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Herbivorous plants that consume falling leaves
I've just seen a report about specialized herbivorous plants which build special traps to catch falling leaves from trees above them.
The only thing, which I'm missing is the correct name of this plant. Do you have any idea what plant(s) could this be?

Welcome to Biology.SE. Did you try to go through the wikipedia list of carnivorous plants?

You seem to misuse either of the term 'carnivorous' or 'vegetarian' in your title! You should have a look at the wikipedia entries for vegetarinism or carnivores

The term "herbivorous" plants would be a more accurate description of the plants that you are asking about.

You say you're missing the 'correct' name of the plant - does that mean the report gives an 'incorrect' (common) name for it? If so, could you post it?

Some bromelias growing up in the trees in tropical rainforests catch falling rainwater and probably leaves to extract nutriens. See here. Is that what you mean?

@RHA: Note that Bromeliaceae only grow in South American rainforests. They do not occur in Asian and African rainforests.

If you've "just" read that "report", maybe in newspaper or magazine etc, you could provide some more specific information, such as if they've provided any common-name, locality, botanic garden(sometimes) or any-other specific features. Plant kingdom is very huge, and a "report" usually is something not-popular or not well-known (otherwise it will not be reported). So the information provided here,  does-not lead to a specific direction.

Most plant utilize the rotten, humic matter in the forest floor. Rotting  (biodegradation) of fallen leaves, twigs etc. is a key source of  nutrients (manure) in soil, and it is an way of re-use of atoms.

@AlwaysConfused Well I would like to provide more information. But I've seen these documentation on a flight, and I just woke up a few minutes before this part of the documentation has been shown. Due to this fact, I couldn't provide much more information. Sorry :-(

After all, I found the answer myself.
The special plant I'm looking for is the Nepenthes ampullaria. It has developed away from the "normal" carnivorous plants to a more detritivorous species.
Nepenthes ampullaria has specialized her pitcher to catch falling leaves from trees above her.

Many plants do this, with varying degrees of specialization - for some it is perhaps incidental, others have evolved this strategy to gain nutrients (often water as well). You are probably thinking of bromeliads, a diverse group of plants in which many species have specialized leaves that form cups at the base to collect water and litter. These structures, a type of phytotelmata, have similarities to some carnivorous plant traps.
These tank bromeliads are able to efficiently absorb nutrients from animal or plant matter which falls into the tank:

Considerable absorbed nitrogen is mobilized in the rosette center. Tested bromeliads appear to be well equipped to utilize minerals and organic nitrogen originating from tank-impounded plant and animal debris as nutrients.

This litter catching habit occurs in other lithophytic and epiphytic plants, i.e. those which don't grow in soil, because it allows them to capture nutrients when growing on rocks or trees. Examples include the staghorns/elkhorns and basket ferns:

They form a characteristic 'basket' that collect litter and organic debris, hence the common name. The collected debris decompose into humus, providing the plants with nutrients it would otherwise not have received from being suspended above the ground.

Thank you @nicfit! But it's not a bromeliads plant. I have them on my own in my home. But the plant I've seen was definitely no bromeliads. But thanks to your post, I've found the real plant I'm looking for. Thanks a lot.


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How can some enzymes work faster than the diffusion rates of the molecules it catalyzes allow?
Quoting Wikipedia: "Some enzymes operate with kinetics which are faster than diffusion rates, which would seem to be impossible." Which are those enzymes and how can they be so fast?
One example is catalase which Lionel Milgrom discusses in Water Journal no. 7.

Is this a homework question?

No. I ask since some surfing didn't give any answer.

Diffusion rates of what? Please provide some explanation in your question. As it is now, the question is unclear.

What is the source of your assertion?

@WYSIWYG I presume he's referring to diffusion-controlled reactions and diffusion limited enzymes. It's a rather standard concept in enzyme kinetics.

@David Here is one such claim: "One of these enzymes, superoxide dismutase, actually catalyzes reactions FASTER than the diffusion-controlled rate. That's because the active site is surrounded by charged residues that attract oppositely charged substrate molecules!"

OK. Now we know what you are talking about. I can't imagine there are many more — there's obviously something about the chemistry that allows the enzyme to develop such an extreme kcat.  I imagine you need to surf kcat to find others. Not many of us have a "Guinness Book of Records"  mindset.

Here is one article trying to explain why catalase is faster than diffusion rates allow. https://www.researchgate.net/publication/316504611_Why_is_catalase_do_fast . Please open this question.

Is this more of a chemistry question? I asked the same question in Stack Exchange Chemistry without reactions: https://chemistry.stackexchange.com/questions/118608/how-can-some-enzymes-work-faster-than-the-diffusion-rates-of-the-reactants-allow

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Why don't phage vectors lyse mammalian cells?
I have read many articles on bacteriophages (like the lambda phage1) being used for transferring genes into mammalian cells, but none of them mention any sort of lysis of the cells even though in bacteria, lysis would occur. Of course, killing the cell would beat the purpose of the gene transfer, but why doesn't the bacteriophage kill the mammalian cells? Has there been any research on lysis of the mammalian cells with phages?

Lambda phage undergoes lysogenic cycle where host cell is not lysed immediately, it becomes a prophage and divides along the host cell. It causes lysis when exposed to UV or some other chemicals.

@JM97 are there any bacteriophages that do lyse immediately?

why doesn't the bacteriophage kill the mammalian cells?

Phage are molecularly equipped to infect only their bacterial hosts. Consider the barriers that a phage needs to overcome in order to replicate and lyse a eukaryotic cell:

The phage needs to get its genetic material into the cell, whose membrane has a vastly different lipid and protein composition compared to a bacterial cell.
The phage genetic material (assuming DNA) needs to translocate to the nucleus. There's no cytoplasmic RNA polymerase to carry out transcription.
The phage DNA needs to be bound by nuclear RNA polymerase. Bacterial/phage promoters have different motifs than eukaryotic promoters and will likely not be bound the eukaryotic transcription initiation complex.
The phage transcripts need to be translated, and the viral proteins need to self-assemble to produce new viral particles.

Under normal conditions, phage λ can carry out none of these steps in mammalian cells, save instances of cytosolic import via energy-independent endocytic mechanisms which may incidentally overcome barrier #1.1
In the linked paper,2 highly modified versions of phage λ are used to deliver a construct encoding firefly luciferase (luc) into mouse cells in vivo and human K562-αvβ3 cells in vitro. These λ variants contain recombinant components from mammalian viruses that help them to perform the desired functions in mammalian cells:

A high-affinity αvβ3 integrin binding protein (3JCLI4), engineered from human FNfn10 for enhanced binding and endocytosis into αvβ3-positive cells.3 This addresses barrier #1.
A domain from the HIV-1 Tat protein fused to λ capsid protein gpD enhances mammalian cell entry 4 and permits nuclear translocation.5 This addresses barriers #1 and #2.
A reporter gene cassette for luc expression driven by a human cytomegalovirus
promoter (CMV) that can serve as a site of transcription initiation by mammalian RNA polymerase II. This addresses barrier #3. Further, this construct is made such that only genes directly regulated by the CMV promoter are transcribed when "infecting" the mammalian host,4 so only luc is expressed and not the full repertoire of phage genes.
It's not entirely clear from the text of the linked study whether this is true of their λ variants, but the original paper describing the λ lysogen they utilize 4 includes gpD constructs fused with integrin-binding peptide RDG, the heparin-binding domain of vitronectin, and the nuclear localization signal of simian virus 40 T antigen, each of which serve to enhance λ entry into mammalian cells and/or nuclear translocation.

Moreover, WT λ produces holins and endolysins to permeabilize the host cell wall in the final stage of lytic infection.6 Even if they were expressed in mammalian cells, these proteins are evolved to degrade bacterial cell walls, not eukaryotic cell membranes.
All of this to say that bacteriophage lack the molecular machinery to infect and replicate in mammalian cells, and that even phage that have been engineered to enter mammalian cells lack the components to engage in productive infection.

References

Huh H, Wong S, St Jean J, Slavcev R. Bacteriophage interactions with mammalian tissue: Therapeutic applications. Adv Drug Deliv Rev. 2019 May;145:4-17.
Lankes HA, Zanghi CN, Santos K, Capella C, Duke CM, Dewhurst S. In vivo gene delivery and expression by bacteriophage lambda vectors. J Appl Microbiol. 2007 May;102(5):1337-49.
Richards J, Miller M, Abend J, Koide A, Koide S, Dewhurst S. Engineered fibronectin type III domain with a RGDWXE sequence binds with enhanced affinity and specificity to human alphavbeta3 integrin. J Mol Biol. 2003 Mar 7;326(5):1475-88.
Eguchi A, Akuta T, Okuyama H, Senda T, Yokoi H, Inokuchi H, Fujita S, Hayakawa T, Takeda K, Hasegawa M, Nakanishi M. Protein transduction domain of HIV-1 Tat protein promotes efficient delivery of DNA into mammalian cells. J Biol Chem. 2001 Jul 13;276(28):26204-10.
Vivès E, Brodin P, Lebleu B. A truncated HIV-1 Tat protein basic domain rapidly translocates through the plasma membrane and accumulates in the cell nucleus. J Biol Chem. 1997 Jun 20;272(25):16010-7.
Young I, Wang I, Roof WD. Phages will out: strategies of host cell lysis. Trends Microbiol. 2000 Mar;8(3):120-8.

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How do developing neurons become tuned to fire only on receiving specific inputs?
Research has uncovered neurons that seem to "listen" for specific inputs and fire only when these inputs are received. For example, neurons in the visual cortex may fire at a higher rate when visual stimuli of a particular orientation is presented, and may not fire for stimuli of other orientations.
Are there any good models on how neurons develop this tuning for specific inputs? Could anyone provide links to good papers or other resources?

The only "good model" I know of is hebbian plasticity* or hebbian theory, here's a link: https://en.wikipedia.org/wiki/Hebbian_theory
Usually what we mean by neurons "listen for" or are "tuned for" or even "like" a particular stimulus is that spiking activity in those neurons is significantly increased (or decreased) in the presence of that stimulus as compared to equal amount of time in the absence of it.
*Plasticity refers to the capacity of the brain to change both the strength of connection as well as number and configuration of connections.

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Transport of newly synthesized proteins to cellular organelles
In the nucleus the DNA is transcribed and processed to mRNA which is translated into proteins in the cytoplasm. What happens between the time a protein is made and that when it reaches the cellular organelle in which it functions? How is it transported to its destination?

You want to read about transcription and translation. In the nucleus the DNA is transcribed into RNA, which then leaves the nucleus. The processing of the RNA and its translation into proteins happens in the cytosol outside the nucleus.

RNA processing also occurs inside the nucleus because the introns need to be removed (only exons code for the protein)

I have changed your title and simplified (and corrected) the content of your question so that it focusses on the question you clearly wish to ask. If I have misunderstood you, please say. A good answer to this question will, in my opinion cover a range of organelles and cellular and sub-cellular locations, as well as perhaps touching on post-translational modifications.

Mature RNA is translated into proteins by the ribosomes.  Ribosomes bound to the ER (endoplasmic reticulum) translate proteins that are bound for export from the cell.  Free ribosomes, which are found in the cytosol, are used for structures within the the cell (http://www.brighthub.com/science/medical/articles/110037.aspx)
Proteins made on the ER are sent to the Golgi apparatus, and are packaged there for transport out of the cell. (http://www.ncbi.nlm.nih.gov/books/NBK9838/)
As far as I know, the proteins made by free ribosomes remain in the cytosol and are incorperated into certain organelles or pathways upon contact with specific other proteins or signalling molecules.

Mark can you add some references - we always appreciate that on this site... even for things that are very elementray

This answer is very limited in scope, as well as being unsupported by references, as Vance writes. I'm down-voting it until you improve it.

Mark: sort of (on the last point). Maybe worth mentioning https://en.wikipedia.org/wiki/Signal_peptide

Sorry about that, I updated it with the references.

Nucleus: DNA transcribed to mRNA.
mRNA is sent out of the nucleus and into the cytoplasm.
Ribosome: Site of translation. Amino acids are placed in accordance with the mRNA codon (triplet of mRNA sequences). Folding is done as the protein is formed.
Once the protein is complete, the golgi apparatus is responsible for packaging and exporting it.

try adding some external sources to back up your claims - i know it may seem like this is basic knowledge, but it is good practice for others to be able to follow your answer and rationale.

This is an incomplete answer as the Golgi is only involved in the processing of secreted or membrane proteins.

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Is it safe to consume foods that are hot enough to scald your skin if you touch it with your hands?
Coffee is usually served at temperatures that would burn your hands if it spilled on it.
Is the inside of your mouth not affected by the same biological process as that which causes your skin to burn?

I think this is more of a physics question: the volume of a single sip (about 20ml) is so small that it cools down before it damages the lining of your mouth. If you put a couple of drops of coffee at the same temperature on the back of your hand it wouldn't burn you either, but if you dipped your hand in it would be a different story.

But when you sip it, the first second of contact the water doesn't have a chance to cool yet. I don't think 20 ml of 180° won't burn you

To be honest 20ml was probably an overestimate (caused by not yet having had my coffee) - when drinking very hot drinks I suspect a sip is considerably less than 5ml. And I frequently burn my mouth on hot coffee despite this.

(Ha ha) But the question is about water temperature that your mouth feels comfortable with but is still nevertheless too hot to touch. Are you, or why aren't you, damaging your mouth

@larry909 I think several factors work, such as 1. mucous layers and moisture help to cool it, and 2. a habit to sip hot drinks cause desensitization and Callosity. Personally, I do-not like to drink very-hot drinks as others do, but if in certain occasion (winters / tourism hurry) I drink hot beverages for several successive days, some desensitization take place.


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Relation of conformational entropy and protein folding
I'm trying to figure out the relation between conformational entropy and protein folding.
I read the following in Lehninger, Principles of Biochemistry (6th edition):

Most of the net change in free energy as weak interactions form within a protein is therefore derived from the increased entropy in the surrounding aqueous solution resulting from the burial of hydrophobic surfaces. This more than counterbalances the large loss of conformational entropy as a polypeptide is constrained into its folded conformation.

In this context the meaning of conformational entropy is that the higher the stability of the proteïn is the lower the conformational entropy is (I think).
Why does the surrounding entropy increases because of the burial of hydrophobic residues?
Why does the burial of those hydrophobic residus couterbalances the large loss of conformational entropy?
I think maybe because the unfolded protein has more conformation then the protein when it's folded because of the hydorphobic core, it lowers the possible conformation because the hydrophobic interaction restrict the possiblities. Am I right?

I have tidied up your question. Don't leave unnecessary space that makes people have to scroll to see answers in the context of your question.

This question is an example of important general problem in chemical biology: “How does an ordered system arise without violating the second law of thermodynamics?” Berg et al. address this in the following manner:

The Second Law of Thermodynamics states that the total entropy of a system and its surroundings always increases for a spontaneous process. At first glance, this law appears to contradict much common experience, particularly about biological systems. Many biological processes, such as the generation of a well-defined structure such as a leaf from carbon dioxide gas and other nutrients, clearly increase the level of order and hence decrease entropy. Entropy may be decreased locally in the formation of such ordered structures only if the entropy of other parts of the universe is increased by an equal or greater amount.

Your question is about the spontaneous folding of proteins. You ask:

In this context the meaning of conformational entropy is that the higher the stability of the proteïn is the lower the conformational entropy is (I think).
Why does the surrounding entropy increases because of the burial of
  hydrophobic residues?

Comments on your interpretation: Do not use the term ‘stability’ in this context. It is not a thermodynamic term and its meaning is imprecise. If we think of entropy as the degree of disorder or randomness, then we can see that Conformational entropy is used by the authors to mean the entropy of the protein as a random coil which can adopt many different structures. This has clearly a greater entropy than the folded protein with (to an approximation) a single structure. The adoption of the folded structure is thermodynamically favoured because it represents a state of lower energy (specifically Gibbs Free Energy) compared with the random coil structures, but entails a loss of entropy.
My answer: The surrounding entropy increases for the following reason. The surrounding entropy is that of the water molecules vibrating and interacting with other water molecules by means of the δ+ and δ– charges on H and O, respectively. In a system containing a protein with a random coil, the movement of these molecules is restricted by the hydrophobic side-chains they encounter, hence limiting the entropy, as it were. When the protein folds into a globule with polar residues on its surface, the vibrating water molecules are less restricted in their movement and hence have a higher entropy.
Further you ask:

Why does the burial of those hydrophobic residus couterbalances the large loss of conformational entropy?
I think maybe because the unfolded protein has more conformation then
  the protein when it's folded because of the hydorphobic core, it
  lowers the possible conformation because the hydrophobic interaction
  restrict the possiblities. Am I right?

My Answer: I have explained that in general terms above, in response to your first question. If you want a quantitative, mathematical justification you’ll be pushed to find one. Assuming that there are no other factors involved, we assume that it must be so because of the second law.
Comments on Your Answer: I don’t understand what you mean by “it lowers the possible conformation”. You can decrease the number of possible conformations — you cannot "lower possible conformation”. I assume English is your first language. You must try to use it more precisely if you are going to write about science (as well as checking your spelling, grammar and capitalization). If I were marking this paragraph as an exam answer I would put a line through it as unintelligible. The key thing is that you are comparing a single conformation of the lowest energy involving specific weak interactions and a polar surface, with a number of conformations which expose hydrophobic residues and restrict the free vibrations of the water molecules.
Further Clarification
The diagram below illustrates the problem:

The protein is changing from a disordered to an ordered state so, its entropy is decreasing:

ΔSprotein = x ,  where x < 0

Whereas the water is changing from a more ordered to a less ordered state, so its entropy is increasing:

ΔSwater = y ,   where y > 0

and

ΔStotal = ΔSprotein + ΔSwater = x + y

If ΔSprotein + ΔSwater = 0 (x + y = 0), we would say that the increase in entropy of the water counterbalances the increase in entropy of the protein. For the folding to occur spontaneously, the total entropy must increase (ΔStotal > 0 , i.e. x + y > 0) and we would change the previous statement to  “more than counterbalances”.

Thankyou for your explanation and critic! However I still don't understand what they mean with "counterbalances"? @David

@RickBeeloo — I've added further clarification. (Hope I haven't got any of the > and < the wrong way round.) Glad you took the criticism in the right way. It was direct (some would put it stronger) but it was intended to be constructive.

Everything is clear now, thanks a lot! @David


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Difference between dysentery and bloody diarrhea
The difference between diarrhoea and dysentery is quite clear; but the appearance of blood in stool or bloody diarrhoea is a very confusing term when compared with dysentery. Are they different in the amount of blood or their etiology or pathogenesis or something else. I searched a lot in the internet and medicine and pathology books but nowhere I could find a straight answer. If anyone knows about it please reply with proper reference and values (if its about the amount).

I think dysentery is always associated with infection but bloody diarrhoea can happen because of many other aetiological reasons. (Although, etymologically, dysentery just means an upset gut).

I am not too sure that's why I am commenting. I'll verify if this is true and then post as an answer.

Diarrhoea
Diarrhea is loosely defined as passage of abnormally liquid or unformed stools at an increased frequency. For adults on a typical Western diet, stool weight >200 g/d can generally be considered diarrheal. Diarrhea may be further defined as  acute  if <2 weeks,  persistent  if 2–4 weeks, and  chronic  if >4 weeks in duration.
~Harrison's principles of internal medicine, 20$^{th}$ edition, page 261.

Dysentry
Dysentery is bloody diarrhoea, i.e. any diarrhoeal episode in which the loose or watery stools contain visible red blood. Dysentery is most often caused by Shigella species (bacillary dysentery) or Entamoeba histolytica (amoebic dysentery).
~WHO definition

One can also follow WHO definition of diarrhea for practical purposes but still I mentioned it from Harrison as it is more specific and quantified.
'Blood in stools' generally describe visible blood in stool, and the quantity of stool passed here can be normal like in upper GI bleeding if compared to diarrhoea or dysentry.
Diarrhoea can be classified into four major categories: Secretory, Osmotic, Malabsorbtive, and Exudative, in which exudative diarrhoea show such features of bloody stool.(~ Robbins basic pathology 9$^{th}$ edition page 577).
In fact, it is also clearly mentioned in Harrison in the topic of diarrhoea that:-

Invasive bacteria and  Entamoeba histolytica  often cause bloody diarrhea (referred to as  dysentery).

Conclusively, bloody diarrhoea and dysentry are the same.

If anyone thinks that there is some issue with this answer please do suggest me by commenting on it, this will help me to improve writing posts next time.


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Do all nerves in the body end at the tongue?
I saw this someone but have  searched on google to affirm or deny it, but didnt find anything on all nerves ending in the tongue. Please help

No, nerve endings are where they communicate with muscles (motor nerves) or the ends are where information is sensed, like touch or taste (https://en.wikipedia.org/wiki/Free_nerve_ending).
You could probably say that all nerves start in the brain but they spread out and end everywhere. http://www.innerbody.com/image/nervov.html

No all nerves do not innervate the tongue.
Out of the 12 pairs of cranial nerves only three nerves innervate the tongue; the pharyngeal part of the tongue is supplied by the glossopharyngeal nerve (IX) and the oral part is suppled by the lingual nerve [a branch of the mandibular branch (V3) of the trigeminal nerve (V)] and by the chorda tympani [a branch of the facial nerve(VII)]. Apart from them the intrinsic and extrinsic muscles of tongue is supplied by Hypoglossal (XII).
The rest of the eight nerves along with C.N IX, V and VII have different extracranial destinations.
For e.g.- The first cranial nerve originating from olfactory bulb of fore brain reach the olfactory mucosa in the upper part of the nasal cavity.

P.S. To understand the extracranial course of cranial nerves read this wikipedia page.
Besides here's a diagram that roughly illustrates the major areas of innervation of Cranial nerves.


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Why do the fastest runners tend to be black?
If you watched the last Olympics like me you probably also observed that most medallists in running events were black. Why is that? I discussed this with university grad friends and researchers and we only came up with hypotheses but nobody had an actual explanation. Is it cultural, genetic, other reasons or nobody really know?
Update:
Sprint and distance running requiring different attributes for being the best, let separate this question in two parts: 1) Sprint (i.e. 100m) and 2) Distance running (@Forest already provided a great answer for this).
Note: I know this question can potentially bring disrespectful answers/comments, but I'm hopeful that this site and its members can answer this interesting question. Otherwise, I'll simply erase my question.

Related post: Athletes: nature vs. nurture?

Matthew Syed covers this in his book "Bounce", which I highly recommend. In summary: Many of the fastest runners are not only black, but also Kenyan, and not only Kenyan but from a specific village in Kenya. This village has a training track at a high altitude, and also the entire village hero-worships all fast runners, which encourages people to really give it their all from a young age.
Your question is more general, but I imagine there are many effects like this in many communities of people (Syed also points out that all the top UK Table Tennis players are from one neighbourhood)

I wanted to know why 0 swimmers were black. My darker friend said he'd ask at the next meeting of black folk, but he hasn't gotten back to me yet.

@Chloe luckily for you the scientific paper I've quoted in my answer (see below) also talks about the swimming disadvantage for black people. See http://www.witpress.com/elibrary/dne-volumes/5/3/454 Whether it's right or wrong is another story but that's an hypothesis.

@Chloe uh, a black American won gold in swimming.

The title of this question isn't asking the same thing as the body of the question. "The fastest runners tend to be black" is not the same as "Black people tend to be fast runners".

@Chloe: See also Why Simone Manuel’s gold-medal swim in Rio was so historic -- "Manuel overcame a fraught history between Black people and water, which ripples across nations."  Apparently part of it stems from people thinking segregation in pools was easier to justify than in other places, because pool water could spread ... stuff ... between people.

@PeterCordes OK but that was the 50's & 60's. How does it explain why there aren't more recently? It seems the peak athlete age is 20, so anyone born after 1996 would have pool access. What about NBA or NFL? Darker skins dominate that sport for decades. And what about other countries, like Jamaica? @ BruceWayne Cool.

@Chloe: read the article. Cultural inertia takes a while to overcome.  If your parents don't swim at all, they're less likely to sign you up for swimming lessons, etc. etc.  Also, I said "part of it is...", because there are of course other factors.  e.g. some sports cost more to participate in, and wealth inequality is racially biased.  And sports heros of your own race and/or background might be more likely to inspire you to take up a sport.  And other factors beyond that.

Specifying between sprint and distance running would be helpful, the attributes for being the best are very different between the disciplines - as it stands it's a little broad hence is attracting answers that make sloppy generalised statements rather than providing useful evidence and theory

Black-peoples/ any other community evolved in extreme environments; evolved through much more stress (like, deficit of food, scarcity of water, predators like lions, extreme hot and cold climate); so in-general, those-peoples are in-general (not individual, but in general), more advanced in muscular work, than peoples evolved in soft environment. The black-color (high-melanin) is an adaptation against scorching sunlight of certain extreme climates

It's an interesting question and one that has been asked before. NPR did a story in 2013 on this topic, but their question was a bit more focused than just "why are so many black people good runners?"
The observation that led to their story wasn't just that black people in general were over-represented among long-distance running medalists, but that Kenyans in particular were over-represented. Digging deeper, the story's investigators found that the best runners in Kenya also tended to come from the same tribal group: the Kalenjin.
I'm not going to repeat all the details in that story (which I encourage you to read), but the working answer that the investigators came up with is that there are both genetic traits and certain cultural practices that contribute to this tribe's success on the track. Unfortunately, from the point of view of someone who wants a concise answer, it is very difficult to separate and quantify the exact contributions that each genetic and cultural modification makes to the runners' successes.
Pubmed also has a number of peer-reviewed papers detailing the Kalenjin running phenomenon, but I could only find two with free full-access and neither had the promising title of "Analysis of the Kenyan distance-running phenomenon," for which you have to pay. Insert annoyed frowning face here.
I did a quick search of some Kenyan gold medalist runners in the 2016 Olympics and sure enough, several (though certainly not all) are Kalenjin. I'm less sure about the Ethiopian runners, since most research that I found online seems to focus on the Kenyans, but I'd feel safe hypothesizing that something similar can explain their dominance at the podium.
So, the short answer to your question is that it's not just "black people" who dominate the world of competitive long-distance running, but that very specific subsets of people (who, as it turns out, are black) do display a competitive advantage and that both genetics and culture account for much of this advantage.

Nice answer, I did listen at the Radio Lab podcast (http://www.radiolab.org/story/runners/) about this story few years ago and this is actually what sparkled my interest. It answers the long distance running, however my question is more related to the sprints (i.e. 100m). In Rio, male and female medallists were black but none of them were from Africa (Males = 1st Jam, 2nd USA, 3rd Can; Females = 1st Jam, 2nd USA, 3rd Jam). Maybe we'll need more studies about Jamaican sprinters?

@MudWarrior Gotcha - I didn't look into the sprinters. At a passing glance, I don't see a trend similar to the Kalenjin/distance runner effect. Would have to do a bit of research to even see what hypotheses to look into. Eeeenteresting...(mad scientist laugh)

Very nice answer for a question that could turn ugly very quick.

@gaborous Thanks! I try to keep things classy and on-point. Partly, it comes with the terrain. I'm a science journalist, which demands some tact when reporting certain topics. :-)

@MudWarrior - Jamaica is not necessarily a meaningful factor - the genetic lines that affect things likely far predate the arrival of ancestors of those runners to Jamaica within last 500 years, and you can't know if the specific winners actually did ultimately descend from Kalenjin ancestry just by where they are born in 21st century.

@Forest I found a source for the paper you mentioned: https://www.researchgate.net/publication/264745551_Analysis_of_the_Kenyan_Distance-Running_Phenomenon

@DVK This has nothing to do with Kalenjin, sprints and long distance running are absolutely different. Sprinters are descendant of West African people (often brought as slaves to America).

@Koga Thanks & good find! The paper provides some nice quantitative background to the Kalenjin/Kenyan/Ethiopian distance runner story. It would be really nice to find something that integrated these results with some of the cultural practices that probably contribute to the Kalenjin's (and others) success. That would be a pretty interesting read.

Take a look at Will Grover's answer here, I will cite the genetic diveristy explantion here, I think that sounds the most logical:

Genetic Diversity
  This is my favorite answer, and the one that makes the most sense to me: Africans are more genetically diverse than other groups; in fact, they find that the further you are from Africa, generally the less genetically diverse you are. So you would expect to see some groups who are faster than others, or slower, stronger, smaller etc. Massive Genetic Study Supports "Out of Africa" Theory. There is a great Fresh Air podcast that describes this as well (thank you Jay Hobson for providing the link!) Talent Or Skill?: Homing In On The Elusive 'Sports Gene'

Because of more genetic diversity you will have more "choice" when it comes to natural selection. Maybe because those people were there first they were exposed to threats which required more strength or speed. So maybe that's the cause— I'm just guessing.
Update
I Found another interesting theory:
African people have most of the time another type of muscle fiber(Type II) instead of Type I. Appeareantly Type II is more reddisch --> more hemoglobin --> more oxygen --> more endurance. take a look at this article.

Good suggestion @Rick Beeloo. I also found another hypothesis (see my answer below).

Interesting theory, but wouldn't we then expect that they would dominate other sports that can be "found" in primitive societies? I wouldn't argue that it will help soccer or pentathlon, but various throws, jumps, swims and perhaps weightlifting should be affected as well, no?

@Ordous, increased variation means you're more likely to find somebody with genetics appropriate for the task; reduced variation means that if the local genetics are appropriate for the task, you've got a larger pool to draw from (and are more likely to find someone who's especially good at the task).

How does the genetic diversity of Western black people (say Jamaicans) compare to that of Western whites (e.g. Americans)... Black populations outside of Africa often come from recently bottlenecked populations

Also your answer is mainly just text lifted from elsewhere with a guess pinned to the end of it, so it's a downvote from me as I don't think it's a good quality answer (if you improve it I am happy to make it an upvote)

Every answer is based on text elsewhere no one knows everything at birth right? But I understand your critic. @rg255

I had heard rumours that most people don't know much at birth, but that doesn't make the text good quality or useful in the context - the text is not particularly good at providing any explanation

Although if we overgeneralize, the genetic diversity argument may be true, it is so bland that in any other case, we would not accept it. Problem with genetic diversity is that most of it is in neutral alleles. When speaking about particular trait, this answer is just not sufficient. One group with higher genetic diversity could have low diversity in particular trait, while other group with smaller overall genetic diversity could be highly diverse. It depends on particular evolutionary pressures.

@FloriOn Edits are always welcome, but do not remove critical content. Now the reader needs to lookup the article and even search the corresponding text which makes it really cubersome. Further everything is coming from a source, then you could just write see: this, this and this, doesn't make sense right?

@RickBeeloo Still better than reading straight up false informations. Also, I think you have linked the wrong article, as it doesn't have to do anything with the topic you wrote.

I also found this hypothesis from a scientific paper which suggests that asian and white people have a lower center of gravity than black people. See the general explanation:

Blacks tend to have longer limbs with smaller circumferences, meaning that their centers of gravity are higher compared to whites of the
  same height," said Adrian Bejan, Jones' co-author, an engineering
  professor at Duke University. "Asians and whites tend to have longer
  torsos, so their centers of gravity are lower."

Update:
Here's an excerpt from the abstract that explains this idea:

The world records in running tend to be set by black athletes and in swimming by white athletes. We show that this phenomenon is predictable from physics. Locomotion is a ‘falling-forward’ cycle, in which body mass falls forward and then rises again. Mass that falls from a higher altitude falls faster, down and forward. In running, the altitude (L1) is set by the position of the center of mass above the ground. In swimming, the altitude is set by the upper body rising above the water, and it is proportional to H – L1, where H is the height of the athlete. The anthropometric literature shows that the center of mass in blacks is 3 percent higher above the ground than in whites. This means that blacks hold a 1.5 percent speed advantage in running, and whites hold a 1.5 percent speed advantage in swimming. Among athletes of the same height Asians are even more favored than whites in swimming but they are not setting records because they are not as tall.

That link (and the link therein) don't actually provide any evidence that center of gravity affects running speed, or why it would. The hyperlink that should point to an article about center of gravity height and foot speed actually links to an article about joint stress and running shoes.

Thanks @Matt I didn't clicked the links while reading it. It's fixed now, I've added the actual study link and it's even open access!

I thought it was generally accepted that the reason fast people run fast is because of a greater proportion of fast-twitch muscle fibres.  Why this appears to be more common in black people I do not know - maybe Rick Beeloo's answer is correct??  Any suggestion that it's to do with body geometry is heading down a very murky path in my opinion.

Also note that, up until Bolt's success, it was generally accepted that a sprinter shouldn't be too tall - tall athletes cannot accelerate out of the blocks as quickly and, in the 200m, cannot run the bend as successfully.  Most top sprinters are around 6ft (Johan Blake 5'11", Justin Gatlin 6'1"), Bolt at 6'5" is several inches taller than almost all of his competitors.

@Mr_Thyroid Thanks for your input, it's not my intention to head down a murky path. I only wanted to point a published study from (what seems to me) a well-known and respectable scientist. I didn't hear about the fast-twitch muscle fibres yet, if you have time, can you make it an actual answer (including references)? This could be a quite useful input to this discussion.

You relate limb length with center of gravity, but... one might think that speed would correlate with length of stride which would correlate with limb length, and speed would also correlate with step rate which would correlate (inversely) with mass at the extremities. In other words, longer lighter limbs can be moved through each step more quickly and cover a greater stride with each step, adding up to a faster run.

@AnthonyX I think you should look at the abstract of the scientific paper I've cited, it's pretty self-explanatory. But you're right, the quote from the "news paper" I used is somewhat confusing.

And that helps or hinders how?

@BobJarvis I've updated my answer to better explain this idea.

Scientists say it is because coloured people have higher centre of gravity in comparison to their white counterpart.
Using law of locomotion,researchers found that black sprinters have 0.15 seconds advantage over their white rivals due to higher centre of gravity,meaning they fall to the ground more quickly between each stride.
Conversely, having a lower than average centre of gravity helps white swimmers as their speed is determined by height they can get above the water
Source:Physics Spectrum Magazine edition April,2016, Arihant publication
           Page number:45

authors: Bob Jarvis - Слава Україні

authors: Vladimir F Героям слава


text:
Continuous EEG: Where does pronounced power peak at 38 Hz come from?
I'm pretty new to EEG analysis. I measured EEG on six scalp positions over night. When I plot the power of the frequencies, I get the following:

What I want to explain (and didn't manage to) is the origin of the 38 Hz peak in my case.
The most important steps to arrive at my graph were (using Python-MNE):

band-pass filter of data (1 to 45 Hz)
resampling from 512 Hz to 200 Hz

Then for every of the six channels:

cut recording into consecutive segments of 2 sec duration

exclude segments if:

maximum allowed voltage step of 50 µV is exceeded
activity is lower than 0.5 µV
maximum and minimum amplitude exceed +/- 200 µV
maximum absolute difference of values in the segment > 200 µV

further:

retain only segments that are ok for all electrodes
randomly choose 15 such good segments (all electrodes) from every participant
calculate FFT for every 2 sec time segment for every electrode and participant
calculate mean of all these FFTs
plot

My question is: is someone familiar with such an artifact at 38 Hz? Where could it come from? These are the things I already checked:

it is pronounced in every participant
it is pronounced in every electrode
eye movements are unlikely since this peak is there after filtering out horizontal eye movements via ICA
electrical devises are unlikely since they should peak at 50 Hz
it is pronounced when segments are 6 sec instead of 2 sec
I also used a notch filter at 50 Hz instead of the bandpass filter, with the following result (here the individual 15 segments are shown, but the 38 Hz peak is still there):

Does someone have an idea where this feature could come from?

Someone taught me how to make a more informative plot without preprocessing the data. It thus seems like this artifact is 12.5 Hz apart from 50 Hz and therefore has something to do with the line noise from nearby electrical devices. The same pattern happens at 150 Hz.


text:
What is the anatomical term for a two jointed leg?
Allow me to apologize in advance for the layman's terminology.
I'm wondering what the anatomical term for a cat- or a goat-style hind leg is.
Cats, goats, t-rexes, and many many other animals don't have human hind legs (i.e., with one knee / one pivot point). They have two pivot points, with one bone going down, then another going back-ish, then another going down again.
I've googled and googled for the answer, but I'm completely at a loss as to what this is called! Is there any name for that style of leg? I'm sure there's a lot of variation inside the category, but there is a category, correct?

? cats have knees and hips as well... https://animalcorner.co.uk/cat-anatomy/

Welcome to Biology.SE!
I think you are talking about plantigrade, digitigrade and unguligrade.
Please note that the number of joints in mammals does NOT vary, but only the relative length (and shape) of the different parts of the leg.

A Plantigrade walks on the sole of the foot. 'Sole' translates to 'planta' in Latin hence the name.

Examples: Human, squirrel, raccoons, ...
Below is a chimpanzee skeleton

A Digitigrade walks on the digits (the toes).

Examples: dog, cat, hyena, ...
Below is a cat skeleton

An Unguligrade walks on the nails. 'nail' translates to 'ungula' in Latin hence the name.

Examples: cow, reindeer, goat, ...
Below is a cow skeleton

I think the final point you make (about the actual structure being invariant) is a major one and should be moved to the top so it isn't missed. The rest works well as an explanation of how that can be in spite their apparent dissimilarities.

I agree with you. I moved it on top. I thought the same when writing the answer but did not really know how to format. Hope that looks good enough. Feel free to edit to improve the format if you want. Thanks

I'd say that sentence placement, being immediately followed up with a side-by-side comparison chart, is perfect.

WOW I never noticed that they're all technically the same thing! That was more than helpful and extremely interesting! Thanks so much!

So amazing, thank you

Birds are also confusing for a lot of people.

Specifically, they assume that birds only have a two-jointed leg and therefore their knees "bend backwards."

However, like all tetrapods, the leg structure and number of joints doesn't really change a whole lot:

 Copyright Scott Hartman 2011
The confusion is a result of the fact that -- similar to what @Remi.b points out in his answer -- birds are generally digitigrade animals. [see here].

In the case of the "backwards bending" bird knee: that's really the ankle joint.

The bird knee joint between the femur and tibiotarsus points forwards, but is hidden in feathers.
The bird ankle joint between the tibiotarsus and tarsometatarsus points backwards.


text:
What percentage of human excrement is toxic if ingested?
I have been considering food production, waste management and 3D food printing, particularly during space exploration. This led me to wonder if human excrement could be processed into raw materials for printing healthy food.
What percentage of human excrement is considered toxic to humans if the toxins were ingested in the quantities in which they were excreted? I am referring only to excrement produced by humans not infected with diseases of any kind.

The dose makes the poison. In other words, everything is toxic, which include all the stuff that you can find in human excrements.

You can possibly narrow down to - what components of human faeces are toxic at even lower concentrations that should be removed when faeces are to be recycled.

Do you think that would make it more likely people would look at the question or answer? Only 23 views so far. :/


text:
Is it possible to identify this chrysalis?
At least I believe it's a chrysalis. I found it hanging from my gate the other day.
I'm in Western Arkansas:

More photos here

Could you provide approximate size? (or is it too late? :p). Also, if you have nay additional photos they would be helpful.

it's about 1.5". I actually posted this elsewhere, I forget the exact species but it's the kind that glues sticks and bark to itself as camouflage.

My guess is a bagworm (Thyridopteryx ephemeraeformis). University of Arkasnsas has a page about these "pests"

@theforestecologist yes, that was it

Wayne or @theforestecologist why don't you write an answer and mark it as resolved?

Based on the image and location, I'd say you've got the chrysalis of a bagworm moth (family Psychidae) or some related species of case-building moth.
There are over 1350 species of Psychidae, and I am not certain of the exact species.
Caterpillars of this family are known to create protective cases out of local debris. Because this debris can vary, so too will the appearance of the case. Different species likewise prefer to use different materials. Sticks, leaves, tree scales, etc. have all been known to be used in their chrysalii. As a result, Googling for images should produce a wide variety of chrysalis structures. Here is one example using Eastern Redcedar scales in NC:

The University of Arkasnsas has a locally-relevant page about Thyridopteryx ephemeraeformis, one species that is often considered a "pest".


text:
Why does rapid decompression make you lose useful conciousness so fast?
I was watching Smarter Every Day's episode on hypoxia, and it had an interesting chart that suggested that at 35kft, you have less than 10 seconds of useful consciousness.  This number seemed low, and I'd like to know why.
I have two pieces of evidence that make me question the chart (even though I know Destin from Smarter Every Day doesn't make mistakes lightly):

I can hold my breath after an exhale and function for well more than 10 seconds
It seems to me that the vacuum of space would be the ultimate test for how long you can sustain consciousness without oxygen, as the vacuum of space literally strips oxygenated blood as it passes through the lungs.  Wikipedia cites sources claiming you go unconscious in under 14 seconds, and a case of accidental vacuum exposure that resulted in a loss of consciousness in 15 seconds.

So why is it that the "useful consciousness" table seems to contradict these datapoints?


text:
Besides fruits and milk, what other things in nature are "intended" to be eaten?
Besides fruits and milk, what other examples are there in nature where it is beneficial for a species to have some part of its biomass eaten by others so that it evolved to produce nutritious parts to be eaten by other organisms? For example, plants having animals eat their fruits as a means of transporting their seeds.
Update.
I think there are at least two philosophically different scenarios that interest me.
One is when the substance is intended to be eaten by the same species (example: milk).
The other is when it is intended to be eaten by another species (example: fruits).

I agree with @Arnb below, this is not a bad question. Will edit to clarify.

Thanks to @Roland's edit the question now makes sense. It is an interesting question. I am removing my close vote, my now obsolete comment and +1

Difficult to define "intended" seeing as there is no intent in evolution - lactation provides for offspring, fruit is taking advantage of heterospecifics to spread seed, nectar is an incentive which makes animals aid pollination, all photosynthetic plants convert sunlight to edible energy but is it "intended" for using within the plant or could it be an evolutionary precursor to "intent" to feed conspecifics and heterospecifics?

Let's say intent means both the food stuff and the interaction evolved by selection with benefits in both species. Did evolution intend for fruit production? Maybe the fruit around the seed was a good way to provide a nutrient rich early environment, or helps the seed float in water to spread it, and then animals came along and started eating them

This is similar to an egg, the egg provides a nutrient rich environment for the chick to grow, humans (and other species) came along and started eating them.

@rg255 well nutrient storages are not quite intended to be eaten. Otherwise, nuts or potatoes or body fat should be counted.

@Remi.b seems it is closed now.

There are plenty of examples! Here is a short list

Defence ("Eat that so that you don't eat this")

Evisceration. It is the ejection of internal organs so that predator eat them but not the prey entirely. (sea cucumber does evisceration)
Lizard's tail being fragile on purpose

Parental care

Milk
Regurgitation
Sexual Cannibalism (as it is often hypothesized as benefiting the male also as he indirectly nourish his offspring)
In haplo-diplontic species, one of the two generation can be much bigger and can transfer its nutrient to the other generation (offspring), such as in moss for example.

Mutualism

Nectar
Fruits
Honeydew produced by aphids to attract ants which protect them from predators
Ant breeding fungi

Symbiosis

Lichen
Root nodule

Social behaviour

Honeypot ant (if we are happy to consider the honey stored in the ant for a long being part of the ant biomass).

Human related

The researcher in parasitology that feed his mosquitoes with his own blood!
Crops (and other things) under artificial selection. It is here just cases of mutualism where humans is involved.

Another point which you may incorporate: Plants also produce another kind of nectar (extrafloral nectar) to attract ants and other insects which protect them (plants) from herbivores.

I don't think evisceration of sea cucumbers is actually intended to feed and satisfy the predators (as per wikipedia). It is for trapping and immobilizing them.

I did not use the word "biomass" in the original question.

Please don't editorialize in your answers. If you want to respond to a particular member or comment, use a comment. Otherwise, use [meta]. That's what it's there for. I realize we were just discussing this, but at this point there are two answers (one is mine) against your point of view with a total of 7 upvotes, and one answer (your own) which has been downvoted (disagreed with) once. If you want to speak critically about the post, please use comments like everyone else. I won't downvote your post this time, but it's an option in the future.

@MattDMo I removed the section 'Semantic issue in the post'. I really find this refusal of any discussion of semantic in answer silly but it looks like the majority of user like it this way, so I will just comply to the majority. Thanks for the comment then! Without this section, it will be likely to have discussion in comments of the kind as those we have underneath Arnb answer though. Btw, I upvoted your comment by mistake :)

I found this question very interesting. Let me explain. In the course of evolution, all organism developed properties (may be structural, functional or other) to protect themselves from predators. It may be by mimicry or development of some defensive or offensive methods. There are only a few exceptions to that - where the organism allows other organisms to eat its body parts. In the question the "intended to be eaten" indicates this. With this sacrifice surely the organism gets some survival advantages of itself or its children. Fruit and milk are among these rare examples.
Another example should be nectar of flowers. Plants make nectar so that bees visit flowers to drink it and unknowingly spread the pollen.
There should be other examples also.
Please note the tag "evolution".

So, one seemingly should add honey, anything else?

What about mushrooms?

@Anixx  nectar, not honey.  Honey is produced by bees as food storage for their colony, and they certainly are not intent on giving it away to other species. Hence all the angry buzzing when beekeepers harvest their hives.

Please don't editorialize in your answers. If you want to respond to a particular member or comment, use a comment. Otherwise, use [meta]. That's what it's there for.

There are only a few except to that where the organism allows other organisms to eat its body parts. This is complete anthropomorphism. A plant doesn't "allow" other creatures to eat its body parts - it either evolves a defensive mechanism against a particular class of creatures, or it doesn't. It "decides" nothing. Some plants are toxic for some creatures and perfectly safe for others, or have some toxic parts and not others (take rhubarb as an example). Did the plant make a choice to do that? Of course not. It just happened.

I used first person in my answer for the sake of simplicity. Otherwise I had to say "in the process of evolution the plants with their seeds covered with edible fruits got naturally selected with respect to other non-fruit-bearing plants of same hierarchical category. The primary purpose of the fruit is its edibility. In other words fruits are evolutionarily selected  to get eaten. " To avoid this long and complex sentence I used terms such as " allows" in my answer. I didn't use "decide" in my answer. So MattDMo please keep it out of quotation marks.

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

In many species (crickets, salamanders, newts, arachnids, moths) males provide a nuptial gift in the form of a spermatophore which aids the female if consumed (normally via additional nutrition, but in some species the package may contain toxins that make the female less susceptible to predation).
Also, @Arnd mentions nectar in the context of encouraging fertilisation but extrafloral nectaries are believed to have evolved specifically to produce nectar for consumption, in this case by insects that will attack herbivores and thereby indirectly protect the plant.
You could make a case that bitter or toxic secretions that are intended to discourage predation have evolved specifically to be consumed, but I suspect that's not really the way this question was intended.

"You could make a case that bitter or toxic secretions that are intended to discourage predation have evolved specifically to be consumed, but I suspect that's not really the way this question was intended." - yes!

I think cannibalism in caterpillars is an example. Especially the larvae of the Lyceanidae, but also anthocharis cardamines are canniballistic. The caterpillars often find themselves on a plant that is too small to sustain more than one of them. Cannibalism is then beneficial to the species, because one butterfly is better then ten starved larvae.
As cannibalism also makes the caterpillars grow faster, it could (hypothesis, not proven afaik) be a survival strategy (or semantically more correct: trait).


text:
What is delayed compliance in blood vessels?
What I understand is it is a permanent stretch of the vessel wall. Is this true or does it mean something else?

Please start with the tour: https://biology.stackexchange.com/tour and the help section: https://biology.stackexchange.com/help with particular emphasis on asking questions.

First let's consider what compliance means:

C = compliance
ΔV = change in volume
ΔP =  change in pressure

Delayed compliance
The response of a blood vessel to a sudden change in pressure. When the volume and so the pressure highers in the blood vessel the vascualar wall will stretch. As the wall of the vessel stretches the pressure inside the vessel will fall. So an increase of compliance is the result(look at the formula ΔV will get higher because the wall stretching will make the vessel larger at so the volume bigger and the pressure less). this change in compliance is what they call delayed compliance.

I don't really think you can speak about permanent because it's a dynamic process.


text:
Thin layers or laminae that make up a single summer band in tree ring, what are they?
I took the photograph below of some tree rings. Each division on the ruler is 1 millimeter:

Each tree ring (the areas between the pizza crusts) represents one seasons worth of growth. The growing season is from about March to October. My question is about the small lamellae or dark bands that make up each ring. I have placed a green box around one set of these bands. What are they?
These small bands all seem to be the same width, so tree rings that are wider (good years) have more of them, and rings that are narrow (drought years) have fewer.
What are these bands?

Not as a confident answer but as a comment... to provide image.
The wood TS looks like ring-porous, Oak (Quercus sp.) wood (Not as identification but anatomical features are comparable).
The dark bands (radial here) seems to be xylem fibres, and bright bands (radial here), seems to be xylem parenchyma.
This is a magnified image of wood of post oak (Quercus stellata). .
Source, URL http://www.wood-database.com/wp-content/uploads/post-oak-endgrain-zoom.jpg
where it seems to me

If there is anything wrong in my knowledge, inform me and feel free to downvote this answer. If any better answer comes, I'll delete this answer.

My question is about the schlerenchyma. Why does it have a banded appearance?

I'm not sure in my labelled diagram about they are xylem fibre or something other, so I kept a place of doubt in my pictured-comment. However, though a certain repeating pattern helping here to all-sort of tissues distributed uniformly, maybe behind the exact radial-banding patterns there is no specific 'purpose'. All phenomena have 'cause', but some phenomena can have no 'purpose'.

or may be there is some purpose/advantage

These are the annual rings that are usually found in areas /regions where environmental conditions are not uniform throughout the year.
These are formed due to the activities of cambium (bundle of vascular tissue in plants showing secondary growth).
In spring it is lighter in color and has lower density whereas the autumn wood has high density and dark in color with higher density.
Spring wood - High activity, produce large no. of cavities
Autumn wood - Low activity, less lumens and cavities.

Read the question more carefully.


text:
Can someone identify this mushroom?
I found this monster on my lawn in New Hampshire USA, with a pileus that measures about 8.5 inches across. My mother has threatened to eat it unless I can demonstrate that it's poisonous, so any help identifying it would be greatly appreciated. I should mention that the mushroom is a slightly richer more brown than the fluorescent lighting suggests.
My best guess so far is an armillaria of sorts.

Cheers!

I doubt it is an armillaria. They usually grow in groups at the trees or dead strunks and have a darker centre. But being  European, I am unfamilair with American species. Depending how fond you are of your mother, I would strongly advise against eating an unidentified mushroom.

Do not eat any mushroom unless it is fully identified.  The results of a mistake can easily be fatal.

mgkrebbs is absolutely right. Some more information that might help with the ID is details of substrate it was growing on (or an in situ photo) and a spore print. That may be enough for an expert to ID it.

It is so big and beautiful

@mgkrebbs And even photographic evidence is an 'inderect' evidence and could be insufficient.

This is most likely a member of the genus Amanita, judging by the vellum traces on the cap, remains of a ring (2nd photo, under your thumb), free white gills.
What we are missing for a better id is the base: is there a volva, a bulbous end...? Please dig out your mushrooms instead of cutting them off.
Also, the colour is significant: are there pinkish tinges (-> A. rubescens?) or is it just brown?

Good shout. It think it looks a lot like Amanita porphyria

I don't recall any pinkish tinges. In any case since I haven't given enough information for an exact id, and the general consensus that it is most likely an Amanita, I will accept this as an answer. Thank you!


text:
Is it true that pigeons became less afraid of humans in recent years?
My grandfather had told me when I was a kid that at his time the pigeons would not approach humans closer than about 15 meters. At the time he said it the pigeons were approaching us not closer than approximately 1.5-2 meters. And now I often have to make efforts so not to step on a pigeon who hinders my movement along a street.
This is in Europe.

I think it is possible that populations can change their behaviour rather fast, but "Europe" is too big to make a statement about. For example I did an image search for "city pigeon 1950s" and got pictures like this one: https://s-media-cache-ak0.pinimg.com/736x/3a/38/34/3a383400d1749e7b1019bc90bdcb43f1.jpg

If it happens, it is very normal. Just like taming the animals, due to continuous presence of human-beings they could shift from their known behavior or may go through desensitization. https://en.wikipedia.org/wiki/Desensitization_(psychology)#Effects_on_animals.

I've seen this phenomenon in some populations of sparrows and squirrels in certain places of India. Especially shockingly in  some tourist-spots, temples and crowded areas. Some of the populations are even easy to touch or capture!!! probably they are nearly 100% desensitized


text:
Can this system of mutual promoting and repressing proteins be simulated using Gillespie algorithm?
Consider an axon of length $L$ with the soma located at $x=0$ and the tip located at $x=L$.
We assume that there is a constant input of Kinesin motors to location $x=0$ coming in from $x \le 0$.
Assuming that all Kinesin motors travel at the same speed $v$, the proteins reach the location $x=L$ after a time $\tau = \frac{L}{v}$.
At $x=L$, incoming Kinesin motors induce Dynein motors to travel from $x=L$ to $x=0$.
Assuming that all Dynein motors travel also at the same speed $v$, they reach the Location $x=0$ after a time $\tau = \frac{L}{v}$.
At $x=0$, incoming Dynein motors inhibit Kinesin motors from travelling to $x=L$.
Thus, we get a negative feedback.
My question:
Can this system of mutual promoting and repressing preoteins be simulated using Gillespie algorithm?
I already simulated it with a mathematical model of delay-differential equations, but as this model doesn' t show all effects, I would like to try using Gillespie algorithm.

Why don't you just try it and find out?

Yes Gillespie's algorithm has been used to study such feedbacks. Are you also modelling diffusion? In that case you should also incorporate Brownian motion.

Yes, I' m also modelling diffusion. Thank you for your help!


text:
How correlated are the lengths of tendons in different part of a human body?
How correlated are the lengths of tendons in different part of a human body?
E.g., if the we consider two humans, A, and B. Human A has a patellar tendon of length 2 cm, and human B has a patellar tendon of length 1 cm, i.e. twice shorter. Should we expect all tendons in human A to be approximately twice larger than in human B?

I couldn't find studies analysing clearly enough tendons size, but a couple of sources show that they are probably correlated:

One study found correlation between dimensions of Achilles'tendon and other ankle tendons (see table 2).
Another study found correlation between height and dimensions of some tendons (see table 2).

Anyway, since correlation is not very strong, I doubt if the effect found is just the obvious correlation of dimension of all body parts to the general dimension of body - that is, bigger people tend to have bigger tendons, bigger bones, bigger livers, and so. It would be interesting to do a regression analysis of tendons dimensions taking in account body dimensions and other tendons dimensions. This way we could be able to see if people with some bigger tendon (compared with people of the same body size) tend to have other bigger tendons.


text:
Correlation between threat and odour, taste
Is there any sort of correlation between threat and taste/smell?
Are we evolved such that things which are harmful to life taste and /or smell bad and things(food) which are useful to us taste, smell good?
How far this conjecture correct?

interesting question, if that's true the additives in food messed everything up

Seems true. Bitter chemicals are mostly "not normal food-component"

All-sorts of organisms apply their all sense-organs (what-ever a chemical receptor or not), to distinguish between beneficial vs dangerous.

The compounds that smell bad to us are often the same ones produced by the anaerobic metabolism of bacteria, such as hydrogen sulfides or butyric acid. These types of compounds are the ones that make excrement and rotting food smell bad, and if something is giving is giving off a lot of them it's a pretty good signal to not put it in your mouth. Vomit also has quite a lot of butyric acid in it, so we may be particularly sensitive to it.
Plants produce toxic compounds to stop herbivory, many of them taste bitter. Alkaloids are often toxic and uniformly bitter, terpenoids are another example.
There's nothing obviously different from a chemical perspective in chemicals that smell bad. Butyric acid is just a 4 carbon chain with a couple of oxygens on the end and reeks, while the compound propanediol (which is 4 carbons with an oxygen on each end) is used in deodorants. If a compound has a strong smell or taste to us, it is because that compound has been important to us during our evolution. That doesn't mean it's a perfect indicator; cheeses can stink and be totally edible, but that's because the compounds in that cheese usually are a sign of something dangerous.


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Why is Capsaicin injection not used instead of nerve surgeries for pain?
High concentration capsaicin kills c & a-delta nerve fibers permanently or at least long term.
This has been known for 30 years.
But capsaicin is only used in creams and patches, and not for injecting direcly into nerves, and people resort to nerve surgeries like nerve blocks, razor-damaging nerves, or rhizotomy to cut the nerve partially or fully. All of these options affect not just pain functions, but overall sensory functions.
On the other hand, capsaicin destroying c & a-delta fibers just affects pain.
So why is no one interested in capsaicin injection as an option before cutting nerves?

Mine god Capsaicin is the pungent, burning component  of chili (Capsicum sp, many edible cultivars) fruits. If it is injected, the patient should at-least feel severe burning pain. Even a very little concentration should be toxic enough because if I cut green chillies ,  even-after washing the hand with soap, If in that-day mistakenly rub eyes with that-hand, it cause burning pain and lots of tears... however no or only a little burn is felt on my adult finger skins.

As a food-tradition, often the labourers and farmers eat very pungent foods containing high amount of chilli, and once I've read a theory that it is due to a painkiller activity of capsaicin. Capsaicin is NOT an anaesthetic-type of painkiller, but the exact-Opposite. According to terminologies of herbal medicine, it is "Counter-irritant" (https://en.wikipedia.org/wiki/Counterirritant), mostly a psychological effect, and partly due to increased fluid circulation. If injected, it would increase the inflammation, nothing better.

There is a simple answer to your question: it might cause a massive inflammation-like response and it might also hurt really, really badly.
Capsaicin activates heat receptors which are not only involved in heat reception (that would cause the pain as TRPV1, the receptor, is strongly activated at temperatures higher than 43 degree Celsius - accordingly, it will feel like burning from inside) but also in sensing inflammations within the body. That means that your body will think it has to take strong and immediate action if capsaicin enters tissues directly, flush out a bunch of neuropeptides and actually might start destroying the affected tissues.


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Are plants actual oxygen factories?
Is the oxygen exhaled by plants during the day compensated by inhalation of carbon dioxide at night?

Green-plant respirate (O2 ---> CO2 ) throughout day and night. But the total rate of photosynthesis (that happens only at day) throughout world is so greater than respiration of animals+plants for (day+night) is so grater, that  CO2 can't accumulate. speed of photosynthesis is greater than the plant's own respiration otherwise it could not be able to accumulate foods and  grow.

The confusion takes place because it is not about stoichiometry (chemical arithmetic) or balance; but it is about reaction-rate (speed) with time.

In night, the plant do-not intake any CO2. You can consider them like animals when it is night.

Are you confused about "dark-phase" of photosynthesis (where CO2) is taken? The term is misleading and another synonym for it is "light independent phase". All school-textbook on photosynthesis-chapter; mentions it so-far I can recall.

If you block the light; there would be a deficit of pre-requisit-compounds for another-phase (so-called dark-phase).  So with turning off light, within very short, momentary time the dark-phase stops. Dark-phase (light-independent phase) though indirectly, dependent on light.

Both phases of the reaction, i.e. 1.  the light-phase and 2.  light-independent-phase, both take place only in presence of light. On dark, both turns off.

All green plants do Photosynthesis as well as Respiration.
Plants respire during the day and night, but they only photosynthesis during the day when it is light:
there is equations for aerobic respiration and photosynthesis:
C6H12O6 + 6O2 → 6CO2 + 6H2O (aerobic respiration)
6CO2 + 6H2O → C6H12O6 + 6O2 (photosynthesis)
In terms of reactants and products, they are the reverse of each other. In terms of gas exchange:
Process        -------Carbon dioxide    -----------------Oxygen
Respiration     -----------Out  ----------------------------    In
Photosynthesis  -------In         ----------------------------    Out

Photosynthesis is only in the presence of Sunlight . So it occurs only during the day .
For photosynthesis they require Carbon Dioxide gas ( CO2 gas )
This gas enters the leaves through tiny pores on them called stomata .
The byproduct of photosynthesis is Oxygen gas ( O2 gas )
It is either passes out through the same stomata OR used for respiration

For respiration they require O2 gas .
It enters the leaves through the same pores or stomata .
The by product of respiration is CO2 gas .
During day time it is immediately used for photosynthesis .
During night time the CO2 gas is released in the atmosphere

Net gas exchange
The net (overall) effect depends on the time of day and the light intensity. Photosynthesis doesn’t occur at night. When there is no photosynthesis, there is a net release of carbon dioxide and a net uptake of oxygen.
If there is enough light during the day, then:
the rate of photosynthesis is higher than the rate of respiration
there is a net release of oxygen and a net uptake of carbon dioxide

(consider CAM plants)
in a plant using full CAM, the stomata in the leaves remain shut during the day to reduce evapotranspiration, but open at night to collect carbon dioxide (CO2)
https://en.wikipedia.org/wiki/Crassulacean_acid_metabolism#During_the_night

this link help you understand the process better by simple language :
http://www.bbc.co.uk/education/guides/zxtcwmn/revision/1

It's impossible for a plant to use more oxygen in the long term. As @BlueFoxy explained, whenever a plant is using oxygen it is to oxidise sugar ($C_6H_{12}O_6$). These sugars were made by the plant itself using $CO_2$, $H_2O$ and sunlight, so it can't oxidise more sugar than it produced in the first place.
If the plant is growing then some of the carbon removed from $CO_2$ will be used to form the plant's tissues, causing a net increase in oxygen in the atmosphere. If the plant isn't growing it'll probably be oxygen neutral.
There are probably some weird parasitic plants that break this pattern by stealing other plants' carbon, but in general the rule holds.

"There are probably some weird parasitic plants that break this pattern by stealing other plants' carbon" - Monotropha uniflora is parasitic on mycorrhizal fungi, so does this indirectly.

@arboviral Cuscuta reflexa or anysuch parasitic plant would be more direct example because they donot require mediators like mycorrhizal fungi.

@AlwaysConfused good catch - I'd forgotten about dodder. However, Cuscuta reflexa can actually photosynthesize a bit; a species which is thought to be entirely dependent on the host plants for nutrition such as C. europaea would be an even better example.

@arboviral Thanks I did not knew C. reflexa can do little amount of photosynthesis. Great info!


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What is recemose inflorescence?
In recemose inflorescence

Main axis continues to grow,
The flowers develop in acropetal succession ,
Opening of flower is centripetal

But according to definition

Acropetal succession : flowers opening in succession from base to apex
Centripetal : the younger flowers are towards the centre and the older towards the outside...

I can't understand that if lower flowers or flowers towards centre open first then they should be older but according to above statement flowers at base are younger. Is there other concept that I don't know?

Inflorescence is a flowering shoot that bears more than one flower. There are two types of inflorescence Cymose and Racemose. Of the two types of inflorescence Cymose inflorescence is more primitive and Racemose is derived. (Parkin 1914)
Racemose
In this type of inflorescence the main axis does not end in a flower, but it grows continuously and develops flowers on its lateral sides in acropetal succession (acropetal (adj.) - of leaves or flowers; developing or opening in succession from base to apex ).
Acropetal sucession is observed in raceme, the simplest racemose
inflorescence.

Now Capitulum or Head, it is another type of racemose inflorescence in which

the main axis or receptacle becomes suppressed, and almost flat, and the flowers (also known as florets) are sessile (without stalk) so that they become crowded together on the flat surface of the receptacle. The florets are arranged in a centripetal manner on the receptacle, i.e., the outer flowers are older and open earlier than the inner ones.

In the following L.S. of sunflower you can see the disc florets developing/opening in centripetal manner.

P.S. I'm not a botanist but a candidate of B.Sc Zoology. I had Botany as my additional subject so I answered it from my knowledge.

I'll add more information as soon as I'm free.


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Thermodynamics of spontaneous protein folding: role of enthalpy changes
I'm trying to get clear why protein folding occurs spontaneously.
$$\ce\Delta G=\Delta H-T\Delta S$$
According to thermodynamics the ΔG should be negative for a process to occur spontaneously.
When a protein folds the ΔS (Entropy) is decreasing, because the protein gets more ordered. However I think the forming of the bonds (disulfide and other weak interactions) counterbalance this unfavourable rising entropy by forming an enthalpy (ΔH) which thus would result in a negative ΔG.
However I saw some other explanation online which didn't apply the Gibbs free energy formula to the protein but instead to the water. Because the water is more ordered when the protein is unfolded it would be favourable according to the second law of thermodynamics to fold the protein because after folding the water molecules can move more freely --> higher entropy -->negative ΔG --> spontaneous folding.
So my question is which of these two (or maybe both) are the cause of the spontaneous folding of proteins?

I have edited the title to avoid confusion with a related question that focuses solely on the entropy change. Hope that is ok. If not revert it.

Summary

The first explanation is commonly encountered.
The second explanation cannot be correct, as it stands, as it ignores the free energy change in the protein.
A modification of the second explanation (perhaps what was intended) is that it is necessary to consider the protein folding and change in the water as being coupled, in which case the overall free energy change — the sum of the two considered separately — is the determinant of protein folding. The assertion would then be that a negative free-energy change in the water system is the deciding factor. This view has been persuasively advocated on the basis of experimental measurements.

Free energy change in individual transformations
It is standard practice in biochemistry to consider the Gibbs Free Energy of transformation of the sort A → B in isolation in determining whether it will proceed spontaneously. A chemical reaction for which ΔG is negative may generate heat (i.e. have a negative enthalpy change (ΔH) ) which affects its aqueous surroundings, but it seems justified to consider the reaction in isolation as there is no sense that the change in the vibration of the water molecules is driving or coupled to the reaction.
This approach has been applied to the structural change of protein folding with the conclusion (consistent with the first explanation) that the change in enthalpy (ΔH) is sufficient to produce a negative ΔG and hence drive protein folding (Citation 1, below).
Free energy change in coupled transformations
Many biochemical changes involve transformations which individually have a positive free energy change, but are made possible by coupling to another reaction with negative free energy change, of greater magnitude:

A → B , ΔG1 = +x
C → D , ΔG2 = –y

If y>x and these two reactions are coupled (generally through a complex reaction path on an enzyme) , then we have:

A + C → B + D , ΔGoverall = –ve

See also Berg et al.
Although one can reject the second explanation in the question as it stands because it ignores the free energy change in the protein folding, perhaps it was intended to mean that the folding of the protein (A → B) should be considered as coupled to the change in the environment of the water (C → D), and that the negative ΔG for the aqueous environment made a greater contribution to the overall ΔG than that for the protein folding.
Is it valid to consider these two systems as coupled? In the original version of my answer I argued against this point of view, but am no longer convinced by my own arguments. The water environment is clearly essential for the hydrophobic effect — the burying of the hydrophobic residues in the centre of the protein away from the water. This is evident if one considers the same protein in a hydrophobic environment such as a cell membrane — it would not fold. In membrane proteins it is hydrophobic residues that are exposed to the lipid bilayer and it is their interiors that sometimes have hydrophilic channels.
So in this coupled system, what is the determinant of the negative free energy change? Minikel (Citation 2, below) asserts that there is no net enthalpy change for the protein folding, and it is the entropy effect on the ΔG for the aqueous environment that drives the folding. He indicates that this view is supported by differential scanning colorimetry and, although he doesn’t cite references, there is a recent (if rather complex) review of this topic by Christopher M. Johnson.
Citation 1: Assertion of role of ΔH of protein
The following explanation, taken from Essential Biochemistry, treats the protein folding in isolation and asserts that change in enthalpy is sufficient to produce a negative free energy change:

The folding of a protein also provides an example of the "ΔH" and "–TΔS" terms competing with one another to determine the ΔG of the folding process. As described above, the change in entropy of the protein as it folds is negative, so the "–TΔS" term is positive. However, in addition to entropic effects there are enthalpic contributions to protein folding. These include hydrogen bonding, ionic salt bridges, and Van der Waals forces. An input of thermal (heat) energy is required to disrupt these forces, and conversely when these interactions form during protein folding they release heat (the ΔH is negative). When all of these entropic and enthalpic contributions are weighed, the enthalpy term wins out over the entropy term. Therefore the free energy of protein folding is negative, and protein folding is a spontaneous process.

Citation 2: Rebuttal of role of ΔH of protein and assertion of role of water
The following explanation, taken from on-line lecture notes of  of Eric V. Minikel of Harvard University, rebutting the point of view above:

An incorrect and simplistic view of protein folding is as follows. An unfolded protein has high configurational entropy but also high enthalpy because it has few stabilizing interactions. A folded protein has far less entropy, but also far less enthalpy. There is a tradeoff between H and S here. Note that because ΔG = ΔH - TΔS, increased temperature weights the S term more heavily, meaning that higher temperature favors unfolding.
That entire explanation only considers the energy of the protein and
  not that of the solvent. In fact, hydrophobic domains of a protein
  constrain the possible configurations of surrounding water (see
  explanation above), and so their burial upon folding increases the
  water’s entropy. Moreover, it turns out that the hydrogen bonding of
  polar residues and the backbone is satisfied both in an unfolded state
  (by water) and in a folded state (by each other). Therefore enthalpy
  is “zero sum,” and protein folding is driven almost entirely by
  entropy.

thankyou great explanation! I understand your point "it would seem very diffucultto specify how many water molecules were affected".However thermodynamics usually calculates the free energy of the total system, so this confuses me a little bit. @david

I think you are right to be confused and even sceptical about my answer. The warning signal is the personalization in “In my opinion…” and “I find…”. Why should you or anyone else care about my opinion? And the fact that I was writing in that way suggests that I was trying to use my authority in lieu of a convincing argument. I have now modified my answer so that it no longer rejects coupling of the changes. Apologies to anyone who has already up-voted my answer — do feel free to withdraw your vote.

I found an explanation about considering the solvent(water) in protien folding thermodynamics (http://www.cureffi.org/2014/09/05/molecular-biology-02/) it's at the bottom of the page,maybe you are interested @david. It looks like the solvent is important.

@RickBeeloo — Pretty convincing, despite having to take his word for "it turns out". Need to revise my answer again, but it may have to wait until tomorrow.

I have revised my answer once more, including the source cited by @RickBeeloo.

If you change the solvent will a given  protein still fold spontaneously?  One could argue that the only biologically relevant solvent to use is one with the pH, osmolarity, and concentration as intracellular cytoplasm (you could also include the inside of the endoplasmic reticulum).  In ethanol, or olive oil the same protein might night fold spontaneously.  So the solvent is paramount for setting the context of your question. What you call folding, others might call "being pushed into shape by the solvent." The hydrophobic effect is crucial (see Tanford's book of the same name--a classic).


text:
Mechanics of Peregrine Falcon Dive Pull Up
There are loads of information on how fast the Peregrine Falcon dives, but aside from having specialized lungs, eyes, etc... to survive the dive.
What mechanics does it use to pull out of such a dive, specifically after it has hit it's prey.
My take is that it uses its momentum to loop back in a U-shape, understand that by changing the angle of attack, this generates the necessary drag & lift to pull out of the dive saftely.
My question is how effective is this & can a larger bird pull this off assuming it has all of said mechanics?


text:
Which area of neuroscience\biology deals with the effects of genetics and drug discovery based on brain microcircuits?
So the title I chose might be a bit too broad or even misleading compared to the specific example I have in mind, but I couldn't choose something longer or more specific than that, so I apologize if that's the case!
Due to its close connection to Autism Spectrum Disorders (ASD) and even some personality dimensions in psychology and my interest in these topics, I was reading an article about the reward circuit (cortico-basal ganglia reward network: microcircuitry, Susan R Sesack and Anthony A. Grace, 2010) which in my opinion is a pretty nice article and as the title suggests talks about the different parts of the cortico-basal ganglia network mostly at a fairly high level of detail (e.g. nucleus accumbens, ventral tegmental area, prefrontal cortex, etc), their interconnections, some physical characteristics of those interconnections, the associated neurotransmitters for the different parts and connections, and some of the functional implications of these topics, and also presents a couple of nice diagrams depicting the afferents and efferents of this circuit. as far as I understand and perhaps obviously, most of this data comes from primate and mouse data, however I would imagine there could be a lot of similarity in humans, and we also approximately know from cognitive neuroscience or other disciplines the general function of some (if not most) parts of this circuit.
The question that came to my mind is, which area of neuroscience or biology deals with modeling and simulating this circuit at this level (not necessarily at the neuron to neuron level) to understand it better, and also understand the effects that genetics or environment could have on it, so that ultimately we might for example come up with a treatment for ASD? is it more related to systems neuroscience, computational neuroscience, systems biology, or even bioinformatics and computational genomics?
Thanks in advance!

Basically you are sketching a situation where:

Brain circuits are modeled (Computational Neuroscience), which often depends on anatomical (Neuroscience, Biology), structural imaging and functional imaging (Neuroimaging) and electrophysiological data (Electrophysiology). Various other disciplines may come into play (Histology, Pathology, Anatomy, etc.).
Genetic (Genetics, Molecular Biology, Cell Physiology) and environmental effects (Behavioral Psychology, Medicine, Psychiatry) also encompass a wide list of expertise, out of which a small handful is mentioned in bold.
The realm of drug discovery harbors Medicine, Toxicology, Organic Chemistry, Pharmacology, perhaps even Physics and likely a host of others.

In short, your question could, perhaps, better be phrased as 'What Biomedical fields of research disciplines are not related to Drug Discovery?

Thanks for the answer. I know all those fields you mentioned might be related to the problem I sketched, however, perhaps I should have explicitly said I meant which field is more directly related, or which field could have the final or biggest contribution to this problem?

@en1gmatic I think this answer addresses your question perfectly, it isn't possible to say "more directly related" or to know where the final contribution will come.

@BryanKrause - thanks for that reply. I'm growing slack in replying on comments - a sign of the dreaded 'I've stopped caring' phase evident in a lot of longer-time users in the Stack network. I'll try to reply more often :-)

No worries - just trying to settle an unanswered question that should be marked answered that got bumped to the top.

@BryanKrause - You're right at the place where Bach-y-Rita worked, right? I've visited Madison a while ago for a visit to Wicab, Bach-y-Rita's commercial legacy.

@Christiaan At the university, yes, but I came here after his death and did not know him; there is a room used for graduate and undergraduate courses in neuroscience and seminars named after him, and his lab continues doing similar work under the direction of other faculty, though I don't know those individuals well either. It's a big place :)


text:
SNPs in the Human Genome
I read online that they have found around 10 million single nucleotide polymorphisms (SNPs) across individuals in the human genome [1]. However, this number includes all SNPs found in all people who have been sampled and does not tell us much about SNPs in any single person.
I was wondering instead how many SNPs there are in a single person on average. I had trouble finding trustworthy evidence about this question.

I was wondering how many SNPs there are in a single person on average

A SNP is a polymorphism in the population, it is not a thing a haplotype can carry. Each individual has a given variant for any given of the SNPs (except for cases of sequence deletion).
It is possible though to say how many SNP a diploid individual in between its two haplotypes but I doubt this is where you interest was. Ewens smapling formula gives expectation and distribution under an infinite alleles model, panmictic population and absence of selection.
Other statistics that make sense include the average number of deleterious mutations pre individual or a few other things or how many new mutations a couple transmit to their offspring,... But asking how many SNPs an individual carry on average makes little sense.
Note as @Chris said, by stating 10k SNPs in the human genome, you seem to under-estimate the number of SNPs.
EDIT
In the comments, you further

Would it make more sense to consider a rough minimum and maximum?

The answer is no, it would not make more sense. Consider the definition of SNP by wikipedia

A single nucleotide polymorphism, often abbreviated to SNP (pronounced snip; plural snips), is a variation in a single nucleotide that occurs at a specific position in the genome, where each variation is present to some appreciable degree within a population [My emphasis]

The term population is key here. The concept of SNPs (or of polymorphism to be more general) makes only sense if you can make comparisons. A single individual does not have any polymorphism (to the exception of the one between his two sets of chromosomes).
If we step back and think of different species it might become more intuitive. Think of the number of pairwise differences between two species. It does not make any sense to ask "how many pairwise differences is there between a blue whale?" You need to say "how many pairwise differences is there between a blue whale and a wolf". Similarly, you cannot say "How many SNPs is there 'between a single individual'" (to the exception again of the consideration of the differences between the two sets of chromosomes), you need to consider a group of individuals.

"But asking how many SNPs an individual carry on average makes little sense." It does make sense. Heterozygosity in individuals is a useful proxy for genetic diversity in the population.

We can sure compare the two haplotypes (as I said in the second paragraph). This is not heterozygosity (nor observed heterozygosity) but just an average number of pairwise differences between haplotypes within each individuals. I just doubt this is what the OP was after but maybe I am wrong in the OP's intentions.

My field of expertise is Computer Science. I have started a bioinformatics project which input would be a vcf document of SNPs (of a human individual). I'm interested in the average for practical and optimisation reasons, rather then biologic scientific reasons. But as you stated, it makes no to consider the average. Would it make more sense to consider a rough minimum and maximum?

@BARJ Please see edit. Hope that helps.

There was only one source I was able to find, It stated that each genome contains 1 SNP every 1000bp. (Take a look here). However I have no idea if this source is reliable

Your number is too low, the 1000 Genomes project lists roughly 15 Mio SNPs (see reference 1). To find out how much SNPs humans have on average (this depends of course on populations, where this can differ), you often find that on average 1 in 1000 nucleotides is altered if you compare two human genomes (or the other way round: They are 99.9% identical).
The problem with this number is that it is quite old and can be traced back to a publication from 1991 (see reference 2), which compared 75.000 sequences nucleotides from 49 loci. Since this was before the complete sequence of the human genome was known, I would treat this number with some caution.
The newest number I found on this is from publication of the human genome. They estimate the number a little bit lower, at about 1 in 1300 bases (see reference 3).
What could be done with the data from the 1000 Genomes Project is to download the data from the individual samples, map it against the reference genome and see, how many SNPs per individual occur. I am not sure if nobody did that or if I simply overlooked that.
Based on this data there are somewhere between 2,3 and 3 million SNPs (1:1000 or 1:1300 respectively) present in each human genome. According to the 1000 Genomes project (reference 1), the rate of newly occurring SNPs is $1\times 10^{-8}$, meaning that there are between 20 and 30 new SNPs occuring per generation.
References:

A map of human genome variation from population-scale sequencing
Low nucleotide diversity in man.
Initial sequencing and analysis of the human genome.