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Is glyphosate carcinogenic?
I'm trying to understand if glyphosate is carcinogenic. The information in internet is very confusing. There are many ecological oriented websites which claim it's carcinogenic which I suppose they could be biased, but also news websites stating that World Health Organization says "it's probably carcinogenic". In the other hand the European Union seems to sustain it's not, and it extended its license of use in a "heated debate". is it known if glyphosate is carcinogenic or not, or just there isn't enough evidence to sustain one thing or the other?

The substance that have to be used in conjunction are very problematic, so many glyphosate-containing formulations are suspect. Glyphosate itself is not under direct suspicion, but the drive for a ban aims for the substance itself nonetheless... Glyphosate and the products containing it are linked, as the only valid(=big) exposure studies naturally come from producs in use. Nobody will douse thousands of people in pure G just to get epidemiology statistics... The problematic additives need (?) to be there because G alone does tend to not stick to plants, threby loosing much of its power.

So, if the experts of the WHO and the EU cannot agree, do you really expect someone on this list to be able to resolve the problem? This is a question and answer site, not a discussion site, so even though the question is important I have voted it off-topic. I suggest you read discussions of the topic from authoratitive sources, such as this recent one in Nature.

@David Actually I do. I've seen completely ridiculous researchs with zero scientific credibility and evidence from Harvard itself, which is supposed to be the most prestigious university or one of the more importants. Also I've been seen completely ridiculous and pseudoscience claims from WHO in other subjects. So I wouldnt be surprised if this issue was treated with little scientific strictness in favor of economic interests by WHO, European Union and any other "prestigious" entity and someone here with facts and real science could point in the right direction

There is a difference between potential and risk. That's why different agencies came to different conclusions.
The IARC (International Agency for Research on Cancer, a body of the WHO) assesses the potential of a compound to cause cancer. They go through the research that point into this direction and if there is any hint that any dose of the compound might cause cancer they have to rate it accordingly. If you go through the IARC report on glyphosate, you find that a lot of the studies they looked into did not actually find a link between glyphosate and cancer in humans. Nevertheless, there are some studies that show that high doses of glyphosate can result in cancer in animals. So, the IARC had to conclude that glyphosate has the potential to cause cancer. They put it into the category 2A (probable carcinogens). In the same category you find red meat, hot beverages and being a hairdresser, because these things have the potential of causing cancer.
Agencies like the FDA, EFSA etc. are assessing the risk of cancer from "normal" glyphosate exposure. While it seems to be possible to get cancer from "too much" glyphosate, we are only exposed to a tiny fraction of that dose. While it's unavoidable that small amounts of glyphosate residues are found in our food, these amounts are most probably not harmful. At least, that's what most research concludes. The dose makes the poison. While eating fresh organic berries does not pose any risk to harm you, they naturally contain small quantities of chemicals that have the potential to harm you at high concentrations. Your body itself makes small amounts of compounds that have the potential to harm you (e.g. Formaldehyde).
That's why the debate is so heated. Environmental activists are taking the cancer potential assessment of the IARC and turn it into a risk for the consumer, which is untrue. If they would work with the same energy against other group 2A carcinogens, we would have to close down barber shops...
So, does glyphosate has the potential to cause cancer? Probably yes.
Does this provide a risk for the consumer/farmer? Probably no.

The research on Glyphosate and cancer is ambiguous however the journal Nature published a paper on January 9, 2017 that found that rats fed ultra-low doses of glyphosate developed non-alcoholic fatty liver disease. The article is: Multiomics reveal non-alcoholic fatty liver disease in rats following chronic exposure to an ultra-low dose of Roundup herbicide

First: This article is not published in Nature, but by the "Nature Publishing Group", it is published in "Scientific Reports". It has another big red warning flag attached to it, as one of the authors is Eric Seralini, who has already been proven to produce bad papers about the connection of Glyphosate and cancer in rats. His credibility in this field among serious researchers has gone below zero and I trust him as far as I can throw my car. Some of these had to be retracted due to bad conclusions and methods and he has followed a clear (political agenda) to which he fitted his experiments.


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Results of self-administration study about pain in honeybees?
There research on nih.gov about ability of bees feel pain. But I can't understand their conclusion. Could you provide necessary excerpts here from those study so it would be clear what conclusion they've got ?
And that research was granted by This research was funded by ARC Discovery Grant DP140100914. Does it mean that we shouldn't completely trust it ?

The paper shows that honeybees prefer sucrose (sugar) solution to a sucrose+morphine (pain reducing) solution. They find that injuring the bees (i.e., potentially causing pain) does not change the relative preference for sucrose vs. sucrose+morphine, but they do eat more overall when injured.
They indirectly conclude that because the bees do not seek a pain reliever they may not feel pain of the type that, for example, mammals do. This is not the same as the ability to detect noxious stimuli (nociception), which insects definitely have, it's more about the emotional/behavioral impact. They cite some evidence that morphine could potentially have similar pain-relieving effects in insects as it does in mammals due to changes in behavior caused by morphine, but of course the interpretation of their results depend very strongly on whether this is accurate or not.
ARC is the Australian govt's funding mechanism. They don't have any commercial ties to the results of research so there is no reason to have any skepticism particular to the funding source: everything has to be funded by someone.

Thank you very much. I would mark your answer, but I'm not allowed to.

source: Stack Exchange

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Can a vaccine or antidote be administrated via gases or sprays?
On TV or in movies a gas or spray containing a vaccine/cure/antitoxin is released and everybody is saved. Is this something plausible in real life? Specific examples would be appreciated.

Yes. This has been possible since the 1990's. In the US recently, the flu vaccine was recently offered as a nasal spray.
There is current research being done to aerosolize several vaccines. Public health officials have an interest in this method due to it being less expensive to produce, more people can receive the vaccine in a shorter time frame, and less need for infrastructure.
In India, they have started to give children aerosolized versions of the Measles vaccine. From research published in 2015 in The New England Journal of Medicine, scientists were reviewing how effective the aerosolized version is against the vaccine given subcutaneously. Even though the group's statistically analysis of the children's seropositivity, a method derived from previous studies, demonstrated  the aerosol vaccine was statistically "inferior" to vaccines given sub-q. However, both groups of children had the same protection from the Measles.
https://www.nejm.org/doi/full/10.1056/NEJMoa1407417
https://www.ncbi.nlm.nih.gov/pubmed/12656420
https://www.jimmunol.org/content/196/12/5014

There are a number of currently used aerosolized vaccines throughout the world. Generally, these are studied and administered in single individual doses. There are advocates for the use of larger, sealed exposure chambers for rapid administration of vaccines to large numbers of people, possibly in the field, for example in a tent like this figure from the earlier linked reference.

The primary barriers for a general release of a vaccine or other medication as, e.g., an aerosolized spray, would be ethical (difficult to get consent from all potential exposed individuals) and dose related (difficult to ensure a specific safe and effective dose).
The closest natural experiment I'm aware of would be the use of live attenuated Sabin oral poliovirus vaccine. Unlike other currently used vaccines, the Sabin vaccine is transmissible. In developing countries, vaccine is transmitted from vaccinated individuals to un-vaccinated individuals through the fecal contamination of food and water, using the same route that wild type poliovirus is transmitted. This can result in extending immunity beyond those who directly receive the vaccine. You could conceptualize this as blanketing a local population with vaccine. It's not without problems, though, because in cases where the overall initial vaccine coverage is low, circulation of the vaccine can eventually result in reversion of the reservoir of previously non-virulent (attenuated) vaccine to a virulent type. This is how you get vaccine derived polio outbreaks, and one of the reason not to use transmissible viruses as vaccines.

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how many spores are needed to "infect" a wall?
There's cardboard box in my room that used to be in another room that had mold all over the walls and it still smells moldy. This probably means the air in my room is polluted with mold spores.(right?)
If only a few spores stick to my wall could this "infect" the wall?
How many spores are actually needed to start infecting the walls in my room?
I threw that cardboard away, but I still wonder about the remaining spores

How big is this "wall" and what is it made of? Does it have a lot of moisture? There are multiple parameters here and hence your question is broad.

Yes, the box likely had many fungal spores attached to it since it smelled “moldy”. This doesn’t mean that your room will definitely be contaminated because spores often wait for ideal conditions to germinate. There are fungal spores in the air we breathe all the time, so if those haven’t already colonized your wall then adding the ones from the box are unlikely to cause any problems.
If you do see spots appear, they can be easily removed with a damp paper towel, generic home cleaner, or diluted bleach.


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What parts of the visual system could be responsible for a fixed, monocular scotoma?
Light enters the cornea, crosses the lens, hits the retina. Electric sinal travels from retina through the optic nerve, reaches the chiasma, crosses and makes its way to the visual cortex.
My question is: given a fixed, absolute scotoma in one of the eyes, what parts of the vision could be at fault?
Initially, I believe the cornea/lens couldn't be, otherwise the scotoma wouldn't be absolute and fixed. Moreover, I suspect that, after the chiasma, signals from the same visual position are joined, so, the problem couldn't be after it, otherwise the scotoma would be binocular. As such, am I right to conclude that a fixed monocular scotoma could only be caused by issues on either the retina, or on the optic nerve?

Yes. You're right.
A scotoma only affecting one eye (i.e., one that is not perceived when one eye is closed) is diagnostic of a lesion upstream from the optic chiasm.
See Brust's Practice of Neural Science, Fig. 3-2. The figure demonstrates a full cut, with complete blindness in one eye, but the principle is the same for a scotoma.

Great answer! But could I ask just a quick confirmation? Notice this image. By the way it is drawn, we could conclude a small lesion on the highlighted area would cause a monocular loss of the right field of the right eye. That was the source of my confusion. Can I just assume this image is misleading in that sense, and that any lesion that far would result in binocular vision loss?

@MaiaVictor Yes, the image you link to in your comment is misleading. Any lesion at or downstream from the optic chiasm is going to present as a binocular loss. The optic radiations (from the LGN of the thalamus to the visual cortex) are not structured in such a way that a lesion would impact only one eye. This is one of the few absolutes: a monocular loss must be upstream from the chiasm.

Actually, I think this may be a counter-example to the answer, although seemingly extremely rare.

By the way, do you happen to be a doctor? If so, is it reasonable to ask here for a recommendation? It has been very hard to find competent doctors.

@MaiaVictor that is a fascinating article. Thank you for sharing. I appreciate the trust in asking me for a recommendation, but it wouldn't be appropriate on this site. Most doctors are quite good, but we all make mistakes every once in a while.

I agree. In the case you're willing to make a recommendation, please update your profile here with your professional contact info! Thank you very much again.


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High pressure cryonics
In this link, it is suggested to use high-pressure cryonics to freeze living cells, tissues or small organism as opposed to various and potentially toxic anti-freeze agent. The core idea is that over a certain pressure, ice is anamorphic and will not form ice crystals. Thus, organic manner will not be destroyed by said crystals.
Detailed information about the proposal can be found at this link:
https://www.benbest.com/cryonics/pressure.html
I have considering self-financing the experiment. Could anyone chip in with some advice? Do you see any red flags, design tips, etc.?

I’m voting to close this question because it is: 1) unclear, 2) appears to not be about biology as defined in the [help], 3) requires following an external link to understand, and 4) solicits opinions and advice instead of requesting a fact-based answer. Each of these alone is sufficient reason for closure. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and delete or [edit] your question accordingly.

The linked material seems quite old. High-pressure freezing of cellular and tissue samples for electron microscopy is now routine, automated machinery is commercially available: Leica EM ICE
I have used this machine's precursor, EM PACT2, it was able to vitrify samples up to 200 microns in diameter. The new machine is likely to have the same size limitations. Rather than pressure, what prevents the formation of ice crystals is rapid cooling; nanometer-thin samples can be vitrified at ambient pressure. Increasing the pressure slows crystal nucleation down, so heat has time to exit larger samples. The sample size cannot be increased arbitrarily, though; high pressures need a strong vessel, and thick walls will insulate the sample, preventing rapid cooling. In the EM PACT2, the copper tubes used to contain the sample would occasionally rupture from the applied pressure. Use of exotic materials might allow higher pressures with similar thermal conductivities, but it's unlikely you'd be able to reach the millimeter scale, even.

One premise of the full proposal is that the freezing process should avoid the formation water crystals which prevent structural damage of membranes and proteins and keep the integrity of the life organism being frozen under high-pressure cryonics.
I have not seen a discussion on the thawing process which I always thought was a problem for example when thawing cells for in vitro cell culture.
For the design I would try small with for example mammalian cells like HeLa. Maybe full organisms like worms or flies for "tissues" and "full organisms".


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How do our eyes see an inverted image?
How exactly do our eyes see an inverted image of what we are looking at?
Does it have something to do with the shape of our lens (i.e. convex)?

This isn't particular to eyes. Anything without mirrors would show the same behavior.


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If life began at sea, why organisms are less salty than the sea?
We may take it for granted that a fish, a seaweed, or clams are not too salty to eat, although the sea around them is salty. I know about the existence of a mechanism which prevents their body from becoming as salty as the sea itself, but this raises an important evolutionary question.
As life evolved from single-celled organisms, those organisms started as very simple cells with the bare essential metabolic functions. Possibly their DNA had no nucleus, and obviously they could not (yet) balance the salts within their body. In theory, this would say that their metabolism should have evolved to function is a salty environment. Yet, we see that this is not the case of modern organisms.
Which of the following scenarios describe the evolution of marine creatures with no excess salts in their body?
1- Metabolism may have started in a salty environment, cells have later "discovered" that less salt makes metabolism more efficient, and therefore the energy expended to clear-out the salts is worth the effort.
2- The time it took for salts to accumulate in the seas allowed marine creatures to adjust to a gradual increase in salinity.
3- Fresh water bodies (Rivers and lakes) are better suited for life to evolve. Eventually, some of the rivers will pour into the sea with all their content, including any living thing facing the challenges of salty sea water. This article mentions "ponds", but larger bodies of water are a better means of transporting those organisms to the sea.
What do we know about the timeline of changes in oceans salinity vs. timeline of evolution? Do we have fossil records that show the salinity content of the organisms?

Many biological processes require regulation of the salts (or more precisely ions) in fluid compartments of an organism. These processes include muscle contraction, filtration of the blood by the kidneys, and so on. Without these processes, a fish would certainly be dead. So it's not necessarily that regulating ions aids evolution or metabolism, nor that the sea changed salinity - the reason is that many biological processes required for an organism's survival wouldn't work without proper regulation of ions.
One such important process is active transport. In essence, by creating gradients of ions across a cell membrane, you can let the flow of ions into the cell drive other processes. This is a bit like how the flow of water through a water wheel can drive other machines.
I've never come across any reference to a cell with an ion concentration of its intracellular fluid greater than that of the ocean, though I'd slightly doubt that to exist since it would disrupt active transport. I'd also doubt that you could discern the ion concentrations of any fossilized cell since ions need to be dissolved, but how would you see this in a fossil?
I'm not sure whether I've completely answered your question, so let me know if something's still unclear.

I'm not sure that we take it for granted that marine organisms  are substantially less salty than seawater.
As to my knowledge, elasmobranchii, e.g., sharks, and echinoderms, e.g., sea urchins, have osmolarities that are quite near seawater (~1000 mOsm). I expect a careful investigation would show many other kinds of marine organisms are similar.

yes, you both understood my question well. The starting point was the need to regulate ions concentration by active transport. The assumption was that even for a single-celled, not all metabolic features have evolved in just one step. Before active transport ever evolved, organisms may have been restricted to a narrower range of habitats. So would they be restricted to bodies of fresher water? This may be a key issue in the debate whether life may evolve under the ice cover of Europa, one of Jupiter's moons.


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Identification: Stinging walking/flying skin cells
Here I was, sitting in the veranda, minding my own business. Kids were playing outside, and I wasn't in charge of watching them. While browsing my stack overflow feed, I felt a pinch in my left arm. Like a very tiny needle just fell from the sky and decided to 'bug' me in my free time.
I looked at the spot where it hurt and saw a minuscule insect. It looked like two shedded skin cells crawling around slowly. Just very flat and small. What surprised me is that it kept hurting for approx 30 seconds afterward.
Not knowing what it was, I decided to get the camera. But how to photograph such a tiny creature, if you do not have the proper gear. Thankfully my wife remembered a trick where you can turn around the lens of the camera (if it's detachable), and take a picture while holding the lens firmly against the body. This way you get a sort of macro. Very difficult to hold it steady and to focus, because the focus field is extremely shallow.
Nevertheless, I managed to take some shots, and now my question is.. what is this stingy little buggy? I obviously let it live after the photoshoot and most likely it's a very common insect, but I've just never seen it in my life. Especially not something that stings like that.
Ah yes, apparently it can fly. Little bugger (literally) tried to flee the scene a couple times.
Additional info:
Origin: Romania, Targoviste (DB)
Date/time: 06 July 2018, 18:30, sunset
Warm sunny but windy day, still warm, 25 degrees Celcius

That is a Lace bug (Hemiptera). Family Tingidae. https://en.wikipedia.org/wiki/Tingidae.
From Wikipedia: "Lace bugs sometimes fall out of trees, land on people, and bite, which, although painful, is a minor nuisance. No medical treatment is necessary."


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"Blood circulation". Why blood bleeds in atmosphere ?
If our body's blood pressure is 120 mm-Hg then why blood goes out of our body in 760 mm -Hg pressure if we have cuts?

In your example the blood pressure is  actually 120 + 760 = 880 mm Hg. So , higher than atmospheric pressure.

That's actually the gauge pressure that we measure. Gauge pressure is the amount by which the pressure measured in a fluid exceeds that of the atmosphere. So, when we say that our blood pressure is 180mmhg, it's wrong. In reality, the blood pressure is (180+760)mmHg inside the blood vessel, and our blood pressure exceeds atmospheric pressure by 180mmhg.


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Wasp using plant fibers in old carpenter bee hole (Indiana USA)
Location: Indiana, USA
Every spring, carpenter bees make a few holes in our exposed porch wood.  This year, we observed a woodpecker removing three 1+ cm white grubs from one of the holes after a week or two (this hole is on the underside of a porch rail).  Interesting enough.  But now, I observed some kind of wasp carrying plant fibers into the same hole, so I guess it is using it as a nest.  Here's a picture of the wasp, and also of the wasp disappearing into the hole with large green piece of grass (at least it looks like grass - definitely a strong flyer).  The hole is about 8 mm across, and the wasp body about 1.5 cm.  Anyone know the species of this wasp?

Update: Here is the apparently completed nest:

Perhaps it is the four-toothed mason wasp.

The plant material now consists of about 30 fibers, looks like a piece of a paint brush sticking out of the hole.

Are you sure both pictures are of the same wasp?  The wasp in the first picture has a white stripe on it's abdomen and the wasp in the second picture doesn't. Another reason that they don't look the same is that the legs of the wasp in the first picture don't look like they belong to the same wasp as the one in the second picture.

@peter Yes, they are the same wasp.  The stripe is hidden in the 2nd picture due to the angle. I have several other pictures of somewhat lower quality than I posted here.  Thanks for your interest!


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how long do chaperone proteins take to fold a protein?
how long do chaperone proteins take to fold a protein?


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Experimental methods to demonstrate coupling of GPCRs
How would you experimentally demonstrate receptor coupling through each of the G proteins, Gs and/or Gi?


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Are there macrophages in the blood vessels and within the blood stream?
Monocytes are phagocytes that "evolve" or "differentiate" into macrophages. I read that there are monocytes in the blood stream and vessels and that macrophages are found mainly in other tissues and in the lymphatic system.
My question: are there macrophages (and not merely monocytes) in the blood vessels and within the blood stream? And if there are, are they numerous there or sparse?

Usually, monocytes and neutrophils are present(there are other cells like Lymphocytes and other leukocytes), the only time a macrophage will be present is when inflammation occurs, I suspect this is due to the large size of the macrophage, it would be difficult for it to travel in the bloodstream, as it is quite big, compared to the small size of a monocyte. During inflammation, vascular dilation and permeability increase, which makes it easier for cells and proteins to diffuse across the endothelium.
A source that macrophages are present in all tissues: https://www.researchgate.net/publication/227897252_Macrophages_in_the_embryo_and_beyond_Much_more_than_just_giant_phagocytes
A source that talks about all the leukocytes and lymphocytes present in the blood normally: http://www.histology.leeds.ac.uk/blood/blood_wbc.php

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

Macrophages are white blood cells and I’m pretty sure that leukocytes are present in blood that flows throughout the body and hence they are found in tissues. Typically, more number of macrophages are present in the blood when there is some form of invasion by bacteria or virus.

This answer is less specific than the question (leukocytes vs. macrophages).


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what are some examples of how evolution's limitations prevented species from climbing to the absolute highest peak on the fitness scale?
In this answer, the author argued that plants are green instead of red or any other color because of some  limitations of the evolutionary process. what are other examples in which the physical and functional characteristics of an organism were a direct result of limitations of evolution?

What does "absolute highest peak on the fitness scale" mean? There really is no such thing, unless perhaps you think of a biological grey goo sort of scenario.

The "limitations" of evolution is somewhat subjective, but a couple of the important ones include random mutation, "greediness" (chasing short-term advantage), and environment.
Evolution is a complex process by which mutations occur which either 1) benefit an organism, increasing reproductive success or 2) harm the organism, decreasing reproductive success, or 3) cause no noticeable change. Over time, these collected mutations bring about significant phenotypic changes. There's no goal or underlying purpose, though. In your example of plants, chlorophyll could certainly have evolved a structure that absorbed light in different wavelengths, but they ended up doing just fine with their current absorption spectrum.
Another example is the difference between the vertebrate eye vs the octopus eye. For mammalian eyes, the optic nerve covers part of the retina. This is commonly known as the "blind spot", and has obvious negative consequences. For Cephalopods, on the other hand, the optic nerve is located behind the retina, so they have no blind spot.
Both of these examples are the result of random mutations coinciding with ideal (or non-ideal) environmental situations. The author of the post you cited is accurate to say that evolution is not an engineer, working towards a goal. The only goal of evolution is "What maintains life?" It's merely millennia of trial and error, and occasionally calamities occur, causing extinctions and loss of genetic potential.
I really think ANY characteristic of any species you care to name could be considered a result of evolution's limitations.

The term you are looking for is evolutionary baggage.
An easy example is the crappy color vision in mammals and to a lesser extent primates, for a long time mammals were only small nocturnal insectivorous (or at least that is all that survived),  during this time mammals lost two of the light sensing pigments in cone cells, leaving only two, primates had a strong enough pressure that a mutation creating a new pigment was favored giving use three, however two of them are very close to each other and overlap, and a whole portion of the spectrum is still invisible to us (ultraviolet) but non-mammals can see it. Birds see colors everyday you and I will never see.
Another mammal example is we turned the gene that would let us keep growing new teeth into control genes that give our teeth complex shapes, which was an advantage to our ancestors who were tiny short lived insectivores, but now mammals can't just grow new teeth to replace old ones like everything else can. there is no way to get these genes back without re-evolving them from scratch or giving up genetic controls on tooth shape, the first is simply to unlikely to occur and the second would be too detrimental.


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Does night mode on iPhone really help?
Okay so I know that night mode is supposed to filter out blue light that is bad for the eyes, but is it really more helpful than annoying? At night I do use it when I’m on the phone but it doesn’t make sense to keep it on during the day when it’s bright outside does it?

Helpful for what?

To protect your eyes from high energy light waves?

Different colors mean different wave lenght and energy, as displayed in the picture.
Using Planck's theory, the shorter the wave is, the more energy it carries.
On day light, all these wave lenghts are present, including UV from sun. With no sun-light, your eyes aren't hit by those, so there's no need of using higher energy waves (that's exactly how night mode on iPhone works, using only lower energy waves).


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What is the motivation behind fluorinated pharmaceuticals?
From what little research I've done, it appears that a significant portion of modern psychoactive drugs are fluorinated in one way or another (for example, Buproprion, Fluvoxamine, or any number of other antidepressants).
What is the motivation behind the addition of these groups? My initial guess would be that it either increases blood-brain barrier clearance or reduces the drug's metabolism, but I've been unable to find papers supporting either idea (or papers on the subject at all, for that matter). Any books/papers illuminating the subject would be greatly appreciated.

Fluorine has a combination of unique chemical properties, which makes it very useful in drug design :

It is small, such that replacing a C-H with a C-F is often possible, from a sterical point of view. Halogens, which share some of the other desirable properties of fluorine, are much larger.
It is very electronegative: it will attract electrons strongly, which allow polarising, stabilising or destabilising various moieties.
It is not found in natural products (except for trifluoroacetic acid), which means our metabolising apparatus, result of evolution by exposure to such products, can have difficulty dealing with it: thus ut makes drugs more resistant to degradation.

With these properties, you either start with fluorine in mind, to make  molecules that mimics transition state of reactions involving non-fluorinated compounds (thus, enzyme inhibitors), or mimic the peptide bond (but not cleavable as easily); or you add it later to a compound that already work for additional activity, or less clearance.
There are many good books and reviews, but you could start with this one.


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Technique to test antibiotic resistance in a bacteria in presence of another compound
so I have to 'quantitatively' assess a bacterial strain for its antibiotic resistance property (it is a specific antibiotic) in the presence and absence of another compound alongside antibiotic. What technique or protocol can be followed?

It sounds like you might employ a "Disk diffusion test" described in this Wikipedia article.  It could be done with and without the secondary adjuvant compound and be quantified by measurement of the varying diameters of the resulting zones of bacterial inhibition.
https://en.wikipedia.org/wiki/Disk_diffusion_test

thank you that was very helpful but the page does not describe how to add adjuvants in the equation. I googled for it and still couldn't find a satisfactory answer

I suppose you would add them to the mueller-hinton when making the plate, a few for each concentration of the other compound you want to test. Then run the disk diffusion as usual.

Eliane B - obviously.  The question involves the addition of a potential adjuvant (other compound).  It's addition can be determined by the experiment.


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Immune System - B-cell receptors
How do the B-cells, which are a part of our body, develop antibodies against antigens of the outside world (outside of our body), which they don't even know about? Is it just a random match?

This is an excellent question. You are on the right track with the random match idea. B-cells (as a group) develop receptors that bind every possible antigen and then get rid of the receptors that match antigens in our body. Some textbooks are a little more careful in their language, though, and say almost every possible antigen.
See Alberts

The preimmune repertoire is apparently large enough to ensure that there will be an antigen-binding site to fit almost any potential antigenic determinant

I'd note, though, that we've yet to identify an antigen that can't be bound by an antibody.
The process by which an individual's set of B-cells is able to generate all these different B-cell receptors was discovered by Susumu Tonegawa. He was given a Nobel prize in physiology or medicine for the discovery in 1987. You can read about it at nobelprize.org.
In broad strokes, each B cell has multiple copies of different types of gene segments that make up the B cell receptor. When the B-cell develops, it selects one of each kind of segment at random and pastes them together. At the level of the human organism, this generates an awful lot of diversity, but not quite enough to produce receptors that bind every possible antigen. The additional diversity is produced by adding or deleting additional DNA bases at random.
This produces a new problem, though, because with B-cells that have receptors that would bind every possible antigen, we would end up attacking ourself. The details here are the answer to a new question, but the basic answer is that B-cells that would recognize self are selected against, leaving us with a complement of B-cells that have receptors that bind literally every possible antigen that is not self.
Lauren Sompayrac has an excellent introductory book on the immune system that makes these very difficult concepts much more approachable. It's called How the Immune System Works, and I highly recommend it.
Here's a diagram from that book, showing the random selection and pasting together involved in one of the parts of an antibody (the heavy chain):

So, can there be B-cells that are identical to each other during the development of B-cells ? What can be the number of a particular B-cell before we get attacked with pathogens ?

@ShawnDypx Sompayrac estimates that, with 3 billion circulating B-cells, in the pre-immune state you have about 30 B-cells with the same antibody (at that point, a B-cell receptor, or BCR). The way the B-cell finds its antigen, and the clone, or set of B-cells with the same BCR, expands and produces a response is fascinating. It takes about 7 days. Again, I highly recommend Sompayrac's book.

Oh I didn't know that. I'm new here. Thanks for letting me know. I will do it.


text:
Construct picture of person's face from DNA
Would it be possible to construct a picture of a person's face from his/her DNA?

Apparently so:
http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1004224
Did you not try a google search before asking?

There's a TED talk from a top researcher on that subject, his answer is YES the science of that is advancing alot. https://www.ted.com/talks/riccardo_sabatini_how_to_read_the_genome_and_build_a_human_being


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What is the benefit of oxygen tanks to persons trappped in an enclosed space?
When people are enclosed in an air-tight space, the levels of carbon dioxide will rise to lethal levels (hypercapnia) long before the oxygen is exhausted (hypoxia).  For example, the astronauts of Apollo 13 were in danger because the carbon dioxide scrubbers in the lunar module were inadequate.  They never "ran out of oxygen", even though the oxygen tank of their service module exploded.
What would be the benefit to supplying such persons with tanks of additional oxygen?  It seems to be a futile gesture to me.
The reason I ask is a news story ongoing for several weeks.  Twelve children and one adult have been trapped by water in a cave for several weeks.  At the time this question was written, four boys were already rescued.  Officials have repeatedly expressed concerns that the "oxygen is running out" and are placing oxygen tanks in the cave.  Is there any benefit to this, or are officials simply ignorant of human physiology?

By breathing oxygen from a tank you can reduce hypercapnia. As Astrolamb below also indicates; O2 eliminates CO2 from the body; it's a balance

The quantity of CO2 is less important than concentration. By increasing the quantities of O2, you decrease the concentration of CO2, thus reducing hypercapnia.

@AliceD: That's a great solution, until your tank runs out.  Then you are back to breathing the ambient air, which now has even more CO2 than you started with!

@DrSheldon, alas yet obviously, nothing in existence today lasts eternally

@Astrolamb: Increasing the amount of O2 (or other gases) would hypothetically work, but wouldn't it be far more efficient (e.g. doubling the ambient air volume to halve the pCO2) and practical to use a CO2 scrubber?

CO2 scrubbers are very costly compared to the relative ease by which oxygen is generated. Additionally, they are far more efficient when scrubbing high concentrations of CO2, such as exhaust gases, than the lower concentrations of ambient CO2.

The big issue in the case of the cave is that it is a temporary thing. O2 only needs to be supplied until the trapped people are rescued, and scrubbers are too expensive relative to O2 costs to be used for such a temporary situation. This is hugely different from, say, the ISS, which is intended for long-term occupation. For the ISS, using scrubbers is much more practical.

@Astrolamb, good answer - you might as well compile your comments into a full-blown answer, makes perfect sense. Just add a few web links here and there and it would receive my upvote for sure.

I'd add that we don't know the dimensions, ventilation conditions, altitude, and other important aspects of the chamber in this case. A cave is a very different environment from a lunar module. It is certainly not air tight.

"...or are officials simply ignorant of human physiology?" You assume much.

@Astrolamb: The cost aspect is good point.  Also, oxygen tanks are more likely to be on-hand than CO2 scrubbers.  However, neither of these have to do with the "running out of oxygen" claims of the press.  Then again, during Apollo 13 the press incorrectly first reported the astronauts "running out of oxygen."

I'm confused - how does having more oxygen tanks NOT have something to do with running out of oxygen?

@Astrolamb: Do we genuinely know if the oxygen is running out?  We have press reports, but the press has been wrong before, as it was in Apollo 13.  We can't assume that the O2 concentration has actually been measured.  I have yet to read an actual value of O2 concentration, nor have scientific terms such as "hypoxia" been used.

I think that to the uninformed public, high CO2 concentrations is effectively equivalent to "running out of oxygen", so comments from the press are moot. I'm sure the officials have consulted people who actually know what they're talking about.

I don't believe they are supplying oxygen tanks to reoxygenate the cave...they are supplying oxygen tanks to be able to ferry people over 1 km underwater. They feel pressure to do this quickly because oxygen levels are dropping and presumably CO2 levels are rising in the small space the individuals are in. Separate issues, likely confused in news.

@BryanKrause that's what I thought too (the oxygen was for diving, not for the boys while they're sitting in the cave), but in this cbc report it sounds like they actually ran an $O_2$ line into the cave.

@DanHall Thanks for that source, I had looked briefly and didn't find ; I also had thought of natural CO2 sequestering in a cave system and I think your answer covers that well. I wonder, too, if by "oxygen line" they really just mean "compressed air" as in a typical mine ventilation system.

@BryanKrause I wouldn't be surprised if they did (mean compressed air rather than oxygen)

"They never "ran out of oxygen", even though the oxygen tank of their service module exploded." The oxygen tanks in the service module exploded, but they still had the oxygen tanks in the lunar module, which provided sufficient oxygen for the "quick return" flight path back to earth. It wasn't like they survived four days on the ambient oxygen in the cabin at the time of the accident. To sustain life you have to have both a supply of oxygen and a way of limiting $CO_2$ concentration.

There are a couple of ways to answer your question. If we assume the cave is an air-tight chamber, we've entered the domain of a very specialized field in medicine, so I can't speak as authoritatively as I'd like there, but lets start, with the fact that the cave is not air tight.
It's a cave
A cave is not a submarine or a lunar module. It is not air-tight, but in a large environment with various types of gas exchange. The cave may already have it's own $CO_2$ scrubber of a sort, since common minerals reversibly bind $CO_2$. I expect there is a whole science around $CO_2$ cycles in, e.g., limestone caves, but the point here is there is likely a sink of some sort for the $CO_2$ produced by the boys. For example, I think we could reasonably speculate that the following equilibrium in a limestone cave would be driven to the right with additional $CO_2$:
$CaCO_3 + H_2O + CO_2 \rightleftharpoons Ca(HCO_3)_2$
Why would you give oxygen?
Here I can speak authoritatively. I'd refer you to both of West's excellent texts (Respiratory Physiology and Pulmonary Pathophysiology) for further reference.
Lets clear up a misconception in the comments. It is correct that we're concerned about the concentration (typically expressed as partial pressure) of gas, not the amount. It is not correct that $O_2$ eliminates $CO_2$ from the body. This can be confusing, but it is a misapplication of Dalton's law to human physiology, based on a misunderstanding about where and how the gas is exchanged. By Dalton's law, you can reduce the concentration of $CO_2$ in a container by increasing the concentration of some other gas (e.g., $O_2$). If $CO_2$ is accumulating in the cave (rather than being taken up by the environment), then delivering compressed gas with no $CO_2$ would decrease the concentration of $CO_2$ in inspired air. Inspired air, however, is not the same as alveolar air or arterial or venous gas, and the human body is not well modeled as a container full of various gases.
While it is true that when $CO_2$ is retained in respiratory acidosis, arterial $P_{O2}$ must go down by whatever amount arterial $P_{CO2}$ goes up, it doesn't work the other way around. Delivering a higher $F_{iO2}$, or fraction of inspired $O_2$ does not cause an inverse change in arterial $CO_2$. This ends up being fairly complicated, and a full discussion is beyond the scope of this question. Let me just emphasize that supplemental $O_2$ specifically treats low $O_2$ (or, in a very specific case, $CO$, carbonmonoxide, poisoning). High $CO_2$ is treated by increasing ventilation. In fact, there are a few special cases where supplemental $O_2$ actually increases a patient's $CO_2$ levels, two of which involve hypercapnic respiratory failure. We do give $O_2$ for hypercapnic respiratory failure, but it is given to treat the associated hypoxia, not the hypercapnea. The only way to decrease $CO_2$ is to increase ventilation. This is a very important concept in critical care and respiratory medicine. I'd refer you to West Pulmonary Pathophysiology, Chapter 10, or any critical care textbook.
So, back to the reason you might want to give oxygen...
CNN reports that oxygen levels in the cave have reached 15%. If the atmospheric pressure of the cave is 760mm Hg, then the $P_{O2}$ in inspired air is about 107mm Hg, ((760 - 47 for water vapor) * 0.15, see West Respiratory Physiology, or any physiology text). At 600mm Hg (equivalent to an elevation of ~2000 meters) $P_{O2}$ in inspired air is 83mm Hg. This is low, and could start to be a problem (leading to hypoxemia and hypoxia), depending on the ability of the boys to compensate (again, see West, either respiratory physiology or pulmonary pathophysiology). If the $O_2$ levels in the cave continued to drop, or if the boys weren't compensating well, then it would be reasonable to give supplemental oxygen to treat their hypoxia, regardless of what the $CO_2$ levels were.
But if $O_2$ was low, wouldn't they also have to have high $CO_2$?
I'm not an expert in cave ecology, but it doesn't seem that strange to me that the rate of $O_2$ consumption by the boys could exceed the environment's capacity to produce or release $O_2$ from organic sources, dissolved sources, or ventilation, without their rate of $CO_2$ production overwhelming the environment's $CO_2$ sink. I have no good evidence one way or the other for this speculation.
What if it is an air-tight container?
Atmospheric $CO_2$ is on the order of 400ppm, or 0.04%. Normal levels in the body are 5% (40mm Hg / 760). We rely on this gradient to dump the $CO_2$ produced by cellular respiration using ventilation, but can still operate, with difficulty, with 5% $F_{iCO2}$. Serious problems (same reference) occur at higher levels. Again, in this particular case we're beyond my personal expertise (Dammit, Jim, I'm a doctor, not an aerospace or submarine doctor!), but in an air-tight container without a $CO_2$ sink, if $CO_2$ levels were higher than 5% and rising, I'd expect you would need to directly address $CO_2$. If it's a small container, adding other gases from pressurized canisters, or pumping gases in would decrease the $F_{iCO2}$ by Dalton's law, provided you could overcome the rate of $CO_2$ production by the boys. If $CO_2$ had accumulated in the boys blood (hypercapnea), they would (need to) increase their ventilation as well, adding more $CO_2$ to the chamber.


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Are microtubules in centrioles helical, like they are when in isolation?
Microtubules tend to be of a helical structure, do microtubules in centrioles also have a helical structure?

The centriole is composed of nine circularly arranged triplet microtubules, one complete microtubule (the A-tubule) onto which two additional partial microtubules are assembled (the B- and the C-tubules, respectively. )
What are the structures of A, B and C respectively, are they helical?

As far as I'm aware, microtubules that are composed of the same constituents will always be structurally identical. This will probably help you:
https://en.wikipedia.org/wiki/Centriole There's a couple of nice diagrams

plenty of diversity,
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5662251/


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The difference between Mast Cells and Basophils
While reading the Wikipedia article on Mast cells, I came across something that confused me. What is the major difference between a Mast Cell and Basophil?
They both seem to do the same exact function: triggering the inflammatory response. The only difference I can pick out is that Mast Cells are kept resident in a tissue while basophils move around.
Is this the only major difference?

There are differences. This article is a little old, so advances may have been made, but try reading through it. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2847274/


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What's going on when roots turn green and grow into the air?
You're looking at a hibiscus and an orchid growing in the same pot. I'm curious why the hibiscus started growing green roots into the air. Or am I looking at a third plant that somehow made its way into the pot?
July 27th
All it does is branch and get longer.

There are no leaves and the shoot doesn't thicken or turn to bark.

A new sprout appears every few days.

Is the hibiscus so root bound it's trying to escape the pot?

July 9th

While I'm not familiar with hibiscus (too cold & dry where I live), it's perfectly normal for many plants to spread by underground roots, which spread out from the parent plant a bit, then send up a new shoot.

I found this article online that does describes hibiscus plants as having a "spreading" type root system that will also form new shoots away from the parent plant ... http://homeguides.sfgate.com/type-root-hibiscus-have-49085.html
I also noticed that you have an attached orchid with aerial roots attached to the hibiscus plant.  If you are misting the orchid roots periodically, you may be dampening the surface soil in the pot and encouraging the growth of shoot forming spreading roots on the hibiscus plant to develop and grow upward.

I haven't seen any leaves on the green shoots. And the stems are flimsy. Wouldn't a new plant look something like a seedling? I do water the orchid every day, and the shoots started a few months after adding the orchid to the pot. I had been pulling out the shoots but I'll let them grow now to see what happens.

See if they develop leaves.  It could also be a combination of new environmental conditions (including low light) that would cause them to look like they do.


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Why are there multiple sequences for the same segment for an individual "strain" of influenza?
I am looking at the genome of the influenza virus being used in the flu vaccine 2017-2018: A/Michigan/45/2015.
When I look below at the individual segments, there are 4 sequences for each segment - shouldn't there be only one for a single "strain"? Is this due to rapid mutation rates? Or is it that they are including both positive and negative sense of the virus?
Edit: sorry, link here:
https://www.fludb.org/brc/fluStrainDetails.spg?strainName=A/Michigan/45/2015(H1N1)&decorator=influenza

It looks to me that the website you're looking at is mostly taking publicly available data from Genebank (the NCBI repository for sequence data) an collects it to form an overview.
For your question this means that there are 4 available sequence datasets for the A/Michigan/45/2015 influenza strain - they are likely very similar but based on the reported segment length not quite identical.

Or is it that they are including both positive and negative sense of the virus?

If you mean the positive and negative strand of the DNA, then no - since the sequence of these two is always complementary the Genebank repositories only stores the forward sequence.
You can also see that the 4 different datasets have similar Acession numbers:
KY117020 - 27 (Passage M1/C3)
KU509700 - 07 (Passage E1)
KU933490 - 07 (Passage E3)
KY090607 - 14 (Passage M1/IR)
You can look up more details for these accessions on the genebank website:

It seems that all 4 datasets came from the same publication
... which apparently was never published (so it's not available online), but it might be part of some WHO program?
The main difference of the 4 datasets I can find is the passage of the strain. I'm no virologist, so I'm not quite sure what it means, but in cell biology passage describes the time a certain cell line has been in (in vitro) culture.

This is pretty typical for influenza, and reflects the ambiguity of "sequence" when talking about rapidly-mutating RNA viruses. Such viruses exist as a "cloud" of variable sequences; a single replication of influenza is likely to contain variants at every single site of the genome.  That also allows the virus to undergo extremely rapid natural selection, including during laboratory passages (which are obviously not performed using infected humans, but might be in various cell types, or very often in eggs).
A common scenario for an influenza isolate (especially one that, like MI/45, is used in vaccines) would be to swab someone's nose, use the swab to inoculate an egg to prepare a stock virus, send that stock to several other labs, grow a subset in cells, have another lab grow some in their cells or eggs, and so on. If it's used in vaccines, it might be made into a reassortant with a different (less virulent) backbone, but the surface genes would still be termed MI/45. Each lab would sequence the virus, often at multiple steps in the passage; and at each step, there's an opportunity for the virus to either undergo selection, or simply to drift, and change its sequence. Or, of course, if may not change, and identical sequences might be deposited into the databases, perhaps starting at slightly different points depending on each lab's sequencing protocol.
Many viruses are only sequenced once, perhaps as the original isolate or as an early passage, because there's no reason (or capacity) to look further at the tens of thousands of isolates that are taken every year, but where there's a reason to look at an influenza virus more than once, standard protocol is to re-sequence it each time it's used. I can guarantee that there are far more than just 4 sequences of MI/45 out there, probably there are more like 400 that have been done world-wide, it's just that there's no point in depositing all of them.


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Book about ordination in ecology
This is a question I posted on Cross Validated few weeks ago but no response has been given so far.
I am looking for a book that would cover a lot of different ordinations techniques (indirect gradient analysis e.g. PCA, CA, DCA, MDS, nMDS but also direct gradient analysis e.g. CCA, CCorA, RDA) with applications in ecology (with R would be better) and mostly focusing on these methods.
I think " Numerical Ecology " by Legendre & Legendre (https://www.elsevier.com/books/numerical-ecology/legendre/978-0-444-53868-0#) would be relevant but it seems to cover a very extensive number of topics. Any other idea ?

I took a class in ordination methods a few months ago and found the following books helpful in better understanding the various techniques:
Multivariate Statistical Methods: A Primer by Brian Manley https://www.crcpress.com/Multivariate-Statistical-Methods-A-Primer-Fourth-Edition/Manly-Alberto/p/book/9781498728966
Correspondence Analysis in Practice by Michael Greenacre (this is somewhat more in-depth for forms of CA) https://www.crcpress.com/Correspondence-Analysis-in-Practice-Third-Edition/Greenacre/p/book/9781498731775
Multivariate Statistics for Wildlife and Ecology Research by McGarigal, Cushman, and Stafford https://www.springer.com/gp/book/9780387988917
Numerical Ecology is really excellent, even if it covers a broad number of topics. I focused on the ordination methods and found it to be very straightforward. Check out the McGarigal et al. book if you are interested in seeing examples of application in ecology.

You might also want to consider:

Tree diversity analysis by Kindt and Coe 2005. Freely and legally available here. Not very deep but nice and crisp introductions + its free.
Numerical Ecology with R by Borcard et al. 2018;
https://link.springer.com/book/10.1007%2F978-1-4419-7976-6
Little brother of Legendre and Legendre 2012. Excellent book with many examples in the R language. Also very up to date as it was released this year.
Analyzing Ecological Data by Zuur et al 2007; https://www.springer.com/us/book/9780387459677. Also a nice book covering the basics of ordination in ecology.


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Why is AMR not widespread?
we know that resistant strains (MDR, XDR, PDR) have arisen in single incidents around the globe but why are these bacteria not common and not spreading quickly as humans keep using antibiotics and killing the non-resistant strains which these Amr strains have to compete for resources. One might say that they ARE spreading but my question is why is the increase in population so slow. compare it with malaria parasite 'plasmodium' which despite being a higher organism with slower reproduction cycle kills so many.

@iayork answered your question perfectly. May I suggest you mark it the answer, or clarify your question. See: https://biology.stackexchange.com/help/someone-answers

Natural selection is environment-dependent. A mutation that makes an individual more fit in one context, might make it less fit in a different context.
The mutations that make bacteria more fit in an environment where they're exposed to antibiotics generally make them less fit in a "natural" environment where they don't have to deal with antibiotics. That means that MDR bacteria are often out-competed by their less-resistant competitors, unless they're in the "right" environment for them, such as a hospital or an infected, antibiotic-treated patient.
Some references:

Barnett M, Busby SR, Mitchison DA. Tubercle bacilli resistant to isoniazid: virulence and response to treatment with isoniazid in guinea-pigs and mice. Br J Exp Pathol 1953; 34:568–81.
urgos M, Deriemer K, Small PM, Hopewell PC, Daley CL. Effect of drug resistance on the generation of secondary cases of tuberculosis. J Infect Dis 2003; 118:1878–84.
Davies AP, Billington OJ, Bannister BA, Weir WR, McHugh TD, Gillespie SH. Comparison of fitness of two isolates of Mycobacterium tuberculosis, one of which had developed multi-drug resistance during the course of treatment. J Infect 2000; 41:184–7.
Gagneux S, Long CD, Small PM, Van T, Schoolnik GK, Bohannan BJM. The competitive cost of antibiotic resistance in Mycobacterium tuberculosis. Science 2006; 312:1944–6.
Li Z, Kelley C, Collins F, Rouse D, Morris S. Expression of katG in Mycobacterium tuberculosis is associated with its growth and persistence in mice and guinea pigs. J Infect Dis 1998; 177:1030–5.
Middlebrook G, Cohn M. Some observations on the pathogenicity of isoniazid-resistant variants of tubercle bacilli author. Science 1953; 118:297–9.
van Soolingen D, Borgdorff MW, de Haas PE et al. Molecular epidemiology of tuberculosis in the Netherlands: a nationwide study from 1993 through 1997. J Infect Dis 1999; 180:726–36.

In addition, the M. tuberculosis complex, except for M. canetti, had lost the ability to do horizontal gene transfer. Resistances thus arise by point mutations or indels, a comparatively slower route than in other species of bacteria.


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How are Antibody and T-cell receptor different?
Since the helper T-cell bonds with specific antigen presented by dendritic cell and that same helper T-cell also activates B-cell by bonding with antigen presented by B-cell, it made me think that the antigens presented by both of them should be same.
If that specificity is true, then what's the difference between an antibody and T-cell receptor? Because both T-cell receptor and Antibody are specific to an antigen.

I'm not sure if this is a homework question, but either way it would help if you state why you need help answering these questions and what you have found so far.

Hi Shawn. You should try narrowing your question. You're asking about antigen presentation and about antibodies vs. T-cell receptors. These are both broad questions in and of themselves. I'm not sure how one would write a good answer to your question as it is currently phrased.

B cell receptors (BCR) work on a similar paradigm, but a different mechanism than the TCR completely, structure aside. When a B cell encounters an antigen that binds to it's BCR, the receptor-antigen complex is internalized where it's processed onto class-II MHC.

Source: UP Manila Lecture, Marilen Parungao (link)
The peptides have to be processed to ~22-residue fragments to load on MHC-II, and the whole antigen is thus fragmented on the extrinsic processing pathway. To be specific, one antigen becomes many different peptides on many different MHC-II on the same B cell. You can imagine this produces some diversity among peptides suitable that at least one Th cell with similar specificity might bind. Class switching and somatic hypermutation that the B cells undergo help them attain greater utility and specificity, and the membrane-bound BCR is alternatively processed so that the c-terminus domain traffics antibodies to be secreted (2).
On the other hand, the TCR is specific with a little wiggle room to a particular MHC-I or II loaded peptide, with the exception of yδ T cells which have been shown to be largely MHC-independent (3). The same situation follows, however, that your antigen presenting cell or APC has many different peptides of the same antigen loaded on MHC, just as cells expressing MHC-I might, which means that the T cells are also not recognizing the same exact peptide sequence. Since they originate from the same antigen, however, your cytotoxic and helper T cells can be specific for the same "target."


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What is going on with these buccal epithelial cells?
A pooled saliva sample from a 70 year old male. What is happening with these cells?

Are these cells undergoing normal apoptosis?
In the video, the cytoplasmic movement looks liquefied and jelly-like (A).
B looks more granular, with small vacuoles that seem to have bacterial activity in them (what could this be?).
Elsewhere in the sample were completely detached, intact nuclei.
Could this be indicative of diabetes? http://www.jdrntruhs.org/temp/JNTRUnivHealthSci1133-9277352_023437.pdf

The cell you've marked "B" is dead, as is common in cells in a saliva sample. The particular path to cell death is very hard to say with an unstained light micrograph, but the fact that you have a dead blebby cell in a saliva sample is not diagnostic or indicative of anything.

If there is a relatively high abundance of them in saliva, could it be indicative of oxidative stress/lipid peroxidation/ROS?

@SMc The count of dead/live buccal cells in saliva is not useful diagnostic information

Thanks. Could you share what signs in a stain might indicate a particular path to cell death?

@SMc generally, you'd at least want an H&E stain to help identify the eosinophillic and basophillic elements. You can read more about a variety of different ways pathologists identify different pathways to cell death here

Thank you very much for the info and link, exactly what I didn't know I needed. Much appreciated!


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Functional Difference between the Distal Promoter and Enhancer Region
According to the Wikipedia article on eukaryotic promoter regions, the distal promoter is:

Anything further upstream (but not an enhancer or other regulatory region whose influence is positional/orientation independent)

What is the difference between the regulatory region and the distal promoter? Does the distal promoter region have a greater effect on the rate of transcription?
If so, is the determination for what has a big enough effect to be a distal promoter subjective?


text:
Large nocturnal butterfly with red and black hindwings
Location:
Central Poland, urban environment.
Size:
Around 4 centimeters long.
Time:
Early July.
Images:

That is a moth, in the family Erebidae. It is in the genus Catocala. Wikipedia has a nice page on Lepidoptera of Poland. https://en.wikipedia.org/wiki/List_of_Lepidoptera_of_Poland
including all the Catocala there.

It looks a lot like Catocala elocata.


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Killing more attractive mates -- intersexual selection strategy?
Is this the affinity or core part of intersexual selection (males fighting for access to females)?
If females are bound to flock to objectively more attractive man 'A' in the majority of cases, would killing him put odds in your favor? It's all relative, no? If a guy is better looking than you and you kill him, he's obviously no longer better looking and alive -- so he can't reproduce. If you killed every better looking man than yourself, wouldn't you become the next best looking man? Sounds about right.
But is this not the core reasons for mating? Kill off all the good looking men and then you're hottest.
Since no guy alive can be more attractive than you, you have sex with all of the women. Not crazy.....?
I mean in theory of course..... we know what makes men sexier -- jaws, cheekbones, eye shape, height, size/muscles, symmetry, facial width to height ratio, skin complexion/coloring/etc. So yeah....

I suspect this question hasn't been downvoted because it suggests murder as a strategy, but because it's not well formulated as a question. What exactly are you asking with "So yeah..."?

It's not a form of intersexual selection; it's an intrasexual selection strategy.

This is why there are fights between males for dominance (and having access to females) in many species. Humans have survived all these years through cooperation. So, no, its a bad idea.

The obvious flaw in this (as applied to humans) is that once the more attractive males discover that you are killing them off, they are likely to gang up and kill you instead.  Futher details likely could be found on the Law site :-)
This would seem to have a serious flaw as a general strategy, too.  Sexual attractiveness would seem to correlate with general fitness, so that if you try to kill that more attractive male (without the sneaky means of killing that technology provides), there is a good chance that he'll wind up killing you instead.

If a guy is better looking than you and you kill him, he's obviously
  no longer better looking and alive -- so he can't reproduce.

Animals can't go around shiving each other.  This less attractive bird or whatever probably can't kill a healthy member of its species without a brutal fight.  They might both end up dead.
Have you thought about what happens to the population numbers as the "kill my rivals" gene becomes more common widespread?
Anyway, we already have plenty of species where one male keeps a harem of females.  And yes, they do get attacked by others seeking to take over their mates.


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why don't antibiotics reduce our weight?
I know that a significant weight of the human body (in Kgs) is contributed by microbiota. I also know that antibiotics can often be broad spectrum and kill all the bacterias regardless of them being good or bad for us. So why doesn't antibiotic courses reduce our weight as the microbial population must've been demolished?

How do you know for a fact that the weight of the human microbiome is in kgs? Billions of microbial cells of micrometer dimensions still wouldn't weigh a kilogram, let alone a few kgs.

You suppose that antibiotics, even broad spectrum antibiotics, kill a significant fraction of bacteria. This is simply not true. Many species will be unaffected, and even amongst the sensitive ones, many individuals survive. These replicate very quickly to replenish dead ones.

The microbiome isn't simply bacteria. It also comprises fungi and archaea, which are insensitive to antibiotics

First, you present as fact that antibiotics therapy (say AT) does not reduce weight. To show this fact, a study must weigh persons before AT and after. Confounders to this measurement are 1. weight differences because of bladder content (up to around 1 liter urine = 1kg), 2. weight differences because of bowel content (100g-200g), 3. Food weight (up to 2kg and more). High salt foods can cause water retention that can easily reduce your urine output one day by 500-1000ml (=g), increasing it with the same amount the other day. So your confounders can add up to +/- 4kg easily. But what you want to measure is a change of 1kg.
This means that you need to account for all these. I don't know any study that did this. Please cite such a study before presenting as fact that there is no weight loss from AT.
Assuming there is no weight loss, there are several hypotheses that can be advanced: from the fact that no antibiotic (even broadband) can kill all bacteria, the remaining bacteria in the gut may simply feed off the highly nutritional content of those bacteria cells that were killed. Note that although we know which bacteria of those that we can cultivate in a lab are susceptible to AT, we don't know at all about those that we can't grow, and that is the majority of bacteria in the gut.

Other factors are that many diseases cause loss of appetite, vomiting, diarrhea, &c, all of which would cause weight loss.

We do account for all these things during phase I trials, but you're correct that you can't sterilize the gut. See my answer

Antibiotics can cause weight loss, though, especially as they are used in the clinically, they are more likely to cause weight gain than weight loss.
This Lancet Infectious Diseases review is not a very good review in general, but it does catalogue many of the weight related changes in response to antibiotic therapy. You could use the references as a good place to start.
Re: @RStephen's answer:

This means that you need to account for all these. I don't know any study that did this.

Having run several phase I trials, I can tell you that we do account for all these factors. These trials are done to demonstrate safety and determine the pharmacokinetic properties of a drug (absorption, distribution, metabolism, and excretion). We keep volunteers in house, and ins and outs are carefully monitored. When we control intake, if weight loss does occur, it's water loss (through diarrhea) or water loss and decreased absorption (again, with diarrhea).
@RStephen was correct, though, that you're not going to get weight loss due to elimination of your microbiota. It is simply impossible to sterilize the gut. You can throw as much heavy artillery as you'd like at it, but the best you can do is change the composition.
Clinically, though most sick patients gain weight when you treat them, weight loss is not uncommon after broad spectrum antibiotic use (often clindamycin or metronidazole) typically with GI side effects (nausea, anorexia, diarrhea). When it's due to changes in the bowel flora, it can be overgrowth but not sterilization. You can read about that in this excellent JAMA review

With a quick read of the first review though, I only found evidence about later weight gain and not short-term, as the OP is asking. Additionally, most human studies cited therein are about correlations between obesity and bacterial concentrations, focused more on what the effect of antibiotics is on obese people (table 2). Perhaps you should also note why there is weight increase (quote from same review): "Beneficial effects of antibiotics in relation to weight gain probably arise through treatment or prevention of disease."

Overall, I am not convinced whether antibiotics intake affects body weight either way in the short-term like the OP is asking, when adjusting for all other factors (previous body weight, condition etc).

@vkehayas I would never quote from that review. It's bad. Part of my job is teaching interpretation of medical literature to medical students and residents. The references, though, are a good place for background reading. The clinical fact that sick people (with infections) gain weight when you treat them (with antibiotics) is from my experience and clinical education. It is so basic, I don't have a reference at hand to cite. It's similar to the fact that a fever will go down (and may actually be mediated by the same factors, e.g., IL-1).

@vkehayas the answer to the OPs question, reformulated, do antibiotics destroy all bacteria in your body and cause weight loss because of it, is categorically no. I'm sick, on leave, and bored. I've found answering these questions helps relieve the boredom, and I hope they're helpful. You'll notice I typically answer questions I have good background knowledge on, and provide additional reading for background. I don't go hunting for sources to support each statement I make. That's boring, and likely to lead to a bad answer. Literature you're unfamiliar with is easy to misinterpret.

@DanHall thanks for answering but the fundamental question of why? is not dealt with here. when antibiotics are known to lay havoc on our microbiota why is the logical argument (i belive it is) is failing ?


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3cm Worm Found in a Glass of Tap Water - please help identify

3cm Stripy Worm Found in a Glass of Tap Water - please help identify. The worm was found in the beginning of July in a glass of tap water, in Ireland. It was about 3cm long, had a round shape and was moving quickly. It had no legs.

Welcome. Don't you by any chance have a better quality picture?

I don't have a better picture unfortunately...

You need stereo microscopes to take a better picture with more resolution.


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Identify the fluff that I have found in tea
I have just opened a new pack of a black Pu'er tea that I've bought at the local store selling it by weight, and found a piece of fluff in there. To me it looks much like some kind of a bird fluff. It might also actually be a plant fluff, but somehow I doubt it. Probably it was white originally, but being so long in contact with the tea made it a bit browner.
Of course it spoiled all the impression of the tea. Now I wonder if I should drink it, or even keep buying at the same store. The worst thing is that their supplier is one of the major suppliers of Chinese tea in our country, and this is not the first time I find something hairy in it. The last time it was a human hair.
The questions:

Please help identify what it is (I don't mean a particular species of whatever it is, but at least what is it? Bird fluff, plant fluff, synthetic fluff?)
Would you still drink your tea if you'd find such things in it? Like, should it be safe, or is there any risk in contracting some terrible infection or a virus in case if it comes from a bird?

Here are some photos that I've made:

It also very much looks like this picture I've found in the internet, but failed to find a proper description of what is it actually (the most bold one was that its a swan fluff, but I can't imagine how a swan would come in contact with the tea):

It definitely appears to be a down feather. Identifying a specific species would almost certainly require a specialized lab to examine it. I don't think your tea supplier has good quality control.

It's kind of hard to tell from the picture, but maybe it's a variety of Milkweed seed-pod that got into the tea?


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Hamilton's rule: When to change the equation?
So, in class, my teacher gave two examples of using hamilton's rule. Let b= 4 and c=2.5.
The first was whether altruism would evolve between two diploid full siblings given these values. Since r=1/2, the equation was (0.5)(4)-2.5.
The second question was the same but from a daughter to her mother. He used (1/2)(4)- (1/2)(2.5).
I was confused as to why the teacher outlined this difference. I know that it has to do with the asymmetrical and symmetrical relatedness concept but don't know the details.
Would it continue to apply to grandparents and aunts/uncles as well?


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Do decibels matter if the sound is outside human hearing?
I bought a dog training device that emits sound at 25K hertz and 130 dB. Can this damage anyone’s hearing since they can’t hear it?  Also is it possible for an infant to hear in the 25K hertz range?  Thanks

Your dog training device produces what is called ultrasonic noise. Children can hear in the 25 kHz range, though they may not develop that ability until they are school aged.
This review has a good overview of the literature around ultrasonic noise. They draw the conclusion that it's hard to isolate the effect of a particular frequency or frequencies exactly, but there is some inconclusive evidence that noise at the frequency and dB of your dog training device could cause hearing damage and have other negative effects. In several countries, you're above the admissible range, but this is for longer term exposure.

We are starting a Bioacoustics Stack Exchange for people interested in the studies of non-human animal sounds and the impacts of sounds on animals. Please join us!
https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=YjZmYjUxYzJkNDI1YmY5NDk3NzdhMzViMmZlNzI4ZDdiYTAyMWQxNTM5ZWFiNzRhODNkMmFiMzIxZjI3MmY1N_gFvrICTvBsmYNJ2ptRM6lIZEAV-VGkXtIwNyVDja680


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In centrioles, what type of fibers connect the triplet microtubules?
In a centriole, each "arm" (a triplet microtubule) is attached from its A-tubule to the C-tubule of the adjacent arm. What is the type of fiber that connects each arm ("connecting fibrils" in the image below)?

Winey M, O'Toole E. 2014. Centriole structure. Phil Trans R Soc B 369:20130457

Cross-sectional images of centrioles and basal bodies show a linker between the A- and C-tubules in many different organisms... Surprisingly, candidate molecules serving as constituents of these linkers have not yet been identified.

That's as of 2014. I don't have the time right now, but I'll try at some point to find if there are more recent developments.


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What happened to ProteomeCommons.org?
ProteomeCommons.org seems to once have been a resource for raw proteomics data. Thought, the website now offers gardening tools. It seems to be hacked. Does anyone know whether the data is still available somewhere?

According to Lars Juhl Jensen on a Biostars forum,

The Proteome Commons Tranche sadly shut down around 2013 due to lack of funding. It is a good example why important bioinformatics infrastructure needs dedicated funding and should not have to operate out of research grants for individual groups.

I have no quibble with your answer but feel the part of the quote regarding the need for dedicated funding is naive and simplistic. The fact is that it is difficult to get grant funding for web resources in the first place, but even more difficult to get extensions as granting bodies like to fund new projects. Thus KEGG got cut back and started charging for database access, and FlyBase likewise and is asking for subscriptions. This is a complex problem with no easy answers.

They seem to have lost the domain name. I believe all the data from that project is now on the UCSD site


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What is protein secondary structure?
Could someone please clarify what is protein secondary structure:
https://en.wikipedia.org/wiki/Protein_secondary_structure
I believe I understand the primary structure, I am not sure what's the difference between secondary and tertiary structure. Tertiary structure seems to be 3d structure of a polypeptide but I am not at all clear about the secondary structure.

Can you clarify your question? what do you know about protein secondary structure and what are you having a hard time understanding?

@DanHall I am studying the structure of protein and while I believe I understand the primary structure, I am not sure what's the difference between secondary and tertiary structure. Tertiary structure seems to be 3d structure of a polypeptide but I am not at all clear about the secondary structure. Does this help?

edit your question to include that  :)

Proteins are made up of long chains of amino acids covalently joined together. The order of amino acids is the primary structure of a protein. In physiologic conditions, these long chains of amino acids fold into three dimensional shapes. The terms secondary and tertiary structure are used to refer to specific aspects of the three dimensional shape.
tl;dr what's the difference?
Both secondary and tertiary structure refer to the three-dimensional shape of a protein. Secondary structure is the regular repeating patterns, generally stabilized by hydrogen bonds between the NH and CO groups of the peptide backbone. Tertiary structure can be thought of as the way secondary structural elements fold together to create the overall shape of the protein.
Secondary structure
Secondary structure refers to regular repeating patterns stabilized by hydrogen bonding between the NH and CO groups of the peptide bond. Typically textbooks will focus on the $\alpha$-helix and the $\beta$-sheet.
Berg biochemistry has some useful diagrams demonstrating these secondary structures. The first is an $\alpha$-helix. The side-chains are represented by green balls here. Notice the orientation of the NH and CO groups, which stabilize this structure:

The $\beta$-sheet forms a very different secondary structure, but it's also stabilized by hydrogen bonding between NH and CO groups of the peptide bond.

Tertiary structure
Tertiary structure is the larger three-dimensional structure of a protein in its environment. It can be useful to think of tertiary structure as the way different secondary structural elements fold together to form the full, active protein. Notice in this figure, also from Berg, the way the elements of secondary structure (the $\alpha$-helices) fold into an overall three dimensional shape that can nicely cradle the heme group.

Secondary structure proteins are repeating chains of alpha helixes and beta sheets like spider silk.
Tertiary structure proteins are globular proteins, like enzymes.

All proteins have both secondary and tertiary structure in physiologic conditions. These terms do not refer to different proteins. They refer to different aspects of their structure.


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Do breasts size depend solely on fat amounts?
I've read the first answer here on quora and it suggests that (not during pregnancy and breastfeeding) breasts differ in size only due to the amount of fats. However, there can be firm or soft breasts of the same size and this is somewhat disputing the claim. Also, women with firm breasts can find it painful when their breasts are squeezed while those with soft breasts are less likely to have the same experiences.
So, what makes breasts firm or soft given the same size?

You are asking two different, but related questions

Does breast size depend solely on fat amounts?

First, breasts are made up of skin, blood vessels, ducts, fibrous tissue, and fat. There is variation between individuals and within an individual the relative composition changes with age, nutrition, and hormonal status. The size of each of those elements will determine the overall size of the breasts.

What makes breasts firm or soft given the same size?

We don't know, but it's not fat. You can determine the relative amount of fat in breast tissue (fat is black, or radiolucent, other structures are white, or radio-opaque) using mammography. There is even a term for the ratio of non-fatty structures to fat (mammographic density) but physical findings by trained examiners regarding the firmness or softness of breasts do not correlate with the relative composition of a breast. This is tricky because breast density as it is defined in mammography is relative amount of non-fatty structures compared to fat, but you can't predict the mammographic breast density with physical examination of the breast.

It is interesting that biologists do not know it, since somehow men prefer firm breasts, I thought women with firm breasts were somehow more fit, than those with soft breasts (given everything else the same, including their size).

@rus9384 funding agencies don't give a lot of grants to study men's preferences in women's bodies

Okay, there even is a research, even cited on wikipedia, so, I'm correct. https://en.wikipedia.org/wiki/Physical_attractiveness#Breasts

@rus9384 you misinterpreted my comment. I meant funding agencies are not going to give a grant to study the composition of an attractive vs. unattractive breast. They will give a grant to study aspects that make it more difficult to diagnose breast cancer with a mammogram. This is why it is not surprising that we don't know what makes breasts feel firm or soft on palpation, but we do know what makes breast cancer harder to diagnose with a mammogram.

I thought it's because of lack of methods to do it (well, actual cutting breasts, of course, is a straightforward way to do it, but juridically problematic one).

Breast density reflects the amount of fibrous and glandular tissue in a woman’s breasts compared with the amount of fatty tissue in the breasts, as seen on a mammogram.
On a mammography report, breast density is assigned to one of the following four categories:

The breasts are almost entirely fatty (about 10% of women).
A few areas of dense tissue are scattered through the breasts (about 40% of women).
The breasts are evenly dense throughout (about 40% of women).
The breasts are extremely dense (about 10% of women).
Women in the first two categories are said to have low-density, non-dense, or fatty breasts. Women in the second two categories are said to have high-density or dense breasts. About half of women who are 40 years old or older have dense breasts.
This mammographic density doesn't correlate with physical density on a clinical exam. You can have mammographically dense breasts that feel soft to the touch and vice versa.


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Is an X ml dose of a drug at 50% bioavailability roughly equivalent to a 2X ml dose at 25% bioavailability?
For the sake of simplicity, assume:

The two doses are the same drug metabolized in the exact same way, and the only difference is the amount that reaches the bloodstream (and thereafter the brain).
This drug is only meant to influence the brain, so differing concentrations in various organs don't matter.
This drug is short-term and nothing lingers in the body after it has been excreted or broken down.

My understanding is that bioavailability means the proportion of drug that reaches the bloodstream. So, all things being equal, does that mean an administration of a drug will be twice as potent if the bioavailability is doubled?

All things being equal, does that mean an administration of a drug will be twice as potent if the bioavailability is doubled?

Bioavailability is initially taught, and sometimes reported as a proportion, $F$, the concentration in drug in plasma under a test condition (typically oral administration) over the concentration of of the same dose of the drug under a reference condition (typically IV administration).
In the simplest case, under zero order kinetics (the rates of all reactions that cause a change in concentration of the drug are independent of that drug's concentration), you can substitue $F\cdot D$, for a dose, where $F$ is the bioavailability and $D$ is the dose (see equation 2-16 in Goodman and Gilman's The Pharmacological Basis of Therapeutics, Chapter 2).
So, for your question, you can write down the state with equal plasma concentrations, $0.5\cdot D_1 = 0.25 \cdot D_2$, which reduces to $2D_1 = D_2$
Potency is a hairy term, defined in many different ways (some with more hand waving than others), but lets say for the purposes of this question that potency is the oral dose $D$ required to produce a measurable effect, $E$, and relative potency is the oral dose of formulation 1, $D_1$ required for a set effect, $E$, over the oral dose of formulation 2, $D_2$ for the same effect (modified from Goodman and Gilman Chapter 3). So, if the effect of your drug is directly proportional to its concentration in plasma ($E = kC$), then yes, the formulation with twice the bioavailability will be twice as potent.
I was going to write a long treatise on why this is not necessarily going to be the case, but since you were so specific about all things being equal, I'll just say this: bioavailability is often not reducible to a single $F$, which is why the FDA requires a lot of information on Bioavailability. This is for good reason, because kinetics are often not zero order, and even once we get to plasma concentration, the concentration term that drives efficacy can be $AUC$, $C_{max}$, time above a threshold, and sometimes even hard to correlate directly to plasma concentration at all. But, in the simplest case, all things being equal, your answer is yes.


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Factors That Would Promote Eusocial Development In Mammals?
What would cause mammals to evolve to be more eusocial, like the naked mole rat did? What advantages does eusociality give in such scenarios?

Welcome to Biology SE! Your question as it stands is more appropriate for Worldbuilding SE. Perhaps if you could rephrase it to ask about a biological question that can be answered with evidence it would be better received here. For example, are you interested in the ecological conditions with which eusociality is correlated? Even so, some prior research from your part is typically required in our site.

What?
Eusociality in mammals can be defined by the following criteria:

reproductive altruism (which involves reproductive division of labor and cooperative alloparental brood care);
overlap of adult generations;
and permanent (lifelong) philopatry (stays (or returns) at (to) breeding ground).

Why?
Burdo et al. (2000) state that eusociality in mammals is a special case of monogamy, involving prolonged pair bonding for more than one breeding period. They argue that eusociality in mole-rats evolved from a monogamous mating system where cooperative brood care was already established. A tendency for group living is considered to be an ancestral trait in some genera of mole rats. The solitary lifestyle seen in some other genera is assumed to be a derived trait.
The aridity food-distribution hypothesis (AFDH) suggests a causal relationship between cooperative foraging for patchily distributed resources and the origin of eusociality. This theory states that limited nest sites or patchy resources leads to benefits of staying within the natal group, including reduced dispersal risk, and the possibility of inheriting the natal nest (Plowes, 2010).
How?
In proximate terms, in eusocial mole-rats either puberty is assumed to be developmentally delayed so that under natural conditions most animals die before dispersal is triggered. If genetic relatedness among siblings is high, then philopatry would not invoke an appreciable loss of fitness, especially if the cost of dispersing is higher than staying within the natal group. High genetic relatedness is more likely in a monogamous mating system or a highly inbred population (Burdo et al., 2000).
References
- Burda et al., Behav Ecol Sociobiol (2000); 47(5): 293–303
- Plowes, Nature Education Knowledge (1010); 3(10): 7