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Why does the formula for blood velocity hold true?
v = Q/A
where
v = velocity (cm/s)
Q = blood flow (ml/s)
A = cross sectional area (cm2)
So the greater the cros sectional area, the lower the velocity, assuming that the cardiac output is a constant for a individual.
But i dont understand the formula content wise, why do you get the velocity by dividing Q by A? I do understand that the units are correct, and you get cm/s as final unit.
Can anyone explain this, perhaps graphically?

In the capillaries the A must be extremely low, yet why is the velocity so small? My book says that you have to add all capillaries up, but you cant do that, since you would get the velocity of an extremely big pipe, which isnt that of a capillary?
Thanks in advance for answering.

Very relevant link https://journals.physiology.org/doi/full/10.1152/advances.2001.25.1.44

In the capillaries the A must be extremely low

For a single capillary yes, the area is small.
However, these statements are not referring to a single capillary! They are referring to the entire capillary bed when it says "the capillaries". There are many many many capillaries and their total cross-sectional area is large compared to other vessels. Blood doesn't flow through each capillary in series, it's flowing through them all in parallel.

So if it flows parallel then the Q gets divided into many capillaries, making the nominator in the formula extremely low, and the area  in the denominator as well since it is a capillary. So the velocity decreases, since Q decreases more than A decreases for each capillary.

Is this true?  c

@excellence Yes, that's true, but I think the best way to think about it is to just think of the "A" as the area for all the capillaries (so, A = N * a, where N is the number of capillaries and a is the area of one capillary). The total A is larger for the capillary bed than it is for, say, the arterioles (this is what your figure shows in the blue line). It doesn't matter what N or a is to determine velocity, just N*a.

So the book is just avoiding to explain in mathemathically, which causes confusion and i had to spend lots of time finding out what was going on

@excellence No I think they're explaining it just fine, you just need to notice that the Y-axis on the right is total cross-sectional area, not for a single capillary. If you missed that point I can see how it would be confusing, though.

Well in reality the capillaries are not bundled together an can NOT be seen as just one big blood vessel, but rather a lot of minuscule capillaries with an extremely small Area. What I mean is, how can you say the blood speed is very low there, because of a huge Area. As i said: the velocity decreases, since Q decreases more than A decreases for each capillary. Why didnt they just show it like this, after all, A doesnt increase but LITERALLY decreases, and Q does too, but much faster. The result is a low velocity. AM i right?

@excellence No, you are not right. "A" here is the total cross sectional area. That's what's plotted on the Y axis and is labeled as such: "Total cross-sectional area". This total area is large in the capillaries, which is why velocity is slow there. For the purpose of calculating the velocity as presented in this chart, yes you can consider it as one big blood vessel, and that's what they are doing. They are considering the entire capillary bed together, just like they are considering all the arterioles together, all the venules, all the larger veins, etc.

@excellence, In reality the capillaries are all bundled together: at one end by the arterial vessels back to the aorta, at the other by venous vessels on to the venae cavae,  A, the total area, literally increases as you move from the set of large vessels to the set of capillaries.  The total blood flow per second through the aorta is the same as the total through the capillaries, so the blood is flowing much more slowly through the capillaries because of their vastly larger total area.

thanks for clarifying everything, very helpful

The trick here is that 1 mL = 1 cm3 (or cc).  So if you divide cm3/s by cm2 the result will be in cm/s.  What that means is that the blood volume has three dimensions - if you picture the vessel as a simple "box", then it has widths in two dimensions, which define a cross-sectional area, and then the third dimension is the distance that the blood has moved past, through the vessel, in order to define the three-dimensional "box" of blood that has moved past as the blood moved that distance.
The principle should be familiar from the phrase "still waters run deep".  A stream that flows rapidly in a shallow cascade over rocks can abruptly become quite slow at a deep hole, as a great depth and breadth of water is sharing the work of moving forward.


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Have scientists tried to communicate with Sperm whales?
I see lots of passive studies of sperm whale click "language", usually focused on fingerprinting to identify groups and individuals. There's application of deep learning, and all sorts of advanced analysis. However, I haven't found any examples of scientists actively producing their own clicks and trying to elicit responses from whales. It seems to me that successful interactions would push our understanding of the clicks forwards much faster with a bit of a debug/test cycle.
Have studies like that ever been done? If so, can I please have links/references to the papers? Thanks!!

There has been a study / rescue attempt of a group of male sperm whales a few decades ago, where female sperm whale codas (a type of rhythmic communication clicks) where played from an underwater transducer in order to entice the males and lure them from an area of confined waters and into deeper water.
According to this study1, the playback was not successful in terms of getting the whales out to deeper water, but on one occasion, one of the sperm whales made a close approach to the playback sound source. A variety of sounds were produced by the sperm whales, but no codas were recorded.
References:

Goold, J. (1999). Behavioural and acoustic observations of sperm whales in Scapa Flow, Orkney Islands. Journal of the Marine Biological Association of the United Kingdom, 79(3), 541-550. https://doi.org/10.1017/S0025315498000666

You're right that there have been few playback studies assessing the response of sperm whales to sperm whale clicks. A couple of studies have shown a response (reduced foraging, returning to surface[1,2]) when killer whale vocalizations are played in the presence of sperm whales.
As an acoustician focused on odontocete echolocation clicks, I field a lot of questions about communicating with whales and when we're going to "get there" or "figure out what they're saying". Based on the title of your question, I'm not sure whether you envision the end goal of playback experiments to be getting us to the level where we could communicate specific messages to the whales themselves. If that is what you mean though, I think we're probably a long way off from that, and I'm not sure whether or not it's possible. It is not a guarantee that the way we use language and the way sperm whales using vocalizations are compatible enough for us to truly communicate.
If you mean communicate more in the context of understanding what types of clicks mean by playing them at the whales and observing their response, i.e., when we play clicks of type A, the animals always come to the surface, so clicks of type A must be some sort of surfacing cue, that's also very complex. For one thing, to draw conclusions you'd likely have to conduct experiments in a wide variety of locations/different groupings of animals, which gets expensive fast. Additionally, as animals are difficult to observe at sea in most cases, you have to factor in the added expense of equipment such as satellite tags that would be required to understand the animal's response to the sound, as you likely couldn't rely on simple visual observation. I'm not saying these efforts wouldn't be feasible, but to my knowledge these are some of the reasons why they may not be more common.
References:
[1] Curé, Charlotte, et al. "Responses of male sperm whales (Physeter macrocephalus) to killer whale sounds: implications for anti-predator strategies." Scientific Reports 3.1 (2013): 1-7.
[2] Isojunno, Saana, et al. "Sperm whales reduce foraging effort during exposure to 1–2 kH z sonar and killer whale sounds." Ecological Applications 26.1 (2016): 77-93.

Project CETI (Cetacean Translation Initiative) is designed precisely to understand sperm whale vocalizations. https://www.projectceti.org/
Check out recent talks by Ellen Garland and Shane Gero about Project CETI with the SETI institute. Note - SETI is trying to find intelligent life in the universe, while CETI is focused on whales here on earth.
https://www.seti.org/event/seti-talks-whales-their-song-their-culture-another-intelligence-earth

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Estimate sex-specific survival from mark-recapture data using multi-site, sex-specific cormack-jolly-seber model?
I am interested in identifying sex-specific survival rates. I have a long-term dataset of individually marked birds from one breeding colony. Of these, I am able to genetically sex a subset. Additionally, I have access to mark-recapture data on nearby breeding colonies and so can estimate emigration from my target breeding colony. However, I am only able to sex individuals from my focal breeding colony.
My research project addresses both survival and dispersal (permanent emigration). So I'd like to disentangle these as much as possible and look at effects of sex. One approach is to only model the subset of birds I'm able to sex. Another approach would be to model all individuals, including unknown sex, and apply the techniques in Nichols et al. (2004) to apply probabilities of "male or female" to unknown-sex birds (I may be summarizing that poorly).
Can I use a multi-site model if I only include individuals marked on one colony, but do have data for permanent emigration to other colonies? Would it make sense to use a multi-site model with all individuals from all colonies but only have sex information from one colony?
Thanks in advance!
Nichols, J.D., Kendall, W.L., Hines, J.E. and Spendelow, J.A. 2004. Estimation of sex‐specific survival from capture–recapture data when sex is not always known. Ecology 85(12):3192-3201.

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What is Lysoferrin?
I was going though my Guyton and Hall Medical Physiology when I came across the name of an antibacterial lysosomal enzyme - Lysoferrin. It said that Lysoferrin "binds to iron and other metals that are essential for bacterial growth." I looked across the web to find some context about it but found every site quoting the exact same Guyton lines. Some more information about this enzyme would be a real help.

Have you looked to see if your text provides any primary references to their claim? I'm wondering if this is just an outdated term for something else. From the description, It sounds a bit like Lipocalin-2. Lactoferrin and Ferritin are also iron-binding proteins that can be unregulated during infections, but they both serve other functions in maintaining iron homeostasis.

A Japanese patent filed by Raymond Jay Bergeron, Jr JP2000514089A notes lysoferrin as the siderophore
N1, N4-bis (1-oxo-3-hydroxy-3,4-dicarboxybutyl) diaminobutamate. The US counterpart of this patent, jointly filed as US application No. US08/783,306 and later issued as US 5,739,395 covers rhizoferrin in its embodiments. So it seems that the term lysoferrin is just another name for rhizoferrin, perhaps a translation aftefact?
Rhizoferrin Drechsel, H. et al.  (1991) Biol. Metals 4:238–243 has the following structure .
Edit: Just to be clear, lysoferrin is not an enzyme, but the siderophore pictured above.
Here’s from Wikipedia:

Siderophores are small, high-affinity iron-chelating compounds that are secreted by microorganisms such as bacteria and fungi and serve primarily to transport iron across cell membranes, although a widening range of siderophore functions is now being appreciated. Siderophores are among the strongest soluble Fe3+ binding agents known.


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Sensitivity vs. Limit of Detection of rapid antigen tests
I'm comparing a bunch of SARS-CoV2 rapid antigen tests:

Source
Columns 4 and 6 list the values for sensitivity and limit of detection (LOD). How come that a test with a several times lower limit of detection can have a worse sensitivity?
As an example, consider tests #2 and #4:
#2 - Sensitivity: 97.7% - Limit of detection: 2.0*10^2.4 = 502 TCID50/ml
#4 - Sensitivity: 91.4% - Limit of detection: 2.5*10^1.8 = 158 TCID50/ml
Shouldn't these values correlate, i.e. the more sensitive a test is the smaller the amount it is still able to detect?

Not necessarily. Sensitivity and specificity are decision criterion-based measures. They are not actually separable from another, they are a consequence of choosing a threshold at which to say "the test reports positive" or "the test reports negative", a consequence of this binary result. As such they are weighed against each other. You can always make a test with 100% sensitivity as long as you always report "Yes". You can always make a test with 100% specificity as long as you always report "No".
Similarly, you can define what it means to have reached a limit of detection, but this need not be the same trade-off as the one you use for sensitivity and specificity. For example, you might declare this as the point where your readout is "significantly greater"  than baseline in a collection of known positives vs known negatives. But if you set your decision threshold right at that level of detection, you may still have, let's say, only 50% specificity at that level and accept too many false-positives, so you set a different decision criteria.
They are apples and oranges, there is no reason they need to correspond.

Thanks for your answer! So which value is more indicative for the quality of the test? Say, I have two tests with the same sensitivity, but one has a much lower LOD - or - two tests with similar LOD, but one has a higher sensitivity (all other parameters being similar, incl. specificity). How to make a decision?

@david There isn't enough information to make that decision. Probably all of the tests on your list are statistically equivalent, unless there are substantial discrepancies in how they were evaluated. For example, you could get an artificially high sensitivity if you tested only very saturated target samples. You would need much more extensive real-world evaluation than I am aware of anyone having on hand as of yet.

Also, making a test report always "Yes" doesn't make it 100% sensitive if it gives false positives most of the time, does it? Sensitivity measures the true positives, so one cannot simply "tweak" the reported sensitivity by relaxing specificity, right? Example: If my test reports "Yes" every time it encounters aqueous oxygen, this doesn't make it 100% sensitive (it could very well be 0% sensitive by completely failing to detect the antigen in a deoxygenated solution).

@david Sensitivity is "true positives"/"actual positives". If you always report Yes, you will have 100% sensitivity: you report every actual positive as true positive. You will also report a lot of Yes when it is an "actual negative", but this doesn't hurt your sensitivity, it hurts your specificity. A test that always says "Yes" has 100% sensitivity and 0% specificity. You're right that this isn't a very good test, but just knowing sensitivity doesn't help much with that.

Are you using "true" and "actual" as synonyms or are you saying that sensitivity = true pos./actual pos.?

@david A "true positive" is a positive your test says is positive that is truly positive. This is standard terminology. "Actual positive" isn't standard terminology, usually people just say "positives", but I'm using it to indicate the number of positives in the sample. So it's the latter equation you write. In this terminology you could also write "actual pos = true pos + false neg", since false negatives are the positive cases that are falsely marked negative.


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What is the minimum water consumption for Arabidopsis and other plants?
I'm working on a project to design a self-contained plant growth environment for germinating and growing plants in space. It's important to know the absolute minimum amount of water and nutrients required to keep the plants alive and healthy over the course of 30 days, since we have very little space to store the water.
The plan is to use a single water reservoir to feed three separate growth chambers by injecting nutrient-rich water directly into a soil medium, similar to the ISS Veggie environment. We want to find out how much water we need to inject and how often.
I've looked over the literature as to what previous astrobotany projects have done. While they are typically very clear about the nutrient composition of the water, I have yet to find one that clearly states how much water the plants were given, and how often.
I focused my search on Arabidopsis thaliana to start, but ideally we would like to know water requirements for all major groups of small plants.
This seems like it shouldn't be a difficult question to answer. What am I missing?

The plant will intake water to keep constant internal water pressure to compensate for evapotranspiration. However, the evapotranspiration will not be a simple universal number.
The evapotranspiration rate strongly depends on temperature, air humidity, water tension inside the plant you want to keep (may it wilt?) and also the radiation received by the plant (PAR - photosynthetically active radiation) and also the air flow. In longer time that will also depend on the ventilation of air in your box. That means how fast water vapour escapes the air from your box and whether any of it condensates.
Also, how much water evaporates from the soil itself? That depends on soil properties, air temperature and also air flow.
A common model for evapotranspiration is by Jarvis and Stewart but is most often used for trees. You can read about interesting measurements of evapotranspiration at Whole plant open chamber to measure gas exchange on herbaceous plants.


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is blood anaerobic?
I was wondering if anyone knows whether there is free molecular oxygen in the blood?
My reasoning would be that oxygen is too reactive to be left alone in the blood, that's why it is transported in a little metal box called hemoglobin. Because of this, blood serum ought to be anaerobic(I know that some immune cells produce reactive oxygen species to kill off microorganisms, but let's ignore this for now). Is this correct?
for those who downvoted the question try to find the answer by googling it. All it shows is anaerobic blood culture of bacteria.
Who said this is homework? I'm probably three times as old as you are and you go flagging this as homework? really? get a life.

Oxygen presumably does dissolve in blood.  At least nitrogen does (as any scuba diver could tell you), and I don't know why oxygen should be different.  And a quick search shows it does dissolve in blood, but only about 2% of the amount carried by red blood cells: https://www.ncbi.nlm.nih.gov/books/NBK54103/


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Is my understanding of the Bergmann's rule correct? (mass is secondary)
According to Wikipedia, Bergmann's rule applies because animals living in colder areas have greater  surface-area-to-volume ratio. If I understand that correctly, the advantage of the bulkier bodies of the polar animals isn't really about having a greater mass but about having a shape more closer to a sphere - which usually means having a greater mass.
Am I right?

No, your argument seems to be flawed. Sphere’s surface-to-volume ratio is proportional to the radius, and a small sphere may have worse ratio than a bulky irregular body.

@jmster That's exactly what I don't seem to get. Isn't size relative? Like how come the ratio is different for a small ball and a big one. The way I see it, the size only tells us comparison to human metrics like meters. Let's say there's a planet A with a ball 1 meter wide and there's a planet B which is twice as big so the humans who live there say the ball is 0,5 meter wide even though it's the exact same size as ball A. Can you please explain how come "size" matters as a seemingly arbitrary parameter?

Heat transfer and many other physical processes depend on the molecular structure of the materials. The molecules on a big planet are not proportionally bigger than on a small planet, that's why you cannot expect everything that happens on those planets to scale up linearly.

@jmster Right, thank you! Both of the occasions when I was explained the rule involved the presenter mentioning that surface of a sphere grows with square of the ratio which rightfully didn't make sense to me as the explanation.

A couple of things. First, SA:V is lower in colder environments (see the similar "ecogeographic rule," Allen's Rule, Wikipedia. Second, SA:V and mass are two somewhat independent traits are the result of somewhat independent evolutionary mechanisms. Temperature affects mass, temperature affects SA:V, but SA:V does not affect mass.

@ChrisMoore Thanks, If I get you correctly, you confirm jmster's comment that the Bergmann's rule applies because it takes more molecules to build several small rabbits than to build one rabbit of the same mass?

@Probably : Not exactly. I am meaning to state what I have in the last sentence: temperature affects mass and temperature affects SA:V, but SA:V does not affect mass or vice versa.


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Why is the mRNA not damaged at -70 C temperature Corona vaccine?
Why is the mRNA not damaged at -70 C temperature Corona vaccine?
Need for -70 degree temperature for Corona vaccine
I assume that if I, for example, were to freeze, say, a chicken egg after heating to room temperature, the protein binding would be destroyed.
What mechanism, process or substance ensures that at -70 C mRNA is not damaged? Or is this a natural property of the mRNA itself?
As I understand it, random errors in the conformation of DNA, RNA and proteins often lead to information distortion.
https://translate.google.com/translate?sl=pl&tl=en&u=https://pl.wikipedia.org/wiki/Konformacja
Sorry for My English.

An egg is an egg. A molecule is a molecule. If you ask this sort of question you need to set out a chemical reason why a molecule should be harmed by freezing. Do you have one?

Yes I have one: https://translate.google.com/translate?sl=pl&tl=en&u=https://pl.wikipedia.org/wiki/Konformacja
Auto translated from polish.

Maybe you want to ask here or chem SE a simple q like "how do cryoprotectants work for preserving RNA?" instead of offering your theories. Conformational isomerism (which you've linked to in Polish) doesn't seem to have anything to do with that... (I should also say here that the vaccine is not just mRNA, but mRNA contained in lipid nano-particles [LNPs], so some of the freeze-thaw effects on cell-like structures may matter too. But as far as I can tell cryoprotectants are used even for "unwrapped" RNA preservation, so you may start with asking about that.)

Why is the mRNA not damaged at -70 C temperature Corona vaccine?

Actually they use Sucrose as cryoprotectant.
https://medicalsciences.stackexchange.com/questions/25289/why-use-sucrose-rather-than-glucose-in-an-injectable-vaccine/25290


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Can you recognize this larvae that came from a human nose? (probable nasal myiasis?
Those larvae came at least four different times from the nose (inside - from the mucosal) of a 60 year old man from a tropical area in South America. He lives and works in a city with a tropical climate. On another occasion a living insect came out of his nose, the picture is also attached.

Approximately how big are the larvae and (presumably adult) insect? Did he find all of these around the same time (over the span of hours/days) or were there longer intervals between them?


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Multiple fission and spore formation

I came across this question today. In the B diagram, zoospores of chlamydomonas is given. Now my doubt is, are the zoospores formed by multiple fission or spore formation? If it is by spore formation, isn't spore formation and multiple fission the same thing when it comes to unicellular organism i.e chlamydomonas? If it is the same thing, why isn't option c correct in the question I attached?

I will answer later, so I can provide a good ref. The issue is whether this shows the result after fission (asexual)  or meiosis (sexual). Showing 9 daughter cells is a bit unfair..2,4,8,16 would be better. After meiosis the 4 daughter cells can also continue to divide by mitosis before release.

But zoospores are produced asexually, so meiosis isn't possible. Also is multiple fission produced by mitosis or amitosis?

All the organisms shown in the figure reproduce asexually. (A) is Penicillium in which non-motile conidia are produced singly or in chains. Organism (B) is Chlamydomonas in which reproduction occurs by zoospores. In Hydra (C) and yeast (D), asexual reproduction takes place by budding.
Mutliple fission and Spore Formation are two distinct processes where in:

Multiple fission can be explained with the following diagram:

Multiple fission is a process of asexual reproduction in which a single organism splits up into multiple organisms or daughter cells of similar type under favourable conditions like availibity of food and suitable environmental conditions.

Spore formation can be explained with the following diagram:

Spores are tiny microscopic hard unicellular sexual bodies which are always suspended in air. Under suitable environmental conditions they settle down and grow into new plants. Above given is a structure of rhizopus(bread mould) reproducing through the process of spore formation. Each rhizopus consists of a globular structure at the top known as the sporangium which consists of spores. When the favourable conditions arrive then the sporangium bursts and the spores get suspended in the air. Soon they settle on the moist bread particles, leading to the formation of new rhizopus plants.


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Nucleotide Sequence
So i am from an IT and my sis who is doing medicine asked for my help on this question i have no clue where to start actually. Please Help. So the question is:

What is the nucleotide sequence for vibrio cholerae bacteria or
treponema pallidum bacteria? or any other related bacteria?

After the nucleotide sequence is got, is possible to use BLAST (https://blast.ncbi.nlm.nih.gov/Blast.cgi) to align and compare a query DNA sequence with a database of sequences?
Please correct me wherever i'm wrong and thanks for helping

I think this is more suited to SE.bioinformatics.

Yes it is possible. That's what BLAST is for. The nucleotide sequences can easily be found by searching the NCBI Nucleotide database.

There are at least 102 genomes of the bacterium Vibrio cholerae that have been sequenced. For example, Vibrio cholerae 01 biovar El Tor strain N16961 has two chromosomes spanning 4,033,464 bp in which its ORFs code for 3,827 proteins and 122 RNAs. Check here The DNA is available at NCBI as entries AE003852 and AE003853.
There are at least 11 sequenced genomes of Treponema pallidum. For example, Strain Fribourg-Blanc has 1,004 protein genes and 54 RNA genes distributed over 1,140,481 bp genome. NCBI DNA sequence entry NC_021179.1
I suppose one may align multiple sequences of whole genomes if that's what intended, but I do not advise it unless one is ready to curate the results. Instead, I recommend studying a given open reading frame using its DNA sequence, or better yet its corresponding protein sequence. BLAST should be quite helpful in finding similar sequences to compare to.


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Review paper on gene expression regulatory mechanisms
I'm a junior grad student in bioinformatics with CS background. I am involved in a project around discovering gene regulatory networks in some data, which got me curious about the gene expression regulatory mechanisms in eukaryotes. I found this page on Nature, which looks super helpful:
https://www.nature.com/collections/pfdsgqgzck
But it does have 27 review papers listed there. Are there any review papers you could suggest that sums up/introduces different regulatory mechanisms and regulatory factors (CTCF, chromatin accessibility, TFs, enhancers, promoters, lncRNAs etc) in a more global overview?
Thanks!

That page looks to be a promotional effort for their review articles, organized by recency and selected by some keyword like 'regulation'.


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Is chromatic aberration related to the spectral sensitivity of the human eye and can it cause "relative myopia" and "relative farsightedness"?
in the text below, the authors equate chromatic aberration and the spectral sensitivity of the human eye. Aren't these two very different phenomena though? They also propose a so-called "relative myopia" and "relative farsightedness". Are these claims valid? Does chromatic aberration even pertain to the human eye? I can only find sources that discuss this phenomenon within the field of photography.
I would very much appreciate any citations that debunk this text.
Here are my summed-up points that I, as an amateur without any formal education or training in ophthalmology, find problematic. I think that the text:

equates chromatic aberration and the spectral sensitivity of the human eye – which are two very different phenomena
proposes that chromatic aberration (which is a property of a lens) happens in all human eyes and it causes a so-called "relative myopia" and "relative farsightedness" – terms I cannot seem to find online. Would not this result in all of us seeing blurred colourful fringes and haloes around objects, just like you can see in a photograph taken by a camera that strongly exhibits chromatic aberration? I can't find a study to support my point though.
states that the human eye is most sensitive to the yellow-green wavelength range because this range is most predominant in the Sun's spectrum – but isn't it so because the weighted function of the spectral sensitivity of our cones simply lies around 555 nm? Maybe these studies might help, I am not sure [1,2]. They also vaguely state that this yellow-green range has "the most favourable effect on humans" which is confusing, what does that mean? For example, "favourable" during the night certainly is light devoid of blue and green wavelengths that suppress melatonin secretion [3,4,5] – so "favourable" is debatable without being specific.

The text:

When designing lighting, the chromaticity of the light used must be carefully considered. Due to the predominant yellow-green component in sunlight, the human eye is most sensitive to the yellow-green wavelength range and this light also has the most favourable effect on humans. On the contrary, red or blue light of the same intensity is much more difficult to perceive. In the eye, light with a high proportion of blue wavelengths falls in front of the retina, causing so-called relative myopia; on the contrary, light with a high ratio of red wavelengths falls behind the retina and causes relative farsightedness. This phenomenon is also called chromatic aberration (also a chromatic defect or colour defect) and it is necessary to keep in mind when designing the lighting systems or electronic displays.

The text is not published anywhere, it is an excerpt I got sent which I translated into English.
References
[1] Stockman, A., & Sharpe, L. T. (2000). The spectral sensitivities of the middle- and long-wavelength-sensitive cones derived from measurements in observers of known genotype. Vision Research, 40(13), 1711–1737. https://doi.org/10.1016/S0042-6989(00)00021-3
[2] Hofer, H., Carroll, J., Neitz, J., Neitz, M., & Williams, D. R. (2005). Organization of the human trichromatic cone mosaic. Journal of Neuroscience, 25(42), 9669–9679. https://doi.org/10.1523/JNEUROSCI.2414-05.2005
[3] Brainard, G. C., Hanifin, J. R., Greeson, J. M., Byrne, B., Glickman, G., Gerner, E., & Rollag, M. D. (2001). Action spectrum for melatonin regulation in humans: Evidence for a novel circadian photoreceptor. Journal of Neuroscience, 21(16), 6405–6412. https://doi.org/10.1523/jneurosci.21-16-06405.2001
[4] Al-Naggar, R. A., & Anil, S. (2016). Artificial light at night and cancer: Global study. Asian Pacific Journal of Cancer Prevention, 17(10), 4661–4664. https://doi.org/10.7314/APJCP.2016.17.10.4661
[5] Bonmati-Carrion, M. A., Arguelles-Prieto, R., Martinez-Madrid, M. J., Reiter, R., Hardeland, R., Rol, M. A., & Madrid, J. A. (2014, December 17). Protecting the melatonin rhythm through circadian healthy light exposure. International Journal of Molecular Sciences. MDPI AG. https://doi.org/10.3390/ijms151223448

Which of the references actually contains the text you quote - 1?

@MattDMo it is not an English text and it does not come a from a published work – it is just something I got sent.

OK, then you need to [edit] your question clarify it. All quotes need to have attributions.

There are two phenomena described in the quoted text, and while there is some relationship between them, they are indeed distinct:  spectral sensitivity of the human eye, and longitudinal/axial chromatic aberration of the eye resulting from variation of refractive index of the lens by wavelength.  I found the following on Physics.SE:
https://physics.stackexchange.com/questions/12602/do-eyeballs-exhibit-chromatic-aberration
which links to this interesting page:
https://www.telescope-optics.net/eye_chromatism.htm
Note that the existence of such aberration is a purely optical phenomenon, but biologically, the structure of the eye (in particular, the distribution of retinal cone cells, and neural processing) compensates for the resulting perception to a significant extent.
That said, I think the way the information is explained in the quoted text is not particularly clear, as it sort of jumbles the concepts together.  If you want to learn more, do a web search for key phrases such as "human spectral sensitivity" and "human lens dispersion."


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How long to breathe (the equivalent of) all of the atmosphere?
I have done some rough calculations of how long it might take humanity: approx 80,000 years (that's taking Earth's population as 7.5 billion, 11,000 litres a day of breathing, the weight of 1 litre of air at sea level at 1.225 grams, and the total weight of the atmosphere at 5140 trillion tonnes)
Please let me know if my calculations are massively out!
My question for you is admittedly much more complicated to answer - how long would it take all animal species combined to breathe the equivalent sum total weight of the atmosphere? and how long would it take all life combined (also including the weight of air of respiration in plants, fungi, algae, etc)?

Volume is probably not the best way to think about respiration for most of life on Earth, as it only really applies to animals with lungs (a small proportion of earth's biomass). Instead, it would make more sense to think about rates of respiration in terms of oxygen demands. With that in mind, an average human needs around 0.85 kg of oxygen per day (according to NASA). So, the annual oxygen needs of the human population would found by multiplying 0.85 kg/person/day by 365.25 days/year and 7.5 billion people to get ~2.3e+12 kg of oxygen per year.
For a crude estimate of how long it would take to use up our atmosphere's oxygen at that rate, we could simply divide the total capacity of oxygen in the atmosphere (~1.4e+18 kg) by the annual oxygen demand of the current human population (2.3e+12 kg), to get a rough estimate of 600,000 years for Earth's current population to use up all of Earth's current atmospheric oxygen (note that both calculations require some pretty dubious assumptions, but the problem already seems to start that way if I'm reading it right).
For an even cruder estimate of all life on earth, we can again take the Atmospheric Oxygen capacity (~1.4e+18 kg) and divide by the annual oxygen flux from atmosphere to biosphere (~3.0e+14 kg) to get around ~4700 years. (note that this assumes no flux from the biosphere back into the atmosphere, and also assumes that lithospheric flux is negligible.)
If you want to go further and calculate how long it would take for just animals to use up an atmosphere worth of oxygen, you could start by looking at how Earth's biomass is distributed, and make some more assumptions about the oxygen demand of other animals compared to humans following this same idea that I've used above.
Capacity and Flux estimates came (via wikipedia) from (Walker JC (1980) "The Oxygen Cycle". The Natural Environment and the Biogeochemical Cycles), but there are probably more up-to-date estimates available somewhere. The general idea would be the same.

Thankyou for the answer @MikeyC, those numbers from the oxygen cycle wiki page are really interesting too. Our initial figures are closer than they seem... as I was calculating the total amount of air that passes in and out of our lungs, only approx. 5% of which is taken in as oxygen... which should make my number 20 times less than yours, not 10 times less, so I will check that when it comes to doing the math more thoroughly....

I've started towards a way to figure out an answer - 1 litre of CO2 weighs 1.964g at NTP, and the amount of CO2 in one litre of air is about 0.04%. So one litre of NTP air contains 0.0007856g of CO2.

An adult tree (yes, very generic!) can take in about 21kg of CO2 per year, or 21,000 grams. 21000 / 0.0007856 = 26731160. So an adult tree must process at least 26 million litres of air a year (and that is assuming it is being 100% efficient, which it won't be... humans take up about 5% of available oxygen that they breathe, not sure what the rate is for stomata...)

There are an estimated 3 trillion trees on Earth. 3 trillion x 26 million = 8.1*10^19 litres .... however, I now realise I had the atmosphere in the units of tonnes, not litres...

... So that would be 9.92 x 10^19 grams of air, or 9.92 x 10^13 tonnes of air. Which is about 100 trillion tonnes of air, if I have understood the conversions right

If we take a totally wild guess of 10% for the efficiency of CO2 uptake of the air in the stomata of trees, that would bring the figure to 1000 trillion tonnes. That would mean it would only take 5 years for all the trees on Earth to filter the equivalent of the whole atmosphere!


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Tree identification in the Caribbean
I live in Puerto Rico and I'm trying to identify this tree and if possible how to kill it since it is infested with termites.
https://i.stack.imgur.com/2TfN5.jpg
Tree

Closer view of flowers and leaves. The rectangles on the floor are about 3mm x 6mm.

Seed pod

Hi Rick. Please copy your images directly into your post. Linking to external photos is not appropriate for our site due to the propensity for such photos to later become unavailable. Posts should be complete in and of themselves. [Edit] your post to include these photos, update with some measurements, and please provide more specifics about location/habitat. We'll be happy to try to help at that point. (see here for more guidelines). Thanks.

Google lense I.D. Program works on nearly all european and north american trees, bark and flowers, and many tropical ones. try it...

Google lense said either Saussurea obvallata or eucalyptus... I doubt it is.

@aliential I STRONGLY disagree with your statement about Google Lens, as it is, in my experience, patently false. From what level of botanical expertise are you coming from? The issue with such programs is that users are typically not equipped in any way to recognize/challenge the accuracy of results. I have only tested Lens out of curiosity for accuracy, and my personal take is that it is rarely accurate when it comes to IDing organisms (e.g., trees). Complicating this matter is that many species are no longer differentiated based on easily-identifiable gross morphological characteristics.

First discovery was a photo of a golden egg bug...100% ok was amazed. Second task was a split gill mushroom... 100%... then monkshood... 100% correct, and lense also manages various leaves and flowers, especially horticulture and unique patternings. I had very high accuracy for  common and morphologically peculiar and specific photos. Yes it though this pages photos are a mantis... awful. But the images are blurred... i recommend trying lense on certain types of targets like flowers and fruits, it can be very worth the 10 seconds of time involved. Try lense on photo of g egg bug.

Also, it got dogwood the first time and i read that Oetsi had dogwood arrows. That ID took me only 10 seconds. The photos have to be very identifying and only for well documented easy  species.

The photos of this tree indicate that it is a horseradish-tree (Moringa oleifera). See https://rngr.net/publications/common-trees-of-puerto-rico-and-the-virgin-islands as well as google searches of that species. Killing the tree will do nothing to eradicate the termites as they will just move onto another source of food.

Thanks for answering this question! We appreciate when new users with expert knowledge begin answering questions! Please update your post, however, to include more information about why your ID is correct. Given the propensity for external links to go defunct, we ask that your answer here can adequately stand on its own in explaining both the correct answer and your rationale. Support as a link is fine (and citing/linking sources is preferred/required), but please capture some of the relevant detail from your external source in your post itself. Thanks!


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Is there any commercial vector technology platform for boosting recombinant protein production?
I am a novice in biomedical industry. Our team would like to search new vector technology for boosting recombinant protein production. It's difficult to google a firm that provide those plasmids.
Dose anyone know if one exists?
Thanks!

What exactly do you mean with "new vector technology"? Vectors to transfect cells in order to have them produce proteins isn't exactly a new technology. Also: Which kind of protein (posttranslationally modified or not), which kind of cells?

Sorry for the misdescription. I mean engineered vector, such as ProteoNic 2G UNic™ technology platform, to product mAbs in CHO cells.

Why is it so hard to Google this topic? I'm sure there are guides out there to help people decide which expression system might be best for them.


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After removing the stigma from a flower, specifically the Crocus flower, does it eventually grow back or does the plant die?
After removing the stigma from a flower, specifically the Crocus flower, does it eventually grow back or does the plant die?  The reason why I am asking is I am trying to find a way to mass produce saffron.

Welcome to Bio.SE! Please limit each post to a single question and demonstrate your own research effort. See our [tour] and [help] for more information. We will be glad to help if 1) you [edit] your post to focus on a single question and 2) you explicitly demonstrate some of your own research effort (i.e., where have you already looked for an answer and what did you find out?). Failure to follow-through with these edits will likely result in downvotes and post closure, so please take a moment to [edit] accordingly. thanks!

Someone will find the pigment genes and engineer them into another crop like wheat or corn. that's the only solution. So if you want to do some crispr then that project would be worth a lot, but it's legally a minefield. saffron is a multi million dollar business and people with degrees in botany are trying to do the same as you, they have lots of tricks like molecular engineering and polyploidy by colchicine. https://www.actahort.org/books/650/650_31.htm

Neither.  (From personal experience growing a few saffron crocus in my garden.)  Like other bulbs (or in the case of crocus, corms, to be technical), the saffron crocus has an annual life cycle.  The bulb sends up leaves & flowers according to seasonal* cues.
The flowers will die whether or not you pick the stigmas. Indeed, the stigmas are usually the largest and most pickable just at the point when the flower is about to start senescing anyway.  At that point the plant is about to go into winter dormancy anyway.
The plant does not die, but stays in a dormant state over the winter, then grows leaves in the spring.  My experience, though, is that they will eventually deterioriate over several years unless the corms are lifted and divided.
The problem with mass production is not growing the plant: it grows readily in many areas of the world - but the labor-intensive harvesting needed.  The stigmas need to be plucked individually, and carefully.  Growing in a greenhouse would be possible, but uneconomical, since you need lots of plants to provide commercial quantities.  (70,000 plants for 1 lb/0.45 kg of saffron, per Wikipedia: https://en.wikipedia.org/wiki/Saffron ) It's unlikely that you could speed up the annual growth/flowering cycle enough to matter.
*Saffron crocus (C. sativus) is a bit unusual in that it flowers in the fall rather than spring.

Thank you very much for your answer!  But couldn't we build a massive greenhouse in Arizona, provided we have enough water, plant the corms in trays of soil, and divide them along a very slow and long assembly line.  The workers can sit comfortably along the narrow bottom-neck, listen to music and talk to each other while separating the saffron by hand?

@Michael Lee: I don't think (though I'm by no means an expert) that would be technically possible, since you couldn't speed up the annual cycle that much.  It sure wouldn't be cost effective.  I think you might have better luck genetically engineering bacteria to produce the specific chemicals you want.

You are correct in saying we cannot speed up the annual cycle, that I understand is six weeks, but I am frequently off on my numbers.  Build a massive saffron green house in Arizona, if we can provide it with enough water, grown in trays, and passed along parallel conveyor belts, pick the stigma by hand with workers seated comfortably, and treated humanely, I know this will work, and those chemists and biologists, who think bacteria is going to get us out of this mess we are currently in, are currently out of their minds!

@Michael Lee: No, the annual cycle I meant is not six weeks (that's approximately the fall blooming time), it's a year.  The corm is dormant in winter, sends up leaves in spring which nourish the plant.  The leaves may die back in summer, as it enters a second dormant period.  Environmental cues of some sort then trigger the fall bloom.  You might be able to speed that up a bit, but IMHO not much.  WRT workers, what's "humane" about sitting in a greenhouse all day, picking those thread-like saffron stigmas?  I'd rather be out in the fresh air, at least.


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In which reactions of glycolysis is magnesium involved?
I am currently studying the metabolic pathways for biochemistry and I am not quite clear in which reactions of glycolysis magnesium is involved.
So I have now found out that magnesium is present in the three ATP-dependent reactions (1st, 3rd and 10th reactions), but also in the 2nd, 7th, 8th and 9th steps.
According to this diagram:

In our university we have been tought, that Magnesium is present in all ATP reactions, but also in Step 2... this is what causes confusion for me:

Ok, have you found out what purpose magnesium can have in molecular reactions?

@Chris ok thank you for the hint, i should and will do that now.

@Chris I know that magnesium is used to regulate the movement of minerals across cell membranes. But what does it specifically in glycosis?

The general answer to this question is "all reactions involving ATP". This is covered in answers to another question.

please check my edit, why is it involved in Step 2

What is the source of your figure with magnesium ions required for the PGI reaction? The paper reporting the crystal structure of PGI and the protopedia page have no involvement of magnesium ions in the mechanism of the reaction. I have no reason, therefore to believe this is true. Furthermore, you should ask your University why they are filling your head with miscellaneous facts (or fictions) instead of teaching you to understand the principles of glycolysis.

In the 1st step where glucose is converted to glucose-6- phosphate by the enzyme hexokinase, in the 3rd step where fructose-6-phosphate is converted to fructose-1,6-bisphosphate by the enzyme fructose-1,6-bisphosphatase and in the last reaction where 2 phosphoenolpyruvate is converted to pyruvate by the enzyme pyruvate kinase.. In this 3 reaction Magnesium is needed as they are ATP dependent reaction and Magnesium stabilises the ATP in this reaction and help the reactions to proceed faster.


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Is there a known efficiency rate for CO2 capture from ambient air in photosynthesising plants?
When humans take in air to their lungs, we capture about 5% of the total quantity of the air as oxygen (which in turn equals about 24% of the available oxygen in the air)
Is there an equivalent rate for plants when photosynthesising (or a rate for any one specific plant?). I.e. if a plant had a given amount of air pass through their stomata, what percentage of the available CO2 is used by the chloroplasts?

Stomata should be compared to human alveoli, not the lungs. Also the lungs are pumps with heavy circulation whereas the plant heomoglobin is passive. The oxygen will tend to be carried by a metabolite whereas the CO2 can diffuse straight into the transportation medium, and the exchange depends on the gaseous gradient near the internal stomata surface.

I understand that trying to compare leaves/stomata to lungs/alveoli is problematic. However, I guess it would be possible to measure the amount of air that passes through a plant organism in a given period of time, and to measure the CO2 levels before and after in a sealed environment, and calculate from there? I guess there must be a lot more variables given it is a passive process in a non-homeostatic environment (like the lungs are) - but I maybe an efficiency range would still be possible?

I've started towards a way to figure it out - 1 litre of CO2 weighs 1.964g at NTP, and the amount of CO2 in one litre of air is about 0.04%. So one litre of NTP air contains 0.0007856g of CO2.

An adult tree (yes, very generic!) can take in about 21kg of CO2 per year, or 21,000 grams. 21000 / 0.0007856 = 26731160. So an adult tree must process at least 26 million litres of air a year (and that is assuming it is being 100% efficient!). Please let me know if I have done my calculations right


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Does alcohol really helps to get substances get faster into the bloodstream?
I saw the video where Arnold Schwarzenegger cooks some protein cocktail and adds Austrian Schnapps to the mix, saying that it's to make everything get faster to the blood. Is it true or some kind of a joke?
One person said this:
Alcohol inhibits protein synthesis, which is necessary for muscle building. It affects Glucose, which is needed for energy and recovery, so in this aspect it'll stunt your recovery and energy. For workouts, it dilates your blood vessels forcing blood into limbs and leaving core colder, what this means is that you'll loose performance. The article mentions that this mainly affects endurance
He says about effect of alcohol, that's a good question too.
And what about actually getting stuff faster into the bloodstream?

The total conclusion of all studies of alcohol is that moderate alcohol consumption has no beneficial effects on health. Some studies said a bit of alcohol is good for you... Most alcohol is metabolised by an enzyme in your liver cells known as alcohol dehydrogenase (ADH). ADH breaks down alcohol into acetaldehyde, and then another enzyme, aldehyde dehydrogenase (ALDH), rapidly breaks down acetaldehyde into acetate. Some people drink the wrong alcohol for covid... which ADH enzyme instead turns to Acetone or Formaldehyde.

About 20% of alcohol is absorbed right through the stomach after drinking.  This means alcohol could have a rapid effect on other aspects of digestion.  Specifically, it could affect the rate of gastric emptying, which would then affect how quickly other food is digested.  I found one paper which I think supports a faster rate of emptying, but another that says the rate of emptying is reduced.  This one says it is the sex of the volunteers that determines this.  They actually went on to look at the menstrual cycle.  Did I say this was one of the weirder batches of PubMed results I've seen lately?  You can find many more studies of alcohol and gastric emptying on PubMed, examining disease conditions and animal models.  I suspect that overall, considering the small sample sizes and heterogeneous results, it would be easiest to classify this use of alcohol among the myriad natural supplements for which there is "insufficient evidence of efficacy".


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Why did the indigenous peoples of northern Asia and America not evolve the same physical characteristics as people of Nordic ancestry?
I was watching DW's documentary on the Arctic the other day, and I was struck by how the indigenous peoples of the far north seemed - visually speaking - to fit into two categories. On the one hand, there are the peoples of northern Europe, with their pale skin and their preponderance of blue-eyed and blond-haired individuals. On the other hand, there are the Yakuts, Inuit, Aleuts and many more, whose physical similarities - they all seem to share an East Asian-looking bone structure, as well as black hair, deep brown eyes and a skin tone akin to white coffee - belie vast differences in language, culture and belief. Why did northern Europeans evolve these distinctive physical traits while other northern peoples did not? It's probably worth noting that the physical and temporal separation between, say, the Finns and the Nenets is much less than that between the Yakuts and Inuit.
It might be helpful to approach this by splitting up the different characteristics:

Pale skin: Of all the physical characteristics, pale skin seems to confer the most obvious advantage: better absorption of sunlight, and the various benefits connected therewith. Although I've not carried out any kind of systematic analysis, non-Nordic northern peoples do not seem to have a lighter skin tone than their southern neighbours (i.e. the Chinese, Japanese, Native American, etc peoples).
Blond hair and blue eyes: These are the most striking physical differences between Nordic and non-Nordic northern peoples, however it's not clear - at least to me! - what advantage they confer in high latitudes. Is it just blind chance that these characteristics evolved in northern Europe, and not in, say, Central America? If it's not blind chance, why did these characteristics evolve in northern Europe, but not in other northern regions?
Other characteristics: I have read that there are other characteristics, e.g. greater height, associated with high latitudes. Do Nordic and non-Nordic northern peoples have any of these characteristics in common? If there is divergence here, how might it be explained?

Regarding eye colour - remember that ecological selection isn't the only form of selection - sexual selection could potentially have played a role in the spread of blue eye colour, which could explain why it occurs in some populations and not others.

I'm also curious as to why this was downvoted - it seems like a reasonable question to me.

I did not downvote, but I'll hypothesize some possible reasons that others did: 1) why questions (especially regarding evolution) tend to be unanswerable outside an opinionated-scope (off-topic here), 2) multiple questions are being asked (posts should limit to a single question), and 3) numerous statements are made as matter of fact without providing support (we ask that all askers explicitly demonstrate adequate prior research on their own part). The current close votes are for too many questions, so I'd suggest the author (@tom) start by editing the post to limit to a single question.

@theforestecologist seems reasonable, thanks for the explanation.

Equatorial people can reach 1m90 average, i.e. regions in Africa. Statement 3 is wrong? ... statement 1 can relate to vitamine D. 2x UV blockage gives half vitamine D input, restricting inland populations and migrations. Statement 2 has many subtleties, blue eyes is a different thesis.

Why do Native Americans, East Asians, and circumpolar groups (i.e. Inuit) look so similar?
A lot of the reasons why Native Americans and east Asians look more similar is that they are more closely related, genetically speaking. Although there's been a lot of intermarriage between east Asian population and the rest of the Old World since then (not to mention the post-Columbian genetic history of the New World), Native Americans all descend from one to three populations of Paleolithic east Asians that migrated east across the Bering Strait. It is perhaps to no one's surprise that most trees of human genotypes typically find New World natives as a whole to form a group sister to East Asian groups.
Blond hair
The reason blonde hair is so common among Europeans and rare among most other places is that the mutation that produce blonde hair originally occurred somewhere in Europe (or possibly the parts of Asia near Europe) and has yet to spread widely. Red hair, in turn, is a mutation of the mutated gene that causes blond hair. Neanderthals had red hair, but it appears to be due to a different gene than the one that causes red hair in humans.
Blonde hair is not unique to Europeans. Solomon Islanders have it too, but it appears to be from a mutation in a different gene than Europeans.
Blue Eyes
As with blond hair, blue eyes are the result of a mutation in the human genome. The gene that causes blue eyes has been linked to a mutation that occurred in an individual that lived nearly 10,000 years ago on the north shore of the Black Sea, hence why the highest concentrations of people with blue eyes live close to that area (e.g., Scandinavia).
The thing is many of these genes may not confer any selective advantage, they may be neutral genes that arose due to genetic drift. For example Harding et al. concluded that the mutation which cause red hair confer no selective advantage in temperate climates, though they increase the risk of skin cancer in tropical latitudes. Similarly, the epicanthial fold may be linked to a gene that promotes hair growth but confers no selective advantage on its own. The same is probably true of other mutations, though I haven't dug through the literature to find precise examples.
This is the reason why pale skin and blonde hair are rare outside of the high latitudes. In temperate to polar latitudes they're harmless novelty genes and may even aid in vitamin D absorption, in subtropical to tropical latitudes they get rapidly removed from the gene pool due to being a one-way ticket to skin cancer.
Notably, part of the reason people from far western and far eastern Europe seem so different is because you aren't looking at the people in between. People in central Russia, central Asia, etc., show a mixture of traits. In fact, the Wikipedia page for red hair shows a young Uyghur girl from western China with both red hair and an epicanthial fold. Epicanthial folds are also increasingly common as you go west to east across Eurasia, they show up to with some frequency in eastern European populations like the Sami.
Height
Actually, normally people at the highest latitudes are shorter than those at lower latitudes (i.e., the Inuit), because shorter bodies help retain heat better.
Height is also highly variable and is often more subject to nutrition than genetics. If you look at a map of which countries are the tallest and shortest it maps more closely to GDP than it does gene flow. I'm reminded of a story of what happened when a large number of Guatemalan Mayans emigrated to the United States between the late 1970s and early 1990s. Guatemalan Mayans are some of the shortest people known, but this turned out to be due to poor nutrition growing up. Children of the original immigrants from Guatemala living on a more calorie-rich Western diet ended up being nearly 10 cm (almost four inches) taller than most Mayan children of that age.
Notably, the average height in Japan, China, and South Korea has skyrocketed over the last fifty years due to the increase in living standards.

Great answer! The only thing you've not quite convinced me on is height. Obviously, a lanky (for want of a better term) individual is going to retain heat less well than a short stocky one. But, if everything is in proportion, then surely a taller individual will retain heat a bit better than a shorter one? Bergmann's rule seems to have some things to say in favour of both sides of our disagreement.

@TomHosker That's the thing. Everything isn't in proportion. People of the far north have shorter limbs and more "barrel-like" torsos than people further south. This tends to make them shorter, but stockier. This difference is more noticeable in humans because we're bipeds, so a change in leg length greatly affects perceptions of size (since height is the unit we use to measure it)

If you look at the Wikipedia image from their lovely article on human migration, you'll notice that after arriving from Africa, some humans went west and others went east.  The ones who went east went on to most of the arctic regions, except in Western Europe.  The physical differences between these groups probably can be explained as random variation, though we may never know what social and environmental factors (such as the behavior of predators or prey) might have driven adaptive changes.
Previously some might have suggested different levels of Neanderthal ancestry could be involved, but this seems even harder to credit in light of recent evidence that all humans have a small but significant degree of Neanderthal heritage.


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Calvin cycle- combining three "turns"
In the common Calvin cycle diagram, it is commonly stated that "three cycles are combined to show the production of 1 molecule of G3P".
How does the G3P molecule escape from this cycle in one of these turns?
Is one carbon atom "released" from this cycle at each turn and the G3P forms in another reaction?
Or alternatively,
is the G3P released at the end of the three "turns"? If this is the case, then shouldn't this diagram represent only one "cycle" of the Calvin cycle?
[1]: https://i.stack.imgur.com/mzizw.jpg

Your question is unintelligible without reference to a diagram. Please revise your question accordingly, and phrase it so that it addresses a biological problem, rather than the interpretation of a particular mode of presentation in a specific text.

Not quite sure I understand what you are asking; the cycle is clearly not closed, there is a reactant entering and a product leaving, as well as interactions with other cycling molecules as ATP/ADP and NADPH/NADP+.

This is a great question - the secret in a nutshell is that five three-carbon G3Ps are turned into three five-carbon RuBPs at the left.  This involves a lot of making change with sugars - see the Wikipedia article section on the regeneration step.  You might also compare the pentose phosphate pathway.  I should submit an answer but I'm not feeling energetic enough to write out all those steps right now ... which is presumably how this textbook author felt!


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Do humans have any biological adaptations to eating cooked food?
Humans have been cooking food for at least tens of thousands of years. The presumed reason why cooking took root in nearly all human cultures is that cooked food is easier to digest. However, cooking food can also generate toxic compounds such as polycyclic aromatic hydrocarbons, which would not be found in the uncooked version of the food. Considering that humans have been eating cooked food for such a long time, I am wondering whether humans evolved any adaptations to eating cooked food, e.g., that certain types of foods, when cooked, are more toxic to our closest relatives (great apes) than they are to humans, because we have more ability to metabolize the toxic compounds.

I'd say that tens of thousands of years is too short a time on an evolutionary timescale to develop any adaptations. On the other hand, social learning did take place, in teh sense of learning of what can and cannot be eaten, how it should be cooked, etc. One could thus make an interesting study of how local cuisine has evolved via selection (what is available and edible), random drift (accidental trials and ideas whiel cooking), and other evolution-like forces.

@Vadim its really not, just look at the evolution of lactose tolerance in human populations that kept cattle.

Fair point. Indeed, if domestic animals had enough time to evolve into new species, so could humans. It is still not clear what are the evolutionary pressures here: I'd rather expect more random drift than adaptation.

Humans are incredibly good at processing maillard compounds, which include both beneficial and mildly toxic byproducts of cooking. Humans are better at breaking them down than other animals. This is presumed to be an adaptation to eating cooked food. Malliard reactions are also a good indicator of when most plant and animal products are safest to eat via cooking, (browning) which may explain why humans on average show a preference for them or even adaptations to detect them. we are also learning that one place animal testing may be problematic is in dietary tests becasue of this.
extra reading on hominid adaptations to diet

Adaptation implies selection. In other words, the claim is that those uncapable of digesting cooked food would have lesser chances of survival. On the other hand, more random drift is quite possible. A somewhat similar case is the increase of the number of women in need of cesarian section - it is not a adaptation to an evolutionary pressure, but result of removing such a pressure.

@Vadim no a trait to be better at doing something is also is also an adaptation. very few adaptations have lethal alternatives, they are just better than the alternative. humans are better at digesting cooked food than any animal tested, due to known unique enzymes, that is adaptation. https://onlinelibrary.wiley.com/doi/abs/10.1002/evan.21498

https://en.wikipedia.org/wiki/Adaptation
What you are saying that people became better at digesting cooking food (adapted) without any insensitive to do so. What could be an adaptation is if people began using cooked food, because they are better at digesting it. Also, the link that you provided emphasizes the role of the gut mircobiome, which is in a big part acquired during lifetime (apart from what we get at the birth, which is still not genetic).

@Vadim NO, incentive does not mean do it or die. incentive or in biological terms "advantage" comes from well having an advantage.  If Jon is better at digesting cooked food that Bob he has a distinct advantage, he is getting more nutrients and fewer problems from the same foodstuffs. Cooking was a part of the hominid diet long before Homo sapien evolved. Also only one link refers to gut microbes, that is the one that lists many factors.

advantage in evolutionary terms means producing more offspring - either by living longer or by doing it more frequently or in bigger numbers. If Bob produces as many miserable Bobs as Jon happy Jons, neither has particular advantage.

@Vadim if you don't understand how greater resource access constitutes an advantage I can only suggest you ask a few questions about evolution. This is pretty basic evolutionary biology.. To use an very basic example, why do herbivores have longer guts than carnivores?

I understand how greater resource access can be an advantage, but it doesn't mean that it always is. I am simply trying to help you clarify things. Your argument about humans being able to digest cooked food better is a solid one, but it needs to be correctly interpreted from the evolutionary standpoint.

There seems to be evidence that cooked food intake regulates different genes than raw food in mice. Apparently these genes also tend to be human specifically expressed (more precisely, their overlap is more than expected by chance) [1]. While this is not a dramatic finding, it does show association between cooked food and genomic changes that evolutionary adaptation implies.
As for toxicity of certain edible foods to non-human primates, I do not know the answer but I would not expect toxicity. Rather, high metabolic demand of humans might have required more protein based diet which is safer when cooked.
1 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4860691/


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What data would Meselson and Stahl have expected if DNA replication was dispersive rather than semiconservative?

What data would Meselson and Stahl have expected if DNA replication was conservative rather than semiconservative?

Answer:
In the first generation, there would be two bands, one of light density and one of heavy density. In the second generation there would still be two bands, one of light density and one of heavy density.
Question 1:
In the second generation, are the heavy-density bands getting closer to the end of the test tube, and the light-density bands closer to the top of the tube, than the first generation? (due to the larger number of DNA molecules)

What data would Meselson and Stahl have expected if DNA replication was dispersive rather than semiconservative?

Answer:
In the first generation, there would be one band, one of intermediate density. In the second generation there would still be one band, one of intermediate density.
Question 2:
Are the bands closer to the top of the test tube in the second generation than the first generation?
(Because DNA molecules would become lighter)
If this model was approved, could we see this change in the test tube? (Between first and second generation)

A few baseline ideas should be understood. 1. The assumption is made that Meselson and Stahl's cell line at the start of the experiment contains DNA composed entirely of the $N_{15}$ isotope. 2. DNA with a greater proportion of $N_{15}$ isotope is denser than DNA with lesser proportion of $N_{15}$ isotope. 3. Higher density DNA sinks lower in the test tube than lighter density DNA. (Same density DNA sinks to the same level.)
Q1: Let's follow 100 parent (generation 0) cells. If DNA replication was conservative, after they first replication (generation 1), we would expect 200 DNA strands. 100 strands come from the "parent" cells and are entirely composed of $N_{15}$ isotope (the conserved template strand). The other 100 strands come from "daughter" cells and are entirely composed of $N_{14}$ isotope (the newly synthesized strand). After the second replication then, we would expect 400 DNA strands. 200 strands come from the "generation 1" cells and share their DNA composition: 100 strands of $N_{15}$ isotope and 100 strands of $N_{14}$ isotope. The other 200 strands come from "daughter" cells and are entirely composed of $N_{14}$ isotope. Thus, in both generations, there are only DNA strands of 100% $N_{15}$ isotope and 100% $N_{14}$ isotope. The only difference is that the second generation has proportionally more DNA STRANDS composed entirely $N_{14}$ isotope than the first. Because the proportion of $N_{15}$ isotope and $N_{14}$ isotope in an INDIVIDUAL strand determines the strand's density, and because the strands in both generations comprise of 100% $N_{14}$ isotope strands and 100% $N_{15}$ isotope strands, the bands visible in the two test tubes are at the same level. They do not move closer to the ends of tube.
Q2: Yes this is correct. The first generation's DNA would all be ~50% $N_{15}$ isotope/~50% $N_{14}$ isotope strands. The second generation's DNA would all be ~25% $N_{15}$ isotope/~75% $N_{14}$ isotope strands. Strands of proportionally less $N_{15}$ isotope are lighter and thus closer to the top of the test tube.


text:
Are sensory mechanoreceptors and mechanical nociceptors the same type of neurons or are they different?
I always supposed the neurons / receptors which transmitted touch and pain were the same, since they react to stimulus which are the same but with different intensity, and they just sent a stronger signal in the case of something that has to be interpreted as pain. Though recently I've read some articles that imply they aren't, even so they don't say it directly. Reading more information I found this,

A nociceptor ("pain receptor") is a sensory neuron that responds to
damaging or potentially damaging stimuli by sending “possible threat”
signals.
Types and functions
Mechanical nociceptors respond to excess pressure or
mechanical deformation.

Nociceptor
Then,

Are sensory receptors neurons?
Receptor cells are specialized neurons

Are sensory receptors neurons?
And finally,

Sensory receptors are primarily classified as chemoreceptors,
thermoreceptors, mechanoreceptors, or photoreceptors.
Mechanoreceptors detect mechanical forces.

Sensory receptors
This doesnt give me a definitive answer, but it tells me both "sensory mechanoreceptors" and "mechanical nocireceptors" are neurons which responds to pressure/ mechanical forces. Are they supposed to be the same types of neurons named differently by different authors, or are they different types of neurons?

Short answer
Nociceptors are different from mechanoreceptors.
Background
Mechanoreceptors in the skin have specialized dendritic regions that facilitate their specific role in sensing different types of mechanical force, e.g., pressure receptors (Merkel’s disks) versus vibration receptors (Pacinian corpuscles and Meissner's corpuscles). See Fig. 1 for schematic representations of these types of receptors (Iheanacho et al). By contrast, pain receptors (or nociceptors) do not have specialized dendritic regions and consist of free nerve endings that respond to harmful mechanical forces (Purves et al., 2001).

Fig. 1. Skin receptors. source: Teach Me Phsyiology
References
- Iheanacho et al., Mechanoreceptors. In: StatPearls. Treasure Island (FL): StatPearls Publishing (2020)
- Purves et al., eds. In: Neuroscience 2nd ed. Sunderland (MA): Sinauer Associates; 2001. Nociceptors

I don't know if this directly answers your questions, but I think some confusion may stem from an underlying misconception of receptor vs receptor cell.
In most contexts (though not this one), 'receptors' do not refer to cells. Receptors are proteins on the cell membrane that transduct some signal/stimulus to the cell. Sometimes a "normal" peripheral neuron will have end processes that contain receptors that pass the signal directly to the neuron. Other times, a special 'receptor cell' is present. These cells are labeled as mechanoreceptors or nociceptors. The difference here is that a "standard" neuron is responsible for signal gating and propagation, whereas a receptor (cell) is primarily responsible for converting an external stimulus into a chemo or electrical signal recognized by "normal" neurons (or other cells).

Edit: As noted by AliceD's answer, different receptors have different proteins and thus have different mechanisms. To add, "nociceptor" and "mechanoreceptor" are categories. There are many different receptors that are nociceptors and many different receptors that are mechanoreceptors. Furthermore, nociceptor is a category of 'function' - it describes that the receptor responds to a pain/damage stimulus. A mechanoreceptor is a category of 'mechanism' - it describes how the receptor works. These categories are not mutually exclusive, and there are indeed nociceptors that are ALSO mechanoreceptors. (E.g. "Joint nociceptors are classified as high threshold mechanoreceptors" (source)) But not all nociceptors are mechanoreceptors and not all mechanoreceptors are nociceptors.

Added. As I understand it, cells that are both nociceptors and mechanoreceptors seem to be classified as one or the other depending on the use/field of research. In cases investigating the mechanisms of nociceptors, it seems they may be distinguishing the two to separate "other" mechanoreceptor from mechanical nociceptors as the mechanisms are indeed different.

"high-threshold mechanoreceptors respond to stimulation of higher intensity, and are a type of nociceptor." From the ever-so-very credible source of lumenlearning.

In any case, after revisiting op's question, I think your answer is more what op is looking for: the two are certainly not the same thing. We're sort of arguing semantics here, as some nociceptors are technically mechanoreceptors by definition, but few people would ever refer to them as both.

so, there are different types of mechanoreceptors, some will detect touch,  others will detect harm, those last ones are also called nociceptors? Or did I get it wrong?

Yes, that is correct.
Normally, people would not refer to them as such though. They would be one or the other. If it detects harm, regardless of mechanism, it will be recognized/addressed as a nociceptor only.


text:
Is it likely that humans will evolve to be less affected by dangerous food additives or tobacco smoking chemicals?
I recently had a discussion with a few colleagues about food additives and there were two major "arguments" about how some of these affect the human body in the long term:

some food additives will become less dangerous to humans, they evolve. The same rationale for smoking. The only similar thing I know to support this would be the ability humans gained to drink non-human milk.

the first argument is very unlikely to hold because in the vast majority of cases these substances do not affect reproduction and thus people getting sick and/or dying in their 50s+ is not affecting the evolution (food additives and smoking allow one to have children that can reproduce).

Neither of those involved has any in-depth knowledge of how evolution works in these cases and I am wondering if any of these arguments make sense from a biological point of view.

This is a really hypothetical question, since it assumes that particular food additives, or the practice of smoking tobacco, will be around for long enough to actually have an evolutionary effect.  But most additives have only been around a couple of generations.  Even widespread smoking was only around for a century or two. and is in decline most places.

Evolutionary effects only show up when they have a strong impact on the number of descendants that are produced.
Any disadvantageous effects due to things like food additives and tobacco appear to be quite small with respect to the ability of people to produce children and grandchildren. Moreover, since humans are social animals whose reproductive success is strongly determined by their social relations, there may be all sorts of other effects that interact as well, such as tobacco use being socially desirable or undesirable in particular (sub)cultures.
Thus, there is virtually no chance of evolutionary effects showing up before cultural or technological changes render the issue moot by changing the nature of the environment against which evolution would occur.

Probably not, if for no other reason than tobacco companies and other drug producers have been intentionally breeding their plants to produce stronger and stronger doses of the chemical so that their customers can get a stronger high. It's just another form of biochemical arms race.
As an example, there was once a species of caterpillar that fed on a drug-producing plant, either tobacco, cannabis, or coca, as part of its natural lifecycle, incorporating the toxins into its body. The modern, selectively-bred versions of this plant are so toxic that this caterpillar, which was once specialized to feed on this toxic plant, can't handle it anymore and can only feed on wild, non-cultivated plants. Sadly I have been unable to locate a reference with the exact species.


text:
How to do manual Saccharomyces tetrad separation with minimal equipment?
I would like to separate the four ascospores from individual asci by manual microscopic manipulation without at micro-manipulator and a basic dissecting microscope capable of 600X total magnification and a fine needle. Is this possible? My guess is that human hands would not be steady enough. But what did they do before micro-manipulators were commonplace?

Careful centrifugation can separate tetrad from individual spores. Do you mean breaking up the tetrad and isolating individual spores.

Yes, I mean breaking up the tetrad and isolating individual spores. I am trying to do this without buying much equipment. There are complete yeast tetrad separation systems that are $$$. A micromanipulator mounted to a microscope  with 600X magnification seems to be the preferred method. I'm wondering if anyone has experience doing this technique with as little expensive equipment as possible.


text:
Do partial (nighttime) curfews curb the spread of epidemics (and via which mechanisms)?

Do partial (e.g., nighttime) curfews curb the spread of epidemics?
What is the (epidemiological) mechanism by which partial curfews curb the spread of epidemics?
Is there evidence from past or present pandemics that this works?

Related questions

This question in SE:MedicalSciences asked about nightly curfews 8 months ago, but with a focus on economic and other effects. It cited evidence that curfews failed for economic reasons during Ebola outbreaks. It did not elaborate why limiting the time everyone can go to a shop would magically lead to less many people being in the shop at the same time. The only (non-accepted) answer to the question is speculative and concludes that the author is not sure if curfews are effective.
The same question was cross-posted here in SE:Biology and closed for that reason (cross-posting). There appear to have been some comments but these were deleted when the question was closed.

Related Research
The only papers on the topic i could find are two papers in the context of the Ebola epidemic in Liberia in 2014/2015. Both papers unfortunately focus on public health policy and not on the epidemiological merits of the measure:

Kirsch et al. 2017 (mentioned above)
Blair et al. 2017

The standard SIR- (and SIS-, SEIR-, ...)-Models predict a reduction of the infection rates when social interactions are reduced. This is obvious and not in doubt. Some common infection prevention measures (working from home, suspension of inter-regional travel, social distancing, restriction of contacts between households, closure of social gathering places) are designed to do this. In the case of partial curfews, it is not clear to me, if this (reduction of social interactions) is the objective and by what epidemiological mechanism that objective (reduction of social interactions) is meant to be achieved with partial curfews.
Why would a nighttime curfew not curb (possibly increase) the spread of the epidemic
People are still allowed (and will still) go to shops, do exercise etc., but if they have to do it at specific times, they are more likely to bump into each other. Human nature may even cause people to congregate in shops just before the curfew time (because you realized that you're out of pasta or so). So this might actually make it easier for the virus to spread.
Why would a nighttime curfew curb the spread of an epidemic
I am not sure; this is why I'm asking.
Some very far-fetched possibilities I could think of:

Making illegal gatherings inconvenient while being easy to enforce?
Reducing service personnel working away from home?
Forcing people to stick to the regular workday sleep cycle even while staying at home to prevent mental health issues which would lead to more people attending hospitals?

Context (Why is this relevant?)
Several countries have declared night-time curfews or are considering these to tackle the current wave of Covid-19 outbreaks. This includes, among many other countries, France, Germany, Spain, Hungary, Tunisia, South Africa.
For some measures, the objectives are clear and obvious: social distancing, closure of restaurants, bars, workplaces, schools etc., self-isolation of infected people and their contacts, face masks, vaccination, etc. Last year Spain took this policy to the extreme by assigning specific time slots to specific demographic groups.
However, I do not understand what good nighttime curfews would do - or other part-time curfews for that matter - unless the curfew is complete, 24 hours a day every day (i.e., everyone except for essential personnel locked in their homes, like in Hubei in early 2020).
To be clear:

I do not dispute that limiting social interactions helps.
It is easy to see that a full (24 hour every day) curfew should effectively halt the spread.
I am not asking about effects on mental health or on the economy.
I am specifically asking about the epidemiological rationale behind imposing nighttime curfews.

Edit (Jan 29 2021), note regarding the Covid-19 curfew in the Netherlands in on January 23 2021.: The Dutch government claims "Research has shown that night-time curfews help to reduce the spread of the virus." This suggests that there is scientific evidence, but they do not detail what evidence that is, what the underlying epidemiological mechanism is, or where it can be found and reviewed. They only add that the Dutch curfew between 9pm and 4.30am "will prevent people from visiting each other and gathering in groups". At the same time, "visiting each other" remains explicitly permitted in the Netherlands during day-time, although for only one visitor at a time. (Yes, the Dutch curfew is the one to which some violent Neonazis and Antisemites in the Netherlands responded by rioting and looting. I would like to point out that the Dutch curfew and the riots etc happened only after I asked this question and that I have no sympathy for those responsible, although I would still like to understand how exactly night-time curfews are supposed to help.)

@David This answer on SE:Biology Meta suggests that epidemiology is on topic here. While you may argue that restrictions such as curfews are unrelated to epidemiology, I specifically asked about the merits of a specific policy from an epidemiological perspective. Also, there was a similar question earlier (linked in the OP) that was closed not for being off-topic but for being cross-posted. If everyone agrees with David, please go ahead and close or delete. But I have to admit, I am a bit shocked by the level of anger in David's comment.

I don't speak for David, but do share his frustration that many of the posts in this site are completely inappropriate and often seem to involve no thought on the part of the poster. He may seem harsh, but he is not attacking you personally. Your post does have on-topic parts. but you've buried them in questions about intentions (e.g. the title). I encourage you to rewrite to focus on a single concise biological question. The [tour], [ask], and other [help] pages for more details on what is expected.

@tyersome Thank you. I tried to rewrite the question to focus it on the epidemiological question. I am sorry that people are frustrated about many off-topic and inappropriate posts. But may I just reiterate (MattDMo said that yesterday) that the tour and how-to-ask do not state to a lot of detail what is or isn't on topic. I looked it up on SE: Biology Meta (see link above) and posted believing that what I was asking was actually on topic.

I think Skeptics.SE would likely take up the specific claim by the Dutch government. I think the biology side of the epidemiological question here is pretty superficial. The intent of the curfew is to reduce contacts between people, particularly contacts between people who are not already in contact at other times of the day (like family members). This is pretty obvious and has little to do with any underlying biology. The extent to which it is truly effective seems like a different question that isn't itself related to biology.

I'd add that I don't think the rationale for the specific policy is epidemiological, but that the policy makers agree: "limiting social interactions helps." Their goal is to make this happen with as little impact as possible, which is a political and economic calculation.


text:
Can someone identify this tree in Playa Del Carmen, Quintana Roo, Mexico?
I just noticed this tree in Playa del Carmen in Yucatan. It was swarming with bats, the bat seem to be eating either the fruit or the flowers of the tree. Any idea what it is?

Please provide approximate sizes of the leaves, fruit, and tree as a whole. Mentioning more specifics about the location (e.g., did you find the tree along the road, in town, in a wooded area, etc.) would be helpful. Finally, updating your post with clearer photos (of leaves, bark, and fruit) would all be ideal and likely would result in a more accurate ID. Thanks

You might also check out 101 YUCATAN TREES (Conrad, 2015) for a site with some decent photos and data for trees of the Yucatan.

This looks more like a fig tree...

The photos are blurred. We need a pic of the bark and of the fruit, sliced. Does it have pips or a nut? Perhaps a Palaquium variety, i.e.  Palaquium Gutta, which is for producing latex/rubber, because it's in a garden and its a useful commodity plant previously grown in south america. Perhaps slice and study the fruit for a better ID.
Latex plants attract bats.
You can check the bark for latex.
https://youtu.be/6DJHD91VKKY

your proposed species is native to Malaysia! (not Mexico). Actually, the entire Genus is native to Southeast Asia / Oceania (see here). What makes you think this is correct? Please update your answer with more convincing information. Thanks!

I'm quite aware of that! Corn is native to the US and quite a few million hectares are found in Eurasia. Cultivacion y laminado de caucho natural! https://youtu.be/6DJHD91VKKY besides i'm not certain, it's just a lead, he can check the bark. Otherwise its perhaps related to avocado. He has to check the fruit. We can't guess much from the blurry photos.

My guess is as good as the photos, which are not very accurate. the info fits though, quote: Palaquium gutta — The ripe fruit, but not the seeds, is eaten by fruit bats. ... its growing in a garden beside a wall, we commonly see many non native plants in gardens and cities.

Understandable. My concern is that many users and visitors coming through our site just look for whatever is written as answers and often don't think in terms of "this is a guess based on low quality starting info". As such, someone (including the OP) might just assume you're giving the "right answer". I think we all need to be very clear and explicit when we're guessing. I don't think you make that clear on the post, so please edit to clarify. I would suggest adding some additional context based on your comments.

Something like "based on your low quality photos, I'd guess it's ___ because ___. Although it's not native, ___ are some reasons I still think it's possible. You could check the bark or other characteristics to be certain. Perhaps you could investigate related species in your area. I'd recommend starting your investigation with species related to avacado because ___" something in that style let's us see inside your head and whatever expertise or research you bring to the table without judging your response to be definitive and allows a jumping off point for the OP. Please consider editing. Thx

The photos are blurry, the fruit isn't photod, neither is the bark, nor the petiole angles along the branches. It's perhaps a correct ID, and it taught me about plant latexes, and encourages proper identification of plants using bark, and fruit dissection. People identify non-native plants in gardens very regularly on Stack, I get 95 of my species ID's correct. so at least i tried. 95% is not bad. so i will leave the answer and Ill ask a colleague with zoology and botany degrees from Cambridge who works in the Amazon rainforest.

It's funny cos my dad was a forest ecology lecturer at oxford for about 46 years and i'm just randomly ID'ing stuff which is hard to ID and not even getting it, and then a forest ecologist is telling me off. That's the actual title of my dad's job "Forest Ecology tutor" but he is a prof at humanities and human ecology not forestry which was just a BSc. Wee-ird.

I'm not telling you off. I'm asking you to provide more detailed support and to be explicit + clear about how you got to your answer and how others should interpret and use your info. 2.There's no reliable method for judging ID accuracy here, so I'm not sure how you got 95%. 3. It doesn't matter who you/your acquaintances are or what any of you know -- your post should be detailed, explicit, and cited. See meta. 4. I'd advise not answering unclear ID posts unless they're edited. 5. Watch the language

not a fan of stentors thanks. chill out it's an adult website and i'm 42 not 2. the marking system is there for a reason. The OP isn't interested enough in this page to post more precise information therefore this ID is not likely.

If the ID photos are not updated with bark photos and fruit photos, it doesn't do justice to the people who volunteer to ID it, so if there is a problem with this page, it's the lack of flowers/fruit/bark photos essential for me to  update the post.

Right, that's why I advised not answering unclear posts. If the OP won't/can't update with clearer photos or more detail, then the best answer anyone can give is more likely not accurate (because IDing something is HARD if it's not clear what you're IDing!). Ask the OP to clarify, vote to close, and move on. If you think guessing or adding a formalized line of thinking would be useful to others, then by all means provide an answer. However, make it clear that your answer is approximating some species based on XYZ characteristics. You've taken this approach, but I'm asking you to expand/clarify


text:
Which Hawaii bird makes this call at night?
I'm on Big Island right now and keep hearing this bird starting at 6-7PM every night: https://voca.ro/18XEepbDmpCy. Which bird could it be?

Thanks to the magic of Reddit I was able to figure out that this is the Coqui frog rather than a bird. Apparently its an invasive species on Big Island and attempts are underway to eradicate them.