text:
Enzyme Inhibitors: Using in vivo in yeast
I find listed on the Sigma-Aldrich site a large list of enzymes & corresponding inhibitors. e.g. For the enzyme squalene synthase the inhibitor listed is "Zaragozic acid A trisodium salt"
Would this mean that if I added the right amount of this chemical to, say, a Yeast cell culture I might expect to get reduced activity of Squalene Synthase which is native to yeast and catalyses the transformation of FPP to Squalenes.
Would this even be a reasonable thing to try if I had a goal to block Squalene synthase? Or am I interpreting how these inhibitors ought to be used incorrectly? Can they be used with in vivo cultures at all?

This is usually the way this kind of inhibitors are used. There needs to be a way that they come into the cells (if they stay in solution and cannot reach their target they will be useless), but then they inhibit their targets.
What usually needs to be done is to determine which concentrations are needed in the cell culture (or the medium) to be effective for the inhibition but not to harm the cells. Therefore I usually use different concentrations of the inhibitor in culture and then measure the outcome.
To find the right concentrations, see if there are some recommendations from the manufacturers. Otherwise you will probably have to dig through Pubmed to find some starting point.

Thanks! Any thoughts on what concentration range might be reasonable to attempt with Zaragozic acid for inhibiting Squalene synthesis in yeast? Also, do you think yeast cells would pick it up?

Honestly: I have no idea. Are there any recommendations by the distibutors? Otherwise you will probably have to dig through Pubmed to find suitable concentrations. If there is nothing, you need to try it.


text:
Why are not all species hermaphrodites?
If a hermaphrodite animal (like slug, snail, etc) finds a partner they can mate immediately.
If another animal with "normal" reproduction (lets say a mouse) finds a partner they can only mate if they are opposite genders.
So it seems logical that the hermaphrodite way of reproduction is more successful than the "normal" way.
But it is not, as far as I know all higher developed species are using, the standard way of reproduction (male and female).
Why? What are the disadvantages of hermaphroditism?

The group of fish known as hamlets https://en.wikipedia.org/wiki/Hamlet_(fish) are simultaneous haermaphrodites, like snails. Many other fish are sequential hermaphrodites, but that is probably outside the scope of your question.

in brief - its quality not quantity.  sort of like asking 'why do we bother getting married and buying houses when we could just hook up at a bar every weekend?'  hermaphrodites can reproduce more easily, but other organisms invest more in their offspring and also often have a harder time getting around to mating.  no judgments here, just trying to make it pretty plain.

Firstly I'll clarify that you are talking about simultaneous hermaphrodites rather than sequential hermaphrodites (1st one sex, then the other e.g. the limpet Patella vulgata).
It is perhaps easiest to address the question by countering it and asking why dioecy (2 sex systems/2 gonochoric types e.g. male and female) is better? As you have pointed out there are obvious advantages to being a hermaphroditic species such as more chance of mating - more likely to provide an advantage at very low population densities where interactions are infrequent.
There are two key disadvantages of hermaphroditism which I will briefly cover but have been discussed in this paper and probably other costs.
The first is energy costs. Maintaining the capacity to produce male and female gametes will be more costly than maintaining one. This gives the hermaphrodite a fitness disadvantage because energy is rarely an infinite resource. Therefore at higher population densities, when mating opportunities are not rare, the gonochoric individuals will have a higher fitness because they have more energy. Monogamy is also analogous to rare encounters but true monogamy is rare (1 partner for life).
The second disadvantage of hermaphroditism is self fertilisation. This will cause an increase in homozygosity and lead to inbreeding depression (reduced fitness).
So you are right to some extent...

the hermaphrodite way of reproduction is more successful than the
  "normal" way.

...but the conditions which give rise to an hermaphroditic advantage are restricting. Overall, the above costs, combined with the obvious complexity of evolving the ability to produce male and female gametes, the ability to both fertilise and be fertilised, pregnancy and birth, and mating systems, mean that it is often more beneficial to be a dioecious species. Thus dioecy evolves.

EDIT: Question Raised by @Single_Digit

I have been pondering this question for a while and I get what RG255
  is saying. I'm just not sure I entirely buy it. Take earthworms, for
  example. They are simultaneous true hermaphrodites (as far as I
  understand). The anatomy doesn't have to be that complex*. They simply
  have two genital openings (one for eggs and one for sperm) and they
  line up in a "69" (excuse the vulgarity) position. This should, in
  theory, minimize the inbreeding depression. However, it doesn't
  eliminate the maintenance of two sets of reproductive systems. But
  most organisms are not internally fertilized mammals with wildly
  complicated systems of internalized embryonic care. Most species lay a
  pile of eggs that a male squirts sperm on or squirt eggs while the
  male squirt sperm and then they hope for the best.
I would think the advantages of simultaneous parenting (after all,
  many MANY species' males don't provide much in the way of child care)
  and its fitness advantage would vastly outweigh the burden of a second
  set of reproductive organs.
With that said, I don't have a better explanation, but I find the
  question a very interesting one. The linked article is pay-walled,
  aside from the abstract, but I still disagree with some of its tenets.
  To me true hermaphroditism should be very common (I realize it isn't)
  in species that don't need two parents to raise offspring, but do
  benefit from some (as in one parent's) parental care. I recognize that
  it would do little to help species that merely dump gametes and leave
  because specialization of one reproductive system would likely do the
  job better and both genders equally contribute under that type of
  system.
So, RG255 convince me! Clearly there are good reasons, since gender
  (or asexual repr) is the norm, but I need more/better evidence.

Yes I realize they would need separate internal anatomies for each type of gamete, but still...

My response:

You have presented one example of hermaphroditism and used that as
  evidence that all species should be hermaphrodites. Earthworms are
  small slow creatures living in soil, I don't imagine they have high
  rates of encounter, and therefore low rates of encountering the
  opposite sex, therefore hermaphroditism would be favoured as discussed
  above.
Further, you say most species are external fertilisers (do you
  have a reference for this?) and therefore it is not costly be a
  hermaphrodite. I don't see your logic there, the cost is not
  necessarily to do with the cost of bearing child, producing &
  maintaining the gonads and gametes is also a costly process. I would
  argue that this is extremely complex. This is not just on a
  morphological level but also physiological: in non-hermaphroditic
  species the sexes have very different, and often, conflicting gene
  expression and hormone production patterns. Hermaphrodites would not
  be able to optimize to the fulfilling both the male and female roles.
Finally, you pointed out that the worms do not inbreed. Inbreeding
  avoidance does not have to be the cause of the hermaphroditism
  persisting, if the environment/other factors favour hermaphroditism. I
  never said that both were simultaneously necessary.
I hope this
  clarifies it for you, if not please expand as to why, I am on here
  because I want to help people understand biology properly!

Further response from @single_digit:

Well fair enough about my external fertilizers comment. I don't have a
  reference, but I was thinking all multicellular life and I'd have to
  imagine that when you factor in plants, that external fertilization is
  relatively the norm (as is hermaphrodism (dioecy) for the plants). As
  to earthworms, I disagree about your description of them. Their
  densities are actually pretty high, so I'd wager they encounter each
  other frequently, so I'm not sure where that leaves them in terms of
  pressures for hermaphroditism. Your point on the physiologic/hormonal
  issues of maintaining the systems is one I haven't previously
  considered. I honestly don't have any clue as to how daunting (or
  simple) that is, but I'd imagine that the sophistication of the
  systems would play a pretty key role. Makes me wonder how much this
  has been researched in true hermaprhodites. I suppose the main thing I
  keep coming back to is the overwhelming disadvantage gender has in
  terms of potential to create offspring. Males in many (most?) species
  essentially act as little more than sperm donors, thus half the
  individuals have effectively zero fitness. That just seems like an
  overwhelming advantage for hermaphrodites.

My Response

Why do you consider half of the individuals to have zero fitness?
  Fitness is widely accepted as the number of offspring a parent
  produces because this is directly related to number of copies of their
  genes passed to the next generation. Sperm donor type males achieve
  increased fitness by mating as do females - with out the male they
  would never be fertilized. The key disadvantage of dioecy is the
  halved (assuming equal sex ratio) frequency of potential encounters
  that could lead to mating. The general disadvantages of
  hermaphroditism are inbreeding depression and high cost & complexity.

Single_digit:

Zero fitness isn't exactly correct, but if we look at parental care as
  conveying a survival advantage for K selected species, and huge
  numbers of offspring conveying an advantage for r-selected species
  (obviously the type of env affects this) does a deadbeat dad really
  optimize for either of these? Passing on genes is fine, but if
  offspring survival is low, does it matter? Does it simply boil down to
  the maintenance of two repr systems plus decreased fitness from
  inbreeding vs the increased reproductive success from extra child
  care? Or is there more?

My response:

r/K selection theory has generally been disregarded in the
  evolutionary biology community due to the substantial evidence against
  it so it is unhelpful to think of selection in this way. As long as
  the 2 sexes strategy is more successful at passing on genes than a
  hermaphroditic strategy it will (should) prevail. Dioecy will be more
  successful if the hermaphroditism introduces to much cost through
  production and maintenance of sexual organs/gamete and inbreeding
  whilst not attaining substantial gains from higher potential mating
  frequency.

@Single_Digit

Interesting about r/K selection. I hadn't heard that. Do you have any
  links? I'd be curious to learn more there. I incorrectly earlier made
  a comment about dioecy where I meant monecy. But this seems to beg the
  question, why is monecy/hermaphroditism so much more prevalent in
  plants? Obviously there are different survival pressures, but I'd
  think the same basic principles would apply as in animals, but the
  condition seems to be far more common than in animals.

My Response

I seem to remeber there being a reason in plants, don't
  have time to look it up right now. The work about r/K selection was
  Reznick/Stearns/Charlesworth. Reznicks is the most recent and more
  overview type paper - best place to start:
  http://www2.hawaii.edu/~taylor/z652/Reznicketal.pdf

also want to add that hermaprodites are not found in larger animals because the reproductive system becomes more complicated and difficult to maintain.  sexual dimorphism is a much better advantage when you have live birth with amniotic sacks, umbilical cords etc.

@rg255 Thank you very much, this is a great answer! Sorry if my question does not contain many hard-to-spell words but I'm not a biologist and my first language isn't english, I'm just curious about everything :) And yes you're right, I was talking about simultaneous hermaphrodites. :)

That's fine, it was easy to understand! great question, really got me thinking & I study sexual selection!

belated reply, but I think that sexual dimorphism is the bigger motive.  It's easy to evolve ways to avoid accidental self fertilization, and production of male gambits for a female is a relatively trivial addition to her energy investment in eggs, so even a minor mating chance as a 'male' would warrant the cost to hermaphroditeism over pure female.  The big distinction is that males could evolve to be even better males, better compete for rights to make with multiple females etc.  A strong hermaphrodite will always choose to mate as male over female, so why not adapt to be better at that role

The book "The selfish gene" gives an answer for you to get ideas from to make your answer. It's obvious that for almost any species that reproduces sexually, it wouldn't be any less advantageous to produce a kid the same way but asexually. For each sexually reproducing species, if it evolved to reproduce asexually, it would be an advantage to do away with males if the species had separate genders and do away with the male parts the species is hermaphrodite. I think it would be better for you to explain that and then answer why not all sexually reproducing species are hermaphrodytes.

Your comment makes little sense to me - could you clarify?

@Timothy Asexual reproduction gives a huge advantage in the short term, but not the long term.  Without the exchange of genes asexual species tend to stay stagnant with little evolution or change.  Which, by itself, is fine if your genes are spread.  However, it means that you have no ability to change with your enviroment.  The moment your enviroment changes, or a new disease evolves that attacks the species, the species will suffer significant death or even extinction due to it's inability to adapt to the change fast enough.  Thus asexual species die out faster then sexual ones.

I'm not at a biologist, but I have a pet theory I'd like to throw into the ring: hermaphroditism tends to be unstable in a similar way to strong sex skews.  Imagine species A where 90% of offspring are female; at moderate population density, the 10% male population will be more than sufficient to maintain the females, and having 90% of the population able to breed will out-compete another species with a 50/50 distribution.  However, a mutation which tends to produce more males will tend to become more common, because the males of species A reproduce much more often than the females.  Eventually, this stabilizes at roughly equal frequencies for the sexes.
Back to the hermaphroditic species C, imagine that a mutation led to a variant which had a flawed female reproductive system, meaning it could not lay as many eggs when fertilized, but it had some other advantage which made it better at mating: perhaps by diverting energy from the female systems, it was slightly larger and stronger and could intimidate others, or perhaps it put this energy into a stronger immune system.  Eventually, the population evolving in this direction could lose its ability to lay eggs or birth young entirely, and instead focus entirely on being better at finding mates to impregnate.
Looking at it from the other side, if some individuals de-prioritize that side of things and instead concentrate on being the best egg-layers and care-providers possible, that could be a stronger evolutionary position than trying to be equally good at both roles.  Eventually, this split would produce recognizably male and female subgroups.
If this idea has already been proposed and either taken seriously or shot down, I'd appreciate any pointers to further reading.

I have been pondering this question for a while and I get what RG255 is saying. I'm just not sure I entirely buy it. Take earthworms, for example. They are simultaneous true hermaphrodites (as far as I understand). The anatomy doesn't have to be that complex*. They simply have two genital openings (one for eggs and one for sperm) and they line up in a "69" (excuse the vulgarity) position. This should, in theory, minimize the inbreeding depression.
However, it doesn't eliminate the maintenance of two sets of reproductive systems. But most organisms are not internally fertilized mammals with wildly complicated systems of internalized embryonic care. Most species lay a pile of eggs that a male squirts sperm on or squirt eggs while the male squirt sperm and then they hope for the best.
I would think the advantages of simultaneous parenting (after all, many MANY species' males don't provide much in the way of child care) and its fitness advantage would vastly outweigh the burden of a second set of reproductive organs.
With that said, I don't have a better explanation, but I find the question a very interesting one. The linked article is pay-walled, aside from the abstract, but I still disagree with some of its tenets. To me true hermaphroditism should be very common (I realize it isn't) in species that don't need two parents to raise offspring, but do benefit from some (as in one parent's) parental care. I recognize that it would do little to help species that merely dump gametes and leave because specialization of one reproductive system would likely do the job better and both genders equally contribute under that type of system.
So, RG255 convince me! Clearly there are good reasons, since gender (or asexual repr) is the norm, but I need more/better evidence.
* - Yes I realize they would need separate internal anatomies for each type of gamete, but still...

Well fair enough about my external fertilizers comment. I don't have a reference, but I was thinking all multicellular life and I'd have to imagine that when you factor in plants, that external fertilization is relatively the norm (as is hermaphrodism (dioecy) for the plants).
As to earthworms, I disagree about your description of them. Their densities are actually pretty high, so I'd wager they encounter each other frequently, so I'm not sure where that leaves them in terms of pressures for hermaphroditism.
Your point on the physiologic/hormonal issues of maintaining the systems is one I haven't previously considered. I honestly don't have any clue as to how daunting (or simple) that is, but I'd imagine that the sophistication of the systems would play a pretty key role. Makes me wonder how much this has been researched in true hermaprhodites. I suppose the main thing I keep coming back to is the overwhelming disadvantage gender has in terms of potential to create offspring. Males in many (most?) species essentially act as little more than sperm donors, thus half the individuals have effectively zero fitness. That just seems like an overwhelming advantage for hermaphrodites.

You have presented one example of hermaphroditism and used that as evidence that all species should be hermaphrodites. Earthworms are small slow creatures living in soil, I don't imagine they have high rates of encounter, and therefore low rates of encountering the opposite sex, therefore hermaphroditism would be favoured as discussed above.

Further, you say most species are external fertilisers (do you have a reference for this?) and therefore it is not costly be a hermaphrodite. I don't see your logic there, the cost is not necessarily to do with the cost of bearing child, producing & maintaining the gonads and gametes is also a costly process.

I would argue that this is extremely complex. This is not just on a morphological level but also physiological: in non-hermaphroditic species the sexes have very different, and often, conflicting gene expression and hormone production patterns. Hermaphrodites would not be able to optimize to the fulfilling both the male and female roles.

Finally, you pointed out that the worms do not inbreed. Inbreeding avoidance does not have to be the cause of the hermaphroditism persisting, if the environment/other factors favour hermaphroditism. I never said that both were simultaneously necessary.

I had to break that up in to small sections because there is a character limit. I hope this clarifies it for you, if not please expand as to why, I am on here because I want to help people understand biology properly!

Glad to see that my question keeps people thinking... thanks guys!

Why do you consider half of the individuals to have zero fitness? Fitness is widely accepted as the number of offspring a parent produces because this is directly related to number of copies of their genes passed to the next generation. Sperm donor type males achieve increased fitness by mating as do females - with out the male they would never be fertilized. The key disadvantage of dioecy is the halved (assuming equal sex ratio) frequency of potential encounters that could lead to mating. The general disadvantages of hermaphroditism are inbreeding depression and high cost & complexity

Zero fitness isn't exactly correct, but if we look at parental care as conveying a survival advantage for K selected species, and huge numbers of offspring conveying an advantage for r-selected species (obviously the type of env affects this) does a deadbeat dad really optimize for either of these? Passing on genes is fine, but if offspring survival is low, does it matter? Does it simply boil down to the maintenance of two repr systems plus decreased fitness from inbreeding vs the increased reproductive success from extra child care? Or is there more?

@single_digit r/K selection theory has generally been disregarded in the evolutionary biology community due to the substantial evidence against it so it is unhelpful to think of selection in this way. As long as the 2 sexes strategy is more successful at passing on genes than a hermaphroditic strategy it will (should) prevail. Dioecy will be more successful if the hermaphroditism introduces to much cost through production and maintenance of sexual organs/gamete and inbreeding whilst not attaining substantial gains from higher potential mating frequency.

@rg255 Interesting about r/K selection. I hadn't heard that. Do you have any links? I'd be curious to learn more there.  I incorrectly earlier made a comment about dioecy where I meant monecy. But this seems to beg the question, why is monecy/hermaphroditism so much more prevalent in plants? Obviously there are different survival pressures, but I'd think the same basic principles would apply as in animals, but the condition seems to be far more common than in animals.

@single_digit I seem to remeber there being a reason in plants, don't have time to look it up right now. The work about r/K selection was Reznick/Stearns/Charlesworth. Reznicks is the most recent and more overview type paper - best place to start: http://www.esajournals.org/doi/abs/10.1890/0012-9658%282002%29083%5B1509%3ARAKSRT%5D2.0.CO%3B2

It's actually quite simple if you consider the following two points:
1.Males only have to mate with TWO MORE individuals in each reproductive cycle to outcompete a hermaphrodite.
2.mobility is important and this gives male-only animals a big advantage.
I can't see anyone clearing expressing this already but apologies if someone has.
Simple animals generally produce a lot of eggs to pass on their genes to as many offspring as possible. However this slows them down, when looking for a mate, in spending time laying their eggs, and in expended energy producing the eggs.
In such a hermaphroditic population, eventually a male will randomly evolve that doesn't bother to produce eggs. Providing that this gives it an advantage over its hermaphroditic counterparts, such that it can mate with at least two more egg-laying individuals in the time taken for the hermaphroditic version to produce and lay its eggs, then this male-only version will produce more offspring sharing its genes than the hermaphrodite would. This means that more of the next generation will also be male only.
This ensures that males always exist (at least at some percentage of the population), as chances are they will mate with many more individuals than their slower hermaphroditic competitors and pass on their genes more successfully. Simple.
(This is probably also the reason that most plants are hermaphroditic, as mobility is not a factor.)

Welcome to BiologySE. We always appreciate references to accompany answers as a way to add legitimacy as well as allow other users less familiar with the subject to read for more information.

The non-hermaphroditic sex systems I'm most familiar with arise from hermaphrodite populations. Suppose a male-only mutant arises, it can cheat the hermaphrodite system by putting its reproductive energy into the "cheap" sperm and fertilising many eggs, instead of sharing the energy burden of expensive eggs and cheap sperm. the male-only out-competes the hermaphrodites and so over generations this male-only trait spreads. the male + hermaphrodite population has an excess of males, selecting for any female-only mutant to do well. Suppose a mutant female-only arises. She Put all her energy into egg production, so there are more and/oor better eggs. A female-only outc-ompetes a hermaphodite if there is an EXCESS OF MALES. A female-only does less well than a hermaphrodite if there is a male/female balance
So, in hermaphrodite species, we see avenues to the formation of a male-only and female-only subpopulation

Hi Stephanie! Welcome to Bio.SE! Please update your answer by citing reputable source(s) of support for your claims. Otherwise, your answer is likely to be downvoted or deleted. Thanks!

This is a bit expressed in an unclear way but I think it solves the problem.
I think the reason is simply that if you have all the hermaphrodites being difficult about their mates they will evolve fast because the best mates will mate more and the worst won't mate a lot. But if the hermaphrodite individual is hard to get, it also  won't be motivated to pursue sex and it will be hard for the 'best' individuals to mate more cause they will be too hard to get.  So the requirement to impress while also being hard to get are contradictory in non differentiated individuals. In most animals, the difference in libido of the female versus that of the male can solve this paradox. One has to show they have good genetic material (the male) and the other just have to be hard to get. This is pretty shitty for females, but nature often is. I think the fitness of this difference almost disappears in monogamous species where both have an advantage if they are hard to get. So we can hope hermaphroditism is not an advantage only for an intermediary stage of evolution but can become one again in higher species. This would alleviate some of the sexual conflict.

The female & male organs compete against each other.  A stud hermaphrodite has little incentive to have female organs.  A human stud who can have 1000s of kids would be slowed down considerably if he\it had to spend 9 months\year being pregnant & raising infants & it's costly to maintain female organs.

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text:
Why doesn't the spinal cord get thicker the further up we go?
The cervical and lumbar enlargements exist on the spinal cord as a result of the increased nerve input/output required for the arms and legs respectively.
However, I don't understand how the enlargements could exist by themselves without the rest of the spinal cord getting thicker.
The following is an exaggerated view of what I think a spinal cord should look like. The cervical region needs to be thicker as it has to accommodate the original nerves from the legs (blue) AND the new nerves from the arm (red). There are now ~2x as many nerves needed to go to the brain - thus the spinal cord above the cervical area should be twice as big. It is not - it just enlarges around the cervical area and returns to normal.
Why does the spinal cord not get thicker the further up we go? Doesn't it need to accommodate more nerve fibers and thus be thicker?

Try this on a piece of paper: sketch out an outline of a human body, with head, arms, and legs. Start drawing fibers that travel from the brain to each of those areas. What does your "spine" that you draw end up looking like?

@BryanKrause I understand that there  will be branching out from the central cord - is that what you're getting at? I'm asking why won't the central cord itself get thicker

Do you see how your drawn spinal cord (not the outline, the bundle of "wires") got thicker where your red lines come in? That's the cervical enlargement.

Also yes some nerves do go to the spine then turn around and go right back, look up something called a "reflex arc".

@JohnHon I think this is a good question for someone just starting out learning about this system such as yourself (+1), but in fact, many nerves play a role in reflexes (especially for our sensitive and highly mobile limbs! ) without traveling to the brain. As John says above, read more into reflex arcs

@BryanKrause Yes I do see how it got thicker, but my question is that in diagrams it looks like a bump not a sustained increased in thickness. Given that there are now more nerves that must run to the brain after the cervical area, I don't see how the thickness of the spinal cord does not increase all the way to the brain (not just locally in the cervical area)

You might consider that the primary function of the spine is structural.  That it also contains nerve bundles is secondary.  In humans, it needs to support the weight of what's above it (for a standing human), but it evolved from mostly quadrupedal ancestors.

Posting as an comment because I lack sources: from what I understand the spinal column does not just relay data like wires.  It does processing.  So its diameter need only grow enough to support the "bandwidth" needed to talk to the brain.,

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text:
Why does oestrogen go from inhibitory to stimulating LH/FSH?
Typically in the menstrual cycle, oestrogen is released from the follicle. The oestrogen goes on to the hypothalamus to have an inhibitory effect on releasing more GnRH and LH/FSH.
However, when all the other follicles in the ovaries have died/atrised, the oestrogen acts as a stimulatory hormone. It increases FSH and LH secretion, to create the LH surge.
Why is this? How can one hormone go from being inhibitory to stimulatory?

"...suddenly the oestrogen acts as a stimulatory hormone. It increases FSH and LH secretion." What estrogen? What causes menopause? Why does FSH increase with menopause? It's easy to google and what you find will show you where you took a wrong turn in your reasoning.


text:
Protein phosphorylation in the cytoplasm. Typical time scale?
Is there a typical protein phosphorylation rate in the cell cytoplasm under physiological conditions, or at least an upper-bound?
Suppose a protein $A$ is being phosphorylated into $A^*$ with the first order reaction
$A \to ^k A^*$
where $k$ is the reaction rate ($k$ unit is $\rm time^{-1}$).
In reality a phosphorylation reaction involves multiple agents (protein, enzyme, ATP) and multiple reactions, therefore cannot be accurately mapped onto a first order reaction. However this makes sense if we are only interested in the order of magnitude of $k$. According to this first order reaction the evolution of the $A$ concentration is given by
$$
\frac{d A}{dt}=-k A
$$
and therefore $1/k$ is the time scale at which $A$ vary.
So my question can also be formulated as: suppose that at a given time a cytoplasmic protein $A$ starts to be phosphorylated into $A^*$. What is the typical time scale at which the concentrations of $A$ and $A^*$ reach their equilibrium values?
From few things I read it looks like it is of the order of seconds or minutes or hours, and 1 second seems to be an upper bound. Any references?

Phosphorylation is not a first order reaction, it always Protein + ATP -(enzyme)-> Protein-P + ADP  (in rare cases a different Phosphate carrier might be used as well). While the concentration of ATP is somewhat kept stable, you shouldn't/can't assume it doesn't matter.
Otherwise I'm not sure, the Brenda database might have some numbers for Kinases, but getting 'average' or upper/lower bounds might be tricky

Sure it is not a first order reaction, but to some extend you can always look how fast the concentration of the unphosphorylated protein (A) changes with time and get the coefficient $k$ which will be your "effective first order rate", that will be function of ATP, enzymes, etc. That is just to get roughly an order of magnitude.

@Nicolai I just edited the question, I hope it makes more sense in this way.

yeah, I think with the edits it's much clearer why you would assume a first order reaction in this case. Did you take a look at the Brenda database for some kinases (phosphorylation enzymes) and possible reaction values? I'd also assume that depending on the kinase (not so much the target), the order of magnitude for k might be very different.

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text:
How Mitochondria differs from Prokaryotes(probably regarding energy production)?
In other words, what evolutionary advantage is offered by mitochondria to eukaryotes(probably regarding energy production), which prokaryotes themselves cannot evolve or do?(here I am assuming that mitochondria evolved from prokaryotes)
I seemingly found some answers in the below article. Will love to hear the opinion of others regarding the same.
http://blogs.discovermagazine.com/notrocketscience/2010/10/20/the-origin-of-complex-life-it-was-all-about-energy/#.WYXsH4h97b0

Your question is somewhat unclear. Are you asking what selective pressure there was for endosymbiosis?

That's a pleasant article, but you might want to add the relevant parts (the "answers" you found) to the question.

If you mean "why do we have mitochondria instead of our cells doing the work themselves"
Then I can think of several answers.
First, oxidative phosphorylation must take place within an organelle, and requires specialized cellular machinery to occur.
So either a prokaryote can wait a couple million years to evolve these structures, or it can ask its friend to do it, and HE is specially evolved to do just that.
Like the way you hire a plumber when your toilet gets clogged, instead of going to plumber school yourself.
Also, oxidative phosphorylation has to do with oxygen.
Oxygen, when busted apart, can form unstable molecules called free radicals that are essentially bleach.
These molecules zoom around smashing up anything they touch including DNA.
So the host cell says "better you than me!"
Remember how I said you need an organelle for oxidative phosphorylation?
This is why. So all the "bleach" gets contained.
Two very good reasons why we evolved to rely on a separate organism instead of just making our own breathing organelle.


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Why are the products of Meiosis 2 different?
In Meiosis I, 46 chromosomes crossover. These mixed chromosomes then split off into new cells. In these new cells, Meiosis II occurs, where these mixed chromosomes have their chromatids ripped apart.
What I'm confused about is why does Meiosis II produce 2 different new cells if you're just separating 2 identical chromatids? Is it because when crossing over the genes makes the both chromatids different?

would someone care to explain why the downvote? I think this question meets community guidelines

Indeed, this is all due to the crossing over between different alleles. For example, put the case of one cell that contains 2 chromosomes, one from the mother and another from the father. Each chromosome contains two alleles: Ab (mother) and aB (father).
The first thing that they will do is divide into two chromatids each one getting to: Ab[1M] (one mother's chromatid) and Ab[2M] (second mother's chromatid) and the same for the father aB[1F] and aB[2F]. Notice that the chromatids still joined by the centromere.
Now, the crossing over comes: in this case, if the A[2M] from mother's chromosome gets exchange with a[1F] of the father's chromosome, we get: Ab[1M], ab[2M], AB[1F], aB[2F].
As you see, when they segregate you will get 4 different cells with two alleles: Ab, ab, AB and aB.
I hope this answers your question.


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Do biologists use the word "solubilize" to mean "dissolve"?
I work with biologists who often use the word "solubilize" to mean "dissolve".
Is this correct usage? I keep correcting them (I'm not a biologist, but I help with writing), and we've argued about it. Not all are native English speakers, so I've been attributing it to that. But maybe they're right. I want to know.
The context here is pharmacology - taking drugs in powder form and dissolving them in a vehicle for dosing lab animals.
I thought "solubilize" means to make something more soluble by adding (for example) soap. (for example: https://www.thefreedictionary.com/solubilisation ).
But they use "solubilize" to mean "dissolve". That usage doesn't seem to be standard English, but maybe it's normal usage as a term of art in pharmacology.
Is it?
For scientific writing in pharmacology, what is the standard usage? When we mean (standard English) "dissolve", which word should we be using, in order to be clearly understood and conform with standard professional terminology?

Added: Some of the commenters seem to misunderstand what I'm trying to ask, so I'll try to clarify.
I can read dictionaries as well as you can, and Google is my friend, too; I'm not asking what the standard dictionary definitions are (I already know).
I'm asking about how working biologists, English-speakers, use these words.
Do practicing biologists/pharmacologists use these terms differently than the standard English definitions? Are these "terms of art" in those fields, with a different definition? Or not?
Some of my colleagues insist that, in their field of biology/pharmacology, the word "solubilize" is used to mean what the dictionary says "dissolve" means. Are they correct, or are they mistaken (presumably because they're not native English speakers)?
I'm not a biologist and so don't know from personal experience. The people I work with are biologists but not native English speakers, so I'm not convinced they know either.
Thus, I'm asking here.

I've been asked for a sample sentence re how it's used. I don't see how that affects the answer, but here:
"Diphtheria toxin (List Biological Laboratories, Cat #150) was solubilized in sterile water at 2 mg/mL, aliquoted, and frozen at -20 C."
Is this correct usage or would "dissolved in sterile water" be better?

I think you'd need a more concrete example than "I work with biologists" for anyone to judge this.

@David I'm not trying to be critical - I just want to know how the word is used by biologists, so I can use the word in our writing that will be understood best.

@BryanKrause This is mainly in the context of dosing drugs. We start usually with a compound in powder form, then stir/heat/sonicate/mix various other things (vehicles) to produce a dosing solution. Not being a biologist, I'd call that "dissolving". We write a report about what we did - should I call that "dissolving" the drug, or "solubulizing" it? I'm not trying to be a language Nazi; I just want to be understood clearly.

@nerdfever.com so you could say that you are making things more soluble by stirring/heating/sonicating them? Why would a chemical treatment (soap) differ from a physical one (heating)?

@MaximilianPress I don't know - the soap reference was something I found in a dictionary. I'm asking about how working biologists use these words. I'm not a biologist and I don't know; the people I work with are not native English speakers, so I don't trust what they think about it.

If you take Maximilian’s question to be rhetorical, it’s worth considering. It sounds like, in your context, both terms could be appropriate.

Sometimes 'solubilize' is a more precise description of a process, even though 'dissolve' would technically be correct. For example, I write a protocol where a user must solubilize a compound in ethanol before adding it to a growth medium. I could correctly say 'dissolve' instead of 'solubilize' here, but 'solubilize' provides a more complete description of the process by giving a context clue as to why it's dissolved in ethanol first. There are also situations where only one of those words is correct. Siderophores solubilize ferric iron, but don't dissolve it.

I think I found an answer at Science Direct where multiple definitions are provided, among one from Thomson (2012):

Solubilization is the action of certain chemical reagents on organic materials (such as animal or plant tissue) that effects a structural breakdown (or digestion) into a liquid form that can then be directly dissolved [...]

and from Lau (2011):

Solubilization is the increase in solubility of a poorly water–soluble substance with surface-active agents. The mechanism involves entrapment (adsorbed or dissolved) of molecules in micelles and the tendency of surfactants to form colloidal aggregations at critical micelle concentration levels.

From these definitions I understand that solubilization is a process to make something dissolvable. The process of dissolving thus happens after the solubilization (definition #1) or during the process of solubilization process (definition #2). Thus, solubilization and dissolving are separate processes (definition #1) or dissolving is considered a part of the process of solubilization (definition #2).
So admittedly, at this stage I am unsure to what exactly the two terms mean exactly, but they are certainly not interchangeable terms.
And regarding your comment

...that it's not unusual for experienced biologists themselves to be unsure which is the proper term here. Even native English speakers

I totally second Bryan's response

Language is messy, scientific terminology included...

This is because terminology tends to stick after having been adopted widely, even if it proves to be incorrect. Consider for instance the fact that current always flows from + to - in schematics, but that electrons definiely choose to go the other way around. Scientific terminology is messy indeed.
References
- Lau, Preformulation Studies. In: Handbook of Modern Pharmaceutical Analysis: 173-233
- Thomson, Handbook of Radioactivity Analysis (3rd ed.) 2012: 575-623

Thanks, but I can read dictionaries, too. That's why I've argued over this with my colleagues. I'm looking for answers from experienced biologists who know how the terms are, in practice, used in the field.

@nerdfever.com Pretty sure AliceD is in fact an experienced biologist. I would consider myself one as well, and this answer is probably as close as you are going to get to an "official definition". At the same time, I guarantee you this term, like many others, may not be used strictly. Language is messy, scientific terminology included. So, getting back to my old comment (which I didn't really explain), you need better context for the description you give for anyone to judge the "correctness", but I highly doubt anyone would confuse the meaning in context.

@BryanKrause Thanks. I'm interpreting that to mean that it's not unusual for experienced biologists themselves to be unsure which is the proper term here. Even native English speakers.

@nerdfever.com It's hard to even argue what the proper term is when you haven't given an example; you say your colleagues use "solubilize" to mean "dissolve" but it seems just as likely to me that they mean "solubilize" and you think they mean "dissolve". AliceD has explained they aren't quite interchangeable yet their meanings are a bit intertwined.

@BryanKrause I did try to clarify the question. It now includes "taking drugs in powder form and dissolving them in a vehicle for dosing lab animals." What other context would be helpful?

@nerdfever.com An entire sentence where the term is used would be helpful. I can't see how that would be difficult to provide, but if for some reason it is, maybe at least a specific drug and a specific vehicle, so you can construct your own sentence "we solubilize (specific drug A) in (specific vehicle X.Y mM Z in PQRS)"

@BryanKrause I don't see how the specific drug and vehicle affect the answer, but I've added an example sentence to the end of the answer. My colleagues and I have debated this - I think "dissolved in" is more appropriate here, but others disagree. Does this make things clearer?


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Infrared emitting diode eye safety
I'm thinking of creating my own laser tag system and am a bit concerned about the eye safety aspect. Most of the homebrew system I've seen use the TSAL 6100 diode(http://www.vishay.com/docs/81009/tsal6100.pdf).
From what I've gathered from hobbyist forums it should be totally eye safe. However the math doesn't add up, my math could be wrong, read probably is, but I couldn't find any conclusive data that would disprove it. Also I cannot manage to factor in what effects lenses would have, which are a must to keep the beam from having to large a spread. Here are my calculations.
First off using the inverse suqare law and a TSAL running at 1Amps (from what I've read most players run it at 1.5 Amps) at the minimum distance of 200mm we get the following result:
Ee = 1.5W/sr / (0.2)^2m = 37.5W/m^2 (the 1.5 W/sr is from the TSALs datasheet at 1A)
The irriadiance of 37.5 is a bit high, but it's still under the 100W/m^2 safety limit for the cornea.
The same equation done at a distance of 100mm however yields an Ee of 150 W/m^2 which is above safety levels. Assuming you don't point a tagger in your face and start firing of shoots you'll be safe.
What I'm curious about is how a lens affects the safety characteristics. Assuming a lens with a focal length of 100mm. Won't the irradiance be the same with the irradiance at a distance of 100mm from the IRLED.
My math and understanding of the principals could be wrong, but I was curious if anyone could put my mind at ease.
I've also made a rough calculation of the retinal hazzard.
R(lamb) = 0.33 rad
(angular subtense) alpha= 5mm/200mm = 0.025 rad
We'll use an alphaeffective = 0.011rad and that gives us an emission limit for the radiance of 545mw/mm^2/sr
and our iriadiance is Lir = 1500mw/sr * 0.33 / (5mm)^2 = 99mw/mm2/sr
that's way below the limit, but if we modify that active light source to 1mm it becomes 495, which is skirting the line.
(the tec doc doesn't define an active light source size, at least I couldn't find it so I used 5mm )
Again the above calculations are for a source without a concentrating lens. What would happen if we added a lens in the mix? Would it stay in the safe zone? How does pulsing the diode effect intensity? I'm guessing it lowers it, but if anyone could manage it, I'd like a numerical demonstration that it brings it closer to safer bounds.
The above calculations are based on the folowing OSRAM paper (http://www.osram-os.com/Graphics/XPic2/00052113_0.pdf/Application%20Note%20Eye%20Safety.pdf), which explains the principles involving

I built a NIR LED light for use with a raspberry pi NIR camera. It worked well, and I probably got it my eyes several times with 25 LEDs. I'm not blind yet. But I know you don't have a look away reflex in the NIR range, so if you accidentally flash yourself, you might not realize it until it's a problem.

Re: the pulsing issue, I can say for sure that if the LED is pulsed at the same power, the effective brightness will decrease. This is how many torches implement their "brightness switch" mode.


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Are there known functions of AST, ALT, and amylase in the blood?
A number of enzymes can be measured in the blood or plasma that aid in the diagnosis of certain diseases. For example, patients with particular liver diseases may have elevated aspartate aminotransferase (AST) and/or alanine aminotransferase (ALT) levels in the blood. These enzymes are normally involved in biochemical reactions of metabolism that interconvert amino acids with other metabolic intermediates - that is, biochemical reactions that are common within the liver cell. Also, patients with pancreatitis frequently have elevated amylase and lipase levels, which are digestive enzymes normally secreted into the gastrointestinal tract. During pancreatitis these enzymes are released into the blood, rising and falling with the resolution of pancreatic damage/inflammation.
Pathologically, the tissues that are damaged in these diseases (liver and pancreas, respectively) are the source of the elevated enzymes. In healthy individuals, however, these same enzymes are still found in low concentrations in the circulating blood. What is the source of these enzymes that are found in low circulating concentrations? Is it still those same tissues (e.g. AST/ALT from the liver)? Is this secondary to "normal turnover" of cells within those tissues? Or, alternatively, are these enzymes secreted into the blood to serve a particular function?

For example... There is a freely available manuscript by Arnold and Rutter published in the Journal of Biological Chemistry (1963) that discusses experimental evidence for active amylase secretion from the liver during an isolated liver perfusion experiment. Amylase continues to be secreted, even in the absence of other enzymes that would otherwise indicate liver damage (suggesting that the amylase is intentionally being secreted for some unknown purpose). This is an paper from almost 60 years ago - do we know what some of these enzymes like AST/ALT and amylase do in the plasma? Or are those functions still unknown?

These enzymes, while useful markers of disease, are not only produced during the disease state, and are not only produced in one organ. It is therefore not surprising that there are always low levels released into the biochemical milieu that is the blood. If there are not even low levels of the enzymes then that might indicate that the organ is not doing it's job properly.
I'll approach this from a veterinary viewpoint but I imagine it is much the same in humans. My preferred source for information about veterinary clinical pathology is Cornell's EClinpath site.
The major tissue sources of AST are liver, skeletal muscle, and cardiac muscle. A small amount is produced by erythrocytes. In lesser concentrations it is also found in renal epithelial cells and brain tissue. It therefore should be no surprise that low levels are found in blood. It is not difficult to picture a small amount of leakage from erythrocytes in the normal state, even without pathologic haemolysis, given the regular turnover of cells and permeability of erythrocytes – although I suspect this is a minor source. Just due to the fact that the liver's normal function is to deal with many cytotoxic compounds, even in the completely healthy patient there always is going to be some low level of hepatocellular damage. As a result, a very low serum level of AST might be indicative of a poorly functioning liver (e.g. with a chronic hepatitis).
Among veterinary species there is considerable variation in the clinical usefulness of ALT. For example, it is a very useful indicator of liver disease in dogs and cats, much less so in horses. Much like AST, ALT is also produced in liver, muscle, kidney, and erythrocytes.
Amylase is known to be produced by cells in the pancreas, salivary gland, duodenum, ileum, ovary, and testes. Of course, the pancreas produces the most of this enzyme, which is why it is somewhat clinically useful (though I can't say I like it much at least for veterinary species).
The bottom line is that these enzymes play an important role in biochemical reactions of many different tissues. While the enzymes may be produced in predominance in one tissue, they have the same function (at a biochemical level) in all these tissues (i.e. they convert the same reactions). I view it more as a difference of the tissue need for these enzymes rather than a difference in function between tissues.

Harry - I guess my question bluntly is "is there any evidence that these enzymes (like AST, ALT, amylase) are intentionally secreted from healthy, non-damaged tissues? This is what is alluded to in the JBC article, but I've never heard any evidence for this in my experience.

@Vance I'm not sure, and I couldn't find any studies that specifically track these enzymes from their source in healthy patients. But I guess the point of my answer is that, for example, healthy functioning liver tissue might by definition of its function lead to mild hepatocellular damage and thus AST/ALT leakage. I understand this isn't a completely satisfactory answer so I hope that someone can come up with some numbers for us.


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How long can an infant human hold his/her breath as part of the "dive reflex"?
Various other questions on the site have talked about the Diving Reflex, which is also known as the Mammalian Diving Reflex. This reflex is observed in mammals of various species, but also in human adults and infants. A number of studies have been done examining the diving reflex (e.g. Advances in Physiologic Education).
If you've ever observed an infant submerged in water (e.g. at a swimming pool) who has this reflex it seems so amazing because the baby will spontaneously hold his/her breath while submerged.
Are there any estimates of long an infant will hold his/her breath as part of the dive reflex?
Obviously this is dangerous to try and test this in the real world, but I'm wondering if anyone has any idea. This reflex seems so remarkable to me because unlike the adult human who knows they shouldn't breath in water, I would think that the baby doesn't know that at such a young age.

It's life threatening because water enters the stomach of infant.

@JM97 what is life threatening about water entering in the stomach? I'm not following what you're saying.

The infant will drown , and it doesn't know how to swim.

when my 3 month old son was in swimming lessons he would spontaneously hold his breath and go underneath the water just fine... actually 10-15 times in a 30-45 min time frame...and he's doing just fine - do you have a particular source that you get your information on this?

The glottis is spontaneously sealed off and the water entering the upper respiratory tract is diverted down the esophagus into the stomach.   ( https://en.m.wikipedia.org/wiki/Infant_swimming#Infant_swimming_or_diving_reflex )

@JM97 correct, but that doesn't mean the infant will drown just because some water enters the upper GI tract


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What is the proper anatomical name of the "band of Richer" that wraps around the quadriceps femoris?
There's this fascial band called the band of Richer that wraps around the quadriceps femoris muscle above the knee (in this illustration, look for it near the left knee). It seems to stem from the iliotibial tract. I could only find the term "band of Richer"/"Richer's band" from artistic anatomy sources, and it sounds like this particular fascial band is named after Paul Richer. Even though it seems to be noted in some sources meant for artists, surprisingly lots of them completely miss this very visible surface feature. In the photo next to the illustration you can clearly see parts of the vastus medialis above the knee bulges out because something is tying it tightly above.
So what is its proper name, if there's such thing? Is it simply "band of Richer"? What about its Latin name?

Suprapatellar tract (Kollmann). Yes, it does exist, but it isn't a ligament, as some illustrations in art anatomy books are trying to indicate.
The name Richer's band, is a term that emerged in art schools. Early 20th century books on Artistic Anatomy have this term imprinted as convention. You'll find it in Arthur Thompson, U. Parkes, Eugene Wolff, Faringdon Moses, and others, where the name of Richer's band is used (published before 1930). Only some of these authors have described it anatomically, but in all cases only partially. Up to the point of the appearance of Joseph Sheppard's Artistic Anatomy, this Richer's band had steadily grown into a thick and firm tendon. For the sake of art students, it has always been important to inform about this "band", since it has an effect on the exterior surface form of the thigh, which can be observed in the live model, as well as be admired in Greek sculpture of the classical period. Richer's band merely served as an explanation for this surface phenomenon in the art studio, and the term has never been used in medical books on anatomy. However, it has beed discribed in one way or another in anatomy books. Sobatta illustrated it, Julius Kollmann described it in his book, Plastische Anatomie, and so on. Kollmann calls it the suprapatellar tract. (Plastische Anatomie des menschlichen Körpers, third edition).

The reason why this thickening in the fascia of the thigh became known as "Richer's band" is because Dr. Paul Richer, collaborator and friend of the Anatomist Dr. Paul Poirier, made a clinical description of it in the last decade of the 19th century, Paris, to explain once and for all what causes the indentation in the skin covering the vastus medialis a few fingerbreadths above the kneecap.
Dr. Poirier, in the multi-volume edition of "Traité d'anatomie humaine, publié sous la direction de Paul Poirier (et A. Charpy)", in the volume on myology, illustrated mainly by Paul Richer, makes brief mention of this thickening band of the aponeurosis of the thigh, adding that he would be going back to this matter soon. In the anatomical illustrations of the lower extremity in this volume, done by Richer, this band had been meticulously added, but no further mention had been made to it in the text.
Poirier writes on page 286,
"je reviendrai plus loin sur les détails que présente cette partie antérieure de l'aponévrose fémorale, renforcée en bas par une band. arciforme (V. fig. 152)"
Translated, "I will come back later to the details of this anterior part of the femoral aponeurosis, reinforced below by an arciform band (see fig. 152)".
Poirier, who was a close friend of Richer's, it seems, had left it to Richer to coin it in his own words.
So we find in Richer's Anatomie Artistique, 1892, the following sentence,
"Il existe à trois ou quatre travers de doigt de la rotule une condensation des fibres transversales de l’aponévrose, formant un véritable faisceau ou ruban aponévrotique, que je  propose de désigner sous le nom de fibres arciformes inférieures de l’aponévrose fémorale.  (PL. 68, 70 et 71.)"
Translated, "Three or four fingerbreadths from the patella, there is a condensation of the transverse fibres of the aponeurosis, forming a real aponeurotic bundle or ribbon, which I propose to call the inferior arciform fibres of the femoral aponeurosis.  (PL. 68, 70 and 71.) "
But in Richer later book, published as an advanced course at the l'Ecole de Beaux-Arts, Nouvelle anatomie artistique du corps humain. Cours pratique et élémentaire, 1906, a more detailed description is given, which may serve as filling the gap left in Poirier's previous text.
On page 71 Richer writes,
"L'aponévrose d'enveloppe du quadriceps présente une disposition spéciale qui joue un grand rôle dans les formes extérieures de la région. (PL 24, 25, 26 et 27.)  Il existe, à trois ou quatre travers de doigt au-dessus de la rotule, une condensation des fibres transversales de l'aponévrose fémorale, formant un véritable faisceau ou ruban aponévrotique qui mérite de prendre le nom de ruban des vastes. En effet, ce ruban aponévrotique obliquement dirigé embrasse dans sa courbure l'extrémité inférieure des deux vastes, le vaste interne et le vaste externe. L'extrémité externe, épanouie en éventail, se confond avec le fascia lata, pendant que l'extrémité interne, formée de fibres plus condensées, croise le vaste interne suivant une direction perpendiculaire à celle de ses fibres charnues, à deux travers de doigt de son extrémité inférieure, passe ensuite sur la tubérosité fémorale interne et descend au-devant du couturier, avec le tendon duquel ses fibres s'entre-croisent à angle aigu.  Aux points où ce faisceau rencontre les cloisons aponévrotiques intermusculaires interne et externe, des fibres se détachent de sa face profonde qui descendent le long de ces cloisons pour aller s'insérer avec elles aux divisions inférieures de la ligne âpre. De sorte qu\in véritable anneau ostéôfibreux se trouve ainsi constitué, anneau disposé dans un plan transversal et incliné de haut en bas et de dehors en dedans, et enserrant étroitement toute la partie inférieure du muscle triceps."
Translated, "The envelope aponeurosis of the quadriceps has a special arrangement which plays a major role in the external shape of the region. (PL 24, 25, 26 and 27.) Three or four fingerbreadths above the patella, there is a condensation of the transverse fibres of the femoral aponeurosis, forming a veritable bundle or aponeurotic ribbon which deserves to be called the ribbon of the vastus. In fact, this obliquely directed aponeurotic ribbon embraces in its curvature the lower extremity of the two vastus medialis and the vastus lateralis. The outer end, spread out like a fan, merges with the fascia lata, while the inner end, formed of more condensed fibres, crosses the vastus medialis in a direction perpendicular to that of its fleshy fibres, two fingerbreadths from its lower end, then passes over the medial femoral tuberosity and descends in front of the sartorius, with the tendon of which its fibres cross at an acute angle.  At the points where this bundle meets the internal and external intermuscular aponeurotic partitions, fibres detach from its deep surface and descend along these partitions to be inserted with them in the lower divisions of the linea aspera. In this way, a veritable osteofibrous ring is formed, arranged in a transverse plane and inclined from top to bottom and from outside to inside, tightly enclosing the entire lower part of the triceps muscle."
Thus was born, the band of Richer.

I woud like to add on a personal note, that I chatted with a retired surgeon from Germany regarding the suprapattelar tract. I said that I was glad to see it being mentioned by Kollmann, although it is a rarity that presents more interest to painters and sculptors that to the medical profession. He reassured me however, that since the knee joint is a particularly difficult joint in surgery the suprapattelar region mentioned by Kollmann is well known by medical professionals since special attention is required in this region during operations. I therefore refute the previous answer given by kmm

There is no such ligamentous or connective tissue structure as depicted in the linked image. This is a visual artifact created by the border of the vastus medialis or just a fanciful artistic interpretation. Based on 25 years of teaching human anatomy, I suspect the latter, because the artist's image shows this band much more proximal than the distal extent of the vastus muscles.

Here is a link to a photo of a dissection of this region that shows no structure there.
Indeed, Gray's Anatomy's list of eponymous structures does not list it:

There is actually quite a lot wrong with that drawing. The rectus abdominis extends too far superiorly, which really shortens the thorax.

So what do you think is causing the vastus medialis to bulge out? I know this is a very old source, but I learned about this Richer's band from a very modern anatomy course, with very modern photographic evidence. This band behaves very similarly to the extra tendon from the biceps brachii that wraps around the hand flexors, causing them to bulge out. And this is not the only source either, in Paul Richer's Artistic Anatomy (Anatomie Artistique), it's also mentioned in diagram in passing, strangely enough, as "Richer's band".

Also I'm not quite sure what you mean by "the rectus abdominis extends too far superiorly, which really shortens the thorax". I think if you overlay the diagram onto the photo it's not even that far off, the measurement seems to line up well. Doesn't the rectus abdominis extend all the way to the fifth or even fourth pair of ribs, right above the bottom of the gladiolus, as the diagram depicts?

It's just the distal extent of the muscle as it grades into the quadriceps tendon. The muscle can hypertrophy with exercise, but the tendon won't, so it gives the appearance of a band. I have dissected easily 400 lower limbs and have never seen anything like this. There is no retinaculum-like structure (which is what think you are describing) at that position in the lower limb.


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Is the human iris concave or convex?
Most drawing and 3D modeling tutorials show the iris to be concave. But all the diagrams I Googled show the iris is at best flat, otherwise even a little convex (discounting the optical distortion in photographs). So is it concave or convex?
Edit: Just to be clear, the question only concerns the concavity of the iris. The reason I mention drawing and 3D modeling here is that because it's such a common practice to make the iris explicitly concave in a somewhat exaggerated way, which is at odds with countless profile diagrams of the eye that I could google.
For example, this video (at about 5:52) even says that "it is convex according to anatomical diagrams, but I like to draw it as if it is concave". Or in this video (at about 7:46), the modeler pushed the concavity of the iris quite far, it's like a deep indent.

I'm not sure I understand the question. When I searched for diagrams of the iris, I usually saw cuts of the eye in the medial plane. The few ones which showed a frontal view of the eye showed the iris as a regular circle. You presumably draw eyes from a frontal viewpoint, which also tends to show a circular iris. So where is the discrepancy? Can you post an image from a tutorial with a concave iris and a diagram with a convex iris?

I didn't really say anything about at which angle I'd draw the iris, because it's not very relevant. I said "most drawing and 3d modeling tutorial show the iris to be concave", meaning that regardless of the view angle or the viewpoint, you'll always have to take into account that it is concave. Thus, when you draw, even in front view, remember to to shade as if it is concave; when you model an eyeball, don't forget to make it concave.

An iris is three-dimensional. A drawing is two-dimensional, so it represents a cut through the three-dimensional object. For many three-dimensional objects, some cuts are concave and others are convex within the plane of the cut. So it makes the question clearer to explain in which plane you are looking for convexity or concavity.

@rumtscho By "concave" and "convex" I simply mean the general tendency, nothing too deep into the weeds of whether some cuts of it could be concave and others are convex. All I care about is whether the iris tends to poke forward toward the cornea ("convex") or recede backward away from it ("concave"), and all that seems to have been easily understood by the answerer below. We could argue all day about how 3D objects manifest in space, but I think the general idea of the question is clear enough.

Thank you! I came up with several different definitions of "convex" and "concave" that would be consistent with your question, and didn't know which is the right one. Funnily enough, it turns out none was the one you had in mind - the explanation of poke forward to the cornea/recede backward is exactly what I was missing.

Iris curvature seems to be dependent on the state and health of the eyes.
See Prevention of blinking alters iris configuration in pigment dispersion syndrome and in normal eyes :

Initial iris configuration was concave in all eyes with pigment dispersion syndrome, whereas in control eyes it was concave in four eyes, planar in four eyes, and convex in two eyes.

Other resources :
Accommodation-induced changes in iris curvature
Ultrasound biomicroscopic analysis of iris profile changes with accommodation in pigmentary glaucoma and relationship to age
Quantification of Iris Concavity

Nice answer! +1

It seems they can be all three of them. Convex, concave or flat.
Was wondering the same thing and ran some searches on google to come across this:

I find it more convincing to have it concave in my artistic preference.
Ref.>
https://www.aao.org/disease-review/gonioscopic-grading-systems

Welcome to Biology.SE. Please take the [tour] and consult the [help] pages for advice on [answer] and [ask] effectively on this site. In particular, please do not post text as images. Copy and paste the text into your question. Images are not searchable, and can not be interpreted by screen readers for those with visual impairments. Use the [edit] link to modify your question. See this for more information. In addition, this seems to duplicate an already existing and better answer — your time could be better used on unanswered questions.


text:
RFLP Pedigree question
A relatively frequent, completely penetrant recessive disease variety of mutations in the gene. The gene has been recently cloned. Analysis of the region flanking the gene reveals that the population has at three (3) RFLP (this is a type of DNA marker; they are not SNPs so have much larger sizes) alleles in this region. The sizes of the RFLP alleles are 7, 10 or 13 kb in length. Shown here are two small pedigrees of families in which affected individuals are shaded in black. The size of the RFLP alleles each individual carries is shown below the pedigree. enter image description here

Question: If the male child from the left pedigree marries the female child from the right pedigree, What is the probability their child will be a carrier?
I said that there isn't enough information to tell since the parents genotypes are unknown.

I said that there isn't enough information to tell since the parents genotypes are unknown.

It seems like you are misreading the diagrams since you say the parent's genotypes are unknown.  All 8 individuals in the two pedigrees have the same information given for each, appearing in the eight columns directly beneath the eight individual's symbols.


text:
Are there any solid inorganic compounds that are part of the human body?
I'm more interested in parts physically attached to the body, if that makes sense.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, your question doesn't seem to make sense as currently written — the title is asking about solids, but your examples are liquids. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

bone and teeth are calcium phosphate.

@tyersome Sorry, I corrected the error.

@John Thanks. I'm surprised I did not think of that

Calcium carbonate stones in the utricle and saccule of the vestibular system are pretty interesting (I think they could be what you're looking for).  They are part of the response to acceleration; if they're messed up, you can get vertigo.

Neat! That works just fine, thanks


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Biophysically, how to change from a tonically firing neuron to an occasionally firing one?
In terms of membrane properties, size and neuronal biophysics (assuming no change in incoming excitation), how can a tonically firing neuron become (say during development) an occasionally bursting neuron?
Any references would be appreciated.


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How likely will 2 normal bacteria "attack" each other if they infect the same parts of your body?
I read this interesting article online about how deadly bacteria are known to attack other deadly strains of bacteria.
https://www.google.com.sg/amp/s/phys.org/news/2013-02-deadly-bacteria-remarkable-precision.amp
I am wondering how normal bacteria that infect us like those that cause strep  throat and so on also have the capabilities to attack other bacteria and how feasible it is to use this as a treatment for bacteria infections by introducing harmless strains od bacteria to fight pathogenic versions (maybe like probiotics?)

Mixed bacterial populations, where not engaged in some kind of mutual or commensalistic relationship, are constantly at each others throats over resources. Even then, sometimes it's just rate of growth isn't terribly bad for each commensal. Not just nutrients, for example, but also precious space to colonize or attach to. There's a good review here, and among some of the tactics direct killing by antimicrobial production is an option. You also have other factors, however, such as secretion of molecules that impair attachment or quorum sensing. Also, virulence factors that give a competitive edge such as evading immunosurveillance (encapsulated B. anthracis strains vs unencapsulated, for example).
So here's the hard part: you want to engineer an attenuated bacterium that goes in and attacks a pathogenic strain. While I'm sure possible, you would certainly need to ensure that what you take away to attenuate your strain doesn't gimp it in vivo. You also need to realize that your target pathogen is very capable of simply "changing" itself to avoid dying to the engineered strain. Once your mechanism of action has been defeated, your product has been defeated. I think that it's fundamentally different from commercial virus-based products like T-VEC, as well, due to the level of variability.
One of my thoughts is your strain needs to be able to compete with the pathogen in the first place to stand a chance, which may be difficult if you cut out too many virulence factors trying to make it "safe."


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Can fish live in the dark completely?
I have got 6 pet fishes in an algae ridden  tank.  My plan is to place the tank completely away from sunlight so the algae dies.  How would this affect my fish?
Edit: Just checked all my fishes died today.  Either its the lack of light or just that i forgot to add the chlorine removal or water pump.

@Remi.b why would it be?  I just want to kill the algea not the fish

@Remi.b I don't disagree that this sounds ill-advised, but I am also curious what would make it actually illegal.

Probably depends on the kind of fish: there are some fish that live in the ocean depths, or in caves.  You might also ask whether the darkness would actually kill the algae, or just make it go dormant until the tank is placed in the light again.

Why not just get some snails to eat the algae?

Or clean the tank once in a while?

What kind of fish were they? Was there algal bloom?

Excessive algal bloom is normally because of sunlight and lots of iron/phosphate/chalk/ micronutrients in the water: tapwater that causes limescale... I lived in a house where the water caused massive algal blooms out of control. if you switch to rainwater on the contrary it keeps the water transparent for a long time. Try goldfish first. they are very tough. I had dead fish when i was young and later i kept puffer fish and exotic fish very easily by not keeping the aquarium like a child.

all you have to do to keep the water good in difficult times, is change half of the water and clean the water pump. dont use tap water unless it is very soft water (no limescale). the solution is to use good water, not to put your fish in the dark until the algea dies. and don't use anti-chlorine, use natural water which didn't have industrial treatments.

As noted fish live in the dark , to the extent that they no longer have eyes.As noted the algae will just go dormant until there is light. I use plants to compete with the algae for nutrients , works well. Algaecide is not a long term solution. I expect you could find some lights which have very little output in the frequencies/ spectrum needed by chlorophyll ( and block any sunlight) but you still have light to see the fish.

There are lots of fish that live in environments without any light (below 1000m in the ocean there is no useful light for vision), however most aquarium fish have not evolved to live in those sorts of conditions. In the future, I think your best bet would be to remove the fish, clean the tank, and then try to manage your nutrient inputs so that the algae doesn't grow out of control.

Fish can live in the dark completely however they will potentially have no source of food at most Algae cannot reproduce without sunlight.
Some new research has been conducted where algae can gain energy from other means apart from the sunlight including dim light from hydrothermal vents deep in the ocean. https://indianapublicmedia.org/amomentofscience/photosynthesis-without-sunlight/


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Sexual reproduction in organisms with 1 parent
An organism that carries out sexual reproduction with itself,  for example a flower with both the anther and stigma,  does it actually contain 2 sets of genes in order to produce genetically dissimilar organisms or do it just leave the offspring to become genetically dissimilar through random crossing over during miosis?

Your second piece is correct: dissimilarity is produced through meiosis.
from The evolution of meiotic sex and its alternatives

Strikingly, almost all forms of uniparental reproduction do maintain
  meiosis, but abandon just outcrossing. Hence, the paradox of sex in
  eukaryotes must focus on the purpose of meiosis.

What do you mean by abondoning outcrossing?


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Use of progesterone in preventing ovulation?
I have heard that progesterone in contraceptive pills or interuterine devices have been known to prevent ovulation. How is this possible since the LH and FSH are only affected by oestrogen not progesterone (am i wrong?)  Also,  my textbook says hormonal intrauterine devices contain progesterone to lessen uterine lining but doesnt the uterine get maintained by progesterone ?
Edit : I have yet to receive a satisfactory answer... Help anyone?

I'm voting to close as homework because explanations on how progesterone pills work are freely available from many sources, and as such it doesn't seem like this answer was very well researched.

@BryanKrause I have already done research on contraceptove pills but could not find any website specifically explaining how progesterone inhibits pregnancy

Did you try wikipedia?

When progesterone alone is used as a contraceptive it is assumed that the oestrogen level is endogenously maintained by the follicular cells.

Yes mainly oestrogen and only little does progesterone inhibits LH or FSH secretion.
LH surge is the principle stimulator of ovulation.

However,experimental work has suggested that immediately before the LH surge occurs, there is probably a sudden depression of estrogen...and this might be ...that leads to LH surge
  [source: Textbook of medical physiology A South Asian Edition- Guyton & Hall]

If progesterone or progesterone-oestrogen combinations be given before ovulation then feed back inhibition of LH surge occurs.This would lead to contraception by anovulation.

Progesterone is only known to proliferate the endometrial lining.

However, administration of progesterone or oestrogen -progesterone combinations after ovulatory phase helps to achieve high concentration of these hormones ,much before the normal time required to attain peak levels due to endogenous secretions alone.
This helps to depress the FSH -LH secretion by feedback inhibition very quickly causing involution of the corpus luteum and early shedding of the endometrium termed as breakthrough bleeding
REFERENCE:

reference site
Textbook of Medical Physiology A South Asian Edition-Guyton & Hall

This might and must be known to you that progesterone is known as the pregnancy hormones as it maintains the endometrial lining to Slough off  the  baby along with the corpus luteum (strata functionalis) and thus maintaining the pregnancy   and as far as the contraceptive pills and IUDs' are concerned they contain PROGESTIN i.e synthetic progesterone which inhibits LH production and hence anovulation  which is a type of we can say contraception  (prevention ) from pregnancy ;)÷

This answer needs citations and editing for English usage/grammar; there are randomly capitalized words, very unclear wording leading to incorrect statements, etc. It doesn't meet the standards of an answer on Biology.SE.


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How do Rab proteins ensure specificity in vesicle transport?
From this paragraph, from Molecular Biology of the Cell 6th Edition, the author makes it quite clear that Rab proteins are important for the specificity of vesicle transport and that Rab proteins are used as molecular markers that identify compartments. They also make it clear that for many membrane fusion events active Rab proteins are required on both sides of the reaction. What is not clear to me is how Rab proteins ensure specificity?
The author is not clear on how Rab proteins ensure specificity. The only way I can imagine this happening is that Rab proteins on the target membrane recognise Rab proteins or other molecular markers on the vesicle and only bind to appropriate markers, but the author does not clearly state this in the text.

Specificity in targeting is ensured because all transport vesicles display surface markers that identify them according to their origin and type of cargo, and target membranes display complementary receptors that recognize the appropriate markers.

What 'surface markers' and 'complementary receptors' is the author talking about here? Due to the position of the sentence in the paragraph below I'm inclined to think they are talking about Rab proteins and SNAREs.

To ensure an orderly flow of vesicle traffic, transport vesicles must be highly accurate in recognizing the correct target membrane with which to fuse. Because of the diversity and crowding of membrane systems in the cytoplasm, a vesicle is likely to encounter many potential target membranes before it finds the correct one. Specificity in targeting is ensured because all transport vesicles display surface markers that identify them according to their origin and type of cargo, and target membranes display complementary receptors that recognize the appropriate markers. This crucial process occurs in two steps. First, Rab proteins and Rab effectors direct the vesicle to specific spots on the correct target membrane. Second, SNARE proteins and SNARE regulators mediate the fusion of the lipid bilayers. Rab proteins play a central part in the specificity of vesicle transport. Like the coat-recruitment GTPases discussed earlier, Rab proteins are also monomeric GTPases. With over 60 known members, the Rab subfamily is the largest of the monomeric GTPase subfamilies. Each Rab protein is associated with one or more membrane-enclosed organelles of the secretory or endocytic path- ways, and each of these organelles has at least one Rab protein on its cytosolic surface. Their highly selective distribution on these membrane systems makes Rab proteins ideal molecular markers for identifying each membrane type and guiding vesicle traffic between them. Rab proteins can function on transport vesicles, on target membranes, or both.
Like the coat-recruitment GTPases, Rab proteins cycle between a membrane and the cytosol and regulate the reversible assembly of protein complexes on the membrane. In their GDP-bound state, they are inactive and bound to another protein (Rab-GDP dissociation inhibitor, or GDI) that keeps them soluble in the cytosol; in their GTP-bound state, they are active and tightly associated with the membrane of an organelle or transport vesicle. Membrane-bound Rab-GEFs activate Rab proteins on both transport vesicle and target membranes; for some membrane fusion events, activated Rab molecules are required on both sides of the reaction.

I read this article and it states that;

For its functions, active Rab5 must be localized to both endocytic vesicles and early endosomes.

In this case I can understand how Rab proteins ensure specificity in that Rab5 on the target membrane will only interact with an endocytic vesicle if it has Rab5 on its surface. But is this always the case? Will Rabs on a membrane always require certain Rabs or other molecules on the surface of a vesicle in order to tether and dock the vesicle? If not I can't see how they are providing specificity to transport.

This is a very long question. I appreciate that you have done your research on this, but not perhaps in human psychology: next to nobody will make the effort to read it. Whatever background you wish to provide, you need to start with a clear and precise statement of your problem. If you can’t do that, forget it.

My previous question was deleted for not being long enough. The question is quite simple really. How do Rab proteins ensure specificity in vesicle transport? Will the effectors of certain Rab proteins only interact with specific other Rab proteins?


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How long could Jack Sparrow and Will Turner survive underwater with a row boat over their heads (Pirates of the Caribbean I)?
How long could Jack Sparrow and Will Turner survive underwater with a row boat over their heads (Pirates of the Caribbean I)?
This scene would be physically infeasible due to buoyancy issues (http://kwc.org/mythbusters/2007/11/episode_92_pirates_2_row_boat.html). One may try to solve this by loading the boat itself with some heavy weights.

Here, the question is about the physiological feasibility - how long they can last with the air in that row boat. The question occurred to me because I have seen people in forumns claiming 2 people could not have made that journey with the air present in that space. But I don't think this is an issue.

+1 2 people downvoted your post without any reason and your question is fine and I think it is very interesting.

This is my attempted solution that I would like to share and verify.

Volume of air.
Assume dimensions of the boat (modeled a cuboid) = 4m x 1m x 0.5m
Thus Volume of air, V = 2 m3.

Acceptable limits of air composition
Carbon dioxide (CO2) poisoning will happen far before there is any risk of running out of oxygen (O2).
Referring to https://en.wikipedia.org/wiki/Carbon_dioxide#Toxicity & https://en.wikipedia.org/wiki/Hypercapnia#Tolerance, I am taking up to 5% concentration of CO2 as acceptable for the duration of the underwater walk.

Actual air composition calculation
3.1. Initial air composition (https://en.wikipedia.org/wiki/Atmospheric_chemistry#Atmospheric_composition):

O2 (initial) = 21%
CO2 (initial) = 0.04% (or 400 ppm)

Thus, for 2 m3 of air (= 2000 L),

O2 (initial) = 420 L
CO2 (initial) = 0.8 L

3.2. Final air composition (Based on acceptable limits above, final concentration of CO2 = 5%). Thus:

O2 (final) = 16%
CO2 (final) = 5%

Thus, for 2 m3 of air (= 2000 L),

O2 (initial) = 320 L
CO2 (initial) = 100 L

Thus, we have time until the 2 people (Jack and Will) have exhaled 100 L of CO2.
3.3. Time taken to exhale 100 L of CO2 (by 1 person).
Composition of exhaled air (https://en.wikipedia.org/wiki/Breathing#Composition):

O2 (exhaled breath) = 17%
CO2 (exhaled breath) = 4%

Volume of exhaled air per breath (https://en.wikipedia.org/wiki/Breathing#Gas_exchange) = 350 mL.
Thus:

O2 (exhaled breath) = 17% of 350 mL = 59.5%
CO2 (exhaled breath) = 4% of 350 mL = 14 mL

Thus, Volume of exhaled CO2 per breath = 14 mL
Assuming 15 breaths per minute,
=> Volume of exhaled air per minute = 15 * 14 mL = 210 mL
=> CO2 exhalation rate = 210 mL / minute
Thus time taken to exhale 100 L of CO2 (by 1 person) = (100 L) / (210 mL / minute)
= (100 * 1000 mL) / (210 mL / minute) = 476 minutes.
=> time taken to exhale 100 L of CO2 by 2 people = 476 / 2 minutes = 238 minutes ~ 4 hours.

Thus, Jack and Will will be able to last 4 hours breathing from that air under the row boat before the air concentration of CO2 reaches 5% (and O2 reaches 16%).

You've not taken into account that the CO2 dissolves in the water, the surface area of the water, the rate of dissolution. Also... maybe additional O2 from the water? (I'd need to check that). That would need to be balanced-out against extra metabolic and muscular use of oxygen from the effort expended.. Just a thought.

@ARogueAnt. As long as the pO2 is different in the water and the air there will be a net diffusion between them. pO2 of the water will be roughly equivalent to atmospheric pO2 at the surface, where air and water are mixed.

Glad you took the time to answer your own question. It's a well-laid out answer. Good job! I agree with the previous comment about CO2 (though I'm less convinced the oxygen pressures will make a big enough difference to matter). Anyway, the reason for my comment is that I wanted to additionally point out that 15 breaths/min might be reasonable while at rest, but these two individuals would likely be breathing faster (i.e., producing more CO2 per minute) given their activity. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4818249/ suggests 40-60 breaths/min is more normal during exercise.


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When did humans or their ancestors gain the instinct to take shelter?
I was going to ask if seeking shelter in a constructure dwelling or natural formation was instinctive to modern humans or if it is a learned sociatal behaviour.  By shelter I mean seek routine issolation from elements by being "inside" some structure or formation that encloses the individual or group on multiple sides and above.  A small shelter would be expected to trigger Claustrophobia and being outside of a shelter would be expected to trigger Agoraphobia in people that experiance such conditions.
It was highlighted that "nest building" is considered a part of a shelter instinct.  I am looking for when this behaviour develops not just during child rearing (as many birds do) but routinely (as great apes do with bedding).  Unlike forming a bed in an open space it seems common place for modern humans to form their beds inside a shelter and to choose to perform many other actions in this shelter such as eating.
Perhapse the first part of that should be to ask if there are any current or recent groups of poeple that do-not routinely occupy a shelter?
Many nomadic peoples seem to go to the trouble of transporting shelter with them but perhapse some do not if there is not an environmental driver to do so.
Not knowing where to look I did some searching and found a couple of websites that dicuss human instincts but not all of them list sheltering as instinctive so perhapse that is still debatable?
Herding but not sheltering is mentioned on Wikipedia.  Shelter is mention in this Harvard Business Review article about How Hardwired Is Human Behavior? but it seems that we could learn to shelter driven by other instincts.  This website was one of the more prominant ones to list seeking shelter as instinctive but I would not call it a reliable source.
Following on from that would be the harder question of when did the instict to shelter first evolve in humans or an ancestory of humans if it is instinctive?
I am not looking for a calendar date but whether there is some point in the ancestry where it is possible to say these early humans did prefer indoors and these ones did not.  We often hear about finds being located in caves which suggests those humans were sheltering in the cave.  I would accept those as signs of habbitation inside a shelter.
It seems obvious that other mamals like Rabbits and Foxes instinctivey live in burrows or dens either perminantly or following a "Nesting Instinct" but it is not so clear for humans it seems.  I could find more references to humans having a "Nesting Instinct" so perhapse that is where the instinct began or maybe it is the limit of it in humans.  There are examples of nesting or sheltering in fish speacies to so it is clearly something that develops multiple times in evoluionary processes, unless the Nesting Instinct is common all the way back to some aquatic species long ago for our line.
Sorry this is a bit rambling and not well resurched.  I have no background in biology, sociology or the study of human evolution so I am a bit stumped as to where I would begin to look for an answer.
I did look into the H2DB from a suggested similar question but noting in there seemed obviously linked to shelter to me besides "conditioned place preference (CPP)" & "housekeeping ability".  Housekeeping being a predominantly female trait could suggest a genetic factor in shelter, possibly from earlier "nesting" instincts?  Although I would have thought both male and female might have some protection of mate & young instincts beyond those for our habbit of forming herds or family groups.

Why must seeking shelter have evolved in humans? As you note, mammals (and other vertebrates) routinely seek shelter. So humans likely do this because they inherited it from their ancestors.

@kmm I am unsure how how to correctly ask about humans or their earliest known ancestors.  AFAIK there are no modern day relatives that do more than make a bed so it seems to be something specific to our line.  Could you suggest how I best rephrase the question in a way that would widely be understood to include everything running up to a "modern day human" in our genetic lineage?

Nest-building, which you are arguing is no more than making a bed, is considered part of shelter behavior (and therefore all great apes shelter). Either you're going to need to be much more specific on what "shelter" means, or, more likely, you'll have to recognize that pretty much every evolved trait, including behaviors and even those that are encoded culturally rather than genetically, occurs gradually, so there is no way to put a date on such a thing.

@BryanKrause I have tried to improve my question to make clear that by "shelter" I mean some kind of "indoors" instead of "outside".  We find remains of ancestors in caves which suggests to me sheltering indoors of a kind.  If there are certain ancestors that are only found outside of caves that would be an indicator of when to me. Not concrete as we only get small numbers of finds but it would be a start.


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gene inversion and DNA directionality
The directionality of the DNA goes from the 3-prime end to the 5-prime end.
Thus, the inversion of a gene would connect a 5-prime to a 5-prime. How could that be?
Maybe inverting a gene also switches between the two strands of the DNA?
Thus, if one stand goes from 5 to 3, and the other goes from 3 to 5,
Inversion would make the first go from 3 to 5, and the other from 5 to 3,
And then each strand would be able to connect to the other?
Does inversion both changes direction, and switches stands?
If not, then how is gene inversion possible?
Thanks!
edit:
My main question arises from the contradiction between:
1) The DNA has a direction (3-prime to 5-prime).
2) inversion inverts the direction.
Thus, my question is: How can an inversion mutation happen?
How can a piece of the DNA, after being inverted (i.e., it is now in the wrong direction), connect back to the DNA?

Hello and welcome at Biology SE! can you please clarify your question? It might be only me but it's hard for me to figure out what do you mean by inversion and 'different strands go from'. You also have multiple questions can you please narrow it down

Thank you!
I updated my question to narrow it down to the main thing that bothers me.

Draw yourself a sample gene of say 10 base pairs marking 5’ and 3’ ends of the strands. Invert it — voila! Hint — I wrote base pairs and strands.

As you know, chromosomal DNA has two strands, with each strand running in opposite 5' <-> 3' directions.  When a chromosomal segment is inverted, both the 5'->3' sequence and its complementary 3'->5' sequence from the other strand are inverted together.  When reattached to the two strands it came from, the segment will have effectively switched its orientation on both strands by switching strands.  This happens exactly because a 5' end must mate with a 3' end.  This diagram should help make this clear (although it shows a duplication with inversion instead of an inversion in place):

Source: Wikipedia Commons

Awesome! Thank you!