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How does Golgi's neural histological stain work?
What is known about the targets of Golgi staining of neurons? Are larger neurons more likely to be stained? Are specific cell types more susceptible than others?
The current wikipedia article says the mechanism is still not fully understood. What is preventing us from using the advanced molecular biology techniques to understand the process?

Some background information.
First of all one should notice, that Golgi staining belongs to so-called morphological types of stainings in neuroscience, where the actual anatomy of different neurons is revealed (compared to other techniques, like Ca-imaging or potential imaging).
Second, Golgi staining is a type of silver staining, there the sedimentation of silver or its salts (here: silver chromate) reveals the morphological traits of the cels.
And, third, Golgi staining is applied to fixed preparation. This means that the tissue (normally a brain slice) is pre-treated (here: with formol) to kill all cells and arrest every biological process.
What is known about the targets.
The common description of the target is quoted as "a limited number of cells at random in their entirety". This is the essence of Golgi staining:

Only single cells are stained, therefore there is no impediment from adjacent cell staining while deriving the morphological structure of the cells (very important for light microscopy where you have integrated input from different depths).
The cells are stained randomly, there is no known preference among neuronal cells for Golgi staining and I haven't seen any other types of cells in CNS stained with Golgi, therefore it is quite specific for neuronal cells (and leaving macro- and microglia, astrocytes etc. intact).
The cells are stained in their entirety, meaning that the complete cell is stained very nicely, showing detailed arborisation of dendritic tree, that was very important in studying of Purkinje cells in cerebellum.

Are larger neurons more likely to be stained? Are specific cell types more susceptible than others?
Golgi staining is used mostly for brain slices (I have never seen or heard its application for other tissues). Traditionally one of the biggest cells here are pyramid neurons (NA, ACh-ergic) and one of the smallest are interneurons (often GABA-ergic) -- both are amenable to Golgi staining (reference) and there is no seemingly clusterization of stained cells by their size or transmitter type.
What is preventing us from using the advanced molecular biology techniques to understand the process?
I can name several reasons for this:

Since Golgi staining is applied to fixed preparation the tissue is already "damaged" (formol leads to dessication of cells and shrumping), therefore it is difficult to use some fine mollecular biology methods to investigate these tissues.
There is no way to tell which cells get stained beforehand. And as long as  the microcrystallisation of silver chromate is started it can't be (easily) stopped and reversed. Therefore it is difficult to look at what caused the staining afterwards, then the whole cell is impregnated with silver.
I think there were no real attempts to crack the mistery of this staining: how intersting it might be, this seems to be an interdisciplinary question on the brink between biology and chemistry. So, maybe one day somebody will look into it and explain everything.

Nice answer, but I'd take issue with the statement that Golgi stain is neuron specific.  Golgi method does stain glia, e.g. Ramon y Cajal's retinal drawings often include Muller glia: http://webvision.med.utah.edu/imageswv/CajalMuller.jpeg


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Why does so much variation exist within species?
My last phrasing of this question did not go down well, so I will try again.
The genotype of species is not always the same. If you ask yourself why not all of these possible expressions except one have died out, a natural answer is each genotype occupies a specific niche: For example, different eye colors might be found attractive by different kinds of people. If the the genotype for one eye color became more rare for some reason, other individuals with this genotype had a higher mating chance; the frequency of that genotype would get pushed back up.
But there seem to be genotypes (for example, having zits) that don't occupy any niche at all. Why didn't they die out?

I'm still not convinced we are quite 'there' with this question to be honest.  Firstly I don't think acne can be considered a genotype (although there may be genetic factors).  Are you talking about adult persistent acne or transient teenage acne (which 80% of 11-30 year olds are affected by)?  Similarly I don't really understand your example with eye colour.

Agreed, acne is a phenotype, not a genotype. Also it's possible that, in some cases, acne is an effect of Antagonistic pleiotropy, and as such, would have no need to occupy any particular acne-related niche to propagate well..

variation generally is proportional to the number of individuals in the species and how quickly it has been increasing in number over time.  so some species, with small numbers in recent history have relatively little variation.  in that light the question doesn't make as much sense.

First of all, your assumption is incorrect: those are not genotypes and they do not occupy specific niches. You are talking about phenotypes (eye colour) or in the case of acne, not a trait at all.
I'll answer the question I think you're asking: why does biological variation exist?
Variation is constantly being generated by mutation, errors in the replication of the genome of an individual. If a mutation occurs in the gametic cells, it affects the genotype of the offspring. By affecting the genotype, it may or may not have a discernable effect on the phenotype. Where a gametic mutation isn't fatal, it has a chance of becoming established in the population when that mutant individual breeds. That chance is increased the further along the gradient from harmful to beneficial that effect of that mutation is.
Variation also exists because development responds to environmental factors, not just genetics. Different individuals grow in different environments, and have unique combinations of factors influencing many traits.
The reason variation persists is because, except under conditions of extreme selective pressure or genetic bottlenecks, many traits have no impact on survival or fecundity (reproductive success) or are determined only partly by genetics. Height, for example, only has a very slight impact on fecundity within quite a broad range of heights. It is partly genetically determined, and partly determined by environmental factors such as diet (Eckhardt et al. 2005), exposure to toxins during development, muscular development etc.
If height were the key factor in human mate selection, we might see a gradual reduction in the range of heights, and a gradual increase in average height. However, what we see in reality is that height has changed through human history in concordance with economic factors like social status, inflation and war (e.g. Steckel, 2001), suggesting that nutrition is a major determinant.
I know it wasn't your choice of example, but for more detail on the effects of natural selection on human height, see this question.

It sounds like you're also trying to ask the question, "how can non-adaptive or maladaptive traits evolve?" and that you're not necessarily interested in acne specifically.  The following are just a few examples.
It is possible that a gene that contributes to an undesirable trait, might also play a role in a strongly desirable trait. The classic textbook example of this is the gene involved in sickle-cell anemia, which causes the disease in homozygous individuals and is almost asymptomatic in heterozygous individuals. Since the gene helps with resistance to malaria, heterozygous individuals are actually better of than those with no mutation of this gene in areas where malaria is prevalent.
However, this is not the only way a less than optimal genotype can persist. A gene may only produce an undesirable trait in combination with certain other genes, and there may not be enough selective pressure for it to be eliminated form a population.

I think there are two elements to this answer. To cut to the short answer skip to the bold summary at the bottom...
Firstly, genetic variation exists because of mutation. Genes get mutated every generation, the . Larger populations will have more mutants within them because: more individuals = more nucleotide base pairs (C's G's A's and T's) = more potential sites of mutation. However mutation is not likely to explain the persistence of variation because mutation rates are very low (1 in 100,000 to 1,000,000 gametes have a newly mutated loci at any individual locus) and singleton alleles have only a 50% chance of reproduction (assuming no selection) so are likely to be lost by drift (Falconer & Mackay, Intro to Quantitative Genetics 1996).
You also talk about acne, which is likely to have a large component of environmental variance. Therefore you should remember that not all phenotypic variance is genetic its source and it is  highly likely that an individual trait has some degree of environmental variance component. Simplistically:

Phenotypic variance = genotypic variance + environmental variance

So the bigger question is why does variation persist? There are many potential causes of this which continue to be widely debated. Essentially it seems paradoxical because selection should reduce variation as it drives the fixation of all loci to the fittest allele. However, selection is transient, both spatially and temporally, and is not efficient against rare alleles (especially recessive alleles because they are hidden by dominant traits - e.g. disease "carriers"). Another important point is that some mutations will be neutral, therefore remain unaffected by selection.
In the spatial context, this means that selection is not always favouring the same allele in all places a species inhabits. Selection might be different based on the where it is occurring (within a species, traits like fur would be beneficial to populations in cold climates but not to those in warmer climates - here I am assuming that the sole effect of fur is to improve the ability of retaining heat).
Temporally there are also key elements. Principally, over time selection changes. Again sticking with my fur example, climates change. Ice ages come and go bringing with them different selection coefficients for fur growth.
Another variance in selection can be sexually antagonistic selection, where different alleles are favoured in either sex. In this case selection does not deplete variation but instead maintains it. It has recently been shown that sexual antagonism is prevalent throughout the genome.

the divergent reproductive strategies of the sexes could promote the
  maintenance of sexually-antagonistic variation (Sharp & Agrawal 2012... yesterday!)

Other hypotheses suggest mechanisms by with selection can maintain variation such as assortative mating.
Long story short, you stated that you expect variation to reduce as a consequence of selection. However genetic variation persists for many reasons, and can even be maintained by selection in several ways. Furthermore, phenotypic variation which is what you actually describe with your acne example (and I with my fur example) can be caused by non-genetic components of variation.
.
Suggested reading:
Cox & Calsbeek 2009, Sexually Antagonistic Selection, Sexual Dimorphism, and the
Resolution of Intralocus Sexual Conflict.
Falconer & Mackay 1996, Introduction to Quantitative Genetics.
Singh & Krimbas 2000, Evolutionary Genetics: from molecules to morphology.
Sharp & Agrawal 2012 (in press, accepted on-line version released yesterday, print may be 2013) Male-biased fitness effects of spontaneous mutations in Drosophila melanogaster, Evolution.
Innocenti & Morrow 2011, The Sexually Antagonistic Genes of Drosophila melanogaster, PLoS Biology.
Arnqvist 2011 Assortative mating by fitness and sexually antagonistic genetic variation, Evolution. (also see his book sexual conflict).

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Why is polyploidy lethal for some organisms while for others is not?
Polyploidy is the multiplication of number of chromosomal sets from 2n to 3n (triploidy), 4n (tetraploidy) and so on. It is quite common in plants, for example many crops like wheat or Brassica forms. It seems to be rarer in animals but still it is present among some amphibian species like Xenopus.
As I know in mammals polyploidy is lethal (I don't mean tissue - limited polyploidy). I understand that triploidy is harmful due to stronger influence of maternal or paternal epigenetic traits that cause abnormal development of placenta, but why there is no tetraploid mammals?

Excellent question! A topic of active research and without clear consensus, as far as I remember from some talk.

Great question, plenty to talk about here (give me a few days).

Looking forward to it, @RichardSmith!

We were told in a lecture that odd polyploidies were usually lethal because the third homologuous chromosome disrupted alignment during meiosis.

Diploidy is an adaptive regulatory mechanism that is not necessary to multicellular life.  Plants and cancer cells are notriously unregulated in ploidy count.

Great question, and one about which there has historically been a lot of speculation, and there is currently a lot of misinformation. I will first address the two answers given by other users, which are both incorrect but have been historically suggested by scientists. Then I will try to explain the current understanding (which is not simple or complete). My answer is derived directly from the literature, and in particular from Mable (2004), which in turn is part of the 2004 special issue of the Biological Journal of the Linnean Society tackling the subject.
The 'sex' answer...
In 1925 HJ Muller addressed this question in a famous paper, "Why polyploidy is rarer in animals than in plants" (Muller, 1925). Muller briefly described the phenomenon that polyploidy was frequently observed in plants, but rarely in animals. The explanation, he said, was simple (and is approximate to that described in Matthew Piziak's answer):

animals usually have two sexes which are differentiated by means of a process involving the diploid mechanism of segregation and combination whereas plants-at least the higher plants-are usually hermaphroditic.

Muller then elaborated with three explanations of the mechanism:

He assumed that triploidy was usually the intermediate step in chromosome duplication. This would cause problems, because if most animals' sex was determined by the ratios of chromosomes (as in Drosophila), triploidy would lead to sterility.
In the rare cases when a tetraploid was accidentally created, it would have to breed with diploids, and this would result in a (presumably sterile) triploid.
If, by chance, two tetraploids were to arise and mate, they would be at a disadvantage because, he said, they would be randomly allocated sex chromosomes and this would lead to a higher proportion of non-viable offspring, and thus the polyploid line would be outcompeted by the diploid.

Unfortunately, whilst the first two points are valid facts about polyploids, the third point is incorrect. A major flaw with Muller's explanation is that it only applies to animals with chromosomal ratio-based sex determination, which we have since discovered is actually relatively few animals. In 1925 there was comparatively little systematic study of life, so we really didn't know what proportion of plant or animal taxa showed polyploidy. Muller's answer doesn't explain why most animals, e.g. those with Y-dominant sex determination, exhibit relatively little polyploidy. Another line of evidence disproving Muller's answer is that, in fact, polyploidy is very common among dioecious plants (those with separate male and female plants; e.g. Westergaard, 1958), while Muller's theory predicts that prevalence in this group should be as low as in animals.
The 'complexity' answer...
Another answer with some historical clout is the one given by Daniel Standage in his answer, and has been given by various scientists over the years (e.g. Stebbins, 1950). This answer states that animals are more complex than plants, so complex that their molecular machinery is much more finely balanced and is disturbed by having multiple genome copies.
This answer has been soundly rejected (e.g. by Orr, 1990) on the basis of two key facts. Firstly, whilst polyploidy is unusual in animals, it does occur. Various animals with hermaphroditic or parthenogenetic modes of reproduction frequently show polyploidy. There are also examples of Mammalian polyploidy (e.g. Gallardo et al., 2004). In addition, polyploidy can be artificially induced in a wide range of animal species, with no deleterious effects (in fact it often causes something akin to hybrid vigour; Jackson, 1976).
It's also worth noting here that since the 1960s Susumo Ohno (e.g. Ohno et al. 1968; Ohno 1970; Ohno 1999) has been proposing that vertebrate evolution involved multiple whole-genome duplication events (in addition to smaller duplications). There is now significant evidence to support this idea, reviewed in Furlong & Holland (2004). If true, it further highlights that animals being more complex (itself a large, and in my view false, assumption) does not preclude polyploidy.
The modern synthesis...
And so to the present day. As reviewed in Mable (2004), it is now thought that:

Polyploidy is an important evolutionary mechanism which was and is probably responsible for a great deal of biological diversity.
Polyploidy arises easily in both animals and plants, but reproductive strategies might prevent it from propagating in certain circumstances, rather than any reduction in fitness resulting from the genome duplication.
Polyploidy may be more prevalent in animals than previously expected, and the imbalance in data arises from the fact that cytogenetics (i.e. chromosome counting) of large populations of wild specimens is a very common practise in botany, and very uncommon in zoology.

In addition, there are now several new suspected factors involved in ploidy which are currently being investigated:

Polyploidy is more common in species from high latitudes (temperate climates) and high altitudes (Soltis & Soltis, 1999). Polyploidy frequently occurs by the production of unreduced gametes (through meiotic non-disjunction), and it has been shown that unreduced gametes are produced with higher frequency in response to environmental fluctuations. This predicts that polyploidy should be more likely to occur in the first place in fluctuating environments (which are more common at higher latitudes and altitudes).
Triploid individuals, the most likely initial result of a genome duplication event, in animals and plants often die before reaching sexual maturity, or have low fertility. However, if triploid individuals do reproduce, there is a chance of even-ploid (fertile) individuals resulting. This probability is increased if the species produces large numbers of both male and female gametes, or has some mechanism of bypassing the triploid individual stage. This may largely explain why many species with 'alternative' sexual modes (apomictic, automictic, unisexual, or gynogenetic) show polyploidy, as they can keep replicating tetraploids, thus increasing the chance that eventually a sexual encounter with another tetraploid will create a new polyploid line. In this way, non-sexual species may be a crucial evolutionary intermediate in generating sexual polyploid species. Species with external fertilisation are more likely to establish polyploid lines - a greater proportion of gametes are involved in fertilisation events and therefore two tetraploid gametes are more likely to meet.
Finally, polyploidy is more likely to occur in species with assortative mixing. That is, when a tetraploid gamete is formed, if the genome duplication somehow affects the individual so as to make it more likely that it will be fertilised by another tetraploid, then it is more likely that a polyploid line will be established. Thus it may be partly down to evolutionary chance as to how easily a species' reproductive traits are affected. For example in plants, tetraploids often have larger flowers or other organs, and thus are preferentially attractive to pollinators. In frogs, genome duplication leads to changes in the vocal apparatus which can lead to immediate reproductive isolation of polyploids.

References

Furlong, R.F. & Holland, P.W.H. (2004) Polyploidy in vertebrate ancestry: Ohno and beyond. Biological Journal of the Linnean Society. 82 (4), 425–430.
Gallardo, M.H., Kausel, G., Jiménez, A., Bacquet, C., González, C., Figueroa, J., Köhler, N. & Ojeda, R. (2004) Whole-genome duplications in South American desert rodents (Octodontidae). Biological Journal of the Linnean Society. 82 (4), 443–451.
Jackson, R.C. (1976) Evolution and Systematic Significance of Polyploidy. Annual Review of Ecology and Systematics. 7209–234.
Mable, B.K. (2004) ‘Why polyploidy is rarer in animals than in plants’: myths and mechanisms. Biological Journal of the Linnean Society. 82 (4), 453–466.
Muller, H.J. (1925) Why Polyploidy is Rarer in Animals Than in Plants. The American Naturalist. 59 (663), 346–353.
Ohno, S. (1970) Evolution by gene duplication.
Ohno, S. (1999) Gene duplication and the uniqueness of vertebrate genomes circa 1970–1999. Seminars in Cell & Developmental Biology. 10 (5), 517–522.
Ohno, S., Wolf, U. & Atkin, N.B. (1968) EVOLUTION FROM FISH TO MAMMALS BY GENE DUPLICATION. Hereditas. 59 (1), 169–187.
Orr, H.A. (1990) ‘Why Polyploidy is Rarer in Animals Than in Plants’ Revisited. The American Naturalist. 136 (6), 759–770.
Soltis, D.E. & Soltis, P.S. (1999) Polyploidy: recurrent formation and genome evolution. Trends in Ecology & Evolution. 14 (9), 348–352.
Stebbins, C.L. (1950) Variation and evolution in plants.
Westergaard, M. (1958) The Mechanism of Sex Determination in Dioecious Flowering Plants. In: Advances in Genetics. Academic Press. pp. 217–281.

(I'll come back and add links to the references later)

It's a really great answer. Just a few remarks:

In next to last point you probably mean diploid gamets (gamets from tetraploid individual)
In frogs, if polyploidy changes male vocal aparatus, then it also have to change polyploid female preferences. Otherwise polyploid males would be avoided also by females of the same ploidy and it would be even more difficult to establish polyploid population.

You're absolutely right on both points Marta. Regarding the second point, the key thing is that polyploidy affecting the males' calls creates a situation where it is possible for a female to distinguish a polyploid male from a non-polyploid, which if there was a non-trivial rate of polyploidy arising would then lead to selection for polyploid females which preferred the polyploid males. Without a change in traits for polyploids there is no selection.

This answer was worth the wait. Excellent and thorough!

Beautiful answer.. I actually had the same question and referred Mable. Only if I could stumble upon this earlier! +1

Plants have a simpler anatomical structure than mammals (is anatomical the right word, or would physiological be more appropriate?). Mammals on average don't have more genes than plants, so my understanding is that this additional complexity is the result of finer and more complex regulatory mechanisms.
When you remove or duplicate an individual gene in an organism, that organism must compensate somehow. The more complex the regulatory system, more likely that even small perturbations will cause severe defects or even lethality.
Extend this to the scale of a whole genome, and it shouldn't be surprising that polyploidy is lethal for a lot of organisms. It find it extremely fascinating that it's not lethal for some organisms, but it makes sense that organisms with simpler regulatory mechanisms would be more successful handling a genome duplication event through gene subfunctionalization, neofunctionalization, etc.

This was one of the first ideas suggested when it was historically discovered that many more plants than animals exhibit polyploidy. However, it is not the explanation. I will expand on why it is incorrect when I post my own answer later. As a side point: whilst plants could be argued to be anatomically more simple than animals, they are not physiologically more simple. Animals have different constraints, environmental challenges and adaptations than plants, but ultimately are not more complex.

Thanks for answer. I also thought about it. But it is hard to measure how complex is an organism and among verebrate polyploidy also occure. Maybe amphibians are not so smart as we are, but are they really so much simpler?

@RichardSmith If there is any time to draw up your answer, it is now. I am interested in what you have to say!

@DanielStandage My finals finish on Wednesday, after which I will be back here to answer all the questions on my to-do list, starting with this one :)

In animals, polyploidy is not tolerated and very few polyploid species
  are known to exist. Those that do exist are usually asexual,
  parthenogenetic, or hermaphroditic. Most of the problems resulting
  from polyploidy occur during synapsis of homologues during prophase I.
As plants do not have a chromosomal mechanism for sex determination,
  synapsis and subsequent disjunction is not as great a problem. In
  fact, most plants are monoecious.

These paragraphs are taken from these lecture notes from an Emporia State University genetics course.
Supporting information looks to be present in Why Polyploidy is Rarer in Animals Than in Plants (H. J. Muller, The American Naturalist, 1925), but I didn't get a chance to access the article.

Thank you for your answer. The issue of reproduction of polyploid species is also very interesting, but my question was rather why some organism survive polyploidy (even if they cannot reproduce), while for other it means death at early stage of development. The last article you've quoted may be quite out of date, but I don't have an access to it either. (that's pity, becouse I'm curious what people thought about this issue at the beginning of XX century).

@MartaCz-C: Do you mean, at the beginning of the X diploid century?

My point in stating what is below is to emphasize even when polyploidy is present in closely related species there is a question of why an organism can survive one ploidy event but not another and why tolerance of polyploidy varies among similar organisms?
Several species of deciduous azaleas are tetraploid. Closely related diploid deciduous azaleas are more than happy to accept pollen and produce seedpods. We have attempted such crosses many times and they almost always success in terms of seedpod development.
Tetraploid deciduous azaleas on the other hand are very reluctant to accept pollen from diploid deciduous azaleas. We have attempted such crosses nearly 100 times without success.
However producing seedpods and producing viable seeds are of course different. Some crosses of diploid X tetraploid produce 1 or only a few viable seedlings (We have never gotten none to date.) while others produce viable seedlings measured in dozens while still others produce hundreds of viable seedlings. In some instances, the same diploid parent will produce many more viable seedlings from one tetraploid parent than from another.
To date all seedlings of diploid X tetraploid have measured as triploid using flow cytometry. Most seedlings appear to be sterile but some are fertile and occasionally some are very fertile to the point of setting open pollinated seed.
When these triploid seedling are successfully crossed with tetraploids, we get what appears based on flow cytometry to be triploids, aneuploids between triploid and tetraploid, tetraploids, and pentaploids. The few pentaploids old enough to flower appear to set seedpods when crossed with tetraploids.
In elepidote Rhododendron which has only diploid species, hybridizers over the last 150 years have had very limited success in producing polyploid elepidote Rhododendrons (less than 100 named hybrids) despite amazing success at creating and naming complex interspecies crosses (more than 20,000).
In other words, the pathway from diploid to polyploid can be a struggle for an organism even when polyploidy is present in closely related organisms.
Yet even the human lineage underwent polyploidy events. Humans were not simply created having 46 chromosomes. There is nothing to say that an organism or a set of organisms unable to tolerate almost all polyploid events are therefore unable to survive all polyploid events.
References
Rules of Engagement: Have Pollen—Will Travel by John Perkins · Sally Perkins in Azalean 2010
Ploidy level estimations in deciduous and elepidote hybrids of Rhododendron by José Cerca de Oliveira, Mariana Castro, Francisco J. do Nascimento, Sílvia Castro, John Perkins,Sally Perkins, João Loureiro in Jornadas Portuguesas de Genética, Coimbra, Portugal; 05/2011
Weighing in: Discovering the ploidy of hybrid elepidote rhododendrons by Sally Perkins, John Perkins, José Monteiro de Oliveira, Mariana Castro, Sílvia Castro, João Loureiro in Rhododendrons, Camellias and Magnolias, Royal Horticultural Society, Editors: Simon Maughan, pp.34-48 2012

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How many times did terrestrial life emerge from the ocean?
Evolution is often mistakenly depicted as linear in popular culture. One main feature of this depiction in popular culture, but even in science popularisation, is that some ocean-dwelling animal sheds its scales and fins and crawls onto land.
Of course, this showcases only one ancestral lineage for one specific species (Homo sapiens). My question is: Where else did life evolve out of water onto land?
Intuitively, this seems like a huge leap to take (adapting to a fundamentally alien environment) but it still must have happend several times (separately at least for plants, insects and chordates, since their respective most recent common ancestor is sea-dwelling). In fact, the more I think of it the more examples I find.

I doubt we know the precise number, or even anywhere near it. But there are several well-supported theorised colonisations which might interest you and help to build up a picture of just how common it was for life to transition to land. We can also use known facts about when different evolutionary lineages diverged, along with knowledge about the earlier colonisations of land, to work some events out for ourselves. I've done it here for broad taxonomic clades at different scales - if interested you could do the same thing again for lower sub-clades.
As you rightly point out, there must have been at least one colonisation event for each lineage present on land which diverged from other land-present lineages before the colonisation of land. Using the evidence and reasoning I give below, at the very least, the following 9 independent colonisations occurred:

bacteria
cyanobacteria
archaea
protists
fungi
algae
plants
nematodes
arthropods
vertebrates

Bacterial and archaean colonisation
The first evidence of life on land seems to originate from 2.6 (Watanabe et al., 2000) to 3.1 (Battistuzzi et al., 2004) billion years ago. Since molecular evidence points to bacteria and archaea diverging between 3.2-3.8 billion years ago (Feng et al.,1997 - a classic paper), and since both bacteria and archaea are found on land (e.g. Taketani & Tsai, 2010), they must have colonised land independently. I would suggest there would have been many different bacterial colonisations, too. One at least is certain - cyanobacteria must have colonised independently from some other forms, since they evolved after the first bacterial colonisation (Tomitani et al., 2006), and are now found on land, e.g. in lichens.
Protistan, fungal, algal, plant and animal colonisation
Protists are a polyphyletic group of simple eukaryotes, and since fungal divergence from them (Wang et al., 1999 - another classic) predates fungal emergence from the ocean (Taylor & Osborn, 1996), they must have emerged separately. Then, since plants and fungi diverged whilst fungi were still in the ocean (Wang et al., 1999), plants must have colonised separately. Actually, it has been explicitly discovered in various ways (e.g. molecular clock methods, Heckman et al., 2001) that plants must have left the ocean separately to fungi, but probably relied upon them to be able to do it (Brundrett, 2002 - see note at bottom about this paper). Next, simple animals... Arthropods colonised the land independently (Pisani et al, 2004), and since nematodes diverged before arthropods (Wang et al., 1999), they too must have independently found land. Then, lumbering along at the end, came the tetrapods (Long & Gordon, 2004).
Note about the Brundrett paper: it has OVER 300 REFERENCES! That guy must have been hoping for some sort of prize.
References

 Battistuzzi FU, Feijao A, Hedges SB. 2004. A genomic timescale of prokaryote evolution: insights into the origin of methanogenesis, phototrophy, and the colonization of land. BMC Evol Biol 4: 44.
 Brundrett MC. 2002. Coevolution of roots and mycorrhizas of land plants. New Phytologist 154: 275–304.
Feng D-F, Cho G, Doolittle RF. 1997. Determining divergence times with a protein clock: Update and reevaluation. Proceedings of the National Academy of Sciences 94: 13028 –13033.
 Heckman DS, Geiser DM, Eidell BR, Stauffer RL, Kardos NL, Hedges SB. 2001. Molecular Evidence for the Early Colonization of Land by Fungi and Plants. Science 293: 1129 –1133.
Long JA, Gordon MS. 2004. The Greatest Step in Vertebrate History: A Paleobiological Review of the Fish‐Tetrapod Transition. Physiological and Biochemical Zoology 77: 700–719.
 Pisani D, Poling LL, Lyons-Weiler M, Hedges SB. 2004. The colonization of land by animals: molecular phylogeny and divergence times among arthropods. BMC Biol 2: 1.
 Taketani RG, Tsai SM. 2010. The influence of different land uses on the structure of archaeal communities in Amazonian anthrosols based on 16S rRNA and amoA genes. Microb Ecol 59: 734–743.
 Taylor TN, Osborn JM. 1996. The importance of fungi in shaping the paleoecosystem. Review of Palaeobotany and Palynology 90: 249–262.
Wang DY, Kumar S, Hedges SB. 1999. Divergence time estimates for the early history of animal phyla and the origin of plants, animals and fungi. Proc Biol Sci 266: 163–171.
 Watanabe Y, Martini JEJ, Ohmoto H. 2000. Geochemical evidence for terrestrial ecosystems 2.6 billion years ago. Nature 408: 574–578.

This is explained at the linked paper, but it's interesting to notice that there are four different arthropod colonizations of land: myriapods, insects, arachnids, and isopods.

What is also cool is that some animals (pulmonate molluscs, mammals, etc) have re-colonized the ocean back from the land.

@NoahSnyder, also Brachyura, it seems?

Richard's answer is fantastic, and I'm not going to be as thorough.  But here's some other examples:

Turtles (which did sea to land to sea back to land!)
Gastropoda (snails and slugs)
Tardigrada (water bears)
Onychophora (velvet worms)
Planaria (flatworms)
Annelida (annelid worms)

Together with Richard's examples that includes all the examples of terrestrial animals given at wikipedia.

75% of questions about the awesomeness of life, the answer includes tardigrades.

The venomous snakes of Australia are all in a single family, Elapidae. These are thought to have descended from a single sea-snake colonization event, so the sequence would be sea->land->sea->land.

@ChinmayKanchi Fascinating!  If it turns out snakes originally emerged in the sea that'd be sea->land->sea->land->sea->land!  (Though my understanding is that currently early snakes being burrowers is more likely.)

It's highly likely that all extant reptiles derive from a terrestrial ancestor because of the egg physiology. As far as I'm aware, not a single reptile lays eggs that can hatch in water.

@ChinmayKanchi: I'm not sure how that's relevant.  Certainly basal amniotes were land-dwellers (that's the first land).  But early snakes may have been aquatic (and closely related to Mosasaurs) which would give the second sea.  Then basal Elapids would then give the second land, the sea snakes the third sea, and the Australian Elapids the third land.  Anyway, as I said current evidence is towards a fossorial origin of snakes against an aquatic origin.

Ah, now I understand. Almost a shame snakes are thought to have originated fossorially, really.

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


text:
What is the average Leg-to-Foot Length/Width Ratio?
I'm making a program that estimates a probable size (widest width and longest length) for a human's foot given the length and width of the leg to which it is attached. However, try as I might, I can't seem to find the average foot-to-leg size ratio. Does anyone know this? It would be even better if you have different ratios for males and females.
As a note, I don't want to know that this varies depending on certain circumstances, just a good average number that will let me generate people who aren't grossly out-of-proportion

A brief study I conducted of my peers (10 people of varying genders, ages, and races, all about average body type) revealed a rather consistent foot-to-leg length ratio of 1:3 for males and females (variance is insignificant), and width of 2:3 for males and 1:2 for females.

Insignificant at a glance of after Chi-Squared with regards to the foot-leg ratio of males/females? How big was your sample?

@RoryM It was brief; sample of about 10 people ages 18 to 25. I didn't quite have the time to do an expansive study of peoples' legs since yesterday :P

poor effort - I'd have expected at least 100,000 samples in 24 hours!!  You might want to include that information in your answer to help future visitors from google etc =)


text:
Can a living organism run on electricity?
Each time I'm too lazy too cook I think it'd be cool to be able to just plug myselt into an outlet. Yet I know it is not possible - I need amino acids and a lot of other stuff that electricity can't replace.
Can some simple organism live on electricity alone or is it just fundamentally impossible?

No; the problem is, as you pointed out, that no organism will manage to multiply, grow or even sustain itself without absorbing matter to create new cells and fill metabolic losses.
Even photoautotrophic organisms which get energy from light (which is in fact an E-M wave, so pretty close to electricity) collect matter from the environment -- plants for instance seem to grow out of nothing, but in fact gather significant part of their mass from atmospheric CO_2.

While true in practice there is nothing fundamental that prevents an organism from maintaining itself using a source of pure energy. Take the planet as a whole as an “organism”, it sustains itself with only an input of solar energy; all material is recycled. Of course it could not grow under such a situation

The cells would have to produce glucose directly from electricity. If we figured that out we could also solve our energy crisis.

I don't see how producing glucose from electricity solves the energy crisis; I would have thought that we want to produce electricity from glucose (efficiently) to do that.

I was mainly making a reference to the storage issue with clean energy generation.


text:
Does consuming sodium benzoate (preservative E211) cause problems during pregnancy?
There seems to be strong evidence to support the claim that sodium benzoate (E211) causes hyperactivity in young children, e.g. Bateman et al. (2004) and McCann et al. (2007).  This leads me to consider whether or not E211 is harmful during pregnancy.
A study by Mowafy et al. (2001) found a slight decrease in survival rates for pups of pregnant rats given sodium benzoate; they also found a more significant drop in mean weight of their pups.
Question: Could the consumption of sodium benzoate by the mother be harmful during human pregnancy? How would this be the case?
References:

Bateman, B., Warner, J.O., Hutchinson, E., Dean, T., Rowlandson, P., Gant, C., Grundy, J., Fitzgerald, C. & Stevenson, J. (2004) The effects of a double blind, placebo controlled, artificial food colourings and benzoate preservative challenge on hyperactivity in a general population sample of preschool children. Archives of Disease in Childhood. [Online] 89 (6), 506 –511.
McCann, D., Barrett, A., Cooper, A., Crumpler, D., Dalen, L., Grimshaw, K., Kitchin, E., Lok, K., Porteous, L., Prince, E., Sonuga-Barke, E., Warner, J.O. & Stevenson, J. (2007) Food additives and hyperactive behaviour in 3-year-old and 8/9-year-old children in the community: a randomised, double-blinded, placebo-controlled trial. The Lancet. [Online] 370 (9598), 1560–1567.
Mowafy, A.R., Darwish, A.M., El-Kholy, S.A. & Abdel-Mohsen, S.H. (2001) Effect of food preservatives on mother rats and survival of their offspring. The Journal of the Egyptian Public Health Association. 76 (3-4), 281–295.

This is really a medical question, which are off-topic here.

I think if you reformulate this scientifically in terms of teratology it might be a great question.  Right now, in addition to being on the medical advice side, as Mad Scientist has pointed out, it's framed in a bit of an alarmist fashion.

Alright, so here's an edited version of it; nothing about my personal reasons for asking the question.  (I'm not really sure how to add in "teratology").  As per the general rules of these sites, if you think you can improve the question (and not change the overall meaning) feel free to edit.

@DouglasS.Stones It's a good edit.  I'm personally unsure of the scientific correlation between an agent that might cause hyperactivity and one that might cause harm to a fetus, but it provides a lead-in for your question, so I think you did the right thing.

There is some evidence to support the idea that sodium benzoate may be detrimental to the development of the foetus:

TERATOGENIC EFFECTS: Classified POSSIBLE for human.
DEVELOPMENTAL TOXICITY: Classified Reproductive system/toxin/female, Reproductive system/ toxin/male [SUSPECTED].

MSDS for Sodium Benzoate
This has been shown experimentally in rats by Minor & Becker in 1971.  They introduced high doses of up to 1000 mgkg-1 intraperitoneally and recorded reduction in foetal weight and "gross anomalies".  Whilst I struggled to find a copy of their original paper, it is referenced in the Catalog of Teratogenic Agents1 (Thomas H. Shepard).
There is some evidence to refute this, however.  The Acceptable Daily Intake limits on sodium benzoate is a maximum of 5mgkg-1, at this dose there is no noticeable effect of exposure. (2,3)  The latter paper by EC food safety standards goes further:

There appear to be sufficient studies to conclude absence of teratogenic potential, with an overall NOAEL* for developmental toxicity of 500 mg/kg bw/day, based on effects on fetal weight.

*(No observed adverse effect level)
So the consensus from the food safety bodies suggests that E211 should not pose harm to an unborn child in the quantities allowed to be present as an additive.

1 Emire, Ronald J. "306: Benzoate, Sodium." Catalog of Teratogenic Agents. By Thomas H. Shepherd. JHU, 2004. 44-45. Google Books. Google. Web. 10 Feb. 2012.
2 Nair, B. "Final Report on the Safety Assessment of Benzyl Alcohol, Benzoic Acid, and Sodium Benzoate." International Journal of Toxicology 20.3 (2001). International Journal of Toxicology. Web. 10 Feb. 2012.
3 Scientific Committee on Food. Opinion of the Scientific Committee on Food on Benzoic acid and its salts. Rep. 24 Sept. 2002. EUROPEAN COMMISSION HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL. 10 Feb. 2012


text:
What is the total number of rounds of cleavage during mammalian embryonic development?
That for frog is 12, but what about mammalian embryos?
I cannot find the exact number anywhere.

I just have an intuation that the number of rounds of cleavage differ between different mammalian, since human seems to have more than 100 rounds, need to verify still from Gilbert.

It's not a totally answerable question, since some types of cells are going to divide more times than others.  But for an estimate, take as a starting proposition that there are 1 trillion cells in the adult human body. [1]  The average weight for a human is 62kg. [2] Average birth weight is about 3.4 kg.  [3]
So that implies roughtly (3.4/62)* 1 trillion = 55 billion cells in a newborn.
You then take the log base 2 of 55 billion, which gives you the exponent you have to hang on 2 in order to get 55 billion, which is about 35.  Then add one for that additional cell division to get from one to two cells == 36 divisions.
Of course I'm just using math, not biology, so your actual reality may vary.  Certainly some cells will reproduce more often than others, maybe cells actually grow in mass instead of dividing (i.e., baby cells might have less mass than adult cells) so the baby-cell-count could be off, lots of possible sources of error.
[1] http://www.nichd.nih.gov/publications/pubs/fragileX/sub3.cfm
[2] http://en.wikipedia.org/wiki/Body_weight#Average_weight_around_the_world
[3] http://en.wikipedia.org/wiki/Infant#Weight


text:
Does Amphibian embryo's blastocoel become a primitive yolk sac without yolk?
The mammalian blastocoel becomes yolk sac without yolk according to my professor. I have not found any evidence that such a thing happens in amphibians like frog.
I need to be able to compare and contrast cleavage and formation of blastula in amphibians and in humans.
My thoughts raised another question.
My friend says that blastula exists only when blastocoel exists.
2. Is the thing without blastocoel but with yolk sac the blastula?

Amphibians are produced externally so they do not get proteins and ATP from the mother during their maturation and differentiation. This means that they must have some way to get those things to protect themselves and survive.
The way that they get these things is yolk. Amphibians start to have yolk-filled endoderm during blastulation, [page 9, Gilbert, Developmental Biology].
I am considering the frog here as an example of amphibian. To know that things need energy to survive and that they must get it somewhere, you can deduce this solution. So nutrition and external "hatching" or development outside of female is the key here.
The overall answer to the question:
The organism must have a yolk sac, since it has yolk.
The second question seems to be an idealized one.
Without blastocoele but with yolk-sac suggests me that the blastocoel has developed already to yolk-sac. If that is the case, then I would call the thing gastrula, since for instance some species' ectoderm develops into yolk-sac. I assume that the question refers with "yolk-sac" to complete yolk-sac, not to the developing one during gastrulation.
If it is about developing yolk-sac, I would say that the cell is still blastula but is developing to gastrula. The yolk sac is not ready until gastrulation is complete.

I'm not overly convinced about getting ATP from yolk.  Perhaps glucose or other respiratory substrate but cellular metabolism is still internal?

@RoryM You are correct. I am not either overly convinced about getting all of the ATP from yolk, probably some - do not know, need to verify. There must be glucose around to get it the most of ATP. Cellular metabolism should be internal, since no mother around, but do not know about possible bacteria or other culture helping the thing. - Need to verify.

if you're happy with the answer that you have posted you should consider marking it as accepted =)


text:
How reversible is DAT upregulation from long-term ADHD medication use?
A mechanism for ADHD stimulant medication tolerance has now been found. See http://neurosciencenews.com/adhd-medication-patient-brains-adapt-dat/.
Here's the thing though: what exactly is the "signal" that the body uses to interpret whether or not it needs to upregulate the amount of DAT (dopamine transporter) that exist? Is it a dopamine-based signal  that somehow then gets carried to a transcription factor that gets carried to the nucleus for additional transcription?

http://www.longecity.org/forum/topic/54091-how-reversible-is-dat-receptor-upregulation-from-long-term-adhd-medication-use/

First the boring (but most important part) looking at the study:
It is important to critique the study design FIRST to see what kind of information we can actually obtain from this study. This is a meta-analysis of cross-sectional studies (meaning there is no record of change over time) that include a variety of age ranges of ADHD patients (some on treatment, some not) who were compared with age, gender and IQ-matched non-ADHD people to measure DAT levels in the stratum measured with PET and SPECT.
What they found:
There were very heterogeneous results from all the studies, there was no statistically significant difference between DAT in ADHD and normal (note that they use the word "trends"). The only thing statistically significant that they found was that there was a wide spread of DAT in the ADHD population, and that exposure to treatment accounted for half of this spread (variance).
What can we say about this?
This is not a very conclusive study, but studies like this are often necessary to merit doing higher resource intensive studies.  This study did not reach statistical significance in it's primary outcome, and on further search was able to only find a single outcome of significance. My summary of this would be: maybe this could represent a method of medication tolerance.
To answer your question
If hypothetically this was the cause and I had to make up a possible method of transcription control, I would say something similar to your answer. I would guess there is some transcription factor that is inhibited by dopamine in the cell. When there isn't dopamine (b/c it is being blocked from returning), it would somehow become active and start transcribing the gene for DAT.
Disclaimer
I am not a neurobiologist, this is my opinion after reading the article. Feel free to add to my comments

Reference:
Fusar-Poli, P., Rubia, K., Rossi, G., Sartori, G., & Balottin, U. (2012). Striatal dopamine transporter alterations in ADHD: pathophysiology or adaptation to psychostimulants? A meta-analysis. American Journal of Psychiatry, 169(3), 264-272.[Link]

Do they speculate a possible mechanism within the body of the paper?  Quoting that would strengthen the answer.


text:
What is the tRNA gene copy variation between different yeast strains?
I just started working on predicting steady-state protein levels from different codon usage bias measures. I have whole-genome sequences (it's NGS data) from different strains of S. cerevisiae and S. paradoxus and I began to wonder if it's possible that different strains of the same species could have different copy numbers of tRNA genes? If so, would this be detectable in the sequencing data (presumably the reads were mapped onto a reference genome so maybe this copy number variation would be lost)?

What type of sequencing data do you have? Are we talking about RNA-seq or DNA?

I would reask this question on BioStar. They may have better ideas than we mere experimentalists.

see
tRNAomics: tRNA gene copy number variation and codon use provide bioinformatic evidence of a new anticodon:codon wobble pair in a eukaryote. Iben JR, Maraia RJ. RNA. 2012 Jul;18(7):1358-72. doi: 10.1261/rna.032151.111. Epub 2012 May 14.

I'd take that computational angle and run the sequence data through tRNAscan-SE (Lowe & Eddy, Nucl Acids Res 25: 955-964). Ideally, you'd install this locally. This tool is what the UCSC folks use and it has been the best known, most widely used tRNA predictor for years. It's what we all used on Arabidopsis thaliana genome annotation back in the late 1990's.
There is also a genomic tRNA database that may have many of the predictions you seek, at least for some of your species/strains.

I don't think this will work since it's NGS data assembled against a reference genome. In fact I ran tRNAscan-SE and all strains have exactly the same tRNA GCN as the reference strains but this is a consequence of the assembly process.

It sounds like you should try a De Novo assembly. That might be tricky since you don't have any paired-end data but that might be able to discover any novel contigs.

I like @bobthejoe 's suggestion. I never intended that tRNAscan-SE would be run against an assembled genome. Depending on the size of your reads vs. the size of a typical tRNA gene, you may be able to input the reads themselves into tRNAscan-SE. If coverage of each genome is deep enough, try that de novo ass0embly. Also run the unassembled reads from each strain through tRANscan-SE - perhaps these are indeed those extra copies of the tRNA genes you're searching. Lastly, are there any gaps in an assembly where known tRNA genes are? I still think my suggestion would work.

I don't think the coverage is deep enough (1-4x) for de novo assembly but I'll try running tRNAscan-SE on the unassembled reads and maybe try to see if there's a difference in coverage of some tRNA genes which would suggest that duplicated genes have been mapped on the same locus.

I would use an RNA microarray to look at those difference instead of sequencing. To delicately amplify your tRNAs in an unbiased manner would be a tricky molecular biology endeavor. I wouldn't be surprised if there were detectable and significant differences. Those experiments will be able to confirm your hypotheses regarding codon usage bias.

The data I have is for over forty Sc strains so it wouldn't be possible to do those experiments within my timeframe/budget. I'm limited to computational approaches and my best guess was that some copy number variation detection algorithm could be applied to the raw read data.


text:
Is this mammalian embryo blastocyst, gastrula or only phase between them?
The picture shows the formation of early blastocyst and late blastocyst.
The middle embryo has embryoblast.
My professor says that blastocyst in general has embryoblast and trophoblast.

Embryoblast is the inner cell mass but the thing has none of it.
The last embryo does not seem to have inner cell mass anymore.
Is the last embryo in the picture anymore blastocyst?
The given thing seems to be "the single layered blastocyst that will give rise to gastrula", Wikipedia Gastrulation. The given stage seems to last very short time. It probably should be called phase between blastocyst and gastrula so that the thing is not blastocyst and not gastrula.
What is the right name for the given thing in mammalians?

Again, the thing (2) is idealized and probably does exists at all. It is an idealized picture. It is really a mistake to call such a thing blastocyst like Wikipedia does. The thing should be fixed not to confuse other people.
There should be real pictures instead of such idealized ones.

At undergraduate level you should not rely on Wikipedia. Good textbooks and journal articles are much better sources.

Completely true. Wikipedia has confused me a lot. I will rely on textbooks now on. I just love my Gilbert's textbook and Albert's biology book. They explain things so that I understand it.


text:
What does entering of sex chromosomes to gametes mean during meiosis I?
I am reading one answer about meiosis:

During meiosis I, the sex chromosomes separate and enter different
  sperm or egg cells (gametes).

I assume that sex chromosomes refer here to homologous chromosomes that experience crossing-over after meiosis that is exchange of genetical information.
Meiosis I refers here to female meiosis I and to male meiosis I.
In both cases, homologous chromosomes separate resulting in haploid cells after meiosis I.
These homologous chromosomes enter sperm or egg cells according to the writer, which I cannot understand, since the given chromosomes, now sister chromatids after meiosis I, do not enter physically anything, they just divide into haploid cells, gametes, after meiosis II.
What is the meaning of the word "enter" in the given sentence?
I am confused by the word "enter".
I am assuming that the word refers to enter something physically which is not the case in my opinion here.

After meiosis I, the resulting cells are haploid, not diploid, but they have 2n chromosomes.

@GerganaVandova So meiosis I is the stage where male (XY -> X and Y) and female (XX -> active X and inactive X). So the resulting cells are haploid.

So that mean that there is no halving of chromosomes anymore in meiosis II, since it is done in meiosis I. Cells are throughout meiosis I haploid, while haploid only after anaphase in meiosis I.

Ok, I am not sure anymore whether the inactivation of the female X chromosome happens right away from anaphase I.

X-inactivation occurs post-fertilization, only if fertilized by a X-carrying sperm. In meiosis I, HOMOLOGOUS chromosomes (meaning your mom and dad's copy of your genes) separate. In meiosis II, SISTER CHROMATIDS (i.e. copies of your mom's or your dad's chromosomes) separate.

@jp89 X-inactivation seems to happen in two places: at the end of meiosis I and then somewhere during meiosis II. - In the former case, there are two daughter cells. The other of the cells gain very little cytoplasm, while the other much. The other with very little cytoplasm will be the polar body.

And then finally the polar body from meiosis I divides to two new polar bodies while the secondary oocyte divides to ovum and one new polar body. So one ovum and three polar bodies. - Ok, the main question still unanswered. - Ok, I will do it, since the answer seems to be that "become" different sperm or egg cells.

@Masi You have some flaws in your logic here. The first polar body does not divide into more polar bodies. Once a polar body, always a polar body. At the end of female meiosis II, your total products is 2 polar bodies and 1 mature ovum.

@Masi And to address the question of X-inactivation, x-inactivation only occurs in diploid XX cells under regulation of the XIST gene from the non-inactivated X chromosome. When homologous chromosomes separate in meiosis I, x-inactivation cannot occur since the XIST gene product from either the paternal or maternal chromosome cannot act on the other X chromosome because they're simply not in the same cell anymore.

@jp89 Are you sure about polar bodies? - If so, then this must a mistake again in Wikipedia and in my lecture materials too: http://en.wikipedia.org/wiki/File:Gray5.svg The picture suggests for instance that the primary polar body can divide again to two polar bodies.

@jp89 The thing does not seem to be so simple: "Sometimes the first polar body undergoes the second meiotic cell division." - Ok, but how that is possible? - The primary polar body is haploid. How can it divide again meiotically and be still haploid? - I would think that mitotic division is needed to have two more polar bodies from the primary polar body.

@Masi See here (http://www.uic.edu/classes/bms/bms655/lesson9.html), here (http://www.ncbi.nlm.nih.gov/books/NBK10008/#A4696) and here (http://faculty.stcc.edu/AandP/AP/AP2pages/reprod/oogenesi.htm). There's also a great diagram in my medical genetics book but it's not on the internet.

@Masi Even if the first polar body divides, it still divides meiotically. It retains it's haploid nature because in meiosis II, sister chromatids separate rather than homologous chromosomes. It is separation of homologous chromosomes (in MI) that results in reduction of ploidy.

I seem to now understand the sentence. I read the clause in other words:

During meiosis I, the sex chromosomes of the gametogonia separate in
  anaphase I and II and become eventually different sperm or egg cells
  after cell differentiation and maturation: male spermiogenesis and
  female maturation into ovum.

Female thing does not seem to have a special name for the maturation thing.
Female does not seem to have differentiation part at the last part similarly as male, since only one ovum is formed after the sequence of events.
Sex chromosomes refer to your parents genotypes. [jg89]
Problem seems to be solved now.
I would not personally use the word "enter" in a such sequence. It is a shortcut. Better would be "enter eventually" or "enter after a sequence of events". I prefer explicity instead of implicity.

Ok, I am not sure whether the last female step has anything to do with differentiation. It seems that it just a maturation step, since there will only be one ovum, while 4 male spermatozoa where the differentiation makes sense. I will fix it. Please, reply if I am wrong.


text:
Does Human Female Meiosis II occur after fertilization with sperm?
I am reading the answer and I am getting confused by the sentence:

At the end of meiosis I females have two daughter cells and meiosis II
  only occurs if and when fertilization occurs by a sperm cell.

The clause suggests me that meiosis II starts after the sperm has ignited the fertilization process in female: I do not know how that exactly works.
Wikipedia says:

The process of fertilization involves a sperm fusing with an ovum.

So female meiosis II must happen before the sperm fuses with the ovum.
Sperm must ignite some process in female that puts female meiosis II going on before sperm can fuse with egg. Is that right? How is that going to happen?

Does this mean that the sperm fertilises a cell with 46 chromosomes instead of 23?

Primary oocytes are formed prenatally and reain suspended in prophase of meiosis I for years until the onset of puberty. An oocyte completes meiosis I as its follicle matures (during ovulation) resulting in a secondary oocyte and the FIRST polar body. After ovulation, each oocyte continues to metaphase of meiosis II. Meiosis II is completed only if fertilization occurs, resulting in a fertilized mature ovum and the second polar body.
So in short, the egg is stuck in metaphase II until fertilization.

Do you mean that the egg is stuck in metaphase II already before the sperm comes? - Does the egg remain in metaphase II a couple of days each month?

Yes, the secondary oocyte stays in metaphase II throughout ovulation until fertilization. Upon fertilization, the ovum and the third polar body form. If no fertilization occurs, the secondary oocyte (still in meiosis II) is expelled via menstruation.

I am considering know which follicle is at metaphase II here http://biology.stackexchange.com/questions/1205/is-secondary-follicle-or-graafian-follicle-arrested-in-the-second-metaphase-of-o

Meiosis, as you know, have two stages, Meiosis I and II. The oocyte is arrested during metaphase II of MEOISIS II. This arrest is facilitated by a complex called "Cytostatic Factor" (CSF).
After fertilization, the sperm induces a rise in intracellular calcium ion which activates and enzyme, Calmodulin Kinase II. This complex, through a series of phosphorylation and ubiquitination, degrades the CSF comples and in turn, activates APC (Anaphase Promoting Complex). APC will then degrades cyclins, securins and this will promotes the completion of Meiois II.

Sperm must ignite some process in female that puts female meiosis II going on before sperm can fuse with egg.

I think the statement is a bit incorrect. The sperm will ignite (I prefer induce) the above changes and fuse at the same time. Because, what starts all the process above is part of the sperm's cytoplasm that need to be assimilated into the oocyte's cytoplasm.
I hope this clears it all up. Or if you are interested, I can provide the long list of signalling pathways that leads to zygotic development.

Provide a link to the long list?By the way: crossing over is in the "grandma's womb"?

Did you mean "long pathway" or long list? I'd still be interested.  Without knowing I guess induction means setting apart one "haploid" single strand of the egg - must be  - diploid, double strand. As I am into viral infection and how that relates to multi cellularism (CoV-19 induces Syncytia!) this to me as if some "single stranded" "haplo" transfects a regular double stranded host and puts itself in place of the regular second strand. -- So, what happens to the second DNA strand of the female egg DNA? It should "budd off" as a haploid cell with a membrane.

Untill puberty the follicles grown from primordial to antral stage (secondary folliccle) and oocytes are arrested in diplotene of profase I of meiosis I, without polar body, with a nucleous called germinative vesicle. After puberty, with gonadotrophis, they can grow more and ovulate. With LH surge they are stimulated to continuing meiosis and they lose the nucleous and became metafase I oocytes (MI) and extrude the first polar body to became secondary oocytes (MII oocytes) just before ovulation. So, the Graaf folicle, last stage of follicular development, has a secondary oocyte arrested in metafase II. Only after ovulation and with fecundation it is possible to escape from MII arrest and extrude the second polar body.

Nice answer. +1. A referencecwould be nice.


text:
Chicken Genome what are the LGE 'chromosomes'?
The chicken genome identifies two "LGE" sequences in the chicken genome.  Are these distinct chromosomes or some highly variable sequence from the genome that is put in a separate sequence? I'm thinking they are not really separate chromosomes.... It would be great to know a little bit about their biology.  the papers didn't seem to help me.

LG stands for "linkage group". It seems the Chicken Genome Sequence group (Hillier et al., 2004) allocated several linkage groups (alleles or genes which tend to be inherited together) to the microchromosomes (tiny chromosomes typical of birds and reptiles), in this case called "linkage group E64" and "linkage group E22....". There are a load more microchromosomes which are the ones numbered 28-31 and 33-38 which haven't yet had their sequences resolved (Burt, 2007).
References:

Burt, D.W. (2007) Emergence of the Chicken as a Model Organism: Implications for Agriculture and Biology. Poultry Science. 86 (7), 1460 –1471. Available from:  [Accessed: 8 February 2012].
Hillier, L.D.W., Miller, W., Birney, E., Warren, W., Hardison, R.C., Ponting, C.P., Bork, P., Burt, D.W., Groenen, M.A.M. & Delany, M.E. (2004) Sequence and comparative analysis of the chicken genome provide unique perspectives on vertebrate evolution. Nature. 432 (7018), 695–716.

So this makes them a little bit like the 'random' chromosomes in the human builds i guess.


text:
Does electricity cause damage on a cellular level?
As I understand it the mechanism of death when a mammal is electrocuted is that the current disrupts the SAN/AVN in the heart causing it to fibrilate or arrest.  That's on a macro scale, however.  What damage, if any, does electricity cause on a cellular level?  I've noticed some sort of moss or lichen growing on the third rail of the train lines so I'm aware that they must be able to cope with the current, do they have adaptations ot allow this or is it just that they are not connected to the earth?

Regarding the moss or lichen on the third rail on British train lines: there is no current passing through the moss/lichen as they are not completing a circuit. They are just sitting on one connector. If another connector passed over them, completing the circuit across them, then a current might pass across them for a very short time. But I doubt they grow on the top of the rail (which is the contact part in the UK system) as that is constantly being polished smooth by the contacts from trains sliding across it.
Regarding cell damage: Apart from fibrillation in animals, and burns caused by Joule heating, electricity does cause cellular damage.
At low frequencies (<10kHz), electricity disrupts cell membranes and makes them much more permeable (we actually harness this when we use electroporation to transform bacteria). All organisms rely on electrochemical potential differences across membranes for their metabolism (Berry, 2002). The exact effect is dependent on the previous electrical state of the cells, for example the electrical potential difference across the membrane, and on the surface area to volume ratio of the cell (greater volume relative to surface area leads to more disruption). In any case, extreme electroporation can cause solutes to flow in or out of a cell, and generally disrupt the balance of solute concentrations and cause organelles and other bodies to move out of a cell. When the electrical stimulation stops, the contents are then fixed in a disrupted state. The cell then has to expend enormous amounts of ATP using ion channels and transport proteins in an attempt to reinstate the necessary chemiosmotic potentials, and in doing so exhausts the entire ATP supply and goes into biochemical arrest (no metabolism occurs), which is when a cell is dead. Dead cells break apart because there are is no maintenance occuring.
At higher frequencies (10-100kHz) proteins become permanently denatured. Many proteins carry charges which give them an overall polarity. When placed in an electric field, the proteins reorient themselves and will undergo conformational change to achieve the optimum dipole moment in the direction of the field. Ion channels and pumps are particularly sensitive to these disruptions (since their charges are crucial to their function).
Rather than provide lots of references, there is one excellent review from which I drew all this information, and which you should read for more of the physical detail (Lee et al., 2000).
References:

Berry, S. (2002) The Chemical Basis of Membrane Bioenergetics. Journal of Molecular Evolution. [Online] 54 (5), 595–613. Available from: doi:10.1007/s00239-001-0056-3 [Accessed: 9 February 2012].
Lee, R.C., Zhang, D. & Hannig, J. (2000) Biophysical injury mechanisms in electrical shock trauma. Annual Review of Biomedical Engineering. [Online] 2 (1), 477–509. Available from: doi:10.1146/annurev.bioeng.2.1.477 [Accessed: 9 February 2012].

I did think it was more likely to be physics rather than biology for the third rail.  Really interesting answer though!

Well, to add a bit of biology to the third rail part: lichens often have a very low moisture content, being poikilohydric they can withstand extremely low moisture for a long time. And since water is the medium of conduction during electric shock of an organism, there's a good chance that lichens would be less sensitive than most organisms to electrocution.

Great response; I learned something today! I also have a vague sense that, over time, flowing current through tissue can deplete the buffering capacity of the system and lead to pH changes, with all sorts of biochemical consequences; don't quote me on this but I think cardiac pacemakers switched from unipolar pulses to biphasic pulses to help avoid that kind of problem.


text:
Why should I degas my gel solution for polyacrylamide gels?
In protocols for polyacrylamide gel electrophoresis (PAGE) I often see instructions to degas the gel solution by putting it under vacuum for 10-15 minutes before polymerizing the gel.
I usually don't do this, and when I tried it once I couldn't see any difference. So I'm wondering what exactly the degassing is meant to achieve and how big the effect should be.

What effect is degassing the gel solution supposed to have?
How important is degassing to achieve good gels?

Any literature that examines the effect of degassing would be appreciated.

The reason for degassing your gels is to remove oxygen. Oxygen in the gel interferes with polymerisation, slowing it down and making it less consistent, so degassing makes it faster and more uniform.
From the EncorBio SDS-PAGE protocol:

Polymerization is quicker and more uniform if you degas the first three solutions for a few minutes in an Ehrlenmeyer flask on a house vacuum prior to addition of the last three reagents. Molecular oxygen inhibits polymerisation by reacting with the free radical SO4- ions, which is actually the reason why PAGE gels are poured in tubes or between plates and not in open top horizontal apparatuses, as can be done with agarose. Also it's a good idea to layer some isopropanol on top of the gel as this prevents oxygen getting in and inhibiting polymerisation.

Oxygen can also lead to oxidation of protein products, which might be crucial if you then want to extract the products and use them for something else (e.g. Sun & Anderson, 2004).
Finally, having bubbles in your gel can distort the results and make them less reproducible, as the bubbles will not form consistently with each repetition and they disrupt the physical medium of the polyacrylamide. So another purpose of degassing is to ensure repeatability.
The Bio-Rad acrylamide polymerisation info sheet has the best info I could find:

The formation of polyacrylamide gels proceeds via free radical
  polymerization. The reaction is therefore inhibited by any
  element or compound that serves as a free radical trap
  (Chrambach 1985). Oxygen is such an inhibitor. Oxygen,
  present in the air, dissolved in gel solutions, or adsorbed to
  the surfaces of plastic, rubber, etc., will inhibit, and in extreme
  cases prevent, acrylamide polymerization. Proper degassing
  is critical for reproducibility. Therefore, one of the most
  important steps in the preparation of polyacrylamide gels is
  the evacuation, or “degassing” of gel solutions immediately
  prior to pouring the gel. This is done by placing the flask of
  gel solution in a vacuum chamber or under a strong aspirator.
  In some cases, a vacuum pump may be required.
Buffer stock solutions and monomer stock solutions are usually
  stored at 4°C. Cold solutions have a greater capacity for
  dissolved oxygen. The process of degassing is faster and
  more complete if the gel solution is brought to room
  temperature (23–25°C)‚ before degassing begins.
  Furthermore, if a cold gel solution is placed under vacuum,
  the process of evacuation tends to keep the solution cold.
  Pouring a gel with a cold solution will have a substantial
  negative effect on the rate of polymerization and on the
  quality of the resulting gel.
Polymerization in which riboflavin is used as one of the
  initiators calls for degassing. The conversion of riboflavin from
  the flavo to the leuco form (the species active in initiation)
  actually requires a small amount of oxygen (Gordon 1973).
This explains why polymerization initiated primarily by riboflavin
  can be completely blocked by exhaustive degassing. However,
  oxygen in excess of that needed to convert riboflavin to the
  active form will inhibit polymer chain elongation, as it does in
  reactions initiated only by ammonium persulfate and TEMED.
  Thus, while degassing is still important for limiting inhibition,
  it must not be so extensive that it prevents conversion of
  riboflavin to the active form. For polymerization initiated by
  riboflavin/TEMED, or riboflavin/TEMED/ammonium persulfate
  systems, degassing should not exceed 5 min.
A consequence of the interaction of riboflavin with oxygen is
  that riboflavin seems to act as an oxygen scavenger. This is
  supported by the observation that the addition of riboflavin
  (5 µg/ml) to stacking gel solutions containing ammonium
  persulfate/TEMED initiators results in cleaner, more uniform
  polymerization at gel surfaces exposed to oxygen (such as
  combs). The same effect could likely be achieved by more
  thorough degassing of solutions without riboflavin.
Whether using chemical polymerization (ammonium
  persulfate/TEMED) or photochemical polymerization
  (riboflavin/TEMED or riboflavin/TEMED/ammonium persulfate
  initiators), reproducible gel quality and separation
  characteristics require careful attention to gel solution
  temperature before degassing, and to degassing time,
  temperature, and vacuum. These parameters should be
  kept constant every time gels are prepared.

Sorry for the long quotes, but they are pasted here in case the original sources disappear.
References:

Sun, G. & Anderson, V.E. (2004) Prevention of artifactual protein oxidation generated during sodium dodecyl sulfate‐gel electrophoresis. ELECTROPHORESIS. [Online] 25 (7‐8), 959–965.

I have to say this is a very well laid out answer. In most applications of typical western blots conducted in our lab, we do not degas the gels and the results are very good. We do make the gels in tubes and pour between plates, effectively removing most of the oxygen from the reaction.

I have been running gels with different Acrylamide/Bisacrylamide ratios recently. People usually work with 1:37.5, 1:29 ratios which are commonly used for DNA and Protein gels. I have noticed that when you work with lower ratios 1:200 - 1:500, degassing becomes fundamental to guarantee reproducible resolution of my proteins. If I don't degass the mix in one of these gels some of the proteins I am resolving (which migrate really close to one another) won't separate well enough. Also, the time it takes to polymerize the gel can go from 20 to about 45 minutes if I don't degass the solution beforehand.
Degassing solutions with normal 1:29, 1:37.5 crosslinker ratios doesn't, in my experience, seem to have much of an effect other than having quicker polymerization times. Perhaps it makes a difference with lower concentration gels (8-5%), but I honestly wouldn't worry too much about this if I was routinely running 10-15% gels and reproducible resolution wasn't a concern.


text:
Is it necessary to conduct a power analysis before beginning an experiment?
I know that power analysis is the statistically valid way to ensure you use the correct numer of samples or repeats in an experiment. But I have never seen any biologist actually conduct a power analysis. Mostly, researchers seems to use a rule of thumb (three technical, three biological replicates is a common one).
Should I be doing a power analysis each time I design an experiment, or can I just use one of the common biology rules of thumb? If not, what are the consequences for the validity of my results? And is there a situation where I will be required to use power analysis, which makes it advantageous to get used to doing it now?

You've already gotten a decent answer to this, but I'll provide my own thoughts on the subject.
Yes
It's necessary. It is absolutely something you should do before beginning an experiment, and preferably something you should do in collaboration with the person who is going to be helping you analyze your data. To address a couple points:

You'll see all kinds of researchers doing all manner of sloppy things when it comes to statistics and data analysis. Reading some journals makes me groan. You won't necessarily find it a problem for your field, but one should ask oneself if the goal is merely not to get called out by your peers, or to actually run a well designed experiment.
The consequences to the validity of your results lie in an increased risk of Type II error - the incorrect failure to reject the null hypothesis, or in slightly clearer English, finding no effect when an effect exists in reality. Which means, if you run an under powered study, you run the risk of doing the entire experiment, finding nothing, and being wrong. The consequences of that are myriad - first, it likely harms your chances to get published, as null results are often quite difficult to get into press. Second, if it does get into press, you've managed to get an incorrect finding into the literature, which will then be propagated in meta-analysis, reviews, and the minds of impressionable future readers. And then there's the chance you'll abandon a potentially productive line of inquiry because you couldn't be bothered to do power analysis.
One thing to also consider is that not having conducted power analysis somewhat limits your ability to chase after interesting sub-findings. If you've built your experiment on a shaky foundation, and then want to do a second analysis on a sub-set of your results, you almost certainly don't have the power for it.
There are times when you'll be required to do power analysis. If you do research that's clinically relevant, and you ever want it to appear in one of those journals, you may very well be required to show you had a properly powered experiment. And many grant applications require you do so. Even if they don't require it, some people will do a napkin math estimation of your power if they don't see it appearing in your application anywhere.

sjcockell is partially correct. To do power analysis, you at least need to have some notion of the effect measure you're likely to see. And these are indeed just estimations of what you'll see. But in nearly all circumstances, you'll likely have some ideas already. Are there similar experiments you can draw from? Your own pilot studies? A "feel" born of experience in your particular system?
It's also trivially easy to calculate power under a number of difference scenarios, to ensure your experiment is sufficiently powered if things go considerably worse than expected. For example, in a study I once did the power calculations for, we weren't sure what the ratio of exposed to unexposed subjects would be. So I ran it over a large range:

Which left me with the confidence that even if I was in my "worst case" scenario, I'd have reasonably good power at realistic effect sizes.
That's the true strength of power calculations. They'll tell you things about your study. What you need. What doesn't matter. Whether or not before you spend time and money pursuing an idea if you have a reasonable chance at success. Sit down with someone, take an hour or two (at most for a simple experiment) and do it right. Or ask CrossValidated for advice.

Great answer, thanks. I accepted this one because it answered the precise points in my question.

In order to calculate power, you need to know the variance of the data being collected. You can only estimate this prior to actually gathering the data itself, so any a priori power calculation is itself just an estimate.
This is why sometimes you will see small studies being conducted as pilot studies (for example, see (1)), which enable variance to be more accurately determined, and a true power calculation to be performed.
Knowing the power will enable you to state the probability that the effects you are observing are real (at a given sensitivity). The better idea you can get of this False Discovery Rate, the more solid the conclusions you can draw will be (so it is almost always a good idea to calculate it, but it is not always a feasible thing to do).
(1): Power and sample size estimation in microarray studies, Lin et al., BMC Bioinformatics 2010, 11:48.

Thanks for your answer. That covers quite well why one might do a power calculation. How commonly are they used though? They are not usually mentioned in papers - is that because they're too commonplace to mention or because nobody does them?

I think it is often because they are not done as much as perhaps they should, not because they are done and left unreported. On a related note, in the course of doing some work this afternoon I discovered http://www.poweratlas.org/ - of which I was previously unaware.

OK, I'll make sure I always do them in future  - I'd prefer to set an example than follow a lazy trend. I will actually be doing a lot of transcriptomics in the next year or so, so that link will come in very useful when thinking about power analysis for it.

@sjcockell: the link is for comressing machines now...

Due to my own woeful ignorance on the subject, I have been reading up on statistical methods recently. From what (little) I understand, the real answer to this question is:
Yes, but only if you are doing Neyman-Pearson hypothesis testing
and
Absolutely not, if you are using Fisher p-values
That is, the question isn't formulated correctly, because power analysis is only valid under one statistical framework (Neyman-Pearson). And you are probably not using that framework.
In my experience, most experimental biologists use Fisher's p-value, which gives the probability of the data (or more extreme data) assuming that the null hypothesis is true. Under Fisher's framework, among other drawbacks, there is no quantitative measure of the test's power. However, it has the benefit that it allows scientists to do something close to what we would like to do--that is to draw conclusions from evidence obtained in individual experiments.
The Neyman-Pearson framework does included the idea of a test's power, because you must formulate an alternative hypothesis as well as desired alpha and beta error rates before starting your experiment. However, it mostly denies us the ability to make inferences from individual experiments, and for that reason appears less suited to experimental science. To quote from Goodman (see below), under Neyman-Pearson, "we must abandon our ability to measure evidence, or judge truth, in an individual experiment."
There is no clear right frequentist framework, although what is clear is that you cannot mix Fisher and Neyman-Pearson. Finally, although it doesn't really address your question directly, it seems wrong not to mention Bayesian methods as an alternative to these two frequentist frameworks, which comes with its own baggage.
Further reading from people that understand this much better than me:
Michael Lew's answer to "Setting the threshold p-value as part of hypothesis generation" at Cross Validated
Michael Lew's answer to "What are common statistical sins" at Cross Validated
Hubbard, Raymond, and M. J Bayarri. “Confusion Over Measures of Evidence (          p’S) Versus Errors (α’S) in Classical Statistical Testing.” The American Statistician 57, no. 3 (August 2003): 171–178.  (Working Paper PDF)
Arguments for Bayesian statistics:
Goodman, Steven N. “Toward Evidence-Based Medical Statistics. 1: The P Value Fallacy.” Annals of Internal Medicine 130, no. 12 (June 15, 1999): 995–1004.
Jaynes, E. T. Probability Theory: The Logic of Science (Online version of some parts)


text:
Why do cucurbits produce so much fluid when their stems are cut?
When carrying out some germination tests on species in the Cucurbitaceae, I notice that young plants of this family produce a lot of clear fluid when they are dissected. Most plants I dissect do not produce any fluid, even ones which appear to be turgid and have large cells. Why do cucurbits do this, and what's the fluid?

So do daffodils.

Members of the Cucurbitaceae family (squash, pumpkin, cucumber, melon etc.) are unique* in that they possess two distinct phloems, see figure below. The fascicular phloem (FP) is the main transport conduit, and more closely resembles the phloems of other plant families. Its role is to transport photosynthates and other nutrients (Turgeon & Oparka, 2010).The extra fascicular phloem (EFP), is more minor and has an atypical composition for a phloem. Although we have been aware of this dual phloem system for centuries (Crafts, 1932; Fischer, 1883, 1884, 1886), it is often ignored!!
The minor strands of EFP have been found to be the source of the extreme bleeding observed in cucurbits (Zhang et al., 2010). However this excessive bleeding has meant that cucurbits are a very popular model plant for phloem composition studies, since copious amounts of phloem contents are easily accessible. This is problematic since we now know that the exudate originates from the atypical EFP strands, making it a poor model (maybe is isn't even a phloem at all)!
The reason that the EFP does not block upon wounding is that it lacks blocking and sealing mechanisms (such as P proteins and pectins), which usually exist in order to protect the phloem from damage or disease, and to prevent the loss of vital metabolites. The fact that these are not present in EFP, along with the fact that EFP is rich in defensive proteins (Walz et al., 2004), may suggest a defensive role for this secondary phloem. Its anatomical placement around the vital vascular transport conduits supports this idea.

*No others are known, but could definitely exist.
Bibliography

Crafts, A. S. “Phloem Anatomy, Exudation, and Transport of Organic Nutrients in Cucurbits.” Plant Physiology 7, no. 2 (1932): 183–225.
Fischer, A. “Das Siebröhrensystem von Cucurbita.” Berichte Deutsche Botanische Gesell 1 (1883): 276–279.
Fischer, A. “Neue Beiträge Zur Kenntniss Der Siebröhren.” Berichte Über Die Verhandlungen Der Königlich-Sächsischen Gesellschaft Der Wissenschaften Zu Leipzig, Mathematisch-Physische Klasse 38 (1886): 291–336.
Fischer, A. Untersuchungen Über Das Siebröhren System Der Cucurbitaceen. Berlin, 1884.
Turgeon, R. and Oparka, K. “The Secret Phloem of Pumpkins.” Proceedings of the National Academy of Sciences 107, no. 30 (2010): 13201 –13202.
Walz, C. and Giavalisco, P. and Schad, M. and Juenger, M. and Klose, J. and Kehr, J. “Proteomics of Curcurbit Phloem Exudate Reveals a Network of Defence Proteins.” Phytochemistry 65, no. 12 (2004): 1795–1804.
Zhang, B. and Tolstikov, V. and Turnbull, C. and Hicks, L. M. and Fiehn, O. “Divergent Metabolome and Proteome Suggest Functional Independence of Dual Phloem Transport Systems in Cucurbits.” Proceedings of the National Academy of Sciences 107, no. 30 (2010): 13532.

Looking through some papers it is not clear to me that botanists actually know why this should be the case, and I am sure that you are more qualified than me to comment on this Richard! However, there's some discussion of this in Zhang et al. (2012).
These authors argue that the "exudate from curcubits is copious" because of physiological adaptations due to their growth habit - i.e. they are vines and as such often require the structural support of other plants. Vines compensate for a lack of a supporting stem structure by having xylem vessels that are wider than comparable freestanding species  and "high hydraulic conductivity" (which is a measure of how readily water will flow through pores - in the case of curcubits - very readily). Similarly, sieve tubes and sieve pores are very wide compared to species in other families. Since these sieve tubes have such a large cross-section, they do not readily self-seal.

The Origin and Composition of Cucurbit Phloem Exudate
C Zhang, X Yu, BG Ayre, R. Turgeon - Plant Physiology, 2012 - Am Soc Plant Biol. 158, 3

See also:

Why vines have narrow stems: Histological trends in Bauhinia (Fabaceae), Ewers, F., Fisher, J, Oecologia, 1991, 88, 2


text:
What is the eye muscle status when you stare at distant view through a glass wall?
The book said when you look at object close to you, the eye muscles contract and vice versa. I wonder what will be the status of the eye muscles when I stare at distance view (such as a mountain) inside an office through a glass wall. The mountain is far away but the glass wall is close to us. In this case, does the eye muscles relax?

In the situation you describe, the eye would be focused on the distant mountain.  This would mean that the lens would be stretched and thin in order to minimize the focussing power of the eye.  Therefore the ciliary muscles would be relaxed.
When you are looking out of the window, it is possible to make a conscious decision to focus on the window pane itself (thus adjusting the focus to be more powerful as the ciliary muscles contract), however then the distant object will be out of focus and uncomfortable to look at.
This is because the light rays reflecting from the mountain are barely affected by the pane of glass, hence its transparency.

I think this answer is correct that the transparency of the glass makes it irrelevant to how the eye focuses through it. However, the relationship between the ciliary muscles and near/far focus as stated here is reversed, or at least confused. The muscles contract when focusing on near objects.

To increase long range focus, the ciliary muscle is relaxed so that the zonular fibres flatten the lens. This flattening increases the focal distance and far away objects appear sharp.
The process is reversed when increasing short range focus.
In your example you are watching out of the window into distance. To see the mountains sharp you need to increase range focus and this means relaxing the ciliary muscle. This is also the reason why it is recreative for your eyes to watch into the distance after hours of computer work for example.
The window itself does not play any role because your focus is not on the window pane but somewhere in the distance.


text:
Why do we add salt when precipitating DNA?
All the DNA extraction protocols I have seen involve adding salts to the extraction buffer. What is the purpose of the salts? What happens if they aren't included?

The role of the salt is to neutralize the charge of the DNA's sugar phosphate backbone.  This makes the DNA less hydrophilic (less soluble in water).
Ethanol has a lower dielectric constant than water so it's used to promote ionic bonds between the Na+ (from the salt) and the PO3- (from the DNA backbone) causing the DNA to precipitate.

since precipitation is one of the methods to purify biomolecules, which separate them from the other components in the solution.


text:
How do I clean and calibrate pipettes, and how often should I do it?
I work in a lab where all the pipettes are shared. We often have visiting students who come and use the pipettes for a short project. So when I work with them, they might have been handled by other people several times since I last used them. This leads me to worry that they might have been mishandled, or become less accurate somehow.
How do I clean and calibrate pipettes? And how often do I need to do it?

How often you should calibrate your pipettes depends on the tolerances of your application. For some applications, like quantitative PCR setup, one may care a great deal; for general lab work, one can probably be less particular. You can get a sense of how accurate your pipettes are by pipetting DI water onto the platform of a sensitive (and calibrated!) balance. Comparing the random and systemic error you get while doing that over several trials to the specifications published by the manufacturer will give you a good idea of whether pipette calibration will help and help give you a sense of how much you care. Note also that the error may vary with the volume; you should test error over the entire volume range you intend to use the pipette for.
How to clean and calibrate pipettes is specific to each design. Some pipettes, like Gilson's, are not intended to be calibrated by the user. Others are. The pipette user guide published by the manufacturer should tell you.
For some demanding applications, even well-calibrated and well-handled micropipettes may not be sufficiently accurate. In particular, I've made standard curves by serial 10-fold dilution for quantitative PCR both a) relying on my micropipettors to be correct and b) trusting pipettes only to get me into the right ballpark, and intentionally undershooting and correcting volumes with sequentially smaller pipettes until the reading on the balance is correct, if that's at all clear. In both cases I was using 900 ul of diluent and 100 ul of the previous dilution, which I feel are comfortably large volumes to handle. I found that the latter curve gave me noticeably better regressions.

Just a small note that hasn't been mentioned elsewhere.  Pipettes remain in calibration longer when reset to their maximal volume when not in use.  This is because it allows the spring (or other compression device) to relax fully and not be forced to stay in a compressed position.  This is an oversight I see in labs all the time, and something I always add to SOP's.

When doing a recent investigation into methods of quantitatively determining the concentration of aspirin in solution I found these procedures helpful.  They are a rough guide; design and procedure will vary by model.  It may be wise to check the manual that came with it, however in summary:
Calibration

Performed at least once per week
Performed in a room of the temperature indicated on the glassware (or at the very least in a room where the temperature will not fluctuate during the calibration).

For example a pipette I was using was a 10ml graduated, the procedure for which was:

Rinse the 10 mL pipette with 10 mL of water. Pipette 2 mL into a tared vial containing water on a 2-place balance. Document the weight. Set the pipette to 5 mL, pipette 5 mL into the vial and document the weight. Set the pipette to 10 mL, pipette 10 mL into the vial and document the weight.

However procedures are given in the linked document for pipettes down to 100μL.   Then compare the values from the mass with the acceptable values in the appendix.  A calibrated pipette will give ±1% of the mass indicated in the appendix, for example the pipette I described above:

1.98-2.02 g
4.95-5.05 g
9.90-10.1 g

Cleaning can be achieved by pipetting up and rinsing with distilled water (in my case) or more likely for your case 'nanopure' water.