text:
Why does cutting onions cause tears?
Why does cutting onions cause tears? From a couple of sites, I found that it is because of sulfuric acid produced by onions. But I could not find more details. What is the biochemical pathway by which onions cause tears? Also, which compound is responsible for it? If it is enzyme-catalyzed reaction, can we just stop the production of this enzyme without causing any side-effects?

Your last sentence refers to the Vidalia Onion, IIRC.  Lacking sufficient sulpher, it doesn’t produce significant quantities of the irritating sulfoxide.

Related advice: https://cooking.stackexchange.com/q/567/28937

Interesting question! The cause of tears and itching is the chemicals produced by onion (Allium cepa). Lets go into some details.
Onions, coming from the family Liliaceae (also containing garlic, chives, scallions and leeks) store compounds known as amino acid sulfoxides, and the one we are talking about here is S-1-propenyl-L-cysteine sulfoxide (abbreviated as PRENCSO), also calles isoalliin (due to its similarity with alliin found in garlic). When onion is damaged (cut, chewed, etc.), an enzyme alliinase converts PRENCSO into 1-propenyl sulfenic acid. This compound is then converted into propanethial-S-oxide by an enzyme lachrymatory factor synthase (earlier this reaction was considered spontaneous). The reaction looks like this:

Propanethial-S-oxide is the major cause of the flavor and aroma of onion. However, it is a volatile compound i.e. vaporizes very quickly. When its vapors reach the eye, it causes tears because of being a lachrymator (aka tear gas) i.e. as soon as it comes in contact with cornea, it triggers a nervous response which leads to activation of lachrymal (tear) glands.
PS: when propanethial-S-oxide comes in contact with cornea, a small amount of it reacts with water to form sulfuric acid. This sulfuric acid is the cause of itching and irritation in eyes due to onion. Also, scientists are now trying to genetically either modify or stop the production of lachrymatory factor synthase enzyme to produce tearless onions. This (modification) has even been achieved to a high efficiency, as another answer discusses. However, making tearless onions could prove harmful to the crop in several ways, as discussed here.
EDIT: As asked in comments, I will add some details about how the sulfuric acid is produced from the reaction between propanethial-S-oxide and water.
The only resource I could find giving some details about this was Marta Corzo-Martínez, 2014. They summarize the complete pathway in the following diagram:

After applying some common chemistry principles, the concerned reaction turns out to be:
$\ce{4~C_3H_6SO~+~4~H_2O \rightarrow 4~C_3H_6O~+~H_2SO_4~+~3~H_2S}$
As you see, one of the products of hydrolysis of propanethial-S-oxide is hydrogen sulfide ($\ce{H_2S}$). Just like $\ce{H_2SO_4}$, $\ce{H_2S}$ also causes irritation in the eyes (its effect on eyes has been well documented, see Lambert et al, 2006 as an example). Thus, the produced $\ce{H_2S}$ only increases the irritation and itching in the eyes caused due to $\ce{H_2SO_4}$.
BONUS: Another interesting point here is runny nose. propanethial-S-oxide is actually the compound responsible for the smell and flavor of onions. But, it causes tears by exciting the lachrymal glands i.e. reflexive lachrymation. propanethial-S-oxide excites the trigeminal nerve (the fifth cranial nerve) causing activation of lachrymal glands. Interestingly, the nerve endings of trigeminal nerve are also present in the nose, along with the eyes. So, this compound can also activate the lachrymal glands from your nose, and since the lachrymal duct is joined from eyes to nose, you can also experience runny nose along with tears and irritation in eyes.
References:

Propanethial-S-oxide | University of Bristol
Alliin | Wikipedia
Tear Gas | Wikipedia
Timothy William Lambert, Verona Marie Goodwin, Dennis Stefani, Lisa Strosher, Hydrogen sulfide ($\ce{H_2S}$) and sour gas effects on the eye. A historical perspective, Science of The Total Environment, Volume 367, Issue 1, 15 August 2006, Pages 1-22, ISSN 0048-9697, https://doi.org/10.1016/j.scitotenv.2006.01.034
Encyclopedia of Perception, Volume 1 -
E. Bruce Goldstein,
SAGE, 2010
The Neurology of Lacrimation – How an Ear Infection Can Cause Dry Eye -
by Noelle La Croix, DVM, Dip. ACVO

I'm curious about the sulfuric acid. The oxidation number of S is rather low in propanethial S-oxide, are you certain that sulfuric and not sulfurous acid is produced? I know about the relatively low stability of the latter.

This is due to a lachrymatory agent called as syn-propanethial-S-oxide.
The process goes as follows:

Lachrymatory-factor synthase is released into the air when we cut an onion.
The synthase enzyme converts the amino acids sulfoxides of the onion into sulfenic acid.
The unstable sulfenic acid rearranges itself into syn-ropanethial-S-oxide.
Syn-propanethial-S-oxide gets into the air and comes in contact with our eyes. The gas diffuses through the air and, on contact with the eye, it stimulates sensory neurons creating a stinging, painful sensation.
The lachrymal glands become irritated and produces the tears.
Tears are released from the tear glands to dilute and flush out the irritant. In this case it is to reduce the effects of sulfuric acid,a chemical that could damage the eye if it was not for the tear reflex that renders the sulphuric acid largely harmless.

So, we can stop tear production by not irritating our eyes by using the onions which produce less irritants.

Through a single genetic transformation in onion (Allium cepa), a crop recalcitrant to genetic transformation, we suppressed the lachrymatory factor synthase gene using RNA interference silencing in six plants. This reduced lachrymatory synthase activity by up to 1,544-fold, so that when wounded the onions produced significantly reduced levels of tear-inducing lachrymatory factor.

Sources: https://www.loc.gov/rr/scitech/mysteries/onion.html
https://www.ncbi.nlm.nih.gov/pubmed/18583530

Interesting. I was wondering, though, if it has to come in contact specifically with the eyes? As it seems for myself that the smell alone (well, the irritating gas actually) starts the tears, and the painful feeling comes from my sinuses rather than the eyes? I also noticed I sustain the feeling much longer if I pinch my nose. Yet that might be confirmation bias ^^

@spectras I believe so; I have a pair of goggles that I wear when cutting onions and it seems to prevent the effect.

Just because it's a random thing I learned working in fast-food for 3 months at the ripe age of 16 before being fired, soaking onions in ice water dramatically reduces irritation. Maybe the ice isn't needed, can't recall.

@ChrisSchneider As temperature decreases enzyme activity and diffusion decreases.

@chrisschneider also the propanethial-S-oxide and sulfuric acid are water soluble, so it prevents their vaoprization

@spectras In my experience, your observation is not confirmation bias, it's simply true. Whatever causes the tears, it makes its way through the nose. Pinch your nose for good (f.ex. with a clothespin and from the start to the end of the process) and there will be almost no tears at all. I got this tip from someone who cooks all the time, I tried and it just works.


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What is meant by "complexity of carbon sources"?
My biology book states

"life on earth depends upon carbon based molecules, most of these food sources are also carbon based. Depending upon the complexity of these carbon sources, different organisms can then use different kinds of nutritional processes"

Please explain this statement.

They mean complex arrangement of the carbon atoms in the carbon sources.

According to me Plants are autographs and they make their own food by the process called photosynthesis and they take Carbon dioxide and water directly from air and roots so Thor the simple diffusion is taking place so they are not that much complex than us so they use simple nutritional process

@Tanushka - On Stack Exchange we are looking for informed answers supported by citations, references or links. This allows users of the site to judge their validity. Please read the tutorial before posting or answering.

Consider all the different types of carbon molecules one can find on earth.
Proteins.  Sugars like cellulose and starch.  Alkanes like methane and tar.  CO2.  Alcohols.  A boatload of variety.
Now think of how each one is used or can be used by an organism.  I will chow down on a potato.  And some alcohol. Termites eat cellulose.  Anaerobic bacteria use methane.  Plants eat up the CO2.
One carbon nothing eats is CaCO3 or limestone.  I am not sure why.  Oh - also diamond.  Not many things can metabolize a diamond.  Although maybe they don't get the opportunity to try...

Have in mind that CaC03 and diamond (as well as graphite, nanotubes, carbonic acid, cyanides, carbon dioxide etc) are inorganic compounds, despite having carbon (actually, diamond is not even a compound, but just an allotrope of C).

@gerardo Furtado  CO2 is also technically an inorganic compound.  But lots of things use it.   "Complexity of carbon sources" I think encompasses traditional concepts of inorganic and organic.

Consider that all the various carbon compounds mentioned can react with oxygen (perhaps including other things in the reaction) to produce energy and CO2.  CO2, OTOH, requires energy from sunlight for plants to turn it into more complex carbon compounts.  Simplistically, CaCO3 is like CO2 in that it would require energy to metabolize, but most of it sinks to the ocean floor where there's not a lot of sunlight.

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sort: votes


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How do trees communicate in the "Wood Wide Web"?
I read on The New Yorker - The Secrets of the Wood Wide Web that trees communicate with each other through electrical impulses sent through their roots. Through these impulses they can ask other trees for some nutrient if they are getting it in insufficient amount or warn the other trees about an upcoming pest attack. This phenomenon is termed as the Wood Wide Web.
So how do trees distinguish in different types of impulses that they receive if they don't even have a brain? And does this process show any resemblance to nervous system in animals?
Additional YouTube video: Trees can talk to each other, but how?

Welcome to SE Biology. It is a good idea to do the guided tour before you make your first post as it will familiarise you with how the site works. (You also get a badge, which is how I know you haven't). As a non-botanist I would still be very sceptical about the proposition in your question, so I would wish to see the evidence for it. You should therefore include a link to where "online" you read about it. Otherwise it may be closed as "unclear".

@David I have included 2 links one of a YouTube video on the topic and another link which I saw. Thank you.

Good. As I've put a space between your main question on the link to improve presentation.

Nowhere in your clickbaity source article is the word electrical found.

@Mindwin https://www.icr.org/article/7700 here see this link

Why do you think a brain is required to interpret communications? Single-celled organisms communicate with each other using chemical signals. And organs within larger organisms communicate using hormones and nerve impulses, but the organs don't have brains of their own.

@Jasmeetsingh Membrane depolarization, which is what those pages call electrical impulse, does in fact happen in (some) plants. However, in this link on your comment above, the phenomenon is not related to your first link (mycorrhizal networks), that's another process. What Mindwin said, and what I also say in my answer, is that in the article linked in your question there is no mention to electrical impulse.

Since it is very much relevant to the context here, sharing a book which has a lot to offer about trees and how they communicate and socialize.
The Hidden Life of Trees: What They Feel, How They Communicate—Discoveries from a Secret World by Peter Wohlleben I read it sometime back - a lot of interesting insights and thought provoking - and makes you realize why trees and forests are important part of human life.

This does not provide an answer to the question. Once you have sufficient reputation you will be able to comment on any post; instead, provide answers that don't require clarification from the asker. - From Review

I have to say: when you claim that "trees communicate with each other through electrical impulses sent through their roots", you're thinking about Avatar.
Joking apart, what you call wood wide web is the mycorrhizal network.
Mycorrhizal fungi are well known to botanists and ecologists. They are the fungal partner in the mycorrhiza, which is a symbiotic association between a fungus and a plant.

Mycorrhizal hyphae (white) in a root
The novelty about this mycorrhizal network is that, as it was demonstrated, plants can use it to exchange some chemical substances. And, in certain cases, this exchange can be used to improve disease resistance.
However, there is no electrical impulse in this process.
According to Song et al. (2010):

In theory, plants can also communicate with each other through underground common mycorrhizal networks (CMNs) that interconnect roots of multiple plants. However, until now research focused on plant-to-plant carbon nutrient movement and there is no evidence that defense signals can be exchanged through such mycorrhizal hyphal networks. Here, we show that CMNs mediate plant-plant communication between healthy plants and pathogen-infected tomato plants (Lycopersicon esculentum Mill.). After establishment of CMNs with the arbuscular mycorrhizal fungus Glomus mosseae between tomato plants, inoculation of ‘donor’ plants with the pathogen Alternaria solani led to increases in disease resistance.

This other research demonstrate that the mycorrhizal network can be used to warn neighbouring plants of aphid attacks (Babikova et al., 2013):

Here, we show that mycorrhizal mycelia can also act as a conduit for signalling between plants, acting as an early warning system for herbivore attack. Insect herbivory causes systemic changes in the production of plant volatiles, particularly methyl salicylate, making bean plants, Vicia faba, repellent to aphids but attractive to aphid enemies such as parasitoids. We demonstrate that these effects can also occur in aphid-free plants but only when they are connected to aphid-infested plants via a common mycorrhizal mycelial network. This underground messaging system allows neighbouring plants to invoke herbivore defences before attack.

In both cases the mycorrhizal networks play an important role in exchanging chemical substances among the plants.
The network has a dark side too: it can be used to deliver allelochemicals from one plant to another, greatly increasing allelopathy. According to Barto et al. (2011):

Common mycorrhizal networks (CMNs) form belowground networks that interconnect multiple plant species; yet these networks are typically ignored in studies of allelopathy. We tested the hypothesis that CMNs facilitate transport of allelochemicals from supplier to target plants, thereby affecting allelopathic interactions.

Finally: don't rely on media to get scientific information, specially in these times of alternative facts. Sometimes you can get good information in the media, but good and accurate information is way harder to find (an example is this BBC page about the mycorrhizal network). However, in defense of that page in The New Yorker, there is no mention to electrical impulses.
Sources:

Song, Y., Zeng, R., Xu, J., Li, J., Shen, X. and Yihdego, W. (2010). Interplant Communication of Tomato Plants through Underground Common Mycorrhizal Networks. PLoS ONE, 5(10), p.e13324.
Babikova, Z., Gilbert, L., Bruce, T., Birkett, M., Caulfield, J., Woodcock, C., Pickett, J. and Johnson, D. (2013). Underground signals carried through common mycelial networks warn neighbouring plants of aphid attack. Ecology Letters, 16(7), pp.835-843.
Barto, E., Hilker, M., Müller, F., Mohney, B., Weidenhamer, J. and Rillig, M. (2011). The Fungal Fast Lane: Common Mycorrhizal Networks Extend Bioactive Zones of Allelochemicals in Soils. PLoS ONE, 6(11), p.e27195.

Thanks for the editing, I totally missed the italics after the copy/paste... I'll still edit this several times, finding my grammar mistakes.

+1 For the content. Also, the media always seems to over-hype scientific results. They are trying to sell something, after all. One of my favourites: Chicken grows face of dinosaur.

I'm surprised that a reputed magazine like The New Yorker can deliver over-hype scientific results

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Where can I find a diagram of cortex connections?
Has anyone come across a diagram (2D, 3D, maybe even interactive) of the connectiontions between cortex regions? Especially, the diagram should display the strength and direction of those connections (but not every single axon). I am interested in information like "Brodmann area 7 receives heavy connections from area 1,2,3 and 17,18", displayed in a neatly arranged way.
If there is no diagram that fulfills my need, is there another source of information, like a table, where I can find that sort of information?
Edit: After some more research I found this paper which contains some interesting diagrams in its appendix. However, this paper does not describe the human brain.

http://www.humanconnectomeproject.org/ might be a good point to start, I have not found a table of the sort you asked for, though.
I don't know whether this information was ever put together in the systematic way you are asking for. At least I never came across it in any of the lectures I've had or conferences I've gone to. For most contexts, it is not just important to know whether two brain areas are connected, but how exactly. Which cell types? Which cells exactly? etc. At this point, the information becomes too complex to be contained in one table. Thus: the connectome project.

Haha that's coool ! My new science project... Pickle brain in paraffin, then robotically slice it into micron thin slices which are imaged with an Epson Perfection scanner at 9600 DPI (2.6 microns).  write a simple computer program which can scan the data and compile a complete neural map of a brain in 3D space so that it can be viewed transparently by a computer in every dimension. every slice would take 3 minutes so that's 200 days to measure a human brain at 2 microns and 10 days for mouse brain. obviously it would not be in vivo.time to buy an epson and pickle a sheep.

The Human Connectome Project looks at imaging the functional pathways in the brain and might include some answers to your question:
http://www.humanconnectomeproject.org
Here is an article in Nature about the project:
https://www.nature.com/articles/mp201792

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What do I need to do to make a Reverse colorblind image?
As a 15 year suffering from moderate Protan colorblindness, I've wanted to find any advantages of colorblindness. I discovered there are Reverse colorblind tests, which only colorblind people are able to see the objects. This has fascinated me, and I want to make one of my own. How can I do this? Since I cannot tell the difference between the colors only visible to colorblind people an their normal vision counterparts, how could I do this without buying a pair of Enchroma colorblind glasses so that I may see it with both visions?


text:
What kind of fish is this (Florida, USA)?
What kind of fish is this? It was caught in Florida (USA) in a canal and was in a group. It was about 5 or 6 inches in size.

What is its size?

5 or 6 inches or so I believe

It looks like an immature bass of some kind. The Shad mentioned below usually have a pigment mark behind the gills and don't have the second set of dorsal spines behind the major. Then again, the split in the tail is not usually that pronounced in bass :(

So after much more time on this than I should have, I am pretty confident this is a silver jenny (Mojarra).
Silver Jenny, Eucinostomus gula

"The Silver Jenny, Eucinostomus gula, whose common Spanish name is
  mojarra Española, is a species in the Mojarra or Gerreidae Family,
  known collectively as mojarras in Mexico. Globally, there are eleven
  species in the genus Eucinostomus, all of which are found in Mexican
  waters, seven in the Atlantic and four in the Pacific."

Dorsal fin structure, tail fin split, location of ventral fins and gill fins all match up, as does color.  So does the faint stripe from top of gill to back of fish. The last clue was the protrusible mouth.
I'm surprised you found it in a canal, as it is a saltwater fish. Were you close to the ocean?  From the link above:

The Silver Jenny are an abundant schooling species that are found
  seasonally in shallow coastal waters over mud bottoms in mangrove
  lined lagoons and creeks in waters that are between 11oC (52oF) and
  28oC (82oF) at depths up to 175 feet. Juveniles are found in seagrass
  beds. They may also enter freshwater. They are known to make seasonal
  migrations to off-shore warmer waters during the cooler months for
  wintering and hibernation returning to coastal waters in the spring
  for breeding. They reach a maximum length of 23 cm (9.1 inches). They
  are benthic feeders that probe the bottom with their protrusible mouth
  consuming bivalves, crustaceans, ostracods and detritus. They are a
  poorly studied species and very limited information is available about
  their behavioral patterns.

Last Link here


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Why do scary situations make our skin crawl? Why do we have goosebumps in such situations?
I do not see why should scary situations make our skin "crawl". In scary situations, we supply less blood to our skin (which makes it paler), so shouldn't its activities reduce? Goosebumps should take up some energy to raise the hairs. Shouldn't that energy be conserved?

Goose bumps are based on a pilomotor reflex where tiny muscles at the base of hair follicles contract, which leads to the "bumps" and also raises the hair in the follicle.
It's often explained as a vestigal reflex, dating back when our ancestors had more hair than the modern human. The "puffing up" of fur has two effects, which today still both can be observed:

Raised hair traps air in the fur, thus minimizing heat loss in the cold.
Raised hair (often combined with certain postures) makes an animal appear larger, thus intimidating an opponent or predator. This is the scenario you mention in your question.

Cats are champs at the raised hair / look large trick.


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What happens when lightning strikes us? How is it fatal?
How does a person die due to lightning? Is the cause of death similar to that due to electric shock? Why do minor shocks don't show similar effects in small magnitude (like paralysis in that part)?

Minor shocks definitely can paralyze a part!  Get on youtube and watch videos of people who cant let go of electrical wires or who are hit by tasers.
Paralyzing a part does not kill you.  Lightning can kill in two ways.

Arrhythmia.  Having arrhythmia or asystole is what kills most people hit by lighting.  As regards lesser shocks - the handymen who are hanging on to a live wire and can't let go (because their hands clamp down) can stay that way for a while.  Eventually the current produces an arrhythmia in the heart and that is what causes death.  If someone goes down this way from lighting or a lesser shock, you might be able to get them back with CPR.

When you see a whole herd of animals killed by a single strike, that is why. The heart is sensitive.  I do not understand why people's hearts do not similarly stop when they are hit with tasers.  I think sometimes they do.

Resistive heating.  Lightning can burn you.  Mostly the electricity goes over your skin and concentrated at conductors, like your phone.  That hurts but won't kill you.  Lightning going thru you can burn you on the inside which can damage your organs.  That is rare.

https://www.cdc.gov/mmwr/preview/mmwrhtml/00052833.htm
https://en.wikipedia.org/wiki/Lightning_strike


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Why does Helium make your voice change?
When we breathe in helium and then speak, our voice changes drastically. Does it happen only due to helium or can happen if we use other gas? What factors of the gas does our voice depend on (like density, temperatue etc.)

Any gas less dense than the mix of N2 and O2 we call "air". The precise explanation is too complex for biology SE, here it is at Physics SE: https://physics.stackexchange.com/questions/122353/why-does-our-voice-sound-different-on-inhaling-helium

Helium is not as dense as air, and when your vocal cord vibrate with the helium, it vibrates at a higher frequency, making your voice higher. sulfur hexafluoride Is Denser than air, making your voice deeper.


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Is there a theoretical maximum on the number of sexes a given species can have?
Background: To the best of my knowledge, most sexually-reproducing species of organism have two sexes, although there are also sexually-reproducing species of organism (flatworms come to mind) which have only one sex. (Depending on one's definition of sex.)
Many species of fungi are both sexually reproducing and apparently have more than two sexes. (Depending on one's definition of sex.)
There are also species of lizards with more than two biologically determined "gender morphs". It is even more debatable than in the case of fungi whether these morphs should be considered separate "sexes" or not, since their mating compatibility network is bipartite.
Question:
Is there a theoretical maximum on the number of sexes a given species of organism can have?
Elaboration:
There would also be a lot of different possibilities -- already with three sexes, one can imagine at least two different means by which sexual reproduction could occur -- any one of three combinations of two individuals from two distinct sexes (most likely in "rock-paper-scissors" fashion), or the combination of three individuals from all three distinct sexes.
How, for example, might either of these two scenarios be maladaptive compared to sexual reproduction of two individuals in species with two or fewer sexes?
I am asking about species with more than two sexes/mating types in general, not necessarily about situations where more than two sexes are involved in a single reproductive event. (Contrast with this related question.) I am also not restricting to animals, or even multi-cellular organisms, or even eukaryotes, since these restrictions might affect the answer. (Contrast with this related question.)
Note that this answer to the second related question implies that we should expect the mating compatibility network of anisogamous sexually reproducing organisms to be bipartite. But note that, as in the example of the side-blotched lizards, this doesn't necessarily preclude having more than two sexes, nor does it give a theoretical maximum to the number of possible sexes. And since I don't want to necessarily restrict to anisogamous sexually reproducing organisms (i.e. isogamous ones would also be fine), then that answer also does not provide a theoretical maximum for isogamous sexually reproducing organisms either.

Why was the question down voted?

I just upvoted it, now it's back to zero (and OP got 8 points). Too bad this was closed: I have an answer explaining that there is no limit to the number of sexes when there is no syngamy and therefore cytoplasmic inheritance, like in protozoa conjugation. Actually, there is no mention to animals in the question's title, it just say organisms.

By the way, flatworms have two sexes, which happen to be (in some classes but not all) in the same individual.

@Remi.b Can you explain why this is a duplicate? I already explained in the question why it isn't a duplicate. Admittedly I didn't explain it very well, but I did do so.

@GerardoFurtado Maybe you could give a summary comment? I would obviously love to hear your thoughts; this question has been bugging me a lot.

@Remi.b All of my examples are animals, that is true, since I am most knowledgeable about animals, but my question is not restricted at all to animals or mammals (as the "duplicate" question supposedly is). The answer to that question explaining the topic of anisogamy is only a partial answer, since it explains why, for special organisms the mating compatibility network would have to be bipartite, but not necessarily restricted to two nodes (as the example with the lizards suggests). But the example of fungi mentioned also makes clear that these assumptions don't hold generally for

arbitrary organisms http://blog.mycology.cornell.edu/2010/06/02/a-fungus-walks-into-a-singles-bar/ But even if they did, that answer itself would, again, not necessarily preclude having more than two sexes, it just would force the compatibility network to be bipartite (as is the case for the side-blotched lizards). So then the question, even in that special case, would still be unresolved by the answer to the other question.

@Chill2Macht That being the case, I suggest you edit your question, making it clearly that the question is about organisms in general (as the title is), not only animals, so we can cast reopen votes. Also, you may want to clarify if you're talking about organisms or species. Thus, I'd do something like "Is there a theoretical maximum on the number of sexes a given species can have?"

@GerardoFurtado I like your suggestion for the title, my only reservation/qualm being that I don't  necessarily want to preclude organisms for which the concept of species is more-or-less ill-defined.

So, we have a problem here: do you want to know if a given species can have more than 2 sexes, or if a given organism can express more than two sexes (be it at the same time or not)? They are tottaly different questions. The species in my (future) answer, for instance, have 8 sexes, but each individual has only 1 sex.

@GerardoFurtado Definitely the former, if a given species (each individual organism expresses only one sex or combination of sexes at a time) can have more than 2 sexes. Although to be fair, if a given organism of a species can express more than 2 (combinations of) sexes throughout its lifetime, then that must mean that the species as a whole has more than 2 (combinations of) sexes, so the latter option would be a special case of the former. But anyway my point being that I am most interested in the full generality of the former (a given species).

Ok, I just casted a reopen vote. However, I believe the best idea is just forgetting about this question and posting a new, fresh one.

I reopened the post! @GerardoFurtado Feel free to post your answer. I note as a comment only that the post is a possible duplicate of Why do only two sexes exist for animals?

Well, your question as a whole is quite broad, with a lot of sub-questions or items (and some inaccuracies, as in the case of flatworms) . That being said, in this answer I'll address only your main question (and nothing more), which is ipsis litteris:

Is there a theoretical maximum on the number of sexes a given species of organism can have?

All the content in this answer is based on this excellent book from Michael Majerus, Sex Wars: Genes, Bacteria, and Biased Sex Ratios:

Unfortunately, I don't have my library anymore and I can't find this book online. So, instead of (boringly) quoting the author, I'll try to summarise his hypothesis. Of course, to a better explanation, you can read the book itself.
Let's start supposing that you're pretty comfortable with the concept of sexual reproduction and sexual types, which I think you are.
Suppose we have two sexual types, called A and B. They have receptors in their gametes' membranes, in such a way that you cannot fusion A + A or B + B gametes, but you can fusion A + B gametes. If the A gamete could fertilize another A gamete, you'll have all gametes in a given gonad fertilising each other, which makes no sense. So, will assume that a given sexual type has mechanisms to avoid fertilising the same sexual type.
So far, what I described is the common system with two sexes, be them "+ and -" or "male and female", it doesn't matter.
Now, let's suppose three sexual types: A, B and C. For this to work, their membrane receptors must be such that A can recognise B and C, but not A. This is theoretically possible (although it is a mess genetically speaking). Thus, the possible matings are:

Sexual type A → A + B and A + C;
Sexual type B → B + C and B + A;
Sexual type C → C + A and C + B;

A system with 3 or more sexes has obvious advantages. Right now, for instance, in a population with two sexual types and the same sex ratio, one has 50% (1/2) of the individuals in that population as potential mate. But, supposing a sex system with 5 sex types (A, B, C, D and E), any individual would have 80% (4/5) of the individuals in that population as potential mate.
So, why cannot we find sexual systems with more than two sex types?
The answer is: we can, but not among species which perform fertilization (animals, plants, most of fungi, most of algae etc...).
This is the problem: in fertilization, or syngamy, the gametes don't simply join their nuclei. It's more complex than that: there is cytoplasmic inheritance, or extranuclear inheritance.
To keep the example among animals, the group you said you know best: mitochondria in the zygote comes from only one gamete (the female one). That happens to avoid what we call heteroplasmy, which is the presence of more than one type of organellar (mitochondrial, in this case) genome in the zygote.
In sex systems with only two sexual types the rule is very clear: "mitochondria comes from this one, but not from that one". That's it, case solved.
But what happens with our system with three (A, B and C) sexual types? If you define that when A mates with B only A donates the mitochondria and, similarly, if you define that when A mates with C only A donates the mitochondria, who donates the mitochondria when C mates with B? Do you see? There is no possible rule here!
Therefore, cytoplasmic inheritance is, probably, what avoids the evolution of more than 2 sexual types.
How can we support this claim?
Let's find what happens in species that perform sexual reproduction, but no fertilization (and, therefore, don't have the cytoplasmic inheritance problem). The best example are protozoans that perform conjugation.
Tetrahymena is a well known example. In these protozoans, according to Umen, 2013:

An individual Tetrahymena cell expresses one of seven possible mating types (I–VII) that it faithfully and indefinitely maintains during vegetative propagation. After mating each new exconjugant has a recombinant micronucleus formed from its two parents. However, rather than just expressing one of two parental mating types, the sexual progeny of Tetrahymena undergo a kind of genetic roulette that allows them to choose at random up to seven possible mating types. (emphasis mine)

So, we have sex mating types. How that system works? According to Cervantes et al., 2015:

The unicellular eukaryote Tetrahymena thermophila has seven mating types. Cells can mate only when they recognize cells of a different mating type as non-self.

Thus, if you belong to sexual type I you can mate with someone that belongs to sexual types II, III, IV, V, VI or VII. The same way, if you belong to sexual type II, you can mate with someone that belongs to sexual types I, III, IV, V, VI or VII, and so on...
The record, however, probably belongs to the basidiomycete Schizophyllum commune, with more than 28.000 sexual types! (Whitfield, 2004) To support the idea that cytoplasmic inheritance is in fact the main factor that avoids more than 2 sexual types, it's worth noting that biparental mitochondrial transmission is quite common in fungi (Barr, Neiman and Taylor, 2005).
Sources:

Majerus, M. (2003). Sex wars. 1st ed. Princeton: Princeton university press.
Umen, J. (2013). Genetics: Swinging Ciliates’ Seven Sexes. Current Biology, 23(11), pp.R475-R477.
Cervantes, M., Hamilton, E., Xiong, J., Lawson, M., Yuan, D., Hadjithomas, M., Miao, W. and Orias, E. (2015). Correction: Selecting One of Several Mating Types through Gene Segment Joining and Deletion in Tetrahymena thermophila. PLOS Biology, 13(10), p.e1002284.
Whitfield, J. (2004). Everything You Always Wanted to Know about Sexes. PLoS Biology, 2(6), p.e183
Barr, C., Neiman, M. and Taylor, D. (2005). Inheritance and recombination of mitochondrial genomes in plants, fungi and animals. New Phytologist, 168(1), pp.39-50.

This is a great answer, thank you! However, I should note that, since species with two sexes evolved from hermaphroditic ancestors (e.g. https://www.sciencedaily.com/releases/2008/11/081120171328.htm), it makes more sense to say that hermaphroditic species have only one sex, rather than each individual displaying two sexes (which is a very anthropocentric point of view). Also, the claim that species undergoing fertilization don't display more than two sexes is also untrue. For example, isogamous fungi are known to have more than two mating types.

http://blog.mycology.cornell.edu/2010/06/02/a-fungus-walks-into-a-singles-bar/ Isogamous organisms do undergo sexual reproduction via fertilization rather than conjugation: http://www.yourarticlelibrary.com/reproduction/sexual-reproductions-in-animals-syngamy-and-conjugation-biology/26755/  The side-blotched lizards are anisogamous, yet have more than two gender morphs (but a bipartite mating compatibility network). That being said, the argument presented is accurate if we restrict to anisogamous organisms (and recognize the possibility of bipartite networks with more than two nodes).

For example, Schizophyllum commune, which is mentioned in the answer, does undergo fertilization, but it is isogamous. http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.0020183 It is not a protozoan, and it does not undergo conjugation. It therefore has to deal with cytoplasmic inheritance. Therefore, the underlying premise of the answer (that cytoplasmic inheritance prevents the development of more than two sexes in all species undergoing fertilization/syngamy) appears to be generally incorrect, and partially correct only for anisogamous organisms.

This webpage better confirms the fact that Schizophyllum commune undergoes plasmogamy http://botit.botany.wisc.edu/toms_fungi/feb2000.html i.e. joining of cytoplasm during mating. So the information described in the paper http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.0020183 regarding the problem of number of sexes and cytoplasmic inheritance seems unfortunately incomplete, since it seems to fail to adequately explain or address isogamous fungi. Note also that it mentions that Hamilton and Hurst were unable to confirm their hypothesis.

In the paper you linked to http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.0020183 , Professor Michiels (at the very end) also states that he believes that two-sexed animals evolved from hermaphroditic organisms, again supporting the claims that hermaphroditic species should be considered as having one sex. That being said, as the paper makes very clear, the definition of the word "sex" is actually very muddied, such that the number of sexes which a given species has depends entirely on one's choice of definition, which is a matter of opinion, not of fact.

1: hermaphrodites have two sexual types, saying that hermaphroditic species have only one sexual type makes no sense. 2: You don't know if Schizophyllum has heteroplasmy.

1: hermaphrodites have one sexual type, which diverged into two types in descendant lineages. Saying that they have two sexual types is what makes no sense -- a single individual, per definition of sexual type, can only display one sexual type -- only species, can display more than one. Anthropocentrism appears to be clouding your judgment. 2: I am not 100% certain that Schizophyllum commune has heteroplasmy, but the page http://botit.botany.wisc.edu/toms_fungi/feb2000.html strongly implies that it does undergo plasmogamy. If you want, I can e-mail the author to confirm.

More than a decade after he devised it, Hurst's is still the leading hypothesis explaining the number of mating types in a species. But experimental evidence remains frustratingly elusive. “I wouldn't say I was entirely satisfied,” says Hurst. “We've got all these ideas, and they turn out to be quite hard to test—there's no simple thing one can do on a single species.” There are species where the uniparental inheritance of organelles is not so strictly enforced, says Hoekstra, such as yeasts and plants. “It's not easy to see if selection [on organelles] is strong enough,” he says.

What I have to say I already said. I suggest, actually I beg, that you unnacept my answer, so other people can write theirs. I already spent too much energy on this, way more than I should. Best regards.


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Odds to clone a parent
I was asking me something weird, and I thought you might validate or not my theory.
Hypothesis: A brother and a sister have one chance over 78 billions to clone one of their parent if they procreate
Here is my method:
I have 23 chromosomes from my mother, and 23 from my father. My father has 23 * 23 = 529 combinations of chromosomes in his "gametes". If my experience is willing to work, I need to have the exact opposites of my father chromosomes than my sister ones. That means that we can't have any of my father's chromosome in common with my sister. That makes approximately 1/529 * 1/529 = 1/279 841.
Then, if I decide to procreate with my sister, our child needs to have the 46 chromosomes back from my father. So the computation stays the same and I will have 1 chance over 279 841 to make it so.
1/279841 * 1/279841 = 1/7.8*10^10

My question is: Is my theory valid? If not why? If yes, that will make a hell of a story at parties...
Thank you for your scientific answers and have a nice day!

For starters, you're ignoring recombination.

...and mutations

Assumptions
You are ignoring recombination and mutations. If you were to add these things, then this probability would be extremely smaller. In apparence, it would be infinitely smaller. It makes no biological sense to make such assumption but for the sake of the argument, let's assume only segregation happen. We will also assume that the parents are completely unrelated to start with (see @BryanKrause 's comment below).
For on given pair of chromosome
First, for a given chromosome number, both parents must each transmit a different chromosome to each offspring. This happens with probability $\frac{1}{2}$ per parent and therefore $\frac{1}{4}$ for both parents. Then, if the brother transmit the maternally derived chromosome, then the sister must transmit the maternally derived chromosome as well (and vice-versa). This occurs with probability $\frac{1}{2}$. So for a given pair of chromosome the probability to clone the parent pair of chromosomes (assuming no recombination and no mutation) is $\frac{1}{4}\frac{1}{2} = \frac{1}{8}$.
For the whole genome
The probability of this to happen for all 23 pairs of chromosome is $\frac{1}{8}^{23} = 1.69 \cdot 10^{-21}$, that is one chance out of a 1.69 thousands billions billions.
As you ask for the odds, note that for such low probability the odds ratio is pretty much equal to the probability.

Side note: your probabilities would be greatly improved if your parents, grandparents, great grandparents, and so on down the line were also each others' siblings. I wouldn't suggest it. Eventually you'd be down to just mutations, but even clones will have de novo mutations.


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Is it feasible to grow edible crops for lawns?
Is it possible to grow some type of plant that functions well as a lawn (e.g. is somewhat grass like), but that is humanly edible?  Would anything that currently exists fit this role?  For example possibly spinach or lettuce might work somewhat, but probably wouldn't be ideal.  If not, could we bioengineer something to fit that role?  I am thinking if we can, this could solve world hunger!

It's a bit off-topic for biology, but there are a lot of economic problems with distribution rather than scarcity of food. In many places where hunger is a problem, it is more profitable to sell cash crops to developed countries or to use crops as animal feed than to sell to impoverished neighbors. Grasses are probably as good as anything to grow in a lawn, if those grasses were fed to animals to free up other space for people. That isn't really the problem, though.

@Brian Krause as far as the distribution problem goes, I wonder if this could be grown anywhere in the world?  Different plants would probably be required in different environments.  Even in deserts, cacti can grow, but they would not make for a good lawn unless significantly bioengineered.

@canadianer Chives is definitely on the right track!  I think of chives more of a spice, but it certainly is grass like and edible.  Now, question would be if it is edible in large quantities, like the majority of a person's food intake?

Just a curiosity: in some languages, like mine, there is no distinction between lawn and grass (we say "I'll mow the grass" instead of "I'll mow the lawn". Thus, defining grasses as all plants from Family Poaceae, the most important edible crops are grasses/lawns: wheat, rice, maize, sugarcane, barley, oats, rye... of course, a lawn made of wheat or maize is not exactly aesthetically pleasing.

Green leafy vegetables tend not to have much in the way of usable calories, so spinach and lettuce wouldn't work, However I think what you are going for is rice... it is the seed of a type of grass and is a staple in much of the world's diets. Now if I can toss my opinion in here, we would be even better off if we stopped fearing GMOs, as we could grow rice that had more nutritive value, such as golden rice, or strains of rice that required far less water to cultivate.

@Bryan Krause: Also hunger tends to be a localized, sporadic thing, often caused by drought or other unusual weather.  That would affect the edible lawn as severely as the field crops.  Also most people with lawns and a disinclination to use large amounts of herbicides seem to have a pretty good crop of dandelions, which are edible.

There are lots of things that you can eat that you could grow as a lawn.  That probably are growing in your lawn now.  My yard is about half violets and they are edible.  Purslane is a delicious succulent lawn weed.  Grab some, rinse it off and eat it.  It is crunchy!  I am telling you from experience you can eat a lot of it and you will not get sick.

Purslane image from here.
http://www.livescience.com/15322-healthiest-backyard-weeds.html
This backyard weeds link says lambs quarters are edible and I did not know that.  They are also volunteers but I did not know they were good for anything and so I was pulling them up.
We are surrounded by things we could eat and which our ancestors ate all the time but which we do not eat.  If you are in school, Johnathan, and this sort of thing interests you it would be a stellar project.  You have all summer to grow weeds in pots and then at the science fair you could have people taste them.

Very nice!  Looks like there are several good candidates here and that such a thing might be feasible, thank you for your answer!


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Is it possible to consume O2 via a pill form to inhibit the need to breathe?
Just wondering if it would be theoretically possible to consume oxygen via O2 pills, in the effort of being able to hold one's breath without limit.
Totally just curious.

Ask yourself two questions: where do pills go when swallowed and where does gas exchange occur?

No, then add more 'no's. The change from solid to gas would explode whatever structure it was in.

You mean solid oxygen exists?! Even if it does, you won't be able to hold it in your hands, leave 'eating' it for future. Also, you need to note that the urge to breath comes from increased CO2 concentration in blood, its got nothing to do with oxygen.

The problem is volume and surface area for gas exchange.  The volume in a pill is puny compared to the amounts you pull in and out breathing.
But could you use something other than the lung for gas exchange?  The colon has a lot of surface area and the small intestine even more.  Maybe if you flooded your gut with an oxygenated fluid like that liquid fluorocarbon the mice breathe, or even oxygen saturated water you could get some of that out via your intestinal villi.  Dragonfly larvae do something like that, performing gas exchange with their rectums.  You would need to exchange the liquid at least as fast as you breathe, getting all the depleted liquid out and new oxygenated liquid in.
Some of those high colonic machines work like that, as I understand: fast in and fast out.  People might not notice you were holding your breath because they were distracted by the churning machine with the hose up your trouser leg.  Maybe you could pass out cards or wear a T-shirt explaining what was going on because you would still have to breathe to talk and that would ruin it.  If you do this would you please post video and link it up here?  Thanks.

The volume of gaseous O2 compressed into a solid the size of a pill would be awesome indeed.


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α-β Interfaces of Hemoglobin
I am trying to learn the interactions that hold the hemoglobin tetramer together, and the conformational changes induced at various allosteric sites. So far, what I know is this:
The tetramer can exist in relaxed state (R-state), or tense state (T-state).
The R-state favors oxygen binding, while the T-state favors oxygen release.
At the C-terminus (a histidine residue) and the 40th residue (aspartate) of the β-chains, and the 146th residue (histidine) of the α-chain, there are two salt bridges. When red blood cells are present in tissues (with a pH of 7.2), the formation of both bridges are favored. When both bridges are formed, the T-state is favored.
The second residues of the β-chains are also a histidine. (This is near the N-terminus). This residue participates in an ionic bond with 2,3-BPG. At the 82nd position, there is a lysine residue that also participates in this bond. (This is a little over half-way down the amino-acid sequence). By binding 2,3-BPG, the T-state is favored.
On the binding of oxygen to a heme-group, the iron atom moves to the center of the protoporphyrin ring. Attached to the iron atom is yet another histidine. This histidine is attatched to an α-helix that is attached to the terminal-carboxyl of the α-chain. By moving the α-helix, a conformational change is induced in the other subunits to shift the structure to the R-state.
What residues of which subunits are the α-carboxyl termini in close spatial relation to, and how does this movement induce the R-state? And which residues hold each dimer together, and how do they affect the R- or T-states?


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Infer distance since duplication from tree?
Question
I have a really simple question, but I'm not able to figure it out.
I made a tree (using BLOSUM62). Here is a part of the tree:

How can I calculate the distance till the duplication event occured between HBD en HBB?

just for HBB 36.21 and for HBD 38.79
or 38.79 + 36.21 = 75

More info
I determined if this set of sequences follows a molecular clock, and indeed this was the case. So I determined the rate at which these sequences envolve. If I can determine the distance between HBD and HBB I can devide this by the rate to obtain the time since the duplication event happened.

How could you calculate this one?

Assuming a molecular clock, the distance between the sequences and the duplication event is 75/2 = 37.5. Ideally, these sequences should have the same distance from the internal node (under a clock), and you could use a model that explicitly assumes a clock -- which will lead to ultrametric trees.  One example is the program promlk (or dnamlk) from the phylip package. A faster alternative would be the  UPGMA method, which also gives you an ultrametric tree.

How could you calculate the one from the image I added? Because this one is before another duplication event.

In this case, and in general, I strongly suggest you to use a method that forces an ultrametric tree -- that is, a (rooted) tree where the sum of branch lengths to the root node is the same for all leaves. In your newly added figure there's more than one way to weight the nodes (assuming, of course, a clock). You could or  find the avge distance of the first internal node (191+151/2) and then do the same again (result +38 is one and 182 is the other), or calculate avge between 182, 191+38, and 151+38. I do not recommend either averaging, preferring strongly a clock-aware estimation.

One last question. I estimated the rate based on a NJ tree using BLOSUM62. If I make a tree using UPGMA for example, it won't be valid to use the rate calculated using BLOSUM62 NJ rigth? Because this will other scores at the branches

If by that you mean that you used BLOSUM62 to calculate the pairwise distances and then used the resulting pairwise distances matrix as input to NJ, then you can just use UPGMA instead of NJ, and use the branch lengths from this tree. (Both NJ and UPGMA are using the same original info, i.e. the pairwise distances; only that UPGMA forces the tree to be rooted, ultrametric.) The branch lengths will be different, however, and in some cases even the topology. But you are assuming that the molecular clock is valid, and then UPGMA should work.

You may have done this already, but I would however use a maximum likelihood framework (e.g. protmlk). The branch lengths would, again, be different, but would be in general more reliable since ML takes into account reversals, site-wise convergence, etc.

First of all thankyou for you help! So what I can do is: MSA of these sequences, calucalting a distance matrix (using MEGA e.g.?), making an UPGMA tree, calculate the rate of change (plotting branch distance vs milion yeasrs since divergence and set up a linear regression) than using this rate (if it follows a molecular clock offcourse) to date the duplication events? Is the right way to go?

I guess so, yes!


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Mental Symphysis
Why dow we consider mandibular symphysis(symphysis menti) as type of Amphiarthrosis that too of symphysis variety, eventhough it lacks movement and cartilage at joint?
Why don't we consider as Synostosis (a type of synarthrosis)?

Why downvote???

What is the source saying that the mandibular symphysis is an amphiarthrosis?

All symphysis are amphiarthrosis. See https://en.wikipedia.org/wiki/Symphysis

Maybe wikipedia is wrong and/or incomplete.

No, many different sources too say so. See this: https://www.google.co.in/url?sa=i&rct=j&q=&esrc=s&source=images&cd=&cad=rja&uact=8&ved=0ahUKEwiRwqzUjvzTAhVJP48KHVO6AaQQjhwIBQ&url=http%3A%2F%2Fwww2.highlands.edu%2Facademics%2Fdivisions%2Fscipe%2Fbiology%2Ffaculty%2Fharnden%2F2121%2Fnotes%2Fart.htm&psig=AFQjCNFTkbPWP72aNKaHrWWFUht_we-hqw&ust=1495288708303622

Lots of vertebrates have unfused mandibular symphyses.

Hmm, that makes sense.


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What is the main difference in chromatin fiber and chromonema?
What I understand is both are coiled version of DNA along with histone but are termed different based on their degree of condensation. My question is when do we call it chromonema and when chromatin fiber? Do we consider 30nm fiber as chromatin and 10nm fiber as chromonema or something else?

10nm fibres are seen only by electron microscopy,while chromonema fibres refer to chromatin fibres visible by light microscopy. See this paper. 10nm or 30nm fibres are thus much, much smaller than chromenema fibres. There are likely several layers of organization (like 100nm and 200nm fibres) before you get all the way up to chromenema fibres.


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Three foramen lying in one vertical plane
In the human skull we can see that 3 foramina named as supraorbital notch(foramen) , infraorbital foramen and mental foramen share a common vertical plane.
Is there any surgical significance of for such a geometry or its just a coincidence?

Well, your cranial nerves all leave the brain just off center on both sides..

Many a times surgeons make use of geometries, so I ask the question. As far as I know all those foramen contain blood vessels too in addition to nerves.

Why pick only those three? Include all the foramen (like the foramens magnum and spinosum) and you'll see that they are oriented by function, not some forced geometric orientation.

I think you have taken it in a different way. My question does this geometry is made use by surgeons. It's made clear in the comment to theforestecologist.

@JM97 If that's what you mean, you should edit your question.

yes, edited. have a look at it.

Can you explain what you mean by "surgical significance"? They lie in roughly the same plane because humans have flat faces, and that fact might be useful. It's not clear what the question is.

I want to know whether this geometry is exploited during any surgical procedure or in craniometry.


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Fermentation of bananas
I may have access to huge quantities of freshly picked bananas. Searching the web, I have found that the sugar content of the average banana is 14g of fructose (could stand to be corrected on this) which should in principle allow for fermentation. The bananas are in no way processed. My questions now are:
(1) How suitable are bananas for ethanol or methanol fermentation?
(2) How exactly is the fermentation workflow? I presume the bananas would be chopped?
(3) considering point (2) what effect would the banana skin have on the fermentation process? Would it be better to ferment the whole fruit including skins or remove the skin before fermentation?
Hope someone can help

Welcome to Biology.SE. I edited your question to improve the structuring and clarify a bit. Please feel free to further edit or re-edit.

How to make banana wine seems like a good start: http://www.celebrationgeneration.com/blog/2011/10/13/how-to-make-homemade-banana-wine/comment-page-1/

I'm voting to close this question as off-topic because this question isn't about biology, even if it induced a solid answer.

Fruit Moonshine is quite desirable :)
Peel the bananas. Good workflow here:
http://www.moonshiners.club/banana-moonshine-recipe/
It takes considerable work especially in large quantities. Furthermore, check legality and read up on methanol poisoning.  Don't poison yourself!

That's impressive!

Is it too late to change my username to Banana Moonshine?


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what is the meaning of VIP-cre::LSL-TOM::SOMGFP(GIN) mice?
I am reading the following paper and the researchers use

"VIP-cre::LSL-TOM::SOM-GFP(GIN)"

mice (page 4) for multi cell patch clamp and

"VIP-cre::LSL-TOM and SOM-cre::LSL-TOM"

mice injected with AAV1 for two photon calcium imaging.
I have tried to look it up in the web.
I understand, for instance, that AAV1 is an engineered virus, and that CaMKII is a promotor, that TOM is a red fluorescent protein, GCaMPis created from fusion of green fluorescent protein with other peptides etc.
However, I have a dificulty in putting together the pieces and understending the whole meaning of "VIP-cre::LSL-TOM::SOMGFP(GIN)" (and the other mice types memtiond).
For example:

Take a VIP-Cre mouse. Does it mean that every VIP neuron in this mouse contains a Cre sequence in it's DNA?
What about other neurons, can they contain Cre also?
When they inject AAV1 virus to VIP-cre::LSL-TOM mice, does this mean that all neurons get the virus? including the VIP and SOM neurons?
Say I have an "VIP-cre::LSL-TOM::SOM-GFP(GIN)" mouse. I understand that VIP cells will be colored red and SOM cells will be colored green. So, why the VIP cells need the Cre promoter and the SOM cells don't?

I'll be greatfull if you could answer some of these questions, of refer me to a suitable reference. I looked a lot but the references that I find are lab references with technical details and numbers. I didn't find anything specific for this mice types that contains explanations.
Thank you!!

I think I can help explain all but your 3rd question.

A transgenic mouse will typically have the genetic construct in all cells. Unless you get a chimeric animal, which is screened for during the making of the mouse.
VIP::Cre means that the promoter of VIP was used in front of the region of DNA that encodes for Cre recombinase.  Note, the animal still has the endogenous VIP gene that makes VIP. This is an additional construct. The intent of this kind of system is to limit the expression of Cre recombinase to only the cells that would also be expressing VIP.
LSL stands for Lox-Stop-Lox cassette. LSL:TOM is the gene that encodes for tomato red protein with a premature stop in the transcript such that it never makes a correct protein (and no red).
If Cre is expressed in a cell with the LSL-TOM construct, it will recombine the LSL and remove the stop codon, thus enabling the creation of functional tomato red transcript and fluorophore (protein). Again, this construct is in the DNA of ALL cells, but the recombination event (and subsequent expression of function TOM) will only happen in the cells that are also expressing Cre recombinase. And for a VIP::CRE mouse this only happens in VIP expressing cells.

Your questions:
1) Actually every cell in the animal has a VIP::Cre (excepting blood of course or sex cells that got the non transgene allele during meiosis. This is because usually the cre genes are kept at Hets during mouse mating).
2) All neurons (and all cells; see answer 1) will contain the genetic construct VIP::CRE.  The intent is in the VIP::CRE mouse, only cells that would express VIP would express Cre recombinase.  This means that other tissues in the body that express VIP should also fluoresce red in a VIP::CRE/LSL-TOM mouse.  As an aside, all cells that normally make SOM should also be making GFP in the SOM::GFP mouse, but every cell will have the DNA transgene.
3) This question is outside my breadth of knowledge. I've done lots of work with transgenic mice, but other than looking up that that viral construct has something to do with calcium and imaging in neurons, I am not sure.
Per Bryan Krause: "...the expectation is that it will infect most if not all cells, not even just neurons, but it is using the 'synapsin' promotor which is neuron-specific (but would be expressed in both VIP and SOM cells, as well as other neuron types). Presumably the authors are using calcium imaging to detect activity across a whole mixed population but then using tdTomato to identify one subpopulation or the other, depending on which animal is used."
4) For VIP-cre::LSL-TOM::SOM-GFP(GIN).   As written, this would imply the expression of Cre is necessary to activate transcription and encoding of tomato red in VIP expressing cells. But that GFP is already active in SOM expressing cells from day one of development.
Some uses of Cre-Lox systems are illustrated here. This picture from that website demonstrates graphically what is going on with a LSL construct.
Your system has tomato red instead of lacz and is using VIP expressing cells as a targeted system.

For (3) the expectation is that it will infect most if not all cells, not even just neurons, but it is using the 'synapsin' promotor which is neuron-specific (but would be expressed in both VIP and SOM cells, as well as other neuron types). Presumably the authors are using calcium imaging to detect activity across a whole mixed population but then using tdTomato to identify one subpopulation or the other, depending on which animal is used.


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How can one calculate "probability of possessing a ‘perfect’ profile" from "typical optimal genotype frequencies"?
Can anyone please explain how the "Probability of possessing a ‘perfect’ profile" was calculated from "typical frequency of optimal genotype" in Table 1 in this paper?
Paper link here

They appear to have simply considered each allele independently. This means that if there are say 2 alleles for a trait, and they are both present at a frequency of 0.1 in the population, then you have a 0.01 chance of having both of them. This is probably an okay assumption for their purposes (in reality some might be linked and would associate non independently). Their point is simply that as the number of alleles go up, having all the best ones becomes increasingly unlikely.

Makes sense, but still I am not able to figure out the math here. Can you please be kind enough to take an example from this table and explain how the probability was calculated?

seems like i cracked it .. thank you so much for the explanation


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Zinc finger nuclease specificity
If I want to make sure that a ZFN cuts at only a certain position in a genome, how many subunits would I need to ensure this?
If the human genome is roughly 3 billion base pairs, we need a sequence that is 16 base pairs because 4^16 exceeds 3 billion (if my thoughts are correct). But then I don't quite understand how the subunits of the ZFN come into this.

How unique and complex is your cut site?

Hello! I dont have a specific sequence, it is more a general question of how many you would need to really specify a cutting. Can you help?

This sounds like a homework question where you need to find the length of a sequence that has a probability of occurring once in the genome.

@canadianer Exactly, so if the human genome is roughly 3 billion base pairs we need a sequence that is 16 base pairs because 4^16 exceeds 3 billion if my thoughts are correct. But then I don't quite understand how the subunits of the ZFN come into this..

If you want to be a bit cheeky then the answer is that it does not matter anymore as everyone doing real science have moved on to Crispr/Cas9. https://en.m.wikipedia.org/wiki/CRISPR

The human diploid genome is ~6.5 billion bp, so you need to find the length of a sequence that has a probability of occurring only once (assuming the sequence is completely random):
$4^n=6.5\cdot10^9$
$n\cdot log(4)=log(6.5)+9$
$n=\frac{log(6.5)+9}{log(4)}$
$n\approx16.30$
According to this article, each finger of a ZFN recognizes 3 bp, which means you'd need $\frac{18}{3}=6$ fingers to probabilistically recognize a unique site. Interestingly, the article also says:

The requirement for dimerization is a great advantage for this reason: because a monomer is not active, cleavage does not occur at single binding sites. The cleavage reagent is assembled only at the target if the fingers have adequate specificity, and the combined requirement for binding two proteins brings the overall specificity into a very useful range; e.g., two three-finger proteins specify the location of 18 bp, which is sufficient, in principle, to pick out a single target, even in a complex genome.

Thank you once again! You have been very helpful many times! :)

Stupid question: isn't it sufficient to consider the haploid genome because one can approximate the sequence of the second set with the first set of chromosomes? (@O.kth: if you are happy with the answer, please up-vote and accept, thanks!).

@O.kth You're welcome. If this (or other) posts have answered your question, please mark them as accepted by clicking the checkmark next to the answer (and up-vote). It seems I've actually answered several of your questions and you haven't accepted any of them :(

@AlexDeLarge Not stupid at all. I assumed for the calculation that the entire genome was random, which is of course not true (especially when considering homologies between the chromosomes). A more accurate calculation could certainly be made but, fortunately for this question, the answer will be the same.

@canadianer sorry for that, I often forget but I think I have accepted and upvoted all of the good answers I've gotten now! :)


text:
Does an increase in cancer cell traction forces increase metastasis of the cancer cells?
I am not very familiar with biology, but I have read some articles about cell traction forces lately, where the cells are cancer cells. I found this very interesting, so I thought it might be nice to read about the relationship between cell traction forces and metastasis for cancer cells. I thought that an increase in cancer cell traction force should indicate that there would be more metastasis. I have looked at two references, but one of the articles says that increasing the cell traction force increases metastasis [Kraning-Rush et al. (2012)], while the other says the opposite [Indra et al. (2011)]. Both are experimental articles.
My question is therefore:
Is it correct that most often, an increase in cancer cell traction forces would increase metastasis, or should it most often decrease metastasis?

The second link cannot be accessed without login. Could you provide an accessible link at least to the abstract (maybe NCBI)? Thanks!

@AlexDeLarge http://pubmedcentralcanada.ca/pmcc/articles/PMC3870281/

You have pointed out in your question that two different research groups have differing conclusions about your question.  The answer is not known which is why they are studying it.
Their differing results probably turn on how cell traction force is defined and the experimental system used to measure it.  It may not even be consistently ture - for example metastasis via the lymphatic system may be mediated by different properties than metastasis through the bloodstream or local tissue invasion.

Thank you for your reply! Okay, that makes sense. Do you have some references about that metastasis via lymphatic system or bloodstream might give different different conclusions on the force exerted from the cells?


text:
Why does the "all-or-none" principle hold true for only single nerve cell, and not a bunch of nerve cells?
I've read this from wikipedia:

... This relationship holds only for the unit of tissue; for nervous tissue the unit is the nerve cell, for skeletal muscle the unit is the individual muscle fiber and for the heart the unit is the entire auricles or the entire ventricles.

https://en.wikipedia.org/wiki/All-or-none_law
I know about all-or-none principle but i don't understand this statement. What it is trying to imply? I am not sure my question title is reasonable because of my less understanding.

The "all-or-none" principle refers to the roughly accurate concept that neurons fire all-or-none action potentials, individual muscle fibers contract fully or not at all, etc.
If you have a population of, for example, 5 neurons, the population response is no longer all or none, even if the individual units follow the principle. You could have 0, 1, 2, 3, 4, or 5 cells firing an action potential together (the definition of "together" is somewhat vague; depending on the location/function of a neuron you could consider spikes within 1 ms to be synchronous or you could consider spikes within 100 ms to be synchronous, for example). The more units you have, whether they are neurons, muscle fibers, etc, the more "smooth" the possible outputs are.
The reasons for different numbers of cells being recruited could be differences in thresholds, but it could also be from different inputs to each of the units, different firing histories of each of the units, etc. This arrangement allows for more "analog" responses both within the nervous system and at muscles, because the strength of a signal or the strength of a contraction can be regulated by how many neurons participate, or how many muscle fibers are contracted.
One everyday example of the importance of this system is your grip intensity when holding an object. If your grip was all-or-none, you would not be able to handle a disposable coffee cup without crushing it. By using a population response rather than a single neuron connected to all the fibers in a single muscle, the nervous system can control the strength of a muscle contraction. The same principle applies within the CNS, where population activity can encode seemingly continuous representations of features like colors, frequencies, sizes, etc, despite an underlying code that is all-or-none at the single unit level.


text:
Recombination frequencies
I have been learning about recombination frequencies, but an still getting a bit confused despite having gone over many of the links in Google regarding them. I was wondering if someone could verify whether the following is correct.

To calculate recombiation frequencies and thus create a genetic map from this, you have to have true breeding parents for two or more different genes.
You have to cross these parents, so that you have an F1 generation consisting only of heterozygotes
You then have to backcross the F1 individuals with either of the parents. If these genes are all located on different chromosomes you will just get independent chromosome segregation and therefore a 50/50 chance of each allele occuring with the other one in the progeny. Whereas if they occur on the same chromosome, then in the F1 heterozygotes the alleles from each parent will only segregate differently into the gametes if recombination occurs.
To calculate the recombination frequencies we therefore take the number of offspring for which the combination of these two alleles is different from that observed in the parents- we call these the recombinants.

Is this correct?

This answer is mainly copy-pasted from my answers here and here.
The importance of polymorphism
To understand what generation to backcross, it is central that you understand why we need polymorphic loci.
If at least one locus is homozygous
If a recombination event happens between two loci where at least one is homozygous, then you would not see anything. Consider for example the following strand sequences in a diploid individual
-----A-----B----
-----a-----B----

Whether a recombination event occurs or not, the two possible chromosomes passed down to an offspring are
-----A-----B----
-----a-----B----

Therefore, you cannot tell whether recombination has occurred.
If both loci are heterozygous
Now consider the following individual
-----A-----B----
-----a-----b----

If no recombination event has occurred between the two loci of interest then the two possible chromosomes that will be passed down are
-----A-----B----
-----a-----b----

If on the other hand a recombination event has occurred between the two loci of interest then the two possible chromosomes that will be passed down are
-----A-----b----
-----a-----B----

Therefore, you can tell whether a recombination has occurred or not.
Statistics of recombination
There is a tiny bit of maths below. These equations are mainly for curiosity as one can understand the answer without understanding the maths behind it.
Definitions of $r$ and $M$
You are getting confused between two different statistics

The rate of recombination $r$ between two loci

$r$ is the probability for two sequences found at two loci to remain in the same gamete after recombination occurred. This probability cannot be greater than 0.5 ($0 \le r \le 0.5$).

The distance in Morgans $M$ (or more commonly in centiMorgans) between two loci

$M$ is the expected number of cross-over that occurs between the two loci.

Morgans and centiMorgans
You will note that I talk in Morgans rather than centimorgans which is unusual in the literature but it helps at conveying the intuition of what it means. if $M= 150$ centiMorgans $= 1.5$ Morgans, then the expected number of cross-over between the two loci is 1.5. Below are some more explanations on these two definitions with some drawing :)
Case study with loci A and B
While $M$ and $r$ are closely related, they are not exactly the same thing. Consider the following sequence with the loci A and B
---[A]------------------[B]---

Let's assumed the two loci are very far apart and $M=2$. The probability of having exactly $k$ crossovers is therefore given by a Poisson distribution with rate $M=2$
$$P(k) = \frac{e^{-M}M^k}{k!}$$
Let's say for a given case that $k=1$ (a single cross-over occurred). This cross over is represented by a "/" below
---[A]-------------/----[B]---

Here clearly the two sequences at loci A and B will be separated. Let's say now that $k=2$ (two cross-over occurred).
---[A]---/-----/--------[B]---

Here, even if crossovers have occurred, the two sequences at loci A and B will remain together. Only the sequence in between the two cross-overs will come from the homologous chromosome.
Relationship between $r$ and $M$ - in words
You might see it coming from the previous section. The probability $r$ of these two loci A and B to be separated via recombination is the probability of an odd number of recombination events to occur between them (knowing that $M$ is the expected number of cross-overs).
Relationship between $r$ and $M$ - in equation
Let's calculate first the probability $p_{even}$ that an even number of cross-overs occur. This probability is just
$$p_{even} = \sum_{k = 0}^{\infty}{e^{-M}M^{2k} \over (2k)!}$$
, where I just added the constant $2$ before $k$ at both the numerator and denominator. With some algebra and trig, one can show that
$$p_{even} = \sum_{k = 0}^{\infty}{e^{-M}M^{2k} \over (2k)!} =
e^{-M}\sum_{k = 0}^{\infty}{M^{2k} \over (2k)!} = $$
$$e^{-M} \: cosh(m) = e^{-M}\left ( \frac{e^{M} + e^{-M}}{2}\right ) =
{1 + e^{-2M}\over 2} $$

As, $r = p_{odd} = 1 - p_{even}$,
$$r = 1 - {1 + e^{-2M}\over 2} = {1 - e^{-2M}\over 2}$$
Here we go! We have our relationship between $r$ and $M$! Let's graph it
Relationship between $r$ and $M$ - on a graph
I just graphed the above equation in Mathematica (Plot[y = (1 - Exp[-2 M ])/2, {M, 0, 5}])

Here is the same graph but zoomed on lower values of $r$ and $M$ (Plot[y = (1 - Exp[-2 M ])/2, {M, 0, 0.1}])

We clearly see from the graph that for low values of $M$, as $M$ increases $r$ increase quasi linearly ($M≈r$). For greater values of $M$, $r$ still increases but slower and slower until reaching an asymptote / plateau at $\frac{1}{2}$. $r$ is indeed bounded between 0 (when $M=0$) and $\frac{1}{2}$ (when $M=\infty$).
Note, the fact that the sum of probabilities of every even $k$ in a Poisson distribution is always lower or equal to 0.5 is an interesting math fact in itself!

Some of your math was incorrect, as mentioned [in a comment] in the other post that you referenced, so I corrected it. I kept it simple and straightforward, using only common trig identities of $cosh(x)$.

Yes that's how it works as far as I know
Because the theory part is pretty straightforward.of the genes are on the Same chromosome, the chance of them being separated in segregation during meiosis is lower
Consider a simple example
---------A--b--------------c----d-e---------------------------------f
Let this be a rope with 6 point a b c d e f
If I were to make a random cut anywhere here, the chance that a,b will get separated is much lower than a,f....because a and f are so far apart that any cut in the middle will ensure them to be separated.
If u look at it again...the chance of d,e to be separated is EXTREMELY low
This is the principle of LINKAGE
Now let me say gene a stands for tall, b for blue and f for bushy...(don't judge the characters)
Now if this is a part of a chromosome on the parent, and meiosis is taking place
We all know that crossing over too is a phenomenon involved here
Now during crossing over.....a and f are bound to get separated for sure, so they will be independently assorted, obeying the law of Mendel
But when we talk about a and b, they may or may not get separated in the various gametes
The closer they are, the lesser chance of them being separated and thereby, higher chance of them occurring in the same gamete and therefore, higher chance of them being expressed in the same offspring(assuming they are dominant)
lets assume we cross blue tall(dominant) with green dwarf(recessive)
As you know f1 will be blue tall(no incomplete or co dominance please)
Now if I take this blue tall and cross it with parental green dwarf
You will have very high number of blue tall and green dwarf(remember, there are alleles of SAME GENE....AND OCCUPY SAME LOCI)(therefore.....high chance of both occurring together in the same gamete)
Therefore the number of recombinant you get will be very low(blue dwarf and green tall........as the chance of these characters entering different gametes is very low)
Therefore we can conclude that higher the number of recombination....higher the chance of the genes segregating which implies a greater distance between the genes)
Therefore a higher recombination frequency implies a higher distance between the 2 linked genes
I hope u have understood the concept and are not struggling to byheart it as a force
Thanks


text:
Is there any species (subespecies?) whose DNA or RNA contains only in stem-loop structures?
I am a computer-scientist working in nucleic acids from the perspective of Formal Language Theory. I am dealing with several papers that analyze the Stem-Loop structure of DNA.
I would like some solid reference that confirms (or negates):
1) The existence of these structures
2) The existence of a (species, subespecies, ...) whose DNA or RNA has been confirmed to have strings which are a pure stem-loop structure.

The existence of stem loops is well established, so I'm not sure what kind of paper you're looking for in that regard. There are even crystal structures. As for your second question, it seems exceedingly unlikely.

I'm not sure this analogy will be helpful (and I'm sure someone could poke holes in it), but you are somewhat asking for 1) Confirmation that a car with wheels exists, and then 2) Asking if there is a car that is only wheels.

@BryanKrause I'll cite you :D

The existence and importance of stem loop structures is well documented.
I'm not sure what the second question means exactly. If you mean 'an organism that has at least one stem loop, try HIV. The MS2 system is also a stem loop binding protein that's used as a tool a lot in biology, I suggest googling it.

The second question means if there is any organism whose DNA or RNA has been documented to have at least one strand which is only a stem-loop, not a stem-loop contained within a larger strand. I suppose the answer is no.

But anyway, I would like to cite a paper stating something like  " (...) it has been observed that stem-loops always appear embeded in larger strands (...)"

@D1X Ah I think I might realize now your misconception...stem-loops are typically quite short relative to genomes, from a few base pairs to a few tens of base pairs, versus even viral genomes that are at least several thousand bases and the smallest bacterial genomes in the 100s of thousands. You won't find a citation saying what you state because it's sort of obvious from the underlying math: you could find some papers on the largest stem-loop structures and smallest genomes to make your point, though.


text:
growth limit on muscle
Is there any biological limit on muscle growth in human body, one can keep pushing body and keep growing more and more muscle but somewhere it must become diffcult for body to sustain those cells right?

Funfact: Actually there is no increase in number of muscle cells, they only get hypertrophied when the muscles become big.

@JM97 but sure larger cell need large energy reserve to stay alive , so it can go to infinity?

But there may be a limit above which they can't show hypertrophy?

@AlwaysConfused thats exactly my question, just for fun ,"CAN I TURN INTO HULK if keep wprking out :P

Natural athletes have to deal with MSTN gene.

The MSTN gene provides instructions for making a protein called myostatin.
This protein normally restrains muscle growth, ensuring that muscles do not grow too large.

Just look at the top natural athletes. There are a lot of them who train for 20+ years and still can't be as large as those athletes who take steroids. Here are some examples of professional natural athletes(Bobby Pandour, Georg Hackenschmidt)

With steroids you can exceed all natural limits up until your body meets its boundaries, often accompanied by serious health issues.


text:
How are commercial steroid hormones produced?
Does someone know how oestrogens and androgens used for treatment are made? Is it with a GMO bacteria? Is it chemistry?
Thanks

Welcome to SEBiology. Before posting a question it is expected that you first try to find the answer by other means, e.g. an internet search. If the results of this are unsatisfactory then you should explain this in your question. In this case a Google search for  "Commercial production of steroid hormones" will bring up plenty of leads. You might also ask yourself when the contraceptive pill was introduced in relation to when genetic cloning techniques and how many genes would have to be expressed in bacteria to allow steroid synthesis.

In this recent review you can find fascinating information on all aspects of this topic. It's dense in sterol structures and chemical interconversions, but that's what you have to expect. This is my précis.
Direct isolation from primary biological sources This was the heroic phase of research in this area:

Androsterone was first isolated from the urine of policemen. Quickly, however, it became evident that natural isolation of hormonal steroids would not satisfy the demand, as, for instance, in 1931, 15,000 L of urine yielded only 15 mg of pure androsterone. Similarly, 4 tons of sows' ovaries were needed to isolate 12 mg of estradiol, while extraction from 625 kg of sows’ ovaries produced 20 mg of progesterone.

[edited by removal of citations]
There are still some commercial processes in this class:
Premarin contains estrogens produced from the urine of pregnant mares.
Chemical transformations starting from steroidal sapogenins of Dioscoreae (yam) These processes still make a contribution but there is a limiting availability of the starting plant material. Apparently important in China.
Direct total synthesis
This section describes chemical routes, but there don't seem to be any commercial processes
Chemical synthesis from cholesterol and phytosterols Phytosterols are plant sterols, available from e.g. soy bean oil, rape seed and paper pulp industrial waste. They can be chemically converted to steroid hormones, as described in the review, but there don't seem to be any commercial processes.
Microbial conversion of phytosterols
Bacteria can convert plant sterols into useful products. Mycobacteria seem to be particularly useful.

Today, more than 1000 tons of steroids are produced annually from phytosterols by microbial transformation, alone.


text:
Sex differences in response to food deprivation
This question was inspired by a casual conversation with friends the other night. Some of us had noted that women tend to eat smaller meals more often (snacks, fruits etc) while men eat larger portions more infrequently. Also, several of the women said to be sensitive to food withdrawal, getting very hungry after a few hours and experiencing low blood sugar symptoms (even fainting in one case) if not eating regularly, for example if skipping lunch. Men (including myself) seemed to be less affected, often skipping meals without noticing.
This was a highly unscientific investigation with a tiny sample size :)  just based on our personal stories and friends we know. It could, of course, reflect attitude/perception/habits rather than actual biological differences. It should also be said that not everybody agreed -- some men also stated that they felt sensitive to food withdrawal. But there are of course known differences in metabolism between the sexes, so it doesn't seem entirely implausible. It might also be related to different body mass, muscle mass, etc.
So my question: is there any scientific evidence that women and men react differently to short-term food withdrawal? Here short-term would be, say, up to 24 hours, as when skipping breakfast and/or lunch. Are there any data on differences in blood glucose levels after food withdrawal, for example?

Don't know about people, but can tell you about fruit flies if you're interested.

@David,  sure, if there are differences in other species that's interesting too.  (Though I'm not convinced flies are the best model for this  ;-)

No, I agree — not a good model. As there are distinct male/female patterns for activity, the expression of genes for enzymes that metabolise sugars (such as the maltase family) show pronounced sexual dimorphism.

Well, there are at least some studies that indicate that men and women have different metabolic response to fasting... but to give a decent answer would require a large litterature study... Here is a paper concerned with blood level glucose albeit with 36 hours of fasting. https://academic.oup.com/jcem/article-lookup/doi/10.1210/jc.2007-0552

I have no significant sample size either, but in my peer group behaviour is directly opposite. Males are constantly snacking and get cranky fast when skipping meals, females eat more regularly, but also do sometimes skip a meal without problems.

@JeppeNielsen,  thanks for the paper link, it's very helpful!

There are very few studies about the gender-based differences in response to food deprivation in humans (or at least I didn't find many such reports).
In one of the papers, Sodersten et al conducted a research on 30 (17 women and 13 men) high school-aged subjects. After a short-term fast (skipping 2 successive meals), males consumed much more food while women actually ate less, when compared with their respective baseline quantity of meal. They suggested an inherent difficulty for women to compensate a period of fasting by increasing their food intake. They, thus, concluded that fasting might be more risky for women than men as this may start them down a self-sustaining pattern of reduced calorie intake. You can see the reference from Yamada's Textbook of Gastroenterology.
In another study, Soeters et al, 2007 showed that after a period of fasting for 38 hours, women had low plasma glucose levels than men, although they have higher amount of free fatty acids in plasma. They suggest that women are somehow protected from free fatty acid-induced insulin resistance, probably because they prevent myocellular accumulation of ceramide.
A yet another study, by Wu et al, 2011, touches upon the point that the relation between kilojoules consumed and kilojoules utilized is different in men and women. They also state that women consume less kilojoules per kilogram lean mass and store more fats in their body, especially during gestation period, as compared to men (I'm obviously not comparing the gestation period). This finding can, in a way, support the observations by Sodersten et al (see first paragraph).
If you want a more detailed report, you can have a look at this report from United Nations University (old website) by Sara R. Millman and Laurie F. DeRose. They discuss in detail why and how women and children are considered the vulnerable groups in times of long-term food deprivation since they are more likely to express hunger and have more serious probable consequences of hunger in times of food scarcity.
If you can expand your terms a little bit, there are (comparatively) many such studies on rats and other animals. For example, Sarookhani et al, 2014 measure the effects of food deprivation on formalin-induced nociceptive behaviors and $\beta$-endorphin and testosterone concentration in rats. You can find many such studies quite easily. However, I'll keep searching and adding more related studies on humans here.

Thanks, these are very useful pointers. It does seem like there is not much data out there.  (Hmm, now I'm thinking of doing my own study :)

@roland sure, I'll be happy to read it ;)

There is a big body of literature in one specific instance of fasting: Ramadan. While not as nicely controlled as most fasting studies there certainly have been a lot of parameters investigated and if there are any differences between men and women.
A quick Google scholar search unearthed this article by Finch et al. with the following in the abstract:

Rated hunger increased substantially during the daily fast, and hunger was higher for the women than the men during the earlier days of Ramadan, whereas later, on average, fasting levels of hunger were very similar for both sexes

But I agree with Jeppe Nielsen, you will have to do a long thorough meta-analysis to come up with solid statements, sample size appear rather small.


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How EGDS (endurance genetic distance score) is calculated?
Can anybody please make me understand how EGDS5 has been calculated to 40.8 in this paper at page#31?
The formula has been described in this paper but when i tried the same, I am not getting the same results.
According to paper describing the formula:
$EGDS = 100 - \frac {100\cdot d} { n \cdot w }$
where
$n =$ number of studied polymorphisms
$w =$ score given to worst genotype
$d =$ euclidean distance calculated as follows
$d = \sqrt{ \sum_{i = 1}^{n} (2 - x_i)^2}$
$x_i =$ genotype score of corresponding polymorphism
$2 =$ optimal genotype score
here is what I tried. Given below is the genotype score of 5 genes:
$ x = (1,1,1,1,0)$
$d = \sqrt { (2-1)^2 + (2-1)^2 + (2-1)^2 + (2-1)^2 + (2-0)^2 }$
$= \sqrt { 1 + 1 + 1 + 1 + 4}$
$= \sqrt 8 \approx 2.82$
Now, $EGDS5 = 100 - \frac{ 100 }{ 5 \cdot 4 } \cdot 2.82$
$= 100 -  5  \cdot 2.82 $
$= 85.9$
which is not equal to 40.8.

In my opinion, there must be something wrong with the formula given in the paper. The rationale behind the conversion of $d$ into the range 0-100 is stated in the papera as follows:

An EGDS9 of 100 represents an “optimal” endurance genetic profile,
  that is, all GS’s are 2. In contrast, an EGDS9 of 0 represents the
  “worst” possible profile for endurance genetic profile, that is, all
  GS’s are 0.

So what they are basically saying is that they want
$d_{max} = \sqrt{\sum_{i=1}^n(2-0)^2} = \sqrt{4n} = 2\sqrt{n} \Longrightarrow EDGS_n \stackrel{!}{=}
 0$
$d_{min} = \sqrt{\sum_{i=1}^n(2-2)^2} = \sqrt{0} = 0 \Longrightarrow EGDS_n \stackrel{!}{=}
 100$
So let's just define EGSD as the percentage of reaching the minimum possible distance:
$EGDS_n =100 \cdot \frac{2\sqrt{n} - d}{2\sqrt{n}} = 100 \cdot \left(1 -\frac  d {2\sqrt{n}} \right) = 100 - \frac {100\cdot d}{2\sqrt{n}}$
Which gives us a formula very similar to the given. (Actually their formula is just missing the squre root in the denominator).
Let's apply this formula now to the case of the other paperb in discussion:
$EGDS_5 =100 \cdot \frac{2\sqrt{5} - \sqrt{8}}{2\sqrt{5}} \approx 36.754$
Not quite 40.8, but closer. Now, what if we assume the people in the other paper used this formula but made a mistake when calculating d, getting $d = \sqrt{7}$?
$EGDS_5 =100 \cdot \frac{2\sqrt{5} - \sqrt{7}}{2\sqrt{5}} \approx 40.839$
Interestingly, the other score 33.8 comes from apparently calculating
$EGDS_4 =100 \cdot \frac{2\sqrt{4} - \sqrt{7}}{2\sqrt{4}} \approx 33.856$
In their table, there are actually five rows but the last row has no value in its column?
I would say these are just bad papers, IMHO.
References
a Meckel, Yoav, et al. "Practical uses of genetic profile assessment in athletic training–an illustrative case study." Acta Kinesiologiae Universitatis Tartuensis 20 (2014): 25-39. (http://ojs.utlib.ee/index.php/AKUT/article/view/11961)
b Ben-Zaken, Sigal, et al. "Genetic profiles and prediction of the success of young athletes’ transition from middle-to long-distance runs: an exploratory study." Pediatric exercise science 25.3 (2013): 435-447. (https://www.ncbi.nlm.nih.gov/pubmed/23877193)

Thank you! I've been trying to make sense of this for over an hour. Now I have to spend an hour forgetting about it.


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Where does craniocaudal closure of anterior neuropore start?

Closure of the cranial neuropore is bidirectional, and final closure occurs in the area of the future forebrain. Closure of the caudal neuropore is strictly craniocaudal and finishes at the level of the second sacral segment.

This is what Larsen's Embryology says. I understand that neurulation starts somewhere in the area of the first five somites and then proceeds in both directions - cranial and caudal. The caudal neuropore is closed on day 26 by neurulation in this direction.
But, the cranial neuropore is closed not only by this cranial wave of neurulation but also by another one incoming craniocaudally and the point where they both meet is of final closure. (hence bidirectional)
My doubts - pls correct if any of my interpretations are wrong. Where is this second craniocaudal wave originating? Where is the final point of meeting (I suspect linea terminalis or anterior commissure) ? Could anyone post a picture or a reference to understand this visually (both waves of neurulation)?
PS. I am not talking of primary and secondary neurulation. Which is different and concerns the caudal eminence.

Where is this second craniocaudal wave originating?

It begins in the prosencephalic region adjacent to the chiasmatic plate.

Where is the final point of meeting (I suspect linea terminalis or anterior commissure) ?

Cranial linea terminalis represents the zone of closure of cranial neuropore.

Could anyone post a picture or a reference to understand this visually (both waves of neurulation)?

Sources:
1: https://www.ncbi.nlm.nih.gov/pubmed/11948562
2: https://goo.gl/RLmQcj

Thanks!  A picture is truly worth more than a thousand words! I was breaking my head for so long, only if this pic was put into the books!

Links for them can be found in gray's anatomy.