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How does the brain store information?
In all electronic devices with the possibility of saving there are tiny magnets that can store your data by the state they are in. In general, there has to be something changed to store information and independent observer should be (theoretically) able to read all the stored information just from one state of brain.
I think keeping some signal in circuit would be really nutrition expensive (through the ion pumps that create the electro-chemical gradients).
So how does a brain store the information?

@AliceD I deliberetaly chose two different words to suggest some different type of storing, even though I see no difference since brain seems to be a bunch of neurons. The only meaning of just "neurons" version I can imagine is as question how do nutritions get to the right neurons and that I think is pretty clear.

Let me clarify: Neurons as units of the brain store information e.g. by LTP. This single-neuron-level learning in e.g. hippocampus has been well-investigated. The brain is yes, a 'bunch of neurons' but information storage at the brain level is highly complicated. In its simplest form the hippocampus stores info for ~24h whereafter it is stored in widespread areas in the cortex. How it is retrieved from there is pretty complex and pretty unknown afaik. The pitch of the answer to the title (Basic electrophysiology) is hence completely different from your concluding sentence (Cognitive Sciences)

I still don't understand the meaning of the question only with neurons, but OK, I'm going to rewrite it.

Probably - does @WYSIWYG 's linked question answers yours? It does seem an exact duplicate to me.

@AliceD I think yes. I really like the idea of connecting your sensations to recieve every information. Only thing I think is different is my circuit or state dilema with which I'm still not sure. Does LTP and LTD work like 0 and 1 state for neuron or are there some circuits switched to long-term synapse which allows the signal come out only if some neuron has "flipped the switch" by some signal from the outside?


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Do biological phenomena follow Gaussian statistics?
I have recently entered the life sciences (from physics).  I am concerned about the use of p values in the life sciences literature.  For example, in this article, they test 9 - 12 rats in a control group and compare it to an experimental group.  They use p values to claim that their results are statistically significant.  This type of use of p values seems to be very common in the literature.
So here are my concerns :

Why is it so often assumed that biological measurements follow a normal distribution?  To my knowledge, this isn't known a priori.
From my physical intuition, it seems quite challenging to claim "statistically significance" when using such low sample sizes.

Yes, if/when you can apply the central limit theorem. Things like body mass/size etc are influenced by many relatively independent atomic factors, hence you can apply the theorem. But don't fool yourself into thinking that normal distribution is all we've got in biology. Binomial, Poisson, beta and gamma distributions are highly common in genetics and bioinformatics.

1) this is really an emprirical question; sometimes it is, sometimes it isn't. Even if the "real" process is poisson, a normal distribution can still be a fairly accurate approximation. 2) intuition based "significance" and the technical concept of "statistic significance" needs to be clearly separated. If assumptions are met, an analysis might produce statistically significant results, while still being weak with rather shaky results.

Healthy skepticism is a great thing, especially in biological research. Also remember that in Biology, models are often imperfect approximations for the questions studied. That doesn't mean they aren't the best that we can do given the current limits of technology, but it is something to always have in the back of your mind when you read biological publications. There are countless examples or studies that produced significant results in rodents but collapsed in human trial. Also, in vitro tissue cultures can be fraught with assumptions that cannot be extrapolated to the organism.

Answers to this question are right, but I miss someone mentioning that there are tests to assess if your data follow a normal distribution, although those test aren't powerful if your sample is small.

kmm's answer is correct; I just want to add some of my points on what kind of data should follow Gaussian distribution.

Unless you know from observation that a process doesn't follow a
  Gaussian distribution (e.g., Poisson, binomial, etc.), then it
  probably does at least well enough for statistical purposes.

I won't fault kmm for this statement because what they said is what happens prevalently. This is practically what all biologists do, but this is an incorrect approach.
Gaussian should not be considered a default distribution. This may lead to incorrect inferences. Usually the experimenter has an idea of what kind of data they are measuring and what distribution is the data likely to follow. If you are unsure of the underlying distribution then you should go for non-parametric statistical tests.

What kind of data follow Gaussian distribution?
According to the Central Limit Theorem, the distribution of the mean (expected value) or sum of several samples of independent and identically distributed (IID) random variables would follow Gaussian distribution. The random variable itself can follow any distribution but if you measure the mean several times using repeated experimentation, then the distribution of the mean would be Gaussian.
From the Wolfram site:

Let $X_1,X_2,...,X_N$ be a set of N independent random variates and
  each $X_i$ have an arbitrary probability distribution $P(x_1,...,x_N)$
  with mean $\mu_i$ and a finite variance $\sigma_i^2$. Then the normal
  form variate:
$$X_{norm}=\frac{\displaystyle\sum_{i=1}^N x_i-\sum_{i=1}^N \mu_i}{\sqrt{\displaystyle\sum_{i=1}^N \sigma_i^2}}$$
has a limiting cumulative distribution function which approaches a
  normal distribution.

The wikipedia page on CLT is also quite good. You can have a look at it too.
Usually in biological experiments we measure some property, lets say expression of some gene. When you do several replicates, and there is no specific underlying mechanism that would generate variation (i.e. the errors are purely random), then you would get normally distributed values. Note that this applies only for the sample means. In certain cases, we assume that the variation in the value of a variable is because of some random fluctuation and therefore consider these variables to be normally distributed (not their means but the values themselves); for e.g. the weights of mice which are fed and raised equally. This is just your assumption which constitutes the null hypothesis.
Another point to note is that the variable that is expected to follow normal distribution should essentially be continuous in nature. Some discrete variables can be approximated as continuous but one should have a good reasoning of doing so. For example population sizes, though discrete, can be assumed continuous if the sizes are large.

Poisson distribution is unique and is a discrete distribution. Certain kinds of phenomena result in Poisson distributed RVs. These phenomena should basically be Poisson processes. See this post for details. Poisson distribution basically models the probability of N events in a given time interval for some given rate of events ($\lambda$). This rate is also called the intensity of the distribution.

Binomial is another unique discrete distribution. Genotypes resulting because of Mendelian segregation of genes, for example, follow this distribution. It basically models the probability of N number of events in some M trials. In binomial distribution there are only two possible outcomes. Multinomial distribution is a generalization of binomial distribution with multiple outcomes.

Since both Poisson and Binomial are discrete distributions they should not be confused with normal distribution. However, under certain conditions especially when the number of trials in Binomial distribution is high and binomial probability = 0.5 then it can be approximated as a gaussian with same value of moments. Similarly, if the intensity (rate) of Poisson distribution is high or the time interval is large, the distribution of the Poisson RV can be approximated to Gaussian (with same value of moments). In these cases, the value of the mean goes up significantly, thereby allowing a continuous approximation.
Many datasets show power-law like/skewed normal distributions and people often make the mistake of assuming them to be normal. An example (from my experience) is the expression of all the genes in a cell. Very few genes have high expression and many genes have low expression. This also applies for degree distribution of nodes in some real networks such as gene regulatory network.

In summary you should assume Gaussian distribution when:

Variable is a measurement of a value which is repeated several times from identical samples
Variability is expected to be random in the control case (in t-test, when you reject null hypothesis you are actually saying that a certain variable does not follow the normal distribution assumed under the null hypothesis)
Variable is continuous, or discrete with large sample size

You raise two issues, both of which might be better suited for stats.SE, but I think the questions are suitably biological to warrant an answer here.
Do most biological processes follow a Gaussian distribution?
Unless you know from observation that a process doesn't follow a Gaussian distribution (e.g., Poisson, binomial, etc.), then it probably does at least well enough for statistical purposes. While ~10 observations isn't enough to test the distribution accurately (and those tests are pretty flawed anyway), as long as the values are approximately normally distributed, then you probably meet the assumptions of most general linear model-type statistical test (t-test, ANOVA, linear regression). These tests are fairly robust to deviations from normality, so in a sense, as long as the values are close enough to normal, the test is fine (which says nothing about the interpretation of the results).
Is the pervasive use of p values warranted? Is there problem with small sample sizes?
Although certainly not the first to raise the alarm about p values, Ioannidis's (2005) paper sounded most loudly. The central idea is that, in science, there is a strong tendency to only publish "significant" (but whatever definition of significance you use) results. Thus the literature is rife with false significant results. For example, if only 1 in 20 experiments yield significant results, the other 19 are not likely to be published. Yet those 5% might represent 95% of the literature, and thus we have a strong bias in the literature. All of those "significant" results can't possibly be correct.
Statistical inference from small sample sizes are also quite problematic (e.g., in neuroscience; Button et al., 2013). There has been a recent push toward including effect sizes for estimated parameters and simply reporting confidence intervals (which will be suitably wide for small sample sizes).
Many of the failings of statistics are summarized in Statistics Done Wrong: The woefully complete guide, which I don't have any affiliation with except that I enjoyed reading it.
The paper you link is pretty deficient in what you might call modern statistical analysis. What they could improve:

Run (and show the results of) an a priori power analysis to establish that their sample sizes are adequate
Include effect sizes of the estimated parameters
Include confidence intervals for estimated parameters
Use one of the many available multiple comparisons procedures to control familywise type I error rates.

It's incumbent on reviewers of papers to ask for these things if the authors do no supply them willingly.
There is no way around the small sample size in many studies, so it's possible that there isn't much they could do to change the sample size. Those who work with humans or animals are under pressure to keep sample sizes as small as possible while maintaining adequate power. However, they could show that what they have is sufficiently powerful.
Button, K. S., J. P. A. Ioannidis, C. Mokrysz, B. A. Nosek, J. Flint, E. S. J. Robinson, and M. R. Munafò. 2013. Power failure: why small sample size undermines the reliability of neuroscience. Nature Reviews Neuroscience 14:1–12.
Ioannidis, J. P. A. 2005. Why most published research findings are false. PLoS Medicine 2:e124.

I really don't agree with the first part of your answer, "Unless you know from observation that a process doesn't follow a Gaussian distribution ... then it probably does".  The burden of proof should be the other way around: unless you can clearly motivate why your data should be normal distributed, you should concede that it might not be, and use a nonparametric method.

You are right to be suspicious. I would contend that, in most situations, hypothesis tests based on the normal distribution are not appropriate. If hypothesis testing is needed, a permutation test should almost always be used.
As WYSIWYG points out, there is no reason to assume a measurement is normal distributed without strong a priori knowledge. The central limit theorem is the standard argument for assuming that the mean is approximately normal distributed, but I would say that it is not very helpful in practise, because the convergence can be very slow: if your data distribution is far from normal, you need a large number of samples for the mean to be approximately normal. How many? Impossible to tell, since we don't know the data distribution! So in practise, the approximation can be very bad, and then the test will be completely off. This applies not only for the t-test, but for many parametric tests that rely on the normal approximation, such as chi-square tests.
Fortunately, there are better tools nowadays. The permutation test does not require the normal distribution assumption; the results are always valid, regardless of the data distribution. It is easy to carry out with today's computers, and simple to understand. This is a good book on permutation tests (and other resampling methods).
Ronald Fischer and his contemporaries that developed the normal theory in the early 1900's were perfectly aware that permutation test was a much better solution, but it requires extensive calculations, which was simply not possible back then. So the normal test was developed as a poor man's approximation to the exact permutation test. But today, we have no need for this approximation anymore, as our powerful computers can perform even large permutation tests in the blink of an eye.
Then why do people stick to the approximate normal tests still? Sadly, I think they are routinely used only because most biologists know of no other tools, and simply follow tradition. A historical reason behind the normal assumption in biology is a classic argument by Fischer, concerning population genetics: if a phenotype is affected by a large number of genes, and their effects are additive, then the phenotype variable is a sum of many random variables, and by the central limit theorem it should be approximately normal. The classic example is height, which is indeed closely normal distributed in the population. But this reasoning applies to genetics of natural populations, not laboratory experiments.
Then there is the whole debate about whether hypothesis testing (and p-values in particular) should be used at all, regardless of which test you use. Other answers touched upon this. I won't go into it, but it is a very important topic, and I would recommend this excellent article from Nature, and references therein.
http://www.nature.com/news/scientific-method-statistical-errors-1.14700f

The willingness to publish only significant results has a second consequence to add to bias on publications. Since power of parametric tests is usually larger than power of equivalent non parametric tests, often results are significant only if parametric tests are used - usually needing to assume a Gaussian distribution. Therefore, researchers willing to publish are highly incentived to assume normality.

Can you please justify shortly the benefit of permutation tests? What do you want to answer with them? How can they help to identify the possible distributions in biological data?

Permutations tests are commonly used to test difference in mean / median / etc between two sample groups. They require only very mild assumptions (e.g. independent sample) and are applicable to virtually all data distributions.  Estimating the actual underlying distribution is not necessary (and rarely feasible).

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What happens when we eat excess fat?
The fats in our body are stored in fat cells. When we over eat fats does the size of our fat cells increase, are more fat cells generated, or do we "throw out" excess fat?

This is a really broad question, are you interested in fat storage? Fat metabolism? Lipocite creation and apoptosis? Fat apsortion?

The question is about fat cycle versus sugar cycle. Doing a research about low fat diets versus high fat diets

The number of fat cells, or adipocytes, in adult bodies remains constant. Therefore, consuming more fat only increases the size of the fat cells not the number. After reaching the age of about 20 years the average number of fat cells is closely related to body mass index.
On the other hand, the adipocytes in children increase in number as more fat is consumed. This explains why people who became fat as children have a harder time shifting their weight as adults.
A study on obese adults who went through surgery to decrease the amount of food intake showed a reduction in their body weight by 18%. While the average size of the fat cells decreased, the number of fat cells remained the same.
This doesn't mean that the same fat cells are active throughout your lifetime. Adipocytes normally die off and are replaced by new cells. One study shows that fat obtained from liposuction of people who were exposed to radioactive materials from atomic bombs in the Cold War showed a decrease in radioactive material stored in the cells which indicates replenishment of fat cells over the years.
So when adults intake excess fat, their fat cells increase in size. The average number of their fat cells is correlated with body mass index. However, when children eat excess fats they exhibit an increase in the number of fat cells.
For more information see: http://www.nature.com/news/2008/080505/full/news.2008.800.html

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How and why are cells irradiated in human-rodent hybrid cell biology?
When human-rodent hybrids are made the amount of human chromosome in the hybrid can be reduced by irradiation. Why and how exactly is this irradiation step performed?

"Why and how exactly is it performed?" Are you specifically asking about irradiation?

Im asking chiefly why it is done

And the principle behind it

I've made an edit that tries to specify that a bit better.

Human cells are irradiated with X rays (to fragment the DNA) and then fused with rodent cells. This is useful for mapping because closely linked markers are more likely to appear in the same hybrid: there is a lower probability of radiation induced breakage between the markers because they are close together.


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Is it possible there were multiple origins of life? And, if so, why did the one which became the common ancestor between all organisms prevail?
I have learned that all currently-living organisms come from a common ancestor, which I theoretically understand. However, my professor in a class mentioned that there is a chance that there were multiple origins of life, but that all the creatures living today all came from the same one and the others died. How can we be sure that before the other origins of life died, they didn't somewhat evolve, and the species from that origin didn't just evolve in convergence with those of this one since through natural selection both would need similar characteristics to survive on Earth?

That is an interesting idea. Are you sure that your professor was saying that all life today descends from several ancestral cells, or that ancestral life was eradicated many times before our ancestral cell came into being?

Closely related: http://biology.stackexchange.com/questions/14175/why-did-abiogenesis-only-happen-once

It is interesting that all forms of life use the same genetic code. The nucleotides composing DNA and RNA are universal. Eric Lander, geneticist from Harvard/MIT cites this as evidence for evolution from a single ancestor. I think your instructor may be saying that it's possible alternative adaptations for initiation of life may have occured and perhaps not worked out. They become just another of nature's experiments that ended in extinction. I seem to recall reading somewhere all but 2% of species have ended in extinction.

I believe that the answer to this question would be that we cannot tell for certain that there were multiple origins of life.
In order to determine that there were multiple origins of life, we would almost certainly need to look into the molecular biology side of these organisms, since convergent evolution makes it extremely likely that these differently originated organisms would be very close to each other in outward appearance. However, the basic molecular machinery would have much less of such selection pressures, allowing them to be maintained.
However, this would be impossible if the organisms have already gone extinct, as fossilisation generally does not preserve the structures of the proteins and DNA (or equivalent information storage molecules) that are used by the variant organisms.
If such an animal was alive, however, it would then be possible to determine the animals' variant origins by detecting a specific biochemical trait that they alone possess. For example, an animal which used D-amino acids for its proteins would certainly be determined to have originated from a different common ancestor.


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There are 6 classifications of CFTR mutations. Is a causal relationship to the sweat test known?
Cystic fibrosis (CF) is caused by mutations in the gene for the protein cystic fibrosis transmembrane conductance regulator (CFTR).
The CFTR mutations are classified in 6 classes.
The sweat test is used to screen for CF. With the following boundaries:

<= 29 mmol/L = CF is very unlikely
30 – 59 mmol/L = intermediate possibility
=> 60 mmol/L = CF is likely

Can I make assumptions from the sweat test in which category a patient may belong? Or can I even make assumptions about a specific mutation?

The results of the sweat test are due related to the total abundance of functional CFTR protein in the plasma membrane, so different classes of mutation that similarly reduce the total amount of functional CFTR would have similar sweat test results.


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Do RBCs need oxygen?
How do our red blood cells (RBCs) get oxygen? Do they even need it? They have no nucleus and no organelles, so I think they don't need it.

Their cytoplasm contains hemoglobin, a protein that carries oxygen. Here is a quote from wikipedia :https://en.wikipedia.org/wiki/Red_blood_cell                                  ..................   " Erythrocytes consist mainly of hemoglobin, a complex metalloprotein containing heme groups whose iron atoms temporarily bind to oxygen molecules (O2) in the lungs or gills and release them throughout the body. "............

the energy for RBC is from glycolysis, so I think they don't need oxygen. At least, for the energy they used.

Erythrocyte metabolism is unique in that the mature erythrocyte
  contains no mitochondria and therefore no Krebs cycle! Instead the
  energy needs of the RBC are met largely (95%) by anaerobic glycolysis
  in the two pathways: Embden-Meyerhof + Hexose-monophosphate.

+

Virginia University source

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method for DNA extraction for human mucus(nose) or earwax?
What is a simple method for extracting human DNA from nose mucus or earwax?
I tried googling for methods for DNA extraction for human nose mucus or earwax and couldn't find any. I assumed that if one can extract DNA from hair, which has few cells with non intact nucleus'  then the same could be done with earwax, which also has few cells or mucus? The simpler the method, the better, given I am an undergrad with low experience.

i dunno xD but how much in mass of "material" you have. You can purify  DNA from raw leaves from the plants for example, so I guess if you are able to homogeneize your sample and provided you have 1)the equipment and reagents necesary (isopropanol, ethanol, sterile water a centrifuge) and 2) there is simply enought DNA material in the sample to begin with you could give it a shot. Anyway I completely dont know, i d try it if google hasnt said otherwise i guess.. anyway SE i summon you

@Katz            I could wager i could collect the samples from my own nose and ear. And i do have access to those materials. So are you stating that a tradition extraction method for something like spit or hair would be suitable?

why do you want to do this btw xD

Just curious if I can do it as a side project, since I will have access to human primers for PCR and possibly have leftovers.

try oral mucosa as DNA source then, i am totally convinced that you should get routine protocols online to do that with PCR as a goal.

@Katz           I have a protocol for spit, id rather get something specifically for "boogers" and "earwax".

why? the DNA is the same so it wont matter to do PCR. anyway if it is a must, i guess as i said you can try with the classical DNa estraction method and see

Let us continue this discussion in chat.

im sorry just saw it, anyway im kinda busy and cant really. but anyway i dont have anymore to say i guess, just try it if you feel so and see what happens. good luck!


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The heart of a Pigmy Shrew beats 1300 per minute then why is it so fast?
A pygmy shrew is such a small animal. Even with such fast heart beats their average life span is 1.5 years. So can we consider faster heartbeats to not be good for health?

Edit: I think for rodents in general, a short life span is preferable, since they are more along the lines of an "r-selected species". https://en.wikipedia.org/wiki/R/K_selection_theory#r-selection

I think that if the the heart beats faster then it brokes down very easily. So, a medium heart beat is related with a medium life and etc.

There is a correlation between the heartbeat and the life expectancy as you can see below.

(source: medcan.com)
This relationship is not linear (the y-axis is on a logarithmic scale) and is negative, that is, the faster is the heart beat, the lower is the life expectancy. You'll note the outlier (human) that has a life expectancy that is twice as high as you wold expect from the regression. This shift toward the right is caused by medicine, food quality and hygiene.
Correltation vs causation
Note that correlation doesn't imply causation. Typically, you'll notice from reading the species names on the first graph that species that have a fast heartbeat (and therefore a low life expectancy) are small in size.Allometry  is the study of the relationship of body size to shape, anatomy, physiology and behaviour. You might want to have a look at the wiki page.

can we consider faster heartbeat is not good for health?

No! it is wrong to think from from those data that the shrew (that has low life expectancy and fast heartbeat) that if they were to have a slower heartbeat, they would live longer. This is wrong. Shrews have the heartbeat they need to have. If one shrew (due to a mutation or some environmental developmental effect) had a slower heartbeat, it would die very early.
In other words, such inter/species correlation doesn't tell anything about intra-species correlation. To reuse the example of the relationship between mass and life expectancy: Body mass and life expectancy are positively correlated among species (see above) but the mass at which life expectancy is maximized in humans is average. The below graphs shows the relationship between body mass and Relative Risk (RR) of coronary heart disease.

(source: revespcardiol.org)
Health ≠ life expectancy ≠ adaptation
Life expectancy, health and high fitness (biological sense) are three concepts that are eventually related but that are very different. While life expectancy can compare health in inter-species comparison, it makes little sense to compare health of different species. Note also, that natural selection may well favour short lifespan (as suggested by @RioSiv, you might want to have a look at life-history r/K selection theory).

Where are you getting the figures that the livespan of a dog is greater than 25 years? I wish this was the case, but it is unfortunately more along the lines of 10 to 12 years with larger breeds being shorter.

Sorry... missed the part about r/K... Deleted the other comment.

@AMR hum.... good point. Looking at the two figures, there seem indeed to have some weird values for life expectancy. They may consider the world records as averages very much depend on conditions/country. I don't know. The pictures were found on Google Image (there are tons of such graphs with the same crazy values for the dog). I am at home now, I don't have access to the peer-reviewed articles.

Can any one help me with my another question about lips ?

You should NOT use comments to attract attention to other posts. I know nothing about human physiology and can't help you with your lips question. If you want to increase your chances to get an answer you can try to motivate people with a bounty but you'll have to wait 2 days after the question has been asked to be allowed to use a bounty (more info here).


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Online Database for PPG (Photoplethysmography) signals (both Infrared and Red light readings)
I am looking for an online Database for PPG (Photoplethysmography) signals for SPO2 (oximetry) analysis. I have tried several sources but they only have single datasets labelled "PLETH" and not individual IR (Infrared) and Red Signals. Please help me find such database or let me know any workaround for this.

It may be me, but I don't understand all these acronyms.

I edited to question

Thanks! I'll not pretend knowing the answer, but at least I know it's about measuring oxygen :) I retracted my close vote.


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How do birds avoid mid-air collision?
Across from me there is a large flick of Pigeons and Ravens that like to nest on the roof. They swoop and dive and fly all over. Sometimes the whole flock lifts off at once. My question is, how do they avoid running into each other? Certainly they can't see every bird around them, can they?

I think, the reason would be the same as, when flocks of birds like starlings, etc. do not run into each other while making patterns. They can un-group and regroup with complete harmony. So, maybe the concept behaves the same with different types of birds as well. Or, maybe they have some kind of natural radio wave signaling due to which they are capable of preventing flying into each other.

They can't see all the birds that are around them as some are hidden behind the others. However, I don't think there is anything so extraordinary; they watch around, have good reflexes and can change direction very abruptly. There is no need for some kind of special sensing abilities to explain bird flocks.
3 simple rules
One can simulate a flock of birds with 3 simples rules:

Adapt your speed on the speed of the other agents

$$\overrightarrow v_{i,1} = \frac{1}{K_L}\sum_j^K\overrightarrow v_j (t) - \overrightarrow v_i(t)$$
, where $K_L$ is the number of birds in the Large area of perception, $\overrightarrow v_j (t)$ is the speed of a given bird in the large area of perception and $\overrightarrow v_i (t)$ is the speed of the focal individual.

Attraction

$$\overrightarrow v_{i,2} = \frac{1}{K_L}\sum_j^K\overrightarrow p_j (t) - \overrightarrow p_i(t)$$
, where $\overrightarrow p_i(t)$ and $\overrightarrow p_j(t)$ are the positions of the focal bird and of a bird present in the large area of perceptio, respectively.

Repulsion

$$\overrightarrow v_{i,3} = -\frac{1}{K_s}\sum_j^K\overrightarrow p_j (t) - \overrightarrow p_i(t)$$
, where $K_s$ is the number of birds present in the Small area of perception.
Then, to update the speed of the birds you just sum up those 3 contributions:
$$\overrightarrow v_i(t+1) =  \overrightarrow v_i(t) + \overrightarrow v_{i,1} + \overrightarrow v_{i,2} + \overrightarrow v_{i,3}$$
see boids for more information.
My point in descrbing this algorithm is that you can get the emergent behaviour of a bird flock out of very simple rules.
Bird Collision
If birds don't often collide each others (what I assume but honestly I don't know much), note that it is estimated that 100 millions birds that die every year after colliding a window (see here). Birds also collide with power lines (ref) and wind turbines (ref).

When they are flying together as a flock, they anticipate the flock's behavior and react accordingly. earthsky.org/earth/how-do-flocking-birds-move-in-unison
And when they are just flying around, but not in a flock, the concept is the same as how we humans don't collide into each other when we are walking. Although birds fly faster, they also see farther
(eagles and other birds of prey can see four to five times farther than the average human can), which means that they have a longer distance to react.

But how about when they fly together? They're really close as they fly.

When they are flying together as a flock, they anticipate the flock's behavior and react accordingly. http://earthsky.org/earth/how-do-flocking-birds-move-in-unison

@YvonneLiew I think the flying together part answers the question better, you should edit your answer to include that citation.

Schooling and flocking behavior is actually very interesting stuff. The real answer- many of the things mentioned already (speed of processing, good reflexes) but there's still much to be found out. Computer analysis is helping enormously, and also helping to create robot flocks. Here's an article of scientists finding out more. Unfortunately, that article's from 2009, but I also read about it in "Complexity: a guided tour". Anyone have something more updated?
some neat flocking robots- there are many other similar projects lately

Sitting in stadium full of thousands of people looking around we notice that just about everyone is in our line of sight.  Flocks of birds also always seem to follow a pattern involving maintaining this global line of sight.  Even as the flock is flying straight ahead, changing direction, taking off or landing the the individual birds seem to move and adjust the pattern to maintain this line of sight to the maximum possible.  The seem to follow this logic even while on the ground pecking grain.

Can you add some references to this claim?


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Can mutation rate be increased for instance by mutagenesis targeting the DNA polymerase?
I am studying a non-cultivable bacterium living in an insect host, and I would like to generate some random mutants of this bacteria while preserving the insect.
I am wondering if one way to do so might be to use directed mutagenesis directed towards the bacterial polymerase, which would leads it to increase the error rate.

Does any one has already seen a study with this kind of approach?
Does any one knows or guess another way to obtain some random mutants of the bacteria while preserving the host insect?


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Can flow cytometric analysis differentiate between a parent contributing longer chromosomes versus multiple smaller chromosomes?
For flowering plants, can flow cytometry of seed from muti-generational interaction of two species and their offspring help us decide if wide differences in genome size for the two species and their offspring is a function of differences in chromosome count versus chromosome length?
Flow cytometry of seed allows us to examine the contributions by the 2 parents to the resulting offspring from generation to generation.
The basic premise is flow cytometry scores for the offspring of "triploid" intermediates would distribute differently if the issue was length versus count. Fine distribution would indicate "aneuploids" because of counts whereas wide distribution would indicate length because length differences are concentrated in only a few chromosomes.
This basic premise proved faulty since flow cytometry scores indicate fine distribution (genome size scores reflecting every potential aneuploid between triploid and tetraploid) but documented chromosome counts indicate the issue is length.
What are the normal distribution patterns in terms of genome size for multigenerational offspring between 2 species having wide differences in chromosome length?
.

This is not a homework assignment. This question is motivated by actual flow cytometry results from a large number of samples for a large group of closely related Rhododendron species. I have been unable to find any good information on how the barriers to species interaction differ when the issue is chromosome number versus chromosome length. If there are straight forward textbook answers to this question, I would love to be guided to resources that provide insight to the answer.

I would recommend that you mention the flow cytometry protocol that you used (PI staining??). You need not elaborate on how you ruled out endoreplication. Just a short summary is enough. Focus on your main question.

@WYSIWYG How can a question be off topic as a homework question when I have not taken a biology course since freshman year high school 1966? I do not know this biology forum well enough to say this question is not off topic but this is not a homework question and the question is motivated by actual flow cytometry findings for Rhododendrons on 2 different continents.

Please see our homework policy. Homework does not just mean homework in a course. For any problem, research or otherwise, the OP should show some effort towards the answer. I see that you have edited to add your effort but your question is too long and is difficult to read. Please retain only relevant sections and then this post can be reopened.

@WYSIWYG  Have focused attention to the basic premise of why I incorrectly thought flow cytometry could address the question of length versus count. Appreciate your efforts to refine this question to address the question of what is wrong with that basic premise,


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How did the double circulatory system evolve from the single circulatory system
I already learned how the mammal circulatory system (double circulatory system) evolved from the reptilian circulatory system. How did natural selection evolve the reptilian circulatory system and the amphibian circulatory from the fish circulatory system (single circulatory system)? Did the reptilian circulatory system evolve from the amphibian circulatory system? If so, how? http://www.shmoop.com/animal-movement/animal-circulation.html shows what the fish, reptilian, and mammal circulatory system look like and https://universe-review.ca/I10-82-circulatory.jpg shows what the amphibian circulatory system looks like.


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Staining cells for FACS at 4 degrees or ambient temperature
I'm sorting a 293 derived line. One thing that is worrisome for me is cell viability after the sort. Usually I have been staining and washing at room temperature (on the benchtop) on a nutator. I have been reading that most sorting procedures indicate that you should be doing this at four degrees in the dark. It is my understanding that this helps with clumping, but is this at the expense of viability? Does the cold cause these cells to apoptose?
Currently my procedure is the following -
Using HBSS + 1 mM EDTA + 1% BSA (sort buffer) I suspend approx 10-15 million cells per/mL.

Stain with primary
Spin at 300 x g for 5 minutes
Add 15mL of sort buffer, spin again
Stain with secondary in 1 mL of sort buffer
Wash x2 with 15mL
Strain
Sort

One thing I can do to minimize cell death is do a live/dead stain (we just added that capability). The other thing I read was to use 50% FBS in your collection tube.
The other thing that might be of concern is that if we are doing many sorts, then some of the tubes may be sitting in sorting buffer for a long time in the queue. How long is too long?
Lastly, we use puromycin and blasticidin as selection markers for our libraries and we usually add these right to the sort after we replate. Should we wait a while?
Thanks for the advice

Low temperature will arrest all cellular processes. The cell will not undergo apoptosis or division, or carry out any other metabolic process. What are you staining the cells with?

You have several questions, please try to limit your posts to one question each. That being said, I'll try to address each of your concerns.

Does the cold cause these cells to apoptose?

No. The purpose of staining at 4°C and washing with cold buffer is twofold - to maintain viability (all cellular processes slow down at lower temps) and to prevent receptor internalization. This second point is especially critical as you're using a primary and conjugated secondary, which I really wouldn't recommend for sorting unless absolutely necessary, for example if the antibody you're using isn't available in a directly-conjugated format.

One thing I can do to minimize cell death is do a live/dead stain (we just added that capability).

Live/dead stains are generally a good idea, but make sure the stain you're using isn't cytotoxic. L/D should always be the last staining step before running your samples. A better way (if your sorter supports it) is to use forward scatter (FSC) and side scatter (SSC) height and area measurements to discriminate single, appropriately-sized cells, then gate on them first before gating on your antibody stain (FITC or PE or whatever your secondary is).

The other thing I read was to use 50% FBS in your collection tube.

I'm not sure how much that will help, especially 293s, which are pretty tough. Just make sure you're diluting the collected cells enough in medium to bring the serum percentage back down to 10%.

if we are doing many sorts, then some of the tubes may be sitting in sorting buffer for a long time in the queue. How long is too long?

As long as your samples are kept in the dark on ice or at 4°C, they should be fine for several hours at least (I wouldn't go overnight, though). Also, make sure your collection medium is chilled, as it can shock the cells to go from 4° to 37° too rapidly. Collect your sample, plate it, then put it at room temp or in the incubator (depending on your workflow) and let it warm up that way.

Lastly, we use puromycin and blasticidin as selection markers for our libraries and we usually add these right to the sort after we replate. Should we wait a while?

Nah, don't worry about it. You can wait if you want, or add it right away - I would lean towards adding it more quickly than not, so you don't give unwanted cells any chance of growing out.


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hummingbird feeders - is sugar water healthy for them?
The top results on google for DIY hummingbird feeder suggest a white-sugar solution for the feed.  In humans we make a big deal about processed sugar vs. the sugar you get from, say, eating a piece of fruit.  Does this matter for hummingbirds?  Their metabolisms so high, it makes me wonder if this is relevant.  Maybe it is not!  But I would like to know.

It is likely especially the lack of nutrients in sugar water that is present in honey that will be deleterious. Just like feeding ducks bread impacts health negatively, because there's nothing of use in there for them.

You should only use white sugar. Anything else (honey, brown sugar etc) can harm them. Hummingbirds get their nutrition from bugs. Lots and lots of bugs.

@AliceD I think a more accurate statement would be "no trace chemicals", since the carbohydrates in both foods are extremely useful to animals.

@Pungh0li0 The first half of the statement is unsupported, and the second half is patently false (hummingbirds subsist on nectar, not insects).

Here's a relevant study showing (Anna's) hummingbirds lost weight but had no behavioral changes eating nothing but sugar water for 10 days. Obviously in the wild hummingbirds will have access to much more than just your hummingbird feeder. I'm sure it also varies with species. http://www.sciencedirect.com/science/article/pii/0300962992906435

@CactusWoman Is 10 days long enough?

@MarchHo I thought that hummingbirds only ate nectar too, but a quick google search informed me that insects are part of their diet too.

@GoodGravy Thanks for the correction and TIL.

Hummingbirds absolutely eat insects, and HONEY and BROWN SUGAR are a huge NO NO.
  The following is a statement from: http://wildbirdsonline.com/index.html

Every year, as more studies are completed, we learn more about
  hummingbird life and diets. However, we find that some people think
  that hummers can survive on nectar alone. Nectar provides quick energy
  to sustain their extremely high metabolic rate and little else. This
  is important enough that the shape of the bills of hummers have
  evolved in partnership with the flower shapes that they frequent.
  Consequentially, there is a wide variety of hummingbird bill lengths
  and shapes among the more than 300 species that exist.
There is another critical food source for the hummers. Essential
  vitamins, minerals, amino acids, proteins, oils and fats, fiber, etc.
  all come from the insects they eagerly consume, not the nectar. Their
  preferred insects include, but are not limited to: small beetles, true
  bugs, weevils, flies, gnats, mosquitoes, aphids, mites, leafhoppers,
  flying ants, and parasitic wasps. Their favorite insect food source is
  the spider and harvestmen (daddy long legs). Some ornithologists
  estimate that spiders are between 60% and 80% of their diet.

But there are lots of other resources for you to find accurate information about feeding hummingbirds.

Hummingbirds eat nectar, which is a high sugar solution. You're assuming that they'll eat sugar water instead of insects.I would assume the sugar water feeders act as a substitute for nectar, and the humming birds will prey on insects all the same.  Is there any evidence for this either way?

Also, why is brown sugar such a big no-no (genuinely interested, not rhetorical)?


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Meaning of 'forms of free energy'?
I was doing a practice exam paper and it asked for different 'forms of free energy'. I am a physicist rather then a biologist so 'free energy' to me means Gibb's Free Energy:
$$G=H-TS$$
But I cannot see how you would could have different forms of this. So is my interoperation of 'free energy' right and how can we have different forms of it?

Can you provide the exact context i.e. the complete question in the practice paper?

@WYSIWYG it was a biophysics paper and it simply said 'Give the main forms of free energy', which I guess is not very helpful, but the question came with no context apart from this.

AFAIK, there are two types of free energy: Gibbs free energy and Helmholtz free energy (A=U-TS). However, Helmholtz free energy is almost never used in biophysics or biochemistry. Energy minimization principle in biochemistry always assumes constant temperature and pressure of the closed system.   HFE is used when pressure can change. The other two thermodynamic potentials are Internal Energy and Enthalpy. Anyway, without the context it would be difficult to answer this question.


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Why can humans feel electricity?
What evolutionary process has provided humans with the ability of feeling electric current? Besides lightning and electric eel, what natural hazards include electricity that poses a threat to humans?

Electrical currents stimulate neurons aspecifically. For example, the BrainPort artificial vision device conveys visual information through electrical stimulation of mechanoreceptors in the tongue. Similarly, cochlear implants and retinal implants convey acoustic and visual information through electrical stimulation of the inner ear and retina, respectively. The list goes on. Bottom line is, none of these organs (tongue, ear or eye) evolved to process electrical stimuli. And in fact, there are no specific current or voltage sensors in man. Electric currents aspecifically stimulate neurons, causing them to fire. When sensory afferents are activated in this way, sensory perceptions are generated.
In case of lightning (electrical shock to the skin) it is mainly pain and heat receptors that mediate the sensation. In the case of the BrainPort, it is the tactile receptors on the tongue that are mainly stimulated (taste perceptions are rare). In case of cochlear implants it is auditory nerve fibers and in retinal implants it is optic nerve fibers that are stimulated. Hence, various, and in fact all, neurons can be stimulated by electric current.
Note that sharks feature Ampullae of Lorenzini. These sensory organs are electroreceptors, which allow sharks to sense the bio-electrical fields of prey under water.

Electricity directly stimulate neurons. You have to understand that neurons basically work via electric currents , which occur due to a difference in membrane charge. So when you give electricity to a neuron, you basically give electrons to the extracellular membrane, which makes it much more negative compared to the intracellular or the stuff that is inside the membrane. This offsets the concentration gradient that kept the careful balance until now, and then neuron fires. Anyway, i hope you got that. Note that you can't directly "feel" electricity, or electrostatic force. That is impossible, nature has not given us the mechanism to do so. What you feel is a direct consequence of electricity interfering with the functioning of your muscles and nerves.

Electricity is essential in order to control and coordinate neurons and skeletal muscles activities. You should imagine a neuron as a very complicated logic port of an electronic circuit, that receives information through its dendrits from other neuronal cells and then integrate this information in its body. If the spatial and temporal summation of inhibiting and stimulating signals is overthreshold, then at level of the first part of the axon, there is the creation of the all-or-null response of the neuronal cell: the action potential. In general, there is the simultaneous activation of the voltage-gated sodium channels that elicit spikes spreading them along the whole axon that is connected to other neuronal dendrits or skeletal muscle cells. These ones, receive and integrate in the same manner the stimuli sent to them. As you can easily imagine, external electric stimuli, like electrostimulators or instrument used by neurologist to analyze neuronal and muscle activities in diagnostic tasks are able to alterate the natural electric potential present across the cell membranes of these excitable cell types and response to this  electric field. Indeed, cells possess and actively keep an electric potential among the two sides of the phospholipidic bilayer of the cell membrane of about -70mV. This one is due to the asimmetric distribution of ionic species (sodium, potassium and chloride mainly) sustained using chemical energy obtained from exogenous sources. Thus, in general, our cells are not able to feel electricity directly but every phenomena, either phisical or chemical, able to alterate the electrical equilibium (homeostasis) of the cell membranes induce a response at inner cellular level leading, for example, to neuronal cell response or skeletal muscle contraction. You can think to the use of defibrilator to treat cardiac arithmias that send to the hearth strong current pulse-wave, that in case of fibrillation or ventricular tachycardia is frequently capable to restore normal cardiac activity and save life. Also pacemaker acts in a similar manner. Some pathologies like ALS, Alzheimer's, Parkinson, Myotonia involve also alteration of this electric mechanism leading to modified capacity of the cells to handle and interpret these electric message. In electrophysiology research, external stimulation of cells by electrodes (see patch clamp technique) is used to test the effect of drugs to treat these pathologic conditions.
Finally, I can say that evolution didn't give us the ability to feel electricity, instead it has been adapted as a cellular-level instrument handled by cells to communicate and integrate (or store in brain) stimuli and information.


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Function and Mechanism of Height Genes
I have an inquiry regarding the exact function of height genes.
To my knowledge, although they are heavily regulated by epigenetic factors, height genes can have either an "on" or an "off" allele, and the probability of the person being "tall" shows positive correlation with the number of "on" height genes alleles he has.
However, I could not find any resources showing the exact function or mechanism of these genes' function. Do these genes code for a specific protein when they are "on"? And if there are any, how do these proteins increase the probability of the person being "tall"?
Thank you.

Can you link to the sources that postulate "on/off" genes or to what some of those genes might be? That would help potential answerers follow the paper trail to the function of those genes.

There is no such thing as "height genes". There are, however, genes that have a quantitative effect on height, such as SHOX which interacts with bone development. Others have a dominant effect, like EGF3, which causes achondroplasia when it is mutated. However, the expression of genes that control growth is highly regulated by environment and epigenetic factors. It would really help if you linked some kind of source, or some group of genes.


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Why are potassium channels slower than sodium channels?
I am relatively new in the subject of biology. I have a strong mathematical background and in order to get into the field of computational neuroscience, I am trying to get some biological background.
I am reading about the general mechanism of action potentials in neurons.
I understand that an action potential starts with a fast entrance of sodium into the postsynaptic cell. Since the potassium channels are slower than the sodium channels, potassium starts flowing out of the cell only around the peak of the action potential, thereby hyperpolarizing the cell's membrane potential.
What is the mechanism that causes the potassium channels to activate slower than the sodium channels? Does it involve differences in the behavior of the suitable neurotransmitters? Because I didn't manage to find transmitters or couples of transmitters and receptors which activate potassium channels, but not sodium channels (or sodium channels and not potassium channels).

Slower can mean two things: slower conduction or slower response.

Just a correction: the action potential does not begin with the entrance of sodium into the postsynaptic cell. This ionic flow changes the overall voltage potential of the cell, and the action potential begins at the axon hillock or just adjacent to the axon hillock, where the sum of all such inputs may start the depolarization known as the action potential.

You have to understand how the integral proteins work. $Na^+$ channels are fast while $K^+$ channels are slow and long lasting in terms of conductance. $Na^+$ channels are voltage gated, via the S4 domain which is blocked by $Mg^{2+}$, while $K^+$ conductance is not voltage gated most of the time.

Short answer
The activation kinetics of Na+ channels are faster than K+ channels.
Background
Voltage-dependent channel gating basically occurs through three possible states of the channel: open, closed and inactivated (Fig. 1).

Fig. 1. Gating of a voltage-activated sodium channel. Source: Balseiro Institute.
Basically, ion channels are protein pores in the membrane. Upon depolarization, the pore opens, which is a process with fast kinetics in Na+ channels and slower kinetics in K+ channels (Lacroix et al, 2013). K+ channel activation is in the order of 6 times slower than Na+ channel activation. The slower inactivation of K+ channels allows sufficient Na+ to flow in the cell for the depolarization phase of the action potential to develop (Fig. 2).

Fig. 2. Action potentials and underlying Na+ and K+ currents. Source: Dundee Med Student Notes.
After opening, the channel is inactivated, which can occurs through a physical "protein-plug" as shown in Fig. 1, or through conformational changes in the pore. This inactivation again is fast in Na+ channels leading to a transient spike in the action potential, and deactivation is slower for K+ channels (K+ channels do not inactivate, but rather deactivate). This inactivation step results in the refractory period of a neuron (silent period after firing). The channel is then de-inactivated and converted to the closed state, after which the channel is again ready to participate in another round of firing.
Note that neurotransmitters do not activate voltage-gated channels directly. Neurotransmitters can activate ion channels, but those are ligand-gated ion channels, such as the nicotinergic acetylcholine receptor, AMPA receptor or NMDA receptor (Purves et al., 2001).
References
- Lacroix et al, Neuron (2013); 79(4): 651-7
- Purves et al., Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates (2001)

What would be the difference between an "inactivated" and a "deactivated" channel?


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Is disease transmisson through milk consumption or meat consumption considered direct or indirect transmission route?
From an epidemiological point of view, is consumption of raw milk or meat considered as indirect or direct transmission ? Let's take the example of bovine TB. Is consumption of unpasteurized milk considered as direct or indirect ? IMO since milk is a tissue (liquid tissue but still), it is part of the cow, then how could you go more direct than eating the infected animal ?

Direct transmission is through direct contact with the infected person with no intermediary or vector. The Ebola virus and AIDs virus are examples. Indirect would be malaria spread through mosquitos, plague via rats, etc. The common cold spread through droplets in the air could seem indirect, but because of the proximity required, the CDC website lists it under direct. The CDC will provide reliable information for a lot of questions regarding infectious disease.


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Can a stationary eye with a moving pupil exist?
I am making a sci-fi web-comic set on an alien world and I thought up an idea for an eye that works much like an eye from a mammal, but instead of moving the whole eye, only the pupil moves. This idea sprouted from the eyes of mantis, though their moving pupil is possible because of their compound eyes, I would like to know if my idea could be physically possible. (And yes I know this is a strange question compared to others on this site).

Although this is an interesting question, it doesn't look like it can be answered without being opinion-based. Perhaps this fits better on Worldbuilding.

what do you mean with "physically possible"?

What I mean is can there be a structure capable of this function.

Also, thanks for the forum recommendation I'm new to these and your help is much appreciated.

Mmmm.... You wish to know whether theoretically an eye could exist that features a moving pupil? Everything is possible, right? I think this question is too theoretical and will give rise to primarily opinion-based answers. I vote to close.

@Jesse There is a Stack Exchange forum where questions such as yours are not only welcome, they are actively discussed. It is Worldbuilding SE. You should join that SE and post this question there. It is populated with creatives who are trying out ideas as well as trying to find out how scientifically accurate their ideas are. There is also a Science Fiction & Fantasy SE where this question would likely generate a discussion, but I would try Worldbuilding SE first.

@Jesse also think of the function of an eye and the pupil. The pupil is an aperture that regulates the amount of light that is allowed to enter and project onto a photo sensitive surface, it the eye's case the retina. The retina is tuned mostly in the center of the rear curve of the eyeball. Moving the pupil would change the plane of the projected image and would be reflected on a different spot on the eyeball with likely a certain amount of diffraction as the lens is still set to focus on the rear of the eye...

... Now if your alien life forms evolved to see white light when their pupil was centered but then had other focal planes that allowed them to see more sensitively in the infrared spectrum or with another positioning and ultraviolet spectrum, then maybe a shifting pupil would be an interesting device to harness this ability. It could be analogous to night vision goggles only built into their eyes, where they can shift their pupils to see under different conditions.


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How octopus develops its imitation skill?
I've watched one documentary about a Mimic octopus which they can imitate another animals in several form e.g. a Lion fish, a Sea snake, a Flatfish, etc. My question is how these octopuses can have these such skills? Imagine that they can not see themselves via a mirror but their imitation is so perfect.
What is a theory behind this?

well other animals do imitation and sometimes cant see themselves, the wikipedia describes two types of mimicry that it exhibits: https://en.wikipedia.org/wiki/Batesian_mimicry  and  https://en.wikipedia.org/wiki/Aggressive_mimicry

There are even theories that some squid and octopuses have monochromatic vision, yet have the ability to change colour. Go figure!

I am confused about the use of the tag evolution in your question. Are you interested in the physiology of mimicry in octopuses or about the evolution of the mimicry?


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Are genes on the 5' to 3' strand only?
I confused myself during studying, and wanted to confirm something. Since transcription via RNA polymerases only takes place in the 5'to 3' direction, that would mean that that 5' to 3' strand is the only one that contains the information to be translated later into a protein or mRNA or w/e.
So then the 3' to 5' strand would NOT contain any genes, but just the base pair complement to them? Or am I thinking of the concept of a gene wrong?

There is nothing called the 3' to 5' strand. Both strands are have the same polarity but the DNA helix is anti-parallel. Both the strands contain approximately equal number of genes. Sometimes the transcription from both the strands can overlap, leading to production of antisense-transcripts.
So RNA polymerase will read the other strand from its 3' to 5'.

Both strands have a 5' and 3' end. Some genes will be on one strand and some on the other. The coding sequence will always be 5' to 3', but RNA polymerase reads the template 3' to 5' to polymerize mRNA.

So then since RNA poly reads 3' to 5', both strands can be parent strands depending on whenever RNA poly stops?

depends on the gene, the location of polII interacting elements and the location of specific transcription terminator sequences. There is usually just one parent strand per gene, but bidirectional transcription is known of http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2576438/


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

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

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

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

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

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

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

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

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

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

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

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

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

bald balding baldness.

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


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Differential gene expression analysis between species
I have RNA Seq data from mouse and human skin ( 2 replicates each) and want to compare the expression of the orthologous genes to find any which are differentially expressed.
I have quantile normalized the gene expression matrix across all 4 samples (2 mouse + 2 human). I eventually want to calculate the log fold change in expression of all orthologous genes between the 2 species. However before I do this, I should control for gene length, right? Will this be enough to give me an idea of the differentially expressed genes or should I be employing more sophisticated methods?
Any comments would be helpful. Thanks a lot.

This might be better suited at [stats.se].

It depends on what type of data you have, really. There are methods developed solely for quantifying relative expression based on count data, such as using edgeR or limma-voom.
You don't need to correct for gene length to estimate fold-changes of relative expression, what you need to do is normalise by library size first (and in the process obtain log2 ((counts + 0.5)/1e+06) and then, following quantile normalisation, you can just calculate mouse - human or human - mouse to give you an estimate of fold change.
I still would recommend using something a bit more sophisticated like limma-voom for this task, though, because that also will enable you to get stuff like false-discovery rates for your fold changes.

I have count data. However the reason I am hesitant in using packages like edgeR or DESeq2 is because they are meant for comparing expression of same gene between 2 conditions. I on the other hand want to compare the expression of orthologous genes (diff genes with diff lengths) between 2 species.  Also if I am doing quantile normalization (i.e. imposing the same distribution on all samples), do I still need to control for library size?

Yes it is the norm to control for library size and then quantile normalise - you always need to control the number of counts for how many reads were sequenced per sample.
Orthologs with different lengths should be fine - I mean, in any case limma-voom for instance estimates gene level differential expression without consideration of isoforms (which have different lengths). Orthologues can technically be regarded as variants of the same genes so maybe give it a go.

Thanks for your answer. But the fact that limma ( & other count based methods) does not account for diff transcripts is a limitation (e.g: if gene A transcript 1 has 20 reads in condition A & gene A transcript 2 has 20 reads in condition B, it will not find transcript 1&2 as differentially expressed...whereas depending on the gene this can be biologically relevant.) this is why I am hesitant to use these methods for my analysis.

You are going to run into similar problems anyway if you are comparing orthologues by fold changes alone - the only way to get round this is to derive exon specific counts,  in which case limma has a diffsplice function to check for differential splicing.
or you could use RSEM to estimate counts for comparable isoforms in your organisms and then instead of gene counts use isoform counts.


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Why does all life use the same macromolecules in their genetic code?
There is no biochemical constraint of any sort, so why doesn't some other code work? Why is it specifically RNA/DNA?

possible duplicate of Why did abiogenesis only happen once?

You are asking two relatively different questions in your post. I'd suggest to restrict your post to only one (and expand on it).

I don't think it is a duplicate of "Why did abiogenesis only happen once?". The question above might be reformulated as: "Why hasn't any lineage evolve to use a different genetic code than the ancestor (or than the other lineages)".

"If it ain't broke don't fix it?" If there were organisms that used other genetic codes then it would seem they are now extinct; species that used this code had the most progeny surviving to reproduce. New, random mutations that modify some aspect of the translational apparatus, and that would yield a slightly different code, are presumably lethal.

There is an interesting biochemical question underlying this question: "Why are nucleic acids better than other polymers for our genetic code?" That's what I've answered anyway!

@GoodGravy "Why are nucleic acids better than other polymers for our genetic code?" There is no answer to it.. There can be many different polymers that can be equally good or even better. Good also is a very subjective term.

@WYSIWYG I try to address why RNA might have been originally preferred in my answer. I'll expand on that though. The main thing is that you're limited to abundant polymers, and of those RNA was preferable for early forms of life for some reason.

Preamble
Any answer regarding the origins of our biochemical evolutionary origin will be reasonably speculative given that this is a very hard question to scientifically test and this field is generally understudied to say it is pretty much the most fundamental biochemical question. But there are a few reasons why RNA makes sense as the prime genetic molecule compared to other established macromolecules present in the primordial soup, and also there are good reasons why DNA superseded it as genetic storage for most cellular organisms.
In summary, the alternative abundant polymer macromolecules that came from the primordial soup aren't as versatile as RNA, and over time DNA was used more over RNA due to it being a more reliable information storage molecule.
We must remember though that the conditions that lead to the genesis of RNA is a much tougher question. There are an unfathomable amount of combinations of chemicals that could have facilitated an evolutionary process. @WYSIWYG made an excellent comment regarding why this is an almost impossible question to answer definitively:

...Why is there a phosphodiester backbone used rather than
ether, amide, carboxyl ester or any other kind of linkage? Or why
purines and pyrimidines, why not naphthalene ring heterocycles? Why
imidazole, why not oxazole or furan? You cannot reason this out in a
reverse manner.

Therefor in this answer we will be discussing RNA and other bio-polymers that were established in abundance from the very early primordial soup, not the original genesis of such biochemicals. What made each of them good vessels for an evolutionary process?
A genetic code macromolecule needs the following features:

Stable.
Variable structure.
Expandable.
Replicable.

RNA has all these and doesn't rely on a biological system for reproduction of the RNA molecule.
RNA world.
Let's not forget that DNA is probably not the first one along and there was an RNA world before the cell as we know it. Even today many viruses particularly make use of ssRNA.
RNA was a good molecule because it was a polymer made of 4 base monomers that could bind with other polymers to make any array of compositions of the base components and was spontaneously replicable. This allowed a primordial form of molecular evolution as we know it today. It is able to carry more varied information than other abundant macromolecule polymers.
RNA can also carry out functions in a similar way a protein might, including catalysis. No known sugars or other macromolecules are able to demonstrate the same level of variability and versatility as RNA, although deoxyribosymes have been artificially designed in laboratories.
This probably gave it a good chance at establishing itself as the first molecule to trigger biogenesis, and this lead to nucleic acids being established as the fundamental molecule of molecular evolution.

DNA chemical structure.
Eventually RNA evolved into more complex structures and DNA broadly superseded RNA as a storage device for genetic information in cellular organisms primarily due to the increased stability DNA offers over RNA. If we take a look at DNA specifically we see a very good data storage mechanism for a couple of reasons.

Intra-strand hydrogen bonding and different chemically structured sugar group makes a more stable overall structure.
More rigid grooves allow proteins to bind at particular sites.
Again, it's a polymer of variable composition.

Alternative coding macromolecules.
What are our other options from the biological polymers?

Carbohydrates. The glycocalyx coats most cells in our body, and clearly sugars (specifically polysaccharides and glycoproteins) are an expandable, information rich molecule. However it relies on proteins for assembly in the same way proteins do, so it never really got the chance to be that prime molecule.
Lipids. A brilliant expandable polymer, and many are spontaneously expanding in the right conditions, but generally lipids cannot carry as much "information" in the polymer (pretty much just varying lengths of CH2 groups).
Proteins. Too complex and not spontaneously replicable. They rely on other systems for production (except in some rare examples, although they arguably still rely on a complex biological system).

There can be infinite comparisons. Why take only lipids and proteins for comparison. I can ask why phosphodiester bond as a backbone and not ether, amide, carboxyl ester or any other kind of linkage. Or why purines and pyrimidines, why not naphthalene ring heterocycles. Why imidazole, why not oxazole or furan.. You cannot reason this out in a reverse manner.

@WYSIWYG excellent point. I think we are talking about different things though, and my answer isn't clear enough. You're talking about the genesis of the primordial soup, I'm describing how RNA was a better vessel for evolution given other established bio molecules. I will edit later to tidy up this point.

One of the things that you left off of your list as to why DNA is more stable is the 2'-hydroxyl of ribose is reactive and can induce strand breaks where the 2'-hydride of deoxyribose is not a center of reactivity. RNA degrades more rapidly than DNA simply because of the chemical structure of the sugar it is made from.

The interesting thing about evolution is that Mother Nature does not go back to the drawing board and start with a completely new design. Evolutionary changes happen in tiny increments. Faced with a problem like the appearance of oxygen in the atmosphere, evolution did not redo the whole genetic structure of plants. It tinkers. So we ended up with a wasteful and inefficient system. But it works.This kid does the most wonderful humorous video explaining this. Just google Rubisco tubes.

That is an evidence that all the creatures share a same ancestor from evolution.
About the origin of the genetic code, scientists proposed some hypotheses to explain it.

Chemical principles: From the experiments, scientists found that some amino acid have a selective affinity to certain triplet codons.
Biosynthetic expansion: The original creatures may produce amino acids as by-products of metabolism, and then some of these function into the genetic coding. Evidences show that fewer different amino acids were used in the past than today.
Natural selection: The goal of the genetic coding is to minimize the mutation. Some scientists assume that ancient life may have longer codon than triplet codon, such as quadruplet codon, but quadruplet codon have more error that triplet codon, and then only the triplet codon can survive.
Information channel:  This hypothesis suppose that the process of genetic code translation is an error-prone information channel. The organisms wanted to inherent their genetic information accurately and efficiently and stay away from the genetic noise. Genetic code should be influenced by three evolutionary force: the needs for diverse amino acids, for error tolerance and for minimal cost of resource. Finally, the genetic coding amino acids become nonrandom.

I'm not sure how this answers the question of DNA and RNA being used to carry our genetic information. You're describing general theories about ribosomal translation. I think point 4 might be on point, but even in that point I don't quite understand what you are getting at entirely.


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Do birds emit infra-red radiation?
I'm an electronics engineering student and I am going to use a sensor that detects infra-red emitted by birds that invade rice paddies.
Do birds emit infra-red radiation?

Anyone here can correct me, but I think that all living organisms emit infrared, since all organisms undergo metabolism (respiration? converting food to energy? what's the correct term?) which releases heat, and hence infrared radiation.

Some birds emit more infra-red radiation than others so it's worth bearing that in mind and testing sensitivity (likely involving field study - sit and compare what the sensor detects to what a good bird spotter detects). I saw a documentary a while back where they showed ptarmigans through thermal imaging cameras, they were barely visible, I tried to find an image but couldn't. Obviously where there are rice paddies its unlikely that birds will be quite as well insulated though... It's  not just a problem of do they produce heat, but also how well they retain it

Short answer
Birds emit infrared.
Background
Objects with a temperature higher than the background emit detectable infrared (IR). Endothermic (warmblooded) animals keep their body temperatures at around 37oC and given the relatively cool temperatures at the earth's surface, endotherms generally emit more IR than the background. Endothermic animals include the mammals and birds, but also some fish.

Infrared image of a hummingbird. Source: Nature Conservancy.
Note that dinosaurs were probably not ectothermic (coldblooded), but they are believed to have been mesotheroms, that is somewhere in-between ecto- and endothermic (Grady et al., 2014).
Also note your IR recordings will benefit from lower temperatures and reduced light-pollution from the sun, hence your recordings will be better at night than during daytime.
Reference
- Grady et al., Science (2014); 344(6189): 1268-72

Nice Answer. You all but told them they probably would want to use a beam and sensor, sort of like the ones that automatically keep an elevator door from closing when the beam is broken than trying to detect the thermal signature of the birds themselves. They would likely be too fast and too small to register on an infrared sensor, especially considering rice paddies are often associated with hot climates.

@AMR - Thanks for the appreciation and also thanks for an interesting add from an engineering perspective. I think IR sensors come in various flavors. For example, hyperspectral cameras can be able to resolve quite some detail, but I am not sure about how fast they are.

Technically, all objects emit infrared, not just those "with a temperature higher than the background". It's true however, that to photograph such an object with any sort of contrast, one would need the temperature to be higher.

@nbubis thanks for that. I corrected my answer.

I would expect all animals, and possibly all living things, to emit infrared as metabolic reactions tend to be exothermic, even if the animal is ectothermic.  The question is that if the difference between the animal and its environment is enough for you to be able to actually detect it.

Dinosaurs is a very broad term which includes both the ancestors of birds as well as modern reptiles. But that analogy stretches as far to say that a bird is a modern dinosaur and a reptile is a modern dinosaur but a bird is not a reptile. Both of their ancestors lived during the cretaceous period and tend to get lumped together.
Another analogy would be that dolphins, bats, and humans are all modern-day mammals. But a dolphin does not fly and humans do not live underwater, etc.
Modern-day birds descended from a group of dinosaurs called theropods which were warm-blooded dinosaurs.
See here for more information:
http://www.abc.net.au/science/articles/2010/11/23/3073903.htm
To be specific to your question, if it is an endotherm then it will emit some level of infrared radiation, as this is their primary means of avoiding overheating.
Interestingly, some birds are actually warmer than humans at 102-112F:
http://animals.mom.me/signs-parakeet-cockatiel-birds-cold-8448.html

Minor nit - dinosaurs are typically not construed broadly enough to encompass the ancestors of any modern non-avian reptiles. The closest modern reptile to the dinosaurs (and birds) are believed to be the crocodilians, but the non-dinosaur pterosaurs branch between crocodillians and dinosaurs/birds on the evolutionary tree, meaning crocodiles - or any other reptile - aren't descended from anything which would count as a true "dinosaur" to a modern paleontologist.

In current technical usage by people who study these things, birds are dinosaurs. Classics usage now becomes "non-avien dinosaurs".  Reptiles are not dinosaurs.  Reptiles are not a mono-clade and don't follow "always will be" rule.

Every object hotter than 0K emits infrared radiation. Many object absorb and reflect, re emission infrared radiation (usually lower frequency). For detect bird need some difference with background object's infrared radiation, like different intensity, spectral, phase. One person above show use intensity (at night ground/trees become cool emit less radiation than birds). If need find birds during day, and ground hot, birds appear darker than ground.
Can also use multiple infrared sensors together detect different frequency (like visible light, infrared light have frequency range) different object have different infrared color. Also, if rice paddies have water, reflected infrared light is polarized but reflection from bird is random, maybe can use this help find bird when they fly. I think sky UV and visible light also is polarized (bee use it for navigation), I guess infrared light from sky is polarized too.

Typically an animal must be 2.7°C warmer than its surrounding environment, to trigger a detection.
Are you talking about herons that hunt frogs or small birds that forage seeds?
The distance of an animal from the camera’s PIR sensor and its body mass, varies the magnitude of infrared radiation, which affects the ability of the PIR to trigger an image.
So PIR triggers perform well for large and medium sized mammals, but do not reliably detect ectotherms (reptiles, amphibians, and invertebrates) or smaller mammals.
I'm drinking a beer while i write this so I can answer well, and by unabashed plagiarism: here is a complete review of some PIR technologies, which is biased towards their 3mm laser sensor called HALT: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5628828/
Personally i'd say forget about complex electronics for this project! just take a slow exposure image every seconds and pass the image stack through pixel processing code to search for bird sized dots and lines.
Birds in paddies should be easy to detect, because they come down from the sky which has a light background and they move at relatively high speed. So a computer can easily recognize the trails against the sky and classify them by size. You can therefore use a very cheap time lapse camera trap which takes 1000ds of pictures a day, at a cost of perhaps 1 gygabites per day, and do comprehensive statistics on bird movement around the paddy fields. Infra red? home made? i'd say forget about it, image recognition digital signal processing is more thorough.
here are some pics from here

Recently I programmed image stacks, and it was very much fun because it was 2d and 3d graphs. to sequence through an image file is 12 lines in U3D. To loop through the pixels is another 12 lines, so all you have to do is write conditions. to save relevant images to another area. That said, you have 1 minute exposure images all day, you will have 600 images a day to sort through manually.


text:
What are the differences and similarities between fimbriae and adhesins in microbes adherence factor?
Adherence factors in microbes is to attach to a host cell or to an extracellular matrix.
So what is the difference and similarities between fimbriae and adhesins?

Fimbrae is a catch all term to denote the hairlike projections on many gram-negative and some gram-positive bacteria, but exludes flagella. Adhesins are a subtype of fimbrae that serve as organs of attachment to cells or mucosal surfaces. Another type of fimbrae are pili, functioning in conjugation, the transfer of DNA from one bacterial cell to another  (Koneman, I can't even find the year on this crazy book. Used to be the bible of determinitive bacteriology. So many hours.)


text:
How long is saliva viable?
Does anyone know if saliva can stay viable for about 5 days, before it gets suspended into a DNA genealogy vial for testing?
Background: My brother wants to do a DNA genealogy test at a US testing facility. The country he lives in doesn't allow it, however. For some reason FedEx has no problem with shipping his saliva to me in the U.S. The fastest they can do is 4 days. Will it still be viable to test? Or will it have gone bad somehow? He wants to ship it tomorrow.

Saliva buffer usualy provides stability at RT for month or even years. Genotyping companies like 23&me use collection kits like Norgen's (https://norgenbiotek.com/product/saliva-dna-collection-preservation-and-isolation-kit) which allows to store the sample up to 5 years.
So my advice would be: get the spitting vial at your place, send it as regular mail to your brother, and then ask him to send it back to you once filled with saliva. By doing so you won't have to worry about temperature.
Sending fresh saliva should be ok if your brother sends it refrigerated (4°C). I keep fresh cells up to at least one week in the fridge in proper medium, and saliva is a pretty decent buffer and has some antimicrobial properties.


text:
Why perform imputation?
Genetics datasets contain measurements for millions of single nucleotide polymorphisms (SNPs). Some (usually small) percentage of these values are of low confidence, and are labeled as missing values. It is common to impute these missing values using statistical relationships within the high-confidence samples as well as relationships mined from public datasets. This makes sense, to get an estimate of what that small percentage of missing data likely is in reality.
Sometimes, analyses are performed that impute up to a much larger number of SNPs - for example, a genotyping platform might measure 2.5 million SNPs, but imputation is performed to get a larger sample of 6 million SNPs. My question is, what value do the extra SNPs that were never even measured have from an analysis point of view? When performing feature selection or predictive analysis, it would seem that the imputed SNPs are really just encoding statistical relationships that are present in the dataset to begin with. What does it mean to find a highly associated or predictive SNP in the imputed set?

In GWAS we are interested in understanding which SNP has a causal influence on a specific phenotype. At the moment large scale studies are carried out by genotyping arrays. For each SNP we put on the array, we measure the alleles present in the patient.
The cost of genotyping obviously depends on how many SNPs we would like to measure. So the problem when designing a genotyping array boils down to: What SNPs do we put on such an array so that we get most information out of it.
To answer that question it is important to realize that SNP alleles are not independent. SNPs that lie in the same haploblock are highly correlated. So measuring one of these SNPs is often sufficient to predict the alleles of other SNPs that are in so called linkage disequilibrium. When designing a genotyping array, we probably do not want to measure all of those highly correlated SNPs, because we gain very little information. Instead may want to measure just few of them and then impute (predict) the alleles of the correlated ones from population study data.
So back to the GWAS analysis. From the SNPs on the designed genotyping array we now predict SNPs that are associated with the phenotype. Say after our statistical analysis we found an associated SNP. But from the design of our array we know that there may be highly correlated SNPs that we did not measure. All of them will also be statistically associated. If we do not impute, we may come to the wrong conclusion that we already found the true causal SNP. In fact, there may be many and finding the correct is often very difficult.

To add to the other answer, an additional reason is that there are different genotyping microarray platforms (chips) with non-overlapping and different numbers of SNPs. In order to make sense of data from multiple chips, or to run GWAS on a dataset with multiple chips, you would want to impute. Otherwise, the sets of variants you are looking at are different.


text:
Are multi-chain proteins synthesized as one biological unit?
Are multi-chain proteins (especially homo/hetero-dimers) synthesized together as one overall unit or are they separate monomers which bind together at some point after synthesis, and are there any relevant factors to know about this process?

Big broad question. Each protein is slightly to greatly different. Generally they are individually folded and brought together by chaperones or proximity.

The question is fine in my opinion.

Are multi-chain proteins synthesized as one biological unit?

Sometimes yes but mostly not.

Some proteins are synthesized as one long polypeptide pre-protein which is cleaved by some proteases to yield multiple chains. After cleavage the intramolecular interactions become inter-molecular or inter-chain interactions. Insulin is a good example of this (See the figure below).

In other cases the chains are synthesized as different polypeptides which (with or without processing) subsequently associate with each other. In case of homo-multimeric proteins, the polypeptides are made by the same mRNA.

Nice answer from WYS. I would have been inclined to say that the ribosome translates one polypeptide and any associations happen post translation. Insulin is interesting in that one polypeptide is produced and then cleaved to form components of the protein so that one could say multiple parts are made at the same time if I understand this correctly. Generally the complexities of a protein are introduced after the ribosome has done its job of translation to form one string of amino acids. Protein interactions are a matter of great interest now. I'm not sure one can say any protein is formed independently but is more part of a large ochestra.


text:
What would happen if most the fat in your body was rapidly converted into energy in 2 minutes?
It all started out as an argument I had with my friend.He said that "it would be the equivalent of catching a fire and burning"
But all I thought would happen is that you would now be very hyper because you have a lot of energy in you body.
Please scientific answers only.
I also happen to be in the 11th grade and I dont do bio, but I knew this would be the best place to post the question.Please dont use scientific concepts I would not understand.
You guys are probably going to ask me to give an example of a way through which it might happen. So here is one way I have come up with:
Lets say the AMPK protein malfunctions and causes all the cells to release all this energy.

I would love to read an "xkcd what if" answer to that question

It depends, but you're going to die.
Specifically, it depends on how fat you are. Even Andreas Munzer is going to die. At only 3% body fat, burning all his fat (9kcal/g) would "only" increase his internal body temperature by 270 degrees C. Factoring in the energy required to boil off his body moisture and adding in body heat leaves Andreas at  ~200 C or so (pretty unevenly distributed) minus whatever heat he could give off through his skin in two minutes. He's definitely dead, but probably not on fire. The flash point of animal fat oil is about 300 C, so most of his body probably isn't going to be hot enough to burn on its own. There will probably be some smoking, though.
The average body fat percentage is more like 22%(for males), and the numbers there are unequivocal. That person is going to catch on fire, as their body temperature is going to go up about ~1800 C after boiling off all the water. That's enough to melt your titanium hip implants.
In short: you'll die pretty quickly, and then you might catch on fire before your two minutes are up, unless you're Andreas Munzer or another professional bodybuilder.


text:
What is the "leaky valve" between the esophagus and stomach?
When someone talks about there being a "leaky valve" between the esophagus and the stomach, what is the exact biological structure they are talking about?
This would be a structure that, when malfunctioning, causes stomach acid to leak into the esophagus.

The structure is called the lower esophageal sphincter:

Basically, its function is to prevent the contents of the stomach, including stomach acid, from "backwashing" into the esophagus. The stomach is protected from acid by a protective layer of mucus, while the esophagus is not, so any number of medical issues which cause problems with this sphincter may lead to erosion in the esophagus, which is quite painful and can lead to serious long-term consequences if not addressed.