Why are the genomes of Humans 99.5% the same?

In a genome that is 3 billion base pairs, a difference of 0.5% works out to a difference of 15 million bases. When a single base change can change the amino acid sequence of a protein, that can add up to a huge amount of diversity, which is what we see over the nearly 8 billion humans on the planet, and the 99.5% sameness is why we are linked together so closely as a species.

How can the lack of diversity be explained?

  Nothing in Biology Makes Sense Except in the Light of Evolution.

The above quote was made by the evolutionary biologist Theodosius Dobzhansky. What this basically means is that you need to take a look at your question from the perspective of evolution and natural selection.

The first thing you need to note is that there is evidence to suggest that modern humans went through a population bottleneck. What that means is that at a certain point in our history, there were very few individual members of our species alive and this can account for the "lack" of diversity that we see in our genome. The number that is quoted is as low as 10,000 individuals left alive after the supereruption of the Toba volcano about 75 thousand years ago.

That means that there were very few mating pairs left, and that significantly reduced the genetic diversity of our species. This is known as Founder Effect.

  Founder effects

  A founder effect occurs when a new colony is started by a few members of the original population. This small population size means that the colony may have:

  reduced genetic variation from the original population.
  a non-random sample of the genes in the original population.

So if we use an average of 20 to 25 years per human generation, we are only looking at about 3,000 to 4,000 generations since there were maybe only a few thousand breeding pairs of humans. Contrast that with bacteria which can go through three to four thousand generations in less than a week, and you can begin to get a feel for why there is so much sequence homology (sameness) in the human genome. See Bottlenecks and founder effects at UC Berkley's Understanding Evolution site for more information.

You also should understand that any changes that are deleterious will be under strong selective pressure. This may not mean that the organism may not survive to reproduce, in may just mean that on average, they may be less successful; fewer offspring that have fewer offspring in comparison to the rest of the population. At some point that lineage may go extinct, either because the change makes it very difficult to survive, or the offspring make less desirable mates and eventually don't get the opportunity to reproduce.

Any changes that disrupt a vital gene will likely be fatal and will lead to spontaneous abortion or if the mutation was sustained in a sperm, then the inability of that sperm to survive to fertilize an egg, so the sperm that was heavily mutated may just never make it to the egg. The average number of sperm in a single human ejaculation is about 250 million. And yet only a single sperm makes it to fertilize the egg, and that is assuming that a fertilization event takes place. There is an incredible amount of selection that goes on in the act of procreation, even before we get to development.

Why the 99.5% to 0.5% figure might be misrepresentative of the population as a whole.

Another thing that you will want to think about is how the 0.5% to 99.5% number was arrived at. The referenced in the question links to a Wikipedia article Human Genetic Variation. The reference provided for this was from a New York Times article about J. Craig Venter, In the Genome Race, the Sequel Is Personal - Wade, Nicholas. September 4, 2007. The quote that is references in Wikipedia is:

  Biologists had estimated that two individuals would be identical in 99.9 percent of their DNA, but the true figure now emerges as much less, around 99.5 percent, Dr. Scherer said.

The 0.5% figure is provided as a quote from Stephen W. Scherer, who was a coauthor of this paper, The Diploid Genome Sequence of an Individual Human, Levy, et.al. PLoS Biology; September 4, 2007. DOI: 10.1371/journal.pbio.0050254. From that paper the following quote is found:

  Inclusion of insertion and deletion genetic variation into our estimates of interchromosomal difference reveals that only 99.5% similarity exists between the two chromosomal copies of an individual and that genetic variation between two individuals is as much as five times higher than previously estimated.
  - The Diploid Genome Sequence of an Individual Human, Levy, et.al. PLoS Biology; September 4, 2007.DOI: 10.1371/journal.pbio.0050254

So at the very least, the statement was made in a peer reviewed article. However there are some problems with this.

The first is the method of the paper. It looks at a single human genome, that of Dr. Venter, and is used to draw the conclusion of 0.5% difference between any two individuals. And the comparison is made based on the analysis of differences between Dr. Venter's maternal chromosomes and paternal chromosomes. Let's look at what the problems might be here:

It is a huge leap of statistical faith to assume that a single genome is representative of the nearly 8 billion genomes out there.
Dr. Venter's genealogy is English on both parental lineages. We have to remember that there was another population bottleneck in middle ages Europe caused by outbreaks of cholera and the Black Death. This fact may imply that Dr. Venter's lineages are genetically close and that if his lineage were more diverse, say Indigenous Oceanian and English, they may have found a much higher percent difference between maternal and paternal chromosomes.

  The donor's three-generation pedigree is shown in Figure 1A. The donor has three siblings and one biological son, his father died at age 59 of sudden cardiac arrest. There are documented cases of family members with chronic disease including hypertension and ovarian and skin cancer. According to the genealogical record, the donor's ancestors can be traced back to 1821 (paternal) and the 1700s (maternal) in England. Genotyping and cluster analysis of 750 unique SNP loci discovered through this project support that the donor is indeed 99.5% similar to individuals of European descent (Figure 1B), consistent with self-reporting.
  - The Diploid Genome Sequence of an Individual Human, Levy, et.al. PLoS Biology; September 4, 2007.DOI: 10.1371/journal.pbio.0050254

Dr. Venter is male. The Y-chromosome was problematic to sequence, and you cannot really do a comparison between it and the X-chromosome. How would the genome of a woman compare?

  The Y chromosome is 59% covered by the one-to-one mapping due to difficulties when producing comparison between repeat rich chromosomes. In addition, the Y chromosome is more poorly covered because of the difficulties in assembling complex regions with sequencing depth of coverage only half that of the autosomal portion of the genome. The X chromosome coverage with HuRef scaffolds is at 95.2%, which is typical of the coverage level of autosomes (mean 98.3% using runs). However it is clear that the X chromosome has more gaps, as evidenced by the coverage with matches (89.4%) compared with the mean coverage of autosomes using matches (97.1%). The overall effects of lower sequence coverage on chromosomes X and Y are clearly evident as a sharp increase in number of gaps per unit length and shorter scaffolds compared to the autosomes (Figure 3). Similarity between the sex chromosomes is another source of assembly and mapping difficulties. For example, there is a 1.5-Mb scaffold that maps equally well to identical regions of the X and Y chromosomes and therefore cannot be uniquely mapped to either (see Materials and Methods and Figure 3). From our one-to-one mapping data, we are also able to detect the enrichment of large segmental duplications 10 on Chromosomes 9, 16, and 22, resulting in reduced coverage based on difficulties in assembly and mapping (Table S3).
  - The Diploid Genome Sequence of an Individual Human, Levy, et.al. PLoS Biology; September 4, 2007.DOI: 10.1371/journal.pbio.0050254

There is another thing that you need to remember and that is the history of the Human Genome Project. Dr. Venter developed a new method of sequencing and became a commercial competitor to the International Human Genome Sequencing Consortium project. While the International Human Genome Sequencing Consortium project beat out Dr. Venter's enterprise(8), it's approach, to use an amalgamation of the DNA of many donors, some of whom had their DNA included and some who did not, to preserve anonymity, Dr. Venter circumvented this by performing the sequencing on his own DNA. When his team was beat out by the International Human Genome Sequencing Consortium, he doubled-down, invested more time and effort and came up with the sequence put forth in this paper, which had a higher degree of resolution than previous efforts. The paper is making an argument for the value of their technique over the techniques being used by the International Human Genome Sequencing Consortium and is trying to make a claim of the superiority of their method. The data being presented is likely factual, but because of this history you have to look at the paper, the methods, and the motives behind it.

It is only 15.5 years since we had a full draft of a Human Genome Project produced by the International Human Genome Sequencing Consortium. In order to sequence that genome samples were taken from a few hundred individuals. Small stretches of the DNA were sequenced and then all of those pieces were put together in computer. That means that there was a lot of averaging that happened. So by default, the most prevalent base in the population of volunteers at every position was chosen. That means that that should be representative for the rest of the population as well.

When we make statements about comparisons in datasets as large as the human genome, more often than not we are looking at known, small subsets of the genome, and we are extrapolating by statistical methods based on that fact. One thing you learn as you read science papers, and not just science news articles, is that you always need to look at their materials and methods to determine how they arrived at their data and headline numbers. It is often quoted that we have only a 1.5% difference between Humans and Chimpanzees, however when you look at those papers the comparisons were done only on areas of the genomes that lined up well. That isn't to say that there isn't a remarkable degree of similarity between us and our nearest living evolutionary relative, it is just that there is more to the story than the headline.

Also, we don't have that many full genomes sequenced to compare to one another, as a percentage of the 8 billion people alive today. While we have representations from most a vast majority of the ethnic groups identified, we may be missing families with novel lineages.

Another thing that you need to think about is that many of the areas in the human genome are repeats and structural elements that do not encode for genes of affect gene expression. Things like telomeres, which protect the ends of chromosomes, and centromeres which are the attachment points on chromosomes that make sure that the are distributed properly into newly divided cells. These elements tend to stay the same because the proteins that bind to them require that sequence specificity in order to function properly, so those are regions were almost every ones DNA will be the same, and not just between humans. These elements often are very similar in most vertebrates.

We also need to consider structural RNAs. These molecules have functions within the cell that require that there sequences be highly conserved (unchanged). Ribosomal RNAs, Transfer RNAs, Small Nuclear RNAs all rely on their specific sequence to fold properly in order to perform their task in the cell. A single base change can change the folding of these elements and as a result they will loose their function, which means those cells won't be able to produce proteins properly which means that the cells will die. If this is happening in germline cells, then they are not going to be involved in fertilization so any mutations there will be passed on.

I could go on and on, but the take away is that it isn't surprising that there is very little sequence diversity on a percentage bases within the human species, but there are many caveats to that fact as well.

Edit: Significant edits to add relevant, referenced information to back up answer.


Is there a consensus on the CaMV 35S minimal promoter sequence?

In case anybody ever has the same question: I found the answer in this paper by Ow et al. 1987 (fig1)
http://www.pnas.org/content/84/14/4870.full.pdf

Just to clarify, I did not want to boost expression of the enhancer element in my algae, it needed boosting in tobacco protoplasts/leaves.


Would a clone of myself have exactly the same development (character, appearance) as me?

No, your clone would differ from you. Actually such clones exist in humans also. Monozygotic twins are clones. They certainly look alike but they definitely differ in some respects.

Understanding why this is true require one to understand the concept of heritability from the field of quantitative genetics. You should definitely have a look at the post Why is a heritability coefficient not an index of how "genetic" something is?. The main reason why you would differ is because our phenotype (personality, appearance, etc...) also depends on the environment we experience.


Do some genes follow Rock-Paper-Scissors model of dominance?

A quick search gives this same question in this Reddit post.

Apparently, there is not yet an existing example of such dominance of three alleles on one another.

That said, if you're interested in rock-paper-scissor patterns in nature, then you will be interested in the side-blotched lizard. It has three genetically encoded male "sexes", that also determines their behaviour. At a population level, the three sexes follow a rock-paper-scissor pattern of successful sexual competition, in that orange-throated individuals can outcompete yellow-throated ones, which can outcompete blue-throated ones, which can outcome orange-throated ones. A simulation has been carried out to model the underlying genetics, but that model doesn't involve a rock-paper-scissors pattern of genetic dominance.


What are the short/long term effects of chloroquine on fundamental cell processes?

This paper provides many experiments about changes to the endosomal system and autophagy and should be a good starting point.
Most of the treatments are done in the 5h to 24h range typical for cell culture studies. In theis relatively short time frame Chloroquine is well tolerated by cells. However, long term treatment will very likely be different.


Few examples in which placebo looks effective even if it isn't (Wikipedia):

The condition, for example, common cold heals on its own in participants who received a real drug and in those who receieved a placebo.
In psychological and other conditions in which the participants are asked only how they feel after the treatment, some of them may just think that they feel better.
Sometimes neither the real drug nor the placebo work, but the condition has a naturally fluctuating course, so it looks that they both work.


Carl Sagan's ideas on the self-extermination of technological civilizations

It sounds like what you may be referring to is Fermi Paradox:

The Fermi paradox — or Fermi's paradox — is the apparent contradiction between high estimates of the probability of the existence of extraterrestrial civilizations, such as in the Drake equation, and the lack of evidence for such civilizations. The basic points of the argument, made by physicists Enrico Fermi (1901–1954) and Michael H. Hart (born 1932), are:

The Sun is a typical star, and there are billions of stars in the galaxy that are billions of years older
With high probability, some of these stars will have Earth-like planets, and if the earth is typical, some might develop intelligent life.
Some of these civilizations might develop interstellar travel, a step the Earth is investigating now.
Even at the slow pace of currently envisioned interstellar travel, the Milky Way galaxy could be completely traversed in about a million years.

-Wikipedia: The Fermi Paradox
In 1966, the book Intelligent Life in the Universe originally written by I.S. Shklovskii and extended by Carl Sagan "speculated that technological civilizations will either tend to destroy themselves within a century of developing interstellar communicative capability or master their self-destructive tendencies and survive for billion-year timescales."(4)
This review of the book written by E. J. Öpik, questions what, if any, factual information was presented.
In 1983, Sagan cowrote an article for the Quarterly Journal of the Royal Astronomical Society with William I. Newman entitled The Solipsist Approach to Extraterrestrial Intelligence that also addresses the issues of the self-extermination of technological civilizations.


Why are plants unable to take up Phosphorus directly in their organic form like Phytic Acid?

I am not a plant biochemist but would make a couple of points that may or may not be relevant or helpful.

The living organisms that preceded plants had evolved a wide repertoire of systems for transporting ions across membranes, involving variations on a few general designs. Given the importance of inorganic phosphate in living organisms, phosphate transporters would have evolved early on.
Phosphate may have been more abundant in soil before sophisticated evolution of plants led to secondary metabolites like phytic acid. If this were the case it would explain why roots developed phosphate transporters.

This is not to say that it is impossible for organisms to develop transporters for more sophisticated molecules — there are many such examples — but in this case such a development would only be expected if there was such a lack and intense competition for phosphate that it would convey an evolutionary advantage.

This sort of question is always a matter of conjecture. One imagines there is a tipping point when the difficulty of developing a new system is outweighed by the advantage it would bring. This clearly hasn’t happened, but which of these factors is most important is difficult to say (for me, at any rate).


Almost philosophical question about controlling a pest/plague

Biologists are certainly not afraid to exterminate pests and plagues in the wild. See: smallpox and polio. However, such exterminations are nearly impossible and very expensive. See: smallpox and polio. In both cases extinction is through  extensive vaccination, preventing the disease from having any hosts to live in. To achieve this you need to vaccinate a huge fraction of the human population for quite some time.

Practically, how would you go about exterminating an agricultural pest? A beetle, for example? Perhaps an army of men, forming a cordon the width of the united states, turning over every rock and every tree from the west coast to the east coast. With a high net or something to prevent beetles from flying over the cordon. And some method for dealing with cities and roads and tunnels and things, because if you miss only five or six they'll be back soon, depending on life cycle and offspring numbers. Or if you forget Canada.

And to use a biological solution to a biological problem, consider myxomatosis and the Australian rabbit problem. Rabbits were(and are) a pest, myxomatosis is a rabbit plague that has a 99.99% fatality rate and is fiercely infectious. Sure enough, myxomatosis wiped out the rabbit population. A few years later the rabbits were back but now the survivors were resistant to myxomatosis.

I would argue that it's a scientific thesis based on hard lessons biologists have learned about doing 100% of anything. There are many biologists with moral precepts against the extinction of pest species. It's a bit of a moot point, however. The only reliable method of extinction is habitat destruction. Whether that's immunizing all the humans or cutting down the rainforests, it does work. It's just usually impractical.


What is this creature? Where can it be found?

The creature in the man's hand is a baby eel. Giveaways: it has fish eyes and the flattening of the tail. The lower right picture suggests it's a vertebrate (i.e. not a worm.)

Exactly which eel it is is unclear, but you can read more about it in the linked article. Indeed, your first picture appears in the article.

  These transparent wonders are not a species, but rather they are the second stage in the life cycle of a number of eel species in the family Anguillidae. This particular specimen is an American eel, Anguilla rostrata. For the rest of the post I'll focus on the life cycle of this species for simplicity's sake.


Short answer: Indeed the proteins in our body are based on amino acids from external food sources. BUT, proteins up-taken from food are ALWAYS disassembled first into amino acids, through specialized enzymes, proteases, (for instance Pepsin in the stomach's gastric juices and Tripsin in the pancreatic juices), during digestion, in the alimentary canal, (gut). This enables the body's liver to build the proteins most needed by the organism itself, through the processes of transamination, that allows conversion betwixt amino acids, and deamination, that removes N2 from the amino acid, (let's say the "amino" part is removed, and then expelled as urea), to excrete amino acids in excess. In addition this breaking down of external proteins is necessary, since they can act as labels for pathogens, and external organisms in general, and thus would soon be destroyed by the immune system if reused straight away.


Is sexual reproduction outside the same biological family possible? Has it ever occured successfully?

Interfamilial hybrids have never, to my knowledge, been recorded occurring naturally (without human intervention).

In plants, somatic inter-familial hybrids have been produced for a wide variety of species pairs in the lab (e.g. between carrot and barley; Kisaka et al. 1997).

In animals, there are some historical reports of hybrids between chickens (Mathis & MacDougald 1987) or peafowl (Serebrovsky 1929), both in Phasianidae, and guineafowl (in Numididae). The animal example meets your condition of being outside the lab, although they were produced by breeders.

Refs

Kisaka, H., Kisaka, M., Kanno, A. & Kameya, T. (1997) Production and analysis of plants that are somatic hybrids of barley (Hordeum vulgare L.) and carrot (Daucus carota L.). TAG Theoretical and Applied Genetics. 94 (2), 221–226.
Mathis, G.F. & McDougald, L.R. (1987) Evaluation of interspecific hybrids of the chicken, guinea fowl, and Japanese quail for innate resistance to coccidia. Avian Diseases. 31 (4), 740–745.
Serebrovsky, A. (1929) Observations on interspecific hybrids of the fowl. Journal of Genetics. 21 (3), 327–340.


Why is the GULO pseudo gene expressed in humans?

I suggest thinking about this from a different direction — something like: "What selection pressure is there for loss of expression of the GULO pseudogene?"

When thinking about that question note that the expression level is very low (less than 1 transcript in a million in the tissue with the highest level of expression.

In general, evolution is messy and I think your null hypothesis should be that this as a vestigial trait.

In other words, unless you can show that there is a significant cost for the low level of expression seen from this pseudogene there is nothing to explain.


To me it looks like some kind of feline with mange.

It is unlikely to be a Lemur given the lack of thumbs on said animal. And this is India not Madagascar. Lemurs are only found on Madagascar.


The Hoechst 33342 dye is similar to DAPI in that both are UV-excited, minor groove-binding, and emit signals proportional to total DNA content. Both are maximally excited around 355 nm and emit around 460 nm.  A UV light source is required, which may harm the cell. However, this is only a risk with Hoechst, as DAPI requires the cells to be fixed and/or permeabilized, which is incompatible with life. DAPI is more stable, but Hoechst is brighter. Both are subject to photo-bleaching after long exposure.

There is another newer DNA dye called DRAQ5 that makes up for all of the issues I mentioned earlier - it is bright, quite photo-stable, can be used in live cell imaging, and its excitation and emission wavelengths are in the far red end of the spectrum, meaning that no UV is needed. I found a good comparison chart at http://www.biostatus.com/product/draq5/live_cell_comparison_chart/ if you're interested. I have no connection to them, by the way, I've just used DRAQ5 a lot in the past.


Is magnetic resonance microscopy appropriate for investigating ion-channel flow?

Clarification
I am unclear of your aim. What feature of elecrophisiology do you want to characterize?
What do you mean by large scale? E.g. Micrometers (μm),  Milimeters (mm) or Centimetres (cm).
Magnetic resonance microscopy imagings at Micrometers (μm).
Answer
An established way to observe neuron propagation is the use of calcium imaging. You can take a video under a fluorescent microscope to observe (Not measure) elecrophisiology. Also I believe this technique may provide the 'larger scale' you are seeking.
More On Calcium Imaging:
https://www.cell.com/neuron/comments/S0896-6273(12)00172-9


Why do we have more sweat glands in our palms?

You sweat much stronger in the palms of your hand and the soles of your feet, because they contain a much higher density of eccrine sweat glands. According to Sato et al., (see reference 1) there are something like 64 glands per cm² on your back, 108/cm² on your forearm and 600-700/cm² on the palms of your hands.

This is thought to have different reasons: First, sweating is an important way to control the body temperature.
Sweat works as a defense by anti-microbial peptide dermcidin, it is also seen as am important way to maintain the conditioning of the skin and as well as a lubricant for contact surfaces. (references 2-4)

Sweating is controlled by the sympathetic (autonomic) nervous system, and can be triggered by acetylcholine and adrenaline. This explains why you get wet palms when coming into stress.

References:

Biology of sweat glands and their disorders. I. Normal sweat gland
function
Systematic review focusing on the excretion and protection roles of
sweat in the skin.
Dermcidin: a novel human antibiotic peptide secreted by sweat
glands.
The human eccrine sweat gland: Structure, function and disorders


Is missing Q wave characteristic for Wolff-Parkinson-White Syndrome?

In Wolff-Parkinson-White syndrome, the normal Q wave is usually masked by the preexcitation action potential which produces the delta wave. Despite this, missing Q wave is not a diagnosis criteria of the syndrome, and up to 70 percent of the patients show a negative delta wave which causes differential diagnosis problems because it is confused with Q, according to Emergency Electrocardiography.

  When the delta wave is negative, this simulates a Q-wave. This is known as a pseudo-infarction pattern, and is seen in up to 70% of patients with WPW.

And this negative delta wave also helps in determining action potential origin, according to Medscape.

  A general rule is that Q waves (negative delta waves) point away from the earliest site of ventricular activation, which is typically the insertion point of the bypass tract.

No, you can't categorize PRS complexes as WPW syndrome. In fact there is no PRS complex. A classic ECG of WPW will show a shortened PR segment and a widened QRS (or RS or RSr' or however it looks) complex.


Constant or variable number of chiasmata during recombination?

There is a large amount of variation in the distribution and number of chiasmata or crossing overs (COs). The total number of chiasmata per cell can vary within the same organism.
Where chiasmata occur along the chromosome is also not consistent cell to cell. Hotspots are 1-2kb regions that experience elevated recombination compared to neighboring genomic regions. A way to think of the distribution of COs is that ~80% of recombination happens in hotspots which comprise ~10% of the genome.

Recombination depends on the chromatin context, so chiasmata are rare near the centromere and positive interference results in chiasmata being spaced out along the chromosome. A good prediction of total chiasmata number per cell is at least 1 per chromosome. Some researchers argue that one CO per chromosome arm is more accurate.

Below is a link to a good article that expands on some of the ways recombination varies in humans.
http://www.nature.com/nrg/journal/v8/n1/abs/nrg1947.html


Finding protein motifs by running sequence analysis in protein BLAST

MOTIF search
First of all this is not possbile in BLAST (at least nog direclty).
There are a lot of tools to search for motifs in your sequence. I think a good way to start is to use MOTIF search. This searches for motifs in your sequence based on infomration in: Pfam, NCBI-CDD, PROSTIE PATTERN and PROSITE PROFILE (you can select which of these you want to use). Further you can also use INTERPRO (which also searches through serveral database, note that INTERPO searching can take a while but will give a nice graphical view). If you want to find new motifs you can use MEME (as suggest by @mxwsn). However to do this you have to find (or have) a set of sequences which resemble your seqence to find motifs. Because off course the algorithm is not able to find motifs in one sequence because it needs to compare a set of sequences to find some frequently occuring motifs, which could be of your interest.
So to summarize you can use MOTIF search (or INTERPRO etc...) to find motifs in your sequence which are already known. Or gather a set of sequences and find new motifs in them using MEME or a similair tool.

However, how did you conclude that your sequence is a Zn-dependent alcohol dehydrogenase? Because BLASTing the sequence you provided will give matches with this enzyme but only covering ~17%. Nonetheless a good way to find information about your sequence is indeed to find motifs and compare the sequence with HMM's or PSSM's of known proteins.
For example MOTIF search will give these results:

PROSITE:
    Zinc-containing alcohol dehydrogenases signature.
PFAM:
    Zinc-binding dehydrogenase
    Alcohol dehydrogenase GroES-like domain
AND A LOT MORE>>>

Searching PFAM will give you this:

Notice that the second domain (Zinc-binding dehydrogenase) is not completely present, more information can be seen in the detail overview:

I would advice to also take a look at how important these "missing" residu's are (e.g. using a MSA and look at conservation). Because your sequence could contain these domains but that does not necessarily mean that this IS A Zn-dependent alcohol dehydrogenase. It could be non-functional for example.


Cerebral/Cerebellar Cortex versus Deep Nuclei

"Cortex" is a more general anatomical term for the outermost layer of a structure. It applies to both the cerebral and cerebellar cortex gray matter, as these are gray matter structures on the outsides of their respective parts of the brain.

Nucleus is also a more general term; in the context of neuroanatomy, it refers to a cluster of cell bodies. Typically we refer to CNS clusters of cell bodies as nuclei, and in the periphery they are called ganglia, though there are some odd exceptions like the basal ganglia (you referred to the basal nuclei in a comment, which are the same structure, but are almost always called the basal ganglia, whether or not that term is the 'best' term).

White matter, in general, is nervous tissue that appears white because it is primarily "fatty" from the lipid bilayer of cell membranes and consisting of processes like axons (especially myelinated ones) and dendrites rather than cell bodies.

I'm not aware of anyone who would call the cerebral cortex (or cerebellar cortex) a "nucleus": these areas are not shaped as clusters of cell bodies, they are shaped as sheets. The distinction is really only an anatomical one, so it makes little sense to use "nucleus" in a more general term to mean "nervous tissue consisting of cell bodies": we already have a term for that, "gray matter," and in most cases interesting to science we are talking about something more specific anyways.

I'd further say that these distinctions are really only gross anatomical ones, as one can have cell bodies outside white matter, and areas of gray matter like neocortex also include a mostly-white layer of axons and dendrites in "layer 1" but we still treat this as gray matter with respect to the whole brain.

Ultimately it doesn't matter: don't take anatomical terms more seriously than the things they are describing.


What kind of spider is this? First time I have ever seen one

It appears that you have a leafcurling sac spider:

They are observed all over east and west north america:

Here is the eye arrangement from bugguide:

I labeled with arrows the two thin dots at the top, which are eyes that point upward, which are easily visible in your picture. Would need a front-facing photo to see the rest of the eyes.
The spinneretes out the back of the abdomen are also diagnostic of clubionids.
The colours can span dark yellow to light brown, and the jaws are dark and sometimes the entire front face is dark as well.
A gallery of clubionids filtered on only Canadian observations is here:
https://inaturalist.ca/taxa/121774-Clubiona/browse_photos?quality_grade=any&place_id=6712


electrostatic charge of viruses, especially Coronaviruses

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology! I'm glad we encourage such questions from curious people who want to learn more.

Via: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4213776/#!po=1.19048

  All viruses are coated with proteins and contain genetic material which can either be DNA or RNA. Since both nucleic acids have phosphodiester bonds, the genetic material provides a partial negative charge to the virus. The viral nucleic acid genomes are wrapped in proteins that can be neutral, negative, or positive in charge. Therefore, the net charge of a virus depends upon the cumulative charges of the genetic material and the protein.

So the electric charge of a virus particle depends on the constitutive parts of the virus of interest; particularly if enveloped or non-enveloped; the outward-facing heads of the phospholipid bilayer membrane of an enveloped virus will carry a negative charge.

Two references in the above paper may help with a deeper dive into the subject:

Lodish H. et al. Molecular Cell Biology (ed 4.). (W. H. Freeman, New York, 2000). (Google Scholar)
Michen B. & Graule T. Isoelectric points of viruses B. J Applied Micb. 109, 388–397 (2010). (PubMed) (Google Scholar)

I couldn't find any papers on the electrical properties of novel coronavirus specifically. But looking into SARS-CoV may be suggestive of general properties. Its envelope proteins have a positive charge that help with targeting and infecting ACE2-expressing cells (https://clarivate.com/wp-content/uploads/dlm_uploads/2020/01/CORONAVIRUS-REPORT-1.30.2020.pdf).


Do You Need Vitamin B12 To Utilize Folate

B12 is not necessary to utilize folate but it is necessary to replace B12 before repleting folate as otherwise you can induce subacute combined degeneration of the cord.  There are multiple mechanisms of folate absorption from the small bowel and large bowel which don't require B12.

Geographic tongue is not caused by B12 deficiency, and the actual cause is not known.  It does cause raw beef tongue.

You don't normally need to prescribe mega doses of folic acid with methotrexate.  Common doses are 5 mg per week, and 0.8 mg daily, though some physicians don't bother using folic acid at all.  Although folic acid was commonly prescribed because it was believed that methotrexate works by virtue of its ability to antagonize folic acid, it is now known that this is not true. It works as an adenosine antagonist, and so you can take the folic acid on the same day as the methotrexate if you wish.


What is the biggest facultative anaerobic metazoan known to science?

I think a tapeworm is your best bet. For tapeworms specifically, I found this textbook, Animal Physiology: From Genes to Organisms, which claims:

  Active facultative anaerobes include some parasitic worms such as tapeworms that can survive without oxygen indefinitely...

I was not able to find any primary research on the subject either @WYSIWYG (other than a paper from 1951 that doesn't seem to be available anywhere), but if the textbook's claim holds, I can't think of anything larger than a tapeworm.


Does body temperature affect human lifespan?

I am assuming that you are referring to a baseline human cooled to a core body temperature of 30C from birth. I am also assuming that you are ignoring the fact that the environmental temperature (and thus the temperature of the extremities) has to be much lower than 30C to cause a core temperature of 30C. Thus, I am ignoring hypothermia-based gangrene, necrosis, and extremity loss.

If you had a normal human with a 30C core temperature starting at birth, I have doubts that it would live any longer than a human at 36.8C. Unlike flies, which are ectotherms, humans need to have a more or less constant temperature to successfully complete most of their metabolic processes efficiently. Since humans are not built to withstand extremely low temperatures, it is likely that lowering the core body temperature to 30C will cause it to have organ impairment, causing organ failure, followed by death. Though you might be able to "fool" the brain on thinking that 30C is normal, it is unlikely that the organ functions can follow. It could be possible to breed successive generations of humans in ever-lower temperatures, but it is unlikely for a baseline human to withstand such a large temperature drop. Sensory neuron adaptation =/= bodily adaption. However, lowering the core human body temperature by 1-2 degrees (typical of sleep) may have a chance of altering a human's lifespan in a more meaningful way. Though cooling may prolong the lifespan of temperature-conformers and single-celled animals, it is unlikely that the same can be said for endotherms. Endotherms have had biological processes that run on a fixed temperature for a long time already.  One more thing: @Hermann: Their core body temperature may not have been much lower than the baseline.


How does collaboration on reconstructing metabolic networks work?

A bit of a preface:

A lot of this large scale collaboration (which I would maybe rather describe as the work of a whole [sub]field over a given time frame) often ends up in some sort of database. Really, there A LOT of those in modern biology - and often with minor but sometimes important differences. One of those would be the level of curation: are results gathered automatically from other sources, or always manually checked before being added? Another thing about databases is that (with certain exceptions of course) they often are only relevant for specific sub field, in some cases this can mean that only one lab maintains a website with a databases that is used by a few others, but that's it.
What I'm trying to get to is that there isn't really a 'one size fits all' solution and that especially the size of your field will impact which kind of solutions are both feasible and actually useful.

Now to answer your actually state question (as far as I can):

Most known biochemical pathways (including the metabolic ones) are described in the KEGG database. Initially this project was started by a single lab (and is still run by that group as far as I can tell), but of course it contains a lot of published information from other sources (I couldn't find information on how they update the networks in the database, you may have to read the papers for this). The database can also be accessed remotely, so it allows people to use the same network for a given reaction, and by incorporating sequence data it also has information on which organisms even contain the given enzymes in the network.
One thing the database does not contain is information about dynamics in the network. In this case I think most groups will generate and publish their own models (e.g. based on ODE's).


What sauropod genera had a double row of chevron bones in the tail?

It's fairly common. It is believed to have evolved two times independently, basically in both groups presumed to use their tails as weapons. Both Diplodocoidea and Euhelopodidae have species with forked chevrons and evolved it independently. It is fairly diagnostic since it is not seen outside these groups.

Source

Independent half chevrons (two rows of individual elongated splints of bone, one right, one left) pop up in many groups but double beamed chevrons are something different: the ends of the chevrons are joined, creating a single solid structure. In some parts of the tail they are separated into right and left halves (these are not very unique), but the joined ones are taxonomically significant. These are not chevrons dwindling into nothing along the tail but changing structure in a specific structurally significant way.


Lobed Nuclei still count as One nucleus?

Yes. Lobation is when a nucleus deforms, but it is still a single compartment. How the nucleus deforms can be helpful in roughly determining the cell type by visual inspection.


Could a large constrictor kill a small animal?

Constrictors doesn't have uniform body circumference from head to tail. They coil around the prey accordingly. In your example, if the prey is very small, it just swallows. If its little big, it coils a little bit (check some videos like this) say two turn coil. This will only cover top half feet of constrictor's length which is of lesser diameter than the body.

So basically, they crush the prey and perform a kill. Its not a necessity for any constrictor to use its entire body to coil around a prey. They adjust their coil level to control the prey.


Identify orange-brown, teardrop-shaped insect in central Europe that was found indoors

I think it may have been a tick of some kind, one that had already fed and was round (hungry ticks are sort of flat).  I couldn't say exactly what species.
I'm not sure, but that's the only thing I can think of that matches this photo.  I'm no professional, so another person here may be able to do better.
Ticks have eight legs (they're vaguely related to mites, and, even more distantly, to spiders), so I was puzzled at first by you saying it had six legs, but possibly what you thought were its antennae were its other pair of legs?  (Ticks have no antennae).
https://en.wikipedia.org/wiki/Tick


Is there any disease in common between human and insects?

It is always difficult to prove that something does not happen, so I will restrict myself to saying that I know of no examples and think it unlikely that there will be a common viral or bacterial disease of human and insects.

Viruses are not limited to a single host, but the typical host range of mammalian viruses would not appear to extend to insects, as far as one can tell from the literature — see e.g. the Wikipedia entry on Virus.

  Viruses are by far the most abundant biological entities on Earth and they outnumber all the others put together.[134] They infect all types of cellular life including animals, plants, bacteria and fungi.[3] Different types of viruses can infect only a limited range of hosts and many are species-specific. Some, such as smallpox virus for example, can infect only one species—in this case humans,[135] and are said to have a narrow host range. Other viruses, such as rabies virus, can infect different species of mammals and are said to have a broad range.[136] The viruses that infect plants are harmless to animals, and most viruses that infect other animals are harmless to humans.[137]

Likewise for the host range of bacterial pathogens, judging from articles such as an article by Baümler and Fang in the Cold Spring Harbor Perspective on Medicine.

One general molecular reason for expecting a limited host range that would exclude insect/human pathogens relates to the means by which the pathogens enter the host cells. Quoting, for example, from the abstract of an article by JM Casasnova:

  To initiate the infective cycle, the viral genome must therefore translocate from the viral particle to the cytoplasm. Via distinct proteins or motifs in their outermost shell, the particles attach initially to specific molecules on the host cell surface. These virus receptors thus mediate penetration of the viral genome inside the cell, where the intracellular infective cycle starts. The presence of these receptors on the cell surface is a principal determinant of virus host tropism.

The membrane proteins that act as receptors generally differ between related members of a species, but mutations can allow the viruses to cross species barriers. However the extreme difference in cellular structure and biochemistry between insects and humans make it unlikely that this could happen, even if the cell type and protein still exist in common. Consider, for example viruses such as Hepatitis A, B and C which infect the human liver. My own favourite insect — Drosophila melanogaster — does not have a liver as such, its functions being served by the insect fat body.

I am less familiar with other aspects of the viral life cycle that relate to physiology (my background is chemical) but these clearly differ and would affect modes of transmission, for example respiratory and sexual.

These latter considerations will also apply to pathogenic bacteria. As an anecdotal conclusion to an imperfect answer, I would mention the bacterial diseases of silkworms that affected the French silk industry in the 18th century. There are several accounts of Louis Pasteur being called in to eradicate the disease but these contain no suggestion that the workers breeding the worms contacted the disease.

Tribute to Pasteur for ‘saving’ the silk industry at Ales, nr. Nîmes, France


It closely looks like Tibouchina urvilleana* or any other Tibouchina species. You can have a look here.

[Source:Wikimedia common]

  Tibouchina urvilleana is a species of flowering plant in the family Melastomataceae, native to Brazil. Growing to 3–6 m (10–20 ft) tall by 2–3 m (7–10 ft) wide, it is a sprawling evergreen shrub with longitudinally veined, dark green hairy leaves. Clusters of brilliant purple flowers up to 10 cm (4 in) in diameter, with black stamens, are borne throughout summer and autumn.[Source]

*Credits to @RHA for suggesting the right species.


A VERY interesting question that I had to think a lot about, and frankly I couldn't come up with an answer.

Nevertheless, this article may have.

https://www.statnews.com/2020/03/19/coronavirus-survives-on-surfaces-how-to-protect-yourself/

"Viruses covered in “envelopes” have the most trouble surviving outside a living cell. On surfaces, the surrounding light, heat, and dryness break down the envelope, killing the virus. (Porous surfaces pull moisture away from viruses that land on them, accelerating the destruction of the envelope.) Most rhinoviruses have such envelopes; so do some influenza viruses. Norovirus doesn’t, enabling it to last longer in the environment."

Here are the author's relevant credentials.

Sharon Begley, senior science writer, covers genetics, cancer, neuroscience, and other fields of basic biomedical research. She was previously the senior health and science correspondent at Reuters, the science columnist at the Wall Street Journal, and the science editor at Newsweek. Among her favorite awards are an honorary doctorate from the University of North Carolina and the Public Understanding of Science Award from the Exploratorium in San Francisco.


Can a cell receive multiple copies of an insert when using different MOIs?

Yes, if you use a high enough MOI, you'll start to get double infections. Usually, anything >1 MOI will guarantee a high chance of double infections. If you're using a high MOI and only seeing single inserts, it might be due to your cells being difficult to transfect. If you look at this site: https://manuals.cellecta.com/lentiviral-construct-packaging-and-transduction/v10a/en/topic/lentiviral-titer-calculation it should give you a general reference for what % double transfected cells you should see. The difference between transfected cells and MOI % should estimate double infections assuming 100% efficiency.
Some cells are less efficient at being transfected, and it's a good idea to get a functional titer on your target cell line which is very easy if you have a fluorophore in the plasmid you're trying to insert.
I reread what you're getting at, and it's generally accepted that MOI under 0.4 won't give you double transfections.


P=(250 × 2 + 500)/1500 = 0.66
Q=500/1500 = 0.33
Your friend was right, you miscalculated P because forgot to add the alleles coming from the heterozygotes.


Are there any animals that celebrate communally?

An event causes us to perform some sort of celebration that is motivated simply by joy and not any sort of survival instinct.

Celebrations usually mean large group activity but a play can be considered an event which is simply by joy and not any sort of survival instinct, and hence would fit your question. One can easily spot their pet playing around with objects when they are sitting around, busy in something 'boring' for the pets, like - reading a newspaper. But here it can be argued that pets have learned to do this to get the attention of the owner, and hence associated benefits.

Well, plays of pure enjoyment have been documented in wild animals too.

  I once observed a young elk in Rocky Mountain National Park, Colorado, running across a snow field, jumping in the air and twisting his body while in flight, stopping, catching his breath and doing it again and again. There was plenty of grassy terrain around but he chose the snow field. Buffaloes will also follow one another and playfully run onto and slide across ice, excitedly bellowing “Gwaaa” as they do so (Canfield et al. 1998).

Certainly, there was no motive here apart from having fun.

I would encourage you to go through this article - Bekoff, M. (2000). Animal Emotions: Exploring Passionate NaturesCurrent interdisciplinary research provides compelling evidence that many animals experience such emotions as joy, fear, love, despair, and grief—we are not alone. BioScience, 50(10), 861-870.

Speaking of the celebration, such as - birthday, or the largest homo sapiens gathering Kumbh Mela, I would also be interested to know of some group of animals doing it periodically.

Reference:

Canﬁeld, J., Hansen, M. V., Becker, M., & Kline, C. (1998). Chicken Soup for the Pet Lover’s Soul. Deerﬁeld Beach, FL: Health.


Why is trypsin digestion required for proteomic studies?

Trypsin digestion allows you to cut proteins into smaller polypeptides, masses of which can be determined by mass spectrometry and then translated back into possible amino acid sequences. Trypsin cleaves after specific amino acids. Altogether, this allows you to identify proteins.


What species is this black, blue and white bird?

That bird is commonly called a magpie. The only species found in Alberta is Pica hudsonia. You can see a reference image on the left and their distribution throughout Canada on the right:

[source]

Interestingly, it is one of the only non-mammals studied that is able to recognize itself in a mirror. In fact, these and other corvids are thought to be some of the most intelligent species on Earth.

You mentioned that you didn't hear them chirp. These birds are actually quite loud and about fifty of them used to wake me up every morning. Have a listen (not my video).


You have found Smerinthus ocellata, the Eyed hawk moth. It is name comes from the eyes on the hindwing, which do not show at your photo. It is known to show these eyes if disturbed, to scare of attackers.

Photo from wikipedia commons:

The forewing shows considerable variability, as you can see here


Do river sharks (genus Glyphis) have reduced rectal glands for salt removal?

I contacted Richard Pillans, the primary author of the article linked to in the question. He told me that he did not know whether the rectal gland was reduced. Researchers are hesitant to capture and dissect the freshwater sharks because of their endangered status.

He did tell me that they have gathered much more data on the movement of the sharks since the 2009 paper was published.  Apparently, river shark is a bit misleading (my words, not Dr. Pillans). Glyphis does occur in freshwater (no salt) but tends to be found in the middle range of brackish water. Brackish water is considered to be anything that is not purely freshwater nor purely salt water, with typical values between 0.5 and 30 parts per thousand (ppt). Freshwater is 0 ppt and open ocean salt water is 35 ppt, the equivalent of 35 grams of salt in one liter of water.

If Glyphis is found primarily in the mid-range of brackish water, then I would expect the rectal gland not show signs of reduction. Pillans and Franklin (2004) showed that rectal gland mass of brackish water bullsharks (Carcharhinus leucas) in Australia did not differ significantly from either freshwater or saltwater individuals.  So, pending further evidence, I would conclude that Glyphis, which in the same family as bull sharks, probably does not show rectal gland reduction.

  Pillans, R.D. and C.E. Franklin, 2004.  Plasma osmolyte concentrations and rectal gland mass of bull sharks Carcharhinus leucas, captured along a salinity gradient.  Comparative Biochemistry and Physiology, Part A 138: 363-371.


Appropriate Buffer for electerophoresis of DNA & Protein TBE or TAE?

I have had good experience using a lithium boric acid buffer from Faster Better Media. I use it for RNA gels, but it's advertised for DNA gels. I don't think it can do protein, but I've never tried it. I'm not an electrician, but higher conductivity may be the opposite of what you want. The lithium boric acid buffer claims to have less conductivity than a tris based buffer, allowing you turn the voltage up much higher while producing less heat. The higher voltage pushes the DNA down the gel faster, and keeps the bands sharper. My RNA gels take 30 minutes to run, used to take 3 hours. Of course, those slow gels used a MOPS based buffer and formaldehyde to denature the RNA.


There are several plants in the family Apiaceae with these kind of thin leaves, and some smell strong and/or are used as herbs in the kitchen. This must be Fennel  Foeniculum vulgare, because you describe it's smell as anise. Dill looks similar, but smells different. Fennel is indigenous to the mediterranean, but planted all over Europe.

It can be quite big, but on poor, rocky soil might remain small.

Picture of fennel from Dutch wikipedia:


How do neurons inverse an action potential?

The University of Texas site where you obtained this picture states in section 6.7:

  What about the transmitter substance that is released by the inhibitory interneuron in the spinal cord? The transmitter substance is glycine, an amino acid which is used frequently in the central nervous system as a transmitter that produces inhibitory actions. It is not the most common, however. The most common transmitter with inhibitory actions is gamma amino butyric acid (GABA).

Glycine receptors activate a chloride-selective transmembrane channel, which is predominantly expressed in the spinal cord and brain stem (Rajendra et al, 1997). Chloride hyperpolarizes the neuron, thereby inhibiting the motorneuron controlling the flexor muscle, and thereby facilitating the extensor muscle to contract. If the opposing flexor muscle would not be inhibited, the extensor muscle would be counteracted and the knee jerk reflex would be less efficient, if present at all.

Typically, an inhibitory interneuron will only release inhibitory neurotransmitter. In the example here, the opposite circuit to bend the knee would activate the flexor muscle. This would be accompanied by opposite events. However, the inhibitory F neuron above in your figure would not reverse its action though, it will simply be silent, thereby allowing the acetylcholine from the E neuron do its job. In more general terms, neurons cannot reverse their action from inhibitory to excitatory. Their outputs are typically simply the release of a pre-defined vesicle pool, which is a yes/no event without further qualities. In other words, an inhibitory neuron will be inhibitory and it cannot change the nature of the neurotransmitters released (excitatory versus inhibitory) based on different inputs.

Reference
- Rajendra et al, Pharmacology & Therapeutics (1997), 73(2): 121–46


Is COVID-19 claimed to get less deadly over time? If so, why?

While the data are much too sparse and noisy to give an answer about what is happening to COVID-19's virulence (the technical term for the "deadliness" of an infectious disease), or to forecast what will happen to its virulence in the future, there are indeed theoretical reasons that one might expect the virulence to decline in the future.

There is an entire theoretical literature on the evolution of virulence (e.g. see Read 1994, or see Wikipedia); Robert May and Paul Ewald are two researchers who contributed seminal ideas. The basic idea is that infectious 'organisms' (including viruses) may face a tradeoff between their ability to produce lots of infectious particles (e.g. by replicating faster within the host) and the length of time that they can stay in the host before it dies or activates immune defenses sufficiently to end the infection. In this case, some intermediate level of virulence may evolve.

Evolution of virulence in ways predicted by the theory has been observed in the real world in such diseases as myxomatosis (a viral disease of rabbits). The theory has also been suggested to apply in HIV and syphilis.

The actual forecast can depend on many details of the biology and epidemiology of a particular organism. If COVID-19 happened to have a higher-than-optimal virulence in humans at the time of emergence, we could expect its virulence to decline over time. It could also decline if epidemic control was applied in such as way as to differentially affect more-virulent strains; this has been suggested by Tang et al. on the basis of the pattern of mutations in different strains, although their logic has also been criticized on Twitter by an expert in genetic epidemiology, and now by a more official rebuttal by McLean et al. (with some back-and-forth discussion between the authors and critics).

This explanation doesn't include the possibility of host evolution, which is theoretically important but not really relevant to COVID-19 — it would only happen over many generations, and only if the epidemic was so severe that it was a significant overall cause of death or failure to reproduce ...

Tang et al. "On the origin and continuing evolution of SARS-CoV-2", National Science Review, nwaa036, https://doi.org/10.1093/nsr/nwaa036 .
Read, Andrew F. "The evolution of virulence." Trends in microbiology 2.3 (1994): 73-76.


Whole Genome Sequencing and B Chromosomes

You can use differences in coverage (number of reads mapping to certain regions in reference) to infer if there is a B chromosome.


Check out the Desert Kingsnake (Lampropeltis getula splendida).  It is native to New Mexico.

Source: Desert Kingsnake (wikipedia)


What is the pathogenuc mechanism of brown pigment lipofuscin in muscle atrophy?

Simple answer: Atrophy through autophagy.


Inheritance simulator not working properly

There are a couple of things going on here, I think. Let's start with simple conditional probability:
import random

sim1 = [random.choice([0, 1]) for x in range(1000)]
sim2 = [random.choice([0, 1]) for x in range(1000)]
for locus in range(1000):
   if sim1[locus] ==sim2[locus]:
     match+=1
print(match)
# prints 492

In other words, even two completely independent samples from [0,1] with uniform probability are expected to match about half of the time (492 / 1000 ~ 50%).
So you are correct, the problem lies in your fashion of encoding the data. When you are talking about "similarity", what I think you mean is "identical by descent". This is distinct from "identical by state", meaning what actual alleles you have.
Two individuals can be identical by state at a large number of loci without any significantly close family relationship, if they are members of a population without a lot of common alleles. This is close to what we mean when we say that humans are all 99.9% identical to each other- this is because most of the positions in the genome have very little variation. So, if you choose two people who have no common ancestors in the last 1000 generations, they will still be identical by state for >99% of their loci. This is the real lesson that your simulation is showing you, I think!!
If you want to show identity by descent, you will have to choose a different encoding. Using e.g. nucleotides will still run into the problem that very frequently the nucleotides will be identical by state in unrelated individuals, whereas what you actually care about is "did this allele originate from the exact same ancestor". So you want some way of guaranteeing (or nearly so) that every ancestor contributes a distinctive, unique allele that you can always distinguish. For example, the following code will produce a "unique" identifier that could be used for each founder individual (e.g. every time you call Person():
import uuid
unique_id = uuid.uuid4()

So really, what your Person.get_random_dna() method should do is something like this (minimal modification to your code):
        def get_random_dna(self):
            unique_id = uuid.uuid4()
            return [unique_id for x in range(CHROMOSONE_LENGTH)]

You may need to fix something else as well, I have not actually run this.


What is the preferred way to abbreviate amino acids?

In my experience neither is preferred.

When simply presenting a protein sequence, e.g. in the context of a database of proteins encoded by a genome, then the one-letter code tends to be used.

When showing an alignment of a DNA sequence with the encoded protein sequence both can be used, although personally I prefer the one-letter code for this too because I don't like squished-together text like LysAlaTrpLeu.

In papers referring to an individual residue in a protein I would say that the three-letter code would be more likely to be used.

When referring to a mutation (or,  rather, an amino acid substitution) you might see Leu129Gln or L129Q.

And, by the way, I use L for ligand and have never found it to be confusing. If the reader of your text is sophisticated enough to know that L is leucine then I think they would be able to tell from the context that you were using L for ligand.


Why do eukaryotic organisms have introns in their DNA?

There is still a lot to be learned about the roles introns play in biological processes, but there are a couple of things that have been pretty well established.

Introns enable alternative splicing, which enables a single gene to encode multiple proteins that perform different functions under different conditions. For example, a signal the cell receives could cause an exon that is normally included to be skipped, or an intron that is normally spliced out to be left in for translation (the Wikipedia article on the subject has a basic overview of the possibilities). This would not be possible, or at least would be much more difficult, without the presence of introns.
In recent years, we have discovered that RNA molecules (especially small RNAs such as siRNAs and miRNAs) are much more involved in regulating gene expression than previously thought. Often the small regulatory RNAs are derived from spliced introns.

There is probably more, but essentially introns enable a finer level of regulatory control. Biological complexity is often not the result of having a larger complement of genes, but of having additional layers of regulation to turn genes on and off at the right times. Prokaryotic genes are often organized into operons, and a single polycistronic mRNA will often encode multiple proteins from multiple adjacent genes. Since the biological processes required to sustain microbial life are much less complicated than those required to sustain eukaryotic life, they can get away with much less regulatory control.


What is the meaning of "Rb is in the active state"?

The terminology of "Rb is active/inactive" refers to the activity of inhibiting E2F.
So active Rb inhibits E2F, while inactive Rb doesn't inhibit E2F.
With regard to Rb and phosphorylation - the story seems to be more complex ([1] describes Rb as an enigma).
According to [2] (this quote is from the summary of the paper by eLife):

  Narasimha, Kaulich, Shapiro et al. now present biochemical analyses of
  Rb proteins that show— completely unexpectedly—that the cyclin D
  complex adds just one phosphate group to Rb during the G1 phase,
  although this group can be added to one of fourteen different sites.
  The resulting 'mono-phosphorylated' Rb varieties can each sequester
  different transcription factors and stop them working.At the
  restriction point, many more phosphate groups are then rapidly added,
  and the Rb protein is inactivated by a different cyclin. This
  cyclin—called Cyclin E—then drives cells into the next phase of the
  cell cycle. Establishing how cyclin E is activated is a priority for
  future research.

+ 3. Wikipedia's Cyclin-dependent kinase (CDK) page says:

  By definition, a CDK binds a regulatory protein called a cyclin. Without cyclin, CDK has little kinase activity; only the cyclin-CDK complex is an active kinase.

Wikipedia's Protein kinase page says:

  A protein kinase is a kinase enzyme that modifies other molecules, mostly proteins, by chemically adding phosphate groups to them (phosphorylation).

And here is a nice visual explanation from Life: The Science of Biology (10th edition):

So both "active CDK" and "active cyclin-CDK complex" (and according to the other answer, also "active cyclin") refer to the case in which a cyclin is bound to a CDK to form a cyclin-CDK complex, such that the CDK might phosphorylate some substrate.
(I didn't mention the cell cycle here on purpose, as I am not an expert, and so I am wary of claiming that an active CDK always pushes the cell cycle forward. If I understand correctly, we still don't know exactly how each cyclin-CDK complex affects the cell cycle.)

As for your last question:

  In general, Maybe one can say that binding (Rb with E2F or Cyclin with
  CKD) means activation and disconnecting means inactivation?

As mentioned above, you could say that about a cyclin and its CDK.
Unfortunately, you can't say that in general. E2F here is a counter example (it is inhibited when Rb binds to it and activated when Rb disconnects from it).
However, you could say that in general, when something binds to a protein, the protein might change its shape, which might lead to activating or inhibiting some function.

[1] Dyson, Nicholas J. "RB1: a prototype tumor suppressor and an enigma." Genes & development 30.13 (2016): 1492-1502.

[2] Narasimha, Anil M., et al. "Cyclin D activates the Rb tumor suppressor by mono-phosphorylation." Elife 3 (2014): e02872.


It does seem oddly phrased, but is still understandable. The paper explains how the combination of low zygotic transcription and increasing amount of DNA due to rapid cell division can function as a switch to trigger the mid-blastula transition. Before this event, most factors in the cell are of maternal origin (ie they are not being expressed in the zygote) and are thus in limited supply. As cell division progresses, the stoichiometric ratio between these factors and DNA decreases until, eventually, there is more DNA than these replication factors. At this point, you could say that the DNA has titrated the replication factors in that there is no unbound form left. This is analogous to the equivalence point of acid-base titrations commonly encountered in first-year chemistry courses.


Why must DNA be packed into chromosomes during mitotic phase?

A chromosome is simply a length or segment of DNA. Bacteria have few structural proteins on their DNA, and they have one circular chromosome. In humans, before DNA replication, the nucleus contains 46 strands of DNA, i.e. chromosomes (22 chromosomes in two copies and usually two X or one X and one Y for males and females, respectively). All chromosomes are DNA that is bound by histone proteins that are organised in nucleosomes, approximately every 147 base pairs.

What you are referring to is a condensed chromosome in metaphase, which confusingly in humans is actually an X shape consisting of 2 identical chromatids, structurally condensed and joined at the centromere to form a duplicated chromosome.

The duplicated chromosomes must condense and join before the cell can divide because a tangle of 96 chromosomes as chromatin would be almost impossible to organise and separate properly. The joining of identical chromosomes and compacting process allows all the 46 compacted and duplicated chromosomes (i.e. 96 chromatids) to simply align along the spindle apparatus that forms in centre of the cell during mitosis, and have separation of the chromatids during anaphase so that each of the new cells has a full set of 46 chromosomes.


At what point during an organism’s lifespan do mutations occur?

I'm assuming this question is primarily interested in heritable mutations, given the evolutionary nature of the link you shared. Only mutations in germ cells are heritable, so it will vary between males and females.
Female germ cells are formed in utero. Oogenesis in humans and is pretty much finished by 20 weeks gestational age (there's some debate about this, but it seems to be the current consensus view). So any heritable mutations would need to happen during gestational period. Note that that gestational age number probably varies quite a bit for different animals, but I think it's generally completed before gestation is completed (in mammals at least).
Males produce gametes via spermatogenesis continuously throughout life. So, for modeling purposes, you could probably use the age at which they conceive (though the sperm actually take a couple of months to mature).
One thing I'm unsure about is whether or not aging in the male affects the mutation rates in sperm, but might be something for the OP to look into.


Do brain cells regenerate in the adult brain?

Short answer
Neural regeneration in the adult brain is confined to two localized hot spots, namely the hippocampus and the anterior lateral ventricular wall. Establishing connectivity between new cells and existing neurons is mediated, at least in part, by the growth cones present on axonal tips of newly formed cells. The growth cone responds to various stimuli and guides the axon towards it new target.

Background
As to your first question: Also adults can regenerate brain cells, albeit in a few restricted, specific regions of the brain. A continuous level of neural regeneration occurs throughout adult life in at least two locations. The first is the subgranular zone of the dentate gyrus of the hippocampus, the region of the brain involved in learning and memory. The other is located in and near the anterior lateral ventricular wall of the cerebral cortex. While neurogenesis in the adult hippocampus is relatively limited, the subventricular zone is thought to continuously replace interneurons in the olfactory bulb (Clarke, 2003).

Studies have shown that neurogenesis folloing neuronal cell loss due to injuries occurs only within the germinal structures mentined above, and not in cortical or striatal structures. Even when neurogenesis in the striatum (but not cortex) has been reported following ischemic injury, the resulting neurons survive only a short time. Hence, under normal circumstances structural or functional recovery in non-neurogenic brain regions is limited (Hallbergson, 2003).

Re-establishing connectivity between new cells and the existing tangle of neurons in the neurogenic regions of the brain is complicated. An important structure in this regard is the growth cone (Fig. 1); it is present in developing axons that are not yet synaptically connected. They are motile structures present on the tip of the growing axon and guide axons to their synaptic targets. They control the cytoskeleton and determine the course and rate of axonal outgrowth. Neurons and growth cones can detect a variety of external signals to establish neuronal migration and neurite outgrowth. A key in this process is chemotaxis. Several classes of molecules, e.g., secreted factors, adhesion molecules and cues from the surrounding extracellular matrix and adjacent cells are involved in the process of neuronal pathfinding and growth. To advance over larger distances however, gradients are insufficient and neurons use mechanical cues (durotaxis). For instance, neurite outgrowth has been shown to be affected by the mechanical stiffness of the substrate. Glial cells have been shown to be softer than their environemnt and neurons preferentially seem seek out glia to grow to (Lu et al (2006); Park (2002); Pawlizak (2009)).

Fig. 1. Fluorescently labeled growth cone on the tip of an axon. source: wikipedia

References
- Clarke, Bone Marrow Transplantation (2003); 32: S13–S17
- Halbergson, J Clin Invest. 2003 Oct 15; 112(8): 1128–1133
- Lu et  al., PNAS (2006); 103(47): 17759-64
- Park, et al., Bioessays (2002); 24(9): 821-7
- Pawlizak, Thesis, University of Leipzig (2009)


What is the best method to check for differential gene expression in large dataset? I want to identify aging differentially expressed genes

A standard pipeline for DGE would be Salmon for (pseudo)mapping + DESeq2 for statistical analysis.
Salmon is one of a set of modern, fast and accurate mapping software. Requires a transcriptome to be defined.
DESeq2 is a mature R (Bioconductor) package which can handle reasonably complex designs, including time series, but not mixed models. The vignettes are pretty thorough. It can handle data from pseudomapping software as well as data generated using more traditional methods, e.g. Star + FeatureCounts.
Using a pre-made RNAseq statistical package is a much better idea than trying to do, e.g. a Poisson/Neg.bin GLM manually for each gene (even though ultimately this is what DESeq2 does).
(agree this question is a better fit for SE Bioinf)


Which organs in the body are responsible for measuring temperature?

Human thermo detection comes from a protein, expressed in high levels in the nervous system.
As per comments, there are a group of transmembrane proteins called transient receptor potential cation channel subfamily V (TRPV) ion channels that can detect temperature changes. Although the exact mechanism of the protein remains unclear, a study published in Nature 2010 showed that a protein called TRPV1 opens and closes to allow increased or decreased sensitivity to temperature change.
There is no specific organ that is responsible for temperature detection, however TRPV1 is expressed in high levels in the nervous system.


Evolutionary biology is a highly quantitative science and offers a fair amount of predictive power. However, at the same time, there are plenty of things that we are completely unable to predict.

What are we good at predicting?

There are plenty of things and it is impossible to list them all. Here are a few examples of things we can predict.

Number of pairwise differences (or other measures of molecular differentiation) do we expect between two lineages that recently split in a given number of years.
Number of pairwise differences between individuals coming from the same population.
Number of mutations of given fitness effects (whether beneficial or deleterious) do we expect to accumulate over a given period of time in a population. We can predict the age of a lineage.
Predictions about the evolution of multicellularity, sociality, etc. in lineages that are limit-cases (relating again to our ability at a short time only).
Speed of evolutionary change as measured in Haldanes or in Darwins (these are units) (from knowledge about the genetic variance).
Predictions about the heterozygosity of a population and the loss of heterozygosity through time.
predictions about the gene flow, migration rate or strength of selection.
Predictions of the consequences on fitness that a change in population size may cause.

Generally speaking, we have good predictive abilities at short time scale OR for neutral sequences OR for conserved sequences (strong purifying selection).

In short, we can predict a lot of things but by far not everything yet.

Main complications in doing predictions in evolutionary biology

I would suggest decomposing the reasons why predictions can be hard into the following categories. However, I might well forget something and one could argue that my semantic is less helpful some other semantic.

Environment

One issue related to making predictions at long time scale is that the environment changes through time in a way that we are not able to predict accurately enough yet.

Noise (incl. genetic drift)

I am not here talking about measurement error or sampling error (these are statistical concepts you may want to check if you don't know them), I am talking about the stochastic process that is inherent to biological systems such as the randomness of mutation processes and genetic drift.

Genotype-phenotype map

We have too little understanding of molecular genetics in order to be able to predict how different specific mutations would affect the phenotype. As a consequence, today we still have very little predictive power about the evolution of a phenotypic trait that is currently totally inexistent.

Complex systems

For example: demography affects evolution which affects the social environments, which affects demography which affects the pattern of species competitions which affects the evolution of another species which affects its demography which affects the evolution of a third species which affects the demography of our first species, etc... These kind of complex systems are often mathematically not tractable.

Parameters

We often don't know the exact parameters of the lineage we are interested in. There is a lot of measures to take to be able to make predictions and we often don't have the money (or the time) to make all these measurements (assuming we are able to accurately measure them). For this reason, we are often relatively good to make predictions for a few model organisms but pretty bad for the vast majority of species.

Applications of evolutionary biology

There are not a lot of applications of evolutionary biology for the moment but still, there are some proving its predictive power. These applications include

medicine and epidemiology (incl. evolution of resistance)
artificial selection and other techniques mainly to improve crops (e.g. nuts)
Various search algorithms such as the genetic algorithm

Note, my answer was partially recycled from this other answer of mine

Answering directly in your text

  It seems like almost any observation can be explained by current evolutionary theory

This is wrong. You should learn more about evolutionary biology (starting with Understanding Evolution by UC Berkeley for example) and you will understand why it is wrong. I can't make a whole introduction to evolutionary biology in a single post.

  Is there any example of someone developing a rigorous framework or model of how evolution works?

Yes, there are thousands of such models depending on the exact evolutionary process of interest. Just to give you a feeling of it, you could have a look at any book recommended on the post Book recommendation on population/evolutionary genetics?. If your knowledge in math is a little weak, then you might want to have a look at the introductory book A Biologist's guide to mathematical modelling in evolution and ecology (Otto and Day). While this book is quite introductory, I would still recommend starting with an even more introductory course as suggested above.

Standard mathematics methods used in evolutionary biology include branching processes, birth-death processes and other Markov Models, mathematical statistics and probability theory, diffusion equations, approximation theory, ...

On a side note, you would note that the development of statistics is very much related to evolutionary biology. This is true historically but is still true for the development of modern statistics. Just to cite one person, Ronald Fisher was an evolutionary geneticist (one of the fathers of the modern evolutionary synthesis) and he invented some of the most used statistical tests (t-test, anova-F-test, Fisher's tests).


How many of the four meiotic daughter chromosomes of a homologous pair can be recombinant via crossover?

There can be and often is more than one crossover per chromosome in meiosis, but how many crossovers occur can depend on the species, sex, age, environment, and which particular chromosome is involved1,2,3. For example, humans typically show 2-3 crossovers per chromosome, but females often show higher recombination rates than males.

However, the structure you drew seems unlikely due to a phenomenon known as crossover interference, which suppresses the occurrence of closely spaced crossovers4,5. See also this historical introduction from Nature.

In Drosophila melanogaster, males do not make any crossovers6. In contrast, females show an average of around 1.2 crossovers per chromosome7. This means that most tetrads have just one crossover, but some will have more and this second crossover can occur between any pair of chromatids. Thus, there can be from two to four  recombinant chromosomes, but most commonly there will be two.

(Note that this last reference (7) is a 2018 review article on this subject and could be a good place for you to start learning more once you've mastered the basics of this subject — figure 1 in particular seems directly relevant to your question.)

References:

Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell. 4th edition. New York: Garland Science; 2002. Meiosis. Available from: https://www.ncbi.nlm.nih.gov/books/NBK26840/
Fledel-Alon, A., Wilson, D. J., Broman, K., Wen, X., Ober, C., Coop, G., & Przeworski, M. (2009). Broad-scale recombination patterns underlying proper disjunction in humans. PLoS genetics, 5(9).
Wang, Z., Shen, B., Jiang, J., Li, J., & Ma, L. (2016). Effect of sex, age and genetics on crossover interference in cattle. Scientific reports, 6, 37698.
Berchowitz, L. E., & Copenhaver, G. P. (2010). Genetic interference: don't stand so close to me. Current genomics, 11(2), 91-102.
Otto, S. P., & Payseur, B. A. (2019). Crossover Interference: Shedding Light on the Evolution of Recombination. Annual review of genetics, 53, 19-44.
John, A., Vinayan, K., & Varghese, J. (2016). Achiasmy: male fruit flies are not ready to mix. Frontiers in cell and developmental biology, 4, 75.
Hughes, S. E., Miller, D. E., Miller, A. L., & Hawley, R. S. (2018). Female meiosis: synapsis, recombination, and segregation in Drosophila melanogaster. Genetics, 208(3), 875-908.


Is there an evolutionary reason for the 5 electron transport complexes in plants and animals?

Your latter assumption is the best we have so far, to my understanding.
Here are a few excerpts from "Early Evolution of Photosynthesis" published in Plant Physiology, October 2010 (emphasis mine):

There is suggestive evidence that photosynthetic organisms were present approximately 3.2 to 3.5 billion years ago...
Overwhelming evidence indicates that eukaryotic photosynthesis originated from endosymbiosis of cyanobacterial-like organisms, which ultimately became chloroplasts (Margulis, 1992). So the evolutionary origin of photosynthesis is to be found in the bacterial domain.

And then there's the abstract from this paper: "Do photosynthetic and respiratory electron-transport chains share redox proteins?"

In purple nonsulfur bacteria and cyanobacteria, there is close interaction between the photosynthetic and respiratory electron-transport chains, which share identical redox proteins.

Purple bacteria and cyanobacteria are some of the oldest known lineages (>3BY, whereas Mitochondria parallel Eukaryotic origins at about 1.4BY - and the endosymbiosis which created Chloroplasts probably came after [plants have both Chloroplasts and Mitochondria, whereas most Eukaryotes just have Mitochondria]), and since the respiratory chain and photosynthetic chain share identical proteins in cyanobacteria and purple bacteria it's not a huge leap to assume that - yup - the 5-protein structure is probably the template used by both Chloroplasts and Mitochondria because of a common source.


Why are killer whales found in the Gulf of Mexico smaller than ones found in the Pacific?

Animals living in colder climate / environment are larger because this way they have better body surface / volume (mass) ration thus they're more resistant to cold. Animals living in warmer areas are smaller thus they have larger body surface compared to their volume(mass) to dissipate heat easier.
Check this wiki page for more details.


Is there a standard way of measuring culture nutrient levels in real time?

Enzyme-based sensors for taking real-time measurements of growth substrates do exist. In brief: an enzyme degrades the substrate and thus changes the local redox state which is detected electronically (example glucose sensor). There's no guarantee that the substrates that you want to measure can be measured using such sensors. Also I think those sensors are fairly expensive and are tailored to specific conditions (ie it's not as simple as dipping the sensor into your culture medium). Practically speaking I think systems using these sensors are limited to monitoring just a small number of substrates.

LCMS or GCMS is the standard method for measuring concentrations of substrates. LC or GC  (without the MS) may be possible, but probably not since there are are many components to culture media and so lots of overlapping peaks. Using this method is labor intensive (lots of samples), likely to be low resolution (temporally), and the equipment is pretty pricey, but if you have access to an LCMS and are willing to put the time in to become an LCMS expert then this is a good option.

Culture based methods using minimal media supplemented with substrates is an option, these experiments may achieve the same thing as real-time monitoring of substrate concentrations. If you have access to a plate reader this will be so much easier. The speed at which different substrates are consumed, and the order in which they are consumed can be inferred by measuring the growth rate of the bacteria and the final population size/dry weight of the culture.

I mention this culture-based method because, although it's not exactly what your question was about, it's much cheaper than the other options and much more established (and in my opinion more fun: you get a great feel for how the bacteria grow and what media they like, and the graphs look great).


How do catalase and other antioxidants neutralize free radicals?

Catalase (hydrogen peroxide oxidoreductase) does not actually quench free radicals. It catalyzes the conversion of hydrogen peroxide to water; the former is a source of a free radical, not a free radical in itself.

This is the proposed mechanism of action of catalase: First one of the oxygens is deprotonated by at the active site of the enzyme. Then the Iron atom that is bound to heme forms a co-ordination complex with the deprotonated oxygen and pulls it away from the other oxygen. As a result the O-O bond breaks.

Free radical quenchers/antioxidants react with the free radicals and form non-toxic products.


Poisonous plants, animals, mushrooms: is this always a kind of defense?

Developing anything by the body takes energy so generally only useful products are conserved. If some sort of mutation caused an organism to produce some sort of by-product that also happened to be toxic to its predators, then that organism is more favored to survive. No species ever starts producing something with the intention of toxicity in a predator/consumer of said species.

These xenobiotics that the plant/animal produces then can either be selected for because they're useful in whatever pathway they are a by-product of. Or they can be conserved because then this by-product has a defense use, regardless of whether the pathway its part of is necessary. Or both could happen, it could be doubly selected for.


If my sunglasses provide "100% UVA/UVB Protection" why can't look directly at the sun?

The damage to your eye does not only come from UV exposure, but also from infrared (IR) radiation. Your eye contains a lens that focuses the incoming rays to a narrow point. This point would get very hot if you looked directly into the sun. This is comparable to focussing the sun on a piece of paper with a magnifying glass, it would start to burn. Also, the rods and cones in your retina are only tolerant to a certain exposure of visible light.

Source: https://eclipse.gsfc.nasa.gov/SEhelp/safety2.html


Why does vaccine development take so long?

Roni Saiba's answer does a good job of explaining what goes into current vaccine development and why it takes so much effort, but I want to directly address the question of why we can't just grow some virus, kill it with UV and have a protective vaccine.
The answer is that not all immune responses to viral antigens are helpful in fighting infections of that virus. In some cases it can be harmful; antibodies to dengue virus of one serotype will attach to viral particles of another serotype but aren't able to inactivate them. The attachment of antibodies to active viruses makes their absorption by cells more efficient, and infections where this antibody-dependent enhancement occurs are more severe than first-time dengue infections.
Some viruses have evolved mechanisms to capitalize on this. The reason we need to get a new flu shot every year is that influenza viruses present a "knob" at the end of their glycoprotein that can change its structure and still retain function. This part is much more 'visible' to the immune system than parts of the virus that can't tolerate changes, so the immune response to this variable part outcompetes and prevents an immune response that would provide long-lasting protection. Conserved stalk-targeting vaccines are being intensely investigated for this reason. SARS-CoV-2 may have a immune-faking mechanism as well: the "spike" glycoproteins responsible for binding the ACE2 receptor and entering the cell convert to their post-binding form prematurely part of the time. Antibodies that bind the "post-fusion" form of the protein don't inactivate the virus, and this form sticks out more so may serve to compete for immune attention with the pre-fusion form that would provide protection if bound by antibodies.
In this last example, we can see that a vaccine made of killed SARS-CoV-2 virus particles would be useless if all of the spike proteins had converted to the post-fusion state. The mRNA vaccines therefore don't encode the natural spike protein, but a mutated version which can't convert to the post fusion state as easily:

S-2P is stabilized in its prefusion conformation by two consecutive proline substitutions at amino acid positions 986 and 987

In conclusion, viruses and the immune system are very complicated. Simple vaccines work for some viruses, and don't work for others. When they don't work, the reason is always different, but hopefully I've communicated some general understanding of the background issues.
EDITS:
This doesn't relate to the rest of my answer but I want to respond to Ilmari Karonen's and there is not enough room in a comment.
Looking at the timeline for SARS-CoV-2 vaccine development gives a very misleading impression of how long it takes generally. This is because ~90% of the development work was already done before COVID-19 was ever identified, in the 18 years since the SARS-CoV-1 outbreak started in 2002. Vaccines against SARS were developed and tested up to phase I trials, but couldn't proceed further since the virus was eliminated. I discussed this in a previous answer to a similar question, but to expand/reformat, here's some of what we knew and had available on March 17th 2020, when the "covid vaccine timeline" begins:

Identified the receptor as ACE2, and knew that antibodies targeting the receptor binding domain (RBD) of the spike protein neutralize the virus. Protocols to test that these were also true of SARS-CoV-2 were already developed and validated. Without this there would have been a lot more trial-and-error experimentation and false starts with vaccine candidates that looked promising but didn't pan out in testing.
Animal models. There is no naturally-occurring model organism for COVID-19. This is a subtle point because other animals can be infected with the virus, and some develop morbidities because of it. However, these are different enough from what we see in humans that something that protects against the reactions we see in the animal can't be assumed to protect against the reactions that cause problems in humans. For SARS, researchers developed transgenic mice that used the human version of ACE2, and showed that the disease they got from SARS were analogous to the disease humans got. This took several years, and the colony was still available when the virus causing the outbreak in Wuhan was identified as SARS-like and researchers started looking for animal models. As an aside, in an interview on This Week in Virology that I can't find right now, one of the maintainers of that colony said they were months or weeks away from shutting it down and euthanizing all the transgenic mice when the pandemic began, so if funding had been just a bit tighter we probably would not be having this particular conversation now.
How to stabilize the pre-fusion form of coronavirus spike proteins had been determined from work on SARS and MERS vaccines.

In addition to these, a large amount of miscellaneous knowledge about coronavirus functions and the immune reactions to them had been accumulated, and this sped up development, and increased confidence in results, which allows vaccine candidate production and testing to proceed more aggressively.
Historically, vaccine development has taken years or decades of research after the need has been identified. Testing is still longer in many cases, but the current case is very unusual.


What would be the shortest and optimal method of extracting human cells for PCR? Is there a colony PCR like protocol for human cells?

I am not confident in my reply, but the article linked below has methods for DNA extraction of various human sample types( blood, hair, urine, Cheek)

For what its worth, my professors always told me DNA extraction was more of an art than a science, and one has to tinker to get it just right.

Maybe for something really quick, you could try a protienase K "squishing buffer" and then boil it for like 10 mins in the buffer and then try running PCR.  I am just an undergraduate though so take my words with a heavy grain of salt.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3792701/

Here is how they gathered the buccal samples:
buccal swabs:

  five healthy adult volunteers were recruited (age range, 22–35 years),
  and demographic information, including age, health condition, sex,
  population ancestry, hair color, and hair treatments, was collected.
  The volunteers recruited were asked to rinse their mouth with tap
  water, 30 s before sampling of buccal swabs, to avoid the
  contamination as a result of food particles. For each individual, both
  sides of buccal mucosa were wiped with a cotton swab for 15 s, and a
  total of five samples was collected in 500 μl 10 M Tris-HCl, 10 mM
  EDTA, 2% SDS, containing 1.5-ml microcentrifuge tubes. Isolation of
  DNA from cotton swabs was performed.

Here is a copy paste, hyphens are mine.

DNA Extration:

  Buccal swabs:

  -samples were suspended in 500 μl lysis buffer [10 mM Tris (pH 8.0), 10 mM EDTA, and 2.0% SDS], and 50 μl 10% SDS, followed by 5–10 μl 20
  mg/ml proteinase K

  -incubated 1–3 h at 56°C until the tissue was totally dissolved

  -The DNA was then extracted from each sample with an equal volume of phenol:chloroform: isoamyl alcohol solution (25:24:1) and mixed gently
  by inverting the tubes for 3 min.

  -samples were then centrifuged (Eppendorf 5415R; Hamburg, Germany) for 10 min with 10,000 g (4°C),

  -upper aqueous layer was transferred to a fresh, sterilized microcentrifuge tube.

  -RNase A (10 μl of 10 mg/ml; Fermentas, Thermo Scientific, Germany) was added, and the solution was incubated at 37°C for 30 min.

  -Equal volumes of chloroform:isoamyl alcohol solution were added and centrifuged (Eppendorf 5415R), again with 10,000 g (4°C) for 10 min.

  -The upper aqueous layer was transferred to a sterilized microcentrifuge tube, and double the volume of chilled isopropanol
  (Merck, Whitehouse Station, NJ, USA) was added, along with one-tenth
  volume of 3 M sodium acetate, and chilled at −20°C for 1 h for
  precipitation.

  -After 1 h, the sample was centrifuged (Eppendorf 5415R) at 10,000 g (4°C) for 10 min.

  -After decanting the supernatant, 250 μl 70% ethanol (Merck) was added, and the pellet was dissolved; the mixture was centrifuged at
  10,000 rpm for 10 min, and the supernatant was decanted gently.

  -The pellet was air-dried under laminar air flow, and the dried pellet was resuspended in 50 μl nuclease-free water or 1× 10 mM Tris-HCl, 1
  mM EDTA, pH 7.6 (TE), buffer and frozen at −20°C or at −80°C for
  storage.