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Is it possible to live without iodine? (sea plants, seaweed or fish?)
I’ve come across a few other people asking this question on different forums such as on Quora, and Reddit…
With my current understanding, we evolved from sea creatures which is why we still need iodine in our system.
The RDA is 150 mcg, 220 for pregnant women.
Isn’t this amount of iodine something a person can get merely from sea plants and sea animals?
Do land animals need such a high amount of iodine as well, and are a majority of them iodine deficient? Unless there is some way for them to get iodine from land plants. Or are we supposed to eat iodine rich soil?
If sea plants and sea animals are a required for proper iodine RDA, this implies that they should be staple foods within our diets.
Sorry for all the questions.

Thyroid Hormone is needed by nearly every cell in our bodies, and without it, we would die. And, as @David said, Iodine is an integral part of the hormone. As a requirement for vertebrates, it is also found in vertebrates (whose products and flesh we consume) as well as in their diets. The majority of vertebrates today are not iodine deficient, but in the past, humans were moreso than they are today.

saying sorry does get around the one question per post policy, I suggest looking up the goiter line to get a lot of answers at once. Iodine is only limited in specific environments.

@John I lean towards a mostly vegan diet. So it interests me that unless a vegan eats seaweed, supposedly they aren’t getting enough iodine. But I can only assume that realistically if an environment has soil that is rich in iodine then sea plants wouldn’t be a requirement.

that's a problem with a vegan diet, IE without and meat, dairy or eggs. non-sea plants in general are low in iodine. most animals including most herbivores get them from the same places we do eating animals or eggs.. Or they are bulk plant feeders and make up for it with sheer volume and eating plants that would be toxic to us. keep in mind a 100lb deer will eat almost 10lb of vegetation a day plus the occasional bird or egg.

Iodine is a component of the thyroid hormones, thyroxine and triiodothyronine, so it is indeed a human nutritional requirement.
According to this Harvard University webpage, milk (especially), eggs and other dairy products are sources of iodine, as well as fish, mentioned by the original poster. In addition, in advanced countries iodine is added to table salt to help combat iodine deficiency.
Although iodine is also added to the diet of dairy cows, I have read that iodine is also present in their natural food. Iodine enters the soil from marine spray in coastal areas, and from rainfall further inland, and is retained by metals in the soil. It can therefore be taken up by plants. However I do not know which plants that would constitute a natural bovine diet are particularly rich in iodine or why that would be so.

I am not so sure that the cows that are being eaten regularly see any of their "natural food" ever, as they are not maintained on grass.

@CaroZ — It's their milk. You have to approach these things from a historical viewpoint — when dairy farming emerged originally the cattle would certainly have been maintained on grass. As for the contemporary situation in factory farms, iodine is actually added to animal feed, so supermarket milk in Britain and the US is, in fact, a good source of iodine.

Thanks for the answer! I lean towards a mostly vegan diet. So it interests me that unless a vegan eats seaweed, supposedly they aren’t getting enough iodine. But I can only assume that realistically if an environment has soil that is rich in iodine then sea plants wouldn’t be a requirement.


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Understanding certain limited biochemical impacts of egg yolk
I am researching the use of isolated egg yolk lecithin (EYL) in food preparation. I am interested in its ability to act as an emulsifier without having ancillary negative impacts. I am aware that some people have negative dietary reactions - intolerance (as a separate issue from allergic reaction) to egg yolks. So my question is whether the components in isolated EYL are the same ones that typically result in dietary intolerance or are there other, different components in "natural" egg yolks that might be a cause, where EYL might typically be clear of them.
In attempting to research this on the Internet I have found few details on the chemicals/compounds in egg yolks, let alone which are prone to dietary intolerance. Most of the material I find deals with egg allergies (frequently lumped together as related to "whole eggs, egg yolks, or egg whites"). There are some articles specific to egg whites because of their use in vaccines. That, however, is not helpful for my question, both because of their focus on egg albumin and the allergy issue rather than intolerance from ingestion.
As I had a previous question "closed" for being "off-topic" because appearing to seek answers to medical questions, I want to clarify that I am only after greater granularity concerning egg yolk composition and digestibility so I can do further research.

You'll need to identify research indicating that a phenomenon of egg yolk intolerance that is not an allergy 1) exists, and 2) is sufficiently well-defined to attempt to find a mechanism. Otherwise there is no biological question to answer.

Thank you @Bryan Krause. I now understand how to reformat the question.

I would also consider moving your post to SE Biomedical Sciences where I imagine people are more familiar with the medical conditions you mention.

Thank you for the suggestion @David

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Can cells straddle different anatomical systems in the body?
I'm reading Periphery by Moses V. Chao, and the author explains that the peripheral nervous system consists of the portion of the nervous system outside the brain and spinal cord. But, if I understand correctly, the cell bodies of motor neurons are in the spinal cord (or even further upstream?), whereas the nerve fibers themselves are just bundles of really long myelinated axons going all the way from the spinal cord to the nerve endings. So these seem to be cells whose cell bodies are part of the central nervous system, but whose axons are part of the peripheral nervous system. Is that how neurologists think about it? I would have thought things would be subdivided in a way that each cell is in one system or another.
I see this related question, but I don't think its answer is a clear answer for this question. That answer does seem to suggest that the cell bodies of the motor neurons are part of the PNS, not the CNS, even though they're physically in the spinal cord, but it's not really explicit about that point.
Alternatively, it's perfectly reasonable to have overlapping systems. I'd just like to know the way the lines are drawn.

The answer in your link does answer your question: "The distinction [central vs. peripheral] is slightly arbitrary... the most important part is that together they are parts of the nervous system, rather than being distinct systems..." IOW, yes, the motor neurons are just long mylinated anons.

Does this answer your question? Why are spinal nerves considered a part of PNS while the spinal cord is a part of CNS?

The answer in the link says: " 'CNS consists of brain and spinal cord, and PNS consists of everything else.' That's really it. The distinction is slightly arbitrary, I'd think of them as the central (nervous system)..." I could read that answer two ways. One is that the cell bodies of the motor neurons aren't really considered "part of" the spinal cord, since those cells are part of the PNS. The other is that the bodies are part of the spinal cord, and it's only the axons that are part of the PNS.

Have you considered the ganglia? This might be what's tripping us both up re. our communication.

Yes, but I don't think all peripheral nerves go to them. Do they? Also, it occurred to me that, if the nerve itself is only the bundle of axons and not the cell bodies, then that other answer did answer my question, but then my question becomes, "Is a nerve just the axons, or is the collection of cell bodies part of the nerve too?"

"Nerves" needs a definition, I think. I think of nerves as the long fibers that transmit impulses from the center to the periphery, and vs. versa. Those consist of axons and the cells that myelinate them. That's different (to me) than a neuron. And yes, all impulses go through ganglia except at C1, I believe. My memory of neuroanatomy has long ago degenerated into simple stuff. Apologies, I should let the neuroscientist(s) answer this.

Answering my own question:
Yes, cells can straddle anatomical systems in the body.
In particular, the spinal cord is part of the central nervous system while spinal nerves are part of the peripheral nervous system, as described in this question. And nerves are bundles of axons, supported and held together by additional cells. The cell body to which the axon belongs is not part of the nerve. Instead, for spinal nerves, it's a part of the spinal cord and hence in the CNS.
It was surprising to me that the boundaries of anatomical structure don't always correspond to the boundaries between cells, but that makes sense when I consider that the field of anatomy began as a macroscopic endeavor, a scale on which it makes sense to treat the boundary between nerve and spinal cord as the point where they meet.
Thanks to anongoodnurse who basically led me to this answer in the comments.

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Peptide fragment software in mass spectrometry
I am trying to study peptide fragmentation in mass spectrometry.
My goal is to find software with which I can retrieve the molecular structure of the peptide and see the a,b,c fragments.
I found these two online tools.
Pep draw & Fragment Ion Calculator. Ι entered a short sequence and I retrieved the m/z values for the a.b.c and x.y.z values in a table.
Is there any software /online tool that I will add a peptide sequence and automatically generate the chemical structure? I want this image generated but for my peptide sequence instead of the side chains.

By "generate automatically the chemical structure" do you mean the 3-d structure of the fragment peptide? If you google "predicting 3d structure of peptides from sequence" you'll find references to a bunch of software that attempts to do this, the PEP-Fold server for example. Of course as the fragment gets larger the problem gets harder, and you end up needing Alpha-Fold.

@CharlesE.Grant I just edited my post. Maybe now is more clear what I am searching for.


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How is it known that there are only three macronutrients: proteins carbohydrates and lipids?
It is stated here that in human nutrition, micronutrients are nutrients required generally in less than 100 mg daily quantities whereas macronutrients are required in gram quantities. It is widely stated that our macronutrients are carbohydrates, lipids, and proteins. How was it shown that these are the human macronutrients and that we don't have other macronutrients?
One answer to this similar question on Quora suggests that ethanol or ketones could be considered macronutrients. Ethanol is mentioned in this article, though ketones are not. Other sources I saw didn't clarify.

there aren't, there are four, carbohydrates, lipids, proteins, and water.  Also ethanol and ketones are not even essential nutrients much less macronutrients. you are getting downvoted for not reading your own source.

What about nucleic acids?

i read the sources john, but thanks for the input

if nobody knows, does anyone know a resource where i could hunt this down?

Summary
The question is based on the misconception that the term “macronutrient” originated as a scientific definition, to which entities satisfying this definition were assigned. In fact it was a default term used as a distinction from compounds falling into the earlier category, “micronutrient”, and was used initially to encompass the three specific classes of food that had been established to be sources of energy through decades of nutritional research. Hence there was no question of whether there “should” be more macronutrients. The term is not a scientific definition, and today is used in different ways so that anyone using the term needs to clarify what it should be taken to mean in that particular context.
Food Energy and the history of Nutrition
Scientific studies of nutrition, dating the late 18th century, were initially concerned with chemical structure, metabolic fate and energy produced by different foods, and this is described in a short readable article by Ned Stafford in Nature (2010) 468, S16–17.
By the end of the 19th century protein, fat and carbohydrate had been established as the chemical fuels that supplied energy from the diet, and the energy values (in terms of the, now obsolete, calorie) had been established by Atwood, using his respiration calorimeter.
Micronutrients
The next phase of nutritional research was concerned with constituents of the diet that did not supply energy, but were nevertheless essential for health. The first of these were the vitamins,  organic molecules that in many cases turned out to be cofactors for enzymic reactions. The term, vitamin, introduced in about 1912, was a contraction of “vital amine”, although the chemical description “amine” does not apply to some of the essential organic molecules later assigned to this class.
Later still came the discovery that certain non-organic molecules were essential dietary components, especially metal ions such as copper or selenium, sometimes known as ‘trace elements’ or ‘mineral nutrients’. These were not termed vitamins because of their non-organic nature, but the need to refer to all non-energy supplying dietary requirements together led to the employment of the portmanteau term, ‘micronutrient’. The first mention I can find of this in relation to human nutrition was in a US Senate report of 1954, although it had been employed extensively in relation to plants from 1940, and the word is most frequently used in a botanical context.
The introduction of the word ‘Macronutrient’
The first recorded use of the word ‘macronutrient’, in relation to human nutrition, was in a 1968 article in the Archives of General Psychiatry. The term only appears in the title of the article (“Comparison of macronutrients in the diets of psychotic and normal children”), although it is clear from the tables therein that it refers to carbohydrate, protein and fat. It seems likely that it was (or had already been) coined by analogy with — and in contrast to — micronutrient, as it was shorter and appeared more elegant than ‘energy-producing food’. Indeed the Oxford English Dictionary entry includes this contrast:

1968– Physiology. A nutrient belonging to one of the three major food
groups (carbohydrates, proteins, and lipids) required by animals, esp.
as opposed to a vitamin or mineral.

It should also be mentioned that the term had been in agricultural/botanical use since 1942, but embracing a quite different set of compounds (nitrogen, phosphorus, potassium etc.).
Distinguishing scientific definitions from descriptions
In my opinion the root problem in the original post is confusion between terms that are scientific definitions from those that are merely descriptions. For example, a chemical term like amine is rigorously defined and indicates a class of chemicals to which any with a structure satisfying its definition (‘contain a basic nitrogen atom with a lone pair’) will be assigned. Hence any list of amines will be expanded by inclusion of newly discovered compounds. In contrast, scientific descriptions (at least in this context) start with a collection of known entities and assign a name to encompass them. This, I submit, is the case with ‘macronutrient’. It not a definition, but a term assigned to carbohydrates, proteins and fats, as a group.

Thus, one answer to the question:
“How is it know that there are only
three macronutrients…?” is
“Because that is what the word was
introduced to describe”

But…
…context is all. As already stated, in plant science the term has a quite different meaning, and those who feel that they should regard the term as a definition, redefine it to exclude ethanol, for example, on the basis that it is not essential. In practice, all that is necessary is to make it clear how one is going to use the term. The FAO food and nutrition paper 77 — Chapter 2, for example, merely states “Analytical methods for alcohol, which can be a significant source of energy in some diets, polyols and organic acids were not discussed, and hence no recommendations for methods are made.”

So an alternative answer to the question:
“How is it know that there
are only three macronutrients…?” is “Because that is how macronutrient
has been defined in this context.”

or, as Humpty Dumpty said:

“When I use a word it means just what I choose it to mean….”
Lewis Carroll — Alice in Wonderland

Thank you! This historical context is elucidating, and I did not realize macronutrient is a non-technical descriptor of molecules where we usually get our food energy. This led me to this page (https://en.wikipedia.org/wiki/Food_energy) which states, "However, the direct calorimetric method generally overestimates the actual energy that the body can obtain from the food, because it also counts the energy contents of dietary fiber and other indigestible components..." It also discusses polyols and organic acids, and I have this follow-up question: What gives me food energy?

@imrobert — Your concerns about simple bomb calorimetry are understandable, and were the subject of another question on this list, which I recently addressed in this answer.

Thanks, this is also helpful. If I take away "The amount of energy a food molecule gives me is the amount of energy it contributes to my TCA cycle" is that ok with you?

@imrobert — A few changes to that: "The amount of energy a food molecule gives me is the net amount of energy it produces from the TCA cycle, fatty acid breakdown and glycolysis." 1. "Net amount", because it may use some energy (as in the elimination of N from amino acids), 2. "Produces from" as your present formultion makes it sound as if the TCA cycle needs energy, that food produces. In fact the TCA cycle is a way of breaking down 3C molecules in a way that converts their energy (ultimately) to a useful form, rather than heat. 3. To cover carbohydrates and lipids.

@imrobert — But I would say, more technically “The amount of energy a food molecule gives me is the net amount of energy, in the form of ATP, that can be produced from oxidation reactions in the body.” Just as the heat energy from burning wood is produced by  its oxidation, the energy for movement, growth etc is produced from oxidation of foodstuffs. Although a little is generated directly in particular reactions, most is generated in two-step process. First the reactions use an oxidizing agent NAD, which is reduced to NADH in the process. cont...

...cont Then there is a complex system in the mitochondrion, where the energy in NADH is used to form ATP from ADP through reoxidizing it to NAD. Not so simple. Explaining that is what put bread on my table for many years.

Can I know in advance how much energy a given molecule will give me via oxidation?

@imrobert — I imagine it will depend on your personal characteristics. Exercise physiologists and nutritionists are the people that are involved in this sort of thing. I really don't know — It's certainly not my field.


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How exactly are the eye color genes related?
How exactly are the gey (maybe aka EYCL1?), bey(2?) (aka EYCL3?), HERC2, and OCA2 genes related to each other? There are numerous sources that explain eye color in terms of OCA2's role in the creation of melanin and the probable role of HERC2 in regulating its expression, and many Punnett squares invoking the gey and bey genes to explain inheritance (with the appropriate caveats regarding evidence of numerous other genes that also play lesser roles), but the relationship between the two is never really clarified.
Is the bey2 gene an alias for OCA2, or is it merely an unphysical phenotype that is likely coded (in part?) by OCA2 genotypes, or a pairing of specific HERC2 and OCA2 codings? What about gey?

There is polygenic inheritance of eye color as well.


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Why are trees so symmetric?
Many trees have a quite symmetrical overall shape. Some are extremely symmetric. Yet when you look at the branches and limbs of any tree their distribution seems completely random. Often even the trunk will bend or divide. So how does the overall shape attain symmetry?
I understand that there is gravitotropism and phototropism acting, but it seems to me that then if one branch extended outside of the general canopy it should grow even faster as it is more exposed to sunlight, thus producing a more irregular shape.
What mechanisms are working here?
There must be some kind of negative feedback (I'm a retired engineer) or inhibitory mechanism that slows growth on the more exposed branches.
I can understand that a spruce or similar would be so. If all the branches grow at the same rate, those lower on the tree will be longer, having had more time to grow and you'll naturally get a triangular shape, but this is not what captured my attention.

"...if one branch extended outside of the general canopy it should grow even faster as it is more exposed to sunlight, thus producing a more irregular shape." Are you sure this doesn't happen? (It won't happen with one branch, but it will generally on that side of the tree.)

if you think trees are mostly symmetric you need to go look at more trees, and then look up phototropism. a unobstructed tree with light levels the same in all directions will be symmetric sometimes, otherwise no so much.

@anongoodnurse That's true. I have two maples in my front yard growing close together. There are no branches that grow on the sides of the trees facing each other - and yet the two trees together make one symmetric whole.

In PA the sun spends a lot of time in the morning and evening in the north half of the sky during summer thanks to the Earth's tilt.

@BryanKrause You're right. Never realized that.

Perhaps set a condition of trees growing without light obstruction and high wind. Conifers are very simmetric and so are other trees. You should read about the chemical signalling which tells each cell it's distance from the trunk and how targeted growth is promoted.

@Rich - I built a house in the middle of acres of woods, clearing the site myself. Ten years later, the trees left standing on the entire periphery of the clearing grew into the clearing so much that I had to cut them down to regain the sunlight I originally had. I don't think I'd have known it was so dramatic if I hadn't seen it myself.

@bandybabboon That is the sort of information I was looking for. Can you give me a reference for this type of chemical signaling?

Does this answer your question? How do trees manage to grow equally in all directions?

@NilayGhosh Yes, that's a very complete answer. Thanks. Knew there had to be some kind of regulatory feedback going on.

Not an answer, but the history of people investigating spiral patterns of plant growth may be interesting to you.


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Why are there only 3 types of data (0,1,2 ) in some GWAS tables?
I am wondering about the format of raw genotyping data in a GWAS article published on 21 December 2023, the supplementary data contains a table named "Diversity_genotyping_raw" (inside Supplementary Data 1), which is shown below:

The table contains samples as the leftmost column, with the Affymetrix array variant specifiers as the top row.
It seems to be the single nucleotide polymorphisms among the varieties used in the experiment.
My question is: why are there only $3$ types of data ($0,1,2$) in this table, while there are $4$ nucleotide types?

@David I've edited it a bit to see if it might help the question

@BigMistake — That's good. That's how SE is supposed to work, allowing questions to be improved by editing. Thank you. I'll delete my previous comments.

Yes, that's an interesting question. The short answer is that most variants only have two alleles, and even though you can be heterozygous at a position in two different ways, both of these result in the same genotype.
We can have A, T, C, or G at a position.
Since there are two chromosomes, we could have many genotypes: AT, AC, AG, CG, GC, etc. However, most of the base pairs in all mammal species are the same. Only a small fraction have even one alternate allele. That is, most positions just have one letter in them in all humans (and animals), and there isn't any other letter anywhere in the population to make an alternate genotype. However, sometimes there is this extra letter available in the population. This is what we call a "variant." Since this is somewhat rare for there to be a variant at a position, it is even rarer that there are more than one variants at a single position. GWASs therefore usually only consider the case where there is one variant. That is, there are two possibilities for the DNA "letter" at that position.
Let's imagine these are C and T. The possible genotypes are C C, C T, T C, and T T.
T C and C T are the same genotype, because they both have 1 C and 1 T.
This means that there are three unique genotypes for the case where there are two variants. This is where the 0, 1, 2 coding comes from. 1 refers to the heterozygotic position (C T or T C, in our example).
In reality, it is possible to have more than two variants. These are called multiallelic sites, and they are not uncommon, but they are rare enough to not be worth the trouble of including in GWAS, so they are either excluded or split up into multiple alleles, each with two variants. There is some work on modeling these more effectively.

Thank you very much for your answer. This leads to another question: why is it that in some database (for example https://www.ncbi.nlm.nih.gov/genbank/), only one nucleotide sequence is included while there are 2 chromosomes?

@anonymous67 Look at BLAST. When dealing with different species, or the whole genome of a species, it's easier just to have one copy as the variants are rare. It's just a choice. Some databases don't require variants for the analyses which require alternate alleles


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Trying to understand sleep
I don't understand sleep.
Before, I naively thought it was related to some kind of 'energy' or 'wakefulness' resource that gets depleted as time goes by without rest.
But that's not it, higher activity levels don't make you sleep sooner, they might make you more fatigued and it might correlate with sooner sleep onset but the relation is not 1:1, more activity doesn't equate to earlier sleep, in fact many times it might do the oposite.
Even plants follow some regular pattern of higher and lower activity levels, but seems more related to the environment and resources available.
Maybe we sleep because of the day-night cycle? we adapted to live in daylight, so by specializing we focus our biological resources, and during the night what we do is sleep to limit the consumption of those resources (metabolic rate slows down during sleep) because doing anything else is not useful, we are not adapted for being nocturnal.
So basically sleep is like some kind of instinctual behavior, sleep is induced by the body, the body actively makes us sleep. But then, why do perform so poorly if we don't sleep? a consequence of our adaptations to that day-night pattern? If sleep is only an induced physiological behavior, Why if we stay awake a lot we risk our health? is this dependence on sleep an accident then?
My question is this. If we consider sleep as a behavior actively induced by the body, akin to an instinct, rather than the depletion of a physiological resource (I think this is true), why does insufficient sleep result in adverse health effects, such as those observed in conditions like fatal familial insomnia?

Stack Exchange is for specific questions and specific answers; can you narrow your post to one specific question about sleep?

Why are the two options "depletion of a resource" and "learned behavior"? Clearly sleep is not learned.

Yes, I imagined someone might misunderstand that part. I never said sleep is learned, but seems similar, like an instinct, but probably doesn't fit the definition. I think the question is if a biological system requires intrinsically periods of less activity (not only regular sleep) to maintain proper functioning indefinitely. We have the confounding factor of the sun periodic effects, which caused even fruit flies to have an internal 24h clock, and this relates to the existence of sleep. If life evolved in a place with no periodic effects and constant resources, would sleep exist?

"Learned" and "instinct" are opposites, so yes it's quite weird to use one to describe the other.

Sure, maybe "like an instinct" is better than "like a learned behavior"

Do existing Q&A like https://biology.stackexchange.com/questions/324/why-did-the-process-of-sleep-evolve-in-many-animals-what-is-its-evolutionary-ad answer your question? If not, can you clarify why not and what your specific question is?


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Has perturbation theory been applied to mutation process frameworks?
For example, imagine this Feynman diagram:

This is analogous to mutational homoplasy.
When comparing haplotypes, there are many possible tree topologies. Under maximum parsimony, we ignore suboptimal tree paths which certainly occur sometimes in reality. For example, imagine the following two haplotypes:
1: C A T T G
2: C A T A A
There are two mutations that make these different.
Maximum parsimony may infer this intermediate, not directly observed haplotype:
C A T A G
If we move from 1 to 2, the tree looks like:
C A T T G --> C A T A G --> C A T A A
However, the following is also possible:
C A T T G --> C A T A G --> C A T T G --> C A T A G
Or:
C A T T G --> C A T T C --> C A T A C --> C T T A C --> C A T A C --> C A T A C --> C A T A G
The not-directly-observed haplotype is analogous to the virtual particle. The directly observed haplotypes are the non-virtual particles. One could construct Feynman diagrams that look similar except have haplotypes instead of particles.
It is possible to imagine that some less-likely haplotypes actually are more harmonious with the observations. It seems that perturbation theory may help.
I don't have completely formalized thoughts on this. I am wondering if this has actually been used before to make a mutation process framework (e.g., an improvement to the infinite alleles model).

@David Thanks, fixed. I try to follow the rules but I don't know what all of them are yet

No problem. The way SE works as a question and answer site is a bit hard to fathom initially, but I hope you persist as your expertise can clearly be of benefit. One key thing is that it is not a discussion site with a dialogue between someone with a question and someone who has an answer. The questions are supposed to be of use generally (and some of them are), discoverable by web searches. And that is why you find reference to the OP (original poster), acknowledging that a question may be edited and that it doesn't "belong" to whoever posted it, but the group in general.

this is basically the argument behind maximum likelihood tree inference. Parsimony can lead to a lot of issues, as argued in the classic Felsenstein paper (linked).
Here is a brief paper discussing a particular improvement to the max likelihood method for tree inference in which substitution rates among sites are allowed to vary, which is another critical factor affecting tree topology estimation in a ML framework that can lead to the different mutational paths you show. I think it's a good entry point showing the value of ML over parsimony in incorporating multiple possible mutational paths with different interpretations (topologies).
If you are talking purely about cases in which the infinite alleles model isn't appropriate, I wrote a review on this topic a few years ago (see box 1 for some mutational paths very similar to the one that you present).
I am not sure how perturbation analysis fits into this or what the Feynman diagram means.


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Have there ever been "half-twins" who were halfway between siblings and twins?
Have there ever been two human siblings who were 75% or more genetically related?

Yes.
A case of semi-identical twins was reported in 2006. These twins share 100% of their maternal alleles and 50% for their paternal alleles. It's hypothesized this arose from a double fertilization of the egg, followed by the formation of two 46XX/46XY twins.
Another hypothesized mechanism of twinning involves the fertilization of a polar body (essentially when the egg divides prior to fertilization; polar bodies are a normal part of meiosis, but aren't usually able to b fertilized). This would give the twins the same maternal chromosomes, but different paternal chromosomes. However, this type of twinning has not yet been observed.

Though your question doesn't make sense to me, I believe the answer is Yes. See the following paper about "sesquizygotic" twins:
Gabbett, M.T., Laporte, J., Sekar, R., et al. 2019. Molecular support for heterogonesis resulting in sesquizygotic twinning. New England Journal of Medicine, 380(9):842-849.

Sesquizygotic multiple pregnancy is an exceptional intermediate between monozygotic and dizygotic twinning. We report a monochorionic twin pregnancy with fetal sex discordance. Genotyping of amniotic fluid from each sac showed that the twins were maternally identical but chimerically shared 78% of their paternal genome, which makes them genetically in between monozygotic and dizygotic; they are sesquizygotic. We observed no evidence of sesquizygosis in 968 dizygotic twin pairs whom we screened by means of pangenome single-nucleotide polymorphism genotyping. Data from published repositories also show that sesquizygosis is a rare event. Detailed genotyping implicates chimerism arising at the juncture of zygotic division, termed heterogonesis. opens in new tab, as the likely initial step in the causation of sesquizygosis.

It's possible this could have resulted from two sperms fertilizing one egg!

Probably, yes.
According to this paper, siblings have a mean of 0.50146 relatedness with a standard deviation of 0.03761. This means that this is an event which is 0.25/0.03761 = 6.6471683063 standard deviations above the mean, a near-7-sigma event. This occurs once in 66,937,665,852 (67 billion) events. However, there have been around 100 billion human births. This means that yes, there have probably been humans siblings who are closer to twins than normal siblings.
(This assumes there is no kurtosis causing platykurtic behavior.)
There is a 78% chance that this has happened at least once for every 100 billion human siblings pairs, or about about 1.5 times in human history assuming there have been about 100 billion unique sibling pairings.

Your source belongs in the question, as evidence of an attempt to answer your question is required on this site.

@anongoodnurse Where is that rule written for this site? (Genuine question, I can't find it.)

https://biology.stackexchange.com/help/how-to-ask

There's also this: https://biology.stackexchange.com/help/self-answer

I think the logic needs to be expanded here. The one-in-67-billion event is between two siblings, not between all humans. You'd need to account for the distribution of sibling counts (e.g. an only child doesn't count, two siblings only count as one pair, but four siblings create six pairs).

@Darlingtonia Yes, exactly. I don't expect great data to exist on this for early humans, but I would imagine the average number of children to be above 3.


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What is the term for a missing feature in a descendant that was present in an ancestor which defines a clade?
Examples include:

A snake does not have legs, but is still considered a tetrapod as it is a descendant of animals with four legs
Bdelloidea (class of rotifera) can only reproduce asexually, but is still considered an animal as it has ancestors that reproduced sexually
Star fishes have pentaradial symmetry, yet they are considered bilateralians as their ancestors were bilaterally symmetrical

I've changed the headline from What is the term for a missing feature in a descendant that was present in an ancestor and defines a clade? because it could be read as saying the feature defines the clade. Since clades are defined by an ancestral organism and not a particular feature, I changed it to read in an ancestor which defines a clade?, which I presume was intended.

The earliest snakes still had limbs: https://www.nationalgeographic.com/science/article/a-fossil-snake-with-four-legs

Loss-based apomorphy or apomorphy?

Secondary loss?


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What animal this bone belongs to?
I recently found this bone on the balcony of my house.

In case it helps, my house is in the northwest of Spain next to a park in a coastal city, and size is 15-20 mm.
Does anyone know what animal it could belong to and what part of it it is?

Could you please edit in the size of the bone  - it looks like it is very small, given that you appear to have it on the palm of your hand.  Size gives us important clues about what sort of animal we might be looking at.

Seems shaped like a fish jaw, are you anywhere near the ocean/sea?

Edit my question adding more info, thanks comments. There are seagulls in the park, it is possible that they bring things from the sea.


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If a protein has multiple globular domains with flexible peptide linkers in between, how do they fold?
Do they fold independently of each other or synergistically? If we express these globular domains separately, would their structures remain the same?
I came up with an easy way to test it. Many RNA viruses like HIV and coronaviruses encode multiple proteins in one peptide which folds into a polyprotein with multiple globular domains. The globular domains are then separated by the viral protease. Can we express these proteins separately and compare their structures with native ones?

This question is not a mere curiosity. Many proteins have multiple globular domains which makes structure determination difficult because these domains are very loosely joined together. It would be much easier if we can solve the globular domains individually instead of solving the whole protein at once.

I don't think there is any one answer, it probably varies. One data point is the capsid protein of phage p22. If its "I-domain" is removed, the rest of the protein fails to fold. That is maybe more of an intrinsic part of the protein than you meant, though.

Do they really fold into a polyprotein with a structure that has been determined? I thought that autoproteolysis occurred rapidly. And please provide examples of proteins with multiple domains that make structural determination difficult? In any case, expression and crystallization of parts of proteins is widespread. I certainly wouldn't draw any general conclusions from the polyproteins of RNA viruses.

Many proteins are shaped like a sausage. For example, the L proteins of nonsegmented -ssRNA viruses have a large RdRp/capping core and a flexible CD-MTase-CTD tail. The L proteins of VSV and rabies are tightly packed which enables us to solve all 4 domains with cryo-EM, while others’ only have the core resolved because the tail is too floppy. https://www.annualreviews.org/doi/abs/10.1146/annurev-virology-111821-102603

So I came up with an idea. If the CD-MTase-CTD tail can’t be resolved, would it be a better idea to remove it? Cryo-EM solve protein structures by averaging millions of images of identical particles, while the flexible tail only add noise to the images. If the flexible part is removed, the remaining is must easier to align.

Yes, as David mentioned, it's common to perform x-ray crystallography or Cryo-EM on a truncated version of the protein of interest. NMR is also done on smaller fragments or domains.

A broad interpretation of the question
The question refers to the “folding” of proteins. This term — and the associated biological problem — is often used in the rather specific sense of the attainment of a structure with a particular thermodynamic minimum free energy. I take the intent of the  OP (original poster) to be whether, or to what extent, one component of a polyprotein influences the structure adopted by another by physical association. I shall extend the question to that as I think an attempt to answer it will be more interesting and rewarding.
The general and the specific
I do not think one can assume that there will be a single answer to the question that will be true for all polyproteins. Nature is seldom so obliging, and there is no guarantee that what may be true for a polyprotein translated from a viral RNA will also be true for one translated from a cellular RNA. Even within these categories it would be prudent to consider things on a case by case basis.
The answer in summary
Comparisons of the sort suggested have been made in certain cases or are implied by the accumulated work in others. In the polyproteins of both RNA virus and cellular biosynthetic complexes the evidence suggest independent folding in many cases. However in some viral polyproteins, particular pairs of protein domains may be have as a single folded protein in precursors to proteolytically cleaved subsequent forms.
Viral polyproteins
Comparisons of the sort suggested by the OP have, in fact, been performed, although not on complete viral polyproteins — rather restricted to examining possible interactions of particular subsections of the latter. I can see two reasons for this:
Practical Difficulty. I am not aware of any viral polyprotein that has had its total structure determined. This may be because large protein assemblies are generally difficult to crystalize, or because the flexibility of the linkers may mean most do not adopt a single structure, or because even if they do they may not maintain it for any length of time before proteolysis occurs.
Insufficient interest in the question. I suggest that most virologists would assume that the sole or primary reason for synthesis of RNA virus proteins as a polyprotein is that the mechanism of eukaryotic translational initiation precludes polycistronic mRNAs (in all but a few cases not relevant here), and the way the linkers space the protein domains suggests that they fold independently of one another. Furthermore, the unrelated nature of many adjacent protein domains (polymerases, proteases, structural proteins) — and the non-conserved organization of neighbours — gives no reason to suppose that they interact in any way. There is a long history of the crystallization of individual RNA viral proteins expressed from artificial constructs including only the open reading frame of the viral RNA, as exemplified most recently by the expression of Covid proteins for research and vaccine development. This also suggests that individual proteins fold independently.
Comparison studies on partial viral polyproteins
Nevertheless, it has been recognized that — and there has been considerable interest in the fact — the viral polyprotein system has been refined and adapted to the infection. In some cases, for example, there is a process of protein maturation by successive proteolysis, with intermediates having functionally different properties to the mature end-product. For this and other reasons structural analysis and comparisons of parts of the polyprotein have been performed with different viruses and proteins, some of which were reviewed by [Yost and Marcotrigiano in 2013].(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3660988/)

One example (from this review) is the 3C/3D precursor of poliovirus, in which the two components are well separated (above) and, to quote, “Overall, the structures of 3C and 3D alone are very similar to their counterparts in the 3CD precursor.“
The preceding result may be the one anticipated, but the nsP2/nsP3 precursor of Sindbis virus illustrates a quite different situation. Here the two proteins components interact strongly in the precursor (below), suggesting that after proteolysis a rearrangement of the structures or interaction with some other protein might occur. Suffice it to say that the situation is complex and remains to be resolved. However a comparison of with the structures predicted by alphaFold might be informative.

Cellular Polyproteins
The situation with cellular polyproteins is rather different. These relate synthetic pathways in which the enzymes catalysing successive steps are organized into a pipeline. In the (relatively few) examples the eukaryotic version is a polyprotein, whereas the prokaryotic equivalent is a multi-enzyme complex of similar, but distinct, components. In contrast to the viral polyproteins, there seems no a priori reason for a polyprotein in this case, and, indeed, this is not subject to (natural) proteolytic cleavage.
Polyproteins of this type have been crystallized only relatively recently, although there are several structures of individual components and prokaryotic equivalents. I shall consider two examples.
The first is enzymes of the shikimate pathway, responsible for the synthesis of aromatic amino acids. In bacteria, such as Escherichia coli, this comprises seven individual enzymes, but in lower eukaryotes such as Neurospora crassa a polyprotein of five of these, the arom complex, is employed. (Higher animals lack the ability to make aromatic amino acids, and plants use separate enzymes encoded by the chloroplast genome.)  The structure of the arom complex polyprotein was determined for the thermophilic fungus, Chaetomium thermophilum, by Verasztó et al. A feature of this polyprotein is that the individual enzyme domains move and function independently of one another with little effect from their linkages. Although many structures have been reported for the individual enzymes of the complex, these differ between species, and I can find none for C. thermophilum in the protein data bank. Hence the exact test proposed by the OP has not been carried out, but the indirect evidence suggests independent folding. A structure, from Candida albicans, has subsequently been reported.
The second example of a cellular polyprotein is the enzymes of the fatty acid synthase pathway in mammals, and the homologous  polyketide synthases in bacteria (only few of which synthesize fatty acids). The first such structure was reported by Maier et al. in 2008. The porcine complex is shown below, and has a more open and flexible design than the arom complex, that seems to have allowed insertion and deletion of different catalytic domains during evolution. Again, this argues in favour of independent folding of individual components, although I am not aware of direct comparison with individually expressed fragments. I suspect that there might be structures available to do this, although I haven’t had the time to examine this further myself.

I would conclude by noting that although the individual components of these cellular polyproteins interact with one another to cooperate in the biosynthesis, the flexibility they exhibit allows transfer of the growing substrate from one component to another.

This is a much more extensive update to my initial answer, now, I think justifying acceptance. However criticism and additions are welcome. I would like to look for structures of individual FAS enzymes, and do some work with alphaFold, but do not currently have the time.


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Visibility of a spiders web from a distance
Given that the diameter of a spiders web is, for instance, far smaller than a thread of cotton. Why are spiders' webs so visible from a distance?
What property of spiders' webs makes them so obvious (in the right lighting!)?
I guess I'm asking, is their visibility something that could be leveraged to create highly reflective surfaces that outperform current standards?!

Are you referring to spider webs with dew on them? Otherwise I think I'd argue that spider webs are not particularly visible, and being not particularly visible is important to their function of capturing prey that would likely avoid the webs if they were easily seen.

Thanks for the answer. No I mean in dry conditions. However, interesting you should mention dew, there must be an evolutionarily advantage for why they are more visible when adorned with dew, and thus aren't hydrophobic?

Another Q&A to read when thinking about why certain traits do or do not exist in light of evolution: https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont

Can you provide some evidence that spider's webs, when dry, are more visible from a distance than other substances of similar thickness?

I can't provide any evidence for that. However, having got older I see cobwebs before I see other "threads" of a greater thickness, so I assumed they're must be some property of web that makes this possible.

I think this is actually a physics question. I forget the name, but for every material (and yes, apparently every material) there is a range of angles where the material becomes reflective. This angle might be so close to 180 degrees and the range so small that you never notice it though.

Clearly you've never walked face first into a spider's web in the woods.


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Why is the expected time to coalesce the same as the ploidy times inbreeding effective population size?
The expected time to coalesce, in generations, is the same as the ploidy (e.g., 2 for humans) times Nef, the inbreeding effective population size, under coalescent
theory. Why?
Both ploidy * Nef and the expected time to coalesce are equal to the summation from generation $t=1$ to infinity of (t(1-((1/(ploidy * Nef)^(t-1) * (1/(ploidy * Nef)))))), or written more prettily:
$$\sum_{t=1}^{\infty} t\left(1-\left(\frac{1}{\text{ploidy} \cdot N_{ef}}\right)^{t-1} \cdot \left(\frac{1}{\text{ploidy} \cdot N_{ef}}\right)\right).$$
Why, and what does it mean to have an "infinite" generation (in the summation)?
The time to the last coalescent (of two gene copies) is ploidy * Nef.
If you multiply this whole summation by the number of pairs of genes, the result is a new summation which represents the sum over generations of the probability that coalescence occurs in the t-th generation, or the probability of the first coalescence occuring within t generations.


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If protein is mostly used by the body for purposes other than extraction of energy, why are calories from protein relevant?
Non-biologist speaking here. As you can probably see from the title, I'm having trouble wrapping my head around concepts related to the body's energy balance amd the role of macronutrients. Let me explain in more detail.
If a person consumes excessive amounts of calories for a certain period of time (i.e. more than they need) they will start to gain weight in the form of fat. Conversely, an extended caloric deficit will lead to weight loss. So far, so good.
Now, each macronutrient has a certain amount of calories per gram of nutrient - if I'm not mistaken 1 g of protein has 4 kcal.
On the other hand, according to different sources that I've been reading lately, the body does not really use protein for energy gain unless in extreme circumstances. In other words, carbohydrates and fat can readily be "converted" to ATP for energy gain while the conversion of protein into glucose and then ATP is very inefficient. At least that's my understanding, if there's already a misconception here feel free to correct it.
Proteins are mostly used to build and repair different structures in the body. I will use the reparation and buildup of muscle tissue as an example. And here comes my main question: if proteins aren't being "burned" by the body to extract energy in the form of ATP, why are the calories consumed in the form of protein really relevant? In other words, if the protein that I eat is being used by the body to build stuff such as muscle, haemoglobin etc. and not being burned, why do I care about the calories that protein has? Why will excess protein calories make me fat?
I obviously "know" that calories from protein matter, but I don't understand why this is the case. I feel like I'm really not grasping something essential here. I hope that the question is clear and that an interesting discussion could follow. If anyone could give a more detailed explanation of what's going on in the body in this scenario, that would be much appreciated.

Relevant to what? Please provide context, i.e. a scientific source in which the energetic values of different foodstuffs are presented with implied relevance to something. Be aware that this site cannot provide dietary advice as questions about medicine and health are specifically off-topic. Also note that this is a question and answer site, not a discussion site, nor is it intended to replace standard textbooks in which metabolism is described for those wishing to know "what's going on in the body". Please cite the texts that you have consulted.

I tried to give an answer "in the spirit of your question," so to speak, but feel free to ask for more biochemistry

Preamble
I had not intended to answer this question as I felt it lacked the clarity required for this site. However I now think that it is necessary to correct the assertion that “protein has to be converted into glucose to generate energy”, especially as this is echoed by the answer from @ThatGuy. I shall clarify the question by interpreting the word “relevant” primarily to mean general “purpose” or “utility”, and shall consider this in relation to the Food and Agriculture Organization of the United Nations (FAO), one scientific body that has published values for energy values of nutrients.
Summary

The dietary nutrients carbohydrate, fat and protein can have
different metabolic fates in the body depending on individual
circumstances. The assumption that “protein is mostly used by the
body for purposes other than extraction of energy” does not apply
in many circumstances.

Energy values for food are concerned only with the situation in which the nutrient is used to produce its maximum biological energy yield as ATP, using the appropriate metabolic pathways.

These values  are not simple bomb calorimeter values. They are calculated separately for protein, carbohydrate, and fat, taking into account their different metabolism. For proteins this takes into account the different metabolism of the 20 amino acids, although it should be emphasized none of these need to be converted to glucose to generate energy.

There are several different purposes to which these values can and are used, but the FAO is primarily concerned with their use to assess basic nutritional needs and their fulfilment in the countries of the world in which malnutrition may occur.

The FAO and standard energy values for nutrients
As mentioned above, I will consider this question in relation to the FAO, the Food and Agriculture Organization of the United Nations, a body that has produced energy values of different nutrients — values that appear to be used by government organizations and commercial food groups in many countries. The source of my information is this report on the subject, produced in 2003, to which the reader is referred for fuller details.
What did the FAO envisage that the results of their work would be used for?
To quote from Section 1.1 of the report:

assessment of the energy needs of countries… living under
different circumstances;
assessment of food availability within regions and countries;
assessment of the potential ability of available food supplies to meet a country’s … needs,
assessment of individuals’ diets (although the recommendations are not meant for this purpose));
as a basis for food labelling, with implications for consumer information/education about specific foods, regulatory compliance regarding nutrient content and claims, and trade.

This should answer the original poster’s concern with the “relevance” of energy values. The purpose envisaged was clearly with energy requirements in countries in which energy malnutrition was a problem, not affluent Western countries suffering from easily preventable diseases caused by overconsumption of food (although they are not irrelevant in the latter).
Did the FAO take into account the different metabolic fates of different energy supplying nutrients?
Yes. It was constituted of personnel who, unlike the poster, were biological scientists with a sound understanding of the physiology and biochemistry of metabolism. To quote from section 1.3 of the report:

“Energy requirement recommendations remain “theoretical” and of little practical value until they can be related to foods… Two pieces of information are needed in order to translate individual foods, and ultimately diets, into energy intakes that can be compared with the requirement recommendations…
…amounts of components must be converted into energy content using an agreed set of physiology-related factors that correspond to the energy-producing potential of the components in the human body. Thus, in order to make accurate estimates of energy intake, it is essential to have energy conversion factors for each component that denote the energy per gram for that component. However, it has long been recognized that the energy contents of protein, fat and carbohydrate differ, both inherently in the compounds themselves and owing to their different digestion, absorption and metabolism.”

So the scientists on this body were well aware of the problems in producing energy values for different nutrients, and the paper considers proteins, fats and carbohydrates separately and in detail in sections 2 and 3 of this report. For each of these (and for different sources of the same constituent) they produced separate values of various measures, with final values in Section 4.
However the value of 17 kJoules per gram protein (=4kcal/g)) quoted by the original poster is the FAO value of Net Metabolizable Energy (NME) — i.e. the energy produced in circumstances when all the protein amino acids are oxidized to produce ATP. This is relevant to individuals in protein equilibrium but in net energy deficit.
(The overall energy values they suggest for fat is 37 kJoules/g, and for carbohydrate 17 kJoules/g).
Summary of metabolite interconversions in obtaining metabolic energy from proteins, fats and carbohydrates

The diagram above is my own attempt at a biochemical summary for the situation when carbohydrate, fat or protein are being solely used to generate energy. Although some ATP is generated directly in one pathway, most of the carbon skeletons are oxidized in the TCA cycle, shown. Not shown is the NADH produced in the TCA cycle and its oxidation in the electron transport chain to produce a proton-motive force which drives the conversion of ADP to ATP — a molecule that can be considered as a source of metabolic energy.
In the energy-deficit scenario carbohydrates are converted to glucose, then to pyruvate in glycolysis (with some direct generation of ATP) and then to Acetyl CoA which for oxidation in the TCA cycle.
In this scenario fat (triglyceride) is converted to fatty acids and glycerol, the latter feeding into glycolysis, and the former being oxidized to Acetyl CoA, and hence to the TCA cycle.
In this scenario, in which they are not required for protein biosynthesis, each of the 20 amino acids from protein undergoes different metabolic conversions, as shown. All these can lead to the TCA cycle, and, as is evident, none involve conversion to glucose†. (The removal of nitrogen from the amino acids, actually consumes energy, but this is allowed for in the FAO calculations.)
Analogy (for those that find them useful)
If I buy a gold trinket in an antique shop it will (in Britain at least) bear a hallmark indicating the purity of the gold. If I am interested in keeping the piece until the price of gold increases and then selling it for its gold content (perhaps after melting it down) then the hallmark information is of primary relevance to me. If, however, I am interested in the trinket because of its beauty or because it may be a rare piece from a famous designer, the hallmark, although reassuring, would have little “relevance” to my purpose.
Even shorter analogy (to demonstrate my sense of humour)
One man’s meat is another man’s poison.

†The misconception about protein and glucose may have arisen in the following way. In extreme starvation the primary metabolic consideration is to supply the brain with glucose, on which it is absolutely dependent. To do this muscle protein is broken down to amino acids, some of which (e.g. those in the diagram that go to pyruvate) can be converted to glucose in the liver by the reversal of glycolysis (gluconeogenesis). However in a normal diet this is unlikely to happen because there will be a plentiful supply of glucose from carbohydrate, and it is certainly not the scenario in which energy values of protein are calculated.

Thank you for the detailed answer, this cleared up some of my misconceptions. In retrospect I should not have asked this question on this site because it is too "unscientific", or at least I should have formulated it more precisely.

When I asked why the calories from protein are "relevant", I meant why their energy value of 4 kcal/g should be counted when keeping track of consumed calories (in a diet for example). My reasoning was that bodybuilders, for example, require high amounts of protein merely to build their muscle mass – therefore the caloric value of their protein intake is irrelevant as they do not metabolize this protein to gain energy but rather build body tissue with it.

On the other hand the reasoning often promoted in dieting tips is that they need to keep track of every calorie they consume – regardless of its origin – to avoid eating more calories than they need, otherwise they will gain fat. Apparently this misunderstanding is very common since it is very often asked on numerous forums. I resorted to this forum not because I wanted dieting tips but rather because I wanted to understand the mechanisms behind protein metabolism in this scenario, but you are right, this question probably doesn’t belong here. I apologize

Side note: A biochemistry professor answered this question (asked by someone else, not me) on a non-scientific forum called quora (https://www.quora.com/Why-count-calories-from-proteins-if-they-are-not-intended-to-be-used-as-source-of-energy-but-to-build-and-repair-body-tissue, answer by Mark Roseman). I also found his answer very interesting and in case anyone with the same misunderstanding as me is reading this, go read Prof. Roseman's answer and the comments to his answer on that site.

I should also note that your answer sparked a deeper interest in biochemistry. I found some very good textbooks that I am hoping to study soon if I have the time to do so. I know that comments shouldn't be used to say "thank you" here on stack exchange, but in this occasion I'll do it anyway: Thank you David for catalyzing my interest in a very fascinating scientific discipline!

@ilovemaths — Thank you for your kind remarks. Good luck with biochemistry!

Think about it this way: if you're compiling a budget or asset report then you want to know about cash flows - income vs. expenditures - regardless of what form that "cash" might take. Sometimes, you want to know how much "cash at hand" you have, and you'll count only the most liquid assets, but often you'll also need to know the total value of any assets that can be converted into cash at all - not just stocks and bonds, but real estate, let's say, and a lot of other possible in-betweens.
In that they are used here (in the context of nutrition), calories are basically like energy currency with varying degrees of liquidity. You might have some assets, like carbs, which are like publicly traded stock shares that can be fairly easily converted to ATP with little commission. Proteins, then, might be more like specialized assets. But the crucial point is, proteins are still energy assets. When you are evaluating your wealth for the purposes of taxes or to take out a mortgage, the bank/IRS will still want to know your net worth considering any property contributing to that net worth. Because proteins can be converted to energy, they still add up to the overall energy budget.
Imagine you have a financial portfolio where you're investing more into stocks (proteins) than what is optimal for your growth targets. The same way that if you have excess cash in your financial portfolio (after meeting your investment and savings goals), you might invest it into more stocks or bonds, the excess energy provided by proteins will need to be stored somewhere.
In the body, consuming more protein than needed for muscle repair and other functions leads to excess calories. Since the body sees this as an "excess cash flow," it converts proteins into glucose (sort of- the details are complicated) and stores it as fat (which is, in our parable, like the savings account).


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How to keep primary human cancer cells alive in vitro and derive a cell line?
I am studying a human cohort of patients treated with neoadjuvant immunotherapy before surgery, of whom we have pre- and post-treatment biopsies as well as the resection. In one patient's resection, we discovered a population of less differentiated resistant cancer cells, which excluded immune cells (even though the rest of the lesion was extremely infiltrated). We profiled these by spatial transcriptomics and indeed do find similar cells in our scRNAseq samples of both the pre- and post-treatment biopsies. All very interesting stuff. I'm super curious to figure out how these cancer cells manage to exclude immune cells. The scRNAseq data gives a hundred interesting leads that /could/ reasonably contribute. However, in the end it's lacking experimental support.
Here's the kicker: We still have primary dissociated cells from the pre- and post-treatment biopsy. All cells that weren't used for scRNAseq were frozen in standard freezing media (1 PRE vial, 2 POST). Thus, I essentially have three shots at thawing these cells (pre- and post-treatment biopsy, unless somebody has a tip on how to safely split frozen vials), and attempting to culture and immortalize them. Here comes the issue: Nobody at my institute has experience with this, everybody says that it's hard and with a low chance of success (I somewhat agree). I still think that it's worth a try and that preparation is key here to increase the chance of success.
I am trying to read online resources about primary cancer cell culture (which does seem hard) and also do find various commercial offers of companies that claim good successes with their numbers, but also wanted to turn to the labrats here and ask for advice or hints on where to look/who to ask. So thank you for any and all suggestions!

Way too broad; there are entire book chapters about this.

I'd highly recommend finding an experienced collaborator.

@BryanKrause Thanks for the suggestion. It crossed my mind before but brings additional complications (which might be too much with the current time constraints)

It is very hard - you have a tiny chance of success normally. It's been many years since I last did something similar, but IIRC about 1/10^6 cancer cells will grow, but the vast majority of these will not make it to cell line transformation stage. You also have to consider removal of other non-cancer cells from this process; fibroblasts will grow very well under most conditions.

@immunoLogical My expectation is that the alternative to dealing with those complications, whatever they are, is failure of the attempt at best, and embarrassing or fraudulent results otherwise (e.g., you'll think you were successful but actually you only succeeded in growing some contaminant instead). See bob1's comment as well.


text:
Which position do retro aldol reactions occur in (comparing glucose and fructose)?
Regarding glycolysis, my text states:

What is the biochemical rationale for the isomerization of glucose 6-phosphate to fructose 6-phosphate and its subsequent phosphorylation to form fructose 1,6-bisphosphate? Had the aldol cleavage taken place in the aldose glucose, a two-carbon and a four-carbon fragment would have resulted. Two different metabolic pathways, one to process the two-carbon fragment and one for the four-carbon fragment, would have been required to extract energy.

I am trying to understand this and I found this diagram. It seems that glucose undergoes a [4+2] retro aldol reactions but fructose undergoes [3+3]. Why is this? What determines which position a retro aldol decomposition occurs in? Is there any particular reason glucose could not undergo [3+3] decomposition?

If you have found a diagram, please present it in your question, as questions here should be self-contained. Also give details of your text. I suspect, however, that your question — when properly formulated — may attract more responses on SE Chemistry.


text:
Is it possible to consider chlorophyll a as an accessory pigment?
I understand that chlorophyll a is the primary light-capturing pigment. However, in last week's exam, one of the questions asked whether chlorophyll a can function as an accessory pigment.


text:
What makes cherry blossoms so delicious? Does this delicious molecule (or molecules) have some function in the blossom? Does saliva activate it?
My friend showed me a news item about a monkey (or macaque) recently (early February) seen in Taiwan eating cherry blossoms. I assumed it must have been eating caterpillars or other insects that eat the blossoms, but a quick search in google found a related video shot in Japan Monkey Eating Cherry Blossoms in Slow Motion.
So a few days ago I tried a few. I pulled off the petals (since the monkey also seemed uninterested in them) and when I first started chewing I tasted nothing but inert vegetable matter.
But then over about 15 to 20 seconds of chewing the little blossom bodies I noticed it first became bitter, then slowly increasing taste of what I describe as "Black Cherry" flavor, but without any sweetness. It continued to get stronger and more delicious, and I did not want to stop!
That day I'd chewed (and eventually swallowed) about a dozen blossoms and felt absolutely wonderful; like I had been treated to a real delicacy.
note: The cherry trees planted and cultiated for their decorative blossoms in the early spring are not the same as the trees that yield commercial cherries. I'm told their fruit is quite sour.
Question: What makes cherry blossoms so delicious? Does this delicious molecule (or molecules) have some function in the blossom? Does saliva activate it?
It's possible that it's stored in structures that take time to break down during chewing, but I got the impression that a chemical reaction was taking place, perhaps a bit like how starch becomes sugar as we continue to chew on bread.

slightly related (and currently unanswered) Why Japanese cherry trees blossom so early in spring?

just asked in Cooking SE: Are cherry blossoms ever used in cooking for their flavor? Is there a preference between ornamental and agricultural varieties?

There actually is a study in the Nature magazine identifying the volatile (in the sense that they easily evaporate, as most aromatic substances do) organic compounds in cherry flower essential oils (basically a liquid cherry flower "extract" in which these volatile organic compounds are enriched by a process similar to distillation) the researchers made from cherry flowers from four different cultivators.
In the study, you find a table.
It contains a list of the volatile organic compounds found, including
how much they found in the essential oil created from the cherry blossoms from each cultivator, respectively.
I copied (one copy-paste suffices) the table into a spreadsheet program (LibreOffice Calc), and then added a column with the average share (probably wrt. weight, see study for details) of the respective volatile organic compound found (averaged over the four oils the scientists made from the blossoms from the four different cultivators), and sorted the table by that column.
The compounds with the largest average share are:

compound
average share [%]
taste

Ethanol
15.8600
it's alcohol

(E)-2-Hexenal
11.4725
like green apples

Benzaldehyde
10.4025
like cherries

Dimethyl sulfide
5.7000
savory

Acetaldehyde
5.4625
tart flavor, like green apples or dry cider

Linalool
4.0625
flowery and citrus like flavor

Followed by compounds with shares of less than 2.8%.
Now the question remains which of these are most important for the cherry blossom taste you observed.
Regarding this, I would like to remark the following:

benzaldehyde and linalool probably play a major role, as you described the taste as black cherry like, and according to this article, benzaldehyde, linalool and eugenol are the most important constituents of the cherry taste (eugenol was not found in the essential oil, and methyleugenol only had a very small share, see the original table).
Ethanol probably only has little effect on the flavor, as it has not that strong of a flavor to begin with, and may even have appeared in the study in such large quantities just because the blossoms were not handled quickly enough and rotted a little, so that possibly, in fresh blossoms, one would find much less ethanol.
Dimethyl sulfide possibly only has little effect on the flavor of fresh blossoms, as it's savory taste doesn't fit the taste you described and the quantity found in the study may similarly actually mostly be the result of the blossoms rotting (as dimethyl sulfide indicates bacterial contamination when brewing).

Explaining the time delay:
Obviously, the compounds are at first contained in the cells of the blossoms (mostly in the vacuoles of the cells). It takes time for the chewing to destroy those cells and for the compounds to leave the destroyed cells and enter your saliva by diffusion, possibly explaining the short time delay.
Safety of eating blossoms:
As you see, those blossoms contain a variety of organic compounds, some of which are actually poisonous in still quite small amounts.
I don't know in what amount, if any, those cherry blossoms you ate are safe to eat, maybe they are totally fine, maybe they are fine in small enough amounts, and maybe those specific cherry blossoms are downright poisonous. This may even depend on details, maybe some cherry blossoms are safe to eat and others aren't (considering that table for example, one of the cherry blossom essential oils tested had 0.54% coumarin, while another had none, and coumarin is poisonous). Please ask someone qualified whether the cherry blossoms you eat are safe.

What a wonderful, thorough, fact-based, well-supported, and informative answer! Also, you emphasize a really important point - don't just eat stuff! A video of a monkey eating one kind of cherry blossom in Japan is not an indication that I should feel safe eating a different kind in a different place. Consider me suitably reminded. :-)

In the linked paper's introduction, this caught my eye: By volatilization, the smell of some flowers not only generates a signal to stimulate the immune response to self-heal but also has an important role in plant resistance to various stresses¹⁸

¹⁸ is Potential applications of glucosyltransferases in terpene glucoside production: impacts on the use of aroma and fragrance who's abstract includes "It is now well established that odorless glycosides represent a significant pool of aroma precursors in plants where they act as preformed but inactivated defense or attractive chemicals." Perhaps that's why it takes circa 15 seconds of chewing before my perceived "black cherry" flavor starts to kick in (which is part of my question)

Possible, but it may also simply be the time it takes to extract the aroma by chewing...

I ate a few more a few days ago and paid careful attention. They start out tasteless after many seconds of chewing but then turn first bitter for several seconds before the deep, satisfying "black cherry" flavor kicks in, so I slightly edited the question to reflect this as I don't think it affects your answer. Also fyi I've just asked in Cooking SE: Are cherry blossoms ever used in cooking for their flavor? Is there a preference between ornamental and agricultural varieties?

As an aside, cherries (Prunus avium) and almonds (Prunus dulcis) belong to the same genus. Stonefruit kernels contain cyanogenic glycosides known to be toxic in large amounts, so some caution is warranted. That faint almond smell is more than sweet. See: https://repositum.tuwien.at/handle/20.500.12708/4851?mode=full


text:
Why Laramidia is more rich in dinosaurs than Appalachia?
Most of the North American dinosaurs are known from Laramidia - the sub-continent western to the Western Interior Sea. From Appalachia, far less dinosaurs are known. However, looking at maps, Appalachia was bigger in area while Laramidia was a relatively narrow band stretching from Alaska to south Mexico.

Why there are more dinosaurs known from Laramidia and not from Appalachia?
I can think of several reasons:

Laramidia had richer dinosaur fauna indeed. Then I ask: why?
Discovery bias - West America has better sites for digging fossils: wide open badlands without obstructions such as forests and vast construction, which prevent digging.
Preservation bias - Laramidia had better conditions for preserving fossils.

I'm no expert, but I think from my readings (possibly from reading Mark Jaffe's The Gilded Dinosaur) it's #2 almost entirely.

Its not, there are just more trees over Appalachia.
its easier to find fossil in dry climates which have more exposed bedrock and sedimentary rock. We find plenty of fossils in Appalachia just mostly in mines and other large scale excavation. Any place with little to no vegetation is best.

If you want to know why arid climates are better for finding fossils, there is an existing question about that.
https://earthscience.stackexchange.com/questions/13331/why-are-many-fossils-found-in-deserts/13337#13337


text:
Claim in article about why insects are attracted to light
In this article they are addressing the reason insects are attracted to light when they say

Heat radiation as an attractive component is refuted by the effect of LED lighting, which supplies negligible infrared radiation yet still entraps vast numbers of insects.

I don't see why attraction to LEDs shows they're not seeking heat. Could they for example be evolutionarily programmed to associate light with heat? So that even though they don't encounter heat near/on the LEDs they still "expect" to?

Do you have any reference to support your hypothesis? Bear in mind that the insects in the article are nocturnal. Until recently the only substantial light at night was the reflected light from the moon - not a lot of infra-red from that. How do you explain that the mechanism you propose might have evolved given the environment they evolved in?

@JiminyCricket.My example is only an attempt to provide a logical possibility that shows their conclusion doesn't follow from their premises.

Your right to question it, but it doesn't end there. There's a 2016 post here, the first answer might be of interest to you.

Then there's the idea that female moths are visually interesting at near-infra-red wavelengths which seems to have some support and there's: Physiological basis of phototaxis to near‑infrared light
in Nephotettix cincticeps which  suggests limited, but some possibility of (near) IR being visible to some insects.

Please be aware that this is a question and answer site, not a journal club for discussion of papers on external sites . Questions should be about biology and of general interest. Your simplistic criticism of a conclusion in a long and complex paper is not that. An appropriate question might be "How are insects attracted to light?". For this reason I am voting to close.

The BBC just has a layman's article on exactly this paper: https://www.bbc.com/future/article/20240215-why-insects-are-drawn-to-artificial-light-at-night

They're looking for and describing proximate relationships (see e.g. https://en.wikipedia.org/wiki/Proximate_and_ultimate_causation).
If the light isn't warm and insects still move towards it, that means they're not using heat to make the decision where to move. They're not saying anything about the ultimate underlying motives, just the immediate proximate mechanism.
Their alternative model is that it's based on orientation to the sky, by which insects point the top of their body (dorsal surface) toward light; if the sky is bright that would keep them oriented back-upward, but if it's a point source near the ground keeping their back towards the light causes them to fly in circles around the light:

Our guidance model demonstrates that this dorsal tilting is sufficient to create the seemingly erratic flight paths of insects near lights and is the most plausible model for why flying insects gather at artificial lights.

So, if you want to propose heat-seeking as a better hypothesis, you'd need to provide data that would explain why this dorsal facing tilt would make sense for an insect seeking heat.

Thank you Bryan!


text:
Water potential problem
$$
\begin{align*}
\text{Left cell} \qquad& \text{Right cell} \\
\Psi_w=\pu{-1400 kPa} \qquad& \Psi_w=\pu{-600kPa} \\
\Psi_p=\pu{600 kPa} \qquad& \Psi_p=\pu{800kPa} \\
\Psi_s=\pu{-2000 kPa} \qquad& \Psi_s=\pu{-1400kPa} \\
\end{align*}
$$
This is the data given, and we have to find the water potential, solute potential and pressure potential at equilibrium. I can't seem to find any website or video for solving these types of questions.
I tried and got the answer equilibrium water potential to be about -1000 kPa, but it seems there can be multiple answers of solute and pressure potential.
So my questions are:
In this problem, are there multiple answers for solute and pressure potential, and is my water potential answer correct?

How is this a question about biology?

It is in my biology textbook. And I think it's part of A level biology course as well.

Biology is the study of life. Your question makes no reference to any living organism. It also presents the problem as a graphic which is not permissible as it cannot be indexed and discriminates against those with visual deficiencies. Please take the trouble to write out your question properly making the biological context clear, and explaining how you arived at your answer. If the question is in a text book (please name it) then one would expect it to include the necessary information for solving the problem. What did you find there?


text:
What is the part between the eyebrow tail and above the eyelid called?
I need to know that anatomical name of the portion of the face between the eyebrow tail and the eyelid, as highlighted in red in the image below, as I need to refer to that particular area in writing succinctly and specifically and without any ambiguity or elaborate description. Upon thorough digging, I have found out that the lacrimal glands (responsible for producing tears) are present underneath the skin of the highlighted part but I fear that lacrimal fossa (where the aforementioned gland is contained) is not the correct term for the highlighted portion as refers to the specific part of the human skull and definitely not the highlighted skin-area pertaining to facial anatomy.
Further brainstorming has got me to the conclusion that the best way to denote these areas in a succinct, unambiguous way without being too "technical" is through "left/right brow bone" but I feel that there is a better/more-specific term for this.
Thanks in advance.

The answer to this question can be found buried deep in the occuloplastic surgery literature.*
It's called... the upper eyelid. (!) Nowhere was it listed in numerous facial surface anatomy illustrations. I first encountered the name of the specific area here. It refers to how facial tissue ages.

The drooping brow and inelastic skin combine to cause upper eyelid tissue to drape over the lid margin, often obstructing the superior visual field.

The "eyelids" in common medical parlance usually refer to the structures that (normally) glide over the eye when blinking. The "eye" normally refers to the actual eyeball.
The occuloplastic literature, though, is necessarily more specific. The upper eyelid is the area between the eyebrow and the eyelid, the lower eyelid is the area that gets saggy in the elderly. The "eye" is the whole kit and kaboodle limited by the forehead above and the cheek below.
Droopy upper eyelid:

This is a YouTube video of a Beverly Hills oculoplastic surgeon who, along with another plastic surgeon, has a show about botched plastic surgery (I believe it is called Botched.) In the video, you see him run his index finger over the area you asked about repeatedly, calling it the upper eyebrow (oops) eyelid.
*Seriously. It took me a while to find it.

This area could be referred to technically as the zygomatic process of the frontal bone. The frontal bone is the top/front part of your skull that comes down to the orbits of your eyes. It connects to the cheekbone (or zygomatic bone) via a protrusion (or process) forming the orbit of the eye. This is also a name for the skeletal anatomy rather than the skin you actually see, but I'm not sure there will be another specific term that doesn't refer to the anatomy of the skull itself.
For a less technical term, you could call it the upper/outer orbit of the eye. That will also refer to the bone, however, and may refer to a location above or below the eyebrow depending on if you're furrowing or arching your brow.

Regarding your suggestion to call it the "upper/outer orbit of the eye", would calling it the "brow ridge" or "supraorbital ridge" pinpoint to the area without making it too technical and avoiding ambiguity caused by your suggested term? Would really love your further inputs and suggestions on this!

@hecate Both of those would refer to the ridge over the eyes, but wouldn't be specific about lateral location. The brow ridge would span from temple to temple going over the nose, but wouldn't specifically refer to the outer parts of it. "Outer brow ridge" might be close enough without being too technical.

No one refers to it that way ("zygomatic process of the frontal bone"). It's also not referred to as any part of the orbit. Link to a reasonable source, please.

@anongoodnurse It is a technical anatomical term. https://en.wikipedia.org/wiki/Zygomatic_process

Also, please note that on this site, we request that folks support their answers with reliable sources. Otherwise the answer is subject to deletion.


text:
What is the difference between digesting sugar and carbohydrates?
To understand where I'm coming from, first some commonly distributed (mis?)conceptions:
(Obviously to be taken with a big grain of salt because they are somewhat contradictory)

Sugar is bad for your health, because it goes into the blood quickly and thus creates a blood sugar spike upon consumption.
Snacking often is bad for your health, because it puts the body in a state of permanent digestion and keeps blood sugar high.
Carbs are better than sugar because they release the glucose over time a supposed in a spike.
Slow carbohydrate food (food that is supposed to release the glucose extra slowly, due to the chemical composition of the carbohydrates inside, or the physical structure of the food?) is better than carbohydrates, because it releases the glucose even slower.

Now the second one and the other three ones are somewhat contradictory, because if it was solely about the peak glucose levels, snacking should be healthy (which it probably is not), so something's off...
So I'd like to know:
What are the biological differences between the digestion of sugar and different types of carbohydrates as constituents of different types of food in humans?
Edit:
For more context:
I would like to understand what the most important aspects of carbohydrate digestion are, in order to be able to conclude a diet that helps me optimize my health from that.
I am very well aware that:

Sugar is carbohydrates.
Many carbohydrates will eventually be broken down into sugar.

I am also aware that "carbohydrates can be bad".
What I do not understand is how exactly "carbohydrates are bad".
In particular, I got confronted with three viewpoints:

High average blood glucose levels are bad.
High peak glucose levels are bad.
Snacking is bad.

Which seem to go in different, rather contradictory directions.
Also, Studies partially supporting either viewpoint can be found:

Study considering hemoglobin A1c levels
Study considering peak glucose levels
Study considering snacking

Which leaves the non-biologist asking themselves which is the "major effect" (certainly, there will be some truth to each position, but the question is which one(s) got the "main point"), and if there are any other important effects to be considered, hence this broad question here, so I understand, from a biological standpoint, what happens to the carbohydrates when I eat them, so I can conclude for myself how to adapt my diet for "optimal" health.

Sugar is a carbohydrate. If you want scientific answers to your questions, you'll have to start with scientific sources that make these specific claims. Anyone can claim whatever they want is good or bad and write a book about it, that doesn't mean it's right or useful for anything besides selling the book.

This site is for students of biology and biology professionals. Its purpose is not to provide textbook information for non-biologists. If you wish to learn about the metabolism of carbohydrates you need to buy a textbook and study it.

@BryanKrause I added some studies as references, as expected, you can find studies to argue either way, so who "got it" then : (

well for a start, cellulose is fiber and is not digestible so yes different carbs are digested in different ways, but I suggest breaking this into 3 different questions since otherwise you are asking for a dissertation on carbohydrate digestion. Also several have already been asked and answered. https://biology.stackexchange.com/questions/31352/do-blood-glucose-spikes-contribute-to-insulin-resistance-or-is-prolonged-elev?rq=1

The level of detail of a Wikipedia article would suffice : )

If your goal is to have "a diet that helps me optimize my health", then I suggest talking to a doctor, specifically a nutritionist. If for some reason or another that is not possible, I would suggest reading articles on trustworthy sites, such as www.cdc.gov or www.who.int. Just so you know, pretty much everything you described is about blood sugar levels, which your body does a very good job maintaining using insulin and glucagon. The condition of this regulatory system not working is called diabetes. If you are not diabetic, then daily calories is much more important than blood sugar level.

The problem is there is conflicting information out there, and the CDC and the WHO each have a track record that is neither abysmal nor perfect, just like most other sources too, so I don't trust either side, and try to gather as much information as possible, with a coherent big picture drawing from multiple sources as primary goal, because if things from different sources fit together well, they are more likely to be true.

That being said, I will of course also consult a nutritionist.

I do not see any conflicts in the sources you cite. There is no reason a snack can't cause a blood sugar spike for example. If you are after nutrition guidance there are lots of guides that do not require an understanding of sugar metabolism. Basically, eat lots of plants, avoid added sugars and excess fats, eat a varied diet.

Scope of Answer
The original poster provided ample context for his question, which related to health considerations. It was perhaps for this reason, among others, that the question had not received an answer at the time of writing: questions relating to medical or health advice are off-topic here. However, his actual question is primarily biochemical:

What are the biological differences between the digestion of sugar and
different types of carbs as constituents of different types of food in
humans?

Although this might be answered with a little internet search, I felt it would be hospitable if someone offered him an answer to this — and this only.
Definitions
The basic sugar unit is a mono-saccharide, those of relevance to this question being hexoses or pentoses, having six or five carbon atoms, respectively.
What in non-technical language is called sugar, refers to a specific molecule, sucrose, which is a disaccharide of covalently-bonded glucose and fructose.

What in non-technical language are referred to as dietary carbohydrates generally refers to the storage polysaccharide of plants such as potato and other root vegetables, rice, and other cereal crops used to make bread. This is a homo-polymer composed solely of glucose units.

Summary of the differences in metabolism
Arising from these definitions, the following differences in metabolism emerge:

Different enzymes (amylase for these polysaccharides, sucrase for saccharose) are used to catalyse the hydrolysis of the linkages between the monomeric units.

Absorption in the gut is different for glucose and fructose, as is transport into cells.

Both glucose and fructose are (or can be) metabolised to pyruvate. However fructose is first metabolised to fructose 1-phosphate, and only enters glycolysis at the triose phosphate stage. A consequence of this is that it by-passes any regulation that occurs for the metabolism of glucose after conversion to glucose 6-phosphate. (In addition, glucose 6-phosphate has alternative metabolic possibilities not shown).

Postscript
This provides the framework for considerations of the consequences of dietary intake of sucrose, which are not part of the question and off-topic here, as already mentioned. Despite that, this topic has been addressed in questions in SE Biology, as well as elsewhere on the internet. I try not to offer advice to others (nor to take it from strangers). However my wife, whose advice I am sometimes obliged to take, professes the following:
“All things in moderation, and moderation in all things.”

Nice answer. Also fits very well with other information I recently acquired.


text:
How much effort is it to establish a cytotox assay for cancer cell lines against a small number of possible compounds?
I am currently testing a series (5-10) of small molecule compounds against an enzyme that are intended as inhibitors. This enzyme is meaningful for cell proliferation.
Until now, nothing was active and therefore I could try to test the new molecules in a cytotox assay, to test if they are of any medicinal value. It is known, that these compounds have multiple modes of action and inactivity against the discussed enzyme does not necessarily mean that they are fully inactive.
I am wondering how complicated this is and if you're a beginner on this how long does it take to set up a growth inhibition or viability assay. Currently me gathered experience on protein expression and aspetic technique. But I have no experience with cell culture and sterile bench. My cell lines of interest are melanoma cell lines and or various brest cancer cell lines that are commercially available from multiple known suppliers. Do you think it would be possible to test this in a couple of weeks? I am willing to work 7 days per week if this will speed up the process. What is a realistic time frame to get first results? I would work with commercial inhibitors as control. I have no idea how time intense this process might be and would be interested about your insights.

Do not forget https://xkcd.com/882/ and https://xkcd.com/1217/

The answer to this is, of course, "it depends". There are quite a few factors at play here. As you don't seem to be experienced at cell culture yet, I strongly recommend that you find someone experienced to teach you. It is not something that is easy to pick up, as problems in cell culture (e.g. low-level contamination, cross-contamination, old cells, overgrowth, under-seeding) can be subtle and difficult to identify without experience.
It will take at least 4 weeks for experience to kick in, and cells aren't like bacteria in that they won't grow overnight to suitable levels for sub-culturing/experimentation; it'll take days to weeks of growth from a frozen vial to having enough to work with. This takes time alone. You'll need to be in some weekends anyway; when cells need to be split or fed, that's when you'll be in!
It takes time to learn the characteristics of each cell line, how fast it grows and how it behaves under certain conditions. If you get the conditions wrong, it will invalidate your experiment. Many cell lines will tolerate quite a bit of mishandling (e.g. growing to too high a density), but others will stop growing if you seed at too low a density and/or they become too confluent. This varies from cell line to cell line and even cell lines within a single type (e.g. melanoma) can be different from others.
You also need appropriate media for each cell line - many culture media use phenol-red as an indicator dye, but this is an estrogen analogue, which can affect growth of hormone-sensitive lines (often the case with breast cancer lines for example). Some lines are sensitive to glucose concentration or need a special supplement to grow. Knowing these sorts of things are critical to your experiments and is where experience kicks in. You will need to start by looking up the growth conditions of each cell line you plan to use.
Once you are experienced, it can be a fairly simple process. With enough cells and the right equipment (e.g. repeat dispense function multi-channel pipettes), I can easily set up 20 or more 96-well plates for viability assays (IC50 style) in a day. There are lots of other options on assays too, how long they take and what read-outs (MTT/XTT?, neutral red? cell count? luminescence or fluorescence-based) you use are variables too.

Thanks. I am now actually working of these experiments yet. For me, the biological part is not the challenge but the synthesis of Activa compounds. For the viability test I want to use the MTT assay. When it will show some.effect on the cells I want to proceed with apostosis tests and than metabolite studies by LC MS/MS. Keep thumbs pressed that my compounds will kill cancer cells.