text:
How to preserve tissue DNA without using formalin?
Except using formalin to preserve human corpse for autopsy. I heard from the news that technique damages the DNA in the organs
Question:
Suppose corpse will be investigated next by another juridical unit
Do we have any other techniques which are better than this?
For example like freezing in the fridge. Because police office needs all above questions to complete his case.

Welcome to SE Biology. I think this question is off-topic as it's clearly not about biology. I don't think there should be an autopsy tag.

@Michael_A I got it. I just update my question to be more focusing on DNA preservation.

you may want to look into actual police preservation techniques, formalin is only used for certain organs after removal in special circumstances, not the entire body nor all samples.

I'd suggest removing all mentions of investigators and murder; it distracts from your title question about preserving DNA without using formalin. You have provided three numbered questions that an investigator might want to answer but 2 and 3 are not about biology.

@Michael_A I have updated my question and remove 2 and 3 out because it beyonds the scopes of SE Biology


text:
What is the signal conversion from hair cells to cochlear nerve cells?
If I understood correctly, inner hair cells generates a graded potential (receptor potential), this potential maps the stereocilia deflection. On the other hand, the cochlear nerve cells transmit action potentials to the brain.
The question is how and where the graded potential is converted to action potentials. In particular, as action potential signals are characterized by the interval between triggers, how are the sound properties (power and frequency) mapped into this interval?

Short answer
Sound level is coded in spike rate, frequency is coded by a place-frequency map.
Background
Spiral ganglion cells (SGCs, the secondary sensory neurons making up the auditory nerve) are continuously firing cells in a healthy ear (they fall silent when the hair cells degenerate, leading to deafness). In fact, their base frequency in silence is pretty high. The only thing the hair cell input does is lowering, or elevating the threshold and hence affecting firing rate. During a sine wave stimulus (a pure tone), the stereocilia of the hair cells deflect in one phase, and inflect on the other. One phase hence depolarizes the SGC, the other hyperpolarizes it. This generates a near-perfect representation of the sine wave input at low frequencies. At high frequencies the SGCs may skip a phase or two, but because multiple SGCs are involved, the population code is still stochastically spot on.
Sound level is coded in spike rate, frequency is coded by a place-frequency map (Müller, 1996). The base of the cochlea codes high frequencies, the apex low frequencies. Hence, loudness is coded by every SGC, while frequency determines which SGC is activated. An informative overview of hair cell signalling is provided in Fig. 1.

Fig. 1. Hair cell transduction. source: Pasadena City College
References
- Kandel et al., Principles of Neural Science, 4th ed.
- Müller, Hear Res (1996), 94(1-2): 148-56

source: Stack Exchange

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

sort: votes


text:
Can one see flickering of a light bulb at 50 Hz?
Yesterday I had a BBQ with some friends. The sun had already set and the only light source left (besides some ambient light from the world around) was a low energy light bulb.
After a while I started to see lighting changes in the faces of my friends and the number plates of their cars. It felt like someone toggled the light very fast. When looking at the wall or the light directly I didn't notice any flickering.
In my country the power grid is running at 50 Hz. Is it possible that I actually saw the flickering caused by the alterations in the power grid or am I just going insane?

Sub-question - had you been drinking alcohol?  I'd guess that would have slowed down your reactions/perceptions though.

@Criggie No intoxication whatsoever - funcact: my friends asked me the same question when I told them :D

You didn't mention if this was an incandescent bulb. If so, it seems the filament's brightness wouldn't change that much during a 50 hz cycle, but it's possible.

It is actually not hard to detect on-off flicker at 50 Hz with your eyes even in well-lit surroundings. Simply flick your line of sight across the flickering light source, and you will see a regularly spaced sequence of images for a split-second in your visual field. There are even some electrical lights that oscillate between different wavelengths, and such a technique will allow you to see it. Also, even if you do not do this on purpose, you may notice the effects when you shift your gaze or during the natural saccades of your eyes. But incandescent bulbs hardly flicker, as @rcgldr said.

@rcgldr It was some sort of energy saving bulb (Not sure which type, but not LED). Not a incandescent bulb.

@Timo - possibly a CFL (compact fluorescent light) bulb (usually a coiled tube). CFL bulbs could change intensity nearly instantly, but there's usually some capacitance in the circuitry which would reduce flicker.

@user21820: This is quite noticable (at least for me) with LED car tail lights, especially at night when I'm a bit tired.  Sometimes traffic signals & advertising signs, too.  Part of it, I think, is that they often use pulse width modulation to control the light intensity...  Also note that a bad or failing LED or CFL bulb can flicker.

@jamesqf: Yes indeed. Especially those that deliberately pulse on and off, but what I found interesting was that some fluorescent tubes that give 'warm light' are not monochromatic, and I discovered it exactly by flicking my line of sight across them, the first time accidentally.

I seem to recall reading multiple times statements from autistic persons who claimed they could see fluorescent light bulbs flicker. (I have a child on the spectrum. This would have been when he was preschool age, and he is now 18, so it was some time ago.)  IIRC the thinking was, it's not so much that very few people can see this but that most of us have learned to filter/ignore it.  We live in the US so this would have been 60 Hz.

Doesn't appear to be mentioned in the answers: your peripheral vision is much better at noticing movement that your focused/central vision.  This is why you noticed it "out of the corner of your eye" but when you looked at it directly you couldn't see the change.   Old CRTs have been mentioned and it was quite obvious if you put two side-by-side (and 1metre/3feet apart) and looked at one: the other would appear to flicker but not the one you were looking at.

You can definitely see if a lightsource is continuous or flickering, by observing rapid motion. Wave a bright (like, white) object lit by that source in front of your face. With flickering light you'll notice multiple separate images.

It might be that it's a very cheap LED light, and uses only a half wave rectifier instead of a full bridge. This means every other wave is turned off, and the lamp spends at least half its time completely switched off. This also makes it flicker at half the frequency it would with a full bridge rectifier.

Short answer
Yes, the flickering of a light bulb may be noticeable, and yes, that's directly related to the mains frequency. However, since the flickering of a bulb is about two times higher than the temporal limits of our visual system, it is unlikely to be perceivable.
Background
The temporal resolution of the visual system can be quantified in a number of ways. As you are referring to a relatively simple flickering stimulus, the critical flicker fusion frequency is probably the most relevant. At a certain critical frequency, a flickering stimulus will appear as a continuous stimulus. This critical flicker fusion frequency limit is around 50 Hz, but variable between 5 - 50 Hz, dependent on the lighting conditions (Kalloniatis & Luu), see Fig. 1 below.
For example, the turn signal of a car is obviously flickering (flickering in the 1 Hz region). But an object displayed on a standard flat-screen computer seems steady. A monitor's refresh rate is typically 60 Hz, which is indeed above the critical flicker fusion frequency (Holcomb, 2009).
However, the good old CRT screens can sometimes seem to be flickering. The mains, as you indicate, is indeed 50 Hz (Europe, Australia) or 60 Hz (US), and indeed the flickering is at this frequency. Similarly, well functioning fluorescent tubes seem to flicker on occasion (when they are reaching their end they start to flicker too, but that's because of a failure of the device rather than the mains frequency peaking through). Due to a similar effect, light bulbs may seem to flicker too. However, because of the sine wave characteristic of the mains alternative current, featuring two peaks per wavelength (a negative and positive peak, the flickering of a light bulb is actually two times the mains frequency, or 100 - 120 Hz. This is quite far above the critical flicker fusion limit and hence will likely not be noticeable.
It's interesting to see that you mention that it was around sunset. Scotopic vision (night vision) is mediated mainly by the rod photoreceptors. The rod visual system mediates gray scale vision at low-lighting. While spatial resolution is poor, it's very well adapted to process fast-moving stimuli. Hence, the flicker fusion frequency under scotopic viewing conditions may indeed be higher; i.e., flickering of light bulbs may not be perceived during the day (Federov & Mkrticheva, 1938). Nice add-on there.
To add to this as alluded to in the comments, whether the flicker of mains-grid powered appliances are actually visible depends on a lot of factors other than flicker frequency. CRT screens, for instance, may have improved phosphors that have delayed response times, 'smearing' out the flickering into invisibility. In other words, it's not a simple matter of 'ON' and 'OFF'. Likewise, light bulbs heat up and hence the temperature difference might not be noticeable to us, as the temporal flickering depends on heating and cooling of the wire.

Fig. 1. Flicker fusion as a function of stimulus intensity. Note that the shape of this graph means that photopic vision is less sensitive to temporal changes; the intensity scale relates to the stimulus intensity, as alluded to in the other answer. Scotopic vision to promote the temporal resolution of vision in the sense mentioned in this answer alludes to the ambient lighting conditions conditions. source: Kalloniatis & Luu (2007)
References
- Federov & Mkrticheva, Nature; 142: 750–1
- Holcomb, Trends Cog Sci 2009; 13(5): 216-21
- Kalloniatis & Luu, WebVision, chapter "Temporal Resolution" 2007

Great answer, thanks! I think, besides your point, if the sun weren't already set, it would have inferred with the light from the light bulb anyway, making it impossible to notice. Glad I'm not going crazy :D

To add a data point, with CRTs I had to go up to around 80Hz or so - 85 being one "standardised" (VESA) refresh rate. Anything less and I had a sense of the flickering "out of the corner of my eye".

LCDs generally are better, even at 60Hz, but I had the privilege of using three Hanns·G monitors in $JOB[-2]. They would operate at 75Hz, and got rid of the semi-permanent mild headache I'd had previously.

@WillCrawford - Part of the flicker effect from a CRT depends on the persistence of the phosphors. The greater the persistence, the slower the rate at which the phosphors light decays, Greater persistence is good for flicker but, can cause blurring of virtual objects moving across the screen. Some fixed field entry monitors, where scrolling wasn't used, like the green monochrome IBM 3740 terminals, had a persistence around 1 second, which allowed for very crisp fonts and no apparent flicker. For many standard CRT monitors, the flicker goes away at around 75 hz.

@WillCrawford - continuing, CRT televisions with interlace, only update "pixels" about 30 times a second, but flicker is usually not an issue. The persistence of the phosphors used on CRT televisions is designed to avoid flicker at these lower frequencies.

I'm aware of what causes the effect. I think the persistence of my retina (or nervous system) may be a little lower than normal :o) [and I've used terminals like the ones you mentioned]

TV is ~25fps here the other side of the pond, so flicker is more noticeable on older CRT-based equipment.

And however it was designed, I seem to be particularly sensitive to "flicker" (older energy-saving bulbs and many office fluorescent tubes give me headaches, quite apart from the way they exacerbated my impaired colour vision).

It should be noted that the eye's ability to detect flicker (raid movement) also depends on the angle under which light enters the retina, because there are 2 different kinds of detector cells. Cone cells in the center (i.e. under sharp angles, head-on) are good at differentiating color, while rod cells at the outer edge of the retina pick up light from the periphery of the visual field and are better at light/dark differentiation and movement detection. You can test this IRL by looking at a sublty flickering light source - the flicker will be more noticable when viewed from the side.

The measurements shown in the graph are for the fovea. Some people report being able to detect flickering only in their peripheral vision, which is mostly rods, which matches your suspicion that the rods may have higher flicker fusion frequency.

A lamp flickers at 2x the mains frequency, i.e. 100 or 120 Hz, and that is typically not noticeable to human eyes. It is visible to chicken and insects.
That being said, a low quality lamp or a lamp at end-of-life may also flicker at 50 or 60 Hz, and you will notice. It depends on the brightness, so an area illuminated by the lamp may not seem to flicker.
A simple way to suppress the flicker of a 60 Hz CRT is to put on sunglasses. The chemistry in your eyes is slower at low brightness, this makes the flicker less visible. The invention of 100 Hz CRT TV (I was involved) was necessary for allowing higher brightness.

+1 for your A lamp flickers at 2x the mains frequency, i.e. 100 or 120 Hz. Can you add sources? I adapted my answer to allude to this effect too. Thanks.

A 50 Hz true-sine wave will pass through zero amplitude twice per cycle: once going toward its positive extreme (climbing through zero), and once going toward its negative extreme (falling through zero). (I'm ignoring bias voltage here.) The entire cycle is from e.g. zero with slope X all the way to zero with slope X, but two zero-passes happen, at slope X and slope -X. So the instantaneous voltage will be zero 100 times per second for a 50 Hz AC waveform (120 times/second for a 60 Hz AC waveform). I don't know the extent to which this actually impacts the intensity of the lamp's light output.

While you are correct about the sine wave and the math, I dealt with this same issue with a set of LED Christmas lights.  The LED lights are wired in a simple series, and they only get forward voltage 60 times a second (60Hz in my location). Since LEDs only work with voltage flowing one way, the flicker is very noticeable in my peripheral vision, but not straight on.  If the OP was using cheap LED lights, it's possible this same thing was happening.

@JPhi1618: LED drivers can use a diode bridge and a smoothing capacitor. Which means only cheaper LED lamps ought to have significant variation in luminous flux over the mains cycle.

@RedGrittyBrick, oh, yea, of course they can and most LED bulbs I have seen look great with no flicker, but on the extreme cheap end, like the string of lights I have, there is nothing done to smooth out the light or reduce flicker.  Sorry if it seemed like I was talking about all LED bulbs.

Let's say there is a point source of light (it could be a lamp or a highly reflective object) that undergoes large, rapid intensity changes, say 50-100 times a second.
If you quickly move your eyes while it's in your field of vision, it will trace out a path across your retina. Some sections of this path will receive little light, while others will receive a great amount. What you see will look like a dashed line. (The flicker fusion frequency is irrelevant because it refers to fixed points in your field of vision. In this case we are dealing with many spatially distant photoreceptors.)
Let's say it takes 0.15 seconds to "flick" your eyes from right to left. This means a light flickering at 100Hz would be broken up into 30 "off" sections and 30 "on" sections during this time. So in fact you would be able to detect frequencies much higher than 100Hz. (This could make an interesting Arduino experiment.) I have noticed the effect when my laptop varies the brightness of its charging light using PWM. As it "darkens", the dashes in the dashed line get shorter, and vice versa.
But let's put this in context. The conditions you describe mean that:

There is a big contrast between reflective objects and the background
There is a big contrast on some objects when the lamp is at its brightest and at its darkest (assuming a LED lamp without smoothing capacitors, the objects could receive virtually no light from the lamp for certain periods)
The objects are not "point sources"

This means that whenever you move your eyes around, a quick succession of bright "ghost" objects will additively combine in your field of vision. The effect will probably look like a sped-up version of strobe lighting. The same will happen with moving objects (e.g. someone waving a hand). But if you fix your gaze on a stationary object you will probably not see flickering.

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text:
Question about the quantity of orchid species and genera
One flower which I am reminded of is the orchid and conjointly, the Orchidaceae family. I am surprised when discovering there is an abundance of species and genera, hence I would like to know the exact number. Moreover, what is the reason, is this a quality resulting from angiosperms?

The Plant List records 27,801 accepted species names in 899 genera within Orchidaceae. This estimate probably differs a bit between authorities. For example the Angiosperm Phylogeny website records 26,000 species in around 880 genera. Regardless it is I think the most speciose angiosperm family.
The explosive diversification of orchids, like the diversification of angiosperms, has been a big study point for evolutionary biologists. A lot of explanations center around the wide array of floral morphologies which you can find in the group, as well as (although not independently) the evolution of a whole range of pollination strategies. Other factors include evolving in a tropical environment and the evolution of CAM photosynthesis in the group. You can find more details in, for example Givnish et al. 2015


text:
Very frequent multiple births in humans
18th century Feodor Vassilyev is said to have had children by two wives, each of whom only ever had twins, triplets or quadruplets. His first wife has 16 sets of twins, 7 of triplets and 4 of quads; his second had 6 sets of twins and 2 of triplets. Is there any known plausible biological explanation for this, or do we have to dismiss it as a fabrication?
I could understand a woman's body being unusually susceptible to multiple births. I can't find information on whether these women tended to have monozygotic or polyzygotic offspring, but neither option seems unviable to me. However, since it's unlikely two of Feodor's sexual partners would share such a trait, one would think to attribute it to him. Presumably there would have to be a mechanism by which paternal DNA can trigger embryo fissions, in which case I imagine the offspring would be polyzygotic.

The probability of having twins is hereditary (see this non-peer review source of information)

Risk factors for dizygotic twinning are related to multiple follicular development, and include maternal family history, ethnicity, geography, maternal parity, maternal age, and, of course, use of assisted reproductive technology. There may be a genetic component to monozygotic twinning as well, but that rate is fairly consistent across populations. Other risk factors, such as diet and supplementation, have been proposed, but the data are less robust. There are some interesting studies demonstrating geographic clusters of twinning, but these tend to be demographic clusters that are associated with other risk factors.
Though a higher risk of twinning can be transmitted from a father to his daughters, the father's family history of twinning is not a significant risk factor (for his own children to be twins). To clarify -- if a man has a family history of multiple births, his children are no more likely to be twins than the general population, but his daughers are more likely to give birth to twins. This study is one example of the studies that have shown a significant independent association between maternal family history and twinning, with no significant independent association with paternal family history.
As far as the case of Feodor Vassilyev is concerned, many people have lived on this earth, making very unlikely events in a single instance more likely to have ever occurred. I would say this case is either a hoax or a rare chance event. There is no modern data I'm aware of that would support a paternal genetic reason that this particular man produced so many multiples.


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Friendly Spider found at home, London
What kind of spider is this? It was very friendly and shy, we spotted it inside our house and we carefully took it to the forest. Hope it will be a nice environment for this kind of spider... One of my kids loves to play with spiders and I would like to be advised on what kind os species he can approach or not. Thanks in advance.

Thanks, Jason, for decoding the image! Why was it coded? Would like to know how to avoid it next time.

Just to be sure: is it London, UK you are located at?

London, UK yes.


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Mushroom Identification
I live in central Ohio and found these mushrooms growing on our 10 acre property. What is it and are they edible?

Do you have any picture showing the size? And especially the underside of the umbrella?

In addition to showing the underside of the umbrella, it would also probably be helpful to be more specific about the property, and where on the property they were found. In the middle of a lawn? On some mulch? By a tree or stump? Clustered together?


text:
Umbrella term for agonist, antagonist, inverse antagonist, etc.
For most receptors there exist different ligands that induce different responses. Depending on the response these different ligands can be classified into different groups such as agonists, antagonists, inverse antagonist, etc.
My question: is there a term that summarizes all of these different concepts?
I'm looking to express something like the following: 'addition of a methyl group to the phenyl ring changed its X from agonist to antagonist.'

activity

"addition of a methyl group to the phenyl ring changed its activity from agonist to antagonist"

A technical word that encompasses agonists, antagonists etc. is effector, defined in the Wikipedia entry as follows:

Effector
In biochemistry, an effector molecule is usually a small molecule that selectively binds to a protein and regulates its biological activity.

However ‘effector’ does tend to be used more in regulation of enzyme activity than signal transduction. I suggest this is preferable to the term ‘activity’, suggested by  @DeNovo as it is the targets of agonists etc. that exhibit the biological activity that one may be considering, rather than the agonists themselves. Such effectors modulate the activity of other molecules, so one could even consider using the term ‘modulator’, described in a Wikipedia entry — for the particular case of allostery — as follows:

Allosteric Modulator
In biochemistry and pharmacology, an allosteric modulator (allo- from the Greek meaning "other") is a substance which indirectly influences (modulates) the effects of a primary ligand that directly activates or deactivates the function of a target protein.

However I would definitely not use a noun of this sort to convey the idea of your sentence.
I find that more complex and clumsy then necessary. Far better, in my opinion, to express yourself in simpler terms and more directly.

“Addition of a methyl group to the phenyl ring changed it from being
  an agonist to an antagonist.”

or

“Addition of a methyl group to the phenyl ring changed its action from that
  of an agonist to that of an antagonist.”

However ‘effector’ might be useful as a portmanteau description of agonists etc. in circumstances when you are listing things.

"Portmanteau - A word formed by merging the sounds and meanings of two different words" - American Heritage Dict.; "A word blending the sounds and combining the meanings of two others, for example motel (from ‘motor’ and ‘hotel’)" - Oxford Living Dictionaries

@mgkrebbs — Umbrellas at dawn! I referred to a portmanteau 'description'' not a 'word'. I use British English Dictionaries that include the definition in the sense I used it (and have used it all my life). Thus, Chambers on my iPhone has "Adjective: Combining or covering two or more things of the same kind". And Cambridge has the example "The Official Secrets Act was described as a piece of portmanteau legislation, covering everything from nuclear weapons to army boots" and also  has an example with the word "motivation".


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What is the highest range mosquito can be detected via Microphone?
Just wondering when a mosquito attack at night I can hear it around my head, shoulders upper corps. Is it any statistic how far our ears or a microphone could detect it is nearby?

In accordance with the article Using mobile phones as acoustic sensors for high-throughput mosquito surveillance mobile phone microphones can detect moscitos in 10 to 100 mm range (depends on a model). In an empty room mosquito can be detected at approx. 3 m (Sound Pressure Level).


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What Does Transcription Factor E25 Activate When a Cell is Transitioning from G1 to S
Cyclin D/ CDK4 phosphorylates Rb allowing for the activation of transcription factor E25 during the G1 phase of the cell cycle. Supposedly, this transcription factor then activates as set of genes helping the cell to enter the S phase.
My question is what genes do E25 exactly activate? Are there any associated pathways with these genes involved in transitioning the cell from G1 to S?


text:
Where does NADP+ come from?
Trying to understand Photosynthesis better. I understand the NADP+ is reduced to NADPH in light dependent reactions and NADPH is then recycled back into NADP+ in the Calvin cycle. What I don't understand is where does the NADP+ come from initially?
Specifically I am asking with regards to its presence in the stroma within the chloroplasts of a plant cell. Where do plants get NADP+ from in order to assist in the production of sugar?

The simple answer is that plants synthesize it in the same way as they do most other cellular molecules. You can find the details in standard texts. However, I assume that is not what you are after. If so, you need to explain — at present your question is unclear, at least to me.

Niacin (better known as vitamin B3) and nicotinamide are both precursors of the coenzymes NAD and NADP in vivo. As you can see below, the biosynthesis of NADP+ proceeds as follows, when nicotinamide combines with a basic ingredient, a sugar phosphate:

The sugar phosphate precursor can also form AMP and GMP, also important molecules in the cell, when it reacts with the nucleobases adenine and guanine (A and G from the 'ladder' that bridges the DNA helix).
Just as an additional funfact, some bacteria such as Plasmodium falciparum and Toxoplasma gondii cannot synthesize nicotinamide themselves, because they lack the genes for it. Instead, they salvage the enzymes from eukaryotic hosts. This is an example of an incomplete biochemical toolkit giving rise to parasitism.


text:
Why do humans lose subcutaneous fat tissue with age?
Why exactly do humans lose subcutaneous fat tissue with age?
It appears that we either lose fat cell volume or we might actually be losing the number of fat cells with age.
One hypothesis is that as the vascular system weakens with age, the fat cells on the perimeter of the body shrink and die because they don't have enough blood flow to sustain them.  The problem with this hypothesis is that subcutaneous fat loss is very gradual and starts during young adulthood and continues. It also happens in very fit individuals too.
Another hypothesis I read before was that subcutaneous fat is loss because of a drop in estrogen levels after menopause.  This hypothesis doesn't explain why men lose subcutaneous fat with age.  Also, women start to lose fat on their hands and upper cheeks long before menopause starts.

Another thing to mention is that not all mammals have this issue. Whales retain their subcutaneous fat well into old age.

Short answer
We do not loose fat (cells) as we age; on the contrary - we tend to gain fat by about 1 or 2% per decade. The place where it gets stored does change; instead of going into subcutaneous regions, it gets stored around the abdomen. A sex hormone imbalance might be the cause of this gain in visceral fat.
Background
What a coincidence! I just finished an article in the Sci Am May issue of this year (2018) on exactly this topic, literally just minutes ago.
In young folks, fat tends to accumulate under the skin, while in older folks this tends to shift to accumulation of fat around the abdominal viscera (the internal organs). Bottom line: we don't loose fat overall, we just store it elsewhere. What's more, as we age we store more fat as our base metabolic rates drop.
Why this happens is no known, but there are some interesting findings:

Sex hormones are involved; women in menopause (estrogen levels drop) gain more visceral and belly fat and loose it around the hips (they go from pear to apple);
However, a drop in estrogen is not the cause, as certain ailments lead to belly fat in young women with plenty of estrogen;
Androgen-using females (transgenders) gain more visceral fat.

These findings together have lead to the idea that a sex hormone imbalance might be the cause. However, some findings counter this idea:

Afro-Americans have less visceral fat, while Asians have more;
Blocking FSH results in less visceral fat, which may have other mechanisms of actions than estrogen.

Reference
- Wallis, Sci Am May issue 2018

Children have low estrogen and very little central abdominal fat (usually).

The question I'd ask, though, is whether the accumulation of fat is actually due to age, or whether it's a side effect of sedentary, inactive lifestyles increasing with age.  E.g. this guy doesn't seem to have a lot of subcutaneous or visceral fat: https://www.adn.com/sports/2018/07/23/73-year-old-sets-new-standard-for-old-runners-at-western-states-ultramarathon/

How sad, you didn't get a response. You got a person saying that people don't lose total body fat with age (which you never claimed, or ask about), and a person saying that visceral fat gain isn't inevitable with aging. Neither of these answers deals with your question. I think it's a common psychological flaw in humans that, when they can't answer a question, they produce a random unasked-for question from the same semantic field. Unfortunately, I also can't provide a thorough response, but I will try to at least narrow it down:
To my knowledge, the reason is not vascularization; decrepitude of peripheral vascularization was suspected for a time, but we have seen that the predilection sites of fat loss readily take fat grafts, and those fat grafts that survive the initial post-transfer phase are "permanent". Since both transferred fat and "original" fat would depend upon vascularization, the difference can't be blood supply, but must be something about the local fat itself. As has correctly been pointed out, loss of subcutaneous fat "begins" long before menopause in women. Indeed, it does not "begin" at all (to my knowledge), but rather, the loss is an ongoing process from birth, although interrupted by localized plateauing at times. Another notable feature in facial fat loss is that its predilection sites are also predilection sites for bone volume loss: maxillary and zygomatic regions. To our knowledge, the cellular processes of fat atrophy and bone remodelling are distinct; osteoclasts do not dissolve fat cells. To me, this indicates that it would be a sensible hypothesis that the process of the body removing facial volume is not a predictable side effect from cellular senescence, but rather that it is, like baldness, a programmed event which might be triggered by the epigenetic clock of aging - a programmed event that simply takes aging as its trigger, but isn't itself necessitated by senescence.
On a less fundamental, cellular level, loss of replacement of subdermal fat is realized by loss of function of fibroblasts: https://www.sciencedaily.com/releases/2018/12/181226132847.htm
But of course, this does not explain why the fat cells already in situ are removed. That explanation is still outstanding, I believe.

This fits with my understanding of the subject nicely. Welcome to the site Dr. K. Please take our [tour] and refer to the [help] for guidance, enjoy the site.

Welcome. There are a lot of unsubstantiated claims in your answer. Can you add more references, most notably in the 2nd paragraph of your answer.

Thank you. In fact, success of fat graft procedure is a common knowledge which does not not require sources, I think. It is easily found in any popular or scientific source on facial rejuvenation surgery. But I edit a source for predilection sites of bone and fat loss.


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Neuron connectivity- how are they connected physically
If Neurons are only connected through synapse and there is no physical connection,  how are they just suspended in brain layers?

Neurons are suspended, as you say, in an extracellular matrix. Brain tissues are a little bit more specific. Here I quote a few summaries from literature to answer and give your a perspective on your basic question. In bold I highlight important statements which differentiate the brain's ECM from the ECM found elsewhere in the body.

Barros, Franco & Müller, 2011: An astonishing number of extracellular matrix glycoproteins are
  expressed in dynamic patterns in the developing and adult nervous
  system. Neural stem cells, neurons, and glia express receptors that
  mediate interactions with specific extracellular matrix molecules.
  Functional studies in vitro and genetic studies in mice have provided
  evidence that the extracellular matrix affects virtually all aspects
  of nervous system development and function. Here we will summarize
  recent findings that have shed light on the specific functions of
  defined extracellular matrix molecules on such diverse processes as
  neural stem cell differentiation, neuronal migration, the formation of
  axonal tracts, and the maturation and function of synapses in the
  peripheral and central nervous system.
Ruoslahti, 1996: The extracellular matrix of the adult brain
  tissue has a unique composition. The striking feature of this matrix
  is the prominence of lecticans, proteoglycans that contain a lectin
  domain and a hyaluronic acid-binding domain. Hyaluronic acid and
  tenascin family adhesive/anti-adhesive proteins are also abundant.
  Matrix proteins common in other tissues are nearly absent in adult
  brain. The brain extracellular matrix appears to have trophic effects
  on neuronal cells and affect neurite outgrowth. The unique composition
  of this matrix may be responsible for the resistance of brain tissue
  toward invasion by tumors of non-neuronal origin.
Dityatev et al. 2010: The extracellular matrix (ECM) of the
  central nervous system is well recognized as a migration and diffusion
  barrier that allows for the trapping and presentation of growth
  factors to their receptors at the cell surface. Recent data highlight
  the importance of ECM molecules as synaptic and perisynaptic scaffolds
  that direct the clustering of neurotransmitter receptors in the
  postsynaptic compartment and that present barriers to reduce the
  lateral diffusion of membrane proteins away from synapses. The ECM
  also contributes to the migration and differentiation of stem cells in
  the neurogenic niche and organizes the polarized localization of ion
  channels and transporters at contacts between astrocytic processes and
  blood vessels. Thus, the ECM contributes to functional
  compartmentalization in the brain.

Neurons are also contained within a matrix of glia cells, which outnumber neurons by a considerable margin: https://en.wikipedia.org/wiki/Neuroglia https://www.scientificamerican.com/article/the-root-of-thought-what/

@jamesqf This idea of glia vastly outnumbering neurons has been challenged and refuted. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5063692/

@Bryan Krause: Perhaps so  - I'm only going by what I've read in texts - but regardless of absolute numbers, glia cells do form a significant part of the matrix in which neurons are embedded.

@jamesqf Yeah that's fair, just challenging the 10x number that is often repeated and rarely supported. The non-somatic components of neurons are also very important and probably more likely to be overlooked.

It's true, neurons in the brain are really sparse within an extracellular matrix. But I would like to say that there exist several type of synapsis.
The first one, to which you referred is the chemical synapse connecting the synaptic button of first neuron with the post-synaptic membrane of the second neuron. Thus in that case, you think there isn't a direct contact of pre and post synaptic membranes but the electrical signal is converted and transmitted as neurotransmitter through the synaptic cleft. To note, both axons and synaptic cleft are "covered" by other cell types, a particular type of glial cells, the Schwann cell that causes the saltatory nature of the electric signal across the axon and, at level of the synapsis, acts in order to reuptake the released neurotrasmitters.
The second type is the electrical synapse. In this one, post and pre-synaptic compartments of neurons are phisicaly connected by gap junction: these are structurally made by two hemi-channels called connexons and makes the cytoplasms to communicate and thus the electrical signals continue to diffuse thanks these connections. In that case the connection between such cells approach within about 3.8 nm of each other creating a mechanical and electrical continuity (Sheriar G.Hormuzdia et al., 2004)
Thus, when you say "neurons are only connected through synapse and there is no physical connection" it's quite simplistic. In reality, also the chemical synapsis are "connected" mechanically by a large number of cell adhesion molecules that acts in order to make and modulate the connection between neurons. For instance these include neurexins and neuroligins or Ig-domain proteins etc (Missler M, et al. Cold Spring Harb Perspect Biol. 2012). Indeed, the pivotal differences between electrical and chemical s. is the ways by which neuronal cells communicate. In the latter, the distance between pre and post synaptic membranes is wider with respect to the electrical one.

Welcome. Can you mention your sources such that other users can background read on your material?

Absolutely yes. I will improve the answer with some bibliography.

I just noticed the inline reference. Best practice is to add a subsection with literature and include the link (e.g., to pubmed or the pdf). +1

I understand. The next time I will change strategy. However I added another reference inline. I hope it will be useful for the other  users. Thanks for the suggestion.

Have you seen histology of brain tissue? Neurons are not "sparse" at all in the brain. Space is a serious constraint for the nervous system. Your points about the physical connections of a chemical synapse are very important though, thank you for that part of your answer.

Yes, you're right. What I mean is that extracellular matrix and glial cells outnumber neurons. I used "sparse" instead of "immersed" to simplify. However connection molucules between chemical neuron's synapses is strong important inorder to allow synaptic plasticity (for instance glutamatergic synapses long term potentiation and/or depressions or synaptic selection/deletion during development of neuromuscular junctions)


text:
How many different colors can a normal human distinguish?
I am not talking about asking a person to sit for 10 hours to separate one color. I want to know is the normal person in a normal life.  How many different colors can a normal human separate?

What do you mean by "separate"? Do you mean "distinguish"? If so what has sitting for 10 hours to do with it. Please clarify your question, indicate its relevance to biology and why you wish to know something like this. See the Help on "How to ask a good question".

Right. Distinguish. From biological point of view, each human can classify 10 millions of color. However, that is not usual. People may need to take very long to classify between two very close color. That situation is not a normal situation.

What do you mean by "normal human" and "separate"?  A lot of it is simply training: If you include say interior decorators as normal humans, they can separate and give names to perhaps dozens of shades lke bone, eggshell, cream, ivory, linen and ecru, that most of us just call off-white.

For example, a jpg image use RGB with 256 color intensity. A total of 16.78 millions of combination.  Note, those are color intensity not color depth. But this gives us the general idea of human can separate will be less than color depth X light intensity = 16.78 million combination, because computer monitor are normally used. I want to know about the color depth of human vision in normal use!!

Values like this are determined via careful psychophysical experiments in the lab. You're asking about 'everyday life' or something? You need to carefully define what you are after then. This question is unclear, open to debate and as a consequence opinion-based and therefore offtopic in its current format.

I remember trying to find research on this subject some years ago, and the best data I could find said the range of human color vision was about 10,000,000 colors. Unfortunately, the article (which I cannot now find) didn't say how this number was reached, but I believe it was based on the response curves of the cones and didn't take into consideration whether or not the brain combines input from the cones as well as the rods to determine colors, which I believe it does. If anyone finds some definitive research, I'd find it very interesting. And I do not think this question is off-topic.

Just to correct a comment from the poster. The 16.8 million colours that can be represented in an 8-bit RGB image tell you nothing about human colour perception. (And colour intensity — whatever its relevance here — is the extent of difference from grey.) The jpeg algorithm reduces image size by reducing the number of colour on the basis that the human eye cannot distinguish (or does not notice) the difference between very similar RGB values. Although the basis of the answer to your question will be biological, your question isn't really biology in terms of SE Biology.

@David It is a biology question. I think that you do not live in USA because your colour has an 'u'. What is the traffic light color in your country? Almost all traffic light in the world have red color, it is because red trigger warning signal in the brain. My 2 hours ago comment was to use an approach to explain to people a possible direction of thinking. We could have different angle to analyze a problem.

Interestingly the answer appears to vary by culture, A lot like sounds it appears it is partially effected by what colors people are taught to distinguish between. http://imbs.uci.edu/~kjameson/ECST/Kay_Cook_WorldColorSurvey.pdf

I may not be in the US, but I live in the country where traffic lights were first introduced. My point is that you could ask the average speed of a cheeta and get an answer, but the question isn't really what we are after on SE Biology. That would be a question of the type, "Why is a cheeta faster than a horse?", where a useful answer would be in terms of body structure, musculator or whatever. Likewise, the question of how we discriminate millions of colours is much more pertinent than whether it is 1 million or 10 million.

@ Giordano Fearghas: The use of 8-bit color depth in JPEG & mainstream computer displays isn't really linked to how many colors a human can distinguish, but on hardware considerations.  8 bits fit in a byte, 3 color bytes plus an alpha (transparency) channel in a 32-bit word.  Increase color depth, and you double the amount of memory & bandwidth needed. making your system uncompetitive except for special purposes.  (Especially in the past, when memory &c was much more expensive.)  Nowadays greater depth is sometimes used: many digital cameras can do HDR (High Dynamic Range) photographs.


text:
What happens when pure chlorophyll A absorbs blue light?
When pure chlorophyll A is put in the presence of only blue light, what happens? My guess is that the extra energy is released as heat/kinetic energy, and then the electron has dropped to the lowest energy state above the state that would normally release red light when UV light is shone. Then, it would drop to ground state and release red light as normal. Is this correct? The reasoning behind this is that UV is even higher energy than violet/blue light, so the same phenomenon should happen, except with less kinetic energy added. On a side note, what is the next electron state after the one that sends out red light?

chlorophyll a or chlorophyll b?

chlorophyll A. 15char


text:
What accounts for the apparent lack of biodiversity in "bamboo forests"?
While hiking on the Hawaiian island of Maui, I passed from a forest with normal variety in trees and other flora, to a "bamboo forest" area in which the only plants that I could see were bamboo.
This was surprising to me! Why does only bamboo (appear to) grow in this area?
The assumption I'm making is that bamboo forests happen elsewhere in the world, not just in Maui.

Mostly the fast growth shades other trees, lateral rhyzomes, mats of undregradable leaves, other factors may contribute. It invades ecosystems mostly vecause its cylinder hollow geometry gives it a massive height / to weight and sunlight monopoly. The roots are very dense, they may also strangulate other plants while also growing high.


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Is existence of different alleles for a gene a result of mutation?
I would like to understand evolution. Here are a few questions

Why are there different alleles for a  gene?
Is the different alleles of a gene are mutated versions of a gene?
Why selection pressure favoured the existence of more than one alleles?

technically all existing genes and alleles are the result of mutations.

I would like to understand evolution

The best way to do so is to start an introductory course on evolutionary biology. Consider having a look at evo101 for example.

Why are there different alleles for a gene?

Because mutations bring variation. Note that not all genes are polymorphic. In other words, there might be genes for which, all individuals in the population share the same allele.
The existence of this genetic variance is absolutely central to the whole concept of evolution. In short, mutations increase genetic variance while natural selection and genetic drift reduce it.

Is the different alleles of a gene are mutated versions of a gene?

Yes

Why selection pressure favoured the existence of more than one alleles?

In the exception of cases of balancing selection (e.g. heterozygote advantage, negative frequency-dependent selection), selection does not yield to the existence of genetic variance, rather the opposite in fact. Selection "selects" for a given allele, which in turn reduces the genetic variance. Mutations bring new genetic variance in populations and selection reduces it. Genetic drift (another "driver of evolution") also reduces genetic variance.

drift within subpopulations could theoretically maintain variation in the population as a whole, I think, by randomly fixing different alleles ... (don't have a reference)

1. Why are there different alleles for a gene?

Variants of a gene are called alleles. In other words, an allele is one of the possible forms of a gene. If there is genetic variation in a population (and in all species, there is variation), then there are multiple alleles.
Evolution reflects changes in DNA sequences and allele frequencies within a species over time. These changes may be due to mutations, which introduce new alleles into a population. New alleles can also, for instance, be introduced in a population by gene flow, when two populations that carry unique alleles breed together.
2. Are different alleles of a gene mutated versions of that gene?

Yes.
3. Why does selection pressure favored the existence of more than one allele?

This question is unclear and/or poorly-stated. Are you asking why there is variation in a population? The answer is that, in spite of the fact that DNA replication (copying) is high-fidelity and quite accurate, it is imperfect. This means that over a long lineage of inheritance, new alleles will emerge, and their frequency in the population will change. Also, DNA accumulates damage and mutations occur due to chemical factors. DNA is not a perfectly stable molecule. Mechanisms of repair of DNA exist but are imperfect. It is impossible for a species to maintain perfect genetic identity, especially over prolonged periods of time, when mutations accumulate.
If you are asking why variation (or more strictly, diversity) is favorable for a species, here is an excerpt from the Wikipedia entry on genetic diversity, which explains it concisely:

Genetic diversity serves as a way for populations to adapt to changing
  environments. With more variation, it is more likely that some
  individuals in a population will possess variations of alleles that
  are suited for the environment. Those individuals are more likely to
  survive to produce offspring bearing that allele.

There is also an important difference between diversity and variability to consider. Diversity is the total number of genetic characteristics in a population. Genetic variability is the generation or presence of genetic differences between individuals of a population. Variability is introduced through migration events, homologous recombination during meiosis, and other things.
Addendum/protip: asking why is often less fruitful than asking how. The how is mutation. The why makes me want to include thermodynamics and statistical mechanics as an explanation, which is definitely an unnecessarily complicated explanation.

The terms genetic diversity (aka. expected heterozygosity) and genetic variance are well defined. I had never seen the terms genetic variantion and genetic variability being stricktly defined. I have always used the term genetic variation is a loosely defined way. The definitions you're providing seem a bit unclear to me. Would you mind indicating your sources?

The vision that genetic variation is favorable to a species is neglecting the genetic load (typically mutation load and drift load) it is causing.

Sorry, I meant diversity and variability. Thanks for the fix.

Oh... so the definition should rather be Genetic diversity is the fraction of individuals that are heterozygote in the population as expected by Hardy Weinberg rule or If 'p' is the frequency of one allele at a biallelic locus, then the genetic diversity is defined as 2p(1-p). When you say "variabiility", did you mean "variance" or does the term "genetic variability" has a commonly accepted definition I am unaware of?

See here and here and here for commonly accepted definitions of genetic variability. I disagree with your proposal to edit the definition; it does not clarify anything, or help pedagogically. Diversity is a simple concept in ecology and genetics and does not require rigorous analytical definitions unless the term is defined so in a rigorous, analytical context. As you can see, the question is far from advanced.

And variance is a purely statistical concept and has no meaning with regard to biology per se. Unfortunately it is often loosely and inappropriately used as a synonym for variation.

1.why there are different alleles for a gene?

alleles of a gene are mutated versions of a gene

why selection pressure favoured the existence of more than one
  alleles?

Reason
1) No reason. Allele is both not 'selected for' nor 'selected against'. The allele do not cause detriment or advantage. It is a neutral mutation. An example is ear lob, connected or not connected. It does not affect hearing. It builds up in a population by chance due to the founder effect.
2) It has an advantage but only in heterozygous form.
Example Sickle cell anemia. In homozygous form this allele is quite lethal. However in heterozygous form (ie pair with the normal allele), it confers resistance to the malaria parasite. So selection does favour the sickle cell anemia allele but only to a point. Once the allele becomes too common in the population it is selected against, as the probability of homozygous individuals of sickle cell allele occurring becomes more common.
3) Because allele is selected for in some parts of organism's ecological range.
Example human skin colour. Human range from poles of the earth to the equator. And thus are exposed to varying light intensity. At the equator, dark, almost black pigmentation is favoured as it protects against sun damage (ie sun burn) and skin cancer. Up in the temperate region, fair almost white skin is an advantage as it allows better absorption of the limited UV light for vitamin D and folic acid production, which is required for bone and limb development. Different light intensity selects for different levels of skin pigmentation. So we have several skin alleles.

Does this mean that existence of unaffected alleles are example of silent mutation?

There is no such thing as an 'unaffected' allele. Alleles are simply variants of genes. Some alleles are favorable, some are unfavorable, some are (un)favorable only in the presence of other alleles. Some have no effect on survival and reproduction, so there exist no active selective pressures. Silent mutations create new alleles which are functionally identical - i.e. the resultant protein is the same. However, even silent mutations may affect the way the DNA or mRNA behaves, or how it is regulated (e.g. how RNA interference may work through microRNAs) and thus its abundance in the cell.

In general, a gene can have more than two alleles (except genes of the Y chromosome) at a specific locus of the chromosome. Alleles are different forms of the single gene, which takes the same place on homologous chromosomes and exhibit variations in the production of the gene product. This means, at the functional level, alleles of the same gene will interconnect in several ways, which result in variations in the type of dominance and occurrence of different phenotypic effects with different allelic combinations. Read about alleles on the biology site.

Please take the [tour] and then consult the [help] pages for additional advice on [Answer] and [ask] effectively on this site and then delete or [edit] your posts accordingly. In particular, this is poorly written, misleading, and doesn't appear to add anything to the previous answers.


text:
Is it possible to calculate the evolutionary response to nonlinear selection gradient as a change in variance of phenotypes?
I often see the breeders equation written like this:
$R = h^2s = \frac{V_a}{V_z}s = V_a\beta$ or $\Delta \bar z  = G\beta$
But is it possible to get something like this:
$\Delta \sigma_z  = G\gamma$
In this case, it would be the change in variance of the population due to nonlinear selection.
Basically, it would me that the response of selection is a direct measurement of the change in $V_z$. So to come back to this equation: $R = \frac{V_a}{V_z}s$, it would mean that $\gamma$ is related to $V_z$ somehow. But is there a way to predict what would be the response?
Is it possible to also predict the total response of a non-linear selection gradient if there are multiple traits?
When one wants to calculate the total response to selection, it is needed to account for the correlated effect of selection on other traits (correlational selection):
$R_1 = V_{a,1} *z_1 +\text{COV}_{V_{a,12}} * z_2$
$R_2 = \text{COV}_{V_{a,21}} * z_1 +V_{a,2}* z_2$
In matrix form:
$
\begin{bmatrix}
    R_{1}    \\
    R_{2}
\end{bmatrix}
=
\begin{bmatrix}
    V_{a,1}       & \text{COV}_{V_{a,12}} \\
    \text{COV}_{V_{a,21}}       & V_{a,2}
\end{bmatrix}
* \begin{bmatrix}
    \beta_{1}    \\
    \beta_{2}
\end{bmatrix}
= \boldsymbol{R}=\boldsymbol{G} \boldsymbol{\beta} $
How would that be translated to non-linear selection?
EDIT:
I think this answer is here:
$\Delta \sigma_a^2 = \frac{\sigma_a^4}{2}(\gamma - \beta ^2 )$
But this equation predict a change in genetic additive variance not phenotypic variance. Would it be possible to simply take $h^2=\frac{V_a}{V_z}=\frac{\sigma_a^2}{\sigma_z^2}$ and get the change for phenotypic variance?
This could also represent an answer:
$\boldsymbol{G}^* -\boldsymbol{G}=\boldsymbol{G}(\boldsymbol{\gamma}-\boldsymbol{\beta}\boldsymbol{\beta}^T)\boldsymbol{G}$

By non-linear selection, do you mean cases where fitness of an individual is a non-linear function of its phenotype or do you mean cases where fitness of an individual depends upon the genetic diversity in the population?

That's what I mean:
$w = \alpha_0 + \beta X + \frac{1}{2}\gamma(X-\bar{X})^2+ \epsilon $
w: fitness, $\beta$ is the linear selection gradient and $\gamma$ is the nonlinear selection gradient. Like in Lande Arnold 1983.

Now, if you would predict the response of selection on the next generation of phenotypes, you can use the breeders equation as shown above. But what about the nonlinear selection gradient $\gamma$? Can we predict it?


text:
What is this? In Florida. Found in plant bed under rosemary tree that gecko' enjoy hiding aloe plants also growing.

Species identification of round soft outer shell

Could you please add the size/diameter of this object?

Possible duplicate of Is this a plant or a fungus?

I only know this because I have seen them before in the tropics, but this is probably Clathrus ruber (Wikipedia).  So interesting!
EDIT: Also mentioned in these questions 1 and 2 so perhaps this will get marked as a duplicate.

Clathrus spp. is a good call but Clathrus crispus  is common in Florida. Still an up-vote.


text:
Volley theory and sound amplitude/power
Assume a pure tone (single frequency) is listen, lets say 2 kHz. If I understand correctly the temporal theory (aka timing theory), in a cochlea neuron the action potentials create a signal that will have one spike for each single tone cycle with the exception of some gaps due to the minimal interval between neuron triggers.
Volley theory extends previous model to a set of neurons. The union of triggers in all neurons of the set will have at least one spike per cycle (with few exceptions). In other words, the base frequency of the signal composed as the union of triggers of all neurons in the set will be the same frequency than the one of the incoming sound.
My question is, if in this model the trigger intervals is used to encode the sound frequency, and taken into account that usual models for neuron activity only take into account intervals between action potentials (all-or-none), how sound amplitude (power) of the sound is translated to the nerve signals. That is, the differences in the nerve activity caused by two tones of same frequency but different amplitudes/powers, assuming frequency/volley model.

It's complicated.
The simplest explanation is that sound amplitude/level/loudness is encoded by the number of participating units, including off-best frequency cells that get recruited when amplitudes are high (the concept of 'tuning width' is helpful to understand). Loud sounds will recruit cells of a wider best-frequency range with high coincidence, for example (see Carney, 1994).
In some experimental paradigms, this hypothesis holds; in others, it does not. It is most likely that the perception of loudness is quite context-dependent and also depends on background, the presence of energy in other frequencies, and adaptation.
Similar to how absolute brightness is not all that perceptually useful (and therefore humans display incredible invariance over very wide brightness ranges), loudness is probably perceptually most useful in terms of relative loudness: sounds that are getting louder may be approaching, for example.
References

Carney, L. H. (1994). Spatiotemporal encoding of sound level: Models for normal encoding and recruitment of loudness. Hearing research, 76(1-2), 31-44.
Heinz, M. G., Issa, J. B., & Young, E. D. (2005). Auditory-nerve rate responses are inconsistent with common hypotheses for the neural correlates of loudness recruitment. Journal of the Association for Research in Otolaryngology, 6(2), 91-105.
Neuhoff, J. G., McBeath, M. K., & Wanzie, W. C. (1999). Dynamic frequency change influences loudness perception: A central, analytic process. Journal of Experimental Psychology: Human Perception and Performance, 25(4), 1050.
Relkin, E. M., & Doucet, J. R. (1997). Is loudness simply proportional to the auditory nerve spike count?. The Journal of the Acoustical Society of America, 101(5), 2735-2740.

"Best frequency" is not a term related to the place theory? It applies also to volley one?

@pasabaporaqui They aren't really competing theories anymore, rather the one that predominates depends on the frequency range you are considering. Certainly people can still argue which is important for some of the intermediate frequencies, but that's more a niche argument. But in principle, louder sounds will induce synchronous volleys over a wider 'place' on the cochlea. Not even an extreme proponent of volley theory would try to argue that the cochlea is not tuned in space.


text:
What animal is this bone from?
10.5 ounces, found laying on ground, central California coast.

This is the cannon bone of an adult artiodactyle.. The size points towards sheep or goat.


text:
Examples of humans intentionally introducing non-native species where everything went well?
It's easy to find examples of humans introducing non-native species to solve some problem (e.g. for food, to control the population of a pest), but later regretting it as the introduced species upsets the ecosystem.

Rabbits in Australia
Mongooses in Hawaii

Are there any examples of this going as expected?
I guess, since I'm really interested in how well humans can predict this sort of thing, what I'm looking for is examples of a situation where there were no unintended consequences. (Rather than beneficial, but unintended, consequences).

Would species that were introduced by humans with out a specific purpose (except Oh, that one looks nice. Let's take it with us.) count as an answer? Or would you limit your question to problem solving (food, pest control) as stated in your first sentence?

Probably most major food crops (other than corn/maize) in the Americas.  Cows seem to have worked out fairly well (I mean open-range or pastured cattle, not the problems associated with industrial feedlots).  Horses are a bit more problematic, but I'd argue that most of the problems actually stem from the decimation of potential predators.

Almost all domestic species would count, the intention was to replace the native ecosystem and that is what happened. The problem with "unintentional" is you have who's intentions. The people who introduced wild boar to the US didn't care what damage they caused, they wanted to be able to hunt boar.

The best examples are for when non-native pest species arrive, and then a search for their natural enemies in their native countries is undertaken to bring them back and control the invaders. This is called "biocontrol", and there are many examples of it going well, under carefully controlled conditions. https://biocontrol.entomology.cornell.edu/success.php
However, you are right to note that it is very difficult to predict.

Fascinating to hear about this working well all the way back in 1889!


text:
What is the difference between pseudorumination and coprophily?
Can someone please explain me difference between these two terms. any help is appreciated.

Ruminants (e.g. cows) is a classification of animals based on its digestive tract, so these are the animals having four-chambered stomacks. Pseudoruminant (e.g. hippopotamus) have three-chambered stomacks in comparison with ruminants. Coprophilous usually applied for different types of fungi that grow on animal dung.


text:
Can you eat cancer cells without risk?
Afaik GMO products are not a real risk to health of course if they do not contain toxins.
But how about cancer cells? Like say rhabdomyosarcoma which is more or less a muscle cancer found also in cows.
Likewise, meat breweries use stem cells, but wouldn't cancer cells just grow faster?

Cancer cells themselves are not effective transmissible agents of disease in humans. Unlike infectious pathogens, there is not a suitable receptor for adhesion at an exposed or accessible site, a suitable environment for replication, and adaptions for immune escape by the tumor cells. There are exceptions in other species: tasmanian devil, dogs, and clams. Importantly, in all of these cases, transmission to another species has not been demonstrated. Eventual transmission to another clam species may be more likely to occur, though, because, unlike vertebrates, they are not known to have a self/non-self recognition system.
Humans, though, do have a self/non-self recognition system.  Even if we ignore the requirement for receptor binding and invasion, consider what happens when cells from another species, and even another human, are surgically implanted. Without immunosuppression, these non-self cells are rapidly attacked and destroyed.
With immune suppression and surgical implantation, though, you can see transmission of cancer. Donor-related tumors in transplant patients are still rare, though the low frequency of transmission may be due, in part, to screening. The fact that we see this at all demonstrates the significance of transmission route and immune escape.
Cancer cells do, of course, metastasize within a single human individual. In order for a tumor seed to successfully metastasize it does need to evade the immune system, find an environment suitable for replication and adhesion. This, however, requires tumor associated cells, non cancerous cells that regulate the microenvironment to make it favorable for growth and replication. You can read about them in Hanahan and Weinberg's 2011 review.
The requirement for tumor associated cells and a permissive microenvironment might be why, in a problematic series of experiments at Sloan Kettering in the 50s, when subjects were inoculated with tumor cells, the procedure resulted in growth of the new tumor, recurrence after excision, and death in some cases where the subject had pre-existng cancer. Transplantation into healthy subjects (yes, they did this) resulted in nodules that spontaneously regressed. This experiment has since been interpreted as evidence for immune system control of transplanted tumor system in healthy individuals, as compared to growth and progression in a receptive niche in a cancer patient. In this example as well, you have eliminated the need for a natural mechanism for adhesion and invasion, and these are same species cells.

HeLa cells (which are of course derived from a cervical cancer) have actually been injected into humans to see if they would grow; they grew briefly but were promptly rejected. Similarly, surgeons have on occasion accidentally stabbed themselves and inoculated themselves with the human tumors they were operating on.
Injecting human cancer cells is a far greater risk than eating non-human cancers, and even in that case the risks seem to be very low.
There have been rare cases of people with profoundly suppressed immune systems (organ transplant recipients) allowing a transferred tumor to grow, so (though of course the risk there is vastly higher than merely eating a cell) it's not completely impossible.
Pragmatically, it's very likely that everyone who's eaten, say, chicken has unknowingly consumed some chicken tumors.


text:
Identification of red, plum-like fruit (probably from Southern Russia)
My parents are currently on a holiday in St. Petersburg (Russia). They sent me this photo of plum-like fruits they bought on a market there (toilet paper for scale, I guess).

The fruits are 20-30mm long, have a big stone, taste sourly like red currant (based on my fathers opinion) and are supposed to come from Southern Russia (don't know where this information is coming from).
Can you please help to identify them?

Can't be certain from the picture, but they look a lot like Cornelian Cherry (Cornus mas: https://en.wikipedia.org/wiki/Cornus_mas ).  However, the ones in my garden (western US) don't ripen until late September/October.
Perhaps they could return to the market, and ask for the Russian name?

I think that's it. The pear shape, the red color, the acidic taste, the origin... everything fits. Of course this can't be verified, but I consider this question answered. Thanks!

I don't notice an acid taste with mine, more of an astringent, mouth-puckering taste until they're fully ripe, when they turn deep red, start to wrinkle a bit, and almost fall off the bush by themselves.  That said, I don't think they're at all good eaten fresh. but they make really great jam and fruit leather.  Search the web for recipes :-)


text:
ID of a purple fungus in Virginia
Could someone tell me a bit more about this fungus found growing in a nearly straight line in the lawn in a wooded area of Virginia, USA? It seems rather fragile, maybe a bit "dry"

This is not a moss, but a fungus of the family Clavariaceae. Most likely this is Clavaria zollingeri, commonly known as violet coral, but there are a few resembling species. Microscopy might be needed to be entirely sure.
The species is saprotrophic, so it grows on the woody debris in your picture.


text:
Why do humans lose subcutaneous fat from the extremities with age?
Why does fat tissue die and shrink on the hands, knees, and lower legs of most people as they age, even when they are overweight?
In most people, their bone definition becomes much more visible around their extremities.
I'm aware I asked a similar question before, but the previous question wasn't specific enough.
Why do humans lose subcutaneous fat tissue with age?
With age, humans store more visceral fat because of multiple factors that include physical inactivity, higher FSH levels, androgens, a drop in estrogen in women, and other factors.

what makes you think they do?

Bones of the extremities become much more visible with age. The bones of the upper face also become much more visible. Its very apparent on the back of the hands, the feet,and outter sides of the knees.

Are you sure that is not just due to  a loss of skin tone.

It doesn't happen to everyone.  Skin by itself is very thin without any subcutaneous fat underneath it. People do lose fat in these areas with age.


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What is this row of pits along the "upper lip" of theropod skulls?
Consider the row of pits visible in the "upper lip" area (and to some extent, the "lower lip" too) of this T-Rex skull at the Palais de la Découverte, Paris (picture from Wikipedia):

I noticed similar pits in a Deinonychus skull a few weeks ago when I visited the American Museum of Natural History in New York:

What are they?

They are called Nutrient Foramen which are innervation of blood vessels and nerves, you see the same thing in reptile and bird skulls (mammals tent to pack it all into one or two large openings). They feed blood vessels and nerves to the gums, lips, and face.
Dinosaurs do seem to have more of them, but size making them more noticable is also a factor. The increase in dinosaurs may be involved with pressure sensitive scales as seen in crocodiles or alternatively something like lips, or both. Here is a great article on them. Paleontologist are hampered here becasue the related animals are birds (who have beaks) and crocodiles (which are entirely scaly). So it is hard to pin down exactly what a dinosaur oral facial anatomy would look like.

Excellent; and great link!


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Are turkish hazelnuts edible?
The title of this question is Google suggestion verbatim, when I tried to write it. Yet, I found no answer specifically for Turkish hazelnuts.
Turkish hazelnut is a tree and it's fruit looks different from normal hazelnuts growing on hazelnut shrubs.
One such tree is planted close to my house, so I was wondering if I could eat all the nuts on the ground.

First off all let me say something about this tree.

Turkish hazelnut (Corylus colurna) is a slow growing pyramidal tree approximately around 25 m (82ft) tall, with a stout trunk up to 1.5 m (4 ft 11 in) in diameter. Leaves are deciduous, rounded, 6-15 cm long and 5-13 cm across, softly hairy on both surfaces. Corylus colurna is actually the largest species of hazel. The name Korylos (korys) comes from Greek and means helmet. The tree is dioecious.

Nuts are about 1-2 cm long, surrounded by a thick, softly spiny and bristly involucre (husk) 3cm diameter. The nuts are born in cluster of 3-8 together. The nuts mature in September and are edible, with a taste similar to common hazel (Corylus avellana). The nuts have a very hard shell, approximately 3 mm thick, which it makes them a little hard to open. Nut production is very irregular and occurs every two to three years.

Source
https://en.wikipedia.org/wiki/Corylus_colurna
http://www.missouribotanicalgarden.org/PlantFinder/PlantFinderDetails.aspx?taxonid=277856
https://www.chicagobotanic.org/plantinfo/tree_alternatives/turkish_hazelnut


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List of proteins by number of amino acids / chain length
Is there any protein database online where I could obtain a list of proteins ordered by the length of their chains / number of amino acids, starting from the shortest, as well as to see their amino acid sequences?
I'd like to start from the short & simple protein structures to see how their particular sequences of amino acids translate into their folding shape, and what those short chains are capable of doing in organisms. (I heard about the LILs, but they are artificially-generated and consist of just two amino acids, Lysine and Isoleucine, so not much variety to study in there :q )
But I'm quite new to these databases, they present a lot of details, but usually not the one I'm looking for, and one has to know what too look for first to get any meaningful information :q

I like this web quite good :)

@aaaaaa: as I said, I'm quite new to those databases, I'm still trying to figure out how to use them. I know some of them, but they don't seem to have any way to list proteins by chain length, starting from the shortest.

@L.Diago: Yup, this one seems nice, especially the pictures ;) And I see there's an option to search by sequence length. Unfortunately, I can only set the minimum and maximum length, but I don't see any way to order the search results by chain length. There's a "residue count", but I'm not sure if it's the same, since I get some weird resuls :q

Have you reviewed the extensive literature on prediction of protein structure? You wouldn't be trying to reinvent the wheel, by any chance?

You can find the data you need in the Protein Data Bank.

Since 1971, the Protein Data Bank archive (PDB) has served as the
  single repository of information about the 3D structures of proteins,
  nucleic acids, and complex assemblies.
The Worldwide PDB (wwPDB) organization manages the PDB archive and
  ensures that the PDB is freely and publicly available to the global
  community.

Each of the PDB member organisations provides the same data with a different interface:

PDBe,
PDBj,
RCSB.

In general, you either query the database through one of the web interfaces, or you download all the data and search it locally. In this case, the RCSB website has the option you asked about (sorting by the residue count):

Alternatively, you could download:
ftp://ftp.wwpdb.org/pub/pdb/derived_data/pdb_seqres.txt
and parse it and sort it as you wish.
This file has sequences of all chains in the PDB entries.
But since your goal is to find the relationship between the sequence and the folded structure, you should probably start from reading about the protein folding problem and about methods used in protein structure prediction.

@SasQ Can you please tune down a bit? You have now three comments flagged and deleted for rudeness, which is not something well liked here. All others: If you want to discuss excessively, please move over to the chat and do not do this in the comments. Thank you.

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

It's worth pointing out that many proteins, and especially "short" ones, are going to be human, computational, or experimental error, or will be intentionally trimmed down from the native version to make it easier to crystallize or otherwise handle. That may not be a problem if considering folding, but relying too much on annotations and descriptions may well be misleading.

In the UniProt Knowledgebase, you can have your proteins sorted by protein length, e.g. in this query for all human proteins with a cross-reference to PDB:
https://www.uniprot.org/uniprot/?query=database%3A(type%3Apdb)%20AND%20organism%3A%22Homo%20sapiens%20(Human)%20%5B9606%5D%22&columns=id%2Centry%20name%2Creviewed%2Cprotein%20names%2Cgenes%2Clength&sort=length
Default sorting is by query score, but if you click on the black triangles in the table headings, e.g. for sequence length, you can have them sorted by other criteria.

I think this answer is better than the PDB one for the question as it was asked, i.e. with no requirement for structures. Firstly, you'll get more data. And secondly, you won't just get proteins that are biased by the composition of the PDB.


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Can anyone identify these flowers?

I'm mostly interested in the maroon and white ones in the center, or the purple and white ones in the front left corner.  They were in bloom in a garden in July at the Buffalo Harbor.  Any help would be appreciated!!

Welcome to SE Biology. Given that these are garden plants it might be worth searching on SE Gardening. If you can't find an answer there you could pose the question there. Also, you need to provide more information about the location.

They look like petunias to me, but this is far from my area of expertise

The sign agrees. They are petunias. The specific variety of the red ones is raspberry swirl. I don't know the specific variety of the purple ones.

Yea I saw the sign after I'd posted, but couldn't see an option to delete the post

@BeckieMaryland no worries! It was a little hard to spot. I didn't post it to shame you or anything, just to provide evidence for my answer :)

@BeckieMaryland take a look at the help for someone answers. If you feel like this answers your question, you can accept it by clicking the gray checkmark next to it.

The violet ones are called Violet Star Charm Petunias and the maroon ones are maybe Madness Burgundy or Easy Wave Burgundy.


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Myoglobin in meat
When looking at the reason why some meat is white and the rest is red, I found out it is down to the levels of myoglobin as higher levels of myoglobin are found in "slow twitch" muscles.
I have also seen that myoglobin is not the same as haemoglobin, so what is the source of myoglobin?  Does it come from the blood?

Myoglobin is a protein made in muscle cells. It is similar to hemoglobin, a protein made by blood cells. The answer you linked helps explain the difference, which it sounds like you understand. The source is simply the ribosomes in the respective cells that express that protein. The color in both blood and uncooked or rare meat is due to the heme group in hemoglobin and myoglobin respectively.


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Can mushrooms spontaneously die?
These are called mushrooms I believe, had been growing on my door for a few weeks. It's monsoon here. Last night I took a picture of it and it looked like this . Today when I woke up it became like this: . All this within 12 hours. I'm pretty sure nobody touched the fungus so I'm inclined to believe this was spontaneous.

nice door! if you want to prevent mould on a door, the least you can do is infuse it with bleach. I imagine the TV has moss on it and the bath has ducks in it.

Of the thousands of shaggy manes I have seen ( and eaten most) , I never saw one growing directly on wood , nearly always they grow in grass .

Those shaggy manes are very fast rotting mushrooms

There are several fungi that autodigest  their lamellae  to release spores. Yours seems to be one of them. Due to the black liquid they release during autodigestion, they have the common name inkcap.
As an example, read this Wikipedia article about Coprinus for more details.

It is said the mushrooms deliquesce when they liquify fairly suddenly. Note that the edible version of that mushroom is always nice until the first gray tones appear in the gills, at which stage they are past their prime and way less palatable... they are only worth picking when completely white and when the mushroom is completely closed, otherwise you have to cut the dark bits off. And there are unpleasant copy cats of the same mushroom so you must ID them well. take the spores of shaggy ink caps, mix them with flour and water in a blender, and throw them around some overturned decayed ground

Actually the coprinus comatus ( pictured) , gets pinkish before grey. I have eaten them with traces of pink, no problem.

Actually "shaggy mane" is the common name in US ; inkys and micas are other closely related species.


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This looks like a mushroom is it eatable?
This looks like mushroom it's white and there are insects feeding on it....it seems to be growing on a cascabela thevetia

Could you please add the location and season, where this fungus grew?


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How long does each of the stages in meiosis take?
For each stages of meiosis (i.e. Interphase, Prophase I, ...), I wanted to know the time between each stages either in percentages or minutes. However, while I could find the cell cycle for mitosis like the image (original link), I couldn't find such thing for meiosis. Does anybody know anything about this?

If you take a look at the figure directly above the image you posted in the link you posted, you'll see a very different set of figures.

It turns out, time spent in different phases of the cell cycle depends on species, cell type, and conditions, specifically, the presence of cell cycle regulating signals like cyclins. You can also read about that in the link you posted.
Meiosis is similarly varied. For example, in a female human, oogonia start meiosis while the female is still a fetus. Meiosis is then arrested in prophase 1. Further progression in meiosis doesn't occur until puberty at the earliest. Spermatogenesis in a human male, on the other hand occurs over a 64 day period. Since oocytes sit in prophase 1 for ~ 13-50 years, they will have a very different proportion of time spent in each phase. You can read about this in Costanza Physiology, chapter 10.


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Apolipoprotein B48 and fat storage
Can chylomicrons formed in the intestine, with apolipoprotein B48, transport lipids to adipose cells for storage?

Fatty acids originating from  chylomicron  triacylglycerol  are delivered mainly  to  adipose  tissue,  heart, and muscle (80%), while ~20% goes to  the liver. - source: Harper's illustrated biochemistry.

Lipoprotein lipase which is present in wall of blood capillaries anchored to endothelium by negatively charged proteoglycan chains of heparin sulfate requires phospholipids and apoC2 for its activity to take place.
Hydrolysis takes place while the lipoproteins are attached to  the enzyme on  the endothelium. Triacylglycerol  is hydrolyzed progressively through a diacylglycerol  to  a monoacylglycerol  and finally to  FFA plus glycerol with the help of lipoprotein lipase.  Some of the released free fatty acid return to general circulation bound to albumin but the bulk is transferred to peripheral tissues like adipose tissue, muscles of heart etc.
Fate of chylomicron
The lipase activity results in loss of 70%-90% of triacylglycerols and apoC2.(source: Harper's illustrated biochemistry) The remnant chylomicron is then taken up by liver by receptor mediated endocytosis. Here cholesteryl esters (present in concentrated form after loss of most of triacylglycerol) and remaining triacylglycerols are hydrolysed and metabolised.

Do you know what proportion of the fats in chilomicrons of dietary-origin get transported to what kind of tissue? I mean the parts that don't go to the liver - "adipose tissue, heart, and muscle (80%)". How much of that goes to adipocytes?

@Abu Dhabi It depends on surface area of distribution (by blood vessels ), need for utilisation of fatty acid and many other factors.

Do the "20% to the liver" refer to  "... after loss of most of triacylglycerol) and remaining triacylglycerols are hydrolysed and metabolised"?  In other words: 20% of triglycerides in chylomicrones go to the liver? Any other easy reference on that?


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Synthesis of adenosine diphosphate?
Where does the ADP come from? As in before ADP was made from ATP and visa-versa how is it conceived that they appeared in nature?

You can't synthesize ADP from just hydrogen; it also requires carbon, oxygen, nitrogen and phosphorous.

Cool so step 1, carbon oxygen nitrogen and phosphorous are all created through fusion from products up from hydrogen. That star eventually yields iron and explodes, what happens next?

Adenosine diphosphate is a nucleotide, specifically a purine nucleotide, since it contains a double ring. These nucleotides are synthesized by cells from amino acids and other nutrients in a rather long and complicated biochemical pathway. You can find information about this pathway in any biochemical textbook, or see this page in Wikipedia.

Your answer is inadequate because it assumes the preexistence of the product.

@kpie  No, it doesn't.  The purines are synthesized from simpler building blocks, like amino acids.  I suggest you read up on the biosynthesis pathway.

ATP -> ADP provides energy at several junctures of the pathways you referenced. like you can't synthesize IMP without ATP, and you can't get credit for answering this question without actually answering it. I'm pretty much looking for someone to layout their theories on life and here you are diminishing the question with your ego.


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What is the source of the fat in adipose tissue?
I have heard the opinion that all of it comes from de novo lipogenesis of carbohydrates, but I'm skeptical. Is there evidence either way - either that dietary fat definitely gets stored in the adipose tissue, or that it never does, and all of it is from carbohydrate transmutation?

The proximal source of adipocyte lipids is mainly fatty acids from circulating lipoproteins (1) after hydrolysis by lipoprotein lipase (LPL).
LPL is activated by ApoC-II, which is present in hepatic-originating VLDL and IDL lipoprotein, but also chylomicron of direct dietary source. Insulin, secreted after meals, stimulates LPL production by adipocytes.
Thus the ultimate source of these lipids is both hepatic lipogenesis (from other substrates like glucids) and dietary fats.
Lipid transport in blood, for reference purpose (Michal G. Schomburg D., Biochemical Pathways, 2012)


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Could being exposed to excess UV in the arctic lead to a human eye color change? If so, what is the mechanism?
The CBS News article Expedition Antarctica: A father and son's journey to save the planet says (in part):

Thirty-two years ago, Robert Swan made history as the first person to walk to both poles. Even as a young man, these grueling expeditions took a harsh toll on his body. Passing directly beneath the hole in the ozone layer, Swan's face became badly burned and his eyes even changed color. But the Arctic explorer now says that all of that physical duress pales in comparison to the agony of watching his son go through the same experience 32 years later. (emphasis added)

Skin color change can happen after exposure to UV light. From Wikipedia:

Melanin is a natural pigment produced by cells called melanocytes in a process called melanogenesis.

Question: Can the human eye really change color due to excess UV light from the Sun, in this case through a polar "hole" in the ozone layer? If so, what is the mechanism?

above: "This winter, Barney and Robert Swan became the first explorers to ever trek to the South Pole surviving exclusively off of renewable energy." Robert (the elder) is on the right. From here. Credit: SHELL-Technical Partners

I find this a pretty bold statement from this article. The second this, I would like to see at least before and after pictures. Additionally, the color of the sons eye doesn't seem to bright to me.

@Chris pigments can degrade and change color from exposure to UV or even blue light, so it's certainly plausible, but I would think that eye protection usually used in sunlit, reflective, snowy conditions would have prevented this. I'm going to ask for a better source for this in The Great Outdoors SE right now, and I'll keep an eye on answers and comments there and here. I understand it's important to avoid the false premise in a question so if I can't get this resolved shortly I'll delete the question until I can. Thanks!

"Credit: SHELL-Technical Partners " is it real?  Because that it is not so trust worthy but still i look forward to some answer here.

I've just asked Has extended exposure to sunlight and UV in the arctic or antarctic ever caused someone's eyes to change color?

@uhoh I will look into this later. Exposure to UV also promotes pigmentation, which puzzles me a bit here. Yes, the eyes are pretty sensitive to UV radiation and sunburn there is pretty painful.

@Chris possibly related: https://www.independent.co.uk/news/science/british-scientists-discover-reindeer-eyes-change-colour-from-gold-to-blue-over-course-of-the-seasons-8916008.html

@L.Diago As far as the SHELL-Technical Partners goes, check out the Shell Corporation video The South Pole Energy Challenge which is also found here which comes from this answer to my question looking for additional information on this.

@Chris some results! outdoors.stackexchange.com/a/20291/12619 Still no hard data yet, but "bleached his eyes and burned his face" does seem to have some plausibility, as mentioned here update: Ah, I've just found this: https://edition.cnn.com/2015/03/04/tech/mci-brown-eyes-blue/ and also https://www.techly.com.au/2014/12/03/want-change-eye-colour-brown-blue-possible-via-laser/

@uhoh Interesting. I actually looking through the journal databases now, lets see, if there is something.

It's a four year old question and so far nothing definitive, but the September 30, 2022 BBC Future article How our eyes can change colour throughout our lives includes the following quotes from David Mackey, professor of ophthalmology in the Lions Eye Institute at the University of Western Australia.
Unfortunately there is no smoking gun here, yet.

Through apparently spontaneous change or through mishap or illness, our eyes can change colour in surprising ways.

But, surprisingly, our eye colour doesn't always remain constant throughout our lives – in fact, a wide range of external influences can change it, from injury to infection and sun damage. And sometimes the change appears to happen spontaneously.

It may be a similar story for eye colour, he suggests, with greater quantities of pigment building up in the months or years after birth. "The main pigment in the eyes is melanin and it's the way that melanin is distributed that gives you the different eye colours," he1 says. "Simply classifying them: you've got blue eyes, some people also talk about grey but really it's a variant of the blue, then you've got the hazel and green combinations, and then you've got the brown, and that can be slightly brown or extremely brown. All of that's related to how much melanin is there."

Higher levels of melanin can have a beneficial function in intense sunlight – as in the skin, the pigment offers protection from sun damage.

In irises with little melanin, the blue colour comes from the way the fibres of collagen at the back of the iris scatter light, in the same way that the sky appears blue because of way light is scattered in the atmosphere.

As to why some children's eyes express more melanin over time, this remains mystery, says Mackey.

"We actually don't know what influences those colour changes," says Mackey, but there could well be an environmental factor at play. "You can almost say that for everything there's an interaction of genetics and environment, even for things we think of as totally genetic or as totally environmental," says Mackey. "But what environmental factors could influence it? We don't really have that data for the general population."

1David Mackey, professor of ophthalmology in the Lions Eye Institute at the University of Western Australia.


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Is the mutation rate in pseudogenes higher than in coding regions?
Coding genes are subject selective pressure that are not present for pseudogenes, that would suggest that pseudogenes have a higher mutation rate than coding regions. If so, how much higher?

It is important to distinguish between the rate of mutation, which is a biochemical process, and the rate of fixation, which is a population process whereby an allele with a particular mutation becomes fixed (present in all individuals) in the population. Relaxed purifying selection, such as that experienced by genes undergoing pseudogenisation, affects the fixation rate of mutations because new variants are not being filtered from the population by purifying selection. The mutation rate itself is probably constant, unless some other factor is at play.
In response to comments, I will say this: if functional constraints on the gene are relaxed to the point where all mutations are selectively neutral, then the process of mutation and substitution can be modelled by neutral theory and the expected rate of substitution (or fixation) is the same as the rate of mutation. This rate is dependent on several factors - lineage, life history, etc., and the difference between this rate and the fixation rate for a given coding region is dependent on the severity of functional constraint on that region.

OK, but the poster obviously means the fixation rate of mutations. The answer is obviously yes, but if one is going to answer here shouldn't one provide experimental justification?

Actually @David I have found that the distinction between those two in relation to questions around functional constraint is a pretty common misconception, especially as the question specifically states "mutation rate". As the poster is new, I have no way of gauging their prior knowledge.


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ID of this flower/plant and origin if possible
Hello again all you helpers out there!
So this plant or flower is found in Virginia (USA) rural area mainly woodland and grassplains, when it comes up, it rarely last for very long, so with a photo of the plant in its glory, i hope some of you could tell me, what kind of plant/flower it is and where it came from, thank you very much and have a great weekend!
/Beo

I assume you mean Virginia, USA, so I've edited that. Feel free to change if you mean Vancouver or whatever.

Look like a Spider lily (Lycoris radiata):

Source: NC State University

Yea it does look like that one, thank you for your answer, ill try and read up on this one.