First, it's been estimated that the narrow-sense heritability of facial morphology is about ~60-90% (Martinez-Abadias et al 2009, Weinberg et al 2013, Liu et al 2012), so genetics is likely to be a greater influence than environment. But actually, the molecular genetic understanding of cranio-facial morphology is quite poor relative to other quantitative traits.
There's a list of genes from Wu et al (2019) which have been implicated and replicated across studies, but it's likely that there is a substantial amount of population specific differences in the effect size of different genes. The most replicable gene is PAX3 (which encodes a transcription factor).
As for the actual molecular genetics, it's complicated. Here are some quotes from a review (Weinberg et al 2018):

As with most common traits [61], the implicated variants from the
above facial GWAS tend to reside in noncoding (regulatory) regions of
the genome. Many variants at the 15 aforementioned facial loci were in or near
enhancers known to play a role in human craniofacial development.

An important finding from this study was that the effects of genetic
variants on facial morphology tend to be highly specific, even within
a single structural component like the nose. Another important finding
was that variants at these 15 loci tended to show preferential
activity in human cranial neural crest cells—a critical cell
population for building the face.

As for a more specific example, Adhikari et al (2016) peformed a GWAS on admixed Latin Americans and identified a significant association in the EDAR gene (well studied and known for being at high frequency in East Asian populations and influencing ear wax type, follicle/gland type and teeth formation). EDAR has a general role in the development of ectodermal tissues (such as the skin).
They found that the variant in EDAR was associated with reduced chin protrusion. Other studies have also shown that EDAR variants influence the cranial morphology in mice (using knockout studies). Functionally, they propose that:

The impact of the Eda pathway on mandibular morphology has been
interpreted as resulting from epithelial–mesenchymal interactions
during mouse craniofacial developme

References

Martinez-Abadias, N. et al. Heritability of human cranial dimensions: comparing the evolvability of different cranial regions. J. Anat. 214, 19–35 (2009).
Weinberg, S. M., Parsons, T. E., Marazita, M. L. & Maher, B. S. Heritability of face shape in twins: a preliminary study using 3D stereophotogrammetry and geometric morphometrics. Dent. 3000, 1 (2013).
Liu, F. et al. A genome-wide association study identifies five loci influencing facial morphology in Europeans. PLoS Genet. 8, e1002932 (2012).
Wu, W., Zhai, G., Xu, Z. et al. Whole-exome sequencing identified four loci influencing craniofacial morphology in northern Han Chinese. Hum Genet 138, 601–611 (2019). https://doi.org/10.1007/s00439-019-02008-6
Weinberg, Seth M., Robert Cornell, and Elizabeth J. Leslie. "Craniofacial genetics: Where have we been and where are we going?." (2018): e1007438.
Adhikari, Kaustubh, et al. "A genome-wide association scan implicates DCHS2, RUNX2, GLI3, PAX1 and EDAR in human facial variation." Nature communications 7.1 (2016): 1-11.


Dermestidae, Reesa vespulae; wasp nest dermestid
http://pestcontrolcanada.com/5965-2/


Does sleep duration vary for animals based on time of the year?

Yes, people, as well as animals regulate their drowsiness by light. There's a well known experiment conducted by Michel Suffre on himself in 1972. When he spent a month with no light and no information about the time, his sleeping cycles prolonged up to 48 hours.


How are sound waves amplified while traveling within the cochlea?

Short answer
Sound waves are, technically, not amplified in the cochlea. The answer to your question, however, is that outer hair cells amplify the acoustic signal in the cochlea.

Background
To answer your question what mechanisms exist that amplify sound within the cochlea - none.

What is amplified within the cochlea is the traveling wave that moves across the basilar membrane. The cochlear amplifier is mediated by the outer hair cells. These outer hair cells are thought to be able to contract and extend when the basilar membrane moves and thereby amplifying the traveling wave (Fig. 1).

The middle ear ossicles as you say do amplify the acoustic sound, but they are situated in the middle ear, as is the tympanic membrane, which also amplifies sound by funneling a large contact surface onto the small stapes footplate.This is not the answer to your question, as they are all middle ear structures.

Fig. 1. Inner ear structures (Fettiplace et al., 2001)

Reference
- Fettiplace et al., 24, Trends Neurosci (2001); 3: 169-75


What is the rate of mRNA decay in saccharomyces cerevisiae?

Here is my best attempt at answering this question:

The median mRNA degradation lifetime is roughly 20 minutes in the case of yeast. Also, the total transcription for RNA pol II in a yeast cell growing in standard conditions is about 60200 mRNAs/h. I am going to go ahead and suppose that the transcription rate is constant throughout time. Thus we have that total transcription rate is equal to 1003 mRNAs/min. Furthermore, I am going to make the rough approximation that all mRNAs live exactly 20 minutes. Therefore, mRNAs will start degrading after 20 minutes. In one hour, 1003 mRNAs will degrade every minute for 40 minutes. It follows that the rate of mRNA decay in yeast is roughly 40120 mRNAs/h.


Yes. It is quite simple actually. Do this inside a clean laminar hood:

Take a clean sterile scalpel blade or any other sterile long object. 1ml pipette tip would also do.
Cut the agar on your plate. Scrape off cleanly.
Put it in a sterile glass bottle.
Heat in microwave
Add kanamycin
Pour back

Another solution is to coat the agar surface with kanamycin just like spread plating. Check the appropriate concentrations.


How did the huge dinosaurs cope with gravity and loads on bones, etc.?

Assuming that gravity was essentially the same (other answers to this question notwithstanding), very large dinosaurs were dealing with the same forces that they would today. There are two clades of dinosaurs in which gigantism evolved, Sauropoda (quadrupdeal sauropods) and Theropoda (including T. rex). Each "solved" the problem of large size in different (but also somewhat similar) ways.

The main reason why large size was not a problem was that, if posture changed to align the forces between the animal and the ground, the bones are compressed. Bone is very strong in compression.

Theropoda

Theropod essential operate as a see-saw, with a large muscular tail balancing a large head. As such, they did not likely use much active muscular force to balance. The analogy is a human standing. Just standing, you don't need much muscle force to balance.

Hutchinson and Garcia (2002) showed that, because of a lack of plausibly large leg musculature, T. rex could not run. For a range of postures, they estimated how much muscle would be required to balance the animal and found that running behavior was unlikely.

Hutchinson, J.R. and M. Garcia. 2002. Tyrannosaurus was not a fast runner. Nature 415:1018-1021.

Sauropoda

Sauropods show many similar adaptations as elephants, the largest extant land mammals. Their limbs were held upright (erect), which requires less energy for balance. Some sauropods had air-filled bones, which would also lighten the skeleton. Wilson and Carrano (1999) document the evolution of posture through sauropod evolution from a biomechanical perspective.

Wilson, J.A. and M.T. Carrano. 1999. Titanosaurs and the origin of “wide-gauge” trackways: a biomechanical and systematic perspective on sauropod locomotion. Paleobiology 25:252–267.


As @skymnige said it is definitely Black garden ant (Lasius niger)


Does knowing the sex of each of a couple’s first N children have any marginal value in predicting the sex of child N+1?

For those who are interested in sex ratio bias itself, the enWikipedia article is pretty good.

As for predictive power, a Bayesian might tell you that by knowing a couple can and did have a male/female should improve, if only slightly, your belief that their next would be the same.  It's by no means predictive and probably largely indiscernible from random chance, but hey it's something!

More to the point, at the very least you might as well just guess their next child will be a son.  As the link above will tell you, the human sex ratio at birth has varied but in general males are more likely to be born - somewhere around 1.03 to 1.08 males per female.  Here's another in-depth study, from 2005, dealing with the last few decades in the US.

That study has Figure 3 (below) and Table 3, which show the raw birth ratio over successive births, and the data are pretty clear: successive births reduce bias.

Those numbers are way more clear than I thought they would - just watch those means move!  I wish there were more information on the variances - clearly there's more down by the 8th child - but that's pretty solid.  Here's another study from Denmark in 1999 doing some of the same stuff (Denmark was popular for this work).  They include the absolutely fascinating Table 2 (below), which breaks down the odds of giving birth to a male given whatever came before.  Which, in the end, is as predictive as you can get, right?

Basically, it's sort of what you'd expect: the more females you have, the more likely you are to have another female; the more males, the more likely the next is a male.  They used about 1.4 million kids but there are some interesting oddities in that table at the extremes.  The best chance for a male?  Your fifth kid, following FMFM.  Best for a female?  Your fifth, after MMMF.

There are some definite issues that can twist the data, particularly when families have another kid to try to get a child of a specific sex.  If you can tease out some of those environmental factors, you'd be better at guessing; still, I wouldn't bet the house on it.  Memorize that table but, when in doubt:

Guess male
Lotta females first?  Maybe guess another one.
A bunch of males?  Guess another male.


Is there a kind of 'rule' which decides whether the male of female is bigger?

In short, there is not a rule of thumb whether a given species will have bigger males or females. In some cases females are larger (often insects, invertebrates or fish), in other cases males are larger (often mammals and birds) but even these generalizations have exceptions (Ralls (1976)).

When a males and females of a species have morphological differences other than differences in reproductive organs, this is called sexual dimorphism. These dimorphisms can be thought of as adaptations which have evolved due to a specific evolutionary pressure.

In males, larger sizes can evolve from sexual selection on males in competition with other males for mates. Simplified, the bigger males are better competitors. In females however, larger sizes can evolve from a number of different pressures, but rarely due to competition for mates. More common pressures resulting in larger females are rearing success, competition for resources other than mates.

Whether males or females of a species are bigger is certainly not random, but rather a precise outcome of numerous trade-offs and benefits of being bigger.


What is the use of crystallized Photosystems from cyanobacteria?

The main purpose of crystallizing a molecule or molecular complex like a  Photosystem is usually to provide a crystal for X-ray crystallography.  A crystal has its molecular components arranged in a structured systematic repeating pattern, and this repeated pattern allows the X-rays to reveal the 3-dimensional shape of one of the components.  Knowing the shape is of biological interest as it suggests how the molecules perform their function.


Question about phylogenies and DNA sequencing

Genes reflect a phylogeny of their own. So no, the genes for "shape" (if they existed) would be very different between dolphins and sharks. Every single gene in a dolphin is more similar to its homologous counterpart in a cow than to any gene in a shark. Gene by gene, or with the entire genome, it would not matter. The similarities between sharks and dolphins are due to convergence. Convergence make sense in that there is selective pressure to have streamlines bodies to swim through the water. It is possible for genes to converge as well, but the nucleotides would differ, just as the fins on sharks and dolphins differ.


Origins of transcription factors and RNA Polymerase

This is one of the main features of the RNA World.
What I mean by that is, RNA not only acts as a repository of genetic information, it also acts as an enzyme. This enzyme is known as Ribozyme. Ribozyme confers a self-replicating property to RNA, leading to the hypothesis that RNA might be the ancestor to the present day self-replicating genetic material.


Are there any known consequences of the right-handedness of the DNA double helix?

The short answer is no, there currently aren't any visible macroscopic asymmetries in some organisms traceable to DNA's handedness.

The long answer is still no, but I want to clarify that this "no" is more of a "not really". This is because there can be potentially drastic consequences when left-handed DNA is present in a cell in addition to the traditional right-handed DNA.

Let me explain. First, left-handed DNA is officially called Z-DNA. Right-handed DNA, which is the normal DNA configuration, is named B-DNA. There's a third type of DNA, which is also right-handed, that is called A-DNA. A-DNA is essentially super-coiled B-DNA.

Z-DNA isn't that unusual, and it is regularly found in human cells in addition to B-DNA. One study, done in yeast, found that Z-DNA can act as a nucleosome boundary element. Another study, by Kwon and Rich, found that the consequences of Z-DNA weren't as benign. The vaccinia virus requires Z-DNA to bind to a key protein that has anti-apoptosis activity. When Z-DNA does this, apoptosis is effectively blocked.

Furthermore, Z-DNA has been found in patients suffering with Alzheimer's Disease. Suram, et al., found that the hippocampus of severely affected AD patients used Z-DNA instead of B-DNA. This change in the DNA coil has potentially drastic consequences with regards to gene expression.

Finally, the presence of Z-DNA antibodies were found in patients that suffered from Systemic Lupus Erythematosus (SLE). Lafer, et al., describes how non-SLE patients do not have these antibodies, which suggests that Z-DNA is involved in the clinical manifestation of SLE.

So, with those thoughts in mind, yes, there can be visible asymmetries traceable to DNA handedness. In fact, some tumors depend on genes that have Z-DNA domains (one study by Alan Herbert found that it was about 40% of tumors on their panel). While this isn't really what I think you're asking, it's technically true as tumors do qualify as visible asymmetrical phenotypes traceable to DNA handedness. Diseases associated with Z-DNA could also technically qualify as since they're diagnosable, they're visible in that manner.

Regardless, there is currently no proof that the handedness of our DNA actually causes any real macroscopic phenotypic effect in the developmental stages of life. The reason why left-right asymmetry happens in organisms is due to asymmetric gene expression, not the direction of the DNA coil. This review by Michael Levin talks explicitly about how the left-right borders are established in embryonic development, and there is nothing regarding the direction of DNA's double helix.

Nonetheless, DNA handedness is still a rapidly developing field. I anticipate that more research on these subjects will quickly become available. But as of now, no. Snails shells are not right-handed because of the right-handedness of their DNA.


Can the extinct Chinese Paddlefish be revived?

Informally speaking, there is no real/good way to bring back extinct species. Especially sexually reproducing species; you'd need to revive a male and a female at the very least, and these are markedly different genomes due to unique sex chromosomes.
Some 'bad ways' exist though; in principle, if you found a perfectly preserved nucleus (the organelle that holds genomic DNA of most eukaryotes), it may be possible to insert this nucleus into a sibling or sister species (e.g. wooly mammoth nuclei into denucleated elephant zygotes). This would be the cloning approach. However, you then run into practical issues. You have to guarantee that this embryo will implant itself, which itself is not always the case. The nucleus and chromosomes must also be intact enough (which may not be the case after storing them, e.g. in ice, which may require thawing which often damages cellular structures) to create a rather healthy, fertile organism that will breed at a sufficient rate to restore a stable population. These and many more complications will reduce your chance of rescuing an extinct species to near-zero. Even then, one could argue that it is an incomplete de-extinction because you've only substituted the genomic DNA, and not other parts of the genome (e.g. chloroplast or mitochondrial genomes) which are part-and-parcel of the genetic signature that makes a species a species.
Alternatively, you can create hybrids where fragments of DNA from extinct species are brought into the genomes of similar existing species, by molecular methods such as recombination using CRISPR/Cas9. Here though you are only creating hybrids, not reviving extinct lineages. The extent to which you could do this is also limited and you would have to increasingly troubleshoot why a hybridization didn't work the more host genome you replaced with the extinct species' genome. Transgenesis using individual genes (say, transfering an enzyme into a new organism) is quite plug-and-play, but replacing entire chromosomes would be near impossible to pull off, not least because you would have little insight into why things aren't working - only that they aren't.


connect three coding sequences with IRES

You might be interested in the Foot and Mouth Disease 2A Peptide, a self-cleaving peptide sequence that can be inserted in between two proteins. The proteins are translated as one sequence, but cleaved at the 2A peptide to form 2 proteins. If I'm reading the source right, they used 4 genes in a row with 2A peptides between them. The 2A peptide has the advantage of being much smaller than most IRES elements, while being more reliable than IRES or internal promoters.


It is a safe bet that a "worm" as you describe in a ripe guava or any other ripe sweet fruit is a fruit fly.

from http://www.greenharvest.com.au/PestControlOrganic/Information/FruitFlyControl.html

Fruit flies are attracted to any ripe sweet fruit.  They are also attracted to vinegar and alcohol - both produced by yeast in and on the fruit, which is the high protein food that the fruit flies are really after in the fruit.

from
http://homeguides.sfgate.com/treat-fruit-flies-guavas-30550.html

  When ripe, guavas emit a pungent, musky odor that attracts fruit
  flies. Fruit flies lay their eggs beneath the fruit's skin, and the
  maggots feed on the flesh. The damage causes guavas to rot. Fruit fly
  infestations often spread quickly, but prompt treatment can get
  populations under control.

The fly large actually speed the rotting of the fruit by moving yeast around on their bodies.


thick filaments slide over thin as cross bridges are formed by thin filament which slides thick filament and sandwich like structure is formed and Z-line disappears


What’s the Difference Between Grass and Sedge?

Short answer
Sedges have edges, and they're in different families.
See Minnesota Wildflowers for a great summary with images.
 Long answer
Both are in the order Poales, but they are in different families:

Grasses = Poaceae (of the graminid clade)

Sedges = Cyperaceae (of the [non-monophyletic]1 cypirid lineage)

Some anatomical differences:

 Compiled using info from here and here

 Source: New York Botanical Garden

 Citations
 1. Bouchenak-Khelladi, Y., Muasya, A.M. and Linder, H.P., 2014. A revised evolutionary history of Poales: origins and diversification. Botanical Journal of the Linnean Society, 175(1):4-16.


Why is DNA double stranded and RNA single stranded?

Though this is a basic question (a few google searches will provide all answers) and you have asked a lot of questions, I shall answer them one-by-one.

Why is RNA single stranded (and not double stranded like DNA)?

dsRNA is less stable than dsDNA.  See this: http://en.wikipedia.org/wiki/RNA#Structure. An important structural feature of RNA that distinguishes it from DNA is the presence of a hydroxyl group at the 2' position of the ribose sugar. The presence of this functional group causes the helix to adopt the A-form geometry rather than the B-form most commonly observed in DNA. This results in a very deep and narrow major groove and a shallow and wide minor groove. A second consequence of the presence of the 2'-hydroxyl group is that in conformationally flexible regions of an RNA molecule (that is, not involved in formation of a double helix), it can chemically attack the adjacent phosphodiester bond to cleave the backbone.
RNAses are very common.  Most critically, in biological systems, the presence of dsRNA is a signal of viruses and active transposable elements, so ssRNA is an easy way for the host cell to distinguish foreign elements.  Yes, that was an oversimplification and ignored functional dsRNA, but even then, dsRNA likely evolved from systems to foreign elements.1

Why is DNA double stranded (and not single stranded like RNA)?

Firstly, the 'information' part of DNA is the nitrogenous base, as opposed to the pentose sugar or the phosphate residues. In a single-stranded molecule, this important part would be exposed to the cellular environment, providing more opportunity for it to be mutated by the various chemicals there. In a double-stranded configuration, however, the two nitrogenous bases are locked within the complex, facing each other in the centre of the molecule. This organisation helps to safeguard them from local mutagens.

Secondly, having two complementary strands facing each other fundamentally means having two copies of the same thing placed right next to each other. This allows for proof-reading. George C. Williams summarised this beautifully in his pithy passage (from "The Pony Fish's Glow" (1997)) (recall that adenine [A] on one strand should always bind to a thymine [T] on the complementary strand, and visa versa; likewise cytosine [C] always binds to guanine [G], and vice versa i.e. Charagaff's rule).2

Source

What is the difference between DNA and RNA?

A complete table of differences can be found here (sadly I can't create a table in markdown) along with this image:

How are roles of DNA and RNA different?

RNA has several different functions that, though all interconnected, vary slightly depending on the type. There are three main types of RNA:

Messenger RNA (mRNA) transcribes genetic information from the DNA found in a cell's nucleus, and then carries this information to the cell's cytoplasm and ribosome.
Transfer RNA (tRNA) is found in a cell's cytoplasm and is closely related to mRNA as its helper. tRNA literally transfers amino acids, the core components of proteins, to the mRNA in a ribosome.
Ribosomal RNA (rRNA) is found in a cell's cytoplasm. In the ribosome, it takes mRNA and tRNA and translates the information they provide. From this information, it "learns" whether it should create, or synthesize, a polypeptide or protein.

DNA's genes are expressed, or manifested, through the proteins that its nucleotides produce with the help of RNA. Traits (phenotypes) come from which proteins are made and which are switched on or off. The information found in DNA determines which traits are to be created, activated, or deactivated, while the various forms of RNA do the work.3

EDIT- As you've asked another question in comments, I will add it here:

Why is DNA preferred over RNA as genetic material?

DNA offered several advantages over RNA so was chosen by natural selection to represent higher beings:

DNA was chemically more stable than RNA so it was possible to maintain greater length of DNA in comparison to RNA. RNA has hydroxyl group (OH) present on the 2’ carbon. This hydroxyl group invites hydrolysis reaction and so it was not possible to maintain long length RNA molecule. This hydroxyl group was absent in DNA leading to stability of DNA molecule.
DNA was more capable in handling self-repair during replication process due to the presence of Thymine instead of Uracil. It was due to the fact that often cytosine was changed into uracil due to the deamination. Now in case of RNA it was impossible for cell to know if uracil should be present there or not but in DNA since Uracil is not all present so it was quite easy to identify the error and rectify that.
DNA also offers more information security because of the double helical structure.4

A comparison of molecular structure of DNA and RNA from here

References:

https://www.quora.com/Why-is-RNA-single-stranded-in-general-and-not-double-stranded-like-DNA
http://medicguide.blogspot.in/2008/07/why-is-dna-double-stranded-but-rna.html
http://www.diffen.com/difference/DNA_vs_RNA
https://www.quora.com/Why-was-DNA-chosen-to-be-the-genetic-material-instead-of-RNA
http://www.atdbio.com/content/2/Molecular-weight-and-mass


How only one follicle develops into graffian follicle?

It doesn't mean only one follicle maturates within a lifetime of a woman. For every ovulation only one follicle maturates from the batch of primary oocytes stored within the ovary. Before a female is born, all the primary follicles are arrested in the diplotene stage of prophase I. Still, we do not know exactly the mechanisms that let only one follicle to release a mature egg cell, but studies have shown why it possibly happens.

Granulosa cells surrounding the oocyte have receptors for FSH (follicle-stimulating hormone), FSH activates the production of aromatase, which transforms testosterone produced under the influence of LH (luteinizing hormone) in cells of theca interna into estrogens. Estrogens activate expression of LH receptors on the surface of granulosa cells and further stimulate the production of LH. The more LH activates thecal cells, the more estrogens are produced in granulosa cells and that at the same time increases production of LH receptors on granulosa cells.

FSH also stimulates granulosa cells to proliferate, providing the whole follicle with a large number of FSH receptors and increased production of aromatase and at the same time stimulates the follicle to finish meiosis I. Eventually one of the growing follicles will have enough FSH and LH receptors on the granulosa cells to become able to respond to large surge of LH, which results in ovulation. The rest of the follicles that started to develop degenerate due to insufficient number of FSH and LH receptors. The fact that FSH and LH concentrations drop rapidly after ovulation also halts the development of remaining follicles.

The follicles that did not receive enough FSH, won't grow to the point, where granulosa cells start expressing LH receptors and they won't pass through the 1st meiotic block, therefore they still may be activated in the next month. Those that did pass the 1st meiotic block but couldn't be ovulated, will degenerate.

It is still unclear whether there are some additional mechanisms that help the atrophy of underdeveloped oocytes.

Sources:

Larsen's Human Embryology
https://kjcscientific.wordpress.com/project-excalibur/


Why cannot there be multiple sources for same species origins?

This is a very fundamental, and in my opinion, interesting question. You might not find many sources that directly cover this question because it is hard to test. If speciation did happen in two separate locations and the resulting species were so similar that they could breed with one another and not the original species, how would we be able to tell if the species originated in separate locations and that the new species didn't just travel to the new location? Below I'll try and explain why it's safe to assume they probably didn't have different locations for speciation.
Thought Experiment
Here is what happened in hypothetical land. Species X exists in happy land. Individuals of X then move to water land. Some more individuals from X move from happy land to H2O land (very similar to water land). Species X undergoes speciation in water land to species Y and speciation of X also occur in the H2O land to species Z.
Can Z and Y be the same species with different origins where the niche conditions are the same?
As you can imagine, the longer after geographical isolation the more mutations occur and the less likely it is that the new species will be able to breed successfully with similar species.
Although the two environments may seem identical, ecology is notoriously complex and chaotic, and so in reality as far as ecology is concerned, they are very different environments. Even the slightest difference between niches will naturally select different traits that could make Z and Y sexually incompatible.
Furthermore, when dealing with the geographical origin, you must assume that there was geographical isolation between the two speciation event locations. Since there is typically no contact between Z and Y species, there is no selective pressure to remain genetically compatible and given enough time, they will become unable to breed.

Humans
There is a contentious claim that ancient humans bred with chimpanzees after both speciation events from our common ancestor to humans and chimpanzees. Broadly I think this has now been dismissed. However, it is reasonably well accepted that in a more recent "Tolkien-esque" world humans bred with Neanderthals.
But ultimately I don't think there is a single example (I am thoroughly open to being proven wrong!) in the natural world of two similar geographical isolation events driving exactly the same species to evolve and both versions of the new species are more genetically similar to one another than they are to the origin species. The odds are just too slim even if to us the conditions seem identical.


How do we know the presence of light when our eyes are closed?

Short answer, your eyelids does not block all light. Since they are only a thin layer of skin, the light is able to pass through although not completely obviously. Since the eyes are still completely functional when you close them, only covered by the eyelids, you are able to see when light strikes your face.


The other inhibitors work on other processes, as you already noticed. There is almost no difference between the conditions when they are added and the corresponding condition when they are missing, suggesting those other processes play no role in the observed phenomenon. Eliminating those other processes makes it more believable that actin polymerization is important, rather than being one of multiple factors.

Moreover, often cell will adapt to an inhibitor by increasing or decreasing other kinds of activity. For example, it could be that actin polymerization inhibition prevents amoeba from eating. In this case, because any imaginable motive mechanism requires energy, starving amoeba may become unable to move, even though it was not using actin for movement. In order to refute such scenarios, where actin polymerization is not directly inducing movement, and where cytochalazine does not inhibit movement directly mechanism, supplementary experiments were performed.

DNP induces something similar to starvation, yet, in these experiments, did not abolish movements when given alone. Nor did DNP rescue movement, because the combination (DNP + cytochalazine) is virtually identical to cytochalazine alone. In both circumstances, DNP did nothing, thus showing that ATP depletion is not influencing movement. This is proof that actin polymerization is directly causing amoeba movement, and not an indirect ATP-mediated effect. Similarly, cytochalazin's effect is independent of protein synthesis, once more supporting the hypothesis that actin polymerization is important on its own.


How verified experimentally is the Marginal Value Theorem for viruses?

I'm not an expert but it seems purely theoretical. There are some fairly basic criticisms that can be made of this model. First it assumes that viruses tend to optimize propagation, a perfectly reasonable assumption. The clear prediction is that propagation rate should be inversely related to mortality rate. Quickly checking a list of the most common viruses shows you that this relation is not that strong, if there at all. The second issue is that R0 is a very abstract measure. Viruses do not propagate in a straightforward manner. Rabies relies on animals biting each other, HIV sexual contacts, etc. On average each virus will still have an R0, but I'm not sure it is so sensible to assume it will trade-off with mortality as it relies on the animals behavior (although with rabbis for example the animal behavior is actually modulated by the virus itself to increase propagation). Lastly epidemics usually start with a zoonotic disease randomly mutating and jumping species. They often have quite different effect on different species so here again I am not sure it is completely reasonable to assume that the mortality rate of a virus will tradeoff with infection rate.

It's still a useful tool to think about how viruses should behave. As you noted there also are criticisms about the MVT to describe animal foraging. But mathematically, under some assumptions, it is the optimal solution. So any deviation you see from that tells you your assumptions were wrong.


What kind of technology is required for plant seed DNA printing?

As Chris mentioned in his comment, 'printing' DNA from scratch (i.e. synthesizing a long strand de novo) is expensive and difficult. Unfortunately, the process of GMO creation is not as simple as assembling a beautiful DNA sequence on the computer, printing it, and then inserting it into a cell. Here's a related question about de novo sequencing. Plant biologists, please correct me if I'm wrong but I don't think it's a trivial matter to grow a plant from a single cultured cell.

Your third question reminds me of DNA programming, which is an amazingly cool, developing field. Many companies (including Microsoft) are funding research into DNA circuitry and biological computing, making computers out of biomolecules. Here's an interesting paper that will tell you more. What you may be most interested in is the branch of DNA programming that seeks to identify discrete protein-coding and otherwise functional DNA that can be utilized as a sort of "programming language" to build a new organism. One of my past supervisors recently joined this field and I'm a little jealous. Overall, this is a very new field so there is much to be accomplished and very little is technically possible, although the principle of GMOs is really just an optimization of an existing organism.

In summary, the answer to all three of your questions is: No, not very well. But we're trying.

Most likely this isn't something you'll be able to pick up in your spare time in order to have a cool plant to grow on your fence. It's very expensive and very difficult (in some cases, maybe even impossible). However, there are so many unknowns in this area of research and everything you propose is reasonable in theory. Let me know if you figure it out. I would love to code my own garden.


Why are there relatively more predators on the land than in the oceans?

I wouldn't say conditions on land are poorer... just more unstable, less predictable over a span of a million years. And an unstable environment appears to be one of the factors in the evolution of human intelligence. ie the environment changes faster than evolution can adapt the body... so one solution is to adapt the animal's behavior which requires intelligence.

That said, dolphins too are plenty intelligent. Octopus also are quite good puzzle solvers.. but are short lived.

As for predator -prey ratio https://www.mcgill.ca/newsroom/channels/news/why-arent-there-more-lions-254873 Here is something to read. Predator-prey ratio appear to be govern by the rate of growth of prey items

And prey in the ocean has a faster turn around in the ocean.. so there are more predators in the ocean than on land. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4240998/.


Is there a website that shows population sizes?

You can access the Imperial College global population dynamics database.  They will have time series data at specific locations.  http://www3.imperial.ac.uk/cpb/databases/gpdd
There is a sister database as well that might be useful. http://lits.bio.ic.ac.uk:8080/litsproject/

These contain several hundred time series, and you can see a paper that used them here:  http://onlinelibrary.wiley.com/doi/10.1111/j.1461-0248.2011.01702.x/abstract


Where do I purchase a fly with the collagen tagged?

There are some more places other than what Bez has already mentioned.

See here.

However, tagging collagen may be a problem. Collagen undergoes a lot of post-translational modifications including hydroxylation and end clipping. It forms a unique structure (triplex) and adding tags may compromise its structural integrity. You can try Masson's trichome stain instead, which is used to stain collagen — a very cheap alternative.


Do whales ever just hang out on the surface breathing?

Whales often hang out on the surface for a while, for a number of reasons. Sometimes it is for curiosity, sometimes to socialize with other whales, and sometimes simply to rest.  The particular sort behavior that you are describing sounds like logging, where the whale basically rests, often for an extended period of time, with its back slightly out of the water, looking sort of like a floating log.


Won't natural selection miss the overall minimum of a function?

What I think the question is "Why wouldn't an organism be more efficient from selection than the environment demands?"  Please let me know if I'm hitting the mark here.

A scenario suggested by the question is this: If there is selection pressure on say an animal to resist a disease, and then it evolves two resistance systems to the disease.  This could be an immune response and a taste for a certain plant containing compounds with remedial properties.  If either system is adequate to resist the disease, hasn't selection gone above and beyond what is needed?

If so, the answer is either not recently, or all the time.

First, for 'not really' you have to consider the importance of competition.  Reading about the Red Queen's Hypothesis is helpful here.. First there is a natural random mutation rate, which can cause one of the system to become less effective.  Or if the disease is also changing to increase its efficiency, then either one or both of the defense mechanisms in this case would fail from time to time.  Then having two systems would not be too much. There is a clear benefit to having redundant systems of resistance here. For both these broad categories of reasons, you have much redundancy and interdependence among the genes which create traits in living things (phenotypes).  Because of the background mutation rate, traits which are not needed disappear relatively quickly; because of competition, those which convey an advantage, even if a small one, have a strong likelihood to stay in the gene pool.

now: "all the time" There are cases where traits are exhibited that are not efficient though. Evolution works over generations, typically selection influences traits on the order of 10s of generations and the population can show traits which are not helpful if the environment or the competition has changed drastically.

An example of this is the current obesity epidemic in the developing world. The sudden availability of cheap food has caused those people who have access to become obese.  This is because they have a heavily reinforced trait to save up fat because humans experience famines regularly.  Its going to take a long time before efficient energy storage in human beings is lost.  In the meantime, people are not living to reproducing age at the same level of fitness they might have.

I want to add a note on genetic algorithms.  The difference between genetic algorithms to achieve the same efficiencies as biological systems are worth thinking about:

As far as failing to find a global minimum, natural selection usually has many more samples.  A typical selection experiment with flies or worms often have thousands or tens of thousands of individuals screened.  GA models of reasonable complexity have usually a few score at most - am I right?  A bacterial or yeast experiment can have 10^9 individuals.

The genetic system of the chromosome itself is tremendously complex.  We can't even model itself and so the product of millions of generations of selection already will has a heretofore unmodelable response to selection.
The typical selection environment is equally undefinable, so a survey of living things in a complex environment has unpredictable effects.  While most of us think as laboratory experiments as being less complex, its not completely true.  I was at a talk recently that mentioned how E coli K12 seems to have diverged in various laboratory environments despite the fact that its mostly been in frozen stocks since being isolated in the mid 20th century.


In humans and animals beard growth is usually restricted to males, since it's dependent on hormones (testosterone or, specifically, according to wikipedia it's dihydrotestosterone). By no surprise it starts growing during puberty.

But why?

Growing a long beard is costly concerning the necessary resources but also because of a potential handicap. Being able to afford a nice beard is showing dominance among males and attractiveness for females. It could be seen as a direct display of high testosterone levels. This is comparable to peacock feathers. They are very impractical, but have great value for showing dominance and attracting females.

I think, there are many psychological theories around to explain the attractiveness of beards. Some might also be meaningful in animals. Apart from cultural, religious or hipster beard trends, we generally consider old men with long beards as wise and knowledgeable. In animals the beard might also signal social status in groups, additionally to male dominance and sexual attraction.

Further reading:

Importance of hair in humans and hormones involved
Sexual attraction of beards in humans
Trustworthiness of bearded men
Intrasexual competition influencing sexual dimorphism (here: size)
Sexual selection
Costs and benefits of male hair (lion mane)


Continuous EEG: Where does pronounced power peak at 38 Hz come from?

Someone taught me how to make a more informative plot without preprocessing the data. It thus seems like this artifact is 12.5 Hz apart from 50 Hz and therefore has something to do with the line noise from nearby electrical devices. The same pattern happens at 150 Hz.


Enzymes alter the rate of a reaction by lowering activation energy; they have no effect on the reaction equilibrium ($\ce{K_{eq}}$). Since $\ce{K_{eq}=\frac{k_f}{k_r}}$ and $\ce{K_{eq}}$ is constant, an increase in forward rate ($\ce{k_f}$) requires a corresponding increase in the reverse rate ($\ce{k_r}$). Intuitively it may help to think that the same effect an enzyme has on lowering the energy of the transition state in the forward direction should also be present in the reverse direction. Whether or not the reaction actually proceeds in reverse depends on the free energy difference between the reactants and products and their concentrations (among other things). See this answer for a great explanation.

Because their reactions are in equilibrium ($\Delta G\approx0,\ce{K_{eq}\approx1}$), many enzymes in the glycolytic pathway also catalyze the reverse reaction in gluconeogenesis.

[image source]


Effective integration time of a typical neuron is in the order of 10-100 ms. You might want to look into this classic paper (read it with a critical mindset):

Shadlen, M. N. and Newsome, W. T. (1994). Noise, neural codes and cortical organization. Curr. Opin. Neurobiol., 4:569-579.

Or some biophysics book like:

Biophysics of Computation by Christof Koch


Why is ACE2 not used as drug against covid?

There's a Cell pre-print by Monteil et al. (DOI: 10.1016/j.cell.2020.04.004) which argues that human recombinant soluble ACE2 protein can competitively bind to SARS-CoV-2 virus and reduce its ability to infect and replicate:

  Here, we report that clinical-grade human recombinant soluble ACE2 (hrsACE2), which has already been tested in phase 1 and phase 2 clinical trials (Haschke et al., 2013, Khan et al., 2017), can reduce viral growth in Vero E6 cells by a factor of 1,000-5,000. Moreover, we show that human blood vessel organoids and kidney organoids can be readily infected, which can be significantly inhibited by hrsACE2 at the early stage of infection.

Though it is not perfect, in that other factors and receptors may be implicated in infectivity:

  Our data now show that this clinical-grade human ACE2 molecule - but not mouse soluble ACE2 - can significantly inhibit SARS-CoV-2 infections and reduce viral load by a factor of 1,000-5,000. However, as observed in antibody neutralizing experiments of many viruses, the inhibition is not complete, though clearly dose-dependent. This may be due to the fact that there might be other co-receptors/auxiliary proteins or even other mechanisms by which viruses can enter cells, as had been initially proposed for SARS (Jeffers et al., 2004; Qi et al., 2020).

One person is right to comment that these are in vitro studies. In other words, they treat cell cultures on the functional equivalent of a Petri dish: Vero cell lines or simulations of human tissues (organoids), and they see what happens.

The in vitro studies are useful and important but it is a big step from those to 1) treating people in vivo — designing a drug that can actually and safely target the virus where it infects respiratory and renal tissues — and, 2) making and distributing that drug in quantity, cheaply, safely, etc.

But the larger point of these studies is to show that scientists are definitely thinking about the mechanisms by which the virus infects cells, and to see if there are ways to interfere with and limit the virus, by doing so.

Like your thought to use ACE2, some researchers have looked at other viruses, like poliovirus and HIV, to see if there are similar soluble ligands that they can bond to antibodies and deliver safely to humans, as a general therapeutic idea.

They found that HIV-1, which uses binding to the CD4 receptor as a means to infect T cells, could develop mutational resistance to soluble CD4 and use other mechanisms to cause infection. But by adding a second receptor CCR5 to the immunoglobulin, other researchers were able to limit the ability of HIV-1 virus to evolve resistance to both receptors, which provides some possibility of this approach as a vaccine, down the road.

These issues all complicate use of receptors as a way to "fake out" the virus. But it is an avenue being explored, especially for this virus during a time of emergency.


They ate other Solanaceae species.  This University of Florida info page gives an excellent overview of the species, including its hosts (emphasis mine):

  Potatoes are the preferred host for the Colorado potato beetle, but it may feed and survive on a number of other plants in the family Solanacae, including belladonna, common nightshade, eggplant, ground cherry, henbane, horse-nettle, pepper (rarely), tobacco, thorn apple, tomato, and its first recorded host plant: buffalo-bur.

The naming history is a bit weird — being neither originally from Colorado or associated with potatoes — but hey, that's science.


Measure of environmental impact on phenotype

In between a long comment and an answer...

For a review of the theory behind the causal variables of phenotype, one might want to have a look at Biology Why is a heritability coefficient not an index of how “genetic” something is?.

One can investigate the impact of a specific environmental variable onto the phenotypic variance but the environmental as a whole is typically computed as whatever is left when other sources of phenotypic variance have been explained. As such you might want to read about estimations methods for heritability and maybe esp. the post How do heredity and regression to the mean work with respect to intelligence?.


The structural model of a protein is obtained using both experimental data and prior knowledge about geometry of macromolecules. As a structural model is refined, interatomic distances are also restrained. So, the C-N distance isn't really predicted. Alternatively, knowledge about this distance is used to construct reasonable model.

In response to the comment below I'll cite Rupp's Biomolecular Crystallography, the most comprehensive book on this subject. Refinement and restraints are covered in Chapter 12, Model building and refinement.

  An observation does not have to be an experimental observation
  (measured data) specific to the particular structure, but can be any
  type of general prior knowledge regarding molecular stereochemistry.
  Known stereochemistry can be exploited and implemented in
  macromolecular refinement in the form of geometric constraints and
  restraints. [...]

  We know from accurate and precise small molecule and peptide fragment
  structures [...] that bond lengths and bond angles show distinct and
  relatively narrow distributions around their mean positions. [...]

  Refinement programs read restraint target values specific for each
  residue and each ligand molecule from restraint library files, which
  are subject to continuous empirical update.

The value given in this book (Table 12-1) for peptide bond C-N is 1.336 Å with variance 0.023 Å.


One thing to remember when you uproot a plant is that some of the smallest structures break off most readily. What you will usually see after uprooting the plant are the largest parts of the root structure, but there are often smaller parts which have broken off.

Root structure is highly variable, but the general idea is that one or more primary trunk-like roots strike out toward the most important water sources, and from those primary roots, smaller roots branch out to more broadly extend the reach of the root system. Depending on the size of the plant, there may be several levels of branching, just like you might find in the top of the plant.

Generally, the nutrients that the roots need to absorb come to the plant with the water. They become dissolved in the water and the roots receive them along with the water. Dirt is chunky, not usually homogenous. So there may be more of the nutrients a plant needs in one area than another, or water may flow more easily through one area than another. The roots are able to grow in the direction of what they need, which is why you will occasionally find strong roots actually breaking into plumbing to get at your water. Mostly, it is water that they seek out, because the nutrients are dissolved in the water, but the plant may also show preference for a more nutrient rich stream over a larger, cleaner water source. The roots seek out what the plants need over the long term as they grow in one direction or another. For many plants, by the way, this means a simple strategy of simply growing straight down (a tap root), because that's almost always where they find more water with more of the right stuff dissolved into it. This is similar to the fact that many plants grow as tall as they can because that's where they will find the most sunlight, though the general idea is to grow leaves wherever that light might be captured.

Wherever the primary roots land themselves, the smaller root branches extend into the space to absorb as much as they can. They have to be greedy, because there may be days or even weeks when the ground gets very dry, so they have to get while the getting is good. If one of these smaller branches finds itself in a particularly sweet spot, the plant grows that branch more than its neighbors, which is part of how it places its largest root branches in the best spots.

Another very interesting part of the story of how the plant covers the maximum area of soil is symbiosis. I recommend further research into mycorrhizae, especially if you are a gardener. It's absolutely fascinating, and an important part of the story of how plants absorb nutrients and water.

I know less about the microscopic porous cellular structure of the roots. They essentially serve the same purpose as our stomachs and there are some loose similarities to be drawn, but of course, plant tissues, made of plant cells, which have a cell wall are very different from animal tissues.


I have to say that this seems like a really odd approach to figuring out your diet.  The question of whether insulin increases satiety has been more specifically studied in the literature, as has the satiety generated by equicaloric portions of various kinds of foods, as have the actual effects of various specific diets in human feeding studies.  If you do a bit of digging, I'm sure you can find studies relating high/low GI diets to medically important outcomes (weight loss, blood lipids, fasting insulin levels, etc.), as opposed to their effect on one proposed satiety/fat regulation hormone (leptin).  Your approach also ignores leptin and insulin sensitivity, which might be as important as the levels themselves.  As someone concerned with which foods to actually eat, empirical studies of actual diets seem like the best place to look.

Anyway, here are a few relevant citations to help answer your question:

This study found a increase in serum leptin levels in type I diabetic children who started insulin therapy:
Flück CE, Kuhlmann BV, Mullis PE. "Insulin increases serum leptin concentrations in children and adolescents with newly diagnosed type I diabetes mellitus with and without ketoacidosis." Diabetologia. 1999 Sep;42(9):1067-70.
http://www.ncbi.nlm.nih.gov/pubmed/10447517

A slightly smaller study asked the same question, and found no increase in leptin levels:
McCormick KL, Mick GJ, Butterfield L, Ross H, Parton E, Totka J. "Leptin in children with newly diagnosed type 1 diabetes: effect of insulin therapy." Int J Exp Diabetes Res. 2001;2(2):121-7. http://www.ncbi.nlm.nih.gov/pubmed/12369715

An in vitro study of rat fat cells does indicate a direct increase in leptin secretion/production when given insulin:
Barr VA, Malide D, Zarnowski MJ, Taylor SI, Cushman SW. "Insulin stimulates both leptin secretion and production by rat white adipose tissue." Endocrinology. 1997 Oct;138(10):4463-72. http://www.ncbi.nlm.nih.gov/pubmed/9322964 http://endo.endojournals.org/content/138/10/4463.full

...and in human fat cells:
Wabitsch M, Jensen PB, Blum WF, Christoffersen CT, Englaro P, Heinze E, Rascher W, Teller W, Tornqvist H, Hauner H. "Insulin and cortisol promote leptin production in cultured human fat cells." Diabetes. 1996 Oct;45(10):1435-8. http://www.ncbi.nlm.nih.gov/pubmed/8826983

Leptin levels are positively correlated with insulin levels and BMI (presumably as a proxy for fat mass?):
Lambrinoudaki I, Christodoulakos G, Panoulis C, Botsis D, Rizos D, Augoulea A, Creatsas G. "Determinants of serum leptin levels in healthy postmenopausal women." J Endocrinol Invest. 2003 Dec;26(12):1225-30. http://www.ncbi.nlm.nih.gov/pubmed/15055477

Thierry Thomas, Bartolome Burguera, L.Joseph Melton III, Elizabeth J. Atkinson, W.M. O'Fallon, B.Lawrence Riggs, Sundeep Khosla, "Relationship of serum leptin levels with body composition and sex steroid and insulin levels in men and women" Metabolism Volume 49, Issue 10, October 2000, Pages 1278–1284 http://www.sciencedirect.com/science/article/pii/S002604950041783X

This study found a positive relationship between changes in insulin levels and leptin levels, though it sounds like only in women. (I don't have the full text to check, and the abstract was ambiguous):
Widjaja A, Levy JC, Morris RJ, Frayn KN, Humphreys SM, Horn R, von zur Mühlen A, Turner RC, Brabant G. "Determinants of within-subject variation of fasting serum leptin concentrations in healthy subjects." Exp Clin Endocrinol Diabetes. 2000;108(3):208-13.
http://www.ncbi.nlm.nih.gov/pubmed/10926318

So based on an incomplete and cursory literature search, it seems likely that injecting insulin increases leptin production, as do some other activities that tend to increase insulin.  The evidence for causation in humans is not totally clear cut, though suggestive.


Can viruses be used to extract oil from algae?

Viruses hijack the hosts translational machinery, forcing the host to downregulate translation of other proteins in favor of viral proteins. Your cells will eventually lyse, but in the meantime they would not be producing the enzymes required to make whatever product it is you're trying to get, likely resulting in low yields that are contaminated with virus.


Why eyes don't get heated while converging sunlight into retina?

If you look straight at the sun, you do burn your retina, in the same sense as you get burnt by contact to a hot surface: living tissue is full of water, so the burning process does not look the same as for dry paper e.g., and the harm will be done long before combustion.

To go a  little further, the first layer of retina in vertebrates is made of so-called Muller cells, which conduct the light as optical fibres do to the photoreceptor cells, but it has also been argued that they can in some measure filter too strong light in order to protect photoreceptors. See http://www.pnas.org/content/104/20/8287.full

These cells are also strongly vascularised, which allows to regulate its temperature. You can read http://creation.com/mueller-cells-backwardly-wired-retina-v-dawkins


Species-ID: What is this thing attached to my wall (California, USA)

This is very likely a chrysalis (or pupa) stage of a lepidopteran.

A similar looking example belongs to the giant swallowtail butterfly (Papilio cresphontes).

 Source: Bill Frank

P. cresphontes is found in southern California [source], so it would not be unreasonable to find it in Simi Valley.


How do S and L cone cells sense colors like deep blue and red beyond their peak?

The answer is actually present in your chart: color perception depends on the ratios of activations of different photoreceptors. For example, as you go "more red" from 575, the responses of the Green photoreceptors are falling off more quickly than the Red ones. The same is true for any colors in between, and on the other end, where 400nm light would activate only the blue receptors, whereas at 445nm there would be some mix of activation of the green.

From the context of Fisher information it is actually interesting that photoreceptors don't actually provide much color discriminability at their peaks.

For example, around 575 nm, the "red" photoreceptors actually don't provide very good color discrimination: the response to 565 or 585 is going to be almost identical, for example. The way you can perceive a difference, though, is that the response from the green photoreceptors will be very different at those two wavelengths (just consult your chart!). In vision, as in all the other senses, the information is really held in the slopes!


Is agriculture really a net contributor of greenhouse gases?

The issue is that it is not always a cycle, when you drain wetlands or burn forests to make more farmland that's not a cycle that is permanent change. A change that can continue having effects for centuries. Then of course you have petroleum fuel used to run tractors and the production of fertilizer which are often not cycles either but pure extraction.

One of the reason the number varies so much is because of disagreements about what falls under agriculture, does the fuel used to run a cargo ship moving bananas count? How about mining equipment used to extract minerals used to make fertilizer? Many simply forget to include things like peat bogs or changes in soil bacteria.

For instance draining a peat bog releases tremendous amounts of carbon, as a functioning net carbon sink is changed into a carbon producer. Sometimes this happens as water is diverted to farmland but often it is done just on purpose to get more farmable land. Exact impacts vary from place to place leading to wide ranges of estimations further complicating it.


Why is Turner syndrome rarer than Klinefelter syndrome?

First of all, they are not caused by the same mechanism. They are both aneuploidies, but the mechanism is different.

Turner syndrome happens when one of the gametes (most commonly father's) lacks a copy of X chromosome, or the X chromosome is heavily damaged. This means that while normal women have two X chromosomes, Turner women have only one, and nothing else.

Klinefelter syndrome happens when one of the gametes retains an extra copy of the X chromosome. This way a Klinefelter man has two X chromosomes and Y chromosome instead of one X and one Y.

As you can see - the Turner woman is lacking some genetic information, while the Klinefelter man has too much of it. Generally, having too much genetic information is much easier to survive than not having enough of it, so this explains the relative difference on the most basic level.

But, you might say, what about Barr's bodies? Don't the women use only one X chromosome in each cell? And wasn't Y chromosome almost empty?

Yes, these are an important consideration for these two syndromes. In each cell of a women's body one of the X chromosomes is inactivated and folded into a Barr's body. This inactivation is random, so part of the cells keep mother's and part of the cells keep father's X chromosome active. The trick is that the Barr body is not entirely inactive (Genes That Escape From X Inactivation). Only about 15% of the genes are active, but just the lack of them is mostly lethal (Turner fetuses are usually aborted, Wikipedia quotes olny 1% surviving until birth), and accounts for the health problems and deformations in Turner women.

A Klinefelter man has two X chromosomes in addition to his Y chromosome, so one of the chromosomes inactivates into a Barr body. The presence of Y chromosome directs his body to develop into a male pattern, but at the same time, the existence of Barr's body with those still active genes, causes his body to develop also feminine features. There is little to cause spontaneous abortion.


Is there any possible way to take a DNA test without using blood in humans?

Yes, we don't have to use blood to extract DNA for testing.
There are many resource we can use include: hair, buccal swabs and urine. And it seems hair can provide good quality of genome DNA.

Here is the paper you may interested: A Simple Method of Genomic DNA Extraction from Human Samples for PCR-RFLP Analysis


Are there any culinary fruits that are not botanically fruits or accessory fruits?

I think there aren't any, with two tentative positive results. Of course, it is hard to prove a negative. But here are my arguments:

Logic. there is little reason for this to happen. A culinary fruit is supposed to be sweet, and plants tend to store sugars in their botanical fruits, not in other parts (although by this logic, there should be tuber-fruits too).
Source checking. I went through two books intended as comprehensive reference works in the kitchen, The professional chef and McGee On Food and Cooking. They don't list a (culinary) fruit which I could identify as a botanical non-fruit, with one contentious case. Note that On Food and cooking's chapter on vegetables is structured according to plant part, and it has a subchapter called "fruits used as vegetables" - but it does not have a chapter of "vegetables used as fruit" or similar.
Language. People tend to mix up the two categories of "culinary fruit" and "botanical fruit" until the difference is pointed out to them. While they don't follow the correct botanical definition of fruit, a plant part seems to have to check the "used by the plant for reproduction" check box to be called a fruit, to the point where many words related to "fruit" evoke a harvest-like image such as "to come to fruition", or also words for "barren" in many languages which literally translate to "without fruit", e.g. the German unfruchtbar. So even when a food fulfills the "plant part" and "sweet snack" criteria, it is not called a fruit if it's not (commonly perceived as) a seed container.

The contentious case coming from the books is rhubarb. The professional chef lists it as a fruit, while McGee calls it "a tart stand-in for fruit" in the vegetable chapter, and mentions it again in the fruit chapter, as "a vegetable that often masquerades as a fruit". Kitchen terminology is by no means standardized, so if you were to question random cooks about rhubarb categorization, I guess you'd get a mixture of "a fruit" , "a vegetable" and "I don't know" answers.

An idea I had while writing the answer: maybe you can count ginger. Ginger has many uses in the kitchen, but it is available as a candied snack, which is else only common for fruit. McGee lists it as a spice, although he explicitly speaks of "the dried spice" without giving a category for the fresh rhizome. I think most cooks won't dub ginger "a fruit" but would be willing to include candied ginger in a bowl of mixed candied fruit.

Some petals and leaves are also made into jams, which would support a fruit categorization. Nevertheless, I've never heard of them being referred to as fruits. Prominent examples are rose petals, violet petals and verbena leaves (although one could argue that preserving verbena produces a herb jelly, not a jam).

This answer encompasses Western cooking traditions. It is possible that other cuisines have a different view of what a "fruit" is - for example aloe is frequently used in sweet preparations, maybe the leaf flesh is eaten as fruit somewhere.

So in the end, it comes mostly to your willingness to stretch the definition of a culinary fruit. It is certainly not the case for the most commonly eaten fruits.


Is there a preferred sleeping position for humans?

The enWikipedia article summarizes the best/only real research on positions that I am aware of.  I read a book in high school (that is to say it was old and I have no idea what the title was) that claimed that the semi-fetal position was the best, as it supposedly maximized protection without compromising breathing too much.  I can't say I've seen anything that would indicate your head's direction actually matters, except as it depends on the position of the rest of your body.  Do you mean facing North or the door?  That's some Feng Shui stuff or something similar, which is meaningless.

In terms of which side to sleep on, there is actually an answer!  Well, maybe.  Sleeping on your left side aggravates heartburn more than sleeping on the right side1, but sleeping on your left may be somewhat associated with heart problems.2  From what I can read from the studies, the heartburn one sounds more causative, but then again dying is worse than a little heartburn...  In the end, though, about the only thing that matters is that sleeping on yours side can lower the amount of snoring (annoying) and sleep apnea (unhealthy).


Do bacteria with multiple flagella move faster than bacteria with a single flagella?

Note: in the following I'm going to focus on E. coli, which is the best understood system for bacterial flagellar movement. It would be interesting to compare uniflagellate bacteria and bacteria that have a fixed number of flagella. However, I know about E. coli and I think there is something interesting to be learned just from them, so I'll continue.

You're in luck that you asked this question when you did: a very cool paper (1) was published just last year addressing your question. They find that the number of flagella has only a small effect on bacterial motion, but to understand why requires some background (A lot of the following background comes from this paper, which summarizes it pretty well).

I would argue that E. coli movement is one of the best-understood examples of cell movement we have, with excellent, high-resolution, quantitative data being generated for over 40 years now (the king in this field is Howard Berg at Harvard, if you want to learn more just read a recent review from him).

E. coli have a variable number of flagella, from one to ten or so. They operate in a bundle, but this bundle is highly dynamic due to the way E. coli moves. Rather than proceeding continually a straight line like a car, E. coli moves by a series of starts and stops called a run-and-tumble: the bacteria moves in a straight line for a short amount of time (a run), and then it stops in its tracks and changes direction (a tumble) before starting off again (2). At a first pass this run-and-tumble behavior is essentially diffusion, the bacteria covers a lot of ground without going anywhere on average unless there's some food nearby, in which case the run-and-tumble is slightly biased so that the bacteria drifts toward the food.

As I said, during runs the flagella are bundled together and all turning counter-clockwise. A tumble happens when the bacteria sends a signal to the flagella to start turning clockwise. This breaks apart the flagellar bundle and sends all the flagella in different directions. Up until the paper I mention above, it was still not clear exactly how many flagella need to start turning clockwise before the bundle breaks up and a tumble commences.

Now you can see why having more flagella might not necessarily be a good thing: you might be able to move faster during the run (though this is not obvious to me, given the sometimes unintuitive nature (3) of low-Reynolds number fluid dynamics) but at the same time the flagellar bundle will be more sensitive to break-up because with more flagella come more opportunities for one to start moving counter-clockwise and mess things up.

As the authors of the above paper (1) find, it turns out that there are correlations between the actions of different flagella in a bundle, so that a bacteria with many flagella effectively acts like a bacteria with fewer flagella. The result is that the overall pattern of run-and-tumble is not much affected by the number of flagella; you might argue that number of flagella has a minor effect on bacterial movement.

On the other hand, you might be interested not in the net movement of a bacteria, but just on its speed when it's moving forward, in the run phase. Unfortunately I wasn't able to find any good measurements of the run velocity of a bacterial cell as a function of number of flagella. But hopefully given this recent paper, maybe such measurements are on the horizon!

(1) Mears PJ et al. (2014) Escherichia coli swimming is robust against variations in flagellar number. eLife 3:e01916.

(2) Turner L et al. (2000). Real-time imaging of fluorescent flagellar filaments. J. Bacteriol. 182(10): 2793-2801

(3) Purcell EM. (1977). Life at low Reynolds number. Am. J. Phys. 45: 3-11.


Folate, or rather its active form tetrahydrofolate (THF), is a coenzyme that carries a 1-carbon group. The carbon group can occur in various redox states: CH3-THF (methyl-THF), CH2-THF (methylene-THF), CH-THF (methenyl-THF) or CHO-THF (formyl-THF). These can be interconverted by a variety of enzymes, and are used by cells to synthesize a number of products, including nucleotides and methionine.

MTHFR (methylene-THF reductase) converts CH2-THF into CH3-THF. The CH3-THF form is the most abundant folate in blood, and is therefore considered the "transport" form of folate. CH3-THF is also the form used to synthesize methionine, in the reaction

CH3-THF + Homocysteine $\rightarrow$ THF + Methionine

catalyzed by methione synthase (gene symbol: MTR). This enzyme requires cobalamin (B12) as a cofactor. Actually, the reaction occurs in two steps,

CH3-THF + Cobalamin --> THF + CH3-Cobalamin
CH3-Cobalamin + Homocysteine --> Cobalamin + Methionine

Loss of MTHFR leads to deficiency of CH3-THF, causing methionine synthase to run out of substrate, and homocysteine to accumulate. Lack of the B12 cofactor also blocks methionine synthase, and it should be clear from the reactions above why supplementing with either CH3-THF or CH3-cobalamin can alleviate the problem (at least in theory). I would guess the phenotypes seen in this condition is mainly due to lack of methionine though, rather than excess homocystine, since methionine is required for a variety of methylation reactions in cells.

This is a simplified view. There are many other interactions between B12 and folate; for example, the methinine synthase reaction is needed for cells to take up and store folates, and therefore B12 deficiency can create a folate deficiency as well. See for example http://www.ncbi.nlm.nih.gov/pubmed/6115113 and http://www.ncbi.nlm.nih.gov/pubmed/10466189 for further reading.


On which date did the official name change of Lactobacillus sanfranciscensis change?

Lactobacillus sanfranciscensis first shows up in pubmed in Gänzle et al. (1998). They reference Trüper and De'Clari (1997) for the name Lactobacillus sanfranciscensis. The latter say:

  As none of them makes sense in the nominative apposition construction,
  we hereby correct these names to forms that are in agreement with Rule
  12c as follows.

  ...

  Lactobacillus sanfrancisco ("the city San Francisco") is corrected to Lactobacillus sanfranciscensis (adjective: "from San Francisco").

That issue of Int J Syst Bacteriol was published 1 July 1997, so I guess that's your date.

References

Gänzle M G, M Ehmann, and W P Hammes. 1998. Modeling of growth of Lactobacillus sanfranciscensis and Candida milleri in response to process parameters of sourdough fermentation. Appl Environ Microbiol 64(7):2616–2623.

Trüper H G, De'Clari L. 1997. Taxonomic note: necessary correction of specific epithets formed as substantives (nouns) "in apposition." Int J Syst Bacteriol 47:908–909.


No, p53 and other tumor suppressor proteins do not belong to Cyclin dependent kinase(CDK)family. p53 blocks the cell cycle by promoting the synthesis of Cyclin dependent kinase inhibitors (CKI proteins). These CKI proteins bind with the Cyclin and CDK complex and inhibit the cell cycle at G1 checkpoint.

(Image Source:  https://www.khanacademy.org/science/biology/cellular-molecular-biology/stem-cells-and-cancer/a/cell-cycle-regulators)

p53 also plays role in activating DNA repair enzymes and if DNA is not repaired, p53 will promote apoptosis, so that defective DNA is not passed on.

These all proteins are structurally homologous to p53, so together they are known as p53 family.

(Via: https://www.frontiersin.org/articles/10.3389/fonc.2014.00285/full)


How are smell and taste in fish differentiated?

Short answer
One way to distinguish between the olfactory and gustatory system in fish is by their  anatomical differences. For example, olfactory receptors are clustered in the nasal region, while gustatory receptors are scattered in the head region and beyond. In turn, olfactory information is sent via a single cranial nerve to the brain, while the gustatory system includes three cranial nerves.

Background
The olfactory and gustatory system both receive their inputs through chemoreceptor cells. The chemoreceptor proteins in both systems are G-protein coupled receptor systems. However, the olfactory and gustatory systems are anatomically separated.

The olfactory end organ is in fish comparable to that in humans, namely sensory epithelia situated in nostrils. The olfactory receptor cells form axons that are grouped into the olfactory nerve (cranial nerve I). The nerve innervates the olfactory bulb, where its axons synapse onto mitral cells. Mitral cell axons group into the olfactory tract that projects to the telencephalon in the brain.

Schematic of olfactory system of a fish (not all structures shown). Source: Global Warming Australia.

The gustatory end organs are less well anatomically localized. The taste buds can be found in various structures including gills, barbels, fins, oral cavity and pharynx, dependent on the species. Unlike the olfactory system, gustatory information is transmitted to the brain via three separate cranial nerves: facial (cranial nerve VII), glossopharyngeal (cranial nerve IX) and vagal nerve (cranial nerve x). Normally, the facial nerve innervates taste buds on the extraoral surface, the glossopharyngeal on the anterior part of the oral cavity, and the vagal nerve on the pharynx. The facial and vagal nerves respectively terminate in the facial and vagal lobes in the medulla. The glossopharyngeal nerve terminates in a dorsal medullary region between the facial and vagal lobes.

Reference
- Hara, Rev Fish Biol Fisheries (1994); 4: 1-35


Does applying sugar to the tongue taste buds releave sugar withdrawal symptoms?

Theoretically if you could somehow activate the G-protein-coupled receptors (GPCRs) corresponding to sweet stimuli without absorption of the sugar into the bloodstream than it may be possible to "trick" the brain. (See this review to learn more about how taste signaling works). However, the process of absorbing sugars into the blood stream begins in the mouth (see this question), so testing your idea would be nearly impossible.


Meaning of letter "c" in description of mutation: "Homozygous c.195C>G; (p.Cys65Trp)"

I typed "c dna mutation" in Google and this article was the first hit:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1867422/

The "c" denotes coding DNA, which given the context of the amino acid mutation having the letter "p", this makes sense.


Relation between OD with different microbial growth

Difficult to say with the information you have given. Here is a paper on the subject if you are interested. The relationship between OD and cell count depends on morphology and size, which in turn depend on culture condition, strain, etc...


For human IgG1 and 4, the only inter-heavy chain disulfide bonds are the two in the hinge region. IgG2 has 4 disulfides in the hinge, and IgG3 has 11:

There are intra-heavy chain disulfides in the Fc region, and of course there are non-covalent bonds between the two heavy chains (as well as the light chains) to maintain structure, but aside from the hinge region the only other inter-chain disulfides are between heavy and light.

Here is an interesting review of classical (determined in the 1960s) and non-classical (more recently discovered) disulfide bond formation and structure in human IgGs.


The animal is very suggestive for Dog whelk-like mollusc removed from its shell.

I try to mark the organs, do not rely on these marks as an absolut.

Testis
Renal vein
Gill
Mantle
Prostate
Osphradium

10 and others - digestive and reproductive systems, cannot mark precisely.

Digestive gland

source for comparing etc


How to restrict a BLAST search to include only a few protein sequences?

The gene identifiers that you get in BLAST output depends on the identifiers used during the BLAST database construction. So you may not find the exact identifier you are looking for.

For restricting the BLAST results to a smaller set of proteins/nucleic acid you can choose either of the two:

Make a database with the fasta sequences of the proteins/nucleic acids that you want. You have to install BLAST and run it from the commandline. Use makeblastdb to make the database. Now you align your queries against this database. Note that now your e-values would not be the same as what you would obtain from a search against the bigger database.
As you said in the question, you can parse the results later. You would have to know what identifiers were used in the blast database that you searched against. ExPASy-BLAST would most probably use the UniProt IDs (there is an ID convertor in the UniProt website to map UniProt IDs to other IDs). If you use NCBI-BLAST (nr database) then you would need to know the GenBank IDs.


How is the mRNA transported out of the endoplasmic reticulum?

The proteins mediating the transport of mRNA out of the nucleus (nucleoplasm/karyoplasm) are called "karyopherins" and belong to the nuclear pore complex family.

Prior the creation of the final form of mRNA, various proteins are attached to the so called pre-mRNA and a mRNA-protein-complex is built (co-transcriptional). Some of these proteins carry factors for splicing and processing, later RNA-binding proteins are added. (RNA binding proteins such as $Npl3p$, $Gbp2p$ and $Hrb1p$ (serine/arginine-rich proteins) accompany mRNA out of the nucleus. )

After mRNA processing mRNA export is initiated by dephosphorylation of $Npl3p$, leading to binding of $Mex67$ (Saccharomyces c.), forming a complex that interacts with the nuclear pore complex.

That is the way mRNA is able to leave the nucleus.


Concentration of a specific promoter in a cell?

In a diploid organism there are two copies of DNA which means two copies or "molecules" of promoter in the entire cell. The volume of a typical eukaryotic cell (HeLa) would be 2.25×10-12 litres (Zhao et al. 2007, BioNumbers).

$$\text{Concentration }(M)=\frac{\text{Molecules per cell}}{\text{Avogadro No.} \times \text{Volume of the cell }(l)}$$

This comes to around 1.4758×10-12 M for 2 molecules of promoter. Accordingly, you can calculate for a haploid cell, multiple alleles or prokaryotic cell.

You can also assume a 2-compartment model with nucleus and cytoplasm as two different compartments. In this case, the DNA would be localized in the nucleus and therefore its effective concentration would be higher in the nucleus. You can look up nuclear volume in BioNumbers and plug that in the above formula to obtain the effective concentration.

Zhao, L., et al. "Intracellular water‐specific MR of microbead‐adherent cells: the HeLa cell intracellular water exchange lifetime." NMR in Biomedicine 21.2 (2008): 159-164.


How correlated are proximally related CpG sites in human DNA?

I've got to dash off so I won't be able to give a fully in-depth answer today, but this basically boils down to the concept of CpG islands.  Something like 70-80% of CpGs are methylated in humans, so if they were randomly scattered around the genome there is already a pretty high chance nearby CpGs are in the same state.  However, because of CpG islands, CpGs of similar state are indeed grouped together, depending on promoter activity (to simplify things a bit).

That being said, if you look for articles that cite your article, a plethora of useful references show up.  In particular, this bad boy has a handy figure 1 which displays the overall landscape.  Maybe that's too broad of a view, but in general, like methylation patterns cluster together; otherwise, there'd be no such thing as a methylation pattern!  This paper has a neat figure which sums it all up nicely:

Basically, it's usually high-methylation or low-methylation; rarely is there anything in between.  There's a lot more in there so I'd recommend going through some of them; I'll try to get back to this later.


Does the brain have a clock and can it be sped up?

While the brain is often compared to a computer (sometimes even rightfully), one key aspect people often overlook is that the brain is inherently analog, whereas computers are inherently digital:

All a computer really does in any single operation is to combine 0's and 1's really really fast - and the faster it's able to do that, the faster it will generally be.

A brain however, fundamentally works by combining a multitude of signal inputs with varying strength's and each single operation (encoded by a single neuron) will give output depending on the weighted sum of all inputs.
Such a 'single operation' in itself is reasonably fast, whats make a brain 'slow' is the propagation of the signal to next neuron/operation: Brains are orders of magnitudes bigger than computer chips and instead of metal/wires they use concentration gradients to propagate the electrical signals. Of course it's possible to increase the speed on individual connections between neurons by insulating them, which nature already does.

However, you can't just 'overclock' the whole brain, because there's simply not enough space to add 'full insulation' to every single connection between two neurons (of which there a lot: ~100 billion neurons, with a couple thousand connections each) and because electrical signal propagation by concentration gradients will always be slower than by wires.

I guess if would replace all neuronal connections with metal wires and some concentration gradient to power/voltage/frequency converter using nanobots, you could potentially speed up the brain - or just built cyborgs instead.

Also, not really what you asked  -  but there IS a clock in the (mammalian) brain and changing it speed, will seriously mess with your day/night or sleep rhythm.


What part, roughly, of the carbon in a plant comes from the soil? As opposed to the atmosphere?

Only a small fraction of plant carbon is soil-derived: e.g. from Majlesi et al 2019:

although the majority of plant C was obtained from atmosphere by photosynthesis, a significant portion (up to 3–5%) of C in plant roots was derived from old soil"

(in an experiment with Scots pine and reed canary grass).
As laid out by this review of C4 photosynthesis, the primary reason for differential isotopic make-up of C3 and C4 plants is that the biochemical pathways they use fractionate isotopes differently — not because the plants' requirements are different.

Because of the very different
affinities of Rubisco and PEP
carboxylase for CO$_2$ , C$_3$ and C$_4$ plants
differ in the carbon isotopes that they
assimilate. While most atmospheric
CO$_2$is made up of ${}^{12}$C, a small fraction
includes ${}^{13}$C. Rubisco has a fairly high
$K_m$ and hence low affinity for CO$_2$, and preferentially fixes ${}^{12}$C. The ratio of ${}^{13}$C
to ${}^{12}$C ($\delta^{13}$C) in a C$_3$ plant is thus much
lower than the ratio in the atmosphere;
the carbon in structural and storage
carbohydrates contains much less
${}^{13}$C. PEP carboxylase has a lower
$K_m$ for CO$_2$ than Rubisco and hence
a higher affinity; as a consequence it
discriminates much less against ${}^{13}$C
than Rubisco does, so that the $\delta^{13}$C
is appreciably closer to atmospheric.

Majlesi, Soroush, Jukka Juutilainen, Anne Kasurinen, Promise Mpamah, Tatiana Trubnikova, Markku Oinonen, Pertti Martikainen, and Christina Biasi. “Uptake of Soil-Derived Carbon into Plants: Implications for Disposal of Nuclear Waste.” Environmental Science & Technology 53, no. 8 (April 16, 2019): 4198–4205. https://doi.org/10.1021/acs.est.8b06089.


Null hypothesis of Chi-square test for independence

It might help if you first ask yourself what the independence test is for in plain English, you are testing to see if one categorical variable has
an influence on another. In other words, if a person (or whatever)with attribute X (for example, is bald) are they significantly more/less likely to have attribute Y (like being allergic to penicillin) than someone who does not have attribute X.

So in your example the alternative hypothesis would be (in words): the ratio of males with attached ear lobes compared to males without is equal to the ratio of females with attached ear lobes compared to those without.


Are all chromosomes equally susceptible to mutation?

terdon is spot on with the recombination hotspot comment. Mutations are often associated with recombination (information gets lost during crossing-over, so DNA repair is necessary, which of course can introduce mistakes/mutations). It's a fact that there areas in certain chromosomes where recombination happens much more often than other areas of the chromosome. So it follows that chromosomes with more hotspots would likely have higher mutation rates than other chromosomes, on average. This does raise the point, though, that perhaps it's not the mutation rate of the entire chromosome that matters-maybe mutation rates at a more-local level (such as near a hotspot or far away from a hotspot) are more worthy of consideration for your question.
Also, I imagine that sex chromosomes have much lower levels of polymorphism than autosomes. This doesn't have to be because of a lower mutation rate, though: another explanation would be that deleterious recessive mutations on the X chromosome would be purged more easily than on autosomes because their phenotype appears in males (who don't have a second allele because they don't have another X chromosome, so the deleterious phenotype can't be "hidden" like it would in a heterozygote).


When did death due to aging first appear?

(Not an evolutionary biologist, but I couldn't resist :)

I don't think your premise is correct. In (symmetric) cell division, we should consider that the old cell "disappears" and two new cells appear; neither of the two daughter cells is the parent cell, they are both descendants of it (hence the term "daughter cells"). The parent cell is gone. Therefore, at least for symmetric cell division, the lifetime of a cell equals the length of a cell cycle. So cells are not immortal --- only the cell lineage is.

Asymmetric cell division (as in stem cell division, not budding) is more tricky. Here it might seem as if there really is an immortal cell (the "stem cell") generating "mortal" offspring. But I think the situation is really the same as in symmetric cell division: most of the cell cycle mechanisms are identical, and again two new daughter cells are generated, and the parent cells disappears. The asymmetric part is that only one of the two daughter cells are "permitted" to continue the line. Again, the cell line is immortal, the cell is not.

But this is still true in higher organisms: the germline is an immortal line, while the somatic cells are not. So the key difference between higher organisms that have a clear life span and unicellular organisms is the appearance of cells that do not generate offspring, but instead support the cells that do.

I'm not sure there is a sharp transition from single cells to the germline/somatic cell situation. Intermediate cases are found in all sorts of single-celled organisms where certain cells "decide" that it's better to support their (genetically identical) neighbor in some way to rather than divide themselves; these are a form of "somatic" cells. All sorts of community behavior in bacteria and other microorganisms could be viewed in this way. During evolution this behavior has gradually got encoded into the DNA itself, with more and more sophisticated "support systems". Higher animals are really just the latest version of this, where the entire body is really just a support system to ensure survival of the germline.

I would suggest reading Richard Dawkin's books on this subject, especially The selfish gene. They are well written and quite accessible.


Semantics aside, I think the OP wants a group of animals which are  grouped together as related and which are extinct.  I propose trilobites.  They are no more but at one time they ruled the earth.

from https://en.wikipedia.org/wiki/Trilobite

  Trilobites ( /ˈtraɪləˌbaɪt, ˈtrɪ-, -loʊ-/;[2][3] meaning "three
  lobes") are a fossil group of extinct marine arachnomorph arthropods
  that form the class Trilobita. Trilobites form one of the earliest
  known groups of arthropods. The first appearance of trilobites in the
  fossil record defines the base of the Atdabanian stage of the Early
  Cambrian period (521 million years ago), and they flourished
  throughout the lower Paleozoic era before beginning a drawn-out
  decline to extinction when, during the Devonian, all trilobite orders
  except the Proetids died out. Trilobites disappeared in the mass
  extinction at the end of the Permian about 252 million years ago. The
  trilobites were among the most successful of all early animals,
  roaming the oceans for over 270 million years.[4]


Bone conduction . Different from the normal hearing phenomena in humans?

Prologue: Bone conducted signals are considered to be evoked by the perilymph fluid moving back and forth out of the cerebrospinal cavity, via the cochlear aqueduct, towards the scala tympani. And not by mechanical deformation of the cochlea. “the fact that the bone conduction phenomenon is actually the result of the push-pull movement of the perilymph fluid instead of the presumed deformation of the bony structures.” some text to refer:
Applying physics makes auditory sense.

I am affiliated with this book. I am the co-author of the Appendices.

Year Article Author(s) Source
2010 1 Applying physics makes auditory sense : a new paradigm in hearing
Abstract  |  Full-text Heerens, W.C., Ru, J.A. de Medicine (2010), pp: 1-74

pp: 13:
Objections against the existing bone conduction signal transfer hypothesis: The common model for the transfer of a bone conducted signal is based on the vibration of the temporal bone. However, both the material and the construction of this bony envelope are extremely rigid, while the cochlear shape of the cavity excludes the possibility that parts of this cavity can function as the hypothesized resonators. Therefore, sound stimuli cannot be transferred in such a manner. Certainly not the weak vibration signals with pressure variations of approximately 20 mPa, equal to a pressure variation of
0.2 x 10^-6 atmosphere that are generated by a normal sound stimulus of 60 dB SPL. Hence ‘bone conduction’ must have a cause other than the deformation of the rigid petrous bone that forms the cochlear bony envelope.

The physiological structure data:

• The walls of the cochlear envelope are extremely rigid. Hardly compliant to not compliant at all. So bone conduction based on deformation of that envelope is not possible.

I assume that it is clear, without further explanation that the petrous bone can be regarded as a non-deformable body when confronted with the extremely weak impact of acoustic signals.  We see that for a completely normal 60 dB SPL sound pressure signal, clearly showing that the vibrations of bone in the cochlea offer only extremely small, and therefore completely negligible contributions.  It means that we are talking about deformations which is therefore completely negligible as a possible mechanism for signal transfer. I dare say, no waving arm statements.  Contributions that all result in deformations comparable to an incredibly small fraction, are all leading to naught, one cannot escape the conclusion that there must be another cause for the phenomenon of bone conduction.

Bone conducted signals are considered to be evoked by the perilymph fluid moving back and forth out of the cerebrospinal cavity, via the cochlear aqueduct, towards the scala tympani. And not by mechanical deformation of the cochlea.

pp: 47: It has been established that the rigid cochlear envelope is hardly deformable. This leads to the realistic hypothesis that the ‘bone conducted’ sound signals evoke stimuli by means of a similar process to those of the airborne sound stimuli, namely by means of a push-pull movement of the perilymph, in this case, out of the cerebrospinal cavity via the cochlear aqueduct.

pp: 19-21: Bone conduction: As the petrous bone is the toughest bone in the human body, it is practically impossible for deformation to occur through the vibrating movements that are caused by acoustic pressure changes. Therefore, there must be another means for this signal transfer. A bone conduction audiogram – apart from a reduced transfer of especially the higher frequencies – is not fundamentally different from a pure airborne tone threshold audiogram. It follows that the perilymph movement within the cochlea must somehow also generate the bone conducted signal transfer. And indeed there is such a possibility. The scala tympani is directly connected with the cerebrospinal cavity by means of the cochlear aqueduct, which has its opening in the vicinity of the round window. The cochlear aqueduct enables the perilymph to move backwards and forwards between the cranial cavity and the cochlear channels (scala tympani and scala vestibuli). The perilymph in this cranial cavity is exposed to the alternating pressures caused by the sound induced vibrations of the shell shaped cranial bones that are located in the front and the back of the skull. As a consequence of Newton’s fundamental law of motion we know that when a larger amount of fluid inside the skull must be brought into motion, the effect of these stimuli will be smaller for the higher frequency contributions than for those of the airborne stimuli for similar frequencies. Furthermore, the stapes introduces the airborne signal that results in a backwards and forwards motion of perilymph, in opposite phase to the back and forth motion of perilymph along the
basilar membrane, which is evoked by bone conduction. This results in a slight reduction of the airborne signal, which actually is the stronger of the two stimuli.

pp: 19-21: The alternating movement of perilymph between the cerebrospinal cavity and the scala tympani via the cochlear aqueduct will also be partially directed towards the round window. This splitting up into two directions of the perilymph movement creates a reduced perilymph velocity in front of the basilar membrane, and finally results in a reduction of the bone conduction signal. The rate of reduction depends on the mobility ratio between the oval window and the round window. A further decrease in round window mobility, related to the mobility of the oval window, results in a higher perilymph
movement in front of the basilar membrane, which evokes a higher bone conduction signal, while an increase would result in a lower one.

pp: 19-21: This hypothesis that bone conduction consists entirely of the push-pull movement of perilymph from the cerebrospinal cavity via the cochlear aqueduct, and is evoked by the vibration of the shell shaped bones of the skull, while the rigid temporal bone does not deform at all, is just one logical step further than the functional possibilities indicated by others.