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Can a human actually be "frightened to death?"
I've been watching some classic horror movies as of late, and a trope I see in many of them is where a person will see the big bad monster and "die of fright." I'm curious, for the average person, could this happen? Or would it require a prior medical condition of some kind?

The people whom this happens to consider themselves average people.
The thought is that catecholamine surge caused by the event triggers some predisposition to cardiac arrhythmia - maybe inherited, maybe due to medicines.  People predisposed to this sort of arrhythmia probably do not know that is the case, and consider themselves to be average people.  It would seem that the victims of this are not average and have some sort of predisposition to that problem.  There is a lot of interest in figuring out who there people are in advance - not in the context of being frightening to death but in the context of SUDEP - sudden death in epilepsy.  Epileptic people sometimes just die, presumably for cardiac reasons, but there is no way of knowing who among this large group is at risk.
In the following abstract the frightening thing is being restrained.  Other circumstances that produce a catecholamine surge can do it too.
https://www.ncbi.nlm.nih.gov/pubmed/25628339

Med Sci Law. 2016 Apr;56(2):85-90. doi: 10.1177/0025802414568483. Epub
  2015 Jan 26. Sudden cardiac death with stress and restraint: The
  association with sudden adult death syndrome, cardiomyopathy and
  coronary artery disease.
Krexi L1, Georgiou R2, Krexi D1, Sheppard MN3. Author information
  Abstract OBJECTIVE: The aim of this study was to report on sudden
  cardiac death (SCD) during or immediately after a stressful event in a
  predominately young cohort. METHODS: This study used retrospective
  non-case-controlled analysis. A total of 110 cases of SCD in relation
  to a stressful event such as altercation (45%), physical restraint
  (31%) in police custody (10%), exams/school/job stress (7.27%),
  receiving bad news (4%), or a car accident without injuries (2.73%)
  were retrospectively investigated. The majority of the subjects
  experiencing SCD were male (80.91%). The mean age was 36 ± 16 years
  (range 5-82 years). Twenty-three cases (20.91%) were psychiatric
  patients on antipsychotic medication. RESULTS: Fifty-three per cent of
  cases died with a negative autopsy and a morphologically normal heart,
  indicating sudden adult death which is linked to cardiac
  channelopathies predisposing to stress-induced SCD. Cardiomyopathy was
  found in 16 (14.5%) patients and coronary artery pathology in 19 (17%)
  patients, with atherosclerosis predominating in older patients.
  CONCLUSIONS: This study highlights SCD during psychological stress,
  mostly in young males where the sudden death occurred in the absence
  of structural heart disease. This may reflect the proarrhythmic
  potential of high catecholamines on the structurally normal heart in
  those genetically predisposed because of cardiac channelopathy.
  Structural cardiomyopathies and coronary artery disease also feature
  prominently. Cases of SCD associated with altercation and restraint
  receive mass media attention especially when police/other governmental
  bodies are involved. This study highlights the rare but important risk
  of SCD associated with psychological stress and restraint in
  morphologically normal hearts and the importance of an expert cardiac
  opinion where prolonged criminal investigations and medico-legal
  issues often ensue.

I guess by "average" I mean average health

Edit that quote. Please. better yet, summarize in your own words what's important, then support it with a snippit. This is too much copypasta. Also, how does the abstract support your comment about restraint?

If I edit a quote it is not a quote any more.  I summarize in my own words at the top.   As regards restraint, the question was about being frightened but the persons suffering sudden death underwent a range of catecholamine-inducing events including non-scary ones.  I suppose the car accident would be frightening also.


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What does enzymatic equilibrium in % represent?
I am studying an enzyme which can catalyse a chemical reaction in both directions. The paper I am looking at is mentioning a thermodynamic equilibrium of 1% in the synthase direction.
What does that mean more intuitively? I am mostly confused by the percent unit as I expected a constant rate without unit...
My guess would be that under these specific concentrations of substrates/products, the enzyme is catalising 1 synthase reaction and 99 inverse reactions for each 100 reactions it is catalising. In other words, the equilibrium constant K of the synthase reaction under these conditions would be 0.01.
Is that correct?

Please provide an exact quotation in your question with a link to the paper so that anyone interested can check the context.  My guess would be the same as yours, if you are reporting verbatime, but the terminology seems most non-standard to me.

You are correct in stating the relative rates of the two reactions.  What may have you confused is the percent sign in the statement.  The percent sign is not a unit in the sense that you are taking it.
What you have in a simple reaction like you are examining are two opposing rates of reaction.  The rate of a catalytic reaction, like others, usually depends on the concentrations of at least some of the reactants in the direction under consideration.
At equilibrium, by definition, the concentration of every material involved in the reaction is unvarying.  Otherwise, the reaction would not have reached equilibrium yet.  What that also means is that the rates of the forward & inverse reactions are equal at equilibrium.  So what does the statement signify?   It means that thermodynamically, the synthase reaction is the more unfavorable direction.  That is, at equilibrium, the product concentration of the synthase direction will be in the minority.
The statement involving the percent sign is just giving the ratio between the [arbitrary] forward direction, here stated as the synthase direction, and the inverse reaction.  The percent sign is just a mathematically short way of stating that the number stated is parts per hundred.
The equilibrium constant K is exactly the same ratio, stated as a decimal value rather than a integer per hundred.

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Reward pathway sequence of events
So I've been reading a lot of papers on the reward pathway. But since I'm not schooled in any relevant knowledge I'm having trouble grasping the chain of events. Most papers detail just bits and pieces, but not the full sequence of events.
I'm trying to grasp how the error prediction signal works.
This is my guess so far:
Players:

Photosensitice cell A
  Light processing neuron B
  Dopamine neuron C
  Motorneuron D

Event:

Light strikes A
A triggers B
B spikes after N triggers.
B triggers C
C spikes after N triggers.
C keeps repeadetly spiking for as long as its internally coded reward size/duration expectation.
D receives predecition triggers spikes causing action.
  Reward comes, neural connections are strengthened.
  If reward doesnt come in predicted time connection degrades.

Am I correct in this deduction or way off?
How does the actual reward get communicated? By dopamine release in blood?
By the same neurons that coded the reward prediction? If so, how do those exact neurons get triggered to release reward?

just within the visual processing you will have many neurons processing the information before it goes on to other areas. after all, you are not afraid of a black dot at a certain location of your retina, but of the spider (or whatever). Your 'neuron B' is not a single neuron, but a whole brain area. However I don't know how far up in the processing cascade a signal goes before the information spreads to other brain areas. It might also differ between signals depending on their abstractness. e.g. I expect that being afraid of speaking in public will involve more/different processing.

i understand that, i tried to simplify the process to understand what happens within the reward pathway. Error prediction signal, reward.  How those two are communicated by an event source, and unrelated reward trigger. I see food, i get appetite. Food is in mouth, im happy. How does the food in mouth, hot relaxing bath, sunlight on face get translated to a reward signal to the neurons that were triggered by the prediction signal

I think it's too much to explain the whole reward circuitry here. You would be best off searching for review articles about reward pathways. For example, searching something like this on pubmed: https://www.ncbi.nlm.nih.gov/pubmed/?term=reward+prediction+signal+review There are several results that answer your question but do note that this is still an area of active research, it is possible to present hypotheses but the full circuitry is not perfectly known, because there are multiple contributing pathways.

@BryanKrause I realize it's a lot to explain in one answer, but it's really hard to find one article that summarizes the path from a to be in a "flowchart" type of style. They usually just focus one one piece, making it really hard to figure out how it all fits together as one coherent piece. Ideally i'd have a simple flowchart that would explain in very rough gist how the current theories are how a trigger ends up in a response and how an error correction signal works in it all.

Essentially that's what I remember, but there can be a lot more steps between A and C, i.e. more pathways interacting in different systems to produce an associative memory. Pavlov's dogs is the classic example:
1: Pavlov rings bell, dogs hear bell
2: Pavlov feeds dogs, (dogs rewarded)
3: Repeat 1 and 2 for a few days.
4: Ring bell, dogs will salivate and expect food, even if no food is on the way.
So, in the skull, the dogs are making a link between hearing a bell and a reward.
Dopamine is released at dopaminergic synapses, the limbic system is probably the best understood part of the memory/reward system, particularly the mesolimbic pathway for reward.
Neurons get triggered by presynaptic neurotransmitters, some require convergence of signals to reach threshold and trigger an action potential. Connections are strengthened by long-term potentiation, which has been argued to be the basis for memories, but that's a massive topic I'm not qualified to discuss.
I haven't heard of the "error prediction signal" before, might be a new discovery/thinking that I'm a bit behind on.

Yes indeed error prediction signals have been discussed for decades now, it is not a new concept. I appreciate the attempt at an answer but there is really very little here that actually answers the question, instead you are explaining a behavioral paradigm. Everything you say is correct, though. I think the original question is just not answerable in a SE format, it is much too broad and the circuitry is not fully understood yet.

It is a bit of tangent but one current idea is that humor itself exists as an error correcting mechanism. a way of dealing with pathways that make bad predictions

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Can any organisms see non-electromagnetic radiation?
Some examples would be cosmic rays, neutron radiation, alpha radiation, beta radiation, muon radiation, and antimatter radiation.
Some related questions: How is non-electromagnetic radiation detected, and would it ever be evolutionarily beneficial?

Welcome to Biology.SE! Is any of these radiations naturally found in a habitable space? If no, then evolving ability to detect it would be senseless. And how would an organism know that it can see something that is not found nearby anywhere?

@another 'Homo sapien', thanks. Off the top of my head, I can think of high-altitude birds & bacteria, organisms living near nuclear reactors & radioactive waste deposits, and organisms living in uranium mines.

When people are exposed to radiation they can see flashes of light. An astronaut on board the MIR space station has told about this when he had to take shelter during a solar storm in a room with thick shielding. The light flashes are caused by protons moving through the brain, causing spurious electric signals in the visual part of the brain. So, you could say that you can become a walking Geiger counter when exposed to radiation.

Increase in the mutation rate (single and double strand breaks) caused by those radiations is harmful for most life forms on earth.

What exactly is antimatter radiation? Things like positrons are not gonna make it very far through our matter atmosphere. As for the rest, about the most any creature can detect is the noxious effects. I am not aware of any species which can directly "see" such radiation. It wouldn't be particularly advantageous anyway, since there are very few places on Earth where the radiation levels are not (relatively) constant. Perhaps in time, organisms like radiotrophic fungi may evolve to have more sophisticated detection mechanisms (though they use electromagnetic radiation, specifically gamma rays).

What do you mean by see. Just detection will be enough?

Some fungi have radiotropism; they grow toward radiation sources. Melanin-expressing (melanotic) fungi migrate toward radioactive sources, which  enhance their growth. According to this paper.

These Melanotic fungi inhabit some of the most extreme habitats on earth such as the damaged nuclear reactor at Chernobyl and the highlands of Antarctica, both of which are high-radiation environments.
Radiotropism was triggered primarily by gamma radiation, but it is possible that both alpha and beta radiation could be  “ sensed ” by the fungi as well.

It seems like these melanotic fungi can detect gamma and beta or alpha that they can use as energy source.


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Have there ever been as many mammals as there are now?
I apologize for the weird question, but based on a Google search it looks like this topic hasn't been discussed before. I'm hoping that enough information about population biology is stored in the fossil record to answer this question.
Humans have wiped out a lot of animals in a very short time, but I realized that mammals might be doing very well.
First off, humans are mammals, and there are 7.6 billion of us. That's quite a lot. I don't believe any other animal species of our body size has such a large population.
Second, humans have pets. A lot of them. And they're almost all mammals. Everywhere we go we take our cats and dogs with us. Many of them become feral and multiply prolifically.
Third, our livestock. With the growth of human civilization came the growth of meat consumption, which, naturally, meant a lot more cattle. I think I read somewhere that cattle are contributing more to global warming than cars, through burping.
Lastly, and probably most importantly: rodents. Cats chased us everywhere because rats chased us everywhere. They thrived on the grain we grew and their population exploded to the point that they became a global pest, and possibly humanity's greatest enemy.
So, my hypothesis is that there are more mammals now than ever before in the history of life. Not in terms of species diversity, but in terms of headcount. If this is true, it would be remarkable, since the rest of the Animal Kingdom is currently suffering through a mass extinction.

Interesting question. At first, my knee-jerk answer was "yes". But then I saw you were talking about individuals, and not species. Humans have certainly skewed the numbers, favoring domesticated species, and eliminating others.

During the ice age, when there were many great plains, there must have been a staggering number of  prairie dogs, lemmings, gophers etc. I don't have time for an in-depth literature search but it appears that studies focus on biomass and less on numbers.

There can be perhaps 10 trillion rodents and bats on the planet, so the humans and livestock probably are small compared to a rainforest rodents and bats. The biggest bat colony is 40 million, they decline without unmanaged forests, can reach 4-10 bats per hectare, and the world population might normally be in 10s of billions, save for the use of pesticides and deforestation.
Here's a bit of maths to say that we have erased 1 trillion rodent habitats through monocultures and ploughing. Every cow and sheep field would have previously supported 10-20-50 times more rodents, and they aren't adapted for pesticides and ploughs.
37% of the world's land is farmed
Extent of total cultivated land in 2006: 1.5 billion hectares.
If there were 14 mammals per km2 of farmland, then we have displaced 20 billion mammals.
If the pristine habitats previously supported 1 rodent/mammal every 5m2, we would have destroyed the homes of 2000 mice,voles,shrews,squirrels and other mammals by hectare, that's 3000 Billion mammals (worst case scenario) due to monocultures and farming, and 1000 Billion in a best case scenario. Bangladesh rice farms and UK fields both are hostile to mammals.
A 20g mouse for 5m2 comes to the same as one human for 15 square kilometers. A mouse only needs a 3g of seeds/roots/beetles/snails per day to survive, that's about a kilo per year. "blue oak, interior live oak, and black oak respectively produce 2955, 1074, and 616 kg/ha of tree canopy" invertebrates provide 100-300kg/ha.
Perhaps we have erased 1 trillion mammals in the amazon alone.
https://www.worldatlas.com/articles/list-of-primates-by-population.html
Also we have depleted the fish stocks. It is reported that in medieval times, the seas heaved with incredible amounts of dolphins, whales and fish stocks, pristine seal and dolphin numbers could have been about 1 billion. Perhaps today it's about 1/4 of that.
If i had to bet all I own on your theory, I'd say it happened at another time in the previous 60mn years, probably not today.

It looks like this comes down to rodent population. I'm surprised the density can go as high as 10mice/m^2 in any large area. Source?

I had a hard time finding any sources that compare mouse density in woods to their density in farmland. But my intuition was always that mice benefitted from human expansion. We wiped out their big predators and left wide open row crops for them to munch on. This back-of-the-napkin calculation gives a ridiculously high mouse count for one agricultural region. Also, consider their introduction as invasives in places like NZ.

I was researching it a bit fast, I did mice m2 in and the first page i had was 10/m2 so i added that, I have edited it. sciencenordic.com/rodent-population-swings-remain-mystery
Sep 4, 2015  70 to 100 rodents for each 1000 m2 of forest floor in southern Norway. a cold country with slow growing forests and smaller tree seed harvests. primeval forests have heaps of dead wood everywhere and masses of seedfall.

I did a bit more research. I wouldn't say it's a certainty that more farmland means fewer rodents. This study found a maximum density of 379 rodents/ha in an Ethiopian wheat field. However, this other study found a maximum density of just 35 rodents/ha in an Ethiopian forest.

Of course, these are just two papers, and maybe another two papers will give the complete opposite result. In any case, do you have a source for the 2000 rodents/ha figure in your first post? I looked around, but never found a density that high.

there's an uphill climb to find references. To refactor your query into a clearly quantitative and thoroughly numerate study, is whether a family of mammals has ever been beyond the 1 trillion and 1/2 trillion figures. in nyc they dont know if there are 1/4 or many million rats. In rodent surveys they have to use traps with vole escapes because the voles die of hunger, and they run after mice with radio antennas in fields. they still dont know.

fields and irrigation, when arranged into en eischer rodent waterfall tower, dont use space and light efficiently to support a maximum of nesting sites for animals, we reduce complexity and age of all habitats and skew the mammal numbers towards smaller numbers of overgrazing large mammals. this is the best list of mammals i could find, no bats and rodents on there... i have to say i'm jammed on the rodent survey synopsis summery of current research on historical national mammal figures :) .https://en.wikipedia.org/wiki/Lists_of_organisms_by_population#Mammals_(Mammalia)


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Is there a reliable estimate of the number of cells on Earth?
A quick Google search didn't turn up any reliable sources. An awkward Cosmoquest thread gives a rough estimate of 10^25 to 10^32, but this is just a bad extrapolation of the number of cells in a human body. Also, I recently learned that we don't even know the number of cells in humans to good precision.
Has anyone ever made a serious attempt to figure this out? If not, does anyone here want to make a quick calculation?

Do you want to count human cells, animal cells or really ALL cells (including bacteria & archea), because these are different orders of magnitude & difficulty

@Nicolai All cells, anywhere and in any organism.

All eukaryotic cells or do you count bacteria as well? Do you count viruses?

All cells, including bacteria and other prokaryotes. Viruses are not cells so they don't count.

I'm voting to close this question as off-topic because it relates to the Guinness book of records, not biology.

@david although this question is off-topic, I don't think it is related to Guinness book in any way :P

@another'Homosapien' — A manner of speaking. You might also term it a "Freak Show" question. This sort of question is asked for no reason other than to be able to respond "wow". It is the very antithesis to science.

I disagree strongly with the people saying this is off-topic, or that it is simply a "wow-factor" question. I think knowing at least an estimate of the number of cells on Earth is important to understanding the environment we live in and just how rare multicellular life is.

I also disagree strongly with those disparaging this question. I think it is an excellent one. I think the burden should be on those who want to avoid answering it to explain why they don't think ecology and evolution have any important extensive properties.

Okay so I looked around a bit, and there are surprisingly few papers related to this question.
This paper is the best I cold find, but it's almost 20 years old. There's also this one, which slightly updates the other one, but they both focus on bacteria. For those the total number is estimated to be somewhere in the range of $10^{30}$.
For humans the latest published number is $3.72 \times 10^{13}$, so even with a few billion in total ($10^9 \times 10^{13} = 10^{22}$) we probably don't even matter for the total cell count. Since smaller more abundant animals have a much lower number of cells, they probably don't matter either.
Now to the only thing I'm not sure about: plants
The number of plants on earth is really elusive, only more elusive is the number of cells per plant. This study claims around 3 trillion ($10^{12}$) tree's on earth. Since tree's are bound to have (many) more cells than humans, we're probably getting closer to the number of prokaryotic cells by now (I guess the number of 'tree cells' will be somewhere around $10^{27}  - 10^{30})$.
So far I didn't find anything about grasses or other plants (neither numbers nor cell counts), so it's really hard to say whether these matter or not.
This study seems to give an average number of cells per growth ring in tree's, but I'm not sure how to get a number of cells / tree from that.
In total the estimated number of bacteria ($10^{30}$) is probably a good measure for the number of cells on earth. Even if plants manage to come to that level, the order of magnitude will probably not change (by much).

It doesn't seem that surprising to me that there are few papers on unanswerable trivia.

About $10^{30}$ prokaryotes (Whitman et al. 1998).
It is an extremely vague estimates of course! Not that every eukaryotic cell contain about $10^3$ mitochondria, so of course eukaryotic cells would have to be negligible in counts even if you consider only the mitochondria. I don't know if Whitman et al. 1998 counted bacteria but it does not change much given the accuracy of their estimate.

Highly related posts

How many organisms have ever lived on Earth?
How many eukaryotes are there on Earth?

$10^7$ is way to low for the number of eukaryotic cells. There are ~7 billion ($10^9$) humans on earth, and we definitely have a large number of cells to multiply with that.

Thanks for your help. Indeed, $10^7$ was an estimation of the number of species from M. Lynch. I rewrote the number without thinking. I removed the estimate.

Thanks for your help. Indeed, $10^7$ was an estimation of the number of species from M. Lynch. I rewrote the number without thinking. I removed the estimate.


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How does alzheimer's affect an octopus, particularly relating to their multiple brains?
From what I have read, Octopus' have multiple brains rather than a single one like in humans. They are also affected by alzheimer's, and so an interesting question arises:
Do Octopus' get alzheimer's in one brain, or are all affected, and can they shut off a single brain if it gets the disease?

I have no idea. Was hoping someone knowledgable could give a full rundown but if not will have to research this sort of thing :-)

Welcome to Biology.SE. This is an interesting question. Could you please add a reference about Alzheimer's in Octopus?

Pathology due to Alzheimer's disease is primarily because of the loss of neurons which cannot be repaired. Many organisms can actually regenerate their brains because they have active adult neurogenesis (which is reduced to a few small regions of brain in most mammals).


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Protein/ligand affinity databases?
Is there any database that contain binding affinities reported in litterature for different proteins and ligands?
I have checked uniprot already and it does not seem to included any binding affinity data, for several well characterised receptors such as the human insulin receptor.

You could try this or this. I haven't used either, but searching for a protein that I work with gave disappointing results.

Brenda has a LOT of values from literature than can indicate binding (KI, IC50, Km), but only for enzymes not for proteins in general.

@canadianer I think it just gives binding of (pharmacological) small molecules to proteins. I just searched stat1 to see if it gives the binding energy of stat1 with its receptors. It doesn't. It rather considers stat1 as a target and returns two small molecules. So, I guess there is no good database for binding affinities.


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Is it possible to temporarily paralyze someone through the use of electric signals or focused ultrasound?
I've been reading about how it is possible to send signals to the brain using focused ultrasound or electrical impulses. It is possible to make someone see a certain shape or color by stimulating different areas of the brain. I was wondering whether or not it would be possible to temporarily shut off a person's motor functions by for example, sending signals to the cerebellum or perhaps intercepting them before they can travel down the spinal chord.

With in-depth study and research, it would be possible on 1 person. However, it's unlikely that this type of technology could ever be weaponized.
Nerves and neural networks are particularly known for having unique calibrations per individual. Even if you can decipher every neural communication protocol on a test subject, the signal protocol would be at least slightly different on others, even for crude movement control.
Mind control would be several orders of magnitude harder - each person's brain is different.
Most neurons communicate through neurotransmitters rather than electricity, completely ignoring your control scheme.
Even if none of these barriers existed, people could always block them using "tinfoil hats".

Yes. Those weapons exist, they are called Electroshock weapon, the most famous of which is the taser.
Tasers spill much ink in the media. You have probably already seen their use (and misuse) in videos.

Thank you for answering, but this isn't quite what I meant. I am talking about a non-painful non-invasive procedure that can prevent movement for a desired period of time. For example, this could be used as an alternate method to sedation in a patient that is having violent involuntary convulsions, or whose movements would otherwise need to be suppressed in order to deliver treatment.

I have no sources for this, but I guess the "impact" you need to immobilize a human with this type of method will never be non-painful.


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What is the symbiotic relationship between truffle fungi and their host trees?
I understand that truffles share a symbiotic relationship as they reside among the root systems of host trees, but I cannot find any material that specifies the details of such a relationship. In other words, what exactly do truffles get from their host trees, and what do they provide in turn?

Some mushrooms can fix nitrogen from the air like oyster mushrooms and Frankia, and Truffles may do, I don't know, and truffles are symbiotic with huge microorganism colonies which can breathe nitrogen, so it's a 3 way resource exchange, Trees, Mushrooms and Bacteira, making sugar from sun, decomposing organic matter into smaller molecules, and breathing nitrogen via microorganisms.   this video taught me about truffles a few months ago: https://www.youtube.com/watch?v=XMNM7AYcSLU

A truffle is the fruiting body of a subterranean Ascomycete fungus, predominantly one of the many species of the genus Tuber. Truffles are ectomycorrhizal fungi and form symbiotic relationships with the roots of several tree species including beech, birch, hazel, hornbeam, oak, pine, and poplar.
Mycorrhizal symbiosis is a mutualistic association between a fungus and the roots of a plant (usually a tree) in which (typically) the fungus obtains energy in the form of carbohydrates from the plant, and the plant gains the benefits of the mycelium's higher absorptive capacity for water and mineral nutrients, partly because of the large surface area of fungal hyphae, which are much longer and finer than plant root hairs, and partly because some such fungi can mobilize soil minerals unavailable to the plants' roots. The effect is thus to improve the plant's mineral absorption capabilities.
Based on the quote below from the website of a truffle nursery in Australia (http://trufficulture.com.au/what_are_truffles.html), it sounds like truffle symbiosis is a completely standard mycorrhizal symbiotic relationship.

The truffle coats the tips of the tree roots to form mycorrhiza which
  act as an extension of the tree's root system. The tree provides the
  truffle with a source of photosynthesised carbohydrates, and in return
  the fine, thread-like filaments (mycelia) of the truffle, extract and
  trade soil minerals and nutrients which would normally be unavailable
  to the tree. Thus the mycorrhiza is able to increase the effectiveness
  of the trees roots, enabling the tree to grow in soils which would
  normally be too nutrient deficient to support them.


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Concerning Rabies can an animal feeding on rabid bat transmit right away?
Playful kitten found biting and toying with a dead bat. Lets say the kitten nips and plays rough with a human right after biting and toying with the bat.
Will a potential rabies virus transmit from the mouth of the kitten into the human being that it may still harbor the virus from the bat?
Putting aside the fact that the rabies virus takes days to weeks to infect the kitten, can the virus cross contaminate from the mouth or nails of the cat if the feline was playing with the corpse?

Yes, there is a possibility that a kitten can transmit the virus if that kitten had fresh infected bat blood or saliva on it's claws or teeth and gets it directly into your eyes, nose, mouth, or a wound. It's very rare and exceedingly hard to prove, however. These are called non-bite exposures.


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Can a virus be transmitted from a sweating person out to another person?
In the sport of Jiu-Jitsu, close contact with many partners is common. Many times these partners are sweating profusely (Yuk), which in turn drips on the other person sometimes into the eyes, nose, and yes mouth. I am just wondering if viruses can enter in this way.

Sweat per se, at the source, is not likely to be contaminated with bacteria or viruses. However, that's a moot point, because as soon as it's produced it's on contact with the sweaty person's skin, which is invariably coated with bacteria and potentially with viruses. Sweat can therefore act as a medium for transferring infectious agents between two hosts.
Examples of this are described in Contact transmission of vaccinia virus from smallpox vaccinees in the United States, 2003–2011:

Among adult male cases, the most frequently reported activities associated with vaccinia transfers were wrestling, grappling or sparring (n = 18) [12,18–20]; household interactions (e.g., sharing towels, clothing) (n = 6); unspecified “contact” (n = 4); and football or basketball (n = 3).

(Vaccinia virus is the vaccine for smallpox. As such it's far less dangerous than smallpox itself, but as an ancient vaccine it's also much more dangerous than the vast majority of modern vaccines, and exposure to large concentrations of the virus in an uncontrolled setting is potentially risky.)

In short, yes. Virus particles, or bacteria on one persons skin can end up being in the sweat that is transferred from one person to another. They can also be transferred by direct physical contact though, so the sweat isn't the only source of transfer.
I will caveat that a healthy person shouldn't need to worry about the amount of harmful bacteria in sweat as the numbers will be so low that their immune system can take care of it fine.


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Are bacteria incapable of producing cytokines such as interleukins?
As far as I understand, bacteria cannot produce cytokines such as interleukins. However, I have not read an explanation as to why they cannot. Perhaps it has to do with an evolutionary limitation. Yet, if this is the case, why would bacteria be incapable of acquiring new functions such as cytokine production during their evolution, especially intracellular bacteria which reside within immune cells. If bacteria have not been able to acquire this function, then maybe it has to do with a biological constraint (size of the proteins, amino acid composition, machinery or bioenergetic capacity). If anyone knows the exact reason or has a knowledgeable explanation I would really like to read it. Thanks.

For what reason should they produce interleukins? To attract immune cells?

@Chris IL-10, for example, is immunosuppressive. It should not be surprising that pathogens can produce immunomodulating molecules, including cytokine homologs. I'll post an answer later.

Agree with Chris above - what functions would cytokines play when produced by a bacterium? I'm not familiar with whether or not bacteria make cytokines (of why they would)... maybe there could be some sort of theoretical role for making 'decoy' cytokines as a way to throw off the endogenous immune system. Just a random though that I have no data to support...

It seems especially pertinent to point out from the start that many cytokines are anti-inflammatory/immunosuppressive. The immune system has evolved to remove pathogens from the body, and normally these cytokines act to deactivate the immune response once an infection has been cleared. It should not be surprising that pathogens have co-evolved defences to the immune system, including interference with cytokine networks and even production of anti-inflammatory cytokine homologs, ostensibly to subvert the immune response. Below are but a few examples of this.

Viruses
Kotenko SV, SAccani S, Izotova LS, Mirochnitchenko OV, Pestka S. 2000. Human cytomegalovirus harbors its own unique IL-10 homolog (cmvIL-10). Proc Natl Acad Sci USA 97(4):1695-1700.

Many viruses exploit the strategy of using homologs of cellular cytokines or cytokine receptors to shield virus-infected cells from immune defenses and enhance virus survival in the host. The presence of virus-encoded homologs of cellular proteins may be an indicator of the importance of these cellular components in immune mechanisms for combating this virus in vivo. A number of herpes viruses harbor homologs of IL-10. Epstein–Barr virus (EBV)-encoded IL-10 (ebvIL-10), the first viral homolog of IL-10 identified, shares many but not all of the biological activities of cellular IL-10 and may play an important role in the host-virus interaction. In addition to EBV, another virus, the Orf poxvirus (OV), which can infect humans, has its own IL-10 homolog, ovIL-10.
...
IL-10 has several immunosuppressive activities that would be favorable for CMV, such as down-regulation of MHC class I and II expression, inhibition of production of inflammatory cytokines, and interference with antigen presentation. Murine CMV infection induces transient early expression of IL-10, which plays an essential role in MHC class II down-regulation. EBV infection causes expression not only of ebvIL-10, but also of human IL-10. We demonstrated here that human CMV encodes its own functional IL-10 homolog, which is expressed by CMV-infected cells. Thus, it seems likely that herpes viruses acquire many advantages by using IL-10-specific biological activities either of virus-encoded or host IL-10s.

Parasites
Ouaissi A. 2007. Regulatory Cells and Immunosuppressive Cytokines: Parasite-Derived Factors Induce Immune Polarization. J Biomed Biotechnol 2007(4):94971.

Another intriguing aspect in the parasite relationship is the fact that parasites could release factors that mimic host cytokines. For instance, (1) hydatid ﬂuid fractions mimicked IL-1, IL-2, and IL-6; (2) an IFN-γ homolog that binds to the IFN-γ receptor and induced change in lymphoid cells has been identiﬁed in an intestinal nematode; (3) two homologs of the human macrophage migration inhibitory factor (MIF) have been characterized in the human parasitic nematode Brugia malayi and termed Bm-MIF-1 and Bm-MIF-2, both having functional properties similar to the MIF human counterpart; (4) Toxoplasma gondii releases cyclophilin-18 (C-18) that signals through the chemokine receptor CCR5 leading to the IL-12 synthesis by dendritic cells and a strong protective response; (5) the tapeworm Hymenolepis diminuta has been shown to express an IL-12-like peptide, one of the suggested hypothesis being that the peptide could act as a competitive antagonist for the IL-12 receptor, thus contributing to the general immunosuppression.

Bacteria
I have not found such explicit examples of bacteria producing cytokine homologs. However, their ability to produce immune modulating, paracrine signalling proteins, which is essentially the definition of a cytokine, is well known. The following reviews are quite extensive and provides numerous examples:
Wilson M, Seymour R, Henderson B. 1998. Bacterial Perturbation of Cytokine Networks. Infect Immun 66(6):2401-2409.

In recent years it has become apparent that bacteria produce many molecules which have profound effects on the capacity of leukocytes and tissue cells to produce selected cytokine networks. Thus attention will have to switch from the current view of the host cell as the only controlling factor in cytokine biology, once the bacterium has stimulated this cell, to one in which the bacterium, by modifying its exported or structural molecules or by direct interaction with the cell, can directly modify cytokine networks.

Henderson B, Poole S, Wilson M. 1996. Microbial/host interactions in health and disease: who controls the cytokine network? Immunopharmacology 35(1):1-21.

Recent cytokine transgenic knockouts demonstrate that the normal benign response to commensal gut microflora becomes a lethal inflammatory state in the absence of the cytokines interleukin 2 or interleukin 10... We propose that the ability of the multicellular organism to live harmoniously with its commensal microflora must depend on mutual signalling involving eukaryotic cytokines and prokaryotic cytokine-like molecules. Such interactive signalling sets up non-inflammatory cytokine networks in tissues which form the background on which responses to infectious microorganisms must be built and related... It is now clear that bacteria contain and produce a large number of diverse molecules which can selectively induce the synthesis of both pro-inflammatory and immunomodulatory/anti-inflammatory cytokines.

Finally, the mechanisms by which bacteria can co-evolve such cytokine-like molecules is discussed in this review:
Stebbins CE, Galan JE. 2001. Structural mimicry in bacterial virulence. Nature 412(6848):701-705.

Recent studies have begun to reveal that many bacterial pathogens mimic the function of host proteins to manipulate host physiology and cellular functions for the microbe's benefit. This is in contrast with the strategies used by some pathogens that involve microbial products with activities lacking clear counterparts in eukaryotic cells. Here we consider recent structural work that provides unique insights into the mechanisms of host mimicry by bacterial virulence factors. In some cases, these factors are homologues of host proteins that have been incorporated into the genome of the pathogen and subverted for its benefit. In others, convergent evolution has produced new effectors that have no obvious relationship to host factors. However, although hidden at the sequence level, the determination of the crystal structures of several bacterial factors and bacterial–host protein complexes has revealed the presence of mimicry at the molecular level.

Bacteria don't produce cytokines naturally (while some might be 'useful' for immune suppression, bacteria can't use human genes/DNA, which has introns, and the chance to randomly come up with a gene that makes the correct protein would be astronomically low).
However, bacteria CAN produce cytokines, if they are engineered to so: here is a company that sells various cytokines, many of which they produce in E. coli. To make this work the company had to remove all introns from the cytokine producing genes and add a bacterial promoter to the gene.
The only thing, which is needed for some human molecules to work (e.g. antibodies), that bacteria can not produce (at least with current technology), are glycosylations of proteins. I checked it quickly and it doesn't look like cytokines are glycosylated (at least in principal, there are very likely some exceptions).


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Why does our body absorb toxic substances or toxic concentrations of a substance if it is capable of regulating gastrointestinal absorption?
Our gastrointestinal system is filled with regulatory molecules that place brakes in the absorption process. For instance, the food that we consume daily is filled with harmful substances that our body does not absorb, and these substances are later excreted. However, when ingesting poison or a potentially poisonous substance at high quantities our gastrointestinal system ends up absorbing these poisonous substances in sufficient quantities (if present) to kill us. Why can't these regulatory mechanisms not entirely prevent the absorption of toxic/poisonous substances that can cause us harm or death?

Is there a  specific substance you are thinking about?

regulating is not the same as control entirely, your skin is proof against many materials but DMSO or mercury pass right through it.

Yes Arsak, any pharmaceutical drug, for instance Ibuprophen. If any person ingests enough Ibuprophen,the pharmaceutical will no longer be therapeutic, as it would get absorbed in sufficient quantity to cause toxicity.

Thanks for the insight John. However, the gastrointestinal tract, contrary to the skin is under more scrutiny in terms of absorption regulation. We rarely abosrb substances through the skin, but continuously need to regulate which substances are absorbed or excreted in the gastrointestinal tract. Hence, my question. Why can't the gastrointestinal put a momentary full stop on absorption, say for 2 hours. Is it so important for continual absorption to occur that it cannot be stopped?

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Possible for bacteria to burst container?
This is kind of a thought experiment, but are there any conditions under which bacteria could multiply enough to burst the container they're in?
Thoughts so far: Bacteria often need oxygen to multiply, but I believe not always? They need a food source, but perhaps despite that mass already being present they might still have a larger overall volume afterwards?
For the sake of this question, I'd like to be fairly loose with the word "container", i.e. not necessarily something solid glass or even solid for that matter, but at least closed. Perhaps I could have bacteria in a bubble and they could burst that?
Thanks for indulging!

some bacteria can convert solids ot gasses so they can generate things that could burst a container.

thanks @John, do you know if there are bacteria that could still burst a container without producing gas? i.e. purely from the volume of the bacteria themselves? (I'd imagine they'd need to consume a fairly dense food supply)

Yes. Bacteria (and fungi) can digest sugar to produce CO2 gas. The latter occupies more space, and can burst contains such as closely sealed bottles (e.g.: for a bacteria / yeast co-culture: http://kombuchahome.com/how-to-prevent-your-kombucha-bottles-from-exploding/ )

thanks @tsttst! Do you know if there are bacteria that could still burst a container without producing gas? i.e. purely from the volume of the bacteria themselves? (I'd imagine they'd need to consume a fairly dense food supply)

@MartinKlvana they couldn't acquire more mass, but could increase in volume/pressure to outgrow it, much like a shaken can of soft drink (but in this case I'd prefer to focus on a case not involving gas evolution)

(Kombucha) Bottles exploding is related to unfermented sugar and active yeast remaining in the bottle at a temperature typically above 50F. Bacteria (acetobacter) are not busy without the presence of oxygen. Lactobacillus may be active but they produce low amounts of CO2 slowly.
Pressure - which may cause bottles to explode - is very temperature sensitive. At 42F the CO2 in the bottle will be contained within the liquid. The warmer it is the more the CO2 expands to the headspace. That same amount of CO2 at 42F just may explode the bottle at 100F
Temperature is crucial both for the activity of yeast (produces alcohol + CO2 in equal amounts) and for the Pressure.

Welcome ed kasper. Please take our [tour] and refer to the [help] for our guidelines. This represents a complete explanation. Answers are expected to show their references, to support why they are correct. You can improve this by [edit]ing to add these. Enjoy the site.


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Suitable writings for self-study in general biology/chemistry
I have recently commenced a graduate education in mathematics. Since I am currently attending extra classes in programming, which are not included in my education, my institution will not let me attend further courses in biology. Hereby, my question is simple:
What are suitable writings for self-study in general biology/chemistry? By general, I mean somewhat of an university-level introduction of mentioned fields.
My level of knowledge is slightly above "advanced" high school chemistry/biology.
(I apologize for my bad english, I'm Norwegian.)

I recommend any Schaums Outline book on the matter. I've read several of them and, although there are books that are better and more specific in many instances, they follow a very easy to grasp format that is common to all other Schaums Outline books.
Therefore, they are a great start for self-studying any subject. The main good point is that, as they are not too dense, the chances you'll leave the book half-through, and stop studying in general, decrease a lot. They will increase your curiosity and understanding, so after reading them you should be ready to read more dense books later on.
I want to clarify that they are not equivalent to "for dummies" books at all. Although they are not dense, they are written assuming you are not dumb and under the principle of being able to make you pass your tests without attending classes. So they are serious books made for practical purposes; no pretence whatsoever.
Particularly on Biology, there are several books:
Schaum's Outline of Biochemistry
Schaum's Outline of Biology
Schaum's Outline of Microbiology
Schaums Outline Of Genetics
Etc. You can learn about any science with them, really.
I'll leave a link with more details on the one in Biology:
https://bookstore.lsue.edu/schaums-outline-biology
They have books on many other sciences. They are designed for self-study.

The post you are replying to is four years old. Furthermore this is a site about specific problems in biology that can be answered in an objective manner. Book recommendations are not that.

Welcome and thanks for your answer. Can you add links to the resources you mention, and in specific those that deal with Biology? Can you also expand a bit on what Schaums Outline exactly is? It seems a book series of some sort? Happy to upvote when you've added these details. Thanks.

@AliceD I think you are wrong to welcome a subjective answer to a book recommendation request which you yourself find lacking, and which is to a question that does not even explain the background knowledge of the poster. It seems to me that this sort of question — like many on Covid — would be better dealt with by a comprehensive answer on Meta, listing sources that are suitable for particular situations, their scope and required background. Allowing posts here encourages subjective material which isn’t of any use to anyone.

Please read the [Tour] carefully to find out who this site  is intended for and what sort of questions are suitable here. Also read the help on writing good answers. It is not our concern if people end up here for the wrong reasons. It is our concern if they then do not conform to the site’s guidelines. If they are not toId, they and others will continue to do so. I have voted to close this old question, but four more votes are needed. If you can answer one of the many scientific questions in your area of expertise, your contribution will be welcomed.


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What is difference between the malaria (cross) types?
When the doctor does the diagnose she says "you have malaria. 2 crosses". Now, I've heard those crosses go from 1 to 5, and historically I've had from 1 to 4, but I wonder: what is the difference between them?
Also there's this popular thing of people saying that an odd number is more dangerous than an even number. Is this scientific or something?
Cheers


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CD4 Proteins & Antigen presenting cells
If Helper T-Cells express CD4+ proteins on their surface to bind to MHC Class ll proteins on antigen presenting cells, why do antigen presenting cells also have CD4+ Proteins?

This question has been asked previously. You can click on this link to get furthur information - https://biology.stackexchange.com/a/67948/11647


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Training Data for Secondary Protein Structure prediction using neural network
I am trying to find some training dataset for prediction of Secondary Structure of Protein. I am having problems finding them online.

The standard benchmark dataset is the one from Lindahl, which consists of 976 × 975 target-template protein pairs.

Lindahl, E. & Elofsson, A. Identification of related proteins on family, superfamily and fold level. Journal of molecular biology 295, 613–625 (2000).

It is for example used in the following articles:

Improving Protein Fold Recognition by Deep Learning Networks
Improving protein fold recognition by random forest

Another resource is SCOP: Structural Classification of Proteins.

Nearly all proteins have structural similarities with other proteins and, in some of these cases, share a common evolutionary origin. The SCOP database, created by manual inspection and abetted by a battery of automated methods, aims to provide a detailed and comprehensive description of the structural and evolutionary relationships between all proteins whose structure is known. As such, it provides a broad survey of all known protein folds, detailed information about the close relatives of any particular protein, and a framework for future research and classification.


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Why facet cells/umbrella cells of uroepithilium are sometimes multinucleated?
Why do are they multinucleated and why only some cells, why not all?

Can you add a source where you obtained this information? Is it a question on the human urogenital tract or of some other animal?

The source is 'Textbook of HUMAN HISTOLOGY' by Inderber Singh and yes, we are talking on human uroepithilium.


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Chewing and weight loss/gain
I have a burning question. I have read many articles which say that chewing food properly, therefore longer, till you have a liquid-like texture, is causing you to eat less calories. However, it causes you to absorb more nutrients. If you would eat the same amount of food. Would chewing make a difference in your weight gain/loss?

I'm assuming that what they are referring to is really not about chewing more, but rather eating more slowly. There is a lot of research that shows that satiety (not necessarily feeling 'full', but feeling satisfied/no longer hungry) is delayed relative to actual eating, so that if you eat more slowly you tend to feel just as satisfied despite eating less. Therefore, that claim is completely predicated on the assumption that you will not eat the same amount of food by chewing more. They should really be more precise, but vague diet advice seems to sell books/get views.


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Nonpancreatic digestion of tryglicerides
In an answer about coconut oil I can read

the digestion of coconut oil does not involve in the Pancreatic digestive enzyme system

In both primary and secondary school I have learned that fat needs to be processed by pancreatic lipase as tryglicerides can not be absorbed.
Are medium-chain tryglicerides an exception (they can be absorbed), are there other (nonpancreatic) lipases in human digestion system, or is the linked answer wrong?

There are two possibilities concerning the further metabolism of MCTs: the glycerides are absorbed and immediately transported through the portal vein to the liver whereupon they are oxidised to release energy.
Alternatively, dependent on the size of the MCT, ranging from hexanoic acid tails to dodecanoic acid tails, it may undergo the standard catalysis by pancreative lipase to form monoglycerides, diglycerides and free fatty acids.
More information regarding the physiological effects of middle-chain fatty acids may be available from: https://academic.oup.com/jn/article/132/3/329/4687297


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Is there a durable surface that ants can't pass?
I'm looking for a surface, that will be impassable for ant's yet not poisonous or easily decaying.
One idea is water - they really can't cross that. But water easily dries and is quite uncomfortable.
Is there something their legs will find uncomfortable? Something spiky for example?

Fluon is a substance that people use to make artificial ant nests. It is similar to teflon in property and fluon coated surfaces are too slippery for ants to cross. See here.

I've found that ants do not walk through petroleum jelly. It is also convenient, as it isn't too messy, and can be whatever shape you want. I use it to keep ants from climbing into my hummingbird feeders. Make sure the area you treat is wider than the ant is long.

Vinegar is something that the ants will not walk through,due to the fact that the vinegar overwhelms their senses.


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Does nature have a mechanism to turn charcoal back to usable carbon?
I have in past asked this about ash, but apart from ash most fires - whether natural or fires in stoves - leave a bunch of charcoal as well. When I was sifting old compost last year, I could identify the layers where the fire pit contents were dumped in - but not by ash, as it really mostly dissolved and disappeared, but by charcoal (and also nails sadly).
In those layers, there were chunks of charcoal as well as larger partly decomposed pieces of wood covered by charcoal.
So, since no wildfire is perfect to the point of burning all organic matter perfectly, what happens to the charcoal after wildfires - or to the charcoal that is dumped with ashes to composts and gardens? Carbon is extremely chemically stable unless you set it on fire, so is there anything that can oxidize it in nature?
If not, is the soil in places of common wildfires rich in pure carbon crystals from millennia of fires and regrowth?

https://www.natureworldnews.com/articles/51463/20220620/430-million-year-old-charcoal-deposits-oldest-wildfires.htm, https://www.sciencedirect.com/science/article/abs/pii/S1871174X20300172, https://pubs.acs.org/doi/10.1021/acs.energyfuels.1c01559. I would suggest researching "biochar".

Short answer - not really. Charcoal as almost pure carbon is fairly inert, not readily available and can remain in the environment almost indefinitely. This is evidenced by charcoal in rocks from the Silurian period (~440 million years ago). We also find evidence of forest fires in the form of charcoal in almost all time periods since this point.
I've personally picked charcoal out of buried soils that is at about 2000 years old from volcanic eruptions - admittedly there the top layers might well have been sterilized by the heat of the pyroclastic flows, so not a perfect analogy.
However we can identify domestic camp sites from Neanderthal and other early human species for the past ~160,000 years, mostly from ash and charcoal presence.
Edited to add: in the case of biochar and similar products, the charcoal is used to act as a reservoir for the nutrients (charcoal is really good at absorbing things a la activated charcoal), which can be taken up into the microstructure of the charcoal and released as the plant rootlets and/or mycorrhizae invade. The charcoal also provides a looseness to the soil allowing greater aeration, better drainage and allowing roots to penetrate to a greater depth. These all help plants to grow well.


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How does peanut pollination work?
I got curious about peanuts and when I found some photos on the internet, I could see they have flowers. However peanut fruit is underground.
How does pollination of peanut flowers affect the fruit underground? Or are there two kinds of fruit, one from flower and one from the underground?

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

@John Where exactly is the explanation? Do you really think I didn't check wikipedia before asking?

Under the heading botany, it explains the entire process.


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Would wasps ever give up on defending their nest against live threat that ignores them?
When I accidentally disturbed a wasps' nest, it was an unpleasant experience. They got everywhere - under my clothes, in my hair etc.
However, in the aftermath - since I'm not allergic to their stings - I observed that apart of some sores on many places on my skin and the racing heart, there's no real damage.
So that made me wonder. If a creature either couldn't feel the stings, or just decided to poke the nest without destroying them regardless of the stinging, would the wasps just give up eventually?
What I mean is, if I just took a stick and poked the entrance ignoring any pain, would they keep stinging until they exhausted themselves to death, or would they just call the defence off and ignore me after a while?

Every wasp acts as an individual so if you disturb a nest, all the wasps that are alarmed will empty their sting on you, that can as many stings as there are wasps. They woudn't call the defense off in any reasonable time. It's not a very rational question. Bears do destroy bee hives, but they have evolved to handle it. I disturbed a hornets nest 10 days ago in a huge black pine tree which i started climbing. Fortunately I didn't get stung by a hornet, even though I had a bike and a track near which is handy for an escape.

@com.prehensible If you keep poking and do not destroy the nest, it must end somehow. Either they exhaust themselves to death or they start to ignore you. That's what I was wondering about.

Yes, but it partly depends on the wasps' perception of "threat". I have had several stings over the years, fortunately one at a time . In E TX the red wasps seem very aggressive , as often as not I do not even know where they came from when I was stung. This year I had 4 stings in 6 days , from small black wasps- something new.. I believe they were "spider wasps" as the stings were very painful and swelling lasted more than 2 days unless treated.  Again , I had no idea I was near them.


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Why is metabolism of ethanol catabolism? Could it be also detoxification?
Detoxification is the physiological or medicinal removal of toxic substances from a living organism, including the human body, which is mainly carried out by the liver. Additionally, it can refer to the period of withdrawal during which an organism returns to homeostasis after long-term use of an addictive substance. (Source: https://en.wikipedia.org/wiki/Detoxification)

Ethanol is metabolised in liver with ADH, which oxidises ethanol to acetaldehyde. The latter is a toxic substance and can cause tissue damage, therfore, it must be further oxidised by ALDH to form a non-toxic product, acetate.
Ethanol can be an addictive substance.

Why is ethanol metabolism catagorized as catabolism? Could it also be detoxification (according to the assumptions above)? Why not?
Is ethanol metabolism a catabolic metabolic pathway because it provides NADH and acetate (which can be activated to acetyl-CoA) for anabolic reactions? Or is there another reason?

These are somewhat loosely defined terms, but I would say catabolism is any metabolic process that extracts energy from a substrate. Ethanol conversion to acetate (via alcohol dehydrogenase; see this schematic) is an oxidative pathway which extracts energy in the form of NADH, so yes, it is a catabolic pathway.
I guess you can also call this process detoxification, since it removes a (mildly) toxic metabolite. Anyway, I think the "classification" of a pathway is less important than understanding the actual biochemistry.


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What is a good set of notes to study human's eye mathematically?
I want to learn about the human eye. I could read a lot of online literature about it.
However, ideally I would like to study human's eye by solving some maths exercises. I suspect people have done this before. How would we have glasses otherwise?
Maybe you know good maths notes + PROBLEMS that would give me an insight into how an eye works?
The notes don't have to comprise a whole course. One chapter is enough, as long as there are some maths exercises attached.


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How a pathologist would analyse this H&E image?
I am working on a project which involves writing computer software to analyse histological images. A typical image looks like this:

It is a Hematoxylin and Eosin stained biopsy of breast cancer tissue.
Being a programmer without biology background, I would like to get insight into how a pathologist analyses such images.
More specifically:

Which cells are cancer cells and which are regular cells?
Can an invasive margin (a curve marking the boundary of cancer invasion into the tissue) be seen in this image?
Can a pathologist provide a TNM classification looking at the image? If yes, what would be the T, N, M, G values for this image?

A single image is not enough for a TNM classification. This system requires knowing the size of a tumor (T), the degree of spread to new-by lymph nodes (N), as well as information about metastasis to other organs and tissues besides the lymph nodes (M), none of which are apparent from a single H & E stain image. Also, histological scoring often requires the user to scan around a slide and review many different fields of view. You'll probably want to collaborate closely with a skilled clinical pathologist for the project you've described.

@MikeyC what can be inferred from such image?

@MikeyC i.e. if a single image is not enough for classification, why is it taken?

My histology experience was looking at inflammation and necrosis in animal tissues, which is why I kept my reply to the commets section. I really only know enough about this to know that I would seek expert collaborators if I was doing what you're try to do. Histology often needs to be evaluated in context. A single image might be enough to identify cancerous or pre-cancerous cells, but you'd also need something like X-ray images to determine a T score along with additional biopsies or lab tests to determine N and M scores.

Here are some reviews I came across that might help give you a sense of similar applications being explored.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2910932/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5556681/


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How to get a list of kinases that phosphorylated a particular protein?
I am analysing the protein SF2 (also named as SRSF1). In the database, it is shown that this protein is often phosphorylated at the 189th tyrosine residue.
I want to know which proteins could have phosphorylated the protein at this site. Is there a way to figure this out using databases? What about getting a list of proteins that phosphorylated SF2 at any site?

I use PhosphoSitePlus too. I use it in combination with ELM as it finds linear motifs and generally gives a good generic candidate.
The literature if not. Checking all close homologues sometimes pays off.
Checking protein protein iteraction databases such as StringDB or IntAct may help too, but that gets very iffy —XL-MS (a smoking gun) is rare and does not pick up low concentration enzymes like kinases.
(A note: this question ought to have been asked in bioinformatics SO)


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How do we know which Eulerian path corresponds to the DNA sequence?
Bioinformatics textbooks explain one method to reconstruct the whole DNA
sequence from multiple reads. The method builds a graph and finds a Eulerian path in it. The Eulerian path corresponds to a DNA sequence.
However, the graph can contain more than one path. How do we know which path corresponds to the actual sequence?

If the DNA sequence contains repetative elements, and your reads are not long enough to resolve them, you won't know if you have the right path.  Usually you split your results into contiguous regions whose sequence you are confident in.


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Protein structure prediction using PSSM? Or not?
I have been studying protein structure prediction algorithms. A lot of recent work uses something called the PSSM, the position-specific scoring matrix.
I think that what a PSSM does is to build a 2-D matrix of all possible residue pairs in a protein, then scores how likely it is that the two residues mutate in tandem. Co-evolution of two positions which are far from each other in the primary sequence are an indication that they are in contact. When one residue in a contact pair changes, that generally destabilizes the protein, and the other residue in the pair is under selective pressure to compensate. Knowing this gives you a good start on building the protein contact map.
Do I have that right?
If that is correct, then this technique of protein structure prediction depends on having many examples of proteins in a homologous family. You need nature to do a lot of sampling for you. And you need to dredge up massive numbers of homologs from genomics projects. I've read that creating the multiple sequence alignments for PSSM work is computationally intensive. If I understand the process correctly, I can see why.
My main question is: what can protein structure prediction models built using PSSM do, when there isn't a PSSM?
For example, the Top7 protein is a fully-novel protein fold that does not have any homologs in nature. It was created in 2003 using RosettaDesign software. Rosetta's protein structure prediction algorithms predate PSSM as far as I know. Sixteen years later, there are exactly six variants of Top7, all of which have been made in the laboratory. That hardly sounds like enough data for a statistically-valid PSSM, and in any case, the variants were not naturally selected.
If you don't have a PSSM, is it even possible to enter your sequence into a model that expects one?
Thanks for your input.

I think you are making PSSMs out to be much more sophisticated than they really are.
A PSSM is merely a scoring matrix — it gives position specific scores for each residue at a given location.
There is no explicit pairing of interacting residues though that does sound like an interesting approach ...
You can learn more about PSSMs from many sources on bioinformatics including NCBI.

Thanks for your quick reply, tyersome.  If the PSSM is an N x 20 matrix, you're right, it can't really do what I thought it does.  So is the PSSM distinct from the "co-evolutionary methods" that I'm reading about in this recent post on Google's AlphaFold? (https://moalquraishi.wordpress.com/2018/12/09/alphafold-casp13-what-just-happened/)  I don't have enough characters to post a relevant quote from the article in this comment, so I'll continue in another one.

Quote from (https://moalquraishi.wordpress.com/2018/12/09/alphafold-casp13-what-just-happened/): "CASP11 began to show life because of the introduction of co-evolutionary methods, but just barely because most FM targets had shallow multiple sequence alignments (MSAs), which are required for co-evolutionary methods. CASP12 was when the power of these methods finally got demonstrated, and CASP13, even when excluding AlphaFold, showed further progress due to the widespread adoption of deep learning in co-evolutionary methods."


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How lion can carry the cub without harming it?
We can see in the picture that lion is carrying its cub by the scruff of its neck without causing harm to it.

The skin of the felines has geneticaly evolved in such a way that the parent can do this.
Its strong and stretchy in the neck area.
Moreover, the cub enters into an obedient state.

Too complicated. I was going to answer but know I would get "dinged" because people on here seem to prefer the complex over the simple. The answer is "They don't bite down". Thats it. You can prove it to yourself. Put your finger in your mouth, and close your teeth around it. What keeps you from biting your finger off? : Intent.

@KarlKjer — Answer in answers or not at all. Comments are explicitly not for answers. It's a pretty naive question that demands a straightforward answer. If people 'ding' you just shrug it off.

just try to "ding" a human and see where is going :)


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Are all/most/any membranes comprised of lipids from the smooth ER?
I'm attending an introductory high school course to cell biology. Based on my understanding, lipids – the building blocks of membranes – are formed in the smooth ER. Are all/most/any membranes comprised of lipids that are formed in the smooth ER? If not, where do the lipids of membranes come from?

It sounds like we're mainly interested in phospholipids here, as they're the main component of cell membranes. Since your question didn't specify, we'll talk about Bacteria/Archaea and Eukarya separately
Bacteria/Archaea
Here, the answer is fairly intuitive. Bacteria and Archaea don't have endoplasmic reticulum, so they can't synthesize phospholipids in it. In this case, it seems like they create fatty acids directly from enzymes in the midst of the cytosol.
Eukarya
Here, the answer is a bit more complex. Fortunately, there are some good reviews about the topic that answer the question. Here, they talk about the entire phospholipid biosynthesis pathway and only mention the ER as an organelle, although it's worth noting that there are several sub-locations within the ER where specific groups are added. However, they fail to distinguish between rough and smooth. In another source, they mention not only the ER but also the mitochondria as having some ability to synthesize phospholipids. That's pretty cool, in my opinion.
TL;DR:
Bacteria and Archaea certainly don't rely on the smooth ER for lipid synthesis. In eukaryotes, there are several areas where lipids can be made but the smooth ER does seem to be the main source.


text:
IgA-s in an immune system vaccined intramuscularly against Hepatisis A
As IgA are immunoglobulins associated with secretion and mucosis membranes, I am interested whether after intramuscular vaccination with Hepatitis A vaccine IgA antibodies will be produced by the immune system before an actual infection?
Also, would they be secreted into breast milk, intestine lumen etc. before the infection coming in a traditional (gestational) way?
Or does it take to have the antigen presented at the mucosis mambrane to start IgA production or secretion?

Antibodies are produced after exposure to cognate antigen.
Remember that B cells start off expressing membrane IgM and/or IgD. IgA requires class switching recombination at the B-cell receptor locus to the IgA isotype. Further differentiation of the B cells to antibody-secreting plasma cells results in soluble IgA production and immunologic memory to the antigen. Whether you'll get IgA, IgE or IgG antibodies against the vaccine will largely depend on the signals they get in the muscle, however (Figure 1). I think IgG is largely a result, since the tissue antiviral response is often interferon gamma (Figure 2).
The importance of intramuscular vaccination is outlined here, just in case it wasn't apparent.

Figure 1. Activated helper T cells that can recognize the same antigen mediate the class switch by providing co-stimulatory signals and cytokines. Source

Figure 2. Class-switching continued. Source: Parham, The Immune System, 4th Ed.

Then I see it is unlikely to have IgA produced after vaccination, am I right? As a side note - the linked paper seems to compare only muscle/fat injections, but no oral delivery.


text:
Does Penicillium roqueforti produce penicyllin?
I have recently discovered that blue cheese is produced with Penicillium roqueforti. As I know that some Penicillinum sp. produce penicyllin I wonder whether it is produced by P. roqueforti too?
The Wikipedia article does not mention penicillin, it mentions "compounds that can be employed as antibiotics" instead.
However the article on P. glaucum also do not mention penicillin, while P. glaucum is mentioned in the article on the history of penicillin.


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How likely is to develop an infection from a single virion entering a single cell?
Is there any research (including mathematical or computational modelling) regarding how likely it is to infect an organism starting from a single virion entering a single cell?
I am interested in any virus and any multicellular organism (including immunocompromised).

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

This is called the Independent Action Hypothesis, described here:

The Independent Action Hypothesis (IAH) states that pathogenic individuals (cells, spores, virus particles etc.) behave independently of each other, so that each has an independent probability of causing systemic infection or death.

Zwart et al. (2009) tests this theory, and their results support the hypothesis that a single virus particle can infect a cell:

The ‘independent action hypothesis’ (IAH) states that each pathogen individual has a non-zero probability of causing host death and that pathogen individuals act independently. IAH has not been rigorously tested. In this paper, we (i) develop a probabilistic framework for testing IAH and (ii) demonstrate that, in two out of the six virus–insect pathosystems tested, IAH is supported by the data.

The modeling done in this paper may be worth reviewing.

See also this paper showing that for influenza in two pigs cages with one contagious it is usually two PFU that caused the infection is the second one, where in a PFU all the virions have (almost) the same genome. The other question is once a viable virus entered the correct cell, what is the probability that it succeeds in finding the right organelles membranes and achieving its replication. The answer is mainly how to translate PFU/ml into number of viruses/ml.


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What is the mechanism responsible for long-lasting detectable antibody titers?
As I understand, when naive B cell encounters antigen matching its receptors and is activated by a T helper cell, it can either differentiate into 4 plasma cells, produce a lot of antibodies and commit apoptosis, or into 2 memory cells waiting to be activated the next time they encounter the antigen.
On the other hand, IgG can be detected for a long time after infection.  As antibodies decay, there must be long-term production of IgGs to keep their level constant.  What is the mechanism behind that if there is no following infections?

Great question. Maybe the answer is simply that these assays are sensitive enough to detect basal levels of IgGs that memory cells continue to produce in the absence of an infection.

@DouglasMyers-Turnbull If not activated memory cells can secret antibodies, that actually answers my question.


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What species is this spider?

A friend of mine saw this monstrosity in Taiwan. The photo isn't very clear but you can't blame her considering it was the size of her face. Wanted to know what species it is so I know where they spawn and to stay away from those areas.

I believe this is called Nephila pilipes.
You can refer to Wikipedia for more information

Link only answers are generally discouraged on the stack exchange sites. You can improve the answer by expanding on it.

Not sure how to expand on it. He asked for the name of the species and I answered.

@Casanova You could mention features that make this species identifiable.


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What kind of experiments could you do to see which end of a microtubule is most dynamic?
I'm stuck between two ideas. Not sure which one of them would be best.

Do a FRAP on the middle of a MT. If it grows from the + end, that section will remain dark. If it grows from the - end, existing fluorescent tubulin will be pushed into the photobleached area. However, how would I be able to tell if the middle region is dynamic using a FRAP?
Introduce GFP-Tubulin into a cell. See where existing microtubules begin to fluoresce as new subunits are added.

Do either of these sound reasonable? Any better ideas?

This sure seems like a homework assignment. The methods for experiments like these were all published by the early '90's

As i remember, it has been shown that MTs are virtually indestructible in the middle. I'd say both sounds reasonable, but as soon as you start planning experiment, you get into trouble. FRAP seems most likely to succeed. Another one is FCS -- see where in the cell GPF-tubulin is most stable, e.g. closer to soma or axonal terminal (in neuron)


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the range of interleukin 2 and 12 that can be used to activate nk-92 cells
I am one of the biotech students. I want to know the dynamic ranges of interleukin 2 and 12 that i can use to activate the NK-92 Cells.
    thank you

If you have the resources you should ideally titrate your cytokines. You'll find that cytokines from different vendors may exhibit varying stability or availability in vitro, but also that you obtain varying levels of activation. Standard NK-92 culture conditions are 100-300 IU/mL IL-2 in RPMI1640 medium, 10% serum and 2mM L-glutamine (or 1X GlutaMAX, life technologies). Activation levels depend on how much you want to activate them. Interleukin-12 I'm fairly certain is standard at 10 ng/mL, but should also be titrated.
There's actually a relevant paper with a fair titration looking at granzyme expression at different concentrations of IL2, IL12 and IL15, and different timepoints. They note that NK92 cells show response at 100, 500 and 1000 IU/mL IL2, and at 10-30ng IL12.


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Evolution and different number of chromosoms? (a non-biologist)
I understand that a species becomes a different one slowly and in a continuous way. However, the different number of chromosomes is bugging me. Chimpanzees, for example, have 48 chromosomes whereas humans have 46.
I have few guesses which haven't satisfied me at all:

The species are not that different, despite of their different
number of chromosomes, and capable of breeding. The offspring is
somehow healthy and is also capable of breeding. But doesn't that
make the offspring sterile?
The other possibility is, at some point multiple offspring in a
    population formed with, say, 46 chromosomes and the breeding took
    place among them. Even though it doesn't sound impossible to me, what are odds really?

Can someone provide an insight to a non-biologist?

It depends on which chromosomes are extra... For example, neanderthal and humans have different numbers, and it's the X and Y chromosome for them that differs. so only female humans which mate with a male neanderthal could have a viable chromosomal balance. The chomosomes can work in sets of three technically, they are called trivalent chromosomes. https://biology.stackexchange.com/questions/15727/examples-of-animals-with-different-number-of-chromosomes-that-can-interbreed

I'm not sure how the evolution of populations works out, but it's well known why humans have 23 chromosome pairs rather than 24 -- our chromosome 2 is the result of a fusion of two ancestral chromosomes, which remain separate in the great apes.  See for example https://www.ncbi.nlm.nih.gov/pmc/articles/PMC52649/

Possible duplicate of Evolutionarily speaking, why do humans have 46 chromosomes

You formulate guesses but what is the question you are trying to address? Does the post Evolutionarily speaking, why do humans have 46 chromosomes answers your question? I am voting as unclear for the moment.

I think you are overthinking the problem. Think of chromosomes as parking lots and genes as cars. Just because there are different numbers of parking lots, doesn't mean cars no longer need parking spaces - they have to park somewhere! In the specific example of humans versus chimps, two "parking lots" were joined together so there are technically less parking lots, but there is still enough room for all the cars. Perhaps I've stretched this analogy too far...

Speciation doesn't happen from one generation to another, it is a slow and continuous process, and for each changing that is kept by natural selection, there are millions of changes that resulted in less functional phenotypes and were negatively selected, and another million of changes that were lethal hence soon aborted (e.g. a mutation that causes an embryo to die even before a fruit or animal can get any development). So it might be possible that many chromosome number changes are taking plane in many organisms, but they  never will estabilsh in their populations. On the other hand, some numerical changes (and all the genetic processes that follow any change) may result in a good fit, and the individuals survive, establish and reproduce. But keep in mind that it is a slow and continuous process.
Theoretically, if among Chimpanzees, multiple offsprings outcome with 46 instead of 48 chromosomes:

In a theoretical scenario: They could be able to reproduce only among themselves (the 46-chromosomed-individuals) and, with time, accumulate some differences in relation to the 48-chromosomed-Chimpanzees, and them they would be named as another species.
In a theoretical scenario: In some conditions, they might be able even to reproduce with 48-chromosomed-Chimpanzees (e.g. if this numeric change resulted from fission of one chromosome, and when the two gametes meet, the two half chromosomes of one parental pair with the whole chromosome of the other one... That is not probable for animals, but happens a lot in plants)
If you are asking if they 46-chromosome chimps would crossbreed with humans... well, I believe they have accumulated too much differences in their genotypes and thus would no be compatible even if they have the same chromosome number. It happens that having the same number is not the most important factor allowing or preventing species to crossbreed. There are many barriers to hybridization, e.g. the lack of biochemical recognition between egg and sperm resulting in no embryo formation... in cases that embryo is formed, it may not develop, it may develop poorly, or it may develop but the offspring comes out compromised and live shortly. Another example that chromosome number does not prevent crosbreed is the mule, which is the offspring of a female horse (64 chromosomes) with a male donkey (62 chromosomes). That's because even having different chromosome numbers, they are still quite simmilar in a genetic perspective.

All that sayd, the odds that Chimps would loose two chromosomes, stablish in the population and reproduce with humans are really really really low... I would say that's impossible. But simmilar phenomena are possible and even quite common in plants (just so you know that it exists)
If you want to learn more about chromosome number changes, I recommend this link: https://www.ncbi.nlm.nih.gov/books/NBK21229/
(Modern Genetic Analysis. Griffiths AJF, Gelbart WM, Miller JH, et al. New York: W. H. Freeman; 1999.)

I think your answer is wrong and unclear -1. Wether your answer answers the question is hard to tell as the question is unclear as well (not your fault). Here are a few critics. Evolution really takes place in a slow and continuous way this is rather wrong! What do you call numerical changes? I don't understand the sentence if among Chimpanzees, multiple offsprings outcome with 46 instead of 48 chromosomes. You seem to think that chimpanzee are humans's ancestors which is wrong. the odds are really really low for Chimpanzees the odds for what?

I'm surprised how poorly I seem to have expressed myself...when I say that evolution is a slow process, I mean that it does not occur from one generation to another... By numerical changes, I mean disploidy... And I don't see what in my answer made you think that I believe chimpanzees are humans's ancestors, but if you got this impression I clearly expressed myself poorly... Thus it's important to remark that humans and chimpanzees share ancestors (as we do with all the extant life, by the way).

I'll edit this answer tomorrow, thanks for pointing out so many things to improve

No worries, misunderstanding is not so uncommon. You are making a hypothetical scenario where chimps lose a chromosome pair and this feel weird to me given that the reason for why there is a mismatch between human and chimpanzees chromosome number is due to a fusion in the human lineage (Ijdo et al. 1991). Btw, welcome to Biology.SE!

Yes, this feels very very weird... But I got from his question that he was asking about the odds of multiple chimps loosing one pair, establishing in the community and reproducing  among themselves... And this is a crazy hypothetical scenario for chimps... But things like this do happen in life... It's even very common in plants... And also, do you think humans would really match chimps if they loose 2 chromosomes? I think they now have too much differences, numeric compatibility wouldn't be enough for them to reproduce and have fertile offspring.. (Btw, thanks! =])

@GerardoFurtado, maybe you can help me improve this answer, Professor... what I mean is that the fact tha in a population one individual was born with a small difference, that doesn't mean a new species has evolved

Absolutely. I guess since the question mentions "one species becoming another one", I took speciation as evolutionary process and used the world evolution improperly. Thank you, Professor.

I think it is probably worth noting that humans did not evolve from chimpanzees as the question and answer imply. In fact, the most recent anthopoid ancestor of both chimps and humans had a diploid karyotype with 50 chromosomes, according to Stanyon et al. (2008) in the journal Chromosome Research.

I never said that humans evolved from Chimps! They only have common ancestors


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Organisms that do not wish to reproduce
Are there any organisms that do not want to reproduce?
As humans, there are people who do not want to reproduce with the opposite sex. Do any other organisms replicate this behavior? Also, why does this behavior exist? If the end goal of an organism is to reproduce, why has evolution allowed organisms that do not want to reproduce to exist?

Are you talking about homosexuality?

See also: Which species has the highest proportion of homosexual individuals? and Can animals, like monkeys, be homosexual?

Hydra dont age and only have sex when food is scarce to leave spawn for next season. they devide. komodo dragons dont need sex to have eggs, whiptail lizards, marbled crabs and many many other animals are asexual: https://www.cuteness.com/article/animals-use-asexual-reproduction some 10 pc of rams, male sheep, stick insects, sawfish, snakes ... search for asexual animals. parthogenesis.

@Remi.b — The poster did not mention homosexuality. Have you never encountered heterosexual couples that don't want to have children and are able to fulfill their wishes through contraception. The question is silly in attributiing human emotions to non-human animals, but it is not about homosexuality.

@David You're right. I'd think however, that the answer remain similar I would guess. It will be hard to talk about 'will of having babies' with heterosexual couples in animals.

@David You're right that I was asking this question with homosexuality in mind, but the explanations there gave me the answer i was looking for. Thank you!

Animals and especially female animals might not "want" to reproduce when circumstances are bad for babies.  Pregnancy and rearing of infants is a big commitment of resources for female mammals.  If a female is under stress, or sick she might avoid having sex even though she could get pregnant because evolutionarily that was a winning strategy for her ancestors - committing the physical and nutritional resources to a pregnancy and fetus unlikely to survive current circumstances puts the mother and subsequent pregnancies at risk.
A more extreme example is the Bruce Effect.  Pregnant females exposed to the pheromones of a strange new male "decide" not to reproduce - their bodies resorb the fetuses.  Presumably this is because the new male is a risk to the fetus and they would do better calling off the doomed project, and possibly having a new litter with the new male if he shows up.
Weirder is the circumstance of parents that kill and sometimes eat their young.  That happens in mammals, birds, fish and others.  It is hard to see how this sort of thing advances genetic fitness - it seems like a crossed wire or misfire of some sort.  Certain animals, however, seem to do it all the time; hamsters come to mind.  Maybe stress causes weird behavior?  In any case this too would seem like a case of deciding not to reproduce.


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Can chromosomal crossover undo itself?
If I have alleles AB on one chromosome and ab on another, and if A and B are far from each other (and also a and b), then there is a lot of chromosomal crossovers happening. If I crossover 7 times, will I end up with the same chromosomes as if I cross over once?

Are you asking if the chromosomes can remain entirely identical or just with respect to AB/ab?

Good thinking. Yes, it is theoretically possible. It is often modelled like this. Have a look at this answer for the maths.
Note however, that to my understanding (and I might be wrong) there is typically either 0 or 1 crossover per pair of chromosomes as cross-over is directly related to the way homologous chromosomes bind together during prophase I of the meiosis by the synapsis. My confusion lies in the fact that, I think, there are sometimes (often?) several synapsis per chromosome pair. Hopefully, someone else will be able to clarify this for us.
As a consequence, the genome-wide recombination rate in humans is almost exactly 23 in humans (Wang et al., 2012). So in practice, such mulitple crossover would very rarely (if ever) happen.

See also.

My experience trying to recombine transgenic constructs in Drosophila is in line with 1 crossover per chromosome being common and >1 extremely rare.

That's quite an interesting question. Crossing over occur during meiosis, there can be more than one in a chromosome indeed. Let's say two crossing over occurs in the same chromosome (the one with your markers A and B), if they both occured in between your markers, you will see no difference. As you said your markers are far from each other you have a good probability to observe that. If your markers were close, your chance to observe a double crossing over is really low.
Also, there is some mechanisms preventing two crossing over to occur too close from each other. I can't tell you exactly what it is about. There is a type of Crossing over not subject to this rule though...
Double crossing over can be an issue when working on genetic maps (using crossing over to determine the order of marker on map). As if this occur we have no way to choose between 0 crossing over or 2 crossing over (meaning markers are actually far from each other.
If you want more explanation about this wide topic, I would suggest you to read this scientific work. They are working on removing inhibition for crossing over and achieve to multiply the number of crossing over by 9 in Arabiodpsis!

Synapsis is the pairing of homologous chromosomes, one from each parent. Crossover occurs following synapsis. The points at which crossover occurs are called chiasmata, and appear to be genetically determined.  However, it seems that they are not always at the same locations on homologous chromosomes from different individuals.
That said, the likelihood of crossover being reversed on one chromosome would depend on a series of lucky coincidences and some serious inbreeding, but could conceivably happen.  For crossover to be reversed on all chromosomes would be staggeringly unlikely.


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Do oranges have traces of starch?
This is for a chemistry experiment, so I just want to know if there are small traces of starch in oranges, and not whether or not I should eat an orange for its starch content, or something to that extent.

If it is related to chemistry, it would belong to Chemistry.SE

Sources are varied. This paper studies starch in oranges (I can't access full paper). However, here authors mention that oranges contain practically no starch (beware, images are upside down). They refer to work by
Stahl A.L., Maturity studies of citrus fruits, 1938

and quote this work saying "starch content was measured to be 0.07-0.13%" in pulp of Pineapple oranges. Compare that to 22% of potato starch amount (dry mass).

According to Healthy Eating, oranges contain 8.98g of sugar but does not contain any starch:

The natural sugar found in fruits doesn’t create such a big response
  because it's balanced by the fruit's fiber content. One banana has
  14.43 grams of sugar, compared to only 8.98 grams in an orange. The biggest difference between the two is in the amount of starch each
  contains. The orange doesn’t have any, while the banana has 9.42 grams
  of starch.

I’m not sure how trustworthy these websites are. This one, for example, says that oranges do have starch.


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Can somebody identify this insect?
It has transparent wings which covers the body like an armor. It has shining red orange colour.

I found it in the western ghats of kerala.

Now, that's an interesting insect. But, we post pictures here on the insect, and it's likely a better photo is needed (but not absolute.)


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What is the field of view of humans (not just fixed angle eyes)?
What is the human field of view also counting the maximum vertical and horizontal eye movement (rotation), with the head still.
It is unclear from this question whether the answer relates to the field of view from both eyes when a person is looking at a fixed angle or also what he/she can see if the head won't rotate but the eyes will.
What is the field of view for the human eyes?
There are many articles and diagrams online as well but they too don't make it clear whether the eye rotations are also taken into account or not and it is just the FOV at any given moment at a given eye angle.

Pretty sure the question you linked assumes fixed head position and includes eye movement. Eye rotation is taken into account.

@Diio - why do you assume that?

I don't know if this is what you're looking for. Your picture is top-down – view from the top, looking down at a head. Here's a picture from the first person point of view:

Field of view
The human field of view is restricted mainly by the pupil size and the nose, and has a
significant overlap, which is shown in Figure 31 (p.62)

Figure 31 The field of view of the left and right human eye. The angle is measured from
the head’s forward axis. Note the influence of the nose on the fields

Found at https://www.researchgate.net/figure/The-field-of-view-of-the-left-and-right-human-eye-The-angle-is-measured-from-the-heads_fig21_277476286, where a full PDF is also available.