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

Explanation: The question examines if taste can be triggered by electrical stimulation. The document on BrainPort technology supports this, demonstrating how the brain interprets electrical signals on the tongue as sensory data, confirming electrical stimulation can induce taste sensations.

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**Short answer**
_Yes_ , taste sensations can be generated electrically. However, we cannot
taste electrons themselves, as taste-receptor proteins on the taste receptor
cells are not activated by electrons. Instead, electrical currents stimulate
taste receptors _directly_ by depolarizing the cell membrane, without the need
of activation of the proteins that normally bind ions or molecules.

**Background**
There is a medical device called the **[ BrainPort
](http://www.wicab.com/#!brainport-v100/ee7ds) ** that electrically stimulates
the tongue (Fig. 1.) The device is marketed as an electrotactile vision
substitution device. Basically, it captures images of the outside world with a
glasses-mounted camera and these images are translated into electrical stimuli
presented on a 20 x 20 electrode array. That array is embedded in the tongue
display unit (aka intra-oral device, IOD). The IOD is worn on the tongue.

[ ![BrainPort V100](https://i.sstatic.net/Bd7S4.jpg)
](https://i.sstatic.net/Bd7S4.jpg)
Fig. 1. BrainPort V100. source: [ TuWindowsMundo
](http://www.tuwindowsmundo.com/brainport-permitira-ver-a-estadounidenses-
ciegos/)

It typically generates electrotactile sensations, like [ champagne bubbles
](http://www.techtimes.com/articles/62220/20150621/fda-approves-
brainport-v100-a-gadget-that-allegedly-help-blind-people-see-with-their-
tongues.htm) . However, some subjects do report [ metallic **taste**
sensations ](http://www.techtimes.com/articles/62220/20150621/fda-approves-
brainport-v100-a-gadget-that-allegedly-help-blind-people-see-with-their-
tongues.htm) when using the device. In fact, [ Lawless _et al._ (2005)
](http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1307523/) * investigated the
electrically evoked metallic-taste in response to anodic stimulation of the
tongue directly and confirmed the anecdotal reports obtained with the
BrainpPort device that electric stimuli evoke metallic-taste sensations.

Physiologically, taste receptor cells sense certain compounds (salts, acids
etc.) due to activation of receptor molecules on the cell's surface. In turn,
activation of receptor molecules depolarizes the cell membrane which
eventually lead to neurotransmitter release and activation of secondary
neurons that transmit the signal up to the brain (Fig. 2). Electrical stimuli
**bypass** the receptor molecules and _directly depolarize the taste receptor
cells_ .

Given the anatomy of the taste receptor system in the tongue (Fig. 2), I am
inclined to believe that the taste receptors are stimulated directly, and not
the secondary neurons, because they are situated in deeper layers.

[ ![Neural gustatory receptor pathway](https://i.sstatic.net/eUfBu.jpg)
](https://i.sstatic.net/eUfBu.jpg)
Fig. 2. Neural pathway of the taste buds on the tongue. Note that the
secondary neurons transporting the taste information to the brain are situated
in deeper layers than the taste buds. Source: [ Universe Review
](https://universe-review.ca/R10-16-ANS06.htm) .

Note that [ taste receptors ](https://en.wikipedia.org/wiki/Taste_receptor) do
_not_ sense electrons. Rather, larger ions or molecules may stimulate them and
cause a [ **depolarization** ](https://en.wikipedia.org/wiki/Taste_receptor)
of the receptor cell, in turn activating the secondary neuron via a chemical
synapse.

**Reference**
**-** [ Lawless _et al_ ., _Chem Senses_ (2005); **30** (3): 185–94
](http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1307523/)

**Acknowledgment**
*Credits for the [ Lawless _et al_ . (2005) ](http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1307523/) reference go to @CMK


Question:
Hot water and bacteria
I know that it is common to say, "use hot water when washing your hands" or when you've got a cut, "wash your hands with warm water," etc. I was wondering, why is this the case? Since bacteria grow in warm environments, you would think that it might be beneficial for bacteria. Is this just another myth or is this actually true?

Explanation: The inquiry questions hot water's effectiveness against bacteria. The selected document was chosen because it addresses common beliefs and scientific findings about water temperature's impact on bacteria removal.

$\begingroup$

The bacteria wouldn't see any benefit from the warm water in the ~30-60
seconds you're washing your hands, neither would hot water "sterilize" your
hands at temperatures you could tolerate. The reason you wash your hands with
hot water is because the hot water+detergent soap mix is better for removing
oil and dirt than cold water+detergent, which is supposedly where bacteria
reside.

Interestingly, there was a study published saying that washing with hot water
doesn't have much of an effect on bacterial load. [ Hot water for handwashing
--where is the proof? ](http://www.ncbi.nlm.nih.gov/pubmed/15824636)
(Laestadius and Dimberg, 2005). I'd be interested to look more into their
methods but the paper is behind a paywall and I don't have access at home.

Also, this paper, [ Water temperature as a factor in handwashing efficacy
](http://onlinelibrary.wiley.com/doi/10.1046/j.1471-5740.2002.00043.x/full) by
Michaels _et al_ . is open and shows no evidence that hot water is any better
than cold water for removal of microbes.

> [W]ater temperature exhibits no effect on transient or resident bacterial
> reduction during normal handwashing with bland soap.


Question:
Why does my room suddenly look 'reddish'? My eyes seem to adapt to color
To get the context of this question clear, I would like you to walk through some parts of my house.
We'll start with one of my rooms as it appears normally - area Y
As evident, this part of my house has a creamish tinge to it, also the balcony door is open which further gives this room a yellow tint. Nothing special. I'll call it "area Y" (for yellow)*. Let's move on.
area G
Here we arrive in another part of my house which has greenish/blue shades acting as a sunlight blocker. This gives this entire place a greenish/blue tint as shown. (Ref. "area G")
So, now let's visit the area Y again. I am always surprised with what my eyes now see. This. {1}
enter image description here
You see, the same room, same lightning, yet the room now looks much more reddish than before! That's what intrigues me, why does it happen? Why my eyes suddenly become sensitive to red color?
I am not a biology student but I do know that our eyes have cones which specialize in color perception, and that there are different types of cone cells to perceive different types of colors (If I remember my high school biology correctly).
So, I somewhat get a feeling of what's happening inside my eyes (or the brain perhaps?). I suspect that as I go to area G, my eyes 'adapt' to the dominance of bluish/green light, either by decreasing pigment of blue cones or by increasing pigment of red cones, which makes my eyes more sensitive to the other end of visible light spectrum (red-yellow), causing an 'outburst' of red coloration in area 'Y'. Since pigments need time to degrade, by the time the red color pigment of my cones decreases, its activity is less than normal. It may be increased as the blue pigment's activity is less than normal and I see a reddish tinge for few moments.
This was a pure hypothesis from my part, but it seems correct to me. But why do my eyes even adapt to blue color? Why can't my eyes be unbiased towards colors?
{1} Obviously I photoshopped the red tint in the image how else could I have replicated my vision? Though it's not the most accurate description of what I see it's still a very close approximation.

Explanation: The inquiry about a room's reddish appearance after exposure to different colors led to selecting a document on afterimages, explaining visual perception changes due to prolonged color exposure, directly relating to the observed phenomenon.

$\begingroup$

**Short answer**
The phenomenon you describe can be explained by the **[ negative afterimage
effect ](https://www.scientificamerican.com/article/bring-science-home-
afterimages/) ** , which indeed is elicited by adaptive processes in the
_retinae_ .

**Background**
In the retina there are three types of color photoreceptors, called cones.
They are sensitive to red, green and blue, respectively. Colors are processed
in the retina through a process explained by the **[ Hering model
](https://psych.ucalgary.ca/PACE/VA-Lab/colourperceptionweb/theories.htm) ** .
This model assumes that there are two sets of opponent colors, namely red -
green and blue - yellow (Fig. 1).

This model assumes that in the red-green opponent channel the red cones
inhibit the output of green cones and _vice versa_ . In the blue-yellow
channel the blue cones inhibit the green/red (= yellow) cone output and _vice
versa_ .

Now look at the visual illusion shown in Fig. 2. This illusion nicely
illustrates the effect. After looking at the image for half a minute, your
cones adapt to the color input. Particularly relevant to your question is that
the green cones adapt to the green and become less responsive to green (this
happens when you are in your _"greenish blue shade acting as a sunlight
blocker. This gives this entire place a greenish [blue] tint as shown. (Ref.
'area G')."_ Now this in turn lowers the green inhibition of the red-half of
the red-green opponent channel. In turn, when you enter your _"part of [the]
house [with] a creamish tinge to it, [] 'area Y' []"_ the green channel will
not inhibit the red-half and everything will have a reddish hue to it, akin to
looking at the white half of the illusion after 30 seconds below.

**Reference**
**-** _[ Sci Am ](https://www.scientificamerican.com/article/bring-science-
home-afterimages/) _ , October 2013

[ ![Hering](https://i.sstatic.net/sGqRR.png)
](https://i.sstatic.net/sGqRR.png)
Fig. 1. Hering model of color vision. Left panel: brightness coding. Right
panel: opponent colors code for color, namely the red-green and blue-yellow
channels. source: [ Bio.SE
](https://biology.stackexchange.com/questions/26216/advantage-of-opponent-
color)

[ ![After image](https://i.sstatic.net/Rdyvq.jpg)
](https://i.sstatic.net/Rdyvq.jpg)
Fig. 2. Visual afterimage illusion. Look at the fixation dot in the middle of
the tripartite circle on the left for 30 seconds. Don't look away. Now look
instantly to the white part on the right. If you don't see much, or only
vaguely, try again. Blinking may help to shortly enhance the illusion. source:
_[ Sci Am ](https://www.scientificamerican.com/article/bring-science-home-
afterimages/) _


Question:
Why do adults lose hearing at high frequencies?
Children and teens can hear high pitched sounds that adults can't hear anymore. Why do adults lose high-frequency hearing?

Explanation: The question probes why adults experience high-frequency hearing loss. The document was chosen for its explanation of presbycusis, the age-related hearing loss, detailing its causes and differentiating it from other types of hearing loss, directly addressing the user's query about adults losing high-frequency hearing.

$\begingroup$

Hearing declines with age and, typically, high frequencies are affected first.
**Age-related hearing loss** (or _**presbyacusis** _ ( [ Kujawa & Liberman,
2006 ](http://www.jneurosci.org/content/26/7/2115.full.pdf+html) )) is
progressive and starts at the highest frequencies and as a person ages the
lower frequencies are affected. The reduction in hearing sensitivity is caused
by the **loss of hair cells** . Hair cells are sensory cells in the inner ear
that convert acoustic vibrations into electrical signals. These signals are
transmitted to the brain via the auditory nerve.

Because of the **tonotopic organization** of the inner ear (the _cochlea_ )
one can conclude that presbyacusis develops from the basal to apical region.
The following schematic of the cochlea from [ Encyclopædia Britannica, Inc.
](https://www.britannica.com/science/inner-ear) nicely shows the cochlear
tonotopy (i.e., high frequencies in the base, low frequencies in the apex);

![cochlea](https://i.sstatic.net/ERAIB.jpg)

As to your question **why the basal region is more sensitive to aging** \-
that is a very good and interesting question that has **not been answered, as
far as I am aware** . What is known, however, is that the basal regions of the
cochlea are also more sensitive to the damaging effects of **ototoxic
antibiotics** such as kanamycin ( [ Stronks _et al_ ., 2011
](https://www.google.com.au/url?sa=t&rct=j&q=&esrc=s&source=web&cd=3&cad=rja&uact=8&ved=0CCkQFjAC&url=http%3A%2F%2Fwww.researchgate.net%2Fprofile%2FHuib_Versnel%2Fpublication%2F47660604_Effects_of_electrical_stimulation_on_the_acoustically_evoked_auditory-
nerve_response_in_guinea_pigs_with_a_high-
frequency_hearing_loss%2Flinks%2F0c96053cd1c55581f2000000&ei=JYe8VJjTO-
PPmwX_4oGQCA&usg=AFQjCNHO_pbdR5L3pW2btsnZGDdtEo-
iLA&sig2=S1nw5B9anvl__Iwy7eNgLA&bvm=bv.83829542,d.dGY) ) and other
aminoglycosides, and some **chemotherapeutics** such as cisplatin ( [ Schacht
_et al_ ., 2012 ](http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3596108/) ). In
low doses these compounds specifically target the basal regions over the
apical ones (at high doses the whole cochlea is affected).

Perhaps the **specific anatomy and circulation** causes the basal region to be
affected more by these chemicals. For example, blood flow may be enhanced
basally whereby environmental and food-based chemicals may enter the basal
region more readily (educated guesses, I can dig up references of authors
posing these possibilities if necessary). This scenario may also contribute to
presbyacusis, since it is quite imaginable that years of exposure to various
substances may cause accumulation damage specifically to the basal parts of
the cochlea.

In addition, since high frequencies are coded in the basal region, and given
that sound enters the cochlea in the basal region (see picture below), **all
sounds** , including damaging loud low-frequency stimuli **first travel to the
base** on their way to their point of processing.

![Cochlea structure](https://i.sstatic.net/M9fxb.jpg)

Because sound is analyzed as a travelling wave, sound travel stops at that
point where the frequency matches the cochlear characteristic frequency. There
the wave quickly dies out due to cochlear filtering ( [ Mather, 2006
](http://www.psypress.com/cw/mather-9781841696997/) ); see the first picture
above. In effect, more apical parts of the cochlea are exposed less frequently
to (damaging) sound stimuli, while the **base of the cochlea is exposed to all
sounds entering the inner ear** .

Hence, **chemical exposure and acoustic wear and tear** may be more prominent
in the cochlear base, which can explain why **presbyacusis starts at the very
high frequencies and progresses to low frequencies** (upward in the cochlea)
from there.

**References**
**-** [ Encyclopedia Brittanica* The-analysis-of-sound-frequencies-by-the-
basilar-membrane ](https://www.britannica.com/science/inner-ear)
**-** [ Kujawa & Liberman, _J Neurosci_ 2006; 26:2115-23
](http://www.jneurosci.org/content/26/7/2115.full.pdf+html)
**-** [ Mather, Foundations of Perception, 2009
](http://www.psypress.com/cw/mather-9781841696997/)
**-** [ Schacht et al, Anat Rec Hoboken 2013; 295:1837-50
](http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3596108/)
**-** [ Stronks et al, Hear Res 2011; 272:95-107
](https://www.google.com.au/url?sa=t&rct=j&q=&esrc=s&source=web&cd=3&cad=rja&uact=8&ved=0CCkQFjAC&url=http%3A%2F%2Fwww.researchgate.net%2Fprofile%2FHuib_Versnel%2Fpublication%2F47660604_Effects_of_electrical_stimulation_on_the_acoustically_evoked_auditory-
nerve_response_in_guinea_pigs_with_a_high-
frequency_hearing_loss%2Flinks%2F0c96053cd1c55581f2000000&ei=JYe8VJjTO-
PPmwX_4oGQCA&usg=AFQjCNHO_pbdR5L3pW2btsnZGDdtEo-
iLA&sig2=S1nw5B9anvl__Iwy7eNgLA&bvm=bv.83829542,d.dGY)


Question:
Did neanderthals need vitamin C from the diet?
Modern humans need to get vitamin c from the diet, because we do not make it ourselves. Did neanderthals produce vitamin c? At what point of evolution exactly was this ability lost?

Explanation: The question explores whether Neanderthals required dietary vitamin C, referencing humans' inability to synthesize it. The document details the evolutionary loss of the GULO enzyme, responsible for vitamin C synthesis, in primates, including humans, making it relevant for understanding this genetic change's historical context and its impact on dietary needs.

$\begingroup$

Humans can't synthesize vitamin C due to a [ dysfunctional enzyme
L-gulonolactone oxidase ](https://biology.stackexchange.com/questions/401/why-
do-humans-not-produce-vitamin-c-like-other-mammals) , or "GULO".

From [ Wikipedia ](https://en.wikipedia.org/wiki/L-gulonolactone_oxidase) :

> Loss of GULO activity in the primate order occurred about 63 million years
> ago, at about the time it split into the suborders Haplorhini (which lost
> the enzyme activity) and Strepsirrhini (which retained it). The haplorhine
> ("simple-nosed") primates, which cannot make vitamin C enzymatically,
> include the tarsiers and the simians (apes, monkeys and humans)

All of our relatives under Haplorhini, including monkeys and apes, are unable
to synthesize vitamin C; that would certainly include neanderthals.


Question:
Why can't humans drink sea water?
It would seem to be a huge evolutionary advantage for an animal to be able to drink sea water rather than have to rely on fresh water, and it's provably not impossible due to the existence of sea mammals that must filter the sea water somehow.
Could someone explain to me any likely reasons that this is the case?

Explanation: We can use the relationship of different concentration of particles dissolved in body fluid to answer this.

$\begingroup$

For humans, our blood and other tissues have a salinity which is less than
that of sea water. The [ osmolarity of blood is 275-299mOsm/L
](http://bionumbers.hms.harvard.edu/bionumber.aspx?&id=100803&ver=1&trm=osmolarity)
, while the [ osmolarity of seawater is ~1000 mOsm/L
](http://bionumbers.hms.harvard.edu//bionumber.aspx?&id=100802&ver=5) .

The major reason we need to drink and excrete (sweat, breath and urine) water
is to rid the system of waste- i.e. water soluble chemicals or heat we do not
need. The kidneys do a lot of this work and they need a reasonable osmotic
potential to help them.

The osmotic potential is the tendency of molecules, for instance salts, to
diffuse from one reservoir of liquid to another. The kidneys burn metabolic
energy (food) to create a slightly higher concentration of waste chemicals
into the bladder/urine. Other organs will fail or also work to maintain a
local salt concentration (e.g. any nerve cell which depends on Na+/K+
concentrations to transmit their signals. But the kidneys are the gatekeepers
of salinity in the body. They work hardest (and can get injured) when there is
more salt in the water we drink. If you drink sea water you will quickly find
your kidneys overworked and not really functioning.

That's why salt water will tend to make you thirsty (if you can drink any at
all). Most people will gag when they drink even a little sea water, much less
a glassful.

[ Sea mammals actually eat their fresh water.
](http://www.scientificamerican.com/article/how-can-sea-mammals-drink/) They
rely on the fluid they get from fish to keep their salt balance. Its true that
some animals like fish and molluscs etc have adapted other means of keeping
their salt balance in check. Its just also true that its a lot of work to keep
this ability and when animals move away from the oceans, they quickly lose
that ability.


Question:
Is monogamy a human innate behaviour?
As the question states, got curious and I was wondering if monogamy is an innate human behaviour or is it because of how we built society (religion, traditions, etc.)?
Let's say we go back in time, would we see humans settling down with a single partner at a time and caring for their children as a couple for life or would they reproduce with several leaving the mothers with their children?
Thanks!

Explanation: We can look for evolutionary factors of why people might cheat to address this question.

$\begingroup$

Humans are believed to be mostly [ serial monogamists
](http://www.sciencedirect.com/science/article/pii/S0376635700001182) with a
noticeable components of secret [ cheating
](https://books.google.com/books?hl=en&lr=&id=I20uPfEjsNQC&oi=fnd&pg=PA93&dq=humans%20serial%20monogomist&ots=C7WGV3D8gI&sig=b9N73PxR0LquC6pLzrKTe75aFXI#v=onepage&q=humans%20serial%20monogomist&f=false)
. Serial monogamy means most will have a single partner at a time but will
likely have several partners throughout their life, there is however an under
current (~15%) of hidden cheating in most studied populations. Also I say
mostly becasue human behavior is plastic and nearly every possible combination
exists, albeit in small numbers. Males do have a stronger [ tendency
](http://www.tandfonline.com/doi/abs/10.1080/00224490409552211) to seek
multiple partners at the same time, which makes biological sense.
like many social species you really have several mating strategies coexisting,
often in the same head. Our large brains allow for more [ flexible
](http://www.tandfonline.com/doi/abs/10.1080/01614576.2000.11074334) approach
to strategies.

In other animals exclusive (one mate forever) monogamy is exceptionally,
almost breathtakingly rare, (not counting animals that only ever mate once).
The Azara's night monkey is one of the few that has been backed by genetic
research. Almost every monogamous species ever studied either has some rate of
cheating, or is serial monogamous.


Question:
Are single-celled organisms capable of learning?
I've read that the amoeba is capable of learning. Since these protists have no nervous system, it's safe to assume that even highly simplified learning mechanisms of the Aplysia are miles off in the evolutionary distance.
How does this species learn? I would presume that there is a complicated chain of receptor mediated transcription regulation, but what are the specifics? What types of receptors does an amoeba have to sense its environs?

Explanation: This can be proved if we can show that orgranisms can adapt to its surroundings.

$\begingroup$

I'd like to know what is the reference for amoebic learning. I cannot comment
directly on this, but there is some evidence for "adaptive anticipation" in
both prokaryotes and single-celled Eukaryotes which do not have a nervous
system.

In the case of E. coli, it has been [ shown
](http://www.nature.com/nature/journal/v460/n7252/abs/nature08112.html) that
the bacteria can anticipate the environment it is about to enter. E. coli in
the digestive tracts of mammals will typically be exposed to initially a
lactose, and then later to a maltose environment as the bacteria pass down
through the animal tract. This suggests that upon encountering a lactose
environment, maltose operons are induced. I.e., upon encountering lactose,
maltose is anticipated. This suggests a "genetic memory" of the sequence of
sugar types where lactose is always encountered before maltose.

Further cultures (500 generations) of E. coli in the absence of maltose but in
the presence of lactose reduced the maltose operon activity to negligible
levels, suggesting that this is an adaptive prediction of environmental
changes.

_Mitchell, A et al._ , **Adaptive Prediction of environmental changes by
microorganisms** , 2009, 460, 1038


Question:
Why does hair turn grey or white, and why does it happen later for some?
The question is pretty simple: what is happening molecularly when hair turns grey or white? I would imagine that it is due to the lack of a particular compound. I'm also interested in why some people's onset of grey hair happens much later than others.

Explanation: This can be explained by loss of particular cells when aging.

$\begingroup$

Each individuals [ hair colour ](http://en.wikipedia.org/wiki/Hair_color) is
determined by the particular pigment they produce (called melanin - the same
stuff in your skin that makes you tan).

As the body ages this pigment (produced by the melanonocytes - cells that
reside in the hair follicle) is produced less and less, until the hair is no
longer coloured, and appears grey.

This is unique to each individual because it is a genetic (and therefore
highly heritable) trait. Because it is in no way linked to mortality there is
no selection pressure against greying hair.

The _reason_ that the pigment is not longer produced is the [ gradual
depletion of the stem-cell pool with age
](http://www.ncbi.nlm.nih.gov/pubmed/17917134) . This is common to many
tissues, hair follicles being just one. As the 'pool' of stem cells is
depleted, the melanocytes are no longer replaced as frequently, and thus less
pigment is produced as we age.


Question:
Can a human be made with ovum but without sperm?
This article says that scientists were successful in making a mouse using only a sperm and no egg (ovum). The article also states that this procedure could be applicable to humans.
However, I want to know why didn't they try with only an ovum?
Can a human be made only with an ovum, i.e. without sperm?

Explanation: Discussion of asexual reproduction solely from eggs in humans can directly address this problem.

$\begingroup$

Nice question! It is actually very difficult to do so because humans,
obviously, are far more complex than some animal species which naturally show
parthenogenesis. Just to mention, there are female-only animals also present
in nature, such as [ New Mexico whiptail
](https://en.wikipedia.org/wiki/New_Mexico_whiptail) , which reproduce only by
parthenogenesis, meaning that it is not as impractical as one might think.

There have been many parthenogenesis tests on mice and monkeys, but they
usually result in abnormal development. This is because mammals have imprinted
genetic regions, where either the maternal or the paternal chromosome is
inactivated in the offspring in order for development to proceed normally. A
mammal created by parthenogenesis would have double doses of maternally
imprinted genes and lack paternally imprinted genes, leading to developmental
abnormalities. It has been suggested that defects in placental folding or
interdigitation are one cause of swine parthenote abortive development.

During oocyte development, high metaphase promoting factor (MPF) activity
causes it to arrest at the metaphase II stage until a sperm fertilizes it. The
fertilization event causes intracellular calcium oscillations, and targeted
degradation of cyclin B, a regulatory subunit of MPF, thus permitting the
oocyte to proceed through meiosis. The most precise and exact mechanism is not
known yet.

But this does not mean that it is not possible. Actually, it has been done
quite a few times; [ once
](http://online.liebertpub.com/doi/abs/10.1089/clo.2007.0033) on June 26, 2007
by International Stem Cell Corporation (ISCC), and [ once
](https://www.theregister.co.uk/2007/08/03/hwang_parthenogenesis/)
(controversially) on August 2, 2007 by Hwang Woo-Suk. Even the procedure for
parthenogenesis (in swine though) in lab is available. To initiate
parthenogenesis of swine oocytes, various methods exist to induce an
artificial activation that mimics sperm entry, such as calcium ionophore
treatment, microinjection of calcium ions, or electrical stimulation.
Treatment with cycloheximide, a non-specific protein synthesis inhibitor,
enhances parthenote development in swine presumably by continual inhibition of
MPF/cyclin B As meiosis proceeds, extrusion of the second polar is blocked by
exposure to cytochalasin B. This treatment results in a diploid (2 maternal
genomes) parthenote Parthenotes can be surgically transferred to a recipient
oviduct for further development, but will succumb to developmental failure
after ≈30 days of gestation.

[ ![swine parthenogenesis](https://i.sstatic.net/MIhux.jpg)
](https://i.sstatic.net/MIhux.jpg)

The major problem with parthenogenesis in humans is the abnormal development
of embryo. This has been accounted by a phenomenon known as genomic
imprinting. Genomic imprinting is the epigenetic phenomenon by which certain
genes are expressed in a parent-of-origin-specific manner. For example, if the
allele inherited from the father is imprinted, it is thereby silenced, and
only the allele from the mother is expressed. The death of diploid
parthenogenetic or androgenetic mammalian embryos is determined by the absence
of expression of the genes of imprinted loci of the maternal or paternal
genome, which leads to significant defects in development of tissues and
organs. How this exactly works is not known yet, but it is supposed that it
evolved to prevent parthenogenesis. Bi-parental reproduction is necessary due
to parent-specific epigenetic modification of the genome during gametogenesis,
which leads to non-equivalent expression of imprinted genes from the maternal
and paternal alleles. Thus, genomic imprinting seems to be ineffective during
normal reproduction.

As a side note, in the article you refer to, the researchers did not just _mix
two sperms and produce diploid zygote_ or something like that. In the
procedure, they injected a normal sperm to the above explained abnormal
embryo, which later on proved to be viable. They, thus, showed that these kind
of embryos can also become viable if they get fertilized by a sperm within
time.

_**References:** _

  * [ Abnormal development of embryonic and extraembryonic cell lineages in parthenogenetic mouse embryos; Karin S. Sturm, Margaret L. Flannery, Roger A. Pedersen ](http://onlinelibrary.wiley.com/doi/10.1002/aja.1002010103/full)
  * [ Parthenogenesis - Wikipedia ](https://en.wikipedia.org/wiki/Parthenogenesis)
  * [ Patient-Specific Stem Cell Lines Derived from Human Parthenogenetic Blastocysts; E.S. Revazova, N.A. Turovets, O.D. Kochetkova, L.B. Kindarova, L.N. Kuzmichev, J.D. Janus, and M.V. Pryzhkova ](http://online.liebertpub.com/doi/abs/10.1089/clo.2007.0033)
  * [ Genomic imprinting is a barrier to parthenogenesis in mammals; Kono T. ](https://www.karger.com/Article/Abstract/90812)
  * [ Genomic Imprinting and Problem of Parthenogenesis in Mammals; E. S. Platonov ](http://link.springer.com/article/10.1007/s11174-005-0040-8)
  * [ Mice produced by mitotic reprogramming of sperm injected into haploid parthenogenotes; Toru Suzuki, Maki Asami, Martin Hoffmann, Xin Lu, Miodrag Gužvić, Christoph A. Klein & Anthony C. F. Perry ](http://www.nature.com/articles/ncomms12676)
  * [ Stem cell fraudster made 'virgin birth' breakthrough; Silver lining for Korean science scandal; 3 Aug 2007, Christopher Williams ](https://www.theregister.co.uk/2007/08/03/hwang_parthenogenesis/)


Question:
Why doesn't water enter my body through my anus or genitals when swimming?
So when we swim, we can make water not enter through our nose and mouth, simply by holding our breath. However, the mouth and the nose aren't the only cavities. What about the anus and the genitals? They obviously can't "hold breath", so how do they stop water from entering?
I thought the reason is gravity, but then, people would be killed when diving because your butt is facing up, against the gravity.
Another explanation might be that the internal pressure is higher than the external one, but I fail to recall any organ that creates the pressure..

Explanation: To solve this problem, we can find out which muscles control the valve of our anus.

$\begingroup$

For the same reason that when you urinate or use the toilet, you have to exert
pressure and urine or faeces just does not simply leak out when you stand up.
The urethra seals shut when the [ urethral sphincter muscle
](http://en.wikipedia.org/wiki/Urethral_sphincter) s relax. Similarly [
Sphincter ani externus muscle
](http://en.wikipedia.org/wiki/Sphincter_ani_externus_muscle) seals shut in
the anal canal when there is no antagonistic force. So water can't just simply
enter our body in such huge quantities that we die. It is possible to get more
water through your anus with some pressure which is what happens when you get
an enema.


Question:
Could viruses be used as antibiotics?
Could we use viruses that only affect bacteria to act as antibiotics?
The more bacteria, the more times the virus divides, so the stronger it gets. Is this practical?

Explanation: We can check if there is a certain kind of treatment that utilizes this methodology.

$\begingroup$

> Could we use viruses that only affect bacteria to act as antibiotics?

Yes. The specific class you're referring to is called a "bacteriophage".

There's quite a bit of research going on surrounding phage therapy as a stand-
in or replacement for traditional antibiotics. Here's a [ Nature Biotechnology
article from 2004
](http://www.nature.com/nbt/journal/v22/n1/full/nbt0104-31.html) that
discusses your very topic.

It is practical, carries some risks (mutations being a known and accepted
risk), and I wouldn't be surprised to see phages in practice now or sometime
soon.


Question:
Why does UV radiation from the Sun cause skin cancer?
What is the specific mechanism makes non-ionizing UVA and UVB radiation carcinogenic? Can lower energy light, like visible light, be carcinogenic because of this mechanism, or is there some kind of threshold within spectrum at which electromagnetic radiation does not induce cancer in humans?
Ionizing radiation can be mutagenic, which can cause cancer. However, this only applies to high-energy electromagnetic radiation with photon energies exceeding about 5 eV, or about 248 nm. (The FCC defines this threshold even higher at 10 eV, or about 124 nm!) These photon energies correspond to UVC, which is blocked thoroughly by the atmosphere, meaning Sunlight does not appreciably contribute to the ionizing radiation we receive on Earth. Therefore, the mechanism with which solar UV radiation induces cancer must be different from higher energy electromagnetic radiation, right?

Explanation: Discussion of a certain DNA damage induced by ultraviolet light can explain this.

$\begingroup$

Rather than 'breaks' caused by high energy radiation, UV radiation causes
chemical modifications of the bases ('letters') that make up DNA. There are
four bases in the DNA alphabet abbreviated to A,T,G or C belonging to two
classes. A & G are guanines while T & C are pyrimidines.

When you have pyrimidine bases next to each other on a DNA strand, they can
react to form photoproducts or pyrimidine dimers. These block transcription
and replication and need to be repaired by nucleotide excision enzymes (only
route in mammals) or photolyase enzymes (plants, many other organisms). TT
dimers are the most frequent but dimers with a C cause more trouble as they
can be imperfectly repaired causing a transition mutation. If they don't get
repaired in time they can cause stalled replication which causes all kinds of
trouble and can result in mutations that lead to cancer. You can find more on
the [ wiki page ](https://en.wikipedia.org/wiki/Pyrimidine_dimer) .


Question:
What is the difference between added sugars and natural sugars in processed foods?
While buying juices, I came across two options, one with no added sugars, one with added sugars. The one with no added sugars had 11 grams of sugars, the one with added sugars had also 11 grams of sugar.
Hence my wonder, does it matter what is the source of your sugar intake, whether it is naturally occurring or artificially added?
I generally don't worry about how sweet something is as long as it’s natural, like mangoes are very sweet, but my mind tells me it’s a fruit hence healthy and I am neither diabetic nor fat, so mangoes are ok for me. But still I don't eat candies or other man-made sweet stuff because my mind says it’s artificial. Is my mind right or wrong?

Explanation: We can try to find a measurement standard of food that gives different values for different types of sugars/

$\begingroup$

One of the ways to measure the _impacts_ of sugar in different foods is with
the [ glycemic index ](https://en.wikipedia.org/wiki/Glycemic_index) , which
is a measure of how quickly blood sugar rises after eating. Faster rises in
blood sugar are thought to contribute to the development of diabetes and
possibly contribute to weight gain, though as with most nutrition science the
specifics are very difficult to study due to the difficulty of conducting true
randomized trials over a long time period (people just won't stick to eating
what a study assigns them to eat) and a vast array of potential individual
differences in digestion and metabolism.

Generally, the glycemic index for a piece of fruit will be low despite
containing sugars, because fruit also contains other things like fiber which
slows the rate at which sugar is absorbed. Adding just sugar to any food will
always increase the glycemic index, because added sugar isn't coming with
anything to slow it down.

Sugar in juices are typically going to be absorbed quickly, whether the sugar
came from the fruit (like an apple juice) or is added (like a lemonade),
because you're typically removing the parts of the fruit that slow digestion
(the fiber) when you make juice. If you have some hypothetical glass of juice,
process it to magically remove just the sugar, and then add that much sugar
back in, no, it won't matter that the sugar is now considered "added" versus
not.

Labeling of added sugars is just intended to help you identify foods that have
extra added sugars; it does not help you identify if the natural occurring
sugars in something are going to contribute to a rapid increase in blood sugar
or not. Manufacturers can use different tricks to avoid their sugars being
considered "added", such as blending apple juice with a more sour fruit (the
apple juice is mostly there to add sugar, yet isn't considered "added sugar"
because it isn't added as sugar, it's added as sugary juice).


Question:
Do large animals often evolve into smaller animals?
There are several examples where the largest animals were killed off preferentially due to a major ecological shift:
The KT extinction event
The Holocene extinction, as well as the major megafauna humans killed off
The common ancestor of modern mammals is thought to be "shrew-like" in size, and it differentiated into most of the large animal species in the world today. I imagine that a similar statement can be made for dinosaurs. In general it seems that a major extinction event is likely to be best weathered by smaller creatures which can later, over time, increase in size to fill the niche that larger animals, and evolution dictates it will be profitable to do so.
Does this limit large animals to only the branches of the tree of life? Any given set of (Multicellular) species obviously share a common ancestor that is much smaller than them. Is it possible for many species to share a common ancestor that is considerably larger than any of them?

Explanation: An evolutionary rule on size of animals can address this problem.

$\begingroup$

Your question brings up several important issues with regards to the evolution
of body size. The rationale for concluding that the ancestral mammal had a
small body size is that all of the taxa in that area of the tree tend to be
small. In contrast, if all of those taxa had been cow-sized, then the most
parsimonious conclusion would be that the ancestral mammal was cow-sized.

##  Identification of ancestors is difficult

Identification of a fossil species as _the most recent common ancestor_ of a
pair of sister taxa is exceedingly difficult. The way that different species
are diagnosed in fossils in by their unique derived characteristics ( [
autapomorphies ](http://en.wikipedia.org/wiki/Autapomorphy) ). So if a fossil
is found with no autapomorphies, then it is plausibly an ancestor (i.e., at
the split between two sister taxa). Some would argue that if you don't find
any autapomorphies, then you just haven't looked closely enough.

##  Cope's Rule

The idea that lineages tend to evolve toward larger body size is known as [
Cope's Rule ](http://en.wikipedia.org/wiki/Cope%27s_rule) , named for the
paleontologist Edward Drinker Cope. The success of Cope's Rule has been highly
variable, with some lineages following and others not ( [ Polly, 1998
](http://www.jstor.org/stable/2897758) ).

Some clades following Cope's Rule

  * Early reptiliomorphs ( [ Laurin, 2004 ](http://dx.doi.org/10.1080/10635150490445706) )
  * Pterodactyloidea ( [ Hone and Benton, 2007 ](http://onlinelibrary.wiley.com/doi/10.1111/j.1420-9101.2006.01284.x/abstract) )
  * Most Cambrian-Devonian marine invertebrates ( [ Novack-Gottshall, 2008 ](http://dx.doi.org/10.1666/0094-8373%282008%29034%5B0210:EBTICM%5D2.0.CO;2) )
  * North American canids ( [ Van Valkenburgh et al., 2004 ](http://www.sciencemag.org/content/306/5693/101.short) )
  * Mesozoic birds ( [ Hone et al., 2008 ](http://onlinelibrary.wiley.com/doi/10.1111/j.1420-9101.2007.01483.x/full) )

Some clades not following Cope's Rule

  * Early stegocephalians ( [ Laurin, 2004 ](http://dx.doi.org/10.1080/10635150490445706) )
  * "Rhamphorhynchoid" pterosaurs ( [ Hone and Benton, 2007 ](http://onlinelibrary.wiley.com/doi/10.1111/j.1420-9101.2006.01284.x/abstract) )
  * Mesozoic birds ( [ Butler and Goswami, 2008 ](http://onlinelibrary.wiley.com/doi/10.1111/j.1420-9101.2008.01594.x/full) )

Note that many results depend on the methods used.

##  Evidence from experimental evolution

Several studies have addressed body size evolution in vertebrates both
directly and indirectly. MacArthur ( [ 1944a
](http://www.jstor.org/stable/10.2307/2457976) , [ 1944b
](http://www.jstor.org/stable/10.2307/2458253) ) directly selected for large
and small body mass in laboratory mice. Within 8 generations, mean body masses
had increased or decreased by over 50%. Even when body mass is not directly
selected upon, mass can change in a correlated way. [ Selection for high
levels of voluntary activity
](http://www.biology.ucr.edu/people/faculty/Garland.html) has led to an
approximately 25% reduction in body mass.

Based on these studies, evolution of body size (larger or smaller) is
certainly possible within relatively few generations.


Question:
Is any known plant magnetic?
Is there a plant (not a microscopic type but one that is visible to the naked eye) that has so much iron (or magnetite), cobalt, or nickel in its body that it can attract a magnet?
In this case "attract" would mean that a person holding a small magnet next to the plant can feel a small attraction between the magnet and the plant.

Explanation: Discussion about magnetism in bacteria can be associated to this problem.

$\begingroup$

There was a 2011 [ study
](http://authors.library.caltech.edu/23694/1/Corsini2011p13835J_Appl_Phys.pdf)
where they used a sensitive atomic magnetometer to try to detect a plant's
magnetic field. They stated that:

> To our knowledge, no one has yet detected the magnetic field from a plant.
> Biochemical processes, in the form of ionic flows and time varying ionic
> distributions, generate electrical currents and time-varying electric
> fields, both of which produce a magnetic field. However, contrasted to
> muscle contraction and brain processes, which have a characteristic time
> scale shorter than one second, plant bioprocesses span several minutes to
> several days and the expected magnetic field from such processes is
> correspondingly smaller.
>
> Measurements with a sensitive atomic magnetometer were performed on the
> Titan arum (Amorphophallus titanum) inflorescence, known for its fast
> biochemical processes while blooming. We find that the magnetic field from
> these processes, projected along the Earth’s magnetic field, and measured at
> the surface of the plant, is < 0.6 lG.

So according to this, no, you wouldn't be able to sense the magnetic field
from a plant with a magnet.


Question:
Can plants get cancer?
I can't think of any reason why plants wouldn't be able to get cancer, but I've never heard of a plant growing a tumor. I've also never seen a plant with a noticeable abnormal growth. Can plants get cancer?

Explanation: This can be explained by a specific type of cancer-like disease in plants.

$\begingroup$

Yes, plants of all sizes can have cancerous growths.

_Agrobacterium tumifaciens_ , the causative agent of crown gall disease,
produces what is called a tumor. See this [ link
](http://en.wikipedia.org/wiki/Agrobacterium_tumefaciens) for detailed
information on these growths. Alternatively, use a plant physiology textbook
to look up the above terms. (Here, is where a textbook is better than a single
abstract in PubMed.)

I am certain that you have seen such growths on trees, such as [ this
](http://www.motikon.com/curiosities/galls/) . Other smaller versions can
occur on smaller plants - on stems and leaves, for example. The plant builds
up tissue around the _A. tumifaciens_ infection in an effort to isolate and
contain the infection and its effects.


Question:
Why are fearful stimuli more powerful at night?
For example, horror movies appear to be scarier when viewed at night than during broad day light.
Does light have any role in this phenomenon?
Are there changes in hormones at night versus during the day that makes fear stronger?

Explanation: We can try to find out whether the brain's response to sudden or threatening stimuli is stronger in the dark.

$\begingroup$

**Short answer**
The increased fear responses during the night are believed to be mediated by
elevated corticotropin-releasing hormone (CRH) levels in the brain that drive
the fear responses in the amygdala.

**Background**
Fear responses can be experimentally assessed by recording the **[ startle
reflex ](https://en.wikipedia.org/wiki/Startle_response) ** . For example,
loud noises can evoke gross startle responses in rodents (whole-body startles)
and more subtle responses in humans (eye blinks).

In **nocturnal animals** , it has been shown that **startles** are facilitated
by **bright light** . In contrast, **fear responses** in humans, a **diurnal
species** , have been shown to be **stronger in the dark** [ (Grillon _et al_
., 2007) ](http://www.sciencedirect.com/science/article/pii/S0006322307005574)
.

In the rat, the light-enhanced startle has been associated with the **[
hypothalamic–pituitary–adrenal axis ](https://www.mind-body-health.net/hpa-
axis.shtml) ** (Fig. 1). Specifically, light exposure has been shown fear
mediated by corticotropin-releasing hormone (CRH) [ (Grillon _et al_ ., 2007)
](http://www.sciencedirect.com/science/article/pii/S0006322307005574) .

[ ![!\[!\[HPA](https://i.sstatic.net/80z0p.jpg)
](https://i.sstatic.net/80z0p.jpg)
Fig. 1. HPA axis. source: [ Wikipedia
](https://en.wikipedia.org/wiki/Hypothalamic%E2%80%93pituitary%E2%80%93adrenal_axis)

The HPA-axis is affected by the circadian clock and therefore exhibits a
pronounced daily rhythmicity. The HPA axis is activated by hypothalamic
release of CRH, which stimulates the secretion of adrenocorticotropic hormone
(ACH) from the anterior pituitary. ACH triggers the production of cortisol by
the adrenal glands. Cortisol, in turn, provides negative feedback and shuts
down HPA-axis activity by binding to corticosteroid receptors in various HPA-
axis structures, e.g.the hypothalamus (Fig. 1). As a result, cortisol levels
show a robust diurnal rhythm that runs in opposite phase with CRH. Cortisol in
humans peaks at the time of awakening and drops to its lowest levels around
bedtime, whereas the opposite is true for CRH [ (Miller & Gronfier, 2001)
](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3035930/) .

The **startle reflex shows a diurnal variation roughly opposite to the rhythm
of corticosterone and in phase with CRH** . Specifically, **startle responses
in nocturnal animals such as rats are highest during daytime** (their passive
phase) when **CRH is peaking** , and corticosterone is at its lowest.
Conversely, startles are lowest during the night (their active phase) when CRH
levels are lowest, and corticosterone levels are high. **In man, a diurnal
species, exactly the opposite pattern is observed** . Hence, s **tartle
responses are thought to be endogenously modulated by the circadian system** ,
most likely via effectors of the central pacemaker such as the **HPA-axis** [
(Miller & Gronfier, 2001)
](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3035930/) .

In rats, **administration of exogenous CRH enhances the startle reflex** and
blocking of the glucocorticoid receptors which produces a blockade of negative
feedback, also increases startles. Conversely, **blocking CRH receptors
decreases the startle response** , as does corticosterone administration [
(Miller & Gronfier, 2001)
](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3035930/) .

CRH receptors are expressed at various brain centers, including the **[
amygdala ](http://neuroscience.uth.tmc.edu/s4/chapter06.html) ** . The
amygdala is a key structure in the **[ limbic system
](http://neuroscience.uth.tmc.edu/s4/chapter06.html) ** , the emotional
control center of the brain. The amygdala is specifically associated with
anxiety and fear responses. Indeed, it is thought that **CRH receptors in the
amygdala are responsible for the fear-promoting actions of CRH** [ (Grillon
_et al_ ., 2015)
](http://www.nature.com/npp/journal/v40/n5/full/npp2014316a.html) .

Hence, **it is not darkness or light _per se_ that mediate fear responses.
Instead, it is the circadian control of the HPA axis that controls the daily
variations in fear responses ** .

**References**
**-** [ Grillon _et al_ ., _Biol Psych_ (2007); **62** (10): 1183–6
](http://www.sciencedirect.com/science/article/pii/S0006322307005574)
**-** [ Grillon _et al_ ., _Neuropsychopharmacol_ (2015); **40** : 1064–71
](http://www.nature.com/npp/journal/v40/n5/full/npp2014316a.html)
**-** [ Miller & Gronfier, _Psychophysiol_ (2006); **43** (3): 297–301
](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3035930/)


Question:
Why is loud music much louder after pausing and resuming it?
If I pause a sufficiently loud song (in headphones) for several seconds, then resume it, I perceive it as deafeningly loud, even painfully. Yet, if I first lower the volume, resume, and then gradually increase it over a span of as little as two seconds, there's no problem.
Like turning on lights when someone's sleeping, but for ears that were awake six second ago.
Why does this happen?

Explanation: This question can be answered by a particular brain working mechanism

$\begingroup$

Hearing is capable of [ sensory adaptation
](https://en.wikipedia.org/wiki/Neural_adaptation) such that prolonged
constant stimulus is perceived as less intense. In hearing, the adaptation to
loud sounds is called [ acoustic reflex
](https://en.wikipedia.org/wiki/Acoustic_reflex) and is mediated by two
muscles: the [ tensor tympani muscle
](https://en.wikipedia.org/wiki/Tensor_tympani_muscle) and the [ stapedius
muscle ](https://en.wikipedia.org/wiki/Stapedius_muscle) . Both of them
involuntarily and quickly contract when a loud sound comes to the ear in order
to minimize any possible hearing damage.

However, they do not respond _immediately_ , which you observed yourself.
Depending on the loudness and the frequency of the sound, the **response
time** generally ranges from several tens of milliseconds up to several
hundreds of millisecond  1,2  . Therefore, gradually increasing the loudness
gives the reflex enough time to respond and decrease the sensitivity of your
ear.

* * *

1  Bell, A. [ _A fast, "zero synapse" acoustic reflex: middle ear muscles
physically sense eardrum vibration_
](https://www.researchgate.net/publication/324646308_A_fast_zero_synapse_acoustic_reflex_middle_ear_muscles_physically_sense_eardrum_vibration)
(2017)
2  Narayanan, R. [ _Characterization of Acoustic Reflex Latency in Females_
](https://www.semanticscholar.org/paper/Characterization-of-Acoustic-Reflex-
Latency-in-Narayanan/1c94d15df6496418b792ad9639eaaaa53a1aa65f) (2017)


Question:
Why does sex last so long?
I wonder why (especially human) sex lasts longer than just a few seconds?
My thought is that the shorter it takes a man to ejaculate, the lesser is the risk that he gets interrupted by a rival or a predator. Therefore, men who ejaculate quickly get an evolutionary advantage in the long-term.
But, as human sex lasts several minutes, I'm obvioulsy wrong with my argument. Anybody knows why?

Explanation: The phenomenon can be explained by a theory about sexual selection.

$\begingroup$

**Want to improve this answer?** Add details and include citations to explain
why this answer is correct. Answers without enough detail may be edited or
deleted.

There are plenty of animals with brief procreative periods, as you suggest. In
chimps, sex takes 10 to 15 seconds - much less time than humans. So the
question is really why have humans evolved to be different?

I don't think any of the answers based on fitness are particularly compelling.
It's not like sex feels like running a marathon or less physically fit people
can't manage to ejaculate in their partners so it seems unlikely that the
lengthy sex act serves to distinguish fitter individuals.

Instead, I think the difference probably lies in the pair-bonding role of
sexual activity. Humans form unusually long-lasting, typically monogamous or
largely monogamous, bonds that function to provide the support needed during
the lengthy childhood that humans undergo. The prolonged, and highly
pleasurable, sex act likely functions to help maintain these bonds in order to
keep the couple together and provide the stable support needed to maximise the
chances of successfully raising a child to adulthood.

Unfortunately, to the best of my knowledge, there is no high quality empirical
evidence that would convincingly answer the question so any answer must be
somewhat speculative.


Question:
How do ants follow each other?
I was observing ants in my house.They all were going in a straight line and also some of the ants were coming back through the the same line.
I took some water and rubbed the line with my finger, then the ants were not able to follow each other. Looks like they were confused.
My assumption is that they may had secreted some chemical .
Am I right ? If yes, then which chemical is that and how it is secreted?

Explanation: Excreted chemical substances from ants can explain how this works.

$\begingroup$

The chemical we are talking about here is called pheromone, trail pheromone to
be specific.

> A pheromone is a secreted or excreted chemical factor that triggers a social
> response in members of the same species. Pheromones are chemicals capable of
> acting outside the body of the secreting individual to impact the behavior
> of the receiving individuals.  [ 1
> ](http://www.medterms.com/script/main/art.asp?articlekey=12896)

Pheromones are of mainly 9 types (13 exactly, but 4 not so common) which are:

  * Aggregation pheromones
  * Alarm pheromones
  * Epideictic pheromones
  * Releaser pheromones
  * Signal pheromones
  * Primer pheromones
  * Territorial pheromones
  * Trail pheromones
  * Sex pheromones
  * Nasonov pheromones
  * Royal pheromones
  * Calming pheromones
  * Necromones  [ 2 ](https://en.wikipedia.org/wiki/Pheromone#types)

Ants, and many other animals, use trail pheromones to mark their trail as a
guide for others in their gang. Other ants, catching the signal of trail
pheromone, follow the way it goes and reach their gang leader. Trail
pheromones are volatile compounds, so it is not very likely that you would see
ants following the exactly same path tomorrow or a week later. All ants
release trail pheromones, so as long as ants are going through that path, the
trail signal will keep getting stronger and will also tell lost ants "Hey,
bro! We are going this way. Don't you want to join us?" See, for example, here
[ 3 ](http://lifeinwireframe.blogspot.in/2010/08/ant-algoithms.html) :

[ ![trail pheromone working](https://i.sstatic.net/CY95e.png)
](https://i.sstatic.net/CY95e.png)

In the beginning, different ants follow different paths, but as soon as an ant
finds the shortest path, all ants join it on that path, due to which
pheromones on other paths evaporates and finally, they all walk in straight
line.

Of course, trail pheromones are very useful for organisms who have lost their
way home, but you know, other organisms, like their predators, are not just
sitting and watching them. Some predators can also catch pheromones and find
out where the whole team is going, to attack them all at once. Such chemicals
are known as kairomones. See this  [ 4
](https://en.wikipedia.org/wiki/Kairomone) :

> A kairomone is a semiochemical, emitted by an organism, which mediates
> interspecific interactions in a way that benefits an individual of another
> species which receives it, and harms the emitter.

Semiochemical is just a type of pheromone which a species X releases, but a
species Y can also respond to its presence. Its just like when you walk on
road and say "Whoa! Seems like a pizza delivery van just passed by"
(obviously, smell of pizza is not by a pheromone ;)

The trail pheromones released by army ants can also be detected by a blind
snake or a forest beetle, leading it right inside their nest. Obviously, all
semiochemicals are not bad. Chemicals like synomones (helping both species)
and allomones (just the opposite of kairomones) are also present  [ 5
](http://io9.gizmodo.com/these-pheromones-get-the-animals-that-secrete-them-
kill-1695437937) , but they are beyond this question's scope.

**References:**

  1. [ Medical Definition of Pheromone ](http://www.medterms.com/script/main/art.asp?articlekey=12896)
  2. [ Types of Pheromones - Wikipedia ](https://en.wikipedia.org/wiki/Pheromone#types)
  3. [ Life in Wireframe - Ant Algoithms ](http://lifeinwireframe.blogspot.in/2010/08/ant-algoithms.html)
  4. [ Kairomones - Wikipedia ](https://en.wikipedia.org/wiki/Kairomone)
  5. [ These Pheromones Get The Animals That Secrete Them Killed ](http://io9.gizmodo.com/these-pheromones-get-the-animals-that-secrete-them-kill-1695437937)


Question:
Why does strenous exercise cause vision of "lights"?
I had a hard climb a week ago. I got so tired then any time I closed my eyes I saw these lights inside my head. I see these lights almost every time that I run fast or some thing like that. What are they and where do they come from?

Explanation: This can be explained by the common phenomenon of seeing lights when eyes closed.

$\begingroup$

This is a common phenomena which most of us come across. Seeing flashes of
light, stars and other shapes in the eyes occur when the body goes through
stressful activities. For example while you are climbing the blood flow will
be more to other prominent parts like hands and lower waist so brain and eyes
will get less supply of blood as well as nutrients. Hence those flashes or
stars are visible to us. This phenomena is called "Phosphene" and a phosphene
is a phenomenon characterized by the experience of seeing light without light
actually entering the eye.

[ Wikipedia/Phosphene ](http://en.wikipedia.org/wiki/Phosphene) gives an
explanation for occurrence of Phosphenes:

> Phosphene is "seeing stars", from a sneeze, laughter, a heavy and deep
> cough, blowing of the nose, a blow on the head or low blood pressure (such
> as on standing up too quickly or prior to fainting). It is possible these
> involve some mechanical stimulation of the retina, but they may also involve
> mechanical and metabolic (such as from low oxygenation or lack of glucose)
> stimulation of neurons of the visual cortex or of other parts of the visual
> system. ![enter image description here](https://i.sstatic.net/yD2EH.png)

So seeing flashes of light can be due to:

  1. Blood shifting.
  2. Low blood sugar(causes weakness).
  3. Head trauma.
  4. Headache.

So to summarize this thing, we should have enough nutrients, water supply to
the body whenever we come across stressful activities. Phosphenes are
temporary stuff which do not harm eyes.


Question:
How does the brain train its neural network?
One question that came up learning how artificial neural networks are working was how the brain can train its neural network?
When we say we have an artificial neural network, the problem behind it is a typical, but uncommon minimizing problem. The math behind it is logical and pretty easy. But it's math, so an computer can calculate it by doing millions of iterations. But the brain can't do that (I would be surprised)
So, how does the brain solve this task. Trial & Error, we don't know or is there an even more complex system behind it?

Explanation: We can try to find a theory that explains how neurons work together to learn.

$\begingroup$

The answer to this question is probably [ Hebbian Learning
](https://en.wikipedia.org/wiki/Hebbian_theory) .

Hebbian learning can be nicely summarised with "Cells that fire together, wire
together". So basically the synapses of neurons are strengthened if they fire
in sync, and weakened otherwise.

One can easily see that a) this kind of local learning mechanism makes a lot
more sense for the brain then some global method like gradient descent and b)
this mechanism leads to [ stable representations of patterns
](https://en.wikipedia.org/wiki/Autoassociative_memory) .

In artificial neural networks this kind of learning is modelled in [ Hopfield
networks ](https://en.wikipedia.org/wiki/Hopfield_network) and [ Restricted
Boltzmann Machines ](http://blog.echen.me/2011/07/18/introduction-to-
restricted-boltzmann-machines/) .

Of course this simple rule barely scratches at the surface of what goes on in
the human brain, when we are learning something. A complete picture would
probably involve complex feedback mechanisms of inhibitory and excitatory
connections between neurons, functional modules of neurons, and different
parts of the brain.

But I fear these details are not yet well understood …


Question:
Why does mouldy food make you sick?
Bread gets mouldy pretty quickly. My parents (both of whom are nurses) throw out a loaf of bread after a spot of mould is seen (because "if you can see one spot, it means the whole thing is covered in mould spores") because they say you'll get sick if you eat it. The USDA also has a handy chart on it's mould page telling you when you should discard food with mould on it.
Is it the mould itself that makes us sick or is it something that the mould is releasing?
What are the mechanisms that cause us to feel sick after eating mouldy food?
The USDA says that there can also be bacteria along with the mould on the the food - is this what is really making us feel ill?

Explanation: We can try to explain this by finding out the exact substance that makes us sick.

$\begingroup$

One of the most common toxins in mouldy food/bread is [ aflatoxin
](https://en.wikipedia.org/wiki/Aflatoxin) .

The exposure to high amount of aflatoxin can lead to [ acute aflatoxicosis
](http://www.fda.gov/Food/FoodborneIllnessContaminants/CausesOfIllnessBadBugBook/ucm071020.htm)
with fulminant hepatic failure and even death.

While mild exposure to aflatoxin could be asymptomatic, it is better not to
take a chance considering possible complications (citation from the link
above):

> Aflatoxins produce acute necrosis, cirrhosis, and carcinoma of the liver in
> a number of animal species; no animal species is resistant to the acute
> toxic effects of aflatoxins; hence it is logical to assume that humans may
> be similarly affected. A wide variation in LD50 values has been obtained in
> animal species tested with single doses of aflatoxins. For most species, the
> LD50 value ranges from 0.5 to 10 mg/kg body weight. Animal species respond
> differently in their susceptibility to the chronic and acute toxicity of
> aflatoxins. The toxicity can be influenced by environmental factors,
> exposure level, and duration of exposure, age, health, and nutritional
> status of diet. Aflatoxin B1 is a very potent carcinogen in many species,
> including nonhuman primates, birds, fish, and rodents. In each species, the
> liver is the primary target organ of acute injury. Metabolism plays a major
> role in determining the toxicity of aflatoxin B1; studies show that this
> aflatoxion requires metabolic activation to exert its carcinogenic effect,
> and these effects can be modified by induction or inhibition of the mixed
> function oxidase system.


Question:
Does taking a shower have the same effect on muscles as warming up?
When playing sports, coaches and trainers are always very clear that it is necessary to warm up and stretch. But sometimes athletes sometimes want to get an extra stretch in and don't want to go through the hassle of warming up.
Will taking a hot shower warm up muscles or does an athlete sctually have to do physical exercises like jogging in order to be ready to stretch?
I know this sounds like a question I could go on the physical fitness SE, but I'm really hoping for an answer involving thermodynamics and I doubt I'll get that there.

Explanation: This is related to a phenomenon where blood vessels are widened in muscles

$\begingroup$

Hot shower will definitely affect your muscles health. Hot water shower
results in [ Vasodilation ](http://en.wikipedia.org/wiki/Vasodilation) ,which
will decrease the vascular resistance and allows blood to flow easily through
the blood vessels. As the vasodilation (increase in diameter of blood vessels)
allows blood to move without resistance and which in turn nourish the tissues
with sufficient oxygen and nutrients. Also it affects in the removal of
metabolic wastes from cells. There is another process called [
Vasoconstriction ](http://en.wikipedia.org/wiki/Vasoconstriction) (decrease in
blood vessel diameter) which makes the blood vessels to contract and may lead
to increased blood pressure.

There is a technique called as Heat therapy which will be effective in muscle
and body health.

> Heat therapy, also called thermotherapy, is the use of heat in therapy, such
> as for pain relief and health. It can take the form of a hot cloth, hot
> water, ultrasound, heating pad, hydrocollator packs, whirlpool baths,
> cordless FIR heat therapy wraps, and others. It can be beneficial to those
> with arthritis and stiff muscles and injuries to the deep tissue of the
> skin. Heat may be an effective self-care treatment for conditions like
> rheumatoid arthritis.
>
> Heat therapy is most commonly used for rehabilitation purposes. The
> therapeutic effects of heat include increasing the extensibility of collagen
> tissues; decreasing joint stiffness; reducing pain; relieving muscle spasms;
> reducing inflammation, edema, and aids in the post acute phase of healing;
> and increasing blood flow. The increased blood flow to the affected area
> provides proteins, nutrients, and oxygen for better healing. [ Reference
> ](http://en.wikipedia.org/wiki/Heat_therapy)

While taking a hot water bath we are just making our muscles and tissues
nourished, which means the muscles will be in a healthy state for expansion
and contraction. So it is recommendable to take a hot bath before exercising.


Question:
Are two eyes necessary for 3D vision?
It has always been my understanding that humans have two eyes so that we can have 3D vision: the left eye sees more of the left side of an object than the right eye and vice versa. This helps us to estimate depth among other things.
Now when I close one eye, I still am able to perceive depth. I assume this is because my brain fills in the blanks For how long does this work? Do people eventually lose the depth perception (or at least it diminishes significantly) when they lose a single eye?
If so, how low does it take? If not, clearly we are capable of perceiving everything with one eye. Why do we then have two (besides redundancy and a larger field of view)? What is considering the evolution of man better in having two eyes as opposed to one or three, or four,..?

Explanation: The mechanism of how our brain can combine information received from the left and right eye answers this question

$\begingroup$

It seems like you suffer from a misconception. "The left eye sees more of the
left side of an object..." is not how distance perception works. Otherwise we
wouldn't be able to estimate the distance from flat objects, such as traffic
signs and shooting targets.

The actual mechanism is parallax estimation, or [ Binocular disparity
](https://en.wikipedia.org/wiki/Binocular_disparity) . In a nutshell, the
closer an object is to your eyes, the bigger the difference of its position on
the left and right eye's retina will be.

You may perform a simple experiment: find a place where several parallel wires
hang in the air: a train line or aerial phone/power line. Look at the wires
normally, and they will appear just as black lines in the sky, with no
distance perception. Now tilt your head to the side, and you will instantly
gain a feeling which one is closer, and which one is further away. Why the
difference? Because any shift of a horizontal wire gives the same picture,
meanwhile for vertical wires the difference is obvious.

When you close one eye, your brain loses the ability to estimate parallax.
However, it is left with several options:

  1. Visual cues. If one object overlaps another, it's obviously closer. If two objects look the same but one is smaller, it's probably further away (or a child). If you know the expected size of an object (a mountain/a horse/a fly), you may get the feeling of distance as well.
  2. Focusing distance. When you focus your eye on a near and far object, the feelings are different.
  3. Memories. You remember what you've seen with two eyes.

Of these, only (3) depends on previous binocular vision. (1) and (2) are
available even to those who were born with one eye. However, parallax
estimation is much faster and more precise. With a single eye you will be able
to hit a fly on the wall, but catching it in the air will be extremely
difficult.


Question:
If human eyes watch an area, what's the shape of its capturing shape? Rectangular? Half spherical?
A normal camera can capture a rectangular image. If human eyes watch an area, what's the shape of the captured region? Rectangular? Half-spherical?

Explanation: This is related to how eyes see objects that are not in the center of our gaze

$\begingroup$

The capture area of the eye is a bit fuzzier and harder to define than that of
a camera.

A camera captures consistent, fully detailed data right up to the edge of its
sensor, and no data at all beyond it. Captured data is clipped by an ideally
uniform sensor, augmented a bit by the lens, and is well-defined during design
and manufacturing.

The eye can capture higher "resolution" near the center of its capture area
and also has very little information about color near the edges (see also [
Peripheral Vision ](http://en.wikipedia.org/wiki/Peripheral_vision) ); so it's
not quite as clean cut depending on your goal of "capture area". The eye also
has a bit of a " [ blind spot
](http://en.wikipedia.org/wiki/Blind_spot_\(vision\)) " near the middle, which
our brains basically Photoshop out. Additionally, it varies from person to
person.

The _effective_ capture area would really depend on your application (e.g. the
"capture area" for, say, reading text, would be narrower than the area for,
say, detecting motion).

Here is a typical diagram for a single eye, showing just the ability to see
something in that area (does not show details related to peripheral vision
quality):

![enter image description here](https://i.sstatic.net/0zByD.jpg)

Here is a typical diagram for both eyes combined, the solid white area is the
overlap:

![enter image description here](https://i.sstatic.net/LfiSe.jpg)

Both of those images are from a [ 1964 NASA report
](https://web.archive.org/web/20170124045754/https://vision.arc.nasa.gov/personnel/al/papers/64vision/17.htm)
detailing aspects of the human visual field. If you want the detailed answer
to your question and more, you probably want to take a look at that.

Note that our field of vision is very wide, those diagrams may not do it
justice. As an experiment, close one eye, stare straight ahead and hold your
arms straight out to the sides. Wiggle your fingers and slowly bring your arms
forward until you can just see your wiggling fingers in your peripheral
vision, and you will get an idea. As an added experiment, hold a piece of
paper with text on it, and repeat the same experiment until you can read the
text - this region will be extremely narrow and will give you an idea of how
the quality of vision changes across the field. Also try with a colored object
and bring it in until you can clearly identify the color.

There are also some simplified mentions of it in wikipedia:

  * [ http://en.wikipedia.org/wiki/Field_of_view#Humans_and_animals ](http://en.wikipedia.org/wiki/Field_of_view#Humans_and_animals)
  * [ http://en.wikipedia.org/wiki/Human_eye#Field_of_view ](http://en.wikipedia.org/wiki/Human_eye#Field_of_view)
  * [ http://en.wikipedia.org/wiki/Visual_field#Normal_limits ](http://en.wikipedia.org/wiki/Visual_field#Normal_limits)

A good set of search keywords is [ "human field of vision"
](https://www.google.com/search?q=human+field+of+vision) . There is also a
nice related article entitled [ The Camera Versus the Human Eye
](http://petapixel.com/2012/11/17/the-camera-versus-the-human-eye/) .


Question:
Is blood regarded as an organ?
It consist approximately 7 percent of body weight.
By definition organ is composed of multiple tissues. Blood is a fluid, a circulating tissue.
Therefore can we call this fluid system a liquid organ?

Explanation: We can first figure out whether blood is a tissue and then check whether a tissue is a organ

$\begingroup$

Blood is considered a type of [ connective tissue
](http://en.wikipedia.org/wiki/Connective_tissue) (sometimes). However, an
organ is formed of multiple _different_ tissues. Thus, blood is a tissue, not
an organ.


Question:
Seeing strange things in light
I have noticed that if you look directly at tubelight (I have only white ones in my home) and close your eyes little, you see little random shaped colourless things sometimes with slow speed and sometimes with falling down.
They are shaped like circles with something in between and in chains of random length.
My father has also seen them. So, I am sure I am not imagining things. What the hell are they?

Explanation: This can be explained by a special substance in our eyes

$\begingroup$

Those are [ floaters ](http://en.wikipedia.org/wiki/Floater) . These are
objects floating in the vitreous humour that fills the eyeball. They typically
look like:

![Floaters](https://i.sstatic.net/c4K1H.png)


Question:
Why doesn't the cell membrane just...break apart?
Forgive me if this is a silly question. I can't understand the basics. Why doesn't the cell membrane just break apart? What's keeping the layers in the phospholipid bilayer together? I know that the membrane is embedded with proteins and lipids, but I still can't wrap my head around the "why". Are the hydrophobic interactions in the middle "stronger" than the hydrophilic interactions on the outside? What's keeping the individual phosphate heads together instead of, say, one of them just drifting away due to a nearby water molecule?

Explanation: This is due to a certain type of force that holds them together

$\begingroup$

The membrane bilayer is held together by hydrophobic forces. This is an
entropy driven process. When a greasy or hydrophobic molecule is suspended in
water, the water molecules form an organized "cage" around the hydrophobic
molecule. When two hydrophobic molecules come into contact, they force the
water between them out. This increases the entropy because the freed waters
don't need to be organized into the cage. Lipid bilayers have many many many
hydrophobic lipids that squeeze out a lot of water and greatly increase
entropy. The polar phosphates allow the water to interact with the surface of
the membrane, without a polar head group the lipids would form a spherical
blob instead of a membrane.

Read [ this section on wikipedia
](http://en.wikipedia.org/wiki/Entropic_force#Hydrophobic_force) for more.


Question:
Why do dog's eyes glow green on a photo?
Taking my current profile picture as a prominent example:
Dog's eyes glowing green in camera
This photo has been taken with flash. As I gather, this is the same effect that makes a human's eyes glow red on photos, namely the reflection of the flash at the choroid and then passing back through the retina.
The retina is full of bloodvessels and the blood inside them gives the reflected light it's reddish color.
If it's the same effect, why is the color different?

Explanation: A special layer of tissue in the eyes of some animals can explain this

$\begingroup$

Dogs, cats, and many other mammals have a [ Tapetum lucidum
](http://en.wikipedia.org/wiki/Tapetum_lucidum) which reflects light back
through the retina to help with night vision. Humans don't have this layer.
The tapetum is probably reflecting green light that would have normally been
absorbed.


Question:
How to make a fake auditory signal?
My question is about making fake auditory signals. The ear collects sounds from the environment, which are transformed into a neural signal by the hair cells in the inner ear. This signal is sent through the auditory nerve to the to brain, where it is decoded into a hearing sensation.
Now can we make fake signals and feed them into the auditory nerve to bring it to the brain? E.g., instead of the ear collecting sound, could we use an electrical instrument for collecting sound and convert this signal into a neural signal in the auditory nerve?

Explanation: A device that aids people with hearing loss to gain sound perception can answer this

$\begingroup$

Devices that bypass the hair cells in the inner ear and directly stimulate the
auditory nerve are called **[ cochlear implants
](http://www.nidcd.nih.gov/health/hearing/pages/coch.aspx) ** . Cochlear
implants are used to treat deafness caused by the loss of hair cells in the [
cochlea ](https://en.wikipedia.org/wiki/Cochlea) . The [ hair cells
](http://www.ncbi.nlm.nih.gov/books/NBK11122/) are the sensory cells that
convert sound vibrations into electric neural signals ( [ Purves _et al_ .,
2001 ](http://www.ncbi.nlm.nih.gov/books/NBK11122/) ). With state-of-the-art
devices, the better performing implant wearers are able to talk over the
phone(!) An exclamation mark is in place, because it means they can understand
the spoken word _without the need for lip reading or sign language_ . Hence,
cochlear implants are the answer to your question, but they definitely are not
designed to generate fake signals. Instead, they are used as an effective
treatment for deafness and are capable of transmitting meaningful speech
information.

Cochlear prosthetics consist of an array of typically 20-24 electrodes that
are inserted in the [ _scala tympani_
](http://www.britannica.com/science/scala-tympani) of the cochlea. The inner
ear is [ tonotopically organized ](https://en.wikipedia.org/wiki/Tonotopy) ,
which means that high frequencies are coded in the base of the cochlea, while
low frequencies are encoded in the tip. Hence, each electrode stimulates a
separate frequency band (Fig. 1). By using a microphone and sending the
acoustic signal through a filter bank, a number of auditory frequency bands
can be obtained equal to the number of electrodes in the implant. After this [
speech processing
](http://biomed.brown.edu/Courses/BI108/2006-108websites/group10cochlearimplant/pages/speechprocessor.htm)
step, the acoustic frequency bands are converted into trains of biphasic
pulses. These pulse trains are sent to the electrodes in the cochlea, which
then activate the auditory nerve directly, effectively replacing the
degenerated hair cells in the inner ear [ (Stronks, 2010)
](http://dspace.library.uu.nl/handle/1874/44671) .

![CI](https://i.sstatic.net/FFAQh.jpg)
Fig. 1. Cochlear implant. Source: [ Mayo Clinic
](http://www.mayoclinic.org/tests-procedures/cochlear-implants/care-at-mayo-
clinic/treatment/prc-20021470) .

**References**
**-** [ Purves _et al_ ., Neuroscience (2001) 2  nd  ed.
](http://www.ncbi.nlm.nih.gov/books/NBK11122/)
**-** [ Stronks (2010). PhD thesis, Utrecht University
](http://dspace.library.uu.nl/handle/1874/44671)


Question:
Why do we go blind for a few seconds after switching off the light?
At night, when I switch off the lights, I always seem to go blind for a while. The room becomes pitch black and I am unable to see anything. After a while, however, my vision slowly recovers and I start to see things around me again. I always have to wait a while before my vision returns to that functional state.
I am interested in knowing the mechanism behind this phenomenon. What do we call it?

Explanation: This is related to a mechanism of how eyes adapt to transition to a dark environment

$\begingroup$

**Short answer**
The eyes need to adapt to the low lighting condition after you switch off the
lights, a process called _dark adaptation_ .

**Background**
The process behind the reduced visual function when going from bright ambient
light to low-lighting conditions is caused by a process called _[ dark
adaptation
](http://www.cns.nyu.edu/~david/courses/perception/lecturenotes/light-
adapt/light-adapt.html) _ . The visual system works on a huge intensity scale.
The only way to do that is by **adapting to ambient lighting intensity** .

The sensitivity of our eye can be measured by determining the **[ absolute
intensity threshold ](https://en.wikipedia.org/wiki/Adaptation_\(eye\)) ** ,
i.e., the minimum [ luminance ](https://en.wikipedia.org/wiki/Luminance) of a
stimulus to produce a visual sensation. This can be measured by placing a
subject in a dark room, and increasing the luminance of the test spot until
the subject reports its presence.

**Dark adaptation** refers to how the eye recovers its sensitivity in the dark
following exposure to bright light. The sensitivity of the visual system
increases approximately 35 times after dark adaptation.

Dark adaptation forms the basis of the **[ Duplicity Theory
](http://www.cambridge.org/fi/academic/subjects/life-
sciences/neuroscience/duplicity-theory-vision-newton-present) ** which states
that above a certain luminance level (about 0.03 cd/m2), the cone mechanism is
involved in mediating vision, called photopic vision. Below this level, the
rod mechanism comes into play providing scotopic (night) vision. The range
where two mechanisms are working together is called the mesopic range, as
there is not an abrupt transition between the two mechanism.

The dark adaptation curve shown below (Fig. 1) depicts this duplex nature of
our visual system. The sensitivity of the rod pathway improves considerably
after **5-10 minutes in the dark** . Because after you switch off the light
the rod system is still inactive, you are unable to perceive much. The reason
why rods are inactive is because they are said to be photo bleached. **[ Photo
bleaching ](https://en.wikipedia.org/wiki/Bleach_and_recycle) ** refers to the
visual pigments in the rods and cones to become used up because of the high
light intensities when the light was still on. The pigment needs to be
regenerated and that takes time.

[ ![adaptation](https://i.sstatic.net/q7gIe.jpg)
](https://i.sstatic.net/q7gIe.jpg)
Fig. 1. Dark adaptation curves of rods and cones. Source: [ Webvision
](http://webvision.med.utah.edu/book/part-viii-gabac-receptors/light-and-dark-
adaptation/)

**Reference**
**-** [ Kolb _et al_ (eds). Webvision. The organization of the retina and the
visual system (2012) ](http://webvision.med.utah.edu/book/part-viii-gabac-
receptors/light-and-dark-adaptation/)


Question:
Why Do Most Humans & Cats Have Blue/Bluish Eyes At Birth?
I've read that the eye color at birth for most humans and for cats may not always be the the true genetic color at first. This is due to the lack of melanin in the iris. This makes sense as there is no light in the womb to stimulate the production of melanin.
My question(s) though is:
Why does the lack of said melanin produce a blue/bluish colored iris?
Why is it not say green, red, clear, etc?

Explanation: This is related to a phenomenon caused by light interacting physically with something

$\begingroup$

The blue colour is an example of [ **structural colour**
](http://en.wikipedia.org/wiki/Structural_color) , caused by light interacting
physically with something. Some examples of structural colour are the
iridescence of insect wings and body surfaces (usually caused by repeating
chitinous structures), and of certain birds feathers, as well as the non-
iridescent colours of the blue and yellow macaw.

In the case of the eye it is the stroma of the iris that is responsible. This
is a network of fibrous tissue which scatters light. When light is scattered
in this way (Rayleigh scattering) it is the short wavelengths which are most
scattered. So when you look at the sky (away from the sun) you are seeing
diffuse blue light created by this scattering in the atmosphere. In the case
of the iris what you are seeing is light reflected from the eye being
scattered within the iris, creating the diffuse blue colour. As you say in the
question, everything else is down to melanin.


Question:
How do trees communicate in the "Wood Wide Web"?
I read on The New Yorker - The Secrets of the Wood Wide Web that trees communicate with each other through electrical impulses sent through their roots. Through these impulses they can ask other trees for some nutrient if they are getting it in insufficient amount or warn the other trees about an upcoming pest attack. This phenomenon is termed as the Wood Wide Web.
So how do trees distinguish in different types of impulses that they receive if they don't even have a brain? And does this process show any resemblance to nervous system in animals?
Additional YouTube video: Trees can talk to each other, but how?

Explanation: The question is asking about a particular communication network system between trees

$\begingroup$

I have to say: when you claim that _"trees communicate with each other through
electrical impulses sent through their roots"_ , you're thinking about [
Avatar ](http://www.avatarmovie.com/index.html) .

Joking apart, what you call _wood wide web_ is the [ mycorrhizal network
](https://en.wikipedia.org/wiki/Mycorrhizal_network) .

Mycorrhizal fungi are well known to botanists and ecologists. They are the
fungal partner in the mycorrhiza, which is a symbiotic association between a
fungus and a plant.

[ ![enter image description here](https://i.sstatic.net/c6q5zm.jpg)
](https://i.sstatic.net/c6q5zm.jpg)

Mycorrhizal hyphae (white) in a root

The novelty about this _mycorrhizal network_ is that, as it was demonstrated,
plants can use it to exchange some chemical substances. And, in certain cases,
this exchange can be used to improve disease resistance.

However, there is **no electrical impulse** in this process.

According to Song et al. (2010):

> In theory, plants can also communicate with each other through underground
> common mycorrhizal networks (CMNs) that interconnect roots of multiple
> plants. However, until now research focused on plant-to-plant carbon
> nutrient movement and there is no evidence that defense signals can be
> exchanged through such mycorrhizal hyphal networks. Here, we show that CMNs
> mediate plant-plant communication between healthy plants and pathogen-
> infected tomato plants ( _Lycopersicon esculentum_ Mill.). After
> establishment of CMNs with the arbuscular mycorrhizal fungus _Glomus
> mosseae_ between tomato plants, inoculation of ‘donor’ plants with the
> pathogen _Alternaria solani_ led to increases in disease resistance.

This other research demonstrate that the mycorrhizal network can be used to
warn neighbouring plants of aphid attacks (Babikova et al., 2013):

> Here, we show that mycorrhizal mycelia can also act as a conduit for
> signalling between plants, acting as an early warning system for herbivore
> attack. Insect herbivory causes systemic changes in the production of plant
> volatiles, particularly methyl salicylate, making bean plants, _Vicia faba_
> , repellent to aphids but attractive to aphid enemies such as parasitoids.
> We demonstrate that these effects can also occur in aphid-free plants but
> only when they are connected to aphid-infested plants via a common
> mycorrhizal mycelial network. This underground messaging system allows
> neighbouring plants to invoke herbivore defences before attack.

In both cases the mycorrhizal networks play an important role in exchanging
chemical substances among the plants.

The network has a _dark side_ too: it can be used to deliver allelochemicals
from one plant to another, greatly increasing allelopathy. According to Barto
et al. (2011):

> Common mycorrhizal networks (CMNs) form belowground networks that
> interconnect multiple plant species; yet these networks are typically
> ignored in studies of allelopathy. We tested the hypothesis that CMNs
> facilitate transport of allelochemicals from supplier to target plants,
> thereby affecting allelopathic interactions.

Finally: don't rely on media to get scientific information, specially in these
times of _alternative facts_ . Sometimes you can get good information in the
media, but good and accurate information is way harder to find (an example is
this [ BBC page ](http://www.bbc.com/earth/story/20141111-plants-have-a-
hidden-internet) about the mycorrhizal network). However, in defense of that
page in The New Yorker, there is **no** mention to electrical impulses.

Sources:

  * [ Song, Y., Zeng, R., Xu, J., Li, J., Shen, X. and Yihdego, W. (2010). Interplant Communication of Tomato Plants through Underground Common Mycorrhizal Networks. PLoS ONE, 5(10), p.e13324 ](http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0013324) .
  * [ Babikova, Z., Gilbert, L., Bruce, T., Birkett, M., Caulfield, J., Woodcock, C., Pickett, J. and Johnson, D. (2013). Underground signals carried through common mycelial networks warn neighbouring plants of aphid attack. Ecology Letters, 16(7), pp.835-843 ](http://onlinelibrary.wiley.com/doi/10.1111/ele.12115/abstract;jsessionid=86C8C2836F37DF3DFCB5A4211E445087.f03t04) .
  * [ Barto, E., Hilker, M., Müller, F., Mohney, B., Weidenhamer, J. and Rillig, M. (2011). The Fungal Fast Lane: Common Mycorrhizal Networks Extend Bioactive Zones of Allelochemicals in Soils. PLoS ONE, 6(11), p.e27195 ](http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0027195) .


Question:
How does a neuron change as you learn?
I am currently taking a course called "Introduction to Machine Learning with ENCOG 3", and I have a question about how well the Artificial Intelligence (AI) algorithm for a "neural network" corresponds with how an actual neuron works.
In the course, they model a neuron like this: AI implementation of a neuron's algorithm
x1, x2, etc. are voltage inputs, the wij are weights. The inputs are multiplied by these weights and summed up by the neuron. The neuron then has an "activation function" which then takes the sum of weighted inputs and calculates an output, typically a value between 0 and 1 (or between -1 and 1). You can think of the wij as representing dendrites (a higher weight means a more dense and thus conductive dendrite), and the output of the activation function as the voltage that gets sent down an axon.
The AI neural network algorithm creates a kind of intelligence by modifying the weights (wij shown in the picture).
My first questions is: Is this a good approximation as to how neurons actually work? That is, do our neurons "learn" by changing the weights (dendrite density, conductivity)? Or, is there some other mechanism that is more important (e.g. do neurons learn by changing their activation or summation functions?)
My second question is: If neurons really do learn by changing the density of dendrites, then how fast does this happen? Is this a fast process like DNA replication? Does the neuron quickly generate (or decrease) dendrite density when it receives some kind of biochemical signal that it needs to learn now?
I understand that much of this might not yet be known, but would like to know how well the AI algorithm corresponds with current theories on biological neural networks.

Explanation: A theory which explains how neurons behave when we learn things can explain this

$\begingroup$

**With respect to your first question** , that model isn't intended to take
time into account, but is based on [ Hebbian learning
](https://en.wikipedia.org/wiki/Hebbian_theory) with the goal of
computability. It's generally used in simple pattern recognition situations
where each case has no bearing on the next. The learning portion is performed
ahead of time during the training phase. For example, a [ deterministic
](https://en.wikipedia.org/wiki/Deterministic_algorithm) perceptron isn't
permitted to change after training. In contrast, the [ Biological Neuron Model
](https://en.wikipedia.org/wiki/Biological_neuron_model) is much more complex,
and uses a variety of [ ordinary differential equations
](https://en.wikipedia.org/wiki/Ordinary_differential_equation) to integrate
the _cumulative_ behavior of neurons _over time_ . As such, those models are
non-deterministic and don't see as much practical use outside of
experimentation.

**To address your second question** , neurons themselves don't "learn." A
single neuron is essentially meaningless. Learning is an emergent process
created by the interaction of several systems at once. While one influencing
factor is connectivity (zero for no connection, non-zero for the inhibitory or
excitatory connection which emulates both [ synaptic
](https://en.wikipedia.org/wiki/Synaptic_plasticity) and [ non-synaptic
](https://en.wikipedia.org/wiki/Nonsynaptic_plasticity) ), what you might call
short term learning can also be performed by existing clusters of neurons,
without any change in connectivity. Biologically, this is what must occur
_before_ any of the comparably slow process of tissue remodelling can take
place, and the computationally equivalent process is only possible in time-
aware models like the aforementioned Biological Neuron Model.

Take, for example, someone who wishes to learn to play guitar. When they begin
playing, existing clusters emulate the desired behavior as best as they can.
These neurons act as the functional scaffold that initiates and drives the
neuroplastic process. Playing becomes _easier_ because this scaffold becomes
more efficient as new connections (shortcuts) are created, existing
connections are strengthened, and irrelevant connections are inhibited. The
improved scaffold in turn allows further improvements. [ Newborn neurons
](https://en.wikipedia.org/wiki/Neurogenesis) may also [ migrate
](https://en.wikipedia.org/wiki/Neuroblast) to the area, though the how, why,
and when of that process is unclear to me. This "behavior emulation" or "short
term learning" process used in practicing the guitar, or whenever a novel
situation is encountered, must be primarily governed by excitatory and
inhibitory neurons' influence. Otherwise the whole process cannot even begin.

**Further reading**

  * [ Parameter estimation of a spiking silicon neuron. ](http://www.ncbi.nlm.nih.gov/pubmed/23852978)
  * [ Synaptic plasticity, memory and the hippocampus: a neural network approach to causality ](http://www.nature.com/nrn/journal/v9/n1/full/nrn2303.html)
  * [ Signaling mechanisms in cortical axon growth, guidance, and branching ](http://journal.frontiersin.org/article/10.3389/fnana.2011.00062/abstract)


Question:
How does a tree trunk sprout and grow after being cut?
After I cut trees into logs and remove the branches in winter, they start growing. They sprout out and grow completely normal looking stems and leaves and maintain them all summer. The sprouts mostly appear around the cut branches. Sometimes they last all winter and grow for another year. How does it find the energy and water necessary to maintain and grow these stems without ground connection and a water source?

Explanation: We can find out the tissue formed on the cut piece that allows growth of new organs.

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This is basically the same that happens after [ pruning
](http://en.wikipedia.org/wiki/Pruning) and involves a basic hormonal
regulation mechanism in the plants.

What happens is that the cut piece of the wood forms a new [ meristem
](http://en.wikipedia.org/wiki/Meristem) which allows the growth of new
organs. What’s important is that there is no other growth happening nearby,
since that would hormonally inhibit any further growth. This is why such
growths happen once you’ve cut the wood, not before (on the healthy stem).
This inhibitory effect is known as [ apical dominance
](http://en.wikipedia.org/wiki/Apical_dominance) , which has now been
disabled.

As to where the energy and water comes from, to some extent it is stored
within the branches themselves. That’s why you need to dry them before being
able to use them in a fire. However, this growth is pretty limited. Further
water is probably collected by condensation of water vapour in the air.