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.

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 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!

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.


text:
What is/are the molecular differences between HDL and LDL cholesterol?
Why exactly is HDL-cholesterol good for us and LDL-cholesterol bad for us. It has been well-established that LDL-cholesterol is associated with atherosclerosis and that HDL-cholesterol helps remove excess LDL-cholesterol from the circulation. From a biochemical view, however, what is the difference between the molecules that causes this difference?

I would like to just leave this as a comment, but don't have enough reputation to do that. If you want an extremely thorough treatment of cholesterol and lipoproteins with tons of references, you should check out Peter Attia's fantastic set of 9 blog posts on the subject starting here.

First of all, we should specify that there is no such thing as "HDL-cholesterols" and "LDL-cholesterols". On the same note there is no such thing as "good cholesterol" and "bad cholesterol": cholesterol is just one molecule, with this chemical structure

What blood tests generally report is HDL-C and LDL-C, that is the amount of cholesterol in HDL or LDL respectively (again, cholesterol is always the same molecule, whether in an HDL or in an LDL).
HDL (high density lipoprotein) and LDL (low density lipoprotein) are lipoproteins, aggregates of proteins and lipids that can carry, amongst other things cholesterol.
There are 5 major types of lipoproteins, called chylomicrons, VLDL, IDL, LDL, and HDL and are distinguished by their size, density and the proteins they are composed of.
The main function of lipoproteins is that of carrying lipids (=fats) around the organism in the blood. The problem is that lipids are not soluble in water (try to pour some oil in a glass of water) and blood is mainly composed of water. Lipoproteins, on the other hand, have a hydrophilic (="water-loving") exterior and a lipophilic (="fat-loving") interior, like this:

In the picture, the "balls" represent proteins, called apoproteins, and the C represent cholesterol and T tryglicerids, which are both lipids.
As you can see, all the fats are inside the lipoprotein, but the exterior, being soluble in water can be easily dissolved in the blood.
The biochemistry of lipoproteins is quite involved and I will not go into details here (but please leave a comment if you want further explanations) but, to simplify things:

HDL bring lipids from the periphery back to the liver
LDL bring lipids from the liver to the periphery

It is very important, at this point, to note that lipids are a physiologically important part of our organisms. All the cells in our body contain lipids: the membrane of each cell in the body is made up of lipids (called phospholipids) and also contain cholesterol. In fact, cholesterol is extremely important for the correct functioning of the body as, for instance, it is used as the base to make many hormones (the so-called steroid hormones, such as estrogen, progesterone, cortisol, testosterone etc).
However, too high levels of lipids, particularly cholesterol, are not beneficial, as high cholesterol levels have been in fact linked to many cardiovascular diseases, which we hear a lot about these days.
So, because HDL tend to remove the lipids from the circulation and bring them back to the liver they can be considered as some sort of "cleaners", that remove excess cholesterol from circulation.

+1 for noting that there isn't a molecular difference.

Better answer than I could have ever hoped for!

Just to add that associations of high cholesterol with CVD are still not clearly established and probably never will be, as there is also good evidence against. This doesn't diminish that high fat diets (= probably more calories than you need) will lead to overweight with all associated risks.

@rwst: surely, I have simplified a lot the problem, I do not know the literature about CVD well enough to put appropriate refs., but if you do, please feel free to add another answer, I wasn't trying to be exaustive!!

I feel unsure about liver cells taking back LDL and/or IDL as well. In that sense LDL/IDL should be differentiated from "HDL tend"(ing) "to remove the lipids from the circulation and bring them back to the liver." If you ever get back to your answer  - I'd be interested in removal of LDL as/in the form of IDL or even VLDL by the liver.

Your question is about the molecular differences between LDL and HDL.
The  way you formulate, asking about differences on the molecular level,  draws the attention to the surprising fact that the molecular structure is not that different as the big differences in physiological function may make you assume. Your question is valid, as textbooks list different contents of cholesterol, triglycerides and proteins, but do not elaborate on differences in structure of - for instance - "molecular markers of LDL". Similar to different classes of antibodies (IgM, IgG, IgA...) there seems to be a very similar structure to all transporter lipoproteins.
Conversely, to illustrate, the word "chylomicrons" may mislead to thinking of those as "micelles" or being very distinct from those  lipoproteins termed  HDL, LDL,IDL and VLDL. However, they also belong to the class of lipoproteins the function of which is transport of lipids, and they are more similar in molecular structure as labeling suggests.
Interestingly, a similar question on Stackexchange Chemics has been refered to your question. That might illustrate the above: any relevant differences do not relate either to the load of the lipoproteins or to their differences in coating or core proteins (that exist), but any difference is in biology that,ironically, very much corresponds to "labeling": which lipoprotein in contrast to the other derives from which organ, which one addresses and unloads at which kind of target cells.
To sum up: differences are neither differences in load nor coat but are differences in send and receive signalling which are differences, as it turns out, of apolipoproteins.
Thus, the ligand on LDL to
"LDL-receptor"
is key difference "literally",
which is remarkably reflected by the fact that the LDL-ligand on LDL-molecules is the biggest protein known, called
Apo B-100.
Anwswering your question: it is expression of Apo B-100 protein, that distinguishes LDL from HDL on the molecular level in respect of pathogenicity.
Conversely, the apoA-I protein may be considered distinguishing feature of HDL (see, for instance,  quote down below, Verghese et al.)
What's more, and may come to a surprise, is the fact that there is no one and the same HDL or LDL molecule, both terms denote classes of proteins; it seems that no single "LDL-cholsterol" is like any other "LDL-cholesterol". See, for instance, Kontush et al.,2014 Structure of HDL: Particle Subclasses and Molecular Components.
Relevant feature of those proteins are their receptor ligand proteins.
LDL-receptor downregulation is the key cause of  atherosclerosis (No known other detrimental effects of cholesterol).
From Nobelprize.org
"Brown and Goldstein have discovered that the underlying mechanism to the severe hereditary familial hypercholesterolemia is a complete, or partial, lack of functional LDL-receptors. In normal individuals the uptake of dietary cholesterol inhibits the cells own synthesis of cholesterol. As a consequence the number of LDL-receptors on the cell surface is reduced. This leads to increased levels of cholesterol in the blood which subsequently may accumulate in the wall of arteries causing atherosclerosis and eventually a heart attack or a stroke."
Note that hereditary disorder is not the only cause for LDL-R downregulation: "LDL receptors are downregulated by increased cellular cholesterol to prevent sterol engorgement, which is a characteristic of cells in atherosclerotic lesions." From: Biochemistry of Lipids, Lipoproteins and Membranes (Sixth Edition), 2016
The way you put your question draws attention to the fact that there is no corresponding downregulation of HDL-receptor.
Search on Wikipedia for "HDL-receptor" results in: "The page "HDL-receptor" does not exist." Presumably, no trivial knowledge that Nobel prize laureates Goldstein and Brown discovered  a whole family of so called "scavenger receptors".
What would happen if the HDL-receptors was downregulated (to  compare  with LDL downregulation)?
The "molecular difference" seems surprisingly unclear then: both HDL and LDL do carry cholesterol (It is  the very same molecule in both HDL and LDL). If too much LDL leads to depositon of cholesterol, same deposition might be made  by ("too much") HDL - your question is valid in that respect.  Downregulation of receptor distinguishes LDL from HDL.
There is one answer to a related question on Stackexchange that seems to exactly fit, in regard of the distinguishing role of Apo B100, quote: "Because LDL contains only the ApoB protein, it is less easily recognized. Thus, more LDL lingers in the blood.", with further reference about the pathological effects. If any  (distinguishing) molecular mechanism other than Apo-protein-signalling presumably protecting transported lipids from oxidation or degradation existed, it would had been mentioned.  Apo-B100 makes the difference.
The essential molecular feature of LDLs is the  LDL-receptor-ligand Apo B-100 which binds to LDL-receptors (on cells of adipose tissue) in contrast to HDL-receptor-ligand to HDL-receptor (on liver cells, surprisingly, however, not only on liver cells) - the latter known as "scavenger receptor class B type I"
which is  barely mentioned in  Wikipedia  (not having done intensive searching, admittingly:  there should  not be found in literature any discussion or even mentioning on  downregulation causing common disease, cp.Rigotti et al., 1997, A targeted mutation in the murine gene encoding the high density lipoprotein (HDL) receptor scavenger receptor class B type I reveals its key role in HDL metabolism: "(...) hepatic overexpression dramatically lowers plasma HDL." - wheras  only the  knock out experiment this paper is about is  cause for downregulation. Presumably, there is no downregulation of HDL receptor that would correspond to LDL-receptor downregulation.
On Apo B-100 as distinctive molecular marker see, for instance, Encyclopedia Britannica:
"LDL contains a single apoprotein and is the principal carrier of cholesterol to the peripheral tissue as both the free sterol and esters. The discharge of the lipid contents of this complex requires the recognition of the LDL B-100 apoprotein by a receptor located on the surface of recipient cells. When the protein is bound to the receptor, the receptor-LDL complex is engulfed by the cell in a process known as endocytosis. The endocytosed LDL discharges its contents within the cell, and B-100 is degraded to free amino acids that are used to synthesize new proteins or are metabolized as an energy source. The elucidation of the process of cellular uptake of LDL by Michael Brown and Joseph Goldstein earned them the Nobel Prize for Physiology or Medicine in 1985."
There is one more aspect to your question in the context of this answer.
The term "scavenger" (for HDL, not LDL) hints to the fact   that another difference between HDL and LDL lies in   LDL being degraded in lysosomes after uptake (by adipose tissue cells), whereas HDL is being recycled after  "touch down" on  HDL-receptor, i.e. not even uptaken by liver cells.  Please let me add this tentative thought: Thus, as there seems to be no "feedback" loop for LDL; the liver producing LDL (which start as so called VLDL, by the way) might not downregulate LDL-synthesis if target tissue downregulates LDL-receptors.
You may  skip the following further tentative thoughts of mine:
According to Voet et al, Biochemistry, the receiving of LDL via LDL-receptor by adipocytes leads to those "shedding" cholesterol (which seems to be picked up by "scavenging" HDL). See, for instance,   Verghese et al., 2007
"In the presence of HDL, composed of human apoA-I and phosphatidylcholine, adipocytes release cholesterol in a lipoprotein-dose and time dependent fashion."
This might be considered recycling of cholesterol (brought from liver to storing tissue by LDL and back again to liver on HDL, as delivery of fatty acids to storing tissue allows those to release cholesterol). In an evolutionary tentative concept, cholesterol as a molecule in itself  might once have been the very transport vehicle to transport lipids and fats from and to cells (see above: HDL is not even endocytosed, in very contrast to LDL-receptor-uptake, when it returns to liver cells, still cholesterol enters the liver cells. HDL leaves the receiving "scavenging receptor" as it is; it is some taxi; my analogy is to cholesterol). This idea leads to considering the sheer quantity of loaded  cholesterol as presumably distinctive: any quantity surmounting a level defined as upper limit for "taxi function" might be unloaded (or oxidized in scavenging funtion). This seems coherent with the existence of "remnants": there are LDL or VLDL-remnants and chylomicron remnants which the liver receives cholesterol  by. On a molecular level, there might be a difference in relative or absolute quantity of cholesterol, between LDL and HDL, reflecting that HDL as such "is" a remnant in the sense that it recyles cholesterol in "remnant quantity/thus quality". (There do exist LDL and chylomicron remnants, however, there is no such term or thing as  HDL remnant, to verify). By the way, counterintuitively, cholesterol is arguably considered "amphophilic", cp. source cited in comment to question and quote Encyclopedia Britannica above that mentions "sterols and esthers" as vehicles of cholesterol transport. Moreover, uptake of free fatty acids by adipose or muscle cells (that is the form derived from VLDL after lipase took on) seems not very well established in its mechanism. Cholesterol, then,  is known to be the distinguishing feature of animal cell walls in contrast to plant and procaryote cell walls. Cholesterol in cell walls might - by "softening" - enable heterotrophic cells to absorb free fatty acid (derived form autotrophic (plant cells, unsaturated fats)) without use of any - yet unknown - membrane transport canal or receptor mechanism. Please let me add one more argument that seems surprising: target cells of adipose tissue are made to "shed" cholesterol by LDL-receptor signalling. "On the other side" these target cells of LDL "take on in"  - and keep - cholesterol and lipids (from degration of LDL). There might be some feedback loop of receiving lipids and shedding free cholesterol that is - in evolution - still independent of APO-B100-LDL-receptor signalling, and downregulating the LDL-receptor  solely might interconnect both levels or regulating free "chole-sterols" in blood, or, if cholesterol is a former instrument of uptake as proposed, in interstitial fluid.   Thank you for having allowed this tentative thinking.
To sum up:
Lipoproteins resemble each other  in molecular structure and transported forms of fat/cholesterol more than the acronymes HDL/LDL may suggest.
The relevant difference lies in   their ligands, which address different target cells: ligand to "LDL-receptor" (which HDL does not seem to have or has to a much lesser extent)  is decisive in pathogenicity as there is "LDL receptor downregulation"; there is no physiological (in vivo) HDL downregulation.
Distinguishing molecular feature thus appears to be Apo-B100 molecule, which is the largest protein of the body.

Self-comment on   "... as delivery of fatty acids to storing tissue allows those to release cholesterol" - This leads to some other question: What is the role of  insuline on LDL-expression by adipocytes (and hepatocytes), as fatty acid delivery by VHDL should be enhanced by insuline (more LDL-Rs), and, because VHDL is precursor of LDL, any cholsterol  uptake via LDL is necessarily combined to fatty acid uptake via VHDL transport. In (diabetic) starvation less LDL-R, more release of cholesterol to HDL - and, question, more release of fatty acids by LDL-R-storage tissue.

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text:
How was the diversity between ethanol fermentation and lactic acid fermentation evolved?
Quite simply, some organisms metabolize glucose under anaerobic conditions via Glucose->(2) Pyruvic Acid->(2)Ethyl Alcohol. Some organisms, however, metabolize to lactic acid.
When did such a process (lactic acid) arise biochemically from its related (ethanol) fermentation, and how was it selected for? i.e What were the advantages?
Also, can someone create the glycolysis or fermentation tag?

First, it is not clear from the physiology or biochemical information alone to determine what evolved from what. The intermediate pyruvate is always there, so lactose dehydrogenase (LDH) and pyruvate decarboxylase (PDC) could have each evolved anytime, and there are good reasons for both:

LDH: the reaction pyruvate + NADH/H+ = lactate + NAD+ + 25 kJ/mol is highly exergonic, i.e. produces heat
PDC: the reaction pyruvate = acetaldehyde + CO2 (and with ALD present) acetaldehyde + NADH/H+ = ethanol + NAD+ where ethanol is poisonous to other species

Add to it that there are organisms like Sch. pombe that have both enzymes, so can do both reactions, your questions should be rather:
How has the enzyme LDH evolved?
The enzyme is similar to malate dehydrogenase, both form a family. They belong to a group of enzymes that all have a NAD(P) binding domain, so it's not too far-fetched to state that LDH and MDH evolved from another enzyme with NAD(P) binding domain.
http://www.ebi.ac.uk/interpro/IEntry?ac=IPR016040
How has the enzyme PDC evolved?

Protein sequences of pyruvate decarboxylase (PDC) derived from cloned
  yeast (Saccharomyces cerevisiae) and bacterial (Zymomonas mobilis)
  genes were compared with each other and with sequence databases.
  Extensive sequence similarities were found between them and with two
  others: cytochrome-linked pyruvate oxidase from Escherichia coli and
  acetolactate synthase (ilvI in E. coli; ILV2 gene in S. cerevisiae).
  All catalyse decarboxylation of pyruvate using thiamine pyrophosphate
  (TPP) as cofactor. General overall similarity suggests common ancestry
  for these enzymes.

cited from abstract of
Green, Jeremy. "Pyruvate decarboxylase is like acetolactate synthase (< i> ILV2) and not like the pyruvate dehydrogenase E1 subunit." FEBS letters 246.1 (1989): 1-5. http://www.ncbi.nlm.nih.gov/pubmed/2651151?dopt=Abstract

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text:
Does sour food cause sweating?
While eating sour food or candy, I start to sweat if it's sour enough. My body feels much hotter although my actual temperature is the same, my forehead starts sweating a lot and I feel like it just got twice as hot wherever I am.
Is this a biological phenomena or is my DNA just stupid? Is it somehow related to the digestive system, that sour food is harder to digest?

In general, sweating is caused by too much heat, even if you're not aware of the heat. This can happen if the bowel moves and so raises the core temperature. Such movement is often accompanied with sweating, and since you only feel the normal temperature on the skin, it is cold sweat. But at the same time your core is hot so you think it's cold, but it will later mix to normal.
Anyway, it points to unusual bowel movement. This can be due to food allergy or, in a milder form, in food intolerances which are quite common. When it comes to sour ingredients, they are often in fruits, so I'll make a shot in the blue and say that you have a food intolerance against some fruits. You can check this hypothesis by trying chemically pure acetic acid to sour your food. If that doesn't result in sweat/hotness then it's probably the fruits.
http://en.wikipedia.org/wiki/Food_intolerance
The Wikipedia points even directly to salicylate in fruits but I think you cannot exclude allergies against essential oils like limonene and such. Plants are really chemistry factories and not all is well that you can get with them.

I do happen to have some fruit allergies, I had no idea it could be connected. I'll try to get my hands on some acetic acid and test what happens like you said. Thank you!

Note that usual vinegar may trigger a grape intolerance/allergy and even seemingly "chemical" acetic essence may be in part extracted.

I don't think this is a normal physiological response, but I would seek medical advice to be sure.
I did a quick literature search with keywords "sour", "food" and "sweating" and came up with one article about SUNCT syndrome. SUNCT syndrome is a short-lasting, unilateral, neuralgiform headache syndrome with autonomic phenomena on the symptomatic side. In other words, 3 patients of 6 studied, suffered headaches and sweating on one side of their forehead only. It seems to be predominant in males, with a mean age of onset around 50 years. The attacks are strictly unilateral, generally with the pain persistently confined to the ocular/periocular area. Most attacks are moderate to severe in intensity and burning, stabbing or electrical in character.

Kruszewski P, Zhao JM, Shen JM, Sjaastad O. SUNCT syndrome: forehead sweating pattern. Cephalalgia. 1993 Apr;13(2):108-13.

The only symptom I recognize from the ones you mentioned would be the sweating. I get no headaches or pain whatsoever. It could be SUNCT syndrome but as the main symptoms are missing I doubt it is. Thank you for your time and effort!

That's alright, it was a stab in the dark.


text:
What preceded ATP synthase?
ATP Synthase is ubiquitous throughout life on earth and so most probably evolved within the last universal common ancestor (LUCA) before that lineage diversified into the various kingdoms of life.
It is suggested that the functional domains comprising the ATP Synthase complex were cobbled together from pre-existing sub-units, each with with a related activity (e.g. the union of a proton motor with a DNA Helicase with ATPase activity), which seems reasonable, although a bit vague in the details.
The fact that a primitive ATP Synthase arose in the first place suggests that ATP already had a central role in cellular metabolism and so begs the question, what preceded ATP Synthase in the role of generating ATP in the LUCA cell?

ATP Synthase is NOT ubiquitous throughout life on earth. It is lacking from most anaerobic organisms.

There are metabolic processes in which ATP is synthesised without the involvement of ATP synthase. The best examples are, in fact, two steps in the glycolytic pathway, catalysed by phosphoglycerate kinase and pyruvate kinase. This is why, in the absence of any aerobic metabolism, many organisms (like yeast for example) can grow quite happily, producing two molecules of ATP for each molecule of glucose that is metabolised.
Presumably this process is what enabled ATP to gain its central role in energy metabolism without any need for an ATP synthase.

We don't know much about early evolution of life. However it is believed that energetic molecules (analogous to ATP) may have evolved before everything else. These energetic molecules may have driven different metabolic reactions (which need not be catalyzed by big protein enzymes). Also, it is believed that natural chemical gradients would have been used by primitive life-forms to obtain the energy.
You can have a look at this article. I am pasting the list of references/recommended reading mention in this article so that you may search for them individually even if this article is not accessible any longer.

- Allen, J. F. The function of genomes in bioenergetic organelles. Philosophical Transactions of the Royal Society of London B: Biological Sciences 358, 19–37 (2003)

- Efremov, R. G., Baradaran, R. & Sazanov, L. The architecture of respiratory complex I. Nature 465, 441–445 (2010) doi:10.1038/nature09066

- Lane, N., Allen, J. F. & Martin, W. How did LUCA make a living? Chemiosmosis in the origin of life. Bioessays 32, 271–280 (2010) doi:10.1002/bies.200900131

- Lane, N. & Martin, W. The energetics of genome complexity. Nature 467, 929-934 (2010)
- Martin, W. & Russell, M. On the origin of biochemistry at an alkaline hydrothermal vent. Philosophical Transactions of the Royal Society of London B: Biological Sciences 362, 1887–1925 (2007)
- Mitchell, P. Coupling of phosphorylation to electron and hydrogen transfer by a chemi-osmotic type of mechanism. Nature 191, 144–148 (1961) doi:10.1038/191144a0
- Orgel, L. Are you serious, Dr Mitchell? Nature 402, 17 (1999) doi:10.1038/46903
- Russell, M. J. First life. American Scientist 94, 32–39 (2006)
- Silverstein, T. The mitochondrial phosphate-to-oxygen ratio is not an integer. Biochemistry and Molecular Biology Education 33, 416–417 (2005)

Is this really a chicken–egg question? It just seems to be asking whether a simpler method of ATP generation preceeded the ATP synthase and if so what. Isn't this actually acknowledging the solution to the real chicken/egg problems with ATP, such the need for ATP in the synthesis of the adenine ring of ATP? Your list of references is very useful, but can I suggest you provide more context by naming the "energetic molecules" you mention.

@David point taken. The energetic molecules that I mention haven't really been identified. It is just hypothetical. This is probably mentioned in one of the references. Nonetheless, I'll try to look up and provide some more context asap.

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text:
Why are the Galápagos islands so special?
Why did Darwin formulate his theory of evolution just after his visit to the Galápagos islands? Why were they so special from an evolutionary point of view?

Charles Darwin formulated his theory after travelling the world aboard the Beagle, here's the route. He found the Galapagos Islands particularly inspiring,

'The natural history of this archipelago is very remarkable: it seems
  to be a little world within itself.'

This is a more detailed account of his relationship with the Galapagos islands, and there is also a book called "Voyage of The Beagle" (I think it is available as a free kindle download) which is basically his diary.
A big part of the reason it is so famous is because of "Darwin's Finches," which are 12 species of finch on the island that have all evolved to specific niches. This is one of the classic examples of evolution. Darwin noted the differences between the birds, thinking they were of different families, but it was later discovered they were all finches and the differences had evolved because of factors like the food they eat (seed eaters had fatter beaks.. etc).
The Galapagos islands offer opportunities to study evolution and adaptation because the islands are distant from the mainland, have differences between the islands, and migration between the islands is difficult. Studies like this one (which I happened to be reading at the time of the question being asked whilst writing a manuscript) are an example of how cool a place it is!

I want to point out that Darwin did not notice about the finches as everybody thinks until the captain of the Beagle (Robert Fitz Roy) pointed that to him. Also it was after a lifetime of collecting evidences not only from his voyages but from experiments in his own house and contributions from colleagues that he developed his theories, many years after his voyages. Which doesn't diminish his contributions at all. He made one of the greatest contributions to biology and human knowledge in general ever.

upvote for that last paragraph.  Among his other accomplishments Darwin also established the use of Islands to study evolution. Other islands do have these properties, but the Galapagos are nicely isolated from the mainland.

absolutely, he was very lucky to find such a place!

You suggest it, but it actually took Darwin many years of intensive study after the voyage to fully formulate his ideas on evolution and natural selection. The question suggests more that the Galapagos Islands provided a Eureka moment, and it was more that it provided him evidence that gave him insight many years after his visit.

Galápagos islands are one of few islands with a unique fauna and flora. This can only happen when the distance to other land is great enough, and when the island exists long enough that flora and fauna could grow (volcano islands are sterile for a long time).
Now Galápagos is even more unique because it is comprised of several islands that are distant enough that some animals cannot cross the distance like small birds. That leads to a unique fauna and flora that also differs between islands, so you can see differences just by visiting the next island. This made it practically a museum of evolution.


text:
what are the mechanics of sweating?
The causes of sweating aside, i.e. I'm not interested in which and how nerve signals are transmitted to sweat glands. But I would like to read a detailed account on what a sweat gland consists of, what it does when not sweating, but esp. what happens when a sweat nerve signal arrives. Is there a good free review or can you give one?

Go to the International Hyperhidrosis Society's website www.SweatHelp.org and look in the Know Sweat section. If you don't find what you want there, ask their top docs: Dee Anna Glaser, MD at St Louis University; or David Pariser, MD at Eastern Virginia Medical School.

Myoepithelial cell contraction initiates glandular release from most exocrine glands developed from the ectoderm. These are the cells that exist in the glandular epithelium.
At the distal end of the glanduar coil, an isotonic plasma filtrate gets actively transported into its lumen. As you move down the coil, close to where it connects to the duct, absorptive cells remove NaCl to make sure the sweat is hypotonic when it reaches the surface of the skin. If you view these cells where staining for alpha tubulin or beta actin, you will see they have abundant levels of myofillaments, something uncharacteristic of epithelial cells. Hence Myoepithelial.


text:
The probability of indirect human fertilization?
What is the probability of conception in situations when sperm isn't directly ejaculated into the woman's vagina, like:

The man's or the woman's hands come into contact with sperm, for example when removing a condom. (Perhaps after washing them,) the hands later touch vagina, for example during foreplay to another intercourse.
The man and the woman taking a bath together, the man ejaculates into the water.
The man ejaculates on the woman's body, perhaps on or around vagina but not inside. (In this case it could also make a difference whether the woman has shaved pubic hair or not.)
The man ejaculates during receiving oral sex, (perhaps the woman rinses her mouth), the couple kisses, the man performs oral sex to the woman.

In all these situations, it seems possible that a tiny amount of sperm is eventually transferred into vagina indirectly. And since just a single cell is enough to fertilize, it seems that there is non-zero probability of conceiving.
How much care need to be taken to prevent conception in such situations? Does simply washing sperm away with water (+ soap perhaps) eliminate it?
If you think of similar situations that are similar, please don't hesitate to add them.

Some outlandish claims of pregnancy: http://www.liveleak.com/view?i=e79_1351515813   and    http://www.museumofhoaxes.com/hoax/archive/permalink/the_case_of_the_miraculous_bullet    and    http://www.newspitter.com/2012/01/09/woman-gets-pregnant-after-having-intercourse-with-dead-man-in-a-mortuary

I don't have answers to all of your questions, but here is one example of a highly unusual conception via the gastrointestinal tract: http://blogs.discovermagazine.com/discoblog/2010/02/01/ncbi-rofl-thats-one-miraculous-conception/.
To cut a long story short, a woman born with a congenital defect that caused her to have no vagina was stabbed in the abdomen when her boyfriend found her performing fellatio on another man. She was taken to the hospital and patched up but a few months later:

Precisely 278 days later the patient was admitted again to hospital with acute, intermittent abdominal pain. Abdominal examination revealed a term pregnancy with a cephalic fetal presentation. The uterus was contracting regularly and the fetal heart was heard. Inspection of the vulva showed no vagina, only a shallow skin dimple was present below the external urethral meatus and between the labia minora. An emergency lower segment caesarean section was performed under spinal anaesthesia and a live male infant weighing 2800 g was born…

The article concludes that:

A plausible explanation for this pregnancy is that spermatozoa gained access to the reproductive organs via the injured gastrointestinal tract. It is known that spermatozoa do not survive long in an environment with a low pH (Jeffcoate1975), but it is also known that saliva has a high pH and that a starved person does not produce acid under normal circumstances (Bernards & Bouman 1976). It is likely that the patient became pregnant with her first or nearly first ovulation otherwise one would expect that inspissated blood in the uterus and salpinges would have made fertilization difficult. The fact that the son resembled the father excludes an even more miraculous conception.”

wow. That's all I can say...

Strictly speaking of course, this is not an answer to the question but still, +1 :).

Very very very very small. Next to impossible, millions of sperm cells start the journey and only a very small fraction of the sperm produced make it as far as the egg if "inserted properly." The vagina is a very hostile environment - to prevent infection - and this means very few sperm make it far enough. We produce in the order of 200-300 million sperm and it estimated that less than 1000 make it, so that is a 0.000005 chance of each sperm cell making it far enough.
There is also a benefit to travelling in such large number (each sperm is less likely to be destroyed by dilution effects, one sperm cell vs the entire human reproductive tract stands no chance). The numbers I am giving may be a little out from the correct ones, it's a while since I did my undergraduate module in sperm biology... I'm sure more accurate numbers will be  in this recommended reading
Further to this remember that not every attempt at fertilisation is successful even when doing it the right way, couples often try multiple times. If it takes 100 attempts to fertilise the egg just once the that is 1 in (100*200,000,000) sperm being successful.
Basically, if someone says they got pregnant sitting on a toilet seat that must have had sperm on it, or some other ridiculous claim, then simply don't believe them.

The man ejaculates on the woman's body

This won't lead to fertilization, as explained in the other answers, however, often times it happens after unprotected sex, meaning the penis was inside the vagina without a condom.
During intercourse, there is the pre-ejaculation fluid, that might arrive long before the actual ejaculation, and as answered here and here, it might contain sperm. The chances might not be very high, but it is possible.
To sum this up: while there is no indirect fertilization, some of the processes described in the question might mean that actions that took part before did lead to fertilization.


text:
Is there any biological reason for humans to rest after x days of work?
A lot of people live in a 7 day cycle, where 5 days of work are followed by 2 days of "rest". Vacations and holidays can increase the time available for resting.
Is there any biological reason for humans to rest after x days of work? Can this be explained by the buildup of by-products of metabolism, like Homocysteine?

No, it's explained by Family, a very complex stuff :)

Don't forget, humans rest every day when sleeping. Whether you are at work or not, your body is still active, still "working".

Sleep is circadian in nature, with this question I'm trying to understand if there are other, longer term cycles that I don't know of yet. The wikipedia article on circa-septan cycles is a stub: http://en.wikipedia.org/wiki/Circaseptan

The 7-day week is a recent innovation. The Romans used an eight day week. The Incas used a ten-day week. I don't know of any evidence that prior to the last ten-thousand years people followed anything other than solar (daily and annual) and lunar (monthly) cycles.

7-days weeks is specific to the cultures tracing back to traditions in the Mediterranean region (Judean, Roman, Egyptian, etc.) and is mainly preserved in Chistian and Arab cultures. Other cultures had weeks of different length or in some cases no days of rest at all (Japan?). Note also that there may be more psychological rather than physiological reasons for taking a day of rest - certainly in the Jewish tradition.

I think your main assumption is not true -- we do not really rest on weekends.
I do not know many people who only rest on weekends. Usually this is the time for socializing, doing home-related work, physical activity (sports, hiking), spending time with your kids, all of which is often almost the opposite of a rest.

This is what I'm trying to find out - if there's a reason to take it slow once in a while and relax,  purposefully not working. I'm sure with the pace of modern life people cram their weekend to the brim and then wish they did not have to sleep. But this does not appear to me to be the nature's way. I can't think of an animal that is as active at all hours of a day as humans are

My point is that with few exceptions, weekend is not the time to "take it slow and relax".

@Alex, Sheep spend 15% of their time sleeping, the rest is either active foraging or chewing cud.

Our bodies work in cycles.. Circadian cycles that refer to our daily routines. We need sleep every night, eating at night affects us differently than if eating in the morning, etc... all because our bodies functions work in these 24 hour cycles...
Now, beside the circadian cycles, our bodies also have circaceptan (or 7 day) rythms. For example, our immune system picks every 7 days (reason why the 7th day after a transplant is the most likely one may reject the organ). This 7-day cycle is also observed in other life forms...
But, read for yourself:
 a seven-day cycle has been found in fluctuations of blood pressure, acid content in blood, red blood cells, heartbeat, oral temperature, female breast temperature, urine chemistry and volume, the ratio between two important neurotransmitters, norepinephrine and epinephrine, and the rise and fall of several body chemicals such as the stress coping hormone, cortisol. "In fact," Perry and Dawson note, "weekly rhythms appear easiest to detect when the body is under stress, such as when it is defending itself against a virus, bacterium, or other harmful intruder. For example, cold symptoms (which are really signs of the body defending itself against the cold virus) last about a week. Chickenpox symptoms (a high fever and small red spots) usually appear almost exactly two weeks after exposure to the illness.:" [Susan Perry and Jim Davson, The Secrets Our Body Clocks Reveal, (New York: Rawson Associates, 1988) p. 22.]
Doctors have long observed that response to malaria infection and pneumonia crisis peaked at seven days. Organ transplants face similar crises as the body's immune system attack the foreign organ. Campbell explains: "When a human patient receives a kidney transplant, there is a rhythm of about seven days, a predictable rise and fall in the probability that the body's immune system will reject the new kidney. A major peak of rejection occurs seven days after the operation, and when a serum is given to suppress the immune reaction, a series of peaks occurs, with increasing risk of rejection, at one week, two weeks, three weeks and at four weeks, the time of the highest of all." [Jeremy Campbell, Winston Churchill's Afternoon Nap, (New York: Simon and Schuster, 1986). p. 76]
So, in answer to your question... it makes a lot of sense that if so many of our body functions have 7-day rythms, we would feel a biological need to slow down and allow our bodies to rest, rejuvenate....

Searching for "circaceptan rhythms" didn't yield so many results. Do you have any additional references?

Did the doctors discover the circaceptan (7 day) cycle on people who live in the modern system of a 7 day working week? Because it would be funny that they found a 7 day circadian rhythm in people who have a 7 day week. And the animals in that study, did they live near to cities that operate and pollute in 7 day variables, or were these animals out in the proper wildernesses where humans don’t venture too much and so there is a chance the 7 day human week isn’t smelting buried into their bones by us?


text:
Determining if a specific proline is cis or trans in the protein?
While peptide bonds usually adopt the trans conformation, peptide bonds to proline can exist in either cis or trans conformation. The isomerization between cis and trans is slow, and has been shown to be the rate-limiting step in folding of certain proteins.
What methods can be used to determine the conformation of a specific proline in a protein?

Sarkar et al.(2007) Proline cis-trans Isomerization Controls Autoinhibition of a Signaling Protein. Molecular Cell 25, 413–426 (DOI 10.1016/j.molcel.2007.01.004), available here.

The authors report on the interactions between two SH3 domains of the Crk adaptor protein. Basically they find that the linker which tethers these two domains contains a proline which interconverts between the cis and trans conformations, and that this interconversion determines the interaction between the two domains. They follow isomerisation by using NMR.
Cis-trans peptidyl-prolyl isomerization is a subtle change, and I don't think that you will find a way of following it in a specific protein that is simpler than this, unfortunately.

i'd agree - the most common method is to determine the structure


text:
Is "tonic activity" common for neurons firing in the brain?
I've been reading about Dorsal Raphe Nucleus, a serotonin- rich part of the brain. I noticed mentioning of "tonic activity" - regular pulsing that releases neurotransmitters. On top of this "tone" the nucleus can fire bursts of spikes(action potentials?) that further increase neurotransmitter concentrations for a short time.
Is this kind of tonic firing common throughout the brain, or is it DRN specific?

Most neurons that have been studied have spontaneous activity. Tonic firing is common in sensory neurons as well as cortical neurons. However, this could be very biased since it is difficult to study neurons that are silent in vivo. In vivo studies are blind, meaning that we usually do not see which neurons we are recording from. This is known as the "dark matter" problem (ref 1).
Also, it is known that there are homeostatic mechanism for maintaining average firing rate. Basically, if a neuron doesn't fire much, then the input sensitivity of the neuron increases to produce more activity (ref 2). But we don't know how widely this can be applied.
References:

Shy Shoham, Daniel O’Connor, Ronen Segev. How silent is the brain: is there a "dark matter" problem in neuroscience? Journal of Comparative Physiology A: Neuroethology, Sensory, Neural, and Behavioral Physiology, Vol. 192, No. 8. (1 August 2006), pp. 777-784  doi:10.1007/s00359-006-0117-6
Gina G. Turrigiano. Homeostatic plasticity in neuronal networks: the more things change, the more they stay the same. Trends in Neurosciences, Vol. 22, No. 5. (1 May 1999), pp. 221-227, doi:10.1016/S0166-2236 (98)01341-1


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Virucides - Herbal and otherwise, for HHV6 type virus or any inner-cell virus
Does anyone know where I can find a reliable list of virucides (not anti-virus) that can be used by humans? This virucide must be able to affect viruses that are already inside the cells. St John's Wort is considered a virucide along with it's other properties, for example.


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Is there such thing as "meters per calorie" for living organisms?
I'm interested in learning if there's some way of quantifying the organism's metabolic efficiency associated with movement.
It seems to me that some organisms would be more efficient than others at using energy. For mechanical systems, there are clear metrics of efficiency, for example "miles per gallon" or "liters per 100km". Is there a similar metric that converts calories into how far an organism can go?
Thank you for your input!

This isn't what I'd call metabolic efficiency. Metabolic efficiency would be calories per gram of some standard nutrient(s). When you're converting calories into movement, it's more a matter of mechanical efficiency.

Halsey & White (2012) Comparative energetics of mammalian locomotion: Humans are not different. Journal of Human Evolution 63:718–722

This paper presents a comparison of the metabolic cost of walking and running in humans, Australopithecus and other mammals.  They use a parameter NCOT (net cost of transport), whose units are ml O2 consumed m-1. The inverse of this parameter would be related to your metres per calorie.
The authors quote an NCOT of 12.77 ml O2 m-1 for a walking human. Using a value of 4 kcal g-1 for glucose, I calculate that this NCOT is equivalent to 14.6 m kcal-1.
Here I found an energy consumption value of 5.8 kcal min-1 (for a 73 kg man) walking at 6.4 km h-1, which translates to 18.5 m kcal-1.
Incidentally, according to the authors of the paper:

The predicted net cost of transport (NCOT, ml O2 m−1) of mammals is related to mass (M, kg) according to 0.54M0.70.


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What is the difference between xDNA and yDNA?
Wikipedia states that:

xDNA contains expanded bases, in which a benzene ring has been added, which may pair with canon bases, resulting in four possible base-pairs (8 bases:xA-T,xT-A,xC-G,xG-C, 16 bases if the unused arrangements are used). Another form of benzene added bases is yDNA, in which the base is widened by the benzene.

In this context, does widened and expanded refer to the same thing? If so, what would be the exact different between yDNA and xDNA.
NOTE: I am not referring to the X and Y chromosomes.

In fact, I just discovered the answer to the question in this article: http://www.aseanbiotechnology.info/Abstract/21026349.pdf. I will answer within the next few days unless someone beats me to it.

yDNA came first:

Lee & Kool (2005) A New Four-Base Genetic Helix, yDNA, Composed of Widened Benzopyrimidine−Purine Pairs. J Am Chem. Soc. 127: 3332-3338

As seen in this Figure from the paper it is a DNA consisting of T and C substituted with yT and yC, widened analogues.

xDNA came next (also from the Kool lab.):

Lynch et al. (2006) Toward a Designed, Functioning Genetic System with Expanded-Size Base Pairs: Solution Structure of the Eight-Base xDNA Double Helix. J Am Chem. Soc. 128: 14704-14711

As seen in this Figure from the paper, xDNA consists of an 8 base system A,C,G,T,xA,xC,xG,xT.

This field is reviewed in:

The XNA world: progress towards replication and evolution of synthetic genetic polymers
  Pinheiro & Holliger (2012) The XNA world: progress towards replication and evolution of synthetic genetic polymers. Current Opinion in Chemical Biology 16:245-252


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Difference between mice and rats
What is the actual biological difference between mice and rats? Are they actually the same thing with two different names depending on appearance (are they all mice for instance and we call the larger ones rats or vice versa) or is there some fundamental difference in their genetics?

Different species by definition have different body chemistry, else they could mate. However, identity on the gene level is probably similar to the man/ape difference of 98 per cent, so MOST body chemistry is identical.

To compute exactly which genes are new in one of the species vs. their ancestor, you could use orthology data from omabrowser.org

How can anyone upvote such a dreadful question? It should have been closed years ago as showing lack of any effort by the poster to answer it himself. Allowing this sort of question drags SE Biology down into the gutter!

Mice (Mus) and rats (Rattus) are definitely separate species, by whichever definition of species you choose to use. They are genetically distinct, and both genera are members of the clade Muridae, along with Acomys ("spiny mice") and Gerbillus ("gerbils").
Moreover, what we call colloquially "mice" and "rats" encompass a great deal of variation within rodents. The genus Mus is one of several subgenera with ~15 species.
A recent phylogenetic study of rodents by Blanga-Kanfi et al. (2009), revealed that Mus and Rattus are sister groups, meaning that each is the other's closest relative. The image below from the paper above shows the complete tree. Muridae is about 2/3 of the way down in blue.

Nice answer. +1

True rats and mice are rodents that constitute part of the subfamily Murinae in the family Muridae. The Old World house mouse is Mus musculus, the brown rat is Rattus norvegicus, so they are members of two different genera in that family. It is estimated that they split from a common ancestor 12-24 million years ago. Just to put that in perspective, the rodent lineage (including rats and mice) and the primate lineage (apes, monkeys, humans) diverged about 80 million years ago.
You can read an NIH News Release about the rat genome here, which is my source for these divergence times.
The names 'rat' and 'mouse' are also used in the names of many other, more distantly related, rodents such as mole rats and dormice.
Added later:
Response to @rwst comment under the OP. Here is a relevant quotation from the NIH source that I cite above:

The new analysis also underscores the fact that while rats and mice look very similar to the human eye, there are significant genomic differences between the two types of rodents. For example, some aspects of genomic evolution in the rat appear to be accelerated when compared to the mouse. According to the new analysis, due to the unusually rapid expansion of selected gene families, rats possess some genes not found in the mouse, including genes involved in immunity, the production of pheromones (chemicals involved in sexual attraction), the breakdown of proteins and the detection and detoxification of chemicals.


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Does the brain and the body use the same energy source (glucose/ATP)?
I've heard that the brain consumes quite a lot of oxygen and energy, compared to the rest of the body. What I'm interested in is if this is the kind of energy and oxygen that the rest of the body competes for?

For example, does running divert resources from the brain to the
muscles, leading to decreased cognitive performance?
Does digesting food divert resources from the brain to the gut?

Does the heart rate or blood pressure have anything to do with how much resources, like oxygen and energy are available to neurons?
Thank you for your input!

Running involves quite a bit of brain resources.  Coordination, balance, obstacle avoidance, etc..  So the total energy requirement for running would have to include the need of the muscles and the brain or running wouldn't occur.

You can grab any university level text on human physiology and you will find that the brain is a unique organ for cellular respiration. The brain is only capable of using two metabolic subtrates: glucose for oxidative phosphorylation (producing ATP) and ketone bodies.
Exercise does indeed divert blood flow toward the muscles. After all, they are undergoing higher levels of respiration and need nourishment. Your body will always balance muscular needs and the needs of the brain and the rest of the body. Similarly, digesting food has a similar response, although this is more involved. Eating food has a autonomic reflex to increase blood flow to the stomach and digestive tract to facilitate the processing and distribution of nutrients.

Diverting blood to the gastrointestinal tract doesn't necessarily mean that less blood flows to the brain - it could be other organs that are "deprived". And even if blood flow to the brain were to be reduced this doesn't mean that the supply of glucose would become limiting in any way since the difference between arterial and venous blood glucose is quite small - the brain would just need to extract more glucose from the blood that was available.

Quite right. I should have clarified that I did not mean to imply that the brain is deprived, just that the pattern of blood flow changes.

While in general the answer is "yes", the brain does use the same type of resources as other parts of the body, you cannot from that alone derive conclusions about the brain competing with other organs. Also, I think that cognitive performance is not a function of availability of resources. In fact, the moment that the brain lacks crucial resources like oxygen, it simply shuts down. But you don't faint when you start running (if you do, go see a doctor). "Power-saving mode" for the brain is not "reduce IQ by 20 points", but "just make sure the body is breathing and shut down everything else".
Also, I do not think that digesting food requires any comparable amount of energy that it would require the brain to give up on some of the oxygen it needs.


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Recombinant protein fraction in E. coli
If a protein is heterologously expressed in E. coli under the T7 promoter, what fraction of the total protein concentration in the cell is the heterologously expressed protein? What could be its concentration at most? Does it strongly depend on the size of the protein or are there certain size thresholds for low/high expression?

Miroux and Walker (1996) Over-production of Proteins in Escherichia coli: Mutant Hosts that Allow Synthesis of some Membrane Proteins and Globular Proteins at High Levels. J Mol Biol. 260: 289–298

The authors report on problems of over-expressing membrane proteins in E. coli using a T7 (pET) system. They isolate mutant strains which show improved levels of expression compared to the parent strain, BL21(DE3). In their Table 1 they document levels of expression of 17 proteins including, as a control, GFP. GFP was found as a combination of soluble and inclusion body protein at a level of 37 mg L-1 in BL21(DE3) and 140 mg L-1 in one of their mutant strains (C41(DE3)). The highest level of expression that they observed was 300 mg L-1 for bovine OSCP.
Unfortunately the authors document neither the total protein content, nor the cell density of the cultures that they analysed.
Let's assume that the cultures were 10e9 cells mL-1 = 10e12 cells L-1.
According to this source (citing Neidhardt F.C. Escherichia coli and Salmonella: Cellular and Molecular Biology. Vol 1. pp. 14, ASM Press 1996), the dry weight of an E. coli cell is 2.8e-13 g
The generally accepted figure for protein as a fraction of dry weight in E. coli = 0.55
I calculate from these numbers a value of 1540 mg protein L-1. For the three protein expression levels described above this means:
GFP in BL21(DE3) = 2.4%
GFP in C41(DE3) = 9.6%
bovine OSCP in C41(DE3) = 19.4%
I conclude (from these numbers, and from personal experience) that overexpression levels are highly variable, and are going to be strain and protein-dependent. Values in the range of 1-20% total cell protein may be anticipated.

Interesting. I had an intuition that protein yields would exist (all other conditions being equal). I was not expecting the difference to be as wide a margin as 20% of total cell protein.

I also had a feeling that the protein concentration should be more uniform, especially for the same protein (GFP in this case). I also imagined it would not be lower than 40%.....

Well, the % estimate is clearly a little uncertain because of the assumptions that I had to make about the cultures, but the protein yields in BL21(DE3) range from 2-65 mg L-1 (and expression was undetectable in four cases). I have added a link to the paper.


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Has anyone ever sucessfully translated xRNA or yRNA?
I've recently been researching the subject of size-expanded nucleobases in alternative genetic sets. Many papers describe the, at least, partial success in replicating xDNA and yDNA, as well as transcribing them, as suggested here.

At the same time, studies on polymerase replication and transcription of oligonucleotide sequences reveal that chemical entities other than the typical nucleoside triphosphates can be tolerated to varying degrees.

My question is can the cell's molecular machinery, including ribosomes and tRNA, possibly lead to translation of xRNA or yRNA? Would the translation product yield the traditional 20 amino acids? Have this ever been attempted?
References to original papers would be appreciated. Thanks!


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What are evolutionary implications of contraception and reduced childhood mortality rates worldwide?
I've heard the following idea this morning: Before the introduction of contraception, humans conceived quite a lot of babies (there was little to do to avoid that), but the population was kept in check by very high childhood mortality rates. This mortality rate ensured that only the fittest survived.
The idea seems common sense, but I decided to investigate if this is really true. I know that for evolution, even 2000 years should be an instant.
I did some research, for example the worst childhood mortality rate currently in the world is around 17.5%, which is still about half of what it was in "developed" countries during the 1700s, according to the table below. But looking at the wikipedia map of childhood mortality, it seems that a baby nowadays has only around 1-3% chance of dying before adulthood, because even the weakest baby can be kept on life support long enough for the danger to pass.
What are the implications of reducing childhood mortality rates worldwide on human evolution? Maybe evolution is a wrong term to use here. Would it be fitness as species? I'm particularly interested in how this relates to developmental defects and genetic disorders. Is there any evidence that people who lived in a world without contraception and with high childhood mortality rate were more physically or mentally fit?
Here's an paper that deals with the subject and the table is from the paper below:
IS CHILD DEATH THE CRUCIBLE OF HUMAN
EVOLUTION?

I think that technically, there's no such thing as natural selection reducing fitness (except due to random chance). What we're doing is changing the environment to which humans are adapted. This means that we may see an increase in traits that reduce infant robustness against disease and injury, but that increase fitness or reproductive success in adults. Of course, we'll also probably see an increase in traits that decrease infant robustness with no compensatory benefits, but that's because we've created an environment where those don't reduce fitness.

Before the introduction of contraception, humans conceived quite a lot of babies (there was little to do to avoid that), but the population was kept in check by very high childhood mortality rates. This mortality rate ensured that only the fittest survived.

Woh! Let me stop you there. No, high rates of childhood mortality do not ensure that whom Natural Selection is acting upon are the "most fit." That title is given to individuals who are able to survive long enough to breed.
Many, many conditions that affect humans do not interfere with a person's growth or ability to perform physical or intellectual feats - but can definitely reduce or completely eradicate a person's ability to reproduce. These individuals are evolutionary dead-ends, and thus - while they survive in the environment - are not "fit" in the context of this topic.

What are the implications of reducing childhood mortality rates worldwide on human evolution? Maybe evolution is a wrong term to use here. Would it be fitness as species?

What it means is that populations will rise. As populations rise and intermingle, alleles get spread around. Perhaps rarer alleles become more common, or more common alleles become rarer. We're talking about Hardy-Weinberg equilibriums in the allele frequencies. However, with populations large enough true equilibriums are impractical to reach.
The more pragmatic explanation is that more mutations will arise, they'll be passed around, rare mutations will see more exposure, and humanity - in a very general sense - becomes more diverse genetically until a Selective Pressure is applied. Until there's a detriment to having a particular gene, there isn't a need to eliminate it from the population.
Your example is children who are too weak at birth to live outside of an NICU for their first few months - well, because we're capable of providing such care, until that care goes away it's not negatively affecting us. If it comes with an additional cost - say that, for whatever reason, premies can't digest mother's milk until the 8-month mark, then Natural Selection would pressure humans to evolve so that only 8+ month or older babies are born.
There's no evidence of significant pressures in human populations at this time, though. At least not in politically stable and technologically apt countries, although in areas undergoing long-time drought or other dangers it is seen. Sickle-Cell Anemia is though to be an adaptation to rising Malaria rates - which was quite fatal until medication was devised to treat it in the last 50 years or so (not even a blip in evolutionary terms).

Is there any evidence that people who lived in a world without contraception and with high childhood mortality rate were more physically or mentally fit?

Not that I can think of or find easily. While there are detriments associated with being born prematurely, and some evidence that women waiting until they're late 30's and men until they're 60 or older can negatively affect their gametes and consequently the development of any children born from them - it's been such a short time since the introduction of hormonal contraception and modern medicine that we may not see results tangible results for hundreds of years. Although condoms have been around for several hundred years, and there's been no associations with condom use that I can think of.
In the short term, what it has done is affect the ethnic diversity of countries. For the first time ever, Hispanic births have outnumbered Caucasian births in 2012 in the United States. Other countries, mostly European countries, are seeing declines in birth rates - which means their populations will decline with age or be compensated for by immigration. Higher birth rates, however, are associated with lower income brackets or very religious communities - both of which are associated with ethnic Minorities, at least in the United States. So while minority populations have more kids, they do so on fewer resources which may negatively affect their children in the long-term, whereas higher-earning segments of the population might have fewer children later in their lives, but can provide a much more stable environment and opportunities to continue that success.
One thing that hormone-centered birth control has done, however, is eliminate rape as a viable form of passing on one's genes. As gruesome as it might be to consider, pregnancies as a result of rape can produce "fit" offspring. It is a legitimate reproductive strategy in nature, and is in humans... unless the woman is using contraception. In the long-term this will probably show some interesting results (nominally an enhanced "Female Choice" effect - which is already evident in human evolution), but nothing right now.
It's also worth considering the ability for humans' increasing abilities to manipulate our own genome. At this point, we're nearly able to remove detrimental genes at-will and replace them with more effective versions. Because of this bio-engineering ability, the generations after ours might never be susceptible to inherited diseases - or they might all hop on the trendy "genes" and end up completely identical to each other. That's part of the fun of being human, though; we're very messy when it comes to Evolution. We tend to muck things but up good. :)

Thanks for an informative answer! It seems that common sense is not always true when evolution is concerned. Where do I sign up for trendy genes? ;)

@AlexStone I wouldn't say Evolution goes against common sense, per se. A lot of people simply haven't had a thorough education concerning Evolution via Natural Selection, so it's easy to come to misunderstandings. As for Trendy Genes, I'd say give it about 20 years and a celebrity endorsement!

Well , Ime sorry but sometimes a question have to be rephrased in order to reach the ''elefant in the room''  : The important question is if the existence of contraceptives in itself wil change the direction  of human evolution . After the invention of contraceptives the meaning of ''survival of the fittest'' is something very different , from now on the RESISTANCE to the effect of contraceptives becomes the dominant factor in determining fitness for suvival .
 This resistance can be compared to the resistance develped by a population of insects being subjected to a targeted poison :  before or later the population will develop some kind of resistance , even in cases where this can only be achieved by a complicated and indirect mecanism .
  Humans can achieve such resistance in several ways easy to imagine , and probably also in others very hard to imagine .
 The most obvious is by cultural adabtion , by developing a culture that prevents the efects of contraceptives . This can already be seen in the demografic growth of several population groups dominated by strict compliance with a beliefsystem damning contraceptives... . Many would argue that this has nothing to do with genetics , but actually a very strong case can be made for the opposite position .
 A less obvious way to devellop resistance is selection for a maternal or parental instinct , operating seperately from the sexual drive which has been ''poisoned'' .  In any population , even with an extemely low birthrate , there will always be a few individuals who will have lots of children , no matter what .  Given time enough ,and especially in a low-bithrate population , this behavour will be selected again and again until the underlying genetic mecanism  will cause it to be come  truely hereditary .  Such is the lessons of  selective breeding towards a derirable quality in  everything from horses to tomatoes , and there are  no reason to believe  humans to be different .  The million dollar question is how many generations this proces wil take ....

This is highly speculative and doesn't answer the question.

It also seems to muddle up genetic evolution evolution and cultural evolution, let alone the complexities of gene-culture co-evolution.


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Do crocodiles age?
I was watching a talk by Michio Kaku and he mentioned that crocodiles (or possibly alligators, I forget offhand) don't actually age -- they can die, but they essentially go through no aging process beyond adulthood
Can anyone link me any sort of detailed information on this?

Well, this needs to be broken down into two parts. Do Crocodilians age (undergo senescence), and are Crocodilians immortal (will only die of external causes)?
Are Crocodilians immortal?
 - No. They appear to live about as long as humans before they die.

Measuring crocodile age is unreliable, although several techniques are used to derive a reasonable guess. The most common method is to measure lamellar growth rings in bones and teeth—each ring corresponds to a change in growth rate which typically occurs once a year between dry and wet seasons. Bearing these inaccuracies in mind, the oldest crocodilians appear to be the largest species. C. porosus is estimated to live around 70 years on average, with limited evidence of some individuals exceeding 100 years. One of the oldest crocodiles recorded died in a zoo in Russia. A male freshwater crocodile at the Australia Zoo is estimated to be 130 years old. He was rescued from the wild by Bob Irwin and Steve Irwin after being shot twice by hunters. As a result of the shootings, this crocodile (known affectionately as "Mr. Freshy") has lost his right eye.

Do Crocodilians undergo senescence (show signs of aging)? Well, if this study from "Gerontology" written by Patnaik BK in 1994 is to believed... Maybe not.

Evidences and mechanisms of rapid or negligible senescence in reptiles are still fragmentary and unclear... neither the increase in mortality rate and accumulation of lipofuscin nor the reproductive senility have been shown conclusively in ageing reptile populations.

So, while Crocodiles and Alligators (both Crocodilians) definitely have a finite lifespan, because they just continue to grow it's hard to tell how long they have left until the day they die.

Good answer, but I strongly disagree with the definition of immortal as "will only die of external cause". Immortal means that it does not die, whatever the cause. If they only died of extrenal causes it would just mean they they could not die of old age.

@nico - Which is precisely why I defined it in my answer. Talk to any Highlander fans, and Immortal means you can only die by having your head cut off - which also differs from your definition. :)

Let's stick to the definition of the dictionary which is (OED): "Not mortal; not liable or subject to death; deathless, undying; living for ever. In wider sense: Not liable to perish or decay; everlasting, imperishable, unfading, incorruptible.". Immortal is just the wrong word to use in this context.

Similarly in Tolkein, elves are immortal but can die in battle or from heartbreak.  Both uses of "immortal" are common, and so MCM did the right thing by clarifying which way he was using it.

@nico I don't think theres a need to be that pedantic about the definitions if they are defined in the question and in general. After all Turritopsis nutricula is called "The Immortal Jellyfish" and I'm pretty sure they aren't bullet proof.

@Good Gravy: [un]fortunately in biology definitions are extremely important. In any case let's stick to the question, which states that they die, i.e. they are not immortal. The question is whether they do not age which is a completely different thing biologically speaking. For instance, do crocodiles show signs of cellular aging, like telomeres shortening? Sorry but if we want to talk about elves or Highlanders I am very happy to do it, just not on a biology Q&A site. As I said before, I have nothing against MCM answer, just pointing out that the term immortal is misplaced here.

I would like to point out that, according to dictionary.com at least, immortality is also definable "not liable to perish or decay." More importantly, I have had several discussions about immortality with my colleagues (we study aging and lifespan) where we take immortality to mean "not dying of intrinsic causes" i.e. not dying of old age. This is because defining immortality as being immune to extrinsic causes (predation, environmental change, asteroid collisions etc.) is a highly improbable scenario due to the innumerable possible extrinsic causes.

Other than external causes, what are the causes for a crocodile to die? Does an increase of aging increase the chances of organ failure?

I believe that to define something as immortal as being limited to total imperviousness to death is to reduce that term to being meaningless.  Immortality is meant only to mean an imperviousness to death from old age.  If you drop a vampire on the surface of the sun, they will cease to exist, but that doesn't mean that they're not immortal.


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How can the Ames test detect a human carcinogen?
Using the Ames test, we add a mutagen to auxotrophic salmonella with mutations in the histidine pathway and rat liver extract to simulate metabolism.  How would we know if the carcinogen is a human carcinogen or not?
I'm guessing that if a mutagen showed no growth without the rat liver extract, but then growth with the rat liver extract this would mean that it is a human carcinogen. Is this true?

The Ames test aims to find out if a chemical (not yet known to be mutagen) is indeed a mutagen, either directly, or following treatment with liver enzymes (which may metabolise a chemical to mutagenic derivatives during "detoxification"). As you explain, the test involves looking for reversion of various histidine auxotrophic strains of Salmonella.
If the chemical is found to mutagenic in the Ames test then there is a good chance that it will be a carcinogen because of the link between mutagenesis and cancer. In practice further unrelated tests are needed to eliminate false positives.
In this review of the method

Mortelmans & Zeiger (2000) The Ames Salmonella/microsome mutagenicity assay. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis. 455: 29-60

the authors state that:

...there is a high predictivity of a positive mutagenic response in the Ames test for rodent carcinogenicity...ranging from 90% to 77%...