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What is the effect of a pure-oxygen environment on a plant?
Just read What's the effect of oxygen deficit on plants? ; and wondered whether the opposite would have any effect on a plant.
That is to say, if a potted plant were placed under a bell-jar and the air within replaced by pure oxygen would the plant starve? If the environment/soil were loosely radioactive, would it make a difference?

why would radioactivity make a difference?

@RichardSmith: Guesswork on the radioactivity bit; wondering whether the combination of the environment in which cells are liable to uncontrolled change may be driven by an environment which threatens the survival of the plant as a whole.

Ask yourself, where would the plant take the carbon for construction of all kind of molecules, most important the cell membrane and cell wall of newly divided cells. Plants do not eat! So they have to get their carbon from somewhere else.

Liable to starve then, I guess ...

If the plant is potted, thre could be co2 from the soil, as well as from plant respiration. But at such high o2, photosynthesis would be inefficient.

As hinted in other answers, the key problem with a pure oxygen environment would be the inability to photosynthesise caused by the absence of carbon dioxide.
The overall equation for photosynthesis (the process in which energy from the sun is harnessed to fix inorganic carbon dioxide into organic molecules that  are of use to the plant) is:
6CO2 + 6H2O → 6O2 + C6H12O6
The carbon dioxide required for photosynthesis is obtained from the atmosphere by diffusion through stomata on the leaves.  Therefore if the atmosphere contains no carbon dioxide (i.e. in the scenario you suggest) photosynthesis would not progress, meaning glucose used by the plant in respiration would not be replaced.
This would eventually lead to the cessation of cellular respiration due to a lack of reactant.  This would cause the plant to die.

It leaves the possibility that glucose for respiration only is taken from the cell wall/membrane, something that e.g. Mycobacteriae actually do.

The plant could still photorespire which means it is unlikely to die. It's impossible for it to grow, but it won't die(right away, or maybe at all).

Keep in mind, there is a chance that a growing plant in a sealed environment with pure oxygen WOULD SURVIVE because of the carbon dioxide discharge of aerobic bacteria in the soil. Consider that by the time a seed would sprout, the soil bacteria would have already had days to a week to metabolize CO2 as a waste product. This question depends on manifold variables (chiefest of which dealing with the environment and especially the size of the biome).


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How does a new species survive without suffering inbreeding?
Just what the title states. The thought came from reading When has an organism evolved enough to be called a new species?
I'm probably wrong but I understand new species happen sporadically rather than in whole-sale lot during breeding season. Is the new species capable of breeding with members of its parent species? How does a new species survive inbreeding initially?

I guess you should define "species" first. It`s kinda tricky term and at least in my opinion "child species" overlap with "parent species", "sister species" and so on.

Well, speciation is a process, not a single event thing.
Usually what happens initially is geographic isolation of some members of a species, so in that sense the inbreeding is something that is influencing and you can also think of it as causing the speciation process. The presence of special harmless or semi-harmless disadvantagious mutations - which increases in frequency from this isolation - influences how the species is going to evolve, but eventually shapes this species to better cope adapt to some environment, or evolves the new species out of existence.

This is indeed a very good question, that I have spent a long time thinking about myself.  My take on this is that there is indeed a very close relationship between inbreeding and speciation, but that inbreeding actually PRECEDES speciation ! The key to this rather counter-intuitive point of view is that inbreeding actually has several advantages, including that of resulting in cleaner genomes in those offspring that survive inbreeding depression.
In populations that have high degrees of inbreeding, because of, for example, small sizes of populations, or high tendencies to self fertilisation, the recessive mutations that cause inbreeding depression will be progressively eliminated, and there will consequently be very little inbreeding depression.
In such a context, there will thus be no barrier to exploiting other advantages of inbreeding such as reducing the cost of sex, or keeping together advantageous gene combinations. Small groups of individuals would thus be better off breeding among one another than with the ancestral stock, leading to speciation.
If you are interested, or just intrigued, by this kind of concept, I invite you to read the rather long essay I wrote on the subject (The existence of species rests on a metastable equilibrium between inbreeding and outbreeding. An essay on the close relationship between speciation, inbreeding and recessive mutations, Etienne Joly, http://www.biologydirect.com/content/6/1/62 ).
And please do not hesitate to get in touch with me directly  by email ( atnjoly(at)mac.com ) if you have comments or any further questions after reading this essay.

Is it possible to divide your post into paragraphs to make it easier to read?

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Are there any studies on the fertility levels of humans/mammals as a function of their stay at Antarctica?
Wikipedia, and Space.SE seem to indicate humans become infertile in space due to the increased exposure to cosmic rays. Knowing as we do that Antarctica is holey, and subject to increased radiation (atleast UV if not broad-spectrum), I find myself wondering whether any studies on fertility were ever conducted on that continent.
So ... Are there any studies on the fertility levels of humans/mammals as a function of their stay at Antarctica?

I haven't been able to find a study on fertility, but it would be important to note the difference between radiation considered.  The dangerous radiation discussed in both of your links are cosmic rays as you noted.  Our main defense against this sort of radiation is the earth's magnetic field.  The hole you are talking about is in the ozone layer, which is much more important in UV protection than cosmic ray protection.  The amount of incident cosmic rays is slightly more at latitudinal extremes due to the deflection away from the equator by the magnetic field, but this is only 1.5 to 2 times greater, see fig. 8.
Unless we figure out how to punch a hole in the magnetic field as well, the main threat in the arctic is skin cancer from UV, not infertility from cosmic rays.

Agreed on your final remark. A study would still be atleast partially relevant with the ATS coming up for renewal in a decade or so ...

I've found a number of health-related reports but none of them have mentioned radiation in that way.  Only radiation-related health issues I could find is this, which is fascinating.. apparently the US ran a nuclear reactor in Antarctica for a decade from the early 60ss to early 70s.  It was complete with 438 malfunctions and a rather sizable spill.  http://www.vbdr.org/meetings/2012/Presentations/McMurdo_Station_Nuc_Reactor_Final_Report-Sec6-OCRed.pdf

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Is a minimum size/complexity necessary for an organism to exhibit territoriality?
A follow-up to Is territoriality only the domain of the male of a species?
I've seen a large butterfly chase a different kind of butterfly around - it may, or may not have been territoriality. Is there a minimum scale of size, sentience(?) an organism must attain to exhibit territoriality?

With some bacteria (e.g.. Bacillus subtilis) when food gets scarce they will start trying to kill their neighbors. (See this arstechnica article) This appears to be a fight to the death between children and parents. That's a kind of territorial behavior, selectively applied only when there are not enough resources to go around. As there is no "recognition" of a specific territory being defended, just wherever the bacteria is currently, this might not meet a strict definition of territorial behavior. But the only thing simpler than bacteria are viruses.
Come to think of it, I bet there are viruses that, once they infect a host cell, will change the cell's membrane or metabolism in a way that reduces its chance of being infected again by a similar virus. Such 'behavior' could be compared to defending a breeding ground. Can't find any examples though.

+1 for the viruses. http://www.pnas.org/content/109/44/18078 ;)... But I don't really think that article is really an example of territoriality.

Without some selective defense of something, I don't see any indication that the small virus behaves territorially. But a virus that infects a virus is still a pretty neat thing.

This is pretty cool; I've +1'ed it for now. If another answer doesn't come through in a day let me then flag this as correct.


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Why does this illusion work?
This is another image I found on Google+

All lines are absolutely straight, parallel and perpendicular but why does it appear to have a curvature?

Related: How does this illusion work?

I think this question is a better fit for CogSci.SE than biology. Even in the answer, both references are to the psychology literature.

The lines are NOT perpendicular. You can see this by noting that the left side spans 12.5 squares but the right only 12.

Like these questions :) Many of these illusions come from Prof. Akiyoshi Kitaoka, a japanese Psychologist and expert for Gestalt Psychology. On his website you'll find some more fascinating illusions and questions to ask here ;)
The illusion above is named Cafe Wall illusion and the newest model to explain those illusions is the contrast-polarity model. Short explanation from his webpage:

The paper explained it better to me:

Kitaoka, Pinna, and Brelstaff (2004) proposed a phenomenal model to
  explain the Café Wall illusion, which stressed the importance of
  contrast polarities of a solid square and its adjacent line segment.
  When a dark/light square is accompanied by a dark/light line segment,
  the apparent tilt is the direction of contraction of  the square angle
  (Figure 18a,b). In contrast, when a dark/ light square is accompanied
  by a light /dark line segment, the apparent tilt is the direction of
  expansion of the square angle (Figure 18c,d).

This explains why you perceive a tilt. If you position the smaller squares now in distinct edges of the big squares, you can achieve 2- and 3-dimenional illusions. Here you see a increasing of the tilt due to more smaller squares:

Here you can see that the positioning of the smaller squares is critical to achieve the 3D effect of the orignial bulge effect in your question:

Notice that Gestalt Psychology is a non-reductionistic theory approach and investigates mainly the phenomenology and underlying Gestalt Laws of visual perception. How these Gestalt Laws developed on a deeper level is a question of neurobiological evolution similar to, "why have some species of apes color-vision and some not". The ellipses in the explaining picture above show you, that our cognitive visual machine somehow tries to group divided objects (square and line of same contrast/brightness) in one line and we see a tilt. I'm guessing here, but this is probably due to cognitive brain algorithm that saves things and objects we see and perceive mainly by countor and shapes, rather than pixel by pixel like a computer and digital camera do it, which of course don't perceive any tilt or 3D illusion in any of those trick images :)
Read the papers for more explanations and examples, not behind a paywall:
Apparent contraction of edge angles, A Kitaoks, Perception, 1998
Tilt illusions after Oyama (1960): A review. Kitaoka, A,  Japanese Psychological Research, 49, 7-19.

Very nice answer.


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What percentage of people today would likely be descendants a man born 4,000 years ago?
Assuming a particular man was born in  southern Mesopotamia, around 4,000 years ago, and was significant involved in a major religion.

To what degree (if any) of accuracy could his descendants be traced?
What percentage of the global population is likely a descendant of the man?

This question comes from a comment on sister site.

I don't think most people are really able to trace their entire family tree that far back. But Avraham is so many generations ago, I would expect that either nobody in the world is his descendant or nearly everybody in the world is

I'm voting to close this question as off-topic because it is not about biology.

If you are asking about any random person then it depends on a lot of factors and hence the question would be broad. If it is specifically about one person then it cannot be answered without having adequate and reliable archaeological evidences. Also, in that case the question is not really on-topic here.

To what degree (if any) of accuracy could his descendants be traced?

I don't really understand this question. To what degree can we trace its descendants given we know what from this man? Do we have a blood sample?

What percentage of the global population is likely a descendant of the man?

If $N_0$ was the population size 4,000 years ago and $N$ is the population today, then the expected number of descendent of any given person is simply $\frac{N}{N_0}$. However, there is a huge variance and this is where things get more complicated.
As coalescent processes are geometrically distributed (well approximated by an exponential distribution if we assume that the population is large; more info in this answer), then the variance in coalescent times is equal to the expected coalescent time.
The expected coalescent time in a diploid population of constant size $N$ is $2N$. Of course, the assumption of constant population size doesn't hold for humans due to the recent demographic explosion. When the population size is increasing the genealogy looks like a star as coalescent events are rarer and therefore, it is more likely for a given individual living in the past to live descendant today (Excoffier et al. 2009). However, I don't know how to calculate coalescent time in expanding populations.

Remi, You could start by ruling out Indigenous Americans, Australians (and associated islands), and sub Saharan Africans. Then the Y-Chromosome is pretty conserved. Genetic anthropologists could likely look at the distribution of Y-chromosomes native to that region of the Middle East and then determine the frequency of that Y-chromosome appearing in samples through out the rest of the word. I don't think that you can really look at today's Raw population, as we have had too many depopulation events over the last several thousand years. Plague, wars, famine, monastic orders, etc.

Working out the percentage of woman would be a total craps shoot. You don't have the option of using mitochondria, as the vast majority come from the mother, and with Meiotic recombination, working out the patrilineal X-chromosome would be near impossible.

Does the $N_0 / N$ formula make sense? Should it be the inverse? What if $N_0$ is very small, don't you expect a given person from the 4 k years ago population to have more descendants?

Yes, you are right. Thank you for noticing the small mistake. I fixed it.


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Should we be looking for extra-terrestrial life on comets?
I have just read What elements are a possible basis for life? and I find myself wondering whether instead of seeking advanced life-forms at remote locales a La SETI, and perhaps fundamentally differently, we ought to be looking for similar microscopic life forms on comets that pass off-and-on.
Granted, a comet may be near absolute 0 for a lot of the time, but microscopic life-forms are known to be capable of surviving lean periods by using a cyst, for instance. As far as the rest is concerned, comets probably contain some amount of ice, and hence water, too. Similarly a comet's sprint around the sun could provide some limited amount of gravity/mass too.
So, should we be looking for life on comets?

Yes we should be and we are! Scientists have been analysing cometary material - but its a challenging task. The problem with looking at meteoritic material from comets on Earth is that it is generally contaminated with material from Earth. In addition, meteorites get physically altered during their passage through the Earth's atmosphere due to the high temperatures of re-entry.
So, the trick is to send missions to the comet. However, then the difficulty is in designing a mission that can analyse samples in situ. NASA's Stardust mission got around this by sample return to Earth. The probe visited comet Wild-2 and found the amino acid glycine among other interesting organic compounds. However, no evidence of life was found (metabolic products, organisms etc.) Further missions to comets (and asteroids) are planned, but they are not going to explicitly look for life.
Elsila, J.E., Glavin, D.P., & Dworkin, J.P. 2009, Meteoritics and Planetary Science, 44, 1323

Changed inorganic to organic, i assume that is what you meant. I apologise if it wasn't.

thanks @terdon that is what I meant! mind you, they found some very interesting inorganic compounds too ...

I imagined so, that's why I asked about the edit :).

This is a cool idea and definitely we have found a lot of the chemicals important to life are associated with comets which have a lot of water too.
Another issue besides the v. low temperatures on comets, when they warm up to the sun are not long lived so I wonder if the a shorter lifespan would be an issue when they are seen in the temperate zones of the solar system.
Still any cometary mission should try to do a biological survey when such things are more economical.  Right now even high profile missions like the current Mars missions are not spending any time looking for bacteria as we know it, but rather for other indications that life unlike our own might be there.  Its been very cautious going for xenobiologists so far.


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What protocol does the nervous system use?
I just read How does an inhibitory synapse communicate to the cell body of a neuron? and found myself asking this question ... hopefully I'm not asking the same thing
Any body possessed of a nervous system probably has hundreds of neurons. At one end of the neuron is the nervous system, at the other - the organ.
A neuron is connected to several others in the vicinity through it's dendrites.
When a 'signal' (for want of better word) is put on the system bus - how does a neuron know whether it has to act ( contract/relax it's associated muscle/organ ) on the signal, or pass it on ( forward ) after amplification of the signal, if necessary?
Is there something like a chemical protocol to identify the target neuron/group-of-neurons that form the destination?

Sensory neurone is the protocol I guess.

An analogy to a computer bus can easily mislead you. Neurons do not communicated via a multiplexed "bus" with different targets; rather the complex connectivity of the neurons itself works as a computing device as a whole. The area study for understanding the communication among neurons is called "neural coding".
If you are talking about just the motor and sensory peripheral nerves, they innervate specific targets.

I'm confused; does this mean that a neuron can identify what is meant for it's action without the signal itself carrying some kind of identification?

@Everyone, no it means that most neurons are hard wired for a specific task. Activating them results in a task-specific signal. That said, information "can" be encoded in the signal. Different chemical pathways in the neuron can be activated depending on the incoming signal, the same neuron can react in different ways to different neurotransmitters for example.


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In Japan, the official average body temperature is 36.0 °C. Why so different from that of Europe?
The Japanese Wikipedia states that the average human body temperature is 36.0 °C (here,"ヒト").
The statement references the data from the Japanese government.
Actually all of my Japanese friends think the same.
A body temperature of 37.5 °C is considered a serious illness in Japan, justifying absence from work.
Most other countries' sources cite 37.0 °C as an average.
Is there a biological explanation for this apparent discrepancy?

Here is a somehow related article you might want to read. http://www.health.harvard.edu/press_releases/normal_body_temperature

Hi Remi.b: Interesting, feel free to propose it as answer! I see two points: 1) Well-accepted means are erroneous 2) Mean depends on the group's age and potentially other parameters.

I won't pre-empt @Remi.b but the English Wikipedia's got a good breakdown of the variations.

36.0 °C is what I was taught when very young, but then it got to 36.8 °C. Actually, my own normal temperature is more like 36.1 °C and I am not japanese. As I literally only had a real fever once in my life, 37.5 °C would be a pretty serious condition for me. For my cousin, who gets a fever with every light cold, it would be kind of normal. So, there is a lot of variation even between related people.

already been answered on http://skeptics.stackexchange.com/questions/10309/do-japanese-people-have-a-lower-body-temperature-than-caucasians

Put every subject(both male & female) in the same environment/conditions, and take multiple temperature readings via oral, rectal, by ear, and under the arm routes. Make comparisons by sex, route of measurement, age, race. As well, the use of different thermometer types, ranging from the old "gold standard" glass mercury rectal thermometer/oral thermometer, thru the digital, ear type and electronic probe types such as FILAC and IVAC with respective oral/anal probes should be considered as there are always questions as to which is the best to use.

Factors that can lower body temperature:

low environment temperature
low metabolic rate
hypothyroidism

I couldn't find any relevant study addressing the Japanese people situation, but:

There is significant variation in metabolic rate in humans, independent of differences in body size, body composition, age, and gender. Although it has been generally held that the normal human "set-point" body temperature is 37 degrees C, these interindividual variations in metabolic rate also suggest possible variations in body temperature [1].

And here's a factor that increases body temperature:

The present experiment investigated the effects of skin pressure by foundation garments (girdle and brassiere) on the circadian rhythms of core temperature and salivary melatonin. [...] The results suggest that skin pressure by clothing could markedly suppress the nocturnal elevation of salivary melatonin, resulting in an increase of rectal temperature [2].

Whether there are differences between Japanese and other people in metabolic rate and /or clothing behavior remains unclear.

References:

Rising R, Keys A, Ravussin E, Bogardus C. Concomitant interindividual variation in body temperature and metabolic rate. Am. J. Physiol. 1992 Oct;263(4 Pt 1):E730-4. PubMed PMID: 1415692.
Lee YA, Hyun KJ, Tokura H. The effects of skin pressure by clothing on circadian rhythms of core temperature and salivary melatonin. Chronobiol. Int. 2000 Nov;17(6):783-93. PubMed PMID: 11128295.

Kinda surprised this answer got the bounty and is the most upvoted. While it describes factors related to human body temperature, it completely lacks any connection between these factors and Japanese people. It simply does not answer the question.

The discrepancy can be partly explained by where the temperature was measured from since the human body temperature ranges from 36.5 and 37.5 °C. For example it is 36.8 ± 0.4 °C when measured under the tongue (http://en.wikipedia.org/wiki/Human_body_temperature). Additionally The body temperature of a healthy person varies during the day by about 0.5 °C (0.9 °F) with lower temperatures in the morning and higher temperatures in the late afternoon and evening, as the body's needs and activities change.

Do you have any references for that (temperature in various parts of the body and methods of measuring in different countries)? It would be quite important to cite them in this case...

@daniel Where did you read that?

I was thinking "front" is a part of a head above an eyes: http://en.wikipedia.org/wiki/Forehead Sorry I am not native English.

Oh! Your English is very good. That's why it didn't occur to me. Cognates are tricky. No problem.

This study states a 0.35 degrees difference between a japanese and a malaysian, 36.95 and 37.3, it's alot.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3929238/
The following study states states a 0.15 degree difference measured with similar precision,
https://www.ncbi.nlm.nih.gov/pubmed/20824480
This graph shows that the human body temperature is 36.2 at rest in the morning/at night and 37.5 in the middle of the day. : http://millar.bio.ed.ac.uk/andrewM/WE%20book99/Part2-examples.html#tth_sEc8.3.4.2
That may account for the 1 degrees difference in Japanese studies, they measure first thing in the morning/ after 4 hours of fasting and rest/at night, and japanese body temperature of 0.15-0.35 lower that some other ethnic groups.


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What makes alcohol harmful to mammals?
During the alcohol metabolic pathway, harmful by-products are made like acetaldehyde, hydroxyethyl, superoxide anions, and hydroxyl radicals. How do these toxic compounds harm our tissues? Many of these intermediates are the compounds that are responsible for hangovers, but are they also the molecular cause of liver damage?

This answer gives a nice explanation of hangovers.

Thanks! I've tweaked the question so that it's not a duplicate.

It wasn't a dupe before either, just figured you might be interested.

That particular sentence was a bit 'dupy' when I read it back. The other answer was interesting though! I'll stick to clear liquors if I don't want to feel so bad in the morning! It seems we are still unclear of the actual cellular damage. The article mostly discusses the dehydrating factors. Hopefully someone will be able to post newer answer with more molecular information.

Superoxide radicals , basically damage the lipid bilayers. affecting the efficient gradient.
for example H+ ion gradient across lipid bilayer in ETC is very important. this gradient is affected if superoxide radicals are present.


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Why do plants produce so much more sugar than they use?
I recently asked the question, "Do plants need O2 to consume energy they've stored via sugar?" to which @canadianer responded, "Yes, plants require oxygen to generate ATP from sugar. However, they generate far more sugar (and O2) than they use." Why do plants produce all that extra sugar, especially given that sugar is thermodynamically expensive?
One reason, I believe, is to produce fruit and so recruit animals to help with reproduction. But are there others?

Plants store sugar as starch and use it to make cellulose (for their cell wall). It's also important to realize that sugar is only one of the products of photosynthesis. The Calvin cycle produces 3 carbon molecules which can feed into other metabolic pathways such as for amino acid or nucleoside synthesis. Basically it's the source of all carbon in plants.

I just realized my other comment may have been misleading. Of course they use all of the sugar they produce, just not as energy.

@canadianer, you write, "They use all of the sugar they produce, just not as energy." Why use such an energy-expensive substance for cell walls? Doesn't the high energy content make it more appealing for animals to eat the plant?

possible duplicate of Do plants need O₂ to consume energy they've stored via sugar?

@kuzzooroo Building anything is energy expensive. Anabolic processes are energy expensive but they are essential for survival. Cellulose cannot be digested by all animals. Herbivores got the ability to metabolize cellulose in animals much later than the development of cellulose cell walls in plants, in evolution. (Actually herbivores rely on bacteria to do that)

Almost no higher animal has cellulase. Some rely on intestinal bacteria to digest the cellulose. Some animals ingest their feces to get the carbohydrates obtained by broken cellulose as the actual digestion of cellulose is in the colon where glucose can't be absorbed.

@WYSIWYG There are insect herbivores that produce cellulase themselves. It is rare overall (most rely on symbionts, both bacteria, fungi and protozoa), but spread in many insect orders.


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Do plants need O₂ to consume energy they've stored via sugar?
This question came up as I work my way through the answers to another question I just asked.
My understanding is that plant photosynthesis looks something like this (though with lots more going on under the hood):
$$\ce{6 CO_2 + 6H_2O + light -> C_6 H_{12} O_6 (sugar) + 6 O_2}$$
(source)
and that the primary functions of the sugar are to store and transport energy. If that's true, then there's something fishy about the familiar view that plants need CO2 to breathe and produce O2, while animals need O2 and produce CO2. Doesn't a plant need just as much O2 as an animal would when it (the plant) gets around to consuming the sugar it has produced? Doesn't consumption of the sugar take you back to the original reactants?

Yes, plants require oxygen to generate ATP from sugar. However, they generate far more sugar (and O2) than they use.

OK, produced one further follow-up, Why do plants produce so much more sugar than they use?

Plants need sugar not only for energy but also for synthesizing essential metabolites and building blocks including cellulose (used in cell wall), glycoproteins and 5-carbon sugars for nucleotides.
As already mentioned by canadianer, plants respire by oxidizing sugars. This happens mostly during the night. However photosynthesis also produces ATP and therefore plants are not strictly dependent on respiration for energy. Moreover the fixed carbon in the form of starch makes up an energy reserve (like fats and glycogen in animals).


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How do we perceive acceleration?
Today me and my friend were coming on motor bike and I was sitting opposite direction because I was holding something in my hand (and it was fun :P). When he started bike I felt very high acceleration. I asked him to go slow however he said he is going with regular speed. Then out of curiosity, me and him tried different velocities and different accelerations while me sitting on either direction of acceleration and opposite to it. To my surprise I 'perceived' more acceleration when I was sitting opposite to direction of acceleration. While searching how we perceive acceleration, surprisingly it is not very well known. I found following explanations,

We overestimate arrival time ( ref: this )
Endolymph from Vestibular system ( ref: Wiki ) [Not exactly acceleration but rather balance]
Interpolated motion segments ( ref: this )

My question, Is it just visual perception or special mechanism for detection of acceleration? In any of these cases, why I was feeling more acceleration while siting opposite than in direction of acceleration? [ My initial guess is because I didn't have any support and visual cues were messed up ]
Update:
I found this post but I didn't get any satisfactory answer from book referred in answer.

Interesting question. However, it is unclear to me whether the question is on the perception of acceleration (a), the perception of velocity (v), or both. In  other words, did you perceive both a and v to be higher when sitting in reverse? Moreover, are you confident it has nothing to do with you being uncomfortable in reverse position on a bike? Personally, I would find it awkward and perhaps even scary to sit in reverse. Last, did you switch places with your friend? Any additional data, or is this an isolated anecdote?

I don't think we visually perceive acceleration. We just estimate it. However, we can perceive acceleration because of the vestibular system. Am I right @AliceD ?

@WYSIWYG - we most definitely obtain visual cues of acceleration visually. Ever sat in a train and the train besides you started moving? No inner ear involved, yet you felt you were starting to move away. You are correct that the inner ear is the end organ responsible for perceiving physical acceleration, but not velocity.

@AliceD but I don't think I can visually differentiate between acceleration and uniform velocity with reference to a stationary frame. Also, acceleration can be felt because it exerts force on mechanoreceptors.

@WYSIWYG - The latter example is pressure, not acceleration technically. The former depends I agree..

This book chapter talks something about visual perception of acceleration. Can't access it now. Also, it is quite old and I am not sure if it is very reliable.

@AliceD Yes, we switched positions. He also felt similar. Maybe you guys can also try :P. I did feel change in acceleration. It was hard to control precisely but we checked by changing bike speed from 0 to X in Y seconds.  Change in velocity was little bit crude. It was just checking (rather 'feeling') velocity when bike has achieved constant speed.

@WYSIWYG, to avoid bias from visual cues, We changed bike speed within certain time frame to keep acceleration same between observations.

@Dexter What if you close your eyes? Did you try that too? To eliminate visual contribution. Moreover I guess we would be more cautious towards backward acceleration because it may give a feeling of falling.

Oh, that is nice suggestion. We didn't try closing eyes. So unfortunately, there was always some visual cue. I will try sometimes tomorrow.

Personally I think the phenomenon is caused by higher cognitive processes, as I am unaware of the otoliths in the inner ear responding differently to various directions of acceleration. Instead, I think the novelty of the situation may be more important, which might even hold eyes closed.

The otolith detect linear acceleration (http://www.ncbi.nlm.nih.gov/books/NBK10792/). The semicircular canals detect angular acceleration.

My question, Is it just visual perception or special mechanism for detection of acceleration?

Acceleration is a synthesized conclusion from a multitude of systems.
Most prominent is the Endolymph system you already mentioned:

As you accelerate, the endolympth and the otoliths within (small, calcified deposits) pass over the hair cells and produce action potentials which travel to the brain. The higher the magnitude of acceleration, the more action potentials will be sent.
This is also where dizziness comes from, as the endolymph and otoliths do not come to rest at the same rate, momentarily giving the brain two different interpretations of what acceleration you're experiencing.
There is also the Doppler Effect:

Based in the cochlear system of the inner ear this time, instead of the vestibular system, the doppler effect is interpreted by the brain and gives a very rough interpretation of both velocity and acceleration (if the velocity of the object happens to be changing).
Then there is the entire visual side of things. Motion blur and the speed at which the perception of objects change size are large contributors to our sense of visual acceleration, but almost all of this is done via complex manipulation of visual data in the occipital and frontal lobes.
There are also countless minor contributors: skin and join tension (the sensation of weight due to acceleration), ease of breathing, sensory cells in your hair if your hair is exposed to the open air while acceleration, blood pressure sensors (and numbness when the body can't compensate), etc.

In any of these cases, why I was feeling more acceleration while siting opposite than in direction of acceleration?

My guess would be because your body is more visually attuned to facing the same direction as the acceleration, and when you were facing the opposing direction your mind overcompensated in an effort to protect you since you probably don't get a lot of opportunities to rapidly accelerate backwards over distances of more than a few feet.
Your brain might also have been panicking a bit because you couldn't see where you were going (usually very bad), and the heightened sensory state made the magnitude of the acceleration feel greater.
These are my best guesses, however. If someone has an academic source, please feel free to edit this answer!

I didn't get Doppler effect part .

@Dexter -- The doppler effect is the change in pitch of a sound due to the velocity of its source. If the source of a noise is moving, the sound waves in the direction of its velocity/acceleration are condensed (higher pitched), and those in the opposing direction are elongated (lower pitch). You can tell if something is heading towards or away based on that. A classic example are race cars or racing bikes, whose engine noises change pitch to an observer despite constant speeds: https://www.youtube.com/watch?v=qyxvPiOqEiE

Are I know what Doppler effect is. I was wondering how that is playing role in perception of acceleration ?

The otoliths are not responsible for dizziness. The moving endolymph is. The endolympoh in turn does not recognize acceleration, but direction of movement afaik.

@AliceD - "the endolympth and otoliths..." I specified both. The otoliths are partially responsible. The vestibular system is designed to track 3-axial movement (XYZ), and the frequency of action potentials changes depending on how many hairs are open and how "open" they are. Unless I'm very, very incorrect, the vestibular system tracks acceleration in addition to vector.

@Dexter -- The doppler effect comes into play with echoes made by your bike's motor, too, and other sounds as you passed by their origins.


text:
How statistically significant was the "sweaty T-shirt" experiment?
An Overview of the Experiment.
In 1995 there was an experiment that involves young people smelling T-shirts worn by another gender and rating their preference. The researchers found that people preferred shirts belonging to people with a dissimilar Major Histocompatibility Complex (MHC). Another interesting finding was that this preference reversed for the women 'sniffers' that were using oral contraceptives.
Here is a link to the wikipedia entry.
These findings were reiterated by a study in 2005.
My Question.
I'm very ignorant in the subject of pheromones, particularly in humans. For those of us not 'in the know' a result like this seems like magic! I want to get a better grasp on how set in stone pheromone preferences like this are.
Unfortunately I do not have access to these articles at the moment. The actual statistical difference in populations isn't mentioned in the abstracts  (the cynical sceptic alarm bells are ringing!) other than the 2005 one stating that the total sample size was 58, which sounds low given that the total population is split into two.
Generally I'm looking for any supporting or opposing critiques of the study, specifically I want to know more about the statistics of the studies.
My question is:

What statistical validations and scores appear in these studies?

I also am willing to accept answers discussing validation in similar studies. I'm after a number or quantification for how consistent pheromone preferences are.

Proceedings B keeps classic papers like this one behind its paywall twenty years after publication? For shame, Proc B! For shame!
For those looking for a free (but legal) source, JSTOR has the 1995 paper available here (free account-registration required):
http://www.jstor.org/stable/50182?seq=1#page_scan_tab_contents

First, let's consider the original Wedekind et al (1995) study.
Sample sizes seem reasonable, if the effect is not very noisy:

[...] 49 female students (average age: 25.2 years, s.d. = 4.0) and 44 male students (average age: 24.7 years, s.d. = 2.6) [...]

... and the statistical design accounts for individual differences in a fairly robust way:

[...] women were asked to rate the odours of six T-shirts each, three of them worn by men who were dissimilar to the rating woman's MHC (average number of dissimilar HLA-antigens = 5.9, s.d. = 0.26), and three worn by men who were more similar to it (average number of dissimilar HLA-antigens = 2.7, s.d. = 0.74). We tried to present every T-shirt as often to MHC-dissimilar women as to MHC-similar women (average difference of presentations to thc two groups: -0.02, s.d. = 0.73). The presentation was random in every other respect [...]

Rather irritatingly, although the study design involved asking women to rate at least three attributes of the smells (sexiness, pleasantness, and intensity) the study performs a bait-and-switch in its results:

The scores for sexiness are not shown in the figures as they were highly correlated with pleasantness (all scorings: r = 0.85, n =  294; for women who do not take the pill: r = 0.87, n = 186; for women who take the pill : r = 0.83, n = 108, p always << 0.001)

This is a bait-and-switch because even if A correlates with C, and B correlates with C, we do not know that A and B correlate with each other. Of the three measured attributes, 'sexiness' arguably has the most direct bearing on mate-choice. Because analysis for 'sexiness' is not presented, the paper ends up telling us much less than it could have about the relationship between MHC relatedness and mate choice.
The results for 'pleasantness' and 'intensity' look like this:

One further piece of analysis is presented: some number of the female subjects seem to have reported that particular smells reminded them of their partner or ex-partner; or reminded them of family members. Mentioning that a shirt smelled like a partner or ex-partner happened more frequently for MHC-dissimilar shirt smells (~17% vs ~9%; p = 0.038, two-tailed Fisher exact test). Oddly, no written response-collection is described in the methods, so I can only assume that these assessments were ad-hoc.
If this was all of the analysis that had been done on the topic, my assessment would be: this is amongst the many published research findings that are probably false. My main concerns would be that

Not all of the collected data are presented;
The most directly-informative contrast is not shown;
No adjustments for multiple comparisons are made on the statistical tests;
The data that are shown are very noisy, and sample sizes are not huge, raising concerns that the tests are underpowered;
The authors conduct tests based on data-collection which is not detailed in their methods, raising concerns about p-hacking.

And now, the 2005 paper!
Right off the bat, this paper cannot possibly replicate the findings of the Wedekind (1995) paper, because Wedekind et al found significant preferences for dissimilar MHC odours in women not taking the pill, and significant preferences for similar MHC odours in women taking the pill. In this study:

[...] we did not distinguish between, in our statistical analysis, women who were taking oral contraceptives from women who were not.
[...] Nine female participants (31.03% of female subjects) were taking oral contraceptives.

Sample sizes are smaller than Wedekind 1995 in terms of number of participants, but larger in terms of number of contrasts, because this experiment had two different sample types (sweat odour and urine), and had men smelling women as well as women smelling men. Within-individual effects are not modelled, so there is a potential for (e.g.) a small number of generically good-smelling individuals with rare MHC alleles at the population level to bias the analyses - whereas this potential bias was accounted for in Wedekind by performing within-individual correlations. The sample-sizes look like this:

The analysis was a series of Chi-squared tests, for data collected in four different sessions: one with men smelling female urine, one with men smelling female body odour, one with women smelling male urine, and one with women smelling male body odour. All chi-squared tests returned non-significant results with the exception of women smelling male body odour, for which the Chi-squared table looks like this:

So, this study didn't find the same result as the Wedekind study, but then, it couldn't find the same thing as the Wedekind study because of the way the analysis was performed, so that is no surprise. The authors claim that they found a significant effect of MHC relatedness on odour perception, but only in the proportions in the hard-to-interpret 'indifferent' response category. I am inclined to disagree. The authors presumably conducted 16 contrasts (a test of independence and three goodness-of-fit tests in each of four treatment types), and found one instance of p < 0.05. I would argue that the one 'significant' result is best explained as a failure to account for multiple comparisons.
Ending notes
If these two papers were the only things that had been published on MHC-directed mate preferences in humans, I would be far from convinced that the claimed effects were real.
however...
These are far from the only papers on the subject of MHC-driven mate-choice in humans. Wedekind and Füri (1997) conducted an analysis with very similar experimental design to Wedekind et al (1995), but arguably better statistical analysis, and found the same direction of association as Wedekind et al (1995), albeit still with a fairly high noise-to-signal ratio. Subjectively, this goes a reasonable distance towards making me think that the findings of Wedekind et al (1995) were not just a statistical fluke. I'm still not utterly convinced, but certainly more convinced than I would be if Wedekind's final paper on the topic had been the 1995 publication.
MHC-driven mate-choice has also been investigated using facial preferences and mate choice surveys. The combined evidence (across odour preference, facial preference, and mate choice surveys) is reviewed in Havlicek and Roberts (2009).

This is exactly the amount of depth and overview I was after. Thanks for putting up with a relatively vague question. If you do get time to finish your review of the 2005 paper I'd be very interested to hear about it.

@GoodGravy: Answer updated with thoughts on the 2005 paper and a mention of other related analysis. You might be particularly interested in a 2009 review. Enjoy!

The problem with mentioning the other papers that weakly support a link between MHC and mate choice is that it assumes there are no negative studies that were rejected, or never written up. The ease of performing these experiments (in the sort of sloppy, half-assed way that the 1995 paper was done) and the pop-culture attractiveness of the experiment, says to me that it has almost certainly been repeated many times, with negative results that were not published because the experimenters didn't get the results they and publishers wanted.   It's almost certainly not real.

@iayork: I think you are right to have concerns about the file-drawer effect, but I wouldn't dismiss the idea entirely. Of the odour-associated studies, the Havlicek and Roberts (2009) covers five studies with a 'disassortative' result, one with an 'intermediate' result, and three non-significant results. No 'assortative' results. To me, this hints at a weak effect and underpowered studies. I'm unconvinced that 'assortative' findings are unpublishable - the discussions in the 'non-significant' papers say 'regional structure?', which could be spun into 'assortative in this population'.

Keep in mind that the original impetus for these studies -- the idea that MHC is involved in mate choice in mice -- is now mostly disproved; it's linked instead to MUPs.  Admittedly there are some wild species where there's still a possible link, but with a weak theoretical underpinning, terrible experimental design, and a likely huge file-drawer effect, I'm more than skeptical.

@iayork That mouse disproving story sounds interesting. Could you cite something to that effect?

There are multiple papers showing this. The most recent is The Genetic Basis of Kin Recognition in a Cooperatively Breeding Mammal (Curr Biol. 2015 Oct 19;25(20):2631-41. doi: 10.1016/j.cub.2015.08.045); work dates back to at least 2007 (Curr Biol. 2007 Dec 4;17(23):2061-6. Epub 2007 Nov 8.)

@bshane has already provided an excellent answer to the question. However, I just found a recent review published in Molecular Ecology (Winternitz et al., 2016) in which the authors performed a phylogenetically controlled meta-analysis on MHC-dependent patterns of mate selection in humans and non-human primates. They used studies from seven primate species and looked at 30 studies (both observational and experimental) with a total of 58 effect sizes.
Short answer | Conclusion:
Winternitz et al. (2016) conclude that their data suggest a significant preference for mates with higher MHC diversity in humans that seems to be conserved across primates. Diversity here means heterozygosity in MHC loci.

An overview of their major findings:
First, a few words on the methodology. In principle, one needs to disentangle actual differences in the outcome of mating from error/random noise. To do that, they estimated heterogeneity in effect sizes, accounted for study ID and phylogeny effects on heterogeneity, and - for the residual unexplained heterogeneity - constructed meta-regression models with which they identified mediators of the respective effects.  Effect sizes are given as Fisher's normalized correlation coefficients $Z_r$ that is loosely similar to the correlation coefficient $r$ (they refer to ecological literature and claim that $r \approx 0.1 \rightarrow Z_r \approx 0.1$ is a small effect, $r \approx 0.3 \rightarrow Z_r \approx 0.31$ is a medium effect and $r \approx 0.5 \rightarrow Z_r \approx 0.55$ is a large effect). They then used mean posteriors and highest posterior densities (HDP, as 95% confidence intervals) to estimate $Z_r$, i.e. an assessment of how strong the mediators influence the effect. If highest posterior densities do not overlap zero, they consider the finding as a (significant) real effect.
Here is a list of what they found (HDP always in parentheses):

There is a statistically significant preference of MHC-diverse (i.e. a preference for heterozygosity in MHC loci) mates in humans ($Z_r$ = 0.153 (0.020 to 0.283), ten effect sizes). This preference also is a (non-significant) trend in primates (humans and non-humans combined) for preferring MHC-diverse mates ($Z_r$ = 0.128 (-0.064 to 0.373), 17 effect sizes). The preference is stronger in females than in males which is known from several vertebrates.
Across primates there is no significant tendency for favouring mates with MHC-dissimilarity (0.044 (-0.178 to 0.289), 37 effect sizes), even though the direction of effect sizes hints at MHC-dissimilarity rather than MHC-similarity.
For humans, there is larger variation to that point. They found effect sizes that indicate choice of both MHC-dissimilar (see above point, also true for humans) and MHC-similar mates ($Z_r$ = -0.022 (-0.107 to 0.073), 31 effect sizes). The latter may rather be an artifact of assortative mating with respect to ethnicity: effect sizes of MHC-similarity were only significant in ethnically heterogeneous populations, not in homogeneous populations. Further evidence for this comes from the fact that this is only true for observational studies, but not in experimental studies that tend to control for socio-cultural biases.

One needs to note that, in general, their reported effect sizes of MHC-related mating preferences in primates are weak (MHC-dissimilarity $Z_r$ = 0.044, MHC-diversity $Z_r$ = 0.153). But nevertheless interestingly, they report a significant effect for choice of mates with heterozygous MHC loci in humans. And - this kind of blew my mind just a little bit - they cite some literature that suggests that heterozygosity in general and of MHC loci in particular is not only reflected in body odour but also in other features like facial morphology.

I have seen many studies on that matter, but I am far from convinced that MHC really effects mate choice. Reasons for this are the following:
 - iayork mentioned it already, the premise for the studies about mice mate choice has been disproved.
 - In population level, almost every one of the studies find no evidence to support MHC based mate choices in general population.
 - Perception studies done in the area have what I consider serious problems in replicating the results. For example, wedekind's both studies feature same smellers and t-shirt wearers, but their answers are not the same as in the first study.
 - The latest perception study cannot replicate wedekinds results and the methods are almost the same.
So we have a hypotese, which has lost its original premise (mice mhc based mate choices), first studies doesnt replicate the results with same individuals, there are only couple of population level studies that suggest disassortative mhc mate choices and the latest study cannot replicate the first two perception studies.
On an individual level, these studies are kind of silly. If the effect is true, how can you discriminate between partners who are dissimilar or similar, if you would score them 5/10 or 4/10. The same applies to the brazilian study: your probability of percepting your partner as indifferent or unpleasant changes based on your HLA-similarity from 50% to 60% in different scenarios. Your overall chance of being 2-3 HLA-similar with this sample is about 10%.
I am just worried about these studies as media picks them up. Some people may come up with anxiety over their partners smell, which is quite silly because with over 50% probability you may be completely dissimilar with your partner regarding HLA, but one still perceives his/her odour as indifferent or unpleasant.
bshane and iayork, do you have any comments of the subject at hand?

can you add any kind of references or external sources to support your claims?

https://www2.psy.uq.edu.au/~uqbziets/Havlicek2009%20MHC%20correlated%20mate%20choice.pdf
Page four one can see population studies. Assortative/ns outnumbers disassortative 4/1
page 5, 6 and 9
https://www.ncbi.nlm.nih.gov/pubmed/26412134 Is the study about rodents.
And the part from the individual level I logically deducted from the results of Santos and Wedekinds work.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2519788/
http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1000925
The latter of the studies proves that the first one is debunked.
Gipharts study of Dutch families cannot be replicated by Nordlander later.

Under-referenced, primarily opinion-based and probably incorrect post. -1


text:
How can Valonia ventricosa cells get so big?
Valonia ventricosa are single-celled algae that range between one and few centimetres. In rare cases, they can reach sizes exceeding 5cm. They range from grass-green to dark green, and some are even a blackish colour.

Weirdly, a lot of the literature covering these organisms seems to be pre-1950. This X-ray crystallography project in 1937 identified key structures in the cell wall of V. ventricosa:

It is found to consist of layers in which the cellulose chains in any
one layer are inclined to those in the preceding and subsequent layers
at an angle which is on the average rather less than a right angle.
The two sets of striations on the layers of the wall correspond closely to the
meridian and spiral directions of cellulose chains, while the
extinction directions, being defined both by the directions and by the
relative proportions of the two sets of cellulose chains, lie in
variable positions between. The development of the rhizoids has been
investigated and found to be associated with regions of the wall
adjacent to the poles of the spiral.

Although the authors hesitate to speculate on their function, has any progress in the field suggested the fibres identified in this 1948 Nature paper be involved in sustaining such a massive cell (Figure below)?

So it seems like the cell wall structure has been categorised long ago. But what allows these single-celled organisms to get so big? Is it the plant-like cell wall, or something else? I was under the impression that cells would burst or collapse well before reaching this size.

the problem is diffusion: 1) maybe cytoplasmic streaming via cytoskeleton? You'd need to somehow add bulk flow in order to correct for the limits of diffusion. 2) Also I'm guessing an immensely large vacuole in the center, thus keeping the layer of cytoplasm really thin in order to permit diffusion to be the dominant form of transport... all guesses here... I'm too lazy to actually read about this algae...

From what I could find, it seems like people aren't interested in publishing things about why its big. http://jmicro.oxfordjournals.org/content/early/2014/01/23/jmicro.dft083.full Is the most recent relevent paper I can find and again, it just discusses the cell surface strcture as analagous to plants. Nothing about how it aids the cell to achieve such sizes.

weird gaps in the literature... perhaps to motivate you to find your own and examine it under the microscope...

Its a bit expensive for me to get to a reef where these things grow :P But also it seems like thats all anyone has done and it doesn't tell them much. They have used crystallography, electron microscopy, atomic microscopy etc. From what I can tell all they have learned is that it looks pretty normal for an algae. My guess is that there needs to be something special in the cytoskeletal structure, but hopefully a specialist will come along and tell me why thats a silly idea!

Ventricaria ventricosa (previously called Valonia ventricosa) is not exactly a single cell. It has a coenocytic structure with multiple nuclei and chloroplasts. As Jasand Pruski correctly guessed the organism possesses a large central vacuole which is multilobular in structure (lobules radiating from a central spheroid region).
The entire cell contains several "cytoplasmic domains" with each domain having a nucleus and a few chloroplasts (See the figure below). Cytoplasmic domains are interconnected by cytoplasmic "bridges" that are supported by microtubules (like in axons). The peripheral cytoplasm (whose membrane is overlaid by the cell wall), is only about 40nm thick.

Fluorescent confocal micrograph of a cytoplasmic domain. From Shepherd et al. (2004) Protoplasma 223: 79–91. Here, n is nucleus c is chloroplast and v is vacuole.

So these are not huge cellular balloons that can burst easily. Nonetheless a huge structure like this is susceptible to injuries by shearing forces of water currents and by other organisms like fish which may try to feed on them. These organisms have some mechanisms other than the cytoplasmic organization that allows them to cope up with injuries:

When the outer membrane ruptures, then the cytoplasm contracts with the help of actin filaments that are attached to the former. Subsequently the membrane fuses, protoplasts form and then cell wall is regenerated. This movement is likely to be triggered by extracellular calcium.
A single cytoplasmic domain with nucleus and other essential organelles can regenerate an entire organism.
A muclilagenous layer made up of sulphated polysaccharides coats both the vacuolar and extracellular surfaces. During injury it impedes the movement of water and ions (by retaining them in the form of a gel) and therefore acts like a plug.

Other organisms like this (siphonous algae) also have similar mechanisms. Some even employ calcium carbonate to maintain rigidity.
REFERENCES:

Shepherd et al. (2004) Protoplasma 223: 79–91
Menzel (1988) Protoplasma 144: 73-91

Ah, fascinating! I'm familiar with coenocytic in terms of fungal hyphae structures. I'm still impressed at the shape of it, most of these other structures are still thin in one plane or another. Just to clarify anecdotally, these organisms are "solid" like a golf ball rather than hollow like a football?
I also read that crabs like to munch on them!

@GoodGravy They are not really solid because there is a central cavity i.e. the vacuole. See figure 2b-e in the first paper. From the optical sections it seems that the "cellular zone" is ~7µm thick. So they are indeed like footballs, with an outer layer (cell wall) the bladder with a central cavity. However unlike the bladder the cellular layer is relatively thicker and organized.

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


text:
Why do many DNA solutions contain additional compounds?
DNA solubility data in only water is scarce.
A previous question asked for a quantification of DNA solubility in water. It seemed like it would be easily answerable, however isn't quite that simple since no data seems to exist for DNA solubility in exclusively water.
Even the small amount of data about water was in the context of washing away organic compounds from the solution. This got me thinking. DNA is in an aqueous solution in biological situations, and is usually handled in aqueous solutions in labs. So why is solubility data so scarce for pure water? What is important about organic compounds for DNA solutions?
Why are other additives important for laboratory DNA solutions?
So my question is why is DNA dissolved in exclusively water seemingly "uncommon" in laboratories? Is there something about pure water that is bad for DNA storage? Is it that functionally DNA never needs to be in water because it is inaccessible to proteins? Or have I misinterpreted the lack of solubility data; water is common-place and no data exists because there is no need?
I imagine PCR is where most of the data on DNA solutions exists. What about the polar organic solvents/compounds makes them important for DNA solutions?

I routinely dissolve minipreps and maxipreps in water or Tris buffer. It is most certainly not irrelevant in laboratories. PCR can't use water as the buffers are necessary for the activity of the polymerase.

@MarchHo Thanks for the insight. I think the idea of buffers probably also goes beyond PCR. I didn't intend to dismiss water as irrelevant - I just wanted to highlight there is little/no research that has been done on water as a solvent by itself.

Double-stranded DNA, with its strongly polar sugar-phosphate backbone, is negligibly soluble in non-polar organic solvents. Could you please provide a link or cite a reference where they dissolved any nucleic acids in non-polar solvents?

@GoodGravy DNA is evolved to function in aqueous environment. Perhaps it may dissolve in other polar non-aqueous solvents but I don't think non-polar solvents can dissolve it. As you might already know, even polar non-aqueous molecules like ethanol precipitate DNA (It precipitates with acetone too- I tried it a few times as a fun experiment).  Which solvents are you talking about?

Thanks for pointing out the "non-polar" mistake. I meant polar: ethanol for example.

@GoodGravy But DNA is never dissolved in any non-aqueous solvent. DMSO and formamide are used in PCR but not as solvents.

@WYSIWYG Ah I see your point. Your point also re-enforces why it's so weird to me;  no pure water solubility data seems to exist despite DNA being dissolved almost exclusively in aqueous solutions. Some other compound is always present. I cannot believe that there has never been a control done on DNA solubility in pure water.

http://www3.idtdna.com/pages/support/technical-vault/faq-old/application-support/storage/faqs/2011/07/01/what-is-the-maximum-solubility-of-dna-in-water-(weight-unit-volume-unit)- How about this.

DNA dissolves perfectly in plain water - there are no other additions needed. The reason you use Tris-EDTA  buffer is that is better for storage. About what other organic compounds are you thinking?

The only organic solvents I have used with DNA/RNA are isopropanol and ethanol to precipitate the DNA, and phenol:chloroform mixtures to extract proteins away from the DNA. I always resuspend the precipitated DNA in an aqueous solvent, sometimes just nuclease free water. It's not the best storage solution, but I don't have to store it forever.

The question received a -1. Do folk see it as being too broad, or simply unclear as it stands?

I'd like your reference for claiming that many DNA solutions contain organic solvents, Aside from extraction and clean-up procedures which utilize the differential solubility of cellular components to isolate DNA, most laboratory procedures (all of them that utilize DNA + enzyme reactions) are performed in aqueous solutions. While there are a few exceptions (highly concentrated synthesized oligonucleotides, perhaps large quantities of genomic DNA in a low volume), DNA is soluble in water at relevant storage and working concentrations for the vast majority molecular biology experiments.

Isolated DNA and RNA are stored in water or Tris-EDTA for the reasons mdperry mentioned. The addition of other solutes to various reactions (ATP, Mg2+, various buffers, etc) is to provide for the enzyme acting upon DNA. Enzyme activity can be highly dependent on temperate, salt concentrations, pH, etc. The concentrations and compositions of the substrates and salts added to reactions involving DNA are optimized for enzyme activity.

@InactionPotential I see the problem. I think I put focus on the wrong thing and perhaps semantically called additives solvents (which is incorrect). I'll edit this to remove any inaccuracies. I'm simply asking why pure water seems to not be used (and according to mdperry, ssDNA is temporarily in pure water).

DNA in pure water.
The only time that nucleic acids would encounter pure water would be in a laboratory setting--for example after an oligonucleotide is synthesized in vitro, the protecting groups are removed from the reactive atoms in the finished sequence and the final product is cleaved from the supporting matrix.  At that point you can lyophilize (freeze dry) the ammonium hydroxide solution, and resuspend the single-stranded oligo in pure water.
Additional compounds enhance heavy oligomer solubility.
However, as noted in the comments, nucleic acid solubility, particularly high molecular weight DNA, like genomic DNA,  is enhanced in solutions with dilute monovalent cations. 10 mM TrisHCl, pH 8.0, 1 mM EDTA suffices for almost every application. The EDTA inhibits any errant DNAses, and also slightly inhibits microbial growth.
Compounds act as pH buffers.
Tris is not the best biological buffer but has high solubility and is relatively cheap and stable. If the solution becomes too basic the DNA strands will melt, and if the solution becomes too acidic the purines will start to deaminate.
DNA never experiences pure water in biology.
From the moment that DNA is synthesized in a cell until that cell dies and its DNA is ultimately degraded, it does not encounter a pure water environment.

Good explanation. I would reiterate in your answer (in addition to your comment above) that DNA is maintained and used in an aqueous solution. Organic solvents (phenol:chloroform) are used primarily to separate DNA from other water soluble cellular components (proteins, RNA). PCR and its variants, restrictions digests, thymidine kinase... reactions of interest performed on DNA in the laboratory are performed in aqueous solutions, they may utilize different buffers to maximize enzyme activity, but water is the solvent.

This answer does an excellent job at explaining a lot about why other compounds are important and when DNA might be in pure water. It's odd to see that even ssDNA appears in pure water. Exactly what I wanted to see, thanks!

I've added some headers. Feel free to roll back if you want.

And as user137 said, DNA does dissolve in pure water. I dissolve PCR products in nuclease free water sometimes (especially if I need huge amounts of the sample for some downstream step).

While physiological experiments could be conducted without organic solvents, chemical syntheses of DNA or analogs, chemical modification of DNA, and purification after chemical reaction could be performed in the presence of organic solvents. Such experiments are not directly relevant to physiology, but we use chemically synthesized DNA and DNA analogs. In addition, chemical properties of DNA in the presence of organic solvents may tell how DNA behave in physiological conditions.
People doing PCR and/or molecular biology may not be interested in the solubility of DNA, because under the condition they are using, the concentrations are far less than the saturated condition.


text:
How does membrane potential vary between intraceullar membranes and the cellular membrane?
Question
Does each type of membrane have a different membrane potential? I'm especially interested in answers that can cite academic papers that have attempted to measure membrane potentials.
Discussion
I've asked about the composition of membranes before , and although I recieved some information, I didn't get all the information I was after. This isn't a problem with our community but rather with the field at large: the popular thinking is membranes are membranes are membranes (mostly due to the difficulties in studying membrane biophysics experimentally).
This is how wikipedia defines membrane potential:

Membrane potential (also transmembrane potential or membrane voltage)
is the difference in electric potential between the interior and the
exterior of a biological cell. - Wikipedia

This isn't strictly true. Intracellular membranes also have membrane potentials as one can imagine, and there is some unverified information regarding compartmental pH values. This is why I am interested to find out if there have been studies attempting to quantify this across the cell membrane, and across different subcellular membranes.

Yes, various intracellular membranes do have potential differences, but as you can imagine they are more difficult to measure experimentally, so in general data on this is scarce.
Summary

Mitochondrial membrane: 150mV-180mV with negativity on the matrix side. Seth et al 2011
Endoplasmic reticulum membrane: 75-95mV with negativity in the ER. Qin et al 2011, Worley et al 1994
Golgi: No notable membrane potential. Schapiro & Grinstein 2000
Lysosomal: 20mV with more negativity on the cytosolic side. Koivusalo et al 2011

Discussion
The mitochondrial membrane potential is probably the best studied case. This is the potential difference over the inner mitochondrial membrane, between the mitochondrial matrix and the intermembrane space; it is about 150mV (more negative on the matrix side). There is also a potential difference between the mitochondrial cristae (folds of the inner membrane) and the matrix which is used to drive ATP synthesis; it is probably larger than 150mV, but this is still poorly understood I think. The outer membrane is permeable (has pores) so there should be no potential difference between the intermembrane space and the cytosol.
For the endoplasmic reticulum (ER), there is little data available I think, but there are some estimates based on measurements of ion transport, which gives a value of about 75 to 95 mV (more negative inside the ER). Probably this depends a lot on the situation, as the ER is involved in regulating ion homeostasis (notably Ca2+).
For the Golgi apparatus, this study found that no potential difference vs. the cytosol, based on the movements on H+ and counterions.
Lysosomal membrane potential has been measured directly, giving values of about 20mV (more positive inside).
For the nucleus I don't know of any data, but I would assume there is no potential difference here, given that the nuclear membrane has large pores.

Add plasma membrane? This will be most variable amongst all membranes.


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How many residues can a reliable ab initio structural model contain?
A recent question on ab initio that I answered involved touching on the limitations of ab initio modelling. A review from 2009 put forward that typically only in the order of 100-110 residues could be reliably modelled.
7 years after that paper: I just attended a pre-publication presentation in which a 400+ residue structure had been modelled using I-TASSER. The speaker claimed it was reliable and it did fit well in the biological context, but it still needed experimental validation. Unfortunately they had no in silico validation scores to hand so I had no handle on how seriously I should take the model.
Ultimately, my question is how many residues can I-TASSER (other modern ab initio brands available!) reliably handle for a typical globular domain with today's technology?

Year on year reliable ab initio predictions are becoming more common for longer proteins. 400 residues is not an unfeasible length. Of course, loops still remain more of a challenge than helical and sheet secondary structures.
At CASP13, the Google DeepMind team used AlphaFold to produce a good quality model (T0594) of a 774 residue protein which is a WD40-repeat of RFWD3 (6CVZ).
All of their CASP13 entries are here.


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What is the transmembrane 'Positive-Inside Rule' nowadays? Has the definition changed over time?
First definition.
Two publications by von Heijne in 1989 and 1992 coined the 'Positive-Inside rule' and showed it's practical value in topology prediction of transmembrane helices. It was clearly defined and evidenced that in bacteria the positively charged residues more commonly were found on the "inside" of a membrane (the cytoplasm rather than the periplasm).
Recent Literature.
However it seems the field has moved away from the idea of "inside the compartment" to "inside the cytoplasm" as more data became available. In a 2006 review even von Heijne describes some transmembrane helices as abiding to the positive inside rule because their positively charged residues were inside the cytoplasm, although never explicitly backtracks on the original definition. A similar review in 2007 by von Heijne offers a more definitive refinement of the rule, however removes the concept from being applicable to subcellular membranes.

...the loops connecting the helices differ in amino acid composition, depending on whether they face the inside or outside of the cell (the “positive-inside” rule).

We are now faced with an awkward rule that doesn't account for proteins elsewhere in the secretory pathway or in the other organelles. All those proteins are inside the cell.
More recently still large-scale analysis of transmembrane helices from different biological membrane surfaces, Sharpe et al., 2010 and Baeza-Delgado et al., 2013, show the clustering of positive charge being cytosolic rather than discussing it in terms of the inside of the compartment. Both of these papers still say that they corroborate with the positive inside rule.
Question.
To me it seems that the definition is somewhat sloppy and can broadly be used to say "inside the cytoplasm", despite publications being reluctant to define the rule clearly. Has the definition ever explicitly been changed, or has the field silently changed what "inside" means? ... Or have I completely misinterpreted something? How do the organelles fit into any of these definitions?

I think you have misunderstood the "inside" part of the "positive-inside rule". Perhaps because "inside" is indeed an imprecise term (but now it is history and cannot be changed ;) ). In order to understand it a bit better it helps to think about the topology of the membrane. During synthesis most membrane proteins (ignoring peroxisomal and mitochondrial proteins, which are a whole other topic) are inserted into the ER membrane by the Sec translocon. The parts of the membrane protein that are exposed to the lumen are matured by the ER and Golgi apparatus to be presented on the extracellular surface. Secretory proteins (those that will ultimately be exported from the cell) are made in similar way except they pass entirely through the translocon and end up in the ER lumen. Therefore, the lumen of the ER (and consequently the lumen of other endomembrane compartments) are topologically consistent with the extracellular space, "outside", and not the "inside" of the cell. Perhaps is is easiest to see in a picture (borrowed from here: http://www.bioon.com/book/biology/mboc/chapter12/figure12-4.gif)
Coloured in pink are compartments whose topology is consistent with the "outside" and coloured grey are compartments whose topology is consistent with the "inside". So, for membrane proteins found in the endosome, for example, amino acid residues in the lumen are actually "outside" not "inside". It is true that this may not be immediately clear to those not steeped deeply in the field. As the initial studies used bacteria, which do not have membrane-enclosed subcellular compartments, "inside" was simple and made sense. Perhaps "positive-in-the-cytoplasm rule" would have been more accurate. Hope this helps!


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Transcription takes place from the 5’ to the 3’ end of the m-RNA. Why?
Only one side of the DNA ladder is copied (the sense side). The sense side starts with a 3’ end. This means the corresponding mRNA will have to assemble starting from the 5’ end. This is my initial thought, but can someone expand on it? Also, is this explained by why replication is performed in the 5' to 3' direction as suggested by this thread: Why is DNA replication  performed in the 5' to 3' direction?

Is the DNA template strand the same as the DNA sense strand?

No. Suppose your mRNA sequence from 5'to 3' is AGUC. Then, TEMPLATE strand is 3'-TCAG -5' but coding and sense strand is 5'AGTC3' i.e. complementary of the template strand and to the mRNA. This is a bit tricky so let someone else confirm this....

It seems as though the nomenclature for DNA sense and template strand can be same or differentiable as suggested by this: http://www.sci.sdsu.edu/~smaloy/MicrobialGenetics/topics/chroms-genes-prots/temp-strand.html

it is not about RNA or DNA.. the chemistry of the polymerases and the substrates (NTP) cause this directionality.

I had read about template,sense and coding from  here

I have also seen  the authors of my textbooks  use the same nomenclature.

The reason why the polymerization of DNA/RNA strands only happens in 5' -> 3' direction is because the polymerases can only add new nucleotides a the 3'OH-group of the existing strand linking it with the 5'-C of the next nucleotide.

The argument put forward at the link provided by @Cloud, that the DNA strand with the same sequence as the mRNA might be called the template strand because it is translated into a protein is illogical. The "template" referred to in the phrase "template strand" is the template for transcription - even the transcription of a sequence which will not encode a protein, rRNA for example, requires a template.


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Why spin live fruit flies in centrifuge?
I was reading this article about the evolution of monarch butterflies’ resistance to cardiac glycosides: These Butterflies Evolved to Eat Poison. How Could That Have Happened?
And this passage made me curious:

The researchers put the mutant flies in a centrifuge and spun them for ten seconds. Afterward, the flies were overwhelmed by seizures for several minutes.
Ordinary flies, by contrast, immediately walked away from the laboratory carnival ride. Flies with the other two resistance mutations were also unharmed by the procedure.

Given that normal fruit flies are usually unharmed by the centrifuge, what made the researchers decide to spin the flies? I’m not a biologist, I’m a software engineer. So I’m just guessing that it might be a standard lab procedure when studying fruit flies. Assuming the researchers didn’t know the flies with mutation 122 alone would experience seizures, what do researchers usually expect to gain from spinning live flies in a centrifuge?

Correction of Poster’s Source
The article cited mistakenly refers to centrifugation, however the actual procedure used in the work — Karageorgi et al. Nature, 2 Oct 2019 — is vortexing, as illustrated in Fig. 3 of the paper below.

What is meant by standard lab procedure?

There is no such thing as standard lab procedure. There are standard
  lab procedures for performing certain kinds of experiments or processes.

In studying the effect of mutations on the behaviour of live fruit flies one devises laboratory procedures that are, if at all possible, cheap and easy to perform on many animals. All laboratories have vortex mixers of the type illustrated, as these are used to speed up dissolution of solutes and to disperse (resuspend) solids which have been precipitated by centrifugation — perhaps the source of confusion as the flies would likely have been put in centrifuge tubes as these would be appropriate (although the flies were not subjected to centrifugation).
Why vortex flies?
The vortexing is what is apparently called a ‘Bang’ assay — a means of testing flies for neurological seizures. The authors state:

To investigate this, we phenotyped monarch lineage knock-in flies for neurological seizures upon shaking (bang sensitivity), a common phenotype in hypomorphic Na+/K+-ATPase mutants29,30

Without consulting references 29 and 30, it seems clear that the authors were expecting cardiac glycosides to produce neurological seizures, and used a simple technique that had been used previously by others to assay this.
So, yes, if you are interested in these aspects of fly physiology vortexing may be a standard laboratory technique, but, no, other fly labs (e.g. those studying the gut) don’t start the morning by saying:

“Lets take the new mutant for a spin”.

Awesome! I did pull up the actual paper and tried to find the word “centrifuge” (and related forms). No wonder I couldn’t find it!

I don't know the exact history, but I wouldn't be surprised if this started as "shake them in the tube a little bit" maybe even initially as a complete accident, and the mechanical option was an attempt to standardize a bit.

In the field of Drosophila neuroscience, vortexing is also a standard treatment to disorient flies, for some decades already. It is, for instance, used in assays for measuring motor functions following a 'reset', or looking at orientation based on mechanosensation, vision and olfaction, and also as a punishment or an aversion stimulus in classical conditioning/learning studies. Vortexing is an easy and reproducible way to standardize what is essentially just vial shaking. Also crucially, centrifuging is a very common lab misnomer for vortexing (source: my experience in quite a few labs).

@SPr — I've never encountered the confusion you mention. I suppose it depends on the type of lab and perhaps nationality. In the biochemical labs I worked in the use of ultracentrifuges and large centrifuges was so central (long before the small desktop centrifuges were developed) that nobody would refer to a vorted mixer (the original was a "whirlimixer") as a centrifuge. It only appeared in the early 60s, whereas Morgan reported the use of the centrifuge to inflict changes on Drosophila eggs in 1902.

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


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Why do men grow facial hair?
Ancestral facial hair.
Our closest ancestors, the chimpanzee and bonobo, both grow facial hair around the mouth area. What is noteworthy is that this is the case in both males and females of the species.
Female chimpanzee with facial hair:

Dichotomy of facial hair in humans.
Our own species has a notable dichotomy in facial hair between males and females. I'm interested in what broadly speaking are the theories on facial hair. Could it be as simple as sexual selection over tens, or hundreds of millennia?
A previous answer eludes to a sexual selection direction, but my question is primarily why do human females not grow nearly as much facial hair as their male counterparts? Is this just a typical sexual dichotomy? I suppose here I am interested at a molecular level - is beard growth absent, or suppressed in women?
Speaking physiologically androgen is a hormone that drives hair growth and this hormone is more prevalent in males. Although females do have vellus hair coverage on their face, the thicker androgenic hair isn't typically present. A cursory search didn't reveal to me if this is due to less follicles in the first place so androgen would have little effect, or less hormone release.

To answer the question "Why do men grow facial hair" I think three smaller questions are raised:

What is the point of facial hair? (If there is any beyond sexual selection...)
What selected thick androgenic facial hair out of human females?
At a molecular level, have females lost the "facial hair gene", or gained a "facial hair suppressor gene"?

Why exclude "they look dashing"? That's sexual selection at work.

@canadianer I'm guessing that we didn't have vogue telling us that beards and tweed is a winning combo over evolutionary time scales. Without being facetious you have a point and that all the literature comes up with that I have found. It is absolutely reasonable that it's sexual selection.

@what In this question I am making the case that ancestrally, the closest species to us have no dichotomy of beards between sexes. Humans evolved this dichotomy. I'm pretty sure black populations have bearded males, and less bearded females as well as white populations. Also the cold doesn't explain why or how females lost the facial hair. If anything, that would be a selective pressure to keep facial hair for women.

@what The idea of chimp vellus facial hair is somewhat interesting. If anything this would complicate things - how has androgenic hair evolved in males, and not in females.

Hormones explain the sexual dimorphism.
Expose females to androgens and they develop masculine facial hair.  See hirsutism.  Also research:

... women’s intermediate facial follicles respond to men’s higher androgen levels by synthesizing more hair over several days ....

I don't think this is a complete answer, but I know that historically hair, like horse tail has been used as a part of armor, because it is flexible and difficult to cut through (see dragoon helmet picture).
Protection could be one of the primary purposes of facial hair in human males, who are more likely to experience aggression or be hunters.

I think @feetwet has given a good argument why the facial hair in females are suppressed rather than absent.
Facial hair signal sexual maturity and play role both in inter-sexual selection (attracting females, like peacock's tail) and intra-sexual selection - demonstrating dominance over other members of the same sex.
Another "hairy" trait also exclusive to males is baldness. For example:

Both male facial hair and male pattern baldness are genetically based, suggesting that they contributed to fitness. The multiple fitness model provides an evolutionary interpretation of the social perception of male pattern baldness and beardedness in terms of the
multidimensional meaning of physical maturational stages. Male facial beardedness is associated with the sexual maturation stage and is hypothesized to signal aggressive dominance. Male pattern baldness, by contrast, is associated with the next stage of physical maturation, termed senescence. Pattern baldness may signal
social maturity, a non-threatening form of dominance associated with wisdom and nurturance.

bald balding baldness.

A factor to add is also whiskers... most mammals have whiskers leftover from nocturnal sensing and fast-bite-reactions. For example felines that don't see well from upclose can use their whiskers in the final phase of an attack.
The age of mammal facial hair being up to 80 million years ( rodent carnivora divergeance ), the genes are more deeply encoded as very useful elements of mammal anatomy, and they tend to stay, plus the other factors described above.


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Do people with congenital analgesia feel cold?
There are a few diseases that cause an insensitivity to pain. This question asks about the relationship between the cold and pain, which got me thinking:
Is shivering a response driven by the sensation of cold, or a response to the pain associated caused by the cold? This is easy to work out by considering people that do not experience pain.
The key here is if people with congenital analgesia (AKA CIPA, CIP) shiver then we may assume that it is the sensation of the cold, not the pain and the cold, that causes the shivering.

Do CIPA patients shiver in the cold?
Does this mean that the shivering is caused by sensation pathways or
pain pathways?

Disclaimer: I am not an anatomist and do not claim to have a working knowledge of the nervous system. Please point out any and all obvious errors in this question that might explain why this wouldn't be the case in the comments or as an answer if its a big error.

There's an awful lot on hyperthermia in CIPA individuals, but not a lot on hypothermia. My personal expectation would be a delayed reaction due to cold misperception, but an induced shivering response as core body T drops below critical values, because shivering is a motor reponse.

Thats interesting to note. I suppose hot things are more dangerous to CIPA sufferers than cold things, so thats where the research goes.

Interesting question. Here what I think (I am not an expert in congenital analgesia so take it with a grain of salt).
The pain provoked by an high temperature is mainly transmitted via the receptor TRPV1 (a Ca2+-channel nocireceptor) while cold sensation is driven by TRPM8 and possibly, for noxious cold, via TRPA1 (two similar types of Ca2+-channels). Those receptors are known as the temperature sensors. As an anecdote, TRPV1 is what give you a pungency sensation when eating spices while TRPM8/TRPA1 give you the cooling sensation from mint.
Mechanical pain is transmitted via other receptors, including TRP channels, but this is not fully understood at the molecular level.
As far as I know, the encoding of pain, and more generally physiological sensations, in the brain are also not yet fully understood but it is very likely that the pathways taken by TRPV1 differs from the one taken by TRPM8/A1 which would suggest that it is possible that CIPA individuals experience high-temperature pain and cold differently at the molecular level and therefore might respond, to some degree, to one but not the other. This also probably applies to mechanical pain vs temperature-driven pain.
I would actually not be too surprised if CIVA people shiver even if not feeling any temperature sensations. Would be interesting to have the opinion or even better the observations of experts in this field.
P.S. I know this is not a definitive answer but I have not enough reputation to comment.


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Alternatives to CFU plating for measuring number of viable cells?
I am hoping to measure growth rates of a bacterial culture in several growth conditions. I am concerned that these growth conditions may cause cell death, which would lead to a decreased correspondence between optical density and number of live cells, so I want to independently measure the number of live cells. I understand that plating serial dilutions of a culture and counting the number of colonies to calculate the Colony Forming Units (CFU) per mL is the gold standard for measuring the number of viable cells. However, I have seven different conditions I want to test in parallel, and making 3+ plates for each condition (to do serial dilutions) and taking measurements at several points in the growth curve leads to a lot of plates. In general this method seems more labor intensive than what I need. I am mostly doing this as a sanity check, so it seems like a lot of work just for a sanity check.
My question is: are there any alternative methods to CFU plating for measuring cell viability, given that I am doing a lot of experiments in parallel? I don't have access to a FACS machine, so cell sorting won't work. I have read this question on measuring live cells in algae. I'm not sure that a hemocytometer is the right alternative for my particular high-throughput application (though you could convince me otherwise). The best answer to this question would compare from experience the precision, accuracy, sensitivity, and ease of use of this alternative method with CFU plating.
Thanks!

Even small cell counters are available. Stain cells with trypan-blue and you can count viable cells. I think invitrogen supplies this machine.

I've only used it for mammalian work, but the Cedex HiRes Analyzer from Roche is pretty sweet. From their docs you can analyze particles from 1-90 μm in size (the cells I work with are about 20 μm), and there are a ton of configuration options depending on your needs. As long as your cells can be stained with Trypan Blue (it's been a long time since I've done bacterial work, pardon my ignorance) to look at viability, then this machine should work quite well. When set to Maximum (i.e., the analysis takes as long as possible), I get results in less than 4 minutes per sample - and this includes about a minute for the sample to settle in the flow cell. If you lower the sensitivity, you can get results faster.
Basically the way it works is you take 300 μl of your liquid culture (diluted if you think the concentration is too high), and add it to a sample cup. Put all your cups in the tray, fill out the sample info and analysis options in the MultiRun screen, and hit Start. The machine includes all the reagents onboard, so it mixes the Trypan Blue with your samples, then injects the proper amount into a flow cell. The sample is allowed to settle, then a high-resolution image is taken of the entire length of the flow cell. Then, depending on your sensitivity settings, a certain number of frames are taken from the full-length image and analyzed. An average count is then generated based on all the images, and your final numbers are spit out. You can then print or save a report of the cell counts and viability.
The software comes with some analysis tools as well, so if you keep multiple cultures going over time with different growth conditions, you can aggregate the data for each one and generate graphs of cell counts, viability, cell size, etc. - there are at least 10 or 20 parameters to choose from. All the image analysis options are configurable, so if you look at the results and think the machine is picking too many dead cells, or not enough, you can change the parameters to your liking, and save the options as a custom analysis type.
One option I like that would beat the pants off CFU-based counting (besides the drastically-reduced time) is the fact that the machine can detect aggregation of the cells. One issue with CFUs is that it's hard sometimes to know that a certain colony really arose from just one parent cell - if you let the colonies grow long enough you may be able to tell based on size, but it's a tough call. Since the Cedex is looking at the cells themselves, it doesn't matter if they're aggregated or not, as they'll all get counted (assuming the aggregation particle doesn't contain a huge amount of cells, like 50+, that can't be resolved by the software due to occlusion of the image).
I don't know how much these guys cost, so depending on your budget you may not be in the market for one, but if you're going to be doing a lot of counting then one of these is invaluable. I'm sure other companies make similar instruments, but I haven't used them, so I don't know how they compare to the HiRes. I do know that the person at my company that was responsible for buying the HiRes is very good about researching possible alternatives, so this one is probably as close to the top of the line as we could find, for the needs that we have.
Good luck with your counting!

Thanks for the detailed, well-explained answer! I'll have to check whether Trypan Blue works for bacteria; from my initial investigation it seems so. I'm a bit leery about buying a whole machine to do this, but at some point if I want to beat tedious (and cheap) CFU counting I'm going to have to get real and buy something; if it could be done better than CFU with similar technology, it would have been done before!

A company called HemoGenix offers a CFU alternative/replacement assay. It's called HALO PCA (progenitor cell alternative). We have used it with great success. It does, however, require an instrument. We use a bioluminescence plate reader, but it looks like they also have kits for fluorescence and absorbance readout.

Welcome to Biology.SE! A little more detail about the procedure would be very helpful.