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Solubility of DNA in water
This would seem to be an easy to answer question, but I was unable to find an answer (in g/L) for generic double-stranded DNA or plasmid neither on Google nor on BioNumbers. I would expect the solubility to vary slightly based on the sequence or length, but it probably wouldn't affect it very much due to the relative hydrophobicity of the bases.
I know I have made solutions of plasmid maxipreps of at least 1µg/µl, and the Nanodrop DNA quantifier datasheet has a maximum DNA detectable limit of 15µg/µl, but can anyone find a source for the maximum solubility level of generic DNA? For example, the solubility of a specific plasmid of approx. 5kb in length would be a good ballpark answer for this question.

I think that we need to dig around for maximum molar concentrations of DNA for this question.  I know that you can't spec a sample above 100g/L (ug/uL), and that to test high concentration giga preps I've had to do serial dilution of the sample for accurate reads.  I've consistently made giga preps that were concentrated to 10+g/L but those were in buffers, not water.

@AtlLED do you have a protocol for the giga prep kit if you used one?

https://www.qiagen.com/us/resources/resourcedetail?id=399337ce-2fb3-495a-b2f3-e35a17f61cab&lang=en  and also http://www.mn-net.com/Portals/8/attachments/Redakteure_Bio/Protocols/Plasmid%20DNA%20Purification/UM_pDNA_NuBoEF.pdf  At high concentrations, the prep becomes much more like a syrup/has an increased viscosity.

This is just a back-of-the-envelop thought experiment: A human cell has  approximately 6 billion bases, meaning that there are app. the same number of - charged phosphate bonds in the backbones of the helices. If you were to say arbitrarily, for argument sake, that you needed 10 water molecules to solvate the negative charge of the phosphate bond, then you would only need 1.8 femtoliters of water to solvate the DNA from a single human cell. The human genome weighs about 3.6 picograms, so if this accurately represented the solubility of dsDNA then it is equivalent to 2g/mL.

This makes sense, because when you think about how absolutely small a cell is and how much water its even smaller nucleus contains, even in this minuscule amount of water, DNA and associated proteins are still solvated, then you get an idea for just how much DNA can be solvated in water. We can easily see small fractions of a drop of 1 µL of water with our naked eye (as you mentioned a nanodrop machine), but we need a decently powerful microscope to see the nucleus of a human cell, and yet all of that DNA is still solvated. It will take a huge number of 5kb plasmids to saturate water.

@AMR Arguably, most of that DNA is bound to chromatins instead of being solvated in water.

Chromatin is linear dsDNA and its associated proteins. Why would that make it any more soluble than naked DNA? Hydrophilic/Hydrophobic interactions will sequester the hydrophobic regions of the molecules from the water molecule. The cell is an aqueous environment, by definition all of the hydrophilic portions of the molecules are solvated in water.

@MarchHo I think that the likely reason that you cannot find an answer to your question is that DNA is a variable molecule. A plasmid will behave differently to linear DNA. A large plasmid will behave differently than a small one. Whether you are dealing with chromatin or whether you have digested the proteins and RNA and are left with naked dsDNA will make a difference. Oligonucleotides are single stranded and will had different solubility. Even small fragments of dsDNA will likely have different solubility than an entire chromosome.

@AMR I asked specifically for the solubility of a 5kb plasmid.

What is your concern related to the solubility of a 5kb plasmid?

The point of my last question was that unless there is a specific reason for needing the solubility of a 5kb plasmid, then the answer of it is soluble in water, is sufficient for almost any application that you will use that plasmid in. It is sort of like with NaCl. Its solubility is 359g/L, for most every application, soluble in water is all that is needed to be known. An E.coli cell is 10^-15L, but they still have enough volume with everything else taking up that volume to replicate tens to hundreds of 5kb plasmids. The point is the DNA, being a charged molecule is highly soluble.

DNA is a bit more complicated than some molecules due to it's length and composition variability.
In water.
According to Integrated DNA technologies:

DNA oligos can be resuspended to a near maximum concentration of 10mMolar; to achieve such a high concentration will require a lot of vortexing and it may take up to a day for the oligo to go into the solution.

DNA is a polar molecule and as far as I have experienced dissolves in water very readily. However there doesn't seem to be an exact quantifiable number for DNA solubility in water. If I correctly understand it, this paper claims that a 200,000Da-8,000,000Da oligonucleotide is soluble in water, however they never quantify this. An answer on a related question pointed out that high molecular weight DNA oligomers, like genomic DNA, is enhanced in solutions with dilute monovalent cations.
Cleaver & Boyer (1971) have some data on this, however it is somewhat outdated, and they were only using this solubility to demonstrate dialysis in water was capable of desalting the oligonucleotides.

Oligonucleotides larger than 5 bases in length remained within the dialysis
bag (Fig. 2) and losses of 10% and 40% occurred for tetra- and trinucleotides,
respectively.

There is a lot of work done on optimal temperature and pH for solubility of DNA so perhaps a more specific query might throw up some results.
In ethanol.
Ethanol precipitates at least 10–20 % of all classes of oligonucleotides. Oligonucleotides longer than 15–16 nucleotides are precipitated to about 65%.

Can you explain why organic solvents are likely to be needed? It seems that DNA is less soluble in isopropanol and ethanol (which are used in DNA extraction) than water, so making the solvent less polar might appear to have the opposite effect.

Hmm... Not sure. It could be to do with the fact that recovering DNA from water could be difficult. I have opened another question for that: http://biology.stackexchange.com/questions/35601/why-do-dna-solutions-contain-organic-solvents

@243 pointed me to a site with the answer you were looking for. I've edited it in.

The link you provide to genscript is for peptide sequences which can have  different solubility properties depending on amino acid composition. Peptides sequences can potentially be far more hydrophobic than DNA.

@InactionPotential You are absolutely correct - this was the wrong server entirely. It is removed and I will re-add it when I find the DNA solubility server.

@MarchHo Other organic compounds are often present because they are used in precipitating the DNA from other molecules in a solution, as a buffer, or for washing detergent from the solution. I think little data is available on DNA solubility because it dissolves very readily, and only the solubility of additional compounds are "important" as they, as you infer, decrease the solubility.

There is a bit of a problem using the IDT number of 10mMolar to think about the solubility of DNA. First off Oligos come single-stranded, so that is a different molecule from a plasmid. Secondly, there is a large amount of salt in the dehydrated microtube they send you. So your resuspension ends up being a buffered solution and not just pure water. Both of these will effect the saturation point.


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What is cross-immunoreactivity, and how does it impact vaccine development?
What I understand about cross-immunoreactivity is that the antibody induced by one specific antigen is also fairly effective against another antigen. How would this be used for vaccine development?
Moreover, cross-immunoreactivity is related to epitopes. And how is how is cross-immunoreactivity defined among epitopes? Are variants of a specific virus hypervariable region some kinds of epitopes? What does antigenic convergence have to do with cross-immunoreactivity? Any comments or directions to further references are greatly appreciated.

Welcome to Biology! I tried to edit your question to clarify. What do you mean with "And how is it defined among epitopes?" - How is what defined (i.e., where does 'it' refer to)?

how is cross-immunoreactivity defined among epitopes? thanks for your help.

Probably this article will help you somewhat. http://www.jimmunol.org/content/189/9/4602.full It is hard to find anything in the topic. Probably with further search... Btw this molecular mimicry is the cause of many autoimmune diseases. http://scholar.google.com/scholar?start=20&q=cross-immunoreactivity&hl=en&as_sdt=0,5&as_ylo=2011

I edited the question again a bit using your comment. Feel free to make further additions or clarifications! Thanks. +1

Cross-immunoreactivity is just as you stated where an antibody that is specific to one antigen may recognize another antigen. I don't think this term is widely used as I see cross-reactive or broadly reactive more often. With regards to vaccines against viruses, cross-reactive immune responses are very important to establish an immune response that is effective against varying strains. Using Influenza as an example, an antibody that recognizes the HA protein of the H3N2 strain and also recognizes the HA protein of the H1N1 strain would be cross-reactive. If we had a vaccine capable of this we would not have seasonal flu.
Epitopes are specific regions on the antigen that are recognized by T cells or antibodies. They are the specific area on the protein structure that is recognized. Thus, for a response to be cross-reactive that specific structure must be present on both antigens. Epitopes could be located in any region of the protein, viruses will often have a region that is highly antigenic and highly variable to trick the immune response into focusing on the highly variable region rather than the more conserved regions.
Antigenic convergence is related to the sequence space available to the virus. Since viruses have limited space  for genes the amount of possible variation is limited as a single point mutation can have a large effect on the virus. Taking this into account some predictions could be made on how the virus might evolve. If the virus is evolving in such a way that there might be conserved epitopes, those epitopes might be important for cross-reactivity. Here is a paper on antigenic convergence in Hepatitis C. http://www.nature.com/articles/srep00267
This is a paper focused on flu, but it outlines the ideas surrounding cross-reactive antibody responses.
http://www.ncbi.nlm.nih.gov/pubmed/26175732

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What is the difference between sequence, reads, and contigs of genetic material?
Can someone explain the differences between sequence, reads, and contigs of genetic material such as DNA, if possible with an example?
I am new to bioinformatics, and I have not found any conclusive answers for all these concepts on the web.

Welcome to Biology! Is this question with regard to a specific research area such as DNA?

yes, I think so. Regard to DNA, DNA sequence

Aren't contigs short for contiguous bp sequences ?

My understanding of those three words as follows:

sequence is a generic name describing order of biological letters (DNA/RNA or amino acids). Both contigs and reads are DNA/RNA or aa sequences
reads are just a short hand for sequenced reads. Usually sequenced reads refer to somewhat digital information obtained from the sequencing machine (for example Illumina MySeq) and stored in the fastq file with quality scores per base. Reads are usually short. However "short" changes rapidly. Right now MySeq produces reads anywhere between 50-150 base pairs long (bp). From a single run (it will really depends on the run) you can get millions of reads, where each read will be set bp size e.g 100bp long. All reads are stored in a single fastq file per replicate, where all reads in that file are usually of uniform size e.g all 5 million reads are 100bp long.

As a bioinformatician your first job is to identify where about those reads come from. Depending on the experimental goal and on what sort of sequencing you were doing e.g DNA-seq or RNA-seq you may or may not encounter contigs.

contigs are simply reads that have been assembled together. For example if you are doing de novo transcriptomics. Then you would:

purify your transcript from a tissue and send it off for sequencing
get your fastq files with sequenced reads, that are all short reads
(e.g 100 bp)
assemble those 100bp reads into a longer contig that hopefully will resemble your individual transcript

@vvilp no probs. as an aside here is a cool pdf I found somewhere on internet http://helix.biology.mcmaster.ca/3S03.pdf. it might help you with your bioinformatics learning

I have taken a look at PDF. Nice tutorial! Thank you

@vvilp I'm glad it helped. by the way here is the link http://biology.stackexchange.com/questions/31546/book-source-for-learning-bioinformatics-focused-on-genomics where I found that pdf file. There might be some more useful info for your bioinfo

I'm going to say the same thing as @Serine but in a slightly different context. Let's take an example where you want to compare smoking persons against non-smokers.
In this context, you'd want to take a DNA sequence of smoking persons.  However, due to technology limitation you won't get a single DNA sequence from the sequencing machine. You'll get millions of short overlapping DNA sequences known as reads.
We need an assembler to "map" the reads and compare them with a reference genome. In this example, the reference genome could have been the human HG38.
The assembler would need to merge the overlapping-reads into a set of non-overalapping regions, known as contigs.

Usual aligners do not assemble reads.

Sorry, I meant mapping.

Thank you Student T. Now I know the mainly difference between reads and contigs

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What are the mechanistics of stinging nettles?
There is a lot of research on why nettle extracts causes skin irritation and a stinging sensation. However, I cannot find information on how the extract is injected in human skin. Similarly, I haven't been able to find information on  how the pressure is built up in the trichome, nor how the silica tip is inserted in the skin.
Suggestions for articles or books on this topic are welcomed.

Does this answer your question, or is it too unspecific: Wikipedia: Stinging plant?

sorry..but it's too unspecific....but thnx...neways...

There found formic acid,  some neurotransmitters which include Acetylcholine.

The stinging hairs (trichomes) of the common North American nettle (Urtica dioica) are sharp, pointed cells. These nucleated cells are embedded in a base of smaller epidermal cells. The shaft of the trichome is composed of silica. Upon touch, the tip breaks off, leaving a sharp tip similar to a hypodermic needle. The hollow trichome penetrates the skin, and toxin from the base is injected into the skin tissue. The stinging toxin includes a mixture of histamine, acetylcholine and 5-hydroxytryptamine (Online Textbook of Natural History).

Left: schematic of a stinging cell, or trichome of a nettle. Right: trichomes on the stem of Hesperocnide tenella. Source: Online Textbook of Natural History
I couldn't find any info on trichome pressure. It may be that the toxins are released passively. Otherwise, high concentrations of dissolved matter may attract water in the base, increasing the pressure (much like turgor present in many plant cells).

thanx...but this I'm afraid is really a general statement....are there any scientifc studies or experiment demonstrating this??...upvoting the ans...because of the pic & for your effort...but the answer is ...I am sorry to say...incomplete...

@souvikbhattacharya - The information comes from an online Textbook, but I haven't found specific primary research on it. My answer is the best I could do.

no no....I understand....there really is no study from this mechanistic angle....I was just double checking...neway you provided a crucial detail....so thanks again for that...


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Why aren't genetic triplets roughly evenly found in DNA?
Sorry, the page I linked to is huge and you'll need to do a text search for "CG" to find the part I'm talking about.
I found a graph on this page (http://www.oftenpaper.net/sierpinski.htm) showing that the eight DNA sequences including CG, i.e. four *CG and four CG* sequences are much rarer than the others in a human X chromosome. I realise that this is only for one sample of a human X chromosome (not even all human chromosomes) but I was wondering why this is? Obviously, if *CG is rare CG* will be too.
From my limited understanding the equivalent RNA sequences would be *GC (redundant codes for four amino acids) and GC* (the only codes that produce Alanine). According to the Wikipedia page on Alanine it accounts for 7.8% of genetic amino acids, well over the average.
Is this representative across all DNA? Across all human DNA? What does DNA have against coding CG sequences, even if only in the X chromosome? Do other chromosomes have an abundance of CG sequences but are rare in others?

http://en.m.wikipedia.org/wiki/CpG_site

Or https://en.wikipedia.org/wiki/CpG_site for desktop computers.

No, it's not specific to the X chromosome. It's a general trend. CG sequences are underrepresented in mammalian genomes. In fact, the very nucleotides C and G are underrepresented. Instead of the ~25% you'd expect by chance, the real numbers for the human genome are (calculated on the hg19 version of the UCSC human genome):
N: 234350281 = 7.5702%   <-- N means unknown
A: 844868045 = 27.2917%
C: 585017944 = 18.8978%
T: 846097277 = 27.3314%
G: 585360436 = 18.9089%

If we break this down by chromosome (chrM is the mitochondrial genome which should probably be ignored here), we get:
chrM    A:5113 (30.9%)  C:5192 (31.3%)  T:4086 (24.7%)  G:2180 (13.2%)  N:0 (0%)
chr1    A:65570891 (29.1%)  C:47024412 (20.9%)  T:65668756 (29.1%)  G:47016562 (20.9%)  N:0 (0%)
chr2    A:71102632 (29.2%)  C:47915465 (19.7%)  T:71239379 (29.3%)  G:47947042 (19.7%)  N:4994855 (2.1%)
chr3    A:58713343 (29.6%)  C:38653197 (19.5%)  T:58760485 (29.7%)  G:38670110 (19.5%)  N:3225295 (1.6%)
chr4    A:57932980 (30.9%)  C:35885806 (19.1%)  T:57952068 (30.9%)  G:35890822 (19.1%)  N:0 (0%)
chr5    A:53672554 (30.2%)  C:35089383 (19.7%)  T:53804137 (30.3%)  G:35129186 (19.8%)  N:0 (0%)
chr6    A:50554433 (29.5%)  C:33143287 (19.4%)  T:50533923 (29.5%)  G:33163423 (19.4%)  N:3720001 (2.2%)
chr7    A:45997757 (29.6%)  C:31671670 (20.4%)  T:46047257 (29.6%)  G:31636979 (20.4%)  N:0 (0%)
chr8    A:42767293 (29.9%)  C:28703983 (20.1%)  T:42715025 (29.9%)  G:28702621 (20.1%)  N:0 (0%)
chr9    A:35260078 (29.3%)  C:24826212 (20.7%)  T:35243882 (29.3%)  G:24813259 (20.7%)  N:0 (0%)
chr10   A:38330752 (28.3%)  C:27308648 (20.1%)  T:38376915 (28.3%)  G:27298423 (20.1%)  N:4220009 (3.1%)
chr11   A:38307244 (29.2%)  C:27236798 (20.8%)  T:38317436 (29.2%)  G:27268038 (20.8%)  N:0 (0%)
chr12   A:38604831 (28.8%)  C:26634995 (19.9%)  T:38624517 (28.9%)  G:26617050 (19.9%)  N:3370502 (2.5%)
chr13   A:29336945 (30.7%)  C:18412698 (19.3%)  T:29425459 (30.8%)  G:18414776 (19.3%)  N:0 (0%)
chr14   A:25992966 (29.4%)  C:18027132 (20.4%)  T:26197495 (29.7%)  G:18071947 (20.5%)  N:0 (0%)
chr15   A:23620876 (23%)    C:17247582 (16.8%)  T:23597921 (23%)    G:17228387 (16.8%)  N:20836626 (20.3%)
chr16   A:21724083 (27.5%)  C:17630040 (22.3%)  T:21828642 (27.7%)  G:17701988 (22.4%)  N:0 (0%)
chr17   A:21159933 (27.2%)  C:17727956 (22.8%)  T:21206981 (27.3%)  G:17700340 (22.8%)  N:0 (0%)
chr18   A:22465380 (28.8%)  C:14838685 (19%)    T:22489493 (28.8%)  G:14863671 (19%)    N:3420019 (4.4%)
chr19   A:14390632 (25.8%)  C:13478255 (24.2%)  T:14428951 (25.9%)  G:13511145 (24.2%)  N:0 (0%)
chr20   A:16523053 (27.8%)  C:13107828 (22%)    T:16725227 (28.1%)  G:13149412 (22.1%)  N:0 (0%)
chr21   A:10422924 (21.7%)  C:7160212 (14.9%)   T:10348785 (21.5%)  G:7174721 (14.9%)   N:13023253 (27.1%)
chr22   A:9094775 (17.7%)   C:8375984 (16.3%)   T:9054551 (17.6%)   G:8369235 (16.3%)   N:16410021 (32%)
chrX    A:45648952 (30.2%)  C:29813353 (19.7%)  T:45772424 (30.3%)  G:29865831 (19.8%)  N:0 (0%)
chrY    A:7667625 (29.9%)   C:5099171 (19.9%)   T:7733482 (30.1%)   G:5153288 (20.1%)   N:0 (0%)

As you can see, C and G are consistently less frequent than A and T across all chromosomes. The exception is the mitochondrial genome but that is not the genome of a vertebrate. So, overall, A and T occur almost 10% more often than C and G. But why does this happen?
As far as I know, the reasons are not entirely clear. Some factors that affect this, however, are:

The C of the CG dinucleotides can be methytlated. Methylation is a chemical modification of the nucleotide and plays an important role in the regulation of gene expression. The regulatory sequences that control the way that genes are expressed (promoters), are often rich in CG sequences (these localized overrepresentations of CG are called CpG islands) which enable the control of the associated gene's expression by the mechanism of methylation (which can "turn off" a gene). Not the kind of thing you want to have occurring randomly in your genes.
Methylated Cytosine (C) is often converted to Thymine (T):

This would result in a gradual loss of C in favor of T. This theory had long been considered to be the main reason why CpG is so rare in mammalian genomes, but see the next point.
I found a study from 2004 [1] that shows that, among other things, there is no correlation between CpG and TpA shortages, suggesting that the deamination of Cytosine to Thymine is not enough to explain the phenomenon.

I should also point out that the fact that Alanine represents  7.8% of all aminoacids in proteins does not say anything at all about the frequency with which its codons appear in the genome at large. Only ~2% of the human genome (genes are ~5% and exons, those parts of genes that are translated into proteins, only ~2%) actually codes for proteins so it is only in that 2% where you will see this overrepresentation (if one exists) of Alanine.
In conclusion, yes, the CpG shortage is a general feature of the human genome and not of chromosome X, but the precise reasons for this are not yet entirely clear (as far as I know, anyway).
References

Jabbari K., and Bernardi G., Gene 333:143-149, 2004


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Programmatic way to differentiate homodimers from heterodimers?
For pdb files is there a simple programmatic way to determine if the file is made up of homodimers or heterodimers.
I have many files so an online tool or some psuedocode/scripts would help more than manually assessing each one.

Could you provide us with an example? Preferably one that is a homodimer and one that is a heterodimer.

I don't think this post deserves closing. I have tried to tidy up the question so its easier to understand. Correct me if I am wrong, but is OP asking if there is a programatic way to check if in a dimer both monomers are either the same or different?

Have you tried simply checking the sequences? same sequences for proteins = homodimer... I have distant memories of pdb fileformat, but as far as I remember individual protein chains are stored separately, but I may be dead wrong on this one.

How comfortable are you with scripting?

There was a recent discussion on this sort of question in meta. What you're asking here is not actually about biology, but about programming. Furthermore, as it stands this question could be interpreted as a "give me the codes" question. What have you tried so far?

I'd just compare the amino acid sequences of the individual protein chains. With some leeway for residues not observed in the density, ie only require 90 or 95% sequence identity, or ignore gaps.
This will not tell you anything about whether the dimer (if you observe several molecules in the asymmetric unit) is actually real. For that, you'd need to do an experiment, literature research or see whether software like the PISA-server could give you a clue.

In case you want to write your own subroutine,
1. Scan the whole .pdb file for number of chains present, if multiple then proceed.
2. Create index_counter for each amino acids of a single chain.
3. Now, For SINGLE chain. While you scan for each amino acid perform a i=i+1 operation for that specific amino-acid_counter.
4. Compare the amino-acid_counter between/among the chains.
5. Exact match = homomer or non-exact match = heteromer.
Hope you get the logic.

I think you will run into trouble with real live PDB-files here - often there are gaps in the sequence because they were not observed in the electron density, or the numbering is inconsistent. I would suggest to rather extract the sequence from the PDB-file and align them (eg using fasta).

@Gerhard yeah! but that depends on how good is the resolution and R-free value of your .pdb is. When you are talking about analyzing .pdb you are supposed to take a higher resolution <1.6A. This covers all the atoms vwd radii(except H), no atom-missing issue is possible. Literature says.

A) if you limit yourself to anything better than 1.6A, there are not many structures left, and (according to Murphy) most likely not the proteins you are interested in. B) whether you have gaps and missing parts in a crystallised molecule is not necessarily down to resolution and Rfree (although there is a correlation). Some parts of a molecule - in particular loops - are simply more flexible and hence disordered in the crystal - no resolution in the world will make these appear.  C) Could you post the reference you mentioned - quite interesting as a crystallographer.

It's a general methodology as reported in every data-mining literature, that's why I emphasized on resolution. And as per my experience, I found that if you have a higher resolution, then random coils(most of the time) shows fluctuating occupancy, but still be present. Although you are right, some gaps stays sometimes(specially in multidomains proteins). However the subroutine can be configured to eliminate any structures with breaks and analyze further. But to reach publication quality I think high-res is always needed. -  it's always nice to see a crystallographer around.


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Doing a medical study on yourself?
What research guidelines is a person legally mandated to follow if they want to do medical experimentation on themselves?
There is a large amount of variation in the types of medical experiments so I wanted to ask people focusing on the change in practice as a function of the type of medical experimentation you do in the biological sciences (e.g., drugs, blood samples, tissue regeneration, testing medical equipment), including invasive and non-invasive studies. This question seemed almost equally suited to academia and biology SE, but given the focus on different types of biological experiments I felt this might be the more suitable site.
I am most interested on research practices in the United States, and anything touching FDA regulations would be great.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3298919/ seems to be a very relevant paper.

I can't cite any sources, but self experimentation is far less likely to be regulated than trials on other people. We had a seminar speaker who was giving high doses of some molecule his lab was working on to himself and looking for side effects. Unfortunately I can't remember his name or his molecule. He did say that the university committee on human subjects didn't care if it was just himself.

And you are not going to be a able to statistically prove any thing with just one individual. There will be inherent bias in the experimental design, and ultimately worthless imo.

Barry Marshall had drunk a solution of H.pylori to "prove" that it causes ulcer !

@RoverEye A self study could still be very useful in the case of a type of study that would be providing a massive stream of data even if conducted on one individual.

This is perhaps too broad because there are a huge number of experiments that one could do to themselves, each with its own legal minefield (e.g. taking drugs), and as already mentioned it would be a massively flawed study and wouldn't contribute a great deal to the scientific community

@biogirl sure, I remember. But that was more of luck and the experiment itself (he postulated) wont end up killing him. I personally feel that it is more of a statement rather than an experiment (yes, I know its published in a peer reviewed journal, but still). You cant do that, with the way science has grown since then.

There's also the guy that did the knuckle cracking on one hand to him self for years...

@rover eye I agree. Doing experiment on one individual does not prove anything. But it amuses me to see to what length scientists can go to prove themselves :)

One of the cornerstones of research ethics worldwide is the Nuremberg code, which was formulated shortly after the Second World War and set off by the cruelties performed by the Nazi Doctors. The Declaration of Helsinki, which is currently widely used as the guiding principle of research ethics, was directly inspired by the Nuremberg code.
Interestingly, article 5 in the Nuremberg code reads, and I quote:

No experiment should be conducted where there is an a priori reason to believe that death or disabling injury will occur; except, perhaps, in those experiments where the experimental physicians also serve as subjects.

Basically what this tells you is that when you are a physician, you are not only ethically allowed to experiment on yourself, even when you can reasonably expect death may follow, you are even allowed to put others at that risk(!) Admittedly, it does not specifically talk about non-physicians. Nonetheless, with regard to your question, this Nuremberg article implies that self-experimentation is allowed, regardless the risks.
Annas (2010), rightfully argues that, even where risks are minimal, prior ethics committee review of research should always be sought, if only to confirm the reasonableness of the risk assessment and regardless whether investigators are subjects.
The problem then becomes whether self-experimentation (an experiment done by the investigator on himself or herself only) must be reviewed and approved by an ethics committee before it is conducted. Here Annas (2010) concludes that:

[...] When an investigator proposes to experiment only on him or herself, that activity is not properly categorized as research at all, but as self indulgence (or, some may say, self abuse). Trivial interventions masquerading as research studies are primarily a source of amusement.

Although I do not necessarily share the concluding accusations against self-experimentation, I do share her view that self-experimentation should not be regarded as proper scientific research, and therefore should not be subject to ethical review.
Reference
Annas, BMJ (2010); 341: c7103


text:
Getting read size less then specified in parameter file Flux Simulation
I have tried to use flux simulation tool to generate simulated RNA-seq data.
I gave the following parameter file to flux-simulation shell script
## File locations

REF_FILE_NAME   cElegansAnnotation.gtf
GEN_DIR         chromFa

## Library preparation
# Expression
NB_MOLECULES    5000000
TSS_MEAN    50
POLYA_SCALE     100
POLYA_SHAPE     1.5

# Fragmentation
FRAG_SUBSTRATE  RNA
FRAG_METHOD UR
FRAG_UR_ETA     350

# Reverse Transcription
RTRANSCRIPTION  YES
RT_MOTIF    default

# Amplification
PCR_DISTRIBUTION default
GC_MEAN      NaN
PCR_PROBABILITY  0.05

# Size Filtering
FILTERING   NO

## Sequencing
READ_NUMBER 1000000
READ_LENGTH 100
PAIRED_END  YES

# create a fastq file
FASTA           YES

According to this parameter, flux-simulation should have given reads with length 100. However when I look at the output, I have seen that reads with less then length of 100 are also included in my  fasta file:
>chrI:47472-49416W:Y48G1C.12:3:651:351:594:A/1
CGTCGAAATTAGTGATATTTTTATCGGGAATCGGTCCGTGTGGTTCTCCGGTGAATATTCGATTCGTTGTGGAGACACGAGATCGCTGGGGTCCAAGGAC
>chrI:47472-49416W:Y48G1C.12:4:651:394:467:S/1
TACGCGACAAAAATGGGAAACCGAATCGCGTTTTTTGGCTTCAAGTACAAGTTATTCAGAATCATCAAAATGGG
>chrI:47472-49416W:Y48G1C.12:4:651:394:467:A/2
CCCATTTTGATGATTCTGAATAACTTGTACTTGAAGCCAAAAAACGCGATTCGGTTTCCCATTTTTGTCGCGTA
>chrI:47472-49416W:Y48G1C.12:5:651:126:142:S/2
AGTTGTAAAAGCGGATT

So, is there anyone how could I fix it?

I think it gives a distribution of read lengths. Not all reads would be 100nt. Even in actual experiments you observe that. Can you add a graph of read length distribution. You can use histogram in matlab, python or R.

@WYSIWYG thanks for reply, I'll add it tonight, actually, I could handle with different size of reads but they have to be longer than a specific length. Could it be possible?

You can remove the small reads before mapping. fastx_toolkit has that option or otherwise just do this: awk 'NR%2==1{h=$0} (NR%2==2) && (length($0)>x){print h"\n"$0}' fastafile.fa


text:
The dominance variance on a single locus
I was reading the book "Genetics and Analysis of Quantitative Traits", by Lynch and Walsh. I how the covariance between two individuals with IBD $\Theta$ gets divided into just the additive variance and dominance variance component, even in the simple $1$ locus case.
Here my understanding of the modelling (for the simple one allele case):
Given a genotypic value $G_{i,j}$ of mean $0$, $i,j \in \{0,1\}$ we find numbers $\alpha_0$ and $\alpha_1$ minimising the least squares of the following form $\mathbb{E}(G_{i,j}-\alpha_i-\alpha_j)^2$, where the expectation is over the population.
We next define the error terms in each case as $\delta_{i,j}=G_{i,j}-\alpha_i-\alpha_j$. From the properties, viewed as functions of the population $\alpha_i$ is independent of $\delta_{i,j}$, and both have
mean $0$.
The claim made in the book is that given two individuals, with IBD $\Theta$ and probability that the genotype is equal $\Delta$, the covariance of the genotypes $G_{i,j}$ and $G_{k,l}$ is given by,
$$\text{cov}(G_{i,j},G_{k,l}) = 2\Theta \sigma_A^2 +\Delta \sigma_D^2,$$
where $\sigma_A^2= \text{Var}(\alpha_i)$, and $\sigma_D^2 = \text{Var}(\delta_{i,j})$.
Expanding the LHS of the expression, showing that $\mathbb{E}[(\alpha_i +\alpha_j)(\alpha_k+\alpha_l)] =\Theta \sigma_A^2$ is quite easy. It also seems to follow from the  that the the terms $\mathbb{E}[(\alpha_i +\alpha_j)\delta_{k,l}]=0$ from independence of errors from the $\alpha$.
On analysing $\mathbb{E}[\delta_{i,j}\delta_{k,l}]$, we see that if both genotypes are equal, which occurs with probability $\Delta$, then this reduces to $\sigma_D^2$. This gives us a term $\Theta \sigma_D^2$. Further, if both $i,j$ and $k,l$ are not IBD then the covariance is $0$. However when one of the two alleles are IBD, then it is not clear to me that this the covariance will still be $0$.
The book seems to claim that unless both alleles are IBD,  $\delta_{i,j}$ and $\delta_{k,l}$ are independent. I do not see why this is the case. Am I missing anything here? I'd appreciate any help wrt this.

@rg255 : It is chapter 7 on page 143-144. They handle the multiple allele case, but I was simplifying it to the single allele case here.

It looks like I could solve the question. My understanding is as follows.
Let $(X_1,Y_1)$, $(X_2,Y_2)$ (corresponds to $i,j$ and $k,l$ in the question) be the genotypes of two individuals
 at some location. We assume that neither individual
 is in-bred. In this case define,
 \begin{align*}
  \Delta_7&= \text{Pr}(\text{Both alleles $\{X_1,Y_1\}$ and $\{X_2, Y_2\}$ are IBD}),\\
  \Delta_8&= \text{Pr}(\text{Exactly one allele pair of the four pairs is  IBD}),\\
  \Delta_9&= \text{Pr}(\text{ No IBD between the two individuals}).
 \end{align*}
 $\Delta_7$, $\Delta_8$ and $\Delta_9$ are calculated from the pedigrees.
 For example, for non-twin siblings, $\Delta_7 = \frac{1}{4}$, $\Delta_8=\frac{1}{2}$,
 $\Delta_9 =\frac{1}{4}$.
We note that the IBD coefficient (also called kinship coefficient) $\Theta$ is
 \begin{align*}
  \Theta = \frac{1}{2} \Delta_7 + \frac{1}{4} \Delta_8.
 \end{align*}
 Also the fraternity coefficient, $\Delta =\Delta_7$.
Thus we have that the covariance between the genotypic
 value of two individuals is given by
 \begin{align*}
  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)] =& \Delta_7 \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{both IBD}] + \\
  &\Delta_8 \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{one IBD}] + \Delta_9  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{no IBD}].
 \end{align*}
Further note that,
 \begin{align*}
  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{both IBD}] &= \mathbb{E}[G^2(X_1,Y_1)],\\
  &= \sigma_A^2 +\sigma_D^2.
 \end{align*}
\begin{align*}
  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{no IBD}] &= \mathbb{E}[G(X_1,Y_1)] \mathbb{E}[G(X_2,Y_2)],\\
  &=0.
 \end{align*}
\begin{align*}
  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{one IBD}] &= \mathbb{E}[(\alpha(X)+\alpha(Y_1)+\delta(X,Y_1))(\alpha(X)+\alpha(Y_2)+\delta(X,Y_2))],\\
  &=\mathbb{E}[\alpha^2(X)] + 2 \mathbb{E}(\alpha(X) \delta(X,Y_1)) + \mathbb{E} [\delta(X,Y_1)\delta(X,Y_2)],\\
  &= \frac{1}{2} \sigma_A^2 + 2 \mathbb{E} [ \alpha(X) \mathbb{E}[\delta(X,Y_1) | X] ] +  \mathbb{E} [\mathbb{E}[\delta(X,Y_1)|X]\mathbb{E}[\delta(X,Y_2)|X]],\\
  &= \frac{1}{2} \sigma_A^2.
 \end{align*}
Thus we have that,
 \begin{align*}
  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)] =& \left(\frac{1}{2}\Delta_7 + \frac{1}{4}\Delta_8\right) 2 \sigma_A^2 + \Delta_7 \sigma_D^2,\\
  &= 2\Theta \sigma_A^2 + \Delta \sigma_D^2,
 \end{align*}
 which is as claimed.


text:
If the haploid prothallium of a fern fertilizes itself into a diploid sporophyte, does this make all ferns clones?
From what I understand in the alternation of generations in ferns, mature spores germinate into a haploid prothallium. But how does this gametophyte produce recombinant gametes if it itself develops mitotically from a haploid spore? And if the gametophyte produces its own (haploid?) eggs and sperm, how does it ultimately produce a diploid sporophyte with the same number of chromosomes as its parent? If the haploid prothallium fertilizes itself, that means it possesses two identical copies of its parent's chromosomes, which themselves are identical - there is no outcrossing between plants. So are all ferns genetic clones? Why even bother with meiosis if you don't have a recombinant mixing of alleles? Or do I have this totally confused?

No, it would not be accurate to label them clones, and the organism still goes through sexual reproduction even if they are selfed. Selfed offspring would get two copies of the "same" chromosome (when selfed within the same prothallus), when the parent might have two chromosomes of different origins, and there will also be recombination during meiosis (during spore production in the sporangia), which will alter the chromosomes. And even if all selfed offspring from the same prothallus will carry that same chromosomes, different prothalli from the same parent will carry different chromosomes, which means that all offspring will not be identical. So to label selfed ferns as clones wouldn't be accurate, since the offspring wouldn't be genetically identical to their parents and offspring from different prothalli would also not be genetically identical. The situation is similar to e.g. monoecious plants that lack self-incompatibility (especially those pollinated by wind), where selfing will be common. The difference in ferns is that all gametes on the same prothallus will carry the same chromosomes.
Also note that some ferns have mechanisms to avoid self-fertilization, and that many species have a mixed mating strategy that allow both selfing and outcrossing, usually with higher fitness in outcrossed individuals.

In ferns (and seed plants) the dominant, largest stage of life is the diploid sporophyte. Within the sporophyte, meiosis occurs producing haploid spores. These spores are dispersed and grow into the small haploid gametophyte, AKA the prothallium. The gametophyte produces haploid gametes - both egg and sperm coming from the same individual, usually. The sperm fertilizes the egg forming a diploid zygote, which grows into an adult sporophyte.
This image should help. Let me know if anything is unclear

I suppose what's confusing me is if the prothallium is if fertilizing itself, then it must have two identical copies of the its parent's chromosomes, which themselves are identical. So is there is no recombinant mixing of alleles? Are all ferns essentially clones of one another?

@BRZA The resulting zygote is not a clone. First off, the prothallium is not necessarily always fertilizing itself: sperm from one prothallium can fertilize an egg from a nearby prothallium (if the weather is wet to allow the sperm to be mobile). So, the prothallium does not have two identical copies of the parent's chromosomes. The prothallium has one recombinant copy of one of the sporophyte's chromosomes: by the time the prothallium has formed, meiosis and thus crossing over have already occurred. Even if the resulting gametes from the same prothallium fertilized each other [cont]

[cont] the resulting offspring would not be genetically identical to the parent due to the crossing over that has already occurred

It has already been mentioned that different prothalli have a different mix of chromosomes, and that in some (yet not all) ferns a single prothallus doesn't fertilize itself, e.g. because male and female gametes aren't produced at the same time.
I want to add that one prothallium usually only produces one sporophyte.
So even in cases with self fertilisation, you only get clones if the gametophyte produces several sporophytes.

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


text:
Do High Iron Stores (but within the healthy range) Make Sun Exposure Damage Worse?
Ultraviolet damage from sun exposure is related to the creation of free radicals. Iron is often involved in exacerbating damage by free radicals.
Having lower iron stores is associated with reduced risk of diabetes. Could having lower iron stores reduce UV-related damage from sun exposure?
=========================================================================
I add some references after being asked in the comments:
On iron and free radicals: Iron, Free Radicals, and Oxidative Injury
UV-light and free radicals: Ultraviolet light-induced free radical formation in skin
About high ferritin making diabetes worse:
"Compared with those in the lowest quartile, subjects with diabetes in the highest ferritin quartile were 55% (P = 0.029) more likely to have microalbuminuria."
Source
Elevated serum ferritin levels predict new-onset type 2 diabetes

Can you add some references for your claims?

Chris, I added some references in the question.

Your references seem to have nothing to do with UV related damage.


text:
What does the term "relay competent" mean?
I was reading the article of Dallon & Othmer (2010) which deals with cell aggregation in Dictyostelium discoideum. In the introduction of the paper it is said that cells becomes "relay competent". I googled for the term but could not find a good explanation for it.

After a period of starvation they become chemotactically sensitive to cyclic adenosine 3 , 5- monophosphate (cAMP), as well as relay competent.

Can someone help me understand this term?

If you read the lines immediately following your quoted line (on p.391, left column, last paragraph in the linked article) it becomes clear what relay competent means (and I quote):

As a result, the cells sense and move toward a source of cAMP, and they relay the signal as well by secreting cAMP. [..] After about 8 h of starvation randomly located cells, called pacemakers, begin to emit cAMP periodically (Raman et al. 1976), the chemotactically competent cells move toward these pacemakers, and eventually the entire population forms a mound-shaped aggregate of up to 105 cells.

In other words, starvation makes cells move toward cAMP by chemotaxis, and  makes them secrete cAMP as well, which factually relays the cAMP signal back to other cells that are also attracted to cAMP due to starvation.


text:
Evolutionary advantages of wet nose of cats and dogs?
Everyone knows that some animals, at least cats and dogs, keep their noses wet and cool. But why did they evolve it? What evolutionary advantages does it provide? Smell-sensing cells need cooling for precision, may be? Or the liquid dissolves smellful gases into itself, simplifying analysis this way? Or may be it just simplifies cleaning the nose from the previous sniffing act?

there's a lot of information to be found with a quick google search - you're risking having the question closed due to poor research effort.

The OP is asking for an accurate answer, although his research seems little but he just put some intuitions. I don't think this would be down voted.

Why did it evolve ?

Mammals with rhinaria tend to have more acute olfaction, and the loss of the rhinarium in the haplorrhine primates is related to their decreased reliance on olfaction, being associated with other derived characteristics such as a reduced number of turbinates.
The rhinarium is very useful to animals with good sense of smell because it acts as a wind direction detector. The cold receptors in the skin respond to the place where evaporation is the highest. Thus the detection of a particular smell is associated with the direction it came from.
  The rhinarium is adapted for different purposes in different mammals according to ecological niche.
In aquatic mammals, development of lobes next to the nostrils allow them to be closed for diving. In mammals that root, the rhinarium often develops into a hard pad, with the nostrils off to the side. In the elephants it has become a tactile organ. In the walrus, it is covered with stiff bristles to protect it during foraging for shellfish. In many animals the form and purpose of the rhinarium remains to be elucidated.

Essentially it is the case of having a better sense of smell provided by the extended surface area, which has evolved to fit whatever the organism in question needs. I'll update this when I find this in a few more papers.
I took this from the wiki:
http://en.wikipedia.org/wiki/Rhinarium
How does it work ?

A model of the canine nasal airway, developed from a 3-D
  reconstruction of high-resolution magnetic resonance imaging (MRI)
  scans, was used to study the aerodynamics of canine olfaction.
  Simulation results reveal that a unique olfactory airflow pattern
  exists within the canine nasal cavity during sniffing that is critical
  for efficient olfaction.
Calculations show that this novel olfactory airflow pattern provides a
  crucial residence time for odorant absorption in the sensory region
  and promotes spatiotemporal fractionation of odorant mixtures along
  the olfactory epithelium.
The canine nose functions similar to a chromatograph that imposes
  odorant-specific deposition patterns upon the thin mucus layer
  covering the nasal cavity....The results show that deposition patterns
  are primarily influenced by the intricate olfactory flowfield and the
  odorant solubility in the mucus layer.
Highly-soluble odorants are quickly absorbed near the entrance to the
  olfactory region, and thus do not reach the periphery with significant
  concentrations. In contrast, insoluble odorants are deposited more
  evenly and may even exit the olfactory region without being completely
  absorbed. Predicted odorant deposition patterns correspond with the
  anatomical organization of olfactory receptors known to occur in
  keen-scented (macrosmatic) mammals, providing a mechanism that helps
  explain the excellent olfactory acuity of the dog.

In short the mucus on a dog's nose 'pre-sorts' smells by trapping the passage of some odour particles more than others along the nose, with different types of molecules being picked up at different "depths" in the nasal cavity.
You can read about it here:
Craven, Brent, Gary Settles, and Eric Paterson. "The Aerodynamics and Transport Phenomena of Canine Olfaction." APS Division of Fluid Dynamics Meeting Abstracts. Vol. 1. 2008.
Lawson, Michael, et al. "Odorant Transport and Deposition in the Canine Nasal Airways." APS Division of Fluid Dynamics Meeting Abstracts. Vol. 1. 2009.
Craven, Brent A. A fundamental study of the anatomy, aerodynamics, and transport phenomena of canine olfaction. ProQuest, 2008.

A downvote because it is a wiki copy-paste. You are perhaps rightfully making a lmgtfy point here, but you could at least add a personal concluding sentence that directly addresses the question. Please ping me as I am happy to retract downvote and/or upvote once edited

@AliceD sorted.

Great! Thanks. Now I could simply skip the wiki stuff and read your answer :)


text:
Can DNA test of my grandparent's brother reveal my heritage from that branch of the family?
I'm thinking about doing that DNA test on all my grandparents to know where their genes come from. They are getting very old and I don't want to let the opportunity pass to gather more knowledge about my heritage, something I find very interesting.
One of my grandparents died long ago, but he still has a brother and I was wondering if DNA testing him would reveal relevant information about my heritage from that branch of my family tree. Obviously all of his genes come from family of mine(his parents) but not all of his genes are the same as my grandparent's. Just how should I look at his tests to find information about my heritage?
By the way can I really trust these sort of tests?

if he is the brother of your grandparent then his DNA has some degree of probability that it is identical by descent to that of your grandparent - siblings on average share half of their DNA, though theoretically could share 0-100% of their DNA. Given how broad this is and that it borders on product/service recommendation, while seeing very little in the way of a proper question about biology, I am downvoting

I can take the recommendation part off even the name of the company, but my question is pure biology

I disagree that this question is too broad. It is asking for a very specific case of the genetic tests which need to be carried out to determine the relationship of less closely related relatives.

@rg255 you should develop a little and post your comment as an answer.

As Rayoub's answer points, you are likely to share a random part of your genes with your grandparent's brother, and therefore analysing his DNA won't tell you where all your genes come from, since he has some genes you don't have and you have some genes he doesn't have.
However, I understand that you aren't that interested on your particular genes, but on what genetics can tell you on the history of your family - that is, to shed light on who were your ancestors and where they came from. Then, if your grandparent's brother was your grandparent's full brother, his ancestors are your grandparent's ancestors and therefore analysing his DNA can be as useful as analysing your grandparent's DNA.
In addition, since your grandparent and his brother doesn't share all the same DNA (likely just about 50% for full brothers) and each of them just have a 50% of each of their grandparent's DNA, if you could analyse DNA from both a grandparent and one or more siblings, you would be able to gather more information. In fact, you would be getting closer to get the same information you could have got from analysing your grandgrandparents'DNA.

You should be able to learn some things about your family's heritage from your great uncle's DNA, but, if you're looking to find out about where they lived previously, a stable isotope test might be useful. However that would only he able to tell you where that individual (and siblings who were with them) lived, but nothing farther back. I know your question is 4 years old at this point, but maybe this is something helpful.

Wouldn't you need bone or tooth samples? That sounds rather invasive for the living.

Welcome to Biology.SE. We're looking for long answers that provide explanation, context, and include references to reliable sources. Don't just give a short answer; explain why your answer is right with appropriate citations. Answers that don't include explanations may be removed. Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly.
@JiminyCricket. — Ridiculous! I'm sure he wont mind "donating" an otolith ...


text:
What is the point at which abiogenesis is complete and evolution begins?
Is the minimum criterion for life a single cell?  It seems that self-replicating RNA is not enough, but I don't know.
What would be the most basic cell that could fit this criterion and what cells today would be most similar?

Even though it is short, this question is really broad. To answer this you need to get into the definition of life (e.g. the line between "protocells" and cells) and minimum definitions of a biological cell. Also note that you can have evolution in the absence of life, see e.g. Evolutionary computation - all that is needed is variation, selection, heritability and reproduction.

I agree with @fileunderwater. Perhaps the following questions may help you to specify this question into something that can be realistically answered: http://biology.stackexchange.com/questions/22008/simplest-biological-organism/22009#22009 and http://biology.stackexchange.com/questions/1663/are-cells-really-the-basic-unit-of-all-life/1666#1666

@AliceD I agree that it should be refined, and parts of the question is probably a close duplicate to the first Q you linked. For the second question, is also unclear whether the comparison should be against the origin of life (~LUCA) or basic cells that can live under current environmental conditions - the external conditions have changed quite a bit.

Related: Can scientists create totally synthetic life?, How did the first self replicating organism come into existence?, and probably others under the [tag:abiogenesis] tag.

Thanks for the comments everyone!  I didn't realize the line was so fuzzy.  I guess I never would have thought of self-replicating RNA as life but it seems that are people that define it that way.

Why is this too broad? - there is a process called abiogenesis and there is a process called evolution.  I assumed the line is clear, perhaps the answer is that's it fuzzy as the answer below discussed and I commented. It could be that the answer is relative based on the definition of "life", but that itself could be the answer.

Yehosef, one problem is that your question is essentialistic/semantic.  The way you've phrased it suggests that there is an inherent importance to the words "abiogenesis" and "evolution", when in science, the words are just tools used to communicate ideas.  There is no fundamental answer because it all depends on how you choose to define those terms.  In science we use operational definitions for things, and the facts are empirical, stemming from measurements.  This question is like saying "what is life", where the answer is "it's a word with a somewhat arbitrary definition", if you follow.

@TrixieWolf - I understand better what the with issues with the question are and how I might phrase it differently to get the answers I'm looking for.  What now?  I could delete the question, but I think the discussion here is valuable because others may have the same question.  I guess I'll leave it and the powers that be can close it or do whatever they want.

@Yehosef You can just leave the question as it is. Since the question has an upvoted answer it cannot be deleted by you, and, as you say, the discussion can useful for later visitors.

I think it's a mistake to assume that there is such a point. All plausible seeming models of abiogenesis currently under consideration involve evolutionary processes long before they reach the stage we'd consider alive.
Evolution will occur whenever there is (a) replication-with-error and (b) selection (simplifying slightly). This is the case with a self-replicating RNA. It is replicating, but those replicates can be imperfect. Imperfections in replication that improve its ability to replicate will be favoured. That's evolution.

thanks for the clarification.   It seems abiogenesis will go from raw elements until self-replicating molecules and then will combine with evolutionary-type processes until there is "life"(which I'm assuming is at least some self-contained cell) at which point abiogenesis is "done".  Is that the right track?

Yeah, that's it. Although even then I'd be wary of assuming that there is a single clear line dividing life from non-life, so the exact end point of abiogenesis will be ill-defined.


text:
Does anxiety about weight or eating cause people to become overweight?
A while ago I saw this TED talk about the futility of dieting. The speaker suggests that a body maintains a homeostatic weight point and returns to that weight after dieting has stopped:

Turns out the brain is an incredibly efficient regulator of body
  weight. Isn’t weight loss about how much you eat versus how much
  energy you burn? Nope, it’s not that simple an equation: it turns out
  that hunger and energy use are controlled by the brain, mostly behind
  the scenes, and this unconscious force is stronger than mere
  willpower. The brain has its own sense of what your body should weigh
  — no matter what you believe — called the set point, which has a range
  of about 15 pounds. While lifestyle changes can shift your weight
  within this range, it’s much harder to move outside of it.

The speaker suggests that once she gave up dieting, she actually lost weight. Since then I've seen a number of other anecdotal reports of people losing weight once they let go of the need to diet and started to "eat anything they wanted".
This makes me ask - does anxiety about weight and attempts to control one's eating cause people to put on weight? In other words, if there's some unresolved anxiety issue in one's life, does it cause the human body to start preparing for hard times by storing extra fat?

yes, anxiety can changes hormonal state of our body,which may reduce catabolic enzyme that leads to grow more fat. So, anxiety may be a cause of over weight


text:
Can pandas hunt for meat?
Recently, I learned that pandas have a carnivore's digestive system but that it exists almost exclusively as a herbivore. If pandas hunted would they be able to find meat in their environment? Can't think of any reason why they would 'evolve' to eat only bamboo if this was true. It's like 2 million years ago some bears decided they wouldn't hunt, hibernate or even roar and are slowly committing suicide.

Keep in mind that evolution is not directed. The bears didn't "decide" anything. Natural selection operates when certain genes confer certain traits that end up increasing fitness of the organism. As it happened, for pandas in their environment, eating bamboo and not hibernating were traits that were beneficial, so they persisted in the population.

My question was why becoming bamboo eaters was beneficial. Is there no game in the environment that they can hunt?

Why all the downvotes? I find it quite an intriguing question, given that they are on the verge of extinction.

i was interested because pandas do still eat meat from time to time for example when they find a dead carcass. They are still omnivores. So I wondered if they are too lazy to hunt for live meat, lost the instinctual skill or there is no game in their habitat.

I find the first two options very unlikely since as far as I know humans are the only animals that don't live instinctively.

And while pandas are assumed to be docile and cute, they attack humans just like any other bear.

First: My opinion on why the question has received that many down votes
There were many down votes to this question, not because the question is no of interest. The question actually makes sense and is interesting. The post attracted those down votes because the post and the comments of the OP shows little understanding of evolutionary processes. Here are some issues:

some bears decided. Evolution is not directed. There is no conscious decision from any species (except humans, see eugenics) on how to evolve.

as far as I know humans are the only animals that don't live instinctively. I am not sure there is a common definition of the word "instinctive". But I very much think that the vast majority of people would suggest definitions that forces us to accept that humans behave instinctively. And if the definition would accept that human can sometimes not behave instinctively, then the definition will very likely accept that some animals behave instinctively.
why they would 'evolve' to eat only bamboo. Why did you use quotes?

Eventually the question may show lack of effort as showed in the fact that the OP is stating the 2MYA the panda and the other bears diverged, while it was rather about 36 MYA (according to onezoom and even a bit older according to this reference). This paper however shows that pandas had an omnivorous acenstor 7 MYA only suggesting that pandas modern day diet has evolved less than 7 MYA. More information below.
I don't think that those evident misunderstandings deserves receiving down votes (not sure though).

Can't think of any reason why they would 'evolve' to eat only bamboo

I had a quick look and I didn't find any good answer to your question. It seems that:

In nature pandas has diet consisting almost uniquely of bamboo (ref). They can eat any of the 25 species of bamboo wiki.
Pandas have a digestive track that is very short (like most carnivorans and unlike most herbivorous). Because of their short digestive track they eat a lot (between 9kg and 14kg of bamboo per day!) and they poop a lot (40 times a day) wiki!
As a consequence of its diet, the panda spend little energy and avoid any effort wiki.
Pandas seem to have evolved so that it is able to digest cellulose with the help of bacteria (ref, ref). According to wiki and BBC this microbiome is not herited from the mother but is acquired later in life (it is quite common to see that). This paper suggests that having such a fast transit prevent the ability to absorb other nutrients and therefore limits the benefit of having a more diverse source of food.
pandas size and mouth are adapted to their diet. They have a large size and a round face with powerful jaw wiki.
We actually know what genes are responsible for food preference in pandas (ref). The mutation for the "I prefer bamboo" allele is estimated to be 4.7 MY old (consistent with skull observation ref).
According to many comments online and according to wikipedia (but I couldn't find a trustful reference), as observed in zoo, pandas can eat other stuff when available. Citing from wikipedia While primarily herbivorous, the giant panda still retains decidedly ursine teeth, and will eat meat, fish, and eggs when available.

Given the amount of information we're having there may be tons of possible scenarios. It is possible for example that there is inter-species competition in the wild for access to prey. It is possible that there was for some point a very low density of preys and pandas has shifted their diets. Once, pandas had evolved some features of herbivorous species, they would get stuck there and not be able to get back to a meant based diet (stuck onto a local optima on the fitness landscape). There might be many different explanations involving patterns of competition, parasites, sexual selection, etc... And it seems that we haven't been able to disentangle between all of these.
Hope that helps!

I admit the term that of "decided" was wrong. I know evolution is not conscious. My main point was that a species with so many traits negative to survival shows that survival of the fittest is not a hard rule. Census evidence is now showing minor hope that pandas may not be facing extinction since poaching has been reduced since the population has even INCREASED 17% over last 10 years.

You post positive evolution mostly related to diet. I can post negative aspects related to reproduction also. Did you know that females select only one mate during the tiny heat period and will let all cubs but one die usually?

here is my blog re it although u will see me assuming spiritual awareness behind evolution though i dont really believe. Just that survival of the fittest is not a hard rule. There is survival of the unfittest too. https://epilepsydubai.wordpress.com/2015/05/22/panda-evolution/

Yes. The question was not about panda's biology in general (and hopefully because it would have been too broad) so I did not address pandas reproduction. Btw, many species have similar pattern of letting all the cubs but one dying. Cub cannibalism is not rare either. The expression "Survival of the fittest" was coined by herbert Spencer who has little knowledge about evolutionary biology. Intuitively, "survival of the fittest" relate to the process of natural/articial (eventually sexual as well) selection.

In those terms, then the adage "survival of the fittest" is indeed not a hard rule as not being the only rule, or if stated more correctly, natural selection is not the only process governing evolutionary processes. However, your simple observation of pandas lifestyle is not a demonstration of those other processes. Evolutionary biology is a big field of science. For example, I am personally working in the subfield of population genetics working on the evolution of the species range, the process of range expansion and the evolution of the mutational effects.

I strongly recommend that you make some readings in basic evolutionary biology before writing stuff online that will just allow misunderstanding to spread. Here is a good introductory source of information to learn about evolutionary processes.

My simple question was if pandas have prey they could hunt as omnivores in their environment as they were actually omnivores. Somehow, that was responded to by a post about positive adaptions of the panda. I understand evolution well enough. I just think pandas prove that a species with an accumulation of negative traits can survive too. So mutation doesnt always have to be benficial even in large amounts.

Do not feel offended but: No, you do not understand evolution well enough. positive adaptation is not a thing. mutation doesn't always have to be beneficial sounds really weird. Most mutations are indeed neutral or deleterious. People make a Bachelor in Biology, then a Master and PhD in Evolutionary biology and spend 25 years studying evolutionary processes. Evolution is more than what you think it is. You don't need to have that level of knowledge to ask a question on this website but don't rush to conclusion without understanding contradictory arguments.

To cite few examples of basic concepts you may not know about: Fst, Muller's ratchet, probability of fixation of neutral allele present at frequency $x$, heritability in the narrow sense, post-zygotic reproductive isolation, character displacement, Hamilton's rule, Wright-Fisher model of genetic drift, Zaahavi handicap principle, horizontal gene transfer, phenotypic constraints, etc...

I notice that noone has really attempted to answer my actual question. Only try to change my concepts on evolution. That's fine. I believe people are entitled to their beliefs. I shared mine too but was not trying to project it onto others. I was certainly not trying to disprove evolution. If anything, when the this thread devolved into evolution, instead of my question, I only suggested that growth of species that seem unfit to grow seemed possible. If anyone can answer my OP, please do so.

Let us continue this discussion in chat.

At approximately the same time that they switched to a primarily herbivorous diet, pandas lost the ability to taste "umami," or "savoriness." We don't know whether this happened before or after the dietary change, but the umami flavor is a strong attractant for other meat-eating omnivores, like humans. It signals instinctively that a food is exceptionally valuable and should sought out and prioritized over other available food. This is why your mouth waters more at the smell of a steak than the smell of a carrot. Unable to distinguish this quality by smell/taste, pandas would be less inclined to go to the effort to hunt down or scavenge meat, compared to just stuffing readily available but almost inedible bamboo into their craws for sixteen hours a day, even though it often gives them serious indigestion and limits their ability to travel or reproduce.

Hi Edie. Welcome to Biology S.E. :)..any chance you could back up your answer with a (couple of) source(s)? I would recommend to have a quick read through the BioSE Tour (https://biology.stackexchange.com/tour).. in doing so you'll also earn your first badge.


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Are blood vessels organs?
Are blood vessels classified as organs? Organs compose of 2 or more tissues and perform a certain function. Blood vessels have 3 different tissues and perform a function (transport blood), yet I do not see them being identified as an organ. Why is this? Are they organs? Or do they hold their own classification?

Did you copy the question from here?

@Cornelius, no need to ask. That is a copy/paste.

@Cornelius - nice find. Wouldn't this issue be a nice one for Meta? It looks like rep mining to me? I retracted my upvote. I might be downvoting if OP doesn't respond.

@AliceD I believe similar issues were discussed on Meta.SE, but I can't find the question now. Anyway I consider we should focus on giving better answers than the ones on Yahoo, where, again, the best answer is a copy-paste from Wikipedia.

@AliceD btw,  ain't hematology a bad tag for this question? The question is not about blood pathology.

@Cornelius - It is a bad tag; I just added terminology and wavered to delete hematology. Thing is there has to be some tag linking it to the vascular system - what about blood-circulation? +1 for your answer btw

http://meta.stackexchange.com/questions/256933/what-to-do-if-a-question-is-crossposted-from-a-non-stackexchange-website

Artery and veins are organs, but capillaries are not.

The cardiovascular system is usually lumped together as an organ. So blood vessels would be included here but you are right in that this is a bit strange being that it includes the heart and the vasculature.

I don't know if they are classified as organs, but basically, blood vessels match the criteria for being organs.
Quoting SIU School of Medicine:

Blood vessels are basically tubular organs found within other organs.

Biology Reference states the same:

Even the glands within the integument can be considered organs; any gland is primarily secretory epithelium surrounded by connective tissue for support and protection. Likewise, the blood vessels and nerves in these organs are organs unto themselves.

Yes blood vessels can be called as organs. They are part of organ system. By definition an organ is one which is made of different tissues and contributes with other organs to a specific function in the body. Here blood vessels are made of different tissues like smooth muscle, epithelial tissue, elastic tissue etc.


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Pavlovian Conditioning And Synesthesia
I have been reading about Pavlovian brain conditioning and it seems that documented cases are mostly limited to motor reflexes (like conditioning an eyelid to close when hearing a tone) or taste aversion . Basically information flowing through Cerebellum and Hippocampus. Are there proofs or scientific studies about the limitations of such conditioning? Or studies about what can be associated and what not?
Let's imagine for example that a subject looks at a black neutral screen and whenever some tone is played, the screen turns bright red. After an intense conditioning would it be possible that this subject, when blindfolded would see some red when hearing that same tone?

Probably more suited to the cogsci SE: http://cogsci.stackexchange.com/

This has been attempted, with some success, though on grapheme-color synesthesia, rather than sound-color synesthesia. Beyond conditioning, there have also been somewhat successful attempts to induce synesthesia through various psychoactive drugs. In both of these cases, however, the effects are temporary and generally weaker than genuine synesthetic perceptions.
There have been no studies (to my knowledge) about which associations can be induced and which cannot. I would say that sound-color might be a difficult association to generate, simply because no one would like to site and stare at a flashing screen while listening to various sounds, and it also predicates on the patients' ability to distinguish sounds, which can vary wildly from person to person. The grapheme-color experiment had the treatment group read materials with certain letters colored, which was much easier to implement.
This raises the question of whether synesthesia can be classified as a low-level interaction between typically non-interacting parts of the brain, or if it operates on a higher cognitive level (i.e. ideathesia).
See the article for details about the grapheme-color study:
"Pseudo-Synesthesia through Reading Books with Colored Letters"

Thanks this article is very interesting. Too bad they didn't achieve color perception


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Recent classification for parasitoid (ecological relationships)
I'm about to present an exam about ecological interactions in biological control. Although the position of some groups is clear, in the case of parasitoids they are included sometimes as predators, some others as parasites, while sometimes they are included like an own group. For example, in this paper they
 are included as parasites, but I wanted to know if there is a more recent reference or classification for these groups (Trophic strategies,
animal diversity and body size Kevin D. Lafferty and Armand M. Kuris).

While both parasitism and parasitoidism are both classifications of predation, parasitoids differ from parasites as they [parasitoids] kill their hosts.

A related question I asked some time ago covering why parasites kill their host received some great answers.

I think the wikipedia article defining parasitoids has it right on this one. The term is, and should be flexible and it's definition defined by context. i.e Case by case definitions are made obvious in the literature.

Patently there is no point to trying to draw arbitrary lines of distinction between such vague, and often variable, life histories. In each ecological or ethological study, the terms applied should reflect the facts in the contexts relevant to the matter in question. Such studies need not in all cases use the identical terminology, and there is no reason they should.

This means that you should always describe the life cycle even if you call the organism a parasitoid. There is too much variation between seemingly similar organism life histories to use a strict and specific term.
For those struggling to see the link from the question, they suggest a parasitoid can be measured as a parasite that reduces host fitness to zero:

... they are also quite different from these other parasites,
  in that, similar to a predator, they must kill their host.

A recent (2015) review on Whiteflies refers to Hymenoptera as parasitoids of Whiteflies because the Hymenoptera are parasitoids as larvae as they kill the Whiteflies and then become free-living adults.


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Terminology regarding cross-immunoreactivity
After reading an article, I saw expressions like "cross-immunoreactivity among epitopes", "cross-immunoreactivity among variants of virus", "immunological reactions among pairs of peptides" and so on.
I wish to verify my following understandings:
An epitope is also called antigenic determinant, and it is part of the antigen that is recognized by the antibody. An epitope, then, is a part of a virus variant. Peptides are short chains of amino acids. Thus, we can talk about the immunological reactions among peptide-pairs, because the virus variant itself is a protein, which is composed of peptides? Did I understand it correctly?
Moreover, I saw a sentence like "this antibody is against a few variants while reacting with all tested peptides", so I guess reacting here includes against? Reacting may include other situations, right?

Everything you state is correct, except that I disagree with your statement that a "[...] virus variant itself is a protein, which is composed of peptides.
A virus is typically composed of a protein capsule with genetic material on the inside. So technically, a virus is not a protein, but its outer shell is composed of proteins. Further, a protein does not necessarily have to be composed of (multiple) peptides - it can be a single amino acid chain.


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Why are bacteria immune to snake poisons?
In a test I was asked why bacteria are insensitive to snake toxins.
Is it their membrane that provides a barrier to the toxins? Or do snake poisons have specific targets and thus cannot bind to bacteria?

All bacteria definitely aren't immune to snake venom. Infact they're very much susceptible to damage from snake venom eg (P Samy, R., et al. 2012). DO you have a specific bacterial strain in mind?

Short answer
Many snake poisons target specific proteins not present in unicellular organisms.
Background
The question is admittedly broad but the idea behind this question is pretty much what you indicate in your post - many venoms target specific proteins and do not simply destroy their target by, e.g., disrupting gross cellular structure (like alcohol does for example). Instead, they target specific molecules that are essential for the survival of their prey.
Snake toxins can be categorized according to the organ systems they target, namely :

the central nervous system
the cardiovascular system
the muscular system
the vascular system

Central nervous system toxins are carried by elapid snakes like cobras, kraits and the taipan. Typical targets are the nicotinic acetylcholine receptor and the muscarinic acetylcholine receptor. Blockade of these receptors at the neuromuscular junctions resulting in death by asphyxiation. Acetylcholine receptors are not present in bacteria.
Cardiovascular toxins are pretty diverse and include things like angiotensin-converting enzyme inhibitors (leading to a drop in blood pressure) and glycosaminoglycans (the sulphated carbohydrate moieties that occur abundantly in cells of cardiovascular tissues) binding proteins that lead to cardiotoxicity. Again, the targets are specific molecules involved in heart function and hormones, stuff not present in bacteria.
Muscular toxins include those that bind specifically to the sarcoplasmic reticulum of muscles or interfere with specific second messenger systems messing up muscular function. Again, quite specific targets not present in bacteria.
Lastly, typical vascular system toxins include anti-coagulants such as protein C activators and inhibitors of prothrombin complex formation. Again, specific targets.
Reference
Koh et al., Cell. Mol. Life Sci (2006); 63: 3030–3041

Venoms from vipers contain high amount of proteolytic enzymes (serine proteases). Many of them act by cleaving fibrinogen and thereby causing blood clot (ref). There is a likelihood that some of these proteases may affect other proteins also. In a study conducted by Bottrall et al. (2010), it was shown that snake venoms do have a general proteolytic activity. The best among tested was the venom of the viper Bitis arietans. However, its activity was significantly lower than the positive control which consisted mainly of trypsin and proteinase-K.
So the venom may have a little effect on the membrane proteins of bacteria.
But it might require extended treatment by venom to digest these proteins compared to that by stronger proteases like proteinase-K.
However, there are indeed reports on antibacterial activity of snake venoms (Stiles et al., 1991; Perumal Samy et al., 2007; Charvat et al., 2018). But the enzymes responsible for the antibacterial activity are phospholipase A2 and L-amino acid oxidase, and not the proteases.


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What is the contribution of the cockroach to the ecological environment?
I've read a lot about cockroaches but was unable to find how they contribute to the ecological environment. Does anyone know?

What do you mean with "contribute"?

They make more cockroaches. They also feed things that eat cockroaches, eat things that are eaten by cockroaches, and transmit microbes that are transmitted by cockroaches. Et cetera.

Their main contribution to my kitchen ecosystem is that they keep the floor clean.They do that mostly at night, a nice example of co-evolution.

Short answer
Cockroaches are an integral part of the food chain.
Background
Cockroaches are an important source of food for a number of organisms, such as arthropods, birds, and mammals. As such, they are an important part of the food chain. Cockroaches also play an important role in nutrient recycling. Most species of cockroach are detritus feeders and with the help of endogenous cellulases play an important role in degrading plant material. Some species, such as Cryptocercus, feed directly on wood and play a major role in lignocellulose digestion in temperate forests.
Reference
 - Bell et al., Integr Comp Biol, 2008; 48(4): 541-3

They don't have to "contribute" as such. All they have to do is survive and pass on their genes to their offspring. Any benefits that they have (in terms of detritus cleaned up, etc.) or harms that they cause is purely coincidental.
There's no "desire" on the behalf of species to make things "better". All they "do" is try to survive in their existing environment but not make it "worse" for themselves. A species wouldn't survive very long if it ate all of the food in an area or if its waste products polluted the area to such an extent that they couldn't survive.
However, that doesn't mean you can simply remove a species from an environment and not cause actual harm to that environment. The environment includes all the other species that co-exist and they have all evolved in the presence of each other. This means that other animals have evolved to cope with the fact that cockroaches prey on them, others have evolved to eat cockroaches. Remove the cockroaches and the population of the first species will explode and that of the second will collapse. This will have knock on effects to other species in that environment and so on.

You must read this article:

“Most cockroaches feed on decaying organic matter, which traps a lot
  of nitrogen,” Kambhampati said. “Cockroach feeding has the effect of
  releasing that nitrogen (in their feces) which then gets into the soil
  and is used by plants. In other words, extinction of cockroaches would
  have a big impact on forest health and therefore indirectly on all the
  species that live there.”

http://www.huffingtonpost.com/2012/06/21/cockroaches-good-environment-nitrogen-cycle_n_1614913.html


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What is the difference between electrons and energy?
I'm studying microbiology right now and I have come across something confusing to me. I thought electrons provided energy to the cell by being incorporated into reducing powers and eventually driving the synthesis of ATP. However in classification of microbes energy sources (photo, chemo) and electron sources (litho, organo) are separate.
Is there a scenario in which the source of electrons and energy are different (besides phototrophy)?

This is not a biological question and if you are studying microbiology, then you would have also learnt basic physics. I am voting to close this question.

I'm voting to close this question as off-topic because it is not about biology but basic physics.

I think there is an interesting question hidden here, but the formulation is throwing us off. Something on the lines of which energy sources does the cell use other than redox reactions of ATP. We could try translating "what does energy do that electrons can't do" as "what do other cellular energy sources do that ATP synthesis/cleaving can't" or something similar.

@rumtscho I still cannot understand what the actual question is. I am interpretting it like this — how different sources of energy translate to ATP production?

Electrons and Energy are 2 completely different thing. Electron is a class of negatively-charged sub-atomic particle. Energy is a concept, that is "ability of a system to do some work". You could consider it as "unstability" of a system

A system, contain the more energy, the more it is prone to do a work, the more it is unstable, the more it is prone to achieve someother more-stable conformation. Such as if you keep a spring relaxed, it contains a less-amount of energy. But if you press or extend or bend it than its normal-conformation; it contains more energy. If you release it, the energy comes out and perform certain work, say shot a bullet.

Just like pressing a spring cause a change in its energy-level; any change in a molecule's structure (bonding) (chemical-change) and conformation (in simple language, shape-change without change in bond-connectivity) (many of the physical-changes); cause change in energy level.

Chemical change occur due to change in electronic configuration of atoms

Since living-creatures made up of atoms; the biological works (requiring energy), take place through chemical-change (i.e. electron-configuration change.). But electron is not same as energy.

Sometime for ease of stoichiometric (chemical-arithmetic) calculations, the number of certain chemical-species (say electron, H+, NADPH, NAD, ATP, etc are considered as a packet, containing certain amount of energy, in certain particular pathways or processes). But they are not themselves energy. The are matter

Question is closed. So I couldn't answer. Read my 6 successive comment above as an answer. You need to understand well enough the basic school-level chemistry and physics before learning advanced science. However, no question is bad, rather avoiding ask question is bad.

You're basically confusing the fuel source with the energy it produces. For example, a car burns gasoline. That doesn't mean that gasoline is energy, only that gasoline can be used to produce energy. Similarly, a cell uses electrons in the production of ATP (source):

In the image above, electrons (symbolized by the flat arrow going from $\mathit{NADH}$ + $H^+$ to $\frac{1}{2}O_2$ + $2H^+$) flow from NADH-Q reductase (I) to cytochrome reductase (III), to cytochrome oxidase (IV). The electron flow across these complexes causes the pumping of hydrogen cations (protons) through the membrane to the extracellular space. This, in turn, produces a pH gradient and membrane potential which are used to drive the synthesis of ATP (by the $F_1F_0$ ATPase), which can be broken down to release energy (source):

So, electrons are needed1 to produce ATP and ATP can be thought of as energy storage. When ATP is broken down to produce AMP and Phosphate, energy is released in the form of heat. This is why ATP is considered as "energy currency". Neither ATP nor electrons, however, are "energy" themselves2. No more than gasoline is.

1 Are used, anyway. There are other choices.
2 No more than any other form of matter, at least. You can, actually, think of matter as condensed energy but that is really squarely in the realm of physics and not biology.


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What is peptide mapping?
After searching online for peptide mapping to my understanding it can be treated as the fingerprint of the protein. It is obtained at the end of several chemical processes and it helps to understand the protein being analyzed.
Does this method operate in "sequence space" then? If so, what exactly is the relation of the two?

I slightly edited the question for clarity. Feel free to roll back.

Shimadzu explains peptide mapping as follows:

Peptide mapping involves selectively cleaving the individual target [proteins] using an appropriate enzyme or chemical and analyzing the peptide fragments obtained using HPLC [high-performance liquid chromatography] or another suitable method. [... I]dentification of the peptide fragments separated by LC [...] [can be done] using amino acid composition analysis, N-terminal amino acid sequence analysis, or mass spectrometry.

As such, it does not provide a sequence of amino acids. Instead, you get a specific set of peptides of different sizes, dependent on the method used, that in turn can be used for protein fingerprinting.


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Recommend any Molecular lab LIMS (Laboratory Information Management System)
We are looking to develop or customize a LIMS for our molecular lab. Do you know of a LIMS that you've used in a molecular lab before, or one that could be used.
Thanks for the help
(Edit)
Some of the attributes we'd like to store include:
    Patient information (Name, demographics, test ordered)
    Sample information (Accession #, Case ID, sample type (blood,bone, etc.) )
    Test information (Kit used, Kit lot #, associated expiration date)
Ideally this is Software as a Service so its usable on multiple operating systems.

What are your precise requirements? online/offline ? Lab notebook or it should handle inventories also? Linux or MS or cross platform?

We use Quartzy to manage all of our lab supplies and reagents. As far as I know though, this does not allow you to also store things like patient records, or lab notebooks.

What kind of management? Orders? Stocks ??

I just added some additional info. Hope this helps clarify


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What is the distance between the sciatic nerve and the colon at the closest point?
Is it possible that a full colon impinges on the sciatic nerve? Is there anything that physically separates the sciatic nerve from the colon?

Short answer
Sciatic nerve pain cannot be caused by a full colon.
background
The sciatic nerve runs at the back of the pelvis down the the leg. The sciatic nerve exits the spine from the lumbar spine to S3 in the sacrum (Fig. 1).

Fig.1. Left: sciatic nerve overview. Right: Sacral plexus. Source: Manchester Bedford Clinic
Hence the sciatic nerve does not come into contact with the bowel and intestines located ventrally in the abdominal cavity (Fig. 2).

Fig.2. Left: sciatic nerve in detail showing dorsal location. Right: Intestines ventrally situated in abdominal cavity. Source: Manchester Bedford Clinic and University of Maryland
Pain in the sciatic nerve (sciatica) is often caused by compression or entrapment by muscles, tendons, and other soft tissues along the nerve path Manchester Bedford Clinic.

I appreciate the extensive answer with the nice diagrams. However, it doesn't actually answer my question: just how far is it between the sciatic nerve and the colon at the closest point?

Alas, I cannot provide you with an absolute distance measure.

And I appreciate it! Do you have a particular source that backs your statement that "Sciatic nerve pain cannot be caused by a full colon"? It appears to me that they might only be an inch or so apart, and if tight muscles in the area can cause sciatic pain, a full colon should be able to at least contribute.

The figures showed me they (nerve and colon) were physically separated and across various websites sciatic nerve pain is not associated with the intestines: http://www.mbmyoskeletal.com/learning/sciatica/


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Do DNA supply houses maintain a watch list for dangerous oligos (Anthrax, Smallpox, etc.)?
The recent work by DeLoache, et al. on a synthetic opiate-precursor production pathway in yeast has generated a lot of scare stories in the media about people homebrewing heroin as easily as they would beer.
In connection with DeLoache and coworkers' research, the New York Times has claimed

Their DNA could be put on a watch list, as sequences for anthrax and smallpox are, so any attempt to buy them from DNA supply houses would raise flags.

I have never heard of such a watch list, and a thorough googling turned up nothing relevant save for the NYT article itself. Does this watch list exist?

I have heard about this before. But this is kind of pointless when you know how to handle and manipulate DNA. Besides that, it is not trivial to puzzle a virus together.

@chris But this is kind of pointless when you know how to handle and manipulate DNA. Yeah, that's my real question: how could such a list even work? How would it handle silent mutations? How would it handle SNPs, or other mutations easily fixed with PCR? Combinations of SNPs?

I think it will hold off people with no real knowledge. It won'T be a big hurdle for everybody else.

Cross-posted to Skeptics. In addition, while the smallpox genome might be within reach of gene synthesis, having an anthrax genome does not bring you any closer to synthesising an anthrax bacterium.

i encountered same question. nowadays you can order very big piece of dna custom-made. some viruses are <10Kb so they are easily synthesized. anthrax is 5Mb and smallpox is around 180Kb, so those are hard to produce in vitro

I guess the fear is not necessarily to have someone produce a viable virulent anthrax from a DNA sample, but to have them introduce virulence factors of those watched pathogens into previously harmless organisms they could easily buy and grow.

@aandreev While the whole bacterial genomes are far larger than a typical gene synthesizer can sell, DNA for the dangerous parts, like the botulism toxin protein, are small enough to be made. These could potentially be inserted into some other bacteria, like E. coli pretty easily. If you can do a little more work, you might be able to get into a cold or flu virus.

@aandreev Additionally, positive strand single stranded RNA viruses have genomic RNA that works as mRNA. If you had the DNA for the virus, and made the RNA through in vitro transcription, that RNA would be enough to infect cells and make virus, assuming you could get it into cells, which is still pretty hard. But maybe the RNA could be produced and stored more easily than the whole virus.

it seems to me that problem of producing virulent/pathogenic (i might mix terminology here) agents from scratch (via ordering DNA pieces and cloning) is medium to hard, but definitely doable. question is does companies check sequences and report to FBI

@aandreev I think they do. You could always get the smallpox sequence and submit it to genscript for synthesis. If the FBI comes knocking on your door, let us know before they send you to gitmo.

@user137 sure thing

I don't know how generally such things are followed, but in at least one contract gene synthesis provider's FAQ, they address this issue, and mention two such government-provided resources:

Q: Does GENEWIZ have a procedure in place to address potential biosecurity
          concerns for gene synthesis projects?
GENEWIZ is fully aware of all risks and benefits associated with gene synthesis research. With the knowledge that gene synthesis technologies have the ability to enable de novo reconstruction of dangerous pathogens, GENEWIZ employs rigorous quality control policies and procedures to safeguard against abuse of the genes we synthesize. GENEWIZ actively monitors the Screening Framework Guidance for Synthetic Double-Stranded DNA Providers [link], drafted by U.S. Department of Health and Human Services (HHS), as well as the Select Agents and Toxins list put forth by the U.S. Government.


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Can the Hebbian theory apply to Inhibitory Neurons
If I understand the basic Hebbian theory, when a neuron fires a pulse to another neuron and this pulse causes the target neuron to fire then the delta energy sent from the initial neuron to the target is increased. (Making it easier to trigger the target cell)
With this in mind is there a way for an inhibitory neuron to increase the delta energy it applies to a target neuron (reducing the excitation level of a target neuron).
If the inhibitory neuron never triggers the target then I would assume it would never increase the decrease in energy it sends to the target.

We now do have mathematical models for LTP. I think Hebbian theory is an oversimplification if we see those models.

≈Yes, it's easy to conceptualize at a simple ganglionic circuit. A really good example is (I believe from Kandel's lab)demonstrated by Aplysia's gill withdrawal reflex. Repeated stimulation causes reduced EPSPs in motor neurons that innervate muscles that cause the withdrawal reflex. However when you apply a electric shock to the tail, the snail will immediately regain withdrawal reflex sensitivity. The tail sensory neuron response activates the serotonergic facilatory interneurons which have multiple IO with sensory and motor neurons.
And don't forget, interneurons can inhibit other interneurons leading to disinhibition.
For most LTP work you're probably ok using Hebbian models. Make sure to keep in mind that in more complex systems like cortical circuits.  there are some modes of communication that don't always play well with Hebb's Laws: gliotransmission, retrograde transmission, neuropeptides/GPCRs, and activation of perisynaptic receptors/receptors on adjacent cells.

Could you elaborate on why neuropeptide/GPCRs may not fall within the Hebbian category ?


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Zoology - Help identify the kind of spider
Yesterday, I bought a banana tree (Musa Basjoo) from a local supermarket.
Today, I noticed a hive of small spiders on the tree.
I do not know where they came from, so I am curious to identify these small creatures.
I am living in Flossenbürg, Bavaria, Germany.
Can someone help me identify the kind of spiders that are depicted on the photos?
A picture of the tree, it is still in front of my house door, planted in a pot:

A near shot of the spiders that are "dwelling" on the tree:

Not too sure but it seems like the european garden spider- Araenus diadematus

[ Image source ]