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Why don't viruses reach broad concentration outdoors in a city like allergens?
Why don't airborne viruses reach concentrations that infect most people vulnerable outdoors in a city the way an allergen can cause inflammation to everyone sensitive to it.  Both are (often) microscopic airborne biological particles produced by a bunch of scattered organisms.
Obviously my assumptions are wrong.  Even at the height of Delta or Omicron Covid variants it was generally considered safe to be without a mask if you were alone and outside.  The question is which assumptions are wrong?:

Does particle size mean that allergens stay near the ground and dilute less?
Are there just nowhere near enough organisms emitting at once to matter?
Does the life cycle of a virus just prevent enough people from being infectious at once the way a whole species of tree will start producing pollen?
Since producing virons isn't a normal function of a body are they just produced massively less than something like pollen from a tree?
Is the immune system so powerful that it's easier to trigger an allergic response than an infection to establish a foothold?

Why don't people catch colds like allergies.

If you had the birch tree in your room instead outdoors you'd also have a much higher concentration of birch pollen, especially if you go through it with a wind machine occasionally ;-).

2, 4, 5, and 6.
6 being that the UV light (from the sun), fluctuations in temperature, humidity, wind etc mean that the virions are decayed relatively rapidly for most virus species.
To address (1): In general a virus, such as SARS-CoV-2 or influenza is about 100 nanometres (0.1 micrometres (μm)) in diameter, whereas a pollen is about 10 μm (sizes in links for the respective viruses) - the virus is 100x smaller, but is largely spread through droplet transmission. Droplets are comprised of typical nasal secretions (i.e. snot) and/or saliva and those of about 5-100 μm in size are relatively dense and fall to the floor rapidly. Less than 5 μm can float for quite some time1 but rapidly dehydrate and lose virion integrity, so can't cause infection.
(2) and (4) Infections produce a lot less virus than a tree does pollen. A typical allergenic tree like a Silver Birch (Betula papyrifera) can produce about 2 million pollen grains from a single catkin - up to about 2 billion grains per tree. Multiply that by the number of trees, and you'll get some idea of the number of pollen grains for that species alone. On the other hand an infected person has about 7 million virions per millilitre (ml) of saliva. However, not all of each ml is turned into droplets when speaking and it turns out that only about 37% of 50 micrometre droplets will contain a single virion, and that this drops to 0.37% for 10 μm droplets (see ref 1). This means that each infected person at their infectious peak is only producing putting a tiny proportion of the virus they contain.
(3) and (4) Sort of - plenty of people can be infected at once, as you will have seen during the waves of infection, but once sick they aren't out there walking around constantly emitting virus into the environment, they are in bed, at home or in a hospital (assuming they are following good public health advice). This also ties into the answer for (1) - the droplets just don't last like a pollen grain can. Pollen's purpose is to travel to find a new flower to fertilize, so trees that are wind pollinated have a selective pressure to produce pollen that can last in the environment and still fertilize another tree. Viruses don't have the same selective pressure because transmission relies on "close" contact of a mobile organism - not a tree that sits in the same place and the closest one might be miles away.
(5) How an infection takes place is multifactorial - you need the conditions to be just right for transmission to take place, and a big enough dose of virions to cause an infection (often for things like Influenza or Adenovirus this is in the 3-10 virions range), you then need it to hit the right tissue in the body and evade the immune system. All pollen has to do is hit a mucosal membrane (nose, mouth, eyes etc) for there to be an immune cell there to activate the immune response.
Long story short infection is much harder to do, produces less virions and has lower likelihood of happening.
1: Stadnytskyi V, Bax CE, Bax A, Anfinrud P. The airborne lifetime of small speech droplets and their potential importance in SARS-CoV-2 transmission. Proc Natl Acad Sci U S A. 2020 Jun 2;117(22):11875-11877. doi: 10.1073/pnas.2006874117. Epub 2020 May 13. PMID: 32404416; PMCID: PMC7275719.

I'd be interested in the sensitivity of organisms to allergens. After all, an allergy is an overreaction: The body is excessively sensitive to the allergen. Extreme cases are, I think, powerful allergen detectors. Any specific information on that?

Sorry for nitpicking, but is viruses are 0.1um and pollen is 10um, than 100 times smaller, not 1000 times

@BrunoPérel quite right, I have fixed it.

@Peter-ReinstateMonica That would make a great separate question. I'm no immunologist at all, but I believe that it is down to repeat exposures to the antigen and the body being able to rapidly identify/respond. However, that doesn't explain things like nut/peanut allergies, which can respond to single exposures of tiny amounts.

In another answer elsewhere on StackExchange, a poster estimated that there might be something like 100 g to 1 kg of SARS-CoV-2 virus worldwide, and that's an estimate of all the virus, including what remains in the bodies of infected individuals, not just what makes it to the outside world.
I'm not certain of the accuracy of that estimate, but consider that a single pine tree can make a couple kilograms of pollen. Even if it's off by a couple orders of magnitude, the simple answer is there isn't nearly as much virus out there as there are environmental allergens.
Anecdotally, there's enough pollen during the right season that if I leave my windows open, there is a light, greenish-yellow coating on surfaces near windows. The comparison just isn't anywhere close.

Wouldn't the difference in mass between a pollen grain and a virus complicate this comparison?

@HarrisonPaine if we accept the 100x difference in diameter between pollen and virus cited in bob1's answer above, the difference in mass would be on the order of 100^3 or 1e6. But there are on the order of 1e12 trees in the world (https://www.science.org/content/article/earth-home-3-trillion-trees-half-many-when-human-civilization-arose), not to mention the other pollen producing herbaceous plants so the dimensional analysis still would suggest many orders of magnitude more pollen grains than virus particles from one particular pathogen.

To add to the discussion -surface area probably has more of a relationship than mass. Viruses often have a certain number of antigenic proteins on the surface, constrained by protein geometry of the capsid (though this doesn't apply to SARS-CoV-2 or influenza), but I don't know about pollen.


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What types of sounds do sperm whales produce?
Sperm whales produce echolocation clicks, what are the other types of clicks and other sounds they can produce?

Welcome (again). You'll find that when you browse the help centre it'll point out the need for showing your own research when asking a question. Since you self-answered (encouraged, though not usually so quickly done!), then showing research in the Q seems redundant - on this occasion.

There's an article here about that: https://www.nature.com/articles/s41598-021-84126-8

Sperm whales produce echolocation clicks, known as usual/ regular clicks (Madsen et al., 2002) and buzzes/ creaks (Gordon, 1987), while they are actively foraging underwater. These are distinguished from other types of clicks based on the repetition rate (known as the inter click interval).
Sperm whales also produce slow clicks (Gordon, 1987), surface/ coda creaks (whitehead, 2003), rapid/ fast clicks, and chirrups. These sounds are thought to be used for communication and/ or to scan conspecifics.
Non click sounds include squeals, pips, short trumpets, and trumpets (Pace et al., 2021).
References:
Gordon, J. C. D. The behaviour and ecology of sperm whales off Sri Lanka (Doctoral dissertation, Darwin College, Cambridge, 1987).
Madsen, P. T. et al. Sperm whale sound production studied with ultrasound time/depth-recording tags. J. Exp. Biol. 205(13), 1899–1906 (2002).
Pace, D.S., Lanfredi, C., Airoldi, S. et al. Trumpet sounds emitted by male sperm whales in the Mediterranean Sea. Sci Rep 11, 5867 (2021). https://doi.org/10.1038/s41598-021-84126-8. Available from: https://www.nature.com/articles/s41598-021-84126-8
Whitehead, H. Sperm Whale: Social Evolution in the Ocean (The University of Chicago Press, Chicago, 2003).Return to ref 8 in article

Nice one. Please take our [tour] and refer as and when to the [help] for guidance. Enjoy biology.

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Can electricity be harvested from the soil around plants?
This is a rehash of a question I originally wrote on Skeptics which got moved to Physics, but I'm really after an answer from a biological perspective.
A device called the E-Kaia is making news by claiming to harvest enough electricity from the soil of a pot plant to charge a phone. They claim they can draw 600mA from the soil, which actually wouldn't charge most smartphones in the 1.5 hours they claim in the article (thanks Physics.SE!).
Is there really electricity in the soil around a plant? I can't imagine there being 600mA there for the taking in the soil of a huge tree let alone a pot plant. Maybe it isn't electricity in the soil but some other kind of energy or chemical that can be extracted to generate electricity - it sounds like the lemon battery experiment, which relies on a chemical reaction.
And surely, even if there was electricity there, extracting all of it would damage the plant?

Actually this is a chemistry question. If you put an anode and a cathode in an electrolyte and a salt bridge, you should get a current. If I remember anything about plant biology (which I really don't) nitrogen fixers should be able to pump Nitrogen to bacteria at their roots that convert it to ammonium, which is a cation and nitrite which is an anion. Add some water and you probably have enough of an electrolyte to generate a current of electrons, though how much and if it is efficient enough to charge anything, I don't know.

The question in its entirety sounds like off-topic. I suggest that you can break down the question into subquestions which can individually be on-topic in either physics, chemistry or biology. For biology, your question should be on the lines of whether soil bacteria can create electrochemical potentials of the order of 100mV. Note that even this is a broad question because this all depends on soil type, temperature, mineral/water content and the microbiota.

Electricity may be indirectly generated from plants through the use of a microbial fuel cell, in which biologically-catalyzed chemical reactions are used to drive an electrochemical cell.
A non-technical description of the technology can be found here.  The basic idea is that plants produce organic compounds, which are broken down by soil microorganisms to produce carbon dioxide, electrons, and hydrogen ions.  Ordinarily the hydrogen ions and electrons combine with oxygen to form water, but there are various ways to divert the electrons to travel through an electrical circuit before the oxidation reaction takes place.  This flow of electrons (electricity) can be used as a power source.
This technology is still in its early stages but the process has been demonstrated in some laboratory proof-of-concepts:

Strik, David P. B. T. B.; Hamelers (Bert), H. V. M.; Snel, Jan F. H.; Buisman, Cees J. N. (2008). "Green electricity production with living plants and bacteria in a fuel cell". International Journal of Energy Research 32: 870–876. doi:10.1002/er.1397.
De Schamphelaire, Liesje; Van den Bossche, Leen; Dang, Hai Son; Höfte, Monica; Boon, Nico; Rabaey, Korneel; Verstraete, Willy (2008). "Microbial fuel cells generating electricity from rhizodeposits of rice plants". Environmental Science and Technology 42 (8): 3053–3058. doi:10.1021/es071938w.

The E-Kaia company has not released enough information to say whether their product is in fact a plant microbial fuel cell, a simple earth battery, or a mere scam.

Can you cite the claim that the product is in fact a microbial fuel cell?

@MarchHo  Based on the company's Facebook page, the product uses a "biocircuit" to "capture the residual energy of plants" (in other words, it runs on "woo").  The Daily Mail article implies that the technology is similar to the plant-e technology, which is definitely a microbial fuel cell.  The other possibility is that the E-Kaia product is a simple Earth battery and the plant plays no actual role in power generation.

@MarchHo I have revised my question to primarily address the larger question "Can electricity be harvested from the soil around plants?"

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Co-dependency between carbohydrates, fats and protein in the mammalian diet?
Following up from the question Are carbohydrates an essential component of human diet? I am interested in knowing more specifically how carbohydrates, fats and proteins are linked in the mammalian diet.
For example, cats and other obligate carnivores eat mostly protein, so I imagine that protein has to be converted first to fat and then to glucose and other carbohydrates that the body needs. Does that mean cats are in a state of ketosis constantly? Do cats have special metabolic tuning to optimize on this metabolic pathway?
Human variations seem to suggest that such tuning exists. For example, (historic) eskimoes when fed carbohydrates tend to be especially likely to suffer from obesity and diabetes. This would suggest that their bodies are tuned to exist on protein and fat. What is this tuning?

What makes you think that cats consume mainly protein?

@AlexDeLarge The way that my cats growl at me if I try to take meat away from them.

But meat does not mainly consist of protein. Adult cats have a 26% (dry weight) protein maintenance minimum.

@AlexDeLarge Did you read the web site you just linked? It says a typical steak has 36g of protein and 7g of fat and 0 carbs. If we exclude bones, the typical mouse is made of 85%-95% protein and 15%-5% fat (depending how fat/starving the mouse is). Human athletes have less than 5% body fat, sometimes as little as 2%. All the rest is bone and protein.

Oh, yeah, you might be right. I actually did not think about that the non-protein parts could mainly have zero nutritional value. ;)

Or maybe Inuit are just prone to obesity if they overeat like all Asians

@GrahamChiu First of all, I was referring to all arctic Eskimoes, not just Inuits. Second of all, a lot of Inuits aren't Eskimoes. Third of all, Inuit tribes are located in Canada and Greenland, neither of which is in Asia.

I should have said Mongoloid

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Maximum solar irradiance per plant species
I'm looking for a table or database specifying by plant species, the maximum solar irradiance it can tolerate, but seems not a straightforward search on most engines or open access botany databases. Anyone has any useful reference?
Also I'm assuming that solar irradiance and not heat, is the factor that will kill the plant via leaf burn, but maybe I'm wrong, and heat distress may kill the plant before... or impede the plant development. Any clarification on this will be useful too.
At the concrete example, I'm finding that a hazelnut (Corylus avellana) can't develop at direct sunlight in my location (middle of Spain), as its leaves seem to burn each year, as the solar radiation seems a bit too much for it. I'm planning planting the next ones at the shade of a stone pine (Pinus pinea) to relieve the irradiance from the central hours of the day (If the are good companion trees would be another question)
But you got the convenience of having this information for as much species as possible, to successfully setting plants and avoid killing them, thanks to anyone that can help.

Welcome Greco. For your interest: we have a [gardening.se] stack for you to enjoy too.

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Why this decay term in Anaerobic Digestion Model?
I am reading about the AM2 model, which appears to be a simplified version of the ADM1 model
for modeling anaerobic processes.
The author of this doctoral thesis extended the simpler AM2 model by introducing hydrolysis. Given a substrate state variable $S_1(t)$, he then proceeds as follows:
$$\frac{dS1}{dt}=D_{in}(S_{1in}-S)-k_1\mu_1X_1+k_7\left(k_{dis}X_c-k_{dec,X_1}X_1-k_{dec,X_2}X_2\right)+k_8\left((k_{hyd,ch}X_{ch}-f_{ch,X_c}k_{dis}X_c)+(k_{hyd,pr}X_{ch}-f_{pr,X_c}k_{dis}X_c)+(k_{hyd,li}X_{li}-f_{li,X_c}k_{dis}X_c)\right)$$
The variables $X_1,X_2$ describe the chemical oxygen demand of acidogenic and methanophobic bacteria. The variables $X_{ch},X_{li},X_ch$ describe the chemical oxygen demand of the hydrolized composite $X_c$.
I do not understand the underbraced parts:
$$\frac{dS1}{dt}=D_{in}(S_{1in}-S)-k_1\mu_1X_1+k_7\left(k_{dis}X_c-k_{dec,X_1}X_1\underbrace{-k_{dec,X_2}X_2}\right)+k_8\left((k_{hyd,ch}X_{ch}-f_{ch,X_c}k_{dis}X_c)+(k_{hyd,pr}X_{ch}\underbrace{-f_{pr,X_c}k_{dis}X_c})+(k_{hyd,li}X_{li}\underbrace{-f_{li,X_c}k_{dis}X_c})\right)$$
Unfortunately I have not been able to reach the author. Why would we substract the underbraced terms? Imagine a scenario, where $k_8=0, k_{dis}=0$. In that case, the substrate concentration $S_1$ could become negative just because of dying bacteria (the $k_{dec}$ terms). That does not make any sense to me.
Does it make sense to you?

I would start be asking simple questions. Does your imagined scenario make sense (biologically and/or practically)? Are there organic substrates with these characteristics (a zero disintegration parameter ({k_dis}) and a zero yield coefficient for proteins, lipids, and carbohydrates)? And if so, why would you feed them into your anaerobic processor? Perhaps my lack of expertise in the area is just preventing me from understanding why the scenario you described is problematic.

Thank you for the answer. The continued substraction of available substrate from for example dead biomass (decayed bacteria) strikes me as peculiar. You are right, I will more deeply investigate these basoc questions


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What are the implications for a small bird flying at high altitudes?
Are the aerodynamics of a bird flying at high altitude significantly different than a bird flying at low altitude? I would imagine a bird adapted for low, short flights (such as between bushes and trees) would have a difficult time flying at a higher elevation. What sort of air patterns are the wings of a high-flying bird adapted to mitigate or take advantage of? For instance, I imagine cross-breezes are strong and more frequent, meaning a bird with wings suited for low altitudes would have to flap much more to avoid being pushed around.
For this question I'm only really concerned with the aerodynamics. Obviously a high-flying bird will also be adapted for less oxygen in the air and flying for longer without needing to eat, but that's slightly out of the scope of this question.
Apologies if this is a repeated question, I couldn't find anything relevant here/elsewhere.

75% of earths total mass of air is below 11 kilometers and it is mainly birds with large wings that can reach this elevation of 10 km +.


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Is there any biological evidence corroborating a historians' claim that the 1918 "Spanish flu" originated from China?
A 2014 History article says

According to new research by a Canadian historian, the 1918 flu outbreak that killed 50 million people originated in China. [...]
Humphries found medical records indicating that more than 3,000 of the 25,000 Chinese Labor Corps workers transported across Canada beginning in 1917 ended up in medical quarantine, many with flu-like symptoms. The influenza ripped through the Canadian guards and soon took root in North America. [...]
The mystery of the origins of the “Spanish flu,” is not totally solved, however. “Only DNA testing of samples from these earlier outbreaks can truly confirm or deny the theory,” Humphries acknowledges.

His evidence/argument seems based entirely on the movement of people and occurence of these outbreaks of some kind of flu among Chinese Labor Corps. Has there been any biological research on these earlier outbreaks, proving or disproving a link to the later "Spanish flu"?

I see there's a (more recent) 2016 paper by GD Shanks which disses the idea, to the extent that it might have been the source of the Spanish flu in Europe

Laborers and soldiers from China and Southeast Asia recruited during the First World War by Britain and France have been suggested as the origin of the 1918 influenza pandemic in Western Europe. This study aimed to review the available data to better understand the sources and origins of the 1918 influenza pandemic, and clarify whether, in fact, there was an Asian connection to its onset. We reviewed official mortality lists from the Commonwealth War Graves Commission and the French Ministry of Defence for all-cause (Britain) and pneumonia/influenza (France) mortality, respectively. The results indicated that influenza mortality (estimated 1/1000) in Chinese and Southeast Asian laborers and soldiers lagged other co-located military units by several weeks. This finding does not support a Southeast Asian importation of lethal influenza to Europe in 1918.

I also see that a 2019 review by Worobey, Cox and Gill is more directly dismissive of the idea that Chinese laborers could have transported it through Canada, but again on a historical argument:

Our view is that attempts to pin down the exact location of the first cases of any influenza pandemic are fraught with difficulties, and, for at least two of the three hypotheses noted above there exists strong contrary evidence. The simplest objection is to the idea that Chinese labourers were responsible for the spread of the pandemic virus. Crucially, Shanks [16] showed that influenza cases among Chinese and Southeast Asian labourers and military recruits lagged, rather than led, cases among other groups in the same locales. Moreover, Chinese labourers were also shipped to Europe from the East via Suez or the Cape, although these routes were rapidly abandoned in March of 1917 in favour of transporting them across Canada [10]. Finally, although the Chinese workers were reportedly transported across Canada in sealed trains, it seems unlikely even under this harsh scenario that the virus would not have initiated detectable spread in Canada if these individuals really were the original hosts of the pathogen.

In their 2019 review, Worobey, Cox and Gill also point to the 2014 genetic analysis of Worobey, Han and Rambaut as the "state of the art" in terms of genetic knowledge on the Spanish flu, in which they argue it was more probable of "Western hemispheric" origin.
More reserved, a 2019 review in Science Translational Medicine (by Taubenberger, Kash and Morens) says

Phylogenetic analyses have also been used to model 1918 virus origin but have yielded different dates for the estimated origin of the pandemic virus (36, 76, 79, 80). Until pre-1918 influenza A virus sequences become available, reconciling
the dates of the origin of the 1918 virus phylogenetically will remain difficult. It seems highly unlikely on epidemiological and biological grounds that a virus expressing the pandemic H1 HA, with its inherent virulence, could have widely circulated in humans much before 1918.

(In there, ref 80 is Worobey et al. 2014.)
I guess that means there's no other/biological research on this putative China link presently, but I'm leaving this as an "open question".

I see someone voted to close this "homework question" for showing "no effort" when it basically contains its answer... and I'm pretty sure I've put far more effort into it than the average question here does! The "usuual welcoming" on Bio SE is amazing!

@David: Ehh?? This is not even about the coronavirus. I guess TLDR...

@David:  I'm not seeing the problem.  The question is if there's proof based on DNA or other medical evidence that the 1918 Spanish influenza originated in China.

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical or social aspects of biology. For one of these reasons I think that your question regarding virus epidemiology is off-topic here. Question of a medical nature might be on-topic at SE Medical Sciences. Otherwise you are advised to consult more appropriate reputable sources for such information, some of which are listed here.

@David that strikes me as a quite restrictive definition of what SE Biology should be about! Viral epidemiology, even for a human virus, is squarely within the domain of a big-tent discipline like "biology". This isn't a question about medical aspects of influenza, but a question about evidence for different interpretations of available data, and a request for other sources of data. It isn't Fizz's fault that some of the available data are historical in nature.

“What SE Biology should be about.”  Your or anyone else’s opinions on that are not to the point in this instant. I refer to what the site IS about — defined by others, but to which all users are beholden. Please read my meta post if you wish to understand my motivation.

Hm, not finding a specific post of yours on meta. And I'm not sure what the restrictions on what the site is about are, if they're not these: https://biology.stackexchange.com/help/on-topic. I would put this question squarely in the "on-topic" category based on what it says there, maybe there is something else I'm supposed to be looking at. Yes, this is just an opinion of mine. But with all respect, I don't see the value in gatekeeping a topical and well-researched question, even if it's on the edge for the site (which I don't believe this one to be).


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From where did the selfish gene get its selfishness?
This is in reference to the book The Selfish Gene by Richard Dawkins. Further,

Because there is a law such as gravity, the universe can and will
create itself from nothing. Spontaneous creation is the reason there
is something rather than nothing, why the universe exists, why we
exist. It is not necessary to invoke God to light the blue touch paper
and set the universe going.
— Stephen Hawking and Leonard Mlodinow, The Grand Design, 2010

What was the spontaneous creation that led to this selfish gene?

This is a very introductory question to evolutionary biology. While the book "The selfish gene" is very pleasant to read and directly offers some key notions of modern evolutionary biology, it offers little to no introduction to the basics of evolutionary biology (which is not its goal). I highly recommend that you have a look at a short intro to evolution such as Understanding  Evolution by UC Berkeley for example.
Below, I give a very brief answer to your question but taking an intro course to evolutionary biology would probably be more helpful.
What is evolution?
Evolution is a change in allele frequency in a population through time.
An allele is a variant of a gene (or any other sequence at any locus). A locus is a position in the genome.
How do alleles come to existence?
Alleles are created from previous alleles, through mutations. The process of mutation is random in the sense that the effect of the new allele is "unknown to the organism" which creates this allele. The mutation just occurs and it just has some effect on the phenotype and the fitness.
What are the forces of evolution?
There are a number of forces that affect evolutionary processes such as genetic drift, migration and natural selection for example.
What is natural selection?
Natural selection is the change of frequency of of the alleles at a given locus caused by differential fitness among the individuals carrying the different alleles.
Why one ought to expect that altruism should not exist in nature?
Here the term selfish and altruism are defined in terms of fitness effects. An altruistic individual is one that is performing a behaviour (or having some other phenotypic trait) that is positively affecting the fitness of an individual of the same species while decreasing its own fitness.
Imagine an individual (let's call him the "actor") that has a mutation causing him to be altruistic (in opposition to being selfish). Such "actors" will have a low fitness while its neighbours will take advantage of the altruism of the "actor". There is therefore a differential in fitness between those that are selfish (higher fitness) and those that are altruistic (lower fitness) which ultimately yields a decrease in the frequency of the alleles causing the altruistic behaviour until it completely disappears from the population.
The above paragraph explains why one would expect that altruism should be absent from nature. However, the story is definitely not that simple. But this extension is a story for another time. You will have to understand the difference between "true (lifetime) altruism" and "false altruism", you will have to learn some game theory and finally Hamilton's extension of game theory.
What Dawkins means by selfish gene
In his books, Dawkins uses "selfish gene" often to refer only to genes that are causing meiotic drive (which might be confusing) and to talk about the existence of intra-genomic conflict. There are various mechanisms that can cause meiotic drive. You can learn more about that in Haid and Berstrom 1995, Jeanike 2001 or Jeffrey and Neuman 2002 for examples.

The existing answer provides a very thorough discussion of evolution, which is actually the biological part of the question. I will address  more literally the spontaneous creation part ("What was the spontaneous creation that led to this selfish gene?" - OP) and touch a bit on how the first self-replicating molecules came into existence.
Remark: Note that the authors of the quote in the OP are both theoretical physicists - indeed, the question here is more about "how life emerged" rather than "how it evolved".
Symmetry
Spontaneous creation is a reference to a concept known as spontaneous symmetry breaking in physics, as emergence in philosophy, and as self-organisation in chemistry. One could think of a symmetric universe as a place where chemical elements (or elementary particles) are distributed uniformly over the space, regardless of where we are or which direction we look at. (This is a simplified vision of what is understood by symmetry in physics, but it suffices for the purposes of this discussion.) Obviously, this is not what our universe looks like: patches of very dense matter, such as stars, alternate with vacuum, some parts are extremely hot and others are extremely cold, etc. Things get even more complicated when we look at highly organized dynamic matter, such as the living organisms.
Symmetry breaking
All this complexity is a result of a chain of symmetry breaking events. The interactions between the particles, chemical elements, etc. make the symmetric states unstable, and so they disintegrate into the less symmetric ones. Exactly which less symmetric state is chosen is a matter of accident - e.g., a mutation defining a new direction of evolution an emergence of a new trait is accidental.
Example: particles and anti-particles
As an example: every particle has an anti-particle, so one could have expected that the world contains equal number of protons and anti-protons, as well as of electrons and positrons (anti-electrons). Yet, in practice the atoms are made of protons and electrons, and there are very few anti-atoms made of anti-protons and positrons in the universe. This is the result of a symmetry breaking event that happened some time shortly after the Big Bang, when the symmetry between the particles and the anti-particles was broken.
Example: chirality of organic molecules
As a similar but more biologically minded example, one can think of the chirality of organic molecules. When these are artificially synthesized, one usually ends up with an equal proportion of the molecules of both chiralities. Yet, only one chirality is encountered in the living organisms. This is a result of another symmetry breaking event, somewhere at the time when the first self-replicating molecules had emerged and those of one chirality, by pure chance, gave rise to living organisms, while the others were less lucky.
Emergence and evolution of micromolecules has been also analyzed as a symmetry breaking event, notably by Manfred Eigen, although this requires more abstract notion of symmetry.
Order from disorder
While it is fair to say that we understand well how symmetry breaking comes about in non-living matter (in physics and chemistry), and how evolution happens (in biology), it is not immediately obvious that the scientists agree on how the non-living matter becomes a living one. The interdisciplinary nature of the question certainly complicates it. Prigogine and co-workers believed that the dissipative structures were the answer, but Phil Anderson disagreed. Perhaps one could reproach Dawkins and his brand of militant atheism for hiding under the carpet the unanswered scientific questions, for the sake of fighting creationists (who are arguably a minority even among the religious folks.)
References

Erwin Schrödinger, What is life?
Manfred Eigen, Self-organization of matter and the evolution of biological macromolecules
Phil Anderson, More is different; More is different - One more time
I. Prigogine and I.Stengers, Order out of chaos: Man's new dialogue with nature, Nicolis and Prigogine Self-organization in nonequilibrium systems: From dissipative structures to order through fluctuations.
P. Anderson and D. Stein, Broken symmetry, emergent properties, dissipative structures, life: are they related?
Kauffman, The Origins of Order: Self-Organization and Selection in Evolution

there is no difference between living and non-living matter, it is all just chemistry.

@John the degree of organization and complexity. I know that appeal to authority is a logical fallacy, but note that all the people that I named are Nobel prize winners (Schrodinger, Phil Anderson, Prigogine, Eigen).

@John why do you think biology texts refer to a cell as the elementary unit of life? Are viruses alive?

crystals are far more ordered  than living tissue and a rock is just as complex, they are all part of the same spectrum of chemical interactions. living and nonliving matter are both results of the exact same laws of chemistry interacting in the same ways. None of the papers you link claim otherwise. the rest are books by people with no expertise in the subject. a nuclear physicists opinion on the fundamentals of biochemistry is as bad as a biochemists opinion on the fundamentals of  nuclear physics.

Is ice a rock? Is pluto a planet? Is cereal a soup? Is a taco a sandwich? is self replicating RNA alive? Is a single member of a sexual species alive? human subjective categories have no impact on the function of matter. This is the reason there is no universal definition of "alive" or "life" because there is a continuous spectrum of matter that both living and nonliving matter fall on. cells are the elementary unit of life as defined as things made of cells.

@John crystals have very simple symmetries. The fact that chemical reactions are the same says nothing about complexity Anderson's More is different discusses why everything is not reducible just to fundamental interactions. Importantly, live systems take energy and use it to decrease disorder = to construct themselves, contrary to normal direction of entropy; this is something that non-living matter cannot do (unless artificially designed for this purpose).

nonliving matter decreases disorder all the time, every endothermic reaction decreases disorder, it does so at the expense of creating more disorder somewhere else, just like living things. the formation of solid salt due to evaporating water is a decrease in disorder for the salt.

@John very good, we found some common ground. Do you know what is a heat engine?

Yes they exist naturally too, the Hadley cell is an example of a self organizing naturally occurring heat engine. technically the mechanical energy exerted by freezing ice is also a heat engine. self replicating molecules are also technically heat engines.

@John indeed, but these are very simple examples of ordered behavior. Living things have many more levels of complexity. In a way, one can say that there is a continuous increase of complexity from non-living to living matter, and one cannot draw a sharp distinction somewhere.  This is explained in my answer  and the references.

It is not even mentioned in your answer, in fact your answer says the opposite.

@John "All this complexity is a result of a chain of symmetry breaking events." I suggest that you read my answer more carefully and look up the references before further discussion. Less aggressive attitude is also welcome.

@John note also the question that I am answering: "What was the spontaneous creation that led to this selfish gene?"

@John I have added Kauffman's book to the list fo references - this is probably more accessible to people with biological background.


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How to understand Aposematism and Batesian mimicry
EDIT I want to understand the reason for intense animal colors. I.e. I don't want to understand the variety of the colors, just the intensity.
The Wikipedia page for Cethosia biblis says, the intense colors are a "warning" to enemies, which means the enemy is warned by the colors that eating that butterfly may result in death.

[...], while the intense color of the dorsal sides of the wings is a warning
  to predators that the Red Lacewing has a bad taste, deriving from the
  poisonous host plants of the caterpillars.

In general it would make sense to me, that animals have learned something like "intense colors means danger". Although, I don't know how good animals recognize colors, but that would be another question.
But poisonous animals don't have necessarily intense colors. E.g. Sydney funnel web spider is very poisonous, but doesn't have intense colors, while on the other side some very intense colored butterflies are not poisonous like explained here. As a result, the explanation given in the wikipedia article doesn't make sense to me. I estimate it very unlikely, that animals learned something like "intense colors means danger", because there are of course examples where this is not true.
Therefore, I don't think the "Golden poison frog" has survived because his enemies recognize his intense colors and conclude "eating this frog will result in death" are hence hesitated to eat him.
My question is: Why does wikipedia say then, the intense colors of Cethosia biblis are a warning for their enemies?
PS: I just found the correct terms for my thoughts ("aposematism" and "batesian mimicry" and are reading now the appropriate wikipedia article. I didn't knew them when I've asked this question.
PPS: to avoid confusion: @DavidBlomstrom answered this version of my question https://biology.stackexchange.com/revisions/42554/2

The question is hard to understand because it is a a bit poorly phrased. I would advice that you 1) start you sentences with capitalized letters. 2) Introduce a quotation before actually quoting. 3) Clarify the intention behind the use of " around the term "warning signal" or just remove them. 4) Clarify what you mean by "warning signal" 5) Don't use ==> but use language to express causation. 6) Clarify what you mean by "survival of the scar" 7) Use capitalized I for the first person in singular.

Make sure you make sentences. For example this: I mean, i doubt a simple "survival of the scar", because of the colorful, but not poisonous animals. is not a sentence. Being ESL (which I also am) might not help. I am voting to close as unclear.

While I don't understand the question I suppose that your question (assuming you know what you really want to ask) is very broad and is something Why are there so many colors?. As you are talking about toxic animals, you might want to focus on them and try to understand why they are colorful. Btw, poisonous and toxic are not synonym.

thanks for the feedback, i've updated my question accordingly. @Remi.b why are "poisonous" and "toxic" not synonym? The cambridge dictionary lists "poisonous" as alternative term for toxic.


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How quickly new infectious viruses can be identified and isolated today?
Say, tomorrow, a previously unknown disease (with non-unique symptoms) starts spreading: With the techniques we have today, how quickly can we find out which virus might be the root cause?
I am asking this, as I was reading this article about the discovery of HIV:
https://www.pasteur.fr/en/research-journal/news/40-years-hiv-discovery-virus-responsible-aids-identified-may-20-1983
Apparently, it took several years after the epidemiologic observation of AIDS till HIV is isolated and identified as the root-cause. In the case of SARS (2002), this process took less than 5-months:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7112372/
And more recently, for SARS-CoV2, (apparently) it took only 12 days from the first announcement to the genetic sequencing of the virus:
https://www.who.int/news/item/27-04-2020-who-timeline---covid-19
Compared to months/years, identification of the COVID 19 virus within days looks impressive: In the future, can we expect to routinely identify any new infectious virus within days? or cost/effort for these techniques still limit their wider and routine usage?

Here's a hit: technology, specifically sequencing.


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Identify caterpillar
Hi i live in the Nilgiris region of South India and I found this fellow on one of my Lemon Grass plants. About 8-10 cm long with fine hair all over.
Let me know what species this could be. Thanks


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How to generate PDB file for custom single strand DNA squence(46 bp)？
I need to generate a pdb for ssDNA to research the interaction of DNA and proteins.
I will really appreciate if you can please guide me.
Thank you all for your time.

A related question on SeqAnswers does not seem to have meaningful current answers.
However, a question on ResearchGate points helpfully to this RNA structural modeling server (RNAComposer) that might be useful, once you create secondary structure predictions. Secondary structure is not enough to predict information needed for a PDB.
An alternative somewhat older path to a PDB for RNAs would seem to be MC-fold and MC-sym.
Granted: most of this is for RNAs, which will have a somewhat different structure and mode of folding.
The toolkit seems a little less rich for DNA, but you can still use tools such as ViennaRNA for secondary structure prediction, and there do seem to be some recently published tools for DNA structure prediction (see also here).
There are some further DNA/RNA resources here that may be helpful.


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In mRNA translation, why are there so many factors?
When the small ribosomal subunit binds to mRNA’s 5’-cap, it looks for the complex of three eLFs bound to the poly-A-binding protein (PABP), which circularises the mRNA.  It is then this circular mRNA that the small ribosomal subunit binds to.

In low-nutrient environments, 4E-BP1 binds to PABP, inhibiting it from binding to the 5’-cap complex. I high nutrient environments 4E-BP1 is phosphorylated.

Why (what benefit is conferred?) are the eLFs there?  Why not just have the PABP bind to the 5’-cap to initiate transcription?  And why 4E-BP1?   Why not just phosphorylate PABP directly?
I mean I know that as is, PABP isn’t set up to be usefully phosphorylated, but why is it this way?  It seems a whole bunch energy and resources wasted making these extra proteins, and more room for things to go wrong, more DNA that has to be made and carried around with no mutations and transcribed and translated correctly.

The eukaryotic initiation factor (eIF) proteins are necessary for the ribosome to translate the mRNA. The main benefit is that they, when present, make it easier for the ribosome to find the AUG sequence, which is the start of the protein (as shown in this diagram) by "helping" the Methionine t-RNA find said sequence.
The reason why the mRNA doesn't bind to the PABP directly is for translation regulation. If the mRNA needed to just bind to the PABP and the mRNA for a protein is made when there is more than enough protein, then amino acids are being wasted to make the already abundant protein. If there exist some factors that can control the translation of protein, then the cell can better control protein translation.
Why 4E-BP1 is phosphorylated instead of PABP is because it evolved that way. I know that isn't a satisfying answer, but cells don't really evolve for efficiency, but for "good enough". If it is enough to survive, then why bother changing it?
I hope this answers your question!
Citation for Paper with Diagram: https://biosignaling.biomedcentral.com/articles/10.1186/s12964-020-00607-9


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H is the set of all possible Diplotypes that are consistent with genotype data
I am new to Biology.SX. I have a statistics background, and have almost zero knowledge in genetics. I am trying to understand some things related to genetics in a certain paper of biostatistics.

Haplotype data were simulated using the haplotype patterns and frequencies (shown below) for 5-SNPs along a dabetes susceptibility region on chromosome 22, reported in FUSION study.

I know that haplotypes can be represented as binary sequences. I wonder why all the possible $2^5$ are not present here. (?)
The paper also says that

Let $G=(g_1,\ldots,g_M)$ denote the unphased genotype data for the $M$ loci. $\mathcal{H}_G$ denote the set of all possible diplotypes that are consistent with the genotype data $G$.

If a subject carries at most one copy of the causal haplotype '01100', it belongs to dominant genetic model, if it carries two copies of this haplotype, it belongs to recessive model.

The set $\mathcal{H}_G$ is not clear to me. While computing the likelihood, I need to know $\mathcal{H}_G$. Any help or suggestions?

Disclaimer: Like the OP, I know very little about genetics and I suppose other people in the site can give better answers than me. Anyway, since the question has been unanswered for months I'm posting my answer. Hopefully someone will improve it.
Just beware that "possible" in this context doesn't mean all haplotypes that we can imagine. As the paper says, "$\mathcal{H}_G$ denote the set of all possible diplotypes that are consistent with the genotype data $G$" and that is an additional restriction that allows just some diplotypes - the seven ones listed, not the 32 we can imagine.
Furthermore, please notice that sum of frequencies in the table equals 1, therefore there can be no more haplotypes in the set.
However, it would help if you linked the source where you got those data and quotes.


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What DNA has the most info for getting a person's likeness?
I understand that DNA can come from hair but also from other places.
Let's suppose a person gets their DNA mapped by a company (there are some companies claiming to offer analysis of DNA.. e.g. maybe $200 and maybe some may send the DNA on a DVD)
I understand from this link that human DNA should fit on a DVD
https://stackoverflow.com/questions/8954571/how-much-memory-would-be-required-to-store-human-dna
Would it be possible to get a person's likeness..  if not now, then in future, based on the DNA I might be able to get sent to me digitally.
And presumably the DNA of a 28 year old would be the most ideal for getting (in a computer program) the likeness/image of that person at 28 - the age the DNA was taken?
I hear of the cost of sequencing the human genome to be millions or billions.. Is that more about scientists figuring out what the DNA does, rather than capturing it all?
For example, if I got my DNA captured by a company for $200, then in 50 years time or the future when technology develops, could I use it to produce a likeness of myself?    Or would what a company would send me, not really be all my DNA or be vastly insufficient to create a likeness?
I'm interested in if the kind of test that copmanies off for $200 provides all the information to create an exact replica.
Is a complete replica of a person possible in theory? (e.g. if in future they have a machine to build somebody from DNA) (with the information gathered and that could be sent to the customer by a DNA test for $200, or is it impossible even in theory because the DNA collected and sent is insufficient?)
I'm more interested in the possibility of (in theory) getting a really good likeness, than the personality of a person.
If a company only collects Saliva, is that just a fail.. would they need hair too and DNA from all sorts of human parts, in order to get a good likeness? or better likeness?  Or would it not matter whether it's the hair or the saliva?

Basically you mean cloning a person? Yes, theoretically possible. The DNA is (more or less) the same in all of a person's cells whether from saliva, hair or other tissue. Also, please clarify exactly what this $200 test is.

@vervet somewhere like https://www.23andme.com/   turns out they charge $100  though it doesn't say they send the DNA.  I will have to research further,  I guess since as you say, all DNA of a person whichever part it's from is much the same it shouldn't cost the earth to get all my DNA on DVD so if they can't do it then some company can at reasonable/similar cost.

23andme do not do full genome sequencing. They test a relatively small number of markers (single nucleotide polymorphisms or SNPs) in your DNA, to determine relationships between individuals and deep ancestry.

In addition to vervets' point, you seem very confused about DNA.
Your DNA essentially is the same in almost every cell, throughout your life.   You will get the same sequence from cheek cells at age 28 that you could from a blood sample as an infant.

@vervet ah thanks, got it.. so whati 'm looking for is full genome sequencing which is mentioned here https://en.wikipedia.org/wiki/$1,000_genome   and is $1000 as of Jan 2014

@swbarnes2  You write "You will get the same sequence from cheek cells at age 28 that you could from a blood sample as an infant" <-- Though what about epigenetics.. where genes change over time due to environment.  Or genes getting damaged with age, or how smoking changes your genes.

The raw DNA sequence, the sequence of ACGT will not change.  Your standard DNA sequencing won't chart epigenetic modifications.

I just voted to close because the question is getting too broad including epigenetics. It should be focused and perhaps trimmed down to remove the fluff leaving the essence. Happy to remove the downvote once clarified.

Except for Red Blood Cells, every somatic cell contains two copies of the autosomal chromosomes and a pair of sex chromosomes, either XX or XY (Assuming an average human being) One set is maternal and one is paternal
Some lymphocytes actually recombine their chromosomes, so their DNA will be functionally different to all of the other somatic cells in the body.
Gametes undergo Meiosis and will be haploid, only containing one copy of each autosomal chromosome and one of the sex chromosomes
Cells accumulate mutations over time. The closest you could probably come to an exact clone of a person is if you harvested one of the cells from the eight-cell stage of development. The other seven are able to go on and produce a viable and healthy person. The harvested cells DNA would be the closest to the DNA that combined in the fertilization of the egg. The next closest would likely be stem cells from cord blood. Then probably neurons, as they tend to divide the least.
As the link you posted said, ATCG can be represented in a two bit code, so for about 6 billion bases, you would need about 1.5GB of storage (You need to capture both sets of chromosomes in order to produce a person).

There are places where you could compress the data. Telomeres could be removed and just added back after the fact, as there is likely a standard length for each chromosome of the six nucleotide repeats.
Though you could have a minimum of a two bit code, you would really need a larger data set. You would need metadata, so things like polarity of DNA and chromosome number.
You might also want data about the alleles of each and every gene, that way any errors could be fixed. If you are making the DNA from a data set, there is no sense keeping any genetic defects or diseases in the sequence when you remake it.

Craig Venter, one of the protagonists of the Human Genome Project has a company that is able to produce synthetic DNA for a whole organism. They have reportedly produced a synthetic bacterium, so in theory, they could print DNA from a database and recreate an entire genome, though at what cost and how long I am not sure.
The Original sequencing of the Human Genome did cost Billions of Dollars, however today's sequencing machines can produce an entire genomic sequence more in the range of thousands of dollars. I am not sure if they have broken the $1,000 threshold yet.
Most of the commercial companies do not produce full genomes. They likely do not even sequence a full exome (The areas of all genes that make up the coding sequences of mature mRNAs). They likely do some form of polymorphism analysis to determine if for any given gene you have certain allele other than the Wild Type allele. In this kind of analysis, you do not really need a full sequencing to determine what gene a person has, you only need to identify areas of key differences to determine what is what. That being said, the data collected by a commercial genetics company would likely not be sufficient to recreate an entire genome.
Another important factor is Epigenetics. Just because you have the entire base sequence of the person, doesn't necessarily mean that synthetically creating all 46 of that person's chromosomes would give you the necessary material to transfer into an enucleated oocyte to then produce a new person. You would likely also want to capture the epigenetic encoding as well as the full genome. The epigenetic code that you would likely want would be from one of the cells from the 8-cell stage of development I mentioned earlier. While we have been able to clone adult mammals by nuclear transfer, those animals have had issues with cancer and premature aging. This may have something to do with telomeres, but it also may have something to do with the epigenetic code in early development.
There are other considerations in development as well. There is exchange of nutrients between mother and fetus during development. There is also a sharing of immunity and probably hormonal signals from the mother that can effect development.
Also women are mosaics. A woman would also have the added challenge that every single one of her cells has one of her two X chromosomes inactivated, so depending on which one is inactivated, at random, will determine which of the two X alleles she will be expressing in that cell. It is very possible that her clone would be different from her in appearance.

That is a pretty extensive list. I probably have missed some things. One thing I have definitely left out are all of the structural proteins of chromatin and how to package the DNA into a nucleus. We do not yet understand all of the mechanisms to compact DNA down into a nucleus, so we would have to answer all of those questions before we could figure out how to print and package the DNA to make a clone of a person from a database of their genome.
As we have not currently cloned a human, then it is difficult to say if it is possible. Things that we can do, even in other mammals do not always translate to humans and human cells. There would also be significant ethical hurdles to overcome and based on the current sentiments, it is unlikely, even if we have the technology, that society would allow human clones to be produced.

Neurons undergo a lot of somatic mutations mostly due to L1 retrotransposons. It creates somatic heterogeneity in them. Cells with least number of somatic mutations would be the germ cells.

@WYSIWYG can you post sources. I would be interested in reading more about that. Also which germ cells are you referring to?

You can have a look at this post. I posted a reference there. Germ cells mean spermatids or oocyte progenitor (but most oocytes undergo meiosis at a very early stage and are arrested at metaphase). But you are right that the cells from ICM would be the best but I guess it would be difficult to collect them.


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Why DNA polymerases don't have helicase activity
RNA polymerases have intrinsic helicase ability, while DNA polymerases don't.
I am curious why DNA polymerases evolved in such a way that they lack the ability to unwind DNA.

Does this answer your question? Why do some bad traits evolve, and good ones don't?

Welcome to SE Biology. Please take the time to  finish reading the [Tour] and read the Help section on Asking Good Questions. Two things we require  of posters is clarity and evidence of previous research on the subject. You do not make it clear whether you are aware that there is a separate helicase involved in DNA replication and, if you are, whether you have thought about the differences between DNA-dependant DNA and RNA synthesis. Furthermore, evolution can lead to different solutions to the same problem, when asking why is fruitless.

@tyersome — I don't see how the referenced question is relevant to this one. We are not dealing with bad traits, but different methods of dividing labour in relation to highly evolved fundamental systems of nucleic acid synthesis.


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In traditional plant cloning, why do we require two different vectors (plasmids)?
So I was recently taught cloning in plants and I came to wonder what is the need to first put the gene of interest in the entry vector plasmid and then the final vector plasmid before finally transforming agrobacterium? Can someone make it make sense to me?

Welcome to the site. Please visit the [help] and take a [tour]. If you could explain (edit into your question) which cloning procedure you are using in detail it would help us to know exactly which methodology you are using. In addition, this site has a requirement of evidence that you have had a go at answering this question for yourself, otherwise it will be closed as homework.

There are a lot of different vector systems and some have 2 components, so including the details for your vectors would help. As bob1 notes, reading the material for that system might allow you to answer the question yourself.

If you mean the binary system using the Ti plasmid:
The main issue is that on the massive Ti plasmid there is a difficulty locating unique restriction sites (see section "Introduction of Genes into Plants by Using Agrobacterium"):

However, Ti plasmids are very large and T-DNA regions do not generally contain unique restriction endonuclease sites not found elsewhere on the Ti plasmid. Therefore, one cannot simply clone a gene of interest into the T-region. Scientists therefore developed a number of strategies to introduce foreign genes into the T-DNA. These strategies involved two different approaches: cloning the gene, by indirect means, into the Ti plasmid such that the new gene was in cis with the virulence genes on the same plasmid, or cloning the gene into a T-region that was on a separate replicon from the vir genes (T-DNA binary vectors).

Both of these approaches mentioned involve a two-step cloning procedure for using the entry vector to add the payload to the Ti plasmid.

Edited to link ref and add quote.


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Genetics... Translocation
Can a Translocation of chromosomal parts occur between an autosome and an allosome?
If it occurs in between allosomes,what could be the effect of Robertsonian Translocation between an X and a Y chromosome considering the fact that the small product of a Robertsonian Translocation is mostly lost!??!

Can a Translocation of chromosomal parts occur between an autosome and an allosome?

In short, yes. A quick scan of a few abstracts gives both clinical and model organism examples.

[I]f it occurs in between allosomes,what could be the effect of Robertsonian Translocation between an X and a Y...

It seems Robertsonian translocations are not ubiquitous amongst the chromosomes and only involve 13, 14, 15, 21 and 22.
HTH.


text:
Embolism risk in cancer
Why is there an increased risk of embolism in any malignancy? I studied that malignancy is a risk factor for pulmonary embolism. Can someone explain me the exact mechanism under which malignancy produces emboli?


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Resources for the study of the environment of Laramidia in the Late Cretaceous
I'm looking for resources (book, web, article, etc.) to learn in detail about the environment of Laramidia in the late Cretaceous, including flora, fauna, landscape, and climate. My goal is to get a picture of what it would be like to step out of a time machine into the North American West during the Maastrichian not long before the mass extinction event that ended the dinosaurs, and hopefully get an idea of how that environment varied by region. So far I've only been able to turn up a few brief articles, and some dense scientific reports (which I read the relevant parts of, but as a layman working without the benefit and context of professional knowledge have been of limited use).
I'm aware this question has some crossover with Earth sciences. But as it might fit pretty well on either site, and I've seen you folks answer more paleontology questions, I'd be grateful if you'd entertain it here.
How can I effectively research the environment of Late Cretaceous Laramidia? (Information directly about Laramidia is also very welcome, if secondary.)


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What does it mean for a type of plant to "vegatatively dominate" as opposed to "taxonomically dominate"?
I'm reading Plants and the K-T Boundary, by Douglas Nichols and Kirk Johnson. On page forty-seven the authors write the following: "By the Campanian many floras were vegetatively co-dominated by angiosperms, conifers, and ferns, but taxonomically dominated by angiosperms."
My first intuition was that this means angiosperms, conifers, and ferns were equally dominating the available resources in many ecosystems, but that at the same time the angiosperms had become more evolutionary diverse. But I'm very new to reading about paleobotany, and biology in general, so I thought I'd better check that. Thanks for your time.
What is the difference between vegetative and taxonomic domination in the above example?


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Do the individual claws of a bear have names?
The question seems pretty self-explanatory (if perhaps a little odd). Anatomical names or colloquial names are both appreciated, especially the latter if they exist.

I would be surprised if they do!
Bears have 5 clearly visible toes per paw. You could just name the claws based on the fingers it is on (thumb, index, middle, ring, pinky).


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Fish Carcass Identification
Can anyone identify the species of this fish carcass?
This photo was taken in Brooklyn, NY. The fish would have presumably been in Gravesend Bay.

The large lozenge-shaped scales suggest me it could be some sturgeon species. The location is compatible with what Wikipedia says:

In North America, they range along the Atlantic Coast from the Gulf of Mexico to Newfoundland [...]

Specialists may be able to refine a little more the identification, based on location and visible features.

I asked on reddit too and got the same answer, so I think you’re right. Thanks!


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What flower is this grown in Southern China
It is grown in Tropical Southern China. It is not wild.

Google image search, first result, thinks that your photo is a mexican petunia. I find the color fairly specific, and the leaves fairly dark, so i tried a google image search: https://www.google.fr/search?q=mexican+petunia&num=100&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiwm8vigNjdAhVjc98KHeOiAgQQ_AUIDigB&biw=898&bih=461#imgdii=DDoju-SfrCdmOM:&imgrc=xC36dN7qAGPh0M:

Google images sais that it's a mexican petunia, I think it's right due to the good focus of your image, and the different attributes of the photo.
http://www.gardenality.com/ImageViewer/?id=2116&IUID=3&RID=88#imageId=2116


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What is this Peacock-like creature?

In the below picture I believe  bird in the foreground is a female. The one that opens the wings is the male.

Please [edit] your question and give us some more details. How big is this animal? Where did you see it? What sort of habitat? Most importantly, what makes you think that isn't a peacock?

It looks like male Great Argus (Argusianus argus) displaying to a female. The circular markings on the male pheasant's secondaries are pretty distinct. The specific epithet argus refers to a hundred-eyed giant from Greek mythology.

I think you're right, the answer could be improved with a link of some sort & a note to the effect it's a species of pheasant wouldn't hurt either :)


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What spider is that in south of Brazil?
I'd like to know if it is possible to identify the spider in the photo below.

In fact, as shown in the next picture, it is very small.

Location: South of Brazil.

I've seen a very similar cephalothorax pattern before, but I'm not sure where. Perhaps in the Zoropsidae, but I'll have to go look through my books and get back to you.

It would help if you could see how many eyes it have. It helps a lot in spider identification.

This is Arachosia praesignis, a kind of ghost spider from the Anyphaenidae family.

(Photo source: https://inaturalist.ca/observations/150348963 )
See this paper for representatives of both the male and female specimen of this species, plus additional species of the Arachosia genus:
https://www.biotaxa.org/Zootaxa/article/view/zootaxa.3932.1.1
(Available free on ResearchGate: https://www.researchgate.net/publication/273951397_Taxonomic_revision_of_the_American_spider_genus_Arachosia_Araneae_Anyphaenidae#fullTextFileContent )
The paper reports the distribution consistent with where you found it:


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Blood Group Notation
In a textbook, I encountered a notation used when writing blood groups down, which was "I" with the blood group type as a superscript. I was curious as to why the letter "I" is used in this notation and what it means. E.g. Iᴬ and Iᴮ.
Thanks.

Those are names of alleles involved in the ABO blood group system. The “I” stands for isoagglutinogen which is an antigen that causes agglutination of blood cells when reacting with a specific antibody (an isoagglutinin).


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Is osteoid an uncalcified substance?
I recently learned about Osteoid (the substance secreted by osteoblasts during intramembranous ossification), and I read that it was an "unmineralized organic component of bone."
Now, does this mean that Osteoid is un-calcified?? I don't know if I can equate unmineralized with uncalcified but I just wanted to make sure.


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Using formulas to explain why contraction of blood vessels leads to increased blood pressure
I know, I know this is probably a question too simple to be asked on a forum like biology stack exchange. Problem is, I looked many places and can't seem to find a more mathematical approach to explain why the contraction of a BV leads to increased blood pressure (BP).
The main formula i'm looking at is Flow = Pressure/Resistance. In addition, Flow = Area x velocity so Area x velocity = Pressure/Resistance. As the BV constricts, the radius, ie. area, decreases, and so the pressure decreases. But clearly, that is not the case.
What am I missing here?

Basic physiology questions are my personal favourite +1...anyways have you tried it this way (I'm supposing):area decreases, so flow decreases (possibly because resistance (R)  increases in the blood vessel)...now to keep the flow constant the pressure (P) needs to be increased...what I 'm trying to say is that P increases to counter reduced flow as R increases.

There is an important missing assumption in your statement, I've added it in italics:

Contraction of blood vessels leads to increased blood pressure if total flow stays constant.

All you need is your first equation:
Flow = Pressure/Resistance
Decreasing the radius increases the resistance. If flow is constant, then pressure has to increase to get the same flow through the smaller vessel.


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How do you read the histone code?
I took it upon myself to research how methylation/acetylation affects histone tails via post-translational modifications. However, I find myself confused about how to "read" this histone code, specifically for the Euchromatin.
My problem is that there are both acetylations and methylations. Does that mean that the methylation of lysine 4 will cause that portion of the chromatin to be condensed, but the acetylation of the lysine 9 and so on will cause that portion to be decondensed?

The "histone code" is not like the genetic code where one codon in an ORF always is translated to a single amino acid. It's closer to something like GC content or CpG islands: a single instance doesn't tell you anything, but enrichment over some finite window may be biologically significant.
You may want to review the basics, starting with the Wikipedia page on the histone code. In particular read the paragraphs at the end:

Every nucleosome in a cell can therefore have a different set of
  modifications, raising the question of whether common patterns of
  histone modifications exist. A recent study of about 40 histone
  modifications across human gene promoters found over 4000 different
  combinations used, over 3000 occurring at only a single promoter.
  However, patterns were discovered including a set of 17 histone
  modifications that are present together at over 3000 genes.[13]
  Therefore, patterns of histone modifications do occur but they are
  very intricate, and we currently have detailed biochemical
  understanding of the importance of a relatively small number of
  modifications.


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What goes on in the muscle during static exercise?
Starfish opens mollusc's shell by applying static force for several hours. Mollusc gets tired and cannot hold shell closed.
Muscles spend some energy even when static exercise is done. But it is not necessary to waste energy when there is no movement.
For example, steel spring can create static force for years without with zero energy consumption.
Where does energy go in muscle during static exercise and is it possible to create "spring-like" muscle?

Looks like starfish blocks water so mollusc is starved for oxygen. It could be actually the main cause of starfish victory in this example.

The force in muscle contraction is generated by myosin cross-bridge cycling.  When a muscle contracts without shortening, this is called isometric contraction. Hypothetically, if the myosin cross-bridges could stay in a state where they are bound the to actin, then the muscle could maintain isometric contraction without expending energy. However, in skeletal muscle, myosin will continue to progress through the cycle as long as there is some ATP available, and this cycle consumes ATP. Additionally, ATP-driven calcium pumps have to be constantly moving calcium into the sarcoplasmic reticulum during isometric contraction in order to balance the flux of calcium out of the sarcoplasmic reticulum that is triggered by nerve signals. All the energy released by ATP through both processes is ultimately dissipated as heat.
Smooth muscles (like those lining blood vessels and intestines) can maintain a spring-like state, since they need to stay contracted for long periods of time. This occurs when phosphorylation of the myosin light chain prevents myosin from dissociating from the actin, so the cross-bridges stay bound to the actin. [detailed explanation]
Rigor mortis in dead animals is an example of isometric skeletal muscle contraction without energy expenditure. This happens when the muscle depletes its ATP shortly after death, so the myosin cannot un-bind from the actin.


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What is the conjugation capacity of the liver?
Our liver conjugates 250-300 mg bilirubin per day under normal circumstances but it is capable of conjugating much more. What is the upper end per day after which it won’t be able to conjugate leading to increased unconjugated bilirubin in serum?

Welcome. What have been your research efforts to answer this question so far? Cn you share it with us?

I’ve looked everywhere I’m dying I need help :(

If you mean that in the very real sense, then you should speak to a member of your medical/surgical team as questions regarding personal medical advice are off-topic here. If it's just an expression of frustration of not being able to find what you're looking for, then I get it. The limiting factor (or a limiting factor) seems to be the process of glucuronidation by the enzyme glucuronosyltransferase (UDPGT), the rate of production of the enzyme being limited. That should be a starting point for research.


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Can you identify this seedpod (Malvaceae)?
I collected this seedpod from a plant I was pretty sure belongs to the mallow family (Malvaceae). Location = Central Europe. Unfortunately I lost my picture of the whole plant. Can you help me to identify the genus/species?

Welcome to Biology.SE. Please [edit] additional detail into your question based on the detailed tag info page. In particular, it could be helpful to have: 1) a size estimate of this fruit; 2) a description of the whole plant — ideally including the arrangement and positioning of the fruits/flowers, but even herb vs. bush would help; 3) more geographical specificity; and 4) some idea of the environment the flower was in (e.g.s: marsh, grassland, forest) — including other plants you could recognize, dryness, and elevation.

Lavatera trimestris (flower became-fruit & dried & exposed and seeds are dispersed)

You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion.


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How similar are polyembryonic plant siblings to each other?

I successfully germinated all the seeds I found in a Yuzu fruit. From about half of the seeds there are 2 little plants growing, like in the picture. I understand this is due to the occurence of polyembryony, which is quite common in the genus Citrus.
My question: Are the two plants growing out of the same seed more closely related (= more genetically similar) than two plants growing out of different seeds (of the same fruit)?


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The direction of the flies(Housefly)
Why do flies move crosswise and polygonally? Does the length of the flight path and the angle they turn mean?

I assume this was observed in a small room and the turns were when they approached an obstacle. They use optic flow for obstacle avoidance which kind of explains the straight lines. The retracing might be just be a neural adaptation to not get stuck in a space while still largely still traveling in the intended direction. Was the opening in the curve the direction of the door that the fly entered the room through.

This was observed in a small room. All the doors were closed. I watched this for over an hour. Don't they get tired?

Air is much more viscous when you're the size of a fly than when you're larger which makes flight much less energetic. It's more like they're swimming than flying. If my understanding of Reynolds numbers are correct, a fly in air is swimming 5000 more than a human is in water (Reynolds number being the ratio of inertial to viscous force and it being around 1 million for a human and 200 for a fly).

Thank you, @DKNguyen


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What are some experimental techniques to identify binding partners?
What experimental techniques can be used to identify binding partners for a given protein? I know that if you have some candidates that may bind to a given protein, then you can use techniques such as pull-down or coimmunoprecipitation to determine whether the protein binds to those putative binding partners. But can you screen for its binding partners when basically there is no knowledge on what the given protein might bind to?

Welcome to Biology.SE, Cactus. I think the operative search term is protein-protein interactions. Googling how to detect protein protein interactions gives multiple websites that list and describe many methods.

BioID comes to mind.

I will
(1) obtain antibody of said PROTEIN (search catalog or custom-made).
(2) pull down said PROTEIN with antibody and techniques you mentioned.
(3) identify other proteins in the pulled-down complex with following method:

(From here) There are two main methods of amino acid sequencing:
mass spectrometry and Edman degradation with a protein sequenator.
Automated Edman amino acid sequencers are offer convenient analysis of
polypeptides of up to 50 amino acids long. This process is generally
characterized by seven steps:

Break apart disulphide bridges in the protein with a reducing agent
Separate the protein complex and purify the chain(s)
Determine the amino acid composition and terminal AAs per chain
Fragment each polypeptide chain
Recreate the AA sequence using these fragments
Repeat with different fragment patterns to mitigate errors

Identification via mass spectrometry is increasingly preferred as it
overcomes many of the established limitations of Edman degradation.
But there are various techniques within protein mass spectrometry that
make amino acid sequencing via MS techniques harder to define in
brief.


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Why does the amount of adipose tissue contribute the most to the total body water amount in humans?
I don't quite get this concept. An obese individual will have a greater fat content in their body, and thus will have 45% water in their bodies (for example), versus a slim person that will have 75% of body water and a much lower fat level.
Is this because fat is made up of about 10% water, so the more fat you have in your body, the more water it "takes up" from the entire body water supply of your body?

Are you sure of your numbers? Can you name a source?

I am getting these numbers from my professor's notes, Dr. Melissa A. Vollrath, and she got them from the textbook Vander's Human Physiology: The Mechanisms of Body Function (14th edition)

Fat mass does not take up water.  It brings with it less water percentage than lean mass and so a person with more fat mass will have relatively less % body water.  Additional mass as fat contributed relatively less water than additional mass as lean tissue.
Consider a 50 kg individual who is extremely lean.  From your numbers, if this individual is 75% water (will will assume lean tissue is 75% water) that is 50 * .75 = 37.5kg water and 12.5kg nonwater body mass.
Now this 50 kg individual puts on 50 kg of fat.  The fat is 10% water (from your numbers) so an additional 10 kg of water.  This individual its now 47.5kg water and 52.5 nonwater; since this obese person weighs 100 kg now she has 47.5% water, similar to your example.
Suppose instead your 50kg person grew up into a 100 kg performance athlete.  Still no fat.  She is still 75% water because the lean tissue has 75% water.
It has to do with the % water each type of body mass brings with it.  This is with no special knowledge; using just the numbers in your example which is what your professor wants you to use.

Considering 100 kg fat or lean person - fat seems to substitute water? Water instead of fat?

@PeterBernhard - it is % water by weight of biological tissue.  Biological tissue lean or fat has some % water.  The % water is greater in lean tissue than in fat tissue.

no chatting: interesting you mention "athlete", as "obese" just put on more absolute kg weight than the lean ones (non athletics).

All living cells have water content. Fat tissue is made up of living cells, but fat cells have much more triglyceride and lipid content than water content. So fat tissue still has some water content even though it is mostly made of lipids.
An obese person should have more total body water because of this, and also he/she will usually have more muscle mass in the lower body as well.
The obese person will have a smaller percentage of water relative to their mass than a lean or muscular person would.


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Ipsilateral vs contralateral side of body
I know that the dorsal columns carry ipsilateral information. Is this fact relative to the dorsal column in question?
If I want to talk about the right dorsal column, then the right side of the body would be considered ispilateral. But, if i then go on to talk about the left dorsal column, does this mean that the left side of the body is now considered ipsilateral?

Yes. Ipsilateral and contralateral always have to be relative to something; ipsilateral means "same side" and contralateral means "other side" - you can't really be the same or other side of something unless you have a reference point.


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Picture of a camel's red blood cells
I'm an art student in need of a little help. I'm looking for microscopic pictures of camel's red blood cells, I need their shape for an art project.
The pictures I find on Google seem a little sketchy as in "is it reeeeeally camel blood or is it from some other animal?" kind of sketchy.
I have tried looking further on the net and in books, but without any luck so far. I hope there is someone out there who can help, thanks for reading anyway!

Do you expect a camel red blood cell to have a drastically different shape than the red blood cells of other mammals? Why don't you just consider any picture of red blood cell?

Instead of using the answer section for comments, please do this in the comments. You can always comment on your own questions. If the answers suits you, it would also be nice if you would accept it. This brings some extra reputation to the person who wrote it and is a thank you.


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Normalizing Metabolomics data
First time posting. I recently started working in the field of metabolomics. I have semi-quantitative (not absolute concentration) LC-MS data from in-vitro cell experiments under different experimental conditions.
What is the best way to normalize the data so that I can compare across experimental conditions correctly ( + across different cell types)? I've found many people scale their data using different methods (pareto scale, auto scale, zero mean)  each of these leads to different results when I run something like a PCA between experimental groups.
Thanks.
Jon

Scaling is not the same as normalization.  You have empirically discovered how scaling affects PCA, and it's purpose is to control whether large peaks dominate the analysis or not.
Normalization on the other hand is typically done when samples were in a solvent and the concentration could vary due to the extraction method, the hydration of the tissues etc.  So normalization tries to compensate for these varying concentrations.
Normalization would normally be applied across the peak intensity vs time dimension.  Two typical normalization schemes are 1) normalization to constant sum (usually 1) and 2) Probabalistic Quotient Normalization which uses a slightly more complex approach (and is frequently preferred).  I don't work with LC-MS data, there may be other methods that are preferred with this type of data.  Whatever software you are using probably has several options built-in.
Probabalistic Quotient Normalization is reported in F. Dieterle et. al. Analytical Chemistry vol. 78 pages 4281-4290 (2006). The exact same mathematics are called "median fold change normalization" by Nicholson's group, reported in K. A. Veselkov et. al. Analytical Chemistry vol. 83 pages 5864-5872 (2011).


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Acquiring Covid-19 vaccination through kissing with viral vector vaccinated person
The mechanism of COVID-19 viral vector based vaccines (AstraZeneca - Vaxzevria, Johnsen, Sputnik V - Gam-COVID-Vac, Johnson & Johnson - Janssen, etc. ) is delivering the genetic information of the corona virus through adenoviruses.
Would it therefore be possible to get "infected" by droplets (f.e kissing) with the manipulated adenovirus from a viral vector vaccinated person and consequently acquire the same vaccination?

No, this is not possible, as the vectors used for the vaccination cannot replicate anymore. Some of the genes necessary for this step have been removed from the viral genome to prevent the uncontrolled spread and replaced by the spike protein which is used as the antigen for the vaccination.
To replicate the virus in the production process, a special cell line with a plasmid carrying the genes necessary for the viral replication has to be used, afterwards the virus is purified and outside of these special cells not able to replicate.
For an overview about the adenovirus type 26 based vaccines, see here:

Vaccines based on replication incompetent Ad26 viral vectors:
Standardized template with key considerations for a risk/benefit
assessment

I'd add that there are vaccines for other viruses that are made from attenuated viruses, but this type of vaccine is not used in SARS-CoV-2.


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What kind of spider is this from Sydney, Australia?
I was cleaning the pool when this guy crawled on my foot. I hit him away and noticed a bite mark. I managed to snap a photo of him.

I went to the doctor because I was worried it was a funnel web and she told me to just keep an eye on it, ice it and take anti histamines if it itches.
I have a tiny bit of tenderness in my foot.


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What are the principles of stem cell engineering?
Suppose you want to convert the skin cell into a pluripotent stem cell. I know there are a few genes that were identified for this purpose (a recent Nobel Prize). But apart from finding such genes, it also seems to involve maintaining the right environment, such that some critical receptor doesn't get triggered and alter the entire expression. It also seem to involve ensuring gene expression stability after the change has occurred. Could someone add to this? What are the broad paradigm ideas in stem cell engineering?

The roles of the reprogramming factors Oct4, Sox2 and Klf4 in resetting the somatic cell epigenome during induced pluripotent stem cell generation

Current reprogramming technology, pioneered by Takahashi and Yamanaka
  1, was built on several seminal advances in the field of
  developmental biology. First, nuclear transfer experiments
  demonstrated that a somatic cell nucleus could be epigenetically reset
  to an early developmental state [2]. Second, cell culture conditions
  were developed that allowed for the isolation and culture of
  pluripotent cells, termed embryonic stem (ES) cells, from the inner
  cell mass of the human and mouse blastocyst [3,4]. Finally, study of
  these cells and of early embryonic development led to the
  identification of factors that were ultimately able to reprogram mouse
  embryonic fibroblasts (MEFs) to the iPS cell state when ectopically
  expressed, albeit at low frequency.
Reprogramming of somatic cells is a multistep process that culminates
  in the expression of pluripotency genes such as Nanog. Although
  morphological changes occur at early and intermediate stages of
  reprogramming, pluripotency gene expression is only induced during the
  late stage and indicates faithful reprogramming.
The core reprogramming cocktail, consisting of the transcription
  factors Oct4, Sox2 and Klf4 can be augmented by the
  addition of factors that enhance the efficiency of iPS cell
  generation

Its a multistep process in which much research is still needed,

The frequency with which somatic cells convert to iPS cells is
  typically below 1%. Therefore, much effort has gone into improving
  reprogramming.

specially to increase efficiency of iPS cell generation

The ability of cells to pass through the cell cycle has also been
  shown to be an important determinant of reprogramming efficiency.
  Knockdown or gene deletion of p53, p21 or proteins expressed from the
  Ink4/Arf locus allows cells undergoing reprogramming to avoid the
  activation of cell cycle checkpoints and cellular senescence, leading
  to greater iPS cell formation [21],24-27].

Gene expression changes during reprogramming

First and foremost, stem cell therapies are cell therapies that, in the US, are regulated by such agencies as FACT (foundation for the accreditation cell therapies), CAP (college of American pathologists) and the FDA (food & drug administration). Manufacturing must be compliant under GTP (good tissue practice) and GMP (good manufacturing practice) standards. Even the labeling of products is moving to the harmonized system ISBT128, managed by ICCBBA (International Council for Commonality in Blood Banking Automation). The take-home point here is that everything is tightly regulated, and produced under rigorous standards of safety, conformity and documentation. Not everyone is FACT accredited, but the benefits are becoming of increasing importance, especially to insurance providers (ref). The therapies are costly to manufacture, to be certain. The two FDA-approved CAR-T immunotherapies YESCARTA and Kymriah run around $500,000.
So you have a number of types of stem cell therapy. Bone marrow transplantation is considered a stem cell therapy, and then you have therapies that involve human embryonic stem cells (hESC) and human induced pluripotent stem cells (hiPSC).
In terms of hiPSC, groups have been successful both in culturing with transcription factors such as Oct4, Sox2, Klf2 and so forth, and in using sendai virus to deliver these transcription factors directly within the cell (thermofisher's Cytotune®-iPS Sendai Reprogramming Kit, youtube video).
We can also see, however, that stem cells can be obtained elsewhere and don't necessarily need to be induced. You can source hESC from embryos and cord blood, and hematopoietic stem cells (HSC) can be mobilized from the marrow with a drug cocktail (like plerixafor and GM-CSF) and harvested with apheresis.
So just for a real-world example of what you're thinking: Papers on the production of glucose sensitive insulin-secreting ß cells from hESC using carefully controlled culture conditions have been published (ref), and companies have taken advantage of this technology. Subdural implants using this system are in clinical trials right now. They produce the ß cells from hESC by controlling the cultures:

Source: 1,2
The transcription factors along the bottom of the figure, which I've pasted together from two sources, shows what transcription factors should be active at that stage. The identity of the final product can be surmised from a combination of what transcription factors should and should not be active. It's also important to realize that there will be off-target cells, but that the process should be validated to ensure on-target cells stay within an acceptable range as defined during pre-clinical development.
Manufacturers would also need to test for the purity, sterility, endotoxin and potency of their cells. Potency assays have become something of a prerogative for the FDA, since anyone can produce a cell, but how can they say it's effective or does what it's marketed to do? An example potency assay might be two cultures, one with glucose and one without, does one secrete more insulin than the other? You'd pick this assay because the proposed mechanism of action for ß cells is they respond to glucose, and secrete insulin.
For sterility, they sell some good kits like BacT alert aerobic and anaerobic test bottles, mycoplasma testing kits, you can also do culture plates and gram stain. Products that don't exhibit 100% sterility can't be infused, and so it generally follows that exceptional releases can be made for many other issues by a physician, but contamination will stop a cell therapy product dead in its tracks.
You're also right in that cell therapies which involve a gene modification step need to look at such things as transduction efficiency, live virus titer, expression of molecules related to the transduction and so forth. The sendovirus kit referenced above is a fair pick because as they demonstrate, after several passages the non-integrating virus titer is negligible. For human administration, in the CAR-T space, the FDA has required that studies where CAR-T have been infused follow patients for 15 years after treatment to study the effect of infusing virally-transduced vectors. I don't think that there's a clear answer as to whether the virus is an issue. You're also right, however, that it's necessary to test the stability of the transduced gene(s) , especially through passaging, holding and cryopreservation. All of this is nicely outlined here.


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Is there any disease that is proven to originate from malfunction of alternative splicing or post translation changes in the genome?
The most common diseases with genetic origin like muscular dystrophy seem to originate from issues with the primary structure of the DNA itself. Also it seems to be somewhat controversial as to whether alternate splicing of a single gene is actually a functional process, rather than biomolecular noise. In that context, do we know of any disease where the primary structure of a certain gene is normal, but the end products are not.

Misconceptions etc. in the Question
There are several misconceptions and erroneous or unclear statements in this question, which first need to be dealt with.

Whether or not muscular dystrophy is a common genetic disease, depends on whether you think 1 in 3500–6000 male births is common. I would term it ‘well-known’.
It is not controversial whether alternative splicing of a single gene is a ‘functional process’ (whatever that may mean). One well studied and unequivocal example is in sex determination in Drosophila melanogaster — see the Wikipedia entry for Alternative splicing and my own answer to a question on this list.
Alternative splicing of a gene involves splicing sites that may or may not be part of the spliced transcript (the mature mRNA). The title of the question asks for diseases of malfunction of alternative splicing, whereas the body of the question refers to a normal “primary structure” for the gene. I shall assume that examples in which there are mutations in splice sites that are in introns — and hence not in the mRNA or the protein — satisfy the criterion. However enhancer mutations will also be considered.
The reference to “post-translational changes in the genome” in the title does not relate to the rest of the question or make much sense to me. I shall ignore it.

Examples
There are several reviews on this topic, but I shall confine myself to the first that I found from an internet search — one entitled Splicing mutations in human genetic disorders: examples, detection, and confirmation by Abramowicz and Gos in J Appl Genet. 2018; 59(3): 253–268. Table 1 of that paper list examples of genetic diseases extending to three pages (perhaps easier to read online horizontally here) which include the following:

congenital cataract
Neurofibromatosis type 1
Ehlers-Danlos syndrome
Succinyl-CoA:3-ketoacid CoA transferase deficiency
Becker muscular dystrophy
Familial dysautonomia
Cystic fibrosis
Androgen insensitivity syndrome
Fabry disease

The mutations causing the aberrant splicing include mutations in the donor or acceptor splice site, intron variants, and exonic and intronic splicing enhancers. The results of these mutations include exon skipping, cryptic exon inclusion, and alteration of the relative frequency of occurrence of different spliced transcripts.

+1. Maybe you could also find examples of diseases caused by splicing regulators, so that primary sequences of targets may be completely normal including splicing sites.

@KaPy3141 — I agree, that would be good. Now finding the time...


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Why does Anti-A antibodies make type-A blood type clump?
A-type blood has B-antibodies; it also clumps anti-A antibodies are inserted. Why is that? The blood has no antibodies against the A-antibodies to make clump in this way.

When an antibody meets its antigen it will bind it. So if you add anti-A antibodies to A blood, these antibodies will bind the red blood cells. Because of its Y-shaped form, each antibody can bind two epitopes. These can be located on the same red blood cell, or on two different. If they are located on two different, this leads to cross-linking of two blood cells. Since this happens many times, the blood cells will clump. The whole process is called hemagglutination.
See the image (from here) for illustration:

The so-called ABO blood grouping is based on the antigen-antibody reaction, where anti-A antibodies circulating in the plasma will bind to cells possessing antigen-A and cause clumping, or agglutination. A deadly situation since the red blood cells will be unable to circulate.
A person's blood group is designated according to the antigens found on the surface of their red blood cells. Type A blood means type A antigens are on the surface of the red blood cells. Type B - the same. Type AB - the same. Type O blood means there are no type-A or type-B antigens on the red blood cell's cell membrane/surface, theoretically making them the universal donor of red blood cells, but not their plasma if it contains anti-A, or anti-B, or both anti-A and anti-B antibodies, that can bind to their pair antigen type.
Persons of type-A blood mean that their red blood cells exhibit the antigen-A on their red blood cell membranes/surfaces, hence these persons can safely have anti-B antibodies circulating in their plasma to avoid agglutination. Type-B blood therefore means that the plasma may have anti-A antibodies safely.
Blood matching is further complicated by various blood antigen systems that have been found to be clinically significant, for example the Landsteiner blood antigens.