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Can erythrocytes Function without plasma?
my title is not very specific. So i will proceed to clarify it.
I am trying to make sure that the only blood cells in a sample are Erytocytes, since i want to evaluate their metabolism, I am aware that they don't have Mithocondria and thus catabolize Glucose into Lactate, (I belive I am not making false statements, however if any corrections pop up please give me a heads up.)
Thus a way I thought of getting rid of leucocytes was through centrifugation, erythrocytes would be at the bottom of the flask and if We got rid of Supernadant (plama and fine layer of leucocytes), we would have a much purer sample of erythrocytes.
My question is: Do they stil carry out their metabolism, so i can a posteriori evaluate it, even after centrifugation and gettting rid of the plasma. Or evaluating the lactate production afterwards would be impossible? I know there are more easier and methodic ways of getting rid of leucocytes(irradiation that destroys all nucleated cells and leucoreduction by filtracion, for example), but this is somewhat hypothetical, and i need to know the final answer in these circumstances.
Thanks in advance :)

@user1136 I apologize for my absolute statement, nothing is ever black or white, I was aware of the HMP shunt, but i failed to see the affect of it in the metabolism since it take 6 molecules of R5P to produce 5 molecules G6P, the net lactate would be bigger if there was no shunt, hypothetically. As for most of the references given about erytrocyte metabolism it was most fun reading them and I discovered things that will almost certainly help me in future studies, even if not, they were very fun to read.

@user1136 However i failed to understand one of your previous statements."And 'reserves' of 2,3-DPG can give rise to a 'burst' of ATP production, especially in stored RBC", do you mean that  the Lubering-Raport pathway will lower net ATP count, or that a considerable ammount of stored 2,3BPG will enter the Glicolytic pathway in media res are produce more ATP and lactate out of the blue?

@user1136 Thanks for the +1! The only implication of the of storage of blood I withdrew from your references was “A practical application of the DPG story was
the realization that the increased oxygen
affinity of blood during storage is due to
destruction of DPG." in the citation classic article by Benesch & Benesch. Much obliged about the information you helped me in on another question I also had! :)

Erythrocytes need more than just glucose in order to function and, they also need a extracelullar medium who shares the same osmolarity, so placing your red blood cells into a medium that solely has glucose will be problematic. If you solely want to evaluate the lactic fermentation carried out by erythrocytes on a short period of time, then you can add the blood plasm on your centrifuge tube (which will be in the superior layer) to the newly separated erythrocyte fraction. This way, we make sure your extracelullar medium not only has every metabolite needed, but is also isotonic with respect to your erythrocytes. If you're planning on evaluating this pathway for a considerable amount of time (days, perhaps), then you, most likely, will have to prepare a solution with glucose that is isotonic with respect to your red blood cells.

Welcome to Biology.SE! This looks like a good answer, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

They need glucose, they absorb that from dissolved particles in water (the plasma). So if you isolate the cells, you'd have to put them in a medium with sugar and so on. It would be analogous to the medium they exist in before you centrifuge them, I think.

Thanks your answer was was most insightful!

If you're interested in what drives osmosis (really, not the "concentration gradient of water"), feel free to have a look here,
http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.618.291&rep=rep1&type=pdf

Wow i did not know that, I will certainly look into it! Much Obliged!!

I discovered it just a few weeks ago, and it was published not too long ago, in 2009. Have not seen any earlier references. The short story is, the membrane is what drives osmosis, acting like a pump. That might sound weird, it does initially, but water organizes into a 4th state at membrane surfaces (or broadly speaking "contact zones"). This 4th state is analogous to ice but without the hydrogen ions to bond the lattice sheets vertically, those ions are instead excluded (ionized). Colloids affect the thickness of these gel-layers, and a concentration gradient forms for H+.


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A poor man's COVID-19 vaccine?
If person A is infected (COVID-19) and person B is not, could the following work as a vaccination?  Person A exhales (coughs?) into a a transparent bag.  The bag is radiated for a long time with a strong ultraviolet (UV) light as is found in some residential well-water systems.  Person B inhales the contents of the bag.
I am curious mostly about how virus particles are damaged at the molecular level by UV light and how this relates to how vaccines are manufactured today.

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical aspects of biology. I therefore think  that your question on dealing with the coronavirus outbreak is off-topic here. You are advised to consult more appropriate reputable sources for such information, some of which are listed here.

@David Respectfully, my question is simply "Is this (a UV-light vaccine design) possible?"  "COVID-19" is just a modifier (it could be any pathogen).  I sat for minutes deciding whether to post this on Medical SE, but it's the DNA damage that's in question and how the body would respond to it, so I posted here.  And judging by your background, in relation to the last sentence of the question, I'm surprised you didn't offer an answer!

Short answer: probably not.
Long answer: for your body to build immunity against something, it needs to identify it as something harmful to you. Otherwise, how would it know if this is just some random particle in your environment that it should ignore? There are molecular clues that your body uses to recognize better whether something is likely a pathogen (that means it should try to build immunity against) and those are some of the additives (known as adjuvants) present in man-made vaccines.
Also, the route of administration is also important. Things that you eat or breath in are triaged by the waldeyer ring because maybe you just ate something that is alive, but not exactly a pathogen. Dysfunctions in this process (thinking a normal protein is part of a dangerous pathogen) is believed to be one of the possible causes of allergies. Injecting it into your blood-stream often makes it more effective (but there are exceptions: polio vaccine however can be orally administered).
A nice read about this topic is this: The dichotomy of pathogens and allergens in vaccination approaches.
This is perhaps a must read on this topic: What to expect of a good vaccine and how to achieve it.
I'm not really sure what else to tell you. The process you described is a part of the manufacturing of some vaccines, so you are on the right track. But vaccines are hard to make, you can't do it for every disease and involves a lot of experimenting.

As a layperson, I always thought vaccines were damaged, non-functional pieces of the original pathogen.  The body would then recognize these fragments as something to attack.  Perhaps that's incorrect thinking.  Thank you for the links, though.  It will take me a while to get through them.  Initially, I don't see much about the use of ultraviolet light in the design of vaccines in them, but they might point me in the right direction.

source: Stack Exchange

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

sort: votes


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Can someone donate antibodies?
Consider the following scenario:

Person A has been infected with some virus (for example, SARS-CoV-2)
Person A has recovered

From this scenario, I assume Person A has managed to develop antibodies for SARS-CoV-2. If so:

For how long, after recovery, would Person A have antibodies for the virus running in their blood?
If Person A donates blood to Person B, would Person B have better responses against the virus, by using  the antibodies received along the blood from Person A? (assuming the donation is successful without issues)
Is there any paper / study building upon this idea for combating SARS-CoV-2?

Notes:

I am not expecting exact quantitative answers to these questions. I just want basic understanding for reasons this could or could not work.

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical or social aspects of biology. I therefore think  that your question on dealing with the coronavirus outbreak is off-topic here. You are advised to consult more appropriate reputable sources for such information, some of which are listed here.

@David Sorry about that. Is there another SE in which this topic would have been more appropriate? Also, I have to point out that your comment about SE being "not a discussion site or a site for floating ideas" is also off-topic, since I know that very well and did not call for any discussion and asked directly answerable questions, to which in fact I answered myself.

You could try SE Medical Sciences. However there is a very good article in today’s Financial Times (27 March) on the subject. I’m a subscriber to the paper edition, but you may find it on line. You’re probably entitled to three free articles. If you are not familiar with the FT do not be put off by its name. It is the foremost British serious newspaper (with US and European offices). In times like these you need to know where to find reliable information.

@David Thank you!

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, each question should be posted separately — this improves the chances that you will get answers for each question and makes the answers more accessible for future users. In addition, each of those questions must be appropriate for this site! ——— We also 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!

Does this answer your question? How does the body respond to blood donation; are there any possible risks?

Question 1

[...] antibodies [...] can last anywhere between a few weeks to a few months. The antibodies themselves though (which are proteins) definitely don't last forever (like all proteins). Eventually certain suppressor cells kill off plasma cells after the response has taken its course, and all that remains are a few memory cells, which are reactivated again should the pathogen invade the body in the future.

Source
Question 2 and 3
Yes.

Here is an article from Johns Hopkins University.
Here is a paper by Arturo Casadevall and Liise-anne Pirofski mentioned in the above article and published on the Journal of Clinical Investigation on March 13, 2020.

Fun fact: I was about to say in the question that I tried to research but didn't find anything. But I decided to make a last attempt, and actually found the answers...

Please note that while answering your own questions is completely fine, you should first fix (where possible) and/or delete the problematic sections of your question. ——— In addition, link only answers (what you provide for your second and third questions) are not acceptable — answers should not require other users to follow links (links also often break rendering the answer completely useless in the future). Please consult the help pages for additional advice on [Answer] effectively on this site. Thanks!

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Can far-UVC light be safely used as germicide? (help understanding a paper)
I've been trying to familiarize myself with the literature on far UVC light as a germicide.  My question mostly pertains to figure 4 of this paper. The paper investigates the efficacy of 207 nm light for killing MRSA without damaging human cells.  Figure 4 shows that you can get 4 logs of cell kill for MRSA with relatively little damage to human cells.  The authors treat this as a very promising result.  This is where I'm confused:  Yes 207 nm light kills MRSA selectively, but it still kills a lot of human cells: to get 4 logs of MRSA cell kill, you need a fluence that kills 80% of human cells.  Killing 99.99% of bacterial cells while also killing 80% of human cells seems obviously not good enough.  But the authors don't touch on this point: They just point out that it kills 5000x more MRSA cells than human, and interpret the result as promising.  What am I missing here?

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology! I'm glad we encourage such questions from curious people who want to learn more.
There is another paper here that discusses using a similar frequency range of UVC radiation (207-222 nm) as a biocide:

The biophysical reason is that, due to its strong absorbance in biological materials, far-UVC light does not have sufficient range to penetrate through even the outer layer (stratum corneum) on the surface of human skin, nor the outer tear layer on the outer surface of the eye, neither of which contain living cells; however, because bacteria and viruses are typically of micron or smaller dimensions, far-UVC light can still efficiently traverse and inactivate them.

Safety perhaps derives from the relatively exponential damage that far-UVC light can do to bacteria and viruses, while the layers and types of human cells that would get exposed are surface cells and mostly already dead or expendable. A 20% constant survival rate of vulnerable cells may be an acceptable trade-off, as those cells which are vulnerable would not typically be exposed (short of a wound or other exposed tissue, maybe), while the figure you cite suggests that you can raise the intensity of UV light linearly and kill exponentially more MRSA (or other disease-causing bacteria).

First of all a disclaimer, I am not an expert in this subject, but I have read these studies and came to this understanding. There might be a chance I get a lot of stuff wrong.
From another paper by the same authors, this time regarding 222nm UVC:

We have previously shown that 207-nm light emitted by a filtered krypton-bromine (Kr-Br) excilamp has bactericidal efficacy while being minimally cytotoxic to human cells in a 3D skin tissue model in vitro (7) and in a hairless mouse skin model in vivo (8). Thus, continuous exposure of the wound to far-UVC light during surgery may inactivate the microbes alighting directly onto the surgical wound from the air.

This shows the limited scope of its use presented by the paper as a way to sterilize the air immediately around the surgical site instead of sterilizing the surface of the patient, though it might also mean that further uses are not researched enough.
Also, it is important to analyze how the far-UVC affects human cells. In the 2013 paper you mentioned, Buonanno's team tested 2 methods of irradiating human cells with 207nm far-UVC. The figure you quoted is the dosage response curve of normal human skin fibroblasts, which are located in the dermis of human skin. In the experiment, these cells were cultivated on petri dishes and irradiated directly with UV light. This is not what you would normally expect when a person is exposed to UV, as the epidermis covers these cells and shields them from far-UVC radiation.

Normal human diploid skin fibroblasts (AG1522) were obtained from the American Type Culture Collection (Manassas, VA, USA) ... Briefly, cells were trypsinized within 5–10 min of exposure, suspended in growth medium, counted, diluted and seeded in 100-mm dishes with numbers resulting in ∼100 clonogenic cells per dish.

This brings us to the other method of measuring the effect of irradiance on human cells, which is the use of a 3-D human skin model, aka lab-grown human skin. The skin sample was then irradiated, after which they measured the amount of by-products caused by UV degradation present inside the nuclei of the epidermis. The results show almost undetectable levels of UV damage by-products, even at 150 mJ/cm^2, the dose which resulted in a 4.7-log reduction of MRSA and a 0.9-log reduction of dermal cells. These results are consistent with the cited literature that far-UVC will not penetrate the epidermis far enough to reach the cell nuclei of the first layer of skin.

In terms of the safety of 207-nm UV light, the lack of induction of typical UV-associated pre-mutagenic DNA lesions in the epidermis of a 3-D skin model is again consistent with biophysical expectations based on the limited penetration of 207-nm UV light, and consistent with earlier studies using 193-nm laser light [23].

So there you go, it turns out the far-UVC might kill 88% of non-skin human cells on the first layer, but the same dose will kill 99.998% of MRSA bacteria. The same team behind this paper has since went on to test 222nm UVC, live mice, as well as against H1N1 aerosol, and the studies show even more promise in this regard in requiring far lower irradiances to achieve a 4-log reduction in those microbes.

What a great contribution to the site!


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Antibacterial soap impacts on septic system?
What impacts do antibacterial soaps have on septic systems?
I know that septic systems rely heavily on bacteria (especially regarding the breakdown of wastes by bacteria), so it seems as though antibacterial agents surely could do some harm to septic systems. Is that the case?

One of my students in my Environmental Science class asked me this question, and it seemed very much worthwhile to post the Q&A to Bio.SE!

Fortunately, this is not a real problem, as you do not need antibacterial soap anyway. It has many other downsides, and regular soap washes away bacteria just as well.

@cody, very true. Antibacterial soaps are bad for long-term human health, and no evidence suggests that antibacterial agents improve soap efficacy. The US FDA has a quick article explaining why you should skip antibacterial soap. An article from Harvard in 2017 further explains the negatives, why the FDA has banned common antibacterial agents, and how/why normal soap works just fine!

Wouldn't the antibacterial soap be diluted beyond the point of effectiveness, and then biodegraded?

I have dry skin and eczema, and my UK doctor prescribes an antimicrobial lotion which is also a soap substitute to be used in washing, called Dermol 500. It contains benzalkonium chloride and chlorhexidine dihydrochloride. I am advised to use it instead of soap and as a moisturiser, especially after bathing or showering.

@CodyGray the craziest thing is people asking for antibacterial soap to avoid a coronavirus infection...

You can do a simple test using a bottle and a serynge... Divide your sceptic volume by 1000 or something, use a similar bottle, and take yoru septic mix from your drain... Fill the bottle with pond slurry, potatos, organic matter that you want to measure decomposition of, let the bottle kick off bacterially for a week at room temperature, and then add 1/4 of the bottle little by little in the relative amount soap that you use... My suspicion is that antibacterial soap will de-activate in about 10% of the tank, leaving 90% of it working normally. In some setups, it will have little effect.

The quick answer is: Yes, it can cause harm.
Think about it...The septic system (both the tank and your drain field) rely on bacteria, and antibacterial soap is not designed to kill only specific species of bacteria. In other words, antibacterial soap can kill a whole range of bacteria, and that certainly includes the bacteria needed in your septic system.
According to University of Arizona Cooperative Extension (Farrell-Poe, 2018):

The use of “antibacterial,” “disinfectant,”or “sanitizing” products in the home can and do destroy both good and bad bacteria in septic treatment systems. “Normal usage” (according to directions) of these products will destroy some beneficial bacteria. Fortunately, the normal bacteria population within the septic system is sufficient and adequate to quickly recover. Significant treatment problems, with conservative use, should not occur. Excessive use of these products in the home can cause significant and even total destruction of the bacteria population. Normally, the use of any single product or single application will not cause major problems.
However, the accumulative affect of using too many such products and excessive application may cause serious problems and damage to the septic system.
It appears that some alternative systems may be more affected by “antibacterial” products than other systems. Additional and more conclusive research is needed.

You can find additional info about antibacterial agents in septic tanks as well as discussion about the effects of the common antibacterial agent, triclosan, on septic tanks here: Svenningsen et al. (2011) and Kirjanova et al. (2014).

 Works cited:
Farrell-Poe, K., 2018. Antibacterial Products in Septic Systems. The University of Arizona Cooperative Extension fact sheet
Svenningsen, H., Henriksen, T., Priemé, A. and Johnsen, A.R., 2011. Triclosan affects the microbial community in simulated sewage-drain-field soil and slows down xenobiotic degradation. Environmental pollution, 159(6), pp.1599-1605.
Kirjanova, A., Rimeika, M., Vollertsen, J. and Nielsen, A.H., 2014. Retainment of the antimicrobial agent triclosan in a septic tank. Water science and technology, 70(4), pp.586-592.

This is interesting. Is it really significantly different to the effect any detergent would have on bacteria? I would guess all soaps kill most bacteria simply by disrupting cell membranes. Is that not the case?

@terdon I would expect it's not significantly different. However, based on the limited sources I could find on the topic (and their own consistent reminder that this topic is under - researched), it looks like there is a measurable difference due to antimicrobial agents. I've just reported what evidence I could find. To be honest, I didn't explore the literature for studies looking at detergent impacts, and perhaps doing so could further inform and improve my answer. If you have any suggested starting points, please feel free to pass on the suggestion or update my response accordingly.

I don't have the faintest idea! Your answer just made me wonder, is all. I didn't mean my comment as criticism.

@terdon No worries - I didn't think you meant it as criticism. I was just hoping not to have to start at ground 0 for exploring a topic for which I have limited existing knowledge! :p. I recognize that my post is a superficial scraping of existing literature, so the post can definitely be improved with additional resources and info. And I hope someone can hep with that. This was -- in my mind -- quite an interesting question my student asked me, and I quite honestly wish I had more time to dive deeper into it!

@terdon triclosan et al have more effects than soaps have; but I'd agree that it's true that it's not significantly different to the effect of any detergent... however it's worth noting that this simply means for a bacteria-based single home isolated septic system like in that picture you should also be selective with what detergents you use. Some forms of septic systems are "dead" and do not care about bacteria, but if you choose to rely on bacteria (which allows for designs with smaller tanks and less draining), then you need to properly select all chemicals that go into your wastewater.

@Peteris if you can find some reputable sources to support the various claims you make, this comment could be converted into an informative 2nd answer :) .

Can the bacteria mutate to a form that is not killed by the antibacterial agent?

@CJ please ask your question in a new post. Comments are not for questions. See the [help] section for more info


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What causes the overactivity of keratin production and expression in the cells of the nail bed/ nail matrix after some traumata?
What is the cellular mechanism of traumatic(sterile) onychodystrophy(hypertrophy)? I.e one hits his toenail and has it removed twice( once after the first trauma and then again 3 years after the first removal) by a surgeon, because it got crooked and grows back dystrophic(extremely thick and dark) without any signs of infection.

Could it be an explanation that elements of the cytoskeleton extend even deeply into the nuclei of some cells and directly, mechanically influence DNA transcription. I think the mechanism is shifting proteins of the chromatin to expose genes to RNA polymerase. If this happens in cells of the nail matrix, it could explain accelerated production of keratin in response to mechanical stress.


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Spider identification (Caribbean)
I live in the Caribbean (Puerto Rico) and found this spider in my garage. Is it venomous?
It measures about 8 inches as a whole.

Please provide a more specific location. Country is necessary, but even more specifics (town/city, local habitat that your garage is surrounded by, etc.) are helpful. Thanks.

It appears to be a Banana Spider:

... a male Heteropoda venatoria, also called a Banana Spider. The female is a more robust spider with shorter legs. This is the spider that is responsible for the rumors that tarantulas come into the U.S. with bananas because they are often spotted emerging frrom a bunch of bananas in a fruit store in the North. This Giant Crab Spider is usually the culprit. The species is found in all tropical regions, its range extending clear around the world. It is very abundant in all tropical seaport towns, being transported in trading vessels. Its chief food is cockroaches. The female carries her eggs beneath her body. According to this site it is also called the Huntsman Spider.

https://www.whatsthatbug.com/2003/11/11/banana-spider-from-peurto-rico/


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Based on morphology alone, what type of claw does the Tyrannosaur have?
I understand that the exact use of Tyrannosaur Rex's claw is a mystery, or at least debated. I also understand that claws can be used for a variety of different purposes, selective pressure adapts their morphological to be better optimized for certain tasks. Some are used for hunting and killing, like large cats' claws, some are used for digging, like bear's claws, while others are used for climbing, like squirrel's claws.
My question is, all other clues and bits of information about if and how T. Rex might have used its arms, what 'type' of claws did it possess? I'm not asking, in this question, about its arm, the arm's musculature, its mouth or jaw, or about any of the rest of the animal. Based on the morphology of the claw alone, and comparing it to known uses of similarly shaped claws, what types of tasks were the claws geared towards?

unfortunately they have fairly generic claws, they are not specialized enough to point to a use. They are curved enough to be used to grasp something but that is true for their ancestral line too so there is no sign of a specific directional selection.


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Do animals suffer in agony or pain the same way like homo sapiens suffer?
When an animal suffer in agony or pain, do they feel it the same way as homo sapiens or human beings?
I saw a documentary where it showed that while the child cattle were being slaughtered mother cattle were crying. Is that really crying or is it just secretion of tears from tear glands like it always happens?
Do they have the sense to feel suffering like we suffer? If it is true then is the sense of suffering prevalent among all the animals equivalently?

https://www.youtube.com/watch?v=PZG0MgCSZ2g

@AlexReynolds Thank you. That answers my question.


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How does SARS-CoV-2 spread from cell to cell in the lung?
This virus exits the cell using exocytosis after assembling golgi vesicles which contain the virus by fusing with the cell membrane.
In the case of infected pneumocytes, I imagine that the virus could then exit into the alveolus and infect other pneumocytes using again the interaction of the S protein with ACE2 or it could exit into the blood and spread to other pneumocytes in a 'miliary' fashion like TB.
Is either or both the main mechanism of spread in the lung?
Does lymphatic spread play any role?

I'm voting to close this question as off-topic because it was cross-posted to MedicalSciences.SE. In the future, please choose a single site to submit your question to. Cross-posting is rude.


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What are these flowers on Kerguelen?
What are these plants, which resemble short pink sunflowers, in this photograph from Kerguelen island?

This is acaena magellanica which is also called "Buzzy Burr" or "Greater Burnett". See these images for comparision (from here and here):


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question about cat's claws?
ok so I went and read this website:
https://www.yourpetsbestfriend.com/your_pets_best_friend/2010/03/why-cats-sharpen-their-claws.html
So I have some questions to ask:

how many times does a cat has use its claw to lose its razor-sharpness and become like this?

when a cat scratch a tree or any hard objects, it sheds its worn outer sheaths and will become like this: (the big one is before it sharpen, the small one is after). I heard that there claws have layers like an onion, so how many layers does it has on its claw? how many times can it do this in one day, i mean can it do this sharpening method everytime or it has a limit?

this question could use of clarity and research.

New horn sheathes continually grow throughout a cat's life. The mechanism is described in depth in the following:

The structure of the cornified claw sheath in the domesticated cat (Felis catus): implications for the claw‐shedding mechanism and the evolution of cornified digital end organs (2009)

The highly complex architecture of the cornified claw sheath is generated by the living epidermis that is supported by the dermis and distal phalanx. The latter is characterized by an ossified unguicular hood, which overhangs the bony articular base and unguicular process of the distal phalanx and creates an unguicular recess. The dermis covers the complex surface of the bony distal phalanx but also creates special structures, such as a dorsal dermal papilla that points distally and a curved ledge on the medial and lateral sides of the unguicular process. The hard‐cornified external coronary horn and proximal cone horn form the root of the cornified claw sheath within the unguicular recess, which is deeper on the dorsal side than on the medial and lateral sides. As a consequence, their rate of horn production is greater dorsally, which contributes to the overall palmo‐apical curvature of the cornified claw sheath. The external coronary and proximal cone horn is worn down through normal use as it is pushed apically. The hard‐cornified apical cone horn is generated by the living epidermis enveloping the base and free part of the dorsal dermal papilla. It forms nested horn cones that eventually form the core of the hardened tip of the cornified claw. The sides of the cornified claw sheath are formed by the newly described hard‐cornified blade horn, which originates from the living epidermis located on the slanted face of the curved ledge. As the blade horn is moved apically, it entrains and integrates the hard‐cornified parietal horn on its internal side. It is covered by the external coronary and proximal cone horn on its external side. The soft‐cornified terminal horn extends distally from the parietal horn and covers the dermal claw bed at the tip of the uniguicular process, thereby filling the space created by the converging apical cone and blade horn. The soft‐cornified sole horn fills the space between the cutting edges of blade horn on the palmar side of the cornified claw sheath. The superficial soft‐cornified perioplic horn is produced on the internal side of the unguicular pleat, which surrounds the root of the cornified claw sheath. The shedding of apical horn caps is made possible by the appearance of microcracks in the superficial layers of the external coronary and proximal cone horn in the course of deformations of the cornified claw sheath, which is subjected to tensile forces during climbing or prey catching. These microcracks propagate tangentially through the coronary horn and do not injure the underlying living epidermal and dermal tissues. This built‐in shedding mechanism maintains sharp claw tips and ensures the freeing of the claws from the substrate.

is it possible to put your answers on the numbers of my question, please


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Can catecholamines degrade back into tyrosine, or, is synthesis irreversible? (in human body)
Catecholamines like dopamine, noradrenaline and adrenaline are broken down with enzymes that catalyze the reaction. Can they degrade back into tyrosine (a conditionally essential amino acid), or is the synthesis of catecholamines like adrenaline irreversible? (in context human body, but, broadest possible phylogenetic or biochemical context welcome in answer.. )

What do you mean by “are broken down with enzymes that catalyse the reaction”? Which reaction?

A glance at the relevant BioCyc entry tells us that each reaction in the catecholamine biosynthesis pathway is irreversible. The standard free energy change of each reaction—again from BioCyc—is given below.
\begin{array} {|r|r|}
\hline
\text{Reaction} & \Delta _r G' ^{\circ} \text{ in kcal mol}^{-1}\\
\hline
\text{Tyrosine hydroxylation} & -93.0 \\
\hline
\text{Decarboxylation of DOPA} & -3.09
\\
\hline
\text{Hydroxylation of dopamine} & -67.9
\\
\hline
\text{Norepinephrine to epinephrine} & -10.5
\\
\hline
\end{array}
Note that all the free energy changes are negative, i.e. all reactions are irreversible under physiologic circumstances. (For the last one, there is a simple explanation: S–adenosylmethionine is a powerful methylator [1].)
Another aspect is worth a mention. Under physiologic conditions, the reversibility of a reaction depends not only on the free energy changes involved, but also on what happens to the reactants and products. A large supply of reactants, or rapid removal of reaction products, can make the reaction physiologically irreversible. Applying this principle to the catecholamine biosynthesis pathway:

A steady supply of oxygen is available from the atmosphere—this drives the tyrosine and dopamine hydroxylation reactions in the forward direction.
The dihydrobiopterin produced by tyrosine hydroxylase is scavenged by reduction to tetrahydrobiopterin, which further takes part in the tyrosine hydroxylase reaction [1].
The carbon dioxide produced by DOPA decarboxylase is exhaled out.

This further adds to irreversibility.
Of course, as mentioned by @user1136 in the comments, it is theoretically possible to have a "reverse" pathway by coupling to ATP hydrolysis. However, I could not find any such pathway in database searches.
Summary: To the best of my knowledge, humans cannot convert catecholamines back to tyrosine.

Reference

Nelson DL, Cox MM. Lehninger principles of biochemistry. 6th ed. New York: WH Freeman and Company; c2013. Chapter 18, Amino acid oxidation and the production of urea; p 695–730.

@user1136 True. But I could not find any such reaction for tyrosine. The only reaction in humans that favours tyrosine biosynthesis is (to the best of my knowledge) hydroxylation of phenylalanine.

@user1136 — The poster asked whether the synthetic pathway was reversible. This answer gives the correct response. Whether there is a pathway for degradation is a completely different matter. I imagine there is, but it is not the reverse of the pathway for synthesis, any more than the reaction of ribonuclease is the reverse of that of RNA polymerase. (No NTPs in the former, in case you hadn’t noticed.

I do believe it's irreversible.  When catecholamines have done their duty, they are degraded by COMT and MAO into products that are excreted in the urine.
I'll make an example out drugs that are MAO inhibitors.  The enzyme MAO participates in the degradation of dopamine, NE, and Epi.  MAO-A inhibitors are non-selective and used for depression/anxiety because their inhibition will increase levels of dopamine and NE (this might help show that there is no reverse reaction, because we don't see an increase in tyrosine).  MAO-B inhibitors are dopamine specific, and therefore used in parkinsons which is a disease of low dopamine.
Hope this helps!


text:
Protein content in chemical composition of different phyla?
The protein content in the human body is roughly 15%, what are the percentages for other organisms? Bacteria, plants, fungi, protozoa, etc.

It can vary greatly and what you are asking is a shopping list of different values.
A spore is very high in protein. Bacillus subtilis (you may have seen slime on old bacon?) is by weight mostly carbohydrate (i.e. slime). etc.

Also, 'Bacteria, plants, fungi, protozoa, etc.' are not phyla. A phyla is a rank between kingdom and class. What you mean is clade or phylogenetic group —'protozoa' are not a clade (polyphyletic).

phylogenetic group and phyla are interchangeable, depending on semantic framework you use (they describe large clades, if you prefer word clade), but clade works as word. yes protozoa are polyphyletic.


text:
Why does DNA have two sets of bases?
DNA has two sets of bases. Why is this the case? If one gets mutated, does the other as well?

Can you please clarify what you mean by "two sets of bases"? Are you asking about the paired strands of a double stranded DNA molecule? Purines vs. pyrimidines? Something more obscure? ——— The way you have phrased this question suggests that you don't have a background in molecular biology — if this is true you may find the resources in the following comment to be helpful.

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.

Does this answer your question? Why is thymine rather than uracil used in DNA?

One could argue that any informative polymer must have more than two different monomers in its primary structure in orden to contain biological information. One could make an analogy to having a language in which any word contains two letters. Any word contained on such languague, like aaaabbbbb or ababababa for example, would essencially be devoid of information, as we can predict the the sequence of letters. So it is clear that if DNA was to be the molecule carrying the genetic information of a particular cell, then its primary structure must contain more than two different monomers. Now, asnwering why exactly does it use 4 different nucleotides is quite hard.
When you use an even number of nucleotides, all the nitrogen bases can have its complementary base, which allows for the formation of two or three stabilizing hydrogen bonds, in sort of a one-to-one relationship (cytosine to guanine and adenine to thymine). These hydrogens bonds can form because the functional groups of the complementary bases are arranged in space in such a way that allows the formation of these stabilizing eletrostatic interactions. If DNA used any odd number of nucleotides, like $3$ or $5$, this one-to-one relationship would not be possible, since you would always have an extra base without a complementary partner. If DNA uses $3$ different nucleotides, let's say, thymine, adenine and cytosine, we can see that in this example, cytosine lacks a complementary base to bind to. The same can be applied to an usage of $5$ different bases, and in general, to an usage of $2n + 1$ bases. Then, the extra base must bind to a non-complementary base and form a much weaker interaction with it, as the functional groups of the bases will not complement in space well enough, which will decrease the stability of the molecule. So, we can see that, any DNA molecule that used an odd number of nucleotides would be far more unstable than any other that used an even number of nucleotides.
Now, in terms of an even number of nucleotides, from above, we can see that DNA could not use $2$ different nucleotides, as it will hardly contain any biological information. The usage of an even number of nucleotides that are greater than $4$, such as $6$ or $8$, seems to be quite unfavorable, as this would imply that we would have to recognize hundreds of different codons. If we pick greater even numbers than these two, the situation only becomes worse, as the number of codons would exponentially grow ($n^3$) into the thousands. So it seems that using $4$ different nucleotides is, by far, the best pathway to take in terms of stability and practicality.
As for the second question, no, a gene mutation on a particular base will not necessarily alter the complementary base, but it will affect the number of hydrogen bonds the pair can form, and therefore, the stability of the molecule.
NOTE: Credits to Bryan Krause for his insight.

There is another big problem with having 3 or 5 nucleotides that you seem to be missing...

Yes, you are right!


text:
What kind of hot pink eggs are these?
I saw a dozen or more clusters of what I think are insect eggs attached to a few vertical sticks protruding from a small pond, and a few more to stalks of grass nearby. Location is in Hsinchu County, Taiwan, end of March, fairly good weather these days in the neighborhood of 15-22 C.
Each cluster consist of a group of roughly 150 spherical hot pink colored eggs stuck to a surface, each about 2.5 to 3 mm in diameter. One group was deposited almost completely around a stalk of grass on land next to the pond, and several others were deposited on the side of a stick from a fallen branch sticking out of the water.
Questions:

Is it possible to identify what kind of insect produces such clusters of eggs?
Is there any explanation possible for the "hot pink" color? I suppose it could be a general "don't eat me" signal like these big juicy red bugs but it's such an artificial looking color, I've never seen it anywhere in nature, at least that I can remember.

click images below for full size:

update: This answer suggests that snails are the likely culprits, and so I returned to the scene of the crime today and caught them red-handed, or in this case "pink-footed".
Click for full size; the larger snail is about 5 centimeters in diameter.

 caught red-handed, or in this case "pink-footed"

Great post that received a great answer!! :). +1 to both!   I've closed as duplicate due to a very similar post from Singapore a year ago. I think linking these 2 posts in this way is most efficient for site bookkeeping. However, if you think that your post and/or species is sufficiently different and maintaining your question as a unique post is useful, then I could possibly be persuaded to reopen. (though, again, I think linking as dupe works best).

@theforestecologist I'm all for keeping all our pink egg questions in one basket ;-) Based on the answer I revisited the pond a few hours ago I took some much better photos of the snails there which are likely the culprits. I was going to accept the answer and then post a supplementary answer with them, but maybe I will just update this question with two more photos. Since it's now closed and it complements rather than complicates the existing answer, does that sound okay?

I think making a clearly "Updated" portion of your answer with photos of the snail species is appropriate. However, if you think your new info/photos suggests a different species than the one suggested in the previous answer, I'd be happy to open the post back up -- a unique ID to species is reason enough to let you post a unique answer :).

@theforestecologist I've added the additional snapshots above and left a message under (at)tyersome's answer. I'm no expert but it certainly looks like these are those. Thanks!

Those appear to be the eggs of a species of apple snail in the genus Pomacea, probably the introduced invasive golden apple snail (Pomacea canaliculata), but there are at least two other candidates1,2.
You can learn more about this species and the problems it causes from this Columbia University webpage.
For comparison — Figure 3 from "The identity, distribution, and impacts of non-native apple snails in the continental United States"3.

Egg masses of introduced and native Pomacea in the continental U.S. a. P. haustrum, b. P. diffusa, c. P. canaliculata, d. P. paludosa, e. P. insularum. Scale Bar:5 cm.
References:
1: Yang, Q. Q., Liu, S. W., He, C., & Yu, X. P. (2018). Distribution and the origin of invasive apple snails, Pomacea canaliculata and P. maculata (Gastropoda: Ampullariidae) in China. Scientific reports, 8(1), 1-8.
2: Yang, Q. Q., & Yu, X. P. (2019). A New Species of Apple Snail in the Genus Pomacea (Gastropoda: Caenogastropoda: Ampullariidae). Zoological Studies, 58(13).
3: Rawlings, T. A., Hayes, K. A., Cowie, R. H., & Collins, T. M. (2007). The identity, distribution, and impacts of non-native apple snails in the continental United States. BMC Evolutionary Biology, 7(1), 97.

Wow, thank you! I never would have imagined that those were snail eggs. I don't have a close-up but I did notice that the pond is full of small snails. Below the big image there are two smaller images that will display full size when clicked. If you look at the one on the left there are dozens and dozens of snails at the bottom of the pond and there are snail trails everywhere. I don't suppose it's just a coincidence. This is probably not the first invasive snail I've posted here either! What are these four large snails doing?

Type "b" looks like eggs of the variety in the aquarium trade in the US.  I found they needed to have a very humid atmosphere to hatch.

Thanks again for your answer! I've revisited the pond and took some photos of the snails in proximity to the eggs. Apart for being covered in algae the do seem to match the shape of the "golden apples" though in this case with the algae they look more like green apples!


text:
Why do ants raid the house in summer when it is hot, but in cooler months they don't come in?
Over summer the ants invade our house, including our kitchen. In winter and the shoulder seasons they are not to be seen.
I can think of a number of possible reasons for this, including:

they are cold-blooded, and need heat from the outside atmosphere (similar to flies), making winter too cold to go outside for ants
ants need water, and tend to run short on it in summer when the temperature is higher, so travel further for water
the higher temperatures cause aromas from food crumbs to effervesce more strongly, and so ants are attracted to a stronger smell
ants natural natural nest cycle means they run their food supply low in summer and they need more

My question is: Why do ants raid the house in summer when it is hot, but in cooler months they don't come in?


text:
electrostatic charge of viruses, especially Coronaviruses
I am searching for (and failing to find) literature about the electric charge (+/-) of viruses, specifically the Coronaviruses.  I am aware that it is a complicated issue, including interaction of pH and electrostatic charges, etc.  However, I note that electrostatic charge of various materials is investigated for barrier protection, suggesting that there are normal average or overall charges for viruses.  Can anyone comment on this?
Especially, I want to know, at neural pH, are Coronaviruses more likely to adhere to a negatively or positively charged surface?
Thanks.

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology! I'm glad we encourage such questions from curious people who want to learn more.
Via: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4213776/#!po=1.19048

All viruses are coated with proteins and contain genetic material which can either be DNA or RNA. Since both nucleic acids have phosphodiester bonds, the genetic material provides a partial negative charge to the virus. The viral nucleic acid genomes are wrapped in proteins that can be neutral, negative, or positive in charge. Therefore, the net charge of a virus depends upon the cumulative charges of the genetic material and the protein.

So the electric charge of a virus particle depends on the constitutive parts of the virus of interest; particularly if enveloped or non-enveloped; the outward-facing heads of the phospholipid bilayer membrane of an enveloped virus will carry a negative charge.
Two references in the above paper may help with a deeper dive into the subject:

Lodish H. et al. Molecular Cell Biology (ed 4.). (W. H. Freeman, New York, 2000). (Google Scholar)
Michen B. & Graule T. Isoelectric points of viruses B. J Applied Micb. 109, 388–397 (2010). (PubMed) (Google Scholar)

I couldn't find any papers on the electrical properties of novel coronavirus specifically. But looking into SARS-CoV may be suggestive of general properties. Its envelope proteins have a positive charge that help with targeting and infecting ACE2-expressing cells (https://clarivate.com/wp-content/uploads/dlm_uploads/2020/01/CORONAVIRUS-REPORT-1.30.2020.pdf).

Does it really mean that viruses are not electrically neutral (i.e., they are essentially ions) or is it mostly disbalance of charge, i.e., polarization and higher electric moments?

Many viruses appear to have an average isoelectric point (pI) that is below a pH of 7. This means that, at the pH of water, such viruses carry a net negative charge. Other viruses with a pI greater than 7 have a net positive charge. A pH-based separation column can be used for purification. https://sfamjournals.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2672.2010.04663.x https://pubmed.ncbi.nlm.nih.gov/18778829/ https://en.wikipedia.org/wiki/Chromatofocusing

sorry, I didn't realise at first that you are talking about viruses in a solution, rather than isolated viral particles.


text:
What are the trade-offs between polymerase chain reaction (PCR) vs Loop-mediated isothermal amplification (LAMP)?
I've heard that LAMP could be a good alternative to PCR for DNA strand amplification and detection because the equipment required is cheaper, more portable, and the amplification is faster since all happens at a single temperature.
Since this system has clear advantages, I'm curious what are the downsides that prevent it from completely overtaking PCR/qPCR?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5862059/ mentions some disadvantages:

However, this technique has some limitations. Complexity of multiple primers’ designs for multiplication of new gene regions and selecting the suitable regions in the gene sequence for efficient design of primers, complicated product having cauliflower-like structures with different sizes, lack of commercial kits based on LAMP technique and complexity of this method mechanism are some of its drawbacks limiting its popularity among the researchers; and it not as common as PCR-based method.

but they just don't seem that important compared to the large benefits for diagnostic usage.
For example, from this video https://www.youtube.com/watch?v=L5zi2P4lggw I understand that more primers are needed, but is it that hard to "just create a few more primers"? Aren't those just deterministically determined from the target DNA of interest in this  case?
I can see why the cauliflower structures matter for certain applications, e.g. I guess those messy strands are not going to go through an Oxford Nanopore pore for sequencing, but do they matter when we just want to know if the DNA of interest is present or not?
Related articles:

https://www.researchgate.net/post/What_is_the_difference_between_a_PCR-RT_and_loop-mediated_isothermal_amplification_LAMP
https://www.ncbi.nlm.nih.gov/pubmed/22051073

I later learnt that there are other isothermal amplification amplification schemes out there as well, maybe  I knew about those I would have asked a more generic isothermal question:

RPA
which is apparently used in Abbot ID NOW system according to this and is being used for Covid-19 diagnostics.
HDA
NASBA
NEAR
Strand Displacement Amplification

Having to use more primers is definitely one of the big reasons. Primer design is difficult and time-consuming, and even more so if you're dealing with similar targets. For instance, if you're trying to differentiate closely related bacterial strains, having to design primers for 6 or 8 regions instead of just two is going to lower your ability to differentiate the strains. It's even worse if you're working with viruses - these mutate quickly and therefore your LAMP primers will fail to amplify the virus sooner than normal PCR primers.
LAMP is good because it's cheap and portable, but there are portable PCR thermocyclers starting to be produced (eg. miniPCR, Biomeme) and so diagnostically speaking, it's a lot easier to just use existing PCR primers that have been validated and are widely used, instead of creating new primers that you'll have to validate all over again.
The primers again are important if you're trying to amplify multiple targets - it's a lot easier to create degenerate or consensus primers for a standard PCR than it is for LAMP, and also easier to distinguish multiple target bands on a gel, which isn't possible for LAMP.
It can vary, but in my personal experience, I have always found Taqman-based PCR to be more sensitive than LAMP. You can't use Taqman probes with LAMP. You also can't use LAMP for cloning, and melt-curve analysis isn't possible with LAMP, which is useful for detecting primer dimers and diagnostically for distinguishing between targets.
So, LAMP is good because it's cheap, requires less equipment, can be done in the field with minimal reagents, and tends to be more robust than PCR as it is less prone to be affected by inhibitors. This means it is great for in-field diagnostics in developing regions. But there is a range of things PCR can do that LAMP can't, and the complex primer design alone will prevent it from overtaking PCR.

Nice answer teaelleceecee.  Conventional PCR primers ultimately misfire against a mismatched exclusive target especially if it is at high copy #.  Multiply exclusive mismatched LAMP primers won't do that. True that viral mutations may stop such a LAMP assay.  Design in conserved sequence may help with this. Microfluidic systems will allow for "multiplexing" using geographic separation, which could allow for multiple amplimers to overcome the former challenge.  There are tricks to achieving single copy LAMP.  PCR suffers from inhibitor retarded polymerase being slowed down such that it doesn't reach the opposing primer site before denaturation.  In LAMP, there is no denaturation step, which mostly explains its robustness to inhibition.


text:
Do we know of any "species ending bugs"?
Are we aware of a "bug" (virus, bacterium, prion, ...) that has completely exterminated an entire species? Either through direct observation or maybe some form of archeological evidence? If not, are there realistic scenarios where this could happen?
I am primarily interested in cases where the disease was the driving factor of extinction of an otherwise well established and healthy population, but examples of species that were in bad shape to begin with are welcome as well.
My understanding is that this is unlikely, since very deadly infections tend to burn out or evolve towards being less deadly. Killing your host is not conducive to your survival. But maybe it would be possible to reduce the number of individuals so much that reproduction became problematic. I imagine a species confined to an island or something might be susceptible.
I'm asking this because in an interview I saw, an epidemiologist said that his usual research interest are "bugs with species ending potential". The interview was on COVID-19 so he didn't elaborate on what he meant by that or give any examples.
For the special case of humans, I was able to find this article that claims such an event to be unlikely, but I suppose we are the best equipped species that has ever existed on this planet to deal with such a threat.

Can you provide a link to the interview and the name of the epidemiologist? Have you tried looking at some of his papers or his website (many academics have one devoted to their research)? Those would seem like good ways to find out what kind of microbe(s) he might have in mind ...

@tyersome Have been looking for that since I asked the question. Had watched so many interviews that it took a while. It was actually the interviewer (Sam Harris) introducing the interviewee Amesh Adalja: https://youtu.be/E9vIUtXa9ug?t=150 . He mentions a bird flu with a 60% case fatality rate becoming highly infectious for people but no details.

Not a species, but the Gros Michel was almost driven to extinction by a fungus. Apparently the now-dominant variety of bananas is also being attacked by fungus and isn’t doing so well. The other noteworthy thing here is that these bananas are sterile and must be asexually reproduced by humans (creating clones of no genetic diversity).

From the vantage point of other species, humans might be considered "bugs" in the sense that we are organisms that are causal in the ongoing extinction of numerous species. We're doing a pretty good job of it, so far:

The included extinctions span numerous families of plants[4] and animals, including mammals, birds, amphibians, reptiles and arthropods. With widespread degradation of highly biodiverse habitats such as coral reefs and rainforests, as well as other areas, the vast majority of these extinctions are thought to be undocumented, as the species are undiscovered at the time of their extinction, or no one has yet discovered their extinction.   The current rate of extinction of species is estimated at 100 to 1,000 times higher than natural background rates.

Well, maybe you can interpret the question like this, but it is not what I meant at least :-). I mean none of the species we exterminated could be classified as hosting us.

@user1136 That's an interesting theory and it would definitely be an answer to the question.


text:
Does there exist a reagent that can only be precipitated by Haemoglobin and nothing else?
I recently read Sherlock Holmes and in the book A Study In Scarlet, Holmes says to Watson that he has discovered a reagent that can only be precipitated by Haemoglobin and nothing else. I know about the Guiacum test but is there any other test like I have discussed above as the Sherlock Holmes test.

This very point is well addressed by Laura J Snyder in Sherlock Homes: Scientific Detective (a great read) where the author challenges the view that Conan Doyle is the 'father of scientific crime detection' and argues that the new science of forensics actually influenced Conan Doyles' writing, rather than his novels being the inspiration for the new emerging discipline.
Furthermore, not all his claims were scientifically valid, and the 'infallible test for bloodstains' is a good example.
The relevant passage is as follows:

Let us examine, for example, the ‘infallible’ test for bloodstains Holmes is presented as having ‘invented’. By1887, when A  Study  in  Scarlet was published, many researchers already shared the desire for such a test; this desire was not satisfied until the turn of the 20th century,when the spectroscopic method was developed.
A modern chemist has noted that the method Holmes describes – one which would precipitate a brownish dust and change the color of blood in water to mahogany – would need an acid to increase the oxidation rate, as well as a material to be oxidized. By examining the possibilities for the ‘few white crystals’ and the ‘drop of transparent fluid’ that Holmes uses, this chemist suggests that the ‘Sherlock Holmes test’ would probably have had a sensitivity similar to the guaiacum test that Holmes derides as being ‘clumsy and uncertain’[15].
Moreover, Holmes’ test does not distinguish between human blood and the blood of animals– a problem that, by 1887, was considered an even larger concern than the sensitivity of the blood tests currently in use. A solution to this problem did not arise until the work of Paul Uhlenhuth in 1901 [16].

The two references quoted in the above passage are:
[15] Gerber, S.M. (1983) A study in scarlet: blood identification in 1875. In Chemistry and Crime: From Sherlock Holmes to Today’s Courtroom (Gerber, S.M. ed.), pp. 31–35, American Chemical Society (Columbus,OH, USA)
[16] Thorwald, J. (1965) The  Century  of  the  Detective (Winston, R. and Winston, C. trans.), Harcourt, Brace and World


text:
If rabies always kills its hosts, must there be some animal that is an asymptomatic carrier?
I searched a lot on the Internet, but I am not clear about the spread of the rabies virus. As I understand, rabies kills any animal it infects—cats, dogs, foxes, bats, humans. If it kills all of its hosts, then where does it stay?
So, if all rabies-infected animals die, but in order to transmit the virus, every rabid animal has to bite some other animal or have rabies without symptoms, must there be some animal that is an asymptomatic carrier?

This is an interesting question, and it's been subject to a fair amount of research. From an epidemiological perspective, most rabies outbreaks have been studied in dogs. Among domestic dogs, the R0, or basic reproduction number, of rabies is usually quite low—estimated to be around 1.2 in rural sub-Saharan Africa, and <2 in most historically observed cases [1] (though a particularly bad epidemic in Osaka had an R0 of ~2.42 [2]). This implies that, among dogs, it's quite possible for rabies to spread faster than it kills its hosts, but can be entirely eliminated in dogs by mass vaccinations (see [1] and [2]).
But your question is still valid—if, say, the virus infects all the dogs in an area, and they all die, shouldn't rabies disappear from that area? There's some debate as to where the virus keeps hanging out. For one, there is some circumstantial evidence [3] that the fatality rate in dogs is not 100%, but actually closer to 85%. However, this doesn't necessarily explain the reemergence of epidemics, since for the virus to spread, it needs to get to the dog's saliva, by which point the dog is likely exhibiting lethal symptoms [4][5]. Dogs sometimes being asymptomatic carriers is a tempting explanation, but remains a "highly speculative" possibility [6].
To answer your question, let's look at a place where rabies outbreaks can cause severe economic losses—the livestock farms of South America and sub-Saharan Africa. Vampire bats, the hematophagic suckers, can bite over half of the animals in at-risk zones [7], which house some 70 million head of cattle. Since bats are very well-known sources of infectious disease—in fact, they're known to be hosts of 10 out of 11 recognized Lyssavirus species, including the rabies virus [8]—they've been a tempting explanation since 1911, when a bat-borne rabies outbreak in Brazil was first diagnosed [9]. [9] continues to say this:

An idea that vampire bats may be asymptomatic rabies carriers, shedding the virus in their saliva for months, was popular during initial studies of vampire bat rabies (16). However, in a well-documented experimental study by Moreno and Baer (17), the disease in vampire bats was similar to rabies observed in other mammals. The bats that developed signs of disease and excreted the virus via saliva soon died, whereas those that survived the inoculation without clinical signs never excreted the virus or had it in the brain as demonstrated upon euthanasia. More recently, the asymptomatic excretion of RABV in the saliva of experimentally infected vampire bats, which survived the challenge during at least 2 years of observation, was documented again (18). Clearly, this phenomenon requires additional investigation.

This is all I've been able to find so far. If I had to bet, I'd put my money on bats being the asymptomatic carrier that you're looking for, with a solid $n=14$ paper to back it up [13]. However, when it comes to established scientific consensus—well, I'm not sure there is one.

This looks like a good answer and you've done a nice job of providing supporting references. However, please include the complete reference information since links (even to good journals) can and do break. One easy way to get that information is to search for the paper on Google Scholar and click on the ‟ symbol to get reference information. This is a good example of how to format references. ——— Also, will you please clarify what you mean "n = 14 paper"?

@tyersome, I think the  "n = 14 paper" refers to the paper at the "[13]" link, whose abstract describes an experiment using 14 vampire bats. The "solid... to back it up" appears wryly facetious since not only is 14 a small number of subjects, only 3/14 survived the rabies challenge and lived for years.


text:
Is it true to say that the more an organism is smaller, the faster it's going through evolution?
As someone who never formally learned biology, I assume that currently;

The number of species of (non Archaea) Bacteria
The number of species of Algae
The number of species of Plankton
The number of species of Bivalvia
The number of species of Poaceae
The number of species of flowers
The number of species of mushrooms
and of many other sets of species

Are all vast (from hundreds to tens)
Is it true to say that the more an organism is smaller, the faster it's going through evolution (hence, is generally more genetically varied)?

See also answer to this question: https://biology.stackexchange.com/questions/10645/rate-of-evolution-of-population-of-long-lived-individuals/10658#10658

I think that you are talking about what are sometimes called "rates of evolution", see also https://www.thenakedscientists.com/articles/questions/do-smaller-organisms-evolve-faster. That wiki is a collection of info of interest mostly to specialists, but the blog post may be helpful.
The short answer is that there is a strong negative correlation between mass of an individual organism and rate of evolution, in terms of years or whatever. But there is not necessarily a causal relationship there.
People can argue that there is such a causal relationship, because the life cycles of small organisms are shorter, and more generations means more mutations, which means more evolution is possible. In the classic example, E. coli reproduces every 30 minutes under good conditions, whereas humans reproduce every 30 years. This is sometimes true but not always.
Alternately, there are bacteria such as Micrococcus that are smaller than E. coli but divide more slowly, and by this same logic must therefore be evolving more slowly than the larger bacteria. So there's a lot of variation.
As another counterexample, bacterial cells can form spores that undergo stasis for tens of thousands of years, then wake up under better conditions and go about their life. During that time, elephants are evolving much faster than the bacterial spores- even though outside of that time the bacteria are dramatically faster.
Another confounding issue is that the different groups you name are of dramatically different ages. Bacteria are probably ~4 billion years old, and have had tons of time to diversify. Even if they had the same evolutionary rate as elephants, you would still expect more species in bacteria than you would in flowering plants, which are ~200 million years old. So measuring evolutionary rate in terms of "number of species" is quite misleading.
Yet another issue is that evolution may not happen at a constant rate. This is a normal assumption people make because it makes life simpler, but there is a certain amount of data that suggests that a lot of large evolutionary changes happen very quickly, and then there are periods of relative stasis; this is sometimes called "punctuated equilibrium" or "saltation". An example of this is the so-called Cambrian Explosion. So even though one group A may have gone through 1/2 the generations of group B in a unit of time, it may have gone through 10X the "evolution" in terms of changes to body shape/other characters.
So, it's complicated, and there's a large field of research in evolutionary biology that is trying to answer these kinds of questions. Your assumption is broadly correct in terms of agreement with the data, but it's not clear that smallness per se is what makes evolution happen more quickly.


text:
Can mold grow on copper pipes?
Couple months ago noticed something was literally, for lack of a better term, eating paint off of lead pipes.  And I noticed joints in copper pipe seemed to be "leaking" flux. Now all the water in my house causes lips and tongue to feel as if they have cold sores or anesthesised.  taste could be rusty.

Not mold. But you may be getting metal poisoning, get good advice. Seriously.

Welcome to Biology.SE! 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). ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

Copper inhibits growth of organisms. See " Antimicrobial properties of copper" in Wikipedia.


text:
Difference between rate of elimination and clearance?
I honesty don't get the difference. I need a simple explanation so that I can grasp it.
Rate of elimination is

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Clearance is a measure of the volume of plasma from which something is removed, per unit time. For instance, it could be 2 mL/min, meaning that every minute, a two-milliliter of drug plasma is cleared. In other words, it is the rate of drug elimination divided by the plasma concentration.
Remember that the elimination rate is in units of inverse time, so dividing it by inverse volume gets you volume over time, which is the standard dimensionality of clearance.

Thank you! It finally clicked.


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What are the exact characteristics for something to be considered a novel virus?
I've heard viruses being referred to as "novel" - is there an exact definition for what this means?

"Novel" means new, as in never been seen/identified before, that's all.


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Can an infectious diseases come from a plant?
Coronavirus, HIV, 1918 Flu, etc. They all come from animals. Do any infectious diseases (in humans) come from plants? More specifically, are there viruses that infect plants that can mutate to infect humans?

Could you please clarify your question. Are you asking whether plants can be vectors for infectious agents such as E. coli O103, which only infects animals, or are you asking whether there are viruses that infect plants which can mutate and infect humans?

Edited question. The second part: are there viruses that infect plants which can mutate and infect humans?

Thank you for your clarification. It seem that my interpretation of the question was the correct one.

Question

“Are there viruses that infect plants that can mutate to infect
  humans?”

Answer
None appear to have been reported so far. It is difficult to provide supporting evidence for an assertion that they do not exist, but a recent review on the relationship between plant and animal viromes does not include any examples, and our general understanding of the mechanisms by which viruses infect organisms and cells suggest that this is unlikely. There are, however, examples of plant viruses replicating in the insect vectors that transmit them.
Evidence
In 2011 Dolja and Koonin of the NIH published a review in Current Opinion in Virology 1 322-331 entitled Common origins and host-dependent diversity of plant and animal viromes. In this they considered:

“…three distinct scenarios for the origin of related viruses of plants
  and animals: i) evolution from a common ancestral virus predating the
  divergence of plants and animals; ii) horizontal transfer of viruses,
  for example, through insect vectors; iii) parallel origin from related
  genetic elements.”

The very fact that there was a need to argue for a relationship indicates the assumed distinction between animal and plant viruses, and indeed they write:

“…plants are not known to support reproduction of dsDNA viruses and
  retroviruses.”

The only reference in the whole article to an actual biological relationship between animal and plant viruses is the following:

“Strikingly, viruses of the order Mononegavirales and the family
  Bunyaviridae… can also reproduce in their arthropod vectors.”

The paper referenced in support of this statement is by Hogenhout et al. and was published in the Annual Review of Phytophathology (2008) 46 327–359, and is entitled Insect Vector Interactions with Persistently Transmitted Viruses. From this it emerges that there is a class of plant viruses called persistent propogative viruses which replicate in the circulation of their insect vectors, in contrast to most types of circulative viruses. The insects involved include the leafhopper (illustrated below in Fig 1 from that review) and the thrip.

Schematic representation of persistent virus transmission by a leafhopper. Viruses that are transmitted in a circulative persistent manner do not replicate in the insect and usually enter the salivary glands from the hemolymph. In plants, replication of circulative viruses is frequently restricted to the phloem tissues. In contrast, most propagative viruses replicate in several plant tissues and in different organs of the insect vectors ( yellow arrows) and may enter the salivary glands either from the hemolymph or from other connecting tissues, e.g., the nervous system or trachea.
It is not clear to me whether the virus is in any way detremental to the insect vector — certainly it is not the primary target of the virus, and replication can be regarded as allowing it to survive longer before the insect transmits it to the plant.
Today insects, tomorrow people?
The very fact that persistent propogative insect viruses can replicate in their animal vectors raises the question whether the insects could somehow transmit them to human beings. In an answer to a different question on whether insect pathogens can infect humans I have argued that the absence of examples in situations where people come into close contact with insects and the  difference in anatomy and molecular structure of cell membranes makes this unlikely. In the present case we are not even talking about an insect pathogen, but a plant pathogen.

This is a great biological question! I'm glad we encourage such questions from curious people who want to learn more about modern biology.
Much as other animals can be vectors for diseases that infect humans, plants can be vectors for pathogenic infectious agents.
You may occasionally read news stories of disease-causing strains of Escherichia coli which contaminate vegetables and force product recalls. There is currently a CDC advisory to not eat clover sprouts, as an example, because of contamination with E. coli O103, a strain which can cause a variety of health problems (including kidney damage, in severe cases).
This kind of contamination is becoming more common, largely as a consequence of how we produce food:

Fresh fruits and vegetables once were thought to be relatively free of disease-producing pathogens. In recent years, however, outbreaks of foodborne illness linked to fruits and vegetables have become more common. These outbreaks come from produce grown both in the United States and in other countries. Outbreaks have been linked to Escherichia coli O157:H7 and Salmonella on apples, lettuce, cantaloupe and sprouts; Listeria monocytogenes on cabbage and cantaloupe; Shigella on parsley and lettuce; and Cyclospora on imported raspberries.
Changes in microorganisms have undoubtedly contributed to this increase, as have changes in growing, harvesting, distribution, processing and consumption practices. Listeria monocytogenes, Clostridium botulinum and Bacillus cereus are naturally present in some soils. Their presence on fresh produce is not uncommon. Salmonella, E. coli O157:H7, Campylobacter jejuni, Vibrio cholerae, parasites and viruses can contaminate produce through raw or improperly composted manure, irrigation water containing untreated sewage or manure, and contaminated wash water. Contact with mammals, reptiles, fowl, insects and unpasteurized animal products are other sources of contamination.

Wash your fruits and veggies!


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Do proteins contain phosphorous? If its true then how alfred hershey and martha chase used the statement that proteins do not contain phosphorous?
I hv heard about phosphorus that it is a constituent of certain protein, although we know that no amino acids have phosphorus... and if its true then how Alfred hershey and Martha chase experiment got acclaimed whose base of the experiment was that "protein doesn't have phosphorus"??

This should answer part of your question.

Yes some of the proteins contain phosphorus but in the experiment (Hershey and chase experiment) they used bacteriophage it's protein sheath contains carbon,hydrogen,nitrogen and sulphur while the DNA in the bacteriophage contains carbon,hydrogen,nitrogen and phosphorus(in the acid) so they selected this for that experiment moreover sulphur is absent in the DNA but phosphorus is not so one can conclude that DNA is the thing that was transferred
Reference:NCERT

Yes, None of the amino acid contain phosphorus in its side chain, but it is introduced during Post translational modification. This helps in stability and proper functioning of proteins. (Via:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3415839/.
As, phosphorus is main building block of nucleic acid not proteins, so its usage in production of new bacteriophage will represent utilization of phosphorus in nucleic acid synthesis.Further using the blender experiment, Hershey and Chase separated the protein coat of bacteriophage  from its nuclei. And then introduced this nucleic acid into the bacteria,
 and found that it can reproduce to synthesize new viruses. And this proved that nucleic acid is responsible for transmission of genetic information.
 (Via: https://embryo.asu.edu/pages/hershey-chase-experiments-1952-alfred-hershey-and-martha-chase)

It is true that no amino acids contain phosphorus, but due to post-translational modifications some proteins can be phosphorylated. In addition, there are enzymatic proteins such as glycogen phosphorylase b, which are relatively inactive protein, and the change to the active forms (glycogen phosphorylase a) can be carried out by the action of phosphorylase kinase (Lehninger. Principles of Biochemistry. 5th Ed.)

Your first sentence suggest that all amino acids contain phosphorous — is that what you intended?


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Zinc, zinc ionophores and viruses
I see that scientist are sometimes trying to use so called "zinc ionophores" to get human cells to take up more zinc. Zinc is believed to sometimes reduce the ability of viruses to replicate, maybe depending on what type of virus it is. Some zinc ionophores are readily available as dietary supplements. I am thinking first and foremost on quercetin and Epigallocatechin gallate (EGCG).

Is there any way to test how "open" ones zinc-channels into the cells are?
Is there any research done on how much a person typically would need to consume of a certain ionophore to get a descent amount of zinc in the cells?
Zinc tablets are available as dietary supplements. Is there any point in taking those if you want more zinc into your cells or is it more or less pointless if you are lacking ionophores?

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It is not pointless.  Some zinc will get in.  But only a small fraction of the zinc you take.  In the short term, relatively high doses of zinc (like twice the RDA) should be okay.  You could take them with green tea, which includes ionophores.


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Why is Homologous Recombination (HR) more frequent at long sequence repeats?
I'm studying plasmids in bacteria (E. coli), and trying to understand the well-cited phenomenon that recombination frequency increases with longer repetitive sequences. I think this also applies to eukaryotes.
In my (potentially misguided) current view, HR can occur between two DNA duplexes either during or after replication (?). As I imagine it, the new DNA duplex will have near identical homology to the template duplex (from which it has just been replicated), meaning that sequence homology is widespread across the entire molecule. This would mean that sufficient homology between sister chromatids can be achieved anywhere (?), negating the trend for 'long sequence repeats'.
So, why is there a focus on long repeats promoting higher recombination frequencies? Is my view on when HR happens misguided?

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HR rarely occurs at all in normal somatic cells, because multiple different mechanisms try to prevent this from happening between sister chromosomes during mitosis; the implications of this recombination can be detrimental to the organism. Instead, in eukaryotes, HR normally occurs during Meiosis, in the formation of Gametes, which will recombine anyway. This actually has a beneficial effect because it increases genetic diversity of offspring, thereby promoting evolution.
As for how homologous repeats enhance HR, it is a rather simple mechanism. Basically, you have the two homologous strands side by side, and you have this extensive repeat section in the middle. The thing is, because the repeat section is so long, and because of the fact that it repeats, really any repeated sequence anywhere along that section can cross over with any repeated sequence on the other strand. This increases the availability of HR sites, as well as increases the number of possible outcomes, therefore increasing the probability that HR will occur. Plus, as the number of repeats increases, the number of possible recombinations increases exponentially, making HR on long repeats much more likely than other cases of HR
I hope that satisfactorily answers your question.

Thank you - this all makes sense. I since realised I was trying to figure out how HR occurred specifically in the context of DNA replication, and therefore wanted to make sense of 'which strands were which' in a potential HR process. Through a combination of this answer and chatting to other people I figured it out :)

I should add for those wondering where I got stuck: DNA replication can stall at any point, promting the repair machinery to get it 'back on track'. One of the ways this happens is through HR. This may require dissociating a newly paired nascent strand for it to be a potential substrate for strand invasion of the duplex on the other side of the replication fork. Reasons for homology are then as you described.

I'm not sure what you mean by "repetitive" sequences because homologous regions don't have to be repetitive, but the relation between long homology regions and increased HR efficiency is due to the mechanism. HR in yeast is achieved by strand invasion of single-stranded DNA (perhaps generated by DNA damage or self-induced in the case of meiosis) at another DNA duplex. The longer the homology region, the more complementary base pairing and the stronger the bond. Conversely if the homology region is short then the bonding is not so strong and the single-stranded DNA will probably get displaced by the other strand in the duplex thus reducing HR efficiency. I believe it's similar in E.coli.


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What is this fossilized claw found in a Belgian forest?
What is this fossilized claw found in a Belgian forest? It is 14.5 cm long and 2.5 cm in diameter.

What are its dimensions?

Why do you say it is fossilized?

Looks like the proximal end of a rib of a large mammal (cow, horse, deer). Without information about how large it is, it is not possible to get closer to an identification. It's not a claw and very likely not a fossil. It just looks old and dirty.
Here's a horse rib cage (from https://www.rodnikkel.com/content/saddle-tree-blog-from-shop-and-desk/the-rib-cage/):

Ribs in the 4-7 range seem to be a good match for shape but not as much for roundness.

It is 14.5 cm long and 2.5 cm in diameter

This isn't my area, but how can you tell that it isn't any other elongate structure from a large mamal? For example, why isn't it a horn/antler?

That's the distal end of an antler of some deer. You can tell because the texture is smooth and glossy, all wrong for a rib, and has that flange at the end which looks very different from the uncinate processes you see in some ribs but looks a lot like the flanges you see on some deer antlers. The more rugose, "veiny" texture near the base is also typical of deer antlers. My guess is that it's either a red deer (Cervus elaphus) or roe deer (Capreolus capreolus) antler fragment.
It's not a claw, because it lacks a clear flexor tubercle, articular facet, etc.

The cross-section is also very typical of a deer antler. This is what a deer antler looks like in cross-section.


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Does the Abbott ID NOW coronavirus test return a positive result if you take it while you're still in the incubation period?
It seems like Abbott's ID Now test works by detecting the virus directly as opposed to checking for antibodies? If the test result is negative does that mean you don't have the virus? Or does that not rule out a recent infection with the virus that has not yet reached a level high enough to be detected?

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This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology! I'm glad we encourage such questions from curious people who want to learn more.

It seems like Abbott's ID Now test works by detecting the virus directly as opposed to checking for antibodies?

Yes, the ID NOW test performs a quantitative real-time RT-PCR assay to amplify reverse-transcribed viral RNA, specifically targeting the SARS-CoV-2 RdRp gene.
The product insert for the COVID-19 test for the Abbott ID NOW product describes the "analytical sensitivity" or "limit of detection" (LOD), which describes the true positive rate.
The LOD described in the product insert is the lowest amount of viral genome in the collected sample that you need to get a true positive in 95% or more of administered tests, in units of "genome equivalents per mL".
This is effectively the minimum number of copies of viral genome per mL of assayed sample needed to give a true positive in 95% or more tests. Its LOD (125 copies/mL) is comparable with other tests (example).
A false negative can result if there is insufficient virus copies in the sample, or if there is test material contamination or the test is not performed correctly.
This assay includes positive and negative controls, which help to identify potential problems with how the assay was performed. Controls are important, given the many millions of tests that will be done to identify infected carriers of SARS-CoV-2 — the assay must be done correctly and without contaminants, in order to give the best statistical odds for the correct diagnosis of those who will be tested.