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Why don't viruses reach broad concentration outdoors in a city like allergens?
Why don't airborne viruses reach concentrations that infect most people vulnerable outdoors in a city the way an allergen can cause inflammation to everyone sensitive to it.  Both are (often) microscopic airborne biological particles produced by a bunch of scattered organisms.
Obviously my assumptions are wrong.  Even at the height of Delta or Omicron Covid variants it was generally considered safe to be without a mask if you were alone and outside.  The question is which assumptions are wrong?:

Does particle size mean that allergens stay near the ground and dilute less?
Are there just nowhere near enough organisms emitting at once to matter?
Does the life cycle of a virus just prevent enough people from being infectious at once the way a whole species of tree will start producing pollen?
Since producing virons isn't a normal function of a body are they just produced massively less than something like pollen from a tree?
Is the immune system so powerful that it's easier to trigger an allergic response than an infection to establish a foothold?

Why don't people catch colds like allergies.

If you had the birch tree in your room instead outdoors you'd also have a much higher concentration of birch pollen, especially if you go through it with a wind machine occasionally ;-).

2, 4, 5, and 6.
6 being that the UV light (from the sun), fluctuations in temperature, humidity, wind etc mean that the virions are decayed relatively rapidly for most virus species.
To address (1): In general a virus, such as SARS-CoV-2 or influenza is about 100 nanometres (0.1 micrometres (μm)) in diameter, whereas a pollen is about 10 μm (sizes in links for the respective viruses) - the virus is 100x smaller, but is largely spread through droplet transmission. Droplets are comprised of typical nasal secretions (i.e. snot) and/or saliva and those of about 5-100 μm in size are relatively dense and fall to the floor rapidly. Less than 5 μm can float for quite some time1 but rapidly dehydrate and lose virion integrity, so can't cause infection.
(2) and (4) Infections produce a lot less virus than a tree does pollen. A typical allergenic tree like a Silver Birch (Betula papyrifera) can produce about 2 million pollen grains from a single catkin - up to about 2 billion grains per tree. Multiply that by the number of trees, and you'll get some idea of the number of pollen grains for that species alone. On the other hand an infected person has about 7 million virions per millilitre (ml) of saliva. However, not all of each ml is turned into droplets when speaking and it turns out that only about 37% of 50 micrometre droplets will contain a single virion, and that this drops to 0.37% for 10 μm droplets (see ref 1). This means that each infected person at their infectious peak is only producing putting a tiny proportion of the virus they contain.
(3) and (4) Sort of - plenty of people can be infected at once, as you will have seen during the waves of infection, but once sick they aren't out there walking around constantly emitting virus into the environment, they are in bed, at home or in a hospital (assuming they are following good public health advice). This also ties into the answer for (1) - the droplets just don't last like a pollen grain can. Pollen's purpose is to travel to find a new flower to fertilize, so trees that are wind pollinated have a selective pressure to produce pollen that can last in the environment and still fertilize another tree. Viruses don't have the same selective pressure because transmission relies on "close" contact of a mobile organism - not a tree that sits in the same place and the closest one might be miles away.
(5) How an infection takes place is multifactorial - you need the conditions to be just right for transmission to take place, and a big enough dose of virions to cause an infection (often for things like Influenza or Adenovirus this is in the 3-10 virions range), you then need it to hit the right tissue in the body and evade the immune system. All pollen has to do is hit a mucosal membrane (nose, mouth, eyes etc) for there to be an immune cell there to activate the immune response.
Long story short infection is much harder to do, produces less virions and has lower likelihood of happening.
1: Stadnytskyi V, Bax CE, Bax A, Anfinrud P. The airborne lifetime of small speech droplets and their potential importance in SARS-CoV-2 transmission. Proc Natl Acad Sci U S A. 2020 Jun 2;117(22):11875-11877. doi: 10.1073/pnas.2006874117. Epub 2020 May 13. PMID: 32404416; PMCID: PMC7275719.

I'd be interested in the sensitivity of organisms to allergens. After all, an allergy is an overreaction: The body is excessively sensitive to the allergen. Extreme cases are, I think, powerful allergen detectors. Any specific information on that?

Sorry for nitpicking, but is viruses are 0.1um and pollen is 10um, than 100 times smaller, not 1000 times

@BrunoPérel quite right, I have fixed it.

@Peter-ReinstateMonica That would make a great separate question. I'm no immunologist at all, but I believe that it is down to repeat exposures to the antigen and the body being able to rapidly identify/respond. However, that doesn't explain things like nut/peanut allergies, which can respond to single exposures of tiny amounts.

In another answer elsewhere on StackExchange, a poster estimated that there might be something like 100 g to 1 kg of SARS-CoV-2 virus worldwide, and that's an estimate of all the virus, including what remains in the bodies of infected individuals, not just what makes it to the outside world.
I'm not certain of the accuracy of that estimate, but consider that a single pine tree can make a couple kilograms of pollen. Even if it's off by a couple orders of magnitude, the simple answer is there isn't nearly as much virus out there as there are environmental allergens.
Anecdotally, there's enough pollen during the right season that if I leave my windows open, there is a light, greenish-yellow coating on surfaces near windows. The comparison just isn't anywhere close.

Wouldn't the difference in mass between a pollen grain and a virus complicate this comparison?

@HarrisonPaine if we accept the 100x difference in diameter between pollen and virus cited in bob1's answer above, the difference in mass would be on the order of 100^3 or 1e6. But there are on the order of 1e12 trees in the world (https://www.science.org/content/article/earth-home-3-trillion-trees-half-many-when-human-civilization-arose), not to mention the other pollen producing herbaceous plants so the dimensional analysis still would suggest many orders of magnitude more pollen grains than virus particles from one particular pathogen.

To add to the discussion -surface area probably has more of a relationship than mass. Viruses often have a certain number of antigenic proteins on the surface, constrained by protein geometry of the capsid (though this doesn't apply to SARS-CoV-2 or influenza), but I don't know about pollen.


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Animal specific names with non-alphabetic characters
I'm part of a research team that investigates and documents native bee species, and we identified one of our Andrena specimens as A. w-scripta. With over ten years of experience in insect and ray-finned fish taxonomy, this is the first animal species I've EVER seen with a hyphen in its name. Google didn't turn up any other examples, and now I'm curious if anyone here can point me towards other names with non-alphabetical characters!
I've dabbled in plant taxonomy and seen a few hyphenated specific names in that kingdom, but those naming conventions are pretty different from Animalia's, if I'm not mistaken.

Not too rare in plants. Carya carolinea-septentrionalis and Smilax bona-nox both quickly come to mind. I think this question is too broad -- is your intention for people to just provide an infinite list of species names that match your description?

That is my intention. This question was so much fun I had to sign up for stackexchange and mention my own personal findings.
I wasn't sure how to go about investigating the subject in my own. I stumbled on A. w-scripta by pure coincidence and had no idea how to find more species or even the ICZN's conventions regarding punctuation! I feel like I'd need to learn R to effectively approach questions like these.

Short Answer
Very few hyphenated specific epithets (i.e., species' names) exist due to the regulatory body (the ICZN) that governs the nomenclature code for animals. The code has multiple rules preventing hyphens and other marks/punctuation from being included in animal binomial names. If such marks originally existed when the species was first described, the ICZN code even recommends removing/updating those marks in all but 1 instance.
Hyphens are only allowed if they separate a letter used to describe some physical characteristic of the animal and the letter needs to be separated from some other word describing the letter.

Example: Polygonia c-album is retained because this butterfly has a white ("album") shape on its wing shaped like the letter "c."

Long Answer
According to the International Code of Zoological Nomenclature from the International Commission on Zoological Nomenclature (ICZN), usage of a hyphen or other marks is not generally accepted in a specific epithet. There is 1 specific instance in which hyphens are permissable.
See relevant excerpts from the Code below (with bold text being my emphasis):

Article 27. Diacritic and other marks:
No diacritic or other mark (such as an apostrophe), or ligature of the letters a and e (æ) or o and e (œ) is to be used in a scientific name; the hyphen is to be used only as specified in Article 32.5.2.4.3.

First, let's look at Article 32.5 more broadly to see its scope in removing characters followed by some sub-articles demonstrating common instances in which hyphens are not appropriate.

32.5. Spellings that must be corrected (incorrect original spellings)

32.5.2. A name published with a diacritic or other mark, ligature, apostrophe, or hyphen, or a species-group name published as separate words of which any is an abbreviation, is to be corrected.

32.5.2.2. In a compound species-group name published as separate words that are deemed to form a single word [Art. 11.9.5], the component words are to be united without a hyphen.

32.5.2.3. In a compound species-group name published as words united by an apostrophe or a hyphen, the words are to be united by removing the mark concerned (but see Article 32.5.2.4.3).

32.5.2.4.4. If the first element is a Latin letter or group of Latin letters not identifiable as fitting into the preceding three categories, punctuation (if any) must be deleted and the components united.

Etc.
Finally, Article 32.5.2.4.3 indicates the only instance that hyphens can be used:

32.5.2.4.3. If the first element is a Latin letter used to denote descriptively a character of the taxon, it must be retained and connected to the remainder of the name by a hyphen.

Example. c-album, in Polygonia c-album, so named because a white mark on the wing of the butterfly is similar to the letter c.

BONUS: Plants
Note: hyphens in plant scientific names is more common.

E.g., Carya carolinea-septentrionalis, Smilax bona-nox, Ribes non-scriptum

The reason? The International Code of Nomenclature for algae, fungi, and plants doesn't have as strict of rules preventing their usage. For example:

60.11. The use of a hyphen in a compound epithet is treated as an error to be corrected by deletion of the hyphen. A hyphen is permitted only when the epithet is formed of words that usually stand independently, or when the letters before and after the hyphen are the same (see also Art. 23.1 and 23.3).

20.3. The name of a genus may not consist of two words, unless these words are joined by a hyphen (but see Art. 60.12 for names of fossil-genera).

23.1. The name of a species is a binary combination consisting of the name of the genus followed by a single specific epithet in the form of an adjective, a noun in the genitive, or a word in apposition (see also Art. 23.6). If an epithet consisted originally of two or more words, these are to be united or hyphenated. An epithet not so joined when originally published is not to be rejected but, when used, is to be united or hyphenated, as specified in Art. 60.11.

There's also ICNAFP Article 23.3:

23.3. Symbols forming part of specific epithets proposed by Linnaeus do not prevent valid publication of the relevant names but must be transcribed.

Ex. 2. Scandix ‘pecten ♀’ L. is to be transcribed as Scandix pecten-veneris; Veronica ‘anagallis ▽’ L. is to be transcribed as Veronica anagallis-aquatica.

source: Stack Exchange

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

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If a HIV+ person gets COVID, will it result in more mutant virus?
High schooler here.
What is the probability of the coronavirus evolving to gain traits of HIV/any other virus from a person suffering from both ailments?
As COVID virus enters cells that are already infected by other virus, what determines which of the two virii will survive and what mechanism governs what traits surviving virus will adopt/integrate?

Welcome to Biology.SE. I’m voting to close this question because it: 1) doesn't demonstrate that you've done the expected prior research (see also the "homework policy"), and 2) asks multiple questions (the second of which is much too broad). These are both reasons for closure and downvoting. Please take the [tour] and consult the [help] starting with [ask] for details of what is expected.

Similar viral strains allow genetic transfer hence recombination. The recombined strain can be selected from the original strains by its better or worse characteristics.
This does not happen in HIV x COVID-19. They are dissimilar and none of the recombinants has been observe to exist.

There is a probability of similar viruses gaining each other's genetic traits while replicating. This is known as horizontal gene transfer. This also happens in viruses, where double infections can allow genetic material between two strains to be exchanged while replicating. As the example you mentioned, the SARS-CoV-2 (the name of the virus; COVID-19 is the name of the syndrome/disease) has evidence of horizontal gene transfer between pangolin coronaviruses (Wang, Pipes, and Nelsen, 2020). Currently, there is no evidence that horizontal gene transfer happens between HIV and SARS-CoV-2 probably because they are too dissimilar.
We have seen the "how" of these things happen. Then, "what" governs the survivability of those recombination strains? Remember, recombination is a mere game of chance, there are combinations which are poor fit and some better. For poor recombinants, its viral characteristics are poorer than its origins, hence it fails to spread. On the other hand, a "better" strain is more fit (as in Darwinian fitness) than its origins, hence it spreads quicker. It's viral characteristics, both the poor and the better, selects itself from its peers. This is the idea of natural selection.
You can check this article by Li, et. al. (2020). They explain the recombination of bat and pangolin coronavirus (which may be the genesis of SARS-CoV-2), is under further purifying selection. This causes the SARS-CoV-2 strains to show the severe and widespread viral characteristics as we see today.

This part is not a continuity of my answer, however some reflection of my perspective. Welcome to SE Biology. To better understand the answer, you can first read a good introductory biology book, such as Campbell BIOLOGY. Then, you can start delve in the articles I mentioned in the answer. If you meet a difficult part inside the explanations, we are eager to help.
I am glad you are interested in these topics as a high-schooler, and hope you continue your interest in tertiary education. I personally enter biomedicine after trying to understand a then tumor misdiagnosis when I was in HS.

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


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What is the name/type/species of this insect?
Facts:

Found in a bathtub in western Washington (state) (the pacific northwest).
3/16-1/4" long, 1/8-3/16 thick.
Gray colored.
No elongated noise but two antennas.
No pets in home, older 1969 build (vented crawlspace).
Found on main floor (crawlspace underneath).

This seems like a weevil or a carpet beetle. Most interested in making sure it’s not harmful.

Hi. Species ID questions need to include a photo, size, location, and as much other information as possible. See here. If you update your post with such information, it can be reopened and you'll be able to receive an answer.

In the meantime: act fast to find your open or damaged container of stored cereal grains, pasta, or similar.

Related: https://biology.stackexchange.com/questions/69598/small-black-slow-moving-insect-showing-up-in-the-home

@theforestecologist thank you. Post updated.

This is much better, but is there any chance of getting close-ups (from multiple angles)? Borrowing a good camera with a macro lens or a phone with a better camera would make it much more likely you can get a precise answer.

@tyersome we released the insect to the wild. I'll use the suggestion on the next one!


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Can we infer the orientation of a moose's head from the teeth patterns on tree trunks?
Background
I am interested in studying the distribution and patterns of behaviour of moose (Alces alces).
Moose chew bark off of the trunks of trees, especially Populus tremuloides. See some of the following examples:
Older

iNat 114539552
iNat 114538310
iNat 114537859
iNat 114537795

Newer

iNat 114539470
iNat 114539399
iNat 114538848
iNat 114538783
iNat 114538569
iNat 114538481
iNat 114538387
iNat 114538247
iNat 114537633
iNat 115635455

Often the teeth marks are at a diagonal, which could be quantified with an inclinometer. In my imagination I see them applying most of the force downward with their top jaw teeth. I also suspect that for higher up parts of a trunk that are chewed that the inclinometer angle would be steeper due to the moose reaching up at a more acute angle with respect to the trunk. This could be confirmed quantitatively by measuring the height of the chewing from the ground and comparing to the chew angles at each recorded height.
The markings may depend on the type of tree. The examples given above are all on aspen trees and show lots of teeth marks, but this video Moose eating bark shows a moose both chewing and pulling in order to get bark off a maple tree. The iNaturalist observations from above are from a similar area, but this video Moose Eat Poplar Tree Bark is unlikely to be from the same area but also shows lots of teeth marks.
Question
Can we estimate the approximate orientation of the head of the moose relative to the tree trunk based on the chewing marks?

Note: This video How Humans Became (Mostly) Right-Handed claims that some information can be inferred from scrapes on surfaces. However, this considered scratches on teeth by (presumably) tools rather than scrapes on trees from teeth. This comparison is only analogical because the reasoning and methods could be quite different.

it might be possible from actual tooth marks but you don't have pictures of any of those. the a pic of the missing park probably can't tell you anything.

@John Suppose I can go back to this tree that clearly has teeth marks on it. Can you describe a method for taking those field measurements and from those estimating the head orientation?

Your best bet it to actually observe and record the feeding behavior then take detailed photographs of the tree, specifically close up shots that could actually show the marks left by teeth. then you can directly compare the two. tooth marks can often show the orientation of teeth by the marks left by the gaps between teeth. the fact moose only bite a very small portion of the bark they strip should work in your favor. keep in mind much of the stripped bark is imply pulled from the tree with only an initial bite to start it.


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How I can find the list of transcription factor proteins involved in transcription of a specific gene?
I want to get the list of transcription factor proteins involved in the transcription of the human SIRT1 gene. How can I access that?

Can you tell us what you have tried so far? My first instinct would be to check the literature.


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Calculating bacterial mutation rate
I'm reading Molecular Biology of the Cell by Alberts et. al and at one point, the authors mention:

One finds that a single gene that encodes an average-sized protein (~$10^3$ coding nulceotide pairs) accumulates a mutation (not necessarily one that would inactivate the protein) approximately once in about $10^6$ bacterial cell generations. Stated differently, bacteria display a mutation rate of about three nucleotide changes per $10^{10}$ nucleotides per cell generation [emphasis mine].

I'm trying to figure out how they came up with the numbers in the text stated in bold. Here's what I have so far:
According to the first sentence, we have $\frac{1}{10^6}$ mutations per $10^3$ nucleotides per cell generation. So per $10^{10}$ nucleotides per generation, we have $\frac{10^{10}}{10^3}\times\frac{1}{10^6} = 10$ mutations, which is not the 3 that they mention. What am I missing here?

One mutation per 10,000 bases per 1,000,000 generations.
1 mutation / 103 bases / 106 generations
= 1 mutation / 109 bases/generation
= 3 mutations / (3*109) bases/generation
= 3 mutations / 109.5 bases/generation
Since all these are rounded approximations, if you started with more precise numbers and round at the end (always round as your final step!), it would be very easy to get 3 mutations / 1010.

Thanks for the answer. Why can't you just jump from the 1 mutation / $10^9$ bases/generation step to deduce 10 mutations / $10^{10}$ bases/generation i.e do what you did but multiply by 10 instead of 3?

@AnIgnorantWanderer I made it 3 to match their estimate. I assume they say 3/10^10 rather than 10/10^10 because that's closer to their actual estimate if they don't round too early.


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Seeds of fruits
Some fruits  ( like watermelon , pomegranate,  etc ) have their seeds spread out throughout their bulk . Also , there are fruits which have seeds at their centre of symmetry ( like apples ) .
Is there any theory or mechanism which explains that why and which type of fruits possesses the type of arrangements of seeds inside their bulk ?

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

In addition, biology is rarely (at least at this stage of knowledge) a matter of distilling rules — to make this an answerable question (for this site) I think you should focus on a single type of fruit and start by figuring out the botanical name for that type (e.g. pome). You can then use search terms like "development fruit pome" to learn more and then ask a clear, focused question based on what you've learned if and when you get stuck.

I looked up and worked on it by asking to my teachers . They told that this may be due to weather , climate and geographical factors.

Sorry I missed your reply — your teachers's answers don't really seem at all helpful to me. Please note that asking good questions is a skill that one needs to work at. If you lack the time for or interest in improving this question (see previous comments for details), please delete it. This will prevent you from losing reputation (and can lead to loss of the privilege of asking questions) due to downvotes and closure.

@tyersome Hello , what I want was an answer not reputation. However , don't close it please.

Ultimately the decision of whether to close is up to the community. If you improve the question then it will be left open and is more likely to receive an answer ...

@tyersome Then please suggest me that how can I improve . What shall I omit and add to my question to improve it?

I already did that in my first two comments ...


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Do photosynthesis and respiration violate the law of conservation of energy?
I don't know, if it's a physics question, biology or chemistry question but anyways here it is:
I have been taught that to produce one molecule of glucose in photosynthesis, 18 ATP molecules are used up, but that in respiration, oxidation of the same glucose molecule releases 38 ATP molecules. I just can't seem to wrap my head around it. Where are these extra 20 ATP molecules coming from (or in other words extra 20 units of energy)?
I know there's a whole lot of reactions occurring in the cell that utilize energy, but the reactions of photosynthesis and respiration are reversible and I don't think the path to make or break glucose actually matters with respect to the amount of energy used or released in the processes. Glucose always remains glucose so of course writing the same reactions in reverse orders shouldn't change the energy used/given out in the reaction.
I really can't understand why it should it depend on the path by which glucose is used or made as many people have told me.
So in my opinion these two processes do seem to violate the law of conservation of energy, so please help!

"Does X violate the law of conservation of energy?" -> No.

The same question with physics-minded answers: https://physics.stackexchange.com/q/707262/247642

@EricDuminil For X that actually happens, that is. It's very much a good sanity check for when you're developing a new hypothesis :D

As for "it should always give X amounts of energy regardless of 'the path'" -- not related to this question directly, but you'll find that aerobic vs. anaerobic can make a huge difference when trying to get energy out of molecules. ;-)

@EricDuminil It would be better if questions like this started with "Why doesn't" instead of "Do", because I suspect the OP doesn't actually wonder if it violates the law of CoE, but rather wants to be enlightened as to what is really happening.

With slight adjustments to the scientific wording, what the poster states is in effect:

“…to produce one molecule of glucose in photosynthesis, 18 ATP molecules are used up hydrolysed”

and

“…oxidation of the same a glucose molecule releases phosphoryates 38 ADP molecules to ATP”

These statements are both correct…
…but the logical fallacy arises because the first one is incomplete.
In the context of energy production and utilization, it is essential to add:

…and 12 molecules of NADPH are used (i.e. oxidized to NADP)

This is because 1 molecule of NADPH is energetically equivalent to 3 molecules of ATP.(Oxidative phosphorylation will convert NADPH + 3ADP to NADP+ + 3ATP).
Hence it takes 54 ATP equivalents to synthesize a molecule of glucose, but one only gets (approx) 38 molecules of ATP from oxidizing glucose.
If you think right back to the light reactions of photosynthesis, the photons of light energy are used to do two things — phosphorylate ADP to ATP, and to reduce NADP+ to NADPH.

Where are these extra 20 ATP molecules coming from (or in other words
extra 20 units of energy)?

The sun.  They are provided by high energy photons emitted by the sun.  Those photons excite electrons into being in a higher energy state, and that higher energy electron state is harnessed and changed into high energy chemical bonds, like in ATP.

The 18 ATP comes from the sun. The extra 20 ATP doesn't.


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Can all plants be reproduced through vegetative propagation?
I have learned that plants can be reproduced or propagated through vegetative parts but there is a question in my mind if we can each method for all  types of plants. I don't know if all  plants have cells which can proliferate and differentiate into other tissue types. Do these vegetative parts have such ability. Is it true for all of them?
Can we grow all type of plants from all vegetative parts( i.e, roots, stem and leaves)?

We ask that questions here show some evidence of prior research; as-is, your question is exceedingly broad. Can you share what you've learned already? What's the purpose of the question?

A point to start your research which challenges the assumptions that you're questioning would be chlorella - a single celled genus of algae with no differentiated cell types.


text:
Maximum solar irradiance per plant species
I'm looking for a table or database specifying by plant species, the maximum solar irradiance it can tolerate, but seems not a straightforward search on most engines or open access botany databases. Anyone has any useful reference?
Also I'm assuming that solar irradiance and not heat, is the factor that will kill the plant via leaf burn, but maybe I'm wrong, and heat distress may kill the plant before... or impede the plant development. Any clarification on this will be useful too.
At the concrete example, I'm finding that a hazelnut (Corylus avellana) can't develop at direct sunlight in my location (middle of Spain), as its leaves seem to burn each year, as the solar radiation seems a bit too much for it. I'm planning planting the next ones at the shade of a stone pine (Pinus pinea) to relieve the irradiance from the central hours of the day (If the are good companion trees would be another question)
But you got the convenience of having this information for as much species as possible, to successfully setting plants and avoid killing them, thanks to anyone that can help.

Welcome Greco. For your interest: we have a [gardening.se] stack for you to enjoy too.


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Gas exchange in the alveolus
When our teacher was talking about the gas exchange inside the alveoli, he mentioned the flow of air and the flow of blood was going in opposite directions so that there always would be a concentration difference.
Because of this the gas exchange between the alveolar space and capillary continues and reaches ~99%.
I could not understand how the air would always go in the same direction so I researched the topic. All resources I found state that when the air enters the alveolus there is a pressure gradient for both oxygen and carbon dioxide between the capillary and the alveolar space.
But I found nothing mentioning the opposite direction of flow for air/blood.
So does that mean gas exchange for oxygen and carbon dioxide stops when diffusion equilibrium is reached?
(I'm not a native English speaker so I hope this question makes sense.)

I think that is about fishes, and most aquatic creatures. They exchange gases from their gills. Most advanced animals have blood vessels in their gills that flow on the opposite direction to the water that is flowing through the gills.

Welcome to Biology.SE. Please take the [tour] and consult the [help] starting with [ask] for details on using this site, which promotes self-learning with some expert help. See also the "homework" policy. Please [edit] this down to a single question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. ——— In particular this seems like the sort of question your teacher could best answer ...

oxygen will go into the blood and co2 will go into the alveola never the oposite.

@trondhansen Bingo. I'm sure that's what the tutor meant.

@cc12amu This seems to be the case. I dont think my teacher would get it wrong. Probably my sleep-deprivated brain is recalling the whole thing very differently, thanks for the answer.

is down voting answers the best peole at this part of SE can do,had it not been better to make an answer that correct the mistakes(if any)in the other answers?

The air in the alveoli has a higher oxygen concentration than the blood, and the blood has a higher carbon dioxide concentration than the air. Due to this concentration gradient, the carbon dioxide will diffuse from the blood to the air, and the oxygen will diffuse from the air to the blood. My guess is that this is what your teacher referred to as "opposite flow".
However, you are right in noting that this flow will eventually reach equilibrium, and gas exchange will cease between the air and the blood. This is where the role of the lungs come in. The lungs constantly exchange carbon dioxide rich air for oxygen rich air, and hence the gas exchange continues happening. Cellular respiration also converts the oxygen rich blood to carbon dioxide rich blood.

Difference in the Partial pressures of Oxygen and Carbon Dioxide in the alveoli and blood capilariess respectively cause respiration.

In alveolar blood, PO2 is low while PCO2 is high, whereas in atmosphere its vice versa, so it diffuses out to the atmosphere.

In capillary blood, PO2 is high and PCO2 is low, whereas in the cell its the opposite, so it diffuses into the cell.

Even if the diffusion equillibrium is reached, the negative pressure gradient of the lungs make sure that there is a constant exchange of gases.
You are good at observing that bro. I didnt even this of that when i studied respiration.


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Are there irreversible metabolic reactions that can happen in opposite ways depending on the cellular conditions?
Irreversible reactions are thermodynamically irreversible, not microscopically irreversible. "Irreversible" here means the reaction happens "out-of-equilibrium". It is a macroscopic property.
Being (thermodynamically) irreversible doesn't mean that a reaction cannot be inverted if conditions (temperature, pressure, concentration of species) change so that the reaction then spontaneously proceeds in the opposite direction as in the previous conditions. In other words, a reaction can happen irreversibly (spontaneously) in one direction in given conditions, and happen irreversibly (spontaneously) in the opposite direction in other conditions.
Are there any known (reported) examples of metabolic reactions that are found to happen in opposite directions depending on the conditions in which a given cell or cell type is found, and that happen thermodynamically irreversibly in either case? I have found reactions that happen irreversibly in opposite directions in different cell types (although I am not sure the reactions are irreversible in the respective cases):

Lactate dehydrogenase catalyzes the interconversion of pyruvate and lactate with concomitant interconversion of NADH and NAD+. It converts pyruvate, the final product of glycolysis, to lactate when oxygen is absent or in short supply, and it performs the reverse reaction during the Cori cycle in the liver.

Ref.: Lactate dehydrogenase (Wikipedia)
But I am wondering about a case where such inversion can happen in different conditions or states for a given cell or cell type.
[Note: see also the discussion in the comments for clarifications if needed.]

Reversibility of biochemical reactions
The general view of the way “irreversibility” is regarded in biochemistry is well summarized by the respected enzymologist, Athel Cornish-Bowden:

“Mathematically and thermodynamically there are no irreversible
reactions in chemistry, and all enzymes catalyse reversible reactions.
All reactions have finite standard Gibbs energies, which is just
another way of saying that they all have finite equilibrium constants.
Nonetheless, for an enzyme like pyruvate kinase, with an equilibrium
constant of the order of 105, one may feel that this is just a
mathematical nicety and that the thermodynamic necessity for the
reverse reaction to be possible has no practical consequences for cell
physiology, and in practice many metabolic reactions are
conventionally regarded as irreversible. This typically means that
they have equilibrium constants of the order of 1000 or more, though
when the mass action ratio in the cell also strongly favours the
forward direction a reaction with a substantially smaller
equilibrium constant than this can be regarded as irreversible.“

[my emphases]
The standard textbook example of this is the three reactions of glycolysis — hexokinase, phosphofructokinase and phosphoenolpyruvate carboxykinase — that are regarded as effectively irreversible, a view supported by the fact that gluconeogenesis (the overall reverse process to glycolysis) employs separate enzymes for these steps. To quote one such text, Biochemistry by Berg et al.:

“However gluconeogenesis is not a reversal of glycolysis. Several
reactions must differ because the equilibrium of glycolysis lies far
on the side of pyruvate formation.“

The text then elaborates on the enzymes and lists the standard free energy changes of the reactions they catalyse (ΔG0′) as in the table below, to which I have added the equilibrium constants (K′eq) calculated for the same ‘standard’ conditions.

Reaction
K′eq
ΔG0′ (kcal/mol)

Hexokinase
1.32 x 10–6
–8.0

Phosphofructokinase
1.25 x 10–5
–5.3

PEP carboxykinase
1.11 x 10–3
–4.0

The PEP carboxykinase value is consistent with the border value of Cornish-Bowden, above.
So, in my opinion, the question becomes whether there are any examples of reactions at this thermodynamic borderline that are reversed under certain physiological circumstances.
Examples of reversal of very thermodynamically unfavourable reactions
I feel that there are probably other examples I should know of, but will be happy to add any that others can supply to make a community answer. However at the moment the only one that comes to mind is the carbonic anhydrase reaction:

HCO3− + H+ → CO2 + H2O

which has an equilibrium constant of the order of 10–3. (I have found values of 1.7–2.7 x 10–3.)
The situation is complicated because of the equilibrium between bicarbonate and carbonic acid, and between dissolved and gaseous carbon dioxide. However, the striking fact is that in the tissues the enzyme catalyses the conversion of carbon dioxide produced in metabolism to bicarbonate:
Tissues: CO2 → HCO3−
whereas in the lungs the reverse occurs in order to allow the carbon dioxide to be removed from the blood:
Lungs: HCO3− → CO2
What drives the ‘unfavourable’ conversion of carbon dioxide to carbonate in the tissues? One factor must be the high concentration of  CO2; another must be the lower pH, which, of course, represents an increase in the concentration of hydrogen ions. Both of these are a result of oxidative metabolism in the tissues.
Footnote: Lactate Dehydrogenase
I see that the poster has edited his question to refer to lactate dehydrogenase. The value of ΔG0′ for LDH is –6 kcal/mol, so it falls into the ‘irreversible’ category biochemical reactions, although, strangely, this is seldom, if ever, mentioned. I don’t see what the poster has against this example. Liver cells can perform glycolysis and form pyruvate and they certainly convert lactate to pyruvate, so the same cell is subject to different circumstances (high blood lactate concentration v. low blood lactate concentration) when catalysing the reaction in opposite directions.

I think another aspect of biology/biochemistry that is missed by those coming from more of a chemistry background is the ability of biology to not only chain multiple reactions to make the "reverse of irreversible" more unlikely, but also to effectively make unavailable the products for reverse reaction by shipping them out to other compartments, sometimes seemingly for 'free' unless you consider a much larger thermodynamic problem. CO2 clearance is an example of one of these, taking advantage of cheap bulk gas flow and the low, biologically unsaturable environmental CO2 concentration.


text:
What types of sounds do sperm whales produce?
Sperm whales produce echolocation clicks, what are the other types of clicks and other sounds they can produce?

Welcome (again). You'll find that when you browse the help centre it'll point out the need for showing your own research when asking a question. Since you self-answered (encouraged, though not usually so quickly done!), then showing research in the Q seems redundant - on this occasion.

There's an article here about that: https://www.nature.com/articles/s41598-021-84126-8

Sperm whales produce echolocation clicks, known as usual/ regular clicks (Madsen et al., 2002) and buzzes/ creaks (Gordon, 1987), while they are actively foraging underwater. These are distinguished from other types of clicks based on the repetition rate (known as the inter click interval).
Sperm whales also produce slow clicks (Gordon, 1987), surface/ coda creaks (whitehead, 2003), rapid/ fast clicks, and chirrups. These sounds are thought to be used for communication and/ or to scan conspecifics.
Non click sounds include squeals, pips, short trumpets, and trumpets (Pace et al., 2021).
References:
Gordon, J. C. D. The behaviour and ecology of sperm whales off Sri Lanka (Doctoral dissertation, Darwin College, Cambridge, 1987).
Madsen, P. T. et al. Sperm whale sound production studied with ultrasound time/depth-recording tags. J. Exp. Biol. 205(13), 1899–1906 (2002).
Pace, D.S., Lanfredi, C., Airoldi, S. et al. Trumpet sounds emitted by male sperm whales in the Mediterranean Sea. Sci Rep 11, 5867 (2021). https://doi.org/10.1038/s41598-021-84126-8. Available from: https://www.nature.com/articles/s41598-021-84126-8
Whitehead, H. Sperm Whale: Social Evolution in the Ocean (The University of Chicago Press, Chicago, 2003).Return to ref 8 in article

Nice one. Please take our [tour] and refer as and when to the [help] for guidance. Enjoy biology.


text:
Why does the Corpus Luteum produce more Progesterone than Estrogen?
In the human ovarian cycle, follicular cells produce only Estrogen in high concentrations (to my knowledge). Yet after ovulation and formation of CL, which should be the remnant follicular cell mass, it is seen that Progesterone is secreted in higher concentration, along with some estrogen. Is this due to some structural change, or is it the effect of LH, or something else entirely? This may have an obvious answer, so I apologize in advance for my ignorance, since it is my first time using this website.

Welcome, Sriram! What did you find when you googled this? You need to show an attempt to answer this. (Hover over the down vote arrow.) Some people take offense at this. Isn't this a Q&A site? Yes, but it's an "advanced" Q&A site, so to speak. This requirement is puzzling to many, but it is not personal or meant to make you feel "less than". We do (often gladly) answer even basic questions that show research. Every site has a culture; this is ours. We're not trying to be unwelcoming. Please edit to include what you found. It's a good question, basic for an endocrinologist, but hey... ;-)

@anongoodnurse 8 months late, but still haven't found any good information. The internet is telling me the purpose of the change in hormones (to prepare the endometrium for implantation), but not the actual cause - as in some physiological change in the Graafian follicles, or external stimulus etc. However, there are articles that mention how and why an LH surge occurs and promotes ovulation, but that's not the hormone that I'm interested in.

Sriram, I would love to help you, and will, but you must provide a quote and a link to a relevant article. I googled, "Why does the Corpus Luteum produce more Progesterone than Estrogen?" and got a perfectly good scientific article that discusses all aspects of the corpus luteum high up on the first page.


text:
The animal with the fastest hair growing rate
we know that human hair usually grows about 1/2 inch a month.
My question is what is the species with the fastest hair growing rate? (including fur for example).

Welcome! What did you find when you googled this? You need to make/show us an attempt to answer this. (Hover over the down vote arrow.) Many people take offense when informed that they need to show their attempt to answer this question first. Isn't this a Q&A site? Yes, but it's an "advanced" Q&A site, so to speak. This requirement is puzzling to many, but it is not personal or meant to make you feel "less than". We do (often gladly) answer even basic questions that show research. Every site has a culture. This is ours; we're not trying to be unwelcoming. Please edit to include what you found.

I'd love to be able to give some info on that topic, unfortunately it's an overlooked field of science. I found that hair growth speed depends on the area of the body and is regulated by cortisol, and that Asians have faster growing hair than Africans.


text:
Role of Bone marrow in T- lymphocyte development?
After I have read this statement in my textbook :
"Both bone-marrow and thymus provide micro-environments for the development and maturation of T-lymphocytes."
I have been searching for some detail on internet but I had found that only thymus is involved in maturation of T-cells while bone marrow in involved in maturation of B-lymphocyte.
So I'm bit of confused what exactly is the case .

T cells arise in the bone marrow, as that's where the common lymphoid progenitor cells are (they also give rise to B cells). However, their development and maturation - TCR gene rearrangement, positive selection, and negative selection - occurs in the thymus1.
I suppose that one could say there is a micro-environment for developing T cells in the bone marrow, as that's where they originate, but pretty much all development takes place in the thymus. Your textbook's statement is misleading at best, although I would say it's just wrong.
It's worthwhile to note that some mature T cells do take up residence in the bone marrow as part of immune surveillance, and micro-environments do form with other cells as part of that, so perhaps that may be what your book is referring to.
Reference

Kumar BV, Connors TJ, Farber DL. Human T Cell Development, Localization, and Function throughout Life. Immunity. 2018;48(2):202-213. doi:10.1016/j.immuni.2018.01.007


text:
How do I know if the claims of a scientific paper are generally accepted?
I am looking for information about the use of glucosamine and  chondroitin for treatment of back pain and disc degeneration. A paper published in Military Medicine in 1999 reported some beneficial effects, but newer papers (references needed) do not support these conclusions.
How do I search for more recent papers that cite this older paper, to decide what the current medical consensus is?
Glucosamine trial (negative results):
https://smallpdf.com/result#r=a595b512d3b25e41aabe7f3179ba8a4b&t=share-document
Chondroitin Sulfate trial (negative results):
https://smallpdf.com/result#r=b82b6b31030bfb6dffd6261a48153fe7&t=share-document
Glucosamine and Chondroitin Sulfate(good results but not conclusive)
https://smallpdf.com/result#r=626038b39e87cc64baab274e1d053871&t=share-document
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC165439/

It might be beneficial to also link to the more recent studies that contradict the older one.

Welcome to SE Biology. Please finish reading the [Tour]. I appreciate that your first language is English, but I think you should reconsider the use of the word "debunk. Do you want to know whether anyone has published a critical analysis of the paper showing that it is flawed — that is what I would take "debunk" to mean — or do you want to know what the current scientific/medical consensus is? People can disregard the conclusions of a paper without proving it flawed. I've cleaned up your presentation a bit.

Use the word “review” in the search terms. A review article will have references to all the useful papers.

@AgnesianOperator you are right sorry I've added the sources of the conflict, Thank you

@David Thank you David for the correction, it is a way more properly to ask, but what I would like to know, if there is a study that take that as a reference (because it is one of the oldest of this topic) and claims like ("We have followed the methods of this papers in a large trial but the outcome its different")

Papers provide evidence for or against various hypotheses, but no one paper is ever a definitive statement on an issue. It is expected that different trials will have different outcomes, both due to differences in the studies themselves (different inclusion/exclusion criteria, different study population, different dose/procedure, etc) and random statistical variation.
It's also very important to recognize that most studies are designed to test whether there is sufficient evidence to reject a null hypothesis of no effect. Failure to reject that null hypothesis does not mean that there is no effect, it means that the results aren't different enough from what you'd expect to see if there was no effect. It may be that there is a smaller effect than the study was powered to detect. Also, consider that a properly powered study generally has a true-positive detection rate of somewhere between 80 and 90%; that means, 10-20% of the time when there's a real effect of the expected size, the study won't be able to conclude there is a significant difference.
So, when there are multiple studies with different results, how do we decide what is "right"? Well, scientific consensus is built over many studies. In clinical research, the best evidence is when you have not only clinical evidence of an effect, but also an understood biological mechanism. At just the clinical level, though, studies can be combined through techniques of meta-analysis. Meta-analysis combines results from multiple studies, weights them by the size/quality of the study, and makes a comprehensive quantitative estimate from the covered literature. If you want to look for scientific consensus on something, you often want to look for recent meta analyses of that topic. In the medical field, there are also often consensus papers written on particular topics. Here's an example:
Priori, S. G., Wilde, A. A., Horie, M., Cho, Y., Behr, E. R., Berul, C., ... & Tracy, C. (2013). HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes: document endorsed by HRS, EHRA, and APHRS in May 2013 and by ACCF, AHA, PACES, and AEPC in June 2013. Heart rhythm, 10(12), 1932-1963.
These statements are written by a bunch of scientists/physicians gathering together and comprehensively reviewing literature on some topic. They typically will weigh not only evidence for effect like in meta analysis, but also consider the implications of treatment options including costs, side effects, and the consequences of getting it wrong (for example, if a treatment following a wrong diagnosis masks some other condition that then goes untreated).

@BryanKrause has given a good general answer to this question.
One specific approach (which the poster may or may not already have taken) is to look for links on the publisher’s webpage to subsequent papers that have cited the one of interest. In this case the page shows that there are 107 papers in Web of Science citing the article in question. It also gives direct access to Google Scholar and Crossref. Click and go. Happy reading!

Thanks David, you do answers the originally question but, Bryan answer's is the apparently correct for the new question

@RodParedes — no problem. Better to accept his answer. But a gentle suggestion about your English. You have a peculiar tendency (as I’ve never met it before) to put the letter “s” at the end of verbs. I realize it’s tough, but if you are going to communicate in science you need to improve your English. Or cheat, like I do in Italian. Prepare your text in a word processor. Select the text and set the language to English, and then run a grammar test. Think about the errors flagged (the suggestions may not always be right) and check in your basic language reference.

Use google scholar and have a look at the papers that have recently cited it by filtering for the year the citing paper was published.
https://scholar.google.com/scholar?cites=17068797659415407733&as_sdt=2005&sciodt=0,5&hl=en
More broadly it's often taken that more citations is a positive, though this is impacted by all manner of phenomena and a high citation count could be due to papers negatively reviewing it!

PubMed has a similar feature (https://pubmed.ncbi.nlm.nih.gov/?linkname=pubmed_pubmed_citedin&from_uid=10050562)


text:
How are the receptors in the thalamus weakened/shut down during sleep?
During sleep, GABAergic inhibition of the thalamus occurs and along with that, it should "block" our senses. Are the receptors weakened, or completely shut down? If they are weakened, what is the exact process that can hinder their function? If they are completely shut, how can we still have the ability to hear during sleep and wake up as a result?

Sleep research is a big field and the answer to your question can take many forms and fill libraries. Having said that, it is not so much inhibition of the thalamus per se, but a change in firing behavior that results in a decreased relay function of thalamic neurons afaik. Specifically, during stages of sleep, or in phases of reduced consciousness where thalamic relay of sensory inputs to the cortex is blocked, the thalamocortical neurons are entrained in slow oscillatory bursting behavior, resulting in more synchronized, slow-wave EEG (Fig. 1). This intrinsic slow wave, bursting activity in the thalamocortical network effectively reduces the ability for peripheral sensory input to reach the cortex via the thalamocortical fibers. This explains the unresponsiveness of people with slow wave EEG to external stimuli.
Slow-wave EEG is most prominent during deep sleep. By contrast, during active wakefulness these neurons fire more chaotically, very much dependent on their inputs, resulting in the EEG rich in high frequencies. A succinct overview is given here on the site of McGill University. Fig. 1 shows the dependency of thalamocortical neurons and cortical neurons in cats (Fig. 1A) and rodents (Fig. 1B) during different vigilance states. The figure is taken from a rock in sleep and epilepsy research, namely David McCormick.
Because the thalamocortical neurons are so occupied with their rhythmic bursting, phasic input from the thalamus may not be relayed. However, stimuli strong enough to push through / override the oscillatory behavior may still result in cortical activity in the sensory regions.

Fig. 1. Slow wave sleep in cats (A) is associated with slow oscillations and spindle waves (equivalent to the K complex in man). The waking state is characterized by rhythmic activity at  higher (gamma) frequency range. In mice (B), mere inactivity like cessation of walking is associated with an increase in slow rhythmic activity. (C) Schematic of thalamocortical circuitry responsible for the generation of rhythmic activity. The slow oscillation and gamma frequency oscillations are generated within the cortex, as an interaction of excitatory and inhibitory neurons. Spindle waves are generated during sleep in the thalamus as an interaction of thalamic reticular GABAergic neurons and thalamocortical relay cells. source: McCormick et al. (2014)
Reference
- McCormick et al., Curr Opin Neurobiol (2014); 31: 133-40


text:
Coniferous tree with alternating bunches of short needles (Toronto area)
What species of tree is this?

Location: East of Toronto, zone 6; urban
Date of photos: May 10, 2022
Diameter at breast height: ~18 inches
Height: ~30 ft

And to help you sufficiently appreciate the excellent answer below, behold — The Larch

 Short Answer
Larix laricina, commonly called Tamarack or American Larch is a deciduous conifer with short-needle-like leaves arranged in bunched fascicles in a alternating (sometimes whorled) arrangement around short stems. The tree is the only species of Larix native to the Toronto region.

 Larix laricina stem  Source: UWGB Herbarium
 Long Answer
This is a larch tree in the genus Larix.
These deciduous conifer trees characteristically have fascicles, or bunches, of short, needle-like leaves arranges in whorls around their stems. They grow in northern forests (deciduous conifer forests, boreal forests, and northern alpine forests) in temperate cold zones. (In fact, larches grow farther North than any other tree species!)
There are 3 North American Species and 9(-11) Eurasian species. Of those 12(-14) species, only 1 species, Larix laricina (Tamarack) is native to the Toronto region:

From Wikipedia:

Larix laricina (Du Roi) K. Koch – Tamarack or American larch. Parts of Alaska and throughout Canada and the northern United States from the eastern Rocky Mountains to the Atlantic shore.
Larix lyallii Parl. – Subalpine larch. Mountains of northwest United States and southwest Canada, at very high altitude.
Larix occidentalis Nutt. – Western larch. Mountains of northwest United States and southwest Canada, at lower altitudes (Pacific Northwest).

 Range map for Larix laricina. Source: Wikipedia
BONAP range maps for Larix species confirms Larix laricina as native to Toronoto, but it also suggests evidence of the European species Larix decidua as an exotic.

We can rule out Larix decidua because the bark is neither smooth nor fissured (see Wisonsin Horticulture), the twigs are not gray or yellow (see the NAS Field Guide to Trees1), and the needles are neither reaching lengths of 4 cm (see Wikipedia) nor (from my quick count from your image) achieving clusters of 30-60 needles per fascicle (see USFS).

Larix laricina, commonly called Tamarack or American Larch, then, seems like the most likely species.

Range: Canada (including Toronto ; see above)

Bark: rough and scaly (USFS)

Leaves: 2-3 cm needles (wikipedia) bunches into fascicles containing 10-20 needles (USFS).

Twigs: reddish-brown (NAS Field Guide to Trees1)

 L: Larix laricina fascicle with leaves. R: Larix laricina stem  Source: UWGB Herbarium
Your image is just a tad too blurry and my screen a tad too small to see your needle detail. A better image of the needles and an image focused on the bark would only further help to corroborate my answer.

 1. Little, E. L. (1980). National audubon society Field Guide to North American Trees: Eastern Region. Alfred A. KNopf, New York.

Thanks very much! If you click on my photos to zoom in (on a full PC computer screen), are they still to blurry? You might need to click on them a second time...to fully zoom in.


text:
Could water soluble dyes be directly absorbed by a plant's / tree's xylem?
Amateur woodworker / hobbyist here, I enjoy using colorful or exotic wood species, the issue is that many of these species are rare, expensive, endangered, hard to grow, or otherwise difficult to obtain.
What I'm wondering is... is it possible to directly introduce dyes or color to a young tree slowly over time, either through directly exposing the internal rings to some kind of dyed water while its growing, or by somehow getting around the root's natural filters? (People have tried to grow plants in just dyed water, but the roots are able to filter most of it out)
It would be interesting to have a plank dyed with a more saturated color than is naturally possible, without treating it and introducing dyes after the wood has been felled.
Often times treating wood can damage specific properties of it, some dyes and treatments can make the planks virtually useless for sanding or staining, and reintroducing water or other fluids can cause warping and other damage to the wood.
If a natural, water soluble dye existed within the wood from the start, it might be possible to get around some or all of those issues.
I'm just wondering if this is even possible, and if so, how it could be done without killing a tree..
This is more of an idea then an experiment, but it would be interesting to try.

You could try using a small weed or hydrophilic species like willow and hydroponics. For bigger trees it would be possible using some obscure metholodology and highly cumbersome.

I don't believe it's possible; the roots have selective permeability. Try this: add food dye to water (darker is better), use it to water a cut stem and a rooted plant. The cut stem will take it up. The rooted plant will not.


text:
Why this decay term in Anaerobic Digestion Model?
I am reading about the AM2 model, which appears to be a simplified version of the ADM1 model
for modeling anaerobic processes.
The author of this doctoral thesis extended the simpler AM2 model by introducing hydrolysis. Given a substrate state variable $S_1(t)$, he then proceeds as follows:
$$\frac{dS1}{dt}=D_{in}(S_{1in}-S)-k_1\mu_1X_1+k_7\left(k_{dis}X_c-k_{dec,X_1}X_1-k_{dec,X_2}X_2\right)+k_8\left((k_{hyd,ch}X_{ch}-f_{ch,X_c}k_{dis}X_c)+(k_{hyd,pr}X_{ch}-f_{pr,X_c}k_{dis}X_c)+(k_{hyd,li}X_{li}-f_{li,X_c}k_{dis}X_c)\right)$$
The variables $X_1,X_2$ describe the chemical oxygen demand of acidogenic and methanophobic bacteria. The variables $X_{ch},X_{li},X_ch$ describe the chemical oxygen demand of the hydrolized composite $X_c$.
I do not understand the underbraced parts:
$$\frac{dS1}{dt}=D_{in}(S_{1in}-S)-k_1\mu_1X_1+k_7\left(k_{dis}X_c-k_{dec,X_1}X_1\underbrace{-k_{dec,X_2}X_2}\right)+k_8\left((k_{hyd,ch}X_{ch}-f_{ch,X_c}k_{dis}X_c)+(k_{hyd,pr}X_{ch}\underbrace{-f_{pr,X_c}k_{dis}X_c})+(k_{hyd,li}X_{li}\underbrace{-f_{li,X_c}k_{dis}X_c})\right)$$
Unfortunately I have not been able to reach the author. Why would we substract the underbraced terms? Imagine a scenario, where $k_8=0, k_{dis}=0$. In that case, the substrate concentration $S_1$ could become negative just because of dying bacteria (the $k_{dec}$ terms). That does not make any sense to me.
Does it make sense to you?

I would start be asking simple questions. Does your imagined scenario make sense (biologically and/or practically)? Are there organic substrates with these characteristics (a zero disintegration parameter ({k_dis}) and a zero yield coefficient for proteins, lipids, and carbohydrates)? And if so, why would you feed them into your anaerobic processor? Perhaps my lack of expertise in the area is just preventing me from understanding why the scenario you described is problematic.

Thank you for the answer. The continued substraction of available substrate from for example dead biomass (decayed bacteria) strikes me as peculiar. You are right, I will more deeply investigate these basoc questions


text:
Has anyone seen/read interspecies competition that is different at spatial scale for the same group of animals?
I work at a highly fragmented wildlife sanctuary in North Borneo, Malaysia. We have 8 species of hornbills here and from our observation they've grown to be less territorial in terms of where they forage for food. Our friends in the mainland of Malaysia have observed differently - these hornbills are territorial even in the areas they forage, rather than just during breeding season or around their nesting trees.
Do you think the limited resources for space and food where I work force them to be less territorial than their counterparts that live in areas with more forest cover (thus more space and food)?
I'd love to hear or read more observations like this from different areas, if any of you have anything to share.


text:
Is there a resource/paper containing information about which co-activators are often associated with a given transcription factor?
Given a list of human transcription factors, I would be interested in which co-activators they are often associated with.
I imagine that one could combine co-expression, pull-down, and other kinds of data to get an idea 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, your question isn't focused, isn't clear, and shows no evidence of the expected prior research — all of these are reasons for closure and downvoting. Please [edit] this to focus on a narrow (i.e. answerable in this format) question, tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions.

In addition, if you provide context (e.g. you are trying to develop a bioinformatic tool to do X) you are more likely to get a useful answer. In addition, depending on context this question might be a better fit for [Bioinformatics.SE], but if you think so please do not crosspost, instead request migration or delete from this site before reposting (with more details as described above) there.

related chapter:  Coactivators  •Encyclopedia of Cancer, 2008• Vol.1, p.714-714

useful information:  https://www.mdpi.com/2072-6694/12/8/2296/htm

This website can be used to search for protein interactomes:
http://www.interactome-atlas.org/
might help you.

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.

Most eukaryotic TFs (transcription factors) are thought to act by recruiting cofactors (Reiter et al., 2017).

“Coactivators” and “corepressors,” are cofactors and these are mediators of TF effector activity.

Do you mean you need the information of cofactors?


text:
How to reduce PPi concentration in blood samples by PPase
I have some samples of whole blood that are a little bit expensive and I want to significantly reduce the concentration of PPi in the samples by causing a reaction. I don't have any experience in practical chemistry, but I understand that in theory, there are enzymes that can hydrolyze pyrophosphate into orthophosphate (e.g. inorganic pyrophosphatase).
I see that I can purchase inorganic pyrophosphatase suspended in 3.2 M ammonium sulfate solution, (pH approximately 6), from yeast, on Sigma-Aldrich and in theory converts 1 micromol pyrophosphate to orthophosphate per minute at room temperature (in the presence of Mg-ions). For my purpose, the reduction in pH is not a problem. I am more concerned about whether PPi concentration would actually go down, or if I could expect cell lysis or other effects to occur, causing PPi to rise.
Can I use this reagent to reduce the measurable PPi concentrations in the blood samples? And if so, how would I do it?
EDIT: I am doing an experiment with bacterial growth in plasma, and comparing with serum deficient in pyrophosphate. I want to have a rough idea of the appropriate way to hydrolyse the PPi.

I guess it might be helpful to know the reason you are removing pyrophosphate? Like this paper suggests, pyrophosphate activity might be inhibited by compounds present in blood, and it would help if you tested on a different sample while monitoring the pyrophosphate level as they do in this paper

@PrashantBharadwaj I added the information that you requested.

@MikkelRev, you mention whole blood, plasma, and serum. Which of these are you ultimately using as your bacterial growth medium? This will affect the steps of your protocol.

Bernhard et al. 1 describe a method for the treatment of human plasma with yeast inorganic pyrophosphatase. The PPase-treated plasma is used as both a diluent and a negative control in their PPi conversion assay. The use of a salt solution as a secondary negative control confirms the depletion of PPi from PPase-treated plasma samples. I've quoted their protocol and validation steps below, but here is my summary:

Centrifuge whole blood and transfer supernatant. This serves to remove most of the cells from the plasma fraction.
Filter plasma with 300 kDa filter. This will remove any remaining cells so the amount of PPi contributed by any cell lysis is negligible.
Add PPase and mix by inversion. The authors do not supplement the plasma with Mg2+ nor any buffers.
Incubate for 30 minutes at room temperature.
Filter plasma with 30 kDa filter. The recombinant PPase from NEB has a mass of 71 kDa 2, so this step likely serves to remove PPase from the plasma, which would confound the use of PPase-treated plasma as a diluent for PPi measurement.
Aliquot and freeze PPase-treated plasma.

Generation of Pyrophosphatase-treated Plasma
For human plasma, blood drawn from donors (everything at room temperature) was spun down at 3500 rpm for 15 min, and plasma was then transferred to a 15-mL tube. Then, 2 mL of plasma was filtered through a Centrisart® I 300 kDa mass cutoff filter at 2500 × g for 30 min. The filtered plasma was transferred to a fresh 1.5 mL Eppendorf AG tube. Yeast inorganic pyrophosphatase (PPase; New England Biolabs Inc) was added at 1:1000 plasma, mixed well by inverting 4 times, and incubated for 30 min at room temperature. Five hundred microliters of PPase-treated plasma was filtered through a Nanosep Centrifugal Device With Omega Membrane 30K (Pall Corp) at 13,200 × g for 5 to 10 min. The PPase-treated, filtered plasma was frozen at −80°C in 500 µL aliquots. A new stock was made every 2 months.

Assay Description and Validation
The assay utilized ATP sulfurylase to convert PPi to ATP, which was then detected by a luciferase/luciferin luminescence detection kit. The luminescent signal is directly proportional to the amount of ATP present; the assay is a semiquantitative assay (regulation 493.1256(d)(iii) of Clinical Laboratory Improvement Amendments of 1988). Target analyte of assay validation was PPi. The specimens were human platelet-free plasma samples. The low limit of detection was 0.15 µM; the quantitative range was 0.15 to 10 µM. Normal ranges, determined by testing PPi levels of 50 healthy adult volunteers (50% male), were 1.43 to 7.40 µM (unpublished data). For validation and clinical testing, a standard curve was generated for each run by titrating measured amounts of PPi in PPase-treated pooled human plasma. The PPi standard curve was prepared by diluting powder PPi in water; thus, concentration was equal to 1 mM PPi final. One millimolar of PPi was diluted 1:100 in PPase-treated donor plasma and mixed well. Defined concentrations were achieved by serial 1:2 dilutions in PPase-treated donor plasma. A negative control of Hank’s balanced salt solution alone and PPase-treated pooled human plasma were included on each assay plate. Each concentration was run in triplicate.

References

Bernhard E, Nitschke Y, Khursigara G, Sabbagh Y, Wang Y, Rutsch F. A Reference Range for Plasma Levels of Inorganic Pyrophosphate in Children Using the ATP Sulfurylase Method. J Clin Endocrinol Metab. 2022 Jan 1;107(1):109-118.
https://www.neb.com/products/m2403-pyrophosphatase-inorganic-yeast


text:
Why are drug dosages so high in some mice studies?
On reading through some research on the effects of certain drugs I often come across staggeringly high dosages such as in this paper:

Römer, B., Pfeiffer, N., Lewicka, S., Ben-Abdallah, N., Vogt, M. A.,
Deuschle, M., ... & Gass, P. (2010). Finasteride treatment inhibits
adult hippocampal neurogenesis in male mice. Pharmacopsychiatry,
43(05), 174-178.

The paper says:

After 2 weeks of acclimatization all
mice received at an age of 12 weeks an identical treatment with
either finasteride (100 mg/kg) or 2-hydroxypropyl-ß-cyclodex-
trin as vehicle [32]. A single daily injection was administered
subcutaneously during 7 consecutive days.

To give context, a standard dosage of Finasteride for androgenic alopecia is 1mg per day orally and 5mg for benign prostatic hyperplasia. The dosage listed in the paper would be equivalent to me taking 7200mg per day via injection.
I see this sometimes in drug research and I imagine this is done to force an effect and see what that effect is. Are they inferring that the effect scales linearly and that the standard dose has 1/7200th the effect?
What is the reasoning behind this approach?

Mice are simply different from humans; they have different metabolism, different lifespan, different body size.
Generally, for a first order approximation, one might scale simply by body weight to account for body size, expressing dose in units of "drug/body weight". Among humans, that can work fairly well, though fails in several cases:

Kids, and especially young children/infants, whose metabolism differs a lot from adults

By sex, since body fat percentages differ on average between men and women

For the obese, especially for drugs that partition differently in different tissues.

It fails for mice, too; most typically the dose per weight to get the same level of effect in mice is much higher than for humans.
An alternative is to adjust based on body surface area, though that isn't something easy to measure, so typically we still express and adjust doses among members of the same species by weight. However, you can use a rough estimate to come up with some constant cross-species conversion factors. Nair and Jacob, 2016 recommend a 12.3X higher dose per weight to adjust for surface area differences between mice and humans (they have a whole table for other species, too).
Ultimately, the appropriateness of any adjustment depends on precisely what drug you're talking about and how exactly that drug is metabolized. Drugs may also have different affinities for target receptors in different species, which may lead to additional conversion factors. These things can only be worked out with specific study.
There can also be experimental reasons. When doing a study for safety, it may be preferable to study doses much higher in animals than expected for use in humans, both because the sample sizes in an animal study are going to be far smaller than the population sizes exposed to a pharmaceutical drug that is approved, and because the tolerance for risk in humans is far lower than the tolerance for risk in the animal study. If you give a drug at 10x or 100x the effective dose and it doesn't cause problems, you can be far more confident going into clinical trials that there isn't a lurking disaster (of course, bad safety results still happen). You may also plan to give the drug to people for years on end; a mouse can't live nearly that long, so a higher dose over a shorter time might help build an understanding of the safety profile, or at least an approximation. It of course isn't quite as simple as giving a drug at 100X the dose for 1/100th the time, but moving in that direction may be preferable to testing a drug in a mouse for only a week that is used in humans for years.
Additionally, when screening drugs for some effect, it may be easier to test a lot of drugs at high doses in small samples, find which ones do something like what you're targeting, and then experiment further with the dose.

One more point that applies to the specific example you gave is that bioavailability can vary depending on how a drug is administered. Generally, IV is the most direct route with the highest bioavailability. For mice, intraperitoneal injections are also used that typically have high bioavailability, since IV injections can be a bit complicated. Oral bioavailability is typically lower, since the drug may be modified to inactive form in the digestive tract, especially in the acidic stomach environment, or through liver metabolism before reaching systemic circulation. Subcutaneous typically has the least bioavailability and slowest systemic uptake. Of course, for drugs that are intended to be modified, the effects of different administration routes can be opposite (for example, a drug that is more potent after liver metabolism, or a drug that reacts with stomach acid to its active form).

Nair, A. B., & Jacob, S. (2016). A simple practice guide for dose conversion between animals and human. Journal of basic and clinical pharmacy, 7(2), 27.


text:
Is Eastern diamondback rattlesnake swimming is an adaptation?
Is Eastern diamondback rattlesnake swimming is an adaptation?
I read that they are capable swimmers. Can we consider that as an adaptation?

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

I think a better question is." Are there any snakes that can't swim?"


text:
Are there human genes that make a cell die when they undergo copy-number alterations?
I am trying to understand if there are known genes in the human genome where copy-number should be stable at a diploid level for the carrier cell to live.
I.e., are there lethal deletions or duplications of specific genes in the human genome? I would imagine "house-keeping" genes might be needed for the regular processes within a cell, but I could not find any reference online on specific studies on the matter. House-keeping genes defined as in this article.
E.g., when looking for "lethal heterozygous deletion genes human allele copy number", I mostly found articles regarding tumor-suppressor genes, so I'm not sure I am using the right keywords.
The genes I am looking for should be exclusively from the human genome.

Why "exclusively from the human genome"?

To make the question more specific. I am currently working on the human genome and, even if genes conserved across different organisms might be interesting, this would be out of scope for this specific question, I think.

Would you consider a translocation/insertion event as a candidate? Say a specific gene (geneA) is reverse transcribed and inserted into a different location of the genome, disrupting an essential gene (geneB). This would result in geneA having a copy number of +1 and it would be deleterious since it disrupts geneB, but it wouldn't strictly be a case where the fact of a change in copy number in and of itself is deadly, it's only because of the specific place where the copy was inserted. For deletions, the answer is trivially yes, house keeping genes being a prime example.

@terdon, thanks. Regarding the translocation/insertion event, I believe this is interesting but not exactly what I'm looking for, since I'm looking for genes where disruption in their copy number is deleterious. Regarding house-keeping genes, is there a validated set of genes that can be used in this case? For example, where the disruption of a gene copy number is verified by different methodologies?

I don't know, but I would guess you should be able to find things at least from mouse knockout studies and you could then translate to human. For obvious ethical reasons that sort of experiment is frowned upon on human subjects and you'll never find actual cases in the wild since any embryo carrying this wouldn't have been born in the first place.

The issue with mouse orthologs seems that "Comparing documented phenotypes of null mutations in humans and mice, we find that >20% of human essential genes have nonessential mouse orthologs. These changes of gene essentiality appear to be associated with adaptive evolution at the protein-sequence, but not gene-expression, level" from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2383943/ . Additional information on "essential genes" can be found at http://origin.tubic.org/deg/public/index.php/index

This also looks interesting: https://www.science.org/doi/10.1126/science.aac7041

A gene is defined as "essential" if its complete loss of function results in a complete loss of fitness (Hart et al., 2014). In practice, a prenatal lethal phenotype is typically the criterion for essentiality.
Homozygous deletion ($CN = 0$) is one of the copy number states that can lead to complete loss of function for a gene, therefore, in theory, if a cell undergoes homozygous deletion on one or more "essential" genes, this CN state might be lethal for the cell.
Some useful resources for "essential" genes are at:

https://www.science.org/doi/10.1126/science.aad7925
https://www.embopress.org/doi/full/10.15252/msb.20145216
https://www.science.org/doi/10.1126/science.aac7041
https://www.science.org/doi/10.1126/science.aac7557
http://origin.tubic.org/deg/public/index.php/index
https://en.wikipedia.org/wiki/Essential_gene

I am not sure how different CN states can be assessed for cell lethality.

Why the downvote?

Personally, I don't see how this answers your original question. You ask for genes that are lethal to cells if they suffer copy number alterations (-2, -1, +1, +2 etc), whereas your answer talks about essential genes who are only lethal when completely lost by the cell.

Completely lost means homozygous deletion, which is copy number alteration. This was the only case that I found described in the literature - probably because is more easy to assess with currently available orthogonal assays. I agree that the answer is not complete, but it is the best that I could find in the literature, so I still don't understand the downvote (which implies that the answer is not useful - or out of scope - which in my opinion is not in this case). I am open to choose another, more complete, answer - if that exists. I removed the acceptance to the answer if it helps.

I get your point and agree. Removed my downvote. Sorry for that!

No worries, I totally understand your point-of-view. Just I know that questions with downvotes are usually ignored by the reader even if they are reasonable, and I wanted to share and learn about this topic :)

Btw, I don't have an answer to your question, but you might want to read about gene dosage. The Wikipedia article is short, but seems to have some relevant references that could be a good start. Not sure how much you will find for human genes though...

Thank you, I am somewhat familiar with the concept, but I never reviewed it in depth - and forgot to use this keyword in this case. I will look into the references.

There is some evidence that even in a heterozygous null state some essential human genes are haploinsufficient, e.g. it is lethal when fewer than two functional copies is present.
For example, this paper pooled cells after introducing knockout edits in a variety of genes, and measured relative growth in the pool, identifying a number of genes that are quite intolerant of loss of one copy (~600 according to one expansive estimate).
Additionally, this paper abstract notes that there are some 3,000 haploinsufficient genes, which is somewhat more expansive than the previous estimate. I don't have access to the paper so I am not sure where that number comes from. This paper screened mice and humans for various flavors of essentiality, coming up with various estimates for haploinsufficiency, mostly on the order of a few hundred genes.
I would expect that some of this extends to the full loss of one gene copy, but I don't have direct evidence for a "copy number" type genomic alteration yielding essentiality-haploinsufficiency. This paper does comment somewhat on haploinsufficiency in CNVs, but does not appear to consider essentiality.
This paper also considers haploinsufficient and "triploinsufficient" genes with notable phenotypes in humans, though again I think that they are more interested in disease phenotypes than in essentiality.


text:
Do Mannose and Galactose yield the same products as Glucose when oxidized?
I just started learning about sugar metabolism, when I saw how other monosaccharides enter the glycolytic pathway. Mannose enters glycolysis as fructose-6-phosphate at the expense of 1 ATP, then pretty much follows the same reactions as glucose. On the other hand, Galactose enters glycolysis as Glucose-6-phosphate then would also follow the same reactions as glucose. Does this mean that both of these monosaccharides yield the same products as Glucose? Or is there something I am missing?
I apologize if the answer to this is obvious; I can't seem to find online references that give the net yields for other monosaccharides, so I just wanted to be sure.

The answer to this question is yes. And it is obvious to anyone familiar with metabolism. I hesitated to give a formal answer, but I hate answers in comments, so let me supplement this with some ‘principles’ (in so far as there are any principles in biology) for those less familiar with metabolism (as we all were once).

To a cell, fructose 6-phosphate is fructose 6-phosphate, so its metabolic fate is likely to be the same, regardless of its source. It will be dealt with according to the activity of the enzymes that can catalyse the reactions of F6-P. (These may, however, differ in different cell compartments, as enzymes and concentrations of reactants may differ there.)

Central metabolic pathways such as glycolysis are complex and highly evolved to do their job well. They are found throughout all kingdoms of life†. It is economical to feed minor substrates into them, rather than duplicate a full pathway. Hence the additional pathways for dealing with minor sugars will be those converting them to intermediates of glycolysis, and it is these where metabolic diseases of sugar metabolism are found.

† This doesn’t mean that they are all present in every organism or in every cell type of a multicellular organism. Just that their distribution is such that that (supplemented by other arguments) we consider them to have appeared early in evolution.

Thank you for answering sir, I actually tried to examine how other sugars aside from glucose enter glycolysis and initially thought that there should be no difference in their yields as compared to glucose, but I got confused since I saw a couple of online resources that says galactose yields 0 ATP in glycolysis.

@JoshArceno — You are welcome. I imagine that you must have misunderstood the articles you mention, as galactose is half of the disaccharide, lactose. As the function of lactose is to provide nutrition for sucklings, common sense would suggest galactose oxidation would result in net generation of ATP.


text:
Why is $H_{S}$ divided by $H_{T}$ in Wright's $F_{st}$ equation?
$F_{st} = H_{t}-\frac{H_{s}}{H_{T}}$, where $H_{T}$ stands for expected average heterozygosity in the meta population and $H_{S}$ stands for expected average heterozygosity in the sub-population.
As I understand it, $H_{T}$ is the heterozygosity assuming that all of the sub-populations are from the same population and if it's true, there would be no gap with $H_{S}$ (if it's in Hardy-Weinberg equilibrium).
Than why is it divided again with $H_{T}$? Is it some kind of standardisation? I don't think it's necessary.
Why can't it be used like heterozygosity of population of meta population (variation of meta population)/heterozygosity of sub populations (variation of sub-populations) somewhat like F-value of F-test.
Also why is it done with expected heterozygosity, not with observed heterozygosity
I'm talking about fixation index and as I know, there are some other formulas for fixation index but this one is commonly used
uwyo.edu/dbmcd/popecol/maylects/fst.html

There are multiple distinct statistics called "Fst". What are you referring to specifically?

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.

I'm talking about fixation index and as I know, there are some other formulas for fixation index but this one is commonly used
http://www.uwyo.edu/dbmcd/popecol/maylects/fst.html

$F_{ST}$, as defined by Nei 1973, is $F_{ST} = \frac{H_T-H_S}{H_T}$ and not $F_{ST} = H_T -  \frac{H_S}{H_T}$. It is, to my knowledge, equivalent to to original Wright's definition $F_{ST} = \frac{var(p)}{\bar p}$, where $var(p)$ is the mean (over all loci) variance (over all subpopulations) in allele frequency and $\bar p$ is the mean (over all loci) mean (over all subpopulations) allele frequency. Other formulations exist, either considering population weights or considering specific bias in estimate (e.g. Weir-Cockerham)


text:
Does a 2-year-cycle species exist?
Many species sleep for an entire season or travel from one continent to another every year. For all species I know all of these recurring events occur in a period of one year. One might refer to these species as 1-year-cycle species.
I wonder whether there are any 2-year cycle species. For example one that travels to some place not every but only every other year or sleeps for an entire year, before becoming active again.
I don't know any and I just started to wonder whether there is an evolutionary argument for this.

There are some polar/high altitude animal species (insects IIRC) that will hibernate until conditions are right, sometimes more than 1 year.

Welcome to Biology.SE. Are we to assume you are only interested in animals? Are you interested in examples like @bob1 suggests where organisms have prolonged often highly variable dormant periods? Please [edit] your post to answer these questions, and also tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

Are you aware of insects that have 2, 4 and even 9 year cycles, some of which swarm regularly with many years interval?

Interesting, thanks for pointing this out! But @LifeInTheTrees this is very much answering the question, as it is a periodic process. Can you maybe provide the name of the species and I'll accept the answer

Biennial plants come to mind. There's also 2-year cicadas. (There's also 13 and 17 year cycles -- periodic cicadas (see https://biology.stackexchange.com/a/100721/16866 and https://biology.stackexchange.com/a/9241/16866))

biennial migration
In sharks (Naidoo et al. 2017):

C. taurus females undertake a biennial migration along the east coast of SA of approximately 1000 km from their gestation grounds to their pupping grounds in the south, so they are not exposed to any single point source of pollution such as a marine outfall or an industrialised harbour for lengthy periods.

biennial life cycles
Semivoltine, biennial are good search terms for answering this question, e.g.: https://scholar.google.com/scholar?q=semivoltine+biennial
As other answers have suggested, most of the examples we find this way are insects living in relatively cold environments where it may take more than one year to complete a life cycle (I haven't come across any examples where the life cycle is always biennial — generally these species have univoltine (one generation per year) or faster life cycles in warmer climates and semivoltine/biennial cycles in colder climates.
e.g. Sota 1996:

Two closely related Leptocarabus [beetle] species overwintered as larvae in the first winter and as adults in the second and later years; one species occurred at altitudes from 750 to 2200 m, and its life cycle changed from annual to biennial in the subalpine zone. The other smaller species occurred from subalpine to alpine zones and had a biennial life cycle.

evolutionary argument
This is somewhat hand-wavy, but it appears that most examples of biennial life cycles/migration occur in organisms with sufficiently rates of growth (in the case of insects) or resource acquisition (in the case of sharks) that they cannot manage to complete their life cycle or reproduce in a single year, so must delay until a second year. (These organisms also live in environments that are sufficiently seasonal that they must synchronize with the annual cycle in some way.)

Naidoo, Kristina, Anil Chuturgoon, Geremy Cliff, Sanil Singh, Megan Ellis, Nicholas Otway, Andre Vosloo, and Michael Gregory. “Possible Maternal Offloading of Metals in the Plasma, Uterine and Capsule Fluid of Pregnant Ragged-Tooth Sharks (Carcharias taurus) on the East Coast of South Africa.” Environmental Science and Pollution Research 24, no. 20 (July 1, 2017): 16798–805. https://doi.org/10.1007/s11356-017-9281-1.
Sota, Teiji. “Altitudinal Variation in Life Cycles of Carabid Beetles: Life-Cycle Strategy and Colonization in Alpine Zones.” Arctic and Alpine Research 28, no. 4 (November 1, 1996): 441–47. https://doi.org/10.1080/00040851.1996.12003197.

Albatrosses have biennial breeding and sabbatical years where they can travel 120,000 km on their 4m wings: https://www.nature.com/articles/srep08853
There are very many species of arthropods which stay in a grub stage 2,3, 4 up to 17 years. Seven species of North American periodic cicadas swarm every 13 or 17 years locally at the same time. https://en.wikipedia.org/wiki/Periodical_cicadas?wprov=sfla1
https://entnemdept.ufl.edu/walker/ufbir/chapters/chapter_12.shtml

Sure, insects in particular are incredibly diverse and while some have multi-stage life cycles which can extend over years, others reproduce multiple times a year.
Common/popular examples of the former are the periodic species of cicada that take 13 or 17 years to emerge as adults, or the woolly bear, which remains as a caterpillar for possibly several seasons, depending on the time it takes to grow, before becoming an adult. If you're looking for exactly a 2-year cycle, a woolly bear in the right conditions would qualify.
Another example is the spruce beetle; like the woolly bear, growth time depends on conditions, but the two-year cycle is most common.
There are so many species of insects that it's likely examples could go on and on and fill books.


text:
How long does an Audiomoth acoustic logger record for?
I'm wanting to record bat echolocation calls using an Audiomoth recorder. However, I can't find out anywhere how long these recorders can record for on a full charge.
What is the longest duration someone has deployed these recorders for, for the purposes of recording bat echolocation, and at what duty cycle (recording continuously, or just at dusk for a few hours?)
Additional info in the comments:
They operate using 3 AA batteries.

Audiomoth is apparently the designation of the circuit module, could you tell us what power-supply you're using?

They operate on AA batteries (3x)...

AA batteries vary in capacity by a factor of more than 6 times (Wikipedia). This is a tricky on-off-topic question, because we need to establish things which are more suited to our [electronics.se] stack. I'll try anyhow. With the most powerful batteries, the tech spec sheet indicates you should get just a shade under 3 days/nights continuous use - but the device can be programmed to go into sleep-mode making it maybe 6 nights in total. Can you code?

when recording high sample rate and continuously through the night (e.g. around 8hrs), then they will last about 3 nights or so.  If you sample discontinuously then you will obviously get a longer deployment time. The new firmware also provides a triggering mechanism that will allow much longer deployment times - see here:
https://www.openacousticdevices.info/support/announcements/audiomoth-configuration-app-1-7-0-firmware-1-8-0
Also - useful advice on Audiomoths generally is available at Tessa Rhinehart's GitHub (https://github.com/rhine3/audiomoth-guide) and at Wildlabs.net.

I use Audiomoths for recording bats. If you are looking for continuous recording, depending on your sample rate (you want your sample rate to be at least twice the highest frequency you expect to record--256kHz should be good if you are in the US/Europe) you should be able to get 3 nights. The key here is the word "should." I've had batteries and Audiomoths do weird things in the field, so if the data are critical, I strongly recommend having redundancy if that's an option, meaning two Audiomoths recording at the same time. I also recommend changing the batteries at least one day earlier than when you think they should last until.
Another thing related to your question: consider where you place your Audiomoth and if a curious squirrel/raccoon/deer might chomp on it and affect your recording duration. Speaking from experience, I highly recommend the hard case.

You can also add an external battery pack with a little soldering which can make the devices last much longer. e.g. https://twitter.com/freaklabs/status/1529915274853502980

@macster110 You beat me to it - was about to post the same +1

With an earlier version of the Audiomoth (v 1.1.0), I had continuously recorded at 384 kHz with duracell rechargable batteries, followed by another round with duracell ultra batteries. The latter lasted the longest for around 2.5 days. So it fluctuates based on the types of batteries recommended and some commercial rechargable batteries usually have a faster drain life.
More recently, Akiba from Freak Labs (https://twitter.com/freaklabs/status/1529915274853502980) has been experimenting with extending battery life using an external battery pack. So this could be a possible solution if suitable.