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What reasons allow for women to outlive men?
It is a well-known fact that women tend to outlive men.
I often hear people unscientifically stating that men generally generally die younger because of the higher stress encountered in their work lives. I would personally immediately rule this out, as who's to say that that women's (past) home lives just weren't as stressful? Also, shouldn't we see a narrowing of difference in age with the recent gender equality issues? Since the trend in question still occurs in virtually all countries of the world, I think it's safe to assume that the phenomenon is purely physiological.
I am curious as to the most sound scientific theories or known reasons for why women typically outlive men. Finally, I understand that aging in itself is not a process that's completely understood, and thus am not expecting a "complete list" of factors.

In a study on longevity in 121 countries, women tended to outlive men by about 5 years [1]. The suggested causes for this are numerous, some of which are temporally, geographically, or culturally specific.
On the terminology, sex tends to refer to the absolute biological differences, whereas gender relates more to differences in perception/lifestyle (for instance, socio-economic differences).
Evidence
In a study on Greek centenarians the authors found that women outnumbered men (1.68:1), with men having a higher likelihood of smoking, and thus are more at risk of smoking-related illness and mortality (historically this was more true than today) [2]. This is also true for alcohol consumption. The authors also report that having a first degree relative who was also a centenarian is associated with longevity (highlighting the importance of genetic factors in lifespan determination).
There is also evidence that the rate of telomere shortening (number of cell-divisions until cell-cycle arrest) is sex-specific [3].
rwst cites an interesting paper, that presents evidence that suggests male hormones may decrease lifespan [4]. This may be due to differential onset of atherosclerosis and cardiovascular disease, caused by exposure to different sex hormones [5].
In a review on the brain/behaviour specific aspects of differential ageing between the sexes, the authors discuss differences in brain anatomy and cognitive (and emotional) functionality between the sexes [6].
Remarks
This is by no means an exhaustive list of the reasons for differences in lifespan between the sexes in humans. There are likely to be many other causes, such as men tending to have more 'risky' behaviours, and possibly other unknown genetic effects, such as having 2 X chromosomes, vs. XY.
References

Møller, A. P., et al (2009). Why men have shorter lives than women: effects of resource availability, infectious disease, and senescence. American journal of human biology : the official journal of the Human Biology Council, 21(3), 357-64. doi:10.1002/ajhb.20879
Tigani, X., et al (2011). Gender differences in Greek centenarians. A cross-sectional nation-wide study, examining multiple socio-demographic and personality factors and health locus of control. BMC geriatrics, 11, 87. doi:10.1186/1471-2318-11-87
Barrett, E. L. B., & Richardson, D. S. (2011). Sex differences in telomeres and lifespan. Aging cell, 10(6), 913-21. doi:10.1111/j.1474-9726.2011.00741.x
Min, K.-J., et al (2012). The lifespan of Korean eunuchs. Current Biology, *22(18), R792-R793. doi:10.1016/j.cub.2012.06.036
Pérez-López, F. R., et al (2010). Gender differences in cardiovascular disease: hormonal and biochemical influences. Reproductive sciences (Thousand Oaks, Calif.), 17(6), 511-31. doi:10.1177/1933719110367829
Kryspin-Exner, I., et al (2011). Geropsychology: the gender gap in human aging--a mini-review. Gerontology, 57(6), 539-48. doi:10.1159/000323154

Update
Just been reading this interesting paper by Maklakov, et al (2013, BioEssays) titled "Evolution of sex differences in lifespan and aging: Causes and constraints", which presents a more evolutionary/genetic argument for the differences.
Abstract
Why do the two sexes have different lifespans and rates of aging? Two hypotheses based on asymmetric inheritance of sex chromosomes (“unguarded X”) or mitochondrial genomes (“mother's curse”) explain sex differences in lifespan as sex-specific maladaptation leading to increased mortality in the shorter-lived sex. While asymmetric inheritance hypotheses equate long life with high fitness, considerable empirical evidence suggests that sexes resolve the fundamental tradeoff between reproduction and survival differently resulting in sex-specific optima for lifespan. However, selection for sex-specific values in life-history traits is constrained by intersexual genetic correlations resulting in intra-locus sexual conflict over optimal lifespan. The available data suggest that the evolution of sexual dimorphism only partially resolves these conflicts. Sexual conflict over optimal trait values, which has been demonstrated in model organisms and in humans, is likely to play a key role in shaping the evolution of lifespan, as well as in maintaining genetic variation for sex-specific diseases.

@LanceLafontaine just been reading this article which is very interesting

Although many studies have shown that there are trade-offs between
  longevity and reproduction, whether such trade-offs exist in humans
  has been a matter of debate [1,2]. In many species, including humans,
  males live shorter than females, which could be due to the action of
  male sex hormones. Castration, which removes the source of male sex
  hormones, prolongs male lifespan in many animals, but this issue has
  been debated in humans [3]. To examine the effects of castration on
  longevity, we analyzed the lifespan of historical Korean eunuchs.
  Korean eunuchs preserved their lineage by adopting castrated boys. We
  studied the genealogy records of Korean eunuchs and determined the
  lifespan of 81 eunuchs. The average lifespan of eunuchs was 70.0 ±
  1.76 years, which was 14.4–19.1 years longer than the lifespan of
  non-castrated men of similar socio-economic status. Our study supports
  the idea that male sex hormones decrease the lifespan of men.

Brand new article!
Kyung-Jin Min, Cheol-Koo Lee, and Han-Nam Park: The lifespan of Korean eunuchs. In: Current Biology, Volume 22, Issue 18, R792-R793, 25 September 2012

Are they really saying that the lifespan of their control samples (i.e. men with testes) was only 51-56 years? That is worryingly low - I suspect that something else may be going on there .. ?

Very interesting though!

They are talking partly about mediaeval times, the Chosun dynasty from 1392 to 1910. http://en.wikipedia.org/wiki/Joseon

Ahh! That makes sense then :-) Even so, it would be interesting to know if they accounted for things like syphilis which might make sense in the context of this study. OK, I should read the paper ...

I'd also add that differences in the lifestyles of eunuchs compared to non-castrated men may influence these findings. Eunuchs likely had a special, maybe even pampered, role in society. The other men likely were engaged in dangerous work. Recall that industrial and work-related accidents was one of the top 120 killers (in the USA) well into the 20th century.

But they compared with "men of similar socio-economic status", as quoted. If you think they did this wrong, you must first cite how the details of the comparison.

The testosterone effect mentioned by @rwst is an exciting new discovery, but there may be a deeper answer which is an evolutionary adaptation.  There is a theory called the grandmother effect that tries to guess why women live often quite a long time after menopause.
Longevity in women doesn't make a great deal of sense from the standpoint of selection, since a lifespan past popping out the little ones wouldn't really increase fecundity.
As you might guess, having a parent around for a long time after a human child is born might increase the number of offspring that reach the age.  The grandmother effect surmises that females have a stronger, more direct relationship with offspring and can contribute directly to the viability of her offspring even after she stops having children herself.  Grandfather's probably don't enjoy this benefit as much because they are thought to contribute less to the offspring.  You have to remember that over the length of human history men's tendency has been to be a little more distant because of the difference in parental certainty.  while it can be very low for fathers, it is pretty much zero for mothers.
There are other adaptive arguments for human gender biases in longevity.  Men are going to try to contribute to their older age fertility by producing offspring later in life too.  Still, women do tend to live longer than men.
It would be surprising if the grandmother effect were the only reason women live longer then men, but it sounds like a stronger selective effect to me and men can probably evolve longer lives by taking an interest in their offspring longer.  This would have to be on an adaptive scale - over the entire population though.
Individual variations in longevity can of course be more important than these effects, but these theories try to explain the bias.


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Are there genetic similarity between humans and pigs that don't exist in chimps?
Chimps are our closer relative.
Any genetic similarity between humans and chimps must exist on the common ancestor.
Pig branch out sooner. So, any genetic similarity between humans and pigs must be on common ancestor between humans and pigs. That must be on common ancestor between humans and chimps.
But chimps may evolve differently.
Hmmm... I am confused.
Actually is there any?

This is a great question. Looking forward to the answers.

For those wanting to answer: Here is a closely related question that share many similarities ;)

Yes there are!
I think it would make more intuitive sense to you if you would have switched the words chimps and humans in your question:

Are there genetic similarity between chimps and pigs that don't exist in humans?

Then, you would directly answer, of course, there are genes concerning bipedalism, brain (FoxP2 for example), digestive track (adult production of lactase for example) and so, and so… which are different in humans but might not have much reasons to be so different between pigs and chimps. Those mutations occured on the human lineage after the split between human and chimps.
To answer your question:

Are there genetic similarity between humans and pigs that don't exist in chimps?

Yes. Most of these difference are due to mutations that occurred in the chimps lineage after the split of the original lineage into human lineage and chimps lineage.
The following are improbable but would also allow to explain such similarities:

Genetic admixture or introgression between human and pig after humans and chimps lineages splitted.
Convergent evolution.

Maybe pigs and human got the same beneficial mutation that never appeared in the chimps lineages.
Maybe pigs and human, due to the fact that today live in cold climates evolved the sequence ATTCGCTGA which cause them to produce a more efficient shivering!

This question doesn't make a lot of sense.  Humans, chimps and pigs are all eukaryotes, share a lot of sequence similarity due to common ancestry.  We are all vertebrates, we are all placental mammals.  So there is a lot of similar sequence between us, more than we have with lizards.
So humans, chimps and pigs all have a common ancestor. Is it possible that there are some sequences where the human versions have drifted farther from the common ancestor than either chimps and pigs have?  Sure, it's possible but probably not very common.
Here's link to ensembl's page on one random gene, the transferrin receptor.  You can see the % identity between the orthologues of a number of species.  Chimps and humans are 99% identical.  Pigs are 76%.  All the primates whose transferrin sequences are known are in the 90's percentage wise, the other mammals are not nearly so close a match.
http://www.ensembl.org/Homo_sapiens/Gene/Compara_Ortholog?db=core;g=ENSG00000072274;r=3:195754054-195782085;t=ENST00000360110
Here's another gene, where the gene has changed much less over time, but pigs are still not as similar to human as chimp
http://www.ensembl.org/Homo_sapiens/Gene/Compara_Ortholog?db=core;g=ENSG00000138379;r=2:190920423-190927455;t=ENST00000260950

Perhaps what Jim Thio is interested in is the xenografts from pigs to humans..

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What is this crow eating, and is it a common part of the corvid diet?
Here's a picture (by Rob Curtis) of a crow carrying and eating the corpse of what looks a bit like a small hawk or falcon:

Other pictures clearly show the crow is eating the dead bird. This image shows the underside of the head and beak; this one shows its legs, which are grayish.

What bird is being eaten?
Is this bird a usual part of the corvid diet? Or did the crow just opportunistically scavenge a dead bird?

Crows are omnivorous, and will eat almost anything they find or can kill.
In this case the prey looks like a Yellow-Shafted Flicker.

I would add that most corvid are scavengers, and there are also some that are "specialized" at that, such as the Carrion Crow (Corvus corone).

Also, do you think the crow killed the woodpecker (rather than scavenging it)?

@Mechanical snail - I don't think that there is any way that anyone could know the answer to this question unless they were a witness to what happened.

I agree with @AlanBoyd that we cannot know for sure but I would say it is unlikely that a crow could catch and kill a healthy flicker.  So just based on that, it seems more likely it scavenged it.

The crow looks like it is just admiring the dead flickers' colors. I think it picked it up in the way it would pick up any colorful thing. The flicker probable died by flying into a window.

It's eating a flicker woodpecker. And yes, it did kill it and is eating it. Crows and ravens are omnivorous but also predators. They will opportunistically kill any small prey they can catch. Most birds are too quick for a crow, but flickers and all woodpeckers are notoriously slow flyers. It's about the only type of bird that is both small enough and slow enough for a crow to catch. Attached are some images of crows as predators.

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Why are spinal nerves considered a part of PNS while the spinal cord is a part of CNS?
So from my common understanding, CNS consists of brain and spinal cord, and PNS consists of everything else. But the spinal nerves - the nerves connected to the spinal cord - why are those considered part of the PNS? And another clarification - spinal nerves are COMPLETELY DIFFERENT than the preganglionic neurons of the sympathetic nervous system?
Thanks for all your help.

I recommend that you stick to one question per post unless the different questions are interconnected to a great extent.

CNS consists of brain and spinal cord, and PNS consists of everything else

That's really it. The distinction is slightly arbitrary, I'd think of them as the central (nervous system) and the peripheral (nervous system): that is, the most important part is that together they are parts of the nervous system, rather than being distinct systems; the central/peripheral difference is fairly minor, especially if you are thinking primarily of the somatic part of the peripheral nervous system (that is, not the autonomic part) relative to the associated part of the CNS.
The peripheral part of the nervous system is not protected by the bones of the skull and spine, does not have the protection of the blood-brain barrier (specialized endothelial cells and astrocytes that limit transmission of molecules between CNS and the blood circulation moreso than in other tissues), and myelination is mediated by cells with a different morphology: Schwann cells in the periphery vs. oligodendrocytes in the central. That's about it.

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Is it normal to see yeast cells stacked in the Z axis when counting yeast?
I just got started with yeast cell counting and was surprised to observe yeast cells that are at different z axis depths at 400x. That is, by adjusting the focus (not the x/y stage) I can make some cells go into view as others go out (there is some overlap in some cases but not always).
Is this normal? It means that I will have to count at probably 2 different depths which I haven't seen anyone else talk about. I had assumed everything would be visible at a single depth.
It is possible I did something wrong like not properly seating the cover slide. My filling technique, based on some videos I watched, was to breathe on the cover slide and the hemocytometer, place the cover slide on and slide it around a bit, and then touch the dropper to the edge of the slide to fill the chamber (I did not observe any obvious overflow/overfill).

Did you wait for the cells to settle or did you look immediately after loading the volume?

I looked immediately but I also looked over different time periods--probably up to 10 minutes... and did not notice any change in stacking.  I did however notice that the yeast cells start dying off over time with the stain creeping into formerly live cells--so I'm not sure I'd want to wait very long either.

That sounds very odd. Yeasts are very hardy and in my experience I can dilute them 1:100 in sterile water and let them sit for an hour on the bench but I never observe a significant drop in colony forming units, let alone observe them dying under the microscope.

I should mention the yeast were not that healthy--I was just using an old sample to test the technique--that may explain why they seemed to die quickly.  I did counting more recently on a healthy sample and did not have any issues (and there was only negligible Z axis stacking for a couple budding cells).  I'm guessing I didn't properly seat the cover when I had the problem originally.


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How is satiety measured?
I am aware of satiety only through experience, rules-of-thumb and possibly myths. For example: white bread is not filling, a pasta meal can be filling but because we "burn" carbs quickly pasta itself is not, and I personally find fruit in the melon family filling. (But that could be because I hate them ;) )
Is there a formal measure of satiety? How does it work?

Can you clarify your question, actually it is not really clear for me what you are asking.

I am aware that the wording is not especially good for biology, but I had to migrate. The feeling of satiety has nothing to do with cooking, and the human physiology of eating food is strictly off topic on cooking.se. It is probably a bit more confusing because the OP imagines something which doesn't (and cannot) exist: some kind of universal scale saying that pasta is X times more filling than bread. But an explanation how the feeling of satiety emerges, as the reason why the scale doesn't exist, can be quite interesting.

Satiety is complex, and there are several kinds of satiety, all of which come into play in different circumstances. Things that decrease or halt our eating are called satiety signals. Different satiety signals are put out by different substances (carbohydrates, fats and proteins) as well as by things like gut stretching and other signals. There is also a psychological component to override satiety signals (company during meals, appearance of food, cost, etc.). The best measure of satiety may well be when a person stops eating a given meal. In lab conditions, the meals are carefully calibrated, but people (and animals) can feed as long as they desire to (ad lib).
Historically, satiety was thought to be the end product of serum glucose, available energy based on body heat, fat utilization by the liver, and the generation of ATP and other energy-rich molecules by the liver and/or brain. For the most part, these hypotheses have not withstood the test of time.
Three major signals influence food intake: satiety signals, adiposity signals, and central effectors. For the sake of simplicity, I'll deal only with satiety signals. Satiety signals (SS) arise from the GI tract and related organs during a meal, and influence eating behavior by activating peripheral nerves passing from the GI tract to the brain, or by recognition by brain receptors.[1]
As food interacts with the lining of the stomach and intestine, gut peptides and other signals that coordinate/optimize the digestive process are secreted. The signals that inform the CNS function as satiety signals. Different signals are secreted in response to carbohydrates, fats, and proteins, and it's the specific mix of signals that informs the brain as to what precisely has been eaten.[2]
Cholecystokinin (CCK) is the most extensively studied gastrointestinal satiety hormone. It is secreted by cells in the duodenum and jejunum in response to ingested fat and protein in chyme (food plus gastric fluid). Giving CCK IV decreases ad lib meal size, while blocking CCK receptor sites will increase ad lib eating per meal.[3][4]
Carbohydrates and fats as the most effective stimulators of Glucagon-Like Peptide (GLP-1) and Peptide YY (PYY). IV GLP-1 decreases meal size by promoting early satiety.[5] Within the CNS, PYY is detectable in the hypothalamus, medulla, pons, and spinal cord.[6]
Enterostatin is a protein which is broken down into a digestive lipase and a five-peptide fragment (Ala-Pro-Gly-Pro-Arg (APGPR) in humans). The appetite regulating effects of APGPR in the brain are specific to high-fat or fat diets but not towards diets rich in protein or carbohydrate.[6][7]
Amylin decreases meal size in rats, probably through the same pathway as CCK. Oxyntomodulin (OXM) and pancreatic polypeptide (PP) are also meal terminators. Pre-prandial subcutaneous administration of OXM to overweight and obese humans over a 4-week period resulted in a significant reduction in body weight of 2.3 kg, compared with 0.5 kg for the placebo arm.[9]
This is a growing field, and there is more suspected, and more to prove. But one can see that there is no one measure of satiety.
[1] That satiety signals come from the stomach and beyond was shown by "fake eating", that is, diverting swallowed food from the stomach by creating a fistula. If food is allowed to enter the stomach, satiety signals are elicited; if not, eating continues for a long time.
[2] Gastrointestinal Satiety Signals I. An overview of gastrointestinal signals that influence food intake
[3] Gastrointestinal hormones and satiety
[4] Rats with spontaneous mutations of the CCK-1 receptor (called
OLETF -Otsuka Long Evans Tokushima Fatty- rats) eventually become obese
during their lifespan.
[5] Glucagon-like peptide-1 promotes satiety and reduces food intake in patients with diabetes mellitus type 2
[6] Introduction to Gut-Brain Interactions
[7] Enterostatin inhibition of dietary fat intake is dependent on CCK-A receptors.
[8] Amylin decreases meal size in rats
[9] Gut-Brain Interrelationships and Control of Feeding Behavior

nice answer.. can  you expand on the role of hypothalamus..

@WYSIWYG - I can, but this answer is long enough. :) If you want to ask a separate question, I can do that.


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Why does sexual selection evolve beautiful features?
I have a very raw understanding of sexual selection:
Say a group of females of a certain species "like" some feature of a certain groups of males; by "like" I mean some behaviour that makes this group of females tend to mate with males having this feature, then the females are selecting their genes which make them feel appealed to males with the feature, and then this process becomes exponent since the group of females becomes bigger and forces the population of males to have this feauture, until an equilibrium is reached. I know this also happens with the roles interchanged.
My first question is, why do females tend to like males that have high amounts of these features, more than the average in the population?
My second question is, why do the end products of these selections are such beautiful features? Perhaps this may sound a little arrogant but I don't understand how an animal can appreciate this beauty, I suppose this is to make some sort of selection of healthy males.
Thanks

I think this may answer part of your question: http://en.wikipedia.org/wiki/Sexual_selection#Exponential_growth_in_female_preference

Hey! Welcome to Bio.SE :) This is certainly a good question. However, it requires a very broad explanation of how sexual selection works, so it seems unlikely that you will get a full answer that clears all of this up. It would probably be a good idea to read the Wikipedia article and see if that makes the issue more understandable to you. If you have any more specific question then, pleasea do ask here!

In regards to the "beautiful features" part, your Q2, Dan Dennett explains the issue well here: http://www.ted.com/talks/dan_dennett_cute_sexy_sweet_funny.html

I don't mean to be rude, but yes your second question is very arrogant and anthopocentric. Why would you think humans have a monopoly on beauty appreciation and emotion? The tails of peacocks just happen to coincide with human aesthetics, but a proboscis monkey's nose or elephan seal's blubber are just as beautiful to the right set of eyes.

I think I can expand on the answer by @boo2060.
The evolution of female mate choice depends on females achieving higher fitness by choosing certain males over others. At the broadest scale, there are two mechanisms by which this can occur, direct benefits, and indirect benefits.
Direct benefits
These are material things that (surprise) directly benefit the female. This might be the provision of food by the preferred male, access to a good territory or shelter that is under the control of the preferred male, protection by the preferred male, that sort of thing. Females will accordingly favour male traits that advertise potential direct benefits. These might include male size/condition/colouration, or even built structures like those of the bowerbirds. Basically, these traits show that the male knows how to look after himself, and by extension, he knows how to look after her (as males in good condition generally inhabit the best habitats and will offer the best protection and parenting).
Indirect benefits
These don't do much for the female, but they increase the genetic quality (and thus potential fitness) of her offspring. This is a much more complicated area of mate choice, and can be split into a bunch of (non-exclusive) hypotheses (below). And of course, attractive males may well offer both direct and indirect benefits.
Sensory bias: Males may, by chance, possess a trait that holds intrinsic appeal for a female. The best explanation might be that it mimics the colour or shape of a food source (e.g. fruit) that the animal eats, and thus the animal has pre-evolved preference for that colour or shape (e.g. red patches). From that point, males with more of that trait, whatever it is, will tend to be more attractive, for no rational reason. This hypothesis is sound, but is currently lacking good empirical evidence.
Fisherian sexy sons: This can in fact lead on from an initial sensory bias. Females may choose males that they find 'sexy', because their offspring will also be sexy, and thus be successfull in reproduction. This can lead to 'runaway' selection for sexier and sexier sons, at considerable survival cost for males. In this case, natural selection and sexual selection work in opposing directions.
Indicator mechanisms: This is the handicap principle or 'good genes' principle. If a structure is costly to produce or maintain, or increases the risk of predation, and yet the male possessing it is still alive, he must have good genes to have withstood such a handicap. It may also advertise that the male is not infested with parasites. The extravagant plumes of birds may be largely explained by this one, but also sexy sons and sensory bias.
Genetic compatibility: Individuals seek partners that are genetically compatible. A certain proportion of the fitness of the offspring depends on the specific combination of genes (i.e. it's not additive), and individuals that can signal or detect signals in such a way that they can choose compatible partners will have an evolutionary advantage. The best example is scent (e.g. preference for dissimilar MHC immune genes - see the human t-shirt experiment).
These mechanisms are well known in theory, but not always well-supported by evidence (yet). This is probably the best reference.

Of course 'beautiful' is a subjective, human concept. But we probably appreciate a lot of 'beautiful' things (like a male bird of paradise) for the same reasons as other species. We like shiny things, colourful things, delicate things. These also happen to be the best indicators of health, and are most likely to exploit existing sensory biases. Fascinating topic.

Hello @atrichornis, thanks for your answer. As you can see in my question I have a "Fisherian" view of sexual selection, this seemed a little arbitrary, as almost any feature could be seen as "selectable", and with your explanation of sensory bias I get a better understanding of why beautiful features end up being selected.

Yep, the current consensus is that for the evolution of a sexual signal (e.g. ornamentation) to occur in the first place, it should exploit sensory biases, AND/OR be costly for the male to maintain and so serve as an indicator of health. Mathematical theory suggests that either one can be enough, provided that there is some mechanism (i.e. cost) that prevents low-quality males from 'cheating' by pretending to be healthy. If males can cheat, the system breaks down, because females can no longer use it as a basis for choosing, and males possessing this trait no longer have an advantage.

Nice highlighting of indicator mechanisms.  That seems to be the best match with the "beauty" term used in the question.

I'm not completely certain about the vocabulary used in this context so let me know if you wish clarification
There are a few hypothesis why females care about the sexual features of males, the two most prominent are:

The sexy son hypothesis states that a sexually attractive male will have sexually attractive offspring which, in turn, is also more likely to mate. This way a female choses to maximize the chance to pass on it's genes to next generations.
The good genes hypothesis says that males who can afford to develop features that do not benefit their survival but are only for the purpose of sexual selection are healthy, strong and fit. If not, they would not spend resources on sexual attractiveness.

But why are all these features beautiful? Well, the purpose here is that they are beautiful, in terms of attractive, to the recipient of the message: the potential partner. We as humans may find these features also beautiful, as is most likely the case with the colourful feathers of the peafowl. But what about the antlers of deer? Beautiful, dangerous? This is subjective for us ..

Have you got any sources?

I was rather thinking of how many attractive features convey a sense of fertility and lack of genetic abberations.

I thought I had my books at hand before I wrote the answer but in the end I didn't find them .. so apart from my experience and a quick verification on the Internet the sources are still to add.

I'm not aware of a study quantifying features that are considered being subdue to sexual selection. I think that rather the potency of one feature communicates fertility, health etc - I'm not an expert on evolution though .. your thought is interesting.


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What is the difference between a circular and a cat's-eye (slit) pupil?
I've been to local zoo the other day and one lizard caught my attention: its pupils are circular, which, I thought, is not usual for reptiles. Turns out it is, but now I can't find any explanation on why some animals have one kind of pupil and others have the other. Lizards can have both, and so can snakes. The only difference I have found is that circular pupil can't shrink quite as much as a cat's-eye pupil, but that hardly explains why circular pupil even evolved in the first place as I don't see any advantage to it.
Ideas?
P. S. Fish only have circular pupils so that shape is older, right?..

Circular pupils are always functionally superior to vertical pupils; a slit does not correctly focus light from all directions whereas a circular pupil does. If you observe cats when they're hunting at dawn and dusk*, they have big, circular pupils; it's only when they're in bright light that the pupil shrinks to a slit. So why have vertical pupils at all? Because, as you mention they're capable of letting a more controlled range of light into the eye.
Thus vertical slits let you be active in a wider range of light conditions at the cost of poorer vision in bright light; whilst circular pupils continue to function well in brighter light but at the cost of not allowing such a large range of control over the amount of light entering the eye.
It is then easy to see why you get both kinds of pupil: circular pupils are favoured by animals that are typically active in bright light and need good vision under these circumstances; vertical pupils are favoured by animals that are primarily active in low light but need some ability to see in bright light.
*- it's often stated that cats are nocturnal, this is untrue; cats are crepuscular - that is they are most active at dawn and dusk.

I have thought about it, but don't understand how exactly non-circular hole negatively affects vision. For example: a heavily used сamera  lens can often have a broken iris, which takes irregular shape. The only clearly visible effect of this is the shape of unfocused background lights and other bright points. it doesn't worsen the sharp part of image in any immediately visible way. That's why I've discarded this reason when thinking of pupils.

Your mention of cats hinted that vertical pupils have to do with night vision, and indeed they do.
The retinas of cats and other nocturnal animals are very sensitive to even the tiniest amount of light. This can make their eyes hurt when exposed to bright sunlight. So their pupils have to shrink as much as possible in the sunlight, and, as you pointed out, vertical pupils can shrink more than circular ones.
EDIT: People pointed out in the comments that cats have vertical eye pupils only in bright sunlight. In low-light conditions, the pupils expand to a circle.

It was my first (and only) idea that nocturnal animals have vertical pupils. It didn't confirm, though, there are lots of nocturnal animals with circular pupils. So, not all nocturnal animals have vertical pupils. I didn't think of it the other way, though - all animals with vertical pupils might be nocturnal. Have to check it, thanks. P. S. I am somewhat familiar with photography and the second theory doesn't make sense to me. Depth of field (DOF) is something you only need to be concerned with at short distance.

Why can vertical pupils shrink more than circular ones? Isn't the lower limit on pupil size always 0?

@Kevin: how do you imagine a circular pupil shrinking to 0? Where will pupil tissue go?

The pupil is an opening in the iris, not tissue: http://en.wikipedia.org/wiki/Pupil

@Kevin: I didn't realize... Still, muscular system for circular pupil seems less trivial and more restricting

Your alternative explanation makes no sense: animals with vertical pupils have these pupils expand to circles in low light conditions so the slit is not used during night vision.

I will remove the alternative explanation (which is not mine but a research study I linked to), people come up with many arguments against it.

@VioletGiraffe "Still, muscular system for circular pupil seems less trivial and more restricting." I think you might be forgetting that animals also have sphincter muscles that can pretty much close completely.

In bright light, a cat can also squint, thus approximating a circle with a square-like aperture. So a vertical pupil is not that much of a liability to focusing. The same cannot be said of a horizontal pupil (unless the eyelids are vertical). Additionally, a vertical pupil might optimize detection of horizontal movement, which is likely an advantage in hunting prey on the savannah.

How does a vertical pupil help to detect horizontal movement?

I think I'm in error there. It would be a horizontal slit according to wikipedia on pupil. If someone can confirm, I'll fix my response, or else delete that point.

With more digging, I found contradictory evidence. http://www.graphic-fusion.com/beyondbokeh.htm - so I don't know the correct answer. I am inclined to believe the photography based info more strongly.

@SmokeyVW thanks for the link to the bokeh examples pages. I had the question of how a cat (or a vertical line pupil animal in general) would see and that link showed exactly what I was looking for.

There was a study published this last year (2015) that suggests that the pupil style of an animal is related to its strategy for predation. This means that land animal pupils evolved as adaptations to the niche that they filled.
The study distinguishes between herbivorous, active, and ambush foraging behaviors. Ambush predators tend towards vertical pupils, where as active predators (those that chase down and kill their prey) tend more towards circular. The pupils of herbivorous foragers tended to be mostly horizontally-elongated as is the case with goats. Eyes also tend to be forward set in predatory animals and more at the side of the head in prey animals.
In Why do animal eyes have pupils of different shapes? Banks, et. al. Science Advances
07 Aug 2015: Vol. 1, no. 7, e1500391 DOI: 10.1126/sciadv.1500391 It is suggested that

AbstractThere is a striking correlation between terrestrial species’ pupil shape and ecological niche (that is, foraging mode and time of day they are active). Species with vertically elongated pupils are very likely to be ambush predators and active day and night. Species with horizontally elongated pupils are very likely to be prey and to have laterally placed eyes. Vertically elongated pupils create astigmatic depth of field such that images of vertical contours nearer or farther than the distance to which the eye is focused are sharp, whereas images of horizontal contours at different distances are blurred. This is advantageous for ambush predators to use stereopsis to estimate distances of vertical contours and defocus blur to estimate distances of horizontal contours. Horizontally elongated pupils create sharp images of horizontal contours ahead and behind, creating a horizontally panoramic view that facilitates detection of predators from various directions and forward locomotion across uneven terrain.

Figure 1. Why do animal eyes have pupils of different shapes? Banks, et. al. Science Advances
07 Aug 2015: Vol. 1, no. 7, e1500391 DOI: 10.1126/sciadv.1500391

I see one possible advantage to round pupils. A slit pupil gives higher visual acuity vertically than horizontally because of diffraction and when a slit pupil is very nearly shut, there's high diffraction in the horizontal direction giving poor horizontal visual acuity. A round pupil on the other hand gives a creature the highest visual acuity in all directions for a given area of pupil. A smaller pupil is better for reducing chromatic aberration but chromatic aberration can be pretty much neglected because for any creature with evolutionary pressure for sharp vision in all directions, good accomodation will ensure at least one wavelength of light focuses onto the retina forming a sharp image because the sun emits a continuous range of wavelengths.


text:
What does Ercc1-/- / DAT-Cre+ mean?
I really need to know what Ercc1-/- / DAT-Cre+  mean. I think the 1st part means that the mice don't have the Ercc1 gene (knockout). But what about DAT-Cre+?
This question arised from reading the following paper: "Inefficient DNA Repair Is an Aging-Related Modifier of Parkinson’s Disease" (Sara Sepe et al).
Ercc1-/- / DAT-Cre+ mice are mentioned several times, For e.g.:

Ercc1−/−DAT-Cre+ mice are viable and normal at birth. At 26 weeks of
  age, specific deletion of Ercc1 in DA neurons mice elicits reduction
  in tyrosine hydroxylase (TH) immunoreactivity in the SNpc and in the
  striatum (Figures 1A and 1B). Aging profoundly exacerbates SNpc DA
  neurons reduction, as evidenced in 52-week-old Ercc1−/−DAT-Cre+ mice
  (Figure 1C). Damage is limited in DA neurons and other populations
  remain unaffected, as indicated by unchanged NeuN immunoreactivity
  (Figures 1A and 1B). Overall, these findings demonstrate that Ercc1
  function and NER are essential to preserve integrity of the DA
  circuits in time.

Sorry to bother you again but you should add the link to the paper. Moreover, copy pasting the text is better than pasting an image, for better searchability and rendering. I have done the both for you this time.

I have answered your question but the answer was pretty obvious. They mention it in the paragraph just before your excerpt. You should have read the paper more carefully. Questions like this ("homeworks") without adequate effort from the asker are generally not appreciated and put on hold.  "Homework" is interpreted to mean any academic or other assignment, test preparation, or task given in relation to a class, educational setting, or self-learning.

Ercc1-/-DAT-Cre means the mice with Cre recombinase mediated conditional knockout of Ercc1 in the DA neurons. DAT-Cre is the mouse strain that expresses Cre recombinase from the promoter of Dopamine transporter.

Cre-recombinase:loxP (Cre-loxP) system was used to generate mutants
  with targeted deletion in dopamine transporter (DAT)-expressing
  neurons. Specificity of Cre recombinase activity was validated using a
  lacZ reporter that confirmed expression in DA neurons of the SNpc and
  not in other cell types, such as serotonergic neurons of the Raphe
  nucleus (Figure S1).

From supplementary information:

Conditional mutants were generated using the Cre-recombinase:loxP
  (Cre-loxP) system and crossing a strain carrying an Ercc1 allele
  flanked by loxP sites (Ercc1fl/fl), with a strain expressing the Cre
  recombinase under the control of the specific Dopamine Transporter
  (DAT) promoter (Zhuang et al., 2005). We validated the specificity of
  Cre recombinase activity by generating DAT-Cre+ROSA26-lacZ reporter
  (Soriano, 1999), which confirmed expression in DA neurons of the SNpc
  and not in other cell types, such as serotonergic neurons of the Raphe
  nucleus (Supp. fig. 1)


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How to derive the deactivation time constant in this model of Acetylcholine Receptor state kinetics?
I came across this simple analytical expression of time constant of deactivation in Elenes et al., 2006. How does one derive this expression
$$\displaystyle\tau_\text{deactivation}\approx\frac{1}{D_+ + 2j_- + \frac{\alpha_2 2k_-}{\beta_2+2k_-}}$$
for the model given below.

 An allosteric reaction mechanism for the muscle AChR. C, O, and D denote the closed, open, and desensitized conformations of the channel, whereas A denotes a molecule of ACh. For simplicity, only one of the (probably several) desensitized conformations is included in the model. Also, the two neurotransmitter binding sites are assumed to be functionally equivalent and independent and, therefore, the two possible monoliganded configurations are considered to be functionally indistinguishable. These simplifications have no consequences on the interpretation of our data. The red arrows indicate the rate constants that, according to Eq. 1, determine the kinetics of the macroscopic current decay upon stepping the concentration of ACh from saturating to zero (i.e., during channel deactivation).

The material is esoteric, but I am hoping someone will be able to answer. The same paper also mentions that deactivation time constant is the reciprocal of
$\frac{\alpha_2 2k_-}{\beta_2+2k_-}$
and references Colquhoun and Hawkes, 1982. This reference will take quite a while to grasp completely.

I just checked the linked paper and the paper that it refers to. Both of them do not explain how the expression was derived. No supplementary methods also. You may find the derivation (not the final one, still) in the 1981 paper but you need to spend some time on it and perhaps read a bit about continuous time Markov chains. This is certainly beyond my scope and if we don't get a reasonable answer from anyone else then we may migrate it to [math.se] or [physics.se] and try our luck there.

I'm trying to solve the system, but I'm having some troubles with the mathematics. On the meantime I recommend reading the chapters of Colquhoun and Hawkes in the book Single Channel Recording specially the Q matrix cookbook. These are a digest of their papers.


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What species is this mosquito-like insect?

I found this in my room in Serbia. It's not a local type of mosquito that I'm familiar with, so I'm very interested. It flies like a fly but it looks like some kind of mosquito. I am looking forward to seeing what this could be.

Where are you from? could help track it down

I am in Serbia, Europe. :)

This is a dance fly, family Empididae (broad sense; two or three groups are extracted for the narrow sense), but beyond that I can't go (I don't have the Palaearctic identification keys).  If you were in North America I'd be halfway confident calling it a species of Empis, but there are a lot of them (and the genus is also found in your neck of the woods).

Wow,thank you so much,it looks like this is it :)

@ArthurJFrost You could make an answer out of your comment.

@Arthur I think Empis is not unlikely in Europe too.

@Remi.b, I'd prefer not going further than I have already; as I said on May 1 there is information I'm missing, and it's possible that even if I had it, the photograph here might not be detailed enough to use it (the key for this group in Manual of Nearctic Diptera, volume 1 [see the Entomological Society of Canada website; they have that in PDF] require at least a stereoscope for effective use, even when the animal is fairly large).

@рüффп No, the text is about Russia. But in Russian Russia is written Россия. In Serbian and in Macedonian it is written Русија. Due to its wast territory, providing Russia as location wouldn't be very helpful.

@ArthurJFrost well, you've clearly established yourself as a knowledgeable entomologist on Bio.SE, so it's fairly doubtful others will be able to provide a better answer (without themselves having the appropriate key). I think providing a write-up detailing the family would be a more than acceptable answer here. You could "improve" the answer by discussing typical characteristics to look for to identify genera/species in this specific family and possibly a citation/link/title to a potentially useful key. Sounds like a comment about Empis is warranted here, too.


text:
Application of molecular dynamics simulation (or alternatives) for the full pathways of protein interactions?
If one would like to control the biological system (e.g. to treat disease or aging/senescence) then one should introduce the drugs in the system, that initiate complex protein interaction pathways that (in final) generate the necessary proteins that induce the necessary biological mechanisms without adverse side effects from additional outcomes.
I am reading https://www.ncbi.nlm.nih.gov/pubmed/29139324 article about application of molecular dynamics simulation to the drug discovery but this article is essentially about simulation of one - target protein/molecule. My question is this: are there methods (molecular dynamics or others) that simulates the processes in the extended protein pathways that are induced by the one or more initiating molecules/drugs? It should be quite complex simulation, but nevertheless nothing less is expected from computational drug discovery and engineering.
I am quite confused. Maybe there is no need for such simulation at all? The databases of protein interactions just provide the more or less complete picture what protein interactions leads to what new proteins or structural updates of participating proteins and there is nothing to simulate - there is just empirical or predicted knowledge about what molecules leads to what other molecules/structures and one just extract the relevant pathway (starting from the drug coming close to the initial proteins) from the database and that is it?

MD is used for studying structural changes. Simulation of biochemical pathways involves the kinetics (you are not really looking at how enzyme structure changes when it binds to substrate). You can certainly pool all the modelling strategies together to make a hybrid multiscale model.
There are many people who work on such kind of modelling approaches. You can search multiscale modelling and check out recent reviews. This is a somewhat recent (2016) review on multiscale modelling of pharmacokinetics-pharmacodynamics.


text:
Why can't the brain and red blood cells use fuels other than glucose?
The question is rather straight forward: I have always been curious as to why, but cannot find an explanation online.
I can imagine that the mechanism is different for each, but why does brain tissue and red blood cells use specifically and only glucose for energy metabolism?

None of the answers below go to the core of the problem. Sure, several systems have been shut off or turned down in neurons and erythrocytes limiting their fuel types. The more important and possibly unanswered question is why these cells evolved this way. See also this related question on the brain.

In the case of red blood cells: human erythrocytes (red blood cells) have no mitochondria. Since the mitochondria are the cellular site for oxidative metabolism of fatty acids, erythrocytes cannot oxidise fatty acids to release energy. The erythrocytes also cannot fully oxidise glucose (to carbon dioxide and water) because this is also a mitochondrial process, so they have to rely upon anaerobic glycolysis. The end product of anaerobic glycolysis is pyruvate, and erythrocytes reduce this to lactate (to recycle the NADH that is produced during glycolysis) and then export this lactate into the blood for further metabolism by the liver.

The brain and heart can take advantage of ketone bodies when the amount of glucose is low.  These are byproducts of fat metabolism and can be converted to acetyl-coA via the citric acid cycle.
Overproduction of these products can cause pathological conditions:

When the rate of synthesis of ketone bodies exceeds the rate of utilization ,their concentration in blood increases , this is known as ketonemia. This is followed by ketonuria- excretion of ketone bodies in urine. The overall picture of ketonemia and ketouria is commonly referred as ketosis. Smell of acetone in breath is a common feature in ketosis.

There is quite a bit of evidence that the brain normally uses lactate produced by astrocytes as a source of energy. http://www.nature.com/jcbfm/journal/v25/n10/full/9600127a.html

@nico Sounds like that could almost be its own answer.  I wasn't aware of that.

unfortunately I know about the topic only superficially and right now I do not have time to go through the literature

Lipid catabolism provides energy mainly through fatty acid beta-oxidation. This process goes through a spiral of four mitochondrial enzymatic steps: one is catalyzed by the mitochondrial trifunctional3-ketoacyl-CoA thiolase (gene HADH). The activity of this thiolase is very low in neurons, explaining the brain need of alternative energy sources. Yang et al., JBC 1987. As previosly mentioned, developing erythrocytes eliminates mitochondria trough autophagy (mitophagy), therefore they became unable to efficiently perform lipid catabolism.

But why the activity of the thiolase you mention is low in neurons? Has it any functional purpose?


text:
Why oldest trees are all around 4k years old?
In christianity stackexchange I saw someone discussing young earth creationism.
One of the evidence they show is that the oldest tree, if measured by ring counts, are around 4k years.
Which, according to YEC, correspond to the Noah's flood.
Yes there are trees that are 10k years old. However, YEC doesn't believe in carbon dating. I wonder what ring counts do those tree have.
Is there any other reasonable explanation why oldest trees are 4k years old besides some massive catastrophe to all trees 4k years ago?

You might be interested in this.

Actually,   the oldest trees  are  almost 5000  years old. See here

You could argue on the same grounds that the world is only 200 years old. After all, there are no 200 year old people! What they are missing is that trees have natural lifespans too.

You can also use dendrochronology, matching ring patterns in the oldest parts of living wood to dead wood to extend the record back past 10,000 years: https://en.wikipedia.org/wiki/Dendrochronology  Also, if those old trees are supposed to have been around "forever", why do they produce seeds?


text:
What is the difference between prefrontal cortex and frontal lobe?
They are both in the front. Looks like they're the exact same thing.
Is one part of the other?
What?
Why is it called prefrontral cortex? What does pre before frontal mean? Before front?

Please don't spam the same question, especially when you already got an answer and when your question was criticized for its simplicity and lack of effort. Prefrontal and frontal lobe are not the same thing, though prefrontal cortex is located in frontal lobe.

It's not the same question. Okay where else should I ask this sort of questions?

The answer says that prefrontal cortex is called such because it is behind the prefrontal bone that doesn't even exist in modern mamal. I seriously doubt the only answer. I think understanding etymology of certain anatomical term would help many people tremendously in remembering those terms.

Yes it is the same question. If you doubt an answer, address those doubts on the original answer, don't make a new identical question. Prefrontal cortex was named well before modern neuroscience by an anatomist who was familiar with animals of all sorts and apparently chose to make an analogy in naming, which is quite common in anatomy.


text:
What's the evolutionary benefit of stress and cortisol?
Stress and cortisol lower immunity and increase hard disease.
But why is it that way?
If that's true then we shouldn't be stressful at all.
What's the benefit of stress then?
Why do we (and most mamals) response to stress by lowering immunity? How do people that lower their immunity due to stress survive "better" in the gene pool?

Acute stress occurs. It is impossible to enter the world without it. Cortisol is part of the physiologic response. This question could be improved by researching the role of cortisol in response to acute stress and explaining what you don't understand.

Consider a stress:  you have been bitten by a wolf, and it wants to bite you more.
Your body responds (among other things) with a surge of cortisol.
The cortisol
1:  Blunts immune response.  That inflamed hip you have needs to not slow you down.  That chronic cough needs to go away.  That stuff can wait.  You need to RUN.

Blood sugar goes up.  RUN!
Platelets go up.  You need to stop bleeding.
Repair / anabolic mechanisms are suppressed.  That stuff can wait too.
Testosterone levels plummet. Do not try to impress the ladies, you with your bleeding wound.  RUN!

The idea is that a stressor warranting a surge of cortisol is temporary.  Once you have found a safe cave the cortisol wanes and you can lick your wounds and build back your body.  Artificially elevated corticosteroid levels (from pills, or a steroid secreting cancer) are indeed tough on the body because of suppression of immunity and anabolic processes.
When people today talk about "stress" with jobs and grumpy roommates, it is not stress on the same level as a wolf attack.  Serious heavy duty stresses are what the glucocorticoid system evolved to handle.

The requirement for cortisol in response to acute stress remains important today. Illness, surgery, injury, and childbirth require high levels of cortisol.


text:
Can a crowded mitochondrial membrane limit O2 uptake?
The mitochondrial inner membrane is crowded with proteins (electron transport chain complexes, ATPases, etc.). As the proteins are packed more and more densely in this membrane, the diffusion of any molecule through the membrane should decrease, since there are less "gaps" for it to go through. I have no idea if this effect is insignificant for the entry of O2 into the mitochondria.
So my question is: Can O2 entry into the mitochondria become limited due to the high density of proteins in the mitochondrial inner membrane?


text:
Can a plasmid cause cancer?
Can a plasmid cause cancer?
According to wikipedia, plasmids are normally present in bacteria

They (plasmids) are normally present in bacteria , and sometimes in eukaryotic organisms such as yeast [(my translation)]

Let's say we inject yeast (by digestive tract) into a H. Sapiens (we will be focused in the yeast's plasmid only). Is it possible for plasmids to get into eukaryotic cells presents in the digestive tract?

Is it possible for plasmids to get into eukaryotic cells presents in the digestive tract? is a completely different question

Canonically, bacterial plasmids will not replicate in eukaryotic systems, due to a lack of the necessary control (regulatory) elements which will lead to expression.
It is possible though to construct shuttle vectors that can propagate in prokaryotes and eukaryotic cells (e.g. yeast or mammalian cells like the immortal HeLa cervical cancer-derived cell line).
What you are specifically asking is whether horizontal (lateral) gene transfer between prokaryotes and eukaryotes occurs, and whether it has an effect on the eukaryotic cell. This 2016 paper is an excellent and recent article discussing this question.

Can a plasmid cause cancer?

It has never been demonstrated, to my knowledge.

Is it possible for plasmids to get into eukaryotic cells presents in
  the digestive tract?

Very few bacteria can penetrate a healthy intestinal lining. However, in many  disorders of the gastrointestinal system, such as in inflammatory bowel disorders, the intestinal lining is compromised, which certainly allows the passage of prokaryotes and/or DNA into human circulation. However, a functional transfer of plasmids from prokaryotes to eukaryotic cells is not demonstrated. Whether the hypothetical transfer would lead to carcinogenesis is also not demonstrated.

A wide variety of intestinal bacteria leave their compartment and cause disease at other sites. This happens all the time.  Often enough that there is at least one patient in your local hospital for exactly this reason right now :)

I want to understand what you mean, the comment is unclear in intent. Gut microbes cause disease all over the body, but can they cross a healthy intestinal lining and the gut-blood barrier? And can you give an example of a disease 'at other sites' caused specifically by gut microbe infiltration, so we are on the same page? Gastroenterology is a very rich field and it's not my strongest point and the specifics are, well, quite specific. Cheers!

The intent of the comment is to correct an error in your answer. Pathogenic enterobacteriaceae often penetrate the intestinal lining. This is a common cause of sepsis, endocarditis, meningitis, and a rare cause of pneumonia (pneumonia that cultures positive for enterobacteriaceae is more often due to aspiration). Certain types of gastroenteritis are caused by invasive infection as well. Your gut is a good barrier most of the time, but gut and mouth bugs often get through. Sometimes the result is transient bacteremia. Sometimes it is disease.

I stand by the statement that very few bacteria penetrate healthy intestinal lining. Perhaps I should have mentioned it is known that even in healthy individuals, there exist small amounts of viable bacteria in the urine and in healthy blood, even though, in medical circles, both are typically referred to as sterile environments. And, as you say, if any lining is compromised, bacteria and other microbes will certainly access circulation.

the statement you're standing by is unsourced and disagrees with my medical and infectious disease specialist training, my clinical experience, and basic textbooks on medical microbiology, internal medicine, and infectious disease.

Look, you wrote an otherwise good answer with an error in it. I'm trying to help you make it a better answer. :)

Clearly we are talking about different things. Help me understand: you're talking about special, medical cases in which bacteria pass from the lumen into the body. I don't doubt that. And I'm talking about the general case, where a healthy intestinal epithelium is, albeit a rich bacterial niche, an entry barrier for organisms even as small as bacteria. From Medical Microbiology, ch. 95: Microbiology of the Gastrointestinal Tract: Once the mucosal barrier is breached, bacteria penetrate through the intestinal wall into the normally sterile peritoneal cavity and its surrounding structures."

Happy to help :) You are correct. A healthy intestinal epithelium is an entry barrier for pathogens. The thing to remember, though, is that, while normal physiology (barrier holds) is normal, pathological processes are common. That barrier is violated in every living human. Sterile compartments are sterile, not just because of barriers, but because of active clearance mechanisms within the sterile compartment. Consider, for example, the neutropenic patient. One of the most common complications in these patients is gram negative bacteremia of enteric origin.

Bacteria get through. When they do, if we have enough WBCs, they clear them (among other mechanisms), which involves bacteria getting into eukaroytic cells. Your answer is good. Horizontal transfer of a plasmid from a prokaryote to a human would be an unexpected and exciting finding. The final point you try to make supporting that argument is just a little off because of a common misunderstanding (held by many very smart and accomplished people), which I expect you hold because you just haven't had the very specific education that would help you understand how often pathologic processes occur.

these are not special medical cases, they are common, everyday medical cases that have occurred in every living human :)

Very good! Upon review, my last sentence could be misinterpreted, or worse, could be misleading - I've adjusted it to clarify that it's not an in principle case but an in practice case of prokaryotes passing into human circulation. I hope it will be clear to anyone reading that prokaryotes are found in what is referred to as 'sterile' bodily fluids, and they become especially prominent and potentially problematic if barriers and/or clearance mechanisms are compromised. Glad we rounded it up and added a few supplementary points as an addendum for others to peruse. Cheers!

good edit. I'm still not going to upvote, though, because you still seem to misunderstand that this statement: Very few bacteria can penetrate a healthy intestinal lining is incorrect. A wide variety of bacteria can penetrate a healthy intestinal lining, and they do so in the absence of prior gastrointestinal disease. The blood compartment, for example, stays sterile because WBCs clear those bacteria. The physical barrier is only part of the mechanism. A sterile compartment stays sterile because of active clearance mechanisms.

Your rudimentary statements are correct. However, what you now (finally clearly) stated is absolutely far from being correct and has never been demonstrated. Provide sources if you make strong claims like A wide variety of bacteria can penetrate a healthy intestinal lining, and they do so in the absence of prior gastrointestinal disease. Some reasons below:

(i) only a very small fraction of total bacteria cross the lining even when the entire barrier is disrupted to an extreme extent. (ii) only a very small fraction of bacteria functionally equip hemolysins or other known toxins to lyse enterocytes or disrupt tight junctions, or affect their shape in order to penetrate the lining. (iii) even affected enterocytes purge their contents into the lumen (Chassaing et al. 2017) (iv) even inflamed gut linings, like in colitis, are permeable only to small molecules, and permit no access to bacteria.

(v) in the vast, vast majority of gastrointestinal issues (i.e. abnormal conditions) what is known and demonstrated to occur is the expulsion of water and other small molecules, activation of the nervous and endocrinological system but not the entry of bacteria. (vii) bacterial encroachment has not been observed nor documented in any person who is not disposed or immunocompromised. in fact, it is only observed in diseased people, and only in very limited parts of the digestive tract. My two cents: Very small fractions of very few types of bacteria rarely cross a normal gut lining.

I've been saying the same thing ever since my first comment. Many species of bacteria leave the GI compartment. I see this all the time in clinical practice. Certainly the dose is small, but it happens often. The gut is not a perfect barrier. Active clearance mechanisms are also needed in order to maintain sterile compartments. If you would like me to answer more thoroughly than I have in this long back and forth comment section, feel free to ask a question.

I see this all the time in clinical practice reveals bias, no? Unlike anecdotal medical practice, I'm sure you understand very well that biology, and also epidemiology, rely on experiment and statistics, and the very central concept of random sampling. This determines the healthy norm. By way of example: pulmonary embolisms are not the norm, they are extreme events, and no internist making the case that they happen to everyone if they live long enough should convince us that thrombogenesis is a frequently-occurring, healthy, normal occurrence in lung vasculature. Let's agree to disagree.

I seem to be failing to communicate the issue here, because you keep misunderstanding. For your analogy, sepsis would be the pulmonary embolism, bacteria escaping from the GI compartment and being cleared by the immune system would be clot formation. Clot formation happens often. Bacteria are often stopped by the immune system rather than the epithelial barrier. We know a barrier is not sufficient to prevent enteric bacteria from disseminating to other sites. I'm well aware of the importance of appropriate statistical methods. I teach those methods to residents and other physicians.

Your statement was in the context of an argument about bacteria somehow not being near eukaryotic cells on a population level. The relevant frequencies here are not the average or most common state of the GI tract. This is a pathophysiology question. Does this happen with a frequency that could cause disease? That's the question.

I agree with your conclusion (I don't believe plasmid transfer between prokaryotes and humans occurs), but your barrier argument doesn't make sense in this context exactly because this is already a well established mechanism for pathogenesis in infectious disease. Here, the identification of enteric pathogens in many body compartments in clinical practice is exactly the kind of data that counters the argument "bacteria can't do this because they don't cross the barrier". You do not need to establish, e.g., the prevalence of positive blood cultures in a healthy population.

In addition to understanding the importance and role of random sampling, if you want to progress in your field and do good work, you need to understand which class of data allows you to draw which conclusions and what kind of evidence supports, suggests, or opposes what kind of hypothesis.

Let us continue this discussion in chat.


text:
Can you make sperm and eggs from the same person using in vitro gametogenesis?
In a recent popular science article there is a discussion of the potential disruptive technologies that could become available with in vitro gametogenesis (IVG). Using skin cells you will be able to create either sperm or eggs. Thus, using stolen cells from Brad Pitt (simpler than getting his sperm) will allow a woman to have a nonconsensual child of him. What is not mentioned in the article and thus my question: Does this technique currently allow, (at least in mice), to make sperm from a female and eggs from a male? If that is the case, what will be the result of fertilizing sperm and egg from the same individual: a clone, a genetic "sibling" (not an identical twin), or neither of them?

Related post http://biology.stackexchange.com/q/27736/3340 (it is older than the IVG paper but some points are still valid).

Thanks guys from your comments. Also, feel free to edit the title if the edit I just made is still misleading.

Possible duplicate of Does a man contain all the genes needed to make a woman?

At present (early 2017) the answer is No.
The trick to make spermatid like cells (ie they are not real sperm cells and need to be injected into an oocyte to accomplish fertilization) from ES and iPS in a dish was just achieved last year http://www.sciencemag.org/news/2016/02/new-method-grows-sperm-dish
The trick to make oocyctes from stem cells is not as complete and still requires an lab grown ovary to complete the process. http://www.sciencemag.org/news/2016/10/mouse-egg-cells-made-entirely-lab-give-rise-healthy-offspring.
The methods above still use ES cell of the appropriate gender. Female ES cells to make oocytes. Male ES cells to make sperm.  No info on female ES cells being driven to make sperm or even spermatid like cells.
That said... we have this paper http://news.nationalgeographic.com/news/2004/04/0421_040421_whoneedsmales_2.html, where a mouse is genetically engineered to produce oocytes that have imprinting patterns similar to a sperm. This genetically modified oocyte is then forced to fuse with a normal oocyte. Success rate was very low. 371 fused oocytes, 10 live births, 1 surviving to adulthood.


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Effect of zero selection (pressure) on the population health
Evolution naturally produces better features: stronger muscles, teeth and minds. Killing the weakest, evolution wipes defective genes out of populations.
The mutations are necessary for advance. However, they are random and, thus, mostly negative. Right? How does the nature eliminate them from the population?
I see that one mechanism is polygamy: male have higher mutation rates. They tend to reproduce as much as possible. Female have lower mutation rates, they couple with only with best men and contribute much more to their offsprings. So, men generate as much random solutions as possible, whereas the role of female is to conserve the best of them. This means that the most of the male (bad mutations) die unreproduced. This eliminates the bad mutations and favours the progress of good qualities. The higher animals started to form harems and tournaments over their ownership. This further fosters the elimination of weak men and profileration of strong genes. However, human monogamy has disabled this selection mechanism. Best men are dedicated to only one woman. Other women cannot mix their genes with other good genes from previous generations. They are forced to look at the low quality men, who carry degenerate mutations. Might be it is monogamy that makes us human but it implies that all genes reproduce.
Yet 100 years ago it was not a big deal since we still had another filter: our grandfathers were born in families that had normally 10 children (I am speaking about Russia) and only 2-3 survived until reproduction (the population increased really slowly). I bet that those who survived had really good health: thanks to the bad health and immense selection pressure, the negative mutants are eliminated immediately and population maintains a perfect genome (aka biologic health). Killing more weakest in the current generation improves the health of next generations.
However everything has changed during the 20th century. The advances in economy and medicine have almost eliminated the selection. The selection pressure has relaxed to essentially zero so that everybody survives and leaves the same amount of offspring (and some scientists are even concerned that degradatory individuals leave more offsprings than the prosperous ones). We have even eliminated the infant mortality. We use baby incubators so that the people with the weakest health could survive and reproduce as normal and we are proud of it. It may sound strange but the mutation rate has not changed at all. Does it mean that the human genome is in danger?
I see the situation like you have inherited a perfect mechanism and decided not recovering it from the inevitably adverse action of entropy, that degrades it constantly. There is a constant chance, d, that every good gene is affected by a mutation. It is a fraction of healthy genes that will fail passing to the next generation. This will leave only (1-d) genes healthy in the next generation. The fraction of healthy genes will melt like 1, (1-d), (1-d)², (1-d)³, an so on, with every generation.

You see the fraction that stays healthy over generations. It decays exponentially. Any utility turns into entropy (aka garbage) exponentially, if not protected. Is this model correct? How quickly does this dissipation go? What is d? Let's assume absolute survival and equality in the reproduction rate among all groups people. How many generations is needed to lose 50% of good qualities?

I need to point out one thing, natural selection does not bring species to perfection.  The best mutant may not be selected for many reasons.
When you have no selection pressure then you have neutral evolution concurring and what takes over instead of natural selection is genetic drift.  Genetic drift is just sample error.  Say you have 1,000 individuals in a population and all of those individuals reproduce, in the next generation all the genotypes would be in the next population.  Now imagine if you only had 10 individuals in the population and only 5 of those individuals were randomly selected to produce 10 individuals in the next generation (the parents die every year).  There is no selection pressure but just by chance some individuals reproduce and some don't.  If you do this over and over again what you will see is that some genes become fixed in the population, meaning that there is no other genotype in the population.
This fixation at small population sizes can occur with either beneficial or deleterious mutations.  Obviously if a mutation is very deleterious the individual will die but slightly deleterious mutations can become fixed in the population as well.
There is an entire field of biology devoted to this study.  It is called population genetics.  The probability for fixation for an allele is its proportion in the population.  This proportion can be calculated by 1/2N, where N is the population size.

Even if a species lives in abundance, there is still an evolutionary arms race: who reproduces the fastest? Even slight advantages in reproduction rate multiply over the generations.
There are, however, cases where selection pressures on specific traits have vanished. For example, for fish living in caves, there is not selection pressure to be able to see, and they lost  their eyes. A more complete discussion can be found in this paper: "Relaxed selection in the wild" -- see also this summary with a funny cover image of a species living in abundance.


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Why do you need you room dark for melatonin release?
There is a light pollution movement that says lighting at night obstructs melatonin production. They say:

What makes you fall asleep are changes in the level of the hormone
  melatonin circulating in your body. During the day, light stimulates a
  part of the brain. This brain part (known as the suprachiasmatic
  nucleus) tells the pineal gland to decrease the melatonin level when
  it is light out and to increase it when it is dark. The brighter the
  light, the bigger the decrease and the darker the dark, the bigger the
  increase of melatonin. By making your days lighter and your nights
  darker, you can improve both the quality of your sleep and the amount
  of time it takes you to fall asleep.

and recommend all kind of protection against the light,

Dark Nights: Make your nights as dark as possible. Draw the curtains,
  close the shades and keep the lights off. Try a sleep mask if you
  can’t get eliminate enough light. The darker your night, the quicker
  you will fall asleep.

Do I sense the light by the whole skin surface or only open eyes? If you sense by eyes, which are closed during the sleep, then what is the problem?
In other words, the question is: is the sleep mask sufficient for melatonin secretion or you need to cover the skin?
update What if I close only one eye? I tend to do this when the blinding sun shines. Does such light eject melatonin?

Close your eyes and look at a bright light. Close your eyes in a dark room. See the difference?

Do they give any reference whatsoever about that (I mean improving sleep quality etc)?

So, the question is: is the sleep mask sufficient for melatonin secretion or you need to cover the skin?

The release of the hormone melatonin is responsible for the feeling of sleepiness. It is released by the pineal gland and production starts when the light fades, as it's production is inhibited by light stimulation of the retina, the onset of the production is called dim-light melatonin onset.
Read more about this at this previous answer.
This study on blind people will show you that the light entering the eyes is the (main at least) regulator of melatonin rhythms. They took blind people, 19 of whom could perceive light and 30 who could not, and showed that 14 of 19 light perceivers had normal melatonin rhythms while 23 of the light-blind people had abnormal or unclassifiable rhythms.

Do you mean that the skin surface is not responsible? Then, why do they recommend the face mask only as the last resort? Why do they want the lights off in the first place?

@Val The quotes you put don't recommend "an eye mask as the last resort," but I assume the more you do the more light you can prevent the better - living here in Sweden I can tell you that blinds and curtains being closed and lights being switched off does not mean you will get darkness during the summer nights - an eye mask is a very effective measure.

@Val I've also added a little about an interesting study on blindness and melatonin production


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Can GENESIS simulation software be adapted to other types of tissues?
GENESIS simulation software http://genesis-sim.org/ is designed for neurobiological systems and it is able to inculude in the simulation the different resolution levels - starting from the molecular interaction and ending with neuronal interaction. My question is - can GENESIS be applied to other tissues, are there efforts to do this and what kind of adaptations should be made? I guess that GENESIS is already capable to include full diversity of the molecular interaction patterns that are common to all cells. But some tuning is necessary for models at the cellular and multi-cell level? I guess that there is lack of dedicated GENESIS-level software for other tissues and systems.

Perhaps you can "switch off" the specific neuronal pathways to simulate a normal cell. However, I cannot comment much without knowing the details of the model used in the software. However, you can try this software called virtual cell. It also allows importing different models created by different people, from a repository.

I'm only vaguely familiar with GENESIS but can't imagine using it for non-excitable cells, since the core is the differential equations you use to simulate membrane potential. You could certainly use it for other excitable cells like immune cells to study just those properties, but if you were interested in, say, muscle, you'd probably want a whole other set of dynamics not incorporated. Maybe they've added more detailed molecular interactions since I looked last and maybe you can provide a more specific link to what you are thinking about so we don't have to dig through the docs.


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Why does 4-thiouracil labelling to map RNA-binding proteins cause a T-C change?
I am now reading a paper about the purification and identification of mRNAs and its RNA binding proteins by using UV crosslinking and immunoprecipitation. I came upon this sentence which puzzled me

Up to 28% of all uridines present in 3' UTRs showed diagnostic T-C
  changes in the protein occupancy profiling sequence reads. This number
  is reasonably high, considering observations that typically only one
  of a few uridines in RNA binding sites when substituted by 4SU,
  crosslinks to proteins.

What I do not understand is why does 4-thiouracil (4SU) labelling in the cell show T-C changes. Would the uracil-adenine base pairing not be affected?
How does the 4SU labelling really work?

The technique used in that paper is called PAR-CLIP (Photoactivatable Ribonucleoside-Enhanced Crosslinking and Immunoprecipitation; see Ascano et al., 2012 and Spitzer et al, 2014). This technique involves substituting uridine (U) with 4-thiouridine (4SU) or substituting guanosine (G) with 6-thioguanosine (6SG). The rationale behind using these modified bases is that they improve the efficiency of RNA-protein crosslinking. Moreover, PAR-CLIP uses 365nm UV instead of the 254nm UV used in the conventional crosslinking. However, the crosslinking process causes the loss of the sulphur atom causing the U to be read as C during reverse transcription. Likewise, 6SG gets read as A.

Ascano et al., 2012


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Rethinking SARS-CoV-1 and MERS-CoV deadliness after lessons learned from SARS-CoV-2
SARS-CoV-1 case fatality rates were about 9% and MERS-CoV case fatality rates were over 30%.
And now there is a newly discovered MERS-CoV relative, which some scientists have warned may be only one or two mutations away from making the jump to humans, and might be as deadly as MERS-CoV in humans.
But in the case of the SARS-CoV-2 pandemic, we've found that our initial CFR was higher than the true IFR. Can we expect that the CRFs for SARS-CoV-1 and MERS-CoV are similarly misleading? Are we able to estimate IFRs for these coronaviruses any better now that we have so much experience with SARS-CoV-2?

The CFR for SARS and MERS is calculated from the numbers of infected and died prople from the disease. Since both cause severe disease and as far as I know asymptomatic disease is not happening there (though I might be wrong) I don't think the numbers are way off.

If you have additional information relevant to your question please edit it into your post (comments are ephemeral and often overlooked). Adding sources to your question would make it stronger as would making the title more focused — as written it sounds like you are trying to start a discussion, which is expressly off-topic for this site. However, I encourage you to find sources in the medical literature or other reliable sources — the news media, even when they are trying to be honest, often oversimplify or make significant factual errors.

CFR is always higher (or at least as high) as IFR, since not every infection results in a symptomatic case. With SARS-CoV2, asymptomatic infections (or nearly asymptomatic one) are a big problem as they make contact tracing so difficult.

The reason CFR and IFR were off for this pandemic were that we had no idea of the full scale of the infections early on - pretty just those that turned up at hospitals and based on symptoms alone (i.e. no tests available). Once tests were developed and we could test anyone who was identified as a case or a contact, then the numbers rapidly fell and became more realistic.
Not so with SARS and MERS, where as far as we know most people get sick and were isolated so we can definitively say the CFR and IFRs. As SARS is no longer around, the CFR and IFR are known definitively.
Sero-prevalence (note this doesn't indicate infection necessarily, but exposure to the virus in some form) has been measured1 and found to be very low for MERS at around 15/10,000 in Saudi-Arabia. For SARS sero-prevalence was about 0.1%2 in asymptomatic people from those exposed to SARS-CoV-1 infected patients.
1: Muller. Lancet Infect Dis. 2015 May; 15(5):559-64.
2: Leung . Epidemiology & Infection, Volume 134, Issue 2, April 2006, pp. 211 - 221


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An alternate cure for AIDS?
Is is possible to cure AIDS patients by using white blood cells of blood cancer, by fooling HIV to attack a false target?
Is it possible to wrap HIV in a physical boundary, such that it has no interaction out side the wrapper, so the functionality of the cell will not be affected by HIV?. Since all cells in out body are replaced within three years, after 3 years, the HIV affected victim will have fresh HIV free cells.

So you're trying to cure pest with cholera? Leukemia also causes problems with the immune system (since mainly only one clone is maintained) so this wouldn't be a good idea.

why not give a try in a worst case?

Because HIV can be controlled for quite a while with the actual medication. And who will be the person conducting these experiments? This is unethical.

The reason AIDS develops is that your normal run of the mill immune cells are plenty potent enough to kill off all of your Helper T-Cells that are infected with HIV, so now you want to let loose killers that are not necessarily specific to cells infected with HIV that will lay waste to everything else?

What would you choose when your treating physician gives you the option: leukemia or antiviral treatment? HIV is not lethal anymore these days, at the least life expectancy can be substantially prolonged. Admittedly, treatment is life long and not a cure, but you'll live.
Leukemia on the other hand, is life threatening and needs immediate treatment. Treatments for leukemia are primarily chemotherapy, and perhaps radiation therapy, biological therapy, targeted therapy, and stem cell transplant, all of which are by no means guaranteed to be curative.
But interestingly: a Berlin leukemia patient with HIV was actually cured after receiving chemotherapy and having received HIV-resistant stem cells to repopulate his white blood cells (Source: Medicine Net). The donor carried the relatively rare mutation called CCR5delta32. People with this mutation lack functional CCR5, the protein that HIV most often uses to enter cells.
Why is this not a standard treatment? The Berlin patient serves as a good example, because the patient suffered intestinal and neurological symptoms due to the chemotherapy. And besides being dangerous in itself, chemo is truly a grueling experience to go through. And in fact, this patient was the only instance in which this approach was followed (Source: Medicine Net).

Then why not try the vice versa: treating Leukemia with HIV?

@JohnyRoyan - All cancerous cells need to be killed off. AIDs infects many, but not all.

At least we can have a try, no ?

@JohnyRoyan - trying new treatments needs careful risk-benefit analysis as well as ethical consideration. Given the grave dangers associated with leukemia, and minimal chance of success, both will not have a positive outcome I'm afraid.

is it possible to wrap HIV in a physical boundary,  such that it has no interaction out side wrapper, so the functionality  of the cell will not be affected by HIV. Since all cells in out body are replaced within three years, after 3 years, the HIV affected victim will have fresh HIV free cells?

No. See this answer to 'How fast do different organs turn over cells?' and this answer to 'Why is an HIV infection considered “incurable”?'.

I wouldn't say it's not lethal. Just because people can survive a decade or more with treatment does not mean it will not kill them.

@forest, thanks, I have toned down that statement.


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How does a virus reach its host, it is always passive?
We know that viruses are non motile and cannot metabolise, and that it enters the host cells via binding to the receptors. But how exactly it reaches the host
(that is, how it go from the transmission medium (e.g. the aerosols) to actually make contact with the cells in the host)
If it rely on simply diffusion to bump into the host cells' receptors, what makes the odds high enough so that such proliferation strategy is efficient enough to ensure the virus to multiply and proliferate?
In addition, once it has released its DNA into the cell, what helps the DNA to reach the nucleus and not drifting randomly within the cell for a long time, that is, is there exist mechanisms or transportation pathways that actually guide the DNA from the perimeter of the cell through the cytoplasm in the middle and towards the area where the nucleus lie?

Different viruses have different modes of spreading- some are water borne, some are transported via aerosols, some are sexually transmitted etc. Your question is a little broad. You should narrow it down.

A textbook could be written to answer your last question--agree with WYSIWYG that you should narrow your question

it is called statistics. Virus or DNA do drift around randomly, but a) there are a lot of DNA/viral particles and b) when virus binds, it stays (so as DNA). And waiting time is not too high

@WYSIWYG I have narrowed down the question by elaborating that I am interested in the pathway on how the viral DNA move from the perimeter of the cell through the cytoplasm to the nucleus, and, how once the virus reach the host via aerosol etc. how they actually made contact with the cell to enter them
.At the time of the edit, it seems aandreev might have provided an/the explanation and Chris have provide a more detailed explanation

There are a number of different ways to spread a viral infection. Some viruses sit on surfaces (or infected persons) "waiting" for someone to touch and take them up, this is called smear infection. Other viruses are airborn inside of small droplets distributed by coughing or sneezing. These are inhaled and can then cause a new infection. Other viruses are transmitted through our body fluids (blood, semen) and either need a wound or can be transmitted sexually (for example Herpes or HIV). Other viruses are transmitted by animals which bite humans (Dengue and rabies would be examples here). Have a look into the Wikipedia for more details and examples.
Additionally viruses are produced in vast numbers by their hosts with most viral particles never reaching a new host. This strategy helps a lot to transmit further.s
For entering the nucleus (which is an obstacle) the viruses use the nuclear pore complex (NPC). Depending on what virus tries to enter the nucleus, different strategies are used. Some viruses are too big and release their DNA through the NPC into the nucleus, while others can pass through and some get stuck inside and release their DNA/RNA at this point. A last group uses the time during mitosis when there is no nucleus. See this figure (from here)
and also the references below:

References:

Virus strategies for passing the nuclear envelope barrier.
How viruses access the nucleus.
Viruses challenge selectivity barrier of nuclear pores.

Some virus DNA or RNA might wait cell division to get into nuclei. For example retrovirus genome is not integrated to the genome of the host cell until cells are divided. However, lentivirus does not need to wait for cell division, because one of proteins in lentivirus binding to virus RNA genome has a nuclear transport signal.


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(Aquatic gastropod) Physae identification
I need help to identify a physa.
What are the identification keys to make the difference between:
 physa fontinalis,

physa marmorata
, physa acuta (syn. Physella acuta)
The difference that can been seen with the eyes, no microscope, and except their biotope? (As they are in my house, not in their biotope)
differences or identification criteriae? What are the right organs to check of the difference in eggs, etc.
There is a variability of color in snails, and a variability of sizes. One specimen in some conditions can be much bigger or smaller than the average, so it's very difficult to identify them.
Some aquatic naturalist here?
Important remark: I don't guarantee the pictures are accurate, the site posting the picture may have confused physae!
I got physae from a vendor, some have a pale body and a more yellowish or partially yellowish shell, some have the tip ot the antennae dark, and have a dark shell and a dark body. The vendor had them together, and it seems they interbreed, but I'm not sure if it's only one ssp or 2. I see nowhere color mutation of physae on the internet.


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Calculating Protein Concentration from Kilo Units (KU)
I am looking to purchase Pyruvate Kinase from the Sigma Website, they state the volume in Kilo Units (KU) i.e. 1, 5 or 25 KU. It also states there are 350-600 units / mg protein.
Does this mean one unit is one protein? so 1KU is 1000 units of protein?
What is the relationship between the KU and mg? and how can I use this relationship to calculate my concentration in um or mg.

EDIT
In this paper (look at the methods section) they calculated the concentration of 25,000 units of calmodulin in 0.5 ml to be approximately 75um which is 40,000 units/mg. How did they calculate this?

The figure of 350 - 600 Units per mg refers to the specific activity of the enzyme.
The Unit is International Unit or IU and is usually defined as that amount of enzyme that will catalyze the transformation of 1 micromole of substrate (or product) per min, under defined assay conditions (such as pH, temperature, substrate concentration, presence of Mg++, etc). It is thus a measure of activity.
When the enzyme is pure (no other extraeneous proteins present), the specific activity provides important information about the catalytic capacity of the enzyme.
It is usually calculated by measuring

the activity of the enzyme preparation under defined assay conditions
the protein concentration of the same enzyme preparation (using, say, the Lowry or Biuret method for protein estimation).
Alternatively, if the E(1%, 280) is known (see below) and the enzyme is pure, measurement of the absorbance at 280 nm gives a very good estimate of protein content (and the enzyme may be recovered 'unharmed' at the end of the measurement).

Thus, taking a figure of 450 Units/mg for the specific activity of pyruvate kinase,
25 KU (25 Kilo-Units, I presume) contains 500/9 mg (~55 mg) protein.
I notice that the Sigma product sheet provides a figure for  E(0.1%, 280) = 0.54.

This means that a 1 mg/ml solution of the protein will have an absorbance at 280 nm of 0.54

E(0.1%, 280) can be used as a very convenient measure of the protein content provided that the enzyme preparation supplied by Sigma is pure.

A 'rule of thumb', useful when the E(0.1%, 280) is unknown, is that a 1mg/ml protein solution has an A280 of 1.

Thus if, say, the A280 (absorbance at 280 nm) of the resuspended lyophilized powder is 1.08 and you have 5 ml of this, the protein concentration is 2mg/ml and you have 10 mg of protein in total.  You may wish to assay the enzyme yourself to determine an accurate specific activity.
The EC (Enzyme Commission) Number may also be of interest.  For pyruvate kinase (EC 2.7.1.40) see here.
For a great ref on PK (pdf may be downloaded) see here (Ainsworth et al.)

For your second question, I do not have access to that paper from home.
However, if calmodulin has a specific activity of 40 000 Units/mg,
 25 000 Units is equivalent to 0.625 mg; this is in a volume of
0.5 ml.  Therefore, the calmodulin concentration is 1.25mg/ml.
Taking the molecular weight of calmodulin to be 16 000,
then 16 000 mg /ml (theoretical) would be a 1 Molar solution.
Thus a 1.25 mg/ml solution is about 78 micromolar.

As far as I can see, "25 000 Units is equivalent to 0.625 mg; this is in a volume of 0.5 ml. Therefore, the calmodulin concentration is 1.25mg/ml."  is correct?

From the page linked from your link:

Unit Definition
One unit will convert 1.0 μmole of phospho(enol)pyruvate to pyruvate
  per min at pH 7.6 at 37 °C.

So, the unit is defined by activity, and there is no way to know how many molecules or milligrams of protein are included

What about in the paper I referenced? They calculated the concentration of calmodulin to be approximately 75um.

After some serious thinking it is possible to calculate the mg. On the website it states there is 350-600 units/mg protein. So if I bought the 1KU to work out the mg and assuming I receive 600 units I would divide 600/1000 = 0.6 mg. I completely missed the obvious here.

You can obviously calculate the moles or weight by purifying the enzyme and weighing it...

@TomD: sure, but that's the way one would do it!

@TomD: I am not saying HE should do it, I am saying that is one method to do it. The Biuret method would also work, although it only gives you an approximate concentration. If weighting is not an option MS or similar should do.

@TomD: well, I let the nice people at Sigma do the tedious work for me :D

direct protein concentration measurement is a lot easier