text:
Is there a molecular basis to intelligence?
Is there any explanation, gene(s) or whatever detected, that are co-related or explicitly related via mechanical bio-molecular (or at any other level) models that explain the higher or lower intelligence found in different individuals of Homo sapiens?
If so, which and how do they work?

Good question. IMHO, I don't think that there's a "intelligence gene". There's a meta-analysis about it here

Just as a potential starting point for your search: this not a review, but it contains a general discussion on the issue of intelligence heredity and underlying mechanisms - Natural history of Ashkenazi intelligence

As a Drosophila biologist, I will attempt to address the above question by giving an examples from the Drosophila field. When this paper (http://www.ncbi.nlm.nih.gov/pubmed/7720066) in Cell came out, it sent shockwaves around the world since it showed a molecular mechanism by which production of cAMP and activation PKA, effects CREB transcriptional activation and in turn formation of the long-term memory (LTM) in flies. Some of these CREB over expressing flies could learn a task after simply one try whereas wild-types had to do it several times! This work was later followed by mouse studies (http://www.pnas.org/content/100/18/10518.full.pdf) and comparisons to RTS patients were made. At that time there were discussions of CREB being responsible for intelligence however now there is nice nature review/meta-analysis paper (http://www.nature.com/srep/2014/140225/srep04176/pdf/srep04176.pdf), which says there are no evidence connecting CREB and IQ. This paper performs a literature based investigation and identifies several candidates that are testable and can act as biomarkers for intelligence related therapeutic approach to mental retardation. According to their screen dopamine and norepinephrine pathways seems to be important in IQ-related biological processes.
Hope this helps!

When doing studies on genome-wide associations, you WILL find an association between a "gene" and pretty much anything (gene A causes preference of vanilla ice cream over chocolate). So, yeah, there are many associations (and correlations), but there is no single "molecular" cause for intelligence; no matter how strong the 'statistical' association is, causality is hardly ever known for complex traits.


text:
The mechanism of mechanoreception?
I am interested in knowing the molecular mechanism behind mechanoreception/mechanotransduction (i.e. mechanism behind receptor potential generation on mechanical stimulation). I know that most mechanoreceptors (touch, stretch, pressure etc) respond to mechanical modification of plasma membrane or of some external projection embedded in plasma membrane. I want to know the molecular basis behind this mechanical transduction.
Also, the sensory hairs in lateral line sense organs of fishes, and equilibrium and auditory sensation in animals involve generation of receptor potential when the steriocilia( or any equivalent extracellular projection), externally embedded in gelatin, bends in specific ways, another example of mechanotransduction.
(I don't know if all these receptors function with slight modification of the same basic framework or all of them operate with distinguishable mechanisms. If the latter is true, I just want one example of how molecular mechanism might bring about mechanoreception.)

See this article on mechanotransduction and especially the cartilage section.

I wonder how exactly mechanical stretching can ope ion channels.

i think it distorts the channel ...

A mechanical stimulus can act on a tissue with elastic and viscoelastic properties in two ways [1, 2]:

distort the cellular membrane which leads to opening of ion channels.
create tension on the extracellular matrix or cytoskeleton, to which a ion channel is bound, thus leading to opening of the channel.

Stretch-activated ion channels opening leads to the formation of an action potential, if there is enough ionic flow to trigger depolarization [1, 3].

References:

Wikipedia contributors, "Stretch-activated ion channel," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Stretch-activated_ion_channel&oldid=606349902 (accessed July 12, 2014).
Grigg P. Biophysical studies of mechanoreceptors. J. Appl. Physiol. 1986 Apr;60(4):1107-15. PubMed PMID: 2422151.
Wikipedia contributors, "Mechanotransduction," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Mechanotransduction&oldid=593605473 (accessed July 12, 2014).

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text:
How likely is it that Earth has millions of different species?
I know that the probability of life existing on a habitable planet is pretty slim. But, how likely is it that it hapenned millions of times in the same planet? Or was it only a few species that evolved into millions of other different species over time?

Hello! I am not sure I understand your question. Do you mean: "How many times did life originated de novo (from non-living things) on earth?". If this is your question, you might want to change your title which is misleading. We have the feeling that you ask about how many species exist today.

I mean if life is  very rare to happen spontaneously how do we have millions of different species?

Because of speciation (evolutionary process by which one species becomes two!). Would something like this answer your question?

We can be reasonably certain that ALL species that exist today share a common ancestor, a common origin. Every single species we have even encountered, for example, uses a long chain of nucleotides (DNA or RNA1) to store its genetic information. If life had arisen through multiple independent sources, we would expect to find different solutions to the problem of passing genes to offspring.
To put it another way, all forms of life we have found can be placed in one of three main classes (superkingdoms): eukaryotes, prokaryotes and archea. All other types of life come under one of those three categories (viruses are special and not really considered alive2):

Now, any organism we have ever seen uses the same basic systems of storing its genetic information. In fact, there are even certain genes that are conserved (similar in sequence) across all domains of life (see my answer here for some examples). That is why this version of the tree has a common root. All lines start from a single original line (commonly known as the Last Universal Common Ancestor, LUCA).
In summary, all the evidence we have points to a single origin of life. There are too many shared features to assume multiple origins. Despite their enormous diversity, all organisms share certain very basic systems.

NOTES

As far as I know, only certain viruses use RNA instead of DNA, all truly living creatures use DNA. Even if I'm wrong about this, the differences between RNA and DNA at this level are small enough that the common origin still holds.
See here for more in why viruses are not alive.

Another proof of the common origin of life is the use of (almost) the same codons for coding proteins. Or that the sequence DNA -> RNA -> Protein is also always the same.

@Chris well, there are actually at least 20 different genetic codes (granted they don't change that much) so I did not want to use that one. Good point on DNA->RNA->Protein though.

I know that there are some differences. But given that the three kingdoms seperated quite a long time ago, its pretty amazing, that we can still translate human proteins in E.Coli and they are functional. And the difference is quite small if you think about the sheer number of species.

@Chris absolutely, I agree. I just didn't want to use it as an argument (though I would if debating another biologist) since there are actually some differences.

Thats a good point. :-)

um, reverse transcriptase, anyone? (biochemistry) A polymerase that catalyzes the formation of DNA from RNA; found in retroviruses.

@Susan, actually found in many species, encoded by repetitive elements like LINES and ERVs etc but in none of them is it used to drive the expression of native protein coding genes nor does it change the fact that the flow of information is from genotype to phenotype via RNA: DNA->RNA->protein.

The fantastic number of species that one can observe today is not a fixed value. This number changes over time. These changes are not caused by De Novo origin of life but by two processes which are:

exctinction

Process by which a species disappear

speciation

Process by which one species (or one lineage) becomes two.

Therefore the absolute change in number of species equals the difference between speciation and extinction.
$$\delta_{species} = speciation.rate - extinction.rate$$
There is a ton to say about extinction and speciation and it would take several books to tell you about this science. If you want to study the subject a bit further, I would suggest you to first grab a book of general biology or an introductory book in evolutionary biology before jumping into a book that talk about speciation and extinction.
One can map how speciations events occurred frmo a unique common ancestor in order to create the diversity of life you can observe today. Such mapping are called Tree of Life. Here are the roots of the tree of life of living things on earth. You can spot Animalia, Fungi and Plants on the far right of the picture. The Common ancestor of all living things on earth is called LUCA (Last Universal Common Ancestor).

As a sidenote: The concept of species itself accept several definitions.

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text:
Can pets catch the cold?
Last night I was drying my cat with a towel after shenanigans in the rain and she sneezed!
Questions

Can cats/dogs/hamsters or other pets catch the cold?
How quickly do they recover?

I know from my own practice that lab mice can catch a cold. The get infected, are less active and sneeze. It takes them a few days to clear this. That was the reason we where usually not going into our mouse facility when having a cold.

@Chris I guess that is quite revealing! Quite interesting actually, I suppose we can then catch it off them too?

I am not sure. Our immune systems share similarities, but they are not completely indentical - something very important to keep in mind when you want to to immunological experiments on model animals. Especially when it comes down to surface receptors of cells (important when a virus wants to enter a cell) there are slight modifications possible which can inhibit an infection.

Yes they can. The viruses that cause a cold include rhinoviruses (up to 80%), coronaviruses and influenza (together accounting for much of the remaining 20%) and a small percentage of adenoviruses. When discussing cross species transfer, influenza is the most important to discuss as it is a fairly common cause of the "common cold".
Influenza A has humans, pigs, bird and horses as its host. Different influenza strains have different hosts. Influenza can recombine if two strains infect the same host (antigenic shift) and also mutate (antigenic drift). With a combination of these influenza can and has numerous times crossed the species barrier which has caused the major flu pandemics as well as swine and avian flu. It's this reservoir that makes these viruses so hard to eradicate. When we are the only host such as in polio virus, it is a lot easier. Pigs don't adhere to national flu guidelines.
Comparing recovery times, all mammals are roughly similar although due to our slightly more evolved immune system as well as social factors of knowing what to do when we are ill we recovery very slightly earlier.

The influenza virus doesn't cause a cold. It causes influenza. Colds are cause by completely different virus families (Rhino-, Entero-, Corona-, Mastadenoviridae to name only a few). The influenza belongs to the orthomyxoviruses. The other thing: Viruses do not cross necessarily species borders again, when they did this once. This ist mostly a matter of chances and contact and doesn't happen too often (luckily for us), since zoonotic viruses are usually pretty dangerous.

@Chris Influenza causes around/up to 20% of "common colds". I have updated my answer to reflect this. Also Rhinoviruses are part of the Enteroviridae family. Also the question was whether it is possible which it is, but I agree that it is fairly rare. Whether it is dangerous is another question, initially they often are as they are maladapted. As time goes on they are less dangerous which is something that is hypothesised may occur with HIV.


text:
Is there a downloadable list of all species along with their traditional classification?
I'm looking for a downloadable list of all known (or better said, online documented) species in this straightforward format, as an example the European Frog:
Kingdom: Animalia
Division: Chordata
Class: Amphibia
Order: Anura
Family: Ranidae
Genus: Rana
Species: Rana temporaria
I'd like to have this list offline in a structured text or database format that I can parse. If such a list has other useful attributes (credits, distribution, common names), it is welcome, but the above is the absolute minimum I need. I know there are more taxonomy levels in the above system (Species 2000 & ITIS Catalogue of Life: April 2013 ), but I only need these basic 6.
I have been looking at several collections and am having difficulty getting the data that I need. Either the database is incomplete, not accessible as a database, has complicated data structures, or has poorly described and slow web APIs that I cannot rely on.
Conceptually, it seems to me that http://www.catalogueoflife.org comes closest to my needs, yet their download is a tool, not a database. I do see the download has a MySQL folder containing lots of files, but I don't know how to reconstruct it into a database. It seems also that they pulled the page to describe the database download.
As simple as my question seems (I'm not a biologist, so I assumed it was simple), I have wasted several hours coming up empty. I was wondering if anybody has done the work to provide basic species info in an understandable format as requested?
As for species completeness, the 1.3m of Catalogue of Life sounds really good, as I'm currently basing my system on Wikipedia, which only has 180k species.

you might want to have a look to www.tolweb.org

Have you ever found what you needed?

Extant only, or all known life? because xtinct life tends to mess with that form of classification, which is why it is included less. .

you have another issue as well,  taxonomic classification is less helpful for cross group comparison (some classes for instance are inside other classes) so many larger "tree of life" projects tend toward phylogenetic classification instead, it makes for clearer coding.

Second John. Possibly there are some reasons to use Linnean classifications, but the phylogeny is the actually useful data artifact. The hierarchical taxonomy is more of a crude heuristic, sounds like a painful exercise to make it play nicely.

ITIS
To expand on the answer from @Rodrigo, the Integrated Taxonomic Information System seems to be a reasonable answer. It gives you a database of every taxonomic node in the Tree of Life™ and each node has a Taxonomic Serial Number (TSN). You can download the data as a database or even just use the tables as pipe-delimited text files.
For example the file vernaculars tells us that the TSN for European frog is 173444. By looking in the file longnames, we can see that the complete name for 173444 is Rana temporaria. Finally, the file hierarchy, tells us that the complete hierarchy for 173444 is:
European frog:
→ Animalia
→ Bilateria
→ Deuterostomia
→ Chordata
→ Vertebrata
→ Gnathostomata
→ Tetrapoda
→ Amphibia
→ Anura
→ Ranidae
→ Rana
→ Rana temporaria
You may download the ITIS data in several different formats from https://www.itis.gov/downloads.
Example data from some of the files.
If you downloaded the MySQL Tables data from https://www.itis.gov/downloads/itisMySQLTables.tar.gz, here are some of the useful files you'll find.
vernaculars
The first two fields of vernaculars contain the TSN (Taxonomic Serial Number) and the common name for a node. Some common names map to a single TSN and not all TSNs have common names. Some examples:
50|bacteria|English|N|2015-03-02|159942
14092|mushrooms|English|N|2004-01-28|11529
14092|pore fungi|English|N|2004-01-28|11534
14092|rusts|English|N|2004-01-28|11539
183798|Domestic Cat|English|N|2007-08-15|111781

You can read the file dropcreateloaditis.sql to see what the other columns mean.
longnames
The file longnames contains only two fields, the TSN and the complete "scientific" name of the item. For example:
50|Bacteria
14092|Basidiomycotina
183798|Felis catus

hierarchy
The first field of the file hierarchy is the entire hierarchy, from tip to tail, for the TSN in the second field represented as a sequence of TSNs separated by a hyphen (-). E.g.,
50|50|0|0|14789
555705-936287-623881|623881|936287|2|415
202423-914154-914156-158852-331030-914179-914181-179913-179916-179925-180539-552304-180580-552363-180586-183798|183798|180586|15|0

Of course, those TSNs can be looked up in the longnames table to convert to something human readable. Using that, here is what the first field of the last line above actually says,
Animalia → Bilateria → Deuterostomia → Chordata → Vertebrata → Gnathostomata → Tetrapoda → Mammalia → Theria → Eutheria → Carnivora → Feliformia → Felidae → Felinae → Felis → Felis catus

synonym_links
The synonym_links file contains a list of obsolete TSNs and the current TSN which should replace them. For example, the TSN for the vernacular mushrooms is given as 14092 (Basidiomycotina). However, that TSN is not in the hierarchy file. Instead, synonym_links points us to use 623881 (Basidiomycota), which works. Here are some synonym entries:
51|50|2015-03-02
14092|623881|2004-01-28
552455|180586|2007-08-15

Example script
If you have access to a UNIX machine (MacOS may work), you can look up any common name by using a simple script I wrote. It will print a taxonomy, just like for European frog above. You can cut and paste the following commands into your terminal to try it out.
① Download the data
    wget https://www.itis.gov/downloads/itisMySQLTables.tar.gz
    tar -axvf itisMySQLTables.tar.gz
    cd itisMySQL*/

② Download my lookup.py script
    wget https://tinyurl.com/yyld2mm4 -O lookup.py
    chmod +x lookup.py

③ Run the script giving it a common name
    ./lookup.py human
    ./lookup.py domestic cat
    ./lookup.py love-lies-bleeding

④ Sample output
    human:
     → Animalia
     → Bilateria
     → Deuterostomia
     → Chordata
     → Vertebrata
     → Gnathostomata
     → Tetrapoda
     → Mammalia
     → Theria
     → Eutheria
     → Primates
     → Haplorrhini
     → Simiiformes
     → Hominoidea
     → Hominidae
     → Homininae
     → Homo
     → Homo sapiens

Have you tried NCBI?  Try this link:
http://www.ncbi.nlm.nih.gov/taxonomy

Sorry, but there's several problems with this answer. It's a different classification, it only has 10% of species, and as far as I can see, there is no database.

@Ferdy: yes there is http://www.ncbi.nlm.nih.gov/guide/taxonomy/

Have you tried ITIS?
http://www.itis.gov/
I once used their database. It was in MS Access format.
EDIT: Now they updated their site, and you may download PostgreSQL, MySQL, SQLite, among other formats: https://www.itis.gov/downloads/

try this one as well:
http://www.catalogueoflife.org/DCA_Export/archive.php
the document with the taxonomy is the taxa.txt document

I suspect you will struggle to find what you are looking for.  However, you could break down your search criteria into smaller chunks to come up with some more successful (but still incomplete) results.  For example, species of what?  Do you really want ALL species (e.g.  Bacteria, Archaea, Eukaryota)?  Do you want just species that are currently alive (extant) or all species that are know to have existed at some point?  Do you want sub-species?
Once you have decided on such things, you may be better off searching for individual country databases.  If you do decide you want ALL species, I suggest you break down each search into smaller chunks - such as 'mammalia'.

He actually don't need to do that. There are a few options to download a full database, as you can see in the other answers.

If you want Reptile data sets these are downloadable files here is the link http://www.reptile-database.org/data/ or if you want a wider and easier search there is https://www.gbif.org/ you might need to sign in though
but in my experience the best data sets for animal species are:
GBIF
and REPTILE DATABASE

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text:
reason for "not for diagnostic use" advice in protocols
I read "not for diagnostic use" in every protocol i saw. why is it so?
which differences have the kits and material that are used for diagnostic purposes?

the FDA has to approve diagnostics - a rigorous and expensive process.  Its a legal distinction, but also one which conveys a significant level of usefulness and reliability.

The quality controls (GMP, GLP and so on) which have to be implemented for diagnostic kits are also ways more complicated, what makes these kits more expensive.

Yes definitely - it takes years and $millions usually.  and its effectiveness has to be clear and reproducible.


text:
Phospholipid Bilayer structural reversal
What would happen if the phospholipids in the phospholipid bi-layer were reversed, the fatty acid tails now facing outwards and the phosphate heads facing inwards? I'm assuming this will not affect the protein channels, but perhaps the loss of cholesterol in the structure of the bi-layer. Would this then mean that the fluid mosaic model no longer holds?

Why should protein channels not be affected ? Even if they are not reversed, environment around them will change which will have a disastrous effect.

I guess that it true, but the point here is to make the inference in the bi-layer structure after the reversal. What would it's characteristics be, and how would it's functions be altered?

DO you mean to ask that if we assume nothing in the proteins change(eventhough that isn't realistic), what will be the impact of reversal of the bilayer ?

For a start, let's just not consider the protein channels unless absolutely necessary.

its easy to do this by the way -just mix the lipids into oil

This would have quite dramatic consequences. The layers are ordered in the way they are, because of their polarity. In the way they are ordered, the hydrophobic tails are inside and directed towards each other, the hydrophilic heads are orientated to the outside and inside. Since both sides of the membrane are surrounded by aqueous solutions, this is necessary to allow a contact between solution and cell membrane and to allow an exchange of molecules between them. If the layers would be oriented the other way, this contact and exchange wouldn't be possible. Proteins channels in the membrane wouldn't be possible as well, since the intermembrane domains are composed preferrably of amino acids with hydrophobic sidechains, while the domains on the outside of the membrane contain more hydrophilic amino acids.
A turn like this would need a completely different composition of life - meaning it couldn't be based on water like it is.

Your answer is sufficient to an extent, @Chris, it implying that the fluid mosaic model is made no longer possible. However, I do not understand why the phosphate heads point outwards while the fatty acid tails point inwards if there was to be diffusion of lipids into the cell. It is conventionally known that lipids dissolve into the phospholipid bi-layer, but how would this be possible as there are phosphate 'heads' present? Imagine a lipid wanting to diffuse into the cell, how will it pass through the phospholipid bi-layer if the phosphate heads are hydrophilic in the first place?

You have to think about how fats (or fatty acids) travel through the blood stream: As small droplets (or micelles) which are organized in the same way: Hydrophilic part outside, hydrophobic part inside. They can fuse with membranes (or are actively taken up) and can so be transported to the cells.

Can you explain how fatty acids travel through the bloodstream or provide a source where I can read further on this matter? Are you referring to 'blood lipids'?

A nice source is the Wikipedia article on blood lipids.

I may have misheard previously that lipids "dissolve" into the membrane. Is it sufficient to say that they fit through the gaps in the Phospholipid bi-layer, therefore not repelled by the phosphates? Do protein channels come into affect this process at any stage?

The lipids travel in form of complexes with proteins which can then dock to the cells via special receptors (the interaction between Apolipoprotein E and the LDL receptor would be such an example). This can lead to the take-up of the lipids by the cell (for example for further break-down) or also into the membrane (for example for cholesterols).

Someone has thought this was a very good question and performed an MD simulation on spontaneous bilayer assembly. There, lipids start in random orientations. The ordered bilayers we know and love spontaneously assemble in under 100ns.
So if the lipids were jumbled up (or even reversed), the would probably reform fairly quickly. I wouldn't imagine that it would do the cell much good though...

If the layer is opposite,then there wont be any cytoplasmic liquid(cytosol) inside the cell, as tail is Hydrophobic.If there is no cytosol,then no function of the cell.Even it becomes difficult to pass substances through the cell when layer is different.

Do you have any source for your answer ?


text:
Photosynthesis: What Powers the Splitting of Water?
The splitting of water is an endergonic (non-spontaneous) reaction, and thus would require energy (chemical work to be done) in order to happen.
In Photosystem II, an enzyme catalyzes this splitting, but where does it get the energy from? Does it use ATP?

I'm kind of confused too. I see that either light or an enzyme powers it.

@jasonszhao An enzyme never powers a reaction on its own, it requires an energy source by non-spontaneous reactions. Which is usually ATP or NADH. By the current reaction the energy is coming from photons, but it is stored in multiple intermediers before getting near to the water molecule.

Catalysis is about reducing the free energy barrier (aka. activation energy) of a reaction, so it does not require any energy. In photolysis (e.g. splitting water) you get the energy from the absorbed photons.
The exact process is called the Joliot-Kok cycle:

Figure 1 - Joliot-Kok cycle - source

So the photon separates the charges on the P680, after that the activated P680 activates the Yz intermedier, which forces the enzyme to the next step (Sx) in the reaction.

2012 - Transmembrane Electric Potential Difference in the Protein–Pigment Complex of Photosystem 2
2006 - The Manganese-calcium oxide cluster of Photosystem II and its assimilation by the Cyanobacteria

The overall process comprises three types of reaction sequences: (a)
  light-induced charge separation leading to formation of the radical
  ion pair P680+QA(-) ; (b) reduction of plastoquinone to plastoquinol
  at the QB site via a two-step reaction sequence with QA(-) as
  reductant and (c) oxidative water splitting into O2 and four protons
  at a manganese-containing catalytic site via a four-step sequence
  driven by P680+ as oxidant and a redox active tyrosine YZ acting as
  mediator.

2007 - Photosystem II: structure and mechanism of the water:plastoquinone oxidoreductase.

So the process does not involve ATP or NAD or something like that just the "redox active tyrosine YZ". ATP and NADPH are created after the PS2 part of photosynthesis.

Figure 2 - Light-dependent reactions of photosynthesis - electron transport chain - source

The photolysis of water is about storing the energy coming from the photons (light) in ATP and NADPH. In the Calvin cycle the cells use the stored energy to reduce CO2 into carbohydrates. For instance glucose can be delivered to the cells in the root, which can use it as food.

So is energy required? Is it catalyzed or powered by light, or both? I don't believe you made it clear.

@jasonszhao I think it's clear. It is catalysed by enzymes and powered by light.

Hmm we could connect PSII directly to a proton exchange membrane fuel cell, so we could convert light to electric current probably more efficiently than the current technologies.

The electrones which are generated from splitting water are later used to split CO2.
The general formula is:

The Photosystem II does the first part of the reaction by splitting up water and transferring electrons to plastoquinone and also by generating H+ ions. Water gets oxidized (spends electrons) in this reaction, CO2 in the end is reduced (receives electrons). 4 photons are needed for splitting 1 water molecule and 8 photons to liberate one molecule of oxygen. For green plants the energy for this reaction comes completely from light. In the process the energy of the electrons is also used to generate ATP, not to use it.
A more detailed view can be found in the schematic diagram "Z-scheme" in the Wikipedia page on photosynthesis:

The figure shows the flow of the electrons and the points when they are brought to higher energy levels by light. The energy of the light is then converted in a proton gradient which is then used to generate ATP.
Its also possible to exchange the role of the oxygen with sulphur, the energy source is then usually heat. This is done by sulphur reducing bacteria in the deep sea in the vicinity of black smokers.

What's the difference between liberating oxygen from water and splitting water? 2) The OP asked how the water splits, not why it splits. 3) The OP also stated that an enzyme splits water. I can confirm this from the Bio textbook by Miller and Levine, "Enzymes on the inner surface of the thylakoid membrane break up each water molecule..."

@jasonszhao The difference between splitting and liberating are semantics. Chemically you use the energy of the light the split the water molecule in its parts.

Other two of them are describing very details and these are good answers.
Lights are the energy source, activating the enzymes to split $\ce{H_2O}$. When a chlorophyll in photosystem II reaction center absorbs light energy, an electron is released. This is the activated state energized by lights and has enough energy/ability to suck up electrons from $\ce{H_2O}$.
$\ce{2H_2O \rightarrow 4H^+ + 4e^- + O_2}$

Water oxidation chemistry of photosystem II
Light is indeed the energy required for the process to occur! The photosystem chlorophyll involved is P680. The light energy excites an electron to a higher level, and this electron is captured by pheophytin, forming P680+. The redox potential for P680+ is huge, 1.3V, and it becomes a very strong oxidizing agent, regenerating it's lost electron from water during the oxygen-evolving process. The electron that went to pheophytin ends up transferring to QA, then to QB (these are involved elsewhere).
So now, the P680+ oxidizes this redox-active tyrosine residue called Yz by taking an electron. This forces the Yz into a radical state Yz*. As the article goes on to provide, data showed the Yz hydroxyl group pKa to be greater than 9, meaning it should be protonated at physiological pH. As a result, in concert with the electron transfer outlined above, a proton is donated from Yz* to a nearby base: histidine 190. In this manner, Yz* is capable of quickly oxidizing the nearby tetranuclear manganese cluster. An oxygen-evolving complex is formed by Yz, Mn4, Ca, Cl, and a couple of additional amino acids. Yz oxidizes the manganese cluster resulting in transition states denoted S1-S4:

The heavily oxidized Mn cluster then oxidizes water to return to an S0 state, forming O2 as a part of the process.
The authors detail:

We propose
  that O–O bond formation occurs in the S4 state via nucleophilic
  attack on an electron-deficient MnV=O species by
  a Ca2-bound water molecule... O–O bond formation begins by bringing the second
  substrate water closer to the MnV=O in an SN2-like reaction
  (S4 state in figure 2). We propose that this occurs
  through contraction of the Mn–Cl bond upon formation
  of the high-valent MnV=O moiety.

In conclusion, we see light powers the reaction, but it is mediated by protein. The net reaction is an oxidation of a metalloenzyme complex which essentially rips the hydrogens off of water molecules to return to it's standard state. The article used for this answer was the best explanation, with a lot of details, that I could personally find, but it is from 2002. If someone has a more accurate explanation let me know!


text:
How much influence does toxoplasmosis have on personality and intelligence?
Latent toxoplasmosis affects up to 1/3 of the human population and up to 40% of the population in Australia.  I have heard that latent toxoplasmosis has many significant undesirable effects on personality, such as decreased novelty-seeking behaviour, and decreased intelligence quotient.
While these changes are statistically significant, I'm wondering if anyone knows the magnitude of these personality and cognitive changes, since a statistically significant result doesn't necessarily imply that there is a large difference in personality between those who are infected and those who aren't infected.  Also, can one succeed in an academic career path if one becomes infected with toxoplasmosis?

Do you have some sources for this wide-spread infection? Would be interesting to read.

Heaps of sources, have to go now, but i'll post later.  Just search on google or google scholar in the mean time if you want to.

@Chris in France pregnant women are routinely tested for toxoplasmosis, since contracting it for the first time during the pregnancy may pose risks to the child.

@Kenshin scientific research or simple interest in studying can be also characterized as a "novelty-seeking behaviors" ;)

I believe its the other way around - humans may engage in riskier and more novel behavior when infected... which is the most interesting part of the story.  Its not cut and dried, but I think its quite possible that risky behavior increases.
T. gondii is a parasite whose typical life cycle includes both mice and cats as hosts.  The transmission involves the mice being eaten by a cat.  Mice infected with T gondii will tend to lose some interest in being sheltered in close spaces and wander out into open spaces.  They also lose their fear of cats.   That is a permanent change even if the mice are cleared of the parasite.
Other animals, such as humans are secondary hosts - they can become infected by handling or close proximity to cat feces, who have a nearly 50% (45.6%) infection rate themselves. As a result toxoplasmosis is very common in humans.
Toxoplasmosis has been found to increase novelty seeking and increases risk seeking behavior at least in men.  Its been shown to contribute to higher automotive accident rates, schitzophrenia and suicide.

Thus, the men were more likely to disregard rules and were more expedient, suspicious, jealous, and dogmatic. The personality of infected women, by contrast, showed higher warmth and higher superego strength (factors A and G on Cattell's 16PF), suggesting that they were more warm hearted, outgoing, conscientious, persistent, and moralistic. Both men and women had significantly higher apprehension (factor O) compared with the uninfected controls.

The correlation between toxoplasmosis and lower intelligence is a matter of debate, at least in this review I cite.  Its still not clear whether it is a sociological correlation - do smart people just handle their cat poo more carefully or not at all? This more recent study shows that some factors might make infected humans more intelligent and some researchers see toxoplasmosis as a transformative factor in humans ability to generate and use technologies.
I do see those links suggesting less risky behavior too.  Some say that the increase in traffic accidents is related to lower muscular coordination for instance.  There is evidence on both sides, but looking at what T gondii does to mice, I would bet that some risk behavior will increase.  As such, I'd guess that researchers as such might have a slightly higher rate of toxoplasmosis, but maybe you will do a study and help figure this out!
That being said - anyone who tries to link a single phenomenon; host-parasite interactions; a drug; a gene; a mutation to a phenotype with a simple description is definitely oversimplifying.  The mapping from biological activity to english (or any other language) is hopefully conscious of the caveats of such talk.

Thanks for your answer shigeta.  I find it interesting because many of the links I had seen say it lowers novelty seeking behaviour.  http://www.sciencedirect.com/science/article/pii/S0301051103000759.  http://web.natur.cuni.cz/~flegr/pdf/toxonovelty.pdf

let me add a comment in the answer here - you are right of course, but its not a simple yes/no thing.  I'll be a little more clear about this.

It is my understanding that toxoplasmosis can increase productivity and the brain's ability to understand things. It is when there is a toxo flare that behaviors can become irrational and angry. Knowing this can help as well as being in touch with when you are experiencing a flare. Knowing what range you have, if its active, and what supportives you will need to get it under control should help.
The Revolving Therapies have the best chance of putting folks into remission according to the following information:
*Together with the result of the checklist, the significantly positive Toxoplasma LTT overruled the result of the antibody assays and justified prescribing a combination therapy from the beginning on. This resulted in a good amelioration of symptoms. When the effect of this therapy decreased after 10 days, the significant toxoplasma LTT result backed the decision for a Revolving Therapy, which finally led to a very good remission of all symptoms. *
https://en.toxoplasmachronic.com/2-faelle-mit-positivem-ltt?fbclid=IwAR2VknK1asw1OoWuedVpRi_TOGaxjDsf6LxWoLM7HKPfxZaHe3AIf1YI5N4

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


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Autoimmunity and central tolerance
Where in the body are self antigens important? In terms of central tolerance and autoimmunity, but also in terms of T cell activation?

Could you clarify a bit? What do you mean by important? Most problematic? Most relevant? I assume the body you refer to is the human one?

This was a question in a PhD defense so I can only add my own interpretation. It's in the mouse and by important I mean anything really, relevant for proper development, where defects may lead to autoimmunity, and/or poor activation...I'm not entirely sure.

There can be many responses. They are important for alloimmunity (so by transfusion, transplantation, etc...), for recognizing pathogens, cancer, virus, etc... By T cell activation, the regulator T cells recognize these antigens as self, and prevent the autoimmune reaction.
I guess they were thinking on MHC1 and MHC2. MHC1 shows the inside of the cells, so e.g. by viral infection or cancer non-self oligopeptides (from degraded proteins) bind to MHC1. These non-self antigens are recognized by CD8+ T cells, which destroy the affected cells. MHC2 is used by APCs to present possible pathogens to CD4+ T cells in a similar way.

Self-antigens are not recognized by the body. This is due to self-antigens being presented to the immune system of the body during the embryological development. Any immune cell which recognize the pattern are destroyed during the intrauterine period, preventing the emergence of Auto-immunity in the Life-time.
Self-antigens become important in the following situations:

There are self-antigens, called cryptic antigen, which are not presented to the immune system during embryologic development. These antigens generally are not present on the cell surface or they are present behind a barrier which is usually not penetrated by the immune cells. Eg.: The sperm antigens are not usually exposed to immune system as the sperms are behind the blood-testis barrier. Other such barriers are blood brain barrier, blood retina barrier, etc...

This is important because if for some reason (infection, trauma, etc...) such antigens get into the general circulation they will cause an immune reaction leading to autoimmunity

Self antigens play a role in graft rejection and transfusion reactions. This is mediated specially by the T-cells. This is the reason why transplant patients receive life-long immune supressants and cross-match is done before transfusion
Self-antigen non-recognition also means non-self antigen recognition. This is the basis of cells infected with viruses or tumor cells getting destroyed. As the new protein peptides (viral or mutated regular proteins) presented by the MHC 1 are not recognised as self, such cells are destroyed protecting the body
The corollary of 3 is that any pathogen which resembles the self-antigen are tolerated and active immunity does not come into play i.e. the epitopes that are recognized as self do not cause any immune response
Some pathogens have antigens that closely resemble human antigens. When T-cells mount response against such antigens, a specific sub-clone of T-cell or B-cell (which are activated by the T-cell) may gain the ability to act against the body cells (due to mutations in the hotspots of the anti-topes) that have antigEns resembling the pathogens. This is called molecular mimicry. A well established disease that is due to this mechanism is the Rheumatic Heart Disease. Post-streptococcal Glomerulonephritis is also another example.

That is the old model of the immune system. There are many other models, which are closer to the reality. E.g. many self recognizing cells become regulating cells instead of dying, and a lot of non self cells (microbes) can be tolerated by the immune system until they don't cause cell death and other messy things... By auto immunity, not just the molecular mimicry is the problem, e.g. a single T cell can have different receptors, so one of the receptors can be self recognizing, while the others can recognize a pathogen, and so on... Immunology is very complicated...

I see, I think I have to read on the newer models then. Can you suggest a good source?

http://scholar.google.hu/ :-) I have the same problem, I read mostly reviews and scientific articles, probably dissertations if have more time. I don't know of a book which is up to date. E.g. none of the ones I checked, mention gasotransmitters, which is a relatively new topic in immunology. Wikipedia is often incomplete, or sometimes even completely wrong. I'll try to make an own wiki, but I have too many tasks: developing programming framework, learning stock exchange indicators, learning data mining, learning immunology, making training plans, etc... 24h in a day is simply not enough. :S

Please let me know if you've found a book worth to read!

http://en.wikipedia.org/wiki/Danger_model Be aware that wikipedia is not a reliable scientific resource, so if you want to learn this in depth, you have to find scientific articles and reviews in the topic.

I think there are no set models (completely proven models). I can't read Hungarian though! Thanks for reference. Will post a book if I find one

Ohh sorry :D http://scholar.google.com (was redirected automatically by google)


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Why temporal lobe is called temporal?
http://en.wikipedia.org/wiki/Temporal_lobe
Does this have something to do with tempo (time?)
Temporal lobe is behind (posterior) to frontal lobe, inferior to parietal lobe and is in front of occipital lobe.
Why it's called temporal?

The temporal lobe is in the temporal region of the head, near the temples of the skull, hence the name. It's name does not relate to it's biological function, it is mainly involved in processing language, visual memories, and emotions. The medulla oblongata is one region of the brain that deals with a lot of the "tempo" type functions (tempo as in keeping rhythm) such as controlling the heart beat and breathing rate.

Temple indicates the side of the head behind the eyes.

The different etymologies of temporal can be found on this wiki article

yes, temporal in this sense has a different etymological root to tempo.

is temporal means sideways?


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Does amylolysis occur in vegetables if stored below 0⁰ Celsius?
Assume that we have a plant, e.g. kale, which is prone to amylolysis if not harvested during a frost period.
If it is harvested and put in a household freezer, such that it is frozen solid slowly enough for cell walls to burst, will the amylolysis stop, or will it still occur? Will it occur if it is kept in a fridge in the 0-4 Celsius range? If it does not occur while the vegetable is frozen, will it start after thawing?

I think it will be at least delayed. Enzymes habe an optimal temperature at which they work best. I don't know this for this special amylose, but at 0°C it will definitely be much slower. The rate of the enzyme will not be zero though...

@Chris interesting. I thought that maybe my question is too silly to ask, and half expected to get an answer saying "once the cell plasma is frozen, all biological processes cease because enzymes, hormones etc. can't move around".

I was thinking about 0°C, not freezing. When you freeze the plants, the enzymes will be not functional. The backside is that you probably break cells with the freezing and set free the enzymes.

@Chris what do you mean by "set free the enzymes"? Does this mean that they will start converting the starch upon thawing independent of ambient temperature, because they are free now? I am afraid my mental model of the whole process is very incomplete. You will certainly break cell walls, this is very noticeable with thawed vegetables.

With "set free" I mean that the enzymes can work not only inside the cell but also outside, since the interiour of the broken cells is set free. This is especially a problem when you work with lysed cells and protein degrading enzymes. Its probably no problem here.

Yes. Freezing would practically stop all biochemical reactions. Household freezer can maintain -15⁰C so that would work. However, freezing also damages the cells if cryoprotectants are not used. But I guess that is not your concern.


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Confused at what is happening with these action potentials
Ok so for a bit of a background, I am doing a science project looking at the action potentials of the earthworm. I anaesthatized the worms then hooked them up to a spiker box (http://backyardbrains.com/products/spikerbox) and stimulated them.
This is an average result:

What I am confused about is why the action potential goes negative first before then going back up. From my readings online, I thought that the action potentials were meant to go up first then travel down and then continue on its course. If it helps I used a program called audacity to record the action potentials.
Thanks very much guys. Sorry if I'm not being clear. Just ask anything if you need more information!

Nice graph. What happens when you reach the top of the potential (when you depolarize the membrane) that you need to go back to a resting potential to be able to stimulized again. The membrane gets "neutralized" and this reaction often over-shoots and goes below the resting potential, which is quite normal. Before reaching the normal resting potential there will be no further activation. The Wikipedia article on the "Action Potential" contains a more complete explanation.

This answers why it hyperpolarizes after reaching the peak but why does it hyperpolarize BEFORE the action potential ?

In the graph above? My guess would be that two pulses of activation come directly behind each other.

Sorry for not responding (christmas stuff). @Chris - could you please expand that a bit more? Oh a bit more information about the earthworm incase this influences how it goes negative first: they have 3 main nerve cords carrying the action potentials, 2 of them carrying the signals down the worm and the other transmitting them to the front. Would this at all influence it?

Do you record the impulse from one isolated nerve or is it possible that you record more than one?

Hm that is possible. Because the equipment I was using was not specifically "designed" for worms (it was designed for cockroaches) I have no way of knowing. If you go to the website that I have put here it has a photo of the pins which you put into the worm. However, if it is true that the results are being influenced by the other nearby nerves sending their signals, why is it the same for all the action potentials I recorded? I have around 50 photos which are almost identical to the one above (length wise).

Ok, that makes it unlikely. I was simply thinking about explanations for this signal.

Hm damn. Im really trying to figure this out I'm presenting this project at the national science fair in  2 weeks and I need an explanation :/  is it at all possible that it is just that the earthworms nervous system acts differently? Could it possibly be that (just making something up here) in the earthworm there isn't that polarity that is present in other axons? Maybe there is an even distribution of sodium and potassium ions on either side of the axon?

Did you ever get an answer to your question? I know this may be too late now, but I was noseying around and spotted it, so I'll take a stab nonetheless. I could be wrong, but I suspect what you're seeing here may be an extracellular representation of an action potential (and/or it could be a filtering artefact, see below). From the video on the spikerbox website, it looks like you place the electrodes (nails?) into the animal and hope to get close to axons and see spiking activity. Correct me if I'm wrong.
From a brief reading of the literature it would appear, under optimal conditions, the waveform of the extracellular action potential (EAP) is dependent on the cell type and location of the electrode along the neuron (this paper illustrates this nicely). As you move away from the soma and down the axon/dendrites, you tend to see this more prominent initial spike, as you see in your recordings. This is due to the ionic conductances and timings of channel openings. So that's one possible explanation...

Here's the other: the signal is filtered in some way. I notice in your figure your signal is very smooth without any noise and your EAP very long (assuming your x axis is seconds), which suggests to me your acquisition rate is quite low and/or being filtered. I've attached an image of an EAP I acquired (from a cell soma) a while back (with an acquisition rate of 10Khz, i.e. I 'sampled' the signal 10000 times per second to get the trace). They're all the same EAP on the same scale with different types of filters applied. The original signal is the one on the left; note all that baseline noise. The middle one is a low pass filter of 2KHz (gets rid of signals higher than that). The right hand one is a 750 - 1000 Hz band pass filter. This type of filter does funky things to signals if used incorrectly (such as in this example!). It basically only allows signals within a given region and gets rid of signals outside of it. What you end up with is the signal on the right, which looks suspiciously like yours!
So I'd hazard a guess and say it's a problem due to how the system collects and filters data. BUT, there could be a biological basis for it too.
However, there is one thing that does confuse me, and that is the polarity of your waveform. I would normally expect the prominent point of your EAP to be pointing downward. I have two suggestions as to what may be the cause of this:

You're actually measuring currents here; the units for your Y-axis would help answer that one.
Some grounding issue.


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Can humans transdermally absorb minerals from ocean water, and if so how much?
According to several studies quoted here, chemicals can be absorbed by the skin transdermally, at least under certain conditions.
When it comes to elements in seawater like sodium, magnesium, potassium and iodine, is it possible for a human to absorb them transdermally in this instance?
If it depends on various conditions, (such as length of time spent in the ocean, physiological factors (e.g. intense swimming vs. gentle bathing), temperature of the water and their respective effects on skin porousness or other factors affecting transdermal absorption), what would be they be?
And if it can indeed be absorbed (e.g. from open water swimming), are the amounts significant to even measure alongside that of recommended levels for human dietary intake by advisory bodies such as FDA for those mentioned elements, or is it an extremely small amount much smaller than dietary levels of mineral intake?

I found this article where swimming in the ocean reportedly cured a lady of psoriasis. http://realrawfood.com/article/magnesium-principles-and-practices-transdermal-therapy

There is not very much transport of ions or water through the upper layer of the skin, mainly responsible for that is the stratum corneum (SC). Through this layer you will get only with small lipids and also substances which are able to penetrate the lipid layer of the cells like chloroform or DMSO. I think therefore that it is pretty unlikely that you can take up noteworthy amounts of ions (which would have to pass through the lipid layer of the cells which is highly hygrophobic) through the skin. Have a look at these publications:

Routes of ionic permeability through mammalian skin
Skin permeabilization for transdermal drug delivery: recent advances
and future prospects.

Interestingly this is different for other animals. The pacific hagfish is able to resorb organic nutients through his skin, see this article or this publication:

Adaptations to in situ feeding: novel nutrient acquisition pathways
in an ancient vertebrate

I doubt it would be efficient. Your skin is a tight, water proof membrane designed to keep water and ions and other molecules inside while keeping the outside out. The molecules that are absorbed through the skin tend to be hydrophobic organic molecules. Ions, which any dissolved salt in water would become, do not easily pass through cellular membranes or your skin. If your skin is damaged, it may have tiny holes, which would allow ions into your blood. If the link provided in the comment can be trusted ( realrawfood.com... ), and I'm skeptical, the psoriasis could have caused the damaged needed to let ions in, but I AM HIGHLY SKEPTICAL OF THESE CLAIMS. There is nothing magical about the ions in seawater. You could dissolve the same salts in distilled water and fill a bath tub with it and achieve the same non-results.


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Paired-end mapping exercise
Pair-end mapping (PEM) is a technique that allows to detect structural variants in DNA by obtaining paired-end reads and the comparison of their positions in a reference genome.
Then among libraries that had insertion of 500bp, 2kb, 10kb and 40kb which one would you pick to detect the following inversions?
a) an inversion mediated by inverted repeats of 20 kb at its breakpoints
b) an inversion with clean breakpoints (no inverted repeats)
c) an inversion mediated by inverted repeats of 1 kb at its breakpoints

My guesses:
a) 40kb, as if it were to be smaller than the inverted repeats length, the pair ends may align inside and nothing would be detected
b) Medium size, as if it is too small it wouldn't probably cover the area desired, and if it were bigger it would overlap too much (anyway data is needed for and answer is a blind optimization)
c) 2kb. same reasonings as a) and b).


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Standard Classification of Disease
I am working on a project for health center. It involves the creation of a database of all diseases. Currently I want to classify disease on the base of their category based on international standard.
Did anyone know where i can find one, I did a lot of research but was only able to come across this which seem not very useful to me: ICD

The two I know of off the top of my head are

OMIM : Online Mendelian Inheritance in Man. This is very good and very well organized but only deals with inheritable diseases, no infections etc.

Human disease ontology. From their webpage:

The Disease Ontology has been developed as a standardized ontology for human disease with the purpose of providing the biomedical community with consistent, reusable and sustainable descriptions of human disease terms, phenotype characteristics and related medical vocabulary disease concepts through collaborative efforts of researchers at Northwestern University, Center for Genetic Medicine and the University of Maryland School of Medicine, Institute for Genome Sciences.

The DO is probably perfect for your needs.

I don't know if you're also interested in mental health issues, but the DSM (Diagnostic and Statistical Manual of Mental Disorders) is the standard typology for that subject area.
edit: I see that the Disease Ontology that @terdon lists also has mental health as a category.


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When was it determined that Type 1 Diabetes is an autoimmune disease?
I just found out today that type 1 diabetes is an autoimmune disease.  When was this discovered?

It probably would help people answering the question if you could link or quote from the source where you found this out.

This question has two answers: The difference was first described in 1936 by Harold Percival Himsworth, which described it in this article.
At this time it was established that there are two forms of Diabetes, one sensitive to insuline while the other is not.
The terms Diabetes type 1 and 2 where established somewhere between 1974 and 1976, for details see the review "The discovery of type 1 Diabetes".

Thanks.  From the "discovery" article it appears the autoimmune theory really solidified around 1974.

It takes a while until such a concept is widely accepted.


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Transcription takes place from the 5’ to the 3’ end of the m-RNA. Why?
Only one side of the DNA ladder is copied (the sense side). The sense side starts with a 3’ end. This means the corresponding mRNA will have to assemble starting from the 5’ end. This is my initial thought, but can someone expand on it? Also, is this explained by why replication is performed in the 5' to 3' direction as suggested by this thread: Why is DNA replication  performed in the 5' to 3' direction?

Is the DNA template strand the same as the DNA sense strand?

No. Suppose your mRNA sequence from 5'to 3' is AGUC. Then, TEMPLATE strand is 3'-TCAG -5' but coding and sense strand is 5'AGTC3' i.e. complementary of the template strand and to the mRNA. This is a bit tricky so let someone else confirm this....

It seems as though the nomenclature for DNA sense and template strand can be same or differentiable as suggested by this: http://www.sci.sdsu.edu/~smaloy/MicrobialGenetics/topics/chroms-genes-prots/temp-strand.html

it is not about RNA or DNA.. the chemistry of the polymerases and the substrates (NTP) cause this directionality.

I had read about template,sense and coding from  here

I have also seen  the authors of my textbooks  use the same nomenclature.

The reason why the polymerization of DNA/RNA strands only happens in 5' -> 3' direction is because the polymerases can only add new nucleotides a the 3'OH-group of the existing strand linking it with the 5'-C of the next nucleotide.

The argument put forward at the link provided by @Cloud, that the DNA strand with the same sequence as the mRNA might be called the template strand because it is translated into a protein is illogical. The "template" referred to in the phrase "template strand" is the template for transcription - even the transcription of a sequence which will not encode a protein, rRNA for example, requires a template.


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Colchicine addition to cells

When is colchicine added to dividing cells for karyotype studies?

I know that colchicine inhibits polymerization of microtubules.
2 So, why should it stop the cell cycle at metaphase when microtubules have already assembled and the next step(anaphase) requires depolymerization rather than polymerization ?

colchicine is used to synchronize the cells.. so whenever you add it, the cells will eventually be arrested at metaphase.

Colchicine inhibits the formation of the microtubules by binding to tubilin and rendering it unavailable for the polymerization. Thats why the cells get arrested in the metaphase and can not go on further in the cell cycle and divide. For chromosome studies this is very useful since this is the phase where the chromatin is most condensed and can be viewed best. It inhibits the positive side producing the microtubules to prevent it from moving to the negative side, in cell division.

I would like to point out that copying from wikipedia without mentioning it as a source is not allowed here.

Sorry, but I haven't looked up this in Wikipedia. Since I have done this stuff myself in the lab I know the background. But I can remove the answer.

In fact I should say sorry because I thought that I had read that exact lines on wikipedia. I looked it up and you say the same thing but not in the same exact words. I really am sorry , I should not have written the comment without confirming.

Fine for me, such things happen.

Thanks. I have one question : I still do not understand why binding tubulin would lead to arrest at metaphase. By metaphase, the whole spindle is complete so why will anything that does not allow polymerization to occur affect this ? Doesn't only depolymerization happen after metaphase ?

@biogirl When the cells are in the metaphase they have their spindles and can divide. But in cells, which are not, the spindle apparatus can not be build (because the tubulin is not available for it) and the cells get stuck in what I would call early metaphase (there is no further differentiation for this step, so its all called metaphase). The cells get ready for dividing (chromatin gets condensed and so on) but the cells can't go on.

let us continue this discussion in chat

@biogirl there is a cell cycle checkpoint for the full formation of the mitotic spindle, and a cell poisoned by colchicine will never pass this checkpoint, hence it will never progress to anaphase.

@chris When exactly is colchicine added for chromosomal studies ?

There is no exact timepoint, since the cells are not synchronized in respect to their growth phase. You simply add it to the proliferating cell culture (meaning the cells are still in the growth phase). You can find a protocol here.


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What is a phospho-protein binding domain?
Is this just a domain that binds proteins that have been phosphorylated? And it mediates signalling between an activated/phosphorylated protein? How is this significant with BRCA1?

Do you have some reference that you're reading, or some more context?

A phospho-protein binding domain binds phosphorylated proteins. For which purpose it does this, depends on the protein. To tell more about it, more background would be nice.

This is a very large topic but I will try to partially provide an answer. Now your question has three parts as far as I understand it.

Do phospho-protein binding domains only bind to phosphorylated proteins i.e. is that their sole (observed) function.
What roles do phospho-protein binding domains mediate.
Function of BRCA1 phosphorylation/phospho-protein binding

Just to get some basics out of the way, there are three amino-acid residues in a protein that can become post-translationally modified by phosphorylation, including serine, threonine and tyrosine. Now the purpose of protein phosphorylation ranges from activation/deactivation signals to binding and changing cellular localisation i.e. recruiting a protein to different part of a cell. Now tyrosine phosphorylation, which I know by far the most about is capable of all the above. So if you think about a receptor tyrosine kinase (RTK) such as epidermal growth factor receptor (EGFR), once a ligand such as EGF binds to it, it becomes tyrosine phosphorylated (activated) through its intrinsic tyrosine kinase activity. Once tyrosine phosphorylated, many proteins are capable of binding to tyrosine-phosphorylated RTKs such as Grb2 to induce a signal downstream of RTKs. So as you can see, phosphorylation of RTK affected cellular localisation of GRB2. Excellent Ras signalling review by Karnoub & Weinberg, 2008 Nature reviews (Fig 5). Grb2 binds to phospho-RTKs through a specific domain called Src-homology 2 (SH2) domain, which provides a platform for other proteins such as Son of sevenless (SOS) which is a GEF to bind to it and induce RTK signalling through Ras. So in the above case the role of phospho-protein binding domain (SH2) is to change cellular localisation of multiple proteins and mediate signalling.
Now I'm no expert in BRCA1 but just had a quick look and it seems serine phosphorylation of BRCA1 may be responsible for its recruitment to the DNA site of damage and if serine residues in BRCA1 are mutated, the protein will no longer get phosphorylated, which may effect its recruitment to the DNA sites of damage, which may affect its DNA damage response function (Clark et al 2012 Comput Struct Biotechnol J). Now BRCA has a phospho-protein binding domain called BRCT, and that is also thought to mediate DNA binding and binds to phosphorylated and non-phosphorylated proteins. So BRCA1 phosphorylation and phospho-protein binding is though to be important in its function (Clark et al 2012 Comput Struct Biotechnol J). So to answer your question in short, phospho-protein binding domains such as BRCT do not necessarily bind to their target proteins through phosphorylation.
Hope this helps.


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Is light required for seed germination?
Is light required for germination of every seed? If not, why don't some plants require it? Is there any difference in the quality and duration of light required ?
It would be interesting if someone could give both  physiological and evolutionary reasons.

Given that germination often happens underground, the answer seems trivially “no”, doesn’t it?

@konrad My first thoughts were the same ! but then I came across  an experiment in which they had exposed seeds to different wavelenghts of light  and they got difference in no of germinated seedlings.

The riddle can be solved by realising that different plants have different requirements, and that some requirements are “soft” – i.e. not absolutely necessary but nevertheless beneficial. I’ll let somebody else with more knowledge provide a more in-depth answer – my comment wasn’t meant to imply that this is a bad question.

Botany was long ago, but if I remember correct, the germination happens usually underground as the seeds contain enough material to supply the developing plant for a while. When it comes through the surface it usually needs light to do photosynthesis to grow further. Most seedlings orientate towards the light.

The short answer is that many species do require light for germination (either to initiate germination or to break dormancy). Some require light of a specific wavelength, and some don't require light. Still others actually require absolute darkness, or the absence of specific wavelengths.

@KonradRudolph in many species, germination can happen underground but not so far that light doesn't penetrate.

Here's a partial answer, based more on common-sense then in-depth knowledge:
Physiological. One reason light is not required immediately is that many seeds are in essence bundles of stored energy (as carbohydrates, I suppose). This is what makes them attractive food for birds, squirrels, humans, etc. When they're able to escape that predation, the growing plant can use that stored energy, rather than relying only on sunlight.
Evolutionary. Seed dormancy can be a powerful tool for fitness – seeds that can remain dormant and germinate during favorable conditions could have a much higher survival rate. These conditions vary from simple: "spring" to more complex: "after having passed through the digestive system of a certain animal"; "after a forest fire"; "when there's a gap in canopy cover / less competition for solar energy". The cues that seeds "read" in order to try to break dormancy and germinate during these times therefore vary among species. Within species, there are probably often a number of cues, and as @Konrad Rudolph suggests these are probably all relatively "soft", or at least act in complex interaction with one another.


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How does a prophage leave the host cell's genome?
I understand that, unlike a prophage, a provirus never leaves the genome, but I don't understand how the prophage "leaves".

The prophage is usually activated by cellular stress (bad nutrient conditions, toxic environment and so on) or cell damage.

This is explained reasonably well at the Wikipedia entry for phage λ, which is the prototype lysogenic phage. Basically, integration occurs by site-specific recombination between the attP region on the phage genome and the attB region in the host genome. This means that in the prophage form the phage DNA is flanked by direct repeats. Excision involves the reverse process - recombination between these direct repeats. Excision is promoted by the phage-encoded Xis and Int proteins in combination with the host protein Ihf. The regulatory cascade which links cellular stress to this recombination event is detailed at the linked page.


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Determining limiting nutrients from a graph
The question was
Which of the following statements is supported by these data?
A. Phosphorus was the first limiting nutrient followed by nitrogen.
B. Nitrogen was the first limiting nutrient followed by phosphorus.
C. Phosphorus was limiting but nitrogen was not limiting.
D. Nitrogen was limiting but phosphorus was not limiting.
E. Neither nitrogen nor phosphorus was limiting.

The answer was B: Nitrogen is the first limiting nutrient followed by phosphorus, but I do not know why. I thought it would be only phosphorus as the Nitrogen values are always greater than the control values.

The control graph shows the baseline against which we can compare the other graphs. It is the graph without any changes, and hence is the graph in which one of the nutrient is limiting.
In the graph for +P, there is no rise in biomass and the graph resembles the control. This shows that Phosphorous is not the first(initial) limiting nutrient, as its addition did not affect the biomass production.
The +N graph shows a significant rise in biomass, indicating that N was indeed the initial limiting nutrient. On its addition, the biomass production increased.
The +N and +P graph shows a higher biomass than +N and the control. This indicates, that while  N was established to be the first(initial) limiting reagent, addition of Phosphorous also significantly improves the biomass yield, and hence P must also have become a limiting nutrient once N was added and its limiting effect removed. That is the reason why +N+P graph is higher than just +N graph. If phosphorous would not have been limiting even on addition of N, then the +N+P graph would have resembled +N graph.


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Current human behavior as a genetic heritage
People: I have doubts about genetic heritage, but let me explain the context which has shown up this doubt for you: I was debating about sexism and the following question were put on the discussion: What kind of behavior, most of them come from men, is cultural and social, and what is a genetical heritage from our ancestry? Because I have a feeling that plenty of these behaviors that can be considered, maybe not correct, but at least justifiable. If you have some literature about this subject I would greatly appreciate it.

This is the subject of an entire field - evolutionary psychology http://en.wikipedia.org/wiki/Evolutionary_psychologist

All phenotypic traits have some part of the variance which is explained by the environment and  some part that is explained by the genes. The heritability is then defined as:
$$H_N = \frac{V_{genetic}}{V_{phenotype}} = \frac{V_{genetic}}{V_{genetic}+V_{environment}+V_{interaction. gene.environment}}$$
where $V_{genetic}$ is the Variance in phenotypic traits due to genes, $V_{phenotype}$ is the total phenotypic variance, $V_{environment}$ is the variance due to environment and $V_{interaction. gene.environment}$ is the variance due to interaction between genes and environment.
So your question (if I understand it correctly) should rather be a list of phenotypic traits (behavior) and ask what is the heritability of each trait in the world-wide human population (or on a given subset of the human population).
I think, there is no objective manner of defining a given phenotypic trait. You should chose subjectively, some behavior, define it accurately and then ask the question what is it's heritability.
Moreover, it is quite hard to measure a behavior. It is much easier to estimate the heritability of height in humans.
There are several different methods in order to estimate heritability of a trait. See this wikipedia article
Some of these experiments are not feasible on humans for ethical reasons. Some others are quite limited and are quite expensive. I don't think we have many studies that quantify the heritability of behavioral traits in humans but I might be mistaken.
As said by @AlanBoyd, there is a field called evolutionary psychology that deal with this kind of question. To my knowledge this field is mostly a purely theoretical field and therefore, it does not quite allow to measure heritability.
A good start into this science would be the wikipedia article which seems quite complete.  I can give you some books but I haven't read most of them. Here and here are introductory books in the field. I think this book is a classic in the field. I read this book and it is quite interesting. There are actually many books in this field. The best think you can do is maybe to typewrite "evolutionary psychology" in amazon.
As a sidenote: If you enter in the field of evolutionary psychology you might as well be interested by memetic evolution (evolution of culture). Here is a classic book on the subject.
Be careful in these fields, I think that some ideas do not deserve to be considered as part of science while other do!

Thank you, it helped a lot. Those articles and books that you recommended will be a good start. As i'm not from the biological field of science, so these kind of subjects makes me a little bit confused. I'd ask more especifc questions, but i'll read those material first, maybe it will clear some things to me. Thank you again, guys.


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How far does the diaphragm stretch when it contracts?
How far, exactly, does the diaphragm stretch during tidal breathing, and what is the maximum length it can stretch? I have been wondering about this for the entire day today, and I can't seem to find an answer.


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Why is dimethyltryptamine (DMT) released during death?
Many times I've come across a theory that the meaning of life itself is procreation - we simply live in order to make our species exist as long as possible. In the light of this theory, units like homosexuals or infertile people are totally useless and there's no really reason for them to exist from biological point of view. Though it's pretty obvious that in order to make us want to reproduce, something like joy of having sexual intercourse and life in general has been created. That's why units who only lack in ability to reproduce do live and most of the time they're fine.
Evolution doing adjustments in us in order to make us feel happy during our life seems to be understandable, but what about death? I've read that during death, a larger amount of DMT substance is being released in the brain - compound which is known from it's psychedelic effects, which in most cases are euphoric. It looks like we're not meant to feel 'bad' while dying, which is nice, but my question is - is it known why? What could be the evolutionary reason to create this mechanism? The unit which is about to die is not going to be useful anymore, so why bother? I'd like to somehow understand logic behind this.

As with many such questions, it may be impossible for us to infer why this trait evolved.

are there any studies backing up this claim?

Homosexuals enjoy the all masculine environment of military and have less worry about escaping to go back to their family. The reasoning that individual and group fitness are dissociated is lacks depth, because survival of humans has been tribal, not just individualistic, since prehistory. For the DMT claim, a reference or concise claim would be less vague.

The issue I suspect you are struggling with is the anthropomorphization of the evolutionary process.  Evolution is an optimization process driven by random mechanisms...i.e. there is often not a "reason" for why certain things are the way they are.  Evolution is not a conscious "designer" that produces things with a specific goal in mind...it simply "picks" the best random alteration and enhances it.  If there is no "best mutation", then there is no selection pressure to drive change overtime.
For example, one can ask, "Why do humans have 5 fingers on each hand, instead of 6 or 4?"  There is no answer, because the question itself is nonsensical.  Humans have 5 fingers simply because there is no pressure to drive a change to 6 or fingers, and so it boils down to randomness.  There is no "reason" humans have 2 arms, as opposed to 4.  That particular trait just randomly happened to be the one which became dominant.
So, to return to your question of "Why does the brain release DMT when dying?", the answer is that there IS no answer.  There is no selection pressure for or against that trait, it just happens.  As to the mechanism itself, I suspect that there is just a global breakdown of function in the brain, leading to a dump of ALL neurotransmitters.  When the reuptake pumps fail, the neurons just dump their contents into the extracellular space.  The result is pleasant hallucinations, giving the impression that humans are not "meant" to feel pain when dying.  Imposing that kind of rationale, however, is simply creating meaning out of chaos.  If you watch TV static long enough, your mind will start to see patterns which aren't there, simply because the human mind is "wired" to find patterns in chaos in order to better understand the environment.
To wrap this up, I suppose the answer to your question is that the brain is finding meaning in meaninglessness, simply because that is what the brain does.  We look for patterns to make sense out of our environment, which sometimes leads to spurious conclusions.  There is no reason that the brain hallucinates when dying, but there IS a reason that this trait appears to be a built-in mechanism.
I hope I was able to shed some light on the issue.  Or at the very least, not confuse you further :D

I disagree with all of this except the part about evolution not being a conscious designer. You are arguing that genetic drift accounts for a large proportion of evolution. This is the opposite of the current understanding informed by genomics and transcriptomics. For example: http://onlinelibrary.wiley.com/doi/10.1111/j.1558-5646.2007.00308.x/.
It is highly likely that there is a reason (i.e. a proximate cause) for DMT being released at death, but it may not be direct, and it may be impossible for us to infer it with current information. The same is true for having 5 fingers and 2 arms.

The point I was trying to get across is not that random genetic drift accounts for the bulk of traits seen in organisms. My point was that assigning a "purpose" to an observed trait is often faulty logic because it presumes a "goal" to evolution. The only goal in evolution is higher reproductive fitness, so attempting to find a cause for other perceived goals is impossible. One could easily imagine humans having 6 fingers per hand, and you would be hard pressed to identify the specific fitness advantage to actively (and specifically) select for 5.

As such, it would be faulty to presume there must be a selection pressure there, when it could just as easily be random. Basically, to argue that a given trait is selected for, you first need to demonstrate how that trait significantly improves that organism's reproductive fitness. I think you would be hard-pressed to identify a reproductive advantage to the "DMT dump" trait. That's not to say it's impossible for there to be an advantage. Just that there is no evidence or hypothesized mechanism for an advantage.

@AndrewBonnell I can't really say I'm satisfied with the answer. I believe it's too much of a coincidence to be happening just because. I might be wrong, but I think it's just not known yet, therefore the best explanation is that it's a random thing. Anyway, thank you very much for the answer.

@PiotrChojnacki: I would like to comment on the use of the word 'random'. There is some randomness in creating mutations and drift-like processes, and there is some non-randomness in the selection process (almost definitely, there was some kind of non-random force involved in creating pentadactyl limbs, or DMT release in the dying brain). To call the outcome of this random again is very, very confusing. What Andrew Bonnell is talking of is contingency which has a 'randomness'-component but fits way better to describe the notion that it simply 'happened to be that way, and not the other'.

Dimethyltryptamine have been identified as normal constituents of human blood, urine,cerebrospinal fluid.Dimethyltryptamine is an  N-methylated indoleamine derivative, a serotonergic hallucinogen.It apparently acts as an agonist at some types of serotonin receptors and an antagonist at others.DMT is traditionally associated with indigenous Amazonian people, who consume a bitter decoction of at least two types of plant material, known as ayahuasca.
DMT is capable of transporting the user, within seconds, to what appears to be a fully autonomous alternate reality.
There is term called consensus reality the world we live in an imagination of our brain. DMT is capable of building this alternate reality with which in normal circumstances we don't feel or perceive it. DMT can cause such dramatic shifts in consciousness, such that completely novel worlds appear.Our brain use various approaches,to create a mental field which gives a unified world and these two can be classified as functional segregation and integration. As humans we are very much visual creatures and the cortex region of our brain helps us in doing that. Our brain continues to develop, changes throughout life and across the span of evolutionary time. It becomes absolutely critical in determining how the brain interprets and categorizes sensory information and thus builds the consensus world and we reach a point where our brain can create or is capable of building worlds without extrinsic influence or data.
These are the findings that were reported from the DMT studies
1.Hallucination—visual, physical, auditory;
2.Entering other realities, sometimes including having contact with other sentient beings, which were described as true or real experiences rather than hallucinations;
3. Lucidity;
4. Affective distortions;
5. Ineffability;
6. Extreme intensity;
7. Spirituality, learning, or being taught about truths of the universe or self;
8. Distortion in sense of time, space, self;
9. Sense of familiarity
This is also being reported by research group.
- Merry-go-rounds, fairgrounds, clowns/jesters, circuses;
– Mischievous or playful elves/dwarves/imps;
– Insectoid and reptilian creatures, aliens;
– Futuristic hypertechnological buildings and cities;
– Complex machinery, hyper-advanced technology;
– Being observed and/or experimented upon;
– Unknown places apparently on Earth.
So due all these mechanisms and effect of DMT I can say that when we are on the verge of our death our brain produces DMT in higher amounts in order to ease the pain which I assume and at the same time the alternate reality or the alien reality is something which is not yet thoroughly investigated. So I would say if an alternate world exist where humans go after death then DMT is the molecule which helps in doing it.

This doesn't answer the question. The question asks why DMT being released at death would be selected for evolutionarily.

It is proven that dmt does exist in human body, but claims about large amount of its release are not proven. But it has been proven that it does protect neurons under hipoxic conditions, so if it was true, it would make you survive just a little bit longer until something saves you from suffocation.
My biophilosophy professor had a theory, that this would explain personality  change of people who have had a near death experience. His reasoning was that it is hard or impossible to encode how selfish you should be in a society, and if you are too selfish, others will bring you near death, and this will change your personality to be more selfless. This is advantageous both to the individual and to the group.


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Are there free electrons in muscles, hair, or skin?
Electric shock occurs upon contact of a (human) body part with any source of electricity that causes a sufficient current through the skin, muscles, or hair.
In metals many electrons are said to be delocalised (i.e, electrons are not bound to any of the atoms). Around one electron per atom is said to be unbound to atom in mettalic lattice. So there will be motion of electrons due to thermal energy, however due to their random motion, there won't be such a significant current produced. When electric field is applied across them there will be motion of electrons in a particular direction, causing significant amount of current. In case of insulators, due to bound electrons we can't expect current through them.
When our body becomes a part of electric circuit, current is said to pass through our skin, muscles, or hair. Does it imply that there are free electrons in skin, hair, or in muscles (like those in metals)?

conduction rarely involves free electrons usually - charge can move through a chain of capture/ionization events.

Our body contains a lot of salt and which act as electroyte,so when we comes in contact of electric source then the electrolyte helps in the conduction of electric current through out body,

Free electron is just one type of charge-carrier. Once can also have other types: such as anions and cations to carry charge from one place to another. Therefore causing a current to flow.
Even if skin and hair lack "free electrons" like metal and semiconductor, we definitely have a great amount of anions and cations in our body. One example would be -- as krushna mentioned in his answer -- is $Na^+$ and $Cl^-$ ions from common salt in our body.
Now, not all (type) potential can cause a great deal of current to flow in our body. The 12V lead-acid DC battery definitely does not cause any perceptible current to flow through our body; no matter how many free ions we have on our skin. On the other hand, 440V AC live wire will cause a great harm if we touch it even with dry hands.
If I were to model my skin, I would go for a RC circuit with high R and high C attached in series. Put the appropriate values and simulate this circuit using a circuit simulator after applying test voltage across it. The Human Body Model for capacitance, as defined by the Electrostatic Discharge Association (ESDA) is a 100pF capacitor in series with a 1.5kΩ resistor. Since we have a capacitor in series, it prohibits DC current to flow through it. This is one reason why X Volt of AC is much more harmful than X volt of DC voltage (AC passes through capacitor easily).


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Is this maritime plant a species of zostera?
This photograph was taken on the intertidal mudflats at Lindisfarne, Northumberland, UK today. It was about 40m from the shoreline at low tide. Is the green plant a species of zostera? Can anyone help with the identification?

This question appears to be off-topic because it is about plant identification. These questions are usually asked on Gardening and Landscaping Stack Exchange. This topic is not found in the following appropriate topics listing in the Help center: 1) General questions about biological concepts 2) Questions about the biological mechanisms behind medical conditions 3) Questions about techniques in a biological or biochemical laboratory

It certainly looks like a Zostera species.  The ones that appear in the UK are Zostera angustifolia, Zostera noltii, and Zostera marina.  Its hard to tell exactly which species this one is without size information and knowing the conditions of the bay.  Z. marina has the broadest leaves at around 5 - 10 mm, whilst Z. angustifolia has leaves just 2 - 3 mm broad.  Is 40m around the mid-water mark?  If so I would hazard a guess this is Z. angustifolia.  Z. marina tends to stick to areas permanently covered by the sea (sub-littoral) whilst Z. noltii likes much more sheltered conditions than the middle of the bay, tending to stick to the upper shore.
Hope that helps!


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Is the empty GI tract a hollow tube with air inside, or is it generally collapsed until food is eaten?
I have heard that "air in the GI tract" results in flatulence and burping etc, however I initially assumed that the "empty" GI tract was a hollow tube filled with air anyway.
So on an empty stomach (or "empty" GI tract rather), does the GI tract collapse due to the pressure in the surrounding cavities, or is the GI tract normally a hollow tube filled with air, and flatulence merely a result of "excess" air?

Under normal circumstances the stomach and GI tract have very little "gas" in them - whether it be flatus, air, CO2, or anything else - and so are essentially collapsed with the walls against each other. However, gas is continually being produced by the microorganisms that inhabit our gut, and can also come from swallowing small amounts of air, fizzy drinks, etc., so the environment is never 100% gas-free. A typical person produces on the order of 500-1500 ml (0.5-1.5 liters) of gas per day.
If you're interested, the Wikipedia article on flatulence is a good introduction.

If you look below you can see two X rays. One with bowel obstruction on the right and a normal on the left. On an X ray air bubbles are black as indicated. Under normal circumstances as you can see there is very little air in the stomach and GI tract, although more frequently there will be some in the stomach due to fizzy drinks or reactions involving stomach acid producing gas in our stomach. That air later on in our GI tract tends to be a mix of carbon dioxide, methane and other waste products that bacteria in our gut have made. As Matt said, we produce quite a substantial amount of gas (500-1500 ml) per day. In an obstruction all of this can collect and further increase as microogranisms are in contact with the food for a longer duration as well as more enzymatic breakdown. And this can be seen in Figure 2.


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How do detergents get in hydrophobic membrane interior?
According to Molecular And Cellular Biology (Stephen L. Wolfe),

Membranes disperse almost instantaneously if exposed to a nonpolar environment or to detergents, which are amphipathic molecules that can form a hydrophilic coat around the hydrophobic portions of membrane lipids and proteins in water solutions.

This might be a stupid question but... if detergents can 'form coats around hydrophobic portions' of membrane-suspended molecules, they must, somehow get in the hydrophobic membrane interior... right?
How do they get in the membrane interior? Do they form clusters like endocytic vesicles? What happens after they form hydrophilic coats around hydrophobic molecule regions?

It depends on the concentration, but at higher concentration the detergent molecules build so called micelles, where the hydrophobic "tail" is orientation into the inner part and the hydrophilic "head" is orientated to the outside. This allows the micelle also to fuse with the membrane and then to desintegrate it.
This illustration from the Wikipedia shows the schematically:

Its from the surfactant article, which has more details.

The membrane is dispersed by detergents.  But the detergents, under the right concentrations and conditions (salt, pH, et) form micelles with smaller curvature than the lipids that compose cell membranes.  With some luck, they can form a small hydrophobic micelle bubble around the protein.
This figure is depicts detergent micelles around a membrane protein's membrane bound regions, hopefully without distorting the shape of the protein!

Since you asked in the comments, here is a picture of the electron density of the detergent micelle in ompF Porin crystals - the detergent density is blue the protein is red.  For a while in the mid 90s through maybe a few years ago there were a reasonable number of simulations including detergent molecules.  The mobility of the chains in the micelles means that no specific model structure would be accurate, but it can help understand the electromagnetic environment of the solvent in cases which are important like charge transfer in a photoreaction center or the dynamics of transport through an import/export protein.

Thats a great image.

thanks. If you want to see a more true to life one, many membrane proteins have visualized detergent micelles in simulations and in the crystal unit cell.  I'll add another image above.

sorry... haven't been in SE for months; and DO please show me that image! @shigeta

actually the last image there is a good example... the blue density is all micelle in a porin unit cell.  protein is red


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How Much Longer For The Gene For Blue Eyes?
In the year 1900 roughly 50% of the people in the United States were homozygous for the gene for blue eyes. By 1950 the number had dropped down to 30%. Just now, (2013) barely 12% of the people living in America are homozygous for the blue eye gene.
Given the current rates of third world immigration into the United States. When will the last blue eyed man and the last blue eyed woman conceive a child with blue eyes? Should people with blue eyes bring reverse discrimination suits?
Reference:http://www.boston.com/news/globe/living/articles/2006/10/17/dont_it_make_my_blue_eyes_brown/ By Douglas Belkin

Do you have any reference for this 50% value? I highly doubt it, since blue is a recessive allel.

Agree with @Chris,you should give a reference for every data that you have put !

@user10739 could you paste the quote - the link is behind a paywall

If you come through the first link via Google, you can read it: https://www.google.de/#q=%22Don%27t+it+make+my+blue+eyes+brown%22+boston+globe

You added something to the question about reverse discrimination suits, but I don't see any other reference to discrimination. What is the alleged discrimination being inflicted upon blue-eyed people?

The 'alleged discrimination being inflicted upon blue-eyed people' is a collection of social policies in the United States leading to their extermination.

Never.
Even if the country arrives at the unlikely day when there is no one alive in the United States with the blue eye phenotype, there are still plenty of people with the unexpressed recessive gene, and if two of them get together, those genes can combine to produce another blue-eyed child. If this happens twice, with one boy and one girl, and they happen to meet when they are in college and say "Hey cool, you have the same inexplicably rare kind of eyes as me. I think I want to marry you." then any children they have will also be blue eyed.
So even if the day came when you couldn't find a soul in the world with blue eyes, you will still never know if you've seen the end of them.