text:
What is the speed of human immune reactions?
It's easy to find general lists of immune systems: innate/adaptive, complement, phagocytes, B/T cells, and so on. Annoyingly, they are very skimpy on quantitative information regarding the speed of these reactions and that matters a lot.
I'm wondering how long after for example bacteria entering the body, do immune systems kick into action? I'm guessing the complement, clotting, and local phagocytes are the fastest but I could not find actual times required.
I found speeds for some immune systems but not for most. This recent recent study on the immune reaction against SARS-CoV2 has a rough time course with dendritic cells early and antibodies from activated B cells in weeks. This more detailed time course, also for Covid, shows the IgM peak at around 2 weeks ("The majority of patients appeared to have seroconverted by day 14").
Ok, but what about all the other processes? How fast can an innate immune cell hone in via chemotaxis, how fast are T killer cells on the scene upon viral infection, how fast is the complement or clotting cascade really, how does antibody production vary in speed between triggers and individuals? I hope you can point me towards any data that might shed light on this. I appreciate any leads.

As a possible lead: hit-and-run viruses, such as those related common cold, give up before the the adaptive immune system kicks in. This is how they avoid forming immunity in the hosts. And this is about a week time.

Don't forget allergic reactions.

Thanks, Roger. That's very interesting.
@DK: I guess immune overreactions = allergies often come in after the real defense work is done, don't they?

I just point that out because your post was talking in terms of weeks, whereas allergic reactions take minutes

Although it's focusing on mechanical injuries, Time Course of Immune Response and Immunomodulation During Normal and Delayed Healing of Musculoskeletal Wounds provides a number of time points for specific immune responses along with references. That should get you started.
This article is looking specifically at musculoskeletal injury situations rather than infections, and suggests that both the types of cells/responses involved and their timing can vary in other situations or infections. For the injury situations, they summarize:

Such injuries are associated with local inflammation and typically
heal in the following order of events: inflammatory phase [0–7 days
post-injury (dpi)]; regeneration phase (4–14 dpi); and remodeling and
repair phase (14–>28 dpi).

Answers shouldn't entirely depend on outside resources. You certainly don't need to recapitulate the whole reference, but can you include enough content so your answer would stand alone?

I see your point, but in this case the OP seems to be asking for so much detail that a partial recap or summary would be insufficient. The article is a review, so is already digested/summarized.  I'll try to add some more to the answer.


text:
Is this a nymph of a Zelus renardii or Zelus luridus?
My mom found this insect on one of her plants, and she would like to know what it is and whether it is dangerous or harmful. I've done some research and I think it is a nymph of a Zelus renardii, but it could also be a nymph of a Zelus luridus, although the latter is usually found only in North America. Can anyone tell me which one it is, or at least whether it is indeed one of these two?

Some more info:

It was found in Milan, Italy, a few days ago
It was on a geranium, where it can find the larvae of a butterfly called geranium bronze (Cacyreus marshalli)
She's also found two more insects like this one on a Pittosporum
She has seen it by day
The body is mainly light-brown with some yellow and orange spots
The legs are also light-brown, with some darker spots that seen from very close are actually spikes (see the last picture)
The length of its body is around 1 cm, and it is arched upwards
I've uploaded some more pictures here. You can ignore the "Not sharp" folder. In the "Sharp" one (which are mostly not that sharp either, but it's the best I have) there's a cropped picture next to each of the full-size ones. Those that I have attached here are chosen among the cropped ones.

Great question -- thanks for the detail! :)

I agree this look like images I've seen of Zelus species nymphs, and I have no reason to immediately rule out Z. renardii. Though, nymphs of many of the Reduviidae look quite similar to me, and I feel like I've never seen a comprehensive guide to thoroughly/methodically distinguishing nymphs (especially from an internet photo). This is made more complicated given that Zelus is one of the most diverse genera in the Reduviidae family, so narrowing to species within the genus is difficult (i.e., time-consuming) for me. (I assume an expert specializing in these insects would know much more than me).
The purpose of my post is simply to point out that Zelus renardii has been found in Italy, while I can't find evidence that Z. luridus has.
Pinzari et al. (2018) provide a detailed recording of Z. renardii in Italy. They also note that (at least as of 2018), Z. renardii is the only member of this genus found in Europe:

The only species of the genus that has been so far re-corded  in  Europe,  is  Z.  renardii  that  has  been  found  in  Greece (Davranoglou 2011; Petrakis & Moulet 2011; Si-mov  et  al.  2017)  including  the  island  of  Crete  (van  der  Heyden 2015), Spain (Vivas 2012), Italy (Dioli 2013b), Turkey (Çerçi & Koçak 2016) and recently Albania (van der Heyden 2017). In Italy, Z. renardii was recorded only twice in the towns of Rome (Dioli 2013b) and Bari (Cor-nara et al. 2016), and never reported anymore. In this note, we add new records for this species in Italy.

As you can see above, Dioli (2013) first recorded Z. renardii in Italy in 2013.

A quick narrowed map search on inaturalist that focuses solely on the European continent suggests that, as of December 20, 2021, Z. renardii continues to be the only species recorded in Europe.

 Pinzari, M., Cianferoni, F., Martellos, S. and Dioli, P., 2018. Zelus renardii (Kolenati, 1856), a newly established alien species in Italy (Hemiptera: Reduviidae, Harpactorinae). Fragmenta entomologica, 50(1), pp.31-35.
 Dioli P. 2013b. Zelus renardii (Kolenati, 1856) (Insecta Heterop-tera Reduviidae). Quaderno di Studi e Notizie di Storia Natu-rale della Romagna, 38(133): 232–233.

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text:
What is the scientific name of this green insect/bug?

(Picture from Internet)
I want to know the scientific name of this insect. They are very small in size and they do not like to stay at one place so taking pictures is hard. Following are some information which will help in identification.

Location: India
Size: Miniscule. About some millimeters
Color: Green. Sometimes a black dot appears on its wings
Survive during the post-Monsoon duration i.e. Late July to October. Hence sometimes referred to as Post-Monsoon bugs.
Attracted to lights. Large number of those swarm around any source of light
Causes a great deal of damage to crops
Does not bite but causes local itching on contact with skin
The name in our native language roughly translates to "green insect" (because of green color)

From the google search I did,guess they are green leafhoppers.
To find more on the leafhopper of the second half, this link should help .Reach the site and give a search on green leafhoppers in the searchbar.
Well,there are a large no of leafhoppers under the family Cicadellidae and I believe the ones in the picture differ.
If my findings are correct,Cicadella viridis is the scientific name of the leafhopper of the 1st half,the second one comes under Nephotettix sp.
Hope it has helped!

Please take the [tour] and then consult the [help] pages for advice on [Answer] effectively on this site and then [edit] or delete your answer accordingly. In particular: 1) copying content from other sources is plagiarism; 2) do not post text as images — images are not searchable, and can not be interpreted by screen readers for those with visual impairments; and 3) answers should include supporting references (primary literature is best).

Please don't post text as images. You can rewrite key points from the source in your own words while citing the original source of the information.

I did some research based on your info and found that indeed they are diffierent typrs of planthoppers/grasshoppers. 1st image is Cicadella viridis which is primarily present in Europe, so let's exclude that. The second one is one of the species under Nephotettix genus. The image I included might be Nephotettix nigropictus or Nephotettix virescens, the latter one most likely.

To complete this post, I want to include my answer based on my research which will server as a complementary answer to @BactiPrabha's answer.

As @BactiPrabha pointed out, they are "green leaphoppers". There are different types of leaphoppers which implies that the 1st image and 2nd image are not same.
The 1st image is Cicadella viridis. This species is present in most of Europe and in the Indomalayan realm which does not match with my location. So let's exclude that.
The 2nd image is one of the species from Nephotettix genus and from the characteristics, it could be either Nephotettix nigropictus or Nephotettix virescens, the latter one most likely. Along with N. cincticeps, they are the most common Asian pest species in this genus and causes diseases like tungro disease in rice. Hence they are also called "Pest of Paddy".
For more information, go through these links:

https://www.cabi.org/isc/datasheet/36200
https://agritech.tnau.ac.in/crop_protection/rice/crop_prot_crop_insectpest%20_cereals_paddy_2.html

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What do you call members of a same species that show some morphological differences depending on their environment and/or diet?
What do you call members of a same species that exhibit a number of morphological differences depending on their environment and/or diet?
I was thinking of the term "different phenotypes," but I am not sure whether this applies.
I would like to apply it in the field of entomology.
EDIT
The ensuing discussion has funnelled the question down to:
When to use the term "phenotype" vs. "morph"?
I am also attempting to synthesise the different viewpoints in a tentative answer below. Comments and some amount of leniency are welcomed.

we would call that normal, the exception are rare and noticeable.

I think that "morph" is a substantially generic term that it would cover environmental as well as genetic variation. A cursory google search suggests that this is common practice in zoology:

a paper on lizards,
one on ants,
another on ants.

This paper discusses the phenomenon in general using the term "polyphenism", in the context of the phenotypic plasticity literature. That last link is to a review paper titled "Polyphenism in insects" (Simpson et al. 2011), which uses the term "morph" extensively.
This suggests to me that this is a well-known concept in entomology and no one will be angry/surprised when you use this term.

The ensuing discussion and additional reading shows that the delineation in usage between the terms "phenotype" and "morph" is not always clear cut.

An organism's phenotype results from two basic factors: the expression of an organism's genetic code, or its genotype, and the influence of environmental factors. Both factors may interact, further affecting phenotype. When two or more clearly different phenotypes exist in the same population of a species, the species is called polymorphic. A well-documented example of polymorphism is Labrador Retriever coloring; while the coat color depends on many genes, it is clearly seen in the environment as yellow, black, and brown. [Source]

According to the above, morphs would be clearly different phenotypes.
However, the difference in fur colouring in dog morphs is solely the result of the genotype and not at all the environment.
Polyphenism → Phenotypes, Morphs

Biston betularia caterpillar phenotypes on, respectively, birch (left) and willow (right), demonstrating a colour polyphenism as a result of its environment and diet.
Polymorphism → Morphs
Whereas the dark-morph or melanistic jaguar does not result from an adaptation to its environment or diet.


text:
"Free space" volume in the nucleus
Take a mammalian cell, say a HeLa cell for concreteness. If a molecule (e.g. a transcription factor) enters the nucleus, what is the effective volume that it can explore/access there by free diffusion? That is, the total volume of the nucleus minus the chromatin, etc.

I'm not sure this is a clear (or answerable) question without more detail — it also would be improved by you telling us: where you've looked for answers, what you do know about the topic, and where exactly you still have questions. ——— One example of a problem with the way you've worded your questions is that chromatin isn't an impenetrable solid, which is why molecules including proteins like transcription factors can directly bind to DNA! ——— It also likely to help if you provided some background about why you care about this number.

No, the question is clear and perfectly answerable: what is the subvolume of the nucleus that a molecule can access by free diffusion? A ref for the total nuclear volume is easy to find (e.g. bionumbers). In Alberts et al., Essential cell biology (5th ed.), question/answer 5-2 estimates that 18% of the nuclear volume are occupied by DNA + histones. That's all so far. Any type of cell would do as a guideline.

Please [edit] your post to include the relevant information from your comment and add complete reference information. Comments are ephemeral and often overlooked and so should only be used to discuss improvements for posts. ——— Some examples of why this question isn't clear: 1) chromatin is not a solid — and the porosity is dynamic; 2) volume will fluctuate depending on what the cell is doing (for instance with cell-cycle state); and 3) even within a single cell the "free volume" is going to vary depending on the molecule that is diffusing.


text:
What type of animal is this?
There was a leaking fire hydrant across a sidewalk. On the other side was a lake. The fire hydrant water was streaming across the sidewalk.
I saw it swimming in the sidewalk away from the side of the lake to the fire hydrant.
What is it?

Could you give us some idea of scale, it's about 18 cm long on my computer screen, I'm sure that's not right.

Welcome to Biology.SE. Identifications questions should include: 1) the location (e.g. country and region — the more specific the better) where you observed this organism; 2) the species-identification tag; and 3) an estimate of the size of the organism. Click on or hover over the 'species-identification' tag for details. Please [edit] your post to include this essential information. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site.

Likely a dragonfly larva, but I don't know the specific type. They live in water and eat anything they catch like small fish.

This is incorrect. It's a mole cricket

They live in water ?

They do not. They live underground. Likely flooded out of its underground hole and seen seeking drier ground. (Alternatively, it could have already been aboveground and just gotten caught in the deluge).

I must agree with you , but I made a close guess.

Second: This is not a dragon fly instar.


text:
Looking for a way to create a video or animated image of a series of segmented lines with cells in ImageJ
I considered asking this on software recs, but felt that the biology community would know better if ImageJ was capable of doing something this way, so I'm asking here.
I'm trying to do a project with ImageJ to model the movement of the flagellum of a Euglena cell. I have an MVI video file of a Euglena cell whipping its flagellum and I converted it into a series of TIFs. Then, I used the segmented line tool to draw over the flagellum so that each image has a "skeletal" line over the flagellum. What I want to do now is put the images together to construct a moving image that would act as a simplified model for the original video, but I don't want the background of the cell to be visible - just the skeletal lines. I want to fix one end of the line on a graph as the origin and be able to play the series of images back-to-back so the viewer will be able to focus solely on the movement of the line to more clearly visualize the cell's movement. It should look something like this:
https://blogs.mathworks.com/pick/2010/08/13/animating-double-pendulum/
I've considered using MATLAB, but I don't know if it can actually do it under the conditions I've laid out. I hope what I said makes sense because its a little difficult to put into words. Is there a way to do this in ImageJ or MATLAB, or do I need a different program entirely?
Thanks in advance!

I think you're better off asking in a software forum as this isn't really a question about biology.

Or as a more specific alternative to @Armand suggestion, SE Bioinformatics, where people may be more familiar with the software.

Thank you. I was going back-and-forth with whether to post here or software recs, but I didn't think they'd know much about ImageJ. I've asked a similar question like this before and the recommendations I got there weren't really suitable for data analysis so I thought an answer was best from people who work in STEM. I didn't know there was an SE Bioinformatics so I'll try there.

I’m voting to close this question because it doesn't seem to be about biology as defined in the [help]. As suggested by @David it might be a better fit for [Bioinformatics.SE], but please do not crosspost, instead request migration by flagging your post for moderator intervention and explaining what you want and why.


text:
Are there life forms that freely fly in the atmosphere?
Are there (unicellular) Earth lifeforms that most of their life fly high in the atmosphere without contact with surface? For instance, in clouds, etc?
If so, at what max altitude have they been detected?

From @jakebeal's keyword "aeroplankton" you could go to https://scholar.google.ca/scholar?hl=en&as_sdt=0%2C5&q=aeroplankton+altitude

Are you only interested in unicellular examples, or do you mention that just as a suggestion?  If you’re interested in multicellular examples too, then common swifts (and some related species) seem to qualify.  They nest and roost at the surface during their brief breeding season, but barely if ever during the rest of the year: “Our data show that swifts are airborne for >99% of the time during their 10-month non-breeding period; some individuals never settled […]”— from https://doi.org/10.1016/j.cub.2016.09.014

@PLL but what do they drink and eat? They need to land.

@Anixx: Unless you’ve seen other research contradicting the paper I linked (which all sources I’ve found seem to agree with), it seems clear that they don’t need to land during the non-breeding months.  They feed on insects in flight; I don’t know whether they get their moisture requirements from their food, or clouds, or dipping into ponds/rivers while in flight (some birds do that, but I’ve not heard of swifts doing so), or something else.  EDIT: quick searching suggests they get moisture mostly from rain/clouds aloft, and sometimes from skimming surface water.

In response to answer the max altitude part of the question: https://www.space.com/microbes-fungi-space-station-identified.html although I couldn't say for certain that this is the maximum they have been detected.

@Frog this is irrelevant

@Anixx Consider fish, most of them are denser than the medium that they live in but many never "land" (while alive). Air is just an edge case.

@Anixx how so?  It seems entirely relevant.

It sounds like you are talking about aeroplankton, a general term for a wide range of tiny life-forms borne on the wind.
While some of these are essentially passive while airborne (e.g., pollen, spores), others like arthropods and microbes are quite capable of being active in the air as well. In essence, anything that can be easily swept up by the wind can be swept up as high as the wind will take it, often all the way to the jet-stream, and kept aloft for a potentially long time before being deposited elsewhere in the world.
For many of these species, this is a key part of their life cycle and dispersal strategy, and as such they are well adapted to survival at altitude.
The density of available resources at altitude, however, is extremely low, and thus, to the best of my knowledge, there has not yet been any species discovered that primarily lives high in the air, as opposed to merely transiting at altitude before landing elsewhere.

Pollen, spores, and their like do not "fly" and being "swept up by the wind" isn't like "flying…" particularly not "freely…"
How could "flying" - even "gliding" - not involve wings and how could "wings" not rule out anything "unicellular"?

@RobbieGoodwin: The OP explicitly suggested “unicellular” in the question, so they clearly meant “fly” in a very general sense.

@PLL That's a big leap of faith and if you have that strong a belief in your powers of assumption, leap away!

Apparently yes. Caveat: the experimenters are are potentially biased because they believe in panspermia (the idea that life came to Earth from outer space), which is clearly fringe. However, I don't think that invalidates the detection of the three new species, only the interpretation.

(PhysOrg.com) -- Three new species of bacteria, which are not found on Earth and which are highly resistant to ultra-violet radiation, have been discovered in the upper stratosphere by Indian scientists ... In all, 12 bacterial and six fungal colonies were detected, nine of which, based on 16S RNA gene sequence, showed greater than 98% similarity with reported known species on earth. Three bacterial colonies, namely, PVAS-1, B3 W22 and B8 W22 were, however, totally new species. All the three newly identified species had significantly higher UV resistance compared to their nearest phylogenetic neighbours.

The samples were collected at 20km to 41km altitude.
The article doesn't say if the bacteria land. Most probably, we don't know.

Is panspermia "clearly fringe"? I am not an astrobiologist, but my (admittedly limited) understanding is that it is a perfectly valid, if unproven, hypothesis that is taken seriously as a possibility in the field. I see 103 results for "panspermia" in the International Journal of Astrobiology, a perfectly respectable peer reviewed journal published by the Cambridge University Press.

@terdon as far as I know, it's fringe compared to abiogenesis. Some of the scientists involved (Chandra Wickramasinghe & Jayant Narlikar) also have a rather spotty reputation, being behind theories such as the quasi-steady state cosmology and the COVID-came-from-space hypothesis which are also fringe.


text:
Why are humans rarely preyed on?
I did a bit of research and noted that some animals such as alligators can indeed digest humans. However, in a lot of cases, they actively avoid humans (bears, alligators, boas). Intellectually, yes humans are responsible for a lot of stuff (e.g. guns and habitat destruction), but on an animal's level, we're just a walking sack of meat with legs and arms.
This question sort of hinges on the idea that it would take too long a while for evolution to tell animals to avoid humans such that they're doing it now (feel free to tell me otherwise with an explanation as to how).

Tell that to Tanzanians. Predatory animals don't avoid humans.

First, I think you have a major misconception about prey selection being entirely evolutionary and driven by instinct.  Animals learn. Mammals, in particular, learn from their parents and/or other pack members, as well as from personal experience.  So wolves, lions, or other large predators develop a culture of humans not being good prey.
Second, many predatory animals tend to be opportunistic hunters.  They want to acquire their dinner at minimum cost to themselves.  They don't want to risk injury by engaging in a stand-up fight with something of comparable size.  Adult humans are pretty large creatures.
Third, and perhaps the most important, is that humans have learned to deal with large predators.  Even before the invention of modern weapons, they learned to avoid places where the predators might lurk.  For instance, if you visit Florida or parts of northern Australia, you're well-advised not to go swimming.  Even so, there are about 1000 deaths per year from crocodiles & alligators: https://en.wikipedia.org/wiki/Crocodile_attack

Its also worth noting humans have put some extremely strong pressure against predators that seem humans as prey and live near humans, Its worth noting predators that attack humans are wither hard to kill (semi or fully aquatic) live in places humans rarely live, or are extinct or close to it. humans have wiped out dozens of large predator species.

In support of learned behavior, animals that attack or kill humans (e.g. grizzlies) are hunted and destroyed, because, well, they tend to repeat that behavior once learned. If they weren't destroyed, there might be a whole lot more predators of humans around.

@anongoodnurse: The learning works the other way, too.  Consider dogs and skunks.  Most of my dogs have had a skunk encounter when fairly young.  Almost all of them learned not to repeat it. (Except my current dog, who needed two.  But then, he's not the smartest puppy in the litter.  Still chases bears, despite a rather unpleasant experience with one.) So even if the predator is just driven off, rather than killed by humans, it learns that there are easier meals to be had.


text:
Where in the cell does this enhancer RNA knockdown take place?
In Pnueli et al., 2015, they knock down an enhancer RNA using RNAi, testing whether it is a mere byproduct or whether it has a key role in the enhancer's function. They find their system works: the siRNA knocks down the enhancer RNA that it's targeted to, enabling further study. Hooray!
... but I've read that RNAi and the RISC work outside the nucleus, and intra-nuclear effects are further downstream and indirect (example: Gosline et al. assume that effects on introns are indirect). I assume the paper's not wrong, so what's going on?

Conventional wisdom is wrong or incomplete: RNAi can work inside the nucleus too.
Pneuli et al.'s enhancer RNA gets exported to the cytoplasm and then re-imported to act on its target gene.
Something else?

Pnueli, L., Rudnizky, S., Yosefzon, Y., & Melamed, P. (2015). RNA transcribed from a distal enhancer is required for activating the chromatin at the promoter of the gonadotropin α-subunit gene. Proceedings of the National Academy of Sciences, 112(14), 4369-4374.
Gosline, S. J., Gurtan, A. M., JnBaptiste, C. K., Bosson, A., Milani, P., Dalin, S., ... & Fraenkel, E. (2016). Elucidating microRNA regulatory networks using transcriptional, post-transcriptional, and histone modification measurements. Cell reports, 14(2), 310-319.

Are you sure an antisense RNA against this enhancer RNA uses the cell’s microRNA RISC system? I don’t know, but a priori would expect not.

I have no idea. What else would it use?

Hybridization? When antisense RNA was first introduced the microRNA Dicer system was unknown, and the strategy was based on the idea of inactivating mRNAs by hybridization. The reason I would not expect such antisense RNAs to use the Dicer system is that they do not have the imperfect stem-loop structure of the natural substrate. I may be wrong as this is not a technique I have used, but you should check it out before assuming your assumption is correct and there is a problem with the paper

Would hybridization lower concentration of the target RNA as measured by e.g. qPCR? Or would it affect activity without altering concentration?

FWIW, the system they describe using is shRNA, which I thought worked via RNAi. That's what wikipedia says anyway. If it's more complicated than that, well, that's basically my question.

RNAi can happen in the nucleus as well. This is better documented in C.elegans but there are some references supporting nuclear RNAi in mammalian cells too:

https://doi.org/10.1073/pnas.1707440114
https://doi.org/10.1016/j.celrep.2013.12.013
https://doi.org/10.1093/nar/gkv1305


text:
How does the phosphorylation state of 4E-BPs affect translation of nuclear-encoded mitochondrial transcripts?
A 2020 review paper about mTOR (ref. 1) says:

because biomass accumulation demands vast reserves of energetic currency, mTORC1 enhances translation of nuclear-encoded mitochondrial transcripts through 4E-BP1 to expand the ATP production capacity of the cell

The above quote cites a 2009 paper (ref. 2) that says:

Upon DR mitochondrial protein density increased 25% in control flies, while in d4E-BP null mutant flies there was no change

(DR stands for "dietary restriction", which is known to inhibit TOR, which is an inhibitor of d4E-BP, if I understand correctly.)
These two really confuse me, as it seems to me that ref. 1 cites ref. 2 but says the opposite.
To spell it out: It seems that everyone agrees that active (i.e., non-phosphorylated) 4E-BPs inhibit translation, but ref. 1 claims that the inhibition is strongest for nuclear-encoded mitochondrial transcripts, while ref. 2 claims the inhibition is weakest for these transcripts.
As far as I can tell, the claim by ref. 1 is also supported by two other papers: A 2012 paper (ref. 3) that says:

gene silencing of 4E-BP1 up-regulated the protein expressions of all RCs and the action of 4E-BP1 appeared to be specific to these mitochondrial proteins.

And a 2013 paper (ref. 4) that says:

Whereas 4E-BP1/2 depletion did not affect polysome distribution of β-actin mRNA (Figure 6B, upper), it prevented the Ink1341-induced shift of TFAM and ATP5O mRNAs toward lighter polysomes (Figure 6B, lower). Therefore, 4E-BPs act as major mediators of mTORC1 on translation of TFAM and ATP5O mRNAs. Accordingly, asTORi decreased ATP5O and TFAM protein levels in control, but not in 4E-BP1/2-depleted cells

Finally, I found a 2017 paper (ref. 5) that seems to make a claim similar to the one ref. 2 makes. It says:

cold inhibits translation in general, but the synthesis of proteins destined to the mitochondria is selectively preserved, resulting in a cellular enrichment of these molecules.

and:

4E-BP can be phosphorylated at multiple sites but phosphorylation of Thr37/Thr46 by the mammalian target of rapamycin (mTOR) acts as a priming event required for further phosphorylation. Cold exposure increased the proportion of nonphosphorylated protein, largely at the expense of the primed fraction [...] Taken collectively, our observations suggest that reduced ambient temperature induces a physiological state comprising posttranslational modification of 4E-BP—resulting in a lower proportion of the phosphorylated isoform primed for inactivation—and a switch from global protein translation toward mitochondrial metabolism and efficiency.

So my question is:
Is it really that refs 1,3,4 say one thing, and refs 2,5 say the opposite?
If yes: Has anyone offered an explanation to resolve the seemingly contradicting results?
References

Liu, Grace Y., and David M. Sabatini. "mTOR at the nexus of nutrition, growth, ageing and disease." Nature Reviews Molecular Cell Biology 21.4 (2020): 183-203.
Zid, Brian M., et al. "4E-BP extends lifespan upon dietary restriction by enhancing mitochondrial activity in Drosophila." Cell 139.1 (2009): 149-160.
Goo, Chong Kiat, et al. "PTEN/Akt signaling controls mitochondrial respiratory capacity through 4E-BP1." (2012): e45806.
Morita, Masahiro, et al. "mTORC1 controls mitochondrial activity and biogenesis through 4E-BP-dependent translational regulation." Cell metabolism 18.5 (2013): 698-711.
Carvalho, Gil B., et al. "The 4E-BP growth pathway regulates the effect of ambient temperature on Drosophila metabolism and lifespan." Proceedings of the National Academy of Sciences 114.36 (2017): 9737-9742.


text:
Red and White Flower or purely Pink? Phenotype of a Flower Species with a Co-dominant Trait
As I understand it, co-dominance is when both genes in an allelomorphic pair produce both their effects equally on the organism in question whilst incomplete dominance applies to an instance where a mix of the effects of two alleles are present — i.e. where one allele is not completely masked by the other.
However, I had this notion challenged by the following paragraph I obtained from a reputable online source:

Carnation plants show co-dominance for the anthocyanin gene. There are two alleles:
$F^A$ – allele for anthocyanin pigment (red flowers)
$F^N$ – allele for no anthocyanin pigment (white flowers)

[...] a carnation plant heterozygous for this gene would yield pink flowers [...]

Shouldn't the phenotype of the flower be red and white as opposed to being pink, as the alleles have been said to exhibit co-dominance? Anything I am probably missing out on?

EDIT
I have bountied this question because I think I have a major hole with my understanding on this topic somewhere; to give you some perspective, I am a High-School Sophomore currently on an introductory course in Mendelian Genetics/Inheritance.
I read through @swbarnes2's answer where they say:

In the case of flowers, if you have two different alleles for the same pigment gene, you will see a blending, because all the pigment-making cells will produce from both alleles.

In such a case (if this always happens), where do the ideas of codominance and incomplete dominance come in? According to my textbook, the following terms are defined as:

If both genes of an allelomorphic pair produce their effects in an individual (i.e neither allele is dominant to the other) the alleles are said to be co-dominant.

Incomplete dominance applies to a case where the effect of the recessive allele is not completely masked by the dominant allele (in this case, I assume, a blending would occur)

(I do get that this may not apply to carnation plants, but would it be safe to follow the phenotypes predicted by my textbook definitions for all other cases?)
Hope someone could clear my doubt; I am extremely confused to read (in the comments section) why co-dominance would not mean both colors/phenotypes are shown simultaneously — like being red and white (as opposed to them mixing into pink).

"from a reputable online source" -- I appreciate your direct quoting of the source, but could you also provide a link to it?

What color does red and white make?

Mix them together & I'd expect pink. But that's purely for incomplete dominance, isn't it? Should be white & red (individually) when it's co-dominant

@BryanKrause I understand Shane's concern. Incomplete dominance is typically taught as as a blending of phenotypes (red + white = pink), whereas co-dominance is taught as the simultaneous expression of two phenotypes (red and white banding). This may be outside the scope of the question, but is seems like the genetics of anthocyanin pigmentation in carnations are in reality more complicated than presented in Shane's question.

@acvill I mean really, all the notions about dominance are outdated in modern molecular biology; they're good tools for understanding Mendelian genetics where one has access only to lineage information and not any molecular biology, but once you know more they are rarely actually meaningful distinctions. I think that's what's happening here; there's a blending between the understanding of the phenotypes as colors, and the understanding of the phenotypes as enzymatic reactions. I guess that's probably what an answer should explain, I do think I have a better idea now of where OP is coming from.

@BryanKrause I agree, though someone new to genetics doesn't have that insight, and your first comment came across as dismissive. Maybe this question concerning the molecular basis of incomplete dominance is relevant.

@acvill Thank you for the link; I took a look at it, but there wasn't much in there I could really understand, being a high school student!

Re: "why co-dominance would not mean both colors/phenotypes are shown simultaneously" Not mentioned here is the scope of the phenotype. Is it one flower? One cell in a flower? The whole plant? As Bryan mentioned, often "the notions about dominance are outdated in modern molecular biology". The red and white patches in your flower photo seem to me to be an example of "variegation" rather than co-dominance.

As I think other commenters have implied, I think that you are applying the definitions from the textbook more strictly than the writers of the textbook. In practice the dividing line between these things is not always so clear. A cleaner example of codominance might be one allele which affects color (red) and the other allele affecting something else, like pattern of expression- e.g. pigment only at the tips. In this case you can enumerate the combinations (all red, red tips, all white). Mechanistically I think this situation is rarer (?) but it's clearer for the definition.

Unfortunately, that nomenclature is kind of old-fashioned; it predates our understanding of what's going on at a molecular level.  Don't get hung up on the language.  Lots and lots of genes and alleles just don't fit into the paradigm of dominant and recessive, and trying to force them to fit doesn't really work.
In the case of flowers, if you have two different alleles for the same pigment gene, you will see a blending, because all the pigment-making cells will produce from both alleles.  There really is no such thing as "white" pigment; either it's causing a color outside the visual spectrum, or it's a broken version of a gene in the pathway that should be making a color-absorbing molecule.  We would usually more properly refer to this as "haploinsufficiency".
If you had blue and red alleles, it would likely make a purple flower, not one that was blue in some patches, red in others.
For something like blood type, AB blood cells make both A and B molecules on their surface (O is broken), but AB is just as good as A in terms of causing an immune reaction; there is no alteration in phenotype due to the lower dose of each allele.

This is not co-dominance, it is the result of either a transposon or a viral infection, similar to the tulip-breaking virus.
https://en.wikipedia.org/wiki/Tulip_breaking_virus

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Friend..you got the meaning of co dominance and incomplete dominance correct... but let me make co dominance easy... its just like mixing colors on a color plate...think it just like that.... otherwise in real sense both colors are indivisually expressed but being expressed in equal amount and with uniformity they appear as pink... other example could be ABO Blood group in humans....as for refrence https://www.genome.gov/genetics-glossary/Codominance hope it helps..

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Can wasps see under moonlight?
It appears that the best time to attack a wasp nest is in the middle of the night. Their venom might terrorize us (my five-day old sting remains swollen and is starting to have red bumps in an area the size of a tennis ball), but at least our eyesight is superior. If we attack while they are asleep, or at least resting, we have our best chance of escaping unscathed—or so the online pundits claim.
The nest in question is at the edge between the wall and the roof protrusion. Because it is 8 feet off the ground rather than on the ground, it would appear to be a paper wasp nest. But because it is covered with paper and the individual cells are occluded, with the entrance at the bottom the only visible path leading inside, it may well be a yellow jacket nest.
Maybe it's futile to attack the nest in September. One might as well let them be. The nest will anyway be deserted in October when the temperature starts to freeze overnight. But it's never too early to prepare for next Spring.
I could choose a night when there is absolutely no light—not even moonlight—but then I myself would need to use a flashlight, providing them with the means of pursuing me. Or I could choose a full-moon, or near full-moon, night, and then I can see and they can, perhaps, not see.
Can wasps see under moonlight?

The false assumption here is that all animals are as dependent on vision as humans. Insects, in particular, make great use of chemical senses. The reason people say attack at night is not so they can't target you. It's to get as many of them as possible on the first strike so they have fewer to retaliate with.

From my experience in the field, they are pretty adept at flying around in pitch black abandoned farmhouses.

No.... probably not... wasp cannot see at night... their scotopic vision{dim light vision} is not well develop so before sunset they return back to thier nest... so at night.. probably you can get them all together... rather then hunting for each indivisually...for reference https://sciencing.com/how-to-identify-wasps-bees-13406632.html hope it helps..

Welcome! Thanks for providing an answer. Whilst the information may be correct, we prefer answers to have some kind of citation or reference to back up statements made. If you could add something like that, it would be great. Thanks.


text:
Does ribonuclease processing of pre-crRNAs happen co-transcriptionally?
I understand CRISPR-mediated bacterial immunity to occur in the following simplified steps:

A CRISPR array is transcribed from promoters in the leader sequence to yield a precursor CRISPR RNA (pre-crRNA).
The pre-crRNA is processed by ribonucleases (e.g. Cas6 in Type III systems) to create mature crRNAs.1
crRNAs are loaded into Cas proteins to create an active CRISPR-Cas complex.

My question pertains to the timing of steps 1 and 2. Is there any evidence for co-transcriptional processing of pre-crRNAs? Put another way, must the full pre-crRNA be transcribed prior to its cleavage by ribonucleases, or can single crRNAs be cleaved from the 5' end of the nascent pre-crRNA. My understanding is that cas6 recognizes and cleaves at the base of the repeat stem-loop,2 and that these stem loops form spontaneously after a repeat is transcribed, so my hunch is that co-transcriptional pre-crRNA cleavage probably can occur, though I'd like some evidence from the literature to support/refute my intuition. I realize mechanisms of CRISPR immunity are quite diverse, so I'd appreciate references pertaining to any CRISPR system.
Some search phrases I've tried in Google:

co-transcriptional processing of crRNA
co-transcriptional cleavage of crRNA
crRNA processing concurrent with transcription
ribonuclease processing of nascent pre-crRNA
cas6 proximity to elongating rna polymerase

References

Carte J, Wang R, Li H, Terns RM, Terns MP. Cas6 is an endoribonuclease that generates guide RNAs for invader defense in prokaryotes. Genes Dev. 2008 Dec 15;22(24):3489-96.
Sokolowski RD, Graham S, White MF. Cas6 specificity and CRISPR RNA loading in a complex CRISPR-Cas system. Nucleic Acids Res. 2014 Jun;42(10):6532-41.

What difference will it make in the systems you are considering if there is co-transcriptional processing?

It may not make a difference. This question pertains to my research interests and has implications for the interpretation of my data.

I don't know the answer myself, but if it would make a difference in the interpretation of your data, it seems like that might be a good hook to build off of.

Thanks, @jakebeal. I'll take that into consideration if I don't get any answers in the next few days.

I originally posted this question in an attempt to understand a pattern I observed in my sequencing data. In the time since, I've formalized my interpretation as part of a manuscript, now posted on bioRxiv.
Some background: we performed precision run-on sequencing (PRO-seq) on bacterial cells derived from human stool samples. In short, PRO-seq involves supplementing permeabilized nuclei (or cell lysates, in the case of bacteria) with biotinylated NTPs, such that endogenous RNA polymerases incorporate biotin onto the 3' ends of nascent transcripts. Transcripts are then precipitated on streptavidin beads and sequenced, revealing (1) which genomic features are being actively transcribed and (2) the genome-wide and strand-specific positions of RNA polymerase with base-pair resolution.
Looking at the PRO-seq reads mapping to our metagenome-assembled genomes, we observe a wave-like pattern at loci annotated as CRISPR arrays. Figure 3 from our preprint gives one example:

(A) Coverage of PRO-seq and RNAseq reads across a CRISPR array in a US2 Prevotella sp. contig. Shaded boxes represent repeats. The large black arrow in each panel represents the leader sequence containing a putative promoter. Small black arrows in the “PRO-seq 5’ end” panel correspond to the predicted site of crRNA cleavage proximal at the base of the repeat stem loop.
(B) Predicted crRNA repeat secondary structure. The black arrow points to the phosphodiester bond that is likely cleaved by Cas5d during pre-crRNA processing, which marks the same position in the repeat as the small arrows in (A). The sequence logo shows perfect conservation of the repeat sequence for this array.
(C) PRO-seq captures nascent transcription of cas5d upstream of and contiguous with the CRISPR array.

Looking specifically at the position of the 5' ends of PRO-seq reads (bottom panel of A), we noticed a pile-up at the same position within each repeat corresponding to the putative crRNA cleavage site at the base of the repeat stem loop (arrow in B). Notably, transcription across this array coincides with transcription of a cas5d endoribonuclease gene upstream of the array (light blue rectangle in C).
Coming back to the title question...

Does ribonuclease processing of pre-crRNAs happen co-transcriptionally?

... I believe the answer is yes. Wave-like transcriptional profiles at CRISPR arrays are not a novel observation (see Figure 1 from Richter et al. 2012), but, importantly, our data include only nascent transcripts. This implies that crRNA cleavage by Cas5d is concurrent with pre-crRNA synthesis, at least in this human-associated Prevotella species.

Very nice answer as usual. Unfortunately the link for your manuscript doesn't seem to work (I'm being sent to a "DOI Not Found" page).

@tyersome thanks for catching that. Fixed


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Boost of Janssen COVID-19 Vaccine increasing Immune Response to Vector
I have been looking for published, or even pre-print, data that evaluates the serological response to a boost of the Janssen COVID-19 Vaccine against the adenoviral vector Ad26 rather than the intended SARS-CoV-2 spike protein target.
Vector-targeting immune responses are a generic and known issue with adenovirus vectors. Janssen has made the claim that Ad26 is superior to Ad5 in this regard, but while increased response to the target epitopes is obtained in boost (though slight in my opinion), a frank discussion or display of differences in anti-vector response is not covered in any of the references:

In contrast to Ad5-based vaccines, a similarly clear impact of
natural- or vector-induced pre-existing immunity to Ad26 on vaccine
immunogenicity has not been observed to date in clinical studies.
Results from clinical trials assessing repeated administration of
Ad26-based vaccination approaches showed that a second or subsequent
dose of study vaccine was able to boost humoral and cellular immune
responses to HIV antigens (Ad26.EnvA, study IPCAVD001; and
Ad26.Mos.HIV, APPROACH study; even in the presence of high Ad26
neutralizing antibody titers induced by the first dose.
Similarly, naturally occurring Ad26 neutralizing antibody titers or
Ad26-targeting T cell responses at baseline were not associated with
decreased immune responses against the vaccine antigen. (DOI)

Not destroying your target immune response with a boost is not the same thing as a meaningful boost to response or a lack of boost to vector.
I was hoping to find a report on changes (or lack there of) reaction to any Ad26 proteins via Western, ELISA, or any acceptable protein interaction assay for individuals after both prime and boost with Jansen vaccine.  Generic reaction to the vector, even related ones, would be apricated if a clear division in prime and boost responses were present.
Most studies that use the vector (an example with RSV that I know had the problem but was unreported) seem to avoid discussing it altogether.

For ChAdOx1 https://www.thelancet.com/article/S0140-6736(20)32466-1/fulltext#figures  (should be quite similar for Ad26)

@reuns I was looking at that, with figure 7 being on point but not clearly to me showing if 7a actually covered the significant difference at boost (would love to see that data broken down by the cohorts in #1).

I think figure 7a is after first dose because at day=0 there is no neutralization

@reuns D0 is definitely the prime/first dose. The schedule was to get boost at D28, and considering it goes to D56, one presumes it covers the boost.  The problem is that they didn't divide out by which group was boosted, so any difference on that division is hidden.

@armand I wasn't meaning to reject your edits, I was already editing it myself.  Concerning the meta question, I can understand taking out the first paragraph, but I do not think it is unsupportable opinion

Re: "Similarly, naturally occurring Ad26 neutralizing antibody titers or Ad26-targeting T cell responses at baseline were not associated with decreased immune responses against the vaccine antigen" I interpret this to mean that the vaccination response (e.g. higher Ab levels) against the vaccine antigen was not weaker even in those with pre-existing naturally occurring anti-Ad26 responses. What wording underlies your "Not destroying your target immune response with a boost ..." comment?


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Do you know what kind of bug this is?
I have tried to find a similar picture online, but can’t seem to find any.  Does anyone know what kind of bug this is?
It has been on a penstemon plant for about 3 days.
I am located just outside of Portland, Oregon.  It’s been on the same stem, only moved from one side to the other.  There have been about a few dozen honeybees around it, feeding on the flowers, and the bug hasn’t moved.  Also haven’t seen them feed on the plant.
Any ideas?
Body is similar to a ladybug, but I haven’t seen markings like this.

Welcome to Biology.SE. Please [edit] your post to include as much of the following essential information as you can — this will improve your chances of getting a good answer: 1) clear closeup photos of the organism (photos from multiple angles if possible); 2) the location (e.g. country and region — the more specific the better) where you observed this organism; 3) habitat information — e.g. what other plants are near; and 4) an estimate of the organism's size. ——— Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site for details.

You're welcome — since you don't seem to be getting much response here, you might want to try other sites that specialize in identification — (e.g.s: iNaturalist and BugGuide.

Short Answer
Looks like the 4th instar of Thyanta custator, the Red-shouldered stink bug, a type of stink bug found in Oregon.

 Oregon Dept. of Agriculture
Long Answer
Definitely a nymph of some species of true bug (order Hemiptera), most likely in the suborder Heteroptera (i.e., the shield bugs, stink bugs, assassin bugs, etc.) and family Pentatomidae.
For example, see these photos of nymphs of similar species:

 From L->R: Podisus maculiventris, Troilus luridus, Glaucias amyoti, Cosmopepla lintneriana, Carpocoris purpureipennis, Murgantia histrionica
Using yet another species, Piezodorus lituratus, as an example, you can see how a Pentatomidae nymph typically develops to maturity:

 Source
As to your species...
Your specimen's physical appearance (i.e., black/white body with yellow band and centered red spot) appears to match that of the 4th instar of Thyanta custator, the Red-shouldered stink bug.

 Oregon Dept. of Agriculture
From Oregon Dept. of Agriculture:

Nymphs are dark brown to black. Early nymphs have two distinctive pale spots on
opposite sides of their abdomens and appear hairy compared to other stink bug nymphs. Thyanta custator is very closely related to T. pallidovirens and they are morphologically indistinguishable, but there is chromosomal evidence that they are separate species

Your 2nd image does appear to have some "fuzziness" around the body's edge -- possibly this hairiness?

This species is listed as living in Oregon:

Oregon's Dept. of Agriculture provides this resource showing common stink bugs found in your state. Species include: Perillus bioculatus, Banasa dimidiata, Chinavia hilaris, Chinavia hilaris, Chlorochroa rossiana, Thyanta custator, Cosmopepla conspicillaris, Cosmopepla uhleri, Cosmopepla intergressa, Cosmopepla lintneriana, Holcostethus abbreviatus, Holcostethus limbolarius, Holcostethus tristis, Trichopepla aurora, Antheminia remota, Brochymena affinis, Brochymena quadripustulata, Euschistus conspersus, Euschistus variolarius, Halyomorpha halys, and others as possible specimens.


text:
the effect of aquatic photoautotrophs on CO2 concentration in the air
The CO2 concentration in the air is more strongly influenced by the northern hemisphere than the southern hemisphere. A given explanation is that the northern hemisphere contains more terrestrial photoautotrophs. Does that mean that the effect of aquatic photoautotrophs on the CO2 concentration is much weaker than that of terrestrial photoautotrophs? If so, how is it so?

the obvious guess would be that it's because the terrestrial autotrophs affect the atmosphere directly while aquatic ones can only directly affect CO2 in the ocean; and mixing between the ocean and atmosphere is much slower than mixing within the atmosphere itself

@timeskull i guess guessing is the least usefull thing one can do on a science site.


text:
How is Vitamin D deficiency linked to multiple sclerosis?
Numbness and tingling in various parts of the body can be linked to the deficiency if vitamin D in one's diet. Also, multiple sclerosis has Vitamin D deficiency as one of its risk factors. How exactly are they related? MS is an autoimmune disorder. What exact role does Vitamin D deficiency play in here?

I don't believe this is known mechanistically to any great degree. Mayo Clinic has an easily understandable post about this.
In summary, the evidence for a relationship is that vitamin D levels correlate with occurrence of MS (high vitamin D intake is associated with less occurrence of MS in individuals; populations further from the equator have less vitamin D and more MS) and that vitamin D in individual MS patients can influence their symptoms and disease progression. Knowledge of those relationships does not require any mechanistic understanding.
The review by Sintzel et al (2018) is another source for these general epidemiological associations and evidence for a possible causal relationship of low vitamin D in MS. Mechanistically, however, they only mention general relationships between vitamin D and the immune system, not any known specific mechanism of the involvement with MS. Autoimmune disease is somewhat notoriously complicated, so I don't find this particularly surprising. The review they cite, Mora et al 2008, takes a more general look at the relationships between vitamin D and immune function, which are highly multifaceted and involve both up- and down-regulation of different cell types involved in different aspects of immune function.

Mora, J. R., Iwata, M., & Von Andrian, U. H. (2008). Vitamin effects on the immune system: vitamins A and D take centre stage. Nature Reviews Immunology, 8(9), 685-698.
Sintzel, M. B., Rametta, M., & Reder, A. T. (2018). Vitamin D and multiple sclerosis: a comprehensive review. Neurology and therapy, 7(1), 59-85.


text:
Do egg-whites dry as right-handed helices?
Do egg-whites dried at cool temperatures form mostly right-handed helices, and if so is there an explanation for this? Because there is so much (mostly crystal-related) research a quick search did not turn up anything. Below is an image at low magnification (400x).

Maybe the coiling reflects aggregate properties of proteins that make up the albumin? If someone has a cite that would be welcome.
Edit: different spiral from same batch. This one apparently left-handed.

It could be something unrelated to biology - like rotation of the Earth.

@RogerVadim: In that case Australians should see left-handed helices...maybe so.

Forgive my pedantry, but isn't this a left-hand spiral? (Growing from the center that is). Related paper gravity.

@ARogueAnt::  that's a good question. it appears to me that that spiral travels toward the slide (away from the viewer). if that is true we have to begin at the closer end and follow it away (clockwise). if we begin at the center and assume it's going away from us then yes, it's left-hand. the visual evidence--(1) the larger coils are closer and (2) they cover some of the smaller ones. but i am not certain.

instead of anonymous downvotes, maybe let me know how i can improve the question?

@daniel I tried fighting against downvoting and particularly anonymous downvoting. Here is my highest downvoted metapost on the subject ;)

@RogerVadim: Wow. Nicely downvoted! I was thinking of posting on meta- but you have expressed my opinion for me.

@RogerVadim: The one virtue of anonymous downvoting is that it gets one used to the real world, in which reputations are made and unmade in secret meetings.


text:
What is the difference in the function of tractus rubrospinalis and tractus corticospinalis?
What is the difference in the function of tractus corticospinalis and tractus rubrospinalis? I know, that they begin in different parts of the brain, but from what have I read on the internet*, I can't see any difference in their function. The only difference I can see is, that tractus rubrospinalis is having impact only on the upper half of the body, but still this isn't difference in their function (at least on the upper part of the body).
Edit:
* for the rubrospinal tract I have read

The tract is responsible for large muscle movement regulation flexor and inhibiting extensor tone as well as fine motor control.

and for the corticospinal

The primary purpose of the corticospinal tract is for voluntary motor control of the body and limbs.

Both are from wikipedia, but this is just because it is was the fastest source of something in english. I learned it from sources in my language so I can't post them here, but I understood it very similarly as it is on the wikipedia.

Can you perhaps add a short quote (with references) on what you've read about each and why that makes you think it's the same?

@BryanKrause, sorry, rn I don't have time, but I'll do it about an hour later. BTW, I also don't think, that they do the same thing, I just also don't know what is the exact difference. This is the reason, why I am asking. Anyways, thanks for tip how to improve the question.

@ARogueAnt., humans, there is the human-biology tag.

Fair enough, I'd missed that.

Assuming those quotes are from Wikipedia (and wherever you quote from it's always important to cite your source), did you happen to read the sentence before the first one, and the paragraph after the second?

@BryanKrause, Yep I did. For the sentence, yes, it is smaller, but I am asking if (and if yes, what) there is something different in what kind of things they do, not just, that one is smaller and the other is bigger, so it can transfer more informations. And for the paragraph, yep, that is my mistake, I forgot to say it, but I am asking only on the motor part of it's function.

Before the first: "It is one of the pathways for the mediation of involuntary movement, along with other extra-pyramidal tracts including the vestibulospinal, tectospinal, and reticulospinal tracts." After the second: "After patients are lesioned in some part of the pyramidal tracts, they are paralyzed on the corresponding side of the body. However, they can re-learn some crude, basic motions, just no fine movements.[2] This implies that the connections to these tracts are crucial for fine movement, and only partial recovery is possible if they are damaged."

Oh sorry, so we were probably referencing to different senences. This is probably the answer, so thanks.


text:
Can the SAME histone tail have both H3K4me3 and H3K27me3?
I'm studying bivalent promoters and enhancers. I understand that the same region of genome can have both H3K4me3 and H3K27me3.
But can they occur on the same histone tail?
Please provide me with a reference to support your answer.

This paper suggests that people have tested if two proteins can bind on a histone tail that contains both epigenetic marks. This implies that indeed both markings can be on the same tail.
"Next, we investigated if a histone tail bearing both H3K4me3 and H3K27me3 marks can be combinatorially recognized by SHL."


text:
On the origin and evolution of vaccinia virus
I was browsing Wikipedia and learned that vaccinia virus, the basis of the smallpox (variola virus) vaccine, was originally thought to be derived from cowpox but was later discovered to be a separate species in its own right. Genome sequencing shows that it is most closely related to the distinct horsepox virus†.
My question is whether vaccinia virus was already a separate species when it was first taken and propagated for smallpox vaccines or if was originally a strain of horsepox (or some other unknown pox virus) that only became a separate species after passaging over many years.
† I have consulted the article in Wikipedia and the ICTV 9th Report's section on Poxviridae for background information to this question, but they do not provide a definitive answer.

Thank you for providing a background to this, but could you please clarify your question. Are you asking 1. Does vaccinia exist in the wild as a pox virus infecting a species that has not been identified? or 2. Did vaccinia once exist in the wild infecting such an unknown species but the species or virus has died out? or 3. Is vaccinia derived from an extant pox virus such as cowpox, but has changed so much (e.g. like dog breeds) that its source is not clear? Or something else. But please edit your question so that this is clear and avoid the unhelpful terms, "artificial" and natural.

A quite different question of clarification. Your statement about infectious strains of vaccinia puzzles me. I followed up your reference but cannot find anything about vaccinia strains. Can you give a page reference. There is a phylogenetic map at https://talk.ictvonline.org/ictv-reports/ictv_9th_report/dsdna-viruses-2011/w/dsdna_viruses/75/poxviridae-figures which shows vaccinia most closely related to cowpox strain GRI-90. Also note that horsepox etc. are poxviruses in their own right, not strains of vaccinia.

@David
I'm trying to ask if vaccinia would have existed without humanity. I suppose another way of phrasing it would be "did the vaccinia virus exist before the 1790s when the strains for vaccines were first isolated".

As for the use of the use of natural and artificial I'm using natural to mean "would still have happened even without human actions" and artificial to mean "only happened due to human actions". If that's unhelpful I'd be fine replacing them but unfortunately you haven't given me any terms to replace them with. I can't replace them without any examples of what words would be better yet still communicate what I'm trying to say.

For the  about infectious variants I was trying to preempt any answers which cited those as examples of natural strains as we have no proof they are natural as opposed to strain which escaped from the lab. Wikipedia lists six member viruses for vaccinia three of which are infectious, two of them have pages, buffalopox and rabbitpox, while the third, the Cantagalo virus, has no page and requires googling.

As for the phylogenetic map, could it be that the map just doesn't show enough detail for any strains closer than GRI-90? Wikipeida says that the closest relative is horsepox with a 99.7% genetic similarity and has two citations supporting it.

For the last sentence, yes I know that, that's why I'm asking the question. I want to know if the mutations that made them distinct enough to be separate species evolved naturally or if it only happened due to generations of selective breeding by researchers developing smallpox vaccines.

As you probably know from other SE lists you are on, the aim of SE is to get good questions and answers, and therefore users are encouraged to improve both. As @bob1 had produced an answer that addresses the general question of the origin of vaccinia, I thought it most useful to edit your question in concert.

The answer is that we don't know for sure. All we know is that at some point in the process of developing the vaccine, what was thought to be cowpox, was not in fact cowpox, but was rather what we now know as Vaccinia virus.
Part of the problem here is that the vaccine process was not entirely scientific in its development, there were multiple sources from multiple locations around the world developed more or less independently using an inoculation process (by Jenner's method, just copied). In many cases, before the development of heat-stable vaccines the method of carrying the vaccine to other parts of the world was to transport a live animal infected with a pox virus (I don't have evidence for this, but it is mentioned in "The greatest killer: smallpox in history" by D Hopkins 2002.
The history, as I mentioned is murky. As Baxby wrote in 1977:

Smallpox vaccination was established long before the nature of viruses was known and therefore very little is known about the number of poxviruses circulating in the 18th and 19th centuries.

and as Razzell 1999 also noted:

The main English vaccine (the Lister strain) was sent from Cologne some time after 1871 and is reported to have been taken from a Prussian soldier suffering from smallpox... ... Many of the English vaccines in the 1850s were derived from the inoculation of cows with smallpox and as Baxby has pointed out the most recent evidence suggests it is not possible to produce vaccinia through the variolation of cows.

In addition, Schrick et al (2017) sequenced a 1902 vial of vaccinia vaccine, finding that it clustered with horsepox, noting that Jenner also suspected as much in his 1800 publication, several sections being devoted to the similarity between horsepox and cowpox and the transmissibility between the two such as the below:

In the month of November 1797 my horse had diseased heels which was certainly what is termed the grease and at a short subsequent period my cow was also affected with what a neighbouring farmer who was conversant with the camplaints... ... No other person milked the cow but the lad above mentioned I am firmly of opinion that the disease in the heels of the horse which was a virulent grease was the origin of the servants and the cow's malady

In conclusion: we don't know, but it seems likely that somewhere along the way a horsepox was used and with repeated passaging either in animals or in people, the virus developed into vaccinia as we know it now.

This is a useful answer to the general question of the origin and evolution of vaccinia virus. The question as posed seems concerned with semantics and does not do your answer justice. I shall attempt to edit it. Another questions that comes to mind is that what makes cowpox cowpox and horsepox horsepox is that they infect cows and horses, respectively. So, is it known whether vaccinia will infect cows and horses?

@David - Thanks for the edit, I read the question as being more or less along the lines of you edit. I don't know off the top of my head as to whether they cross species. I suspect so, as most PoxV are capable of it, albeit with limited infectivity.

@David - I'll edit in more information into my answer when I have time - there's quite a bit to this.

It is often good to just take the genbank sequences and do your own tree. Here I just chose a random region of vaccinia reference genome (50000-55000), blasting to get the 500 closely related strains, mafft, iqtree. Result: the vaccinia virus clade is very diversified and contains a few horsepox, buffalopox, rabbitpox strains, and it falls into the diversity of some cowpox clade.
So the main thing to elucidate is the reason for this wide diversity of vaccinia, ie. first selecting a few sequences representative of the early strains, before all the lab/passage work.
The most basal sequence seems to be AY313848 (Acambis clone 3, named CL3 in this paper).
This paper is probably a better start.
There are good chances that it depends on the chosen genomic region, so that the question of vaccinia's origin is more complicated than it seems.


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Why ions created in our body doesn't give any sensation of electric shock?
We know almost every cell in human body uses ions specially nerve cells , still why we are not getting shocked by those ions ?

Curiosity is an excellent thing, if you want to know more about nerve transmission and the general functioning of the nervous system, you're going to need to do some research on your own. By all means ask questions here, but once you've done some research yourself and understand a bit more about what it is you're asking. The Wikipedia article on the subject has lots of background and many links to follow, I'm sure you'll find it very interesting.

Quite apart from the fact that those ionic potentials are what we feel WITH, they're on the order of 70-80 millivolts.  Would you expect to be shocked by say a common 1.5 volt battery?  Or even the 12 volts of an ordinary car battery? Even the ordinary sort of static electricity shock, such as you might feel from stroking a cat on a dry day, can be thousands of volts.

Hi , I also want to know how this ionic small electrical signals transforms into a something sensible , like light, sound, touch etc . We don't feel any current , we feel colors , cry of a baby etc . Why is that?

@Koushik Pal: The only real answer is that nobody really knows.  We know a good bit about how stimuli - light, sound, pressure, &c - get transformed into nerve impulses (which BTW aren't really electrical signals, they're waves of membrane depolarization along nerve fibers), but almost nothing (AFAIK, anyway) about how the brain converts them into the various qualia that we experience.  It's a queston that exists in the terra incognita between neurobiology and philosophy.  As for feeling current, ask how the 1.1-1.5 volt currents of your CPU got transformed to this text :-)


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How can I accurately determine how much someone likes a sound?
I was thinking about this question the other day. My first instinct was to evaluate the dopamine levels before and after listening to a tune. I proposed this to my friend in the medical field, and she said that it might not be the best way to assess how much someone likes a sound, since dopamine is released when the body feels pleasure. However, she can't think of an alternative. Is there a good way to do this? Preferably something that is feasible to do on human subjects in a non-lab environment (although this might be a lot to ask). Thanks.

You've rejected "ask them"?

@swbarnes2 Of course that is a possibility, but I was thinking of something more accurate than good/bad.

Whether they've actually bought the CD/MP3? Or concert tickets &c?  And on the other side, how much they'd pay for earplugs if trapped in a (pick your genre/artist) concert?

@jamesqf I was thinking less of a song, more of a tune, but thanks anyway

@TheBestMagician: What's the difference between a song and a tune, though?  Unless you mean that a song is sung by human voices?  But even then, it's possible to enjoy that simply as music.  I certainly don't understand Gaelic or medieval French, and I struggle with Latin & even Middle English, but I enjoy songs sung in those languages.

The gold standard would have to be to ask. Any other physiological parameter would just be based on correlation with what people report.


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Where is the location of cutin or cuticle in the plant leaf
Cutin's main role is to prevent the the plant leaf from water loss, cutin is thick in shape , but I need to know where is the location of it ,for example is it in the lower epidermis or in the upper epidermis ?

Welcome to Biology.SE. The Biology.SE community has agreed that 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. Under researched questions may be subject to down-voting and closure. Please take the [tour] and consult the [help] starting with [ask] for details.

Cutin is a waxy substance comprised of a mixture of two or more oliphatic acids. It is secreted onto the whole above-ground surface of the plant: leaves, stem, flower-buds. As such, it covers the whole of the outside of the plant - excepting the stomatic openings which serve to enable wanted moisture loss.
It's secreted by the epidermal layers of the tissues and has served to enable the plants to evolve beyond the marine environment in which they originated in excess of 450 million years ago. It provides a hydrophobic coating, preventing unwanted moisture-loss from the plant.
Cuticle is the name given to the coating of the leaves, cutin to the chemical mixture it comprises.


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Does Chewing Food Properly Ensure that we gain Less Fat?
We recently went to a fast-food corner and I was told by my sibling that even if we chew a burger properly(slowly) converting it into a fine bolus, then it would not affect the amount of fat gained by the body as much as we gain when we normally(hastily) eat a burger.
I ,on the other hand, don't believe in the above statements. I think that it will at least have a better impact with regards to weight loss.
So who ,among the two of us, is correct ?

the only result of chewing for a longer time is that the food on your plate will be colder at the end of your meal.

I think you are misunderstanding reasons for weight loss advice for slow eating/excessive chewing. Slow chewing is promoted because it reduces apetite not because slowly chewed food is digested differently. Slow chewing reduces the objective amount of food people eat before thay subjectively feel full. For standard sized meal it reduces amount of snacks later.


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Is it possible for a brown cat to birth an orange kitten?
I have a brown (cinnamon) cat, I assume her alleles would be b’b’ and oo. She was bred with either a black male (B_ o) or an orange male (__ O), or both if it’s possible for her to have carried the black cat’s sperm with her for a while until she met the orange cat. I can’t remember how long, I was eight or nine when this happened. She had five kittens, an orange female, an orange male, two black males, and a cinnamon male. From my understanding, it shouldn’t have been possible for her to have two orange kittens, let alone for one of them to be female, with either male. However, I have only taken two genetics classes! So, how could this have happened?

Edit: cat coat color genes:
Primary coat color alleles: B- black, b- chocolate, and b’- cinnamon. B is dominant to b is dominant to b’.
Orange coat color alleles: O- orange, o- not orange. These alleles are carried only on the X chromosome. If the cat has OO or OY, they will be orange. If the cat has Oo, they will be tortieshell. If they have oo or o, the primary coat color will be displayed.
If my cat (b’b’ oo) mated with the black cat (B_ oY), the kittens should have been 50% black and 50% dependent on the second allele of the male, either black, chocolate, or cinnamon. None should have been orange.
If my cat mated with the orange cat (_ _ OY), the kittens should have been 50% non-orange males and 50% tortie females. None should have been orange.
I’m unsure about the black cats’ statuses as tabbies, as it can be hard to tell, and the black cat was a stray that we don’t have photos of to even try to check, but the brown cats and orange cats were all tabbies. None were dilute, none had white patches, etc.
It is possible for cats to be intersex and for this to affect their coloration (XXY is how we get male calicos and torties), so perhaps the male orange kitten was OoY, but that would have made him a tortie. For there to have been an orange female or orange XXY male they would need two ‘O’s, which would not have been available to them. Or perhaps the female was just O? But I feel like the odds of there being two intersex kittens in the same litter must be very low. Plus, she had no other physical anomalies (she went thru a series of tests including ultrasounds, x-rays, and a CAT scan to diagnose a well-hidden tumor later in life and nothing strange came up internally either). The orange tom could not have been XXY, as this causes cats to be sterile. Also, the only mutations I have found that causes oo kittens to be orange also tend to cause a shift in coat color during kitten-hood, which none of the kittens experienced.
My cat:

My cat with the orange female and short-haired black male:

The orange female grown up:

The orange male grown up:

One of the black males:

Here is that same black male grown up, he’s the only one of the family with long fur!

Here is the other black male, you can see the stripes on their legs a bit as babies, not so much grown up:

The brown male:

And lastly, here is my cat and her brother as kittens, you can see he also had faint stripes. All of the kittens in their litter looked like either one of them and their mom was brown as well:

I don’t have pictures of either toms, one was a stray and the other was a farm cat. I do have a picture of my cat's mom and her litter if anyone is interested in that.

What breed of cat did you have?

@classy_BLINK Sorry, she’s an American shorthair! All three of them should be/have been American shorthairs.

It would be very helpful if you also add her picture in question.

Welcome to Biology.SE. I think you will get a better response if you elaborate on what lead you to your conclusions about your cats genotype (and what alternative genotypes you have considered). As someone with a genetics background, but who isn't current on the genetics of cat coat color (and no time to read up on that) I would personally find it helpful if you laid out the logic of why you think orange kittens are impossible.

@tyersome Thank you! I added in some more clarification.

@classy_BLINK I had to go searching, but I got pictures of momma and all the kittens!

Cat coat color is controlled by many genes not just two and at least partially environmentally developmentally triggered. so its not entirely genetic on top of being genetically complex. worse some genes are unknown and some other genes are sex linked so will not express in some sexes.

If Momma cat is photos 1 and 2 then what you have there is a tabby cat - these have agouti hairs and the Agouti colour alleles. Agouti means that they have bands of colour on the hairs. I don't know if this means that they also carry other colour alleles.
In addition, I believe that cats are superfecundators (fertilization of multiple eggs from separate acts of sexual intercourse), which means that if they mate with more than one male during the fertile period, then they can have multiple fathers for one litter, as is discussed in this article.
So - yes, it is possible that there are more than one father associated with this litter, and that there are some underlying genetics that can also result in this.


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What is the meaning of harboring cryptic in below sentence?
Tissue culture became more widely used at this time because of the introduction of antibiotics, which facilitated long-term cell line propagation, although many people were already warning against continuous use and the associated risk of harboring cryptic, or antibiotic-resistant, contaminations [Parker, 1961].

I’m voting to close this question because it is off-topic (english language usage rather than biology as defined in the [help]) and demonstrates a lack of the expected prior research — an internet search would have turned up relevant definitions for both of these words.

The natives are more friendly here

Harbouring, using harbour as a verb and in this meaning containing/hiding (see 3rd and 4th definitions at Harbour)
Cryptic = hidden/difficult to find - this is how the word is often used in biology, particularly zoology.

So it means containing hidden contamination.

Yes, that is correct.


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Do the genes for external viral epitopes mutate faster than for viral machinery (e.g. Proteases)?
To fight SARS-COV-2 we use vaccines which train our immune system against viral epitopes like the external S(pike) protein. Since these structures change a lot, would it not have been a better idea to develop drugs which inhibit viral replications (such as protease inhibitors do with HIV)?
I know that vaccines make sense, but couldn`t it make sense to give such antivirals a shot?
Coronaviruses caused quite some trouble within the last years (SARS, MERS), to focus on more genetically stable structures would make sense. Who knows, perhaps there is going to be a new pandemic in the near future....
My question is, are these structures really genetically more stable? And If so, why are there no drugs yet? I know drug development takes normally quite long (over a decade). Why is it more difficult to develop antivirals than to develop vaccines?
Best wishes,
Mourinho_1

Yes, this is correct for (at least some) viruses. E.g., in HIV pol and gag genes are singificantly more conserved, while the genes responsible corresponding to proteins involved in viral attachment to cells. Some elements even explicitly have word variable in them, such as variable loops.

Thanks a lot for your answer. I have some issues finding a paper about this. Could you help me out? I would highly appreciate it.
Best wishes, Mourinho_1

As I have already mentioned in the comments, the mutation rates are indeed different, at least in some viruses. As an example we can take HIV, where pol, gag, and other genes essential for viral replication and interference with the cellular machinery are singificantly more conserved than the env gene, coding for the viral envelope.
Mutations vs. substitutions
To be more precise, one has to distinguish between the mutation rates and the substitution rates. The former are actually pretty much the same along the genome, since they are determined by the chemical processes. These are the rates that one observes in an in vitro experiment where virus is allowed to replicate for one generation, and thus the question of the viability of the new virions does not arise.
Substitution rate is what one measures in vivo, since mutations in the genes needed for replication, such as the polymerase gene, result in "dead" virions, which are present in the blood samples at negligeable concentrations. On the other hand, the substitutions in the envelope gene, which are responsible for the constant adaptation to the host, present much higehr variety.
As a consequence, when looking for the articles on the subject, it makes more sense to look for fitness rather than mutation rate data. Such as, e.g., right panel of figure 5 in this article:

Thats so cool! Thanks a lot!

My understanding is that if you look at the viral genome population and do a mutational analysis, generally there isn't a lack of mutations, substitutions etc in those conserved genes, it is purely that the viruses that are mutated at those essential sites aren't viable and don't produce an infection in subsequent hosts, hence the conservation.

@bob1 Not sure how this differs from the difference between the mutations and the substitutions as explained in my answer. Btw, I liked your answer - mine was intended just to give one example.

@RogerVadim there isn't much difference - it's the old quasi-species problem but I believe you can measure it outside of a single-cycle infection process. I like your answer too - it's a lovely example of a classic virology problem, that I hadn't considered in my answer.

The answer is that drugs and vaccines do different things.
Drugs treat the problem (sometimes before it starts - this is known as a prophylactic), whereas vaccines are intended to prevent the problem from starting in the first place, so vaccines are a form of prophylactic themselves.
One of the problem with drugs is that the vast majority of them have some side-effects, some serious, some not. In many cases, long-term taking of a drug will result in some damage to the taker. How serious this damage is depends strongly on the drug, how long it is being taken for, and how much is being administered.  Vaccines, on the other hand, are generally well tolerated usually being comprised of either proteins from the species of interest or weakened/inactive forms of the pathogen they are preventing. Vaccines encourage your body to prevent harm from an invading pathogen by giving it something to recognize before an actual infection happens.
Vaccines are generally developed against parts of the infecting organism that the body can see - in the case of enveloped viruses (like SARS-CoV-2 and Influenza), this is the bits that poke through the viral envelope, such as the S (spike) protein or HA/NA of influenza.
These sites do change a lot and the virus is under selective pressure to evade the antibodies that bind to these sites, leading to breakthrough infections. However, the same happens for drugs - the virus is again under selective pressure from the drug, so drug resistance happens. Indeed, we have seen this happen in real-time with influenza, where the first generation of anti-influenza drugs (called Amantadines) are no longer effective because of changes in the proteins they target.
As it so happens, there is one drug for SARS-CoV-2 called Remdesivir. This is a nucleoside analogue, that pretends to be one of the nucleobases that comprise the genomes of RNA viruses, and it is effective against a range of RNA viruses. However, check out the side effects part... Resistance to this drug has been observed in the lab for SARS-CoV-2 and other viruses. You might think that it would be pretty hard to develop resistance to something that behaves as part of your genome, because the proteins that process the genome are fairly stable - they can only tolerate a few changes before they are no longer functional, but we still see resistance developing because there is some wiggle-room.
Drugs are being developed to target stable parts of the genome or bits that can't be mutated for a range of viruses, but it is very difficult to do because it requires massive screening of compounds for effectiveness, then screening for toxicity/side effects etc in the host(s), then further development to make the drug deliverable in a form that the body can uptake and transport and finally clinical trials.

Since viruses typically hijack much of the cell's own machinery, and even viral-encoded proteins are often closely related to similar functional proteins of the cell, it's difficult to identify an anti-viral that doesn't also have a negative effect on the cell. With bacterial infections, bacteria have important components (like cell walls) that are missing in human cells and so can be targeted with more impunity. Many antibiotics target such bacterial-specific molecules.

@Armand Yes exactly. However, people are working on developing drugs for things like the influenza RdRP active site, which can't really mutate without losing functionality, but it's really really hard to do, and there's still evidence of resistance mutations.


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Identification of huge larva in South Tyrol
On a sunny autumn day (19.09.2021) i saw a huge green larva crossing the street facing a wineyard. The picture was taken near Bozen, South Tyrol (22 °C that day). It is at least 14 cm long and 2 cm thick. It is entirely green, besides black and yellow stripes at each "segment" and with black spots at the lower part of the body. Additionally there is an red/black anal spine.
I would have guessed it is some kind of Acherontia atropos, but i am not entirely sure.

Is that a green horn catepillar? Don't know anything about them or if that is even what they are called but when I saw that photo that name came into my memory somehow. Google seems to correct that term to hornworm catepillar. 4 inches. Similar pattern too.

Sure looks like tomato hornworm, Manduca quinquemaculata or similar tobacco hornworm M. sexta, but Manduca is an American genus.  Agrius convolvuli is European and similar larva, but seems to have a stripe connecting the slashes of the segments.

After some additional research, i would agreelso conclude its one of the larval stages of Agrius convolvuli , which looks pretty similar. So i guess mgkrebbs was right. A friend of mine, working as an agricultural entomologist said, that especially the black stripes of the larva can change during the developement.


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Why does the body lose enzymes over time?
I recently started my GCSE Biology course where I spend the next two years learning and preparing for my GCSE. One of the questions I have is that I was told that enzymes are recycled every time they are used. So why do people sometimes refer to developing an enzyme deficiency?

There are conditions (genetic) such as enzyme deficiencies, but the chances of you meeting someone with them in your lifetime (unless you specialize in this medical field) are infinitesimal. I'd take what people have to say about themselves with a pinch of salt - as claiming bizarre medical conditions comes into fashion frequently, particularly since the advent of Wikipedia. That being said, you never know.

@ARogueAnt. Glucose-6-phosphate dehydrogenase deficiency is an obvious exception. (Such individuals (over 400 million worldwide) are sensitive to fava beans, for example)

Good point, now I think more about it, digestive enzymes relating to dairy come to mind too, so developmental pathway differences fit also. @user338907

Proteins are fairly fragile molecular machines. They are subjected to environmental and intentional degradation all the time. There is quite a bit of variability across different protein types in how long they last, but none are permanent. Chen et al 2016 write:

For example, RALB is a GTPase, and is involved in a variety of cellular processes including gene expression, cell migration and proliferation, and membrane trafficking. The half-life was measured to be 9.4 hours in this work. IGFBP1 is insulin-like growth factor-binding protein 1, which is a well-known secreted protein. It has a very short half-life of 0.3 hours inside the cell because it is secreted after synthesis. The distribution of all protein half-lives is shown in Fig. 4b. The bin at 9 hours (half-lives between 8 and 10 h) contains the greatest number of proteins. The majority of the proteins quantified have half-lives within the range of 4–14 hours. About 6% of all quantified proteins (49) have half-lives <4 hours, while 51 proteins have long half-lives (>14 hours); the median half-life is 8.7 hours.

When someone talks about enyzmes being "recycled" in a reaction, they're contrasting between enzymes that participate in a reaction but yet are not consumed in that reaction, and other chemical species that do in fact become consumed in the reaction. That doesn't mean that an enzyme is indestructable, just that it isn't used up in the reaction itself.
Similarly, a wine glass is not used up in the process of drinking wine. It's recycled every time it's used. And yet, in the course of being used or even just sitting on the shelf, a wine glass is subject to degradation in the environment at some rate. If you never ever purchase another wine glass, or at least don't purchase them as often as they are broken, you're likely to over time develop a deficiency.
For normally functioning proteins in normally functioning cells, the proteins that are degraded are constantly being rebuilt from scratch. To have a deficiency would require something in the process to go wrong: either degradation is too fast, or something along the chain from DNA -> RNA -> translated protein -> post-transcriptional modification and transport is slowed down or incorrect.

Chen, W., Smeekens, J. M., & Wu, R. (2016). Systematic study of the dynamics and half-lives of newly synthesized proteins in human cells. Chemical science, 7(2), 1393-1400.


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Did Dinosaurs have a neocortex?
Did dinosaurs have a neocortex in their brains? If not, when did it come into existence?

Dinosaurs did not have a neocortex - but many of them might have had something neocortex-like.
The neocortex does, in fact, appear to be a uniquely mammalian brain structure.  However, birds are dinosaurs, and although birds do not have a neocortex they do have complex brain structures that appear to be fairly similar in function.
The neocortex and analogous bird brain structures do appear to have derived from the same base, which means that somewhere after the amniota split, at least some fraction of dinosaurs did in fact possess those neocortex-like structures that we still observe in birds today.
Since information about brains does not fossilize well, we still know very little about dinosaur brains. As such, it's not currently possible to know whether all dinosaurs had such brain structures, or if it only emerged in the group that we now know as birds.

There is some evidence for the bird structure in at least maniraptorans, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4262302/ but the issue with definition does make it weak at best.

Interesting! Thank you for your time


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Identifying substance in body fluid (serum, urine)
I have a large number of serum and 24 hour urine samples from a collection of individuals on many consecutive days. Some of the samples contain a 'large' amount of a substance that has a brown color. The concentration is large in the sense that there is a visible discolouration in those samples. I want to identify the most abundant molecules that are causing the discolouration with some degree of accuracy.
Is it possible to analyse by chemistry methods?

I’m voting to close this question because it doesn't appear to be about Biology as defined in the [help]. This seems like it would be a much better fit in either [Chemistry.SE] or possibly [MedicalSciences.SE]. However, please do not crosspost, instead either request migration or delete from this site before reposting.

Of course it is!

Dipstick urinalysis?

source
The urine dipstick has a bunch of squares, each with a chemical analysis ready to go.  The dip will semiquantitatively show you what is in the urine.  My bet would be hemoglobin but various urine dipsticks will have various substances on there.  A dipstick will detect hemoglobin which will come out of any blood cells once they lyse on sitting in storage for a while.  Free hemoglobin can be in fresh urine too if a person is hemolyzing.  Another brown thing could be bilirubin.  All detectable with chemistry.
A serum chemistry lab will quantify many different things in serum - again bilirubin would be my bet as a common component of serum.  You can look for almost anything and a clinical lab can run a chemistry test to determine presence or quantity of that thing.
Chemistry tests could miss nonchemical microscopic brown things.  Bacteria or mold could contaminate your specimens, or there might still be red blood cells present.  You could look for these things under a microscope.