text:
Why do spiders hang up dead bugs?
I used to think the reason we see a lot of dead bugs wrapped and hanging on spider webs was that they get caught by spiders and after the spiders are done with the bugs they leave them there. But I have had a few spiders trapped in a plastic bottle and that assumption no longer seems correct. I haven't found any articles online that sufficiently address this.
I notice that the spiders in the bottle actually actively work to make web to hang up dead bodies, even if the bodies are much larger than them in size and are not their prey. For instance, there was a pretty sizeable spider in the bottle when I trapped a few newcomers. The large spider had been dead in there for weeks. I was just too lazy to get its body out. The newcomer spiders were much smaller but they soon worked to wrap up the dead body of the large spider and hoist it so it didn't stay at the bottom. The same also happened with the body of a moth several times their size. House spiders in general don't attack other bugs that outsize them or even their own size because they only attack bugs they can pin down. So the moth died of natural causes in the bottle-starvation I assume, but its body was also hoisted. Why do they do that?

I think that spiders like organisation. It can also be that they hang up bodies that they don't feed on so they attract predators for those bodies that they can actually feed on.

Spiders can eat things much larger than themselves, one of the advantages of a liquid diet. even after a spider has fed on something a husk is left behind.

It seems they do that to save food for later, at least that is what this source suggests. Could also be a sanitary thing, if the bug is dead for some time. Please be nicer to the invertebrates around you!


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How do colorblind people see the back of their eyelids?
When people close their eyes, they still see and they see the back of the eyelids, in colorblind people, they see the back of their eyelids differently, how do colorblind people see the back of their eyelids?

Welcome to Biology StackExchange! How do you see the back of your eyelids, and what makes you think that anything would be significantly different for color-blind people?

The eyelids are translucent, if we face the light, we a reddish color and if we don't face the light, we see a quite not black color, with colorblind people, they see the back of the eyelids differently.

So if the lit eyelids are "objectively" slightly reddish, then color-blind people perceive them the same way as they perceive other slightly reddish objects–given the type of colorblindness they have. Why would seeing the eyelids be any different than seeing other objects?

Color blindness varies as much as skin color, some have the genes from both parents, so the results vary. Generally, the difference in color balance can make a red seem more attenuated or brown compared to other colors in a scene, or a blue or green depending on the type of genes they have. It's a comparison of many individual experiences and interpretations of vision, including a psychological interpretative balance.

source: Stack Exchange

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

sort: votes


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Where can I find a video of human cells reacting to cold water vs warm?
I have the following lists:
Hot Water Effects on Human Cells:
When human cells are exposed to hot water:

   Denaturation of Proteins:
   The proteins within cells denature,
   losing their normal three-dimensional structure.

   Cell Membrane Damage:
   The cell membrane can be damaged by heat.
   The lipids in the membrane become more fluid.

   Increased Metabolic Activity:
   Increase the metabolic activity of cells.
   Can lead to cellular stress and even cell death.

vs.
Cold Water Effects on Human Cells:

    Reduced Metabolic Activity:
    Slow down the metabolic activity of cells.
    This is one reason why hypothermia can be life-threatening.

    Cell Membrane Changes:
    Cell membrane to become less fluid,
    potentially affecting its permeability and functionality.

    Ice Formation:
    Extreme cold can cause ice crystals to form
    within and around the cells.

But I really want to see these up close under a microscope.
The temperatures don't have to be extreme. Just like mildly cold ice water vs. a warm shower. When the cold water hits a cell do you see it like bounce off? When the warm water hits a cell do you see it enter the cell?

You can't see these changes easily under a microscope.  It is a challenge to add heat or cold to cells on a microscope in a manner that you might see, unless you have the right equipment.
You might see protein denaturation - it's like an egg cooking, but because the cells are so small, it happens very fast and you aren't left with a residue, the cells detach before this happens or just disintegrate. For this to happen you need to be heating above about 55 - 65 C (131 - 149 F) for observable denaturation - this is about the same temp as egg white denatures (IIRC 61 C/141 F), but some proteins denature much earlier. Part of the reason it is so difficult to see is the range of temperatures it happens over, so the process is spread out.
Membrane fluidity is not something you will see at all unless you are making specific measurements of it - the cells just don't move enough for you to notice the difference between warm and cold. Water doesn't "bounce off" or enter cells because of membrane fluidity - it enters through protein channels called aquaporins - you can't see these either, far far far too small for light microscopy.
Adding water to the cells (note - cells don't like water in general, mammalian cells need isoosmotic conditions with some salt to keep them happy or they undergo osmotic stress and pop, which you might see, but it isn't dramatic at all). As they are already in a liquid - Have you ever added hot water to cold - how much difference do you see? How would you know when the cold/hot water reached the cells?

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


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How can saliva neutralise acids produced by bacterial cells in our mouth if it is itself acidic in nature?
My school textbook makes the following claim:

This means that saliva must be basic. However, I learnt that the pH value of saliva is about 6.8, which would surely make it acidic. How can the above point be correct then?

even if an acid is 6.0, it's reaction with other acids depends on the quantity, so a lot of the mild acid can react with an amount of the stronger acid.

Saliva is neutral, not acidic (6.8 is very barely acidic), and is a means to carry the acid away physically, and is also much less acidic than acid produced by bacteria, so is still effective in neutralizing.

Also substances with higher pH can act as bases against substances with lower pH. If I remember right, alcohol acts as base when warmed with carboxylic acid in esterification reaction. Enzymes are very sensitive to change in pH so that probably reduces bacterial activity.
https://youtu.be/UGs0hrIkjss

Saliva also has anti microbial properties and might kill bacteria or hinder their growth. https://en.wikipedia.org/wiki/Wound_licking


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What torque can the human wrist take?
Say you are holding a rod in one hand with your tumb on one side and the rest of your fingers on the other. What amount of torque could be exerted onto the rod (with the axis of rotation being around your forearm) before the average person's wrist starts to hurt?
I am asking this because from my calculations it seems like mine can withstand 115Nm which seems unreasonably high. On top of that all studies I can find only measure with the axis of rotation in line with the rod itself.
I hope you guys can help me out, thanks for the effort beforehand.

"...before the average person's wrist starts to hurt?" There is no "average" person (imo); there are males and females, there are various ranges of mobility due to hormones or genetics, there is well developed and poorly developed musculature and connective tissue and everything in between, etc. There are averages in a group of similar individuals, e.g. '30 y.o. white males in good health'. Averages don't really mean that much when it comes to one individual's characteristics. (I know it sounds nit-picky, but it's true.)

@anongoodnurse, that seems fair, but what kind of range can I expect it to be in? Because the 115Nm that I got don't seem plausible.

TBH, I don't know. Speaking medically (where most of my expertise lies), it doesn't matter. I can imagine how stupid that sounds, but it's true. I do think an orthopedist or a physiatrist can answer that with some authority, but I don't think we have one on this site. Sorry to be of so little service.

The technical terms you should include in literature search are "pronation" and "supination". This article seems to measure exactly this. Also, please let us know how you derived your estimate of 115 Nm. You might have made a (trivial) mistake somewhere.

@Domen - Those are extremes before damage occurs; the OP just wants to know at which point it will start to hurt.


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What is the magnification of this microscope image?
I mistakenly forgot to write down the magnification of this lobster egg image.
I do know that each division on the graticule is 20 microns, as I calibrated it using another duplicate graticule: the actual sizes of the graticules are 5mm long with 100 divisions, and I lined it up so that the installed graticule in the eyepiece spanned only 40 of the 100 divisions of the graticule on the base plate. I believe this meant the installed eyepiece graticules divisions represented 20 microns.
I can see that the eye spot on the egg is 29 divisions, so it is 580 microns long.
Is it possible to determine the magnification with this information?

If you know the size (check the literature to see if your calculated size is close to expected for the egg), you generally don't need the magnification - you simply put a scale bar on the image representing sensible units.

Hi @bob1, thanks for your response but i need to report the magnification in this case. Would you know how?

It's impossible to say from an image on the internet - images scale with different display formats/qualities. If you have the original image and can display it at the 1:1 scale, then you can do an approximation. The internets tell me that a lobster egg is ~1/16" or 1.58 mm in diameter, so you could work it out that way.

How about taking another image of another lobster egg (or even the same egg)?  Try to find a setting/magnification where the same zoom of the resultant image with the same image resolution will give you a similar visual representation.


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Where do the bones of dead animals go?
I've spent quite a bit of time in the wild, but I've seen little to no bones lying on the ground.
Large bones such as skulls, spines, horns, hooves are not eaten by any other animals, and even microorganisms. thanks to which they can persist for decades on the ground surface. Especially in hot and dry climates, steppe and desert regions, as well as in the arctic.
Therefore, it should be expected that a large number of bones will be found on the surface of the soil, also underground in the topsoil.
But nothing like this actually happens.
Where do the bones of dead animals go?

Can't speak for all bones everywhere, but bones get eaten quite often. When I lived in the woods, I could see a carcass disappear bit by bit in a matter of days - far too quickly for disintegration - leaving only the hardest bones bare on the ground.

Same here, weeks later the remains would be visible only as glints of ivory through the overgrowth of ivy. After an autumn's leaf-fall, nothing the next year. Still there if you dig. I found a pig's lower jawbone, teeth and all thrown out of a rabit's burrow - decades old, not seen until the rabit found it in the way of its home-building efforts.

Does this answer your question? Why don't we find animal corpses and skeletons all throughout the woods?

Even a superficial Google search will tell you by the title of the hits you get that bones are eaten, e.g. my top hit.
Osteophagy simply means bone eating. I'm not sure why it applies to herbivores in particular; maybe because it seems to be strange behavior in an herbivore, whereas it's expected in a carnivore.
Phosphate is crucial to life, but isn't abundant in 'edible nature' (plants, etc.). It is abundant in bone, however, and because it is crucial to growth and energy production, animals eat bones however they can. Some animals, e.g. those without teeth, will swallow small bones whole. Carnivores and capable omnivores will crush susceptible bones by chewing on them; herbivores will just grind away at them and consume the bits they can generate.
From Wikipedia, a cow chewing on a bone.

How about a squirrel?

Or a deer eating human bones:

This answer could be longer, but why go on? The answer is obvious.
Osteophagia: How Wild Animals Use Supplements

The O.hypothesis has the right to be, but I do not think that it is able to explain everything completely.
Let's start with O. is noted in a limited number of animal species, not in all.
It also follows from the context of the article that this is more a deviation variant due to adverse conditions than the norm.
An example would be  domestic animals that get along just fine without eating bones, because the food usually contains sufficient amounts of phosphate.
( more detail in  the next comment)

Another example, rabbits can eat the corpses of relatives.
But this happens only in conditions of critical hunger. Under normal circumstances, they never behave like this.
The situation is the same among people.
Herbivores cannot eat fresh bones, their digestive system is adapted for this.
We are clearly talking about heavily decomposed bones that have already lain for several years.
There are a few more interesting facts about this but I'm going to describe them in the following questions on the site.

@VladimirOrlov - It's not aberrant behavior, and it's not limited. True, if a diet is adequate in phosphorus, osteophagy decreases. But in nature, diets are not adequate in phosphorus. Carnivores prefer fresh bone, herbivores dried bone. Both want to eat bone. Mice and rats eat bone. One buzzard's diet is 70-90% bone. Mammal bite marks have been found on dinosaur bones. Something is not true because one prefers it to the truth. The "truth" is what is supported by the evidence. There is an adult rabbit corpse on my lawn. I love to observe nature, so have not removed it. ...

...I found it because a buzzard was on my lawn. Three days ago, it was freshly dead and didn't smell so good. Today it has been reduced to fur and a few vertebral bones and a mandible. That is evidence to me that the bones do not just get covered up. I have only seen the buzzard at it, but am not watching it 24 hours/day. I suspect creatures have been eating it bit by bit.

the rabbit is a fairly small animal, so it is not so surprising that it was eaten.
But there are much bigger animals and their bones.
in Tibet there are customs of sky burial, when the corpses are fed to the vultures.
but there the bones are specially crushed and even after that some of them remain lying on the ground.

@VladimirOrlov - Your point being?

this only happens to a small minority of bone. The first thing google kicks back is rarely the whole story.

@anongoodnurse I haven't any acceptable hypothesis. There's no reasonable explanation for this facts.

What about arm and leg bones, hips and skull, which only a hyena can chew on? And regions with high calcium content, like clay and limestone soils? Only about 50% of regions have calcium depleted water, soil and vegetation,  https://www.researchgate.net/figure/A-Map-of-calcium-hardness-as-calcium-carbonate-for-North-America-Note-that-calcium_fig2_236942539

@bandybabboon - Calcium isn't the problem; phosphorus is. Long bones get eaten (what bone do you think that bovine is eating?) The hardest bones break down eventually or not. The majority get eaten. And it's not only hyenas that are great at breaking bones.

@anongoodnurse, where i live there are just foxes and pigs, and only pigs can eat big bones, a horse femur is giant.

@bandybabboon - Which is it? First you said only hyenas could eat long bones, now you include pigs. What is the bull above eating, a dinosaur digit? Why don't you provide sources for your answer, instead of arguing with mine?

@anongoodnurse you're answer is great, The question specifically refers to large bones such as skulls, spines, horns, so I'm being logical. Skulls are huge bones and don't just fit in the leverage part of the jaw towards the molars, and horse femurs are pretty big too. I find a lot of skulls compared to other types of bones in the forests, so I think that osteophagy concerns stick-like bones. https://www.google.com/search?q=equus+femur&tbm=isch

@bandybabboon - Fair enough; I may have overread the question. I agree that the cranium is the most likely bone one will find in areas where animals live and die. Some vertebrae, but many get broken and eaten. I disagree with long bones; once in a while I'll  find a femoral head with the cartilage chewed off. For many years I had 28 acres, mostly wooded, with all kinds of carnivores and an abundance of deer. Yet on my walks through the woods, I never found long bones, vertebral bodies or antlers. I often found fur and feathers.

they rot, get eaten, or get weathered away. Under extremely rare circumstances they fossilize.
What you are talking about is called bone taphonomy.

You can do a simple experiment yourself, put hooves or bones partially buried in dirt in your yard and check on them from time to time, depending on where oyu live what happens will vary quite a lot. Paleontologist and forensic scientists have studied this a lot to understand fossil and human remains respectively.
What happens to them

Normal erosion processes and soft tissue decomposition break the bone in to smaller pieces. The same thing that breaks down rocks breakdown bone just faster. Physical and chemical weather all work on bone. Bone is soft and permeable as rock goes so it weathers very quickly.

Bacteria, insects, fungi, plant roots, or other organisms break them down and eat them. You can prevent this by drying the bone out and keeping it away from soil, (soils keeps the bone moist and makes it easy for those things to reach the bone) Bone like any organic material rots, oxygen and water make it happen faster and bigger organisms can eat them faster.

You can see the same thing with any organic material which is why we dry meat and fruit to preserve them. Also why we cover organic materials like leather or wood in oils to keep them dry. or cover them in poisonous chemicals just like you can do with bone, it slows down their decomposition. in really dry places or conditions with no oxygen bone can take very long to decay. A cow skull defleshed and nailed to a barn in the desert will take a very long time to decay centuries or longer, a bone left on the jungle floor wet and covered in dirt and leaf litter will be gone in months, assuming you can keep things from eating it, (bone is a high demand resource in forests where phosphorous is in high demand).
Different materials decompose at different rates. Under absolutely perfect conditions the bone does not decay completely, creating a fossil. I personally have pulled unfossilized mammoth bones out of clay rich desert soil in Wyoming, the bone had all the structural strength of dry rotted wood, any handling caused bone to flake off, but it was still a complete mammoth leg bone, its decay had been severely slowed by dry, cold, anoxic conditions. We do find lots of buried bone in the right environments.
Soils is not static
If you put bone on top of soil it will not stay on top of the soil. soils turns over due to thermal, erosional, and biological forces. things get buried, see frost heaving and soil creep as examples. Soil is not static it is always on the move. Deserts in particular tend to be highly erosional, which is why we look for fossil in deserts,  new rock is constantly being exposed and destroyed.
Now deserts and cold regions do have much slower rates of decay which is why you can find remains that are decades or even centuries old in such places. Bones are found in bogs and permafrost for instance.  things like sunlight, temperature, abrasion, weather and such can all breakdown bone. Also you vastly overestimate how many animals there are in such places, even if all their bones did not decay they still would not make up a noticeable portion of the topsoil. in places where the animal remains are that common they do make up a significant portion of the soil we call those coral sand beaches, where mechanically broken up animal shells make up the majority of the soil.
Sources about bone decomposition and diagenesis
https://pubmed.ncbi.nlm.nih.gov/20646883/#:~:text=Abstract,or%20as%20long%20as%2030.
https://www.scientificamerican.com/article/dust-to-dust/
https://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1061&context=nebanthro
https://www.jstor.org/stable/2400259
https://www.sciencedirect.com/science/article/abs/pii/S003101821630164X
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8224596/
Sources about soil and erosion turnover
https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/soil-movement
https://www.sciencedirect.com/science/article/abs/pii/B9780123864734000014
Bonus
Great simplified of review of decomposition.

Your first link is about buried bones: "The burial of remains below the surface has been found to effectively shut out many of the most destructive decaying agents, such as the natural elements and insect and animal activity. the other links are irrelevant, the third being only about soil, and do not support your answer (or the comment you left under my post.) I actually did the experiment you suggested inadvertently by leaving a dead rabbit where it was found. Three days later, almost all of the bones were gone. Supervoracious topsoil, maybe?

@anongoodnurse I added a few other sources for all manner of bone decomposition and diagenesis. I also ogranized them a bit more. I have done the experiment thousands of times to study early stages of fossilization. I never said osteophagy does not occur just that it is only one small part of a large variety of things that break down bone.

Let's look at the decomposition of a corpse as a whole.

Fresh
Bloat
Active decay
Advanced decay
Dry state

You can skip to the dry state, which answers your question specifically.

A prerequisite to studying decomposition is knowing that decomposers break down organic material by secreting enzymes turning it into dark liquid form that's possible for them to absorb. Foul gases are produced in the process.
Also, it's best to think about decomposition as a bunch of processes caused by several agents happening and progressing at the same time.

When you hear fresh state, think of anything that ends with mortis:

Algor mortis (decrease of body temperature to ambient temperature)
Rigor mortis (temporary stiffness of muscles due to decreased ATP which is required to relax muscles until decay starts)
Livor mortis (pooling of blood at the site closest to the ground)

Bloat happens because gut flora starts breaking through the wall of the gut. The wall is normally protected by the epithelial cell layer which has a high rate of shedding and regeneration. Since regeneration stops, flora can now bypass into the underlying tissue and start feeding on the body from the inside which results in the formation of

Gas (has foul smell)
Liquid (dark purge fluid that leaks through orifices because of increased pressure from gases in the intestine)

Autolysis also starts where lysosomes containing lysozymes break up and release the hydrolytic enzymes which break down tissue so skin slippage may occur.

Liquifaction by decomposers continues causing darkening and loosening of the exterior.
Blowflies are attracted to the foul smells (even the smell of excrement) and thus, approach the corpse early and lay their eggs which hatch releasing maggots that feed on the corpse.
Several species of insects also start feeding on the corpse but that starts later.
Adipocere (corpse wax) may also form from decomposition of fat preventing further decomposition.

In advanced decay, most tissue has liquified and loosened.

What remains from the corpse is the dry or skeletonised state. Dry here indicates that all the liquid produced from the action of decomposers has been taken up and what remains is the hard tissue, bone or the skeleton.

If the skeleton becomes covered in soil, scavengers (animals) do not eat it and it breaks down in acidic soil over a long time period.
If the soil is neutral, it takes much longer time for this to take place.
If the soil is

dry, anoxic or slightly alkaline (unsuitable for decomposer activity)
salty (has minerals which can form long-lasting hard structures)

the bones may fossilize.

When you study archaeology, you dig and find everything becomes buried very fast through burrowing and overgrowth subsidence. You can find a lot of bones when you walk a minute away from the beaten track, and very rarely on paths, often gray and beige. Humans very often move nice skulls as trophies.
Skulls provide a microclimate for moss, ants, beetles, plants, low-wind zones and snags to collect leaves. Humans like to pick them up and move them, rodents gnaw them, the jaw tumbles away, bug and bird droppings, acids and humidity dissolve them, frost cracks the pores.
Plants compete for space and grow around bones and hide them. Bugs dig networks of burrows and make the soil cave in a bit, worms place middens on the sides, A hoof or a femur will be covered by wild grass in 3-5 years, a horse skull in 10-20 years.
In the arctic there aren't horses, cows, deer, only seashore megafauna. Bones get snowed over. Else they are subject to freeze-thaw weathering, water stays in the pores of the bones, freezes and expands every day, and erodes them.
In the forest, leaf fall and sticks accumulate 1-5cm every year, trees fall over, the soil is alive with fungus mycelia and bugs, It's also quite an acid environment. Bones would be expected to stay uncovered for less than 15-20 years.
In the desert, there aren't lots of big animals, and the bones can last a very long time there, we can find awesome cadavers in regions of low biological, geological and glacial activity.
Human transportation near paths
Scavenging
Animals hide away when they are ill
Gnawing
Moss
Freeze thaw
Geological activity
Subsidence
Glacial activity
Sand dunes
Trampling by other animals

I'm not sure what's going on with the last paragraph. Also, -1 for not mentioning osteophagy. If this answer were all there was to the fate of bones, we'd be buried in bones, which is clearly not the case.


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Estimating the diameter of all earths biomass as a sphere
I am working on an educational resource about the relative scales of resources compared to the earth. Attached is an example of the earth compared to various elements contained within, as well as a comparison of the sum of all water and the atmospheric gasses (at standard temperature and pressure).
Such images are great for creating a sense of scale and displaying the fragility if earth's ecosystems.
I want to also include spheres of wet biomass, which I would imagine to be quite small.
However, when I do math I am faced with spheres that seem too small.
I did the math based on 3 methods and got answers of 6km to 14km diameter, based on Metric Ton estimates of 1.57E+12, 1.38E+11, 1.00E+12
Two folks on Quora estimate 10km diameter.
My questions are these:

What is the appx wet biomass of all plant and animal life on earth?
What is the appx density of it such that it can be converted to volume?
Is it really so small? I am used to being humbled, but this seems excessive. :-)

No need to be humbled. If you think about most life exists in a very thin layer about 150 m thick (about the max height for of the tallest tree species (~120 m), and about as deep as roots penetrate (~25 m)) on the surface of the planet. There's very little biomass that we know of much below the surface or up in the air.

I would be so sad if you made this calculation based on plants and animals alone. Bacteria make up the Second largest component of earth's biomass at ~70 Gt C (~15% of total biomass), mostly in the deep subsurface. Then Fungi (12 Gt C), Archaea (7 Gt C), Protists (4), and finally Animals (~2.5Gt C). Animals are barely more than a rounding error. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6016768/

The following calculation is a very rough estimation to get the sensible order of magnitude.
In 2018, Bar-On et al. estimated the total biomass on Earth at about 550 billion tonnes $(5.5\times 10^{14} \, {\rm kg})$ of carbon, $80 \,\%$ of which is stored in plants. $70 \,\%$ of this plant biomass are stems and tree trunks, which are mostly woody.
Let's assume that the whole biomass is in the wood. The authors suggest that the carbon content should be multiplied by a factor of 2 to get the dry biomass. Assuming that the average water content of wood is $80 \,\%$. This gives us the total wet biomass of $$m=2\times(1/80 \,\%) \times 5.5\times 10^{14} \, {\rm kg} = 1.4 \times 10^{15}\,{\rm kg}$$
Approximating the density of wood at $800 \, {\rm kg/m^3}$, we calculate the diameter of equivalent sphere:
$$ V = \frac{4\pi}{3}\left(\frac{D}{2}\right)^3 \implies D = \left(\frac{6}{\pi} V\right)^{1/3} = \left(\frac{6}{\pi} \frac{m}{\rho}\right)^{1/3} = 15 \, {\rm km}$$
Even though we made quite a few assumptions, note that the diameter of sphere scales with mass as $D \sim m^{1/3}$. This means that if we over- or underestimated the total wet biomass by a factor of 2, the diameter of the sphere changes only by a factor of $2^{1/3}\approx 1.26$, e.g. $D \approx (12-19)\, {\rm km}$.

There is also another interesting visualization published, although it uses the carbon biomass and not wet biomass.

Beware: The article estimated the biomass as 550 gigatons of carbon. However, biomass is not just carbon. As noted in the methodology of the paper, you can multiply the estimate by a factor of 2 to get dry mass; still, the OP is asking for wet biomass.

thanks, yeah i saw that and i was too hurried to account for it, i just corrected it.

Thank you! I appreciate the help.

@bandybabboon, I have edited your answer to more clearly state all the assumptions and include calculations. I hope you feel that my edit improves your answer, but you may of course reject it :)


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What are these worm-like creatures?
I was reading a book in the balcony and I encountered these animals. They look like worms but I don't know if they are worms or insect larva.
I investigated a little and I found a dead pigeon at the balcony of the upper floor which had a lot of these creatures inside its body.
They have a black thing under their skin near the head and they move like drunken people on the ground.
Also, at the mouth they have a tiny black proboscis-like thing (not present in the picture).
Are these worms or insect larva?

most likely fly larvae, also known as maggots, don't know which species.


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Are DRB3 DRB4 and DRB5 different genes or different version of the same gene
From what I understand, an individual can hold up to two HLA-DRB345 alleles (but can be less) that can each be HLA-DRB3, HLA-DRB4 or HLA-DRB5.
However, since HLA-DQB1 and HLA-DQB2 are entirely different genes and we have two alleles for each of those two genes necessarily, I'm struggling to understand if HLA-DRB3/4/5 are three different genes or three different "version" of the same gene.
Similarly:

Are HLA-DRB3/4/5 located at the same place on the chromosome?
What about the people that have neither HLA-DRB3 nor HLA-DRB4 nor HLA-DRB5? Is there no genetic code at the place where other people have it?
Why is there only DRB3 on the "maps" of chromosomes like this one (http://www.biorigami.com/wp-content/uploads/2014/11/MHC1.png) and never the three of them (I wanted to know what "orders" they were in).

Finally, wikipedia states:
DRB1 is expressed at a level five times higher than its paralogues DRB3, DRB4 and DRB5 but doesn't provide a source. Would someone know about a scientific article or an entry proving this?

The reference to DRB3, DRB4, and DRB5 as paralogues of DRB1 indicates that these are different genes. However, as paralogues they share essentially the same structure, having presumably originated from a gene duplication at some point in the past.
From Wikipedia:

DRB1 is present in all individuals. Allelic variants of DRB1 are linked with either none or one of the genes DRB3, DRB4 and DRB5.

Particular alleles ("versions") of DRB1 are linked with one of the other DRB genes, or none of them. Linked genes are often located near each other on a chromosome, such that recombination rarely breaks the linkage between them. DRB1 and the other DRB genes are found on human chromosome 6 within several kilobases of each other. (Unfortunately, that link will only be valid for 90 days; a screenshot is below.)

So, for this region of chromosome 6, some alleles carry a particular version of DRB1 and a copy of one of the other paralogues, and other alleles for this region carry a different version of DRB1 without another paralogue. Since we all carry two copies of chromosome 6 we all carry two copies of DRB1, plus 0, 1, or 2 copies selected from the other paralogues.
Are HLA-DRB3/4/5 located at the same place on the chromosome?
They are located nearby DRB1, and each of them are "upstream" by about the same distance.
What about the people that have neither HLA-DRB3 nor HLA-DRB4 nor HLA-DRB5? Is there no genetic code at the place where other people have it?
Correct, they carry a deletion relative to chomosomes with one of the paralogues.
Why is there only DRB3 on the "maps" of chromosomes and never the three of them?
DRB3, DRB4, and DRB5 do not occur together on a chromosome. They are essentially different alleles, except they're alleles of a chromosomal region and not of just a gene.

Thank you so much, I have two follow up questions though: 1/ about your link, why can we only see DRB3? Is it because the person which was sequenced only has DRB3? When I  search for DRB4 I see the same (DRB4 and DRB1 but neither DRB3 nor DRB5) https://i.imgur.com/XoIRVjf.png? 2/ when you say "Correct, they carry a deletion relative to chomosomes with one of the paralogues.", does that mean that some people have literally thousands of nucleotides less than others? I thought the deletions were always very small like 1 or 2 nucleotides, but I guess I was mistaken.

Also, the "3800K", etc .. of HLA-DRB1 don't map between my screenshot and yours, is this because alleles are not always at the same "place" depending on the individual sequenced?

You can only see DRB3 because the chromosome shown (NT_167248.2) only carries DRB1 and DRB3, the one you show (NM_021983.5) only carries DRB1 and DRB4. As far as I can tell DRB3/4/5 don't occur together on the same chromosome, they just happen to be in the roughly the same place relative to DRB1. My hypothesis is that something like DRB1 existed prior to the other DRBs, but at one point got duplicated so there were two DRB1s adjacent to each other. This pair persisted in the population and the new DRB eventually differentiated somewhat from DRB1 becoming, say, DRB3.

[hypothesis continued] At a later time or in another part of the population a similar duplication occurred, but now the new DRB differentiated in a different way to become maybe DRB4. Since the new DRB3 and DRB4 appeared independently, they're not together on a chromosome. For that to happen there would first need to be someone carrying both DRB3 and DRB4, and then recombination would have to occur in just the right way for their offspring to get a chromosome with DRB1, DRB3, and DRB4.

Yes, different people can differ in their genetics by thousands of nucleotides. Either insertion/deletions (indels) or changes in the order or placement of genes. Once the differences are large enough they usually aren't referred to as just indels anymore, but a broader category of "structural variants". Capturing the diversity of structural variants is a major goal/challenge for the human genome project.

I understand! Lastly, just to be sure, the chromosomes identifiers (NM_021983.5, NT_167248.2) are basically sequences from actual humans for which we sequenced the whole chromosome?

Yes, or at least a large chunk of a chromosome.


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Is it physically impossible for a male Anopheles mosquito to bite?
I know that malaria is spread through female Anopheles mosquitos as they require a blood meal to survive and that male ones do not bite and they survive off of nectar, etc.
But is it physically impossible for a male Anopheles mosquito to bite an organism infected with malaria?
If it is physically possible, then doesn't that imply that there can be a chance, albeit a small one, that they can have Plasmodium in their gut?

Just making sure - physically possible and therefore plasmodium or physically impossible and therefore no chance of plasmodium?

@bob1 I want to know if it is physically possible and therefore plasmodium.

It is physically possible to kick a football on the surface of Mars. Does that help you know whether or not there are footballs on Mars?

Thanks - the wording was confusing with the physically impossible one one line and the no words indicating either way on the next.


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what frequency is the mosquito's whine?
I read on Wikipedia that mosquitoes make the sound they make by beating their wings-- when they are flying, and that the average frequency of the wing beats are about 600 hz.   I went and listened to a 600 hz tone and that is way too low.  Not even close to the sound a mosquito makes.  So I went and found this, which shows the average number of wing beats per second for 29 different species of mosquites:  https://www.researchgate.net/figure/Wingbeat-frequencies-for-29-mosquito-species-Bars-mean-wingbeat-frequency-are_fig1_351489590
and they showed frequencies that were on average EVEN LOWER than 600 hz.  Only one of the 29 species had a frequency higher than 600 hz and that one was only about 750 hz.
But when I listen to pitches of sounds, like from here:https://muted.io/note-frequencies/  the sounds that are even close to what a mosquito sounds like, are more like 2000 hz or 3000 hz.
What am I doing wrong?

Look for a spectrogram of a mosquito buzz, and read about harmonics.

yeah look at waveform as well. try spectrograph too. https://www.google.com/search?q=mosquito+waveform&tbm=isch here's a frequency spectrum:  peak is indeed at 1000 https://www.researchgate.net/publication/8521026/figure/fig1/AS:280254565371909@1443829303583/Waveforms-produced-by-a-female-An-gambiae-in-ssight-top-The-waveform-signal-was.png


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What is this color on mycelium?
i cloned yellow plearotus ostreatus to an agar petri dish, i used potato solution to make the agar.
the first 5 days the mycelium was growing in a tomentose growth and everything was right, the 6th day i started having yellow color in the center of the petri dish.


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Is there a paradox in the field of immunology for the elderly patients?
Say you have an 80 year-old. You can spray anti-bacterial in their door knobs, keys, floors, walls, bathroom. So now less-bacteria. But by doing that, you weaken their immune system, so if they're back in a higher-density bacteria environment, they are now weaker then if you didn't put them in the sterile environment?
Obviously, this paradox does not apply to toddlers, which is the best time to expose someone to bacteria/viruses.

You do not weaken the immune system by removing bacteria. Additionally, with the methods available at home, you will not be able to kill all bacteria. So this is nonsense.

@Chris it's like that for me with allergies. If I'm not exposed to cats for a while, I get re-allergic to cars. If I don't eat ice cream for a year, I end up gassing a lot when I have ice cream for the 1st time. If I don't read while in motion, I'll eventually get motion sickness from reading again.
Isn't our body constantly fighting decomposition, so constantly fighting bacteria from taking over our body? So what do you think happens when our body is put in a sterile environment, and then put back in the previous environment?

@NealConroy nothing, your examples are allergic (aka abnormal ) reactions and lactose breakdown which has nothing to do with the immune system.  one way to treat allergic reactions is controlled exposure thus reducing the immune system response, if we went by that example it should make the immune system stronger. But neither is good model for how the normal immune system works.

@John well why is it when we die, the bacteria take over and eat our flesh? Because we are no longer fighting it. So basically, when we are alive our body is constantly fighting against decay.

To borrow a phrase that was widely heard during the last three years: "Immunology is complicated". You seem to be assuming it functions similarly to a muscle that atrophies with disuse. This is far too simplistic.
For example, I was immunized against smallpox when I was three or so. I've never been exposed to smallpox and I'm in my sixties now, but the odds are that I retain strong immunity to smallpox. To highlight just one of the immune subsystems, there is a class of immune cells called Memory B cells. Their job is to "record" chemical signals from pathogens you have encountered, either from infection or vaccination. These cells then hang out in your blood for decades. If the Memory B cells encounter that pathogen again, they activate and interact with other parts of the immune system and vastly accelerate an immune response to kill off the pathogen.
Notice that I said "odds". There are many probabilistic aspects to the immune system. When you get vaccinated or sick with an infection, you will generate millions of Memory B cells targeted at that infection. As I said, these cells can remain dormant in your blood stream for decades. As you age, some of them will die off, and if you are unlucky, enough of them may die off that they may not be able to respond effectively to their target pathogen. The gradual dying off of Memory B cells, is just one aspect of the overall decline of the immune system with age. In other situations older folks may still have well functioning Memory B cells, but the other systems that do the actual killing may have become weakened and ineffective. This is the motivation for being particularly careful with sanitation around the elderly: they may no longer be able to mount a strong immune response even to pathogens they've seen and fought off many times before.

If I'm not exposed to cats for a while, I get re-allergic to cars. If
I don't eat ice cream for a year, I end up gassing a lot when I have
ice cream for the 1st time.

Your experience may very well be an example of the ability of the immune system to form long-lasting "memories". Note that it isn't the cat hair or the ice cream itself that causes the unpleasant symptoms, it's your immune system's response to them that causes the problems. At some point you were exposed to cat hair and your immune system erroneously decided it was pathogenic, and "memorized" how to recognize it so it could mount a response the next time it encountered it. However, it seems that continued exposure to small doses of an antigen can eventually convince the immune system (at least temporarily) that the substance is OK and doesn't require an immune response. Exactly how this happens is not well understood. This isn't a case of the immune system "forgetting" how to deal with a threat, it's more like it remembering all too well its first impression.
An excellent popular book on the immune system and its complexities is "An Elegant Defense".

Charles, 1st off I thought allergies, and bodies immune system to bacteria and viruses, are separate? My allergies to cats is just red eyes and blowing nose. So, yes, I asked an immunology professor, your environment changes, your allergy-immune system changes. Somehow, bacteria and virus immune system retains a lot longer.

Like I said, "Immunology is complicated". Allergies and responses to pathogens differ, but do involve shared subsystems of the overall immune system. The "memory" for allergens also involves Memory B cells, but usually of a different subtype, than handles pathogens.

Charles, but the part that is much more complicated in immunology is allergies, as opposed to bacteria and viruses. Immune system to bacteria is pretty straightforward, immunity to viruses is rather moot, as viruses change over time. It'd be interesting to see what kinds of things our immunity loses quickest to least. Could very well be motion sickness.

"Immune system to bacteria is pretty straightforward" need citation! Here is a research project for you: tell me how many classes of cells are involved in the human immune response to a bacterial infection. "immunity to viruses is rather moot, as viruses change over time": some do, some don't, as is also the case with bacteria (that's why we're having to deal with anti-biotic resistant strains of bacteria now). "Could very well be motion sickness." OK, you've lost me now. Motion sickness doesn't having anything to do with the immune system (cont)

Charles, I was allergic to acts, at age 12, got my1st kitten, was allergic to it for a day and a half. Then slept with the cat for 6 years, then moved out for college at age 18, at age 19, came back to mom's house and allergies to cat all over, and this time, it took weeks to get over. But lose it within a year. Same thing with motion sickess. 1 time, I read something so interesting while in a bus, that when I got off the bus, I had to throw up. But the next day, I was able to read while on bus/train no problem, so played video games. But within a year, had to start all over... Viruses seem to

Viruses seem to change 50% in about 4 years, so it seems to be much easier to keep track of bacterial immunity. But I don't know a good example of it. As winter colds are caused by viruses. By the way, regarding motion sickness, I constantly threw up in the car at age 4 over long-distance highways, so got immune to that quick. I have a feeling, if I went to jail for a year, and come out, rode a public bus, I'd feel dizzy. But I ride the bus every day. If I don't ride the playground swings for a while, it feels a little dizzy too.

Motion sickness is caused by a conflict between neural input from the vestibular system and your visual system. It is sometimes treated with anti-histamines, but that's simply to suppress your impulse to vomit.

With respect Neal, you're telling your self 'just-so' stories linking your issues, and you are fixating on things like "Viruses seem to change 50% in about 4 years" that simply aren't true. Rather than spin your stories explaining a sample set of 1, I urge you to do some reading on the subject.

Charles, viruses specifically for rotavirus and norovirus, that cause gastroenteritis.

Let us continue this discussion in chat.

I seem to have lost my ability to post in the chat, here's my reply: Charles I didn't change my point. The sickness from sewers was the 2 viruses. And after 4 years, I got sick again at some 50% intensity, hence my logic. I realize now the microbio professor is not the immunology professor. Though the immunology professor should know more about microbio than the microbio professor knows about immunology, so I know now to ask the immunology professor. Which I lost touch of. But they did back my allegation on cats, that my allergies to cats was lost after losing exposure for over a year.

I also seem to have problems tagging people @Charles E. Grant


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What is the origin of the name Crassostrea gigas (pacific oyster)?
Context
I am looking for a source that reveals the origin of the name "Crasssostrea gigas". This is an oyster also known under the common names giant oyster, Japanese oyster, Pacific oyster and Portuguese oyster (amongst others).
What I've looked into so far
WoRMS and molluscabase both refer to "Thunberg 1793" page 140, but that refers to Ostrea gigas:

I did find information on the recent change from Crassostrea to Magallana (https://doi.org/10.2983/035.036.0301), but that does not refer to the origin of the Crassostrea gigas.
Question
What is the origin of the name "Crasssostrea gigas"?

Are you interested in the etymology of Crasssostrea?

Well, would be interesting as well, but ultimately I am looking for a reference where the name is used to describe this specific oyster. I.e. how "Ostrea edulis" has a reference to Linnaeus 1758, p. 699

Etymology. From Latin crassus (“thick”) + ostrea (“oyster”). Genus: Crassostrea; Sacco, 1897

As I see it, it went down like this:
1753: Linné describes the genus Ostrea
1793: Thunberg describes an Oyster as gigas and puts it in that genus
-> Ostrea gigas (Thunberg, 1793)
That is the original description and should be the original name of the type specimen.
Over a hundred years later...
1897: Frederico Sacco forms a subgenus (sottogenere) Crassostrea in the Genus Ostrea (Linné, 1753). It is not considered a subgenus anymore, today it has the rank of a genus.
So at some point, Ostrea gigas was taken out of Ostrea (this genus still exists) and into the Genus Crassostrea (or maybe into the Subgenus Ostrea (Crassostrea)).
It says here that Crassostrea gigas is a homotypic synonym of Ostrea gigas, so that also backs up that it was "just" a matter of nomenclature.
I could not find the original source that describes the basis of changing the genus. The earliest source I found mentioning Crassostrea gigas is from 1952, Adresses delivered at the Convention of the National Shellfisheries Association (page 82) and there is a reference to findings of Schaefer 1937. So if you look for that you might be able to go back and pinpoint the origin of it at some point.
The entire new Magallana Genus from 2016 (Crassostrea gigas Thunberg, 1793 is its type taxon) is also an interesting read, it seemed to have evoked quite a spat amongst malacologists.
Maybe you can find something in the Biodiversity Heritage Library that helps with your question.

@nika identifies the original description of the species as Ostrea gigas Thunberg 1793. They also identify creation of the subgenus Crassostrea Sacco 1897, which I believe, according to the rules of zoological nomenclature, simultaneously created the genus Crassostrea.
Ostrea gigas was placed in the genus Crassostrea by Gunter (1950). Previous authors had recognized O. gigas as part of the subgenus Crassostrea, but it looks like Gunter is the first to recognize Crassostrea gigas (Thunberg 1793) as belonging to a separate genus.

Awesome, thanks! It was fun looking into Crassostrea's history and it bugged me that I didn´t find the complete answer


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Proportion of cell layers in the different areas of human cortex
I am looking for any scientific paper or book which could help me find the different proportion of layers across the different areas of the human cortex. I am working on a research project which includes investigating the areas with the highest proportion of layers 2 and 3 of pyramidal neurons. I have an idea of what some of these areas are, such as dorsolateral prefontal cortex, but I could not find any comparative material which describes the layer composition of the cortex area by area. Most of the papers I've come across either about an individual area and its cytoarchitecture, or about specific neuronal layers without comparing each area with respect to them.

You might check out the Allen Institute.


text:
Is inhibin hormone secreted by corpus luteum in females?
In females, I have studied that corpus luteum secretes mostly progesterone, but some of estrogen, relaxin and inhibin too. But in some of the books they say that inhibin is not secreted by corpus luteum. Can someone please explain.

In human females, inhibin is secreted by the granulosa cells of the primary oocyte which inhibit FSH secretion ,resulting in the stoppage of follicle maturation until activin ,again secreted by granulosa cells activate FSH activity .

I think this doesn't answer the question.

So inhibin is secreted by primary oocyte and not corpus luteum?


text:
Are organisms that are genetically modified with a deletion classified as "transgenic"?
Imagine you delete a genomic region in a zygote with a CRISPR plasmid to generate an F1 animal with a genomic deletion.
The animal should be considered transgenic because of the presence of the plasmid DNA. But in the nuclear DNA, no foreign DNA has been introduced, it's only had a segment removed.
But when F2 are produced from two such animals, are they considered transgenic? They shouldn't inherit the plasmid DNA from their parents, right? And they have no foreign DNA in their nuclei.
In my own project, we used "transgenic" mice that bore a genetic deletion. But they also had the Cre recombinase or LoxP sequences in their genomes, hence they'd qualify as transgenic despite the deletion. But what about when there are no foreign sequences introduced, only deleted?

In Australia, gene deletions still count as genetically modified. See “the office of the gene technology regulator”


text:
modify PCR steps to include a ligation
Imagine a multiplex PCR in which after the extension step, the dsDNA is nicked and requires a ligation reaction to repair the nick before the next denaturation step. So the steps would be:

Denature
Anneal
Extend
Ligate
steps 1-4 X 30

There are thermostable DNA ligase enzymes available (best activity at 65C), which don't get heat-inactivated by the high temp at the denaturation step.
It seems like this should work, but I can't find any info on anyone trying this. Any ideas?

I don't get this. Why would you nick the dsDNA?

@Chris it's a multiplex PCR with 3 primers. Two flanking and one mutagenic in the middle. Assuming all 3 primers anneal, the polymerase will "bump into" the dsDNA in places where the other primers are hybridized (and either continue polymerizing or not depending on whether it's a non-displacing enzyme), but not covalently link the two ends. So before the next denaturation step those two pieces need to be ligated together. So the nick is an unfortunate byproduct of the PCR design that necessitates ligation. Now I'm doing in it separate rxns. I'd like to do it all in the same iterative reaction

Ah, thanks. There are two problems I could imagine: First: The reaction may be hard to optimize in terms of the needed temperatures for annealing and the enzymes to avoid by-products. Second: Buffers needed for the different enzymes are incompatible. Or it is simply much easier to simply take the whole PCR reaction in the end, add some ligase and incubate it for an appropriate amount of time, so nobody ever bothered.

yes, the buffer compatibility was my main concern. My guess is that the ligation should be fine in the presence of pcr buffer, since as you mention, people just add dna ligase to their pcr rxns, post-pcr. But whether pcr is inhibited by ligation buffer I don't know. Looking at the buffer compositions it at least seems like it's worth a shot. Do you agree? Temperature I'm not so worried about, as there are ligases available with high optimum temps, i.e. right around my target annealing temp. They don't have inactivation temps, so my guess'd be that they won't mind high denaturation temp steps

If the buffers are compatible (especially for the magnesium content), you could give it a shot. The Taq shouldn't have much activity at these "low" temperatures, so at least you shouldn't have to expect some unexpected here :-)

In case this helps anyone, I found a technique called Gap Ligase Chain Reaction which includes both a thermostable ligase and a DNA polymerase enzyme in the same reaction:
Ligase Chain Reaction (LCR) --Overview and Applications (Wiedmann et al.) PCR Methods and Applications
Amplification of Chlamydia trachomatis DNA by Ligase Chain Reaction
Preliminary Evaluation of the Ligase Chain Reaction for Specific Detection of Neisseria gonorrhoeae
Detection of point mutations with a modified ligase chain reaction (Gap-LCR)


text:
Is there a detailed model of the resonance of the basilar membrane and excitation patterns of hair cells?
I've read that it's generally understood that deeper parts of the cochlea are sensitized to lower frequencies, and regions closer to the oval window are sensitive to high frequencies. In a sense, a frequency distribution is converted to a spatial distribution along the length of the cochlea.
Is there a precise model that can predict exactly where excitation will occur along the basilar membrane? I.e., can we compute, with relative precision, exactly how to convert between a frequency distribution to a spatial distribution of hair cell excitation?
I'm well aware that a Fourier transform breaks down a sound into constituent frequencies, and if the cochlea were perfectly idealized, that would suffice to take a Fourier transform and then map the result to the basilar membrane. But we're talking about a biological system, which is certainly not ideal. It's not a given that what actually happens is anything like a Fourier transform.
A few things that I'm not sure how to answer are:

The basilar membrane is coupled to itself. If one part of the membrane is vibrating, presumably the adjacent areas are too. How is the vibration isolated into frequencies down to the level of precision that we know humans can distinguish?
The wavelength of sound in water at audible frequencies is much much longer than the length of the entire (unrolled) cochlea. To what extent (and how) are phase differences actually relied on by the mechanism?
The vestibular and basilar canals are coupled at the tip of the cochlea, and there will be a phase difference between them, and this will be involved in the vibration of the basilar membrane. How does is this phase difference involved in the spatial distribution of basilar membrane vibration? (Is there any impedance mismatch at the opening between them?
Will there be wave reflections that matter?)
A pure "Fourier transform" mapping of frequency to length along the cochlea does not explain why harmonically related sounds are also perceived as related by the listener. This phenomenon would be well explained if frequency ω also excited 2ω, 3ω, 4ω, ... modes within the cochlea, so that harmonically-related tones would have very similar patterns of excitation (and thus similar perception). How might this be modeled? Has this been looked at?
I have read that it may be true that hair cells are capable of motion (!?) and may be individually tuned to mechanically resonate at particular frequencies. Is this true? If so, how is this involved in the distribution of hair cell excitation? How much is known about the mechanism/dynamics?

What are the best models/research about this question?

Too many questions in one post here.

Ni, G. Modelling Cochlear Mechanics (2014) looks like a nice review to begin with. Also, searching for "biophysics of cochlea" will give you many results.


text:
Does poop have protein?
Popular health advice suggests that one shouldn't consume >30g of protein at a time (without a gap of ~3 hours, or otherwise depending on the type of protein), because only so much can be digested at a time.
This seems wrong to me? Shouldn't the protein just form a backlog? Where does the protein go? And if this were true, couldn't people just lose weight by consuming all their meals in one go?
I was under the impression that poo doesn't contain any macronutrients (apart from some occassional indigestion, or fats not absorbed on a high-fiber diet), just fibre and water. Perhaps it has to do something with protein synthesis, and the amino acids get excreted in urine?

Trivially, feces contains cells and cell waste, which necessarily have proteins. You may want to narrow your title and question to discuss the persistence of dietary protein in the human GI tract.

I wouldn't start with popular health advice as a basis for understanding anything.

perhaps try some before your exercise sessions and see if your gain weight? were you thinking of starting a line of poop protein supplements for gyms?

Human stool, on average is about 25% solids and 75% water. Up to 54% of the dried solids consist of bacterial biomass, of which protein comprises up to 50% (1). This is pretty consistent with other research that stool contains up to 25% protein (dry weight) (2), although there is still debate over how much of that is attributable to undigested protein and how much is bacterial biomass.
Basically all dietary protein is absorbed in the duodenum and proximal jejunum (3), so, pretty much just the first half of the small intestine. And, since the food you eat only spends a finite amount of time in this region of the gut, protein uptake is likely limited by transporter density and also by the kinetics of gastric and pancreatic enzymes that break down large dietary proteins into small, absorbable peptides and amino acids.
Lastly, when your body does uptake more protein than it needs (or can utilize) at a given time, it doesn't just backlog (there is no storage form of protein in humans). Instead, it's catabolized and used to generate glucose or ketone bodies, which can eventually be stored as glycogen or fat. These processed also generate a significant amount of ammonium waste, which is converted to urea in the liver and excreted in the urine, putting extra strain on the kidneys.
References:

Rose C, Parker A, Jefferson B, Cartmell E. The Characterization of
Feces and Urine: A Review of the Literature to Inform Advanced
Treatment Technology. Crit Rev Environ Sci Technol. 2015 Sep
2;45(17):1827-1879. doi: 10.1080/10643389.2014.1000761.

Volk T, Rummel JD. Mass balances for a biological life support
system simulation model. Adv Space Res. 1987;7(4):141-8. doi:
10.1016/0273-1177(87)90045-7.

APUS: An Introduction to Nutrition 1st Edition (Byerley); Chapter 5.4: Protein Digestion, Absorption and Metabolism. https://med.libretexts.org/Courses/American_Public_University/APUS%3A_An_Introduction_to_Nutrition_(Byerley)

Interesting. So where does the bacterial biomass protein come from? Does bacteria convert fiber into protein?


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Vine has simple and compound leaves
What kind of plant is this?

Some leaves are compound (leaves of three). Other leaves are simple.

Located in an urban garden in the shade; east of Toronto, Ontario, Canada (July 30, 2023).

Woody vine crawling up a fence. Vine has feet that stick to the fence.

Related posts: (30 feet away on the other side of the lawn; all are different specimens)

Is this poison ivy? (Aug 2, 2022)
Is this plant in my urban garden poison ivy? (Jul 20, 2023)

Edit:
This plant/location in the garden is especially hard to photograph. It's hard to reach, dark, and surrounded by thorny brambles. And there are lots of different species of plants in the same spot; it's hard to tell what leaves are attached to what plants when viewing a photograph.
Rather than take another dark, poor-quality photo during the day, I made a video at night with a bright light. I tried to show that there are lots of differently-shaped leaves attached to the same plant. Some leaves are simple leaves. Others are compound leaves of three.
YouTube video

Does this answer your question? Is this poison ivy?

leaves in 3s is your key here. Definitely poison ivy (again)... see your other question, look at the attachment of the vine to the fence and the leaf arrangement.

As a novice, my guess is Boston Ivy (Parthenocissus tricuspidata).

Eastern Poison Ivy vs Boston Ivy
Boston Ivy: A deciduous woody vine native to east Asia, introduced in North America. Established in numerous scattered locations, mostly around urban areas. It is a close relative of the native Virginia creeper.
Middle leaflet has no stem or a short stem not much longer than that of side leaflets.

Plants can have both compound (trifoliate) and simple leaves. Some leaves have two side leaflets fused to create a two-leaflet leaf.


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What is the function of smelly sweat in primates?
I remember one, sweltering day in Malaysia, I was climbing the very long staircase to a Buddha statue in a cave, when I suddenly felt enveloped in an overpowering smell of sweat. My first thought was that I must have forgot to wash, possibly for several weeks, but then I realised that I was in the middle of a troupe of monkeys.
And now I've come to wonder what the function is of this very characteristic smell. There seems to be connection to sexual maturity, since children don't start producing the smell until puberty, and the overwhelming base of evidence I collected that day, seems to suggest that this may be universal among primates.
Has any research been done into the function smell of sweat, socially or otherwise?

Why do you think it has a function?

It might not have a function. But maybe it's there as an indication that one should clean themselves to prevent disease. We similarly developed smelling dead bodies and excrement as foul to stay away from them because they can cause disease despite other animals like blowflies being attracted to these smells.

Sweat does not smell much on its own, its the bacteria that eat the sweat that smell.

@user438383 Well, mostly because it only really starts at puberty. The fact that other primates also smell strongly suggests to me that this an adaptive trait that goes several million years back; and although we in modern society find the smell rather offensive, it is not actually smell you connect with decay. I believe more in the idea that it signals adulthood and perhaps that you are ready to fight for your territory or group, which may explain why we now try to mask the smell with deodorant, since we live rather stressful lives in dense cities.

@j4nd3r53n thats fine, it's just always good to question whether a trait is really adaptive has a function or whether it's just a random byproduct of something else. Often things can appear to be adaptive when they are really just nothing :)

It's a tricky query to answer, so here's some prelim info and someone can be more specific from there:
Apocrine glands are a type of sweat gland found in certain mammals, including humans. These glands are responsible for producing a thick, odorous sweat that is involved in various physiological and social functions. Here are some key characteristics and functions of apocrine glands:
Location:
Apocrine glands are typically found in specific areas of the body, such as the armpits (axillae), genital region, and around the nipples in humans. In other mammals, they may be located in different regions depending on the species.
Odorous Secretion:
Unlike eccrine glands, which produce a watery and odorless sweat, apocrine glands secrete a thicker sweat that contains proteins, lipids, and other compounds. When this sweat comes into contact with bacteria on the skin's surface, it can lead to body odor.
Activation:
Apocrine glands are activated during emotional arousal, stress, and sexual activity. The sympathetic nervous system controls their secretion, and hormonal factors can also influence their activity.
Scent Communication:
One of the primary functions of apocrine glands in mammals is scent communication. The odorous sweat they produce contains unique chemical compounds that can convey information about an individual's identity, reproductive status, and social position to other members of the species. This is particularly important in social species where scent marking and recognition play a crucial role in group dynamics and hierarchies.
Sexual Signaling:
In some species, apocrine gland secretions may play a role in sexual attraction and mate selection. The distinct scents emitted by individuals can serve as cues for potential mates to assess each other's fitness and genetic compatibility.
Developmental Timing:
Apocrine glands are not fully functional until puberty in humans. Their activation and development are influenced by hormonal changes during adolescence.
Associated with Hair Follicles:
Apocrine glands are associated with hair follicles, and their ducts open into the hair follicle canal. This is in contrast to eccrine glands, which release sweat directly onto the skin's surface.
Here's a ref from nature stating that human primates may use sweat pheromones to communicate:
https://www.nature.com/articles/npre.2008.2561.1.pdf
Primates, especially those living in social groups, rely heavily on communication to maintain social bonds, establish hierarchies, and coordinate group activities. Scent plays a crucial role in primate communication, and sweat scent could have evolved as a means for individuals to convey information about their identity, reproductive status, and emotional state to other members of their group.
mate selection in primates can be influenced by olfactory cues. Scent signals emitted through sweat may allow potential mates to assess each other's genetic compatibility, overall health, and reproductive fitness.
the scent-marking behavior using secretions from sweat glands may serve as a way to establish territorial boundaries and prevent conflicts with neighboring groups.
The odor produced by sweat may play a role in avoiding predators. For example, certain primate species may produce alarm pheromones through their sweat, signaling danger to other group members.
Sweat scent in primates could be a remnant of their ancestral heritage, where scent communication was crucial for survival and reproduction.
incidentally, horses, dogs, deer, they also have strong pheromones.

Thank you for the article, +1. So it seems pheromones have an effect, even in the absence of smell. But evolution wouldn't have favoured sweat that would produce this characteristic smell when broken down by skin microbes, I think, unless the smell itself was important. Perhaps it amplifies the effect of pheromones?

To elaborate slightly on the existing answer in which mention is made of 'genetic compatibility', there are many compelling studies which indicate a strong preference for dissimilarity in class 1 HLA alleles between human mating partners, and that this dissimilarity is readily detectable in the body odour of respective individuals.  The link below 1 is to one such study; and the following paragraph is its abstract.

The major histocompatibility complex (MHC, called HLA in humans) is an important genetic component of the immune system. Fish, birds and mammals prefer mates with different genetic MHC code compared to their own, which they determine using olfactory cues. This preference increases the chances of high MHC variety in the offspring, leading to enhanced resilience against a variety of pathogens. Humans are also able to discriminate HLA related olfactory stimuli, however, it is debated whether this mechanism is of behavioural relevance. We show on a large sample (N = 508), with high-resolution typing of HLA class I/II, that HLA dissimilarity correlates with partnership, sexuality and enhances the desire to procreate. We conclude that HLA mediates mate behaviour in humans.

Interestingly, there are also allied studies which demonstrate that the use of oral contraceptive hormones disrupts this sensitivity, and one such example is cited by the study linked.
There is clearly a heuristic argument that this dissimilarity favours a broader range of immunological memory in any viable offspring; and this hypothesis is explored in the 'Wikipedia' articles on 'Major Histocompatibility Complex' and its subsidiaries on 'sexual selection'.
To address the comment inquiring upon a causative basis for this phenomenon in the relation between MHC or HLA type and body odour, the latter section of that 'Wikipedia' article makes the following observation and cites the relevant study.

MHC may be related to mate choice in some human populations, a theory that found support by studies by Ober and colleagues in 1997, as well as by Chaix and colleagues in 2008. However, the latter findings have been controversial. If it exists, the phenomenon might be mediated by olfaction, as MHC phenotype appears strongly involved in the strength and pleasantness of perceived odour of compounds from sweat. Fatty acid esters—such as methyl undecanoate, methyl decanoate, methyl nonanoate, methyl octanoate, and methyl hexanoate—show strong connection to MHC.2

I might add here that perhaps the most consequential determination of these sorts of studies is the finding that hormonal contraceptives such as the OC pill effectively inhibit any olfactory sensitivity to this potentially important dissimilarity in HLA type.
Consider for example the implications of less than optimal breeding matches arising under the influence of these hormones and of this manipulation of female fertility on a massive scale, the persistence of which culture in the face of such evidence -- arguably in order merely to sustain the putative bodily autonomy of women in the illusory form of a simple pill -- defies reason.  Common sense alone informs us that practices of this kind invite sociological and even biological calamity.
Influence of HLA on human partnership and sexual satisfaction
Infuence of MHC on odour perception of 43 chemicals and body odour

Does this have any relationship to the perceptible odor of sweat?

@Bryan Krause. The particular study cited rather correlates a preference for body odour between individuals in a mating couple with the dissimilarity found in their respective class 1 HLA types, than to attribute a direct effect of MHC type on such body odour.  However, there are other studies which demonstrate this effect, and I have amended the answer accordingly. to say that If it exists, the phenomenon might be mediated by olfaction, as MHC phenotype appears strongly involved in the strength and pleasantness of perceived odour of compounds from sweat.: fatty acid esters,


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Anticodon Translation Question

Could somebody please explain the answer for (c). I assumed that since transcription started at the bolded/underlined T/A base pair, the second codon would be UCU? Thanks!

Welcome to Biology StackExchange! Beware: Transcription and translation are two very different processes. Transcription indeed begins at the bold&underlined T/A, but translation begins at the start codon.

Hi! Thanks for your response. If it were to begin at the start codon, wouldn't the second codon be TTT and the anticodon would be AAA? Where does the answer, CCU come from?

This is a question best understood carefully and in parts. We know that transcription begins at the bolded AT pair, and that once transcription begins we are looking for a translation start codon (i.e., ATG).
From the transcription start, we have the sequence as follows:
5' TGCAGAGATGAGGAAAA...AGT 3'
Here is the start codon for translation:
5' TGCAGAGATGAGGAAAA...AGT 3'
If our start codon is there, then the next codon would be 5' AGG 3'. We know that an anticodon is the complement of the codon, so it would be 3' UCC 5'. However, we normally write sequences in the 5'to 3' direction, so that's how we get 5' CCU 3'.
I think another commenter was right in that you seem to be mixing up transcription and translation. The start codon refers to translation start, not transcription start. Make sure to slow down a bit and read the question, as it even gives you that information in part B ("give the first ten nucleotides of the transcript and box the start codon for translation").


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Behavioural experiment on Nasonia Wasps
I want to see how two male Nasonia vitripennis interact with each other. I have been using enamel paint on their heads to distinguish them, but I am wondering if any other methods of marking them would be less invasive. Any ideas?

I’ve previously used Posca pens to mark wasps during experiments - I think that’s going to be about as non-invasive as you can get without using some kind of advanced video tracking techniques. But this was on much larger paper wasps than Nasonia which are much smaller.


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Is it possible to identify a kind of scorpion based on a photo of its dried body
Somebody at my university have came back from a vacation trip and brought back a dried body of this small scorpion.
Can you identify it for me?
This is a very tiny (?) scorpion, if I may say so. I can't provide the exact measures right now, but I'd say that the whole body was 7-8 centimetres long. Maybe 10 cm with its tail straighten up.

Is is endangered of extinction? Is transporting it illegal? Can it be dangerous (when alive)? Lethal (I've heard that the smallest scorpions' bite are the most dangerous / more dangerous then much bigger counterparts' bits; but that might be some kind of urban legend).
Unfortunately, I don't know whose belongings is this, so I cannot ask for a location where this dead scorpion was found. It was simply lying in university's kitchen as... I don't know what. A trophy?
All I know is that it is 100% not a native species. I am from Poland, eastern Europe and we definitely have no scorpions here. Due to to too low temperatures and the climate being very unfriendly for that kind of animals.

Definitely not small at 8 cm - that's a large one. No expertise at all, but there are scorpions in Europe (Spain, Italy(?) Greece, even the UK (whether it is Europe or not aside)). Likely to be a common species (as that's usually what people find).

Spain, Italy and Greece are all much, much warmer than Poland so that would fit into my theory. United Kingdom is on the other hand pretty much in the same temperature zone and climate like Poland. So, it seems that I must revise my thoughts and... watch my steps! :) Thanks!


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Why are deformable cancer cells associated with being more malignant or dangerous?
So I was watching a lecture that talked about circulating tumor cells/cancer stem cells, and the professor mentioned that deformable cancer cells tend to be more dangerous to us. Why is this so? Does it have to do with the cells' physical ability to metastasize or intravasize better? Is it possible deformable cells are more resistant to drug therapy? (The latter suggestion sounds kind of crazy to me but if anyone has insights, a potential answer, or a research paper on it, I'd really appreciate it!!)

What was the exact term the professor used? "Squishy cancer cells" is unlikely to yield good results on searching. Try deformability and metastasis.

I don't know for sure, but it could be something similar to what happens to RBCs where continuous peroxidation takes away their deformability so they break more easily and are taken up by macrophages when they get old. Deformable cancer cells may be similarly more stress resistant.

essentailly those cells are "stickier" because they are deformable and can adhere to a new site to begin growing easier. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386247/ and https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386247/


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What caused these shallow depressions in a European forest?
Recently, in an eastern European forest, I came across many depressions in the ground of a regular round shape, with a flat bottom and vertical walls.
Many were filled with water.
Some were obviously dug recently.
At the same time, there were no traces of excavated soil nearby.
I have no idea what kind of creature could do this, and why.
Has anyone come across something like this?
What it is?

Welcome to the site. Where in the world were these photos taken? - I'm guessing Eastern Europe from your name. Could be soil sampling for a science study.

@bob1 yes, you're right, it's Eastern Europe

Another, more cynical, suggestion - any rare/valuable/collectable plants in the area?

Or elephants? ;p

@bob1, "Another, more cynical, suggestion - any rare/valuable/collectable plants in the area?" I did not see anything like it there, although I looked carefully enough, because I picked mushrooms.
besides, it is unlikely that the correct shape of the pits will be important for thieves

Could be that something was burried there... I like to dig out historical artefacts (others call it junk :D) and those holes made me think of when I dig out an old pot or something like that, that is laying in the ground.

@nika I agree, though there most people would leave the soil behind and perhaps pile it to the side, which we don't see here. This was why I was suggesting perhaps plant collectors or someone doing a soil survey.

@nika I did not specify the number of artifacts. there were about a hundred of them, or more. many could simply not visible, because the grass was overgrown.
this is a young forest on the territory of an abandoned boarding house, so the presence of antiquities in the soil is very unlikely.

It looks like a horse hoof print in soggy ground.


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Why don't water cuttings die of root asphyxia?
Root asphyxia happens when there is not enough oxygen available for the roots, for example when the soil is clogged with water.
However it is common to do water cuttings where roots directly develop in water.
In this scenario, how is it possible for the roots to develop in only water without asphyxia, but they die of asphyxia in waterlogged soil?

Look up dissolved oxygen in water. In mud, other organisms compete for O2.


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Would anaerobic glycolysis create more ATP than aerobic respiration
I know the fact that anaerobic glycolysis is first step of aerobic respiration.
If fast twitch muscles use anaerobic glycolysis to get 2 atp at rate that 100 times faster than oxidative phosphorylation according to this Wikipedia site:

It replenishes very quickly over this period and produces 2 ATP molecules per glucose molecule,3 or about 5% of glucose's energy potential (38 ATP molecules).[4][5] The speed at which ATP is produced is about 100 times that of oxidative phosphorylation.

This means that it may be even more than 100 times due to other steps in aerobic respiration.
My question is would anaerobic glycolysis create more ATP than aerobic respiration in the same time interval , because if we consider that aerobic respiration creates 38 ATP molecules in x time then according to the previous Wikipedia site, I mentioned before anaerobic glycolysis, would be able to create 200 ATP molecules in x time which is much more than aerobic respiration.
What I don't get is that, it is said that aerobic respiration creates more ATP than anaerobic glycolysis?


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Why do short hairs get longer with age?
I know that short hairs such as eyebrows, eyelashes, nasal hairs will stay a certain length because the lifespan of the follicle only allows them to grow to a certain length.
My question is why do those hairs start to grow longer and longer with age?


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Average surface area of the outer portion of a human skull
I tried Google. I tried Bing. People don't seem to measure the surface areas of skulls much. I was only curious before. Now I need to know. I don't really wants to know about the face of the human skull, just the top, sides, and back "flat" portion of the skull. What is the surface area of this?

Welcome to BiologyStackExchange. Sometimes you have to search through primary sources (e.g. research articles), for example using Google Scholar: Sholts, S.B. et al. Variation in the Measurement of Cranial Volume and Surface Area Using 3D Laser Scanning Technology (2010)

your gonna have to get the linear measurements and do the math yourself, the skull is such a complex shape, surface area is not a useful measure so it is not recorded much and your guidelines are too vague for a meaningful estimation. .that or find a good 3d model and extract the data.


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Does blunt end have a hydrogen bond?
I am an undergraduate student of biology.
I saw a lecturer online, who said that sticky ends makes phosphodiester and hydrogen bonds cut. (also here).
But why blunt end just makes phospodiester bonds cut?
Thank you for answering.

Welcome to Biology StackExchange! Do you know how the structure of DNA looks like, and where phosphodiester and hydrogen bonds are located? Did your lecturer show you an image of sticky-ends and blunt-ends cuts?

Does this help? @ https://www.ncbi.nlm.nih.gov/books/NBK21129/

@BrendanDarrer thank you for sharing with me, but unfortunately the book didn't contains the answer that i'm looking for.

@Domen hi, thank you for your warm welcome. Yes i know the structure of DNA looks like and where are the bonds located. My lecturer shows me how the sticky-ends and blunt-ends looks like using GAATTC strand (for sticky-ends) and CCCGGG strand (for blunt-ends). Can you please enlight me about this cause i really need to know. Thank you so much

Have you found the answer or are you still looking for one?
In short - Hydrogen bonds occur between the 2 strands, whereas phosphodiester is within the each strand. so a sticky end has a few overhang nucleotides on one strand that are absent in the other strand, hence the hydrogen bond is missing..

Hi! i'm still looking for the answer. But thanks to you, your answer kinda enlight me. Thank you.


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Can you identify this marine organism?
I found this in a beach located at Magnisia District in Greece. I found many more like this stuck in rocks, this however was loose. It was a bit hard and very smooth to the touch. It didn't seem to move.
The date I found this was 3rd of August 2023.

What are your first thoughts? Your first guess? On the name of this marine organism?

Looks like some kind of sponge or snail/mollusk type animal or plant?

@BrendanDarrer I believe it's a kidney sponge, although I am not sure.


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How pitch of a DNA Helix is 3.4 nm?

How pitch of a DNA Helix is 3.4 nm?
In the image that I have attached, the numbers with prime represent the number of base pair and normal numbers represent the number of gap elements between two base pairs. Everywhere to calculate the pitch (have 10 base pairs), number of base pairs (i.e. 10) is multiplied with length of gap element between two base pairs (i.e. 0.34 nm). BUT, to calculate pitch, the total number of gap elements should be multiplied with length of one gap element, Hence, the length of pitch should be 3.06 nm instead of 3.4 nm.

Welcome to Biology StackExchange! No, you have to include a space around basepair when thinking about one repeating unit. Think about it this way: If one pitch contains 10 bp, then half a pitch contains 5 bp, and the length should be one half of the whole pitch, right? But this isn't compatible with your calculation, because $\frac12 \times 3.06,{\rm nm} = 1.53,{\rm nm} \neq 4\times 0.34,{\rm nm}$. Perhaps it's easier to see why you have to count this way if you include half of space above and below.

@Domen "No, you have to include a space around basepair when thinking about one repeating unit"         Sir, with "space around basepair" do you mean the empty spaces left above bp 1' and below bp 10' (i used ' to show my numbering).

Those aren't empty spaces except in your diagram, they're the continuation of the chain in each direction.

i've tried to answer a related question here that somewhat includes this answer. https://biology.stackexchange.com/questions/112909/calculating-pitch-of-b-dna/113805#113805


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Is there any research on episodic-like memory in reptiles?
I've been studying the area of episodic-like memory in non-human animals and our old reptile cousins seem to be really underrepresented (or not represented at all). Is there any research that I am missing? Anything that would point to reptiles remembering what, where and when of an event? The only papers I could find were related to spatial memory (what & where), like this:
Rapid learning of a spatial memory task in a lacertid lizard (Podarcis liolepis) - by Enrique Font
Also here: @ https://doi.org/10.1016/j.beproc.2019.103963

Have you tried google scholar? if you go trough the papers that cited the one you mention you will get some related research.


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Statistical significance set at $p < 0.05$ or $\alpha = 0.05$?
Obviously, both refer to the same thing. But, which is more correct/more common in biomedical papers? By alpha, I mean alpha level (Also see one). (And, should it be $p < 0.05$ or $p = 0.05$ if it's not alpha?)

Definitely α; α is the threshold you set, p is the probability you measure, you compare p to α. If α = 0.05, then you consider p < 0.05 significant. See e.g. https://en.m.wikipedia.org/wiki/P-value
I wouldn't necessarily let a majority of biomedical papers sway you one way or another with statistics, because the stats in so many of those papers are sub-ideal in that area. Biologists and physicians do not get enough statistical training relative to its importance, especially as you go back decade by decade.
I don't think confusion with other distributional parameters is plausible if you are describing a threshold for statistical significance - there is only one meaning in that context.

Definitely p = 0.05, this is because α is a parameter, e.g. in the gamma distribution and therefore avoids any confusion. The gamma distribution models over-dispersion for example mutation rate heterogeneity across a gene.
α = 0.05 is a bit low for α in e.g. a gamma distribution but it is certainly possible, usually its >0.1.

I think we are talking about a different alpha. I mean this: https://www.google.com/search?q=alpha+level

Indeed but it avoids any confusion.


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Start codon and 5' codon
Here it says:

For amino acid-based systems, the start codon of the mature protein is
labeled codon 1. The codon 5' to this is numbered -1.

So, I assumed the START codon is either -1 or 0.
But, when I align sequences on the HLA-A gene, both amino acids at positions -1 and 0, aren't a methionine which I thought was the only start codon possible.

There is however a Methionine at position -24.
Am I missing something? What are these amino acids numbered from -24 to 0. I've heard it's the "signal peptide", but cannot find any source about it, and I'm confused about the help page of this website. Any help is appreciated.

Beware, the manual says the start codon of the mature protein is labeled codon 1. Proteins undergo post-translational modifications and processing during which chemical modifications or protein cleavages happen. HLA-A has a signal peptide (see UniProt) which is 24 aa long. The term mature protein denotes the protein after processing, namely after the removal of signal peptide.

Thanks for the clarification. So is the start codon of the mature protein not necessarily a Methionine?

Correct. Protein is synthesized in its nascent form with methionine as the first amino acid. Later, the signal peptide is cleaved away, and therefore some other amino acid becomes the first one in the mature protein.

I understand, so almost all proteins are synthesized in their nascent form with methionine as their first amino acid but some have a signal peptide that is later cleaved away?


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Found these bugs on a sticker in an old shoe box. What are they?

What are these bugs? I found them in an old shoe box on a sticker that was sitting on the carpet.

Hi, those pictures are really blurry. It would be helpful if you tried to take better photos, also with a scale to have a better understanding of their size.

I updated the photos, hopefully that is easier to see. Thank you!


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What's the significance of DNA replication (S phase) before Meiosis?
From what I'm able to understand, Meiosis should end up with haploid cells with chromosomes having single chromatids (I don't know why it's necessary, but alright)
I understand that meiosis has a slightly different interphase than in case of mitosis, with basically no G₂ phase.
My question is then, why does the DNA / Chromosome replicate / duplicate before meiosis?
If DNA doesn't replicate before meiosis (during S phase of interphase), meiosis 1 can still occur. But this time we'll directly end up with haploid cells with single chromatid chromosomes.
Does double division in meiosis has a biological significance? Does it ensure better (less erroneous) division or something similar?
Possible (Unhelpful) duplicate questions:

Why there is replication of DNA before meiosis?
What is the purpose of two cell divisions in meiosis?


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What is this insect (or spider)?
Location: Vienna, Austria
Date: July 18th
Daytime: around 5pm
Begaviours: none, unfortunately. Just walking
I take these to be six legs and some kind of appendices. But I am not entirely sure.

This is a true bug larvae - thus, an insect - you correctly counted six legs :)
Characteristics of true bug larvae are the combination of the rostrum, the wing pockets and the dorsal scent glands (although the latter both are hard to see on the photos).
I suspect the specimen to be a member of the family Coreidae as it exhibits typical (larval) characteristics of this family: a rhomb shaped body and long legs and antenna. Also spines are a common feature of this family.
Although a bit hard to tell from the photos, I find it to be most similar to Coreus marginatus, a common species in Central Europe.
Comparing two of the specimen's photos with those showing C. marginatus from a similar perspective, shows that - besides the general habitus and coloration - the number and position of the dorsal spines (2 x 2 central and 2 x 3 lateral) match well.
Also, the antenna are relatively large in comparison to the body (compare also this photo).
In comparison, a Leptoglossus occidentalis larvae (as this species was suggested in another answer) would have a generally more elongated habitus with thinner antennae. And, most strikingly, L. occidentalis larvae have a more-than-body-long rostrum.
For comparison, here are more photos of...

European Coreidae here or here
C. marginatus larvae
L. occidentalis larvae

Image source (in reading direction):
B. Schoenmakers CC-BY-3.0 |
B. Schoenmakers CC-BY-3.0 |
B. Schoenmakers CC-BY-3.0 |
Slimguy CC-BY-4.0

I think it could be this animal. It is the nymph of Leptoglossus occidentalis, the Western Conifer Seed Bug.
It fits in terms of size and the greenish-brown colour of the abdomen. Also the position of the spikes and the long antennae are a match, eventhough the antenna look a bit more flat and broad in your picture and less hairy.
This invasive species is originally from the US. It was first recorded in Vienna in 2006.