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Why is it important to have a restriction point? (G1-S phase control)
Why have eukaryotes evolved to control G1-S phase?
Surely if you could control G2-M phase very well, you will not get an excessive proliferation?
Thanks for your help.

The reason you want a check point in the transition from the G1 phase of mitosis to the S phase of mitosis, is that the cell needs to make sure that it synthesized all of the necessary proteins, and accumulated the necessary compounds with which to have DNA synthesis begin AND complete.
The transition from G1 to S is a point of commitment for the cell. There is no turning back at that point. It either needs to faithfully replicate the entire genome or it should die. An incompletely replicated genome would be disastrous for the cell.
If it tried to arrest and go backwards it would likely have too many copies of certain genes and those gene products would likely cause lethality to the cell. You would end up with all sorts of errors and breaks where replication forks collapsed. It would basically be death for the cell. What would be even worse would be if this cell was actually able to avoid the death signals, and at some point enter the cell cycle with all of these damaged chromosomes and you are looking at the possibilities of cancer.
If it arrested and then proceed to G2 and M and somehow got through those checkpoints, then you will have two daughter cells with incomplete genomes. Again if they could survive at all, then likely end up becoming good candidates to proceed down the road to cancer.
That is why G1 needs to be completed properly before the cell commits to replication. It is a point of no return and needs to be tightly regulated for the benefit of the multicellular organism.


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What is the effect of the wavelength on the spectrophotometric measurements of protein?
Does the wavelength setting affect the absorbance reading of a spectrophotometer? For example, if I am using a spectrophotometer at 550 nm to determine the protein concentration of my samples, would my results be different if I analyze them at 500 nm?

I don't understand your question, can you clarify it?

The change in absorption due to concentration (Beer's Law) is the most at the wavelength of maximum absorption. But using another wavelength should give you similar results, but they would be so accurate.

correct me if I'm wrong. The change of the wavelength would result in a lower absorption, but it will be similar to the one with the bigger wavelength.

Molecules will have a certain range of absorbance with a peak at a certain point. A wavelength longer than the peak absorbance and shorter than the peak absorbance will result in more light being recorded by the detector. You can determine peak absorbance by taking several readings of the same sample  and varying the wavelength of the spectrophotometer. you will need to make very small changes around the peak to find the exact peak wavelength, but you should be able to find it this way. On the opposite sides of the peak, absorbance will fall off to near 0 if you have calibrated for solvent.

@AMR perfectly described what I mean by wavelength of maximum absorption. You should do your analysis at this wavelength. But if you do it at another wavelength, then it will give you similar results but the result would be less accurate.

In addendum, keeping the wavelength around the absorption maximum for the light-attenuating species avoids introducing error into Beer's Law. There are limitations to the law, outlined here where we can see that around the lambda max, there's little change in absorption per unit wavelength:

In case B, this would end up returning a bad extinction coefficient! You can experimentally determine this point either by testing the solution at different wavelengths or more accurately, running a program where the machine goes through it's entire wavelength range and measures absorption for you. You'll get a parabola where the maximum is your lambda max, so it's solvable by calculating the maxima if necessary (take the first derivative, set y'= 0, solve for y when x = (y'=0) for the associated ordered pair). You also want to be careful when you're using something like the Bradford assay where the bound form of the dye shifts the lambda max!

Nice information +1. However, in an experiment I would not expect the wavelength of the incident light to change (if the light is monochromatic). Also, I do not understand Figure B. Why would absorbance vs concentration become non-linear for non-λmax wavelengths?

I think this is the explanation here. As far as the math goes I'll admit I'm not actually 100%!

Light absorption happens because of interaction of light with electrons (in a way) such that the energy of the light is transferred to some electrons that moves them to a higher energy state.
As per quantum chemistry (Bohr's model of hydrogen can be referred for a basic understanding), there are distinct energy states (solutions of the Schrödinger equation) and there are no intermediate levels. Therefore, to excite an electron to a higher energy level the energy of the incident light should match the energy gap between the ground state and the excited state.
In a molecule, there are different electrons, that reside in different orbitals and environments; only a few electrons can be exited by the energy that UV-Visible range of the electromagnetic spectrum can provide. These electrons are typically referred to as chromophores. You should refer to a book on spectroscopy for more details. A molecule can have multiple chromophores and each may absorb a different wavelength.
Having said that, there are energy bands (multiple closely spaced energy levels) in the molecule instead of fixed energy state which allows absorption in a range of wavelengths around a value at which the absorption is maximum. The wavelength vs absorption graph will give a peak at the maximum (which usually looks symmetrical but not always necessarily be so).

 From ChemWiki

The width of this absorption band would differ between different chromophores; so in your hypothetical case, some chromophore which has an absorption maximum at 580nm may absorb 530nm while another chromophore with same maximum, may not.
The Beer-Lambert's law will hold for all wavelengths that can be absorbed i.e. the absorbance would be proportional to the concentration of the molecule (unless there are complex phenomena like energy transfers that may be dependent on concentration; this is unlikely in dilute solutions).
As a practical suggestion, I would say that if your spectrophotometer has fixed options then choose the wavelength that is closest to the absorption maximum.
If you see the above example graph and let's say your aim is to quantify nitrophenolate in a mixture of nitrophenol and nitophenolate. Then a measurement at 350nm instead of 400nm would give you erroneous result. In other cases a 50nm difference may not matter (for e.g. measuring at 450 for the nitrophenolate). It all depends on what you are analysing. You should know the molecule that you are analysing.

The Bohr model is only valid for hydrogen. However the Schrödinger Equation takes into account all the rest... so I would probably edit, to just mention Schrödinger.

From Chemistry 8th Ed - Zumdahl & Zumdahl "At first Bohr's model appeared very promising. The energy levels calculated by Bohr closely agreed with the values obtained from the hydrogen emission spectrum. However, when Bohr's model was applied to atoms other than hydrogen, it did not work at all. Although some attempts were made to adapt the model using elliptical orbits, it was concluded that Bohr's model was fundamentally incorrect."

@AMR We are not even arguing which is the best atomic model. I had mentioned Bohr's model because it is easy to understand for a beginner in spectroscopy. Though it is obsolete, the fundamentals that describe energy levels are not incorrect even though they are applicable only for hydrogen atom. I cannot take the OP through a course on quantum mechanics. Nothing that I had said is misleading I guess; however, for your satisfaction I made the edit :)

I would probably have mentioned something about conjugated systems reducing the energy of the photon needed to get the electrons to change energies, resulting in "absorbing" longer wavelengths and probably not worried about mentioning Bohr and the Man with the Cat, as the OPs lab exam is more likely to have a question about why PNP can absorb light in the visible spectrum that about quantum theory,... but then that is just me.

@AMR Conjugation is just one case but there can be several ways including splitting of orbitals, interaction with solvent or other dipoles in the molecule, etc. That will go in a different direction altogether. Best to avoid that IMO.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

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Does opening the lid of the spectrophotometer affect my results?
If I'm performing an experiment using a spectrophotometer and I mistakenly forgot to close the lid on the spectrophotometer, would that affect my results?

ambient light from the room can leak into detector and create artifact in reading. best way to test it is to record absorption without sample and open lid.

It depends on the construction of the spectrophotometer, the wavelength of light you're detecting, and the sensitivity/accuracy that you're demanding of the result.
In the past I have used spectrophotometers which were completely missing their sample lid, with no appreciable detriment to the result. Several things were in my favor, though. The light path from the sample to the detector was suitably collumated, such that any light that wasn't coming from the sample was blocked. I was attempting to detect far UV wavelengths (e.g 260 nm), for which there is little to no ambient source - attempting to detect a wavelength at the peak of a fluorescent light wouldn't have been as successful. I also didn't need highly accurate results, and I was able to dilute my sample such that it fell within a region (~50% absorbance) that is least sensitive to small changes in the amount of light being received.
In your case? If you can retake your measurement "properly", then I'd recommend doing so. If not, you can run some tests (like user aaaaaaa suggests) with some other similar sample, seeing if the absorption readings for that wavelength are affected by having the lid open.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Are mitochondria alive?
I'm working on an assignment for my IB biology class and some assistance would be highly appreciated. I've read several articles and I still haven't quite gotten the answer I'm looking for. I have to write a one page summary on whether or not Mitochondrion are alive or not.

Think about the definition of a living organism... Does it reproduce, or some kind of growth? Can it live by itself?

Mitochondria are symbionts that are no longer free living. Some of there essential genes have been incorporated into the hosts genome and some remain within the mitochondria themselves. After billions of years of coevolution, they have, for the most part become organelles, and are considered to be organelles. You could not lyse a Eukaryotic cell and grow mitochondria. But Eukaryotic cells need mitochondria to function efficiently.

The definition is a matter of philosophy and not everybody agree. And typically "can it live by itself?" would be a pretty misleading question given that it would exclude all parasite from the realm of living things. If you push the concept of ecological interdependence a little further it would even yield any living individual to be excluded from the realm of living things. A wolf for example is not a living thing just because it depends on its preys and on the plant that is producing its oxygen (and other species with which it has a relationship).

@TanMath, you have just given a 50-50 scenario. They can reproduce, as that is how the cell gets new mitochondria, but they cannot live by themselves as some of their key genes have been transferred into the host genome, so vital proteins can no longer be synthesized but the mitochondria.

@Remi.b. Free living in this case implies having a complete genome. Mycoplasmas have extremely small genomes, but they have all of the genes that they need to function. Humans cannot synthesize all 20 amino acids and need oxygen and other things from our environment, but our genome allows us to interact and survive within that environment. Mitochondria have transferred many of their genes to the host genome. They do not have the genes they would need to produce the essential gene products that they would need to survive in say an enucleated cell, such as an RBC.

@AMR I was reacting to Can it live by itself? in TanMath's comment, not to free living in your comment

Welcome to Biology.SE
Fields of interest
The assignment you have to write has a little bit to do with Biology and a little bit to do with Philosophy! The question of what is alive and what is not depends on the very definition of what is a living thing and this question is not of interest to biologists but only to philosopher.
How to nail this assignment
Therefore, for your assignment you will need to understand what a mitochondrion is (the Biology part) and to understand how do the different definitions of life apply to the mitochondrion (Philosophy part although you will need some knowledge in Biology to understand the relevance of these definitions).
What is a mitochondrion?
This question is too broad and cannot be answered here. Make sure to have a look at the wikipedia page. In short:

mitochondrion contain DNA
mitochondrion is the result of a bacteria that has somehow been internalized into a bigger cell (it is a symbiont). This is why today mitochondrion contain DNA. It is therefore not exactly an organelle like others. Note that plants, in addition to having mitochondrion, they have plasmids that are also consequences of a similar process of internalizing other form of life.
mitochondrion DNA evolve (of course)
mitochondrion are basically the energy factory of the cell.
mitochondrion are not able to live by themselves outside a living cell (to my knowledge).

Definitions of life
It is important to understand that the definition of life has absolutely no impact on biology and is nothing but a question of nomenclature.
There are a lot of definitions and I can't cover all of them here. You might want to have a look at this wiki page. The previous link lists the most common properties we think about when thinking about the definition of life.

Homeostasis: Regulation of the internal environment to maintain a constant state; for example, sweating to reduce temperature.
Organization: Being structurally composed of one or more cells — the basic units of life.
Metabolism: Transformation of energy by converting chemicals and energy into cellular components (anabolism) and decomposing organic matter (catabolism). Living things require energy to maintain internal organization (homeostasis) and to produce the other phenomena associated with life.[49]
Growth: Maintenance of a higher rate of anabolism than catabolism. A growing organism increases in size in all of its parts, rather than simply accumulating matter.
Adaptation: The ability to change over time in response to the environment. This ability is fundamental to the process of evolution and is determined by the organism's heredity, diet, and external factors.
Response to stimuli: A response can take many forms, from the contraction of a unicellular organism to external chemicals, to complex reactions involving all the senses of multicellular organisms. A response is often expressed by motion; for example, the leaves of a plant turning toward the sun (phototropism), and chemotaxis.
Reproduction: The ability to produce new individual organisms, either asexually from a single parent organism, or sexually from two parent organisms,"with an error rate below the sustainability threshold."

Related questions
The question of whether viruses are alive is a very common one. Here are two Biology.SE posts on the subject:

why-isnt-a-virus-alive
changing-the-definition-of-life


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Why are viruses considered microbes?
My question is simple. Why is a virus considered a microbe? Considering a microbe is considered to be a "living" unit of life, which viruses are not.

"Life" is either a) arbitrarily defined or b) poorly defined.

Who considers a microbe to be "a living unit of life"? Do the people who use the word "microbe" use strict scientific definitions of life? In my experience, "microbe" is not a scientific term (although it may have been one once), it's a folklore word for "tiny bugs which make you sick". When a grandma tells her grandchild "cover your mouth when you sneeze, you're spreading microbes everywhere", she neither knows nor cares whether a biologist would classify the microbes as alive. Your question seems to need no biologic answer, but an epistemological one.

I think these sort of questions arise because we are generally too lazy to properly define terms. I've asked a similar question before: "Why isn't a virus alive"? We need to carefully define "life" every time it's brought up: Genetic code? Membranes? Ability to replicate? High cognitive power? Each has problems & caveats, but without a measurable feature, it's a moot discussion. I'd suggest reading The Seven Pillars of Life by Koshland, 2002.

Some recently identified viruses are considered alive due to their more complex organisation such as mimiviruses. Take a look at This it's pretty interesting.

What is a microbe?
A microbe (or microorganism) is a microscopic organism. Anything that is considered alive and that is small enough is called a microbe.
Note that this definition has two issues.

There is no universally accepted definition of life.
There is no universally accepted size threshold for being called a microbe (to my knowledge). I would go with a threshold of about $10^{-5}$ meters.

Is a virus a microbe?
A virus IS and IS NOT alive depending on the definition. Note btw, that the definition of what is alive is not a matter of Biology but a matter of Philosophy. Most of the time, viruses are considered as not being alive. It is important to understand that the definition of life has absolutely no impact on biology and is nothing but a question of nomenclature.
If you want to call a virus a living thing, then yes, viruses are microbes. As stated on the wiki article:

Some microbiologists also classify viruses (and viroids) as microorganisms, but others consider these as nonliving.

You can find a discussion of why viruses are generally considered as not being alive here.
Unit of life
The concept of "unit of life" has not much meaning in biology and, to my experience, is most often used as a nice image for teaching young students what a cell is. Most of the time that I heard of "unit of life" (mostly when I was in secondary school and eventually high school) was used to describe a single cell making up a multicellular individual such as a cell of your blood for example and not a unicellular individual.

Viruses are not alive until they are inside the body of the host organism (plant or animal). Viruses are active once they are inside the host and reproduce inside the host. They are a link between living and non-living.

Viruses are small bits of genetic code in a protective covering. Viruses are not "alive," that is, they cannot replicate, unless they are inside another organism. A virus is definitely too small to be seen without a microscope. Since viruses are so small (tinier than bacteria) they may be considered microbes. However, since they are not "alive" outside of a host organism, it is debatable whether they are really organisms at all. For convenience since they are neglected in other areas of biology, viruses are discussed in microbiology. Most viruses are known because they cause disease.

The claim [some organisms] are not "alive," that is, they cannot replicate, unless they are inside another organism is pretty bas IMO because following this logic, an endosymbiont cannot be a living thing. Plasmodium wouldn't be a living thing for example. Note also that stating Viruses are not alive reduces the discussion to a single definition while several exist (it has the advantage to highlight the result most common definition though)

@Remi.b: My personal definition, as a theoretical ecologist, is that if you can meaningfully study its ecology and evolution, then it's alive. :) That easily includes viruses. Of course, if you define "ecology" and "evolution" broadly enough, that definition can also cover a lot of things we would not usually consider alive, such as languages and ideas. I'm not really sure if that's an argument for or against it.

@IlmariKaronen As a theoretical evolutionary biologist, I like your definition! However, it is not the most common definition. In any case, I think pretty much everybody agrees that excluding from the realm of living things, everything which reproduction depend on other life forms is quite a bad idea!


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How to write 100% phenotype ratio?
I am not quite sure how to write 100% out come for the phenotype ratio after using "Punnett Square". The result from the each alleles, the dominant allele completely(100%) took over the recessive allele.
How can I express my phenotype ratio?
(Let's say....Purple flower→dominant White flower→recessive)

Phenotype/ Purple flower 1: White flower 0
Phenotype/ Purple flower 4 :white flower 0
Phenotype/ Purple flower 4

I am voting to close because It is a question of language and not of biology.

You could write "ratio of purple to white flower 1:3" I suppose. Also you should clarify whether you want to express such ratio in a sentence or as a list of such ratios.

Note btw, that there are a few typos in the title of your post.

I understand the how to express the ratio of the our come of 1:3.....but I was not quite sure how I should do to express when the outcome is 100%......I guess I could do with "Purple flower4: white flower 0".....!?

...sorry about the typo....

Oh... maybe I misunderstood your question then. The question might be about basic math and not language. A ratio of white to purple of 1:4 corresponds to 25% white flowers and 75% purple flowers. Does it answer your question?

thank you for your help...yes, that is true that it is 1:4...., however, my instructor was using this ratio of 2:2:0 when we did multiple alleles....I thought there are rules about how to create "Bio ratio" using "Punnett Square".....so.....if it is 100% outcome of the genetic cross, it will be 4:0....hmmm, still little confused....

@Remi.b Just to clarify, a ratio or 1:3 (not 1:4) corresponds to 25% white and 75% purple flowers.

The phenotype ratio would be 4:0.
You did not include the complete example including the genotypes, but an example that might produce this result is:
P is a dominant allele that produces purple flowers, and pp homozygotes are white.
    P    p
  -----------
P | PP | Pp |
  -----------
P | PP | Pp |
  -----------

The genotype ratio is 2:2:0 (2 PP : 2 Pp : 0 pp) meaning there are 50% PP and 50% Pp.
The phenotype ratio is 4:0 (4 purple : 0 white) meaning there are 100% purple and 0% white flowers.
To keep things simple, you do not need to reduce the ratio to the lowest terms (in other words, the sum of the numbers in the ratio should equal the number of boxes in the Punnett Square). It would not, however, be incorrect to reduce the genotype ratio to 1:1:0 and the phenotype ratio to 1:0.

Thank you so much for your help! Especially giving an example of genotype.! I can clearly see the difference now. And yes....I should have given my example a lot more clearer....
one more worries....the way I should answer fully...is going to be...
" purple flower 4 : White flower 0" for the phenotype...? If you could help me once again....

@Runa I do not understand what you are asking now. It is a matter of preference whether you reduce the ratio to lowest terms (that is 1:0). However, from your comments it appears your instructor is keeping things simple by making sure the number of boxes in the Punnett Square add up to the sum of the numbers in the ratio, which is why I suggested the best answer is 4:0.

Yes...you are very correct...
My worries are not about the number anymore but how to express"Biology term ratio"(Thanks you as you explained, it made all clear for the number.) it is just about how to answer the question, how to write....(I was not sure if there were the big rule about "how to write the biology term of the ratio")...I guess I am little like " being-worry-too -much"...


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How to determine suitable Cysteine mutations?
In the lab, I'd like to generate a dimer of a protein via disulfide bonds. The interface between the two looks as follows:

Now, in the interface, there isn't any cystein I could use to dimerize the two, so I'll introduce some (bacterial transformation). But which place would be the best to introduce them? Probably not the alpha-helices or beta-sheets. But is there a general method to find the best linking site? Maybe there are program to calculate an energy minimum? Or is there a nice heuristic?
Here  a picture of a close-up of the interface.

Ive had success with Disulfude by Design, though it doesn't tell you how the suggested mutations will affect protein structure.

You need proper bioinformatics analysis to get predictions on this. Do molecular dynamics simulations for such calculation. One of most famous free tool is GROMACS.


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What was Protein G named after?
Protein G (the bacterial antibody binding protein) is often used to pulldown antibodies, for example in chromatin immunoprecipitation (ChIP) experiments.
However, I was unable to find a site describing the history of the said protein, and how the name of Protein G came about, due to the fact that the similarly named (but completely different) G protein came up higher in search results.
What was Protein G named after? For example, Protein A was named after the antibody fraction in which it was found, and G protein was named because it bound GDP and GTP.

This paper seems to suggest that protein G is so named because it was isolated from group G streptococci.

@canadianer is correct. Group G comes from Lancefield serum type G and it was a method that used to be used to classify bacterium and Group G Streptococci could be identified using this method. The protein was isolated from G148 S.aureus. Canadianer should post as an answer. +1

G148 is a Streptococcus strain. I incorrectly used the Genus and Species for Staphylococcus aureus in my prior comment. Protein A was isolated in S.aureus, Protein G in Streptococcus G148.

As @canadianer mentions in his comment, Protein G is more than likely named after the human group G strain of Streptococci, G148.

Protein G, a bacterial cell wall protein with affinity for immunoglobulin G (IgG), has been isolated from a human group G streptococcal strain (G148).

Purification and some properties of streptococcal protein G, a novel IgG-binding reagent. - Björck et.al.
Protein G is a  Streptococcus protein that can bind the the Fc portion of the Immunoglobulin G protein. While it is similar to protein A, it was found to have better binding affinities to the different varieties of heavy chain constant regions of IgG molecules.
The G comes from Lancefield grouping. Lancefield grouping was a method that used to be used to classify bacterium. Group G Streptococci could be identified using Lancefield serum type G and that is how they received their classification.


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What kind of tortoise is this?
Can you help me to ID this tortoise? It was walking around near to my house and then my mom found it, so we'd like to know more info. Its Straight Carapace Length is about 5+ inches. Found it in mid-Mexico (Guanajuato state). Most part of the year we have a warm weather.

Where do you live?

@canadianer just edited the question.

Could you please post the number of toes on the hind legs when you have a chance? Thanks.

The front end of the plastron (the flat 'ventral' part of the shell) is hinged, so that the turtle can enclose itself almost completely, a characteristic of box turtles.

Box turtles are turtles of the genus Terrapene native to North America (United States and Mexico). They are also known as box tortoises, although box turtles are terrestrial members of the American pond turtle family (Emydidae), and not members of the tortoise family (Testudinidae). The twelve taxa which are distinguished in the genus are distributed over four species. They are largely characterized by having a domed shell, which is hinged at the bottom, allowing the animal to close its shell tightly to escape predators.

Your turtle certainly has a domed shell. There is a lot of wear and tear on the shell, but not so much on the plastron. Box turtles can live 100 years.
From the lack of coloration on the top part of the shell and the paucity of markings on the plastron, I think it is either a Three-toed Box Turtle (Terrapene carolina triunguis), or a Mexican Box Turtle. The Mexican box turtle can grow slightly larger than the Three-toed box turtle. I can't really tell them apart. Boxturtles.com might help.

Their appearance is similar to that of the Three-toed Box Turtle.

The three-toes refers to the hind feet (which can also have four toes, to make matters worse.)

Three-toed box turtles have a domed shell which grows to an average 4.5 to 5 inches in length. The record shell length for this subspecies is 7 inches. The highest part of its carapace or upper shell is more posteriorly positioned than in the other subspecies. The dorsal and limb coloration is commonly completely absent, although some dark blotches are common in adult turtles. These areas more often being a uniform olive green or tan color.

From another site:

Shy and quiet are the traits of a Three-toed Box Turtle, both in its personality and in its coloring. Unlike the bold patterning and color seen on other eastern box turtles, the color of this species is quite subdued. Occasionally there will be a Three-toed that is more brightly colored, but for the most part they are a fairly uniform olive-brown to brown or horn color.

See also Reptiles & Amphibians

Thanks for your response, will update with the number of toes as currently  later as I'm out of town but this was a really good first approach to know it.


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Serotonin activity with short 5-HTT promotor region and depression
So after reading a few studies (1,2) it seems that a shorter promotor region for the serotonin transport protein may be associated with increased likelihood of developing depression after stressful life events.
I'm still an undergrad but this would seem like it would lead to less transcription of the protein leading to more serotonin at the synapse. My understanding is that this should then lead to some sort protection against mood disorders not the increased likelihood of them like the studies suggest. Is someone able to explain what I'm missing here?
Thanks,
Zane


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What are the key differences in giant and large unilamellar vesicle preparation processes?
I have to study my peptide's folding on membrane mimetic (model membrane) by circular dichroism spectra. Now I'm looking for suitable methods for preparation of vesicles: LUV, SUV, GUV- large, small and giant unilamellar vesicles.
I have studied several methods but I am having a hard time grasping the key factors that affect the resulting vesicle size (LUV, SUV, GUV, etc.)
Any pointers are greatly appreciated.

Giant unilamellar vesicles (GUVs) are made by methods like hydration of phospholipid membrane generally by use of some solvent , use of electric current, combining small vesicles etc.
large unilamellar vesicles (LUVs) are made by methods like evaporation with low concentration of phospholipid, dialysis etc.
Small unilamellar vesicles (SUVs) are made by methods Injecting solution spontaneously, microfludic methods etc. There are many methods reviewed extensively (just search in pubmed you will get lot of them)
Now coming to your question, factor which affect sizes are depends on method you are using. I will list out few, rest you can check in references of each method I gave above. Most of times these methods will have all kinds of vesicles. Success of these methods relies on which method gives you highest proportion of vesicle size you desired.

Microfludic method - total flow rate, ratio of solvent to aqueous phase (Kastner et al 2014)
Electric method - rate of application of electric field (Angelova and Dimitrove 1986)
Hydration method - amount of phospholipid, evaporation rate (Lasic 1988)

Besides all of this, basic physics behind this explained here like energy difference shown below
(Image taken from (Lasic 1988))


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E.coli division and its DNA replication
E.coli divides in 20 minutes and its DNA replicates in 38 minutes .Kindly explain.


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Protein modification and ATP consumption
According to wikipedia there exists a lot of ways to modify a protein (post-translationally). Just to mention few: phosphorylation, dephosphorylation, glycosylation... While phosphorylation requires an ATP molecule, the reverse reaction, dephosphorylation, does not.
How about the other process?
Do all modification respect this scheme (i.e. one transformation consumes ATP but the reverse transformation does not)?
If not, I am particularly interested to know if one transformation and its reverse transformation both requires ATP.
Thank you

ATP is adenosine triphosphate. The reason protein phosphorylation usually consumes ATP is because the ATP contains the donor phosphate group. Some other post-translational modifications have ATP-dependent steps (e.g. ubiquitination), but not most (e.g. acetylation). As you say, there are a lot of ways to modify a protein post-translationally, so why not look at the wikipedia pages for the various modifications to see which ones have steps that require ATP?

I don't think there are any which have direct ATP involvement in both steps. Indirect dependence may be there.


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Where does the inverse seconds unit come from in the association constant?
I'm working to determine Kd(s) kinetically by generating association and disassociation curves.  Kon (association constant, or on-rate) is in inverse seconds multiplied by inverse molar.  I get that the molar comes from concentration, but where do the seconds come from?

First order association reaction:
$$\ce{A + B <=>[k_f][k_r] AB}$$
Rate of association (units: concentration per time) = $k_f\times[A]\times[B]$
 Since [A] and [B] are concentrations and LHS is conc. per time the units of $k_f$ has to be such that it gives conc per time when multiplied by conc2 ([A] ×[B])  Which is conc-1 × time-1
Rate of dissociation (conc. per time) = $k_r\times[AB]$
 Therefore units of $k_r$ would be time-1.
Dissociation constant is actually $\dfrac{k_r}{k_f}$; Its units therefore would be conc.


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Hemiptera sp preimago?
Which species of Hemiptera is this preimago, seen in 2015 in Rome?

Can you please download the image from flickr and upload it here? You can credit flickr and the photographer.

What is the question?

I am the photographer. Can you help me identifying this species? Thank you again! Elena

@Elena You should add the picture here. And you should edit the question to add details such as geographical location, environment type, climate, habitat or whatever you can tell about the organism. Have a look at other [tag:species-identification] questions.

I think this is an Aphid because it has long, thin legs and two-jointed, two-clawed tarsi and resemble the Russian wheat aphid very much. They are very common in temperate zone and is a major plant pest.
Here's how the Russian wheat aphid looks:

Source:Website of tasmanian government


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How does one predict the methylation pattern?
Suppose, we have a double stranded DNA like

5' AGCTAGGAGAGACCAGGTTCC 3'
3' TCGATCCTCTCTGGTCCAAGG 5'

Where would the methylated cytosine be? Is there any randomness?

It is usually at CpG however there are non-CpG methylations too. It is not easy to predict. You can however use machine learning by training from existing experimental data.


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What sort of seed pod is this?
My son found this floating in a stream in Massachusetts, in the northeastern US. It was intact when he found it, but he cracked it open to see what was inside. I did some Google image searching, but couldn't find anything. Any idea what it is, and where it came from?

Are there any trace of a hole through which a bug could have entered? The content looks messy. Can you isolate seed ?

@bli no, there weren't any holes in it. I haven't dug around in it, but I can take a look for seeds when I get home from work.

Looks like a gall such as an oak gall.

Looks like a gall. was it delicate and lightweight? If so I'd guess it belongs to the oak apple gall wasp

It's actually not a seed pod, but rather a gall (see here or here for more info about galls). Specifically, it most likely is a gall belonging to the Oak Apple Gall Wasp (Amphibolips confluenta). You can read about this species and its gall here.

Yes, it was quite light for its size, and I suppose "delicate" could be used, but it was certainly difficult to cut open :)


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Species-area relation graph
When species richness is plotted vs area, the graph follows the equation : log S = log C + Z log A where Z is the slope of the line. Z values are usually in the range of 0.1 to 0.2 but if very large areas like entire continents are analyzed, the slope is much steeper. (0.6-1.2).
Why is it so ?
(Here S = species richness and A= area under consideration)

Interesting question. Can you please add some reference and eventually two graphs that show different slope depending on the range of areas used? Note also that if $C$ designates a constant (which I think it does), then $log C$ is a constant too and could well just be replaced by $K$ (or just write $C$). You should also make clear that $S$ is species richness and $A$ is the area even though it is quite intuitive.

@Remi.b The full log notation is useful to highlight that the basic relationship is a power law: $S = CA^z$

Perhaps because when analyzing large areas, adjacent masses of considerably different climatic conditions are successively bought under analysis, and will hence increase the richness faster than compared to small areas where increasing the analyzed area is still more likely to be confined to the same geo-climatic zone. Just speculations, though. Will get back with a better answer.

Right, @Satwik Pasana. Also consider that evolutionary history becomes increasingly important when you're looking at large areas.

@satwik pasani That makes sense. Actually when I had asked the question I had a wrong notion of what species richness is but now what you say seems logical. Add it as an answer !

@Hav0k Could you elaborate a bit ? Do you mean to say that larger the area, more are the chances that a larger no of species would have evolved in it ?

Well, not exactly. I meant that when you increase area, at some point you will likely add regions that share different evolutionary histories and thus add disproportionally more species, thereby increasing z. Imagine you start with a small area in North America and increase its size until it encompasses all of NA. Now there is no more area in NA to add, so you start adding parts of South America. These species assemblages differ drastically from North American ones and even small increases in area will yield many new species --> your z increases.

@hav0k ok yes. That is a really good explanation too.

What are the data points in the relationship you are thinking about (the "samples")? The number of species vs area for each continent or species richness vs area for subsamples ( or nested samples?) taken at the continent level? Relatively often, slopes of mainland areas or well-connected islands are smaller than slopes for more isolated island groups.

@fileunderwater species richness vs samples of increasing area

Either way, you should add a reference to back up your basic claim (steeper slopes for continent-level samples).

@biogirl Also, what taxa are you considering? To me, it is still also unclear whether you are asking about a species-area relationship where the data points are entire continents, or large-scale species-area relationships within continents (nested or otherwise).

@fileunderwater My question is just a general one. I am asking about large scale species area relations within continents.

Z value is a fitted constant and it ranges between 0.1 to 0.3 regardless  of the region or taxonomic groups.i.e. the slope is almost similar .Among larger areas like continent,the slope tends to be much steeper.becoz, Larger the area larger will be number of species(species richness),for larger areas the Z values tends to be 0.6 to 1.2.(NOTE:if Z is less,lesser area is enough to capture more species).


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C-myc/anti-myc Ab Interaction with Fusion Proteins
I am going to prepare a c-myc fusion protein with the following configuration:
(28-residue signal sequence)-(c-myc)-(GGSGGGSG Linker)-(Protein of Interest (POI))
POI is a transmembrane protein and the 28-residue signal sequence is needed for membrane incorporation in ER.
My concern is the disruption of the c-myc/anti-myc Ab interaction due to the fact that c-myc being fused on both ends. Does anyone have any experience or reference with a similar construct?

After some further research, I found papers reporting successful co-immunoprecipitation experiments with POI-myc-His fusion proteins.
Moreover, I figured the signal sequence will be cleaved by signal peptidases which will leave the c-myc tag exposed on N-terminus with only an extra residue. I don't think that one extra residue will create a problem.
Here's the tool I used to figure out where the signal sequence will be cleaved:
http://www.cbs.dtu.dk/services/SignalP/
Here are the references for POI-myc-His experiments:

DOI: 10.1016/j.cub.2006.08.085
DOI: 10.1073/pnas.97.2.668


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Applications of shortest path problem
The shortest path problem is the problem of finding the shortest path between multiple nodes. What are the applications of the shortest path problem in biology?
A simple google search gives me this - http://mutage.oxfordjournals.org/content/30/2/191.full.pdf
This, unfortunately is under a paywall.
Apart from that article, I can't find anything else useful.

Why the downvote?

There are several applications. This question is too broad. (Not my downvote btw)

@WYSIWYG like? A simple google search doesnt give me anything...

look for "bioinformatics" instead of "biology". ;-)

The classic application is analysis of graph data. For example, protein-protein interaction networks or gene regulatory networks and the like. There are various types of data that can be presented in the form of a network and network analysis is an integral part of Systems Biology.
Another example is determining the similarity of functional annotations from the Gene Ontology. One of the ways of doing so is finding the shortest path between two nodes in the GO graph.
Or, for a more concrete example, I recently published a paper where I examined various features of a particular group of proteins. One of the pieces of information I used was how central these proteins were to the network and, for this, I measured how often they served as a node in the shortest path between two others.
The simplest way for you to find more example is to go to PubMed and search for "shortest path":
https://www.ncbi.nlm.nih.gov/pubmed/?term=shortest+path

Thank you for your answer... Can you please give me a link to your paper?

@TanMath here you go, but it won't help you much. The shortest path analysis was a tiny part of the work, I only mentioned it because I happened to have done this recently. Your best bet is to go on PubMed and search for "shortest path".

Hace you seen my latest question about influenza? Do you know anything about that?


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What is the silencing mechanism of AGO1,AGO3 and AGO4?
I read that this proteins lack of slicer activity, so what mechanism do they use to perform gene regulation?

Just the presence of a large protein complex in the 5'-UTR of an mRNA can prevent ribosome binding and therefore translation. I'm not saying that that is the actual mechanism, but it's plausible.

Ago(s) of what organism? I presume you are talking about mammalian Ago. I am asking this because Ago proteins with same name may not be orthologs; for e.g. Drosophila Ago3 (along with Piwi and Aub) belongs to the Piwi family which in vertebrates includes Piwi, Piwi-like and Piwi-2. Also, there are differences between Ago1&2 of Drosophila and mammals. Plants have many Ago proteins (even C.elegans)

Paper by Zinovyev and colleagues in the paper "Mathematical modeling of microRNA‐mediated mechanisms of translation repression" find that there are reports to 9 different mechanisms of miRNA-regulation.

Here we are reviewing available experimental data on all reported mechanisms of microRNA action, grouping them in a way which elucidates the main details supporting each of these proposed mechanisms.

Here is a list of the mentioned mechanisms:

M1: Cap-40S Initiation Inhibition
M2: 60S Ribosomal Unit Joining Inhibition
M3: Elongation Inhibition
M4: Ribosome Drop-Off
M5: Co-translational Nascent Protein Degradation
M6: Sequestration in P-Bodies
M7: mRNA Decay
M8:  mRNA Cleavage
M9: Transcriptional Inhibition Through microRNA-Mediated Chromatin Reorganization Following by Gene Silencing

Also here is a link to the Pubmed entry of the article:

Perhaps you could briefly summarize the mechanisms.

And could you add a proper citation with a web link? -1


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Why do some bacteria have an asymmetric replication?
Our teacher said that Bacillus subtilis has an asymmetrical replication fork.
I know that this happens only in some strain of the bacteria . She asked us to find an explication for this mechanism , but all that I was able to find is that the chromosome is more compacted in some areas, therefore it slows the replication .
Are there other reasons?

Are you sure that your teacher was not referring to asymmetric replication as in asymmetric cell division? B. subtilis undergoes asymmetric cell division, whereby the two daughter cells have different fates, in this case during sporulation. Are you at a college level? If so, then there is this article. It might be a little too advanced if you are not at the college level. If it was in fact replication, then it is likely that she wants you to explain leading and lagging strand synthesis.

The replication fork itself is always asymmetric. This is true for all organisms and is due to the fact that DNA polymerases can only add nucleic acids to the 3'-OH end of DNA. This leads to different mechanisms for the replication of the so called leading and lagging strands. You can find more details on wikipedia https://en.wikipedia.org/wiki/DNA_replication
Most Bacteria have circular chromosomes that they usually replicate using two replication forks. Both forks start from the origin of replication and progress in opposite directions to meet at the replication terminus which is opposite to the replication origin on the circular chromosome. Each replication fork replicates about half of the chromosome. We talk about the left replicore and the right replicore. I assume that your teacher was referring not asymmetry in the replication fork itself, but to asymmetry in the size of the replicores. In B. subtilis the left replicore is 196 kb longer than the right replicore (J Bacteriol. 1993 Feb; 175(3): 741–749.). I do not know whether there is any evolutionary explanation for this, but mechanistically it is caused by the fact that the terminus of replication is not placed opposite to the origin of replication on the circular chromosome.


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Polymerase Chain Reaction Questions
First question is about why we use primers in PCR. It requires two reasons. I know only one reason though. It is so that DNA polymerase can attach to primer and make a copy of nucleotide from there. But i don't know what is the other reason.
Another question is about why the primer bonds to 3' end of the DNA you want to copy. and explained why. I really have no clue for this one. Plzz help.

"why the primer bonds to 3' end of the DNA you want to copy. and explained why. I really have no clue for this one." How did you get to learning about PCR and not learn that DNA is antiparallel? DNA always has a polarity. Single stranded DNA has a 5' to 3' polarity. So do primers, which are just short ssDNAs.

We use primers in PCR because we are mimicing natural processes. DNA polymerase cannot act without primers. It needs primers to start it's work. Binding of molecules happen by chance, so the more there are of your primer, the more likely it is that it would bind to any given string of complementary DNA. DNA replication occurs in the five prime to three prime direction because phosphate doesn't allow the reverse reaction.

When a new nucleotide is added on to a growing DNA molecule, the reaction takes place on the hydroxyl group at the 3' end. The 5' end is a phosphate group, so it can't add there. It always has to add to the OH at the 3' end, so we say DNA always grows from 5' to 3'. Alcohols are fairly reactive and are intermediates in a number of reactions, if that helps you to remember.

Beside helping Taq to add dntps to the growing strand
Primers minimize the risk of mishybirdization as they are designed specifically for a specific region of DNA

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


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num_tol_term in PeptideProphet result
What is the meaning of the num_tol_term attribute in a PeptideProphet (pep.xml) search_hit?
<search_hit hit_rank="1" peptide="DATDDFEDVGHSTTAR" peptide_prev_aa="K" peptide_next_aa="A" protein="Traes_5AL_64120ED6B.1"
    num_tot_proteins="4" num_matched_ions="9" tot_num_ions="30" calc_neutral_pep_mass="1735.7364" massdiff="-0.0269"
    num_tol_term="2" num_missed_cleavages="0" is_rejected="0" protein_descr="| AT2G32720.1 | member of Cytochromes b5">

Found the answer in the PeptideProphet paper: number of tryptic
termini (NTT)

This number, which can be 0, 1, or 2, measures how
  many of the peptide termini, on the basis of amino acid sequence,
  are consistent with cleavage by trypsin.


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Do all different types of neurons serve different roles?
I know from my basic education in neurology that the brain has various sorts of neurons. These are usually bunched into 3 different categories (sensory, moto and interneurons).
I read in a recently published book, and papers on modern neuroscience that there have been thousands of different types of neurons identified in the brain. Does this mean that there are different types neurons each dedicated to a very specific task in the brain? If that is true, then what is each individual neuron's job (a few examples would be sufficient)?

Short answer
Neurons were (and still are) often identified based on their histological features (e.g., by Cajal). In turn, the structural hallmarks of neurons are often related to their specific functions.
Background
The question is broad and difficult to answer without restricting to some example types of neurons. As you say, about 10,000 types of neurons have been identified. Their roles are often obscure. I will restrict the answer below to a few examples of neurons with relatively well characterized histological features and relatively established functionality.

Fig. 1. Examples of neuronal cell types. A. Purkinje cell B. Granule cell C. Motor neuron D. Tripolar neuron E. Pyramidal neuron F. Chandelier cell G. Spindle neuron H. Stellate cell.source: Ferris (2012)
The Purkinje cell (Fig. 1A) receives large amounts of input in the cerebellum, integrates it and sends it away to deeper layers. Hence, as an integrator, it has an elaborate input side (large dendritic tree) and a single output axon. The basic  function is similar to the pyramidal cell in the cerebrum (Fig. 1E) and their appearance is hence similar.
On the other end of the spectrum is the spindle neuron (Von Economo neuron, Fig. 1G), which is believed to receive simple input and generate simple output and is built for speed. Less integration allows for faster responses. Hence, its dendritic tree is much less elaborated than the Purkinje cell (cf. fig. 1A) (Allman et al., 2011).
As a last example: the Chandelier cell (Fig. 1F); these neurons have axons that form elaborate collaterals that are believed to form local inhibitory connections in the cortex to keep (excessive) stimulation in check; hence their output is more elaborate, with relatively simple input. Dysfunction is believed to be associated to epilepsy (excessive stimulation) (Inan & Anderson, 2014).
References
- Allman et al., Ann N Y Acad Sci (2012), 1225: 59–71
- Inan & Anderson, Cur Opinion Neurobiol (2014), 26: 142–48
- Purves D et al. (eds.) Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates (2001)
Source
- Ferris, 2012, Sci Am blog


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How can I fit the A595 of my unknown samples to the data?
While I was conducting the Bradford Assay experiment to determine the concentration of my unknowns, I ended up by having an A595 for my unknown samples that is higher than the A595 of the standards. How can I resolve this issue?
wishes.. Micheal.

Just find out slop of your standard curve and then calculate unknown concentration from that. this might be helpful to you.

When you run a bradford assay the bound form of the dye shifts the absorption max to 595nm. This is what your spectrometer should be set to when you're running the assay. You make a standard graph because you can calculate an extinction coefficient ε from the slope of the graph. Beer's law says that A = εcl where your path length is determined by the cuvette you used, and c is your concentration. So you take your absorption that you obtained and solve for c! Canadianer makes an excellent point below, however, so make sure your methods make sense!

You could, depending on what you are doing, extrapolate your standard curve to include the absorbance of your samples. This, however, is not recommended since absorbance is linear only within a certain range. It's best to dilute your samples so that they fall within the range of the standard curve while also ensuring that your standard curve is, in fact, linear.


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What is the name of this plant, from Bangladesh?

This is a small plant from my backyard. I have found the flower closes in the evening.

You would like to compare it with a related species which is also common in the same locality. http://biology.stackexchange.com/questions/50513/want-to-identify-plant-and-flower

what could be the butterfly on the first image?

This plant belong to Malvaceae, and the yellow flowers open towards morning to mid-day.
This plant is most-likely Sida rhombifolia or may be Malvastrum tricuspidatum .
From broad leaves it seems not Sida acuta
Check epicalyx ( made up of bracteoles)... is there is no epicalyx then Sida rhombifolia.
If epicalyx is 3, it is Malvastrum tricuspidatum
look also https://en.wikipedia.org/wiki/Sida_rhombifolia,
https://books.google.co.in/books?id=Roi0lwSXFnUC&lpg=PA258&ots=N7DNvrN4UL&dq=malvastrum%20tricuspidatum%203%20epicalyx&pg=PA258#v=onepage&q=malvastrum%20tricuspidatum%203%20epicalyx&f=false
Epicalyx of Malvastrum tricuspidatum :

C= Corolla (all petals), K= Calyx (all sepals), E= Epicalyx the bracteole

3 bracteoles

I'd recommend adding an explanation of how to check the epicalyx and elaborating on 'if epicalyx is 3' (I know it's in the link but it's good practice to put this in the answer).


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Why don't we have two hearts?
The human body is amazing. But there seems to be some evolutionary changes that appear to not make sense regarding redundancy.
While not necessarily the primary reason for their existence, the human body has a great deal of redundancy.

Two eyes.
Two arms.
Two legs
Two ears
Two nostrils
Two lungs
Two kidneys
Two sets of teeth
A very large liver that can work in part.
Two brain hemispheres that can (to some degree) do the work of the other.
An appendix that is not critical.

But why do we not have two hearts? It would seem like a good idea to have two smaller hearts, together they work above optimally, but survival would be possible with one.

Having two of almost all of those body parts is absolutely better than one i.e there is no redundancy. Even if a smaller liver can sustain a human, a bigger one is more tolerant to potentially harmful toxins. The brain can reassign parts of the brain to an incredible degree after a hemispherectomy, but not completely depending on age and type of trauma. It also looks like our appendixes are important for our digestion system too.

Two atria and Two ventricles....

One esophagus, one trachea, one stomach, one spleen, one thymus, one small intestine, one large intestine, one thyroid, one spinal cord, one diaphragm, one penis (apologies to those with Diphalia), one tongue, one vagina, one clitoris, one cervix, one uterus, one urethra, one umbilicus, one rectum, one anus... what's your point?

@AMR If you're referring to my comment re: two is better, I should have prefaced it with the ancestral symmetry answer. This question is flawed in my opinion because it assumes symetrical anatomy has absolute redundancy. These symmetrical body parts work together to perform optimally with their partner and are not redundant. The question requires a fairly speculative answer based on false assumptions that we may never be able to scientifically test.

@GoodGravy oh heaven's no... I was not commenting about your comment... It was an observation about the question...

@AMR I see now! Still, I should have given my first comment more context.

OP. How would you coordinate two pumps in order to maintain proper fluid pressure? Or get them to respond in unison to fight or flight hormones? Imbalances would likely create eddies in the blood vessels that could lead to air embolisms or clots. Even for normal function, you would need the timing to be exactly correct. How would you propagate that impulse between the separated organs? All of the examples of duplicates are capable of working independently, though, as @GoodGravy said to perform optimally, they work together. The two hearts would need to work together perfectly to work at all.

@AMR there are other animals that have more then one heart. Worms for example have 5 hearts. I agree a worm is simple in comparison but it has obviously found a way to work with more than one heart.

@AMR also while we do have 1 of lots of other things there is normally a very good reason why there is only 1. Such as the space needed to have it, or the energy required to keep it working.   In the case of a heart it would be possible to have two smaller hearts and maintain a fully working system that could cope with some damage. Also two smaller hearts may work better as they don't need to be as powerful as they are only pumping blood "halfway" around.

Two arms working together is clearly better, And is probably the reason we have two. But four would be even better! but we don't have four. We don't have four as it would be too bulky and too expensive to maintain. Thats a good answer for arms.     But that douse not explain a single heart.

And clearly one heart is good as that's why we have one heart. But there must have been a good reason to stick with one and not develop two. The point is not to say evolution is wrong. its to answer why it chose what it chose.

It is not about redundancy. There are evolutionary and developmental  reasons why we have two eyes or two legs and one heart. However just to give you short examples, two eyes are better than one because of our binocular vision while we have two legs because of its locomotor energetics.


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Why do earthworms have 4 hearts?
I was reading about earthworms and came to know that they have 4 hearts.
Why is there a need for a 4 heart system? What advantages would it have over a 1 heart circulatory system except for pumping more blood obviously.

The earthworm heart is not really like a vertebrate heart. They are not that efficient. More like valves you can say.

"pumping more blood obviously" Is it obvious? To me it is more obvious that there are way more factors in blood flow than the number of hearts. An interesting factoid though, I didn't know about this! You learn something new everyday they say, thanks.

Today suddenly many people are concern about heart :P


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Why do we laugh?
Why is it that the reaction we get from absurdity is laughter? Everyone does it, even babies. Is there a reason why it is our instinct to laugh when we see or hear something absurd/humorous

I don't mean to be flip (well, not too flippant anyway), but one of the most profound things hidden in a Calvin and Hobbes strip - and there were quite a few profound things hidden in C&H - had to do with the evolution of a sense of humour, This is the strip I'm referring to: http://imgur.com/s0fZX

That is brilliant

There is a really good TED talk on this.

@biogirl is talking about this - https://www.ted.com/talks/sophie_scott_why_we_laugh?language=en

The book Inside Jokes by Hurley has the only idea for why humor and laughter evolved I have heard that actually made sense biologically, Including why it is so rare, it is only valuable to very intelligent species as a way to internally assess credibility of beliefs.

Like so much of biology, we just don't know!
I'll preface this answer by disappointing you; this answer doesn't entirely answer your question. That's because this is a pretty big mystery in research and a fascinating topic. I'll start with a couple of quotes that maybe explain why!

"If you search on the Web of Science database for papers on the emotion of fear, you’ll get back 6,477 published papers. Search for papers on laughter and you’ll get a paltry 175."

-Sophie Scott 2015
In other words, the lack of research into laughter possibly is because research usually tries to solve a problem. Generally, laughter isn't perceived as a problem and is relatively seldom investigated. Notably, there is a symptom called the Pseudobulbar affect. It describes someone that laughs (or cries) uncontrollably.

"Analysing humour is like dissecting a frog; few people are interested, and the frog dies of it."

-Elwyn Brooks White 1941
Why do we (as humans) laugh?
The consensus in the community of researchers seems to be that we laugh because it strengthens human social connections.
Counter-intuitively, it's not always because we find things funny. The linked article implies that although it's not exactly clear why we laugh, laughter is a form of seemingly non-deliberate social interaction that doesn't interrupt or replace speech, but adds to it. We laugh in addition to talking.
The evolution of laughter.
As you mention in your question, even babies laugh. Laughter is clearly not unique to humans, let alone human adults. Most social mammals laugh and there are lots of studies on ape laughter and a niche field in "rat tickling" which studies laughter in rats. Jaak Panksepp even found that rats can be bred that love to be tickled! That article also discusses the science surrounding laughter and the links laughter has with increasing neurogenesis. This implies that laughter emerged a long time ago even on an evolutionary timescale and contributes in a very real way to the wiring of our brain. It's not clear why this happens.
There is a popular but unfounded theory put forward by the philosopher John Morreall that laughter originated as some sort of group "the danger is over" signal after the flight or fight response.
Going back a step; what is laughter?
To fully place laughter in the context of our social constructs, we must first understand what laughter is. Unanimously, all types of laughter are non-verbal expressions of emotion (and above there is a reference to how laughter fits in around language, enriching it). These positive non-verbal auditory signals have been shown in primates to be involved with mirroring the emotions of others. At a higher level, there are different types of laughter in our social world ranging from Schadenfreude to laughter based off of specialist interest, all of which seemingly have different triggers, varying numbers of potential participants, and social purposes.
Another question is raised as people can interpret the authenticity of laughter. This study found that people can very easily perceive an inauthentic "polite tittering" from an "explosion of mirth". This highlights that why-ever we laugh, laughter has a complex and under-appreciated social underpinning in humans that we don't yet understand.
Personal views
To me at least, laughter may be the result of primitive non-verbal emotional communication and lie-detection; part of the intra-species evolutionary arms race of big-brained social mammals in terms of altruism and lying. For example, I would laugh, and I would gauge the state of you by seeing if you laugh too, and then I can act on how I think you feel; be it altruistically or selfishly. You would need to be able to tell if my original laugh was testing you, or genuine.
With that tool as a basic premise, one can imagine how such a wide variety of functions arose from a simple two-party status check.

If it's a social interaction that doesn't explain why we laugh when on our own (and often feel better for it!)

@Jez To counter that: it's usually much easier to find things funny when in a group.

@Jez Sophie Scott describes having problems in an anechoic chambre whilst trying to record isolated laughter from individual people laughing on their own.

@SmallLegend I just wish there was a review or something so that we laugh because it strengthens human social connections. can be referenced.

It is not known for sure. But I find Hurley and Dennett's theory very convincing.

Our brains are engaged full time in real-time (risky) heuristic search, generating presumtpions about what will be experienced next in every domain. This time-pressured, unsupervised generation process has necessarily lenient standards and introduces content - not all of which can be properly checked for truth - into our mental spaces. If left unexamined, the inevitable errors in these vestibules of consciousness would ultimately continue on to contaminate our world knowledge store. So there has to be a policy of double-checking these candidate beliefs and surmisings, and the discovery and resolution of these at breakneck speed is maintained by a powerful reward system - the feeling of humor; mirth - that must support this activity in competition with all the other things you could be thinking about.

I realize that the writing style is dense, and the quote requires some knowledge of their assumptions, so here is an explanation.
Pre-pre-explanation: What is a mental space?
A mental space is one of the modern assumptions of how humans organise the knowledge in their heads. I won't spend time explaining how it differs from other assumptions such as scripts. It is probably best introduced by thinking of fiction. When you watch Star Trek, you can easily think within the "Star Trek universe". You know that within this world, it is possible to beam up people, that money doesn't matter but dilithium crystals do, and so on. Your head holds a description of this world, and you can do logical reasoning to infer things which are true within this world.
A mental space is such a "world" within our head. It is rarely as elaborate as the Star Trek world. It is just a compartmentalization of our knowledge of our surrounding world, such that we can hold contradicting views of the world at the same time. This is useful, for example, when we consider whether we should hurry up for work: we can conjure up a mental space representing our day if we arrive at work on time, then a contradicting one where we arrive late, and compare them.
Pre-explanation: Why we find things funny?
Our heads are constantly carrying around innumerable mental spaces, some we actively think about, others buried in memory. And all the time, we are learning new information, which may or may not be true. It is in our best interest to incorporate true information into appropriate mental models (a mental model is a complex of theories which explain to us how something works), and discard false information. For example, when a Star Trek episode introduces the Tribbles species, we have to incorporate the information that Tribbles exist as true in our "Star Trek canon" mental space and possibly our "What I'd do if I were a Starfleet officer" mental space, and keep it as false in all other mental spaces.
What Hurley and Dennett are proposing is that our brains know how to evaluate information for truth value (or at least consistency with a mental model). This job is, like most jobs in the brain, too computing intensive for the conscious mind. But when it gets done, the conscious mind has to be informed about the computation result. This information arrives, as with all other conclusions of the unconscious computation, in the form of a feeling - in this case, the feeling of mirth. So, if you find something funny, it is a sign that the mental space you just built (which contains this "something") is incongruous and should be abandoned as untrue.
Explanation: Why we laugh?
We are social animals. It will frequently happen that we are all receiving the same new information from outside as our herd comrades. And out in the jungle, we frequently evaluate new information as being a possible danger. Is this rumbling a tiger? When a herd member has computed the signal and his sense of mirth has told him that the "this is dangerous" mental space is internally inconsistent, the automatically triggered laughter will inform other herd members that the situation is safe and they can relax. This is what makes laughter contagious and pleasant (although they have additional arguments for "pleasant" - basically, a reward without which we wouldn't be inclined to go through the resource-hungry heuristic computations).
Summary

We feel something is funny when we consider a proposition which turns out to be untrue,

especially also when we consider a potential danger and it turns out that we are safe.

We laugh when something is funny as a signal to others that "things are not what they seem to be",

especially that a danger we may all be evaluating is not dangerous.

Arguments for the above theory
I only had the space here to present the content of the theory. For the arguments why they believe this theory to hold, and how it compares to multiple competing theories, please see their book. It is a truly fascinating read.
Hurley, M. M., Dennett, D. C., & Adams, R. B. (2011). Inside jokes: Using humor to reverse-engineer the mind. MIT press.

Truly insightful, never thought of it like that. Thank you sir

I'm confused. You started with a philosophical description of the mind and then concluded that because we are at ease when we hear laughing that there is some sort of pavlovian response that makes us feel safe when laughing. Perhaps I am oversimplifying, but the argument feels circular and very unscientific. Expanding from one of your points, there is an interesting point about jokes being funny because they don't match expectation. I think it was Ricky Gervais who first put that to paper.

To clarify on why this seems like a circular argument: The conclusion is it's own evidence. The premis is not empirically tested and the essay on the mind relies on assumptions, misconceptions, and oppinions aside from being heavy in anecdote. Your reference is about our sense of humour, which is not necessarily the same as laughter as most of the other answers tackle. Sorry to be so blunt; I do think that this is an interesting answer to read, it's just that I don't see the value in using "fluffy" descriptions in neuroscience, particularly when it's implied as set-in-stone fact.

@GoodGravy of course I couldn't replicate all the arguments of a whole book here. Sure, the theory comes from philosophy and is based on pure reasoning without any direct "empirical testing" as usual in neuroscience. But in the book, it is applied on many jokes and different humorous situations, and is shown to fit better than the other existing theories, including the old oversimplified "don't match expectations". Also, the premise from which it starts is the best we have. Theories about "do we think in scripts, frames, cognitive spaces", etc. are established and tested as far as we can.

Oh, and another thing: there are no arguments in my answer, except the one connection from humor to laughter. I needed this space to simply explain the claim of the theory. I did not attempt to reproduce any of the evidence for it - if somebody can do this in a reasonable length of text, I am not this person. The book I am speaking of uses 3 pages to explain the above, and another 370 to present arguments for it. So of course you won't feel convinced of the theory being true just by reading this answer - don't expect this, or take it as evidence that the theory is not true.

@rumptscho People have seldom investigated laughter because it's not a "problem" to be solved rather than because it's impossible to test. To leap to philosophical reasonable hypotheses as the absolute truth before we have pushed the limits of empiricism seems premature. This isn't exactly theoretical multi-verse physics yet, it's just messy neuroscience! As you say, the mind-space theory fits many humorous situations; Platos world of forms fitted really well too. Remain skeptical until there is conclusive data. Why should we be afraid to say that we don't know?

@GoodGravy 100% of science is simply hypotheses which best fit what we have observed so far. Nothing in science is proven as the absolute truth, that's the point of it. This is why have the theory of evolution, not the gospel of evolution. Also, looking at a branch of science which does its empiric research differently than yours and declaring it "not empirical" is short sighted. To sum it up: I am not afraid to say that we don't know much about laughter and humor. Neither is the author of the book I cite. But I am convinced that we have a good, stable theory here, not idle musings.

Science is hypothetical, but not all hypotheses are scientific. The multi-verse is an unscientific hypothesis for example (hence my reference to it). But I do not think that the science of laughter has reached that point since it remains scientifically testable. There is if anything too much data (hence it's messy).

In the case of laughing, there has been barely any research on this data. As it stands, the hypothesis you present is unscientific as it cannot be tested; it sounds contextual, abstract, and verbose. I hope I'm not coming across as short sighted, I'm trying to be pragmatic; "how do we test what laughter is?" rather than "Laughter might be X." Why settle for that hypothesis when there are scientific hypotheses available in the field? This answer doesn't reflect any uncertainty in the same way your comments do.

@GoodGravy First, how do you know that this hypothesis is unscientific, when you don't know either how it was derived, nor what scientific evidence there is for it, and how much it incorporates the findings you referenced in your own answer? You are making assumptions without having the information necessary to judge. Second, "this answer doesn't reflect any uncertainty"  - why? The first thing it says is "It is not known for sure". And the second says that the rest of an answer is a theory I have found convincing after having read the argumentation its authors have for it.

Conceptual blending, & other cognitive semantics aren't testable & are more akin to metaphor. I've seen it recently in computer development, and essays in cogsci, but not biology. If a study shows mental spaces are used in brains, or if they are linked to laughter, using experimental data please share it (my cursory search didn't come up with anything). I thought your first line is refering to laughter, not mental-spaces? You go on to assuredly discuss mental spaces before laughter again. It could be clearer I suppose.

Why do we laugh?
The leading research on why we laugh is done by Robert Provine. He has even written several books on the topic. His theory is that laughter was a primitve form of communication that evolved. For example,he and some graduate students listened in on average conversations in public places and made notes. And in a survey of 1,200 "laugh episodes," he found that only 10%-20% of laughs were generated by anything resembling a joke. The other 80%-90% of comments that received a laugh were dull non-witticisms like, "I'll see you guys later" and "It was nice meeting you, too."[1].
Reason
One reason could be is that it is to make other people nearby feel good and charismatic. It is used to show you like them. It is a social signal[1,2 3]. What would support this is the fact that laughter occurs more in social situations in front of a person[4].
Another, more older hypothesis is thaf the first human laughter may have begun as a gesture of shared relief at the passing of danger. And since the relaxation that results from a bout of laughter inhibits the biological fight-or-flight response, laughter may indicate trust in one's companions. Again, this is a type of social signal.[3] Plus, this may be the reason why laughter has evolved to be contagious. Again, the fact that laughter occurs in a social situation supports this hypothesis as well.
Note that laughter isn't just a human phenomenon. It is also a mammal thing. As @GoodGravy mentioned, rats do laugh when they are tickled. But also primates laugh, especially when they play. Also, this is a social situation.[2, 4]
Summary
In short, laughter is a more primitive, ancient form of communication. We laugh as a social singal, not to say something is funny. Humor is not always the cause of laughter. It has to do with social situations. It is to show support and liking for the people around you. It is to make the atmosphere more charismatic and happy.
Really, the point I am trying to get is that laughter is a primitive form of communication in social situations to show support and likeness to others.
Your question is a great one and I enjoyed researching on this topic.
References
[1] - http://www.webmd.com/men/features/why-we-laugh
[2] - https://www.ted.com/talks/sophie_scott_why_we_laugh?language=en
[3] - http://science.howstuffworks.com/life/inside-the-mind/emotions/laughter2.htm
[4] - https://postmediavancouversun.files.wordpress.com/2009/03/extra1.pdf

@SmallLegend if you like it, you can upvote and accept my answer... If there is anything on this subject you want to know, I can continue researching and add more details..


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Purpose of antibody wash
It is common practice after surface staining cells for flow cytometry analysis to wash the antibody out of solution before analyzing a sample. I have tried analysis with and without washing the antibody out and notice no significant difference by flow. So is there a reason people do this step that maybe I'm just not noticing?

I'm not 100% sure but I was thinking it's to avoid getting weird background from cross-reactivity with the unbound antibodies, as in when they bind to any labelled secondary antibodies.

@Kendall So in this case there are no secondary antibodies. But if there were, I could understand, as extra primary in solution would just soak up the added secondary.

Two reasons for antibody wash:

To limit non-specific epitope binding. All ABs have specificity.  Washing is usually trying to remove weaker binding to non-intended targets.
For flow, excess AB that is not bound, if also pre-conjugated to a fluorophore, may allow for excitation of the fluorophore while going through flow even though the antibody isn't bound to the cell type of interest.

If you had a very specific AB, and very little excess, you may not notice a thing. I'm sure there are additional reasons; these are the two that immediately come to mind based on my own flow cytometry experiments.


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Bootstrap question

I have a question about bootstrapping:
The way that I understand it is that each number represents how well a given node is supported. So in the diagram presented, we can see that the "Seal-Bear-Cat" clade is fairly well supported with a bootstrap value of 87. From that, the "Seal-Bear" clade has a bootstrap value of 95, making it quite well supported within the larger clade.
My question is this: Does that 95 for the "Seal-Bear" clade refer to the idea that that given relationship is a true 95, and therefore very well supported, or is it a value of 95 within 87, making it a true value of somewhere closer to 83 for the overall tree?

Welcome to Biology.SE. Your title could more accurate (and then attract more users). It is typically pointless to use the word "question" in the title given that obviously the post contains a question.

The term bootstrapping is a concept of statistics that is much broader than its particular application to phylogenetics. Bootstrapping refers to the process of sampling iteratively your own sample in order to approximate the sampling distribution and calculate confidence intervals.

Bootstrap support is merely the percent of bootstrap iterations that support the clade, it doesn't account for tree hierarchy.

where is this slide from? Could you give us some references? Bootstrapping can be used in many contexts as @Remi.b pointed out.

I've voted to close the question unless more contexts can be given.

I don't have any references on me, but the answer is the "95". You may be pretty confident that seals and bears are each other's closest relataive, but you might be less sure about the placement of the cat (maybe it's more closely related to pigs? It's not, but you get the point)

If the values on the branches indeed represent bootstrap supports, they indicate the percentage of times a clade has been obtained in a set of trees computed from resamplings of a starting data matrix. This is irrespective of the topology within the clade or outside it, because this is merely a count of bipartitions (a branch corresponds to a bipartition of the taxa in the tree).
I think there is no real sense in multiplying bootstrap percentages along a tree, contrary to what the end of your question suggests.


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Absorbed dose from a CT scan with relation to radiation accidents
I read somewhere that the average CTDIvol in CT scans at hospitals is ~40 mGy. This translates to the 'radiation intensity' at the center of the person, and can also be roughly interpreted as an 'absorbed or equivalent dose', but this is not the organ specific absorbed dose.
From medical literature, particularly the life span studies of RERF,  I read that at 2500 meters the 'absorbed colon dose' was about 5 mGy [1].
Out of curiosity, I tried to figure out at what distance you would have to be from the epicenter of Hiroshima, to get the same level of 'absorbed colon dose' as the average CT Scan.
To convert, the ~40 mGy to 'absorbed colon dose', you use a tissue weighting factor [2]. The tissue weighting factor for the colon is 0.12. So, this means, the average CT Scan results in an 'absorbed colon dose' of ~40 mGy * 0.12 = ~4.8 mGy.
I realize there is a different concept of 'effective dose' that calculates risk of cancer based on organ type and organ weight scanned. That is not of interest for my calculations.
As far as purely 'absorbed dose' of the organs is concerned, is it accurate to say that the the average CT scan has the same effect on a person's organs as it would to someone standing just outside 2500 meters from the epicenter of Hiroshima?
[1] http://www.rerf.jp/general/qa_e/qa2.html
[2] https://www.euronuclear.org/info/encyclopedia/t/tissue-weight-factor.htm

Good question, maybe one for the Physics Stack Exchange site? If I was standing 2.5km from the epicenter of Hiroshima the effect it would have had on my organs (especially my colon) would probably result in them emptying themselves. CT scan doesn't seem to do that... Usually. :)


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Does the number of nodes determines the rate at which a neural signal is transmitted?
I know that the the bigger the neuron's diameter is, the faster the neuron signal is transmitted. This makes sense according to the proportionality of resistance to the inverse of area and thus, in physics, there is lower resistance in wires that have bigger diameters (cross-sectional areas). I can imagine that this is the same logic for our neurons as well because they are like wires. I also know that the more myelinated a neuron is, the faster the neuron signal travels too because myelination acts as an insulation that reduces resistance in signal transmission.
But then, my question is: does the number of nodes matter and affect the rate at which a neural signal is transmitted? Can you please help explain why or why not? Let's say for example, that two neurons have same amount of diameter and myelinated sheaths hypothetically, but one of them has more nodes. Does that number of nodes of ranvier make the saltatory conduction faster?

The number of nodes is a trade-off between speed of conduction and reliability. The fastest transmission would be where nodes are spaced at roughly the maximum distance to trigger sufficient depolarization at the next node - however, small changes in ionic concentrations or channel densities could lead to failures, so in practice the nodes are typically a bit closer.
The slowest transmission would be to have no saltatory conduction at all.
(I mean these to be general principles; one could probably design a hypothetical system with very close nodes that is actually worse than having no saltatory conduction, and there is probably a perfect edge case where nodes that are spaced at the maximum distance are slower because of membrane time constants)
The reasons for this are: that travel between nodes is very fast, regeneration at nodes is comparatively slow. However, there is a maximum distance for reliable transmission, so we can't simply have one long stretch containing no nodes in between.
edit: references were requested. This was off the top of my head so I would suggest any introductory neuroscience textbook, Purves is a preferred one of mine, but this will run you significant $ if you are not/have not been a student in a neuroscience course. The Wikipedia articles for https://en.wikipedia.org/wiki/Node_of_Ranvier and also for Saltatory Conduction both look good to me, though they do not address the specific issue in detail. This brief Neuron review is more appropriate to the specific question asked, though I am not sure people without an academic library subscription will have free access: http://www.sciencedirect.com/science/article/pii/S0896627300803232

can you provide some references to your answer? we always appreciate outside literature/references

Saltatory conduction is faster, because between nodes, the action potential skips the intervening distance. There, passive spread of charge takes over, which is much faster than channel-mediated conductance which is restricted by protein gating mechanics as passive currents can travel with speeds approaching the speed of light (through metal wires that is).
The optimal internode distance for speed of action potential transmission is that distance where the depolarization currents just do not die out before reaching the next node through passive charge conduction. A bit further, and the depolarization current of one node doesn't reach the next due to current leakage. A bit shorter and more nodes are necessary per unit of axon length, slowing down saltatory conduction as more (slow) ionic channel conductance will replace passive current spread.
In other words, your notion that more nodes speed up transmission is incorrect. On the contrary, less nodes speed up transmission. The extreme case is no nodes at all, where a continuous channel density lines the axon (an approximately infinite number of nodes). This would boil down to to normal, slow action potential transmission.
Further reading
- Saltatory conduction of nerve impulses
- Why is saltatory conduction faster than continuous conduction?

Your answer is the same as the question you cited http://biology.stackexchange.com/questions/8282/why-is-saltatory-conduction-faster-than-continuous-conduction which has been negated by the answer to it.

@Hans - what do you mean? My answer is redundant; my answer is inferior; the question is a dupe? Answer above does contain additional info.

I am saying your statement is confusing and possibly self-contradictory.You say "on the contrary, less nodes speed up transmission." That is incorrect as is answered by the cited answer. There is an optimal positive, non-unit density of nodes, less or more of it slows the transmission speed. The statement "the extreme case is no nodes at all, where a continuous channel density lines the axon (an approximately infinite number of nodes)" contradicts itself: no nodes at all vs continuous, infinite number (imprecise, do you take the size of a channel into account?).

I say that a continuous array of channels is slower

You are not responding to all my points which point out all the confusion/contradictions in your answer. Are you going to respond to those point by point? As for your last comment "I say that a continuous array of channels is slower", it is again unclear: slower than what?

@Hans - updated


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What kind of mushroom is this?
I picked it this evening beneath an oak, in France, Nantes :

I tried an image search with Google, and it seems I picked a finger of a dead hand :)

What is its name, and is it edible?

Did you try the image search after cropping the fingers out of the target!

@DavidLeBauer No I didn't, I'll give it a shot!

@DavidLeBauer Interesting!

:-) a dog! No, I suspect Coprinus comatus or similar. Did you keep them around? Did they turn black and inky?

@DavidLeBauer I forget it in the fridge, a black juice came out of it and turned all of my roommates crazy. So yes.

The shape, colour and scales on the hat suggest something in the genus Coprinus.
Some species are edible, but it is not recommended to have them with wine.
I would not advise you to eat them without further live identification by someone knowledgeable. Photo identification is not reliable.

Coprinus comatus gills will start to turn pink then to black liquid in a couple days . That would confirm identification so next time they come up in the same area you will know what they are . Certainly looks exactly like them ; I have eaten many pounds of them.


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How is the volume of the dialysis buffer decided?
Is there a specific ratio between the volume of enzyme solution in semipermeable membrane bag and the volume of the buffer outside the membrane bag? I have been looking for a specific formula or general rules to decide on the volume of the buffer outside the membrane bag but to no avail. There must be general rules to determine the volume. It can't be come up with out of thin air. What common criteria are there to determine the volume as well as the time for the dialysis?

You can calculate the final concentrations of solutes in your sample after dialysis, assuming complete equilibration, with C₁V₁=C₂V₂. This formula also tells you that it is more efficient to dialyze, say, twice in 500 mL instead of once in 1 L. I typically dialyze several times in 500 mL because it seems like a reasonable beaker size.

In case I wasn't clear: you can calculate solute concentrations as mentioned above and then use this information to plan the volume(s) to use in your dialysis, depending on your specific needs.

By "solute", do you mean the enzyme, imidazole, salt, or something else?

A solute is anything dissolved in a solvent, so all of the above and more. The point of dialysis is to remove something unwanted from your sample. You decide what concentration of that something is tolerable for your experiment and dialyze accordingly.


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Is it possible to stop yourself from going into shock?
https://en.wikipedia.org/wiki/Shock_(circulatory)
I was helping someone move a refrigerator down steps and it slipped while I was holding a sharp corner and it sliced my finger and there was continuous blood flow. Soon after, I started feeling light-headed and was shaking and felt like I was about to pass out or have an attack, but I could not allow myself to appear weak, so I fought against it mentally and I got past it without anyone observing any signs. Did I avoid circulatory shock? Did pure mental dedication allow me to surpass such a thing?

Is it possible to stop yourself from going into shock?

There are different types of shock: hypovolemic, cardiogenic, anaphylactic, septic, neurogenic, etc.
Can you prevent yourself from going into shock by virtue of pure willpower? No. You cannot override the body's reactions to decreased oxygen to the brain any more than you can will yourself out of the flu.
The early signs of hypovolemia (blood loss), though, can be confused with those of vasovagal syncope (simple fainting). Both involve dizziness/lightheadedness, cool or clammy skin, and a decrease in blood pressure. However, with hypovolemia, your heart rate increases to compensate for the lowering of blood pressure (which eventually leads to shock), whereas with vasovagal syncope - which can occur with sudden fear - your heart rate drops, which is what causes your blood pressure to fall.
Passing out due to blood loss depends in part on how rapid the blood loss is (the more rapid, the earlier on might pass out) and the volume lost. To lose enough blood to pass out, a healthy, normally hydrated person would need to lose about 2 liters of blood (or 20% of one's blood volume); maybe 1.5 liters if it happens quickly enough.
Regardless of whether it happens slowly or quickly, if enough blood is lost, shock will ensue. No amount of willpower will stop it.
Interestingly, the sight of blood or having your blood drawn are frequent triggers of vaso-vagal syncope.
What you experienced is commonly called pre-syncope: the feeling of lightheadedness as though one might blackout, but consciousness is preserved.
Vasovagal syncope
Hypovolemic shock
HEMORRHAGIC SHOCK

+1, but I have heard an MD telling that she would faint when blood loss occurred with herself/her loved ones while she wouldn't faint when performing surgery in the OR. I guess I have the same thing - I fainted when a doctor drew blood from my baby, but I am totally sure I could draw blood without problems from someone else I didn't know. I don't faint when they do it to me either. There is something going on in terms of will power / professionalism /emotional involvement that may keep one from fainting.

There was a fellow medical student in my class who would faint at the site of anyone's blood, his or someone else's, every. single. time. Unfortunately, the profs had no sympathy, and we witnessed him pass out during most of our hematology labs where pinpricks were needed. The thing with you is emotional - you are more concerned about your child than yourself. That's not at all uncommon in parents. We often tell parents to avert their eyes when doing bloody procedures on kids. (My adult friend passed out when I was ministering to her daughter's cut in my kitchen. And she's stoic.)

@AliceD, Fainting due to a small loss of blood (50 mL?) during blood drawing is not caused by shock, but by a vasovagal syncope triggered by pain and looking at blood. In this reaction, the vagus nerve temporarilly slows down the heart rate, which causes a drop of blood pressure and hence fainting. You may be able to learn to prevent such a reaction. In hypovolemic shock, you lose a lot of blood (700 mL+), which again causes a drop of blood pressure. You can't convince yourself that you did not lose blood; still your psychological reaction to blood loss may aggravate or postpone shock a bit.

I seriously doubt you lost 750mL of blood, the 15% where they wouldn't even treat you, according to your linked article, which is the equivalent of a full bottle of wine, from that cut. Even if you had sliced your finger off completely, I doubt that you would have lost that much blood. You would need to sever an artery...
750mL is less than two units of blood that you would give donating blood, and they are hardly concerned with putting anyone into shock at a blood drive.
You likely had a vasovagal response (syncope) to the sight of the blood.
Now if you were in a car accident and the guard rail had impaled you....


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Identification of a moth

It is from Bangladesh. Is it hawk moth? I am not sure. Please help.

Looks like a small Sukhoi plane :P. Jokes apart, this doesn't look like a hawk moth. I know that this moth is from Bangladesh since you mentioned that in other posts but it better to always keep your question complete with all necessary information.

Do you have think this picture is enough for visually identify it (at least at genus level)? Otherwise I gotta hunt this guy :P

It looks like a Hesperiidae (Skipper), not a hawk moth (Sphingidae). There are more than 3500 species of skippers worldwide though, and I don't know what species this is. However, I'm sure that somebody who knows butterflies in Bangladesh could identify this to the genus level.
One suggestion/guess/starting point might be Baoris pagana, but this is merely based on a quick glance at skippers found in India.

(picture from http://www.ifoundbutterflies.org/)


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NCBI EUtils. Get Homolog infromation using Gene ID
How to retrieve homologs information in xml or json format from NCBI using gene ID?
I tried one URL:
http://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=homologene&geneid=9&WebEnv=???&query_key=???

I dont know what to add in question mark regions

I'm voting to close this question as off-topic because it is a pure programming question better suited for BioStars.

I think the default format is xml. See more about EUtils here.

From Entrez Programming Utilities Help [Internet]:

Input: Any Entrez text query (&term); Entrez database (&db);
  &usehistory=y; Existing web environment (&WebEnv) from a prior
  E-utility call

To avoid the error messages, web1, and key1 can be used as terms (these are usually being used to associate with other searches), however this returns no data, probably because the ID you supplied was simply "9", and it remains unclear exactly what you're searching for in the context of other queries.
For example:
esearch.fcgi?db=<database>&term=<query>&usehistory=y

# esearch produces WebEnv value ($web1) and QueryKey value ($key1)

esummary.fcgi?db=<database>&query_key=$key1&WebEnv=$web1

So whilst view-source:eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=homologene&geneid=9&WebEnv=web1&query_key=key1 is a valid query, it's not pointing to anything.