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What modern insects are not (flying OR descended from flying ancestors)?
What modern insects are not flying or descended from flying ancestors?
(I read somewhere that 99% are, so of course I instantly became curious which aren't. xD )
EDIT:  Sorry, I should have been clearer: I meant examples of modern insects with no flying ancestors.

To make sure I understand your question: You want examples of non-flying insects which ancestor was flying. Or in other words your want examples of insect lineages that lost the ability to fly?

Sorry, insects with no flying ancestors. Edited.

Do you ask for examples of non-flying insects which ancestor were flying? In other words do you ask for examples of insect lineages that lost the ability to fly?
The ability to fly arose with the clade called the Pterygota. All species from this monophyletic taxon come from ancestors that had once the ability to fly.
For nonflying species with no flying ancestors, you can navigate back in Tree of Life and look at the other two clades in Insecta: Archaeognatha and Thysanura.
For nonflying species with flying ancestors, you can look within Pterygota on Tree of Life, and you can find many non-flying species in the following clades for example:

Hemiptera (bugs, aphids)
Coleoptera
Siphonaptera
Many Vespoidae (clade contained in the hymenoptera)

EDIT:

Did Flying only evolved once in insects?

Yes it did evolve once only. At the start the ancestor had 3 pairs of wings that are though to have evolved from gills or from the sclerites (competitive hypotheses) of the prothorax. the most anterior pair of wing was lost. The diptera lost a second pair of wings (the posterior ones) that degenerate into halteres (particularly easy to see in crane flies). The insects that perform the most "primitive" fly are the Odonata (dragonflies and damselflies). These insects can move their wings independently which is not the case of other flying insects because the way their wings are attached to the rest of the body has changed.

So flying only evolved once in insects, eh? (That is, all flying insects have a single common ancestor, which was the first flying insect ever.) Interesting!

Wow, this tolweb.org site is awesome, thanks! I see it's only the orders Archaeognatha and Thysanura that have no flying ancestors.

3-winged insects? Cool! Do we have many fossils?

And if we're not sure whether the wings came from "sclerites" or gills, does that mean we don't have any fossils of the presumably gliding ancestor of this first flying insect?

Yes, there are some fossils (especially those coming from a famous fossil site in great britain) and there still exist a 3-winged species that live on trees that use their wings to head their fall toward the trunk when they let themselves fall to avoid predators. This species might hold the ancestral trait of first winged insect species but it is not sure. Unfortunately, I don't remember where I found these information. There are several points that are still unclear in the evolution of flight in insects (such that which organs developped into wings).

Do we know if this gliding "pre-first-flying-insect" ancestor was terrestrial, or if it developed flying even before it left the water...?

Fossil records does not allow to know which organ developped into wings. If I am not mistaken, there was one study who should that given the position of the wings compare to I don't remember which structure, it is likely that wings developped from gills. And one study who showed that the molecular factor causing wing devlpoment is a factor also causing sclretie development suggesting that wings come from sclerite. But I am not sure of what I am stating

Well, that's a good question too! Because the living habitat is only poorly correlated with the phylogeny, it is sometimes hard to really know what was the ancestral stat of a given clade. If you take the example of the most "primitive" flying insect, the Odonata, you'll realize that eggs and larvea live in water. But more "primitive", non-flying insects mostly lived on earth. And the ancestor of all Hexapoda lived on earth. But more recent flying species do not have larvea that live in water.

Now I realize looking on tolweb.org that the phylogeny is actually quite unclear and the info I had in mind might be wrong. I am not an insect specialist and I don't provide any reference. So please consider I might missing some important point or even saying some mistakes.

This all very interesting (really) but I don't understand it getting accepted since it doesn't appear to be an answer to the question from OP - modern insects with no flight in their ancestry.

@AlanBoyd Oh, right, now that you mention it, I answered my own question in the second comment ("it's only the orders Archaeognatha and Thysanura that have no flying ancestor"), but I did that in a single step from the link Remi.b gave me, and my question was stupidly ambiguously phrased at the time, so... yeah.

Silverfish, also known as Lepisma (order Zygentoma), does not fly and does not descend from flying ancestors.
It's close to Archeognatha, which don't fly either nor descend from flying ancestor.


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Where can I find the metabolic network for the human erythrocyte?
Where can I find the metabolic network of the human erythrocyte (red blood cell), in SBML format? The red blood cell metabolic network is a model that's usually employed in the literature [see refs below] to demonstrate mathematical techniques of analysis of metabolic networks.
Despite this common use, I haven't been able to find a metabolic network of the human erythrocyte in SBML format, which is commonly employed for these networks (for example, in the BiGG database, http://bigg.ucsd.edu/) because it is easy to use with the COBRA package (http://opencobra.sourceforge.net/).
So, anyone can tell me where I can find an SBML model of the metabolic network of the human red blood cell?
References where the red blood cell metabolic network is used:

Wiback, S. J., Famili, I., Greenberg, H. J., & Palsson, B. Ø. (2004).
Monte Carlo sampling can be used to determine the size and shape of
the steady-state flux space. Journal of Theoretical Biology, 228,
437–447. doi:10.1016/j.jtbi.2004.02.006
Braunstein, A., Mulet, R., & Pagnani, A. (2008). Estimating the size
of the solution space of metabolic networks. BMC Bioinformatics, 9, 240. doi:10.1186/1471-2105-9-240
Jamshidi, N., Edwards, J. S., Fahland, T., Church, G. M., & Palsson,
B. Ø. (2001). Dynamic simulation of the human red blood cell
metabolic network. Bioinformatics, 17(3), 286–287.
Kauffman, K. J., Pajerowski, J. D., Jamshidi, N., Palsson, B. Ø., &
Edwards, J. S. (2002). Description and analysis of metabolic
connectivity and dynamics in the human red blood cell. Biophysical
Journal, 83(2), 646–662. doi:10.1016/S0006-3495(02)75198-9

The model used by Jamshidi et al. can be found in the BioModels database with acession no. MODEL1103210001  http://www.ebi.ac.uk/compneur-srv/biomodels-main/MODEL1103210001
A more recent model has also been described in Bordbar et al. iAB-RBC-283: A proteomically derived knowledge-base of erythrocyte metabolism that can be used to simulate its physiological and patho-physiological states. BMC Systems Biology 2011, 5:110 The model file in SBML format can be downloaded from the Additional Files section (http://www.biomedcentral.com/1752-0509/5/110/additional) or BioModels (http://www.ebi.ac.uk/compneur-srv/biomodels-main/MODEL1106080000).

What about the model used by Wiback et al? The paper has the stechiometric matrix, but in pdf format, which is useless.

Indeed, I couldn't find any model file for that. I wouldn't call it completely useless though. If you are using for example COBRA Toolbox or CobraPy, you can construct the model yourself from the matrix, then save it to SBML. I'd expect to use a couple of hours.

source: Stack Exchange

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How usable is the Human Metabolic Model to predict biomass?
In order to use the Human Metabolic Model for Flux Balance Analysis of specific cancer cell lines, we would like to know what sort of flux values have been determined for the Human Metabolic Model.
Basically, how usable is it to predict biomass production in humans (to some extent)?  If it is not very good for this, what other options are there?
Thanks very much!

Firstly, it is important to remember that Flux Balance Analysis computes theoretical performance limits, i.e, the theoretically optimal behaviour of the system with respect to the objective and constraints. When growing bacterial cells growing in culture evolve under selection pressure for biomass production, the theoretical limit on biomass production may indeed be approached, see for example Ibarra et al: Nature. 2002 Nov 14;420(6912):186-9. (http://www.ncbi.nlm.nih.gov/pubmed/12432395) and Fong & Palsson: Nat Genet. 2004 Oct;36(10):1056-8 (http://www.ncbi.nlm.nih.gov/pubmed/15448692).
How closely other systems can be expected to approach optimality should be considered on a case-by-case basis, and the constraints should be realistic. In humans, you would for example expect that the physiology of the persons (blood glucose levels, etc.) would greatly affect the growth rate of any cancer cells, in addition to the structure of the tumour (especially blood supply). For cells growing freely in culture, one might expect FBA to be easier to apply.
For HeLa cells growing in culture, the results of at least one study suggests agreement between experimental and FBA-predicted growth rates: See Resendis-Antonio et al: Modeling core metabolism in cancer cells: surveying the topology underlying the Warburg effect. PLoS ONE, 5 (2010), pp. 1–11 (http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0012383)
Whether the precise biomass production rate is predicted or not may actually not be so important, and there has been considerable interest in applying FBA to studying various aspects of cancer metabolism. Here are some papers that may be of interest:
Ashwini Kumar Sharmaa, Rainer König. Metabolic network modeling approaches for investigating the “hungry cancer”. Seminars in Cancer Biology 23:4,2013, 227–234 (http://www.sciencedirect.com/science/article/pii/S1044579X13000436) (Review)
Shlomi et al.: Genome-Scale Metabolic Modeling Elucidates the Role of Proliferative Adaptation in Causing the Warburg Effect. PLoS Coputational Biology 2011 (http://www.ploscompbiol.org/article/info%3Adoi%2F10.1371%2Fjournal.pcbi.1002018).
Lewis & Abdel-Haleem. The evolution of genome-scale models of cancer metabolism. Front. Physiol., September 2013 (http://www.frontiersin.org/Journal/10.3389/fphys.2013.00237/full). (Review)
And a relevant Master's thesis: Computational Metabolic Modeling of
Cellular Growth: From Bacteria to Cancer. http://www.cs.tau.ac.il/thesis/thesis/Benyamini.pdf

As usual, awesome answer.  Thanks very much for your input!

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What are good data on the Human Metabolic Model and where can I get them?
Trying to get a good SBML representation of the Human Metabolic Model for use in Flux Balance Analysis and drug targetting (i.e. gene knockout) simulations.
What are good sources for these data?
Thanks very much!

As far as I know, there is no one model officially known as "the Human Metabolic Model", but the Recon 2 model, described as a "consensus" model and the most comprehensive to date in Thiele et al. 2013, A community-driven global reconstruction of human metabolism (http://www.nature.com/nbt/journal/v31/n5/full/nbt.2488.html) is available at http://humanmetabolism.org/?page_id=75
Tissue-specific models are also available. See for example  Wang et al.:  Reconstruction of genome-scale metabolic models for 126 human tissues using mCADRE. BMC Systems Biology 2012, 6:153:

Interesting.  Yep, I have found Recon 2, but I am also having trouble matching the drug therapies against it (I assume I should do that through figuring out which genes are knocked out by each therapy and trying to match them with the model).  Tissue specific models sound interesting.  Thanks!


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Is the regulation of lactose operon different between Gram + and Gram -?
I know that in E. coli the lactose operon is shut down by CAP protein when binding cAMP. Is this true also for Gram positive bacteria?

I know it's stupid but I answer my own question, for those who are interested.
It is different.  CAP protein regulates lactose operon only in Gram -. In Gram + the presence of glucose shuts down the operon with another mechanism: the TCRS that relies to concentration of fructose 1,6 phosphate.

It is not stupid to answer your own question! It is actually encouraged on every SE site :)

Its not stupid at all. You saved our time


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How to convert nanogram to picomole?
I have lets say 10ng/uL of RNA. How can I convert it to picomole?
I need it to calculate how much magnetic beads I need. This is the product: http://tools.lifetechnologies.com/content/sfs/manuals/dynabeads_m270_sav_man.pdf
I do not know how much beads should I use.

Do you want the the concentration or the pc/ul? Also what is the mass of your RNA?

To make the calculation, you need the mass of the DNA. What would also work is the sequence from which you can calculate (or estimate, depending on how exact you need this) the mass.

The thing is I have no idea about the mass. It is a pool of transcripts from a specific cell (they are biotinylated) and I need to pull them out with magnetic beads.

Average molecular weight (MW) of a ribonucleotide = 340g/mol
Size of RNA = x
MW of RNA = 340*x g/mol
moles of RNA needed = y * 10⁻¹² moles (1 picomole = 10⁻¹² mol)
mass of RNA needed = 340*x*y*10⁻¹² g
Conc of RNA = 10*10⁻⁹ g/µl `(1ng =10⁻⁹g)
Volume needed for y picomoles = (340*x*y*10⁻¹²)/10*10⁻⁹ = 0.034*x*y µl
If your RNA is biotinylated then add the MW of biotin to MW of RNA

I don't think it would be appropriate to take account of the biotin, since the RNA concentration (ng/ul) has presumably been estimated by a method that only measures RNA.

yeah thats true.. Plus with a big RNA the biotin tag won't matter..

Thanks for all the answers. The thing is RNA is containing biotin for every uracil that it has.(TU-Tagging method: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2783170/) I decided to use an estimated amount of beads since I do not know the amount of biotinylated RNA in my sample.


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Why prefer $MgSO_4$ over $MgCl_2$ in recipies
Many molecular biology recipes use MgSO4 (and not MgCl2). Is there indeed a preference? If so, why?

Can you specify which recipes you mean? I am aware of a number of polymerases like Pfu which prefer $ MgSO_4 $. I haven't found a reference for that now, but its probably the same: The chloride ion interferes with the enzymes reaction.

My guess is its the solubility properties of the anions.
Chloride ions can precipitate with some metals that might appear in a complicated buffer or medium. And yes they could even compete with enzyme binding.  Sulfate will remain in solution with just about anything.
There are exceptions, but if you're making a buffer you're probably going to do better if you use the general solubility rules.

Are you sure about the insoluble chloride salts? I recall only a handfull of them, mostly with ions, which are not common in cells like titanium or silver. For sulphate I agree completely.

Although calcium sulphate is only sparingly soluble.

added a link... this is chem 101 so nearly every book has a mention of some form of counter-ion solubility rules.

@AlanBoyd A number of sulphates is nearly insoluble.


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DNA sequence from the middle of a gene
Someone gives you a short DNA sequence that comes from the middle of a gene.
5'- TCTAACTGATTAGC -3'
3'- AGATTGACTAATCG -5'

From this sequence, determine the following:

Is the promoter located to the left or right as the sequence is written?
Is the sense strand the top or bottom strand?
What amino acids are encoded by this gene fragment?

The only thing I have been able to come up with, is that since this is from the middle of a DNA sequence I need to choose a frame with no stop codons.

The two segments you provide are not complementary to each other. Is this a typo or a part of the actual question?

I've edited the sequence to repair the 5' and 3' ends of the bottom strand, which are now as was shown in the original version of the question.

Gene doesnt essentially mean protein coding

TCT AAC TGA TTA GC
T CTA ACT GAT TAG C
TC TAA CTG ATT AGC
AGA TTG ACT AAT CG <<< this is the ORF
A GAT TGA CTA ATC G
AG ATT GAC TAA TCG
If the sequence comes from the middle of a gene we assume it should encode an open reading frame.
For this sequence only 1/6 frames does not include a stop codon (shown above in italics). So in standard format, with promoter to the left we can write the ds sequence as:
5'-AGATTGACTAATCG
3'-TCTAACTGATTAGC
Since this is homework I'll leave the rest to you.

Since the ORF has no stop codons, does that mean it is the template strand?

The open reading frame is the strand of DNA with the same sequence as the mRNA (with T>U). RNA polymerase makes that RNA using the other DNA strand, which is the template strand. If the dsDNA sequence is written in the conventional way with promoter to the left then the top strand is the coding strand and the bottom strand (running 3'>5') is the template strand.

Don't we want the template strand to have no stop codons? Cause when we are reading the template strand making the mRNA we don't want to encounter a stop codon.

For example if we use 3'TCTAACTGATTAGC as the template strand when the polymerase reaches TGA, it would stop right?

Or do stop codons only stop the mRNA was making proteins. It doesn't stop the DNA replication?

@itsSLO I would like to tell you a couple of things. 1. Stop codons do not stop transcription of mRNA, it will stop only the translation of mRNA. 2. Here, we are taking the sequence with no stop codons only because the question says that the sequence taken  is from the middle of a gene. So, if we take a sequence with a stop codon the mRNA from rest of the part of the gene will not be translated.

On the sequence alone, you can answer neither of these questions because:

from the sequence alone you don't know anything about the gene or the
promoter.
the same is true for the orientation
and the codons, since you don't know if the code is in frame or not.
If one base is cut-off from the original sequence, your codons shift,
and don't show the original code. The sequence has 14 nucleotides
which will not ressolve into a short amino acid sequence.

You can probably identify the gene using BLAST and then see, where the sequence is located and answer the questions. I tried to blast the sequence, but it is too short to give a definitive answer.
So the first thing, you need to do is identify the sequence (gene and the organism where it comes from), then you can do the rest of the work.

Yeah this was all that was given for the problem. Nothing else.I was thinking you can determine the frame by choosing one without any stop codons.

Thats right. Alan showed what can be done, but the rest is problematic.


text:
Do vitamins help our memory?
It is commonly believed that vitamins can help our memory.
Is this really true? What is the biological basis of this?
Is there any specific research paper on the subject?

Welcome to Biology.SE. You should try your question on skeptics.SE where you can provide any NOTABLE claim and they will tell you whether your claim is supported by scientific evidences or not.

Why the close votes? The question was a bit "bare", sure, so I edited it a little. In any case I think it fits this site very well.

There seems to be no effect of vitamins. This paper ("Preventing cognitive decline in healthy older adults." found no evidence for herbal supplements, vitamins or fatty acids improve cognitive functions.
There seems to be some evidence ("Preventing Alzheimer's disease-related gray matter atrophy by B-vitamin treatment.") that a cocktail of hig dosed vitamins including folic acid, Vitamin B6 and Vitamin B12 can slow Alzheimer's disease. But: The benefits were only seen in participants which had high blood levels of homocysteine. This amino acid is linked to a higher risk of heart disease for which the B vitamins are postive for the outcome. So this might only be helpful for people with too high homocysteine levels.
And its questionable if high doses of antioxidants (like vitamin A or E) are not only not helpful, but can cause actual damage. This is due to the fact that they catch up reactive oxygen species, which might otherwise trigger the cell to go into apoptosis and prevent it from becoming a cancer cell. Here is the paper: "Antioxidants accelerate lung cancer progression in mice.".


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Aren't current explanations for the evolution of human cooperation a little too reductionist?
Lately, I've become a believer in the limits of reductionist explanations especially in areas like complex systems and biology. So, without wasting any more time, I'll get to my question..
Whenever we think of something like cooperation, the most common explanation that comes up is that of genetic fitness. It is said that evolution would have selected for psychological mechanisms of cooperation because it is beneficial in a society in which reciprocity is possible. You scratch my back, and I scratch yours. Add to the mix the ability to name names, and reputation becomes a kind of proxy signal for fitness.
Now, the major problem I have with this is does it all have to boil down to fitness? Can't it be a phenomenon that is culture-specific? Different cultures go to different lengths to help a stranger. Yet, we all share the same evolutionary history. This seems like a strong indicator that cooperation can't be reduced to one's genetic or reputational fitness alone. Should the study of cooperation be handed off to the anthropologists?

All animals are not humans ! So handing over to anthropologists - Bad option !

Sorry, I should have been more specific that I meant human altruism.

Ok! then I completely agree with you. Human altruism is  far more complex than other animal altruism. (I also suggest that you edit your question to be more specific)

You have to define altrusim here.  In evolutionary biology altruism often refers to an evolutionary adaptation where some individuals in a species are unable to reproduce, supporting a breeding caste.  e.g. ants and bees. Humans do not do this. I think you are actually thinking of what biologists call Cooperation.

Inclusive fitness proponents will tell you that this explanation is completely wrong, by they way (without being an expert, I tend to agree).

Interesting question!
I think that in terms of 'tribal' fitness, altruism would be strongly selected for, as communities would tend to be quite small (relative to, say, a town today). In modern civilization cultures have developed differing levels of altruism, but I imagine this is a result of upbringing rather than inherent differences in tendency toward altruistic actions.
So in my opinion you cannot rule out altruism being selected for because it is clearly an advantage (in terms of survival / fitness) in smaller communities - we just don't live in that kind of society any more; people don't have to be altruistic to get by, and this kind of mind-set can 'evolve' culturally, outside genetics. But on the whole I would still argue that most people are inclined toward altruism - ether because they feel naturally inclined to help others, or feel that by helping others some benefit (such a reputation) would be bestowed upon them (the former may be the same as the latter, but at an unconscious level).

There are many various model used in order to explain evolution of cooperation. Here is a small list:

kin selection
group selection (levels of selection)
lineage selection
Reciprocity

direct
indirect
network

Memetics

People from many different background study social evolution including

mathematicians
biologists
philosophers
computer scientists
paleontologists
…

Social evolution is studied through fundamental science (using mathematical modelling and computer simulation) or by looking for common trait among species that are very social. For example, it seems that having a high extrinsic mortality rate "helps" a species evolving altruistic behaviors. Or sex determination mechanism such as haplo-diploidy seem to be important too. There are many experimental studies on human behavior too.
The field you referenced to ("Can't it be a phenomenon that is culture-specific") is called memetics. A meme (named by analogy with the word gene) is a cultural unit which reproduces according to their "memetic fitness" and mutates. There are lots of computer simulations on the subject and there are several empirical observations such as the evolution of a joke.
I think that none of the field we manage to think it would help explaining the evolution of cooperation is neglected. There are several articles who investigate the co-evolution between genes and memes. I don't know any of them who focused on the question of altruism. I have to confess that I have never read any article who considered the combined effects of several models from several fields in the study of altruism. But I don't think we have a sufficient level of understanding of each field in order to combine these models. For example, it's been argued that kin selection and group selection is actually the same process.


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Which direction are wild beehives combs oriented?
Is it on the North-South axis, the East-West axis or some other orientation?

I've usually observed wild Indian Bees (Apis cerana) orient their hives in an East-West direction. The entrances are usually oriented towards the Sun.
This is purely from my own observation (in South India) and not from any research.

So are the combs parallel or perpendicular to the E-W axis ?


text:
Mutation rate in viruses
Mutation rate is a phenotypic trait that evolves. The process of evolution of such kind of traits are often referred to as evolvability. I am wondering about the evolution of the mutation rates in viruses. For the purpose of this question, I'll focus only on viruses that do not possess DNA polymerase. Because the replication of the viral DNA is performed by the molecular machinery of the host cell (eukaryote or not) it seems rather impossible to me for a virus to evolve its mutation rate. Is it correct?

Do we have any evidence of adaptive mutation rate in viruses?
Is there a correlation between the mutation rate of the host and the mutation rate of the virus?
Could the virus evolve some structure (or codon bias) of their DNA/RNA in order to adapt their mutation rate?
Is there another mechanism allowing a virus lineage to adapt their mutation rate?

What do you mean by "adaptive mutation"?

Thanks for the question, I though I might have been unclear. I meant "adaptive mutation rate". The trait is the "mutation rate" and I am asking whether this trait has been shown to evolve "in an adaptive manner" or evolve in order to reach some optimum. This might probably also be phrased by: "Do mutation rate in viruses genetically coded" Does it make sense to you?

I think so, yes.

Just as a point of correction, some viruses technically encode viral DNA polymerases.  Reverse transcriptase in retroviruses is a DNA polymerase, and Hepatitis B (https://en.wikipedia.org/wiki/Hepatitis_B_virus_DNA_polymerase) also has a DNA polymerase, although admittedly hepadnaviruses are weird.

@Armory Very good point, thank you! I edited my question in consequence.

Really interesting question.
I am not sure, if the mutation rate is something "actively done" by the virus. I think its more a byproduct of vast replication after taking over the host cell. Mutations with a negative effect are deleted, those with neutral effects will be there, and those with positive mutations will be selected for. This paper looks interesting in this context: "Viral Mutation Rates". Looking for related publications on the site, I found this two:

Rates of evolutionary change in viruses: patterns and determinants.
A short introduction to the origin and molecular evolution of
viruses.

The whole list is here.
Answering your second question: There is obviously no connection between the mutation rate of the virus and the host. I have found this paper ("Rates of Spontaneous Mutation") which gives some pretty interesting numbers. In short: The rate of mutation for DNA viruses is much higher than for eukaryotic cells and for RNA viruses 2-4 orders of magnitude higher than for DNA viruses.
At least RNA viruses encode for some own polymerases, the reverse transcriptase. Depending on which these have a proof-reading (exonuclease) function they induce more or less errors.


text:
Smoking, cancer, correlation between quitting smoking and increased immediate risk
There is "proof" out there today that suggests smoking is directly linked to cancer. I cannot argue against that, for the evidence in favor appears strong, and the evidence against is lacking. I'll happily sit here and agree that smoking increases the risk of cancer. This question, however, is not about how smoking increases the risk of cancer, rather how stopping smoking might increase the risk of cancer.
Consider what I know so far:

Cancer is caused by mutant cell growth.
Mutant cell growth is believed to be caused by chemicals in the smoke
Smoking itself stunts growth, thus slowing the cell growth rate

If the growth stunt is severe enough that it will reduce the cell growth rate by 20%, one might assume this would take some weeks (let's say 8 weeks, sounds reasonable to me, though I lack knowledge of the subject) to recover. This will likely be some scale and will gradually decrease to somewhere near 0.
Further to this, the risk of cancer is not directly related to the lung, but it is believed to be caused by chemicals entering through the lung into the blood, and travelling around the body, causing cancer in various organs.
Consider that the cell growth is probably linked (in the lung, at least) to chemicals "surrounding" the existing cells, this explains why smokers run short of breath. This partially explains the growth stunt side of smoking. Perhaps this happens body-wide, I don't know.
Then consider what will happen when one stops smoking. The cell growth rate will begin to radically and unexpected increase as the growth stunt is suspended, meanwhile chemicals will still exist in the blood and organs which will be perverting cell growth causing mutant (cancerous) cells. At this point the body is unprepared and settled into its routine of slowly generating cells, but now it is generating them faster and is struggling to keep up. Energy is lacking in areas, and there is further cause of mutant cells to grow and even to be allowed.
Surely, given this reasoning, it might be understandable that stopping smoking increases the immediate risk of cancer, though reducing the long term risk?
Does anybody know, or can anybody find reasonable proof that any part of this argument is flawed? Is there any research to suggest that there is or is not an immediate increased risk? The one thing that people never mention in the side-effects of quitting is the risk of immediate body failure through a variety of means (I've known people to come with flu-like symptoms then find they have cancer weeks later). Is this really unexplored? Or is the nanny state trying to hide it from smokers to prevent them from damaging their health further?

I think solid evidence of this going to have to come from an animal model, because you couldn't really need to do the experiments required in humans.  One important note is that smoking tends to only slow proliferation in the lung epithelium [mechanism debated], not systemic cell division.  The carcinogens that are introduced into the blood through smoking are found through out the body, so your hypothesis is probably limited to lung cancers only.

Interesting that there is still a glimpse of hope at the end of this tunnel. What I'm really thinking is that although there are some very dangerous chemicals in tobacco smoke, there may also be some very useful ones. Maybe these could be applied properly, and instead of being used to scare people away from smoking, be used instead to try to treat cancer and perhaps other similarly developed disease. People are always so negative, there must be benefits to tobacco, in similar scale to what people suggest about cannabis.

To summarise your argument, cancer is a disease characterised by uncontrolled cell division of mutant cells. Smoking decreases cell division, thereby smoking decreases risk of cancer. Furthermore, stopping smoking increases growth rates, thus there's an immediate rise in risk following smoking cessation.
Cancer is NOT caused by cell division. Smoking does NOT cause cancer by cell division. That's the flaw in your argument. What's happening is that cell division ISN'T being controlled. Let's propose that smoking does indeed stunt normal cell growth. The carcinogens in tar from smoking are still floating around causing mutations in the DNA. Most of DNA doesn't code for very much, but some parts of it codes for genes which control cell division. If these genes mutate then cell division is no longer controlled by these genes and hence there's uncontrolled cell division a.k.a cancer. Once these cells are dividing in an uncontrolled fashion, smoking isn't going to limit their growth. That's because this cancer has developed in the presence of these toxins that limit it's growth and despite this it's still managed to occur.
And then that cell growth stunting may actually be causing cancer to occur. White blood cell function is impaired by smoking, these cells usually target cancerous cells and destroy them. Without being destroyed, there's a higher chance of cancer.
And then I could go further, usually cells grow older and die. Maybe smoking by stunting growth of these cells leads to cells that last longer than they should. These cells accumulate mutations and become cancerous, where else they otherwise would've been recycled.
Smoking however has been linked to improving the symptoms of some diseases. Just not cancer.

Interesting take on it, though you have slightly contradicted yourself. Cancer is caused by uncontrolled cell division, understood. But you previously said cancer is not caused by cell division. Well, one of those statements must be untrue, and one must assume the first is that. I was looking at cessation devices, and considering how much more productive these may be if they were combined with some chemicals which, similarly to tobacco, could stunt cell growth over the period in which the smoker still retains nasty chemicals from the cigarette smoke. Do you still believe this is not plausible?

To further that, it would make sense that cell division being limited by chemicals in cigarette smoke is also likely to stunt growth of cancerous cells. Unless this is being performed by the body reacting and trying to control cells in a manner to which it has become accustomed, the chances are this is being done by the chemicals in smoke itself, which as far as I'm aware operate on most human tissues. If that's the case, how unlikely is it, really, that those cancerous growths cannot be stunted similarly to regular cells? Unless the mutation is incredibly severe I suspect unlikely.

You've interpreted my answer incorrectly. Cancer is defined as uncontrolled cell division, but its caused by ONE cell which has mutated sufficiently to divide uncontrollably. This cell mutates because of tobacco which damages DNA. Smoking most likely does stunt growth of cells. However this increases the chance of cancer as healthy parts of the body are likely stunted more than cancer cells. These healthy parts include white blood cells. Without stunting these white cells could eradicate the one cancer cell before it divides uncontrollably. If things still don't make sense, let me know.

One thing is pretty clear and needs not to be debated I think: Smoking is pretty unhealthy and can cause cancer. I see a number of misconceptions here:
First you assume, that a slower cell division is something you want to have. Most cell of the adult human body do no divide at all (or only at relatively low rates). Some cells have higher proliferation rates belong to the hematopoietic system, the gut, the mucosas of the body and the skin. These cells need to be able to proliferate in order to fulfill their function. Other cells are dividing to replace cells which went into apoptosis or had to be replaced, but this can not be compared like the growing rates of kids.
Then, cell growth is highly restricted and controlled for good reasons. I did a short search for articles describing slower cell growth by smoking. What I found does not favor the idea that slowed cell growth might be beneficial. This paper for example ("Cigarette Smoke Induces Cellular Senescence"), shows that lung fibroblasts are going into senescence and are not able to do necessary proliferation for lung maintanence.
Then, even if cancer is defined (among other things) to be a fast proliferating, uncontrolled growing mass of cells, its not enough to simply let cells grow, to be able to call them cancer cells. To be able to grow as a cancer cell, the cell needs to change genetically and pick up a number of mutations which allows them to escape the security programs of the body. These are apoptosis and the immune system and its not an easy task. Most cells with the potential to become cancer cells get caught on the way. For the way, how cells become cancer cells, this webpage is pretty interesting.
Stopping to smoke does not cause more problems for you body, it reduces them. The number of dangerous substances delivered to your body is reduced, as is the chance for them to cause harm (lower concentrations). It will take quite a while to get rid of them though, for tar in the lung this can take several years.


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Why is Portuguese man o' war considered a colony?
The wikipedia entry on the Portuguese man o' war says:

... the Portuguese man o' war is ... not actually a single multicellular organism but a colonial organism made up of many highly specialized minute individuals called zooids. These zooids are attached to one another and physiologically integrated to the extent that they are incapable of independent survival. (emphasis added)

This is contradictory. If it's got multiple cells, and those cells are highly specialized to the point of being incapable of surviving on their own, then how does that differ from a multicellular organism? That last sentence seems like it describes the cells in my body.
In fact, the entry colonial organisms says:

The difference between a multicellular organism and a colonial organism is that individual organisms from a colony can, if separated, survive on their own, while cells from a multicellular life form (e.g., cells from a brain) cannot. (emphasis added)

So, is the Portuguese man o' war a colony or a multicellular organism? And if it's a colony, can its zooids survive independently, the wikipedia text notwithstanding?

Very related question:- http://biology.stackexchange.com/questions/8745/polymorphism-in-cnidarians

Physalia and Siphonophorans in general are multicellular Metazoans.
But the whole discussion is about modularity on the level of individuals: Siphonophorans are colonial organisms, which means they are composed of multiple individual polyps and medusae. This is in fact quite common among Hydrozoa, but in Siphonophora the degree of integrity and function division among the components is of extraordinary level.

I'll buy this, but it doesn't change the basic question. If they are so integrated, why aren't they simply considered a single organism like us? They derive from a single fertilized egg. They divide asexually from that egg. The individual cells take on specialized roles physiologically and structurally. Only one set of cells reproduces. Nothing about any of this suggests colony to me. Am I missing something? To me it just seems that because there are individual polypoid cells, people are hesitant to say it is one organism.

I don't know, what you mean by "polypoid cells": individual modules here are zooids. No one is hesitant to call Physalia "one organism", but it's a colonial one, a very integrated modular animal. It is colonial from the morphological, developmental and evolutionary points of view.

For me, as a layperson, this answer doesn't explain much. I suspect a proper answer is hidden somewhere behind the statement "It is colonial from the morphological, developmental and evolutionary points of view.", and it makes me wonder whether saying that it is "not a single animal" (in contrast to, say, me an my cells/organs, which are a single animal), is more a matter of taxonomy than ontology.

I think the Wikipedia entry on Colonies in biology is helpful. It writes:

...a colonial organism can be distinguished from a conventional
  multicellular organism by the looser association and repeating nature
  of its component subunits—perhaps with specializations, but still
  visibly similar. The components can also be recognized as organisms in
  their own right by comparison with evolutionarily related free-living
  species. For example, the Portuguese man o' war is a colony of four
  different types of polyp or related forms. These four types can be
  readily seen to be analogs of one another (or of immature stages), and
  also of related free-living cnidarians such as jellyfish.

If I interpret this correctly, the Portuguese man o' war seems to be descended from colonies of less specialized organisms, in a way that, say, jellyfish are not. Of course, we are all descended from colonies of single-celled organisms, but I think it's clear that being a colony on the level of the man o' war is an unusual thing and worth getting a special label.
I also like the label "colonial organism". I don't know how standard that is, but it seems to recognize a man o' war is a single organism in a real sense, even though it is structured as a group of specialized parts that maybe were more obviously separate organisms in the evolutionary past.

I'm not a professional biologist, but I just did some research, because I had the same question. It's frustrating how poorly this commonly-cited fact is explained to laypeople.
The biggest difference between a man-o-war's zooids and the cells of a multicellular organism, in principle, seems to be that each zooid is itself multicellular. And one of the things that makes them intuitively seem more like organisms than cells is that they're not microscopic - my understanding is that more or less each of the knobby and tentacly things hanging down from the bottom of the man-o-war is a single zooid (the balloon on top is also one zooid).
I would think that the fact that they can't survive being separated makes them something less than individual organisms - they are analogous to cells in many ways, but another level up in complexity. But as someone else said, this kind of system is common among marine creatures, and it seems that the convention is to call them separate organisms.
Hope someone will correct me if I got anything wrong, but I'm pretty certain that what I wrote here is essentially correct.

Welcome. Thank you for your answer. We ask answers to be backed up by credible references. Answers ideally don't need correction from the community - they answer the question. You might benefit from taking the tour, and a close look at the page on answering questions in the help center  might prove beneficial.

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Prevalent large (>=90kDa) maintenance protein/loading control
I was wondering if anyone had recommendations for good, large (hopefully 100kDa+), control proteins that would be present in most mammalian cells.  I'm working mostly with tissue samples from humans and mice, and airway epithelium in particular if that matters.  So far the best I've thought of is HSP90, but that is far from ideal for a number of reasons.  My target proteins are between 125 and 210 kDa.  To improve resolution, we've run pretty much everything under 90kDa off the gel.
That removes the old standbys like actin or GAPDH.  I understand that the protein levels could vary between cell types for a good loading control target.  Bonus points if you know a good antibody clone to it.

How about RNA polymerase subunits - some of these are large. (In E. coli I used to use beta-beta prime for the same reason. Not particularly abundant but very distinctive.)

@alanboyd Not a bad idea, I'll give it a try.  Most of these will be testing effects from infections with RNA viruses, so this might look interesting anyway.

Vinculin!  I love our grad-students, I can't believe I didn't think of it last night.
Also, awesome chart, even if it's from a company.

Thats a pretty useful chart. Bookmarked for later use.

@Chris I thought about replicating it here, but it seemed too much like stealing


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How do neurons send electric pulses even though they are surrounded by liquid which is mostly water?
I just thought about the fact that people move through electrical pulses traveling through neurons in the brain and muscles through the body. Here is what i know: the body is full of 97 or more, percent of water. the thoughts we have and the moves we make are a result of electrical impulses within the neurons and cells.
  My question is why the water does not disperse the impulse and or make it completely ineffective. My personal guess would be that each neuron is made of or has an outer layer of electric resistance material that( is it conducts) electricity.

You might want to begin to look at ion pumps and channels (plenty of good wiki articles).  Remember pure water is not a good conductor but with ions it becomes so.  In biology, signals are propagated by the control of ions across membranes and other gradients.  Have a look at action potentials as well.  I'd answer this but I know there are some really good nuro people on here and I'm not one of them.

Ooh, even more interestingly, how do we control ions, hormones and catalysts?

read about synapses

We are not made of 97% water https://en.wikipedia.org/wiki/Body_water

Neurons have sodium, potassium, as well as some calcium channels all over the surface of the cell (I'm giving a very generalized explanation here). The "electric pulses" that you are mentioning is more of electrostatic potentials generated from the interactions of cations and anions flowing in and out of the channels. Water at the specific pH surrounding the cations is a good conductor of these electrostatic interactions.
You have to remember that there are large negatively charged anion proteins inside the neurons which attract the cations (sodium ions for example) to rush into the cell. Once threshold is reached all gates open and an action potential is produced.


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Solubility of Forskolin in ethanol
I am interested in using forskolin in cell culture medium. Does anyone know how to make solution of 10 microM forskolin in 5% ethanol or less. I would like to avoid using DMSO as a solvent.
Thank you. L.

Sigma gives a solubility of 200 microMole in water containing 2% ethanol.
They state:

Forskolin is soluble in water (with 2% ethanol) up to 0.2 mM by first
  dissolving in ethanol at 5 mg/mL and doing subsequent dilutions with
  water.

The datasheet can be found here.

Thank you for you answer. We will probably try that,even though we tried to avoid the part where we would first dissolve it in absolute ethanol, as it gives some concerns toward inhibition of its ability to raise cAMP levels. Dont know if that is a genuine concern.

I don't remember the last time we prepared forskolin, but I don't remember this was a problem.


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Why do mammals in the wild retain the "trait" of menstruating with blood?
This question intrigued me a lot since if animals in the wild did have menstruation with blood flow, wouldn't all that blood be attracting every other predator in the vicinity?

Yes they do, most if not all mammals menstruate. Any dog owner can confirm this for example. Please research and try to answer your question before posting here. A 5 minute search for "mammal menstruation" for example would have answered it for you. If you want to know why that does not call in predators, [edit] your question accordingly.

Edited the question. I wasn't able to find why they would retain this trait.

I've always wondered the same thing about crying babies - would attract predators.

I would guess that the answer is something like this: ever since the development of the placenta enabled females to carry their offspring longer and to develop more fully.  Upon birth they were stronger and/or their brains were more fully developed (in the case of humans).  The increased gestation time, made possible by the structures of the womb and placenta is probably an adaptation whose advantages are much greater than the increased risk from menstruation once a month.
Some anthropological studies indicate that in preindustrial societies that women do not menstruate very much as adults though.  If you subtract out the time that they are carrying infants and nursing, which both prevent menstrual cycles, females will miss years of menstruation with only a few months in between. I would assume this is a factor in the risk of menstruation for many animals.

Yeah! I guess in the wild most mammals will miss quite a lot of menstrual cycles.


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Does adding milk to cereal make it harder for our body to absorb the vitamins and minerals from the cereal?
I add about 3/4 cups of Blue Diamond almond milk (unsweetened) every morning to a single serving of Cheerios. The milk contains filtered water, and I read that drinking water with food at the same time makes it harder for the small intestine to absorb the nutrients from the food. Has this been verified?

This topic is more appropriate for http://skeptics.stackexchange.com/

Do not migrate this to skeptics please. You've read it where? How does this apply when you're eating say a tomato, most of which consists of water. As do 90% of all foods you eat.

And by which way should water hinder the absorption?

Overall, no it doesn't. Cereal is made in a way that it's expected consumers will consume it with milk. Here's a list of some important fortifications added to cereal and milk effects on absorption.
Riboflavin: No. Affected most strongly by light.
Iron: Yes. Calcium can affect absorption. Milk causing a deficiency is rare unless it is being used as a breast milk substitute in babies.
Thiamin: No. Unless you are drinking alcohol with your cereal.
Folic acid: Milk is a source of this!

What about zinc?


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Is endoderm visible in the germ layer?
This picture is my drawing about germ layer - not embryonic folding as I wrote initially.

Where exactly is the endoderm here in the picture?
The known things

Ectoderm
Neural tube
Notochord
Endoderm - Where is this?
Somite
Somite leg
Intraembryonic coelom
Embryonic somatopleura
Embryonic splanchopleura (lateral mesoderm)
Endoderm
Mesoderm (intraembryonic)

Ok so that's not the best picture, but I think it would be along the bottom of the top wall there.  Want to give us a few clues with the parts you're sure of?

Another strong possibility is that you're missing it in the inside of 2.

@AtlLED I added clues to the body of the question.

umm... you do note you have endoderm twice, once as 10...

Again you may or may not want to further clarify what slice and when in the germ layer you are looking (might make this a better question). After thinking about it, I think you were going for neural tube and chorda formation (which is exactly what I DDG'ed to pull that image).

I think you're going for a view of tube formation, in which case, here's a good image:

Lateral plate mesoderm
Intermediate mesoderm
Somite mesoderm
Chorda
Endoderm
(Reference)

Again in your drawing I think you correctly have it labeled as 10, and don't really need to put it twice.

Thank you! Of course, I had mistake in numbering and then started to think where the missing number should be, since all known parts were already taken.


text:
Phylogenetic tree
I want to find the conventional phylogenetic tree of human, mouse, C elegans and drosophila, without all the other organisms.
Do you know where can I get it?
thanks,
Noga

Are you looking to make one, or find one that someone else already made?  I have a feeling that you wouldn't find one pre-made and that at best you'd have to do some deleting.  You might also expand on what your end goal is, as I have a feeling a graph-kernel diagram might actually show what you want better.

I made some trees based on few enzymes and i want to compare them to the conventional tree.

If you just want to check something, use the whole tree, you have all the information there. Just ignore the species you don't care about.

Every tree is an hypothesis of relationships.

This isn't a complete answer, but to get things rolling.
I think I see what you want; a comprehensive "correct" tree you can compare your single alignment tree to?
I can think of a couple of responses to this.  Firstly there is no perfect way to make a phylogenetic tree. Aside from all the different distance metrics you could use and algorithms to sort large trees, the data you use can also vary depending on what you want to do.  You can compare some conserved genes for long distance comparisons or highly mutable sequences for close distances, but which are subject to noise.
That being said a tree comparing ribosomal RNA is a phylogenetic standard.  As are trees derived from multiple genes. If you want to see if your genes are unusual you can run a few other genes through the same comparison and see if the trees vary substantially for your gene. Because the animals you compare are so far apart on the tree the relative comparison will be pretty close to the tree you've made.
If you are trying to compare the tree quantitatively to some master tree, that will be a demanding task.

You can go to Wikispecies and find the species page for each organism, e.g. the Mouse page.  On there you can click on the Taxonavigation box Expand button and see the group names for the organism.  Comparing the names for each organism will give the closest common ones, which gives you the tree.
However, for the tree between the mammals and the other two, you might want to have a look at the Tree of Life Web page for Bilateria.  Your three groups fall into Deuterostomia, Arthropoda, and Nematoda; for these you'll find a tree for these three groups.  (Actually two trees, but for your groups they amount to the same thing.)

I would not recommend Wikispecies as a reference for phylogeny: taxonomic system is not identical to (our current understanding of) phylogenetic relationships. I'd not recommend Wikispecies at all, since it is currently occupied by a single moderator.

If you accept the nowadays prevailing Ecdysozoa-hypothesis the relationships are as follows:
               ____ Drosophila
              |
        ______|
       |      |____ C. elegans
       |
  -----|       ____ Human
       |      |
       |______|
              |____ Mouse

According to the more traditional views (the Coelomata-hypothesis):
         _______________ C. elegans
        |
    ----|     __________ Drosophila
        |    |
        |____|       ____ Human
             |      |
             |______|
                    |____ Mouse

(Note that these trees have the same unrooted topologies)


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Best way to automatically link Gene Entrez ID with Gene Symbol in TCGA
I am trying to figure out how to link Gene Entrez ID with Gene Symbol, for TCGA dataset.
So far, I have found this ftp directory with Gene info updated daily.
But, for Entrez ID 728661, I have found two different mappings:

here symbol is RP11-345P4.4;
here, and in gene info downloaded from ftp above, symbol is SLC35E2B while RP11-345P4.4 is in the field 'locus tag'.

Since I am a newbie I am bit confused about this thing. And, while I think they can be synonyms, I need to know if there is a best practice to use in this case, and if I need to implement some script on my own to do it automatically.
Thanks

To be sure, if I understand you right: You want to have a list with the Gene ID in one column and the corresponding Gene symbol in the next?

It is best to use the Standard Gene Symbol (HGNC) or Refseq IDs. Some Refseq IDs may be of this form NM_xxxx.x (where x is a number). In such cases remove the . and the following number. Sometimes same transcript can have more than one refseq ids- in such cases use the shorter id (not a universal rule though).

@Chris yes, I want the unique mapping between the two ID, is it possible?

@WYSIWYG Thanks, I think I am going to use the HGNC symbol. Could you please explain, if you know it, why the two symbols differs? HGNC is the standard   for Gene Symbols? Thanks

Do you have this list with the IDs? If so, you can use Biomart from Ensembl to convert it.

Thanks, I will try it as soon as possible. Could you please write that as answer? So if it works I can vote it and accept it..


text:
Pathway mediates nitroglycerin-induced relief from angina pectoris
what kind of Pathway mediates nitroglycerin-induced relief from angina pectoris,please provide some idea...

This looks like a homework question. Can you please show what you have done so far to find an answer?

@Chris I missed my class so I really had no idea how to approach this question I did some literature search but it was confusing ..

The effect of nitroglycerin on the cardiac tissue is similar to nitric oxide (NO),  which forms in the endothelium of blood vessels from arginin metabolism products.
So, the general scheme can look like this:
R-NO2 is converted to R-NO outside of the cell (glutathion-SH-dependent reaction). NO is lipophilic and rapidly penetrates into the cell where it activates guanylate cyclase. From this moment you can see the resulting influence on myosin and actin on this picture:


text:
M-type potassium channels by muscarinic receptors
How does the closure of M-type potassium channels by muscarinic receptors result in increased excitation of the target neuron?

Closing of the channel through muscarinic receptors involves activation of phospoholipase C and depletion of membrane phosphatidyilinositol-4,5-bisphospate which is needed for the channel to stay open. Once the channel is closed,  potassium, which is a positive ion accumulates inside the cell eventually depolarizing it or lowering its threshold for activation. Thus, blocking the extrusion of K ions results in excitation of the target neuron.
See this for more:
Brown, D. A., and Constanti, A. (1980). Intracellular observations on the effects of muscarinic agonists on rat sympathetic neurones. Br. J. Pharmacol. 70, 593–608.


text:
Is Rheumatic fever more Chronic than acute?
It follows from the complication of S.pyogenes' pharyngitis.
I am thinking how the inflammatory response behaves: acute or chronic or something between.
I think chronic disease is better description here than acute, however not sure.
What is the type of inflammatory response in the Rheumatic fever?

the inflammatory response it autoimmune reaction, thus it occurs 4 weeks after the Strep infection.
please, look at the picture from the "Nature" -

So it is chronic, since not rapid.


text:
How does the brain know where a signal came from? What is the addressing system
I am an electronic engineer so I am thinking about this from an electronics outlook.
How does the addressing system work, As I see it, the nervous system is small parallel branches attached to larger "serial" lines (spinal cord).
The serial line is then attached to the brain, but how does it then figure out where the message came from and then get the message back to the place it came from.
If I were to build a robot I would have an addressing system with each message and maybe some kind of error checking to make sure the messages don't become corrupted, but as it's not an electronic system I don't see how the brain could possibly do this. unless it is a fully parallel system and there is a single wire going from every sensor back to the CPU..

The brain knows where a sensory signal came from by what neuron is doing the signalling.  The incoming neuron is dedicated to signals from one source and, since it is not shared by other sources, does not need to have an encoding as to what the source was. When your toe touches something, the sensation causes a pulse which, amazingly, travels along a single nerve cell (neuron) up to the brain stem.  That neuron has its nucleus at a dorsal root ganglion located by the spinal cord, and has a fiber (axon) that extends to the source (toe) and another extending up to the brain stem.  This pathway is called the PCML pathway and the Wikipedia article has some readable details.  This page has a schematic and tabular summary, while this site has a good descriptive overview.
If a robot were built along the same sort of design, to determine what was happening at 1000 places in its body, it would have 1000 wires running to its central computer.  You probably wouldn't choose to use such a design, but then you probably wouldn't be designing a robot that has to build itself from raw materials.

That is exactly the answer I was looking for, thank you so much. So it is literally a fully parallel system. So extending what I said below, does every sensation reach the brain or are some so, meaningless that they don't need much processing. E.g. Hair, stuff like that. Beacuase if so does that mean there's millions of axons and neurons

If you perceive a sensation, it had a path; the signaling is indeed massively parallel.  Some sensations are processed in the periphery and a derived signal sent on to the brain; The density also varies (the hands have many nerves, the back, few). There is also peripheral processing like the knee reflex.  Also there are nerves that have little or no flow to the brain; see autonomic nervous system.  If this answer is what you wanted, you can accept it by clicking the checkmark to the left.

Is it precisely 1-to-1? The number of somatosensory neurons < axons in spinal cord to brain? I don't think this is absolutely true, but not sure. For example on your back, you have a very coarse sensation, but there's no missing area of sensation. To save bandwidth, it is plausible that there were some converging signals in the spinal cord level.

Isn't this simply a circular reasoning? The essential question must be: How does the brain know 'which neuron is doing the signalling'? The answer must be of meta-sensation, something like self-recognition. Though I think no one in the world can really answer it..

your question is a little bit difficult to answer in the current forum format, however I'd suggest you reading about Reflex arc  - from this you can understand consequence of the events in simple reflex on the level of spinal cord (i.e. monosinaptic pathway) and very complex reflexes managed by multiple neural cells (neurons).
A classic example of the reflex -

If you want to dive into the very complex explanations you should read some textbook and probably not forums.
Probably, you'd like to know what the potential of action is....

Thanks for the answer but as I see it these are all just connections and how the conduction works, but somehow the tip of my little toe can send a variety of messages to the brain and it knows exactly which toe and which sensation, there must be some kind of addressing. Biology is so complex

I have just noticed this similar post http://biology.stackexchange.com/questions/550/how-does-a-brain-distinguish-stimuli where the top comment says the way the brain distinguishes is largely unknown.

the messages come from specific receptors and along any pathway there are interconnections for different regions. Your question is complex, so we cannot answer before you'll be more specific...

Well okay a specific sensation, is the brain processing the movement of hairs and does it know the location of every single hair. Well obviously it does because if you touch it lightly I know exactly where I was touched.. Or do you mean something else by specifics?

considering hairs you're a little bit wrong - the brain join skin regions in quadrants and each quadrant has about 1cm sides, thus you cannot differentiate 2 touches inside the same quadrant


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What's the best way to measure/calculate the size of a light beam at the sample of a microscope?
I am using a microscope with an LED derived light through the epi-fluorescent port of a microscope.  I know that the "field of view" for a given objective is equal to the field number/magnification but I don't know that this is the actual area of illumination on the sample.  In my case, I am using a 40x objective with field number 26.5.
Secondly, if I were to use a pinhole filter between the light source and the back of the objective would this limit the area of illumination so long as the pinhole was smaller than the f.o.v. dimension?
I would be grateful for any answers, most of the information I can find on beam size at sample is related to spot size calculations of resolution.

Well you can always use a piece of white circular paper and draw the outline of the light onto it since it should be visible. This is a quick and dirty method that can be improved by taking a photo of the light with a camera if you have one and then comparing the distance of the edge of the paper measured with a ruler to that of the circle of light.


text:
Difference between Fulminant and Acute Meningococcemias
Fulminant seems to mead rapid.
There is however some articles with both phrases: "fulminant meningococcecemia" (about 5000 Google matches) and "acute meningococcecemia" (about 3000 Google matches).
I am thinking Neisseria meningitidis and its pathogenesis

Portal entry nasopharynx (pili)-> attach epithelium cells -> bloodstream (bacteremia); upper respiratory tract infection -symptoms; may be asymptomatic in transient flora; fulminant meningocococcemia (regardless of meningitis)

What is the difference between the two diseases?

When we say "Fulminant meningococcemia" we mean failure of adrenal glands due to haemorrhage of infectious origin, or Waterhouse–Friderichsen syndrome
and acute is related to time of signs appearance, opposed to chronic disease.

Can we say that all fulminant diseases are acute? In this case, the fulminant disease seems to acute.

in medicine there are not 100%, so we only can say that most of fulminant infections are acute, but sometimes chronic bacteremia or chronic wounds can lead to fulminant deterioration in the host

This answer is incorrect. Fulminant does not refer specifically to adrenal hemorrhage. It's a general adjective describing the explosive course of a disease process.

Both fulminant and acute are adjectives that describe a disease course. The previous answer by @ilan is incorrect. Fulminant does not specifically refer to adrenal failure, despite the association between meningococcemia (which often has a fulminant course) and adrenal hemorrhage.
Fulminant relates to onset, speed of progression, and severity. A fulminant disease process is sudden, rapidly progressing and very severe. Diseases processes described as fulminant are often lethal if not immediately treated. Meningococcal bacteremia, classically described as purpura fulminans, is one example.
Acute relates mostly to onset. Here the earlier answer by @ilan is correct. Acute, as opposed to chronic, refers to a disease process with a short course, or a short term phase of a disease process with a longer course (as in an acute exacerbation of a chronic disease process).
All fulminant disease processes are acute, by definition. When referring to bacteremia with Neisseria meningitidis, the use of the descriptor acute or fulminant does not indicate a different disease. So I suppose the direct answer to this question is that there is no specific difference between fulminant and acute meningococcemia. They are not separate diseases, and both terms could correctly be used to refer to the same case.


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Systemic sensory confusion?
Sometimes when a person gets touched on one part of the body they feel it else where and may think it came from a different part of the body. What causes this? Other examples are similar to why you can trick your self into thinking your arms are heavier than they really are. another would be that you can close your eyes and move in circles up and down your arm slowly and then when you guess where u are touching your hand is higher or lower than expected. What causes these things?

The situations you describe involve what is called proprioception or the feedback to the brain of where your arms and limbs are in space. As APengioun mentioned, this is a complicated undertaking and if information is restricted, for example eyes are closed then the sense of where your limbs are gets messed up. As for your title, it's not really neuronal confusion as it is confusion of the sensory system if you can call it that. This includes sensory neurons from your limbs as well as central neurons in the brain that further process your information.

When our brain works out where a part of our body is in relation to another part of our body, or in relation to anything for that matter, we combine:

visual information
information about how much our muscles are contracted
how much our joints are contracted
different forces being applied on our arms/legs or other body parts
where it remembers we used to be
how much force we applied to move where we wanted to move
where we would therefore expect to be
and many other things

That's quite a few things that our body relies on! The one that's most fine tuned is our vision. Let's face it, whatever we are actively doing with our hands requires the most skill and knowledge of where our hands etc. are. It is also the system that we rely on the most. But other systems are helpful to make sure we don't fall, grabbing on to things and making sure we reflexively contract the opposite muscles to prevent falling, stop us dropping things and lot's more. It doesn't matter if they're not accurate, they just need to be fast and in doing so they can't be extremely exact.
When we don't use vision, we rely on these other things. They're made to quickly adapt (e.g. hold a shopping bag for a while and when you let go your arm feels light or when you get out of a swimming pool your body feels heavy) and it is important that they do this to allow their functions as listed in the last paragraph.


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Genome Assembly Using Reads
I'm taking an online bioinformatics class and I am stuck on a problem. The resources I have found don't help that much. Here is the problem:
"Assemble the error-free reads from a circular genome on the dataset below. You do not need to consider the reverse complement of the reads.
Dataset: CGTTCT CTAG GACGT TAGAC
As the reads do not have the same length, convert the reads to 4-mers using the approach proposed by Idury and Waterman."
I believe this means I need to convert this into sets of 4 characters each. Do I simply break them up by taking the first 4 characters and last 4 characters like this?
CGTTCT: CGTT --> TTCT
CTAG: CTAG --> CTAG
GACGT: GACG --> ACGT
TAGAC: TAGA --> AGAC
And end up with a new dataset of: "CGTT TTCT CTAG GACG ACGT TAGA AGAC"?
Or is there more to it than that? Thanks for any help.

I would guess that it would be all 4mers. In this case that would mean that CGTTCT would also yield GTTC. But as I say - this is a guess.

It does in fact mean all possible 4mers. I don't know how much material you get from the course, but they refer to this paper: http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.79.6459&rep=rep1&type=pdf

To be sure I'm understanding correctly, does that mean the new dataset should be: "CGTT GTTC TTCT CTAG GACG ACGT TAGA AGAC"?

Actually the new data set will be,
for k = 4 (k-mer value)
CGTTCT -> CGTT GTTC TTCT
or

Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874646/


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Why there is a very high drop in pressure from arteries to arterioles?
Laplace law explains why the pressure is the same in aorta and arteries (100).
I am thinking why there is so big drop in pressure when going from arteries to arterioles (40-60).
Why there is a great drop in pressure from arteries to arterioles?

While correct, @AndroidPenguin 's answer is only part of the explanation. By far the main reason of the pressure difference is that the peripheral circulatory system has two main compartments:

a resistive compartment, represented by arterioles
a capacitance compartment, represented by capillaries

The reason for the abrupt pressure fall from arterioles onward is precisely that this is the main function of the arterioles: they contract and dilate to adjust capillary pressure. Since a good part of capillary function depends on exchanges along oncotic pressure gradients, hydrostatic pressure cannot be allowed to stay too high in the capillary compartment. So in conclusion, @AndroidPenguin gave you the physical reason, but mine is the physiological reason.

This answer makes sense for me too! Thank you for your answer!

The vessel diameter is the most principal determinant to control resistance. Compared to other smaller vessels in the body, the artery has a much bigger diameter (4 mm), therefore the resistance is low.
In addition, flow rate (Q) is also the product of the cross-sectional area of the vessel and the average velocity (Q=AV). Flow rate is directly proportional to the pressure drop in a tube or in this case a vessels, although there are other factors of blood vessels that contribute towards the difference in pressure drop in bifurcations of blood vessels. These include viscosity, length of the vessel, and radius of the vessel.
Factors that determine the flow's resistance as described by Poiseuille’s relationship: ∆P=8µlQ/πr4:
∆P: Pressure drop/gradient µ: Viscosity l: length of tube. In the case of vessels with infinitely long lengths, l is replaced with diameter of the vessel. Q: flow rate of the blood in the vessel r: radius of the vessel
Assuming steady, laminar flow in the vessel, the blood vessels behavior is similar to that of a pipe. For instance if p1 and p2 are pressures are at the ends of the tube, the pressure drop/gradient is (p1−p2)/l =∆P.
In the arterioles blood pressure is lower than in the major arteries. This is because velocity of flow is increased with decrease in diameter and vice versa.
Source: http://en.m.wikipedia.org/wiki/Blood_pressure_drop_across_major_arteries_to_capillaries
This is important as for efficient exchange at the capillary bed pressure and flow need to be much lower.


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Difference between Cary-Blair and Amies transport media for Staphylococcus and Streptococcus?
I normally use Amies medium, but I today heard that Cary-Blair is also possible.
When should you use Cary-Blair medium?

This site (no connection) states (my emphasis):

Unlike Cary-Blair Medium, which is almost exclusively associated with enteric transport, both Stuart and Amies Medium have been widely used for the transportation of a diverse range of clinical swab samples from sites including the eye, ear, nose, throat, skin, genital tract and wounds.

This is very general. I am interested if there is any advantage of using the other in some circumstances. I think if you use Amies transport medium, you do not need to use Cary-Blair transport medium in most of the cases.

I put this up because it clearly states that Cary-Blair medium is used for enteric samples. Whether you should use it for that purpose is not explained. Presumably the Staphylococcus and Streptococcus you refer to are not samples of that type, so you would use Amies.


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Primer design and BLAST E value stringency
When searching for misprimings I have been told that an e value that is higher than 0.01 is ok and will produce no significant amounts of mispriming. Yet I searched some and it would seem that the e value threshold limit is dependent upon the "amount of information" in the database.  Indeed I found that some papers cite as values lower than 0.07 to be significant already.
What are the criteria you use at times to judge this issue, and how do I know when to lower or increase my stringency when running a routine BLAST for the purposes of designing primers?

I never used BLAST for primer design, but often for finding out where a sequence came from.
From the FAQ of the NCBI:
http://www.ncbi.nlm.nih.gov/blast/Blast.cgi?CMD=Web&PAGE_TYPE=BlastDocs&DOC_TYPE=FAQ
"The lower the E-value, or the closer it is to zero, the more "significant" the match is. However, keep in mind that virtually identical short alignments have relatively high E values. This is because the calculation of the E value takes into account the length of the query sequence. These high E values make sense because shorter sequences have a higher probability of occurring in the database purely by chance. For more details please see the calculations in the BLAST Course.".
What they say in the papers is true, the size of your database matters in deciding how significant the match is. I can imagine that for primer design you want to be more careful with the E-values, as they often fall under: "because shorter sequences have a higher probability of occurring in the database purely by chance".
I hope this helps to make your decision for deciding your threshold, otherwise please give more information.

This NCBI page offers a primer design tool which appears to incorporate a specificity check run via BLAST. However it seems to base stringency upon degree of mismatch rather than an e value.


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Rate of cell division in humans
On average, how many cells divide each day in a human being?
How long does a cell wait before dividing itself ?
I have tried to look on the internet but surprisingly the answer is difficult to find..

Thats pretty hard to answer, since the proliferation rate of cells is pretty different. For example heart cells hardly ever divide while cells of the hematopietic systems do this pretty often.

This is very difficult to answer since the rate of cell division is age and also health dependent.

My first thought was this:
According to Wikipedia (citation provided)

Between 50 and 70 billion cells die each day due to apoptosis in the average human adult. For an average child between the ages of 8 and 14, approximately 20 billion to 30 billion cells die a day.

For every cell that dies a new one must be born, so there must be at least between 50 and 70 billion cell divisions to replenish these cells in an adult human (no net growth).
But then I remembered erythrocytes. Wikipedia again:

Adult humans have roughly 2–3 × 1013 (20–30 trillion) red blood cells at any given time, comprising approximately one quarter of the total human body cell number

and...

these cells live in blood circulation for about 100 to 120 days

So approximately 1% of erythrocytes are destroyed every day and must be replaced. That's 2-3 x 1011 cells formed every day, which dwarfs the cells replenished due to apoptosis (5 - 7 x 109).

Through this process [erythropoiesis] erythrocytes are continuously produced in the red bone marrow of large bones, at a rate of about 2 million per second in a healthy adult.

I like the answer, but there is a problem with the math. 50-70 billion cell is 5-7 x 10e10, not 5-7 x 10e9. It is still larger than the 2-3 x 10e11 number of the blood cells by a factor of about 4, but not by a factor of about 40 which is the result of the original calculation.

Thanks for spotting that Len.  So the sentence that says 'That's 2-3 x 10e11 cells formed every day, which dwarfs the cells replenished due to apoptosis (5 - 7 x 10e9).' should say 'That's 2-3 x 1011 cells formed every day, which is ~4 x the cells replenished due to apoptosis (5 - 7 x 10e10). Not sure about the protocol here, do I edit my answer?

It's also important to note that starting point of this estimate of 50-70 billion cells has no reference in the wikipedia. D'oh! So the whole thing is on very shaky grounds. I've tried to find a paper for this statement but have come up empty so far.


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What indices can we use to describe fitness landscapes?
We usually talk of smooth or rugged fitness landscape.

Are there any (standard) indices to measure the "structure" of fitness landscapes?

For example, one might consider the mean epistatic interactions (over all possible combination of loci)

This paper uses 4 metrics for discreet landscapes.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240586/
Deviation from additivity: How much your genes interact (normalized). Fitness in a purely additive landscape with three genes, for example, is F=f(x)+g(y)+h(z) where f,g, and h are each functions of one variable (the x,y, and z "genes"/coordinates). Deviation measures how far from additivity the fitness is. Higher is not always rougher but it is "trickier" since the effects of changing a gene depend on other genes.
Peak fraction: The % of points that are local peaks (discreet landscapes only), higher is rougher.
Tree component: The % of points that have at most one neighbor of higher fitness. Lower is rougher and indicates that there is a choice as to which direction to travel.
% monotonic paths: The fraction of paths (of all possible shortest paths from a given point to the peak) that don't go downhill. This calculation is averaged over all starting points in the landscape (excluding the peak). Lower is rougher.


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Does recombination increase the additive genetic variance for fitness?
On this article, first column, eighth line of the introduction:

By bringing together favourable alleles from different chromosomes, sex and recombination increase the additive genetic variance for fitness [..]

Can you please help me understanding why does recombination increase the additive genetic variance for fitness?
Note: In reaction @mgkrebbs comment, I think that given the subject of this article, when talking about different chromosomes, the authors actually referred exclusively to homologues chromosomes. My question concerns the second part of this sentence anyway: "Why does sex and recombination increase the additive genetic variance for fitness"?

Here is another question on the same article

This is a little tricky.
First of all lets be clear about 'bringing together favorable alleles' (or any alleles) represented by site mutations on 2 chromosomes:
--------A------------------
             X
------------------B--------

If the two dashed lines are two copies of the same chromosome, then a recombination event at X may produce:
--------A---------B--------

Allowing both A and B to be passed along to offspring.
Any given case of recombination might actually harm resulting offspring. But in cases where A and B together are beneficial, over the course of generations you will find AB genotype combinations show up more frequently in the population because of selection and competition.
Firstly each individual variant experiences some selection for fitness and many are lost.  Because of this, recombination will typically put two or more such variants together onto a single chromosome.  Recombination allows for individual mutations of benefit to pool together and collect into a single place.  This multiplies the chance that stronger combinations of mutations will show in the gene pool.  This increases the fitness variance - the most powerful combinations are more beneficial than any single variant alone.  On the other end detrimental combinations will also make some individuals exceptionally weak.
So its not just recombination, but recombination and selection which create favorable combinations of alleles in populations.  The link you give discusses how when selection is not strong, recombination is not so great, but we never seem to lose recombination where these conditions don't hold sway.
By comparison, consider a simple case where recombination does not occur where there is an A genotype and then one waits for B to show up on the same chromosome by random mutation.  That would take perhaps thousands or even millions of generations before such a thing happens at random.  Recombination is a powerful accelerator of evolution.

thank you. As I understand your answer, you explain the advantage of recombination just as it has been considered by Muller. But if I am not mistaken you don't address the question of why the additive genetic variance (you actually don't use the words "variance") increases thanks to recombination (or thanks to the combined effects of recombination and selection). Can you try to further elaborate your answer so that it explains why recombination causes an increase in additive genetic variance.

I don't think this response addresses the quote since this concerns crossing over.  The quote says "bringing together favourable alleles from different chromosomes", which doesn't involve crossing over.

"In meiosis and mitosis, recombination occurs between similar molecules (homologs) of DNA. In meiosis, non-sister homologous chromosomes pair with each other so that recombination characteristically occurs between non-sister homologues. In both meiotic and mitotic cells, recombination between homologous chromosomes is a common mechanism used in DNA repair." http://en.wikipedia.org/wiki/Genetic_recombination

@sigeta I agree with you shigeta. But I don't think your answer answers my question. I understand that if a highly beneficial mutation occurs before another beneficial allele on the same chromosome had time to reach fixation, then these two mutations can only be found in the same individual if recombination occurs. This concept is also conveyed by Gould when saying that "selection creates the fit". But I still don't understand why the additive genetic variance for fitness increases as a result of recombination.

Its tough to write answers here - remember that responders want to explain terms to other readers as well as the poster or they get complaints.  I thought I'd answered your question though.  Beneficial recombinations are among offspring; the vast majority of recombinations are probably less fit or have no substantial effect on fitness. Over time selection brings those combinations into common occurrence in the gene pool.  I didn't explain how selection works... maybe i need to define that in detail too?

Well the issue I'm struggling with is the idea that fitness variance is greater in a population where recombination occurs. This is not intuitive to me. I understand that recombination allows to bring to fixation several mutations that occurs in different individuals in roughly speaking the same time (It actually depends on the probability to occur in a chromosome already bearing the mutation which depends on the time difference between the two mutations and the selective coefficient of the first according to Haldane's law 1-P = exp((1+s)p).

@shigeta But why does this process increases fitness variance? I am not sure my comments will help finding out what point I am missing. I might still have some difficulties with Fisher's fundamental theorem although I asked a question about that some times ago. If you can pinpoint what I am missing, please try to edit your question to add some elements. Thanks a lot for your help.

I added a little bit here, but I'm not sure what the tie in to Haldane's rule is explicitly.  Haldane's Rule applies to specific cases where there is interspecies breeding and relates to speciation. Can you put in some links if you have any?  Or perhaps i've helped with what I've put up here.


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Meiosis vs. Mitosis
Meiosis is a type of cell division that reduces the chromosome number from 2n to n to make gametes viable for reproduction in humans. I know that during meiosis, there is independent assortment and crossing over that occurs, which help to make more genetically individual organisms.
My question is, why don't haploid gametes go through mitosis to reproduce instead of diploid germ cells going through meiosis to create more gametes, without considering crossing over and independent assortment? This is just my opinion, but meiosis seems like a much more energy intensive process. After the germ cells go through meiosis once to create the gametes, I do not see why the gametes don't then just multiply via mitosis (again, not considering crossing over/independent assortment.)
Is there any specific reason, other than to create more genetically diverse people, that gametes do not undergo mitosis to multiply rather than germ cells undergoing meiosis to make more gametes?
Sorry if my question is confusing, I'm just curious to what the reason is. It's probably something obvious I'm not seeing myself. :)

I think this is a great question, but it is based on two questionable assumptions: (1) that meiosis is more energy-intensive than mitosis; and (2) that energy efficiency is a key driver in evolution.

Couldn't fit in a comment...
To me, your question sounds like "what are the possible advantages of sexual reproduction over asexual reproduction?" but in the meantime you're saying that you're not interested neither in the advantage of recombination nor in the advantage of "independent assortment". I don't quite see what you mean by "independent assortment" in this context.
I just want to say some words about some "proximate" possible explanations of the evolution of sex. It's been suggested that meiosis have evolved in order to repair damage in double stranded DNA. Also, it's been suggested that meiosis is important for the problems of telomere length also.
You might be interested to have a look to the evolution of bi-phasic life cycles and, more globally speaking to the evolution of sex.

I'm not interested in the advantage of recombination because I want to know if there's anything beyond that that makes meiosis more advantageous than mitosis. Also, I was always taught that "independent assortment" referred to how chromosomes line up independently of one another in Metaphase 1 before they split into separate cells. Is that term incorrect? Is it just a term used to help students learn the process? I guess I never really questioned the terminology before..

So, you're interested in what I called "proximate" explanations? Or we could call them physiological explanations. If yes, I'll let someone further develop these kind of explanations.

Yes! Please. Sorry for not being clear initially.

I would suggest that the key here really is the variation produced from meiosis. Every gamete produced from meiosis is genetically unique. This gave rise to variation, which is the raw material for evolution. Meiosis would give a selective advantage in this way, therefore it could have allowed organisms to survive and pass on their genes.


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Isopropanol precipitation of DNA - duration and magnitude of cold storage
DNA prep protocols often include a final precipitation step with alcohol, often isopropanol, where the DNA must be kept in the alcohol, at a low temperature such as -20C or -70C, often overnight.
What is the point of keeping it at low temperature? Is lower better? At what point do you see diminishing returns?
What about the time? Is overnight really necessary, or would, say, an hour suffice? Do lower temperatures result in quicker precipitation?

For the precipitation you use different reagents: First you add salt under slightly acidic conditions to make sure that the DNA precipitates in a less polar environment. This is achieved by adding alcoholes like ethanol or isopropanol.
It is commonly thought that a incubation at low temperatures enhances the results, but this is interestingly not true. There is a paper from the Bethesda Research Laboratories which is called "Ethanol Precipitation of DNA." which analyzes these relationships (temperature, time and alcohol concentration) in great detail, its definitely worth reading.
Figure 1-3 from this paper shows the influence for Ethanol (but I am pretty sure that this is not much different for isopropanol):

I would prefer ethanol precipitation to ispropanol whenever possible. Isopropanol co-precipates salts, so you have to wash a few times with 70% ethanol and it is less volatile than ethanol, so the drying step takes longer. Its also less effective cleaning organic compounds like phenol away and sometimes the pellets are harder to see.
On the other it can be useful when you have to deal with large volumes, since you only need 0,7 volumes of isopropanol compared with 2,5 volumes of ethanol.
Precipitations with Isopropanol are usually not incubated but centrifuged directly after mixing. Here is a protocol from my lab (which originally came from Qiagen, if I remember correct):

Adjust the salt concentration, for example, with sodium acetate (0.3
   M, pH 5.2, final concentration) or ammonium acetate (2.0–2.5 M,
   final concentration).
Add 0.6–0.7 volumes of room-temperature isopropanol to the DNA
       solution and mix well.
Centrifuge the sample immediately at 10,000–15,000 x g for 15–30 min
   at 4°C
Carefully decant the supernatant without disturbing the pellet.
Wash the DNA pellet by adding 1–10 ml (depending on the size of the
preparation) of room-temperature 70% ethanol. This removes
co-precipitated salt and replaces the isopropanol with the more
volatile ethanol, making the DNA easier to redissolve.
Centrifuge at 10,000–15,000 x g for 5–15 min at 4°C
Repeat the washing and centrifugation steps once more.
Carefully decant the supernatant without disturbing the pellet.
Air-dry the pellet for 5–20 min (depending on the size of the
pellet).
Redissolve the DNA in a suitable buffer.

It seems that overnight incubation is absolutely superfluous based on Fig.2 - or am I mistaken?

Thats how I read it and how we do it. I have never had any problems with short incubation times.

Why can you conclude that overnight incubations are superfluous when they only examined conditions up to 10 minutes? The 5-minute difference between incubating for 5 or 10 minutes seems pretty minor compared to the possibility of incubation for 15+ hours. In general, I'm not so sure I can rule out that temperature might also have a better effect if the samples were left for 15 hours as opposed to 10 minutes.

Because you should be able to see a difference between 0 (simply mixing) and 10 minutes. And its also my own experience with fits with this data.

@Chris I find your experience more credible than Fig. 2. What if the amount of precipitate over time looks like a Michaelis-Menten curve (http://dwb4.unl.edu/Chem/CHEM869K/CHEM869KLinks/www.curvefit.com/1952b0e0.gif change x-axis to time and y-axis to amount of precipitate)? Then a lot would rapidly precipitate out, but a significant fraction might take a long time to come out in a short time; you wouldn't necessarily see the difference between 5 min and 10 min, but you might notice a difference after 15 hr.

I agree that for most applications, Fig. 2 shows that waiting a short time gives reasonable yields. But without seeing the data point for 15 hours, you're extrapolating, I can imagine plausible scenarios where that extrapolation could be false, and if you care about getting as much of your sample as possible, I would want to see evidence that waiting 15 hrs doesn't improve yields before I take that out of my protocol. Your experience with this seems more credible to me, although have you done the experiment where you compare yields from just mixing the sample and leaving the sample overnight?

The freezing at -70C, how long do you recommend it ?

@AnuragMishra 20-30 Minutes, longer is not necessary.

Is it okay to use Sodium Chloride, instead of Sodium Acetate ?

That depends on the pH you are working at. If it is already slightly acidic, than NaCl is usually ok. If not, use sodium acetate to make sure that the DNA gets enough protons. This reduces the solubility. One thing: If you have a lot of questions, please ask a new question with it and not as in the comments below other questions.


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Can viruses be used to extract oil from algae?
I read that one hard step in algae oil extraction is to rupture (or fracture) the cell walls to get the contents inside. Some people use chemical methods; some use sonication or mechanical forces.
I wonder why nobody is talking about using viruses to accomplish this task? Viruses destroy the cells and release clones of itself. Some article states that there are plenty of unknown viruses in seawater. I'm sure a major part of it infects algae.

Another major concern would be containment. Let's say you start producing industrial amounts of virus that you engineer to quickly causes the lysis of algae (we'll ignore mutations).  Where are you going to grow that where it wouldn't also be open to insects, birds, or even wind.  You could move this entire operation in a green house, but then you start to loose your major provider of energy in the first place--the sun! Again it could work, but is unlikely to yield what you want.

Viruses hijack the hosts translational machinery, forcing the host to downregulate translation of other proteins in favor of viral proteins. Your cells will eventually lyse, but in the meantime they would not be producing the enzymes required to make whatever product it is you're trying to get, likely resulting in low yields that are contaminated with virus.

A virus has to infect the cell, take over the cell machinery to make more virus, and then is might lyse the cell.  And then you have to wait for more virus to do that again to more cells, and you have to keep the algae alive all that time.
Chemical or mechanical shearing would be much faster, and you don't have to run the risk of virus floating around and getting into stocks that you don't want to kill right now.

But we could use a lot of virus to shorten the time it takes for all the cells to get infected, the virus can just be reused from a previous batch so it's cheap to produce.
Mechanical shearing would be inefficient if you want to fracture cells that small, and chemical methods require recycling and they are expensive in the first place. Virus is using the energy of the cell itself to do the fracture, and afterall the purpose of making oil from algae is to use the cell to produce energy, it's still a net gain.

Consider where you'd get all that virus. Purify it out of the lysed cultures you just made? The viral lysis takes longer, results in less product, and requires an additional virus recovery step. If you're making energy, it's probably more efficient to run the sonicator off the extra yields you get from sonicating your algae instead of using viruses.