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Effect of closed eyes on balance?
Suppose you want to stand on one leg. Doing it eyes open is not that difficult, but doing it eyes closed seems to be difficult. Why?

@Bez No. I think this is an interesting question which is related to the neuroscience and the functioning of small brain. Some neuronal pathways are closed when you close your eyes. Some people also cannot do this when eyes are closed - it is impossible if you have severe damage in your inner ear etc caused by falling.

@Masi Then it would be great if a case study or population study to that effect is referenced by the OP since at the moment this question is based on the opinion of the OP!

@bez definitely not one for skeptics for me - it's a fairly well known phenomenon

@Bez It is based on his intuition, not just opinion. There is much logic in his thinking. No reference need to be done if the user does the thinking themselves. Very well known phenomenon also so I think this is recalling event from his deep memory and wanting an explanation for it. Completely acceptable question here, I think.

@Masi Is correct.  This is a fairly common neurological test.

Balance is tricky and depends on a lot of things, including, to some degree, your sight. Balance is achieved and maintained by a complex set of sensorimotor control systems that include sensory input from vision (sight), proprioception (touch), and the vestibular system (motion, equilibrium, spatial orientation); integration of that sensory input; and motor output to the eye and body muscles. Your vision helps you see where your head and body are in relationship to the world around you and to sense motion between you and your environment.
Very simply put, to blindfold someone is to take out the contribution of vision to balance. So, if the other systems involved in balance are off even a bit, blindfolding someone will interfere with their ability to keep their balance, even on two legs, let alone one.
Here are those systems in more detail.
Proprioception. In your joints, muscles, tendons, skin, and other areas, you have proprioceptors, that tell your brain where yoor aody parts (arms, legs, etc) are in relation to self in space. Because we live on a planet with  gravity, even if we are blindfolded, if we are standing correctly, our feet will sent our brain signals that will in turn allow the brain to judge our position in space with regard to gravity and we will keep our feet firmly planted on the ground in a way which will maintain us upright in a constantly regulated position (if we sense less pressure from the bottom of our right great toe, we will adjust by leaning forward and to the right a bit until out=r brain says, "ok, right there!" This happens from all the skin and joint proprioceptors responding at the same time. Notice that once vision is blocked, our bodies become relatively very still; we focus on our balance. We move tentatively.
As people age, they lose some of their propioceptive abilities. That's one of the reasons for falls in the elderly.
Inner ear. In our inner ear are the semi-circular canals, three on each side, which are oriented at ~90° to each other so we cover 3 dimensions. In these canals is fluid which sloshes about when we move our heads, change directions, bend over, etc. The fluid moving about is detected by fine hair-like projections on the sensory cells lining the canal called stereocilia - like a wave would be detected by your leg in shallow ocean water. These semicircular canals help us to remain oriented in space. Now, the semicircular canals are also attached to otolith organs - two chambers which are concerned with gravity. They have fine crystals in them - called otoconia - which move according to our head's position with relationship to "down", or gravity.
If we stand perfectly still (probably not possible without support), everything is read by the vestibular system (the semicircular canals and the otolithic organs) as normal, and we stay upright (there is a constant communication between our vestibular system and our brain). So, when blindfolded, we can stay upright even if we shake our heads, bend them forward or back, etc (within reason). As we age, things can degenerate in this vestibular system, which affects our balance, and results in more falls in the elderly. (Diseases in the young can also affect this.)
Vestibulo-ocular Reflex. A complicated system which reflexly coordinated input from your vestibular system and your vision in head movement. If someone suddenly turns your head, your eyes will move in the equal and opposite manner, that is, your eyes will stay focused on the object on which they were focused just before your head was moved. This system is what allows you to easily keep reading something while you shake your head from side to side (not the case if you move the print side to side).
When things start going wrong (in a very slow manner) with your vestibular or proprioception systems, your eyes can help compensate by orienting you to the horizon, etc., in a manner, correcting for some 'off' calculations in your vestibular system. Vision helps us to identify orientation with respect to gravity, determine direction and speed of movement, etc., to a much lesser degree than the other systems described but enough to have an impact. So, in people whose vision is failing, either their other systems have to be in really good working order (e.g. why young blind people aren't always falling over) or they have problems with falling.
The Human Balance System (easy)
Researchers find diminished balance in those with poor vision (easy)
Balance (easy)
Visual influences on balance
Baloh and Honrubia's Clinical Neurophysiology of the Vestibular System
 By Robert William Baloh, Kevin Kerber, MD
Somatosensory Systems
Vestibular Occular Reflex


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Increasing/decreasing signal intensity in Western blotting
So I was in class and my professor was explaining western blotting. It seems as though there's more than one way to increase or decrease the signal intensity. He presented us the challenge to discover different ways this can happen. As hard as I look all I can find on the internet or even in google scholar is just certain chemicals like 'signal enhancer' and that's it, nothing remotely specific. Legitimately I do not propose this as actual homework, in fact it's just a curiosity I have. Therefore I ask the scientific community what, if any, are conditions that one could increase or decrease the signal intensity in western blotting? I understand what western blotting is, anyone can find this on wikipedia, but conditions that could increase or decrease signal intensity?

There are several different places in a typical Western blotting protocol where conditions can be altered to modulate signal intensity. The first is the amount of protein loaded - more protein will give a stronger signal, less will give a weaker signal. However, too much protein can result in indistinct bands, increased background, lane distortion, and other issues.
The next condition to change is the amount of primary antibody and the incubation buffer. More primary may lead to an increased signal, but too much can give higher background. Some antibodies give a better signal when diluted in BSA, others when diluted in nonfat dry milk. Generally, milk will give you a cleaner blot, but may reduce the signal. Incubation time can also affect specificity and signal intensity - some antibodies will fully bind with a 1-2 hour incubation at room temperature, others require an overnight incubation at 4°C.
The third condition to alter is the amount and type of secondary antibody. Increasing the amount of secondary may increase signal, but again may result in increased background. There are also different types of secondaries, depending on your detection system - HRP for chemiluminescent detection, AP for colorimetric, fluorescent tags for imaging systems, etc. These have different sensitivities, but can also result in increased background, depending on the other conditions of the protocol.
Finally, the type of detection system can affect sensitivity. For example, when using standard HRP-conjugated secondaries, there are numerous different ECL substrates with widely varying sensitivities. Here is a list of different systems available from Thermo/Pierce, ranging from standard ECL to Femto.
So, while Western blotting seems like a fairly straightforward procedure, there are many places to optimize the conditions to get the results you're looking for.

Wow I was sort of close with some of this yet so far away.  That is amazing, you must work with western blot on a regular basis?  Curiously, could I get a reference from you as to where or how you got this?

@Fistula I worked for an antibody company for over 6 years doing antibody preparation, QC, and tech support, so this answer is just a quick distillation of my knowledge. I can talk for hours about Westerns, if you're so inclined :)

This is a good answer @Fistula

One thing that others have not mentioned yet is that the time of the wash can affect the signal. If its washed longer than the usually required 5 minute three time wash, this could result in a reduced (decreased) signal.
Reference:
http://www.cellsignal.com/common/content/content.jsp?id=western-trouble

Additionally to the points in the answer @mattdmo has given, it is possible to enrich the protein of choice before the gel run. This can either be done by using tagged proteins (possibly with the cleavage of the tag before loading) or by doing an immunoprecipitation of your protein. The later is interesting when you have only low concentrations of your protein present in the cell. What you basically do is to bind an antibody to the protein, the bind the protein-antibody-complex to a column or beads, wash away (in theory, practically you are not getting all the other proteins away) and then load the sample. Depending on the enrichment, you will be able to see a band, where this is not possible without immunoprecipitation.
Then washing and blocking of the blot plays an important role. Usually you use milk powder to prepare the blocking solution, as this is quite cheap and works pretty well. But it can give quite a high background and make problems with phosphoproteins (not necessarily though). Sometimes it's better to use more expensive solutions like BSA for blocking the membrane. The washing is also critical, depending on how stringent you wash, you will loose signal and influence the background. Here you can play with different concentrations of detergents as well as with different detergents.
Additionally you can get a lot of different signals in the detection. For chemolumincence based detection you can either use x-ray films (which are rather unsensitive) and have problems with strong bands outshining neighbouring weak ones. They are also harder to quantify, as the linear range in which more intensity corresponds with more signal is limited. With chemoluminescence you can also use special highly sensitive CCD-cameras (which are more sensitive and have a much higher linear detection range) or phospho-imager plates (special plates, which store the chemoluminecent signal on a light sensitive plate and which are read out with a special scanner).
The latest development in the detection technology are infrared scanners for which you use secondary antibodies coupled to a dye which fluoresces at infrared wavelength. These scanner are extremely sensitive and also allow the usage of two differently labelled secondary antibodies at the same time, which can be very handy in analyzing protein interactions. You will need primary antibodies from different species, though. The modern detection techniques also have the advantage of delivering digital files, while films need to be scanned before further use in publications.

Also a good answer @Fistula

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Can a human acquire a memory of an animal?
I would like to know if it's possible for a human to acquire an animal memory.
I mean, animals store their memories in their brain, right? And so do we, humans, store our memory.
So, is it possible to cut off an inch (or something like that) of an animal brain,
also to cut off an inch of a human brain, and to replace that animal brain-piece in the missing part of the human's brain?

No, it can't be done for a lot of reasons. Here are just a few.
1) Memories are stored in electrical pathways, not the the cells themselves. You don't have 1000 memories in a chunk of brain that contains 1000 neurons. If you don't get the entire pathway, you won't get the memory.
2) Once a nerve is cut, it won't fuse with another cut nerve. All you'll have is a chunk of dying animal brain in your head. Even if a skilled neurosurgeon united the blood vessels of your brain to those of the chunk to keep it alive, the nerves themselves wouldn't become a working part of your brain. All you'd have (at best) is a useless chunk of another animal's brain sitting where your now-missing chunk was.
3) Animals are different from us. Your body would recognize the different-animal brain matter as foreign, and would make antibodies to it and reduce it to mush (if one didn't die of infection before then).

@ShadowRealm if this answered your question, please indicate as such by clicking the check mark next to it (it will turn green). Please see What should I do when someone answers my question? for more details.

Do we even comprehend memory that well? Cause from what I know we don't.

The other answer has been deleted but I think raised an important point specific to the original question : "is it possible to transfer animal memories into a human's mind." This answer answers the more broad question : "is it possible to physically transplant one brain's memory into another person's brain."  If we assume that memories are in no way transferable, then there is no need to distinguish between human-to-human vs animal-to-human. But if we accept a science-fictional possibility (think Dollhouse) for human-to-human, are other animals still too foreign to transfer?

@Anthony - I'm not aware of how memories were transferred in dollhouse. Can you explain?

It's pretty silly. "Dolls" undergo a procedure where their brain is "wiped" and special hardware is installed, making their memory "storage" like a blank floppy disk. Meanwhile, a source mind can have their minds mapped to get their mind's "image" mapped and copied into some storable format. This image can then be loaded to the doll's brain. Think of it as "copy as image" and then printed to reformatted disk.

It's interesting that through the ages, our brains have been compared to the latest technologies. Descartes compared the brain to a hydraulic machine. Freud likened emotions to pressure building up in a steam engine. The brain later resembled a telephone switchboard and then an electrical circuit before evolving into a computer; lately it’s turning into a Web browser or the Internet. But the brain isn't like a computer. If it's wiped, truly wiped of higher functions, we would not be able to reprogram it, or reboot it, or replace it. What was there before would be gone forever.

Is there a citation for the memory stored in electrical pathways? I didn't know human memory was figured out.

@vajra78 - just out of curiosity, where/how do you think memories are obtained/kept? Here's one small example. Intracellular Correlates of Acquisition and Long-Term Memory of Classical Conditioning in Purkinje Cell Dendrites in Slices of Rabbit Cerebellar Lobule HVI

I don't know. But electrical pathways run across the cells. It is clear that networks of neurons store memories. I can't find one nice study done using a new type of optical technique to turn memories on and off in a mouse model. Even so with all the research no one would bet their life on understanding how a memory is stored. There could very well be molecular structures associated with those networks allowing for differentiation. Something must make one network standout from another.

Also instead of transplanting nerves, what if the signals were routed via a wire. The thing is you would need the references from the animal mind. I'm jumping here but I would wager that a complete memory references memories from the sense and emotional regions in the brain. Very much like a relational database. But I wouldn't bet to much money.

@vajra78 - I would wager with you.

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Ebola immunosupression and infection
I was wondering... If Ebola attacks immune cells and causes immunosupression, then shouldn't we see death in Ebola patients due to secondary infection?

Secondary infections does not matter when you bleed to death... Btw. I hate this ebola hype, it is a relatively insignificant lethal virus, nothing more.

Yes, we should. But Ebola doesn't completely immunosuppress us, or there would be no survivors.
Ebola kills by overwhelming the body before enough antibodies are formed to fight it.
If you're one of the survivors (as about 40-50% are, more with good care), you'll have antibodies to Ebola in your blood which might help someone else infected with Ebola.
If you're not one of the survivors, it's still likely you'll have some antibodies, but the shock your body goes into from all the dead cell products in your blood (which - overly simplified - causes a cytokine storm -> leaky capillaries -> fluid balance problems -> end organ failure -> death).

So the Ebola virus replicates too fast for the immune system to handle?

I wouldn't quite put it that way. I'd say, rather, that in many cases, the host dies of the damage done by the virus before an immune response adequate to destroy the virus is mounted.


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What's up with all the vague protocols?
I have lost count of how many protocols I've seen, including those supposed to be professionally written (such as manuals that come with kits from well known brands, or methods sections of papers in respected journals), that outright fail to give unambiguous instructions. Some common examples are:

Give centrifuge speed in RPM instead of RCF, and not say what rotor or centrifuge it is.
Say to spin a sample at "maximum speed".
Use subjective time periods, e.g. "incubate briefly" (is one minute brief enough or does it have to be five seconds?)
Subjective quantities, such as "get a good amount of cells" (!!!)
Give time ranges without explaining the consequences of the choice, such as "5-10 minutes" (is it 5 or 10? which one???).
Say "mix well", without specifying if vortexing is okay.
Say "mix well, don't vortex", and don't explain what mixing technique I'm supposed to use.
Give urgent-sounding warnings, such as "don't touch the pellet!", without explaining what happens if I do it or how to fix it (do I need to start over? will I just get 5% lower yield?).
Give urgent-sounding warning, without explaining how to actually heed the warning ("dry the pellet, but do not over-dry it!")

It is in fact extremely rare that I ever see a protocol that has none of these issues. It almost never happens.
It is extremely important that scientific results be reproducible, and it seems like you are opening yourself up to a lot of trouble with an ambiguous protocol. What if somebody fails to reproduce your results, not because your experiment wasn't legitimate, but simply because you left out some crucial detail from the protocol you gave them? You would look bad, and for no good reason.
So why is it so common for protocols to be ambiguous? Is there some nuance to this that escapes me, or do people just not care? How do you follow a protocol that left out crucial information so as to be impossible to follow? Or are you supposed to have amassed a sufficiently vast reservoir of practical knowledge that you can draw on it to "fill in the blanks" on the fly?

As a counter argument to the hold: I am specifically interested in the personal experiences of researcher who have encountered this problem far more often than I have (perhaps I have failed to communicate this adequately). I am hoping that these anecdotes will be useful to me, and other novice experimentalists like me. As such, I think it can qualify (perhaps with some revisions) as a good subjective question.

I agree. This is more a meta question for biology research, so I don't think it's completely off-topic.

@Karolas Incidentally, the "boring lab questions" have always been a bit of an unclear case as to whether they fit. I believe a Meta discussion concluded that it's best to include them here, as opposed to say Academia@SE or a separate SE site. That said, the hold appears to be not for topicality, but subjectivity (and to be honest I don't understand how it's opinion based, but that's another matter).

This is too long for a comment, so I post my thoughts about this here:
This falls into different important parts here: One is an insufficient understanding of the techniques on which the method is based. This makes it hard to decide which steps are important and which are not. One prominent example would be the use of EDTA in DNA gel running buffers. This recipe originated from RNA research (where you need the EDTA) which where then simply used for DNA as well. Since it worked somehow, it was never really changed.I have seen enough people in the lab clinging to old photocopies of protocols without knowing why they do certain steps.
And the other (connected) issue is that protocols are usually passed down through labs. Things are then done in a certain way because they have always done in this way (with some changes in the protocol probably not even documented) and are not changed. People are even told to use the exact routine, even if this makes absolutely no sense.
In publications there may also be another thing which comes into play: The fear that someone uses the own methods and will then be faster than the own group. At least some groups only publish incomplete and vague methods because of this reason. Then it's a thing of space: There are character limitations in publications and when you need to save a few hundred characters when the article is too long, it's much easier to shave the methods than the discussion.

Thanks, this a quite informative comment/answer. The EDTA example is a very good one that I had noticed myself. I'll wait for other answers, since the question is probably more useful as "What do you do if a protocol is vague?" rather than "What is the reason for protocols being vague?".

@Superbest As I said, it's more like a comment, but too long for it.


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Why does the 'Positive-inside Rule' exist?
Gunnar von Heijne's Positive-inside Rule seems to have been around for a couple of decades and underpins a lot of what we know about transmembrane topology. It is used to predict the topology of a given transmembrane domain, typically a helix.
My question is what are the physicochemical, or biochemical explanations for this rule? Although the literature talks about it in depth and has many examples of the rule being employed, I can't seem to find anything about the "behind the scenes" explanation.

Isn't  the electrostatic polarity across membrane enough for the explanation to you?

@243 It would be if there was a negative-outside rule, which it turns out that there is! I found many examples of the negative-outside rule, but they were statistically masked by the rarity of negative residues.

There are not much explanations available, as far as I can see. The best explanation that I have found is that the positive charge allows the orientation of the protein in the membrane. The orientation for membrane proteins is important as a lot of them are transporters which have a dedicated transportation direction. The same is true for receptors, which transport a signal from the outside to the inside of the cell. Most of the positively charged arginine and lysine residues are found in loop regions which are located between transmembrane regions (often hydrophobic helices).
References:

Topogenic signals in integral membrane proteins.
Positive charge loading at protein termini is due to membrane protein
topology, not a translational ramp
The Positive Inside Rule Is Stronger When Followed by a Transmembrane
Helix
Membrane-protein topology

Proteins insert  according to the positive inside rule because positive charges tend to stay in the cytoplasm.  Cells tend to have an electrostatic polarity across the membrane boundary that will hold the positive area inside, and because  higher pK values make the positive areas harder to deprotonate, these interactions tend to make the protein stay that way.

Please add some references!


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Prevent biofilm formation on moist surfaces
I have an indoor fountain with lots of water. What are the most common microorganisms in this kind of moist environment, and what are the standard way to prevent biofilm formation by them? I thought of copper and/or salt as general cheap disinfectants so far.

Bleaching powder can also be used but it can corrode metal parts. Salt will also aid in corrosion. You can try little bit of phenol or other aromatic disinfectants.

By salt about 3-4000 ppm is recommended. It starts to corrode most of the materials above 5-6000 ppm (from non scientific source). I read that cleaning it with acetic acid and using distilled water could work either. Algae is an usual microorganism in this kind of environment.

Distilled water is costly.. It will accumulate minerals and dust soon. You can occasionally use bleaching powder to clean it up. Better than acetic acid. Chlorination is commonly used technique against algae (bleaching powder is calcium hypochlorite).

Don't pools use chlorine tablets?

@Superbest This is an indoor fountain, and chlorine have an odor, so I wouldn't use it if not necessary. I stay with the salt (about 10-15 g/L), and see what happens. The fountain is 2 days old and does not get too much light, so I hope it won't bloom for a long while.

You can use some antibiotics or germicide or alcohol...they prevent the formation by interfering with the attachment or adhesion and expansion of immature biofilms..

Antibiotics degrade quickly. You would spend a lot of money on them if you regularly treat the whole water reservoir. Alcohol needs to be at a very high concentration (70%) to have bactericidal effect.

Antibiotics are expensive, and I don't want to nurse AB resistant strains. Germicide is a broad term... Alcohol is expensive as well, and will vaporize very fast. At least I get drunk ;-)

@inf3rno you could also use ion coatings...

How can I do that?

@inf3rno I think it comes as a spray... It's about $30...

Never heard of it...

@inf3rno http://www.righttoolusa.com/p/Sonus-Ion-Paint-Coating-55330570.html?gclid=Cj0KEQiAwaqkBRDHx6rzxMqAobgBEiQAxJazJ3jzHjOpHllIxRodywVckR6v5iXnefsLg0IlCPNgfYoaAofh8P8HAQ

@inf3rno it's kind of expensive...

@TAbraham Not exactly what I wanted, but would be good surprise to my father for xmas.


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Why should plants transform glucose into sucrose before transporting it to other parts?
I've learned that plants transform glucose into sucrose before sending it into phloem. But the process seems to be complex and energy comsuming. Why should plants do it? Is it really necessary?

Glucose, fructose and galactose are the three dietary monosaccharides. Glucose and Fructose are  simple monosaccharides found in plants. A monosaccharide is the basic unit of carbohydrate and the simplest form of sugar, glucose are aldose and Fructose are ketose.

If the carbonyl is at position 1 (that is, n or m is zero), the molecule begins with a formyl group H(C=O)-, and is technically an aldehyde. In that case, the compound is termed an aldose. Otherwise, the molecule has a keto group, a carbonyl -(C=O)- between two carbons; then it is formally a ketone, and is termed a ketose. Ketoses of biological interest usually have the carbonyl at position 2.
  http://en.wikipedia.org/wiki/Monosaccharide

Whereas Sucrose is a disaccharide composed of glucose and fructose. A disaccharide is more complex than monosaccharide, more complex compounds like oligosaccharides and polysaccharides exists. Sucrose synthesised within the cytosol of photosynthesizing cells is then available for general distribution and is commonly trans located to other carbon-demanding centers via the phloem.
Sucrose and starch are more efficient in energy storage when compared to glucose and fructose, but starch is insoluble in water. So it can't be transported via phloem and the next choice is sucrose, being water soluble and energy efficient sucrose is chosen to be the carrier of energy from leaves to different part of the tree. Another problem exists,   glucose is highly reactive and this may result in some intermediate reactions while transporting glucose. Being a complex structure, sucrose is not as much reactive as glucose. So plants uses the sucrose as a medium to transfer energy. Inside the cells, sucrose is converted back to glucose and fructose. Energy is yielded when it is needed. So plants transfer glucose and fructose in the form of sucrose in order to:

Increase energy storage
Efficient energy transfer
Removing in between reactions

References

Carbohydrates
Sucrose & Starch Biosynthesis
Sucrose Metabolism
Sucrose and starch synthesis
Disaccharide

there is no free glucose in the photosynthesis. Stop to spread that myth. The net product is G3P. The end products of photosynthesis are sucrose and starch, but never glucose. Do you test glucose in the leaves? No... it is always for starch. ;) The G3P is converted to sucrose and other molecules, for example, thiamine. Glyceraldehyde 3-phosphate occurs as a reactant in the biosynthesis pathway of thiamine (Vitamin B1), another substance that cannot be produced by the human body. Part of sucrose is then translocated to the phloem. Starch is stored in the stroma of chloroplasts. It is also stored in the amyloplasts in the roots, stems cells after sucrose suffers a conversion to starch.

Welcome to Bio. Could you post a reference to support your statement?

See very first statement in https://en.wikipedia.org/wiki/Calvin_cycle

During Calvin cycle, 3 molecules of CO2 combine with RuBP acceptors to form 6 molecules of G3P. 1 G3P molecule exits the cycle and goes towards making glucose while the other 5 are recycled, regenerating 3 RuBP acceptor molecules.
Plants do synthesise glucose.

This seems more like a comment to the foregoing answer. Some link would come in handy. Thank you!


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How does the cornea breathe during sleep?
The cornea is not supplied with blood vessels and so exchanges gases directly with the atmosphere. So how does it breathe during sleep when our eyes are closed?

As you noted, the cornea needs oxygen, yet it's not vascular. It needs to get it's oxygen supply from diffusion. In the daytime, diffusion occurs from air through the tear film covering the cornea.
The cornea spends about a third of it's lifetime under closed lids. At night, the tear film remains intact and is continuously replenished. The inner aspect of your eyelids, called the palpebral conjunctiva, are highly vascularized, with capillaries just below the surface (and accessory tear ducts and tiny mucosal glands to keep it moist).
When you sleep, oxygen (and nutrients) diffuses from the palpebral conjunctival capillaries through the tear film to your cornea.
The blood vessels in the palpebral conjunctiva are more permeable than most other capillaries and contribute fluid and nutrients to tears by leaking plasma. The surface epithelial cells are also a source of tear fluid because of a special arrangement of the cells such that there is more intercellular space allowing fluid, antibodies, and other plasma constituents to the surface of the conjunctiva.
This very issue was of great concern to ophthalmologists when people started wearing extended-wear contact lenses.
The Conjunctiva and Lacrimal System (www.eyecalcs.com/DWAN/pages)
Organization of Capillaries in the Primate Conjunctiva
The Conjunctiva—Structure and Function (oftalmologia/enciclopedias)
The oxygen tension and temperature of the superior palpebral conjunctiva
Facts About the Cornea and Corneal Disease (cool article)

If the palpebral conjuctiva doesn't work properly, can it cause blindness ?  Are there any reported cases ?

@biogirl - yes, it can and does cause blindness, most commonly in dusty, sandy, dry climates.


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Neuron Growth and Regeneration
Are nerves and/or neurons able to grow and repair after damage, but not regenerate? Is this specific to humans? I have heard of people being paralyzed, but after much therapy are able to use their legs again. Is this just through the creation of new connections from healthy nerves, or is there nerve repair to an extent?

the following is true for humans, I dunno about other animals:
schwann cells in peripheral nervous system can rebuild a severed axon if the perineurium of the nerve fibers are sutured together ... the same is not true for oligodendrocytes in the central nervous system. Thus only peripheral nerves can regenerate and not nerves located in the central nervous system (ie. spinal cord or brain).
surgical nerve regeneration after a nerve is severed is not the only possible form of nerve regeneration, another example would be when the facial nerve is damaged by bells palsy and then it regenerates itself. so a fun example of what can go wrong is when some of the nerves switch when they regenerate, so your brain thinks it's doing one thing, but since the nerves switched when they regenerated, it does the other. The example would be "crocodile tears syndrome", it has nothing to do with crocodiles (thats just the name) but rather this is where the facial nerves salivation fibers get switched with the crying fibers... so when they eat they cry...
as for neuro-rehabilitation in people suffering paralysis, this is a broad question. As I understand it, if it's the spinal cord thats cut then it will never regenerate, but if its a nerve that left the spinal cord (a peripheral nerve) than it may possibly regenerate. Here are some specific conditions:
Also it could be a temporary thing like Guillain-Barré syndrome where the immune system (hyper sensitized by a previous campylobacter bacteria or CMV virus, or for some other reason) temporarily injures the peripheral nerves and then after about 2 weeks they recover)
also there is there are drugs and toxins which are temporary, so one your body metabolizes/excretes (bile or urine) it is gone: botulinum toxin (from bacteria Clostridium botulinum), curare (south american plant poison), the many chemically modified versions of curare produced by pharmaceutical used in surgery to relax the muscles, and the list goes on for drugs/toxins. Again, drugs/toxins are temporary.
Stroke, though in the central nervous system, might be able to be rehabilitated since maybe everything wasn't destroyed (even though what was destroyed was destroyed permanently), and the patient can salvage what is left and use their neuroplasticity to try and use their brains slightly differently to be able to recover.
ALS, affects the ventral horn of the spinal cord... this one is irreversible at least today.
there are many other causes of paralysis which may nbe reversible or irreversible
glossary

schwann cell= the fatty cell that wraps around an individual nerve in order to myelin ate it... myelination being the fatty insulating of axon so they send electric signals faster...
axon= a projection off of the cell body that sends an electrical impulse to the end of the nerve that ultimately communicates with the target nerve/muscle/gland/etc
perineurium= outside protective sheath composed of connective tissue covering many nerve fibers
oligodendrocytes= the equivalent of a schwann cell, but in the central nervous system, it myelinates many nerves, unlike the schwann cell which only myelinates 1 nerve.
nerve fibers= a collection of many nerves running together
facial nerve= facial nerve innervated the muscles of the face and there are 2 facial nerves, one for each side of the face. the facial nerve doesn't only do face muscles, but also taste, salivation, and tear formation
bell's palsy= when the facial nerve stops working and half the face gets droopy... there are a lot of possible causes, like virus bacteria, and many many noninfectious causes...

That is really helpful and interesting, thank you!


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PCR cycle problem
IF I began a PCR cycle with 5 copies of a particular DNA section, and copied the section by PCR, for 6 cycles, how many copies of the DNA (include the originals) would I have by the end of these cycles? Explain or sketch out your reasoning.
Edit: I think it is 315 copies (5+10+20+40+80+160 = 315) after 6 cycles right?

What do you know about PCR? Especially about the double rates?

I think it is 315 copies after 6 cycles right? I did some research haha

Then you should redo you research. How do you come to 315?

uhh I did 5+10+20+40+80+160= 315

This is exponential - you double the number of molecules in each step. See my answer below.

PCR ideally doubles the number of amplified DNA molecules in each cycle. So after the first step you have 10 molecules, after the second 20, the third 50 and so on. The formula for the calculation is:
n × 2cycles = number of molecules
n is the number of molecules you start your PCR with, cycles is the number of cycles used.
In your case this would be: 5 × 26 = 320 molecules of DNA.

hmmm so it goes 10, 20, then 50? How does it go to 50 for the third cycle?

No. It goes: 10 - 20 - 40 - 80 - 160 - 320. You double the amount of DNA molecules in each step, you are not adding them up.

so in the first cycle the 5 turns to 10? and then you start doubling it up? btw the formula up there I can't seem to find it on the internet, did your teacher teach it?

Yes, since you start with 5 DNA molecules, the first round goes up to 10.


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What percent of the population has some form of synesthesia?
Data I am trying to get my hands on:

What types of synesthesia (e.g. Grapheme-color synesthesia,  Chromesthesia, etc.) are most common across the population?
What percent of population has that type of synesthesia?

It would also be great if there's geographical (genealogical) data on what types of synesthesia are more common to what areas.
What percent of the population has what type of synesthesia?

The phenomenon
Synesthesia is a neurological phenomenon in which a stimulus in one sensory or cognitive pathway triggers an experience in another.  Some hallmarks:1

It tends to be developmental, arising early in childhood.
It is involuntary.
It is stable over time (i.e. the same stimulus leads to the same sensory experience).

Epidemiology
The best paper I found on the issue is by Simner et al, 2006.2 The authors first review prior literature on the topic and then describe their own methodology and study addressing the question of prevalence. Regarding prior research:

Estimates of the prevalence of synesthesia have diverged widely....estimates range from 1 in 4.....to 1 in 25000 - 100 000.

Not so helpful.
They point out some problems with prior studies: one group of surveys relied on self-referral and made the (conservative) assumption that all non-responders to an invitation to participate were non-synesthetes. Another set of studies avoided this problem by questioning every member of a participant pool but established the prevalence only “subjectively” (their wording, although I note that this is an inherently subjective phenomenon!).
Simner's own group used a validated survey questionnaire about specific synesthetic experiences (the specificity and prior validation of this overcoming the  "subjective" aspect in their view). They found an overall prevalence of 4.4% for any type of synesthesia. Importantly, the male: female ratio was not significantly different from 1 in this group, in contrast to many prior studies which have found a marked female predominance, ranging from 2:1 to 5:1 (references in Simner's paper for those interested).
Modalities of experience
To address your question about the types of sensory experience involved, I turn to a more recent review article1 that compiled results from multiple studies. In this report, grapheme-color type synesthesia was most common (86%). These participants see a number or letter and experience a particular color in association. This was followed by followed by time-space type (62%), a group who associates units of time with a particular space relative to their body.  The third most common was music-color type (41%), which is fairly straightforward. The majority experienced more than one type (clearly, given the percentages).
Here is a graph showing the percentage of the cohort who reported particular synesthetic experiences, grouped according to the category of inducer:

Note that the most common type mentioned above, grapheme-color, includes all three of the first categories - "digits," "letters," and  "words" on this graph. Although only the inducers are listed here, the most common associated perceptions were indeed color (97%), followed by spatial configurations (62%). In most cases the color was static (73%) but in some people it moved in a specific direction (16%).

Niccolai V1, Jennes J, Stoerig P, Van Leeuwen TM. Modality and variability of synesthetic experience. Am J Psychol. 2012 Spring;125(1):81-94.
Simner J1, Mulvenna C, Sagiv N, Tsakanikos E, Witherby SA, Fraser C, Scott K, Ward J. Synaesthesia: the prevalence of atypical cross-modal experiences. Perception. 2006;35(8):1024-33.


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How long does it take for a cricket to die at subzero temperatures?
I am on a number of reptile groups and I often hear freezing recommended as a humane way to get rid of surplus feeder insects.
However, they can also revive if you don't leave them in there long enough.
If I had a bag of crickets and put them in the freezer, how long would it take for them to die in this way?

The actual paper that the linked article cites never mentioned about freezing the crickets:

We examined CCR (Chill Coma Recovery) in G. pennsylvanicus exposed to 0 °C. The time
  required for crickets to recover movement of the abdomen and legs
  increased exponentially with the duration of exposure to 0 °C; after
  more than 12 h of cold exposure, recovery time reached a plateau at
  ca. 15 min

And this is how CCR is performed

A total of 60 crickets were placed individually into 14-mL plastic
  tubes and cooled from 25 °C at 0.25 °C⋅min−1 and held at 0 °C for 2–42
  h. At 2-h intervals (first 24 h), and every 6 h thereafter, four
  crickets were placed on their dorsum in a Petri dish at room
  temperature. Times of four indices of chill-coma recovery were
  recorded: (i) first foreleg movement, (ii) first hind leg movement,
  (iii) initiation of abdominal contractions (active ventilation), and
  (iv) righting. Foreleg and hind leg movement were identified as a
  coordinated directional movement of the limbs, distinct from twitches
  of the limbs observed during rewarming. If crickets had not righted
  within 3 h of removal from the cold, they were considered to have
  incurred chilling injury that precluded recovery.

So, the crickets were never actually subjected to subzero temperatures or freezing or even cold shocks.
How long it takes to die depends on the freezer temperature; based on personal experience I can say that they die in ~10min @ -20⁰C.
Didn't find much information on crickets but according to this paper Drosophila will die in less than 2 hours at -5⁰C upon transferring them to the cold temperature directly (cold shock). However, if the larvae are "hardened" by keeping at +5⁰C before cold shock, their survival chance increased — the temperature required for killing them in 2h (Lowest Lethal Temperature) reduced. Now cricket is bigger than Drosophila but the surface area is also higher. I cannot do more than speculate at this moment (you can apply complex heat transfer equations and see how the rate changes with the size).

Thanks, that's useful info. Obviously completely different conditions to simply throwing them in the freezer then.

@starsplusplus yes. That would subject them to cold shock and they would die sooner. Also, during freezing the tissues would be damaged; they won't come back to life (very few organisms can tolerate freezing; they produce cryoprotectants). Please accept the answer if it answers the query (the tick on the left). You can upvote as well if you found it useful.

I found the information you provided helpful because it addressed the fallacies in the article's reporting of the paper. However, my actual question was "How long do crickets take to die?" and you only have a single line addressing that which is based on personal experience. If you could expand on that and preferably include some references I would be happy to upvote. :)

I also prefer to leave it a couple of days before accepting an answer, so as not to discourage further answers. I've seen this encouraged on multiple SEs for that reason; hope you don't mind.

I used your answer in a footnote to my other answer here and credited you.


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How was the resemblance between apes and humans explained in pre-Darwinian biology?
Humans and apes have somewhat obvious similarities, these must have been apparent to natural philosophers before the possibility of a common ancestry was first proposed in the mid-1800's. These proposals were not formally made in Darwin's On the Origin of Species (1859), but his general ideas of common ancestry were built upon in Thomas Huxley's Evidence as to Man's Place in Nature (1863) and then Darwin's The Descent of Man (1871).
How was the resemblance between apes and humans explained prior to this shift in thinking?

The time before Darwinism, people believed life as an entity which is created rather evolved. But there were great biologists interested in the relationship between species, who deliberately thought of evolution ideas and some of them believed in ape-human similarities and placed humans and apes in same group.

In 1699, Edward Tyson, an English anatomist, dissected an ape specimen(chimpanzee) and showed that its anatomy closely approaches ours.But he didn't established any relationships between humans and apes. It was first done in 1738 by Swedish scientist  Linnaeus in his book Systema Naturae .After that in 1759, Lamarck, a French naturalist  who was Darwin's predecessor in general theory of evolution, stated that humans were derived from up-right walking apes.

In 1759, just half a century before Darwin was born and precisely one hundred years before he published his famous book , "Origin of Species", Linnaeus, the great Swedish scientist, discovered that man was a mammal. He then placed man in the Order of primates, which means literary the first, or the highest,order of mammals.It comprises all the monkey like forms, including the man-like apes.
  Reference

References
Primate Evolution and Human Origins - Russel L. Ciochon & John G.Fleagle
Human Evolution: A Guide to the Debates - Brian Regal

It seems Aristotle discovered this prior to Linnaeus: "The monkey, as has been observed, is furnished with a tail. In all such creatures the internal organs are found under dissection to correspond to those of man." (Historia Animalium II.9, courtesy this comment).

Richard Owen, a leading British naturalist noted for his opposition to Darwinian evolution, defended a form of "Old Earth creationism" where an intelligent agent has its designs continually improved over long periods of time. Common features were not the result of common ancestry, but common design.

The concept of evolution was widespread even before Darwin. For instance, Linnaeus, Lamarck and Erasmus Darwin (C. Darwin's grandfather) all expressed evolutionary ideas.
Another interesting example is the German philosopher Immanuel Kant, which appears to have had rather well-developed ideas about evolutionary change, a common origin of life, that also included humans:

The agreement of so many genera of animals in a certain common schema, which appears to be fundamental not only in the structure of their bones but also in the disposition of their remaining parts,—so that with an admirable simplicity of original outline, a great variety of species has been produced by the shortening of one member and the lengthening of another, the involution of this part and the evolution of that,—allows a ray of hope, however faint, to penetrate into our minds, that here something may be accomplished by the aid of the principle of the mechanism of nature (without which there can be no natural science in general). This analogy of forms, which with all their differences seem to have been produced according to a common original type, strengthens our suspicions of an actual relationship between them in their production from a common parent, through the gradual approximation of one animal-genus to another—from those in which the principle of purposes seems to be best authenticated, i.e. from man, down to the polype, and again from this down to mosses and lichens, and finally to the lowest stage of nature noticeable by us, viz. to crude matter. And so the whole Technic of nature, which is so incomprehensible to us in organised beings that we believe ourselves compelled to think a different principle for it, seems to be derived from matter and its powers according to mechanical laws (like those by which it works in the formation of crystals).

(from: Kant. 1790. Critique of Judgment, MacMillian 1914 (translated by Bernard), https://www.gutenberg.org/ebooks/48433)

In contrast, Immanuel Kant found abiogenesis quite absurd and contrary to reason, according to the book "Life's Ratchet: How molecular machines extract order from chaos".


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Why are nausea and dizziness such common side effects from medication?
Why are nausea and dizziness such common side effects from medication?  If you go through your medicine cabinet and look at side effects, those might just be on every single bottle.  Is there some system in the human body that is very sensitive to any disturbance and causes nausea and dizziness?

This is very broad. Can you narrow it a bit down by naming specific medications? Additionally you have to understand that the information sheets provided by the companies are not medical, but legal information sheets. They have to name every side effect which occurs in a certain time frame after the intake.

I don't know I think the question is meant to be broad. An answer addressing the pathophysiology of these symptoms could have merit

Some medications because they are taken orally do cause nausea. Many medications, because they have an effect on blood pressure, or are central acting in some way, do cause dizziness. However, nausea and dizziness in particular are two highly subjective symptoms which are difficult to quantitate or verify, and which can occur with simple anxiety or stress. Several more such highly subjective and difficult-to-verify symptoms are numbness, tingling, headache, insomnia, fatigue and difficulty concentrating, all of which can be brought on by stress.
Switching for a moment to a drug with a measurable side effect of beta-blockers: erectile dysfunction (ED). In a study of men treated with beta blockers, the patients were separated into three groups with the following results:
a) the group who were not told the name of the medicine nor informed of the ED side effect had the lowest incidence of ED (3.1%)
b) the group who were told the name of the medicine but not informed about the ED side effect had a 15.6% incidence of ED
c) the group who were told the name of the medicine and informed of the ED side effect had the highest incidence of ED (31.2%)
Hypervigilance is an increase in attention to bodily cues or symptoms for any reason. It has been well documented in many studies that if you give one group of people a list of possible negative side effects, and another group a list of possible beneficial effects, then give both groups placebos (usually a small coated sugar or cornstarch tablet), the first group will experience negative effects while the second will feel better. The negative expectation producing a negative side effect is called the nocebo effect (the opposite of the placebo effect).
Interestingly, recent studies where anti-anxiety medications were administered before the nocebo dramatically decreased the nocebo effect.
For ethical reasons, in all clinical trials of drugs, patients in the treatment group and the placebo group must be given an extensive list (standardized) of possible negative side effects, introducing a negative expectation into both populations.
Two of the most common negative side effects in both groups are dizziness and nausea. Therefore, they must be reported as possibly occurring side effects with the medication.
This is not to say we're all imagining things. Nocebo effects have been correllated with reproducible effects on functional MRIs. They have a basis in reality, even if it's caused by negative expectations.
It's a problem being discussed a lot now by medical ethicists.
The influence of the nocebo effect in clinical trials
Avoiding Nocebo Effects to Optimize Treatment Outcome

anongoodnurse's answer is very thorough, but I would like to add one additional thing:
Nausea is in many ways the body's "default reaction" to anything being out of order with the body's chemistry; since most such things would once have been caused, the vast majority of the time of the time, by eating something toxic (or at least biologically active, and therefore probably toxic in large doses), which means that regurgitating stomach contents had a decent chance to expel the toxin and therefore save the person's life.
Because the effects of the medication are fairly light compared to toxic doses, the body rarely goes as far as actually throwing up (although people on prophylactic antiretrovirals, as one example, may disagree); the stimulus to do so is weak, so we feel only weak to moderate nausea rather than nausea strong enough to throw up.


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Does physical exercise following lack of sleep increase the risk of sudden cardiac death (SCD)?
Is there any scientific evidence supporting the hypothesis that physical exercise following lack of sleep increases the risk of sudden cardiac death (SCD)?
The only relevant research I could find is: Reddy PR, Reinier K, Singh T, et al. Physical activity as a trigger of sudden cardiac arrest: The Oregon Sudden Unexpected Death Study. International journal of cardiology 2009;131(3):345-349. doi:10.1016/j.ijcard.2007.10.024. However, it only points out that 5% of the SCD cases in the sample took place during vigorous physical activity, which does not directly answer my question.
I am not a biology professional, so please pardon me for any misunderstanding, and, when possible and reasonable, please avoid using too many biological jargons in the answer.

The closest I found: Acute sleep deprivation is associated with increased QT dispersion in healthy young adults. A surrogate endpoint, but a plausible one given that long QT is one of the more common causes of SCD during exercise. Research in the general population using the endpoint of SCD itself is nearly always retrospective and plagued by reporting bias.

I am probably not the best person to answer this, but I know of someone who had heart issues while training for a marathon while working long hours as a white collar worker. He also had trouble falling asleep a lot, even if he was feeling tired. This was probably because he was so pumped up at the time. He told me that sleep exercises helped him though..

Sleep is an important aspect of our life. Sleep disorders are acute due to their effects in physiological and mental health of a person.Sleep occupies nearly 30% of our daily life and people were gradually decreasing the sleep time in order to adjust their busy schedule. According to the United States National Sleep Foundation, adults need to sleep 7-9 hours each night. The decrease in sleep time contribute mostly towards cardiovascular disease, including hypertension, coronary artery disease(CAD),risk of arrhythmia, stroke etc.
The circadian and dirurnal rhythms influence the neural circulatory control causing the changes in heart rate, vascular tone and blood pressure. The REM(Rapid Eye Movement)sleep and nonREM sleep affects the cardiovascular system. Researchers found it important that normal sleep is a complex and dynamic process with profound effects on cardiovascular homeostasis.
Insufficient sleep is a stress stimulator that acts through the sympathetic nervous system elicit changes in blood pressure, heart rate and barroreflex setpoint.
Sleep deprivation is a state of having less or no sleep which is a major reason for cardiovascular diseases.Which may cause
Inflammation
Cardiovascular disease is mainly driven by atherothrombosis, which is an inflammatory process. Increased levels of C-reactive protein(CRP) and interleukin-6(IL6) have been implicated as the predictors of cardiovascular disease risk.Both CRP and IL6 have been found elevated in both totally and partially sleep-deprived subjects.Inflammatory cells such as monocytes and neutrophils were also found to be elevated during acute sleep deprivation, supporting that sleep deprivation is an inflammatory process.
Endothelial Dysfunction
Endothelial Dysfunction has been reported after a combination of sleep deprivation and stress, also increased heart rate, blood pressure are reported in sleep deprived subjects may result in Endothelial Dysfunction.
Hypertension and Stress
Hyper tension and stress hormones are released by the body when lack of sleep occurs, this results in elevated bloop pressure and may lead to CAD.
CardioArtery Disease
The American Cancer Society , the Almeda County study and Partinen also showed an increased risk of CAD in subjects who reported sleeping 4-6 hours a day.
Diabetes Mellitus(DM)
Diabetes Mellitus is a major risk factor for CAD and it has been underlined from several studies across past decades that sleeplessness can result in DM.

A sudden cardiac death is highly probable for a person who follows increased physical exercise and decreased sleep durations. For a sleep deprived person the risk of cardiac diseases are so high, then for some one who spend lot of time exercising can cause chronic cardiac problems. Physical exercise and over training can cause more stress hormones and increased heart rates, these factors along with prolonged sleep deprivation can cause serious cardiac diseases or even sudden cardiac death.

Levels of cortisol (the "stress" hormone) are elevated for long periods of time.
The body spends more time in a catabolic state than an anabolic state (perhaps as a result of elevated cortisol levels).
Excessive strain to the nervous system during training.
http://en.wikipedia.org/wiki/Overtraining

References

Critical Care Nursing: Synergy for Optimal Outcomes - Roberta Kaplow
Sleep Deprivation and Disease: Effects on the Body, Brain and Behavior - Matt T. Bianchi

You've brought in some interesting theoretical reasons why one might wonder about an association between sleep deprivation and SCD, but to my knowledge this research has been either 1) in chronic sleep deprivation (CAD, DM, HTN) or 2) in acute sleep deprivation using surrogate endpoints (cytokines, HTN - though the latter is certainly a good surrogate). To conclude that A sudden cardiac death is highly probable... for the OPs scenario of exercise after acute sleep deprivation seems like a leap.

@Susan:I have edited to "prolonged sleep deprivation", I personally know cases of SCD due to heavy exercise and lack of sleep. I have claimed that "highly probable" not always possible. So its really a highly risk situation for a person following these appetites. Thank you for your valuable suggestions.


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Long-term effects of antihistamines on mind and CNS
Can maybe someone share knowledge or guesses on the following questions:

Does the prolonged use of antihistamines cause long-term effects on mind or CNS?
Are there any known evidences of their influence of formation of CNS or personality when taken at a young age?
Generation-II antihistamines are said to be next to devoid of sedative effects since they selectively block just the H1-receptors. However, they are reportedly potentially mind-altering. How is this possible?

This question appears to be off-topic because it is not really a biology question

@GriffinEvo: can you suggest a more suitable stack exchange site? I have not found a site on biochemistry or anything more suitable...?

Not really - it's medical and there's no stack exchange site for that. I know it's not personal medical advice,  but it's not really a question of biology either

@GriffinEvo: yes, well, I agree.. sad but discussion on "medical" SE site has faded out: http://meta.stackexchange.com/questions/229495/stack-exchange-website-for-medical-questions ... well, maybe it is possible to move this question to http://cogsci.stackexchange.com/ ? does it seem more appropriate?

I think a medical SE is untenable because it generates a lot of risks - the people answering questions and offering medical advice aren't necessarily medical professionals, there's a lot of people out there looking to take advantage of those in need and a lot of people offering incorrect advice (with good intention) which might prevent someone from getting the correct treatment.

@GriffinEvo: what do you think about moving this question to cogsci SE site? If you think this could be done, then how can I do this?

I think the Mods have to do migrations - @kmm ?

@GriffinEvo: also, maybe you could propose a more appropriate site (not an SE site) to ask this? I am not into biosciences myself, so I do not know that segment of internet very well, but maybe you have some clue... I would really appreciate an advice since the question is important to me and is persisting in me for several years already.

These questions are ok for me but cannot answer them at the moment. Voted to reopen. However, very big chunk here and too much side tracked. You could reformulate your questions since the pharmacological sides of antihistamines are well known. All antihistamines pass BBB (1st gen most, 2nd gen less while 3rd gen very very little because antimetabolite of 2nd gen). These are Pharmacodynamic! Histamine can be released from all tissues ("hist"). So the drug primarily affects in all your tissues. Long-term effects have not been studied in no standardised situation. Immunosuppressed case neither.

I think you should split this question to many separate questions and then provide links between them: Ph.dyn antihistamines, their penetration of BBB and Pharmacology; long-term study about Ph.dyn antihistamine (take 2nd gen etc cetirizine) and Epidemiology in some standardised setting; same long-term study with some immunosuppressed patients; effect of 2nd gen antihistamines on cognition ... (think some parameter); etc. Personal medical advices are not provided in this site, since there are so many factors which we cannot consider publicly here and many other reasons too.

@GriffinEvo cogsci says it's off topic there too because of the personal medical orientation. I think it would be fine here or there (1) as separate questions and (2) as more general scientific questions as opposed to personal experience.

I edited and removed any personal info and basically stripped it down to a few sentences. The questions, however, are very broad and it may now be nominated for re-closure, if re-opened, but I think it deserves a chance.

And actually, the nature of the question may make it suitable for Cognitive Sciences SE. Specifically, question 2 could be deleted here and re-posted on Cognitive Sciences SE? This would kind of narrow down the question here as well.

Good edits so far, some comments though: The third questions suits Skeptics SE better (and if you insist on posting it here I want a source for "However, they are reportedly potentially mind-altering." and it should be a second separate post). The first and second are ok questions for here but may be better served by splitting in to two separate posts.


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Long term storage of agarose-ethidium bromide gels that have already been cast
I have come up with what I thought was a clever idea: Store the agarose gels I pour, and only cut as many lanes as I need to run later, minimizing wasted agarose (and wasted effort/time) when I need to make many electrophereses using a small number of lanes.
I realized that over time, the EtBr would diffuse out of my gel into the buffer that the gels are kept in. Since I add 2 µl of EtBr to 50 ml gel, and the gels were kept in 400 ml TAE buffer, I added 16 µl EtBr to the buffer, reasoning that now concentrations are equal and no net diffusion will take place.
However, after several weeks, I noticed that the EtBr signal from the gel is severely weakened. What can I do to fix this? I can see the following options:

Use higher concentration of EtBr in the buffer (how much?)
Change buffer weekly, adding fresh EtBr every time
Cover the transparent container with aluminum foil to prevent hypothetical photobleaching

Which one is most likely to solve my problem? Should I just give up, and throw away gels that are older than a day or two (I want to avoid this option, because of the record keeping needed to track when the gel was last made)?

What I've seen is to keep a bottle of agarose gel, then heat it up to melt, pour what you need into a gel caster, add your ethidium. This way your large gel stock doesn't get contaminated with ethidium and you don't have to worry about loss of ethidium signal.

@user137 I am saving cast gels in order to avoid the hassle of melting and casting a gel everytime I want to run some samples. The bottle of agarose only saves me the work of weighing the agarose, which is quite insignificant in comparison.

did you see a reduced signal using the same DNA conc or construct after running it several weeks later in a gel containing no previously run DNA band? I think EtBr can photo bleach so just use fresh buffer with fresh EtBr. Even with a stock EtBr you are meant to wrap it around foil! Old gels are generally not good since they can become quite hard and fragile in my experience so using fresh gels is always best.

@Superbest You could store pre-cast gels without ethidium and then post-stain, but you'd end up with more ethidium waste to worry about.

@Bez Yes - what I do is, first make a gel with normal EtBr and wells etc., then put the gel into TAE buffer with EtBr in the buffer, keep it there for a few weeks, run. I'm comparing equal amounts of ladder, and it seems like my signal from a two week or so old gel is maybe 30% of a fresh (or 1-2 days old) one.

@user137 Yes, also an option. However, I want to specifically "pre-stain" - ie, apply EtBr after the gel is fully cast and ready to use, but before it is actually loaded with DNA. I am only asking how to accomplish this with minimal signal loss (your suggestions make sense - but which ones do I actually need to do?). If it is impossible, a good explanation for why would also be acceptable.

I have been told in order to maintain a gel I should keep it in a cold and dark place wrapped around a wet towel! But I think its the photo-bleaching which is the problem! so soak it in new buffer with fresh EtBr after you run your samples. Didn't you start getting mould in your buffer with gel in it for weeks?

Come on @Superbest it takes an insignificant amount of time to weigh and pour gels. Pour it before you settle down to check mails or facebook :P

@Superbest see my answer I've had to work through this before. Also if you are trying to save gels after they have been run you can use a gel dryer (one of those food vac bag kitchen utensils you can buy at Target work just as well as the $5000 commercial gel dryers fyi

@WYSIWYG true this is trivial but if your prepping a lot of gels like for 400 students for an undergrad teaching lab, it's a lot easier to cast them, cut them and store them.

To increase storage life: after gel solidifies, dampen it with running buffer. Wrap the gel in polyvinyl chloride. Place in plastic container with a lid. Store in fridge in dark. It will last for a year as long as you re-dampen it with buffer each time you access it. Don't keep it submerged in buffer as the etbr will diffuse out. this is probably the cause of your problem. Notice when you order precast gels (either agarose or acrylamide) they are sealed and only a small vol of buffer is added to keep it hydrated. Additionally, the etbr and EDTA in the buffer helps prevent most mold growth although I have seen black mold grow a few times at around a year.
You can always spike the buffer with etbr adding it directly to the electrophoresis chamber before you run the gel (etbr doesn't even need to even be in the gel for it to work) although I find you get a little more sensitivity with the etbr in the gel. If you spike it be sure to mix and let it sit for about 20 min for the etbr to diffuse.
If you are trying to cut down on cost you are probably using a higher grade agarose than you really need for the application your doing so I would take a look at that
If you end up needing to store gels for rna work, add plain old Clorox bleach to a final concentration of 1% to your TAE gel just after microwaving. It sounds crazy but it works extremely well. You will completely inhibit RNAse and your rna bands will look nice!!!. The bleach also helps  with storage of the gel.

OP has already stated that the concentrations of EtBr inside and outside the gel are identical.

@MarchHo To be sure, just because they are identical doesn't mean there will be no net diffusion.

I can confirm storage of the bleach gel as well - not only that, but despite not taking care to keep the bleach gel away from RNAse contaminants (keeping in the same box as normal gels, dirty electrophoresis tank) my RNA ran and stained just fine.

I think I have some evidence that the key factor is light.
Since asking this question, I changed the buffer for fresh TAE-EtBr (same concentration as in my gels) moved my gels from a well-lit area into a closed, opaque box so that they remain in darkness. After 1 week, I ran equal amounts of my ladder in the stored gel, as well as a fresh gel. The results (old gel on left, new gel on right) show very little difference in signal - I conclude that blocking the light is sufficient.

I'm not quite sure what you are doing. Are you running the whole gel each time and cutting off the lanes you've used, or only putting the lanes you desire into the tank and leaving the rest outside?
If the former then the ethidium bromide will be leaching out of the gel because it is positively charged so each time you apply a current to it some of it leaves.
If the latter, I'm not sure why you are storing your gel in buffer at all. Wrap it in clingfilm to stop it drying out and store it away from UV light to avoid the ethidium degrading.
Frankly, however, I'm not sure why you think this will be a big timesaver? You can store pre-melted agarose with ethidium bromide added for a period of weeks and pouring a fresh gel doesn't take a significant amount of time.

It's the latter. I have a big gel stored in a container (easier to open and close than film), and I cut off lanes I need and run only those lanes.

authors: Ольга Фарина


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Is this a carpenter ant?
I stumbled upon a few hundred of these swarming around two different places in my living room today. They kind of look like a carpenter ant to me, but I'm not sure.
Also, I'd love to know how you identified the ant.
// EDIT, per a helpful suggestion, I'm in Los Angeles, CA, US. We just had rain come through within the last 4-5 days and it has since dried up.

Welcome to biology stack exchange. With insect identifcation it often helps to know a little about your geographic location.

No, this is not a carpenter ant...it's possibly a Pavement Ant (Tetramorium
caespitum) - only it's a male & hence winged....for identification...follow these guidelines-

Pavement ant workers are small, l/8-inch to 3/16-inch
  long, and blackish brown with light-colored legs and two spines at the
  end of the thorax. A distinguishing character, visible with a hand
  lens or microscope, is the series of fine parallel groves on the head
  and thorax

This is completely wrong. It cannot be a Tetramorium because there is no post-petiole between the thorax and the abdomen, and it is not a male but a queen as you can deduce by the absence of external reproductive organs at the end of the abdomen and by the fact the the head is fully developed with eyes relatively small compared to the head and mandibles entirely developed. The concave thorax indicates that this ant is from the genus Camponotus, also known as carpenter ants.

Hymenoptera, Formicidae, Formicinae, Camponotus sp (queen). "Carpenter ant"
The unique segment between the thorax and the abdomen indicate this ant is in the subfamily Formicinae; the color pattern, the shiny cuticle and the concave thorax indicate this ant is from the genus Camponotus. It has wings so it is either a queen or a male, and you can exclude that this a male by the absence of external reproductive organs at the end of the abdomen and by the fact the the head is fully developed with eyes relatively small compared to the head and mandibles entirely developed.


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Deeper Learning in Physiology?
I am a Pharmacology and Toxicology major at a large state school. I was only required to take physics I and II. (algebra based)
At first I thought that was fine, but I soon began to realize that I can't just memorize like my professor and book asks me too, but I need to go in-depth.
So my question is this, I am looking for a way to learn the "physics and chemistry behind physiology" or deeper that what we are taught?
For example, say we are taught that atherosclerosis can cause aneurysms and that aneurysms can rupture.
But what we aren't taught is that blood flow through a closed vessel is constant, so any dilatation in the mid-length will increase the cross-sectional area and decrease the fluid velocity to maintain flow.
In accordance with Bernoulli's principle, the decrease in velocity is met with an increase in pressure, which increases wall tension. Vessel integrity is already compromised from the three layer degradation. So now you start to see this great positive feedback loop whereby atherosclerosis damages the vessel wall causing it to dilate, which increases the pressure, which causes it to dilate further, which damages the vessel wall further, etc, etc, until the aneurysm finally ruptures. (I did not write this example, but it is an example of how I would like to learn it.  I would like to know how the author of that explanation came to that conclusion or what kind of book would explain in heavy detail.)
The question I am asking how can I learn the "science" behind the physiology?  I'm a type of learner that needs to know the how and why.  Will I need to take more physics classes?
** Sorry if I posted in the wrong section, I am new to stack exchange!

It is very easy, use google + pathophysiology and read some articles in the actual topic. There are a lot of pathophysiology books as well (some of them pretty expensive). Another way to do an online course.
Just a simple search about your example:

It is known that AAAs are characterized by destruction of elastin and
  collagen in the media and adventitia, loss of medial smooth muscle
  cells with thinning of the vessel wall, and transmural infiltration of
  lymphocytes and macrophages. Atherosclerosis is a common underlying
  feature of aneurysms. However, atherosclerosis is not the primary
  driving factor in the development of AAAs. Atherosclerosis is a
  disease that is widespread throughout the vasculature, however
  aneurysms only form in specific locations and only in certain
  individuals. Additionally, atherosclerosis is primarily a disease of
  the intima, while aneurysm formation primarily affects the media and
  adventitia.

2009 - The Pathogenesis of Abdominal Aortic Aneurysms


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Hydrophobia Outside of Rabies?

RELATED:
Why does rabies cause hydrophobia?
Agony, Hydrophobia and viruses in the light of evolutionary principles

Has hydrophobia been found outside of rabies?
I have only seen it being mentioned as a symptom of rabies.

You are correct that hydrophobia is often considered pathognomonic of rabies. However, I offer for your consideration:
Hydrophobia as a rare presentation of Cotard's syndrome: a case report.1
Cotard's syndrome itself is a bizarre psychiatric condition that the authors of the above paper define well:

Cotard’s syndrome is a rare condition where the central symptom is a nihilistic delusion, which, in its complete form, leads the patient to deny his own existence and that of the external world.

The patient described in this case report harbored delusions that his internal organs were shrinking. He asserted that his abdomen would rupture if he internalized anything. The hydrophobia was secondary to this concern. When given a glass of water he showed a panic reaction and attempted to keep away. Orientation and memory remained intact.
The authors go to length to point out that this was not, in fact, a case of rabies (as thought that were in question at this point!). Also, the patient himself was not aware of symptoms of rabies, ruling out "rabies hysteria" (a hypochondriacal delusion that one has rabies).
Hydrophobia, then, is a rare manifestation of a rare psychiatric disease in addition to the more frequent and well-known association with rabies.

1. Nejad AG. Acta Psychiatr Scand. 2002 Aug;106(2):156-8; discussion 158.

Hydrophobia is mostly attributed to rabies, most of the sources refer rabies as hydrophobia. Technically Hydrophobia is the intense fear of water.

Hydrophobia is an intense, irrational fear of water that can be commonly diagnosed at childhood and should be treated as soon as possible. Certain types of hydrophobia may also appear in later stages of contracting rabies, which would require treatment on an immediate basis.

Also the Wikipedia link for Rabies states that

Signs and symptoms may soon expand to slight or partial paralysis, anxiety, insomnia, confusion, agitation, abnormal behavior, paranoia, terror, and hallucinations, progressing to delirium. The person may have hydrophobia.

So rabies and hydrophobia are distinct and hydrophobia is a symptom of rabies.

Hydrophobia may, however, more readly be confronted with hysteria, acute mania and tetanus.

Hydrophobia is incidental to other diseases, it can be observed, occassionally, in tetanus,hysteria,cynanche,tonsillaris,tracheitis and certain inflammations in stomach. Tetanus is strongly believed to cause intense hydrophobia conditions.How ever, there is always a belief of hydrophobia linked with rabies.

The pathology of Hydrophobia and Tetanus is found to have great similarities and there is a great similarity in the distribution of lesion in the central nervous system as well as a certain analogy in the kind of lesion. The special localization of symptoms of both disease, in the tongue,throat and neck was associated with the special prevalence of the lesions in the medulla oblongata and especially in the neighborhood of the nuclei in the fourth ventricle etc.
Reference :THE Medical Times and Gazette - J & A Churchill

So it is possible to cause hydrophobic conditions when Tetanus is affected and also hydrophobia can occur from mental disorders.


text:
Why estimate linear and full (linear, quadratic, and correlational) selection coefficients separately?

"We then fitted a linear regression including all three life-history
  traits to estimate the vector of linear selection gradients, β, for
  each sex (Lande and Arnold 1983). A quadratic regression model
  incorporating all linear, quadratic, and cross-product terms was then
  used to estimate the matrix of nonlinear selection gradients, γ, for
  each sex. "

This is from the paper Evidence for strong intralocus sexual conflict in the Indian meal moth, Ploida interpunctella. I am not sure why they estimate these gradients separetly rather than taking them just from the one full model - any suggestions? Is this normal or have they done it for a reason?
For some similar work see these two papers:

Gosden et al which seems to use only the linear gradients from one model with sex as an effect.
Stearns et al which uses linear, quadratic and correlational estimated from one multiple regressions model per sex (similar to the main paper I cite first but not using a linear terms only model for the linear coefficient).

I have mailed the corresponding author on the quoted paper to ask why, I will let you know what he says if he replies

This is directly following the advice of Lande & Arnold (1983), saying:

Linear multiple
  regression can be used first to estimate the forces of directional selection, $\beta$, and their standard errors. Then a quadratic multiple regression (16) or (Al), can be used to estimate the forces of stabilizing selection, $\gamma$, with their standard errors. The regression (16) provides the best quadratic approximation to the selective surface (although valid estimates of $\beta$ can be obtained
  only from a purely linear regression, or by using the orthogonal regression (Al)).

The reason is that the estimates of direction selection is influenced by the higher order terms in the full model that includes quadratic and correlational selection, and the linear model therefore has the best estimates of the change in mean value over a generation of selection ($s = \bar{z}_{after} - \bar{z}_{before}$). However, the full model is the better representation of the fitness surface. There are also other methods to approximate the fitness surface.
For the record, I used the same approach in my master's thesis many years ago.

Thanks - what did you do your masters thesis on and who with? (I did mine on multivariate nonlinear selection in a secondary sexual trait hence I should have known the answer to the above, it's just been too long!) Talk in chat?

Actually, after rereading the Lande Arnold paper, this will be problematic only "If the character distribution before selection displays multivariate skewness (non- zero third moments), the linear and quadratic terms are correlated and estimates of β, depend on whether or not the quadratic terms are included in the regression." Thus, if I understand correctly, you can use orthogonal polynomials using poly(x,2) in R or run a model with only the linear and a second model with both the linear and the quadratic term. Is that correct?

The third moment in the sentence means the skewness. Does that mean the same thing as covariance = 0?


text:
Are more animal species edible than plants?
While grocery shopping I was thinking that we restrict ourselves in regard to which animals we eat. I surely don't want to eat spiders and ants, for example, but I know that this is just because of my upbringing. But a lot of plants are actually inedible. So, is my idea correct that we can eat far more animal species than plant species? And if so, why? The reasons why certain plants are inedible seem to me also as rather diverse, like most plants
developed their own special molecule(s) to avoid being eaten by us. :)
I would be interested in some more educated opinion on this thought than mine. Thx in advance.

It is estimated by some that on earth there are

7.77 million species (of which 953,434 have been described and cataloged) of animals
298,000 species (of which 215,644 have been described and cataloged) of plants
611,000 species (of which 43,271 have been described and cataloged) of fungi
36,400 species (of which 8,118 have been described and cataloged) of protozoa.

with 6.5 million species found on land and 2.2 million (about 25 percent of the total) dwelling in the ocean depths.[1][2]
Despite the existence of toxic plants and animals, from the numbers alone it is clear that there are more animal species we can eat than plant species.
This does not take into account population or individual sizes, just species.
[1] How Many Species Are There on Earth and in the Ocean?
[2] How many species on Earth? About 8.7 million, new estimate says


text:
Why do we have to exhale (or inhale) in order to speak?
Every time we speak, sing, or make any other kind of advanced noise with our throats, we exhale, or to put it that way, blow air through our throats. Why is this required? After all, speakers do not need any air blowing through them, they simply vibrate the air and create the vibrations (sounds) they're supposed to.
Why can't humans create (intelligible) sound just by having an organ that vibrates the air around us? Also, are there any animals that can? (None that I can think of at least). Would it be an evolutionary gain, or just rather pointless?
PS:
Obvoiusly we can clap out hands and the like, but that's not what I'm talking about.
Edit: The question is not about exhaling/inhaling, but rather why we need airflow in the first place; why we cannot use a mechanism similar to that of speakers.

Very similar to this but not quite a duplicate because I think this is asking about why the human voice box needs airflow to make sound, and why it isn't like a speaker.

Exactly. I know we can speak while inhaling (and sometimes I do it myself), but as you said: Why do we need airflow in the first place, why cannot we use a mechanism similar to that of speakers?

My guess is that is that our voice box is similar to a resonator. Our vocal chords provide vibrations at multiple frequencies and by adjusting our throat and mouth we change the resonant frequency and select the frequencies that are used to make voice. A simple speaker must be driven at whatever frequency you want, and while this is simple for electronics, it's probably harder for an evolved biological system. It was relatively simple to adapt the existing trachea for sound than to develop a biological speaker.

You can speak inhaling. It just sounds different.

As part of your question, you ask if other animals can create sound without continuous airflow. Many insects (e.g. cicadas and moths) do exactly this by using tymbals. A tymbal/timbal is an external membrane organ that is controlled by muscles or wing movements, that cause the membrane to flip back and forth, creating clicks or other sounds. So in many ways it produces sound in a similar way as loudspeakers, by creating sounds using a vibrating membrane.
One example can be found in this clip, which nicely shows how the organ functions:
Moth Making Sonar Jamming Sounds (youtube)
On this page (in Swedish) you can also listen to slowed-down butterfly sounds from four species.

Here is a list of woodwind instruments. Do you know of any (non-open) reed instrument that produces a note without anyone blowing air through them? Imagine a clarinet being played on someone's lap pouring out a melody. That would be very, very remarkable indeed.
Our ability to produce sound from our throats is in theory like a reed instrument  in music. Let's take the flute.
The flutist blows a rapid jet of air across the embouchure hole. In the flute, the air jet produces an oscillating (vibrating) component to the air flow. Once the air is vibrating, the energy is radiated as sound out of the end and any open holes. The column of air in the flute vibrates much more easily at some frequencies than at others (i.e. it resonates at certain frequencies). These resonances largely determine the playing frequency and thus the pitch, and the player in effect chooses the desired set of resonances by choosing a suitable combination of keys. (More on that here.)
Our vocal chords don't vibrate without the movement of air through them. They just tense and relax to different degrees. There is no sound made if you go through all the motions of saying yes but don't move any air. The moment you move even a small amount of air, you'll get a sound. Furthermore, vibration of the vocal chords is not enough for speech. The noise must go through a chamber where a particular noise will be made to change to resemble speech. Say ahhhhhh and touch the tip of your tongue to the roof of your mouth. The sound is changed significantly. Now, add your cheeks, lips, teeth, and pharynx all changing shapes and you have language.
Our voices are a wind instrument (not like an electronic speaker. For that, look to the electrolarynx). The air column moving across the vocal chords is the air jet. The vocal chords are what sets the air to vibrate. Our "mouth" (all of those I mentioned above" affect the vibrations to produce the desired sound. That's speech.

Would it be possible, and what would be the downsides/upsides of having a sound box functioning like a speaker, not a clarinette? Do we see any examples in the animal kingdom?

@Ludwik - that, to me, is a separate question. I did my best to answer it as written. ')

While appreciating your efforts, it seems to me the that I must have written badly. Re-reading my question, you're right, it does come across as a question about how our speech system works and why we need the airflow, but my intention was rather to ask why we didn't develop "speaker-like" speech boxes, and the upsides and downsides of that. On the other hand, I might ask that in a new question, if other people interpret my text the same way you did.

@Ludwik it is often hard to explain why something evolved one way and not another. But consider that when our far ancestors developed lungs for breathing air, they also got a windpipe with regular airflow. Transforming it into a wind instrument must have required minor changes, compared to evolving a new "speaker system" from scratch. So, we got our vocal chords because they were easy to get.


text:
Terrestrial Vertebrate Limbs
This question is regarding the conversation that took place here: Why don't mammals have more than 4 limbs?. I'm not sure if someone mentioned this and I just missed it, but everyone is talking about two pairs of limbs for all terrestrial vertebrates; what about the case of kangaroos? If we are analyzing this from a locomotion point of view, and tails are being considered limbs, then wouldn't the kangaroo be considered to have five? They use their tail for balance and to push forward in "walking" (not exactly a walk, but I am lacking the proper term at the moment), resting only on the tail and forelimbs as the hind limbs swing forward. Does anyone have thoughts on this?

This has recieved a fair amount of attention recently, as it made it into the lay press, Unique Among Animals, Kangaroos Use Tail as Fifth Leg, Scientists Find

I did not realize that was out there. Thank you for sharing that article!


text:
How does air-liquid interface (ALI) culture work?
For studying diseases, such as chronic obstructive pulmonary disease (COPD), cells are often grown in air liquid interface.
I understand that the common way of establishing this these days is to grow cells in culture well inserts with a permeable bottom, then put medium only in the well and not the insert.
Here is an image from Stemcell Technologies:

The last images implies that the level of the medium is just high enough to cover only the basal side of cells. Is this realistic? Given that the monolayer is a few microns thick, is it really just a matter of carefully pipetting just enough medium? It seems like the error of a pipette is too high for this.
In practice, I am getting the impression that the level of liquid is actually higher than the apical surface of the cells, but it is somehow prevented from seeping out of the well and into the insert. If so, how? The bottom of the insert is permeable; even if you grow cells to confluence, surely there will be a small hole or two somewhere which causes a leak?


text:
Cigarette consumption dose-response function WRT health outcomes
I'm curious how health risks (mortality, lifetime probability of cancer, etc) change with cigarette consumption.  Specifically, treatring cigarette consumption like a continuous variable, rather than a binary for "smokers" and "nonsmokers".  I've got access to academic literature, but I'm not a doctor or a PhD health researcher.  This article states in the abstract that the dose-response relationship between cigarettes and incidence of lung cancer is linear.  This website (CDC) states that "smokers" have a 25-fold increase in risk of lung cancer.
How to reconcile the two?  The latter reports odds ratios, which means that they did a logistic regression, which means that the raw logistic regression coefficient was 3.2.  If the average smoker smokes 20 cigarettes a day, and the dose-response relationship is linear, then the relative risk for someone who smokes one per day should be exp(0.32) = 1.37.  So someone who smokes one cigarette per day would be 1.37 times more likely to get lung cancer than someone who never smoked (on average).
Is this a reasonable estimate?  I can certainly understand why public health types wouldn't promote this sort of conclusion, as smoking one cigarette can be a slipper slope to smoking a lot more cigarettes.

Personal medical questions are off-topic here. Could you edit your question to remove those implications? See http://biology.stackexchange.com/help/on-topic

Its a general population-level question with personal interest.  But if it bothers you, I'll lose the last paragraph.


text:
Should I dilute DNA with water or elution buffer?
I've extracted DNA using a kit and final step is eluted with buffer. If I must dilute my DNA samples, do I use the same elution buffer or can I use milliq water?

Just a note, the Qiagen TE buffer has significant UV absorbance around 230nm. Been too long since I did that spectra to remember exactly how much or what wavelength, so just be aware of that if you need spectroscopic measurements of your DNA. Absorbance at 260nm should be fine.

I would generally recommend using the elution buffer (which is typically Tris-EDTA buffer) or TE-Buffer, as the pH and the conditions stabilize the DNA for a longer time, which is especially interesting when you want to store your DNA.
It also dependent on your downstream application - when they recommend diluting the sample in water (or another buffer) I would follow this advice. In my experience TE buffer is perfect for all molecularbiology applications (cloning, digestion, amplification, PCR, etc.). The EDTA will of course complex bivalent cations, but since the concentration in the buffer is only 1mM and the DNA solution is usually diluted further in PCR or digests, this plays no role in real life applications.

The Quiagen kits I'm familiar with explicitly state that you can use water instead of elution buffer for elution. The choice of continuing to use buffer or water is yours and depends on what you want to do with the DNA and whether the buffer interferes with later steps. Using the buffer is probably safer for long-term storage, but I don't know how much this really matters (I never had any problem storing DNA in water).
If you dilute with water you'll obviously end up with a weaker buffer that might not be able to keep the pH at the specified value. So if you need your DNA at the elution buffer pH, you shouldn't dilute it.

Just to add to the above responses, you are better off not use MQ because if it is contaminated with DNases, then it will digest your construct if it reaches room temperature or 37 oC as you are melting the frozen construct in your hand! TE-buffer is the standard buffer for DNA elusions but make sure your column is compatible with it. For transfection based experiments TE works fine for me!