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Epistasis Involving Multiple Loci
The following problem is from Schaum's Outlines on Genetics, 5th edition, by Elrod and Stansfield.  I'm having some trouble solving it.  It is found under a section entitled "Interactions with Three or More Factors" in the problems at the end of the chapter on Epistasis.

Problem 4.30 (pg. 112):  If a pure-white onion strain is crossed to a pure-yellow strain, the
  F$_2$ ratio is 12 white : 3 red : 1 yellow.  If another pure-white
  onion is crossed to a pure-red onion, the F$_2$ ratio is 9 red : 3
  yellow : 4 white.  (a)  What percentage of the white F$_2$ from the
  second mating would be homozygous for the yellow allele?  (b)  If the
  white F$_2$ (homozygous for the yellow allele) of part (a) is crossed
  to the pure-white parent of the first mating mentioned at the
  beginning of this problem, determine the F$_1$ and F$_2$ phenotypic
  expectations.

In the first crossing, it looks like the type of interaction is one of dominant epistasis between two loci.  So, we could call the alleles for the first locus W and w and the alleles for the second locus A and a.  Then W-A- and W-aa would have a white phenotype, wwA- would have a red phenotype, and wwaa would have a yellow phenotype.  This would be consistent with the ratios provided in the problem.
In order to explain the 9 red : 3 yellow : 4 white, a third locus can be considered with alleles B and b.  Proceeding as above, where we had the locus for W or w epistatic with respect to the locus for A and a, we could have the same locus for W or w epistatic with respect to the locus for B and b.  This time, wwB- and wwbb would be white, W-B- would be red, and W-bb would be yellow.  This would be consistent with the 9 red : 3 yellow : 4 white ratio.
This is where I get stuck.  If the locus for W and w is epistatic in a dominant way with respect to one locus and in a recessive way with respect to another locus, then all onions would be white.  Therefore, I must have done something wrong.  Am I on the right track?
This isn't really a homework problem, despite the "homework" tag.
Here are the answers provided in the text for the problem:

Problem 4.30 (pg. 115):  (a) 25% (b) F$_1$: all white; F$_2$ : 52
  white : 9 red : 3 yellow

Is it necessary to have atleast one common loci for the two crosses? I fail to see that mentioned in the question.

@SatwikPasani: I've added the answers in the text for the problem to the original question (I apologize, it would have been better to do this when the question was first posted).

After reading Satwik Pasani's comment to the original problem, I tried using the hypostatic locus as the common locus in the epistatic relationships, instead of the locus causing the onions to be white.  The following solution fits the answers supplied in the book.
Three loci can be used to determine the colors of the onion, the alleles of which can be denoted by C, D, and E.  Suppose that C and D are each epistatic to E, such that the phontypes of the onion are given as:
cc---- white
--D--- white
C-ddE- red
C-ddee yellow

Then the first crossing in the problem can be given by CCDDEE x CCddee.  The second crossing could be ccddee x CCddEE.


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What exactly are "floaters"?
i was reading this artical after hearing about it on the news, while reading i saw the term "floaters" which made me remember of a recent Family Guy Episode in which there is a joke about them in Peter's vision.
I am wondering, what exactly are they? what is their technical term? and is it possible to remove them permanently (apart from the obvious gouging out your eyes).

When I move my eyeballs around, I see some very faint dark curvy lines(resembling blood vessels) move about with my eyeballs. Those are floaters. I'm not sure if everyone can see them.

Every question regarding floaters that you have asked is answered on the wikipedia page: http://en.wikipedia.org/wiki/Floater

source: Stack Exchange

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sort: votes


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Valid comparison of gene expression between several genes in several cell lines
We have gene expression data (Affimetrix mRNA gene expression results) for several cell lines, over a set of genes.  Our goal would be to be able to compare relative gene expression for genes over the different cell lines.
The method we have thought of so far involves calculating some sort of gene-based average (the expression of a particular gene over all the lines) and normalizing our expression data, grouped per gene, based on that.  However, we are not sure that this is a valid method for obtaining relative expression data from our data set, especially so that we can compare the data from several lines.
Does this seem like a valid strategy?  How is this normalization commonly done?  Should we do something differently to get a better comparison?
Thanks so much!

Perhaps a formal statistical test like ANOVA would be applicable.

This is not an easy task, as there are many factors which you have to take in account. First there are intra-essay differences as slightly different conditions for each set of probes for the repetitions. Then, there are inter-assay differences, as differences in the array slides and so on, this paper ("Analysis of microarray gene expression data") goes into more details.
This articles might be helpful as well:

Multiple-laboratory comparison of microarray platforms
Increasing consistency of disease biomarker prediction across
datasets.
The curse of normalization.
Microarray probe expression measures, data normalization and
statistical validation.

What you could also do is go over the Researchgate, I think there are more people around with a lot of experience in this field.

Thanks a lot.  These are all great tips!  I'll look into the articles and probably head over to Researchgate.

If your data came from a single lab and a standard protocol gcrma normalisation is a good method to use (and comes with the affy R package); if the arrays are of U133A or HGU133plus2 types frozen RMA may be a good method to use. Finally you can check for and control for batch effects using ComBat and use the corrected expression data.

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Is there an antagonistic association between Penicillium and Aspergillus?
Some Aspergillus species appear to like walnuts. My question concerns the association of Penicillium and Aspergillus. No sooner does Aspergillus colonize a walnut (or some other challenging carbon source) than Penicillium seems to move in, eventually killing the Aspergillus colony.
A totally unscientific guess is that Aspergillus is a good colonizer and Penicillium a good opportunist and that this is a common pattern with these two species. Is there any science in this direction? I do recall a sort of well-known picture from an old text in which Penicillium is shown more or less strangling a species of Aspergillus. I didn't think about it much at the time.
The image attached is not very incriminating but the theme is the same. Penicillium are the green hand-like structures strewn about the clover-like Aspergillus. Foot-cell of the latter cropped.
This seems like a simple question but a quick search doesn't reveal a lot, I think in part because this would generally come up as a contamination issue.

It is hard to find any articles on the association between Penicillium and Aspergillus species, although they are both considered two of the most common mold species found indoors.

In this study, the most prevalent spore types detected in both the indoor and outdoor air samples were generally from the Penicillium/Aspergillus group [...] these ﬁndings are qualitatively similar to those observed in other geographical locations, conﬁrming the ubiquitous nature of these fungi.

Although these genera seem to be found commonly, it also has to do with environmental factors, and the relative humidity of the area as well.

Geographical location, climate, and short-term meteorological
  conditions are responsible for outdoor types and levels of fungal
  spores.

As for the association and apparently colonization/opportunistic behaviour of the genera, it seems like there are not any associations between the two, unless perhaps environmental conditions are subject to changing, and different mold species have different moisture/temperature thresholds, although again these mold groups tend to be generalists and do well at a wider range of environmental conditions than other fungi.

A laboratory procedure was developed in which viable peanut seeds were wounded and inoculated with field soil containing natural populations of fungi, then incubated under different conditions of seed water activity and temperature. [...] A. parasiticus colonized peanut seeds at lower temperatures than A. flavus, and cool soil temperatures relative to temperatures of aerial crop fruits might explain why A. parasiticus is found mostly in peanuts.
Other fungi, dominated by the genera Penicillium, Fusarium and Clonostachys, colonized seeds primarily at water activities and temperatures suboptimal for section Flavi species and A. niger.
Eupenicillium ochrosalmoneum frequently sporulated on the conidial heads of section Flavi species and showed specificity for these fungi. The inoculation of wounded viable peanut seeds with soil containing natural populations of fungi provides a model system for studying the infection process, the interactions among fungi and those factors important in aflatoxin formation.

Any associations with different fungi species and their different structures, including, for example, with the conidial heads of Aspergillus seem to be currently under study:

The genus Penicillium comprises species that mostly colonize plant matter. However early reports suggest that several species are capable of parasitizing Aspergillus and sporulating on the conidial heads of the host. More recently Eupenicillium ochrosalmoneum and E. cinnamopurpureum, [...] have been observed sporulating on the heads of Aspergillus species belonging to section Flavi during the colonization of peanut seeds.

Little is known about the host specificity underlying these Aspergillus-Penicillium associations. [...] all species spread across Aspergillus colonies by means of aerial hyphae that grew from head to head. Additional studies are required to clarify whether Eupenicillium and Penicillium species are parasitic or simply epibiotic on their hosts.

+1 This is informative, especially the last. Will wait a while before accepting because it is always risky to assert a negative--the articles you cite appear to support your position.

A year after the fact I found a short passage in Thom and Raper's 1945 text, Manual of the Aspergilli. At page 59 the authors relate that Aspergillus niger colonies are commonly overrun with Penicillium rugulosum which "winds its hyphae within and about the conidiophores, and fruits in a radiating series of short-stalked penicilli surrounding the heads and upper halves of the conidiophores." There is a photo illustrating this on p. 60.

authors: Мирослава Бодь


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What's the worst that can happen from eating too many spicy peppers? Can you die?
Some peppers, such as the habanero or Carolina reaper are extremely spicy, and when eaten in larger amounts than one is accustomed to, can cause some discomfort.
I've also heard anecdotes claiming that pepper spray, if applied with sufficient intensity, can cause death.
What if you were to eat as many spicy peppers as possible, despite the noxious taste? Is it possible to commit suicide in this way (and what would the cause of death)? Would you faint from excessive mouth pain? Would uncontrollable vomiting prevent you from consuming further peppers?

You can die from eating too much of just about anything so the question in the title is pretty meaningless.

@DavidRicherby Right, but at the same time, "can you die from eating too much cyanide?" is not a meaningless question (though perhaps strangely worded).

"die" or "wish you were dead"?

This is more anecdotal than an answer, but I live near a place called Munchies 420 in Sarasota, FL. The guy from "Man vs. Food" failed to eat the "Fire In Your Hole" wings.  One man so far actually did die from trying to complete the challenge. He was resuscitated in the parking lot.  Now that I read your question again, I'm going to make this an answre

The more "dangerous" properties of spicy peppers are chiefly due to capsaicin.
Sigma-Aldrich sells purified capsaicin, for which they provide safety information, including an MSDS. Most of it is the usual, unsurprising set of warnings about irritation to eyes and the respiratory system. However, there are LD50 numbers:

LD50 Oral - rat - male - 161.2 mg/kg
LD50 Oral - rat - female - 148.1 mg/kg
LD50 Dermal - mouse - >512 mg/kg

From this, we can conclude that one would have to eat quite a bit of capsaicin to die. If lethality in humans is exactly the same as rat (which it probably isn't),  a 70 kg human would need to consume about 11 g of capsaicin to reach similar levels of lethality.
The Carolina Reaper, one of the hottest known peppers, averages about 1.6 million on the Scoville scale. Capsaicin amount is related to Scoville heat units, so we can make an imprecise conversion from one to the other.
Using values given in 2 publications (Nwokem 2010 and Al Othman 2011) we can observe the following trend:

So on average, about $6.25 \cdot 10^{-5}$ mg/g capsaicin per SHU. With this, we get $(1.6 \cdot 10^5) \cdot (6.25 \cdot 10^{-5}) = 10$ mg/g, or 1% capsaicin for dry Carolina Reapers. To eat the equivalent of 11 g of capsaicin in peppers, you would have to eat 1.1 kg of dry peppers - which should be a couple of dozen.
So, I think we can conclude that it is relatively "feasible" to consume a dangerously large amount of capsaicin by eating very spicy peppers. However, there are numerous caveats with my reasoning:

Human LD50 and rat LD50 are not necessarily the same.
Toxicity is not necessarily linearly related to body weight.
Peppers have compounds besides capsaicin that contribute to hotness.
It would be very difficult to eat such a large amount of spicy peppers, and various involuntary reflexes would interfere. Even if one were force fed the peppers, I imagine the body would attempt to vomit it up - which brings up the question of how the toxicologists even managed to feed several milligrams of capsaicin to rats to measure the LD50.

This answer is quite incomplete: The quantitative aspects are inconclusive (they rely on rat values), and there is very little qualitative information on how exactly death would occur. I have nevertheless included it here as a way of collecting the relevant information I was able to find, in the hopes that it would help answerers.

1.1kg of dry peppers being a couple of dozen would be a weight of about 50g per pepper -- quite heavy, especially if you mean dried (dehydrated) peppers. These peppers don't look very big. (For reference, it seems that a medium bell pepper weighs about 100g.)

I agree with @Superbest.  This answer is based on rats.  I demand precise, demonstrated research results on what the lethal doses are for a human.  Potential research subjects might be hesitant to participate, but 50 bucks would probably seal the deal.

toxicologists even managed to feed several milligrams of capsaicin to rats to measure the LD50: Purified capsacin (wrapped in something like capsule) could have been provided in a single dose. Quite a nice answer though :)

They can also perhaps do a test in TRPV knockout rats. This would at least eliminate the instantaneous burning sensation of capsaicin. Avian TRPV channels are not sensitive to capsaicin

by TRPV I meant TRPV1.. Moreover chronic exposure to capsaicin causes analgesia. It is important to ascertain the cause of death after capsaicin overdose

If you have cardiovascular problems, then it should be quite possible for the pain cause by spicy peppers to trigger a heart attack via a spike in blood pressure. A similar scenario might occur with respiratory diseases. And of course an anaphylactic shock, if you are allergic.
Apart from such special circumstances, I imagine that it would be nearly impossible to overcome the debilitating effects of capsaicin long enough to consume a lethal dose.

Please include references

wouldn't it do the opposite instead? I would imagine that it would dilate the blood vessels lower blood pressure.


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What is the biological function of nose, underarm, and pubic hair?
What is the biological function of nose hair? In general, can we consider underarm hair and pubic hair to be vestigial structures?

It’s weird that sometimes, that the question lacking basic research or any effort to answer the question at all, rise to top Despite the site’s policies.

@Chemist This is very old (~5 yrs) question. Standards change over time.

From this article I quote

Hair in the nose is one of the body's first lines of defense against
  harmful environmental pathogens such as germs, fungus, and spores.
Another purpose for nose hair is to provide additional humidity to the
  inhaled air. As the air passes through the nasal passages, the mucus
  and hair provide heat and moisture. Humidity is an important factor
  for the rest of the respiratory system, such as the larynx and lungs.
Hair in the form of tiny cilia also draw solid particles towards the
  interface between the nose and throat. Harmful debris is generally
  directed towards the back of the throat and esophagus for swallowing,
  while the filtered air continues towards the larynx and lungs.

If you look on an evolutionary perspective, the arm pit hair follicles as well as pubic hair have a type of sweat gland associated with them, called an apocrine gland, that begins to function at puberty and is widely associated with scent-communication via chemicals known as pheromones (reference).
Some other functions that are associated with pubic hair are:

Keeping the genitals warm.
Drawing attention to the genitalia.
It also decreases friction during intercourse (reference).

The nose hair is definitely not vestigial. As long as the armpit hair (between the body and arm in certain heavyset individuals) and pubic hair serve to reduce friction and male sweat serves to increase female hormones, I wouldn't call them vestigial (reference).

Keeping genital may not appropriate reason,as in male it’s located outside to keep it cool, it could be to reduce friction between genitals and limbs while walking etc

I meant keeping genital warm is the first line

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Why are some chemical dangerous to aquatic environment only?
Recently I was changing the thermal grease on my PC. I have noticed on the back of box, that the grease is not dangerous when ingested or when touched. But there was specifically stated, that is dangerous to aquatic organisms.
What is so special about aquatic chemistry, that the grease is dangerous to them? I would guess that the chemistry of mammals, reptiles, and birds would be quite similar to that of fish.

just a guess, but dissolved in water it may coat the gills and prevent proper oxygen/CO2 exchange...

What type of thermal grease are you using? I think it depends on the ingredients.

From some of the MSDS (1, 2) I come across, a major component of thermal grease is aluminum oxide.
Risk Management for Hazardous Chemicals by Jeffrey Wayne Vincoli states in page 101 that aluminum oxide has both acute and chronic toxic effects to aquatic life; it also states that aluminum oxide has a half-life longer than 200 days in water; finally, it acknowledges that the short term toxicity data for non-aquatic animals are insufficient.
From this, the reason thermal greases have special notification regarding to fishes can be attributed to those following points:

The long half life makes fishes exposure to it longer and therefore makes them more susceptible.
We simply do not understand how aluminum oxide effect non-aquatic animals.

(According to Risk Management for Hazardous Chemicals, bioaccumulation in food chain might not be the concern.)

I have to admit, 'we don't know that it kills land creatures, but it definitely kills fish' is a scary reason to put an aquatic warning on it.


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Why are hens so different from other birds?
Hens lay many eggs during their lifetime (at least, I don't know of one which can lay more eggs) and they can't fly. Compared to other domestic animals it seems to me they are the least capable of defending themselves or escape if it comes to be left alone in open wild. What is their evolutionary story?

Hens can fly, animals that are kept for farming purposes have their wings clipped

Domestic organisms are bred to serve specific purposes for humans. Sheep are bred to produce wool; Cows are bred to provide meat and milk for human consumption; dogs are bred for service and companionship. Since domestic animal do need to survive in the wild in order to reproduce (ignoring feral animals, which is an interesting topic by itself), most of the other aspects of that animal relevant to its survival tend to be minimized.
So one could just as easily point out that there is no other animal that produces as much wool as a sheep, and yet producing copious amounts of wool isn't particularly useful to the animal itself (i.e. other than the fact that humans will tend to select good wool producers for breeding). So sheep are not particularly good at surviving in the wild, and yet they are incredibly successful as a species and are widely distributed, thanks to humans.
In short, domestic hens evolved to produce many eggs in their lifetime because over the past millennia since humans have started keeping them as livestock, humans tended to preferentially breed those individuals which produced more eggs and to eat those individuals which did not. Chickens tended to be kept in pens and guarded by humans or other animals, so the ability to defend themselves or flee from danger was not important to their survival, and in fact, those that did attack their handlers or escape were probably less likely to be bred.
This process is known as selective breeding or artificial selection.


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What happens to fecal matter if it's continually re-eaten?
After class today, the topic of eating one's one fecal matter came up. There was a sharp divide as to how people thought the defecations would change. I realize this is a bit of an odd question but understanding it would help me understand how our body handles waste.
One theory was that the body would continually reuse some elements of the fecal matter such that, eventually and with no other input, nothing would be defecated.
Another theory was that there are elements in the fecal matter that the body would never make any use of, so it would continually get excreted (up until the person died, of course).
Could someone please explain the likely outcome of continually and only eating your own poop (assuming you could stay alive long enough)?

In a healthy person, stool weight depends mainly on the quality and quantity of the diet. The mean stool weight of a normal defecation is about 320 g [1].
Dry weight of fecal matter contains [2]:

30 % bacteria
30 % undigested food and fiber
10-20 % fat
2-3% protein

Let's do the math (the only nutrients in feces are fats and proteins):

20% * 320g = 64g of fats which can release 64 * 9.3 = 595 kcal of energy
3% * 320 = 9.6g of proteins which can release 9.6 * 4.1 = 40 kcal of energy

That's about 650 kcal. 2,000 kcal is a rough average of what people eat in a day. But your body might need more or less than 2,000 [3].
As you can see, fecal matter can't supply enough nutrients. Continuously (re)eating feces and only feces will lead to denutrition, less feces and death.
References:

Seyed Mohammad Kazem Hosseini Asl MD, Seyed Davood Hosseini MD. Determination of the Mean Daily Stool Weight, Frequency of Defecation and Bowel Transit Time: Assessment of 1000 Healthy Subjects
shigeta's answer on What is the composition of human feces?
HowStuffWorks.com. How many calories does a person need daily?

The author seems aware that the person would clearly die from lack of nutrition but is more wondering about the theoretical result. I think you should add that after continuous cycles of digestion, the fat and protein components of faeces would at some point be completely eliminated. So would the bacteria, but while passing through the intestinal environment, new bacteria would inevitably get mixed into the mass again. Thus, the result would be a mixture of undigestible fibre and bacteria.

A very thoughtful response. I guess my further question would be that, with only fecal matter as food intake, would the amount of bacteria and undigested stuff eventually (and theoretically of course) dwindle to nothing? Or would that continue to just be processed and excreted?

@AHungerArtist fibers and bacteria are not processed. Fibers will be excreted over and over again as-is. Bacteria may vary because they are multiplying in the intestine.

Want to add a point that some animals like rabits eat their feces because a single round of digestion is not very efficient.


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Cancer cure statistics questions
I have a question about cancer cure statistics. Many of the cancer literature or databases I have come across speak about 5 year or 10 year survival rates. In this case survival means that the patient with cancer is still alive 5 or 10 years after diagnosis. I am in need of references about the statistics which explain what is the percentage of people in these groups who are in progression-free survival group and disease-free survival group. That is for instance among the cancer patients which survive for some X years, who are completely cured of cancer (which means that the cancer is completely cured and has not reoccured with in this X years).
Update: USA data is preferred
Thanks

So you want to know actual numbers of survivors?

No I want to now the actual number of people among the survivors whose cancer has been completely cured. Survivors also include people who survive for some time with the cancer still in their body.

@Sina Any particular cancer or geographical location you are particularly interested in?

Thanks for the question. I would prefer USA if available. Age stratification would also be very useful.

Does this help? http://www.cancercenter.com/ctca-results/

Check the NCI database

This question seems well fitted for Skeptics.

I would caution you against using phrases such as "completely cured" or even "cured". This goes beyond our technical ability to detect the presence of tumor cells within someone's body. All we can conclude is progression-free survival (i.e. living with cancer that does not get worse) or disease-free survival (i.e.  or no signs or symptoms of the tumor). Many of these data are included in cancer trials along with overall survival rates. Some general statistics for many groups of cancers can be found here: http://www.cancer.gov/statistics/find
And a glossary of terms used in reporting cancer statistics here: http://www.cancer.gov/statistics/glossary

In cancer research, we never talk about "curing" cancer because, as others have pointed out, there is no way of being sure that all of the cancer has been eradicated. You may be interested to consider "Recurrence" statistics which describe the amount of time from when a cancer was treated to when it was detected to have returned.
If you are willing to do some statistics computations of your own, The Cancer Genome Atlas (http://cancergenome.nih.gov/) will let you download clinical datasets that include datasets like recurrence, "Overall Survival" (how long did the person live after being diagnosed with cancer), and others.
You can plug in either recurrence values or overall survival values and perform a Survival Analysis (http://en.wikipedia.org/wiki/Survival_analysis, http://lifelines.readthedocs.org/en/latest/Survival%20Analysis%20intro.html) to see how long people tend to live cancer-free or live in general after their diagnosis depending on their cancer type (or other variable you feel like comparing).

I didn't know this was publicly available now. Thanks this is really interesting.


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How much vanilla will kill a person?
I received a gift that is a jug of Pure Mexican Vanilla. Having never dealt with large quantities of vanilla, it made me curious as to what would happen if a person had too much vanilla.
I understand that the alcohol has a higher toxicity rate and is probably more fatal than the actual vanilla itself, but I'm curious as to what ratio of mass of pure vanilla to mass of the human would be considered fatal.
Also, what is the physiological effect of a vanilla overdose as it pertains to inhibiting critical bodily functions? That is -- specifically what about a vanilla overdose would cause fatality?

You get a present and the first thing you do is thinking about how to kill someone with it?

Why do you think vanilla is toxic?

I'm just not used to seeing Vanilla in the "jug-sized" unit of measurement. My friend said not to drink it all in the same place. Naturally that piqued my curiosity about the fatality of Vanilla.

First question: Is it real vanilla extract? Or is it synthetic vanilla? In the first case, it contains alcohol, but that should it be.

As Paracelsus said: "The dosage makes the poison"

@Chris It turns out that most so-called “vanilla” carried back from Latin America is completely fake, and potentially even dangerous.

Vanillin is the chemical that gives vanilla its flavour and smell [1].

Vanillin is pharmacologically active, causing depressed blood pressure, increased respiratory rate & death due to cardiovascular collapse [3].
Non-Human Toxicity Values [4]

LD50 Rat oral 1580 mg/kg
LD50 Rat ip 1160 mg/kg
LD50 Rat sc 1500 mg/kg
LD50 Mouse ip 475 mg/kg
LD50 Guinea pig oral 1400 mg/kg
LD50 Guinea pig ip 1190 mg/kg
LD50 Rat oral 2.8 g/kg
LD50 Guinea pig oral 1.40 g/kg
LD50 Mouse ip 0.78 g/kg
LD50 Rat sc 1.8 g/kg
LD50 Dog iv 1.32 g/kg slow in fusion.

References:

Wikipedia contributors, "Vanillin," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Vanillin&oldid=613429267 (accessed June 26, 2014).
PATTY F. A. 1963. Industrial Hygiene and Toxicology. Volume II Toxicity, page 1696 (referenced from TOXNET, Vanillin - Human Toxicity Excerpts)
TOXNET. Vanillin

Hm that's really interesting. But would humans react similar or differently compared to animals? Plus it would be interesting - considering the initial question regarding the bottle - which would component would be "deadlier"? I assume the alcohol, but would still be interesting to know.

@Mario - The LD50 Rat oral for Ethanol is 7g/kg.
Surprisingly, the vanillin is deadlier.

@MCM In raw form, yes, but I wouldn't expect the mix to be 50% alcohol, 50% vanillin. There's a reason people enjoy alcohol rather than getting killed by it left and right. ;)

@Mario - People overdose on alcohol all the time. Now sugar or water... yeah. Wiki says "pure" extract would be about 35% alcohol and at least 100g of beans per gallon. So drinking an entire gallon of the stuff might be lethal for most people who weighed 65kg or less from the Vanilla. There'd be approximately 1.32L of alcohol - or about 1000g, also enough to probably kill somebody who weighed 150kg or less. They'd be killed by the alcohol before the vanilla.

Out of interest, I've had a look around a bit and it seems like the most dangerous part of that bottle might be the alcohol.
According to the FDA...

The term unit of vanilla constituent means the total sapid and odorous principles extractable from one unit weight of vanilla beans, as defined in paragraph (b) of this section, by an aqueous alcohol solution in which the content of ethyl alcohol by volume amounts to not less than 35 percent.

(Emphasis mine.)

This is not far away from what Whiskey has. Only that vanilla extract will be a bit more expensive...

@Chris So in this case, ordering "Bourbon" might be a bit vague? ;) The EU actually demands 40% or more (for Whiskey).


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Anatomy suffixes?
Here are some suffixes I want to know their meaning:
-ium: trapezium (carpal bone)
-ius: trapezius  (column muscle)
-ous: Talous and calcanous (tarsal bone)
-alis: Acromialis, Ulnaris (shoulder proccess and bone of forearm)
-ate: Capitate, Hamate, lunate (carpal bones)
What is the difference between tuber and tubercle?
How to know where to use these suffixes, they are randomly given or it has to do with location or something?

I cant even understand what you are asking here. Edit your question please.

These names originate from latin [1].

-ium is the second declension of a noun in accusative (trapezium refers to a bone thus is a noun)
-ius is a genitive adjective suffix (trapezius is the name of a muscle thus being an adjective)
you have written them wrong: talus and calcaneus is correct. They are both nominative nouns.
there is no -alis suffix; it is either -is or -lis. They are adjective suffixes.
there is no -ate suffix. Those are nouns.

Tuber is the latin word for tuberosity. It is the quality or condition of a tubercle (adjective) [2].
References:

Wikipedia, Latin declension
The Free Dictionary by Farlex, Tubercle


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Anaerobic respiration choice in E. coli
Under anaerobic conditions E. coli has two options to generate ATP: fermentation (substrate-level phosphorylation), and respiration (proton gradient, chemisomotic phosphorylation). Which is favored? What determines the choice? If availability of enzymes required for anaerobic respiration is decisive, what regulates them under anaerobic conditions?
I looked into the web but did not find the answer.

E. Coli is not simply aerobic. Nor is it anaerobic. It is facultative, meaning that it thrives in both environments, and can breath with or without oxygen.

Let me first clarify the difference between anaerobic respiration and fermentation.
Literally respiration refers to breathing, but its definition has been extended to include cellular metabolism that leads to ATP generation.
Fermentation, as you said depends on substrate level phosphorylation. Anaerobic respiration on the other hand just means ATP synthesis in the absence of oxygen- in other words anoxic. This happens in several cases in which the terminal electron acceptor is not oxygen but some other chemical species such as $Fe^{3+}$ or fumarate.
E.coli can carry out ETC mediated ATP synthesis both in the presence and absence of oxygen. At high oxygen concentration it uses $O_2$ as electron acceptor, mediated by cytochrome-d. At low oxygen concentration other kinds of cytochromes accumulate and the cell uses fumarate or nitrate as the terminal electron acceptor with the help of fumarate reductase and nitrate reductase respectively. This is an old article but is still quite informative. Check it out.
Fumarate and nitrate reductases are regulated as a part of what is known as FNR regulon. FNR is an oxygen-sensitive transcription regulator. In the presence of oxygen it is inactivated. In the absence of oxygen it activates the fumarate and nitrate reductase genes.
Perhaps in the absence of these alternate electron acceptors, the bacterium totally depends on SLP.

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


text:
Why does the oxygen produced in the photosynthesis come from water and not carbon dioxide?
In the photosynthesis equation:
$$\ce{6CO2 + 6H2O ->[sunlight] C6H12O6 + 6O2}$$
The only place where we have 6 molecules of $\ce{O2}$ is in $\ce{6CO2}$. Then it reacts with $\ce{6H2O}$ to form $\ce{C6H12O6}$ and $\ce{6O2}$ that apparently comes from $\ce{CO2}$. So why do we say that the $\ce{O2}$ produced by plants comes from $\ce{H2O}$ and not $\ce{CO2}$? I don't know if I'm the one who's understanding something wrong or is it the photosynthesis formula which is wrong?

go through this http://www.howplantswork.com/2009/02/16/plants-dont-convert-co2-into-o2/

@The Last Word - great link.

and it's still like this after the edit?

It's funny that the only answer that actually addresses OP misunderstanding, i.e., the difference between the simplified and non-simplified equations, is the one with less upvotes. Again, it's not the only correct answer, but it's the only one that shows the complete (non simplified) equation. In my classroom experience, showing the non simplified equation to the students really help them to better understand that the oxygen comes from the water.

Yeah, but the water might have come from mitochondria that devoured HCOH which came from CO2.

You are missing some knowledge here for sure, photosynthesis is a little complicated at A level, so I will describe it in brief.
During photosynthesis electrons and protons (A hydrogen atom without the electron) are required for a process called the electron transport chain and proton motive force. This happens during the light dependent stage of photosynthesis, (there is also a second light-independent stage called the Calvin cycle, and that is where the CO$_2$ is used), I won't go into detail about what the protons and electrons do (unless you want me to) but you need to know that these come from a water molecule, the water is split using light (photolysis, literally: cutting with light) into two hydrogens and half an oxygen molecule (or an oxygen atom). The oxygen that was released in photolysis is not required for the rest of the pathway, so it diffuses out of the cell.
For why it doesn't come from carbon dioxide, you need to consider the Calvin cycle. In the Calvin cycle, carbon dioxide is converted to glucose by enzymes, using products from the light dependent stage, so 6CO$_2$ are combined over six cycles to form one molecule of glucose. So that is where the CO$_2$ is used as well.
Hope that helped! If you want me to go into any more detail please ask!

Photosynthesis uses chlorophyll (or other pigments) for harnessing photons and water (or other compounds) as electron donor $H_2O = 1/2O_2 + 2H^+ + 2e^-$. After splitting the water it sends the electrons through the further steps of an electron transport chain and at the end it reduces $NADP^+$ into $NADPH$. Meanwhile it increases the $H^+$ concentration outside of a membrane, so it creates a $H^+$ gradient. This gradient can be used to synthesize $ATP$ from $ADP$ using a $H^+$ pump. After that $NADPH$ and $ATP$ can be used to fix $CO_2$ at any time (so that part of the photosynthesis is not light dependent).

Figure 1 - Light-dependent reactions of photosynthesis - electron transport chain - source

Splitting $CO_2$ into $CO$ and $1/2O2$ is possible as well. It can be done enzymatically or due to photolysis. You need similar energy to do that as by water splitting.
After that $CO$ can be used e.g. by shift reaction $CO + H_2O = CO_2 + H_2$ to create an electron donor ($H_2$) and play the same thing as normally. It is possible to reduce $CO$ with an electron donor ($_H2O$, $H_2$, $H_2S$, $NH_3$, etc...) further, and create for example ethanol or carbohydrates like glucose.
Afaik only artificial photosynthesis use $CO_2$ splitting and natural ones prefer $NADPH$ and $ATP$ creation and usage for example in the Calvin cycle, C4 pathway, CAM pathway, reverse Krebs cycle, Wood pathway, etc... I think this is because carbon fixation evolved before photosynthesis. So photosynthesis is just about plugging another energy source into the system.
(In programmer terms the carbon fixation is loosely coupled to the implementation of the energy producing process and the common interface is described with ATP and NADPH creation.
In mobile phone user terms it is like charging your phone's battery (ATP and NADPH storage) from line power or using a solar charger. Both chargers provide electricity (ATP and NADPH) via USB.)
The question is good, what you meant is possible, but afaik. in natural photosynthesis the $O_2$ always comes from the water.
References:

2006 - Photosynthesis in the Archean era.
2008 - When did oxygenic photosynthesis evolve?
2012 - On the photosynthetic potential in the very Early Archean oceans
2010 - Early Evolution of Photosynthesis
1988 - Photoreduction of carbon dioxide by aqueous ferrous ion: An alternative to the strongly reducing atmosphere for the chemical origin of life
wikipedia - Anoxygenic photosynthesis
2002 - Kinetic study of the reverse water gas shift reaction in high-temperature, high-pressure homogeneous systems
The Enthalpy, Entropy and Gibbs Energy of Ion Formation in Solutions
wikipedia - Standard enthalpy of formation
2012 - Splitting CO2 into CO and O2 by a single catalyst
2002 - Molecular Hydrogen as an Energy Source for Helicobacter pylori
2009 - Water-Gas Shift Reaction Catalyzed by Redox Enzymes on Conducting Graphite Platelets
2013 - Leaf-architectured 3D Hierarchical Artificial Photosynthetic System of Perovskite Titanates Towards CO2 Photoreduction Into Hydrocarbon Fuels
2014 - Comparison of CO2 Photoreduction Systems: A Review
2006 - Microorganisms pumping iron: anaerobic microbial iron oxidation and reduction
1972 - Flash photolysis of H2S
2011 - Anoxygenic Photosynthesis
2004 - Time line of discoveries: anoxygenic bacterial photosynthesis
1990 - A reverse KREBS cycle in photosynthesis: consensus at last
2009 - Molecular Approaches to the Photocatalytic Reduction of Carbon Dioxide for Solar Fuels
2014 - Electroreduction of carbon monoxide to liquid fuel on oxide-derived nanocrystalline copper
2012 - Biological conversion of carbon monoxide to ethanol: effect of pH, gas pressure, reducing agent and yeast extract.
2012 - Hydrogen, metals, bifurcating electrons, and proton gradients: The early evolution of biological energy conservation - an exciting article
2005 - Hydrogen-driven subsurface lithoautotrophic microbial ecosystems (SLiMEs): do they exist and why should we care?
2011 - Alternative Pathways of Carbon Dioxide Fixation: Insights into the Early Evolution of Life?
1998 - Hydrogen metabolism in organisms with oxygenic photosynthesis: hydrogenases as important regulatory devices for a proper redox poising?
1975 - Facultative anoxygenic photosynthesis in the cyanobacterium Oscillatoria limnetica.
2003 - On the origins of cells: a hypothesis for the evolutionary transitions from abiotic geochemistry to chemoautotrophic prokaryotes, and from prokaryotes to nucleated cells
2011 - Serpentinite and the dawn of life
2010 - How did LUCA make a living? Chemiosmosis in the origin of life
2012 - The Emergence and Early Evolution of Biological Carbon-Fixation
2012 - Photosynthetic Electron Transport in an Anoxygenic Photosynthetic Bacterium Afifella (Rhodopseudomonas) marina Measured Using PAM Fluorometry
Bacterial Energetics: A Treatise on Structure and Function
2012 - Depth variation of carbon and oxygen isotopes of calcites in Archean altered upperoceanic crust: Implications for the CO2 flux from ocean to oceanic crust in the Archean
2013 - Hydrogen-Nitrogen Greenhouse Warming in Earth's Early Atmosphere
2010 - Aeronomical evidence for higher CO2 levels during Earth’s Hadean epoch
2014 - From Ionizing Radiation to Photosynthesis
2011 - Metal centers in the anaerobic microbial metabolism of CO and CO2
2014 - Evidence and arguments for methane and ammonia in Earth's earliest atmosphere and an organic compound–rich early ocean

I'd suggest you cut most of the references. Nobody is going to read them all (certainly not the poster) and they discourage people scrolling to other, perhaps more succinct answers.

@David I read them all. I think I am still somebody...

@David Btw. I think the problem is with the site. It does not provide a way to collapse a reference list or add it as an attachment.

It’s not about the oxygen!
This question indicates two misplaced concerns. One is with oxygen. I imagine that this is because of its importance to us as animals; however as far as photosynthesis is concerned oxygen is just a waste product. The other is with a chemical equation, which is as informative as the top line of a commercial balance sheet. One's focus should be on the chemical problem and what is needed to solve it.
The problem is making sugar from carbon dioxide
The purpose of photosynthesis is to make sugar from carbon dioxide. Why is this a problem?

The individual carbons in the carbon dioxide have to be joined together with C-C bonds. This requires energy (in the biological form of ATP).
In sugars most of the oxygen atoms are in OH groups. So we need to convert the C=O of the carbon dioxide to C–OH (not throw the oxygen away). This is reduction of the carbon, and requires ‘reducing power’ (in the form of the NADPH) which also requires energy input.

The sun solves the problem by supplying the energy
The energy for creating the reducing NADPH and the ATP comes from the sun in a complex series of reactions that do not involve carbon dioxide. Light of a particular wavelength is used to break a water bond so as to separate charge in a reaction that I will deliberately not balance:
(1) H2O → O2 + H
A complex series of reactions transfer the H (more strictly an electron) between different molecules, eventually reducing NADP+ to NADPH. At the same time an equally complex process builds up a H+ concentration difference across a membrane which provides the energy to convert ADP to ATP.
To reiterate, the reaction uses light energy to generate chemical energy in the form of NADPH and ATP. Oxygen is just flushed down the toilet.
Now for the Lego bricks — so easy we can do it in the dark
Having harvested the energy of the sun we have money in the bank which we can spend whenever we want — day or night — to make sugar from carbon dioxide. The overall unbalanced equation is:
(2) CO2 + NADPH + ATP → C6H12O6 + NADP+ + ADP
but this is actually a complex series of enzyme-catalysed reactions (known as the Calvin Cycle if you must know).
You still want to know the answer?
The oxygen produced in photosynthesis comes from water because this is the molecule in which a bond is broken by sunlight to separate charge allowing synthesis of molecules with reducing power and energy transfer potential. Carbon dioxide is the building block of the sugar and far from breaking a C=O bond, what is needed is for it to be converted to C-OH by reduction of the carbon.

@user1136 — I'm about to take a late vacation. I'll consider the chemical arguments you make regarding reduction of carbon dioxide and respond on my return.

@user1136 — OK, I see your point. Yes, my reference to reducing the oxygen (and even a double bond) was sloppy and incorrect. I have modified my answer to make it clear that the carbon is reduced. Trust it is ok now. If so, we can tidy up the comments.

I read on Wikipedia that basically 3 $O_2$'s come from water in the light reaction, and during the Calvin cycle $H_2O$ is produced from H+ ions and $CO_2$ to make more $H_2O$, which produces more $O_2$ in the light reaction.
Basically, 3 $O_2$'s come from the water and the other 3 $O_2$'s come from $CO_2$-made $H_2O$.
EDIT: The equation is $12H_2O$ + $6CO_2$ => $C_6H_1$$_2$$O_6$ + $6H_2O$ + $6O_2$ so therefore all the $O_2$ is from the water, and the $O_2$ in the sugar is from the $CO_2$, and the supposedly extra $O_2$ left over goes into some new $H_2O$.

It's the only answer that accounted for the discrepancy of "wait, 6 H2O only has 6 O's and so that makes 3 O2's! Also, 6 CO2 will have 3 O2's left over after making C6H12O6! Why does the missing O2 (from H2O) magically appear and the extra O2 (from CO2) magically disappear?"- well, that I could find, anyway.

Actually, I don't know if the plant reuses the CO2-generated H2O, but I know that there is H2O generated by CO2. The equation I saw later was 12H2O + 6CO2 --> C6H12O6 + 6O2 + 6H2O, but they took 6H2O from both sides to simplify the equation, but it adds confusion later when viewed without 6H2O added to each side, and the O2 is explained to come from H2O.


text:
Regarding the NCBI FTP site
I am trying to extract information about SNP data from the FTP server of NCBI. Could someone please explain to me how the directory is organised? There are many many files and folders and I can't figure which contains what. Is there one file which explains the organisation of the ftp site properly? The NCBI help manual did not give much help beyond helping me find species of interest.

Is this the help that your talking about? It is perfectly clear. What can you not figure out?

just a thought - its better to use biopython or some other script library to get what you want, especially if you are trying to get more than one item.

Getting SNP data from FTP Site of NCBI SNP:
It's actually simple to download the data from the NCBI, if you follow the method given by FAQ( as given by @WYSIWYG).
Step 1:
Goto organism FTP: ftp://ftp.ncbi.nlm.nih.gov/snp/organisms/

Step 2
Open your required organism folder:

From here you can download any file you wanted. If you trying to study the whole organism please download any one of the whole folders(ASN.1, rs_fasta, XML(recommended)).
Now,
It's not about the downloading it's about understanding the files which are provided.
files types:

XML files
ASN.1 or Abstract Syntax Notation One
rs_fasta

All of them contents almost the same data, just in different format. It's up to you how your script(preferably Python or Perl) works to get out the import information.

Other way of Download from NCBI FTP:
You can always use filezilla:

Put Host as : ftp://ftp.ncbi.nlm.nih.gov/snp/organisms/
rest Username and Password, etc empty


text:
Why does low temperature make RuBP, GP and TP concentrations fall in Calvin cycle?
In my A level revision guide and places on the internet it states that at low temperatures levels of RuBP, GP and TP all fall. However I don't quite understand how this is the case, because as far as I can see, a reduction in temperature would give the molecules less kinetic energy and reduce the rate of reaction of the enzymes and so there would be no change to relative concentrations, because everything is slower all equally. Could anybody explain to me why all three decrease in concentration at low temperatures?

Enzymes don't universally reduce their catalytic ability when the ambient temperature is lower. Some will be affected more than others. You could probably look up the KM values with relation to temperature if you're curious.

Note that reaction rates depend exponentially on temperature as per Arrhenius equation. So the change won't be linear. Moreover the activation energies for different reactions will be different. $\k=Ae^{-E_a/{RT}} \\frac{k_1}{k_2}=e^{-E_aR(\frac{1}{T1} - \frac{1}{T2})}\\$

@MCM so, if the enzyme to convert TP into the respiratory substrates works faster than all the other enzymes, and given that Carbon Dioxide will diffuse slower in lower temperatures (hence less input), all the levels of intermediates should decrease?

@WYSIWYG that's an interesting equation, I will look into it, I love a bit of exponential decay from physics!

@J_mie6 I missed it then but after a while looked at this question again. The answer to your question requires the model parameters and other reactions. Can you provide the link to the source where you read this?

@WYSIWYG The OCR A level biology textbook I think


text:
On which part of the DNA will the new DNA nucleotide connect?
My question is:

Where will the new DNA nucleotide connect on the (part of the) DNA shown on the picture? Will it connect to the phosphate group?

What does the 5' --> 3' mean?

Thank you in advance.

The numbers come from the numbering of the carbon atom of the ribose in the backbone of the DNA. The ribose is numbered as shown in the figure below:

In the nucleotides the phosphate groups are attached to the 5' carbon atom and new nucleotide will be added at the 3' carbon atom. See the image below:

First you have a OH-group at the 3' position which is then "replaced" by the new nucleotide.


text:
Can we really 'discover' 85% of mammalian viruses?
This virology [blog] discusses estimates of the number of mammalian viruses and the costs of 'discovering' 85% of them.
My question is whether this is not a forlorn hope. The ".632 rule" in statistics says roughly that as we approach n random samples from a large population of size n we will see only about 62.3 per cent of the population. After a point we would begin to see the same viruses again and again. This argument is probably stronger with respect to marine viruses, as they may be even more numerous and sampling at depths could be difficult.
I wonder if someone with experience sampling small organisms from large populations or familiarity with the literature has an idea about the plausibility of seeing 85% of a large population, such as mammalian viruses, by sampling?
If the samples are really random (in some sense) and the population is large, a few computer simulations reveal the power of this rule of thumb.
Edit in response to comment/question:
Like any such estimate, the blog's estimate of 3.6 million is a guess. I am not reproducing the calculation here because it's just speculation.
Having said that, if 3.6 million were correct, we would have to draw about 6.8 million samples to find 85% of the existing viruses, 8.2 million to find 90%, and so on. As the blog notes, the PCR approach detects viruses similar to those we know, so the sampling is worse than random. If we look at the difficulty of finding/using a method that has a reasonable chance of capturing any of the extant viruses, the number 3.6 million looks very big.

How did they know/estimate the total no. of viruses ?

Is there an article you could refer me to for the .623 rule? I was very interested and would like to know more and also could you elaborate how you made the calculations in your edit. Thanks

@Bez: If you go to the Cross Validated site, problem 96739, user603 gives a really good short description of the calculations. He also gives some pseudocode to implement the calculation but you can to it fast by solving $1-(1-1/n)^x = .632$ etc. using the program of your choice. $n$ in this case was 3.6 M and so solving for x we get 3.6 M. If we insert 0.85 instead of .632 we get 6.8M. And so on.

Excellent page, I found the R code on the page very helpful. Many thanks

Regarding the question, I guess it is possible to reach the %85 based on the formula however I think there are two major problems that could affect the percentage. First most of the viruses collected for analysis is probably not collected/sampled at random as (unfortunately) samples are collected when they are of interest e.g disease causing viruses etc. Second is that there are perhaps many places, which have not yet been sampled due to inaccessibility etc. So in short I think it is possible but there are barriers but these are just my thoughts and I could be totally wrong!

@Bez: Yes I think this is all true. And maybe the biggest barrier is the numbers. How to do 7 million random samples. I don't think we're allowed to group results from disparate studies unless they are all following some common procedure.

For some statistical models, see e.g. The Mathematics of Biodiversity (Part 1) by John Baez.
However, in terms of new species, such statistical methods may not suffice - usually also our tools for discovering change. So it might be more accurate to extrapolate number of some kind species we know as a function of time.
For extrapolations (though not for viruses) see e.g.:

Camilo Mora et al., How Many Species Are There on Earth and in the Ocean?, PLOS Biology (2011).

In any case, for viruses (and many other fast-multiplying asexual creatures) defining number of species can be anywhere from tricky to impossible (for fundamental reasons, not only - practical). At best you can try to estimate their time to the last common ancestor. See also links in this discussion on Azimuth.

@daniel Fixed, thanks (sometimes I have issues with copy-paste). BTW: AFAIK OP means 'Original Poster' (i.e. you, in this context), not 'Original Post'.

@daniel I feel overnerded by you (and thanks, it is always good to know). In any case, in the context of Stack Exchange (unlike fora, separating Q from A), I see people using OP when they mean Original Poster (as it is easy to refer to question as 'the question', or Q).

I was thinking about 'outnerded' (it sounds right), but decided to go for 'overnerded' (compare: 'outpowered' vs 'overpowered'). But you are an expert on words here.

OK, here goes. Using MathSE because it's bigger--questions 8623,513239,774176 Poster; questions 708644,272591,350485 Post. I think most refer to poster because it's a service-oriented group. But...

Let us continue this discussion in chat.

Can't--I'm off to the salt mines...


text:
How tolerant are ants to cold?
There was a trail of what are commonly known as sugar ants (small, brown, hyperactive) in my kitchen. Three of them walked onto an ice tray placed in their path.
They only walked a short distance on the ice before being immobilized by cold. I put the tray in the freezer beside a very shallow dish of water. When the water in the dish had frozen (about a half hour later) I removed the tray/ants and let them passively drop onto a warm dry surface. After 2-3 minutes they revived, walked in circles a few times, then headed off to forage (they were released outdoors).
There is anecdotal evidence of ants' tolerance of cold but I was a little surprised by this. Do we know the extent of their tolerance of cold?
I guess it would vary with size and conditions. But an obvious question is whether, having survived freezing at (let's say) 22F, they could survive lower temperatures and/or longer periods of cold if properly handled? There may be cell structures that are sensitive to freezing because they break or change shape but it's already amazing to me that ordinary freezing does not distort water-bound structures in a lethal way.
Thanks for any insight.

As an afterthought-- I would not have done this if I was not quite sure the ants would survive. The result was surprising but more or less expected.

Acclimatization increases cold resistance of ants [1]. They have a strong adaptability to different environments [2].
When it comes to the red imported fire ant (Solenopsis invicta) here are some numbers (from [2]):

When the exposure time was 0.5 h, the survival rate of workers was 15.3% at -14°C. At the exposure time of 1, 2 and 4 h, the entire lethal temperatures for S. invicta were -13°C, -9°C and -9°C, respectively. When the exposure temperature was -10°C, all workers died within 240 min; while at -11°C, it took only 120 min.

References:

Modlmeier AP, Pamminger T, Foitzik S, Scharf I. Cold resistance depends on acclimation and behavioral caste in a temperate ant. Naturwissenschaften. 2012 Oct;99(10):811-9. doi: 10.1007/s00114-012-0963-8. PubMed PMID: 22955370.
Xu YiJuan; Lu YongYue; Huang Jun; Zeng Ling; Liang GuangWen. Cold hardiness of natural populations of the red imported fire ant, Solenopsis invicta Buren (Hymenoptera: Formicidae) in Shenzhen, Guangdong. Acta Entomologica Sinica 2009 Vol. 52 No. 9 pp. 974-983.

This answer is helpful +1. I also wondered how they are able to tolerate this degree of cold and what goes wrong at the molecular level if they don't.

@daniel this is about yeast cells frozen to much lower temperatures, but it says what is happening at cellular level http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1392953/

Your answer together with the comment is I think a complete answer to the question. Will accept in a bit. Thanks.


text:
Single stranded DNA in gel electrophoresis
From http://www.nfstc.org/pdi/Subject05/pdi_s05_m01_01.htm :

... The separation medium contains a denaturant in order that the
  electrophoresis is conducted on single-stranded DNA fragments.
  Single-stranded DNA fragments are more similar to each other than
  double-stranded DNA fragments are to each other. Double-stranded DNA
  produces more electrophoretic diversity due to its three-dimensional
  structure.

Questions :

What is the denaturant they are talking about?
It's mentioned that double-stranded DNA
produces more electrophoretic diversity due to its three-dimensional
structure. Why should dsDNA have more 3-D structures than ssDNA? ssDNA can form hairpins and other structures. Which structures can dsDNA form?

As far as I see, they are talking about standard gel electrophoresis. I have done this hundrets of times for different purposes, but I have never used denaturants. I think the chance of producing unwanted 3D-structures is much bigger when it is single-stranded. This is different for RNA (which is usually not double-stranded). Here denaturating gels, as well as denaturating agent like urea or formamide in the loading buffers are used.

As already mentioned formamide can be used. However formamide has to be incubated with the nucleic acid sample and heated. Urea can be included in the gel (8%). DNA can also be denatured using NaOH. NaOH, however, cannot be used for RNA because it will cause alkaline hydrolysis.
I don't much agree on this point. Though dsDNA can produce diverse structures, as buzrw mentioned, so can ssDNA (in fact more diverse). Moreover, linearization solves the issue of supercoiling. We never compare circular plasmids with each other on the gel. Long linear dsDNAs can form structures but then in such cases gel electrophoresis is not a very suitable method for comparison. PFGE might be a better option in such cases.

Formamide and/or urea most likely. They both lower the melting point
of the ssDNA. This allows the structures to unravel at lower
temperatures. Typically you want to reach for  melting temperatures
around 50° C, and then run the gels at that temperature. RNA is
often denatured with harsher agents, like formaldehyde because RNA
form stronger structures.
ds DNA can exhibit supercoiling which is a very elegant method of
    packaging DNA. This is a huge topic and mathematically derived. It's
    important is mostly due to it's role in gene expression via the
    interaction dsDNA has with proteins it wraps around-his tones.

Note that ds-supercoiled-DNA forms two structures; a plectoneme or a toroid, and can also have combinations of these two. It's interesting stuff. Google "DNA supercoiling" with an image search  and look for a figure that shows the different levels of winding and wrapping:
I'm not very familiar with this source but the figure looks to be on the up-and-up.
Good question


text:
Solunar theory of animal activity
Solunar theory, which states that animal activity in wild (fishes, deer) depends on position of sun and moon in sky.
Based on the solunar calender, hunters seek for optimal time for hunting fishes.
I am wondering that how solunar calender is developed from the sun's and moon's rise/set timing or from their positions in sky? For instance if I know the position of sun and moon in sky how would one forecast the animal activity timings of that day? OR the solunar calender is based on some statistical forecasting?
Thanking you.

by observation!! all organisms have circadian rythm but their behaviors are different. some are diurnal while some are nocturnal

Right ! But my question is more mathematical. I am interested in how we derive the animal activity forecast from the sun/moon data ?

If there is a pattern based activity, you can mathematically model it and make extrapolations so as correctly mentioned above, you make observations, gather data and model it. What mathematical formulations people use I do not know but would be interesting if someone could point to a source. there is a similar version of your question here (http://answers.google.com/answers/threadview?id=295970)

are you looking for the kind of charts that are provided on this website. http://www.solunarforecast.com/

No. The way they find the best day of the month.


text:
Can HIV be transmitted via breastfeeding?
If a pregnant women is HIV positive and she is treated with medicines to deliver a normal child,can she transfer the HIV virus back to her normal HIV free child by colostrum?

possible duplicate of How does a person get AIDS?

The other thread doesn't cover the post-natal infection by breast milk.

Note that is seems that sexually sucking an infected woman's breasts is not considered a dangerous activity.

Yes, it is possible and the chances are pretty high. According to the WHO paper linked below, the rate of partially or completely breastfed children which get infected by this route is about 20-35%, while the rate of children which are not infected and doesn't get breatfed is zero (no surprise here).
The mechanism by which this infection occurs is currently unknown, but it is hypothesized that the virus enters via the mucosa. See these two articles below for more information:

A review of HIV transmission through breastfeeding.
HIV transmission through breastfeeding : a review.


text:
Do women have testosterone?
In a documentary on fitness I saw it was stated that women can't get big like men because of their low concentration of testosterone. If it is true that women have testosterone, where is it made? Why do some women, especially later in life, develop facial hair (though obviously not as much as men)? Do men also have "female" hormones in their body?

Yes, they do. The ovaries produce both testosterone and estrogen. Relatively small quantities of testosterone are released into your bloodstream by the ovaries and adrenal glands. Sex hormones are involved in the growth, maintenance, and repair of reproductive tissues [1].
The serum testosterone level in women with no acne, hirsutism, or menstrual dysfunction is 14.1 +/- 0.9 ng/dL (nanograms per decilitre) [2]. An average adult man has 270-1,070 ng/dL serum testosterone [3].
Men have female sex hormones too. For a prepubescent male, estrogen levels are expected to be between 1 and 3.7 ng/dL. During puberty, normal levels fall between 2.3 and 8.4 ng/dL. Levels for an adult male should be between 2.5 and 5 ng/dL [4].

References:

WebMD, LLC. Normal Testosterone and Estrogen Levels in Women.
Ayala C, Steinberger E, Smith KD, Rodriguez-Rigau LJ, Petak SM. Serum testosterone levels and reference ranges in reproductive-age women.
Alexia Severson. Testosterone Levels by Age. Healthline Networks, Inc.
wiseGEEK.com. What Are Normal Estrogen Levels in Men? (Measurements cited in picograms per millilitre, converted to ng/dL)

Two comments. The first is that you gave a good comparison of testosterone in men vs women. But you only gave the amount of estrogen for men and in (slightly) different units from testosterone, thus marring an otherwise great answer.

Healthy young males have estradiol levels in the area of 20-30 pg/ml.
Also, estrogen is a group of hormones, including estradiol and estrone for example. You shouldn't think of any hormones as women hormones or men hormones really, as both genders have them all, albeit in different proportions, and generated often through different pathways/organs.
this link is the best i could find within a few seconds of a google search:
http://emedicine.medscape.com/article/273153-overview
it will really describe where and what hormones are created where and in what quantities, as well as how and where they can convert within the body into more potent steroids.


text:
How do a particular arrangement of atoms become self aware?
At the simplest level, we're all just atoms, animals, plants and humans alike. But what I don't understand, is how a particular arrangement of atoms such as us can become self aware, and be able to not only understand our environment, but manipulate it to our will? How is that even possible?

well, we have to not think of the atoms themselves. It's the macrostructure that is more important, the cells themselves. It is the interaction of cells that make us self-aware, as they are able to communicate via Cell Signalling. It is like thinking of a computer, it is just a bunch of transistors really, and on their own they are not capable of calculating, but together they form a computer. You have to think of an object/organism as the sum of it's parts

this belongs in a philosophy forum :P

You are skipping too many steps.
$Atom \rightarrow \color{red}{molecule \rightarrow structure \rightarrow cell} \rightarrow organ \rightarrow organism$
The following is a proposed speculation regarding the steps in red on the above:

How life originated and how the first cell came into being are matters of speculation, since these events cannot be reproduced in the laboratory. It was first suggested in the 1920s that simple organic molecules could form and spontaneously polymerize into macromolecules under the conditions thought to exist in primitive Earth's atmosphere. At the time life arose, the atmosphere of Earth is thought to have contained little or no free oxygen, instead consisting principally of $CO_2$ and $N_2$ in addition to smaller amounts of gases such as $H_2$, $H_2S$, and $CO$. Such an atmosphere provides reducing conditions in which organic molecules, given a source of energy such as sunlight or electrical discharge, can form spontaneously. The spontaneous formation of organic molecules was first demonstrated experimentally in the 1950s, when Stanley Miller (then a graduate student) showed that the discharge of electric sparks into a mixture of $H_2$, $CH_4$, and $NH_3$, in the presence of water, led to the formation of a variety of organic molecules, including several amino acids.

Although Miller's experiments did not precisely reproduce the conditions of primitive Earth, they clearly demonstrated the plausibility of the spontaneous synthesis of organic molecules, providing the basic materials from which the first living organisms arose.
The next step in evolution was the formation of macromolecules. The monomeric building blocks of macromolecules have been demonstrated to polymerize spontaneously under plausible prebiotic conditions. Heating dry mixtures of amino acids, for example, results in their polymerization to form polypeptides. But the critical characteristic of the macromolecule from which life evolved must have been the ability to replicate itself. Only a macromolecule capable of directing the synthesis of new copies of itself would have been capable of reproduction and further evolution.
Of the two major classes of informational macromolecules in present-day cells (nucleic acids and proteins), only the nucleic acids are capable of directing their own self-replication. Nucleic acids can serve as templates for their own synthesis as a result of specific base pairing between complementary nucleotides. A critical step in understanding molecular evolution was thus reached in the early 1980s, when it was discovered in the laboratories of Sid Altman and Tom Cech that RNA is capable of catalyzing a number of chemical reactions, including the polymerization of nucleotides. RNA is thus uniquely able both to serve as a template for and to catalyze its own replication. Consequently, RNA is generally believed to have been the initial genetic system, and an early stage of chemical evolution is thought to have been based on self-replicating RNA molecules—a period of evolution known as the RNA world. Ordered interactions between RNA and amino acids then evolved into the present-day genetic code, and DNA eventually replaced RNA as the genetic material.
The first cell is presumed to have arisen by the enclosure of self-replicating RNA in a membrane composed of phospholipids.

Phospholipids are the basic components of all present-day biological membranes, including the plasma membranes of both prokaryotic and eukaryotic cells. The key characteristic of the phospholipids that form membranes is that they are amphipathic molecules, meaning that one portion of the molecule is soluble in water and another portion is not. Phospholipids have long, water-insoluble (hydrophobic) hydrocarbon chains joined to water-soluble (hydrophilic) head groups that contain phosphate. When placed in water, phospholipids spontaneously aggregate into a bilayer with their phosphate-containing head groups on the outside in contact with water and their hydrocarbon tails in the interior in contact with each other. Such a phospholipid bilayer forms a stable barrier between two aqueous compartments—for example, separating the interior of the cell from its external environment.
The enclosure of self-replicating RNA and associated molecules in a phospholipid membrane would thus have maintained them as a unit, capable of self-reproduction and further evolution. RNA-directed protein synthesis may already have evolved by this time, in which case the first cell would have consisted of self-replicating RNA and its encoded proteins.

Source: Cooper GM. The Cell: A Molecular Approach. 2nd edition. Sunderland (MA): Sinauer Associates; 2000. The Origin and Evolution of Cells. Available from: http://www.ncbi.nlm.nih.gov/books/NBK9841/


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Can tubular secretion regarded as local hormone?
Tubular secretion is : The process in which ions and other waste products are transported into the distal tubules of the nephron.
can it be regarded as local hormone??

First of all, I can't understand how can you regard an electrochemical process (tubular secretion) as chemical substance (hormone).
Tubular secretion is the transfer of materials from peritubular capillaries to renal tubular lumen. Tubular secretion is caused mainly by active transport.
Usually only a few substances are secreted. These substances are present in great excess, or are natural poisons. Many drugs are eliminated by tubular secretion [1].
The substances that are secreted into the tubular fluid (for removal from the body) include [2]:

Potassium ions (K+),
Hydrogen ions (H+),
Ammonium ions (NH4+),
creatinine,
urea,
some hormones, and
some drugs (e.g. penicillin).

Tubular secretion occurs from the epithelial cells that line the renal tubules and collecting ducts [2].
Uptake transporters in the basolateral membrane and export transporters in the luminal membrane of renal tubule cells are involved in tubular secretion of their substrates (organic anion transporters and organic cation transporters - these are transmembrane proteins) [3].
Despite considerable advances in the understanding of basic transport pathways and mechanisms involved in the tubular secretion of organic compounds, there is still relatively little information on the regulation of this transport [4].

References:

Wikipedia contributors, "Renal physiology," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Renal_physiology&oldid=608689347 (accessed June 26, 2014).
http://www.ivy-rose.co.uk/HumanBody/Urinary/Urinary_System_Kidneys_Actions_3.php
Müller F, Fromm MF. Transporter-mediated drug-drug interactions. Pharmacogenomics. 2011 Jul;12(7):1017-37. doi: 10.2217/pgs.11.44. PubMed PMID: 21787191.
Berkhin EB, Humphreys MH. Regulation of renal tubular secretion of organic compounds. Kidney Int. 2001 Jan;59(1):17-30. doi: 10.1046/j.1523-1755.2001.00461.x. PubMed PMID: 11135053.


text:
What is the focus distance of a 3D screen?
I've thought long and hard about wheter this is the appropriate section for this question, because I guess it's kind of an interdisciplinary subject.
My understanding of stereopsis (please, correct me if I'm wrong), basically depends of the way we cross our eyes when we attempt to see objects at different distances.
The more "our eyes are crossed", the greater the difference between the images we receive in each eye, which it's more effective to look at closer objects. In order for an object to be in focus, it needs to be at the point where the vision of the eyes intersect (including "at infinity" for very far away objects).
Now, with this mindset, how would such a gadget as Oculus VR work?
It consists of two separate screens (one for each eye) attached directly on an helmet-like device strapped to the user's head. It is capable of convincing 3D representations and has similar features which make it of close interest for gaming and similar applications.
So, my question is: in order to deliver such an illusion of depth, do the users' eyes need to be focused at the screen's distance, or at the represented objects' distance?
Sorry for the long question :P
Thanks in advance!

my anwer is that 3D is usaly in movie theaters with spestil glasses that are black lenes

There are a number of aspects to the perception of a 3D world. While looking into how cinema and TV 3D systems work recently, I found the following Wikipedia articles useful on how the illusion of a 3D world is generated:

Stereoscopy
Depth perception

The articles on 3D Television, 3D film and Head-mounted displays have some coverage of the issues with 3D display systems, since they do not work the same for all individuals.
Generally 3D display systems ignore convergence and accommodation as a mechanism for generating depth and instead depend on parallax and the brain being able to assemble an approximation of the 3D scene without the information from those cues.
In head-mounted display systems such as the Oculus Rift the image focus is usually at infinity.


text:
What are hot spots on human body?
Recently I have just discovered that a certain amount of the mobile phone frequency can be absorbed by human tissues.
For example, this is the SAR info of iPhone 4s:

Head: 1.180 W/kg 1 g
Body: 0.491 W/kg 1g
Hotspot: 0.491 W/kg 1 g

http://en.wikipedia.org/wiki/IPhone_4S
so hotspot means a hot spot on human body right?
Then question is:
What are hot spots on human body?

"Hot spot" does not refer to anything on the human body, but   testing while using the phone's "Personal hot spot" feature: http://support.apple.com/kb/ht4517 See also the documents on "RF exposure info" at https://apps.fcc.gov/oetcf/eas/reports/ViewExhibitReport.cfm?mode=Exhibits&RequestTimeout=500&calledFromFrame=N&application_id=134990&fcc_id=%27BCG-E2430A%27

I think hotspot in that context means the highest exposure amount as this document shows (https://apps.fcc.gov/eas/GetApplicationAttachment.html?id=1544448), which comes from the reference the above wiki page provided.

@ Bez, i don't think so, hotspot mean "if iPhone works as a WiFi hotspot" & the Wi-Fi hotspot can generate WiFi electromagnetic radiation). I opened a WiFi last time & I suddenly feel a litle bit of uncomfortable when sitting next to it so i have to turn it off. (http://www.radiationtalk.com/info/wifi_radiation.php)

The author has listed the Specific absorption rate of radio frequencies and asked about hot spots which is not something associated with the human body and is a mobile phone technology (to my knowledge). The question is just wrong and the author has not made relevant efforts to understand the topic before placing the question.

I vote to keep open. The question is reasonable and easily answerable:"Hot spots" in this context does not refer to anything on the body).


text:
How does guanidium denature DNA?
Guanidium salts like (G-isothiocyanate) disrupt the hydrophobic interactions inside a protein or nucleic acid and denature it. What happens when hydrophobic interactions in DNA are broken? (I don't think it should get ssDNA because guanidium doesn't break hydrogen bonds within molecules)

Guanidium is a chaotrope i.e it increases the entropy in the solution. It doesn't disrupt hydrophobic interactions. Guanidium and urea act by forming hydrogen bonds. They can bond with both the dissolved macromolecule and water. The water molecules are arranged as a shell around the hydrophobic regions so as to contain it, which leads to the reduction of entropy. This containment causes hydrophobic regions to come together and give rise to a pseudo-interaction (hydrophobic interaction. See the figure below). Guanidium interacts with the water shell and disorders it, thereby reducing the hydrophobic effect.
Guanidium can also interact with macromolecules directly, by forming hydrogen bonds. In this process they can disrupt the normal H-bonds in the macromolecule.

So what would its effect be on dna ?

Just think about it: a molecule which can disrupt hydrogen bonds and increase water entropy. What can it do? :)

DNA becomes single stranded ?

yes it would...

It is important to realize that the hydrophobic effect is largely due to the exclusion of water from non-polar surfaces, which increases entropy. This effect is a major contributor to the helical structure of DNA, which effectively brings the bases closer together and excludes water from contacting their hydrophobic rings. Chaotropic agents like guanidine thiocyanate increase water entropy by disrupting its hydrogen bonding network (decreasing it's order) and this makes it more favourable for hydrophobic surfaces to be exposed to water, thus denaturation can occur. Implicit in that process is that GITC is a hydrogen bond competitor, which is also evident when looking at its structure. So, in fact, GITC can disrupt the hydrogen bonds between base pairs and denature dsDNA at high enough concentrations.
That all said, we're ignoring a major component of aqueous solutions that can also form hydrogen bonds with the bases: water itself! So we must ask ourselves that if a compound capable of hydrogen bonding (water) is present, what exactly is it that holds helical DNA together? While base pairing certainly does contribute, the major factors are the hydrophobic and base stacking interactions.


text:
Breaking a gene during recombination
I just started reading about recombination frequencies of genes and related stuff, and can't find an answer to this (possibly naive) question.
Can recombination possibly "kill off" a gene ?
To be more specific, say a gene is located at position $x$ to $y$ on some chromosome.  Then, we are so unlucky that recombination decides to cut off the chromosome at location $x + (y - x)/2$, right in the middle of the gene.
So both halves will get recombined with the other halves of the gene on the homolog chromosome.  If the allele on this chromosome was different, could it result in destroying both alleles of the gene ?  Is there something that prevents this ?

Yes, you could imagine a situation where two functional alleles could produce a recombinant which was non-functional.

chromosome 1 has A and B at positions x and y - functional
chromosome 2 has C and D at positions x and y - functional
Recombination between positions x and y produces A/D and C/B versions of the gene. Either or both of these could be non-functional.

Nothing prevents this from happening, but natural selection will act on the recombinants.


text:
Silene virginica Endangered in FL
Why is Silene virginica, colloquially known as Fire Pink, endangered in Florida? What factors besides human industrialization are affecting its survival there?

Various factors from different sources:
-- Diseases like Anther Smut Disease (reference).
-- Rampant use of herbicides.
-- Invasion of exotic pest species (reference).
-- Spatiotemporal variation in the pollination of Silene virginica by the ruby-throat hummingbird which is its principal pollinator (reference).


text:
Does melatonin change the appearance of humans?
Melatonin (not to be confused with melanin) was sold as a wonder drug during the 90s. I remember images of mice, which supposedly got a more beautiful fur. I would like to know whether the effect is true and whether it also has an effect on humans skin (or appearance in general).
Obviously, googling about melatonin generates a lot of suspicious results.

Melatonin is a hormone produced by the pineal gland located in the brain, and its production is inhibited by light to the retina and permitted by darkness (reference). It has a lot of effects on the body (reference) but I will stick to just discussing its apparent effects on aging and skin.
Melatonin works as an antioxidant and helps in removing free radicals from the body (reference). Research has shown that free radicals could damage the skin (reference), so I would have to conclude that melatonin could have a part to play in maintaining the beauty of your skin.
It is a known fact that melatonin levels in the body decrease from age, and its decrease has been correlated with some of the effects of aging (reference). As you have mentioned in your question, there is research proving that melatonin could decrease the effect of aging in rats (reference). Also melatonin was found to increase the youthful rhythmic activity in a shrew (reference). In the paper titled melatonin and skin aging it has been stated that

In UV-induced solar damage, melatonin distinctly counteracts massive
generation of reactive oxygen species, mitochondrial and DNA damage.
Thus, there is considerable evidence for melatonin to be an effective
anti-skin aging compound.

Moreover in the paper titled "On the Role of Melatonin in Skin Physiology and Pathology", it has been proposed that

Melatonin (synthesized locally or delivered topically) could
counteract or buffer external (environmental) or internal stresses to
preserve the biological integrity of the skin and to maintain its
homeostasis.

So in conclusion, I would have to say that melatonin does have a lot of positive effects on the skin but, given that it is a hormone and there are side effects (reference), it should be used in moderation.


text:
A question about the intersection of evolution and thermodynamics
From this 2014 article in Quanta magazine by Natalie Wolchover there is a quote from a physicist with an intriguing idea about evolution:
“You start with a random clump of atoms, and if you shine light on it for long enough, it should not be so surprising that you get a plant.”
Jeremy England's idea is that the attributes associated with life have a lot to do with absorbing and dissipating energy. He insists he is not saying Darwin is wrong, and that his thermodynamics-based idea in some sense subsumes Darwinian evolution.
(The Quanta article links to a recent paper of England's which is somewhat technical, but deals with bacterial replication and thermodynamics. I include the link to give a sense of his ideas in his own words.)
My question is  whether his idea, taking it at face value, might furnish a better explanation of something already explained in Darwinian terms or fail to account for some detail of current evolutionary theory?
So if someone had a lot of examples of different aspects of evolution s/he might be able to say, "Here is a situation in which the thermodynamics do not work out as England suggests but which is explained in evolutionary terms," or conversely, "Here is something contrary to evolutionists' expectations that seems to be pretty well explained by the thermodynamics." I suspect that there are several candidates and England's paper gives a hint in one direction.
Thanks for any insights.
Some helpful reading:

Thermodynamics, Enrico Fermi (1936) [Dover reprint].
Understanding Thermodynamics, Ness (1969) [Dover reprint].
What is Life?, Schrodinger (1944).
Entropy Production..., Crooks (2008).
Schneider and Kay, Life as a manifestation of the Second Law of Thermodynamics, Math. and Computer Modeling 19 (6-8): 25-48 (1995).

The last paper is a very readable and non-technical introduction to this topic. If one works through the equations in Chapter 7 of Ness and ref. 4 the idea should be quite clear. Basically, systems (both nonliving and living) which are at some remove from equilibrium devise ways to dissipate energy that involve a decrease in entropy, increasing the entropy of the surrounding system.

The paper seems interesting. Thanks for sharing. I'll read it and get back :)

that article is has quite many technical details that i am not aware of.. it would take me an entire day to read through it :P

it is taking a lot of time for me too.. it is fully in thermodynamics jargons... but one of the references is good and I am reading it. It is called Handbook of Stochastic Methods

Getting long for a comment
I can only comment that evolution does not proceed towards thermodynamic optimum. Adaptation is thermodynamic optimization but evolution is directionless. Otherwise the extant species would not suffer from tradeoffs (which they have even in their usual habitat). Establishment of a self replicating cell may be thermodynamically driven and given the conditions, irreversible; macroscopic evolution is like die roll where some states are randomly⁺ selected and eliminated.
⁺Not really random but a complex non-linear function which seems unpredictable
You can imagine a chamber with particles exhibiting brownian motion. Assume that particles have a random size distribution (lets say they are crystals of different topologies). Now if you keep a separator with few holes wide enough for a just one particle of a given size to pass. Then you'll end up getting only few particles of a narrower size distribution on the other side. This no way ensures that these were the most thermodynamically stable particles.

I added a ref. to the question which I think is very helpful. The thermodynamic idea is almost certainly correct. The only question is, how does this idea relate to the idea of evolution when both are addressing the same local situation. Taking the physics idea as stated it can't be completely inconsistent with evolution. The two will point in the same direction most of the time. The question is, when might one do better than the other and why? Your example appears designed to show the two ideas are incompatible but if you read ref. 4 this seems... Quixotic.

I am sorry.. I was a little occupied with other things.. give me some time to think over it.. this is an interesting concept and I have also myself thought occasionally about thermodynamic explanation of evolution. I just echoed in the example what some "experienced" people told me. I'll get back on this.

authors: Виктор шевченка


text:
alpha tubulin molecular weight problem
Is there any academic reference that shows α-tubulin is around 50-55 kDa? The only thing I found is some data sheets from companies. I need the real reference.

The data sheet is a good enough reference. They must have showed a gel picture also. If not then find details of the protein in Uniprot.

The paper titled Identification of α-tubulin as a granzyme B substrate during CTL-mediated apoptosis mentions it as 51KDa and the paper titled Carboxy-terminal amino acid sequence of α-tubulin from porcine brain mentions it as 55,000 Da. Hope that suffices.

This is not so easy to answer, since alpha-tubulin has at 10 known genes in this family (data from Ensembl):

TUBA1A   tubulin, alpha 1a
TUBA1B   tubulin, alpha 1b
TUBA3E   tubulin, alpha 3e
TUBA3D   tubulin, alpha 3d
TUBA4A   tubulin, alpha 4a
TUBAL3   tubulin, alpha-like 3
TUBA1C   tubulin, alpha 1c
TUBA3C   tubulin, alpha 3c
TUBA8    tubulin, alpha 8
TUBAL3   tubulin, alpha-like 3

You can go on the site linked above and choose any of the proteins. I checked TUBA1A, and get a length of 451 amino acids and a weight of approximately 50,1 kDa.

authors: Бану Балапанова


text:
How many recombination events are there per generation in humans?
I'm looking for a reference that tells me how many recombenation events occur in humans from one generation to the next.
Assuming that the human genome is a 3.3 GigaBases long DNA sequence, how many recombination events do you find, and what is he amount of DNA exchanged?
Is it in the order of 0.1%, 1% oder 10%?

Back-of-the-envelope calculation
The definition of the centimorgan is that it is the length of DNA in a chromosome corresponding to a 1% chance of crossover occurring.
In human chromosomes 1 cM  = approx. 1Mbp.
Your value for the length of DNA in the genome = 3.3 Gbp = 3300 MBp
Ignoring complications like the Poisson distribution:
1 cM corresponds to a probability of 1% chance of a detectable crossover. Detectable, because only an odd number of crossing over events between 2 genetic markers can be observed as a recombination, but even numbers instead go unrecognised. Therefore the actual chance of crossing over is doubled relative to the cM value.
If 1 cM = 2% actual chance of crossover, there will be on average 1 crossover per 50 cM or per 50Mbp
Therefore crossovers per human genome = 3300/50 = 66  or approx 2-4 per chromosome
This guess comes near empiric data:
Actual data

This Table, taken from here shows the number of chiasmata by chromosome for 8 human cells. (Note that it believed that there has to be at least one chiasma per chromatid pair since they have a structural role.)
The average chiasmata per chromosome for each chromosome can be estimated by dividing the number in the final column by 8. These vary from (rounding aggressively) 3.5 for Chr 1 and Chr 2, to 1 for Chr 20. So my back-of-the-envelope calculation seems to have produced a reasonable answer.
What is the amount of DNA exchanged? I'm not sure this question matches well with the picture that emerges from these numbers.

"On average, between two and three crossover events occur on each pair of human chromosomes during meiotic division I" according to Molecular Biology of the Cell. 4th edition by Alberts B, Johnson A, Lewis J, et al. For simplicity we will call that 2.5 events per pair.
Each of those pairs ultimately forms 4 gametes. Each event connects one chromosome to another, so each individual event will leave 2 chromosomes with a location where an event has occurred. That means that in the 4 chromosomes in 4 different gametes that are produced from any single pair, there will be (on average) a total of 5 locations where a recombination event has occurred. On average then, each chromosome will have 5/4 or 1.2 locations where a crossover event has occurred.
Each human gamete has 23 chromosomes. Two gametes (1 egg, 1 sperm) unite to form an embryo. That embryo has 23 PAIRS of chromosomes, or a total of 46 (except in cases of certain chromosome abnormality). Therefore a first estimate would be that across a given set of 46 chromosomes, there would be 1.2 times 46, or 55.2 sites where recombination occurred on average.
It is important to note that the question cites 3.3 Giga-basepairs in the human genome. While that may be a reasonable estimate for the size of one complete human genome, each human has two copies of each chromosome and therefore two complete copies of the human genome. Wikipedia states that this is currently estimated to be 6.5 billion basepairs (6.5 Giga-basepairs). This distinction is significant because recombination during gamete formation in females is significantly more frequent than in males, so the genome found in a human egg cell will have many more recombination events than a sperm cell genome, therefore the average is only applicable to the entire 6.5 Giga-basepair genome.
The question about the "amount of DNA exchanged" through recombination is not really valid since total quantity of DNA in each of the four gametes produced in meiosis is exactly the same as the amount that had been contained in the original parent cell after DNA replication (but before meiosis I has produced two daughter cells). No base pair can be said to have been exchanged through recombination or not.

"Each human has two copies of each chromosome and therefore two complete copies of the human genome" - I believe that the term "human genome" refers to both sets of chromosomes together, so that each human only has one human genome.

This is not easy to answer, since it depends on a number of factors. For example it is dependent on the region of the genome (there are hotspots). I found a PhD thesis, which goes into the details here and which also has a ton of interesting references:

The Estimation of Recombination Rates from Population Genetic Data


text:
Why some neurons are tetraploid
Why are some neurons tetraploid, and how does this result from it's ancestor cell ?

Please don't ask multiple questions in a single post. Break them up into separate questions.

I have removed the second part of your  question. If you wish to ask it please make a separate question.

where did you see tetraploid neurons? provide the link to the source.

I didn't know that - interesting question!

Neurons are tetraploid in pathological situations like Alzheimer disease:

Neurons that duplicate their DNA are rarely observed to undergo mitosis, and they remain for long time as tetraploid cells, in accordance with the chronic course of the disease. We have recently shown that cell cycle re-entry and somatic tetraploidization occurs during normal development in a subpopulation of RGCs (retinal ganglion cells), giving rise to enlarged neurons with extensive dendritic trees. Tetraploization in these neurons occurs in response to the activation of the neurotrophin receptor p75NTR by an endogenous source of NGF (nerve growth factor).

Source: Frade JM, López-Sánchez N. A novel hypothesis for Alzheimer disease based on neuronal tetraploidy induced by p75NTR. Cell Cycle 2010; 9:1934 - 1941; PMID: 20436277; http://dx.doi.org/10.4161/cc.9.10.11582

These neurons are generated in response to nerve growth factor (NGF) acting through the neurotrophin receptor p75 (p75NTR), which induces E2F1 activity and cell cycle re-entry in migrating RGC neuroblasts lacking retinoblastoma (Rb) protein. We have also showed that brain-derived neurotrophic factor (BDNF) prevents G2/M transition in the tetraploid RGCs, thus being crucial for the maintenance of the tetraploid status as well as the survival of these neurons. The realization that tetraploid neurons can be readily observed in the vertebrate nervous system has important physiological consequences.
Several eukaryotes are known to undergo endoreduplicative cycles leading to somatic polyploidy, thus increasing cell size in specific tissues. Examples of polyploidy in neurons are known in some invertebrates.

Source: José María Frade. Somatic tetraploidy in vertebrate neurons - Implications in physiology and pathology. Commun Integr Biol. 2010 Mar-Apr; 3(2): 201–203. PMCID: PMC2889987

It's not all pathological. From the same second article cited:

Modern techniques such as flow cytometry, fluorescent in situ
  hybridization (FISH), slide-based cytometry (SBC) and quantitative PCR
  analysis of DNA from isolated nuclei can all reliably quantify the
  amount of nuclear DNA in neurons.11 By using SBC, flow cytometry and
  FISH, we have recently demonstrated that tetraploid neurons exist in
  the normal vertebrate retina, representing a subpopulation of RGCs
  that, in the chick, innervate lamina F in the
  stratum-griseum-et-fibrosum-superficiale of the tectal cortex.12 These
  neurons are generated during the early stages of retinal development,
  soon after they acquire neuronal markers. Indeed, a subset of
  migrating RGCs expressing the transcription factor E2F1, and lacking
  Rb protein, was observed to undergo S-phase and remain in a permanent
  G2-like state. Therefore, endoreduplication, but not alternative
  mechanisms such as aneuploidy or cell fusion,13,14 represents the
  mechanism generating tetraploid RGCs in the vertebrate nervous system.

Can you add what article you quoted this from (either a link to it, or reference to the book or journal where it could be found).