text:
Is the human biological clock genetically programmed or learnt?
Argument favouring learning:
A newborn sleeps for 20-22 hours. But overtime (s)he learns to focus sleeping time to night time, according to his or her needs and family needs. Some sleep from 1 am to 7 am, some from 11pm to 5 am. So it is learnt.
Argument favouring a genetic origin:
Somewhere I read (I don't exactly remember the article) where it was told that the biological clock is not of 24, but of 25 hours. This means that the synchronisation is not maintained with the earth. If it would be learnt, then why is it not in synchrony with the world?

The circadian clock is hardwired at ~25h and reset according to various cues, mainly day/night, but also time of food supply, parents who put you to bed at a certain time, among other things. And kids definitely sleep longer than 6 hours :)

The sleeping time was just an example... Also AliceD, can you give me more details of circadian clock you are speaking of? May be some article. Also, it is not clear what is the answer to the question.

related question: How do humans perceive time?

Short answer
The biological master clock is neurologically and genetically hardwired. The biological clock is not affected by learning. Instead, it is constantly entrained mainly by daylight.
Background
The biological clock is hardwired in the human body and can be traced back to the master clock in the suprachiasmatic nuclei (SCN) of the hypothalamus (Fig. 1).

Fig. 1. The SCN is entrained by environmental light captured by the retina in the eyes. Source: Neuroscience News.
The SCN is an intrinsic oscillator that governs sleep and wake timing, rhythms of temperature, hormones, mood and cognitive acuity etc. etc. These rhythms are entrained to 24 hours by the environmental light-dark cycle primarily via a subset of photosensitive retinal ganglion cells that project directly to the SCN (Fig. 1). Using hormones and neuronal signals, the SCN entrains peripheral clocks of similar molecular mechanism present in many tissues (Pagani et al., 2010).
In humans and other organisms, the timing of 24-hour behavior is governed by the period length of the circadian oscillator. This period is approximately, but not exactly, 24 hours long (circa diem), and ranges from 23.47–24.64 across people (23 hours 28 min to 24 hours 38 minutes) in laboratory conditions (Pagani et al., 2010).
Why is it circa diem and not exactly 24 hours? Note that the absolute length of a day depends on the definition used. For example, one complete rotation of the earth around its axis (the sidereal day) actually takes 23 hours, 56 minutes and 4.1 seconds. The solar day is 24 hours and is defined by the time it takes the sun to make an apparent circuit across the skies. More importantly, there is apparent solar time, sometimes called true solar time, which is determined by the daily apparent motion of the observed sun. It is based on the interval between two successive returns of the sun to the local meridian. The length of a solar day varies throughout the year, and the accumulated effect of these variations (equation of time) produces seasonal deviations of up to 16 minutes.
The length of a day can also be defined in the number or hours from sunrise to sunset, which varies where you are on earth. At the equator every day of the year is exactly 12 hours long. At 50° latitude (e.g., England & Canada) the longest day is 16.5 hours and the shortest day 7.5 hours. At 35° latitude (e.g. many US states and Greece) the longest day is 14.5 hours and the shortest day 9.5 hours. Given that light is the most effective way to entrain the circadian rhythm, it is obvious why the absolute length of the intrinsic circadian rhythm is not important. As long as it is circa diem, it will do.
Reference
- Pagani et al., PloSONE (2010); 5(10): e13376

Good answer. Note however that the complete rotation of Earth on itself is not the definition of a solar day: you want the duration between two occurrences of the sun being at the zenith, and this is 24h. (23h56'4.1'' is the duration before two occurrences of a given star being at zenith)

@Joce - thanks for your suggestion - I will look into this later. Are you saying my information is incorrect then? If so, I will make some edits. Thanks again!

It's not incorrect, but I'd say that the duration of earth revolution upon itself is not relevant : 23h56min is the time until stars are back at the same position, for circadian rhythm it is the time until the sun is back at the same position which is relevant. (Then on top of that you have the "true solar time" correction)

@Joce - I adapted the answer

Is the human biological clock genetically programmed or learnt?

It is genetically programmed.

A newborn sleeps for 20-22 hours. But overtime (s)he learns to focus
  sleeping time to night time, according to his or her needs and family
  needs. Some sleep from 1 am to 7 am, some from 11pm to 5 am. So it is
  learnt.

Sleep clears the brain of toxic metabolic byproducts. A newborn have different sleep requirement than an adult (it would be an interesting question why). The connection with the age is something like this:

- Figure 1. - Sleep requirements by age - ref
So it is not learnt, if they wouldn't sleep enough, they could have health problems or they could even die because of brain damage.

Somewhere I read (I don't exactly remember the article) where it was
  told that the biological clock is not of 24, but of 25 hours. This
  means that the synchronisation is not maintained with the earth. If it
  would be learnt, then why is it not in synchrony with the world?

It is in sync with the world, every morning the blue light resets the clock, that's why we tend to use red light at night.
There is a clock in the hypothalamus (brain), which is entrained directly by the daily light/dark cycle. There are peripheral clocks in the liver, heart and in other tissues (probably in every single cell), which are weakly affected by the light/dark cycle, and strongly affected by the food intake (probably by other factors as well). The sleep/awake rhythm depends on all of these clocks. So it depends on the actual light/dark pattern and the metabolic (feeding) pattern of the individual.

When food is plentiful, circadian rhythms of animals are powerfully
  entrained by the light-dark cycle. However, if animals have access to
  food only during their normal sleep cycle, they will shift most of
  their circadian rhythms to match the food availability.

2008 - Differential Rescue of Light- and Food-Entrainable Circadian Rhythms
2008 - How to Beat Jet Lag: Don't Eat
2006 - Nuclear Receptor Expression Links the Circadian Clock to Metabolism
2008 - Effects of light cues on re-entrainment of the food-dominated peripheral clocks in mammals
2011 - The circadian clock and metabolism
2009 - Food-anticipatory circadian rhythms: concepts and methods
2009 - Rev-erb-α: an integrator of circadian rhythms and metabolism

If they [newborns] won't sleep they would die because of brain damage? Do you have any reference to that? The linked NIH website doesn't mention that. +1 for the reference to food-based resetting

@AliceD I just applied logic, people die because of too much sleep deprivation, but you are right, it is exaggeration, because less, but chronic sleep deprivation can cause just health issues, but not instant death. I'll edit that part, thanks! :-)

@AliceD Edited. Not the best references, but I think it is enough in this case.

Better for sure, great. Can't +1 you again unfortunately :)


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Is this a bedbug?
Does anyone know if this is a bedbug? Or maybe a cockroach? I am located in Quebec, Canada.
If you need a clearer picture I'll try to take one without the glass in the way so my camera can focus better. Hopefully it doesn't escape.

where are you? country/state?

This is a woodlouse (often called a "pill bug" or "rolly polly"). See this answer for an example of an actual bed bug.

I think I can see 5 extremities sticking out under the shield on one side in your image. Hence I think it has a total of 10 extremities. A bedbug, belonging to the class of insects, should have just 6.
I'm pretty sure it's a pill bug (Fig. 1), a family of woodlice (Armadillidiidae), belonging to the isopoda, an order of crustaceans. Crustaceans include the lobsters, crabs and crayfish, to name a few.

Fig. 1. A Pill bug species. source: Natural History of Orange County, CA
A bed bug is an insect and has six extremities (Fig. 2).

Fig. 2. A bed bug species. source: Terminix
So long story short, your species here is not an insect, and hence not a bed bug.
From the limited amount of information you've provided a specific species determination is difficult; there are many pill bugs.

Thank you! After going through some pictures of the different species of pill bugs, I have found a match.

Do you any special reason to say pill bug? From the unclear picture I find that hard so say. It's clearly a woodlouse though.

No, it looks like a woodlouse. They are perfectly harmless to humans, and feed on decaying plant matter. They are also called isopods, roly-polies, or pill bugs.
Woodlouse on Wikipedia

source: Stack Exchange

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Which Papaya (Lechosa) plant (male or female) bears fruit?
I will be planting Papaya fruit seeds and I understand that there is a female and a male plant, so how can one distinguish which are the ones that will bear fruit and which I should just rip up by its roots as I have limited planting space?

@chrisstronks hermaphrodite should be added to the title.

@dustin - I will leave that to PO, or you are welcome to edi the question!

Male flowers have no ovary and do not produce a fruit but females need to be pollinated or the fruits will be aborted falling off when they are about golf ball size (1). Therefore, you will need at least one male or hermaphrodite plant with your female plants so you can manually pollinate the female plants. Also, note that hermaphrodites can pollinate themselves so you will not need another one or a male for fruit.
The article goes on to say that hermaphrodites are the preferred type but under certain circumstances a hermaphrodite can shift to a female.

Cool winter weather or high soil moisture can lead to a shift toward femaleness, where the stamens fuse to the carpels or ovary wall. The re
  sulting fruits become severely ridged (carpelloid, or “cat faced”) and hence are deformed and unmarketable (1).

Home gardeners should take steps to avoid having only a single papaya plant, in case it turns out to be a female. One way to accomplish this is have several plants in the garden, to ensure the possibility that at least one will be
  a hermaphrodite with pollen. If space is limited, allow several seedlings to grow to flowering stage in the same planting spot, and then remove all but the healthiest hermaphrodite plant (1).

that was the fastest answer ever....

@ChrisStronks I am used to math.SX. If you aren't fast, the the question will have 10 different answers before you even develop your approach.

but you don't really answer how the PO can differentiate between the (wanted) females and (unwanted) males.

@ChrisStronks the answer is in the picture on how to differentiate.

@x457812 I miss typed and corrected already. Hermaphrodites don't need the presence of a male to bear fruit. However, the article goes on to say under certain circumstances a hermaphrodite can shift to a female.

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What is Mendelian Segregation and how is it related to the Hardy-Weinberg equilibrium?
I can't find the exact definition of Mendelian segregation. In addition, I am wondering how it is related to the Hardy-Weinberg equilibrium?

I slightly modified the wording of your question. Feel free to roll back if it is not to your liking.

Related: Solving Hardy Weinberg problems

Mendelian segregation is defined on the Nature site, and I quote:

The Principle of Segregation describes how pairs of gene variants are separated into reproductive cells. The segregation of gene variants, called alleles, and their corresponding traits was first observed by Gregor Mendel in 1865. Mendel was studying genetics by performing mating crosses in pea plants. He crossed two heterozygous pea plants, which means that each plant had two different alleles at a particular genetic position He discovered that the traits in the offspring of his crosses did not always match the traits in the parental plants. This meant that the pair of alleles encoding the traits in each parental plant had separated or segregated from one another during the formation of the reproductive cells. [...] We now know that the segregation of genes occurs during meiosis in eukaryotes, which is a process that produces reproductive cells called gametes.

Likewise, the Hardy-Weinberg equilibrium is explained on Nature's website:

The Hardy-Weinberg equilibrium is a principle stating that the genetic variation in a population will remain constant from one generation to the next in the absence of disturbing factors.

So in case of Mendell's experiments, his pea plants showed no disturbance and quite perfect ratios, for example 3:1 green:yellow seed pods:

The Nature site continues on the Hardy-Weinberg principle:

When mating is random in a large population with no disruptive circumstances, the law predicts that both genotype and allele frequencies will remain constant because they are in equilibrium.
The Hardy-Weinberg equilibrium can be disturbed by a number of forces, including mutations, natural selection, nonrandom mating, genetic drift, and gene flow. [...]. This occurs because certain alleles help or harm the reproductive success of the organisms that carry them. [...]. Because [...] of these disruptive forces [...] the Hardy-Weinberg equilibrium rarely applies in reality. Therefore, the Hardy-Weinberg equilibrium describes an idealized state [...].

So to get back to your question on the relation between Mendelian segregation and the Hardy-Weinberg equilibrium: The Hardy-Weinberg equilibrium is necessary for the Mendelian segregation to become phenotypically apparent. So in Mendell's controlled experiments the 3:1 green:yellow pods became nicely apparent as both phenotypes had equal chance of survival.
And to continue the seed pod example, if there were to be introduced a disturbing factor, such as a pest that wrecks havoc in plants with yellow pods, but not in green, the Hardy-Weinberg equilibrium (i.e., Mendell's 3:1 green:yellow) would be disturbed and Mendelian segregation would become less apparent as aberrant phenotpyic ratios would emerge (>3 : <1).

The post by AliceD isn't quite right.
The definitions are correct, but the relationship between both is incorrect. Mendelian segregation won't be affected by disturbing factors, unless the disturbing factor affects the way chromosomes are arranged during meiosis. And no pest should affect that.
So, as the definition says, "This meant that the pair of alleles encoding the traits in each parental plant had separated or segregated from one another during the formation of the reproductive cells. [...] We now know that the segregation of genes occurs during meiosis in eukaryotes, which is a process that produces reproductive cells called gametes." That is correct and means that if you cross two individuals, and obtain a large enough number of progeny, the mendelian traits should maintain a predictable phenotypic ratio. 3:1 between dominant and recessive traits, 1:2:1 between heterozygote traits, and so on.
Now, Hardy-Weinberg equilibrium is a characteristic of a random mating population, if no external evolutionary forces are acting on it (no selection, no migration, no mutation). This is basically an extension of the Mendelian segregation to a population, answering the question: What happens with the phenotypic frequency of Mendelian traits in a population, after random mating? If the population is large enough (infinite in the model), you'd have every possible mating and after one generation, the phenotypic equilibrium would be reached and it will remain constant.
So, in short, Mendelian segregation is the result of the random segregation of alelles during gametogenesis. And Hardy Weinberg equilibrium is the result of purely Mendelian heredity in a population.

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Can rapid eye blinking induce epileptic seizures?
Photosensitive epilepsies are characterized by visually-induced seizures. Flashing-light stimuli are known to induce seizures in some (but not all) patients. My question is whether people with this type of epilepsy can self-induce seizures by rapid eye blinking?

I'd guess not - a strobe light's pulse can last a few milliseconds, while a blink can last a hundred times as long.

Photosensitive epilepsy is often evoked at flicker frequencies of 3-30 Hz, which should be feasible through eye blinking. However, I couldn't find any info on self-induced seizures, and it is not listed in common causes of flash-induced seizures. E.g.: http://www.epilepsysociety.org.uk/. More common causes are computer games, TV screens etc.

@Bez and others - Why is this question put on hold? There isn't any self-referral present? I find it rather interesting and couldn't find anything on it.

This is an interesting question and NOT a personal medical question!

@ChrisStronks reopened for your pleasure.

“Self-induction” in photosensitive epilepsy is a well-described and fascinating  phenomenon. Photosensitivity itself is rare, occurring in only ~5% of patients with epilepsy.1 Among this group it has been estimated2 that 25% self-induce epileptiform activity. The most common methods appear to be passing a hand with open fingers repeatedly across the visual field and, as you query, blinking.
Quoting from a classical paper on the topic by Andermann et al:3

The method of inducing seizures varies
  both in detail and in principle. Light contrasts are always brought about, but they may either be applied to and alternate for the whole visual field—an effect produced by blinking or batting the eyelids and induced by any flickering light—or else the attack is elicited by the spatial displacement of brightness and darkness  over the retina.

This phenomenon is most common in epileptics with established photic triggers, and the scenario triggering an attack is often in the context of bright sunlight. However, this has also been described in epileptics who are not otherwise photosensitive. See, for example, “Seizures triggered by blinking in a non-photosensitive epileptic.”4
Notably, some authors have questioned whether blinking and other “triggers” are actually themselves ictal phenomena (i.e. representing the initial phase of an epileptic event) rather than a form of voluntary self-induction. For more on that hypothesis, see Ames, 1971.5
Presuming that this is, in fact, self-induction as has been traditionally postulated, the question of why such patients repeatedly self-induce seizures is perhaps the most interesting aspect of this. There has been some research2 considering the psychiatric factors underlying the behavior. Quoting Andermann3 again:

The reward a patient seeks by self-stimulation may lie in escape from unwanted situations, in attracting attention, in punishing those around him, or, indeed, in deriving pleasure from the attack.

References

Kasteleijn-Nolst Trenité DG. Photosensitivity in epilepsy. Electrophysiological and clinical correlates. Acta Neurol Scand Suppl. 1989;125:3-149.
Ng BY. Psychiatric aspects of self-induced epileptic seizures. Aust N Z J Psychiatry. 2002 Aug;36(4):534-43.
Andermann K, et al. Self-induced epilepsy. A collection of self-induced epilepsy cases compared with some other photoconvulsive cases. Arch Neurol. 1962 Jan;6:49-65.
Rafal RD, Laxer KD, Janowsky JS. Seizures triggered by blinking in a non-photosensitive epileptic. J Neurol Neurosurg Psychiatry. 1986 Apr;49(4):445-7.
Ames FR. "Self-induction" in photosensitive epilepsy. Brain. 1971;94(4):781-98.


text:
What is the science behind the inaccurate perception of colors?
If I go into a green room (all walls are semitransparent and green) and spend some time - around 10+ min - in there, when I come out all my eyes see is white as pink. I see no (or very few other) colors due to this for a while - around 2 minutes. What is the science behind this? Why do eyes lose color perception in this case?

To explain the neurophysiological background to the existing answers I would like to add the following:
The effect you are describing (pinkish appearance of white) is generally referred to as a negative after image and it is a direct reflection of the color opponency in the retina. The effect is caused by adaptation of the (in this case green) cones in the retina. This adaptation occurs through photobleaching, which means that the chromophore (cis-retinal) in the visual pigment in the cones is converted to the inactive state (trans-retinal). The conversion of retinal forms the basis of the detection of photons by the cones. When you look at a green stimulus for a long time, the photopigment in the green cones is progressively converted to the inactive trans-retinal state and the green cones will stop responding to the green light stimulus. Why then does this lead to a pink'ish (magenta) perception of white? This is because color vision is based on color opponency.
The visual system in the retina is based on three cones: red, green and blue cones.
These cones feed into three channels: a red-green, a yellow-blue and an achromatic (luminance) channel. Note that yellow is formed by adding the red-green color signal, while the achromatic channel is formed by adding the red and green cones as well, where only light intensity information is extracted.
The red-green and yellow-blue channels are opponent channels. For your specific example, the latter is important. Red-green opponency means that at the neural level, red responses cancel green responses and vice versa. Therefore, we are not able to perceive a "reddish green". White is perceived when light activates all cones, such that red cancels green, green cancels red and yellow cancels blue.
However, if the green cone system is adapted due to the green pigment being bleached, the opponency of green is diminished and the red response will dominate. In addition, as the yellow channel will be reduced as well, there will be a bit of blue added as well due to reduced blue suppression, explaining the pink'ish (i.e., magenta) appearance you describe. A nice example of the negative after-effect is the following:
Stare at the colored dots on the girl's nose in the negative photo image below for 30 seconds. Then look at a white surface and start blinking. You should see a non-negative image of the girl (see here for image source).

Reference on the opponency model:
Mather, Foundations of Perception, chapter 12 Colour Vision.

First recall that pink is white minus green, more or less.
Now, your perception can be explained by adaptation: Neurons try to control their gain (amplification factor) to have roughly the same range of output. So if there's a lot of stimuli they like, they will reduce their gain, and vice versa. It can be thought of as a form of fast time-scale homeostasis in this case.
While you were in the green room, your neurons that represent 'green' gets less sensitive to green stimuli due to strong green input (adaptation). Additionally, the 'non-green' representing neurons become more sensitive, since there's less visual stimuli that they like. When you suddenly come out of that room, now the green neurons do not respond as strongly as the non-green neurons in response to white, hence your perception of pink.

I don't think the process is primarily mediated through gain control. Rather, it is disrupted color opponency through pigment depletion.

I like this answer because I always like analogies between electronics concepts (or terms) with human/natural systems and it is easiest graspable answer. Still the depth seekers might not satisfied ;)

@ChrisStronks pigment depletion can be thought of as a form of adaptation. I guess 'gain control' would be a wrong analogy though. Thanks for your comment and answer.

The shift in color is caused by the proteins in your photoreceptors being used up and thus no longer being able to absorb the light.
If you stare at a green wall, you're using up green sensing proteins. When you switch to a white wall you're now seeing more red and blue compared to green, and thus it appears pinkish.
Your brain somewhat tricks you into thinking that the green you're seeing is the same was it was when you first looked at it, but you're actually sensing less of it the longer you look.

Perhaps "temporarily deactivated" or "in a refractory period" is a better term than "used up", as the latter term implies the protein was destroyed by the process.

The cones are definitely not in a refractory state (they don't spike) and, technically, not deactivated either. "used up" is actually pretty apt.

@ChrisStronks Can you explain why they are not, though? https://books.google.co.uk/books?id=ask7iOrvjJIC&pg=PA481&lpg=PA481&dq=color+cone+refractory+period&source=bl&ots=3fU0u3trDO&sig=QaP522JuocfShsu7squ1LIY4h-A&hl=en&sa=X&ei=28uTVPK0PNCv7Aat-ID4Dg&ved=0CDMQ6AEwAw#v=onepage&q=color%20cone%20refractory%20period&f=false is an example of scientific literature using the term.

Refractory periods refer to action potentials causing sodium channels to enter an inactivated state. Deactivated implies regulatory action of some kind. That is not the case. The active cone rhodopsin is simply depleted.


text:
Which wavelength to use to determine algae using a colorimeter?
I am doing a Biology project involving the measurements of the density of algae (Nannochloropsis) using absorbance colorimetry. What wavelength should I set my colorimeter to?
The issue is that there are two types of chlorophyll, each with a different absorbance optimum, there is spectral scatter to consider, as well as UV absorption when going to low wavelengths. What to do?

From Biotek I learned the following:

Spectral scans of algae cultures demonstrate significant absorbance below 400 nm as well as two distinct absorbance peaks at 440 nm and 675 nm (Figure 1). Cell number determination is most consistent when light scatter is used rather than absorbance by cellular constituents. In order to avoid influence from absorbing material 600 nm [is best] to monitor growth.

Figure 1. Absorbance spectral curve of Microcystis aeruginosa suspension cultures.Source: Biotek


text:
Can C. elegans be raised on Lactobacillus as the only food source?
I'm interested in running some C. elegans experiments for educational purposes, but would like to avoid having to grow or handle E. coli.  I was wondering if C. elegans need E. coli specifically, or if they would grow well on most (non-pathogenic) kinds of bacteria.
In particular, I'm curious about whether C. elegans would grow on (either live or pasteurized) yoghurt, including strains such as Lactobacillus acidophilus and L. delbrueckii.
I did a quick literature search and found a few articles (like this) which talk about screening probiotics in C. elegans by adding them as part of their diet, but I haven't been able to find any reference to using them as the only food source.


text:
How many of each structural component of SARS-CoV-2 are there?
I'm interested in the composition of SARS-CoV-2, including how many copies of each protein are present in an assembled virus, as well as the overall mass and density.  There are a few recent papers such as Klein 2020 and Yao 2020 which provide a lot of useful info on the structure of the virus, but they do not completely answer that question.  For example Klein estimates 48 (range from 25 to 127) copies of S, but doesn't say anything about how many copies of M, N or E there are.  I have not been able to find a full answer even after a pretty thorough literature search.  Considering how good molecular biology (and imaging) tools are nowadays, and the importance of the subject, this seems like a pretty astonishing gap in knowledge.
Question: What is the exact composition (stochiometry) of SARS-CoV-2, in terms of how many copies of each building block are present in each virus particle?

Spikes are somewhat easy to see and count on an electron microscope image. Not sure why you think the other ones are just as easy to see/count.

And I'm rather doubtful you'll find a firm answer. Seven years after SARS discovery, there was still disagreement as to its M-assembled structure. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4486061/

Even shotgun mass spec should be able to quantify everything using the quantity of RNA as a reference.  Tools today are way better than in 2011 when the Neuman article was published.  Could you please link any articles that show people trying to do this kind of quantification and running into problems?

@Fizz I agree that it would be hard to get this type of data from SEM.  There may be other options that allow proteins to be counted, for example TIRF or STORM single molecule imaging, or TEM with antibodies conjugated with gold nanoparticles as contrast agent

Probably there are some data of this kind, surely not as exact as in stochiometry. There must be a basis for this picture https://commons.wikimedia.org/wiki/File:Coronavirus._SARS-CoV-2.png?uselang=de . Ah, note that the virus membrane itself is stolen from the host cell and not made by the virus.

@jk-ReinstateMonica Yes, although the virus membrane is budded off from cell internal (organelle) membranes of the ERGIC, not the external cell membrane.  For that wikipedia picture, it originally comes from https://nplus1.ru/, there is a nice article about how it was made (with a bibliography even).  But it doesn't seem like there is an accurate count of M or N in any of the bibliography sources either :)

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text:
Does breathing air containing 3% carbon dioxide gives you a headache?
As far as I know, breathing air containing relatively high levels of CO2 may get you a headache.
I also know that CO2 level in the fruit bodies of peppers can reach levels as high as 3% at certain stages in development (Blasiak, 2006). So clearly it is possible in a natural setting to achieve these high level of CO2, at least in a micro-environment like around the locules of pepper seeds developing in its fruit.
So I was wondering, if we would have to breath air containing 3% CO2, would get a headache if we breath it in?

Do you have the source?  If not, it's hard to know what the number is referring to.

The source: J. Blasiak et al., JASHS 131, 164 (2006). http://journal.ashspublications.org/content/131/1/164.short

To close-voters - I edited the question during the close-vote process to reflect the linked article posted by OP. Please re-consider when voting to close when you your decision on the previous efforts of others as question is changed.

totsha - feel free to change my edits, or roll back when the edited question does not reflect your intended original question any longer.

http://en.wikipedia.org/wiki/Carbon_dioxide#Toxicity
"In concentrations up to 1% (10,000 ppm), it will make some people feel drowsy.[83] Concentrations of 7% to 10% may cause suffocation, even in the presence of sufficient oxygen, manifesting as dizziness, headache, visual and hearing dysfunction, and unconsciousness within a few minutes to an hour.
...
Occupational CO2 exposure limits have been set in the United States at 0.5% (5000 ppm) for an 8-hour period.[90] At this level of CO2, International Space Station crew experienced headaches, lethargy, mental slowness, emotional irritation, and sleep disruption."
So according to this, yes you could breathe it, and yes, you would get a headache."

It would take a lot of peppers to get 8 hours worth of pepper air.

Where there's a will there's a way!


text:
Nature of sight/ color perception?
I am wondering how we perceive color and whether that is dependent on the wavelength of the light, or on something manufactured in the brain.
For instance, if we evolved on a planet orbiting a red dwarf star, would we see colors differently than we do now, given that our sunlight has another wavelength composition?
I know that there have been experiments where volunteers have worn glasses that make them see the world upside-down and eventually the brain corrects this and they see right-side-up again (and have to re-adapt when removing the glasses). I wonder if something similar would happen with color perception.
Does anyone know of any studies done that have tested this?

I'm voting to close this question as off-topic because it is primarily opinion-based, as it is asking about a hypothetical situation. This question may be more on-topic at the [worldbuilding.se] Stack Exchange.

@MattDMo - I think it boils down to whether we can test color perception, or only color sensation. It's an OK question imo. +1 I've refined it a bit.

The color you perceive is ultimately dependent on the relative contributions of the color photoreceptors in the retina, namely the red, green and blue cones. The sensation of color, therefore, is physically determined by the wavelengths in the light source and the absorbance spectra of the cones. Thereafter, the neurophysiological wirings of the retina and the brain take over and these paths are pretty well defined too. However, one cannot say anything about the qualitative perception of someone observing a light source. This is the big difference between sensation (peripheral processes including the retina) and perception (central processes).
To quote the late Bach-y-Rita: 'You see with your brain, not with your eyes.'
Everything we perceive ('see') is a subjective construct devised by our brains. No red dwarf star is necessary to pose the possibility that you perceive my perceived red as green, or vice versa. No experiments can be conducted to prove or disprove a hypothesis like this.
In terms of experiments: we can test stuff like 'up' versus 'down', as with the prisms mentioned in the question. This, because a subject can qualitatively point out where an object is perceived relative to others, and that can be objectively measured. However, we cannot test the subjective quality of color. We can test relative color contributions through color matching experiments (Kalloniatis & Luu, 2012). These experiments will tell you which contributions the red, green and blue cones have in a certain color mixture, but they will not tell the researcher anything about the subjectively perceived color by the test subject in a qualitative way.
Reference
- Kalloniatis & Luu. Color Perception. In: Webvision. The Organization of the Retina and Visual System, Moran Eye Center (2012)

Thank you for taking my question seriously even though it seems kind of silly at first. I thought that maybe if a person was in a different (more mono-chrome) "light environment" that he/she might eventually see more diversity of color as our brains reinterpret the information that the light cones of our eyes gather. I thought that this may be something that could be tested.

@JackR.Woods now I understand your question better, thanks for that. Although I doubt I can add much relevant info,  I can try to edit my answer. If you don't mind I can re-edit the question too and see if anyone else has ideas?


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Why do we have five fingers?
Humans (and other humanoid mammals) have five fingers in each hand.
Curious to know, why five? Wouldn't more fingers be more useful?
Is there any evidence that it used to be different and natural selection caused those with five fingers to survive?

Related post

Thanks @WYSIWYG, missed it due to not knowing "digits" is used to describe fingers and toes.

Cost / Benefit. More fingers need more neurons devoted to controlling and coordinating them which means less neurons for other stuff. And I suspect the amount of coordination need probably increases exponentially which each additional finger. I'd also argue that the fact you can't move your pinky completely separately from your ring finger is a sign we're already on the limit of what we can support. The benefit of a sixth (or seventh, or eighth) finger on the other hand is probably pretty minimal (diminishing returns).

@Matt interesting, if you can elaborate with scientific quotes this might make a fair answer as well. :)

I found an interesting article in Scientific American (Coates, 2005), and I quote part of it:

The condition of having no more than five fingers or toes [...] probably evolved before the evolutionary divergence of amphibians (frogs, toads, salamanders and caecilians) and amniotes (birds, mammals, and reptiles in the loosest sense of the term). This event dates to approximately 340 million years ago in the Lower Carboniferous Period. Prior to this split, there is evidence of tetrapods from about 360 million years ago having limbs bearing arrays of six, seven and eight digits. Reduction from these polydactylous patterns to the more familiar arrangements of five or fewer digits accompanied the evolution of sophisticated wrist and ankle joints--both in terms of the number of bones present and the complex articulations among the constituent parts.

So Coates states that around 360 million years ago there were tetrapods with more digits (6, 7, 8), but that this was reduced to 5 about 340 million years ago. Losing things in evolution is generally relatively simple, yet re-gaining them is hard. So while there is still a tendency for evolution to create species with less digits, there are no examples of land dwelling species with more than 5 digits.
The author reasons that more digits do no good on land as more digits impair locomotion. Most polydactylous species were indeed found to be aquatic.

How do more digits impair locomotion?

@Nit: You need to coordinate all those digits as you walk making the process more complicated.

So, why we do not have three fingers?

Well, doesn't more digits create more traction? That's kind of the whole point of having fingers and toes, that an animal can create more surface are contact with any given object in a controllable manner. However, more digits are also more complex and would require more metabolism to keep alive as well.


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Can androgen-insensitive genetic-males get pregnant?
According to the linked report, people with androgen insensitivity syndrome appear as male, but have both feminine and masculine outer genitalia.
However, I was not able to find out whether their internal reproductive system is functional, i.e., if these people have a functional uterus.
Is it possible for such a person to get pregnant?

A "bug" is basically an insect or a computer software fault. Use proper terminologies. Please try to put in some basic effort. I could have simply said "no humans do not self-fertilize", but it is important to follow some basic discipline. Since you are a programmer and an active SO user, you would perhaps react the same way if I just ask a question without even attempting to code.

I specified the pathology in the question according to your linked report. Without mention of a pathology this question is too broad to my opinion. However, feel free to roll back if it doesn't reflect your original question.

Short answer
People with androgen insensitivity syndrome do not have a functional uterus and cannot bear a child.
Background
Androgen-insensitive genetic males may develop female genitalia and internal female reproductive organs. However, in both partial androgen insensitivity syndrome (PAIS) and complete androgen insensitivity syndrome (CAIS) the uterus is absent, or is present only in a rudimentary form.
The reason for the absence, or rudimentary form of the uterus is the fact that Mullerian inhibiting substance (MIS), produced by the Sertoli cells of the fetal testes is present. MIS controls the regression of the mullerian ducts, and in its absence in XX females, the mullerian system develops into the uterus, oviducts, and upper vagina. However, in XY individuals with CAIS (and likely also with PAIS), MIS is produced normally by the testes resulting in inhibition of the growth of the uterus and fallopian tubes (Oakes et al., 2008).
Reference
- Oakes et al., J Pediatr Adolesc Gynecol (2008); 21: 305-10

@mdperry - you cannot tell by looking who is an XY female, and your comment is misleading. I am not tall, and the two XY females I've known as friends are diminutive and certainly not fashion-model material. They are, in fact, no different from me in appearance, except they can't reproduce, and they are usually on hormone replacement therapy.


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Immediate stroke/seizure Therapy
Can an oncoming stroke/seizure, be stopped by a setup consisting of a brain-computer-interface (BCI) that immediately detects the variation in wave-form, and then another machine that neutralizes the anomaly by sending a measured voltage to select areas of the brain OR by Transcranial Magnetic Stimulation?

Can you please use names (not initialisms)? What is a BCI? Also, stroke and seizure are two completely different entities. You can't stop a stroke with electricity or transcranial magnetic stimulation.

Welcome to Biology SE. Nice qunction - I think the seizure part is an interesting thought. However, how a stroke could be detected by its electrical signature, or how it could be prevented by electrical stimuli seems a bit out of context here, and hardly possible for that matter. Perhaps consider focusing on seizures to give the question focus.

@anongoodnurse (I hope you get a ping - I am mobile) - when giving it a second thought - if it would be possible to transfer a large current and coagulate the impeding rupturing vessel, one could, theoretically, use currents to prevent a stroke? But again, predicting it by electrical recordings seems impossible.

To give a jolt strong enough to coagulate blood in a vessel might do more harm than good... and then there are ischemic strokes (>80%).

@anongoodnurse - I see, practically it clearly doesn't make sense - thanks for this.

This is more of a long comment than an answer:
There have been active research in this area for several decades now. The problem is that once you detect seizure (which is relatively easy), it's usually too late. Therefore, a lot of effort has been to predict epileptic seizures some time before it happens. This has proven quite difficult.
See this review article for the state-of-the-art in 2007:

Mormann, F., Andrzejak, R. G., Elger, C. E., and Lehnertz, K. (2007). Seizure prediction: the long and winding road. Brain, 130(2):314-333.
http://ntsa.upf.edu/system/files/biblio/Mormann-Brain2007.pdf

Yes, these devices and treatment programs are being actively developed. General idea is that epileptic episode follows certain path within the brain. It can start in thalamus, after which sporadic activity spreads into cortical areas, for example motor cortex. There is a number of papers on prediction of epileptic seizure, e.g. Seizure Prediction and its Applications.
The device then will detect initiation of seizure before evident symptoms and provide inhibition via cortical electrodes, microelectrode array (MEA). It seems that currently MEAs are used more for research (recording from tens of neurons), but single electrodes are useful for actual control of epilepsy. Also one can control vagus nerve, which causes parasympathetic response (general inhibition, aka "rest-and-digest"). More you can read here.
Transcranial magnetic stimulation, as I understand, is not portable enough to be useful.


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How did multicellular life evolve?
I can imagine several specialized unicellular beings collaborating. But how does life get from that point to a unique pluricelular being that reproduces into another pluricelular being?

The key is specialization: e.g. some cells specializing in getting food, others in producing something sticky to keep them together. Which cell does what is usually determined by chemical signals: depending on their specialization they produce particular chemical compounds. So if a non-specialized cell notes that one compound is rather low because the specialized type of cell producing it is in low supply then it specializes that way.
While initially all cells are capable of reproduction, at some point there also will be cells specialized for reproduction, whereas the others lose the ability to reproduce to better concentrate on their specialized duty. Hence the other cells do not have an independent existence anymore but exist only as part of the larger organism. When such an organism is then to be considered a separate pluricellular entity is a matter of definition: if it is an entity independent of the original (e.g. capable of moving away)? if sexual reproduction happens?
Wikipedia also has some things to say.

Welcome to Biology SE and thanks for your interesting answer. At Biology SE some references are appreciated to substantiate answers to allow people to validate the answer or for further reading. Thanks.

Ps: although wikipedia is a much referenced source, it is unfortunately one of the most unreliable sources as its contents change continuously. +1 for your answer.


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Why don't myopic people see the world upside-down?

I found this image while reading optical instruments in physics. If we look at the uncorrected rays, we see that the image they outline gets inverted. So why don't people with myopic vision see images as inverted representations?

Could that diagram be exaggerated? Maybe the uncorrected ray in a real eye is focused just in front of the retina rather than in the middle of the eyeball.

@user137 even if that's the case then still it would be inverted, right?

@LucyferZedd - I slightly modified your wording. Please feel free to roll back, it's just a suggestion.

You have misinterpreted the nature of the light rays shown in the diagram in the question.  The two rays are representing light coming from the same (distant) point in the environment, that is, some small feature on an object is reflecting (or emitting) light in slightly different directions and reach the eye separated by a small amount (less than the width of the pupil).  The rays are almost, but not quite, parallel.  The two rays, coming from the same point, should be focused on the same point on the retina (as are the red rays corrected by the external lens).  The spread of the uncorrected rays in myopia or hyperopia sends them to different places of the retina, causing the image to be out of focus, not upside down.
The path of light from an entire scene can be illustrated like this:

As this diagram shows, the image is upside down for all of us, in focus or not.  That the image top is at the bottom of the retina is not especially important -- the cells doing the interpretation could have been located physically located anywhere as needed.

seems, it's not the light rays coming from different parts of the object reflecting the light, but rather the light rays reflecting off of the same part or closely adjacent part of the object but going to different parts of the eye, "misaligned rays"... a quote from opthobook: "punch a small hole in a paper card, and have your patient reread the eye- chart while looking through this pinhole. This technique can actually improve vision by several diopters. It works because the paper blocks most of the misaligned rays that cause visual blur, and allows the central rays to focus on the retina."

Overview
Myopia does not cause image inversion. @mgkrebbs provides an answer with a clearer diagram than the one you have provided that illustrates how only the focussing ability, not the orientation, of an object changes.
However, an image can be inverted by special inversion glasses. Furthermore is that the brain can convert the image to the right way around.
Although myopic vision can't cause the inversion, the answer you're looking for is probably that perceptual adaptation, a phenomenon that occurs to correct our vision, comes into play in cases of inversion. The brain "gets used to" inverted images and what you visualise becomes the correct orientation. So lets say myopia did cause inversion, the person with naturally inverted vision wouldn't experience anything unusual.
Experimental Evidence
The below text from the wikipedia entry describes an experiment with inverting glasses. These glasses contained prisms that flipped the real world image before it reached the eye. Note the experiment was carried out in the in the late 1800s.

On a later experiment, Stratton wore the glasses for eight whole days. By day four, the images seen through the instrument were still upside down. However, on day five, images appeared upright until he concentrated on them; then they became inverted again. By having to concentrate on his vision to turn it upside down again, especially when he knew images were hitting his retinas in the opposite orientation as normal, Stratton deduced his brain had reprocessed his vision and adapted to the changes in vision.

A more recent study by Linden et al., 1999 confirmed the same thing happening with more up to date inverting glasses. The subjects reported slightly different results. Rather than the image being inverted, it was more the case that the subject felt their reality became inverted to match the inverted image. I can't see someone suffering with myopic vision being able to make this distinction since they would only be used to one orientation.
Figure 1 from Linden et al., 1999
On removal of the glasses, the world becomes temporarily re-distorted, but normal vision and perception returns.

How myopic do you need to be to invert the image? I don't notice any problems taking my glasses off, so the image either isn't inverted or my brain adapts within the half a second it takes to remove the glasses.

Undoubtedly interesting, but not relevant to the question; myopia does not cause image inversion.

@user137 I had doubts that myopia would cause inversion except in extremely severe (possibly only hypothetical) cases, but mgkrebbs explains why this wouldn't happen. Here I am just answering a hypothetical about the brain correcting an inverted image.


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Does the nervous system have "routers"?
Does the peripheral nervous system have a system of routers that decide where a message is meant to go based on some kind of address, or does a signal from the brain follow a single, unbroken chain of neurons that starts at the brain and ends at one destination?
For example, let's say my brain wants to send a message to my left pinky, telling it to contract. In the first model, a series of action potentials travel down my spinal cord, reaching a node in my chest. The action potentials encode the "contract" command as well as an address. The node in my chest reads the address, and routes the signal down my left arm. It reaches my left hand, where another node reads the address and sends the signal to my left pinky, where the signal reaches the appropriate muscle, telling it to contract.
In the second model, every single muscle in my body has a particular chain of neurons that runs in parallel to my brain. If my brain wants to send that signal, it doesn't have to specify an address, it just sends the "contract" command down the path that says "Leads directly to left pinky and nowhere else".
If the second model is true, does that mean that the large, visible structures that we call "nerves", such as the vagus nerve, are actually bundles of point-to-point connections?
Anywhere I can find more information about this would be awesome. I'm a comp sci/biochem double major, and really love reading about the body as an information system.

while the second model is correct, at many points along the chain there is a choice of whether or not to proceed (sort of address)... example, the sensory pathway going from the body to the brain, the thalamus is a relay that decidedes whther or not to permit a signal (spatial or temporal summation) that is determining further access up into the cortex... not sure what exactly is coded within the signal and how the cortex communicates with the thalamus to say how strict the gate keeping should be... I suppose the same occurs in the descending sensory pathway that is involved in pain gating...

The second model is the one. No tags, flags, or routers, just a 1-to-1 system.
A striking example of this is are the different effects of spinal cord injury, which depend on the place where the injury occurs.

And I quote from the apperalyzed website:

Spinal Cord Injury Overview
When a person suffers a spinal cord injury, information traveling
  along the spinal nerves below the level of injury will be either
  completely or partially cut off from the brain, resulting in
  Quadriplegia (Tetraplegia) or Paraplegia.
[...] The brain will still be trying to send messages downwards to the
  muscles in the body, known as motor messages. These messages however,
  will be blocked by the damage in the spinal cord at the level of
  injury. Nerves joining the spinal cord above the level of injury will
  be unaffected and continue to work as normal.
Quadriplegia / Tetraplegia [occurs] when a person has a spinal cord injury above
  the first thoracic vertebra. Paralysis usually affects
  the cervical spinal nerves resulting in paralysis of all four limbs.
  [...]
  Paraplegia [occurs] when the level of spinal cord injury [is] below the first thoracic spinal nerve [and leads to] paralysis of the legs and abdomen up to the nipple line, [but] paraplegics have full use of their arms and hands

This example shows that there are strict one-to-one connections (2nd model) and that messages are not simply flagged and routed to their destination via the shortest or quickest route available among a bunch of redundant, ill-defined pathways (1st model). Hence, there is only one way from the brain to the periphery; once severed the message cannot be simple re-routed via parallel lines.
Another example is the make-up of the sensory-motor cortex:

The picture shows that the motor cortex (muscle control/motor output) as well the sensory cortex (sensory input) contain a complete image of the body. Each part of the motor cortex and sensory cortex is devoted to the control or sense of one specific part of the body, respectively.
Nerves are indeed typically bundles of 1-to-1 fibers. For example, the optic nerve contains fibers that carry info from one, and only one well-defined and localized pixel from the retina to the brain.
Principles of Neuroscience by Kandel and Schwartz is a great book with a wealth of info.

authors: Валера Воробьев


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What really is color and how do we perceive it?
How do our brains actually transform the information that the cones in our eyes  receive into the different colors that we can see and imagine?

Related: http://biology.stackexchange.com/questions/39882/are-some-animals-like-dogs-and-cats-color-blind-and-how-do-we-know-that/39890#39890


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How do afferent mechanoreceptors work on the finger pads?
I'm having some difficulty understanding how the afferent signals are sensed in the finger pads. My understanding is that for mechanoreceptors, as the indenting force increases, their effective response also increases. Additionally, as contact area increases, so does the overall stimulus area and hence a larger response amplitude from the mechanoreceptor afferents should be found.
However, the results shown in this article in the Journal of Neuroscience that discusses this physiology shows contradicting results. In this article, the closer the dot spacing (1 mm or less) and the higher the contact area the lesser the receptors seem to fire, and stop firing altogether at about 1 mm dot spacing?
Why would this occur?

I made some edits to your question... not trying to change your question but only clarify it for other users so you can get a good answer from someone.

Unfortunately, this is not a "please hold my hand and walk me through this paper/concept/idea" site. I strongly suggest you take the [tour] and carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and how to ask a good question.

This is a really tough question to answer. I skimmed through the linked paper (authorative authors there!) and the last part of the discussion goes into more detail on this question, including references to other papers. I may get back to this question, but it's going to take me a while. Good question! +1

Can you also pinpoint the figure numbers so that the actual issue is easier to spot?

This took me a while and my apologies - I have to add that it's an excellent article with a set of awesome authors and it was an enlightening read. Thanks so much - I learned a great deal :) I'm actually writing a paper on this stuff as we speak, so questions like this make this site so fruitful :-)

Short answer
Tactile grating stimuli with a higher line density (number of lines per surface area) and applied with an equal force result in a lower amount of pressure per unit of skin area under the grating, and hence smaller afferent responses.
Background
In the Discussion section of the linked article (Phillips et al, 1993) the authors explain on p. 838 (left column) that the reduction in the response of SA afferents (slowly adapting fibers) when grating density is increased is due to the higher proximity of neighboring areas of stimulation, i.e., the lines in the grating stimuli are more closely spaced. The authors reason that this leads to a reduction in the effective stimulus (i.e., compressive strain) at the receptor terminal due to the presence of adjacent stimulus elements that distributes, and hence reduces the skin loads per line.
Reference
- Phillips et al, J Neurosci; 12(3): 927-39


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Can excessive carbonated drink consumption lead to elevated red blood cell levels?
I've recently had a blood test and the results displayed elevated levels of erythrocytes as well as hemoglobin. (As a result my hematocrit levels were also above average)
At my workplace there is a water cooler which also has an option to dispense carbonated water (this is just regular ol' carbonated tap water) and usually over the course of the day I tend to drink quite a lot of the stuff.
Since erythrocytes/hemoglobin deals with O2 and CO2 transport, I was wondering if my daily consumption of carbonated water is a plausible cause for the additional erythrocytes that are being pumped out?

The main regulatory input into erythrocyte production is hypoxia. The response to elevated CO2 levels in the blood (hypercapnia) is mainly to increase ventilation (i.e. more and/or deeper breaths) so that the excess can be "blown off".
I think that some carbon dioxide could pass into the bloodstream from the stomach since gases tend to be quite good at diffusing across membranes, but this would be easily dealt with by the physiological mechanism described above.

Answer: No. How should the CO2 from you stomach get into your blood?
And: Most of the CO2  is removed (by burping) from the solution in your stomach anyway due to the conditions there.


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Where do I get an annotation file for yeast genome with ENSEMBL ids?
Even the annotation files hosted on  the Ensembl site have systematic names (starting with Y..) instead of ENSEMBL ids (starting with EN..).
I bet there would be a place where I can get an annotation file (GFF3 preferably). Please let me know if you know such.

With a further search for the answer, I realised that unconventionally, ENSEMBL ids for yeast start with Y. That is strange. I guess this is because the yeast annotations are primarily maintained by SGD (yeast genome database) and ENSEMBL just hosts a copy of that.
Also these ids are called Stable Gene IDs.


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Orange Fungi on Oak tree
The fungus in my profile pic is bright orange in a ball growing out of the cut off branches scar, also in a necklace.  There are egg shell white broken balls instead of the orange balls-suggesting the orange ball explodes and the seed depart leaving the white shell bottom.

The picture is missing, please add it for clarity.

@Chris look at her profile pic :-)

Too small! Can't see detail! :(

http://leslieland.com/2009/09/hunting-laetiporus-sulphureus-the-sulfur-shelf-or-chicken-mushroom/  I think this is the answer.  I have great pictures, but don't know how to add them.


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What are the reasons which make intron detection uncertain?
Intron/exon sequence detection seems to involve statistical prediction which can at best deliver a guess (until experimentally confirmed) as to where the splice site is.
What are the reasons why there are no deterministic (rather than consensus) sequences which signal the location splice sites?
Trying to answer this myself, I guess the obvious one I can see is chromatin structure, which interacts with how RNA polymerase reads the DNA strand.  If this is the case however, isn't the current way of describing DNA as a sequence of AGCT base pairs fundamentally flawed?  If chromatin structure is actually part of the functional description of DNA, then are there any efforts being made to describe this?


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Spinal cord injury bypass
When the spinal cord is damaged, the connection between the brain and some part of the body may be lost.
To restore this connection, researches are considering either:

Repairing the damaged area so that the spinal cord works again.
Bypassing the spinal cord by connecting the brain directly to the affected part of the body.  This is done by implants in the brain connected directly to electrodes in the muscles creating a new circuit in parallel.

My question is has there been any attempt to bypass only the damaged part of the spinal cord?  To create a bridge over the damaged tissue?

This question is poorly worded and hard to answer as it stands. Consider restating more clearly what you are asking.

Ok sorry I am not a native english speaker, I will try to be more clear

Interesting question!
There has been at least one study that bypassed a spinal lesion site with autografted neuronal tissue (Tadie et al., 2004 - doi:10.1089/089771502320317069). The study participant regained voluntary motor skills 8 months after bypass surgery. The surgery involved the implantation of nerve autografts between the rostral spinal ventral horn and the caudal ventral roots. Regain of motor function was observed after the patient had been paralyzed for 3 years.

Nice answer, I was talking more about electronic solutions but it is still interesting. I cannot access the entire article, what is a "nerve autografts" ?

Nerve autografts are nerve grafts taken from the recipient himself/herself  (auto means 'self' in this context).


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Why is competitive inhibition reversible?
My Biochemistry book mentions that 'competitive inhibition' is a reversible form of inhibition. But given that the inhibitor is blocking the active site and prevents an enzyme-substrate complex to be formed, how can it be reversible?

Not all competitive inhibition is permanently irreversible. Only substrates which bind covalently are irreversible. Something like Narcan(Naloxone) is a competitive antagonist, but it is not permanent.

A competitive inhibitor typically competes for the active site with the substrate. In this textbook case, binding of a competitive inhibitor is reversible, because it binds to the active site of the enzyme, but is also released, making way for the substrate to bind. The affinity of the substrate, as well as its concentration determine the amount of inhibition (Berg et al., 2002).
An irreversible inhibitor may covalently bind to the active site, permanently disabling the enzyme (McDonald et al., 2012).
References
- McDonald et al., Enzymes: Irreversible Inhibition. In: eLS. John Wiley & Sons Ltd, Chichester (2012)
- Berg et al., Biochemistry. 5th ed. New York: W H Freeman; (2002)

In light of this meta post, this might be the single greatest answer of all time. I had a good laugh.

@canadianer thanks :-) It was a bit of an over-reactive response to someone claiming the answer was undersourced (a whole string of comments has been deleted since). Admittedly, it was indeed undersourced, but to me its contents are common knowledge and I didn't even bother to source it. Well, after it had been scrutinized even in a meta post, others began to interfere, mainly long-term residents here who knew I was probably among the last deserving to be blamed for not sourcing his answer :) Eventually it lead to the above result....

The high number of upvotes is totally not representative of its quality, it's just that people appreciate the principle of sourcing answers to that extreme point where it becomes just plain silly :)

@xusr thanks for your input. It sounds like you could write an excellent answer. In the meantime, I have adapted the wording of my answer above to reflect your thoughts. My approach was to give a schoolbook answer to a schoolbook question. Nothing more, nothing less.

It's water under the bridge, but if I were writing a schoolbook answer I would have included a diagram and an equation. School books are the most highly reviewed and edited form of literature. The publishers stand to lose a lot if they get things wrong in a very lucrative corner of the market.


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Electrically facilitated active transport across a membrane
I'm trying to go back to school to do a PhD in control theory, specifically concerned with control of glucose. The glucose system can be controlled using two chemicals: insulin and glucagon. I was wondering if there was any precedent for controlling the active transport of a chemical across a membrane using a tiny electric current. Has this ever been done?
The reason I ask is that I want to avoid relying on mechanical systems that are prone to being bogged down by attacks from the native immune system.
Any knowledge on the subject/recommendations for attacking this problem/alternative subreddits or websites would be greatly welcomed.

Welcome to Biology. Electroporation is an example where DNA is injected into a cell using a (high?) current. But I think it works only with charged particles. Glucose is uncharged.

Thanks for the info. The glucose wouldn't need to be injected anywhere per se, just "let go" from a reservoir into the blood stream.

You may want to take a look at some of the research behind insulin pumps. I don't know the specifics, but I know they use a lot of closed-loop control, and are a fairly active area of research (but potentially difficult to get into--some people have been working on control problems related to glucose since at least the 80's).


text:
What would be required to evolve an animal (non-human) brain to obtain human-level cognition?
Could any animal subject to the right conditions evolve human-level intelligence? Suppose that an artificial intelligence (AI) decided to artificially evolve a population of octopus (don't ask why, its for science) by restricting them to calculated environmental pressures, and over millions of years, the AI manages to produce a relative of the octopus that has a similar level of cognition to humans. Is this possible? If it is possible, what are some steps (in general) that might be required to evolve a complex animal brain (to human-level cognition or beyond)?

I think this question is far too broad and answers will probably be opinion-based/speculative, and have therefore voted to close.

@fileunderwater - I disagree. There are many factors identified that have resulted in the development of the human brain. Particularly the cerebral (neo) cortex is associated with higher cognitive skills; the subcortical structures have been very stable during evolution. No need to close this one. The formulation may be a bit awkward (OP is a computer scientist I guess, explaining the question pitch) but i see no reason for closure.

@AliceD Just because something is answerable in some kind of shape and form(at) doesn't mean it is a good fit for the site. This is spanning from neurobiology to evolution, natural selection and evolutionary constrains, is very speculative, and is asking if this scenario is "possible" (by definition "opinion-based"). I just think it is problematic to keep these kinds of questions open, if we aim to treat all questions in a consistent way. However, users of the site will decide if this should be kept open.

@fileunderwater, you might be right, I agree it is a bit of hazy question... It's just interesting stuff. Perhaps i am biased. Perhaps not. I could make a bash at re-writing this question into something more rigid, but somehow I don't like the idea of that...

Answering the question what is needed for a human brain to evolve starting from a cephalopod brain is hard. However, I can expand on what is thought to have been the driving forces behind the evolution of the humanoid brain (Hawks, 2013):
The species of the famous Lucy fossil, Australopithecus afarensis (~3-4 mln yrs ago), had skulls with internal volumes of between 400 and 550 milliliters, which is comparable to chimpanzees and gorillas. Australopithecine brains started to show subtle changes in structure and shape as compared with apes. however. For instance, the neocortex was expanding, which is an indication that the evolutionary pressure on higher functions of the brain was important.
Homo habilis, the first of our genus Homo, who appeared 1.9 million years ago, saw a modest hop in brain size, including an expansion of a language-connected part of the frontal lobe called Broca's area. The first fossil skulls of Homo erectus, 1.8 million years ago, had brains averaging a bit larger than 600 ml. This shows that language development is a likely factor that has driven evolution of the human brain.
By 500,000 years ago, the humanoid brain reached a volume of about 1,000 ml. Early Homo sapiens had brains within the range of people today, averaging 1,200 ml or more. It is thought that cultural and linguistic complexity, dietary needs and technological prowess took a significant leap forward at this stage, and that our brains grew to accommodate the changes. The shape changes we see accentuate the regions related to depth of planning, communication, problem solving and other more advanced cognitive functions.
Interestingly, in the past 10,000 years of human existence the brain actually shrank. Limited nutrition in agricultural populations may have been an important driver of this trend. Industrial societies in the past 100 years, however, have seen brain size rebound as nutrition increased and disease declined (Hawks, 2013).
Indeed, one of the driving components behind the expansion of the human brain is increased availability of fatty fish to sustain the large amounts of fat needed in a brain - survival of the fattest (Cunnane, 2006).
Although the past does not predict future evolution, a greater integration with technology may lead to further expansion of the human brain (Hawks, 2013).
References
- Cunnane, Med Sci (Paris) (2006); 22(6-7):659-63
- Hawks, Sci Am (2013)

but "what are some steps (in general) that might be required to evolve a complex animal brain"?

The bolded-out points in my answer are some essential human skills on which evolutionary pressure may have had its effects driving evolution (as to the question title: requirements). I have, admittedly, not directly attempted to answer the question what steps are needed. I find steps needed a vague term, and open for various interpretations (spanning molecular level to anatomical levels). Instead, I have focused on the what was important for early humanoids and how did that affect the brain. This is less opinion based from my point of view.


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term for species that produces males only to mate with mother or sisters
In reading about unique reproductive strategies I've run into two closely related and comparatively unique mechanics.  Both involved a female who was born 'pregnant' with at least a male, but the male sole job was to impregnate the mother/sisters prior to immediate death, with the females never mating with a male other then their relative.  Thus, the outcome feels more similar to self fertilization of hermaphrodites then your traditional mutli-sex mating strategy.
I have heard of at least two species that did this.  One in which the son was born along with a batch of females that he immediately mated with, another where the son actually mated with his sisters while still in the womb, and the children would then eat their way out of the mothers corpse to be born (fun stuff!)
I also recall reading an article which said a mother would lay an egg to have a son who would mate with the mother to produce females and then immediately die.  However, this sounds so similar to the Haplodiploidy system that I wonder if the article I had been reading was simply misrepresenting a regular Haplodiploidy system by implying the males would never mate with other females (I read about it awhile ago so not sure, does anyone know if a species uses a haplodiplody system where the male never survive long enough to mate with other females?
I'm wondering if there is a name for this reproductive strategy.  Specifically for any strategy where a male is produced, but only as a means of providing DNA to mother or sisters; with no means to mate with non-familiar entities.

Dont bee's do this to some extent, via producing males for reproduction, and males for working? And if so, would that be considered Eusociality? Sorry if I am way off base, I am an undergrad. https://en.wikipedia.org/wiki/Eusociality

@RoSiv the first example I gave was one involving mites which do not have a eusocial (is that a word?) system.  Bees may do the same thing I described, but if so I think that's separate from eusociality.

@RoSiv - Bees aren't a good example of this as the drones of a hive leave as adults to find virgin queens to mate with. The queen of their hive mated with a drone outside of her birth hive to begin her own colony. She doesn't need to mate again.

The non-random mating of individuals within a population is called Assortative Mating. Mating specifically with individuals that share similar traits is called Positive Assortative Mating. However, sharing similar traits doesn't imply being closely related.
The reproduction by two closely related individuals is called inbreeding. The opposite of inbreeding is outbreeding (a.k.a. outcrossing).
To my knowledge, a mating system where all individuals inbreed doesn't have a special term. Searching google.scholar for mating system inbreeding will show you a lot of articles that talk about mating systems where all individuals inbreed without needing to use a specific term for it.


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Has research indicated how much koinophillia preferences are learned vs insinctual
I'm curious about rather the definition of 'normal', as it affects  koinophillia & mate choice, is something instinctual or learned.  To clarify I'm not asking if koinophillia itself is instinctual (I take that for granted), but instead the definition of what constitutes 'normal' vs 'abnormal' for a species which drives instinctual attraction via koinophillia.
Basically, does the definition of normal get affected by those around an individual as they grow and/or select a mate?  Can a trait that would be considered abnormal for a species be considered accepted or attractive if it is common amongst a small subset that the individual spent time in?  For instance, has any study be done in which an animal grew up among a large number of 'abnormal' phenotype animals to see rather the would later be drawn to mates that look like the peers they were raised around or the more normal appearance for their species?
In fact I'm particularly interested in the case of humans.  Does anyone know if koinophillia and attraction is affected by the environment one is raised in?  For example if someone was born in an isolated island where their populations physical features were rather unique and there was limited genetic variation/gene flow from outsiders but was raised in a family/community of people on the other side of the world with very different physical traits has a study been done to indicate rather they are more likely to be attracted to individuals from their home island, individuals that look like the community the were raised in, or no strong indication either way?


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What niche was humanity theorized to fill before we possesd weapons and coordination to hunt & kill large prey?
I'm really interested in evolution, and for a err 'hobbyist' I think I understand a good bit of evolution and adaptation and the role it has played in many species.
However, I feel I'm rather ignorant about a key period of time in human evolution.  When I try to research it (and I have!) I see discussion of humans-as-ape, right around the time we split off from the bonobo & chimp common ancestor, and then discussion seems to skip to the 'cave-man' era of more advanced stone weapons used to take down larger prey animals along with significant coordination.
There seems to be a time gap between these two points, a time when we did not yet have weapons strong enough to deal lethal damage to fleeing prey, and may not have yet had communication skills to arrange complex ambushes.  I'm trying to figure out what evolutionary niche humans possessed prior to having weaponry for killing large prey.  Were they scavengers, mostly dependent on fruits, hunt smaller prey etc?  I really have no image at all of humanity role or how it evolved during the gap prior to being capable of the coordinated hunts.
The only theory I have heard of is the use of persistence hunting to basically chase prey before it died of exhaustion.  I personally am not that big a fan of that particular theory though (ignoring the massive caloric expense per 'hunt' and difficulty of doing it in stone age, prey species would quickly evolve to not run to exhaustion from otherwise non-dangerous humans rather then constantly letting themselves be killed this way if it was the primary hunting strategy of humans).
I realize that this far in time there is no consensus on exactly how humans evolved or exact roles they may have played.  however, I'm hoping someone could point me to some theories or discussion for how pre-weapon human may have lived?

If I understand your question correctly, I think it would be easier and less wordy to indicate a date and ask about the feeding behaviour of humans at that date. I suppose you are interested in maybe 2.6 millions years ago (right before the invention of tools for hunting).

If you want to keep learning about evolutionary biology, then you might want to have a look at an introductory course to evolution. Understanding Evolution (UC Berkeley) is an online free resource.


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How to prove that pork meat has parasites
I suspect that the pork sold at a certain shop is infected with the parasite pork tapeworm (Taenia solium).
Is there a way I can prove this without special equipment? Would it work to leave the raw meat in the fridge (at 4 degrees Celcius, or higher?) for a week or so and the worms will come out of their eggs and grow big enough for the eye?

Short answer
T. solium infection can be identified in pork meat by visual inspection.
Background
The stage of the life cycle of the tape worm T. solium in pigs is characterized by cysticerci, which is the larval stage consisting of a protoscolex (head) of the tapeworm. Humans are the definitive host, which means they are the species in which the parasite completes its life cycle, reaches adulthood and is able to produce eggs.
The larvae are observable in pork meat, and cysticercosis is generally identified during slaughter when cysts can be seen in muscle or organs (Fig. 1).

Fig. 1. T. solium cysticerci. (A): as seen in infected pork. (B): excised into a Petri dish. The white dot in each cyst corresponds to the scolex. Source: Garcia et al. (2011)
It is not until these cysticerci are ingested by humans that the tape worm starts to develop fully into a meters-long tape worm, as it enters the next and final stage of its life cycle (Fig. 2).

Fig. 2. Taenia life cycle. Source: CDC
Hence, leaving the meat in the fridge will not induce growth, as a human is needed to induce outgrowth of the protoscolex into the mature tape worm.

Reference
Garcia et al., Lancet (2011): 362 (9383): 547–56


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Why did Opabinia have 5 eyes?
I recently read about a fossil called Opabinia. What intrigues me is that it had five eyes. I was under the impression that most features, such as eyes, ears and legs are always even-numbered, i.e., 2, 4, 6 etc. Why did Opabinia have 5 eyes?

Actually, even modern insects have two compound eyes and three ocelli. For example bees, wasps, and ants. The ocelli are "simple" eyes: they generally can't form clear images and their purpose is mostly light metering. From a mathematical point of view, having three ocelli might make sense if light metering is most useful for a 2D space coverage, relative to the posture of the insect in 3D space (because 3 points in a 3D space define a plane).

Short answer
The number of eyes are not always even-numbered. In fact, many present-day lower vertebrates feature an uneven number of eyes.
Background
Eyes can be generally defined as photosensitive organs. Besides the regular paired eyes, lower vertebrates such as fish, amphibians and reptiles feature an unpaired (single) brain structure called the pineal gland, or parietal eye. It is primarily a photoreceptor organ, and its electrical activity changes in response to environmental lighting (Fig. 1). The pineal does not mediate vision, and it is mainly involved in regulation of circadian rhythms (Deguchi, 1981).
Hence, many lower vertebrates can be considered to have 3 eyes. In fact, the blind cavefish Astyanax mexicanus undergoes bilateral eye degeneration during embryonic development. Despite the absence of light in the cave environment, cavefish have retained a structurally intact pineal eye. Hence, cavefish can be said to have a single eye (Yoshizawa & Jeffery, 2008).

Fig. 1. Reptilian parietal eye. Source: review of the Universe.
The mammalian pineal gland is a secretory organ only, and no longer responds to direct illumination. In mammals it is situated deep in the brain and the mammalian skull does not admit light into the brain. Instead, the mammalian pineal needs input from the eyes to regulate the circadian rhythm.
References
- Deguchi, Nature (1981); 290(5808):706-7
- Yoshizawa & Jeffery, J Exp Biol; 211:292-9


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How much heat can a human sustain?
For how long can a human sustain a temperature of 180 degrees Fahrenheit (82oC) without damage in a confined place?
For instance, suppose a person is sitting in a steam-filled room, without external air flow (but with enough oxygen) - how long could one resist the heat before permanent physical damage would occur?

Short answer
Water of 180 oF (82 oC) causes immediate scalding (thermal burn wounds).
Background
The severity of a scald injury depends on the temperature to which the skin is exposed, and for how long. Residential water heaters warm up tap water typically to 120 oF (48 oC). At this temperature, the skin of adults requires an average of five minutes of exposure for a full thickness burn to occur. When the temperature of a hot liquid is increased to 140 oF (60 oC)) it takes only five seconds or less for a serious burn to occur. Coffee, tea, hot chocolate and other hot beverages are usually served at 160 to 180 oF (71 - 82 oC), resulting in almost instantaneous burns that will require surgery (American Burn Association).
How these numbers apply to steam I am not sure, but I think they will be comparable, given that steam is essentially made up of a dense mass of water droplets. Further, the amount of steam obviously matters. Consider these numbers: The temperature in a sauna typically ranges from 160-200 oF (71 - 93 oC) with a low level of humidity (ranging from 5 - 30%). Steam rooms provide moist heat from a water-filled generator pumping steam into the enclosed room. The temperature in a steam room typically ranges from 110-114 degrees Fahrenheit (43 - 46 oC) with a humidity level of 100%.
There is anecdotal evidence of the Russia-born Ivan Ivanitz Chabert (1792-1859), who supposedly entered an iron oven in Paris with a few trays of meat, and stayed there unscathed for 5 minutes at a temperature of 380 degrees F (193 oC). When he re-emerged from the oven the meat was cooked, while the only noticeable effect on him were profuse sweating and a dramatic increase in heart rate (from 98 to 168 bpm).
This experiment shows the remarkable capacity of the human body to reduce overheating by means of evaporative cooling (sweating). However, the effects of steam are far more devastating to the human body than dry heat. Not only does it carry much more energy than hot air, it also prevents perspiration by saturating the air with water vapor.
References
- American Burn Association Educator's Guide

AFAIK the main difference in steam's behavior comes from "latent heat", in which the energy absorbed by the liquid as it changes into gas is released when it changes back into a liquid. But that'll only happen above 100 deg C -> http://scienceline.ucsb.edu/getkey.php?key=1322

Depends highly on the amount of steam in the room. Most if the heat energy does not come from the air, but from the steam that is condensing on your skin. I can tell from my own experience that I regularly spend 20-30 minutes in 80c sauna while pouring more water to the stove every few minutes without getting too uncomfortable (as long as I have water to drink). 100c sauna maybe 10-20 minutes and 120 c sauna 5-10 minutes. If you don't throw any water, you can stay in much longer. It is also worth to mention that people normally are NOT used to this kind of temperatures and will feel uncomfortable much earlier if they are not used to the heat.
I can take an example from the last Finnish Sauna Championships: a Russian guy died and a finnish guy burned 70% of his skin after spending only 6 minutes in 110c sauna. However, a few years back the same guy lasted for 16 minutes in the same 110c temperature without burns. Again, the difference was made by the humidity. In the final, half liters of water was poured every 30 seconds. Half liter per 30 seconds in a small sauna means the air is constantly over saturated with water and it is constantly condensing on the skin without a moment of relief.
Around 50 people die annually in the sauna in Finland. Most of them are either very old (70+), very drunk or/and have an existing disease. Normally you cannot get burns in the sauna as long as you are hydrated enough to sweat and your body is not completely messed up by alcohol. If you pass out in the sauna, your body does not function properly with managing the heat stress. Dehydration in people under the influence of alcohol heightens the risk of hypotension which impairs skin blood circulation.
Here one article claims A 30-minute stay in a sauna with a temperature of 80 degrees C increases rectal temperature by about 0.9 degrees C in adults. If the rise stays constant, a fatal level of hyperthermia (about 5 c increase in body temperature) is reached in around 2.5 hours. This estimation is probably based on a relatively dry sauna.


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Why is chlorophyll green? Isn't there a more energetically favorable color?
Chlorophyll being green means it absorbs light in the red and blue area of the spectrum. Isn't this the high and low energy light? Wouldn't plants get more energy if they absorbed light in the green area of the spectrum instead of the red one?

The reason that chlorophyll is green is because it absorbs other colors of light such as red and blue, so in a way the green light is reflected out since the pigment does not absorb it.
Because life might have been purple:

It is possible that the very first life form to process light may have been purple colored. This would mean it was reflecting red and blue light and absorbing green. In such a scenario this thing if it was the first to produce energy from light would have out competed against everything else. It would have had a population explosion and possibly covered much of the Earth or at least the oceans. Haloarchaea are an example of a simple life form that uses Retinal and Bacteriorhodopsin to produce energy though far less efficiently than photosynthesis. Had this been developed prior to photosynthesis it may have let it spread very far even though it is a less efficient energy production method. A 2% efficiency increase in a market no one has yet tapped is still a huge advantage.
In this scenario because the first thing to use light was using green light it left a niche for another form of life to exploit. That niche would have been absorbtion of the Red and Blue spectrums. Which is the same area plants absorb today. They got so good at their niche that they eventually were able to generate much more energy than the first life form did and eventually out competed for the sun. This niche has worked so well that they never developed a full system for the other spectrums.

Because you could say that good enough is good enough:

The sun puts out a lot of energy. It is possible that there was no need to try and capture all of the spectrum or that it was actually not beneficial to do so. Often too much sun is more an issue than too little. Too much sun and heat can dry out the plant. It is possible that to gain the benefits of photosynthesis there needed to be a reduction in some energy to balance it out. Much like a black car on a hot summer day a black plant might absorb all of the spectrums but also get far too hot. Blue plus red may just be the sweet spot.

However, about your question about colour:

Wouldn't plants get more energy if they absorbed light in the green area of the spectrum instead of the red one?

Plants would probably get more energy if their leaves were black.
Sources:

https://www.quora.com/Why-did-chlorophyl-evolve-to-be-green-as-opposed-to-black-which-would-absorb-more-energy
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691134/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2807594/

That first sentence basically says, "chlorophyll is green because it isn't some other color."

@amarillo feel free to edit my answer.

Absorbing higher energy may also lead to harmful photoproducts.

"Because you could say that good enough is good enough" -- this is perhaps the most important point.  If there was a massive benefit to doing so, plants would likely have evolved to capture the green spectrum as well.  But doing so would probably not help -- a lack of sufficient CO2 to use all the captured energy would almost certainly be the result.

@Yoda Plants already absorb blue, which is more energetic than green.


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Electrocardiogram: Missed beats in presence of Ectopic beats or Premature Atrial/Ventricular Contraction beats
I have been working on analyzing Electrocardiogram data.
So far, i have identified Ectopic beats and Premature Atrial/Ventricular Contraction beats.
I am working on identifying Missed Beat in the Electrocardiogram.
The definition of Missed Beat is:
"The characteristic of a missing beat in ECG is the unexpected absence, together, of P-, QRS-, and T-waves."
My question is, do we have to consider missed beats in presence of Ectopic or Premature beats also ??
For example, if an ECG contains premature/ectopic beats, then should the R-R interval between these beats should be compared to R-R interval between normal beats to search a missed beat ??

After developing and checking the algorithm with simulated ECG data, i found out that premature beats (as the name suggests) itself arrive prematurely i.e. their R-R peak interval is less then the R-R peak interval between normal beats.
In that case, i am considering the averaged interval between normal beats and compare it to the interval between next arriving beats. If that interval is more than twice the averaged normal interval, then i classify it as a missed beat.


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Will the increase in atmospheric carbon dioxide lead to larger insects?
From my understanding, the increase in atmospheric carbon dioxide will also increase oxygen levels. That makes me wonder if in the near future insects will grow larger than they are today, since their maximum size is limited by how deeply oxygen is able to diffuse into their body.

I haven't seen anything suggesting increased oxygen levels. If you've got a source for that I'd be interested.

There is the supported theory that insects during the Paleozoic period were larger in size because of the increased oxygen content in the air.

The study adds support to the theory that some insects were much larger during the late Paleozoic period because they had a much richer oxygen supply.
The Paleozoic period, about 300 million years ago, was a time of huge and abundant plant life and rather large insects - dragonflies had two-and-a-half-foot wing spans, for example. The air's oxygen content was 35% during this period, compared to the 21% we breathe now, Kaiser said. Researchers have speculated that the higher oxygen concentration allowed insects to grow much bigger.

This article is based on a paper published in the American Physiological Society:

It is because when the oxygen concentration in the atmosphere is high, the insect needs smaller quantities of air to meet its oxygen demands. The tracheal diameter can be narrower and still deliver enough oxygen for a much larger insect, Kaiser concluded.

There are similar papers that investigate the relationship between oxygen and maximum potential size, such as this article published in Nature (1999):

The tendency of some animals to be larger at higher latitudes ('polar gigantism') has not been explained, although it has often been attributed to low temperature and metabolism. [...] We have analysed length data for 1,853 species of benthic amphipod crustaceans from 12 sites worldwide, from polar to tropical and marine (continental shelf) to freshwater environments. We find that maximum potential size (MPS) is limited by oxygen availability.

Another paper published in Proceedings further supports this theory:

[...] A variety of recent empirical findings support a link between oxygen and insect size, including: (i) most insects develop smaller body sizes in hypoxia, and some develop and evolve larger sizes in hyperoxia; (ii) insects developmentally and evolutionarily reduce their proportional investment in the tracheal system when living in higher PO2, suggesting that there are significant costs associated with tracheal system structure and function; and (iii) larger insects invest more of their body in the tracheal system, potentially leading to greater effects of a PO2 on larger insects.

The question you propose is very interesting, although I am sure it would take thousands of years for these insects to adapt to this oxygen level change (which in itself, to reach prehistoric levels, would take a long time) and in turn become larger.
This article, based on the original APS paper, seems to think larger insects could appear in the future if the limiting factor (in this case low oxygen levels) is removed.

Image from Biotic interactions modify the effects of oxygen on insect gigantism (PNAS, Chown 2012).

I just realized an implicit assumption in my question. Is it only lack of oxygen that limits insect size today, with their current genetic makeup, or is an evolutionary change also required to take advantage of the increased oxygen?

Although these findings are all based on theory, the general consensus for the relatively large size of ancient insects seems to be linked to oxygen levels in the atmosphere.  There could be other factors related to size, however, with their current genetic makeup I would assume that these physiological changes would not happen in a short period of time - they would adapt slowly with the changing atmosphere, based on the fact that the changes in ancient insects happened over millions of years.


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Muscle force/energy relationship
I found the Hill muscle model, which helps relate the force a muscle can generate to its change in length over time (its "contraction velocity").  Is there a similar model to get an idea of the energy consumed during a contraction as a function of the force generated?

You can calculate the energy consumption using basic physics formulas.
Work = Force x Distance
and the unit of work is the Joule. Therefore if force is a function of change in length then substituting this function in for force in the above calculation we have that work is a function of length.
If you want to talk about energy consumed in terms of calories rather than joules,
1 calorie = 4.184 joules

That's part of it, but what about isometric exercise?

The same physics applies, you are buttressing your muscles but they will still be exerting a force. The resulting distance of movement is small so that you don't notice it, however the force is greater. Work is still force x distance.

But that doesn't help in building a mathematical model for muscle activation.  I want a predictive model for the energy consumed during a muscle contraction, whether it's isometric or isotonic.  Even for only isotonic contractions, if you only account for mechanical work you're entirely ignoring the heat generated.  You'll only get a lower bound on the amount of energy consumed.

Your question asked for energy as a function of force generated. Not as a function of heat and force generated. If you want the total energy used then yes you would have to take into account the inefficiencies of muscle contraction which generates heat. The question then is how efficient are myocytes in converting energy from ATP to force. This a variable quantity see the following paper http://www.ncbi.nlm.nih.gov/pubmed/11350777

Yes, I asked for energy as a function of force generated.  Because muscles can produce force with no net movement, mechanical work is simply not a complete answer to the question :(  Did you read the body of my question, or just the title?

Yes I read the body of your post, and was trying to help with sarcastic comments like that I am sorry I tried.

I wasn't being sarcastic; I'm sorry if you read it that way.  I was pretty specific about what I was looking for in the body of the post, so I was trying to understand where the disconnect was coming from.


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Identify a bird
I have taken this picture of a bird in university zoo in Tel Aviv. It was approximately 25 cm high and seemed to be a flightless species. Can somebody help me identify it?

They fly rather well when they want to.

It's a Black Crowned Night Heron, Nycticorax nycticorax, in my opinion - you can read more about it here. Key to it's identification is the shape of the body and bill, it's characteristic of species from the heron family such as the green heron. The range is right and the red eye is a good clue too.

Thank you, it seems to be a Black Crowned Night Heron indeed. The photographs on wikipedia page helped me to conform this http://en.wikipedia.org/wiki/Black-crowned_night_heron .