That's describing immunofluorescence microscopy, a more labor-intensive way of doing it. I assume ELISA is more widely used nowadays. And they do mention the option of using human cell lines - that would be the better choice as you want to see if there are antibodies against human nuclear proteins/antigens. Animal cells will have homologous proteins/antigens which some of the antibodies would likely still recognize, but human ones would be better. In an ELISA you would just use purified human proteins/antigens.

The body only really makes antibodies against stuff it has actually encountered. So a human would only have antibodies against animal stuff that has come into contact. Under normal circumstances that might be a bit of hair and the like, rather than more intact/living cells or their nuclei (what ANA tests for).

An ANA test on human blood will usually be ELISA and not have anything to do with animal cells. They will probably use secondary antibodies from some animal (mouse, rat, rabbit, whatever floats your goat) just to bind to and detect human antibodies. You wouldn't be mass producing those antibodies in animals though, rather you'd generate some clonal cell lines.

> > > > > The Ptolemy line, from which Cleopatra VII (the famous Cleopatra) descended, had partial Greek ancestry.

I mean they originally were fully Greek, and they did their level best to stay that way through most of their dynastic period. Even when they adopted the local custom of sibling marriage, that would only have reduced the influx of local non-Greek heritage.

> To me this change to start with the more significant number makes sense. But what led to this change in numbering and when did it take place? Did it follow a longer debate? Was there a transition period?

You could argue we're in a stalled transition period. The teens have not been switched - it "should" be teenthir instead of thirteen etc.

>Could a similar transition happen to other languages like german, where at the moment a "two-and-twenty"-style numbering is in place?

I don't see why not, in principle. Some German books even recommended that in the early days of adoption of the Arabic numerals (which are the reason for the confusion - they go in the opposite direction of original Germanic pronunciation of numbers). Martin Luther wasn't a fan though, and that was probably the deciding factor. It's unlikely anyone will decide to switch it around anytime soon, but not impossible.

Your corneas normally perform gas exchange directly from the air (well, via the tear fluid), rather than being supplied by blood, so your eyes would have a bit of a problem if the breathing apparatus did not cover them.

> The immune system can't really specifically remove those foreign elements, though (though there have been arguments that under some conditions it can). In general if a cell contains harmful foreign elements, the immune system rapidly identifies it and destroys the whole cell.

That definitely depends. Systems like CRISPR-Cas and piRNA, for example, are capable of removing foreign elements without damaging the cell.

Of course immune systems vary dramatically depending on the organism you investigate.

Also some potential alternatives, like chimpanzees, are ruled out for ethical and practical reasons.

Yes, the host genome will grow with integrations like this. Genomes are often inflated due to integration of viral sequences and other selfish genetic elements. This helps explain the extreme variation in genome size among eukaryotes.

> They're defined based on presence (or absence) of certain proteins on the surface of red cells.

Presence or absence of certain glycosylations. The proteins are there regardless of blood type.

> > > > > BUT : insulin released is ONLY trigger by glucose level in blood.

That is not true. Other nutrients affect insulin release too, and there are also control systems affecting the beta cells. So the brain experiencing tasting something sweet could absolutely affect insulin release.

It's true that glucose levels are the most direct factor controlling insulin release, but it's not the only thing involved.

> On top of it all the sequence isn't the end all be all, as you can have post-translational modifications (for more search epigenetics) which change how genes behave

What.

Post-translational modifications happen to proteins after they have been translated. It has no direct link to epigenetics.

CRISPR-Cas9 can cut the DNA in cells whether or not they are dividing.

The problem arises if you then try to rely on HDR to insert a sequence at the break. The HDR pathway is inactive in non-dividing cells, so that strategy will not work. But there are other ways to insert DNA in this scenario, for example HITI. And if you are not trying to insert DNA, but just knock out a gene, it will work anyway.

Depends on the gene defect; if it's enough to edit 3% of your liver cells to produce an important protein to circulate in your blood, then it's pretty reasonable to expect to cure that disease with (non-germline) CRISPR/Cas.

If it's something that needs to be fixed in 100% of a certain cell type, especially non-proliferating cells, then that's going to be very tough. And if it's something that acts during development, then fixing the DNA in an adult would do nothing (the body has already been "built" with the wrong "blueprint").

You have multiple options. You can provide the Cas9 gene in DNA form, but also as mRNA. Or simply the protein, usually pre-assembled with guide RNA into a RNP.

Even the Cas9 DNA delivery has multiple options - viral vector, plasmid transfection, it all depends on the use case.

>Normally, when a break happens, there's another copy of the DNA sequence in the cell - remember you have two copies of each chromosome: one from your mom and one from your dad. So the repair mechanism looks for another similar sequence and copies it (oversimplifying here) to patch the hole.

HDR is mainly active in S and G2 phase, where you get up to four copies of each chromosome - two maternal, two paternal. That provides additional templates for repair (or let's say a stalled replication fork ripped both paternal sister chromatids apart - you then still have two maternal templates available).

NHEJ can also be used for insertion, in strategies such as homology-independent targeted insertion (HITI). Because the ends being joined don't have to be homologous, you can co-deliver a linear DNA fragment and have the end joining pathway insert that where the double-stranded break was made.

>• If we let the cells repair it by themselves, will they not just remake the segment we just cut off?

Depending on the strategy used, they often do just that. Afterwards, you can just select the cells that used the repair template with your insert.

>• If we insert a new gene, how exactly do we deliver it? Does it come with the CAS9 and guide RNA complex? Or do we use another enzyme to deliver it separately?

Traditionally it's a separate piece of DNA we deliver. But prime editing actually delivers the template as part of the guide RNA. That only allows fairly small edits though.

Depends entirely on the particular virus or bacterium. Some are handled well by the immune system, some are not.

I think the real difference here is the availability/relevance of antibiotics vs. antivirals for treating certain symptoms. There are some situations where you can use antiviral drugs, but in many cases it isn't considered worth it (or there simply isn't an effective drug available). But we're also coming around to the fact that antibiotics probably should not be prescribed as often/freely as they have been historically.

You freeze cells slowly, which gives water time to diffuse through the membrane and equalize the pressure.

It was a knockout of the gene for CCR5, a coreceptor for (some types of) HIV. That gives resistance to infection. The coreceptor does not seem to be that important, as some people are in fact born without a functional copy of the gene and appear to be normal (aside from resistance to HIV infection).

We just don't really know enough yet to say whether you're better off with or without CCR5, even putting all the ethical issues aside.

There's also eg. beta oxidation of fatty acids. That cyclically generates a double bond, hydrates it, and cleaves off, until the end of the carbon chain. The hydration can use water that came from the electron transport chain, so oxygen that was initially reduced to water can still end up in CO2.

Bear in mind a lot of catabolic pathways hydrate double bonds, and that water can in principle come from the electron transport chain. So that oxygen ends up attached to carbon, and can end up in CO2.

Also pyruvate decarboxylation (by pyruvate dehydrogenase) is not the only place CO2 comes from. The citric acid cycle releases two equivalents of CO2 for each equivalent of acetyl-CoA added. Pyruvate decarboxylation releases one equivalent of CO2 for each equivalent of acetyl-CoA generated, so two thirds of the CO2 comes from the citric acid cycle here (makes sense, since pyruvate is a 3-carbon unit and only one carbon is initially lost as CO2).

No, that's not about the overall correlation - it's well established that Alzheimer's is correlated with amyloid plaques. The question is whether the amyloid plaques are causing the Alzheimer's. That likely fraudulent study showed that expressing this particular form of amyloid-beta in mouse brains led to Alzheimer-like symptoms alongside accumulation of a particular fragment. That was proposed to be an early precursor to the more severe plaques seen later on (or postmortem).

It refers to all DNA, not just coding sequences.

Sequencing all the coding sequences is called whole exome sequencing.

>
> > > > No there are a lot of different types of cells, bacteria has much simpler cell walls so alcohol dissolves them easily.

Human cells do not even have cell walls, unlike bacteria.

If you're thinking of the cell membrane, then I wouldn't say the bacterial membrane is any simpler. The lipids used are slightly different, but that's not a question of simplicity or complexity. And for example Gram negative bacteria would have two membranes, which is more complex than the single membrane of human cells (though we have additional membranes around some organelles).

In any case, alcohol would damage our cells just as easily as bacterial cells. If they were exposed to the same concentration.