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How can I label cryotubes in a way that eliminates the problem of legible hand-writing?
My lab stores biological material (tissue, cells, plasma, serum) in a -130 C, liquid nitrogen freezer. The cryotubes that we use to store a samples are labelled by hand which frequently creates legibility problems.
Its my understanding we can't print out stickers to use as labels because they will degrade in the cold. The solution of putting barcodes on the tubes has been suggested but its undesirable because in addition to the cost and logistic complications; we would have to choose between thawing and refreezing all of our samples to transfer them to new tubes OR live with the nightmare of having both labeling systems in use at the same time; one which humans can read and one which humans cannot.
The ideal situation would be a small, portable machine that can physically label the tubes for us. I'm envisioning:
 - an adjustable clamp to hold the tube in place; ideally with sensors that would infer the shape, size, and position of the area that can be labelled.
 - a very-fine tipped pen attached to a motor that would mimic a printer's line-by-line printing action; this would have to take into account the shape and size of the area that can be labelled
- rollers in the clamp to adjust the available space for labeling
 - a screen/keyboard interface that would display how the label will appear
Does anything like this exist?
Do you have any other suggestions about how to deal with the problem of legible hand-writing on cryotubes?
Please advise if there is a more-appropriate SE site to post this question

One way to get around this problem is to keep similar samples in the same box; for e.g One box per cell type and label the box nicely [easier to write legibly on a big box]. Keep the marking requirements minimal on the tube (for e.g. just dates)

It doesn't seem that "legible hand-writing" would be a problem. Rather the problem is illegible handwriting. Could you have some technician with legible hand-writing just prenumber the tubes?

Barcodes would not be a good solution due to the ice crystal formation when the tubes are removed from storage preventing scanners from working.

This is indeed a problematic point. I have been using machine printed labels for a while now (sometimes with some extra scotch tape around it to prevent it from falling) off, which worked pretty nicely.
However, there is a printer available on the market (though I haven't tested it yet) which claims that they can print on any tube. This printer is called Tubewriter, which is probably also worth a look. The backside is the price, Fisher Scientific lists them around 40.000$, which will make them unavailable for most labs, except for cell banks etc.

Reminds me of this thing

@chris This is affordable but I would want to test the ink around solvents.   http://www.usascientific.com/dymo-450-printer.aspx

@rhill45 Interesting. I didn't know this machine - since it is labelled with "lab" it should probably adress some problems with the durability.

What I find works is to scotch tape the labels to the tubes, they hold up fine in our -70C freezer.
What I did was go into excel 2010, go to View tab, click on Page Layout on the left side, not normal view! Then, go to home tab, select all the cells on the page. Go to the right side of the home tab, hit Format, then Row Height. This lets you set height in real units, I typically enter "10mm". Do the same for Column Width, I like 20mm. Now reselect the page of cells because changing the cell size will push some off the page. Right click the cells and format them to center the text horizontally and vertically. Now you can type your label text into the cells. I suggest font size 8 or smaller so you can fit it all in the cell. To make cutting the labels easier, put borders on all sides of all cells. Just print it out, cut them apart and tape them on your tubes. Sorry microsoft makes it so hard to set the size of a cell in real units.
Just to see if I could, I tried to create a QR code and make it small enough to fit on the 10x20mm label. But my phone can't read it once I print it out at that size. With a better camera and a good printer you could probably make it work. I don't know enough about alternative bar code systems to try anything else.

I hate this problem but I hate even more when I pull up a cryo vial that some one wrote on with a dry erase marker.
Get printable tough tags.
Two options after that, print on them with your laser printer. Can do many at a time.

You can take a step further and overlay the tag with some 3m single sided tape (scotch tape is gonna brittle up from the N2.)
Write on it with a fisher brand solvent free marker. This is the only marker alcohol will not take off!!!

I would love to find the ink in this market and be able to put it in my printer for the tough tags.
I like these types of questions on here.
There are elaborate systems out there like Chris's answer and they are of course preferable. But expensive.
I didn't think to use the QR codes for as mentioned by 1st answer, I may try this.

However, it seems that the Tough Tags are only rated for -40°C.

For OP's application, I would recommend Cryo-Babies, which are rated for liquid- and vapor-phase nitrogen storage at -196°C

We have used Brother P-Touch printers in the stock at work, but our lowest temperature is -80C. It's ideal for making sure the labels go all the way around the vials.

Welcome to Biology.SE! Can you please provide a little more detail? For example, model numbers, links to the product, and images of successfully labeled tubes. I also think you will get a better reception for your posts if you make sure the spelling and word use are correct. Also what do you mean by "in the stock" — it feels like maybe you left out at least one word? ——— You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


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Simulating substitution rate of neutral mutations
I am trying to computationally simulate a population based on the Wright-Fisher model I would like to get to the classic result of the neutral theory of molecular evolution that the rate of neutral substitution equals the rate of mutation. However, the results of my simulations never show that. I will briefly explain my simulation process and how I calculate the mutation and substitution rates. Please let me know if there is something wrong in my procedure.
I have a non-structured haploid population that grows in discrete time steps. I start with a population of N individuals in an environment with carrying capacity K. I use a K-allele model of mutation. At each generation, every individual will reproduce n offsprings and it will immediately die afterwards. A u fraction of offsprings will be chosen randomly to have a single mutation in each generation (u is mutation rate per gene per generation). At each generation, I record how many mutations have occurred and how many mutations have reached fixation in the population (reached frequency of more than 99% of individuals). Thus, mutation rate and substitution rate per generation is calculated as the number of mutations and number of substitutions divided by population size, respectively. With this set up, even with hundreds of repetitions, the rate of fixation will never be as big as mutation rate u.
Where do you think is the problem?
I have struggled with this a lot and I appreciate any help.
Edit:
My code is written in Python. This my pseudo-code:
Parameters: population size, genome_size, mutation_rate, generation_number, fixation_threshold.

'''
Population_size: Here it is 1500
Genome_size: the number of loci that can be mutated. Each locus can be mutated to any of ACTG. Here 10^4
Mutation_rate: number of mutations per genome per generation. Here 0.05
Generation_number: The number of generations that the population grows. Here 1000
Fixation_threshold: The fraction of individuals having an allele in the population so that the allele is considered fixed. Here 0.99
'''

The initial population is created. All individuals are the same without any mutations
A vector to hold the number of mutations and a vector to hold the number of fixations is created

For each generation:
    I determine how many individuals in each generation should be mutated. Here 8.
    I randomly choose  (uniform with replacement) the individuals to be mutated
    For each individual in the population:
        It will produce an offspring. The offspring inherits the genome of its parent, i.e. the mutations of the parent.
        If the individual is among the ones to be mutated, the offspring will receive a mutation that is randomly picked.
            The mutation can be a back mutation
        The individual will die
    I record the number of mutations that occurred (it will always be 8 in this case)
    I record any mutation that has a frequency in the population of more than 0.99 of individuals. This is the number of fixations

I run this code for at least 100 times. I expect that the average number of fixations to be equal to the average number of mutations in each generation, or they converge over generations. Because the neutral theory of Evolution by Kimura predicts that for neutral sites in the genome, substitution rate is equal to the mutation rate.

There's not a lot we can do without your code or at least a pseudocode outline. Why are you expecting the fixation rate to be exactly the same as the mutation rate?

I will put here a pseudo-code outline. I expect the fixation and mutation rates to be equal, because that is what the neutral theory predicts for neutral sites. Am I not correct?

Wait, if I'm reading your pseudo code correctly, each organism produces exactly one offspring and the only way to reach fixation is have all 1500 individuals develop the same mutation independently. Either n, the number of offspring needs to be sampled from a distribution, or you need to sample with replacement from the current population of parents N times to create the next generation. What kind of results are you seeing? From this pseudocode, I expect fixation rates of almost exactly zero.

You are correct. I can either have more than one offspring per individual or sample with replacement. I have tried both scenarios. What I observe when I plot the data is constant mutation rates across the generations, and few burst of fixations. See the image below. The x axis is generations and the y axis is frequency. .

That is about what I expect from your model and simulation. Kimura predicts that the rate of fixation is related to the mutation rate, but that actual relation depends on genetic drift and the distribution of offspring and the population size. The probability of an individual mutation reaching fixation is very small in nearly all cases. The probability of seeing a fixation event is always increasing, but it will never reach the mutation rate(or even really get close in a population of 1500).

Thanks. But the theory does exactly say that k=u, where k is fixation rate and u is mutation rate. It explicitly says that fixation rate is irrelevant of population size, because mutations arise with rate Nu and fix with probability of 1/N, where N is the number of chromosomes.

Do you have a link to the text of the theory?

Yes I used this paper which you have cited yourself.
Kimura, M. (1968). Evolutionary rate at the molecular level. Nature, 217(5129), 624–626.

What an insidious misunderstanding about a single variable. My word. Do you have any other related questions or points of clarification you would like?

Thanks for your help. That was all my problem. With the following procedure, the mutation rate equals the substitution rate: I calculate the mutation rate for each generation as the number of mutations divided by the population size. For all generations, I take the mean mutation rate for each generation. Now for the substitution rate, I divided the total number of substitutions over all generations by the number of generations. This will give the substitution rate per population per generation, which equals mutation rate per individual.

This just got too big for a comment and I think might actually qualify as an answer.
Can you give me a source for what you're reading? According to this, which matches the definitions you are using, K=(Nu)/N=u where K is the substitution rate, u is the mutation rate in the population, Nu is the individual mutation rate, and N is the population size.
I went back to Kimura's original paper in Nature in 1968 and he derives that u(p), the substitution rate in the population, is (almost exactly) the same as the mutation rate in an individual(p). But this follows from a different paper(prolific guy) where he shows that the fixation probability for a given allele is roughly 1/N, where N is the population size. Your individual mutation rate in your model is not u, but Nu.
You are confusing the mutation/substitution rate in the population, which is used for molecular clocks and other things, and the individual mutation rate. If the molecular mutation rate, is say, 1/20 (as you assume in your model) then you are expecting a fixation rate per mutation of 1, essentially. If the substitution rate is going to be the same as the molecular mutation rate, every single mutation must reach fixation. If the same locus mutates twice in the same generation(quite possible with enough individuals), then both must somehow reach fixation, even though the first to reach fixation will necessarily destroy the other.
I hope that helps you sort out why Nu will never equal K, and helps the results of your model make sense.
(sidebar: Nu isn't the raw molecular mutation rate but the individual mutation rate, which is actually higher because while growing to adulthood the average human gamete is involved in about 50 cell divisions, which leads to a few more mutations per person.)

I don't fully understand how your model works
I don't fully understand how you model your population. Is it a standard $oop$ (object-oriented programming) where you simulate each individual? Or is it a simulation where you already use some mathematical model? You could eventually copy-paste your code. it is probably not very long, right? What language did you use? Do you have only one locus? Do you simulate several positions within these locus? Do you allow for back mutations?
It seems that you allow the population size to change over time and I don't quite understand how your parameter $K$ does limit the growth rate though. You should write down some equations about that. In any case, change in population size will modify the probability of mutation fixation.
Here is probably some important modifications to do on your code
It is a bit hard to comment on your simulations without actually seeing some equations or seeing the code but I really think that you'll need two important modifications in your code.

fix population size $N$.
To simulate reproduction, randomly choose (uniform distribution) individuals (with replacement) from the population. The chosen individuals form the new generation. For example:

In R:
new_pop = sample(old_pop, N, replace=T)

or directly
pop = sample(pop, N, replace=T)

In Python:
from random import randrange
new_pop = []
for i in xrange(N):
    new_pop.append(old_pop[randrange(N)])

When you get your results, don't forget that you're talking about a stochastic process and you may want to run enough simulation or enough independent loci in order to be able to compare with the predictions from mathematical models.

Thanks for your answer. I have updated the question and implemented your suggestions to my code. But it does not meet the expectations yet.

source: Stack Exchange

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Identification of small fuzzy flying insect (pic)
These critters were flying around the neighborhood on an autumn evening in Seattle, WA, USA. Their most notable feature was the small amount fuzz on them. They were quite slow in their flight compared to similar-sized fruit flies.
Any ideas?
Here are two close-ups:

One one for size comparison:

I'm having trouble counting the wings. In your image on the right, I can't tell if there is a second wing on the lower edge of the right wing. The left wing is even less visible. If this only has 2 wings, then it's a diptera. But I'd also believe this is a hymenoptera if it has 4 wings. Not familiar with pacific northwest insects.

To me, it looks like a male Aphid (males are winged, and have four wings) from the genus Eriosoma (wooly aphids). The white feathery substance is a wax secretion.
Have a look at Bugguide: Eriosoma, InfluencialPoints: Eriosoma and this page from the Uni of Minnesota for some more info.
A picture of a species from the genus:

I'm with you, and tempted to delete my answer.

+1 : decisive is the wing venation pattern - it's definitely an aphid. By the way, females can also be winged

@har-wradim True that also females can have wings, but my impression is that winged males are more common. I cannot say about this individual though. Females have an ovipositor and males claspers (and often slightly different body shapes), but hard to see in the pictures.

These are known as 'wooly aphids' and are common in the fall. An example is the woolly apple aphid (Eriosoma lanigerum) which do occur in WA. See http://treefruit.wsu.edu/crop-protection/opm/woolly-apple-aphid/

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What is the advantage to neurons being asymmetrical?
Does having a central axon and dendrites result in any advantage compared to if the neuron was symmetrical?

Asymmetry to essential to neuronal function, particularly in the peripheral nervous system. This is because the dendrites of a neuron receive synaptic potentials, which are graded and decay with distance. Dendrites are typically short such that a synaptic potential is still above threshold by the time it reaches the axon hillock (sometimes called trigger zone), so that a subsequent action potential can fire. Axons need to be long (some are up to a meter long, in the leg) to transmit signals long distances in the body. To make a neuron symmetrical, one of these qualities would have to be compromised and neuronal function would suffer as a result.
Source: Principles of Neural Science, 5th ed (2012), Kandel et al. Chapters 1-6.


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Can chitosan affect the absorption of unsaturated fatty acid?
I know chitosan will decrease the absorption of fat. However unsaturated fatty acid, such as DHA, is beneficial. Does chitosan effect the absorption of unsaturated fatty acid?

It seems that there is no difference in the effects of chitosan on the uptake of saturated and unsaturated fatty acids. The study cited below (which has been done on guinea pigs) fed the animals a diet which contained different digestion-resistant fibers (maltodextrin, cellulose and chitosan) and also fats. Then the fatty acid content of the feces was measured afterwards.
Only for the group which got additional feeding of chitosan showed a significant increase in the excreted fatty acids. This was true for the saturated (lauric, myristic and palmitic acid) but also for the unsaturated fatty acids (Oleic, linoleic and α-linolenic acid). This effect is specific for fatty acids, The uptake of neutral sterols and bile acids was not affected in any of the experimental groups.
The second paper suggests that chitosan forms an emulsion with fatty acids under the acidic conditions of the stomach. This emulsion is stable and later excreted with the feces.
References:

Selective in vivo effect of chitosan on fatty acid, neutral sterol
and bile acid excretion: a longitudinal study.
Interaction between chitosan and oil under stomach and duodenal
digestive chemical conditions.


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Does NADH inhibit gluconeogenesis?
I was told in a physiology lecture that alcohol inhibits gluconeogenesis because 'NADH produced from ethanol catabolism leads to product inhibition'.
But is NADH not a reactant coenzyme of gluconeogenesis? It would make more sense if NADH inhibits glycolysis by product inhibition.
So, what is wrong here? Or is it because of some other reason why alcohol inhibits gluconeogenesis and leads to hypoglycemia?

Yes, this is the effect of metabolizing ethanol and also the reason why excess ethanol can lead to hypoglycemia.
Ethanol is oxidized by the alcohol dehydrogenase to acetaldehyde. This reaction consumes one molecule of NAD+ per molecule ethanol oxidized:
Ethanol + NAD+ <=> Acetaldehyde + NADH + H+

Acetaldehyde is oxidized by the acetaldehyde dehydrogenase in a second reaction in the mitochondria to Acetyl-CoA, which produces another molecule of NADH:
Acetaldehyde + NAD+  + CoA <=> Acetyl-CoA + NADH + H+

If you now take a look at gluconeogenesis, there is one critical step which needs NAD+: the oxidation of lactate to pyruvate by the lactate dehydogenase which then cannot be processed into oxalacetate, phosphoenolpyruvate and so on.

Adding excess NADH shifts the reaction equilibrium completely to the side of lactate and also leads to the production of additional lactate, leading to hypoglycemia and lactic acidosis. Excess NADH from the ethanol oxidation inhibits the oxidation of fatty acids in the liver - this process also generates NADH for the production of ATP. NADH signals this process that enough energy is available in the cell. And finally excess NADH also inhibits the malate dehydrogenase reducing the amount of oxalacetate for gluconeogenesis further.

Good explanation

Partially correct. Please allow me to explain. It is mentioned above: "shifting the equilibrium to the production of additional lactate, leading to hyperglycemia..."
It's true that excess NADH production as a result of alcohol consumption inhibits oxidation of lactate to pyruvate via lactate dehydrogenase. But, this leads to HYPOglycemia, not HYPERglycemia, because lactate is not adequately converted to pyruvate to meet the body's metabolic demands.
What are the repercussions?
Less pyruvate created ---> less of its conversion to oxaloacetate, which under normal conditions, would usually traverse across the mitochondrial membrane into the cytoplasm to be converted to PEP via PEPCK. Less oxaloacetate as a result of less pyruvate being shunted towards the gluconeogenesis pathway ultimately leads to HYPOglycemia.
Although ethanol on its own (like if you were to drink grain alcohol) would result in a drop in blood sugar, and this is ESPECIALLY a danger for individuals with Type 1 diabetes. Beer, wine, and common spirits rarely cause a drop in blood sugar because they also provide carbohydrates. These carbohydrates help to maintain blood sugar, if not elevate it on a binge.

Welcome to SE Biology.  I think hyperglycemia was probably just a typo in @Chris post.  It would probably be better to just edit the accepted answer to correct the mistake.

You can simply correct typos in answers. As I have no corrected mine (thanks for spotting it), your answer is obsolete.


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Are there any multicellular forms of life which exist without consuming other forms of life in some manner?
The title is the question. If additional specificity is needed I will add clarification here.
Are there any multicellular forms of life which exist without requiring the consumption (destruction) of other forms of life in some manner? Thus purely on inorganic material.
I do understand that the definition of life is a semantic distinction, so for this discussion I will assume the one Wikipedia provides:
"Life is a characteristic distinguishing physical entities having signaling and self-sustaining processes from those that do not, either because such functions have ceased (death), or because they lack such functions and are classified as inanimate. Biology is a science concerned with the study of life."
I am open to considering alternative suggestions.
Thank you.

Closely related to the question can humans survive without eating life

Many of deep sea organisms eat dead bodies. They do not catch other organisms alive.

Please include the question in the question. The title may or may not be the same, but the question should read coherently without reference to it.

Yes, plants for example!
Autotrophs vs. heterotrophs
Plants are autotrophs while animals and fungi are heterotrophs. Have a look at the Wikipedia articles. In short, autotrophs organisms are organisms that synthesize their own compounds from inorganic compounds. Heterotrophs organisms are organisms that synthesize their own compounds from organic compounds.
Therefore, any multicellular plants are multicellular organisms that "exist without consuming other forms of life" (with the exceptions of carnivorous plants).
Consuming nonliving organic matter
Of course, many life forms feed on organic matter but only on non-living organic matter. Such life forms do not kill to feed. It is the case of all detritivores (such as earthworms) and decomposer such as fungi.
Competition vs predation
As @TechZen said, not consuming other organisms doesn't mean that the existence of an individual of this species is not causing the death of another individual (competition and parasitism that does not involve consuming the other individual).

Aside from blocking out light, how do zooplankton cause the death of other individuals?

Why do you want to take the "light blocking effect" out of the discussion? Zooplankton (by definition) are heterotrophs and therefore they eat other individuals. Zooplankton probably have tons of impact on their environment too (I am not an ecologist as you can tell) that likely affect other species.

Because what do they gain? Are they gaining resources because their numbers are high enough to smother other forms of life? Do they decompose the dead organisms and use them for energy like other plants do if there are dead organisms beneath them?

I don't quite understand your point. Maybe you want to make sure to have a look at the wikipedia entry for zooplankton.

There are multicellular organisms which do not actively eat other organisms, however, there are no organisms who do not kill other organisms, period.
Trees and other vertical plants evolved in the first place in a competition for sunlight. For plants, being in the shade is like smother or starving a human since they literally use sunlight to create and create food and oxygen. Plants carry out complex chemical war against a wide range of other life forms from microbes to other similar plants.
Plants don't eat other organisms, save indirectly, but they do kill.
All multicellular organisms have an immune system that wages and unrelenting slaughter against microbes which in turn are constantly assaulting multicellular organism.
Lastly, every individual organism and probably all strains and species, displace other individuals, strains or species just by existing. No energy is wasted in the biosphere. If something is living in one place or niche and then dies, the energy it was living on becomes available for something else. Conversely, while it lives it prevents other organisms from evolving to fill the niche, or as an individual moving into the physical niche.
Just by our very existence, we kill.

Though there are saprophytic plants which "eat" dead organisms, parasitic plants (like this one: https://en.wikipedia.org/wiki/Sarcodes ) which feed off other plants, and even carnivorous plants that eat animals.

@jamesqf - Doesn't matter, what they eat or were, they displace something else and kill. All multicellular organisms have to constantly kill microbes to prevent being eaten by them.

No, there are no known multicellular organisms that depend exclusively on inorganic material.
Plants have been put forth as examples of multicellular organisms that do not "consume life", but that does not mean they don't depend on organic matter. Plants depend on nutrients found in the soil, and these nutrients come largely from decomposing organic material.
It is now early spring here and the local farmers have started spreading manure on the fields. That manure consists largely of dead plant matter digested (mainly) by cows.
Of course, a plant can live exclusively on inorganic nutrients, if you grow it hydroponically and exclusively give it inorganic fertilizers. Ammonia can be produced from nitrogen in the air through the Haber-Bosch process, and the rest, phosphates, potassium, sulphates etc. can be taken from mineral deposits, but this is rather artificial. Plants are, by and large, completely dependent on organic matter.

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Can radiation equilevant to 1 CT (computer tomography) scan causes significant changes in human body?
I've read that CT scan causes radiation equivalent to few hundreds of ordinary X ray scan. It sound scary at the first look of it but I wonder is it the amount considered significant? Can dosage equal to the 1 CT scan significantly increase chance of developing cancer or other adverse effects?

As a rule of thumb you can say that a CT scan exposes you to a higher dose than a X-ray examination, due to the different techniques. For CT scans a number of single 2D photos is processed into the 3D models. However, the dose strongly depends on what body part is examined. See a part of this table (the complete table can be found in reference 1):

The additional risk for most examinations is low to very low and since we don't get x-rayed on a daily basis this is a risk which can be tolerated. Besides this, there are other exposures to radiation which also accumulate, but where people usually don't hink about it. These are for example smoking and flights at great altitudes. See the answer from @anongoodnurse for some more details on this.

References:

Radiation Dose in X-Ray and CT Exams
The 2007 Recommendations of the International Commission on
Radiological Protection
AAPM Response in Regards to CT Radiation Dose and its Effects

@anongoodnurse The table lists Radiography of the lower GI-Tract with 8 mSv, while a CT of the head is listed with 2-4 mSv.

@anongoodnurse Ok, thanks for the correction. I will change this in the text. So CT gives higher dose exposures than X-rays, if I am not mistaken again?

yes, CT is much higher than plain films. Fluoroscopy is more than CT in most cases.

Xrays are not scans. They are one shot (or a series of a few). Say that a chest Xray (two views) doses you with .1 mSv of radiation. The dose from a standard chest CT is 7 mSv.[1] That is 70 times what a chest film gives you, not a few hundred (though that might seem like quibbling). The TL;DR answer is: no one knows for sure.
Radiation (especially in fetuses -children) increases the likelihood of cancer. Our information comes mostly from atomic bomb survivors, people exposed at Chernobyl, people treated with high doses of radiation for cancer and other conditions, and people exposed to high levels of background radiation, e.g. uranium miners.
Can one CT scan increase your chance of developing cancer? Yes, but how significant that is remains debatable. It depends on a lot of unmeasurable things: genetics, your age, your ability to repair the damage, which area of the body is being dosed, whether there are other carcinogens at work (e.g. viruses or co-carcinogens), etc.
The following are commonly found numbers (which does not mean they're accurate). Given 10,000 people, about 2000 will die of non-radiation related cancers. If you expose those 10,000 people to 10 mSv of radiation, you can expect 5-6 additional cancer deaths in that 10,000 (or .5% increase). [2] However, if you expose someone to 10 mSv twice, with two months in between, the risk does not double.
The average dose of radiation per year from background sources is 1.5-3.5 mSv/yr.[3] [4] Because of our ability to repair damaged DNA over time, it's generally estimated that, from natural background radiation, the risk of developing cancer from background radiation is about 1% of our total cancer risk.[5]
So, let's say that your average CT scan is going to give you 7 mSv of exposure (that's a high estimate). What is your chance of getting a lethal cancer from that? The answer is: no one knows.[6]
Relative risk has be calculated by some. The following all give you a (estimated) 1 in a million chance of dying from that event[7]:

Smoking 1.4 cigarettes (lung cancer)
Eating 40 tablespoons of peanut butter
Spending 2 days in New York City (air pollution)
Driving 40 miles in a car (accident)
Flying 2500 miles in a jet (accident)
Canoeing for 6 minutes
Receiving 10 mrem (.1 mSv) of radiation (cancer)

So, you can estimate that (maybe) the risk of dying from a 7 mSv CT scan is about equivalent to driving 2800 miles.
The point of all this is, no one knows your exact risk of developing a lethal or relatively non-lethal cancer (yes, that does exist) from an imaging study. Most ethical Radiologists will tell you there is no known safe radiation exposure, and that one should avoid unnecessary radiation exposure. While some imaging studies are unnecessary, some of them are not, and the risk of avoiding the study greatly outweighs the risk of undergoing it. What you can do to protect yourself:

ask if an MRI will give the doctor the same information (no radiation, but 2-3x the cost, longer wait)
ask the doctor if the test is absolutely necessary (a lot of tests are ordered to cover one's ass)
ask if there is another way to obtain the same information (e.g. colonoscopy instead of barium study)
get your study from the newest scanners available (radiation can be reduced up to 60% between generations of CT scanners)
reduce conflict of interest: any CT scan ordered in house (or by a doctor that owns a share in the imaging facility) should be questioned (but not necessarily refused.)

[1] XrayRisk.com
[2] USEPA Radiation and Health
[3] Radiation and Life
[4] Higher accumulated doses of radiation might produce a cancer which would only be observed several - up to twenty - years after the radiation exposure. This delay makes it impossible to say with any certainty which of many possible agents were the cause of a particular cancer. In western countries, about a quarter of people die from cancers, with smoking, dietary factors, genetic factors and strong sunlight being among the main causes. Radiation is a weak carcinogen, but undue exposure could certainly increase health risks.
[5] American Nuclear Society
[6] Risks of Radiation
[7] Radiation and Risk


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Visualizing GFP in transgenic rice seeds?
I want to express GFP in rice as a method for differentiating transgenic from non transgenic rice seeds. I want to know if I can visualize them using a hand held UV lamp as the GFP I will be using has a excitation maxima at 395nm. If yes, how is to be done? Do I just flash the UV lamp on the seeds in the dark room and I can see the GFP expressing seeds glowing green?

I don't know about GFP in rice, but I've made GFP expressing bacteria, and they glowed ok on a UV tansluminator usually used for DNA gels. The RFP colonies I made were visibly red even without UV, but glowed good too. A simple UV transluminator would probably be fine, and you should have one for working with DNA anyway.

395 nm is not quite UV, so if you're not getting a strong enough signal (depending on the exact wavelength your transluminator emits, and the excitation profile of your protein), you could try using a purple light bulb. You can sometimes find them in big-box home centers like Home Depot, Lowes, etc., and you should also be able to find them at party stores. BTW, are you using GFPuv?

I am using mgfp5, optimized for plant expression which has excitation maxima at 395nm and 473-477nm(blue).What should I do?


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Organisms using thermal energy as their sole energy source
After seeing this question I remembered that in secondary school we watched a documentary stating something along the lines of "all organisms derive their energy directly or indirectly from the sun. *pause* Well, except a couple of organisms in the deep sea cultures that get their energy from small undersea volcanoes" . Now, after doing a lot of searching I was able to find the 'giant tube worm', however that still indirectly relies on energy from the sun as well as it relies on free Oxygen being available that in the end comes from photosynthesis (if my understanding is correct). So my question is two fold, am I correct in my understanding of the giant tube worm and if so, are there any organisms that function in a way that does not require any energy source beyond geothermal energy?

(PS. I don't have the reputation to tag this chemosynthesis yet, but do think that adding that tag would be useful)

I had to re-read your last sentence a few times to make sure I understood it correctly, but I think that now I do, and I can answer your question.
What you're talking about are thermophiles. They're small organisms that love hot conditions - up to nearly 250 degrees Fahrenheit. They can be found places with a lot of hot water, such as hot springs - and, yes, ocean vents. Many use sulfur as a fuel during chemosynthesis, oxidizing it to make sulfuric acid. They take the energy from the heat source to do this.
Not all thermophiles use chemosynthesis. Those in hot springs may get a lot of sunlight, and they can use photosynthesis. However, those in the deep sea cannot undergo photosynthesis, and are forced to use the energy from the vents to undergo chemosynthesis. In fact, entire ecosystems can be built off them!
Thermophiles may even have been some of the first organisms on Earth. Around the time that life is thought to have first formed, Earth wasn't a very hospitable place. As Ashwini Kumar Lal writes of the first forms of life,

Many of them are evolutionary relics called “archaea”, believed to be among the first homesteaders on the Earth 3.8 billion years ago. They are presumably
  the first version of life on our planet when its atmosphere was devoid of oxygen, and comprised largely of ammonia, methane, water vapour and carbon dioxide. They are microorganisms similar to bacteria in size and simplicity of structure, but continue as an ancient group intermediate between bacteria and eukaryotes. Heat – loving microbes, or “thermophiles”, are among the best studied of the extremophiles that can reproduce or grow readily in temperatures exceeding 45º C, and some of them, referred to as “hyperthermophiles”, are capable of thriving even thrive in temperatures as high as 110º C – more than boiling water temperature.

While we do not know (and may never know) the truth of this hypothesis, it is certainly plausible, given the locations where some extremophiles have been found.

References:
1: Microbial Life in Extremely Hot Environments
2: http://en.academic.ru/dic.nsf/enwiki/18641 (link no longer works, for some reason)
3: Origin of Life
Note: While I list several Wikipedia articles throughout the answer, I did not use them for the information in this answer. I think they're a good starting point to lead you to other sources, though.

It's 1:39AM here, so I will take a look at it tomorrow when my brain is up and running again, but just a very very quick question I can already pose now. So these bacteria do not require any products from photosynthesis? The reason I am asking is that I came across Chemosynthesis as well, but the example chemical process there is "12H2S + 6CO2 → [...]" which requires the oxygen I mentioned in the question. Or is that simply how it works in giant tube worms, but is the process different in some thermophiles? And if so, which (even a single example would be great)? I will be looking through

those references tomorrow, so I might discover more then myself. Just those are the question that came up in me when I read your answer. And PS. I confess, I did do most of my research on wikipedia... as it still is the best encyclopedia that's around.

@DavidMulder I figured; your info on the tube worms was similar to what it said. I, too, love Wikipedia, and sometimes use it for references on Astronomy, but I know Biology is a bit stricter about this sort of thing.

This seems to indicate that some material can come from other organisms - i.e. organic matter.

You may be confusing elemental oxygen (oxygen the element, made in exploding and late-stage stars, comprises almost 50% of the earth's crust by weight) with O2, the reactive oxygen gas. Carbon dioxide contains oxygen, but isn't necessarily produced by photosynthesis. Ditto water, etc etc

This makes no sense. No organism, or any other device, can use thermal energy as an energy source. It is thermodynamically impossible to convert heat to other forms of energy, because it would reduce total entropy.

@Roland The second law is valid only for a closed system. If heat is introduced into a system, work can indeed be done. For example, if you heat water, it can turn into steam, which can then be used to generate electricity. See also thermal energy.

@Roland The second law does not prohibit heat engines from existing; it simply limits their efficiency.

@HDE226868 Okay, that is true; my statement was too general. But heat engines rely on a temperature difference; here we're talking about microscopic processes, and the heat gradient across a bacterium must be minimal.  What would be the mechanism for an enzyme exploiting this? Can you cite any example?

Organisms do not survive solely on heat. The organisms you mention that are (more or less) independent of the sun obtain their energy by oxidizing inorganic compounds, like iron or sulfur. For example, some bacteria oxidize ferrous iron (Fe$^{+2}$) to ferric iron (Fe$^{+3}$), which releases some energy that can be used to "power" the cell. A list of various reactions used by these bacteria is found in this Wikipedia article.
The reason these species exist at hot thermal vents is not because the heat is helpful as such, but because iron, sulfur and other energy-rich inorganic materials are released into the ocean at these sites. The bacteria have adapted to tolerate the heat so that they can harvest the inorganic materials; but they don't benefit from the heat in itself.

The bottom part of your answer is correct but the top part is simply wrong. Heat CAN be converted to other forms of energy and this does not violate the second law but you do need a temperature gradient (https://en.wikipedia.org/wiki/Heat_engine). Every conventional powerplant operates on this priniciple.

See comments above. I don't think there are any examples of microorganisms extracting energy from heat gradients. But I realize you're correct in principle, I have edited the answer.


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Proteins with alpha helices alone and beta sheets alone?
I would like to see some examples of proteins with PDB ID so that I can download and see them in VMD software. I need some proteins with alpha helix only and proteins with beta sheets alone.

You may consider taking a look at the SCOP structural classification of proteins to check all beta proteins and all alpha proteins. As per specific examples and though not belonging to the SCOP classes mentioned above, Porin for a beta protein (PDB:1A0S), and Rhodopsin for an alpha protein (PDB:1F88) are two nice structures to look at.

Very helpful answer.

You can find examples by using the "drilldown" function at the RCSB PDB homepage:
Click on the number 103921 at the top of the page at http://www.rcsb.org then find the "SCOP Classification" section and then e.g. select "All alpha proteins".


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Formaldehyde turns plantar region of feet red?
I'm a freshman med student and I've noticed that on all the feet (and hands) of deceased people that I've worked with, the bottom of the feet always turns red and also the inside of the palm? Why is this?
Thank you.

I haven't seen any cadavers, how red are you talking about?

It might be due to livor mortis, also called postmortem lividity, which is the settling of the blood in the lower parts of the body which in your case might have been the limbs. By time the color can be interpreted as either blue or purple, but given, that not much time has passed it can very well be the reddish color you might have asked, as stated here on page 39:

The first manifestation of livor mortis can be expected 20-30 min following the irreversible cardiovascular arrest, initially as bright-red spots that subsequently become confluent and turn bluish-violet.

Which might better describe your case is the fact, that cold conditions can cause bright red color in livor mortis, as it can also be found on page 39:

Cold conditions, such as keeping a body in cold storage, cause ... bright-red livor mortis.

You can read more about it here or here.
EDIT
I have added references thanks to @Kendall, who provided them.

On these sites it says the extremities turn blue/purple with livor mortis: http://noirtek.weebly.com/embalming.html  and http://deemzet.nl/5/3/3/links.htm (dutch site)

After long time it can be seen as blue/purple as pretty dense amount of blood indeed have a color like that, but earlier it might very well be considered red.

A case study in this text on forensic medicine, page 23, makes note livor mortis may be bright red. Then, on page 40, a table notes bright red livor mortis is result of postmortem cold storage, among other causes like CO poisoning.


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Preservation of human tissue
At my med school we have human samples (body parts, organs, etc.)
They are soaked in some sort of solution for long term storage. I'm quite sure that it's not formaldehyde as that would be really toxic and we're allowed to pick them up from the tubs.
What sort of solution could this be?

I would assume you're using gloves to handle them?

Embalming solutions for cadaver study differ from institution to institution (and are reportedly somewhat different from embalming for funerals, but I'm not sure of those details). Typically embalming solutions for cadavers meant to be stored indefinitely consist mostly of water with lesser but roughly equal amounts alcohol (usually methanol), gylcerin, phenol, and a smaller percentage of formalin/formaldehyde to prevent mold.
A document from Albert Einstein College of Medicine lists:

Methanol: 11.1%
Glycerin: 11.1%
Phenol: 9.3%
Formaldehyde: 1.9%

If you want to know what your institution uses, you should just ask, and they should be willing and able to tell you.

Thank you. That explains why it's okay for us to handle them.


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Active & passive transport question
If an element, ion or molecule is found in a cell is it possible to tell which method of transport was used? for example if a hydrogen or sodium ion was found in the cell could you tell if it got there by diffusion, or facilitated diffusion, or endocytosis, pinocytosis etc? If not could you at least narrow down the number of transport methods it could have used?
I'm very interested in which substances are let throught the cell membrane and by which method.

How should you be able to distinguish how a certain atom or molecule entered the cell? They are not getting a sticker on them saying "got through the Na-K-ATPase".

Welcome to BioSE! As @Chris mentioned, transported atoms and molecules don't typically retain a record of their past history, so just by looking at a molecule in the cell you can't in general tell how it arrived in the cell (an exception might be proteins that have some chemical modification on them that allows them to be imported via a specific mechanism, such as the mannose-6-phosphate enzyme re-uptake system). In order to infer if a molecule typically enters a cell by a particular method, you will have to do several different types of experiments. I'll list a few off of the top of my head. Note to other SE contributors: since this is not my area of expertise, I'm not sure how feasible some of these experiments are, or how they are typically done, so please edit my answer to be more accurate!

Diffusion If you want to know if something can diffuse across a membrane, then the easiest way would be to try it in vitro. One way I can imagine doing this is to use a phospholipid bilayer to separate two compartments: one with your molecule of interest, one without. By measuring the concentration of your molecule that transfers from one compartment to the other, you can see if your molecule can diffuse across a lipid bilayer. Note that this will only tell you if diffusion is possible for your molecule. It may be that cells have ways to actively prevent your molecule from diffusing across your membranes, which you wouldn't be able to know from this assay.
Endocytosis or pinocytosis One way to assess if your molecule is taken up by endocytosis or pinocytosis would be to knock out (genetically or with an inhibitory drug) these processes in your cell and see if your molecule of interest still ends up in the cell. Depending on the context of the molecule you're interested in, you might be able to simply place cells in solution with your molecule of interest and measure the concentration of the molecule outside the cells over time. You could compare how much of your molecule is lost from solution when cells can't endocytose and compare to when they can; if your molecule stays around when cells endocytose, you have some indication that process is necessary. Note that there would have to be a lot of other controls for this experiment as well: e.g. ensuring the effect you observe is specifically caused by endocytosis being inhibited. Since endocytosis and pinocytosis form vesicle intermediates containing your particle of interest, one check to see if endocytosis might be reasonable is to see if you can see vesicles containing your molecule of interest in the cell. Of course, this requires a method for being able to visualize your molecule of interest (maybe it's fluorescent, or can be modified with a fluorescent marker? Or maybe there is a fluorescent protein that binds your molecule and can change color on binding? These things all exist, they just depend on your particular molecule and context).
Transport channels: In a similar vein, how does the uptake of your molecule change when you inhibit or remove from the cell a particular type of channel? You could measure this in a similar way as the bullet point above.
Active vs passive transport: If you wanted to see if uptake of your molecule requires active transport, you could try inhibiting ATP synthesis with a drug and see if transport of your molecule decreases over time. Note that this is in general not good for the cell (really!), so you might also have to have some more controls for this, maybe showing that transport of a molecule known to travel by passive transport is not affected on the timescale you're looking at, for example.

This list is by no means exhaustive, but I hope it gives you a sense of the type of experiments and ways of thinking you might be able to use to figure this out. Some general thoughts:
This tends to be case-by-case. While the type of experiments you might do to determine the mode of transport for different molecules are similar, the controls you will have to do to shore up your conclusions will really depend on the system involved, what type of effect a molecule has on your cells, whether your cell imports and exports this molecule, under what circumstances you might expect the cell to take up this molecule (so you have a way to trigger the cells to take up this molecule for your experiment). I don't know of a completely generic method for resolving this type of question.
Being able to measure abundance of your molecule is important. All of the experiments above rely on being able to measure the concentration of your molecule, either outside of the cell, or inside of the cell. This is often easiest if you can modify your molecule to be visualizable in a microscope or spectrophotometer, but however you do it, you need a good, reliable, robust assay in order to make strong conclusions with this assay.
Controls are really important. Thinking up all the different alternative possibilities and trying to come up with ways to rule them out is the heart of experimental science. Fortunately, it also happens to often be rewarding and thought-provoking! I certainly had fun thinking about this.
Best of luck!


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Why would the stroma have a higher pH during photosynthesis?
Here is a question form my test.

If you could measure the pH of the interior of thylakoids and the
  surrounding stroma during active photosynthesis what would be the
  relative pH of each?

The answer is C.

the stroma would have a higher pH

I understand that proton gradient is from stroma to thylakoid space, but that does not mean stroma would have less protons than thylakoid space, if stroma would have a higher pH, then the proton will never flow from stroma to thylakoid space, right?

Energy from an electron transport chain is used to actively transport protons from the stroma to the thylakoid lumen. Thus the lumen has a relatively higher proton concentration and therefore a lower pH than the stroma.
Higher [H+] means lower pH.
Lower [H+] means higher pH.
Keep in mind that the flow of actively transported protons from the stroma to the lumen is against their concentration gradient. There wouldn't be a net flow of protons this way without active transport.


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Understanding the meaning of $s$ and $t$ in a population genetics equation
Sewall Wright in this article (1937) at the end of page 313 gives the equation:
$$\Delta q = (s+tq)q(1-q) \space\space\space\space\space\space\space\space\space(1)$$
This equation is an approximation who holds only when $t$ and $s$ are small. $q$ is the frequency of allele A. $s$ and $t$ define the fitness of the three possible genotypes AA, AB and BB. I am not sure which genotype has fitness equal to 1 and I don't how $t$ and $s$ define the genotype fitnesses.
Let's assume for example that the genotype BB has fitness of 1. Then, the fitness of the genotypes AB and AA might be given by $1-t$ and $1-s$ respectively or $1-s$ and $1-t$ respectively or eventually by $1-t$ and $1-(s+t)$ (or variants) or even $s$ and $t$ (and opposite) or $st$ and $s$ (and variants). The genotypes fitness might as well be given by $1-st$ and $1-s$ but it would not be make much sense given the assumptions used for the approximation.
My question is: do you know how is the fitness of the three genotypes defined in equation (1)?


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What are the side-effects of long-term liquid breathing?
I just saw a recent Physics question that mentioned liquid breathing (which I had never heard of before) and I started to wonder about its long-term effects. Let's imagine a person underwent liquid breathing for some wacky reason - see the Wikipedia page for some starters - for a long time, maybe a month. What would begin to happen to them? Would any effects be reversible?

I'm pretty sure this has never been done long enough to really know the long term effects of liquid breathing. While the perfluorocarbons used for this aren't considered very toxic, exposure to such large amounts for such a long time could cause some toxicity.

Although I don't believe it's being done anymore, there were studies in respiratory care involving partial liquid ventilation. The perflurocarbons, besides offering a good interface for the perfusion of oxygen, provided a surfactant effects, prevening the alveoli from otherwise collapsing. Search the journals 'Chest' and 'Respiratory Care' for partial liquid ventilation.

Can anyone give a reference to liquid breathing done on an awake animal (or human)?  The only cases I have seen have been animals, in which case I think the prolonged anesthesia is going to be more of a problem.

It depends on the mechanical properties of the liquid you use. If you can find a suitable liquid, i.e. one that has fairly low density and viscosity, and is non-toxic even when inhaled in copious ammounts, then you can have a human "breath" in this fashion for a pretty long time, probably. Of course, these requirements aren't at all easy to fulfil and I'm sure are not the only ones. Also, "getting it right" would require a tremendous amount of trial and error, which is costly (and probably unethical, even in animal studies) and offers very little (if any) benefit, because we already have plent

I vaguely recall David Blaine (a celebrity illusionist/escape artist) considering this to complete a long submersion trick, but he dismissed the concept and commented that the process would intensely painful [Citation needed]. Still unsure if this has ever been attempted by a fully awake human without anaesthetic.

Overview.
This is a very interesting question. The ideas behind this have been around for a while and the methods are covered in great detail elsewhere.
The overall answer to the hypothetical question is rather surprising. There may be actually potential benefits to perpetual liquid ventilation for people with certain diseases. Trials so far have not found side effects in fluorocarbon liquid breathing.
So lets talk about the history of liquid breathing and case studies, then we will move onto the hypothetical situation of liquid breathing indefinitely.
A great review (Shaffer et al, 1992) covers the field in great depth.
@MCM pointed out in the comments that my original answer did no emphasise that animal diaphragms are not powerful enough to move the liquid in and out of the lungs. I should mention now that the below cases all use ventilators to pump the fluid into and out of the lungs. The difficulty of breathing this without a ventilator is emphasised by David Blaine at 4:54 in this TED talk who said it was like trying to breathe with an elephant standing on your chest.
Case studies.
As early as the 1920s, poisonous gas research that lead to the infamous mustard gas found that lungs could tolerate large quantities of saline briefly without damage.
Animals.
Kylstra, the first pioneer introducing the idea of land animals breathing liquids (Kylstra et al., 1962), found mice could withstand 4 hours of 160 atmospheres of pressure.
Clark found that mice and rats could breathe oxygen bubbled silicone oils and survive for a few hours after emersion.
In 1965, he discovered that the fluorocarbon known as FC75 not only supported respiration during total immersion but the mice survived indefinitely in apparent good health.
The most recent study I can find is the partial use of fluorocarbon liquid ventilation in adult respiratory distress syndrome (ARDS) of rabbits. The same improvements in breathing were not observed in saline liquid breathing or conventional ventilators.
Humans.
In humans PFCs were first used successfully in 1989 for the ventilation of young infants near death.

Marked improvement in lung compliance, without a compromise of cardiovascular status was noted in all three patients.

All three infants died of their severe preexisting respiratory complications, but the trial showed liquid breathing can support gas exchange in humans. However developing lungs of infants cannot rely on mechanical ventilators for prolonged periods as nearly a quarter of premature infants of those that do later developed chronic breathing problems.
Biomedical application.
There are a fair few researches and doctors who believe fluorocarbon liquid ventilation has some advantages over gas ventilation. It reduces stress at the area of interfacial surface tension in the distressed, surfactant-deficient lung. This would be ideal and appropriate for ARDS in human adults. A more sophisticated use would be using fluorocarbons as a drug delivery system straight to damaged lung tissue.
(All the above can be found in the 1992 review. There is also data on the different properties of suitable FCs)
Real world potential.

Is perpetual liquid breathing possible? ...And healthy?

So this is where we stand with the case studies; mice can breath liquids indefinitely and stay in good health, rabbits with ARDS survive where breathable gas would not help, and there is a contingency in the biomedical community that it can be better than gas ventilation for medical treatment. To me it seems that there is nothing to suggest a fully grown adult would suffer from breathing liquids. The inertness of the fluorocarbons implies any toxicity would only reveal itself in a timescale of years, and everything else about the compounds pose no danger and may make gas transfer across the lungs easier.
This relatively modest success is perhaps no surprise. The exchange interface of our lungs relies on a mucous (liquid) so the gases can permeate the lung tissue. Expanding on that idea should certainly not rule out the possibility of liquid breathing.
The biggest drawback, besides the cost of a long term experiment and being dependent on a mechanical ventilator, is that these are very small case studies of success. Given the massive amounts of unknowns (particularly for long term studies), switching to  purely liquid ventilation in an adult human could have unforeseen risks and would be considered dangerous by any ethics board (or insurance company)!
On a lighter note, here is a YouTube video of what Maddie, a biology podcaster from the BBC, had to say on the matter of living in total submersion. Lots of skin problems, risk of infection after a few days etc.
Again, a very interesting, albeit understudied, topic!

@HDE226868 -- One thing that absolutely must be said that wasn't addressed is this: All of those human studies used external pumps to move the fluid. Mammalian diaphragms are not designed to move a liquid medium more than a handful of times. They will literally tear themselves to shreds very, very quickly.


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What do we know about the cellular structure, processes, environment, and immediate ancestors of the last universal common ancestor (LUCA)?
I am up for all scientifically sound speculations, and sources are highly welcome. I've looked into this quite a bit myself via scholar.google, the wiki article, and /r/askscience.
I'm really looking for more speculation about physical details of the organism, its environment, and its immediate ancestors.
e.g. How did they (referring to the LUCA and some immediate ancestors) acquire nutrients? What forms of mobility were available to them? How long was it until photosynthesizing organisms emerged?
mods: If this is too open-ended or too speculative, please let me know where I can redirect this question.

As far as I have read LUCA is just predicted to have certain characteristics. It is not physically found. You can have a look at this paper. It is about energy metabolism in LUCA.


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How many traits can a multivariate breeders equation handle?
The multivariate breeders equation (MBE) by Lande predicts the change in a trait $\Delta \bar z$ (response) as
$\Delta \bar z = G \beta$
where $G$ is a genetic variance-covariance matrix and $\beta$ is a vector of the selection coefficients. What are the limitations on the number of traits the MBE can tolerate? Is there a theoretical limit on the number of traits $G$ and $\beta$ could contain? Or does the calculation lose power with increasing complexity?
Theoretically as an example, could I take the expression of 10000 genes, compare them to fitness to to make a 10000 row $\beta$ vector, and generate a 10000 * 10000 G-matrix from estimates of male and female gene expression in some lines, and then put them through the MBE?

(this may be better on or cross posted on maths SE)

I guess there is no theoretical limit on how many dimensions you should have. But it makes sense to reduce the dimensionality of the model if possible. Having too many variables makes a) the system look complicated (and clumsy) b) consumes more computational resources c) in some cases makes the dynamical model stiff (makes it difficult to solve)

This is still fine because it is a linear equation. And 10k x 10k matrix is not that huge for computers these days. But you would end up storing more information than needed.

@WYSIWYG Thanks, I guess there is a trade off to be had, on one hand we want to include as many traits as possible to ensure we have all traits affecting fitness (which is almost impossible, particularly in natural populations, and especially if we consider all ontogenetic and environmental variants). But on the other it becomes rapidly more complex, conceptually difficult and less general in its meaning.

Noting that the right hand side can also be written $\mathbf{G}\mathbf{P}^{-1}\mathbf{s}$, we see that the only theoretical limitation of the multivariate breeders equation is the invertibility of the matrix $\mathbf{P}$. This happens when the measures of two traits are the same for all individuals, making two columns of the matrix the same I.e. It becomes singular.
This theoretical concern can become a practical concern quite quickly when multiple traits are measured. The solution is to effectively consider two traits as one.
The 'power' of the equation, by which I assume you mean something like 'accuracy of prediction', actually improves with the number of traits measured. Indeed, a big concern with measuring only a few traits is that the response to selection on those traits is actually 'caused' by selection on some other correlated but unmeasured trait.


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Do animals have social status as humans in our society?
As our society and it's functioning is closely related to the ones of animals, one question arises: Do animals in nature have social status as humans? People often display it publicly, by buying nice cars, searching for women and partners and so on, accumulating wealth and so on. Does similar things happens in nature? How our behavior is similar to animals?

Are you asking if animals try to show off social status?

Yes, exactly this.

Animals certainly have social status as evidenced in the idea of 'pecking order' or dominance behaviors in canine packs.
I think the more interesting question (perhaps what you are looking for) is whether non-human animals 'dress up' their social order either to deceive others about their standing or reinforce their position in society.
If this is the question, then natural displays don't really count. More specifically, is there evidence of animals 'affecting' a position in 'pecking order' that is not theirs otherwise? Or perhaps ask, ' why do men buy BMWs?'


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The biology behind tree pruning and hedge trimming
I read two contradictory arguments which both seem logical to me, related to the tree pruning and hedge trimming:

You should prune/cut trees only outside the growing season, when the tree is "sleeping". In some countries there is even a law forbidding to cut/prune trees within the growing season!
You should trim the hedges only within the growing seasons, when the tree is not sleeping and thus able to heal the cuts.

Which of these two arguments is true and how are they supported by the plant biology?

The difference has to do with the concept of "thinning and heading" and how plants respond to abiotic damage. Thinning refers to the removal of a branch or shoot all the way back to the node which it originated from. This is the primary type of pruning used on trees - either to limit growth or to increase the amount of light permeating to lower branches. Late winter is generally the best time to do this, just before the tree breaks dormancy, since plant pathogens are generally less abundant. By pruning in late winter, this also reduces the amount of time that the wound is exposed before the tree begins active growth.
In contrast, "heading" refers to the partial removal of a branch, usually 1/2 to 1/3 back to the node.  The purpose of heading is to stimulate shoot growth on the remaining branch - hedges being a primary example. Because new shoots and leaves are desired, heading is usually performed at the height of stem growth (in most climates late spring to early summer).
The biologic processes behind this are complex (botanists are just beginning to understand how plant behavior adapts to predation) but in very general terms, plants respond to damage in two ways: by compartmentalizing the wound; and by stimulating growth on the remaining tissue. Many types of woody plants produce latent (or adventitious) buds, which lie dormant within the cambium tissue. Normally these buds are suppressed by auxin hormones produced in the meristem by active shoots. When the meristem is removed (such as through heading the branch), these buds rapidly develop to produce new shoots and leaves. Most species used for hedges are selected because of this ability.
So long story short: thinning is best performed in late winter, when the plant will quickly be able to seal off the damage while limiting the production of unwanted water sprouts and suckers. In contrast, heading is usually done in early summer, when the hedge can vigorously produce new growth and fill out any gaps.
Some resources:
http://extension.wsu.edu/maritimefruit/Pages/PruningBasics.aspx
http://puyallup.wsu.edu/~linda%20chalker-scott/horticultural%20myths_files/Myths/Wound%20sealer.pdf


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Interpretation of graph from evolutionary biology
I am studying evolutionary biology, and been presented with this graph:

I am having some difficulties understand its meaning. For a start, why is time measured as a fraction of the population size? Also, what does it mean by allele frequency? Does it mean the frequency of a single allele? But if the first caption it referred to 'frequencies'... Any help? :)

I think measuring time in terms of generations means that time is measured in generation time, time it takes an organism to reproduce. In bacteria, this can be 30 minutes, or in humans it's about 20 years. So I would interpret that graph to mean that within 2 generations, allele frequency probability becomes equal. It's been too long since genetics for me to tell you anything more right now.

This graph shows the probability distribution of allele frequency i.e. it displays the density probability of an allele to be at a given frequency. The time is measured relatively to the generation time and expressed in in relation to the population size $N$. t=2N means that 2N generations occurred and of course it doesn't correspond to the same real time if we talk about rats or lions. It would be good to include the text that accompany the figure so that we could understand at what state was the population at $t=0$.

@max0005 Does the answer help you understand the graph?

I assume that the figure comes from a section on genetic drift (since this seems likely), and it shows how the allele frequency will change over time under drift in a diploid population. So in short, each line represents the distribution of allele frequencies in different hypothetical populations, that all started with the allele frequencey p=0.5.
As for your specific questions, as the comment from @remi.b says, t is expressed as generation time since this is the relevant time scale for evolutionary changes. The reason why it is a function of population size, N, is that genetic drift acts more stongly in small populations, since it is essentially a sampling effect. You can see it as a repeated application of binomial sampling. So in small populations different populations will quicky drift away from the starting point of p=0.5, while this takes a longer time in larger populations. The effect of population size is clearly shown in this article from Nature education, where you can see the distribution of allele frequencies after one generation in populations of different sizes.
The change in allele frequencies over time under drift has been modelled by a diffussion approximation (see Kimura, 1955 for the original results). His results show that heterozygozity decreases at the rate of $1/(2N)$ per generation, and after 2N generations the distribution of allele frequencies is essentially flat (if you started at p=0.5). The degree of heterozygocity at time t is given by:
$$H_t = H_0*e^{-(\frac{1}{2N})t}$$
However, your graph does not show populations where fixation has occured (only heterozygous populations), and this proportion will increase over time in the absence of new mutations. So what is missing are bars at 0 and 1, and these will become higher as time goes by (more populations will have become fixed for one of the alleles). It should also be mentioned that these results deal with the effective population size, so $N$ is really equal to $N_e$.
As for the confusion of frequency/frequencies; the graph shows the frequency of one allele in different populations (so the allele frequency on the x-axis), but each line shows the distribution of allele frequencies in different populations. This is probably why you found this confusing.
However, your question is a bit unclear since you haven't described from where you got the graph and exactly what it is supposed to represent.


text:
What are "anchor regions" in the human genome?
I've been reading this paper entitled "A high-resolution map of the three-dimensional chromatin interactome in human cells", about interactome in 3D chromatin.

We next applied the above algorithm to the 518,032 anchor regions in
  the human genome, with each containing one or a few HindIII
  restriction fragments (fragments shorter than 2 kilobases (kb) are
  merged) (Fig. 2a), and uncovered a total of 1,116,312 chromatin
  interactions with a false discovery rate (FDR) of 0.1

Simple questions: what are these anchor regions in the human genome?
How could I group them into types/categories?
Thanks

Good question. Anchor regions are regions that connect to the nuclear matrix. More specifically, in eukaryotic organisms, chromatin is anchored to the nuclear matrix by short DNA sequences of about 100-2,000 bp called matrix attachment regions or MAR. To answer the second part of your question, there are many categories (and opinions about those categories) of anchor regions. The most comprehensive way of categorizing these regions however I believe is by whether they are constitutively (always) or transiently (sometimes) bound to the nuclear structure.

Thanks @rhill45 Where could I find the categories that you mentioned? Could you give me a list or a link to a paper?

From the reading I've done, I think they have been very well catalogued and are still being identified. Here's a 2008 review on MARS.http://genomebiology.com/content/pdf/gb-2008-9-1-201.pdf


text:
Do the light and dark reactions happen at the thylakoid?
My professor said that light reactions and dark reactions happen at the thylakoid. He did not choose the answer that "both reactions happen at chloroplast".
Isn't the thylakoid a part of the chloroplast?

The light dependent reactions involve an electron transport chain with enzymes embedded in the thylakoid membrane. NADPH and ATP are generated in the stroma and water is oxidized in the thylakoid lumen.
I'm not sure if it's correct to say that the light independent reactions occur "at the thylakoid" since, in plants, they could really occur anywhere in the stroma (not necessarily "at" the thylakoid, and certainly not within it). It's possible that the enzymes involved in the light independent reactions are somehow localised at the the stromal side of the thylakoid membrane for efficient use of substrates, but I have no idea if that is actually the case and I don't have time to review any literature.
In plants, all of these processes occur in the chloroplast. However, photosynthetic bacteria don't have chloroplasts so you can't categorically say that the photosynthetic reactions occur only within chloroplasts. Cyanobacteria do have thylakoids where the light dependent reactions occur.


text:
What is meant by a muscle fiber being glycerinated?
I was popped this questions today, "what is a glycerinated muscle fiber, and what is required for its contraction," and had little idea. I'm assuming the question is "what's required for its contraction as compared to normal muscle tissue?"
There's a limited amount of information out there about this. It appears that it is a type of in vitro system requiring special preparation of typical muscle tissue. I was wondering if anyone here had a little more information. Is this something that's just used in teaching lab exercises?

From: http://www.acad.carleton.edu/curricular/BIOL/classes/bio126/Documents/Lab_5.pdf

Glycerination disrupts the membranes of the muscle cells, ruptures mitochondria, and leaches out soluble constituents such as ATP and inorganic ions. However, glycerinated muscle retains the organized structural array of myosin thick filaments and actin thin filaments, actin-associated proteins like troponin and tropomyosin which regulate contraction, and the functional capacity for contraction.

I would expect that because the sample has lost ATP and inorganic ions, you would need to supply ATP (the source of energy), $Mg^{2+}$ (which is necessary for ATP hydrolysis) and $Ca^{2+}$ (to induce the contraction).

this is the answer I was looking for. You may want to double check info the  Mg2+ though, I know free mg+ will inhibit  hydrolysis, while calcium alone can act as a cofactor. Your right though mg will help nucleophillic attack I just think Ca is ok alone, this is one of the reasons why the cell prefers the sarcoplasmic reticulum is quenched with ca2+.

I included the bit about magnesium based on the protocol linked to in the answer. Here is an article discussing myosin catalysed ATP hydrolysis which includes magnesium in the reaction mechanism (http://pubs.acs.org/doi/abs/10.1021/bi052433q). However, I have also found articles describing how magnesium inhibits myosin, so I don't know.

Calcium ions aren't needed (like normal muscle cells), because the glycerination process disrupts the troponin-tropomyosin complex so that the binding sites on the actin are exposed. However, glycerol makes the membrane permeable to small molecules, including ATP. That means that a glycerinated muscle requires addition of ATP so that the myosin heads can actually bind to the binding sites and create cross-bridges.
Magnesium ions aren't required, but they act as catalysts that help the muscle contract more.


text:
Cell targets of Glybera
So we know that there is a first gene therapy drug in the market out there called Alipogene tiparvovec to address  lipoprotein lipase deficiency (LPLD) at a genetic level. Does this genetic drug target all cell types (except germline) that expresses the LPL gene in the human body or simply the parenchymal cells that process fat? I have not been able to find information specific to Glybera.

Glybera doesn't target all cells, and doesn't target fat processing cells. Glybera is adeno-associated virus 1, which normally infects skeletal muscles. Glybera is delivered by intramuscular injection, so the virus easily infects the muscle tissue. The infected muscle cells produce a variant of lipoprotein lipase that has better activity than normal LPL and secrete it into the bloodstream. Once in the blood LPL can interact with chylomicrons and make them smaller.
Here is a paper about viral gene therapy for LPL deficiency, specifically about glybera, but I don't think it's open access.

So does it mean that all muscle tissue associated cells will be targeted and test positive for the new LPL variant?

Probably not all muscle cells. The virus is given by multiple injections into lower limb muscles, most likely only the cells near the injection sites are infected. The virus is also replication incompetent, so it can't copy itself and infect new cells.


text:
What is the scientific and common name of this bug?
Captured this under my stereo microscope. Much more beautiful than appearing on my camera sensor.
Can someone help me identify it and explore more?
Also is it having a compound eye ?
Location: New Delhi.

I'm pretty sure it's a hemiptera, looks like a stink bug, though I don't recognize the color. And yeah, those are compound eyes.

Pentatomidae(http://en.wikipedia.org/wiki/Pentatomidae).
Great pic! can you tell us the geographic location this found?

@DevashishDas New Delhi, I found it near my table lamp on first floor in evening, where I have kept some plants. Then I took a leafe, and gently placed it on it, and photographed under my microscope.   I found that it became stable as soon as it came in contact with the leaf, otherwise it was moving here and there and jumping a lot. And thanks for the link.

@DevashishDas Post your comment as an answer so that it can be accepted by the OP and the question can be closed.

@TheLastWord That's not the answer though, the question asks for species, and pentatomidae is the family name.

Definitely appears to be Pentatomidae (as others have pointed out) due to shield-like, broad bodies. With over 4500 species and larval stages demonstrating significant variability even within species, ID can be difficult without knowing specific fauna, size, habitat, etc.
The OP doesn't list a size, but because OP is viewing under a scope, I assumed this is a fairly tiny species.
I came across this similar-looking unknown species (simply labeled "PK03") of the genus Eysarcoris

 Credit: CBG Photography Group, Centre for Biodiversity Genomics
The Eysarcoris genus is present in India (e.g., see indiabiodiversity.org with example of "two-spotted sesame bug")
A similar species well known throughout Europe is Stagonomus venustissimus (previously classified as Eysarcoris):

 Credit: Jose Manuel Sesma (2016); appears to be originally posted here
I cannot say if either of these species is correct (doubtful), but I think they are closer than the other provided answer.
I'll update if I find anything specific.

It belongs to Pentatomidae family. More on the Wiki page

That's correct, but pentatomidae is the family name, and the question asks for species.

The answer will be more useful for future reference if you add some rationale for your determination.

To answer your other question about the eye:
Yes, shield bugs (Pentatomidae), like most insects, have compound eyes.

Buschbeck and Friedrich (2008)1 discuss this highly conserved trait found in most arthropods.

Also, the red dot medial and nearby the eye? That's an ocellus, a simple eye.

 Oregon Department of Agriculture

1: Buschbeck, E.K. and Friedrich, M., 2008. Evolution of insect eyes: tales of ancient heritage, deconstruction, reconstruction, remodeling, and recycling. Evolution: Education and Outreach, 1(4), pp.448-462.

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


text:
When the mind is highly active, roughly how many neurons become excited in one second?
I'm curios to know how many times neurons send signals in one second when the brain is highly active (Highly active meaning during difficult problem solving, or any task that might bring the brain to it's higher volume of activity).
When the mind is highly active, roughly how many neurons become excited in one second? The question might also be posed as: "How many action potentials might "occur" in the brain over the course of one second during any form of complex mental process?"

Answers accurate to whatever accuracy we're currently capable of would suit my interests.

What do you mean by "happen"?  Synapses can be strengthened by ongoing activity (or weakened by a lack of it), but they don't really appear out of nowhere on that timecourse.

@jonsca It was my understanding that an action potential sent over the axon to connected neuron dendrites had a chance to either synapse or not depending on the strength of that ongoing activity.

I understand my blunder after some research. I'm still curious about what I intended to ask, so I've fixed my question.

Great question. My first assumption is "nobody knows", but a) I'm no expert, and b) you might be able to get somewhere by using 2-photon microscopy data (or something else that measures neural activity in vivo) and making some inferences. See, eg http://cshprotocols.cshlp.org/content/2014/7/pdb.top081810.abstract

Depends on what you mean by active mind. High resolution FMRI can enable you to approximate how many or which (bunch of) neurons are getting activated.

@WYSIWYG I simply mean, any active mind. Someone solving a puzzle, playing a game, etc. Just looking for a maximum-ish measurement.


text:
Recovering Coma patient with theoretical full knowledge of heart function
In coma, there is the medullary depression (stage of agony).
Spontaneous respiration and circulation cease i.e. vasomotor center.
There is no full circulatory and respiratory support.
Assume you could stimulate and coordinate fully the autonomic nervous system of the heart.
You know exactly which pacemaker cells and pathways are blocked in the particular coma patient.
I have in mind Schumacher's case - where you have head injury.
I think you should consider, in his case, the pressure of the head also if you can restore circulation and respiration artificially.
Some neurologists say that it is practically very difficult to wake a person if he has been in coma for six months.
I would like to understand this.
I think it is because of atrophy of muscles and probably something with atherosclerotic changes.
However, I am still interested in your opinion about the theoretical situation - if you can restore heart and respiration centre, can the recovery start?
What are the limitations of restoring the function of the body by restoring the circulation and respiration i.e. vasomotor centers after long stay in coma?


text:
Effects of selection on effective population size
Background
The effective population size ($N_e$) is a central concept of evolutionary biology and is influenced by several parameters. For example: sex ratio bias affects $N_e$ $\left(N_e = \frac{4N_mN_f}{N_m+N_f}\right)$ and varying population size over time influences $N_e$ $\left(N_e = \frac{n}{\sum_{i=1}^n\frac{1}{N_i}}\right)$. There is a post on how overlapping generations influences population size.
Question
Selection also influences the effective population size. Intuitively, I'd expect that the higher is the fitness variance, the lower is the effective population size as fewer individuals contribute to the next generation. Am I right? How (what is the mathematical formulation) does fitness variance influences the effective population size?

From Conner and Hartl's A primer of ecological genetics:

"Any variance in reproductive success among individuals greater than
  random expectations, a commonplace concurrence in natural populations,
  reduces effective population size."

So yes, selection does reduce the effective population size and for the reason you suggest - it removes some individuals from the mating pool/ reduces their contribution to the next generation. Mathematically it can be derived as
$N_e \approx \frac{ 8N_a}{V_m + V_f + 4 }$
where $V_m$ and $V_f$ are sex-specific variances of offspring production (males are often more variable in reproductive success than females).
They give an example of selection affecting $N_e$, in a population of deer 33 males had four times the variance ($V_m$ = 41.9) in reproductive success of 35 females where variance was $V_f$ = 9.1. Thus effective population size was
$N_e \approx \frac{ 8 * (33 + 35)}{41.9 + 9.1 + 4 } = 9.9$
The notation $N_a$ is the actual number of individuals in the population. This can be seen in the calculation of effective population size when the number of males and females are not equal
$N_e = \frac{4 N_m N_f}{N_m + N_f} = \frac{4 N_m N_f}{N_a}$
An example is a population of 80 males and 80 females compared to a population of 70 males and 90 females. Both populations have equal sizes but effective population size is reduced by unequal sex ratios
$N_e = \frac{4 * 80 * 80}{160} = 160 \neq \frac{4 * 70 * 90}{160} = 157.5$

+1 Nice! $N_a$ is just the population size I guess. What does the $a$ in index stands for?

I'll take a look tomorrow, just got home, can't remember why it's $N_a$ as opposed to anything else. @remi.b

edits done @Remi.b

Wow, usually when people say that they "I'll have a look at that tomorrow", it means that they won't never give any more attention to the post. But you actually came back and answered my question in the comments! Thank you

@Remi.b I'm guilty of that a lot, I think I still owe you an answer on evolution of the G-matrix!!!

Note that this is just the effect of non-heritable variance in fitness. Heritable variance can have much larger effects.


text:
What is the result of meiosis?
Is the result of meiosis ONLY the sex gametes (male and female) which later meet to form a somatic cell?
Sometimes I feel as if my book is hinting towards meiosis is the process where sperm cells meet oocytes?? I'm a bit confused.

In principle, Meiosis is only the process in which the haploid egg or sperm are generated. Have a look at this figure, which shows Meiosis I and II (from the Wikipedia):

During Meiosis I homologous recombination between homologous chromosomes can happen, the chromosomes are then distributed normally among the daughter cells. In Meiosis II the cells split again and here the sister chromatids are divided and the haploid gametes form.
In the oocytes the process is in principle the same, but the cells get arrested in the so-called diplotene stage of Meiosis I (picture from here):

In the diplotene stage the chromatin is decondensated and transcriptionally active, this helps maintaining a correct chromosome structure, as the diplotene stage can last up to 50 years. When the cell receives the hormonal signal to enter the fallopian tube, Meiosis I is finished. The resulting cells are not divided symmetrical, building one big oocyte and one polar body containing the second set of chromosomes. Most vertebrate cells are arrested in this stage again until they are fertilized. Then another asymmetrical division is done, leading to a haploid cell with two polar bodies. This oocyte is then fertilized.
This process can happen almost at the same time in a lot of vertebrate species, including humans. This is probably what was meant by your textbook.
For further reading I can recommend: Meiosis and Fertilization from the NIH bookshelf.

It should be notes that meiosis is sometimes arrested in eggs until fertilization.

You are right and I should have looked into the Alberts directly :-) Thanks for the notification.


text:
Is the innate immune system capable of identifying all foreign antigens?
I've been studying immunology on my own lately and I would like to know if the macrophages and the other components of the innate immune system are capable of identifying all foreign antigens.
As far as I understand the innate immune system is responsible for activating the adaptive immune response that will produce antibodies. So the innate immune system should be able to identify new antigens, antigens that the body has never seen before.
If that's the case, how does it work? Does everything "alive", from virus to bacteria, present the same molecular pattern that is responsible for triggering an innate immune response?
Thanks!

Not essentially. TLRs have evolved to identify some common antigens.

TL;DR the huge block of text:

The innate immune system only recognizes certain antigens, called PAMPs.
The activate immune system usually requires the immune system, but it can get around this in some cases.

You're on the right track.
Pathogen-associated molecular patterns (PAMPs)
Innate immune cells such as macrophages and denritic cells (DCs) only recognize certain pathogen-associated molecular patterns (PAMPs), and this occurs primarily through membrane-bound receptors called Toll-Like Receptors (TLRs). Diversity of PAMPs is extremely limited compared to the extraordinary diversity in recognition by the active immune system. However, they include many molecules and classes of molecules that are essential for certain pathogens, such as flagellin, lipopolysaccharide, and viral double-stranded RNA.
To answer some of your question right away, the immune system can't adapt, but it can recognize antigens that the body hasn't seen before, because the set of antigens it can recognize (the PAMPs) are dictated by the genes associated with Toll-Like Receptors and other "Pattern-Recognition Receptors".
Exception 1: T cell anergy
The major link between the innate and active immune systems that you mentioned is through the presentation of antigens to T helper cells in lymph nodes by DCs: DCs present antigens (digested parts of pathogens) to T helper cells through a process called antigen cross-presentation.
When this happens, the T helper cell is activated through a series of chemical exchanges between the DC and the T helper cell, with two that are important to mention here: 1) the T cell recognizes the antigen–MHC class II complex on the DC (called T cell stimulation), and 2) the T cell receives a signal (called co-stimulation). The first signal only requires cross-presentation and recognition by a T cell. But for the DC to release the co-stimulatory signal, Toll-Like Receptors (TLRs) on its surface need to have recognized a PAMP.
With these interactions (plus some more), the T cell will begin proliferating. However, immunology is very nuanced; you can probably find exceptions to every sentence I just wrote (I see a lot even while writing this). It turns out that a T cell can still be activated even without co-stimulation if its own stimulation is strong enough. This occurs through a process called T cell anergy. Activation of an anergic T cell—that is, one that was activated but did not receive a co-stimulation signal—has to do with the autocrine and paracrine nature of a signal called IL-2, which T cells normally produce only small amounts of but produce much more when fully stimulated.
Exception 2: B cells T-independent activation
But T cells are only half of the active immune system. It turns out that B cell activation follows similar rules, though not through DCs. B cell activation usually occurs with help from activated T helper cells (only one that recognizes the antigen the B cell is specific for). However, B cells can become activated without T cell help in two situations: an antigen binds to the B cell receptor and to a TLR, or 2) the B cell receptors become saturated with highly repetitive epitopes. Situation #2 technically occurs without help of the innate immune system.
So you're mostly correct that the active immune system requires innate immune system help, except that there are these two exceptions. And since immunology has so many exceptions, there are likely to be more.


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What would happen if there were no SOX9 in an XY human?
Would testes be produced? If SRY is functional, can it produce other proteins that can direct the production of testes, which may or may not be sterile?

Quoting the abstract of this paper verbatim:

Sox9 is an Sry-box-containing gene that encodes a transcriptional
  activator. During mouse gonadogenesis, Sox9 is detected in the male
  gonad at 11.5 days postcoitus (dpc). At 12.5 dpc, testicular cords
  form, morphologically distinguishing the male gonad from the ovary.
  From this stage onwards, Sox9 expression is restricted to the Sertoli
  cell lineage and persists in the adult. Humans with heterozygous
  mutations in SOX9 develop a skeletal syndrome known as campomelic
  dysplasia. Furthermore, most XY SOX9 heterozygotes show variable
  male-to-female sex reversal, implicating SOX9 in testis development.
  Sox9 heterozygous knockout mice die at birth with a syndrome similar
  to that of human campomelic dysplasia. In contrast to humans, XY
  Sox9+/- mice form normal appearing testes. Germ-line knockout of Sox9
  using a conditional null allele provides a tool for generating Sox9-/-
  mice by simple genetic crosses. However, Sox9-/- mice die soon after
  11.5 dpc because of cardiovascular defects. In vitro culture of the urogenital ridges of XY Sox9-/- results in gonads lacking testicular
  cords and Sertoli cell marker expression, but with the expression of
  ovarian-specific markers. Therefore, Sox9 is essential for diverting
  an intrinsically ovarian program of organogenesis toward testis
  formation.

From MGI page on Sox9:

Null mutant heterozygotes and conditional knockout mutants display
  perinatal lethality with cleft palate, hypoplasia and distortion of
  numerous cartilage-derived skeletal structures, and premature
  mineralization in many bones. Specific conditional knockout mutations
  are sex-reversed.

SOX9 is indeed the factor which is important for the developent of the sexual organs and not only for men, but also for women. Expression of SOX9 regulates the expression of the anti-Müllerian Hormone, which inhibits the formation of the female reproduction system. See reference 1 for more details.
Mutations in or around (in regulatory regions) of the SOX9 gene lead to severe developmental changes and to the genetic disorder "Campomelic dysplasia". The disorder leads to changes in the bones and also in the sex determination, it is often lethal in the neonatal period due to respiratory problems. Have a look into reference 2 for more details.
In mice, the complete loss of SOX9 is embryonical lethal, have a look at reference 3 for details. Although there are no data available for humans (for obvious ethical reasons) I assume that the effect is the same.
Development of testis starts by the activation of SOX9 by the testis determination factor. SOX9 in turn activates a number of other transcription factors (have a look into references 4 and 5 for details) which finally lead to the development of the testis.
Mutations in SOX9 in men (with XY chromosomes) also lead to the reversal of the sex, meaning these individuals will develop female reproduction organs (see reference 4). It has also been shown that female mice will develop testis when SOX9 is induced in these animals (see reference 6). You can also have a look into the OMIM database for an extensive review.

References:

Direct interaction of SRY-related protein SOX9 and steroidogenic
factor 1 regulates transcription of the human anti-Müllerian hormone
gene.
A clinical and genetic study of campomelic dysplasia.
Sex determination: a tale of two Sox genes
The PGD2 pathway, independently of FGF9, amplifies SOX9 activity in
Sertoli cells during male sexual differentiation.
Fgf9 and Wnt4 act as antagonistic signals to regulate mammalian sex
determination.
Sox9 induces testis development in XX transgenic mice