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What is this plant in the Butler, Pennsylvania area?
This is growing in the woods near my house in the Butler, Pennsylvania (USA) area. I have not seen it around before, and I have no idea what is it. What is it? Is it poisonous to pets (or little kids)?

could you comment on two things: What time of year did you take this picture? And were the viney tendrils and green leaves the same plant as either the lighter-colored stem in the middle of your top picture or the cluster of berries? Or are the big stem and berries a separate plant.

That looks like a bit like a Smilax to me, possibly Smilax herbacea.
Make sure you have a positive ID on any wild plant before you eat it, but if this is Smilax it looks like you don't have to worry about it being poisonous: from Flora of North America entry on the genus Smilax:

Smilax has numerous uses. Sarsaparilla, a beverage and medicinal used
  against rheumatism, is obtained from the rhizomes of various species... All species of Smilax are excellent wildlife food and are also browsed, or the rhizomes dug
  and eaten, by domestic stock.

For you, or for other Pennsylvania people, note that the Pennsylvania Flora Project of the  Morris Aboretum is a great resource. You can download species lists by county, and just that and some google image searches can often substitute for a field-guide of your county.
If you want to identify plants the hard way, and are willing to deal with special botanical vocabulary, the Flora of North America that I linked to above is the definitive resource.

Short answer
I would also guess it's Smilax herbacea, but let me go a step further and explain why...

 LEFT: NC State Extension ; RIGHT: SEINet
Long Answer
This does indeed appear to be a species of Smilax, a genus of climbing and sometimes woody plants often found with prickles. The group often picks up the colloquial name "greenbriers," and according to BONAP, 5 of the ~20 North American species are present in Pennsylvania with 4 found in Western PA specifically: S. glauca, S. herbacea, S. hispida, and S. rotundifolia (with S. pulverulenta found in Eastern PA).

 Range map of Western PA Smilax species. Sourse: BONAP
Greater detail of the leaves would be quite beneficial for IDing to a specific species, but we'll try to figure this out with the available data. The nice shots of the umbel-shaped infructescences (i.e., the umbrella-like cluster of berries) are certainly useful. The long length of the peduncle (or main shoot to the base of the fruit cluster) should be able to help us here.
If we take a look at Weakley's Flora of the Southern and Mid-Atlantic States (I'm using a 2013 copy), the first dichotomous break in his key references peduncles of either usually > 4 cm long (clearly the case in the OP's picture) or < 3 cm long. Of the species I listed above from BONAP found in Western PA, only S. herbacea falls under the > 4cm peduncle step in the key.  In fact, Weakley claims that S. herbacea has peduncles 5-8x as long as the subtending petioles (these are the small stalks connecting the fruits to the main stalk). BINGO!

According to Flora of North America (vol. 26): peduncle to 30 cm.

But wait, according to both floras above, the berries are supposed to be blue...
Aha! But fruit on many greenbriers often start out paler green before darkening to dark blue in maturity. According to NC State Extension, the berries are not "available" until August in NC, so I'd guess berries in PA would be even farther behind being farther North. If you took this picture relative recently prior to posting the post (mid July), it would suggest any such fruits are still quite immature and so the pale coloration is not totally unexpected (though yours look particularly pale).

 Northern Bushcraft (see for additional pictures)
 Note: the International Plant Names Index actually lists a number of varieties (though I think a number of these have been separated out as their own species). Gleason and Cronquist (1991) [see here] suggest 3 remain.  I point this out simply because some variability could be a result of variation between these different varieties.

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How to obtain bacteria samples at home?
As the original question went from hold to closed, I thought I would write up a more appropriate question.
How should one go about getting bacterial samples to look at under a microscope at home?  How do professionals do it?  What if I want to look at cool pathogenic species like Salmonella bongori, Escherichia coli, or Bacillus anthracis?

Interestingly enough, PLOS just published an article about culturing Salmonella and other bacteria in field conditions. Here's the link to that paper by Andrews et al., and here's the Scientific American summary

There's nothing "cool" on killers such as Bacillus anthracis. The use of the word "cool" in association with B. anthracis suggests this is probably a kid, wanting to experiment. Or worse. With all the possible dangers involved. I strongly oppose releasing any information on how to culture it and I suggest the answer here being erased.

This is kind of pointless, since this knowledge is not secret. Anyone with access to a well-sorted library or microbial science publications can find out the conditions. Besides that, the real problem is doing this work without training. Most likely nothing (or only contamination) will happen.

I know, but then let them search it from themselves. That kind of "cool" knowledge shouldn't be provided to kids on a golden plate. I will be the first to plea for scienc education for kids, even if that involves some risk. But helping a kid culturing antrax? With all the risks it involves? Him being infected only being the least concern? No.

@guest did you actually read the post? You'll note that there's not specific instructions on culturing anthrax. That language in the question came from the comments and back and forth from the original post. I don't know if it would be on topic but if you wanted to make this a question, maybe a meta, I'd be happy to refute in detail. I don't think that there's any point denying that people will perceive more highly pathogenic species as "cool."

First, and I cannot stress this enough, you should not go seeking out human pathogens if you don't have the appropriate equipment to handle it at the right safety level.  That goes for all pathogens, even ones you might find around your house.
In a professional lab, you might get samples from collaborators, clinical samples, vendor, or really an number of other professional resources.  A well respected vendor as an example is ATCC, but the general public wouldn't be able to "shop" there.
But you really don't need to go far to get a whole host of microbes to study, you can grow them all at your house.  The basics of bacteria culturing can really be broken down to three steps: (1) get a source of bacteria, (2) put some of the bacteria in an environment where they can grow easily, and (3) harvest them to do something useful with them.
(1) Is fairly easy, bacteria are everywhere.  You can swab nearly any surface of anything in your house and come up with microbes (note you might also get some mold/fungi).  In this case (3) is easy as well.  Once you have culture you can streak it across a slide to view it under a microscope (you could also use several proper mounting techniques).  After all, looking at microbes under a microscope is the real goal here!
The only part of this plan that will take some real elbow grease is making your own culture dishes at home, but it's not as hard as you might think.

Making your own culture dishes:
1) The "plates" themselves.

I recommend getting the smallest Tupperware like containers your can
  find that are microwave safe, dishwasher safe, and really make a good
  seal (water tight at the least). They really don't have to be big, and
  you will make your life easier if you buy a bunch to match. They need
  to be super clean. After running them through your dishwasher at home,
  put them all in a boiling pot of water until you are ready to pour in
  your "medium." A mid-low simmer will work

Note that you won't probably be able to have perfect sterile technique at your house, but you should try to do what you can.
2) Your "Medium" or Broth

I highly recommend using pectin as your gelling agent if you can't get
  your hands on some agar. After that comes plain unflavored gelatin,
  but I recommend pectin. You can get it at almost any grocery store and
  my recipe is made assuming that. You can determine how much you want
  to make, just scale up the ratios. I'm going to list things as rough
  volume by volume so you won't need a scale.
i) Make the powder first:

45mL of pectin;
4 bouillon cubes ground as finely as you can (you can get different
  types and results depending on if you start with vegetable, beef, or
  chicken. I recommend starting with vegetable.);
125mL of refined white sugar;
Additives (more on this later)

ii) Mix the powder into 500mL of water.
Before you mix in the powder, heat the water to 50-75oC (mid low heat), but not boiling. Mix the powder in while stirring until
  dissolved.
iii) Bring the mixture up to a boil. Let it boil for about 2 min,
  stirring all the while.
iv) Cover the pot and let it cool for 4-5 min.
You by no means want it to cool down to room temperature, you just want
  to get it a little below boiling. If you are at 55oC or below it's
  definitely time move on.
v) Dip/fill your "plates" 1/3 full of media using clean/sterile
  utensils and seal while hot but not boiling.
You may have noticed this seems an awful lot like canning, and that's
  because it is. Again you want to be as clean as possible in this step
  and of course try not to burn yourself on anything.
vi) Let your media plates set and chill over night in the
  refrigerator.
You really probably only have to wait a few hours if you are anxious
  to get going. You are going to want to store the plates that you are
  not using in the refrigerator anyway. Also if you made a bunch of
  plates, let the cool on a counter before you put them in the fridge so
  that you don't raise the temp of your fridge too much.
Remember the thing about additives? You can play around with adding
  different amounts and different types of salts, vitamins, food, or
  other items to see how they affect the cultures you get to grow. All
  kinds of fun there. First go round, leave them all out.

Now you have your own home made culture plates! The above recipe was empirically tested by my childhood, and repeated by my son's. Not all pectin from the store may be equal, this is with Ball Classic (I have no relation to the company). I'd love to know people's results in trying it, because I might need to re-think how/what I'm doing to get it to work.
Go around your house swabbing things with sterile swabs (you can get these at a drug store), and then streak them out on plate. While it will be a little different with a swab and homemade plate, the idea is similar to what is done here.
Leave your plate in a warm wet place, but not in direct sunlight. Ideal temp is going to be around 37, but you can leave them above and below that and still get things to grow. On top of our dryer is where I leave them.
After a day or so you should have colonies you can streak out on a slide and look under a scope. You will find all kinds of things this way. If you want a more formal way to put things on a slide, you can check out dry and wet mounting from a Google search.
You are actually quite likely to run into E.coli if you sample enough "areas" this way. Obviously don't eat or huff the stuff that ends up growing. Maybe you can post some fun pictures of this if you try it.
As pointed out in the comments, if you successfully get bacteria to grow, then you will need to successfully get rid of them.  I should point that a good set of rubber gloves (that you can bleach and wash after use), or disposable gloves are a really good idea when handling plates that have grown bacteria.

Clean Up

First off, I want to clearly say that this stuff can clog a pipe.
If you tried to grow something on a plate, and you didn't get a colony that you can see with the naked eye (note some microbes might make CLEAR growths) you can probably just scoop the gel into the trash.
Note that I said probably.  If you swapped any part of your body, waste, or that of an animal you must decontaminate even if you didn't see anything grow.  On the plus side decontamination is easy.
If you did see something grow, or you otherwise need decontamination:
First make a 20% bleach solution in a large Tupperware like container (probably don't want to do this is a nice metal pot, but could do it in a junk one).  You can go as low as 10% bleach solution if you sure your bleach is NOT a cheap already watered down brand (like something bought at dollar store).  But just to be sure, I recommend 200mL of bleach in 800mL of plain tap water.
Drop your plates and lids into the bath (with the lid off) and let it sit for 10-15 min.  Then, working under/in the bleach solution with your gloves on, use a fork/spoon to get out the medium (it will be like thick jello).  Do this for all your plates, and you can do more than one at a time this way.
Once you have all the medium out and floating in the bleach, take the plates out and put them in the dishwasher.  Strain out the bleach/medium/funkiness you grew through a cheap colander (I recommend dishwasher safe plastic like PP).  Put what get's caught in the colander in the trash and take the trash out.  Wash the plates, lids, colander, and large container you used for the beach bath.
Slides
Slides present extra caution because they can break or shatter to create sharp edges.  For the most part, if you cover your sample with a cover slip, and seal it with nail polish, you can actually keep your slides indefinitely with little risk.  If you do decide to dispose of them, they should first go into a thick Ziploc bag (use an expensive freezer guard type bag for this) or into a Tupperware you don't mind throwing away.  If you never sealed your sample to your slide, you should also decontaminate the slide in bleach first (as above, with extra caution to not cut yourself).
If you are sophisticated enough to get microscopic photos of the microbes you see, by all means post them up and we'll try to ID them as best we can (many look very similar, and we use genetic or protein markers to get a true ID).

O wow, the formatting did not copy paste well.  If no one does it earlier, I will probably be able to work on the formatting tomorrow night.  I just don't have time right now.  If someone does it for me, thanks in advance.

Just wondering @Atl LED, pectin is of course a solid, so what is the concentration of the pectin solution that your recipe is based on. I've seen a 10% solution - does that sound ok? Or do you mean 45 ml of powder?

@AlanBoyd Crazy enough, I mean 45mL of powder.  If you look at most home cooking recipes they are given v/v, as is the recipe. For example, add 2 tbsp of sugar is a volume measurement.  I think most people won't have good scales at home.  Surely I won't be accosted for going metric here :).

I think this answer needs some information about safe disposal. I don't think you should be growing bacteria without knowing how to get rid of them safely.

@JackAidley Good point.  Decon & disposal added. +1 for the foresight.  Also thanks to the editors, you really saved me some time.

Have you considered growing the bacteria at 25°C to reduce the likelihood of pathogenic bacteria growing?

@MarchHo, Holding a temp accurately close to room temp is much harder than an elevated or refrigerated condition.  Our lab dropped some serious cash for an incubator that can really accurately maintain even 30oC.  At people's home, I just don't think you're going to get that kind of accuracy.  You'll note I said I put them on top of my dryer which tends to be 27-39oC (family is almost constantly doing laundry).

@AtlLED What I mean is that wouldn't it be safer to not place the bacteria in a heated environment, and just leave them in a cool, dry, shady area?

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Doesn't osmosis violate the law of conservation of energy?
Osmosis seems very counter-intuitive to me. I will try to explain my doubt with the following thought experiment:
Consider a huge container divided into two by a semi-permeable membrane. We add equal levels of water on both sides. On one side, dissolve some sugar. After some time, there will be a net movement of water to the sugar containing side of the container. This will increase the level of water on one side and decrease it on the other. If we create a huge hole in the membrane (large enough for both water and sugar molecules), then water will rush from one side to the other, equalizing the levels. If we were to somehow place a turbine at this hole, we could generate quite a bit of energy. Where did this energy come from?

Liked the way you presented it

I'm no thermodynamics expert, but Ill have a go at this.
The energy comes from the original set up, in which you have created a low entropy state. As the diffusion of water molecules equalises their concentration across the membrane so the entropy of the system will increase. This translates to a negative free energy change. That manifests as potential energy stored in the hydrostatic pressure resulting from the changes in volume, which in turn is available to turn the turbine.
So in the case of an experiment of the type described, the energy is derived from the experimenter who sets up the experimental situation in the first place.

Small Addition: free energy changes and the reaction spontaneity is governed by ambient conditions. The semi permeable membrane poses an energy barrier. Given this barrier, osmotic motion, brings down the free energy by entropy maximization (as Alan Boyd said).

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How can I accurately predict proper transgenic protein function/structure from different species?
I am currently building a synthetic system in E.coli, and am often faced with the need to use genes from other distant prokaryotes. I know that myself and most of my colleagues resort to an educated trial and error approach. Besides the obvious (elimination of introns from eukaryotes, codon optimization, genetic relatedness), is there any predictable or semi-rational way of knowing if a transgene for a different organism will function properly in any given organism?

There seems to be something missing at the end of the second sentence.

other things such as the nature of the protein should also be considered (Glycosylation and other PTMs which make the protein functional). Also it is important to make the GC content of the transgene comparable to that of the host. I have heard that certain organisms such as plants silence transgenes with drastically different nucleotide composition (it is something like an innate immune response).

By looking at the sequence only?  This is an unsolved problem.
Its not clear to me exactly what you are looking for, but here are some thoughts...
On a relatively narrow question as to whether any gene you plug into a bacterium, yeast, mouse, goat or other transgenic organism - the rna may not translate into protein in detectable levels or at high enough levels to get the desired result.  changing the sequence of the DNA of the gene for better transcription/translation is a common necessary experimental.
On the broader systems biology level, other cofactors, substrates that are necessary for the function of the gene may have to be engineered in the host organism. That is also an open question.
All this is assuming the gene in question codes for an enzyme to make a new or different amount of the metabolic product from the host organism, a commmon synthetic biology target.  If you are adding signaling pathway components, tinkering with a more specific mechanism in the cell, getting the function you desire could be a lot of work.  E.g. if you were inserting a new ribosomal component or a gene related to mitosis, that would be hard to imagine a priori how it would function in the new cell or if it would just kill it.
Also, Olga Troyanskaya at Princeton CS is working on the related problem of finding the function of a gene by looking at its sequence and cross referencing to other known data. Electronic functional inference is difficult, esp when we have no complete gene functional description of any living organism to start with.


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What is the effect of flash pasteurisation on Maillard reactions or production of AGEs in milk?
Does flash UHTP homogenision and pasteurisation change significantly the extent of maillard reaction in milk compared with traditional batch pasteurisation? If this is significant does this effect the nutritional value of the milk?
Initial research; i have found via my wikisearch  http://www.food-info.net/uk/colour/maillard.htm and on pub med an abstract: J Nutr Sci Vitaminol (Tokyo). 1990;36 Suppl 1:S57-69.Influence of processing on protein quality.
Mauron J.
Source University of Fribourg, Switzerland.  i dont have full access to pubmed papers.
background to question.I have developed a sensitivity or intolerance to UHT and typical homogenised and pasteurised milk in the supermarket and any products with milk solids. I can consume non homogenised batch pasteurised milk from the specialty organic store, thus the curious chemist in me was alert. Either my body doesn't produce sufficient of the necessary enzymes ,ruled out by the latter scenario,  or the composition of the milk has changed in modern high throughput pasteurisation.
In Flash pasturisation we have P.T and V all being varied to increase proximity and likelyhood of collisions of reactants as well as temporary emulsification.
There is another term AGE see http://agefoundation.com

I think this is better off on [biology.se]

This is only an partial answer, as I do not have the time now to look for other references.
In the chapter about milk, Harold McGee's beautiful book "On Food & Cooking" says (pg. 21 of the 2004 edition, bold is mine):

Flavors from cooking
  Low-temperature pasteurization slightly modifies milk flavor by driving off some of the more delicate aromas, but stabilizes it by inactivating enzymes and bacteria, and adds slightly sulfury and green-leaf notes (dimethyl sulfide, hexanal). High-temperature pasteurization or brief cooking - heating milk above 170°F/76°C - generates traces of many flavorful substances, including those characteristic of vanilla, almonds and cultured butter, as well as hydrogen sulfide. Prolonged boiling encourages browning or Maillard reactions between lactose and milk proteins, and generates molecules that combine to give the flavor of butterscotch.

He continues by speaking about the different types of pasteurization, and says (pg.22-23)

The third method of pasteurizing milk is the ultra-high temperature (UHT) method which involves heating milk at 265-300°F/130-150°C either instantaneously or for 1 to 3 seconds, and produces milk that, if packaged under strictly sterile conditions can be stored for months without refrigeration. The longer UHT treatment imparts a cooked flavor and slightly brown color to milk; cream contains less lactose and protein, so its color and flavor are less affected.
  Sterilized milk has been heated at 230-250°F/110-121°C for 8 to 30 minutes; it is even darker and stronger in flavor, and keeps indefinitely at room temperature.

So, it appears as if indeed there may be some Maillard reaction going on in UHT, although it is probably minor (otherwise the milk would be much darker in color, as it is the case for sterilized milk).
The book also speaks about homogenization, but it does not mention anything specific about Maillard reaction there (homogenization is not carried on at high temperatures, so it does makes sense not to have it).
To answer your question:

Does this effect the nutritional value of the milk?

Well, according to this presentation (but, be warned, it does not cite any reference!) it seems that it does, although I don't think the Maillard reaction is specially involved.
http://www.slideshare.net/Aslal_saja/effect-of-uht-treatment
Specifically it says that the irreversible changes that occur are:

Whey protein denaturation (35 to 100% of denaturation of $\beta$-lactoglobulin)
Slight increase in the size of casein micelles
Whey protein-casein micelle interaction
Maillard reactions
Fat globule composition changes (although no changes in nutritional value of milk fat)
Vitamin content changes (20-30% loss in vitamin B1 and B12. Markedly reduced content in vitamin C and folic acid if high level of oxygen were present during the treatment, no changes in vitamins A, D, E and beta-carotene).

It also says that:

Biological value and net protein utilization of UHT milk were lower for stored milk than directly used milk. Lysine loss during UHT is high but not significant to affect milk nutritional values.

I don't know whether the fact that you have problems when drinking UHT milk has anything to do with Maillard reaction or any of the other modifications brought by UHT treatment, and I will not venture in there, as I am not an MD and prefer not to give any sort of medical advice.

Thanks I have my digestion problems are sort by minimizing processed dairy intake and pressed flavours like HVP.

Try:
Food: The Chemistry of its Components (RSC Paperbacks) [Paperback]
Tom P. Coultate (Author)  and What Einstien told his Cook by R.L.Wolke


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Isoprenoid Diphosphate Concentration in Yeast saccharomyces cerevisiae
Isoprenoid  Diphosphate(IPP) is an important metabolites which is precursor in lot of secondary metabolites like Dolichol diphosphate, ubiquinone, prenylated proteins and carotenoid (not synthesized in s cerevisiae).
What is the average concentration of IPP present in yeast per gm ?

Although this information doesn't provide a direct answer to your question, I hope that it sets the scene for what is achievable in metabolic engineering from IPP. It should also provide a jumping off point for further literature research.
This is a fairly recent review of metabolic engineering of relevant pathways in various microbial systems, including Saccaharmoyes:

Ajikumar  PK et al. (2008)  Terpenoids: Opportunities for Biosynthesis of Natural Product Drugs Using Engineered Microorganisms. Molecular Pharmaceutics 5:167–190

The review refers to:

Ro, D. et al. (2006) Production of the antimalarial drug precursor artemisinic acid in engineered yeast. Nature 440, 940–943.

In this work, the introduction of a pathway-specific gene led to the production of 4.4 mg L-1 of product. This was increased to 153 mg L-1 by several manipulations including:
Increasing flux through the pathway by expressing a modified HMG CoA reductase
Decreasing flux into sterol synthesis by downregulation of the ERG9 gene combined with expression of a dominant negative allele of the transcription factor Upc2.
UPDATE
After posting my answer I found this paper:

Huang, B. et al. (2011) Metabolite target analysis of isoprenoid pathway in Saccharomyces cerevisiae in response to genetic modification by GC-SIM-MS coupled with chemometrics. Metabolomics 7:134–146

The paper includes a detailed discussion of methodologies, which I won't go into here.
Although there are no measurements of IPP, in Table 7 they present this result: geranyl pyrophosphate 32 ng ml-1 in a 48 h culture, A600 ~ 2.3. ERG9 disruption increased this to 56 ng ml-1
As far as I can tell these values are presented as ng ml-1 original culture. Using 1 U of OD600 corresponds to 0.41 g of dry cells liter−1 taken from here I calculate a value for GPP of 34 µg g-1 dry weight in the wild-type strain.


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Is recognizing one's own mirror reflection a valid test of animal intelligence/self awareness?
I've been looking at this Ted talk on interspecies internet, and it appears that they have selected a small number of species of animals (dolphin, elephant, and some ape(?)) and are intent on developing interfaces for these animals to be able to connect with other animals over the internet.
From the talk, it appeared as if one of the criteria for animal selection was whether or not an animal recognizes itself in the mirror. This got me thinking - there are many more cats that have access to technology like the internet or TV or cats that have been interacting with touch screen displays. Yet apparently cats cant recognize their own reflection as themselves.
What is so special about being able to recognize one's own reflection? Is it a true measure of self awareness? Does it only appear in animals with larger brains?

I think it is a necessary test of self-awareness. In order to make the connection that "I am the being in the mirror" and that every action I do will be reflected in the mirror (or, vice versa, every action I see the being in the mirror take is a reflection of my own action), one must first have a concept of self. One requires a constant present-tense (at least) story of oneself: "I am doing this. Now I am doing that. Oh look, I am doing this and that guy is doing the exact same thing." And then there's the ultimate realization, "Ah ha! That's me!". That realization would make no sense if the individual has no sense of "me"!
[speculation] On the other hand, perhaps it is too strict. It seems that it would unfairly favor social species, since it requires not only recognizing another member of the species (and being able to associate the anatomy of another member of the species with one's own anatomy), but it may also require the recognition of intent. That latter requirement is complicated by differentiating between intent and compulsion: at some point, one must realize that the being in the mirror isn't trying to copy but rather it always, inevitibly reflects one's motions. So, perhaps a cat is self-aware, in a sense that it has a constant story in its head of what it is doing and what it intends to do, but it cannot easily ascribe intent to other members of the species and thus cannot figure out that the cat in the mirror is automatically mirroring all of its movements. [/speculation]
Herein lies the rub: there is no perfect test for self-awareness; we can cast doubt on any outcome. The best would be if these animals could communicate with us by language. In lieu of that, we have to think of such tests that demonstrate with reasonable confidence that the species carries all of the characteristics that we attribute to self-awareness. I think another good test would be determining whether the species can plan individual actions in the future; in order to say, "first I will do this, then that; finally, that will allow me to do that", it seems like it would reasonably require an understanding of self and the consequences of one's actions. An example would be birds solving sequential puzzles.

The mirror test is definitely useful, but clearly biased toward animals with social intelligence (a notion of self is only useful if there's a notion of other) and also toward highly visual animals.  A mole-rat, no matter how intelligent, is unlikely to use a mirror for much of anything.  Using the same test for animals with very different sensory modalities is bound to fail. For example, see the comments of the following YouTube video.  The user Sluchesi notes:

sticking a piece of post-it paper on my tom cat's head where he couldn't see it without a mirror and while petting him, waited until I was sure he didn't notice it (he didn't respond to it), showed him the mirror and he instantly started trying to get the paper off his head (not the image in the mirror, his own), shaking it and using his paws.

A second user (M. Ransom) did the same test and verified it.  Not quite to the level of scientific proof that you would want to see, but certainly worth a follow-up study by someone who focuses on the topic.  If true, it would indicate that cats probably do have a conception that the reflection in the mirror is them, but place little value on introspection or visual self-concepts.  This might indicate that what cats (and many other animals) lack is not the ability to have a model of self, but to have a model of some other being modeling yourself (i.e., 2nd-order model of self).  This is actually a quite complicated level of modeling: even humans are quite bad at guessing what other people think about them.  However, basically all humans try to do it, even if their guess is often mirror-bias (i.e., other people think about them like they think about themselves).  Given that this is nearly at the limit of average human cognition (3rd order models of other/self are rare and usually limited to strategic games like poker), it seems reasonable that most animals lack this ability.
Having a model of another's conception of oneself is necessary for a being to care what they look like, for instance.  After all, if you can't comprehend that the world attaches importance to how you look, you would be unlikely to develop mechanisms to attach importance to it either.  In that second case, the mirror test may be accurate (i.e., it measures higher order thought), but it is in fact measuring something very different (and more advanced) than what it has been assumed to measure.

The sticky note on head is a good experiment, I will try it!

An interesting anecdote from the book "Merle's Door".  The dog didn't at first appear to recognize itself in small mirrors, but when the human took the dog to an exercise studio with large wall mirrors, the dog saw himself and his human together, and from then on appeared to understand mirrors.  He just needed that extra bit of social context...

To the answer above:  "I am the being in the mirror", one has to ask themselves:  Is it so strange that a cat seeing it's own paw in front of it and recognizing it as it's his OWN, and not chasing it's own tail because it knows it's his and he's not a kitten anymore?
So how much different is that when they come to understand, especially after you hold the cat several times in front of the mirror with you, making the association and he's no longer weirded out?  Many cats making this transition look in curiosity and awe and move on, never really caring that much about it -- much like kids.
Bring a cat into a bathroom with a mirrored wall behind the sinks, when he's dealing with something where the mirror is in his line of sight.  Walk in behind.  When the cat turns around to look at you to play instantly, instead of trying to play with the mirror -- it recognizes that it shows whats behind him.  I have observed this.
If a cat recognizing it's own tail out of it's "perif" is nothing special, neither is recognizing that it's him in the mirror.  He may not be cognitively advanced to think deeper than "Yep, that's me, I have THIS look.  Oh, am I getting fat?" -- they care less about that.
A good test would be to have a cat with whom you can put something on his head and he doesn't care -- unless it's something he HATES by its LOOK.  Once you've established that over and over 100%, and have been able to put it on him without him caring without him SEEING it -- put him in front of the mirror and see if he tries to take it off.
A red dot isn't going to do squat.  They don't give a shoot about things like that.  If you want to know whether they know IT'S THEM, put them in position where there's something they DON'T WANT on them -- and they try to get it off... where it's something they don't mind on them, they don't try to get it off after seeing themselves in the mirror.
Not fool-proof, though.  They may not mind it on them because it's purely how it looks.  They can just walk away from the mirror and they don't have to worry about it.
But back to the original point:  I don't think it's a big deal that they can recognize that it's themselves.  To UTILIZE that for deeper thinking in making connections is another matter.


text:
Is there an instinct-driven body language for birds?
Over the last year or so, I've been observing house sparrows, because they are so prevalent in the northeast US cities. I noticed that a lot of sparrows, even in different cities seem to have very similar body language for communicating. I learned 3 expressions
Here's an example of a sparrow feeding their young. The young bird opens month and flickers its wings in what I can only describe as impatiently.
A sparrow swipes its beak along a surface at its feet - something food related?
A sparrow fluffs its feathers, turning into something like a tennis ball made of feathers.
I'm looking at this video of a sparrow raised in captivity, and it does 2 out of 3 expressions described here.
What interests me is if expressions like these are "local dialects" or universal, thus found across different geographies and times? for example, do sparrows in northeast US use the same expressions as sparrows in Australia? What about sparrows in the United Kingdom in the 1950s?

Cf this question: http://biology.stackexchange.com/questions/2463/is-there-such-thing-as-animal-non-verbal-body-language/2464#2464

In general, animal communication contains both "cultural" aspects and genetic components.
As you suggest, the cultural aspects vary more across geographies and times. The genetic components might vary as well, with genetic differences among different populations, but you'd expect them to be more conservative than the cultural aspects. To make the matter even more complex, if the communication behaviors affect mating; they could in turn have an effect on the genetic components!
This article describes birds raised in captivity that had "maladjusted" songs (which would support both genetic and cultural components), and North Carolina cowbirds raised by Texas parents who grew up with a Texas birdsong dialect (evidence for cultural components). Although the piece is mostly focused on song, I imagine the mechanisms would be similar for body language.

Full disclosure – the author of that linked article is my father.


text:
Can two hammerhead ribozymes simultaneously cleave each other?
I am working on a project in which an XOR gate is being built by having two hammerhead ribozymes simultaneously cleave each other when both are expressed, but have these ribozymes cleave a target transcript when expressed alone. Has it ever been shown in the literature that a hammerhead ribozyme was able to cleave the flanking arms of another ribozyme?

In principle it can. Ribozymes can be designed to target small RNAs too. But unless the ribozymes have highest affinity for each other, they will continue to cleave the target, when both are expressed together. It will cause leakiness of the gate.

@WYSIWYG, I plan on having longer flanking arms and 100% complementarity between the ribozymes, and less so for their target.

[ For the sake of answering a question that is long unanswered ]

Can two hammerhead ribozymes simultaneously cleave each other?

Yes, in principle they can.

two hammerhead ribozymes simultaneously cleave each other when both
  are expressed, but have these ribozymes cleave a target transcript
  when expressed alone.

This may be realized only when ribosomes have higher affinity for each other than for the target. As you said in the comment, inserting few mismatches in the ribozyme-target interaction may work. You may need to notice that since the two ribozymes are complementary to each other but cleave the same target, the target sequences will form a set of two mutually complementary regions. If separated well enough, there may not be much of a problem. From your design strategy I guess that UTRs are the best place to keep the ribozyme target sequence. If you keep both the target sequences in the 3'UTR (lets say), then they may form a hairpin structure, which may interfere in the targeting. So you can insert mismatches that also destabilize the possible hairpin.

Has it ever been shown in the literature that a hammerhead ribozyme
  was able to cleave the flanking arms of another ribozyme?

Not yet. Self cleaving examples are there but not mutually cleaving ones.


text:
Plant anatomy, what are these stem like filaments growing under the flower
The picture below shows what I am talking about. Each flower has one and I am just wondering what they are?

See https://en.m.wikipedia.org/wiki/Spur_(botany)

Looking at this, it looks like a spur. A quite overbreed one, though.

These are "floral spurs" – they usually contain nectar, and are part of the variety of complex flower shapes that orchids and other flowers, like columbines, have co-evolved with their pollinators.
Essentially, in order for the pollinator to reach the nectar down in the base of the spur, it must move into a position where pollen is deposited onto it; then when it moves to another flower, it can transfer that pollen and the plant is able to reproduce.
Of course, long tongues are good at getting nectar from long-spurred flowers, so there is both species filtering for long-tongued species, and presumably also selective pressure within a species for long-tongued individuals. This, in turn, drives selective pressure on the spurs.
Spurs are a classic example of a "key innovation": they have evolved separately in different types of flowers, and when they evolve, they often lead to rapid speciation (because a small change in spur architecture can constitute a barrier to reproduction). (See, for example, publications of Scott Hodges)


text:
Any tool to align whole genome sequence data to another genome and give exon regions a higher mark?
I want to align WGS data from several mammals to one reference such as the human genome sequence. Since in most cases exons should be conserved and spliced in the same way and introns should vary, I want to use a tool that is aware of the annotation of exon and intron.
That is to say that matches in an exon region should have be given a higher weighting than matches in intronic regions.
Also, when a read pair maps to 2 exons, the insert size should be more flexible as the intron length can be vary among different mammals. Since the library insert is less than 2kb for short libraries, the more common situation should be one read on exon and another on intron.
This is different from RNA-seq as I am using WGS data of a whole genome, so both exons and introns are in the reads. And I want to align them to a human reference sequence.

SeqSphere and DNAstar Lasergene software are good

If you are not trying to assemble but just to align each read to the genome, you can use exonerate. On a Unix/Linux platform, once you have installed it run something like:
exonerate -m genome2genome WGS.fasta genome.fasta > out.txt

From the exonerate manual:
          genome2genome
                 This  model  is  similar  to  the  cod‐
                 ing2coding  model,  except  introns are
                 modelled on both sequences.  (not work‐
                 ing well yet)

What I would recommend though, is to align against a reference cDNA dataset, not the whole genome. In that case, you should use this instead:
exonerate -m cdna2genome genome_cdna.fasta WGS.fasta > out.txt

From the exonerate manual:
          cdna2genome
                 This   combines   properties   of   the
                 est2genome and coding2genome models, to
                 allow modeling of an whole cDNA where a
                 central coding region can be flanked by
                 non-coding UTRs.  When  the  CDS  start
                 and  end  is  known it may be specified
                 using  the  --annotation  option   (see
                 below)  to permit only the correct cod‐
                 ing region to appear in the alignemnt.


text:
What gases are needed for humans to breathe?
I will be beginning a science project about sustaining life on space stations. I already know that pure oxygen is harmful for humans but would $O_2$ + $CO_2$ be enough for humans to breathe in or do humans need other gases as well?

For a start, in addition to the International Space Station (ISS), also look at gas mixtures used in scuba diving and breathing gases.

This is a good question, as understanding the minimum requirements of human respiration has many applications beyond that of a space station, extending to future biospheres both on Earth (eg under the ocean) and beyond.

Yes that what my science project is about, it's about sustaining life on Mars so I just needed to know what gasses are required for human respiration respiration

Why not look at the existing space station as an example.  The International Space Station (ISS), a starting article is "Breathing easy on the space station" (NASA), while this article does not discuss the amounts of various chemicals, it looks at the process about how the chemical balance is maintained - an important point related to your question is that carbon dioxide is filtered away.
The second article "Breathing on the Space Station" (e-missions), discusses the actual percentages of each component.  It states that the chemical composition of the space station air is ideally similar to Earth's atmosphere.  With 78% nitrogen, 21% oxygen and 1% water vapour on the space station (Argon is in the Earth's atmosphere, but appears to be unnecessary on the space station).
I hope this helps.


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Is the ratio Brain Mass/Total Mass still considered a valid indicator of intelligence?
I was reading this(1) and it led me back to ask a very basic question (I'm not a neuroscientist).  All the way back to undergrad anthropology and neuroscience courses I remember being taught the general rule of relative intelligence was that one looked at the ratio of the brain mass over the total mass of the animal (or the estimations therein from let's say fossils).
I know a lot of the interesting neuroscience research going on these days does looks into bird brains, particularly within Corvidae.  It would seem that birds are often much more efficient in the abilities they seem to show with considerably less brain mass.  I do realize that birds often weigh very little as well, so perhaps the ratio is preserved?
I also realize that within birds, they see better ratios in more intelligent birds.  But what about the comparison from mammals to birds?
Dinosaurs are often predicted to not be intelligent because of the enormous body size and small cavities for a brain.  Now I realize that some dinosaurs were actually quite tiny, but this is just an example.
Given birds' close genetic link to dinosaurs, could it simply be that they were just doing more with less?  The mammalian brain is a huge caloric burden, so perhaps this would show an efficiency that could be selected for?
Thus as the title suggests, my main question:
Is the ratio of brain mass to body mass still considered to be a valid indication of intelligence of a species in modern (current) neuroscience?  Certainly there are exceptions, but is it still considered the rule of thumb?
EDIT: I also wanted to point out the first article(2) I started to read after formulating the question.  It made me question the usefulness of encephalization in addressing this issue at all, but I don't/didn't feel adequately trained to evaluate the conclusions of the meta study.
Again, this still leaves us comparing within primates, which still leaves me feeling that Corvidae have some really impressive efficiency going on with their overall brain mass.  Which then leads to hope that some dinosaurs could be at least equally intelligent, if not more so (noted that this is complete conjecture).

(1) Front Hum Neurosci. 2013 Jun 6;7:245. doi:10.3389/fnhum.2013.00245. Print 2013.
(2) Brain Behav Evol. 2007;70(2):115-24. Epub 2007 May 18.

I don't know about brain mass to body size, but ratio of neocortex to brain volume is correlated with primate evolution (Figure 3, here). If you subscribe to the view that humans and more closely related primates are more intelligent than more distantly related primates, then that is an important correlate.
I think the issue with this question is that we're still having trouble defining intelligence.

Exactly; the whole brain mass / total mass thing might be a rather anthropocentric test. This will always be the problem in dealing with tests of intelligence, self-awareness, and the like.

+1 I certainly agree that we have problems with defining intelligence, and that even getting theory of mind levels poses problems.  I also enjoyed the reference.  Is the issue then, that across higher taxa (say class) we can't rigorously compare intelligence.

@AtlLED: I would say, yes.  Even if you want to talk about temperament, there's a lot to debate. Here's a review: http://homepage.psy.utexas.edu/homepage/faculty/Gosling/reprints/CDPS99Xspeciesreview.pdf

Short answer
It is mainly synaptic connectivity that determines intelligence, rather than brain size per se.
Background

For a starters, Albert Einstein, considered to have been a reasonable intelligent person, had an average sized brain (Sukel, 2009).
Secondly, there are not only neurons in a brain that determine its size. The brain contains a relative large proportion of glial cells, which perform mainly a supportive function and are not part of the main neural network in the brain. A brain with a larger proportion of glial cells can thus be bigger than another equally sized brain with a higher proportion of neurons (Sukel, 2009).
Thirdly, even the number of neurons per se is not a valid indicator of intelligence. Of course, in the very extreme, an organism with a few hundred neurons like C. elegans (Jabr, 2012) has hard-wired cognitive limitations due to the low number of processing units available to it, as opposed to, e.g., the human brain with some 100 billion neurons. However, scientific studies across several animal species, including humans, have shown that brain size alone is not a valid measure of intelligence. For example, birds with tiny brains have shown to be capable of some remarkable clever stuff, including the use of tools to obtain food. Rather, scientists now argue, it is the number of connections in the brain that matter, i.e., the organization and molecular activity at the level of the synapses is the main determinant of intelligence (Sukel, 2009).
Lastly, as mentioned by others, intelligence is notoriously hard to measure. Species evolved in different environments. Learning to use a tool to dig up ants by chimpanzees is quite a clever thing, but makes absolutely no sense for a humpback whale diving 3 kilometers below sea level in search of giant squid. Intelligence is a relative thing.

References
- Jabr, Sci Am (October, 2012)
- Sukel, Sci Am (October, 2009)

I always heard Einstein's brain was bigger than normal

Considering that as humans had larger brains in prehistoric times, then no, brain size doesn't mean more intelligent.
I aren't well versed into this subject, so I don't particularly know if they could learn better than us, but there are speculations of why their brains were larger than ours.
The most primitive humans, had to deal with a lot of predators, and unnatural things in their environment. Mist of them contained a vast amount of knowledge of what is "bad" or "good", and that was a requirement if they wanted to survive in that period.
As we settled down, and our natural predators became our food, such needs became less and less important.
Maybe they were actually smarter than us.

Welcome to Bio. This is a scientific stack where sources and preferably references to credible papers are considered mandatory. Apart from that your answer seems incomplete as it is commonly accepted that at least part of intelligence is determined by the number of connections present in the brain.


text:
Do animals exist with an uneven total number of digits?
I recently finished reading Contact by Carl Sagan. In the book they talk about a pattern in the transcendental number like pi or e, and comment that it is found in base 10 or however many fingers the race has to count with.
When in the end they find a pattern in pi it is in base 11, which I found a strange choice since I can't think of an animal that has an uneven total number of fingers, and I would think that most evolution would result in a somewhat symmetrical design.
Do any animal exist that has an uneven total number of fingers or equal lim, excluding polydactyly and oligodactyly?

I had a quick look around and I cant see any actual proof that pi has a pattern in base 11 apart from that book ?

The pattern is a fictional part of the book, but the author based a lot of the information in the book on existing scientific knowledge. There for i found it strange that he chose base 11, and I wanted to know if there where some beings on earth that if they where the dominant spice could have evolved to count on an uneven number of lims, but as Brandon pointed out some count in other ways.

cf. http://math.stackexchange.com/questions/460729/what-would-have-been-our-number-system-if-humans-had-more-than-10-fingers-try-t

Your conclusion relies on the supposition that all beings must count using their finger tips (or the most paralogous, "finger-like" limb). In fact, even within humans this is not necessarily true: the Yuki native people of California count in base 8 by counting the spaces between their fingers; meanwhile the Oksapmin people of Papua New Guinea count in base 27 (an odd number!) via counting a range of different body parts. One can easily imagine counting in base 20 by counting on fingers and toes. Heck, the Sumerians used base 60. And here's a scheme for counting in base 16 on your fingers.
So, it's entirely plausible to count in base 11, even when assuming morphological symmetry. The beings just need to settle on precisely which 11 parts of their anatomy to count.
As for your actual question, I am unaware of any species with an uneven total number of fingers and I would be surprised if we found one, based on an argument of developmental symmetry and overall (coarse-grained) evolutionarily conserved development plans within major clades of extant animals.

Really great answer. Thank you for answer what I needed to know and not just what I asked, that is how I personally prefer answer but I see a lot of people who ignore what people need and just answer what they ask for.

Arguably, the Kobon in PNG have a base 11 (body parts on one side), although it's not exactly a base, because they then count a midpoint before continuing to the other side of the body; thus, while "little finger"=1, "little finger other side"=23, not 22. (Harrison When Languages Die).

Harrison also mentions other languages with uneven bases: 3 (Bukiyip), 5 (many languages), and 15 (Huli).

Coscinasterias calamaria, the Eleven-Armed Sea Star! (Although I doubt it has much to do with pi)

Image from Wikimedia Commons

although both C.calamaria and "pi" sound similarly delcious

True, I hadn't thought about the possibility of radial body designs!

Thanks for the answer, hadn't considered that, now can you teach them to count ;)

This has 11 votes, so I refuse to add another. sorry.

this is a good answer since bilateral symmetry is what creates even numbers of digits.

On the other hand, can we count a starfish arm as a digit? I mean, in the case of some alien race with a penchant for counting, the appendage can be anything; that's why I voted for this answer too. But in reference to the original question, it's doubtful (even with the "equivalent limb" clause) that we can consider starfish arms to be equivalent to fingers.

Maybe tube feet are more equivalent to "digits"? Although if you define fingers as "things you open yummy mussels with", sea star arms pass the test.

@ghoppe:  others have brought the total above 11.

@Oreotrephes Fair points; please excuse my moment of pedantry.

The key point here is the radial body design, not whether the arm of a starfish counts as a digit. One could imagine some alien life form with a radial body design of 5 "arms" and 5 "digits" or fingers on each arm. Those would then be true digits and the total count would be 25 - still odd.

I just wanted to say that I believe you're seeing it from a quite anthropocentric standpoint. It doesn't make much sense to search for patterns like even or odd numbers of fingers or limbs.
If evolutionary tends to result in bilateral symmetry, there is no reason at all why the symmetry should be inconsistent - like 4 fingers on one hand and 5 on the other.
Consistent bilateral symmetry will always result in even numbers:

4 fingers x2 = 8
7 ribs x2 = 14
5 toes x2 = 10

The Eleven Armed Sea Star in @Oreotrephes' answer isn't much of an exception to the rule of symmetry, it's just radially symmetric.


text:
Will eukaryotic RNA fold in the same way in prokaryotes?
As far as I know, there are no specific eukaryotic or prokaryotic factors that aid in RNA folding other than cellular environment (salt and ion concentrations, dissolved molecules, etc). Are there any factors to consider when introducing eukaryotic RNA in prokaryotes? Is it possible to predict the proper shape and folding upon introduction to a prokaryotic cell?

Interesting question. Ionic concentrations and temperature will certainly affect RNA folding. There may well be other constraints as well.

RNA chaperones will be different as well. I'm not sure how much the relevant ion concentrations vary, but Mg concentration is certainly a very important factor in RNA folding. And are you asking about secondary or tertiary structure by the way?

@MadScientist, in my specific case I was more interested in secondary structure, but an answer addressing tertiary would be ideal

Fast googling: http://www.nature.com/nature/journal/v505/n7485/full/nature12894.html#ref3 this might help

As you have mentioned ions and temperature affect RNA structure. There are also different types of RNA structures and their dependence on ions are different. Mg2+, as Mad Scientist mentioned, stabilizes duplexes; so do monovalent cations like K+ and Na+. However, Mg2+ favors duplex over quadruplex if the same RNA can adopt both these conformations.
Dependence on temperature is a trivial case.
Ions and temperature should be more or less same for prokaryotes and eukaryotes unless we are talking about extremophiles.
Apart from these factors I can think of two other factors that can cause difference in RNA structure between prokaryotes and eukaryotes:

Osmolytes
RNA binding proteins/chaperones (Already mentioned in comments by Mad Scientist)

Osmolytes
It has been shown that TMAO (Trimethylamine N-oxide) stabilizes RNA secondary structures. The metabolism of TMAO is different in prokaryotes and eukaryotes.
From this paper:

Although eukaryototes can endogenously produce L-carnitine, only
  prokaryotic organisms can catabolize L-carnitine11. A role for
  intestinal microbiota in TMAO production from dietary carnitine was
  first suggested by studies in rats; moreover, while TMAO production
  from alternative dietary trimethylamines has been suggested in humans,
  a role for microbiota in production of TMAO from dietary L-carnitine
  in humans had not yet been demonstrated30-32. The present studies
  reveal an obligatory role of gut microbiota in the production of TMAO
  from ingested L-carnitine in humans (Fig. 6c)

I cannot ascertain that this will affect RNA folding but is possible.
RBP
This is something that you can be certain about. Some RNAs require protein counterparts to adopt a functionally capable structure. In the absence of the protein they may not form the relevant structure. So if an RNA needs Hfq then you have to express it in the eukaryotic system where you want to use the RNA (and converse).


text:
Would it be possible/plausible for a type of spider to fly by weaving web between it's legs to create bat-like wings?
I've been thinking about this lately.  Would it be possible for a type of spider to gain the ability to fly freely by weaving its web between it's legs and creating wings much like those of a bat?
Is there anything like that in nature currently?
Is it plausible at all?

It might glide, but not fly, for the same reason that you can't even if we give you wings, the size is all wrong and you don't have the necessary muscles.

Over time, could the spider evolve the "muscles" and movement in order to sustain flight with these web-wings?

Perhaps but it would no longer be a spider. Your question asks whether a spider could fly without changing its morphology, just by spinning webs between its legs. If you allow it to change form then sure it could, just make it morph into an eagle.

I gotcha.  In the short term the most a spider could do with this is possibly glide.  In the long-term it could gain flight but would be very different than any spider you see today.

They might not fly, but some spiders can "balloon".

It takes more than wings to fly, just look at the poor penguins. The first problem is that simply weaving webs between a spider's legs would probably not generate enough lift to keep her airborne. Flying creatures have a specific body plan that allows them to fly, if you just add a couple of wings to a hippopotamus it won't be able to fly.
On top of that, the spider would not have the necessary muscles to enable it to flap these wings even if they were capable of producing sufficient lift.
While it is theoretically possible (I stress theoretically) for a spider species to adapt over time (long long time) into a flying form, then it would no longer be a spider. So, in answer to your question, no, it is not possible.

Great answer.  I guess with all the changes it would need to undergo, it would be too different from any current spiders.  But it's really interesting to think about!

Very unlikely as spiders don't have direct muscle/exoskeleton connections like insects, it would be a more complicated mechanism for powered flight...
imagine replacing a radial engine in an airplane with and engine that powers a hydraulic pump that then has a mechanism that converts that force to a force usable for flight.

Why have you posted two contradictory answers?

@terdon I had not one, but two theses; and they didn't agree very well, I wrote it as one answer, but it was self defeating.

probably permitted by the laws of physics and biology...
almost anything is possible, jumping spiders move extremely quickly for their scale, and you could easily imagine an evolutionary pathway... spiders already use parachutes: the parachute gets bigger, the line get shorter and controlled by the rear most legs...
maybe it has already happened, there likely wouldn't be any fossil record of it, and spiders have been around for a long time (compared to apes).


text:
What does phasing mean?
What does phasing mean in genetics/informatics? I've heard that a phased file is a file that has genes separated by chromosome, but can someone give a concrete definition of what phasing actually means?

This refers to haplotype phase (aka gametic phase). This essentially means knowing which allele belongs to which copy of the chromosome, or alternatively, which alleles appear together on the same chromosome.
In short-read sequencing, for example, it is difficult to resolve the haplotype of two heterozygous SNPs if they have not been covered by the same read. If you observe A/a and B/b, you do not know whether you have AB + ab or aB + Ab. So you would say you do not know the phasing.
See the Wikipedia links for more information.

Can you shed some light on why this process is called phasing? It reminds of phase as in waves which makes no sense.

phasing is the relationship between adjacent alleles on the same chromosome i.e. if they are in cis or trans configuration. In other words, weather two alleles are indeed on the same chromosome or on different chromosome. One of the reason alleles get shuffled is by process called recombination where chromosome exchange happens. Majority of current methods infer the phase using linkage disequilibrium principle however with advent of whole chromosome sequencing it's possible to determine empirically the phase from related samples. i.e. father, mother, son


text:
Why can't we observe haplotypes directly?
I am completely a noob to biology and DNAs, but recently I am looking into EM-algorithm used in the case of re-constructing haplotypes from genotype data.
I am just wondering what exactly in the process of DNA data collection prevents us from observing haplotypes directly.

I am not completely sure what you mean. In DNA extraction, not even chromosomes are (usually, it is sometimes possible) singled, much less alleles. You have a complete bunch of chromosomes that you shear, most of the time put through PCR, tag with adapters and sequence. Often you actually even sequence several different probes together, so you additionally add a barcode to sort them afterwards. There are sequencing errors and different alleles and you have to figure out which read belongs where ... but this would be an answer, not a comment. Is this what you want to know more about?

To fix the problems that @skymninge pointed out EM (Expectation maximization) algorithms are used which try to find the likelihood of a read arising from a location

The difficulty of reading haplotypes 'directly' lies in the difficulty of reading any long sequence of DNA, and this is for technical reasons.
Short DNA fragments are sequenced using a variety of methods. Gel electrophoresis can pull these fragments apart by length, but all the fragments have to be relatively close in size to get the accuracy needed to tell fragments that differ by one base pair apart. It's easy to separate a 16-bp segment from a 17bp segment easily, but it's much harder with a 516bp segment and a 517bp segment. Modern sequencing can sequence reads up to about 5kbp in length at a time. The 'reads' are then reassembled.
There are next-generation methods(pyrosequencing, etc) that can read a long dna molecule one base at a time, but for practical reasons sequencing an entire chromosome this way is cost and time prohibitive. As a result, there are always going to be fragments that you need to reassemble computationally, no matter how the sequencing is done.

Are you asking why it is difficult to tell whether a cell is homozygous or heterozygous? If so, this is usually a combination of sensitivity of the assay (rtPCR can be optimized for this purpose - at least, I've heard of people doing it). Another aspect of this is that even if the alleles code for different things (eye pigment or something), much of the gene may be similar enough that PCR primers are difficult to construct in a way that they distinguish between the two alleles.
Then again, sometimes you get lucky and there's an EcoRI site right in the middle of one allele, but not the other.


text:
Advantage of being deuterostome
We know that most of the so called "Advanced" organisms are deuterostomes (i.e., development of gut starts from anus). Is there any evolutionary advantage of that? If not, why and how did it evolve?

Just a word of caution: it's very easy to invent "just-so" stories when it comes to speculating about evolutionary advantages/disadvantages. Without rigorous experiments proving the relative advantages of one trait over another, or at least providing quantifiable evidence thereof, it's impossible to do anything more than speculate.

One other note: I would discourage the use of the word "advanced" here; that would imply that increasing complexity is somehow a goal of evolution that natural selection works towards. I would argue that it is a side effect. There are many extremely successful species that never evolved beyond a single cell. Thus, I would prefer to say "complex" here, which is pretty objective.

Your premise is quite doubtful. While you are considering vertebrates as the pinnacle of evolution, you should note that arthropodes, nematodes, annelids and mollusc, wich contain more than 95% of known animal species are, in fact, protostomes.

Rather than thinking about "complexity", I think a better question would be, what selective advantages do protostomes and deuterostomes have, if any, and how are these related to the environments ?

Are protostomes less complex/advanced than deuterostomes? Well, it is true that the sequenced genomes of the fruit flies and Anopheles Gambiae show that these genomes are slightly shorter than the one of the puffer fish or the human. Also, I would like to remind that correlation does not mean causality. Other traits that are associated with deuterstomia/protostomia are likely to explain the observed variance.

I think we have to go back even further.... I think the deuterostome and proteostome are a convergence of a body plans (development of body cavity) of two organism that diverged even earlier. It should be noted that all protostome have spiral cleavage at their 8 cell stage. While deuterostome have a radial cleavage. The cell fate of the blastosome of a protostome is determinate while in deuterostomes it is Indeterminate.

I would speculate that there is no direct advantage imparted by the deuterostomic development process over that of protostomes with regards to the evolution of more complex species. Instead, I would guess that sometime after that split, a series of novel alleles arose in various genes which were eventually fixed and laid the groundwork for future increased complexity. Given the trait in question (increased organismal complexity), I would be certain that these alleles were in mostly unrelated genes and were selected for some other function (in other words, there is no gene encoding a protein that imparts organismal complexity; that trait is, by definition, a complex one!). Perhaps the genes involved in the deuterostome/protostome split were part of this groundwork, given their activity at the base of development, however it would be very difficult to know at this point.

I don't know why I didn't think about this before, but the more likely explanation for the difference in complexity between deuterostomes and protostomes is actually unrelated to that difference. Most of the complex deuterostomes that you're probably thinking of are vertebrates. Vertebrates went through a couple of rounds of genome doublings (tetraploidizations) during their early divergence. The extra copies of all the genes provided fertile ground for evolutionary novelties that seems to have led to some wonderfully complex creatures. It's still possible that the tissue groundwork laid out by the deuterostome developmental process somehow contributes to that complexity, but it would be rather indirect, I think.


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Do primates other than humans have a consistent sleep schedule?
I'm doing some sleep research and would like to compare a human sleep pattern as recorded by a wrist-based actigraph with a "natural" sleep pattern, such as from apes. In an experiment like that, a human wears an activity monitor on a non-dominant arm over multiple days. The monitor analyzes activity pattern and can detect when the user is asleep versus active.
Can someone suggest a research article or a website that did a sleep study of primates (monkeys/apes) either in captivity or natural habitat over multiple days?
I'm particularly interested in how consistent their bedtimes are - do primates go to sleep in the evening whenever they feel like, or do they stick to a more consistent sleep schedule?

This is only a partial answer, but a reasonable starting point.
In a blog-article "The Evolution of Primate Sleep", the author identified 3 main patterns - the third pattern seems most relevant to your question.
What he found was that there are 2 divisions of sleep patterns - several primates, such as some species of lemurs are nocturnally active, whereas apes, gorillas etc tend not to be active at night.  Seemingly adapting to the diurnal cycle.  In the article "Mammalian Sleep Dynamics: How Diverse Features Arise from a Common Physiological Framework " (Phillips et al.), primates uniquely undergo monophasic sleep.

Check out Sleep Architecture in Unrestrained Rhesus Monkeys (Macaca mulatta) Synchronized to 24-Hour Light-Dark Cycles.  From the abstract: "With minor exceptions, most notably a delay in peak delta activity, sleep-wake architecture, regulation, and consolidation in rhesus monkeys strongly resembles that of humans."


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Is this a valid principle of curing HIV?
I have a set of questions actually, it will be very helpful if you answer them in order.

Where does the HIV virus hide (during incubation period)? Let answer be X cell.
Is X cell in the bloodstream?
What parts of the HIV are constant for all its version? (I suspect it's Reverse Transcription Protein, Glycoprotein 120 and 41) Let answer be Y.
Is there a chemical that can destroy Y?
Is Y present in the normal Human body?
If Answer to question 2 is yes and that to question 5 is no can we inject the said drug into the bloodstream so that it can wipe out the virus?

I think that if the answer to 6 were yes, it would have already been accomplished.

@kmm not necessarily, is there a chemical and has it been found are two very different questions.

This sounds like an oversimplified question...

The question shows lack of some basic information on current HIV treatment, which is completely fine in my opinion. Afterall we're here to answer questions. In the end, the question is simply asking what's the problem with treating HIV at the moment.

HIV hides in a number of known cells and unknown cells. Although most of the damage of HIV is caused by its infection of shorter lived cells, long lived cells which it infects includes anything with adequate receptors including memory T cells, dendritic cells, macrophages and some glial cells too. These cells are found widespread in the body from tissues to the blood stream. HIV also infects an as of yet unknown pool, which is thought to be the cause of rebound after HART (Highly Active Retroviral Therapy) is stopped.
The constant parts are not exactly there. Every part of HIV can essentially mutate and does. In functional HIV particles (which surprisingly make up a tiny proportion of total HIV particles in an infected individual), the epitopes you mentioned are mostly constant.
Destroying them is impossible as of yet and hence no cure for HIV. It is hard to destroy a particular protein. We could make HIV that doesn't make these proteins (it would then rapidly mutate until it did, or be non-functional to the point it was an awful vaccine not inducing a particularly adept CD8 response). Otherwise we could block either these proteins themselves or that which they bind. There is a group of individuals with the delta 32 mutation which blocks CCR5 preventing infection, however this is rare. For the most part most individuals are susceptible as CD4 and CCR5 are highly conserved amongst humans. We would benefit therefore from inhibitors of these proteins themselves, however due to glycosylation generally our antibodies are terrible at inhibiting the glycoproteins. Reverse transcriptase inhibitors exist and are in fact very important as part of HART.
HIV came from chimpanzees. In their natural host the HIV equivalent (SIV) doesn't cause immunosuppression. HIV doesn't infect quite a few primates due to restriction factors which do not exist in humans or do not target the same things. Then of course there's the matter of the lack of the correct receptors. There's ongoing research if there's a chemical that does cure HIV however there isn't a subset of individuals where this occurs to study. HIV resistance is normally due to elite control of the virus due to specific genetic features that make the immune system target the best least variable, most deleterious (if HIV mutates them to escape) epitopes. If we could get everyone to respond to these epitopes that would be great (see a billion vaccine trials for HIV) otherwise if we could flush out the cells where it hides latently integrated (our current therapy and the immune system can only target cells where HIV is constantly replicating).

To answer your title question: Yes, that is a valid principle of curing HIV. In fact that's pretty much the basic idea behind treating any infection.

1) HIV strains use a combination of two receptors to enter a cell: CD4 and either CXCR4 or CCR5. It can infect and hide out in any cell which expresses both of these receptors; namely CD4+ T cells and some macrophages.
2) Yes. Except that there are populations of dormant CD4+ T cells in some hard-to-reach tissues such as lymph nodes.
3 & 4) There are currently five strategies against HIV, and each strain may be vulnerable against one of them but not another - or may develop resistance during treatment. This is why HAART (highly active anti-retroviral therapy) always comprises drugs of three different strategies. An article recommended to me on this is Shattock and Rosenberg, 2012: Microbicides: Topical Prevention against HIV. Or in particular, this graphic from the article is a great summary: http://perspectivesinmedicine.org/content/2/2/a007385/F1.expansion.html. Briefly: Drugs either inhibit viral entry into a cell by blocking the receptors mentioned above; or they target the viral reverse transcriptase (two strategies for this one), integrase or protease. *)
5) No - although partial activity by the drugs against human enzymes is the cause of side effects.
6) Yes, and we are doing so already (or rather, take them orally - no need for bothersome injections). The only problem is that the above-mentioned dormant cell populations are already infected and have integrated HIV, but it is not being active and hence not noticed by the immune system and not affected by our drugs. As long as HAART is maintained, viral loads in the blood are reduced to near-zero and the patient is for all intents and purposes healthy (including not transmitting HIV) - any latent virus that activates will immediately be wiped out. However, when HAART is interrupted even briefly, the virus can relapse.

Reaching those dormant populations is the focus of current research. If a person starts HAART very shortly after initial infection, before the virus can reach those populations, it is possible to cure them.
In terms of third world, the problem is not the drugs but getting them to the people who need them (money, transport, distribution, legal systems, civil wars etc.)
*) These are not simply 'chemical X from virus' and 'destroy chemical X'. Our drugs do not destroy the viral particles themselves but prevent them from replicating in a live system. If you mix HIV particles and the drugs in a test tube, leave it for 20min, filter the particles out and inject them into somebody, you will still infect them. There has probably been research into antibodies to target viral particles but I don't know any detail of this.

Here's a list of FDA-approved drugs against HIV: http://www.fda.gov/ForConsumers/byAudience/ForPatientAdvocates/HIVandAIDSActivities/ucm118915.htm


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Cell identification by Body Cells
How do the B-cells and T-cells recognize or distinguish a body cell from a foreign particle?
I suspect something to do with this causes Auto Immune Disorders.

This is an extremely broad question. As a start, I suggest you read about the adaptive immune system, then come back with any specific questions you may have.

http://en.wikipedia.org/wiki/Antigen-presenting_cell is a good starting place, and it certainly does have to do with auto-imune disorders, and every other immune activity that I can think of off the top of my head.

And http://en.wikipedia.org/wiki/Allorecognition.

Self recognizing immune cells become regulator cells, so they can prevent autoimmune reactions (against the self).

Broad question. Summary:
The innate immune system processes everything. When it senses that something is dangerous it tells the adaptive immune system, that is T and B cells, that this thing I'm holding is dangerous (via coreceptors and cytokines).
T and B cells that are specific for this dangerous protein (or sometimes non-protein) are activated.
Ideally T and B cells that react to self proteins are deleted. These are from central tolerance mechanisms when the cells are developing (T and B cells are tested against self proteins; if they react they die) and in the periphery (once they're mature) by them only getting activated by the innate immune system and other mechanisms. There's also T regs which regulate the immune system by preventing any cells that react to self proteins from being activated.
Autoimmune disorders are caused by a break down of these mechanisms.

Good answer Android.
Recognition of self vs non-self is the central theme of immunology.
I wanted to clarify and kind of oversimplify a part of Android's response though...
B Cells and T Cells get their antigen receptors made by DNA rearrangement as immature cells. This is a random process and leads to receptors capable of binding (theoretically) anything. As these cells are developing in controlled environments, anything they see is 'self'. If they react to these 'self' antigens, the cells are eliminated. Later in life, antigen receptor activation turns from a self-eliminating event into an activating event. If all goes well, this mature population has already been screened for anti-self cells, so anything that activates them is assumed to be foreign and therefore a threat.

I often have to reiterate this question in my head to clarify to myself how it works, though I tend to take an approach that asks more: What is different between a part of the body and something foreign which triggers an immune response?
Here is the part that concerns B and T cells:

The adaptive immune system (B and T cells) is based on random genetic reshuffling, producing an 'immune cell army' in which every 'soldier' (every cell) recognises a unique target. This 'army' is so vast in diversity that it covers virtually every molecule that occurs in the world - including those of the own body.
This method requires the elimination of those randomly created cells which recognise the body's own substances. The mechanism of elimination is extremely beautiful and makes great use of the way genetics work: Because every cell contains ALL genetic information for your body (except that in almost all cell types the vast majority of it isn't being used most of the time), it is possible to have a few cells which will simply randomly produce bits that belong to a completely different part of the body. This way, everything that belongs into the body will be present where these specialised cells live - which is the bone marrow and the thymus. Thanks to them, it is possible to test every single B and T cell against everything that occurs in the body - and kill them if it turns out they recognise something.
This is how you end up with an army that only reacts to things which are not part of the body.
In other words, an individual cell doesn't distinguish foreign from body, it simply doesn't react to anything aside from its specific target - which should be foreign if the earlier selection mechanism worked.

Aside from this, the main method by which B and T cells determine whether to activate or not is context, which means two things:

B and T cells require co-stimulation to activate - T cells from the so-called antigen-presenting cells (APCs), and B cells from T cells.
In order to be activated, adaptive immune cells (T cells in particular) depend on the levels of certain inflammatory messengers (known as cytokines) in their environment. In other words, the presence of inflammation is a signal to immune cells that in this location where they currently are, abnormal processes are happening and there may be a need for them to take action. As the reasonable response, they will activate or enter a state ready for activation.

Both APCs and inflammation are mainly provided by parts of the innate immune system, adding another safety barrier with more recognition mechanisms to tell self from non-self.


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Is iodised salt harmful to the lactofermentation process?
I was discussing sauerkraut recipes with someone on IRC a minute ago, and they warned me not to use iodised salt in the process. My first (and so far, the only successful) batch is one I made with iodised salt - I think it's pretty much the default here. Searching the Internet shows roughly equal numbers of answers going either way, from "it doesn't matter" to "it discolours the vegetables" to "it kills the bacteria you want".
Clearly elemental iodine is nasty, as are any of the halogens. But is the iodide ion similarly harmful to the bacteria (and yeasts?) involved in lactofermentation, in the low quantities in which it's present in supermarket salt?

I think it may make a difference depending on which vegetable you're pickling...

This study found no difference in the outcome of sauerkraut fermentation with or without iodized salt:

There was no clear influence of iodized salt on microbial populations.
Stable fermentations were achieved using iodized as well as non-iodized salt.

Welcome to Bio.SE! This is a great contribution. Clear, concise, referenced. Thanks for contributing :)

from wikipedia:

No-additive salts for canning and pickling
In contrast to table salt, which often has iodide as well as
anticaking ingredients,
special canning and pickling salt is made for producing the brine to
be used in pickling vegetables and other food-stuffs. This salt has no
iodine added because the iodide can be oxidised by the foods and
darken them—a harmless but aesthetically undesirable effect.

I have been looking for a concentration, but I suspect it is below the threshold that would harm microflora, as it typically has to be visibly yellow (~6ppm if i remember correctly) to be effective as a contact antimicrobial agent...

The FDA states that for chemical sanitization, "An iodine solution shall have a … [c]oncentration between 12.5 mg/L and 25 mg/L" Food Code 2009 4-501.114(B)(3)
The main concern in pickling seems to be the aesthetic.  "Fermented and non-fermented pickles may be safely made using either iodized or non-iodized table salt. However, non-caking materials added to table salts may make the brine cloudy." National Center for Home Food Preservation


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Earliest ancestor of humans who could integrate into modern society
Assuming the current model of human evolution to be correct, approximately when did the earliest ancestor of humans live, who was intelligent enough, that if raised from a young enough age, could learn the necessary skills to live in today's society:

learn a modern language
learn to read and write
learn to use most common tools and household items
learn to drive a car, use a telephone, a computer, have an average job.

Interesting question but I doubt it can be answered conclusively, we just don't have the necessary data. Also bear in mind that chimps can do all (or at least most) of the above.

@terdon : of course, it is impossible to give an exact date, but I was asking it in terms of orders of magnitude. (5k years? 50k years? 500k years?) And chimps definitely don't fit, not just because they are not the ancestors of humans, but because they can't learn the above skills. Learning it as a circus trick does not count. You can teach a bear to drive a bicycle, that does not mean it will have the skills to live in and integrate into human society.

That's exactly my point, how can you define what is a "circus trick" and what is not? Short of trying this with a real hominid, I don't see how this question could be answered. You could assume that a certain hominid would have been able to do some of these things but you can't know. Perhaps a better question would be which was the first hominid to show a society whose complexity is comparable to ours.

Some of your bullet points are already challenging for many Homo sapiens sapiens. ;)

Interesting question.
The organism would have to be monogamous, that's for sure, otherwise it would be too competitive and it would be a beast - as chimps are. Chimps couldn't integrate into the modern society.
So, monogamy is the prime prerequisite as it's also prerequisite for intelligence. Bipedalism is another obvious prerequisite, as you need an organism with fine motorics of front limbs - and fingers.
For "modern language" you need high intelligence and the ability of abstract thinking. Same goes for reading and writing.
Humans split from great apes between 8 and 4 million years ago. Problem here is that every new piece of fossil of a human ancestor is classified as a new species, so there's very little we're certain of. I'd say the first organism capable of doing the above things existed around 200.000 years ago. Either homo erectus or, more likely, a Neanderthal.

Well... given than mitochondria eve was around 99–148 thousand years ago https://en.wikipedia.org/wiki/Mitochondrial_Eve The human species is at least that old.
So a human baby from 148 000 years ago likely could learn to do all the things listed.
Could  Neanderthal do all those things... Well Neanderthal are not an ancestor species.. more like a cousin species (separation by 500,000-700,000). And from hyoid bone... appears to be able to speak like modern humans do.
http://www.ibtimes.com/did-neanderthals-speak-60000-year-old-hyoid-bone-virtually-indistinguishable-our-own-1559113
So probably yes.. on mastering modern language.
Reading and writing.. well no idea. But then again there are no examples of humans writing older than 3200BC. And the human species is at least 150 000 year old.
However Neanderthals do have a reduced semicircular canals compared to humans. An almost defining feature of Neanderthals.... so Neanderthal were probably less  graceful in 3d space... so probably no gymnastic and kungfu for neanderthal.
Homo erectus... well they have high larynx.. limiting the sounds the they could make. The position is approximate that of a human 2 year old.
The other things on your list... no answer can be given.


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Are there dangers to Teflon and aluminium cookware?
I've been reading some articles on the internet about dangers of Teflon and aluminium to the body.
My family say I'm just exaggerating the situation, and maybe I am, though I'm not sure because not everything on the internet is true. They always tell me that if aluminium were dangerous then why would the government allow the use of aluminium bottles in drinks.
Are there strong references and facts to support dangers associated with aluminium or Teflon cookware? If aluminium or other chemicals enter the body from cookware, are they naturally eliminated, or do they remain in the body?

I was recently taught in a module on chemical toxins that the Al in deodorants was more concerning because it was more readily being absorbed in the blood and that heavy deodorant users had higher circulating levels of Al in the blood.  I'm looking into actual sources now.  This question may also need some rephrasing to be sure it is not a personal health question.

I think that teflon that is still teflon is pretty darned chemically inert... the dangers are in teflon that has been damaged by heat and in the production of teflon which uses horrible chemicals... also Al metal is less dangerous than Al+3 compounds... and even then, most aren't soluble at all, but some give good routes to ingestion especially antacids.

@Daniela Diaz, I've edited the question so as to make it more useful to other users, and taken a stab at answering it below. I hope the edited question still reflects your intentions.

@Oreotrephes Your edition is perfect. Thanks so much.

The US Department of Health and Human Services has a nice set of factsheets on aluminum. In brief, and to specifically answer your questions, they point out that:

Aluminum occurs naturally in air, water, soil, and plants.
The amounts of aluminum that we encounter in pots and pans are considered to be safe for healthy people. Cooking acidic foods in aluminum pots increases the amount ingested, but is still considered to be safe; and it still represents many times less aluminum than in over-the-counter antacids, which are also considered safe.
Much of the aluminum we ingest leaves ones body naturally through the digestive system (that is, feces), and is not taken up into the bloodstream. The small amount of aluminum that makes it to our bloodstream is mostly quickly eliminated in urine. Those with kindey problems may not process this bloodstream aluminum as quickly.

Nonstick pan coatings are a little more difficult, probably because they're so diverse. Cookware isn't even mentioned as a source on the factsheet for perflouroalkyls, the chemical which has been mentioned in connection with nonstick pan health issues. The US Environmental Protection Agency FAQ says:

Consumer products made with perfluorochemicals include some non-stick cookware ... Consumer products made with fluoropolymers and fluorinated telomers, such as Teflon and other trademark products, are not PFOA. PFOA is used as a processing aid in the manufacture of fluoropolymers and can be also be produced by the breakdown of some fluorinated telomers [NB. I assume they mean overheating nonstick pans]. The information that EPA has available does not indicate that the routine use of consumer products poses a concern.

This is one of the articles I read: http://www.globalhealingcenter.com/natural-health/concerned-about-aluminum-dangers/                                              It contains some references and basically my concern is the part where it says that aluminium accumulates in different parts of the body and it causes problems with calcium absorption and demineralization, and also that is bad for the brain.

Well, it's always good to see citations. However, I would approach with a cautious eye any article that ends with an appeal to buy a product from the author.

Teflon® is a brand name for a man-made chemical known as polytetrafluoroethylene (PTFE) and it has been used since 1940s (discovered by DuPont Co.). Perfluorooctanoic acid (PFOA, also known as C8) is another man-made chemical and it is used in the process of making Teflon and similar chemicals (known as fluorotelomers), although it is burned off during the process and is not present in significant amounts in the final products.
Teflon itself is not suspected of causing cancer, but PFOA has the potential to be more of a health concern because it can stay in the environment and in the human body for long periods of time. Studies have found that PFOA is present at very low levels in just about everyone's blood in the US and it can be found at low levels in some foods, drinking water, and in household dust. It can be higher in areas due to contamination. People can be exposed to PFOA from fabrics, ski wax or carpeting which has been treated to be stain resistant. However non-stick cookware is not a significant source of exposure.
Studies in laboratory animals have found that PFOA exposure increases the risk of certain tumors of the liver, testicles, mammary glands, and the pancreas in these animals. Overall, well-conducted animal studies do a good job predicting that cause cancer in humans exposures. But for PFOA, there are clear differences in the way the body of laboratory animals and humans handle this chemical. Because of these differences, it is clear that the process chemical to cause cancer in animals also occur in humans.
Human studies have shown that people with workplace exposure to PFOS have a higher risk of cancer of the bladder and kidneys.
Several national and international agencies studying various substances in the environment, to determine if they cause cancer (carcinogens, substances that cause cancer and help cancer grow). However, at this time, these agencies do not formally assessed whether PFOA can cause cancer. The US Environmental Protection Agency (EPA), an electronic database that contains information on human health effects from exposure to various substances in the environment, has not officially classified PFOA as to its carcinogenicity.
Other than the possible risk of fumes from overheating the pan, there are no known risks to humans using Teflon-coated cookware. When PFOA is used to make Teflon, does not occur (or not present in very small amounts) in a Teflon-coated products. Because the way by which people may be exposed to PFOS are not known, it is not clear what steps to take for people to reduce exposure.
Currently, EPA states:

"Consumer products made with fluoropolymers and fluorinated telomers,
  such as Teflon and other trademark products, are not PFOA. PFOA is
  used as a processing aid in the manufacture of fluoropolymers and can
  be also be produced by the breakdown of some fluorinated telomers. The
  information that EPA has available does not indicate that the routine
  use of consumer products poses a concern. At present, the EPA does not
  recommend any steps for consumers to take to reduce exposures to
  PFOA."

Source: Teflon and Perfluorooctanoic Acid (PFOA) at Cancer.org


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How can haired mammals synthesize vitamin D?
The human body can synthesize vitamin D in the skin from cholesterol, when sun exposure is adequate. But how can haired mammals do it? Do not they need it?

At least the vast majority of adult mammals have hair/fur (not sure if you are trying to make a distinction), possibly all (I will have to check on a hairless adult mammal or mammals that made to adulthood without hair).  Hair is actually one of the defining characteristics of mammals.  So what do you mean by "haired mammals" (humans have hair)?

@AtlLED, I think the OP means mammals whose skin is apparently inaccessible to the UV required for vitD synthesis, i.e. that don't have any exposed skin.

@AlanBoyd Right, I was trying to edit my comment and got distracted (and came back too slow).  OP: Would a polar bear and a dog be an ok example, then, for how different animals do it?

Lanolin is now commercially the main substance used in Vitamin D3 production. It's irradiated with UVB. It's waxy, composed of a variety of waxy compounds, highly water-resistant. Do sheep reabsorb these back into their skin or lick to acquire Vitamin D? A sheep has little skin exposed to sunlight.

According to "Melanocyte biology and skin pigmentation" (Yin and Fisher, 2007), the exposed parts of mammal bodies, such as their noses have melanocytes that can be locations of vitamin D production.
According to this Wikipedia article, the secretions in woolly animals also produce vitamin D.
This is further explored in "Vitamin D(3) synthesis in the entire skin surface of dairy cows despite hair coverage." (Hymoller and Jensen, 2010), where they found that cows synthesise vitamin D all over their body, where they dispute an idea that vitamin D is manufactured in the fur secretions, and ingested via grooming.