text:
Does 1kg of lettuce have more energy than 1kg of beef?
Given that each trophic level of the food chain has a decrease of 90% of available energy, would it be fair to say that 1kg of lettuce has more energy than 1kg of beef? If it's not true, can you explain the reason?

Re: "each level of the food chain has a decrease of 10% of available energy", could you clarify, ideally with a reference? Also, I'm guessing you mean available calories from digestion rather than e.g. fusion energy :)

Here is a source from NatGeo:  "only about 10 percent of energy stored as biomass in a trophic level is passed from one level to the next." https://www.nationalgeographic.org/encyclopedia/energy-transfer-ecosystems/

Thanks for the ref; assuming it's roughly correct, you should probably correct your question to be "a decrease of 90% of available energy", as passing on 10% reflects a loss of 90%.

Reductio-ad-absurdum - is there more energy in a kilogram of Uranium than in a kilogram of water?

Each level of the food chain has stored less energy than the stuff it eats, so I see where you're coming from - but it takes a lot more than 1kg of lettuce to make 1kg of beef.

This situation will only improve once we genetically engineer solar powered cows.

@criggie that's actually a bad analogy. There is more energy in 1 kg of water than in 1kg of Uranium. Fusion releases more energy per mass than fission, don't you know.

@PcMan Actually, E=mc^2, so they both contain the same energy, ultimately (in the same inertial frame, at least).  How much of it you can practically release in various circumstances is a different question.

Talkin about how much energy one can use in various circumstances... a human body will use more energy digesting lettuce than will get from burning whatever it can burn from the lettuce constituents. Whatever nutritional value the particular vegetable has, it is not energy.

@J... it depends which one is higher from the ground… or moving faster!

@Tim That's what the "same inertial frame" was about.  Different depths in a gravity well are different non-inertial (accelerating) frames.  Objects moving at different constant velocities are in different inertial frames.

What about a pound of sugar cane vs. a pound of lettuce?

1kg of beef has more energy than 1kg of lettuce but it isn't directly related to the trophic level energy loss.

Given that each level of the food chain has a decrease of 10% of available energy

You're all mixed up here. What the rule is saying is that if you start out with n units of solar energy, you lose 90% of it for every trophic level it passes through; Only 10% passes through as stuff that "stays around" materially (i.e. used to build the structure of the organism rather than being burned away as fuel to keep it alive). That means that it takes about 10x more energy to produce the same amount of edible calories in beef than it does in vegetables and grains, if they are separated by one trophic level.
It's not talking strictly talking about the energy density in food, but instead about how wasteful it is to produce the food containing those edible calories from the point of view of the total solar energy invested. For the same solar energy, you can feed a lot more people calorie-wise with vegetables and grains than beef.
It's kind of like thinking how many vegetables a rabbit eats over the couple years of its life from birth to when the rabbit becomes food for you. How long could you feed yourself on those same vegetables? Weeks maybe? How long could you feed yourself, if you ate the rabbit? A few days at most. You can imagine all those vegetables weigh more than the rabbit, but supply more energy than the rabbit meat, while the same mass of rabbit flesh has more calories than the same mass of vegetable. The rule isn't talking about calorie density of food.
Obviously, there are complicating factors, such as the actual composition of the food, since that determines calories and nutrition (which isn't related to solar energy).
The reason the same mass of beef has more energy is that 10% that sticks around keeps on accumulating. This is also the reason toxins accumulate in animals higher up the food chain. A little plankton might have a tiny bit of mercury in it, but a small fish might eat a billions of plankton. And, then a large fish might eat a thousand small fish. And, you might eat one large fish. If that mercury stuck around in everything that ate it, all that accumulated mercury ends up in you.

+1 for the rabbit example. Though I do wonder why you didn't use chicken or for that matter cows.

@slebetman I did not use cows because humans can't eat the same food as cows. I used rabbits instead of chickens because I was thinking of vegetables and grains only came to mind afterwards, plus I was watching Non Non Biyori and they were feeding rabbits the same thing that people eat.

Also this is how charcoal has a higher energy density than wood, despite being made by burning wood. Yes, during that burning process some of the energy (carbon content) is lost, but you get rid of so much water and other useless components, that the end product has a higher energy density than the raw materials.

Another complicating factor is that you have to eat 13 kg of lettuce every day.

The technical term of relevance here is "embodied energy", and is just as useful when considering the energy efficiency of EVs and other systems. 1 kg of beef embodies far more energy than 1 kg of lettuce.

The so-called '10% law' is a common, albeit very rudimentary, rule-of-thumb in foodweb analysis. It's commonly attributed to Raymond Lindeman, though he cited a wide range of ratios in natural systems. The point it's trying to make relates to the transfer of energy between trophic levels, not about the energy density of plants or animals in each trophic level.
The '10% law' would generally be parsed as 'it takes 10 kilojoules of energy stored in grass to make one kilojoule of energy stored in a herbivore, and 10 kilojoules of herbivore to make one kilojoule of a carnivore'.
Energy density of various foods is routinely measured. The US Department of Agriculture estimates the energy density of beef (15% fat, broiled) at 10470 kilojoules per kilogram, and the energy density of lettuce (Romaine) at 720 kilojoules per kilogram. One kilogram of lettuce clearly provides less food energy than one kilogram of beef.

The key here is that a "natural" cow - that is, one that grazes in meadows, rather than being confined to a feedlot - uses 90% of the energy in the grass &c that it eats to do things like walk around collecting that grass, avoiding predators, and making baby cows.  Only 10% (or less - I'm just using the "10% law") of the energy extracted from the food it eats gets turned into beef.  But OTOH, humans can't get much energy from eating grass, so would almost certainly use more energy to collect the grass than they'd get from it.

@jamesqf Humans could also grow other things than grass.

@user253751 other things, like cows

@jamesqf A significant proportion of the energy in grass is also needed for digesting grass, at least for ruminants.

@jamesqf that's an answer in its own right.

Plus, humans don't eat the entire cow, but only part of it, so there is an additional loss there that may not be included with the 10% law.

@user253751: In case you haven't noticed, they do :-)  But unlike most of those things, grass (and other forage) grows naturally in many places, with minimal if any human effort.  Cows (and other herbivores) collect the energy in their forage, again with little effort by the humans (or other carnivores) who'll ultimately consume the meat.  What matters is not the trophic energy levels, but the energy profit (gain/expenditure) of the consumer.

The (food) energy in 1kg of lettuce or 1kg of beef depends on each's composition, not on its trophic level. Normally we can digest fats, protein and carbohydrates, but other organisms like certain bacteria and fungi can even digest components like fiber and cellulose than we can't. Water doesn't provide any energy, but is still part of an item's weight, so food scientists normally calculate available energy for people based on the dry weight of fat, protein and carbohydrates, using average calories per g for each of the 3 classes of components.
The trophic levels/food chain 90/10 rule refers to how much biomass is produced in an ecosystem, not the energy content of a certain piece of that biomass.

Dry weight is important to the question, too.  If you've ever made your own dried food, you may have noticed that there's a lot more "food" left after drying meat vs vegetables.  A quick search says about 25% of the mass of beef is non-water, but only about 4% of lettuce.

Note that the decrease in food energy from one trophic level to the next is 90%, not 10%, if only 10% of the energy is actually passed on to the next level.
To compare 1 kg of lettuce with 1 kg of beef is not a very fair comparison for several reasons.

Most cows don't "beef up" on lettuce; they are usually either grain-fed or grass-fed.

Cows don't get their calories directly from the foods they eat to begin with--they eat to feed the bacteria in their stomachs, from which they derive their own sustenance.  (This not being a direct transfer may have some complications in terms of whether one should consider this to be one trophic level or two.)

Because of the energy transfer ratios, the cow will eat many kilograms of food to put on one kilogram of weight.  But in the process, the food is also changed in its form from being mostly simple carbohydrates to having considerably more fat and protein which are higher caloric-density foods.

Clearly, 1 kg. of beef will have more food calories than 1 kg. of lettuce.

I believe your point 2 is intended to cover digestion in the rumen and is indeed a major source of energy for the animal. However, cows do also digest some protein and fats on their own; this source https://extension.umn.edu/dairy-nutrition/ruminant-digestive-system#fat-digestion-1001418 indicates the rumen fermentation provides about 50-70% of the cow's energy. Fats are indeed more energy dense than carbohydrates, but proteins are similar to carbohydrates. It's having more fat and less zero-calorie water that boosts meat calorie density.

@Armand Yes, I'm aware of some of that which is why I used the term "complications".  Yes, fat is about 9 Calories/gram, protein is 4, and carbohydrates initially produce 2 but another pass through the citric acid cycle produces another 2.

The points about feedlots and cow digestion are really distractions, I think.  So consider instead a wild deer that you hunt for meat.  You've obtained a lot of food energy for little effort.

Just to complement @DKNguyen's excellent answer, think about this: if you were raising cows on lettuce, how many cows would you have and how much lettuce would you have? Obviously you could not have more cows than lettuce, because then you couldn't feed them. That's another rule of biology: "you'll eventually always have less predators than prey" (because when the number of prey falls below the number of predators, the predators will starve to death and reduce their numbers). So there you have it: the total amount of lettuce you would have would much more than compensate for the total amount of cows you were raising. The total amount of energy in lettuce would be far superior than the total amount of energy in beef.
But clearly, in the real world, we do not raise cows on lettuce. However, the same principle applies to whatever we use as cow feed.
Side note: I hope that makes you think about how very inefficient (and wasteful) it is to consume meat on such a large scale as we do.

Welcome to Biology.SE. Your post seems to be about the relative amount of energy in higher tropic levels, but that isn't what the OP asked. Please only post answers that directly address the question. This could be a comment, but is not appropriate as an answer. To critique or request clarification from an author, leave a comment below their post once you have sufficient reputation. Comments posted as answers are subject to removal, or you can delete this yourself. ...

... For details about how this site works, please take the [tour] and carefully read through the [help] including what is on-topic and what is not, and [answer] and [ask] good questions.

@tyersome: It IS what the OP asked for.  Specifically "If it's not true, can you explain the reason?"  This answer is a decent attempt at explaining the reason.  (And the base question can be answered with a simple search for the energy contents of beef & lettuce.)

@tyersome I understand how this site works. My answer addresses exactly what the OP asked for. Just like jamesqf said right above: I gave a perfectly reasonable and sufficient explanation for the second part of the question, "If it's not true, can you explain the reason?". If this is not an appropriate answer, nothing is.

@tyersome If this is because I said "to complement Nguyen's answer...", my answer stands alone on its own. In fact I find it simpler and more to the point. I only said I was complementing his answer because he gave a lot of information (not all of which is necessary to answering this) and it's the chosen most upvoted answer, so my answer is likely to be read after his being read.

@jamesqf & CoralBleaching — No the original question was "Does 1kg of lettuce have more energy than 1kg of beef?" — You are discussing what you infer that the question should have been, but I see no evidence that this is correct. This question is based on confusion between the total energy present in tropic levels and the energy density of those trophic levels, but that just makes it an insufficiently researched and poorly thought out question.

@tyersome I think I understand better what you're trying to say. You're telling me I should answer the question in the most literal sense possible. In this case, it would be appropriate only to break down the chemical compositions of lettuce and beef and demonstrate that he's wrong. I'm of a different opinion. I think we should address the context of where the question came from, whether it's ill-posed or not. As a user of this site, I know this saves everybody's time. And the accepted and most upvoted answer is the same as mine, but overcomplicated. You should complain there too.

only about 10 percent of energy stored as biomass in a trophic level is passed from one level to the next.

"biomass in a trophic level is passed from one level to the next" is a lot of words to say that the cow eats the lettuce.  This conversion from lettuce to beef is a lossy process.   Similarly, if you hypothetically continue to farm down the trophic pyramid, growing bears and feeding them your cows, it's likely to take about 10 kg - likely more - beef to produce 1 kg of bear meat.
A 300 kg cow will give about 180 kg of beef. But growing that animal for approximately two years is likely to require about 1,300 kg of grain and 7,200kg of silage/roughage. The "90%" number is a rough approximation; 180 kg is 13% of 1300, the silage or pasture gazing can count for something and bring it reasonably close to the 10% rule of thumb. Intentionally bred animals like some fish or poultry can be more efficient than beef.
The important thing to consider is that when you drive by unimaginably huge fields of grain being farmed 40 feet at a pass by massive combines and wonder how people could ever grow hungry, be aware that we're wasting a lot of those calories by turning them into beef.
As a side note, the cow will (generously) average about 40 liters (40 kg, 10 gallons) of water per day for those 2 years, for a total of (730 days * 40 kg water/day) / 180 kg beef) = 160 kg water actually drunk by the cow per kg beef produced. That's a lot, but that's not counting all the water used to grow that grain and roughage (and lettuce)...generous numbers for that growth is how you end up with insane quantities like 10,000 liters of water per kg beef.  If you assume that the water in the cow's urine is recycled to the water table and that the water that drains into the soil goes into the same aquifer or transpires from the grain goes back into the water cycle, the numbers are much more manageable - but it's still a lot of water. If you substitute for the veggie burger at dinner, feel free to leave the water running while you brush your teeth, you've saved more water than a week's brushing by not consuming that meat.
As a bonus side note: At a high level, both protein and carbohydrates have an energy density of 4 (kilo)calories per gram. Fat has an energy density of 9 calories per gram. However, 1kg of raw beef is not 1000 grams of metabolically available protein, it's actually a combination of water, collagen, elastin, about 200g protein, and about 50g (depending on the cut and cooking process) of fat. Similarly, 1 kg of lettuce is mostly water, quite a bit of indigestible cellulose, and about 30g of actual caloric carbohydrates. So your question could also be interpreted as "Does something containing 30g of carbohydrates have more energy than something containing 200g of protein", and the answer to that is a definitive "no", the former has 120 calories and the latter has 800 calories.


text:
If blood vessels mostly aren't supplied by parasympathetic nerves, how effects through M3-ACh receptors are mediated?
Blood vessels throughout the body mostly aren't supplied by any parasympathetic fibres. But the effects of ACh through M3-ACh receptors would infact release NO (which acts on VSM and causes vasodilation), which is demonstrated after ACh intravenous administration.
My question is how is it physiologically mediated? (i.e. the ACh mediated vasodilation)
*VSM= vascular smooth muscle
*NO= Nitric Oxide
*Ach= Acetylcholine
*M3 (Muscarinic type 3) Acetylcholine receptor

ACh=acetylcholine? NO=nitric oxide? M3-ACh? Might be useful to spell out acronyms/abbreviations the first time you use them (I see you have VSM at the bottom), since odds are the average user of this site is not in your field

Thank you! I've edited the question.

source: Stack Exchange

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

sort: votes


text:
Do any animals mix porphyrins and carotenoids in their pigmentation?
Many animals (particularly birds) use carotenoids or porphyrins in their diet to contribute to the brilliance of their skin/fur/feather coloration. A few even mix melanin in with carotenoids to get more complex colors. But are there any animals that mix a porphyrin with a carotenoid to make their color?

Yes. Here is one example of an annelid worm that does this:

Altogether, the endogenous porphyrinoid pigments of E. viridis appear to be similar in function and origin to the coloured bile pigments of H. diversicolor. It must be noted that biliverdin in this latter species is described as a secondary pigment, since the green coloration is only noticeable when the presence of the worm’s main pigments, namely carotenoids, decline during the reproductive phase and/or in starving individuals7. However, in E. viridis, green pigments are unequivocally predominant, likely being homologous to biliverdin, whereas yellow pigments may be more similar to another product of haem breakdown known as bilirubin (also yellow), rather than carotenoids. In fact, the yellow pigments found in the proboscis and epidermis (see Fig. 2) have quite distinct spectra from carotenoids36.

It seems that the original reference that they refer to is here, performing a relatively straightforward organic extraction and spectrographic analysis of pigments, stating:

Worms thus owe their green appearance to biliverdin, while the yellow, brown and orange pigments also present in the epidermis in most worms are carotenoids.

Biliverdin is a porphyrin.

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


text:
Monogenic disorders vs multifactorial inheritance disorders
There's a condition called SYNGAP1-related intellectual disability which is caused by mutations to the SYNGAP1 gene.
I believe that this is called a monogenic disorder, while disorders that are caused by multiple genes are called multifactorial inheritance disorders. Other examples of monogenic diseases are apparently cystic fibrosis, sickle-cell anemia, and Huntington's disease. Examples of multifactorial inheritance disorders are heart disease, cancers, Alzheimer's, athritis.
The number of monogenic disorders are limited to the number of genes at $\approx20000$, while the potential number of  multifactorial inheritance disorders is then $20000!$ or about $10^{77000}$. This upper bound is not very helpful since I would assume that most multifactorial disorders aren't going to affect anywhere near all genes.
How common is it that diseases/conditions are caused by the mutation to only a single gene? If I pick a random disease/disorder/condition how likely is it that it's caused by only a single gene?
Is there a list somewhere of all known monogenic disorders? If I search "monogenic" in OMIM there are 185 results, of which many don't appear to actually be monogenic. For example, the second result is obesity which is not monogenic.
If I look at Type 1 Diabetes there is only one gene-phenotype relationship which leads me to believe that it's monogenic, but the phenegene graphics shows three genes linked to type 1 diabetes: 600716, 147620, 142410. So not only are there multiple genes linked to diabetes, those multiple genes are also linked to multiple disorders.
The gene that causes sickle-cell is also connected to other disorders. Is this because different mutations in HBB lead to different phenotype disorders, where sickle-cell is one, but sickle-cell itself if just caused by that single gene mutation? I.e. sickle-cell is monogenic, but the responsible gene can mutate in other ways giving rise to other disorders?
Maybe I'm interpreting things in the graph wrong. But, what I'm looking for are gene, disorder pairs like SYNGAP1 where the one gene is linked to one and only disorder. I think what I'm looking for then is not just monogenic disorders, but also "monodisorder" genes.
Is there a way I can search OMIM for these?

Just a note that since different mutations in a single gene can sometimes cause different disorders, the possible number of disorders is not limited to the number of genes. On the other hand, many gene defects will result in non-viability before birth, so will not be seen in practice. There are also disorders caused by chromosomal abnormalities involving duplication/deletion of multiple genes or a chromosome.  Apropos your final question, our knowledge is nowhere near complete, so genes that are today listed as "monodisorder" could easily have additional disorders recognized down the road.

Re: " Is this because different mutations in HBB lead to different phenotype disorders, where sickle-cell is one, but sickle-cell itself if just caused by that single gene mutation? " In general, yes. There are often groups of related but somewhat different disorders for different mutations in the same part of a gene, for example see the beta thalassemias also caused by certain mutations in HBB.


text:
What do ribbon diagrams mean?
What is the higher order meaning of ribbon diagrams like this one? I know the first order meaning is a graphical representation of α-helices and β-sheets, but what else does it mean? Is the protein's function or behavior encoded in there? Do the α-helices helices and β-sheets form a kind of protein alphabet so that a particular arrangement (a "protein word") always has the same function?
An analogy might help: take the word ox. The zeroth order meaning is a circle followed by a cross; the first order meaning is the graphical representation of the sound oks; and the second order meaning is a castrated male bovine.
An English speaker who sees ox reads it as oks and understands it as castrated male bovine. A non-English speaker just sees a circle followed by a cross.
I'm at the non-English speaker level with ribbon diagrams and would like to get to the English speaker level. What does the protein researcher see and understand where I only see spirals and squiggles? Googling hasn't been helpful.

Source

What is the source of the image?

Added source in edit

@zencraft Nice analogy!

Do some research on "protein secondary structure". The figure you include is just trying to show where probably-relevant amino acid mutations are located in the S protein's 3D structure. For example, since an antibody would normally only have physical access to the outside of the S protein, a neutralizing-antibody-evading amino acid mutation buried inside the interior of the S protein is probably changing the overall 3D protein structure rather than just "disguising" a bit of the outside of the S protein by changing a bit of the surface.

I have, and it's not been much help. Another analogy might help: the stuff I've found by googling is like the quadratic formula, I'm looking for higher order understanding, like Galois groups.

There is no higher order meaning.

Ribbon diagrams are a cartoon representation of portions of a polypeptide chain that are engaged in what is termed the secondary structure of proteins — the regular areas of protein structure formed by hydrogen bonding of peptide bonds. These are either individual helices (α-helices) or adjacent flat pasta strips (β-sheets).
An experienced scientist in the field of protein structure can look at the combination of such features and perhaps recognize combinations that recur in proteins of similar function, but there is no — heaven preserve us — code. Ribbon diagrams are just one device for simplifying a complex object.
There are other types of representation that allow appreciation of surface charge, hydrophobicity or individual side chains. An author representing proteins in a paper will choose one (or a combination) that best allows the reader to understand the information he is trying to convey.
Ironically, in the diagram presented in the question they are merely serve as references to indicate the positions in the protein where mutations have occurred.


text:
Darwinism and the idea of being too successful
Is there an example of any animals or insects that have evolved too efficiently and went extinct due to upsetting the homeostasis of their environment? Outside humans.
I was thinking about venomous snakes when a fruit fly landed on me while having a libation in my garden. Then I got to wondering about why, for instance, a fly that eats rotting flesh wouldn't develop a potent neurotoxin on its feet? What a terrifying creature! Then I considered that perhaps a fly could have existed like that but it may have quickly killed all of it's food sources, and, as a result, gone extinct. Are there any known examples like this in animals or insects?

For neurotoxin on the feet, consider that after killing the creature it lands on, the fly would have to wait around for a significant portion of its lifespan for the flesh to rot before it could eat it.

@jamesqf Or it could just be immune to its own toxin. Perhaps more importantly is that its a waste of energy to produce toxin that just gets smeared everywhere you go.

@DKNguyen: I meant that since flies typically live only a matter of weeks, and it takes at least days for flesh to rot, a fly that eats rotten flesh would have to wait around a long time for something it killed to become edible.  It'd be like a lion killing an antelope, but not being able to eat it until a year later.

@jamesqf Flies don't need to eat rotten flesh. They just do because they are scavengers. They eat plant matter too.

Photosynthesis.
early photosynthesizers, which would have been adapted for a reducing atmosphere, drove themselves extinct as they dumped oxygen into the atmosphere as a waste product. They were incredibly successful because they could live off of little more than the three of the most common materials on the planet. Eventually the oxygen built up to the point mostly only oxygen tolerant or later oxygen using organisms survived.
https://pubmed.ncbi.nlm.nih.gov/20731852/

I think this is a good canonical example, though the answer would be improved with a reference.

Going exinct hardly counts for being successful. Let us, take, e.g., Ebola - a virus that is  efficiently transmitted and quickly replocates, but ends up killing most of the hosts. It quickly goes extinct, because there are no hosts lefts for its replication. If Ebola still survives, it is because it infects animals other than humans, for whom it is elss lethal.
A similar example is small pox, which was less lethal than ebola and therefore continued to circulate in human populatiosn for thousands of years... but became extinct once vaccinces were developed.
On the other hand, flu and cold keep circulating in human populatiosn since time immemorial, and it is not likely that they will be going extinct any time soon, becaus ethey have developed a way of co-existing with their hosts.


text:
What are these little brown insects
We have these little insects in our house, they look brown and round to the naked eye, they seem to be somewhat attracted to light since we found a cluster of ~6 on the wall next to a light, otherwise we find them one here and one there.
They are very very small, can barely tell what shape they are without magnification, they look almost like a dot.
Images below are taken with a loupe with 30x and 60x magnification but they are of squashed bugs so not the greatest photos, sorry. Will post pictures of live ones if I find more.
Location: San Jose, California, USA
Full quality images: https://drive.google.com/drive/u/0/folders/15FU-KEzqmXy7s69VfmA1UJoM_o0elWWz

EDIT: added some images of live insect on the wall, no magnification, 30x and 60x to the drive folder.

Great pictures! Can you update your question with your location?

Mist with alcohol for better unsmashed photos.

Woops, this is in San Jose, California, updated question as well.
Also took some pictures of a live insect on the wall with and without magnification and added to the drive folder.

if you can please sit some on graph paper or a ruler to photograph, then their size can be known.

The beetles are about 3mm (1/10 inch) long - so not any wood eating beetle. That's good.
The elytra (wingcase=main body) has parallel lines.
The antennae have the terminal 3 segments enlarged, so not cigarette beetle.
Looks like the drugstore beetle, Stegobium paniceum.
http://en.wikipedia.org/wiki/Drugstore_beetle
If you can easily get a pheromone trap, that will help confirm by catching the male beetles.

Photo from wikipedia.

i looked for pheromone traps for drugstore beetle but can't find them, closest I found was this trap that says cigarette beetle and someone in the comments mentions that it also worked for drugstore beetles, which sounds odd, any thoughts?
https://www.amazon.com/JF-oakes-Pantry-Beetle-Pre-Baited/dp/B006J9IK08

I only found the idea of pheromone traps online - I've never lived in an area that has this beetle as a problem. Anyway, those photos are quite good, see if you can get one of the antennae.

there should be a half decent picture of the antennae in the drive folder, I am hoping to remember to take another one with a ruler next to the beetle, once I have that I will try to repost the drive folder images here as well.
As for the trap, I found one on amazon for $20, will first comb through my kitchen to see if I have an infestation, otherwise they just look lost, a few here and there, some even in the bathroom, not a lot in the kitchen.


text:
What is the density of nacre?
What is the physical density of nacre/mother-of-pearl? I can't find an authoritative figure for it.

According to this article, nacre is composed of aragonite ($\mathrm{CaCO}_3$) and organic matrix (chitin, proteins ...) with a mass ratio $95 \% : 5 \%$. In the supplementary file, they provide densities for each component, namely the density of aragonite $\rho_a=2.95 \; \mathrm{g/cm}^3$ and the density of a generic protein $\rho_p=1.35 \; \mathrm{g/cm}^3$. From this data, we can estimate the density of nacre:
$$\rho_n \approx \frac{1}{\frac{0.95}{\rho_a} + \frac{0.05}{\rho_p}} = 2.78\; \mathrm{g/cm}^3.$$


text:
How it happened that in cactuses the difference between the fruit, the leaf and the stem so much blurred if they were normal plants in the past?
Looking at a cactus may make impression that they evolved separately from other plants, which usually have stem, leaf and fruit.
But the fruit in cactuses has the same structure and surface as the leaf and stem, and grows from leaves. How this could come? Cacti are flowering plants, so should had evolved from normal plants.

cactus have stem leaves and fruit, the needles are modified leaves, the big flat green parts are the stem.

It makes sense if you think of it in terms of water conservation.  Cacti are adapted to environments where there's plentiful sunlight, so growth is limited by water.


text:
Pedigree probability question
The following pedigree shows the inheritance pattern of a trait. From the following, select the possible mode of inheritance and the probability that the daughter in generation III will show the trait.
a) X-linked recessive, probability is 1/2
b) X-linked recessive, probability is 1/4
c) Autosomal recessive, probability is 1/2
d) Autosomal recessive, probability is 1/3

This question is from an examination. The answer key says c) is the answer. I get how c) could be the answer, but I also think a) is a possibility. Please tell me if a) is possible or not.

No, it cannot be X-linked recessive, because in this case, the right-most son would have a trait.


text:
Pedigree probability question - complete penetrance
The inheritance pattern of a common trait that shows complete penetrance is shown below:

What is the kind of inheritance? If III-1 is a carrier, what is the probability of IV-1 (from III-1 and III-2 marriage) showing the trait?
a) Y-linked; 0
b) Y-linked; 1/2
c) Autosomal; 1/8
d) Autosomal; 1/6
It cannot be Y-linked because then II-2 could not have transmitted it to her son. It can only be autosomal (recessive).
Since III-1 is a carrier (heterozygous, Aa):
i)If III-2 is also Aa, the kid will have a 1/4 probability of getting aa
ii)If III-2 is AA, the kid will have zero probability of getting aa
iii)If III-2 is aa(unlikely because it is not colored in the pedigree), the kid will have a 1/2 probability of getting aa.
I am unsure how 1/8 or 1/6 probability is calculated.

You have correctly identified that the trait is autosomal recessive.
Now for the probabilities. We know that:

II-1 is $Aa$ and
II-2 is $Aa$ (because they don't show the trait, but their son does),
III-1 is $Aa$ (because he is a carrier),
III-2 is either $Aa$ or $AA$ (because she doesn't show the trait).

IV-I will show the trait if it is recessive homozygote, $aa$. Because we are not sure about the genotype of III-2, we have two distinct scenarios:

III-1 is $Aa$ and III-2 is $AA$
III-2 is $Aa$ and III-2 is $Aa$

Let's first calculate the probability for each of the scenario. Here, we have to be careful not to fall into the trap by ignoring the conditional probability. The probability of III-2 being $Aa$ is not $1/2$ as we might wrongfully assume from simply drawing a Punnet square of their parents ($Aa \times Aa$). Because we know that III-2 doesn't show the trait, he cannot be $aa$. Therefore, we have to eliminate this possibility from the Punnet square, and we are left with the probabilities $1/3$ for her being $AA$ (scenario 1) and $2/3$ for being $Aa$ (scenario 2).
Scenario 1 (probability 1/3)
III-1 is $Aa$ and III-2 is $AA$.
Their child cannot show the trait.
Scenario 2 (probability 2/3)
III-1 is $Aa$ and III-2 is $Aa$.
Their child will show the trait with the probability $1/4$.
Conclusion
The probability of IV-1 showing the trait is now the product of probabilities for the scenario 2 to be true and the probability for their child to show the trait. Therefore,
$$\text{probability for IV-1 to be } aa = 2/3 \times 1/4 = 1/6.$$
As you see, not being careful about the conditional probability will lead you to the wrong result: $1/2\times1/4 = 1/8$.


text:
Species ID of this giant brain-shaped mushroom? How do its spores escape, there's no "puff" for this puffball!
After several days of rain then a few warm sunny days in northern Taiwan in August, I came across this giant mushroom growing in an open field that's only occasionally mowed.
This mushroom about 18 cm tall and the cap is 20 cm wide. The the very thick base is also 15 cm wide.
The color is beige and white. The cap is wrinkled giving the very rough appearance of a brain.
There were no obvious places for the spores to come out.
There were older ones that had fallen over and had turned dark brown to black.
They feel quite dense.
Questions:

Can this mushroom be identified?
How do its spores escape?

Following up on the helpful comments I've gone back and taken some additional photos of other mushrooms in this large group.
The first was still white, the second had fallen over and turned brown.
I'm thinking that there is something wrong here, there's no evidence of a "puff" or big dramatic dispersal event. They just turn brown, fall over, then turn black.
It seems like a lot of work to go through to make such a huge puff ball, but then not really ever "puff"!

First google result for "brain shaped mushroom taiwan" suggests Calvatia craniiformis, which has variable morphology but many pics look similar to your specimen, e.g. https://www.shutterstock.com/image-photo/skull-puffball-species-giant-white-mushroom-1398120314

@Luigi Thanks! I've posted this for a friend, and since posting they've been searching in Chinese and come across both  C. craniiformis and  C. lilacina found here. Looks like we're getting close. There is actually cooking instructions but I'm not going to be doing that :-) https://i.stack.imgur.com/zPtRs.jpg

https://www.marylandbiodiversity.com/view/4990

Puffballs break open when mature relapsing dust-like spores. When mature they are mostly hollow . When stepped on they make a puff of spore, I guess that is the source of the name.

@blacksmith37 I ran across this image      https://en.wikipedia.org/wiki/File:Purchawka_olbrzymia_i_widelec.jpg of Calvatia gigantea which is said to be a "puff ball" but certainly looks solid in cross-section, and the mushroom in my question feels quite dense and solid, even the ones that turn black, die and fall over intact. I think there's something different going on here. https://commons.wikimedia.org/wiki/File:Old_Giant_puffball_Calvatia_gigantea.jpg I don't have any photos of the dead mushrooms I saw near this one.

@blacksmith37 I'll try to add a photo of a dead, fallen-over mushroom in a day or two when I can get back there. In the mean time here are more cross-sectional images https://www.mushroomdiary.co.uk/2015/09/giant-puffball-calvatia-gigantea/ and also https://doorcountypulse.com/door-to-nature-mushrooms-galore/ There are plenty of slicking and cooking recommendations but I'm not going to be partaking in that.

"A giant puffball is edible if the inside is totally white and even-textured" It sounds like these are not hollow at all.

@uhoh all puffballs are solid when young, hollow when mature.

I found some record size giant puffballs ( like 18" diameter). fried a few slices in butter; tasted like fried butter .  So little or no flavor.

@jmster I've added some photos

@blacksmith37 ditto Do puffballs this big rely on being stepped-on to reproduce?

If this is indeed a giant puffball, the puff comes out of tiny pores in the sporangium (the bit you see), especially as it rolls and breaks apart after maturity. IIRC one of the Attenborough doco's had great footage of this, possibly Private Life of Plants.


text:
How does increased resistance to flow decrease blood pressure?
I have recently encountered this question:

Waldenström's macroglobulinemia is a condition which causes increased blood viscosity due to high protein content in the blood. How would Waldenström's macroglobulinemia influence blood flow and pressure?

(A) Blood flow would be increased, blood pressure would increase
(B) Blood flow would be increased, blood pressure would decrease
(C) Blood flow would decrease, blood pressure would decrease
(D) Blood flow would decrease, blood pressure would increase

My immediate thought was to consider the relationship between viscosity and resistance. If the viscosity of the blood increases, the resistance (to flow) should also increase. According to the equation for vascular resistance:
$$R=\frac{\Delta P}{Q}$$
Resistance is directly proportional to blood pressure. This lead me to believe that the increased resistance should lead to an increase in blood pressure. But even without the use of equations, intuitively, I suspect that the heart should work harder (thus raise blood pressure) if there is resistance to blood flow.
However, the answer key indicates that choice (C) is correct, and that the pressure decreases. How is this possible? The explanation given in the key is:

Viscosity is directly proportional to resistance.
Blood flow is inversely proportional to resistance.
Blood pressure is directly proportional to flow.
If you have increase viscosity, you'd have increased resistance, resulting in less flow, and consequently lower pressure.

There is not enough information in the question to solve it.
The answer key from the original question makes a logical error:

Viscosity is directly proportional to resistance.

This is true. An increase in viscosity increases resistance. Flow and pressure do not matter for this statement to be true. You are correct to assume an increase in resistance.

Blood flow is inversely proportional to resistance.

This is true, but it's missing a qualifying statement: blood flow is inversely proportional to resistance for a given pressure drop. You can only assume blood flow decreases when resistance increases if you also assume pressure stays the same. Maybe this is a reasonable assumption, though I'll note it is not one that you seem expected to make since all the answers involve changes in pressure.

Blood pressure is directly proportional to flow

Again, this is true, but is missing an even more important qualifying statement than the previous one. Blood pressure is directly proportional to flow for a given resistance. Importantly, you know this does not apply because you know resistance changed. If resistance is different between Situation A and Situation B, like in your problem, you cannot assume that flow and pressure change in the same direction from A to B.
What you do know is that
$$R=\frac{\Delta P}{Q}$$
holds. You know that R increases. So you know that the flow decreases if the pressure drop is constant, and you know that the pressure drop must increase if the flow is to remain the same. More generally, you can say "there will be a greater ratio of pressure to flow rate". You cannot solve the problem prompted by the question, which asks you to know the direction of flow and pressure change, without additional information about one or the other. The only way you would get a decrease in both flow and pressure is if the drop in flow is proportionately greater than the drop in pressure differential; nothing in the question suggests this is an assumption you should make.
I would rewrite the solution as:

If you have increase viscosity, you'd have increased resistance, resulting in a greater ratio of pressure to flow rate.

You can only make statements about the ratio with the information given.

Perfect explanation!


text:
Strange yellow flower in shrub Species ID
This is a perennial plant photo taken in Bhubaneswar, Odisha, but I have seen the same plant in Andhra Pradesh as well. It's not exactly woody like a tree, but pretty large shrub [taller than me].

What species is it?

Anything else you can tell us about the plant - the shape/form/habit? is the plant woody or soft? If you are searching include the terms pinnate leaves, flower raceme/racemic

Looks like a type of legume called a senna, though I do not know for certain which species -- see below for a pretty good guess!
Things that stand out about your specimen: most prominent are the erect/many-flowered yellow inflorescences, which are called racemes. You can see narrow green seed pods below your inflorescences as well -- these appear to be winged. Also noteworthy are the pinnately compound leaves with opposite leaflets having emarginate tips and entire margins -- I count 18-22 leaflets on leaves in your second image.
One such species that matches your specimen pretty well is Senna alata, the candelabra bush.

 Credit: Marie Lacouture ; Source: TRAMIL Library

This is a shrub-like plant growing 3-4 m tall, has bright yellow racemes that open bottom to top in the fall, leaves with 18-28 entire leaflets that can sometimes have emarginate tips, and is in-fact named for its winged seedpods (ala = winged).

Although native to the Neotropics, iNaturalist shows many observations of this plant in India.
Other Sources:

Missouri Botanical Garden

N Parks (Singapore)

Weeds of Australia


text:
Does nacre/mother-of-pearl have a greater compressive strength than human bone?
Exactly what it says on the tin: as measured in mPa, does nacre/mother-of-pearl have a greater compressive strength (i.e. it can take getting squeezed more before breaking) than human bone?
I recognize that it's rather brittle and doesn't do well with shear loading, but that's not the question here.

Yes.
According to this article, the compressive strength of nacre is $300{-}500\;\mathrm{MPa}$, whereas the compressive strength of human bones ranges up to around $200\;\mathrm{MPa}$.


text:
Why do the mRNA vaccines for COVID need special lipids?
I've read that the Pfizer mRNA vaccine is delivered to the cell by encapsulating the fragile mRNA into a lipid nanoparticle. However, the lipid has to be PEGylated in order to avoid immunogenecity. Why is that? How does PEGylation reduce immunogenicity in general?

Lipid nano particles are bound by serum proteins, the opsonins which are part of the innate system and are subsequently eliminated from the body by uptake through macrophages.
Binding PEG to the surface of these particles increases their hydrophilicity (and obviously creates a hydrate hull around the particles) and functions as well as a steric barrier. Both measures prevent the opsonins from binding the particles and thus marking them for removal, which extends their half-life (see the references for more details).
References:

PEGylated liposomes: immunological responses
Rationale and Application of PEGylated Lipid-Based System for
Advanced Target Delivery of siRNA


text:
Is the principle of "the least energy" a fundamental principle of evolution? How does it stand with the rule "the one who replicate the most"?
The principle of "least energy" seems to be a fundamental law of the universe (is it?). I probably use the wrong word. I'm just talking about the reason why electrons are filling first the lower level of energy or why chemical reactions happen in a specific direction, or maybe even the "Path of least resistance". Is it a fundamental law/principle or the consequence of another principle (like the weak force)?
This principle also seems obvious in living beings. But how does it fit with evolution? I first thought that between two individuals, evolution will favor the one who needs/spends less energy, but it's not that simple because the "winner" is not the most efficient, but the one who will reproduce the most (replicate its genes). So an individual who is less energy efficient (or needs/spends more energy) but replicates, more will be selected. But the principle seems to apply for two individuals who replicate at the same rate: the one who spends the least energy will be selected by evolution.
So it seems that the principle of "least energy" applies to everything, including the things that replicate (living beings) and their evolution. But it also seems like evolution favors "the one who replicates the most" first and, only after, follows the principle of least energy. But if the principle of least energy is really fundamental, how evolution was able to overtake it and put it in second place?
For example, is it accurate to say, that evolution doesn't necessarily invent the most efficient things/strategy, and fancy stuff because (amongst other reasons) it's stingy, it only follows the path of the least energy?
I feel that I'm handling the problem in the wrong way. Please correct me if that's clear for you.

EDIT: (the question has been close: I can't answer...)
this is a difficult question because it points to (at least) 3 different concept that seems conflicting, but thanks to Joe Daniel and Paul Spencer (from quora) it seems solved.

"living organisms will seek to minimize their energy output in a variety of ways. Those that do so effectively have an edge in survival and reproduction and are thus more likely to continue a population that can evolve." (Joe Daniel) "There is always selection pressure towards the systems that are most energy-efficient" (Paul Spencer)

But in evolution, the one who replicates the most will be selected, even if it's less energy efficient.
"Reproductive success is the filter that creates that evolutionary pressure on all traits, and is more fundamental than anything in terms of evolution itself" (Paul Spencer). "Conservation of energy is a distant second to surviving long enough to get offspring that survive and reproduce" (Joe Daniel)

1+2= If resources are plentiful, an individual can invest more in strategies that are costly, but increase one’s odds of success. If resources are scarce and patchy, the ones who can conserve their energies best may have an edge. (Joe Daniel)

then there is the entropy problem (It wasn't my question, I focus on energy, entropy focus on order, but it answers a part of it) :

The problem: "Biological evolution does cause the system (living organisms)'s entropy to decrease. So, by the second law of thermodynamics, the entropy of the universe (in this case Earth), must have overall increased."(Yolo123)
The solution: Earth is not an isolated system. Life causes entropy of the earth to decrease. This is offset by increased entropy of the sun, which is the primary source of energy for the earth. Overall, the entropy of the universe increases.Canadianer
(What is the difference between entropy and energy? "The more energy present in a system, the more disorder or entropy there will be. [...]  That increase in freedom that corresponds to an increase in disorder is entropy. Entropy is thus a measure of the random activity in a system, whereas enthalpy is a measure of the overall amount of energy in the system." src)
So what about the principle of least energy?
1+2+3= [it] is a theoretical concept explored by several mathematical papers that, on the surface, makes sense, if life was all about the flow of energy. But it’s not. Life is about survival, and that is often not energetically efficient. (Joe Daniel)
(An interesting implication ―which solves the seemingly paradoxical concepts, I was struggling with―: at the individual scale the principle of the least energy pushes the organism to come back to its natural state ―because it's the state that costs the less energy for it). But its natural state does not necessarily follow the 'least energy' for the reason mentioned above.)

It is possible that you thinking of the second law of thermodynamics? It would be best to be clear what that means before considering it in relation to evolution. It does indeed pose problems for cellular organization and life, but not, as far as I can see, specifically for evolution. But at the moment posing a question about something you call a fundamental law of the universe but are not sure what it is does not make a satisfactory question.

@David posing a question about something you call a fundamental law of the universe. If you read carefully, you will see that don't "call" it fundamental law, I say  it seems , then is it? and I ask Is it a fundamental law/principle or the consequence of another principle [...]?. Half of the question is about it... So to summarize, people who don't know the answer, or aren't sure shouldn't ask a question (that sin definitely deserves your downvote).

At present the question qualifies for closure on the following grounds: it lacks clarity, it lacks research, it involves several questions, the first of which belongs in Chemistry, and it has been asked before. There is a fundamental law of chemical thermodynamics and concerns Entropy (not energy) changes. As evolution is not a chemical  process I do not see how it relates to the second law, but see here.

As suggested in these comments, some research (e.g. https://courses.lumenlearning.com/cheminter/chapter/entropy-and-free-energy/ ) should help you better frame your question.


text:
Is lactic acid build up the cause of muscle fatigue or only a symptom?
If your body could magically instantly remove lactic acid as it is produced, would that make you immune to muscle fatigue, or is the lactic acid only a symptom of muscle fatigue and instead exists, at least partially, as a means for your body to measure the stress your muscles are under to keep you from overexerting and damaging yourself? Would your body still have other kinds of immediate and daily maintenance to do to deal with muscle fatigue even if lactic acid wasn't a limiting factor?

Always wondered this.

Accumulation of any biomolecules in any condition can't be a symptom. A symptom is defined as a physical or mental feeling that a person experiences, which can be an indication of disease. Symptoms can be headache, nausea, cough, running nose, change in body temperature and they never show up on the diagnostic tests. So, the accumulation of lactic acid can never be a symptom. However, lactic acid is one of the cause of muscle fatigue indirectly.

As a biochemist I know how lactic acid is normally handled in the body and how it might affect muscle function in circumstances that perhaps did not arise frequently in early man. What I do not know is the medical status of what you refer to as “muscle fatigue”. I doubt very much your ideas about it being a sensor, and wonder whether you are familiar with what is known as the Cori Cycle. However I do not know. Given the lack of response I wonder whether you would be better to migrate your question to SE Medical Sciences, where someone might know about muscle fatigue.

Couple of points:

Removal of lactic acid would only solve the lactic acidosis problem.
Conversion of glucose to lactic acid $\ce{(C6H12O6 \to 2 C3H6O3)}$ only produces two ATP per glucose molecule. You will still miss up to 34 ATP omitting the oxidative phosphorylation step.
Once the free glucose in your cell is exhausted, you will then have to rely on glycogenolysis which is rate-limited by glycogen phosphorylase.
As your glycogen gets depleted, you will have to import glucose (as well as fatty acids and certain amino acids) from the blood for sustained energy production.


text:
Identify bush with white puff and 3 petal flowers, is it poisonous?
Is this one of the poisonous bushes I should worry about? Tiny white puff of flowers along with 3 petal flower.   What is it?

You haven't told us where you live, but it must be somewhere in the Eastern USA, as your plant appears to be the native Hydrangea arborescens.  More info available here and many other places on the internet.

That’s absolutely it!


text:
What's the difference between Kd and IC50?
What's the difference between the equilibrium binding constant ($K_d$) and Inhibitory Concentration 50 $IC_{50}$? They both seem to mark halfway points. Is the only difference that $K_d$ refers to any binding, whereas $IC_{50}$ refers exclusively to inhibition?

For a reversible inhibitor, the relationship between Ki and IC(50) will critically depend on the mechanism of inhibition, and IMO IC(50) values are at best misleading (and at worst meaningless).  Consider a (reversible) competitive inh: the IC50 value determined at a substrate conc equal to Km will be very different to that determined at, say, a substrate conc equal to 10-times Km.  There is a great paper by A. Naqui who explains this very well. For a reversible inh, IC50 only equals Ki if the mechanism of inhibition is non-competitive.

I have expanded on this topic ( a bit too much perhaps) in the section "Reversible Inhibition & IC50. A Brief Comment" of this old answer.  For a much too detailed treatment of reversible inhibition, see this answer

First, let's review the definitions of $K_d$ and $IC_{50}$.
$K_d$
$K_d$ refers to the dissociation rate at equilibrium and is calculated by $\frac{K_{on}}{K_{off}}$. This is the rate at which the peptide is bound to the target protein ($K_{on}$) divided by the rate at which the peptide unbinds or comes off the target protein ($K_{off}$). So when you look at binding curves, it's the 50% bound/unbound point on the curve (the inflection point).

$IC_{50}$
$IC_{50}$ indeed refers specifically to the inhibition of binding or inhibition of a function at which 50% of the peptide is bound and 50% is not bound (or 50% of the function is active and 50% is inactive).
Comparison
In some cases $K_{d}$ and $IC_{50}$ may be very similar values even identical, but in other cases $K_{d}$ and $IC_{50}$ values actually differ.
Pragmatically, $K_{d}$ values generally are considered more "constant" and vary less with changes in concentration of the target protein and peptide. They are more independent from the assay set up and type. In contrast, an $IC_{50}$ value can range depending on the assay set up (not considered constant values). For example, the $IC_{50}$ values in Fluorescence Polarization depend heavily on what "probe" molecule was used and the concentrations of the target protein and peptide.

(+1) [I am not the downvoter]

If Kd has dimensions of concentration (Molarity, say), shouldn't Kd be defined as k-off/k-on? (Kd will be the ratio of a first-order rate constant (k-off) divided by a second-order rate constant (k-on), giving overall dimensions of concentration. For example:  time^(-1)/( conc^(-1) time^(-1)), giving 1/conc^(-1), which is just conc


text:
What is the process by which fluorescent proteins in two photon microscopy are optically stimulated by membrane depolarization?
How does the flow of calcium ions through neurons cause the dyes to activate? The voltage is extremely small, so the dyes have to be extremely close to the neurons, which would disrupt the cells, so is there any additional process?
Fluorescent protein dyes are used, however this article prompted me to ask this question, which might be different:
https://news.berkeley.edu/2020/03/19/high-speed-microscope-captures-fleeting-brain-signals/

What type of dye are you referring to? Can you name one?

There are entire families of fluorescent protein dyes used, so it not a clear cut answer, which is why I am asking this question.

And I'm asking to narrow it down. Are you talking about calcium dyes? Voltage-sensitive dyes? Bath-applied dyes or genetically expressed? SE Q&A should be specific questions with specific answers, not for questions that beg an entire tutorial for an answer.

@C-Consciousness Small correction in your description. Fluorescent protein or fluorescent dye. Not Fluorescent protein dye.

I agree with @BryanKrause here. The question is a bit vague and there are multiple questions in a single question. The title says about membrane depolarization based dyes. Description talks about calcium dyes. Also lack of source validating "dyes close to neurons disrupting the cells". Finally as mentioned above either fluorescent protein or fluorescent dye. Fluorescent protein dye is technically confusing.

They are using a GCaMP, specifically GCaMP6s and GCaMP6f.
This is a genetically encoded sensor. Cells expressing the gene make a protein. The protein is inside the cell, in the cytoplasm. This protein includes a domain that can bind calcium ions. There are lots of other proteins in a cell that bind calcium, too, so this is just one of them.
When bound to calcium, the protein is in a different conformation than when not bound to calcium. When a particular wavelength of light shines on the calcium-bound protein, it emits a photon of a different color. Two-photon imaging takes advantage of a summation trick in that two longer-wavelength (reddish) photons of light combine to provide enough energy to release a single shorter-wavelength photon (greenish).
No voltage or energy from the cell is needed to operate the fluorophore, except the energy used to synthesize the protein originally and the small voltage changes that cause calcium channels to open and allow calcium into the cell. It only fluoresces because of the excitation light used in the microscope.
It would be possible that if you had too much calcium binding protein around it would actually bind enough calcium to interfere with cellular signaling. However, people use these proteins quite a bit and it doesn't seem to affect function all that much. Lab mice who have these proteins expressed throughout their brains all their life aren't any behaviorally different than wild type animals.

Thank you for your answer. This is more of a question related to the fluorophore. As I understand, green fluorescent protein transform ultraviolet-blue light to green light, however I am unclear how the protein do the non-linear photon conversion of infrared light. Could you expand on that? Thank you

@C-Consciousness The wikipedia page I linked on two photon microscopy explains it fairly well. It's not really anything special about biology, it's a chemistry/physics thing about excited states. Two long wavelength photons can have just as much energy as one shorter wavelength photon so it excites the molecule to the same state from which it then emits a photon is the short story.


text:
Resource recommendation: a good book explaining and evaluating the evidence for evolution?
I take a great interest in the intersection between science and religion and evolution is therefore something I often read about. Many of the critics of evolution like to poke "scientific" holes in evolution, perhaps the most common one being that there is simply "not enough" evidence. As someone trained in physics but not biology, I would like a book that is accessible and which summarises the evidence we have accumulated for the evolution of life on Earth. Ideally, I would like a book that remains strictly scientific, without any particular atheistic or religious agenda, and which evaluates each line of evidence rather than simply describing it.
Does anyone have a book recommendation?

I don't think you can do much better than the original: Darwin's "Origin of Species", or failing that, any high school or college biology text.  The "problem" from your point of view is that evolution has for a long time been accepted fact. Modern books would describe evolution rather than argue about it, since at this point trying to convince those who don't accept it is rather like trying to teach a pig to sing: it just wastes your time and annoys the pig :-)

My own favourite, first published in 1958 but with a Canto edition in 1996, is The Theory of Evolution by John Maynard Smith. You can get a 'flavour' of the great man's work here. IMO his book is still one of the very best.

@jamesqf You can obviously do a lot better. Darwin's work was seminal but even ignoring the dated language (his is clearer than most from the period but, nevertheless, language evolves), Darwin's understanding of evolution was simply extremely limited. It's hard to overstate just how much we've learned since then, and, in particular, a modern introduction to evolution is incomplete without discussing evidence from genetics.

Have you tried Berkeley's understanding evolution it is a great supplement for anyone just getting started on the subject. https://evolution.berkeley.edu/evolibrary/home.php

@Konrad Rudolph: But modern texts will (AFAIK, anyway) be written from the point of view that evolution is accepted fact, rather than citing evidence in order to persuade the reader that the theory is correct.

For the love of your own sanity don't read "On the Origin of Species" for a modern reading it is incredibly dry and covers many thing you already know, like that heredity exists, and uses examples you will have no experience with like pigeon breeding, which was very common at the time and nearly non-existent now. Three bloody chapters on pigeon breeding!

I like "The Darwinian Revolution" by Michael Ruse.
It's far more of a history book than a science book. It won't get into the nitty gritty of evidence from molecular biology and modern genetic analyses. What it does do is to chart out how exactly Darwin (and Wallace) came to understand the key features of biological evolution and how the scientific community reacted, both in converting skeptics overnight and hardening a few opponents.
Reading the book, you'll learn how Darwin was a geologist at heart and by training more so than a biologist, and how evolution fits as much into the history of geology as it does in biology. You'll learn how religious thinking was an element to all sorts of competing theories about natural history, with different thinkers taking different approaches and getting stuck in different holes.
You'll also see how Origin was both revolutionary and incremental: really all of the basic concepts were already out there at the time Darwin published, they just hadn't quite been synthesized into a whole.
I think it's a good book to set the table. When considering all the competing theories and evidence, Darwinian evolution comes naturally out of the bodies of evidence collected by others. It explains numerous puzzles that no one else could quite figure out. It emphasizes the places where adherence to faith put up barriers for some scholars in understanding what was otherwise right in front of them. I think it puts more modern opposition to evolution, like "intelligent design", into its own historical context, and after reading it's hard to argue against Dobzhansky: "nothing in biology makes sense except in the light of evolution". It's not that there are particular pieces of evidence for or against evolution, it's that all of biology is the evidence for evolution, and modern biology takes it so much for granted as truth that we hardly notice.
There are reasonable religious arguments to make about the origins of life and the universe itself, but the descent of species from common ancestors and all the phenotypic and molecular connections that link us to all other organisms of life on Earth are unimpeachable.

Ruse wrote a review/afterword of his own book decades after publication, available in PNAS:
Ruse, Michael. "The Darwinian revolution: Rethinking its meaning and significance." Proceedings of the National Academy of Sciences 106.Supplement 1 (2009): 10040-10047.
and another a few years earlier:
Ruse, M. (2005). The Darwinian Revolution, as seen in 1979 and as seen Twenty-Five Years Later in 2004. Journal of the History of Biology, 38(1), 3-17.
if you want to start with something shorter than the original book:
Ruse, M. (1979). The Darwinian Revolution: Science Red in Tooth and Claw.
My copy is of the 1999 second edition, and it looks like there is a newer 2019 version as well.

I can name a few
Your inner fish by Neil Shubin is probably the most inviting for a layman. Just be aware the first chapter is about Shubin personal story and the discovery of Tiktaalik. It is greater starter not because it covers every of lines of evidence but because is covers six or seven specific human centered bits of evidence in great detail. it makes a good starting book if that sounds like your level.
If you want to go into detail, the blind watchmaker by Dawkins is still some of the best in depth explanations of the evidence out there. It also goes into great detail about the part that gives people the most trouble how evolution gives rise to complexity. It also deals with the problems with the lay arguments against evolution. this is the best if you really want to sink your teeth into it and for getting an evaluation of evidence.
If you are just interested in animal evolution Endless Forms Most Beautiful: The New Science of Evo Devo and the Making of the Animal Kingdom by Carrol is you best bet. it is focused on how mutation can change animals by altering regulatory or developmental genes, which is the bulk of evolution in animals. It also delves in many of the modern experiments on such genes which lets you see modern examples of evidence. This is another good one for sinking your teeth into.
As someone trained in physics you may even find a undergraduate population genetics book worth looking into since it will be a more mathematical framework. Although I can't name one off the top of my head.
Evolution: The Triumph of an Idea by Zimmer, is a good middle ground, if you just want a primer on evolution, this is an excellent one. It talks about the modern evolutionary synthesis, the history of evolution and the ideas it is founded on. It is also one of the most accessible books on the subject I have ever seen. If other books are giving you trouble read this first.
DON'T read On the origin of species, is is a dry, dull, long winded book for modern readers, there are three chapters on pigeon breeding for sanity's sake. Darwin was writing an exhaustive book for a different time and many of the chapter are devoted to demonstrating things most modern people already know without question, like that heredity exists.
this question may also be helpful for you. What are the major differences between good study habits for biology vs mathematics?
Also the stated clearly site has some excellent videos on evolution, some of the best out there. I recommend them to my students. It is amazing how much easier a simple animation can make a concept.

I think libraries have been filled on the topic of evolution - it is an immensely broad field of study and can be looked at from a geological time scale (millions of years) to a much smaller scale observable in a scientist's career, since evolution driven by geographical separation can happen over a few generations. Nonetheless I can add my 2 cents worth.
I love the book 'Dinosaurs - A concise natural history' from Fastovsky & Weishampel. Chapter three of this book on dinosaurs features 5 sections that feature many elements that you are after. The sections in this chapter are the following:

Phylogeny
Evolution
Phylogenetic systematics
Cladograms
Logic of science and hypothesis testing

As you can see the chapter builds up to the point where the theory of evolution is explained. It's still a theory, yet the evidence is so overwhelming it's principles are taken as a fact, yet the exact mechanisms behind it and the construction of the 'tree of life' is anything but a fact, but rather based on science, logics and hypothesis testing. The chapter has been really rewarding for me to read and I bet it can help you a lot too. Along the way you'll learn a lot of cool things about dinosaurs too (birds are technically dinosaurs, but flying dinosaurs were not the direct predecessors of birds and so on).
Reference
- Fastovsky & Weishampel. Dinosaurs - a concise natural history. Cambridge University Press. 2010

Recommendation:
A Short History of Humanity by Johannes Krause and Thomas Trappe
Not pure evolution however Johannes Krause is the Director of the Max
Planck Institute of Evolutionary Anthropology and this is a recent book (2021) in a very rapidly changing field of Archaeogenetics.  Covers the extinct species of Neanderthal and modern DNA showing traces of Neanderthal interbreeding with modern humans.

I've read a few on the topic, and what I would recommend would depend on your focus.
For a generally fun, smart, and accessible book on evolution, my favorite is Trilobite: Eyewitness to Evolution, by Richard Fortey.  It's an odd approach to talking about general evolution, but trilobites were around for so long, and they left such perfect fossils, that they teach us a lot about the whole process.  Did you know that when geologists don't know how old a layer of rock is, they often look for which species of trilobite are stuck in it?  Or that they had eyes made of crystal, and were so numerous that the oceans were black with them.
This book broke down evolution for me when I was looking for exactly the clarity that you describe in your question, and allowed me to converse with people in a much more intelligent way.
You might also consider as secondary reading Desmond Morris' The Naked Ape, and others by him. It's more about evolutionary psychology, and is interesting is showing, as he put it, that "Man is not a fallen angel, but a risen ape."  It's really interesting to see how many of our morals, thoughts, actions, cultures, and even gestures come built in from our ape ancestors.  But, psychology is also always a more slippery field, so you may not like some of the assumptions.

If you are looking for something that gives a good overview of all evolutionary processes, I recommend Evolution Unraveled from Randall Harris. The book goes into the best explanation on how evolution could work as observed by science.
For example, as @CaptainSkyfish mentioned with the Trilobites, the book expands on some great questions like how did something with such a complex eye evolve so early?
A great book if you are into coming to heads with what science actually describes around evolution.

Being a physicist myself I would recommend the Gillespie's little book as a crash course on the basic genetic concepts. For the mathy stuff it is worthwhile googling "population genetics" - there are a few excellent sets of lecture notes walking around - such as several version of the Mathematical population genetics by Ewens. Theses might seem not exactly what the question asks about, but to a physicist this would give a rather good idea why genetic models being a lot more serious than most creationists with no math background can imagine.


text:
Number of homozygous recessive offspring
A question from the KVPY-SX examination, organised by the Indian Institute of Science (IISc) in Bengaluru, India, held on 3rd November, 2019.

A plant heterozygous for height and flower colour (TtRr) are selfed
and 1600 of the resulting seeds are planted. If the distance between
the loci controlling height and flower colour is 1 centimorgan, then
how many offspring are expected to be short with white flower (ttrr)?
(A) 1 (B) 10 (C) 100 (D) 400

The answer given by the organising committee, of the KVPY, is (A).
My problem with this answer is that if the alleles are in a cis arrangement*, and the distance between them is 1 cM, then the recombination frequency will be 1% (a good enough approximation in this case, in my opinion).
So, on selfing of TtRr, we'll get;
TR - 49.5%
Tr - 0.5%
tR - 0.5%
tr - 49.5%
So, the probability of getting a homozygous recessive genotype, which we obtain from tr × tr, is (0.495)^2 = 0.245, and hence, we get (0.245)(1600) = 392 offspring approximately, the answer closest to which, is (D).
*By "cis arrangement" of alleles, I'm assuming that the 'T' & 'R' alleles are present on one chromosome, and 't' and 'r' alleles are present on another. (An NCBI webpage explaining this terminology)
Where am I going wrong?
What's the right solution to this problem?

Why do you assume the alleles are in a "cis arrangement"? We typically talk about alleles being linked, but you need to specify which alleles are linked (e.g.s 'T is linked to R' or 'T is linked to r'). Is the former what you mean by "cis arrangement"? Also, have you included the full text of the question? It is quite possible that this is (yet another) example of a poorly worded question ... ——— Also note that this is a "homework" question (see [help] for details about what that means. You've shown the required effort, but you must also include the homework tag on these questions.

@tyersome Thanks for the suggestion; I have included the homework tag now. What I mean by "cis arrangement" is that the 'T' and 'R' alleles are present on one chromosome, and 't' and 'r' on the other. Yes, I've included the full text of the question.

You're welcome. Can you please also edit in answers to the questions I've asked? With the information you've given I'm not sure that any of those answers is correct ...

@tyersome you can consider posting an answer justifying why you are not sure of any of those answers being correct, and  the appropriate approach towards this, given the right (amount of) information.

I don't see anything in the problem statement that allows assuming cis or trans arrangement.

@mgkrebbs What arrangement other than these two can we assume? All I'm saying is that, if the alleles were in a cis arrangement, their answer doesn't hold true. This in itself is enough to invalidate it.

@ShishirMaharana, "enough to invalidate it." -- invalidate the answer? No, the trans calculation results in an expected number between 0 and 1, so the "1" answer would be the best answer in that case.  Invalidate the question? Well, as shown, the question presentation doesn't have enough information to select an answer, so that's crappy.

I wonder if the creators wrongly modified a simpler question and botched the modification? If height and color are unlinked, the number of ttrr offspring should be 100/1600. Perhaps they wrongly decided "we'll make the loci 1cM apart, so the new result will just be the original result x 1%, or 1."

Taking your assumption of a cis arrangement of alleles to be true, here is how I would solve the problem.
A diploid plant heterozygous for height and flower color is selfed.
$TR / tr \times TR / tr$
A map distance of 1 cM means that 1% of meioses will result in recombinant gametes, so we can calculate the expected distribution of gamete genotypes assuming equal probability of the strictly dominant or strictly recessive gametes in the absence of recombination.
$p(TR) = 0.5(1 - 0.01) = 0.495$
$p(tr) = 0.5(1 - 0.01) = 0.495$
$p(Tr) = 0.5(0.01) = 0.005$
$p(tR) = 0.5(0.01) = 0.005$
The expected proportion of homozygous recessive $tr/tr$ offspring is given by the product of the gamete probabilities.
$p(tr) \times p(tr) = 0.495^2 \approx 0.245$
$0.245 \times 1600 = 392\space\texttt{offspring}$
So it seems that your answer is correct and the given answer is wrong.

Since the loci of interest are very close together, a quick way to think about this is to treat the height and flower color loci as a single locus with dominant and recessive alleles $A$ and $a$ (i.e. independent assortment never occurs). This allows us to model the problem as a monohybrid cross of heterozygous plants.
$Aa \times Aa$
The phenotypic ratio of dominant to recessive progeny from a monohybrid cross is 3:1, so you can expect 25% of offspring to be recessive.
$0.25 \times 1600 = 400\space\texttt{offspring}$


text:
How to create long term stock for Bacillus subtilis?
I am trying to create a long-term stock for Bacillus subtilis (Bacterial glycerol stocks). I have looked online for guides and step-by-step tutorials and I found that they don't say where the sample originally comes from.
In my case, I am using Bacillus subtilis subsp. subtilis (ATCC® 23857™) pure from the supplier bottle.
What is the proper procedure to create a long-term stock for Bacillus subtilis using this product?

I worked with B. subtilis WB800 and just used 50% glycerol / 50% LB. I imagine the same would work fine with wild-type.

Do you add the bacteria in the LB before mixing with the glycerol?

No I would prepare the glycerol/LB mixture and autoclave it then create the stocks from log-phase (approximately) plate cultures.

@canadianer Wouldn't you want to use liquid cultures as the source so you can count the number of cells? Or does B. subtilis not grow in suspension? I come from the world of eukaryotic (mostly mammalian) cell culture, so I honestly don't know...

@MattDMo They certainly do grow in liquid culture, but I’ve never used one to make glycerol stocks. Perhaps some do it more carefully than I do but, in my experience, this method was sufficient for my application (protein expression). I imagine mammalian cells are a lot more finicky.

@canadianer Can you turn your comments into an answer so that I can vote it up?

@jakebeal Sure thing, although I’m not sure how helpful it was.

I worked with Bacillus subtilis WB800 and just used 50% glycerol / 50% LB. I imagine the same would work fine with wild-type. I would prepare the glycerol/LB mixture and autoclave it then create the stocks from log-phase (approximately) plate cultures. This method was sufficient for my application (protein expression).


text:
What determines the nucleotides incorporated into RNA by polynucleotide phosphorylase?
Polynucleotide phosphorylase, in addition to its role as an exonuclease, is also involved in the post-transcriptional addition of nucleotides to RNA in a template-independent manner:

“Polynucleotide phosphorylase not only synthesizes long, highly heteropolymeric tails in vivo, but also accounts for all of the
observed residual polyadenylylation in poly(A) polymerase”

My question is:
What determines which nucleotides are incorporated as the process is template-independent?
I have not been able to find any information about this. Is it purely chance?

There would seem to be two possibilities:

The enzyme has differential specificity for different substrate NDPs.

or

The deciding factor is the relative concentrations of the different NDPs in the cell.

Although the structure of the enzyme has been determined there do not appear to be any studies that would distinguish between these possibilities. This is perhaps because most recent attention has focussed on the exonuclease activity of the enzyme.


text:
ID microbe found in moss sample (USA)
I found this microbe after putting a wet moss sample under my microscope. It latched on to a piece of moss and scanned the area around it for prey, and when it didn't find any, it slowly swam away. It's fairly large for a microbe, and it's rectangular with two big green spots. I'm not sure if the spots have any significance (I thought for a second it might be mitosis, but I'm not sure).
Some pictures at 250x and 400x:

Any information would be greatly appreciated!

Are you sure it wasn't just moving in water currents on the slide?

I am not 100% sure on this, but it looks very like a diatom. These are a range of very diverse unicellular algae found world-wide in soil and water environments (salt and fresh). There are a huge number of species (also genera, families etc.).
The reasons I think that this is a diatom are that it has what appears to be a thick transparent wall (photos 2 and 3) and has a "cut in half" shape - where the word diatom comes from (dia divided, tomos I cut). Diatoms are usually between 20 and 200 micrometres long, so 250-400x observation fits fairly well.
I think what you have here is a pennate diatom (see images under "classification"). Some pennate diatoms are motile
There's an image of one that resembles yours here (see second image)


text:
What is the current accepted taxonomy of the Citrus genus, and how do common cultivated fruits fit into it?
I want to learn about the taxonomy of Citrus, and how cultivated fruits fit into it. I know that the history of cultivated citrus fruits is full of hybridisation and that the taxonomic classifications have changed extensively over time, but I'm looking for the most up-to-date and currently accepted classifications.
Kew (Plants of the World Online) has information about which species names are currently accepted and which are synonyms. But there is no information about ancestry or about how cultivated plants fit into those species. Horticulture/agriculture widely use common names, and botany widely uses scientific names, but I'm looking for information that bridges these two areas.
I want to be able to write a full binomial and cultivar (if applicable) name for common citrus fruits. For example:

"Meyer lemon". Is it Citrus × meyeri? Citrus × limon 'Meyer'? Citrus × limon var. meyeri?
"Satsuma". Is it Citrus unshiu? Citrus deliciosa? Citrus × deliciosa? Citrus aurantium var. unshiu? Citrus reticulata?
"Seville orange". Is it Citrus × aurantium? Citrus aurantium var. aurantium? Citrus aurantium 'Seville'?

Researching individual species or cultivars turns up some answers, but they often don't match each other because there are so many different sources. I want a cohesive summary of the current classification for the entire genus. Is there a book or article that can help me?

I don't have any sources for you, but I can tell you you're very likely going to find disagreement about classification,  taxonomy, and naming. Certainly some judgement calls will need to be made on your part, so make sure you're citing your sources and jotting down brief explanations why you choose one over the other. Ideally, you'd find 1 (maybe 2) sources to pull from to mitigate this problem, but if that's the case, then you'd probably not be tackling this project to begin with. Anyways, I'll keep my eyes open for helpful sources. Good luck!


text:
Should a red blood cell in hypertonic solution be drawn with a nucleus or not?
I'm a student at 6th stage in High school from Iraq. I need to draw a red blood cell when it is put in a hypertonic solution; "high concentration of solute and low concentration of solvent".
Do I draw it with a nucleus or not? I think there is no nucleus because the cell has a nucleus only when it is in the bone marrow, but it loses its nucleus later. So when it is put in a hypertonic solution that means it doesn't have nucleus. But my teacher said that it should have a nucleus.

Hello @handsomecat !! Welcome to Biology SE. Yes! you're right. A mature RBC doesn't have a nucleus. However, for this particular activity, the source of the blood sample has to been taken into consideration. If the sample was taken from a vein, the RBC should be enucleated. If the sample was taken from Bone marrow (generally Hip bone) then RBCs should be nucleated.

What species?  Human RBC don't have nuclei but some species' (for instance, birds) RBCs do.  May be the source of confusion.

The nucleus being absent is secondary to what happens with the cell when you put it in a hypertonic solution.  Perhaps you are studying osmosis?

Yes, it's the osmosis..thank you all.


text:
What causes metallic tastes when you receive electric shocks
Whenever I receive small electric charges (most often by, e.g. touching the jack of a plugged in charging cable, or the casing of a charging Apple device), I experience a very distinctive taste in my mouth.
I'm relatively certain that the taste is what is termed "a metallic taste", and some brief googling suggests that this is a common experience when receiving an electric shock.
What is going on, biochemically, in this experience?

FWIW, it's the same sensory experience that I associate with a sudden physical danger shock, such as times when I've been standing on a branch that then broke (I was holding another branch, so was fine, but had a huge fear/adrenaline rush, plus that same metallic taste).
Are they linked experiences at all?

I think adding more support for your metallic taste sensation would add a lot of body to the question. As of now you seem to be asking the community to explain an anecdotal personal observation. Sensation and perception are subjective phenomena and personal anecdotes are not a very solid basis for a scientific question. I can list a quite a few sensations I have repeatedly perceived under various circumstances, yet I hardly find them to be solid enough to raise a question about.


text:
Ingredients in Pfizer vaccine
The ingredients in the Pfizer vaccine have been listed in a number of websites, including government healthcare ones. This site claims that the list includes ALL of the ingredients of the vaccine. Considering that things like sodium chloride have been included on the list, that would seem to suggest that it is indeed comprehensive. The ingredients list is the following:

mRNA
Lipids (including ((4-hydroxybutyl)azanediyl)bis(hexane-6,1-diyl)bis(2-hexyldecanoate), 2 [(polyethylene glycol)-2000]-N,N-ditetradecylacetamide, 1,2-Distearoyl-sn-glycero-3- phosphocholine, and cholesterol)
Potassium chloride
Monobasic potassium phosphate
Sodium chloride
Dibasic sodium phosphate dehydrate
Sucrose

I cannot help but feel suspicious about whether this truly is the full list. For a synthetic medicine, I would expect a much longer list with stabalisers, peservatives, adjuvants etc.
So my questions are: Is it reasonable to assume that this truly is the entire contents of the vaccine, sans water? And, where are the adjuvants? There is no aluminium here.
EDIT: I feel like I have been downvoted because my post gives the impression that I am an anti vaxer. I emphasise I am not. I just really wish to know what is inside these vaccines and how they work, and why the things that I expect to be inside are not. Because vaccine are such a sensitive topic now, it makes sense for anyone posting iformation about them to be very careful about what they include. This extends to publishing incomplete ingredients lists, which are not explicitly said to be complete (so there is no legal repurcusiion) although the wording makes it seem like such. I have no issue with some aluminium being present in vaccines. People consume aluminium all the time when drinking soda pops from cans. But, I do want to be fully aware of everything that is inside of them and how they work, and I think it is reasonable to when you are putting something inside of yourself. As someone with a family history of severe autoimmune conditions, I am also concerned about the presence of other adjuvants and I think justifiably so. Again, this is just to say that I am not an anti-vaxxer at all, but I am all for knowing what is inside a vaccine and how they work. And unfortuantely the scare around vaccines means that it can be hard to get complete information about them, because people with little scientific background may be scared by what they see in a complete list as they don't understand it. Thus it is discretely censored, and I understand why.

An adjuvant increases the immune response to some antigen. No one wants any immune response to any component of these vaccines; including an adjuvant would be silly. I don't see how this question can be answered with any biology, though - you're basically just expressing skepticism about a manufacturer's ingredient list. They'd get in quite a bit of trouble with regulators if it's incomplete.

@BryanKrause I assume you downvoted, which I think is unjustified. I am not skeptical about the manufacturer's ingredients list. I have not seen this published by Pfizer themselves. Rather, by other websites. The reputable ones have not claimed that this is the entire list and could merely be listing the things that they believe are important and/or would not scare the public. Only a non-reputable one has claimed that this is the entire list.

Secondly, I think it is perfectly valid to question why there are not more preservatives/stabilisers (the lipids are some stabilisers, and I think the sucrose acts as a preservative or stabiliser here too). AND, why there are no adjuvants I recognise. As is mentioned in the website below, "many vaccines contain aluminium salts... they act as adjuvants" https://vk.ovg.ox.ac.uk/vk/vaccine-ingredients#Added%20ingredients

The point is that one wants to amplify the immune response such that there is one towards a small amount of viral material. Now I do not know whether the white blood cells directly detect the viral mrna and create some protein/rna 'antibody' against this, or whether the mrna gets into cells and is expressed as an antigen which the white blood cells make antibodies for. I presume it is the latter, since the mrna encodes the viral protein spike specifically. In any case, since little material is injected, amplifying the immune response would be beneficial.

@Meep, I've answered your question. Though it seems like a better question to ask (and the crux of your inquiries) is "Why do mRNA vaccines not require adjuvants, but other vaccine types (like inactivated influenza vaccines) often do?"

@acvill Thank you for the suggestion. It seems like this may be a better way to go, as I think I am getting downvoted as people think I am just another anti vaxer looking for reasons to scaremong people. Not the case at all!

@Meep You do not want an immune response to the lipids or mRNA or any ingredient in the injection. You ideally want the mRNA to enter cells without the immune system knowing anything about it, you only want an immune response to the spike protein that can be used to identify active virus particles. You may not be an anti-vax person but you are really carrying a lot of their baggage.

@BryanKrause Ok thank you for telling me that the immune response is meant to be towards the expressed antigens and not the mrna (I would never have thought of the lipids triggering immune response). This may be why the mrna vaccines do not require adjuvants, just a longer amount of time to create enough antigens from the mrna templates to have a sufficiently large immune response.

@BryanKrause Also, yes it may be the case that I carry anti-vax baggage. I come from a family of scientist turned anti-vaxers. However I am trying to educate myself. My questions are ones of genuinely trying to understand vaccines, and formulate my own opinion as to whether they may be harmful in certain circumstances or no (obviously mass use of vaccines rules out severe harmful effects in the general population). Being attacked like this makes me scared to ask whether it is harmful to the cells which the mrna enters and which express the antigens. From my knowledge of the immune response

these would be detroyed by the white blood cells. I think it is a valid question to ask. I know it is no issue to lose a few cells, but if the mrna gets into many cells, or the immune response goes awry because some cells are expressing thsi antigen, then it can be harmful.

I don't see the point of posting a likely disreputable site and essentially asking "is this right", when one can just access the official materials descriptions from the FDA, the manufacturer, and so forth.  You also baselessly claim "Thus it is discretely censored, and I understand why"  Those are the reasons for my downvote.

@Meep Being destroyed by the immune system is the fate of every infected cell that is recognized as such cell. So you lose a few cells because of the vaccination, however these are easily replaced. The same process (but on a ways bigger scale) happens throughout your whole body (and not only around the injection site) when you are infected with SARS-CoV-2.

@Meep Generally, there is no need for an immune response against mRNA. Free ssRNA is very unstable in cells because of RNAi. There are plenty RNA-dependent RNA polymerases floating in cells that detect (both endogeneous and exogeneous) free ssRNAs, such as mRNAs. These synthesise the complement, and the dsRNA is then rapidly degraded because dsRNA is never functional in human cells. In fact, this system probably evolved as a defense mechanism against infections from ss/dsRNA viruses.

@Meep And, if anything, the production and publication process around vaccines effective (or non-effective) against SARS-CoV-2 shows that there is no discrete, indiscrete or whatsoever censorship. The fact that potential side effects are widely publicly discussed that even occur less often in the vaccinated population than in the non-vaccinated population suggests that there could not be more transparency. In fact, I consider the development and publication of these vaccines to be examplary for a very transparent process (at least on the side of scientists).

@Meep For your interest in scientific evidence on the subject of vaccinations, I suggest you have a look at this excellent blog: https://www.skepticalraptor.com

The source for the linked  article is this FDA factsheet, which gives the following description for the Pfizer-BioNTech COVID-19 Vaccine (emphasis mine):

The Pfizer-BioNTech COVID-19 Vaccine is supplied as a frozen suspension in multiple dose vials; each vial must be diluted with 1.8 mL of sterile 0.9% Sodium Chloride Injection, USP prior to use to form the vaccine. Each dose of the Pfizer-BioNTech COVID-19 Vaccine contains 30 mcg of a nucleoside-modified messenger RNA (modRNA) encoding the viral spike (S) glycoprotein of SARS-CoV-2.
Each dose of the Pfizer-BioNTech COVID-19 Vaccine also includes the following ingredients: lipids (0.43 mg (4-hydroxybutyl)azanediyl)bis(hexane-6,1-diyl)bis(2-hexyldecanoate), 0.05 mg 2[(polyethylene glycol)-2000]-N,N-ditetradecylacetamide, 0.09 mg 1,2-distearoyl-sn-glycero-3-phosphocholine, and 0.2 mg cholesterol), 0.01 mg potassium chloride, 0.01 mg monobasic potassium phosphate, 0.36 mg sodium chloride, 0.07 mg dibasic sodium phosphate dihydrate, and 6 mg sucrose. The diluent (0.9% Sodium Chloride Injection, USP) contributes an additional 2.16 mg sodium chloride per dose.
The Pfizer-BioNTech COVID-19 Vaccine does not contain preservative. The vial stoppers are not made with natural rubber latex.

The factsheet does not mention adjuvants.

Thanks very much for this. The wording is quite waffly though. They do not claim to list all of the ingredients, just other stuff that the vaccine contains. Considering the concern over aluminium in vaccines, they might have reason not to mention it, but have themselves covered by not claiming it isn't there.

You expect a statement like "This is a comprehensive list of ingredients."? No one does that. The wording is succinct, not waffly. The FDA has no reason to exclude ingredients from their fact sheets (e.g. note the mercury content of Fluzone is clearly stated).

I am not. At all. But I do expect more explicit wording. Thank you in any case.

I've edited my comment, sorry for the presumption of anti-vax sentiment. We get a lot of that here. Additionally, the hep A vaccine factsheet clearly states its aluminum content.

Note that the temperature handling requirements act as a preservative, as likely does the sucrose content of the vaccine (dilution occurs only just before administration).  The reason for the lack of adjuvants is covered in the comments under the question.