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Neuroscience of mathematicians
I've tried to google this but everything that comes up are things like "mathematical neuroscience" rather than the other way around.
Specifically, I'm interested in the workings of a mathematician's brain that sets her apart from others. For example, is there evidence to be found in MRI scans or EEG recordings of mathematicians as to why they excel in math?

i think you are looking in wrong direction. Mathematicians are same species as other folks, so look for information on how brain processes mathematics, don't bother with occupation. This article might be of interest: http://phys.org/news11473.html It is not who does math, but rather what brain s doing. Or are you interested in how brains of accomplished mathematicians differ from that of artists?

Thanks for the pointer! That is perhaps more of what I'm looking for. Though I'm much more interested in what happens when mathematicians research more abstract stuff than just numbers, like topological or algebraic reasoning. Do you know any research on those things?

numbers seems pretty abstract to me. Maybe this paper will shed some more light: http://journal.frontiersin.org/article/10.3389/fnhum.2014.00068/abstract

I'm voting to close this question as off-topic because it is a cognitive science question http://cogsci.stackexchange.com/

Most people choose a particular subject not just because of an inherent predilection. You should perhaps study the mathematical savants.

Since when is neurobiology off topic?

Taking the comments into account I have edited the question to give it more focus. Comparing math versus other disciplines cannot be done at the imaging and electrophysiological level as one needs a control group. Both the math group and control group need to be doing the same task. Comparing a musician playing an instrument versus a mathematician solving a complex mathematical problem is comparing apples and oranges.

It's not completely off-topic, but the cogsci SE is a better fit and the question should logically be there to a) ensure it gets the best possible answers and b) gets the right traffic.

@GriffinEvo - Neurobiology questions and their overlap with Biology are hotly debated at CogSci. It is definitely on-topic there, but not because it is a better fit there. This question has a strong neuro-anatomy and neurobiology component and it is a borderline-case. Possibly the neurobiology debate needs to be addressed here at Bio as well. Anyway, I edited the question to make it more scientifically sound.

@AliceD I think it would be a very good discussion for meta - its a part of the SE model to not post the same Q on multiple sites, while both the question, and the site it is on, benefit most by being on the most appropriate site. Personally I'm not sure that it the best way, questions such as this (and many other cogsci type Q's) are suitable for both. I've only raised the close vote because that is how SE is supposed to work, not because I feel the question is massively off topic, just more on topic somewhere else :)

Short answer
People competent in mathematics have been shown to have higher activation of the left angular gyrus according to fMRI. EEG recordings have shown larger activity in the posterior parietal cortex.
Background
I think you are interested in what makes a good mathematician. A brain imaging study by Grabner et al. (2011). showed that the left anterior gyrus was more activated in individuals more competent in math. Specifically, the authors argue that the stronger left AG activity in the more competent subjects reflects a higher proficiency in processing mathematical symbols. The anterior gyrus is involved in mathematical symbol processing.

Left angular gyrus, lateral view. Source: Kenhub Neuroanatomy Atlas
ERP studies (event-related potentials deduced from the EEG) have shown higher activity in posterior parietal cortex in subjects excelling in math (Waisman et al., 2014). This region is associated with algebra and handling mathematical functions.

Posterior parietal cortex among other regions not relevant to the question answer. Source: Live Science
References
Grabner et al. Front Hum Neurosci 2011; 5: 130
Waisman et al., Int J Sci Math Edu 2014; 12(3): 669-96

What type of Algebra? Algebra that everyone learns is a low form of mathematics. Being able to process Algebra doesn't necessary equate to a high competence in math. However, if by Algebra, you mean Abstract Algebra, Algebraic Geometry, Lie Algebras, Sigma Algebras, etc. this would be a different story. So what is meant by Algebra since I would be skeptical to someone simply good in Algebra $x+3 =5$ equates to math greatness.

Quoting from the study: "A computerized test that required of the participants a translation between symbolic and graphical representations of function was designed with 60 tasks (trials) using E-Prime software. [...] The tasks we used in our study are basic items for the Israeli curriculum and were learned by all study participants in a similar way."

I actually think that this is a fairly good compromise. If we delve too deep into higher mathematics the available pool of subjects diminishes rapidly; on the other hand function manipulation is much closer to actual mathematical research than the plain numericity studies that @aandreev has been pointing out in his comments.

@dustin - I tried to keep the answer short and sweet without too much detail on methods. But I am happy to edit.I

@SorcererofDM Israeli curriculum at what level? Even if it is just college math for non math majors, I don't think that reflects a mathematicians brain. If it is high school, that is substantial worse. All subjects should be MS, PhDs, Post Docs, and Professors (hence PhD). Anyone else else shouldn't be referred to as a Mathematician and mathematicians will say MS holders aren't mathematicians either but including wouldn't be wrong.

In the US, the Bureau of Labor Statistics says a Mathematician typically needs a Masters Degree.

@AliceD, it is great, that you use Kenhubs image. But please also use the correct link for source: https://www.kenhub.com/en/atlas/gyrus-angularis

@dustin - the problem, as AliceD mentioned, is that we can't test, say a categorical theorist and a musician, on proving the Yoneda lemma. So we need a task that should use similar faculties in all people, regardless of what occupation they have. Perhaps questions from math competitions would be more appropriate than from the standard curriculum, but olympiad problems are quite different from problems arising from mathematical research.

@SorcererofDM we can't call something neuroscience of mathematicians if the subjects are layman. Would you say neuroscience of doctors (MDs) if we based it on the educational level of anatomy 1?

@dustin - I think we are parsing "neuroscience of mathematicians" differently. You want to find out the difference between fields medalists and the "regular Joe" mathematicians. I'd be interested in this question too, though I can't see an easy way to randomize this, or even how to test this. After all, fields medalists are known for building grand and important theories, not for solving problems in one sitting.

@SorcererofDM I am not talking about field medalists. I am talking about mathematicians. People who simply take a math course are not mathematicians.

@dustin - so now I'm confused. What is the question you are trying to answer? What is the quality about mathematicians you want to extract? Do you want to separate the good mathematicians from the average mathematicians, or to separate mathematicians from nonmathematicians?

Perhaps I was misleading in my previous reply. By fields medalists I simply mean much better mathematicians than the average. I probably should have added "for example" in there.

@SorcererofDM I am not asking any questions. Your title doesn't jive with what you want as an answer. The word mathematician means mathematicians not people who take math courses. They are totally different.

Let us continue this discussion in chat.


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Do electromagnetic waves outside the visible spectrum have any role in photosynthesis?
Does photosynthesis occur only in the visible spectrum? If there is a way to completely remove all other electromagnetic bands from the sunlight, including infrared (IR), will photosynthesis continue to occur?
Is there any known plant (algae, fungi, bryophytes, pteridophytes, gymnosperms and angiosperms) that utilises the other wavelengths for photosynthesis?

Photosynthesis occurs at and around the absorption spectrum of chlorophyll, i.e. at green wavelengths, so in the visible spectrum. This does not mean that other wavelengths are not used, just less optimally.

@ChrisStronks Sorry, I started editing once I saw your comment. It seems your edit clashed with mine. Feel free to edit this version

Photosynthesis only occurs in the visible light.have a look at the absorption spectra of the different pigments involved in photosynthesis, you see that all these pigments absorb light between 400 and 700nm (from a diagram from here):

You see that the absorption spectra of chlorophyll a and b are located from 400 to 500nm and again from 630 to 700nm. The maxima for both molecules are different so that the light is used more efficiently.
The other three important light harvesting pigments involved in photosynthesis (in cyanobacteria and plants) are: Beta Carotene, Phycoerythrin and Phycocyanin. These use different parts of the visible spectrum (hence the different color of cyanobacteria), but they still only use the visible part of the light between 400 and 700nm.
The reason for this can be seen in the figure when you look at the intensity of the sunlight (plotted in black). All photosynthesis occurs in the area of the highest intensity. Wavelengths shorter than 350nm are efficiently blocked by our atmosphere, wavelengths much longer are not transporting much energy.
To shortly answer your question: If we could "switch off" all other wavelengths from the spectrum, there would still be photosynthesis on earth.

Don't we need some infrared to keep the plan warm enough, as otherwise most plants just shut down.

I'm curious, what software do you use to generate the graph?

I haven't made this myself, the source is named above the figure (in brackets).

@IanRingrose sort of? Infrared is more the mediator of heat than the provider. Warm things would emit it if it wasn't around, but a planet illuminated by only gamma rays would still be warm if it had an atmosphere to keep the heat in. It wouldn't exactly be a vacation spot.

Photosynthesis is nearly all visible light. There's usually not enough UV and thermodynamics more or less rules out infrared. Chris covered that pretty spectacularly, but that nearly is significant.
There is some evidence that certain kinds of fungi can use gamma rays or other ionizing radiation for energy, but they're not particularly common. Melanin is used instead of chlorophyll, but apparently 'tooling up' for radiosynthesis(is that a word?) is fairly hard on the cell. It was assumed the melanin was a protective pigment(like it is in humans) and produced only when necessary(also like humans), but these particular ones were discovered growing in the Chernobyl reactor and apparently evolved to continuously produce melanin and absorb ionizing radiation for food. They don't stop producing melanin even on the verge of starvation. Other melanized fungi live in high-radiation environments, like mountaintops and the poles, where there is more UV and cosmic rays and things.
Fun fact aside: Fossilized melanized fungal spores turn up at the K-T boundary when the earth had no magnetic field and therefore higher radiation flux at the surface (see paper linked above and Hulot & Gallet, 2003 for more).

+1 Interesting fact. The word is "radiotrophic" BTW.

I would use radiosynthesis to describe the process of absorbing ionizing radiation for energy, and things that primarily do that for food as radiotrophic, but my spellcheck underlines both as 'not real words' and I'd never heard radiosynthesis before. Chemo/photosynthesis, sure. radiosynthesis no.

You are right, I forgot about this part.

Do you have citation to the fun fact? Great additional answer.

Curiously enough, the paper about radiotrophic bacteria talks a little about that, but they cite in turn Hulot G, Gallet Y (2003) Do superchrons occur without any palaeomagnetic warning? Earth Planetary Sci. Lett. 210: 191–201.

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Have there been studies done to test Immortality of cancer cells in culture?
This website on cultured cancer cells () says cancer cells may be immortal.
I am wondering if there has been any research done to find if cancer cells are really immortal.

How old is the still maintained living oldest culture of cancer cells?
Has there been any research done on replicative senescence of Cancer Cells invitro?

Edit 1:
If there is some data relating to the number of replications the cells have undergone, it will be very useful

The HeLa cell line is undoubtedly the most used and investigated human  immortal tumor cell line. Extracted from a cervical tumor from Henrietta Lacks in 1951 at Johns Hopkins hospital, Baltimore, MD these cells proved immortal and are still used in many, many labs worldwide today. It is the oldest human cell line in use and, therefore, the oldest human tumor cell line (Callaway, 2013).
In terms of senescence of immortal cells; HeLa cells are immortal, and hence do not grow old as such. However, they are subject to mutations and the genetic profile of HeLa cells does change over time. Hence, although they may not be growing old, they do age in the sense that mutations are accumulating in continuous cell lines.
References
Callaway, Nature (2013); 500: 132-3

Will add refs later, I am mobile. Informative website: http://www.nature.com/news/deal-done-over-hela-cell-line-1.13511

Take your time @ChrisStronks

very interesting read Chris, Thanks for the link

More info: http://www.embl.de/aboutus/communication_outreach/media_relations/2013/130311_Heidelberg/

I am not specifically asking for human cancer cell culture @ChrisStronks. Is HeLa the oldest of cancer cell culture (among all species)?

My answer marked (1) should answer this. In other animals I am unsure.

I wanted to know for sure, as data on animal cell lines seem scarce. All I knew was animal cell lines were established and experimented upon way before human cell lines were started. That's the reason for the post

@ChrisStronks CTVT is not a cell line, it is a natural tumour that has become infectious (thereby making it a pathogenic parasite). A good recent example of a retrograde evolution.

@WYSIWYG I removed CTVT from my answer. Thanks.

@WYSIWYG just wondering, how was it determined that CTVT cells belonged to canids? It seems that chromosomal composition varies vastly

@CRags See this paper. They have done genomic analysis and commented that the mutations seem to have arisen because of UV exposure. I guess there were no major chromosomal aberrations to prevent its identification as a canine derived tumour.

@WYSIWYG Thanks for the link, I think I will post a new question to discuss further on this

Added a reference, finally!

I think, a story about Alexis Carrel and Leonard Hayflick is appropriate here.
In the beginning of 20th century a Nobel prize-winning medicist/biologist Alexis Carrel published a series of papers, claiming that growth of a culture of cells of normal somatic differentiated tissue can be maintained indefinitely without undergoing cellular senescence. This wrong result was held for a fact for many years, before being disproved by Leonard Hayflick, who's shown that normal somatic cells undergo a limited number of divisions before dying and immoratlization happens in cancer cells. It's worth mentioning that the cause of Dr.Carrel's error might be attributed to his personality. For instance (quote from Wikipedia):
Carrel claimed the existence of a "hereditary biological aristocracy" and argued that "deviant" human types should be suppressed using techniques similar to those later employed by the Nazis.

So, the results of his finding might be attributed to a version that he's just scared his laboratory members so much, that they started to secretly replace a deteriorating culture with a new one.
I may be rough on the corners and attribute sins to the man, he's innocent of. For a "fair trial" with evidence etc., you'd better address this paper: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1082700/
See also this popular paper: http://www.theguardian.com/science/2015/feb/18/haruko-obokata-stap-cells-controversy-scientists-lie

Terminology involved makes everything lie a bit.
All the "immortality" and so complicate things a bit. We perceive life as life of our individual bodies. Thus if our body is immortal, that means that it is persistent, without us bothering about our individual cells.
But, there isn't any distinction like that in single cell organisms where cells themselves are taken as "individuals". When cell divide, there isn't usually any distinction of which one is "mother" and which one is "daughter". Both new cells are usually the same. So either it may seem that cells are immortal because they are not dying by old age, or that we define new cells as new individuals and thus the old one died to give birth of two new ones.
But we could take certain aspect of this viewpoint on multicellular organisms as well. Our bodies are defacto created by very old cell-line (or in sexually engaged organism, two cell lines) and then this cell-line created vehicle for itself. From this viewpoint, which is not very different from viewpoint taken when speaking about these laboratory cell-lines, whole life is single cell-line. And from this point of view, life itself is immortal.
So the whole problem is that our point of view, on which we define immortality and individuals, is made only for special types of organism, as has no sense when speaking about single cell organisms. Immortality of cancer cells is thus only buzzword.

You're not even wrong

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Bacteria trapped in crystal inclusions found 'alive' after 50,000 years - what were they eating all that time?
The phys.org article Biologists find weird cave life that may be 50,000 years old describes the announcement by NASA Astrobiology Institute director Penelope Boston at the 2017 AAAS meeting$^{(1)}$ of micro-organisms found in small inclusions within crystals of hydrated Calcium Sulphate (Gypsum) that had grown while underwater in a cave in Naica, Mexico. It is estimated that some of these organisms have been isolated within inclusions for as long as 50,000 years, and yet can grow and reproduce when carefully extracted and provided with fresh chemosynthetic nutrients.
(BBC Radio interview with Penelope Boston)
This particular discovery has just been formally announced so there is no peer-reviewed material to read yet, but it's possible someone here in Biology SE attended the meeting or has read further about the announcement.
50,000 years is a long time (for a bacteria, not a crystal), and if I understand correctly the energy source for these organisms is chemosynthesis. Put simply, wouldn't they have eventually used up all their food and died? I'm thinking the crystal is a good electrical insulator and the cave was dark, so there couldn't be external energy sources to replenish the oxidation state of the iron or sulphur or whatever they were eating.
The elevated temperature and ubiquitous radiation would have presented a relentless, potential source for DNA damage mechanisms, and repair would require a constant supply of energy. So I'm guessing there had to be some minimal source of energy to keep them viable, if not actually 'alive' for 50,000 years.
Is this thinking roughly correct? If so, what might that source of energy have been?

Below: Giant gypsum crystals in a cave in Naica, Mexico, from here. Note the person for scale at lower right.

(1) Currently 2017 AAAS meeting links are all re-directing to the 2018 meeting, so I can't find a link to the particular talk or session.

There is no chemosynthesis tag.

now there is one!

Still no publications on this that I can see; at least not with her name associated with them. Closest I can find is this one from 2013

@bob1 Interesting! fyi I've just asked Where does Actino- come from in the genus Actinomycetota?

The question is interesting, but I must say it is too early to say anything. But let me tell you what I can.
Dormancy, first of all, is a state in which all metabolic activities of an organism temporarily stop or slow down, and when saying all, I literally mean it. Dormancy can be considered, in layman's terms, as molecular level of hibernation. Any organism, in dormant state, does perform all kinds of activities, but in super slow motion. Again, we don't know anything about those microbes, so I can just tell the currently known mechanisms by which those microbes could have survived. Gypsum i.e. $CaSO_4.2H_2O$ contains sulfate ($SO_4^{2-}$), so those microbes (let me call them X from now) must be sulfur metabolizing ones to survive. Now, known mechanisms of sulfur metabolism include:

sulfur oxidation
sulfate reduction
sulfite reduction

which are summarized as:
source
Now, with sulfate already available from gypsum (considering dissociation) as:
$CaSO_4.2H_2O \rightarrow Ca^{2+} + SO_4^{2-} + 2\hspace{1mm}H_2O$
The reactions it can perform are sulfate reduction and sulfite reduction. Some of the mechanisms are:
source
In the presence of $CO_2$, glucose can also be formed as:
$12\hspace{1mm}H_2S + 6\hspace{1mm}CO_2\hspace{1mm}\rightarrow\hspace{1mm}C_6H_{12}O_6 + 6\hspace{1mm}H_2O + 12\hspace{1mm}S$
The required $CO_2$ might come from respiration. During dormancy, this process is highly slowed down, so that X may have survived such a long time by just this process.
Again, this is just the known mechanism, X may have evolved other, possibly even more efficient, mechanism. The above example was just to suggest how X could have survived in gypsum crystals for as long as 50K years. We don't know anything about X yet. From the article you cite:

If confirmed, the find is yet another example of how microbes can survive in extremely punishing conditions on Earth.

meaning we don't even know yet whether they are really viable or not.

The life forms—40 different strains of microbes and even some viruses—are so weird that their nearest relatives are still 10 percent different genetically. That makes their closest relative still pretty far away, about as far away as humans are from mushrooms, Boston said.

Now, viruses ain't alive. And 90% similarity means a lot of difference, which means they almost certainly have different mechanisms for survival. At last, I would again remind that it is too early to say anything unless some scientific studies are performed and published.
P.S. talking about energy source, even the heat and radiation from environment could be used as a source of energy. Obviously, harnessing energy directly from external heat is pretty difficult, but when one finds fungi using radiation for growth, then you never know!

This is exactly the answer I was hoping for. Background to put the question in perspective, the possibility of constituents from the crystal itself participating, and a whole lot of caution not to draw any conclusions until the normal business of science takes its course. Thanks! (rad-munching fungi was an eye-opener, I hadn't heard of that before.)

From the radio interview I had the impression that some things were in fact viable, but they may not simultaneously be the 50Ky old things. I'll listen again at some point, and wait for more to be written, and published in the future.

I've just asked this question.

keep in mind the cave in question is so hot humans can only enter it is special cooling suits, and even then only for short periods of time.

@john thats a nice point, but I can't understand how it relates to the question... :/

Under high heat you have a wider array of reactions to work with. Such as Iron sulfur reactions.

@john talking about wider array, it just comes out as a bonus that iron sulfur reactions are also the ones we already know, who knows what kind of reactions could those microbes perform! ;)

Thanks for the great answer! I have a hunch I that shouldn't hold my breath for any conclusions/consensus to be announced soon.

@uhoh yeah, research takes quite a long time, so a better answer might take years or so :)

...and even an answer with new information may not be a "better answer" in terms of being helpful or thorough. These "nonstandard ecosystems" (ones that look different than the rabbit eating the plant and returning nitrogen that I remember from school) are fascinationg!

Why do you presuppose bacteria needed to "eat" something all the time to survive. Let me give you an example-if I take a batch of a billion bacteria, throw it on a meteorite and let it bathe on the "sunshine" in space for a million years, then took it back to Earth, put it in a culture where the bacteria can grow again and out of those billion bacteria a single one was able to restart its metabolism and grow a new colony of billions of bacteria, would you consider it alive all those years it was in space? Especially, when it comes to bacteria, because they are so small they can easily go to huge numbers and if just a tiny fracture of those manage to survive you have Life Immortal.
The matter of Life is it can look quite, for the lack of a better word, "dead" for a very long time and despite not having the "need" to eat anything it can(when given the right conditions)flourish back to its full potential. Life can be pretty resilient and biomolecules remain unscanted for very long periods of time, so the question-"What it feeds on?" can be surmised as-"Can it survive unscented for so long?". And be sometime the answer is-Yes!
You may be interested to read this here and see the original paper here

Please read the question again and note that I've mentioned the molecular mechanism of DNA repair. Unless I'm mistaken these are hydrated - bacteria or some organisms floating around fully constituted in water. Under those conditions, over 50,000 years, I am suggesting at least a minimal amount of energy is needed for repair against inevitable DNA damage. If you can cite a specific known example of hydrated, single cell organisms remaining for 50,000 years with absolutely no source of energy, please provide a link. I write with careful constraints to this specific situation.

As it stands now, your answer wanders all over the place, and isn't helpful. You start out by mis-stating my question and then literally go into outer space from there.

I don't think the space analogy is out of context here but let us not waste any more space with this but will not go further on the topic.

The question is then "Do really the bacteria need an energy source to prevent them from decay, right? Is this your specific question?"

Please try to address the question as written, thanks!

The question is then "Do really the bacteria need an energy source to prevent them from decay, right?" If it is then there are two possible answers-the first is the number of bacteria is big enough and their mutation slow enough to leave survivors after 50,000 years. The other is the possibility of sulfur metabolism discussed in the previous answer. I would also suggest the possibility that these microbes might be able to make spores or synthesize special protectors to prolong their dormancy but as the article goes-we don't know enough about them yet. How about that answer?

@YordanYordanov you've written a nice answer, but you missed a crucial point: situation! The OP wants to know about the specific case of recently discovered bacteria, not a general case. So please try to be as specific about this case as possible, and a +1 from me is then guaranteed ;)

Thank you another "Homo sapiens" but I think the information provided in the source material is too little for now to jump to conclusions. If we can know more about the metabolism or the relationship of these bacteria to other genera I think we can make better suggestions. But the way I see it first we should wait for the formal paper or at least NASA to give us something more about their genetics and taxonomy. How about this answer?

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What kind of tree is this — why do its huge leaves change shape and "grow fingers"?
Edit 2: Confirmation that it's one tree!
Surrounding trees on either side along the sidewalk are completely different, and the ones on the other side of the fence are short and have rounded but far smaller, as well as thicker, dark leaves.
I've taken a 180 degree vertical "panoramic" photograph to show that there are no encroachments from trees with large leaves from behind. I've also included a few more photos of small clusters of leaves coming from a single large branch, again showing all three types of leaves.
Note some of the photos are large, and if you open them in a separate tab or window you can zoom in for additional detail.

I was riding a bike in Taipei recently (November 2017, location in google maps - more views of trees: https://goo.gl/oXPHr3) and I saw two huge leaves on the sidewalk. I stopped to photograph them and realized that they were very different shapes but otherwise looked quite similar. They are both over 40 cm long broad leaves, but while one has smooth edges and is "leaf-shaped", the other has long serrations (roughly 10 cm deep, 5-7cm spacing) on each edge.
I took some more photos of the leaves and branches of this very large tree, and one of the trunk, which looks quite gnarly.
Edit 1: I've cropped and lightened sections of two of the photos where I believe I can show examples where leaves on the same branch exhibit continuous change from smoothed edges to serrated edges. I've used 1 to denote smooth-edged leaves, 2 to denote leaves that show a few "digits" at the far end of the leaf, and 3 to denote leaves that exhibit full "digitization". In each case I think it's pretty clear that they connect to the same branch, and are not from different trees as suggested in the answer. This is strongly (if superficially) reminiscent of the sassafras leave differences.
Question: What kind of tree is this, and why do its huge leaves change shape and "grow fingers"?
It was pointed out to me that Sassafras leaves also come in different shapes with "fingers", I've included one image of those below as well for comparison.

For comparison, here's an image of Sassafras leaves with "fingers", from Landscape Plants, Oregon State University.

It looks to me that one of your pictures (the third) shows an entry to something like a botanical garden. Maybe they even are involved with the planting or care of the trees in front of their doorsteps. It wouldn't hurt to ask there directly. (Assuming this is one of the pictures you took yourself.)

Having different shapes of leaves is called heterophylly. I noticed this in Ficus carica (common fig tree), Hedera helix (Ivy), some Eucalyptus, and, I think, Paulownia. I assume this is something quite common.

@skymningen Oh my gosh! I ride by there often but I've never stopped to see what's actually there. You are right!! There's a botanical garden and a herbarium and things related. Thank you for pointing that out! OK I will have to spend some time in that area and see what I can find out.

@Glorfindel your edit adding a link to Seaworld is not appreciated. https://i.sstatic.net/JaN1Q.png

I'm going to take a stab here.  It looks a lot like Artocarpus altilis or breadfruit.  However, the trunk is a bit gnarly for breadfruit, but maybe that is the result of being a street tree.  Also, I can't find any reliable information about the variation in the leaves (heterophylly) for this species.  However, other species in the genus have entire leaves, so perhaps this is hybrid.  Also, Artocarpus chaplasha does show heterophylly related to light intensity and leaf position (online images suggest your tree is not A. chaplasha however).  I think the climate in Taipei is consistent with Artocarpus too.  If it's not breadfruit, I imagine it is a species from the Moraceae.  Finally, in some of your pictures it looks like there is an adjacent tree (possibly a Ficus or Clusia) mixing in -- those leaves are obtuse rather than acute at the tip.
EDIT:
I'm including one of your photos with the leaves of the tree in question circled in yellow, and what I believe to be the leaves of a different tree circled in red (in case my earlier comments were too cryptic).

EDIT 2:
Here is an excerpt of Fig 1 from Jones et al. "Morphological diversity in breadfruit (Artocarpus, Moraceae): insights into domestication, conservation, and cultivar identification" Genetic Resources and Crop Evolution vol 60 no 1 pgs 175-192 (2013) which shows the diversity of leaf morphology in Artocarpus including some hybrids.  I'm convinced you are looking at one of the species in this genus or a hybrid, and looking at the leaves in the panel for A. altilis there is considerable diversity (phenotypic plasticity) w/i that species, so that may be as close as it can be nailed down.
Finally, I can't run it but apparently there is graphical key to Artocarpus species which might be fun to try.

EDIT 3:
@uhoh has verified that all the leaves in the pictures belong to the same tree, so, it's likely we are seeing heterophylly based on the age of the leaves.  I went back to the reference above, and found this sentence would would seem to be consistent with the young leaves being entire and obtuse (and we've already established that the more mature leaves show a lot of variation): "Leaf characteristics, such as the number of lobes, degree of dissection, size, and shape can vary between young shoots and older branches".  So I think all the observations and literature point in the same direction, namely good 'ol breadfruit.

Sounds good, I'll await your additional impressions once you get the chance.

Added an annotated version of one of the original pictures to show what I believe to be a different tree.

I looked at the Google street view but one can't zoom in that much.  However, the different leaves I marked in red appear to be from the trees behind the fence at the back of the side walk.  I'm sure it will be clear when you can inspect again in person.  Fun puzzle, thanks for asking the question.

Did you have a chance to re-inspect these trees and make a final determination?

I think maybe you took my comment that there appeared to be a different set of leaves in the one pic as a personal affront.  It was not intended that way -- it was just speculation ("... it looks like...") based on a single image (it's not uncommon for trees to be intermixed).  Thanks for re-visiting and affirming your original observation that all the leaves belong to the same tree.  Is it your impression that the leaves with entire edges and obtuse tips are young leaves?  Perhaps that is how they emerge and the serrated edges and mitten-features grow in over time. 1/2

2/2 I noticed the following statement in the article referenced above: "Leaf characteristics, such as the number of lobes, degree of dissection, size, and shape can vary between young shoots and older branches" suggesting they do change over time.

Ah, the persistent trauma of grade school... I edited my answer to include the additional info from the literature reference.

Continuity of the thread... there is a discussion that evolved over time here, and removing parts of it would leave future visitors confused.

Stackexchange answers are not conversations or threads.

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


text:
Questions on DNA structural motifs
In the recent Nature Chemistry paper I-motif DNA structures are formed in the nuclei of human cells (open access link in LATimes) figure 1a shows "Schematic of i-motif and G4 structures."

I'm not a biologist, nor a chemist, so please forgive if the answer to my  questions seems obvious. I've looked at Wikipedia's Structural Motif article but there's little there about nucleic acids.

The length of the unlinked strand seems shorter, is this just because it is a schematic, and in reality the two branches would have the same number of bases?
What does the presence of the dual left and right arrows in G4$\ce{<-->}$ iM in the figure mean in this case? Does it suggest that a single molecule can change configuration back and forth between two distinct structures, or something else?

Double arrows represent reversible reactions. Your question is not really about biology but about the correctness of a schematic. Therefore I shall put this question on hold. BTW, both your guesses are right.

@WYSIWYG thanks for your comment. I'm trying to understand how all those bonds can re-arrange between those two configurations, and if this is actually known to happen. My intended question is to explore how DNA can do this but I wanted to check first if I was interpreting the diagram correctly or not, perhaps I was being overly methodical. If I rewrote to make this clearer, asking if DNA can do this, how, and if it is known to do this (move between these two configurations) would that be potentially on-topic?

Yes, if you edit your question such that it is about how DNA attains a certain configuration then your question is on topic. However, make sure that you are not asking a broad question.

@WYSIWYG thanks for your help, I'll take a day or so and try to do some additional reading.

When you edit the question ping me in the comment or vote to reopen. Ideally, the question should show up in the reopen review queue if it is edited post closure.

To answer point 1: The length of the unlinked strand is not represented accurately, it is shown shorter only because this is a schematic. In reality, the unlinked strand should be the same length, and would have the same number of bases as you have guessed.


text:
How does aging affect fingerprint?
Do fingerprints change as we grow from child to adult? Most notably, what is the effect of the increase in surface area of palms and fingers on the finger print? Does the finger print simply increases in size, and/or does the pattern change?
And what about old age? As the connective tissue in dermis get lax, how is the fingerprint affected?

All the evidence I found says that fingerprints do not change over time. However, I also found a paper from the National Academy of Science of America, which concluded that there is not peer-reviewed scientific report on fingerprints and if and how they possibly change over time. I think this question cannot be answered right now.

Fingerprints form in the womb at 22 weeks and after that, all they will do is expand as you grow. Therefore, it is possible that a fingerprint 22 weeks after conception could be used to identify a 50-year-old criminal.

can you please add a source?

Can you add some references to your answer?


text:
What is the reason behind high resting membrane potential of pacemaker cells?
Pacemaker cells have high resting membrane potentials of -50 to -40 mV, whereas normal cells have their resting membrane potential around -70 mV. Which ions, and what kind of channels are responsible for the high resting potential of pacemaker cells?

According to my knowledge their is a slow influx of sodium ions which causes action potential and during depolarization their is influx of calcium ions and while repolarizing their is efflux of potassium ions. But I want to know specifically what is the reason behind slow influx of sodium at the start of action potential and if their are any other ions involved in this.

The pacemaker potential is interesting (to a biologist) as it involves your typical Na/K channels, Ca channel, as well as a funny current (If) or alternatively called hyperpolarization-activated current.

The funny current is a mixed sodium-potassium current that activates
  upon hyperpolarization at voltages in the diastolic range (normally
  from -60/-70 mV to -40 mV). When at the end of a SA potential the
  membrane repolarizes below the If threshold (about -40/-50 mV), the
  funny current is activated and supplies inward current, which is
  responsible for starting the diastolic depolarization phase (DD); by
  this mechanism, the funny current controls the rate of spontaneous
  activity of sinoatrial myocytes, hence the cardiac rate.

Pacemaker activity (or spontaneous electrical activity) of the
  sino-atrial node is based on the presence of a special phase called
  the diastolic depolarization during the action potential, in which
  cells depolarize spontaneously towards the AP threshold. Animal
  studies (mostly conducted on rabbit heart) have identified that this
  net inward current during the diastolic depolarization phase is the
  result of a complex interaction of multiple inwardly and outwardly
  directed ion currents....

Verkerk, Arie O., Antoni CG van Ginneken, and Ronald Wilders. "Pacemaker activity of the human sinoatrial node: role of the hyperpolarization-activated current, I f." International journal of cardiology 132.3 (2009): 318-336.
Also this

The SAN is a complex tissue with regional differences in morphological
  and electrical properties.Animal studies have revealed that
  pacemaking in SAN cells follows from diastolic depolarization driven
  by a net inward current, which results from an interaction of multiple
  ion currents. Inward currents are activated during diastole:
  hyperpolarization-activated pacemaker current (If), background Na+
  current (Ib,Na), sustained inward current (Ist), T- and L-type Ca2+
  currents (ICa,T and ICa,L, respectively), and Ca2+-release activated
  Na+–Ca2+ exchange current (INCX). Conversely, outward currents are
  deactivated: rapid delayed rectifier K+ current (IKr) and slow delayed
  rectifier K+ current (IKs). The relative contributions of these
  currents to diastolic depolarization are a matter of debate.

Verkerk, Arie O., et al. "Pacemaker current (If) in the human sinoatrial node." European heart journal 28.20 (2007): 2472-2478.
Might I suggest you read up on the papers mentioned above?
You might also be interested in this:
Noma, Akinori. "Ionic mechanisms of the cardiac pacemaker potential." Japanese heart journal 37.5 (1996): 673-682.

The Last reference provided by you was very useful and it had answers to most of my doubts and questions.


text:
Where do most mutations come from, mitosis or meiosis?
According to this (old) paper there are 10 times more mutations during meiosis than during mitosis. One reason for that is that recombination often causes replication error and therefore mutations. However, in many multicellular organisms, germ cells undergo many cell divisions (mitosis during development) before finally undergoing meiosis.
I think that intuitively many people (me at least) think of new mutations* that are transmitted to the offspring as mutations occurring during meiosis. I would like to have a notion of how important are the two processes (mitosis and meiosis) in generating heritable new germ-line mutations in multicellular animals.
Let's consider humans for example. Out of 100 new germ-line mutations transmitted to the babies, how many of those mutations occurred during mitosis (during the development)?

*I call "new mutations", any mutation that is transmitted to a baby but that was not present in any of the two eggs of the parents (even before the parents started the gastrulation).

"Many more mutations occur during meiosis than during mitosis.":  well recombinations, yes but mutations? Are you sure about it. Can you cite a reference for that? This is new to me.

@WYSIWYG I added a reference. The estimate is 10 times as large (I would have expected something more extreme though). Note that it's an old paper.

That is an interesting info. I'm trying to check the articles citing this for any clues on mechanism. One factor in the mutation contribution would be the number of events. A gamete undergoes 1 round of meiosis but the gametocyte would go through many rounds of division. So even though mitotic mutation rate is lower than that of meiosis, the total number of mutations due to mitosis may be higher.

@Remi.b I think we can do better than 1962. Let's fast-forward here to 2014, in the post-genomic era.  I think this paper provides some data relevant to your query: Possible mechanisms for Chromothripsis .

Yes, indeed we can probably find much better results. Note that whether or not the mutation rate is different between a given mitotic and a given meiotic event, the question remains of whether most segregating sites are polymorphic due to mitotic divisions or meiotic divisions.


text:
Are mitochondria transferable between cell types, individuals and species?
I'm curious about what happens when you insert organelles from a cell into another. In particular, mitochondria.
Take two cells from your own body. Somehow extract a mitochondria from one cell and somehow insert it in the other cell.
Will the cell with the foreign mitochondria make use of it (respiration), or will it dispose it?
What if the foreign mitochondria comes from someone else's body?
What if the foreign mitochondria comes from another species' cell?

There is evidence that cells can exchange mitochondria. There are some donor cells that transfer mitochondria to recipient cells via cytoplasmic nanotubes (within the same species). This happens endogenously and triggering factors may include stress.
References:

Pasquier et al. 2013
Ahmad et al. 2014
Wang and Gerdes. 2015
Hayakawa et al. 2016

On interspecies mitochondria transfer.
In a study by Yang and Koob, the feasibility of mitochondrial transplants was studied. Mitochondria isolated from donor cells were initially injected into mouse oocytes/embryos. Then mitochondria, along with a chunk of cytoplasm and membrane was taken out; these cell-like structures were called  mitocytoplasts. Then, these mitocytoplasts were fused with recipient cells (mouse rho0 cells - these lack mitochondria) with the help of a viral fusion protein.
They found that the recipient cells supported mitochondria from the same species (donor species include mouse, rat, Mongolian gerbils and Golden Syrian hamsters).
The success of the "mitochondrial xenograft" depends on how different the species are and as shown in the abovementioned experiment, a donor cell (mouse) would not support the mitochondria from even a closely related species (rat). This incompatibility would primarily be based on the dependency of mitochondria on the nuclear genome which may be different for different species. It is possible that "mitochondrial xenografts" may be accepted; the impossibility of it has not been exhaustively verified.

Interesting stuff. +1 great answer

I'm not entirely sure about cross species organelle transfer (lets focus on mitochondria), but some people have already made three parent babies, therefore mitochondria are at least transferable between individuals of the same species.
The reason for the operation was to cure a disease that was inherent to the mitochondria of the mother (mitochondria always come from the mother, never the father). They used the genetic material from the nuclei of the mother and father, and used the mitochondria of a "foster" mother.
http://www.bbc.com/news/health-31594856

Interesting! But this looks like transfer of the nucleus, rather than transfer of mitochondria. So it doesn't answer the question of whether a cell would accept "foreign" mitochondria I think.

Another keyword for interspecies mitochondrial transfers is "xenomitochondrial". Carlos Moraes' lab is probably one of the the main groups that study this over the years, finding that mitochondria from only some great apes could functionally substitute for human mitochondria in cell lines.
Kenyon & Moraes "Expanding the functional human mitochondrial DNA database by the establishment of primate xenomitochondrial cybrids" PNAS 1997
http://www.pnas.org/content/94/17/9131.short

this is a comment that adds nicely to the pre-existing answers, but is not a stand-alone answer by itself.


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What is the definition of the life biologically ?
I want to know what is the definition of the life biologically , on the other hand ,  what is the definition of the death biologically  ?? However, I think it is a very difficult question to answer .

It is something that has its own metabolism and can reproduce I think.

I'm voting to close this question as off-topic because it is about philosophy.

I am really surprised by the attitude, that the question "what is life" should  belong to philosophy only. It should be at the core of biology! The work of Tibor Ganti comes to mind.

Could not fit in a comment..
The question is off-topic
Biology is the study of life. Without a good definition of life, Biology itself is poorly defined. It appears that there is no universally accepted definition of life and therefore Biology (just like Chemistry and Physics to cite other examples) is a poorly defined field of study. But it is not scientists job to decide whether their work should stand within one category or another, nor whether those categories are natural categories (see prototype theory) or not. It is the job of philosophers and therefore this question is about philosophy and is off-topic here.
Few notes about the definition of life
Most often, philosophers see a continuum from not living to living things and not a clear dichotomy (ref.).
Biologists, most often just assume that bacteria, archea and eukaryotes are living things while viruses, viroids and prions are not living things. This arbitrary dichotomy is based on the concept of metabolism. However, this dichotomy can lead to some limit cases. Typically, considering viruses as not being living things yields to intuitive issues when thinking about macroviruses such as Marseillovirus and Lausanevirus.
There are two questions in your post
Of course, the definition of what is dead is a total different question from the question of what is a living thing. A stone is not dead it is just not a living thing. Even then, the definition of death is of interest to philosophers, not to biologists. You should always try to limit your post to a single question.

Well, that is curious to receive down votes for this comment/answer.

I down voted because I disagree with your opinion. Biology is the study of life; how, then, is a question about its definition off-topic?

because this answer dignifies the question

@canadianer The field of Biology is itself poorly defined. Just like are Physics and Chemistry and it is not the job of scientists to care about whether their work should be considered as being part of one field or another. Typically virology is field that is mostly part of biology although viruses are usually considered as not being living things. This question is definitely about philosophy and there are several philosophy books that discuss this issue as the one I linked in my answer.

@aaaaaa the answer dignifies the question. What do you mean? Is it good or bad?

@Remi.b I mean there are some questions that should not be dignified with an answer because those questions are so low-quality

Oh....that's a good point. I guess I often dignify bad questions with answer (and voting to close in the same time). I feel bad when someone don't get any help. But that's probably not helping them nor the site.

@Remi.b If you can provide an answer, it's good to see! But these answers will attract down-votes because they will of course be fundamentally flawed by the nature of the question - hence the question gets closed.

I am curious what you think about the work of Tibor Ganti. He deals with such questions and such theoretical biology does seem to be a valuable area of research. I don't get the remarks why such questions should not be "dignified" with an answer, or get answers like "it's all up to philosophy" from biologists.

I have never read from Ganthi, so I can't comment unfortunately. What is life? can be rephrased what is the definition of life? and a definition is whatever you want it to be. There is no right or wrong when defining terms. Sometimes, there are commonly used definitions of course but there are no right or wrong definition. You might want to read [this post](Why isn't a virus “alive”?) though.

Note that the question has not been closed for being off-topic but has been closed as a duplicate.


text:
Can my eyes adjust instantly to my friend's glasses?
My eyesight is pretty much perfect, but I noticed that whenever I try any of my friends glasses, from really thin to extremely thick, my eyes seem to adjust to them within seconds and let me see perfectly fine. Is this weird or abnormal, I was just really curious.

how 'strong' are the glasses? i.e. how many diopters? If they are small correctional glasses the distortion of the image to you may be minimal. Thick glasses expectedly are stronger, but just to verify.

@WYSIWYG the question is understandable. Please, take a look on the answer.

@rg255 the question is understandable. Please, take a look on the answer.

The phenomenon you described as "my eyes seem to adjust" is a particular case of accommodation - adjustment of the dioptric power of the crystalline lens to the object's distance.
When you place a lens before your eye, any object seen through this lens will initially appear at a different distance (and of different size of course) and will be blurred at different degrees (i.e out of focus). Thus, to overcome this discrepancy the eye must accommodate.
Now, the amplitude of accommodation is the maximal power which can be added to the current power of the crystalline lens. The younger the subject, the higher amplitude of accommodation he/she has:

Thus, if one young emmetropic person (person 1) wears some other person's myopic glasses (person 2) with a concave lens with minus power to lessen the actual "overpower" of the optic system, and this power does not have the refractive error of person 1's has (less myopia if they have any "hidden" myopia), the eye must accommodate, i.e. by increasing the convexity of the crystalline lens. If the amplitude of accommodation is much higher than the glasses in question, person 1 will easily adjust to these glasses by elimination of dioptric discrepancy.
Thus, Sherlock Holmes could deduce the following:
You are a young person (under the age of 30) with a high amplitude of accommodation.
You have a lot of "four-eyed" friends suffering from myopia.
From these facts the fiction writer could assume even your nationality (developed country) and level of close work (reading books, using computers) your friends are doing but - let's leave those assumptions to writers! :)


text:
What are the differences between a benign tumor and swelling?
What are the differences between a benign tumor and an injury related swelling?
And can swellings due to injury turn into a benign tumor?

Hi @chrisstronks, so what is a swelling?  in another question someone told ne that thats kind of tumor. .. thanks for helping

There is too much confusion of terms here for the question to be answerable.

"Tumor," latin root Tumere is for swelling. If you're looking at a modern definition though, you have to consider the abnormal tissue growth. Yes, injuries may produce a thrombus, embolus, etc. however when you get injured and it swells, that isn't really a tumor. Injury swelling is just a biochemical response, but isn't characterized by cell proliferation.

@Kendall - This would be a fitting answer. I'll edit question and vote for reopening.  Could you turn it into an answer?

@MalicOfSdom - I removed malignancy here, as the step from benign to malignant may make the question too broad. If you are unhappy with the edit roll back. I am just trying to reopen this question. It covers your other closed swelling question as well. Perhaps turn benign vs malignant in a new one?

The term tumor is used in the medical definition of inflammation. However it just denotes a temporary swelling that goes down once the inflammation subsides. This swelling is due to edema (accumulation of fluid). You have to understand that in practice no one uses the term tumor to denote an inflammatory swelling. So the term “tumor” denoting edematous swelling is of historical significance only.
In modern practice the term tumor is used only to indicate abnormal growth of any kind. Either benign or malignant.

In pathology an inflammation is classically described as having the following features:

Tumor : Swelling
Dolor : Pain
Calor : Warmth
Rubor : Redness

Replicated from comment section:
"Tumor," latin root Tumere is for swelling. If you're looking at a modern definition though, you have to consider the abnormal tissue growth. Yes, injuries may produce a thrombus, embolus, etc. however when you get injured and it swells, that isn't really a tumor. Injury swelling is just a biochemical response, but isn't characterized by cell proliferation.


text:
Does learning increase the number of neurons in the brain?
I am attempting to understand neurogenesis related to learning. Does learning increase the number of neurons in the human brain? What would be some good scientific publications to read?

So in other words the number of connections between neurons is just changed? Where could I find some good references for that?

We should probably wait for @AliceD to answer, since he knows the field better.

@WYSIWYG: I am not so sure that it doesn't, and I think it actually does lead to new cells.

@AliceD Not in most cases esp. in adults. There is some neurogenesis in the dentate gyrus which may perhaps be regulated by some hippocampal activity (there is a paper which says that). Another point of view is that neurogenesis might lead to amnesia (this was in science some months back). Anyways I just gave a casual comment- I take it back :)

@user16406 It does happen but in most cases learning basically adds/strengthens the synapses.

Not necessary. Neurons are very complex and dynamic. They can be regulated both pre-synaptically and post-synaptically. I think you should read about neural plasticity. It will give you more insight on how the neurons might be able to "learn" without the need to form new projections to adjacent neurons.
Edit: Perhaps you want an answer specific for the role of neurogenesis in learning, but I still think that reading about neural plasticity will give you a good answer for your question.

0I thought we had something that prevented new neurons from forming and that learning was a change in synapsis. (However, you shouldn't take my word for it. @AliceD

@SolarLunix - Check my answer. There is definitely neurogenesis. also see http://biology.stackexchange.com/questions/25880/can-brain-cells-move/25889#25889

Short answer
Training increases white and gray matter densities in the brain. This may reflect increases in neuronal cell counts especially in the hippocampus. In the cortex, however, such observed changes are probably more reflective of other processes, such as synaptogenesis.
Background
Gray matter is generally viewed as being the neuronal cell bodies, while white matter corresponds to myelinated fiber tracts. Changes in both can be reflective of changes in cellular content, but changes in gray matter are generally more directly related to changes in cell numbers, which you are after.
A striking example of the effects of learning on the brain is observed in subjects that start to learn to juggle. These people have been shown to have increased gray matter density in the occipito-parietal regions (the visual motion areas). These changes are apparent after as little as 7 days of training. Such experience-dependent changes are also observed in white matter. Occipito-parietal regions are involved in visuo-motor coordination, reaching and grasping. There have been a host of other studies that showed similar changes in the brain. For example, taxi drivers were shown to have increased hippocampal volumes.
There is good evidence for adult neurogenesis occurring with learning in the hippocampus. Adult neurogenesis also produces thousands of new granule cells in the dentate gyrus every month, but this is a relatively small increase in total number of hippocampal neurons. Furthermore, although there have been reports of neurogenesis in the mammalian adult neocortex, this is controversial.
Thus, neurogenesis is likely a minor factor in MRI changes, particularly those found outside the hippocampus.
Instead, other factors such as increase in glial cell numbers, synaptogenesis, changes in dendritic structures, axonal sprouting and re-routing and even vascular changes may underly the observed changes in imaging studies.
Note: there is a host of imaging studies available on effects of learning on structural changes in the brain. The referenced review article cites many.
Reference
- Zatorre et al., Nature Neurosci (2012); 15: 528–36

The no. of neurons only increase during development.
As, a person grows, the no. of neurons is constant or decreases (degradation due to injury or other brain diseases). The no. never increases.

Learning anything (say, a phone no.) requires repeated thinking. The thinking can be continuous in the brain or re-induced by revision. Therefore, learning anything STRENGTHENS the connections; not increase in neuron no.
I can't help you with any Scientific Paper. The image was taken from a Textbook.

Without proper references such a strong statement is unfounded. -1

The figure is from Campbell Biology

The number of neurons does not only increase during development.


text:
Oxygenated hemoglobin in MRI
I have read the following sentence:

Because this oxygenated hemoglobin is unaffected by magnetic fields,
  the response RF signal returned to the fMRI scanner is stronger when
  there is more brain activity and therefore more oxygenated hemoglobin
  in that brain tissue.

Oxygenated hemoglobin does not react to magnetic fields, while deoxygenated hemoglobin does. So in my view, if there is more brain activity and therefore more oxygenated hemoglobin, the signal should be weaker because the oxygenated hemoglobin does not react to the magnetic field? Why is it the other way around?

I think that the type of fMRI you are referring to is blood-oxygenation-level-dependent fMRI or  BOLD fMRI.
The principle behind MRI in general is the detection of proton signals from water molecules. The proton signal is generated by magnetizing the protons in tissue, which causes their spin to change. A subsequent powerful radio wave disrupts this spin and the following relaxation phase of the protons to the original state can be detected by MRI. Water, and hence protons are everywhere in the body, including the brain and the blood.
Deoxygenated hemoglobin (hemoglobin without oxygen) in blood changes the proton signal in its immediate surroundings due to the magnetic properties of deoxyhemoglobin. This is caused by the fact that deoxygenated hemoglobin is paramagnetic and decreases the proton signal. In fact, the paramagnetic influence of deoxyhemoglobin has been regarded as noise in structural MRI scans, before its use in BOLD-fMRI became clear. Oxygenated hemoglobin does not have this property.
Radiopaedia has a nice explanation as to exactly how the BOLD signal is used in BOLD fMRI, and I quote:

When a specific region of the cortex increases its activity in response to a task, the extraction fraction of oxygen from the local capillaries leads to an initial drop in oxygenated haemoglobin [...]. Following a lag of 2-6 seconds, cerebral blood flow (CBF) increases, delivering a surplus of oxygenated haemoglobin, washing away deoxyhemoglobin and with it the attenuating effect on the MRI signal. It is this large rebound in local tissue oxygenation which is imaged, as it is accompanied by an increase in the MRI signal. The difference is used to generate the BOLD fMRI response.

So brain activity increases the BOLD signal by picking up oxygen-changes after an increased blood flow to that specific part of the brain.
So your statement [...] If there is more brain activity and therefore more oxygenated hemoglobin the signal should be less strong because the oxygenated hemoglobin does not react to the magnetic field is incorrect, because oxyhemoglobin attenuates the proton signal.


text:
Can a lack of sleep degrade balance?
For years, I've noticed that the day after a night of poor sleep (4 hours or less), my balance noticeably degrades. For instance, while walking 20 feet to the coffee maker, I might stumble into the fridge. Is this a shared experience among humans, and is there a physiological explanation for it?
I have noticed that other functions of my body degrade as well (e.g., my ability to focus), but I am particularly interested in the change in my ability to balance.

Welcome to Biology S.E.! If you need additional assistance, please visit The Help Center. I will warn you, this question may be voted to close as being a personal health question. I will try to support this question to keep it from being closed because this isn't something that just you suffer from.

@L.B. It is not a health question, just an observation.

@AliceD Yep. I was concerned some people may view it as a health question.

Short answer
Sleep negatively impacts attention, which in turn impairs balance control in cognitively challenging situations.
Background
Schlesinger et al. (1998) argue that under normal conditions, postural control appears to be automatic, and to require little or no attention in young, healthy adults during quiet standing with full sensory input. However, postural control appears to require increased attention when sensory integration or motor coordination are required. Examples of such challenging conditions where increased attention is required are situations during reduced or conflicting sensory input conditions, or when one is subjected to balance perturbations. The regulation of attention, in turn, is dependent on sleep, because sleep deprivation causes deficits in attention. Hence, although sleep deprivation per se has little or no effect on standing postural control, it can impair postural balance when one has to perform a cognitive challenging task.
Reference
- Schlesinger et al., NeuroReport (1998); 9(1): 49-52


text:
What is the distance between the sciatic nerve and the colon at the closest point?
Is it possible that a full colon impinges on the sciatic nerve? Is there anything that physically separates the sciatic nerve from the colon?

Short answer
Sciatic nerve pain cannot be caused by a full colon.
background
The sciatic nerve runs at the back of the pelvis down the the leg. The sciatic nerve exits the spine from the lumbar spine to S3 in the sacrum (Fig. 1).

Fig.1. Left: sciatic nerve overview. Right: Sacral plexus. Source: Manchester Bedford Clinic
Hence the sciatic nerve does not come into contact with the bowel and intestines located ventrally in the abdominal cavity (Fig. 2).

Fig.2. Left: sciatic nerve in detail showing dorsal location. Right: Intestines ventrally situated in abdominal cavity. Source: Manchester Bedford Clinic and University of Maryland
Pain in the sciatic nerve (sciatica) is often caused by compression or entrapment by muscles, tendons, and other soft tissues along the nerve path Manchester Bedford Clinic.

I appreciate the extensive answer with the nice diagrams. However, it doesn't actually answer my question: just how far is it between the sciatic nerve and the colon at the closest point?

Alas, I cannot provide you with an absolute distance measure.

And I appreciate it! Do you have a particular source that backs your statement that "Sciatic nerve pain cannot be caused by a full colon"? It appears to me that they might only be an inch or so apart, and if tight muscles in the area can cause sciatic pain, a full colon should be able to at least contribute.

The figures showed me they (nerve and colon) were physically separated and across various websites sciatic nerve pain is not associated with the intestines: http://www.mbmyoskeletal.com/learning/sciatica/


text:
Effect of closed eyes on balance?
Suppose you want to stand on one leg. Doing it eyes open is not that difficult, but doing it eyes closed seems to be difficult. Why?

@Bez No. I think this is an interesting question which is related to the neuroscience and the functioning of small brain. Some neuronal pathways are closed when you close your eyes. Some people also cannot do this when eyes are closed - it is impossible if you have severe damage in your inner ear etc caused by falling.

@Masi Then it would be great if a case study or population study to that effect is referenced by the OP since at the moment this question is based on the opinion of the OP!

@bez definitely not one for skeptics for me - it's a fairly well known phenomenon

@Bez It is based on his intuition, not just opinion. There is much logic in his thinking. No reference need to be done if the user does the thinking themselves. Very well known phenomenon also so I think this is recalling event from his deep memory and wanting an explanation for it. Completely acceptable question here, I think.

@Masi Is correct.  This is a fairly common neurological test.

Balance is tricky and depends on a lot of things, including, to some degree, your sight. Balance is achieved and maintained by a complex set of sensorimotor control systems that include sensory input from vision (sight), proprioception (touch), and the vestibular system (motion, equilibrium, spatial orientation); integration of that sensory input; and motor output to the eye and body muscles. Your vision helps you see where your head and body are in relationship to the world around you and to sense motion between you and your environment.
Very simply put, to blindfold someone is to take out the contribution of vision to balance. So, if the other systems involved in balance are off even a bit, blindfolding someone will interfere with their ability to keep their balance, even on two legs, let alone one.
Here are those systems in more detail.
Proprioception. In your joints, muscles, tendons, skin, and other areas, you have proprioceptors, that tell your brain where yoor aody parts (arms, legs, etc) are in relation to self in space. Because we live on a planet with  gravity, even if we are blindfolded, if we are standing correctly, our feet will sent our brain signals that will in turn allow the brain to judge our position in space with regard to gravity and we will keep our feet firmly planted on the ground in a way which will maintain us upright in a constantly regulated position (if we sense less pressure from the bottom of our right great toe, we will adjust by leaning forward and to the right a bit until out=r brain says, "ok, right there!" This happens from all the skin and joint proprioceptors responding at the same time. Notice that once vision is blocked, our bodies become relatively very still; we focus on our balance. We move tentatively.
As people age, they lose some of their propioceptive abilities. That's one of the reasons for falls in the elderly.
Inner ear. In our inner ear are the semi-circular canals, three on each side, which are oriented at ~90° to each other so we cover 3 dimensions. In these canals is fluid which sloshes about when we move our heads, change directions, bend over, etc. The fluid moving about is detected by fine hair-like projections on the sensory cells lining the canal called stereocilia - like a wave would be detected by your leg in shallow ocean water. These semicircular canals help us to remain oriented in space. Now, the semicircular canals are also attached to otolith organs - two chambers which are concerned with gravity. They have fine crystals in them - called otoconia - which move according to our head's position with relationship to "down", or gravity.
If we stand perfectly still (probably not possible without support), everything is read by the vestibular system (the semicircular canals and the otolithic organs) as normal, and we stay upright (there is a constant communication between our vestibular system and our brain). So, when blindfolded, we can stay upright even if we shake our heads, bend them forward or back, etc (within reason). As we age, things can degenerate in this vestibular system, which affects our balance, and results in more falls in the elderly. (Diseases in the young can also affect this.)
Vestibulo-ocular Reflex. A complicated system which reflexly coordinated input from your vestibular system and your vision in head movement. If someone suddenly turns your head, your eyes will move in the equal and opposite manner, that is, your eyes will stay focused on the object on which they were focused just before your head was moved. This system is what allows you to easily keep reading something while you shake your head from side to side (not the case if you move the print side to side).
When things start going wrong (in a very slow manner) with your vestibular or proprioception systems, your eyes can help compensate by orienting you to the horizon, etc., in a manner, correcting for some 'off' calculations in your vestibular system. Vision helps us to identify orientation with respect to gravity, determine direction and speed of movement, etc., to a much lesser degree than the other systems described but enough to have an impact. So, in people whose vision is failing, either their other systems have to be in really good working order (e.g. why young blind people aren't always falling over) or they have problems with falling.
The Human Balance System (easy)
Researchers find diminished balance in those with poor vision (easy)
Balance (easy)
Visual influences on balance
Baloh and Honrubia's Clinical Neurophysiology of the Vestibular System
 By Robert William Baloh, Kevin Kerber, MD
Somatosensory Systems
Vestibular Occular Reflex


text:
differentially expressed genes of the treated with estradiol samples
I did differential analysis on samples treated (G1E-ER4) with estradiol (differentiation induced by estradiol) and control (G1E).
The genes that I gor as differentially expressed in G1E-ER4 showed following pathways.
I can explain the first five: estradiol causes stress and more hemoglobin is synthesized during cell differentiation, also tetrypyrrole is involved in hemoglobin synthesis. Cell death might also be caused by stress induced by estradiol.
However, I am not sure why I have cell division or starvation etc pathways.What is considered to be a starvation actually?
response to stress (GO:0006950)
heme metabolic process (GO:0042168)
tetrapyrrole metabolic process (GO:0033013)
regulation of apoptotic process (GO:0042981)
cell death (GO:0008219), death (GO:0016265),programmed cell death (GO:0012501)

mitotic cell cycle (GO:0000278), cell cycle (GO:0007049)
cell division (GO:0051301),nuclear division (GO:0000280)
cellular response to starvation (GO:0009267)
positive regulation of GTPase activity (GO:0043547)
regulation of localization (GO:0032879)

Maybe some mTOR crosstalk with your estradiol? As for your starvation and look here, it's hard to tell unless we know what kind of starvation it was, but I suspect it has something to do with the cell division.

Pathway analysis can be a little tricky. Because pathway enrichment is estimated from the enrichment of genes (or miRNA or what have you) that participate in overlapping pathways, certain pathways often show up for reasons that may have little to do with your experiment. Cell cycle related pathways, in particular, come up a lot, since so many genes are "cell cycle-related". These papers both go over this phenomenon in more detail. The second one is behind a paywall...sorry for that. If you can't access it, but want to read it, I'm sure we can figure out a way to send a pdf.
I deal with this a lot in my own research. My usual strategy is to make pathway analysis only one part of the overall analysis. How that works exactly depends a lot on the nature of your project. For instance, pathway enrichment could just serve as a sanity check, to see that other results aren't widely off mark. Alternatively, you might want to put other results in the context of some pathway or the other & having pathway enrichment data would naturally be a part of this.
Regarding the question of what exactly starvation means in the context of your results, it's possible that, if this pathway doesn't make sense in the context of your experiment, then it shows up as enriched because more starvation-related genes came up as differentially expressed. The degree to which that means that your cells were undergoing starvation could be debatable. I would bet money that there's significant overlap between starvation-related gene sets and those related to "cellular stress" & "cell death". Cell death is one common response to serum starvation, for instance.
Hope that helps!


text:
Why is dopamine or a dopamine-receptor agonist not pumped into the brain of Parkinson patients?
I am aware that dopamine cannot cross the blood-brain barrier, but can't it be pumped inside the cerebrospinal fluid via some permanent tube implant? Wouldn't Parkinson patients chose that over succumbing to the disease? Why hasn't it even been ever tried?

Levo-Dopa is used as a first-line treatment of Parkinson's disease. Unlike dopamine, L-Dopa is able to cross the blood-brain barrier. There it is converted into dopamine. To prevent premature breakdown in the gastro-intestinal and circulatory system after oral intake, carbidopa can be co-administered. Also MAO-B inhibitors and COMT inhibitors can be applied to prevent breakdown of L-Dopa in the brain. Oral medication is preferable over invasive intracranial infusion of medication.

Conversion of L-Dopa into dopamine. Source: ADHD treatments.
Dopamine agonists are also in use. Unlike L-Dopa, dopamine agonists are not converted into dopamine. Instead, they mimic dopamine effects in your brain. They aren't as effective as L-Dopa, but they last longer and may be used alongside L-Dopa to smooth the sometimes off-and-on effect.
Parkinson's disease is not fatal, but it can reduce longevity. The disease progresses more quickly in older patients, and may lead to severe incapacity within 10 - 20 years. Older patients also tend to have muscle freezing and greater declines in mental function and daily functioning than younger people. L-Dopa treatment in the long run causes adverse effects, such as dyskinesias, toxicity, or loss of efficacy (Marsden, 1994).
Reference
- Marsden, Clin Neuropharmacol (1994); 17: S2:S32-44

so why do patients die in the end instead of living on "dopamine replacement" ?

@shortage_radeon - L-Dopa is a treatment, not a cure. Parkinson's is a progressive, degenerative and incurable disease, but not fatal. I amended the answer in response to your comment

Quoting a faculty member at Moffitt Cancer Center: sometimes the goal now is to get patients dying with their particular disease, and not simply because of it using the treatments and therapies at medicine's disposal. Cures are remarkably elusive for complex diseases, where effective management strategies exist.

@AliceD I don't think this answers OP's question, which is why dopamine or an agonist cannot be pumped into the brain and thereby cure Parkinsons, or why that has never been tried. I do not know that answer, but I want to know it too. What's interesting is that it has been tried in 2 monkeys

@AliceD ...(you have to scroll through that to find the part on monkeys)  at least once, and for one of them it rescued the motor deficit from an MPTP induced lesion for 9 days before problems with the method caused the pump to stop working. I was somehow both surprised and not surprised that this would work. I'd love to know whether anything more was ever followed up with this sort of approach.

@Chelonian - my answer is that we don't have to with L-Dopa as a treatment. L-Dopa can be taken orally and is converted to dopamine in the brain. Why pump it in? Maybe I'm thinking too practical?

@AliceD I see; yes, if the OP doesn't realize that the DAergic cells eventually all die and L-DOPA no longer helps, that's a good point. But since they do, it is an interesting question to wonder whether some kind of chronically implanted canula could deliver DA to the right targets, thereby keeping people asymptomatic for life (given that it seemed to help that monkey, at least at first), and, if so, why it hasn't been tried in people (or has it?) or at least pursued further in primates? I'm curious.

The blood-brain barrier isn't a bag that surrounds the brain that you could puncture and then inject dopamine. It is a thin layer of cells around every blood vessel and capillary in the brain that mediate transfer of substances between the blood and the brain cells. As such, it is incredibly complex and branched (as complex and branched as the myriad blood vessels in the brain).
In theory, you could inject dopamine directly into the cells of the brain, inside the barrier. But, the dopamine wouldn't diffuse far, and so wouldn't affect anything except for a very small area (millimeters?) around the injection point. So, to get an even distribution of dopamine, you'd need to inject at thousands (millions? more?) of points throughout the brain, and do it repeatedly.
And even with that, there's no guarantee that directly applying dopamine to the brain cells would actually help. In fact, bathing nerve cells in a neurotransmitter seems like a great way to mess up their signal transmission system.

FDA recently approved the duodenal levodopa infusion pump.  Idea is to wear the pump 18 hours a day, removing it at night.  This allows for a small dose of levodopa to be injected through the day.
I can not yet add comments, only new post.
@shortage_radeon The leading causes of death, among patients with Parkinson's, were pneumonia and bronchitis. Swallowing becomes more difficult with time, leading to aspirated liquids into the  lungs.  While a feeding tube can assist, the most effective is working with a Speech Therapist on keeping those muscles active.
Thankfully exercise and diet have huge benefits for those of us with Parkinson's.


text:
What is the human ear's temporal resolution?
What is the smallest sound duration that the human can hear? In other words, what is the lower duration limit for a sound to be translated into electrical signals by the ear?
Suppose the human ear can discern or distinguish between 18 kHz and 20 kHz sounds, this would mean that, if a single wave could  be processed at 20 KHz, the sound duration would be 1 / (20KHz) = 0.00005 second, which would be next to incredible (and probably impossible).
I am particularly interested in the lower duration limit as depending on frequency.
I am expecting something like this (I am not sure)
 Freq   Duration needed to be aware of the sound
 20KHz  0.05S (50 mS)
 10KHz  0.04S (40 mS)
  5KHz  0.03S (30 mS)
2.5KHZ  0.02S (20 mS)

Yes, it is the question. The duration depends on frequency How? Thank you...

I am an engineer too. Take a machine and hit it with a Dirac delta impulse of the frequency you wish to test and see if you can hear hear the frequency. The impulse will be less than 0.00005 secs.

@ChrisStronks I don't think you understand what I mean but my last comment then.

@dustin What OP wants to know is what would be the minimum duration of the stimulus that can generate a stable action potential along the auditory nerve

@chepelucho This study says that minimum duration for an auditory perception is 120-170ms. Note that this is not the physiological duration that elicits a stable nervous signal. This study was done on human subjects who have to report the onset of a sound stimulus. I think you are interested in the mechanistic aspects. Let me search; I'll get back

It would surprise me alot if this wasn't also related to the amplitude/volume of sound, similarly to how our vision works, see "Is it a limitation of the eyes, or the brain, that we can't see a moving bullet?". I also think that you should clearly separate hearing (a subjective impression) from the sensitivity of the ear (e.g. threshold for electrical impulses in the vestibulocochlear nerve).

Our sensitivity is also highest between 2-5 kHz (http://en.wikipedia.org/wiki/Equal-loudness_contour), and this will probably also interact with the temporal resolution of our ears.

@WYSIWYG - I looked at your linked article, interesting! But from my understanding they investigated minimal perceptual duration, which is different from the physical stimulus duration threshold

@chepelucho - I re-worded your question, based on your comments, to improve clarity. Feel free to roll back.

@WYSIWYG Thank you!!!, Please put your link (minimal perceptual duration) in your comment doing the clarification!!! and you have reason: One thing is the sensivity (or resolution) that the brain "knows" about of this stymulus in the ear by sound, and Other thing "Me" be aware as a person.

I will provide an answer in 2 parts. The first part is a theoretical approach based on the absolute possible minimum (my original answer). The second part focuses on experiments in the peripheral auditory system (added edited answer).
PART I: Absolute theoretical minimum (original answer)
As you inquire about electrical signals in the auditory human system I have to say that electrophysiological data at such a fundamental level is scarce in humans. That having said, we can start off by looking at auditory clicks, which are generally the shortest possible well-defined auditory stimuli. The shortest auditory click I was able to find, and which was used in a psychophysical context (i.e., audible to a human) was 10 microseconds (Leshowitz, 1971).
Now, (1) assuming 10 microseconds is the lower duration limit of a click (it may well be lower), and (2) assuming this click duration is representative of the lower limit of a tonal burst duration limit (it may well not be), and (3) assuming you indeed wish to know about/use auditory tones and not clicks, and finally (4) assuming we need at least one wavelength of a tone to fit in this window, then we could present a frequency of 100 kHz, or higher. As 20 kHz is the upper frequency limit of the human ear, we would need at least 50 microseconds for one wavelength, i.e., basically what @Dustin concluded, but it does not end here:
Frequency splatter (Fishbach et al., 2001) limits the lower limit of tonal stimuli. To prevent spectral splatter one needs to incorporate rise and fall times (ramps) onto the tonal stimulus. Hence, again assuming you do want tonal stimuli, an onset and offset ramp of one wavelength each would be advisable (at the very least) and hence 3 wavelengths are needed, increasing the duration of a 20 kHz tone to 3 wavelengths, i.e., 150 microseconds (spectral splatter may not be prevented, but at least reduced).
On top of this theoretical approach, it has to be noted that I started off with taking a click as a starting point. A click, being an impulse signal, basically stimulates the entire cochlea (the inner ear), and hence represents the most powerful auditory stimulus. Pure-tone bursts are, as a consequence, weak stimuli as they stimulate a small proportion of the available hair cells. High sound levels may therefore be necessary for short tonal stimuli, in turn degrading the frequency resolution in the cochlea as excitation spreads away from the characteristic frequencies. Mostly, several milliseconds are used as tone bursts.
Moreover, taking 20 khz is kind of an upper limit, and many folks are not even able to hear 16 khz. An upper limit of, say, 12 kHz would be advisable when grownups are used. This means a wavelength of 83 microseconds and for 3 wavelengths (for ramp times) that means 250 microseconds.
If lower frequencies are needed, this number would increase further.
EDIT: PART II. Phsyiological experiments.
As you are also interested in electrical signals, we might take another approach and start looking at experimental (animal) data. The temporal limits of the auditory system are generally assumed to reside in the ribbon synapse that is situated between the inner hair cells and the auditory nerve fiber (Parsons, 2006):

This synapse is considered to be the limiting factor in the temporal characteristics of the auditory system (Khimich, 2005). By analyzing this synapse using very short tone bursts, it was shown that the vesicles of glutamate (the neurotransmitter activating the auditory nerve fibers that lead the signal to the brain) were released as shortly as 2 ms after tone onset. Tone bursts were 8 - 16 kHz, 10 ms plateau, 1 ms
rise/fall (Khimich, 2005). Note the tone burstduration and rise fall times mentioned in answer PART I.
Indeed, when first spike times in auditory nerve fibers were determined, spikes with the shortest latency occurred just under 2 ms (Heil and Irvine, 1997).

SR in the figure means spike rate, showing that higher spike rates are accompanied by shorter latencies. A1 means auditory cortex neurons, which obviously have longer latencies.
Hence, from these experiments I dare say that 2 ms would be sufficient to elicit at least one spike.
Why then leave part I of the answer? The problem is that the experimental data do not show that a spike wouldn't have been generated at shorter stimuli. The data merely show that with an ongoing stimulus the first spike appears at 2 ms. It does not show whether 2 ms of temporal summation is necessary, and that is why I have left part I of my answer in place, as a theoretical lower bound.
As a side note: the spike rates are highly dependent on loudness levels. Lower sound levels result in longer latencies. Specificaly, acceleration of the stereocilia on the inner hair cells in the cochlea is the primary parameter. The faster the cilia move, the faster the spike response.
References
- Heil & Irvine. J Physiol 1997; 78:2438-54
- Fishbach et al. J Neurophysiol 2001; 85:2303-23
- Khimich et al. Nature 2005; 434:889-94
- Leshowitz et al. J Acoust Soc Am 1971; 49, Suppl 2:462-6
- Parsons. Nature 2006; 444:1013-4

This and other answers use the 20 kHz upper limit as a reference. But to the best of my knowledge (used to teach audio engineering) the hair cells in the cochlea do not discharge at such rate. Rather, the highest rate of discharge is around 12-14 kHz. Perceived frequencies higher than that are the sum component of intermodulation caused by non-linearities.

@Izhaki - discharge rates follow acoustic tones 1:1 only up until 2 kHz at max. After that the auditory nerve still fires in the same phase as the stimulus, but individual fibers skip one or more cycles and fire only in response to one in so many peaks. Overall, the 16,000 fibers do reproduce the stimulus perfectly though. But then, acoustic pitch is primarily a place-code and not so much a rate code.

The average human auditory range is between $20$ Hz to $20$ kHz [1]. How this relates to time is by the definition of frequency.
$$
f = \frac{1}{\text{time in sec}} = \frac{\omega}{2\pi}
$$
where $\omega$ is angular frequency. So if a human can hear a sound frequency of $18$ kHz, then
$$
(18\cdot 1000)^{-1} = 0.000056\text{ sec}
$$
where $18$ kHz is $18000$ Hz.

Abel (1972) reported duration DLs ranging from approximately 0.4 to 80ms for stimulus durations of 0.2 and 1000 ms, respectively. The lowest frequency on average is $20$ kHz but all people are different and some people may hear at a lower frequency.[1]
A different type of auditory temporal resolution can be assessed by measuring the minimum detectable duration of a gap in a continuous sound. The gap detection is in the order of 2 to 3 ms for tones at moderate and high sound
  pressure levels (Exner, 1875; Ostroff et al., 2003; Plomp, 1964). Zwicker and Feldtkeller (1967) reported values of 1.5 ms and 5.0 ms for gap detection in tonal signals and noise, respectively.[1]

Reference:

http://www.usaarl.army.mil/publications/HMD_Book09/files/Section%2019%20-%20Chapter%2011%20Auditory%20Perception%20and%20Cognitive%20Performance.pdf

You calculated the wavelength of an 18 kHz tone. OP wishes to know how long a tone needs to be for it to be audible. The fact that hair cells can discriminate frequencies doesn't mean one wave length is enough to hear it. 20 kHz is not a duration, but a frequency. And you mean 20 Hz.

@ChrisStronks according to Georgia State Universities Physics department, "the threshold of hearing corresponds to air vibrations on the order of a tenth of an atomic diameter."

@ChrisStronks Hz as units 1/time. If you want time, you invert.

Yes that is auditory threshold level. Then there are frequency limits and OP inquires about duration threshold.

@ChrisStronks and at that limit, some people will pick it up.

In your edit you mention difference limens (DL: duration difference) and gap detection threshold (shortest noticeable interruption in a burst), but both are irrelevant for OP's question I'm afraid (which is on minimal duration threshold). It's is all just basic psychophysics.