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Does the cranial dura consist of the periosteum? and if not, then is there a mistake in my textbook?
My textbook (Neuroanatomy an illustrated colour text) states that:

The spinal dura and much of the cranial dura are separate from the periosteum, which forms the inner lining of the surrounding bones.

However, as far as I am aware the cranial dura has two layers, one of which is the outer periosteal layer or the periosteum, so I'm not sure why this is mentioned separate to the cranial dura.
The textbook later states that:

At certain locations, however, such as on the floor of the cranial cavity, the dura and periosteum are fused and the cranial dura is tightly adherent to the interior surface of the skull.

This would make sense if they were referring to the pericranium, but the first quote suggests that the textbook is referring to the outer periosteal layer (or the inner periosteum).
Please could you shed some light on this. Thank you.

First about the terms:

The outer side of the cranial bones is covered by a single layer of  periosteum that is specifically called pericranium.
The inner side of the cranial bones is covered by dura mater that has 2 layers:

the periosteal (or sometimes called endosteal) layer that is attached to the inner side of the bones
the meningeal layer that covers the periosteal layer and, at places, folds into the skull to make extensions

Image 1: Dura mater with its periosteal and meningeal layer (source: Idris Siddiqui, SlideShare)

Image 2: Extensions of the meningeal dura mater (falx cerebri, falx cerebelli, tentorium cerebelli) (source: Wikipedia, CC license)
The cranial dura mater has the periosteal and meningeal layer, but the spinal dura mater has only a meningeal layer, which encloses the spinal cord. Vertebra have no additional periosteal layer. The periosteal layer of the dura mater that covers the cranial bones does not extend to the spinal canal:

The periosteal or endosteal layer of dura mater is simply a layer of
  periosteum that covers the inner surface of the skull. The layer does
  not extend beyond the foramen magnum to become contiguous with the
  dura mater of the spinal cord. The spinal cord dura mater has no
  periosteal layer.
The meningeal layer of dura mater is a durable, dense fibrous membrane
  which passes through the foramen magnum and is continuous with the
  dura mater of the spinal cord. (V. Kekere, Dura mater, StatPearls)

Both quotes from the book mentioned in the question suggest that the periosteum and dura are two separate things: periosteum being a part of the bone (as elsewhere in the skeleton) and dura consisting of a single layer. The other  explanation, which I presented here, is that the periosteum on the inner side of the skull is a part of the dura (its periosteal layer) that has another layer (the meningeal layer). So, they are two ways how you can look at the structure of dura mater, and I believe, the second one is more widely accepted.


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Why is it so important to avoid infection of lacerations to the scalp?
There is supposedly something unique with regards to infections of the scalp, although I cannot remember, perhaps it was to do with the CSF and its build up? I have scoured the internet for hours but have not found an answer.

Sounds more like a question for SE Medical Sciences or whatever it is called.

No, there is noting unique to scalp lacerations (I've repaired literally hundreds of them) except that they bleed a lot more than the usual laceration. Probably because of that, there's a very low rate of scalp laceration infection. CSF is inside the cranium, not in any contact with the scalp.

@anongoodnurse i have found an answer to this question. It is to do with deep lacerations of the scalp specifically though.

The deepest lacerations of the scalp go through the galea and exposes the skull. No lacerations of the skull make contact with the CSF.

Deep lacerations of the scalp that penetrate the fourth layer (area of loose connective tissue) have an increased risk of infection. This is because pus and blood spread easily within it. This can easily pass into the cranial cavity along the emissary veins Therefore, infection can spread from the scalp to the meninges and could lead to meningitis.

Sources for this?

This does not sound right to me. Deep lacerations - the deepest go through the galea - are far from uncommon, and while they are less common than the average skull laceration, I've seen and treated very many. I've never seen an infected scalp wound. Again, scalp wounds are less likely to get infected than other wounds due to very high vascularity. (https://www.ncbi.nlm.nih.gov/books/NBK541038/) While I think this answer is theoretically possible, I assume - as I have never seen it - that it is rare (not that I haven't seen rare things...)

Sorry for the very late reply, but this was answered by my anatomy professor on a worksheet we had to do. Now that you have mentioned the galea, I will email him to ask whether this was a more theoretical question simply for students to see conenction between scalp layers, or if it has clinical relevance, and I'll post an update soon.

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Why can only small molecules pass through the phospholipid bilayer of the cell membrane?
TO put simply: I am just wondering what mechanism or substance only enables small molecules to pass through the cell membrane. Is it cholesterol? My textbooks are not very clear.

The plasma membrane consists of a phospholipid bilayer which separates the internal environment of the cell from the external environment. It regulates the movement of substances in and out of the cell and helps keep a constantly regulated internal environment of the cell.
The plasma membrane consists of a phospholipid bilayer, which, as the name suggests, is made up of phospholipids(lipids that have a phosphate group attached to them.).
The phospholipid has two regions a hydrophilic (water-loving / has an affinity for polar molecules) and hydrophobic (water-hating / has an affinity for nonpolar molecules).

So what happens is these molecules come together and arrange themselves in such a way that it faces the least amount of repulsions. Hence, the fatty acid tails (Hydrophobic part) face inside and the polar part(Hydrophilic part) face the outside, to look something like this.

Now, what happens is that when a molecule has to enter the cell it first has to interact with the polar part of the lipid membrane and then with the inner non-polar part of the membrane to pass through, hence if it is a polar molecule it will face repulsions and will not be able to pass through without the assistance of transmembrane proteins (it doesn't matter whether it is small or large, it simply won't), but, in the case of non-polar molecules, there is no repulsion from the fatty acid part of the phospholipids and hence it can pass through the membrane. When the non-polar molecules are too big some other mechanisms may be utilized (like receptor-mediated endocytosis).
With regard to your doubt regarding the "mechanism" with which a molecule passes through the membrane, in the simplest case, it will simply slip in between the phospholipids and through the bilayer. But, this is, as I said the simplest case, there may be transmembrane proteins which create channels for diffusion (aquaporin is a good example), or as I mentioned earlier they may be taken into the cell by endocytosis, through pumps like the Na-K pump etc.
And also cholesterol acts like a buffer to ensure that the spacing between the individual phospholipids is maintained so that it stays fluid (i.e. to maintain optimum rigidity of the membrane).
This is what an actual membrane looks like in an actual cell:

Hope you got a general idea.
You can refer to Chapter 11 of Molecular Biology of the Cell (by Bruce Alberts et al) if you want a  more rigorous explanation.

Although aquaporins transfer most of the water, simple osmosis can occur with water due to the osmotic pressure and it is very small size.

True. I just wanted to give an example and that was the first thing that came up in my mind. Water is very small molecule and the lipid bilayer is not perfectly impermeable to water i.e. some amount of the water does get in. Once it is in the hydrophobic region, water has to go in as it will face repulsions, leading to the entry of water into the cell

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In the induced fit model for enzyme action, does the enzyme active site change slightly after products form?
The reason why I am asking is because I am looking at a past paper and they highlight that it does. I have attached it below. Could you explain why this is the case.

I am just looking for a quick overview of why this is the case.

I understand now that they are highlighting how during the transition state the enzyme was induced to change shape, but once products formed and left active site, there was further changing of shape of the enzyme active site so it could return back to its original shape - therefore it could be reused again, as in line with the role of an enzyme/ catalyst.

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Can the heart generate its own rhythm independent to the SAN?
My textbook and a revision guide, which I believe is a reinterpretation of the textbook, state that:

The SAN initiates waves of excitation that usually override the myogenic action of the cardiac muscle.
  From the textbook

The revision guide is more direct in its interpretation of the textbook:

The heart muscle is myogenic, which means that it can generates its own rhythm. However, this rhythm is overriden by the sinoatrial node (SAN).

I wonder whether the textbook was interpreted incorrectly, or if in fact the heart can contract independent to the SAN?

Your textbook and review guide are correct, but the missing details may be a little confusing. Yes, the heart has the property of automaticity, meaning action potentials fire on their own at a certain rate, without input from the nervous system. Yes, the SA node typically controls the overall rhythm of the heart because it overrides the rhythm of the rest of the heart.  However, not all cardiac muscle cells have automaticity. Cells in the SA node, the AV node, and to a certain extent, the conducting system all exhibit a physiologic automaticity, that is, they have ion channels that carry what is called a pacemaker current (or sometimes "funny current"), that slowly depolarizes their membranes after each action potential. When this slow depolarization reaches the threshold voltage, another action potential fires. The SA node drives the rate of the heart because an action potential reaches these other automaticity centers, or latent pacemakers, before they would fire on their own. Normal, non-conducting atrial and ventricular myocytes do not exhibit a pacemaker current (except in certain pathological situations), so do not contract independently. So, while the heart muscle is, as your textbook describes it, "myogenic", normal cardiac myocytes (in an intact organ) are not.
This becomes important in cases where the SA node is unable to generate an action potential, is suppressed (is generating an action potential at a slower rate), or other cells with a pacemaker current have increased their rate of firing. In these cases, you can experience an escape beat (a single action potential from a latent pacemaker propagates through the conducting system to cause a heart beat), or an escape rhythm (a series of escape beats).
These are general textbook level principles. You can refer to the wikipedia entry linked above. They are discussed, perhaps more authoritatively, in Lilly's pathophysiology of heart disease. Chapter 1, under electrophysiology, discusses the general principles of automaticity, pacemakers, and latent pacemakers. Chapter 11, under native and latent pacemakers, alterations in sinus node automaticity, and escape rhythms, goes into more detail about the circumstances in which latent pacemakers drive the heart.


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How long would you expect a designed plasmid to remain in a population of E. coli after transformation?
When transforming E. coli with a genetically-modified plasmid, how quickly/often is this plasmid "lost" because of mutation, or horizontal-transfer, or "dilution" over reproduction over several generations?
How often are inserted plasmids lost/mutated/diluted in E. coli? How long would you expect to observe the plasmids' output after transformation?

It depends on a number of variables, like the plasmid you're using, the strain of E. coli, and the culture conditions. Most expression vectors require some sort of antibiotic selection for maintenance. I've been able to cure high-copy-number plasmid vectors in a single overnight culture without selection.

There isn't a simple answer.
There are a lot of factors which can influence how stable a plasmid will be. I'll describe what the main factors are, but to work out exactly how stable your plasmid is, unfortunately you'll just have to test it. I've given links to some studies which do this at the end.
Copy number
Copy number refers to how many copies of your plasmid are present in each cell. This can range from 1-10 for low copy number plasmids, to 300-500 for high copy number plasmids. Generally, low copy number plasmids can be lost easier than high copy number plasmids as there is a higher chance that the plasmid won't be present in one of cells after division. (https://www.nature.com/articles/s41598-017-05219-x)
Plasmid Size
Very large plasmids (in the mega base range) tend to be less stable than smaller plasmids as organisms, especially E. coli, can struggle to replicate them. This means that over time, less of the plasmid will be present in your system. (https://pubs.acs.org/doi/10.1021/acssynbio.0c00008)
Selection marker
Typically, synthetic plasmids will have a selection marker encoded which is used to provide selective pressure for keeping the plasmid. The exact marker used can affect the stability of the plasmid, as some are more effective than others. This paper has a good comparison of two different markers and measures the stability of plasmids for each: https://bmcbiotechnol.biomedcentral.com/articles/10.1186/1472-6750-8-61.
Burden
Plasmids normally contain an insert which encodes your system. Some inserts will have relatively low burden on the cell (for example low expression of a small protein). Others may involve high expression of many proteins, or proteins which are toxic to the cell. Mutations are much more likely in high burden plasmids compared to low burden plasmids. This is because cells containing plasmids with mutations which reduce/stop expression will have a much higher fitness advantage over those cells with unmutated plasmids. Other time, these mutated plasmids will become dominant and eventually you will lose your original plasmid. There's some good reading about cell burden here (https://2019.igem.org/Team:Austin_UTexas/Measurement) and here (https://pubmed.ncbi.nlm.nih.gov/25849635/).
This is anecdotal, but I've managed to run 24 hour experiments with plasmids about 5kb in size containing a low burden insert and without using any selection marker without seeing plasmid loss. I've also had trouble even cloning plasmids of about the same size but with antibiotic selection and a high burden insert without any mutations occurring. So it really does depend on what your plasmid is and what it's expressing.
Measuring plasmid stability
Here are some examples for how you can measure plasmid stability:

https://link.springer.com/protocol/10.1007/978-1-4939-9877-7_16
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3966108/ - This paper describes plasmid stability mathematically
https://academic.oup.com/femsle/article/232/1/45/490969


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Techniques to find out which species are endangered
Most countries have a list of endangered species and international organisations too issue such lists of vulnerable and endangered species.
What mathematical or statistical models are those estimates based on?
Regardless of which techniques the lists use, what are some of the most popular mathematical models to find out whether a certain species is endangered or vulnerable given the population and/or other environmental data in the academic literature? What is the state of the art currently?
Especially, if I want to learn the models at an intermediate and then advanced level (I already have training as an Economics student on mathematical and econometric modelling), what are some books/ other sources you would recommend?

Based on the IUCN Criteria for endangered status there are two broad categories of models to help in determining endangered status. Note that no one methodology is used to determine the status of any species. Rather, a panel of experts consider all available evidence (including numerous modelling studies) and essentially make a determination based on their own judgement.

Range Estimates
Estimating the range of a species uses two primary techniques. The first is an expert range maps drawn by people very familiar with the species distribution, which involves essentially no modelling. The 2nd is ecological niche modelling, aka. species distribution modelling. See 1 and 2 for introductions on the latter. Note that the IUCN guidelines have criteria based on total range size, and well as the amount of fragmentation and patchiness of the range.

Population Size Estimates
Since it is usually impossible to count all individuals of a species, models are used to estimate total populations. These usually fall in the realm of mark-recapture models. There are numerous variations on the basic model form which account for things like an open population, varying birth and death rates, and varying capture probabilities.

1: Elith, Jane, and John R. Leathwick. "Species distribution models: ecological explanation and prediction across space and time." Annual review of ecology, evolution, and systematics 40 (2009): 677-697. https://doi.org/10.1146/annurev.ecolsys.110308.120159
2: Araújo, Miguel B., et al. "Standards for distribution models in biodiversity assessments." Science Advances 5.1 (2019): https://doi.org/10.1126/sciadv.aat4858.

Thanks a lot for your answer, it was really insightful! If it's not an inconvenience, I also wanted to know if panel data on the population estimates are or can be used to predict when would a species likely go extinct in a region. I have heard of predator-prey models in game theory, but have no idea if or how any such forecasting is done empirically. Also if any other techniques are used for forecasting

Wikipedia has an article on the IUCN Red List Categories, There are some formulae there that show how the category is determined.
For example:
https://en.m.wikipedia.org/wiki/Endangered_species_(IUCN_status)


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Research on chicken that cannot feel pain
In was having a conversation about the ethics of vegetarianism, and if it is right to cause pain to other animals.
It is then that I stumbled upon the question, that if, just the way chicken and many other animals have currently been cultured or genetically modified (or by any other means) to have certain desirable qualities (from market and demand perspective) such as the fat content, quality of eggs etc., will it be fine to consume chicken if we also, if possible, raise chicken that do not feel any pain at all (if that is defined, or can we define that?).
I realise that this is not philosophy stackexchange, so I would not ask about the ethics of it.
What I want to ask here is this: is such research taking place (anywhere on earth) to develop breeds of chicken that do not feel pain, if yes I would be thankful to know at least the basics, and if not, do you think it is possible in the near future or what possible approach would you contemplate?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). In particular, you might want to look at the NIH page on congenital insensitivity to pain and consider the effect a similar condition would have on chickens. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

Inability to feel pain seems likely to make an animal accident-prone.

I used to raise chickens (among lots of other animals.) Chicks peck at anything that stands out, they can't help it. They don't do it to be cruel. If another chick didn't get out of the way when pecked, it would get a bloody or bald spot on it, which would attract more pecks, and further injury, etc. Eventually these chicks die of infection. I've seen it happen a lot to a particular kind of chick (called broilers) bred to grow quickly to market size. Unfortunately, they were also dumber than a box of rocks, and didn't get out of the way. Since I didn't debeak chicks...

...the broilers had more than a 50% mortality rate when raised with normal chicks. It was heartbreaking, and I had to isolate the broiler chicks, and never had the heart to eat them though they grew to be very large. They were also very docile, so easy prey for foxes, coyotes, etc. But my point in all this is... pain matters a lot to survival. I doubt a chick without pain would have much chance to survive to adulthood.


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What terrestrial trait makes cetaceans so successful in an aquatic lifestyle?
Intuitively, I would expect that an organism that has lived in the ocean for millions of years and can breathe underwater should outcompete any newcomer that is not fully adapted for oceanic life. It makes sense that there may be some semiaquatic animals that can outcompete fish in semiaquatic niches, such as seals, crocodiles, and diving birds. And I could see there being short-term instances of odd species that manage to colonize an isolated area that happens to lack competition.
But dolphins and whales are extremely successful across the globe, have been around for millions of years, and a large part of their niche overlaps with the much older and also hugely successful sharks, yet they manage just fine. A common explanation of this is "intelligence" but sharks are now known to be pretty intelligent, and even if they weren't, why wouldn't they be?
This isn't the first time this has happened, either.  Aquatic reptiles like ichthyosaurs, plesiosaurs, and mosasaurs, and even modern sea turtles, represent hugely prolific and long-lasting groups of air-breathing, fully-aquatic animals (sea turtles come on land to lay eggs, but this seems more like a flaw than an advantage), suggesting that there is something in particular about land-dwelling that gives animals returning to the sea a natural advantage not found in their piscine counterparts.
Is there anything specific about evolving on land - some particular trait that doesn't generally evolve in aquatic animals - that cetaceans retained after returning to the sea, and that makes them particularly successful in the aquatic lifestyle?

Do sharks show evidence of great social intelligence?

@ARogueAnt. It's not as well studied as cetaceans, but numerous studies suggest the answer is yes https://www.wired.com/2016/11/two-way-radios-reveal-mysterious-social-lives-sharks/ https://www.smithsonianmag.com/science-nature/forget-jaws-now-its-brains-48249580/ https://www.sciencedaily.com/releases/2016/10/161004224218.htm

@ARogueAnt. At any rate, it wouldn't answer the question - if you would say "their intelligence or social behavior," the question simply becomes "why are air-breathers more likely to be intelligent or social than water-breathers".

I'd consider https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont both on its own and as a partial answer to those questions ("why are air-breathers more likely to be intelligent or social than water-breathers") as well as in conjunction with the answer by timeskull. Natural selection operates on variability that exists; not every possible trait is expressed in a way that can be selected for in every lineage.

You seem to missing the effect of phylogeny. Cetaceans are mammals — their advantages don't necessarily have a direct connection to them having terrestrial ancestors, but instead are likely to be because they are mammals. Please also note that what makes aquatic reptiles successful may have nothing to do with cetaceans, so I would avoid lumping them together in one question.

Thermoregulation and echolocation both depend on evolutions that occurred on land and seem to be less accessible to fish than to the ancestors of mammals. The heat capacity of water is much greater than air, so maintaining an elevated temperature in body tissues is both more difficult and less necessary. Still, some fish lineages have independently evolved partial thermoregulation. From the article Warm eyes provide superior vision in swordfishes:

In these animals, warming the central nervous system and the eyes is the one common feature of this energetically costly adaptation. In the swordfish (Xiphias gladius), a highly specialized heating system located in an extraocular muscle specifically warms the eyes and brain up to 10 degrees C-15 degrees C above ambient water temperatures.

Depending on diving depth, temporal resolution can be more than ten times greater in these fishes than in fishes with eyes at the same temperature as the surrounding water. The enhanced temporal resolution allowed by heated eyes provides warm-blooded and highly visual oceanic predators, such as swordfishes, tunas, and sharks, with a crucial advantage over their agile, cold-blooded prey.

Echolocation in mammals is possible due to the mammalian ear, which is summarized in a previous answer. From Ultrasonic hearing and echolocation in the earliest toothed whales:

The advent of echolocation is thought to be a key innovation that supported exploitation of a vast pelagic biomass—vertically migrating organisms, especially cephalopods—and explosive diversification of odontocetes

We are starting a Bioacoustics Stack Exchange for people interested in the studies of non-human animal sounds and the impacts of sounds on animals. Please join us! https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=YjZmYjUxYzJkNDI1YmY5NDk3NzdhMzViMmZlNzI4ZDdiYTAyMWQxNTM5ZWFiNzRhODNkMmFiMzIxZjI3MmY1N_gFvrICTvBsmYNJ2ptRM6lIZEAV-VGkXtIwNyVDja680

Advantages of air breathing over gills? Keeping in mind water-breathing animals could still evolve lungs.
Not being vulnerable to parasites and diseases of the gills, which are obliged to have blood supply close to the water.
Able to colonise water regardless of salinity, able to survive warm water.

Should I answer if I don’t “have citations from a reputable source”?

Air is 20% oxygen. Water at best is 0.01% oxygen. That is a lot more energy to ventilate gills than lungs (ram ventilation still costs energy in the form of extra drag). Also, you can't burn a fire underwater: body heat gets lost in the gills, and the only way large fish keep warm is counter-current heat exchangers and it still isn't as good as lungs.
But unless you are forced to breath air (life on land) evolution isn't innovative enough to develop lungs on it's own.


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In Genetic Engineering, why are we limited to existing creatures when it comes to creating a new species?
So, I don't know much about Biology. Haven't studied it since high school. So please excuse me if my science isn't proper. I'll do my best.
Let's say for example you wanted to make a fire breathing Komodo dragon. Well, from what I understand, it's quite impossible to do because there are no creatures that breathe fire. So you wouldn't be able to gather the needed DNA information for breathing fire.
However, if you wanted to give a Komodo dragon wings, well this would be possible, because there are many winged creatures in this world, so the genetic information you need is available.
What I don't understand is, why couldn't you create or manifest this genetic information artificially in a lab? What stops us from doing that? Say for example, fire breathing?
I'm not particularly interested in the utility behind fire breathing dragons. I'm just using it as an example for my question. Any other features could be added in it's place.

Obligatory not a biologist, I studied physics.
In a very basic way, and ignoring the limits of carbon chemistry, it's all a question of understanding.
If you imagine DNA, and genetics as a whole akin to a language, we're currently barely able to read it, let alone write.
We know the letters of the genetic alphabet, at this point (Adenine, Thymine, Guanine and Cytosine, along with Uracil for RNA), and we're starting understand how to make a few words (genes), but we're still quite a ways away from mastery of the genetic language.
Part of the problem is that some traits have simple mechanisms that go from gene to expression, like how skin colour is largely based on the amount of melatonin in your skin-cells, and how eye colour largely hinges on one or two genes. However, many things are not that simple, from things like autism to adult height, to cancer, most parts of an animal don't hinge on a single gene. This also means that, in your example, we're nowhere close to making a komodo dragon grow wings.
To summarize, we've only barely figured out the genetic alphabet, along with a couple words, but we're nowhere near being able to write whole sentences, nor make up words from scratch.

Be careful when talking about stuff that you obviously don't know. Especially pigmentation and its regulation is a complicated field, although in the end the amount and ratio of the melanin (not melatonin!) is what makes the difference. Getting there is another story.


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Combining MAOIs with Stimulants
Is it dangerous to combine MAOIs with stimulants? According to wikpedia, Parnate, for example, "leads to an increase in the availability of monoamines, such as serotonin, norepinephrine, and dopamine, as well as a marked increase in the availability of trace amines, such as tryptamine, octopamine, and phenethylamine." A stimulant like Vyvanse, for example releases dopamine but doesn't act significantly on serotonin. So would combining the two be dangerous?

This question is closed, but I want to comment for the sake of future readers: yes, this may be dangerous. MAOs are one (of several) ways the body has to remove monoamines. If you simoultaneously increase the availability of monoamines and decrease one of its elimination pathways there may be an excess of monoamines, which may be dangerous.


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Is downregulation of neurological receptors fully reversible, i.e. complete upregulation and resensitization?
Are down/upregulation truly reciprocal mechanisms? After a binding ligand or agonist is removed, such as a prescription medication, is upregulation and resensitization able to occur to a level that exactly equates to and completely reverse and fully make up for any loss of receptors, bonding affinity, etc? Could anything theoretically be permanent? Does time/length of prescription play any role in this, including when prescribed a benzodiazepine (Clonazepam)?


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How to estimate MOI for a complex cell type
I am currently confused about the estimation of multiplicity of infection (MOI), here is an example in a scientific article
in figure 3b, they tested the virus, and get estimated MOI based on this:

To estimate the MOI, we isolated a total of 45 individual neurons from three animals injected with MAPseq virus into the right LC and sequenced the barcodes within each neuron. On average, infected LC neurons contained 1.2 ± 0.1 barcodes each, implying MOI of 0.43 (Figure 3B).

I am confused which equation they used for estimating?
Thanks in advance!

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The new DNA study showing that we have two DNA codes and not only one unique code
I am looking for a study that i read maybe 2-3 years ago that i cant find at the moment.
Scientist has always believed that humans only have one unique DNA code that makes us who we are, but a couple of years ago scientist found that we actually have two DNA codes, something that the scientists called mysterious and that this changed what we always have belived regarding humans uniqe DNA code that makes us who we are, now this was not true anymore with this new finding, since we have two codes which means that who we are could be more complex and not only be information stored in one DNA code. I cant find this study when i look for it on google, do you know which study i am speaking of? i would like to find it again, so that i can see if there is any updates by the scientists, and i also think it is extremely interesting and don't want it to get lost, i forgot to save it in favorites before.

This is not about epigenetics is it? Defenitely know for longer than 2-3 years but otherwise might fit what you're looking for.

Perhaps you are referring to so-called "duons" (dual-use codons) discovered by Stergachis et al.. This paper was published a bit more than six years ago. A recent paper within the last 2-3 years references duons implicated in photosynthesis.
Duons essentially extend the idea that conserved coding DNA encodes proteins, but can in fact also preferentially encode sites which bind transcription factors, at the same time. DNA can code proteins as well as code that controls regulatory regions, which in turn are switches that control how proteins get made.
Disclaimer: I am a contributing author in the linked Science paper.

Thanks but thats not it, im talking about a whole new DNA code beside our orgiginal discovered DNA code. The author speaks about our individual traits not necessarily being defined by our original DNA code and the whole thing being mysterious.

I'm lost. But I hope you find the answer you're looking for.


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Large study showing that attraction to only the same sex has to do with your genes, published where?
Can someone please help me out and find and link me the study from a couple of years ago that showed how only same sex attraction, when the male cant become attracted to a woman, it has to do with genes?, it was a large study and a first of its kind, maybe from 2016-2019, i am not talking about the big study from 2018 by Andrea Ganna about not finding any single gene that explains sexual orientation.

Is it this? https://www.nature.com/articles/s41598-017-15736-4

@AlexReynolds That seems more like an answer than a comment.

No thats not the one. They said that it was the largest study of its kind, and i think they might have mention DNA besides the word genes also but i am not sure, i know it was a very big studie that looked at genes/DNA in a new way. It seems like not many places wrote about it and then the other study by Andrea Ganna came and everybody wrote about that so its hard to find it now i have looked a long time.

Have you looked at the references section in the Ganna study? If this is as large a study as you say, it may well be referenced there, and the date range may help you drill down to what you're after.

Nope its not there, i think the both studies where done very close in time and thats why. Only the Ganna study got any real news.

I'd suggest scanning the reference sections of as many related papers as you can. You have a known time window to limit your search to some reasonable possibilities.

Possibly https://science.sciencemag.org/content/365/6456/eaat7693.long is what you were looking for?  It implicates a few specific genes - the connection to olfaction is interesting (I would suggest it could be fun to look up the vomeronasal organ, terminal nerve, and GnRH).  [Alex Reynolds' suggestion of https://www.nature.com/articles/s41598-017-15736-4 is highly useful for those reading, even if it wasn't what you were looking for.  https://www.sciencedirect.com/science/article/pii/S0091302219300585?via%3Dihub is also potentially useful]


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About how many covid-19 virus particles is required in the human body before infection and sickness follows?
Our immune systems are often able to destroy germs and virus particles.
About how many of them does it take to make a 70 year old healthy male sick ? Any ideas ?

To the best of my knowledge, we don't yet know the infectious dose of the SAR-COV-2 virus in humans. In theory, it only takes one viulent virus particle to start an infection. In practice, it's pretty hard to measure, Published estimates of infectious dose for any pathogen don't often account for differences in age or sex, per se, so it's hard to address that part of your question.
Most of the estimates of SARS-CoV-2 infectious dose I've seen are essentially experts handwaving based on previous coronavirus outbreaks. I'm not saying they're useless, but they aren't necessarily empirical. For reference, there's a perspective article here, with a section discussing infectious dose. They cite an estimate from the 2003 SARS outbreak of 280 particles to cause infection in 50% of the exposed population (ID50). They also point out that this is similar to the ID50 for other animal corona viruses and the common cold in humans.
There's no guarantee that SARS-CoV-2 will be the same, but it's likely to be in the same ballpark.
Referenced:
Imke Schröder, J Chem Health Saf. 2020 May 11 : acs.chas.0c00035. Accessed via PubMed Central, PMCID: PMC7216769

Good research article MikeyC .


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How can I make legal mature female Cannabis plants to Flower in home during March (springtime)?
In December 2019 I purchased 4 Cannabis seeds Legally in Canada.Two of my plants are now about 100 cm tall. I am using wide-spectrum LED grow lights and have fertilized them both. I started with 16 hours light per day and now have cut back to about 12 hours per day.I was told that these seeds were not auto-flowering.These seeds were from Tweed and were labeled "Baker Street Indica". The leaves are all healthy and dark green. Now I would like to stimulate flowering. As our days are getting longer I want to trick the plants into its Fall/Autumn flowering cycle. Any good ideas ?

This question should be asked at [gardening.se].

I'm voting to close this question as off-topic because it is about gardening rather than biology. It may be on-topic at gardening.stackexchange.com but please check their guidelines before re-posting there.

Keep the plants in dark night for 12 h , 13h then 14h per night.
Keep the plants well fertilized with lower N , higher P and K.
Keep well watered with a dry period in between watering.
Keep the plants protected until the plants are ready to flower.


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Species that murder their own counterparts when put in captivity
Mary Midgley writes in her book, Beast and Man (p. 54 in this eBook: https://goo.gl/3NnhtP):

Lorenz gives chilling examples from roe deer and doves, in both of which species stronger members will slowly murder weaker ones if kept in captivity with them[...]

I find this fascinating but I was not successful in finding any more info on this phenomena on the internet.
Can any biologists point me into a good direction? I do not have the work of Konrad Lorenz at hand, and would not know where to exactly look for in them.
Thanks a lot!

Some individuals kill their own offspring (https://en.wikipedia.org/wiki/Infanticide) or eat their offspring (https://en.wikipedia.org/wiki/Filial_cannibalism) or their own siblings (https://en.wikipedia.org/wiki/Siblicide).  See this article about siblicide and fratricide in bacteria:  https://www.webmedcentral.com/article_view/4804.
Other conflict and killing between members of a population occurs in many species, including humans (https://en.wikipedia.org/wiki/Homicide), mice (https://sci-hub.tw/10.1111/j.1469-185X.1991.tb01147.x), and other primates (https://www.sciencedirect.com/science/article/pii/S0140175082920632).
Search "intraspecific killing" on Google or Google Scholar.
See also a similar question here:  Why social animals attack odd members of their own group?


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Why is the macromolecular composition of a human cell seemingly hard to find?
I am trying to find a 3D rendering or list of molecules by volume in a cell (originally I was searching for human, but I'll take any at this point!). I understand the open-endedness of the question: what type of cell? During which phase? Under what conditions? etc.
What I am looking for, if such a thing exists, is as accurate-as-can-be list of structures/particles/macromolecules/ions/etc by volume in the protoplasm.
"Inside a living cell" by DS Goodsell is a step in the right direction but nearly 20 years old at this point.
"Diffusion, Crowding & Protein Stability in a Dynamic Molecular Model of the Bacterial Cytoplasm" is another step in the right direction.
Anything related to this query would be appreciated!
Thanks for your help!

For some components, you can find it here: http://bionumbers.hms.harvard.edu

Your title and question seem to be different. Your title would be off-topic as it is not about biology per se, but as it seems to be a concern I shall comment on it. The reason, I would think, is that modern biology — especially cellular and molecular biology — is not about classification. It is about understanding how things work. So why would any modern biologist do such a thing? Presumably you have a reason for wanting such a list, but I can't imagine why you would want the comparative volumes of all proteins, for example, even if this were known. Perhaps you could explain.

The various data related to dimensions and volumes of structures\organelles\macromolecules and cells themselves could be obtained from BioNumbers. For example, please see in the table below the information on volumes of COS-7 (monkey kidney tissue):

The details can be got at Applying systems-level spectral imaging and analysis to reveal the organelle interactome, by Valm A.M. et al


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How do you keep track of past/new lab protocols?
Does there exist a list grouped my subject (e.g. 'microscopy') for keeping track of what protocols have been designed and used?
Closest I could find is http://www.protocol-online.org/ but it's fairly sparse and out of date.
Any recommendations/tips and tricks? Thanks!

The best match to what you're looking for is probably https://www.protocols.io/, which hosts protocols for free and generates a digital object identifier (DOI). It is not indexed by PubMed or other similar engines, however.
Some journals permit methods papers, but not a high proportion (and it sounds like you're looking for a place to find them, not to send them).

Looks interesting – I had in mind that someone would have built a crawler for finding method papers and indexed them, but perhaps not.


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Can the face bones be "compressed" or forced together? What would happen?
Say someone doesn't like that their maxilla bone is too long because the height of the maxilla affects the placement, position and angle of the mandible relatively.
If one were to apply mechanical force from the mandible underneath the hand (pushing up) while countering the force either with the neck and/or pulling the head forward and down for prolonged periods of time, steadily and consistently, will the maxilla literally move upwards?

Simply put, as I understand it, bones remodeled due to consistent mechanical tension and stress placed on them lifelong as part of osteoblastic/osteoclastic activity and bone metabolism. My question is, assuming my line of thinking here is right, would the maxilla actually move upwards and the mandible will rotate too? How far up can it go before it would affect facial structure in a negative and/or potentially dangerous way, and how long would this take to do if done 1-2 hours per day, 7 days a week with about 1-4 lbs. of consistent, balanced and equalized force?

What's with the premaxilla? What do you think will happen to your teeth? And with you sinuses? And your nasals? 1-2 hours a day won't help anything... This won't act like plastic surgery...

Time under tension has to make some physical changes given enough duration. Doubting that would be doubting the science surrounding bone re-absorption and Wolff's Law.

Yes, there will be some effects... But not the ones you are looking for.. Or are you looking for terrible tooth ache and a missing occlusion? I don't doubt the effects... I work with biomechanics. There's something called the phenomenon of the blind billard player... He only sees the cue ball but isn't aware of the effects on the other balls when he hits the cue ball with the billard cue.

Please don't encourage this kind of question. This is a personal medical question, common among people who frequent incel forums.

It's a serious question and not personal/medical. What does its relation to incel forums have to do with anything? It's a fairly legitimate question about bones/biology/biomechanics/etc.

Bones are remodelled,it's correct but there is a limit too in this remodelling and specially when are doing it manually. Moreover it is very important  to keep your jaws in proper occlusion otherwise this improper way of pressuring and tension creation in your maxilla and mandible will lead to more severe problems in your temperomandibular joint, leading you further to the cranial disorders. Such activities on a daily basis are quite harmful and these definitely don't work like plastic surgery. So, it's better not to perform these or it may lead you to become a regular patient to your dentist. If you are really willing to have such changes then you should consult a cosmetic surgeon.

I get your point, but this is more of a "what will happen" kind of question. Cosmetic surgeons charge money -- this experiment is 100% free so there's an advantage there.

For whom? The dentist?


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Killing more attractive mates -- intersexual selection strategy?
Is this the affinity or core part of intersexual selection (males fighting for access to females)?
If females are bound to flock to objectively more attractive man 'A' in the majority of cases, would killing him put odds in your favor? It's all relative, no? If a guy is better looking than you and you kill him, he's obviously no longer better looking and alive -- so he can't reproduce. If you killed every better looking man than yourself, wouldn't you become the next best looking man? Sounds about right.
But is this not the core reasons for mating? Kill off all the good looking men and then you're hottest.
Since no guy alive can be more attractive than you, you have sex with all of the women. Not crazy.....?
I mean in theory of course..... we know what makes men sexier -- jaws, cheekbones, eye shape, height, size/muscles, symmetry, facial width to height ratio, skin complexion/coloring/etc. So yeah....

I suspect this question hasn't been downvoted because it suggests murder as a strategy, but because it's not well formulated as a question. What exactly are you asking with "So yeah..."?

It's not a form of intersexual selection; it's an intrasexual selection strategy.

This is why there are fights between males for dominance (and having access to females) in many species. Humans have survived all these years through cooperation. So, no, its a bad idea.

If a guy is better looking than you and you kill him, he's obviously
  no longer better looking and alive -- so he can't reproduce.

Animals can't go around shiving each other.  This less attractive bird or whatever probably can't kill a healthy member of its species without a brutal fight.  They might both end up dead.
Have you thought about what happens to the population numbers as the "kill my rivals" gene becomes more common widespread?
Anyway, we already have plenty of species where one male keeps a harem of females.  And yes, they do get attacked by others seeking to take over their mates.

The obvious flaw in this (as applied to humans) is that once the more attractive males discover that you are killing them off, they are likely to gang up and kill you instead.  Futher details likely could be found on the Law site :-)
This would seem to have a serious flaw as a general strategy, too.  Sexual attractiveness would seem to correlate with general fitness, so that if you try to kill that more attractive male (without the sneaky means of killing that technology provides), there is a good chance that he'll wind up killing you instead.


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Territorial behavior in humans?
Do humans exhibit territorial behavior like other primates? I have seen people sometimes stare at others -- notably males -- and then physical fights spontaneously turn up. Is this territorial? It seems it either goes two ways: One person looks at another; the other looks back and either looks away or both look away; or they both hold a stare until one or both erupt in to physical blows and try to dominate the other or fight/assault them. Is this a display of human territorial behavior? I know some chicks do it too.
I've also read that in males more so that staring can be an "alpha" or "dominating" gesture to others -- especially if a stare is held at one in response to them either turning away or provoking a fight.
This can be seen in every area, but possibly more so in clubs, bars, or certain social settings.

What you're describing is not territoriality, but dominance/aggression.

From encyclopedia britannica

Territorial behaviour, in zoology, the methods by which an animal, or group of animals, protects its territory from incursions by others of its species.

Following, this definition, yes territorial behaviour exists in humans. Here are three simple examples drawn from different (western) cultures

You seem to be confusing territorial behaviour with general, aggressive behaviour. Whether or not the behaviours you describe qualify as territorial behaviour requires one to make a psychological study to determine whether the individuals had a notion of territory that they wish to defend.

I'd argue that territoriality can be observed on many scales with humans. At the bar, 1-on-1 conversations with a spouse, between homes, between cultures, between parties during war, nations, the list goes on. It is also peculiar that humans seem to extend territoriality into abstract spaces, such as thoughts and ideologies.
I once read the 2010 book Supernormal Stimuli: How Primal Urges Overran Their Evolutionary Purpose by Deirdre Barrett which argues, details and very elegantly describes our instinctual, territorial tendencies in modern humans. I do not doubt that humans today follow instincts we evolved for our time spent in the African savannahs. The book explains other vestigial instincts too, which evolved and now exist in an artificial environment.
Take a look: https://en.wikipedia.org/wiki/Supernormal_Stimuli


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How to characterize stability of a protein from Trp fluorescence vs [denaturant] curves?
A colleague of mine has taken Trp fluorescence measurements from a dimer in combination with various ligands, over a range of denaturant concentrations.
The idea is that ligands which bind more tightly to the dimer will stabilize it and delay changes in fluorescence. This is what our data look like:

Total fluorescence decreases, probably due to quenching from the denaturant. Papers I've seen using this method show it's possible to calculate the fraction of denatured protein by analyzing displacement in peak emission wavelength. However, they use monomeric proteins with few Trp, whereas I have a dimer with several Trp plus some additional variability introduced by the different ligands.
Additionally, we have data from a scintillation proximity assay that indicates ligand affinity is ordered as 1<...<5 and 6<...<11. Ideally, we would like to replicate this same ordering through the analysis conducted on the data above. I would appreciate any suggestions of methods that will allow us to carry out such comparisons.

Papers I've seen using this method show it's possible to calculate the fraction of denatured protein by analyzing displacement in peak emission wavelength.

Have you tried doing that with your data? What do you get if you plot peak emission wavelength as a function of denaturing agent concentration? If these look like sigmoidal curves (you might need a log scale on the X axis) with a clear upper plateau, then you can apply the method mentioned by these papers because the signal you observe is correlated to the fraction of denatured protein and saturates (this part is important: the signal must saturate past a certain concentration of denaturing agent, because all protein molecules are fully denatured and therefore adding more denaturing agent won't give further signal change; if your signal doesn't saturate, something is wrong).

However, they use monomeric proteins with few Trp, whereas I have a dimer with several Trp

Oligomeric state and number of Trp residues should not matter, because peak emission wavelength is only correlated to the fraction of denatured protein. Total intensity will increase with more Trp residues, but you're not using intensity as a measure of the fraction of denatured protein (and if anything, it's good to have more intensity to begin with given the quenching effect you observe with increasing denaturing agent concentration).

plus some additional variability introduced by the different ligands.

To take care of this concern, you need two controls that:

prove that none of the ligands alters the fluorescence of your protein,
prove that none of the ligands emits fluorescence between 300 and 450 nm, or if they do then you need to measure it to be able to subtract it from your total spectra, in order to recover the protein contribution to the total fluorescence.

For 1, record fluorescence emission spectra of the protein without denaturing agent but as a function of ligand concentration (span a few orders of magnitude) and see if the peak emission wavelength changes with ligand binding (it might change, which means the same assay can yield binding curves and Kd values for your ligands, which could also be useful!). Full ligand titration curves would be the most robust control, but you can simply use the same ligand concentrations as used in the denaturation experiments.
For 2, the simplest case would be that your ligands are not fluorescent, but you cannot simply assume that. Therefore, an important control you also need is to record emission spectra for each of your ligands at the concentrations used in the denaturation experiments, and this at each concentration of denaturing agent (or simply at 0 and max concentration: if there's no difference between these two spectra, you don't need to record one at every concentration in between). If the ligands emit fluorescence between 300 and 450 nm, you need to subtract that from your total spectra to recover the fluorescence arising from the protein only.


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Creating ideal conditions for life
Suppose some scientists built a large vat, sterilised it and filled it with distilled water. Then they start dissolving compounds into the water such as amino acids or what ever they deem conducive to life. They can also control temperature, radiation and other environmental factors.
They periodically capture a sample of the water and examine the results.
Would they be able to inadvertently create self replicating molecules and the precursors to life?
Would this kind of experiment be worth attempting?

There are groups attempting this. Check out this (paywalled) paper from 2010 that tries to see if life could form from such a primordial soup on a simulation of Titan. Plenty of others too!

Suppose some scientists built a large vat, sterilised it and filled it with distilled water. Then they start dissolving compounds into the water such as amino acids or what ever they deem conducive to life. They can also control temperature, radiation and other environmental factors.

Your direct question is whether this experiment would be worth attempting, and as other answers have said, it has been attempted many times.
I'll address the question implied in the title "Creating ideal conditions for life".
You talk of dissolving compounds into water and controlling temperature, radiation "and other environmental factors"; I assume you mean this to imply all the possible variables are being manipulated, but that is not the case. "Being in a large vat" is also an environmental factor, and there is good reason to think that large vats don't provide ideal conditions to develop life at all.
If that sounds silly, consider all the chemical reactions that could be happening in your vat. Chemical reactions are typically reversible: molecules A and B can meet and interact and form molecules C and D, and molecules C and D can in turn meet and interact and form molecules A and B. In a large vat, nothing is preventing all those molecules from meeting and interacting with each other; this leads to an equilibrium, depending on the rates of both reactions, and you'll end up with a stable quantity of A, B, C and D.
Now imagine instead you have two vats, with a system between them that transfers molecule C from vat 1 to vat 2. Now molecules A and B continue meeting and forming molecules C and D, but as that happens C gets transferred from vat 1 to 2, so you get a buildup of molecule D in vat 1 while A and B gradually run out because they keep forming C and D but not being reformed in turn, while in vat 2 you have a surplus of molecule C, so any molecule D that is formed from the interaction of A and B is likely to meet a C to re-form A and B, meaning you'll end up with more molecules A, B and C and very little D.
In other words, you got very different results from the case where everything was in a single vat. The macroscopic and microscopic environment your molecules are reacting in is a variable you cannot ignore.
As for large vats not being conducive to developing life, this 2010 article by Nick Lane, John Allen and William Martin summarizes those issues with the "large vat" experiments, and the "primordial soup" hypothesis in general:
https://onlinelibrary.wiley.com/doi/abs/10.1002/bies.200900131
(full article downloadable here: http://nick-lane.net/publications/luca-make-living-chemiosmosis-origin-life/)

Setting aside the absence of geochemical evidence that a primordial soup ever existed, there are grave difficulties with the soup theory. To give a single example, polymerisation into RNA requires both energy and high concentrations of ribonucleotides. There is no obvious source of energy in a primordial soup. Ionizing UV radiation inherently destroys as much as it creates. If UV was the primordial source of energy, why does no life today synthesise ATP from UV radiation? Worse, every time an RNA molecule replicates itself, the nucleotide concentration falls, unless nucleotides are replenished at an equal rate. UV radiation is an unlikely energy source for rapid polymerisation and replication, and an unpromising initiator of natural selection.
The reason that nucleotides and other organic molecules are reluctant to react further in a soup is that they are at thermodynamic equilibrium. They have already reacted, and the homogeneous soup has no internal free energy that would allow them to react further. Life is not just about replication; it is also a coupling of chemical reactions – exergonic ones that release energy and endergonic ones that utilise it, preventing the dissipation of energy as heat.

That article was in 2010, and those people have been investigating the hypothesis that life began in hydrothermal vents under specific thermodynamic conditions since; Nick Lane recently published the book The Vital Question on the subject, that I highly recommend to anyone interested in how life might have begun.
Their hypothesis for how life formed also implies very different kinds of experiments to try and reproduce it. Putting chemicals in a large vat is one thing, trying to recreate the conditions of a hydrothermal vent is another.
Here is a video of Nick Lane presenting their research; at 30:15 he briefly talks about where they're at experimentally, with a picture of their setup.
https://www.youtube.com/watch?v=PhPrirmk8F4
ETA: Stealing John's comment here:
Creating ideal conditions for life
The experiments described in the article that yielded RNA are also more complex than just dumping molecules in a vat, and the cycles of heating and evaporation described are the kind of energy input and mechanisms to force disequilibrium that can make it thermodynamically possible for those molecules to form. This highlights another variable that can matter, which is variations in the environment over time as well as over space.

That question was asked in 1953 by a classic experiment by Miller and his mentor Urey. You can find it on Wikipedia under "Miller_Urey_experiment"
Basically they zapped basic molecular building blocks to life with electricity and more complex molecules (amino acids) formed.
The experiment, with updates is nicely discussed here.
The experiment showed that the molecules required for life could be formed spontaneously on Earth from lightning. You would need amino acids, but also bipolar lipids, which can spontaneously form compartments. However, attempting to create life this way would not be worth attempting for two reasons, relating to time and scale. First (time), life has evolved only one time on Earth over 4 billion years. Second the scale of the entire Earth over billions of years is a pretty big experimental "test tube". It happened once in all this time, over all that space. A small side-issue; the fact that the codon table is optimized (and pretty universal, with only small differences), such that common amino acids have more ways to make them (more codons), and codons close to stop codons are for rare amino acids. This indicates that some early life experimented with alternative suboptimal codes that didn't make it.

Earlier description in Goethe’s Faust: “Es wird ein Mensch gemacht”. Publication lacks experimental details though.

A much more modern and updated version of the experiment can be found here, https://www.wired.com/2009/05/ribonucleotides/ got all the way to RNA. After all codons are meaningless without nucleic acids.


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Are there regularly spaced connections between caudate nucleus and putamen?
There are a number of images on the Web, most beautifully Visible Body's artwork, which show the caudate nucleus and putamen linked by regularly spaced connections across the barrier of the internal capsule.  Since vertebrate forebrains are treated as having only a few segments (see Michael Carstens, 2017), which seem tough to relate to the C-shape of deep cerebral structures, there is something about such figures that piques curiosity.  In a paper like Heide Hörtnagl et al., 2020 the situation seems less clear to me, but they weren't really focusing on this issue.  Is there a regular/regulated spacing between the connecting bundles, and does it correlate with any other observable anatomical regularity?

"vertebrate forebrains are treated as having only a few segments" - I think you may be overextrapolating from early developmental models (especially those making cross-species/evolutionary comparisons). In any event, that structure wouldn't have any relationship to the pattern I think you're asking about.

These seem to be referred to in literature as "transcapsular" or "caudolenticular" (gray) bridges. My initial thought was that the picture you shared is just some weird artistic rendering but upon seeing histological slides these are quite prominent and familiar to me as part of the basic "look" of these structures in histology. You can see them in any coronal slice through this area, this atlas, "Cross-Sectional Atlas of the Human Head" by JS Park has them labeled though often they are not labeled.

(left image from JS Park; annotations on the right image are mine. There are many more "bridges" than I've drawn but I highlighted the most prominent to compare on the left side. Probably those deeper in the section relative to the camera are showing up a bit faint or blurred. This is also just one histological section, the bridges are found throughout the length of the area where caudate and putamen are located, at least a couple cm)
There may be other terminology, as well, but I'm having trouble finding it.
I see no reason or foundation on which to connect these to any sort of segmentation of the developing vertebrate forebrain. Since resources are sparse it seems difficult to find a reference, but my thought is that this is just an emergent pattern you get as different fiber pathways cross one another, like how your fingers look when you fold your hands together.
Some other references:
Mendoza, J. E., & Foundas, A. L. (2008). The Basal Ganglia. In Clinical Neuroanatomy: A Neurobehavioral Approach (pp. 153-193). Springer, New York, NY.
Nieuwenhuys, R., Voogd, J., & Van Huijzen, C. (2008). Brain slices. The Human Central Nervous System, 137-173.

Thank you for a great answer!  Though perhaps I should have asked a better question...  I don't have ready access to these resources - can you tell from the sections you see whether the number and positioning of the bridges is consistent between individuals, as you'd expect from a regulated structure, or does the number and position vary more randomly as you'd expect from something emergent but unregulated?  Thanks again.

@MikeSerfas In the limited experience I have with anatomy of individual human brains (albeit focused on cortex) I have to say I'm amazed by just how much variability there is. I can't see these structures as having consistent structure but don't have a source to prove that either, only a strong suspicion that if they did have a regulated structure it would be remarkable and highly discussed. I would say though that the artist picture you show vastly underrepresents the number which may be why they appear so orderly.

@MikeSerfas I added a picture of one of the slides I referenced. I think you'll appreciate that they are quite diffuse and scattered, not nearly as orderly as that cartoon suggests, nor are they found in a plane like it appears there.

Oh!  I have seen those in images, but based on the artist's drawing I was expecting larger, rarer connections.  Now I see what you mean.

@MikeSerfas Yeah that was exactly my thought too - went from something I hadn't heard of to seeing a picture and realizing I recognized that from any coronal section of the the caudate I'm quite familiar with the look. I don't know for sure but I'm guessing it's that those fibers are unmyelinated/less myelinated than the rest of the fibers.

@Bryan Krause
Are these caudolenticular bridges not gray matter structures? So, they're not myelinated.

@Akila Not myelinated or at least less myelinated/lower total fat content than the white matter they interleave with.


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What terms or concepts are used to describe the morning metabolic phenomenon involving glucocorticoids, glucose, and blood pressure?
A recent conference report described using a vaccine-based strategy to blunt a surge of high blood pressure that occurs between 5 and 8 a.m.  Apparently most heart attacks and strokes occur during this period, which makes this of special importance.  Presumably this ties in with preceding work showing that ordinary blood pressure medication is more effective when taken in the evening.
When I read about the "dawn phenomenon" (reduced glucose tolerance in type II diabetics) it is often treated in isolation.  Because glucocorticoids are a factor in the dawn phenomenon, it makes sense they could be involved in raising blood pressure during the same period.
This makes me wonder how much more I have missed.  There seems to be something special about the morning period in metabolism, something deserving of some name as fundamental as "sleep".  Yet I don't have one to use, and I don't know why it evolved, how its timing is determined, what its advantage is, whether it correlates with worker productivity, whether early risers and late risers and night shift workers have this period at the same time and so on.  Medical labs typically open at 7:30 a.m. - do they reference the time in relation to any of these phenomena?
Thus the question: what terms or concepts would you suggest to help someone research and pull together existing knowledge about the metabolic changes that occur in the morning?

Hypoglicemia is a rather common condition - often pronounced in the morning, but also not uncommon in the late afternoon (hence snacking), and particularly common in small children: https://en.wikipedia.org/wiki/Hypoglycemia

Morning surge, Prewaking surge, Sleep-trough surge, Rising surge.
Example of article using the terms:
"Morning Surge in Blood Pressure and Cardiovascular Risk"
https://www.ahajournals.org/doi/full/10.1161/HYPERTENSIONAHA.110.157149
This one is interesting in that it lists other articles and the term they used for the period you are looking for.


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Why would pedophilia exist?
From an evolutionary perspective, why would anyone ever be sexually exited by small children who could not possibly have started puberty?
Is it a confusion between some combination of sexual and non-sexual systems?
Is it a evolutionary imperfection?
Or is Darwinian thinking not necessarily applicable to human behaviour?

There are a lot of societal influences in our behaviour and also there is a lot of room, in our complex society, for developing behaviour that are side-consequence of other behavioural features that have been selected. It does not mean that "Darwinian thinking" (whatever that means) is not applicable to human behaviour but only that seeing everything as a result of selection is very misleading (and Darwin never made this mistake, hence why the term "Darwinian thinking" is misleading), maybe esp. when it comes to human behaviour.

I can't imagine this is at all genetically linked, but rather a learned behavior or result of some traumatic experience in the person's own past.

My best guess is that it's probably beneficial in a certain context. This is pure conjecture, but if a child's parents died, the group would raise them, however they wouldn't get the benefit of having a parent to advocate for their interests. If a pedophile took a liking to such a kid though, the easy sexual access might cause the pedophile to have a reason to care about the kid's wellbeing, and the pedophil might for the kid's advancement in the tribe. So basically, one possibility is that pedophilia in a tribal setting creates a natural caste of orphan caretakers.

Additionally, humans use sex as a way to bind communities together, and as messed up as it is, child sexual abuse would have probably been a way to relieve stress and sexual frustration without burdening the group with the risk of another child being born, and would make the tribe's otherwise relatively useless children "useful."

I am guessing on this one, and there may be some good research on it, but I do know that there can be combinations of genes acting on different behaviors, such that if you have a certain combination of 5 genes, you are a nurturing parent (which would be selected for), but when you accumulate more of these tangentially related genes past some threshold, you end up with non-selected behavior. For example, for homosexuality, which has been shown to be genetically heritable, it may be that 5 genes in a suite make you super attractive to women (thus these genes stick around), while 10 genes combine to make you gay. (Note, I am NOT equating homosexuality with pedophilia in ANY sense. Homosexuality if a healthy normal trait for humans. I am just saying that this is a theory about how suites of genes can be individually selected for while some combination of them is non-selective. Similarly, heterozygous sickle-cell genotype produces resistance to malaria, which is adaptive enough to keep the gene around, which is non-adaptive in the homozygous condition.)
In answer to the other parts of your question, humans are absolutely subject to natural selection. Darwin was dead-on correct about virtually everything he said, to the point where it is frustrating for evolutionary biologists today to work in his shadow, because he pretty much got it all right in 1859. "Theory" is the strongest conclusion that science can ever come to, and people have been trying to tear down Darwin's theory for 160 years without being able to put a single dent in it.

Darwin didn't get heredity "wrong". It was not understood at the time by anybody but Medel. The fact that the theory fit Mendel PERFECTLY, even before it was understood (which was the point of the modern synthesis...look it up if you need to) is how science, when you get it right, is predictive.


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How deep could a human swim with SCUBA apparatus?
Using normal SCUBA apparatus and wet suit, how much pressure can the human body withstand? This is assuming that they descend as gradually as necessary for their body to make adjustments. What would be first symptoms that they experience as they descend? And if they descend to the deepest depth that they can reach without immediate permanent harm, how long can they spend at that depth before time related symptoms set in?

It's not a question that has a simple answer.  Do you mean diving with simple compressed air?  Then 130 ft/39 m is the accepted max for recreational divers.  With different air mixes, you can go much deeper.  The other problem is not going deep, though, it's coming back up.  Gas dissolves in the blood at high pressure, and if you come up too fast makes bubbles, AKA "the bends", which can be fatal.  All this and more can be found in the Wikipedia article ttps://en.wikipedia.org/wiki/Deep_diving or through a simple search.

As far as I can find the current world record for "scuba" diving is 1,090 ft 4.5 in set in 2014.
The previous record was 1,044 ft set in 2005 so (as with most human endurance & physical achievement records nowadays) we're most likely at the limit of the possible there.
Barring a few more feet (or even just inches) of course.
Howsoever, that's only normal scuba diving equipment
Deep diving using hydrox and trimix has reached depths of 1,644 ft (1977) & 1,752 ft (1988).
So the answer depends on if you're asking about with normal commercial scuba gear using bog standard compressed air or if you want to include breathing mixes etc to help alleviate the bends.


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What is a good approximate functional form for an equation relating plant growth to sunlight?
Question is in the title.  I've got daily measurements of daily mean shortwave radiation at the surface, and annual measurements of plant growth (some measure, be it height or biomass or something).
I want to fit a statistical model
$$
growth = f(light) + \epsilon
$$
Assume that all other conditions are near-optimal, for simplicity.  What is a good first-order approximation for how to specify $f$?
For example, could it be:

Average daily light over the growing season?
$$
growth = \beta_0 + \beta_1\bar{light} + \epsilon
$$
Average daily light for each month?
$$
growth = \beta_0 + \displaystyle\sum_{months}\beta_m\bar{light_m} + \epsilon
$$
Maybe it's quadratic?

$$
growth = \beta_0 + \beta_1\bar{light} + \beta_2\bar{light}^2 + \epsilon
$$
Obviously something so simplified will never be perfect, but what's a good rule-of-thumb that'd cover most situations reasonably well?

You need to write more about the specific system/plant species you are modelling to get useful answers. Is it a crop plant? Annual or perennial plant? Strongly seasonal environment? Generally, and since it seems like you are not testing a specific hypothesis, you should try several models and see what fits your data best. After all, the goal should be a biological reasonable model that describes the patterns in your data.

Ok, let's say an annual in a temperate climate.

And I take your point that cross-validation is how to do model selection. But domain knowledge is usually the best starting point.


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If it weren't for animals, insects, or people, would plants that produce seeds (nuts, fruit, etc) cease to exist?
I gather that some would or could in theory still be successful, but don't most depend on takers to flourish?

Comments are not for extended discussion; this conversation has been moved to chat.

No
Not all seeds need to be ingested in order to be spread from one place to the other, in fact some won't grow at all if eaten, some need the fruit to help them germinate and sprout after they hit the ground. Nuts simply will not grow at all if you crack them open.
Most plants rely on the wind to disperse their pollen and seed.
Dandelions are a prime example of a plant with wind carried seeds, their seeds can travel for hundreds of kilometres on parachutes before settling down and germinating in the ground, plenty of other weeds and plants go to seed the same way.

Cotton bearing trees produce their cotton so the wind can carry their seeds, like the Cottonwood and many species of Poplar tree.

One of the fun ones is helicopter seeds. Maples, elders and ash trees are among the species that disperse their seeds this way. The seeds will literally helicopter down, and fly great distances on the wind if it's strong enough. Even as an adult it's still fun to pick these seeds up of the ground and drop them just to watch them fly.

Some trees don't even need to go to seed in order to spread and multiply. Poplars are notorious for sending out suckers underground. Their roots systems spread out from the tree near to the surface and sprout suckers that will pop up out of the ground an grow into another tree. Other bushes and plants do this as well, like raspberry plants.
Not even all fruit is intended to be eaten, The fruit of the chestnut tree is sour, and covered in sharp spines that hurt. We used to spin them around and throw them at each other as kids imaging we were medieval warriors wielding maces. The spikes can get rather long and sharp, I've seen them stick to kids that have been hit by them, and after plucking them off they develop a golfball-sized welt covered in lots of tiny puncture marks.

Worst case scenario for plants that spread their seeds via burrs or by being ingested a pooped out elsewhere if animals were to suddenly cease to exist is that they wouldn't be able to disperse their seeds as far. They'd simply drop their seeds beside them, but they would continue to exist.

Thank you, Shem, for your wonderful answer. That puts into perspective fruits and seeds, which I appreciate! :) I had thought of fruits and nuts as being quite dependent on being eaten or carried away, but as you point out, not all are so dependent. Interesting!

I up voted your answer, but since I don't have 15 points yet, I'm not "allowed" to say thank you in such a way. Sorry man

As kids in Hawaii, we had 'burning beans' of this tropic legume tree with beans the size of a quarter that we rubbed on the concrete to get hot and touch another poor kid!  No 1st degree burns at all...

Even edible fruit trees may survive, just look at the osage orange, the only animal that could eat its fruit is long extinct, so not only the fruit that rot away fast enough spread.

I think this question is wonderful.  This is the kind of thinking everyone should find themselves doing everyday.  And, my answer would be, yes, plants would adapt to other ways to disperse seed.  It would take a long time but you bet, if that method of dispersal stopped plants would evolve to use only wind or water to disperse seed.  The dandelion's method would become the norm.  Maple seeds, the little helicopters would become even more impressive.
The problem with your scenario are insects; bacteria, nematodes, fungi and macro soil organisms the millipedes, earthworms...without these decomposers it would inhibit decomposition and thus no food for all the other soil organisms, some plants are totally reliant upon.  Plants would change, evolve into a more survivable organism.
Plants already communicate via chemistry to protect their own species.  When the antelope and other herd beasts in Africa got overpopulated and started to put major stress on the shrub trees, the shrub trees got together and became poisonous and killed entire herds of animals.
I am wondering when plants will turn on us!  Grins...


text:
Which comes first, PCR or Gel electrophoresis?
If I want to find out wither a group of patients have the abnormal BCR-ABL cancer gene, how do I benefit from the PCR and the gel electrophoresis techniques? I'm kinda lost trying to determine which comes first and what is the exact function of each device, I have read the whole gene cloning process in my biology book but couldn't absorb it because it's so complex.

PCR comes first. If PCR works right, then a specific product will be amplified. But you cannot see it in the little plastic Eppendorf PCR tube. That is what the electrophoresis is for. After you run PCR, you run the products on an agarose gel to visualize it (with the help of some flourescent dye). The agarose gel is just to see if the PCR worked.


text:
Chart of intra-species genetic diversity across species / phyla?
I am looking for information on how genetic diversity within a species (not between species) differs between taxa. In other words: Is the "spread" in the genetic pool, if measured, for instance, in terms of single-nucleotide polymorphism (SNP), generally bigger / smaller for some groups of species than for others?
My ad-hoc idea is that species with a stronger phenotypic difference between individuals, like homo, should probably have a higher genetic diversity (higher rate of SNP) than those with lesser phenotypic variation, like, say, Orthoptera (grasshoppers etc.). But I couldn't find any statistics or research on this topic.
I am especially interested in data on far-related taxa. Ideally this would be a chart with comparative data for Sponges, Annelids, Arthropoda, Fish, Mammals (single representatives of these groups), or even Plants, Fungi, Archeae, Bacteria …
I do not look for information on the actual genome sequences, nor on biodiversity, but specifically on the genetic diversity within species from different phyla.
This is my first question here, thanks for you help!

I don't know any resource you can use right now, but one thing you'll need to be aware of is that genetic diversity generally correlates with (effective) population size. This means that species like insects should generally have higher genetic diversity than mammals just because there are more of them in a given population.

You can look at the Heterozygous SNP rates in genome-sequenced species, which is a measure of within species diversity.
You have an example in Figure 4 here:
https://genomebiology.biomedcentral.com/track/pdf/10.1186/s13059-016-1090-1
You can see in the figure that endangered species are plotted (most of them with poor genetic diversity).
Also, I am afraid that your starting hypothesis is not very good. Our species is very poor in genetic diversity and has little phenotypic variation. The human species went through several major bottlenecks during his evolutionary history that reduced their diversity. Even gorillas or giant pandas are more diverse than humans. You have a bias because you are human and are good at differentiating individuals from your own species.
Also a single representative from each group won't suffice as the differences can be huge inside a group. Additionally phenotypic variation is hard to measure in certain groups.
Sorry for being a bit negative

Yes, my ad-hoc hypothesis is probably wrong, as becoming clear after some more research. On the other hand, if including ethological traits into "phenotypic diversity", the grasshopper-human comparison will still hold. But no direct correlation with genetic diversity.
Figure 4 is part of what I am looking for, but it should be inter-phyla.
One runs into a bunch of problems when asking the question as I did, I see. Will try to unsnarl this a bit more when reading on.

Turns out this is in fact a subject in recent discussion: "Understanding why some species have more genetic diversity than others is central to the study of ecology and evolution, and carries potentially important implications for conservation biology. Yet not only does this question remain unresolved, it has largely fallen into disregard. With the rapid decrease in sequencing costs, we argue that it is time to revive it." http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1001388 and some more.

I did not say it was not possible, or not interesting to do it. Simply that humans are not a diverse species. In fact the HSNP value is quite easy to compute from a genome, if it has not already been calculated by the genome consortium responsible of the assembly.


text:
Risks of generating photosynthetic yeast
The paper "Engineering artificial photosynthetic life-forms through endosymbiosis" (Cournoyer, 2022) describes the creation of a new endosymbiosis between yeast and cyanobacteria, which was followed up with "Introducing carbon assimilation in yeasts using photosynthetic directed endosymbiosis " (Gao, 2024).  The organisms are capable of replicating for multiple generations, though the first paper found the symbionts are eventually lost.  The second paper suggests further work; to quote the abstract: "We anticipate that our studies will have significant implications for sustainable biotechnology, synthetic biology, and experimentally studying the evolutionary adaptation of an additional organelle in yeast."  I did not notice any mention of safety, disposal, or BSL levels in these papers.
Suppose that some of these organisms are released in a waterway.  I'm imagining that the cyanobacterium could lose genomic material, become more efficient to maintain, and be retained in the cells by selective pressures.  I wonder if the organisms that evolve from this process would be reasonably efficient but turn out to be less palatable or even toxic to primary consumers (perhaps due to the intended chemical product for which the organism is engineered).  I wonder if this could in turn snap the food web and leave the waterways in a state of disaster akin to eutrophication.  Question: is this concern warranted?  What is the level of risk from pursuing this line of research?

In summary, your concerns are not unwarranted.
This work will result in a formal risk assessment for GMOs and will be sanctioned by the GMO committee. They will assess the risk of GMO escape and associated containment facilities required. For example, any work on Ebola virus is automatically category 4 (cat4), where the investigators use oxygen tanks and full safety "jump-suits". They will shower when leaving the facilities and nothing that enters the containment lab is permitted to leave without high temperature sterilisation, except for the investigators of course.
Accidents happen, African killer-bees terrorise native bee populations in the Americas stemming from a laboratory escape in Brazil. Obviously there other possible escapees, which are both disputed and debated, that are far more dangerous (SARS-CoV-2).
I would personally categorise the risk for this GMO as Cat 2 (regular lab), but I've never sat on a GMO committee. What I would believe is that a GMO escapee would not compete again indigenous yeasts, therefore would not be a threat. If there was evidence to the contrary the work would be escalated to Cat 3: which are difficult to work on and hemmed in by regulations.
The African killer-bee disaster however serves as a warning that assumptions about adaptability and invasive species in a foreign ecoregion can be very badly flawed.

Africanised bees in the USA Scientific American 1993, link maintained by the USDA. The situation has got a lot worse since then.

This answer could be improved with references, links in support of the assertions.


text:
What determines the number of chromosomes an organism carries?
This is an extension of this question about What limits chromosomal length?.
I am wondering what could be the specific reasons behind the number of chromosomes an organism carries. In other words, what drives the number of chromosomes and is there anything "stabilizing" the number of chromosomes.
Of course I am not talking about multiple copies of the same chromosome, i.e. trisomy, but rather the reasons behind the partition of the genetic information into a defined number of chromosomes.
From the question I referred to, chromosomes have an upper length limit which is based on their physical size, i.e basically they must be shorter than half of the spindle arm axis and they probably also have a lower limit. Yet it is unclear to me if any non-random equilibrium exists between chromosome number and length other than just being bound by an upper and lower limit in size.
Also let's restrict this question to diploid organisms to avoid organisms such as the Oxytricha trifallax which has 16,000 chromosomes but is also ampliploid or plants such as wheat which can be tetraploid.
I tried to search in the literature and couldn't find a satisfying answer. Also I had in mind the example of the Hela cells which have completely shuffled chromosomes yet still exactly 46.

With more chromosomes, the cell would need more number of centromeres and telomeres (this unnecessarily increases the size of the genome). Also the metaphase checkpoint has to be more stringent to prevent aneuploidy. This is just a guess though. In general there would be a higher metabolic cost in maintaining a very large number of small chromosomes compared to fewer but longer chromosomes. Additionally meiotic crossover would be relatively difficult with smaller chromosomes

Practically, there is an obvious barrier to changes in chromosome number: haploid cells produced by diploids must contain exactly one copy of each chromosome (or chromosome section, or locus). Otherwise over- or under- expression of genes can lead to dosage problems. Across all of diploids some large groups show strong conservation of number of chromosomes but others seem fairly free to change the number.
An example of conservation are the Drosophilids (fruit flies) where for approximately 100 million years they have maintained five or six chromosomes (search for Muller elements). Incidentally, with a huge amount of intra-chromosomal shuffling of genes "Drosophila 12 Genomes Consortium", 2007, Nature.
An extreme example of changes in chromosome number can be seen between similar species of Muntjac deer . Where in a relatively short time period (of the order of a million years or less (?) - my guess), the number of chromosomes has reduced from 46 to six (Wurster, D. H., Benirschke, K., Jun. 1970). Someone may correct me but I think amongst vertebrates, mammals show particularly fast evolution of chromosome number relative to, say, birds (though more birds also have micro-chromosomes...).
The above changes (or lack of change in Drosophilids) appear to be independent of genome size - so that was a long way round to saying "It's not genome size".
It could be repetitive DNA. The centrosomes (where mitotic spindles attach) of mammals are full of repetitive DNA and for this reason have been hard to sequence accurately (Graphodatsky, A. S., Trifonov, V. A., Stanyon, R., 2011. ). These repeats evolve (in sequence and copy number) and may promote more or fewer spindle attachments. Drosophilids (in general) have fewer repeats but I don't know if this is a diploid-wide pattern [Research anyone?].

Very interesting, thanks! Do you have, by any chances, some direct references I can look at? What I would like to know is if it is solely random recombination that drove those changes which would indicate that the number of chromosomes in an organism would change randomly within some size constrains.

I've added a few refs that may serve as starting points.  When you say "recombination", do you mean recombination (the normal pairing and crossover of homoologous chromosomes during meisois) or chromosome-rearrangement (mutation leading to novel chromosomal structure)?


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How compelling is the hypothesis that dinosaurs were killed by toxic plants?
A friend of mine has recently told me that dinosaurs were "killed by flowers". I was a bit surprised and so I googled. And I did find a lot of recent articles in popular media on this topic, probably based on this. To me it doesn't sound convincing at all, but I'm an outsider. Does anyone think that there's more to that than just a usual journalistic overhype?

Things in the paper that strike me as suspicious
Associating toxic plant defenses with the Cretaceous

Although there continues to be uncertainty about precisely when plants
first evolved toxic defenses, this period of angiosperm proliferation
would seem to be a strong candidate case. (pg 50)

Against this Gleadow and Moller (2014) discuss Cyanogenic glycosides (CNglcs), a class of organic compounds that can kill overgrazing herbivores from cyanide poisoning,

CNglcs are unusually widespread in the plant kingdom. They are found
in the oldest of terrestrial plants (the ferns) and in gymnosperms and
angiosperms.

Similarly, poisonous terpanoids are found in the Ginkgo; Proanthocyanidins, of which oak or wine tannins are a member, is found also in maritime pines; etc. There doesn't appear to be a strong link between angiosperms and chemical defenses against herbivory in plants.
Claiming that the angiosperm proliferations and extinction of dinosaurs are linked in time

The relative co-occurrence of angiosperm proliferation and the
disappearance of the dinosaurs has not gone completely unnoticed.(pg 50)

The diversification of angiosperms occurred starting about 112 MYa for the Monocots, and 100 MYa for the Eudicots, according to De Bodt, et all (2005). From Figure 1 of that linked paper, we can see that both branches of the Angiosperms were approaching their modern diversity by 90 MYa; a time still 25 million years before the extinction of the dinosaurs. 25 million years ago, our nearest ancestor hadn't diverged from the line that would lead to Old World Monkeys, and was probably arboreal. Evolution can do a lot in such a time. Calling these two events linked in time is suspicious, at best.
Using crocodilians as a test case for taste aversion

Since crocodilians are descendent from the same creatures that gave
rise to dinosaurs, this creates the opportunity to evaluate the
tenability of the proposition that dinosaurs went extinct due to an
inherent inability to learn to avoid eating toxic plants.

Reptilian cladistics are far from settled, but I would suggest that crocodilians diverged from dinosaurs by at least the early Triassic. They are almost certainly more divergent from all dinosaurs than birds. Here is what the authors have to say about birds.

However, in contrast to caimans, birds are in fact capable of forming
learned food aversions. (pg 51)

That seems to really undermine the argument here.

Learned taste aversions does exist in crocodilians, if caimans do lack it (unlikely) it is secondary event. http://sydney.edu.au/science/biology/shine/publications/reprints_legal/712hatchling.pdf

Rather than talk to the specifics of this idea, which others have already done well, I'll contextualise it as one anti-consensus view among many. Many. Many.
The extinction of non-avian dinosaurs is the most publicly well-known part of a much larger systemic event at that time, one of the largest extinction events in the last 500 million years. The Cretaceous-Palaeogene extinction event killed something like 70% of Earth's species, and unless the large clade that is the dinosaurs suffered an extinction (excepting some birds) at the same time a lot of other life, both on the land and (which is arguably even better understood from the fossil record) in the oceans, suffered one coincidentally for a different reason, we need an explanation of the pattern.
This was not initially recognised. After dinosaur fossils were discovered, there was a period of about 100 years when scientists didn't think much about why it happened, because "life progresses up a ladder" was a popular idea in biology until surprisingly recently. (Bear in mind that Charles Darwin only lived to see evolution become uncontroversial among biologists, not his model of how it happens.)
Then, from c. 1920-1980, a zillion in-hindsight-stupid ideas were proposed; see here for details, including the toxic plants idea dating to 1976. It's not even the only "something went wrong with the plants they ate" idea. The consensus view (the Chicxulub impact) explains a food chain collapse, which explains why all animals over 25 kg became extinct except for ectothermic marine reptiles (crocodiles and leatherback turtles), whose different metabolism and diet explain why they could get away with being larger. Other plant ideas included "geologic uplift reduced plant supplies on the uplifted terrain" and my personal favourite (among all hypotheses, not just plant ones), "caterpillars ate the plants". Pointing out the fact that butterflies evolved 10 million years too late for that to work, making this more scientifically feasible, feels like taking a sledgehammer to a nut.
In the end, we have to look at "maybe miscellaneous heterodox idea #23 is the real answer" the same way we do when people deny contemporary anthropogenic GHG-driven climate change. The point often missed in both cases is that the consensus view explains an enormous pattern of pieces of evidence, while the rival ideas each contradict something observed, requiring a detractor from the consensus to assert inconsistent ideas to explain it all.

IOW, the culprit was Astrophysics, in the Caribbean. with a great big meteor :-)

No, it's not convincing; angiosperms evolved in the middle part of the dinosaurs' reign, not the end, and toxins evolve slowly which gives herbivores a chance to compensate, also conifers can be riddled with toxins just as easily.
Lastly, the idea that dinosaurs could not learn taste aversion is ludicrous; it is one of the simplest neurological feats, anything with even the simplest brain can accomplish it. Claiming dinosaurs would not be able to do so would require extraordinary evidence and the article provides nothing even slightly convincing.

The "evidence" is supposedly (I didn't check if its true or not) is crocodiles don't have taste aversion now.

@Joshua Which is pretty weak evidence, considering the fact that crocodiles don't usually eat plants anyway, so they don't speak to the neurology of any herbivorous dinosaur.

@Joshua its also wrong, crocodiles have and learn taste aversion, http://sydney.edu.au/science/biology/shine/publications/reprints_legal/712hatchling.pdf