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Where does nitrogen go or come from as its partial pressure in different parts of the lungs decreases or increases?
Here's a table from Guyton and Hall Textbook of Medical Physiology showing the partial pressures of gases in different types of air:

We can see that as the partial pressures of some gases decrease or increase, the partial pressures of the other gases increase or decrease, respectively. Let's focus on nitrogen. The PN2 in humidified air is lower than in atmospheric air because the PH2O in humidified air is higher (I'm not sure if the word "because" is correct here, but I guess it is). The PN2 in alveolar air is higher than in humidified air because the PO2 in alveolar air is lower.
Since partial pressure is proportional to concentration, I believe a gas should go somewhere for its partial pressure to decrease or come from somewhere for its partial pressure to increase.
Where do nitrogen molecules go or come from in the two cases I described? As the PN2 in humidified air decreases, where do the nitrogen molecules that cause this decrease go? As the PN2 in alveolar air increases, where do the additional nitrogen molecules that cause this increase come from?
I'm asking only about nitrogen because I think the reasons should be similar for the other gases (i.e., the PO2 in humidified air and atmospheric air) or are clear (i.e., diffusion into and from the blood for O2 and CO2).

You can't just look at nitrogen and how its concentration changes. Their concentrations all rely on each other. Nitrogen is inert; in your examples it doesn't go anywhere. The partial pressure of N decreases  in humidified air because more water is in the air, making the percent nitrogen fall. The N in inspired and expired air is basically unchanged. We add a bit of moisture to exhaled air.

You can get an answer in the accompanying text in Guyton & Hall that describes your table. It says: "Because the total pressure in the alveoli cannot rise to more than the atmospheric pressure (760 mm Hg at sea level), this water vapor simply dilutes all the other gases in the inspired air. Table 40-1 also shows that humidification of the air dilutes the oxygen partial pressure at sea level from an average of 159 mm Hg in atmospheric air to 149 mm Hg in the humidified air, and it dilutes the nitrogen partial pressure from 597 to 563 mm Hg."

@anongoodnurse If nitrogen didn't go anywhere, wouldn't that increase the total pressure? For example, imagine a container that contains only gaseous nitrogen. This nitrogen creates some pressure. If we added some water molecules, these molecules would too create some pressure. If we didn't remove some of the nitrogen, I think the total pressure would increase, since it would be a sum of the pressures created by the nitrogen and water.

@Domen I saw this explanation and a similar one in Costanzo's textbook, but I didn't understand both of them, unfortunately. In the case of liquids, when you dilute something with water, you increase the volume of the solution. This makes me think the volume of the gas in the lungs should also increase. Sorry, I'm not very good at pure physics.

@Domen I think you should write that as an answer.

@athlonusm Your two comments are related: the way it wouldn't affect the total pressure would be by affecting volume instead. In this case you really shouldn't worry about pressure at all though, just assume it's always the same; it's forced to be the same by the measurement approach, anyways.

@athlonusm - This isn't as much about physics as about straight math, or if you must, algebra. For example, if you have a 900 cc of nitrogen in a big floppy balloon (so, 100%) and you add 100 cc of water. The amount of nitrogen doesn't change, i.e. the N didn't go anywhere, but its concentration dropped to 90%, and H20 goes from 0% to 10%. (<-- that's a tree). You're looking at a tree, when you should be looking at the forest (all the components and how they relate to each other causing percentages of each to change when one component changes.)


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What is the connection between LDL, liver, and saturated fat?
I've been trying to learn about cholesterol, lipoproteins, and fats, but unfortunately, there is an ocean of confusing information on the internet. I don't have any solid background in biology, so this is kind of making my head spin.
I know that Low Density Lipoprotein (LDL) and High Density Lipoprotein (HDL) are carriers of cholesterol in blood. LDL carries cholesterol from the liver to the tissues while HDL takes cholesterol from the blood to the liver.
How does saturated fat increase the cholesterol level in the blood?
Some sites explain that saturated fat affects the LDL receptors on the liver, which inhibits the liver's ability to receive and break down excess cholesterol in the blood. But LDL is supposed to carry cholesterol from the liver to other tissues. So why should the liver have LDL receptors in the first place? If saturated fat affected the HDL receptors on the liver, then that would have made sense, right? But many sites say saturated fat increases LDL cholesterol in the blood.
What is it that I'm missing here?

Welcome to Biology.SE! Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, each question should be posted separately — this improves the chances that you will get answers for each question and makes the answers more accessible for future users. ——— Please also tell us where you've looked for answers — for example by providing citations (to reliable sources) for the background you've provided.

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

I can’t. General normal fat metabolism involving liver, adipose and other tissues, and triglyceride synthesis and transport as lipoproteins is more than enough for me. How diet might distort that and affect cholesterol deposition in arteries is not something I know anything about, and is difficult because it is observational rather than a question of fundamental mechanistic design. Cave men didn’t suffer from arteriosclerosis. You might try asking on SE Medical Sciences.

I think I understand the picture somewhat now. The liver synthesizes both VLDL and cholesterol. Cholesterol is packed (along with triglycerides) in VLDL and send to tissues through the blood. As tissues absorb triglycerides from the VLDL, it changes to IDL and then to LDL. LDL continues to transport cholesterol to tissues across the body. But when there is excess LDL cholesterol in the blood, it comes back and is received by the LDL receptors in the liver. Meanwhile, the liver also synthesizes another lipoprotein called HDL. HDL travels to the cells across the body and receive excess cholesterol from the peripheral tissues, and take it back to the liver for breaking it down.

Welcome Curiouser. Whilst you may be correct (personally, I'm not familiar with this), your answer could be improved by references to  a reliable source which confirms your explanation. Answers without references risk being downvoted or deleted in extreme cases.

Saturated fat does not increase serum cholesterol. I know you can find lots of studies that say otherwise, but its basically a myth that has been propagated since the 1960s, like claiming that the human genome has 24 chromosomes (yes they used to say that). All of the studies I have seen claiming such things are "observational" studies with no controls. A lot of these studies are just BS generated by nutritionists trying to justify why you shouldn't eat eggs and other crazy things.
The intestines are impervious to sterols which have to be digested into more fundamental packages such as phospholipids before they can be transported across that boundary. Phospholipids are not processed by the liver, nor are they a component of serum cholesterol. Virtually all serum cholesterol is directly synthesized in the liver from fructose. This is easily proven (and has been proven) by guinea pig studies. If you feed a guinea pig a carbohydrate free diet which is heavy in saturated fats, their serum cholesterol drops to very low levels. Conversely, if you feed a guinea pig a high-fructose diet, they will develop high serum cholesterol levels. This is strong experimental evidence that serum cholesterol is almost purely dependent on carbohydrates and on fructose in particular (a carbohydrate derivative).

Please add references supporting your assertions. As currently written this comes across as excessively opinionated. In addition, I'm confused by you claiming that sterols are "digested" into phospholipids — this suggests that phospholipids are a component of sterols, which is not correct. Finally, since guinea pigs are not humans, it would be great if you could indicate why those results are relevant (with citations).

@tyersome https://onlinelibrary.wiley.com/doi/full/10.1111/eci.12161 To claim that guinea pigs metabolize dietary cholesterol in a different way than humans or other mammals I think is a specious argument.

I think if you were to reread my comment you will see I made no such claim — I am aware that there is evidence supporting guinea pigs being a good model for human cholesterol metabolism, but that is not known to everyone. I'm trying to make constructive suggestions — please respond by making edits to your post rather than posting links in the comments.

your answer is contrary to the most reliable hospitals, medical universities and dietary associations in the world such as the harvard heath school, mayo clinic and the American Heart Association. But your criticism of observational studies as evidence is spot on, a lot of laymen have been misguided by these studies' findings

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What is the physical dimension of international unit (IU)?
I was skimming through a study [mRNA-based COVID-19 vaccine boosters induce neutralizing immunity against SARS-CoV-2 Omicron variant, page 6, figure 3(A)] on vaccine and I came across the international unit ($\text{IU}$). From what I read, $\text{IU}$ measures the amount of substance adjusted according to biological activity observed. [I studied maths in uni. I only learnt a bit of physics/chemistry/biology in secondary school.]
In dimensional analysis, all units are assigned a physical dimension which is expressed in term of length ($\text{L}$), mass ($\text{M}$) and time ($\text{T}$). For examples, gram has dimension $[\text{g}] = \text{M}$, mole is dimensionless, millilitre has dimension $[\text{mL}] = \text{L}^3$ and molar has dimension $[\text{M}] = \text{L}^{-3}$.
What is the physical dimension of $\text{IU}$?

@ARogueAnt. The $y$-axis of the graph has the label Pseudovirus neutralization (IU/mL). I don't know that it varies according to the substance measured. It's something new to me.

Please link the study

@acvill mRNA-based COVID-19 vaccine boosters induce neutralizing immunity against SARS-CoV-2 Omicron variant, page 6, figure 3(A)

It depends totally on the substance. IUs are decided upon by committee in order to be able to compare formulations.

As you have identified it yourself, the $\rm IU$ is a measure for the "effective" amount of substance, which is one of the seven base quantities in the International System of Quantities. Therefore, in your notation, $[{\rm IU}] = {\mathsf N}$.

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Why does water damage the lungs but amniotic fluid doesn't?
I've read that near-drowning causes lung damage due to water inhalation. How come this is not the case with amniotic fluid? Taking this further, would lukewarm purified oxygenated water cause damage (if hypothetically there was no CO2 buildup in the blood)? Is it the pressure differential and/or movement caused by there being a mix of both liquid and gas inside the lungs at the same time that causes the damage to the lung and alveoli (the motion tearing or crushing alveoli perhaps)? Is it an issue of consistency or temperature? Meaning, if all the air in the respiratory system was instantly changed to oxygenated purified water, would it still cause damage if the water was not the right thickness or temperature? Given the right fluid concoction, is it theoretically possible for full molecular exchange to occur indefinitely in a liquid inside the lungs (both oxygen and CO2)? Can I hypothetically become Aquariumman or a Hairy Porter munching on quality Gillyweed?
I'm very sorry for the long list of queries, but I've searched extensively for the answers to these questions, and yet still haven't found a more detailed answer than what amounts to 'it is normal and healthy for fetuses to circulate amniotic fluid through their lungs, getting water in your lungs is neither of those things, please go see a doctor'. And so that's what I'm hoping to do here. I'd greatly appreciate a more detailed answer from someone who specializes in the respiratory system (being a fan of fishy Superheroes or dodgy Wizards is appreciated but not required). A heartfelt thank you to all who answer my questions, and may everyone who is reading this have many a wonderful weeks ahead! :)

The level of saltiness is critical. Look up Isotonic, compare with hypotonic

You already know that amniotic fluid isn't water. So how is it different? It's an interesting fluid. Tell us what you've learned about how it's different from water. There is no Neonatologist or Pulmonologist here, and if there was, they would not answer so basic a question without evidence (not just guesses or your claim) of trying to find a solution to your question This site requires some research to be shown (hover over the down vote button; it's also a close vote reason.)

Part 1: For proof that my claims of having researched aren't bogus, I shall answer off the top of my head (I've only just noticed the comments). I know that fetal lung fluid is very similar to, and formed from, amniotic fluid (though they're not completely the same), since it has more chlorine (released by the lungs I believe) which is why I indicated purified water in my question. Amniotic fluid itself also has many things in it (enzymes and proteins and such) that facilitates cell growth, which is why I asked whether a special concoction could facilitate molecular exchange. Part 2 cont.

Part 2: I know that some sort of mechanism regulates and maintains the pressure in the fluid in the lungs by releasing the excess, hence my question of whether pressure was an issue. I also know that the sacs that the alveoli are in are very delicate, hence my question of whether the movement could cause damage. As indicated by Wrangler, I know that the amniotic fluid is salty to facilitate chemical reactions, but not so salty as to disrupt cell function. The saltiness also plays a big part in getting the fetal lung fluid out of the lungs just before delivery I believe. Part 3 cont.

Part 3: I have a Fin Econ background and have 0 formalised education in Bio or Chem after grade 10, since I chose physics for my grade 11-12 IBDP. This means all I know about biology after that comes from self research into curious topics in my free time from studying in Uni. This unfortunately severely restricts my ability to understand Bio papers/articles in as much detail as I'd like in a reasonably timely manner. I'm also curious about absolutely everything, not just biology, hence I find myself with a little knowledge about lots of things, rather than in-depth for some, except finance. :)

As you stated, fetal lung fluid is not the same as amniotic fluid, and the direction of fluid flow is from the fetal lung into amniotic fluid/fetal GI tract, not amniotic fluid into fetal lungs. Fetal lung fluid is secreted bu the fetus' developing lungs to keep them expanded. Does this change your question(s) at all?  IOW, amniotic fluid doesn't normally reach fetal alveoli. As to O2 exchange with the right solution, yes, it can occur, but there needs to be a mechanism to circulate the fluid such that O2 is continuously introduced and CO2 removed.

Part 1: Thank you immensely Anongoodnurse for your answer and for such quick replies! However, I was completely certain that fetuses did indeed inhale and exhale amniotic fluid, and that it was only changed (not secreted) into fetal lung fluid by the lungs releasing certain chemicals (such as chlorine) into the amniotic fluid that was being inhaled from around the baby. And I was also absolutely certain that the alveoli/air-sacs were indeed exposed to the fluid as well. Part 2 cont.

Part 2: In fact, I found myself to be so darned certain of these two views that I decided to go back and research them again to see if my memory was failing me and I'd somehow started getting early-onset dementia at 23! (:D) Here're the results of my (admittedly quick and of shallow depth) reconducted research: The Children's Minnesota web page at ChildrensMN.org states that "The unborn baby “breathes” the fluid into the lungs, where it pushes open the air sacs and stimulates them to grow". Part 3 cont.

Part 3: Furthermore, WhatToExpect.com states that "Muscle contractions bring amniotic fluid in and out of the lungs" and that "It may even support the development of alveoli, tiny air sacs on the lungs". This view is supported by many different types of reputable sources as well. For instance, Medical News Today states in a news article that "Developing babies are surrounded by amniotic fluid, and their lungs are filled with this fluid... babies begin taking “practice” breaths. But these breaths... only refill the lungs with more amniotic fluid". Part 4 cont.

Part 4: And also, BabyCenter.com is a parents' help website that states "26 weeks: Baby begins inhaling and exhaling amniotic fluid". These views are even supported by Bio education websites. For example, OpenTextBC.ca is a Canadian education website for British Columbia, and it states that "Fetal breathing movements involve muscle contractions that cause the inhalation of amniotic fluid and exhalation of the same fluid". And another Edu-site called LumenLearning.com has a course that states that "the fetus “practices” breathing by inhaling amniotic fluid in utero".

N.B. Not everything you read on the internet is true.

@ShaptarshiJoarder you should [edit] your question to add all necessary details instead of stating them in comments. Make your question readable, understandable, and self contained so that any user who has a similar question does not need to scroll through comments.

@PolypipeWrangler - Now that few people are looking at this question, it doesn't matter if non-fatal drowning occurs in salt or fresh water, so isotonicity isn't really the issue. People tolerate small amounts of inhaled fluids well enough, but larger amounts can wash away surfactant, and causes shunting.

Thanks for new info @anongoodnurse; in response I read the wikipedia article on pulmonary shunt.

TL;DR: Fetal lungs are filled with lung fluid produced by lung epithelial cells, not amniotic fluid. Amniotic fluid aspiration in utero can be catastrophic. So your question is based on an inaccuracy.

Why does water damage the lungs but amniotic fluid doesn't?

My question back to you is, how do you know that amniotic fluid isn't harmful to fetal lungs?
There is a common misconception that fetal lungs are filled with amniotic fluid. In fact, it's so common that even many physicians mistakenly believe this.
From a book chapter titled Amniotic Fluid: Physiology and Assessment published in 2008, this misconception is discussed briefly:

Because amniotic fluid is more hypotonic than fetal plasma, it is postulated that exposure of amniotic fluid to the fetal alveolar capillary bed results in net movement of water from the amniotic cavity into the fetus. Although radioisotopes have been discovered in fetal lungs after intra-amniotic instillation, this quantity has been small and inconsistent,2 leading investigators to question the actual contribution of fetal respiration to amniotic fluid removal. In fact, surface-active phospholipids originating from the fetal alveoli are found in the amniotic cavity, leading to suggestions that the fetal lungs may actually be a net contributor to amniotic fluid volume.

This, in 2008, despite the fact that fetal lung fluid was shown to be produced by fetal lungs in 1948. (That paper, unfortunately, is unavailable.) By 2018, that misconception was corrected in medical textbooks, e.g. Avery's Diseases of the Newborn, Tenth Edition (2018) in which can be found the following:

Fetal lung fluid is a product of the epithelial lining of the developing lung (Wilson et al., 2007; Helve et al., 2009), averaging 4–6 mL/kg per hour. The resistance imparted by laryngeal abduction results in fluid accumulation to a total volume of 20–30 mL/kg during gestation, which generates an end-expiratory pressure of approximately 2–4 cmH2O. The composition of fetal lung fluid is distinct from that of both amniotic fluid and plasma, as illustrated in Table 42.2.

More succinctly:

During fetal life the lung develops as a liquid-filled organ. This liquid is produced by the fetal lung and leaves via the trachea from where it is either swallowed or enters the amniotic sac. Fetal lung liquid plays a crucial role in the growth and development of the lungs by maintaining them in a distended state.

Fetal lungs produce fluid that keeps the lungs expanded and developing normally. Though there is evidence of diaphragmatic activity as early as 12 weeks gestation, amniotic fluid does not enter the lung with these diaphragmatic movements because the fetal larynx closes during "inhalation" preventing the entrance of amniotic fluid. When it relaxes, a small amount of lung fluid escapes the trachea, some of which is swallowed, and the rest contributes to amniotic fluid.

Fetal breathing movements contribute to the efflux of lung fluid into the AF, but about half of the effluent is swallowed rather than entering the AF.

Amniotic fluid aspiration in utero can cause death because amniotic fluid is loaded with keratinized epithelial cells from the baby's skin and other things that can injure the lungs.
Before the baby's first breath, all the fetal lung fluid is quickly absorbed by the lungs into the interstitial space, allowing for air to enter the lungs.
Edited to add: You wanted a specialist to answer this question.  Well, here is a letter to the editor of Pediatric Pulmonology, a journal about the lungs you referred to in your question, from a Neonatologist,  entitled Fetal lung fluid: Not the same as amniotic fluid. In it, the Neonatologist corrects a mistake by another Neonatologist in one of the articles in this specialty journal! So it shouldn't be a surprise that so many others get it wrong, too.
An exerpt:

However, I wanted to bring attention to a statement in the introduction where the author states that the “preterm infants’ lungs are filled with amniotic fluid”. This is not accurate and appears to be a common misconception, particularly among medical students and junior residents despite recognition of fetal lung fluid as being a separate entity from the amniotic fluid as originally described in 1948 by Jost and Policard.

Thank you so much for this amazingly in-depth and easy-to-understand answer! Finally one of my endless number of curiosities have been quenched. Hope you and your family have a most fantastic week ahead! :)

@ShaptarshiJoarder - Feel free to hit me with another. I learned a fair bit here, too. :)

As soon as I have another biology curiosity that my research can't seem to answer, I'll be sure to do so! It seems fishy wizards shall remain in fiction for now.


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Can mosquitoes be attracted by our voice?
In the dark, mosquitoes use CO2 to find blood host like us. However, 1) they are known to have excellent auditory organs (ref1, ref2) and 2) sound can be heard from any directions, contrary to odors which follow the wind direction.
Do mosquitoes use our voice to find us?

Comments are not for extended discussion; this conversation has been moved to chat.

Keep in mind that mosquitoes main food is flower nectar.  Only the females bite for blood and only to feed their eggs.  Humans are not a primary source for such blood so even though they can hear human speech, singling us out specifically would not be evolutionarily advantageous since they can also get blood from many other sources much more easily than from humans.  We get bit as a crime of opportunity, but we're not a consequential source of blood for mosquitoes.  We're also rather more dangerous to bite than other animals because we're quite good at striking back.

@J... - While some of what you say is true, there are anthropophilic mosquitoes - human loving - which prefer human hosts, e.g. Anopheles species, which transmit diseases such as malaria, and some which use humans exclusively.

@anongoodnurse Well, TIL!

Attraction to voice would explain why my significant other is often bitten by mosquitos, and myself far less.

@dotancohen More likely acetone, lactic acid, and estradiol.

Mosquitoes can hear the human voice. If they use human sound to hone in on us as a source of a blood feed is not known at this time, however research into this has just begun. This is especially useful research because of anthropophilic mosquitoes - human loving - which prefer human hosts, e.g. Anopheles species, which transmit diseases such as malaria, and some which use humans exclusively. If disease can be prevented by understanding the role of voice in attracting anthropophilic mosquitoes, it's well worth studying (even if only to develop mosquito traps.).
Until relatively recently, it was thought that a mosquito's acoustic abilities were very limited, and used mainly to detect the correct species and gender to mate with, as there are over 3000 species of mosquito (176+ in the US alone, the CDC states over 200), and they need to be able to determine which other mosquito would be a suitable mate. Most of the research honing in on their acoustic abilities has centered on males and their ability to detect females, e.g. in order to build traps to attract males to determine the efficacy of sterile male release into the wild,  induce sterility in males, capturing and manipulating males genetically to introduce a dominant lethal gene, etc., hopefully limiting the population of those most deadly to humans without harming the environment. From this 2021 paper:

Early studies focused on mate-seeking male mosquito attraction to female wing-beats (Kahn and Offenhauser 1949), and female mosquito responses to male wing-beat frequencies in the laboratory and field (Ikeshoji 1981, Ikeshoji and Ogawa 1988). The fundamental wing-beat frequencies of male and female mosquitoes can vary by species (Table 2), so there has been interest in their use for surveillance and control efforts.

In the last 15 years, however, after studies emerged that some blood-feeding midges focused on host (or prey, if you prefer) vocalizations, some of that attention has turned to the acoustic capabilities of female mosquitoes. Multiple studies have shown that female mosquitoes known to feed on various species of frogs were attracted to traps using recordings of those frogs, and a few have shown the same in attraction of mosquitoes that feed on birds as hosts. Studies have shown that femaqle mosquitoes can detect sounds within the human vocal range at 10 meters away, and males even further (though male mosquitoes do not feed on blood.) But as of this year, no studies have been completed with regard to the response of female mosquitoes to human voive.

"Studies have shown that femaqle mosquitoes can detect sounds within the human vocal range at 10 meters away".
If you refer to Menda et al 2019, it seems that they exposed a male mosquito (not a female) to sound levels of 70 dB SPL located at 10m away from the loudspeaker (which is far louder than normal-speech at 10m away). Or was you referring to another study?

@Noil - OOf, I read a number of papers, I'm not sure which one(s) I read that in. But it's the hot thing to study now, so I saw that claim several times. I'll  have a look when I get the time again, Thanks for asking. :)

"a few have shown the same in attraction of mosquitoes that feed on birds as hosts" Could you give the sources for this please?

I@Noil - I answered this question a year and a half ago. Don't you think asking me to revisit my research now is a little much?

no worry, it was just in case you knew, I'd be interested about it

@Noil - Thanks for understanding. At my age, when something new comes into my memory, something relatively unimportant is tossed... :p

Mosquitos can certainly hear in the range of normal human speech. They are sensitive to the range of around 150-500Hz, and typical human speech is between 100-300Hz depending on your age and sex (DOI: 10.1016/j.cub.2019.01.026). Whether they use that auditory capability to zero in on humans, I do not know (and could find no indication that this is something known in the literature). I do know that the most important sense for mosquitos to find prey is olfaction.
The frequency sensitivity range surprised me actually. I was expecting the frequencies to be much higher. Some insects like moths are sensitive to ultrasound frequencies which helps them detect bats.
Based on the Göpfert et al. paper you listed, it appears that this hearing range tracks nicely with the sound frequency of mosquito flight. Without knowing really anything about the mosquito literature, I would hypothesize that this is no coincidence. I would guess they use hearing to determine the sex of other mosquitos (males and females produce different flight frequencies) for mating purposes. There is also evidence that their auditory abilities can help them in evasion from predators (DOI: 10.1038/s41598-021-81456-5).


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Does anybody know what sort of fossil this could be?
enter image description here
Found in rural North Dakota. Small rock with black circular indentations.

Welcome to the site. Can you please provide more pictures, with better lighting of the "fossils". It may not be a fossil at all, but rather some sort of inclusion in the rock.  Fossil ID is on-topic for Earth Science SE, but you would need to request migration - don't cross-post!

it looks like marks made by animals living on the stone probably made under water,it is very unlikely to be fossils the rock is rounded most likely when submerged under water.

Thanks guys! Any bit of info helps.


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Species identification: flaky worm
enter image description here
Recently our house got ABSOLUTELY INFESTED with the following creature.
Kindly identify.
Hapitat: damp shadowy regions of our house
Description: The outer flake is probably a shell, the shell is not very soft, not very hard. The smaller ones have really soft shells. I could not photograph it, but the shell houses a really small worm kind of thing that pokes out its head and then graples the wall or something and then pulls it shell to move. Movement speed is pretty small say about 5mm per second at max. The worm was black coloured with pretty undistinct and unclear yellowish rings. The worm thing can produce some spider web kind of thing which makes it stick to walls. I mean it sometimes appears to almost float against the wall/ceiling as it is hanging by its web. The spider web allows it to hang by a couple of millimetres above surface. Multiplies superbly fast like there are 20 new individuals within a day in some of the walls.
My best guess: a pupa of some moth. I spotted some moths flying around it once. Only once, in five to seven years.
enter image description here
[enter image description here
India. A place close to bangladesh. Plains temperature aroung 32 deg celsius in average

Also please do tell how to get rid of these.
Insect inside has no legs. Plus the shell, it appears to have the same colour as the paint of the room. Possibly the flaky shell is made out of the particle of the wall that the insect took up.

It looks reminiscent of Luffia ferchaultella a moth larva - a  lichen eater - but not quite, too flat. I can't find references of that species in India since the 1960s either so I'm not answering but leaving it to the experts to name.

Hmmm.... the species you mentioned does resemble my insect, but my insect is thinner in depth...

I would emphasize that the insect living inside does not have legs... plus there is no lichen in my house

Does this answer your question? What insect is this? (India) See also: this and this. ——— Please note that one part of the research expected of you is that you look for similar questions on this site before posting. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site for details.

@ tyersome yes i could not find these similar answers before thanks for pointing them out


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Advantages of NADP+ dependent Isocitrate Dehydrogenase
I came across a question (Q-5b) that asks:

Isocitrate Dehydrogenase in the [human] TCA cycle is associated with NAD+.
Why does it make good metabolic sense that it should use NADP+? Explain and show why this is so using appropriate structures and reactions.

This interesting paper argues the evolution of NADP-dependent IDH in prokaryotes as an adaptation to the need for growth in acetate. In the case of glucose growth, NADH can be obtained from the oxidative branch of the pentose phosphate pathway; in contrast, for acetate growth, PPP cannot run efficiently and IDH provides the predominant share of NADH. However, this ought to be a really irrelevant reason concerning IDH enzyme in humans since we do not have enzymes like isocitrate lyase etc. to entertain acetate growth!
Standard textbooks in biochemistry (Voet&Voet, Lehninger, et al) do not offer anything relevant except a generic note that NAD+ and NADP+ are respectively favored for oxidative and reductive metabolism. I am unsure about reasoning using this bit of trivia since TCA is an oxidative pathway! Fwiw, a question had been asked in Biology StackE about NADH vs NADPH where the accepted answer restates this.
To conclude, what is the metabolic advantage? Does there exist a way to arrive at the advantage using the fundamentals of biochemistry?

I find the question most ambiguous. The context is presumably human, given the preamble in the exam paper. The first sentence says that ICDH "is associated with" (presumably he means "is specific for") NAD+. The second sentence talks about it making metabolic sense to use NADP+. But it doesn't — only in the cytoplasmic form mutated in tumours, which is not involved in the TCA cycle. I can give an answer to a question on the use of NAD v. NADP in mitochondrion and cytoplasm, but I can't answer a question that appears self-contradictory. How do you understand it? Seems like a typo to me.

Mitochondria also contain an NADP-specific isocitrate dehydrogenase which probably plays no role in the TCA cycle (but not everyone agrees!). See here, for example, one of several seminal papers on this enzyme from the Roberta F Colman group

And, of course, there is also a cytoplasmic NADP-linked isocitrate dehydrogenase. See here, for example

For an interesting take on why there are two pyridine nucleotide cofactors (ie NAD and NADP), see Why NADP? by BT Kaufman, who postulates that " blocking the 2'-position of NAD with a phosphate group, thus yielding NADP, shields a potential pool of pyridine nucleotide cofactor from the drastic effects of ribosylation reactions"


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Why does pancreatin affect the pH of milk?
I just finished a lab for college and I was really intrigued by this. Since we're in a rush to finish the semester on time my professor didn't go into details much she just said something about fatty acids? But I'd like something more in depth because honestly this is the only lab I've liked this semester and it's just fascinating to me. I googled it but it was a whole bunch of other stuff coming up and I want a direct answer on why this happens.
Lab: For the lab, we started out with two test tubes one filled with water and milk and the other with a pancreatin solution and milk. We then added bromothymol blue to each test tube and put it in a warm water bath for 40 minutes then we just recorded our results. We just had to explain what reaction was being used and what would happen with different types of dairy products. For each test tube with the pancreatin solution and milk it changed color usually to orange or yellow, showing that the pH had dropped.
This is NOT for a homework answer I'm genuinely just curious about the mechanics of it all.
Thank you!! :)

Describe the lab a little bit - what did you do, and what did you find?

@MattDMo For the lab we started out with test tubes that we filled with two test tubes one filled with water and milk and the other with a pancreatin solution. We then added bromothymol blue to each test tubes and put it in a warm water bath then we just recorded our results. We just had to explain what reaction was being used and what would happen with different types of dairy products.

@MaximilianPress not really? Sorry but I'd like for something more in detail and most of the responses are people getting mad about it being a homework question.

@wheeinsoup it's true that there are no detailed answers on that question. However, in this community we tend to consider one copy of each question as enough, and the one short answer there probably gives enough information for you to be able to do some research. If you still find something confusing you are very welcome to bring your research and to explain what about it is confusing and we will try to help if we can.

@MaximilianPress okay! thank you for the help :)


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Is raw meat or raw vegetables easier for humans to digest?
Which one is easier for a human digestive system to digest, raw meat or raw vegetables?
I have heard some of my friends who say that raw (or uncooked) meat is easier to digest than raw (or uncooked) vegetables.
It initially sounds absurd to me but then they back their argument with something more logical like, "raw vegetables have cells surrounded by rigid cell walls made primarily out of cellulose which are hard to break by the digestive enzymes".
Are they correct?
Anyway, for simplicity, let's assume on a fine day, a healthy adult eats 50g of raw beef and on another fine day she eats 50g of raw broccoli. Which of the two will she digest faster, provided she didn't eat anything else apart from these foods on those particular days.
My Own Investigation  I tried googling a lot but couldn't find anything that explicitly or even implicitly address my question. Most of the sites (like this one) address "raw food vs cooked food" type questions. However, all of a sudden, I remembered something that I studied almost two years back in my secondary school, class 10th science textbook. I quote the paragraph here,

Access the full chapter here (NCERT Class 10th Science Textbook) and check out 7th line (from top) of the 8th page.
This source further support their (my friends') claim in some manner.

Please clarify what you mean by "easier." Easier as in more mass breakdown, greater absorbing of nutrients, less indigestion,...?

also which vegetable,  all meat is more or less the the same but vegetable covers a huge range of tissue compositions. also almost all herbivores can digest meat, they have to be able to to reabsorb their own dead cells.

it will be wrong to compare human digestion with animals that eat grass(cellulose)and it is not very helpful to compare human digestion with other animals that eat the same diet as us.

@theforestecologist by easier I mean, which one (of equal mass) of the two undergo faster breakdown. And as far as vegetables are concerned, considered a typical mixture of green vegetables that we eat, e.g. cauliflower, cabbage, lettuce, broccoli, etc.

@GauravKumar You should focus on one vegetable. Knowing how well a mix of random vegetables will digest is basically impossible. Maybe stick to comparing broccoli and beef, for example.

@user438383 fine, let's stick to beef and broccoli!


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Stimulus currents and neuronal responses
As I understand it, if a subthreshold current of unlimited duration is injected in a neuron, a passive response is observed, like an RC circuit. The membrane potential is depolarized by some arbitrary amount, before gradually stabilizing due to more and more current flowing through the resistive branch of the circuit.
So yesterday, I was looking at some HH simulators when I noticed that increasing the duration of a normally subthreshold current pulse would allow it to depolarize the membrane to threshold. How is that? Can someone please point out the error in my logic here?
Also to clarify: I am not familiar with the dynamics of the HH model, so please take it as such.

If you inject a current into a model cell with no active components (no voltage-gated channels), you'll see a capacitive response, because that's basically all you have: the membrane acts like a capacitor in parallel with a resistor. Adding a current charges the capacitor and you have an "exponential decay"-shaped change towards a new equilibrium potential.
When you stop injecting current, you'll again have an "exponential decay"-style return to the baseline.
However, the HH model includes active conductances: voltage-gated channels that change state according to voltage. "Action potential" is the name given to a positive-feedback opening of sodium channels: voltages more positive than rest open some channels, which open additional channels, etc. "Threshold" refers to a voltage that triggers a full positive-feedback activation of these channels. Sometimes it's stated to be a particular voltage, but that's not really true; threshold depends on the whole state of the system: voltage and state of all the gates of different channel types.
However, any depolarization will open some voltage-gated channels beyond those open at rest, it's just that up until threshold there aren't enough open to trigger the positive feedback. The reason is that voltage-gated sodium channels don't just open and close, they also inactivate. In the HH model, this is represented by the "h" gate.
If you inject a brief positive current, you'll open some channels and get a little "bump" in the voltage afterwards that then returns to baseline as those channels close/inactivate. If you inject a longer current, you'll open a few more channels and also the "bump" from the open channels will sum with your injected current. If you're right around threshold, that could cause you to exceed the threshold for positive feedback and therefore an action potential.
Though the question is different, a lot of this same reasoning is found in my answer to another question here: Hodgkin huxley neuron not spiking consistently for currents greater than threshold?

Thank you for your prompt answer! I think I get it now. Can you just allow me one more question? It’s been bothering me a bit!

It goes like this: a stimulus current, at the beginning of an AP, depolarizes the membrane towards threshold right? For some reason textbooks always pretend like they don’t exist once the membrane reaches threshold and an action potential fires. So let’s assume that the stimulus current is on, for the whole duration of the action potential. My question is: would that change any of the AP’s characters? For example, increase its amplitude or duration? The one with amplitude specially resonates with me, as I imagine that the current would depolarize the membrane all the time while it’s flowing.

@CalyxOfHelp Happy to answer if you post as a separate question. Would be ideal if you quoted from your textbook or another citable source, and take some steps to think about what the answer might be and describe your thinking (sort of "show your work"). That'll help me write an answer that specifically addresses the gaps you have.

Ok, I'll try to write it soon, thank you!


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Contextual Fear Conditioning
I've been studying memory and I've come along an interesting experiment, where a rat is placed in an environment (context) and shocked, leading to fear conditioning with the conditioned stimulus being the context and the unconditioned stimulus being the shock.
After that, the "cell assembly" formed representing the memory of the environment is stimulated, and the rat freezes as a learned response to the environment.
I'm interested in the mechanism by which activating the context cell assembly causes freezing, and I have 3 ideas as to how that may occur:

The context memory activates the amygdala directly and thus activation of the context memory activates the amygdala
There are 2 memory representations: one for the context in the hippocampus and one for the shock memory in the amygdala, and both are linked together, so activating the context memory activates the shock memory
Both the context and shock are encoded in one cell assembly, and activation of that cell assembly leads to activation of the amygdala

What are your thoughts? Regardless of my ideas, is there a specific known mechanism for this process, or is it still uncertain?
Any insights or clarifications are highly anppreciated! And of course feel free to correct any mistakes I may have made here.
Thanks in advance!

I'm sorry if I may have confused you with using engram! And yes I agree the presence of a shock memory is to be expected. What I find interesting is the proposed interaction of both the shock and context memories. To be honest I was thinking about this question but I recently stumbled across the 2 memories idea so I was pretty excited but uncertain, and so I felt like the input of someone with more knowledge than me in the field would help.

And regarding "engram", do you think there is another better term to use? Perhaps cell assembly, ensemble, or just a memory?

I'm not fully sure I understood but I think the mechanism you're looking for could be related to pattern separation in the hippocampal neurons? Maybe formulating the question in a more specific way would help.

Ok, I'll try to rephrase it. Thanks for your feedback!


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Identification of Mold / Fungus
I am working with some old plaster powder, and a few days after it set (mixed with water), I found that pink mold / fungus appears to be growing on it. See attached photo.
Please help me identify what type of mold this is and if it is dangerous to my health.
Thank you.

Welcome to SE Biology. Personal medical questions are off-topic here..  It would be useful to include your geographic location.


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Can disk diffuson be used, without diluting a broth culture to match a 0.5 McFarland turbidity standard?
In this video, there doesn't seem to be a process of diluting the broth. I'm not looking for extremely accurate test results, all I need is to see if a particular colony is susceptible to the antibiotic. Since it's not a lab project or anything, I only need a Yes or No answer. Does that mean broth dilution can be substituted by making a good lawn? Can I just inoculate my agar that simply?

It depends on what you mean by "susceptible" for the question that you're asking. Fresh broth cultures will likely give you a good lawn, but if you aren't doing anything to standardize the innoculum, it's not really comparable to anything else when you make your determination. So, if you do end up seeing a zone of inhibition, you won't really have any idea if it's actually suceptible in the context of clinical relevance. For that, you'd check a table of clinical breakpoints for that organism, which are determined using standardized protocols most likely involving a McFarland standard. If you look through the linked table of breakpoints, you'll find that some organisms can have a fairly large ZOI diameter and still be considered resistant.
Another consideration is spontaneus plasmid loss. In my experience, passaging a colony into a broth culture overnight is a great way to cure plasmids from their host, plasmids that may carry genes which would otherwise make your isolate resistant to antibiotics. For that reason alone, I think you're better off using some kind of pseudo-McFarland procedure than broth cultures. If you don't have a standard, and don't want to buy one, just pick some colony and mix it up in a mL or so of sterile saline solution until it's a little more turbid than the unadulterated saline solution and make the lawn with that (looking up pictures of the different standards online will probably get you in the ballpark, which is really all the McFarland standard method is anyway).


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What is the difference between "ecological succession" and the term "stage of regeneration", is there a difference between them?
In ecology what is the meaning of the term "ecological succession" and the term "stage of regeneration", is there a difference between them?
Edit 1: Perhaps the term "Stage of ecological succession" is in English "ecological succession".

Where do you find the terms used? It's best to provide some context around questions asked here.

This term exists in Portuguese, I don't know if there is another term in English

Though this site is English-only, if you're taking something from Portuguese and taking a literal translation I think it's important to mention that in the question body. You're probably best off following citations in the Portuguese text to others in English, though.

Second other comments. It would be nice to know if you are talking about restoration ecology, forestry, disturbance ecology, or something else. "stage of regeneration" implies some of the above. There may be terminology that's specific to the field or the type of ecosystem.


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Why and who: named some fish "bashers" (African electrofish taxon "stonebasher")
Folklore question for itinerant elephantfish/electrofish experts happening to see this:Is any stonebasher fish named for a behavior related to bashing...
something or some part of its anatomy against some stone, somewhere? Nonbiologist (so far) or certainly not grad level, so I don't know what mailing list archives or other sites are out there here in English-Interwebs-land.
20 minutes of wikipedia, goog, bing etc yields nothing, but maybe one of the tree-of-life type phylogenome-DB sites has a "history, indigenous and non-scientific names, etc." field? I found none on the sites I looked at (2-3 sites) via footnotes on eng.wikipedia.com references.
Probable possible source might be a print publication from around the period of first characterization of whichever one was named first.
Best imaginable answer would be who saw what on what day when, with an excerpt from field notes, but any reference helps!
Thanks for the welcome! I'm off to read the new member's tour

Welcome to the site. Please visit the [help] and take a [tour] for more information about the site. In particular one of the requirements here is that askers make some attempt to answer a question for themselves. Having said that; common names often don't have a source, unlike scientific names which do have an origin/attribution associated with them. Stonebashers seem to be a informal group from a few genera within one family. None of the scientific names have to do with stone.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

Sorry, and thanks. Just falling in love with this "place" via the Mathematics exchanges, and dived in to add sites without taking individual stacks' tours. Now I know to do that first. (unfortunately un-)common courtesy for the win!

l should have mentioned several general Google searches, which I will now repeat with bing, and any bio/zoölogy or hopefully ichth specific search engines or preprint-server searchlinks those of you who happen to see this may chance to recommend.  I know this is only likely to be easy in places where people who know "folklore" of taxonomic adventurers past, tho'!


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What genetic biomarkers are the best place to obtain histopathological images for the purpose of cancer classification?
I am doing a science-fair project and wanted to know where I could obtain the best possible histopathological images of both non-cancerous and cancerous subjects. I would require roughly more than ~50k images.

It sounds like you might be doing some form of image analysis for features followed by statistical analysis, with needs for a dataset that size. I would suggest looking at what others have done in the past and see if you can find their datasets. For example, here is a recent review. One possible resource might be here. All of this would show up in a google search. If those don't answer your question, feel free to edit your question to explain why.

Do you mean biomarkers (e.g. proteins such as CEA or other biologic substances whose expression/appearance or lack thereof correlates with cancer) or databases? I think some clarification to your question could help others answer your question. Also, for 50k+ images, I think it is likely that you need to partner with an institution to obtain this data.

Maximillian, are you sure the resources of cancer imaging archives that you sent me is trustable? Because it is asking for access to transfer files to and from my computer. Otherwise, these are some really good images for my project and will most likely help me succeed.

The grammar in the title of the question here doesn't make sense to me. "Genetic biomarkers" are not a place. Additionally, "best" depends on some criteria, which are not specified here.

Additionally: At what cancer are you looking? Biomarkers differ widely and are often not very good. Reliable biomarkers for certain cancers are a "one million dollar" question.


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Heat shock proteins in T cells of tumor microenvironment
Analyzing human tumor single-cell RNA sequencing (scRNA-seq) data, I found abundant expression of Heat shock protein (HSP) family genes in T cells. My literature review on "HSPs in T cells" brought a lot of papers. But all those papers are talking about how HSPs in cancer cells suppress anti-tumor immunity through different pathways. I do not particularly see much HSP expression in cancer cells though. Does that mean HSPs expression is not important on T cells or maybe it was not extensively studied from that point of view? Could somebody explain that from biological meaningfulness perspective, please?

Welcome to Biology.SE. I've made a few changes to your post, please check to make sure that I have not accidentally altered your intended meaning. In the future, please make sure you explain all acronyms and abbreviations the first time you use them — they are often ambiguous. Providing links that explain techniques and other relevant source material is also helpful. ——— In addition, can you tell us why your search didn't include "T-cell"? NB: if you are doing "Google" based searches then the "AROUND" operator can be very helpful e.g. "HSP" AROUND(3) T-cell tumor microenvironment ...

... Also, this site works best if you make sure that each post contains a single clear well-focused (narrowly scoped) question — you appear to have more than one question and the last question is both unclear (¶ What is the "that" you want biological meaning for?) and potentially too broad. ——— I encourage you to take the [tour] and consult the [help] starting with [ask] for details — this will help you get up to speed on this site's peculiarities and avoid pitfalls that can lead new users to have a poor experience here.

ok. thank you for the tips! should I ask a new question then?

You're welcome! It is best to [edit] this post so that is a single question and then move any additional questions into separate posts.


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Possible fishbone identification
It's my first post to this forum so I really hope, my question is not misplaced here!
I found this item on the beach La Línea de la Concepción, Spain and it resembles pictures I found of certain spine bones of larger fish. Acutally, I have no idea about any of that and as far as I know, it could be some piece of pottery washed by the sea into this shape.
Interesting is the small "V"-shaped mark. The object is 5.5cm in diameter.
Thx for your helping me identifing this object!

Welcome to Biology.SE. Not an expert, but that is almost certainly not a fish vertebra (try an image search) —  looks like part of a ceramic to me.

agree with Tyresome, the texture is all wrong for a vertebra especially the broken portions, a piece of shell is more likely. bone has a very recognizable porous texture, massive or solid texture like that is either shell or man made.

In addition, the reddish coloration is the result of iron oxide - used in the glaze probably, or possibly iron from the clay. There is also a very clear "V" mark in images 1 and 4 - this has been stamped in. Definitely man-made.

It might be the base of a broken ceramic mug or vase; @bob1 has provided excellent evidence of it's origin. That is a maker's mark (I used to throw pottery before the pandemic and makers marks were required to identify which piece of pottery belonged to whom coming out of the community kiln.)

This is definitely man-made. It has none of the features of a natural (biological) product and several features of man-made.
First - it has impressions on a smooth surface. In nature, smooth surfaces such as the interface between bones tend to be completely smooth, with no impressions or shapes that might cause friction. This has two features that appear man-made - the "V" which appears stamped in and might help an expert identify where, and who (company) made this. On the obverse (image 2) of the V surface are two shapes that appear like blobs or holes (at the "10" and "1" positions; if the object were a clock). I suspect that these are from the manufacture and that this object is made using a ceramic method known as slip-casting, which is where liquid clay (slip) is injected into a mold and allowed to set before firing. This technique produces a form of stoneware which is cheap and highly reproducible, so it is used for most ceramics these days. If you have a mug or plate handy - have a look on the bottom, you'll likely find similar shapes to those on this object (on my mugs it tends to be the bottom of the handle often smoothed a bit). This is where the slip has been injected into the mold.
Second - The reddish coloration on the surface is highly likely to be iron oxide. This could come from two sources in man-made objects. One of these sources is a glaze. In ceramics glazes are often used to create smooth, impermeable surfaces and are frequently made with metal oxides, but this would create a more even surface coloration, so I suspect that it is iron oxide present in the clay from which this was cast. On this object, most of the glaze has worn off, but you can still see the residue inside the "V" mark, which is shiny. This is a clear glaze making it likely to be a lead-glaze. Lead glazes are very commonly used on ceramics for their clear and shiny effect.
Third - this has fracture patterns consistent with ceramics rather than bone. I'm struggling to find things to illustrate this, but ceramics and stones chip in remarkably similar ways, with chips coming off the edges, leaving sharply delineated edges and rounded spall. Bones tend to chip in a more jagged manner.
Fourth - the texture is wrong for bone. Bone texture tends to be porous when broken, but yours looks crystalline (not easy to see in the images though), which is not a characteristic of bone, but might be for something like a sea-shell from a gastropod or mollusc.
Conclusion: Man-made stoneware ceramic, not biological.


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Snake Identification in India
Location: Kharagpur, West Bengal, India.
Time: Near the end of September at around 1:00 pm.
This snake was spotted in a drain near my hostel in Kharagpur, West Bengal, India. Can somebody help me identify this species or at least tell me if it is venomous or not? It is hard for me as I can not distinguish its head from the piece of "trash" in the drain.
After a bit of research, I now believe that this is "Striped Keelback". However, I would like someone to confirm this.

The trash might just be its lunch, a rodent perhaps.

@JiminyCricket. Yes, I was thinking the same thing.


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Is the biomass decreasing?
Is the overall biomass decreasing over time, and if yes, has that trend started within the last say $200$ years (about when industrialization started)?
EDIT. Let me add some of my own attempts to answer this question.
Reasons that the biomass might be decreasing. Humans have such a big impact on the environment that the current era is called the Anthropocene. Species are disappearing in masses. We put a lot of artificial chemical substances like pesticides and herbicides into the ground. All this makes it plausible that the overall biomass is decreasing. However...
Reasons that the biomass might be increasing. Humans are big animals, bigger than most species (and host to many bacteria). Their number has increased sharply in the last $200$ years. The $\text{CO}_2$ that humans output might lead to increased plant growth, and the higher temperatures might make macroscopic life possible in areas with little life.
Bottom line. It might be the case that animal biomass is increasing (due to human population growth), but the total biomass is decreasing because of the intense deforestation in the Amazon basin and other places.

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

Thanks for your hints - will do this!

@theforestecologist I chose to edit the answer, can you re-open it? Or is it preferable that I create a new thread?

Don't focus too much on land-based biomass. The impact of climate change and ocean acidification on plankton causes probably much larger changes of total biomass on earth than anything else.

I think you are looking for Net Ecosystem Production. Biodiversity seems positively related to NEP as e.g. concluded here. As we are causing the sixth mass extinction ceteris paribus the NEP should decline. Other factors that changed over the last centuries may increase NEP e.g. monocultural plantations can yield higher productivity in abundant resource environments.

Now as long as NEP is positive, I would expect the biomass defined as the mass of all living organisms to increase.


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Why aren't iPSC's created in vivo?
As I understand it, induced pluripotent stem cells (iPSC's) can be made using the following (grossly oversimplified) steps:

Take some skin cells (fibroblasts) from the host
Introduce the transcription factors Oct3/4, Sox2, Nanog, and Lin28 using retroviruses to reprogram them into pluripotent stem cells
Reintroduce the reprogrammed cells into the host

I do not understand why steps 1 and 3 are needed, and why the retroviruses can't be introduced directly into the target area to create the iPSC's in vivo. My guesses are:

The culture conditions within an animal body are not sufficient for reprogramming or differentiation (low methylation?)
The retroviruses would die off before they could deliver the transcription factors uniformly enough or in large enough numbers for any meaningful regeneration to occur, either due to the immune system or simply because they are not self-replicating
Because the cells would not be transfected at exactly the same time, and would already be surrounded by many differentiated cells, a newly created transfected cell may immediately differentiate based on its surroundings, causing no noticeable difference compared to the cell being made through un-transfected cell division
I am misunderstanding how reprogrammed cells act, and all reprogrammed cells form a blastocyst from which the actual useful stem cells are harvested
Using the retroviruses directly could cause organs cells to become transfected and differentiate in unexpected ways, harming the host

I am not a biologist so please feel free to point out any and all misunderstandings I may have shown. The transcription factors mentioned are the ones which work on humans according to what I read, but this question is not about humans specifically.
Edit: this question appeared in the Related tab after I posted my question, but wouldn't immunosuppressants or more infectious/illusive vectors circumvent the immune system issue?

I don't know which specific barriers are the most important, but certainly it is not simply trivial to say "immunosuppressants would circumvent the immune system issue". Immune suppression is a terrible, terrible condition to induce. It's done when the alternative is death in short order. That doesn't mean that some people don't live long, productive lives on immune suppressants after e.g. organ transplants, but it's not something you'd choose for anyone that didn't absolutely need it.

But assuming it was induced temporarily (long enough for the targeted tissues to have the transcription factors delivered) in an isolated environment, would it still be effective? I'm not trying to imply it's something to try on a whim any more than if I had said "radiation would circumvent the issue of cancer cell replication", I'm just listing possibilities (not solutions) based on my limited understanding.

Pluripotent stem cells, regardless if they’re of embryonic or iPSC origin, will form a very nasty (and often very deadly) form of cancer called teratoma when present in adult tissue (Wesselschmidt 2011, Choi 2015).
I read from your question that your goal is to regenerate tissue. Although iPSCs were a breakthrough in understanding stem cell biology in general, their use in regenerative medicine is still very challenging, since their embryonic-like state is too multipotent and dangerous. Even adult stem cells (like mesenchymal stem cells, hematopoietic stem cells) are undergoing vast changes until they reach their terminal state. And even they need specific signals to develop into the right tissue type. Even when transplanting stem cell grown organs, one has to make sure that every cell is terminally differentiated, otherwise your new liver might grow something random like a set of teeth. People try to circumvent the pluripotent state to solve this problem (Pushp 2021).
Together, you were right with your last point: even if the direct retroviral transfection would work, there won‘t be directed tissue regeneration but random organ growth.


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How long does therapeutic mRNA last in vivo?
How long does mRNA delivered therapeutically to cells last in the human cell once it's gotten there? I've seen sources say that endogenous mRNA lasts around 8-10 hours in humans, but wasn't sure if anything about the currently used mRNA therapeutics extended their halflife in vivo. For example, some of the COVID vaccines used a human α-globin fragment for one of their UTRs, and similar specifically selected UTRs show up in mRNA therapeutics presumably to enhance either transcription or stability.

This is a very broad question which is unlikely to be answered in this form. Can you please restrict yourself to one question at a time?

@Chris Understood, question scope restricted, thanks

mRNA half-life varies markedly, with a variety of stabilising features (or the reverse). Viral structural RNAs that act as mRNA differ again. Regardless, mRNAs are not transcribed. If you want to know how long a particular viral RNA or a particular vaccine RNA persists, that would be a valid question. Likewise the purpose of introducing particular sequences in vaccines. But at the moment your question seems to me misconceived.


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Can several genes be edited at once and what is the name of that procedure?
In general, if there are multiple genes of interests, or edits at multiple points along a large gene are desired, can several edits done at once (or as many as is possible while minimizing off-target effects), transfecting cells with multiple gRNAs and possibly different Cas variants, or would the edits be done one at a time, with each edit being screened for one after another? Or somewhere in-between where you'd batch edits and screen for them in groups? Mostly interested in base edits and electroporation based transfection, but any information on workflow for editing multiple sites is welcome!
Per bob1, my goal is to edit multiple base pairs on sites adjacent to and within a gene for in vitro mammalian cell lines, to see how those edits affect protein expression.

How you go about it is dependent on what phenomena you are interested in and your reasons for looking at the products. Need more information on your aims to answer this. Also depends on organism.

The workflow you're talking about I believe is called multiplexing. Maybe this  article can help you out.

@pawelekzzz That's exactly the term I'm looking for, thanks! I didn't know the name of it and hadn't seen that term in any of my searches prior, this gives me what I need the find more articles, and the one you link gives a good intro to the concept too, much appreciated.

@bob1 Simultaneous base pair edits on sites, upstream, downstream and mid-gene for in vitro mammalian cell lines, to monitor changes in protein expression

@Gumpf You should edit that into the question. In that case I can see that intermediates might well be useful...

@pawelekzzz you could expand that into an answer.

One of the advantages of CRISPR/Cas9 is that it allows what is called multiplexing. In other words: transcriptional regulation of multiple different genomic loci in one single construct. I'm not sure if other biotechnological methods allow for a different strategy to obtain the same result.
Multiplexing using CRISPR/Cas9 has been documented several times expressing several gRNAs at once. Anecdotally, I can also personally say it works. The multiplexed CRISPR/Cas9 reagents are assembled into T-DNA vectors. This is done through reactions called Golden Gate cloning and Gateway reaction.
Bear in mind I'm talking about plants all this time.

References:
Lowder LG, Zhang D, Baltes NJ, Paul JW 3rd, Tang X, Zheng X, Voytas DF, Hsieh TF, Zhang Y, Qi Y. A CRISPR/Cas9 Toolbox for Multiplexed Plant Genome Editing and Transcriptional Regulation. Plant Physiol. 2015 Oct;169(2):971-85. doi: 10.1104/pp.15.00636. Epub 2015 Aug 21. PMID: 26297141; PMCID: PMC4587453.
Li JF, Norville JE, Aach J, McCormack M, Zhang D, Bush J, Church GM, Sheen J. Multiplex and homologous recombination-mediated genome editing in Arabidopsis and Nicotiana benthamiana using guide RNA and Cas9. Nat Biotechnol. 2013 Aug;31(8):688-91. doi: 10.1038/nbt.2654. PMID: 23929339; PMCID: PMC4078740.

What you should do is highly dependent on what you are looking at and why you want to make those changes. It also depends on which method you want to use
There are quite a few different ways of doing this for mammalian cells. One commonly used way is to have the gene expressed off a plasmid in a cell line that lacks expression of the protein of interest. This means you have an easily manipulable plasmid which you can make and confirm sequence changes easily and quickly. Plasmids are also easy to use and can get results quickly.  However, these are usually non-permanent changes, unless you have a selection mechanism like geneticin and maintain this on your cells. If you don't maintain the selection the cells tend to lose the plasmid. The downside is that you don't tend to get every cell transfected and the percent of cells transfected drop with plasmid size and/or method and can be variable between different transfections and different plasmid preparations. These methods are known as transient transfection and stable transfection respectively. For many sequential changes, looking at intermediates, this is probably the method I would use, but CRISPR/Cas (see below) is also promising.
For targeting of the genome of the cells you are looking at, conventional gene editing techniques by recombination between plasmid and genome are slow and best suited to smaller inserts and low numbers. They tend to have lower success rates and require things like antibiotic selection to ensure that they have happened. This includes things like Cre-Lox recombination. These tend to be quite slow relative to transient transfections and require you to have robust sequence checking methods in place (often done by PCR product size and/or sequencing), but are stable and don't require continued selection once stable. They can be done at a single-cell level and can be site-specific, depending on the method used.
Viral transduction is similar to both transfection and recombination methods. You usually work with relatively easily manipulated virus genomes expressed off plasmids to make the viruses, which are then used to do the recombination/expression. It does tend to have quite a bit of finicky set-up, but is robust and stable once it is working. Lentivirus and Adenoviral vectors are two common methods of this, but there are others.
CRISPR/Cas I don't know a lot about, but I know it is entirely possible to use this method to rapidly make site specific changes in genomes. I think this is the most promising technique for many genetic manipulations in the cell. This is very quick, but requires quite a bit of optimization.
In general, making lots of changes at once is entirely possible, though, as you will have realized from the above, this depends on the mechanism used to make the changes. Just be aware, that if you are manipulating the genome of a host, dramatic changes (i.e. many) might drastically affect the cells in some fundamental manner so that you don't get any cells survive. This is where intermediate steps might be useful, but is something you can choose or not at this point.

Really? :) You provided the animal cells answer, and I provided the, rather succinct, plant cell version.

@pawelekzzz To be fair, you can use the viral method and a bacterial method (Agrobacterium i think?) on plant cells too.

Yes, that's right, Agrobacterium tumefaciens is used in plant cells transformation.

@pawelekzzz excellent, having not worked on plants for over 20 years, good to know my memory of methods hasn't failed on me. Not that I used Agrobacterium at the time, just knew it was a possibility.


text:
Cross correlation metric in ChIP-seq experiments
I found this explanation of cross-correlation metric in ChIP-seq.
Now, the definition of Pearson's correlation coefficient between two random variables $X$ and $Y$ is $$\rho_x = \frac{Cov(X,Y)}{\sigma_x\sigma_y}$$ where $Cov(X,Y) = \frac{1}{n}\sum_{i=1}^n(X_i-\mu_x)(Y_i-\mu_Y)$ and $\sigma_x = \sqrt{\frac{1}{n}\sum_{i=1}^n(X_i-\mu_x)^2}$ (similarly for $Y$).
Given this definition, I am not sure what is being computed when the above link says:

Strand cross-correlation is computed as the Pearson’s linear
correlation between the minus strand and the plus strand, after
shifting minus strand by k base pairs

Following my above notation, what would $X$ be? What would $Y$ be?

I'd read that page in a little more detail. They give an intuition here:

The concept is that if you have a read that maps uniquely on strand x at position $i$ (where $i$ is the starting position); it follows that you will have a read mapping to strand y at position $i+r$. Because the way the counts are stored, with the number of reads starting at each coordinate, you will get a bunch of reads at $x[i]$ and a bunch of reads at $y[i+r]$ that are $r$ distance away from each other.

It's not super well explained, but one presumes based on the explanations that relevant values of $r$ are the read length (how long individual reads are reading off the fragments) or the fragment length (how big the pieces of DNA that go into sequencing library preparation are on average, usually due to sonication or nucleosome positioning, based on how the cells are treated). Thinking about how ChIP-Seq works, you expect that the DNA is in a bunch of fragments of some length, and then you sequence each end of the fragment (of a chemically induced length) on opposite strands with reads (of a technologically specified length):
read1     >>>>>
fragment  --------------------- (length r)
read2                     <<<<<
positions i                   i+r

So you expect that at a certain distance corresponding to the average fragment length, there will be a correlation between reads mapping to the + and - strands some distance apart.
In terms of the statistical method, $X$ and $Y$ are the counts of reads at every position ($X$) and the counts of reads on the opposite strand at every position + some value $r$ ($Y$). Looking at their docs, you then vary $r$ systematically to obtain various datasets $X$ and $Y_r$ (a different $Y$ for each value of $r$) and see at which values you obtain maximal correlations, as shown in their figure where the X axis is $r$ and the Y axis is the corresponding correlation value:
$r$" />
Update
I am less clear on why there is the artefactual "phantom" peak of read length (in addition to the more interesting peak from fragment length), as they call it. That is not well explained by the resource that you linked. I attempted to search the site you linked for more information about the utility of the cross-correlation method, but I was not able to find anything relevant. I find it plausible that read length would introduce some sort of signal, but the mechanism is not obvious (to me).
But as far as I can tell, fragment length is the quantity of interest that is most readily apparent from this method.
If you are interested in the mechanics of paired-end sequencing library preparation that lead to the architecture shown in the monospaced text figure, I would suggest looking into documentation on that subject (one random example from Illumina). If you are interested in chromatin immunoprecipitation (ChIP), which forms the input to the sequencing library prep, I would suggest going and looking at wikipedia. Those are rather different and more fundamental questions, regarding which there exists abundant reference material.

Thank you so much - that is very helpful! That is why there is a peak at the fragment length, for example - because it is when the shifted read1 overlaps most with read2?

Moreover, how is read-length different from fragment-length? You seem to use it interchangeably but the graph has two different labels for them.

Lastly, from what you wrote, I am assuming that read1 and read2 are on opposite strands, rather than the same one? You wrote this is because of how ChIP-seq works, but I was also curious about why this is the case, in case you can help me understand that too (as I have highlighted better here - https://biology.stackexchange.com/questions/110658/questions-about-chip-seq-reads-and-macs). Thank you again - you have been very helpful!

see update @AryanDugar


text:
cancer cell - antigen presenting cell
We all know that if normal cell contains virus inside it, normal cell has mechanism inside it that can detect that it has abnormality inside(virus) and what it will do is present the virus's protein(antigen) with MHC I on its surface, so T-cytoxic cells can kill it.
But cancer cells don't have virus inside. They still look healthy. I mean the cell itself has different proteins(derived from mutation), but cell itself thinks that it's healthy. So would it put anything on its surface with the MHC I ?

If the answer is no, then we got a problem, as it would never, ever be recognized by T-cell to kill it.

If the answer is yes, I guess, it would just put its modified protein, though, in that case, that means that every cell(in our body, even normal ones), they all put their protein representations on their surface. Because if cancer cell(which thinks it's healthy put it, then every cell which is also healthy should put it, seems logical)

Maybe my question should be: What is MHC I exactly ?
In case of normal cells(healthy ones), only MHC I is put on the surface and MHC I is proteins taken from within the cell.
In case of the cell that contains the virus, MHC I is the proteins from within the cell that aren't part of the virus protein. So here on the surface, it puts MHC I and virus protein(antigen) separately(MHC I + antigen).
In case of cancer cell, what is put on the surface ? just MHC I (which are modified proteins within the cell) or we also have somehow MHC I + antigen, but I don't understand how we would have MHC I + antigen combination as the cell doesn't know that it has antigen(thinks it's normal).
What do you think ? I'd appreciate the clear explanation.

This is a really big field. I think that there is a lot of complexity in how the immune system recognizes cancer cells. Yeah there are specific epitopes that get displayed, but I'd suggest just googling "how does the immune system recognize cancer cells", and you will get lots of helpful results like this.

I'm voting to close this as "Needs more focus." @MaximilianPress is correct, this is a huge field, and even a simplified answer would need to be textbook chapter-length in order to be complete.