text:
How can I find a complete human genome file?
I'm trying to figure out how I can download a file that represents the complete human DNA sequence. I don't care too much about the format – I'm able to write C++ code to parse it. FASTA seems like a simple format though. What I haven't figured out yet is where I can find a complete file – I have found what appear to be subsets of genes or other sequences or single chromosomes but aren't there 46 chromosomes to include or are some of those duplicates (i.e. 22 chromosomes + 2 sex chromosomes)?
On this page, I have found this list of files under "Human > Genome assembly: GRCh38" but it appears to be broken up by chromosome or something? If so, would I merge these? My goal is to display all the letters via projector onto a wall and I want to be able to point at it and tell someone, that's all the DNA for a human (not a subset). Also, to double check, it is a "genome assembly" I want right? By the way, I don't care about allele variants right now.
Please consider in your response that I am not familiar with much of the lingo, thank you.

Thanks for all the great answers! They were actually ALL helpful to me.

Non-biologist here stepping in.
@swbarnes2 has a good point pinning the fact that (approx) 3Giga nucleotides to display "on a wall" (as you state) even with a good projector is gonna be a hard task.
You'll need several projectors and a hell of a big wall.
(say you take the smallest readable police setting you'll have each letter take a space of 4*6 pixels which for the whole will bring you to ~[227k x 342k] pixels so around 35k HD-projectors)
Which led me to think of why you would want to do such a thing.
The most plausible of which is : it is for some sort of artistic/cultural intent.
In such case, rather than showing letters (ATGC) I recommend to encode it in binary (00,01,10,11) and make this value code for a colored pixel.
That will leave you with a square matrix of around 57k pixels edge (which remains humongous) of shaded in 4 tones black to white dots.
If you want to go even farther, trichromia stands to the rescue, don't make pixels code for just one nucleotide each.
Make them code for one "pseudo-codon" (triplet) each.
First nucleotide defining the red shade,
Second nucleotide defining the green shade,
last nucleotide defining the blue shade.
(plain and simple Additive color RGB stuff).
-EDIT-
Knowing that the notion of codon is invalid and that any nucleotide (except the leading and trailing 2 of each chromosome) could be part of three distinct codon (depending on wether they are in an intron, exon or even alternatively spliced) we see that this grouping by 3 is not THAT right.
In such case why not take even more liberties ?
Group your nucletides by 12 (3 groups of 4) giving you more depths in the color shades.
-END OF EDITED SECTION-
you'll get a much nicer and significantly smaller matrix of [30k x 30k] (which is still gonna take you a big wall and a few HD-projectors ~150 but at this point you can compress the output with several methods and get merged pixels, yet 150 is far less than 35000).
I know I don't bring actual solutions to the asked question (but I really think @Omen did it pretty well) but I sensed that there maybe here some insight worth handing (at the risk of making a fool of myself)

id think a dynamic display might work, showing segments at a time...

I also considered advising to have a dynamic display (to save even more money on projectors ;p) but it seemed either self-evident or out of what I understand to be the required scope.
Yet it IS probably the smartest way of displaying it all.
It's like displaying a whole book, one should consider displaying it page by page not all of it in a bloated block.

A small niggle...we generally don't call three nucleotides together a codon unless they are actually in the coding region of a gene, and are in the frame that's actually being translated.  Most of the genome would not be in "codons".

As I stated in my message, I'm not a biologist, at most I am a bio-enthusiast.
But that is true indeed. If nucleotides are in an intron (that is not interpreted in alternative splicing) then yes it is not part of a codon.
I'll amend my post.
Yet for the purpose that I described, it can still be part of a non-semantic triplet. After all, if the assumption I stated is right, then grouping nucletides by any numbers, in any way (as long as they are consecutive) would not really matter as it won't be anymore relevant. The DNA in itself is not THAT relevant, it's the way it's gonna be transcripted.

Thank you, this is my favourite answer as it gets to the heart of how I want to use the data. I marked another one as the most direct answer for what I asked. I guess I had a few questions in one.

No problem, glad I could be of any (even vague) help.

but aren't there 46 chromosomes to include or are some of those
  duplicates

First of all, while each person has 2 copies of each chromosome, those copies are 99% identical.  So it would be a waste to repeat the whole thing twice.
Second, the technology is such that it's not easy to generate, say, the whole sequence of a chromosome that came from their mother.  You either get sanger traces which show the two sequences superimposed on each other, or very short reads that are not mixed, but you can't tell which parent generated which fragment.
So in general, a reference genome will just have one consensus letter at every position, even though that's not biologically realistic.  It doesn't much matter what the reference is, as long as everyone knows that it's just a reference.

My goal is to display all the letters via projector onto a wall and I
  want to be able to point at it and tell someone, that's all the DNA
  for a human (not a subset).

Can you really display 3 billion characters like that?

Can you really display 3 billion characters like that? No: assuming a character is ~0.03 sq. in. (about 12pt), it would take 14.35 acres of wall to display 3 billion characters.

For us "metric" readers who wonder, 14.35 acres ~= 58072m² which in turn is a bit more than 5 "large" (internationnal cups) soccer fields.

If you want to merge all the sequences as a single sequence then download the sequence of all the chromosomes and then concatenate them. Simple command for that if you use linux:
grep -v ">" chromosome*.fa > entire_genome.txt
Now it makes sense to separate the genome chromosome-wise because there is no physical connection between one chromosome and the other. Moreover there are many orders by which you can concatenate the chromosomes together which will give you 23! number of genome sequences.
Now you should note that all of this can give you serious errors if you are trying to do study genomic context of any gene. So better go chromosome wise.
If I have interpreted you wrong and what you meant is to have all the chromosome fasta sequences in a single file, yet not merge the sequences then it is a pretty straightforward command.
cat chromosome*.fa > genome.fa
Now, what you download is a reference sequence. You have to find variants etc for your data by controlling your alignment parameters.
And I really don't understand why you want to project it on the wall. There are easier and better ways of analyzing the genome.

If I understand your question correctly, you want a single file, i.e. a single string, which represents the sequence of an entire human genome.  However, there is no such thing.  The human genome is stored in 46 different strings (chromosome), and these strings have no natural order.
The numbers used to refer to the genomes are based on their order when arranged by size.
All operations on the genome (such as copying it before mitosis) happen in parallel, with proteins operating on each chromosome individually.
If you want to represent an entire human genome "honestly", I would say your best bet is to put 46 separate strings on the projector, perhaps running parallel to one another like the code in the Matrix.
If you want to display one big long string, any sequence of concatenation is as (in)correct as any other, so just open the files in alphabetical order and concatenate them all.


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Would intravenous insulin + glucose significantly accelerate glycogen synthesis?
Would an intravenous injection of insulin + glucose result in significantly quicker replenishment of exhausted glycogen stores than an injection of glucose alone?
This is a strictly theoretical question and I'm aware of serious dangers of intravenous insulin (Diabetes Spectrum). It is to help with writing a story in which a quick recovery from exhaustion is needed.
After heavy exercise, during which the glycogen stores are depleted, the glycogen can be replenished fully in about a day by consuming high-carbohydrate meals (PubMed).
According to one study, intravenous glucose stimulates glycogen synthesis, but there is no timing mentioned.
Would adding insulin into glucose injection further accelerate glycogen synthesis and for how much? Is there any minimal time needed for glycogen synthesis regardless of the amount of glucose and insulin available?
The added insulin would probably inhibit the natural secretion of insulin from the pancreas, so does intravenous insulin injection even make sense?

What is the mechanism you presume?  (Do you presume signaling in a feedback loop - or, what you mean is depletion of (elevated) blood sugar?

Concluding from this 1991 PubMed article, intravenous (or subcutaneous) insulin may not stimulate glycogen synthesis more than naturally secreted insulin.

Experiments carried out in man have suggested that insulin may play
  only a permissive role in the determination of splanchnic glucose
  uptake. In a study by DeFronzo et al. (5), in which the plasma glucose
  and insulin levels were raised via peripheral intravenous infusion to
  223 mg/dl and 55 μU/ml, respectively, net splanchnic glucose
  uptake was 1.0 mg/kg per min. The rate of glucose uptake did not
  change appreciably when the arterial insulin level was raised further
  to 191 μU/ml.

So, at insulin level 191 μU/ml, there was no greater hepatic glucose uptake than at 55 μU/ml and hence no further stimulation of glycogen synthesis.
According to Emedicine, insulin levels can increase to 276 μU/ml 1 hour after glucose administration.
Which means that even naturally secreted insulin can reach levels that no longer stimulate glycogen synthesis and there is no point to give insulin by injection to stimulate it.

does intravenous insulin injection even make sense?

No, it does not make sense for two reasons:

Half-life of insulin: Insulin has a half-life on the order of minutes. On the other hand, it takes much longer to remove the blood glucose and turn it into glycogen. This is why people with type 1 diabetes receive injections of microcrystalline insulin subcutaneously to form depots that are released into the blood stream at a slower pace.
The body is able to make its own insulin in time: We are used to large increases in glucose levels, and the pancreas is quick in responding with secretion of insulin. So you are trying to find a solution for a problem that does not exist. Of course, injecting glucose instead of eating carbohydrates raises the blood sugar level more quickly. However, the processes downstream of insulin mobilization take some time too. So it the glucose concentration administered intravenously is too high in the absence of extra insulin, extra insulin will not fix the problem (and the problem could be death).

Intravenous insulin injections exist and can be used to treat severe hyperglycemia https://emedicine.medscape.com/article/2049152-overview . They can be used in emergeny cases in hospitals and not by patients at home, because, yes, they can cause dangerous hypoglycemia.

You did not  integrate that "paradox" into your answer: how can hypglycemia by to much insuline occur if, according to answer, adding more insuline does not add to depletion of blood sugar?

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Why will tissue from identical twin be rejected in some cases?

Also, transplants from one identical twin to another are almost never rejected.
[ Source: Medline Plus ]

Why can a tissue from an identical twin be rejected ?

I don't think there is a reason in identic twins, since they have identic surface antigens on the cells.

MattDMo, I think you're right on.  Also remember the thymus is where T-cell recombination and maturation occurs during fetal development, and rates are highest during neonatal period through pre-adolescent childhood - long after sharing a womb.
The immune system keeps developing during childhood.  It's the immune system that's responsible for tissue rejection in transplant.
In our immune system, T cells attack and kill foreign cells in the body.  They're supposed
to ignore cells that carry molecules belonging to their own body.
T cells go through selection in the thymus during these years to eliminate the T cells that attack their own molecules;the rest of the T cells that recognize foreign molecules are allowed to live.
Next, consider that environmentally-induced epigenetics influence the expression of proteins and other products.  Even twins have different experiences and exposures, so there may be a difference in protein components in their bodies.
Also, this is conjecture, but the same concepts involved in autoimmune disorders (which are another topic entirely) might also be involved in some of these situations as well.

While Epigenetics play a role in the different expression of proteins and is different even between identic twins, the important proteins for determining own and foreign come from the HLA-complex. And these are identic in identic twins (but not in other, even closely related persons).

This was too long for a comment, but I have absolutely no evidence for what I'm about to say :)
It looks like that sentence was a little bit of hand-waving, as the author didn't want to categorically state that identical twin tissue would never be rejected. I suspect that in the early days there may have been reports of organ failure (esp. kidneys) in the recipient that were incorrectly identified as rejection episodes. I suppose there's also the slight possibility that one twin could have a mutation event very shortly after the separation of the twins in utero (when all the cells are still pluripotent) that could somehow change or (more likely) silence one or more of the HLA or other surface antigens involved in transplant rejection. This would almost certainly have to happen when the separated twin was a single cell. The mutated twin would therefore not express an antigen the non-mutated twin did, and if the non-mutated twin donated a kidney or other organ to the mutated one, its immune system wouldn't recognize the silenced antigen and could potentially result in rejection.
Like I said earlier, all pure conjecture :)

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Can plants grow under extreme (>1%) carbon dioxide concentrations?
Related to but distinct from this question due to the concentrations involved.
While small carbon dioxide concentration increases can positively impact plant growth under some circumstances and at the same time negatively affect it under other circumstances, these changes are relatively small (doubling CO2 from 0.04% to 0.08%).
Is there any research on plants grown at extremely high (>1%) carbon dioxide concentrations in the air, assuming Earth atomspheric pressure? For the purpose of this question, assume that the plants are supplied with pH modifiers such as limestone in the soil to prevent soil acidification.

Yes they can, but their normal growth is somewhat impaired. A study by Bugbee and collaborators showed that while the yield of rice and wheat increases with CO2 up to about 0.1% CO2, yield decreases sharply as CO2 climbs from 0.1% to 0.25%. There is a smaller loss in yield as CO2 is further increased from 0.25% to 2%.
One interesting thing to note about the study is that the above results turn somewhat on how "yield" is defined. Bugbee defines yield in terms of the mass of the parts of the plant that people can actually eat. They make a note in the study that the vegetative growth of the plants (the green leafy parts humans can't eat) was not affected by the jump from optimal to super-optimal CO2 levels.

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Is it possible to use microalgae to produce food and live on it?
I know microalgae have not less protein and starch, grow quickly, require less. So, is it possible to use them for producing food (replace rice and wheat) and live on it?
Currently, I only saw people eat it as an extra-nutrition.

I don't see why microalgae couldn't be a main food source (putting aside the taste factor).
It contains many different lipids, carbohydrates, proteins and other essential nutrients that are digestible and would be beneficial to humans. I do know that microalgae has a very high lipid content (hence why they're often harvested for biofuels), but it can nonetheless provide nutritional value (ie. feed a starving man).
However, not how this is completely different from living solely off of microalgae. This likely wouldn't be possible, as us humans cannot synthesize all nutrients that we need from scratch. These nutrients are deemed essential nutrients. This problem usually arises when your diet is too restricted to certain types of food. So whether it's microalgae or any other type of consumable, you wouldn't be able to live by only eating that thing.
Another related problem is that growing microalgae is more difficult than it would seem, as is once again usually encountered in second-generation biofuel manufacturing. Temperature, light, cell density, nutrients, and much more must be precisely managed to obtain a increasingly growing population of microalgae. The pros and cons of farming microalgae for billion of hungry people would have to be contrasted with other current agricultures, like corn, soy and rice.

do you have any idea whether algae don't provide the essential nutrients?  a lot of animals only eat algae.

as i knew, the germany use Chlorellaceae for food during the World war 2, the problem is can we relied on it for long term use

@shigeta different animals have different metabolisms and different essential nutrients. For example,  most mammals can synthesize Vitamin C from other nutrients. Humans and other primates have to find it in the food they eat, they can't synthesize it.

while the nutritional profile can change there are also many microalgae and you would have to look pretty hard to find a microbe that is missing, say an essential amino acid.  its more of a problem finding an occasional compound that might not be healthy for human consumption , say.  in terms of making food nutritionally competent supplementing with vitamins minerals and fats is really common in food. its not technically prohibitive to add a vitamin...

lots of filter feeders would agree with you if their throats weren't clogged with algae.


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Can mosquitos bite in self-defense?
When chasing away wasps or bees there is a danger of them stinging us in self-defense.
Can a similar danger arise when chasing away a mosquito which is otherwise not hungry? I understand that mosquitoes bite to feed (by sucking blood), but do they use their bites in self-defense against large targets, like humans? Mosquito bites can be somewhat painful or at least uncomfortable, and can carry dangerous diseases, making them theoretically viable as a self-defense weapon.

Probably not. An immediate defense against predators requires an immediate response. The sting of Hymenoptera like the wasps and bees has an immediately painful reaction.  In addition, in the eusocial (colony-forming) species, multiple individuals typically contribute to defense of their nest. One sting may not deter a predator or invader but dozens or hundreds of stings would create an immediate deterrent.  See for example this paper by [Breed et al. (2004)] on the defense behavior of honey bees.  Animal bites that are immediately painful, such as an ant bite or dog bite create an immediate response in the organism being bitten. Spines and thorns on plants deter organisms from biting the plant. Odors released by skunks and some insect provide an immediate response.
The bite of blood-sucking mosquitoes does not provide an immediate deterrent. (Not all mosquitoes suck blood.) This paper by Ramasubramanian et al. (2008) provides a detailed explanation of how a mosquito penetrates the skin.  The paper is related to microneedle design but they are using the mosquito as a comparison for painless needle design. Go to page 3 to get a description of the mosquito anatomy and piercing behavior. Comparison of painless microneedle design to the mosquito's proboscis is instructive.
The proboscis is the set of modified mouth parts the mosquito uses to penetrate the skin and suck the blood.  The study states that microneedles that penetrate human skin less than 1.5mm is usually painless or effectively so. These needles have a very small diameter, only about 40-100 micrometers in diameter, similar to the width of a human hair. The mosquito's proboscis is about 1.5-2.0 mm long. The diameter of the various structures used to cut through the skin and suck the blood are all less than 40 micrometers in diameter. Thus, the size of the mosquito's proboscis is so small that it does not cause immediate pain, or the pain is so little that it is an annoyance at best. In addition, the proboscis is weak enough that the moquito may have to probe the skin several times before a spot suitable for penetration can be found.
Finally, only the females of blood-sucking mosquitoes feed on blood and have the penetrating mouth parts. Males do not. They feed entirely on nectar and water. Males would thus not be capable of such defense.

Don't they also inject a painkilling substance into the skin, which allows them to be done sucking blood, before their victim even realises, that they where bitten?


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How was 2019-nCoV (Wuhan coronavirus) identified so quickly?
It seems that from the first few cases to identifying 2019-nCoV as a new disease happened very quickly. How were they able to identify this as a new disease and not an outbreak of a previously known but rare disease so quickly? Side question: How many patients were needed to identify this new strain of coronavirus?
If this question can be answered in the generic case as well (how do any new diseases get identified quickly), that would be good too!

I'm voting to close this question as off-topic because this is not a question about a biological problem that can be answered objectively, which is what this site is about, but a question about historic public health measures taken in China.

@David See https://biology.meta.stackexchange.com/a/4040/10204

Your question has come back because of an edit. The meta link you posted over a month ago is irrelevant to whether a question is off-topic or not. It just expresses the view of individuals who have not backed up their opinions by answering your question. Since your original post there is a resource on information about the coronavirus on meta as a community wiki, which you can find here.

Thanks @David. That meta link doesn't answer my question. It's possible the information is in one of the further links somewhere, but then it's a link only answer. "Please provide the relevant details here."


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Walk me through microsatellite markers and PCR

Three polymorph microsatellite markers are used to try and narrow down the location of a disease locus, with the use of PCR with 2
  flanks on each side of the actual polymorphic area. The PCR product is
  then put on gel.

I need help understanding exactly what is going on here. I understand polymorph as "two or more phenotypes in the same population" as by wikipedia. I don't understand what they mean here.
How is the PCR different with 2 flanks from a normal PCR?
I do understand how the gel works.

you should probably include a link to the paper you are reading.... it will make the question easier to answer :)

It's actually very simple. You misunderstood the term polymorph in this situation.
A microsatellite is a sequence composed of a short repeated DNA motif. A polymorph satellite is then simply a microsatellite varying in length between individuals, i.e. composed of more or less repeats of the motif.
The flanks of the microsatellite are the DNA sequences targeted by the primers.
In essence, using two primers flanking the microsatellite you will amplify this specific DNA region and because it varies in length between individuals you can detect that by simple gel electrophoresis.
Note: Microsatellites can also change in sequence (also called polymorphic regions) as they are prone to a high-mutation rate but in this case you would need to sequence it to know how the sequence differs between individuals.


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Genetic engineering for insulin production
In order to put human DNA inside a bacteria in order to have it create Insulin, from what type of cell would you need to take the gene for insulin?
I thought it should be from any somatic cell, since the DNA is identical, but I'm told it should be only from the pancreas, why is that?

You may want to take a look at the Open Insulin Project.

In short, because the easiest way to get the protein coding sequence of the gene is to create cDNA based on the mRNA, and insulin mRNA is only expressed in pancreatic cells.
Insulin gene consists of two exons. That means, amplifying the genome will not give us a coding sequence -- two pieces of that sequence will be interrupted by a large, non-coding intron.

On the figure above, you see the translated (i.e., coding a protein) sequences represented as opaque boxes. They are linked by a slightly curving thin line -- this is a fragment of sequence that will get excised during mRNA maturation.
To get the coding sequence in a straightforward manner, one can create cDNA from mRNA using a reverse transcriptase. Processed mRNA does not contain the intron. And clearly, pancreas cells express the insulin gene mRNA at very high levels, enabling such a procedure, whereas it is practically not expressed by other tissues.
EDIT: Since I see these comments upvoted, I need to debunk them here:

There are introns and splicing in both, bacteria and archea. Both type I and type II introns are present in bacteria. See this review on bacterial type II introns.
Bacteria also have post-translational modifications, including glycosylation. Once thought to be rare, there is an increasing body of evidence that it plays a much more important role than previously thought. See a paper from a decade ago here.

Just to write it explicitly: Bacteria have no splicing mechanism, so inserting the human genomic DNA into the bacteria will not result in a correct mRNA transcript.

@Bitwise: that is not true -- there are bacterial introns and bacteria have splicing -- but yes, the mechanism is different, so it would not work in a straightforward manner.

@leonardo: again, strictly speaking bacteria do have posttranslational modifications of proteins including glycosylation.

@January I stand corrected, thanks. I thought bacteria only have self-splicing introns without any splicing machinery.

@Bitwise: but you are right -- they don't have a spliceosome, but self-splicing is also a splicing mechanism.


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Why are cats attracted to catnip?
According to wikipedia, the active substance is nepetalactone ($\ce{C_{10}H_{14}O_{2}}$) which has weak sedative, antispasmodic, febrifuge, and antibacterial effects in humans. Why are cats so fond of it? Why do they seem to get high on it?
According to the same wikipedia page, the effect is gene-linked but it does not mention which genes, what they code for or any details whatsoever. Are all felines affected in this way or only Felis catus? What is the biochemical mechanism by which cats are attracted to catnip?

This is essentially answered on Wikipedia:  "catnip", although there is no reference to addiction.

if something is on wikipedia a question you can't ask for the same information on stackexchange? I doubt that this is in the guidelines. We would also need to clear out maybe 20% of our content here.

@shigeta I believe that the policy on StackOverflow is the exact opposite. i.e., answers should ideally be canonical and stand on their own and duplicating information found elsewhere is alright. I can't be bothered to find the meta link at the moment, but it's there somewhere.

what I can see here is that catnip is not addictive and i think cats might not be attracted to it until they actually take it in.. http://chemistry.about.com/od/medicalhealth/a/Nepetalactone-Chemistry.htm

Nepeta cataria(Catnip, Catmint, Catnep) is a plant belongs to the family Lamiaceae.It is a  herb that has been recognized for its medicinal properties for many centuries. Over time it has been used in remedies to cure internal cancer, smallpox and scarlet fever.Also it was believed that a dense growth bordering fields helped to protect crops because of its ability to repel rats.
Major Active Constituents of catnip includes a and ß nepetalactone  citronella , a and ß citral , limonene , geraniol , thymol , and carvacrol  epideoxyloganic acid and 7-deoxyloganic acid

Nepeta cataria has a carminative, anti-spasmodic, astringent and anti-flatulent effect on the gastrointestinal system, particularly on the stomach . It is also a diaphoretic and antipyretic in times of fever . Nepeta cataria is similarly recognized as a tonic, mild nervine, and sedative, with a slightly emmenagogue action . With respects to cats, Nepeta cataria produces an aphrodisiac effect.

http://scu.edu.au/scps/index.php/125/
A research paper published in 1994 states that,

Catnip was  the most promising candidate lures tested. The 'catnip-response' is
  inherited as an autosomal dominant (Todd 1962). In trials, behavioural observations showed
  that 50% of the subjects (including all four domestic cats and 8 of 20 feral cats) showed the full catnip response (B. K. Clapperton, unpublished data). This includes sniffing, licking, rubbing and head-over rolling (Tucker and Tucker 1988). Nine of the remaining 12 feral cats approached and sniffed at the catnip samples. This suggests that, although not all cats are genetically determined to respond to catnip , these odours may act as more general attractants.

http://www.southwestnrm.org.au/sites/default/files/uploads/ihub/clapperton-bk-et-al-1994-development-and-testing-attractants-feral-cats-felis-catus.pdf

When cats inhales nepetalactone it stimulates the olfactory bulb, the part of the brain that processes odors. The olfactory bulb then interacts with the amygdala, the brain region associated with emotion and decision-making, and hypothalamus, which controls a variety of bodily functions. From the hypothalamus, nepetalactone stimulates a sexual response in cats that are genetically predisposed to sensitivity to catnip. (About 20 to 30 percent of cats don't seem to react to the plant.)this is why mostly adult cats shows significant addiction to catnip.

http://www.compoundchem.com/2014/06/08/catnip/

The catnip stimulates an Innate Releasing Mechanism(IRM) in domestic cats that elicits a predictably playful behaviour pattern apparently independent of experience and learning(Ewer,1973 and Leyhausen,1975) ,trans-nepetalactone is reported to produce behavioral respondse in cats.It has been verified by Todd in 1963 that capnip is mediated by Olfactory and not gustatory stimuli.Catnip sensitivity has been related to a dominant autosomal geneand to the estrous cycle by Todd.The reports shows catnip elicits behavioral respondses in domestic and wild cats, but these responses are not shown by female sex.In addition, it has been suggested that catnip mimics a pheromone found in cat urine, however evidence supporting this theory is scant.(Todd 1962)

http://link.springer.com/article/10.1007%2FBF00987747#page-1

Seems to be lots of good information here. However, you need to be more careful about including references and to clearly show when you are quoting from other texts. At the moment this is borderline plagiarism. I'm saying borderline since some of the sources are linked in your answer, but it is not clear that the actual text in your answer has been lifted, see e.g. http://scu.edu.au/scps/index.php/125/ and http://www.popsci.com/science/article/2013-04/catnip-effects-humans


text:
Are the inverse problems of Systems Biology impossible to solve?
I have heard Sydney Brenner give a talk [0] on how the entire program of Systems Biology is suspect because, according to him, a chap named Hadamard showed that inverse problems are impossible to solve, or something to that effect.
I find it somewhat odd that no one seems to be paying any attention to this, and many are blithely carrying along trying to reverse-engineer biological organisms. I personally think that this reverse-engineering effort has its place, but Sydney Brenner doesn't seem to think so, and advocates tackling only the forward problem. Here's an excerpt from an abstract to a similar talk of his:

... This notion of computation is, in my opinion, the only valid approach to biological complexity and is opposed to many of the ideas underlying what has come to be called systems biology, which is very fashionable today. It will be shown that systems biology attempts to solve inverse problems — that is, obtain models of biological systems from observations of their behaviour — whereas, what I call computational biology, continues in the classical mode of discovering the machinery of the system and computing behaviour, solving a forward problem.

Is Brenner simply wrong on this or is there something to his objections?

[0] Sydney Brenner, Much ado about nothing: systems biology and inverse problems, 2009.

I've seen many a computational model that blatantly failed to consider very well known biological constraints and were, therefore, useless.

You might find this note useful - http://www.physics.ox.ac.uk/systems/agarwal/PhilSB.pdf
Also this blog post - http://www.pagev.net/2011/04/is-systems-biology-doomed-to-fail-no.html

Another Brenner quote: "Systems biology is low input, high throughput, no output science" and I fully agree.

First link in my comment is not working now - Updated link is http://web.iitd.ac.in/~sumeet/PhilSB.pdf

The answer is mostly no, and this is not as disruptive a statement as it seems to be.
I think Brenner has a point of course and he is not the only one who wonders whether the systems biology can create a holistic model of living things.  Still I wouldn't take this to mean we should stop doing systems biology research.
At 18:30 brenner illustrates the inverse problem with some examples 1) can you create a drum from only the sounds that come from the drum? (no he says). 2) can you solve the molecular structure of a molecule from a diffraction problem (no he says).
Of course we can do both of these, but the point is valid as we need to have an idea of what a drum looks like.  If we did have even a glance at a drum, this lets us build a model (cylinder of diameter d, height h and with a drum head of a tension t and material properties alpha beta, etc) from the sounds is a lot of work, but it could be done.
The problem of solving a molecular structure from diffraction intensities alone has also been solved for small molecules in the 60s I believe by so-called 'direct methods' which don't work well or proteins and larger molecules.  Still the point is that you had to have a good mathematical model of molecules and diffraction to get to direct methods, MIR, MAD and other diffraction only methods. Sorry I can't go into details here...it might bore you to death if you don't care about crystallography.
In both cases the statement is that you need to have that model - what does a molecule look like, what does an x-ray do when it encounters a crystal? In order to get there.  Which makes total sense and I agree with.
I wouldn't read too much into this though, because in practice this has never been done, yet Bragg started with just the diffraction pattern and drew in models from other fields of study.  Given the nature of the proof described, no scientific discovery has ever happened in a mathematical vacuum and systems biology will not either.
Rather I would read this talk as saying that the models we are using for action are not very good yet.  What is happening is that synthetic biology (engineering approaches), experimental observation, and intensive modeling (the 'inverse' and 'forward' approaches Brenner mentions) are all happening at once and are informing each other.
Its hard to imagine that data from inverse approaches can't be an important part of any solution to biology.  Its also looking likelier that a mathematical model alone of biology will be difficult or impossible to find also.  What is currently (IMHO) working is a framework that is both conceptual (and not entirely quantitative) as well as analytical (mathematical) and data driven.

The problem is that you need good data to do good sysbio, and you need lab work to produce good data. You can't simply rely on electronic annotation of genes and even manual curation introduces too many errors. Then where do you get your enzymatic constants from. It's all garbage in, garbage out.

@rwst v true - really the molecular mechanisms of biology are incomplete in every sense - models, mechanisms, data, observability... to some extent this is true for any major scientific system at first (atomic physics had no idea how large an atom was until early 20th century, and even the motion of the planets was difficult to discuss until adequate telescopes could be made).

The article is well known and discussed amongst systems biologists. It makes a good point - high throughput, observational biology cannot substitute for mechanistic studies that provide causal information.
But we know an awful lot about biological systems already. All systems biologists are using information from the forward approach implicitly when they formulate their models. More importantly however, most systems biologists combine the forward and inverse approach in their work. Models are tested and validated by perturbing the systems, and updated according to the results.
Discussions of these kind often devolve into a debate over the semantics of systems biology, in which it's detractors attempt to define "systems biology" in the most unflattering terms possible.


text:
Is a corpse more flexible than a living person?
I read that the majority of humans have the muscular-skeletal potential to perform the splits that you see many gymnasts perform.  The reason a living person with no flexibility training can not achieve the splits is because the person's central nervous system (CNS) automatically constricts the muscle fibers of the legs when the legs move beyond the person's normal range of motion.  I read that this automatic CNS response is called the stretch reflex, and it is the CNS's way to protect the body from performing potentially dangerous movements.
So my question is: does this mean a body with a non-functioning CNS is very flexible?  For example, if I could not perform splits while I was alive, could someone position my corpse into the splits before the event of rigor mortis?

According to the science in this article: healthunify.com/why-cant-everybody-cant-do-a-split/, not really. Flexibility such as splits are only possible by lengthening the skeletal muscle fibers (in the case of splits, this includes the hamstring and iliopsoas). Which means that splits aren't solely dependent on how your CNS functions.
Furthermore, with death eventually comes rigor mortis where due to the body's chemical changes after death (lack of ATP production etc... https://biologydictionary.net/rigor-mortis/), the body becomes rigid which makes it even more difficult for a dead person to do splits than a live one without seriously damaging the dead person's body/muscles.


text:
Can dogs see infrared radiation, i.e., heat?
I, like most of my fellows, prefer my meals served piping hot. As all know, humans sometimes feed their dogs table scraps. If I put down a small piece of chicken from within a piping hot chicken pot pie and alert my small pet dog that it's for her, she'll stand back 2 or 3 feet away from it for a while before eventually consuming it. I am starting to believe that she only does this behavior when the food I put down is too hot for her. So it begs the question I here pose: are dogs able to see heat radiation from afar?

Welcome to the site. Please visit the [help] and take a [tour] to find out more about what this Stack Exchange site does. In particular note the homework page. Questions on here generally require some evidence of prior attempts by the asker to answer it themselves. So - what does a simple google search for "dogs infrared" bring up. I can see a Nature paper...

Why "see" infrared radiation?  You can feel the heat of a fireplace even if the fireplace is covered by some glass that prevents the outflow of hot gasses. Or, one can sense that the sun is shining intensely even with one's eyes closed.

A dog's nose can even sense weak thermal radiation, as found out recently by researches at at Lund University and Eötvös Loránd University. So strong thermal radiation can be detected from a couple of meters away which would explain your observations.
Citation from this article:

To test the idea, researchers trained three pet dogs to choose between a warm (31°C) and an ambient-temperature object, each placed 1.6 meters away. The dogs weren't able to see or smell the difference between these objects. (Scientists could only detect the difference by touching the surfaces.)
After training, the dogs were tested on their skill in double-blind experiments; all three successfully detected the objects emitting weak thermal radiation, the scientists reveal today in Scientific Reports.
Next, the researchers scanned the brains of 13 pet dogs of various breeds in a functional magnetic resonance imaging scanner while presenting the pooches with objects emitting neutral or weak thermal radiation. The left somatosensory cortex in dogs' brains, which delivers inputs from the nose, was more responsive to the warm thermal stimulus than to the neutral one. The scientists identified a cluster of 14 voxels (3D pixels) in this region of the dogs' left hemispheres, but didn't find any such clusters in the right, and none in any part of the dogs' brains in response to the neutral stimulus.
Together, the two experiments show that dogs, like vampire bats, can sense weak hot spots and that a specific region of their brains is activated by this infrared radiation, the scientists say. They suspect dogs inherited the ability from their ancestor, the gray wolf, who may use it to sniff out warm bodies during a hunt.

Here's the scientific article if you want to dig your nose in a bit further (pun intended)..


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Why are DNA samples stored as biochemical samples and not as binary data?
Why are DNA samples stored in cryogenic conditions as biological (or bio-chemical) samples and not as binary data streams of nucleotide sequences in a hard disk or tape drive?
A few reasons I can hazard a guess at are -

Cost to sequence
Cost of data storage (?)
Reliability  of sequencing?

Is there any motivation - financial or academic to achieve this?

I think it would be really useful if you gave more information about specifically what DNA samples you are talking about and why you think they’re stored cryogenically rather than as sequence data.

@user438383 - I was thinking of the 23&me kind of services and forensic evidence. A DNA of a fugitive can be made available worldwide and matched with active investigations across borders if the DNA were in digital form.

@LordLoh.  23&me does not fully sequence their customer's DNA. Rather they sample some important spots that are known to be informative, and check those sequences. DNA identification for law enforcement generally doesn't using sequencing at all. They rely on  a technology called DNA Fingerprinting. Law enforcement has to hang on to samples so that the defense can examine them with their own experts.

One reason DNA samples are kept is because we might want to do further analysis using them. If we relied on digital records we'd have to synthesize  the physical DNA from the digital record, adding an additional step and possibly introducing errors.
The larger reason is that DNA is not a digital code, it's a large, complex molecule. It happens that many important properties of DNA can be modeled as a simple digital code using the sequence of the four bases, but this is by no means the whole story. For example, in cells with nuclei, the DNA is wound around complex protein structures called histones. The histones in turn can have subtle chemical modifications that have profound influences on whether the DNA wrapped around them is active or not. Furthermore the DNA itself is subject to chemical modifications that aren't usually noted in the standard genetic code. The most important of these is DNA methylation, which again is critical in determining the activity of a region of DNA.
Many people spend their entire careers studying DNA via data streams of nucleotide sequences on computers, but when you have new insights, you often want to test them in a wet lab using physical DNA.

It's also most common to store DNA not as a molecule but as part of an organism that contains all the machinery to make more DNA (and everything else) when you need it; spores, cells, seeds, eggs.

It’s also often not trivial to just synthesize DNA whenever you need it, and this is especially true for larger sequences. Even for something small like an expression vector, one would typically have only the insert synthesized and then subclone and transform it into some organism. All this takes time and money.

The answer by Charles Grant is absolutely correct, especially with respect to our limitations with sequencing DNA of biological origin.
I'd like to add that DNA is also a much more stable storage medium than digital storage. DNA can effectively retain encoded data for at least 2000 years and can still produce living organisms after >30,000 years. Digital storage becomes corrupted within several decades.
DNA also has an extremely high information storage density, and there have been several efforts at encoding digital data as DNA.


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How does a Coronavirus "test kit" work?
A number of countries are using test kits for detecting new cases of nCoV (2019-Coronavirus) and apparently China is running low.
What exactly is in a nCoV "Test Kit" — How does it work?
(Surely they also differ, so in which way do they differ?)

The CDC has made available online its nCoV test kit. Briefly,the kit contains primers and probes for real-time reverse-transcriptase PCR, as well as instructions for appropriate use and (critically) controls and guidelines to avoid false positives and negatives. Kits from different countries may use slightly different primers and probes, though since they are all working from the same sequences and the same principles they should be broadly quite similar.
Explaining how quantitative PCR works and the details of the primers and probes is out of the scope of this SE. A layman's introduction was written by John Timmer at Ars Technica.

According to instructions, the testable specimen include: Respiratory (nasopharyngea, loropharyngeal, broncheoalveolar, tracheal, sputum) and (blood) serum. Can it also be used on urine/fecal  specimen?

Can it also be used on urine/fecal specimen? On the one hand, if you use the kit outside its guidelines, the accuracy, sensitivity, specificity, etc will not be defined. That said, in general conditions for qPCR on most clinical specimens are well understood, and specialists will probably be able to predict conditions that are compatible with the primers. So the answer is probably, It's not recommended for routine lab testing, but specialists with a solid technical understanding will undoubtedly be able to adapt it.

For others like myself who don't know: PCR - Polymerase chain reaction, a technique used to amplify, or make many copies of, a specific target region of DNA.

I don't think you'd expect to find much trace of a respiratory virus in stool or urine.

There are reports that it’s been found in feces, raising the possibility of fecal/oral spread. Unlikely, perhaps, but dismissing it based on weak theoretical grounds seems unwise.

Yes, it an live a long time in stool and urine, please see the links in my nCov Environement question.

SARS was found in stool samples and is thought to be airborne from defecating in a squat position. This may have been an important route of transmission during the SARS outbreak.

"is thought to be" - By whom? Random internet people, or peer-reviewed articles? Frankly this claim looks like racist and ill-informed speculation, and there is far too much of that already on the internet; the last thing SE needs is more of it.

@iayork As little as we all like it, we're operating in a very challenged time at the moment. Many questions and comments are directly taken from non-peer-reviewed research or cutting edge information, research and private communication forums. I'm sure speculation will be dealt with better in a few months as research and pandemic fallout will become more clear.

@not2qubit I'm pretty sure iayork and Matthew Martin were talking about the old SARS outbreak, not the COVID-19 outbreak

There are actually 3+ types of test kits widely used to diagnose diseases caused by viruses. We can check for the nucleic acid of the virus, the antigen of the virus that would cause an immune response or the antibody produced during the immune response of the patient. Since we've already got the whole sequence of the nCoV, the test kits normally used this time (at least in China) fall into the nucleic acid class.
To diagnose a patient with this type of test kit, the patient's nasopharyngeal swab, sputum or alveolar lavage fluid would firstly be collected to get a sample of the virus. Some reagents would then be used to extract the nucleic acid in it. After a reverse-transcription which would produce a DNA sequence based on the original single-stranded RNA gene of the virus, a PCR would be performed to amplify it to a large enough amount to eliminate the interference of other genetic materials in the sample (e.g. human DNA, genes of some normally existing bacteria and/or viruses). Here is where the nucleic acid detection kit would take place: the kit contains several characteristic genes serving as a guideline of the PCR, and it would have two primers that flank the target regions for each gene. The kit would also check if the amplification process goes well: it contains fluorescence molecules whose intensity would increase exponentially with the number of amplification (if target fragment exists in the original sample).
The whole set of the testing process is called qPCR (quantitative polymerase chain reaction, or real-time polymerase chain reaction) and it requires highly precise thermal control and real-time fluorescence measurement. The labs where those qPCR instruments are in also need to be high-standard cleanrooms with negative air pressure in order to ensure that samples would not be contaminated by previously amplified DNA products. Unfortunately, most hospital labs in China are not qualified enough to perform tests of this level and that's why it takes so long to truly diagnose a patient with nCoV, even if tons of test kits are already sent to the infected area.
Recently a new method called POCT rapid detection is being tested and it is said that it takes only 15 min to get the result. This method takes a colloidal gold-based immunochromatographic assay to detect the nCoV antibody produced by the patient. Going through the strip, the material tested would pass through a layer of the colloidal gold marker that binds to the antibody, a detection line that contains the corresponding antigen, and a control line that would change colour once it detects any liquid that contains the colloidal gold. This method feels kind of like a pregnancy test, where two lines are bad (i.e. antibodies is detected in the sample as they bind with antigens) and one line is good. It's much faster than the nucleic acid test and it's easier to apply, but the problem is that you can get false positives or false negatives due to the different amounts of antibodies produced by patients. It can be used as a supplementary method for nucleic acid detection, but for clinical use we may want to be more careful with it.
Hope this answers your questions!

Excellent addition to accepted answer! Welcome to Biology SE!

Can you provide a link describing the POCT method, because it's an ungooglable  general term for Point of Care Test, which I don't think is what you intended.

@not2qubit - not quite excellent, as it is not sourced in any way.

@AliceD I know what you mean, but I think we need to give people a little bit of slack for having to source something that have just very recently become available and possibly not even official or marketed yet. (Also some test kits have already been shown to be very poor with only 60% accuracy etc.)

Apparently they are called Point of Care Test as found in this very nice summary:
Recent advances in the detection of respiratory virus infection in humans.

@AliceD My bad, it's my very first answer on bio SE and I didn't quite know how things work here. Thanks for pointing that out!

There are several proposed tests for 2019-2020 novel coronavirus responsible for the Wuhan outbreak. The main techniques these are based on are:

PCR or qPCR targeted amplification

CRISPR-Cas9 genome editing

PCR-based tests are the current standard for diagnosis of viral infections (as these are faster than protein staining and can be made widely available as a kit). Most tests in use are based on PCR targeting sequences unique to novel coronavirus from the publicly release viral genome sequence. These protocols are recommended by the CDC and kits are commercially available or in development from Novacyt SA, or Liferiver Bio-Tech, or Altona Diagnostics. Before kits were available, various companies such as GeneSig offered primer design or primers specific to 2019-nCov which can be performed with standard PCR or qPCR kits. Bio-Rad has been cleared by the FDA to provide a test using Droplet Digital PCR (ddPCR).
PCR-based tests have the advantage that anyone with experience with standard molecular biology techniques or clinical testing can perform them, they do not need specific expertise in microscopy or pathology. Controls are important but there are still issues with low specificity with these kind of tests. For example, PCR tests for influenza type A (a similar virus) have high relatively false-positive rate for a clinical test. Considering the prevalence of the disease, these should only be used to triage people showing symptoms for further diagnosis. Results should be interpreted carefully. It is difficult to design specific PCR-based tests for viruses as they can mutate quickly (as 2019-nCov has been shown to do), especially in emerging epidemic. Note that as an RNA virus "reverse transcription" is required before PCR can be performed. These tests take several hours and it can take days to get results if a lab has many samples to process.
A proposed alternative is tests based on CRISPR. Several startups are working on this including Mammoth Biosciences in San Francisco and Sherlock Biosciences in Cambridge, Massachusetts. However, further testing is required to demonstrate the performance of these tests and none have been FDA approved yet. The advantages of this approach is that the test could be performed faster during an outbreak or epidemic. This is an emerging technology that has not been thoroughly tested.
Updates
Recently, another testing technique has been announced (in English and Japanese) by Drs Hayashizaki and Usui at the RIKEN institute. This proposed testing technique uses the Smart-Amp2 technology which has been commercially released. This technique is based on cycles of amplification similar to PCR but has the advantages of being more cost effective and able to perform the test as fast as 30 minutes.
We should also bear in mind that these tests are all subject to false positive and false negative results. Many current media reports do not acknowledge this limitation. Any reports based on a single case deserve skepticism due to the inaccurate nature of some of these tests. For example, the State of New York was not using the CDC recommended test in February 2020 due to problems that they’ve identified with it.
Research is ongoing to ensure accuracy. In January 2021, the H.U. Group Research institute reported concerns with detecting mutant variants using the Japan National Institute of Infectious Diseases (NIID) primers and adopted the USA CDC recommendations at the time.
Disclaimer: while I was affiliated with RIKEN when SmartAmp2 was published and have since joined the H.U. Group Research Institute, I was not involved in the development of either technology.
Note: at the time of writing, antigen and antibody tests were not yet available.

https://www.synthego.com/blog/sherlock-crispr-diagnostics#Unlocked suggests that crispr-cas13 (not cas9) is just replacing the fluorescent probe. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5961727/ says the theoretical advantage is that a cas9 based probe needs much smaller concentrations

Less PCR cycles required? Running many cycles can take hours. Of course sample preparation and the RT step will take time as well. I’m not sure but this is the benefit claimed by the companies proposing CRISPR-based tests. I doubt it’s cheaper.

For nCov the sequence amplified by WHO' primers is 100 nucleotides long, they recommand 45 cycles of 45s. Now maybe for more common viruses they need longer sequences ?


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How to find the age of a memory stored in the brain?
Is there any way to find how old one's memory is?
One can find the age of stones, plants, animals, etc. So why not find the age of a memory stored inside one's brain?

Are you referring to previous lives O.o ? Regardless, the question is unclear and should be revised if OP wishes an answer on it.

The fundamental problem here is that we don't even really know how memory is stored.  Even if we did, how do you distinguish a memory from a memory of a memory?   For an analogy, say I stored a file (memory) on my first hard disk, back in the '80s.  For nostalgia's sake, I look at it every year or so, and copy  it to each new machine I buy.  Is it still the same file today?

We are only barely beginning to understand how the brain works, including memory. We do know that it is a very complex thing. There are many different kinds of memory; many different processes are involved in creating and recalling memories. One factor that plays into a naïve concept of "how old a memory is" is that "remembering" does not seem to be a passive activity; instead, every time we remember a memory we re-create it.
Having said that I don't see a theoretical reason why there wouldn't be a way to determine the age of a memory... but we currently don't know it.
Consider that we don't magically know the ages of stones, plants, or animals. We learned to figure it out from studying those things, seeing how they change over time, and deducing ways to use that knowledge to guess their age. For example, people discovered that in many climates trees alternate a growing season and a dormant season, and this results in the trunk having "tree rings" for each year they've lived. They've also seen that animals have specific life cycles and look different (if only in size) depending on their ages, and they can use that to roughly estimate an animal's age. Obviously this depends completely on the animal in question; different animals grow in different ways and we can tell their ages in correspondingly different ways, and not always to great precision.
For most of human history we were completely unable to tell the age of stones. Only the discovery of radioactivity, and that the atoms inside stones transmute into other elements over the millennia and that this allows us to tell how long it has been since the stone crystallized (i.e. the atoms got stuck where they are), enabled radiometric dating.
Similarly with memory, it is completely plausible that once we understand very well what a memory is, what its exact correlates in the brain are, and how those correlates change over time, it will be possible to tell how old a memory is. But we aren't there yet (see some articles at the end for where we are).
And while it's plausible that we'll be able to know the age of a memory once we understand it well enough, it is by no means inevitable. To give a counter-example, there is absolutely no way to tell the age of, say, a water molecule. We understand water molecules extremely well. They form and can be destroyed, so for every water molecule there is a certain amount of time since it formed, i.e. it has an age. But a water molecule is just an oxygen atom linked to two hydrogen atoms; its properties are dictated by chemistry and don't depend on how long it has existed. There is no way to tell the age of a given water molecule just from looking at it. Similarly, computers give a timestamp to a file when they create it, but if they didn't do that I don't think we could tell how long a file had been on the disk just from examining the disk itself. So it is certainly theoretically possible that once we understand how memory works, we'll find that we can't, in fact, know the age of a memory.
Here are some papers on memory to give an idea of what neurobiologists are looking at these days:
The Regulation of Transcription in Memory Consolidation
http://cshperspectives.cshlp.org/content/7/1/a021741.short
This paper looks at the role of DNA transcription in the consolidation of long-term memory (as such consolidation apparently requires new proteins being created)
Structural Components of Synaptic Plasticity and Memory Consolidation
http://cshperspectives.cshlp.org/content/7/7/a021758.short
This paper (more or less the same authors) looks at the structural factors involved in consolidating memories by strenghtening synapses and creating new ones.
The many faces of working memory and short-term storage
https://link.springer.com/article/10.3758/s13423-016-1191-6
This recent (2017) paper discusses "Working memory" and how the field doesn't have a single, coherent definition of that concept yet.
Functional neuroimaging studies of encoding, priming, and explicit memory retrieval
http://www.pnas.org/content/95/3/891.short
This 1998 imaging study looks at what regions of the brain light up in various memory-related tasks, and suggests such imaging studies can be useful to investigate brain function. They were right, but notice how general the areas they see are, and how they only can guess at what might be going on there.
The Molecular Biology of Memory Storage:
A Dialog Between Genes and Synapses
http://teachline.ls.huji.ac.il/72336/sphira/Kandelnobellecture.pdf
This is a very long lecture from 2000 from one of the authors of the above papers, summarizing their life's research on the molecular and synapse-level mechanisms of memory. These paragraphs give a historical overview of how scientists have thought memory works:

In his Croonian Lecture to the Royal Society of 1894, Santiago Ramo´n y Cajal
  proposed a theory of memory storage: memory is stored in the growth of new connections[16]. This prescient idea was neglected in good part for half a century as students of learning fought over newer competing ideas. First, Karl Lashley, Ross Adey, Wolfgang Köhler, and a number of Gestalt psychologists proposed that learning leads to changes in electric fields or chemical gradients, which they postulated surround neuronal populations and are produced by the aggregate activity of cells recruited by the learning process. Second, Alexander Forbes and Lorente de No proposed that memory is stored dynamically by a self-reexciting chain of neurons. This idea was later championed by Donald Hebb as a mechanism for short-term memory. Finally, Holger Hyden proposed that learning led to changes in the base composition of DNA or RNA. Even though there was much discussion about the merits of each of these ideas, there was no direct evidence to support any of them [reviewed in 17].
We were now in a position to address these alternative ideas by confronting
  directly the question of how learning can occur in a circuit with fixed neuronal
  elements. Kupfermann, Castellucci, Carew, Hawkins, and I examined the neural
  circuit of the gill-withdrawal reflex while the animal underwent sensitization or habituation, a form of learning in which the animal learns to ignore an innocuous stimulus to siphon when given with monotonous repetition. (We later also extended these studies to an examination of classical conditioning [20].) Our studies provided clear evidence for Cajal’s idea: learning results from changes in the strength of the synaptic connections between precisely interconnected cells [6, 7]. Thus, while the organism’s developmental program assures that the connections between cells are invariant, it does not specify their precise strength. Rather, experience alters the strength and effectiveness of these pre-existing chemical connections. Seen in the perspective of these three forms of learning, synaptic plasticity emerged as a fundamental mechanism for information storage by the nervous system, a mechanism that is built into the very molecular architecture of chemical synapses [95]

Notice how twenty years ago, this person was saying we can finally begin to answer century-old questions of what form memory storage takes in the brain to begin with.
A Putative Biochemical Engram of Long-Term Memory
https://www.sciencedirect.com/science/article/pii/S0960982216311393
Exciting 2016 article: they've maybe found one place where one memory might be stored! First line of the abstract:

How a transient experience creates an enduring yet dynamic memory remains an unresolved issue in studies of memory.

Same idea in the first line of the abstract of this 2016 article on associative memory:
Neural ensemble dynamics underlying a long-term associative memory
https://www.nature.com/articles/nature21682

The brain’s ability to associate different stimuli is vital for long-term memory, but how neural ensembles encode associative memories is unknown.


text:
What's the evidence against SARS-CoV-2 being engineered by humans?
A couple of colleagues suggested in a discussion that the virus that causes COVID-19 appears to be made by humans, since nature could not have produced such an efficient virus — that spreads so fast and whose patients are contagious quite some time before showing signs of infection.
Since my knowledge of biology is very limited, my only counterargument for such a conspiracy theory was along the following lines:

there is a consensus that the most probable source of the first infection was in an animal market in China.
since that animal market was actually composed of a plethora of animals belonging to various species (mixed with humans), a virus had a bigger chance of evolving a mutation that might infect an individual from another species (a thing that is way less unlikely in the wild since many of those animals do not sit close to each others or next to humans).

Clearly, I have made a little story that might be quite far away from how SARS-CoV-2 infected humans, so I am interested in a scientific arguments to support my cause.
Question: What are the main scientific arguments that can be used to debunk COVID-19 being engineered by humans?
Answers that also include explanations more accessible to laymen are greatly welcomed.

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

At the moment, there is very little scientific literature about this, but I found two papers that address the problem and are fairly easy to understand. You can find them in the references. Reference 1 is probably the most interesting and is the basis for this answer.
Edit: It is also interesting to read reference 2 on the origin of SARS-CoV-2; the article also addresses some of the conspiracy theories.
As far as I can see, there are a few major points taken up by conspiracy theories.
1. SARS-CoV-2 leaked from a lab in which research on the Bat CoV (RaTG13) was done:
Unlikely, since the viruses share only around 96% sequence homology, which translates into more than 1100 sites where the sequence of SARS-CoV-2 viruses is different from RaTG13. The mutations are distributed throughout the viral genome in a natural evolutionary pattern, making it highly unlikely that SARS-CoV-2 is a direct descendant from RaTG13. For comparison, the original SARS-CoV and the intermediate host palm civet SARS-like CoV from which it originated shared 99.8% sequence homology, showing a much closer relation.
2. The S (spike) protein from bat SARS-CoV cannot be used to enter human cells via the human ACE2 receptor and therefore has been adapted in the lab:
This is untrue, since a 2013 study of a novel bat coronavirus was published showing the ability of the virus to enter cells via the ACE2 receptor. See reference 3 for details.
3. The spike protein of SARS-CoV contains a unique inserted sequence (1378 bp) located in the middle of its spike glycoprotein gene that had no match in other coronaviruses:
As shown in reference 4, the sequence comparison of the SARS-CoV-2 with closely related other coronaviruses shows that this sequence is not unique to the new virus but is already present in older strains. It shows some difference due to inserted mutations.
4. The claim that SARS-CoV-2 contains four insertions from HIV-1:
The paper claiming this has now been retracted due to severe criticism, and additionally a renowned HIV expert published an analysis (reference 5) demonstrating that the HIV-1 claimed insertions are random rather than targeted.
5. The claim that the SARS-CoV-2 virus is completely man-made:
To design such a "weapon grade" virus in the lab, the design would usually start from a known virus backbone and then introduce logical changes (for example, complete genes from other viruses). This cannot be seen in the genome of the virus; rather, you see randomly distributed changes throughout the genome coming from virus evolution and not directed cloning. It is more likely that this virus originates from the recombination of a bat CoV (to which it is closely, but not directly related) and another, not yet known CoV in an intermediate host, like the palm civet for the 2003 CoV.
References:

No credible evidence supporting claims of the laboratory engineering
of SARS-CoV-2
The proximal origin of SARS-CoV-2
Isolation and characterization of a bat SARS-like coronavirus that
uses the ACE2 receptor
Is SARS-CoV-2 originated from laboratory? A rebuttal to the claim of
formation via laboratory recombination
HIV-1 did not contribute to the 2019-nCoV genome

The mutations are distributed throughout the viral genome in a natural evolutionary pattern. I don't think this means it wasn't engineered per se. Aren't viruses in research labs often "encouraged" to naturally mutate in a certain direction? It could both be engineered and have a "natural evolutionary pattern."

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

Could you please comment about this paper? "Using the SARS-CoV reverse genetics system, we generated and characterized a chimeric virus..." - this is from the abstract of https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4797993/

If you need more [counter]evidence, there's a newer paper "The proximal origin of SARS-CoV-2" by Andersen et al. (March, 17) that touches on the same topic.
The paper brings up two reasons why SARS-CoV-2 is not "made in a lab". The first is the (relative) [in]efficiency of its spike protein; the second is somewhat more complex to explain and is related to cleavage site in said protein that is usually an indicator of rapid (but natural) evolution; this cleavage site is actually not found in the most related relatives of SARS-CoV-2 (the B-lineage of the betacoronaviruses), but only in the more distant A-lineage. Features related to this cleavage site also suggest that it was probably shaped by an immune system, something unlikely to happen in mere cell cultures.

Our comparison of alpha- and betacoronaviruses identifies two notable genomic features of SARS-CoV-2: (i) on the basis of structural studies and biochemical experiments, SARS-CoV-2 appears to be optimized for binding to the human receptor ACE2; and (ii) the spike protein of SARS-CoV-2 has a functional polybasic (furin) cleavage site at the S1–S2 boundary through the insertion of 12 nucleotides, which additionally led to the predicted acquisition of three O-linked glycans around the site.
The receptor-binding domain (RBD) in the spike protein is the most variable part of the coronavirus genome. Six RBD amino acids have been shown to be critical for binding to ACE2 receptors and for determining the host range of SARS-CoV-like viruses. [...] Five of these six residues differ between SARS-CoV-2 and SARS-CoV. On the basis of structural studies and biochemical experiments, SARS-CoV-2 seems to have an RBD that binds with high affinity to ACE2 from humans, ferrets, cats and other species with high receptor homology. [cites 6 references in support]
While the analyses above suggest that SARS-CoV-2 may bind human ACE2 with high affinity, computational analyses predict that the interaction is not ideal [citing: Wan et al.] and that the RBD sequence is different from those shown in SARS-CoV to be optimal for receptor binding. Thus, the high-affinity binding of the SARS-CoV-2 spike protein to human ACE2 is most likely the result of natural selection on a human or human-like ACE2 that permits another optimal binding solution to arise. This is strong evidence that SARS-CoV-2 is not the product of purposeful manipulation.

Wan et al. indeed mention that

several other critical residues in 2019-nCoV RBM (particularly Asn501) are compatible with, but not ideal for, binding human ACE2, suggesting that 2019-nCoV has acquired some capacity for human-to-human transmission.

Basically what Andersen et al. say is that if someone made SARS-CoV-2 in the lab, they could have made it better in terms of human transmission by using what we knew from previously studied SARS-like viruses, instead of coming up with a completely new and somewhat inefficient solution.
Another argument of Andersen et al. (somewhat similar to Chris' #4), which they only mention briefly is that

if genetic manipulation had been performed, one of the several reverse-genetic systems available for betacoronaviruses would probably have been used. However, the genetic data irrefutably show that SARS-CoV-2 is not derived from any previously used virus backbone.

As I mentioned in my first paragraph, Andersen also discuss that SARS-CoV-2 "borrows" a fairly distant feature, namely a polybasic cleavage site, which is only found in more remote "cousins" of the A-lineage of betacoronavirues:

The second notable feature of SARS-CoV-2 is a polybasic cleavage site (RRAR) at the junction of S1 and S2, the two subunits of the spike [...]. This allows effective cleavage by furin and other proteases and has a role in determining viral infectivity and host range. [...] Polybasic cleavage sites have not been observed in related ‘lineage B’ betacoronaviruses, although other human betacoronaviruses, including HKU1 (lineage A), have those sites.

And if you think this was an international manipulation, the trouble is that we still have no precise idea what that cleavage site does in SARS-CoV-2, although cleavage sites observed in other coronaviruses are thought responsible for cross-species infectivity and also are thought to be related to rapid evolution in highly dense populations.

Neither the bat betacoronaviruses nor the pangolin betacoronaviruses sampled thus far have polybasic cleavage sites. Although no animal coronavirus has been identified that is sufficiently similar to have served as the direct progenitor of SARS-CoV-2, the diversity of coronaviruses in bats and other species is massively undersampled. Mutations, insertions and deletions can occur near the S1–S2 junction of coronaviruses, which shows that the polybasic cleavage site can arise by a natural evolutionary process. For a precursor virus to acquire both the polybasic cleavage site and mutations in the spike protein suitable for binding to human ACE2, an animal host would probably have to have a high population density (to allow natural selection to proceed efficiently) and an ACE2-encoding gene that is similar to the human ortholog.
[...]
The acquisition of both the polybasic cleavage site and predicted O-linked glycans also argues against culture-based scenarios. New polybasic cleavage sites have been observed only after prolonged passage of low-pathogenicity avian influenza virus in vitro or in vivo. Furthermore, a hypothetical generation of SARS-CoV-2 by cell culture or animal passage would have required prior isolation of a progenitor virus with very high genetic similarity, which has not been described. Subsequent generation of a polybasic cleavage site would have then required repeated passage in cell culture or animals with ACE2 receptors similar to those of humans, but such work has also not previously been described. Finally, the generation of the predicted O-linked glycans is also unlikely to have occurred due to cell-culture passage, as such features suggest the involvement of an immune system.

Nice paper, thanks for adding. It shows how fast science is moving.

"The (relative) [in]efficiency of its spike protein" does not make sense as a proof of the virus being of natural origin. By that standard, my first car also could not have been designed by humans.

A conclusive proof of CoV2's artificial origin would be finding lab records or samples dated before the epidemic, or finding an obvious unique marker sequence in the cDNA. To date there is no such conclusive proof.
All other "proofs" I have seen are just hypotheses, and they all can be explained by natural processes too. In fact, if your opponents refuses to consider natural causes, such hypotheses become infalsifiable, like the Russel's teapot: any naturally occurring coronavirus can also be recreated in the lab. Here's an article from 2003 in which researchers describe how they have recreated SARS-CoV using a panel of cDNA fragments, which produced a virus identical to the natural strain (except for marker mutations).
For instance, here's a closer look on the infamous "unique sequence in S protein" (called Receptor Binding Domain) of CoV2, compared to RaTG13 (bat coronavirus) and MP789 (pangolin coronavirus):

source
As you can see, the "uniqueness" of this sequence is questionable if we consider that RaTG13 could have combined with a part of MP789 (in the red frame) and accumulated some additional mutations to produce CoV2. The conclusion that such recombination happened artificially can only be drawn if you see no possibility those two viruses could have met in the wild.
There's also a philosophical side to what should be considered "artificial". Two viruses recombining in the wild is natural. How about two viruses recombining in a market? What about a lab cage or waste?

I'm sure if this claim of recombination is plausible, it would be published somewhere else than a Russian (science?) blog.

To help you with that, the same author has published his views here https://onlinelibrary.wiley.com/doi/10.1002/bies.202000240 This is of course no proof as to whom is right but Andersen's paper has 2000 citations by now,  Deigin's has two.

And by that I mean citations in Google Scholar. Deigin's paper has surely made more of an impact on the right-wing press, e.g. https://spectator.us/virus-causes-covid-man-made/


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Why aren't cat hybrids common?
Why aren't hybrids of different species of felinae (say, hybrid of domestic cat with manul, cheetah, ocelot, puma or panther) widespread? Why were they not artifically created?

I'm not sure why you say cat hybrids are not common. Savannah cats spring to mind. Generally speaking animal hybrids aren't common, because they often have to be produced through unnatural methods. See Felid hybrid for a number of examples. It is true that there have not been reported successful hybrids of Felinae and Pantherinae, but I doubt it is not for lack of trying...

In fact I first read about savannah cat, than read that article about hybrids, noticed the hybrid of puma (felinae) and leopard (panthera) and thought that if such species far away from each other on the dendrogram (the one in the first answer) have hybrid, there may be other hybrids of felinae and panthera. So I wondered why there is no so many diverse artifical hybrids.

@KOLANICH I hadn't heard of the pumapard when I answered, so I added an edit mentioning it. It doesn't appear to have been genetically robust, and at least some people have questioned whether it was a leopard-puma hybrid at all, but I can't find any reputable sources on it. It appears to have been sterile. In general such hybrids are not impossible, but at best unlikely, and as I said in my answer their existence is more surprising than nonexistence of others.

In order to form a hybrid, substantial genetic similarity between the organisms is required. To understand why, the successful formation of a zygote from the gametes of the two parents (i.e. fertilisation) in higher animals like mammals requires that the genomes of the organisms be reasonably similar (or homologous; see for instance human fertilisation). This is because successful development of the fetus appears to require that a very specific combination of genes and proteins be present and in the right relative ratios (it's helpful to remember that the genome is a highly analogue computer (see here also), not just a set of instructions to build an organism) - think of the significant effects of simply having an extra copy of one chromosome in Down syndrome, or the fact that triploidy or quadruploidy are often tickets to the death of the human embryo (and so having half of your genome from two different animals could lead to an imbalance in the proteins required to develop normally). I'll be addressing mainly the feasibility of obtaining a hybrid at all; of course in order to become widespread a hybrid would need to be fertile (although see the sterile mule) which would require even more genetic similarity, specifically in order that the chromosomes from each parent can interact, they have to be similar enough that the proteins regulating this process will recognize them as homologous, and enable a process like chromosomal crossover to take place during the meiosis occurring in gametogenesis.
To answer your question about felinae and panthera first, several panthera genomes have been sequenced, and (see here) the tiger for instance has only 95.6% similarity with the domestic cat and diverged 10.8 MYA. For comparison, human and gorilla have 94.8% similarity and diverged 8.8 MYA, so that puts into perspective why you wouldn't expect a tiger-cat hybrid, or for that matter any felinae-panthera hybrids. Those dates are from the linked paper. (Edit: It appears from wikipedia as referred to by the OP above that there actually is a puma-leopard, i.e. felinae-panthera, hybrid which I wasn't aware of (although all of the reports are old, so there is no genetic evidence to prove that it was in fact a hybrid). I assume this may be an exception to the rule; what I was trying to show is why such hybrids are not necessarily to be expected, and as I said below, I'm more surprised about how many hybrids are possible. It does appear though that this particular hybrid is prone to dwarfism, which indicates that it probably does not have a particularly viable genetic makeup, and I think it was sterile).
With regards to your question about felinae hybrids, if you go to Timetree, then it will tell you that Panthera tigris and Felis catus (domestic cat) diverged 14.4 MYA, and by comparison Aciconyx jubatus (cheetah) and Felis catus diverged 9.4 MYA, so it seems reasonable to suppose that they can't hybridise. (But note that P. tigris and P. leo still diverged 6.4 MYA and they can hybridise: the relatedness of two organisms isn't the only thing at work, and a better measure is the genetic similarity; this paper mentions that hybridisation ability correlates both with genetic similarity and time since divergence). Interestingly, this paper actually indicates that the percentage alignment of the cheetah genome to the domestic cat genome is only 91.1% with 93.6% similarity to the tiger, indicating that the cheetah may be a specialised outgroup.
For a more familiar comparison to all of these, Canis lupus which is the ancestor of the domestic dog, dingo, and the gray wolf only arose around 700,000 YA according to wikipedia, although I do not know the exact sequence similarity. Domestic dogs (everything from chihuahuas to great Danes) only diverged 40,000 YA, so the different cats are only superficially similar by this comparison.
There's a diagram on wikipedia shown below which nicely illustrates the different hybrids within felinae (although some seem dubious), so you can see there are actually quite a lot, and although most of the cats involved haven't been fully sequenced, presumably some of these hybrids cross some of the boundaries which I've mentioned above. They do actually include a successful hybrid between a domestic cat and an ocelot (although I can't find another source for this, so it might not be possible), and a hybrid with a jaguarundi (which appears to be closely related to the cheetah) is described as dubious here. Unfortunately, I don't know if either of those cats has been completely sequenced. Ultimately predicting hybridization is a complicated field.

This image below shows a more detailed phylogeny of the cats to illustrate the evolutionary timescale:

And for a comparison to all of that, this image below (from here) shows the phylogeny of the dog (which you might be more familiar with in terms of hybridisation), and if you realise that the whole part of the tree in B from the bush dog down diverged 9-10 MYA (see here - comparable to the whole cat family) and that the bush dog despite its name is extremely dissimilar to modern dogs (for instance it only has 74 chromosomes compared to the domestic dog's 78), then this will illustrate that the evolution of the modern hybridisable dog family (in C in the image) is tightly packed into a much much shorter time than the entire cat branch. All of the names like D1 on the right are modern dogs.

With regards to your question about artificial creation, I think a point to remember is that a lot of these cats are rare/endangered and although such hybrids are still done, there is also criticism of such proceedings. Anyway, I think a good take-home point is that the cat family is actually very genetically old and diverse. I think it's more surprising how many cats can actually be hybridised.

Terrific answer, +1 seems too little. Welcome to the site!


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Does Remdesivir interfere with human transcription?
Remdesivir is metabolized into a nucleotide analogue. It is incorporated in the viral genomes causing either termination of transcription or a dysfunctional genome. Thus, the new viral particles produces within infected cells are dysfunctional.
However, how does Remdesivir intefere with human transcription, or does it? I'd imagine that a nucleotide analogue could be incorporated into a human mRNA. Can it?
edit: The mithocondria are discussed below. I would also be interested in usual, i.e. nucleic transcription. Is Remdesivir transported into the nucleus? Does human RNA polymerase accept it?

Look at ribavirin, remdesivir is supposedly much less active on human RNA polymerases than on viral RdRp, possibly due to proof-reading mechanisms.

Some liver issues were reported during ebola trials, but you might keep an eye out here: https://clinicaltrials.gov/ct2/show/NCT04292730

Quote from paper referenced by reuns: "In contrast, purified human mitochondrial RNA polymerase (h-mtRNAP) effectively discriminates against remdesivir-TP with a selectivity value of ~500-fold." So it seems that it cannot be incorporated in human mitochondrial RNA. Do you know if it can be transported through the nuclear membrane?

The question in the title asks a medical question — does a drug have side effects — which would be off-topic here, although probably on-topic on SE Medical Sciences. The body of the question asks if the drug affects a particular process in human cells, which is on-topic. Please edit your title to fit your question.

However, how does Remdesivir intefere with human transcription, or does it?
Via https://www.ncbi.nlm.nih.gov/books/NBK548938/:

Nucleoside analogues can cause liver injury by several mechanisms. Most characteristic is a mitochondrial type of hepatic injury that is probably caused by the nucleoside analogue becoming incorporated into or blocking mitochondrial DNA synthesis by the mitochondrial gamma polymerase, leading to a depletion of mitochondria or decrease in their function. Mitochondrial injury can affect multiple tissues thereby causing myopathy, neuropathy, pancreatitis, bone marrow suppression and/or hepatic injury.

Remdesivir trials for treatment of Ebola virus infections included in vitro studies of hepato- or liver toxicity. Via https://www.who.int/ebola/drc-2018/summaries-of-evidence-experimental-therapeutics.pdf?ua=1:

Remdesivir and the parent nucleoside analog GS-441524 were extensively profiled for in vitro cytotoxicity and mitochondrial toxicity in multiple relevant cell types. Both remdesivir and GS-441524 exhibited > 3.5-fold margins in most in vitro toxicity assays. Data from in vitro studies with liver cell culture systems demonstrated that human hepatocytes are susceptible to remdesivir mediated toxicity, likely due to high cellular permeability and effective intracellular metabolism of the drug. Systemic metabolites of remdesivir detected in vivo in plasma do not exhibit any in vitro hepatotoxicity at pharmacologically relevant levels.

However, treatments in vivo did not show much in the way of negative effects:

Single dose of remdesivir IV infusion from 3 to 225 mg was well tolerated with no dose limiting toxicity observed. No treatment emergent AEs were observed in more than 1 subject per arm. No evidence of renal or liver toxicity was observed. All AEs were Grade 1 or 2.
Multiple-dose IV administration of remdesivir 150 mg once-daily for 7 or 14 days was generally well tolerated. No subjects had a Grade 3 or 4 treatment- emergent laboratory abnormality during the study. Reversible Grade 1 or 2 ALT or AST elevations were observed in several subjects without abnormalities in total bilirubin, alkaline phosphatase (ALP), or albumin. There was no abnormality or clinically significant change in international normalized ratio (INR) in any subjects. Remdesivir did not show any effects on renal function in the multiple-dose study.

Stereochemistry of the active portion of remdesivir may help make it less toxic.
Human DNA polymerase selects for or preferentially incorporates right-handed or "D" nucleosides. Nucleosides that are of the left-handed ("L") enantiomeric form will still be incorporated by RNA polymerase and have clinical effect from blocking viral replication, but will less likely be used by the machinery in human cells.
Here is another paper that explores how DNA polymerase selects for the D-enantiomer: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4121797/
Other nucleoside antiviral drugs appear to have L-stereochemistry (ibid.) for this reason, to reduce toxicity, so I'd assume the same about remdesivir, as well. I tried looking through a paper on the organic chemistry of remdesivir synthesis, but I don't know enough about that subject to see whether there was a specific step or steps along the drug's synthesis, which involve separation and purification of enantiomers. Perhaps someone with more expertise there can comment.

Don't you think it is much more about proofreading mechanisms of human polymerases than enantiomers. CoV has a proofreading mechanism but it is much less efficient than ours.

Remdesvir cannot interfere with human transcription as it is DNA dependent whereas viral transcription is RNA dependent. And this drug is adensoine analouge which blocks the addition of further nucleotide performed by RNA dependent RNA polymerase.The RNA dependent RNA polymerase is used to replicate viral RNA-based genomes. This competes with adenosine triphosphate to add into the nascent RNA strand. This substitution results in early termination of RNA synthesis and thus prevents the viral genome transcription.
https://www.sciencedirect.com/science/article/pii/S2352771420300380
And this invitro study has shown that Remdesvir discriminates between viral and human RNA polymerase.


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Health effect of electromagnetic and acoustic waves on brain function
What if any effects are there on brain function from prolonged exposure to electromagnetic or acoustic stimulation?

Welcome to Biology.SE! What research have you done before asking it here?

Nothing formal, just been thinking about some things I've been noticing

Homework questions are off-topic here unless you have shown an effort for an answer. Please show some research effort lest the question is likely to be closed.

The title is very uninformative. The title (which I now have edited) should not state whether you estimate the post will be interesting or not and stating that it is about biology carry no information as everything is about biology on Biology.SE.

https://en.wikipedia.org/wiki/Blast_injury

The question is extremely broad.
Electro Magnetic signals
Even this subquestion is very broad. Electro magnetic signals encompass a lot of phenomenon, some of them represent health risks, some of them don't. It is funny to wish to limit the health effect to brain in your question as to reduce the scope of the question given how variable are difference electro magnetic waves can have on matter overall.
Ionizing radiations
Ionizing radiations will obviously represent health risks. But even non-ionizing radiation can pose health risk.
Non Ionizing radiations
Microwave
You are probably aware that you should not put your cat in a microwave!
Retina damage
Intense light can cause photochemical damage to the retina. See here.
Intense infra-red
High intensity infra-red affect cells (see König et al. 1997)
Cell Phone
Overall, there is likely no impact of cell phone radiation on our health. If there were any, it would be minimal.
See this Veritasium video: Do Cell Phones Cause Brain Tumors?. You should also have a look at the skeptics.SE post Do mobile phones have anything to do with brain cancer?.
Cell phone towers
Likely has no health effect. See Do cellphone towers cause health issues?
Other electro magnetic signals
For more information, you should have a look at WHO > Electromagnetic fields and public health: radars and human health
Sound wave
Some sound can cause hearing loss. The frequency of this sound, the intensity and duration of exposure to the sound are all important in determining the degree of the hearing loss. Have a look at this article from the American Hearing Society for more information.

Please add about sound waves as OP is asking about it too.


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Why is it possible to make yoghourt with lactose-free milk?
The function of the Lactobacillus bulgaricus and Streptococcus thermophilus  cultures is to ferment lactose to produce lactic acid. The increase in lactic acid decreases pH and causes the milk to clot, or form the soft gel that is characteristic of yogurt.
In lactose-free milk, all the lactose was transformed in glucose and galactose using lactase. Is it possible for those bacteria to ferment glucose and galactose instead of lactose? Or is this based on other biological reactions?

Conversion of lactose to galactose and glucose is a part of the bacterial metabolism of lactose. So digested lactose would work.
In fact, it should work for all kinds of 6-carbon sugars as lactic acid is produced from pyruvate (end product of glycolysis). See Wikipedia:lactic acid fermentation.