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What does min mean?
I read that

"trp operon is located at 27 min on E.coli chromosome."

What does "min" mean ?

Min means minutes. Minutes are counted for interruption points since onset of DNA transfer in F-pili-mediated conjugation. The point "0" is not associated with ori, but is close to thr. The total chromosome size is 100 min (time taken for conjugation).
See:

Linkage Map of Escherichia coli K-12, Edition 10: The Traditional Map
Recalibrated linkage map of Escherichia coli K-12

Well.. I am not sure if this 100 minute is for the replication or transfer. I am still confused because this site says it is replication. In fact I did write conjugation first and changed to replication.

in fact replication is much faster in regular conditions.

Yes, 100 min is the time required for the transfer, since replication time itself is ca 40 min.


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Life on other planets
first of all I'm not sure if I should post this here or in the astronomy stack. I think biologist are more likely to answer my question. To make it short:
Why when looking for any sort of life on other planets, we keep looking for similar conditions we call "life friendly", like nice temperature, oxygen level, pressure etc...
Is there some rule in biology that says life can only exists under these conditions? Why nobody supposes that evolution did not have enough time yet on our planet to generate other living mechanisms, and that on other planets even if the conditions are not suitable for us, there might be something well evolved through time there. After all if we can conceive electric robots that can survive to radioactivity and to high pressures and temperatures, why nature shouldn't be able to?

this topic has been discussed several times in this forum. If you search for related questions you'll find them.

technically, early life on earth didn't even need our sun because it didnt use photosynthesis, but for meaningful life you need plate techtonics, mountains and large landmasses, or it's a waterworld. Anywhere which has volcanos and seas should be able to support life, even if the surface temperature is -100 or -220C

If you want to ask a specific question about transistor or metal based life forms, you should check out the chemistry forums. there is a post about silicone there.

We might imagine living things that are very different from what we know. There is no conceptual reason for limiting life in its relation to water for example. Moreover, the definition of what is alive is really unclear. We classified more or less arbitrarily objects we know on earth as being living or not living but this does not give any clear definition of what is life and therefore it would not allow an exobiologist to even know what he's looking for!
But if you had to seek in billion of planets/natural satellite a living creature somewhere where what planets would start looking at? Probably those that look alike yours because you already know that life is possible the kind of conditions these planets offer. I think the answer is as easy as that.

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Was the mitochondrion or chloroplast first?
I still don't  know if the mitochondrion or chloroplast was first? I've looked for it on the internet and in various books but haven't found anything. Does anyone have the answer and a theory which backs up this answer?

Mitochondria evolved before chloroplasts.
We know this because Mitochondria form a monophyletic group: e.g. all life with mitochondria traces back to a single common ancestor (source). Since the group with chloroplasts groups within this clade, it must be the case that either (a) chloroplasts were obtained by an organism that already had mitochondria or (b) chloroplasts were independently lost by multiple lineages within the Eukaryotic clade and then many of these lineages re-acquired chloroplasts by secondary endosymbiosis. Since (a) is a (much) more parsimonious explanation it is the one it makes sense to accept.

Straight and convincing.

I do not have a definitive answer but I can argue that mitochondria came into existence before chloroplasts despite the fact that, between their free living ancestors- $\alpha$-proteobacterium and Cyanobacteria, the latter seems to be older in evolution.
I have following points to support this argument:

The organisms that have chloroplasts also have mitochondria but the converse is not true.
There have been events of secondary endosymbiosis (especially in the Chromaveolata) in which organisms that already contained chloroplasts became endosymbiotic organelles in another host.
There is a very recent case of endosymbiosis of a chloroplast like organelle called spheroid bodies in the diatom Rhopallodia gibba which already has a secondary plastid. See this.

Usually a cell has many mitochondria but fewer chloroplasts. Though this doesn't say much about the evolutionary age but higher number allows more organelle to nuclear gene transfer, considering the limited transfer window hypothesis. More the transfer, more "dependent" will the organelle become on the host.
Even though I claim in the first paragraph that Cyanobacteria is older than $\alpha$-proteobacterium (In fact I dont have a strong reason to support that claim), it doesn't mean that photosynthesis has an older origin. Chemosynthetic pathway and membrane bioenergetics have evolved very early on. Coupling of light to assist these processes, most likely came later when organisms surfaced to the limnetic zone.

The use of molecular oxygen as an electron acceptor evolved some time after photosynthetic processes had made molecular oxygen abundant in the earth's atmosphere. So I think you can make the argument that photosynthesis has an older origin compared to the oxygen dependent metabolism that is performed by mitochondria.

Point taken. But oxygen is not the only electron acceptor... Mitochondria which use $Fe^{3+}$ also exist (one of the $e^-$ acceptors other than Oxygen). So yes, photosynthesis is older than aerobic respiration but ATP-synthase is older than both :)

@WYSIWYG: your third argument doesn't seem very strong.

@har-wradim yes that's the weakest of all :) I mentioned it because it is likely that mitochondria are numerous because they became associated early on. Also considering the limited transfer window hypothesis, the chance of mitochondria to nuclear transfer of genes is easier because of its higher number. Although, one can argue that $\alpha$-proteobacterium was inherently fast dividing than Cyanobacteria and therefore the higher numbers in the cell.

I think you mean "descendants", not "ancestors", and even then, this is probably incorrect. The original endosymiont is probably in a sister clade to the extant bacteria. I also think the single origin of both endosymbionts is the strongest argument, anyway.

According to my knowledge, this was the molecular and cellular evolutionary path of life.

Synthesis of essential building blocks (fatty acids, aminoacids, cofactors...)
Condensation of building blocks
First RNA replicase; RNA genomes (differentiation between genomic and
functional RNA, primitive metabolism)
Ribosomes and first matrix dependent translational machinery
Copying RNA into DNK (rNDP reductase, reverse transcriptase)
PROGENOTES (DNA genome, introns in genes, slow growth, anaerobic
heterotrophs)

From here you have two main branches, organisms with branched lipids, and with unbranched lipids (the first will become archaea, and the latter urkaryotes and Bacteria)
In the Urkaryotes, you have selection of complexity. Their growths is inefficient, and they tolerate extra DNA. Bacteria favored efficient growth, autotrophy and loss of extra DNA.
At this point the endosymbiosis occurred (presumably), and the bacteria became a very specialized parasite. Mitochondria as you probably know, have their own genome which replicates independently from the nuclear genome. Cells and mitochondria became permanently linked when the mitochondria "decided" to relocate parts of it's genome to the nucleus, incorporating it's genome in the host's.
Now we have the first Eukaryotic organisms that are similar to today's. They were heterotrophic, but one more event of endosymbiosis occurred. That was the formation of chloroplasts.
Many people think that autotrophy is more primitive compared to heterotrophy. That simply isn't true. The conditions when these organisms arose were quite different. Building blocks were readily available and plentiful, so the organisms were all "friends" with each other. It is when food became scarce that selective pressure started nudging species into different directions (autotrophy).

Why would a mitochonrion be of any advantage in a world without oxygen?
Chloroplasts evolved to fill the atmosphere with oxygen then mito's exploited that situation.

Welcome. You may have an interesting point, but without sources it's more of a comment than an answer. The more so as your answer seems to contradict the existing answers above. You will need some reputation to place answers, but if you could improve your answer with some more evidence and sources to allow other users to background read on your answer, that would be great.

Chloroplasts did not evolve to fill the air with oxygen, but were acquired symbiotically to allow plants to obtain energy from photosynthesis. This had already evolved in cyanobacteria, which were responsible for the great oxygenation — not chloroplasts in plants. We welcome new users to SE Biology but, please respect other members. Given the detailed and academic responses already received for this question, you might have considered that the previous contributors to this question had some knowledge of this area.

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What are the roles of guanidine-HCl and ethanol in binding of DNA to silica?
I'm trying to understand how exactly the binding to silica gel (in kits) step works and I cannot find any papers which provide an explanation of the physics or chemistry; especially on the way that Guanidine-HCl works.
So lets get them from the beginning.
First of all, we adjust DNA binding conditions by adding a buffer which includes
Guanidine-HCl and ethanol and then we centrifuge our sample. I knew that Guanidine-HCl destroys the tertiary structure of proteins but somewhere I read that also it helps the DNA to bind to a silica column. I searched to find the way that it works but I couldn't find a paper. Also what is the role of ethanol in this step? Is it just to remove proteins and polysaccharides from the sample?

There is an excellent discussion of this in:
Melzak et al. (1996) Driving forces for DNA adsorption to silica in perchlorate solutions. J. Colloid Interface Sci. 181: 635 - 644
I've skimmed the paper, and I'm beginning to understand it, but I don't feel up to actually answering the question yet.

So the whole story as i understood is not clear at all.Here is a abstract on what i got but i am not sure if this is the final answer. In earlier years there was the opinion that the SiO4 molecules had negative charge as the DNA too. So to achieve the binding of them you had use high conc. salt (chaotropic salt) and alkaline pH. In that way some cations from the salt will create a bridge between DNA and SiO4 molecules. In recent studies (Water interactions with silica surfaces: A big role for surface structure) seems that the things doesn't work that way. They predict that SiO4 molecules has

(continue from above) positive charges and the way that chaotropic agent works is by creating hydrophobic environment so to remove the water molecules from DNA and let it bind into silica membrane. As for ethanol...nothing yet. Some companies nevertheless they explain the binding mechanism as i described first.

As far as I know, the ethanol is just a wash in which DNA is insoluble to remove contaminants

Guanidine HCL is a chaotropic salt.  Chaotropic salts are critical for cell lysis and binding to the silica resin. Specifically, Chaotropes have two important roles in nucleic acid extraction

Destabilize hydrogen bonds, van der Waals forces and hydrophobic interactions.

Leading to destabilization of proteins (including nucleases).

Macromolecular structure and function is dependent on the net effect of these forces (see protein folding), therefore it follows that an increase in chaotropic solutes in a biological system will denature macromolecules, reduce enzymatic activity and induce stress on a cell (i.e., a cell will have to synthesize stress protectants). Tertiary protein folding is dependent on hydrophobic forces from amino acids throughout the sequence of the protein. Chaotropic solutes decrease the net hydrophobic effect of hydrophobic regions because of a disordering of water molecules adjacent to the protein. This solubilises the hydrophobic region in the solution, thereby denaturing the protein. This is also directly applicable to the hydrophobic region in lipid bilayers; if a critical concentration of a chaotropic solute is reached (in the hydrophobic region of the bilayer) then membrane integrity will be compromised, and the cell will lyse. [Source]

Disrupt the association of nucleic acids with water.

Thereby providing optimal conditions for their transfer to silica.

Salts can have chaotropic properties by shielding charges and preventing the stabilization of salt bridges. Hydrogen bonding is stronger in non-polar media, so salts, which increase the chemical polarity of the solvent, can also destabilize hydrogen bonding. Mechanistically this is because there are insufficient water molecules to effectively solvate the ions. This can result in ion-dipole interactions between the salts and hydrogen bonding species which are more favorable than normal hydrogen bonds. [Source]

Ethanol, like Guanidine HCL, is a  chaotopic agent.  Ethanol is added for 2 reasons:

Enhance and influence the binding of nucleic acids to the silica.

Interfere with non-covalent intramolecular forces as outlined above.
Reduce association of nucleic acids with water. From Melzak et al. (1996):

Decreaing the water activity in solution through addition of either a chaotropic salt or an alcohol changes the helical structureof B-DNA either continuously to C-DNA or through a sharp  cooperative transition to A-DNA (28). Either transition is  accompanied by a decrease in solvent-accessible surface  area.

The correct concentration allows for washing of the salts from the membrane. [Source].

Citations

Melzak et al. (1996) Driving forces for DNA adsorption to silica in perchlorate solutions. J. Colloid Interface Sci. 181: 635 - 644.


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Is a sequential double transformation acceptable?
Standard protocol states having two compatible vectors being transformed simultaneously during the same procedure. I've come across a situation in which transforming one vector, obtaining results, and then transforming the other is preferable. Is there any reason to think that this wouldn't work? Do I risk losing my first vector upon transformation of the second?

I'd assume that you use different antibiotic resistances for selection, that way you should be able to ensure that both plasmid are taken up successfully.

you do, but some will maintain both plasmids, so the two antiobitics on the plate still should give you want you want.

If the plasmids you wish to transform are very big (more than 20kb), the co-transformation might not be very efficient (you might not get any colonies). Electroporation should work though, as electrocompetent cells are more efficient than chemically competent cells. Alternatively, as you have read, you could transform your first plasmid and select for it, and then make these cell that harbor it competent and transform the second plasmid. As long as you select for the plasmids (with kan/carb/etc resistance marker), the cells that grow on the selective media will keep both of them. If I were you, I would try the co-transformation and then if it doesn't work I would do the sequential transformation.


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How does mutation cause natural selection? and is it common in protists or prokaryotes?
Why is it inevitable that evolution by mutations alone should be a common cause of evolutionary change in most natural populations? And do you expect mutation-driven evolution to be more common in typical protists or typical prokaryotes? Why?

What other causes of evolutionary change are you comparing mutations to? If you get right down to it, every change is a mutation of some sort...

I edited your title because of the close votes- hope this helps - feel free to change this back.

Your question, as I understand it, concerns the relative role (compare to natural selection and drift probably) of mutation in evolution. But evolution is not one process. Mutation and natural selection are processes that influence populations in very a different manners. At first sight, it seems to me that it does not make sense to weight the important of mutation versus other processes such as selection. But again, in what term would weight these processes?

Prokaryotes have very high reproductive rate. So, they develop mutants far more faster than multicellular eukaryotes.

Your question doesn't make a lot of sense.
Mutation is the process whereby new alleles are created, by the DNA chemically changing its sequence.  Natural selection is the process where in a population, alleles change frequency over time due to differing survival rates.  (And there are lots of other kinds of selection, and allele frequencies can change just due to chance, too)
So I don't think "evolution by mutation alone" makes much sense.  In sexually reproducing eukaryotes, variety can be created by mixing and matching different alleles in the population in different combinations, which isn't something that prokaryotes really do, so I guess that's a difference in the importance of mutations between sexually reproducing eukaryotes and prokaryotes.

A good post about "mixing", which means that a population generally harbors multitude of different versions of a gene, called alleles. So one organism, like a human, has a unique combination of which two alleles out of thousands possible represent each gene in its body. Besides this, major changes are often made not so much by mutations as by changes in the level of gene expression. For example, a mutation in one gene that produces a protein important for regulation of the expression of 50 other genes can cause a lot of change in body development (morphology) and physiology by simply affecting the expression level (amount of protein produced) by these 50 genes. In turn, changed levels of these 50 proteins can make substantial changes in the whole protein interaction network in cells. If you think why sharks look different than elephants, for instance, it's much more because of differential gene expression (including the timing of the expression during body development) than differences brought about by mutations causing functional changes in the coding regions of multiple genes.
And yes, mutations only provide raw material for evolution - diversity to select from. Mutations are a supermarket for evolution, selection is what evolution tends to buy more frequently in this supermarket or what's in demand currently. It is thus selection and drift that work to increase the frequency of certain mutant alleles that actually result in evolution.
The mechanism of selection is simple. The functional diversity in populations created by mutations in particular creates different survival rates for particular phenotypes/genotypes based on how well the combination of the alleles representing its genome can create a phenotype that matches environment. For example, in a bacterial population adapted to neutral media there's still a random diversity in the range of pH tolerance. If the medium becomes more acidic, cells that happen to have better tolerance to low pH gradually increase in frequency over time.
The difference between prokaryotes, like bacteria, and eukaryotes (like humans) mostly lies in that due to meiosis eukaryotes randomly shuffle alleles, so that they "intermix" in a population creating more possible phenotypes to select from. Bacteria do not have this mechanism and can only diverge by cell division, creating diversity only by mutations. However, it is not completely true, as now it is well known that bacteria share a lot of genes via horizontal gene transfer - direct exchange of genes between bacterial cells. This process is often aided by viruses. Horizontal gene transfer, just like meiosis, works to shuffle genes in the population, creating more diversity.

Can you break up this wall of text?


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Cosmid genomic library, or genomic cosmid library?
Which usage is better for referring to a "cosmid library of genomic DNA fragments"?

I've always used Cosmid Library but Cosmid Genomic Library is better than Genomic Cosmid Library.

Indeed - comments are better for statements of opinion. In answers, please try to provide reasoning why one phrasing might be better than another.


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How can a YAC be screened against a cDNA library and a cosmid library of genomic DNA to find a gene?
I am reading fw2.2: A Quantitative Trait Locus Key to the Evolution of Tomato Fruit Size (doi: 10.1126/science.289.5476.85).
The authors are trying to find the gene that makes tomatoes bigger. As far as I understand, previous research had narrowed it down to "something" in the region of the genome called fw2.2. They are trying to determine the actual genetic elements responsible (which turns out to be a gene similar to human HRAS).
Supposedly, the big-fruit allele is recessive and the small-fruit allele is dominant.
They say (in section Genetic complementation with fw2.2) that:

They got a YAC containing the fw2.2.
They "screened a cDNA library" with the YAC to find transcripts that were potentially relevant. (How?)
They "screened a cosmid library" of genomic fragments to find the stretch of genome that the cosmid came from. (How?)

It is unclear to me how steps 2 and 3 work. Can someone explain how you can take a YAC, cDNA library and cosmid library to find the gene inside the region responsible for your trait, as these researchers describe?

The YAC contains a segment of chromosomal DNA. By using it as a probe they could screen the cDNA library to find cDNAs derived from that genomic region. This would be done by plaque or colony hybridisation. The cDNA clones thus identified represent the "candidate genes" .
The last step is a little unclear. Clearly they are identifying cosmid clones that map to the segment of interest, but they could be using either the YAC or relevant cDNA clones (could be pooled for this step depending upon their aim) as probes. My guess is that they used individual cDNA clones to find corresponding cosmid fragments so that they could home in on the regions encoding the identified cDNAs.

I am skeptical because firstly the YAC contains one allele, while the cDNA comes from an organism that has the other allele (a detail in the paper). Secondly, this becomes dubious if the gene on the ORF is spliced (like this one). For hybridizing cDNA to cosmids, there is again the potential issue of exons/introns. Or are you saying the cDNA would still hybridize if only a small part of it was complementary?

@Superbest - hybridisation of probe to clone will occur if there is shared sequence. The fact that there might be small differences in sequence (alleles) or missing sequence (no introns in cDNA clone) will be irrelevant. Before transcriptomics this was the standard way to relate genomic DNA mapping to information about transcripts coming from cDNA cloning.


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How do I get a brighter DNA bands
I've been trying to a good contrast for my DNA bands, however I haven't been so successful. I've been running the ladders only to make sure I get a good contrast before further experimentation.
I created the gel using 70mL 1X TAE buffer, 0.84g of agarose (so about 1.2% gel), and 28ul EtBr.
I set the electrophoresis box at 90V for about 1 hour hoping to get a better gel but the results came out looking the same as if I had ran it at 110V.
I've attached a picture of my gel. It was taken with a DSLR, no flash, 20 seconds exposure time.
Any tips would help. Thanks

That is a lot of EtBr. You are using about 30x more than what most people do! You're potentially exposing yourself to a higher amount of a dangerous chemical than usual.

What's the typical amount? My graduate TA told me to run 10uL per 25mL for the gel.

Standard amounts are about 16 ul per 100 ml of gel IF added in the gel solution.

EtBr is a powder that can be made to solutions of different concentrations. So volumes don't make much sense unless the stock concentration is mentioned. Final concentration of EtBr in the gel should be 0.5$\mu g/ml$

EtBr needs to be detected with UV light. Then: What is the concentration of you EtBr solution? @Superbest EtBr is not as dangerous as many people think. Yes, it is an intercalating agent (as most DNA dyes are) but it is not the monster that many people make it.

@Chris Yes. However, I've heard a nice analogy - "it's kind of like smoking a cigarette". I, personally, don't smoke.

Use more DNA. If you add more to your experiment, it will likely show up brighter in the DNA ladder.

I normally use 1-2 ul (depending on whether my gut tells me I have a lot of DNA, or a little that day) in a 70 ml 1% gel (which is probably 60-65 ml after boiling in the microwave). I have no trouble whatsoever seeing ladders and DNA samples of down to 100 ug in wells not much bigger than about 4 mm.
Here are the factors that you can manipulate to alter the brightness:

Amount of EtBr. More is brighter. (However, you already use a lot - using less may even be better because it would reduce background while still saturating the DNA with EtBr)
Amount of DNA. More is brighter. To avoid guesswork, use a ladder and consult the instructions in its manual or spec sheet. They usually have an example picture of a gel, and say exactly how they obtained it.
You messed up. Do other people in the lab get good gels? Ask them to do the protocol with you.
Sample preparation. Are you using a loading dye in the correct amount? Is the DNA diffusing out of the wells? Are you spilling a lot of it when you load?
Band width. Obviously if you load the same amount of DNA in a well 4 times as wide, it will be 4 times fainter.
Strength of UV light. Many illuminators have a knob to adjust the intensity, people turn it down to avoid damaging DNA when gel-purifying restriction fragments. You can also play with intensity, gamma and exposure in a geldoc machine.
Quality of EtBr. I've never actually had this happen, but your stock may be bad for some reason. Ask another lab for a ul or two to easily control for this.
Quality of DNA. Obviously, your sample must actually have DNA in it, and not be degraded. You can check amount and purity easily with a spectrophotometer, but it will not tell you if the DNA has been digested into its component nucleotides (that is usually checked with a gel).
Amount of gel. The crucial variable is obviously not total amount of EtBr, but concentration. Less gel, brighter bands - but you seem to be using a standard gel amount.
Quality of gel. Again, never had this happen, but try making the gel with someone else's reagents.

I can see that you have a ladder in the middle, so at least some DNA is definitely there.
Also, keep in mind that off-the-shelf cameras are not good at imaging the EtBr fluorescence, because the wavelength is a bit unusual. The nice pictures you see in papers are taken with a specialized geldoc machine or a camera with an appropriate filter.

Thanks. As far as taking the picture, I am using a blue transilluminator from io rodeo: link

The blue LED transillumination is the problem.  There is nothing wrong with making your gel, electrophoresis or resolution of bands based on your image. EtBr is best illuminated in the short UV range and is a function of wavelength. It's worth comparing abaorbance ratio for peak UV illumination vs the wavelength of blue LED (415 nm? ). 20 sec exposure is awfully long. What do 100 ms to 1 sec exposures look like?

@leonardo, the pictures with less exposure time look a lot brighter. Here's a picture taken (of the same gel) at .6s exposure time. link. Also, is there another illumination solution that is inexpensive that I can try?

Since this answer was accepted, let me clarify: Looks like the problem is that the wrong illuminator was used. The linked device produces blue light, for use with CYBR Green. For EtBr, you need UV. Probably the signal you did get was from UV bleeding from the blue LEDs of the device.


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Dopamine paradox in schizophrenia
If there is more dopamine action in the mesocortical pathway in schizophrenia, then schizophrenics should always be in euphoric state. Instead, schizophrenics often lack motivation and do not experience pleasure. Why?

Can you provide a reference?

I'm no expert, which is why this isn't an answer, but it may have to do with receptor down-regulation, or an altering of receptor signaling.

Short answer
The dopamine (DA) hypothesis suggests that excessive DA transmission in the mesolimbic pathway in schizophrenia leads to hallucinations and other positive symptoms. It explains the negative symptoms of schizophrenia (flattened affect, reduced motivation) by reduced DA activity in the mesocortical pathway affecting the frontal cortical regions.
Background
You are referring to the dopamine hypothesis of schizophrenia.
The initial dopamine (DA) hypothesis focused primarily on the positive symptoms of schizophrenia, namely the active psychoses, which includes periods of hallucinations and delusions. These effects can be attributed to hyperactivity in subcortical dopaminergic pathways. Specifically, excessive subcortical release of dopamine is thought to increase D2 receptor activation, disturbing the cortical pathway through the nucleus accumbens (Brisch et al., 2014), called the mesolimbic pathway (Fig. 1). These positive effects can be treated quite effectively with the classical, first-generation anti-dopaminergic antipsychotics such as haloperidol and chlorpromazine.
However, there is another important aspect on schizophrenia, which are the negative symptoms. While the full-blown psychoses occur in waves, these negative symptoms are a more continuous and persistent phenomenon. The symptoms include a flattened affect and dysphoria (reduced pleasure in life). These symptoms are thought to occur due to altered prefrontal cortex (PFC) functioning. Specifically, they are thought to be induced by hypoactivity in dopaminergic D1 transmission (Brisch et al., 2014) in the mesocortical pathway (Fig. 1).

Fig. 1. The dopamine pathways in the brain, including the mesolimbic and mesocortical pathway, implicated in the positive and negative symptoms of schizophrenia, respectively. source: Wikipedia.
These two sides of schizophrenia point to an imbalance in DA activity in the brain, namely hyperactive subcortical mesolimbic D2 activity leading to positive symptoms, and hypoactive mesocortical D1 activity in the PFC resulting in negative symptoms. This imbalance hypothesis is the revised DA hypothesis and it is still an accepted working model (Brisch et al., 2014).
However, as noted by others, schizophrenia is a complex disease and it is thought that besides DA, also serotonin, glutamate and GABA play a role (Olijslagers et al., 2006). The current first line of treatment of schizophrenia are atypical neuroleptics, such as Clozapine. Clozapine is a selective monoaminergic antagonist with high affinity for the serotonin Type 2 (5HT2), dopamine Type 2 (D2), 1 and 2 adrenergic, and H1 histaminergic receptors. Clozapine acts as an antagonist at other receptors, but with lower potency. The broad effects of Clozapine are thought to underlie its potent antipsychotic therapeutic effect. It is believed it mainly works through a combination of antagonistic effects at D2 receptors in the mesolimbic pathway and 5-HT2A receptors in the frontal cortex. D2 antagonism relieves positive symptoms while 5-HT2A antagonism alleviates negative symptoms.
References
- Brisch et al., Front Psychiatry (2014); 5: 47
- Olijslagers et al., Curr Neuropharmacol (2006); 4(1): 59–68

No. Schizophrenia isn't a single disease. It is class of psychotic disorders. Dopamine isn't the single cause of psychotic type diseases including schizotype. Many other pathways play a part in the various diseases; Serotonin, Glutamate, Histamine...ect.ect.ect. Genetic, Expressive and developmental factors are all known to play a role too.
Moreover you're not even describing typical symptomatic schizophrenia but a version of schizo that contains depressive features as well. Apathy caused by schizophrenia is a negative symptom a lack of interest in this life. Often we become preoccupied with the pleasures of delusions or hallucinations. The large dose of dopamine associate with a not "evil" hallucination is pleasurable on the order of cocaine. Delusions feel like antidepressants. Apathy caused by antipsychotics is entirely different.

Can you add some references to your answer?

@Chris is that enough or do i need to keep going?


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How to measure quality and quantity of DNA?
I would like to mesure DNA. I quantify the concentration with Qubit fluorometer, but I would like to know also quality of DNA. I try BioAnalyzer (Agilent),but without success. Bioanalyzer measure DNA samples from 100 to 7 000 bp (12 000 bp). Problem is that my DNA is not sheared, I would like to quantify whole mouse DNA. Have you any idea? Thanks!

You can run your DNA sample on agarose gel to see, whether you have significant degradation.
If you are interested in contamination, you can make a standard photometric analysis to assess the 260/280 and 260/230 ratios and absorbance at 320 nm on NanoDrop or even something similar to Eppendorf's BioPhotometer.
In case RNA may be an obstacle for some down-stream procedures, with Qubit you can also measure separately DNA and RNA concentrations and then decide if you have too much RNA and it's worth treating your sample with RNase.

I run DNA on gel...but I need some number for comparison...NanoDrop is probably the best option in my case :) Thanks!


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What does it mean for a chemical pathway to be conserved?
In many papers the MAPK pathway, (along with many others) is referred to as being conserved:
Example: "The mitogen-activated protein kinase (MAPK) cascades are ubiquitous in eukaryotic signal transduction, and these pathways are conserved in cells from yeast to mammals"
example 2 "The Hippo signaling pathway appears to be highly conserved."
What does it mean for a pathway to be conserved?

A conserved pathway is a pathway that exists in a variety of species, by virtue of that pathway being conserved throughout the evolution of those species. A pathway must by neccessity have appeared for the first time in one particular species. If that species gives rise to new species, but the pathway in question is identical or very similar in all the new species, it is sensible to say that pathway has been evolutionary conserved. This may imply that the pathway in its conserved form is important for the fitness of those species.
For some examples, here is a page on evolutionary conserved pathways in Drosophila: http://www.sdbonline.org/sites/fly/aimain/aadevinx.htm

Thanks, so it's conserved as in kept back, in the same way one would conserve a limited energy supply.

@RRs_Ghost I would rather say conserved as in unmodified (over long periods of time and across species).

More in the way that the pathway is found in a wide variety of species.

Good answer. You might add that there isn't really one MAP cascasde in mammals, although textbooks often speak of it as such --- there are several isoforms of each protein in the cascade, and probably many alternate signaling pathways connecting to different things. Which makes the idea of evolutionary conservation a bit more complicated ...

Great answer - would there be a bioinformatic way to query for degree of conservation of  pathway or how do people come up with the definition?


text:
How does sepsis affect heart function?
I have intuition that sepsis with infection can cause:

spastic functioning of heart during systole
heart working spontaneously in snatches during systole
atrial fibrillation
first contraction of ventricles ends earlier
which follows Action potential from A-V node during relative refractory period
weak second contraction
long compensatory pause

which can be recorded as spikes in the time axis.
With arrhythmic (earlier myocardial infarction) patients, sepsis seems to also cause leaking of valves, weakened compliance of vessels and structure of the heart.
So there are creaking sounds in the spectrum spaces.
How do the symptoms of sepsis affect heart function?
I am thinking if it is possible that this leakiness of valves and weakened compliance last only for short term and occurs periodically, during which also the heart pumps more frequently load during extrasystoles.
Assume that everything listed above is possible.

Can temporary acute/chronic inflammation in the heart cause such symptoms such as sudden weakening of valves and only temporary weakened compliance of coronary vessels?
I think the reason can be thromboembolism which is causing the sudden spastic function and weakened function of vessels and heart structures.

While the heart is affected during septic shock, it is the result of the chain of events that occur as a result of a systemic release of the pro-inflammatory cytokine Tumor Necrosis Factor alpha (TNF-$\alpha$) that leads to the "collapse of the circulatory and respiratory system." (Janeway's Immunobiology, 8th Edition) See also Tumor necrosis factor signaling.
When leukocytes, mainly macrophages encounter a pathogen or the antigenic product of a pathogen, pathogen-associated molecular patterns (PAMPs) such as endotoxins or exotoxins, their pattern recognition receptors (PRRs), such as the toll-like receptors, are bound and signaling occurs which stimulates the production and release of pro-inflammatory cytokines. In a localized infection, this is a beneficial response, however when the response is systemic, it will lead to a catastrophic cascade that leads to septic shock and often death.
Under "normal" conditions, TNF-$\alpha$ is an inducer of local inflammatory response. When an endotoxin such as lipopolysaccharide (LPS) is detected by TLR-4 on macrophages in the local microenvironment of an infection, the macrophages are stimulated to secrete TNF-$\alpha$. TNF-$\alpha$ produces the following physiological effects:

Activates the vascular endothelium

The endothelial cells will begin expressing a different assortment of receptors that recruit leukocytes out of the blood and into the tissue
This also allows for increased platelet adhesion to the activated endothelial vessels

Increases vascular permeability

Increased entry of Immunoglobulin G into the infected tissue
Increases entry of Complement proteins from the plasma to the tissue
Increased access to leukocytes and activated lymphocytes for extravasation into the infection microenvironment

Increased fluid drainage to lymph nodes

- Janeway's Immunobiology, 8th Edition; p 101
One of the mechanisms that is beneficial to the local inflammatory response, namely platelet adhesion will become problematic in the systemic response and will lead to multi-organ failure. In the local environment, however, it helps to prevent the spread of infection and shunts fluid flow away from the bloodstream and to the lymphatic system where it will be encountered by the components of the adaptive immune system. Locally:

Another important action of TNF-$\alpha$ is to stimulate endothelial cells to express proteins that trigger blood clotting in the local small vessels, occluding them and cutting off blood flow. This can be important in preventing the pathogen from entering the bloodstream and spreading through the blood to organs all over the body. Instead, the fluid that has leaked into the tissue in the early phases of an infection carries the pathogen, usually enclosed in dendritic cells, via the lymph to the regional lymph nodes, where an adaptive immune response can be initiated.
- Janeway's Immunobiology, 8th Edition; pp 107-108

You can begin to see where the inflammatory response triggered by TNF-$\alpha$ may become a catastrophic problem if it is secreted systemically.

Once an infection spreads to the bloodstream, however, the same mechanisms by which TNF-$\alpha$ so effectively contains local infection instead become catastrophic. Although produced as a membrane associated cytokine, TNF-$\alpha$ can be cleaved by a specific protease TACE (TNF-$\alpha$-converting enzyme, formerly called ADAM17) and released from the membrane as a soluble cytokine. The presence of infection in the bloodstream, or sepsis, is accompanied by a massive release of TNF-$\alpha$ by macrophages in the liver, spleen, and other sites throughout the body. The systemic release of TNF-$\alpha$ into the bloodstream causes vasodilation, which leads to a loss of blood pressure and increased vascular permeability, leading to a loss of plasma volume and eventually shock, known in this case as septic shock because the underlying cause is a bacterial infection. The TNF-$\alpha$ release in septic shock also triggers blood clotting in small vessels throughout the body--known as disseminated intravascular coagulation--which leads to the massive consumption of clotting proteins, so that the patient’s blood cannot clot appropriately. Disseminating intravascular coagulation frequently leads to the failure of vital organs such as the kidneys, liver, heart, and lungs, which are quickly compromised by the failure of normal perfusion; consequently, septic shock has a high mortality rate.
- Janeway's Immunobiology, 8th Edition; pp 108-109

So, as you can see, it is the effect of the depletion of clotting factor, the loss of plasma volume and blood pressure, and the alteration of the blood's ability to clot which likely is leading to the arrhythmic effects that you have observed in the heart.
The figure below summarizes both the localized and systemic effects of TNF-$\alpha$ release.
$\alpha$ can have damaging effects when released systemically" />
- Janeway's Immunobiology, 5th Edition; Figure 2.37
Effects of TNF-$\alpha$ on the heart
There is research from the 1990s and early 2000s that deals with the effects of TNF-$\alpha$ both on the heart and expression of the cytokine in failing heart tissue. Below is a brief selection of those articles. The final reference discusses the link between Toll-like receptor 4 activation and the promotion of cardiac arrhythmias:
From Cardiac-specific overexpression of tumor necrosis factor-alpha causes lethal myocarditis in transgenic mice. Kubota, et.al. J Card Fail. 1997 Jun;3(2):117-24.

Tumor necrosis factor (TNF)-alpha, a proinflammatory cytokine with negative inotropic effects, can be detected in myocardium with end-stage heart failure, after endotoxin administration, and during transplant rejection. Various studies suggest that TNF-alpha participates in the pathogenesis of cardiac dysfunction.
Overexpression of TNF-alpha in the heart leads to severe myocarditis and cardiomegaly. These results support the hypothesis that myocardial expression of TNF-alpha can contribute to the pathogenesis of cardiac dysfunction.

From Dilated Cardiomyopathy in Transgenic Mice With Cardiac-Specific Overexpression of Tumor Necrosis Factor-$\alpha$. Kubota, et.al.
Circulation Research.1997; 81: 627-635; doi: 10.1161/01.RES.81.4.627

That end-stage congestive heart failure is associated with a marked increase in circulating TNF-$\alpha$ levels has been reported by numerous investigators. Furthermore, there appears to be a direct relationship between disease severity and circulating levels of TNF-$\alpha$.
In the present study, we demonstrate that chronic overexpression of TNF-$\alpha$ results in the development of a dilated cardiomyopathy that shows (1) ventricular hypertrophy, (2) ventricular dilatation, (3) interstitial infiltrates, (4) interstitial fibrosis, (5) rare myocyte apoptosis, (6) a diminished ejection fraction, (7) attenuation of $\beta$1-adrenergic responsiveness, and (8) expression of atrial natriuretic factor in the ventricle. Additionally, mice overexpressing the TNF-α transgene had a marked increase in mortality. More than half of the mice that died spontaneously presented with exceptional dilatation of the heart, increased lung weight, and pleural effusion, suggesting that they died of congestive heart failure.

From The role of tumor necrosis factor in the pathophysiology of heart failure Feldman, et.al. Journal of the American College of Cardiology
Volume 35, Issue 3, 1 March 2000, Pages 537–544

In summary, both basic and clinical studies strongly support the hypothesis that myocardial expression of TNF alpha is an important step in the pathophysiologic pathway leading to progressive cardiac dilatation and failure.

From Toll-like receptor 4 activation promotes cardiac arrhythmias by decreasing the transient outward potassium current (Ito) through an IRF3-dependent and MyD88-independent pathway. Monnerat-Cahli, et. al. J Mol Cell Cardiol. 2014 Nov;76:116-25. doi: 10.1016/j.yjmcc.2014.08.012. Epub 2014 Aug 25.

Abstract
Cardiac arrhythmias are one of the main causes of death worldwide. Several studies have shown that inflammation plays a key role in different cardiac diseases and Toll-like receptors (TLRs) seem to be involved in cardiac complications. In the present study, we investigated whether the activation of TLR4 induces cardiac electrical remodeling and arrhythmias, and the signaling pathway involved in these effects. Membrane potential was recorded in Wistar rat ventricle. Ca(2+) transients, as well as the L-type Ca(2+) current (ICaL) and the transient outward K(+) current (Ito), were recorded in isolated myocytes after 24 h exposure to the TLR4 agonist, lipopolysaccharide (LPS, 1 μg/ml). TLR4 stimulation in vitro promoted a cardiac electrical remodeling that leads to action potential prolongation associated with arrhythmic events, such as delayed afterdepolarization and triggered activity. After 24 h LPS incubation, Ito amplitude, as well as Kv4.3 and KChIP2 mRNA levels were reduced. The Ito decrease by LPS was prevented by inhibition of interferon regulatory factor 3 (IRF3), but not by inhibition of interleukin-1 receptor-associated kinase 4 (IRAK4) or nuclear factor kappa B (NF-κB). Extrasystolic activity was present in 25% of the cells, but apart from that, Ca(2+) transients and ICaL were not affected by LPS; however, Na(+)/Ca(2+) exchanger (NCX) activity was apparently increased. We conclude that TLR4 activation decreased Ito, which increased AP duration via a MyD88-independent, IRF3-dependent pathway. The longer action potential, associated with enhanced Ca(2+) efflux via NCX, could explain the presence of arrhythmias in the LPS group.

It would be great to understand in which order the dysfunction of valves and coronary vessels commonly occur. I think that the dysfunction of valves can occur earlier in the cascade of TNF-$\alpha$ than the dysfunction of coronary vessels because the hypovolemia leads to the occlusion of the vessels in the late stages. It would be great to understand the pathway differences of Tumor necrosis signalling between the valves and the vessels.

I extended the Synchronicity of TNF signaling in heart's microenvironments to the thread http://biology.stackexchange.com/q/41981/86

@Masi please see edits with additional information on TNF-alpha and TLR-4 in cardiac failure and arrhythmias.


text:
Normal Frequencies in Heart
I am trying to visualise possible ranges of frequencies from different structures of heart:

different valves and their possible frequencies
heart sounds I - IV and their normal frequencties
what can frequencies be in healthy situation for adult
what can frequencies be in healthy situation for children 4-9 years old

I searched meta-analysis, clinical trials and reviews in PubMed unsuccessfully.
Is there any review article or book about the frequencies from different structures of heart?
Search terms used

frequency heart
frequency heart valve

frequency as in the electromagnetic frequencies I presume?

Yes. Electromagnetic frequencies.

This is a part answer (as this is outside of my field), but the article Self Regulation of the Heart: Natural Frequency and Damping of the
Heart Contractions  (Bahramali et al. 2009) imply that 'normal' frequencies may not be possible to precisely define, due to:

ECG frequency analysis is complicated by the fact that ECG signals are non-stationary, that is, their activity
  patterns change slowly or intermittently as a result of variations in a number of physiological and physical influences.

The article extensively reviews the general frequency analysis, divided into P, Q, R, S and T components.  However, they define 'optimal conditions' (i.e. 'normal and healthy) as:

optimal conditions of the heart contraction as those under
  which the dynamics of contraction shows the best
  agreement with underdamped harmonic oscillation

An example of this is visualised in the diagram below:

this example is provided on the University of Pennsylvania tutorial site ECG Tutorial
In the article Comparison of Power Spectral Density (PSD) of Normal
and Abnormal ECGs (Das and Chakraborty, 2011), note comprisons for the QRS component, as

QRS complexes are chosen because
  it shows distinct differences for different heart diseases

In other words, distinguishing healthy from not-so-healthy.

Thank you for your review! Those mathematical methods used in those publications are insufficient. Data is lost when filtering is used. Power spectrum vs frequencies can NEVER reveal the exact energy patterns of the cardiac frequencies in time.


text:
What is TILLING?
How does TILLING (Targeting Induced Local Lesions in Genomes) work? What is needed to perform a TILLING experiment, and what kind of information can we get out of it?

You can easily get the answer to this question in wikipedia article on TILLING


text:
How does DNA resolve on size exclusion resin?
We generally have a good idea of how DNA separates using agarose gel electrophoresis, how well does DNA resolve on a SEC resin like superose? I get the impression that salt influences where it elutes.
Is it possible to compare the molecular weight of DNA and where it elutes to the molecular weight of proteins and peptides and where that elutes?

It works pretty well and can be used to desalt DNA. The DNA runs a bit different than proteins since it is more a long stretched molecule while a lot of proteins are globular. See this references (the first is about the behaviour of DNA on superose):

Size-exclusion chromatography of DNA restriction fragments. Fragment
length determinations and a comparison with the behaviour of proteins
in size-exclusion chromatography.
Size exclusion chromatography of DNA and viruses: properties of
spherical and asymmetric molecules in porous networks
Size exclusion chromatography of plasmid DNA isoforms


text:
Population Genetics Question

Can someone please help with this question? Here is my working (just in case it is not clear: 1/300*1/30*1/2) but is this actually correct or do I need to multiply by 0.5 once again? I appreciate any help!

Question is: If an Ashkenazi(1/30) and(multiply) French-Canadian(1/30) ....
Where 1/300 came from ?
I duno, I may missing something - but may it be like  that
Parrent1(=1/30 * 1/2)*Parrent2(=1/30 * 1/2) = P(child with both mutations)


text:
What is the energy consumption of the brain?
What is the energy consumption of the brain, and is there a difference in consumption when waking and sleeping?

Do you mean the activity as visible in an EEG? Because the brain mainly uses up energy as far as I know.

I assume that you mean energy consumption.
Talking in round numbers the daily energy requirement of a sedentary human is 2,500 kcal. It's usually said that the brain uses 20% of this energy.
What does this mean in terms of power consumption?
500 kcal = 500 x 1000 x 4.2 J  -[1]
24 h = 24 x 60 x 60 s          -[2]

1 W = 1 J/s

therefore brain power  = [1]/[2] = approximately 24 W

Most of the energy consumed by the brain is used in maintaining membrane potentials so energy is used continuously. I would think that there will be very little difference between waking and sleeping.

One ref for the breakdown of energy costs: Laughlin, S. (2001). Energy as a constraint on the coding and processing of sensory information. Current Opinion in Neurobiology, 11(4):475-480.

The cortical activity pattern is measurably different between rest and sleep states. I think there would be measurable differences.

Adding to this: There is a difference of active vs. inactive brain regions in terms of energy consumption. This is used in PET (positron emission tomography) scans. Here you enrich radioactive glucose in the regions which are more active (=need more energy) and make them visible.

I'm not denying that brain activity will require more energy (to restore membrane potential), I'm just dubious that it will be a very big difference (the brain is active during sleep too). I await an answer that provides evidence about this.


text:
Can excessive carbonated drink consumption lead to elevated red blood cell levels?
I've recently had a blood test and the results displayed elevated levels of erythrocytes as well as hemoglobin. (As a result my hematocrit levels were also above average)
At my workplace there is a water cooler which also has an option to dispense carbonated water (this is just regular ol' carbonated tap water) and usually over the course of the day I tend to drink quite a lot of the stuff.
Since erythrocytes/hemoglobin deals with O2 and CO2 transport, I was wondering if my daily consumption of carbonated water is a plausible cause for the additional erythrocytes that are being pumped out?

Does CO2 increase in the blood when active?

The main regulatory input into erythrocyte production is hypoxia. The response to elevated CO2 levels in the blood (hypercapnia) is mainly to increase ventilation (i.e. more and/or deeper breaths) so that the excess can be "blown off".
I think that some carbon dioxide could pass into the bloodstream from the stomach since gases tend to be quite good at diffusing across membranes, but this would be easily dealt with by the physiological mechanism described above.

Answer: No. How should the CO2 from you stomach get into your blood?
And: Most of the CO2  is removed (by burping) from the solution in your stomach anyway due to the conditions there.


text:
Literature about industrial enzyme application
Can someone point me out to literature (reviews or better workbooks) describing industrial chemical reactions catalysed by enzymes?
What I'm most interested in are case studies of how the output of a reaction on a big scale is optimized with respect to enzyme activity.
Most of the literature I'm finding is about optimization of cell growth, which is not what I'm looking for.

Can you please accept answers, which answer your question satisfactory? This is a nice gesture towards the people who write the answers. You can find all your questions in your User menu.

I'll give you examples I have encountered in talks. There are too many variations and types of applications for me to break out in a comprehensive way.
Example 1: enzyme production.  this sort of application is about optimizing the amount of a desirable enzyme or protein produced from a liquid culture.  Sorry if this is too close to cell growth, but its terribly important.  Small cell cultures are used in research and the genetics of the cells (usually e coli or yeast, but also often a fungus that's been found somewhere) to improve the amount of the desired protein.  The protein may be secreted, which makes it much easier to purify.
Once a good strain is found, the culture is scaled up to thousands of liters, often many kilos of pure enzyme can be produced this way.  Examples: the enzymes that break down fabric for acid washed jeans, the proteases and cutinases which are included in laundry detergent
and insulin.
Example 2: glucose isomerase.  This enzyme is used to produce high fructose corn syrup.  The enzyme itself actually changes fructose into glucose, but by le Chatlier's principle, a glucose syrup under high pressure will be converted to fructose by the enzyme.  This enzyme, produced by an industrial process like that described in example 1 is immobilized onto a resin and packed into large industrial sized columns.  I seem to remember from the talk that they were similar in size to an oil barrel.  Large amounts of glucose rich corn syrup are passed through the column; it comes out about 40% fructose.
Another example (3)  along those lines might be how to use an enzyme with a product.  In an industrial manufacturing process like enzyme denim treatment, the fabric may be washed in a solution including the enzyme.  The process has to be careful to control the amount of enzyme the denim is exposed to and to optimize the conditions so that none of the fabric is ruined but comes out consistently.  The enzyme might be killed by a pH change or heating.  This is essentially chemical engineering and there are courses about this sort of thing at most major chemE departments now.

Your ex. 2 is in the direction of what I'm looking for. I agree cell growth optimization is important, but not relevant for my specific case- the engineering considerations are also not applicable. Do you have more examples of your example 2 type?

Ive added another example - these two examples are immobilized enzyme and heterogeneous enzyme processes that broadly cover a lot of applications.

Google's first hit for me. Also consider invertase  to make soft centered toffee candy. And citric acid and beer/wine.  Although they use microbes, enzymes do the work.

that's a good one @PlaysDice.  fermentation with organisms would include vitamin production, beer brewing, nacho cheese... a whole new frontier.

no probs. I like your answer and didn't want to add mine and dilute yours.  My Google link is a very accessible intro.  OP should now be able to find a reaction and search for literature on its optimization.


text:
Triune brain model
I have heard about the triune brain model in biology class, but my teacher does not know much about it. What I'm curious about, is this model accepted by most of the neuroscientists, or is it just a mere hypothesis? And should I learn more about it? Although I think it's an interesting topic, I won't put efforts in finding all the info on the net, if not necessary.


text:
What exactly is Tinnitus?
What exactly is tinnitus? What is it's cause, and why do some people hear it and others don't?

Although tinnitus is usually described as a ringing in the ear, there's a whole range of tunes, buzzes, whooshing sounds, humming and hissing sounds that are described of as tinnitus. The sounds can either genuinely be there or be perceived to be there. If it is genuinely there it suggests muscles ate at play or some blood vessel disease if the sounds are in time with your pulse, but usually its the latter perceived to be there that presents.
Tinnitus that is perceived and permanent usually suggests damage to your hearing nerve (called the auditory nerve or cranial nerve 8 or vestibulocochlear nerve). The common cause for this we see is patients that have been exposed to loud noises or drugs like certain strong antibiotics which cause damage to the nerve. Other drugs also have a side effect of causing tinnitus. However any ear problems really may cause tinnitus including ear infections, too much wax, getting older, a disease called Mennieres, tumours, neurological diseases, vitamin deficiencies and lots more.
If you're really interested, keep reading. There's a number of reasons why it might occur. Usually patients presenting with it have some degree of hearing loss. Its thought that somewhere along the line the structures are getting more sensitive to sound because through a feedback mechanism. Think of it this way, you speak to someone but they can't hear you so you speak louder and louder until they can. In the same way its thought that the sensitivity is increased and increased to try to restore hearing but the result is audible nonsense sound from abnormal activity i.e. tinnitus.
If anything doesn't make sense, please do say :)

What a wonderful story. I'll have to up vote it.

it is the commonly perceived answer for the majority of humanity...not the one I'm looking for though, so I must decline and stack exchange states that I do not have to accept an answer.  Android has plenty of rep, I doubt 35 more is going to matter.

@Jody Actually my flat mates have decided they will only give me food this week if i get 35 more reputation

More seriously, what are you looking for that I haven't answered?

@Jody: you give a general question, so expect a general answer. All that AP said here seems to be good, correct information AFAIK; tinnitus are symptoms not actual diseases, so it can have multitudes of totally unrelated reasons. If you want a specific answer, please specify what exactly you want to know about tinnitus.

Again, I remind you that I am not required to accept an answer per Stack Exchange Rules, regardless of how good it was answered. I placed a bounty and a hint at what I was looking for and if I get an acceptable answer then so be it.

+1 for giving a solid answer to @AP, but being older I've had friends who have had tinnitus and I'd like to add some notes to try to flesh this out a bit.
I don't think tinnitus is the result of nerve damage usually.  Nearly everybody experiences episodic tinnitus at one point or another.  When exposed to a loud sound or a blow to the head can cause it.
Chronic tinnitus occurs when the sound does not go away and is heard all the time.  This is annoying but incredibly common - nearly 1 to 2 in ten people have an extended period and about 0.5% of people experience tinnitus to the point where it affects their daily life and it doesn't seem to ever go away.
Like headaches, schitzophrenia, depression, and other neurological conditions, the specific cause of tinnitus is not really understood and explanations which are really satisfying are hard to imagine.
While a loud noise could possibly cause nerve damage in the auditory system, it sounds more often the cause is related to a vulnerability in the auditory system that allows the generation of these sounds in such a way that they cannot be tuned out. There have been genetic factors associated with the tendency to tinnitus, implying that physiological factors are in play. Tinnitis can be aggravated by stress, caffeine and smoking, which further implies that nerve physiology has a lot to do with the condition.
Much of the treatment for tinnitus involves amplifying other sounds in other parts of the sound spectrum so that the ringing sound tunes itself out - that the nervous system actually attenuates the sound as it should so that the patient does not consciously register it. Hypnosis and cognitive behavioral therapy have also been touted as well as herbal remedies, diet changes, but attenuation is all the result that is typically expected.
There is a class of tinnitus where a pulsating sound from vasculature near the auditory nerves appears to be a cause.

Apparently some (small amount of) tinnitus is caused by, or at least associated with, otoacoustic emissions. This paper covers the link if you are interested.
If you want a great talk that generally covers the molecular mechanisms behind hearing, I highly recommend this one by James Hudspeth. This covers a ton of material, including otoacoustic emissions, and is very interesting.


text:
Book recommendation on selective breeding?
I am looking for a good book that gives a nice overview of the science and technics of selective breeding. I am particularly interested in the use of population genetics to support decision in this applied field. So do you have any suggestions?

Below are some examples of question that I would hope that book answers.

If the artificial selection is too strong, it is very likely that some beneficial alleles will disappear. How strong do we decide artificial selection to be?
How do we deal with various lifetime?
How do we deal with species that can have only few babies so that we are obliged to limit the strength of selection to keep a stable population size?
How do we make sure to not reduce the immunologic genetic diversity within the population to zero but only to reduce the diversity of genes that influence the trait of interest?
Is it better to wait to be able to measure the quantity of milk in the sisters of a bull in order to infer about the quality of the bull or is it wiser to directly allow the bull to reproduce to speed things up?
How are the estimations of heritability performed?
How do we measure the impact of various environment of the trait of interest?
Which cultural traits should we allow to spread and which should we stop?
How can we use a correlated trait to infer more simply or more rapidly of the amplitude of the trait of interest?
How much outbreeding should we allow?
When is mutation breeding preferable?

and more globally some questions of the kind:

What are the different solution to artificially inseminate?
Can we select on the spermatozoids?
What financial elements should be taken into before creating a breeding plan?
GWA's studies in selective breeding
What is the relative importance of selective breeding and GMO in current economy and in our current ability to improve strains for our purposes?

i would imagine that there are so many solutions amongst the scores of animals and plants that are bred selectively that such a single book does not exist.  selective breeding is a millenia old discipline depending on the culture and the strain and a lot of these genetic terminologies are relatively recent.  The differences between say a sheep and an orchid are so vast I'm not even certain that it would be worth the effort to try to cover all these topics in one volume.

I will Suggest:
Selective Breeding in Aquaculture: An Introduction
Authors: Trygve Gjedrem, Matthew Baranski
ISBN: 978-90-481-2772-6 (Print) 978-90-481-2773-3 (Online)
http://image.slidesharecdn.com/selectivebreedinginaquaculture-anintroductionreviews-methodsandtechnologiesinfishbiologyandfisheries-140725230642-phpapp01/95/selective-breeding-in-aquaculture-an-introduction-reviews-methods-and-technologies-in-fish-biology-and-fisheries-10-1-638.jpg?cb=1406347865

authors: Элл Нейгебауэр


text:
Do you have experience with PacBio?
I prepare a experiment and I found $PacBio SMRT$ as the great way to sequence my PCR products. I find the cost: library preparation 655 dollars + sequencing 435 dollars. It seems very low. Do you have some experience how much of sample can I sequence in one run (by coverage around 30) and if it is really for this price?

If it is a good idea to use PacBio depends a lot on what you want to sequence and what you want to do with the data you get. In short: you get longer reads but about 15% error per base. This means, you will have to cope with those errors, there are possibilities to do that. How much coverage you will get of you sample I cannot tell you, as I do not know what kind of sample you want to sequence.
How much data you get out of one SMRTcell depends also on the chemistry, I think it currently is between 275 Mb and 375 Mb, depending on chemistry. They have a nice brochure you could look at.
Anyway, you probably will have to get some advice by a bioinformatician of you choice on how to design and analyse your sequencing experiment.

I am planning to sequence mouse genes of MHC a TLRs (about 2000 bp). Can you get me a fictitious example about how much sample can I involved by certain covarage?? Thanks a lot! ;)

I have never done this calculation for a sample this small with PacBio. To keep it short, from one SMRTcell you would get 30x coverage of the E. coli genome (no fiction, they have done 3 cells and got 100x coverage). I guess this is a bit oversized for your short samples. Still, I would rather not do any more "virtual" calculations about this, you need to have someone you can talk to who understands your experiment and probably has seen more PacBio sequencing than I have.


text:
condensed protocol for sequencing a portion of human DNA from buccal sample
Anyone have a short & sweet protocol for PCR amplifying a region of human DNA (chromosomal or mt, I don't care) extracted from a buccal sample: including validated primer sequences and preferred method of DNA isolation from a buccal swab. I'm looking for a new exercise to run in my classroom. We would be able to follow the amplification up with Sanger sequencing, done in-house.

Which possibilities do you have for the extraction? Would this be more "lab-like" or more "DIY-bio"-style?


text:
Tapeworms and their effect on humans
I've read that some people in some countries actually use tapeworms as a form of losing weight.  What are the dangers to these people?

I haven't really found much on this topic (besides popular sites) but I can summarize it here:
There are quite some tapeworms (or cestoda), I found numbers of up to 3500 species. They attach to the intestinal wall of the humans and then start to take up predigested food through their skin. With that, they reduce food from their host and start to grow, some get as long as 15 meters!
Some of the worms seem to be relatively harmless (besides stealing food), but this is more true for the first world. In poor countries, where there is not enough food, tapeworms can cause severe malnutrition.
Some tapeworms can migrate into the blood stream and from there into other tissues or organs like muscles, eye and brain. There they can cause cysts which can lead to organ failure and death.
For more information see this CDC webpage and this article: "Biochemistry and physiology of tapeworms.". This popular article is probably also interesting.

An addition to the answer by Chris.
Probably the most dangerous tapeworms for humans are Echinococcus. In humans they form cysts (in a variety of organs including brain) [it's because humans are "interpreted" as intermediate hosts], which can become very large and can cause death when untreated or disrupted.


text:
Is there any documented case in which floating substances led to the introduction of a new species?
Floating substances in the marine or freshwater environment often carry hitch hiking organisms. It is argued that many species may use this dispersal vector to reach new habitats, however to my knowledge there is no hard evidence / no documented case. This may be because of the difficulty to associate an established species with a certain vector of introduction.
By floating substances I refer to natural floating substances such as detached algae, trees or pumice and those of anthropogenic origin such as litter items, detached buoys, etc. (in whatever aquatic environment: sea, lakes, rivers)
Any help to find a reference / documented case study is very welcome!

But not including actual sea-going vessels?

Right, no vessels. Their dispersal capacity, especially considering vessels with ballast tanks, is not readily comparable to other floating "substances" and IMHO better understood.

As far as I know, this is dicussed for the distribution of geckos through the pacific. They are common on quite a number of islands.

im pretty sure it happens all the time - geologically speaking.  @Chris could cite 'Voyage of the Beagle' for the galapagos chapters really

There is a number of reported cases of marine species reaching new locations through "hitchhiking" in recent times. However, it seems harder to find reports of species actually becoming established in a new location through this.
The following articles describe examples of species transported with ocean debris:
In an early study on the dispersal of plastic pellets (3), it was suggested that pellets encrusted with the bryozoan Membranipora tuberculata was transported to New Zealand across the Tasman Sea from Australia. Barring one exception, this was the first time the species was observed in New Zealand waters.
Appendix A of a later article by the same author (1) contains 13 examples of species transported by sea (not necessarily through debris, or invasive), including the previous example. Of it, the author writes that

Later, L. M. Stevens (1992, unpublished data) was to report that [Membranipora tuberculata]
  was abundant on both eastern and western shores around northernmost
  New Zealand.

Thus, this is possibly a case of a species transported on floating debris and subsequently becoming established in a new habitat.
Jose Derraik also deals with the topic in a review (4):

Plastics floating at sea may acquire a fauna of various encrusting
  organisms such as bacteria, diatoms, algae, barnacles, hydroids and
  tunicates (Carpenter et al., 1972; Carpenter and Smith, 1972; Minchin,
  1996; Clark, 1997). The bryozoan Membranipora tuberculata, for
  instance, is believed to have crossed the Tasman Sea, from Australia
  to New Zealand, encrusted on plastic pellets (Gregory, 1978). The same
  species together with another bryozoan (Electra tenella) were found on
  plastics washed ashore on the Florida coast, USA, and they seem to be
  increasingtheir abundance in the region by driftingon plastic debris
  from the Caribbean area (Winston, 1982; Winston et al., 1997). Minchin
  (1996) also describes barnacles that crossed the North Atlantic Ocean
  attached to plastic debris. Drift plastics can therefore increase the
  range of certain marine organisms or introduce species into an
  environment where they were previously absent (Winston, 1982).

Finally, the book Marine Pollution: New Research (2) contains the following passage which ends with the observation that conclusive proof is difficult to obtain:

Drift plastics are known to have introduced exotic marine species to
  several areas (Winston et al., 1997; Deraik, 2002). Winston et al.
  (1997) reported that the non-indegenous oyster Lopha cristagalli was
  fond on plastics wshed ashore in southern New Zealand, and that the
  exotic bryozoan Thalamoperella evelinae was found on plastics washed
  ashore in Florida. Barnes and Milnder (2005) fond the exotic barnacle
  Elminius modestus on plastic debris in the Shetland Islands (Atlantic
  Ocean). The bryozoaen Membranipora tuberculate is believed to have
  crossed the Tasman Sea from Australia to New Zealand rafting on
  plastic pellets (Gregory, 1978). M Tuberculate and the bryozan Electra
  tenella seem to be increasing their abundance on the Florida coast by
  drifting on plastic debris from the Caribbean sea (Winston, 1982
  Winston et al, 1997). Maso et al. (2003) (...) However, attributing a
  marine biological invasion to floating marine debris and not to other
  mechanisms is very difficult in most cases, and available data are
  generally insufficient.


text:
Why do the neuron pathways decussate?
I learn about the brain right now, and there are crossing of neuron pathways everywhere; in the thalamus, the medulla oblongata, the pyramidal tract... And I don't understand why? What is the reason to connect - for example - the right foot to the left part of your brain?

Possible duplicate: Here and especially here.

Crossing or decussation is a lot more robust against wiring errors than their seemingly simpler same-sided wiring counterparts. See here for the research carried out to establish this and for more detail.


text:
Any examples of life forms on Earth that could have survived on Mars or Moon?
Do we know of any living forms on Earth that could continue to live on Mars?

Under the current conditions and without an athmosphere? Hardly imaginable.

Yes, under current conditions and without an atmosphere.

Yes, research studies that were conducted have found that methanogens (microorganisms) are able to survive in conditions similar to Mars (reference). Another study conducted has also concluded that some lichen and cyanobacteria is also capable of survival.  Surprisingly, they were also found to be active (reference).
There is speculation now on whether organisms from earth have been accidentally transported to Mars on the Mars Curiosity Rover which would be funny or a cause of concern, depending on how you look at it (reference).

Interestingly, methanogenes are even more useful for terraforming Mars than plants, because they accelerate greenhouse effect.


text:
List of the biggest companies that work in selective breeding
Looking at this question, I've been wondering, What are the biggest private companies which work in both animal and non-animal selective breeding?
Let me know if Biology.SE is not appropriate for this kind of question.
Thank you

Seeking on the internet I found these two companies Hendrix Genetics and PoultryHub

This varies by the kind of animal or plant. I think one company would rarely do both.
For plants Monsanto comes to mind.  And Syngenta.
I'm not sure for animals.  For beef cattle in the US, this is done by individual ranchers (who may be corporations) that collectively share their genetic data creating a market which can predict the value of a bull.  The market for bull semen can be worth hundreds of dollars per impregnation.
Why are bulls valued at such a greater rate than cows?  Because semen can be preserved, transported and used thousands of times while a cow can only calf one at a time.

Thanks for this answer. I found two companies on the internet (see comment under my question). I'll wait to see if others can bring some other company names. I am surprised that individual ranchers make their own selection without any breeding plan decided at a national level.

in the US that would not quite work.  but the history is that cattle ranchers have been doing this for centuries and a company hasn't quite been capable of taking the business from them.  seed farmers have been okay with buying seeds from central sources for some reason.

you can add perdue chicken to the list too though.  they do breed a specific line of chickens for meat.  they don't let their farmers even hatch eggs.


text:
A question about gag reflex
If left glossopharyngeal nerve and right vagus nerve are intact, but there is a lesion at left vagus nerve, would stimulating the left side of pharynx elicit a gag reflex?

The sensory and motor components are  required (GP and vagus respectively). Similar to the corneal reflex and cranial nerve 5 and 7, if a lesion exists in either the sensory or motor component there will be a defect. In your case, there is no motor innervation on the left due to the lack of the vagus nerve so there is no vagus nerve response.


text:
What are mast cell membranes made out of?
What are mast cell membranes made out of?
What would weaken or strengthen them?
Web searches bring up a lot of information about mast cells but very little on the membrane. And the Wikipedia page is not clear as to whether or not additional calcium or sodium fluoride would improve/weaken mast cell wall strength.

Why do you want to change the cell membrane?

I'm trying to understand potential causes of Dermatographic Urticaria.

Why this happens is unknown (at least after a short look into the literature), but it seems, that anything, that causes stress to the skin can cause this symptome.

Add more information on the context of the question to get a better answer

Cell membranes (not cell walls) are composed of a double layer of phospholipids. The lipids are orientated in the way, that the hydrophilic part of the molecule is oriented to the outside and the inside of the cell and the hydrophobic tail to the inside of the membrane.
See the figure from the Wikipedia:

Embedded in the bilayer are transport proteins, receptor and so on. Calcium and sodium fluoride have no effect on the integrity of the membrane.

So mast cells are the same as all cells in regards to membrane and wall?

@brannon there are no cell walls in animal cells.  They r found in plants and fungi. See d wikipedia page on call walls.

Eukariotic cells only have membranes made of phospholipids. Their protein content and also the flexibility varies between the different cell types. But in general, the overall composition is the same.

Although the Wikipedia page on dermatographism refers to "weak membranes" it cites no source for this, and like Chris, I haven't found any mention of this in a quick look at the literature.
Histamine is usually released from mast cells in response to specific stimuli by a degranulation reaction (internal vesicles fusing with the surface membrane to release their contents) and I would guess that abnormal degranulation is a more likely cause than cell lysis.
In a recent paper (Ralph, JW (2013) Evidence for a role of neural pathways in dermographism. Brit. J. Dermatology 169, 1357–1374) a case is reported of a man who combines dermatographism with a syndrome called "stocking-glove neuropathy". This latter syndrome results in a pattern of loss of sensation in the lower arm. When the dermatographic reaction is triggered in this patient the resulting weal does not extend into the affected part of the arm, suggesting that neural activity is part of the trigger for dermatographism. In other words, in those suffering from dermatographism, sensory nerve activation would somehow result in cross-talk into the pathway for stimulating mast cell degranulation.


text:
Could alpha-numeric taxonomy of fungi make things simpler?
Please feel free to construe this question broadly--I don't see why the question would not apply to branches of biology other than mycology.
If the goal of taxonomy is to create classification of fungi that reflect evolutionary relationships, and if this results in a more or less unmanageable proliferation of names, might it not be a good idea to use a numeric or alpha-numeric system instead of a verbal one? One author estimates there may be as many as 5 million species of fungi (and it may take 1000 years to catalog them). If we did manage to note them all would the result really be useable? The ease of storage and retrieval alone would seem to commend a numerical approach.
I assume someone has thought of this before and I guess viral taxonomy does this to some extent. Are there any proposals like this afoot?
Thanks for any insights.

(First of all the term numerical taxonomy has a completely different meaning. Here you are talking about nomenclature.)
(To make it clear: you are talking about species.)
Simpler for whom?
For humans numbers are much less memorizable than pronounceable and often meaningful words. For database management identification numbers are unavoidable - that's true, because numbers require less disk space and lead to smaller indices and faster access, but that doesn't mean that the text field "title" should be abandoned.
In IndexFungorum, for example, they have id's for every name: e.g. www.indexfungorum.org/Names/NamesRecord.asp?RecordID=228098 for Boletus edulis, but they do not expect the user to use 228098 in place of the name, because that would be inconvenient.
On Mycobank different id's are used: www.mycobank.org/Biolomics.aspx?Table=Mycobank&MycoBankNr_=356530. I'd agree, that would be good to have the same id everywhere, but database managers nicely trace these numbers for us (see e.g. the "Other fungal links" section).
By the way, nomenclature of Fungi is controlled by the International Code of Nomenclature for algae, fungi, and plants. Nomenclature of viral species is still based on memorizable names.

Actually I think I was talking about numerical taxonomy in the context of fungi but this answer was useful. Thanks.

In 2017 Rambold et al. have proposed to cite a taxon name identifier instead of taxon name author citation: https://doi.org/10.12705/665.12 But I very like the proposition of Dubois (2008) to cite year of taxon publication instead of author: https://doi.org/10.1111/j.1095-8312.2007.00900.x

This is actually already done in some contexts.
For instance: yeast (a fungus) is a pretty extensively studied organism, and this means that there are a vast number of yeast strains which are know/used by biologists.  Many of these strains are referred to simply by an alphanumeric string rather than a "verbal" name.  (some examples in link 1)
This is also the case for bacteria, and maybe most of microbiology.


text:
Comment on the introduction to a bioinformatics paper
I've written a paper about DNA sequence analysis. This paper attempts
to use Bayesian modelling for a set of DNA sequences. It will probably
end up either in a statistics journal, or, more likely, in a
bioinformatics journal. My concern is that biologists may take
exception to some of the language in the introduction.
I'm attempting to make a connection between De Novo motif discovery,
and modelling the sequences. Maybe it is a bit of a
stretch. E.g. I use language like "analyzing a set of DNA sequences
with biological significance solely by focusing on the motifs
contained within them potentially discards valuable information, for
example, possible long-range correlations between nucleotide
positions in the sequences." Also, "An alternative, and possibly
complementary approach, is to consider a sequence as a single unit,
and try to do direct statistical analysis on it... This approach is
used in this paper, which does not use Markovian techniques. Instead,
it tries to model correlation structure across the sequence."
So, the question is whether it is better to try to make an explicit
connection at the risk of saying things that are incorrect and
generally over-stretching, rather than just saying (which seems a
little lame) that this sequence classification problem is related to
De Novo motif discovery problem and leaving it at that. Comments?
I include the first few paragraphs of the introduction below. This
includes all the relevant language.
I'm willing to send my current draft to anyone who is interested in
knowing more about the context. I don't want to post a public link to
it, though.

DNA sequence motifs are nucleotide sequence patterns that are
  conjectured to have a biological significance. Often they indicate
  sequence-specific binding sites for proteins such as nucleases and
  transcription factors (TF). Others are involved in important processes
  at the RNA level, including ribosome binding, mRNA processing
  (splicing, editing, polyadenylation) and transcription termination.
  Motif discovery is a very active area of research interest. So-called
  “De novo computational discovery” is perhaps the most popular, where
  given only a set of DNA sequences, an algorithm is used to identify
  candidate shared motifs. This can be thought of as the task of finding
  a set of non- overlapping, approximately matching substrings given a
  starting set of strings. This is a very difficult problem.
From a more general perspective, DNA sequence analysis is often done
  using DNA sequence motifs. It is reasonable to ask the question - what
  makes a sequence a motif? From a biological perspective, a motif is
  simply the smallest identifiable sequence sub- component of something
  larger.  This subcomponent can be thought of as the smallest
  identifiable piece of functionality related to the underlying biology,
  Therefore, sequence analysis often focuses on identifying these
  motifs. However, these motifs are typically very short, so analyzing a
  set of DNA sequences with biological significance solely by focusing
  on the motifs contained within them potentially discards valuable
  information, for example, possible long-range correlelations between
  nucleotide positions in the sequences.  Note also that the statistical
  methods used to identify motifs are typically Markovian, like Hidden
  Markov Models (HMM), which are naturally tailored towards looking at
  small sequences.
An alternative, and possibly complementary approach, is to consider a
  sequence as a single unit, and try to do direct statistical analysis
  on it. This approach is less often used. One reason is that such
  sequences can quickly grow too large, and are not well suited to
  Markovian approaches. This approach is used in this paper, which does
  not use Markovian techniques. Instead, it tries to model correlation
  structure across the sequence.
We do this by fitting a suitable Bayesian model to that set using
  Bayesian model selection. As noted above, our major rationale for this
  model is the assumption that the nucleotide locations of this set are
  correlated among themselves. With this assumption in mind, we
  construct a family of probability distributions to capture this
  correlation information, described in Subsection 2.1.

I'm not technically a biologist, I'm a bioengineer, but even biologists understand the limitations of HMM for motif finding. If you can pick up on long-distance conserved disulfide bridges and that sort of thing, there's value in that. You haven't written anything that'll ruffle feathers that don't need a good ruffling.

@JeremyKemball Thanks for the feedback. Consider writing a formal answer, if you feel comfortable doing so. Not really sure what "disulfide bridges" are, though.

Cysteine residues form -S-S- bonds across long sequence distances. They're a big structural/functional feature, one that's hard to detect with Markov models. So you're not implying anything too off-the-wall. I won't submit a formal answer, because I don't really work in this field. Maybe I'm missing something? Who knows.

Bioinformatics journals can deal perfectly with this type of papers. If you target a journal like Bioinformatics, then you can be as technical as you want (and you probably should). Biologists that read those journals will most likely understand the terminology.
Even traditional experimental biology journals, like Nucleic Acids Research, now include a section for Computational Biology that can be a perfect target for a paper on DNA motif analysis. If you submit to such a journal, however, you have to consider the target audience may be more broad than the typical Bioinformatics journal.
If you aim for Biologists to understand the concepts, you have to accept that there will be Biologists with very variable degrees of understanding of Bioinformatics. For example, as mentioned in some of the comments, some Biologists may understand what Hidden Markov Models are, others, however, may have never heard the term before. I would suggest that if you target a Biology centered journal, try to explain things in very simple terms, connecting the concepts to real life examples. You can use those explanations as introduction to more detailed descriptions. Depending on the journal, you may want to put the technical details, including formulas, in supplementary material. Keeping the technical details out of the main manuscript will make it accessible to general readership, yet having the details in supplementary material will give rigor to your paper and allow anyone interested in your research to check the details.

Hi, I've read this a couple of times, but it does not appear to address my question. You seem to be answering a question I didn't ask, something like where is a good place to place such a paper. I'm asking a fairly specific question (perhaps not too well phrased), which could be summarized by the sentence "I'm attempting to make a connection between De Novo motif discovery, and modelling the sequences.". In a nutshell, I'm wondering if the statements I make in the intro (quoted) would be considered controversial or objectionable.

Hi. Yes, it is possible that I did not understand your problem. I thought the quoted part was as an example of the type of description that you would put. My response was more in the line of how you should generally approach the writing to a Biologists oriented journal. If you are asking whether that specific piece of text should be clear enough to Biologists, then my opinion is that yes. For Biologists interested in transcription factors and other sequence related topics it should be easy to understand.

Right. Well, my concern was not whether biologists would understand it (I think they would), so much as whether they would object to it. :-)

Don't think they would object. I mean, the ones without much knowledge of the theory will appreciate the simplicity. The others, can check the more detailed descriptions. It also pretty much depends on who's your target audience! Maybe I should update my response with some of these thought? What do you think?

Updating your answer sounds reasonable. Part of my question, implicitly, was whether my observations were conventional wisdom. See the comments on my question by Jeremy, which are pretty on target.


text:
what is the effect of soda water on digestion?
what is the effect of soda water on the process of digestion? As it has been seen that after drinking soda the process is increased...I just want to know that what is the chemistry behind this?

do you have source for this observation?

What should happen? It can be slightly acidic due to carbon dioxide which reacted that way. But the stomach is orders of magnitudes more acidic, which makes sure, that the CO$_2$ is removed from the solution.

Soda, anything carbonated causes bloating, which stretches the stomach. Mechanoreceptors in stomach detect the stretching resulting in parasympathetic innervation to GI smooth muscle. This causes an increase in GI motility.

what about chemistry?

I think unless your talking about caffeinated drinks, or drinks that contain a chemical that affect the nervous system, it's negligible. carbonated liquids are acidic, but like @chris stated above, it's moot compared to the pH of the stomach.

Due to presence of hydrogen ion in soda water ,H+ ion Concentration in stomach is increasing (common ion effect) it helps in digestion.

Please extend your answer and provide reputable support for your claims. Unfortunately, failure to do so will result in downvotes or deletion. Please see our [help] page about writing good answers. Thanks!