text:
Why does my room suddenly look 'reddish'? My eyes seem to adapt to color
To get the context of this question clear, I would like you to walk through some parts of my house.
We'll start with one of my rooms as it appears normally -

As evident, this part of my house has a creamish tinge to it, also the balcony door is open which further gives this room a yellow tint. Nothing special. I'll call it "area Y" (for yellow)*. Let's move on.

Here we arrive in another part of my house which has greenish/blue shades acting as a sunlight blocker. This gives this entire place a greenish/blue tint as shown. (Ref. "area G")
So, now let's visit the area Y again. I am always surprised with what my eyes now see. This. {1}

You see, the same room, same lightning, yet the room now looks much more reddish than before! That's what intrigues me, why does it  happen? Why my eyes suddenly become sensitive to red color?
I am not a biology student but I do know that our eyes have cones which specialize in color perception, and that there are different types of cone cells to perceive different types of colors (If I remember my high school biology correctly).
So, I somewhat get a feeling of what's happening inside my eyes (or the brain perhaps?). I suspect that as I go to area G, my eyes 'adapt' to the dominance of bluish/green light, either by decreasing pigment of blue cones or by increasing pigment of red cones, which makes my eyes more sensitive to the other end of visible light spectrum (red-yellow), causing an 'outburst' of red coloration in area 'Y'. Since pigments need time to degrade, by the time the red color pigment of my cones decreases, its activity is less than normal. It may be increased as the blue pigment's activity is less than normal and I see a reddish tinge for few moments.
This was a pure hypothesis from my part, but it seems correct to me. But why do my eyes even adapt to blue color? Why can't my eyes be  unbiased towards colors?
{1} Obviously I photoshopped the red tint in the image how else could I have replicated my vision? Though it's not the most accurate description of what I see it's still a very close approximation.

Your brain does something roughly similar to auto white balance. Use the camera to take WB from the green room, and then shoot the white room - is that what you meant?

is the WB setting available on a smart phone camera? I don't see it in mine.

@Sarthak123 Depends on the camera. Mine lets you set white balance in what it calls "Pro" mode.

Short answer
The phenomenon you describe can be explained by the negative afterimage effect, which indeed is elicited by adaptive processes in the retinae.
Background
In the retina there are three types of color photoreceptors, called cones. They are sensitive to red, green and blue, respectively. Colors are processed in the retina through a process explained by the Hering model. This model assumes that there are two sets of opponent colors, namely red - green and blue - yellow (Fig. 1).
This model assumes that in the red-green opponent channel the red cones inhibit the output of green cones and vice versa. In the blue-yellow channel the blue cones inhibit the green/red (= yellow) cone output and vice versa.
Now look at the visual illusion shown in Fig. 2. This illusion nicely illustrates the effect. After looking at the image for half a minute, your cones adapt to the color input. Particularly relevant to your question is that the green cones adapt to the green and become less responsive to green (this happens when you are in your "greenish blue shade acting as a sunlight blocker. This gives this entire place a greenish [blue] tint as shown. (Ref. 'area G')." Now this in turn lowers the green inhibition of the red-half of the red-green opponent channel. In turn, when you enter your "part of [the] house [with] a creamish tinge to it, [] 'area Y' []" the green channel will not inhibit the red-half and everything will have a reddish hue to it, akin to looking at the white half of the illusion after 30 seconds below.
Reference
- Sci Am, October 2013

Fig. 1. Hering model of color vision. Left panel: brightness coding. Right panel: opponent colors code for color, namely the red-green and blue-yellow channels. source: Bio.SE

Fig. 2. Visual afterimage illusion. Look at the fixation dot in the middle of the tripartite circle on the left for 30 seconds. Don't look away. Now look instantly to the white part on the right. If you don't see much, or only vaguely, try again. Blinking may help to shortly enhance the illusion. source: Sci Am

The reverse-color image ones were fun as a kid.

There's more to it than just afterimages.  The eye (or the brain) does adapt, though I don't know the mechanism.  Perhaps the most obvious case is demonstrated by taking photos at sunset when cross-country skiing.  Your eye/brain knows that the snow is white, and sees it as white, or nearly so.  The camera records a very reddish color, though.

Hering model assumes that red and green are opponents, this should mean that they should complement each other. However, the after-image illusion described at scientific american article I see cyan/blue as red's complementary (afterimage). Though my question is answered both ways, why the contradiction?

@Sarthak123 you describe the sunshades as blue. To me, they look green. Assuming they are green, the negative after image is red.

I think it's misleading to describe the three sets of cones as "... sensitive to red, green and blue, respectively ...".  Each set of cones responds to a wide range of frequencies, to different extents.  In fact, the "long wavelength" cones respond more strongly to green than they do to red.  So it's badly wrong to refer to "red cones", "green cones" and "blue cones".  Other than that, this is a good and thorough answer.

@DawoodibnKareem yes the cone absorption curves are broad. The thing is that the Hering model lies at the basis of sharpening the cone responses, because of the opponencies sharpening their partner's response. So it's not misleading at all. Further, absorption spectra of cones have been the subject of a multitude of questions already. I'm getting tired of posting those good ol absorption curves :-) and in this answer their not essential either. Lastly, the terms red, green and blue cones are used widely in the visual sciences.

@jamesqf: my camera does only record sensor readings, later in lightroom then an image is reproduced that is quite white, since I use proper white balancing settings, just like eyes/brains do.

@jamesqf IIRC it has to do with how synapses can exhaust their neurotransmitters, so they decrease the rate of firing for a persistent stimulus; coupled with the visual cortex compensating and filling in with the last relevant input (the brain “knows” what goes in the holes of our visual field and shows it to us as if our nerves were still transmitting it at full power). That is, IIRC—it's been ten years since biopsych class. I'm sure there's a term for the synaptic behaviour and the visual cortex adaptation, and they're more complex processes than this sketch—a good question to post, perhaps!

@PlasmaHH: But the question there is what's "proper": what the camera records as the actual quality of the light (assuming good sensors, of course), or the illusion your brain has created?

@jamesqf what the camera records is pure physical excitation of a sensor (it really gets complicated if you want to). What you later then do when developing is an interpretation of the data, no matter if you choose the settings to match what you "saw" at that point, or whether an algorithm tries to guess that choice for you. White balance is arguably the most prominent setting for colour rendition here

@PlasmaHH: But that's not really relevant.  (Doing color balancing &c on photos would be better addressed in the Photography site.)  The question is why and/or how the brain performs its internal color-balancing, to create the perception of white even though the light is quite red.


text:
What adaptations does the human body have to handle frequent and sustained changes in orientation?
Most animals are horizontal with the ground.  When they lie down, they get closer to the ground, but their orientation does not change.
Humans, on the other hand, stand up straight and tall, perpendicular with the ground.  And when we lie down, we make a complete 90° turn.  So we spent 2/3 of our day at one orientation, and 1/3 of our day at the exactly orthogonal orientation.
It's difficult to think of many other animals that change their orientation so completely on a regular basis, or spend much time in different orientations.  (Sure, prairie dogs, bears, lemurs, and apes stand upright now and then, and I've seen pictures of whales sleeping vertically, but it's never for long, sustained periods.  Giraffes seem so tall and vertical, but it's all neck and legs — the organs of their body are always horizontal with the ground, and this orientation is maintained when they lie down.  Birds, maybe?)
For humans, regular changes in orientation must surely cause biological stresses, and therefore there must be some biological adaptations to those stresses.
Even non-biologists are aware of plenty of orientation-related malfunctions:
— middle-aged people start to get acid reflux and indigestion when they lie horizontally
— elderly people with certain heart conditions and arrhythmias cannot lie horizontally
— some people are affected by changes in blood pressure when they lie down or stand up
— some people have dizziness or balance issues when lying down or standing up
— knees and feet start to have problems from a lifetime of bearing all the weight
What specific adaptations does the human body have to handle these daily changes in orientation?

I guess posture would be a more appropriate term instead of orientation.

For "— some people are affected by changes in blood pressure when they lie down or stand up" and "— some people have dizziness or balance issues when lying down or standing up
", see the discussions of mechanisms in the Wikipedia articles for Orthostatic Hypotension and Reflex Syncope.

For "— knees and feet start to have problems from a lifetime of bearing all the weight", the protective adaptations will largely be identical to those for any joint - even those that aren't supporting the entire body. This can include processes like the release of Synovial fluid.

source: Stack Exchange

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sort: votes


text:
Why doesn't the soil get depleted after repeated clearing of vegetation?
In my neighborhood, there is a hillside owned and maintained by the local municipality.  The hillside is generally overgrown with vegetation.  Work crews clear out the vegetation multiple times throughout the spring and summer, yet it always grows back quickly.
The workers don't leave the cuttings there.  They haul them away.  So that means the soil of the hillside is losing nutrients.  Yet why does the vegetation always grow back?
Hypotheses:

It all looks like weeds to me, but maybe there is a natural cycle of crop rotation going on that I can't appreciate.  I.e., in year 1 it was all Type A weeds, then in year 2 it was all Type B weeds, then in year 3 it was all Type C weeds, and then in year 4 it was back to Type A weeds again.
Maybe some other natural process is bringing nutrients back to the soil of the hillside.  Bird droppings?  Earthworms?  Insects?  Underground fungus and bacterial colonies?  Small mammal feces?  (I don't think rain runoff is bringing many nutrients because there is nothing but a highway above the hillside.)
Maybe the hillside is getting depleted and will eventually become barren, it just takes a while.  I guess you have to keep clearing, year after year, until it gets down to the very last and most hardy of the weeds before it becomes truly barren and lifeless.

Yes (kind of) to all your hypotheses. You'd benefit, for starters, by reading about succession, pioneer species, plant strategies, nitrogen fixation + plant symbioses (e.g., refer to legumes), and nitrogen content of animal waste

@theforestecologist — If you post your comment as an answer, I'll give you the checkmark.

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IgA complement activation
Recently, I have been reading Janeway's immunobiology and had a question on immunoglobin A. I read that IgA activates the complement pathway using the Fab fragment of the IgA. How does IgA do that? I can't seem to find an information on that in  the book or online.

@anongoodnurse 4th edition.. in Fig 3.20 on pg 102, it mentions that alternative complement pathway activated by Fab for IgA1

In the 2011 edition, compliment activation is discussed beginning in Ch. 10.

Oh, the 4th editions is very old. Even the NIH bookshelf has the 5th edition. Can you link the figure from the NIH edition so we know which one you are talking about?

@Chris in the 5th edition, the figure is 4.16

I found some reports on it (like reference 1) but there is an oddly little amount of publications on this topic. then I found this review in Mucosal Immunology (reference 2, interesting to read) which doubts this activation. It says:

Interaction with complement
IgA lacks the residues identified in the Fc regions of IgG or IgM that
  bind to C1q, and consequently IgA does not activate the classical
  complement pathway. Although several papers have reported activation
  of the alternate pathway by heat-aggregated, denatured, or
  recombinantly generated IgA, this seems to be essentially artifactual,
  and intact native IgA antibodies complexed with antigen inhibit
  complement activation induced by IgG or IgM antibodies. This
  effect is also replicated by Fabα fragments generated by cleavage of
  IgA1 antibodies with IgA1 protease. It is telling that mixed
  aggregates of heat-denatured IgG and IgA activate the alternate
  pathway in proportion to the content of IgG, and that C3b becomes
  covalently linked to the IgG heavy chains, not to IgA. Intriguing
  reports that IgA antibodies promote complement-dependent lysis or
  opsonization of encapsulated bacteria probably also arise from
  facilitation of alternate pathway activation by bacterial
  polysaccharides

It names three papers to underline this (which are number 45-47 in the reference list of the article), which can be found as references 3-5. So the question here is not only how the mechanism looks like, but also if this is real or an artefact.
References:

Activation of complement by human serum IgA, secretory IgA and IgA1
fragments.
Structure and function relationships in IgA
Anti-inflammatory activity of human IgA antibodies and their Fabα
fragments: inhibition of IgG-mediated complement activation
IgA blocks IgM and IgG-initiated immune lysis by separate molecular
mechanisms.
Activity of human IgG and IgA subclasses in immune defense against
Neisseria meningitidis serogroup B.

Janeway says much the same thing in different words. IgA is a very minor player in compliment activation, and even then, only in certain situations.

Roos et al (Journal of Immunology, 2001, reference below) suggests that IgA binds MBL, and activates complement by facilitating the lectin binding pathway for complement activation rather than being a major player in the alternate pathway.
Another group of researchers (Daha et al, in Nephrology Dialysis Transplantation, 2006) discusses a potential fourth method for complement activation, as well as describing IgA nephropathy as a result of both alternate- and lectin-activated complement activity. (second reference)
http://www.jimmunol.org/content/167/5/2861.full
http://ndt.oxfordjournals.org/content/21/12/3374.full.pdf

Your third paragraph is slightly confusing. "Has this been discredited?" and then you provide two sources. Are you asking if those articles have been discredited, in which case that should not be part of an answer but should be raised as your own question? Please try to rephrase to make the intention of your answer clear. Thank you.

I think you're right, AML--I decided just to remove the third paragraph entirely, and let the research articles I quoted speak for themselves.

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text:
Why we shiver/tremble/shake while performing some work which requires high accuracy?
Shivering when nervous or anxious is a common thing.
But, shivering or trembling sometimes also occurs when we are performing a work which requires high accuracy. In such case, our whole body doesn't shivers but a part (usually hand) which is involved with that work shivers. The most common example is threading a needle. It requires great accuracy and you might have noticed that when you are doing so, your hands are continuously shaking which prevents you from accomplishing that task flawlessly. Even when we aren't in a state of nervousness, our hands tremble. It's un-resistable.
Yet another quick example - Try to stretch your one arm and try to keep it straight (have it loose, don't try to force it straight), you might notice that your arm is actually shaking a little bit. You can't hold it exactly straight without moving even a little bit.
It's also noticeable when we try to pin-point a small spot with our hand(finger) without actually touching it. (that finger and the hand as a whole starts trembling)
So, what's the reason? It isn't anxiousness as we shiver even when we are calm.
Perhaps, it's gravity which is pulling our hand down and we are trying to lift it continuously which creates a imbalance? But, then we should shiver always?

If you thread needles often - like a dozen times a day for many days - you will eventually be steady as a rock, because practice improves the process (you will also unconsciously maneuver to steady both hands.) It's not inevitable that all people have involuntary muscle movements with very fine motor skills; it's a matter of ability/practice for most.
The steadying of larger muscle groups like the upper arms - especially against gravity - is less controllable (e.g. threading a needle with arms fully extended), but not even closely outside the realm of possibility. Think of what great athletes, dancers, craftsmen are able to do that is "impossible" for mere mortals.

..and what surgeons can do! +1

@Christiaan - D'oh! Great example!

A trivial example : applying an eyeliner flawlessly :P

Norepinephrine (noradrenalin) is a neurotransmitter and hormone released by the body in situations which, among other things, require focus. This may (partially) explain the shaking hands when focusing.

"The general function of norepinephrine is to mobilize the brain and
  body for action. Norepinephrine release is lowest during sleep, rises
  during wakefulness, and reaches much higher levels during situations
  of stress or danger, in the so-called fight-or-flight response. In the
  brain, norepinephrine increases arousal and alertness, promotes
  vigilance, enhances formation and retrieval of memory, and focuses
  attention; it also increases restlessness and anxiety."

The shaking occurs because the body is increasing burning of energy.  There's not many good links online for this (unsurprisingly google searches of "noradrenalin shaking hands" pretty much only returns 'medical' websites trying to tell people they have a brain tumor), but I think what happens is the muscles twitch as a result of the excess energy release.

"When you suffer from anxiety, your body rushes with adrenaline - a hormone that gives your body a tremendous amount of energy, which - when unused - leads to physical agitation. That causes your hands and legs to shake, often visibly."

Beta-blockers are known to reduce symptoms of noradrenalin and are frequently (if questionably and irresponsibly) used to treat anxiety. We may shake less when we practice a process multiple times possibly because with practice anxiety associated with such tasks (I imagine a surgeon is quite nervous the first time they open up a patient) and the level of focus required (intricate tasks become easier with practice thus requiring less focus) both reduce, therefore reducing the amount of focus-related and anxiety-related physiological changes.

While I would certainly agree that doing fine motor activity under intense focus might be stressful (and cause cortisol and norepinephrine release), intensively focused individuals - as @Christiaan mentioned - can perform fine-motor actions without trembling. While I'm not impressed with his political views, Ben Carson was amazing in the operating theater. Intense focus doesn't necessarily cause norepinephrine release, and inability to perform fine-motor actions smoothly is more likely a muscle control issue overcome with practice. Examples are innumerable.

It's (I believe) more related to neuroplasticity, for example demonstrated by the ability of stroke patients in regaining gross and then fine motor function with intensive therapy. Practice.

Perhaps as one gets more practiced they need less intensive focus and becomes less stressful - I know from my own lab work at the start I needed to focus a lot, now I can do it with my eyes closed! Practice makes most things much easier, thus requiring less intense focus (and meaning less noradrenaline release)

I considered that as well. I think it's likely a combination of stress and ability in differing ratios under different circumstances. :)

@anongoodnurse and rg255 , both of your answers were pretty well written and answer my question to a satisfactory extent but both of you are holding slightly different reasons as the cause. Which one should I consider as the actual cause? Ability to control muscle movement or Norepinephrine release? or perhaps both of them? It's hard to decide the correct answer for me :P

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text:
In the video, "Inner Life of a Cell", what's the empty space between the molecules?
In the video, "Inner Life of a Cell" there's a lot of empty space between the proteins. Is it just a simplification (i.e. they omit smaller molecules)? If so, what are the smaller molecules supposed to be? Or is it just a vacuum small enough to be ignored?
I've done some reading up on it, and found that it's called cytosol which is a complicated mixture of random proteins and molecules.

It is a vast oversimplification. At a minimum the space between proteins will be mostly water. There will be plenty of small molecules, ions, and dissolved gases as well. Also, the cytosol is a pretty crowded place.. Also, it might be helpful if you linked to the video so we can see what you're talking about more easily.

@Loogai you answer the question in your question: "I've done some reading up on it, and found that it's called cytosol which is a complicated mixture of random proteins and molecules." - therefore, it's unclear to me why you've posted this as a question, and unclear what question remains.

I was seeking clarification for the cytosol answer and if the proteins in the video comprise the cytosol, if so the space between them is vacuum. I thought I implied it but I wasn't clear enough. Sorry. Also: "what are the smaller molecules supposed to be?"

If the video were realistic and showed all the molecules in the cell, you couldn't see anything because water would always get in the way.

It could be plasma containing water.

This is a common simplification of videos and textbook illustrations. In reality a cell is much more crowded and there is hardly any space between proteins. You can find a more realistic drawing here (I linked the pictures, because I am not sure about the license).
Regarding the cytosol:
Quoting wikipedia:

The cytosol or cytoplasmic matrix is the liquid found inside cells.
  [...]
  Most of the cytosol is water, which makes up about 70% of the total volume of a typical cell
  [...]
  The amount of protein in cells is extremely high, and approaches 200 mg/ml, occupying about 20-30% of the volume of the cytosol


text:
What is a tardigrade "in tun form"?
While reading this article about tardigrades that had been previously frozen, I came across some verbiage I wasn't sure of and couldn't find any real explanation given the context. The article kept making mention of the tardigrades "in tun form", yet the only references I could find to the meaning of tun dealt with weight or casks (like for holding liquid).
So does tun mean cask (like a casing) in this context?

I was wondering the same thing for a good long while, but I have come to the same conclusion that tuns are a folded-up version of the tardigrade that slows down the metabolism of the creature. >>>Tardigrades are microscopic, yet almost invincible one-celled organisms.-Anonymous

From Illinois Wesleyan University:

One way in which tardigrades have adapted to various types of
  environments, has been to reversibly suspend their metabolism. This
  state is known as cryptobiosis [ 'hidden life' (Clegg, 2001) ] and is a truly deathlike state.
  Metabolism lowers to 0.01% of normal or is entirely undetectable and
  the water content of the body decreases to less than 1%. [...]
The most intensely studied type of cryptobiosis is anhydrobiosis, a
  form of cryptobiosis initiated by desiccation. [...] Anhydrobiosis is an almost complete
  loss of body water and the animal can stay in this state for an
  extended period of time. Tun formation, a vital part of the process [Fig. 1.],
  results in a body that is constricted and folded. The first step is
  invagination of the limbs, longitudinal contraction of the body, and
  infolding of the intersegmental cuticle. Wax extrusion covers the
  surface and may help to reduce transpiration (water loss by
  evaporation). The tun formation process requires active metabolism. [...]

Fig. 1. Tardigrade before and after entering the tun state. Note the decreased body length and infoldings. Source: Media & Society Journal.
Reference
- Clegg, Comp Biochem Physiol B Biochem Mol Biol (2001); 128(4): 613-24


text:
Are there people blind to touch?
There are people who completely blind or deaf. Are there people who are completely blind to touch in a particular area or in the entirety of their body? If not, are there people in whom the temperature modality of touch or the pressure modality of touch is completely absent? It seems that this might be related to congenital insensitivity to pain, but it is not quite the same thing.

USH2A mutations can cause degrees of deafness and partial touch insensitivity in humans. Do those count or is full loss of function a requirement?

@AlexReynolds I thought Usher's syndrome affected sight and hearing only?

There is a paper from 2012 that suggests a mutation in that gene can cause partial loss of touch sensitivity (ref. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3341339/)

Short answer
In a way, yes.
Background
One prime example where the sense of touch is diminished is when peripheral sensory neurons degenerate, which is called sensory neuropathy. Diabetes is currently a common cause of this disorder, resulting from the high blood glucose levels that damages the small blood vessels which supply the nerves. This prevents nutrients reaching the nerves, eventually damaging nerve fibres, which may end up in a disappearance of the nerve altogether (source: diabetes.org).
Sensory neuroptahy can lead to a multitude of complaints, including weakness, numbness and pain, usually in the hands and feet (source: Mayo clinic).It can also lead to the loss of ability to feel pain, changes in temperature and coordination when you lose proprioception is affected. The loss of the sense of pain is dangerous. An often heard complaint is that wounds to the feet are not noticed. If ignored, even minor injuries can develop into infections or ulcers (source: diabetes.org). I fact, my grandmother-in-law recently underwent an amputation of the lower leg, because of a diabetes-related, neglected injury to her toe. It lead to an ulcerating wound and eventually necrosis. At a certain point it caused terrible pain, but the initial wound had gone unnoticed.
A related condition is Carpal Tunnel Syndrome, also called median nerve compression. It is a condition that causes numbness, tingling, or weakness in your hand. It is caused by pressure on the median nerve that traverses a passage in the wrist called the carpal tunnel.
This may not be exactly the answer you are after, as sensory neuropathy mainy causes numbness of the extremities, rather than a complete loss of sense of touch. Remember, however, that blindness rarely results in a complete blackness. Beside the fact that the great majority of blind people are 'only' functionally blind, as they still have rudimentary visual function left, perceptions of phosphenes are in fact really common, and some people even start seeing complete visual scenes with people and objects included (Charles Bonnet syndrome). This is not unlike deafness, where many people still have residual hearing, yet too little to be of any functional use. For instance, people that are eligible for a cochlear implant often still have substantial residual hearing left. Like phosphenes in the blind, tinnitus in the 'deaf' emerges akin to 'phantom' sounds. These 'hallucinatory' sounds are actually generated more centrally by the brain after prolonged deafness. In short, blindness and deafness are relative, the great majority of folks don't lose their senses, they have reduced functionality of them.


text:
Why is active transport needed in repolarization?
During the repolarization phase of an action potential, the potassium ions diffuse out of the cell, and active transport begins.
What I do not understand is why active transport is needed when the movement of ions is not against their concentration gradient?
Since the potassium ions have diffused out in repolarization, only the sodium ions are left in the intracellular space.
The sodium/potassium pump is used to pump 3 sodium ions out and 2 potassium ions in. However, isn't there a concentration gradient as the sodium ions are moving out of the cell, where there are no sodium ions, and thus from a high concentration to a low concentration?
Is it because the active transport allows the imbalance to occur (3 out and 2 in)?

...when the movement of ions is not against their concentration gradient...

This assumption is incorrect: Na+ has to be pumped out of the cell against its chemical gradient (table 1) and against its electrical gradient, given that the inside of the cell is negative (Fig. 1).

...potassium ions have diffused out in repolarization, only the sodium ions are left in the intracellular space

This is incorrect: There are heaps of K+ ions in the cell, also after repolarization. A tiny fraction exits the cell during repolarization.

...moving out of the cell where there are no sodium ions...

This is incorrect; there are Na+ ions out of the cell, heaps in fact. You should be aware that the flux of ions is not an all-or-nothing phenomenon. It is a flux of relatively few ions out of a pool of them. Action potential formation and ion gradients are membrane-bound phenomena. While Na+ may enter the cell during an action potential, there is still a nearly infinite large amount of Na+ left in the intercellular space.

Table 1. approximate ion concentrations in and out of the cell. source: Med Quarterly

Fig. 1. Action potential. source: UC Davis

Okay. Regarding the fact that the movement of ions is "not all or nothing", as during depolarization the intracellular space is momentarily positive compared to the extracellular space, although not all of the sodium ions have diffused into the cell, there is enough to create a positive charge within in addition to the positive charge of the potassium ions?

And so even with the pump actively transporting 3 sodium out and 2 potassium in during the resting potential, there will never be only potassium in the inside and sodium on the outside correct?

@city7lights that is correct


text:
Ebola immunosupression and infection
I was wondering... If Ebola attacks immune cells and causes immunosupression, then shouldn't we see death in Ebola patients due to secondary infection?

Secondary infections does not matter when you bleed to death... Btw. I hate this ebola hype, it is a relatively insignificant lethal virus, nothing more.

Yes, we should. But Ebola doesn't completely immunosuppress us, or there would be no survivors.
Ebola kills by overwhelming the body before enough antibodies are formed to fight it.
If you're one of the survivors (as about 40-50% are, more with good care), you'll have antibodies to Ebola in your blood which might help someone else infected with Ebola.
If you're not one of the survivors, it's still likely you'll have some antibodies, but the shock your body goes into from all the dead cell products in your blood (which - overly simplified - causes a cytokine storm -> leaky capillaries -> fluid balance problems -> end organ failure -> death).

So the Ebola virus replicates too fast for the immune system to handle?

I wouldn't quite put it that way. I'd say, rather, that in many cases, the host dies of the damage done by the virus before an immune response adequate to destroy the virus is mounted.


text:
Difference between protein channels, protein carriers and protein pumps?
I'm revising for my biology exam and I don't fully comprehend the difference between protein channels, carriers and pumps. I know that:

Protein channels do not require ATP (passive transport)
The difference between passive and active transport

My questions are:

Are protein carriers and pumps the same?
I read that protein carriers can perform both active and passive transport, is this true?
But protein pumps always require ATP?

@Christiaan Thanks for the  comment, but I'm specifically confused about the proteins, not active and passive transport.

Usually, when introductory textbooks and tests ask about pumps, they are usually ion pumps, such as Proton pumps or Sodium - Potassium pumps, etc. Carriers usually are used to transport hydrophilic molecules such as glucose through the membrane. Carriers can be both. Passive usually requires another substance, such as sodium where there is a gradient. The binding of the transported molecule will cause a conformation change in the carrier protein that transport the molecule to the other side of the membrane. Have you talked to classmates about their understanding? Study groups are a good idea.

No, carriers are not the same as pumps. Carriers may or may not carry out active transport and pumps always use energy. Carriers, for example, can make use of the concentration gradient of a certain ion built up by pumps to transport other molecules actively against their gradient. For example, the glucose transporter uses the sodium gradient to transport glucose against the concentration gradient into the cell, while getting the energy by co-transporting sodium into the cell along the gradient. The sodium import yields energy. That in turn is caused by the Na+ K+-ATPase, which builds up the sodium gradient using ATP. The glucose transporter is called a symporter, because it co-transports sodium into the cell. An antiporter transports another particle in the opposite direction.
Yes, true. The glucose transporter as explained above is an example of active carrier-mediated transport. Other carriers just mediate passive diffusion of, for example, large molecules that don't fit through channels and won't readily cross the cell membrane.
Yes, pumps always use energy under physiological conditions. The energy source is always ATP.

Will add references shortly.

Good summary. A couple of comments to consider. First, there is not a single type of glucose transporter, which isn't clear from this answer. The one you describe is used in intestinal and renal epithelia, but most mammalian cells use a simple uniporter for glucose uptake. Second, I think that many would consider the proton transport out of the inner mitochondrial membrane, needed for oxidative phosphorylation, to be pumping, but the energy sources there include NADH and oxygen, not ATP.

A small note: There are also carriers that use ATP by their ATP Binding Cassette domain (ABC transporters). The mechanism, however is different from that of the phosphorylation dependent pumps.


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Can we taste electrons?
Why does licking a 9-Volt battery elicits a taste sensation? Can taste be stimulated by electrical stimulation?

I'm assuming stimulating a taste receptor generates a "taste", and there are no taste receptors on your knee. This could be relevant: https://en.wikipedia.org/wiki/Digital_lollipop

Short answer
Yes, taste sensations can be generated electrically. However, we cannot taste electrons themselves, as taste-receptor proteins on the taste receptor cells are not activated by electrons. Instead, electrical currents stimulate taste receptors directly by depolarizing the cell membrane, without the need of activation of the proteins that normally bind ions or molecules.
Background
There is a medical device called the BrainPort that electrically stimulates the tongue (Fig. 1.) The device is marketed as an electrotactile vision substitution device. Basically, it captures images of the outside world with a glasses-mounted camera and these images are translated into electrical stimuli presented on a 20 x 20 electrode array. That array is embedded in the tongue display unit (aka intra-oral device, IOD). The IOD is worn on the tongue.

Fig. 1. BrainPort V100. source: TuWindowsMundo
It typically generates electrotactile sensations, like champagne bubbles. However, some subjects do report metallic taste sensations when using the device. In fact, Lawless et al. (2005)* investigated the electrically evoked metallic-taste in response to anodic stimulation of the tongue directly and confirmed the anecdotal reports obtained with the BrainpPort device that electric stimuli evoke metallic-taste sensations.
Physiologically, taste receptor cells sense certain compounds (salts, acids etc.) due to activation of receptor molecules on the cell's surface. In turn, activation of receptor molecules depolarizes the cell membrane which eventually lead to neurotransmitter release and activation of secondary neurons that transmit the signal up to the brain (Fig. 2). Electrical stimuli bypass the receptor molecules and directly depolarize the taste receptor cells.
Given the anatomy of the taste receptor system in the tongue (Fig. 2), I am inclined to believe that the taste receptors are stimulated directly, and not the secondary neurons, because they are situated in deeper layers.

Fig. 2. Neural pathway of the taste buds on the tongue. Note that the secondary neurons transporting the taste information to the brain are situated in deeper layers than the taste buds. Source: Universe Review.
Note that taste receptors do not sense electrons. Rather, larger ions or molecules may stimulate them and cause a depolarization of the receptor cell, in turn activating the secondary neuron via a chemical synapse.
Reference
- Lawless et al., Chem Senses (2005); 30(3): 185–94
Acknowledgment
*Credits for the Lawless et al. (2005) reference go to @CMK

I have also heard of some device that can produce tastes of different foods via electrical stimulation. I am not sure if this is the same device.


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Why is it necessary to have both cone and rod cells in the eye?
Our eyes have both cone and rod cells. Rod cells measure the intensity of light whereas cone cells identify the colour of the image formed in the eyes. So cone cells must also be able to identify white, black and grey and also their shades.

So it wouldn't have been that much trouble to just have cone cells cells as identifying black and white would have been the same as measuring the intensity of light. Wouldn't it?

Duplicate of http://biology.stackexchange.com/q/42216/3340

@WYSIWYG this question is different

The question might sound different but the answer there completely answers your question. There is no point in repeating the same answer, isn't it. If there is something that is missed out in that answer that your question pertains to, then you can add some details to clarify.

Jen asked that what would white look without cone cells. I wish to ask is it necessary to have both cone cells and rod cells.

Please see Christiaan's answer to Jen's question.

It is pretty much similar but i am still having trouble understanding why rod cells are required. As stated  Rods only mediates the perception of low-resolution gray-scale images, so couldn't the same image be provided by cone cells by only using black, white and gray.

It is clearly mentioned in Christiaan's answer that rods are required for vision in low-light conditions.

First off - both the rod and cone system measure light intensity; both sensory cells increase their responses when excited by more photons (Purves et al., 2001). Hence, your introductory sentence that rod detect luminescence and cones color is incorrect. They are both sensitive to luminescence.
You are correct that rods detect gray scales, while cones perform color coding. Both systems can detect gray shades; while rods are limited to that, cones are not. Rods are very sensitive to light and in a dark-adapted state are capable of detecting a single photon. Hence, they operate under conditions of low-lighting at night and as such they mediate night (scotopic) vision. Cones are photon-hungry and need more light to operate (photopic conditions).

Why have cones? Because color vision helps to detect and differentiate stuff.
Why have rods? Because night vision is helpful.
Why have both? To be successfully equipped to thrive in both light and dark environments.
Do we need them both? No - even nocturnal hunters that don't have rods have been shown to be able to hunt at night. Not only that, these geckos have been shown to be able to detect color in starlight (Röll, 2000). Under these lighting conditions, human retinae rely on the rod system and are unable to detect color.

References
- Purves et al., Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates
- Röll, J Neurocytol (2000), 29(7): 471-84

But in night couldn't we have managed off with just using grayscale vision with the help of cone cells to view images. During night the cones don't work?

our cones don't work at night.

So, as cones don't work at night, we need rods to help us with grayscale images.

@Reptile1234 It's more that you need rods to help you see at night. Not having functional rods results in nightblindness. As you can imagine, not being able to see at night will affect one's ability to survive.


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How many "primary colors" can we smell?
There are many more that three visible wavelength in the visible EM spectrum, and yet we can model any color using only three primary RGB wavelength. Perception of an arbitrary color is equivalent of perception of a linear combination of only three fixed wavelengths that correspond to Red, Green, and Blue.
On the other hand, as far as I know, there seem to be no auditory "primary colors": you cannot fool an ear into believing that it hears an arbitrary frequency by starting with a small finite number of primary frequencies.
The question is about human olfactory sense: is it possible to fool the nose into believing it smells an arbitrary odor by offering a combination from a small collection of "primary smells"?


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How is recruitment of multiunit smooth muscle cells fine tuned if they are innervated by varicosities?
In my physiology textbook (Silverthorn) and on wikipedia it says that:

Multiunit smooth muscle tissues innervate individual cells; as such,
  they allow for fine control and gradual responses, much like motor
  unit recruitment in skeletal muscle.

However, that does not seem right to me. Although potentially each cell could be innervated, they are innervated by autonomic neurons. These neurons use the rather crude method of varicosity innervation. Such neurons recruit all the cells adjacent to its varicosities, not just a few. Hence, does this not mean that there is no 'fine' control of unit recruitment of smooth muscle cells?  Or is there an other way in which recruitment of smooth muscle cells is fine tuned?

Welcome to Bio and +1 for a good question. Could you link that wiki page?

I removed Moreover Silverthorn states that smooth muscle cells are responding in an all or nothing fashion, as I don't understand its relation to the question. Feel free too roll back any edits if any or all of my edits are not to your liking.


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Anatomy of the ear canal
When you insert your finger into your ear, you hit a dead end. You can't insert your finger into the auditory canal. What's this dead end called, the medical term for it?

I think its because auditory meatus is curved, not straight to prevent direct entry of large substances (insects, finger) inside to the tympanum.

Short answer
There is no dead end from the entrance of the auditory canal to the tympanic membrane. The diameter and shape of the object inserted rather determine whether it can reach deep enough.
Background
The above statement can be proved by following examples:
ENT doctors use an otoscope on a regular basis to directly examine the tympanic membrane (eardrum), meaning the emitted light entering the meatus from the otoscope, and the reflected light from the tympanic membrane exiting the auditory meatus are following straight paths.
Another practical example is the use of tympanic temperature to quickly measure core temperature. Again, the infrared light emitted by the tympanic membrane has to follow a straight path out of the meatus, otherwise it would be absorbed.
Lastly, see below picture that graphically shows the relative straightness of the meatus. There is some curvature, but certainly no dead end. A dead end, or hooked region with a sharp angle would be disastrous for hearing sensitivity, as it would block the passage of sound waves to the middle ear.

structures of the ear. source: WebMD.
The finger is simply too wide to enter the meatus to the tympanic membrane. In contrast, cotton buds do readily enter the meatus up until the tympanic membrane and ENT doctors sadly see quite a lot of cases where folks turn in with ruptured tympanic membranes due to excessively deep insertions of cotton buds.


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With over 400 chromosomes, does mitosis in a species of butterfly happen in the same way as in humans?
The beginning of the Ars Technica article Gene editing crunches an organism’s genome into single, giant DNA molecule begins:

Complex organisms have complex genomes. While bacteria and archaea keep all of their genes on a single loop of DNA, humans scatter them across 23 large DNA molecules called chromosomes; chromosome counts range from a single chromosome in males of an ant species to more than 400 in a butterfly.

Thanks to @Remi.b for tracking down Lukhtanov (2015) The blue butterfly Polyommatus (Plebicula) atlanticus (Lepidoptera, Lycaenidae) holds the record of the highest number of chromosomes in the non-polyploid eukaryotic organisms.
Does mitosis happen in this species of butterfly cells, and if so, does the process that separates the pairs take place in a similar way mechanically to the way it happens in mammal cells such as the 23 pairs in human cells even though there seems to be almost twenty times the number of individual chromosomes?
Has the mechanics of this process ever been imaged or visualized?

above: from here and here.

above: " Image of the mitotic spindle in a human cell showing microtubules in green, chromosomes (DNA) in blue, and kinetochores in red." from here

For those who would rightly ask for a reference for the claim that there is a species of butterfly that has more than 400 chromosomes, consider having a look at  Lukhtanov (2015).

@Remi.b Thank you very much for tracking that down! I've added that back into to the question.

Mitosis was displayed in a lot of organism, also in organism with a very high number of chromosomes. Here's an example of the analysis made in a fish with an average count of 280 chromosomes. Look at the metaphasis of a cell with higher number of chromosomes (Acipenser transmontanus):

This doesn't mean that every chromosome is equal to others: there're microchromosomes, acrocentric chromosomes, meta, sub-meta.. So, the size required into the nucleus (because where're obviously talking about eukaryotic cells) isn't strictly connected with the chromosomes number.
The answer to your question isn't a clear "yes" : the high number of chromosome in a butterfly is connected with a karyotype instability, where some cells received a wrong number of chromosomes into an alterated mitosis. Actually isn't fully clear why and how these errors come out. Here's something else about butterfly karyotype and phylogeny.

Thanks for the explanation, link, and image! I just found and put an additional image in the question, and discovered the word "spindle" that I'd been looking for. Mechanically, if there were 400 pairs of chromosomes, I'm trying to understand if there would also be 400 pairs of spindles as well?


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What causes "ear rumbling"?
The video Ear rumbling happens below the range of human hearing demonstrates that the "ear rumbling" sound is actual sound and can be recorded by a sensitive microphone near the ear.
What is it exactly that produces this vibration and how is it radiated as sound waves into the air?
If it is subsonic, then why does it sounds like noise rather than being inaudible?

I'm able to create rumbling in my ears at will. Unlike the poster of the video, I don't need to yawn to do so; I can do it without my face appearing to move. I actually discovered this alongside another ability of mine when I was little: the ability to create warmth flowing from the base of my neck outwards into the rest of my body. After some research I figured out that the warmth I'm able to create is actually part of voluntary piloerection (its use for warmth is mentioned here), while the ability to create a rumbling sound is simply the contraction of the tensor tympani, a muscle in the ear. Voluntary control over either one of these things is supposed to be rare, but I've found claims of several other people online who can do both (example1, example2).
Anyways, Wikipedia gives a brief explanation of how the ear rumbling works, which also specifically mentions "yawning deeply" as a trigger:

Contracting muscles produce vibration and sound. Slow twitch fibers produce 10 to 30 contractions per second (equivalent to 10 to 30 Hz sound frequency). Fast twitch fibers produce 30 to 70 contractions per second (equivalent to 30 to 70 Hz sound frequency). The vibration can be witnessed and felt by highly tensing one's muscles, as when making a firm fist. The sound can be heard by pressing a highly tensed muscle against the ear, again a firm fist is a good example. The sound is usually described as a rumbling sound.
Some individuals can voluntarily produce this rumbling sound by contracting the tensor tympani muscle of the middle ear. The rumbling sound can also be heard when the neck or jaw muscles are highly tensed as when yawning deeply. This phenomenon has been known since (at least) 1884.

It also seems like this type of noise can happen with conditions such as Tonic Tensor Tympani Syndrome.
The tensor tympani connects directly to the handle of the malleus, so I'd assume that's why it can be heard by the person doing it. Apparently this also causes the eardrum to move. This means it's classified as objective tinnitus.
Here are some relevant studies I found:

Voluntary contraction of the tensor tympani muscle
and its audiometric effects
Voluntary Eardrum Movement : A Marker for Tensor Tympani Contraction? (paywall)
Tonic contractions of the tensor tympani muscle: a key to some
non-specific middle ear symptoms? Hypothesis and data from
temporal bone experiments (paywall)

Thank you very much for taking the time to write such a well-sourced answer. This is great!

@uhoh I didn't find it publicly, which is why I was using my school access to read it. Using that link was a mistake; I have edited it to be a link to the abstract.

That looks great, thank you! I'll stop by a library soon and give all of these a good read.

half-way through discussion Lise et. al. says "Voluntary control of the tensor tympani muscle is an extremely rare event." I can make this loud rumbling sound in both ears any time I want just as you describe in your introduction, and yes after 10-20 seconds of continuously doing it it gets difficult just like a muscle is getting fatigued.

I wonder if this is really as rare of an ability as this paper suggests, or if it's simply rarely-reported or rarely-published?

With these you may be able to finally answer What is official term for contraction induced muscle “vibration”?

The rumbling is caused by two middle ear muscles. These muscles are connected to ear drum and staples, if they are activated, they make it harder for incoming air soundwave to push the eardrum, they increase eardrum acoustic impedance so less sound gets to cochlea. This is triggered by loud sounds and it serves to prevent hearing damage, its called acoustic reflex.
All muscles when activated and under tension shiver slightly, this vibration is the rumbling you hear. The reason you hear this so loud is becose the muscles are directly connected to your middle ear bones so the vibration goes directly to cochlea. You may also hear it if you tense up your jaw muscles but it will be alot quieter becose its further away from cochlea. You can also try pressing clenched fist against ear to hear this muscle rumble.
The term subsonic is confusing and vague, its generaly considered to be sound below 20 Hz but the problem is that humans can hear down to about 5 Hz if the sound is 110db loud. Also, while its true this muscle rumble does contain sub 20 Hz sound, it extends above it too, roughly to 70Hz.

Thanks! The vibration is an artifact of some collective behavior of nerve and muscle. If the result is not a pure sine wave but instead was anharmonic and had other noise and random effects, would those end up above ~20Hz?

I am sorry I dont understand what you mean.

I'm thinking that the audible part is not a ~12 Hz (or similar) sine wave, but the random variations or noise in the contractions. Muscles have a bit of mechanical noise when they contract, in addition to the periodic vibration. I'll see if I can find a better word for it. I'm proposing that it's not the very low frequency sine wave we hear, but the random, noisy component on top of it.

Noise is just word for bunch of chaotic sinewaves. You are right, you mostly hear the 40 to 70Hz part, the 10 to 20 Hz part doesnt contribute much to audibility.

https://www.newscientist.com/article/dn11885-muscle-noise-could-reveal-diseases-progression/ links to https://aip.scitation.org/doi/10.1063/1.2737358 but I don't have access right now


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How to clean and preserve a cicada's molted exoskeleton (exuvia)?
I found a good quality molted exoskeleton (exuvia) of a cicada, about 3-4 cm long on the ground. I'm amazed at the completeness and detail, the exit hole is in the center of the back and you hardly notice it. The "claws" on each foot are sharp and you can stick it onto any surface with a bit of roughness.
It had rained and there is some mud on it. I'd like to gently wash it and then keep it.
Are there any particular guidelines or techniques I should know about? Can I just gently swish it around in soapy water and then let air dry, or do I need to take some precautions, or even use some kind of fixative? Humidity is high where I live; anything that can possibly support mold will get moldy if you are not careful!
Sorry I can't add a real photo right now but it looks a bit like the emptying exoskeleton in this randomly chosen photo from here:

Are there any additional tags for this? I couldn't find "preservation" or "specimen" or "collecting"

The exuvia is made of cross-liked chitin, and will not decay. You don't need any special preservatives as all. If you need to get the mud off, just rinse it as you said, in soapy water, let it dry, and you are done. Simple.

Excellent, thank you for your quick reply! It might be good to add a supporting link for the "cross-liked chitin" for future readers, but personally I'll take your word for it.

fyi I've just asked Is the chitin in an insect's exoskeleton cross-linked?


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Difference between LH and ICSH
Are Luteinizing hormone and Interstitial Cell Stimulating Hormone(ICSH) the same?

As far as online dictionaries (Medical Dictionary, Merriam-Webster) and a popular-scientific site on hormones (Your Hormones) go, LH and ICSH are the same. ICSH mainly pops up in the older literature; e.g., Lostron & Johnson (1966) and Louvet et al. (1975). My understanding is that LH is currently the more accepted term for the hormone.
I get the impression that historically, LH has been used in relation to female reproduction and ICSH to the male reproductive systems. In males, LH stimulates Leydig cells in the testes to produce testosterone. In females it stimulates the ovarian follicles to produce oestradiol, and it induces ovulation.
References
- Lostron & Johnson, Endocrinology (1966); 79: 991
- Louvet et al. Endocrinology (1975); 96(5): 1179-86


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Use of restriction endonucleases to analyse Variable Number Tandem Repeats (VNTRs)
The textbook I’m using states that “Ends of VNTR have conserved sequences. These can easily be cut by restriction endonucleases.”
But restriction endonucleases cleave palindromic sequences. Does this mean that the repeated DNA and conserved sequences together form a palindromic sequence?

The general situation regarding using restriction endonucleases to analyse Variable Number Tandem Repeats can be explained with (as well as without) reference to the illustration below.

The original region of DNA in which the insertion occurs will in general be complex (rather than repeated) and conserved to a reasonable extent among H. sapiens. The complex conserved sequence is represented by a gradient of colour in the upper part of the diagram so that the point at which the original copy of the repeat inserted can be identified in different individuals (or alleles), A, B and C, where, for the sake of argument, two, three and four copies have been generated.
The individual repeat unit is relatively short (typically 10–100 bp), so it is relatively easy to find conserved sites for at least one commercially-available restriction endonuclease on either side of the original insertion, but not within the repeat.
The mathematics of this reasoning are quite simple, and I provide exercises on my University website. However, as an example, consider a 4-base pair sequence that is the target for a restriction enzyme. It need not be palindromic, but as most Type I restriction endonucleases are, let’s choose GGCC. The chance of finding this in any tetra-nucleotide is 1 in 256 (4x4x4x4), or, in other words, it should occur in any 256 bp stretch of DNA. (Of course this is just an average of what may be a normal distribution, and overall base composition will affect the actual frequency.)
The net result will be that it will be possible to generate fragments of an overall size such that the flanking regions are not so large that they make it difficult to distinguish differences reflecting different numbers of repeats.
And today?
The polymerase chain reaction (PCR) might well be used instead of restriction endonuclease digestion as, given that the DNA sequence of the region has been determined, one could choose appropriate positions in the flanking regions to generate DNA fragments for analysis. See, e.g. Richie et al. (1999).

The edited question is much closer to what I actually wanted to ask. And the exercises you provided are very useful as well. Thank you so much!!

You are welcome. Although written a few years ago, it is gratifying when students find them useful.


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Why does there have to be two muscles to control the size of the pupil?
In dim light, the circular muscles relax and radial muscles contract to allow more light to enter the eye, and vice versa in bright light.
Why is there the need to have two muscles when probably the circular muscles would do the job itself? Couldn't a single circular muscle be responsible for to enlarge the pupil (muscle relaxation) in dim light and constrict it in bright light (constriction)?

Those aren't biology questions. Those are engineering questions at best and what if questions. Just because something is the way it is in biology doesn't mean it must be that way, but it probably means there are good reasons for it. "Why must DNA have a right-handed helix?" is asking the wrong question to ask.

It's a biomechanical question, and therefore on topic. It can be answered with general knowledge of biomechanics to explain why/how the two muscles are applied in this setting. I'm not a fan of the question given the lack of research effort, but I see no reason to close due to topic choice. @user, please [edit] to show some personal effort to answering the question. Thanks.

Short answer
Agonist / antagonist muscle pairing in the form of the sphincter and dilator muscles in the iris allow for quick and powerful movements of both the constriction and the dilatory response.
Background
Like the (striated) skeletal muscles, the smooth iris muscles come in pairs. Contraction is per definition an active process, and hence it is fast. Take the familiar example of the arm; when the agonist (biceps) contracts, the arm bends. Its antagonist (triceps) relaxes at the same time to give minimal resistance to the motion. The process reverses when the arm is stretched again (Fig. 1).
A similar mechanism operates in the iris to regulate the pupil response (Fig. 2). In this case it is smooth musculature: the sphincter muscle  forms a ring around the pupil and constricts the pupil. The dilator muscles radiate from the pupil such that contraction dilates the pupil. Also here, the action of the dilator is antagonistic to that of the sphincter and the dilator must relax to allow the sphincter to decrease pupil size. Their actions regulate the amount of light that enters the eye as well as the depth of field. The iris sphincter is controlled by the parasympathetic system, whereas the iris dilator is controlled by the sympathetic system (source: University of Texas).
A constriction and relaxation alone cannot do the job, unless some basic tension would exist that would keep the arm continuously bent; in that case a constant muscle tone would be needed to keep the arm fixated somewhere in the middle of its dynamic range. Increased tension would bend it, relaxation would stretch it. However, a decrease in tonus would never allow it to be stretched completely without the assistive force of gravity or another source of power. In addition, it would be a really sluggish process. E.g., using your arms to get up from the ground would be impossible.
In terms of the eye, the pupil response would be fast in the active process, say the constriction, but very sluggish at best in the opposite direction. Viscosity and friction of the tissue might even prevent the antagonistic (dilation in this example) movement altogether, leaving your pupils stuck in a constricted state (in our example), hampering quick adaptation to dark environments.
Reference
- Tudor & Deaconescu, MATEC Web of Conferences (2018); 178(3): 07005

Fig. 1. Arm control. source: (Tudor & Deaconescu, 2018)

Fig. 2 Pupil response. source: Mammoth memory


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In evolutionary history, which came first - neuron or astrocyte?
As research is showing astrocytes role in information processing [1], I am interested in knowing which evolved first - an astrocye or a neuron ?
[1] Santello, M., Toni, N. & Volterra, A. Astrocyte function from information processing to cognition and cognitive impairment. Nat Neurosci 22, 154–166 (2019)

Short answer
Neuroglia evolved after neurons did. The evolution of glial cells coincided with increased complexity of the organization of the nervous system.
Background
Glial cells are supportive cells for neural tissue. As such, evolution of glia before neurons would not be a parsimonious hypothesis, however not impossible.
Glia indeed seems to have evolved after neurons did. Arguably, Ctenophora (comb jellyfish) and Cnidarians (hydras and sea jellyfish) feature the most primitive neural systems known today. They have diffuse nervous systems, characterized by relatively simple semi-independent networks. These networks lack conglomerates of specialized neurons called ganglia, and these animals don't have a brain or a spine such as the chordata have. They also don't have glial cells associated with the diffuse neural networks.
Only until more complex nervous systems appeared later in evolution, i.e., in early Bilateralia (e.g., flatworms and roundworms) supportive cells evolved: the neuroglia.
Reference
- Verkhratsky et al. Adv Exp Med Biol (2019); 1175:15–44

Fig. 1. Evolution of glia accompanies increased complexities of early life forms. source: Verkhratsky et al. (2019)


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Would tinnitus be explained by perpetually-bent/opened hairs in the cochlea?
When I look around for what causes tinnitus and the like, the usual response is "Well, loud sounds and hearing damage" but I feel like that's a little plain and I am curious about the underlying mechanism / explanation on a physiological level.
My previous understanding of how the ear works can be found in my previous question (with a terrific answer by AliceD).
So my question is this: Let's say a really loud, fierce sound occurs - the sort of thing that is said to cause tinnitus. This is equivalent to a really strong pressure wave approaching the eardrum. I imagine it would hit the eardrum, causing it to move violently / harshly, causing a similarly strong movement in the stapes, which is already providing something like a 20x pressure amplification to the cochlea.
So the stapes hammers hard on the oval window of the cochlea, causing a harsh pressure wave through the perilymph / endolymph, also causing the basilar membrane to move very harshly and violently. To me this would imply a fierce smashing/dragging of the hair cells against the tectorial membrane above, possibly causing sufficiently harsh wear-and-tear along the tops of the hair cells, leaving them bent or maybe even chopped, allowing their channels to remain perpetually open.
If these channels are always open, they're always accepting potassium, always creating the action potentials, always triggering the nerves underneath, which would mean the person is always hearing that particular tone all day, every day, 24/7.
Is this more or less what happens, or am I way off in my little thought experiment daydream here? Is this why tinnitus is difficult to cure, because it would require somehow rebuilding / closing up hair cells that are always open?

Thanks for the credits!

What you're describing would likely cause hearing loss, which could later result in tinnitus, but not by the mechanism you describe.
Hair cells transduce sound via remarkably fragile connections between stereocilia. The channels are closed until tension pulls the channels open (see Fettiplace 2011 for a review that covers pretty much all of sound transduction including a detailed description of the tip links and channels involved). Disconnection would result in the channels being perpetually closed, not perpetually open.
Anything like the trauma you describe would irreversibly damage the tip links and sound transmission would fail. There are mechanisms in the ear to prevent this sort of damage, but for sufficiently loud sounds the damage is not avoidable.
@AliceD has another excellent answer on tinnitus specifically here for more realistic mechanisms proposed for tinnitus: What is the mechanism behind tinnitus?. These are all centrally derived in some way. In short, the absence of proper input to the auditory processing parts of the brain results in compensation that induces an illusory perception. Similar sensations are experienced in other parts of the body as well, such as phantom limb.

Fettiplace, R. (2011). Hair cell transduction, tuning, and synaptic transmission in the mammalian cochlea. Comprehensive Physiology, 7(4), 1197-1227.

Thanks for the credits!


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What kind of big bird is this seen walking around Taipei?
I've seen this humorous sign warning drivers to keep an eye out for birds many times, but today I finally realized what it's talking about!
This is a large bird and I've seen it all around Taipei in gardens and green areas. It's not shy of people unless you get too close.
I'd guess it's about 30 cm tall when standing upright, but it often is bend down looking for things to eat. It takes one step at a time, sometimes very slowly, and it's head moves out-of-synch with its body as it hunts for food. I am not sure if it can fly, I've only seen it on the ground, and I've never heard it make a sound.
It's various shades of brown and tan, and just like the cartoon on the sign it has long feathers projecting backwards from its head. That can be seen in the center top of the photo montage.
Any idea what kind of bird this is?
These are cell-phone photos from the closest I could get without it getting nervous.

"Life imitates Art far more than Art imitates Life" Oscar Wilde

Does anyone know what the sign says?

@CDspace I don't have an official translation, but I'm told it doesn't match the humor of the drawing, and says something like "animal crossing; slow speed, pass slowly".

Ah, I see it now. The bird is in the foreground, and not Godzilla size picking up the car

@CDspace actually I believe it's meant to look huge. That's the style of warning signs here, often a little humorous and cartoonish to catch your eyes and not to appear too authoritative.

I am fairly certain that this is a Malayan Night Heron (Gorsachius melanolophus).
Taiwan is listed as one of the countries where the Malayan night heron can be found. Its diet consists of small reptiles, snails, chilopods, arachnids, crabs and insects. This would explain why you have observed it bend down a lot to look for food.
Needless to say you can find more information in the corresponding Wikipedia article.
Here a photo with better resolution:

Photo by: Pete Morris/Birdquest
In addition, here is a link to a video taken in Taiwan. Does this remind you of the bird that you saw?

That's a great photo, yes this certainly looks just like it, thanks! Okay I'll give the article and video a look. Tis one and the one in the video are a little darker than the ones here but that could just be regional variations. Southern Taiwan has some differences in flora and fauna.

You are welcome. I agree, it could well be that there are regional variations or that males looks slightly different to females (sexual dimorphism).


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What is "beto carotene" and how can it turn lakes pink?
The BBC News article Pink lake in Australia attracts and delights tourists describes an artificial salt lake in Westgate Park, Melbourne, Australia that tuns pink around February and then in "late Autumn, until cooler temperatures restore it back to blue."
I am not sure about the autumn part as it's in the southern hemisphere, but my question is about the color change.

Could they mean beta carotene rather than beto carotene?
And if so, does the pigment stay inside the algae or is it released into the water to produce this color change?
And why pink, rather than the orange color we associate with carrots?

In those conditions, the lake's algae produces a red pigment called beto carotene

The lake's pink colour typically lasts through to late Autumn, until cooler temperatures restore it back to blue.

It's definitely a typo and should be beta.

Carrots actually come in a variety of colors, orange carrots is just a fluke of political history and has little to due with beta-carotene.

Note there are other ways to get pink lakes halobacteria dominated lakes (hypersaline) are often pink becasue they don't use chlorophyll but bacterioruberin. Salt itself tends to be pink which can contribute. Lake hiller in Australia is one such lake. https://en.wikipedia.org/wiki/Lake_Hillier

@John see my comment below questioning if "Salt itself tends to be pink".

The "beto" is a typing mistake. Beta is an organic chemistry label referring to a beta-ring of 6 carbons that exists at either end of a carotenoid polymer C40-Hx.
It is localized in the chloroplast. The plants don't really have a mechanism to release pigments, they can re-metabolize chlorophyll. The volvocalean algea Dunaliella salina is used to harvest beta-carotene in Karratha, Western Australia, from salt lakes. The can have 12% beta-carotene as dry-matter content, the highest of any known source.  The squares are probably salt.

the algea afterwards:

There are over 1,100 known carotenoids of which at least 700 have been identified in plants. They include carotene and xanthophylls, and carotene include beta-carotene. The plants and algea use it to protect themselves from intense sunlight and UV's. It is an anti-oxidant.

Pink doesn't actually exist as a color. It is imagined when green and blue light is sensed by the eye, while red is at a maximum. In the lakes, we know there is 80% red and 20% green pigment in the algea. All that is required would be 20% blue to percieve pink. I don't know where the blue color comes from, the sky/water.
Orange is complex for the eye, and so is pink, because we can only see red green and blue.

Oh, this is a thoroughly wonderful and wonderfully thorough answer, thank you!

Hey thanks!  People should be warned that the BBC takes 150 dollars per year in taxes from the 51st state and is keener on hiding state secrets than journalism, it's the same as RT in higher secrecy.

oh-kay.... I've been duly warned ;-)

worth noting that yellow and cyan are actually parts of the spectrum magenta is not. you can have pure yellow wavelengths, not so for magenta.

There are several combined reasons.
first salt itself in such lakes is often pink, so part of the color comes from the salt crust itself. this is more noticeable in more extreme salt lakes where the deposits can be quite thick. It can be due to iron impurities but can also be further dyed by trapped carotenoids in the salt as it is deposited.
Part is also coming from salt loving halo-bacteria which use are not algae but are photosynthetic. They use bacterioruberin and salinixanthin for photosynthesis but not chlorophyll. these are carotenoids and pink, and responsible for many pink salt lakes like lake Hiller. (there is an interesting link between these bacteria and why chlorophyll is so inefficient that is worth reading)
the last is indeed beta-carotene, produced by salt tolerant algae.
In the case of that particular lake algae appears to be the major factor. However there are many pink lakes each caused by a different mix of carotenoids produced by salt loving organisms which depends on just how salty it is.
As for why it looks pink instead of orange, the answer is carrots have other pigments that shift the color further towards orange, particularly yellow pigments. Also water is transparent so mix a pigment into it and you get a lot of subsurface scattering which can shift color towards blue, this is part of the reason water is blue. Purple and pink are artifacts of how the human eye sees color and not "real" colors so when you combine reds and blues you get pinks and purples.

Thanks for your answer! "...salt itself in such lakes is pink..." is surprising to me, I've never heard of pink salt. Your comment also mentions that the salt can be pink but I've never heard of at least an inorganic salt solution that has such a color. Can you support this with a source? I don't see it stated explicitly in the Wikipedia article linked in your comment that it's the salt itself that produces the color.

In solution? Can you find a source supporting that iron makes salt solutions pink? The optical properties of crystals are often affected by dopants (e.g. the variety of colors of diamonds and sapphires) but those effects are related to the crystal structure. Once dissolved, they crystal structure is destroyed and thse effects are no longer relevant.

trace minerals (mostly iron) turn sea salt pink. Not all sea salt is pink but many are.  this is especially noticeable in thick layers of salt. Interestingly you can get darker pink and even red salt  due to a build up of carotenoids in the deposited salt when it is deposited in isolated basins (allowing hyper-saline conditions to persist and the micro-organims to thrive).

Not the solution, the solid salt deposited on the bottom of the basin/lake.

The water in the image is quite opaque, we can't see the duck's legs much less the bottom of the lake. If the lake is saturated such that there are crystals of otherwise soluble salts at the bottom 1) the duck would not be drinking the water (it's incredibly painful to mucous membranes) and 2) they'd be visible near the shore as well where the lake is thin enough to become transparent.

I was referring to pink lakes in general, I stated that the lake in question algae was the major factor.

Okay, maybe it's good to add to the answer that the salt effect does not apply to the question specifically? Are there algae that can live in lakes that are saturated solutions such that there are also crystals of salt at the bottom? I think that saturated solutions are sterile, aren't they? In other words aren't pink salt crystals and pink organisms mutually exclusive?

please read my answer, I already mentioned that these organisms prefer hypersaline conditions. hypersaline solutions are not abiotic, there are plenty of organism that like hypersaline conditions. hypersaline lakes lack FISH which is a very different thing.

Yes going off-site and reading Wikipedia I see that ...extreme halophiles or haloarchaea (often known as halobacteria), a group of archaea, which require at least a 2 M salt concentration and are usually found in saturated solutions (about 36% w/v salts) There will be no ducks drinking that water but I see that it can happen. But I'm not sure that such a saturated lake would look pink because of both iron-doped pink salt crystals at the bottom and simultaneously because it's full of pink organisms. Anyway thanks for the helpful discussion!

read the one about the algae which is a different orgaimsims, that survives in less salty lakes, said lakes are sill MUCH saltier than normal sea water. also look at salt farming in which halo bacteria often take over super saturated brine pools turning them pin, often getting pinker as they become more salty. you will rarely get all there at the same time but it is very possible to have two of them at the same time.


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Identify this insect with a big "face" pattern on its brown fuzzy wings
Hiking in low mountains in northern Taiwan in early May I noticed that something seemed to be looking at me from the ground, and it turned out to be the pattern on an insect's wings.
The wings are fuzzy like a moth or butterfly but they fold back.
There is also a striking face-like pattern on the wings, one "eye" with heavy upper eyelid on each and a "mouth" across both, and it has very long black (or blue?) and white densely-striped antennae or feelers which project straight forward, and it's legs were also black with several white bands. The length from head to wingtips (not counting antennae) was about 2 or 2.5 cm.
I also got the distinct impression that its orientation was not flat (parallel to the leaf's surface) but oriented with its rear high, so that something in front of it could see the "face". I don't have a photo from the side but based on judging things from what is and isn't in focus I think it's pretty clear.
Question: Is it possible to identify this insect with a big “face” pattern on its brown fuzzy wings? Is it also possible to know if the pattern has some underlying structural function within the wings, or is it only for appearance?

I fully admit that I am not an expert on Asian insects but having trawled through various species identification keys and collections I am fairly certain that the insect you observed was:
Deltoplastis commatopa
I lifted the following species description from Wikipedia and I think it matches your description & photo rather well:

Deltoplastis commatopa is a moth in the family Lecithoceridae. It is
  found in Taiwan and the provinces of Jiangxi, Hunan, Hubei and Sichuan
  in China.
The wingspan is 16–22 mm. The forewings are light lilac-fuscous with
  blackish-fuscous markings, edged ochreous-whitish. There is a large
  subtriangular antemedian blotch from the dorsum nearly reaching the
  costa, connected with costa by an angulated mark. There is a large
  triangular postmedian blotch, its base posterior, reaching the costa
  and the dorsum, its apex cut off by ochreous-whitish to form a
  tadpole-shaped mark. The terminal area beyond this irrorated
  (speckled) ochreous-whitish, a blackish marginal line round it. The
  hindwings are fuscous, darker posteriorly.

Here is a screenshot of the entry in the Global Biodiversity Information Facility:

You can see from the entry that several occurrences have been reported (with images) by people in Taiwan.
I also found this Taiwanese biodiversity website (in Traditional Chinese) and thought I would include it here (although I have to admit that I am not able to read Traditional Chinese).


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Does Telomere length shortening with age actually cause our cells to age and stop functioning properly?
The human telomere, a simple repeating sequence of six bases, TTAGGG located at the ends of chromosomes (Moyzis et al, 1988) protect them from degeneration, reconstruction, fusion, and loss. It is believed that  this shortening becomes critical for a telomere on a particular chromosome, which becomes unstable and the cell stops dividing.
Nevertheless, as human dermal fibroblasts of 100-years-old individuals still have a telomere length of 6–7 kb and retain proliferative capacity for about 20 doublings (Allsopp et al, 1992). They have not reached the limit of their proliferative capacity or of telomere shortening even at such an advanced age. The telomere length of human peripheral blood lymphocytes decreases with age and shortens to about 5 kb in some individuals after age 60 years, but no individuals have been found with a mean telomere length of less than 5 kb, even among 100-years-olds. (Vaziri et al, 1993) (Iwama et al,1998)
Does this Telomere length shortening actually cause our cells to age and malfunction?

Yes

"all somatic cells have a molecular clock that leads them to develop a senescence phenotype" Ruiz et al. 2022

Short telomeres cause replicative senescence. Senescent cells upregulate survival factors and do not undergo apoptosis (although they should). Senescence is accompanied by SASP (senescence-associated secretory phenotpye). A cell with SASP will secrete inflamatory (and cytotoxic) factors that attract immune cells, maybe in order to be killed and removed from the tissue. If senescent cells aren't removed (due to a high burden of senescent cells), these inflamatory factors also damage surrounding cells. This accumulation of tissue damage is pretty much what "aging" is.
However, there are other mechanisms that cause senescence/aging: There is also DNA-damage, mitochondrial DNA-damage (causes production of reactive oxygen species), accumulation of protein aggregates, chronic inflammation, etc.
Note that cellular stress (drug therapy, genotoxic stress, irradiation, inflammatory stress, etc.) can accelerate telomere shortening. For example, smoking during pregnancy  reduces telomere length of the unborn child (Mirzakhani et al. 2017)
But still, telomere length is only a  "rough estimate of aging rate and can hardly be regarded as a clinically important risk marker for age-related pathologies and mortality" (Vaiserman & Krasnienkov 2021)
Further reading: Chaib et al. 2022

Yes.
This was demonstrated by showing that re-activation of telomerase (which lengthens telomeres) prevents cell senescence.
The immortal nature of cancer cells can be attributed in large part to their constitutive expression of telomerase.
The mechanisms by which short telomeres lead to / are linked to senescence, aneuploidy, etc.  occurs have been pretty well worked out.

Yes, it's true in eukaryotes after every cell division telomeres shorten by many base pairs. Telomerase is not found in prokaryotes as their chromosomes are circular. So, no DNA is left out for copying.
In eukaryotes, telomerase is found in stem cells.
Note: There are different types of stem cells that exist in humans at every point of their lifetime. But none of them are totipotent(those have the ability to create a full organism)
Thus, telomerase ensures the safety of genetic information by elongating the telomeres.
Mechanism of telomere regeneration given in AP biology...I m posting the link below
https://openstax.org/books/biology-2e/pages/14-5-dna-replication-in-eukaryotes


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Why do we fear the night?
I always feel more afraid in the dark than in light conditions. Is this a common phenomenon in all the people? Does it have biological underpinnings?

This is more a psychology question than a physiology question and is probably better asked at http://cogsci.stackexchange.com/

Possibly related: http://biology.stackexchange.com/questions/55700/why-are-fearful-stimuli-more-powerful-at-night?rq=1

This question was closed as a duplicate as mentioned above, since the OP deemed the other question as a sufficient answer for this one.

Our ancestors were hunted by predators active at night. This is our inheritance, it is not something pathological.


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How do aerobic Rhizobium bacteria survive in root nodules while fixing atmospheric nitrogen?
I read that rhizobium carry the enzyme nitrogenase, which is irreversibly damaged upon the exposure of oxygen. Inside the root nodule of legumes leg-haemoglobin keeps a microaerophilic environment where nitrogenase enzyme can function and molecular nitrogen can be fixed (source: Brock's Biology of Microorganisms).
Shouldn't therefore Rhizobium bacteria die in such microaerophilic condition inside the root nodules?

Welcome to Bio. What makes you think rhizobia are anaerobic environments?

I read that rhizobium carry the enzyme nitrogenase that is irreversibly damage upon the exposure of oxygen, that's why, inside the root nodule of legume plants leg-haemoglobin keeps a microaerophilic environment where nitrogenase enzyme can function and molecular nitrogen can be fixed.

That's interesting to note. +1. I added those details in the question. If you could add the source of that info that would be awesome. Thanks for this question.

The source is 'Brock Biology of Microorganism', it is 14e I believe

Great book! I love that one, especially the edition with the hot water springs in Yellowstone NP :)

TLDR
One hypothesis for survival is nitrate respiration.
Long Answer
Ampount of oxygen available in root nodules is controlled by the host plant by two ways:

By presence of leghemoglobin
By the diffusion resistance
Under anaerobic condition the bacteria survives by making use of denitrification process which could be used to produce ATP under anaerobic conditions.

It is known for a while that, beside nitrogenase activity, in many symbiotic associations between legumes and Rhizobium the activity of nitrate reductase also exists 12. Most of the nitrate reductase ativity has been found to be concentrated in infected bacterial body i.e., bacteriod3. The bacteriod uses the process of conversion of nitrate into nitrite for creating a proton gradient which is inturn used for generation of ATP.
Reference.

Leghemoglobin fan here.  My boy needs equal time with that loser nitrate reductase.  Got another diagram?


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Is hydrochloric acid suitable for pickling food?
I was wondering whether it is possible to pickle food using hydrochloric acid (HCl), rather than acetic acid. I am not very familiar with the biology of the fermentation process involved in pickling and I do not know if HCl would give rise to a suitable environment. Is HCl-based pickling possible? What percentage of HCl should be used?

Short answer
Weak organic acids are more effective for food preservation then strong mineral acids, mainly because undissociated weak acids can cross the cell membrane and disrupt cell physiology from within.
Background
Natural fermented, or pickled materials are traditionally cured in a brine solution (salt, water, sometimes spices and sugar). Desirable anaerobic bacteria convert carbohydrates to acetic acid that “pickle” and preserve the food. The brine protects the vegetables from aerobic organisms. However, most contemporary pickles are not fermented at all; instead they rely upon the direct addition of acetic acid (vinegar, a product of fermentation), and usually heating for additional preservation. This way the acetic acid production through the fermentation process is simply bypassed.
So the basis of the traditional and contemporary pickling is the addition of organic acids like lactic and acetic acids. These small organic acids are known to be more effective against bacteria than inorganic mineral acids like HCl (Rode et al., 2010)
Acetic acid is a weak acid. In undissociated form, it is lipid soluble and able to rapidly diffuse through the plasma membrane (source: World Nutrition Science blog). It is thought that diffusion of acetic acid and other organic acids into the bacterial cell is the main mechanism of action behind its preservative effects. Preservation by acidification is especially effective in certain species of pH-sensitive bacteria such as E. coli and Salmonella. In contrast, strong mineral acids are nearly completely ionized in solution and ions do not pass the cell membrane's hydrophobic lipid bilayer.
The mechanism of action of small organic acids in food preservation are thought to be at least threefold:

Once diffused in the cell, organic acids will dissociate because the internal pH is near or above neutrality and thereby lower the bacteria's internal pH and disrupt cell physiology;
The anionic part of the organic acids, which cannot escape the bacteria in its dissociated form, will accumulate within the bacteria and disrupt many metabolic functions. This is one advantage of using organic weak acids like acetic acid, because they are normal constituents of the cells. Acetic acid and lactic acid for example are both intermediates in glucose metabolism. Accumulation of these metabolites will disrupt the glucose metabolism essential to the cell's survival.
Eventually, upon progressing accumulation, osmotic pressure increases become mechanically incompatible with bacterial life.

Another advantage of acetic acid is that it is a natural metabolite in human metabolism, and because it has been used in food preservation for thousands of years it is not classified as a food preservative, at least in the EU, and can be freely added to foods. Last but not least, acetic acid has a certain taste to it that may be preferable over inorganic acids.
Reference
- Rode et al., Can J Microbiol (2010); 56(9): 777-92

But wouldn't metabolic acidosis become a concern with such inorganic / mineral acids? We can certainly metabolize many of those organic acids (acetic, lactic, citric, etc......) just fine (down to water and exhale $\ce{CO2}$), but I'd imagine those "inorganic" ones ($\ce{HCl}$, $\ce{H2SO4}$, etc.....) could well become more problematic -- especially if one eats too many of those pickles!

Granted -- the body does have ways of dealing with occasional metabolic alkalosis just fine from ingested "inorganic bases" like baking soda & common antacids ($\ce{CaCO3}$), so perhaps the dangers of inorganic-acid metabolic acidosis may be somewhat exaggerated as well...


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How are large snails able to climb trees?
In answers to What kind of hot pink eggs are these? and the linked duplicate I found out that snails that live in the water will climb up a smooth stick or branch to deposit their eggs. Today I saw several large (8 to 10 cm) snails climbing trees both a relatively smooth one and one with considerably rough bark.
How do these large and heavy snails manage to adhere safely to the sides of trees and climb so high? Is it adhesion? Is suction involved?

click images for full size view
above: June, northern Taiwan lowlands in a damp area. They look similar to the species discussed in answers to What are these four large snails doing? below: from What kind of hot pink eggs are these?

The foot of the snail secretes a sticky mucus which allows the snail to climb even the smoothest surfaces. The mucus have two states: one in which it is almost liquid to lubricate motion, and the other - a very viscous one, in which the mucus is sticky and "glues" the snail to the surface. The mucus can alternate between these two states via the pressure the snail activates on it. The gluey state sticks the snail to the surface via adhesion.

Researchers discovered nearly 30 years ago that snail mucus has some unusual properties. It allows the animal to stick to a surface while moving, with the mucus changing its characteristics according to how firmly the snail presses on it.  The slime initially acts like glue, sticking the snail to the surface. But when the snail's foot presses down hard enough on the mucus, it becomes more liquid, allowing it to flow underneath the moving snail. Existing theories assumed that this special characteristic of snail mucus was always necessary for the snail to push off and move forward.

Cited from: https://news.stanford.edu/news/2011/april/snail-slime-trails-040611.html

How does it alternate between these two states? Does this information come from some source?

It comes from Prof. Joseph Heller's Land Snail monograph, which I don't have with me right now. See also the following research: https://news.stanford.edu/news/2011/april/snail-slime-trails-040611.html

I didn't see your comment until now for some reason, it may be that the @reply was necessary. From FAQ see How do comment @replies work? I'm still looking for an understanding of the mechanism that holds these snails against gravity from falling off the trees; is it adhesion, or suction, or a combination of both, or if something else is also involved, so I've added a bounty.

@uhoh The sticky mucus works as a glue, that is: as an adhesive. See https://en.wikipedia.org/wiki/Adhesive

I've adde a bounty, asking for a "more detailed answer". if you think that adhesion is the primary mechanism for climbing trees and suction and/or gripping are less important then please feel free to include that back into your answer post rather than a comment. Thanks!

@uhoh I added it to the answer.


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Roughly speaking how stable are short sections of single-stranded RNA in exposed environments compared to double-stranded DNA?
A search following a recent news item led me to a CDC Morbidity and Mortality Weekly Report for 23 March 2020 which says in part:

SARS-CoV-2 RNA was identified on a variety of
  surfaces in cabins of both symptomatic and asymptomatic
  infected passengers up to 17 days after cabins were vacated
  on the Diamond Princess but before disinfection procedures
  had been conducted (Takuya Yamagishi, National Institute of
  Infectious Diseases, personal communication, 2020). Although
  these data cannot be used to determine whether transmission
  occurred from contaminated surfaces, further study of fomite
  transmission of SARS-CoV-2 aboard cruise ships is warranted.

Identifying bits of RNA does not imply a surface is infectious and that's not what I am asking about here.
This reminded me of answer(s) to Was 14,000+ year old DNA “laying around in cave dirt” protected from degradation, or is it just naturally this robust? which explain that small fragments of DNA can be quite stable in some environments; in some places on Earth the DNA in the soil can be ten thousand years old.
Question: Roughly speaking how stable are short sections of single-stranded RNA in exposed environments compared to double-stranded DNA?
The answer is likely to contain "It depends on..." as did the answer to the DNA stability question, I'm primarily interested in the differential stability between the two.

Because the cited source is a personal communication, we do not know if the extraction protocol used is sufficient to disrupt viral capsids, so it's hard to say whether the RNA recovered was naked RNA or virus-bound RNA.

@PolypipeWrangler that sounds like it could be quite a reasonable and acceptable answer.

Like stretching a rubber band until it breaks, comparing the elastic limits of dsDNA and ssRNA might be useful to do a direct comparison of energetic stability. I haven't found much online about RNA rupture experiments, but looking up ssDNA might serve as an upper bound on ssRNA stability, as ribose is less stable than deoxyribose.

The main difference in stability is due to the very high amounts of RNase in pretty much all fresh biological materials. Naked RNA is easily degraded by just touching it with skin. The first step in most RNA extractions is often to add an RNase inhibitor.
For example, from Wikipedia's Ribonuclease; RNase contamination during RNA  extraction:

The extraction of RNA in molecular biology experiments is greatly complicated by the presence of ubiquitous and hardy ribonucleases that degrade RNA samples. Certain RNases can be extremely hardy and inactivating them is difficult compared to neutralizing DNases. In addition to the cellular RNases that are released, there are several RNases that are present in the environment. RNases have evolved to have many extracellular functions in various organisms.

This covers it nicely, thanks!