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Do self-exciting neurons exist?
I have two questions concerning self-exciting neurons in the brain.

Have directly self-exciting neurons been oberved, i.e. neurons with an axon terminal building a synapse with one of its own dendrites.
Does self-excitation work?

I guess that self-excitation can only work when the following time constants fit to each other:

refactory period of the neuron's membrane voltage (approx 1 milliseconds)
run time of the signal along the axon
refactory period of the synapse (approx 5-6 milliseconds)

I tried to estimate a typical run time by taking a not untypical axon length of 1cm = 0.01m and dividing it by a typical nerve propagation speed of 10 m/sec, getting 0.001 sec = 1 millisecond. Direct self-excitation would not work because the synapse would not be ready when the self-exciting signal arrives.
The other way around: Only when the run time is longer than the two refactory periods direct self-excitation might work.
Once again: Are there known examples of direct self-excitation in the human brain or nervous system?

Short Answer
Yes, autapses exist, though the role of excitatory autapses in particular is unclear.
Long Answer
A lot of your assumptions are wrong for biological neurons (I'm suspecting you have a background in artificial neural networks but that might be inaccurate). These don't directly impact your question of whether these connections exist, but I think they are important for understanding how they could function, which is just as important if not more so.

The 'refractory period' refers to a period in which a cell cannot or is less likely to fire an action potential. Cells can receive inputs freely during their refractory period.
Neurons are not single compartments. Action potentials are generated near the soma, and although they can propagate into the dendrites, synapses out on the dendrites can be fairly electrically isolated from the soma, and synaptic potentials in dendrites can take some time, easily a ms or two, to affect the soma, and they also last for several ms. They can also affect the potency of other nearby synapses.
Although axons can be cms or more in length, dendrites are rarely found and further than 1 mm from a soma in the CNS (there can be exceptions, of course; I am mostly thinking of neocortex), and most dendrites are within 100-200 um from the soma. So travel distances are much shorter than your estimate. However, synaptic transmission itself is somewhat slow, so you can add another .5 ms, and your estimate for speed is quite fast for the brain; the link you gave applies to peripheral fibers and spinal cord to brain transmission only (note they are talking about "nerves"), so your overall estimate of 1 ms from spike to autapse turns out to be reasonable, but for different reasons.
It isn't meaningful to talk about refractory periods for most synapses. Synapses can display short-term depression and/or facilitation but that isn't the same as a refractory period. Only at particular synapses containing a single release site does it make any sense to talk about refractory periods.
Cells are not activated by an individual synapse, with a few exceptions in very specialized brain areas. So just because a cell has been made to fire tells you nothing about whether a particular synapse was activated. In fact, unless that cell has fired previously very recently, you can be confident that an autapse would not have contributed to that particular firing event.

Evidence for excitatory autapses
You specifically asked about self-excitation, but it's important to know that inhibitory self-synapses also exist, and they are much more common between GABAergic inhibitory cells than between excitatory cells (Bekkers, 1998). Inhibitory autapses make a lot of functional sense because they serve as direct negative feedback.
However, excitatory autapses do exist and they may have function significance(Bekkers, 2009), rather than just being rare "accidents" that do little. In Aplysia, for example, there are autapses that cause an excitatory plateau potential during feeding behavior, maintaining activity for a long duration (Saada et al., 2009).
In mammalian neocortex, excitatory autapses have been observed but their function is unclear. Their properties can be a bit different from other synapses (Liu et al., 2013). Spike-timing dependent plasticity would suggest that autapses should shrink and go away, but they don't, which suggests they might have some functional utility, though it isn't understood yet. There are many computational attempts to find some function, which I won't list here but you can easily find by searching a reference like Google Scholar for recent articles about "autapses."
Experimentally, the role of autapses in vivo is difficult to study because there is no specific way to selectively suppress autapses outside of a computational environment, or a reduced prep where individual cells can be activated without activity in the rest of the network.

References
Bekkers, J. M. (1998). Neurophysiology: Are autapses prodigal synapses?. Current biology, 8(2), R52-R55.
Bekkers, J. M. (2009). Synaptic transmission: excitatory autapses find a function?. Current Biology, 19(7), R296-R298.
Saada, R., Miller, N., Hurwitz, I., & Susswein, A. J. (2009). Autaptic excitation elicits persistent activity and a plateau potential in a neuron of known behavioral function. Current Biology, 19(6), 479-484.
Liu, H., Chapman, E. R., & Dean, C. (2013). “Self” versus “non-self” connectivity dictates properties of synaptic transmission and plasticity. PloS one, 8(4), e62414.

Thank you so much, Bryan! But how would you call the period of time that a synapse needs to "reset", e.g. absorbing and/or reproducing the transmitter molecules?

@HansStricker That period of time doesn't exist in a meaningful way, nothing is waiting for that to happen. You can ask another question on that if you'd like (it's a good question) and I'll happily answer, only reason I'm demurring is it's frowned upon to ask/answer new questions in comments because they won't be indexed in any way.

My assumption on refraction times of synapses was from here: http://www.snl.salk.edu/~zador/PDF/1309.pdf:
"[...]  the synaptic refractory period - a brief 5–6 ms period [...] during which the synapse is incapable of transmission [...]"

@HansStricker Can you give a full citation and quote from one of those references? I very briefly looked at three of the papers I think you are referencing and they don't have anything to do with a synaptic refractory period. Again, this all would be better in a new question rather than a conversation in the comments.

Got it, thank you, that's better. They are talking here about very specific low-vesicle-count synapses that contain essentially a single release site. It has nothing to do with the time to clear neurotransmitter out of the cleft or refill vesicles, but just because it takes some time for a new vesicle to get into place at the synapse. I wouldn't generalize that to all synapses. I'll edit my answer to allow some nuance.

It's also important to recognize that connections between two cells rarely involve a single synapse; for a given axon contacting a given cell's dendrites, any one action potential might only cause release at 10-20% of the possible release sites. All of the others remain potentially able to release at the next action potential with no delay; in fact, the probability can be increased due to short-term facilitation.

I agree that this topic is worth an own question. May I contact you before I post it? This is my email adress: stricker@syspedia.de

Let us continue this discussion in chat.

"100-200 um" do you mean micrometer?

@Mockingbird Yes. um is a fairly common shorthand for micron/micrometer in informal contexts due to the similarity of "u" and the appearance of the Greek letter "mu" which is the more formal shorthand.

'plateau potential'?  Do you mean some potential remaining constant over time?

@Mockingbird Yeah, essentially a potential that keeps the cell more depolarized than it would be at rest, but relatively constant (not perfectly constant). It is a common phenomenon in motor systems, for example see wikipedia here: https://en.wikipedia.org/wiki/Plateau_potentials

Also see https://scholar.google.com/scholar?hl=en&q=plateau+potential

Self excitation can also be realized via leaky ion channels causing a constant rate of depolarization. This is for example the case for the generation of the heart beat by pacemaker cells
If you are more broadly interested in examples of self-generated activity, you might also want to look at circadian clocks, which are essentially biochemical oscillators that ultimately modulate firing rates of neurons.

Aside from autapses and pacemaking cells, there are also some kinds of sensory neurons that exhibit a spontaneous resting (constantly depolarizing) activity that helps with encoding stimuli. The benefit of having constant activity is that stimuli can further excite or inhibit this activity, and this can be valuable information.
Sensory neurons such as olfactory receptor neurons - whose function is to detect and relay information about airborne chemicals - also exhibit spontaneous activity. The exact rate probably depends on the olfactory receptors found on the dendritic region of the neurons, which are, as mentioned, leaky. Many other sensory neurons share this property with olfactory sensory neurons.
Example reading on olfactory receptor neurons.


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How extensive was interbreeding among human species?
I have read this article about non-Africans interbreeding with Neanderthals, Neanderthals interbreeding with Denisovans, and Asians interbreeding with Denisovans as well.
Now, I'm wondering what that even entailed.
Were populations of these species cohabitating a piece of land and completely mixing up? Would the humans of that time and place be 50/50?
Or would that just be a single act of interbreeding where an adventurous person had children with another species and those children became a part of the sapiens population?
Do the genetics suggest how much interbreeding happened or can they only say that some interbreeding happened?
Bonus, unrelated question. Does natural selection in any way suggest that mixed species offspring was better adapted to the environment and thus spread so far or can it just be a random event with little effect one way or the other that just spread regardless.

I suggest you remove the "bonus, unrelated question" and ask it separately.

Interbreeding between H. sapiens and neandertalis was quite limited.

Our results indicate that the amount of Neanderthal DNA in living non-Africans can be explained with maximum probability by the exchange of a single pair of individuals between the subpopulations at each 77 generations, but larger exchange frequencies are also allowed with sizeable probability.

--Extremely Rare Interbreeding Events Can Explain Neanderthal DNA in Living Humans

... the interbreeding success rate between humans and Neanderthals was found to be below 2% (Fig. 2, Table 1, Fig. S1, and Table S1). Under demographic scenario A (Table 1), which is based on the most realistic demographic parameters, we estimate this interbreeding success to be even well below 1% (0.51%, mode of black curve in Fig. 2; 95% confidence interval: 0.33–0.89%). ...  If we assume that both species interacted for 10,000 y during the range expansion of modern humans (11), successful admixtures between Neanderthals and humans would have occurred, on average, only once every 23–50 y over the whole hybrid zone to produce introgression levels of 1–3%, which shows that they were extremely rare events.

--Strong reproductive isolation between humans and Neanderthals inferred from observed patterns of introgression
Note that this technically doesn't touch on "interbreeding" but rather addresses successful interbreeding; sterile individuals won't be detected in this approach, and even sub-fertile individuals (whose lineages died out) will be underrepresented.
We have strong evidence that male progeny of sapiens/neandertalis crosses were either sterile or extremely sub-fertile:

These results suggest that part of the reduction in Neandertal ancestry near genes is due to Neandertal alleles that reduced fertility in males when moved to a modern human genetic background.

--The landscape of Neandertal ancestry in present-day humans
And even apart from that, there's good evidence that hybrids were less "fit" (in evolutionary terms) than either parent:

After hybridization, on average, selection appears to have removed Neanderthal alleles from the human population. ...  We find that the bulk of purifying selection against Neanderthal ancestry is best understood as acting on many weakly deleterious alleles. We propose that the majority of these alleles were effectively neutral-and segregating at high frequency-in Neanderthals, but became selected against after entering human populations of much larger effective size. While individually of small effect, these alleles potentially imposed a heavy genetic load on the early-generation human-Neanderthal hybrids.

--The Strength of Selection against Neanderthal Introgression
So it's very likely that the rate of interbreeding, per se, must have been higher than the roughly once-per-generation rate that can be inferred from genome analysis, but most of the hybrids were sterile, or poorly adapted.  Of course, this is exactly what you'd expect from interspecies hybridization; the number of successful sapiens/neandertal hybrids through the millennia of their interactions was probably lower than the number of fertile mules in the past few hundred years.

source: Stack Exchange

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sort: votes


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Why does walking mitigate the urge to urinate?
When feeling a strong urge to urinate humans tend to walk around when e.g. waiting for the current bathroom occupant to get out. Why is that?

This is what we call a displacement behaviour (or displacement activity, the term used by Konrad Lorenz - see below). Funnily enough, that's exactly the same general mechanism involved in the behaviour described in my previous answer here at Bio SE.
In short, a displacement behaviour is a behaviour that occurs when the animal (human beings are animals, of course) faces itself in a situation of conflict: you want to urinate, but you are inside a train, or in a concert, or in the theatre during the best moment of that movie, or the bathroom line is simply too huge.
In that moment, you realize that you need to hold it a bit longer. That's when you start your displacement behaviour.
When people need to hold a very strong impulse to urinate, the most common movements/behaviours are:

stamping the feet
squirming
walking, as you said
humming

Therefore, walking is just one among several behaviours we show when we need to urinate but we can't: there is nothing special with walking in this situation.
Another common displacement behaviours that humans show in other situations are scratching the head, rubbing hands, drumming the fingers or biting the nails.
Konrad Lorenz explains displacement behaviours in his The foundations of Ethology:

When two conflicting motor patterns are activated simultaneously, it can happen that the organism performs a third pattern which may belong to an altogether different system. This curious effect was first described in avocets, Recurvirostra avisetta, by G. F. Makkink, the Dutch ornithologist who called the movements thus elicited "sparkling-over" activities (Über-sprungbewegungen). The accepted English translation is "displacement activities". Although "displacement" means something entirely different in the psychoanalytical literature, this term will be used here.

Further down, giving examples of displacement behaviours in human beings, he says:

Locomotion, too, is often disinhibited in conflict situations; some people tend to walk restlessly to and fro while delivering a speech, and so on.

Sources:

En.wikipedia.org. (2017). Displacement activity. [online] Available at: https://en.wikipedia.org/wiki/Displacement_activity [Accessed 1 Jul. 2017].
Lorenz, K. (1981). The foundations of ethology. New York: Springer-Verlag New York.

So you are saying it's all in the head and there is nothing really happening in the bladder or surrounding muscles/organs to suppress the urge?

Yes, that's what I'm saying. For instance, I don't walk, what I do is swinging from side to side... and also humming, if my bladder is really full.

does displacement behaviour works like massage on pain? I am suggesting like massage suppresses the feeling of pain, walking suppress the need to urinate?

@Mockingbird Yes, that may be the case. When Lorenz described this behaviour he suggested that this could relieve the tension caused by competing urges. However, that doesn't necessary mean that it reduces one of the urges: it reduces the tension between them (the necessity to pee vs the necessity to hold it). In my personal experience all I can say is that it helps me to cope with the urge to urinate.

Is there any concrete research about this?

What do you mean by this? If you're talking about OP's question, it's worth mentioning that Lorenz won the Nobel Prize. If you're talking about your question here in the comments, I'd have to do some research.

@Gerardo Furtado I was talking about my question in the comments.

@Mockingbird That being the case, I'd have to do some more research, as I said. But I believe that the displacement activity doesn't suppress the need to urinate.

Are you sure displacement behavior is the best descriptor for this phenomenon? I have an (unreferenced) feeling that sympathetic/parasympathetic activity is also involved to some extent. They may not be mutually exclusive but it seems somewhat different than Lorenz's displacement activities.

@BryanKrause Displacement activity is the only explanation I know for this phenomenon. I can say something about your hypothesis only if I read it somewhere, which I never did. Thus, feel free to write it.

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How can someone share 50% of their DNA with their parents yet all humans share 99.9%?
I have heard that humans share 99.9% of their DNA with other humans. I have also heard that a child shares 50% of their DNA with their parents. How do I resolve this apparent contradiction? It has been really bothering me.

There was another recent question about this that gave an answer that is equivalent to the answer for your question, asking about Neanderthal DNA in Homo sapiens sapiens, see here: https://biology.stackexchange.com/questions/61147/neanderthal-human-genetics The short version is: they are talking about slightly different things.

See here: https://biology.stackexchange.com/questions/41974/why-are-the-genomes-of-humans-99-5-the-same as well

And here we go with that 99.9% again: https://biology.stackexchange.com/a/61078/24284

Why was the question down voted? I think it is a common misunderstanding. We have already seen such misunderstanding several time on Biology.SE but it is the first time that the origin of the misunderstanding was so clearly phrased. I think it is a good question.

It will be clear with a simple analogy.
You are 50% related to any one of your parent
Let's say you don't have any biology books. You have two friends, Alice and Bob. They each give you a copy of the book Campbell Biology. You now have two Campbell Biology. You have received 50% of your Campbell biology books from Alice and 50% from Bob.
Similarly, you inherit 50% of your DNA from your mother and 50% from your father. You are related at 50% to any one of them.
Two randomly sampled individual are 99.9% identical
Now consider the list of all the copies of Campbell Biology in the world. As there exist different editions, all Campbell Biology won't exactly be the same.
Let's say you randomly sample two Campbell Biology from around the world and you align them letter by letter. What is the expected fraction of the letters that will be identical? If, for example you find the two sentences

Selection is a fitness variance associated to a genetic variance among individuals in a population.

and

Zelection is a fitnezz varianze azzociated to a genetic varianze among individualz in a populazion.

There are exactly 9 mismatches out of 99 characters, that is a 90% similitude.
Similarly, if you randomly sample two humans, align their DNA (a DNA sequence look like ATTTCGCTGTCGAATCGATCGGTA), you'll find that the fraction of mismatch is lower than 0.1%. Therefore, we all share 99.9% of our DNA.
Of course, alining DNA sequences (or normal sentences) is not quite that easy as some sequences (or sentence) can have more nucleotides (or letters) than others but I won't go into the details here.
How do these two measures relate?
Let's say that instead of giving you a book, Alice actually produced a copy of its book and gave it to you. The book you have received from Alice (that is 50% of all your Campbell Biology books) is 100% identical to Alice's book in term of mismatch.
Similarly, the 50% of your DNA that you inherit from your father (or mother) is 100% identical to the copy of the genome found in your mother.
Note however that

Your mother probably made between 10 and 100 mutations when copying her DNA so that the DNA you received from your mother is not exactly 100% identical to your mother's DNA

Similarly Alice could have miscopied her Campbell Biology book that she passes to you

Your mother actually recombined her two haplotypes

Similarly Alice actually had two different editions of Campbell Biology and she mixed them up a little bit before copying the resulting book!

Good answer. +1 But could you add a link between the two? E.g. that the 50% you have from your parents are 100% identical to the respective parent in terms of 'shared mismatches' (disregarding the 60-100 de novo mutations) and that because of this the expected identity between parents and offspring is way higher than between randomly sampled individuals.

@AlexDeLarge Very good point, thank you. I tried to add that. Feel free to rephrase it if you think you can make it easier to understand.


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Identification of store-bought succulent plant
I bought this succulent in the Bronx Botanical Garden Shop, but it was unlabeled. On the photo it is about 4" high:

Can anyone help identify this? Could this be Echeveria haagai? It's indoors in NYC.

Please provide your location as well as where you obtained the specimen. Thank you.

The only reason I have any clue as to what this could be is because I have one that looks exactly like it and, in a stroke of sheer genius, I wrote the name on the bottom of the pot. I think it is some member of x Pachyveria, which are intergeneric hybrids of Pachyphytum and Echeveria. Because there are so many, determining the exact cultivar may prove difficult. Mine is "Blue Pearl" and it looked very similar until it's untimely demise.
You can check out this website to see some different varieties. Actually, some of the Pachyphytum look pretty close too.
Compare w/ x Pachyveria "Cheyenne" (source):

and x Pachyveria "Little Jewel" (source):

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Can you identify this insect for me?
Does anyone know what this is? I have lived in this area of northern Utah, USA for over 30 years and played with insects, snakes and spiders growing up here. However, until this week, I have never seen this insect before, nor anyone else we have asked. Suddenly they are all over our porch, patio, trampoline and house. This one is about the size of a lady bug, but we have seen some about double that size.
At first we thought it might be a beetle, but their shells are not bifurcated. Looking underneath, they have a long thin tube that they fold into their body that appears to be their mouths. We thought a weird tick, but they only have 6 legs. Can't seem to find anything similar online either.
Does anyone know, what it is?

I don't know about species in Utah, but this looks like a shield bug (Pentatomoidea) nymph. So perhaps that could get you somewhere in your search!

Since the back isn't bifurcated, not a beetle and with its long proboscis folded underneath, it's  a plant bug nymph (as in true bugs in the order Hemiptera). Suddenly finding them all over the place means eggs have recently hatched. Metamorphosis doesn't happen with true bugs. Eggs hatch directly into nymphs which are usually, but not always, a small version of the adult and go through a number of moults till adult. But I still don't know what species, sorry.

I found a bunch of similarly looking hatchlings on a plant on my balcony a few days ago. Probably a different species, given that I'm in France. It must be hatching season in the northern hemisphere.

Definitely a nymph of some species of true bug (order Hemiptera), most likely in the suborder Heteroptera (i.e., the shield bugs, stink bugs, assassin bugs, etc.) and family Pentatomidae.
For example, see these photos of nymphs of similar species:

 From L->R: Podisus maculiventris, Troilus luridus, Glaucias amyoti, Cosmopepla lintneriana, Carpocoris purpureipennis, Murgantia histrionica
Using yet another species, Piezodorus lituratus, as an example, you can see how a Pentatomidae nymph typically develops to maturity:

 Source
As to your species...
This site lists Cosmopepla lintneriana, Chinavia hilaris, Podisus placidus, Chlorochroa rossiana, and Sehirus cinctus as species of Pentatomidae that live in Utah. None of their nymphs looks quite right, though your specimen reminds me most of a stripe-less Podisus. That might be a good jumping off place for further digging...

As you can see, there are many species with similar nymphs, and various instars within species even have fairly great variation.

I can't find a great match yet, but I can keep looking. I'll update if I find one.

Plus, what with the shift in climate, insect ranges are shifting too, sometimes drastically.


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Is there any species that cannot reproduce without its symbiont?
I was thinking about humans and machines being symbiotic "species".
So I wonder if there exists in biology a species that could not reproduce without its symbiont.

I don't know why you are bringing up humans and machines but this is a pretty trivial question: yes of course, there are tons of examples.

@BryanKrause While I agree the human/machine bit is superfluous to the question (though it gives background in what the questioner was thinking), if you have "tons of examples", you can (and should) pick some illustrative ones and write up an answer, rather than snarking about its triviality.

@R.M. I meant merely to explain the reason for my downvote, because, as the alt-text for the downvote button notes: "This question does not show any research effort." Poor effort questions should not be answered.

To the exception of many Monocercomonoides (thanks @canadianer for pointing the exception), all eukaryote (incl. animals, plants, fungi and others but excl. bacteria) all have one or more types of endosymbionte (e.g. mitochondria) and cannot function without it. So yes, any eukaryote is an example.

The question of whether at this point mitochondria/chloroplasts/etc. count as separate organisms (and full symbionts) or rather they just originated as an endosymiont but are now just a part of the cell (and thus not technically a symbiont anymore) is one of perspective and thus whether it "counts" is a little fuzzy.

Tell this to Monocercomonoides.

Any obligate parasite would be an example.

An obligate parasite or holoparasite, is a parasitic organism that cannot complete its life-cycle without exploiting a suitable host. If an obligate parasite cannot obtain a host it will fail to reproduce.

How about Leishmania?


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What is this weed?
I first noticed this weed a few years ago, and saw its long, thin, V-shaped bean-shaped seed pods on meter height plants.  The pods start out connected together at the far end, but eventually separate into an inverted V.
If I recall, correctly, the thin pods split open to release very small seeds with a sail.
It somewhat resembles milkweed, but is branched, red stemmed and, of course, has these strange pods.
Location: My back yard, in Augusta County, in the Shenandoah Valley in Virginia.

You'd be better off asking for plant identification at https://gardening.stackexchange.com The people there would be more likely to identify it as many requests for plant identification come in.

My guess is Hemp Dogbane. The milkweed "family" has 140 species; all have milky sap. Add red stems, branching, downward-facing pods, and hemp dogbane comes up.

The flowers are white, not perfectly like common milkweed, and the pods hang down.

A photo with flowers and pods can be found here.
Hemp Dogbane is common throughout the country.


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What is this bird species in India?
I spotted this bird in India a day ago in a park located inside a city. There are no nearby water bodies around the park. The bird is slightly larger than the average person's fist. Does anyone know what species of bird is it?

Ardeidae perhaps?

Please describe the habitat you found it in. For example, in a park, in the forest, near some water, etc. Also please provide an approximate size.

@theforestecologist I've added some details to the post.

Looks to be either a chestnut-tailed starling (AKA grey-headed myna, Sturnia malabarica) or a Malabar starling (Sturnia blythii) in the Sturnidae (or starling) family.

S. blythii was previously considered a subspecies of S. malabarica.

 S. malabarica, Source: universebirds.com

 S. blythii on the left and S.malabarica on the right.
Description: Adults are approximately 20 cm long. They have grey heads/neck, blackish remiges, and reddish-brown (i.e., "rufous") belly and undertail. Their beaks are yellow with pale bluish bases.

The poor coloration in your photo seems to show the base of the beak being a paler grey color (vs. the yellow of the rest). I'm going to guess that this was really at least slightly bluish in hue and the color did not show up in your low-quality photo.

Range: As you can see in the map below, they are present throughout most of India:

 Source: Natural Earth and Myself

According to here, S. blythii is more constrained to just southwest India.

You can see videos of specimens here.
Further References:

Fina a list of most (all?) species of birds in India on Wikipedia.
Here is a good site with hundreds of photos of Indian bird species.


text:
Can DNA fingerprinting tell you if someone has been genetically engineered?
I am writing a fictional novel about an extensively genetically engineered man, unbeknownst to him, who gets into trouble on a regular basis. The man is physically large and strong, very fast (tiger-like hand speed), and he has exceptional sensibilities such as night vision, hearing and smell. The FBI gets some of his saliva from a crime scene and creates a DNA fingerprint from it.
My question/s is: could the technicians/scientists who perform the DNA fingerprinting procedure for the FBI be able to tell that this man is different from other humans? Would it be possible for someone to be human and have a different number of chromosomes? Does all DNA fingerprinting appear as bar codes and mean nothing until compared to a sample?
Please forgive my ignorance on the subject. Thank you for any input.
Chris

Can you clarify what you mean by "different from other humans"? I assume you mean could they tell he was super human, not just tell him apart from other people? If it's the latter then yes, since that's basically the point of fingerprinting.

You could try your question on WorldBuilding.SE, too. I'd expect there are some people there with a background in biology, at least enough to know some of these forensic techniques that are often of interest to the general public. There it would also be on-topic to ask in the style of "I want this to happen in my story, is this feasible?" for example, if you wanted a feasible way for your FBI to start to reveal the nature of this individual. @canadianer's example is about as far as we can go here without straying off topic.

Based on the answers below you could decide to have one or two  modifications that showed up as odd in the fingerprinting which leads to a whole genome sequence being determined. Especially if the story is set in the near future.

Could the technicians/scientists who perform the DNA fingerprinting procedure for the FBI be able to tell that this man is different from other humans?
If by different you mean genetically engineered, it depends on whether the loci tested have been engineered to such an extent that they are substantially different from other humans in order to arouse some kind of suspicion. There are other tests could be done that would show, at the least, that this individual's genome is abnormal.
Would it be possible for someone to be human and have a different number of chromosomes?
Yes, this is called aneuploidy and is the cause of many genetic disorders. Fingerprinting would not detect this.
Does all DNA fingerprinting appear as bar codes and mean nothing until compared to a sample?
DNA fingerprinting looks at sequence length polymorphisms and essentially tells you the length of certain regions of DNA in an individual. In fingerprinting, samples are compared to see whether DNA from two samples come from the same individual. A single sample obviously wouldn't work for this, but that doesn't mean it would tell you nothing.

Just to add, modern "fingerprinting" uses short tandem repeats that are (mostly) free of biological activity, so it seems unlikely that some engineered human would differ from his parents any more than their unmodified children would. And if there are new genes added on a new chromosome, well, those would be completely invisible to the technique unless it contained sufficient sequence similarity with one of the targeted STRs.

To answer the questions separately:
1 - "Could the scientists tell that this man is different from other humans?"
The functional basis of DNA fingerprinting, is to use regions of DNA that are known to be highly variable between individuals, such as micro- and minisatellites (short, highly repetitive stretches of DNA).
This is explained in fairly basic terminology on the wikipedia page for the topic.
As such, if your question means "can this be used to distinguish him from other people", then the answer is yes, absolutely. That's exactly why DNA fingerprinting is used in criminal trials etc.
If the question is "could the stretches of DNA used in the fingerprinting procedure show if someone is 'super-human'" then there are 2 issues I can think of:
The first is up to you:
You have the creative freedom to decide where in his DNA these alterations have been made. If the modifications are not in the areas that DNA fingerprinting would test, then no.
Since the modifications that would give marked phenotypic changes such as sight improvement etc. are likely to need be in coding DNA sequences (the ones that typically give rise to proteins, though this is an exceedingly loose definition), it's probably pretty implausible you'd be changing regions DNA fingerprinting examines. Tandem repeats dont generally have well known or defined biological roles. They're often referred to as 'junk DNA'. Though this term is falling out of favour as we're beginning to realise there are more subtleties to genome architecture.
Secondly, if we assume you do elect to modify some satellite sites, it would be extremely unlikely that this could ever be linked to 'super human' phenotypes. Determining whether or not a mutation, even in a coding sequence, where you can examine the protein product and the organism experimentally, has any biological effect, is still extremely hard to do. Not to mention, a vanishingly small number of spontaneous mutations in a sequence ever give rise to an 'improved' sequence.
2 -"Would it be possible for someone to be human and have a different number of chromosomes?"
Absolutely, this is a well documented condition, generally called aneuploidy. 'Ploidy' is the fancy term for chromosome copy number.
Down syndrome, AKA "Trisomy 21" is probably the most well known example of this. Sufferers are very definitely still human. As the scientific name implies, they have 3 copies (so 1 additional) of chromosome 21. It is also possible to be lacking chromosomes, as well as having additional copies (for example, Turner Syndrome.
3 -  "Does all DNA fingerprinting appear as bar codes and mean nothing until compared to a sample?"
Generally yes, you'd compare 2 samples to obtain an answer. You perform fingerprinting and sequence length polymorphism studies on your 'subject' sample, and on your 'reference' sample, and if they have the same banding pattern, you have a match. It will still contain information though. Those samples could be sent for sequencing for instance, which would tell you to even greater resolution, how similar 2 samples are.
EDIT
Just as a final thought (though getting a bit off the scope of the SE), if you did want the authorities to be able to tell that someone had been genetically modified, you could propose that those microsatellites are changed to something non-repetitive, which would potentially stand out. Or go even further and 'watermark' the genome, much like Venter et. al did, with the first synthetic genome (they incorporated a code to spell out messages in 'junk' regions of the genome).

Adding to what the two other answers have said, normal DNA fingerprinting tests do not tell the researcher how many chromosomes the organism has. That is part of a different process called karyotyping. However, karyotyping is actually surprisingly low-tech, people have been karyotyping for years before genetic sequencing was even a thing. That said, it is unlikely a researcher would think to look for karyotyping unless there was some evidence the subject suffered from a chromosomal disorder like Downs' syndrome or Turner syndrome.

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


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Are viruses more common due to modernity?
Is there any evidence to say whether in the past viruses like the cold virus were less common?  I wonder if high density living and globalisation mean that the cold virus mutates and spreads much more than in the past.
Perhaps in the past, owing to lower population density, slower and less frequent transport, viruses were effectively localised and isolated from the general population?  Of course that might not be true, as perhaps those things have been offset by improvements in sanitation and nutrition?  Perhaps virus frequency is always proportional to population size?

Generally, media was less common, so the knowledge about a virus spreading anywhere else then where you live was less common. But yes, what you mention did lead to some viruses spreading faster and further.

I remember reading a paper about the evolution of Bordatella pertussis (not a virus) and how it was influenced by increasing population density of humans several thousand years ago. I can try and find it again if you think it might provide an answer your question, or are you specifically asking about viruses and relatively recent history?

I'd rather think about it in the way that humans are more common due to modernity and that the abundance of human pathogens is a consequence of this main effect.

@canadianer The core question is about viruses like the common cold as they spread quicker than other diseases, but anything which can contextualise that over the long term is appreciated.

@AlexDeLarge Surely then that's demonstrable somehow?  If viruses correlate with population size, or whether population density and connectivity affects this?

Short answer: there are a lot of viruses, and they're all different. The answer to your question is going to be "it varies by virus". Some of the ways population density and urbanisation affect virus transmission are summarised very briefly below.
Population density
Any pathogen's ability to sustain itself relies on every infection causing, on average, at least one other infection. This is called the basic reproduction number or R0. The transmission rate of a pathogen depends on its transmission mode, but with some modes of transmission (like droplet transmission, a major route of transmission of viruses that cause the common cold) population density is important. There's an excellent explanation of density- versus frequency-dependent transmission here. This means that as people live at higher densities, the potential for transmission of some viruses increases purely because of that difference in density, while it has little effect on other viruses.
Critical community size
However, transmission rate is only part of the story. Assuming infected people eventually become immune, a pathogen can burn itself out before new hosts are born or immunity is lost. Stochastic effects become more important in small communities, and there is a critical community size below which pathogens tend to go extinct. Small or isolated communities cannot sustain the virus causing measles, for example.
Urban environments and transmission (and vector-borne diseases)
Urban environments aren't just higher density, they are different in potentially important ways. For example, some viruses need to be transmitted between vertebrate hosts by arthropod vectors like mosquitoes. If you don't have the mosquito, you can't get the virus. Viruses like yellow fever virus, dengue virus and Zika virus are primarily transmitted by Aedes aegypti, which nowadays breeds preferentially in urban environments, so as urbanisation increases the potential for transmission of these diseases also increases. Without adequate sanitation, the potential for faeco-oral transmission also increases at high population densities, for example. Things like sewage treatment, air conditioning and exposure to wildlife all affect transmission in important ways.
So, basically, it's complicated.


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How is there no limit to a human lifespan again?
It's probably just misconstrued pop science, but I thought a read an article recently that said there's no known limit on how long humans can live. I could have sworn though that there were a few automatic processes that took place though, like that the chromosomes all shorten in length every time they're copied (is there any limit to that? Also, why does that matter?), the retinas in the eyes harden, the metabolism slows down, the heart muscles wears out, etc.
So, how could it be true?

I'm not sure this is a very informative question without the original offending article.
Specifically I think the key is known limit. We here of people living to increasingly long lengths these days, and with regenerative medicine, this could go on for some time. We don't, and probably can't, know a definitive maximum age currently - even if one exists.

The quote is something akin to "ageing is plastic, and not a natural law". However, without the source material, it's hard to know how to answer this question. This video on ageing from one of my lecturers at undergrad might interest you.

Mm, no, it doesn't matter what the source material is here. It's a typical scenario, so if someone actually is accredited they will have the knowledge to speak to the phenomena either way, the same way a physicists doesn't need reference material if someone asks "are energy and mass really equivalent?"

You're probably reading about the recently-published responses to a publication that argued there is a limit to human lifespan.
The original article is Evidence for a limit to human lifespan, and in the June 29 issue of Nature there are five responses to it:

Contesting the evidence for limited human lifespan
Many possible maximum lifespan trajectories
Is there evidence for a limit to human lifespan?
Questionable evidence for a limit to human lifespan
Maximum human lifespan may increase to 125 years

Each of these responses has, in turn, a reply from the original authors.
The arguments turn on fairly intricate details of statistical analysis and database interpretation, and I think it's fair to say that outside experts remain unconvinced either way -- neither the original article, nor any of the five responses, nor any of the five responses to the responses, presents a slam-dunk case for or against a limit to human lifespan.

"It's therefore pretty pointless to discuss mechanisms how lifespan may or may not be limited, since it's entirely unclear if lifespan is limited and that's not likely to change in the near future." - You might reword this to make clear you are talking about the context of this particular question. Understanding whether lifespan is limited from a research standpoint will almost certainly involve understanding the mechanisms first.

I've removed that paragraph until I think of a better way to phrase it

There will be no "limit" to human lifespan, if for humans the "survival function" $l(x)$- the probability, for all subsequent ages $x$, that a newborn will still be alive at age $x$ - never hits $0$, but only asymptotes towards it. (The survival function is estimated by the fraction $l_x = \frac{N_x}{N_0}$, of a group of newborns, who in a cohort study are seen to still be alive at age $x$. For finite cohorts the fraction surviving of course will eventually hit $0$, when the last member dies, even if the idealized survival function does not.)
This is the case for "Gompertzian" survival functions, where $l(x)$ decreases super-exponentially, rapidly approaching but never hitting $0$.
(Gompertzian survival functions are more usually described in terms of their age-specific, instantaneous relative rate of decrease [the survival function's slope at age $x$, divided by its height at age $x$, times -1], which is also called the hazard rate or force of mortality $\mu_x = - \frac{{N'}_x}{N_x}$. For Gompertzian survival functions, the force of mortality grows exponentially with age.)
Human survival functions are roughly Gompertzian throughout most of adult life, although the force of mortality's growth may decelerate in very late life.

This type of logic doesn't apply to this problem. I agree with the responses in @iayork's answer that the original paper has some flaws, but you can't just say "because this model applies at ages we have observed, therefore this is true."


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Do mosquitoes squeeze in?
Practical motivation: I have equipped part of my windows with mosquito nets. Despite not opening the unequipped ones at night, I still have mosquitoes entering my flat. To decide whether I equip all windows with nets, I am wondering whether mosquitoes are likely to take advantage of other ways to enter the place: it is a 3-century old building, and in no way air tight. There is likely to remain gaps of about 2 mm width in many places, both at some edges of mosquito nets (although I could improve on these) but also around front door, etc.
Zoology questions :
Given the strategy I observe for mosquitoes who fly upfront to the net and explore randomly while hitting the net repeatedly, I am not sure they may detect a small opening away from larger ones, or will they?
I am also unsure whether they would squeeze for a distance longer than a few mm, since they do not appear to ever walk or crawl but only fly?


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DNA base pair heading
Does it make ANY difference to which strand of DNA double helix base pair heads? I mean, could base pair AT and base pair TA makes any difference when interpreted by biochemical mechanisms which use DNA?
Double helix has two strands, right? So does pair Adenine on the first and Thymine on the second strand make any difference with Adenine on the second and Thymine on the first?
I am a novice in biochemistry, so please excuse me my ignorance if the question is ridiculous.

Absolutely yes, is the short answer.
All genes are encoded in a  5-prime $\rightarrow$ 3-prime manner on each of the 2 DNA strands of the double helix.
Here's an example of a stretch of the genome from a bacteria that I work on in my PhD:

Each of the blue boxes is a separate gene. You can see they're able to be encoded on both strands, and run in opposite directions.
Consequently, whether a base pair is AT or TA changes the overall sequence, and would affect any gene which happens to span that base pair.

When reading the DNA during transcription, the strand that the gene resides on is called the Template (sometimes "Sense") strand.

The strand is separated by RNA polymerase enzymes, and it then uses the opposite strand of the DNA, known as the "anti-sense" strand, to create a copy of the gene sequence, but in RNA instead of DNA (and Thmidine bases are substituted for Uracil, as in the diagram).
Thus, the polymerase creates a mirror image of a mirror image, restoring the sequence of the original strand, but in it's RNA representation.
Flipping the bases round in the helix would change the sequence in the DNA molecule, and this would be propagated by the enzymes etc. which rely on it for transcription and replication.


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How do animals avoid the problem of inbreeding?
In humans, there are various cultural rules to avoid inbreeding (to the level of paternal cousins, nieces/nephews and uncles/aunts etc)
How do animals such as dogs avoid the problem of inbreeding? They do not have a record of their relatives and there seem to be many siblings in each batch for some animals. How does it work in the wild or among stray animals? Is their DNA somewhat resilient to these genetic disorders?
Likewise, how do birds handle this issue?
EDIT: I am not trying to breed animals, want to understand how it works in the uncontrolled wild when the young leave home early and are scattered.

Is it even a problem?  Especially when you consider the Darwinian effects.  That is, most animals produce far more offspring than needed to keep a stable population, so only the fittest survive to reproduce.  ("Fittest" here being a rather circular definition, as an individual that survives is fit.)  So if an instance of inbreeding produces unfit individuals, they don't survive.  And at the extreme, with a limited population some inbreeding might be necessary for species survival.

@jamesqf yes, I want to know if there is such a case observed in practice. It is known that cheetahs suffer from an inbreeding problem and the genetic makeup of any pair of cheetahs is currently too similar. How about other creatures?

@jamesqf Of course it's a problem. The very definition of "fitness" is based on progeny survival. Progeny represent a large energy investment, so there's should be (and is) strong selection to prevent individuals from generating large numbers of unfit offspring.  As the answer shows, there are in fact multiple mechanisms to prevent inbreeding, so observation supports theory.

@user1952500 There are widespread claims that cheetahs suffer from inbreeding problems but they're not well supported. It's clear that cheetahs are inbred, but very little evidence that it affects their reproductive efficiency. There are well-understood mechanisms by which inbreeding effects can be minimized (flushing of deleterious alleles) and it's likely that cheetahs went through those.

@iayork: That was my point, that there does not seem to be any significant adverse effects from occasional inbreeding.  Based on my (admittedly limited & unscientific) observation of animals & humans, I'm not entirely convinced that there really are effective prevention mechanisms other than dispersal, which of course has more obvious benefits.  Certainly among humans, avoidance of inbreeding seems to be more cultural than biological.  There are examples of cultures, like ancient Egypt, where it seems to have been common, at least among royalty.

Why not ask the question "Are there significant adverse effects from inbreeding"? The answer is "Yes, there are." On the other hand, many people seem to think that inbreeding is an instant guarantee of death, and they're wrong too.  As for prevention mechanisms, many have been put forward in @John's answer; there are far more than dispersal. Also, your claim of widespread inbreeding in Egypt is flat wrong. None of this is appropriate for comments, so ask a question (and read the answers) if you want your misconceptions to be corrected.

The question is interesting. However, it will be impossible to answer accurately for all birds as the mechanisms actually used vary from species to species. So I will give you some information in the general sense.
Recurrent inbreeding reduces inbreeding depression
Inbreeding depression is caused by both

Recessive deleterious alleles that are brought to homozygosity
Some epistatic interaction

In any case, in a population where inbreeding is common, those recessive deleterious alleles and alleles involves in these deleterious epistatic combinations will be washed out (or at least brought to lower frequency) of the population via selection and the population will end up suffering less from inbreeding than a typical outbreeding population. In the extreme, a population of exclusively selfer individuals, such deleterious recessive alleles are brought to extremely low frequency within lineages.
How to avoid inbreeding?
Now, sure animals and plants typically don't have a big book that allow them to tell how related they are to another individual. However, there are other mechanisms of kin detection
Self-incompatibility
For example, in plants self-incompatibility is thought to be relatively uncommon. There exist many mechanism, so I-ll just consider a simple example. Consider a self-incompatibility locus as a specific loci for which if the same allele is shared by both the pollen and the ovule, then no fertilization occurs. This prevents selfing and prevents mating with many of the closely related mechanisms.
Body odour and sexual attraction
Also, there are mechanism that can mediate sexual attraction toward individuals that differ. The classical example is Major histocompatibility complex (MHC) and sexual attraction (vertebrates), where individuals tend to be attracted to individuals that have a different MHC.

I was just curious about dogs because I have seen stray dogs in large numbers in some countries and wondered how they would handle it. I have not seen that many stray cats or other animals. There have been many wild birds as well, hence asked about them. They could apply to any animal in general.

I didn't downvote, but would encourage you not to use the terrible, terrible "research" that claims to show MHC compatibility effects in humans -- the so-called experiments are an embarrassment that showcase virtually every bad research practice there is.

@iayork I did not read that paper. I only went to the conclusion. I did not know, their experimental design was considered so bad. I removed the reference (and the associated claim) and will read the paper to make my own opinion on it. Thanks

The term you are looking for is Kin Detection. which is the methods of recognizing related organisms, important both for avoiding inbreeding and aiding relatives.
There are several known mechanisms.
First they can avoid it the same way humans, they don't want to mate with anyone they were raised with. Humans don't need an understanding of genealogical to avoid mating with kin. Humans have an aversion to to romance with anyone they shared meals with frequently as a child. It is called the Westermarck effect or sometimes reverse imprinting and is part of humans in built kin detection system. It can work with many method just by building a brain that sees those who were around when you were a child as likely kin and thus unattractive to downright sexually repulsive. It is not perfect, it can be confused by adoption or separation, but works fairly well in the natural human setting. in effect their "record" is simply their memory.
Smell is another known method, in animals with better senses of smell than humans can detect certain factors that would indicate relatedness, like genetically controlled urinary proteins or simply smells of familiar and thus likely related individuals. This can work hand in hand with the Westermarck effect. There is even some very preliminary evidence humans may use this method to some extent.
Basic dispersal patterns can also do this by behaviorally programming one sex to travel far from where they are born and the other to not do this, it decreases the chance they will end up mating with a relative.
Now the formalized study of inbreeding avoidance is relatively new, mostly due to the technology making detecting kin for the scientists easier being new, so more and more research will almost certainly find other methods as well.


text:
Where to start understanding chemical principles of human body?
I have no background in chemistry.
What is a good way to start understanding principles of human body - how it works, determine which meals are good or bad for health. Maybe it is not just chemistry, but some other fields, too. I just want to know how human body works, lets say - improve health - but on my own. Knowing just that this is not good for health is not enough for me. I want to build deep knowledge.
I want to know how it is functioning at the lower level (based on chemistry).
Where to start?
(sorry for my incompetence)

Biochemistry requires a strong understanding of (general) biology, molecular cell biology, chemistry and organic chemistry. I recommend beginning with basic chemistry if you're not already familiar.

If you want to start from the chemistry upwards I'd recommend you to either look into a biochemistry textbook (buy or borrow one/get a used one, since they are quite expensive) or look for some (online) courses in that field.
The textbooks I know from university studies are:

Biochemistry (Stryer, Berg, Tymoczko) [possibly downlaodable from here]

Biochemistry (Voet & Voet)
Lehninger Principles of Biochemistry (Cox, Nelson)

The MIT offers quite a few (free!) online courses and there seem to be quite a number of biochemistry ones (I haven't looked into any of them, but I reckon the MIT courses aren't too bad).

I did not find the prerequisities for Biochemistry (Stryer, Berg, Tymoczko). What should I know to start read this book?

@JúliusMarko If I remember correctly (I don't have anything at hand right now) the books contains a few chapters with basic information about the underlying chemistry. Maybe try the link I added to look into it.

Nicolai offered book (and other ressource) recommendations in biochemistry (+1). However, you might want to start with some very introductory general biology. For this purpose the Campbell Biology book is one of the best.
You can find the 11th edition here on Amazon.ca but it is quite pricy but if you can accept a slightly older edition (that will still teach you a lot) such as this one, then you can get away for much cheaper.


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Analyzing Messy Data Files
I was writing some code scripts to analyze some plasmodium spp. using this database. However the names assigned to the various epitopes and other items on the list is very very very disorganized. In some places there are acronyms and other places the full name. Sometimes hyphens replace the spaces for the same epitope name. So I was trying to collect lists of all the different names that are actually synonyms of each other. However there were some words that were added on sometimes that I wasn't sure would count as synonyms:

"xxx" and "xxx, putative" synonyms?
"xxx" and "xxx like antigen" synonyms? (this one made little sense to me as both are epitopes
"xxx" and "xxx 1" synonyms?
"xxx" and "xxx partial" close enough to    be synonyms for sake of
grouping?

I'm rather new at analyzing these sorts of databases. I'm sure I'll find other such messy naming issues and was wondering how to approach such a problem and solve such discrepancies.

The answer of David explains most of the common/general problems you encountered and how to tackle them. In case you don't have anyone more experienced to consult, I'll try to give suggestions for the specific cases you mentioned.

"xxx" and "xxx, putative"
These might synonyms, but the 'putative' indicates that the authors of the entry weren't sure themselves. If you want robust results don't group these together (or exclude the putative ones). If you need more samples, group them but maybe test how much difference it makes.
"xxx" and "xxx like antigen"
I think it's quite likely that many of these will not be synonyms. Many genes and proteins are named after similar known ones ('xxx' - known; 'xxx like' - new gene), but that doesn't mean they have related functions.
"xxx" and "xxx 1"
These could be synonyms. I don't know any examples where two different genes/proteins named like this exist. To be save you should check this on a case by case basis and look up both versions on uniprot or NCBI.
"xxx" and "xxx partial"
You can group these together. You're dealing with peptide  antigens, so fragments of proteins. Therefore partial proteins are not a problem.

Thanks! This answer helped a lot! Both of your answers did! :)

It’s not the fault of the database, it’s the fault of the individual scientists that described the epitopes. O.K. in a perfect world the curators would have gone through the entries and tried to standardize the descriptions. But they probably lack the time or expertise. I sympathize with them.
So what can you do? You have to use your own expertise or that of experimental scientists you are working with and make your own decisions, some of which will be incorrect.
This is a general problem with databases compiled from papers or individual submissions, and is a headache for data mining: misspellings, spaces or no spaces, hyphenated or not, different names for the same entity. Unfortunately there’s no fairy with a magic wand to solve the problem for you.

Thanks! I wish there were some kind of dictionary at least that kind of outlined some of the basic terminology(like when to use and when not to). I guess I've been spoiled by IUPAC in orgochem.


text:
Given an amino acid sequence, how to determine the structure (helix, beta sheet etc)?
Assume there's a short sequence of an amino acids.
MAKMGSKKKAGHGGKEKLENMGE

I am using molecular structuring softwares to look at secondary structure. But it's blackbox method. In plain theory, how to determine what structure the above peptide will fold into? There must be a basic set of rules, prior to all the complex maths, and modelling?
Based on basic rules I also want to know what and how a different amino acid contributes to the formation specificity.  Will add more details.

@BryanKrause that's helpful. But what I really want to know why? Like what bonds, interactions of these amino acids contributes to the specificity of forming helix or beta etc. How it is so. I will update my answer. Cheers.

@benCodigo A lot of that would just be on the wiki pages for those types of structures. eg: https://en.wikipedia.org/wiki/Alpha_helix#Structure

Afaik there are no excat rules for this. The methods are based on (known) statistics of the presence / absence of certain amino acids in helices and beta-sheets (e.g. proline and glycine almost never occur in helices)


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Play Mimicking Normal Behaviour In Cats
I tried to word my question so it will be given serious consideration. Rather than ask in Pets SE (which doesn't have the brightest questions or answers), I feel it's better suited for Biology SE - specifically animal behaviour.
Generally, the play behaviour of adult cats mimic their interaction with siblings when young, and as adults, their hunting behaviour. It's in regard to play mimicking hunting that my question likely fits best.
The stealthy stalk and pounce while playing is almost identical to what's used in actual hunting but with far more playful abandon. Leaping in the air to grab an escaping bird is seen when they leap and grab at a feathered toy that's whipped about. Tossing a small fuzzy weighted toy about mimics how they act when they've caught a mouse. The same with chasing after a small rolling ball.
But there's one play behaviour I can't find an equivalent. It's cats' fascination with a simple dangling string or cord. A person doesn't even need to move it. As long as it hangs and dangles near the ground, many cats can't resist playing with it. (I'm referring to an average active cat, not one of the unfortunate inbred creatures that do little.)
Does anyone know, or can think of, an equivalent natural behaviour that explains this? It's not similar to a mother cat flicking the tip of her tail as that involves tempting movement. But it's the closest thing I can think of. I've given this a lot of thought for a long time. Hopefully, someone else has wondered too and found a reason.
(No tags really fit my question so only one given.)

I dont have any sources for this, but I'm pretty sure this is somehow connected to a hunting instinct. Even though cats probably don't mistake the cord for actual hunting game, they have to learn and train hunting behaviours - therefore it makes evolutionary sense that they react to small movements in the environment (I'm imagining grass rustling) with hunting like behaviour.

Yes, I'm quite sure it relates to hunting behaviour too but what? I have a cord tied to my bathroom door handle. The cord doesn't move but my cat plays with it a lot. I've seen photos of cats playing with cords (as the internet is full of cat photos). I've even seen a photo of a cat happily playing with a rope tied to a horse's halter while the horse just stood there.

Your question is very well worded and it suits Bio SE. However, I'm afraid to say that the whole question is based on an wrong assumption: that the play behaviour is a preparation for hunting or that it's related somehow with adult behaviours. That's not the case. Play behaviours are one of the most complex branches of ethology and cognitive ethology in particular, and today we see play behaviours as complex behaviours that have their own reasons and objectives: it does not improve the hunting skills of the cats. A good answer here would be too long, unfortunately. Besides that, ...

... since it deals with cognitive ethology, the answerer will spend a lot of time and energy to write an answer that will probably attract a bunch of downvotes, not upvotes. PS: you also have the tag "ethology".

Thanks, Geraldo. I understand that any answer to my question would be very complex. I'm not a scientist, of course, but I've read articles dealing with ethology in wild and domesticated animals (which ones I could without a paid subscription to some of the journals). I can understand not all behaviour would be related to hunting but certain play behaviour, while some fit a range of mammals, many are specific to that species only. Do you have any suggestions that could point me to certain publications about cognitive ethology? Or are you allowed to do so?

Sure. This is a good science communication book, accessible to laymen (although very complex sometimes), and it has a chapter about play behaviour: https://mitpress.mit.edu/books/species-mind

I've never heard, read or seen photos of other animals attracting to a hanging cord. I'm curious how and why it proves so attractive to cats but not other animals (as far as I'm aware).

Complex is better as far as I'm concerned. I read science and nedical journals for recreation so I prefer something not readily understandable to most people. I appreciate the link. Thanks.

Gregory Bateson talks about play behavior in Steps to an Ecology of Mind and in Mind and Nature; @GerardoFurtado is correct that play behavior is much more complex than it appears. Not all animals play, for instance, but some play with other species, e.g, cats. Think about that a minute; this is not a simple evolved behavior.

jlawler, I fully realise it's not simple evolved or hard-wired behaviour. I'm not trying to imply it is in my question. But all animals are hard-wired with certain behaviour along with the ability to learn new ones. Often, though not always, new learned behaviour stems from or is related to other more hard-wired behaviour. I'm looking for the background of the dangling cord play (if there is one). Thanks for the book suggestion. Even if my question gets side-lined, I'm grateful for the chance to learn more on my own. I never take anyone's answer as 100% correct without  checking further.


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What is this fluffy bug?
I found this bug (actually he found me) while walking through some bushes in the city (Iași, Romania).
It is a small bug, a quarter of a fingernail, white and a fluff tail. He lays a white fluff on bushes (that is how I meet him, I brushed the bush and got the white fluff on me, when I wanted to clean it off I saw 2 moving on my shirt) and it seems they stay around it. I also found it near the plants, on a stone pavement, but I presume he got lost.

The overall shape suggests a leafhopper or planthopper of some type. I can't identify the exact species. But there are species known to produce white wax structures that might explain the fluff.

Based on the image and on the description, it could be a woolly aphid, a kind of insect that produces filaments of a waxy, cotton-like substance that gives them a fluffy appearance.
The images on Wikipedia aren't convincingly similar, but I found a better reference on abundantnature.com:


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Bug identification: rectangular green and copper creature
I've found a very strange-looking creature on the street of a local park (Russia, Urals). It was 2-3 cm long,  almost rectangular, with green and copper colors, running somewhere with low speed. I've never seen anything like it before. Here's a picture (sorry for the quality):

Does anybody know what this is?

I tried zooming in on this picture and wasn't able to; that having been said, from what I can see you have a mating pair of whatever these are (I do know the order, and think I know the family, but I am having a tough time locating a web-based resource that will help in a deeper identification).

@ArthurJFrost This is an interesting option. I think they would move more chaotically if they were mating (and this thing crossed a road on my eyes), but I'm no expert.

@ArthurJFrost you are correct, I see legs at both ends.

Some sort of Pentatomidae, but that's as close as I can get with this photo.


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What is this liriope looking plant?
They look like monkey grass, in the midst, a tall, skinny stem with bright orange flowers on top.
One of the plants, although it looks just like the others, has pink, purplish flowers instead of orange.
I would like to know what these are so I can start to take care of them properly.

Your question' better suited to Gardening SE where members can identify plants. As it is, I'm an active member there and the identity of these flowers are straightforward. They're all different cultivars of the daylily (plants in the Hemerocallis genus). If you use Google image search, you'll see photos of various cultivars. Basic structure:

Notice the flowers on a branched (or unbranched) scape (tall stem); leaves arise from the base of the plant. Flowers can be single or double (sometimes more); single flowers (as in your lower left photo) have six petals.
While Asian and Oriental lilies are toxic to pets (even the pollen is toxic to cats if they lick it off their fur), daylilies aren't. They're easy to tell apart as the daylily has long narrow strap-like leaves with flowers on stems with no leaves. Asian and Oriental lily have small leaves continue up the length of the stem like this -

This includes Easter lilies.
Daylilies are named for the reason individual flowers lasts only one day. But each stem has many buds on it that continue to mature over a few weeks so will produce flowers for about a month (as some stems don't have open flowers yet when the first stems start flowering).

Hi. I added a picture of a daylily as is customary on this site when identifying. Hope that's ok. If not, please feel free to roll back. :)

Again, I'm thankful for your extra help! I'm still learning what the protocol is (even though I've read through the Help section twice). I don't remember it all so your example helps me to remember.


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Caterpillar(?) in Leaf Cocoon identification - Missouri
A small chunk of leaves fell off of a potted tomato plant. We noticed our cats taking an interest in it once it started moving. Then a little caterpillar poked its head out. What kind of bug is this and should we worry about our plant?

Can you describe its size or take a photo with something for scale?

I apologize, the bug moved shortly after I took the picture and now I can't find it. It was pretty small. The pictures above probably show about 1cm of its body poking out and the diameter of the bug is less than half a cm, I would say.

Larvae making these sort of cases out of found material is typical for Bagworm Moths (Psychidae), but I don't know what species you have in Missouri. But it's a start if you don't get an answer here.

This is the larvae (caterpillar) of a bagworm moth (family Psychidae).

 Source: Wikimedia Commons; Credit: Bernard DUPONT
From Wikipedia:

The caterpillar larvae of the Psychidae construct cases out of silk and environmental materials such as sand, soil, lichen, or plant materials.

There are about 240 genera, so I will leave IDing to lower taxonomic levels up to you. However, based on the striations of the caterpillar and your lcoation, the Evergreen Bagworm Moth doesn't seem like a bad guess...


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Need help identifying multi-colored grasshopper
I was out hiking with my friend when we ran across what I presume to be a grasshopper. It didn't seem very startled by our presence, and we were able to get some pretty cool pictures. I've been having trouble finding out what species it is. I was hiking near Albuquerque, New Mexico, and the grasshopper was about 1 - 1.5 inches in size. It was about midday when I saw it.

Welcome to Biology.SE! Please take the (tour)[https://biology.stackexchange.com/tour]. Can you add some more detail to the post - where you saw this insect, when, and what size it was?

It's what's called a Rainbow or Painted Grasshopper (Dactylotum bicolor).

You can learn more at Bug Guide Species Dactylotum bicolor (where the picture is found) or Wikipedia' article on Dactylotum bicolor. The colour and pattern is very unmistakable.

I edited to add a picture (as is the custom when identifying something. Hope that's ok. :)

Perfectly fine if you edit it. I don't have enough time to help out in that department on SE so if others do, I'm only too happy for the help!


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Does a generator potential pass along a nerve the same way an action potential does?
I have read that a generator potential is a localized depolarization of a membrane. Does that mean that it does not pass along a neuron the same way an action potential does ? If not, then how do generator potentials from multiple rods in our eyes add up (converge) and trigger an action potential in a sensory neurone ?

Generator potentials (GP) are meant to generate action potentials (AP). An action potential results, whenever the level of depolarisation at a particular place crosses a threshold. This "place" is usually the beginning of an axon of a typical receptor, since it is equipped with all the channels required to begin and propagate an action potential. The purpose of the receptor architecture, then, is to make the threshold go off in a naturally meaningful situation.
There are two possible ways this is done. Say the neuron is transmitting information about the location of a stimulus. Then the "naturally meaningful threshold" would be some spatial cutoff, a minimum area that needs to be stimulated for the action potential to go off. Then, the receptor would have several GP-producing dendrites spread out, each generator potential being summed at the meeting place of the dendrites, which happens to be the cell body and the beginning place of the axon. So the individual generator potential in each dendrite will contribute to the sum, which will be summated and the cellular decision-making process (or a crude example of it) be affected as this summation.
Another way is temporal summation, something which has, for example only one GP-producing dendrite and the axon. Then, for the summated potential at the cell body to cross the threshold, the stimulus must stay, or be summated across, for some time-cutoff. GPs have some decay time, before which if another GP reaches there, it adds up. This would be meaningful in things like the presence or absence of a touch, the cutoff preventing against minor fluctuations.
This said, the situation in the eye in much much more complex. There are several layers of neurons and each neuron performs a lot of different functions and has a specialised architecture for it. The Rods and Cones actually produce hyperpolarizations and not depolarisations (theoretically, both are propagated in the same way, but hyperpolarisations themselves do not initiate AP).
To complicate further, most receptor systems alter the frequency of AP and thus have some basal frequency, this modulation also being important for encoding the message.
An image of GP:

Some of this answer is good but it has major problems. Photoreceptors do not fire action potentials, for example. It is also misleading to talk about "10 layers" of the retina in terms of how many "layers of neurons" there are. There are only 3 in the chain: photoreceptors, bipolar cells, and retinal ganglion cells. Amacrine and horizontal cells also modulate the activity in other cells, but they are not part of the serial transmission chain to the brain.

@BryanKrause I never said that they do. I did mention the modulation of frequency at the end of the paragraph as a general complication in several receptor systems. I did mention the 10 layers to only show the complexity, hence the caveat 10 layers of 'retina' and not neurons. Edited in the answer.

It seemed difficult to explain the retinal neural mechanism in a simple way. Hence, the preceding part is a general way in which GP work. Do let me know if anything needs correction.

I would suggest adding that action potentials are transmitted actively (trough activation of sodium and potassium channels), but localized potentials are transmitted passively with a time and space constant (cable theory).


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In which organs is water that we drink absorbed into the blood?
From biology classes I remember that water from food we eat is mostly 'sucked in' (absorbed into blood) in the colon. I guess the same is true for water we drink. But if I eat something, it will reach the  colon after say 4 hours, and if I drink a lot of water, I'd want to go to bathroom earlier than in 4 hours.
So is water absorbed not only in colon?
If it's absorbed in other organs, what % of it would be absorbed in each organ?

The internet is unanimous on this: some absorption takes place in the stomach, but most of the water is absorbed in the small intestine. Try searching Google: water absorption stomach

@AlanBoyd - The internet is not unanimous on anything as far as I know. Which site the information is obtained from matters a lot! (I agree with the small intestine, though.)

@anongoodnurse perhaps unanimous was a little strong, since I didn't check the entire internet (still working on it), but I think you'll find it difficult to find a relevant site that doesn't provide this information.

Role of the stomach in water absorption:
The absorption of much of the ingested water from a hypotonic food already starts in the stomach due to osmotic reasons.
If we study the mechanism of secretion of HCl by the oxyntic cells of the stomach, HCl secretion favours water osmosis from the blood to the lumen both for protective reasons as well as to maintain the osmotic balance of the gastric juice. This is predominantly the phenomenon in a filled stomach.
However, in the empty stomach, absorption of water is relatively more perceptible in the reverse direction upon water consumption.
Furthermore, the pyloric sphincter is usually open to the passage of water and electrolytes to empty to the duodenum. Thus, they may travel to the large intestine for absorption even before chyle. But this too is dependent on the empty or filled condition of the stomach, in which an empty stomach would pass the water and electrolytes in 5-6 minutes whereas in the filled stomach it could take 15 minutes or even more. Thus these factors may cause the early micturition to ensue.
Role of the small intestine in water absorption:
The small intestine, besides the transcellular pathway (through the cells), also facilitates water transport via the paracellular pathway. Thus it is more permeable to water osmosis than the stomach. Furthermore, the small intestinal segments duodenum, jejunum and ileum are differentially permeable to the absorption of different solutes. This facilitates the simultaneous absorption of water according to the osmotic gradient resulting from this differential absorption of the solutes, maintaining isosmoticity with the blood plasma.
However, this also has the implication that, when the digested products from the stomach (chyme) are hyperosmotic, water may flow from the blood in the villus to the intestinal lumen rather in the opposite direction until chyme is rendered isosmotic to the plasma.
Role of the large intestine in water absorption:
The large intestine is the key centre for water reabsorption rather than the stomach and the small intestine because of the following reasons:
a) It prevents most of the paracellular flow of water and electrolytes because of tight junctions, unlike in the small intestine. This prevents the back flow of electrolytes and water from the chyle to the blood.
b) The proximal colon is where most of the water reabsorption occurs as a consequence of major electrolyte intake. This region is highly active in the reabsorption of Na+ and Cl-.
c) It is mainly involved in concentrating the fecal matter, so reabsorption of water and electrolytes becomes its principle function.
For reference:
Textbook of Medical Physiology by Guyton and Hall

Can you recheck your references? Though water absorption does occur from/in the stomach, it is far from the primary site. Also, there is more to the GI tract that the stomach and intestines. There are the duodenum, jejunum, ileum, ascending, transverse and descending colon.


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What type of beetle is this?
I found this beetle in my yard. Wondering what type it is.

Please add the location. By the way, are you in California?

This is probably Prionus californicus, which is a coleopteran native to the American west.
Look at the serrate antennae:

Also, the abdomen looks like the one in your specimen:


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Could these be Mycetozoa?
I found this on a forest in Mexico City. It was kind of a warm day (around 15°C). It had been raining a few days prior and it was quite humid, but not suffocating.
This orange thing was on top of a rotting tree. I thought it could be Dictydiaethalium... maybe.
When I moved it it produced an orange slime.

Your second species ID request (i.e., Lycogala epidendrum) should be asked in a separate question. In general, please do not combine multiple species into a single ID question. Thanks!

Looks like a slime mold perhaps. See here for a picture of Tubifera ferruginosa, a visually similar looking species. EDIT: actually I see you suggest Dictydiaethalium, so you're thinking alogn the same lines as me. I'm no mycologist, so I'll leave the details up to someone else to figure out / answer


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What causes notches in elephants' ears?

What causes the elephants' ear to rip like this?
Is it a natural process as they get old, or it's injuries, like consequence of fighting with other elephants?

A natural process is something quite vague: this is a natural process, but it's not related to the elephant's ageing. Neither is it (normally) related to fighting.
Those notches and tears are caused by the daily activities of elephants, feeding in the bushes. The longer the ear, the more prone it is to damage. On the other hand, thicker ears are less prone to damage.
Day by day, the number and pattern of tears/notches/holes changes.
Curiously, this pattern of tears/notches/holes is used by researchers to identify individuals. Not only that, but also the pattern of the veins in the ears (you can see them in the left ear):

Thus, the same way the tail of a humpback whale or a human fingerprint is unique to each individual, so are the elephants' ears.
Sources:

http://voices.nationalgeographic.com/2013/08/16/name-that-elephant-how-to-identify-elephants-in-the-wild/
https://www.elephantvoices.org/support-now/814-how-to-use-ear-notches-and-tears-to-id-african-elephants-.html


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What, other than genetic factors, influence which individual survives a parasite and which perishes?
What factors other than "good genes" are at play in determining whether one individual survives a parasite and another individual in the same species perishes as a result of the same parasite?  For example, is there variation in the amount of the parasite (not in the amount of parasite species but in the amount of one species) with which an individual is infected and how might this occur?  I'm mainly interested in this first example, but another example:  Might infection occur at different parts of life-history in which vulnerability varies? (I am asking generally about any parasite species and any host species.)  Thank you very much.

@David, thank you for the edit.  Wondering if you have an opinion on the question.  For just one example, take the 1918 influenza crisis that killed 40 million people.  Does it make sense to suggest that some individuals just happened to be exposed but exposed to some dosage that was sublethal?

I am neither a parasitologist nor an immunologist, so these suggestions are only provided as a starting point and may meet valid criticisms from others. However, as your comment mentions the 1918 flu epidemic, a couple of general suggestions.
Assuming that resistance to pathogenic organisms can involve the immune response, then at least two factors that might affect that — and hence resulting mortality or morbidity are:
Nutrition:
It is popular wisdom that undernourished individuals are more susceptible to disease. This might have diverse causes, but there would appear to be an extensive literature on the role of nutrition in the immune response, e.g. this article by  Chandra has been highly cited.
Previous immune challenges: There is, of course, the classic case of milk maids being resistant to smallpox because of immunity provided by the related cowpox. Thus exposure to previous strains of a virus may provide some protection. Speculating widely here, there may also be affects on the non-specific components of the immune response (macrophages and whatever).


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Why do depleted blood veins seem to appear near the surface (or skin) more frequently than blood vessels and arteries?
I could be wrong, but it seems like blue veins generally exist closer to the surface of the body rather than red blood vessels and arteries. And I'm also wondering if this is evolutionary because during an injury, the outside gets damaged first, and I am just speculating that it's more important for muscle tissue to keep gaining blood from less damaged blood vessels than removing already depleted blood that simply bleeds anyway out due to the injury.
Or, if this is simply a trick of the color, that blue veins are just dramatically more noticeable and the first hypothesis is completely wrong.

Short Answer:
The veins you see are special veins right at the surface; major arteries are typically much deeper in the tissue.
Longer Answer:
Great question. Usually veins and arteries come in more or less one-to-one pairings, traveling side-by-side (often nerves accompany them as well). Both types of vessels tend to be fairly deep, because, as you note, damage to blood vessels can be quite problematic.
However, superficial veins, the ones you can typically see right under the surface of the skin, are different. They don't have a direct artery pairing, and they are not the only venous drainage from the areas distal to them.
Instead, superficial veins have a known purpose in temperature regulation. When core temperature is high, the superficial veins are relatively dilated to allow temperature exchange between the blood and outside. When core temperature is low, the superficial veins constrict to cause the blood to flow deeper and retain heat.
A nice side benefit to these superficial veins is that, because they aren't completely necessary for circulation, they can be harvested as surrogate vessels to divert around a blocked artery, like in coronary artery bypass grafting. The saphenous vein from the leg is often used. Superficial veins can also be removed for cosmetic reasons.

References
Webb-Peploe, M. M., & Shepherd, J. T. (1968). Responses of the superficial limb veins of the dog to changes in temperature. Circulation research, 22(6), 737-746.

Nice syrightforward easily understood explanation for those not adept in the physiology or biology.


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How many generations apart can a DNA test for blood relations be valid?
Suppose an American suspects he is a descendant of George Washington and he has a strand of hair of George Washington. Can a DNA test be done to prove that he is indeed a true descendant of the great Founding Father?
How many generations apart can a DNA test for ancestry still be valid?

What research have you done to answer this (interesting) question yourself? You might be interested in the question of Thomas Jefferson's offspring.

i would like to ask: " how many generations of parents can be found from all current people's dna? if all dna of all all current people is got, how many years of past parentship relations can be found from it? " but it is too short. would you like to edit your question that way?


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Background (null) distribution for higher observed frequency of an allele
I am testing the hypothesis that being heterozygote at a certain gene locus, say X, increases the chances of having the good allele of X compared to being homozygote. I have data of more than 6000 individuals with their zygosity for gene X. What could be the background distribution of allele frequency for testing the hypothesis if the observed frequency of good allele is more in heterozygotes compared to one expected by chance.
Thank you so much.

I'm voting to close this question as off-topic because it is not about biology but about statistics (see stats.SE). (Note: see comments under my answer for clarification about the nature of the question).

I don't really understand your hypothesis you want to test. Here are two things that may help you.
Test if allele frequency is the one expected from the genetic and demographic properties
The expected allele frequency is not that easy to calculate as you need much information. You need to know the mutation rate, the population size, the migration rate, assume random mating and most importantly know the selection coefficient associated with this allele. Once you've got all that, you'll find the equation in the old paper Wright 1937.
How to test?
Maximum likelihood ratio test is probably the way to go.
Test if heterozygosity is the one expected from the allele frequency
Now if you want to test if heterozygosity is not the one expected, it is much easier. The expected genotype frequencies are given by Hardy-Weinberg rule (see here for explanation on Hardy-Weinberg's rule and see here for the assumptions of this rule).
In short, for a bi-allelic loci with allele frequencies $p$ and $1-p$ the three genotype frequencies are $p^2$, $2p(1-p)$ and $(1-p)^2$, where $2p(1-p)$ is the frequency of heterozygote.
How to test?
You can simply do a chi-square test or a binomial test.

I ask if being heterozygote increases the odds of carrying a certain allele compared to being homozygote. So can I just compare the allele frequency in two populations (hetero- and homozygotes) using fisher exact t

Oh ok. If I understand you correctly, you have two loci. One for which heterozygosity is the variable of interest, while for the other locus, the variable of interest is the presence / absence of a certain allele is that right?
Sounds like your question is a pure question of statistics, not biology. Stats.SE is the place to go to but I will still try to address your question now that I started.
You can do a simple chi-square test you have the following 2 by 2 chi square table with the count of individuals in each cell
$$\begin{array}{c|c|c|}
 & \text{Homozygote} & \text{Heterozygote} \\ \hline
\text{Allele 1} & w & x \\ \hline
\text{Allele 2} & y & z \\ \hline
\end{array}$$
Now, that works well if you consider only a single, randomly picked allele per individual but that would reduce your sample size. If you pick both haplotype per individual, then I am not sure of whether you might suffer from pseudo-replication. In such case, you could do a logistic regression with a nominal random effect that is the individual ID. They will be better than me at giving you such advice on stats.SE though.

Dear Remi, thank you for the insights. I think my hypothesis is relatively simple but i could not phrase it well at first place. I ask if being heterozygote increases the odds of carrying a certain allele compared to being homozygote. So can I just compare the allele frequency in two populations (hetero- and homozygotes) using fisher exact test?


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Does translation have a way of preventing mismatching between mRNA codons and tRNA anti-codons?
What happens in translation if a tRNA with an inappropriate (non-cognate) anti-codon binds to the A-site of the ribosome carrying mRNA?
For example, what would happen if an ile tRNA with the anti-codon 3'-UAG-5' occupied the A-site when juxtaposed to a met codon: 5'-AUG-3'? This would seem possible to some extent as two of the three  bases pair correctly.
Does something prevent this occuring or are incorrect amino acids removed or the protein degraded?

Welcome to Biology.SE! Although it is an interesting question, its answer can be found quite easily. What research have you done before asking it here?

Its really unclear what you are asking, only three tRNA are present in the ribosome at any one time. The wiki for translation may help you. https://en.wikipedia.org/wiki/Translation_(biology)

John Btw I have edited my question  but still i would like to ask whether right tRNA interacting with the right codon in the mRNA is just permutation stuff.Like what would happen if a tRNA with anticodon AAA occupies the site of the codon with its nucleotides say,GGG.

I have edited this question quite extensively so that it addresses a non-trivial point which I don't believe is off-topic. It may be more sophisticated than the OP intended, but it represents a means of rescuing the question, as one is asked to do.

After the edits I think it's a valuable question +1. Thanks @David for your efforts. If folks disagree with the re-opening feel free to start another round of closure or flag the question.

Summary
Non-cognate codon–anticodon interactions on the ribosome do occur, but do not normally result in misincorporation of amino acids into protein. This is because aminoacyl-tRNA binds the ribosomal A-site in an EF-1A–aminoacyl-tRNA–GTP complex, and hydrolysis of GTP must occur before the peptide bond can form. The non-cognate interaction appears to be unable to trigger this hydrolysis and dissociates from the ribosome.
More Detailed Explanation
The hydrogen bonding between the bases of the mRNA codon and the tRNA anticodon is the basis of the specificity of decoding. It is easy to see that a codon such as 5’-GGG-3’ would form nine hydrogen bonds with an anticodon 3’-CCC-5’, but none with an anticodon 3’-AAA-5’. However, as the question makes clear, the situation is not quite so simple if two of the codon bases form the correct hydrogen bonds. A more telling example is shown below (here with the same tRNA, but different codons), where the difference between a his-tRNA interacting with a His codon and a Gln codon is only the strength of a GU ‘wobble’ base pair, often reckoned to be that of a single hydrogen bond. Certainly there is a difference in energy of the two interactions, but not enough to prevent a significant extent of miscoding.

The answer to this conundrum turned out to be the solution to another long-standing puzzle — that of why GTP is required in the binding of aminoacyl-tRNA to the A-site of the ribosome, which is directed by EF-1A (originally known in bacteria as EF-Tu). The GTP is not required for peptide-bond formation — the energy for that is supplied by the ATP in the tRNA synthetase reaction. It transpires that the role of GTP is in maintaining the fidelity of translation. The hydrolysis of GTP only occurs when the correct tRNA is bound — presumably the conformation of the incorrect interaction does not allow this to occur — so the non-cognate tRNA will eventually dissociate from the ribosome.

It is interesting that the other elongation factor, EF-2 (EF-G), involved in translocation of the peptidyl-tRNA, binds to the same site on the ribosome in a complex with GTP, and that translocation and removal of the deacylated tRNA can only occur after hydrolysis of GTP. It is as if the requirement for GTP hydrolysis ensures that the system is in the correct conformation before the next step of the complex process proceeds.
References
Berg et al. provides a general account, freely available online. A more detailed structural consideration can be found in a review by Nilsson and Nissen, which requires library access.

Thank you so much for taking your time to answer my question!!!


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What is this small insect called?
It is about 1-2 mm long. It also can fly and it stays on the wall.
Location: Lebanon.

Your country/state will help in getting an answer; a more-in-focus photo (if available) would also assist ... the best anyone can do at the moment is "it's a beetle."

It is in Lebanon. That's the maximum zoom my cell have. Sorry. I want to identify them so I can get rid of them.

If you are taking pictures with your cellphone it's usually better not to use the zoom. Cell phones, at least the ones I am aware of, don't usually have a real optical zoom, just a digital zoom. Essentially its the same thing as cropping the center out of a picture and then stretching it bigger. You don't actually get any more information.

It looks to me like a cigarette beetle- they can infest many different types of products so I would definitely check everything carefully. Here's the link I used as a source, you can find more info here: https://www.orkin.com/other/beetles/cigarette-beetles/

Welcome to Biology.SE! Although this answer might prove to be helpful, you still need to add more details and some images for comparison.