantime I also thawed 2 different freezing stocks, but I still have the same problem.
I also tried different pipettes, from 25 to 5mL. But I can pipette like a maniac up and down and up and down... still there are big chunks of cells floating around...

Gibco has an anti-clumping agent verified for CHO cells, as does Lonza, but I like Gibco reagents more. Cells tend to clump for a number of reasons, including extracellular DNA from lysed cells and the presence of Ca and Mg ions (important ions for cell adhesion and aggregation).
You could try these:
1) Wash and resuspend in balanced salt solution without magnesium or calcium. Like Hank's balanced salt solution.
or
2) Treat with DNase I. I think you could go as low as 1 IU/mL for 30min-1hr to bust up a fair amount of DNA clumping. You can do this in a basal medium (like RPMI, DMEM, etc.), or the balanced salt solution. Your medium can contain serum only if the serum has been heat-inactivated as proteases in the serum with inactivate your DNase. Incubate with DNase under gentle agitation at 37°C (I always had a tube rotator in an incubator for this purpose, just put your cells in a 50mL conical and set them to agitate for 1hr. You could also use a heated shaker unit). If you don't have this setup, you can agitate at room temp, but for a little longer perhaps.
and maybe
3) Once of the other obvious choices is to avoid passaging your clumping cells and collect the rest. You can do this by putting all your cells into a flask incl. the clumps, agitate for a moment, and let it sit so that the chunks quickly fall to the bottom, and collect everything but the stuff that fell to the bottom.


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Why are vaccines a successful treatment of allergy?
As I understand the answer to Allergic rhinitis vaccine, the vaccine facilitates immune response against the antigen.
Given that allergy is an overreaction of the immune system against harmless antigens, how can facilitation of the immune response act as a cure (moderate the response or so)?

This is basic and also broad. I see you read this question: https://biology.stackexchange.com/q/30195/5198. Though it is not the same question, it does provide the answer. See also a possible duplicate: How Do White Blood Cells Learn? Or Do They?

@anongoodnurse Indeed, I had read the linked questions. Don't get me wrong, but I think one of us is misinterpreting written text again. Why do you think questions about facilitation of the immune response against a pathogen address moderation of the response against an allergen?

"...how can facilitation of the immune response act as a cure?" There is no mendion of moderation of the immune response in your question. That is a different (and also broad) question.

@anongoodnurse ok, now it is stated explicitly

Still basic (first question) and now too broad.

@anongoodnurse I definitely miss your point. I am not a native speaker, but IMHO there are two question marks, but only one question. Also I can not address the breadth issue.
Let's assume I am not clever enough, so unless you wish to devote a lot of time to explain it, I propose to drop the conversation. The question has been already interpreted as intended and answered.

The theory is that constant and gradual escalation of the administered dose of allergen eventually tolerizes the immune system to the allergen through the induction of peripheral Tregs or IL-10-secreting effectors.
While the purpose of a traditional vaccine against a pathogen is usually to rile up the immune system with and adjuvant or modulators, the idea of allergy immunotherapy is to sensitize the patient to the problematic allergen by implementing chronic exposutre. That mechanism is still poorly understand and is not thought to have immune memory, as the effects of the therapy tail off after discontinuation.


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To what extent is prion aggregation responsible for Alzheimer's disease?
I was intrigued by a description of prions as a factor regarding 'Mad Cow Disease', the epizootic threatening the cattle stock of the United Kingdom and France predominantly.
Understandably, the prion, a misfolded protein causes neurodegenerative damage through inducing an aggregation of prions into a complex capable of converting functional proteins. Disregarding Creutzfeldt-Jacob disease, thus far believed to be a Dementia characterised by the accumulation of prions, I simply seek clarification as to whether the onset of Alzheimer's disease should have a direct correlation with an aggregate of misfolded proteins.
Nota Bene
Although the hypothesis regarding the accumulation of amyloid-derived diffusible ligands, toxic oligomers, may be associated with the prion causing Bovine Spongiform Encephalitis, if any further clarity regarding the direct correlation between these two events in humans would be appreciated.

"I simply seek clarification as to whether the onset of Alzheimer's disease should have a direct correlation with an aggregate of misfolded proteins." This is easily googled (in other words, provide your actual research, not just a question.) "What causes Alzheimer's on a cellular level" should give you all the information you need, or "Alzheimers and prions".

@xusr - I disagree; most basic questions which show no attempt on the part of the OP at finding an answer are not excellent. But you know what opinions are like... everybody has one. (BTW, I never said the cause of Alzheimer's was/is known. The OP asked if folded proteins were the cause of Alzheimer's. I think that's easily googled. And while I'm at it, why don't you post an answer?)

To What extend is prion aggregation responsible for Alzheimers's disease?
Until recently, there was no 'hard evidence' implicating an infectious, self-propagating protein or prion (proteinaceous infectious particle) in Alzheimer's disease, or any convincing evidence that  a prion-like mechanism  is involved in this disease.
However, I quote from a recent review (Alzheimer’s and Parkinson’s diseases:  The prion concept in relation to assembled A$\beta$, tau, and alpha-synuclein) by a leading researcher in the Alzheimer's field:

Transcellular propagation of protein pathogens, reminiscent of the spread of viruses, represents an unprecedented concept of disease. It is now known to extend beyond CJD [Creutzfeldt-Jakob disease], to include AD [Alzheimer's disease]  and PD [Parkinson's disease], which are the most common neurodegenerative diseases.

Pruisner,
 who
 received a Nobel prize
 for his work on prions ('a new biological principle of infection'), was one of the first to suggest that neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease, like Creutzfeldt-Jakob disease (CJD), may be due to a prion, or to a prion-like mechanism. He points out that over 80% of these diseases are sporadic, late-onset, and involve proteins present since birth (see
 A Unifying Role for Prions in Neurodegenerative Diseases
 ).
However, there  is one caveat.  The prion causing CJD, scrapie and kuri may be transmitted from one individual to another, and there is no evidence that Alzheimer's disease or Parkinson's disease may be so transmitted or  are in any way infectious.
What is Alzheimer's disease?
Alzheimer's disease is a neurodegenerative disease, and a disease of ageing, that causes severe dementia worsening over time. It affects 10% of those over 65 years of age, and 50% of those aged over 85  years. There is no known cause, and no known cure.  It is the leading cause of dementia, ahead of Parkinson's disease.  Most cases of AD are sporadic, but a small percentage have a genetic origin (familial AD).
The disease was first described (On certain peculiar diseases of old age)  by Alois Alzheimer in 1906. After histochemical analysis, Alzheimer described  two characteristic abnormalities in the postmortem brain of a 51-year old woman :  the (extracellular) neuritic plaques and the (intracellular) neurofibrillary tangles.
There is a very nice picture of both neuritic plaques and neurofibrillary tangles in Fig 1(A) of Goedert (2005).  For a great summary of the history of AD and references to the above summary, see  A Century of Alzheimer's Disease (2006) by Goedert & Spillantini.
What are the neuritic plaques?
Neuritic plaques are extracellular structures primarily composed of  a small peptide of (usually) either 40 or 42  amino acids known as  the amyloid-$\beta$ ($\beta$A), where the '$\beta$' refers to their tendency to form beta sheets.
This small peptide arises by proteolysis of a much larger protein of unknown function, the amyloid precursor protein (APP). The APP is a trans-membrane protein with  a single membrane-spanning segment, where the N-terminus (28 amino acids) is extracellular. Two proteases are responsible for generating $\beta$A :   $\beta$-secretase and $\gamma$-secretase
Peptide bond cleavage by   $\gamma$-secretase  occurs within the membrane-spanning region of APP and components of this proteolytic complex (the presenilins) are 'major players' in the Alzheimer's story.
It is thought that A$\beta$ is a 'normal' brain peptide, that is it does not arise from 'aberrant' proteolysis, but its function is unknown (Goedert & Spillantini, 2006).
Finally, mutations in the APP gene are known to cause familial AD, but account for only a minority of cases. (Goedert & Spillantini, 2006).
So, the structure of the neuritic plaques is known. They consist of a small peptide of unknown function derived from a much larger trans-membrane protein of unknown function.
And the neurofibrillary tangles?
Under the electron microscope, neurofibrillary tangles have a ribbon-like appearance called paired helical filaments.  It is now known that these structures are composed of a single protein, microtubule-associated protein Tau, or Tau protein  in an aggregated and hyper-phosphorylated state. There is  a very nice picture (electron micrograph) of a paired helical filament in  Fig 1(B) of Goedert (2005)
What is Tau Protein?
Tau is a 'normal' brain protein characterized by Kirschner and colleagues (see here and here)  as a microbutule-binding protein, long before its role in Alzheimer's disease was realized.
In humans, it consists of six isoforms generated by differential mRNA splicing of the transcript from a single gene, and 'imperfect repeats' within the amino-acid sequence are thought to be responsible for microtubule binding.
Mutations in the Tau gene are not known to cause Alzheimer's disease, but are responsible for very rare neurogenerative diseases (taupathies ) such as frontotemporal dementia  (FTD) (Goedert, 2005)
In the 'native' state Tau is phosphorylated, and is considered an intrinsically unstructured protein, (there is no crystal structure available), and it is now accepted that  'hyper-phosphorylated' Tau is the major structural component of the paired helical filament of Alzheimer's disease.
I simply seek clarification as to whether the onset of Alzheimer's disease could have a direct correlation with an aggregate of misfolded proteins
This is where things get interesting.  There is no doubt that aggregated proteins are involved in AD. The case of Tau and $\beta$A attest to that, and the paired helical filament could be considered a misfolded state.  Can either of these proteins act  as a prion and transmit the misfolded state?  That is, can Alzheimer's disease be considered a prion disease, where a 'rogue' form of a protein transmits its 'rogueness' to 'normal' proteins?
In the case  of Tau, it has been shown that extracellular Tau aggregates can "transmit a misfolded state from  the outside to the inside of a cell, similar to prions" by inducing fibrillization  of intracellular Tau .  In addition, aggregated intracellular  Tau can transfer to other cells. (Propagation of Tau Misfolding from the Outside to the Inside  of a Cell)
Testing of the hypothesis that prions or a prion-like mechanism is the cause of AD is a very active field and much more detail and discussion will be found in Goedert (2005).
What are the other 'players' in the Azheimer's story?
There are many 'players' in the modern understanding of AD.  Two further important ones are the presenilins and  apolipoprotein E  (APOE).
What are the presenilins?
Presenilins are part of the $\gamma$-secretase complex, a protease that cleaves trans-membrane proteins including APP. Mutations in the presenilin-1 gene are the  most common cause of familial AD; presenilin-2 mutations also known to cause AD. (See  Goedert & Spillantini, 2006).
And apolipoprotien E4?
A risk factor for sporadic AD is inheritance of the  ${\epsilon}_4$ allele of apolipoprotein E (APOE), a protein of fat metabolism,  but the molecular basis for this is a complete mystery.   (Goedert & Spillantini, 2006, Goedert, 2005). Inheriting a single copy of the APO-$\epsilon_4$ gene more than doubles the  likelihood of developing AD; inheriting two copies increases the risk by 12-fold (see Smith, Dana, 2018)
In what looks like a major advance, gene editing has been used to convert a  APO-$\epsilon_4$  phenotype to one resembling 'normal'  APO-$\epsilon_3$.  For a great recent article, see Scientists Fix Genetic Risk Factor for Alzheimer’s Disease in Human Brain Cells by  Dana Smith (2018).


text:
Is swimming pool water actually a weak topical medication?
I was inspired by this question.
Given that the chlorine levels in swimming pool water are so high that they can seriously harm amphibians, it seems logical that the water should also kill various microorganisms, fungi or skin parasites.
Is the swimming pool water a weak disinfectant? Are there any illnesses for which a doctor would prescribe a full-body bath in a swimming pool for this reason?

No, there are not. If a doctor wanted to treat a patient with dilute chlorine, they could have the patient put several drops of household bleach into a cup of water (or an ounce into a full bath) and soak in that. However, bleach damages skin as well (if you put your fingers in bleach, they feel slimy afterwards. That's dead skin cells that have been broken down by bleach.) So usually we don't disinfect humans (just materials) with bleach. There are less damaging disinfectants for skin and wounds.

@anongoodnurse Your comment is probably a sufficient answer for this question, so maybe you should post it as such so that I can answer.


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What are some potential consequences for attempting to cure Type one Diabetes?
Type one diabetes has been in my family for a few generations. As a carrier and having a mother with the disorder, I've done a lot of research on it. As I am completing my High school Biology course, I've gotte a better understanding of how the disorder may be treated. (Stem cell therapy, gene replacement, etc). Here's a hypothetical scenario: Scientists develop a modified virus that contains a normal person's beta cell genetic makeup, injects it into the pancreas, and reproduces. The virus and beta cells reproduce, and the body detects the virus, but not the beta cells. (or neither, and the virus is not harmful). The beta cells create insulin, and the Diabetes is cured. Would this work, and would this hurt the immune system? Would it be possible for the scientists to blunder and either create too potent a virus or too much of the virus?

A virus is much smaller than a cell. It cannot carry a cell into the pancreas. Just infecting the pancreas with a virus carrying a gene or two (DNA) for islet cells wouldn't do anything worthwhile, and might damage the pancreas. That's why stem cells (whole cells) hold potential.

High school biology apparently failed to teach you that many conditions, like type I diabetes are not classically Mendelian. The term "carrier" does not apply to you...you are just someone with a predilection who hasn't developed the condition (but who might...I have heard of someone developing type I diabetes in college)

Scientists develop a modified virus that contains a normal person's
  beta cell genetic makeup,

How much DNA do you think you can cram into a virus?  Not having the right beta cell DNA is almost certainly not the cause of type I diabetes, anyway.

The virus and beta cells reproduce, and the body detects the virus,
  but not the beta cells.

How do you think the immune system responds when it detects a virus?  Hint, it kills the hosting cell.
A virus that induced a small percentage of pancreatic alpha cells to undifferentiate and redifferentiate beta cells might work...but you would still have the same immune system that went agro on your beta cells the first time.  They might do the same when exposed to new beta cells.  And there is a fine line between undiffernetiated cells and cancerous cells.

This might strike some as ironic, but -1 for the hostility. If you think a question is stupid, bypass it, or DV/VTC it, or comment, but an answer like this one ("High school biology apparently failed to teach you ...", "How much DNA do you think...", "How do you think the immune system responds...", "Hint..." is pretty rude. I sure hope you don't teach students anywhere.

When someone says "Well, I've done lots of research and I don't understand why scientists who are supposed to be experts haven't tried this obvious thing that my research told me should work".  That's a little hostile to the intelligence and integrity of people who do work on researching diabetes for a living.

That's nonsense. With that attitude, as a scientist and a physician, I would be continually insulted by people who don't have my experience. People have ideas and opinions that are ill informed. We are all confident idiots. You can go through life offended or just accept it as a reality.


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How do cells determine RNA types?
I was reading about the different types of RNA polymerases, and I am confused as to how a cell determines which type of RNA it is transcribing.
According to this nature article:

RNA pol I transcribes ribosomal RNAs (rRNAs), RNA pol II transcribes RNAs that will become messenger RNAs (mRNAs) and also small regulatory RNAs, and RNA pol III transcribes small RNAs such as transfer RNAs (tRNAs)

The system as to how the different types of RNA polymerase are selected makes sense to me, the core promoter's sequence determines the affinity of the polymerase to itself.
But, how does RNA polymerase II determine if the transcript is a regulatory RNA or a messenger RNA? Can someone explain that process to me or point me to where I would find it?
Another question: When RNA polymerases I and III transcribe their RNA, what prevents the cell from processing them the same way as mRNA and sending it off to a ribosome with a poly-a tail?

Well remember that an mRNA, the RNA that is destined for the ribosome, has already been processed by the time it gets there. This is done by the splicing machinery, among other things (capping enzymes, for example). But the splicing machinery isn't smart in itself. Rather, the gene has the elements, just like it does to select the RNA Pol it needs, to direct the sort of modification the RNA needs to obtain. The image below depicts two types of RNA transcribed by RNA Pol II and how the processing elements let the modification machinery know how to handle them:

Source


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Eukaryotic equivalent of bacterial tmRNA
According to this Wikipedia article,
tmRNA is only found in bacteria, with its purpose being to “rescue stalled ribosomes”.
This brings me to the question of is there a eukaryotic equivalent of this RNA? If not, how do eukaryotic cells (or any other type of cell) prevent or stop stalled ribosomes?
Every time I search for “eukaryotic rescuing stalled ribosomes”, I am constantly only  presented with references to tmRNA in E. Coli.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5311927/

Googling works fine with a slight amount of persistence: the 6th result for stalled eukaryotic ribosomes is this overview paper.

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


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biological difference between 9 month and 7 month pregnanted humans
it possible baby born when 7 month of pregnancy, and possible when 9 month pregnancy.
what happen in additional 2 month?
what their difference. do they have different something.

The child is still developing, just as the child will continue to develop after it is born. Is there something in particular you have in mind? I don't know much about fetal development, so it may just be me, but it doesn't seem quite clear what answer you're looking for.


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Recent research in bioluminescence powering photosynthesis?
In 2013 there was a Chinese study published on "Bioluminescence as a light source for photosynthesis," which is briefly summarized in this Chemistry World article. There was a question on Biology.SE about a year earlier asking about the feasibility of such (and a somewhat related question for photovoltaics also in 2013).
My question here is if there is any newer research in the area of bioluminescence powering photosynthesis? Bonus if it is even more specifically related to any kind of crop production (so on a larger scale).
Please note:

I am not a biologist (last biology I took was AP Biology in high school a number of years ago).
From the other answers here on Biology.SE, I understand there is inefficiency with the use of bioluminescent light for "powering" things, but I'm still interested in more theory behind it as related to photosynthesis (hence the question about any newer research) for purposes of a fictional work I'm pursuing where sunlight is not an option. As a side question, imagine a "sky" of bioluminescence; would that be enough to grow some level of crops or trees?

Consider conservation of energy: where does the energy for the bioluminescence come from?

@jamesqf Well for purposes of the main question here, from wherever the sources for the bioluminescence get their energy from based on whatever particular source a recent study experimented with. For purposes of my side question for my fictional work, an animal that primarily "feeds" off geothermal heat (of which it has an unlimited supply to feed off of). While that part may be a point of "suspension of belief" in my story, I want to figure out if "reality" confirms that some size/level of normal Earth plants could be grown by the bio-light assuming enough light is generated.

Well, there's physics again :-(  Thermodynamics, this time.  You can't simply feed off heat, you need a temperature gradient.  But assuming you have some way of generating bioluminescence that's strong enough, and of the right spectrum, you can grow plants.  It's no different than using LED grow lights for house plants: https://www.gardeners.com/how-to/gardening-under-lights/5080.html  But the natural bioluminescence I've seen is far too weak.

@jamesqf I'm not sure I follow what you mean by "a temperature gradient" with respect to the feeding, other than are you saying the rate the heat flows into the animal? But this question is not about that aspect. So theoretically, if the bioluminescence was of an intensity/duration equal to an overcast day, then most plants (except perhaps those that really like direct sunlight) would grow fine (if I understand you). The fact that it is bioluminescent light vs. sunlight is not directly a factor on photosynthesis.

By temperature gradient, I mean there has to be a difference in temperature in order to extract energy - just as a rock won't roll downhill if it's on flat ground.  WRT photosynthesis, yes, as long as the light has enough energy and the proper spectrum, the plants don't care where it came from: http://hyperphysics.phy-astr.gsu.edu/hbase/Biology/ligabs.html