text:
Why is some scat in the form of little pellets?
The scat I most often encounter when out and about is from coyotes, black bears, deers and rodents. The deer and rodent droppings I find are in little pellets, what is different about their digestive system or their food choices that produces these perfectly uniform little balls?

According to this article:

The material that cannot be broken down any further, such as
indigestible fiber, passes directly into the large intestine.  Here
water is reabsorbed and the material is passed, making up the round
droppings you see in your rabbit’s cage.  This indigestible fiber is
important in the diet of the rabbit as it helps to stimulate
intestinal contractions, which keeps the chyme moving through the
gastrointestinal tract.

While this article is specifically about rabbits, all herbivores require high quantities of fiber in their diets. Ruminants such as deer have different stomachs, but it is the large intestine, which is commonplace, that these pellets are formed. Fiber tends to clump together (either because the strands are attached or intertwined), and contractions in the intestine as the material is dehydrated cause these clumps to roll around similarly to pebbles in a rock tumbler, causing them to form round pellets.
Carnivores and omnivores have (and need) less fiber in their diets, so this phenomenon is not present in their feces.


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Are there any place in human body that safe to implant things and have large amount of blood run through?
Suppose there was a fuel cell in the size of AAA battery that could convert human blood sugar into electricity. Assume it safe and efficient without causing allergic reaction. But to avoid the risk of it disintegrate and malfunction it should be put in a place that far away to any critical organ as much as possible. It also need to have large amount of blood to supply anytime
Which place in human body would be the best to put that device in?

Wouldn't the answer also depend on the purpose of this implant? You wrote it produces electricity - where is this going to?

My physiology knowledge is pretty thin, but I would guess that 'far away from critical organs' and 'large amount of blood supply' are pretty much diametrical to each other. (unless you don't count large blood vessels as organs or start tempering with stuff like VEGF)

@Marzipanherz In my hypothesis we could use wireless energy transfer with magnetic induction to charge anything outside our body such as cellphone or just implant the cellphone parts in our body

@Thaina I'm not an expert, but you should consider that many body functions are based on electricity as well, and such an implant might interfere with that. Here is a short summary with further references.

@Nicolai I think so, so my question is to ask for a place that if accident happen, the nearest organ would be damaged but that organ should be the one that not make us die too fast. I also suspect that the fat tissue should have some blood supply to but I don't know if it enough

Possibly the safest place for it would be in a dialysis machine, or something similar. But dialysis is not exactly "safe," even if it is often the lesser of two evils - the other one being premature death.

No, there is no safe place.
Devices in contact with blood are subject to thrombosis and embolism. Even devices designed for bio/hemocompatibility are not 100% safe: they are used because the illnesses and diseases they treat are more dangerous than the side effects. Immune responses and platelet activation that occur in the vicinity of a device could also have effects elsewhere in the body, not just in the vessel you could potentially occlude.
Long term, these effects are reduced only because of healing over the exposed surface. You are proposing something which must be in constant contact with blood, which isn't really possible unless you plan to remove and clean it regularly.
On a side note, for the purposes you describe, there are already devices in development based on mechanical motion to do what you suggest (for example, the motion from walking) that are much safer and more feasible than using blood glucose, which is strictly in the realm of science fiction.

Lanzino, G., Wakhloo, A. K., Fessler, R. D., Hartney, M. L., Guterman, L. R., & Hopkins, L. N. (1999). Efficacy and current limitations of intravascular stents for intracranial internal carotid, vertebral, and basilar artery aneurysms. Journal of neurosurgery, 91(4), 538-546.
Wendel, H. P., & Ziemer, G. (1999). Coating-techniques to improve the hemocompatibility of artificial devices used for extracorporeal circulation. European Journal of Cardio-Thoracic Surgery, 16(3), 342-350.
Werner, C., Maitz, M. F., & Sperling, C. (2007). Current strategies towards hemocompatible coatings. Journal of materials chemistry, 17(32), 3376-3384.

My purpose is not just energy harvest (it is one of purpose too). But to have burn calorie and control blood sugar level by disposing it as useful energy without moving at all (which will be good for lazy diabetes people (such as myself)) that's why I want this technology be possible

@Thaina I understand why you might want the technology to be possible; I'm explaining why it's dangerous.

I believe the best place for this sort of implant would be the femoral vein in the upper leg. It's one of the larger blood vessels, and on the return trip so you don't have to be as concerned about oxygen removal from the blood on whatever apparatus you have. You're far away from all non-peripheral organs as well.
I would also question whether such an implant would be worth all the engineering challenges implicit in a long-term implant in a major blood vessel, but that's tangential to the question.

A vein can be worse in some ways because of the risk of pulmonary embolism, or stroke with a patent foramen ovale.

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How a Name is Selected for Binomial Nomenclature
I understand the gist of how to construct a name using the Binomial Nomenclature, but I don't understand how to select a unique name.
My contrived example comes from looking at this:

acaulis: stemless, e.g. silver thistle, Carlina acaulis.

So assuming the naming is <Genus> <Species>, then within the genus say we have 20 species already, which is fairly modest given this description of genus size:

The number of species in genera varies considerably among taxonomic groups. For instance, among (non-avian) reptiles, which have about 1180 genera, the most (>300) have only 1 species, ~360 have between 2 and 4 species, 260 have 5-10 species, ~200 have 11-50 species, and only 27 genera have more than 50 species (see figure). However, some insect genera such as the bee genera Lasioglossum and Andrena have over 1000 species each. The largest flowering plant genus, Astragalus, contains over 3,000 species.

Looking at the Astragalus genus gives some insight to the potential naming conflicts.
But say we have our 20 species in our custom genus. Our genus is called Foo and our species are (translated into Latin):
Yellow
Green
Blue
Shiny
Spotted
...

Now say we discover a new species and the prominent features are that it is both Shiny and Yellow, whereas those previously defined species are only either Shiny or Yellow, not both. So now we have one that is both, and we are having a hard time finding any other distinguishing factors.
One approach would be to call it the Double (diplo-) species, since it is both Yellow and Shiny. So perhaps we add to our list (in Latin maybe "diplopicta")
Foo DualColor (or Foo Diplopicta)

But wait! We already have used this technique (let's say). We look further in the original list and yep it's already there.
Yellow
Green
Blue
Shiny
Spotted
...
DualColor
...

So we can't use that technique. So maybe we go to the location, say it is northern:
Foo NorthernLocation

But wait! We already used that technique too!
Yellow
Green
Blue
Shiny
Spotted
...
DualColor
...
NorthernLocation
...

So now maybe we just try using another feature that we haven't used yet in any of the other species. Maybe this thing also is slightly larger than most of the other ones, and we haven't used Large as a property.
So we add (in Latin):
Foo LargeSize

Then we find some more species and we keep having to try to come up with new ways to get unique names. Maybe we try other things like:

Specific continent.
A feature that hasn't been used yet.
The discoverers name.
etc.

Already it's kind of brittle feeling.
Now let's say we discover a new species in the genus again. But this one is really really yellow. Way more yellow than the previous one we called yellow. And that is it's only distinguishing feature. I would like to know what is done in this situation.
I would like to know, generally, how this process like described above is handled in practice in the real world.
So we have this new yellow thing. Now we want to rename the old species and use Yellow for this one, and come up with something better for the old one. Not a problem if this information hasn't been shared yet. But if it's already been shared all over the world then you can't really change it, at least not with a long and drawn out, carefully managed process.
So we're stuck with the less than ideal name for our new "really really yellow" thing, and we just end up calling it:
Foo CoreyDiscoverer

But at this point I feel like might as well just give it a number ID since there's not really any meaningful connection (though history perhaps is a good enough connection).
Basically I'm wondering how good names are created for things using the Binomial Nomenclature, and how naming conflicts (or the desire to change names) are handled. The example above outlines a scenario that one might encounter when trying to uniquely name species within a genus, and I am wondering how it is handled in practice.
As an example, from here it reads:

If on the other hand the taxon appears never to have been named at all, then the scientist or another qualified expert picks a type specimen and publishes a new name and an official description.

But it doesn't explain how this works, the issues they had to consider as outlined above.

Your question covers a whole field of research, taxonomy, and the answer to the complexity of the naming process and how conflicts are resolved is the subject of very strict and very detailed rules. For example, the nomenclatural treatment of animals is governed by the International Code of Zoological Nomenclature, while the nomenclature of plants, algae and fungi is governed by the International Code of Nomenclature for algae, fungi and plants (paradoxically, fungi are actually more closely related to animals, but however).
These codes have a series of rules governing the ways that new names can be coined, how new names should be considered against old or preserved names, what constitutes a synonymous name, and hundreds of other little things (for example, the Shenzhen code, the most recently ratified code of the ICN, is very, very long).
Some trivia, which might give you some idea of the conflicts which are handled by the code: under the ICZN, tautonyms, which are species names where both the genus name and species epithet are the same (e.g. Vulpes vulpes, the red fox) are allowed, whereas under the ICN, they are not allowed. Species from separate codes can share the same name (see for example the answers to this question), and two species from different genera governed by the same code can share the same species epithet - it is the binomial combination which must be unique.
I am not kidding when I say the rules are really, really detailed, and the minutiae is too much to get into here. If you read the respective codes, you will get some feeling for the rules which are applied.
In regards to the other part of your question, choosing an appropriate name: this is generally at the discretion of the publishing author (unless the name is invalid under the code, then another author may step in to dispute it or correct it). These can come from all sorts of things, ranging from utterly boring and descriptive to pretty funny and facetious. For example, Han is a monotypic genus of fossil trilobite, and having only one member, its sole species is Han solo.
I suspect the reason that most materials don't discuss how this process really works is because it is really, really complicated and often pretty dry. You'll see plenty of examples of new names being coined in journals like Taxon. But doing taxonomy is often conceived as not very glamorous, so doesn't receive that much attention, even though it underpins most comparative fields like ecology and evolution.
As a final note, the reasons that a species will be included in a given genus, or split into its own genus, or several genera will be lumped together into one large genus, are more murky, and related to phylogeny, morphology, final size, etc. These decisions are often also left up to the discretion of the author, unless of course they conflict with the code.

I understand that the rules are detailed. I am more wondering though how you select a good name, not a correct one. It seems they aren't much concerned with "good" names.

@LancePollard what is good? Does it mean a name evocative of appearance, or a name designed to help you remember the system? Does it maximise the stability of the nomenclatural system or help it to reflect more natural groupings? These are all valid questions, and they've been asked as far back as Caesalpinus

Lol yeah, it is a design decision. I guess a good name would be (a) easy to remember and (b) bring up vivid mental imagery.

@LancePollard all well and good until you arrive at some plant taxa that are near identical, or something even more cryptic like red algae or bryozoans.

Exactly! That's what I was wondering about :)

As ever in biology, there are no easy answers :P

@LancePollard Unfortunately, reliably coming up with good names is an unsolved problem, not just in biology, but in general.

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The meaning of and standards for "specimen numbers"
I just read here:

For example, in the research collection of the Natural History Museum in London, there is a bird specimen numbered 1886.6.24.20. This is a specimen of a kind of bird commonly known as the spotted harrier, which currently bears the scientific name Circus assimilis.

I am wondering what exactly that number 1886.6.24.20 means and how to find out more information. It seems it is structured to give some significance, such as perhaps year.month.day.incremented number. Wondering if this is unique to the Natural History Museum in London, or if this is how everywhere does it. By everywhere, I mean every museum. That is, wondering if there is a standard of some sort on how to number specimens.

It is good scientific practice to utilize some sort of consistent structure for sample/specimen identification, but to the best of my knowledge there is no "standard", per se.

In this case, your suspicion of year.month.day.sequential number is correct. The NHM specimen page has an image of the collector's notes:

On line 20, that specimen of Circus assimilis is accessioned, with a note on the right that it is the type for that species.
Generally however, there are no standards for specimen numbers in museums. Many museums that I have studied in have several different numbering or ID systems in use at the same time. Importantly, each specimen is accessioned under the system used at the present time. Sometimes these are later renumbered, sometimes not.
Even in the NHM, there are different schemes in use. Megalosaurus bucklandi, the first described species of dinosaur, is specimen PV OR 2482.
The NHM has 80,000,000 specimens. I'm sure that those doing the cataloging at the start couldn't have imagined the collection would grow to that size, so planning ahead for a single numbering scheme wouldn't even have occurred to them.


text:
The parts of the phylogenetic nomenclature that need to be "unique"
I am not quite sure I have sorted through the diversity of approaches to nomenclature, but I had a specific question to help clarify what is going on. Basically I am just wondering what needs to be globally unique in the name of a species.
I understand how to construct a name using the Binomial Nomenclature, and am under the assumption that this "uniquely defines a species" (for simplicity, not considering all of the variations of subspecies and sub-x ranks). But I am not sure what exactly "uniquely defines" means. In addition, I am not sure if the names of all the different ranks are globally unique, and how the rank names are defined (if they are defined differently from the binomial nomenclature-defined species names) (but this is probably a separate question). This makes it hard to figure out what actually needs to be unique, and what is unique, in these names.
So to start from the top, we have Domains. Wikipedia shows 3 (Archaea, Bacteria, Eukarya). I have seen more in other places, but not too concerned with that currently. First question is, if these names are globally unique. Second (related, possibly separate) question is, if these names are decided according to the same codes as the binomial-nomenclature defined genus/species names, or if they have a different process. I'm not sure if a domain (and later, the kingdoms, phyla, etc.) is associated with one single specimen. I read that for at least the Genus', they have individual specimens that act as the model or reference point for the Genus (not sure if I can call a Genus a clade). So I'm wondering if this technique/requirement/workflow is applied to domains/kingdoms/phyla/etc. That is, there is an individual specimen in some museum somewhere that serves as the type / model for that clade (domain/kingdom/phylum/etc.). That would be interesting and helpful for better understanding how the uniqueness requirement works in the terminology.
So following domains we have Kingdoms. Wikipedia shows 7 of them. Same thing, if these names need to be unique from the Domain ones, and if they are chosen the same way.
Then Phyla has approximately 32 for Kingdom Animalia, 14 for Kingdom Plantae, etc. Same questions here, if these names need to be unique from Domains/Kingdoms/Orders/etc., and if they are chosen the same way (and have the model specimen in some museum somewhere).
Oh, in regards to that model specimen. If it turns out that each clade indeed does have a model specimen in some museum somewhere, that means it must have a genus/species name. This is a big part of the question: wondering if that means that a Kingdom like Plantae actually has a specimem along the lines of Plantae plantae. That would make me confused as to how the clade then gets its name. If there is a thing/specimen called Plantae plantae (used as the model/type representing that clade), then it seems almost circular. Plantae plantae is the name of a species, but it is also somehow [partially] defining the Kingdom Plantae! That is where I get confused. Anyway, back to the other big half of the question, about each level.
So then we have Class, Order, and Family. I see some naming rules now starting to pop up. For example, in botanical nomenclature, they have "-aceae" as the ending of the names for the most part. So this to me says that, yes, they are using the standard binomial nomenclature codes to construct the name of the Family. But there again I am confused, because the Family is only 1 word, whereas binomial nomenclature is 2 words. So don't see how those two fit together. But anyways, Class, Order, and Family start having custom endings to the words in some cases, so it seems to use binomial nomenclature codes.
Then Genus is where it starts to get a little bit more familiar. Still I don't know how the genus names are constructed (that will probably be answered with the above stuff), but I at least know that the Genus is the first part of the binomial nomenclature name.
Then Species has a name, but I guess the "full name" (as opposed to the "relative name") is <Genus> <Species>, rather than just <Species>.
So to summarize, I am wondering
What needs to be globally unique, and in reference to what. My first guess as of now is that Domain, Kingdom, Phylum, ..., Family, Genus, Species, all with 1 Latin name, are all globally unique. So you can't have a Species named the same thing as a Family or a Kingdom. But wait, no that doesn't make sense. So everything from Domain-Genus needs to be globally unique, but Species is only unique relative to the Genus. So you can have Volpus volpus (for example). But you can't have an Order named Foo and a Kingdom named Foo, that wouldn't work (that is my understanding at this point).

Binomial nomenclature does not uniquely define a species unfortunately, there are several duplicates.
The Wikispecies directory shows 5 duplicates: each of this is with an organism from kingdom Animalia and another from either Plantae or Fungi.
Therefore, you could conclude that binomial nomenclature is a unique identifier within a kingdom.

Many of the problems you are discovering are the basis for phylogenetic classification. Without necessarily answering each of your question specifically, I'll mention some of the basics of phylogenetic classification as compared to traditional Linnean classification:

Species are the main "currency". We classify species and species alone.
All taxonomic groups higher than the species level are arbitrary. The Linnean system of Kingdom - Phylum - Class, etc. has no biological meaning. For example, Reptilia and Aves can't both be classes, because birds are reptiles (a class within another class).

These two points alone address most of the questions. There are no general rules (and lots of arguments) for naming clades above the level of species. Clades are names following the main rule of "the most recent common ancestor of [taxon] and all of its descendants". This conveniently does away with all the business about "Supraclass" and "Infraorder" and such.
The implication of this scheme is that there are no (extant) species at the bifurcations, so there is no taxon that is not assignable to a "tip" on the tree. In other words, "we do not find direct ancestors in the fossil record", which basically answers your third question.


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What is the closest relative to odd-toed ungulate?
I have seen about 3 variation of phylogenetic tree about odd-toed ungulate and I don't know which one is really updated or outdated or which one have more backed up theory

First is odd-toed ungulate are closest to even-toed ungulate

https://en.wikipedia.org/wiki/Odd-toed_ungulate#Outer_taxonomy

Second is odd-toed ungulate are closest to carnivore

http://www.ultimateungulate.com/FamilyTree.html

Third is odd-toed ungulate are closest to Hyrax and Elephant

http://tolweb.org/Eutheria/15997
http://www.newworldencyclopedia.org/entry/Eutheria

Second or Third

https://research.amnh.org/paleontology/perissodactyl/node/55

Could anyone please ordering the actual relativity of each branch in the most reliable theory in present. And also could anyone please explain why there was such a very confusion in evolution of odd-toed ungulate specifically?

It would be great to add the sources of the three phylogenetic hypotheses.

The best would be to see results based on the TOL tree of life file, which is about 80 mb open source updated by researchers relative to science papers... TOL is the resource that is most accurate here, but I am surprised that it is not more recently updated.


text:
What species of butterfly is this? Picture taken on 9-18-2018, near Helena, Mt

Butterfly picture taken on the 18th of September 2018 at an elevation of 1800 meters (6,000 feet) near Mount Helena in Montana, USA.

To me it looks like one of the tortoiseshell butterflies (genera Aglais and Nymphaiis) - but I could not tell which one :/

Oh, and just to be certain: I guess "Helena, Mt" is "Helena, Montana, USA"? It might not be obvious to everyone in this international community :)

Yes, Helena, Montana, USA.

That is a California Tortoiseshell google[https://www.butterfliesandmoths.org/species/Nymphalis-californica]


text:
What is this? Found crawling across ground under oak tree. Six arms waving, I broke off 1 trying to pick it up. Less than 1 inch long
Crawled like snail.  No slime trail.  Less than one inch.  Six arms, I broke one off.

Where in the world is that species located? And at which season?

Hi D.J., welcome to Bio.SE! Please add a location, approximate size, and preferably additional (clearer) photos of your specimen. Thanks

That is a Hag moth caterpillar

Don't touch.


text:
why is erythrocyte sedimentation rate higher in females?
erythocyte sedimentation rate should be independent of the sex.
what is the reason behind this sex bias and why does it increase during pregnancy and how does age influence it.

Why would you think ESR should be independent of sex? Do you understand what the test is and what it indicates? What have you done to try to find out why it's not independent of sex?


text:
What kind of snake is this
Found this outside on patio in northern Virginia, Ashburn area, September 2018. It's about 12 inches. Is it a water snake or rattlesnake?

It looks like an Eastern Hognose Snake, which is characterized by an upturned nose and high likelihood of playing dead.
These are described as variable in coloration:

"Two color phases are common in Virginia: (1) a patterned phase (79.6%, n = 98), characterized by a series of 19-27 (average = 23.2 ± 2.4, n = 12) black or dark-brown blotches along middorsal line, with alternating black spots on sides; body color consists of varying combinations of gray, tan, pink, yellow, orange, and red; venter of body and tail immaculate cream to dark gray;"

If you replace the tan in this image (www.virginiaherpetologicalsociety.com) with gray in yours, I think the pattern match and overall body form are very similar:

Another characteristic of Hognoses is their tendency to flatten their necks in a cobra-like fashion when they feel threatened. This is visible on both the picture in the question, and in the answer.


text:
How plausible is it that pesticides and mosquito spraying is affecting insect populations?
I live in Massachusetts and I notice that there are a lot fewer bugs than when I was a child. 40 years ago if you drove around for 4 or 5 hours in the summer the grill of your car would collect a noticeable amount of bugs. Nowadays, I can drive for the whole summer and there is not a single bug on my car. I rarely see a butterfly of any kind. I have not seen a monarch butterfly in years. When I was kid butterflies were omnipresent in any meadow or field. Even 20 years ago I remember cursing all those annoying Japanese beetles flying around. Haven't seen one in years. There used to be huge gypsy moth infestations. Even in off years, you would see the caterpillars plastered all over the sidewalks. Nowadays, sidewalks are all clean, not a single squashed bug.
I thought maybe this was because of mosquito spraying. In Massachusetts for many years we have had these huge mosquito spraying programs that cover every square inch of the state. The method used is what they called ultra low volume spraying or something like that. Even so, I can't see how it would be possible. For example, I saw a schedule for spraying in my county on an each day they would have 5 different towns listed. I don't see how a few trucks could possibly spray anywhere enough insecticide to depopulate 5 towns worth of bugs. I mean in my town alone there are probably a couple hundred roads and many areas that have no road access. How many roads can they possibly drive in one night? It doesn't seem possible, yet there no bugs.
Is there some kind of cumulative effect, or are these poisons so incredibly powerful that they just wipe everything out with even tiny amounts being released? How plausible is it that pesticides and mosquito spraying is affecting insect populations?


text:
What is Modulation Power Spectrum?
I'm reading this paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4562283/ , but I cannot make sense of what MPS nor how should I read the pictures that make use of this method.
The authors say

The MPS, beyond classical representations such as the waveform and spectrogram (Figure 1A and B, upper and middle panels), displays the time-frequency power in modulation across both spectral and temporal dimensions (Figure 1A and B, lower panels). The MPS has become a particularly useful tool in auditory neuroscience because it provides a neurally and ecologically relevant parameterization of sounds

I'm clueless about what the meaning of time-frequency power in modulation across both spectral and temporal dimensions. Can someone provide a brief explanation about this and MPS?

A time-frequency graph also know as a TF distribution, is a spectrogram, a spectrograph, a sonogram, a waterfall display of sound. They are all different names for the same thing. They look like this:
https://www.google.fr/search?q=dolphin+spectrogram&num=100&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiD3vv-9cvdAhUCzhoKHf4jDM0Q_AUIDigB&biw=1429&bih=734
Just as white light contains many wavelengths of colors, sound energy contains bass, mids and high all in the same moment in time, a bit like a water wave has multiple wave sizes, sound energy is the same with sound pressure levels.
Modulation refers to the variation of a simple signal, like tarzan modulates his voice using a kind of tremolo effect, so does a car alarm, and a bird has very varied squeak effects with tremolo effects and also changes from squeaks into clicks into hisses, spectral changes in the timbral quality of the sound. Modulation is a scientific word for the variations of the amplitudes and frequencies of a communications signal.
They write about temporal modulation and spectral(pitch) modulation, it's just hte changes on the time-frequency graphs.
Modulation power spectrum is a relatively obscure field of bioacoustics, it attempts to generalize the fluctuations and patterns of loudness and squeak spectrums into another graph, which is a bit like a secondary time and freqency graph derived from the first sound time and frequency graph, else a 2D graph as in the illustrations, which show sound fluctuation prevalence as an average of the TF graph(a averaged sound fluctuation prevalence of the spectrograph). so, if tarzan's voice oscillates every 1 second, he has a major modulation at 1Hz spectrally, and a minimal amplitude modulation, and they will graph that as a peak as 1Hz on the MPS graph.

We can see on this image that The human speech spectrogram on the top left is mostly at 500HZ, with some S and CH sounds at 2000hz.
For the MPS of the human voice, they have correlated Spectral modulations against Temporal modulations. It is easy to see that the human voice mosly changes at arond 1HZ, same as tarzan's voice, because syllables and pauses take about .5 to 1 second (average words per minute of a human is about 50, average syllables per minute is about 120). So it is easy to see a temporal modulation peak at 1Hz.
The less clear thing is that it is plotted against spectral modulation, which is 2-3 octaves of change, an octave being a doubling of wave speed and frequency. So we can say that the main spectral modulations of the human voice occur over 2-3 octaves at a speed of about 1Hz.
There is a secondary peak, which suggest that there is a change of about 1 octave that occurs at about 200-300 HZ. That is the gruff buzz that you hear in your own man voice, it is about 150HZ and it has about .5-1octave, the base frequency of your voice being 150Hz and various 3rds adn 5ths of an octave, and another octave at 350Hz, seems to be visible from that graph.
tarzan voice: https://www.researchgate.net/profile/Alexandre_Hyafil/publication/283260815/figure/fig2/AS:293940512215079@1447092287682/A-Phase-Frequency-coupling-can-be-mistaken-for-Phase-Amplitude-Coupling-Top-curves-An.png
MPS seems to have been used to study neuron responses in psycho-acoustics.
Neurons interpret sounds using some kinds of complex time and freqency variation(modulation) recognition(resolution) and the researchers use MPS as they say it fits well with the neuron psychoacoustics study.
I would suggest that there are many other ways of measuring psycho acoustic nerve responses and bioacoustics than only MPS, it is an over simplification of sound analysis, and the Digital-Signal-Processing forum on this website will inform you that there are also 100ds of other maths and analysis algorythms that you can run on sound to study Time-Frequency Graphs, and to define sound in many different ways than MPS.
very pure sounds like sine waves make tight lines on a time frequency graph, noise makes very scattered signals at all frequencies, and sounds with many harmonic modes make nice ordered lines of smaller subharmonics that reflect the base frequency of a signal, which resemble echoes of the original sound in parralel with it, and that are on a different frequency.
Time frequency graphs are quite interesting to study and there are probably some studies of bird calls on YT: https://www.youtube.com/watch?v=_FatxGN3vAM

Still not sure if I'm getting it. (1) What (I think) I understand is that MPS graph shows the variation of pitch (spectral modulation) vs variation of time (temporal modulation). So if Tarzan's voice jumps from a tree using his voice with a tremolo effect, and his voice oscillates from 10 to 20 hz every second, should I expect to see at the 1hz a distribution of red to blue from 10 to 20hz corresponding to the change in pitch? (2) Consider the "fall" in the MPS for human speech, nearer to 0, do I see more red because within invervals close to zero voice shows a greater change in pitch?

that's about right. (2)The human voice spectrogram is illustrated as a correlation of spectral versus temporal modulations. We can see at .5Hz the giant peak at the start corresponds to the slow change in words and syllables, which varies by 2-3 octaves of pitch. There is also another peak at 150Hz which corresponds to the gruff tone of a male voice, which varies by 1 octave, and which has 3rd and 5th harmonics and at 300hz, an octave above 150hz. I'll add a bit just under the image with another image of tarzan's vice. given a moment to read the peacks, spectrograms are easy to read.

MPS is the two-dimensional Fourier transform of the spectrogram. Assuming that you know what a Fourier transform and a spectrogram is, the MPS method consists in treating the spectrogram as an image on which to apply the Fourier transform. Thus, one can extract an estimate of the joint modulation on the frequency and temporal domain of a signal. If I attempt to provide an intuitive explanation of how to interpret an MPS, I would say that it allows the researcher to quantify the irregularity of a signal across time and frequency bands.

Here a clear explanation, cheers!
https://journals.plos.org/ploscompbiol/article/figure?id=10.1371/journal.pcbi.1000302.g001

Link-only answers are generally not acceptable on Stack Exchange sites. The link may change or become unreachable in the future, and without a summary of what the link contains this answer would be useless. Please summarize what is in the link (don't just copy and paste) and use the link solely for reference. If you remove the link and the answer cannot stand on its own, it is not a good answer.


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Homology modelling of protein with two identical subunits in its quaternary structure
I am using homology modelling to assign the 3D structure of Torpedo acetylcholine receptor (Unwin 2004, 2bg9 in RCSB) to human muscle nAChR. The problem is, both Torpedo receptor, and human receptor have subunit structure A-B-D-A-E: so a same subunit (A) occurs in the model twice. This seems to cause problems for homology modelling software, as it tends to align the second 'A' sequence over the first 'A' sequence, creating a hole in the pentamer, and not filling it up. Any ideas on how to make sure the modelling software acknowledges the quaternary structure? Below please find a link to a file generated using pdb.gz structure data from Unwin model + a set of corresponding FASTA sequences, and attached picture shows the problem (revealed when alignment is set as shown in the picture, by clicking on the same 'boxes' as in the image). Long story short, I need to get the A subunit to complete the alignment in a different spot than it is automatically placed in, as it occurs in the whole structure twice.
https://swissmodel.expasy.org/interactive/JJ5mQf/models/

I don't know a proper solution to this, but maybe you could try 'hack' it by changing  a few amino acids in one of the two A chains?

Thanks for response: was thinking about it, but as I am planning to use it for docking studies with cell-membrane permeating ligand (so can bind both inside and outside): the original Unwin model is quite shabby on its own, homology modelling isn't really optimal either, and docking is notoriously unreliable, so can't quite see how I could justify this 'hacking' (and thus adding another source of unreliability) in a paper. Furthermore, it seems like a type of problem with relatively simple solution: surely, someone must have thought of this before!

For anyone who will struggle with this problem in the future: The trick is in reading WHOLE of the manual, NOT submitting the whole sequence/badly segmented sequence, and in NOT attempting to input the same subunit twice. It is necessary to upload subunit FASTAs separately as a hetero target, and each subunit ONLY ONCE (so A,B,D,E for A-B-D-A-E receptor), and then search for templates: most probably there is a template with your quaternary structure uploaded somewhere already, and if not, you can choose preferred arrangement afterwards.


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SNP coding for association analysis
I'm working on a project about detecting SNP association with a disease. As I understand, SNP is a single variation of the nucleotide that occurs for more than 1% of the population. However, I couldn't connect this idea with the dataset in hand. The rows in my dataset represent each patient and the columns contain SNP information. For example:
ID  exm355 exm615
1     T_T   A_C
2     T_T   C_C
3     A_T   C_C

I have no idea why the SNP columns contain 2 nucleotides(T_T, A_T, A_C, C_C). As the definition of SNP, I thought it should show only the variant nucleotide or am I misunderstanding anything? How could I interpret T_T or C_C and how could I know which nucleotide is the variation from the common ones in the population?
Thanks all

Without knowing where exactly your data comes from / how its formatted this is hard to answer. Generally the SNP notation with two bases is used to denote both the 'canonical' and the 'variant' base at each of the SNP positions (this would mean that exm355 doesn't have any SNP at ID 2, since its 'T_T'). You should look up which base is variant/canonical in an description of your data/file format

Each chromosome location which has been identified as being a SNP is a location at which more than one nucleotide occurs at appreciable frequencies in the general population.  This means that there are two or more bases which can occur there, so a person's test must show which bases actually occur there in that person's genome.  Since a person has both a paternal and a maternal chromosome of a chromosomal type (a pair of homologous chromosomes), the person has two instances of the SNP location and so two nucleotides to be detected and reported.  Hence your dataset has two nucleotides for each SNP location for each patient.
Just from the reported base or the SNP name you can't tell which is more frequent in the population.  If you need to know that, you must consult SNP frequency data from some other database. (The SNP names in your example, e.g. "exm355" are not familiar; usually SNPs have names like "rs1234567".)


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Exact terminology of natural selection
You don't need to explain to me what the theory of evolution is, or how it works. This question is purely about what exact meaning the word "natural selection" is ascribed to.
There seem to be multiple meanings that are given to the term "natural selection":

The process by which, in a single generation of species, the most fit individuals tend to survive. The "things that are being selected", are the individual organisms, and the "moment that selection took place", is the moment that these individuals reproduced or failed to reproduce, or alternatively, the moment that they died or survived.
The process by which, over many generations, the genotypes that result in highest fitness tend to to be selected for. The "things that are being selected" are the genes, and the "moment that selection took place" is not a single instance in time or a single generation, but a long time-span. In fact, I sometimes hear the idea that natural selection is already selecting for genes even if those particular genes don't exist in any organism. For example, if natural selection is selecting for "height", and there is a gene X that would increase height, then it is said that X is being selected for even if X does not yet exist.

Are both of these interpretations generally accepted?

Natural selection has many different nuances and interpretations different fields. A population-geneticist and an ecologist would give you vastly different answers as would the original text from Darwin. This theory has been constantly refined since its inception, in particular in response to developments in genetics and statistics. RA Fisher in particular has written about this at length. The earlier works of Dawkins also give a good summary on this topic and address common misconceptions.

Possible duplicate of What is the definition of “Natural Selection”?

"...in a single generation of species, the most fit individuals tend to survive.".  This is not correct. "Fitness" in an evolutionary context refers to how many offspring you produce. It has nothing to do with how many pushups you can do.
Yes, individual organisms are selected, and the selection process involves differential survival (to reproduce).
"The process by which, over many generations, the genotypes that result in highest fitness tend to to be selected for. "
This is largely correct.
"The "things that are being selected" are the genes..."  Yes and no. It is individuals that are selected. They live or die, depending on their traits, which are encoded by genes.
Darwin noticed the extreme physical variations that humans could create in dogs, and pigeons by selective breeding. He thought that the same process could occur in nature, and termed it "Natural selection".

I did. It seemed from the error-filled descriptions that you could use some clarification. You set up two alternative definitions, both of which were significantly flawed, as if the true definition had to be one or the other, when the true definition contains elements of both.

Biologist have a unified definition of natural selection. You presented two that no evolutionary biologist would agree with. That people outside the field are sloppy with their terminology does to mean that experts are confused.

You said the most fit survive.

Survival of the fittest lineage, not individual.

Re ""Fitness" in an evolutionary context refers to how many offspring you produce."  Not exactly.  If you produce a lot of offspring, but most or all of them die before reproducing, then you are not very fit (in the evolutionary sense).  Indeed, there are two different paths to success: have lots of offspring and hope that a few survive (like the codfish, which can lay 2.5 million eggs a year, and live 25 years or so), or like many mammals, invest lots of effort into caring for a few offspring.

That is so obvious, I did not think it needed to be stated on a biology site.

"traits, which are encoded by genes" is a little imprecise, though of course I get that we are going for simplicity here. We must accept that there is a mapping from genes to traits, but it is not a simple or linear encoding, otherwise genetic association studies would be more successful than they are; genotype-phenotype maps are complex and highly environmentally responsive (the responsiveness is sometimes encoded in the genes, of course).


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If virus is an inanimate(non-living) structure, why it poses tendency/intelligence to spread itself to others?
A virus has no aim, no agency but just a chemical propagation(DNAs, RNAs). Still, it accounts for millions of deaths and horrible nature.
Rabies, for example, is a very deadly disease with a fatality rate of 90%. One of the terrible symptoms of this disease is Hydrophobia(fear of water). I can surely understand the fact that the victim cannot drink or fear water because virus controls it to as water reduces the chances of transmission.
But why transmit in the first place. If a virus is still aimless like a rock on the ground with the couple of DNAs, how it evolved to replicate and reproduce.
If a virus being inanimate did it, why can't a rock or any other aimless non-living thing do it?

I would consider fungi or plants as pretty unintelligent and aimless as well (although they are living!), but still they are reproducing and growing and have amazing biochemical pathways.  It doesn't need an aim to reproduce, but the capability. And while viruses have the capability, rocks don't have it.

Why does a fire spread?  Or to get a little closer to viruses, why do prion diseases spread?

You're confusing semantics with reality. People referring to viruses as "inanimate" or "non-living" are simply playing silly word games. The terms that people use for viruses tell us about the history of the word "life" or "animate", but do not tell us anything about the virus; in fact, trying to apply these words to viruses is simply misleading, as this question shows.
Viruses have replication machinery, whether it be RNA or DNA, that allows inheritance with variation. These are the requirements for natural selection and therefore viruses evolve and, on a population basis, adapt to their environment (their environment mainly meaning the host they infect).
It should not be surprising that an agent that has co-evolved for 200 million years along with its host is well adapted to that host.
If your question is mechanistically how viruses are capable of doing this, the question is too broad (there are millions of different viruses with different approaches), and asking a more specific question would be helpful.

Related: Why isn't a virus “alive”?

Lets use a metaphor to say that a virus is like a cursed book. The book has milions of copies all around the world in random places. If a person finds the book, and opens it, he will immediately be cursed and will start to make copies of that book, over and over, until it dies. Then the copies of the book will be able to infect new people and this way there will always be copies of the cursed book around. The virus, just like  book, can't copy itself on its own. It needs a person with tools (pen and paper) who can read and write to make copies and distribute them.
In this metahpor the book is the virus RNA (or DNA), the person who read the book is just a random cell (human cell, bacteria, mice cell ...). In the metaphor the 'pen and paper', or the 'tools' to make copies of the virus are ribosomes and enzymes.

why can't a rock or any other aimless non-living thing do it

I'm sorry but this doesn't make sense. A rock does not have DNA. What do rocks have to do with viruses?

how it evolved to replicate and reproduce.

Tricky question. How did YOU evolve to reproduce? It's just a matter of trial and error. In the course of bilions of years nature produced countless viral DNA (RNA) strands, and 99,9999% of them couldn't replicate. The ones who could, did, and we are now able to see them.
Please clarify your answer, especially the rabies part that I didn0t quite understand.

Rocks do not have DNA, what are you talking about ?

I don't know, you mentioned rocks and you suggested rocks have something to do with viruses. Your question not only is very confusing and unspecific but you didn't even reply to our answers and comments.


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Can fruit be affected by antifreeze in soil?
Due to an accident about 2L of car antifreeze (ethylene glycol & corrosion inhibitors) was spilled around the soil at the base of a fig tree. I am wondering if there is any way the antifreeze can enter the fruit? Will soil bacteria break it down over the course of time? I did a web search that indicated that antifreexe can be harmful to plant roots and can stunt their growth. I could not find any information indicating whether it has any chance of actually entering fruit. I wonder if the ethane glycol (ethane 1, 2 diol) molecule is too large to enter the root system. Your advice would be appreciated.
Kind regards
Chris


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Infant immunization
I know that polio vaccine consists of small dose of polio virus itself, which activates body's immunity against the disease. An infant is given a no of vaccines including chickenpox, tetanus, diptheria etc, see here for details. Does all these vaccine work on same principle ie they contain small dose of respective virus/bacteria to activate hosts immunity?

There are a wide variety of different kinds of vaccines. The basic principle is that the human (and more generally, jawed vertebrate) immune system can identify invaders by recognizing and responding to portions of macromolecules on those invaders called antigens. Vaccines use this principle by exposing the immune system to specific antigens ahead of time, so the immune system is prepared for them. There are, of course, many more details about why that is helpful, but I think they're beyond the scope of this question.

polio vaccine consists of small dose of polio virus itself

Vaccines generally don't involve a small amount of the pathogen itself. Current poliovirus vaccines include an inactivated virus (killed with formaldehyde) that cannot reproduce, and several live attenuated viruses, that is different strains of viruses that can replicate, but do not cause disease. The inactivated virus is used in the united states, but the attenuated virus is used in some other countries.
There are several types of vaccines, and none of them involve small doses of the pathogen itself. The key here is exposing the immune system to the antigen, not the pathogen. As with polio, the major groups are live attenuated or inactivated vaccines. There are many kinds of inactivated vaccines. They can be whole killed viruses or bacteria, or just the important parts. Some vaccines are a just subset of key proteins or polysaccharides.
You can read about all these details in the CDC pink book. Chapter 1 discusses the principles and the different types of vaccines. Chapter 18 discusses polio virus.

Small dose of either killed or live attenuated (they are grown in other animals, so they evolve to better infect that animal, making them slower to infect humans) pathogen...yes, that is the general idea behind all vaccination.


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Do chromosomes line up as pairs in mitosis or meiosis?
Here is a question from the book SAT II Success Biology E/M (where the SAT is the exam taken by the American high school students):

Homologous chromosomes line up in pairs in
  (A) metaphase of mitosis.
  (B) metaphase I.
  (C) metaphase II.
  (D) interphase.
  (E) prophase of
  mitosis.

In my opinion, we can definitely eliminate D and E since in both mitosis and meiosis, chromosomes line up during the metaphase.
Then, I would choose the answer choice B because as far as I know, after prophase I -- when the chromosomes are in pairs during crossing-over -- the chromosomes are still in pairs and become separated into the different ends of the cell during anaphase. In mitosis and metaphase II, however, they align along the "equator" of the cell, forming a line of single chromosomes.
However, I am confused here because of my book. Here is its explanation for this question:

The correct answer is (B). In meiosis, the homologous pairs line up as
  individuals in meiosis I in preparation for final segregation in
  meiosis II. Meiosis simply needs to ensure the pairs end up in
  opposite daughter cells in meiosis I. It is in mitosis that the
  homologous pairs line up as pairs, and interphase, of course, is not a
  phase where the chromosomes even appear.

You can see that even though the first line indicates that the answer actually is B, the phrase that's in the cursive contradicts that statement.
I suspect there is a mistake either in the bold or the cursive statement. Could you help me here?

You are correct.  The books explanation is mistaken, and badly written ("the pairs line up as individuals"???)
https://en.wikipedia.org/wiki/Homologous_chromosome

In metaphase I of meiosis I, the pairs of homologous chromosomes, also
  known as bivalents or tetrads, line up in a random order along the
  metaphase plate.

https://www.khanacademy.org/science/biology/cellular-molecular-biology/meiosis/a/phases-of-meiosis

So, during metaphase I, homologue pairs—not individual
  chromosomes—line up at the metaphase plate for separation.


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why and how multi allele gets reported during variant calling in vcf?
This might be a very basic question for many here. With the basic understanding of inheritance, eventhough there is a possibility of multiple genotypes due to multi alleles, the resulting genotype can only have two alleles(paternal and maternal) that way after variant calling, an allele at one position can be homozygous or heterozygous. So there can be max of two alleles, but why do we see multiple alleles at a given position in VCF. I am trying to understand the science behind this. Please help out. Thanks!
chr5    127640782   .   AG  A,AA    .   .   .   GT:AD:DP    1/2:0,28,409:437

Can you please clarify what you mean by multiple alleles at a given position in VCF.? Maybe, you could show an extract of a VCF file to show us what you mean. Are you surprised that in the population there can be more than 2 alleles at a given site?

In your example the 4th column contains the reference allel on the given position. It is not said, that your sample has this. The 5th column contains all alternative alleles found on the given position.
Which alleles are present in your sample is given in the last column by 1/2. This means you have one allel with the first value in the 5th column and one allele with the second value given in the 5th column. You see, that your sample has exactly alleles, but none of them is the reference. This would be indicated by a 0.

A vcf can contain multiple columns representing allele data for multiple samples.  I also see no reason why you could not represent a tetraploid sample's data in a vcf.  One might also have a mix of organisms i one sampe, like a mixed population of bacteria.  If you could get your SNP caller to call a tri-allelic SNP, the vcf format can handle it.

The other possibility I can imagine is that the format is designed to accommodate heterogeneity between individual cells in a sample, and inevitable sequencing errors.
If you sequence a sample from an organism which (mostly) has two alleles at a locus (e.g. A and G), there may still be individual cells which have a C or T at that locus, and there may also be sequencing errors introducing a C or T in reads which were actually an A or G.  The VCF format would then still be able to represent the low-probability calls, in addition to the higher-probability ones.


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Protein Pathways, Superfamilie, Function database/website?
I'm going trough some old data - but I'm running into this problem that all website we used use is not existing anymore.
What I have is a very long list of proteins with accession number (refSeq from NCBI) and the organism that they are from.
So where do I go to for:
1) Finding information on which pathway they are involved in. It would be great to a visualization of the whole pathway as well.
2) There function.
3) Super-family

The UniProt KnowledgeBase (UniProtKB) is the central hub for the collection of functional information on proteins.


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Can anyone help me identify what type of horns these are?
I picked these up at an estate sale a few years ago and now need to identify them for shipping purposes.
They are 29x18x10.5 inches in size.
A friend who works in antiques believes the are over 100 years old based on the wood they are attached to and thinks they belong to some kind of ram. That's all the information I have on them.
Any help would be appreciated.
Thank you.

almost certainly that of a goat (see here, here, and especially here)

Those look very much like "Catalina" goat horns. They're a popular trophy game to hunt, specifically for these sorts of displays. The goats themselves originate in Spain but are commonly found in the United States, now.


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Why so fewer birds in the yard come late summer and early autumn?
We've enjoyed watching birds in our yard this past summer. We're in a suburb, fairly forested, inland northeastern USA hardiness zone 5. As we scaled up the amount of diversity and net primary production around the house, and added a bird feeder, we notice an uptick in various kinds of wildlife. However, we're surprised to see a stark decline in the amount of birds starting around late summer/early autumn.
What could cause the sudden decline in birds in late summer? Is there a migratory trend starting up around this time; it seems early to me for birds to be flying south?
The birds in question include a family of cardinals, occasional blue jay, downy and hairy woodpeckers mid-summer (some are still around), many various sparrows, yellow finches, chickadees, et al.
We continue to fill the bird feeder as usual. We haven't changed anything about our yard routine. We have a rescued feral cat which goes outside and hunts despite our efforts to stop it, and it has killed many mice and a few chipmunks mid-summer, so perhaps the birds have become wary of him and the dead bodies of small mammals left in forested edges around the yard.

One possible cause is Cooper Hawks. We are in east TX and put out a lot of seed ; we had more birds. Fewer in recent months due to the Cooper Hawk(s). Our yard is a buffet for them ,I hear them often, see them occasionally ;they will perch in the under story.  And we hear birds hit the windows as they panic from the hawk ; it happens 0 to 4 times a day. The hawk has developed a technique of diving and after the small birds when they knock themselves out on the windows , the hawk walks on the patio to pick one up. I have been going out after a bird strike and picking up stunned birds and put them in a shoebox for 30 minutes. They usually recover, had a cardinal yesterday. If you are home during the day , listen for window strikes and watch for sudden flights of all the birds. The Sharpshin Hawk is also here but not a problem.......... And there is a degree of randomness to migrations: Some years we get many Goldfinches, Pine Siskins, Robins, and some years a few or none. And birds like Cedar Waxwings are notorious for their unpredictable movements.


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Are there situations where in vivo results work better than in vitro results would have shown?
Basically, if I have poor in vitro cell line results but decided to test them in vivo in a mouse anyway what are the possibilities of having better results in the in vivo live mouse model that I would have never known otherwise from the in vitro results?
Links are appreciated

This is a very broad topic and massively depends on the specifics of your hypothesis.

Differences between in vitro and in vivo results are (unfortunately) very common!
Somehow, all failed clinical trials (and many preclinical trials) are large-scale examples of the discrepancy between promising in vitro and actual in vivo results - which also highlights the fact that even from one in vivo system (e.g. mice) to the other (e.g. humans), there can be significant and unpredictable biological differences. It is the opposite of your case, in which you expect an improvement when moving to live animals, but it is also more common.
By essence, your in vitro culture will be unable to recapitulate key processes like:

Signals provided by the natural extracellular matrix. Your cells are probably grown on polystyrene, but that substrate is far from the complexity of the natural molecules that surround cells in vivo: stiffness, immobilized signaling molecules...
Information provided by other cell types. Organs are formed of many dynamic subpopulations (stem cells, immune cells etc), some unknown, that interact and control cell behavior at the tissue scale.
Fluctuating information like biological cycles and behaviors (circadian rythm, sleep, food intake...)
Many others like for instance immune processes, (de)activation of small molecules by enzymes in unrelated organs (liver) or plasma...

All these factors can change your result in unpredictable ways, making them either better or worse. But, and that is important, more often than not, complex biological systems tend to make things worse, as they introduce extra noise, buffering effects etc. so more often than not, things will not be as good in a real animal as in a Petri dish. It can get better, sure, but it is extremely unlikely!
That is one of the main reasons why people do in vitro work first: it is faster, cheaper and more ethical, and failure in vitro is usually a good predictor of downstream failure in vivo.
Please, don't cherry-pick an answer that tells you otherwise! It's easier and more comforting to think that everything is going to work if you just move to animals, yes, but you will most likely waste time, money and animal lives for identical results. My (unsolicited) advice is to build a better in vitro model, that will reduce the possible differences between cell results and animal models: can you mimic a biologically relevant environment by adding a protein/sugar matrix to your cells? Can you find primary cells that will behave more naturally than immortalized cell lines? Can you make mixed cell cultures to improve the adequation of your model with reality? If you do all this, then your results should be much more reliable and you will have a better idea of what to expect in vivo.


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DNA replication and Protein synthesis
Is DNA replication required for Protein Synthesis or can proteins be synthesized without DNA being replicated?

Sounds like you may not be be very familiar with the basics of DNA and protein synthesis. I suggest you check out Khan Academy, they have some very good videos explaining many aspects of biology (and other subjects)

DNA replication and protein synthesis are very very different processes. The key thing to remember about protein synthesis is that DNA is not directly used; RNA is. When DNA is replicated, it is for reproduction. When it is transcribed, it is copied, with certain changes, into RNA instead. RNA is then "read" by protein synthesis machinery to produce the proteins.
To directly answer your question, no, replication is not required. If you inject some RNA which codes for a protein into a cell, it will be translated into a protein. There are many viruses which exclusively use RNA for their genetic makeup. The RNA is replicated at some point by the host cell's machinery but the RNA can be directly translated into a protein by the host cell as soon as the RNA enters the cell.

If you have a file on your computer hard drive, a document, and you want to translate that document into a different language, do you need to make a copy of the original file before you translate it?
Making a copy of a file is duplicating it, like replicating the DNA in a chromosome.  Translating the document into a different language is “sort of” like translating a messenger RNA into a protein.


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Coacervater were more like Viruses or Cells?

The answer considers them as first formed living cells as they were precursor of life. But they had no lipid bilayer nor any cellular organization, shouldnt they be more like Viruses ,or like Prions and Viriods ??

Do not post text as graphics on this list. It discriminates against people with visual disabilities who use screen readers. This is a homework question and should be tagged as such. You need to put more effort in before an amended homework question would be acceptable. For a start, a reference to "coacervates" is necessary. I for one have never heard of them

@Astrolamb - please do not provide answers-in-disguise as a comment, it deters other users from answering. I have removed your comment.


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Is flowers nectar secreation influenced by bees/pollinators?
Nectar secretion by flowers is influenced by many environmental factors e.g. water supply and air temperature [1].
My question is: do bees (or any other pollinator) influence it too?
I can imagine every bee's visit takes away a certain amount of nectar from the flower. Then following the flower nature, it should produce nectar again (if there are the right conditions, e.g. enough water).
[1] https://www.jstor.org/stable/2468960

In short, yes, it seems many flower species have mechanisms to replenish nectar after removal. For example, in Luo et al. 2014 Journal of Pollination Ecology,  9 of 11 species of plants they studied in the Colorado Rockies showed significant additional nectar production after some nectar was experimentally removed. Furthermore, the magnitude of this behavior was greater for flowers known to be heavily visited by bees:
https://www.researchgate.net/publication/268523373_Stimulation_of_flower_nectar_replenishment_by_removal_A_survey_of_eleven_animal-pollinated_plant_species

Hi Michael. Please provide some summary or other form of support from the source you provide. Simply adding a link without an explanation or summary is not acceptable on this stack site. If the link goes dead, this post literally becomes useless. Please update accordingly to avoid having it downvoted or deleted. Thanks!


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Why do we fall asleep when our eyes are closed?
Why do we fall asleep when our eyes are closed? When we lie down with our eyes closed, eventually we'll fall asleep. Why is that? Is our eyes closing some sort of trigger to our brain that says it's time to sleep?

Why am I sometimes unable to fall asleep, no matter how long I close my eyes? There's your answer: your assumption is wrong.

You're confusing the cause with the effect. The effect is closing of the eyes (and maybe some component of relaxing.) The cause is sleepiness. In other words, when you're falling asleep, the eyes close, not the other way around. You can close your eyes for 24 hours straight, and you might sleep longer out of boredom, but you'll still spend most of the time awake. Closing your eyes doesn't cause sleep.
The reason our eyes close when we sleep is to protect the eyes from drying out and insuring the oxygenation of the corneas.
Take for example truck drivers. They need to keep their eyes open or bad things happen, like death and destruction. Yet, as they tire, try as they might, their eyes flutter closed and off to sleep they go.
Driver drowsiness detection with eyelid related parameters by Support Vector Machine


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Rank-specific rules for taxonomic classification
There appears to be a very specific (although not universally agreed) list of characteristics that describe what a "species" is--and the list applies to ALL species.  Are there similar generic rules or characteristics for the other taxonomic ranks that do not resort to characteristics of existing members of the rank? For example, I've seen "number of lobes on leaves" used to place a particular flower in a particular Family or Order.  Is there anything that applies across ALL Families, or across ALL Orders, etc., of the tree of life?

Somewhat related: How could humans have interbred with Neanderthals if we're a different species?

In short, no. Species are unique, in that they are thought to be biologically real categories that would exist whether there were humans trying to classify them or not. There are a variety of definitions for species, involving fixed characters that imply a lack of gene-flow. However, all higher categories, from genera on up are designed by humans to be able to talk about these groups. Each category is defined by phylogenetic relationships, but taxonomists have wide leeway to decide how broadly or narrowly to subdivide groups. (Lumpers vs. Splitters). For example, all ants are in the same family. Yet all it would take to change this would be for some ant taxonomist to submit a paper that divided ants into however many families s/he wanted to. The peer reviewers would then decide if such a division was reasonable, and once published, it would be the new taxonomy. There are no broad rules, other than peer review. Not age: one family could be 1 million years old, and another, 100 million. Not the magnitude of phenotypic or genotypic variation: some groups are radically different from one-another, and still in the same category, while other groups are heavily subdivided and barely distinguishable.

I would disagree that "once published, it would be the new taxonomy". It would be a new taxonomy. Many taxa have organizations or authorities that confer "official" status on a selected tree for a selected set of taxa. It's true that trees or authorities can go in and out of style, and that they're only as authoritative as the experts in the field who follow them. But in most areas, you can't arbitrarily decide to lump or split something and have it "stick", whether it's peer-reviewed or not. If the science is good and it's reviewed by appropriate experts, then maybe; if not, no.

I agree that the overall answer is "no, there aren't consistent standards for what constitutes a taxonomic level". Perhaps someday we'll be able to say that an animal phylum denotes X years of divergence or Y amount of sequence similarity, but making those same judgements for extinct organisms or microbes is a lot messier. See Wikipedia on bacterial phyla for an example of how taxonomists are still debating whether bacteria should be said to have phyla at all, or whether they're more like kingdoms, or whether we should just use a different word entirely.
However, at the detailed level of one taxon here and one taxon there, evolutionary biologists and taxonomists can work toward greater local consistency. If it's discovered that species X is very different from the other species in its genus, and indeed it's as evolutionarily distant from them as the species in other genera are, then there's a reasonable argument for it to be "promoted" into its own genus. Other taxonomists working on the same group of organisms can choose to use that change as a precedent; and when people revise entire trees at the family or order level, they may be able to apply roughly the same standard throughout. It would be nice to think that through such processes we'll start creeping toward some sort of overall consistency; but I don't think it's likely to happen any time soon across kingdom- or domain-level barriers.


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How many different chains exist within a specific pdb file?
More specifically, if we want to understand the different chains within a protein, is it enough to look at the fourth column of all the lines that start with "ATOM" in a pdb file, and see how many different chain identifiers exist there?

In the PDB format the lines with atoms can start either with ATOM or HETATM.
Chain ID is in column 22, i.e. it is 22nd character of a line that starts with ATOM or HETATM. (Programs that support 2-character chain IDs use columns 21-22 − it's a popular extension of the PDB format).
Yes, the number of different chain IDs is the same as the number of "chains" in the PDB file.
But note that the "chain" from the PDB format is not necessarily a real chain (polymer). It may be a bunch of water molecules or something else.

Thank you for your answer. It’s less confusing now.


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How do molecular biologists determine biochemical pathways?
I'm new to this community, so hopefully this is the right place to ask this question.
I know my question is really general, but in all of my biology courses we are merely taught the chemical pathways of common reactions in cellular metabolism, but we're rarely told how these reactions were determined or discovered. What approaches do molecular biologists take to determine what molecules are involved in what reactions, what order the reactions take place, where they take place, etc.? Some of these pathways involve tons of steps, huge molecules, and a bunch of enzymes and proteins, and I just don't see how anyone could have pieced it all together. For that matter, how is the molecular structure of anything in the cell determined? For example, what was the setup of the experiment that determined that TNF-R1 even existed on the surface of the cell membrane, and that it triggers the apoptosis pathway? Another example is photosynthesis -- I could see how maybe we could find PS1/2, cytochrome complexes, etc. in a soup of blended up cells, but how in the world did we figure out what each one does and in what order?
The average cell is just so tiny and complex that it doesn't seem like there's any feasible experimental design that could lead to the discovery of these things. Please enlighten me!

You might find the answers you seek in the autobiography of Arthur Kornberg: “For the Love of Enzymes: The Odyssey of a Biochemist”

Welcome to SE Biology. What research have you done on this topic? First, molecular biologists had nothing to do with determining biochemical pathways, it was chemists — first called physiogical chemists, then later (in English-speaking countries) biochemists. This should give you a clue how they went about it. How does a chemist study a reaction? How would a chemist determine that yeast converts glucose to carbon dioxide? What's the next step from studying live yeast? And after showing A goes to Z, how would you look to see if there are B, C and D in between? With this in mind, search.

Have fun. Remember, Rome wasn't built in a day, and that the initial slow and limited progress was built upon by others as technological advances allowed new methods to be used. And, though cells may be small, you can get enough compounds (and enzymes out) with lots of them (e.g. yeast cultures, rat livers and kidneys). Enzyme preparations didn't have to be pure to yield information. And at the time the pathways of central metabolism were worked out (before and immediately after WWII) they didn't know anything about DNA (and probably didn't even think about it).

@David It's really quite fascinating how recent (late 20th century) the majority of this information came to light. I've always taken it for granted and assumed it was discovered hundreds of years ago, like many of the things we learn in the classroom.


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Trying to identify the species to which this vertebrae belongs
Found vertebrae in the "graveyard of the Atlantic" (on account of the 5,000+ shipwrecks since the 1520's) off Frisco/Hatteras, North Carolina. Tried searching online but not finding any perfect patches (although some were close with some seemingly minor differences to the untrained eye). Any ideas would be much appreciated. I have images from every angle and can take specific images if instructed on exactly what is needed. This is new for me and I am unsure who to contact if this is fruitless. If (fairly certain) identification is not possible from the image(s) please comment with any suggestions on my next contact.

I don't see any images in your question, so it is completely unclear what you are asking.

Another question about bones refers to this bone ID site which you might find helpful.

Please add more photos (one from top, bottom, front, back and each of the sides) and measurements/dimensions. Thanks.


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Is it appropriate to say "selection of" or "selection for" an allele that evolves by genetic hitchhiking?
In terms of Sober's selection of/selection for distinction, is it appropriate to say that there was selection of or selection for an allele that evolved by hitchhiking?  I am inclined to say selection of.  Is that correct?

I never remember which is which in Sober's terms and I have a hard time finding a reference that would clarify that for me as they are behind paywalls. Would you mind quoting the definitions of "selection for" and "selection of" in your post?

That's a good question and I don't know the answer because they are discussed in Sober's 1984 book, The Nature of Selection, but I do not have access at the moment.

So, your primary question is not so much about hitchhiking but rather about the terminology of Sober.

I suppose so.  Hitchhiking in terms of the terminology of Sober.

The expressions "selection for" and "selection of", their definitions and their usage have been subject to a number of semantic issues throughout the literature. Good and Griffith (1995) is a good read on the subject.
I would argue that neither "selection for" or "selection of" is appropriate to use in the context of genetic hitchhiking because, in this context, by definition, the increase in frequency of an allele is only due to a different locus nearby that is under selection. So an allele that evolves due to hitchhiking is not directly under selection and only changes frequency indirectly due to nearby selection on a linked site.

Could you please clearly define the terms "selection of" and "selection for" so that we can understand why you consider these terms poorly apply to the case of genetic hitchhiking (or of linked selection to be more general).

Yes, sorry! This paper is helpful. I think my disagreement is with the level of selection we are talking about. But I am happy to be corrected! From this reading, Sober's usage seems that "selection for" would be for the trait that improves fitness, while "selection of" would be some trait that necessarily is brought along (e.g. p9 discusses the polar bear). For an allele, I would only say linked selection in order to prevent any misinterpretation of how selection acts at the genome level.

Good and Griffith (1995) that you pointed out was a very helpful read for me. I edited (adding this paper into it among other things). Please feel free to roll back (or re-edit) if you don't like my edit. By the way... Welcome to Biology.SE!


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Interesting examples of models
I am studying the general use of models in biology in terms of methodology, applications, usefulness etc, and I would really appreciate any recommendations of some specific examples of models from any area in biology. Some examples are the logistic growth model or the Lotka-Volterra prey predator model.
It would be nice if you could shortly explain what the model is used for and why do you think it's an interesting case, and give a reference for further study.
Also any recommendation of books on model development and other meta-model questions in biology is very welcome. Thank you.

Biology is a large field of knowledge! As you give examples drawn from population biology (logistic population growth and Lotka-Voltera models), I will assume you are mainly interested in ecology and evolution.
For analytical models used in ecology and evolution, I highly recommend the book A Biologist's Guide to Mathematical Modeling in Ecology and Evolution by Otto and Day. The book assumes a relatively low level of knowledge in mathematics from the reader and walk the reader through most of the most iconic models in ecology and evolution, their analysis and interpretation. The mathematical tools used in this book include linear algebra, equilibrium analysis, analysis of cyclic behaviour, Markov chain and esp. birth-death processes, diffusion equations, probability theory and stochastic models, approximation theory, class structure models (Leslie matrix and more) and, separation of time scales among others.
For books, mainly theoretical, in population genetics, please have a look at the post Books on population or evolutionary genetics?.
As you talk about the Lotka-Voltera model, you will find an intro to this model in the post What prevents predator overpopulation?.

One nice model to use as a example the Hodgking-Huxley model that describe the current through a nerve fiber given a certain membrane voltage. This model describes the sodium and potassium currents that are the basis of the action potential.
Some characteristics of this model are:
This model explains the membrane currents through the activation of "charged particles" in the membrane that allow the passage of ions (K+ and Na+). It was latter discovered that in the membrane there are Na+ and K+ channels that carry these currents (in the original model there was no evidence of the molecular components of theses channels).
The model can reproduce the action potential of neurons.
The model predicts the existence of "charged particles" in the membrane that must move before the channel open, named gating charges. Since this particle move from one side of the membrane to the other, they generate a small transient current ("gating currents"). These where actually measured 20 years after the proposition of this model.
This is a great model because it described mathematically and physically the behavior of neurons and also predicted several properties that where later fond.
You can read more here:
HH model


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Allergy desensitization: what is the mechanism? Could it happen with other immune responses?
Allergy is a type of immune response against an otherwise harmless substance. If I understand it well, the aim of allergy immunotherapy is not to stimulate an immune response like the immunotherapy for for other diseases, but to progressively reduce it by controlled exposition to the antigen. Is the mechanism understood? Could the repeated long-term exposition to an antigen reduce other types of immune responses (to virus or bacteria for example?)


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Are the first humans black
I have been doing some studies and I believe humans where black before they were white. Black has the ability to create all colors where as white derives from no color so white couldn't have been first. What do you think?

Which one would you consider "the first" in your question?

Possible duplicate of How did some humans evolve to be white?

"Black has the ability to create all colors where as white derives from no color so white couldn't have been first" – permanent black skin pigmentation was an adaptation to constant UV exposure of hairless skin. Our furry hominid ancestors didn't have much of a selective pressure to produce eumelanin (the black pigment) in the skin itself, which is why the logic is not as straightforward as you put it in your question.

Related found (after typing my own answer): https://biology.stackexchange.com/questions/61141/why-did-evolution-make-peoples-skin-dark

Welcome to SE Biology. This is a science site for questions and answers based on scientific principles. It is not a discussion site, so that statements like "I believe" and questions like "what do you think?" are good indications that a question is off-topic. I am afraid that supporting your belief with an argument like "Black has the ability to create all colors where as white derives from no color so white couldn't have been first" cannot be regarded as scientically appropriate here. Please re-read the Tour and the help on asking questions.

It very much depends upon what you call "first humans". Before there was any hairless hominids, the skin under the fur might have been very different from the skin colour of a human 30,000 years ago.
It appears that extant sister species of Homo sapiens sapiens tend to have a light skin under its fur according to a number of popular article I could find (e.g. this and that). Here is a picture of a hairless chimpanzee from the St-Louis (Missouri; USA) zoo

It suggests that the MRCA between humans and chimpanzees had a pale skin but please realize that this claim is based upon my research of poor quality references and it contradicts John's claim in the comments.
It sounds reasonable to me to think that humans skin evolved a darker skin when they started to lose fur and when their skin got more directly exposed to sun. Some human lineages have then "evolved back" lighter skin (see How did some humans evolve to be white?).
You can read more about the evolutionary forces controlling skin evolution in this answer.

chimps actually show both skin tones, as well as a selection of "inbetween patterns" although pale is the most common.  Gorilla on the other hand are far more often dark skinned. s we really don't know what skin tone our common ancestor had.

@John I would love a reference for these claims. I failed to find any good reference so that's why I went with popular sources and a zoo picture only.

Tanning does not work the same in chimps as it does humans (or gorilla for that matter), chimps can tan to a completely black color, unlike white humans they actually have the genes to produce dark skin even when pale. Since chimps are forest delling it makes sense savannah living humans might evolve a more permanent solution. http://www.sbs.utexas.edu/levin/bio213/articles/skin_deep.pdf

The first (African) humans with low body hair/fur (compared to apes) almost certainly acquired black skin pretty quickly, probably in a simultaneous process with shedding of hair/fur. This is based on genetic evidence, such as the low variation in the "African black skin gene". From Jablonsky and Chaplin (2010):

The near absence in African populations of functionally significant variation in the coding region of the melanocortin 1 receptor (MC1R), one of the major genes regulating human eumelanin production, indicates the action of purifying selection maintaining dark pigmentation under intense selective pressure (Harding et al., 2000; John et al., 2003; Makova and Norton, 2005). The evidence of functional constraint on MC1R in African populations is unusual in light of the high levels of polymorphism observed at other loci in African populations (Makova and Norton, 2005).  [...]
The loss of body hair in humans was accompanied by enhanced barrier functions of the stratum corneum (Montagna, 1981; Elias, 2005), including the evolution of other epidermal keratins (Chimpanzee Sequencing and Analysis Consortium, 2005; Moll et al., 2008), which reduced the skin’s permeability and improved its abilities to resist abrasion and microbial attack. The rapid divergence of genes responsible for epidermal differentiation was one of the most significant results to emerge from the initial comparison of human and chimpanzee genomes (Chimpanzee Sequencing and Analysis Consortium, 2005). Changes in skin pigmentation also accompanied loss of body hair, and multiple lines of evidence indicate that permanent, dark, eumelanin-based pigmentation evolved soon after the emergence of the genus Homo in Africa (Jablonski and Chaplin, 2000; Rogers et al., 2004).

How quickly this (combined process) happened is a matter of some debate, in particular because we don't know how quickly hair was shed (that also depends on the environment of ancestral hominids, which itself is somewhat contentious) or how quickly a (mostly hairless) species would die out (or evolve) because of skin cancers, in the absence of eumelanin protection. Greaves (2014) summarizes:

Early hominin evolution in East Africa at some 2–3 Ma was associated with a dramatic loss of the body hair development that is retained by our primate cousins. Hair growth was retained on the head—the most UVR-exposed part of the body of a bipedal hominin. Some exotic explanations have been entertained for this dramatic phenotypic shift, including avoidance of fur parasites or of catching fire, a response to wearing clothes or an adaptation to an aquatic way of life. But the most likely major adaptive advantage would have been for thermoregulation or facilitation of sweating and heat loss for physically active, hunter–gatherers in the savannah But what colour was the exposed skin of the first hairless hominins? Not black it would seem. The skin of our nearest primate relative, the chimpanzee, is, under the fur, essentially pale or white with melanocytes restricted to hair follicles. The exposed and relatively hairless face and hands are also white in infant chimpanzees of three Pan subspecies (but black in Pan paniscus) and they become facultatively pigmented with age. It has therefore been considered very likely, albeit not unambiguously so, that the first African hominins to discard hirsutism were also white- or pale-skinned. [...]
Rogers et al. [2004] proposed that, around the time that humans first became hairless savannah-dwellers, the now common allele swept to fixation under the influence of potent environmental selective pressure. They calculate a minimum date for the time since that sweep occurred of approximately 1.2 Myr  which is not too discordant with the time estimate of 1.7 Ma when hominins (Homo ergaster or Homo erectus) were believed to have first inhabited the savannah. The adoption of the more open savannah as a habitat may have resulted from climate change and consequential shifts in forestation and faunal species abundance.

With those estimates there's a 500,000-year gap between moving to savannah and getting black skin. What happened in between is a matter of conjecture. (Neither skin nor hair are preserved in the fossil record.) A more recent study (Tishkoff et al., 2017), which further analyzed black skin DNA variation in Africa, concludes:

Skin pigmentation is highly variable within Africa. Populations such as the San from southern Africa are almost as lightly pigmented as Asians, while the East African Nilo- Saharan populations are the most darkly pigmented in the world. Most alleles associated with light and dark pigmentation in our dataset are estimated to have originated prior to the origin of modern humans ~300 ky ago. In contrast to the lack of variation at MC1R, which is under purifying selection in Africa, our results indicate that both light and dark alleles at MFSD12, DDB1, OCA2, and HERC2 have been segregating in the hominin lineage for hundreds of thousands of years. Further, the ancestral allele is associated with light pigmentation in approximately half of the predicted causal SNPs; Neanderthal and Denisovan genome sequences, which diverged from modern human sequences 804 kya, contain the ancestral allele at all loci. These observations are consistent with the hypothesis that darker pigmentation is a derived trait that originated in the genus Homo within the past ~2 million years after human ancestors lost most of their protective body hair, though these ancestral hominins may have been moderately, rather than darkly, pigmented. Moreover, it appears that both light and dark pigmentation has continued to evolve over hominid history.

And speaking of Neanderthals, it is estimated by Lalueza-Fox et al. (2007), based on genetic evidence, that they developed an arrays of skin colors as well, by a mechanism similar to modern humans:

The melanocortin 1 receptor (MC1R) regulates pigmentation in humans and other vertebrates. Variants of MC1R with reduced function are associated with pale skin color and red hair in humans of primarily European origin. We amplified and sequenced a fragment of the MC1R gene (mc1r) from two Neanderthal remains. Both specimens have a mutation that was not found in approximately 3700 modern humans analyzed. Functional analyses show that this variant reduces MC1R activity to a level that alters hair and/or skin pigmentation in humans. The impaired activity of this variant suggests that Neanderthals varied in pigmentation levels, potentially on the scale observed in modern humans. Our data suggest that inactive MC1R variants evolved independently in both modern humans and Neanderthals.

And if the wide-variation of skin color within Africa (from recent studies) confuses you in relation to MC1R's [gene] lack of variation in Africa (it did baffle me for a while), Martin, Henn, et al. (2017) explain it as:

As
  observed previously, we find a strong correlation between absolute
  latitude and average skin pigmentation reflectance caused
  by melanin content. We also observe that populations with lighter
  skin have reduced variation within any given study: populations
  furthest from the equator have narrower distributions, while
  populations closest to the equator have wider distributions.
  These patterns suggest that selection is acting differently at
  different latitudes. In equatorial regions, strong directional selection
  for darker pigmentation has shifted the distribution means in
  some populations to M indices >90, but with wide variances. This
  is consistent with a ‘‘threshold’’ model (Chaplin, 2004) in which
  the protective benefit of melanin needs to meet some minimum
  threshold but with no penalty to darker pigmentation; alternatively,
  diversifying selection could maintain the wide variance.
In stark contrast, pigmentation in far northern European and
  Asian populations has been under directional selection for
  decreased melanin production, reflected by very narrow distributions.

Great answer, though I find the last citation a bit odd: "We also observe that populations with lighter skin have reduced variation within any given study: populations furthest from the equator have narrower distributions, while populations closest to the equator have wider distributions. These patterns suggest that selection is acting differently at different latitudes." The authors seem to ignore that non-African populations (1) have had less time to diversify and (2) have experienced bottlenecks. These factors should've been pointed out when discussing variation in non-African populations.


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Why do Petri dish lids not fit?
I understand that they are generally "vented", but why such a poor fit? For the batch I bought, the lid and container don't even recognizably go together (like 1/2" difference in diameter). The wind from a box fan could blow the lid off. Even "non-vented" designs appear to have no positive connection between the dish and lid.
Then it looks like the people that do need a positive connection or a seal have to go through a lot of work with tape or wax to seal them.
Seems like a petri dish lid that has a snap, thread, bayonet, or even just friction fit, would be superior. The manufacturing cost differences would be negligible. What am I missing? Thanks!

I would dislike friction fit because I would likely need two hands to open it, whereas now I can just take the dish in one movement, have my tool in the other hand, do the thing, then put it back and pick up the next one. But for storage I often tape them together by 5 for ease of handling, and that prevents accidental opening. Not too much work IMO.

"Seems like a petri dish lid that has a snap, thread, bayonet, or even just friction fit, would be superior" – Petri dishes work by creating a sigmoid path that any particle would have to travel in order to get inside, which is why you don't need a tight lock. From a practical point of view you are supposed to handle (open) Petri dishes in a controlled environment with a rising air flow (preferably in a box or within a small radius of a burning flame) and you should be able to do it with a single hand, because your other hand would be holding something else in the process.

@EliKorvigo, Now I'm curious. Do bio labs really use rising air? I know clean rooms for semiconductors use downward air to help sweep heavier than air particles and bacteria out of the environment. https://en.wikipedia.org/wiki/Cleanroom#Air_flow_principles

Not entire labs, of course. The laminar boxes generate a laminar airflow  directed toward the operator, i.e. a rising airflow. As I've mentioned before, in the old days people used to work within a very small radius from alcohol burners for the same reason (rising airflow). Additionally, old-school microbiologists never fully remove the lid: they use the same hand to rotate the plate and hold the lid above the plate, so that there is only a narrow opening between the lid and the plate during plating.


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Is it possible to create a biological radio?
If someone had taken the genome for a basic single or multi-celled organism, and had the understanding of genetic code to write his own program, is it possible on a fundamental level to create the organelles necessary to emit an electromagnetic signal at a frequency that isn't widely used by modern day electronics (noise concerns)?

Welcome to Biology.SE! This type of question are off-topic here. You might want to give it a try on WorldBuilding.SE

Note: Bioluminescence is a type of electromagnetic signal. Gymnotoid fish use electric signals to communicate (mainyl for courtship if I am not mistaken). Electric discharges (e.g. eels) might count too. Also, any neuron that fires causes an electromagnetic signal. You don't need to do any genetic engineering to get an animal that produce an electromagnetic signal! You should clarify what you're looking for.

Albeit interesting question, what @Remi.b refers to are the additional senses of magnetoception and electroception. However, i think your are talking about something else. Please clarify.


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What does 'kinetically accessible' mean in protein folding?
The hydrophobic collapse model discusses this term in the energetics section. What does this actually mean?

At some point during protein folding, there may exist lower energy states from a thermodynamic perspective (lower ΔG free enegy) which are actually unreachable in a given environment, because the required activation energy is too high. These are kinetically inaccessible states, conversely accessible state are those that can be reached.
For example, that could mean a protein could reach a lower energy state by unfolding a bit, but exposing hydrophobic amino acid even temporarily would require too much energy. So the lower energy state is not kinetically accessible.
This is somewhat similar to the concept of kinetic and thermodynamic reaction products in chemistry.


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Can anyone identify this insect larvae please?

I found thus tiny creature in my shower its about 19mm in length with a see through body and moves much like a caterpillar.

It would be great if you could add some information where this image was taken.

It looks like a Diptera larva, and it is most certainly not a parasite. I've seen many similar larvae in the Limoniidae subfamily.