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Did most pandemics originate from Asia/China?
This question may be on the borderline of well-posed-ness. Let me ask it. Then please tell me if or where it can be improved.
Is it statistically true that the majority of the pandemics or epidemics originate from Asia particularly China? If not, is there a geographic concentration of the origin of pandemics? If so, why?

According to Merriam-Webster Dictionary a Pandemic is:

an outbreak of a disease that occurs over a wide geographic area and affects an exceptionally high proportion of the population : a pandemic outbreak of a disease

Epidemics are considered a smaller scale version of a pandemic affecting a smaller region, community or population. Epidemics are obviously more common than Pandemics for that reason.
COVID-19 is believed to have become a pandemic event because it has affected multiple continents and most if not all Nations of the world. These extent of pandemics though rare in the past may become increasingly frequent as our world continues to become more globalized if further precautions are not continuously developed.
According to this list, Around 5 of the world's Pandemics have likely started or been mainly spread from and within China, They are:

Third Plague - 1885
Asian Flu 1957
Hong Kong Flu - 1968
SARS 2002
Coronavirus Disease - 2019

These are 5 out of the 20 pandemics in the list. Would that count as a majority? Depends on how you look at it. For one country to start so many does make it unique and a possible majority but we must also consider the size of the country's population relative to the rest of the world. For such a large country (currently 1.4 Billion people which is about 18% of the world's population) with a large portion of the population being poor it is almost expected that China suffers more epidemics than most countries.
Pandemics and Epidemics start for a wide variety of reasons (some quick-search articles that explain: 1, 2, 3) and many of these pandemics develop because of unique environments or pathogens existing in 'coincidence' with each other.
Generally, lack of hygiene, low economic wealth, lack of healthcare products including vaccines coupled with a high population are common societal trends for the beginning of an epidemic. However the pathogens have their own characteristics that make them effective at causing an outbreak. This includes but definitely is not limited to: rapid mutation rate, easy transmission such as through air (e.g. SARS) or water sources (e.g. ebola virus), and zoonotic capabilities (being able to infect more than one species such as swine flu).
Two sources that must be strongly suggested to check out for anybody interested in these sort of topics are the Center for Disease Control and Prevention and the World Health Organization

Thank you for your informative answer. Since as you say, the number of pandemics is small, I have added epidemics to the question so as to make any conclusion drawn from the statistics more accurate. Would you like to revise your answer accordingly?

Epidemics may be even more evenly distributed across the world. this link (https://en.wikipedia.org/wiki/Category:21st-century_epidemics) is a quick search of all the epidemics (and pandemics in the 21st century), You may notice some other continents or countries having more epidemics than China such as India. If you look into the 20th century (https://en.wikipedia.org/wiki/Category:20th-century_epidemics) The distribution of epidemics changes drastically with the US having several more than most others.

The reasons I mentioned still remain true. But there is of course unique characteristics of each country and each disease that infects them that makes each epidemic its own study.


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What causes eye strain when viewing any display?
Few everyday experiences:

Staring at the physical paper (or any other sight in nature) doesn't cause eye strain.
Staring at the LCD screen causes eye strain.

Some of the differences in properties I have isolated so far are:

Refresh rate, that how often picture updates itself. For LCD like display, it is finite, but for the physical paper (viewing up, down or turning page) it is instantaneous (infinity),

Most common LCD emits backlight to project image, whereas physical paper reflects light.

Other effects like glare, blue light (harmful light which disturbs sleep cycle)  which is absent in physical paper but present in most of the LCDs.

(3.1) The physical paper doesn't distort contrast or image quality whereas LCD can sometimes. Although I am not sure how giving an inaccurate description (which is a different problem) can cause eye strain.
So I want to ask what makes up a favourable viewing experience from a biologist perspective.

Biologically you need to use soft light if your eyes are forced into a fixed distance on small details, then at least there shouldnt be bright lights all around the small details. 1/Try alt-control-print buttons if you have windows. It inverts the colors white on black. 2/install "gamma panel" you can fix hotkeys to different brightness levels, i.e. I have ctrl-f1 to f5 instantly change brightness effortlessly. 3/dark reader for chrome. fixed eyes. on android say "accessibility"and find the vision/invert colors option... and use n offline reader which reformats text size and colors.

Any task that implies an intense use of the eyes may cause eye strain. The difference between reading paper and staring at a screen may vary from the distance, pauses made when turning the page, etc...
As stated in this link, it depends on the individual. So a favorable viewing experience is any that does not require an intense effort given the particularities of the subject's vision.
"Some people, while concentrating on a visually intense task such as reading fine print, using the computer for hours at a time, or trying to see in the dark, unconsciously clench the muscles of their eyelids, face, temples, and jaws and develop discomfort or pain from overuse of those muscles. This may lead to a vicious cycle of tensing those muscles further and causing more distress. Other people attempting to do similar visual tasks may have no symptoms at all."
https://www.medicinenet.com/eye_strain/article.htm#what_causes_eye_strain

source: Stack Exchange

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

sort: votes


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Why do some plants develop a shiny layer that looks like plastic?
I noticed some plants that look almost as if they were made of plastic and am wondering what and why that is. Here is a sample photo:

My guess is that this might be some sort of waxy cuticle that protects the plant from either water loss or pests.

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


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What's the name of this colorful tiny spider?
Found this colorful spider yesterday in my study. Couldn't find exact match over internet. Does anyone know what spider is this? Is it harmful?

Welcome to Biology.SE! Identifications questions should also include: 1) the species-identification tag; 2) the location where you observed this organism (e.g. country and region — the more specific the better); 3) habitat information; and 4) an estimate of the size of the organism. Please [edit] your post to include this essential information. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

It seems a lot like the 'jade jumping spider'.
The jade jumping spider scientifically known as Siler semiglaucus has been observed primarily in Asia. I notice that the legs and abdomen have similar patterns to this species. As for the feelers and head I'm not so sure, but the dark hair on the front legs makes me more convinced of my guess. Perhaps look at different species that share the same genus to see if there is any other species that looks more similar to your observation.

If you're still not convinced, as a last resort, perhaps take a look at the peacock spider also known as Maratus volans. It's a long shot but maybe you see connections that I couldn't catch from the photo :).

Thank you for the details, Ark.


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What is the exact definition of mitochondrial depolarization?
As I understand as per literature reading and some khanacademy(https://www.youtube.com/watch?v=PtKAeihnbv0&t=315s):
Proton gradient := the gradient created when hydrogen ions moves to the intermembrane space from the mitochondrial matrix.
Mitochondrial membrane potential := the potential energy created by the proton gradient.
Does depolarization mean the loss of mitochondrial membrane potential? The lower the mitochondrial membrane potential, then the more depolarized the mitochondria?
So the way I defined proton gradient and mitochondrial potential is conceptually derived from the so-called proton-motive force used here https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2605959/ and also described here https://www.dummies.com/education/science/biology/the-proton-motive-force/ as an electrochemical force. Thus, my definition is from my rudimentary physico-chemical intuition.

What does “:=“ mean, and where did you get these definitions, which I would consider poor or incorrect? Where have you encountered the term “mitochondrial polarization? To be meaningful you should provide sources and context. If you have read one thing and providing your own understanding of other terms please make this clear.

Sorry, David. This is simply how understood it based from youtube videos and literature reading. So it is my personal interpretation. I posted it so people who have the expertise and who care to correct it, will.

Then perhaps you could modify your question to give a specific source for the use of the term so we can see whether it was used in relation to mitochondria as a whole or just the inner membrane. Also it would be better to rephrase the other sections as "I understand that the mitochondrial membrane potential is..."

Hello David, I've added some of the sources. Thanks!

Ok. I'll see if I can find anything of use to add.

The inner mitochondrial membrane is important for ATP synthesis (oxidative phosphorylation) to occur. Electron transport chains are situated on the inner mitochondrial membrane where electrons traverse the chain across proteins - causing protons to traverse into the mitochondrial matrix. Creating an electrochemical proton gradient.
This is a very interesting topic and is best understood with an explanation of the JC-1 Dye.
Explanation
Mitochondrial membrane potential changes - depending on cellular events.
The dye 'JC-1' is able to indicate mitochondrial membrane potential in different cells.

If there is a negative charge inside mitochondria then the monomers express green fluorescence.
If there is a positive charge inside mitochondria then the monomers form J-aggregates and now express red fluorescence.

The ratio between red & green florescence shows the mitochondrial membrane potential.

A low or negative mitochondrial membrane potential will show more green florescence.
A high or positive mitochondrial membrane potential will show more red florescence.

Example
One event that may influence mitochondrial membrane potential is an increase in reactive oxygen species.
Reactive oxygen species are molecules that damage cells but are also important to regulate cellular activities. Some examples are Hydrogen Peroxide or Superoxide.
In this image cells are stained with JC-1. The ratio of the dye is ~1:1 at basal. As the reactive oxygen species hydrogen peroxide is added and time continues, there is more green. Showing:

A low or negative mitochondrial membrane potential in each of the cells.

Thank you very much. This is helpful. This does agree with the assumption that ROS can induce "damage" to the membrane complexes; hence a low mitochondrial membrane potential, i.e. green fluorescent? May I also know the reference of the image? Lastly, what are your thought on the definition of depolarization?

@TheLast Cipher
"In general, harmful effects of reactive oxygen species on the cell are most often:[18]
-damage of DNA or RNA
-oxidations of polyunsaturated fatty acids in lipids (lipid peroxidation)
-oxidations of amino acids in proteins
-oxidative deactivation of specific enzymes by oxidation of co-factors" - ROS wiki page.
High levels of ROS changes the gradient.
Image Ref: https://www.thermofisher.com/au/en/home/life-science/cell-analysis/cell-viability-and-regulation/apoptosis/mitochondria-function/jc-1-dye-mitochondrial-membrane-potential.html

@TheLast Cipher
Apologies, I didn't have enough room.
A depolarized mitochondrial membrane potential is an indicator of increased levels of ROS. Ref: Thermofisher.com link above.

@Andrew — I have no interest in you or "everything you do", indeed I am generally not aware that I have commented on people's posts previously unless they have very distinctive names. My only interest is to improve answers (and questions) to make them more useful to the community. As you are new here, you may not realize that comments are primarily for asking for clarification or making suggestions for improving answers. That was the point of my remark. Let me reword it. "I suggest you could improve your answer by distinguishing between the potentials of the two mitochondrial membranes".


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How does sleep prevent our eyes from drying out?
If we don't sleep for about 16 hours, our eyes start to get dry, and no amount of eye drops helps. You use eye drops and then you're dry 10 minutes later.
However, after you've slept for 8 hours, your eyes can go another 16 or so hours without drying out.
What specifically happens to our eyes during sleep that prevents them from drying out in the next 16 hours after sleep?
Are there any research papers explaining the mechanics of all this?
The reason I am asking about this is in order to understand whether there are any connections between nasal and eye moisturization.
There's a condition called empty nose syndrome, in which people with reduced nasal turbinates suffer from a range of symptoms and a lot of them have to do with their nose getting dry.
Here's a CT scan of a person suffering from empty nose syndrome in one nostril. As you can see, one of their turbinates has been reduced, and the other one looks normal.

There's something called "the nasal cycle", it's a phenomenon where turbinates swell up on one side at a time in order to "rest", according to wikipedia. Here's a picture illustrating the nasal cycle:

As you can see from the picture, one nostril of this person is mostly closed, due to cavernous tissue being swollen. It is not a disease, it is actually how our nose normally works.
Of course, if you have reduced nasal turbinates, like in the first picture, it is impossible to properly close the nasal airway and expect it to "rest", so that it can start producing moisture again.
Does that mean that our nasal turbinates work in the same way as our eyes do? They have to be closed for a while in order to properly produce moisture?
As I've mentioned before, when your eyes are dry, you can moisturize them, and then they're dry 10 minutes later... It seems to be the same with empty nose syndrome patients. It seems to me that in order to restore normal moisture in the nose we need to have it closed for several hours. I think it is so, but I'd like to first find out why our eyes need to be closed in order to rest. So, I want to find the parallels between nasal and eye moisturization.

When we don't sleep we force our eyes open, blinking less to stay awake and focused. Less blinking means less eye hydration. I've never heard about what you say, can you provide any references to learn about that 16 hours awake limit?

@MarioZ I'm using rough estimates of my own findings. I only mention it because there are 24 hours in a day. Normal sleep should be about 8 hours, that means that we stay awake for 16.

Regarding our eyes getting dry at the end of the day, when we're tired, I think it's common. You can google it. If people don't sleep much, for example, their eyes are red...


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Is there such a thing as an autotroph that doesn't use photosynthesis?
I've heard of photoautotrophs, which are just autotrophs that use photosynthesis. What I'm wondering is if there's any other way for an organism to make its own food that doesn't involve it using photosynthesis?

Chemoautotrophes

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 expect 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, since you can easily answer this using reliable sources online this question seems to fit this sites criteria for "homework". (Note this can apply to questions not assigned as homework.) 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.


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Is "Retinal Glial Cells Enhance Human Vision Acuity" creationist propaganda?
The paper Retinal Glial Cells Enhance Human Vision Acuity is profusely quoted by creationists as "proof" of the "perfect design" of the human eye.
The paper is about biology but published in Physical Review Letters (open access, click PDF). Is it generally accepted as legitimate science, though cited by creationists, or is it thinly veiled creationist propaganda?

I've adjusted the wording of your question to avoid overtly soliciting opinions. In Biology SE we should ask questions that can have fact-based answers. The classic example of the debunking of intelligent design arguments is the flagella motor, looking for a source for that now... Here's one https://youtu.be/jdF-ugdl4mc but just search "flagella motor intelligent design debunked" for more.

@uhoh, thanks. This is my first question here.

apparently these are harder: Determine if a coincident point in a pair of rotated hexagonal lattices is closest to the origin and Can there be an energetically unbounded three-body orbit where escape is impossible due to conservation of angular momentum? which reminds me that I need to post it in MO


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Can twins that develop in separate sacs but share the same placenta be identical?
I have two younger non identical twin sisters. When my mum was pregnant she was told they were both in different sacs when developing but shared the same placenta.
We have done hours of research on the topic, as we have reason to believe they could after all actually be identical.
After all this research we’ve just found a load of fancy names for twins and no information on non identical twins that share the same placenta and are in different sacs.
Another thing that may help is that they are mirror twins.

Welcome to Biology Stack Exchange! I modified the wording of question a little bit to bring out the actual question about biology.

they were both in different sacs when developing but shared the same
placenta

This suggests that they were monochorionic diamniotic twins, which would mean they are monozygotic, i.e. identical.


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Help identifying an insect by its remains
Yesterday i hiked in Bolsena lake, Italy. I felt this insect moving into my ear. So i smashed my ear and this is the result. Please tell me that there are no risks related to Lyme desease or similar.
Sorry for the bad quality of the photo.

It is probably a beetle.
The shape of legs and the two big eyes are an insect thing.
Lyme desease is transmitted by ticks, so i would not worry.

Thank you. One more question: so beetles could own wings?

@FedericoJuvara many (though not all) beetles have wings. They're usually protected and hidden under the elytra when not in use though. Check out https://simple.wikipedia.org/wiki/Beetle#Wings for a picture and more information.

I'll check it out, thank you very much!


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Do SARS-CoV-2 virus particles really travel through filopodia and "emerge from the tips"?
Watching the new University of California San Francisco video Coronavirus forces cells to produce tentacle-like structures that infect neighboring cells I saw

The growths spread out, and coronaviruses emerge from the tips, ready to infect neighboring cells.

The caption on the video page includes the following:

When a cell is commandeered by SARS-CoV-2, however, these same kinases behave in ways that disrupt normal cell function and transform the host cell into a virus factory. Cell division comes to a halt, inflammation pathways are activated, and the cell even begins to produce tentacle-like structures known as filopodia, which protrude from the cell's surface and may serve as molecular highways that help the virus spread rapidly to neighboring cells.

Question: Do SARS-CoV-2 virus particles really travel through the induced filopodia and "emerge from the tips" of at least some kinds of human cells? Are they transported along the microfibers to the ends as part of this process? If so, how is this known? Images here and elsewhere seem to shown the virus particles dotted randomly along the filopodia and other areas of the cell surface as well.

It surely depends on the cell line, is it specific to vero E6 cells and maybe some models of epithelials (Caco-2, HAE, where filopodia are desired) ? There are some images where the virions budding vesicles seem to be exocytosed normally. You can try emailing the authors of 1 and  2.

@reuns I'm too shy


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How do microbes spread from a small place to a very large place?
Bacteria are very small, so they cannot move very far on their own. Viruses cannot move themselves at all. So how does a specific type of bacteria or virus spread from a small place to a very large area (such as the whole Earth)?

Studies of the human microbiome suggest that gut and skin bacteria strains are localized to regions not larger than 1000 km so transport in general is limited. Look at works about ocean microbiology and aerobiology for transport through water and air. If you travel around the world and defecate, then your gut bacteria are extremely lucky.

Birds migrate for thousands of miles, carrying diseases on a time scale of months or less.  With climate shifts, insects and animals shift their ranges on a time scale of hundreds of years or more.  Bacterial spores like anthrax can be in a form that is easily blown around the whole Earth, ready to thrive wherever they touch down. Plant diseases travel with their plant hosts, and over time scales of thousands of years the plants - e.g., dandelions and conifers - can spread thousands of miles of latitude and longitude.

Or for a more topical example, the COVID-19 virus travels mostly by airplane and cruise ship.

@jamessqf technically the vast majority of its "trips" are over distances of <2m, but yes - most long-distance introductions occur via rapid international travel. :)

The answer by @SMcGrew is essentially correct, but let me add a technical term (at least in the context of infectious diseases): the bacteria and viruses a carried by vectors. Since word vector is a kind of overused, even if we limit ourselves to biology, it is also common to be more specific and call the disease vectors.
Vectors are classified into biological vectors and mechanical vectors, depending on whether they biologically interact with the microbe (i.e., they get infected) or whether they are simply carried from one place to another.


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Why is egg white alkaline?
According to Tiefenbacher,

Egg white is naturally alkaline with an initial pH of 7.6–7.9 but in storage the loss of carbon dioxide by diffusion through the shell
increases the pH of the egg white up to about 9.7 with age.

The loss of $\ce{CO2}$ means loss of $\ce{H2CO3}$, an acid with pKa of 6.3. This reduces acid and in a neutral solution pH would approach 7. Since it goes up towards 9-10, what is the base? Albumin is a buffer in biological systems but I don't think it is that strong a base. What is the alkali causing pH of around 9-10?

This question has attracted some oddly out of character negative attention in the comments; let's keep discussions civil, please. If you want to ask for clarification, do so politely; if you think it's a good question, put your efforts toward an answer instead of a comment.

I have provided a link for your attribution and corrected it to the author of the book that is listed in Google books. Please note that Google is not the author of material found using its search engine.

In the terms of the question, this can be regarded as calcium hydroxide, with the carbonate being in the form of calcium carbonate. Calcium hydroxide is a stronger base (pH of aqueous solution at 1mm = 11.27) than carbonic acid is an acid (pH of aqueous solution at 1mm = 4.68), so that 1mm calcium carbonate has a pH of 9.91. (Values from Aquion)
Calcium carbonate is, of course, the constituent of eggshell, which crystallizes out of solution when it is deposited in the uterus. Its presence within the egg white is presumably a consequence of this.
–––––––––––––
I would add that one does not generally regard there being a particular base balancing the carbonic acid: when the hydrogen ions are removed there is an increase in the free hydroxyl ions and hence an increase in pH. The way the question is formulated only really makes sense if one assumes that the egg white acquired extra carbonic acid to reduce the alkalinity resulting from the calcium carbonate/hydroxide.


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Why does exposure to a smell for some time reduce the electrical response of receptor neurons in the olfactory system?
In what way does exposure to a certain smell for some time causes them to loose sensitivity and have a lesser electrical response

You may find providing a little more research/context will help net more useful answers? For example, is there research that shows reduced olfactoy sensitivity is a peripheral phenomenon occurring at the receptors, as opposed to sensory filtering that happens in the CNS? I'm also curious about time scales. Are you interested in long-term exposure and/or chronic loss of sensitivity or more short-term/transient phenomena, like when you get in a funky smelling car but stop noticing after a few minutes?

Both, long term exposure as in you cant tell if you smell bad because ur used to ur smell and short term as in u keep smelling a perfume and u stop smelling it for a short period of time

in what way is that different to any neural adaptation?  https://en.wikipedia.org/wiki/Neural_adaptation


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Cell-autonomous viral defense involving oxidative burst?
I'm looking for a mechanism by which a cell detects a virus (probably a retrovirus) within itself, then triggers an oxidative burst in response. This should all happen within the cell itself, independent of any immune-specific cells outside. Ultimately interested in humans, but any pointers whatsoever would help.

Could you clarify. Do you have any reason to think such a system exists, or is this just a conjecture that such a response would seem to you an effective cellular response?

@David conjecture, based on staring at one of the holes in current theories of aging and asking what would be about the right shape to fill that hole.

Better to do some research into what is actually known, I think. Try intrinsic immunity and respiratory burst. The known examples of oxidative bursts against pathogens occur within specialized organelles in neutraphils, presumably because they would be dangerous in the general cellular environment you envisage.

So, the cell may trigger an oxidative burst in response to pathogen (not specifically virus).
In case of retroviruses, they are hard to detect for the cell (example HIV) as they use the cell machinery for replication and can also stay in inactive latent state thereby not triggering immune response.
Hope you found your answer. Thank you and good day.


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Is the leading strand consistent in the same chromosome with multiple replication forks?
If a chromosome has multiple origins or replication, do those origins necessarily pick the same DNA strand as leading and the same one as lagging, or can they be of opposite orientations, sending replication forks in opposite directions and therefore picking different leading vs lagging strands?

Replication proceeds in both directions from a single origin of replication, so the same strand acts as both the leading or lagging strand for the two different replication forks.


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Could anyone kindly identify this bug for me? Is it harmless?
Details:

Found by a wall/window in Brooklyn, NY in a house not too far from the beach
Rooms walls/windows are dusty and spots of mold growing on wall/windows
size of bug: 2 milimeters

Keywords I've tried in my web search and image search:

True bugs, ticks, types of house bugs, sowbug, stink bugs, insects that live/grow near mold, flat bugs, dust bugs

Any suggestions or ideas would be greatly appreciated.

That particular one is dead, so I guess it's completely harmless, a closer picture with different angles would help a lot to identify it  :)


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What coastal creature leaves braid-like trace that has clear landing and take off points?
6/29 around 8 PM EST (within 40 minutes after downpour) the depicted trace was found in swash zone at Jacob Riis Park in NY. For reference the boot size is 12.


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Help ID snake near Deming NM
This snake is in our yard, south of Deming NM, in Luna County.
Approximate length is about 3 1/2 feet.
It moved slowly at the time, but was being picked on by a couple of medium-sized birds.
It is basically black with a black, narrow head.
The body and snout have pale yellowish markings.  On the body, the yellow is individual scales, so almost spotted.  And on the snout, more like lines or stripes.
I have some good photos, and even videos, but it says the files are too big - need to be under 2 giggleburps or something and I don't know how to do that.

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

Though a full body image would help a lot, I feel certain that it is the desert king snake scientifically known as Lampropeltis getula splendida. This species is seen in most parts of New Mexico and is not venomous. It primarily feeds on rodents, lizards, birds, snakes and eggs.
Here's a link to a website with more details on this species and other snake species of New Mexico: http://www.nmherpsociety.org/reptiles/snakes/lampropeltisgetulasplendida/index.html
Here's a variety of different photos of the desert king snake from different angles (but different ages, sizes and pattern varieties of the same species).


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Why do bees fly inside the gaps between the decoration on the exterior wall of a building and the wall?
My house has decorations around the windows on the exterior wall:
There are gaps between those decorations and the bricks of the building:
During the summer, there are always bees looking for those gaps so they could fly into them while I rarely caught them flying out. I wonder why do they do that? What do they do inside? Is there anything I should do about this situation?
I guess that maybe they want to stay in a cooler place since it's quite hot outside? However, it's also worth noting that they seem to be interested in only one particular side of one particular window since I have never seen this happening to other windows of my house.

Bees often nest in rocks and in soil, i.e. cliffs and rodents nests. Those gaps are a good shelter for a bee, from sun and rain.

@DeltaEnfieldWaid that sounds like the start of an answer.

They just want to escape from.the heat. If there are no trees near your area, the bees can make a hive to live in. The bees don't constantly fly around; they only do so to gather food (or looking for a partner to mate).
Regarding the particular side of window, I'm not sure, may be that part is a little dry or (damp). What I mean is that the microenvironment of that crack may be more likeable to the bees, though that is just my wild guess.
Hope you found your answer. Thanks for reading.


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Bedbug or psocid?
I’ve found a few of these tiny bugs on the windowsill next to my bed. Can anyone tell if it is a bedbug nymph, psocid, or something else?? I’m hoping it’s not the former!
Edit: They were very small maybe 1 to 2 mm

I edited your images to get rid of 99% of the empty area. Can you mention roughly how large these were? There were no identifiable objects in the photos to estimate a size from. Thanks!

See Insect identification - Is this a bedbug? and Questions about insects eating flour and living in the cracks of a wooden cutting boards for a comparison.

Also, please update your post with your geographical location (i.e., what city/country are you in?). All species ID posts should be as detailed as possible to ensure you receive the best and most accurate answer.


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What was the largest flying insectoid pollinator?
Megachile pluto is a large resin bee whose body length may reach 38 mm and a wingspan of 63.5 mm. But that's nothing compared to the prehistoric and extinct Meganisoptera including the Meganeura, which had 'dragonflies' whose wingspan exceeded 70 centimeters!
There are "recent studies" linking animal gigantism in the Paleolithic to the increased atmospheric oxygen content.
Considering the size of some prehistoric insects I can't help but wonder: how big was the world's biggest insect(oid?) flying pollinator?

Define what criteria you're using for big: wingspan, body length, mass, or ?  Also, if the Meganeura were like modern dragonflies, they were probably predators, not pollinators.

Good question. Wingspan might be a fairly good measure, or body length. With no answers so far I'll gladly settle for ANY measure of size at this point.
-- As for the huge dragonflies being predatory? I'll be in my bunker.

keep in mind flowering plants did not evolve until the Jurassic.

Meganeura is from the carboniferous 360Mya, currently the biggest non insectoid is an 8 inch hummingbird. https://en.wikipedia.org/wiki/Giant_hummingbird?wprov=sfla1

Currently the best fit is probably a 28cm butterfly, lepidoptera fossils say its the biggest known insectoid pollinator, although it seems resonable that a 50+ cm lepidoptera can have been around recently.

@aliential: I'd say the largest non-insect pollinator is probably H. sapiens.  It's a learned behavior, though.  For mass rather than wingspan, I'll offer the hawk moths, some of which are indistinguishable from hummingbirds without close examination.


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Meaning of "optical" in "Optical cap, 8X Strip" (used in qPCR)
I'm translating an English document that lists equipment used in a qPCR procedure:

Reagents/Materials

Optical cap, 8X Strip

I googled and found that the meaning of this line is "a strip of 8 caps for PCR tubes". What is the meaning of optical though? I'm not sure how to translate it into Russian.
Does the word indicate the the cap is fully transparent? Or that the cap creates no visual distortion (it is flat)?
Screenshot:

I'm googling but I can't seem to find any definition of "optical cap". It is used in a lot of books and documents as if the term is self-evident, while it's not.

I think it means flat-top, please refer to the article.https://www.thermofisher.com/order/catalog/product/4323032#/4323032

Does the word indicate the the cap is fully transparent? Or that the cap creates no visual distortion (it is flat)?

Yes and yes. As an example of the different kinds of PCR tube caps, refer to the cap options available from Thomas Scientific:

Available with a domed, flat frosted, or flat clear caps for qPCR. [emphasis mine]

For most lab plastics, "optical" refers to the surface between the camera/detector and the sample.  Another example: for plate-based fluorescence assays where the plate reader takes measurements from below  the plate, one might use a Nunc MicroWell 96-Well Optical-Bottom Plate from ThermoFisher. Usually, such plates also have opaque walls to prevent signal bleed from adjacent wells.


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Would BMP7 introduced to a Petri dish with cartilage cause chondrocytes to replicate?
Chondrocytes are the cells that make up cartilage. As I understand it, the best growth factor that signals replication of chondrocytes is Bone morphogenetic protein 7.
If supplied with a sufficient source of nutrients and a growth factor, would those chondrocytes begin to replicate?
If you prepare a Petri dish full of blood and cartilage and add BMP7, would the cartilage start to grow? Are those two questions the same?

Hello and welcome Delaney Fitzpatrick.
BMP7 - Bone morphogenetic protein 7 - Plays a role in cartilage homeostasis.
Chondrocytes - A cell which has secreted the matrix of cartilage and become embedded in it.
Chondrocytes therefore make cartilage. Cartilage unfortunately has a poor regeneration capacity.
BMP7 stimulates Chondrocyte division
Naturally the question then becomes, does BMP7 also increase cartilage production?
A paper from 2009 - Chondrocytes that expressed increased levels of BMP7 in defected rabbit knees showed statistically significant repair when compared to controls.
Although an early study, it does suggest that BMP7 may improve cartilage repair.


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How does salicylic acid work on acne?
There are claims that salicylic acid has an effect on acne. I have done preliminary research and found multiple sources saying:

"Salicylic acid [can] help prevent future breakouts." - https://www.healthline.com/health/skin/salicylic-acid-for-acne
"Salicylic acid penetrates into your skin and works to dissolve the dead skin cells clogging your pores." - https://www.healthline.com/health/skin/salicylic-acid-for-acne
"Salicylic Acid works by opening the pores and killing the bacteria inside." - https://www.reddit.com/r/askscience/comments/tuqt2/how_do_things_like_salicylic_acid_and_topical/
Pointing out that salicylic acid is used to treat acne, but no explanation as to how. - https://en.wikipedia.org/wiki/Medical_uses_of_salicylic_acid
"Salicylic acid modulates COX2 gene expression to decrease the formation of pro-inflammatory prostaglandins. Salicylate may competitively inhibit prostaglandin formation. Salicylate's antirheumatic (nonsteroidal anti-inflammatory) actions are a result of its analgesic and anti-inflammatory mechanisms. Salicylic acid works by causing the cells of the epidermis to slough off more readily, preventing pores from clogging up, and allowing room for new cell growth. Salicylic acid inhibits the oxidation of uridine-5-diphosphoglucose (UDPG) competitively with nicotinamide adenosine dinucleotide (NAD) and noncompetitively with UDPG. It also competitively inhibits the transferring of glucuronyl group of uridine-5-phosphoglucuronic acid (UDPGA) to the phenolic acceptor.", again, with no source. - https://en.wikipedia.org/wiki/Salicylic_acid
"Because BHAs [specifically salicylic acid] are oil soluble, they’ll be able to penetrate deep into the sebum filling up your pores, loosening the gunk to make it easier to remove" - https://fiftyshadesofsnail.com/2015/03/28/how-to-shrink-pores-temporarily-plus-3-pore-myths/
"Salicylic acid dissolves well in vegetable oils." - https://chemistscorner.com/cosmeticsciencetalk/discussion/2514/how-to-dissolve-salicylic-acid-or-aha-acid-in-oil
"Salicylic acid helps ... by dissolving the type of skin debris that clogs pores and causes acne" - https://www.huffpost.com/entry/heres-exactly-what-salicylic-acid-does-to-your-skin_b_578cff25e4b07cc1115aa329

Therefore, the sum of claims add up to that salicylic acid

Penetrates skin.
Dissolves dead skin and skin debris.
Separates skin.
Opens pores.
Reduces inflammation.

If I suppose the anti-inflammatory properties of salicylic acid is well-documented by virtue of being similar to acetylsalicylic acid, then 5) can be intuitive. My remaining questions are as follows.

How does salicylic acid penetrate skin? Which part of the skin? What does it do there? How does it penetrate skin better than other amphiphilic molecules?
How does an acid dissolve dead skin and skin debris? How much acid, at what concentration, at what temperature, and for how long?
Through what mechanism does salicylic acid "open pores"? Additionally, if opening pores is one of its selling points, is it not true that ordinary soap also removes dirt from pores?

Most of the claims above are from unreliable sources. https://scholar.google.com/ might be a better place to search. Since this is a medical topic, https://pubmed.ncbi.nlm.nih.gov/ would also be a good choice. Apart from these, you could look up the references in the Wikipedia article.


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What is the primary cause of death for small animals in urban and suburban areas?
Small birds (sparrows, robins, jays, finches) and mammals (squirrels, rats, opossums, raccoons) are a common sight in many urban and suburban communities with green space. However, I observe carcasses of these animals relatively infrequently.
I imagine that the following are some of the most common causes of death:

Predation (the species I mention are small, and somewhere in the middle of the food chain)
Age-associated decline in foraging ability, leading to starvation
Disease
Fatal contact with infrastructure (collisions with buildings or wind turbines, contact with electricity lines)

I can think of two reasons why we don't see carcasses very often:

predation is the most common cause of death
individuals that succumb to disease/starvation end up in their nests/dens

Is this plausible? Has this been studied systematically, e.g. in populations of birds with tracking bands?

Cats, windows, and cars appear to be the leading causes of avian (bird) deaths:

 Major sources of anthropogenic bird mortality in the USA [from Fig 2b, Loss et al. (2015)]
Cats and vehicles are likely leading causes of death for many small non-avian animals as well.

Loss et al. (2013) estimated that 6.3–22.3 billion mammals are killed by free-ranging domestic cats in the USA each year.

The Wikipedia article for roadkill provides the following discussion of vehicular deaths:

In 1993, 25 schools throughout New England, United States participated in a roadkill study involving 1,923 animal deaths. By category, the fatalities were: 81% mammals, 15% bird, 3% reptiles and amphibians, 1% indiscernible. Extrapolating these data nationwide, Merritt Clifton (editor of Animal People Newspaper) estimated that the following animals are being killed by motor vehicles in the United States annually: 41 million squirrels, 26 million cats, 22 million rats, 19 million opossums, 15 million raccoons, 6 million dogs, and 350,000 deer.

I welcome others to corroborate these claims with a more reputable source in the comments. (I will try to do so myself and will update as I find them.)

DISCALIMER: I was previously only aware of Loss et al.'s work, so the emphasis of my post is on their papers. I did not otherwise search exhaustively for data. Noticeably absent from my post is mention of deaths caused by pest control (trapping and poisoning). I may update this post with more info as I come across it.

 Citations
Loss, S.R., Will, T. and Marra, P.P., 2013. The impact of free-ranging domestic cats on wildlife of the United States. Nature communications, 4(1), pp.1-8.
 Loss, S.R., Will, T. and Marra, P.P., 2015. Direct mortality of birds from anthropogenic causes. Annual Review of Ecology, Evolution, and Systematics, 46, pp.99-120.

It's quite hard to generalize, but this paper seems to suggest anthropogenic mortality increases with body size in mammals. Hence, small mammal mortality would be caused more by predation/competition/diseases than roadkill, imho.
To answer your question why we don't see so many carcasses, I would say that scavenging is very common and i don't see why a 'perfectly fine' protein source should be wasted.

The overwhelming cause of death of small animals ( and deer) that I see is that fearsome predator , the Toyota, Ford, Chevy, etc; AKA roadkill. I am in suburban E.TX. Other than that ,Coopers Hawks are common here and take many small birds. Also barred Owls are common and they are eating something. I think it is politically incorrect to estimate how many birds and bats are killed by wind turbines so those will be difficult numbers to get and they are not located in suburban areas. There are individual studies such as the local college studied the life cycle of Carolina Wrens ; but I doubt you will find anything covering  the range you are asking about.


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Meaning of "standard reactions" in a DNA extraction procedure description
From a DNA extraction procedure description (an in-house pharma document I'm translating into Russian):

Preparation of Standards

All the standard reactions should be prepared at least in duplicates. The template DNA stock (CHO cell genomic DNA) should not be less than 100 ng/μL concentration.

Does "standard reactions" here mean what it says, or does it really mean "reactions with standards" (reactions using standard samples)?
P.S. It is part of a qPCR procedure to quantify host cell DNA content. The company is producing a monoclonal antibody drug and is describing its internal procedures. As a translator I cannot disclose the document in full.

https://meta.stackexchange.com/questions/320052/why-are-images-of-text-code-and-mathematical-expressions-discouraged

How can we possibly know?

In order to quantify a target using real-time PCR, each run must include a standard curve of your target DNA. This is typically done by making serial dilutions of some known quantity of template DNA, with each dilution assayed in duplicate or triplicate on the same plate as your experimental samples of unknown quantity. A standard-curve is also important for determining assay validation statistics like amplification efficiency (reference).

Does "standard reactions" here mean what it says, or does it really mean "reactions with standards" (reactions using standard samples)?

Since your protocol is designed to quantify host DNA, I would interpret the phrase "standard reactions" as referring to the actual qPCR reactions containing standard dilutions, not necessarily to the DNA extraction procedure. The reason there is a specified minimum concentration for the standard template DNA is likley a quality control check to prevent errors caused by degradation of DNA standards during storage or from freeze-thaw activity. The quality of your qPCR data can only be as good as the quality of your standard curves.
Reference:

Real-time PCR Handbook, published by ThermoFisher Scientific (Lifetechnologies.com)

Is this PCR or just DNA extraction and if so, what is the source material?
If it is just DNA extraction, maybe the standard reaction means to extract some given standard sample DNA (CHO cell genomic DNA?) to optimise the yield and reaction conditions.
You would ideally use these same reaction conditions to extract other genomic DNAs.
Also, is the CHO genomic DNA included in the kit?

It is part of a qPCR procedure to quantify host cell DNA content. The company is producing a monoclonal antibody drug and is describing its internal procedures.


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How quickly are plants able to sense changes in light intensity?
Evidently due to the process of photosynthesis, plants are able to "sense" light (as demonstrated by the phototropic response). My question is, how quickly are plants able to perceive changes in light intensity?
I.e. if there is a strong light shining on a plant, and at t=0 the light is switched off, is there some delay τd before the plant exhibits a response to the change in light intensity?

Hi, welcome to StackExchange Biology. While this is an interesting question, it could benefit from a look at these points: 1. 'Evidently due to the process of photosynthesis, plants are able to "sense" light (as demonstrated by the phototropic response)' This statement needs modification as photosynthesis and phototropism are very different processes. (Though one could argue that phototropism evolved to increase the efficiency of photosynthesis.) 2. It would also be nice to include (in the question body) efforts you made to answer the question: what books/sites you read, what you found out.

Hi. As a preface let me apologize for my lack of clarity / background knowledge. Biology is not my field of study, but I have been curious about this question for a while. To address your concerns: 1) By this I mainly meant to indicate that plants evidently do have some pathway for sensing the intensity of light. Phototropism is evidence of this, as it shows that plants have some "awareness" of the location of a light source. 2) I have searched for research relating to the response times of photoreceptors in plants, but have only been able to find information such as absorption patterns.

I should add that some of my confusion comes from not understand the difference between animal and plant photoreceptors. If they are very similar, then it could be inferred that a plant's response time would be very similar to that of a human. However, I imagine there is very little evolutionary advantage for plants to have a fast response time to changes in light when compared to animals.

Thanks for the clarification. Please edit your question body and incorporate your comments into it (in a concise manner). This will improve your question and increase the chances of getting a useful answer.

The delay for UVR8 photoactivation seems to be in the range of picoseconds depending on the wavelength:

Global analysis in terms of a model of parallel decaying
components indicated four lifetimes of 14.7 ps, 370 ps, 1.9 ns,
and 5.9 ns.

The photodynamics of the Trp ensemble in UVR8 can be summarized as
illustrated in Figure 5B. We observe excited state decay in the
few-hundred- picoseconds to nanoseconds time domain to the triplet
intermediate U460.

For a better understanding of photoactivation mechanism times, you can read the following article:
Proton-Coupled Electron Transfer Constitutes the Photoactivation Mechanism of the Plant Photoreceptor UVR8
Journal of the American Chemical Society 137(25) · May 2015


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Calcium reabsorption from egg shell during embryogenesis, how is carbonate neutralized?
As the embryo reabsorbs calcium from the shell, it also reabsorbs an equal quantity of carbonate. Calcium is in quite high concentrations in the body, the same molarity for carbonate causes a very alkaline environment. Carbonate has a pKa near 10, seen in that the egg white in "food eggs" (non-incubated and non-impregnated) becomes alkaline as the egg ages, approaching pH 9 to 10.
Throwing some numbers in there, assuming 2.2 gram of CaCO3, 8% reabsorbed to cause the average 8% thinning documented here (this is also just day 3-5 I think. ) 2.2 gram*8% = 0.176 gram carbonate released. The molecular weight of carbonate is 61 g/mol, 0.176 g / 61 g/mol = 0.003 mol = 3 mmol. If newborn chicken weighs 85 gram, and is 70% fluid, 85 gram * 70% = 60 gram. 60 gram is 0.06 L water. 3 mmol carbonate equivalent to 3 mmol/0.06 L = 50 mmol/L. The solution gets a pH of 11, and if you add 25 mmol/L of hydrochloric acid it is still at pH 9.2.
How is that carbonate neutralized?
At least 1 carbonate ion in 5 can be neutralized by bone formation, since hydroxyapatite has a ratio of 5:1 calcium to hydroxide ions, and, 99% of calcium is in bone (assuming somewhat similar ratio in infant as well. ) What about the other 4?
EDIT: A user David emphasizes that Wikipedia's entry on Calcium carbonate gives a pKa of 9. I based pKa closer to 10 on equilibrium between carbonate and bicarbonate. 9 or 10 does not really change the question that much since its about the huge quantity of base, quite strong in either case. I used http://www.aqion.onl/ for pH calculations giving pH 11. Feel free to use the correct value.
EDIT: Carbonic acid from CO2 from cellular respiration was mentioned. Carbonic acid from cellular respiration is at least part of it. But I don't know if it is all of it or close to all of it. 3 mmol of calcium absorbed (see Crooks, 1973) if average egg volume is 50 mL, molarity is 60 mmol/L, and this is as carbonate which saturates pCO2/H2CO3/HCO3-/CO3^2- as well.
EDIT: Also quite a lot of uric acid created, 2.3 gram per L by day 13, jbc.org/content/70/2/535.full.pdf, molarity 14 mmol/L.
SUMMARY: Bone formation likely takes care of 1 in 5 carbonates. Carbonic acid from cellular respiration, uric acid from nitrogen excretion, both contribute. Other factors?

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

Carbonic acid from cellular respiration, like Trond mentioned, and uric acid from nitrogen metabolism, and, bone mineralization, are large sources of acid, might be enough to neutralize 3 mmol (Crooks, 1973; Tuan, 1986) CO3.
Calculations
3 mmol CO3 in a chicken that weighs 45 gram when newly hatched, 45 gram * 60% = 27 g = 27 mL of water, is 3 mmol / 27 mL = 111 mmol/L. The carbonic acid is likely around 30 mmol/L, and shares an equilibrium with the carbonate ion which might reduce that number. Acid from bone mineralization is 1:5th of CO3, 111 mmol/L / 5 = 22 mmol/L. The upper bound for carbonic acid and mineralization is then 30 mmol/L + 22 mmol/L = 52 mmol/L. This leaves 111 mM - 52 mM = 59 mM. Uric acid is up to 14 mmol/L by day 13 (Fiske, 1926), and, could reasonably increase up to 59 mmol/L.
References
Crooks, R. J., & Simkiss, K. (1974). Respiratory acidosis and eggshell resorption by the chick embryo. The Journal of experimental biology, 61(1), 197–202.
Tuan, Rocky S., and Tamao Ono. ‘Regulation of Extraembryonic Calcium Mobilization by the Developing Chick Embryo’. Development, vol. 97, no. 1, Sept. 1986, pp. 63–74.
Fiske, Cyrus H., and Edward A. Boyden. ‘Nitrogen Metabolism in the Chick Embryo’. Journal of Biological Chemistry, vol. 70, no. 2, Jan. 1926, pp. 535–56.

I was asked by a little notification to provide references. The point is, everyone knows cellular respiration releases CO2, everyone knows uric acid is how uricotelic animals excrete nitrogen, and everyone knows hydroxyapatite is 5 Ca^2+ +3 PO4^3- + OH-, acid excreted during mineralization therefore. The reference I did provide, I can also include the whole APA citation for it, here:
Crooks, R. J., & Simkiss, K. (1974). Respiratory acidosis and eggshell resorption by the chick embryo. The Journal of experimental biology, 61(1), 197–202.

Obviously, reference standards from 20th century aren't ideal way to record information but so there you go.


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What is the defining characteristics of a Gap Species?
For the following competitive exam question: A road is constructed through a tropical rain forest, following which a population of a species of butterflies declines. Which of the following is NOT  a possible explanation for the road causing a decline in the forest butterfly population?
The answer: The Road facilitates immigration of gap-loving species which compete with the forest species
What is the defining characteristics of a 'gap' species?

The previous answer from @Ark Lomas is true to the extent that gap-loving refers to preference of an open habitat. It was found that these species e.g. have improved flight abilities and are in general geographically more wide-spread.
Here is prove:
Ecology of Tropical Butterflies in Rainforest Gaps
J. K. Hill, K. C. Hamer, J. Tangah and M. Dawood
Oecologia
Vol. 128, No. 2 (Jul., 2001), pp. 294-302

Tropical forest gaps are ephemeral and patchily distributed within
forest areas and have very different light environments compared with
closed-canopy forest. We used fruit-baited traps to investigate if
gaps are exploited by more opportunistic butterfly species compared
with closed-canopy forest. Gaps supported a higher diversity of
butterflies in terms of species evenness but closed-canopy sites
contained species with more restricted geographical distributions.
There was little similarity between the assemblages of butterflies
trapped in the canopy and those in either gap or closed-canopy sites,
but the greater similarity was with gaps, and increased diversity in
gaps was partly due to canopy species turning up in gaps. Dispersal
rates (as measured by recapture rates) were higher in gaps and there
was evidence that butterflies in gaps had relatively larger and
broader thoraxes, indicating a flight morphology adapted for faster
flight. These results support the notion of a distinctive gap fauna
comprising more widespread, mobile species. Habitat modification that
opens up the canopy is likely to result in an increase in these
widespread species and a decline in understorey species with
restricted distributions.

a gap-loving species is a species that prefers existing in open spaces such as the gap that the road creates in the rain forest. I can't think of any organism native to rain forests that would be considered significantly gap-loving since most rain forest species rely on the trees and bushes etc... that the rain forest provides which therefore causes them to not prefer being exposed in the middle of a road.


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What is the name of this insect? It is from Punjab, India
What is the name of this insect? It is from Punjab, India.

It seems to be a bug that belongs the family Rhyparochrominae from the tribe Myodochini.
https://species.wikimedia.org/wiki/Myodochini
There are too many species for an inexperienced person like myself to know which particular one this photo belongs to.
These species I believe are known as seed bugs.

Welcome to Biology.SE! For identification questions please [edit] your post to include the size of this creature. The size can be an essential clue for identifications. ———  Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!


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Why is it (allegedly) dangerous to feed ducks with breadcrumbs and pieces of bread?
I used to go down to the local lake all the time with leftover bread and throw little pieces of it to the hungry duckies, who very eagerly fetched it and ate it while happily quacking away.
I thought I was doing them a favour, but apparently, it's bad for them? Can even kill them?
Is this really true, or is this a false rumor spread by people who don't like ducks and want to deprive them of their favourite food?
Why exactly would bread, especially soaked in water, somehow damage wild ducks? Isn't it a very neutral food which feels filling and nice for the ducks? Nobody says that they have to only eat bread thrown from humans -- they can still eat little insects and algae in the lake or whatever they normally/naturally eat.
What exactly can happen? I never noticed any dead ducks or ducks in pain whenever I visited them. They seemed to love the bread and consider it a luxury dish from a fine restaurant from their perspective.

This web page from National Geographic can give you some idea: https://blog.education.nationalgeographic.org/2017/03/27/stop-feeding-ducks-bread/
Also, you can give a look to this page from the Wildlife center of Viginia:
https://www.wildlifecenter.org/problem-feeding-ducks

This question was asked and answered on Skeptics.

the simple answer to this is white bread is carbohydrate(sugar)and not a lot more so it causes malnutition.


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Why do the eyes of this cat have different colours when viewed from different angles?
Why do the eyes of this cat have different colours when viewed from different angles?

Both of the eyes of this cat appear yellow when looking straight at the camera.

However, when the cat looks at an angle to the camera one eye appears green. Unfortunately, the cat is not mine and I don't have many more pictures of it.
I have also noticed that my own eye which appears dark brown from straight on, looks lighter when viewed from an angle.
Why does this happen? Is there a special property of the iris that lends itself to such behaviour? In this website, it is mentioned that the colour of the iris varies with the angle at which it is viewed but no explanation is given.


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Which chromosome of the two contained in a haploid cell goes into the diploid cell after fertilisation?
I am totally new to biology and I have a very stupid question. In the typical representation of meiosis, haploid cells contain two different chromosomes, resulting from the crossing-over process. But diploid cells have two homologous copies of each chromosome, usually one from the mother and one from the father. So, since there are two identical copies of the same chromosome for each parent, it means that each haploid cell brought only one out of two chromosomes into the zygote. My question is: how is this chromosome selected? Is it a combination of the chromosomes contained into the haploid cell? Is it one of the original two, while the other one is discarded in the fertilisation process?
I'm sorry if my question is not clear. Thanks.

Have you looked at Meiosis II, the second part of the process?

I am not sure about where is your confusion. Do you understand that homologous chromosomes are represented as having same size in the image? So the chromosomes in doughter niclei II are definitely not homologous?

Can you provide an image presenting what confuses you? "Haploid" by definition means only one chromosome, so I think there is something off here. Remember in meiosis (re: Bryan), 2n (diploid)-->4n -->2n (meiosis 1)-->1n (meiosis 2, haploid), e.g. https://en.wikipedia.org/wiki/File:Meiosis_Stages.svg. The terminology gets hairy because people don't like calling it 4n before meiosis 1, but that's still what it is.

@MaximilianPress I think a better way to put it would be 2n,2c(diploid)-->2n,4c(DNA replication)-->n,2c(meiosis 1)-->n,c(meiosis 2) since the 2 chromatids are still attached at the centromere after DNA replication.

Thank you guys. I think that my confusion about this representation arises from me thinking that the two same-color chromosomes in the first diploid cell were identical. I hadn't noticed the difference in size. So let us take the first haploid cell from above. The longer chromosome will be the homologous chromosome of the same-size one coming from the other gamete? (The same for the short one)

@Luigi Yes, I think that they usually include more than one non-homologous chromosome in the models to remind us that most (all?) organisms that do meiosis have >1 chromosome in their genome (e.g. humans have 23 chrs in the haploid state). So it's always super important to sort out homologous vs. non-homologous chromosomes before you do anything.

@trinitrotoluene I see the point, but I have always found that logic to be extremely confusing- it looks like the chromosomes come from nothing if you count that way! IMO much simpler to just say 4n, even if they take away my geneticist union card.

@MaximilianPress I guess it just depends on whether you count chromosomes by the number of centromeres or consider the number of chromatids instead

@Luigi Since you were also confused about the colors: The same colored chromosomes represent chromosomes coming from the same parent. So for example red chromosomes came originally from mother and gray from father. Thay do this to show that after crossover there are "mixed" chromosomes - patchwork from both parents.


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Should there be a distance between the terminator of a protein with the promoter of another one?
I want to do an overlap PCR to get the desired gene product I want. Can I put the promoter of the second protein just after the terminator of the first protein, or should there be some distance between them filled with random bases?!


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What is meant by 'proteolytic activation' of a virus?
Noob biologist here. I suspect that at the first stage this means 'activating the virus by lysis of a surface/spike protein'? Seems kind of obvious, but I put it here in case 'proteolytic activation' is not in fact merely a subset of 'virus activation', and means something slightly different.
Second, if the above interpretation is correct, what precisely do we mean by virus activation? Is it the release of viral RNA into the host cell cytosol? This would be my guess, as it is necessary (sufficient?) for replication of viral RNA to commence, and viral replication to occur. Another idea is that 'virus entering host cell' is enough to constitute viral activation, though I suspect some viruses can enter cells and remain dormant there. Hardly seems like activation to me.
Would really appreciate clarification of this terminology so I don't have misconceptions when reading literature.

I don’t think “virus activation” means anything more than making a virus that is in an inactive state active. Why would you think otherwise and that it implies anything more specific? (And, unless you’ve performed some experimental procedure to remove organelles, it’s cytoplasm, not cytosol.) “Proteolytic activation” without any further qualification, only adds the mechanism (I assume you know what proteolysis is), so to find out its likely context I had to Google. You can too, but it’s sloppy writing.

@David but what is the defining difference between an active and inactive virus? What is the necessary process that makes an inactive virus now active? Is it the injection of rna into a host cell? Are the released replicated viruses then inactive until they start infecting other cells? Sorry if I'm being pedantic, but I really want to be clear on what is being referred to in the literature.

My point is there is no defining difference other than the English meaning of the word “inactive”. I hadn’t in general considered viruses having in inactive state, and there are so many different viruses that there can be no commonality. If someone writes “proteolytic cleavage of such and such a virus protein so that it is able to initiate membrane fusion” and thereafter abbreviated this as virus activation, that means something. Otherwise, not. As I wrote, sloppy writing — and incomprehensible too. The Emperor is naked.

Viruses all have some mechanism to enter cells' lipid membranes, and these need to be prevented from activating prematurely. Often this means the virus is in an inert state while it is assembled and trafficked out of the host cell, then activated by some chemical signal such as the low pH of inner endosomes. So "activation" is usually going to refer to a chemical change that removes the barriers to cell entry.
For example; in flaviviruses such as Zika or Dengue, the E glycoprotein that handles most of the host entry functions is assembled while bound to prM protein. Once virions are assembled with E in an inert arrangement, prM is proteolytically cleaved. When the new host cell absorbs the virion into an endosome and lowers the pH to digest it, the E glycoproteins rearrange into spikes that can penetrate the endosomal membrane and induce fusion with the viral membrane. If prM isn't cleaved, the virus can't infect cells. Here's a recent paper that discusses this process, with high resolution structures. For these viruses there are two rounds of activation, and only the first one is proteolytic.

For coronaviruses some cell's surface or endosome protease cuts some part of the viral surface protein (mainly S2' site but also pre-priming at S1/S2, the interaction of both is still unclear) which triggers the membrane fusion


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Why is it that only humans are ashamed of certain critical biological activities
Humans are ashamed of certain activities that are critical to our survival.
Examples: mating, defecation, exposing certain parts of our bodies
This restricts some activities from being performed while others are around (usually only if others are also humans).
Perhaps it is because we are the only species who is capable of feeling ashamed?
What are the advantages of this mechanism in terms of survival as a species?

Welcome to SE Biology. In my opinion this is not the kind of practical biological question that can be answered in an objective manner, but is one the answers to which will be opinions and lie in the area of psychology or sociology. That is why I have voted to close it.

I think there is certainly an interesting biological question underlying the evolution of e.g. fecal avoidance, which has been studied in a variety of organisms (e.g. https://pubmed.ncbi.nlm.nih.gov/24027342/). Unfortunately, when such questions are applied to humans, they often end up descending into telling just-so stories about human evolution.

Some humans are, not all humans, nudity for instance is definitely cultural. Don't confuse your cultures behavior  with universal human behavior.

@John Can't culture have a genetic component?

@RodrigodeAzevedo cultural behaviors generally have no genetic component they are purely learned behaviors. This is easily seen by the behaviors of people raised in drastically different cultures than their ancestry. Humans in general have so little genetic variation claiming anything cultural has a genetic component would require a great deal of evidence.

@John Studies involving identical twins adopted by different families would suggest that it is more complicated than that. A proper definition of "cultural" would be the starting point.


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Is natural selection actually random?
In the Theory of Evolution, two main factors take place:
One is random, which are the different mutations that organisms' DNA suffer. This process adds genetic variability to a given population.
The other one is not random, which is natural selection. It is not random because it will only select  those organisms which are better capable of surviving to the conditions of their environment.
Most likely I am wrong and I would like to be corrected, but I was thinking that, since natural selection depends on mutations and the conditions of the environment, and since those conditions can be formed by random processes, wouldn't it make natural selection as actually random?
I mean, this is probably an over simplistic analogy, but take a group of mammals which suffer a great series of mutations in a short period of time, and separate into two species of mammals: one group of animals with hair and the other group has no hair at all. Suddenly, one day starts to snow. We could expect that the second group would most likely go extinct, while the mammals with hair would survive. Since the weather is based on random processes and since natural selection in this example would be based on the mutations that the animals suffered and the weather as well, wouldn't natural selection be a fundamentally random process?

Note that random processes can have systematic outcomes. E.g. random movement of gas molecules has a non-zero pressure as outcome. (Systems that do not behave in this way, i.e. where random processes do not have predictable systematic outcomes but the outcome stays unpredictable are called chaotic)

You are right in a sense. The processes which generate mutations in an organism are stochastic (not quite exactly random, but in most organisms they are effectively random for all intents and purposes). In terms of population genetics, it is considered that mutations occur randomly across the genome and have an equal probability of occurring at a given base pair.
The environment is also random/stochastic in the sense that it occurs mostly independent of mutations which have occurred. Whether or not it is cold one year is independent of the mutations which have occurred within an organism. (Actually that's not quite correct since organisms can generate their own environmental niches and evolve according to them, but I think that is beyond the scope of this question).
What is not random is how the frequency of genetic variants respond to different environments. This is natural selection. Over the long run, we expect genetic variants which increase the fitness of an organism within a given environment will increase in frequency and vice versa. There is a large body of theory and evidence which predicts how a particular variant may change in frequency in response selection of a particular pressure.
As @jamesfq correctly points out, a nice example of selection being non-random on the macro-scale is convergent evolution. For example, aquatic animals such as fish, certain mammals (e.g. Dolphins) and Amphibians and Dinosaurs have independently evolved streamlined bodyplans in order to conserve energy when moving through the water.

As an example of non-randomness, see examples of parallel evolution, where distantly-related creatures evolve similar forms because of environmental pressures.  E.g. Ichthyosaurs, dolphins, some sharks, and some fish all evolved similar body plans, even though creatures with very different body plans - plesiosaurs, rays - can be successful in the same environment.

Or as another example the very fact you can predict a hairy species to survive better in the cold makes it non-random.


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Why are organs not harvested from deceased cancer patients?
From my understanding, cancer is not contagious, and if a cancerous cell from a patient is introduced to a healthy person, then the immune system of the latter can destroy this cell. In such a case, why are internal organs from cancer patients not used for donation? Is this because there is a small probability of the immune system failing? Isn't there any other way to make these organs usable again?

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

On of the main reasons why cancers are normally not transmissible between different people is basically the same reason as why organ transplants are difficult: histocompatibility.
Every human cell carries a set of human leukocyte antigens on its surface, and (except for identical twins) every person's cells carry a different set of antigens.  Any cells that don't carry these specific antigens are treated as foreign by the immune system and rapidly attacked and destroyed.
Normally, cancer cells carry the same antigens as the host cells they arose from, and thus are mostly left alone by the immune system.  However, when tissue (whether cancerous or not) is moved from one person's body to that of another, the recipient's immune system recognizes the transferred cells as foreign, since they carry the wrong antigens, and tries to destroy them.  In the case of organ transplants, this leads to transplant rejection.
The main ways to avoid transplant rejection are 1) choosing donors that happen to carry a similar set of antigens, either due to a close genetic relationship or just by chance, and 2) treating the recipient with immunosuppressant drugs to prevent the immune system from attacking and destroying the foreign tissue.  With appropriate choice of donor and a well chosen drug regime, the rejection can often be prevents, or at least mitigated  and delayed.
But the same methods that are used and needed to prevent rejection of the transplanted organ will also, just as effectively, keep the recipient's immune system from attacking any other cells presenting the same foreign antigens — including any cancer cells that might have been inadvertently transferred along with the transplanted organ.  Thus, transplanting tissue that might be infected by metastasized cancer cells inevitably risks infecting the recipient of the tissue with the same cancer as well.
Nor is this just a theoretical concern.  For example, as pointed out in Chris's answer, in 2007 four women became infected with breast cancer after receiving organs from the same donor (who was not diagnosed with cancer at the time of her death, and thus qualified as an organ donor).  Three of the recipients died of the cancer, while the fourth survived after the transplanted organ was removed and immunosuppressant drug treatment was stopped, allowing her immune system to fight the foreign cancer.

Ps. The other main reason why cancers don't usually spread from one person to another is that, unlike infectious viruses, bacteria and other parasites that have adapted to the lifestyle of a transmissible pathogen, most cancer cells simply don't have any effective mechanism of getting out of their current host and into a new one.  That's why even identical twins aren't generally at significant risk of contracting cancer from one another through casual contact, even though their cells bear the same antigens.
Even so, a few lineages of cancer cells have managed to overcome both of these obstacles and to survive their original hosts as transmissible diseases.  While no such clonally transmissible cancers are known to naturally occur in humans (the few recorded cases of human cancer transmission arising from organ transplants or other surgical procedures, and rarely if ever leading to secondary transmission), some examples are known in other species.  These include the canine transmissible venereal tumor, a sexually transmitted cancer that infects dogs, coyotes and related species, and the devil facial tumor disease, a transmissible cancer that infects Tasmanian devils and is believed to be mainly spread by biting.

In humnas, HPV is a readily transmitted virus which is commonly associated with cervical cancer. Although you can't really catch cancer via HPV the way you catch a cold, there is significant similarity in HPV DNA and that found in cervical cancer cells.

There are different reasons why cancer patients are mostly excluded from donating organs.

Although the probability of transmitting cancer is small, it is not zero. Also tumors tend to form metastases over time, which spread throughout the body. It is possible that a cancer has formed metastases in other, distant organs, which are too small to detect. Since recipients of organs have to take strong immune suppressing medication to prevent the rejection of the transplant, the immune system might not be able to fight the cancer cells anymore. Because of this medication, transplant patients already have a higher chance of getting cancer, because their immune system does not capture cells when they go rogue. See reference 1 for a more general description and 2 for the detailed report, reference 3 for the higher cancer risk of transplant patients.
Tumors can go dormant when they are treated with chemotherapeutics to evade destruction, but these dormant cells can re-wake. If this happens after the transplantation of an organ, this is obviously bad for the recipient. See reference 4 for details on mechanisms.
Cancer patients who died from the disease have often been treated with agressive drugs like chemotherapeutics. While these attack mostly the fast dividing cells of the tumor, they also have more or less strong side effects on the body. A lot of organs are simply not in the state (or have a strong chance of being in this state) anymore to be transplanted. Nobody wants to transplant a dysfunctional organ. See reference 5 for details.

References:

Cancer Spreads from Organ Donor to 4 People in 'Extraordinary' Case
Transmission of breast cancer by a single multiorgan donor to 4
transplant recipients
Cancer in the Transplant Recipient
Tumor dormancy as an alternative step in the development of
chemoresistance and metastasis - clinical implications
Long-Term Side Effects of Cancer Treatment

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

"Tumors can go dormant when they are treated with chemotherapeutics to evade destruction". Why do tumors have this ability? I mean, tumors don't learn or evolve, do they?

@MatthewChristopherBartsh This is a phenomenon called senescence, look for example into this paper. Additionally tumors can evolve (or single cells do, not whole tumors to be precise) as a chemotherapy exerts a very strong selective pressure.

I had a look at the paper and this one https://pubmed.ncbi.nlm.nih.gov/15814644/, which uses the word 'evasion' (you used 'evade'). Are these words being used in some jargon sense I don't know about, because otherwise it seems to imply intent on the part of the tumor. How could anything like intent evolve in tumors, when they have no gene pool. In fact, if anything cancer should evolve to let the body live, because that way the cancer genes, so to speak, might get passed on. If you see what I mean.

@MatthewChristopherBartsh There is no intent in tumors. Senescence (or call it evasion) happens. It enables cells to survive which might otherwise be killed. Same is true for adaptations. Here you usually have further mutations which give these cells under the treatment conditions an adavantage. This is selection under a highly selective pressure.


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Is magnetic resonance microscopy appropriate for investigating ion-channel flow?
I've been looking into ways to characterize the elecrophisiology of neurons for cell signaling and I came across magnetic resonance microscopy as a tool for gaining images of neuronal activiy at a large scale.
This made me question, is it possibly to take a timeseries video of an active neuron and view the actual signal flow through and outside of it?

Clarification
I am unclear of your aim. What feature of elecrophisiology do you want to characterize?
What do you mean by large scale? E.g. Micrometers (μm),  Milimeters (mm) or Centimetres (cm).
Magnetic resonance microscopy imagings at Micrometers (μm).
Answer
An established way to observe neuron propagation is the use of calcium imaging. You can take a video under a fluorescent microscope to observe (Not measure) elecrophisiology. Also I believe this technique may provide the 'larger scale' you are seeking.
More On Calcium Imaging:
https://www.cell.com/neuron/comments/S0896-6273(12)00172-9

Ah I wasn't aware of calcium imaging I will look into it. To clarify yes, I wanted to know if it is possible to inspect/observe signal propagation through a single neuron.

Excellent, I admire your curiosity.


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What is the mass of carbon dioxide absorbed by an oak tree in one year?
I want to understand the environmental impact of oak trees due to absorption carbon dioxide. So my question is, what is the mass of carbon dioxide absorbed by an oak tree in one year?

What's the difference between '$CO2$' and '$\ce{CO2}$' ? I'm new to SE.

Oh ok, thank you. I have now proposed an edit using that format. Will that be for an equilibrium reaction with k1 and K2 as forward and backward rate constants?

Sometimes, the simple solutions work well: CO2.

It's uncommon (and probably not that useful) to consider this sort of question from a "per tree" perspective. "Per tree" depends greatly on the surrounding environment. Instead, people typically approach carbon fixation from a "per area" perspective.

I upvoted @RodrigodeAzevedo  comment, but neither work in titles on the phone and the Math thingy is unreadable. In any case one has always to ask oneself why not just writing carbon dioxide? It’s not as if there’s any equation involved. So it’s not justified. So I’ll edit it.

@trinitrotoluene: The difference is that some people (and I'm one of them) haven't memorized the keyboard combinations or other gymnastics needed to get subscripts :-)  Just about everyone will recognize what you mean if you write "CO2", though.

This question is unanswerable as it stands.  How big an oak tree, a year-old seedling or the centuries-old oaks of English forests?  What species?   Quercus robur (the English oak again) or the often shrubby Quercus wislizeni found in interior California?  Just to pick two of many species of oak.

@David I have posted a question regarding formatting on meta. Please let me know of the accepted formatting on Biology.SE

Re: Bryan Krause's comment, measurements per hectare are common. However, if you can just estimate average trees per hectare, then it works out. But it still likely depends on the local climate, ecology etc. It also varies across the life term of the tree.
Some estimates have been made, such as in this paper (see Table 4), for Quercus rubra and 2 other hardwood species. They estimate that for the most mature trees, Q. rubra stores ~20 Mg/hectare total biomass, of which approximately half is carbon.
This is a little more than twice the biomass of the 8-year-old tree, so if we just linearly interpolate we could say that a hectare of oak stores ~1 Mg C per year. There are some problems with this- for example, older trees are likely to store much more than that, but it is not clear exactly how much variation there is over the course of an oak's life, and also there is likely variation between the sites in the study.
It is also clear that the other species measured, e.g. American chestnut, are more effective carbon sinks than oaks as young trees.
See the paper or this pop science article on the subject for more information. THere are also a number of papers citing that paper that may be interesting, such as this, this, and this.


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Can the axial length of the human eye decrease?
I understand that the axial length of the eyeball grows until you are around 20 years of age, which is why hypermetropia decreases with age but myopia doesn't. My question is: can the axial length of the eyeball decrease, and does it do so naturally?
I know that certain conditions can cause the axial length to decrease, such as very low pressure or disease, but my question is regarding a normal healthy eye.

Weihua Meng, Jacqueline Butterworth, François Malecaze, Patrick Calvas; Axial Length of Myopia: A Review of Current Research. Ophthalmologica 1 March 2011; 225 (3): 127–134. https://doi.org/10.1159/000317072

This study by Meng et. al. (2011) says that with current research we KNOW that the axial length decreases with age this same point was also in a different study based on the idea of a an emmetropizing mechanism for the adult eye but many people have criticised this study and due to this apparently the studies findings should be taken with a grain of salt but if this is the case why is it that many articles do say that the axial length reduces with age is there another study that shows this?

Scott A. Read, Michael J. Collins, Beata P. Sander; Human Optical Axial Length and Defocus. Invest. Ophthalmol. Vis. Sci. 2010;51(12):6262-6269. doi: https://doi.org/10.1167/iovs.10-5457.

This study by Read et. al. (2010) basically used lenses to create hyperopic and myopic defocus in participants and they measured the axial length of the eyeball after exposure to the blur. They found that the axial length did decrease in the case of myopic defocus and increased in the case of hyperopic defocus in order to create a clearer image by focusing the image on the retina. But if this article provides definitive proof that the eye does in fact change its axial length then why is that people still say it doesn't happen?
Also do we know which mechanisms allow the eye to determine whether it is myopic defocus or hyperopic defocus that is presented to the retina?
Lastly, if the eye's axial length is able to reduce wouldn't myopia have a cure or at least a method to reduce it based on the reduction of the axial length of the eyeball?
https://www.quora.com/How-can-the-axial-length-of-an-eye-decrease-as-they-say-that-it-does-with-ageing

Generally the axial length doesn't decrease:
graph
Although there is discussion of various conditions where it has been observed to decrease, i.e. nanophthalmos, microphthalmos, and retinoblastoma... A review of current research is here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5501611/ quote:
It is considered that the axial length reaches adult length by the age of 13 years, showing no further increase in length. Recent cross-sectional studies found that the axial length in older adults tended to be shorter, suggesting that it may decrease with aging. However, in a recent longitudinal study by He et al., slight increase of the axial length in adults (mean refractive error, −0.44 ± 2.21 diopters) was reported. Conversely, an increase in the axial length in adults with highly myopic eyes is common and has been previously shown in longitudinal studies [5–7]. However, to the best of our knowledge, there have been no studies directly comparing the increase in the axial length in adults with non-highly myopic eyes or highly myopic eyes. In addition, because previous studies on the axial length in highly myopic eyes have not compared between eyes with and without macular complications, their influence on the axial length remains unknown.
Can myopia be treated with a reduction in axial length? Presumably, yes it could, if opticians had figured a way to do it... Do you suggest that a drug or a medical intervention can flatten the entire eyeball a bit? perhaps a drug could but it would reduce the entire eyeball, you'd have to find a way to administer it. Apparently doctors haven't researched that option, but perhaps they will in future. Laser currently seems like a better way.
https://www.google.com/search?hl=en&biw=1706&bih=951&sxsrf=ALeKk01GuiHpl6-_fRp-Bg_UdsYOdqVzbg%3A1596509065944&ei=icsoX9aRObLMgweX6KboCQ&q=%22decrease+in+axial+length%22+of+optical
https://www.google.com/search?hl=en&biw=1706&bih=951&sxsrf=ALeKk03b75zOsA6CN_Ypqdv5v7hqfVWLbA%3A1596509091797&ei=o8soX8ySMIyqUP2dtvgI&q=%22reduction+in+axial+length%22+of+optical&oq=%22reduction+in+axial+length%22+of+optical

Hello, thank you for your answer. I understand that generally the AL doesn't reduce unless a disease is present but I'm slightly confused with the research that I linked above. In the research it says hyperopic and myopic defocus can cause the axial length to increase or decrease respectively, so why is it that we say the AL is unable to decrease am I missing something?

The statement in that paper is contradicted by the paper from 2017 which is a summary of current research, so perhaps they are thinking of eariler on. Teenagers and adults have constant AL.


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Easy and cheap antigen/antibody couple
For an application I need to find a cheap antigen and cheap correspondent antibody. The antigen can be literally any molecule that is cheap and potentially easy to produce and with a correspondent antibody that is cheap and easy to produce as well. I imagine this antigen will need to be a molecule that triggers very easily an immune response to result in a easy to produce antibody.
I have never worked in immunology so I don't know what system antigen-antibody to choose. I know pregnancy test are common so probably the antibody for Human chorionic gonadotropin (hCG) is easy and cheap to produce but I don't think hCG is.
 Are bigger molecules better than smaller ones as antigens? Any suggestion is helpful.

I am not experienced in this field but this could be helpful to you.

I think adding how you expect to use this will get you a better answer. For example, there are many protein purification systems that use protein or peptide tags that are recognized by antibodies, but that may not be appropriate for whatever you are planning ...

Really anything. I  like the avidin/biotin system suggested in the link that @trinitrotoulene shared in the comment. Doesn't necessary need to be antigen/antibody but it is preferable. Interesting the protein purification, I'll have a look since those peptide tags and antibody may be common and relatively cheap.

A good choice is the IgG/anti-IgG pair for cheap, easy to demonstrate/work with system. E.g. Goat-IgG coupled with donkey anti-goat IgG.  Just about any antibody supplier will have these.
These type of systems are the basic primary/secondary antibody bindings routinely used in immuno-assays, blotting etc. These may be mouse IgG coupled with a labeled anti-mouse IgG for example.
Reference
Wilson MS, Nie W. Electrochemical multianalyte immunoassays using an array-based sensor. Anal Chem. 2006;78(8):2507-2513. doi:10.1021/ac0518452


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How would one model a Neutrophil Extracellular Trap with Hookean Springs?
This is a question based in biology but involves a good amount of physics.
Given that a Neutrophil Extracellular Trap (N.E.T) behaves like an aggregate of DNA strands with citrullinated Histones and defensins such as Myeloperoxidase and Neutrophil Elastase, and that DNA itself can be modeled as a Hookean spring (maybe with a variable spring "constant"), I thought that it would be possible to model say a 100 uM X 100 uM Neutrophil Extracellular trap as a network of hookean springs.
I think that this would require one to ascertain the length of the DNA strands incorporated into the N.E.T as well as the configuration of these many strands. The configuration will determine whether the spring constants of each DNA strand are additive (for parallel springs).
Is there some approximation of configuration and DNA length I could use to maybe get one cumulative spring constant for a N.E.T of a given size or is more complex notation required? Also the purpose of my asking this question and even modeling a N.E.T as a network of springs is to gauge the compliance and compressive stress that can be generated by the N.E.T.


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Can we develop a virus which is amicable for us but deadly for SARS-CoV-2 and HIV?
I am not biologist and do not have special education in it etc.
It is know that in the wild, some species have their deadly enemies.
What I am suggesting is can we humans find/create virus that is amicable for us, but super deadly for SARS-CoV-2, HIV etc?
If I am not mistaken, there are plenty of native bacteria/viruses in human body.
As an option can we genetically modify one of them to turn them worst enemy for some kind of viruses like SARS-CoV-2  for restricted amount of time?
P.S
I am not a specialist, therefore I apologize if my questions are too naive.
With regards,
Almas

Viruses are obligate intracellular parasites. They act like a living organism only when they infect a cell. Apart from some protein structures which help them to attach and enter specific kinds of cells, viruses don't have enzyme systems that can be used for activities like "destroying other viruses".
A virus can not infect another virus as this would be a one time action. Viruses infect cells in order to replicate, a virus can't replicate by using another virus. So if you engineer a virus which will attach and destroy another kind of virus, it will be no longer a virus, it will be an unnecessarily complicated antiviral drug.
In addition to this point, you should consider that our bodies have leukocytes (white blood cells) which can identify and destroy viruses. Some kinds of leukocytes also produce antibodies to fight with the infection agents. If you aim to engineer a bacterium in order to fight with a virus inside our bodies, first you have to provide that the bacterium will stay in the tissues of our bodies for a sufficient amount of time and/or its secretions which attacks to the virus will enter and stay at least in the blood stream. It is obvious that this approach is way more complicated and hard to achieve.

This is an interesting question I have not considered, however it does have some caveats.
The ultimate question is how is COVID-19 going to be assaulted? What is the interaction to eradicate the pathogen? If we understand this, we don't need to create a bio-weapon to destroy a virus.
Also if we understand this interaction, we should arrive at a suitable vaccine as a solution. There are many methods to develop a vaccine, as outlined here.
Bacteria and viruses are very different and are in-fact different organisms.
Within our gastrointestinal tract (The hole from our mouth to anus), live approximately 100,000 billion bacteria. Typically viruses - speaking generally - stay with someone for a short time-frame. So you never have more than one at a time really and most people live their life without any viruses.

This does not provide an answer to the question

In fact, there are many gastrointestinal viruses that are present indefinitely, they are bacteriophages that use intestinal bacteria as hosts: https://pubmed.ncbi.nlm.nih.gov/31295677/
However, there are no "virophages" for animal viruses--the closest thing I know of is hepatitis delta virus, which exclusively infects cells that are already infected with the hepatitis B virus. However, while HDV is a "parasite" of HBV in this sense, it doesn't eradicate HBV (doing so would be evolutionarily "stupid" as it eliminates its own host).


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Taking cold shower / drinking cold water after / during training
(I am a new-comer in biology SE so sorry if violated any rules)
Effect of cold showers after intense training
I have read the answer to this question, but it seems there are discussions on the validity there so I am still confused. For me,
Benefits: increase heat loss by conduction on the skin surface, prevent heatstroke.
Disadvantages: thermoreceptors in the skin detect a drop in skin temperature, sending nerve impulses to the hypothalamus. Then the heat gain center is activated and causes vasoconstriction, reducing blood flow just under the skin hence reduce heat loss (&dangerous for patients with heart disease like the answer says). This also reduces sweat production by sweat glands.
Won't this 'chain' of physiological actions reduce heat loss (which is needed after exercise), hence trapping more heat inside the body instead of cooling in the long run? Or am I wrong when deducing the disadvantages?

You're right, It will reduce heat loss.

@ArkLomas OK thanks this means taking a warm shower can make the body return to normal core temperature even faster?

not necessarily, your body has natural methods of cooling and heating itself to stabilize body temperature.
If you have just done exercise, your body will naturally try to cool itself, taking a warm shower to make your body cool itself quicker (via vasodilation etc...)  is less efficient than taking a cold shower.
that said, drinking warm liquids also causes your body to sweat which can serve as a cooling mechanism to counteract the heat conducted from the liquid. but If your body is dangerously warm, a cool drink will probably be better especially if your sweat can't evaporate.