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Can humans ever directly see a few photons at a time? Can a human see a single photon?
I am not asking the following question: Can humans ever see a photon in the same way we see a chair?
My question is: Can a human retina respond to a single photon? If so, how does this happen and why is the retina able to "sense" (detect) a single photon?

Related Quora question

A single molecule of rhodopsin (actually the cis-retinal bound to it) can and actually does react to one photon (Purves et al. Chapter: Phototransduction in Neuroscience).

It has been estimated that a single light-activated rhodopsin molecule
  can activate 800 transducin molecules, roughly eight percent of the
  molecules on the disk surface. Although each transducin molecule
  activates only one phosphodiesterase molecule, each of these is in
  turn capable of catalyzing the breakdown of as many as six cGMP
  molecules. As a result, the absorption of a single photon by a
  rhodopsin molecule results in the closure of approximately 200 ion
  channels, or about 2% of the number of channels in each rod that are
  open in the dark. This number of channel closures causes a net change
  in the membrane potential of about 1 mV.

Photoreceptor cells continuously secrete the neurotransmitter glutamate in dark; with light exposure glutamate release would reduce. This leads to activation of the next line of cells (bipolar, horizontal cells and retinal ganglion cells).

 Modelled relationship between glutamate release and rod membrane potential.  From Witkovsky et al. (1997).

From this model (Witkovsky et al. 1997) it appears that for a change in glutamate release rate, a larger change in membrane potential is needed. Moreover, the depolarization of the photoreceptors has to be sustained for a while so that downstream cells can react (light absorption is much much faster than biochemical processes). The lifetime of an activated rhodopsin molecule is ~40ms in mice (Gross and Burns, 2010) and ~400ms in salamanders (Lyubarsky et al., 1996). We can assume that human eye is more similar to that of mice. There are approximately 40,000,000 molecules of rhodopsin in a rod cell (BioNumbers). The most sensitive of retinal ganglion cells need ~0.04% of rhodopsin molecules per rod cell to be activated (Takeshita et al., 2017).

(b) Absolute threshold of On and Off retinal ganglion cells
Both On and Off RGCs carry rich information about the weakest light
  signals. Off cells are somewhat more sensitive than On cells but have
  a higher error rate in their gap-based coding. The absolute threshold
  for primate On and Off parasol cells in a two-alternative
  forced-choice task is extremely close to the limits posed by the
  quantal nature of light: On parasols reach 75% correct choices at a
  light level corresponding to approximately 0.0008 R* per rod per flash
  (mean, n = 6) and Off parasols at a light level corresponding to
  approximately 0.0004 R* per rod per flash (mean, n = 5).

A single activated rhodopsin molecule would be 0.0000025% of the total. This would be insufficient to activate an RGC.
So, I can make a reliable guess that you cannot actually "see" a photon although one of the retinal photoreceptor cells can sense it. However, I'm still looking for a solid reference that says how many photons are needed (and for how long) to produce a visual response.

A single photon is sufficient to elicit a somewhat reliable response (whether this counts as "seeing" is open to debate, but seems to fit the OP's criterion): https://www.nature.com/articles/ncomms12172#discussion

Another thing to add would be that if our eyes were good enough to reliably grab single photons, we'd have great night vision. Your cats might stand a better chance, though it's much harder to determine if they have actually "seen" anything or not. Moreover, if our eyes were good enough in that regard, we might even have discovered photons and quantum mechanics earlier than we did in our actual history, by trying to figure out why that very dim light gets "staticky".

I've been looking for a reference on how many photons are need for threshold perception, for a while. For some reason the number seven to ten photons knocks around physics teaching circles, but I have no idea where it comes from.

The numbers I remember having heard are 10 photons per second sustained exposure or 100 photons in a single burst

A recent study published in Nature by Tinsley et al. Direct detection of a single photon by humans found that it is possible for dark-adapted humans to respond to a single-photon stimulus, but only rarely. They used a source which created pairs of photons, and used one of the pair to determine whether the subject may have been exposed to a single photon. The subjects were asked to respond whether they had seen a single photon after an event, and to rate their confidence in their response on a scale of 1-3. Of the highest confidence trials, $60\% \pm 0.3 \% \space (P=0.001)$ of responses were correct. Not exactly reliable, but strong evidence that it is possible.
They also interestingly found that the detection efficiency was highly increased if another single photon was emitted in the previous ~3.5 seconds.
As far as mechanisms, I'm no biologist or biochemist so I'll suggest reading section III from Rieke & Baylor (1998) Single-photon detection by rod cells of the retina, which covers it in detail.

Interesting. I just skimmed through the article. The concept does not sound very convincing to me but I'll read it more carefully and check if there have been any replies to this finding.

Neither P=0.001 nor 60% of correct responses sound like proof beyond reasonable doubt.

@DmitryGrigoryev very hard to believe without a molecular explanation.

@WYSIWYG It's definitely open to bias as any psychophysics experiment is, but the paper gives me the impression that it was very carefully undertaken. The concept seems to be essentially the same one that's been used for decades, just with a much better source

I wonder if they broke that down by person? If this was a biological difference, I'd expect the accuracy to vary by person (e.g. one person was 90% correct, another was 30% correct, leading to a 60% overall accuracy)

@NicHartley they state somewhere in there or the supplementals that they didn't have good enough individual-subject statistics to do that convincingly, but that people took a few sessions to get good at it

@DmitryGrigoryev a lot of biology uses p<0.05. At 0.001, its fairly strong evidence that people are better than a coin flip (but still pretty bad!) at detecting single photons.

@mbrig Or perhaps people are good at detecting something correlated with the photon emission (like noise), but not everyone figured that out.

@DmitryGrigoryev they both minimised (sound damping foam, fibre to couple light into room a distance from source) and tested for that. The efficiency of the single photon source is low, because if you crank it up you get significant numbers of multiphoton events. Most trials (92%) actually had no photons, although they would have had every other possible signal that would bias a subject. "in these trials the probability of correct response was not different from the baseline for both the combined and the high-confidence responses (0.505±0.003, P=0.08 and 0.507±0.01, P=0.3, respectively)"

I haven't read the paper but I wouldn't be surprised if the better than chance performance is an example of stochastic resonance.

Technically, we can sense the individual photons. Here is an quote from a cellular biology textbook:
"Absorption of a single photon of light induces a conformational
change in the rhodopsin molecule, which transmits a signal to a heterotrimeric G protein (called transducin ), which activates a coupled
effector." (Karp's Cell and Molecular Biology 8e, 603).
However, we have neural filters (part of evolution/adaptation) that only "see" light if somewhere around 5-9 photons are detected within a 100 ms period. Here is a source for this.
According to that source, this neural filter is actually an evolutionary advantage, as it will prevent unnecessary visual data from being processed (which would add a lot of noise to the "images" we see).
However, something interesting is that frogs can actually detect and see single photons of light. I remember watching a video some time back where it was explained as follows: If a frog is launched to the outer edges of our solar system (where photon density from the sun is very little), time-to-time a single photon will enter the frog's eye, and the frog will see flashes of this light, while seeing darkness when photons aren't entering. You can Google more about these frogs, or read a summary of it on The seeing power of frogs: Frogs can detect single photons of light.
Edit: As WYSIWYG pointed out, frogs aren't so special after all! There are more than one organisms that can "see" (not just sense) these individual photons.
Hope this helps!

@WYSIWYG Hi, I read it from this source for my class last year: http://math.ucr.edu/home/baez/physics/Quantum/see_a_photon.html

@WYSIWYG I guess it's in one (or all?) of those: `Julie Schnapf, "How Photoreceptors Respond to Light", Scientific American, April 1987
S. Hecht, S. Schlaer and M.H. Pirenne, "Energy, Quanta and vision."  Journal of the Optical Society of America, 38, 196-208 (1942)
D.A. Baylor, T.D. Lamb, K.W. Yau, "Response of retinal rods to single photons."  Journal of Physiology, Lond. 288, 613-634 (1979)`

@F16Falcon I just found that the lifetime of activated rhodopsin is longer in salamander than in mouse. Not sure about frogs but photoreceptors of different organisms can have different sensitivities.

@WYSIWYG Yes they can, and the frog was just an example that I wanted to give because it was fascinating to me. I didn't know about other organisms that did this, so thanks for sharing! Also, that is the original document I read (I didn't read the full research papers); Vaxquis is correct.


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What is it called when a dead flower is rotted away and only the veins remain?
I've spotted a flower that is dead:

It looks like most of the tissue has rotted away and only the veins remain.
(Sorry, I don't know the proper name for flower veins).
What is the technical term for this phenomenon?

Retting could be a valid term. But I think that the term "skeletonization" is more common. For instance here is a link to the University of Arizona showing how you would take a flower or a leaf and remove all components, leaving the veins:
Skeletonization
I think that "retting" is confined to the industrial harvesting of plants like flax. I would use the term "skeletonization" to include acts of botanical science in which the veins alone were sought. For instance in the above link the botanist Frederick Ruysch published a method of chemical skeletonization in his book Adversariorum Anatomico - Medico - Chirurgicorum Decas Tertia in 1723.
It also became a form of art and craft in the late 1800's in the United States; "Skeleton Leaves & Phantom Flowers" was published by E.Parrish. I would assume that the end result as a craft would be to display the skeletonized flowers or leaves on a display board.
As a natural, observed event the term skeletonization could be used. But if the  underlying causes such as fungus were considered then both rot, or fungal rot, and skeletonization might be used together in the same sentence. The wikipedia entry skeletonization considers animal decomposition. It's a reasonable and analogous step to use the same term for plants that decompose and leave fibres rather than bones.

I learned something new today! +1

Thats is great! I enjoyed researching it!

I have heard the process that leads to this called retting.

source: Stack Exchange

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

sort: votes


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What determines the direction in which motor proteins go?
I know that kinesin motor proteins move towards the positive (beta) end of the microtubule, while dyenin motor proteins move towards the negative (alpha) end of the microtubule. However, because the microtubule is composed of repeating alpha and beta units in ABABABABAB fashion (as shown in the picture below), what causes motor proteins to move to the positive rather than the negative pole?
For example, if one "leg" of the kinesin is bound to a beta tubulin while the other leg is up and ready to bind again, what determines which alpha tubulin it binds to (since there is alpha in front and in back of the beta tubilin it is bound to)?

While you're entirely correct that the ABABAB sequence is symmetric to a motor protein cruising along, the individual $\alpha$ and $\beta$ monomers themselves are not symmetric along the axis of movement (or any axis at all, as far as I can tell). This produces a polarity that can be seen in the figure below, from the original 1998 paper describing it.

The figure you use above to display the microtubule is slightly misleading in this way; it shows the subunits as blobby spheres. However, the motor proteins are able to distinguish the top of these molecules from the bottom, seeking a unique set of loops and helices to attach to. As it walks, then, the motor protein can only bind to one side (pole) of the subunit and is unable to walk backwards.

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


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Can anyone identify this tiny insect?
Very high magnification, size of a very small ant. Found in Menorca, spain

define "very small ant". One millimeter in length?

I would say 2mm/3mm but that's a guesstimate now as these have gone.

These are Barklice (order "Psocoptera"); the out-of-focus photo will probably forbid going deeper.

That's a barklouse, order Psocoptera. https://en.wikipedia.org/wiki/Psocoptera
It's very hard to identify those to species in a picture.


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Why is there a weevil on top of a beetle?
A click beetle was walking around and there is a weevil on top of it.
Any idea why? I would also like to know the exact species of these insects.
 !
Time: 18:50, place: Netherlands / Noord-Hollands / Overveen / the Amsterdamse waterleiding duinen / it's in the dunes near forest and grasslands near the dunes

Where and when was the picture taken?

That's probably a small male mating with a big female. Like in this photo: https://www.naturepl.com/stock-photo-dor-beetle-geotrupes-stercorarius-smaller-male-riding-on-back-of-image01585111.html

@personjerry No, they are completely different species from different families; Curculionidae and Elateridae it seems.

Just to be clear; for species-ID questions we consider them off-topic (Too broad) if they do not contain time and location (and preferably the environment and circumstances for the observation).

Time: 18:50, place: Netherlands / Noord-Hollands / Overveen / the Amsterdamse waterleiding duinen / it's in the dunes near forest and grasslands near the dunes. Thanks for the family names! I just really wonder why the click beetle was giving a "beetle ride" to the weevil. I thought that maybe the weevil was sucking out the beetle, but weevils only suck on trees right?


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How does the inability to produce vitamin C helped weight gain?
I recently wondered how do dogs cope without vitamin C intake like us.
A few Wikipedia pages later, I learned that our dry-nosed ancestors lost about two-thirds of the gene responsible for vitamin C synthesis some 63 millions years ago. And then this passage:

Johnson et al. have hypothesized that the mutation of the GULOP (pseudogene that produces L-gulonolactone oxidase) so that it stopped producing GULO may have been of benefit to early primates by increasing uric acid levels and enhancing fructose effects on weight gain and fat accumulation. With a shortage of food supplies this gave mutants survival advantage.

(Wikipedia: L-gulonolactone oxidase)
I'm curious about the interaction (GULO/uric acid/fructose effects/fat storage) quoted above.

The effect comes indirectly since lower levels of ascorbate increases urate levels, according to

Arthritis Rheum. 2005 Jun;52(6):1843-7.
The effects of vitamin C supplementation on serum concentrations of
  uric acid: results of a randomized controlled trial.
Huang HY1, Appel
  LJ, Choi MJ, Gelber AC, Charleston J, Norkus EP, Miller ER 3rd.

So the direct weight gain effect is due to increased levels of uric acid.
Further in the chain of events is that

Recent studies show that fructose-induced uric acid generation causes
  mitochondrial oxidative stress that stimulates fat accumulation
  independent of excessive caloric intake.

according to

Diabetes 2013 Oct; 62(10): 3307-3315.
Sugar, Uric Acid, and the Etiology of Diabetes and Obesity
Richard J. Johnson1,2⇑, Takahiko Nakagawa1,3, L. Gabriela Sanchez-Lozada4, Mohamed Shafiu5, Shikha Sundaram6, Myphuong Le1, Takuji Ishimoto1, Yuri Y. Sautin7 and Miguel A. Lanaspa1

Thanks. What remains unclear to me is the GULO/uric acid/fructose effects/fat storage interaction, i.e., the how.

Doesn't the article tell? I can't look into it until after several days, although I am interested in this as well. I think the cure is to restore GULO and urate oxidase. It seems to benefit our health.

I haven't accepted before because I haven't seen the Jul 28 edit you've made, we last corresponded on Jul 26. Thanks for the edit and the reminder.


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If plants "alternate generations" between sporophytes and gametophytes, why don't we say the same of humans?
I've been reading on Wikipedia about how plants alternate generations between a diploid sporophyte (usually the dominant part) and haploid gametophyte (in flowering plants, the pollen and ovule sacs).
Mammals also produce haploid gametes. But in mammals we don't describe the gametes as a separate generation that alternates with the dominant "sporoid." The gametes are just the organism's means of reproduction.
What is it about plant reproduction that warrants describing their gametes as a separate "generation" or "phase"?

Well, I do. But my biologist friends don't find it funny.

There's an old joke that a zygote is just a gamete's way of producing more gametes.

The big difference is that in humans, there is no mitosis in the haploid phase.
There are three terms that are important here:

Haplontic: Most of the life is spent in the haploid phase
Diplontic: Most of the life is spent in the diploid phase
Haplodiplontic (aka. diplohaplontic): About as much time is spent in the haploid phase than in the diploid phase

At the extreme, when there is absolutely no mitosis in one of the phase, then the organism is clearly not haplodiplontic. Haplodiplontic organisms have an alternation of generations.
Note that the term alternation of generations is also used for systems that are much more complex than haplodiplontie. Examples of such complex alternation of generation include many parasites such as the giant liver fluke

Hmm, I guess the follow-up question would be why plants benefit from haploid mitosis, while mammals do not? Is it merely divergent evolution, or is there some conditions that make it more useful for plants or v.v.?

This is a good question but one that is difficult to answer. I don't think a clear consensus has been reached on this question but there certainly are some research (there certainly are some theoretical models at least). I opened a new post (here) to ask this question and we will see if someone can come up with a nice answer

@JAD In addition to the hypothesis in Remi.b's linked question, you can check out one of our canonical answers here: https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont which might also apply to some extent.


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Why does it take 24 hours for tendons to give feedback on whether the loads they received were excessive?
I heard in this interview of Jill Cook (tendon researcher) on https://youtu.be/GKkSp-TlofI?t=230:

Tendons talk to you 24 hours later. So what happens if if I put load on a tendon today, it will tell me tomorrow it's been happy with the load.

Why does it take 24 hours for tendons to give feedback on whether the loads they received were excessive?

In this article, they say that they believe any pain that lasts more than 24h during rehabilitation should be considered a contraindication. No reference was cited for this reasoning. I believe it takes 24h for recovery. My suggestion is that you write to the author herself asking for the relevant reference. You can then post that as an answer. It is unlikely that you would receive an answer here because this is a very specialized topic.

It sounds like the person in the interview was referring to delayed onset muscle soreness, of which there is an interesting wikipedia article


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How to get ants/termites to attack
I am working on ant resistant coatings that are meant to make a material resistant to ants or chewing through them. The question is - how do I get ants to attack the material?
I have considered leaving a plastic bag full of water that is coated in the material outside of an ant hill. Does anyone have any suggestions?

Sugar and grease are strong ant attractors.

It is possible that a sugar solution could work. I would not have expected grease. Is there a specific type of grease that is the most effective?


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Evolution of the haplo-diplontic life cycle
From wikipedia > Biological Life Cycle:

haplontic life cycle - the haploid stage is multicellular and the diploid stage is a single cell, meiosis is "zygotic".
diplontic life cycle - the diploid stage is multicellular and haploid gametes are formed, meiosis is "gametic".
haplodiplontic life cycle [..] - multicellular diploid and haploid stages occur, meiosis is "sporic".

To my knowledge, all mammal species are diplontic. It might even be true for all vertebrates (but I am not sure). In plants and in fungi, there is a much greater diversity of life cycle however. In many (all?) bryophytes for example, the sporophyte (the diploid phase) is multicellular and its life is completely dependent on the gametophyte. This diversity of life cycle lead to the following question:
What drives the evolution of the relative time an organism spend in the haploid vs in the diploid phase of the life cycle?

This post comes as a follow up to @JAD's comment here

I appreciate that English is not your first language, but at 60k you can surely come up with a clearer title and question. How can “relative importance” evolve (either in English or French)? Are you sure your question can’t be rephrased to something like “What determines the relative…”?

By "relative importance", I was referring to the ratio of time spent in the diploid pahse over the time spent in the haploid phase (or the same ratio but in terms of number of mitosis). I chose "What drive the evolution" to clarify my question was about the evolutionary pressures and not about the physiology. I made a few edits but please feel free to edit it yourself if you can improve language and clarity.

I’d rather you do it yourself. I’m sure you’re able to. The title can be simplified because it’s just a title. Think about the question. Two sentences is often the solution.

I just want to report the finding of one paper here. I don't know much about the rest of the literature and can't comment on it.
Otto et al. (2015) investigate this question in sexually reproducing organisms. As I understand it, they assume that the amount of time spent in on phase of the life cycle is proportional to the amount of selection happening in this phase. With a theoretical model Otto et al. (2015) showed that there is a sexual conflict over the length of the haploid phase. Mothers favour a longer haploid phase while fathers favour a shorter haploid phase. The outcome of the model depends upon who is in control of the length of this phase.
For mothers, producing a baby is often costly (see Bateman's principle). As such, the mother might want to ensure that its baby has high fitness. In the haploid phase, deleterious recessive alleles are no masked by their dominant counterpart and hence can be purged out of the population. A long haploid phase, therefore allows purging of deleterious alleles and make the diploid phase more resistant which is in the mothers interest.
Among fathers, the evolutionary pressures are different. Fathers evolve to mask mutations carried by their haploid gametes (e.g., by provisioning with diploid gene products), causing their sperm to be more competitive. As such, a father has interest that the haploid phase is short.


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What is this insect in a cocoon climbing a web?
I found this thing hanging from the framework of my garage yesterday:

The size of the object in the picture was about .75 inches tall by maybe a quarter inch wide. This was taken yesterday in a suburb of Jacksonville, Florida, US in late evening (8:30 pm?).
He was (apparently) using his mouth-parts to draw in what appeared to be a strand of spiderweb, and in about 10 minutes had drawn himself upward, towards the top of the garage framework, a total distance of about two feet.
An additional question would be what is that he's in, a cocoon? a piece of bark or something being used like a hermit crab uses a scavenged shell?
Any help would be appreciated!

You're much more likely to get reasonable answers if you remove the silliness from your question and use an informative title. Also make sure you adhere to the species identification guidelines.

I edited the post to remove the alien nonsense the OP included. I opted to edit the post so to avoid attracting further downvotes given that it's an interesting specimen and the post follows the [tag:species-identification] guidelines otherwise. @Chowzen, in the future please keep your posts professional and to the point. Ideally, when asked to edit your post, you should [edit] on your own to avoid closure. Thanks.

That is, probable, a Psychidae (Lepidoptera), commonly known as bagworms. They build those "bags" with pieces of wood, twigs and leaves, and they protect them from predators and parasitoids. One possible species for Florida is this one: https://en.wikipedia.org/wiki/Evergreen_bagworm


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Are these 2 procedures to fight cancer (cancer "vaccine", and cancer drugs which can attack all tumours) related?
Last year appeared the new of a cancer "vaccine" (not a vaccine in the traditional sense) tested in animals for 4 types of cancer and which worked in 97% of the cases to eliminate already existent tumours.
Cancer Vaccine Trial
Now appeared the new of "cancer drugs which can attack all tumours" to be fast-tracked by NHS.
Game changing cancer drugs can attack tumours
I would like to know if both procedures are based in similar ideas (meaning the second one could have a similar effectiveness to the first one) or if they are completely unrelated.

The first source (Science Direct) says that the "vaccine" treatment stimulates T cells to attack cancer. In general, this treatment is intended for all tumors and has been very successful in studies in mice. Cancer.net and Cancerresearchuk describe cancer treatment vaccines in a bit more detail.
The second source (Telegraph.co.uk) mentions “tumor agnostic” or "tissue agnostic" drugs, which target tumors according to their genetic make-up, rather than the tissue from which they arise. This treatment is intended only for specific tumors with known genetic mutations. Examples of tissue-agnostic drugs are pembrolizumab and larotrectinib, which are approved by FDA for treatment of certain metastatic solid tumors.
So, these are two different ideas and most of these drugs are currently in a research phase.

in complement to Jan's answer, the 2 therapies discussed here are unrelated. The first one stimulates T cells locally at/around the tumor site with TLR ligands and is a class of immunotherapy, while the second one aims at shrinking the tumor cells by targeting some genetic alterations. Note that the second one may induce immunogenicity


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Application of molecular dynamics simulation (or alternatives) for the full pathways of protein interactions?
If one would like to control the biological system (e.g. to treat disease or aging/senescence) then one should introduce the drugs in the system, that initiate complex protein interaction pathways that (in final) generate the necessary proteins that induce the necessary biological mechanisms without adverse side effects from additional outcomes.
I am reading https://www.ncbi.nlm.nih.gov/pubmed/29139324 article about application of molecular dynamics simulation to the drug discovery but this article is essentially about simulation of one - target protein/molecule. My question is this: are there methods (molecular dynamics or others) that simulates the processes in the extended protein pathways that are induced by the one or more initiating molecules/drugs? It should be quite complex simulation, but nevertheless nothing less is expected from computational drug discovery and engineering.
I am quite confused. Maybe there is no need for such simulation at all? The databases of protein interactions just provide the more or less complete picture what protein interactions leads to what new proteins or structural updates of participating proteins and there is nothing to simulate - there is just empirical or predicted knowledge about what molecules leads to what other molecules/structures and one just extract the relevant pathway (starting from the drug coming close to the initial proteins) from the database and that is it?

MD is used for studying structural changes. Simulation of biochemical pathways involves the kinetics (you are not really looking at how enzyme structure changes when it binds to substrate). You can certainly pool all the modelling strategies together to make a hybrid multiscale model.
There are many people who work on such kind of modelling approaches. You can search multiscale modelling and check out recent reviews. This is a somewhat recent (2016) review on multiscale modelling of pharmacokinetics-pharmacodynamics.


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Can the body always find the right antibodies?
If the body produces random antibodies in order to fight a virus, is there a small chance that the specific antibody needed to fight the virus just won't be randomly generated? Even though it is a common virus that normally doesn't kill people?
For example if you have a common cold, is there a small chance that you could die from this just by probability? Whereas someone else won't because they randomly produced the right antibody?

Yes and no. Yes, it's possible that some individuals won't be able to (or happen to) make antibodies to a specific part of a pathogen. But most pathogens are large and complex enough that they have many different targets for antibodies, and it becomes increasingly unlikely that someone won't be able to target any part of the pathogen.
An example is given in Influence of Immune Priming and Egg Adaptation in the Vaccine on Antibody Responses to Circulating A(H1N1)pdm09 Viruses After Influenza Vaccination in Adults. A subset of adults (who were exposed to a particular influenza virus as children) have poor antibody responses to a vaccine to a different strain of influenza virus:

Significantly reduced antibody reactivity to circulating viruses bearing K163Q was observed only in the USSR/77-primed cohort, whereas significantly lower reactivity caused by egg-adapted Q223R change was detected across all 3 cohorts.

(This is not an argument against vaccination, I feel obliged to point out, because the vaccinated people were still better off than unvaccinated, just not as well protected as they could be.)


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Limitations of the Self-Incompatibility Mechanism in Plants
For a given plant species, how many types of S-loci exists to prevent self-pollination? I would like to know how often a plant stops fertilization process by other plants, thinking the pollens belong to itself due to limitations of SSI/GSI.

The answer is going to vary dramatically depending on the species.
Have you checked wikipedia?

An examples suffices.

I think you mean to ask how many self-incompatibility alleles generally segregate in natural populations? (@tyersome gives a reasonable answer). I cannot tell if you instead mean how many different S-locus systems (mechanisms) exist. I am happy to provide an alternative answer if you clarify.

Herrera, Sara et al. 2018 suggest that there are at least 33 S-alleles in apricot.
I believe some species of Brassica have at least 60 S-alleles identified.
However, there are dominance relationships among these alleles, so I don't think you can directly extrapolate from the number alleles to to the rate at which non-self pollen will be excluded.  The frequencies of the different alleles within a population will clearly also affect this calculation.
In addition, different individuals with the same S-alleles are more likely to be closely related, so I would hesitate to classify this as a limitation of the system.
Ref: Herrera, Sara et al. “Identification of Self-Incompatibility Alleles by Specific PCR Analysis and S-RNase Sequencing in Apricot.” International journal of molecular sciences vol. 19,11 3612. 15 Nov. 2018, doi:10.3390/ijms19113612


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Why do urine have a chemical smell after drinking a lot of alcohol (red wine)?
When I've been drinking a lot of red wine my urine starts to have a chemical smell. How do that urine differ from normal urine?
Is that chemical smell a sign of liver issues? When I was younger I don't remember my urine having that smell after or during drinking lots of alcohol.

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Its a very specific question and those are simply not on internet. You should know this.
You misunderstand. If it were a medical issue I would go to a real doctor and not ask sketchy strangers about it. Im asking because of curiosity.

What is your issue about how I formulated the question? Its short and to the point. I see no issue with it. Do you mean I should formulate it as a hypothetical question? That would be ridiculous nonsense and unnecessary.

Some things you can do to conform to our expectations here and to improve the response your question receives: 1) to avoid looking like a personal med question, indicate explicitly (i.e., by linking/citing specific examples) how others have experienced the same thing; 2) be more specific about the smell -- compare it to something; 3) to demonstrate research effort: do an extensive online search for your question (e.g., Google, Google Scholar, PubMed, NIH, etc.,) and explicitly report back where you looked (with which search terms), what you found out, and what you'd still like to know.


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MRI maximum field strength
More tesla = more resolution, is there limit of human body of how much strong magnetic fields it can handle safely which means there is limit to how strong MRI magnets we can use?
Engineering problems aside, could we scan live humans if we had 20 or 40 tesla MRI machine?

What have you found while trying to answer the question?

Technically, higher main magnetic field strength doesn't mean more resolution.  There are three parts to the scanner: 1) main magnetic field, 2) gradient coils and 3) RF coils.
The main magnetic field strength (1.5T, 3T, 7T, 9T, the last two typically more for research) determine more of the signal to noise (in a very simple sense).  This is static - it doesn't ever change.
The gradient coils are what determines the resolution and the rate of switching is the biggest determining factor. There are limits on what they can switch at when used on humans as they can cause peripheral nerve stimulation, vertigo, nausea, metallic tastes etc.
I don't believe static field of 20T etc would be a problem, though there is not much research to prove or disprove that.  The problem would be moving into that field as that will cause the same types of effects as the gradient coils switching.  Even for 7T, one must not run into the scan room as it can cause peripheral nerve stimulation (and some other effects). Currently, I believe the strongest full body human MRI scanner is 10.5T. Another article talks about 11.7T human scanners (one of them is a "head only" scanner. It also has some nice pictures).

Thanks for the nice answer, I think you meant 11.7T.

is there limit of human body of how much strong magnetic fields it can handle safely which means there is limit to how strong MRI magnets we can use?

The 2018 {1} study concluded:

Where feasible, effects are quantified for magnetic fields beyond 7T with the conclusion that there are no foreseen barriers either in the technical or human safety aspects of brain MRI and MRS at fields up to 20T. This conclusion is conditioned on results of recommended experiments to verify the predicted level of physiological effects beyond 9.4T. This technology is predicted to enable quantification of biochemical components of the functioning brain not detectable heretofore.

FYI:

MRI scanners in the United States with teslas
The strongest MRI for small animals — 21.1 teslas — is located at the National MagLab's headquarters in Tallahassee, Florida. (mirror)
https://www.openwater.cc: "Rivaling MRI quality at a fraction of the price and size".

References:

{1} Budinger, Thomas F., and Mark D. Bird. "MRI and MRS of the human brain at magnetic fields of 14 T to 20 T: Technical feasibility, safety, and neuroscience horizons." NeuroImage 168 (2018): 509-531. https://www.ncbi.nlm.nih.gov/pubmed/28179167


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Can crows see in ultraviolet? If so, does their plumage look different in UV?
Apparently birds which appear identical to the human eye can look quite distinct under UV light. Additionally, drab looking birds might have more "spectacular" looking plumage when considering wavelengths outside of the visual spectrum.
Question: In the specific case of crows, (1) can crows see in the ultraviolet range? (2) is the plumage of crows still monochrome when considered in the UV spectrum? Is it dichromatic?
Google seems to return very little about this, although this random person claims that crows can see in UV and their plumage does not look monochromatic under UV, while this article says they can not see in ultraviolet. Neither provides citations for their claims, and I am not familiar with the academic literature on this subject. Any help would be appreciated.
This question seems related inasmuch as crows seem black to the human eye. However, I know that some animals can see in UV, and am curious about whether this extends to crows.

Corvids (and raptors) are reported to not see UV Håstad et. al. 2005.
However, American crows are reported to recognize sex-specific differences in plumage that are invisible to humans Eaton 2006.
Unfortunately, I don't have access the latter paper so I don't know what the basis for that discrimination is or how to reconcile that result with those of Håstad et. al.
You might also find this well referenced blog post that summarizes these results to be of interest.


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What does "dissection-based microscopy" mean as described here, and how can it give genetic information?
The Phys.org article 'DNA microscopy' offers entirely new way to image cells references the new Open Access paper in Cell DNA Microscopy: Optics-free Spatio-genetic Imaging by a Stand-Alone Chemical Reaction.
My question is not about DNA microscopy, but instead about the second kind of microscopy mentioned in the explanation below quoted from the Phys.org article

Until now, microscopy fit into two main categories. The first is based on optics; light microscopy, for example, dates back to the 1600s and relies on visible light to illuminate samples. Scientists have riffed on this approach, even going beyond the visible spectrum. Electron microscopes, fluorescence microscopes, light-sheet microscopes ¬- they're all based on the principle that samples emit photons or electrons, and the microscope detects the emission.
The second category is based on dissecting samples at locations defined by a microscope. Computer programs then stitch together each dissected piece into a complete picture of the intact sample. Optical imaging can offer intricate portraits of subcellular structure and action. Dissection-based microscopy can give scientists genetic information.

I don't really understand exactly what is being referenced by the 2nd paragraph. What is "Dissection-based microscopy" and how can it give genetic information?
The passage seems to repeat a few sentences in the introduction to the Cell paper:

These approaches closely mirror the two ways in which microscopic images have been acquired to date: either (1) detecting electromagnetic radiation (e.g., photons or electrons) that has interacted with or been emitted by a sample, or (2) interrogating known locations by physical contact or ablation (e.g., dissection).

This may shed some light on the question for those more familliar with the techniques discussed, but I still don't understand what technique this is really referring to.
See also NY Times' DNA Microscope Sees ‘Through the Eyes of the Cell’

I guess it refers to optical mapping (https://en.wikipedia.org/wiki/Optical_mapping). However, the text is a little bit confusing, so I am not 100% sure.

@FabioMarroni Okay, I will have a look in the morning. Thanks!


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Polyandry in birds
The Wikipedia article on Bateman's principle states:

Until recently, most bird species were believed to be sexually
monogamous. DNA paternity testing, however, has shown that in nearly
90% of bird species, females copulate with multiple males during each
breeding season

citing two articles. But the Polyandry in nature article says:

Polyandry… occurs in … around 1% of all bird species, such as jacanas
and dunnocks.

(No cites provided.)
Am I correct that the second article should be updated?

"no citation provided" would be the relevant information.

I did work on the Louisiana waterthrush 15 years ago and found some instances of polyandry. Wasn't previously recorded in that species to my knowledge

I think you're confused about the definition of polyandry. Firstly, polyandry normally refers to sustained relationships, not simply mating. In birds this means nest biulding, incubating eggs, and feeding young. If a pair of birds raise chicks in one nest, and neither interacts with another nest of chicks, then they are a monogamous pair - it doesn't matter if there are other chicks with their genetic material.
Also, polyandry normally refers to females taking more than one male partner, while males stick with that single female. The article states that most females "cheat" on their partners but a similar percentage of males do the same.
The dunnocks given as an example often form trios where 2 males and a female collectively raise chicks, with the young having a mixture of paternities. The jacanas have a system where males build nests and females claim up to 4 males, and defends all her nests while the males raise the young. These are very different to the standard bird system, where a female bird may have many sexual partners, but only cares for one set of young.

Do you have a cite for “polyandry normally refers to sustained relationships, not simply mating”? Both https://en.m.wikibooks.org/wiki/Animal_Behavior/Polyandry#Polyandry and
https://en.wikipedia.org/wiki/Polyandry_in_nature start w defn in terms only of mating. Perhaps in parallel with ‘social monogamy’, (see https://en.wikipedia.org/wiki/Social_monogamy_in_mammalian_species#Monogamy_in_mammals),
nest building, etc., could be termed ‘social polyandry’?

It also varies among species. A study by the local college ( Sam Houston , Huntsville TX) found Carolina Wrens were almost monogamous; different from other birds studied . It was years ago and I do not recall what species were in the study.


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Cellular respiration in carnivorous animals
What is the equation for cellular respiration in carnivores as they don’t consume carbohydrates to break down into glucose in the following manner:
Glucose + oxygen -> water + CO2 +energy.
Do they (mammalian carnivores) primarily use ketones to produce energy without using glucose?
Does this mean that glucose is not the only energy source for humans/other animals?
Am I wrong in thinking that every source (protein, fats or carbohydrates) need to be convert into glucose for energy.

Welcome to SE Biology. I have edited your question, primarily to replace the term diet/sports  term "carbs" by the biochemical "carbohydrates". In addition I have tidied up a bit. I would express the opinion that your question is very naive for this site. Although you have received a useful answer, you really need to read a textbook on biochemistry to appreciate this and the topic in general.

Your guess is correct: glucose is not the sole source of energy in the cell!
While cellular respiration is the classic mechanism for energy production (in the form of ATP) in the cell, there's another process that's equally important and a little less well-known: beta oxidation. Beta oxidation is how fats and other lipids in the cell can be broken down to produce energy. In this process, the last two carbons in the long chain are sliced off and transferred to Acetyl-CoA, which can then be used in the citric acid cycle to produce ATP.
Here's the equation describing it:
$$C_{n}acyl-CoA+FAD+NAD^{+}+H_{2}O+CoA -> C_{n-2}acyl-CoA+FADH_{2}+NADH+H^++acetylCoA$$
And here's a good diagram from the Wikipedia page that summarizes it:

Courtesy of Cruithne9 on Wikipedia [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)]
This process is why fats actually have a higher energy density than sugars: 9 Cal/g, as opposed to sugar's 4. It's also why organisms tend to use fats as energy storage - while sugar and cellular respiration is great for immediate energy, fats are stable and energy dense so it's an evolutionarily favored idea to use them for long-term storage.
You're also quite correct that animals don't tend to have a lot of free sugars and carbohydrates, unlike plants. Instead, we've converted those carbs into the fat molecules via the reverse process, fatty acid synthesis. So, carnivores largely get their energy from beta oxidation and the metabolism of fats, rather than glucose.

Ah thanks for the equation. Wondered how the energy was produced ! Cheers


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What is the difference between protein translated by a free ribosome and protien translated by a ribosome attached to endoplasmic reticulem?
There are protiens translated by free ribosomes and proteins translated by attached ribosomes.  But how do these two types of protein differ from each other? I am just talking about a eukaryotic cell. I know that proteins made by free ribosomes do not have a covering but proteins made by attached ribosome gradully have a vesicle around them but I am not able to understand what difference in use does the vesicle make? (I am new here so pls forgive if there are mistakes in my question)

As a newcomer to Stack Exchange Biology, you may not realize that your question has a couple of problems that may result in it being ruled off-topic. The first is that it looks rather like a homework question, for which there are specific rules you can find in the Help. One of these — which also applies generally — is that you should show that you have made an attempt to answer this question yourself. This means doing some research. Try Wikipedia on free and membrane-bound ribosomes.

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!


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Movement of the Thoracic Cage During Movements of the Thoracic Spine
Just for a bit of context: I am trying to create a 3D digital model of the human skeleton as the first step towards computer generated muscle simulation, and as such I want the skeleton to be as anatomically and biomechanically correct as possible. However, I am currently struggling with the movement of the ribcage. I am quite capable in the 3D side of things, but without any medical background I've essentially had to learn everything about the skeleton so far from the ground up.
Whilst there is plenty of information on the internet about the movement of the ribs and sternum during inspiration and expiration, I haven't been able to find any detailed descriptions/diagrams/animations of how the various movements of the thoracic spine (lateral flexion, sagittal flexion and extension, and axial rotation) influence the positioning of the ribs, including in scientific papers (however I can't see that this topic hasn't come up before?).
The only thing I've found for this are three diagrams from this website http://body-disease.com/movements-in-the-thoracic-region/ (bottom right hand corner in each case):

Whilst these diagrams are definitely helpful in showing the general movements and shape, they don't really have the detail that I am looking for: for example the movement of the sternum isn't specified or the exact movements of the ribs and costal cartilage. These diagrams are a good starting point but I can't really work with them - as really I need to understand the four movements of each rib (torsion, calliper, bucket handle and pump handle) where they connect to the thoracic spine in order to create an accurate 3D model.
I would most like an accurate diagram or (even better) an animation of the spine movements with a complete rib cage; however X-ray images, sketches or anything that might provide more information would be useful. Descriptions are also great but as I'm not very experienced with anatomy I may not be able to glean as much information from text as I would from images. Essentially I am not trying to understand the concept of how the rib cage changes, but the specifics of this complex movement.
I know this might be quite a specialist topic (especially given the lack of online information) however I thought I would ask anyway in case anyone knew. Thanks for any information you can give me!
(Also let me know if I've made an error - this is my first forum question)
Edit: after some more digging I've found this image (from http://www.orthotech.ethz.ch/research/musculoskeletal-biomechanics/sarcopenia--implications-of-age-related-muscle-loss-for-spinal-p.html) showing thoracic flexion and extension, which may help in understanding the sorts of thing I'm after. the issue with this image is the fact that the movement of the sternum and costal cartilage is still very unclear:

What benefit can one have from such 3D digital model?

@Jan I want to use the skeletal system as the basis for simulating muscles, fascia and other tissues present in the body to create a photorealistic human which can be used for CGI. The idea is to adjust the different settings of the model (such as muscle definition or amount of fat) to quickly create a vast range of realistic 'humans'. The advantage to conventional 3D modelling would be accuracy (see Weta Digital's 'Tissue' software as a good example). I'm using the open source software "Blender" and I hope to make the system free to use for all if I get it to a point where I'm happy with it.


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Are hybrid-species individuals considered to be of the same species as their parents?
This question arises given the definition of father and mother as seen in the Spanish dictionary composed by the Royal Spanish Academy. Basically it says that a father/mother is a man/woman or a male/female animal that has engendered/given birth to an individual of the same species (Spanish: "especie").
The Spanish word "especie" could also be translated here as "kind", but let's assume it refers to its zoological definition. That definition would be mostly true, but what about mules or ligers?
In the case of mules, they are the offspring of a male donkey and a female horse. A male donkey is considered to be of the species Equus asinus, while a female horse is an Equus caballus. The mule is an individual of the species Equus asinus♂ × Equus caballus♀, but what is exactly that? It is the set resulting from the addition of the two parent species, or is it a complete, new species? In other words, are mules considered to be of the same species of a donkey or a horse? Or what they all have in common is just the genus?

Mules are not a species because they can't reproduce.  The problem seems to be that the dictionary definition doesn't correspond to the real world.

TL/DR We usually don't give specific names to those hybrids.
This is a fairly complicated question, actually, without an easy answer. Hybridization can have different outcomes, depending on how different the hybridizing species are. The cases you mention (liger, mules) actually do not deserve a specific names, because, first, they don't occur in nature, and, second, they are sterile, so there's no reproduction, hence no progeny. This lack of descendants goes against any defenition of species that we have in biology. There are cases where hybrids might become their own species, for example the butterfly Heliconius heurippa appears to be a species that evolved through hybridization between two closely related Heliconius species. There are also many examples in plants and more are being discovered in animals. These cases do receive a species name, because they occur in nature and populations can be predictably found.
Another case, similar to the cases you mention, involve hybridizations that occur in nature, but are rare and the individual rarely has any significance effect on the population. Sometimes those individuals are fertile, but look so different that might not be able to reproduce. Other times they can only reproduce with one of the parental species and if this happens successfully, new alleles can be introgressed into the parental genome. But for what we know, reproductive barriers between species tend to be successful in nature, tend to be broken down with human intervention (captivity, movement of species, among others) and, in most cases, don't have a significant evolutionary impact, except the cases when they do.


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Why don't most life forms show uniqueness in progeny?
I guess everyone must have observed this. Dogs, cats, and most of all insects (including mosquitoes) appear more or less the same.
Why is there so little variation in their offspring, unlike humans, where you rarely find two humans showing even a little resemblence.
Is it the large size of the human genome that allows infinite combination of traits? (seems unlikely, as even small flies like drosophila melanogaster have somewhat large genomes, but show very little variation).

@iayork I'd searched but couldn't find. Thanks.


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Could somebody please tell what tree genus is this?
Leaves of a tree in south Asia:
It is in Pakistan, found in flat land habitats.

South asia is a bit vague. Can you be a bit more precise and what kind of habitat you found it?

Please provide approximate size of leaves. also, if possible, providing additional images/descriptions of the plant is always helpful: closeups of leaves, images of flowers, plant growth size and habit, etc.


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How do receptors lose their sensitivity?
Recently, I learned that one of the causes of Type II diabetes is that insulin receptors on cell surfaces lose their sensitivity due to long-term high exposure to insulin (which occurs as a result of high blood sugar).
How do receptors (like that for insulin) become more resistant to ligands? Is the receptor itself getting damaged? If so, how, and why don't other frequently activated proteins/receptors (like GPCR's) also get damaged? If not, then how does the cell become more "resistant" to insulin?

There are different mechanisms for different receptors, so this is a very broad question. It's usually a negative feedback from within the cells. For insulin resistance, you can check Figure 1 in this article.

The field of insulin resistance is a very active research area and hundreds of research papers on the topic are published every year. There appear to be many mechanisms involved in the development of insulin resistance and to give a full answer might not be possible at this time.

The major celltypes responsible for getting rid of blood glucose are the liver, adipose tissue (fat cells) and the muscles.
The problem of how muscles becomes insulin resistance was solved by a team of scientist led by Gerald Shulman a few years ago.
The mechanism is that incread levels of diglycerides (note that normal fat in the body is in the form of triglycerides) in the muscle  cells prevents/makes it harder for glucose transporters of the type glut-4 to attach to the cell membrane. Thus causing incread levels of insulin in the blood in order to get the muscle cells to accept the glucose.
This seems to be the major reason for how muscle cells become more "resistant" to insulin. It is mostly not the insulin receptors becoming dysfunctional or fewer but diglycerides stopping the insulin receptors from getting the glucose transporters to the cell membrane imparing the glucose uptake. Listen to Geralds Banting price lecture:
https://www.youtube.com/watch?v=TnvmEUUtoZw


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Are there gaps in what our ears can hear?
I know about the hair cells in our Cochlea and it is the movement of the fluid that makes them vibrate. And it is this that activates the transmission of electrical signals to the brain that become sound.
But I've heard that hair cells are each built to detect specific pitches of sound. And if they don't get that particular pitch then they don't transmit.
So as I understand it, we have cells that each respond to one particular pitch and nothing else. Since we have many that each respond to a different pitch, this is what gives us a wide spectrum of hearing.
What I've been wondering is this, if each hair cell responds to one particular pitch, what happens if we try to hear a sound that is in between two hair cells?
Imagine a hair cell that only responds to 1 Hz (and based on my understanding they do) And next to it a cell that responds to a sound at 2 Hz.
What happens if there is a sound that is 1.5 Hz? Can we not hear that sound because it exists in the gap between our hair cells? Or can hair cells cover a wide range so they overlap and cover the gap?
As our ability to hear sound quantised or continuous?
I know that there are sounds so low or high they are beyond our range of hearing but what about within our range of hearing? If someone played a sound that was right in between two hair cells could we not hear it? Is there a finite number of different sounds that we can hear within our hearing range?

Good question. I think clearly the range of the hair cells do overlap, because if I listen to a tone that slowly changes in pitch, such as slowly tuning a guitar or piano string I don't notice gaps where the sound goes away and comes back as I tune the string. Although it would be interesting to know exactly how much they do overlap.

Short answer
No, there are no between-hair cell induced tonotopical gaps in frequency perception.
Background
Young people are able to hear over a frequency range of about 10 octaves, with a frequency resolution of about 0.3% of an octave. So we would have about 2300 resolvable frequencies. This number is dependent on the sound level, as excitation spreads at higher sound levels, but it gives a reasonable starting point to answer your question.
The human cochlea contains on the order of 3,500 inner hair cells. Hence, according to this (highly simplified) calculation, it seems that the number of hair cells is redundant.
In other words, the notion of in-between hair-cell stimulation is stretching the limits of physiological frequency resolution a tad too far.
Reference
- Elliott & Shera, Smart Mater Struct (2012); 21(6):064001
Source
- Cochlea.eu. Cochlea: function

To add to the good answer by @AliceD, take a look at some tuning curves for hair cells, the sound receptors in the cochlea (these happen to be fairly low frequencies and a turtle cochlea, though those details aren't all that important):

Fettiplace, R. (1987). Electrical tuning of hair cells in the inner ear. Trends in Neurosciences, 10(10), 421-425.

The horizontal axis is frequency; the vertical axis is the response of the neurons in voltage. The data are produced by recording responses to a bunch of different pure tones.
What you see is that the cell that is "tuned" to 131 Hz doesn't only respond to 131 Hz, that's just where it responds most. Same for another cell that is tuned "best" to 314 Hz. There would be many cells in between with different best frequencies, and you could take a weighted average of the activity across that population of cells to precisely identify the actual tone.
Generally, the hair cells that actually monitor sounds are some of the most poorly tuned cells in the early auditory system. At higher levels of processing in the auditory brainstem, lateral inhibition improves tuning.

Great answer! And +1 for that ancient graph of Fettiplace ;-)


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Akt phosphorylation at Thr308 and Ser473
I am studying Akt signaling pathway. I know that phosphorylation at both T308 and S473 is prerequisite for full activation of Akt but wonder if phosphorylation/de-phosphorylation of one of them is prerequisite for another. In other words,

wonder if phosphorylation at T308 is required for phosphorylation at S473 or vice versa, or they are phosphorylated independently.
wonder if de-phosphorylation at T308 is required for de-phosphorylation at S473 or vice versa, or they are de-phosphorylated independently (wonder if there is any order of de-phosphorylation by phosphatases such as PP2A between the two sites)

If there is such order, can anyone suggests me some references?


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What kind of insect does chirp like this?
I live in Japan. Recently I hear chirp coming from Wisteria floribunda at every night. Please check this sound that I uploaded for this question.


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Dinosaur bones found
I found a bone in 120 metres under the ground which has nuclear radiation. Can you help me to recognize this bone?

It was found in a clay quarry near Odessa Ukraine.

Not with just that image. You want pictures with something for scale from all sides including the broken section. We need to get a good idea of the shape and size. The formation it is found in would also be helpful but not absolutely necessary. The radioactivity is irrelevant.


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What is violet color?

We have 3 color receptors in our eye, so assuming the above picture is precise we are checking for 3 wavelengths: 450nm, 540nm and 700nm.
Pink for example has an RGB value of

R (700nm): 1
G (540nm): 0
B (450nm): 1

Violet has an RGB value of

R (700nm): 0.5
G (540nm): 0
B (450nm): 1

However Violet has a wavelength of 400nm which is lower than the Blue receptor. So how can it activate the red receptor when red is clearly not active at that frequency?
Does that mean Ultraviolet appears blue to the human eye? Why is it constantly painted as violet in all frequency graphs?

The question was first duscissed here (https://physics.stackexchange.com/questions/486560/what-frequency-is-pink-color) but did not receive the answer I need.

related question. https://biology.stackexchange.com/questions/51870/can-red-cone-cells-actually-see-much-red-light

Ever see a rainbow, or sunlight that's passed through a prism?  The high-frequency end of the visible spectrum is painted as violet because that's what it looks like.

this is a chart of the light activation of the light sensitive cells in the human eye.

see that little blip up on the tail end of the red cone, that minor ranges means the extreme blue end of the spectrum activates blue cones but also has a chance to activate red cones. That is why you can sometimes see magenta tinges in bluest of blue light. There is also a sensitive issue as blue cones are the least sensitive of our cones so it requires a stronger blue light source to activate it than the equivalent light on other cones, since red is more sensitive a strong blue and a weak red source will blend to about equal as far as our eyes are concerned so at the bluest end of the spectrum, where the blue activation is at its weakest it does not take much to activate the blue and red "blip" equally meaning all sources at that extreme end blend into magenta.
Also magenta itself is not actually part of the spectrum, it can be produced in two ways, the first I discussed above, hitting the far end of that little blip perfectly. The second and most common requires light from two disparate and different parts of the spectrum in other words not a single wavelength. It is blue light and red light without green light, it is not a real color but an artifact of how our eyes see light. Your cones can't tell how they are activated just that they are. Yellow and cyan (and every other common human color)on the other hand can be produced by a single wavelength, which may or may not activate multiple types of cones.
You can find more information here

Really impressed by the straightforwardness of the linked article. I quote Einstein here "If you can't explain it simply, you don't know it well enough" Thanks for that!! Fascinating!!!

This is incorrect. There's no bump in the sensitivity of the L cones. This misconception arose from a bump in the X function of the CIEXYZ colour space. But X, Y and Z were never meant to correspond to cone sensitivities.

@OscarCunningham I see... can you edit the answer or write a new one? I am in no position to do so.

So what is the answer to this then? I have never seen that activation spectrum from any other source. If there isn't that hump in the red cone's spectrum, then it seems the OP's question remains unanswered.


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Do the organisms within a lichen communicate with each other?
So you've got your fungus and your algae (or cyanobacteria) (and the multitude of other variations and additions to this two-species symbiosis that lichens present). Do the species that comprise the lichen communicate with each other via chemical or electrical signalling? For instance, could an algal cell "tell" the fungus that it's diseased, thus triggering the allocation of more resources toward pathogen resistance?
And if there is no communication, how have lichens been so successful?

Communication definitely happens, but I don't know of any research into response to disease.
One example are molecules known as lectins that help the fungal partner recognize the correct photobiont (algal or cyanobacterial) symbiont.
Another example are the physical connections between fungal hyphae and photobiont known as haustoria that appear to help the fungus extract sugars from the photobiont.
You should find this review by Piercey-Normore & Athukorala 2017 a helpful place to begin learning more.
Ref: Piercey-Normore, M. D., & Athukorala, S. N. (2017). Interface between fungi and green algae in lichen associations. Botany, 95(10), 1005-1014.

Please expand your answer. Provide a quote, image, or some other useful summary item from the article you link to to demonstrate how it answers the OP's question. Also, due to concerns about links dying, please provide the citation of the article directly into your answer for future reference. (The citation is easily found by typing he paper title into Google Scholar and selecting the citation button (shown as a ") below the search result).

@theforestecologist: Is that more along the lines of what is expected?

@theforestecologist:  Great, thanks for the feedback!


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What trajectory do action potentials take, from initial visual stimulus all the way to motor function?
Say we see a mosquito, and our brain tells us 'hey that's a mosquito, you should kill it.' Then we move our hands and slap/clap it.
The initial visual stimulus is translated to an action potential via the phototransduction cascade. Light hits retinal, bla bla, glutamate release is decreased, turns a few cells on and off, which eventually sends the action potential down the optic nerve through the lateral geniculate nucleus and to the 'final' target, the occipital cortex.
Then, something happens from this point in the occipital cortex, which eventually 'translates' to action potentials beginning in an upper motor neuron (UMN). This UMN located in the  motor cortex of the brain, propagating its message eventually reaching the muscle.
The question is, what happens in this intermediate phase, where visual input lands on the occipital cortex, and then eventually translates to an action potential being propagated at the UMN located in the motor cortex? Do neurons directly synapse from the occipital cortex to the motor cortex? Is there a particular neurotransmitter responsible for communication between neurons of the occipital lobe and motor cortex, or whatever lies in between (glutamate, acetylcholine, etc)?
And finally, the hardest question... light provides a simple stimulus which translates to an action potential, making it the 'origin' of the action potential in this case. But if we close our eyes, and imagine a mosquito, we'll still have activity in our occipital cortex, and willingly provoke the same motor response. What was the stimulus for this visualization, if light wasn't the firestarter? Does some other molecule isomerize cis-retinal to trans-retinal, or affect some other step down the photoreception cascade?


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Long brown needly things fallen from tree?
I was walking next to a row of trees (I think coniferous) and found many of these things on the ground:
A parallel bundle of 2-4 medium-brown needly things, about 15 cm long and 1 mm in diameter, not quite as sharp as a saguaro spine, a bit stiffer than a blade of grass, connected at one end by a darker brown bulb about 3 mm in diameter and 7 mm long. Very easy to pull apart.
What is this thing called?
EDIT: thanks to nextworldplz' answer, here's a picture of what I was describing (turns out to be specifically ponderosa pine needles):

... pine needles?
These are the leaves of coniferous (evergreen) trees. It sounds like they might be from Pinus ponderosa, a species of pine.

Yup, I think that's it. lol. I was originally thinking "aren't pine needles shorter?"

If they are brown, they are dead pine needles.  Unlike deciduous trees, which shed their leaves in the fall and grow new ones in the spring, conifers replace their needles more or less continuously: https://sciencing.com/pine-needles-6455979.html  Needles also vary in length according to the species.


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Viability of Toxoplasmosis oocysts on dry smooth surfaces
This is a weird question. My wife is terrified of contracting toxoplasmosis during pregnancy and I was hoping I could get an expert opinion here to potentially make her feel better.
She recently took the toxoplasmosis test and it came back negative. The next day, we cleaned the house. We have four cats, all indoors, who have intermittently gotten into the trash and licked containers containing raw meat or eaten raw meat that we had bought from the store. We also live in the city, no rats or rodents that they could find and kill. We keep our house fairly clean. There was a smear of dried cat poop hiding under a rug on our tile floor that I cleaned that has to be at least 5-6 months old. I had to really pick at it after spraying it to get it up. She's worried that because she handled the towel I used to clean it up with that she's potentially exposed herself to infection.
How likely is it that old, dried cat poop like that could still harbor viable oocysts? Assuming that it was infected in the first place. Do they dry out and inactivate if they're not exposed to moisture?
Thanks!


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How are monocytes larger than capillaries?
I have read that the average size of a capillary is about 8 micrometers. How is it possible that the 15 micrometer or so monocytes in blood do not block these vessels?
https://en.m.wikipedia.org/wiki/Blood_vessel#Vessel_size
https://www.britannica.com/science/monocyte

They aren't completely rigid and can change shape to squeeze through (see Downey et al).
If they are activated, monocytes can get stuck in capillaries and block them, which contributes to poor circulation following reperfusion after an ischemic blockage (see Engler et al).

Downey, G. P., Doherty, D. E., Schwab 3rd, B., Elson, E. L., Henson, P. M., & Worthen, G. S. (1990). Retention of leukocytes in capillaries: role of cell size and deformability. Journal of applied physiology, 69(5), 1767-1778.
Engler, R. L., Schmid-Schönbein, G. W., & Pavelec, R. S. (1983). Leukocyte capillary plugging in myocardial ischemia and reperfusion in the dog. The American journal of pathology, 111(1), 98.


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Is Dioxin causing Diabetes Mellitus?

Today I was watching a show on Discovery Science (Everything You Need to Know About). In that show they were talking about toxins and venom.
In that they mentioned Dioxin and its effect. And suddenly I heard the unexpected, that Dioxin damages Pancreas!!
Dioxin spreads due to contamination by food & mainly beef (as mentioned in the show).
It is produced mainly because of (chlorinated) burning of fossil fuel, coal,trees,PVC, plastic.
As there is a spike in the diabetes in recent years. And there was a increase in pollution from last few decades.

It looks like Dioxin is culprit which is lurking behind to attack people and causing Diabetes.
Am I thinking right?

Correlation is not causation.  There has, for instance, been a large increase in the consumption of soft drinks in recent years.  There's also been a large increase in the number of personal computers, and of solar panels on rooftops.  Of those four correlations (and there are many others), which is most plausibly linked to diabetes?

Valuable information:- https://www.who.int/news-room/fact-sheets/detail/dioxins-and-their-effects-on-human-health


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Are olfactive indicators always the result of inadequacy in sanitation?
Question
If you can smell the scent of food in a thoroughly cleaned container, does that imply trace amounts of food particles remain?
Scope
It goes without saying that our sense of smell is commonly used in helping identify undesirables in day-to-day life, and as such it's understandable to correlate certain smells to hygiene effectiveness.  However, I'd like to definitively understand whether or not the presence of odorants unequivocally indicates ineffective or insufficient sanitation (in particular, on direct food-contact processing utensils and containers in a commercial/industrial environment).  E.g., coffee mugs with lingering scent of coffee despite repeated washing.
From the standpoint of HACCP/HARPC, I've always been slightly curious about the absence of "smell" as a modus operandi for pre-operational inspection (visual is the go-to).  I've always made the assumption that it simply isn't a reliable sensory indicator (despite visual being the same, in that sense), but I'm not fond of assuming.  I have a physics background, but I am unfortunately a bit lacking in biology / chemistry knowledge (beyond food safety-related microbiology).
Parameters
I'd like to understand from a scientific stand-point: is there an exclusively causal relationship between the two?  Are there possible scenarios where we can detect odorants despite having met sanitation performance standards?  For the sake of this question, I'd like to preclude the hypothetical possibility that "there were traces of debris/microbiological activity/etc., only they were within the tolerable limit defined".
I'm sure there might be a lot of complexities I am glossing over in my question, for which I apologize; e.g., I am aware in the framing of my question, I am holding some prejudice that the hazards of concern are microbiological -- whether pathogenic or not -- wherein the results from an adenosine triphosphate swab may be used as a quantified measure for overall activity.  For the sake of keeping this question from becoming too technical and convoluted to answer, and to also simplify and make measurable the criteria for "sufficient sanitation", please advise from the microbiological stand-point, but if relevant please advise from other standpoints as well (under HACCP/HARPC, the remaining potential hazard categories would be physical and chemical [includes radiological]).
Thank you!

Well that's discouraging to see.  May I ask why the down vote?  I even made sure to carefully read through the help pages here and here and thought I covered all my bases...?

My impression is that someone in the past day has felt like downvoting a significant percentage of recent questions, so the downvote for this question is about par for current submissions.  The question has also garnered a close vote, with close reason "unclear what you're asking", which IMO is not terribly off target.  Despite the amount of verbiage (also perhaps in part because of it), what you're really asking doesn't seem all that clear.  Not that I could answer anyway, but I wonder: any smell? Inadequate cleaning for what? "industrial" when the example is coffee scent from a coffee cup?

Sorry about that!  This is from the standpoint of sanitation at food processing facilities, I work as a food safety practitioner and document coordinator.  The background might be very specific, probably not many people will know what it's like to work at a USDA inspected food plant, hence maybe the terminology I'm using could sound a bit unfamiliar.  What I'm asking though is more generalized and I think can be answered by the community here.  Let me rephrase it: if you can smell the scent of food in a thoroughly cleaned container, does that imply trace amounts of food particles remain?

Or rather, one would assume "yes" in most cases, but are there cases where detecting a scent does not equate to presence of particulates that remain on the surface due to inadequate cleaning?

@Arctiic Trivially, if you detect an odorant then (unless you are imagining things) some of that odorant must exist. How much depends on the particular odorant and who is doing the smelling. From that point, from a food-processing standpoint it depends more on standards than biology, which I think is why some people have issue with the question.

@BryanKrause thank you for expanding on that.  The reason I posted in the Biology community is due to my own lack of basic knowledge on how odorants work; when I say "particulates", I'm referring to protein/lipid/other particles that can and should be removeable following standard wash procedures, of which the ones for concern would be those that would contribute to microbiological growth post-lethality treatment.  With that in mind, I'm unclear as to whether odorants can be, for instance, made up of x type of molecules and have no significant impact to microbiol proliferation, etc.

So in the coffee mug example, if I can still detect the scent of coffee -- the odorant -- then does that signify leaving it at room temperature for 8 hours, I would see a higher TPC count swabbing as-is, versus if I washed it another x amount of times until no detectable scent remains?  Note: I work with meat products and have no idea what risk category coffee grounds have under biological hazards, so that may not have been the best example, it was just the first thing that came to mind.

@Arctiic Nothing left open is sterile. Even a completely clean glass will eventually be contaminated with bacteria, mold spores, etc. This is why I say it depends more on standards than biology: if you want something to be sterile, you have to actually sterilize it which includes sealing it from the outside world in some way (for example, canning processes reach sterility or at least near sterility). However, that level of cleanliness is not necessary for food preparation that is not meant to be kept very long term, so there are standards for food prep cleanliness that are short of sterility.

@BryanKrause Yes, I understand that, our current testing standards are:
APC <100,000 CFU/g FDA-BAM CH.3
Coliform <200 CFU/g AOAC 991.14, 989.10
CP Staphylococcus <10 CFU/g AOAC 2003.07/0.08/0.11


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How to troubleshoot in vitro formaldehyde fixation for nucleosomes?
For an experiment, I am trying to fix the mononucleosomes (100ng) using formaldehyde as crosslinking agent in HEPES buffer. I have been using 2% formaldehyde in a reaction buffer containing 1mM EDTA, 25mM NaCl and 50mM HEPES, pH 7.5 (same as nucleosomes suspension buffer) to fix mononucleosomes.
In my first reaction, I added 100ng of nucleosomes, 2% formaldehyde and incubated at 4degC, 30', then I added 0.4% SDS and incubated for 30' at RT. I observed less intense but equally sharp band for nucleosomes (less smear) as compared to unfixed nucleosomes.
When I performed the same reaction again, the gel showed a huge smear covering the entire lane instead of a sharp band.
I have been reading about the fixation reactions and encountered an emphasis on using methanol free formaldehyde (while I was using 10-15% methanol containing formaldehyde). Do you think that can be one factor for not being able to get similar results?

Same reaction protocol giving undersirable result may simply be because of some sample prep errors. See this protocol. The final concentration of formaldehyde is 1%. Most protocols suggest that formaldehyde be prepared fresh. This is because formaldehyde gets oxidized to formic acid.

Thanks for the suggestion. The chance of adding errors while making the reaction is relatively constant since I prepare it in the same manner, every time (except for the pipetting errors). I agree with you about the oxidation of formaldehyde. The protocol you suggested uses 11% of final formaldehyde, is it because they are using certain mammalian cell lines?

Their fixation buffer contains 11% formaldehyde. They add 20ml of this buffer to 200ml of cell suspension. So final concentration of formaldehyde is 1%.

Yeah, I figured. Thanks though.

Since formaldehyde is the matter of discussion here, I wanted to ask that I have an 1ml aliquot of pure formaldehyde sealed with inert gas in a glass. Now, in one reaction I am only using 10ul from that 1ml. Ideally since these aliquots are for  one time use, I shoud discard remaining 990ul but if I want to store, is there a feasible way to preserve the rest of the formaldehyde while taking care of its exposure to air?

That is a different question and should be asked in [chemistry.se]. That said, I think that most people who do these experiments prepare "fresh formaldehyde" by heating paraformaldehyde solution. You should look at the protocols for more details.


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What animal is this? A bee? red mason bee? (Bee-like with brown/orange fur)
The picture was taken at the Bodensee (Lake Constance) in Southwestern Germany in June 2019. I tried to Google "Bee with brown fur", but the only thing that came up was a red mason bee, and the resulting pictures didn't look quite like this photo
Since I was sent the photo, I don't know the actual size of the insect.

Definitely a bee, I'd guess from the family apidae. Do you have other photos? Getting a good ID will probably require a sharper photo.


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Rice left in water for several months - what biological reactions or growths would occur?
In an attempt to make a hair care product, uncooked white basmati rice was left in an air-tight container half filled with tap water for several months.
When opening the container, the smell was extremely foul and disturbing, one of the most revolting things I have ever smelt.  It was worse than the smell you would usually associate with yeast, alcohol, or mold.  This horrid smell immediately spread to the entire property and took many hours of fan extraction to remove.  It was worse than the smell of sewage.
I rinsed the container used and cleaned it in the dishwasher several times at 75'c.  After several dishwasher cycles, the disgusting smell remains.  It makes me wonder what kind of biological or chemical product has been created that even a dishwasher cannot neutralise or sterilise at high temperatures?  Is this a safe substance?  This is especially concerning as this recipe exists on several hair care forums; is it widespread misinformation caused through malice?
I believe this is a valid scientific question about microbial life so on that basis I would not expect it to be down voted.
The substance looked like water with rice or rice starches dissolved in it; it was murky with a whitish colour.  There was no air bubbles which could be visually observed, although the murky texture could have been caused by micro-bubbles. The smell was very strange, unlike anything I have smelled before.  The closest description I could give is that of sewage, yet it is more disgusting than the smell of sewage if that is relatable at all.

What did the contents of the container look like?

It depends on the microflora in your locality. Difficult to comment unless you describe the smell accurately. In general I would advise against doing anything (in the name of home remedy) of which you have no knowledge.

It is likely a volatile organic compound (VOC) that is released as a by-product of microbial metabolism, although microbes can also produce some inorganic compounds, such as hydrogen sulfide (rotten egg smell). It could be any of a number of compounds, depending on the microbial species and the environmental conditions. The only relevant paper I could find based on a cursory search was by Yanqiang et al. (2013) on volatile compounds released from the anaerobic digestion of food waste in general; based on the results, the odor likely consists of a complex mixture of gases, and may be especially rich in aromatic compounds. Whether it could have any negative health effects is challenging to prove, but you would likely want to avoid exposure.
I presume that your container is made of plastic or at least contains a silicone ring. You can remove odors from metal or glass by washing them, but porous substances like plastics, rubber and the like will absorb volatile compounds, rendering them largely inaccessible to solvents such as water, and will release them slowly over time, which you can perceive via olfaction as you have noticed. If you want to eliminate the odor faster, you will need to accelerate this outgassing process. The way this is usually done is by baking in an oven (optimally in a vacuum, although this is not necessary). The rate of outgassing grows exponentially with the temperature, so you should use the maximum temperature that the material in question can withstand.


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Can I use a basic compound microscope to analyze the ploidy of plant chromosomes?
So, I'm not really any kind of trained botanist. But I do have two things: some dandelion seeds from France, and, collecting dust in my garage along with related accessories, this thing.
Normally, the dandelions growing in an American yard are apomictic triploids, but in Europe there's both triploids and sexual diploids, the latter getting even more common the further south. I'm assuming that, because these French seeds are a specific common cultivar (Vert de Montmagny), that regular sexual selection was used in breeding it, making it a diploid. But I don't know who to ask to confirm this so I may as well do some testing. If it's a diploid, maybe I can do some breeding of my own?
But I don't even know the first step. Are there some parts of a plant that I'll have an easier time finding chromosomes in? What do I put them in to express their DNA and what do they best stain in? Would I even be able to discern the different chromosome shapes without training? I've heard the standard science project way to extract DNA (dish soap, salt, alcohol) damages the chromosomes so that you wouldn't really find them in a microscope; if true I hope there's another way.

If you want mitotic chromosomes then you want to look at apical meristems — probably the primary root from germinating seedlings will be easiest.  Apical meristems are at the growing tips of roots (and shoots) and contain regions of rapidly dividing cells.  Since you can only see chromosomes as separate bodies when they are condensed for cell division this increases your chances of visualizing chromosomes.
However, you will need to stain the roots to visualize the chromatin (material that makes up chromosomes).
This paper has a protocol for staining dandelion root tips, but I don't know whether you can obtain all the necessary compounds.  However, colchicine and para-dichlorobenzene probably aren't really necessary (they will increase the number of cells in mitosis) and are toxic so best to avoid those steps anyway.
Note, it looks like you would also need a 100x oil immersion lens, which doesn't look like it comes with the microscope you listed.
You may also find this paper useful as a starting point for making "homemade" chromosome stains.
Good luck!


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Are there any animal species other than humans & chimps that engage in tribal conflicts?
i.e., between tribes within the specie.
(For chimps, see, e.g., https://news.nationalgeographic.com/2016/01/160130-animals-insects-ants-war-chimpanzees-science.)
Am seeking examples to develop taxonomy of such conflicts, e.g., for resource acquisition, enslavement, etc.

this depends largely on how you define tribal conflict, ants for instance go to war.

Thx — elaborated q to clarify

That does not help clarify. You need to define "tribal conflict" otherwise this is just opinion.

In the introduction of an article by Gavrilets and Fortunato, the authors give (with references) some examples of intra-specific group conflicts:

Social organisms living in stable groups often engage in aggressive interactions with conspecifics from neighbouring groups over territory, mating opportunities and other resources... Examples include border patrols in chimpanzees, raiding parties in spider monkeys, clan wars in hyenas and between-group fights in lions, free-ranging dogs, meerkats, Capuchin monkeys, blue monkeys, black howler monkeys and ring-tail lemurs.

Whether these conflicts (or others, such as ant colony conflicts) meet your definition of "tribal conflicts" you will have to decide.

Thank you -very- much — an excellent article, on point.

Surprisingly, bonobos do. A study from researchers from the Max-Planck Institute for Evolutionary Anthropology back in 2008 and other research found that even though bonobos prefer to solve problems using sex, bonobos fight each other and even other great apes.
The same thing applies to bees. Australia's stingless bees go to war where thousands of worker bees perish and the young from the losing side are dragged out of the nest to die. Slave-making ants raid and attack other ant species. These intertribal conflicts seem to happen in nature due to in-group favoritism that causes certain creatures to favor members of their own phenotype when it comes to companionship and territory defense.


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ATP and Muscle Contraction
I have a question regarding how molecular interactions manifest in physical actions - such as hanging from a bar. To the best of my understanding, when it comes to the contraction of muscles, ATP is required for myosin to detach from actin - terminating contraction.
So, what I'm wondering is when we are hanging from our bar, utilizing our grip strength, we are in a constant state of contraction. However, eventually, our muscles fatigue and we let go. I presume this is because we are running out of energy, but isn't energy (ATP) what was necessary to terminate contraction? Why do we eventually let go of the bar and how is this represented on the scale of muscle fibres?


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How does a ribosome move along mRNA?
I've been reading around Wikipedia recently trying to learn more about various biomechanisms. I’m intrigued by ribosomes — with how small they are, they’re basically chemical machines from what I can tell. I’ve got the general idea of what they do, which is nicely illustrated in the super common GIF below:

My question is how this happens, on a molecular/chemical scale. Even in the GIF, the way the mRNA is being so mechanically fed through the ribosome at the exact-right times seems so deliberate, and I can’t imagine a chemical process that does this so well. It seems like we know the exact protein by protein structure of a few types of ribosome; as such, I naively assume we can work out exactly why and how it does each thing it does. I’m sure it's not a simple question — if it's not really answerable in a stack exchange question, then I guess my question becomes where should I read to learn this.

Your question and tags are fine in principle, so I'm deleting your remark about them. Your supposition that this is a simple question is completely wrong. It is the animated gif that is simple, not least because our knowledge of the process is based on static views of the ribosome. The reality is extremely complex and requires one to read original papers in detail. I doubt anyone could summarize what is known here. I'll see if I can find a decent recent review to point you at.

I've modified your question a little more (restricted the title to a single question and specified messenger for the RNA — mRNA). And give an "answer" with some references.

I agree with David. The exact mechanism cannot be explained here. You need to read the articles/papers on the structural biology of the process. It is also not very easy to understand even for biologists who are not working in that field.

Disclaimer
It is not clear to me that requests for references are on-topic here. In general I would think not, as they are subjective and not about biology per se. I therefore solicit neither votes for, or acceptance of, this answer. I would have used the comment area to provide references, but there isn’t really enough space, so I decided to flesh it out into what follows.
Overall perspective of elongation in protein synthesis
The main concern of the question is the movement of mRNA during translation, so I shall focus on elongation (rather than initiation). Most of our detailed knowledge of the ribosome is based on static ‘views’ of the ribosome at different stages, although there is a paper (reviewed in Nature by Ehrenberg) in which the dynamics have been deduced from millions of time-resolved electron microscopy images. I doubt whether that is what the animation in the Wikipedia article is based, however.
After an introduction to the subject from Wikipedia, I strongly recommend graduating to a good text book. Text books have the advantage over Wikipedia that they are comprehensive, integrated, professionally illustrated and sent out by publishers for review. Berg et al. is probably as detailed as you will find in a general text, the 2002 edition is available online (as are others such as Alberts et al. and Lodish et al.) through NCBI Bookshelf.
Figure 29.24 of Berg et al. provides a static general view of elongation:

You need the associated text to understand this properly, but the step at which the mRNA is thought to move with respect to the ribosome is the penultimate one in the diagram: translocation.
Unfortunately you can’t just read through books on NCBI Bookshelf — you have to search for particular topics. But Chapter 29 of Berg et al. is what you need, and the links to the relevant sections are:

29 Introduction
29.3
29.4
29.5

How exactly does the mRNA move?
The details of the individual steps in protein synthesis are being deduced from examination of high-resolution structures of complexes at different stages. For the student who as able to go beyond the accounts in general textbooks, a review such as that published in 2009 by Schmeing and Ramakrishnan is perhaps the next port of call. But, chemical virgins beware, this is structural biology, and there is no simple answer that you can scribble on a table napkin!