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What is the evolutionary rationale for palm sweating?
Sweaty palms seems to be a reaction to stress, anxiety, etc. For our forest-inhabiting primate ancestors sweaty palms could cause unwanted side-effects such as slipping off tree branches under stressful conditions, like when being chased by a predator.
Why did palm sweating became a reaction to fear, worry, anxiety etc in the course of human evolution? What is the benefit of sweaty palms?

Sweat in response to stress is not limited to palms. Sweat glands just happen to be there I guess.

I guess the question is why do our palms sweat at all(?) because the OP has given an example of when sweaty palms are (possibly) a disadvantage (maybe slightly moist hands grip better). I am not sure of the advantage myself, perhaps because of the absence of hair on the palms they are useful for rapid heat loss which would be further increased if the palm is sweaty.

Many animals use palm or sole-derived sweat for scent marking, so there may have been an evolutionary pressure for retaining sweat glands on the palms. If the negative selective pressure wasn't large enough in primates, then there wouldn't be any reason to lose palmar sweat glands.

When the sympathetic nervous system is aroused, it has historically been for life threat situations, and in those situations historically there have not been a lot of slick things to grip or run on, but rather porous things. Those things, like sticks or rocks, were easier to grip or push off of or climb upon with a little moisture. Think of when you were a kid and you climbed a pole. You wanted your shoes off for that, didn’t you? And you wanted a little sweat because dry feet would slip. Same for if you’re wielding a branch or a bone or a rock as a weapon. That seems, to me, to be the primary

Do the top parts of our hands sweat? I can imagine that sweating palms gave a better grip on certain surfaces that were abundant.

I remember watching a documentary about person with arm transplant. He was complaining about the fact his transplanted arm did not produce any sweat and as result daily objects were often sliping from his fingers. I will try to find the reference.

As @Ben states, every theory of 'why' we evolve a trait is just a guess and never more than part of the story.   But there are theories.
The palms of our hands are a major source of heat transfer out of our body.  For bears it is the nose and pads of their feet, for dogs it is their toungue, for us a major portal for heat out of our body is the palms of the hands.

Black bears are extremely well-insulated animals, equipped with a heavy coat of fur and a thick layer of subcutaneous fat that help them maintain their body temperature as they hibernate through winter. But once spring arrives and temperatures rise, these same bears face a greater risk of overheating than of hypothermia. How do they dump heat without changing insulation layers?
Heller and Grahn discovered that bears and, in fact, nearly all mammals have built-in radiators: hairless areas of the body that feature extensive networks of veins very close to the surface of the skin.
Rabbits have them in their ears, rats have them in their tails, dogs have them in their tongues. Heat transfer with the environment overwhelmingly occurs on these relatively small patches of skin. When you look at a thermal scan of a bear, the animal is mostly indistinguishable from the background. But the pads of the bear's feet and the tip of the nose look like they're on fire.
These networks of veins, known as AVAs (arteriovenous anastomoses) seem exclusively devoted to rapid temperature management. They don't supply nutrition to the skin, and they have highly variable blood flow, ranging from negligible in cold weather to as much as 60 percent of total cardiac output during hot weather or exercise.

Given this, one could see how the palms of our hands are more likely to react to emotional situations where the heart rate elevates and sometimes we get hot under the collar.  The AVAs will
I am not physiologist, but the quote above comes from an article I stumbled upon a few months ago.  They use the AVAs to reduce the swelling associated with exercise and got some amazing results.  I guess that's another story though.

There isn't necessarily a nice neat evolutionary rationale or advantage behind all of the observable traits found in all organisms.
It's perhaps more likely that there simply was not enough selection pressure against having sweaty palms to eradicate it from the gene pool entirely.

I think this should be posted as a comment on all questions that have the title "why does X evolve?" - too often people assume there is some great reason for something to evolve and persist and reason that redundant traits should disappear immediately via selection. However, I don't think this answers the question, there are theories out there such as the answer by @shigeta

It is almost certainly to improve grip.  There is a different type of sweat gland (eccrine sweat glands) in the palms and soles.  The sympathetic nervous system (one feature of which is epinephrine / adrenaline) feeds those glands, so if something is scary or tense they kick in.
Our ancestors were in trees.  Our close relatives still are.  Scary situations often means moving fast through the trees.  Or it is scary because you are about to fall!  Either way you need your good grip: hands and feet both back in those days, or for our great ape cousins.
A little bit of moisture makes hands much more grippy.  Especially if your hands are not very clean.  People sometimes spit on their hands to improve grip.

Because feet and hands touch so many things, I would think that sweat would help act as a protector from various pathogens as well as scent marking, heat transfer, or stress symptoms.  Both the salt and fluid in sweat might wash some pathogens away.

you need to add some background and rationale for your answer - see comment above... otherwise this is not reasonable for this site.

It was advantageous for our ancestor's grip while tree climbing millions of years ago, so the best current theory claims.

Welcome to Biology.SE! It isn't clear that this adds anything to the existing answers. In addition, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. Thanks!


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Gene & Protein nomenclature: N-Myc, c-Myc, et. al
Can someone explain (or point me to an explanation of) exactly what is meant by all the different symbols I see used for writing genes and proteins?
I think I know that for genes, we use an italic font and for proteins, we use a regular font.
I think I've also learned that for human, all letters are in uppercase (eg. SHH) whereas for mouse, only the first letter is in uppercase and the remaining letters are in lowercase (Shh). (From http://en.wikipedia.org/wiki/Gene_nomenclature)
But I'm stumped with all the other "tags" (in quotes because that's how they seem to be used and I don't know how else to think of them) that I see floating around gene and protein symbols.
For example, Myc (MYC?).
I see these three articles in uniprot.org:
http://www.uniprot.org/uniprot/Q99417 for C-Myc
http://www.uniprot.org/uniprot/P04198 for N-myc
http://www.uniprot.org/uniprot/P12524 for L-Myc
These proteins are all in human, and yet their recommended names are not all caps; what's up with that? But even more confusing to me are the "C-", "N-", and "L-" letters prefixed to them. What in the world are those supposed to be indicating?
Are these all fundamentally different proteins (coded by different genes), but maybe related somehow to each other (thus the common three letters, 'myc' even if they are not all the same case and not all upper case as I thought was supposed to be the case in human), and they are just given these "C-", "N-", and "L-" tags to distinguish one from the other? Does one tag indicate an oncogene or a proto-oncogene? Why do I sometimes see "c-Myc" and other times, "C-Myc"? Does the case of the "C-" mean something? Is there some kind of key or legend I can look at to get answers to all these questions? I've found some explanations in Scott Gilbert's Developmental Biology textbook, but it still doesn't give me all the answers I seek here
I just want to understand how these tags and symbols are being used because it seems to me that when I read research papers (of which I've read many), they are used by different authors in different papers in ways that are not consistent with each other. Either that, or else I'm missing something very basic, which is why I'm asking here.
Thanks in advance for any help.

That's a good question, and honestly, the nomenclature for genes and their coded proteins is somewhat abused in scientific literature. For example, when referring to microbes (like E. coli), gene names are all lowercase (eg, lacZ). The problem of protein names is compounded when the protein name is (often) an abbreviation.
With respect to myc, it can refer to the family of MYC transcription factor proteins (of which, c-Myc, L-myc and N-myc are members). More commonly, myc refers to c-Myc, and is the name given to a 10-amino acid segment of human proto-oncogene myc (EQKLISEEDL) and is a common epitope added to recombinant DNA for making fusion proteins.
From what I recall, the initial that precedes myc (in this instance) refers to what form of cancer that myc protein is associated with. I know c-myc comes from a mutation in wild-type myc that becomes constitutively expressed. Wikipedia tells me that N-myc is a neuroblastoma-associated myc transcription factor.

"somewhat abused"? Now that's un understatement if I ever saw one, just pick any five Drosophila gene names. I even have an uncle who named two genes after his dog!

I was being polite. ;) Which genes are those?

Phaedra1 and Phaedra2. Yes I know who Phaedra is but trust me, the genes were named after the dog.

Thank you. Both answers help me a great deal. Preceding initial from associated cancer, so "N-"=neuroblastoma. Didn't know that. Also didn't know about epitope EQKLISEEDL as myc. How to distinguish between epitope myc and gene myc then (aside from context maybe)?

This response is wrong, the answer below from Alan should have been accepted... There's more information in this review article for example

There is a useful set of links to nomenclature guidelines for all of the main genetic systems at this Wikipedia page. Personally, I think that the Saccharomyces cerevisiae system works best: it manages to cover dominant and recessive alleles of a gene, the name of the protein, how to refer to a related phenotype, and the use of a parallel convention for the designation of ORFs.
Unfortunately there is now no going back - there are many different systems and there is no hope of unifying them. When this plethora of naming conventions is combined with the reluctance of so many scientists to stick to the guidelines, we have a recipe for near anarchy.
Edit - On the specific topic of MYC nomenclature:
The v- and c- prefixes come from the early days of oncogene research. Viral oncogenes such as myc and src were found to be related to (derived from?) similar genes in normal cells. Thus v- means viral and c- means cellular.
This can be seen if you peruse the HUGO entries for the four MYC family members encoded in the human genome (extracts below). They all have an approved name which relates them back to a viral oncogene found in the genome of avian myelocyomatosis virus. This was the founder member of this gene family. Thus c-myc was the first myc-related gene found in the human genome, and is the one that is responsible for Burkitt's lymphoma. It is true, as @Leonardo says, that in tumours the expression of this this myc gene in lymphatic tissue changes due to chromosomal rearrangements, but this is not the origin of the designation c-myc.

MYC
  Approved Symbol:      MYC
  Approved Name:   v-myc myelocytomatosis viral oncogene homolog (avian)
  Previous Symbols & Names:   "v-myc avian myelocytomatosis viral oncogene homolog"
  Synonyms:   bHLHe39, c-Myc
  Chromosomal Location: 8q24
MYCL1
  Approved Symbol:      MYCL1
  Approved Name:   v-myc myelocytomatosis viral oncogene homolog 1, lung carcinoma derived (avian)
  Previous Symbols & Names:   MYCL, "v-myc avian myelocytomatosis viral oncogene homolog 1, lung carcinoma derived"
  Synonyms:   bHLHe38, "l-myc protein", LMYC, "myc-related gene from lung cancer", "oncogene lmyc"
  Chromosomal Location: 1p34.3

MYCL2
  Approved Symbol:      MYCL2
  Approved Name:   v-myc myelocytomatosis viral oncogene homolog 2 (avian)
  Previous Symbols & Names:   "v-myc avian myelocytomatosis viral oncogene homolog 2"
  Synonyms:   bHLHe38
  Chromosomal Location: Xq22-q28
MYCN
  Approved Symbol:      MYCN
  Approved Name:   v-myc myelocytomatosis viral related oncogene, neuroblastoma derived (avian)
  Previous Symbols & Names:   NMYC, "v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived"
  Synonyms:   bHLHe37, N-myc
  Chromosomal Location: 2p24.3

Thank you. Both answers help me a great deal. Preceding initial from viral (v-) or cellular (c-). Didn't know that either. Regret that it seems I cannot accept both answers, but thank you both.

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Vaccination and population dynamics of an epidemic
I'm trying to figure out how should a vaccination model be built to correlate with population density, and I'm having problems to understand meanings of the results I receive when I apply theory on specific data I'm provided with.
Theory(i):
The initial phase of an outburst of a disease can be described by an exponential growth
model. The relevant equation is:
$(1)\frac{dI}{dt}=\beta n(1-q)I-\mu I$ where:
$n$ = the population density. Let us measure it in units of $km^{-2}$.
$I$ = the density of already infected individuals in the population; measured in the
same units as $n$.
$q$ = the fraction of the population that is immune to the disease, either naturally of
due to vaccination. Consequently, $1-q$ is the fraction of the population that is
susceptible, i.e., at risk of getting infected. $q$ is a pure number between $0$ and $1$,
and has no units.
$\beta$ = is the transmission rate of the disease. It measures how easily and quickly
the disease can be transmitted from an infected individual to an non-infected
susceptible individual. $\beta$ includes within it both the rate at which encounter
between infected and non-infected individuals occur, and the probability that
such an encounter would result in actual transmission of the disease. $\beta$ has
dimensions of $\frac{1}{time\times density^{2}}$, so let us measure it in units of $week^{-1}km^{4}$.
$\mu$ = the rate at which infected individuals are eliminated from the group of
infected individual, either because they recover, or because they die. $\frac{1}{\mu}$ is the average duration of the infection, i.e., the average time that an individual remains
infected before it either recovers or dies. Let us measure $\mu$ in units of $week^{-1}$.
This equation derives from the differential equation $(2) \frac{dN}{dt}=rN$ where $r$ is called instantaneous rate of increase. It is easy to see that $I$ from equation $(1)$ is equivalent to $N$ from equation $(2)$ and therefore, $r$ for equation $(1)$ will be $(3) r=\beta n(1-q)-\mu$. When we look at equation $(3)$, we see two factors:
$\beta n(1-q)$ - A positive factor(ii)
$\mu$ - A negative factor
Minding the above, when $r=0$, there is no increase in population(iii). From this, we can compute $q_{0}$ which is the minimum fraction of vaccinated/immune individuals in the population that is required in order to prevent the disease from spreading. From equation $(3)$ we can figure out that $q_{0}=1-\frac{\mu}{\beta n}$. Just as $q$, $q_{0}$ is a pure number between $0$ and $1$.
Welcome to the desert of the real (my question):
Suppose we compare two countries with the following data:

Israel: $n=347km^{-2}$, $\beta=0.0015week^{-1}km^{4}$, $\mu=0.25week^{-1}$
Finland: $n=16km^{-2}$, $\beta=0.0015week^{-1}km^{4}$, $\mu=0.25week^{-1}$

When we look for $q_{0}$ for Israel we see that $q_{0}(Israel)=1-\frac{0.25}{0.0015\times347}=0.52=52$% while for Finland we see that $q_{0}(Finland)=1-\frac{0.25}{0.0015\times16}=-9.42=-942$%. Assuming that we've got correct data in the first place, $q_{0}$ is a negative pure numbers which is not between $0$ and $1$.

Do such, and similar results make any sense at all? Especially when they are not between the defined boundaries of the variable.
If they do make sense, what does it mean getting a negative results? How should it affect my vaccination policy?

Footnotes:
(i) Taken from my Populations Ecology lecture slides
(ii) Positive when looking at it from the epidemic point of view
(iii) Of infected individuals

You should ensure that the basic reproductive number for your Finland model is capable of sustaining an epidemic without vaccination.

@EpiGrad In other words, I need to make sure that the epidemic will keep on being at least stable without vaccination?

Yes, that's correct.

According to this we increase μ when we quarantine infected ppl.

I think it does make sense - with a population density for finland that is so low, the disease with such a low beta cannot communicate to enough people to propagate.
The number of people who have this disease will be fewer each week.  I think this makes sense because at 16 / km^2, you can expect that practically nobody will ever see each other.
This is a flawed model though because it assumes that the mean density is uniform.  In a city like Helsinki (2,800 / km^2) you would expect the disease to get caught by nearly everyone in just a week.
Helsinki: n = 94.5%
In Lapland (which has a population density of less than 2/km^2) , the transmission rate (beta) of 0.0015 translates to 0.003 incidents per week.  This is not a terribly catchy disease, you probably have to kiss someone, wear their clothes, or eat off their plate to get it. With only 2 people per km^2 the chances of this happening appear to be poor, though even here families tend to get the disease and the model breaks down.
So to sum up, the model is consistent within itself, BUT it is a baby model and makes some broad assumptions that do not help it describe the dynamics of the disease in a national scope or in a highly detailed scope.  It probably describes the chances balls will collide in a box as well as disease spreading.

So basicly, I shouldn't be strictly bound by 0<q0<1 in this case and use this only when the epidemic is self-sustained even without vaccination (as pointed by @EpiGrad in comment to the original question)?

Yes - this is an important point - if we include the social an economic costs of immunization sometimes we don't do it.  This was the case with tuberculosis.  In Europe, which has more borders and denser population (at the time) they used a vaccine which is effective 60-80% of the time (BCG).  In the US we decided to pass on that and use the skin test for prevention and detection (the vaccine makes you a false positive).  The difference is primarily in the number of patients and the density of the population at the time.

Reading through wikipedia, this looks like a standard deterministic model, but there is a description of multi-compartment models which would account for different populations or different subregions in a model...  http://en.wikipedia.org/wiki/Epidemic_model#Models_with_More_Compartments

"I think it does make sense - with a population density for finland that is so low, the disease with such a low beta cannot communicate to enough people to propagate. " - This is not necessary accurate, it depends on population density, social habits, level of technology, etc... how often ppl meet...

I don't think this model is valid by STDs like HIV.

" It probably describes the chances balls will collide in a box as well as disease spreading. " +1, I agree with that. Btw. do you know of better models?

I can imagine a model that explicitly tracks individuals and disease transmission events would work better.  Its not my field though, I'm just reading what you have here.

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Does the DNA sequence of a butterfly match that of the caterpillar it used to be?
Just had this thought occur to me.
If one were to take a DNA sample(or is it RNA?) of a caterpillar before it became a chrysalis, and attempt to match the sample against one taken after the chrysalis matured to a butterfly, would the two samples come up identical?

By 'signature' do you mean sequence? Is the sequence of caterpillar DNA the same as the sequence of butterfly DNA? And if you do mean this you probably need to differentiate between somatic cells and germline cells in the butterfly.

@AlanBoyd: DNA Sequence is probably what I had in mind. That thing the Ministry of Law use to definitely identify a person...

Sometimes a caterpillar turns into a wasp rather than a butterfly. But then its DNA Is very different! (And it doesn't go on to make more catterpillars)

The genome (entire DNA sequence) of the butterfly would be identical to that of the caterpillar in all somatic cells.  A caterpillar has the genes to produce wings, for example, however at that stage in it's development they are not 'switched on' to make the necessary proteins.
If you were to sample the mRNA produced from transcription of the DNA in the caterpillar and butterfly stages, there are likely to be many differences.  As in the example I previously used, the mRNAs that are translated into wing-forming proteins are more likely to be apparent in the butterfly than the caterpillar.  When saying this, please be aware that I'm assuming that the regulation of these genes is pre-transcriptional - I'm not an expert of butterfly physiology!

Forgive me, but would it be possible for you to elaborate on 'pre-transcriptional' ?

@Everyone there are several points in protein production where regulation can happen to stop it being produced - this happens naturally (for example there is no benefit to producing chlorophyll in root cells where there is no light).  Some of these points are before the DNA is transcribed into mRNA (pre-transcriptional) - if the gene is being suppressed here then there should be no template mRNA produced that could be detected.  If it was being regulated post transcriptionally then mRNA would be present (though likely in small amounts before being degraded).

Alan Boyd's Answer suggests that there is more going on than just gene suppression/expression, however.

@Rory M
Here is evidence for developmental genome rearrangements in Hymenoptera. I have emphasised the relevant section of the Abstract. It is probably premature to assume that similar changes might not happen in somatic cells of some Lepidoptera.

Bigot Y, Jegot G, Casteret S, Aupinel P, Tasei JN (2011) DNA modifications and genome rearrangements during the development and sex differentiation of the bumble bee Bombus terrestris. Insect Mol Biol. 20:165-75.
Abstract
Bombus terrestris is a bumble bee that, like most hymenopteran species, exhibits ploidy-specific sex determination controlled by a single sex gene. Depending on their ploidy and the queen pheromone repression, the imagoes differentiate into three castes: males, workers and queens. Here, we focus on the differences of genome organization that occur during development and sex differentiation. We found that cytosine methylation is a significant epigenetic factor with profiles that can be correlated with both processes. We also showed that two kinds of genomic rearrangement occur. The first consists of important DNA amplifications that have sequence profiles that differ in the different developmental instars and sexes. In the second kind, DNA losses also occur, at least involving the mosaic transposable element B. terrestris mosaic repeat 1 (BTMR1).

True, but the genome sequence is still the same.

@nico I don't understand what you mean. If two cells differ because in one of them a region of the genome is  amplified (e.g. single copy > tandem repeats) then the genome sequences are different. There may be no appearance of DNA with a novel sequence, but I don't think that anyone would argue that the two sequences were identical.

sorry, forget my comment, I had read the quote too quickly and thought it was just speaking about epigenetics.

@AlanBoyd I imagine the germline cells' DNS remains the same?

I would like to expand on Rory's answer.
You can think about the DNA like a very complex book of recipes (genes) for constructing cellular machinery (e.g. proteins). Every genome has a large repertoire of machines that it can construct. For a given organism, all its somatic cells will have the same DNA (more or less, but let's put that aside) since it starts out as a single cell. In spite of this, you can see that cells can have completely different shapes and functions. For example, look at how different a neuron is from a muscle cell or a blood cell in terms of shape and function. In addition, cells can change in reaction to their environment.
Then how is the repertoire the same but the cells completely different?
The solution is choosing which genes to activate. This is the called gene regulation and is an extremely complex system as you might guess. It is to some extent the "brain" of the cell, with which the cells can make decisions and gain its plasticity in biological function. This system operates on many levels, one of them being by controlling transcription, i.e. transcriptional regulation, which controls how much RNA to make from each gene, which will later translate into some level of activation (no RNA means the gene will not be active). This is why the RNA will probably vary widely according to the cell type and cellular state.
In general, each species have a similar DNA sequence give or take some minor variations. The sequence of family members will be even more similar, and the sequence of clones (e.g. identical twins) will be virtually identical. This type of variation is random and thus will not be used as a control system. From this you can already guess that the change from caterpillar to butterfly will be controlled by its gene regulation program, as it is a developmental change, in the same way as a human grows from a single embryonic cell.
That said, it is always possible that some random changes occur somewhere along the way and would cause differences, as biology is stochastic. However, for these to be consistent between all cells in the organism, they would have to happen when the organism is a single cell, which is not the case when transitioning from caterpillar to butterfly.

Here's an interesting story from npr.org, Are Butterflies Two Different Animals in One? The Death And Resurrection Theory.
Apparently some people are proposing a theory that says (heavily paraphrased) that a butterfly is actually two different ancestral species rolled into one. This is the relevant quote:

The old view was that over millions of years, animals evolved this habit of switching from one set of instructions to the other. The new view is that this is not one animal gradually changing shape, but rather instructions for two different animals sandwiched together and this change is so radical, says Bernd, "with no continuity from one to the next, that the adult forms of these insets are actually new organisms."

Far out.

And a chicken is a new organism, radically different than an ovoid, calcium-covered egg.

That's a bit different of a scenario ... or do you look at a carton of a dozen eggs and classify them as 12 living and breathing organisms sitting on a shelf?


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What is the inlet/outlet speed of air going in/out of our mouth during inhalation/exhalation
During inhalation, your alveoli expand, creating a pressure difference between the atmosphereic pressure and our lung sacks and therefore air will flow into the repspiratory airways.
I am trying to find what the (I guess average) speed of this flow is, and therefore estimate the pressure difference. I have spent some time online trying to find this, but I have not got a definite number yet. It should be an order of magnitude of 1 m/s ?

See Speed of Exhalation

I'm thinking this may be hard to answer due to: (1) Different people breathe differently and (2) breath seems to "accelerate" if you will (I start out breathing slowly than end quickly with each breath). So do you mean the average of breath span? Or the average per person? Or the average per person per breath span?

Just the average

Quick clarification firstly, the main change in thoracic volume that causes inspiration is not as a result of the alveoli expanding - they have no smooth muscle lining therefore are unable to spontaneously contract.  They do have some elastic fascia however their expansion is passive. The change is mainly as a result of the diaphragm contracting to become flatter, increasing the space that the lungs can occupy.  The external intercostal muscles also raise the ribs (in adults) which further allows for inspiration.

Figure One: Inspiration and Expiration(1).  "Rib muscles" refers to the external intercostal muscles.
With that being said, the value I think you are looking for is peak expiratory flow.  Peak flow is a common medical measurement that is often taken in the management of patients with respiratory conditions, either as part of their management plan or acute assessment.  Peak flow is a measurement of the maximum speed that a person can exhale at.
As the comments on your question suggest, this varies dramatically between person to person.  Ignoring any pathologies - such as asthma, chronic obstructive pulmonary diseases (COPD) or nerve damage to the diaphragm/intercostal muscles - peak expiratory flow varies primarily with age, gender and height.  These variations are summarised in charts of expected peak flow that are used, amongst other things, to grade the severity of an asthma attack (and consequently how aggressively to manage it).  Charts resemble the following:

Figure Two: Normal values for peak expiratory flow used in UK hospitals - The EU Scale (2)
So if you pick the height, gender and age that you feel is appropriate for your question, you can then read off peak flow in litres per minute.  Then you would need, I think, to work out the area of the aperture (in your case the mouth) to get a speed in metres per second?

Medina B. Brenda's A&P eportfolio: objective 48 & 49: inhalation and exhalation [Online]. 2011 [accessed 2012 Dec 11]. Available from URL: http://blm1128.blogspot.co.uk/2011/04/objective-49-contrast-inspiration-and.html.
Häggström M. File: normal values for peak expiratory flow - EU scale.png [Online]. 2009 [accessed 2012 Dec 11]. Available from URL: http://en.wikipedia.org/wiki/File:Normal_values_for_peak_expiratory_flow_-_EU_scale.png.

Figures 4 and 5 of "Airflow Dynamics of Human Jets: Sneezing and Breathing - Potential Sources of Infectious Aerosols" appear to provide the requested information (Figure 4 is for nasal breathing); the paper also comments that "units of airflow rate (litres per second)"  "are difficult to convert to comparable airflow velocities (in m/s)".

I'm not sure this is a great answer, but since no-one else has stepped up: it will vary a great deal depending on what you're doing.
According to Wikipedia the tidal volume for a breath is typically about 500 cm$^3$, so you can work out the velocity from the time taken for a breath and the cross sectional area of the mouth. The trouble is that the breath rate varies enormously e.g. from resting to running a marathon. Also would you take the cross sectional area of the lips, or the larynx, or some other point in the respiratory tract?
In any case under most circumstances I doubt the limiting factor during an inhalation is the pressure difference. I suspect it's more likely to be how fast the ribs can expand. It seems to me that if I take a sudden breath and try to stop halfway through, the inhalation stops immediately. If the limiting factor were the pressure difference I'd expect the air to keep flowing in after I'd stopped trying to inhale.

But as you expand your lungs, you create a pressure difference between the the ambient air and you lung sacs. . If you stop expanding you will stop creating a pressure difference, therefore stop the flow. The pressure difference reduces as the air flows into your lung sacs, this happens fast I presume, that´s why the flow stops if you stop expanding.

Yes. I guess the point is that the pressure difference is going to be very small. It also won't be the same everywhere in the lungs. I'd guess the main pressure drop in the small tubes to the alveoli rather than in the throat, trachea or bronchioles. So it's the velocity in the small tubes that matters, not the exhalation velocity.

btw... if it takes about 2 seconds to get 500 cm^3 of air into your lung sacs, then Q = 250 cm^/s * (1m/100cm)^3 = 0.00025 (m^3/s). Then the volume flow rate is Q = Velocity * Area and therefore Velocity = Q/Area = 0.00025/(pi*(9*10^-3)^2 = 1 m/s if the cavity of the mouth is approximated as a tube with radius equal to 9 mm. Seems like the velocity is approximately 1-2 m/s


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What to look for when buying a light microscope?
I am a science lover and want to buy a microscope to explore things around me. Like studying cell structures, microorganisms, blood and plants. It would be great if there is way to photograph slides. Just curious to know and explore things around me.
I want to know which features I should consider while buying it?

...and your question is?

To clarify how you could edit your question to make it more suitable for the site, we'd be happier to answer a question asking for an explanation of which features to look out for when purchasing a microscope.

Light. Literally. When I got a microscope as a kid, it was supposed to be lighted with a mirror, which made it hard to find a good setting sometimes. It  was the most frustrating thing about it (for me as a kid).

honestly, save your $,  build your own using parts from Edmonds. Unless your super $$$ not gonna get a very good. this isn't like toyota vs hundae. There are only two manufacturers of microscopes, the prius type (ebay) and the lamborgeini type (zeiss, olympus and leicA). try to get a higher end objective and build your own scope. Optics and light paths are good skills to have too. but i default to @guest below, nice presentation.

Well it depends on the application. First you have to determine what it is that you want to view under the microscope e.g. an organism such as Drosophila or you want to see microscope slides? In the first case you need to by a dissecting microscope, otherwise you need to by an upright light microscope with the appropriate objective lenses, again depending on the application. If you are viewing cells in a flask/dish/plate in a cell culture setting or if viewing a haemocytometer (although not necessarily in the case of haemocytometer), you need to buy an inverted light microscope with phase contrast since you wouldn't be able to view the cells very well with an upright microscope since the goal is to reduce the distance between the objective and the sample for a better view of the samples in cases of dishes or plates. Again the choice of equipment depends on the application. But as correctly said above you need to clarify what you mean in the question.

My advice is always the same: "first microscope? keep it simple, keep it cheap, but nevertheless: buy something usable".
This Olympus GB is, IMHO, "something simple/cheap/usable":

These can be bought here second-hand for anything between € 50 and € 100. It's an uncomplicated stand, easy to overhaull yourself. It permits the use of any optics you would like, it has a nice Abbé-condenser N.A. 1.25. It's heavy,  sturdy and reliable.
These are some of the microscopes I bought second-hand over the last few years. None of those was more than 80 Euro's/US$, except the Diapan (lower right). All were in reasonable condition and ready to use, except one. Notice the build-IN 6V-15W illuminator in the Zeiss GF stand (lower middle), versus the build-ON 12V-100W HAL illuminator in the Reichert Diapan (lower right). See the text:

And if you're handy and not affraid to work it can be even cheaper. This one was for free and it turned out to be one of the best stands I ever had:

Perhaps this can help: it's a (partial) checklist on what to look for when buying a second-hand microscope.
I don't have absolute "no-no's": many problems can be solved, but sometimes it takes a lot of effort, time and cursing...
Sometimes a stand is junk, but it has excellent optics. Or the other way around.
You should take into account that having a microscope (seriously!) serviced/repaired is usually very expensive: a company here, known for their high quality work and their very reasonable prices, asks for a complete overhaul of a microscope genre Zeiss Standard 14/16 a fixed price of slightly more than 700 Euro, spare parts not included... On request they do it on an hourly basis as well: 120 Euro/hour. They do an excellent job, but well... it's not cheap.
1. A first glimpse
Brief examination of a second-hand microscope would take half an hour, up to an hour, depending on how sophisticated it is and on how experienced you are.
You're allowed to be exited and thrilled, but don't loose your critical sense! It's only a microscope. Plenty of those and there are far more important things in life.

Microscope complete, all parts present, all same brand and same
generation (do your homework!). All knobs, screws, gears... present as far as one can see
Suitcase present and in reasonable condition, key present if one is needed, factory certificate present, user manual present
Microscope reasonably clean, no excessive dirt, no severe traces of
corrosion or fungus (if fungus is present, even in very small
amounts: carefully check all optics!). No excessive traces of extremely heavy use. Check aperture diaphragma dial, field diaphragma dial, surface of the stage, x- and y- dials of the stage if present, the surroundings of the focusing knobs, the nosepiece...

Spider webs and dirt on a vintage microscope, stored for decades on an attic. Turned out fine:

Microscope doesn't spread strange smells: fungus, dish soap, cleaning naphta, white spirit, xylene, ethyl alcohol, hexane, greases and/or oils, "creeping oil" such as WD40 or CRC... A microscopes "treated" with creeping oil is about the only absolute no-no I have: these oils do what they're supposed to do: creeping in everywhere, including in the optics
Microscope doesn't show any trace of a fall or a punch. If that kind of damage is present, decent repair should be demonstrated beyond any doubt by official documents only, excluding hearsay: repair costs estimates, invoices, correspondence between owner and insurance company if applicable etc... (observe serial numbers in those documents. They're there for a reason!)

Damage due to a drop in a Zeiss Standard microscope. A cleaning lady dropped it accidently, while cleaning a college lab. Accident and repair were well documented. Replacing it would have been less expensive, but the insurance company insisted on a repair, which was done in the Zeiss factory. Nearly all parts were replaced, except for the base of the stand, as that was considered "cosmetical damage" only. The microscope was equipped with high end optics and the price was modest. A steal:

All adjustments (coarse and fine focussing, nosepiece, condenser height adjustment, aperture diaphragma, field diaphragma, movements of the stage, eventualy present internal magnification changers, Bertrand lenses, polarizers, ... work well over their entire range. Use your senses: sight, hearing and, most important: your tactile sense. Be very aware of "strange things" when using the settings: scratching noises/feel, ticking noises/feel and so on. Might be a minor problem, such as a small lump of dried out grease. Or might be a broken/stripped tooth gear... Very stiff controls, even up to the point of being completely "frozen up" are usually not that big a problem. However, keep in mind it might be necessary to dismantle the microscope completely to solve the problem. That means: dismanteling, cleaning and degraising, regreasing using the right lubricants in the right amounts at the right places, reassembeling and alligning the stand. It's not rocket science, but it is a lot of work! Pay attention to the leafs of iris diaphragms: these should always be dry, and free of grease or oil

Dismanteled coarse and fine focusing controls of a Zeiss Standard. Notice the ingenious construction using a planetary gear:

2. A closer look
3. Microscope under the microscope
Second-hand microscope buyer's best friend: a phase telescope:

"Minor" optics problems...
Seeped in immersion oil and degraded lens kit in a Hensoldt 100/1.30 achromat (awaiting a go for repair, succes unlikely):

"Small scratch" and extensive delamination in an Aus Jena apochromat 40/0.95 (garbage bin):

Unsetting fungal growth in an Olympus 10/0.25 achromat (repaired):

4. Using it
Counting dots/objective testing using test slides: I'm no fan:

Continues: work in progress...

"Continues: work in progress..." please continue, this is very interesting!

Have you seen http://www.microscopy.org/education/projectmicro/buying.cfm?
You can find your answer if you have such questions about buying a light microscope.

What kind of microscope should I buy? But I only have $50-100 to
spend; does that mean no microscopy? What type should I buy? What
features should I look for? I see a lot of other features advertised;
which ones are worthwhile? Can I check lens quality? What about
buying a used microscope? I see a lot of great deals on eBay. Where
do I find these microscopes?


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What vegetation would thrive in the Martian atmosphere?
Most plants require carbon dioxide for their photosynthesis, which Mars has in overabundance.
Would atmosphere composition (let's ignore temperatures for the purpose of this question) of Mars allow vegetation to grow?

Check out the answer here http://biology.stackexchange.com/questions/1242/what-is-the-lowest-pressure-at-which-plants-can-survive

This is not my field by a long shot, so take what I say with a grain of salt. However, this question is very hard to answer because whether or not a plant will grow depends on a great variety of factors. Even if we ignore the temperature as you say, there are other considerations. These include, but are not limited to:

Soil composition, I doubt that Martian soil can support earth vegetation even if its atmosphere could. Plants need various nutrients, and specific pH ranges among other things.
Atmospheric pressure, I am not at all sure that the Martian atmosphere (though it is, indeed rich in CO2) would be enough to drive an earth plant's photosynthesis. Bear in mind that the atmospheric pressure on Mars averages 600 pascals (0.087 psi), about 0.6% of Earth's mean sea level pressure (source). This makes it highly unlikely that unmodified earth plants would be able to thrive there.
Water water water...
Pollinating species. Many many plants depend on other species (e.g. bees or hummingbirds) for their propagation. These would be hard to find on Mars.
Sunlight I don't know if Mars receives enough sunlight at its distance from the sun to drive an unmodified plant's photosynthesis.

Now, that said, it should theoretically be possible to start with some extremophile archaea or bacteria that would over the course of many many many years (at least hundreds, thousands more probably) terraform Mars to make it suitable for human habitation. Specially engineered plants could play a role then but I find it very hard to believe that any existing, unmodified, multicellular plant life of earth origin could survive on Mars.

i know mars soil will not be up to the task as we know it is highly acidic, i'm just wondering about the atmospheric composition alone

@lurscher I'm just pointing out that the atmosphere alone is meaningless. In any case, even if everything else were OK, there is probably not enough atmosphere on Mars to provide sufficient CO2 to unmodified plants.

I'll stick to considering the atmospheric composition, as referred to in the original question: Although there may be some rare exceptions that I can't recall, under normal circumstances all green plants use aerobic respiration with O2 as final electron acceptor for energy production. This means that they require oxygen, which is essentially absent from the Martian atmosphere (0.13%). Even though our hypothetical Martian crop could produce oxygen as a byproduct of photosynthesis, that oxygen would be lost into the atmosphere, and would not be available for respiration.
I believe that under waterlogged conditions some plants can switch temporarily to some sort of anaerobic metabolism as a stress response, but I don't know if this is just to survive or whether the plants can grow in this way - I suspect it is the former.

+1 I said it wasn't my field :). Would the oxygen present in Mars's atmosphere be enough if combined with that produced by the plants themselves?

It took (anaerobic) cyanobacteria one billion years to raise the atmospheric oxygen concentration on earth up to a level that supported aerobes.

I work on photosynthesis in algae, blue-green algae and anoxygenic photosynthetic bacteria.  All would more or less be able to live on Mars in a blow up tent equipped with a simple blow compressor (like some tennis courts in cold climates).  This could be used to raise the air pressure up enough (say 100 millibars) for water to exist in liquid form over a reasonable range of temperatures (Mars atmosphere is about 10 mB, Earth about 1000 mB).  The tent material could be made of UV opague material.  Besides many algae are quite resistant to UV anyway. The light intensity on Mars is no problem.  Most earth plants saturate photosynthesis at about 30% of full sunlight anyway.   Keeping the inside warm enough would not be a huge problem because the Mars atmosphere is essentially a near vacuum and so is a very poor conductor of heat. I do not think it would be all that hard. Low O2 is no problem for many algae. You could grow many higher plants quite easily if the O2 level was resonable.


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Experiments in vitro vs those with dead organisms and fixated tissue
Does the term in vitro necessarily imply that the organism/organs/cells of study are  dead?
If not, is there an alternative latin term to refer to studies of dead biological matter ? (e.g. in Connectomics where the tissue is biologically dead, and has been fixated and sectioned with a microtome)

Ex vivo perhaps? In mortum? :)

Does the term in vitro necessarily imply that the organism/organs/cells of study are dead?
No, in vitro studies are often carried out with living cells - just think of in vitro fertilisation. The nearest I can come up with for what you want is histology, but I think even this encompasses studies of living cells and tissues.


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Are there oligocellular organisms in nature and, if so, what are they like?
I'd think protozoans can be oligocellular, but I haven't found any examples, and I'm curious to know what is the minimum number of cells an organism can have other than a single cell.

Well, do you consider relationships like the Mitochondria and Chloroplasts - who were separate bacteria that became functional organelles - appropriate?

Various colonial and multicellular forms of cyanobacterial species are reviewed in:

Beardall, J et al. (2009) Allometry and stoichiometry of unicellular, colonial and multicellular phytoplankton. New Phytologist 181: 295-309

Nostoc and Volvox are some of the simplest true multicellular organisms known (usually 3-4 cell types), but in both cases the differentiated colonies (filaments in Nostoc, spheres in Volvox) typically consist of hundreds of cells.
The paper below reports the emergence of a colonial form of a unicellular organism. Since there is no evidence that the individual cells within a colony have specialised functions this doesn't really count as 'oligocellular' but it is an interesting angle on the question nevertheless.

Boraas, ME et al. (1998)Phagotrophy by a flagellate selects for colonial prey: A possible origin of multicellularity. Evolutionary Ecology 12: 153-164
Abstract: Predation was a powerful selective force promoting increased morphological complexity in a unicellular prey held in constant environmental conditions. The green alga, Chlorella vulgaris, is a well-studied eukaryote, which has retained its normal unicellular form in cultures in our laboratories for thousands of generations. For the experiments reported here, steady-state unicellular C. vulgaris continuous cultures were inoculated with the predator Ochromonas vallescia, a phagotrophic flagellated protist (`flagellate'). Within less than 100 generations of the prey, a multicellular Chlorella growth form became dominant in the culture (subsequently repeated in other cultures). The prey Chlorella first formed globose clusters of tens to hundreds of cells. After about 10-20 generations in the presence of the phagotroph, eight-celled colonies predominated. These colonies retained the eight-celled form indefinitely in continuous culture and when plated onto agar. These self-replicating, stable colonies were virtually immune to predation by the flagellate, but small enough that each Chlorella cell was exposed directly to the nutrient medium.

Just to add to this, there have now been several other experiments observing transitions form unicellularity to multicellularity in organisms. E.g. see https://doi.org/10.1073/pnas.1115323109. Another article summarizing a number more recent examples of this being experimentally observed is here: https://www.quantamagazine.org/single-cells-evolve-large-multicellular-forms-in-just-two-years-20210922/


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Bacterial cell lysis - what solution to use?
I am trying to determine how quickly detergents act on bacterial cells (cell lysis). I would like to compare some detergents at difference concentrations for bacteriolytic activity. I don’t care about all metabolites inside the cells (proteins, DNA, etc…). Many publications suggest that often more complicated solutions are used. My first thought was to use a simple prepared detergent in PBS or saline for lysing the cells. Do I need a complex solution to lyse the cells?
Could someone please give me a suggestion? Thanks in advance.

What exactly is the purpose of lysing the cells? The "complicated" solutions, as you say, include a bunch of ingredients. The detergent is largely present to dissolve cell membranes (which are lipid-based) and allow for extraction of proteins or other biochemicals from within the cell (and organelles in eukaryotes). There are also two types of detergents: ionic and anionic. Both detergent types will dissolve membranes, but ionic detergents tend to be harsher of the two by strongly disrupting protein structures.
If protein biochemistry is important, then the next most important ingredients will be specific inhibitors of proteases: enzymes which degrade proteins. There are many of these, but some examples include PMSF, EDTA, aprotinin, etc.
Sometimes it is necessary to buffer the pH of lysis solution to monitor protein complexes, or keep a protein natured, or keep DNA in an optimal pH range. General solutions for lysis buffers include Tris-EDTA (TE), PBS, etc. This choice comes down to whether you want a buffer, and in which pH range you wish to keep your lysis solution. Common buffers like TE and PBS are made up for a pH range of between 7-8. There are other buffers that are used for low pH ranges (pH 4-6), but are usually less common.
Lastly, there are ways to lyse cells without using any kind of lysis buffer. One method is to use sonication, which uses directed pulses of high-frequency sound to lyse cells by mechanically shearing them. Another method is to repeatedly freeze-thaw cells from -80°C to 4°C (usually 3 times is sufficient). Lysis in this manner is accomplished by repeated formation of ice crystals which cut open cells, releasing their contents.
If you have a more specific question, one of us can guide you further, but this provides a general overview of what is involved with cell lysis buffers.

I wonder how you plan to measure lysis? You will find that many lysis methods for E. coli incorporate a treatment with lysozyme and EDTA. This is so that lipopolysaccharide (outer membrane) and peptidoglycan layers of the cell envelope can be breached before detergent (usually SDS or Triton X-100) is added to dissolve the inner or cytoplasmic membrane. I suspect that if you added detergent to intact cells it wouldn't be particularly effective, and any cells that were affected would remain as denatured cells which would, for example, still contribute to optical density.
Since they are usually able to withstand bile salts in the small intestine, Gram-negative bacteria can be quite resistant to detergents. For example many Enterobacteriaciae can grow in 5% SDS - see:

Rajagopal, S et al. (2003) Eight Gram-negative bacteria are 10 000 times more sensitive to cationic detergents than to anionic detergents. Canad. J. Mic. 49:775-779


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What is the function of the RNA primer in DNA replication?
During DNA replication, RNA primase puts an RNA primer in the lagging strand. What is the function of this RNA primer? Why can't the enzymes put DNA fragments directly?

DNA polymerases need a primer oligonucleotide (RNA or DNA) - their substrates are an existing 3'-OH group and a dNTP. The primase however is a typical RNA polymerase, capable of initiating polynucleotide synthesis de novo by positioning a complementary ribonucleoside 5'-triphosphate opposite its complementary DNA base. The primase makes an RNA primer that the DNA polymerase can then use for chain extension. The RNA primer is ultimately degraded and replaced by a DNA polymerase.
The rationale for this difference is that DNA polymerases have an active site that is geared towards proofreading and that primerless initiation would be an error-prone process. By having the primers 'tagged' by virtue of them being RNA, it is possible for the replication machinery to use them but then replace them with a high fidelity DNA copy of the template strand.
Edit in response to OP comment:
Synthesis of the leading strand consists of extending an existing DNA. However the leading strand is also originally initiated, at the ori element, with an RNA primer. Once that first initiation event has taken place the synthesis of the leading strand is simply a process of extending that original primer.
Some viruses employ ingenious variations on this theme such as using tRNA primers , or proteins - see Wikipedia.

so why doesn't DNA polymerase need RNA primer in leading strand?

OK.thanks a lot bro....i really appreciate for giving time to answer..:)

Well, if the answer is useful, you might consider giving it an upvote, or even possibly accepting it. Entirely up to you of course - before accepting might be worth waiting for a day or two in case a better answer comes along.

well i tried many time to vote it..but i need 15 reputations. i have 11 now...so the first i will do when i get 15 reptutations is that i will vote this answer...:)

"but then replace them with a high fidelity DNA copy of the template strand" - I would suggest adding that at the very end of eukaryote (linear) chromosomes, there will not be any way to replace the RNA primer with DNA and it will hence be removed along with the leftover sDNA end to which it was attached - resulting in telomere shortening.

@AlanBoyd Just to add to your answer, the leading strand is synthesised from the primer produced by a primase of the opposite replication fork.

It's known that the RNA primase adds RNA , is this RNA ultimately removed?, Or does it stay there?

In simple terms:
Function of the RNA primer: DNA polymerases need a double-stranded DNA region to which they can attach in order to begin copying the rest of the DNA strand. In order to provide this double-stranded attachment site, RNA primers are added by primase, an RNA polymerase which does not require such an attachment site itself.
When DNA replication starts, one primer is needed at the start of the leading strand. The lagging strand will need new primers regularly, and they mark the start of the stretches known as Okazaki fragments.
Why is RNA used instead of DNA?: Adding primers is an error-prone process, and DNA replication must copy the original strand with as high fidelity as possible. Using RNA for primers and then copying the original using DNA means that there is "memory" of which bits of the new strand were originally primers and hence more likely to contain errors (any RNA in the copy must have been primers). This allows removing them, in order to then replace them with proper high-fidelity DNA copies. When this happens, there is double-stranded DNA around the sites where primers were located, allowing DNA polymerases to attach there and fill in the gaps.
Aside from this, I would guess using RNA for priming may be more energy-efficient as RNA is more reactive than DNA.

Can you elaborate on how the use of RNA primers plays a role in high fidelity?

Presumably, when a polymerase attaches, the first few bases are quite error-prone (wobbly attachment to single-stranded DNA, proofreading at this point would risk the polymerase dropping off the strand). Once the first few bases are added, the resulting double-stranded region can provide more stable attachment and allow proofreading to function properly. When done, it would be better to know which bits of the resulting strand were the first few (error-prone) bases, so that they can be removed and re-done with proofreading. Using a different type of molecule for the primer makes that possible.

So basically, is the need for primer in replication because DNA polymerase  requires double stranded region and this primer being RNA helps distinguish the first few bases added which are error-prone?

Rather: being able to distinguish the first bases is good, and one possibility for this is to use RNA for them and DNA for the rest. To implement that, the easiest is to have two polymerases, one which makes RNA and can attach to single strands, and one which makes DNA but can only attach to existing double-stranded regions.


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High protein turnover rate and protease inhibitors?
I work with mice, and I want to see what happens to some specific proteins in the mouse brain after IL-1b injection (intracerebroventricular).
I have a problem: when I measure the mRNA and protein levels, I see that there are some differences between them.
It can be like:  mRNA (upregulated)  Protein (no difference)
Is it possible that these proteins have a high turnover rate? If so, how can I prevent that?
Can I (if it is possible) inject (intracerebroventricular) IL-1b mixed with protease inhibitors?

Scientists are recently finding (or coming to accept the notion) that, at least in eukaryotes, mRNA expression is poorly correlated to protein expression. There are several factors influencing translation regulation, such as siRNA or microRNAs, sequestering mRNAs while they are transported to various cell compartments, and others.  Even after the protein is made, there can be factors interfering with your expression reporter.  And as you mention, it may be degraded faster than you expect.  Cells try to keep proteins at certain expression levels, so if IL-1b is promoting expression without inhibiting the degradation pathway, degradation might kick into overdrive to bring the levels back down to normal.
Trying some protease inhibitors is worth a shot, since it's pretty simple by itself.  It should also increase your protein expression regardless of whether protein degradation is your limiting factor. If this doesn't work, or if it's prohibitively expensive to be sacrificing mice while you're working out a protocol (and is usually is), then I would turn to cell cultures and try and discern where you're getting blocked.  That kind of information will generally make a decent PNAS paper by itself.


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What kind of event would cause the current Mitochondrial Eve to be replaced by a new one?
Apparently all living humans are matrilineal descendants of a single woman who lived 200.000 years ago. She is called Mitochondrial Eve.
But at the time she lived there was a different matrilineal ancestor that all living humans shared. And between then and now I imagine many other women have been Mitochondrial Eves of the human population that lived at a particular time.
What I'm wondering is what kinds of events would cause a different, more recent matrilineal ancestor to become the Mitochondrial Eve of all living humans?
One scenario I can image is that the human population is on the brink of extinction and literally only a few people survive. Because there are so few people alive, I imagine that the chance that they share a more recent matrilineal ancestor is high.
Are there other scenarios possible? Does the chance of a new Mitochondrial Eve emerging decrease if the human population is large (billions) instead of small (hundreds or thousands)? Suppose that the human population will not decrease, is it likely future human populations will ever have a different Mitochondrial Eve than the current population? Does it depend on the amount of people that migrate?
The same questions could be posed for Y-Chromosomal Adam and the most recent common ancestor of all humans, I guess...

An mathematical solution to this question is the Galton-Watson Process. It is formulated in terms of surnames and this situation is very similar. http://en.wikipedia.org/wiki/Galton%2DWatson_process

It looks like the genetic Adam just got replaced... so there you go. http://www.newscientist.com/article/dn23240-the-father-of-all-men-is-340000-years-old.html

The new mitochondrial eve is alive right now.
When humans reproduce, mothers pass their mitochondria to their offspring without a contribution from the father.  As a result, each human can trace back their mitochondrial lineage as an unbroken chain to a single individual woman in the past.  Through random chance (genetic drift) or natural selection women in some mitochondrial lines will pass offspring to the next generation, while others will not.  If a woman fails to pass offspring to the next generation then she represents the end (i.e., extinction) of a particular mitochondrial lineage.  As time progresses more and more of the original mitochondrial lineages will go extinct until all humans represent one remaining linage.
Note that this is a continual process since lineages accumulate differences through mutation of the mitochondrial DNA.  This mutation is the source of the different lineages that that will go forward.  Based on the estimated rate of mitochondrial DNA mutation we can estimate how long  it would take for extant mitochondria to have developed the genetic differences we now see.
If you take a snapshot of this process at one point in time (e.g., contemporary humans), you can use this estimated time to say how long it would take to accumulate the present differences - that is when the line began.  Due to the continual extinction of extant mitochondrial lines, there is some point in the future where if we were to take the snapshot we would estimate that the mitochondrial eve was alive right now.
EDIT based on comment:
The rate that a new mitochondrial eve would be formed is based on the accumulation of mutations in non-coding regions of the mitochondrial DNA (i.e., the molecular clock) which is dependent on the population size only in so far as the probability that a given mitochondrial line will survive when all others go extinct is basically its initial frequency in the population. So in a large population with more initial diversity each line will have a lower probability of succeeding.
Also, if there is no selection for or against a given line then changes in frequency are due to chance (genetic drift). In a large population the effect of drift is smaller than it is on a small population.  So if the population size is small, then the likelihood that a mitochondrial line will go extinct is greater and the rate of a single mitochondrial line succeeding to be the mitochondrial eve is greater.

True, I hadn't thought it fully through...  I edited my answer to remove the references to speciation.

This sounds fair, but I'm left wondering if the rate of extinction of mitochondrial lineages is dependent on the total population. At what rate do humans get a new M-Eve, and which factors influence that rate?

@molf I edited my answer to address your comment.  Hope that helps.

it sounds like you expect all the mitochondrial lineages to disappear in the future.  why would that happen? It has never happened in the past.

@shigeta it has happened in the past.  Mitochondrial lineages are continually going extinct but new diversity arises due to mutation.  Using the rate of neutral mutations we can estimate how long it has taken the population to accrue that amount of diversity, which is the time since that diversity was 0, which is when that lineage arose, which is the estimate of the age of mitochondrial eve.

the question is what would it take before the mitochondrial Eve to be replaced.  there are 7 billion people on the planet.  You are right it might have happened before our current Eve, but do you really believe it will happen at some time in the future?

The mitochondrial eve after the one we have now is probably not alive right now. If the species is around long enough, someone born today might become the new eve, or might not.  Imagine killing off all the women in the world bar two native american ladies. That pushes mitochondrial eve forward to maybe 15 thousand years ago, 'skipping' 185 thousand years of history. We could be 'skipped' in the same way.

One possible scenario would be that a particular woman develops a mutation rendering her much more 'fit' (in the evolutionary sense) than her peers. For the sake of argument, lets take the very simplistic case of an X-linked recessive mutation causing the women who bear it to have say 10 children at each birth. If this mutation is then transferred to the offspring, it will very quickly spread across the entire population.
If this continues for a few generations, the crushing majority of the earth's population will be the descendants of that one woman who carried the original mutation, she would be the new mitochondrial Eve.
I want to stress that this is nothing but a very simplistic thought experiment. Such a mutation is i) very unlikely, probably impossible, ii) likely to render the carrying individual less fit rather than more as each birth would be exhausting, increasing the chances of dying during child birth.

Update:
I have specified that the mutation has to be X-linked and recessive. This means that it will only present a phenotype in women who are homozygous for it, women both of whose parents carried the mutation. This is because, as mgkrebbs very correctly pointed out in the comments below, otherwise her sons would mate with women who are not their sisters and their children would have the mutation but not her mDNA. If the phenotype is only expressed when the mutation is homozygous, only women whose mother carried the mutation (and Eve's mDNA) would show it and only then would a new mEve arise.

Not correct, as such a mutation would pretty much have to be in the nuclear genome, not the mitochondrial genome.  Being on a nuclear chromosome, it would spread to offspring of women who are not her mitochondrial descendants, and thus she would not become  a mitochondrial eve.

@mgkrebbs, huh? Of course the mutation would be in the nuclear genome and of course, by definition, it would pass to her descendants only. What exactly are mitochondrial descendants? Each female egg contains both the mitochondria and the genome of the parent. Yes, the mutation would not be carried by her mitochondria, however, her mitochondria would be carried by her descendants, therefore, she would be the new mitochondrial Eve (although, as shigeta points out, she would still be dcendant from our MEve herself).

But these mutations can ultimately also be transferred to the offspring through patrilineal descendants, right? What factor makes it likely that this woman would become a M-Eve? Was our M-Eve really so different from other women alive at the time?

@molf, not necessarily no. The point is that mitochondria come from the mother not the father. Therefore, if one female has a much greater reproductive success than her peers, and that female's offspring do so as well, eventually ALL individuals will be the descendants of that one female. Since mitochondria come from the mother exclusively, all individuals will have the same mitochondrial genome. Their nuclear genome will be different as it is also affected by the father but that is irrelevant to the point discussed.

This is true but it is not necessary that one woman have much greater fitness.  Even if fitness was equal drift would produce a mitochondrial eve with sufficient time. Just like one player will wind up with all of the money if the poker game goes on long enough, even if they are equal players.

@DQdlM, I'm not sure... Drift will affect the spread of genes through the population. I see no reason why it should afect MEve.

This is how I see it:  if the population has 10 M-lines at equal freq. and fitness.  At each generation the lines will be perpetuated based on their freq.  W/o drift the freq. wouldn't change and no lines would go extinct but drift can raise or lower the freq. of a line by chance so over time some lines will become less frequent and more vulnerable to extinction and others will become more frequent and less vulnerable to extinction.  Given enough time only one line will remain. This is MEve.

@DQdlM, OK, yes, I see your point. However, I am still not sure whether drift is applicable here. Even if the M-lines have equal freq. and fitness, the nuclear genomes of the hosts will not. Therefore, the fitness of the nuclear genotype will affect the spread of M-lines much more than drift. The only way I can see mitochondrial genomic drift producing a new MEve would be if the both nuclear  and mitochondrial genomes were free of any selective pressure and governed by drift alone.

Agreed.  In nature, both selection and drift are going to be acting in concert and it would be very difficult to tease them apart.  My understanding of the MEve concept though is that the estimate is based on the accumulation of neutral mutations in the mito. DNA, so the estimate assumes no selection and only drift.  Selection should speed up the process and MEve would be more recent (assuming it doesn't change direction during the process) - as you point out in your answer.

@terdon, since you say "Of course the mutation would be in the nuclear genome", the scenario would not be likely to make the particular woman a Mitochondrial-Eve.  Suppose she has 5 sons and 5 daughters, then the offspring of the 5 sons are just as likely to carry the advantageous nuclear mutation, and thereby be likely to have surviving descendants, yet the sons' children do not carry her mDNA. The population will not especially favor female-only descendants of the original woman, hence not favor her mitochondria, and not favor her becoming a M-Eve.

@mgkrebbs, I see what you mean, however, even if the mutation is caried by her male offspring, it will make no difference. Since the females of each generation that carry the mutation will consistently have more offspring, eventually the vast majority of the species will carry the mutation. Therefore, her male descendants will mate with her female descendants, thereby spreading her mDNA.

@terdon, yes, "the females of each generation that carry the mutation will consistently have more offspring, eventually the vast majority of the species will carry the mutation" is true, but it is not true that these females need have her mDNA.  Her sons mated with non-sisters, so all their offspring, sons and daughters, will not have her mDNA, yet will have the advantageous mutation to the same extent.

@mgkrebbs, I understand now, you are absolutely right. I have changed my answer to make the hypothetical mutation X-linked recessive.

That would increase the probability that she could become a M-Eve, but does not assure it.  First off, being recessive, none of the woman's children would have any advantage carrying the mutation, since they will mate with non-carriers and so not show the advantage.  (Assume for discussion both her X's have the mutation.) Now note that of her grandchildren, one half of them will be carriers and one half of them not.  Note also that all of the sons' daughters will be carriers (the X coming from her), while [continued in next comment]

...while only half of the daughter's daughters will be carriers (plus half of the daughter's sons).  This means that the most likely first appearance of the fertility advantage is between cousins: a daughter's son and the daughter of either sex child of the original women (excluding unlikely brother-sister matings). Two-thirds of these latter granddaughters are (probalistically) via sons; the other third via daughters.  Thus, 2/3rds will not carry the original mDNA, and thus the original woman is not so likely to become a M-Eve.

What's a more realistic scenario that could happen to allow only one lineage to survive ?

What would need to happen for a single woman's mitochondrial genome to be in all living humans ?
All other women would suddenly or gradually need to be eliminated from the gene pool.   No other woman could enter the gene pool of this future humanity.  So the most likely scenario is one where we would have to be reduced to a single woman at some point.
Genetic isolation was brought up, but the words 'all living humans' doesn't really say 'isolation'.  In isolation, there are other people still carrying on somewhere else.   Here we are talking about only isolation in the sense that the breeders are the only ones left to reproduce.
Even so, any human woman will still be descended from MEve.  That original Eve would still be the mitochondrial Eve, though the genomic record pointing to her would have disappeared.
A completely New Eve could happen if there were a woman unrelated to MEve were to come along, and her offspring were so much more successful than all other women that over time only this woman's daughters were chosen as mothers.  She would be incredibly successful- like all her children were 6'6" and much smarter, attractive etc etc, then the rest of the gene pool could dwindle leaving only 'new Eve'.  This could happen say if we got some Neanderthals going.  They don't seem to be particularly likely to take over though.
This is similar to the scenario where one female lineage simply out-competes all other female lineages to assume the mantle of M-Eve.  This seems less likely to me.  This lineage would have to enjoy an advantage would have to out-weigh all over variants that exist at the time and would ever emerge over the following generations before our new M-Eve's final domination. Given the number of genes and possible variants, in the entire genome, that is statistically really improbable.
As far as a new Y Adam, this sort of thing nearly happened for men.  Just to remind, the Y chromosome is transmitted exclusively from father to son, so a Y Adam would be the only ancestor of all men on the face of the planet.
A national geographic sponsored survey of genomes found that in central asia 8% of all men have the same Y chromosome.  Over all humanity, 0.5% of all men have the same Y chromosome.  The genetics point to the Mongol Warrior King, Genghis Khan whose campaigns across Asia to the doorstep of Europe included him bedding with one or more different women from the conquered peoples every night, one of whom is reputed to have killed him.  Not incidentally killing many men too, eliminating much future competition for his progeny.
Still, all this is a mere fraction of the sort of effect you are talking about.  100% replacement by a single individuals descendants is hard to imagine in less than an extinction like scenario.  Or a new race of superbeings coming from a single individual.  Hard to imagine given the billions of people on the face of the planet now.
Its a little easier to imagine in the case of a new Adam only because a one man can have hundreds or even thousands of offspring in his lifetime.  Even then, Male psychology seems to bring it up more than is rational. Its still extremely improbable (not going to happen).

Its also worth noting that few species have been able to come back from such a small gene pool and number...
Here's a tree of human Y chromosomes. You can see that fat grey blob which are descendants of GK.

Based on the comment to my answer I removed the mention of isolation so I edited out your reference to the part of my answer that no longer exists.

I was also editing - i think i ran over your changes, but i took the reference to you out.

This notion seems to conflict with the hypothesis that our current M-Eve was not the only woman alive at the time. Isn't it so that other contemporary women of our M-Eve do have living descendants, just not matrilineal?

If there were a group of women that were not at all related at the time of origin of the human race, we should see it in the mitochondrial version of the above diagram - more than one tree.  It seems as the human race (and speciation) started with just one event.  On the other hand its interesting that there are theories that neanderthals and denisovans mated with humans after leaving africa, but it doesn't seem to show up here. http://en.wikipedia.org/wiki/Denisova_hominin#Interbreeding_with_modern_humans

It isn't required that all other women be eliminated from the gene pool but rather that through time the individual lineages of mitochondrial DNA (based on some initial variation at a specified time in the past) go extinct.

How do you make a single chromosome go extinct while the rest of the chromosomes breed?

The point is that you do not need to be reduced to a single woman at any point.  If there are x different mitochondrial lines extant right now.  Through time, the proportion of descendants from each of these lines will vary (n/x) and some lines will go extinct (0/x).  Given enough time all lines but one will go extinct (either from selection or drift) and all of the individuals in the population will be the descendants of a single line.  Note that background mutation will mean that the extant variation need not decline through time.

That's true - though I did not really mean say that all the women would need to be removed at the same time, but eventually they would have to exit to achieve the scenario depicted. I think this is what I said though its true not at the top of the entry. This parallel competitive MEve is a lot less likely. I can amend my answer to describe how much less likely that is, although all these scenarios are the stuff of science fiction - more thought exercise than at all likely to happen.

I don't really think it is science fiction as much as a way to think about genetic drift.  It is basically just genetic drift in reverse.  The MEve is just an estimate of how long it took for drift to eliminate the genetic diversity of the population.

let us continue this discussion in chat


text:
How to map the Gene name to its Gene Symbol?
I am learning in Gene data lately so I apologize for the silly questions in advance. I read a paper for a cancer on human which found some important genes. For example, the paper listed one of genes in its name as
gene1:    chromosome 12 open reading frame 52

May I know how I can find its corresponding gene symbol as
C12orf52

Is there a mapping table or  tool I can use ?
Thank you very much,

What species are you interested in?

Unfortunately, protein and gene name mapping is one of the most annoying problems in modern computational biology. There is no surefire way of doing this. Especially from hopeless gene names as the one in the paper you cite. Here are a few services you can try though:

General, text search, useful if you have a gene description (as in the case described in your question):

NCBI Entrez,
UniProt search

Mapping servers, useful if you have an actual gene/protein symbol/name (e.g. P53_HUMAN, AF240684, NP_001119585 etc)

UniProt ID Mapping
DAVID Gene ID Conversion Tool

“one of the greatest problems” – uh.

@KonradRudolph, you disagree? Believe me it is. I don't mean problem in the sense of a scientific problem but of a technical one. Each database often uses its own identifiers, the identifiers change over time, as does the sequence as errors are corrected. For the list of ~15000 proteins (UniProt) I am working with, on average 1-2 identifiers change PER WEEK. Correctly mapping the names between the various databases and other sources of information I use has been the great headache of my Post-Doc.

Well, I agree that it’s a nuisance but we have stable identifiers (= don’t change) and services to translate between the different ones. It’s a solved problem (in that it may still require manual work, but not intellectual work).

@Konrad, unfortunately, the stable identifiers are only good if your input data is using them. If you have to combine interaction data from 15 databases, each of which uses a different ID schema (RefSeq, GIs, UniProt, HUGO, Flybase, Wormbase etc) the identifiers become a very real problem. The translation services are often buggy (UniProt, for example, was not creating unique IDs for each job submission, and was returning my queries mixed up with somebody else's!), limited to certain species or ID types. It may indeed not be an intellectual problem, but it is a very real technical one.

If the original source used the official human nomenclature, you can search the HGNC (HUGO Gene Nomenclature Committee) site.

Just use a genome database such as Ensembl. Paste your gene name into the search box and hit “Go”. The first hit in the result list is what you’re searching for.

It worked. But I am still configuring out how to input a list of gene names not only one at a time.


text:
Hershey and Chase experiment
http://www.youtube.com/watch?v=3QJ4CjFsflA
This is a link to Hershey and Chase experiment. According to this experiment, we conclude that DNA is the genetic material. But how do we conclude that DNA is the genetic material? They only proved that DNA of virus enters into the bacteria, not the protein coat of virus.
The DNA of the virus later destroys the bacteria because the virus reproduces inside them. Does this demonstrate that DNA is the genetic material?

It is a matter of deduction. We know that:

Viruses entering a cell are capable of making more copies of themselves.
The only part of a virus that actually enters the cell is its DNA (or RNA, depending on the virus in question).

Based on these two facts, we can conclude that the DNA ̣--since it is the only part of the virus to enter the cell-- somehow contains the information necessary to make new copies of the virus and is, therefore, the genetic material of the virus.

@MuhammadRafique, I did not mean to push you to accept my answer (it is often a good idea to wait a while in case a better one comes along), I was just pointing out the etiquette on these sites :). Thank you comments are discouraged.

i was not pushed, don't worry....:)...and i didn't know commnets are discouraged, so bye bye...:p

@alanboyd, ouch,thanks for the edit, durned iphone...

This was an important experiment, but did not convince everyone.
Not even Hershey and Chase claimed this conclusion, although it convinced many.  In most mol bio classes or when reading "The Double Helix" you can see how there were lots of facts pointing to DNA, but doubts lingered.  Some viruses contained RNA only and not DNA, but still replicated.  There was also a school of thought which felt that proteins could be the genetic material.
It was Watson and Crick that finally convinced everyone that DNA was the medium of genetic inheritance.  The reasons for this are varied, one of them is probably that atomic structures are so clearly understandable and seem so uncomplicated compared to a wet lab experiment which is built upon so many other experiments.  Questions keep coming up:  "how do you know you shook the flask long enough?", "What if a small amount of residual viral protein got in?"  For every revelation like Hershey and Chase, there are many cases where someone stopped an incubation too quickly or wrote down an illegible number and was found out after publishing.
And you can see how much the structure gave us in one fell swoop: the structure of DNA inspired a mechanism by which replication of the DNA could be produced with some error correction, the central dogma (DNA -> RNA -> protein).  There were several years more effort to demonstrate that the genetic code existed and then parsing out the exact codons and the fact that they were 3 bases long.  But all of this was predicted when the structure was found.  So much clearer as to what is going on.

Perhaps worth adding this quote from Watson: "the Hershey-Chase experiment had a much broader impact than most confirmatory announcements and made me ever more certain that finding the three-dimensional structure of DNA was biology's next important objective. The finding of the double helix by Francis Crick and me came only 11 months after my receipt of a long Hershey letter describing his blender experiment results."


text:
What causes tree lines?
There is an area of where there is a distinct line of only trees on one side and only shrubs on the other (right next to each other). What could cause this?
My attempt: I said there could be a difference in sunlight, but I'm not sure.

could you describe this a bit more?  my first thought is 'landscaping'...

I doubt you are referring to http://en.wikipedia.org/wiki/Tree_line

There are a bunch of possible answers;

On my own property I have such a line.  Turned out it was an old fence line.  One side was farmed intensely for 90 years, the other side left in bush.  The farmed soil is enough different that it doesn't grow good trees.  Even the grass is different.
Another place I have an abrupt line of willows.  That one turns out to be water level from the local creek.
A third one has an abrubt chaange in types of grass.  That one is caused by a clay seam coming to the surface.  Uphill the surface soil is sandy.  Water hits the clay, and moves downhill, coming out at the grass line.
I've seen another one, in the mountains, that I think is due to cold air drainage.  The valley floor and 20 feet up the sides are bush.  I think the cold air settles and kills young trees.


text:
Proteins that are strongly overproduced in E. coli and S. cerevisiae?
I'm looking for some pointers to proteins that produce at really gigantic levels in E. coli and yeast (S. cerevisiae).  Can anyone point to some champion proteins?
Even in inclusion bodies and non functional, just cases where the yield is very high - how much of a given protein can a liter of E. coli or S. cerevisiae make?
I've seen bands on gels like this, but I've probably not seen the champions:

It would be great if you could cite and discuss the plasmid/promoter used and whether codon optimization or other such tricks made a difference.

I think this comment (with respect to E. coli) was addressed here (http://biology.stackexchange.com/questions/5197/recombinant-protein-fraction-in-e-coli). If you're looking to maximize plasmid protein expression, then you'll want a highly active constitutive promoter (eg, CMV), and then depending on codon optimization and many other factors, you might get ~20% by weight of your protein.

thanks for the pointer - I was hoping to get some pointers to specific genes nearer the maximal limit though.  OSCP is promising though - if nobody has anything better than that maybe i'll go there.

@Leonardo, CMV in ecoli probably would be a bad idea ;). I've heard that typically 1/6 of the cell weight would be protein so 20% doesn't sound too crazy.

hehe, just listed a promoter since it's what was on my mind at the time. ;)

The promoter is good information - I have only worked with T7 promotor for protein production I think.

Heat shock proteins - HSP70 and HSP30.
You may also have ribosomal subunits as well.

interesting!  a reference would be appreciated?

Definitely agree. HSP70 is produced in gigantic quantities especially during recombinant protein expression in E. coli. You can get rid of HSP70 by doing a pulldown with denatured protein and ATP.

Here you go:http://www.wikigenes.org/e/gene/e/398343.html


text:
Will climate change affect flower population?
There is a flower population elevated 1000 meters above sea level.  If climate change causes a 12⁰C increase in temperature over the next 10 years, what will happen to the flowers?

Its really hard to say for any given field of flowers and its hard to separate temperature from so many other factors that are accompanying climate change.
For example, rainfall is changing as well as CO₂ levels.  The pH of the rain may change because CO₂ becomes a mild acid when its absorbed into water. The speed at which the seasonal temperatures vary and how cold is the minimum temperature and how hot is the hottest day will cause parasites and infections which kill plants to appear.
To be sure the heat is important, but the timing maybe just as important.  The temperature is causing earlier blooms and later growing seasons.
Each different species is responding differently, but odds are that nearly any given field of flowers is going to feel it.  The temperature is important, but its sometimes hard to guess if its the specific culprit in changes.

Making one change in an ecological system is much like eating one salted peanut.
A:  If you only assume a 12⁰ change (which is really large) then the net effect is not only warmer but dryer. Higher temperatures mean faster evaporation, faster transpiration.
B:  Warmer may also mean that some pest has a limiting factor removed. Look at the problem northern British Columbia has had with Mountain Pine Beatle. The pines are fine with the warmer winters.  But the lack of cold winters has allowed the beatle population to explode.
C:  Some plants are adapted to a large temperature range. Look at the range for dandelion. So warmer temps may make them grow faster and set seed sooner.
D:  Some plants are adapted to a narrow temp range, and will die out.
One of the questions is, "If the change is slow enough, won't they just move up the mountain. In some cases yes.  We can look at turn of the century (1900) photographs of mountains, and we can see the tree line -- both at the top, where it meets tundra, and at the bottom where it meets prairie -- has moved up the mountain.
However it also depends on the soil. And soils neither move fast, nor are created fast.
Example:  Lot of articles think Canada will win big with global warming, because more northerly land will be suitable for farming. Not so. Most of the land that has reasonable soil is already farmed. The soil north of that point tends to be mostly peat moss bogs, and glacial till. In addition over half that country is the Precambrian shield -- endless miles of granite under 2-3 inches of moss and gravel, with bogs and lakes between. The equivalent of a rural gravel road costs millions of dollars a mile to punch through this country.

I don't understand the 1 peanut analogy.

No one eats one peanut.  They eat handfulls.  Similarly making one change in one parameter has a ripple effect through the entire system.


text:
What light intensity starts melatonin release in humans?
I'm interested in whether any studies have determined the intensity of light at eye level that starts melatonin release in humans.
I know that:

melatonin release is suppressed by blue light with peak suppression
occurring at 420-480nanometer range.
This light is registered by Melanopsin, a photopigment in the
eye.
Melanopsin signals the Suprachiasmatic Nucleus, the master clock of the human body.
The suprachiasmatic nucleus makes a decision to suppress melatonin
release in response to blue light observed.

What I need to know is how much light is "enough" to trigger the suppression by the mechanism described above. I've seen a mention of as little as 200 lumens of white light, but do not have any reference to verify that. Additionally, the figure of 200 lumens was given for a typical smartphone screen, not necessarily translating to 200 lumens at eye level.
I'm aware of this experiment involving rats, where the light intensity at eye level was quantified. I'm looking for a similar measurement in humans.
Here's my original question on the subject, but I've learned quite a lot since then to refine the question
I appreciate your input!

Ps. Different numbers for melatonin sensitivity (ex: starting at 420) are because the eye somehow changes the light, thus pure melanopsin responds to less wavelength than through the eye

Not looking for a new answer, just want to award bounty for the great answer already posted

There is a bounty message for that. something like , 'Reward existing answer
One or more of the answers is exemplary and worthy of an additional bounty.'

The question piqued my interest, but after hunting through the literature for a bit, I hadn't found any direct answers.  Then I went back and read the mouse study you cited a bit more carefully. The mouse study only made a reference to mice being affected at 4 lux, ~100x more sensitive than humans.  However, for that number it cited a paper in Science that has a direct answer.

http://www.sciencemag.org/content/210/4475/1267

Melatonin concentrations decreased 10 to 20 minutes after the subjects were exposed to 2500-lux incandescent light and reached near-daytime levels within 1 hour (Fig. 1). After the subjects resumed sleeping in the dark, the melatonin concentrations increased immediately and within 40 minutes were at the levels measured before exposure. The fluorescent light (500 lux) did not reduce melatonin, and there was no change after the return to darkness. In the two subjects who were exposed to 1500-lux incandescent light, melatonin concentrations decreased to levels intermediate between those measured during exposure to 500 and 2500 lux (Fig. 2). The return to normal nighttime concentrations after subjects were exposed to 1500 lux was similar to that occurring after their exposure to 2500 lux. The concentration of melatonin in subjects awakened and exposed to 500-lux fluorescent light did not differ significantly from that measured while they were asleep in the dark.

Since that was the granddaddy study of the subject, I just checked the recent citation list on that page for modern articles.
Using pure blue LED lights at 446-477 nm wavelengths, West et al. measured light intensities necessary to induce melatonin suppression. Table 1 of that study converts LED irradiance/lux into retinal irradiance (uW/cm2) based on mean pupil size.  Figure 2 shows plasma melatonin falling (p<0.05) at 20 uW/cm2 of corneal irradiance (then curve fit to 14.19 uW/cm2). It's at least twice as powerful as white light, which didn't show significant suppression at 40 uW/cm2, but was "numerically similar" to 10 uW/cm2 exposure.  If I've got the conversions right, 20 uW/cm2 is about 136 lux, which is about the brightness of an overcast day or half the brightness of typical office lighting.
http://jap.physiology.org/content/110/3/619.full
As for the discrepancy between the two studies (1500 lux vs. 136 lux), I would blame it mostly on technological advances since 1980.  The original study used gas chromatography. You can see the huge error bars and noisy data in the Figure.  The modern study uses a radioimmuno assay using antiserum, and is presumably far more sensitive.

I was also going to mention a nice review paper that summarizes more findings, but apparently I can only post 2 links as a new user.  So I'll just paste the abstract and citation.

Light is a potent stimulus for regulating the pineal gland's production of melatonin and the broader circadian system in humans. It initially was thought that only very bright photic stimuli (≥ 2500 lux) could suppress nocturnal melatonin secretion and induce other circadian responses. It is now known that markedly lower illuminances (≤ 200 lux) can acutely suppress melatonin or entrain and phase shift melatonin rhythms when exposure conditions are optimized. The elements for physical/biological stimulus processing that regulate photic influences on melatonin secretion include the physics of the light source, gaze behavior relative to the light source, and the transduction of light energy through the pupil and ocular media. Elements for sensory/neural signal processing become involved as photons are absorbed by retinal photopigments and neural signals are generated in the retinohypothalamic tract. Aspects of this physiology include the ability of the circadian system to integrate photic stimuli spatially and temporally as well as the wavelength sensitivity of the operative photoreceptors. Acute, light-induced suppression of melatonin is proving to be a powerful tool for clarifying how these elements of ocular and neural physiology influence the interaction between light and the secretion of melatonin from the human pineal gland.

Photic Regulation of Melatonin in Humans: Ocular and Neural Signal Transduction
Brainard, Rollag, and Hanifin
J Biol Rhythms December 1997 vol. 12 no. 6 537-546

If you need more information, I'd start by checking the papers cited by the second paper. Alternately, there's probably more historical information available by looking at papers which have cited the first one.

This is probably the best answer I've ever received here:) starting a bounty so you can claim it!

@AlexStone if you plan to split and distribute your bounty for each quality answer, that's a great idea indeed.

Thanks! It's satisfying to harness that abstracted science knowledge, dig deep through the literature, and come up with a simple and practical answer. :)