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Monitoring fish growth
I am new to experimental design and would like to perform the following experiment but I am not sure if my setup is correct or not so far. My idea is below.
Let's say you want to optimise the growth conditions for the small fish. You have been using a standard type of food that has worked reasonably well. But now, three new brands of fish food have become available and you want to conduct an experiment to test which food works best and whether it is worth changing to one of the new food types.
Based on previous experiments, you reckon that you will need 10 replicates to have a good chance
of finding meaningful differences. There are aquaria and tanks of different sizes available so you are not constrained by the equipment.
For this experiment, I assume there will three treatments (the three new brands of fish food). I will call them A, B and C. Since we are testing three different brands of fish food, I will replicate the brands of fish food three times so there will be nine tanks used in this experiment in total. I will label them from 1 to 9. Each tank will randomly receive different food brands of food every day.
But now, how will I find meaningful differences in the growth of the fish if I apply different treatments randomly on the tanks? Also, how many fish do you recommend I use for this experiment and how often should I monitor the growth of the fish? Or do you have another suggestion of how I could set up this experiment, help. Your help will be much appreciated. Thanks in advance.

If this is a homework question, please consider using the 'homework' tag, and consult the homework policy here (https://biology.stackexchange.com/help/homework). It will help people give more suitable answers. If you are actually designing this experiment in real life, it would help if you included information about the species and the purpose for which they are being raised.

This is a good experiment!

3 types of food: ok
9 tanks: ok
Apply different treatment randomly - no!  You are right - no way to tell with random.  It is like comparing McDonalds to vegan diet - you have to stick with your diet to be able to tell a difference in the end.  So Tank 1,2 and 3 get food A.  Tank 4,5,6 get food B.  Tank 7,8,9 get food C.  Each tank gets only that food type.
You need to add the same weight of food to each tank.  More food = more weight.  I am not sure how much is a reasonable amount; it depends on your fish.  Get out what looks like a reasonable amount and weigh it.  That is how much food each tank gets each day.  You could weigh a bunch of quantities and set them aside - maybe in an old egg carton?  That will make it easier to feed the fish each day.
Have the same number of fish in each tank. 3?   Ideally fish are same species and all about the same size to start because different size fish might not all gain weight at the same rate.  I am picturing 11-cent goldfish.  3 per tank makes 9 / food type and 27 in all which is good.
You can gauge growth by fish weight.  When it is time to weigh the fish, fill a bowl with aquarium water, put it on the balance and zero the balance.  Now you will get the weight of whatever you add to the cup because balance is ignoring weight of cup and water.  Sweep a fish out of the tank into the bowl and weigh it.  Then dump it back in and repeat with next fish.

If you can tell the fish apart each one can be weighed separately and I think should also be named with a name that starts with the letter of its tank because that is fun.  For example TankB4 will contain Burr, Black Beauty and Buzz.  Tank C7 will have Clyde, Caesar and Coco.

Keep track in your lab notebook of each fish and its weight
Take a photo of each one when you start and one when you are done.  This will make a great poster.

You can weigh fish every day or maybe every 3 days if you think handling them is too stressful.
You can track weight for each fish, average weight for each tank, and average weight for all 9 fish (3 fish / tank x 3 tanks / food type) over time.  You will graph each of these.  You can use Excel or do by hand.

If a fish or 2 die your data will still be good.
Good luck!  I hope you will come back to this idea and post an image of Aloysius, Angel and Aesop, the fish from tank A1.

It would still strengthen the design for treatments to be randomly assigned among the tanks, ideally in a way that is blinded to the person weighing the fish (you keep a key to which tank gets which treatment, decode after data collected). This helps guard againt measurement bias and other possible confunding variable, like where the tanks are located in the room, or the order in which they are fed. You'll also want way more than 3 fish per tank, depending on the stage of development they are starting at. Some fish have very low rates of survival to adulthood.

Per your prompt, there are three new brands of fish food, but...

You have been using a standard type of food that has worked reasonably well.

I suggest you include the "standard" fish food as a control, so that you will have four treatments in all.  Besides that, the experimental framework suggested by Willk is spot-on.


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Why do COVID19 serology tests focus on the nucleocapsid while vaccine efforts focus on the spike?
When I look at the specification sheets for many of today's serology tests like the new Roche test or the Abbott test, they use a nucleocapsid antigen in the test, looking for anti-nucleocapsid antibodies. Given that these tests seem to have high sensitivities toward past infection, it suggests that recovered patients seem to reliably generate an immune response to the nucleocapsid.
At the same time, a lot of the research into vaccines focuses on the spike protein: Moderna is developing a vaccine based on an mRNA coding for the spike protein, CanSino and Oxford combine an adenovirus carrier with a SARS-CoV-2 spike, and so on. I'm having trouble finding any vaccines that target the nucleocapsid peptide.
I'm having trouble understanding this difference. Is it the case that recovered patients reliably produce antibodies to both viral components, but the nucleocapsid is better for testing due to cross-reactivity or other concerns? Or does a natural immune response target the nucleocapsid, while scientists think that the spike is a much better target because it's directly expressed on the cell surface or for some other reason?

N is highly antigenic because N-Elisa works and shows an early and high Ab load. N is hidden inside the virions and  infected cells so it is unclear how anti-N Ab might be useful. The antigen presentation and B-cell maturation (as described in the books) doesn't depend on if targeting the antigen will be efficient. Emphasizing neutralizing antibodies is probably deserved but they are not all, most antibodies simply tag and opsonize the virions and infected cells for destruction by immune cells. S accumulates on the surface of virions and infected cells, a perfect marker

The vaccines will be directed towards a protein/epitope of the virus that creates the most robust immunogenic response, in which the defense system will create an array of antibodies to confer immunity, those antibodies will have to NEUTRALIZE the virus upon entry.
In the case of SARS-CoV-2, the majority of research shows that neutralizing antibodies are directed towards the S1, S2 and RBD proteins which are all part of the S protein.
In this same line, the fact that the body creates antibodies directed towards other components of the virus doesn't mean that they are protective. So creating a vaccine towards those components wouldn't be useful at all.
The reason why those serologic tests target the N protein is probably due to the fact that is highly antigenic. But I'm sure I've seen tests that also target the S protein.

Can you please provide citations for the claims that (1) antibodies directed toward the S protein are neutralizing and (2) the N protein is highly antigenic?

source: Stack Exchange

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

sort: votes


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Can a macrophage differentiate back into a monocyte?
I know that monocytes differentiate into macrophages when they enter the tissues, but do macrophages stay in those same tissues for the remainder of their lifespan, or do they differentiate back into monocytes and re-enter the bloodstream at some point?

No, macrophages can not turn back into monocytes, usually once a monocyte travels around the bloodstream for 1-3 days, it then leaves the bloodstream and travel to a tissue where it will differentiate to a macrophage or dendritic cell. It undergoes a conformational change, this usually happens during inflammation as the macrophages travel over a chemical gradient, macrophages can still enter the bloodstream, however, they won't re-differentiate to a monocyte. So to answer your question directly, macrophages don't stay in the same tissue forever as their life span is pretty long(1-2 months) so most likely an inflammation will occur and force the macrophages to diffuse across the chemical gradient, but they usually patrol around the tissue area where they differentiated.
source: http://www.histology.leeds.ac.uk/blood/blood_wbc.php

This paper found dedifferentiation of macrophages back to monocytes
https://mbio.asm.org/content/10/5/e01743-19
"Bordetella Adenylate Cyclase Toxin Inhibits Monocyte-to-Macrophage Transition and Dedifferentiates Human Alveolar Macrophages into Monocyte-like Cells"
Jawid Nazir Ahmad, Jana Holubova, Oldrich Benada, Olga Kofronova, Ludek Stehlik, Martina Vasakova, Peter Sebo
mBio Sep 2019, 10 (5) e01743-19; DOI: 10.1
Found by searching with keywords macrophage dedifferentiation

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


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How would evolution explain parastitic wasps?
I read this article about wasps that can do "brain surgery" on cockroaches.
https://www.wired.com/2014/02/absurd-creature-of-the-week-jewel-wasp/
How does evolution create such a thing?

The brain surgery along with many of the other steps in the reproduction process seems to be very precise.  Any error here or there could lead to a bad result
Even if by happenstance the first wasp figured out a good way to do brain surgery, how would its offspring know to do the same thing?

Thanks.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In general we encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). In particular, we expect you to look for similar questions on this site before posting — there are many including the one I've flagged. Thanks!

I encourage you to check out some of the online resources available for learning more about evolution. For example, this a useful introduction to evolutionary theory from UC Berkeley.
You might also find a book like "The Blind Watchmaker" helpful for understanding how complex behaviors and structures arise through evolutionary processes.


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What is this yellow sticky excretion from a moth? Details in photos
Saw this moth on some grass the other day and took some bad phone photos. I'd like to know what the yellow excretion is. I believe it is an excretion from the moth (as opposed to for example, some bubble gum someone dropped on the ground), because it was attached to the tail end of the moth instead of its whole body.

I tried to label the pictures as best I could, you may have to look closely. You can only see a tiny portion of the moth wing in the first picture, below.
The yellow thing was quite sticky but not as hard as bubble gum, as it stopped the moth from flying away. It was frantically flapping its wings trying to get away from some ants, which seemed to be very attracted to the yellow thing. At first I thought the swarm of ants were eating the dead moth, but the moth was alive and the ants were more interested in the yellow sticky thing. I got a thin stick and pulled away some of the sticky stuff and the moth was free enough to crawl away, taking the yellow sticky thing with it, leaving a thin trail behind, like when you stretch out bubble gum. It seemed to be very sticky to the moth and my stick, and very tensile, because unlike a spider's web, I was able to draw it out more when I tried to pull it away from the moth to free it.
I am so curious to know what it might be. I don't think it was made by ants, because it seemed to be attached to, or coming from the actual moth, although, the ants did not seem to be stuck to it.

Please add "moths" to the tags if you have enough 'reputation level' to do so.
Thank you

Some moths exude a yellow lymph excretion when they are threatened.
https://www.nature.com/articles/219747a0
The photo is not very clear, It's difficult to see the species of moth. what did the moth do after? did it fly away? If the moth was looking ill, it could be that it had a parasite.
https://www.insidescience.org/news/meet-moth-produces-both-bird-and-ant-repellants

Just going to mark this as the answer as I am satisfied with this explanation. The moth was trying to get away from the ants, but it was unable to fly away or spread its wings. It was rather difficult to get better photos. Thanks!


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Protein half-life regulating gene expression
Are there any instances in real life of protein half-life regulating gene expression? For example, in a cell, Gene A produces a starting population of protein P, after which the expression of the gene is turned off. The starting population then degrades over time. When the numbers of protein P are reduced to roughly half, the transcription of Gene B, which had been repressed until then, is turned on (perhaps a byproduct of the protein degradation acts as a transcription factor for Gene B?)
My apologies if the question does not make sense. I am a sci-fi author, trying to design a synthetic virus for my novel - a bioweapon of sorts. The scenario is that the viral genome, upon making its way into the nucleus of a human cell, goes into a lysogenic phase, where the genes for its replication are turned off.  The virus needs to initiate its replication only after a certain amount of time has elapsed, say X days. X is the half-life of protein P, which is produced by the viral genome while lysogenic. After X days, transcription of the rest of the viral genome is turned on, and the virus starts making copies of itself. Only this time, the copies go straight into lytic mode upon infecting a cell and start multiplying exponentially. My fictional virus has mechanisms to suppress interferon signalling and evade the immune system (for some time at least, until it gets out of control in the host body).
I am aware that some real-life viruses that infect bacteria can switch between the two phases, but the trigger for the switch is always an external event - like UV damage - and not something controlled by the virus itself. In my scenario, I want the virus to behave like a programmed timer, turning itself on after a fixed elapsed time.

Some variation on quorum sensing based autoregulation maybe?

Many processes are mediated by (usually active or catalyzed) degradation of proteins. For example, cyclin proteins are degraded by the ubiquitin pathway as part of the cell cycle, allowing the cell cycle to proceed. They are however helped along on this by catalysis via ubiquitin ligases.
I was not able to find any examples of a "passive" degradation of a protein regulating anything, but it might be very difficult to demonstrate in any biological system that a degradation process was truly passive.
It seems that the main thing you are interested in is epigenetic memory of a cell- e.g. a way of measuring time lapse in a biological system.
It's not exactly the same, but you may be interested in processes like the cyclomorphosis of Daphnia, which are effectively transgenerational epigenetic memory. I'm hazy on the molecular details though.
Another option might be something like a DNA methylation clock.


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Unlike humans, why do plants not have something blood-like to transport $O_2$ throughout their body?
Since plants have a large number of stomata at different parts of their body, they can get $O_2$ at almost every part of the plant and so, they don't need to transport it throughout the whole body whereas in the case of human beings, they can only intake $O_2$ through their nostrils, but a large number of organs throughout their body require it. So it needs to be transported. And for this reason, blood is present.
Let me know if I'm wrong and what the actual answer is.

In plant cells, O2 enters through stomata or lenticels. Then, the O2 molecules are transported to the cells through the process of diffusion. Stomata and lenticels are found all over the surface of plant body, i.e., leaves, stem and root. Because of this, plants don't need blood like connective tissue to transport O2 and CO2.


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Why are these nesting magpies building another nest
Pair if eurasian magpies occupy a nest visible from my balcony. It's the nesting season for them here, and I assumed they have laid eggs. I can't see the eggs directly, but one of the magpies has been regularly sitting inside the nest (at least for last two or three weeks) and they always attack other birds that come too close.
Today, they've started building a new nest on another tree. It's pretty close, the nests are about 20 meters apart. They still visit their original nest.
What does it mean? Is it a sign of nesting failure? Does it mean their original nest is no longer sufficient?

I found an article that explains secondary nests as backups in case of nest usurpation by other birds:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4858914/
This is for black sparrowhawks losing nests to Egyptian geese around Cape Town. They measured number of nests built per breeding pair of sparrowhawks and found it to correlate with number of Egyptian geese present and especially their nest usurpation behaviour.
That article mentions brood parasitism (e.g. cuckoos) as another possibility for other birds, and I've seen references to duplicate nests with eggs in each. ( https://www.tandfonline.com/doi/pdf/10.1071/MU939286a )


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What is the cause of a protuberant belly in kwashiorkor?
Kwashiorkor is a PEM (Protein–energy malnutrition) usually characterised by a pot belly. Why is there a pot belly in the case of a malnutrition? I have found contradictory reasons. This paper says that it is due to a fatty liver. This website says it is due to excess fluid accumulation in the tissues.
I noticed that these children have very skinny limbs. When I pointed that out to my teacher a few years back, she told me that the subcutaneous fat from the thighs accumulates under the belly. I can find no source confirming that, though.
So, what is the cause of the pot belly?

The Gastroenterology paper you cite doesn't mention distended bellies at all.  There is no dispute that fatty liver is a symptom of kwashiorkor.  But the Wikipedia article makes it quite clear that the cause of the distended belly is edema.

The extreme lack of protein causes an osmotic imbalance in the gastro-intestinal system causing swelling of the gut diagnosed as an edema or retention of water.[4]

And:

Compromised fluid recovery results in the characteristic belly distension observed in highly malnourished children.[14]

Here's another source:

To understand the reasoning for this, it is important to know that in malnourishment, the rounded abdomen is not due to fat accumulation. Instead, the water retention and fluid buildup in the body cause the abdomen to expand. This results in a bloated, distended stomach or abdominal area.

The rest of the article goes into more detail on the phenomenon and mechanism of action.
This source seems less authoritative, but also suggests that weakened abdominal muscles (due to protein deficiency) also play a role:

The swollen belly is the result of not only that enlarged liver, but also the loss of muscle mass, which leads to weak abdominal muscles. Together with a weakened lymphatic system that is unable to keep up with the body’s liquid wastes, when those wastes accumulate in the abdomen, the belly becomes distended.

So the author suggests that fatty liver contributes to belly distension, but is not a sole cause.  None of the sources I looked at mentioned fat accumulation as a contributor, but rather eliminated it.

Abdominal distension is common in kwashiorkor, and many reasons have been proposed for it [1,2]:

Dilated bowel loops (because of gas produced by bacterial overgrowth),
An enlarged liver (because of steatosis, i.e. fat accumulation),
Ascites, i.e. excess fluid in the peritoneal cavity (as part of the
generalised oedema of kwashiorkor), and
Weakness of the abdominal wall muscles.

But these are merely guesses. It is difficult to pinpoint one particular cause, since no studies have been done on this. Possibly, each of them contributes to some extent.
Now it is true that children with kwashiorkor have skinny limbs, but it would not be correct to say that their fat has 'moved' to their bellies. They are skinny because they are not getting enough nutrition to make up for their fat and muscle breakdown. The liver fat accumulation, on the other hand, is because the liver too is diseased. It is unable to metabolise lipids as it normally does [3].
References

Klein S. Protein-energy malnutrition. In: Goldman L, Schafer AI, editors. Goldman's Cecil medicine. 24th ed. Philadelphia: Elsevier Saunders; c2012. p 1388–90.
Ashworth A. Nutrition, food security and health. In: Kleigman RM, Stanton BF, St Geme JW, Schor NF, editors. Nelson textbook of pediatrics. 20th ed. Philadelphia: Elsevier; c2016. p 295–306.
van Zutphen T, Ciapaite J, Bloks VW, et al. Malnutrition-associated liver steatosis and ATP depletion is caused by peroxisomal and mitochondrial dysfunction. J Hepatol. 2016;65(6):1198–1208. https://doi.org/10.1016/j.jhep.2016.05.046


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Carotene in Dracaena draco
I'll keep this question straight and simple:
Some succulent plants produce carotene, a red pigment, in response to great heat, turning their leaves red. The dragon blood tree (Dracaena draco) is among the succulent plants. Does it exhibit this behaviour too?

Looks like they do.
What We Know and What We Do Not Know about Dragon Trees?

Numerous phytochemical studies of resins from the Dracaena species
  resulted in the isolation and subsequent identification of sterols
  [135–138], steroidal saponins [110,138–141], lignans [138], and
  terpenoids [131,135,142–144], flavonoids (recently reviewed by Sun et
  al. [129], bioflavonoids [145,146], carotenoids [109,138], and
  aromatic compounds [107,147–151].

Citations are behind a paywall but apparently carotenoids are in the sap.


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Why animals haven’t yet evolve in 2020?
In past when I was born like 1990s I notice most animals haven’t evolved in 30yrs. Example  cats haven’t gain more muscular body as to be strong to defend themselves from predators like well many animals of coyotes, raccoons, possums, red fox, bobcats, birds of prey, wolves and others

Are you looking for the evolution of cats, mammals or animals in general? And what exactly makes you think there is no evolution? Not all changes are visible on spot, especially given that 30 years are not a long time span in context of evolution.

I wonder why so many downvotes for this.

Yeah I'm a bit confused why so many downvotes. I was curious for live chat @Arsak

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, your question needs: 1) clarity, and 2) evidence for the assertion that "animals" haven't evolved. ——— In general, we encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

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

In particular, I encourage you to check out some of the online resources available for learning more about evolution. For example, this a useful introduction to evolutionary theory from UC Berkeley.

But still feral cats of 2020 are new generations from 1990s feral cats that 20yrs later of generations possible over 100 generations had passed since cats breed very quickly in feral life

Evolution takes either many generations or strong evolutionary pressures (or both).  For your example species, domestic cats, 30 years is only about 30 generations.  Most domestic cats (as opposed to feral ones) are bred by humans, and are selected for attributes - call them collectively "tameness" - that make them good house pets.  These attributes are not those which would help as defenses against predators.
Now if you looked at populations of feral cats, you might find them evolving such traits, since they'd be under strong selection pressure.  (Though stealth & avoidance behaviors would seem to be more likely than size & strength.)
Conversely, wild animals can be "evolved" under human selection in a fairly short time, as for instance in the Russian fox domestication experiment: https://en.wikipedia.org/wiki/Domesticated_red_fox  You could also consider the evolution of the coywolf in eastern North America: https://www.csmonitor.com/Science/2015/1108/How-did-a-canine-hybrid-coywolf-emerge-in-front-of-our-eyes
Likewise, if you go to organisms with shorter generation times, examples of evolution, such as antibiotic resistance in bacteria, are quite frequent.  Indeed, if you have been paying any attention at all to recent events, you might have noticed that a variety of coronavirus has recently evolved the ability to infect humans.

But I seen many cats they look and same behavior. My cat was born from the streets so he ten years old. He quite small but seems tough but not really a dog can kill him with one bite :( I mean dogs are stronger, faster, smater high stamina and more resilience then cat. If cat could gain some those then cat wouldn’t have so many predators. I think dogs are smater then cats but cat people not true even though I’m cat person

@John Pass: I strongly doubt that the many cats you've seen are an appreciable fraction of all the cats there are, or that you've made any statistical study of the differences between feral cat populations and domestic cats.  (FTM, search for 'new cat breeds" to see how cats have evolved in recent decades.)  As for dogs being stronger &c than cats, it really depends on the dog. My bear-chasing Plott Hound, yes (except maybe the smarter part :-)), someone's toy poodle, not so much.  And of course there are enormous differences between dog breeds, too.

But the feral cats I seen are small like average size. They lived with coyotes, raccoons and birds of prey. If pack of coyotes chase a cat then the cat is no match to defend themselves. My cat ran out one night because we accidentally left door open he  gotten attack by raccoon at night we took him to the vet he got scars that was few years ago. I turn the lights on the raccoon ran off

@John Pass: Certainly feral cats defend themselves against coyotes. (Otherwise they would all be eaten, no?) They do so by evasion, not combat: climbing trees, going into small holes, &c.  If they were to evolve towards larger size/strength, they would lose those advantages, and would have to become large enough that they would be competing directly with coyotes for that evolutionary niche.

Oh I understand but I seen YouTube videos that coyotes hunt feral cats like 1-2 coyotes is enough to kill them. Cats can’t run long distance compare coyotes

@John Pass: So what you're seeing is evolution in action.  The ones that get eaten by coyotes are the ones that couldn't evade the coyotes, because they e.g. got too far from a safe refuge.  You don't see videos of the cats that don't get eaten because they were smarter, more cautious or whatever, yet these are the cats that will be passing on their genes to following generations.  That's the way evolution works: if all cats (or any other creature) that were born survived to reproduce, the world would soon be buried in cats. "Thus, from the war of nature, from famine and death..."

Like tigers are big cats they been hunted by poachers why they never evolved or adapted to gain more intelligence or smaller sizes to hide or faster bodies or tougher body for gunshots those who did survive by a bullet to next generation

@John Pass: Once again, the really too obvious reason is TIME.  Humans have only had guns for a couple of hundred years.

but its been like 200-300yrs why isn't that enough for evolution

@John Pass: No, it's not.  Why can't you seem to understand this?

You are witness to the COVID-19 epidemic, an example of evolution.
True, there are not weird bipedal cats walking around.  Actually Youtube shows quite a few, but you get my meaning.
But there is a new virus ravaging the world.  Where did it come from?  It came from predecessors that were not so pathogenic for humans, got a purchase in humans, and a new strain evolved.
COVID-19 coronavirus epidemic has a natural origin

Evidence for natural evolution
The scientists found that the RBD portion of the SARS-CoV-2 spike
  proteins had evolved to effectively target a molecular feature on the
  outside of human cells called ACE2, a receptor involved in regulating
  blood pressure. The SARS-CoV-2 spike protein was so effective at
  binding the human cells, in fact, that the scientists concluded it was
  the result of natural selection and not the product of genetic
  engineering.
This evidence for natural evolution was supported by data on
  SARS-CoV-2's backbone -- its overall molecular structure. If someone
  were seeking to engineer a new coronavirus as a pathogen, they would
  have constructed it from the backbone of a virus known to cause
  illness. But the scientists found that the SARS-CoV-2 backbone
  differed substantially from those of already known coronaviruses and
  mostly resembled related viruses found in bats and pangolins.

A rare thing - the evolution of a new and dangerous life form in your time on earth!

I don't understand what you mean on corna virus for a cat? I'm asking about why cats haven't evolved. My cat is ten years old so he was born almost 10-20yrs after i was born in the 90s. My cat and any other cat that was born after 2010, all the same, no extra attributes

The cat thing was a joke.  I believe you have not seen new cat types.  But you have seen or heard of a new virus type.  A new virus has evolved during your lifetime.  Get it?

I understand but I’m asking about cats in streets or feral cats not evolved from predators

@John Pass: And you've been told the obvious reason why there are no readily apparent evolutionary changes to feral cats: not enough time.

Can u explain not enough of time. That’s why I don’t get it. Feral Cats been around 1900-2020 that 120yrs that hundreds of new generations


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Is this a fossil?
My neighbor found this rock and asked for help identifying it as a fossil. Can anyone confirm that it is/isn't a fossil? If it is, what it is a fossil of?
It was found near Lexington, VA, USA, on Short Mountain. It is about 12cm long, 8cm wide and 6cm tall.

City's you please edit your post and add the size of the object and roughly were in the world it was found?

@Arsak Done - I had to approximate the size as I don't have it anymore, but the estimate is probably close enough.

No
It bears no halmarks or indicators of being a fossil, and it does not look like any fossil I have ever seen . it looks like simple chemical weathering.


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Difference between sexual and asexual spore
This Wikipedia article on Spores mentions this:

In biology, a spore is a unit of sexual or asexual reproduction that may be adapted for ....

What is the difference between the sexual spore and asexual spore?
Are they any different on basis of formation, diploid or haploid, role in life cycle?
By Sexual Spores, I mean the spores that arise in the sexual reproduction process and similarly for Asexual Spores, i.e. spores which arise in asexual reproduction process.
To add to the context, this image shows the Sexual and Asexual spores in a certain fungi (Mycelium) life cycle.

I am curious - if this is for an assignment, are you not given sources that contain what your teacher thinks you should learn?  Or are students just turned loose on the internet now?

@Willk this is not an assignment given by anyone to me. I was in fact studying reproduction in organisms and dug into 'spores', eventually I ended up upon the Wikipedia page on Spore (link mentioned in the question). And was curious between their difference. [I have edited the question now]

In the same wikipedia page of spores you cited, you can find that they have said:

Fungi commonly produce spores, as a result of sexual, or asexual, reproduction. Spores are usually haploid..

Again,

Vascular plant spores are always haploid.

So, sexual and asexual spores have no difference in ploidy- both are haploid. (There are exceptions- zygospores in fungi are diploid)
Now, coming to mode of formation, they are different. For example, in Ascomycetes, sexual ascospores are produced endogenously whereas asexual conidiospores are produced exogenously.
Spores that are formed by the process of meiosis are sexual spores and when formed from mitosis are asexual. The term 'sexual' means meiosis is involved.


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What are the methods to quantify the bacterial adhesion rate for the biofilms grown on coupons in CDC or annular bioreactor, non-invasively?
I'm interested to know that if I grow the biofilm on coupons in the CDC bioreactor at a particular shear stress, and after say 48 hours, I take out the coupon from the bioreactor to quantify the bacteria attached to it; what are the commonly preferred 'non-invasive' methods that I can use to do so? Can LIVE/DEAD staining be used in this case?
Additionally, if I want to know the bacterial adhesion rate (when the coupon is still inside the CDC bioreactor, and the baffle plate is rotating at say 80 rpm) at different time intervals (say after 1 hour, 4 hours, 8 hours), without disturbing the coupons, can I do that by using any Imaging technique?
Please let me know. Thank you for reading my question.
Regards,
Grishma

By "non-invasive", do you mean you want to quantify the bacteria in the biofilm in such a way that it can be re-insterted into the bioreactor and continue growing? What exactly are you to accomplish with this experimental design?

Thank you for your response. By non-invasive I mean to imply that can taking the images (without taking the coupons out of the bioreactor) at different time instances be possible. By knowing the growth at different time instances, I'm working towards figuring out the optimum time instance when we can introduce the disinfectant treatments.


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Is there a bacterium that became a virus?

Is it possible for a virus to be a descendant of a bacterium that was not through horizontal gene transfer?

How I think this could happen:
Suppose a species of bacteria lives in an environment where it gets all the resources it needs to reproduce (and let's assume that there will be no major changes in the environment).  That is, if it loses a gene that synthesizes some substance (or regulates some process), it will not be at an evolutionary disadvantage.  Because it can achieve this from the environment.  Even depending on the gene, it can even be an evolutionary advantage, as it can become more efficient when it comes to reproducing.  And I have seen that an experiment was carried out related to this question, it was shown that viruses can lose some genes in an environment where it can naturally find the protein that is associated with those genes.  Thus, there is a chance that this species will become so simple, that it will end up becoming a virus.

The fundamental difficulty with this theory is the bacterium would somehow have to learn to make multiple proteins to encapsulate and deliver the genetic material.  This is a classic chicken-or-the-egg problem for evolution: to iterate and to evolve the mechanism, the mechanism must exist.  This is an open problem for evolution, so I don't want to nix your theory on this aspect alone.  But -- you must realize this idea requires knowledge far outside what we understand well about evolution.  Is it possible? No one knows.  Is it plausible? Yes, but very difficult

Mitochondria and chloroplasts are descended from endosymbiotic prokaryotes that can no longer reproduce outside a eukaryotic host, and in billions of years they've not simplified anywhere near that much. As with @BAMF4bacon's point, this is a non-fatal but significant difficulty.

Could you be a lot more realistic, Raphael?
Your bacterium does get all the resources to reproduce, with no changes in the environment. If it loses (an important) gene it can achieve (this?) from the environment? That could be an evolutionary advantage; it could become more efficient at reproducing?
Then, how did the experiment you saw switch from bacteria to anything about viruses?
Perhaps viruses can lose genes when they find proteins in the environment and how does that change bacteria into viruses?
Is your thesis simply that “there is a chance” or what?

This virology site has a post about a 2017 paper about membrane-vesicled plasmids that act in ways that are theorized to be precursors to how viruses work:

It is likely that the plasmid-containing membrane vesicles are precursors of what we know today as virus particles. It is thought that viruses originated from selfish genetic elements such as plasmids and transposons when these nucleic acids acquired structural proteins (pictured; image credit). Phylogenetic analyses of the structural proteins of many enveloped and naked viruses reveal that they likely originated from cell proteins on multiple occasions (link to paper).
The membrane-encased Archaeal plasmid seems well on its way to becoming a virus, pending acquisition of viral structural proteins.

Though plasmids are not viruses and are not bacteria, bacteria are hosts for plasmids, and plasmids add indirectly to the genetic constitution of bacteria. Expression of plasmid genes can help bacteria survive hostile or extreme environments, and they reproduce along with bacterial chromosomes. Via the Wikipedia link:

Unlike viruses, which encase their genetic material in a protective protein coat called a capsid, plasmids are "naked" DNA and do not encode genes necessary to encase the genetic material for transfer to a new host; however, some classes of plasmids encode the conjugative "sex" pilus necessary for their own transfer.

There are giant viruses that some people think could be degenerate bacteria.
https://en.wikipedia.org/wiki/Mimivirus

Mimivirus shows many characteristics which place it at the boundary
  between living and non-living. It is as large as several bacterial
  species, such as Rickettsia conorii and Tropheryma whipplei, possesses
  a genomic size comparable to that of several bacteria, including those
  above, and codes for products previously not thought to be encoded by
  viruses (including a kind of collagen[20]). In addition, mimivirus has
  genes coding for nucleotide and amino acid synthesis, which even some
  small obligate intracellular bacteria lack. They do, however, lack any
  genes for ribosomal proteins, making mimivirus dependent on a host
  cell for protein translation and energy metabolism.

It is plausible that organisms like this started as cells and dispensed with various things they did not need in their parasitic lifestyle, resulting in something that fits the definition of virus.  Other parasitic bacteria (like those mentioned in the article) lost other unnecessary components but retained such that they still fit the definition of a cell.

Can you reference your claim that "some people think (Mimivirus) could be degenerate bacteria"? Preferably someone with the relevant expertise? The Wikipedia page does not include this point of speculation and it seems likely to be false.

The giant viruses like minivirus may be degenerate free-living organisms, possibly a bacterium but more likely an archeon or eukaryote (based on number of homologous genes).  One paper you might reference is Abrahão [2014] doi: 10.1186/1743-422X-11-120

@BryanKrause - saying it seems likely to be false means you did not check at all past reading wikipedia, and I suspect you are able.   But if not, here is the link to the first hit for mimivirus on google:  https://www.nature.com/articles/nrmicro.2016.197. Here is text from that link: Furthermore, there is disagreement as to whether the large genomes of giant viruses are a result of smaller viruses acquiring genes or of a genome with cellular ancestry adapting to escape the cell nucleus2,9,10,11,12,13.

@Willk It's up to you to provide a complete answer, not up to me to research the entire question for you. It's also not acceptable (and I think of it as academically dishonest) to cite a source for a claim that doesn't make that claim - it makes it look like you have support that you don't have. So far you've only cited Wikipedia which does not make that claim. Please edit proper citations into your answer for claims you are making rather than having them in comments as comments are ephemeral.

@BryanKrause I agree he should cite a source, but do you care to cite a source for your claim that his claim is "likely to be false"? I've tried preliminary research and can't really find much to back up either point... more like a lot of "it's a weird, huge, virus with a ton of gene sequences we're confused about, and some similarities to cells > other viruses... but really we have no clue" - 100% just fishing for good reading because I found this interesting ;) (but it should improve the answer)

@TCooper The Wikipedia page includes statements like "its lineage is very old and could have emerged prior to cellular organisms" and "It has been suggested that Mimivirus and similar kinds are remnants of a "fourth domain" of life, and that other giant virus may represent other ancient domains" as well as being part of https://en.wikipedia.org/wiki/Nucleocytoviricota which are genetically related, so if one of them is derived from a bacterium than they all are. My statement about "likely to be false" was mostly based on OP's own source ranging from saying nothing to contradicting it

I get very skeptical when I see people using citations as support for claims they make when those very citations don't provide any support.

Re "it's up to you": I'm pretty sure that collaboration is more constructive, and answers can be edited by others.(BryanKrause's points are fair, and that "up to me" means "as a moderator", but the tone of this conversation seems to have derailed...)


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How do biologists infect cells with viruses within a lab setting?
I'm writing an experimental proposal as my final paper for my single molecule biophysics class. Part of the procedure I wrote involves intentionally infecting a culture of HeLa cells with SARS-CoV-2 in order to perform a series of tests on it. Are there any readings or articles that you guys can point me to which detail how biologists intentionally infect cells with viruses within a lab setting?

A good strategy when writing a proposal like this is to read the methods sections of papers in the literature. You can probably use searches that include terms like "in vitro" and members of the class of viruses you are interested in studying - both the original SARS virus and SARS-CoV-2 would be good places to start, MERS would also be reasonable. You might not find your answer in the first paper you look at, so expect to look at a few, and expect that you might need to go to a source that is cited by one of the papers you initially read. Note that your instructor likely wants you do to this.

I'm closing this question as Homework because I think getting a thorough answer here would interfere with the purpose of the assignment you were given. I'll let @MikeyC's answer remain because it is helpful but doesn't go so far as to complete your homework for you.

You'll probably want to consider whether HeLa cells are the optimal cell line for acheiving your objectives. This paper shows minimal change in cell viability of HeLa cells innoculated with SARS-CoV and SARS-CoV2, but it's probably a good resource for how cell-culture infections are performed. This paper claims that VeroE6 is the standard cell line for producing viral stocks of SARS CoV-2.
Best of luck with your proposal.


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Can DNA be used directly to determine the age of a mutation?
I've studied that proteins found in a sample as biochemical evidences for evolution. Its variation in structure and configuration can be used to date the age when that mutation occured, effectively dating the sample. But can't DNA be directly used for the process? Proteins also require transcription and translation, increasing error. I think proteins make phylogenetic detection easier, but doesn't transcription and translation give more room for error?

A similar question has been asked previously and I supplied an answer here. Your remarks about transcription and translation errors are irrelevant. One is using the sequences of the proteins that are correctly transcribed and translated. Those that are not will probably be degraded. They will certainly not predominate.

I think that this question for which there are already two answers encompasses yours Comparative evolutionary study: is amino acid or nucleotide comparison more useful?

Dayhoff matrices are a way of looking at the acceleration of evolution in the protein sequences. But why wouldn't you use the genetic code for pseudo time?

Hi and welcome to Bio.SE! I think with a little tweaking this could be a great question, and I am not sure yet if it is a duplicate as David suggests. I have voted to close this question because it is unclear what the question is. I think without an example of the problem, it cannot be answered. What studies that use protein for time have you come across? Are they carbon dating, building a phylogenetic tree, or something else?

Yes, you are right.  Proteins are specified by DNA sequences, so DNA sequencing is a more direct way to obtain essentially the same information.  Note that mutation dating via DNA or proteins is approximate.  It involves a lot of assumptions about continuous rates of mutation, but in fact mutation is a stochastic process and does not have a knowable continuous rate.  The sequence of mutations can be determined with high confidence, but the rate can only be determined approximately.

No. DNA sequencing is an inferior method for evolutionary studies in general because the DNA diverges much more rapidly than protein. There is already a question on this topic. I’ll see if I can find it.

More rapid divergence does not equate to inferiority for evolutionary studies!  It would (ideally) amount to a higher "clock rate", which would (ideally) amount to higher accuracy.

See my answer to the related question which I give a link to in my comment to the poster.

This approximate time is often called pseudo-time.


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Why shouldn't there be any air between lungs and ribcage?
My OL biology textbook says that one of the functions of the pleural fluid between lungs and pleural membrane is that it ensures no air between lungs and rib cage.
But I wonder why air there would cause any problems. I was told that it'd build up there and exert pressure on the lungs but why would it build up there in first place, couldn't it just go out through the mouth or nose? And in case that's really the answer, how does it manage to prevent any oxygen or other gases from getting into the fluid, after all, the pleural fluid touches the pleural membranes cells which require oxygen, won't oxygen diffuse from around them into the fluid?

having air or gas bubbles interacting with the intercostal muscles would be outside of the bodies air cavities which are gas control systems, free oxygen in the body is quite a reactive substance, having air bubbles forming outside of the lungs would be far from peak performance.

The pleural membranes help the lungs to move without friction, they are like water in between glass, the hydrostatic pressure is a low friction system. If you are running with bubbles outside your lungs, it would tend to move around and upwards, it would interact with the muscle tissues and the nerves, the intercostal are well innervated.

The pleural cavity and the airway are separate compartments; there is no anatomical path between them.

(Image source: https://upload.wikimedia.org/wikipedia/commons/0/0d/2313_The_Lung_Pleurea.jpg. Attribution: OpenStax College / CC BY (https://creativecommons.org/licenses/by/3.0))
Thus air in the pleural cavity would not go out through the mouth or nose. But it would make breathing difficult. How?
In a normal human being, the chest wall and diaphragm move outwards to bring about inspiration. Remember, though, that they are separated from the lung by pleural fluid. Since pleural fluid (like most liquids) does not compress or distend to any significant degree, the outward movement of the chest wall and diaphragm tends to create a negative pressure in the pleural space. This in turn expands the lungs. The reverse happens during expiration to increase pleural pressure and contract the lungs. In a sense, the pleural fluid 'couples' the movement of the chest wall to movement of the lung.
This coupling action would be lost with air, which is highly compressible and distensible. The bulk modulus of water (the main constituent of pleural fluid) is 2.2 GPa: about two million times the isothermal bulk modulus of air! With air in the pleural cavity, chest wall and diaphragm movement would do nothing to change lung volume. Rather, the air would happily accommodate to the new volume of the pleural cavity, without any pressure change.
As far as the diffusion of oxygen into pleural fluid is concerned, I believe it does happen (similar to what happens in extracellular fluid in any other location). However, I could not find any data on pleural fluid oxygen tensions specifically. For perspective, the interstitial fluid oxygen tension in different human tissues ranges from 3 to 7 kPa. I'd expect it to be higher in pleural fluid because of its close proximity to alveoli.

The pleural fluid would also have more carbon dioxide.

Pleural fluid is secreted by the pleural membrane and therefore it is not made up of living cells. Usually a trauma to the chest, such as a stab wound, would allow air to enter the thoracic cavity, called pneumothorax.
The problem caused by air building up in the thoracic cavity is due to the movement of the diaphragm and intercostal muscles cannot create a low pressure relative to that of within the lungs pressure, and air rushes into the thoracic cavity instead of the lung to equalizes the pressure. Note that oxygen that enters the thoracic cavity is not usable by the individual, and only the oxygen that enters the lung can. Also, air in the thoracic cavity is not connected to the nose or mouth, or else only little air would enter the lung when aspirating.

I think you got me wrong in the first part, I don't mean the fluid itself is living, I mean it was made or secreted by living cells, which are the pleural membranes cells. And since the fluid is touching them, won't oxygen diffuse into it? And sorry for the confusion, I'll edit my question in that part to make it clearer.

Thanks Philip, I've searched in details about pneumothorax and it seems like my knowledge lacks alot. I didn't realise the role of the pleural membranes in making the lung moves outward and the negative pressure in the pleural cavity. We tend to concentrate at school on the intercostal muscles and kind of ignore the pleural cavity that I became to think that if the external intercostal contract the volume of the lungs would automatically increase, completely missing the role of the pleural cavity.

@Manar lung based breathing is a really strange kluge, that most tetrapods are just stuck with, birds at least found a better solution. You should see what crocodiles have which as a weird hybrid system that has two different ways of working they can switch between. They even move the lungs around the torso to control buoyancy.


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Are there computational models verifying the feasibility that complex biological systems can emerge by random mutations plus natural selection?
I am interested in studying the theoretical feasibility that very complex systems such as the vascular system, the respiratory system, the nervous system, the digestive system, among others, could have emerged by means of random mutations plus natural selection. Are there computational models that have successfully verified (via simulation or other means) the theoretical feasibility of the Darwinian hypothesis that random mutations plus natural selection can indeed give rise to sophisticated systems under the time constraint and the environmental constraints life on Earth probably had to face? What is the state of the art (as of 2020 and later) on this regard?

Yes, those exist.  Look up "Artificial Life" , "Genetic Algorithms"  and "Evolutionary Computation".

Thanks for the search keywords, but do you know if they have been able to successfully simulate DNA mutations in a population and see if new organs or new systems can emerge from that? Maybe asking for a 100% accurate simulation of a biological organism can be too much, but at least an approximate simulation, as close to reality as possible. Do you know if anything like that has been done?

Eyes have been evolved digitally.  I dont know about ohher organs.  Starting from DNA per se has not been done, because we don't yet know how to calculate the process of producing an organ from DNA instructions.  However, the principles of evolution have been extremely well verified digitally as well as in the lab, as in "directed evolution".

Awesome. Can you share some references to learn more about this? Especially on the evolution of eyes digitally.

Here is one.  Really, a Google search will get you pretty far down this road.  https://ieeexplore.ieee.org/abstract/document/8790284


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Optimal bacterial vegetative cell inactivation method(s) after subtilis spores germinated under pressure
I am writing a PhD research proposal and being a newbie in the field I am lost a little bit in the bacterial vegetative cell inactivation methods in foods.
I should propose two main methods to my future reseach team. The strategy is to germinate B. subtilis spores applying the high pressure, and then select one mild method to inactivate them.
My problem is to select max two most appropriate methods between:

Microwaves (MW)
Ozone (O3)
Pulsed electric fields (PEF)
Cold plasma (CP)
Ohmic heating (OH)
Ultrasound (US)
Ultraviolet (UV)
High/Low-energy Electron Beam (H/LEEB)
Chlorine dioxide (ClO2)
CO2 (HPCD, scCO2)

I need to select two methods..., I need to select only mild ones, to preserve the food taste - so I think the temperature should be <60° or max 70°... but what other criteria to take into consideration, being a newbie in this field?
Let's consider one of the method for dry foods, and another for liquids (juices, milk etc).

Are the spores in a food substance?

Yes, I edited the op

First thing to consider for a PhD proposal is the literature. Has someone already done this research, or something similar? Other criteria I would consider: What is the nature of the food substrate in question (solid, porous, wet, dry, cooked, raw, plant or animal based, etc.)? Could anything in a given food product interfear with or prevent any of these methods from working? Is subtilis the only spoilage organism of concern? What's the optimal stage in processing to apply your treatments? Just to name a few.

@MikeyC, there is no more details but I already gave. Let's select one method for liquids and another one for dry foods.


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Is it possible to force Sars-Cov-2 virus to mutate?
The title may definitely be a stupid question since I have no background in biology. I would like to know if the coronaviruses or any other can be manipulated artificially so that they stop spreading among humans and target other animals, for example cats. I like cats but they can spare one of their lives for humanity.
¿Is it possible?
Furthermore, is it possible to create a surface made of articifial cell membranes which is better than human cells for the viruses to stick? As I understand the viruses have no life, which means they are like machines, they have no aim in "life" other than stick. Am I correct?

Have you heard this suggested as a solution? How would you plan to collect all the viruses in all the different people who are infected?

I haven't heard or read anything about this. So your point is each virus is different genetically, correct?

My main point is that you'd have to introduce your mutation in every viral particle, otherwise at best what you've done is create a new virus that infects cats, while not having done anything to the 99.999999999% of virus that you haven't touched.

This idea is conceptually similar to creation of a live attenuated vaccine, where a virus is passaged through some other host (like lab animals or cultured cells). Mutations benefiting infection of the new host accumulate. Hopefully, after enough passages, it's no longer infectious to humans, but still similar enough to help an innoculated human develop immunity to the infectious form. https://en.wikipedia.org/wiki/Attenuated_vaccine


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What does the point in the middle between two numbers mean?

[...] cells were removed to a cover glass and treated with plasma for 2 min, then returned to TS broth and centrifuged for 10 min. Cells were harvested and washed twice with PBS, then mixed with tryptic soy agar. The agar block was fixed with 2·5% glutaraldehyde in 0·1 mol l−1 PBS. Samples were postfixed in 1% (w/v) OsO4 in 0·1 mol l−1 PBS for 2 h at room temperature, washed once with the same buffer, dehydrated in a graded ethanol series and embedded in low‐viscosity medium. Thin sections of the specimens were double‐stained with uranyl acetate and lead citrate...

What does mean this bolded point? Is it a decimal separator, or has other scientific meaning?
If this is decimal point, why is vertically middle aligned?
Source: a recent Korea researchers team article

Short answer
It's a decimal point.
Longer answer
A point in the 'middle' of the neighboring characters is called an interpunct, and was the standard in UK typography for marking a decimal at one point in time (possibly elsewhere as well). You're most likely to encounter it in older issues in UK and UK-inspired journals, and no doubt some have lagged behind the trends for reasons of tradition/stubbornness or whatever else and still use it.
Note that you will also encounter countries that use the comma as a decimal separator; Wikipedia has a list that includes most of mainland Europe and South America, for example.

I live in a country where the comma is decimal separator, this is common in Europe :) Thank you to clarifying that English Men habit )

This is even more strange cause encountered in a recent Korean article )) http://www.surfxtechnologies.com/fileaway-directory/full/067.%20Sterilization%20effect%20of%20atmospheric%20plasma%20on%20Escherichia%20coli%20and%20Bacillus%20subtilis%20endospores.pdf

ah, ok, the article was edited in an UK Journal ) https://sfamjournals.onlinelibrary.wiley.com/


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Can someone identify this bug?
I am looking for some help identifying this bug. I am in southern New Mexico, US. There are a handful of these on the inside and outside of all the window panes on one side of my house. They are about 3mm long. They appear this time of year (late April/early May), stay on the windows for a a week or so and then disappear.  Hard to get a clear picture as they are so small. Any assistance would be greatly appreciated. Thank you!


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Identify the caterpillars
These are the two caterpillar I found at Taipei, Taiwan. Can anybody help me identify the species. The first caterpillar is about 6-7 cm long and the other one 10-12 cm. Thanks in advance!

This is actually not easy - for the first one I am sure that is a caterpillar from order Orgyia and the family Erebidae, but since there is a vast number of different caterpillars on all continents, I am not sure which one it is exactly.
If you look at this image (from here), you will see a striking resemblance:

A lot more information on these moths can be found here.
The second one is most likely Trabala vishnou ssp. guttata, see the image (from here) for comparision:

There seems to be very little information available, some on the Wikipedia page.


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Meaning of "Domain with function to find" (FIIND)
From NALPs: a novel protein family involved in inflammation.

FIIND - Domain with Function to Find.

What is the meaning of this name? Does it mean "Domain with an unknown function"?
I'm translating an article in which this domain is mentioned, and I found three different translations of the term into Russian: "Domain with an unknown function", "Domain with a search function", "Domain with identification function".
I think the first translation is the most logical one, but I'm asking just in case, because I'm not an expert in this field.

The NALP subfamily. Finally, a large subfamily of the CATERPILLAR proteins is composed of 14 NALPs (also called PANs36 or PYPAFs37; FIG 2.) and is characterized by the presence of an amino-terminal PYD. This modular architecture is found in NALPs 2–14 (short NALPs), whereas NALP1 contains an additional domain — which our group has designated FIIND (function to find) — and a CARD, forming a carboxy-terminal extension. With two notable exceptions (NALP1 and NALP3), the NALP genes are located in two clusters on human chromosomes 11p15 (NALPs 6, 10 and 14) and 19q13.4 (NALPs 2, 4, 5, 7, 8, 9, 11, 12 and 13) (TABLE 1). Interestingly, the 11p15.5 region is an important IMPRINTED region and has been implicated in the imprinting disorder Beckwith-Wiedemann syndrome and in various human cancers, including Wilm's tumour38.

In my opinion it is broken English, presumably contorted in this way to provide an acronym.  To find out what the culprits intend it to mean you would need to read the paper. Dictionaries will not help.

I was pretty certain @David's comment was spot on, that this was some one-use funny acronym from just this paper, but a search of Google Scholar suggests that it has indeed been propagated sufficiently to have meaning beyond this paper, while also originating, as these things do, in some clumsy one-off usage.
One of them gives a clear definition that is consistent with what you supposed:

The acronym FIIND (domain with function to find) was coined several years ago to indicate a highly conserved protein region with unknown function[4]

D'Osualdo, A., Weichenberger, C. X., Wagner, R. N., Godzik, A., Wooley, J., & Reed, J. C. (2011). CARD8 and NLRP1 undergo autoproteolytic processing through a ZU5-like domain. PloS one, 6(11).
The paper they cite (reference 4 in the previous quote) is in fact this one:
Tschopp, J., Martinon, F., & Burns, K. (2003). NALPs: a novel protein family involved in inflammation. Nature reviews Molecular cell biology, 4(2), 95-104.
...which probably looks familiar since it is in fact the paper you started from. Importantly, though, this is not a generic term for a domain with unknown function, it's a specific domain which was known to be highly conserved (and since found in several other proteins) - it's just that it's specific function was at the time unknown.
This paper is a recent review of NLRP1 that may also be useful and has some discussions of what has been found of the functions of the FIIND:
Mitchell, P. S., Sandstrom, A., & Vance, R. E. (2019). The NLRP1 inflammasome: new mechanistic insights and unresolved mysteries. Current opinion in immunology, 60, 37-45.


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Meaning of "external demands" in a paper describing the gut-brain axis
From "Brain Gut Microbiome Interactions and Functional Bowel Disorders":

In response to external and bodily demands, the brain modulates individual cells (ECC – enterochromaffin cells; SMC – smooth muscle cells; ICC – interstitial cells of Cajal) within this network via the branches of the autonomic nervous system (ANS) (sympathetic and parasympathetic/vagal efferents) and the hypothalamic pituitary adrenal (HPA) axis.

What is the meaning of "external demands"? What other possible demands can the brain strive to meet by modulating the activity of the neural network of the gut?

From the context, it seems to refer to those demands outside of the human body. i.e. perceptions of the external world. Examples could include a perceived threat, diunal cycles, or stress about that public presentation you're giving later.
If you are about to be chased by a dangerous predator, a sudden urge to poop would probably impair your chances of survival. Luckily, when our sympathetic nervous system kicks in, our GI motility slows down, so our body can focus on surviving the external threat and live to poop another day.


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Why do Centipedes always have an odd number of pairs of legs?
Furthermore, centipedes are within the Myriapoda, a subphylum of arthropods which also contains millipedes. Do millipedes also have an odd number pair of legs?

A definitive answer would require an extensive embryology research across many species of centipedes. To my knowledge, Strigamia maritima is the only centipede whose embryogenesis and segmentation has been seriously studied. I'm afraid you won't find your answer.

@A.Bourgoin noted, you provide a relevant / useful caveat.

Centipedes are part of the group of insects that utilize a short germ-band mode of embryonic development.1  One feature of this type of segmentation is that new segments are added sequentially to the end of the developing insect (the "posterior proliferative zone").  This is in contrast to insects that undergo long germ-band gastrulation, like Drosophila, where all segments are created simultaneously.
Additionally, Myriapoda demonstrate double segmental periodicity, meaning that segments are always added two at a time.  See the following informative figure from Damen 2004 2 --

Figure 2. Segmentation in the geophilomorph centipedes involves a phase of double segmental periodicity. The drawing shows a schematic model for segmentation in geophilomorphic centipedes. Segments are patterned in posterior tissue that does not show overt segmentation. Segments become molecularly defined in entities (coloured blocks) that eventually give rise to two segments each. Before morphological segments become visible, these two-segment entities are molecularly subdivided into segmental units
(dashed lines), which each eventually will give rise to one segment. For instance, at stage I C represents an entity that is refined into two units (C at stage II), which give rise to one segment each (C′ at stage III). This mechanism of segmentation provides a developmental constraint that only allows the addition of segments in bits of two and in this way only allows odd numbers of trunk segments in centipedes.

One would expect, then, to only see even numbers of leg pairs.  Arthur and Chipman explain this discrepancy in their 2005 essay 3 on Strigamia maritima, the most well-studied member of the Myriapoda subphylum.

Of course, if everything happens in twos, we would expect that there would always be an even, rather than odd, number of segments. But this apparent discrepancy is probably not real. It seems likely that the poison claw segment immediately anterior to the first pair of legs is really a modified trunk segment.

As for how Myriapoda add segments two at a time, I direct you to sources like Chipman and Akam 2008 4, though be prepared for some heavy reading on signaling cascades and morphogen gradients.

References

Hughes CL, Kaufman TC. Exploring myriapod segmentation: the expression patterns of even-skipped, engrailed, and wingless in a centipede. Dev Biol. 2002 Jul 1;247(1):47-61.
Damen WG. Arthropod segmentation: why centipedes are odd. Curr Biol. 2004 Jul 27;14(14):R557-9.
Arthur W, Chipman AD. The centipede Strigamia maritima: what it can tell us about the development and evolution of segmentation. Bioessays. 2005 Jun;27(6):653-60.
Chipman AD, Akam M. The segmentation cascade in the centipede Strigamia maritima: involvement of the Notch pathway and pair-rule gene homologues. Dev Biol. 2008 Jul 1;319(1):160-9.

[W]e suggest that the myriapods have developed their unique body plan
  largely by expanding the number of segments under the control of the
  ‘trunk’ genes.

https://dev.biologists.org/content/develop/129/5/1225.full.pdf
In a way, Wikipedia states that the Craterostigmomorpha centipede doesn't: "They have a distinct body plan; their anamorphosis comprises a single stage: in their first moult, they grow from having 12 segments to having 15." Albeit, no source for that.
It seems that they always have an even amount of legs or an odd amount of leg pairs on a genetic level, hoc genes:

https://pubmed.ncbi.nlm.nih.gov/11874918
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4244043

It gets very technical; if you really want to dig deep, perhaps look at the similar articles (after the abstracts) in the sources.


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How can poliovirus and other pathogens lead to permanent conditions if the bodies adaptive immune system is still functioning?
Wont the lymphatic system eventually create antibodies that completely eliminate the virus in the body?

Welcome to biology.SE! I think this question would likely attract a good answer if you include some discussion of what research you've already done. Please take the tour. It seems like there are two major assumptions coded in your question: (1) A functioning immune system should be able to clear poliovirus and (2) in the absence of virus, all damage done by a viral infection should be resolved.  I encourage you to read up on how viruses evade immunity and the etiology of poliomyelitis and the human nervous system.

When polio causes paralysis it's because it has destroyed nervous system cells. Once those cells are destroyed they typically cannot be replaced, so it doesn't really matter what happens to the virus after that in terms of the immune system. See the Wikipedia page on polio:

In around 1 percent of infections, poliovirus spreads along certain nerve fiber pathways, preferentially replicating in and destroying motor neurons within the spinal cord, brain stem, or motor cortex. This leads to the development of paralytic poliomyelitis, the various forms of which (spinal, bulbar, and bulbospinal) vary only with the amount of neuronal damage and inflammation that occurs, and the region of the CNS affected.

The post-polio syndrome may be the result of a persistent infection. Indeed most persistent viruses hide inside neurons and conversely viruses infecting neurons are often persistent (the neuron infection often happens in a minority of patients)


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What did Darwin mean by "degraded flowers"?
One of the chapters of The Origin of Species says that "Certain plants, belonging to the Malpighiaceæ, bear perfect and degraded flowers;" Full passage for context
Do you know which plant characteristic was he referring to? Is this morphological difference still recognized? Is there a new name for it?

Perfect flowers have both male and female parts.
"Degraded" isn't used anymore - just "imperfect".
"A bisexual (or “perfect”) flower has both stamens and carpels, and a unisexual (or “imperfect”) flower either lacks stamens (and is called carpellate) or lacks carpels (and is called staminate). Species with both staminate flowers and carpellate flowers on the same plant (e.g., corn) are monoecious..."
ref https://www.britannica.com/science/perfect-flower
Found by searching for "perfect flower"

I focused on "degraded", my mistake! Thank you very much!!


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Is it possible to reduce maturity time of plants with biotechnology?
I've heard of speed breeding which makes use of optimal circumstances in glasshouses and growth chambers. Is it also possible to shorten a plant's maturity time (i.e. the time it needs from being planted until the time its yield can be harvested) using genetic modifications?

Pick up a packet of seeds at a garden shop. Most will have "days to maturity" . And there will be choices of time(growing season) .Such as a 70 day corn or a 100 day corn. Growing conditions such as moisture an nutrient level have a secondary affects.

Your use of "growing season" is confusing, since it almost always means the length of time plants will grow - basically from the last frost in the spring to the first frost in the fall (for those of us in temperate latitudes).  What you're asking is more often "days to maturity" or "time to harvest".

@AlexReynolds thanks for the reply and links. I also suggest you post this comment as an answer to get some reputation.

@jamesqf thanks for the clarification; I've edited the question accordingly. Is there any other word for what I mean other than "days to maturity" or "time to harvest" (or as I said maturity time)?

Perhaps investigate the families of YUC genes that synthesize the growth hormone auxin (ncbi.nlm.nih.gov/pmc/articles/PMC6941117) and ARF genes (ncbi.nlm.nih.gov/pmc/articles/PMC4737911) that respond to auxin. Auxin overproduction or changes to ARFs might speed growth. But some herbicides are synthetic auxins (e.g. 2,4-D) and work by exhausting and killing weeds (en.wikipedia.org/wiki/2,4-Dichlorophenoxyacetic_acid), so modifying these pathways may have unwanted side effects, depending on the crop.

Independent of the hormone manipulation suggested by Alex Reynolds, perturbation of transcription factor UPB1 has been found to have an effect on plant growth by Tsukagoshi and colleagues -- Transcriptional regulation of ROS controls transition from proliferation to differentiation in the root.
In short, disrupting UPB1 activity in model Arabidopsis roots alters the balance of free radicals, leading to delayed differentiation and continued cell growth. UPB1-deficient roots were faster growing and composed of larger cells. Artificially increasing UPB1 activity resulted in slower root growth.
Taking OP's definition of maturity time --

the time it needs from being planted until the time its yield can be harvested

-- the agricultural utility of this mutation depends on the crop.  If the goal is to increase the amount of biomass as fast as possible, this is likely a beneficial mutation.  If the goal is to decrease the time needed for a plant to bear mature fruit, this mutation would not be ideal, given that disruption of UPB1 activity leads to slowed cell differentiation.


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What is a general timeline to replace stainless steel SS 316 pipes in food industry?
Does the dairy and/or food industry (specifically but not limited to the USA)considers to replace their stainless steel SS 316 or SS 304 pipes after say 30 years or so? Could someone please share their experience or opinion.
I have this question because I wanted to know if the cleaning in place procedures stand ineffective after say 30 years because the metal's surface roughness, hydrophobicity, corrosion resistance would change.
If you have an idea about any beverage industry besides dairy or even meat industry, please let me know. It will be very helpful.
Thank you in advance.

I’m voting to close this question because it is about industrial practices and metallurgy, which are not on-topic for this site. Please consult the [tour], [ask], and other [help] pages for more information.

I would appreciate if this question is still visible. I'm new to this website and all I'm interested in is the knowledge that some users are willing to contribute.I would like to defer and say that this question is not just industrial practices and metallurgy based but it also aims towards people contributing to the food industry. I see one useful response.

Stainless does not "wear out" or deteriorate in general food service , so no replacement. There may be some unusual service that causes corrosion . If that occurs I expect a more corrosion resistant alloy replacement is quickly installed. Keep in mind if there is corrosion ,there are traces of Cr, Ni, Mo going into the food . That would bring lawsuits regardless of any harm. It is hard to imagine any surface texture change ;possible exception of raw foods with entrained sand which might cause polishing of the stainless.

Thank you. I agree with the points you have mentioned, I was thinking if there is a general timeline for the SS 316 pipes, where we can say that after say 3 billion production cycles (or say after transferring 20000 liters of milk per hour for say 50 years) of service in the food processing plants, they start to corrode and needs to be replaced; as opposed to replacing them after say 5 years, where they are not showing any signs of possible mechanical failures or alterations in their roughness. I understand that there are no set guidelines. Your response is greatly appreciated.

There is no deterioration: Infinite life ( as an engineer I  cringe when I use that word). I am sure there are buried carbon steel pipelines that have been in service over 75 years ; much higher corrosion potential inside and outside than SS in food service.

Thank you once again for your response. In that case is there a specific timeline that the industry follows for inspecting the presence of corrosion inside of the pipe? That looks like a reasonable thing to do in this situation. Can you share your experience with any inspection technique used and its timeline followed by the food industry?

In a refinery with carbon and low alloy steels metal loss is expected. So very detailed surveys are documented  both for the refinery and various government agencies.  Usually ultrasonic ; it is important that the UT tests be made at the exact same spot as there are some original variations in wall thickness.  Today very accurate inexpensive UT units are available "off the shelf", Frequency of inspection is determined with experience , from a few month to a few years. For SS food piping , likely every 5 years will be enough.  .

I expect there are organizations that have written requirements and/or guideline for examination.Likely they concentrate on organic contamination but may have NDE for equipment integrity. ASNT American Society for Nondestructive Testing might have something you can use.

Thank you for your helpful responses. Much appreciated.


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Is it possible to make synthetic olfactory receptors?
Are there any electronic engineering technologies that allow people to make synthetic olfactory receptor that generate electrical impulses when exposed to certain proteins or molecules? If not, what are the primary challenges of creating such a device?

Have you performed any prior research - I'm asking, because the question is really broad. Do you mean electronic (macro)devices? or artificially bio-engineered proteins, or cells of some kind?

@AliceD At this point in time, I am interested in any detecting technology that can be customized to detect specific compounds similar to olfactory receptors. I have done some research, but I have not found anything that would be able to link into electronics systems and be reusable like our own nerves. I have done some research (my background is engineering), but it took me a good deal of time to even find anyone who could describe in detail how the olfactory receptors work to detect multiple smells.

Thanks for that, I've edited your post a little bit to clarify that point. and to hat end do you need this technology? For a sensorineural implant to replace the lost sense of olfaction (a biocompatible 'bionic nose')? Or is it more for some kind of computerized detection system that can, and should operate out of the body and 'simply' detect different odors?

My gut reaction is that this feels outside of Biology per se; there are certainly chemical
"sniffers" of a variety of types - can you explain how your question necessarily relates to biology per se? As far as how olfactory receptors work, have you tried introductory-level neuroscience textbooks? It's pretty common for them to have at least a chapter on olfaction.

Depending on just what you mean by "olfactory receptor", this might be an absolutely trivial question.  Ckips that can "smell" for instance carbon monoxide are readily available for a couple of bucks.  Others can smell CO2, alcohol, LPG, the oxygen in your car's exhaust, explosives...

@AliceD - So to clarify my purpose that isn't necessarily pertinent to the question itself: It seems like being able to create a synthetic and readily reusable smelling device that is as powerful as that of a dogs would be a world changing invention. In the medical field alone, there are numerous diseases which dogs have the ability to accurately smell and diagnose instantly. I posed this question to biologist as I thought the only way to create the wide range of detectors needed to get an accurate sensor would be to synthesize a large variety of proteins like our receptors.

@jamesqf- What is a Ckips? I can't seem to find any reference to such a thing...

You might be asking this questions because there has been reports in the news about dogs possibly being able to detect patients infected by COVID19. You can read similar reports every single time there is a new disease or new scary thing. Don't pay attention to it, it only tells you how much people like reading about dogs.

But to answer your question there is a bench of devices that can measure compounds in gases much more effectively than animals. For example photoionization (basically spectroscopy) or chemically. If you know what you want to detect. Usually you don't.


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Why don't we dribble tears through our nose?
Basal tears are tears produced by the lacrimal gland and they lubricate the eye. They are then funneled into the lacrimal sac and then from there into the nose eventually.
If this is the case, why don't we constantly dribble out tears from our nose? Where do the tears go?


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Recommended books and articles on the origin and evolution of sexual reproduction?
I'm interested in learning about the origin and evolution of life on Earth. In particular, one topic that puzzles me a lot as a layman is the evolution of sexual reproduction, since the DNA mutations have to be such that they affect both female and male in a coordinated way so that their reproductive organs match with each other in order to make the sexual reproduction viable. Would you guys kindly recommend me high quality books and peer-reviewed articles on the matter that hopefully can clear these questions out? Thanks in advance.


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Help identifying this bird skull
The skull is 4 to 6 inches long and still has tendons attached. I found this on a beach in central California, which leads me to think it's probably from a seabird. I believe this is from a smaller scavenger bird.

I don't think the photos came through.

Welcome to Biology.SE! Can you please measure the skull and [edit] your post to include the more accurate estimate. 4-6 inches is a very large range and a more precise value may be critical for getting a correct identification. In the future please also proofread your posts and makes sure that the image has been uploaded. Thanks!

Certainly a seabird, with the tubenose. Possibly a giant petrel or one of the other Procellariidae. Please post an exact size.


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Can the activity of a specific gene in a cell artficially be increased?
While there are many gene regulation mechanisms from the cell itself, I was wondering whether it is possible to increase the gene activity in a living cell permanently (so that the protein that it codes for is produced in higher amounts) using methods of biotechnology (i.e. no external factors)? Are there any studies or experiments regarding this topic?

What do you mean by "Using the methods of Biology"? Genetic modification? Breeding? Evidently yes in that case.

@David oh I actually wanted to write biotechnology. So yes, this would include genetic modification. Do you know any studies or experiments using genetic modification to increase gene activity?

I don't particularly want to answer your question as I am not an expert in this field, and others can and will no doubt answer now you have clarified it. However there must be dozens of practical examples in modification of crops and lifestock, these based on earlier experiments with simpler organisms.

Do you want to increase telomerase production with CRISPR?

@Sergei I actually just asked general, but that might be an interesting application

There are technologies available for inducing higher (or lower) gene expression in cultured mammalian/human cells as well as in bacteria. The state of the art is CRISPR-mediated gene activation/repression, where you fuse a transcription activation domain to a Cas gene in a CRISPR-Cas system (usually Cas9), and provide a guide RNA to target genes of interest. This Cas gene is made "nuclease-dead" so that it can only target but not cut or degrade DNA (as opposed to natural CRISPR-Cas systems that do both), and serves to bring the transcription activation domain to your gene of interest, which leads to an increase in transcription of that gene.
Check out this paper for an earlier example of such a system in cultured cell lines. The field has advanced quite a bit since then, and people have successfully activated genes in mouse lines

If you are after large amounts of a particular protein, search "recombinant protein production". It is a huge field.

A sequence is executed with transcriptase. To double amount of signaling or some protein production try doubling the sequence occurrence.

It can be done. I've found this article which describes how cou can use a modified CRISPR-Cas9 mechanism to either repress or activate transcription.


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Humic Acid and PCR
Quite a few papers claim humic acid is an inhibitor of PCR reactions. I understand this is true when working with soil microbes, but how does it qualify to be a PCR inhibitor in general (i.e when not working with soil micorbes)?

In general, when not working with samples from soil or natural waters, you propbably won't encounter high enough concentrations of humic substances to inhibit your PCRs.
If you're just asking about mechanisms of inhibition, humic acids can interact with polymerase enzymes, with nucleic acids (altering primer annealing and template melting temperatures), and they can partially quench fluorescence in the case of real-time PCR (see Overcoming Inhibition in Real-Time Diagnostic PCR). There are numerous sources in this reference if you want to read more about how these different interactions were characterized in the lab.

The chapter is paywalled, but is available for those who can access Researchgate at https://www.researchgate.net/

Thanks! that is really helpful.


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How are human rotaviruses generally transmitted?
I know rotaviruses are double stranded RNA viruses and i am wondering if the human transmission is similar to the modes of veterinary transmission.

Faecal-oral transmission. Ref from https://en.wikipedia.org/wiki/Rotavirus

Ah, that makes sense. Thank you.


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What happens if ace2 from lungs is removed? Will there be any major impact on our body?
when ace2 receptors  are not present in the lungs will we experience any disturbance or suffer from any other problems

Yes, the  renin–angiotensin system is very important. Search about ACE2 knockout mice https://physoc.onlinelibrary.wiley.com/doi/full/10.1113/expphysiol.2007.040014

According to my cursory and unprofessional assessment, the most prominent issue would be hypertension, flanked by excessive retention of water, sodium ions, and chloride ions, due to the boatloads of angiotensin II just sitting around. Potassium ions would be excreted gratuitously, however. The lack of the ACE2 receptors has been (ostensibly) linked to Hartnup disease as well, so make of that what you will.
Once again, I'm not a medical professional, so take my word with a bucketful of salt.

Welcome to Biology.SE! This looks like a could become a good answer if you provided more detail and included supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. A good example of how to format references. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. Thank you!

@tyersome My apologies, I’m new and I come from quora, so my standards are a tad low.


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COVID-19 Infection rate related to population size?
Recently, in the UK's daily government briefing they started showing the graphs that compare national death rates, adjusted by the population size of each country.

I understand the various reasons why comparisons between countries are difficult and might not make sense right now.
I understand that a country's population places an upper bound on the number of people who
can become infected.
I can see why population density might affect the rate of infection.

But, why would the rate of infection be different because of the population size?  Surely, when a virus reaches the shores of a new country, it doesn't think to itself "hey, there are a lot of people here, I'd better spread faster"...?
I hate to sound like a conspiracy theorist, but right now we in the UK might be the worst-hit in Europe, and I wonder if showing these graphs adjusted by population size might be a political attempt to make us look "not quite so bad".
But, I am very ignorant of biology and epidemiology, so maybe there is a sensible reason for adjusting these graphs by population size.  Can somebody explain it to me?
Update: I have noticed that over the last few days, the UK government briefing has stopped including the charts that are adjusted by population size.

Perhaps the rates are similar, but a high rate of testing is revealing more cases.

What really matters is the per-capita infection rate.  2800 total cases in New York City (or London) would be almost negligible.  2800 cases on the Navajo Reservation (or say in the Hebrides) would affect a large part of the population: https://www.abc4.com/coronavirus/navajo-nation-reports-seven-confirmed-deaths-174-positive-tests-from-coronavirus/

It depends on what you want the graph to show you (and not just whether it makes the epidemic look more or less scary).  For example, if viewers are interested in the overall impact of the epidemic, they might want to know about per capita deaths rather than total deaths (here I will only use "rate" to mean "number per unit time" rather than "number per  individuals").
You're right that (1) we don't expect the epidemic growth rate (measured by cases or hospitalizations or deaths) to depend on population size (initially - once enough people have been infected to significantly deplete the pool of susceptibles, the population size does matter) and (2) naively plotting per capita deaths of regions with widely differing  population sizes can be misleading.
A good solution, used by the widely redistributed Financial Times COVID-19 plots, is to plot the time axis as the number of days since 0.1 average deaths (per million) first recorded (obviously you can pick a different per capita threshold); this sets the scale appropriately for regions of different sizes.
For example this chart:

It looks from The Guardian's story that the government's plots are adjusted to "number of days since 50 deaths".  It would seem better to use a threshold based on a per capita threshold (larger countries will hit the 50-death threshold sooner) ...

Thanks!  I was also using "rate" to mean "number per unit time", so your answer makes sense to me.


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Can/have bacteria been engineered to express ACE 2 receptors?
In light of SARS-COV-2 binding to the ACE 2 protein in human cells, I was wondering if any bacteria exist or could exist that possess this membrane protein. If not, do you believe that an ACE 2 like protein https://www.jstage.jst.go.jp/article/jpssuppl/92/0/92_2-YIA-09/_pdf expressed by a bacteria could allow  the COVID-19 virus to successfully attach and be fused into the bacterium?

Could you edit your question so that it is clear whether you ask about expressing a functional membrane attached ACE2 receptor allowing for SARSCOV2 infection, or about simply producing ACE2 receptors with engineered bacteria.

Short answer is no, because the ACE2 receptor is only a trigger (and anchoring point) for endocytosis.
The endocytosis requires many enzymes/proteins which are (as far as I know) specific to eukaryotes. You'd need to express those too in your bacterium and the lack of adequate eukaryote-like transport protein in your bacterium will likely forbid the whole from functioning.

That makes perfect sense, thank you. Do you know of any attempts to get a eukaryote targeting virus to infect a prokaryote?

@user91617 It is not exactly my domain of expertise. If not for pure curiosity, I fail to see why such an attempt would be made. I also noticed I failed to answer the title question : can a bacteria express the receptor : yes, see http://www.ndsl.kr/ndsl/search/detail/article/articleSearchResultDetail.do?cn=NART51710590.

Thank you for the link. As you inferred, my ultimate question would be whether it is possible for the COVID-19 virus to infect a prokaryote such as E. coli (engineered or otherwise).


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What brain regions consume the most energy?
It's well known that the human brain consumes roughly 20% of the body's energy, and that grey matter is much more energy-intensive than white matter.
Beyond this basic information, it seems difficult to search for the total energy consumption of the brain broken down by lobe, or ideally further. For instance, how much power is consumed by the typical hippocampus, averaged over a typical human lifespan?

Welcome to Biology.SE! This is well outside my area, but I think you need to clarify and focus your question. For example, it is well known that energy consumption in different regions varies depending on what the brain is doing.

@tyersome I'm not sure what you mean, but I want the time-average values for a typical human.


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What is the significance of the amplitude of brain waves?
What does the amplitude of brain waves represent and to what neuronal activities is this amplitude related to?
For example, in a hypothetical situation, the frequency of brain waves is kept the same, but the wave amplitude is increased or decreased by some means. What would be the effect on human brain and its activities?
Can resonance related to waves effect human brain waves?

Brain waves are a colloquial term for EEG recordings. EEG recordings are gross potential recordings, in other words, they represent the responses of thousands of neurons together. Much of the background is stochastically determined, meaning it represents, basically, random activity. In other words, oftentimes neurons fire stochastically and they cancel out each others contribution to the EEG, resulting in random ('white') noise.
However, certain parts of the brain do exhibit synchronized activity in certain frequency bands (Fig. 1). Oftentimes a time-to-frequency analysis is necessary to visualize these activities, e.g. by FFT. Certain stages of sleep, most notably slow-wave deep sleep, is characterized by gross synchronized, slow-wave activities across the cortex, showing up in the raw EEG. In fact, simply closing ones eyes has marked effects on the cortical synchronization on the raw EEG. This is caused by the fact that certain swaths of the cortex become synchronized, resulting in more clear responses.
In general, to come to your question, gross potential recordings like EEG thus are plagued by background noise. Synchronized activity increases the amplitude of brain waves and hence increases their amplitude. Amplitude is hence directly related to the level of synchronization. This shows up as larger peaks on the FFT.
What synchronization exactly does to the brain boils down to down to is the classic interpretation of EEG frequency bands (Table 1).

Fig. 1. EEG waves. source: Neurosky

Table 1. EEG frequency bands and their associated mental state. source: Liang et al. (2016)
Reference
- Liang et al., J Sensors (2016), 1831742


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Do we know if dogs are asymptomatic transmiters of sars-cov-2?
Dogs do not use mask when going for a walk nor they observe the security distance. On the contrary, they frequently join their noses, and put their noses where other dogs had put them before or had urinated. So, as they are our pets, it is important to know if they can be asymptomatic transmiters of sars-cov-2. Do we know it? At least, have we tested asymtomatic pets of people infected with sars-cov-2?

Related, and easier to check: do we know if some data associated to sars-cov-2 is higher among people with dogs at home?

It is the opposite, if the human is not infected then the probability that the pet (cat or dog) is positive is very low. To prove the infection they check that the animal is positive for > 4 days, because they are asymptomatic. If they'd find high viral load they would tell it (ie. very low viral load thus animals pets are not contagious). In contrary minks had symptoms and contaminated each other, same for a few tigers.

It may be too early to tell.
Testing of dogs in Wuhan found no infected dogs
"487 dogs including 90 beagle dogs, 147 pet dogs and 250 street dogs during the outbreak of SARS‐CoV‐2 were also tested serological negative."
from https://onlinelibrary.wiley.com/doi/full/10.1111/tbed.13577
This article mentions deliberate infection of five dogs. on this very small sample they suggest that dogs are not likely to become carriers.
"Coronavirus can infect cats - dogs, not so much."
https://www.nature.com/articles/d41586-020-00984-8
found by searching "dog" on LitCovid at https://www.ncbi.nlm.nih.gov/research/coronavirus/

I am assembling sources there https://biology.stackexchange.com/questions/92436/what-are-the-implications-of-tigers-being-susceptible-to-covid-19/92458#92458

I saw your sources too late. LitCovid is a great collection of papers too.