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Is there a way tell apart dinosaurs from similar extinct reptiles?
When I was a child, I thought I knew what a dinosaur was. But, as I grew older, I was told that many of the extinct species that I thought were dinosaurs (dimetrodons, pterosaurs, plesiosaurs, etc.) were not in fact dinosaurs. Is there a reasonably quick way for a lay person to tell apart true dinosaurs from non-dinosaurs without taking up an in-depth, species-by-species study of paleontology?

There are several defining morphological characteristics of dinosaurs. Including their ankle structure and perforated acetabulum, Aka the hole in their hip goes all the way through, as well as a few other minor features. These combined makes it literally impossibly for a dinosaur to take on a sprawling pose without breaking hind leg in many places, this is why you will often see an erect posture given as the reason, but that is a product of these feature not the defining feature itself, there are many ways to achieve upright posture.
Now of course we are moving away from purely morphological definitions, cladistically dinosaurs are defined as The last (most recent) common ancestor of Triceratops horridus and Passer domesticus (common pigeon), and sometimes Diplodocus carnegii as a third, and all of its(the ancestor's) descendants.
A more superficial quick and dirty method is if it is a pterosaur or lives in the ocean it is not a dinosaur, If its limbs sprawl it is also not a dinosaur. I should also include this guys work, since he attempted to create a complete cladogram of every dinosaur, so you can visualize the group.

Could you explain how dinosaurs could possibly be defined as "the last common ancestor...", since birds diverged from the dinosaurs tens of millions of years before the K-T extinction?

Sorry that should say the "most recent" common ancestor,  which is probably closely related to Nyasasaurus. It is worded that way because it is assumed we will never find the exact ancestral species this way any new discoveries can be assessed. If the common ancestor thig is giving you trouble try this, https://evolution.berkeley.edu/evolibrary/article/0_0_0/evotrees_primer_04

I understand the common ancestor bit, what I don't understand is the choice of species.  IIRC Triceratops was a late Cretaceous (group of) species, while birds diverged from theropods sometime in the Jurassic.  But there are dinosaurs going back to the Triassic (e.g.  Nyasasaurus).  So how can "dinosaurs" be defined as the descendants of something that existed tens of millions of later?  Wouldn't there be many dinosaur lineages that coexisted with that ancestor, but diverged earlier and followed different evolutionary paths?

@jamesqf You misunderstand, all the descendants of the common ancestor, not those two (although their descendants would be included). Since those two are from each of the major dinosaur lineages respectively that means the descendants of their common ancestor will include all dinosaurs. Triceratops and birds are about as distantly related as you can get within dinosaurs.

But aren't the ancestors (or at least some of them) of that last common ancestor also dinosaurs?  At least back to the point where they could be confused with reptiles?  Also lineages that branched from the ancestors of that last common ancestor?

@jamesqf No they are not, this how clades are defined. Every organisms on earth shares a common ancestor with every other organisms, the only thing that varies is how far back you have to go. You may want to familiarize yourself with something called cladistics, which is about the only way of defining biological groups that makes even a lick of sense. Wherever we draw the lines is always going to be arbitrary but cladistics is at least consistent in its rules.

Yes, the legs of dinosaurs are directly beneath their bodies. This is more efficient that the sprawling stance of lizards, crocodilians, pelycosaurs, and other mammal-like reptiles. It is likely no coincidence that another successful group, mammals, also have their legs directly beneath them. Also, as far as I know there were no fully marine dinosaurs.

Please provide support for the various claims you make in your answer. Thanks, Karl.

This would hardly seem to apply to pterosaurs and plesiosaurs.

Points of fact do not need to be supported by citation. Also, it does apply to both pterosaurs and plesiosaurs, whose limbs come out from the sides.

There are many examples of "upright" postures among animals you list as having sprawling posture.


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What sauropod genera had a double row of chevron bones in the tail?
I know that Diplodocus is marked by the feature of having a double row of or "double-beamed" chevron bones in the tail, but how diagnostic is this feature if several other sauropods have it? I mean, if there are other genera with the feature, which ones are they, so I know not to confuse them with Diplodocus?

It's fairly common. It is believed to have evolved two times independently, basically in both groups presumed to use their tails as weapons. Both Diplodocoidea and Euhelopodidae have species with forked chevrons and evolved it independently. It is fairly diagnostic since it is not seen outside these groups.
Source
Independent half chevrons (two rows of individual elongated splints of bone, one right, one left) pop up in many groups but double beamed chevrons are something different: the ends of the chevrons are joined, creating a single solid structure. In some parts of the tail they are separated into right and left halves (these are not very unique), but the joined ones are taxonomically significant. These are not chevrons dwindling into nothing along the tail but changing structure in a specific structurally significant way.

Thank you for your answer, but I am still not clear on something. Did you mean to say that ALL genera in Diplodocoidea and Euhelopodidae had double-beamed chevrons? I knew that at least some did, but I am trying to know which genera specifically so I can have a relatively quick and easy way to distinguish the specific genus Diplodocus from the rest of Diplodocoidea (e.g., Barosaurus and Galeamopus).

most Diplodocoidea do (it is lost on some of the Dicraeosaurus who re-evolve short tails) and only a few Euhelopus do it appears to be a an independent evolution. It is hard to say definitively because so many sauropods are known from only a few elements.  It is not a good distinguishing feature simple because it is one of the smaller more easily lost elements.

source: Stack Exchange

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

sort: votes


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What causes the distinct color change in matured leaves in some plants?
Maybe that color change is caused by lower chlorophyll concentration in younger leaves' cells, or chlorophyll a to b ratio differs between younger and older leaves. All I could find is that the chlorophyll a to b ratio in higher plants is 3:1, but there's little data if that ratio ever changes.
That color change is especially noticeable in conifers, but I've seen it in trees belonging to other divisions.

My guess would be that the structural metabolites and waxy cuticle that give these leaves rigidity and protect them from the elements can't be produced in these tips of new growth without stunting their development (note that the branch tip is still green and not yet woody). Conifers have some of the toughest cuticlular waxes in the plant world, and I know that a property of these waxes is that they change the apparent color characteristics of the leaves by reflecting or absorbing certain wavelengths of light (it's what makes the blue spruce blue).

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


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Are "antibodies" and "immunoglobulins" really the same things?
Wikipedia says that NCAM (CD56) glycoprotein belongs to Immunoglobulin (Ig) superfamily.
A the same time, its article on antibodies equates them with immunoglobulins. NCAM is obviously not an antibody, so are these words really synonymous?

See also https://en.wikipedia.org/wiki/Immunoglobulin_superfamily
What you have here is a bit of imprecise terminology, and a language problem equivalent to another familiar one: cats. A lion is both a cat and not a cat, because 'cat' refers both to a family of mammals and to what is more precisely referred to as a 'house cat'. To tell which you are talking about requires context or clarification.
Same thing here: antibodies are referred to as immunoglobulins, which are part of a larger family, the immunoglobulin superfamily, which you might also refer to as immunoglobulins but usually not. They share a name because the immunoglobulins (antibodies) are sort of the 'archetype' of the superfamily. Wikipedia is saying CD56 belongs to the immunoglobulin superfamily - that's clear because they specifically write superfamily - not quite the same as calling them an "immunoglobulin". They're also saying antibodies are called immunoglobulins, but that doesn't mean everything in the immunoglobulin superfamily is an antibody.

I don’t think your cat analogy is so helpful because we can say “a lion is a cat” but we can’t say “NCAM is an antibody”. I would have made the point that immunoglobulin is the technical name for a molecule of precise function, commonly known as an antibody. However “immunoglobulin superfamily” is a term used in structural classification of proteins which have a variety of different functions. It could equally well have been named something  like the Y family, but was named after the first structure of this type to be determined.

@David Eh, it would be better to argue that "we can't say 'NCAM is an immunoglobulin' " - I think that's accurate, in that "immunoglobulin" is only ever used for the antibody, and not in a broader sense to refer to the whole cat family/immunoglobulin superfamily, yet it's still used in that broader sense in the adjective form, e.g. immunoglobulin domain. The point of my answer is that you need to distinguish between the immunoglobulin superfamily and immunoglobulins/antibodies, just like you need to distinguish between the cat family and the household cat.

Whatever. But if you must make an analogy the it should be: Cat is the common name for Felis catus, a member of the family felidae. In the same way Antibody is the common name for immunoglobulin G (generally) a member of the immunoglobulin structural superfamily. But then it doesn't work as nicely. I prefer to stick to pictures of proteins, as in your Wikipedia link. May get round to it myself over Christmas.

@David I'll be glad to see your answer.


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Do beavers' tails hurt from being dragged?
I understand that when beavers walk on land, they drag their tails behind them on the ground. Their tails look quite large and rather heavy, and the ground is often rough - does dragging the tail not cause abrasions and pain for the beaver?

No, it does not, otherwise beavers wouldn't walk with their tails dragging. Here is a picture of the bottom of a beaver's tail:

Found here
and here is a closeup (probably of the top, but they're very similar):

Royalty-free stock photo from Dreamstime
As you can see, the skin looks almost like reptilian scales. It is likely highly-keratinized and is quite thick, as you can see below. Innervation is probably net very close to the surface, like callouses we develop on our hands and feet, so it doesn't hurt to be dragged over sharp surfaces like rocks or thorns. Here is a cross-section of the thick part of the tail close to the body:

Source: Cannundrum blog


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Quantitative Physiology Textbooks Recommendations?
I am currently completing a 2nd year (UK) Mamamilian Physiology Module and a Neuroscience Module. However, my degree is also 40% Maths and Statistics. So in order to learn the content better, I am thinking I may be more suited to a quantitative first explanation before the qualitative description.
I am asking here as I don't want the biology to be glossed over as I am being assessed by Physiology Professors not my Statistics Professor

Has your professor suggested any book as a part of the course?

@RoniSaiba yes the Pocock and Richards Textbooks and points us to research papers in the slides


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Uranium based blood
Here's a hypothetical planet with complex, sapient life and a very weak magnetic field. Could they have Uranium-based blood, much as our blood is based on iron and crab's is based on copper? Deinococcus radiodurans can resist radiation extremely well. Could this hypothetical life do the same? Or would their blood accidentally cause nuclear fission?

Why specifically uranium?

This is an opinion-based question because it is asking about a hypothetical situation. From the [help/dont-ask], avoid asking subjective questions where […] you are asking an open-ended, hypothetical question: “What if ______ happened?” We expect answers to be based on verifiable facts and references, along with subject-related expertise. You may be able to get answers at [worldbuilding.se], but please read through their help center first.

Robert, if you adjust and move this question to WorldBuilding StackExchange (read their guidelines first), perhaps you may have more suitable answers to your hypothesis.

I would say it’s very unlikely. There is a difference between tolerating radiation and incorporating unstable isotopes in your organism. In metazoa, the metal ion serves the purpose of binding to another molecule (a ligand, oxygen) which needs to be moved around within the organism. There is no reason why a rare element with an unstable nucleus would be useful for performing that task. A more abundant, easier to manage element would be selected for.
SciFi speculation: I could envision a cellular mechanism able to harvest energy from the nuclear decay of unstable nuclides. On a planet where the material is much more abundant than it was here on earth during the hadean. This is purely speculative.


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What is the dynamic range under initial conditions?
could someone help me to understand the following sentence better?
It's from the book "A Practical Guide to Assay Development and High-Throughput Screening in Drug Discovery".
And it's about fluorophors used in FRET-assays, for screening of protease inhibitors.
"In contrast to many other FRET dye pairs, both EDANS & DABCYL and Mca/Dnp generate a dynamic range between cleaved an uncleaved substrate, sufficent for the application of such protease assays in HTS and high-throughput compound profiling under initial conditions. "
I'm confused about the last part of the quote "under initial conditions".
What does that mean?
the question summarized "What is the dynamic range under initial conditions? "

I think that they mean initial profiling as the profiling/screening is the subject of the clause.
In this case it would mean that FRET with these compounds has enough difference between cleaved and uncleaved that you can use this difference to tell if it has inhibited or promoted a reaction between your target and its substrate or not in a quick/high-throughput assay for mass screening of potential inhibitors/promoters.

I've read that its common to do HTS screening first with an easy and cheap assay.
Afterwards more complex assays follow, which sort out more substances.
So "initial" in this case would mean, something like: "the first assay to screen for substances?"

@Mourinho_1 that's how I read it.

thanks a lot. I did not consider that it could mean something like this. I would say that this sounds plausible


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Why are babies rarely born with cancer?
Childhood cancer is fundamentally a disease of dysregulated development. Why does it rarely occur during the fetal period, a time of enormous growth and development?

"Childhood cancer is fundamentally a disease of dysregulated development." Can you please clarify what you mean in stating this? I'm a bit confused why you say this; I can think of lots of 'childhood cancers' that seem to be no different than those occuring in older adults. In fact, a number of cancers have a bimodal presentations, one in childhood/adolescence and then again in adults.

Nature tends to turn against cancer not towards it. Cancer exists when cells begin to multiply with abnormal features, without correction. Cancer is the consequence of many many harmful mutations, which inhibit the correct reading of DNA.
Cancer takes time to develop, not months, but years. Also, babies don't have old tissues, so there haven't been as many divisions, or as many opportunities for mutations, as a 5 yr old or a 10 yr old has gone through.
Although rare, Neuroblastoma is a cancer that babies CAN be born with. Nerve cells develop early, week 5 of fetal development.
Perhaps someone else could talk more about the biological mechanisms which really make cancer more a reality for older organisms, but probablistically, it doesn't make sense that a newborn baby would have cancer.
I looked up these links, to try and address your question.
cancer in general
https://www.cancer.gov/about-cancer/understanding/what-is-cancer
why cancer takes time to develop
https://sites.duke.edu/missiontomars/the-mission/cancer/why-do-most-cancers-take-so-long-to-develop/
cancer in babies
https://blog.dana-farber.org/insight/2015/02/can-babies-be-born-with-cancer/


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Can sperm cells penetrate the cell membrane of non-ovum cells?
Sperm cells have tiny bags of enzymes on their tip (the acrosome) which allow them to penetrate the ovum. My question is whether or not the process that allows sperm cells to penetrate the cell membrane is specific to ova, or if it allows them to penetrate other types of cells.
In either case, a quick description of the process would be greatly appreciated!

I was about to ask this question. I just bought a microscope and of course I was looking at my sperm, what intrigued me (even though I have little knowledge on biology) is that I saw a sperm cell incide a another [what looked like] another cell, from my own semen. (Took pictures and recorded with my cellphone!).

It is very possible that the specific enzymes that penetrate the cells can be used to lyse other cells or at least manipulate the plasma membrane. That being said, I don't think that sperm cells can be used to do that because the acrosomal reactions that you discuss are only activated by the presence of the zona pelliculada of the egg cell. Since that doesn't exist in any other type of cell a sperm cell can't be used for Acrosomal enzyme delivery for somatic cells, for example.
If you want to read more, the Wikipedia page about the Acrosome reaction is pretty good.

Thank you for your response. The specificity of the acrosomal reactions to the zona pelliculada was the information I needed.


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how long would oxidation of ammonia solution to nitrates take?
A hot topic among amateur chemists is making nitric acid from ammonia. While not as useful, im interested in making nitrate salts from ammonia as well.
A simple idea is to just infect ammonia solution with soil bacteria and add some fresh grass as source of other necessary nutrients for bacteria. If kept at optimal temperature, how long can i except the process of forming ammonium nitrate to take?

Hi, maybe tell us how far you got and where your research got stuck. A lead can be to search for COMMOX (COMplete AMMonia OXidiser), they do the whole process from ammonia to nitrate.

haven't started the experiment yet, i just wanted to know whether it would take days, week, or months


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Questions about "parasite recursion"
So imagine a parasite of a parasite. Imagine a parasite of that parasite. Then imagine a parasite of that parasite, then a parasite of that parasite, and so on and so forth.

Is there a formal term for this?

How frequent does this occur in nature? If it varies, what does it vary by? How many levels down do parasites typically go?

What is the deepest level that has ever been observed, and with what organism?

Thanks

There actually are virophages https://en.wikipedia.org/wiki/Virophage or satelite viruses https://en.wikipedia.org/wiki/Satellite_(biology), so the level should be at least 4 or 5, maybe more.

Hyperparasitism is one possible term. According to the linked article it is commonplace in certain types of insects, but also in fungi. Apparently the cases of at least three levels are known: a fungus on a fungus on a fungus on a tree.


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

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


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

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

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

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


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Are antibodies removed before blood transfusion
I am an O blood group person meaning, I can donate my blood to all as I don't have any Antigen A and B. But my body does contain antibodies A and B right?
If they were along with the donor blood, wouldn't they cause clotting with the recipients blood?
We spent a whole period over this. My teacher said they probably remove the antibody before transfusion, but I couldn't find much info on that. I postulated that these antibodies can not work outside the donor body for some reason.
Thanks for the help

I quote from the below.
Groups and Red Cell Antigens
by
Laura Dean (page 7). Available at:
http://www.ncbi.nlm.nih.gov/books/NBK2265/
"Red blood cell incompatibility may also occur when the patient's RBC antigens are attacked by antibodies from the donor's plasma. This tends to be a minor problem because of the small amount of antibody present in the donated plasma, which is further diluted on transfusion into the recipient's circulation."
I dont think the antibodies are removed, but in countries with a good medical system I believe the matching blood type is always used.
http://en.wikipedia.org/wiki/Acute_hemolytic_transfusion_reaction

"I dont think the antibodies are removed" But isn't O group still considered universal donor. Thanks for telling me it's only a minor problem

O is universal donor.


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What material is permeable for plant roots, but "impermeable" for fungi & bacteria?
I'm designing an experiment where the roots of the plant will grow in a sterile environment while the shoot will grow in a non-sterile grow room. For this reason the environments of the shoot and the root should have some form of physical separation.
Is there any material that allows roots to grow through it but will stop fungi and bacteria?

root and shoot grow in different directions. Why can't you sterilize your media and cover it with an impermeable material?

I might have found a solution! Kuijken et al. (2015) first germinate seeds in a sterile eppendorf filled with agar and nutrients. They then cut off the bottom of the eppendorf and stick it through the lid of a sterile plastic jar and pad it with sterile cotton. So I guess they are using the agar as a material that is permeable to the roots and "impermeable" to bacteria and fungi.
Kuijken, R. C., Snel, J. F., Heddes, M. M., Bouwmeester, H. J., & Marcelis, L. F. (2015). The importance of a sterile rhizosphere when phenotyping for root exudation. Plant and Soil, 387(1-2), 131-142.


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Can I imbibe seeds before sterilization?
For an experiment I want to germinate lettuce seeds. For logistical reasons it would be convenient to imbibe the seeds by placing them in the cold for 2 days, afterwards I would sterilize the seeds using dilluted bleach. I mostly see people apply stratification or imbibition after sterilization, does the order matter? Would there be a difference for cold treatment (stratification) or wet treatment (imbibition)?

Personal anecdote: Once I planned to sterilize seeds of Silene latifolia for tissue culture but after the first step (washing the seeds in water for an hour) I had to do other things and the seeds did spend the night wet in room temperature. The next day some of the seeds were showing first signs of germination - a little crack in seed coat. I decided to sterilize them anyway, since there was nothing to lose. The result: Some seeds did germinate after sterilization and were fine. Some seeds died. Interestingly, in some seeds the bleach destroyed only the exposed root meristem resulting in rootless seedlings.
I have never worked with lettuce seeds but I would consider questions:

How fast the seeds germinate and what conditions they need for germinating? You cannot sterilize seed that have already germinated.
Could the inbibition change the properties of the seed coat and make it easier for the bleach to pass through and kill the embryo? I suspect not, but cannot be sure.
Wet environment is good for bacteria and fungi growth. "Dirtier" seeds are sometimes harder to sterilize - they need longer exposure to bleach or stronger bleach concentration to completely remove contamination. Stronger bleach or longer treatment can sometimes kill some (especially small) seeds. It is hard to say weather two days of wetness can make any difference. The cold should slow down the bacterial and fungal growth.

At the end of the day I reccomend you to try with few seeds and see the result. Maybe include negative control with usual order of steps. If the survival is the same for both groops you are good to go.


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How does lactate produced in the intestines get transported to the rest of the body?
Some gut bacteria known as lactic acid bacteria(LAB) are known to produce lactate in the intestines and they confer beneficial effects such as enhancement of the immune system, but I assume not all of the lactate stay in the intestines and some of them will get transported to the rest of the body and used by other tissues (e.g. cori cycle). If that's the case, do these lactate enter the circulatory system? Are there any articles reporting it?


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In cell division, are daughter cells "newer" than the parent cell?
I learned that cells go through cell division to generate new cells to replace dead or damaged cells.
Are the daughter cells "newer" than the parent cells? For example, the parent cell has an "age" of 9 days and the daughter cells will have an "age" of 2 days.  Because if they are not "newer" than the parent cells and all have an "age" of 9 days, they will all still die  together at the same time in the end.
For a real world example, skin cells only live a few weeks. But not all skin cells on our body die after a few weeks. So the only logical way I can think of to get around this is that daughter cells are "newer" or "younger" than parent cells. Or perhaps my notion about the "age" of cells is wrong.
And if the daughter cells are "newer", why is that possible?

Hi and welcome to Biology@SE! Have you read about telomeres? In general, you have to define "cell age" more precise, i think

I think you need to read about cell ageing and sort out what you mean by new and how the two do or do not relate and then come back with a properly defined question.

There may be an interesting question here. Cell division can be asymmetric (asymmetric partitioning of the biomolecules and orgaqnelles) and the "age" of the two cells can be different. This is at least known in yeast. Are you asking about something similar?


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N value in a GWAS?
Just like the title says. I am reading about a GWAS but I don't know much about them. I understood most of it but I couldn't figure out what the "n" value was.

Are you talking about n (as written in the title) or N (as written in the title)? The meaning of a variable like this might well vary depending on your source. Can you please indicate your source?

Same question as @Remi.b. The most common use of $n$ is to denote the total number of subjects used in the study. $N$ is also often used to denote the number of alleles.


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Can Females Songbirds Have Male Plumage?
Male birds are colorful for courtship displays, females are dull for camouflage. But, is written in a website somewhere that sometimes, when females birds are sterile, they grow male plumage due to male's feathers being a dormant gene (or something like that, sorry, I'm no professional). Is true? Can it happen? If so, how came? (and I lost the website's link, so I can't post it here, sorry again)

Please would you add a link to the website that you mentioned? That would be useful.

I don't have a link to a reference, but I was told by an ornithologist last week that in the UK, female blackbirds (usually brown plumage and brown beak) can sometimes change to more resemble males later in their lives (black plumage and orange beak).

Unfortunately, anecdotal references are not acceptable even if they come from an expert. Unless there is good statistical evidence, we cannot be sure. It would be super good if you can contact the ornithologist and ask them for a reference.


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What is this snake?

What kind of snake is this? It was sighted in Singapore (South-Eastern-Asia) and was ca. 40cm (~ 16 inches) long.

Could be a Temple Viper (Tropidolaemus wagleri). Hard to tell from the picture, but the head looks spaded like a Temple Viper's and I think they come in the green morph you show


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Why has the human eye evolved to become sensitive only to the visible light?
The human eye has evolved to become sensitive only to visible part of the electromagnetic spectrum. Why? Why is infrared vision disfavoured for us by evolution but not for some other animals? I am not an expert of biology but curious.

First hit on google. There are some complete answers there and elsewhere!

I searched google. I found this answer on quora https://www.quora.com/Why-does-the-human-eye-only-see-the-visible-spectrum-Does-the-fact-that-yellow-is-in-the-middle-of-the-spectrum-have-to-do-with-the-sun It says that "because that’s what we evolved to use to find food and mates, and to identify threats to survival. ". But it doesn't make sense to me. Humans also have survival threats at nights.

99% of all the photons in the universe are from the cosmic background radiation, echoes from the big bang, the rest is infrared, save for 0.001% of the photons which are visible. We can sense IR with our skin, UV requires small eyeballs, and yes i want IR vision.

Actually, it's got nothing to do with evolution or even human biology.
Why?

What’s in a name? That which we call a rose,
  By any other name would still smell as sweet. William Shakespeare.

First, try to define visible yourself. Next look at the definition of it in various respected dictionaries; in our context it means

that can be seen

Consider the case of Goffin's cuckatoo, they can see as far up to as ultra-violet spectrum. They don't speak English (or Portuguese for that matter) but for them visible would mean "what they can see".
So, coming back to your question, even if we had capability to see, say, infrared spectrum, visible would have meant: VIBGYOR + infra. And then we'd have complained about not being able to see bacteria with naked eye :P

I think it's pretty clear the OP is not asking for the pedantic answer, nor does the pedantic answer have anything to do with biology.

@BryanKaruse sorry for that. But OP didn't show effort on their part and the question text lacked necessary specifications. Also, OP admits lack of expertise, a bio-physics answer would be pedantic for OP.

shall I find a cockatoo speaking portuguese on YT? :D


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Can bacteria pick up lethal plasmids?
I am sorry if this question is too general, and does not have any concrete answer.
I was explaining to my non-biology-background friend about plasmids and how they are picked up by bacteria from the remains of other dead bacteria during stressful conditions. This is when this question arose:
Why would bacteria pick up plasmids released from the dead bacteria, as this means that these plasmids either did not help it survive in those conditions, or could have in fact been the cause of their death? This also lead to the question of whether plasmids can be lethal? (I believe there could be, for example plasmids which are translated into proteins which are endonucleases which would probably kill the bacteria, yet I am not sure).
Moreover, if this sort of plasmids exists, then why could we not engineer them specifically and use them as medicine as an “antibiotic”?

You might be interested in this answer, and the other answers to the question.

The ability of bacteria to take up intact environmental DNA is called natural competence.
One problem with trying to take advantage of this in a therapy is that it is not very efficient. Importantly, natural competence is regulated and tends to be activated when bacteria are already stressed. This is also likely part of the answer as to why a bacterium would take up DNA from the outside: if they are already in bad shape, they don't have much to lose. Bacteria growing in non-stressful conditions are less competent, and possibly negligibly so.

Ween et al 2002 compared competence in two bacterial strains, one with a "normal" regulation of competence. At most bacterial concentrations, the "normal" strain showed less than 1% transformation, and this is still in sort of an ideal laboratory condition, where the culture medium is flooded with plasmids. There wouldn't be a feasible way to even approach delivering that much plasmid DNA into a human.
Ween, O., Teigen, S., Gaustad, P., Kilian, M., & Håvarstein, L. S. (2002). Competence without a competence pheromone in a natural isolate of Streptococcus infantis. Journal of bacteriology, 184(13), 3426-3432.

The other big problem is you are working directly against selection pressures. In the case of a plasmid that improves survival (say, one containing a gene that confers antibiotic resistance in the presence of that antibiotic), then the population will more quickly increase the expression of that plasmid, as bacteria with it grow and reproduce while other bacteria die. However, if you have a lethal plasmid, all the bacteria you are able to transform simply die. They don't spread the plasmid by reproducing, and as they die the non-transformed bacteria will continue to reproduce.

This also lead to the question of whether plasmids can be lethal?

Yes, genes in plasmids could be beneficial, neutral or even lethal, although lethal plasmids may have trouble surviving for long since they depend on a live cell for replication.

Moreover, if this sort of plasmids exists, then why could we not engineer them specifically and use them as medicine as an “antibiotic”?

Efficacy aside, they're relatively large, highly immunogenic molecules. Not great properties in an antibiotic.


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Why does absorption (at 260nm) of ssDNA increase with temperature?
In the graph below, I understand why A260 of double stranded DNA would increase with temperature increase, as more of the DNA becomes single stranded (and A260 of ssDNA is higher than that of dsDNA because the aromatic bases are more exposed, which absorb the light).
However, I do not understand why the absorbance of ssDNA also increases... I know that individual nucleotides also absorb more than ssDNA (as shown in "inequality" below), but I doubt that the covalent bonds holding the nucleotides are breaking at 80 degrees centigrade. Would this maybe be the effect of an increase in temperature increasing absorption? (I have read that increase in temperature increases collision of photons hence increases absorbance, but I am not quite sure). Thank you.
"inequality" showing which has higher A260:

single nucleotides > ssDNA/ssRNA > dsDNA

One factor to consider is that "ssDNA" isn't actually a single strand — in most cases it will be a pseudoknot where parts of the strand will pair with other parts sometimes in ways that involve noncanonical base interactions that can lead to three and four strand structures. I would guess that "melting" of these structures is a major contributor to the increase. Will turn this into an answer later when I have time if no else does.

@tyersome It's perhaps just my skeptical side, but I'd have a hard time believing that that accounts for a straight line increase... I'd expect it to follow a similar (though much less pronounced and perhaps left shifted) shape to that which double-strand DNA follows.  That said it's not impossible that the graph is not actually all that representative.  Anyhow I look forward to seeing your answer and sources.

This paper looks at the hydrolysis of DNA during prolonged incubation (up to 36 hours) at 70° C.

Thank you for your insightful answers! I do agree with @rotaredom that if there is melting of stemloops (@tyersome) and other "tertiary" DNA structures within the ssDNA, then this denaturation should also be cooperative, and should follow a similar sigmoidal curve to the dsDNA shown... The paper on hydrolysis (@rotaredom) would mean that there's also single nucleotides, which absorb more. It would make sense in this case if the rate of hydrolysis increases linearly with temperature, as shown in the graph. I'm curious for other interpretations!

The decreased absorbance of dsDNA is in large part due to base stacking interactions. Base stacking still occurs in ssDNA, so I suspect that is why you see a temperature dependence.

It might not have to do with any self-interactions of the ssDNA, but instead to do with interactions between different ssDNA molecules. Just because the strand has no reverse complement doesn't mean it can't have hydrogen bond interactions with other molecules of ssDNA

I suspect this may be a chemical question. Have you checked whether temperature has any effect on the UV absorption of nucleotide bases?

It seems canadianer's intuition is correct --

Base stacking still occurs in ssDNA, so I suspect that is why you see a temperature dependence

-- based on this paper:
Conformational Changes in Single-Strand DNA as a Function of Temperature by SANS
Motivation --
UV absorption-based measurement of DNA melting temperature is reliant on the assumption that the DNA duplex dissociates into the same single-stranded DNA (ssDNA) random coil conformations at all temperatures.  However, calorimetry studies (citations 2 and 3 quoted below) have suggested that temperature-dependent conformational changes occur in ssDNA, too.

Early results from calorimetric studies on the dissociation of a 13-mer DNA duplex have shown, however, that the conformation of the single complementary ssDNA does depend on temperature (2). This was evident in the absolute difference between the heat of dissociation of a 13-mer DNA duplex of 490 kJ mol−1 determined at 74°C determined from differential scanning calorimeter (DSC) measurements and the heat of association of the duplex of −236 kJ mol−1 directly determined at 25°C from batch calorimetry measurements (2). This difference was attributed to the additional thermodynamic contributions from conformational changes in the complementary single strands implied from UV absorption changes upon heating solutions of each of the complementary strands from 25°C to 74°C.
...
More recent results also show a large disparity between the free energies of the dissociation of 10-mer duplexes extrapolated from DSC measurements at high temperature to 25°C and the free energies determined directly from isothermal titration calorimetry measurements on the binding of the single strands of the duplex at this temperature (3). This was again attributed to free energy contributions of the change in the single-strand random coil conformations as the temperature increased from 25°C to the melting temperature of the duplex (3).

Methods --
The authors used a 2 μM solution of 10-mer ssDNA (5′-ATGCTGATGC-3′) in 10 mM sodium phosphate buffer, pH 7.0, containing 0.1 M sodium chloride and 0.1 mM ethylenediaminetetraacetate.  Temperature-dependent changes to this solution were measured by three methods:

Small-angle neutron scattering (SANS) at 10°C increments from 25°C to 80°C.  Normalized scattering data were used to compute the geometry of the ssDNA using the LORES algorithm (PDF).
Optical density measurements (260 nm) between 20°C and 90°C, with a heating rate of 1 K per minute and measurements taken every 30 seconds.
Differential scanning calorimetry with continuous measurements from 5°C to 105°C at 1°C per minute.

Findings and Conclusion --
Taken together, the SANS and calorimetry data suggest that the change in shape of the ssDNA with increasing temperature is due to unstacking of bases, corresponding to an endothermic transition.

... [the ssDNA] undergoes an expansion in the diameter direction that causes a slightly shortened length as the temperature increases from 25°C to 43°C. Then, as the temperature increases further from 43°C to 53°C, it expands in the length direction as the diameter decreases. Finally, the ssDNA increases dramatically both in length and diameter as the temperature is further increased from 53°C to 80°C.
...
These conformational changes correspond to the unstacking of the A and G purines as well as the T and C pyrimidines in 5′-ATGCTGATGC-3′ as the temperature is increased. The unstacking is manifested in molecular motion of the nucleotides in and out of the cylindrical axis (an increase in diameter) and in the stretching of the helix or cylinder (increase in pitch). The increase in the optical density upon melting of the single-strand substantiates the SANS results since the optical density changes indicate exposure of the purine and pyrimidine bases to a more polar (water) environment.

And, as with liliae's figure, the results of the ultraviolet absorbance scan show density increasing with increasing temperature.

Figure 6. Normalized UVM scan of a 2-μM ssDNA solution. The solid line is the least-squares fit of a two-state, A↔B transition model to the data points. The broken horizontal lines are the extrapolated pre- and post-transitional base lines and the broken vertical line indicates the temperature at the midpoint of the transition.

Glad somebody found a paper; great answer.


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What made this, is it an egg sac?
Found this "egg ball" on a gate near a greenbelt north of Seattle, WA. From other posts here, it looks similar to snail eggs, but they do not have the webbing. Two days later I went back out to measure it, but it was gone. Maybe hatched or eaten?

s://i.sstatic.net/tj6gT.jpg

similar: What is this agglomeration of pink cells I found attached to a stone?


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How did animals on Earth survive without plants?
Around 500 million years ago, there were animals on earth, but there were no plants yet. How did animals survive? I'm assuming some of the animals ate other animals, but did some animals eat rocks or something?

Plants evolved around a billion years ago, land plants evolved at least ~800 millions years ago, likely closer to 1200 million years.

Maybe if you cite a source for the claim about particular years that could help someone write an answer explaining where the discrepancy is?

They ate grass, since grass was not classified as a plant back then :)

Since you're a new contributor, I'm going to go ahead and answer this despite the flaws in the question that have caused it to be at -4 when I write this answer (skip to the last paragraph to see what I have to say about that).  The major reason the answer isn't more obvious is that your assumptions about how long plants and animals have been around is incorrect.  Or rather is based on when a particular type of animal life (sea life with hard parts) arose 500 million years ago and comparing it to when complex plant life was able to colonize dry land (about 475 million years ago). Besides the obvious point that animal life in the oceans is  not directly dependent on eating plant life on dry land, there  a larger problem.  You are treating complex multicellular life as the only type of life. It is not.
When most people think of 'animals' and 'plants' they are thinking about complex multicellular life.  Things we can see with our own eyes.  The problem is that this type of life is quite recent.  For most of the history of life on earth, living creatures have been single celled.  While composed of only one cell, these creatures (like animals and plants) could be divided into two groups based on how they got their food: heterotrophs that consumed other things (like animals do) and autotrophs that make their own food (like plants do)
The oldest fossils of single celled life date back to about 3.5 billion years ago. Since these fossils suggest relatively complex communities of multiple types of living creatures, including both heterotrophs (that ate autotrophs or other heterotrophs)  and photosynthetic autotrophs (albeit using a less efficient form  that did not make oxygen but otherwise lived much like plants do today).   We think life originated before that, probably abut 3.8 billion years ago.   Mostly because before 3.8 billion years ago, the earths surface was repeatedly blasted with meteorites and comets sent crashing through the inner solar system by the orbits of the outer planets shifting into their current positions (see https://en.wikipedia.org/wiki/Late_Heavy_Bombardment  )
I draw your attention to the timeline of life on earth within that article and follow it to the article: https://en.wikipedia.org/wiki/Timeline_of_the_evolutionary_history_of_life
By 3 billion years ago, long before multicellular plants and animals, single celled autotrophs were engaging in photosynthesis essentially identical to how plants do today. Even at 3.5 billion years ago,  there were single celled plant-like organisms for animal-like organisms to eat.
Before that?  Classically, it has been thought that the first living creatures consumed the 'soup' of organic (carbon containing) molecules that made the first simple informational and catalytic macromolecules that were the likely basis for early protolife (or one well established idea, read about the "RNA world hypothesis" https://en.wikipedia.org/wiki/RNA_world). Either right about this time or soon thereafter, protocells that could make their own food evolved. Similar to very primitive life living in extreme ecological niches today, these chemoautotrophs likely made food from high energy chemical reactions that take place as a result of geothermal activity.  In places like "black smoker" deep sea vents where single celled organisms use the boiling hot water and highly reactive chemicals dissolved in it to make food that is even today the basis for ecosystems that do not depend on the light of the sun (see https://en.wikipedia.org/wiki/Chemotroph).  In a manner of speaking, these did sort of eat rocks.
By the time complex multicellular heterotrophic life (animals) had evolved hard bits that fossilize well about 500 million years ago (when you incorrectly have animals first evolving),  animals without hard bits had existed for about  500 million more years.  Even when they evolved, there was a 2.5 billion year history of single celled things to eat.  When complex multicellular photosynthetic autotrophs (plants) first colonized dry land about 475 million years ago, some single celled photosynthetic autotrophs had been living there in or near fresh water for about 400 million years  (https://en.wikipedia.org/wiki/Evolutionary_history_of_plants).  And the most basic complex multicellular photosynthetic autotrophs (similar to simple seaweeds today) had been living is marine environments for a billion years (https://www.eurekalert.org/pub_releases/2020-02/vt-1bg022120.php)
So you can see, your question is predicted on incorrect assumptions.  When these are corrected, there is no question at all.  As to why this question is downvoted, the incorrect assumptions likely are a big part of it.  But you may notice that all the key citations I make are from one source.  Wikipedia.  I could easily have made it from primary sources or college level textbooks.  But I used wikipedia for a reason.  You could have done it too. Before asking your question, you probably should have checked to see if what you thought was the timeline of animal and planet development was correct.  You would quickly have found it was not. Stack Exchange, as I understand it, really isn't for asking questions that can be quickly answered with a wikipedia search. And that, I think, is why the question has been downvoted so much.  As to why I answered it anyway, the question seemed genuine and it didn't seem like you were just trying to lazily answer a question from class.  Besides,  I think even a question that isn't ideal can teach.  By answering, I show my reasoning which may help teach a reader how to answer questions themselves or ask a better question next time.
That and I think the issue of people forgetting that most of the history of life on earth is unicellular is widespread and deserves more consideration.  For example,  most alien life we are likely to encounter will look like slime on rocks.  Just like it would have looked to a visitor to Earth for most of our history.  So I rarely pass of a chance to make the point that life is mostly unicellular.

DrRadium. Nice attitude, and spot on about your Wikipedia paragraph. Thanks for contributing here. Hope you stick around and get more involved here.


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How much of male parental matter is still there in an infant organism after birth?
Are the atoms from the father's sperm still there in his baby's cells? Do they get lost during pregnancy? If they are still there, are they in a particular cell? Are they dispersed among many cells? Is it a regular mechanism or a matter of chance?

What do you mean by the term - "The atoms from father's sperm"? Is it chemical atoms or something else?

In most animals, humans included, the normal pattern of fertilization ends up with precisely one sperm contributing precisely two things to the egg: a haploid nucleus and a centriole. That's it. No more physical matter from the father ever enters the baby.
A typical human nucleus is about a 6 micron sphere of material, and a centriole is much smaller, so we're talking about mass in the picogram range. A healthy newborn child is a little over 3 kilograms, so the fraction of paternal atoms in a newborn child is definitely less than $10^{-12}$.
The actual location of those atoms would be fairly arbitrarily dispersed with each cell division, with the biggest chunks being the chromosomes and centriole, which could end up in at most 24 different cells. Don't forget, however, that not all cells in the fetus make it to the baby (some die, some are shed or otherwise disposed of), so some of that paternal matter might well be further lost. Other paternal atoms will be in materials less carefully managed by the cell (e.g., non-chromosomal materials of the haploid nucleus), and so will disperse more evenly and also be diluted by the regular processes of recycling and dilution.
Bottom line: there will likely be a few atoms from the father in the child, but only a vanishingly small fraction.  That doesn't really matter, though, because the information contributed from the father is still in every cell.

The father contributes information just once, doesn't he?

Yes, via that one sperm. The mother also contribute genetic information just once, via the egg (which has a little more genetic information than the sperm, due to the addition of mitochondria). The mother also has, of course, a major impact on development by providing the gestational environment, but the information content of that is difficult to define.

Doesn't the mother contribute genetic information as many times as there cells in the embryo and then in the foetus?

@yewgeniy No: just the once, via the egg, just like the father does just the once via the sperm. After that, the genetic information of both gets replicated. The atoms come from the mother (or, more properly, mostly from her food, delivered to the growing fetus by her body), but they no more deliver genetic information than your dinner gives to you.

"... the genetic information... gets replicated..." by whom?

Cells replicate themselves.


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Which enzymes use ATP?
It is well known that there are many enzymes which use ATP in their function, and any enzyme that work against an energy gradient need to have that energy supplied from somewhere, but just as well there are enzymes that simply work spontaneously and do not require such an influx of energy. However I can't seem to find any sort of list, however brief, that contains examples of enzymes that use ATP and ones that do not, or any indication of their prevalence. I could go one by one through each of the commonly encountered enzymes in the cell, but that would be tedious.
Is there any source where I could find what I am looking for? Or at the very least which of the major enzymes in the protein transcription/synthesis chain require ATP?

This would be such a massive list I can't see why you would maintain such a thing. It's possible someone will have an answer to how to extract it from a bioinformatics database, though.

I agree with @BryanKrause but both he and I gave examples of ATP-utilizing enzymes in our answers to a different question. This might be a starting point. However please finish reading the [Tour] and the help on asking questions here. We are keen on people showing evidence of having tried to answer their question themselves.

I just searched the Expasy Enzyme site for ATP using this search page. Will take you a while to look through them although there were fewer answers than I expected.

Thank you, David's answer was just what I was looking for. However I should have expected the daunting task of picking out a set of examples from that list. Any chance of being able to sort by a criteria like papers cited or times cross referenced, to a get some sense of importance?


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Does an FAD:FADH2 ratio exist in the cytoplasm? (similar to NAD+:NADH ratio?)
I have learned about a lot of enzymes/proteins which are covalently bound to FAD, and use this as an oxidising agent. In vivo, FAD is (almost) always protein bound (very low concentrations of free FMN/FAD [source]). Would an "FAD:FADH2 ratio" make sense (if it isn't free)? I know that the NAD+:NADH ratios in the mitochondria and in the cytoplasm are important, same for NADP+:NADPH (e.g. low NADP+:NADPH ratio in cytoplasm makes the reducing environment for fatty acid synthesis). Is it the same for FAD?


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What relation do glycerol-3-P DH and acyl-CoA DH have with Complex II of the ETC?
I am sorry if this may be a purely definitional/nomenclature question.
Complex II of the electron transport chain (ETC) would be succinate dehydrogenase, transporting electrons to ubiquinone (and forming ubiquinol with the addition of 2 protons).
Both glycerol-3-phosphate dehydrogenase (DH) and acyl CoA DH are integrated in the inner mitochondrial membrane, and form an ubiquinol, which can be used by Complex III of the ETC - very similarly to succinate DH. I was wondering why, then, these 2 enzymes weren't also part of "Complex II" or whether they were just not part of an "ETC complex" because they aren't part of the TCA cycle, or something? Are they in any way also related to the ETC supercomplex/respirasome?
Thank you.


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Can muscles remake pyruvate from lactic acid, or does it have to go to the liver in the Cori cycle?
When the muscle is exercising, and only anaerobic respiration is done, pyruvate -> lactate to regenerate NAD+. Lactate is then transported out of the muscle and into the liver, to regenerate glucose, which is then shuttled back to the muscle (the Cori cycle).
I was wondering whether once the muscle stops exercising, the muscle itself could regenerate pyruvate (using lactate dehydrogenase), or whether muscles always release their lactic acid to the liver? Or maybe there is no way of knowing this (how would this be tested experimentally...).

What would you envisage the skeletal muscle doing with the pyruvate, assuming that the liver had not cleared the lactic acid?

Once there is enough oxygen, I would think that the pyruvate could be used for oxidative phosphorylation.

But the whole point is that the muscles that are used for exercise need an energy source primarily under anaerobic conditions, and have few mitochondria. There is no way of storing pyruvate and in very light aerobic exercise other substrates for mitochondria available.

Oh okay thank you. Would it be possible for you to explain or attach a link about these myocytes with few mitochondria? I always believed muscles had a lot of mitochondria.. Also, would the other substrates for mitochondria in aerobic exercise (which you mentioned) be fatty acids? Thank you very much for clarifying.

I never was a card carrying metabolism man, but I always understood that you could tell a muscle’s metabolism by its colour: red muscle has a good blood supply for oxidative metabolism — hence it would have the requisite complement of mitochondria; white muscle would be mainly anaerobic. Muscles working continuously, like heart and the flight muscle of migratory birds, would need to be capable of aerobic metabolism. And yes, fatty acids can be used by heart muscle, sparing glucose for tissues like the brain. (All directed by the liver.)


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What makes the cytoplasm a reducing environment?
It is known that the cytoplasm is a "reducing" environment, where disulfide bonds cannot form (will soon be reduced to 2 cysteines) [I'm not putting a link as this is a fact in many biology textbooks].
The NAD+:NADH ratio is high in the cytoplasm (around 1000 (725 in this paper)), which should make the cytoplasm an oxidising environment. The NADP+:NADPH ratio is low, making a reducing environment. Also, there is Glutatione Reductase, which should also make the cytoplasm a reducing environment. Which one of these is the underlying cause of this reducing environment? Or is FAD also involved in this?
As an additional question, what does reduce disulfide bonds? Is it using the NADPH or the FADH2 or the glutathione reductase?

The redox buffer in the cytosol is glutathione (reduced GSH and oxidized GSSG), which is present in large amounts (López-Mirabal & Winther 2008 , doi: 10.1016/j.bbamcr.2007.10.013).
Proteins with disulfide bonds are often secreted, since the disulfide bond ensures proper structure outside of the cell. These proteins are imported into the endoplasmatic reticule (ER) that contains enzymes (e.g. PDI) and an oxidative milieu for disulfide bond formation. Thioredoxin breaks down disulfide bonds in the cytosol and is regenerated by TrxR, which in turn is regenerated by NADPH (Bulleid 2012, doi: 10.1101/cshperspect.a013219)


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How does exercising/starved muscle import glucose (released by liver)?
Adrenaline releases glucose from the liver during sport or if starved. This glucose goes to the blood through GLUT2 transporter. But how does it get transported into the muscle cells? GLUT4 is the glucose transporter into muscles, but it is activated (translocation to plasma membrane) by insulin, but when exercising/starved, there is no insulin. So is the glucose transported through some other transporter?

GLUT4 is the major glucose transporter in muscle even in exercise. However, during exercise, it is translocated to the cell surface by contraction-triggered, insulin-independent mechanisms, such as AMP-activated protein kinase (AMPK) activation.
For more, you could read this review.
Note:
'No insulin' is too strong a phrase; exercise and fasting are associated with low but detectable insulin levels. The reference range for fasting insulin in healthy individuals is $<174 \ \text{pmol L}^{-1}$ (contrast this with levels upto $1917 \ \text{pmol L}^{-1}$ one hour after glucose ingestion). Exercise studies have shown levels around $60-80 \ \text{pmol L}^{-1}$.

A nice concise answer, and a most useful reference. However you might comment on the poster’s statement that “there is no insulin”. The concentration of insulin may be decreased, but surely not to zero. Do you know any figures?

@David I edited the answer.

A valuable contribution to the site. Hope to see more posts from you.


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How to derive Hill equation (one specific part)
There is just one specific step in the derivation of the Hill equation for haemoglobin which I can't understand.
Step from: $Y = \frac{(p\ce{O2})^n}{K_d + (p\ce{O2})^n}$
To: $Y = \frac{(p\ce{O2})^n}{(K_d)^n + (p\ce{O2})^n}$
I don't understand where $(K_d)^n$ comes from. (I can go from this second equation to the Y/(1-Y) equation afterwards).

How I derived my equation is the following.
$\ce{Hb.(O2)_n <=> Hb + nO2}$
Hence the dissociation constant $K_d$ should be:
$K_d = \frac{[\ce{Hb}][\ce{O2}]^n}{[\ce{Hb.(O2)_n}]}$
And Y, which is the fractional $\ce{O2}$ saturation would be:
$Y = \frac{[\ce{Hb.(O2)_n}]}{[\ce{Hb.(O2)_n}] + [\ce{Hb}]}$
If you multiply the top and bottom by $K_d$, the following is obtained:
$Y = \frac{(p\ce{O2})^n}{K_d + (p\ce{O2})^n}$
This is where I became stuck. What am I doing wrong?
Thank you very much for your answer.

In your second step $(K_d)^n$ should be $(K_A)^n$.
Where:

$K_d$ is the apparent dissociation constant and
$K_{A}$ is the ligand concentration that results in half occupation

See for example the relevant wikipedia article.

@user1136 Apparent because the association/dissociation reaction is not a single step kinetics.


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Why is sugar absorbed very fast into the blood stream?
Recently, I heard from a pregnant person I know that immediately after she eats something sugary/sweet, the baby starts kicking and moving around, as if reacting to the sugar. She told me (unscientifically) that sugar gets absorbed fast into the bloodstream (and then into the baby), faster than protein for example, which takes a couple of hours to be digested.
However, I know that both sugar and protein must go through the digestive system until the small intestine to be absorbed into the blood. This is done through mechanical action (peristalsis), as well as chemical digestion. Yet I was wondering how there is such a big time difference between the digestion of sugars versus proteins if the path to the bloodstream is the same.
I did a little bit of research and found that there are some glucose transporters in the cheeks, which could explain how glucose is absorbed so fast (in the same way alcohol is also absorbed fast through the cheeks too).
I wanted to ask if theres any other reason or way in which sugar is given so fast to the foetus when ingested by the mother?

In short, sugars are absorbed quicker than proteins and fats because they pass through the stomach quicker and their digestion is simpler.
Sugar can be absorbed through the mouth mucosa when applied as a sublingual gel, as discussed here on Biology SE: Is sugar absorbed into the bloodstream through the walls of the mouth?, but probably in much smaller amounts during usual eating/drinking followed by swallowing.
SUGARS
Not all sugars are absorbed at the same rate.
Glucose and galactose do not need to be digested and can be quickly absorbed in the small intestine via sodium–glucose linked transporters (SGLTs) - sodium acts as a cofactor that stimulates glucose and galactose absorption (Lumen Learning).
Fructose also does not need to be digested but is absorbed much slower than glucose via GLUT5 transporters without the help of sodium (Lumen Learning).
Sucrose needs to be digested in the small intestine with the help of the enzyme sucrase to glucose and fructose, which are then absorbed. Glucose stimulates the absorption of fructose (Food and Agriculture Organization). This means that glucose and fructose from sucrose will be absorbed slower than glucose alone, but faster than just fructose alone.
Lactose needs to be digested to glucose and galactose, which prolongs the time in which they can be absorbed.
The absorption rate of various sugars is reflected in their glycemic index (the rise of blood glucose levels after ingestion): GI for glucose = 100, sucrose = 65, lactose = 46, fructose = 19.
STARCH
Starch is not digested in the stomach, so it can pass through it quickly, and is then, in the small intestine, quickly digested to glucose with the help of the enzyme amylase. The glucose from plain starch is absorbed almost as quickly as when ingested as glucose alone and faster than fructose, sucrose or lactose. This is evident from high glycemic index of foods made mainly of plain starch: cornflakes (81), instant oats (79), potatoes (78), rice porridge (78), white wheat bread (75).
FIBER
Foods high in dietary fiber slow down gastric emptying and thus absorption of nutrients (Faseb).
PROTEINS
Proteins need to be digested in the stomach by the enzyme pepsin (which slows down gastric emptying) and then further in the small intestine by peptidases into amino acids, which can be absorbed. Slow gastric emptying is the main reason for slow absorption of proteins (Diabetes Care, Experimental Physiology).
FATS
Fats are not digested in the stomach but they slow down gastric emptying, so they are absorbed slower than carbohydrates (JCEM, Vivo Colostate).
LIQUID vs SOLID MEALS
Liquid meals pass through the stomach quicker than the solid ones, so glucose from sweetened beverages will be absorbed quicker than from whole fruits (Vivo Colostate, JCEM).


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How do enzymes not change the overall energy change of the reaction they're catalysing if they lower the activation energy?
Based on the Induced-Fit model of enzyme action, enzymes catalyse a reaction by lowering the activation energy of a single forward reaction over and over. But I read that enzymes don't change the overall energy change of the reaction $(\Delta H_{solution})$ they just speed up the reaction.
How can enzymes reduce the activation energy of every forward reaction but still not affect the $\Delta H$? $\Delta H$ is sometimes called change in heat because it is measured in Joules and it's either endothermic or exothermic (this bit is chemistry).
I'm a highschool student and I'm just trying to find out how the required activation energy doesn't affect the energy change for the whole reaction.

Welcome to SE Biology. Please finish the [Tour] and learn how to ask questions here. One of the first things to do is to search for previous postings of the same or related questions of which there are many on the topic. You are incorrect in your recall of what you read. It is the Gibbs Free Energy of a reaction, ΔG, that enzymes do not affect. This is definitely not the same as ΔH:  ΔG = ΔH − TΔS. So your question is invalid as it stands. I would advise you to read (this section of Berg et al.) [https://www.ncbi.nlm.nih.gov/books/NBK22584/] which addresses this topic.

I’m voting to close this question because it is based on incorrect premises.

You're on a valley on one side of a mountain (representing some fairly stable state of your reactants), and you'd like to go to a town on the other side at a lower elevation (representing another stable state for your products, at lower energy than your current state: this is an energetically favorable reaction).
You can go over the mountain: high activation energy to climb up to the top, then you go down the slope to eventually get down to the town.
You can go through a pass between mountains instead: much lower activation energy to get over the pass, then you eventually get down to the town.
Whichever path you choose, you're at the same elevation (energy, $\Delta H$ compared to where you started), with the same products (your location in space), but if you took the pass you've gotten there via a different chemical route that was easier to achieve energetically at the peak.
Enzymes let you take the path through the pass rather than over the top of the mountain. They don't change where you started from or where you're going, so they don't change the overall energy of the reaction.


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How does a product form from a transition state in an enzyme despite the weak interactions being at its optimal
In the book Lehninger Principles of Biochemistry, there is a metal stick analogy to explain why an enzyme being compliment to its substrate would actually make a terrible enzyme.

If the enzyme is complimentary to the substrate, it will form many weak interactions, hence the enzyme-substrate (ES) complex is very stable, meaning it will require more energy to reach the transition state, so very few products are made

If the enzyme isn't entirely compliment to its substrate, it will form a few weak interactions (that allows it to bind to its substrate). This isn't its lowest energy state, as there are still more weak interactions that can occur. The weak interactions will mould the substrate into its transition state. This would mean that the transition state is the most stable state in this environment (I would assume). The thing that I am confused about is that if the transition state would be the most stable state, then why would it go on to form a product? Once the weak interactions mould the substrate, then energy would be released from the substrate, forming a transition state, therefore making the transition state have lower energy than the substrate, not higher, so the reaction profile in the final diagram doesn't really make sense to me. Is there anything that I am missing or not understanding?

I would really appreciate someone clearing up any confusion about this. Thanks.

I'd recommend starting from the diagrams here, since it seems like you understand them. Compare the 2nd and 3rd plots, and use them to explain to yourself why an enzyme that works like the 3rd plot is drawn is better than the 2nd in both the ES and transition states. Then reread the text and think about it as a comparison between those two diagrams rather than the imaginary other case you're thinking of.

I think I've got it now. The energy required to reach the transition state is lower because of 2 things:
-The ES complex is less stable in diagram 3 then diagram 2 (higher energy)
-Once the ES complex has formed, there are still more weak interactions that can occur which provide some energetic driving force towards the transition state, so require less energy to reach there.
Is this right?

That sounds accurate to me! I think it's worth keeping in mind that the "transition state" is energetically not very favorable: it's at the top of all of these charts. So, when describing "weak interactions (that) mould the substrate into its transition state", you're making the transition state more favorable than it would be without those interactions, not necessarily more favorable than a different, favorable state. If you have to jump over a rope, and someone else puts their hand on it to make it lower to the ground, there's still a rope to get over.


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How are testosterone levels distributed among men and women?
Wikipedia tells me that men have 7 to 8 time higher levels of testosterone than women, on average.
Since the hormone is linked with performance in certain athletic events, my hypothesis, which I presented to a disagreeing friend, is that female top athletes in certain fields will have levels above the average male.
I found Why do endocrine profiles in elite athletes differ between sports? (Clinical Diabetes and Endocrinology 2018) which in Figure 10 presented testosterone levels for men and women in a number of olympic athletes:

As you can see in the plot it seems that even in the cohort of olympians there is an overlap, even if small, between men and women. Am I misinterpreting these result? I noticed that the units (nmol/L) are different from those used on Wikipedia (ng/dL), is this somehow important?
So:

Are there information about the distribution of testosterone levels among the general population to help answer the question of the share of women exceeding the average male level?
Am I interpreting the above results correct, are there indeed female olympians with higher testosterone levels than male olympians?

(The mapping between numbers and sport)

Power Lifting (18 M and 1 W)
Basketball (27 M and 14 W)
Football (Soccer; 37 M)
Swimming (100 M and 91 W)
Marathon (1 W)
Canoeing (7 M and 1 W)
Rowing (36 M and 25 W)
Cross Country Skiing (8 m and 9 W)
Alpine Skiing (11 M and 12 W)
Weight Lifting (10 M and 7 W)
Judo (26 M)
Bandy (19 M)
Ice Hockey (38 M)
Handball (23 M and 29 W)
Track and Field (95 M and 49 W)

Did you generate these plots yourself? If not it's good to cite the source. Anyway, if you have the data you can perform a statistical test to see if the differences are significant. Did you try any? Try Mann-Whitney test or student t-test and then you can conclude if the overlap you see is indeed significant.

@WYSIWYG: I attributed the sources, but perhaps not clearly enough (see paragraph before the plot). Thank you for your suggestion, but I think it would be better done with a larger dataset of the general population, this is only for olympic level athletes.

Did the authors of the paper discuss the possibility that some of the athletes  misused testosterone for doping and thus the results might not reflect the "natural" testosterone levels?

As you can clearly see from the data, some women athletes have higher testosterone levels compared to some men even in the same sport. However, this does not negate the statement that a random (or average) female athlete is unlikely to have higher testosterone than a random (or average) male athlete (you can perform a statistical test to check).

To the first question we can look at a paper such as "Estimating age-specific trends in circulating testosterone and sex hormone-binding globulin in males and females across the lifespan" from Handelsman et al.  The figures they provide are:

The top image is of females, the bottom of males.  We can see throughout a lifetime that the top 2.5% of females and bottom 2.5% of males seem to have approximately the same amounts of testosterone.  If we went to the top and bottom 1% there would likely be consistent overlap between the male and female distributions.
I believe you are interpreting the figures correct, although it is important to keep in mind these figures do not include any information on age and are a single point measurement.  To facts that may limit the depth of inference you can make about testosterone levels among the sexes.


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Do de-husked seeds germinate?
As simple as that, lentils beans and other legumes are sold both with and without husk, and often I make beans with the husk germinate in a jar.
Do those without husk germinate as well? Or are they simply dead?
I'm asking this because my girlfriend told me she's using de-husked legumes, but that they take longer and less of them actually do sprout.

De-husking and industrial storage reduces the germ's longevity quite a lot, although quite a lot of germs will still be viable if the humidity and microbial conditions are very stable, perhaps even a year.
De-husking will accelerate this graph:

The husk is designed to keep the germule in peak condition in the wild until whichever season it is supposed to germ, through droughts, rains, cold weather, changes in humidity, predation, infection.
If the germ is de-husked and left in natural conditions, it rapidly loses vitality and deteriorates. In storage it's kept in conditions made to discourage microbes, so it will last longer, but it will absorb ambient humidity changes and deteriorate much faster than with a husk.


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Is there any risk for oranges to lose vitamin C
My understanding is that vitamin C easily undergoes oxidation. But for that to happen, the vitamin C has to be in contact with oxygen, e.g. with air. Therefore an orange doesn't start losing its vitamin C content by just because it's picked from a tree. It keeps that vitamin up to the moment we make juice out of it, when it starts losing it simply because it is dispersed in the liquid which is in contact with air.
That's what I know.
But somebody today told me otherwise, claiming that it's the plant that continuously supplies the orange with vitamin C.
This idea looks a bit silly to me, but I'm not a biologist, so I'm asking.
Incidentally, where in the orange is vitamin C contained? In each individual cell? I was once told that the oranges' cells (well, those that we like to eat and that actually make the juice) are those little drop-shaped things that are contained in the wedges (in a number that I'd say it's several hundreds?). Is that the case?

Isn't that what the covering is for?

@AsekuVena, I've also read that the peel itself contains more vitamin C then the rest

Maybe it is like the colony bacteria, who have their outer bits protect  the inner bacteria ?


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How does PCR mutagenesis add restriction site near the gene of interest?
I have been learning about PCR mutagenesis to add restriction site right next to the gene of interest using a primer that's attached with single stranded restriction site (first image). I have drawn my own diagram (second image) to better understand how this works, but I am stuck at the last step in question mark. How does DNA Polymerase 'insert' the green sequence (restriction site) so I would end up with the gene shown in the bottom?
Thanks for anticipiated response.

[![enter image description here][3]][3]

This diagram would be easier for you to conceptualize if you instead used the actual nucleotides in the restriction sites and green GGAGAA region along with your gene of interest (GOI). I recommend working with the DNA sequences when learning about primer design for various applications. I believe it has led you to be slightly confused with what is the restriction site and what is not in this diagram so I'll walk through it.
At the first step shown, you have your annealing region of the forward and reverse primers binding to the GOI. The overhanging region on each primer contain your restriction sites, which are flanked by the GGAGAA region for these restriction enzymes to have a sequence to "grab on" when you perform a restriction enzyme digest. Note that the annealing region of your primer anneals to the GOI because it has homology to the DNA sequence. Your restriction sites and green "clamping" region do not have homology to your DNA template so they are considered the overhanging regions. It is important to have your annealing regions of both primers of similar annealing temperatures when designing this or you may not have an efficient PCR reaction. I typically use this tool from NEB to design annealing regions of my primers. https://tmcalculator.neb.com/#!/main
Moving forward, these primers are both going to be used in one PCR reaction, not separate. Thus, when the reaction begins, the double stranded DNA template will denature, giving your forward and reverse primers the opportunity to anneal during the annealing phase of a PCR reaction. During the elongation phase, your DNA Polymerase will add complementary nucleotides in the 3' direction of your primers. Now after the first cycle, you have two different products. The forward primer's product has the GOI with a single stranded BamHI overhang on the 5' end, while the reverse primer's product has the GOI with a single stranded NotI overhang on the 5' end.
During the second cycle, after denaturation, the reverse primer with a NotI overhang anneals to the forward primer's previous product with a BamHI overhang. The DNA polymerase then adds nucleotides in the 3' direction of the primer, eventually adding complementary bases to the BamHI overhang. The same is done vice versa with the forward primer and the reverse primer's previous product.
Now after the second cycle, you have the desired products which will be amplified exponentially. Your GOI flanked by NotI and BamHI restriction sites with the GGAGAA region on both sides. This product is ready for a restriction enzyme digest.

Thank you for your thorough explanation. So after every round of PCR, I would have a complementary strand in the overhang region, right? I found this image quite similar to your explanation, and want to check if it's a correct diagram I could refer to. https://ars.els-cdn.com/content/image/3-s2.0-B978012385544200003X-f03-02-9780123855442.jpg

I like your hand-drawn figure. I will do a pictorial explanation starting from that. You are correct in the primer binding and first stage of PCR step. But PCR1 and PCR2 and the final product is wrong.
This is the way you think about it - In each step the primers bind to products extended in the previous steps (+ original template DNA, which is miniscule in comparison after a few cycles). The tails of the primers, that don't bind to the original template DNA are incorporated during extension from the other primer.


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Why does histamine cause bronchoconstriction?
What purpose does histamine-caused constriction serve in lungs during allergies and such, since it's vasodilator in other parts of body. Wouldn't it be more practical to vasodilate lungs so that white blood cells can arrive and toxins can be flushed more quickly.  Thanks in advance

You can think of it as a mechanism of preventing more toxins from getting in. Also note that bronchoconstriction is different from vasoconstriction.

You should think about bronchoconstriction as the constriction of bronchi (airways), not lung arteries.

Basics first: Crash Course
We will be introducing:
Autonomic divisions, Histamine and Vasoactivity (or Broncho-)
Starring: Innervation of the Lower Respiratory Tract
Lower respiratory tract is mostly innervated by the parasympathetic division, it has only scarce sympathetic-receptors there.
So, why it matters?

Autonomic divisions serve as fight-or-flight and rest-and-digest mechanism for the body as to respond for sudden changes.
You are having a good picnic, your body is in a state of rest. Your body is absorbing nutrient and enjoying your day. Blood isn't needed so much on your hands, or skin, or muscle.
This is the Parasympathetic Division
Suddenly a snake appeared in front of you, you scream, you panicked, and you flight away (or fight?). Your eyes dilate (where is that snake!), your muscles work, your respiratory tract dilates, as to prepare to avoid being killed by the snake. Blood rushs in to your muscles, but shunts on your digestion part, as what every you eat doesn't matter.
This is the Sympathetic Division
What matters?

Parasympathetic division only knows how to lock down things.
Sympathetic division can lock things, open things, and so, and so, and so.

How does sympathetic division work with so many things?
It has different receptors which reacts differently on input
Imagine people when reacting to clown: NOOOO and YAYYY
Histamine serves as modulation to outputs of autonomic division, directly or indirectly
Histamine is a broad-response chemical used to respond against an infection. As different cells have different ratio of autonomic division, it can cause dilation or constriction on different places.
One thing to note that, in a nutshell, histamine serves to buffer the work of autonomic innervation. It is entirely up to the regular function of the "autonomics" there to do their business.
Vasoactivity (or Broncho-) is achieved by state of balance between innervation by the autonomic division and local signals
Local signals play a part. A balance of signal determines the effect of innervation.
For bronchi, when histamine puddles, local signal sends stronger input than global innervation. Hence, the parasympathetic takes over.

histamine-caused constriction serve in lungs during allergies

Histamine serves as to protect the lower respiratory tract from inhaled irritants. The lower respiratory tract is innervated by parasympathetic stimulation. Parasympathetic stimulation only knows one command: constrict and strike.
When histamine buffs up the signal, it constricts.

vasodilator in other parts of body

Indeed it is. The vasodilation effect is achieved by GPCR-mediated sympathetic innervation.
Histamine buffs a diverse response of sympathetic division, hence dilates the blood vessels.

Wouldn't it be more practical to vasodilate lungs so that white blood cells can arrive and toxins can be flushed more quickly

In line with WYSIGYG, vasodilation is different from bronchodilation (or constriction). We have noted above that the operators are different, and they serve different functions.
As a note, white blood cells can't just come anywhere they want. Ever seen your nasal mucus being very viscous? That will happen your lung when white blood cells arrive.
White blood cells also cause fibrillation, which succumbs people when does.
It has been a reason why pneumonia and lung-infection related diseases, tend to succumb people by drowning them in "their own mucus".
Another part of sending much things down your lower respiratory part is...
How could you clean the mess up?
The upper respiratory part is the defense capable of trapping irritants by mucus and send the mucus to your stomach.
Bronchus? Not so much. More mucus will eventually drown your lungs.

I invested 50 minutes for this.


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Do nerves work as I think they work and what does that mean for our senses?
Let me start off with a couple of metaphors.
In the third Lord of the Rings film, a signal for help is sent from Minas Tirith to Gondor, using a chain of beacons. When the keepers of one of these beacons sees that the one next to his lit, his orders are to light his own thus passing on the chain reaction. When the last one within sight of Gondor is lit, the message that Minas Tirith wants help is received.
There is nothing conveyed in the fire itself, no information within the flames, the beacons are either on or off. The only reason the beacons convey a message is that the citizens of Gondor know why that beacon would be lit.
Imagine a simple pressure sensor inside a building that is connected by a wire to an electric light on a control panel in a security room. When someone steps on the sensor it completes the circuit which sends electricity straight to the light turning it on. A label on the light says what it's connected to and where it is. So that when the light comes on, the person at the control panel knows someone is in that sector of the building.
But to be more precise, he knows someone has activated that particular pressure sensor, if it wasn't labelled he would have no idea what the message meant.
My understanding of the human nervous system is that it works in the same way. Based on information I learned from children's educational programs as a child and a few bits I picked up since.
Our ears have sensors designed to respond to sound. Each and every one has a direct connection to the brain via a chain of nerve cells. When one of the sensors is sufficiently stimulated, it zaps the neuron it's connected to, this in turn causes the neuron to zap the next one and so on all the way up to the brain.
The impulses/spikes themselves contain no actual information, they are just pure electricity, every spike contains the same amount of voltage. The only reason the brain is able to interpret them is because it knows exactly where each and every chain is connected to. When the impulse reaches the brain it knows it comes from a sensor in the ear that is responsible for a particular level of sound, the brain takes these signals and translates them into the sounds we hear. Nerve cells work something like binary, they are either on or off with nothing in between. The frequency of the spikes going along the chain indicates how intense the sound is. If the brain didn't know where that chain was connected to then the signal could mean absolutely anything.
This is supported by the condition known as synaesthesia where, because "wires are corssed" in the brain there are people who hear colour or taste music.
My questions are, is my reasoning correct? Is this exactly how nerves and perception work? Has this been scientifically proven beyond a doubt? Is there something within the impulses that contains additional information? Are the workings of the nervous system debated in scientific circles? I've been told we've never been able to plug an eyeball or any other kind of human sensory device into a computer so we've never been able to examine it as it's working, is this true?
But most of all, does this mean there are things our senses cannot detect?
I already know there are things beyond our range of vision and hearing and the brain blurrs then together. What I mean is this...
I know that we have different senses in our ears that are designed to respond to higher or lower sounds. Say we have a sensor that responds to a level 1 sound (I don't know the unit of measurement for sound) and next to it is a sensor that responds to a level 2 sound. What happens if we try to hear a 1.5 sound? Is it not detected by the ear because we don't have sensors in that range?
Can we only sense something if we have a sensor for it and are those sensors only built to sense one ultra specific thing?

I'll attempt an answer, but please know you don't have a clear nor defining question to address. This is more suited for conversation or open discussion, and I recommend starting a chat on the topic. Please be wary the question may be put on hold. I'll give it a go and respond from the top down. I absolutely don't think this is going to be fruitful for other people. Here goes:

Our ears have sensors designed to respond to sound. Each and every one
  has a direct connection to the brain via a chain of nerve cells. When
  one of the sensors is sufficiently stimulated, it zaps the neuron it's
  connected to, this in turn causes the neuron to zap the next one and
  so on all the way up to the brain.

Take the example of the eye; the retina is composed of photosensitive neurons, a type of sensory neuron. The inner nose is innervated with olfactory sensory neurons. The cochlea is similarly innervated by neurons. Firstly, you haven't made it clear that the neurons are the sensors. But indeed, the sensory neuron is the first order neuron. The processing of sensory information proceeds through first, second, third and higher order neurons until the information is integrated functionally somewhere in the brain. There exist neurons that modulate the signal along the way (e.g. lateral inhibitory interneurons) that are not on the information highway but rather beside it, regulating the input and output of neurons. It's quite complex, but you have the general gist of the hierarchy of neurons from sensory input (e.g. odor) to output (behavior, response, perception).

The impulses/spikes themselves contain no actual information [...]
  Nerve cells work something like binary, they are either on or off with
  nothing in between.

The exact temporal dynamics of this communication highway between neurons is very important. At some level, auditory volume may be coded by frequency, but this is restricted only to some level. Information is very quickly encoded and the 'raw' information sensory neurons provides becomes processed and transformed quite early in the chain. For instance, you may trigger circuits responsible for reflexes, which are (so-to-speak) dormant until a kind of neural activity activates them. Vision is well described in terms of encoding; at the first processing area of the brain for vision, things are simple, and are progressively more high-levels of encoding as the information is processed; there are regions responsible for motion, color, object recognition, even specialized regions for the recognition of faces, for instance.

If the brain didn't know where that chain was connected to then the
  signal could mean absolutely anything.

Correct. Remember though that the brain is very plastic, and can learn. There are many curious cases in neuroscience where this is apparent. One well-known widely described example: you can wear glasses that invert the world, and this would feel strange. After some time though, your perception would switch the world the "right way up". The retina has been largely unaffected, but the perception and the integration of the information can drastically vary quite independently.

Is there something within the impulses that contains additional
  information?

Remember that there are two kinds of connections between two neurons. Electrical and chemical synapses. A wave of depolarization does indeed travel through a neuronal axis, but in most cases, this does not occur across neurons. Instead, neurons (and related cells such as glia) release chemical messengers (neurotransmitters and neuromodulators) that act as inter-cell signals. These can inhibit or excite the post-synaptic neuron. Simply put, it's not a string of wires; it's a line of wires that interface with each other chemically; at each interface, chemicals must diffuse across the gaps and interact with the membrane-bound sensors found on the receiving neuron. This is not at all binary. And please know we are simplifying the system in order to describe it.

Is this exactly how nerves and perception work?

This is a simplification of how neural circuits work. How perception works is a completely different thing you have not even begun to address. This is a completely different topic of discussion. Bonus link!

But most of all, does this mean there are things our senses cannot detect?

A sensory system can only detect what it can detect. Your skin cannot detect radio waves. Your eyes cannot detect infra-red light. Your mobile phone, similarly equipped with sensors, cannot detect neutrinos.

I don't know the unit of measurement for sound

Decibel (volume) or hertz (pitch or frequency).

What happens if we try to hear a 1.5 sound? Is it not detected by the
  ear because we don't have sensors in that range?

You are describing the spectrum of volume as a graded, discontinuous thing. It's not! And more generally, yes. If your sensors cannot detect something, the organism is oblivious to it. Obvious.

Can we only sense something if we have a sensor for it [...]?

Yes. But you underestimate the power of a sensor such as a photosensitive cell. It can transmit information about the amplitude of the light, and responds to a range of light. Moreover, each photosensor has a response spectrum and does not respond equally to different (although similar) wavelengths of light. More so, if you have a patch of photosensitive cells, you can infer motion, direction, speed, size, distance, and all the merry things we associate with vision. The wealth of information is easy to underestimate.

... are those sensors only built to sense one ultra specific thing?

It depends on how you define specific. The equipment of a neuron in the retina is usually specific (e.g. expression of proteins responsible for light sensitivity) but it's possible to have a neuron that is responsive to several things. Have you ever tried to rub your eyes, and you see phosphenes? Your retina is responding to the increased pressure. You could say these cells are sensitive to light and pressure. That's not ultra specific. You can similarly activate these neurons at short range electrically, or magnetically. That's starting to sound like a pretty unspecific sensor, depending on how you define it for yourself.
I absolutely don't mean to aggravate, I very much suggest you do some readings on the topic. It's one thing to have a pub-level confidence in vaguely worded funfacts about sensory circuits, and another to understand and appreciate the nuances and complexity and the many knowns and unknowns of neuroscience. It's not too difficult to grasp. I would instead ask you to ask about fundamentals before you ask to correct your outlook on biological sensory systems. Books are cheap and the internet comes in handy sometimes, and you may even spare someone else's time!