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If a human takes antibiotics are all bacteria in the body killed?
From my basic understanding, antibiotics kill living things, bacteria for example.
Do the antibiotics consumed by a human-being distinguish between what they kill? Or do they just kill every bacteria they find? And if that's the case, which bacteria do antibiotics find or do they find all bacteria in a human's body? Again, if that is the case, does that mean that after taking antibiotics for a certain time that the human body is free of all bacteria?

No
There are several reasons why this might not be true, as Alexander has discussed. An antibiotic often has a molecular target that isn't present in all bacteria, it's extremely hard to get antibiotics to certain parts of your body, and some bacteria will be defended against a antibiotic attack by biofilms, resistance mechanisms, and sheer statistical probability.
That is not to say that many don't die. Indeed, one of the major causes of Clostridium difficile infection is that antibiotics kill most of your gut bacteria, allowing the somewhat better protected C. diff to proliferate, start producing toxins, and send you to the hospital with symptoms ranging from diarrhea to perforated colon and worse. That disease is a direct consequence of "Antibiotics kill some but not all bacteria in you".

Bloody autocorrect on the new OS grumble

Just a quick answer: No, there is no way to kill all bacteria in your body once they are there. The only way to keep a person sterile is to prevent any bacteria entering the guts during and all time after the birth. Look for gnotobiology and gnotobionts to learn more about these organisms (including humans).
Here are some reasons why:

Most antibiotics have selective action on certain type of bacteria. This is due to the mechanisms involved in their action, permeability through the bacterial wall, their effective concentrations etc. Even broad-spectrum antibiotics have selective action. None is universal (and it is hardly possible to create those).
Antibiotics can't reach all the places in your body. Many bacteria either create some barrier against the immune response or the body eventually builds one. In the worst cases the whole bacterial infection is isolated and petrified (calcifications), as it is the case for tuberculosis and so-called Gohn's complex in lungs.
As long as you are not isolated from the society and secluded into a sterile box you will have a steady contact with millions of bacteria which re-invade your skin and guts. There is no way you can stop it and your gut flora will beging to restore spontaneously.

A follow up point: bacteria actually seems to transfer from mother to baby in the womb, so even birth by cesarian in a sterile environment wouldn't produce sterile babies.  Which is a good thing, since they'd probably die without a healthy established colony.  http://www.ncbi.nlm.nih.gov/pubmed/18281199

I'd also like to add that gnotobionts are not per se germ-free. Gnotobiontic  (from the greek gignoskein, γιγνώσκω, to know) animals have a known flora. Although one could also argue that germ-free animals also have a know flora, namely none.


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Gastric and intestinal gas exchange
A very long time ago, I happened across research into using an oxygenated liquid in the stomach and or intestinal  cavity.  I wondered what further results came about of that research, and am having difficulty finding anything on it.   Is anyone aware of it and it and or  can point me to articles and or research papers done?

Intestinal gas consists of ingested air and gas formed during digestion. Stomach gas consists of  15% oxygen and 7% carbon dioxide approximately; the remaining is nitrogen.
The air that we breathe contains about 21% oxygen; thus some of the swallowed oxygen is absorbed through the blood capillaries present in stomach. Carbon dioxide is synthesized by digesting food using gastric juices. Nitrogen is not absorbed.
The small intestine absorbs some amount of carbon dioxide and oxygen. And the remaining gas is passed further to the large intestine. In the large intestine,  most of the oxygen is removed and carbon dioxide is increased. New gases are produced mainly hydrogen because of bacterial fermentation. And these gases are absorbed by blood and later released via lungs.
Check out following links:
https://katesalevelbiology.wordpress.com/2017/02/14/human-gas-exchange-the-digestive-system-and-breathing/
https://www.gastrojournal.org/article/S0016-5085(19)33654-6/pdf
https://journals.physiology.org/doi/abs/10.1152/ajplegacy.1926.76.1.92
https://nyaspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1749-6632.1968.tb19024.x

Kindly let me know, if these links are useful. I can share whole research articles as some of these links need subscription.

Asking the question here inspired new terms for me to search and I belive I found information on the original article I had happened across where researchers tried to oxygenate pigs by perfusing the abdominal cavity with oxygenated perfluorocarbons.
Penn researchers use the abdomen to deliver oxygen to assist ailing lungs
Link to a research paper.
Peritoneal Perfusion With Oxygenated Perfluorocarbon Augments Systemic Oxygenation

source: Stack Exchange

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Genetic evolution without crossover
Can someone please point me to the origin of the system of coupled differential equations (1) in Section 2 of Shahshahani's book$^\star$?
$$ \dot{x}_i = x_i \sum_{j=1}^n m_{ij} \frac{x_j}{|x|} $$
Shahshahani claims this equation is well known as a simple consequence of random mating and cites Crow, J. F., Kimura, M., et al. (1970). An introduction to population genetics theory, but I have not been able to find the equation there.

This is a dynamical system with $x \in \mathbb{R}^n_{>0}$, and $m$ is a symmetric matrix with constant coefficients. The equation models the evolution of a genetic system subject to selection in population genetics.  The variables represent

$n \in \mathbb{N}$ number of types of gametes in a diploid population
$i \in \{1, \dots, n\}$ labels the types of gametes
$x_i \in \mathbb{R}_{>0}$ number of gametes of type $i$
the unordered pair $\{i,j\}$ represents the genotype determined by the gametes $i$ and $j$
$m$ is the selection matrix and $m_{ij}=m_{ji}$ is the selective advantage of the genotype $\{i,j\}$
$|x| := x_1 + \dots + x_n$

$\star$ S. Shahshahani, A new mathematical framework for the study of linkage and selection, Memoirs of the American Mathematical Society, Volume 17, Number 211, 1979.

Can you please provide enough information in your question so that it can be understood without reading external references? What is the meaning of the variables in the equation?

$m_{ij}$ is the mean number of descendants at the next generation from a single individual carrying $i,j$, so $m_{ij}$ has to be multiplied by the number of individuals carrying $i,j$ at the current generation. $ x_i  \frac{x_j}{|x|}$ is supposed to be that number of individuals. This is a very simplified model assuming perfect mixing between individuals carrying $x_i$ and those carrying $x_j$ and I'm not sure the "unordered" is taken in account correctly. But anyway it gives you a rough idea of what this equation says and how useless/simplified it is.

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Why doesn't my rtPCR reaction work?
I am doing a rtPCR to detect the watermelon mosaic virus (WMV). My set of primers are:

WMV primer forward: 5'-TNGARAATTTGGATGYAGG-3'
WMV primer reverse: 5'-CTGCGGTGGACCCATACC -3'

both of which at the concentration of 10 microMolar.
The first step of my rtPCR reaction was looking for a positive control.
I did the rtPCR against to a field sample (In the NGS results showed a positive against to WMV) and two greenhouse samples (the first one of my greenhouse samples was inoculated with WMV and the second one it was not).
These samples were extracted with good concentrations and integrity.
After that, I did the rtPCR with rt enzyme (from Affinity company).
Following the next steps:

I added 2000 ng of my RNA samples (in different tubes; one of them to one greenhouse sample, another tube for the remaining green house sample and the latest tube with the field sample) with Reverse primer (2 ul) and H2O (until get 12.5 ul).

1.2. I incubated them 65ºC 5' and 25ºc 10'.
2.1.  I added the next volumens for 1 sample: 2ul of my buffer, 2ul of my DTT, 2ul of my DnTps, 0.5 ul RNAsa block and 1 ul of Rt enzyme.
2.2. I vortex them and I incubated them 1 hour 50ºC and 10' 70ºC.
3.1. The PCR reaction was performed with the takara polymerase enzyme.
I added the next volumen per one tube: 2.5 ul of takara buffer, 0.5 ul forward primer, 0.5 ul and primer reverse, 0.5 ul DNTPS, 0.25 ul of taq polymerase and 15.75 ul of watter. All these volume 20 ul I added 5 microlites of my rt samples (2.2 point). I did this process with my remaining two samples.
3.2. Finally I incubated them 98ºC 5', then 35 cicles of 98ºC 30'', 56ºC 30'' and 72ºC 1'. out of the 35 cicles the temperature goes to 72ºC 10'.
I run the gel and I got primer dimmer. What I am doing wrong? All help will be very useful.

Note: These protocol was following by a labmate who got good results with the same field sample. Now I am following the protocol that was written in his notebook.

RT-PCR predates the widespread availability of the World Wide Web; which means bench scientists have been troubleshooting failed RT-PCR reactions for a very long time.  I suggest you find somebody local with such troubleshooting expertise, and learn everything that they are willing to share with you.  I predict this will be both speedier and also time well-spent for your own scientific training.

@mdperry thanks for your advice, but I am looking for someone who can tell me my fault; a short time in one step or whatever

doing more assays I found what was the trouble. I used an oligodT for the rtPCR and then I amplified with my polymerase. Probably my RNA sample had not a linear conformation in the region that my reverse primer must join. The oligo dt bint to the polyA region, typical of this type of potyviruses.

Good!  I am glad that you were able to quickly identify the problem.  I suspect that it would’ve been relatively challenging for remote individuals to figure that out so rapidly.


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Effect of soap on the survival of non-enveloped viruses
As I understand it, non-enveloped viruses are not annihilated by alcohol or have lipid layers to get soluble in soap micelle.
Does soap remove non-enveloped viruses and does hand wash help in their spread?

Yes, hand washing with soap is effective at removing non-enveloped viruses. Here is a study showing that washing with soap is effective at disinfecting norovirus, which is a non-enveloped virus: https://aem.asm.org/content/76/2/394


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

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

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

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

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

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


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Why is it that evolution of organisms had oxygen as their life-supporting gas?
On Earth, gaseous N2 is abundant. However, life began by dealing with O2 and CO2.
What can be considered the major reason for life developing in such manner?

Ambient temperature range, oxygen & water at the same time?

Have you ever tried to do chemistry with gaseous nitrogen?

Life did NOT begin with “dealing” with oxygen. It was anaerobic before the great oxygenation. And if you expressed a chemical question in chemical terms instead of using words like “dealing with” you would be nearer to considering for yourself the chemistry and thermodynamics involved.

$\ce{N2}$ may be abundant, but in the environmental conditions typical of Earth today, and back when life appeared, $\ce{N2}$ is nearly inert. That is, $\ce{N2}$ generally doesn't participate in chemical reactions except at higher temperatures or with special catalysts. $\ce{O2}$ on the other hand can participate in many chemical reactions at temperatures and pressures typical for Earth. At a more fundamental level, the reason for the inertness of $\ce{N2}$ is that the electron affinity of $\mathrm{N}$ is much less than the electron affinity of $\mathrm{O}$.
Think of it this way: Q: why don't we build cars out of tissue paper? A: Because the material properties of tissue paper are a poor match to the material requirements of cars.

Why not use $\ce{O2}$? It's used widely at Chemistry SE.

@RodrigodeAzevedo thanks for the suggestion. I've edited the question to fix that.

I was just wondering whether there is a particular reason to use \mathrm instead of \ce if both are supported.

\mathrm is a generic tag for turning off italicization  of symbols. \ce is a tag specifically created for annotating chemical formula, so the choice of tag helps convey the semantics of the the formatting.

Amusingly, I did not even know that \ce worked outside Chemistry SE until 10 minutes ago.

@Rodrigo de Azevedo: And those of us who don't regularly do chemistry wouldn't even know that :-)

@RodrigodeAzevedo   Better to use HTML  tag as it doesn’t change the typeface. Especially as the question shows no consideration of chemical energetics. Why waste time with it anyway?

@David, you seem to have a rather idiosyncratic model of posting style. I've had my posts edited on other exchanges for not using the appropriate MathJax for chemical symbols. As far as I know there is no preferred style guide for this exchange, so users are free to use MathJax or not as their personal preference dictates.

The method used to achieve a certain typographic effect should be unimportant if the result is the same with different techniques.  In the case of subscripts and superscripts the methods available yield different results — HTML maintains the sans serif typeface and size, MathJax results in serif typeface that is different in size. My recommendation is not “personal preference” but standard biochemical usage as found in e.g. J. Biol. Chem. and Biochem. J. The rationale is that there is no need to make such expressions stand out from the text — they are not mathematical displays.


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What do cats see when they look at 2D, still images?
My cat doesn't like other cats. She doesn't really like anyone that isn't part of our family. So when she sees other cats she will aggressively try and chase them out of her area. She will also do the same to dogs, if she thinks she can take them on (she is a medium-large cat). She used to occasionally go after her own image in a mirror, until she basically gets bored or realizes that the 'other cat' is behind a barrier she can't cross. Nowadays, she appears to have either given up, or realized on some level it is her (I know cats don't have mirror recognition).
However, when presented with the image of a cat, like one on the side of a food bag that is the same size as her, she completely ignores it. I would get it if she dismissed it once she realized it wasn't moving, doesn't smell like a cat, and therefore is not alive (aka, not a threat), but she doesn't even acknowledge it. And the image on the bag isn't of a cat in a field or obscured at all. It's Hill's Science cat food, which is basically a white bag with a forward facing, unobstructed cat on it the same size as an actual cat.
Her completely ignoring it makes me wonder how well she can actually see it. Can she see the details at all, or is it just a dark blur on a white background? I've seen videos of cats playing games on tablets and other 2D surfaces, but those games again feature moving objects on the screen. Given that cats generally have excellent vision for hunting, how well can they see 2D, static images? And if she can see it, do cats really have the cognitive ability to dismiss an image so quickly?

Does she respond to images of cats on a tv screen?

Yes! And to bugs; etc. But again, those are moving. I'm more curious about static images.

Clearly, if she reacts to TV images, the issue isn't 2D vs. 3D, or not only that.  Maybe she's learned that cats that never move and never change perspective even as you move around them are not threats.  OTOH, there has been cross-cultural perception research suggesting that humans have to learn to interpret photos as images of the world.  That conclusion was controversial, iirc, and I don't know where the science stands at present.  If that conclusion about humans was correct, interpreting static photos as reality ought to be even more difficult for cats, one would think.

Maybe, but I just started on this food because of a medical issue she had. She's never seen this image of a cat before, which is why it surprised me!
I focused on 2D, static images because she can react to sculptures. Often she goes and checks them out, a bit aggressive at first until she smells them and realizes that they are made of stone or similar. She just had no reaction to the 2D images, which I found interesting.

So, oddly enough, I found a decent answer in a Business Insider article, How cats see the world compared to humans by Dina Spector. She consulted with a few animal ophthalmologists, and it seems that cats' eyes and brains are more focused on detecting motion, and cannot see a wide range of color. Therefore, it is likely that my little fur-ball cannot even discern that the image on the food bag is a cat at all.
That being said, I did find this interesting article about cats responding to illusory motions, like rotating snakes. However, the sample size for this study was shockingly small.  I may try and show these images to my own cat and see what she makes of it...

Refs
Bååth, R., Seno, T., & Kitaoka, A. (2014). Cats and illusory motion. Psychology, 5(9), 1131-1134.

some additional information https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1970.sp009270

Have you watched this video?

Thank you, @RodrigodeAzevedo for bringing that into my life.


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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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Trying to identify a baby bird seen in Palermo, Sicily
I'm trying to identify a baby bird that i saw in a pond in Palermo, Sicily, Italy. Unfortunately i did not see any parents!
Any help is appreciated.
Thanks,
Robert

It looks like the chick of a Moorhen (Gallinula chloropus) or Coot (Fulica atra), probably the former. Both species are common on ponds.

The moorhen chicks on the picture here indeed have this similar German/Belgian flag coloured beak: https://upload.wikimedia.org/wikipedia/commons/9/9b/Gallinula_chloropus_-Regents_Park%2C_London%2C_England_-chicks-8.jpg

it's a chick of Common Moorhen. Shape and color of the bill allow to tell it apart from the coot's one.
Also the behaviour can help: the moorhen often walks on floating vegetation whereas the coots prefer to swim.

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Phase Transitions of Purified Proteins
Why do solutions of purified protein condense into droplet phases?
I'm trying to understand the protein phase transitions.
Here is the article http://www.cell.com/cell/fulltext/S0092-8674(12)00634-4#
It's on Intracellular Granules as Liquid Droplets

Welcome to BiologySE! Thanks for your question... it always helps if you can give some additional information so others can understand what you're asking. Also, links embedded in the question that re-direct to other sources may be helpful as well.

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how did the domestic dog evolve and was the role humans played in its evolution justified?
Humans have been selectively breeding dogs for a long time. Why do we do it? What are the positive and negative impacts of selective breeding and why do they occur?
I am writing an independent project on the subject >should selective breeding in dogs be allowed<, although I can think of many negatives to artificial selection, from a loss of genetic diversity to health problems for supposedly "pedigree dogs" I am finding it hard to find  positives other than for the development of breeds. I am especially looking for scientific research/papers/books on this theme of selective breeding in order to find  enough scientific information to write a balanced 3000 word essay. I hope this clears up the confusion surrounding the question, I was just looking for help, I did not realise my question would be graded!

What is your question? You are actually asking for a textbook. Please add some details to narrow down to the actual issue.

Welcome to Biology.SE. Why are we performing selective breeding in dogs? is more a question of sociology and human culture than biology. good and bad. The terms "good" and "bad" are subject to personal interpretation and it is therefore impossible to give a scientific answer to this question. For these reasons, I am voting to close as off-topic.

I think if '(both good and bad)' was removed it could be answerable. It does sound like a homework question to me (although of course that doesn't in itself mean it should be closed). I think the biggest problem is there's no evidence of research by the OP before posting.

Selective breeding, or artificial selection, by its very definition is the selection of desirable traits over less desirable ones. Individuals more like the desired phenotype are allowed to reproduce while others are not. Therefore, the reason a breed is selected in a certain way may be because of certain aesthetic characteristics, or speed, or hunting ability etc. For example, Schnauzers might have their beards/moustaches because for many generations breeders have wanted to accentuate this feature.

Artificial selection often causes problems because of inbreeding (an increase in homozygosity) and poorly imposed selection (only the desirable trait is considered, not other bad traits). This is why many dog breeds have associated diseases or health problems.

Image source

The question is of poor quality and it is impossible to offer a good answer to it (IMO). You did a good job at offering some pieces of info that may help the OP though (+1)

there's obvious weaknesses in the question (even after my edits, I wanted to make the question clearer, but the issues of opinion remain because I didn't want to interfere with the OP's intent), there's really not much needed to answer such a question - why do we select for desirable traits? .. because selecting for undesirable traits would be stupid. Hopefully it gives the OP somewhere to start reading about it.


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DNA replication in E.coli
What is the difference between replication and to divide? My A level bio book says that it takes 20 min for E.coli to divide and in next page it's written that E.coli completes replication within 38min.
Moreover, there is a diagram (shown below) which contradicts as what I thought.
Please explain the difference between replication and division.

Your question is unclear. The diagram you show has nothing to do with replication time per se, but with the mechanism. It shows the Messelson-Stahl-Experiment. So please clean up your question and make clear, what your question is.

This diagram shows that to divide frm 1st  gen to 2nd gen it took 20 min but then  i read "E coli completes the process of replication within 38 min, average rate of polymerisation being 2000bp per sec. " but then that dig says that it took Ecoli 20 min to divide... And that is my confusion.. Is replication nd to divide different

Here, replication means DNA replication, while division means mitosis.

I am unsure if I really understand the question. Are you wondering how the rate of DNA replication can be slower than the rate of cell division if every daughter cell needs a chromosome copy?
If so, keep in mind that prokaryotes have different origins of replication on their chromosome so that DNA replication can actually be parallelised. Cooper (1968) presents a mathematical model that is consistent with experimental findings and indicates that when the DNA replication step becomes limiting for cell division, E. coli switches to multiple replication forks, thus decreasing the net time needed for complete DNA replication.
According to that, it is no contradiction that DNA replication per se takes longer than cell division.

Replication refers to DNA replication and division refers to the cell division. Yes it is true that, in E.coli replication can be slower than the division time. This is a well known problem in molecular genetics.
The bacterium copes up with this by having a partially replicated genome during the beginning of the "cell cycle". So there are actually two origins of replication when a new cycle starts. When the replication proceeds you have multiple forks (from the replicated origins). Because of these multiple forks (forks within forks), the replication time speeds up. See the figure below:

 From Fossum et al. 2007
For more details see:
Fossum, Solveig, Elliott Crooke, and Kirsten Skarstad. "Organization of sister origins and replisomes during multifork DNA replication in Escherichia coli." The EMBO journal 26.21 (2007): 4514-4522.

The picture that you have shown is something totally different. As mentioned by Chris, the picture illustrates the Messelson-Stahl experiment to demonstrate the semiconservative nature of DNA replication. Do not confuse that with the above problem. As for the 40min shown from generation-1 to generation-2, in this picture, I feel that it is a misprint.


text:
Why did scientists state that the Omicron COVID-19 variant was a reason to get a booster?
I was watching Vox’s video, Big questions about the Covid booster shot, answered, which references the New York Times article Omicron Prompts Swift Reconsideration of Boosters Among Scientists.
In these sources, it is mentioned that the scientific community used to be mostly against giving a COVID booster shot to the less vulnerable. With the emergence of the Omicron variant, the same scientists who were opposed to booster shots had changed their minds.
However, no complete explanation was given for this in these sources, and my further research led to nothing concrete.
As per my understanding, vaccinations provide protection both by increasing antibodies in the blood (which provides protection for about 2 weeks), or by increasing B cells which would be able to identify the spike protein of the virus and help create antibodies (which provides more long-term protection).
With the SARS-CoV-2 Omicron variant, my understanding is that there were several mutations in the spike protein, which means that B cells may not recognize it or the antibodies might not bind to its receptors. If this is the concern, then how was the Omicron variant a reason for extra doses of the preexisting vaccines?

I think it's important to recognize that scientists "against giving a booster shot to the less vulnerable" had that position for public health reasons of reserving the available doses for those who had not yet received any vaccine.

Just because Omicron has come out, it doesn't mean the others have died down.  They are still about.  Some vaccines may not be effective against omicron but they may be effective against all the others before or even after omicron.  Note that vaccines are not the magic bullet that some govts and newspapers sell it to be - you can still get infected after having the vaccine.  There is no magic bullet.

This came out today (BBC): "Two doses of a Covid vaccine are not enough to stop you catching the Omicron variant, UK scientists have warned. Early analysis of UK Omicron and Delta cases showed the vaccines were less effective at stopping the new variant. However, a third booster dose significantly increased protection to around 75%."

@BryanKrause The scientists against giving the booster shot to the less vulnerable are motivated by the risks to individuals.  "One big reason for the panel’s skepticism: the risk of myocarditis and pericarditis … particularly in men aged 18 to 25. Those  patients, several panelists said, are also at the lowest risk of Covid." https://www.statnews.com/2021/10/14/fda-advisory-panel-meeting-moderna-covid-vaccine-booster/

(note: I'm simplifying things a bit here by only talking about antibodies; I don't mean to downplay other aspects of the immune response, just to keep it focused for a lay audience)
Natural antibody responses by the immune system are polyclonal - there isn't just one antibody to meet one antigen, but numerous different antibodies that may each recognize a slightly different part of the antigen.
Antibody binding (or ligand binding more generally) is also not "all-or-none". We usually describe ligand binding in biology by "affinity". When a receptor has a lower affinity for some ligand, you need higher concentrations of the ligand to saturate the same fraction of receptors (or vice-versa).
You can expect that antibodies raised against a coronavirus spike protein may have lower affinity for spike proteins altered by mutations in a viral lineage. It's also reasonable to expect that the more changes (mutations) there are, the more the affinity will change and the more antibody clones will be affected.
It's still unlikely that every different antibody in a polyclonal response will stop binding completely, but the reduced affinity is likely to equate to a reduced immunity. It's not easy to quantify this at the level of the whole organism, but it's normal to do in vitro binding experiments where you mix a mutated viral protein with some antibodies raised to a previous version. The extent of binding is a good qualitative approximation for how well immune responses will transfer.
Probably the best approach would be to give boosters with a spike closer to the new dominant variant at any point. However, that requires testing and manufacturing and simply isn't going to happen in time to be useful. In the meantime, the best alternative is to be prepared against the next-closest thing. As an approximation, you might say that if binding affinities are reduced by 50%, then if you can double your antibody response you've got about the same immunity.
Previous experience with the delta variant showed that antibodies raised in response to vaccination with the original spike protein still bound, even if they didn't bind as strongly. It seems like vaccinated people had good protection against delta even if it wasn't as good as their protection against the original strains. We can expect the same trend for the new variant, though we'll need further data to understand quantitatively where that protection level is at.

We're getting the first, non-peer reviewed yet, reports and it doesn't look good: https://www.medrxiv.org/content/10.1101/2021.12.07.21267432v2.full.pdf. I need to go through it a bit more carefully, but they are claiming that two jabs of BionTech gives 0% protection from omicron. Apparently, the best results are a combination of vaccine and infection. This is only about omicron and only about several months past the first vaccine, it shouldn't be taken as an indication of the efficacy of recent vaccination.

@terdon 0% protection against what? Infection / transmission / symptomatic cases / hospitalisation / death / all of the above?

@Tim none of the above. This is an in vitro study using blood serum extracted from people with different combinations of vaccine doses. The serum should contain antibodies against the virus, which should be able to neutralize the virus when put in a solution with it. The paper claims that serum from individuals with only 2 vaccination doses (no booster) had no effect on Omicron (but did on Delta). Exactly what such an in vitro study means for the effects in vivo is unclear, but it isn't encouraging. The good news is that sera from people who had had a booster shot did better.

@terdon Interesting. I would have thought a spike that mutated past antibodies completely would also not bind to the same receptor. But I guess that's too much to hope for.

"...not "all-or-none". (...) When a receptor has a lower affinity for some ligand, you need higher concentrations..." - Would like to know about role of concentration in respect of antibodies compared to t-cells and their receptors.

to the above: https://twitter.com/CiesekSandra tells - 8th of dec. 21 - antibody neutralization by 3 doses Biontec 25 percent effectivity after 100 days compared to roughly 90 percent with Delta.

Some Clarification:

Scientist were not opposed to a third dose, they were opposed to the rich country getting a third dose before we vaccinated the rest of the world. The WHO is right to call a temporary halt to COVID vaccine boosters
With Covid immunity either from vaccination or infection weaken with timeIsraeli Study Shows How COVID-19 Immunity Wanes over Time. Thus, a booster shot help your immunity.Immunogenicity and safety of a third dose of CoronaVac

What changed the mind of expert? Even if Omicron is not more dangerous than delta. (dangerous here: For 1000 persons, How many needs hospitalization, ICU, will got sequels and long covid or will die?)
Omicron is "at least time 2" more contagious. In terms of spreading capability, it is a monster. It is estimated that case double each 3 days (All number you are seeing right now will evolve as we get more data).
EDIT: This number is changing as new data emerge, cdc only state that omicron is more transmissible: cdc. The number I gave 2 times more transmissible and doubling every 3 days are from non peer reviewed source, take them with a grain of salt. Other sources are more dramatic, to have the real number science need a bit more time and more data.
Omicron seems to be able to reinfect people infected previously.
All together, those two points are scary. We expect to have a lot of covid case in a shorter time span. Followed by hospitalization with all the negative attached to it. To a degree we have never seen. Yes you heard it right, we expect it to be bad...  Hospital saturation, economic going slow.
In this context, a booster shot may impose itself as a way to preserve life and avoid hospital saturation. Early data show a weak protection to infection from previous infection or vaccination (but everything help in this regard)Omicron likely to weaken COVID vaccine protection. But we still hope that the third shoot preserve from dangerous form of the disease.
Summary :
The Goal of a third shot is to avoid a saturation of the health care system, a lot of people still seem to minimize this eventuality, but it is terrible. It is what cause government to impose shutdown and lockdown.

(Update Dec 15: See update in my 2nd answer below, describing new study based on actual patient data, published in just the last few days, relevant to the current question.)
This answer is a supplement to the answer of @Bryan Krause. It responds to a comment by original questioner @hb20007, who pointed out that
"My question was about the seeming logical contradiction where the concern with the Omicron variant is that it might have too many mutations in the spike protein to be recognizable by existing immune cells, but the proposed solution is extra doses of the same old vaccines."
This comment makes a reasonable point: there might indeed be a 'logical contradiction' if it were true that a booster only provides more of the very same immune response that the previous dose(s) evoked.
But in fact, vaccine doses of identical content not only can generally produce different immune responses in different people: it's also the case that successive doses of the same vaccine can also produce different immune responses in one and the same vaccinated person.  This is fundamentally due to the presence, as part of the normal mechanism of immune response, of a stage that involves random mutations, even hypermutation (followed by selection) of the somatic genes encoding antibody proteins.
When a booster vaccine is given, it not only boosts the quantity of the immune response, it also causes a process called antibody affinity maturation. (See also a recent review in 'Frontiers in Immunology'.) The mutations involved in this process can increase the diversity of the immune response. This mutation round is built-in to the system, so this is 'good' mutation (when it goes to plan*) -- and it is followed by selection of those mutation products that have affinity for the antigen.
As a result, the enhanced immune response after a booster vaccine is not just a 'carbon copy' of the earlier immune response.  As long as the antigen underlying the vaccine retains some relevant cross-reactivity with a variant antigen of concern, there is the possibility of increasing the response against the variant antigen by the booster.
At the same time, it does seem obviously more desirable that the vaccine against a variant antigen should be tailored as closely as possible to any new antigenic identity of concern. The chances of relevant protection are so much the better, as the resemblance between the vaccine antigen and the variant antigen is closer. So far, the experts who have made recent statements, about the value of boosters using the original coronavirus vaccines types, do not seem to be denying (as far as I read them) that a variant vaccine tailored to the mutated variant antigen would be desirable, but they are emphasising the point that the potential utility of the current vaccines is still there in spite of the mutations.
Perhaps a variant coronavirus vaccine will be produced along lines parallel to the annual flu vaccines, where an existing manufacturing and formulation method is repeated for the variant except for the identity of the antigen(s) included. Because of the commonality these are subjected to (abbreviated) testing and regulatory examination.  There may be more happening in the reserach pipelines for the coronavirus than we are currently getting news of -- but we are not there yet, and the only vaccines around appear to be those targeted on a spike protein with sequence close to that of the original SARS-Cov-2.

*(Somatic hypermutation does occasionally suffer genetic accidents, see for example  (https://pubmed.ncbi.nlm.nih.gov/30874354/). But it remains a vital stage in the normal immune response.)

"...there is the possibility of increasing the response against the variant antigen..." Could you please add some reference? That's because there was no specifity "at all" before? Possibility in a literal sense?

@Peter Bernhard  -- I didn't say or suggest there was 'no specificity at all before'. Also, according to my understanding, the reports of reduced effect of the immune response arising from the current vaccines against the new variant are just that, reduced effect, they do not say that there is no binding effect at all. The references I've given about the hypermutation and affinity maturation already appear to provide what you asked.

@hb20007 -- thank you!

No pun intended (globally) drawing your attention to your source "Frontiers...", citing: "Indeed, the periphery may offer more suitable sites for optimization because these regions are typically more flexible and tolerant to mutations than central sites." The more affinity maturation the more cross-reactivity (which is more)? Thanks!

Pathogens (and unfortunately sometimes unrelated things) have antigenic sites. These antigenic sites are responsible for acting as antigens by which an antibody can respond to, or perhaps a larger immune response can initiate. Viruses and pathogens are constantly evolving to try to better hide from their hosts' immune systems, called the Red Queen hypothesis.
One reason why the Omicron variant may be more transmissible than the current Delta variant is because of difference in these antigenic sites. If an immune cell can't recognize a pathogen, the pathogen can sneak by undetected and may later initiate infection. In essence, subtle differences in new variants are what give those variants a potential advantage over each other. This variation is a source of evolution, and you can't forget that viruses are evolving too, just like every other species on Earth. Often, viruses are phylogenetically monitored for their level of divergence to try to plan ahead and determine which viruses are going to be the most troublesome next year.
So, what needs to be investigated now? Well, much research is being done trying to figure out how much conserved information there is between variants, called homology, as well as other factors like hospitalization, virulence, and so on. Depending on how alike Omicron is to Delta will depend on how well our vaccines are against it. If our vaccines have a chance at doing something, then being immunized right now is absolutely crucial in preventing the evolution of future variants and later strains that may be more pathogenic. While it may seem like a time to rest on our laurels, the Omicron variant gives rise to new genetic variation that may result in future evolution and extend this pandemic long beyond what we have the patience for. It is our responsibility to beat out that evolution before it can occur.
But, then again, the immune system is a complicated mess of unintuitive situations, and I would encourage you to read into all of the science a little further.
Here are some resources:
A little bit about the immune system.
About how viruses must balance transmission and virulence (lethality).
How evolution helps us understand viruses.

Be careful: The transmission rate has nothing to do with the immune system. This is a "simple" stick and fit to the receptor which is needed for cell entry. That this is the same as we are vaccinating against has reasons.

I'm not talking about the lock and key model, I'm discussing the evolution of a virus. Viruses with high transmission are weakly selected against in virulence, they can kill people because they spread easily. Viruses with low transmission can't get away with this, and so virulence is selected against. Variants with differences in antigenic sites can become more transmissible. Why? Because the immune system is naïve to them.

This answer has a lot of great information but I feel like it does not completely answer my question. My question was about the seeming logical contradiction where the concern with the Omicron variant is that it might have too many mutations in the spike protein to be recognizable by existing immune cells, but the proposed solution is extra doses of the same old vaccines.

Hey that's fair. Allow me to clarify. Boosters for everyone were previously recommended against so that people who were at high risk had access to them, because their immune responses are typically weak and the level of immunity they achieve isn't as great as say a young person. But now, we have a new variant to worry about, and there's a reasonable chance that, because of evolutionary homology, our vaccines may do something about it. To prevent this variant from spreading and creating another worse variant, it's important to immunize ourselves as best as possible.

@BrownBag: Can you add the information to the answer, please? Comments may be deleted at any time. (But without "Edit:", "Update:", or similar - the answer should appear as if it was written right now.)

@Chris - please would you clarify your comment that "transmission rate has nothing to do with the immune system"? Literally that statement would include claim that transmission rate is the same in a population of non-immunised susceptibles as in a heavily immunised population -- clearly not so.

@terry-s Sure. Omikron is not more transmissable because of the changes, but because it can infect the cells more efficiently and probably because it causes a higher viral load (which is not completely clear at this point to my knowledge). Immune evasion helps the infection but has no effect (or only a minor) on the transmissability.

@Chris You don't think those 'changes' that result in greater infection, or better immune evasion then subsequent infection, have an effect on the susceptible population? As a consequence, this notion implies that the effective reproduction number is not somehow directly proportional to the rate of transmission. I perhaps see what you're saying, that transmission and infection are not the same. But there are implications of increased infection, whatever the mechanism, however the cause, that affect the dynamics of transmission.

This is a second/supplementary answer, bringing newly-published data relevant to the question
"Why are scientists saying that the Omicron COVID-19 variant is a reason to get a booster?" and in particular, why "the proposed solution is extra doses of the same old vaccines" (when initial courses of those original vaccines have shown clear signs of relative ineffectiveness against this new variant).
My earlier answer (Dec 11) tried to describe the part of the normal immune system that enables a booster vaccine dose to generate a diversified immune response, through the intervention of the random-mutation part of the system.
While this describes an in-principle mechanism for booster effectiveness against Omicron in the current scenario, descriptions of mechanism inevitably leave aside an important point : 'how effective' can such booster vaccine doses be?
To answer that, as the old saying goes, "the proof of the pudding is in the eating".  But with the Omicron variant so new, the main scientific results until the last few days had to be based on laboratory-bench testing of blood-serum/antibody samples.
Naturally of great interest is actual clinical data, and within the last week, the original laboratory data have been supplemented by publication of a (preprint) report of a UK-based case-control study surveying actual patients.
Again, since the Omicron variant is still so new, and the Omicron-caused diseases still so recent and perhaps in early stages, the new study is "unable to determine protection against severe forms of disease, due to the small number of Omicron cases so far, and the natural lag between infection and more severe outcomes".  Nevertheless, the new results do show that the indications from the laboratory antibody studies are being confirmed in the early clinical experiences of covid-19 due to Omicron, i.e. the results are showing that booster dosing with the Pfizer-Biontech vaccine gives a marked improvement in protection against the Omicron-caused disease seen so far compared with the effects of either of the previous 2-dose vaccine programs alone.
The report is still too recent to have been refereed, but can be read at "Effectiveness of COVID-19 vaccines against the Omicron (B.1.1.529) variant of concern". The authors come from hospitals and research institutions in London, Oxford and Cambridge plus the national health-security agency. The data analysis was enabled by the UK National Immunisation Management System with details of covid vaccinees.
The authors' introduction cites previous "preliminary neutralisation data" (that is, laboratory studies of antibody inactivation of virus) against the Omicron variant.

"The South African and German studies, as well as unpublished data
from the UK, indicate a 20- to 40-fold reduction in neutralising
activity in sera from 2-dose [Pfizer/Biontech] vaccine recipients
compared to early pandemic viruses, and at least a 10-fold reduction
compared to the Delta variant." Thus the "effectiveness [of available
vaccines] against symptomatic disease with the Omicron variant is
significantly lower than with the Delta variant."

Among those who had received 2 doses of [Pfizer/Biontech], vaccine
effectiveness [against Omicron] was 88.0% ... 2-9 weeks after dose 2,
dropping to 48.5% ... at 10-14 weeks post dose 2 and dropping further
to between 34 and 37% from 15 weeks post dose 2.
Vaccine effectiveness increased to 75.5% ... after the booster among
those who had received [Pfizer/Biontech] as the primary course."

"Among those who had received 2 doses of [Oxford/AstraZeneca], there
was no protective effect of vaccination against symptomatic disease
with Omicron from 15 weeks after the second dose.
Among those who received [Oxford/AstraZeneca] as the primary course,
from 2 weeks after a [Pfizer/Biontech] booster dose, vaccine
effectiveness [against Omicron] increased to 71.4% ... .

"All of the Omicron estimates are subject to significant uncertainty with wide confidence intervals", because of the low number of patients with identified Omicron-caused disease (just under 600 patients between 27 November when Omicron patients began to be identifiable and 9 December when the data were obtained, although Delta patients and test-negative controls in the data came from a larger time-interval and numbered over 56,000 and over 130,000 respectively.
Thus the new study concludes that

"a booster dose of [Pfizer/Biontech] following either
[Oxford/AstraZeneca] or [Pfizer/Biontech] as a primary course" brings
"moderate to high vaccine effectiveness against mild infection [due to
Omicron] of 70-75% ... in the early period after [the booster dose]."

By contrast, for patients without booster doses,

"Our findings indicate that 2 doses of vaccination with
[Pfizer/Biontech,] or [Oxford/AstraZeneca] are insufficient to give
adequate levels of protection against infection and mild disease with
the Omicron variant, although we cannot comment on protection against
severe disease."

"Booster doses of [Pfizer/Biontech] provide a significant increase in
protection against mild disease and are likely to offer even greater
levels of protection against severe disease. As such our findings
support maximising coverage with third doses of vaccine in highly
vaccinated populations such as the UK. Further follow-up will be
needed to assess the duration of protection of booster vaccination."

So the boosted patients in the study experienced very much better protection against Omicron than patients who had only received two doses, whether of Oxford/AstraZeneca or Pfizer/Biontech.
In the US, in reaction to recent results, "Dr. Anthony S. Fauci said Wednesday [Dec 15] ... that “at this point, there is no need for a very specific booster” designed especially to fight Omicron." New York Times.


text:
What are the physiological effects of retinal exposure to 380–400nm light?
There are two categories of sunglasses: UV380 sunglasses block all light with wavelength 380nm or lower, while UV400 sunglasses block all light with wavelength 400nm or lower.
This made me wonder, what are the physiological effects of retinal exposure to the 380–400nm band of light, which is not covered by UV380 sunglasses?
Also, assuming that the 380–400nm UV light does cause eye damage, does any potential pupil dilation caused by the dark tint of such glasses have an effect on the amount of damage caused?

I suggest editing your question to remove all references to possible health effects and just focus on the scientific question of the physiological effects of retinal exposure to 380-400nm light. Make it a science question, not a personal health one.

@MattDMo Thanks for the suggestion, I tried to do just that.

Looks much better.

dunno but long term exposure would increase the risk of cateracts later on, just getting a milky zone on the iris. I think that's one of the main things that sunglasses protect from.

Answering my own question after thorough research:
Definitions
First, I noticed that there is no consensus on where the UV spectrum ends and the blue portion of the visible light spectrum begins.
According to the WHO, as well as to most other sources, the UV spectrum covers the wavelength range 100–400nm (1). However, a few other sources, notably the SCENIHR, define visible light as starting at 380nm (2), hence UV light would be 100–380nm.
Another source, the ICNIRP, directly mentions that the boundary is not clear-cut, “the band 315 to 380–400 nm is designated as UVA” (3) . At least one source refers to the 385–405nm band as the “UV/Visible Radiation Boundary Region” (4).
Tinted Lenses
To address the part about the dark tint of lenses causing pupil dilation, it is first worth noting that not all lenses that filter out UV light have a dark tint.
In fact, clear lenses can actually offer up to UV400 protection (5). There is even some research specifically on UV protection by clear lenses (6).
Back reflection of UV light
UV380 and UV400 are not the only eyeglass specifications relevant to UV protection. There is also eye-sun protection factor (E-SPF®), which was introduced in order to also account for back reflection of UV light from eyeglass lenses to the eyes (7). Therefore, this back reflection should also be taken into account when examining the effects of 380–400nm light exposure on the eye.
The 380–400nm Band
Now let’s get to answering the question.
According to the Texas Technical University Health Sciences Center, 40% of the radiation harmful to our eyes falls within 380–400nm, which they call the “UV protection gap” (8). Another source states that, while 100–380nm light is “very harmful”, 400–460nm blue light can still cause retinal damage and macular degeneration (9). The American Optometric Association also states that blue light, which they define as the range 380–500nm, may cause eye damage (10).
An article by ZEISS Vision Care explains that the UV380 standard was a “pragmatic choice” by the ophthalmic industry, and does not reflect “biomedical realities” (11). The article refers to the 380–400nm spectrum as the “most intense portion of solar UVR on Earth”. I assume the author is referring to the physical definition of intensity of radiant energy, which is the power transferred per unit area, however I am not 100% sure that this is the intended meaning of “most intense”.
I also found an article claiming that the WHO recommends UV protection up to 400nm (12), which again implies that 380–400nm does cause significant retinal damage. However, I couldn’t find the actual WHO publication stating the recommendation.

Hello and welcome hb20007,
I would like to introduce the types of Ultraviolet light to you first.

Ultraviolet A - UVA - 400–315 nanometers
Ultraviolet B - UVB - 315–280 nanometers
Ultraviolet C - UVC - 280–100 nanometers

UV380 sunglasses block all light with a wavelength < 380nm. Blocking most UVA, UVB & UVC.
UV400 sunglasses block all light with a wavelength < 400nm. Blocking all UVA, UVB & UVC.
The first article you attached is poorly written. It states that quality control is at fault by some sunglasses manufacturers. Meaning some sunglasses aren't made right because they do not meet appropriate manufacturing standards. Therefore they are damaging to eyes. Which is true.
The second article is also true.
UV380 sunglasses are fine for UV eye protection, if you would like greater protection from ultraviolet light (all of UVA), then buy UV400 sunglasses.
I talk more about ultraviolet (UV) light and it's cancerous consequences here.
Wikipedia has well-written free scientific information that I would highly recommend.

You did not address the apparent trade-off where wearing UV380 sunglasses dilates pupils but does not fully block UV light. I would like to have more information regarding this point. All I could find was this, which mentions pupil dilation and goes on to say that 100% UV protection is important.

In the original first article you reference, it is the 'Dark lenses' they are talking about that cause dilates pupils. Not the UV380 sunglasses, hope that is helpful.

True, but UV380 sunglasses will also cause dilation while not offering full UV protection. I'm interested to see if there is any research on the effects of the 380nm-400nm UV band on the eyes.

There is no evidence that UV380 sunglasses causes pupil dilation. As for your other question, nothing came up when I searched it on google scholar. It may not be ethical for animal models, and it is definitely not ethical for humans to be exposed to UV light of an exact band. Unfortunately I don't believe this is an area this we as humans know much about.

UV380 sunglasses, as well as any other form of sunglasses, would cause pupil dilation because of their dark tint.

Correct, the dark tint is what causes the pupil dilation. The dark tint the sunglasses they are referring to in that article is from faulty manufacturing - not from their ability to protect UV light < UV380.


text:
What was the breakthrough behind the “sudden” feasibility of mRNA vaccines in 2020?
Several sources describe the initial failures in the realization of a successful mRNA vaccine. E.g., this 2017 article from Stat describes the following problem faced by Moderna while working on one of their mRNA vaccines:

The safe dose was too weak, and repeat injections of a dose strong enough to be effective had troubling effects on the liver in animal studies.

Another Stat article describes a similar challenge:

In animal studies, the ideal dose of their leading mRNA therapy was triggering dangerous immune reactions — the kind for which Karikó had improvised a major workaround under some conditions — but a lower dose had proved too weak to show any benefits.

The work by Karikó was conducted before Moderna and BioNTech were founded, so it does not seem to be the breakthrough that led to feasible mRNA vaccines. I am also aware that one of these companies, Moderna, is secretive about its technology.
However, I would like to learn, at least at a high level, the reason mRNA vaccines are a viable option against COVID-19, while earlier attempts to develop them against other diseases, such as Crigler–Najjar syndrome, were unfruitful.

I am aware of Why weren't mRNA vaccines clinically tried earlier?, which was closed for being opinion-based. However, my question is specific to the biological mechanism behind the breakthrough that enabled feasible mRNA vaccines, so is objective and within the scope of this site.

Your question is about vaccine development and medical application rather than the biology of the method. I would suggest it is more suited for SE Medical Sciences.

@David My question is about the biology of the method. According to the Help Center, “questions about techniques in a biological or biochemical laboratory” are on-topic here.

@David Also, this answer mentions that drug-related questions which “focus on biological concepts or drug mechanisms” are on-topic

Perhaps part of the reason is that Crigler–Najjar syndrome isn't a viral infection, it's an inherited genetic defect: https://en.wikipedia.org/wiki/Crigler%E2%80%93Najjar_syndrome  Then there's a lot more motivation (which means more resources) to find a vaccine for a pandemic, than a treatment for a condition that affects less than 1 in a million.

@jamesqf That's a good point, but I'm trying to understand what biological breakthrough came from the increased motivation and resources.

@user1136 thanks for the link. I will read it and, yes, post an answer if it completely answers my question.

Relevant: https://www.youtube.com/watch?v=XPeeCyJReZw

Answering my own question after reading the 2018 Nature review article “mRNA vaccines — a new era
in vaccinology”
The resources and motivation engendered by the COVID-19 pandemic are a major factor in the development of the first mRNA vaccines approved by national governments. However, before the COVID-19 pandemic, there were recent advances in mRNA vaccine pharmacology, which made everything possible.
Introduction
The Nature review points out that it was not a single breakthrough, but a lot of research that was conducted during the last couple of years.
Demonstrations of protective immune responses by mRNA vaccines against various infective pathogens were published in recent years. In the first one, published in 2012, direct injection of non-replicating mRNA vaccines was shown to be immunogenic against various influenza virus antigens in multiple animal models1. Since then, several studies on animals, and in some cases, healthy human volunteers, have managed to induce protective immunity against rabies2,3, HIV-14,5,6, Zika7,8,9, H10N8 and H7N9 influenza10, and other viruses.
The authors of the review, which was written before the COVID-19 pandemic, believed that “mRNA vaccines have the potential to solve many of the challenges in vaccine development”. Therefore, had the pandemic not happened, it is likely that we still would have seen effective mRNA vaccines being developed, albeit at a slower pace.
Recent technological advancement has largely overcome the main challenges in the development of mRNA vaccines.
The Challenges
1. Instability
Protein expression after the vaccine is administered might be insufficient if, for instance, the half-life of the vaccine is too low, or if in vivo mRNA translation is insufficient11,12.
2. Inefficient in vivo delivery
mRNA vaccine delivery is tricky. For instance, mRNA can aggregate with serum proteins and undergoes rapid extracellular degradation by RNases. Therefore, formulating mRNAs into carrier molecules is often necessary, and delivery formulations need to take into account factors such as the biodistribution of the vaccine after delivery, mRNA uptake, and protein translation rate13,14.
3. Safety
The complexity of modulating the immunogenicity of the mRNA used in vaccines can potentially lead to unwanted stimulatory effects on the immune response15,16,17.
The Recent Advances
1. Optimization of mRNA translation and stability
Sequence optimization techniques such as replacing rare codons with more frequently used synonymous codons18, as well as enrichment of G:C content16, have been examined for increasing in vivo protein expression.
2. Progress in mRNA vaccine delivery
There are numerous delivery methods for mRNA vaccines that have been examined in the literature. In recent years, the limitations of some of these, such as using physical methods (e.g., electroporation) to penetrate the cell membrane, were demonstrated19. On the other hand, progress was made toward the increased efficacy and reduced toxicity of other delivery methods such as cationic lipid and polymer-based delivery13,16,20,21.
3. Modulation of immunogenicity
Recent studies have demonstrated that the immunostimulatory profile of mRNA can be controlled more precisely using a variety of techniques. These include chromatographic purification to remove double-stranded RNA contaminants, the introduction of naturally-occurring modified nucleosides to prevent the activation of unwanted innate immune sensors, and complexing the mRNA with various carrier molecules (this includes novel approaches to adjuvants that take advantage of the intrinsic immunogenicity of mRNA)15,17,22,33.
Apart from the advances in techniques such as purification and the introduction of nucleosides, there was also an improvement in the understanding of when these techniques should be used, based on factors such as the mRNA platform used, RNA sequence optimization, and the extent of mRNA purification under consideration16,24.
References

Petsch, B. et al. Protective efficacy of in vitro synthesized, specific mRNA vaccines against influenza A virus infection. Nat. Biotechnol. 30, 1210–1216 (2012).
Schnee, M. et al. An mRNA vaccine encoding rabies virus glycoprotein induces protection against lethal infection in mice and correlates of protection in adult and newborn pigs. PLoS Negl. Trop. Dis. 10, e0004746 (2016).
Alberer, M. et al. Safety and immunogenicity of a mRNA rabies vaccine in healthy adults: an open-label, non-randomised, prospective, first‑in‑human phase 1 clinical trial. Lancet 390, 1511–1520 (2017).
Pollard, C. et al. Type I IFN counteracts the induction of antigen-specific immune responses by lipid-based delivery of mRNA vaccines. Mol. Ther. 21, 251–259 (2013).
Zhao, M., Li, M., Zhang, Z., Gong, T. & Sun, X. Induction of HIV‑1 gag specific immune responses by cationic micelles mediated delivery of gag mRNA. Drug Deliv. 23, 2596–2607 (2016).
Li, M. et al. Enhanced intranasal delivery of mRNA vaccine by overcoming the nasal epithelial barrier via intra- and paracellular pathways. J. Control. Release 228, 9–19 (2016).
Pardi, N. et al. Zika virus protection by a single low-dose nucleoside-modified mRNA vaccination. Nature 543, 248–251 (2017).
Richner, J. M. et al. Modified mRNA Vaccines protect against Zika virus infection. Cell 168, 1114–1125.e10 (2017).
Richner, J. M. et al. Vaccine mediated protection against Zika virus-induced congenital disease. Cell 170, 273–283.e12 (2017).
Bahl, K. et al. Preclinical and clinical demonstration of immunogenicity by mRNA vaccines against H10N8 and H7N9 influenza viruses. Mol. Ther. 25, 1316–1327 (2017).
Weissman, D. mRNA transcript therapy. Expert Rev. Vaccines 14, 265–281 (2015).
Sahin, U., Kariko, K. & Tureci, O. mRNA-based therapeutics — developing a new class of drugs. Nat. Rev. Drug Discov. 13, 759–780 (2014).
Kauffman, K. J., Webber, M. J. & Anderson, D. G. Materials for non-viral intracellular delivery of messenger RNA therapeutics. J. Control. Release 240, 227–234 (2016).
Guan, S. & Rosenecker, J. Nanotechnologies in delivery of mRNA therapeutics using nonviral vector-based delivery systems. Gene Ther. 24, 133–143
(2017).
Kariko, K. et al. Incorporation of pseudouridine into mRNA yields superior nonimmunogenic vector with increased translational capacity and biological stability. Mol. Ther. 16, 1833–1840 (2008).
Thess, A. et al. Sequence-engineered mRNA without chemical nucleoside modifications enables an effective protein therapy in large animals. Mol. Ther. 23, 1456–1464 (2015).
Kariko, K., Muramatsu, H., Ludwig, J. & Weissman, D. Generating the optimal mRNA for therapy: HPLC purification eliminates immune activation and improves translation of nucleoside-modified, protein-encoding mRNA. Nucleic Acids
Res. 39, e142 (2011).
Gustafsson, C., Govindarajan, S. & Minshull, J. Codon bias and heterologous protein expression. Trends Biotechnol. 22, 346–353 (2004).
Johansson, D. X., Ljungberg, K., Kakoulidou, M. & Liljestrom, P. Intradermal electroporation of naked replicon RNA elicits strong immune responses. PLoS ONE 7, e29732 (2012).
Schlake, T., Thess, A., Fotin-Mleczek, M. & Kallen, K. J. Developing mRNA-vaccine technologies. RNA Biol. 9, 1319–1330 (2012).
Reichmuth, A. M., Oberli, M. A., Jeklenec, A., Langer, R. & Blankschtein, D. mRNA vaccine delivery using lipid nanoparticles. Ther. Deliv. 7, 319–334 (2016).
Fotin-Mleczek, M. et al. Messenger RNA-based vaccines with dual activity induce balanced TLR‑7 dependent adaptive immune responses and provide antitumor activity. J. Immunother. 34, 1–15 (2011).
Rettig, L. et al. Particle size and activation threshold: a new dimension of danger signaling. Blood 115, 4533–4541 (2010).
Kauffman, K. J. et al. Efficacy and immunogenicity of unmodified and pseudouridine-modified mRNA delivered systemically with lipid nanoparticles in vivo. Biomaterials 109, 78–87 (2016).

So in a nutshell, we're just really lucky that this pandemic came along just when mRNA technology had developed to the point where it could be used to make a vaccine.  Otherwise we'd probably facing years more to develop conventional vaccines that might be much less effective.

@jamesqf Isn't China's CoronaVac based on the usual (non-mRNA) technology?

@jamesqf Indeed, one of the advantages of mRNA vaccines mentioned in the review is the capacity of their rapid development and low-cost manufacture. However, I'm not sure how Sinovac was able to develop their CoronaVac, which is a conventional inactivated SARS-CoV-2 vaccine, so quickly.

@jamesqf Lucky? No. DARPA and other agencies have been strategically investing in rapid vaccine development for a decade (including specifically Moderna's mRNA technology, which has been receiving federal funding since at least 2013), because everybody paying attention has known it was only a matter of time before we needed a rapid response like this.

@jamesqf There are other SARS-CoV-2 vaccines using conventional mechanisms that are on the cusp of completion. Pedro already mentioned Sinovac’s CoronaVac. Others are the DNA-based Oxford/AstraZeneca collaboration vaccine AZD1222, as well as the Russian Gam-COVID-Vac (“Sputnik V”).

@jakebeal: Lucky, yes, because COVID-19 or something similar could easily have appeared a decade ago.

This is a good answer, though I'm assuming all of your assertions are backed up by the linked Nature review article.  This would be a much better answer if you directly cited the primary literature referenced in the review, such that the answer is self-contained and does not rely on readers to go to the review itself for citations.

@acvill Thanks, and you are right. I edited the answer to include the citations.

@jamesqf also lucky because it if the advances had been made earlier it could have been used on a non-emergency illness, and taken years to go through the system...

Refering to "increased efficacy and reduced toxicity of other delivery methods such as cationic lipid and polymer-based delivery13,16,20,21."  Have you already read all this and are able to tell if is considered "efficient" if the nano particles not only transfect the cell efficiently (not get lost on their way etc) but also target specific cells, which is also called "tropism". Is there report on progress in targeting specific cells? This definitely matters in respect of cancer cellls, but need not in the context of vaccines. So, is there progress in targeting too?

@PeterBernhard I tried to focus more on vaccines against infectious diseases in my answer here, but the review article I linked also covers mRNA cancer vaccines in the same detail. You can check out the "mRNA cancer vaccines" subsection which begins on page 9 of the article. It also refers to other more extensive reviews focusing on mRNA cancer vaccines.

@hb20007 Thank you! Are you familiar in any other way, by any chance with "nano lipid vaccines cell targeting"? As you are in respect of cancer, you might. Would you think that there maybe none, bedause vaccines may target any cells, it just doesn't matter (in contrast to cancer which needs to be hit?)

@PeterBernhard I assume you are talking about the "cationic lipid nanoparticle" delivery system. According to the review article, it was tested on HIV-1 as well as OVA (ovalbumin-expressing cancer models). Reference #152 in the article is the relevant one; you can probably find more details about this delivery system there.


text:
Predator prey interaction
I went through a line in my textbook which read:

"But for predators, prey species could achieve very high population densities and cause ecosystem instability."

I was not able to understand the meaning 'but for predators'. Can anyone please help me to interpret it's meaning?link to page where this line is mentioned
Edit: In terms of biology, I was unable to understand the meaning of the sentence,  and I wanted to make sure that I don't misunderstand things... And this is why I posted the question.. I feel that the answer given is correct and in case, you find better explanation, please do post.

Can you provide a longer quote and what book it is from? To me, this isn't really answerable at the moment.

@fileunderwater - This is the text I was able to find. Third paragraph under the table.

@GForce yes... This is where I read from... Ncert 12th biology.. Organism and population.. To be precise

I'm voting to close this question as off-topic because it's about English language.

@user24693 You should add this info to the actual question (title, author, and preferably a longer quote.

@fileunderwater  ok... Next time when I post a question,  I will make it sure that I write all the details.. Thank you

@rg255 But I thought questioning it on a biology site would be a better option... As I was intrested in knowing the answer by biology perspective

I disagree with GForce's explanation; the meaning is not that growth of prey populations causes instability in predator species.
The sentence is merely saying that without predation, prey population growth is more likely to be at a level which leads to ecosystem instability. The term "but for predation" means "if it wasn't for the effects of predation". In other words:

"Ecosystem instability can occur when population growth of some species goes unchecked by predation."

See here for more explanation, where this example comes from in which it says that running a red light caused a crash:

"but for running the red light, the collision would not have occurred"

Biologically this makes sense in the sentence you show; without predators a species is limited by its supply of resources, and it can use these resources at an unsustainable level, whereas if you add predators to the mix there is additional extrinsic effects on population size, not determined by ecosystem properties such as space or nutrients.

I agree with this explanation and a practical example of this is the cascading effect of the wolf species canis lupus. Their reintroduction to the Yellowstone national park in the late 90s saw the proliferation of many life forms and also the change in the geological nature of the area, this effect was simply a result of the wolves changing the pathways of the moose species which were initially along the stream banks.

It's essentially saying that high densities of prey species can cause ecosystem instability not only for themselves but also for the predators which prey upon them.
In other words, high densities of prey species not only cause ecosystem instability by competing with each other, but this instability can move up the food chain and affect predators at higher trophic levels. One example would be a high density prey species having a population crash and having a corresponding adverse effect on predators which feed upon them. Without prey to feed on, predator populations would crash as well.


text:
Is there any strong factor against human edible plants being widespread and easy to gather?
While many habitats have plants, fruits, nuts and berries available for consumption by humans walking by, most places (if any?) seem to require significantly more effort than simply picking our food from trees and bushes in order to survive.
Borrowing @BryanKrause's words in a comment below:
"Why don't you find enough things like broccoli, green peppers, almonds, and wheat to support a human population when you are walking in the woods/natural fields?"

because except in the case of fruit plants don't benefit from being eaten so they have evolved a wide range of defenses. You might as well ask why gazelle just don't lie down and let lions eat them.

@John But gazelles graze grass, why haven't either we evolved to eat such abundant food or why haven't any plant species filled that niche? I guess this is a set of rather complex and unanswerable questions…

Because there are already many grazers in africa, and having evolved from omnivores our ancestors could not compete with them. Grass may be abundant but it it rather difficult to digest grazers need to be specialized.  Why haven't plants evolved to fill what niche?

I meant the niche of being easily available food for humans? @John I guess these questions really are unanswerable…

The questions are perfectly answerable if, asked clearly.

Is your question essentially: "why you don't find enough things like broccoli, green peppers, almonds, and wheat to support a human population when you are walking in the woods/natural fields?"

Yes, exactly, @BryanKrause! @John, does this help? Maybe I should add that very quote to my question.

to that the answer is becasue human don't live in those places, of have moved into them only recently. Evolution has no foresight, plants can not evolve for conditions that do not exist yet or have only existed for a few generations, not without a lot of intervention (artificial selection). Note also none of the plants Bryan listed actually benefit from humans eating them without farming.

Oh And I should mention that broccoli is not a naturally occurring plant it is entirely a human invention. even the other plants listed have been modified by humans to be easier for us to eat. A lot of features we prefer in plants make them horrible at surviving outside farming.

Humans prefer the very tenderest of plants as found in shops, which only grow abundantly when there is a lot of rain and warmth: salads, roots, tubers, fruit. Other animals are not so fussy, they have more stomachs and more grinding teeth. So plants that are palatable to humans have very few chemical and physical protections, and are good food for all herbivores. That's why the majority of plants have chemical and physical defenses, cellulose that makes them stringy, hair, tannins and so forth. plants favored by humans are favored by insects and mammals too. harsh habitats that favor slow growth have very few fast growing and low cellulose plants, i.e. mediterranean, where everything is strawy and has spines and strong resins. In cold habitats, juicy low cellulose plants can't grow fast enough to gain advantage by rapid low cellulose growth. In arid habitats, insects and animals covet juicy salad type plants, and they are eaten fast and also grow slower. Only in lush green habitats, i.e. tropics and in temperate climates can indigenous people go for a 10 minute walk and bring home malva, palms, thistle stems, reed roots, vine, and make a salad in a very fast time.

Define "easily available to human", lots of fruit are perfectly edible to humans. Human have only become widespread in the last few million years so there is not enough time to see things specialized in humans via natural selection. Especially since we  are both generalists and for most of the world completely new factors in the environment.
But there are plants that have evolved to be eaten by humans. Wheat, rice, and, maize have done amazingly well by having the right factors to be useful to humans, they are also some of the most common plants on earth now thanks to us.
Artificial selection is still evolution, it's just not natural selection. Humans are generalists and its hard for natural selection to push things to specialize in edible symbiosis with a generalist, especially in as short a time as humans have been around, but artificial selection can do it just fine becasue it is faster, provided the plant in question survives us long enough.
Being useful to humans is also a bit of a mixed bag sometimes it means we spread you over the whole world, such as wheat and dogs, but sometime is means harvesting to extinction like Silphium. Then you have things like avocado which almost went extinct becasue humans killed off their parter animals and almost nothing else could eat them, then we invented farming and decided we liked them and brought them back from the brink. Human intelligence and cultural information sharing means capabilities and technology change so much faster than the speeds natural selection tends to work at, most things just have not had the time to really adapt to how fast we changed the world,  unless we take an interest in forcing them to.


text:
How long can an octopus survive out of the water?
I saw videos of octopuses crawling on the ground and I was wondering how long an octopus can survive when out of the water? Does it depend on either its size (i.e., does a big octopus from deep sea survive longer than a tiny octopus) or the species?

The Pacific Northwest Tree Octopus only needs water during the early parts of its lifecycle; the rest of the time, it can get what it needs from rain or atmospheric moisture.

Umm.. the Tree Octopus bit is a hoax.. If you read a little of the linked page, above, it mentions its natural predators being the Bald Eagle ..and  sasquatch.

Short answer
Under ideal conditions, an octopus may survive several minutes on land.
Background
Octopuses have gills and hence are dependent on water for the exchange of oxygen and carbon dioxide. Gills collapse on land because of the lack of buoyancy (source: UC Santa Barbara). Octopuses have three hearts. Two of these are dedicated to move blood to the animal’s gills, emphasizing the animal's dependence on its gills for oxygen supply. The third heart keeps circulation flowing to the organs. This organ heart actually stops beating when the octopus swims, explaining the species’ tendency to crawl rather than swim (source: Smithsonian).
According to the Scientific American, crawling out of the water is not uncommon for species of octopus that live in intertidal waters or near the shore (Fig. 1). Because most species of octopus are nocturnal, we humans just don't see it often. Their boneless bodies are seemingly unfit for moving out of water, but it is thought to be food-motivated, e.g. shellfish and snails that can be found in tidal pools.
Octopuses depend on water to breathe, so in addition to being a cumbersome mode of transportation, the land crawl is also a gamble. When their skin stays moist, a limited amount of gas exchange can occur through passive diffusion. This allows the octopus to survive on land for short periods of time, because oxygen is absorbed through the skin, instead of the gills. In moist, coastal areas it is believed they can crawl on land for at least several minutes. Mostly they go from pool to pool, never staying out of the water for extended periods. If faced with a dry surface in the sun, they will not survive for long (source: Scientific American).

Fig. 1. Octopus on land. Source: BBC
Your sub questions; I think small octopuses may survive longer, since passive gas exchange is the mode of survival on land. In general, an increase in diameter causes the volume to increase with a third power, while surface increases with a power of two. Therefore, an increase in body size reduces the surface-to-volume ratio and leads to reduced gas exchange. Because passive gas exchange needs large surface-to-volume ratios, I am inclined to believe small octopuses may cope better with terrestrial environments. However, in hot, arid conditions it is likely a bigger one will have an advantage, because it can store more oxygen in its blood.
In terms of species, I have to say I couldn't find any sources going in so much detail on this. Likely, as said, smaller species may do better in cool, moist conditions, while larger specimens may be better off in dry environments.
Reference
- Harmon Courage, Sci Am; (November 2011)

You do realize fish gills are different than octopus gills, your source for their gills not working is talking about fish not cephalopods.

@John thanks for that. The similarities or dissimilarities between gills across species doesn't change the fact that octopuses need water for oxygen.

Found an octopus today which had attached itself to a rock covered in algae during high tide and had failed to swim back out with the receding tide. We found it at low tide, this means it must have been exposed for a long period of time, definately not only minutes. December in North Wales means it was wet, cold, no direct sun (but no rain). The octopus was moist. It was alive and well, just seemed to need to rest: Once we sat it back into the water, it stayed in one spot for a long time, after vigorously swimming there. Size: Body about palm-sized (12cm lenghth)