text:
Is plastic just as good for you as corn?
To specify, I mean plain corn-on-the-cob, not anything processed like corn flakes.
Since one of the main important functions of corn is that it's not digestible, and therefore helps with digestion by loosening feces, would that make it just as beneficial as chopping up and eating a plastic bag?

This question appears to be off-topic because it is not biologically relevant.

Corn is digestible. Plastic is not.

corn cobs are not really digestable, but that still doesn't make plastic good for you

@MikeTaylor then please point me to the most relevant SE

Sorry, I do not know of an SE forum that fits.

@shigeta We digest corn cobs when we eat baby corn. Pigs can easily eat and digest corn cobs. Corn cobs are part of corn silage, which after fermentation is consumed and digested by cows and other farm animals. But still, none of this makes plastic any more nutritious or good for you. :)

the word 'you' seemed to imply human consumption, but it does seem like you have a response started here...

why isn't metabolism biology?  I just don't understand what some people think biology is.

@shigeta yeah some strange ideas about life here

I think I was the first vote to close this question but after considering comments by @shigeta I've voted to reopen and will submit an answer soon.

@shigeta Thanks for your comments. They gave me something to think about.

The part of the corn kernel that is visible in human feces is the outer coat of bran called the pericarp (see this image). This is a common structure in cereal grains like corn and wheat.  However, the bulk of the corn kernal is starchy endosperm, which is readily digestible by humans and provides carbohydrates and vitamins A and C.  The non-digestible (by humans) pericarp does help to keep fecal material soft.
Plastic bags do not provide those same benefits. Studies on human consumption of plastic bags are lacking, for obvious reasons.  However, marine organisms like sea turtles unfortunately consume large amounts of plastic debris (Derraik 2002). Bugoni et al. (2001) found that plastic debris caused mortality for 13% of the green turtles in their study. A review of 408 leatherback sea turtle autopsy records by Mrosovsky et al. (2009) found plastic inside 34% of turtles. The mortality in the sea turtles may be due to the accumulation of plastics in the gut which can block movement of food, alter feeding behaviors, and prevent absorbtion of nutrients.
If humans were to consume chopped up plastic bags, the evidence suggests that instead of receiving the same benefits as we do from whole kernal corn we are much more likely to be harmed. Eat your corn, recycle your plastic.
Literature Cited
Bugoni, L. et al., 2001. Marine debris and human impacts on sea turtles in southern Brazil. Marine Pollution Bulletin 42: 1330-1334.
Derraik, J.G.B. 2002. The pollution of the marine environment by plastic debris: A review. Marine Pollution Bulletin 44: 842-852.
Mrosovsky, N. et al. 2009. Leatherback turtles: The menance of plastic. Marine Pollution Bulletin 58: 287-289.


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Heterozygosity and the Wright-Fisher model
I was reading the textbook Probability Models for DNA Sequence Evolution by Durrett. In chapter 1, he discusses the Wright Fisher model and the coalescent theory which I am interested in.
He defines heterozygosity as the probability that two copies of an allele are the same. In theorem 1.3, he derives the expected value of heterozygousity, but what he seems to derive is the expected value of the probability that two allelles have a common ancestor. This does not seem to be the same as heterozygosity to me. Am I missing something here?

The following borrows from Gillespie, J.H., 1998. Population Genetics: A Concise Guide. The Johns Hopkins University Press. It is a good concise guide, and reduces to some extent the mathematics.
Theorem 1.3 is used to show the decay of heterozygosity in a population due to genetic drift.
Consider alleles in a population.  Two alleles drawn at random can differ by state, meaning they have two different DNA sequences. In other words, they are different alleles. Or the randomly drawn can have the same state, meaning they are the same allele. For alleles that are identical by state, they could differ by origin, meaning they are the same allele from two different chromosomes. The two alleles in a homozygous individual differ by origin (sampled from maternal and paternal homologs) but are identical by state.  Or, two identical alleles could differ by descent, meaning they are the same because they trace ultimately back to a common ancestor.
To calculate heterozygosity, you can first account for homozygosity, the frequencies of alleles that are identical by state. First consider two alleles identical by origin.  If you draw two alleles identical by origin when t=1, the probability that the two alleles are copies of same original allele (from the same chromosome) is
$$\frac{1}{2N}$$
because there was only a single copy of that allele on that one chromosome in the population prior to the round of mating, so it is 1 out of the 2N alleles at time point 0 ($t=0$).  The probability that two alleles identical by state are not identical by origin then is
$$1-\frac{1}{2N}.$$
Therefore, total homozygosity ($G'$) in the population (identical by state) after one round of random mating is
$$G' = \frac{1}{2N} + (1-\frac{1}{2N})G,$$
where $G$ is the homozygosity prior to the round of mating.  Of course, anything not homozygous is heterozygous. So, heterozyosity ($H$) is simply,
$$H=1-G.$$
By substituting the formula for $G$ into the above equation, the equation for $H$ becomes,
$$H' = 1-G' = (1-\frac{1}{2N})H$$
where $H$ is the heterozygosity prior to the round of mating.  This formula represents the change in heterozygosity after one round of random mating.  This can now be expanded for several rounds of random mating. For example, the change from $t=0$ to $t=1$ is
$$H_1 = (1-\frac{1}{2N})H_0.$$
The change from $t=1$ to $t=2$ is,
$$H_2 = (1-\frac{1}{2N})H_1$$
Therefore, the change in heterozygosity from $t=0$ to $t=2$ is
$$H_2 = (1-\frac{1}{2N})^2H_0.$$
This can be expanded to any time $t$ with the equation,
$$H_t = (1-\frac{1}{2N})^tH_0,$$
which you will recognize as Durrett's Theorem 1.3.
In short, in the Wright-Fisher model, two alleles that have a common ancestor are by definition identical by state and so cannot contribute to heterozygosity.
I hope this helps. I was a bit rushed and have not explained this often (mostly to myself in my mind) so if I can clarify something, please let me know.

Thank you for the brilliant answer. I think you have one typo though. Just above the second equation, I think it should be the probability of two alleles do not have the same origin is 1- 1/2N, rather than the probability of two alleles with the same state having different origins.

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What causes skewed ladder bands on an agarose gel?
I frequently ran into an issue where the bands of my ladder become skewed. What causes this?
Here's an example: 0.7% agarose gel, 100V, 60 minutes. Same problem occurs with 1%. I loaded 10 ul of a 20 ul PCR reaction.

As you can see, the problem is not smiling per se. The lanes themselves are fairly vertical and straight. Just the bands themselves appear warped. What could cause this issue?

The ladder and lane next to it look overloaded. Try to use less. Also, if possible, don't use the lanes on the sides of the gels, leave those empty if you can. Are you reusing the buffer? You might need to replace it more often.

0.2u Filter the solutions you use to make your gels, and don't overload the gel, this is overloaded.

@user137 Why do you recommend not using the side lanes?

@Chris It might just be coincidence, but it seems like I'm more likely to get a problem with the ladder if I put it in the side lines. Maybe it's just the electrodes in my gel box, or maybe it was a problem with my early gels before I knew not to overload the lanes, but I avoid the side lanes when possible and have had fewer issues.

I have never seen this problem when the gel box was ok. Boxes which caused multiple gels to run funny usually had problems with the wiring of the electrodes.

Can you please accept an answer which satisfatorily answer your question? This is a nice gesture towards the people who provide the answers. You still have a lot of open questions with proper answers. If the answer is not ok, use the comments or edit the question.

If the ladder is on an edge of the gel, it may be a process of different density as a result of how the gel cooled (or was poured too slowly). I've loaded more DNA loaded in a gel and it doesn't cause this kind of warping for me. It may be the buffer of the ladder is different from that used to make the gel. Your bands don't look particularly sharp, so I would suspect that the running voltage is too high and causing the surface of the gel to heat up and therefore "smearing" the bands. Try running the voltage at 75 V  for a proportionately longer time to see if this solves your problem.

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How long does it take for a hard clam (Mercenaria mercenaria) to reach sexual maturity?
How long does it take for a wild hard clam (Mercenaria mercenaria) to reach an age where they are reproductive? How does fecundity depend on age and size? I've looked at several hard clam life cycles and none of them have this information. They tend to agree that hard clams are long lived and take multiple years to reach a size suitable for harvest. While I am more interested in wild hard clam, please do also share information on farmed hard clam if you have it?

According to Ebersole 1987, Mercenaria mercenaria reaches sexual maturity at two years of age although some individuals can reach maturity at 1 year of age under certain growing conditions.  The mean size of individuals reaching sexual maturity is 33 mm with males somewhat smaller than females.
Ebersole cited a few studies that estimated fecundity of M. mercenaria. The results were highly variable. Individuals of about 60 mm in size released between 2 million and 6 million eggs.  Other estimates were as high as 25 million eggs.  Ebersole also cited a paper by Bricelj and Malouf (1980) where they found a general association of increasing fecundity with increasing clam size.  I don't have access to that paper but a book called The Great South Bay edited by Schubel et al. 1991 discussed the results of Bricelj and Malouf. Scroll to page 45 of the Google Books preview.  They show the mean fecundity and size as follows:
Seed (<48mm): 1.6 million eggs / individual
Little Necks (48-70mm): 2.9 million
Cherrystones (70-79mm): 5.9 million
Chowders (>79mm): 6.3 million
However, the figure on page 45 of Schubel et al., and taken from the Bricelj and Malout (1980) paper, shows a lot of variability in fecundity at different size classes.  Hopefully, the citations in the Ebersole paper will point you to other useful studies. If you don't have ready access to the book, your local library may be able to get it for you on loan.
Literature Cited
Bricelj, V.M. and R.E. Malout. 1980. Aspects of reproduction of hard clams (Mercenaria mercenaria) in Great South Bay, New York. Proceedings of the National Shellfish Association 70: 216-229.
Ebersole, 1987. Species profiles: Life histories and environmental requirements of coastal fishes and invertebrates (South Atlantic). Hard clams. US Fish and Wildlife Service Biological Report 82 (11.75).
Schubel, J.R. et al. (editors) 1991. The Great South Bay.  State University of New York Press, Albany, New York, USA.


text:
Why do rabbits often have white hindquarters?
There are several species of herbivores that have a very visible white hindquarters: several kinds of deer, rabbits, antelopes, etc.
Does the white fur serve a functional purpose, or is it purely random?  Is it defensive enabling them to escape predators, or is it for intraspecies communication?
Examples photos to clarify:

deer
Notice that otherwise relatively well camouflaged animals have visible white fur.

Pronghorn, I have a 2-link limit for the post: http://www.gpnc.org/images/jpegs/animals/flare.jpg

Apparently the most noticeable research on this subject of a rabbit's white behind has been done by Dr Dirk Semmann of the University of Goettingen. He proposes that

these spots actually confuse predators because of their very
  noticeable nature. By focusing on the bright spot, the would-be
  predator ignores the larger body of the animal. Then, when the rabbit
  executes a sharp turn, the spot disappears and the predator has to
  readjust to focus on the camouflaged coat, losing vital seconds
  (reference 1, reference 2).

It could be the same reason for the white behind of a deer. As to why deer flag their tails, there is a paper on the subject which lists 4 possible reasons for the behaviour.
1) Flash behaviour
2) Alarm Signal
3) Cohesive signal
4) Detection signal
More can be read about it in this paper.

It is unknown the reason why vertebrates hair in general varies in pigmentation. In the case of humans our genetic evolution for light and dark hair grew out of an adaptation to our environment. Camo is a key to other mammals so other species have predatory relationships that they must adapt to as well as environment.

Coloration is a diagnostic tool for identifying mammals, but inquiry into its function has lain dormant for almost a century. Recently, the topic has been revived and modern phylogenetic methods have been applied to large data sets, allowing researchers to assess, for the first time, the relative importance of three classic hypotheses for the function of coloration in mammals: concealment, communication, and regulation of physiological processes. Camouflage appears to be the single most important evolutionary force in explaining overall coloration in mammals, whereas patches of colored fur are used for intraspecific signaling. Sexual selection is associated with flamboyant ornamentation in a minority of primates and other restricted mammalian taxa, but to a far lesser extent than in birds. Interspecific signaling among mammals includes aposematic coloration, exaggeration of signals to deter pursuit, and lures for misdirecting predatory attack. Physiological causes of coloration, including melanism, are evident but poorly researched. The relative importance of evolutionary forces responsible for external coloration varies greatly between vertebrate taxa, but the reasons for this variation are not yet understood.

-The Adaptive Significance of Coloration in Mammals

I was asking specifically about the white patch on the bottom of several different herbivores, not why mammals have their colour in general.  If you've seen a wild rabbit running from the back, you know what I mean.  I updated the post with photos.

@Boar yeah the papers I read said we don't know sry wish we did


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Has it been confirmed yet that the DNA found in dinosaurs was really DNA?
I hear different sources claiming different things, bbc said they did, wikipedia says it hasn't which is it?

I have never read from any reputable source that DNA was extracted from some dinosaur bone. They did manage to sequence a few partial proteins like collagen through mass spectrometry a few years back..

Which source says that DNA has been found? I am not aware that any discoveries have been made.

Apparently it wasn't. According to Wikipedia, A study that reported Dinosaur DNA was,

mitochondrial cytochrome b sequences that had apparently been
  extracted from dinosaur bones dating to over 80 million years ago
  (reference).

However, contamination was found in the reported study (reference). Don't expect too much because this is a close to impossible task (reference 1). Most researchers pinned their hopes on DNA surviving trapped in amber resin but even that is not possible (reference).
If interested in cloning a dinosaur, quickly go through this article (or not).

Could an approximation of dinosaur DNA be made by analyzing the genomes of modern birds and trying to come up with a closest common ancestor? If it worked at all, it would probably be closest to DNA for an Archeopteryix, not a Tyranosaur.

@user137 That would be hard or next to impossible I would say. There has obviously been many many mutations  before when an Archeopteryix evolved into the birds of today. Going back means estimating these mutations as well as estimating what genes might have been present or not. There is a limit to these estimations and it would never be accurate enough.


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Immunodominant Peptide
Can someone please explain me the concept of Immunodominant peptide in simple language?? I did read the wiki article but did not understand it clearly. Please help!
(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

This article is indeed written in a complicated way.

If you have an antigen (something foreign for the immune system, for example a virus or bacteria) this consists of many different epitopes (immunogenic regions), as shown in the figure below (from the German Wikipedia, Antikörper means antibodies). The antigens are taken up by special cells of the immune system and processed to get small peptides:

To produce highly specific antibodies, the body has to undergo a specific immune reaction against these peptides. In the beginning of this reaction antibodies usually have a rather low affinity (bind only weak) against their antigen. This is changed by the so called affinity maturation in which the antibodies are mutated to make a variety of different new antibodies. These are then again "checked" against the antigen and the ones with a higher affinity are positively selected.
So antibodies with a strong binding to their antigen are favoured against such which have a less strong binding which can lead the selection of only a few antibodies, even if a complex antigen which has many immunogenic peptides is used. This is positive in the way that these antibodies are very effective in directing an immune response against the virus/bacteria but can be critical if the pathogen has a high mutation rate as this leads to a pathogen which does not have this antigen anymore.

It is about recognizing the intracellular pathogens. Every cell with nucleus splits up some of its intracellular protein to small chunks called oligopeptide (OP hereafter). So if there is an intracellular pathogen inside a cell, then its protein will be split up as well. After that the cell select the OPs it wants to show up on the surface. After an OP is selected, the cell binds it to a protein called MHC1 and sends it to the cell surface. So there is a lot of different MHC1-OP on the surface of every cell with nucleus. An immune cell group called T-cells are recognizing the MHC1 with their T-cell receptor (TCR hereafter). The TCR has a constant part and a variable part. The constant part depends on the species and person, it recognizes the MHC1. The variable part is random, it recognizes the OP. Each (not activated) T-cell has different variable part on the TCR on their surface, so each of them recognizes a different OP set. If a T-cell has strong binding to an intracellular pathogen's OP (IPOP hereafter), then it will be activated and it will destroy the cell infected with the pathogen. If a T-cell has only weak binding to an IPOP, or it recognizes an OP of a harmless own cell, then it won't be activated and it will die after a while, or in the second case it can become a regulator cell, which prevents autoimmune diseases. After the activation the T-cell start to proliferate, it divides many times and these clones try modify their receptor to bind even stronger to the selected IPOP, so they can find and destroy infected cells even more effectively. There is a mechanism in the immune system which prevents the activation of more than a few T-cells with different TCRs against the IPOPs of a single pathogen. So for example against a single pathogen there will be about a dozen different T-cell lines, which recognize a dozen IPOP. These IPOPs are the immunodominant peptides. Ofc. there can be IPOPs which are specific to the pathogen, but the T-cells which recognize them, are not or less activate. Those are the subdominant peptides.
You can find more info about immunodominance on wikipedia.


text:
Is epilepsy more heritable from maternal side?
I am thinking if paternal or maternal genetic line is the risk factor.
Mitochondrial DNA is coming from maternal line.
I do not know the pathogenesis of epilepsy so well that I could answer my question.
Is epilepsy more heritable from the maternal side?

Epilepsy is a neurological disorder characterized by hypersynchronous discharge of neurons .i.e abnormal electrical activity in the brain. Epileptic seizures caused primarily due to i) inhibition of inhibitory neurotransmitter systems such GABA neurotransmitters or ii) Enhancement of excitatory neurotransmitter systems such as nAchR. These conditions arise due to head injury, trauma and genetic factors. But there is no evidence as of now regarding Mitochondrial DNA taking part in inhibitory and excitatory systems. so, epileptic seizures are not specific in inheriting from any side (Maternal or paternal side) as far as pathophysiology of epilepsy is concerned.

I am thinking about the genetic factors, since more genetic factors are inherited from the maternal side because of mitochondrial DNA. If mitochondria play any role in the disease, then maternal side has more role in the pathology of the disease. I have seen one case where the disease spread only through maternal genetics - and do not understand this.


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Do the eyes play any role in producing the visual experiences you have during dreaming?
Sometimes, you remember a vivid picture of a dream that you saw. What is the role of your eye in this experience? Please provide me with the answer that is as simple as possible since I am in Class 10(Grade 10).

Your eye doesn't play a part in your dream aside from giving you the basic images which your brain later used to form the dream. The visual image in your dream comes from your brain itself.

While this may answer the question, it's best to add references, or list the literature you've cited. This is a scientific site. Please format accordingly.

The cerebrum is the centre of any unconsious activities that take place in our body. So there is hardly any part played by the eyes in visualising a dream. The brain does the visualising part

Welcome to Biology SE! While this may answer the question it lacks support from references in the scientific literature. Un-referenced answers may be challenged or deleted.


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Does chromosomal crossover result in a mutation?
Is chromosomal crossover considered a mutation? Would this be a large-scale mutation?

There are many different ways a DNA sequence can change. Labeling a change as a mutation implies that there was a biological process in which DNA was damaged then not properly repaired.

Crossing over during the formation of gametes does not result in a mutation.
Crossing over during repair of a double stranded DNA break does result in a mutation.

Yes. And it is especially considered a large-scale mutation when compared to point mutations which effect single bases.

I disagree with this answer. Have a look at the Wikipedia pages for mutation and recombination. Crossing-over may create new combinations of existing alleles/SNPs but it does not create any new ones. Even if there is a piece of sophistry which can be devised to defend this answer it is neither helpful nor useful to lump these two together as one.

The scale of a mutation is not simply a matter of counting bases. A frame shift mutation from a nucleotide deletion completely changes a translated protein. However, a change in any number of bases in a gene would only affect those bases, not the entire gene. The 'scale' of a mutation is situationally dependent.


text:
Identification of this insect
These insects lived inside the wood of my bed in little round holes. They bite, lеаving very itchy red marks. And when crushed stink really bad. In the picture the lines are notebook lines for size comparison.
   I live in Eastern Europe, so I don't think they are fire ants, if they are ants at all.
Any suggestions would be appreciated!

About how large is it? It looks like you took that picture on a piece of lined notebook paper, but that still can't tell us the exact size of the insect. How many millimeters are between the lines of your paper?

The lines are 8mm appart

If the lines are 8mm apart, the ant is about 2.3mm, making this consistent with pharoah ants and ghost ants.

OP states "I live in Eastern Europe, so I don't think they are fire ants". However, Myrmica rubra, the European fire ant, can be found in Eastern Europe. See https://www.antwiki.org/wiki/Myrmica_rubra and https://species.nbnatlas.org/species/NBNSYS0000009343

This looks like an ant, but I cannot say which species. Their small size, colour, bite and being found indoors made me think of Pharaoh ants (Monomorium pharaonis), but I haven't heard that they smell bad. Ghost ants (Tapinoma melanocephalum) are rather similar and have a foul smell when crushed, and have been found indoors in Europe. They usually have a dark head/thorax and lighter abdomen though. They can also be separated from Pharaoh ants by having a one segmented petiole (the Pharaoh ant has two). A closely related species to the Ghost ant is Tapinoma sessile, which also smells but has a uniform colour (usually darker than your specimen though, see picture at bugguide.net). The petiole not being clearly seen in your specimen points towards the two latter species, or other species with a short/hidden petiole (see hidden petiole at antkey.org). However, these are only a couple of suggestions, and there are probably many other possible species.
Termites have larger mandibles (jaws) relative to their size, and no distinct narrow division between thorax and abdomen (your specimen does). Your animal also has eyes (termites don't) and I think you can spot a long first antenna segment, which ants have (hard to see in the picture though).

Good call on the eyes. I had to zoom in quite a bit to finally see them but they are there.  I think I agree more with your answer than mine.

I have attached couple more pictures. I believe it also has a stinger. (Sorry about the quality, but due to the size of the insect and using a magnifying glass and a cell phone I couldn't make better shots)

While there are some wingless hymenoptera species that can resemble ants, I feel pretty certain that this is an ant. I'm not specialized in ants and cannot determine the species. It might be difficult to get a species determination from these pictures, but you should be able to get a genus from an ant expert. Another option could be Tapinoma sessile, which is closely related to the Ghost ant, also smells, but with a uniform colour (usually darker than your specimen though).

The size of this ant is about 2.3mm, consistent with pharaoh ants.

I can't tell you the species but it appears to be a termite. The Australian Museum explains some of the differences between termites and ants. Termites have straight antennae. Ants have bent antennae with a distinct elbow.  Your insect has straight antennae without an elbow. Termites have a broad waist. Ants have a very narrow waist. Your insect appears to have a broader waist. You also find more at The University of Florida. I'm not an entomologist and I do not live in Eastern Europe so consider my answer with a degree of caution.  If you have a pest control company nearby, you can take the specimen to them for verification, in case it is a termite species capable of home damage.

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text:
What is this fuzzy, black fungus that grew on my plates in the 4⁰C room?
I often find the fungus below growing on my (ostensibly) sterile plates in the 4⁰C room. Presumably it takes a few days to reach this size.
The colony looks puffy and dimpled in the middle, like a chocolate cake. The colony is actually black, but looks grey because of what I assume are hyphae and/or spores on top.
It looks like if I disturb the colony physically spores will be released (I haven't tried this because I don't want to contaminate the whole lab with aggressive spores). I notice that the center of the mass curves upward over time, and after a few more days of growth this colony will probably tear itself apart, leaving a gaping hole in the middle (based observation of similar contaminants on other plates, not pictured).
I suspect this is a very common lab contaminant. It grew to this size in less than 2 weeks, and was at 4C the entire time. I noticed many plates in the same batch/sleeve were contaminated, but each plate had only one colony, so it somehow spreads from plate to plate but not within the plate. What is it?

If anyone has any suggestions for simple but informative, classical microbiological techniques that would help identification (common stains, inexpensive selective media) I would be happy to try them - although it would be hard to justify very involved experiments since this doesn't pertain to my main research (in other words, if this was bacteria, sequencing the 16S would probably be out but a Gram stain is fine - this is very likely not bacteria, but I don't know the equivalents of those methods for fungi). Since identifying species is not really my strong suit, I'd appreciate if you link to a protocol when suggesting methods.
Update: I have found 4 more plates, all LB-Ampicillin, with what I suspect to be the same contaminant. With regard to Alan Boyd's comments, the colony morphology seems to be uniform in several aspects. It is not necessarily flower-shaped as I have claimed, but on the other hand, it never has a halo of satellites (dots) around it either.
Photos of the plates:

View from the top (agar side close to the benchtop) - shows round colony morphology and various stages of growth. Bottom left colony shows small dimple as the mass begins to swell. Top right shows cracks (actually tears) appearing as the mass is distorted by growth. Note that there is never two colonies on the same plate. The plates all came from the same sleeve in a cold room storage.
View of same colonies from the bottom - note star-shaped inward creases which form as the colonies grow and distort the surface.

Aspergillus niger?

@AlanBoyd According to the Wikipedia photo, A. niger colonies have a halo of dots around the main disc. In contrast, mine have very tidy edges (even after the middle bursts), and they are flower-like rather than circular. I don't know if this is significant.

Yes I saw that. However fungal colony morphology is very dependent upon the composition of the agar. But if I was more confident I would have answered, not comented.

@AlanBoyd Perhaps relevant: Besides the LB, I saw this grow on an LB-spectinomycin plate and a YPD plate. Colony morphology was indistinguishable.

I am far from an expert, but looking at similar pictures around the net I would guess for some Cladosporium species.

@skymninge Some photos of Cladosporium appear similar, but none are exactly like this. I think it's a promising possibility, but I'm not sure if it's really Cladosporium.

Just take a sample and do deep sequencing on it. Then compare the results with the genome database.

Sounds like a plan, @StefanGruenwald !

@Superbest, http://synapse.koreamed.org/DOIx.php?id=10.4489/MYCO.2008.36.4.211&vmode=PUBREADER#!po=7.14286. The picture in this study, esp the one from the bottom view, looks very similar to yours. Did you find out what the mold was?

Cladosporium sphaerospermum

I'm voting to close this question because more details are necessary to answer this question accurately, however, this mould seems like Cladosporium.

@WYSIWYG Actually Cladosporium sounds pretty good. I was planning to provide the additional details (eg. microscopy) but haven't gotten around to it yet.


text:
Alternative protocol for evaluating RNA integrity, using a bleach gel
I hate having to run MOPS PFA agarose gels with DEPC and everything just to verify my RNA integrity. I came across an alternative protocol that uses ordinary household bleach in the gel to inhibit RNases and was wondering if anyone here has tried it and what the success was like? Or any helpful insight is welcomed also.
here's a protocol I put together based on what was done in that paper.
For a 50ml gel
IN a RNase-free 250ml Erlenmeyer flask
Mix:
5 mls of 10x TAE that I gave you
42.5mls ultra purified water
0.5g of the agarose I gave you
2.5mls of household bleach (6% sodium hypochlorite, use clorox)
Incubate 5-10 minutes.
Microwave for the minim amount of time on the lowest heat setting that’s needed to completely solubilize the agarose, you don’t want evaporation adjusting your solutions volume
Check your volume with a sterile 50ml serological pipette, if you have lost more than 5% volume I would redo, using less heat.
Add 3µl 10mg/ml ethidium bromide, swirl to mix.
Pour in casting frame, allow to cool, submerge in 1xTAE
Combine 1µg of your total RNA, 2µg RNase free 6x loading dye and q.s to 12µl in RNAse feree water, you can use the water from the qiagen kit for this.
Run at 100V, about 30 min, get  good scanned image of it and use Photoshop to assess the band intensity. The 28S should be twice the brightness  of the 18S in a sample with little to no fragmentation.

I also hated the denaturing agarose RNA gels, but I switched to native gels using Faster Better Media's Lithium Boric Acid buffer at 0.5X concentration, my gels look much better, though I get 2 bands in each lane because it's not denatured. How are you using the gels to check for RNA integrity? If I see a band at the right size I've been calling it good enough and moving on. How precise does a gel need to be?

Looking at the small and large subunits. The large one should be 2x as bright in an unfragmented sample of total RNA. The gel needs to not exhibit any exonuclease activity, not much more than that needed

Maybe that's why I've been able to get away with my gels, I'm making RNA through In Vitro Transcription, you must be isolating it from cells.

You are correct!

What is your ultimate objective? What do you need RNA for? The rigor of the test depends on that. For usual RT-PCR I heat RNA with the 2x loading buffer that contains formamide and run it in normal agarose gel with TAE/TBE at 120V.

Testing RNA integrity for Microarray

Why not just run the RNA on an Agilent Bioanalyzer nanofluidics machine (or something similar)? It's fairly cheap and quick, and I'm sure a lot of core services offer it now. Of course, I am making certain assumptions about funding and technology availability here...

@Cantona'sCollar that's certainly the gold standard but I don't see how it's cheap those chips have a very supposed short shelf life for the bulk you have to buy it in. Also any fluids machine had the potential for disastrous cost.

I don't think bleach can denature RNA. Bleach is an oxidizing agent and it will damage the RNA. Also, the protocol mentions addition of hypochlorite before heating which I think is illogical because heat will decompose it.
For testing RNA integrity you need not make a denaturing gel. What you can instead do is to heat the RNA with the 2xRNA loading buffer that contains 95% formamide and run it in a normal TBE/TAE agarose gel. Heating with formamide denatures the RNA permanently.
Denaturing gels are only essential for Northern Blots.
You can also run your sample in a bioanalyzer to check for RNA integrity and this is always recommended for RNAseq experiments (even for microarrays but I cannot comment much on that because I have never done it and am not aware of the usual practice).

I'm telling you I didn't believe it either but it works quite well. Don't add it to the agarose before microwaving and use 6%. Also the rna will be denatured already from most any purification procedure especially the standard ones that use guanidine. works good for a teaching lab (cheap and easier) and I think this protocol focus's on RNAse removal or inactivation. +1 for the heating recc but I'm weary to heat rna unless it can be flash heated. I may Ty this next time however.

The bleach is not to denature the RNA but to destroy and RNase that might be lurking in your agarose or buffer - heat doesn't kill RNase easily so the boiling doesn't help.  Then just run a normal agarose gel (TAE/TBE or borate) and look at the relative intensities of the LSU and SSU RNA.  The bleach gels work very well for me and I've got very good RNA-Seq results out of RNA analysed this way (I don't have access to a bioanalyser).

Please add some references to your answer.


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Why can't you just take a vitamin? Why you need a healthy diet on top of that?
From what I understand, your body needs certain amounts of vitamins and minerals to maintain health. Why can't we just take enough pills to obtain these vitamins and minerals?

Getting enough food as an energy source would be a problem.

This is more of a biochemistry question and to be honest its a little bit out of my league because I have not had the necessary grad classes to explain nutrition but indeed I will try.
Unknown metabolite cofactors and things like ionization, oxidation and state of matter are the reason that straight up vitamins are rejected by the body and cause really expensive urine and a difficult time otherwise excreting.

Metabolism involves a vast array of chemical reactions, but most fall under a few basic types of reactions that involve the transfer of functional groups. This common chemistry allows cells to use a small set of metabolic intermediates to carry chemical groups between different reactions. These group-transfer intermediates are the loosely bound organic cofactors, often called coenzymes.
Each class of group-transfer reaction is carried out by a particular cofactor, which is the substrate for a set of enzymes that produce it, and a set of enzymes that consume it. An example of this are the dehydrogenases that use nicotinamide adenine dinucleotide (NAD+) as a cofactor. Here, hundreds of separate types of enzymes remove electrons from their substrates and reduce NAD+ to NADH. This reduced cofactor is then a substrate for any of the reductases in the cell that require electrons to reduce their substrates.
Therefore, these cofactors are continuously recycled as part of metabolism. As an example, the total quantity of ATP in the human body is about 0.1 mole. This ATP is constantly being broken down into ADP, and then converted back into ATP. Thus, at any given time, the total amount of ATP + ADP remains fairly constant. The energy used by human cells requires the hydrolysis of 100 to 150 moles of ATP daily, which is around 50 to 75 kg. In typical situations, humans use up their body weight of ATP over the course of the day. This means that each ATP molecule is recycled 1000 to 1500 times daily.

-wikipedia
If you did not like that explanation of cofactors maybe you will this:

Whole foods offer three main benefits over dietary supplements:
Greater nutrition. Whole foods are complex, containing a variety of the micronutrients your body needs — not just one. An orange, for example, provides vitamin C plus some beta carotene, calcium and other nutrients. A vitamin C supplement lacks these other micronutrients.
Essential fiber. Whole foods, such as whole grains, fruits, vegetables and legumes, provide dietary fiber. Most high-fiber foods are also packed with other essential nutrients. Fiber, as part of a healthy diet, can help prevent certain diseases, such as type 2 diabetes and heart disease, and it can also help manage constipation.
Protective substances. Whole foods contain other substances important for good health. Fruits and vegetables, for example, contain naturally occurring substances called phytochemicals, which may help protect you against cancer, heart disease, diabetes and high blood pressure. Many are also good sources of antioxidants — substances that slow down oxidation, a natural process that leads to cell and tissue damage.

-The great Mayo Clinic

So why does the body reject straight-up vitamins but not whole foods?

@user6035 without the cofactors the microbiology is unable to have the chemical reaction that creates the actually useful but quickly degrading nutrition. Sometimes the very chem reaction is as important as the output.

Without cofactors macrobiology shuts down cause it takes lots of filler to make poop and other stuff like tissue regen

We also depend on other organisms that live within our bodies and they have to be fed at various places and times as well

You can't finish a puzzle without all the pieces even if one piece is really big

So the vitamins we take are insufficient? Meaning that they don't contain all the pieces they need to be useful? If so, why is it so hard to create a pill that does have all the pieces?

@user6035 yes ur assertion is correct. Molecules are small and we cannot observe their interactions because physicists are focused on the stars rather than cells. I tried to make a macromolecule camera and I couldn't get help.

I think this calls for a separate question.

I think @Susan's answer provides a more direct answer: energy. This answer discusses vitamins from food vs vitamins from pills, not food vs pills.

@user1357 I'm also not sure that it is fair to say "physicists are more focussed on the stars than our cells". Molecular imaging is a massive, well funded field.  A macro molecular camera is not a trivial feat. Having said that cryo EM is catching up fast with crystallography in terms of resolution.

I think the piece of missing information here is the distinction between macronutrients and micronutrients. The info from Mayo clinic quoted in the another answer addresses some reasons why whole foods might be better than pills for obtaining micronutrients (i.e. vitamins and minerals).  While this may be true, most of it remains to be conclusively demonstrated (arguably). However, one clear reason “why….you need a healthy diet on top of that” is (unarguably) to obtain the fat, protein, and carbohydrates that your body uses to create energy. Unlike the minerals that act as cofactors, these macronutrients are the substrate. They are broken down to create the ATP that keeps everything running and they are built up to create the very structure of the body.

The energy that is consumed in the form of food or drinks can either be stored in the body in the form of fat (the major energy store), glycogen (short-term energy/carbohydrate reserves), or protein. . . to be used by the body to fuel energy-requiring events. *

These are called macronutrients because they are required in gram quantities — hundreds or even thousands of times more massive than the requirements for most micronutrients. As such, they don’t fit in a pill. As tragic as it is, we must keep eating.

*Gibney, M. J., & Nutrition Society. (2009). Introduction to Human Nutrition. Chichester, West Sussex, U.K.: Wiley-Blackwell.

The Question: Why can't we just take enough pills to obtain these vitamins and minerals?
We don't know enough about nutrition.
There are about 45 essential nutrients, which you need to consume to be healthy and live. You can get all of them from food without thinking about them. I'm not sure if currently there are a lot of supplements on the market that contain all essential nutrients. Also, we may currently still not know which all nutrients are essential, so we may miss some when designing multivitamin/mineral pills.
Food is easier!
A healthy adult who regularly consumes both plant and animal foods in reasonable variety and amount does not really need any vitamin/mineral supplements. And you need to eat foods to get calories. Yes, you could make supplements to substitute calorific content; imagine some sort of carbohydrate powder. But why complicate this when food is readily available, much cheaper, and easier?

Why has this been down voted? It answers the question in a way the others don't: why bother? I've made some edits. Feel free to roll back.

TL;DR : Food gives the human body much more than simply vitamins & minerals. A healthy diet is essential to overall healthiness, not just this one aspect of it.
Micronutrients
The component you're asking about - vitamins & minerals - are referred to as "micronutrients", and is only a quarter or so of what the body needs. Micronutrients are the vitamins like Vitamin A, Vitamin B, Vitamin C, etc. but it's also trace elements like zinc, iron, iodine, and many other metals that the body requires in very small quantities.
This is the part of the diet that most people actually overlook, and is what pills like the "once-a-day" vitamin are intended to supplement.
Macronutrients
Much of what we get from food falls in the category of "macronutrients". These nutrients are the actual building blocks of the body - things like fats, proteins, calcium, carbon, hydrogen, etc. A lot of macronutrients are required on a daily basis, and it would be difficult to condense these into a pill form. An average-sized pill would have to be taken 5-6 times a day in order to provide even a less-than-average amount of macronutrients for the average person.
Digestion
The human body is designed to be an engine. The act of eating is hard-coded into human physiology, and the act of digesting food kick-starts a great many processes throughout the body. Digestion is a rather efficient process, and it's one that only works properly when it has enough food to break down. A handful of pills could never fuel this process correctly, since they would simply dissolve in the stomach and never require any kind of breaking down.
Psychological
Lastly, food & drink have a psychological component to them as well. The human brain is wired so that it desires food on a psychological level. The physical act of eating something soothes that desire in a way that a pill never could. One of the greatest obstacles to someone trying to lose weight is this very component - even when their body technically has what it needs from vitamins, supplements, or shakes, this psychological aspect of hunger makes them want food anyway.

Your answer is in Cellular Respiration which is the production of ATP (energy storage molecules). Food is Carbon and Hydrogen. The body needs carbon and hydrogen for cellular respiration. Carbon and Hydrogen are not in vitamin pills they are in food.

Please add some references. This is a great answer overall though!


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What is this vinca like vine?
What is this vinca like vine? Is it poisonous? 62521 USA Illinois

From what region of the world was this photo taken? That can help to narrow down the range of possibilities.

Across the river and down the street from you @MikeTaylor

I think it must be a climbing Euonymus. Given its status as a horticultural weed, it's possible you'll get a more informative response on the Gardening & Landscaping SE.

Wintercreeper, Euonymus fortunei
Given that you're just over in Illinois, here's the page from our Plant Finder database.
In regards to your second question, this factsheet from UMich mentions (and gives citations) for its use as a medicine. Given that, I'd avoid eating it if I were you, but there's not mention of it being especially toxic.

Based on the MO Botanical Gardens information for this region, it seems like a good plant to try to remove to prevent further spreading.

Yeah, it's pretty weedy in my garden certainly, where it tries to climb the trees as in the photo.


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Why do we absorb vitamins better from whole foods than from pills?
We can't rely on pills to provide us our nutrients because we don't absorb the nutrients from the pills as effectively. Presumably this is because pills are lacking components that are required for certain reactions to take place.
Why can't we just create a pill that does have all the necessary components?

I think your premises are wrong. I don't know of any food that is recommended in place of a pill, because it is supposedly better.

Why can't we just create a pill that does have all the necessary components?

I'm assuming you mean micronutrients (vitamins & minerals). A day's worth of macronutrients (energy and building-block providing chemicals - proteins, fats, sugars) are already very abundant and dense - a pill containing a day's worth would be the size of an egg.
Otherwise, we do. There are vitamin/mineral pills which have a very high absorbancy rate (usually those chelated or chemically bonded to various amino acids [words ending in -nate on the label]).
The big problem is that while the vitamins and minerals may satisfy your bare biochemical needs, that is all they do. They will not satisfy a hunger instinct (proteins and fats do that), and there are untold millions of compounds in the untold thousands of plants and products humans can pick up from the market. These compounds usually do not do much, but some are beneficial to our health.
So while multivitamins exist which provide you with a very efficient method of absorbing most of your vitamins and minerals, it's always recommended to get them directly from food since food will provide macronutrients (thus satisfying your hunger), the micronutrients you're curious about, and many potential beneficial compounds which are not necessary.
If you are still interested, Soylent Shakes are an attempt to provide all the micro- and macronutrients the body needs in an easier-to-consume form without all the messy cooking or multivitamin pills. Keep in mind the long-term effects of sticking to such a diet are more or less unknown, but it's as close as we can likely get to an "all-in-one" meal.

I'm assuming you mean micronutrients - Yes, I do.

So does that mean you could eat an diet that isn't nutritious but that fulfills your macronutrient demands, take a multivitamin (satisfying the micronutrient demand), and that would be perfectly healthy? (you said the micronutrients that aren't in vitamins but are in food aren't necessary. could you expand a bit on this?)

Ps: thanks for introducing my to Soylent. VERY interesting. I definitely have to research it some more, but I had no clue this existed and it seems to be a huge step forward for humanity if is indeed healthy.

@user6035 - Yes, you could eat an artificial diet of macronutrients and micronutrients that would satisfy your biochemical needs. It would probably be "healthy" in that you would probably continue to live without issues you weren't already predisposed to. How other chemicals and compounds contribute to our health are unknown (think antioxidants), but have the potential to contribute significantly. However, please consult medical professionals for further info if you intend to pursue this. Due to genetic variation your body might have greater or lesser needs than the recommendations.

Ah ok. Great point about antioxidants. That example cleared up for me what you mean about other chemicals and compounds. I'll continue to investigate before moving forward!


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Why is the current Ebola outbreak different from previous outbreaks?
I don't know if this question has an answer at this time, but I would like to know if there is some biological reason why the current Ebola outbreak is so much more complicated and widespread than in the past. Traditionally it has been initially very virulent and has then has rapidly waned. I hope what I am saying is accurate, and if so why dont we see the same pattern now ?

Can you provide some references/proof for your statements (e.g. fatality rates over time of the current outbreak), and also explain more accurately what you mean (e.g. complicated in what way)?

This is too long for a comment, so I put this in here: The main reasons are sociological. From the data I have read so far, this outbreak (actually these are two independent outbreaks, one in West-Africa and another one -not connected- in the Democratic Republic of Congo) is not exceptionally deadly in terms of Ebola. The death rate is about 60% which is extremely high compared to other diseases, but Ebola had reached up to 90%...
I think the main differences are that this outbreak struck in a much more populated area which has a very poor health care system (if you can call it like this at all). Then it happened in a border region, I recall reports about a traditional funeral of a Ebola victim which infected visitors, some of them crossed the border afterwards.
Then it was completely underestimated in the beginning, because a lot of cases stayed unknown. This led to a wider spreading as people who got sick infected relatives and medical personnel subsequently. And although the reaction has been powered up a lot since then, it is still not adequate to contain the outbreak.
Former outbreaks happened in rural areas which where easier to contain with a smaller number of personal, which is not possible this time. If you want to read further about this, I recommend the blog of Tara C. Smith which has been doing research about Ebola for some time and also worked in crisis response teams.
Especially interesting are these two:

A historical perspective on Ebola response and prevention
Addressing more Ebola myths

You are correct that this seems to be two separate outbreaks, see http://www.who.int/mediacentre/news/ebola/2-september-2014/en/

For some background, it is essential to know that Ebola is actually a group (genus) of ebolaviruses, each with different fatality rates. There are five known species of Ebola, and four are known to cause disease humans (WHO: Ebola virus disease; wikipedia).
The known species of Ebola includes:

Zaire ebolavirus (or just ebolavirus)
Sudan ebolavirus
Bundibugyo ebolavirus
Tai ebolavirus (only one known human case)
Reston ebolavirus (can infect but does not seem to cause disease in humans)

Zaire ebolavirus is the deadliest strain (with Sudan second), and also the one that is causing the current outbreak. A table of all known ebola outbreaks can be found in the WHO report (WHO: Ebola virus disease), which shows that the historical fatality of the Zaire strain has been between 44% and above 90%.
From my limited understanding, when dealing with ebola it is essential for infected individuals to be identified early so that they can get intensive care (most importantly intravenous fluids because of dehydration), but also to prevent further spread. This is probably what has failed during this outbreak, but another problem is also that the size of the outbreak has put tremendous strain on an already weak healthcare system. These outbreaks have also occurred in well populated areas in countries with very weak governments, that also lacked experience in dealing with ebola (both in the administration and among the population).
In many former outbreaks, the initial death rate is very high since early victims are found at late stages of the disease, but when the outbreak is more controlled the death rate drops due to supporting care of infected individuals. I don't know to what extent this has been the case during the current west african outbreak. However, the overall fatality rate of the current outbreak is 52% (tabulated Aug. 28 2014), with 44% in Sierra Leone and 66% in Guinnea (WHO: Ebola virus disease update - west Africa), and this lies well within the normal fatality rate of the Zaire ebolavirus.


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How is it that ionic diffusion is independent of other ions?
This question arises from the explanation of what the resting potential of a cell membrane is. In the Goldman formula, there is no interaction between different ion types.
If diffusion is caused by random movement of ions and collisions, then how is it that the K+ ions do not seem affected by the very high concentration of Na+ ions outside of the membrane? Shouldn't there be an effect due to the fact that outside, the ion concentration overall is higher than inside? How come they are all independent?

Most importantly, the whole Goldman-Hodgkin-Katz model is, well, a model. It is a way we would like to find and explain phenomena, given pen and paper.
Often, scientists build models in order to explain data in hand, but even then, they will have to add something from their imagination. For example, early astronomers saw planets moving differently from stars, and came up with the idea that, you know, planets do not circle the earth, but maybe around some points in space, which in turn circle the earth. That didn't work well, so they created the heliocentric model, where planets and the Earth circled the sun. That was still perfectible, and Newton suggested the planets do not move on circles, but on ellipses. Each generation of astronomers had almost the same data in hand, but chose to make some assumptions in their models.
The same goes with the lack of interaction between potassium and sodium ions: it is a theoretical assumption. As models go, the GHK model is quite good, because it fits experimental findings better than any other model. Its assumptions have a great chance of being true, of reflecting the physical world. I guess you really asked what are the physical facts that underlie the assumption of ion independence. The fact is, you are looking for explanations for a fact that may be or may not be - so any response you will receive is, to a degree, speculation.
My thought is that the number of water molecules (55 molar) that may collide with an ion is far greater than the number of cations (up to a few hundred nanomolar, about 100 million rarer). Perhaps the number of ion-ion collisions is negligible. There is one bottleneck, in the actual channels, but there different species do not meet, because each has its own channels.
Another, more factual, is that the model is imperfect, and independence is more of a wish than a complete truth. Quoting from http://books.google.com/books?id=SmJoSwnwSh0C&lpg=PA353&ots=3fvI19Sk5Q&dq=ghk%20ion%20independence%20fails&pg=PA353#v=onepage&q&f=false : "The rich literature on how ion channels fail to obey the independence principle is reviewed in Chapter 14 of Hille (1991), and some specific models will be studied in the following chapter."

Thanks for this quick reply, which helps to a certain extent. But now that I thought about it for a while... If one assumes that the interactions between cations are negligible, and that therefore K+ diffuses "as if Na+ wasn't there", wouldn't that also mean that inside the cell K+ would hardly diffuse, because... well they don't interact with each other, thus hardly ever collide and thus don't diffuse?

In solution, potassium ions collide with each other as rarely as with sodium ions. The issue is net movement. When looking at a semiporous membrane that allows 1/10 of the ions hitting it, there will be no net movement, if 10 Na ions bumble on one side, and 10 Na ions on the other; nor if you have 100 on one side and 100 on the other. But there is predictable movement, if one side holds 10 times more Na compared to the other side, regardless of absolute numbers, and regardless of the number of K ions hanging around.

Hi Nick, and thanks again for taking the time to help me! I think I finally understand what you mean. Are you saying, that the diffusion is only caused by how many potassium ions hit the channel on either side? That would make sense to me... I had a quick Wikipedia search and found that there are inward and outward potassium channels, so that potassium that hits the membrane from the outside can flow into the cell too. The fact that there are inward and outward channels also helps with all this. Thanks again!

The number of ions moving one way is dependent on the number of ions of that kind. If one in a thousand hits the hole, like the balls in lottery, it matters how many balls one is juggling. More green balls will pass if more greenballs are bouncing. But we have two movements. Most ionic channels allow equal passage both ways.

(continued) The GHK model implies no direction selectivity. GHK does not distinguish permeability for moving K in from permeability for moving K out. (In reality, this assumption is not 100% correct. Rectifying channels make a distinction between directions. So here's another reason why GHK is a simplified model.)

(continued) The net movements is a balance of two movements. The fact that we have the electric+osmotic imbalance makes ion X undergo net leakage towards, say, the cytosol, in physiological conditions. But in the lab, where one can play with concentrations and voltages, most ions will allow net reverse flow.

Thanks Nick! it's all a lot clearer now, very interesting topic I find, much more interesting than they show you in a classroom!

Maybe I'm missing something here (and it's not my area of expertise) but...
the GHK formula includes the parameter Vm which is the transmembrane potential. This parameter is determined by the intracellular and extracellular concentrations of all ions. A high external concentration of Na+ will therefore influence the net movement of K+.
One of the assumptions of the GHK equation is that the ions do not directly interact.

Hi Alan, in the GHK formula, the movement of K+ is independent of the other ion concentrations, you can see this by setting the permeability of all other ions to 0. According to the GHK model, if the ion cannot pass, it will not have an effect on the membrane voltage. But have a look at Nick's answer!


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Which sex is homogametic in side-blotched lizards?
I'm just trying to find out whether the male side-blotched lizard is the hetero- or homogametic sex in side-blotched lizards (Uta stansburiana) - some reptiles are ZW system (female heterogamete) and some are XY (male heterogamete).

Lizards of the genus Uta are apparently male heterogametic (XY) (Pennock et al. 1969). The XY system seems to be the most common mode of sex determination in iguanid lizards (Kasahara et al. 1983).

Kasahara, Y et al. 1983. Chromosome mechanisms of sex determination, G- and C-band patterns and nucleolus organizer regions in Tropidurus torquatus (Sauria, Iguanidae).  Genetica 60: 151-156.
Pennock, L.A. et al. 1969. Minute Y chromosome in the lizard genus Uta (Family Iguanidae). Cytogenetics and Genome Research 8: 9-19.


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How do birds influence brood sex ratios?
This paper concludes that birds can adaptively modulate brood sex ratios. How do birds modulate brood sex ratios? Are they somehow able to influence the sex of their young? Or once young are born, do they provision one sex with more food so that the other sex does not survive?

On a more general level it is possible for parents to influence sex-ratio of broods in a number of ways, and there are other reasons why a brood might have a sex ratio distortion. The paper I've been reading this morning is about side-blotched lizards doing just this. I'll give a quick basic answer just from the top of my head and hopefully someone can give some specific examples in birds.
Bias in gamete production
Assuming XY chromosome systems where the males are heterogametic (XY, females XX) the male can influence the brood sex ratio by producing more or less Y-bearing sperm. Sperm carrying an X-chromosome will always produce daughters and sperm carrying a Y- will always produce sons. The opposite would be true for ZZ/ZW where female gamete type determines the sex, they could only produce Z eggs, therefore only having sons.
Female cryptic sperm choice
A fairly modern idea is that females can selectively fertilise eggs with sperm based on the DNA they carry, this could include whether the sperm is Y- or X-bearing. This idea is thought to explain how females produce daughters from small sires and sons from large sires in the paper I mentioned at the start.
Meiotic drive and sex ratio distorters
Meiotic drive elements may be responsible for sex-ratio distortion in broods. Just like the biased sperm production this can alter the sex-ratio at the gamete level. Genetic effects mean that fewer offspring of one sex than the other are produced. Here is one example where suppressors of the distorter have evolved in the autosomes.
Direct selection by the parents
In the paper you mention above, and with most studies, it is possible that the parents are selecting which offspring to raise after they hatch (or as an egg - it may be possible to determine sex at that point) and if females are more costly to raise and conditions are poor, they may kill/neglect the female offspring early on.
Within brood competition
If one sex is stronger as a chick it possible that the broods could become sex biased in certain conditions which consistently favour one over the other.
Consequence of environmental strain
Similarly to the last two points, if conditions are poor it may be harder for one sex to reach maturity than the other which would result in sex-bias. This is the conclusion the authors in your paper seem to come to.
Environmental effects
As with some reptiles, environment can determine the sex of the offspring. For example, incubation temperature in turtles has a considerable effect on offspring sex ratio. Given how close birds and reptiles are in evolutionary time, and the importance of active incubation in birds, I don't see that it's impossible for the parent to vary some kind of environmental factor in order to bias sex-ratio.
There are certainly more potential mechanisms and some of these ideas are fairly new in evolutionary biology research so there are many unanswered questions. I hope I will have time to find some bird specific examples later.

Sperm production bias will, of course, not work in birds since they have a ZW sex chromosome system, not XY. I suppose the female might be able to similarly bias ovum production, though.

Thanks @IlmariKaronen - I've clarified the answer a little bit. You are of course right, I was just putting in an answer for general brood sex ratio manipulation so forgot to add the ZW specifics.

authors: Светодиодные решения


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Negative role of Placenta
How can a placenta turn hostile to the mother or fetus ?
What are the abnormalities found during placental delivery ?

The placenta does not turn "hostile" to the mother or fetus. Placentation abnormalities can result in harmful situations, but these are a secondary result.
Structural anomalies of placentation:

placenta accreta/percreta: means that the placenta took hold not only in the uterine mucosa, which is the normal state, but through it up to the myometrium (muscle layer, in placenta accreta), or even up to the serosa (outermost uterine layer, in placenta percreta). These anomalies will convey a much higher chance of massive haemorrage at delivery, and therefore are dangerous to the mother.
placenta praevia: placental insertion covers the entrance to the uterine cervical canal, partially or totally. Therefore, the way of the fetus for natural delivery is blocked, and the placenta will tear during labor, causing massive haemorrage.
marginal implantation of placental vessels: vessels linking the placenta to the fetus (the umbilical cord) are implanted on the periphery of the placenta. This causes structural fragility, and a greater risk of bleeding for both the mother and fetus.
retroplacental hematoma: in such cases, the placenta partially or totally loses its hold on the mucosa, and blood fills the space left behind. This is an immediate threat to both the fetus and mother because of the potential for massive haemorrhage and interruption of oxygen delivery to the fetus.

Deleterious side effects of pregnancy:

preeclampsia/eclampsia: misunderstood biological syndrome that causes the classical signs of arterial hypertension, peripheral edema, hepatic cytolysis, and thrombocytopenia in the mother. Eclampsia is all that plus added seizures (in which case maternal mortality is high). This is not due to placentation abnormalities, even if it is true that delivery is the only cure, and can justify a premature artificially induced delivery in extreme cases.
fetal/maternal rhesus factor incompatibility: During labor and delivery, a small amount of fetal blood will come into contact with the mother's organism. If the mother is Rh neg, and the baby Rh pos, the mother can develop antibodies against the rhesus factor. This can cause haemolysis in the newborn, and in grave cases, kernicterus (toxicity of degraded red blood cell metabolites to the baby). While this may threaten the baby to be born, problems are much more common for subsequent Rh pos pregnancies. We check for antibody presence in the mother with the Kleihauer test and give preventive injections of rhesus antibodies to Rh neg mother with a Rh pos pregnancy to decrease the chance that the mother develops her own antibodies.

Other special cases:

molar pregnancy/choriocarcinoma: A structural genetic accident happening on fecundation that can cause the embryo to behave as a type of cancer.
ingesting placental extracts: this is mentioned is another answer here. This has nothing to do with the placenta, but the deleterious secondary effects are due to direct toxicity of the hormones contained in those extracts ingested in an inadapted situation. This is not to say that one should take them while pregnant, because hormonal deregulation would also be toxic in a normal pregnancy.

An abnormal placenta position can lead to increased risk of heavy bleeding during placental delivery which further complicates the process by needing blood transfusion drugs. Anterior placental attachment is associated with increased risk of pregnancy induced hypertension , gestational diabetes mellitus due to dysfunction of lactogen hormone secreted by placenta, placental abruption, intra uterine retarded growth or fetal death.Rh factor incompatibility is a complication during the second delivery. Also, placenta encapsulation(conversion of placenta into capsules) has side effects on mother's health like pelvic girdle pain, constipation or diarrhea , PMS like emotional outbursts.
Placenta is an intimate connection between the fetus and mother but locational abnormalities can make placenta hostile to both fetus and mother. Also, the Rh factor incompatibility stays a major factor in being harmful.

Can you add some references to you answer?

This answer is unstructured, confused, and partially incorrect, and reveals a lack of understanding of the subject. The answerer has good points but mixes things up.


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What is the classification for animals with full tube digestive tracts?
What is the formal name for animals with full digestive tracts, by which I mean a mouth and an anus, and what is the classification for animals that have a single hole for exchanging food and waste?

Animals with a single hole do not form a monophyletic group: metazoa > eumetazoa >bilateria almost all have separate mouth and anus (except notably flatworms which is one reason it does not form a monophyletic group).
As species are not grouped in monophyletic groups by what they don't have (eg. invertebrates do not form a monophyletic group while vertebrates do) there is no particular group. Eumetazoa before the bilateria have a single mouth-anus.

Some echinoderms also have one gut opening- i think brittle star


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Did Darwin ever reach the conclusion that selection will remove variation?
According to simple models of selection the genetic variance in a population should be reduced by selection. (Fisher's fundamental theorem states that the rate at which a population can evolve is limited by its variance). If we select the next generation from one population we will only ever capture as much, and probably only a subset of, the variation that exists in a the first generation.
Did Darwin ever discuss this loss of variation? What did he conclude?
(For now lets ignore the potential roles of sexual antagonism, pleiotropy and such)

A little clarification on my question:
Darwin saw variation in phenotypes, and variation in fitness dependent on phenotype - an effect he called selection. He also saw that this variation was heritable (but did not know how). This is the basic concept of evolution, and is mathematically speaking, the breeders equation:
$r = h^2 s$
He also would have realized that life must therefore have started out as a simple unit, and new variance in traits (and whole new traits) must have arisen over time, i.e. that some kind of changes (mutations) were going on in the heritable information (genes). However, what I'm asking is, did he realize that selection would act to reduce the variation in a population? This would reduce the rate at which evolution can occur over time (Fisher's fundamental theorem - assuming no influx of variance or potential for pleiotropy to maintain variation). Or was it Fisher that first formally discussed the concept of lost phenotypic/genetic variance?

I don't think you can simply ignore mutation like that. Each generation may have its variation reduced by selection but novel variants will also pop up through mutation and copy errors. We'd have to take both rates (that of loss and that of gain of variation) into account to answer this.

Do you mean genetic variance specifically? Since Darwin didn't really know about "genetics" in the same sense as Fisher, I doubt Darwin could have come to this conclusion. Phenotypic variation is another question, though.

@terdon I mean I'm not worried if he considered mutation and other effects which may maintain variation. I mean he realized there is selection, and some kind of heritable information, and therefore did he realize and discuss that selection would take away from the pool of information over time

@kmm yes loss of variation in the information/trait from one generation to the next is what I'm thinking of - mentioning genetic variation was not so deliberate.

This might help

@terdon is right - in practice over time the rate of variation will reach a steady state if there are no environmental changes

After reading your question, I had a vague memory that this subject was indirectly touched upon in "On the Origin of Species", so I did some text searches (in this pdf version I found online). From what I can see, Darwin never used the technical term 'variance' (I don't know how old this use of the word is), but 'variability' is often used, both with regard to accumulated variation but also meaning variation between individuals within a population.
All-in-all, I could not find clear support for the idea that selection will decrease the amount of variation. However, there are number of passages where the subject of variation vs selection comes up (often indirectly), but, to me, these just as often (most often?) indicate that Darwin saw no risk that selection would reduce variation as the opposite. Here are the most interesting passages I could find (searching for combinations of 'variab*', 'selection', 'decrease' etc), with page references referring to the pdf version and a short comment below each quote:

A large number of individuals,
  by giving a better chance for the appearance within
  any given period of profitable variations, will compensate
  for a lesser amount of variability in each individual,
  and is, I believe, an extremely important
  element of success.
  (p. 44)

This is clearly discussing amounts of variation within species, where large numbers can compensate for a smaller amounts of standing variability, by increasing the chance of advantageous mutations.

Nothing can be effected, unless favourable variations
  occur, and variation itself is apparently always a very
  slow process. The process will often be greatly retarded
  by free intercrossing. Many will exclaim that
  these several causes are amply sufficient wholly to
  stop the action of natural selection. I do not believe
  so. On the other hand, I do believe that natural selection
  will always act very slowly, often only at long
  intervals of time, and generally on only a very few
  of the inhabitants of the same region at the same time.
  (p. 103)

Not directly related to selection vs variation, but deals with the rate of evolution vs amount of variation.

But what here more
  especially concerns us is, that in our domestic animals
  those points, which at the present time are undergoing
  rapid change by continued selection, are
  also eminently liable to variation. Look at the breeds
  of the pigeon; see what a prodigious amount of difference
  there is in the beak of the different tumblers,
  in the beak and wattle of the different carriers, in the
  carriage and tail of our fantails, &c., these being the
  points now mainly attended to by English fanciers.
  Even in the sub-breeds, as in the short-faced tumbler,
  it is notoriously difficult to breed them nearly
  to perfection, and frequently individuals are born
  which depart widely from the standard. There may
  be truly said to be a constant struggle going on between,
  on the one hand, the tendency to reversion to
  a less modified state, as well as an innate tendency
  to further variability of all kinds, and, on the other
  hand, the power of steady selection to keep the breed
  true. In the long run selection gains the day, and we
  do not expect to fail so far as to breed a bird as coarse
  as a common tumbler from a good short-faced strain.
  But as long as selection is rapidly going on, there
  may always be expected to be much variability in
  the structure undergoing modification.
  (p. 141)

This is maybe the most interesting passage, which to me indicates that he saw little risk that selection could/would limit variability (see especially beginning and end).

For forms existing in larger
  numbers will always have a better chance, within
  any given period, of presenting further favourable
  variations for natural selection to seize on, than will
  the rarer forms which exist in lesser numbers. Hence,
  the more common forms, in the race for life, will tend
  to beat and supplant the less common forms, for
  these will be more slowly modified and improved.
  (P. 162)

Also on limitations for variation that selection can act on, and the value of large populations.

... firstly, because new varieties are
  very slowly formed, for variation is a very slow process,
  and natural selection can do nothing until
  favourable variations chance to occur, and until a
  place in the natural polity of the country can be better
  filled by some modification of some one or more
  of its inhabitants. And such new places will depend
  on slow changes of climate, or on the occasional immigration
  of new inhabitants, and, probably, in a still
  more important degree, on some of the old inhabitants
  becoming slowly modified, with the new forms
  thus produced and the old ones acting and reacting
  on each other.
  (p. 163)

On the limiting nature of variation, but does not connect selection to decreased variation.

It cannot be asserted that organic beings
  in a state of nature are subject to no variation; it cannot
  be proved that the amount of variation in the
  course of long ages is a limited quantity; no clear
  distinction has been, or can be, drawn between spe-
  cies and well-marked varieties.
  (p. 425)

On variation over the long run.
These are the most interesting sections I found on the subject from my (quick and limited) searches. I hope you find them useful. However, this is only based on the first edition of "On the Origin of Species", and it is possible that it is is modified in later editions or that he touches upon this in his other writings. However, when looking at these particular passages in the sixth edition, I cannot see a major change in his thinking.

I now see that the pdf version I used is unavaliable at the moment. At the Project gutenberg page for On the Origin you can find the first edition as html and the sixth edition as epub, as a complement.

Fantastic research on your answer, from this I would conclude that Darwin wasn't aware/hadn't considered that selection reduces population variation (and therefore reduces the rate at which evolution occurs) I'd credit that observation/idea to Fisher. Would you agree?

My guess would be that it came from the Modern Synthesis, but I cannot say who should be credited for the idea (could be Fisher, Haldane, Wright, Dobzhansky ++). Even if Fisher developed it theoretically, somebody else might have voiced the concept earlier. I do not know the literature well enought to say.

However, I would tentatively conclude that Darwin did not have any well developed ideas on the relationship between selection and within-population variability.

I think Darwin just stuck to the empirical observation that variation exists.  Without knowing about genetics and mutations, he didn't know the mechanism that generates variation, and he knew that he was lacking that, but he knew variation was being generated.


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What about a bat's immune system protects them from Ebola?
Current evidence indicates that fruit bats are a reservoir host for Ebola. Has any research established what is different about their cell biology or immune system that reduces virulence for them?
Failing research on this particular system, do you have an example in another system of how virulence is reduced in the reservoir host?
I'm teaching a cell biology class, so actual examples of modified proteins or enzymes or inflammatory molecules in the reservoir is preferred.

New paper in eLife you might find interesting: Pigot et al. 2014. Mapping the zoonotic niche of Ebola virus disease in Africa. @Chris

@fileunderwater Interesting, thanks for the paper.

The main reason for this is that fruit bats are most likely (I don't think there has been a direct proof for Ebola so far) the reservoir host for this disease. The reservoir host is adapted to the disease and can harbour it for an indefinite time (with recurring infections) without showing signs of an infection or being affected by it. Although it is not getting sick, the reservoir host can pass the disease to other animals.
There is very little known about the immune system of bats, but they seem to be different, so they are not affected by diseases which cause havoc in humans. The following papers go into some details and they are interesting to read:

Bats: Important Reservoir Hosts of Emerging Viruses
Bats and their virome: an important source of emerging viruses
capable of infecting humans.

These papers give an interesting view of the bats immune system. The first article is a short explanation of the most important findings of the second. It looks into differences between species and analyse how the bats immune system may have evolved. Really interesting.

Of bats, flight and immunity to viruses
Comparative analysis of bat genomes provides insight into the
evolution of flight and immunity.
Antiviral Immune Responses of Bats: A Review


text:
What roles do cyclooxygenase, lipoxygenase, and epoxygenase have in signal transduction?
Besides oxidizing fatty acids to form prostglandins, leukotrienes, and epoxides, what other roles do cyclooxygenase, lipoxygenase, and epoxygenase have in signal transduction?

Is this a homework question? Do you have any preliminary ideas?

No. I was reading about how these enzymes oxidize fatty acids in my textbook, but I was curious to know if they had any other important functions in signal transduction. I honestly don't have much of an idea on what else they could possibly do, since I have no previous knowledge on these particular enzymes.

Fair enought. The reason I asked was because your Q seemed to fall under our homework policy. Do you have any special reason to believe that these enzymes have other roles?

I just took a quick look.
These classes of enzymes are important to a family of lipid based molecules which perform intra and intercellular signalling with a lot of medical importance.
Epoxygenases can create epoxides of arachidonic acid,  which can modulate cell proliferation.  Arachidonic acid is a well known second messenger in many tissues in the cell, so these enzymes clearly would affect many signalling pathways.
Cyclooxygenases (COX) enzymes are such important mediators of inflammation signalling that they are the primary targets of aspirin and other Non steroidal anti-inflammatory drugs.
Lipoxygenases oxygenate compounds such as prostaglandins which are downstream from aranchidonic acid (as does COX).


text:
What does "Mutational Variance" mean?
Background
The concept of mutational variance can be found in many articles including this one for example. The mutational variance of a trait number $i$ can be found in the M-matrix in position $m_{ii}$ (in the diagonal). Elements of the off-diagonal represent mutation covariance. For example element at position $m_{ij}$ of the M-maitrx is the mutational covariance between traits $i$ and $j$. More info about the M (and G) matrix can be found here.
Question
What does "Mutational Variance" mean? What does it mean for a population to have a high or a low mutational variance?
Does "mutational variance" refers to:

Average effect of new mutations on fitness (mutational effect) (parameter $s$)
Variance in the effect of new mutations on fitness (variance in $s$)
Average effect of new mutations on phenotype
Variance in the effect of new mutations on phenotype
The increase in genetic variance ($V_G$) due to a new mutation
The increase in additive genetic variance ($V_A$) due to a new mutation
Genetic variance in the population at mutation-selection-drift equilibrium.
Is it a concept that is opposed to genetic canalization?
...

In Pigliucci (2004) (repeated in Hansen (2006)) the mutational variance is defined as being the new additive genetic variance entering in the population each generation due to mutations.
In consequence the mutational variance is not define at the level of the mutation in the sense that we do not care about how many mutations yield to this new genetic variance. So none of the suggestions of possible answers in the OP's question is correct.


text:
Is there a difference between any of these terms for proteins: "crystal structure," "NMR structure," "solution structure," and "complex structure"?
My homework wants me to plot all crystal structures determined per year, but when I search on PDB for all structures, many of the articles say "crystal structure," but some say "solution structure" or even "complex structure." Are all of these considered to be subsets of "crystal structure"?

Depending on who you talk to (typically laymen and scientists who are not structural biochemists), the term "crystal structure" is frequently taken to mean "some determination of molecular structure, whether by actual crystallography or some other means".
For example, a graduate student is talking to her adviser, an immunologist, about the structure-function relationship between a certain viral capsid protein and the peptide antigens they are using to create families of antibodies to the virus. The adviser consistently refers to the recently-published "crystal structure" of the protein, even though the actual study was performed using a combination of NMR spectra obtained from solution, electron microscopy, and quantum mechanical computational chemistry modeling techniques, and no crystals were actually studied.
So, you probably want to talk to your teacher/professor and clarify what s/he is looking for. Most likely, if you're in some sort of undergrad or first-year graduate class, they're just looking for "structural determination" in general, but they may specifically be looking for those models that were generated using actual crystals, so asking is always best.
I should note that there are significant methodological and computational differences when determining structure via X-ray crystallography, various types of NMR, electron microscopy (with or without crystals as the target), so-called "complex" determinations, etc. Find a structural biologist to learn much, much more.

I agree with what MattDMo has said, but just to emphasise - a 'solution' or 'NMR' structure is not a crystal structure. ('Complex structure' probably means structure of a complex. e.g between a protein and a ligand.) To be a crystal structure the structure should be determined using X-ray crystallography.
From the Protein Data Bank home page choose Advanced Search.
Then use the pull-down menu Choose a Query Type: to select Experimental Method. This will automatically populate with the X-RAY option which is what you want - have a look at the other options.
You can then use Add Search Criteria  to append a new field where you can select a date range.

I think it is important to emphasize that there are some differences between the NMR and crystal structures. In NMR, a floppy tail will move freely. One will learn that the tail is floppy, and perhaps localize it. In crystals, proteins are packed very tightly, forcing many tails to sit still. To the observer, it may seem that the tail is not floppy. In conclusion, crystal structures may mislead. But NMR is limited about the size of protein it can work with. One is forced to perform NMR on fragments, rather than full length protein. Cutting may create spurious floppy ends etc.


text:
What's the mechanism behind 'losing heat through your extremities'?
I can understand how if you are not circulating enough (warm) blood, by not moving much while in a cold environment, your extremities themselves lose heat, and become cold - but I don't understand how they (the hands, feet, and head) can make the rest of your body lose heat too.
'Drawing the heat out of your body' (as people have termed it to me) doesn't make sense itself - what is the actual mechanism(s) behind the (exposed, relatively uncirculated) extremities, 'drawing' heat out of the body?
Is it that it merely draws the need to heat those (poorly insulated, circulated) extremities from the existing distribution of heating the other parts of your body, thus lowering how warm those other parts are?
If so, how does that happen? In the case above, where you're not moving the body to circulate warm blood to the hands (or using other warming stimuli like friction), how would 'heat transfer' to the hands occur then? Or does it just indeed slowly 'lose heat' and get colder and colder (which would then lead me back to my question, how would that explain the rest of your body becoming colder as a result of the extremities becoming colder)?

Your extremities lose heat at a faster rate than the rest of your body because they have higher surface area per unit volume. Heat exchange happens at surfaces, so if you have more surface, you transfer heat more quickly. Imagine you have a sphere of water with 1L volume, and a long cylinder of water, also 1L, lets say 1cm wide, the sphere will hold heat longer because it has less surface area per unit volume.
Why does losing heat through extremities cool the rest of your body? Because of your blood. As blood runs through your core, it takes heat from surrounding tissues. The blood carries that heat to the extremities, where cooler tissues pull it away from the blood. It's kind of like how the coolant in your car takes heat from the engine block to the radiator.
When it is very cold, your body will reduce blood flow to the extremities to save heat, making your fingers vulnerable to frostbite. However, it cannot stop bloodflow, those tissues still need oxygen, so you still lose some heat.

It would be good if you could flesh out the answer with an explanation for this: when cold, does it reduce the general circulation levels from the extremities being very cold, or does it actually increase it (even if slightly) due to the 'need' for the extremities/core to be heated more? I guess I'm going off-topic into the realm of the whole hypothermia process at large, but still it would be good to explain that point as it still relates to and would explain the topic slightly more fully. So to sum: when cold and hands exposed, does it reduce core circulation or actually increase it? Thanks!


text:
Origin of the 260/280 ratio?
This is not a duplicate of all the other 260/280 ratio questions, I already know that DNA is supposed to be 1.8 and RNA is supposed to be 2.0. However, this might be more appropriate for chemistry, and will move it if I have to.
My question has to do with the Poly A tails on mRNA. I've been doing in vitro transcription and tailing for a while now and have noticed that the untailed RNA has a 260/280 of about 2.0, like you'd expect, but successful tailing results in ratios from 2.15 to 2.45, with higher ratios correlating to better band shifts on agarose gels, implying a longer tail. I suspect the reason for this is because the adenine has a much higher 260/280 than the other bases, so if you add a lot of adenines to the 3' end of the RNA you add much more 260 absorbance than 280 absorbance.
After seeing this I tried to come up with a mathematical method to estimate tail length based on 260/280, since gels are annoying, while I can get the ratio directly from the nanodrop.
I started by using the 260/280 for each nucleotide, A: 4.50, G: 1.15, C: 1.51, U: 4.00, T: 1.47 source here: 1. I then took the sequence for the Luciferase gene I'm using for mRNA and counted the nucleotides, 449 A, 566 C, 470 G, 374 U. I tried to get the weighted average of the 260/280 for my RNA.
A: 449 x 4.50 = 2020.50
C: 566 x 1.51 =  854.60
G: 470 x 1.15 =  540.50
U: 374 x 4.00 = 1496.00
Sum:            4911.60

Nucleotides: 449 + 566 + 470 + 374 = 1859
Sum / Nucleotides : 4911.60 / 1859 = 2.64

2.64 is clearly not 2.0. Even accounting for the potential effect of pH and ionic strength on RNA 260/280 ( acidic solutions have lower ratios ) I can't explain why the calculated ratio is so high. Even if we assumed an RNA with 25% of each base, the weighted average is still (1.15 + 4.50 + 1.51 + 4.00)/4 = 2.79, even higher than for my real sequence.
Doing the same calculation for DNA, (1.15 + 4.50 + 1.51 + 1.47)/4 = 2.16.
So why don't my calculated ratios for RNA and DNA 260/280 match the "ideal" ratios of 2.0 and 1.8?

I bet it has something to do with base stacking interactions.

Here's one explanation: It's not the base composition that determines UV absorbance (260 nm), but whether the nucleic acid is in a single- or double stranded state.
Promega cites Griffiths biochemical methods that claims that double-stranded DNA absorbs UV less strongly than denatured DNA due to the stacking interactions between the bases.
I think your calculations must be wrong, since you can not expect a polymer to have the same spectrometric behaviour as the sum of all monomers. The absorbance of a molecule depends on its surroundings (like solvent, or nearby chemical groups). Bases within a DNA strand have much less contact to the solvent (H2O) when compared to a single nucleotide. In general, bases in ssRNA (single stranded RNA) and dsDNA interact with each other via aromatic pi-stacking. This affects the energies of the electrons that are responsible for light absorbance.
Most importantly, each base inside a dsDNA strand is engaged with a hydrogen bond from the other strand, which (I presume) significantly shifts electron energies and hence also its absorbance behavior. This might also be the reason why low pH decreases UV absorption of RNA (260 nm), since hydrogen acceptors are protonated just like in the double stranded state.

Seems reasonable in general, but polyA would surely be single-stranded and, hence, unstacked, which would give a higher value than obtained. I just wonder how one gets enough mRNA to do an accurate 260/280.

Pi stacking happens in any single stranded nucleic acid. I presume that user137 somehow accumulated luciferase mRNA using e.g. in vitro transcription.


text:
Protein Isolation from mammalian cells
What non-SDS buffer can I use to isolate protein from mammalian cells? The protein is intended for testing electron transport chain complexes.

Short answer - you will need to use a nonionic detergent. These will dissolve lipid membranes but leave most protein complexes intact, and many proteins in active form.
However there are many of these available and finding the right one for a particular job is a black art.
The usual approach is to start off with something widely-used and not too expensive like Triton X-100. Detergents with glycoside head groups are also widely-used but tend towards the expensive.


text:
Why can't NMR be used on large RNA molecules?
While reading my Molecular Bio textbook, I came across a sentence that stated that NMR cannot be used on large RNA molecules to determine their structure. Why is this? Is it because RNA is single stranded?

RNA usually has pretty complex structures. What causes the problem with NMR however is that large RNAs, such as mRNAs, don't have 1 structure, they have a population of possible secondary structures, and even if small parts of the RNA always have the same local structure, the overall molecule will occupy a variety of forms. The NMR will see a population of structures and won't be able to get good signal. DNA and RNA seem like tempting targets for NMR because the phosphorus in the backbone is NMR active, potentially allowing for backbone structure determination, but this only works on short pieces of RNA that adopts a single conformation.
Unfortunately I don't have sources to cite, only a couple semesters of NMR courses and a year of in vitro transcription of mRNA.