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When to measure resting heart rate and blood pressure for following day-to-day trend?
I'd like monitor my resting heart rate and blood pressure to see how they are affected by regular cardiovascular training and other events in life.
When should I take the measurements in order to reduce day-to-day variations? In the morning or evening? Before or after eating? Right after waking up?
Of course I'll make sure to follow good routines when measuring, but the ones I've found prescribed by hospitals don't state an appropriate time of the day.

I would be very surprised if the time of day made a difference.  I've personally never heard mention of such a phenomenon in discussions with intensive care practitioners (where of course HR and BP are measured constantly).  However this is only the case during rest, this paper (on horses) suggests that there is some difference in HR and BP after exercise depending on time of day.
You are right to attempt to control it however, I suppose.  It doesn't matter when you take your measurements, as long as you take them at the same time each day.
I would say that one of your first suggestions of taking the measurements almost immediately after waking.  Of course you would have to be relaxed as you assembled your equipment then rest for a few minutes in the posture you have chosen (this will matter) before taking the measurements but otherwise I can't see you having too great a problem.

It kind of depends.  If you want to compare apples to apples, check it first thing in the morning.  However, that's going to be at the lowest point. It's also important to know what your blood pressure is during the day, when you're living your normal daily life.  I recommend checking fairly regularly in the morning so you'll know what your true baseline is and whether it's trending up or down, and to "spot-check" occasionally at different times of the day to see how your body is handling the normal daily stress

Actually in my research into circadian events, the hourly differences in blood pressure was the first thing that I found. Based on this, I'd state that there are hourly differences in blood pressure and cardiovascular efficiency.
Because these changes are circadian, measuring these values at the same time every day (ex: 1 hour after wake up time or 1 hour before bedtime) would reduce variation. Just be aware of your caffeine intake - it may skew the measurements.
I do not have access to the scholarly library that I used then, so the chances of finding the article are slim to none.


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Can someone identify this bird?
We recently found a nest in the back garden and a little bird inside. Can you help us identify it? The nest is quite small like the bird so we are wondering whether this is the parent or a baby chick. Is there anything we can do to help it or are we better off leaving it alone?
Update: I'm from the UK, currently in Oxfordshire to be more precise.

Took me a ridiculous amount of time to locate the bird in the picture :L

Looks like a Carolina wren. They are common small brown birds.  The call is a loud three syllable call that sounds sorta like cheeseburger cheeseburger cheeseburger.  Regardless it is certainly better off if you leave it alone.

Well it's not a Carolina Wren, then...

@RoryM still can't find it. Now I'm afraid to keep looking at the picture, lest it be a joke with a monster who pops up screaming. I mean, I know it surely isn't the case, but still...

I'm seeing something like bird at top middle portion of photo.

It looks like a passerine bird, but I can't really tell the species without seeing the whole body. As for what to do with it, your best course of action is to leave it alone. Trust me. Once placed tissue paper over a pigeon's eggs to keep them warm, and the mother crushed them when she landed on the nest because she didn't see the eggs.
If there are eggs in the nest, try noting down what color they are. Passerines have colored eggs.

The bird needs to be left alone; that's the best help you can give it.  Anything more than watching it is liable to lead to nesting failure (e.g. abandonment of the nest).  The bird looks attentive and quiet, and so is most likely an adult keeping the eggs or chicks warm.  The bill suggests a seed-eating bird, but there are large numbers of those (e.g. finches, sparrows, grosbeaks, ...) and I can say little more from the evidence.

This is not really an answer.

@WYSIWYG, it responds directly to the last sentence of the post, to wit: " Is there anything we can do to help it or are we better off leaving it alone?"  It also gives addresses the other question ("Can you help us identify it?") by giving more information than the accepted answer, i.e. by naming three specific possible subgroups of the passerine birds.

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Can one dendrite pass through another?
While tracing dendrites on EyeWire I encountered the following situation. They belong to an Orientation Selective Ganglion Cell.

It's the first dendrite I've noticed with such a clear 'hole' in it, though which another dendrite passes.

Is it possible for one dendrite to pass through another? Perhaps I shouldn't have 'connected' the top part with the bottom part?

I can't think of any reason that would explicitly prohibit a dendrite from travelling through a space created by another dendrite's branching pattern. In non-EM images of dendritic branching patterns I don't think I have ever observed dendritic loops, but of course, that has nothing to do with whether or not they occur. Nonetheless, I think there are more likely explanations for what you are seeing in these particular images.
As shown, the upper and lower parts of the "dendrite" in the first image do not look like a continuous structure. I would guess that you are looking at a synapse or some other contact between two different processes in the first image. The 3-4'o'clock connection in the loop suggests this interpretation. Can you see vesicles in the images around those connections?
The other dendrite that shows up in your second image might be a glial cell or some other cell's dendrite that participates in the synapse. Alternatively, the other dendrite may just be a chance passing of two dendrites that don't interact functionally.
Of course, it could be that you and the computer have just completely misunderstood the data. My understanding of the Eyewire interface is that the computer guides a lot of the identification and doesn't easily allow you to see the surrounding areas so you can't track structures all the way to their sources. In such a situation, it seems probable that you would end up with ambiguous instances like this that you would have a hard time resolving without more information/expertise. But maybe Seung or one his colleagues can come weigh in on that?

"I don't think I have ever observed dendritic loops" ... On the images it did look like a loop, but I've noticed big staining gaps before. "do not look like a continuous structure" I don't know how the 3d model algorithm handles additions, and how much you can rely on it visually, although it does look like the structure is rounded prior to touching, which could indicate it's just a staining gap.

"doesn't easily allow you to see the surrounding areas so you can't track structures all the way to their sources", ... correct. It's mainly just tracing neurons for now, but they are planning to work on other possible tasks as well. I agree that in many cases I am uncertain about what to do, ... hence this question, and your help being greatly appreciated. I'm still very curious to see how the project will evolve.

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Main methods used to predict functional annotations in GO
Can someone provide me some information about the main method used to predict the inferred electronic annotations in Gene Ontology?

This is an interesting question but I suspect that it’s better suited on biostars.org

Thank you for the suggestion, i'll try there. If i obtain answers i will re-post here.

I believe the most common source of electronic annotations comes from analysis of peptide sequences.  A collection of InterPro to GO mappings were created manually and can generate GO annotations.  DNA binding domains of transcription factors would be given "DNA binding" GO annotations say.
This method has its flaws - if the domain detected has evolved away from the function used for the Interpro to GO listing, there is a potential for error in this method.

You can refer the IEA documentation maintained by GO consortium to get an idea about the automatically assigned evidence codes using IEA. Also please note that IEA is different from Computational Analysis Evidence Codes

ISS: Inferred from Sequence or Structural Similarity
ISO: Inferred from Sequence Orthology
ISA: Inferred from Sequence Alignment
ISM: Inferred from Sequence Model
IGC: Inferred from Genomic Context
IBA: Inferred from Biological aspect of Ancestor
IBD: Inferred from Biological aspect of Descendant
IKR: Inferred from Key Residues
IRD: Inferred from Rapid Divergence
RCA: inferred from Reviewed Computational Analysis


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How was the guided daily amount (GDA) calculated?
We are constantly shown nutritional information on food packaging stating this food contains "x" amount of your guided daily amount. A linked to the values is here. How were these values calculated? How do we know that men as a recommendation must not consume more than 2500 calories, 55g of protein 300g of carbohydrate etc...

Many of those values are unfortunately probably made up, or at least meaningless due to the extreme variance in populations.

So not even an educated guess?

Probably an educated guess, I'm sure they funded it on some research... but it was probably not an excessive effort. They knew just as well as everyone that humans vary too much to postulate a general amount of nutrients everyone needs, so it was more important to get exactly what it is - a guideline.

The total calories are not in fact a recommended value - they are an example amount that is derived from some calorie intake that seemed reasonable to someone (I don't know the details). It does not mean that the government is recommending that you eat exactly 2000 calories per day.
The relative content is, however, a recommended value, based on presumably research. So, if you do take 2000 calories a day, then you know how much of it should be fat/carbs/proteins.
I think that there is some controversy about whether the recommended values were influenced by industry lobbying. Moreover, science is definitely not clear on what the optimal food content for a human is, which is why we keep having the different diet fads, oscillating from no-fat to no-carbs.

In the USA, they refer to this as the recommended daily values (DVs) for a variety of nutrients. All I can find regarding these recommendations is that they were calculated for adults and children over 4 years old with a daily energy intake of 2000 kilocalories (often referred to as calories in the US).


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number of RNA pol II molecules in a given human nucleus?
Does anybody have any estimate on the number of RNA pol II molecules in the nucleus of a given human cell? For example, how many RNA polymerase type II protein complexes would there be on average at a given time in, say, a human immortalized lymphoblastoid cell line (LCL)?

it is highly variable even in a single cell type.
Dont know for a human cell but this is the range for ecoli: 1500-11400
check this site out. got this number from there (its quite useful for questions like these):
http://bionumbers.hms.harvard.edu/bionumber.aspx?&id=101440&ver=3&trm=RNA%20polymerase
You can estimate protein copy numbers and there are techniques available for doing so. One of such techniques:
http://www.mcponline.org/content/11/3/O111.009613.long
You can also calculate concentration using traditional techniques like western blot and elisa and calculate approximate copy-numbers (you have to also calculate average cell volume and number of cells for protein extraction.


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Mouse meta-globin mRNA problem

This is an mRNA strand of mouse meta-globin:
5'-ccccagauacggaauucgaau-3'
A) Which small RNA (below) is most likely to regulate expression of
  meta-globin?

5'-auucgaauuuucuaucugggg-3'
5'-ggggucuaucuuuuaagcuua-3'
5'-ccccagauacggaauucgaau-3'
5'-uaagcuuaaggcauagacccc-3'

B) This RNA most likely?

acts as an siRNA
inhibit meta-globin translation
increase meta-globin translation
help transport meta-globin mRNA back into the nucleus

My attempt:
I think A is 2 because the strand is complementary and will bind nicely to the mRNA strand.  For B, I'm between 2 and 3, but cant decide.

I'm going with 1) for A since you need the strand to be the reverse complement.

A) Is this a take-home exam question? 1) Yes, then I can't answer your questions for you. 2) No, well, I'll see if I have time tomorrow to get to it.

@Larry_Parnell this is a problem I found in an MCAT book.  (I'm studying for the mcat)

There are always exceptions but you can consider some general rules.
A is 1 i.e the sequence that is perfectly complementary (2 is complementary but direction is parallel — cannot base-pair), then B would be 1 (siRNA). Reasons (some are just based on general rules of siRNA design):

siRNAs have to be perfectly complementary
The size is also perfect for a siRNA (21nt)
U/A (2-3 residues) at the 5' of the siRNA
U at 10th position
GC content 43% (ideal 30-50%)

See here for guidelines for siRNA design.


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What's the opposite of a thermophile?
Thermophiles, heat-loving organisms, have been a popular topic of research for decades due in large part to the utility of their enzymes in various chemical reactions (Taq Pol single-enzymedly made PCR practical). One of the signatures of thermophiles is that their proteins resist heat denaturation up to much higher temperatures than their mesophilic (middle-loving) homologs.
Is there a corresponding group of extremophiles whose proteins resist cold denaturation down to much lower temperature than their mesophilic homologs? If so, could someone please point me towards a few good literature reviews on the topic? Or at least give me the proper name for this group of cold-loving extremophiles?

there are organisms that survive in cold temperatures - like arctic plankton and fish...don't know their names, but their adaptations tend to be the production of antifreeze proteins.

The term you are looking for is psychrophile or cryophile. There are examples of microbes adapted to very cold conditions in Bacteria, Archaea, and Eukarya. There are also fairly complex animals capable of surviving very low temperatures -  Tardigrades, for example. There are multiple issues that organisms face in withstanding extremely low temperatures - protein denaturation, membrane fluidity, intracellular ice-formation, just to name a few.
There is this review that might be useful to you.

D'Amico, S., Collins, T., Marx, J.-C., Feller, G., Gerday, C. Psychrophilic microorganisms: Challenges for life (2006) EMBO Reports, 7 (4), pp. 385-389. link

You beat me by 20 seconds! I shall defer to you.


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Do any animals other than humans undergo menopause?
Do any animals other than humans undergo menopause?
Also, is there any difference between animals in captivity and animals in the wild as regards menopause? For example, even if menopause has been observed in a captive member of a particular ape species, do individuals of that species typically live long enough in the wild to also undergo menopause?
I guess here's what I'm really getting at: is menopause a common thing in the animal kingdom, or is it only a common thing in humans?

So now we have one answer saying it's common and citing a Nature article, the other saying it's uncommon and citing a Science article.
Let me get my popcorn...

@arboviral Jacques linked to a summary of a paper. The original paper isn't looking at menopause per se, but rather at mammals that tend to live for a long time after menopause occurs. So it seems like the summarizer got it wrong.

Yes. Menopause is common for long-lived mammals. For instance, in the wild, killer whales go in a sort of menopause as reported in 2009 by Ward et al. Front Zool. 2009 Feb 3;6:4. So it is not due to captivity. According to a Nature review, reproductive cessation has also been documented in non-human primates, rodents, whales, dogs, rabbits, elephants and domestic livestock (Packer et al. Nature. 1998; 392(6678):807-11)

As of 2017 you can add false killer whales to the list as well (Photopoulou, T., Ferreira, I. M., Best, P. B., Kasuya, T., & Marsh, H. (2017). Evidence for a postreproductive phase in female false killer whales Pseudorca crassidens. Frontiers in zoology, 14(1), 30. at https://frontiersinzoology.biomedcentral.com/articles/10.1186/s12983-017-0208-y )

The ecological knowledge that older females have gained throughout the course of their lives can be extremely useful for the survival of their offspring. This is sometimes referred to as the "grandmother effect". For example, older females may remember key information about rare events, such as how to avoid/defend against predators, or how to find food/water in times of scarcity.
Check out this paper describing the grandmother effect in humans:
Herndon (2009). The grandmother effect: implications for studies on aging and cognition. Gerontology, 56(1), 73-9.
And in killer whales:
Brent, L. J., Franks, D. W., Foster, E. A., Balcomb, K. C., Cant, M. A., & Croft, D. P. (2015). Ecological knowledge, leadership, and the evolution of menopause in killer whales. Current Biology, 25(6), 746-750.

Only three — humans, killer whales, and pilot whales.  (Reference)

Among long-lived animals, scientists have found only three species that undergo menopause: humans, short-finned pilot whales, and resident killer whales. What makes these species so special? A new study finds that it all comes down to their unique social structures.

Your link is a summary of Johnstone et al, Proc. R. Soc. B 2010. Here's the first couple of lines from their abstract: "Human females stop reproducing long before they die. Among other mammals, only pilot and killer whales exhibit a comparable period of post-reproductive life."

Long post-menopausal life and menopause are not equal. I can assure you that mice undergo an analogue of menopause.

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Consensus codon optimization by organism
Does a public database exist that contains this information? I'm trying to make a simple gene annotation program that will let me input a DNA sequence and then optimize it based on one of these tables using the E. coli preferences, for example.

This sounds like http://www.jcat.de/

That tool is pretty much what I was going for. Thank you.

http://helixweb.nih.gov/dnaworks/ also has this functionality. It also accepts information from the Codon Usage Database. However, I'll love to see any improvements in the field.

Try the Codon Usage Database at Kazusa. You can search by organism. The database contains 35,799 organisms and compiled from 3,027,973 complete protein coding genes (CDS's), but last updated in 2007.

This kind of database is what I was looking for in terms of access. JCat seems like a good tool to do the work for me, but I'd like to try it myself using this database.

Plenty of softwares doing that kind of functionality. A 2007 open access review lists >30 such softwares http://www.ncbi.nlm.nih.gov/pubmed/17882154. However, No correlation between 'most common' codon and recombinant protein expression yield. http://www.ncbi.nlm.nih.gov/pubmed/21102527. Thus, those >30 softwares are pointless.

The second conclusion is interesting. I would have thought perhaps it would make a difference when using microbes as bioreactors and the only quantifiable trait that matters is the yield.


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What is the biology behind a skin "mole"?
Are the dark marks aka "moles" on our skin a patch of dead cells? If so, why is it not cleared over time? In a (probably) similar vein, why do scar marks from injuries remain long after new cells replace the dead cells?
[Feel free to edit out the second question if the answers are unrelated]

A mole is simply a benign tumour, i.e. a proliferated cell growth that hasn’t become cancerous. So moles are not dead cells, they are very much alive. The colour is caused by a high concentration of the melanin, which is also responsible for normal darker skin.
Since moles are tumours, they can – but in most cases don’t – give rise to melanomas, malignant skin tumours, when they lose susceptibility to cell growth regulation and start invading surrounding tissue.
Scar tissue is entirely unrelated and due to regular regrowth of epithelial cells after injury forming a linear collagen structure (as opposed to the skin’s normal collagen structure, which resembles a “weaved“ structure).

A Mole may be a Hamartoma or a benign tumor. A congenital mole is usually a hamartoma, while acquired mole a benign tumor. In a few people mole very slowly grow in size.


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Linkage and LD: quantitative or qualitative?
My understanding is that the concept "genetic linkage" can be expressed in quantitative form, like:
A predisposing gene X was found in close genetic linkage to Y.

And that linkage disequilibrium (LD) is a quality, like being pregnant, you are either in LD or your are not:
A predisposing gene X was found in close genetic linkage to Y and in
linkage disequilibrium with Z.

Is this correct?

Linkage disequilibrium (LD) occurs when there is a non-random association or correlation between genotypes. Note I used the word correlation; this is a quantitative trait.
Some genotypes may well correlate perfectly (R=1), i.e. they are always inherited together. Others may not be in 'perfect' linkage (e.g. R=0.9), but are still considered to be in LD because there is a strong correlation between the genotypes (I think 0.8 is generally seen in published papers as the 'cut-off').
The correlation coefficient is derived from the D' value - this (simply) denotes the observed vs. expected frequencies of the genotypes (whether they are in linkage or not). Therefore either value can be used, but I think it is more common (and more interpretable) to express the correlation coefficient (or to be more precise, the coefficient of determination, R^2).
If you'd like an example: I might be interested to know if any SNPs are in LD with rs10757278 (located on 9p21, associated with heart disease). Using SNAP (by the BROAD) I can input my search, choose my options (e.g. use 1000 genomes data, and an R^2 cut-off of 0.8) and search. ~5 SNPs are found to be in 'perfect' LD (R^2=1), but a further ~40 are still considered to be in linkage with the input-SNP because their R^2 values are above 0.8.
So in summary, both statements can be used correctly, but it is always more informative to state the degree of linkage (otherwise it might be assumed they are in perfect correlation).

This is a good explanation with a fine example. It can be added that the r^2 value can be between 1 (complete LD) and 0 (zero, no LD whatsoever as with markers on different chromosomes). Yes, we and many others use a cutoff of r^2 > 0.8 to denote strong LD. However, values of 0.4 and above are not to be discounted as having no LD.

authors: Bob Jarvis - Слава Україні


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Generating custom human DNA sequences based on traits such as eye colour?
I'm wondering if it would be possible to create software (unless some already exists, but I couldn't find any) to generate human DNA (the base pairs on the double helix) containing genes representing specific permutations (eye colour, hair colour, etc.)?
Basically, something like the "character builder" from those "Saints Row"-style video games, except with actual human chromosomes, enabling you to essentially create a 'custom' human.
Of course, that is assuming that all human DNA has a common structure, and that the entire sequence can either be assembled from individual chromosomes, or by using a reference genome and modifying specific genes/chromosomes according to user input. Is this the case?
One setback here, of course, could be the number of bases in each chromosome, which ranges between 100 million and 250 million, and the (approximately) 23000 human genes - a lot of data to manipulate.

A major limiting factor in such an exercise is the complexity of the biological process under question (eye colour etc.,) and thus, our nascent understanding of these. What I mean is that there is not a single gene that determines a given characteristic, rather it is the complex interaction of a set of genes in different conditions responding to environmental cues and such. We are barely at the level of scratching the surface when it comes to understanding the mechanisms that underlie such outputs. And so, we are long ways off (maybe hundreds of years?) before we can even start thinking about coming up with feasible approaches to such objectives.

We may be long ways off- but really? Hundreds of years? I don't think so. :-)

"maybe" is the keyword ;-)

I'm pretty sure 23&me could already do something pretty accurate for many traits.


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Difference between strand-specific and not strand-specific RNA-seq data
I would like to ask the difference between strand-specific and not strand-specific dataset.
As far as I know, strand-specific data means that we know which strand the transcript is from.
I do not have biological background. Please confirm whether it is correct. If we have a transcript, which is from sense strand, when RNA-seq is producing reads, is that first the cDNA is synthesised. Then this cDNA is used for PCR to amplify the sample? Then the reads generated could be from both strands of the original DNA?
For strand-specific protocols, what is different?
========================================================
Follow up.
Please correct me if I am wrong. There are multiple protocols to produce strand-specific RNA-seq libraries. The basic process is like:

Get the RNA;
Get its cDNA;
Somehow mark the cDNA as sense or antisense when amplifying (PCR?) (here comes the differences between different protocols);
Then REMOVE all antisense (or sense) cDNAs;
Read the reads from clean cDNA library.

The result is that, the reads from this RNA can be used to assemble the sense cDNA. And for not strand-specific libraries, using the reads would be able to assemble both the anti-sense and sense cDNA.
Am i right about this problem? Thanks.

cross post (first closed, then re-opened...) http://www.biostars.org/post/show/43507/charateristics-of-strand-specific-rna-seq-dataset/

It may be worth checking out the paper "Comprehensive comparative analysis of strand-specific RNA sequencing methods".
The most common techniques sequentially ligate different RNA adapters to the 5' and 3' ends of each RNA molecule prior to cDNA synthesis.  You will end up with an RNA molecule that looks like this (where A and B are the two adapters):
  5'-AAAAAA---------------BBBBBB-3'

These adapters are then used for cDNA synthesis and library preparation.  Finally, since each adapter is ligated to a specific end of the RNA the library can be generated in a stand-specific fashion; ie. the reads derived from the antisense strand should align to the antisense strand of the genome.
** Note that there are other variations of this technique but Illumina's protocol is one of the most popular.

Thanks, @GWW. Does it mean that Illumina is going to provide two libraries (one antisense and one sense) to users? Or they just mark every read which sense it is from? When giving reads to customers, have they removed the adapters beforehand? Or users need to remove by themselves?

By the way, I checked the paper... But cannot find much regarding the post-processing of the data...

You mean aligning the reads?

I mean, you said "the reads derived from the antisense strand should align to the antisense strand of the genome", so what would Illumina provide? If they just provide whatever reads, that is not strand-specific, right? They must filter out sense or antisense reads, or they may mark each read as whether it is from sense or antisense strand. Am I right?

No, after alignment the reads derived from the antisense strand should only align to the antisense strand of the genome (the same for reads from the sense strand).  With a standard RNA-seq preparation reads could align to either strand, which prevents you from inferring the actual strand the read is derived from.

Thank you for your patience, @GWW. Yeah, the reads from antisense strand should be aligned to antisense DNA. So given a read, we KNOW that this read SHOULD be from which strand, right?

Yes, assuming that the libraries were prepared using a directional library.


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Is it harmful for someone to consume things full of bacteria if they don't get physically sick from the bacteria at all?
Or as another example - what if you touch a surface that's contaminated with potentially pathogenic bacteria (like the ones at http://arstechnica.com/hardware/news/2008/05/study-keyboards-make-excellent-homes-for-nasty-bacteria.ars) and introduce those bacteria into your body and don't get sick. Then could there be some other damage that the bacteria could do your body? Like, at the very least, maybe promote a not-particularly-noticeable increase in inflammation in the regions where the immune system decides to fight the bacteria? Inflammation only starts to get noticeable when some really high threshold gets crossed.
By "sick", I mean, that the symptoms of the infection become noticeable enough to cross the threshold of being unpleasant to the person carrying the infection. I'm sure that there may be some sub-threshold effects that come in first.
And why is this important? We have to establish some sort of balance between using too much soap/other cleaning agents and not using enough of it. If we use too much, the bacteria could develop antibiotic resistance. And if we use too little, there could be an increase in the types of bacteria that cause chronic infections that don't get noticed, even though some of us might not even get physically sick more.

There is some confusion: bacteria develop antibiotic resistance if we use too much antibiotics. If you use too much soap, what is likely is that your immune system will not find any bacteria and will develop some exagerated response against 'safe' exogeneous material (allergies) or endogeneous material (autoimmune diseases).

It really depends on what you consume, how much of it you consume, and the state of your immune system. Let me give you some examples. Yogourt is full of bacteria, and yet we can eat it without issue. The bacteria likely don't survive digestion, but if they do, they will quite happily live in our intestines contributing to the already existing population of good bacteria.
Streptococcus is a genus of bacteria that contains some species that live all over us. They are on our skin, in our upper respiratory tract and intestine. If the species, S. pneumoniae makes it into our lungs, this can cause a bacterial pneumonia. There are likely few bacteria making it into our lungs on a regular basis, and normally our immune system can fight this off without concern. If we some how become immune depressed or compromised (for a number of medical reasons) then that's when we become symptomatic and ill.
On a more extreme side, if we have a bacteremia it is called a bacteremia. There are benign cases of this every time your brush your teeth and bacteria are able to enter tiny cuts in your gums from the brushing action. A healthy person fights this off. If a bacteremia is left unchecked, because of a lack of immune response or trauma, this can develop into a sepetcemia, a toxic infection of the blood. This can be very life threatening and is quite serious.
In general, we always have bacteria all over our hands which we likely transmit to our food or otherwise ingest. This is normally not a problem, but there is an appreciable risk of getting some kinds of viral or bacterial infection (eg, strep throat or a cold). Washing with soap (and to a lesser degree, using hand sanitizers) minimizes this risk.

Some bacteria produce toxins when alive. The infamous Clostridium botulinum produces botulinum, a very powerful toxin that can cause total body paralysis in very small amounts.
C. botulinum cannot survive the acids in the stomach, but the toxin and the spores can pass through and still affect (kill) you. This is an example of a bacteria that you cannot get physically sick from just eating, but from its by-products.


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Are there examples of PTMs that add different chemical groups (and mass) to different amino acids?
I'm talking about this type of post-translational modifications. What I'm interested in is not whether some modifications can only occur on specific amino acids (that's clear), but if the nomenclature has examples of addition of slightly different chemical groups to different amino acids known under the same name.
Thanks.

Not clear about what you're asking. Are you asking if there is a class of PTM that describes the addition of a variety of chemical groups to a variety of amino acids?

Well, yes. Of course I don't expect this variety of groups to be diverse; maybe just a single deviation for a single amino acid.

The term "methylation" may be what you're looking for, if I understand your question correctly. A CH3 group can be added to one, two, or all three nitrogens on arginine's side chain, for example, potentially resulting in slightly different chiral conformations.


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Why are some plants frost tender?
Why do some plants have the ability to stand frost, while others can't? Does it have to do with the size of the water vacuoles in the plant cells?

Cf. How do individual plants adapt to changes in temperature

All cells are susceptible to cold, but freezing is particularly difficult.  If the water in the cells freeze, it would usually burst the cells (water expands when it turns to ice) and tearing the cell membrane (totally killing it).
Some plants and animals have adapted to colder temperatures by putting antifreeze proteins in their cells.  A lot like adding antifreeze to the radiator of a car, this lowers the freezing temperature of the water in the cell.
So the answer is that some plants have adapted to colder climates with the help of additional genes.  There are other things that have to change too - the chemical reactions in the cell will go haywire when temperature changes too, so lots of genes must make adjustment for a fully cold adapted plant.


text:
Purpose of poly(A)+ RNA?
I am learning RNA-seq analysis. I always encounter this phase "poly(A)+ RNA". After searching, I got this: "Most messenger RNAs contain a poly(A) tail, while structural RNAs do not. Poly(A) selection therefore enriches for messenger RNA. The technique has proved essential for construction of cDNA libraries."
Does it mean that when constructing the cDNA, we always use the ones with a A's tail? Then other RNAs like tRNA are filtered and not used to get their cDNA? I do find some RNAs records on UCSC where microRNAs are included.
When we say poly(A)+ RNA library, what is the difference between normal one? Or normal RNA library is a poly(A)+ RNA library? Thanks.

Note that this isn’t always done: there are RNA-seq protocols which do intentionally not enrich for mRNA and hence don’t do poly(A) selection. After all, we might be interested in other RNA as well (but this is much rarer since most RNA-seq is done as a quantification of gene expression).

One of the primary reasons to use poly(A) selection is to eliminate the massive amount of ribosomal RNA (rRNA) present in the samples.  The alternative is to use ribosomal RNA depletion kits / techniques to remove as much rRNA as possible before sequencing.  Without rRNA depletion a large proportion (~60-80%) of the reads would map to rRNAs.
poly(A) selection also reduces the amount of pre-mRNA in the samples, which reduces the number of intron aligned reads.

Thanks, GWW. So if we are not saying "poly(A) RNA", the reads we get will be largely from rRNAs? And for poly(A) selection, is it going to remove other RNAs like microRNA?

@CaiShaojiang, yes it will not bind to miRNAs

@bobthejoe miRNA can be (usually is) polyadenylated as well.

@KonradRudolph: Not exactly. The pri-miRNA is polyadenylated, but what is (eventually) called the miRNA isn't, so ...

@Steve Correct. Unfortunately, I oversimplified.


text:
Majority of transcripts are from sense strand?
I am wondering whether majority of transcripts are transcribed from the 5'->3' strand? Because I encounter a lot of expressions like "anti-sense transcripts". Could anybody help clarify this? Thanks.

Could you elaborate on your question?  Anti-sense transcripts are also transcribed in the 5'->3' direction.  What type of data are you looking at?

Thanks, GWW. Maybe I was wrong, i thought the "anti-sense strand" as the 3'->5' strand. So you mean, for example, the DNA is "AAAAATTTTT", some transcript could be "AATTT" and some could be "TTTAA"? Could you please further clarify it?

do you have questions after reading http://en.wikipedia.org/wiki/Sense_%28molecular_biology%29 ?

These terms depend on circumstances.
If I give you a sequence .AAATTTGGG
You would say AAATTTGGGis sense strand while TTTAAACCC antisense. So far it's regarding sense and antisense.
And there is no transcript transcribed from 3'-5'.
RNA polymerases work only in 5'-3' direction.

From my understanding sense and anti sense is contextual. If you are looking at a gene from 5'->3'(which is convention) that strand is the sense strand and the complement to the gene is the anti sense strand.
However further along the DNA there could be a gene on the 'original' anti sense strand, if you are discussing this new gene, there is a new context and it is now on the sense strand (oriented 5'->3'), and it's complement on the anti sense strand.
I hope that's clear.

Thanks, @Ben. I found this on Wiki: "The only real biological information that is important for labeling strands is the location of the 5' phosphate group and the 3' hydroxyl group because these ends determine the direction of transcription and translation." May I have this conclusion: the cell is going to read the DNAs ONLY from 5' end to 3' end, regardless whether it is reading the 5'->3' strand or 3'->5' strand? And whichever strand is used as a template to produce the transcript, it is called "antisense" strand? Moreover, when aligning, result "+" means aligned to sense strand?

You are indeed correct, as the antisense strand is used as the template to make the mRNA translation of the DNA sense strand.

Can you link the web page into your answer? Answers should be accompanied by useful resources. Thanks.


text:
Primer design for introduction of restriction sites flanking a gene of interest
I am wondering what the correct method for primer design to introduce restriction sites. Specifically between two methods.
1) Primer first partially hybridises to the gene, has a mis-match where the restriction site and extra bases are on the primer, then has a hybridised site following the restriction site, to DNA upstream of the gene.
or
2) Primer first partially hybridises to the gene, then completely dangling and non-hybridising has the restriction site and extra bases.

The option #2 is most common. Do not forget to add 3 or more additional terminal base pairs for optimal restriction enzyme cutting (source: BioTechniques 1998, 24:582-584)

I think the best way is option #2:
Suppose that your gene of interest is AAAAAAAAAAAAAAAAAAAAAAAGGGGGGGGGGGGGGGGGGGGGGGG
and you want to insert EcoRI restriction site GAATCC
Then your Fwd primer will be  GAATCC AAAAAAAAAAAAAAAA
and your Rev primer will be GGATTC CCCCCCCCCCCCCCCC
But in general, it shouldn't matter which option you choose, as long as you calculate the Tm of only the part of the primer that hybridizes to your template.


text:
During starvation, does the human body do anything to prioritize which organs receive nutrients?
When food is scarce, the body slows its metabolic rate to conserve energy. Are there any other systems or processes that prioritize which organs receive nutrients?

Glucose is prioritized for the brain and erythrocytes over the muscle and adipose tissue, for example, by hormonal control.
The hormones insulin and glucagon respond to strarvation, insulin secretion falling and that of glucagon increasing. The glucose transporter, GLUT4, in muscle and adipose tissue is dependent on insulin, so that in starvation less-essential uptake of glucose to these tissues declines. The glucose transporters of erythrocytes and brain (e.g. GLUT1) do not depend on insulin, so the supply of glucose to these tissues, which absolutely require it, is not cut off.
References

Hormones and Starvation: http://www.ncbi.nlm.nih.gov/books/NBK22414/
Insulin and the GLUT4 Glucose Transporter: https://en.wikipedia.org/wiki/GLUT4
GLUT1, insulin-independent Glucose Transporter: https://en.wikipedia.org/wiki/GLUT1

Could you add some references and good sources for additional further/reading?

Done. Let me know if you think any further clarification is needed.

The glycogen in the liver begins providing blood glucose. Muscle glycogen is used as fuel by the muscles, fat cells (adipose tissue) release fatty acids to manufacture ketone bodies in the liver and to be used by the brain as fuel, and body proteins are converted to glucose.
In short, the body's metabolism shifts to catabolic reactions.
If this continues for too long, you begin to see effects of starvation:

Inadequate tear production
Enlarged/tender liver
Muscle atrophy
Rashes, sores, or peeling skin

In short, deficiencies of energy, protein, iron, and zinc can really mess you up in the long term.

Are you sure this is right: "ketone bodies in the liver and to be used by the brain as fuel".  If I recall correctly the human brain uses glucose as fuel.

Could you add some references and good sources for additional further/reading?

@GabrielFair yes, brain is dependent on glucose and requires some amount of it, but it can get some portion of energy from metabolism of ketone bodies as well, you can see: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874681/  or https://en.wikipedia.org/wiki/Ketone_bodies#Uses_in_the_heart.2C_brain_and_muscle_.28but_not_the_liver.29

The switch from glucose to ketone bodies as the principal blood metabolite accompanies starvation. This prioritizes the heart, which preferentially uses ketone bodies as a fuel (update; actually it's fatty acids, but they're metabolically similar.) This de-prioritizes the brain, which preferentially uses glucose.
[edit]
I was asked for a source. This is definitely in Voet, Voet & Pratt's Fundamentals of Biochemistry, but I vouch for Wikipedia's description.

Welcome to Biology SE!  This is a great answer, but perhaps you could include a reference? (I learned this also in undergrad, but citations are always helpful.)

The brain is the most metabolically active organ and will sacrifice the body for fuel.
starvation is characterised by the catabolism of muscle tissue for gluconeogenesis, and the provision of glucose and amino acids for fuel.
Before this occurs, the liver, when glycogen depleted, will switch from creating glucose, to creating ketone bodies from fatty acids. Ketosis is not starvation.
Ketones are eventually preserved for the brain, heart and lungs, whereas the rest of the body can utilise fatty acids, while certain glucose-dependent organs such as the kidneys will still utilise glucose.
Starvation will only occur when there are no free fatty acids to convert to ketone bodies, and the sacrifice of muscle tissue will begin.


text:
Using the IMGT/GENE-DB service to find RSS
I'm trying to get the data for the Human and Mouse 12 and 23 Recomination
Signal Sequences (RSS), to run a classification algorithm on it. I'm not a
biologist, so I apologise in advance for my misunderstandings and
confusion.
A version of the data is available here, but I thought I would try to
get it from www.imgt.org, if possible. There is also another slightly
different version available for the mouse here.
I'm trying to follow the instructions at IMGT-FAQ to obtain Recombination Signal
Sequences for the mouse.
Here is what I have selected at the search page:
Identification:
Species : Mus Musculus
GeneType: any
Functionality: functional
MolecularComponent: any
Clone name: <blank>

IMGT group: IGHV
IMGT subgroup: any
IMGT gene: <blank>

I'm not clear what "Locus", "Main locus", and
"IGMT group" mean here exactly. Specifically, what is the difference
between "Locus" and "Main locus"?
I think, but am not sure, that IGHV corresponds to V genes in the
Immunoglobulin heavy locus (IGH@) on chromosome 14, where locus here
denotes collections of genes. Clarifications and corrections appreciated.
I would have expected that the IGH locus would correspond to "IMGT group"
entries like "IGHJ, IGHV" etc, and the IGK locus would correspond to IMGT
group entries like "IGK, IGKJ, IGKV", but no matter what I select for
Locus, it does not change the possible entries for "IMGT group".
Running the search gives
Number of resulting genes : 218
Number of resulting alleles : 350
As instructed, I went to the bottom, selected "Select all genes", clicked
on "Choose label(s) for extraction", and selected "V-RS".
I got

Number of results=98

The first few results were
>X02459|IGHV1-4*02|Mus musculus_BALB/c|F|V-RS|395..432|38 nt|NR| | | |
|38+0=38| | |
cacagtggtgcaaccacatcccgactgtgtcagaaacc

>X02064|IGHV1-54*02|Mus musculus|F|V-RS|295..332|38 nt|NR| | | | |38+0=38|
| |
cacagtgttgcaaccacatcctgagtgtgtcagaaatc

>M34978|IGHV1-58*02|Mus musculus_A/J|P|V-RS|554..560|7 nt|NR| | | |
|7+0=7|partial in 3'| |
cacagtg

Ok, now I'm confused. The lengths of the RSS should be 28 or 39. but I
counted lengths of 4,7, 31, 38, and 39. Are the results here not supposed
to contain the 12 and 23 RSS?
So, I must be misunderstanding things here. Possibly many things. Any
explanations and clarifications are appreciated.

I'm not clear what "Locus", "Main locus", and "IGMT group" mean here
  exactly. Specifically, what is the difference between "Locus" and
  "Main locus"?

From the same site:

A locus is a set of IG or TR genes that are ordered and are localized
  in a same chromosomal location, in a given species. […]
   A locus comprises the genes of different groups which participate
  potentially to the synthesis of a polypeptide of the same 'chain
  type'.

Main locus should have been Locus minus the orphons:

A chromosomal orphon set is a set of IG or TR orphons (genes outside
  from the main loci) belonging to a same group and localized on the
  same chromosome in a given species.

However the Main Locus and Locus have the same options; Options for the Locus should have been chromosomes. They must have made a revision in the site but forgot to change the help. I tried setting all the options except any in Locus and selecting all for the Orphons; it yields no result. It works only if you set any in Locus. So it seems Locus option is useless; you can set the Locus as any by default.
 For confirmation it is best to ask the authors.
From the changelog:

16 April 2012

Update of the IMGT/GENE-DB Query page:
The search criteria are organized according to the axioms IDENTIFICATION, LOCALIZATION and CLASSIFICATION of IMGT-ONTOLOGY.
  Addition of new search criteria:

MolecularComponent (IDENTIFICATION)
Locus (LOCALIZATION): includes main loci and chromosomal orphon sets
  Main locus: "all" value allows to search genes of all main loci.
  Chromosomal orphon set: "all" value allows to search genes of all chromosomal orphon sets

For details on the IMGT classification you should refer to this paper.
Fixing a Locus option does not change the IMGT dropdown box option but the results are different. If you try your example and set Main Locus as IGH and IMGT Group as IGKJ you would get no results. It is just a problem of the web interface. Apparently the search works fine.

Running the search
I searched with the exact same criterion as you mentioned and did not get any sequences smaller than 38nt. There must have been some bug which seems to be fixed.


text:
Does the use of "var", "x", and/or "ssp" in a scientific name provide specific information?
What exactly does it mean when a plant has a scientific name that specifies a vairety, for example  Nothofagus solandri var. cliffortioides, or when the name includes an "x", as in Populus maximowiczii Henry x trichocarpa, Populus xcanadensis, or "Crataegus x macrocarpa"?
All of these species are in the USDA Plants database (of plants that occur in the US). There are > 6000 occurences of the string " var. " ~500 occurances of " ssp. " and only a handful occurences of " x " in the database,

Does the x indicate that a plant is a hybrid, and are the varied uses indicate a different meaning?
Does the use of " var " mean that the plant is a variety?

Does it mean that each of these species has been cultivated and/or bred by a human?

Does "ssp"  mean that the plant is distinct yet compatible with others in the species?
is there a way to identify a that a plant is cultivated based on its scientific name?

Does the use of "var", "x", and/or "ssp" in a scientific name provide specific information?
Yes, those terms denote the rank of the taxon in question.
Does the use of " var " mean that the plant is a variety?
Yes, the use of "variety" or "var." in a taxon name indicates it has the rank of variety. There is also "subspecies", "subsp.", or "ssp." to indicate the rank of subspecies.1
Does [the use of "var."] mean that each of these [taxa] have been cultivated and/or bred by a human?
No. Subspecies and varieties are wild taxa found in nature (mostly, some common crops are called species, such as Zea mays subsp. mays).
Does "ssp" mean that the plant is distinct yet compatible with others in the species?
Probably. This is complicated because it gets into species concepts, but some kind of distinctiveness is required, and the biological species concept (where a species is basically defined as being able to interbreed) is popular.
Does the x indicate that a plant is a hybrid, and are the varied uses indicate a different meaning?
Yes. The multiplication sign × is used to indicate a taxon of hybrid origin. Its different placement can indicate whether the taxon is an intergeneric or interspecific cross. If the × glyph is not available, a lower case x is used (though, really, this should be rare these days). The × should occur before either the genus name or before the specific epithet (e.g., the species Populus maximowiczii is just a regular species name that happens to contain the letter "x").
Is there a way to identify a that a plant is cultivated based on its scientific name?
Yes. Names that include quotes (specifically single quotes), non-italicized text, or the addition sign + could all be indications that the plant is a named cultivar (or group, grex, or graft-chimaera).

Since the question references the USDA plants database, I'll limit the answer to plants. Similar rules are applied to animals and microorganisms.
Each entity being referenced is a taxon (plural taxa), that is, a group of populations of organisms that are seen by taxonomists as forming a unit. Taxa are hierarchically ranked, with the highest being kingdom2, such as Plantae (the green plants), the "basic" rank being species, such as Populus maximowiczii, and—most relevant here—ranks below species, such as subspecies and variety.
The rules for how (wild) plant taxa are named are defined by the International Code of Nomenclature for algae, fungi, and plants (the Code). There are similar codes for animals, prokaryotes, viruses, and, interestingly, cultivated plants.
While the Code recognizes that there are an indefinite number of ranks, it gives names for many of them from kingdom down to forma (grouping them as principle or secondary ranks). It also specifies that more ranks can be created by adding a "super" or "sub" prefix to the rank name to indicate a higher or lower level rank, respectively.
Species is the lowest principle rank, subspecies is below species, and variety is below subspecies (and, for completeness, there is forma below variety).
Strictly, since subspecies and variety are different ranks, a taxon could be classified as a variety that itself is a part of a subspecies. In practice this is rare, usually a taxon is assigned to one or the other.3
Besides denoting a different rank, what is the actual difference between a subspecies and variety? It turns out that the biological definition of these terms is basically up to the taxonomist doing the work. Just like there's no set definition of species, there is no set definition for intraspecific taxa. Some taxonomists might basically rank all intraspecific taxa as subspecies or as varieties, depending on their philosophy. Those that use both terms need some recognition that variety is a narrower term than subspecies, but what that looks like operationally is up to the person/group doing the work.4
(However, one should follow the resource they are using. If it's listed as variety in USDA, use variety. It's incorrect to just decide you don't like it and change it to subspecies [for example]; that would require a research publication.)
Species, either members of the same genus or of different genera can sometimes interbreed and form a natural population. One could refer to these by simply listing the hybrid parents in a hybrid formula, such as Agrostis stolonifera L. × Polypogon monspeliensis (L.) Desf.5 One could also formally name the resulting hybrid. In this case the hybrid nature would be noted by placing the × before either the genus or species name. The above intergeneric cross between Agrostis and Polypogon has been given the name ×Agropogon lutosus C.E.Hubb. The name Populus ×canadensis refers to the interspecific cross between P. nigra and P. deltoides.6
The basic unit of cultivated plants is the cultivar, which is an assemblage of plants selected (by humans) for a specific character, and that remains stable through appropriate propagation. The naming of cultivars is governed by its own code. This code only recognizes the terms subspecies, variety, or form, as they apply in the (wild) plant Code. (Note that other groups, such as the Association of Official Seed Certifying Agencies, do consider cultivar and variety to be synonyms.)
An example cultivar name is Clematis alpina 'Ruby'. Note the use of the correct botanical name, the cultivar epithet in plain text, and the use of single quotes. See other examples here.

1The Code recommends the abbreviation "subsp." for subspecies, but "ssp." is very commonly used.
2Kingdom is the highest rank recognized by the Code; there are generally recognized ranks that are higher, such as superkingdom and domain.
3For example, take the taxon Saxifraga aizoon var. aizoon subvar. brevifolia f. multicaulis subf. surculosa Engl. & Irmsch. This has been fully classified to a particular variety, subvariety, forma, and subforma. To refer to this taxon, one would almost always just write Saxifraga aizoon subf. surculosa, and that is in fact it's name as defined by the Code. One would only spell the whole thing out if they needed to give the full classification. Since no other plant can have the same name, there can be no other subforma within Saxifraga aizoon with the epithet surculosa, even if it were to belong to another variety, forma, etc.
4I could include forma in this paragraph, too, but this seems to have greatly fallen out of fashion as a useful rank.
5I've also included the author abbreviations here. They have their own set of rules. Just know they're not technically part of the name, but often included to help avoid ambiguity.
6This could be written as Populus ×canadensis or Populus × canadensis. The × glyph is not actually part of the name, and can be placed for best readability.

Let me clarify my answer since it is lower quality than people may like.  To answer the question, my friend is a horticulist and has given a more detailed answer.
Subspecies is the most generic, taxonomically-defined term one rank order lower than species. The subspecies (either an individual subspecies, or collective group of subspecies) are defined to be genetically or morphologically distinct among other subspecies belonging to the same species, yet still produce viable offspring from interbreeding. For example, every type of dog is a sub-species of Canis familiaris, and all dogs are capable of breeding with each other. Subspecies, abbreviated Ssp, may refer to an individual subspecies type, or a collective group of related subspecies when a distinct subset is difficult to define or unknown.
There are a variety of terms that are analogous to subspecies, when the strict definition does not apply, or a different term has been used historically. For example, a varietal is the botanical term, and refers to a named subspecies. For example, grapes are a family of species, divided into the various subspecies, and a varietal is a specific subspecies that we refer to by a more common or familiar name, such as Riesling, Chardonnay, etc. (Grapes are a slightly different case in which most grapes are produced from hybrids or crosses for reasons of withstanding environmental conditions avoiding insect prey and fungal infections.) Microbiology has yet another distinction, called a strain. Strains are often genetically different, and yet all belong to a species. For example, several E. coli strains exist. In contrast, viruses are also given strain/subspecies names which don't technically fit the ICZN definition of interbreeding. Cultivar is a similar term, also from the field of botany. Cultivar is specifically applied to plants that are grown for some agricultural benefit, and have been bred or altered by humans for some reason.
In short, there is a zoological definition of subspecies set out in ICZN. This definition requires viable interbreeding among subspecies belonging to the same species. The term applies to individuals, or groups, as the context dictates. Analogous terms of subspecies are applied (adapted?) to other realms of biology, such as botany, microbiology and virology, but the definitions are slightly different, but consistent within the branch of biology (eg, viruses can't breed so they don't fit the ICZN definition, but the term applies). Ssp can also be qualitatively used to describe an unknown subset of a species (I've seen this used in microbiology mostly).
Crosses/hybrids are indicated with the "x" in the nomenclature. Since I found this confusing, I'm copying from Wikipedia.

From a taxonomic perspective, hybrid refers to offspring resulting
  from the interbreeding between two animals or plants of different
  species.

Hybrids between different subspecies within a species
  (such as between the Bengal tiger and Siberian tiger) are known as
  intra-specific hybrids. Hybrids between different species within the
  same genus (such as between lions and tigers) are sometimes known as
  interspecific hybrids or crosses. Hybrids between different genera
  (such as between sheep and goats) are known as intergeneric hybrids.
The second type of hybrid consists of crosses between populations,
  breeds or cultivars within a single species. This meaning is often
  used in plant and animal breeding, where hybrids are commonly produced
  and selected because they have desirable characteristics not found or
  inconsistently present in the parent individuals or populations. This
  flow of genetic material between populations or races is often called
  hybridization.

There are some horticultural examples of crosses in which an example of interspecific and intergeneric hybrids, and others, are shown.

I know what words are being abbreviated, and what they generally mean. I am wondering if the uses have clear definitions and consistent use

@David - Ah, that was not clear in your question. The International Code of Zoological Nomenclature is as definitive a naming system that you will find. The definitions are clear, however not everyone uses the system consistently (particularly older literature).

are there definitions of "var.", "ssp", and "x" available? are they used consistently in the ICZN approved list of plant names?

You'll have to find a copy and look through it, and for a specific (sub)species of interest read the literature to see how it is referenced.

I don't dislike your answer, and the recent changes did provide additional information, but it doesn't answer my questions, For example: is the term varietal used only for cultivated plants? i.e. does use of "var" indicate that a species has been cultivated? Also, is there meaning to the different uses of "x", e.g. "Genus x species" vs "Genus species x otherspecies" vs "Genus xspecies"? Finally, is there a biological definition of 'subspecies' - e.g. can subspecies interbreed? Does subspecies have a consistent biological definition, or is it just used to describe distinct populations?

^ edited. All questions have been answered for you.

The ICZN does not cover plant naming, (hence the 'zoological' in the name). I think you mean the ICN (International Code of Nomenclature for algae, fungi, and plants)

This answer is conflating how these terms are used casually with their precise meanings (those used in the USDA database). Dog breeds are not considered subspecies, and the term subspecies is not just any subset of the same species. Grape varieties are actually cultivars, not botanical taxonomic varieties (and varietal is the wine made from a grape cultivar).


text:
Why is hydrofluoric acid so dangerous if it is a weak acid?
I've read that hydrofluoric acid (HF) is extremely dangerous to touch, but what exactly makes it so toxic? It's a weak acid ($K_a = 7.2 \times 10^{–4}$) and dissociates approximately 1/1000 as much as hydrochloric acid does in water, so why is it so much more dangerous? Wouldn't a stronger acid cause more damage? What exactly happens when human skin comes into contact with hydrofluoric acid that causes it to get so badly damaged?

Acidity is not the only dangerous effect a compound can have, fluorine will oxidize almost anything, including oxides. it is highly poisonous to nearly all biological systems.

@John But HF will dissociate into fluoride, not fluorine, surely?

The confusion arises from the term weak, which has only to be interpreted in chemical terms.
Weak acid, as you say, just means that the acid does not readily dissociate, not that its effects are weak! Just to say one, HF corrodes glass, something that not even smoking HCl does.
Wikipedia has a nice summary of HF toxicity (see also the references in the article itself):

Hydrofluoric acid is a highly corrosive liquid and is a contact poison. It should be handled with extreme care, beyond that accorded to other mineral acids. Owing to its low dissociation constant, HF as a neutral lipid-soluble molecule penetrates tissue more rapidly than typical mineral acids. Because of the ability of hydrofluoric acid to penetrate tissue, poisoning can occur readily through exposure of skin or eyes, or when inhaled or swallowed. Symptoms of exposure to hydrofluoric acid may not be immediately evident. HF interferes with nerve function, meaning that burns may not initially be painful. Accidental exposures can go unnoticed, delaying treatment and increasing the extent and seriousness of the injury.
  Once absorbed into blood through the skin, it reacts with blood calcium and may cause cardiac arrest. Burns with areas larger than 25 square inches (160 cm2) have the potential to cause serious systemic toxicity from interference with blood and tissue calcium levels. In the body, hydrofluoric acid reacts with the ubiquitous biologically important ions Ca2+ and Mg2+. Formation of insoluble calcium fluoride is proposed as the etiology for both precipitous fall in serum calcium and the severe pain associated with tissue toxicity.

But how it can penetrates the skin if it is a polar compound? How is it soluble in the tissues?

This suggests transport occurs by non ionic diffusion https://pubmed.ncbi.nlm.nih.gov/6266462/ and as Wikipedia says it is lipid soluble

helpful source, it is about treatment but has a good breakdown of effects. https://www.sciencedirect.com/science/article/abs/pii/S0305417914001508

This question appears to have a revived interest? I would like to clarify this Q&A you don't mind.

HF(aq), like other hydrogen halides, does completely give up its proton to $\ce{H2O}$ but since F is the most eletronegative element on earth, it will pair up with hydronium ion in the aqueous environment, making the proton "less available", at least to a pH electrode. This is one of strongest hydrogen bond known.

$\ce{HF(aq) -> F^-.... H3O+}$

Thus HF(aq) has a depressed pKa in water whilst its "real acidity" can be much higher.

Homo-association of HF only occurs in very high concentration (close to unity). You can estimate the extent of homo-association of anhydrous HF by measuring its conductivity. Anhydrous HF has lower conductivity (<1.6 $\mu$S/cm) than deionized water (~5 $\mu$S/cm) [1] so it's probably not terribly important in driving disassociation of HF, esp in water.
HF causes deep burn, often with a delayed onset because while the skin prevents charged raw hydronium ion from penetrating too deeply, HF or the hydronium-flouride ion pair can be absorbed and releases the hydronium ion (by exchanging with water abundant in tissue) at deeper level. (Thus it's often reported as more painful than other acid burn)
Although fluoride in ppm level is anti-microbial and prevents cavity (by reacting with calcium mineral in tooth), high concentration of fluoride is toxic because, as cited in previous answer, fluoride interferes with calcium metabolism in forming insoluble calcium fluoride. It causes skeletal fluorosis and suppresses some essential metabolic enzymes.
HF is corrosive because of its proton; it's corrosive to bones because of its fluoride. HF corrodes glass and HCl doesn't because silicon tetrafluoride is a more stable complex than the highly reactive silicon tetrachloride. It has little to do with whether the acid is weak or strong.

I am not a chemist and unfortunately I will have to refer to wikipedia, but the ionization constant for HF (10−3.15, according to wikipedia) does not take homo-association into account.
Homo-association is an association between a base and its conjugate acid through a hydrogen bond. This process stabilizes the conjugate base, thereby increasing ionization. Often this behavior increases acidity, especially at high concentrations. In case of HF (double arrows indicate equilibria):
2HF <- -> H2F+ + F− (autoionization of HF)
HF + F− <- -> HF2− (homoassociation)
The formation of the bifluoride anion (HF2−) encourages the ionization of HF by stabilizing and removing F− from solution hence pulling the dissociation equilibrium of HF (HF + H2O <- -> H3O+ + F-) to the right. Thus, the usual ionization constant for hydrofluoric acid (10−3.15) understates the acidity of concentrated solutions of HF.

Although the importance of that would depend on the reaction constants of those three reactions... do you by chance know what they are?

@nico - great comment - but no. I'm just a humble biologist and stumbled upon this info after digging into it. HF is absolutely a strong acid from my perspective and this proves it, albeit just qualitatively. A quantitative answer has not even appeared on chemistry.SE, where a few related questions were posted.

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


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From inflammation to sickness and depression: when the immune system subjugates the brain
Recently, some research, for example this article has proposed that inflammation can cause innate immune cells to produce pro-inflammatory cytokines that act on the brain to cause sickness behaviour.
My questions are:
(1) What medication would potentially help to reduce the inflammation? I am not a biology expert so I do get a little confused reading the research articles.
(2) What are cytokines in laymen's terms? Are they the same as histamines which cause allergies?

Cytokines are essentially signalling molecules of the immune system. Broadly speaking these can be classed as pro- or anti-inflammatory. Pro-inflammatory cytokines promote inflammation, and anti-inflammatory cytokines inhibit inflammation.
Inflammation (again, broadly speaking) is associated with the 'innate' immune response - this is the immediate response by neutrophils and macrophages (among others), and these cells release a variety of molecules designed to damage cells around them. This is great if those cells are bacterial, or damaged host cells that need removing, but not so great if that is 'normally' functioning tissue.
Aging is associated with increased systemic inflammation - i.e. a greater proportion of pro- to anti-inflammatory cytokines. The causes of this aren't entirely certain, but it could be that the adaptive immune response (i.e. the memory T-/B- cells) is not as effective in older ages so the innate response is more important, or that it is just simply left 'unchecked'. Either way, the result this that the pro-inflammatory response can end up damaging host tissues, including the brain, without the corresponding repair instigated by anti-inflammatory cells/cytokines.
Any anti-inflammatory medication (e.g. aspirin, ibuprofen, or glucocorticoids) will, in theory, reduce inflammation, but by suppressing the immune system the risk of infection naturally rises, and there may be unforeseen consequences to prolonged use (the immune system does a lot more than just fend of bacteria - e.g. it is essential for tissue maintenance and regeneration), so I am by no means suggesting the use of anti-inflammatories to protect brain function!


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How many genes do we share with our mother?
Somewhere I have read we share more than 99% of our genes with every other other person and 98% of our genes with chimpanzees. What does this mean? Don't we share 50% of our genes with our mother and 50% with our father?
I've found an another article stating that.

There is a distinct difference between the 'genes' that we share, and the genome (the DNA) that the genes are made of.
All humans (excluding genetic disorders) have the same genes, but the same gene in different individuals may have a slightly different DNA sequence, and this may be manifested in the different traits you can observe between people (eye colour, height, etc) or be ’silent’ (have no observable effect).
So you therefore have 100% of the genes that your mother has.
However, as stated in another answer, you inherit the different 'alleles', or versions, of the genes from your parents, and end up with ~50% of the alleles from each parents (but all the genes).
With regard to species differences; many of the genes we inherit have evolved over millions (in fact billions) of years, and thus many of our genes are present in most other organisms (but in very different forms - the DNA). Chimpanzees are our closest relatives in evolutionary terms, and thus their genes are very similar to ours in the genome (~98% the same). But this only applies to the coding regions! Less than 2% of your genome actually codes for genes - the rest is mostly regulatory (not junk, as it used to be called), and this is where the true inter-species variation lies. So whilst we have ~98% homology in the protein-coding regions, this is MUCH less if you count the whole genome.

Nice answer, +1. Actually, recent analysis of 1000 Genomes data shows that each person has some 25-40 homozygous LOF (loss of function) variants not found in either parent. Thus, one could lower the 100% figure to ~99.9% shared.

How many kinds of genes are there in humans? If we all have same kind of genes, so is it just the combination of these genes that affect our personality?

+1 but you should probably change the word "code" for something else. The great majority of the species on Earth use the same genetic code (I do understand you did not mean it like that but...)

@user103431 I think there are around 23,000 accepted protein-coding genes in humans. We each have a copy of every gene. But at the DNA level the genes can vary ever so slightly, and this is where the different alleles come from (slight variations in the same trait). With regard to your personality, that is another kettle of fish: your genes can certainly affect your predisposition to certain mentalities, but it should be fairly clear that it is your life experiences that mostly affect how you develop, and thus what kind of person you become.
And 'code' is a bit layman, but it is 'correct'

Also, the DNA formerly known as junk is called heterochromatin. This was long thought to be inactive but I believe that is has now been shown to contain protein coding genes, not just regulatory elements (I spoke to Gary Karpen in the summer and think this is where I heard it). It is quite an unknown entity because it is so damned hard to sequence thanks to lots of repeating units!

In addition to the other answers, let me show you a logical error in your reasoning:

Don't we share 50% of our genes with our mother and 50% with our father?

You get 50% of our genes from each respective parent (disregarding mutations for now). But if you shared only 50% with each parent, this would imply that your parents don’t share a single gene:

But your parents do share genes – or rather, alleles1 – which is why the you also share more than 50% of the alleles with each of your parent.

1)  They share all genes.

Very good point! I had not thought it before. I had too the same misunderstanding.

In every cell of your body, you have two physical copies of every gene (ignoring gametes, / copy number variations), one from your mother, one from your father. (Humans are diploid.) That's why it's correct to say that you got 50% from either parent (ignoring the 13 mitochondrial genes that are inherited from the mother only).
The second approach is to look at genes as abstract entities. In the abstract sense, you share 100% of your genes with fellow humans, and more distant species will have a number of different genes. (This difference can be quantified in many different ways.)

I like the physical vs abstract take on this.

glad the mitochondria got mentioned :)

Let's not forget in these explanations about the special case of X and Y genes. If you are a boy, you share 100% of your father's Y chromosome (with a few mutations/transcriptions errors and slight recombinations in between) and a 50% mix of a X chromosome from him and a X chromosome from your mother.

@ogerard: Boys get one complete Y chromosome from the father, and one complete X chromosome from the mother. (The sperm was carrying a Y, and not an X.) Girls get one X from each of their parents. (So no 50/50 mix in the X for boys.)

@Michael Kuhn: Sorry, I was really not correct in the end part of my comment. What I should have written is that the X from their mother is a recombination of the two Xs of their mother. There is a small recombinable part in the Y chromosome but it does not contain the key genes for sex determination.

Say x is the percentage of an allele in your mom (or cousin, or brother). Say c is the filial similarity (brother=.5, son=.5, cousins=.125, etc.) of the allele. Say y is the general probability of having that allele in that population (assuming mom is the same species with you). Say f(x,y) is the expected value of the number of allele that you have.
Then f(x,y)= c * x+ (1-c) *y
In other word. There is no contradiction in the idea that we are 98% similar with monkeys and yet only 50% similar with our own mom.
Here, the world similar is used in totally different sense.
f(x,y) is 99% for most allele. Now let gy(x)=f(x,y) then
gy'(x) is c.
In other word, for every allele your mom have, it'll improve the expected value of you having the same allele by half. For each allele your cousin has, it'll improve the expected value of you having the same allele by 1/8th. That is for the same y. For most y, similarity is 100% nevertheless.
Say Ann, Beth, and Cindy has AA, Aa, and aa alleles.
Then Ann's sons have 25% higher expected value of having A alleles than Beth, and Beth have 25% higher expected value of having A alleles than Cindy. I say nothing of actual probability distribution.
Ann's cousins have .0625% higher expected value of A occurrence than Beth's cousins and .125% expected value of A occurrence than Cindy's cousins
Disclaimer: We do not take into account that people mate with those who are genetically similar but not too similar (i.e. no inbreeding).
Another way to see this is to look at y. For rare genes y is small. Hence.
50-50 is for genes that are rare and family specific. If your mother is color blind (100% carrier), the expected value of the number of color blind carrier is improved by 50%. It doesn't mean you'll be color blind. We'll have to go to the technicality of dominant vs recessive. But that's the idea.
For genes that are NOT rare, say genes that make you have 2 feet and 2 hand, you still share all your mom's genes. That's because everybody have that. Your mom have that, and your dad have that, and so is everyone else, including chimps.
Is this what most directly answer your question?
Again the issue is rarity. For rare genes P(You have it|mom have it) is 50%.
For common genes,
P(You have it|mom have it) = P(You have it and mom have it)/P(mom have it). //By bayesian rule
That is 1/1, which is true.
It's just obvious, probability = 1, that everybody has it.
Source: selfish gene by Richard Dawkins
I am a mathematician. Now prove me wrong.

C'mon. I got the math right here. Is it wrong?

Can someone tell me if I am wrong? I could be the only correct answer here.

Just a note that red/green colour-blindness is X-linked so it's much less common to find an affected female than male.

no body like math here


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What can the timing of human urination tell about the human's physical condition and circadian rhythms?
I've noticed a peculiar phenomenon. A subject drinks 400 ml of water, then observes time until the urge to urinate is felt. The time is 15 minutes. The subject releases water. 14 minutes later another urge to urinate is felt. The subject releases water again.
I'm particularly interested in what kinds of biological systems are involved in timing of such events.
Does the time depend on how full the subject's stomach is? Does caffeine and other diuretics play a part?
Is it time of day (circadian rhythm) sensitive?
Does that predict anything about the suppression/release of diuretic hormones?
What I'm trying to understand is if the timing between human urges to urinate after water consumption can be used to make predictions about the human biological clock and the state of various systems within the body (for example the digestive system).
I will be conducting this experiment at different times of the day. My hypothesis is that at night, when diuretic hormones are suppressed, the timing would be longer for the same amount of water consumed. This is based on my limited research in the area.
Update: I did perform the same experiment at night, the time was 75 minutes for the same amount of water. The experiment was performed at the end of one of sleep cycles, which makes me think that 75 minutes was the duration of the subsequent sleep cycle.
I appreciate your input on the subject, along with any keywords that can help me advance my research in this area.
Thank you!

The fact that urine output (enuresis) and other kidney functions are circadian is well known, just search on pubmed 'circadian urine kidney'. This can be due both to the fact that liquid consumption is less during the night and to the fact that hormones regulating kidney function like aldosterone and plasma angiotensin II are circadian.

Thanks for a great answer! I got a glimpse that this may be circadian from a general scholarly paper, now I know precise keywords that I can search for.

I would suggest a couple of papers
Circadian rhythms in urinary functions: possible roles of circadian clocks? - Noh et al., Int Neurourol J., 2011
Circadian regulation of renal function - Firsov and Bonny, 2010
Neural regulation of the circadian vasopressin rhythm in cerebrospinal fluid: a pre-eminent role for the suprachiasmatic nuclei - Schwartz and Reppert, J Neurosci, 1985


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What happens to a human body once a sugary snack is consumed?
I'm looking to understand the effects of sugary snacks and/or drinks on a human body. I'm particularly interested in the timing of the ingestion versus various hormonal levels that may be circadian in nature. Is the release of insulin circadian in nature?
Scenario 1:
A person eats 50 grams of trail mix- raisins, sugared pineapple, sugared mango.
What happens in the next couple hours?
Which hormones get released and for how long?
Does the timing of ingestion produce different effects (ex: consumed at 11AM vs 3PM vs 8 PM?) on the body?
Scenario 2:
A person eats 100 grams of trail mix and drinks a can of sugary nectar (48 grams of sugar dissolved in water).
Will this cause the sugar "crash"?
Is there some grams per kilogram of weight guideline on how much refined sugar or corn syrup a human body can handle at once?
Thank you for your response or any keywords that may help me search for this information!

The human/animal digestive tract breaks down food chemically (with low pH/acid), enzymatically (like proteases and glycolytic enaymes which break down protein and sugars respectively), as well as symbiotically (bacteria participates in the breakdown of some compounds in the gut).  The results are released into the blood stream for the most of the body to assimilate.
With foods with complex carbohydrates (scenario 1), the results can be only a modest change in the glucose level in the serum.  This depends upon the specific food which you can understand better by researching the 'glycemic index'.  Highly glycemic foods result in rather short term release of simple carbohydrates glucose/sucrose into the blood.  Lower glycimic food contain complex carbohydrates (which are elaborate chains of sugars) which need to be broken up into simple carbohydrates before they are metabolized the the cells.
Foods which contain a lot of simple carbohydrates change the sugar levels in the blood nearly immediately and it can go quite high.  simple carbohydrates are monomers or dimers of sugars.  BTW complex carbohydrates have few pictures on the web, but you can imagine them as chains and networks of many many simple carbohydrates linked together.
Not all simple carbohydrates are used by human beings for energy.  For instance the glycosamine in 'joint juice' is the sort that makes cartilidge, which just to show you how different some complex carbohydrates can be. BTW i don't recommend joint juice, just trying to give a familiar example.  Its unlikely that the glucosamine you drink will be directly used for your joints!
So glucose is the energy currency in the blood.  when the glucose level goes up insulin is secreted by the pancreas which tells the cells to take up the glucose for glycogen (internal cell energy storage in a complex carbohydrate) or to be metabolized directly.  Diabetes results when insulin is not produced (type I) or when the cells stop responding to insulin (type II).
Human tolerance to glucose in the blood is estimated to be up to about 100 mg/dl long term. higher than this on the average is not healthy and can go up to several hundreds and cause lots of degeneration in the kidney, liver, and eyes, and more.  Exercise and fasting increase insulin sensitivity and athletes have blood glucose that is quite low even if they have a sugary beverage.
hope this helps - many keywords embedded within...
One last note.  Fructose, which is about 45-60% of high fructose corn syrup (the rest is sucrose) is almost entirely metabolized in the liver.  This is why fructose can be harmful to people who drink too much sweetened beverages.  With the liver taking in the vast majority of fructose, it tends to make fat out of it, sort of overdosing it to make it fatter than the rest of you relatively quickly.  Fatty liver is a marginally disfunctional liver and can cause health problems down the way.  Abdominal body fat (not on your love handles, but amongst your chest cavity and internal organs) is particularly harmful as it interferes with all sorts of organ function.  Probably something everyone should be aware of.

@AlexStone you're welcome :)


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Is there such thing as a generic "metabolic type"?
A while ago I picked up a book called "Eat right for your metabolic type". The book discussed the effects of the endocrine system on the overall shape and the speed of metabolism.
The book outlined few major metabolic types:

Adrenal
Thyroid (hypo/hyper)
Muscular

The book proceeded to discuss the overall shape of the body, including shape of fingers to help identify the metabolic type and give suggestions on which foods to avoid for a particular type.
The book then gave examples of effects of foods on metabolic types - for example an Adrenal type who eats too much sugar would crash and compensate for this by sleeping.
Since I can no longer find that book in print, I'm interested if there's really such a thing as a metabolic type that can be easily identified ? Are there indeed some foods that people should avoid eating?

In general the answer is yes. However, the degree in which this is true and the degree in which the human body can adjust and adapt to new food types is larger misjudged. I am of the opinion that metabolism is largely controlled by the microbiome. It is largely recognized that the gut biome does adjust depending on diet and will also vary depending on drug intake. From previous meta-analyses, it has been noted that there are three subtypes of microbiomes. In a particularly famous study, it has been noted that Japanese and only Japanese people have the microbiome to digest seaweed due to the remarkable volumes of sushi that they eat.

Very interesting article!

That book was likely crap, but in short the answer is yes, probably there is a genetic basis in the metabolism, with human 'types' that could benefit from a personalized nutrition. The discipline studying these relationship is called nutrigenomics, and the main concept is similar to what is being told for personalized medicine. The bad news is that unfortunately this is not easy to identify, surely not from the form of your finger.

Not from your finger … but possibly from metagenomics.


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Genetic effects on personality
It is said that genes are partly responsible for the choices we make in our life; our genes help to create our environment, and then that environment can influence our personality. So, beside genes, what else is responsible for the other choices? Is there something else at work?

The answer to the question is in the sentence immediately before the question: “the environment can influence our personality.” With that in mind, what’s the real question?

Many genetic studies in this area have found that variation in serotonin receptors associates with differences in a number of personality traits. That one gene, or a very small number, turns up time and time again for something so complex as human personality makes me a bit suspicious.
Other factors at play:
Family dynamics
Culture and cultural norms
Society and societal norms (these could clash with the above two)
Exposures - drugs, toxins, diet, and many others
Traumatic events

The problem you are looking for is called the "Nature vs nurture" debate. Lots of scientists have written lots of books and papers and done lots of studies on the subject. As you can see, the title of the debate already includes the two main concerning factors: nature (genes) and nurture (environment).
These of course each include a variety of ways in which they influence personality. Genes provide the biological basis for your personality, they determine how everything in your body works1. At the same time, these genes build a system that has a life of its own - your brain.
It consists of neurons, and nobody knows how personalitites comes about from them exactly but somehow they do. Neurons reshape all the time in ways that no other cells do. The connections between them, synapses, are formed, destroyed, reinforced or weakened all the time - in response to things that take effect on them, for example the things that you see and hear, smell, taste and feel. A very interesting subject in this field is the study of neuronal networks, giving some insight into how memory and learning may work.
But while this may seem like external factors must then be more important for personality, it depends on the setup provided by your genes how your neurons respond to certain influences - what concentrations of neurotransmitters they produce and secrete etc.
As you can see, the only thing that is really safe to say is that it is not "either or", both definitely play a role.
1But even the biological development of the body has non-genetic influences - at the moment I can think of epigenetic inheritance though this seems to be disputed (see comments). Apart from that as far as I know there are uterine influences on embryonic development. And then there are the more or less obvious external influences such as cutting things off before they develop.

Interesting post! Do you know of any good review papers on the subject of neural networks, and modeling the neuronal reshaping? Or even any citations really!

I recently read "Wetware" by Dennis Bray, which is generally on the topic of intelligence and consciousness. I don't know how well-respected that is but I found it quite an interesting read, even if some of his claims are a bit off in my opinion. I can't offer any papers unfortunately though.

“epigenetic inheritance” in humans is still unproven and has considerable problems (germline–soma distinction, i.e. Weismann barrier, and reprogramming) so I wouldn’t put too much weight on that.

Is this better? :)

Furthermore the genotype of the individual does not represent the phenotype, it is about the expression profile of the genes rather than just their presence.


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Why are melodies/harmonies perceived as pleasurable by humans?
Is there any evolutionary advantage to finding melodies or harmonies pleasurable? Does the ear pick up these particular oscillating waves differently from other sounds, and if so, how does that affect our perception of pleasure? I'm looking for some sort of signalling pathway (most likely involving neurotransmitters I realize).

Why was this asked on Biology and not [cogsci.se]?

There are strong connections between the auditory cortex and the limbic system, which includes such structures as the hippocampus and the amygdala.
A recent paper [1] builds on earlier notions of emotional "significance" of music without any lyrics.  It adds in lyrics, so giving a perspective of which portions of the brain are reacting to which component of the music.

Additionally, contrasts between sad music with versus without lyrics recruited the parahippocampal gyrus, the amygdala, the claustrum, the putamen, the precentral gyrus, the medial and inferior frontal gyri (including Broca’s area), and the auditory cortex, while the reverse contrast produced no activations. Happy music without lyrics activated structures of the limbic system and the right pars opercularis of the inferior frontal gyrus, whereas auditory regions alone responded to happy music with lyrics.

One of the limitations of this particular study is that the subjects self-selected their own pieces, which may limit the reliability of the results.  Of course, defining "happy" or "sad" for every individual is slightly subjective and difficult.  They cited an earlier "pioneering" study which standardized the musical selection between subjects.  Without consideration of the lyrics:

The first pioneer study using functional magnetic resonance imaging (fMRI) by Khalfa et al. (2005) chose a controlled manipulation of two musical features (tempo and mode) to vary the happy or sad emotional connotations of 34 instrumental pieces of classical music, lasting 10s each. Sad pieces in minor-mode contrasted with happy pieces in major mode produced activations in the left medial frontal gyrus (BA 10) and the adjacent superior frontal gyrus (BA 9). These regions have been associated with emotional experiences, introspection, and self-referential evaluation (Jacobsen et al., 2006; Kornysheva et al., 2010).

As an aside to answer your final thought, in cases like this I think trying to jam everything under an umbrella of one "neurotransmitter system" or another can make things overly simplistic to the point where you lose focus of the diversity of receptors expressed.  You can say a system is driven by Dopamine, but D1 and D2 receptors have exactly the opposite effects on the neuron.

[1] Brattico, E., Alluri, V., et al (2011) A functional MRI study of happy and sad emotions in music with and without lyrics.  Frontiers in Psychology, 2: 308.  doi: 10.3389/fpsyg.2011.00308 (free pdf)

(see also, http://www.sciencedirect.com/science/article/pii/S0028393206003083 and related)

In music, harmonies are simultaneous combination of tones or chords that are concordant.
In physics, each note is actually a vibration with defined wavelenght, the concordance can be explained in mathemathical terms, for instance with regard to coincidence of phase oscillation.
In physiology, the ear perceives air vibrations and send them to the brain by means of trains of pulses.
According to some scientists, a music providing regular train of pulses (like harmonic music and rhytmic music) should be more pleasing, probably because of stimulation of the limbic system, as the other answer explains.
Source: Ushakow et al. 2011, Physical Review Letters, DOI 10.1103/PhysRevLett.107.108103
Lay explanation: Why harmony pleases the brain, New Scientist, Sept 2011


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Why is PEG important for efficient yeast transformation?
One way to do an yeast transformation is by using lithium acetate, a single-stranded carrier DNA, and PEG (1). I was wondering why is the polyethylene glycol important for the efficient transformation. How does it affect the take-up of the foreign DNA? Yamakawa et al (2) showed that PEG is essential for the recovery of the cells but I couldn't access that paper to read more about it.
1. R Daniel Gietz & Robert H Schiest (2007). High-efficiency yeast transformation using the LiAc/SS carrier DNA/PEG method
2. Yamakawa, M., Hishinuma, F. and Gunge, N. (1985). Intact cell transformation of Saccharomyces cerevisiae by polyethylene glycol. Agric. Biol. Chem. 43, 869-
871.

PEG causes fusion of protoplast (in general lipid-bilayers)

I found this article that might answer your question: Shigeyuki Kawai1, Tuan Anh Phan1, Emi Kono1, Kazuo Harada2, Chihiro Okai2, Eiichiro Fukusaki2, and Kousaku Murata1 (2009). Transcriptional and metabolic response in yeast Saccharomyces cerevisiae cells during polyethylene glycol-dependent transformation. Journal of Basic Microbiology 2009, 49, 73 – 81 I think this is the correct link:
http://onlinelibrary.wiley.com/store/10.1002/jobm.200800123/asset/73_ftp.pdf?v=1&t=hfux1ljn&s=2c2619c78848056e5a51eacebf4489f34657fec6

It is more of a comment, but I can not add one due to my rep points. In addition to what others have already added, I was also told that PEG helps in stabilising the yeast cells, thereby increasing their recovery. I can not share the Nature Protocol paper from Gietz et al, but this is a book chapter from the same authors on the same topic:
https://www.researchgate.net/profile/R_Gietz/publication/11302160_Transformation_of_yeast_by_lithium_acetatesingle-stranded_carrier_DNApolyethylene_glycol_method/links/0f31753c6bfdf40dc4000000.pdf

http://www.protocol-online.org/biology-forums/posts/26634.html
I found this link - it says 'we don't really know'.  It says PEG binds DNA, I assume shielding the membrane from its negative charge and allowing internalization to happen.
I would guess that the amphipathic nature of PEG, being partly hydrophobic, also helps soften up the membrane.  Interestingly, if you increase the PEG concentration beyond the limits, it decreases the efficiency of the procedure.

I assume it has an analogous function in ligation buffers. There it apparently takes up a large proportion of the volume and thereby increases the chance of interaction between bits of DNA.
In a transformation buffer it should increase the chance of DNA getting into a cell. Unfortunately the only reference I found for this was at Bitesizebio: http://bitesizebio.com/20/5-dna-ligation-tips/