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Compressing structural information in PDB files
There seems to be a lot of redundancy in PDB files.  These files can of course be compressed with general-purpose compression programs like gzip, but I can't help but imagine that these tools are overlooking a significant amount of redundancy in PDB files.  Are there compressors that specifically target PDB files?  If not, what are some aspects of PDB files that are ripe for compression?
Looking at a typical PDB file, some redundancies are immediately apparent.  Other redundancies are less obvious.  Consider this excerpt of two residues from 1MOB (myoglobin):
ATOM    332  N   LYS A  42      16.481  27.122 -10.033  1.00 11.15           N
ATOM    333  CA  LYS A  42      15.926  28.134  -9.159  1.00  8.64           C
ATOM    334  C   LYS A  42      16.970  29.081  -8.512  1.00 16.74           C
ATOM    335  O   LYS A  42      16.687  30.075  -7.799  1.00 11.84           O
ATOM    336  CB  LYS A  42      15.093  27.489  -8.043  1.00 18.03           C
ATOM    337  CG  LYS A  42      13.731  26.888  -8.502  1.00 19.65           C
ATOM    338  CD  LYS A  42      12.679  27.912  -8.953  1.00 17.94           C
ATOM    339  CE  LYS A  42      11.438  27.406  -9.703  1.00 24.82           C
ATOM    340  NZ  LYS A  42      10.474  28.567  -9.803  1.00 19.81           N
ATOM    341  N   PHE A  43      18.218  28.599  -8.544  1.00 12.28           N
ATOM    342  CA  PHE A  43      19.311  29.318  -7.919  1.00 11.81           C
ATOM    343  C   PHE A  43      20.223  30.024  -8.949  1.00 10.95           C
ATOM    344  O   PHE A  43      21.201  29.462  -9.450  1.00 10.08           O
ATOM    345  CB  PHE A  43      20.138  28.301  -7.137  1.00  9.30           C
ATOM    346  CG  PHE A  43      19.494  27.689  -5.877  1.00  9.53           C
ATOM    347  CD1 PHE A  43      19.572  28.376  -4.679  1.00 12.01           C
ATOM    348  CD2 PHE A  43      18.837  26.465  -5.923  1.00 10.54           C
ATOM    349  CE1 PHE A  43      18.993  27.861  -3.536  1.00  9.59           C
ATOM    350  CE2 PHE A  43      18.261  25.959  -4.775  1.00  8.62           C
ATOM    351  CZ  PHE A  43      18.341  26.666  -3.597  1.00  7.89           C

These two residues occupy 1,638 bytes as plain text; when compressed with gzip, they occupy 467 bytes.  For reference, the format of ATOM records in PDB files is defined at wwpdb.org/documentation/format33/sect9.html#ATOM.
Almost all of the data in the above excerpt seems redundant.  The first field (ATOM), second field (atom index, e.g. 332 in the first row), sixth field (residue index, e.g. 42), tenth field (occupancy, e.g. 1.00) and last field (element name, e.g. N) seem clearly extraneous.  The fourth field (residue name) could be shortened from three characters to 1 character, or simply an integer.  I'm not a data compression expert, but I imagine gzip picks up most of this redundancy.
Slightly less obviously, the atom names for each residue also seem unnecessary.  To my understanding, the atomic composition of all residues' backbones will always be the same, and represented in PDB files as "N", "CA", "C", "O".  The same for the atomic composition of the residues' respective sidechains: a lysine sidechain will always be "CB", "CG", "CD", "CE", "NZ" and a phenylalanine sidechain will always be "CB", "CG", "CD1", "CD2", "CE1", "CE2", "CZ".
A subtler redundancy, but one that might increase compressibility a lot, seems like it could be in the atomic coordinates themselves.  For example, in the backbone, would it be possible to deduce each residue atom's X, Y and Z coordinates (12 data points: 4 atoms * 3 coordinates) given only their phi, psi and omega dihedral angles (3 data points)?  Could applying dihedral angles to atoms within sidechains similarly remove the need to explicitly list the 3D coordinates there?
Could "temperature  factor" (the second to last field in the excerpt) be losslessly removed, or compressed in some non-obvious way?  What are some other possible optimizations that could be used to more efficiently compress PDB files?  Are there any obvious grave performance implications of these various compression techniques on the speed of a hypothetical decompressor to convert back to the official PDB format?  Have these questions been answered in the literature or an existing PDB-specific compression program?
Thanks in advance for any answers or feedback.
Edit:
Given that no PDB-specific file compressors seem to be available, I suppose my specific goal is to develop one.  One potential application I see for this is in significantly decreasing fresh times-to-render in certain use cases of browser-based molecular visualization programs, e.g. Jmol, ChemDoodle Web Components or GLmol.  Another application could be decreasing the time and size of data needed to download archives of PDB files like those described here.
This would of course require a way to efficiently decompress the packed PDB files, but this trade-off between decompression time and download time seems like it could be useful in at least some niche applications.
Edit 2:
In a comment, nico asks "How would compressing the file decrease render time?".  Decreasing gzipped PDB file size (e.g. by half or more) and thus decreasing time needed to download the file would decrease the time between when the PDB file was requested from a remote server and when the structure was rendered by a molecular visualization program running on a client machine. Apologies if that use of "fresh time-to-render" in that context was unclear.
A lossless compression could also involve encoding the PDB file to an object (e.g. JSON) that is faster to parse for the visualization program, and decrease render times that way.  Looking around further, if the application only required displaying the 3D structure and not also retaining data about specific atoms and residues, then using a binary mesh compression (e.g. webgl-loader) seems like it would probably decrease time-to-render even more.

Do you have any specific goal in mind? The size of PDB files shouldn't be a problem today, the largest ones I've seen are only a few megabytes, like e.g. ribosome structures or NMR structures with large bundles. Or is this just an exercise to understand the PDB format better?

How would compressing the file decrease render time? And, I agree with @Mad Scientist, we are speaking of a few Mb maximum, so building a compressor from scratch would seem only a nice proof of concept

It sounds to me that apart from the fact that it is PDB files that are under discussion here, this is not really a biology question per se but more of a programming question and you are likely to get better responses from that forum.

Thanks for the pointer.  I asked my original questions to get answers from people knowledgeable in the domain of structural biology on what information in PDB files is redundant and can expressed more compactly.  In addition to providing answers about that, respondents have asked some reasonable questions that were unrelated to the structural biology, and I've answered in kind in my edits.  I would have asked in Bioinformatics, but that forum is still just a proposal.

finally, 5 years later, bioinformatics.SE got into private beta, but it may get closed if it doesn't get more Q&A in the next few days. Structural bioinformatics is underrepresented there, so consider supporting that site by asking a question there.

You are making a few assumptions that are likely not valid for all PDB files. For example:

Residue indices are not necessarily sequential, nor do they have to start at 1
Not all possible residues have 1-letter code equivalents, there are thousands of possible exotic residues, not only the standard amino acids
PDB files are not only used for proteins, but also nucleic acids and small molecules (usually as ligands)
Occupancy can be different from 1.0 if there are multiple conformations represented in the PDB file
The element type is obvious for unmodified amino acids and nucleotides, but not necessarily for more exotic residues (though usually it's easy to identify)
The distances between atoms are not necessarily the ideal distances, so you would need angles and distances to represent the coordinates.

The temperature factor is an experimentally determined value, there is no obvious compression for that. You can safely discard it if you don't need that data, and e.g. it has no meaning anyway in NMR structures.
The advantage of the PDB format is that pretty much every program can (theoretically) handle it, though the implementations vary and subtle incompatibilities can cause a lot of headaches. The size of PDB files is almost never a problem, so there is no significant motivation to improve on the format in that regard.

Those are good points about A) needing not only dihedral angles but also distances between each atom and B) temperature factor being extraneous in NMR structures.
I think the usefulness of compressing PDB files is probably best suited for a separate discussion, but I appreciate this answer.  Definitely informative.

I'm resurecting an old question, but I've heard this question from a few young bioinformaticians and had a couple more points to consider about compressing PDB files.
The first is that many PDB files (including all PDBs hosted on the PDB site) have some 300-400 lines of meta data at the top of the file.  This accounts for about 10-20% of the total file size.  Also many PDBs have ANISOU records, but they're about as redundant.
Second, even if you're dealing with raw coordinate data, I think you're underestimating just how well GZIP already does.  Let's just say half that column data is somehow completely redundant and we can just compress it all away. Next we'll encode the 5 numbers (x, y, z, q, b) in binary using 2 bytes for each number (which isn't even enough room for practical use, but we're optimistic here).  So we've compressed 80 columns to 10 columns, which is 12.5% of the original size. Running gzip on a couple simple pdbs (after grepping out just the ATOM records), it achieves 23.0% of the original size. If we really cared about file size, we could use bzip2 which gets to 16.4%.
Our magical compression tool is only twice as good as gzip, which is nice, but gzip is already four times better than uncompressed pdbs.  If we cared enough, we'd just use bzip2, which is only 30% larger than this hypothetical minimum size. And once we got all the atom specifications back in there, I'm sure they'd be virtually identical.  The bottom line is that bzip2 is already very close to the maximal theoretical compression limit for many kinds of files, especially text files. For genome sequencing data, which is orders of magnitude larger and more redundant, people just made slight modifications of the underlying algorithm.
I've downloaded and analyzed the entire PDB database (a little out of date, but it's 75K structures and 14GB, gzip compressed), and can appreciate wanting to shrink it down further, believe me.  At that level, compression makes a difference in analysis time just reading data off the hard disk (or an NFS server). Fortunately, many (if not most) pdb tools read gzip'd pdbs natively (sadly not the case for bzip'd files). Perl, Python, and every other major bioinformatics language have simple APIs for automatically decompressing gzip'd files as they're opened. Against the ubiquity of gzip, it's not really worth thinking about a small improvement in compression. Again, if we cared, we'd just make everything use bzip2 instead.
The future is more like PDBML, which I kind of despise.  But it's far more complete and easier to parse (given that XML parsers exist for every major language), even if the files themselves are an order of magnitude larger. I don't like them (and mostly XML in general) because they're not human readable in any practical sense. But at the same time I'm not suggesting we just move to a 120 column PDB format just to address PDB format limitations.
Using only dihedral angles would never work either, and not because of numerical precision. There is small but significant variance in bond lengths and angles that would cause coordinates to be off by angstroms by the end of the chain.  It wouldn't help with ANISOU, REMARK, and other records. And it would frankly be a huge pain to write new parsers for.

The PDB file format was specified in the dawn of computing to fit on punch cards. So it has some shortcomings that have led to generations of scientists cursing the fixed-width column format. By now, it has been superseded by an XML-like format: PDBML. Of course XML is less space-efficient than a column layout, so you can see that disk space was not the main concern, but being able to parse the files. Nonetheless, the PDBML page states that they offer three types of download files: "fully marked-up files, files without atom records, files with a more space efficient encoding of atom records" -- so you could check what they do in the latter case.
As for your suggestions: in theory you could use only dihedral angles. However, the numerical errors would accumulate as you go along re-constructing the 3D coordinates, and different software architectures will give you different precision. So: explicit is better than implicit in scientific file formats.

I know the question is old, but for the record: the RCSB PDB is currently working on a project to compress the PDB structural data with a new file format, called MMTF (MacroMolecular Transmission Format).
The format uses MessagePack for serialization and does custom compression, achieving ~ 5x advantage over mmCIF gzipped files. Currently the whole PDB archive fits into 7GB. Most importantly parsing time is reduced dramatically thanks to the format being binary.
You can read everything about it at the website: http://mmtf.rcsb.org

this seems more like a comment than an answer, yes?

@VanceLAlbaugh reading the original post, one of the questions was "Are there compressors that specifically target PDB files?". I'm answering directly to that, only a few years later...


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Cucumber on the eyes
In many spas and salons I have seen people place a cold cucumber on their eyes.
 I think this might be for coolness, but why a cucumber?
And Is it actually for coolness or for something else (like lightening of dark circles, etc.)?

Cucumbers have an anti-inflammatory effect that reduces puffiness. The
  vegetable not only has a high water content, it but it's often stored
  in the refrigerator and comes out cold. This means that the water
  hydrates your skin, and the cool temperature decreases the flow of
  blood to the space around your eyes. Together, additional hydration
  and reduced blood flow can sooth the skin around your eyes and
  alleviate swelling

Source
Also it has silica.

...What does the silica do? It'd also be appreciated if your answer wasn't entirely a direct quote from the article.

@Lance made it cw.

@Mahmud can u please provide some more info?

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Why do human have continuously-growing hair on their head?
Why do hair continuously grow on human heads, while the same doesn't happen on other parts of the human body? Where there are hair, they only usually grow to a fixed length; but they seem to have no limit (or at least a much higher limit) as long as the head is concerned (and the face, in men).
Why does this only happen on humans? When did it start happening? What kind of evolutionary advantage could there be in overly-long head hair, so that humans have them while other primates and mammals don't?

I know there are various questions around about why humans have much less body hair than other mammals; mine is related but different: why are we the only species with so much hair on our head, to the point that they might even become inconvenient if we don't cut them?

There is a limit on hair growth - http://biology.stackexchange.com/questions/1267/why-can-hair-grow-without-limit-while-eyebrow-cannot/1273#1273
As for the rest of your question, we still haven't found the "missing link" in human evolution, so we can't really say "when" because we don't know the stages in-between. As for advantages and disadvantages, well, that seems like it might be more opinion based as I don't know if we can ever know for sure "why".

Thanks for pointing that out; however, even if waist-long hair is the limit for most people (and I know for sure there are exceptions to this rule), the question still stands: why does this only happen on human heads?

@SolarLunix there is no such thing as the "missing link". It's a fallacy dating back to the ancient Greeks, and used by creationists to attempt to disprove evolution. Look it up.

@Massimo Actually, it doesn't really only happen in humans. If you look at a lot of long hair breeds of dogs, there are some that need CONSTANT attention or their coats will become too long and get in their way. As for why it started, that's more of an opinion based thing, it could've been a mutation, or it could've started and continued due to a mating preference.

@MattDMo I wasn't aware, thanks for pointing that out. Is there any research/evidence on how humans evolved? I mean I've read a bit about Neanderthals and other species in the phylum Homo (such as ones who were amazing runners), but I haven't read much more than that.

@SolarLunix check out https://en.wikipedia.org/wiki/Timeline_of_human_evolution and https://en.wikipedia.org/wiki/Human_evolution for starters. And, BTW, Homo is a genus, not a phylum.

@MattDMo sorry, I'd change it but it won't let me edit that comment. Sometimes I get my terms mixed up (thanks for the two corrections)

This post should give some insights on the mechanism of hair length control.

Suggested edit by user @JustinMasters:  "I would like to suggest taking a different approach towards asking questions that have to do with science.  Rather than ask why something happens, try to ask "how" or "what" questions that can provide you with the the information you seek.  "Why" implies reason or purpose in such a way that one can get comfortable thinking about things the wrong way, especially when you ask "why" in a physics or chemistry class. In zoology, most why question about an animal's traits can be answered with fitness to compete for resources or mates." [cnd..]

[cnd..]: "The more interesting information comes from trying to figure out the how. How do the genes / gene expression for hair and fur differ such that hair will continue growing unchecked while fur will grow to a specific length?"

The above comments were a suggested edit to the Q, but I think they fit better as comments, since the edit wasn't a rewrite of the Q but rather suggestions or an alternative perspective.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Can this theory on the evolution of human appearance be flawed?
This is what a friend of mine said:

When there's human offspring, it will look a rough 'medium' between
  the two parents, with it sharing features from the two. well if the
  offspring of one set of parents has sex with the offspring of another
  set, the outcome becomes a 'medium' of those two. So the range from
  what we shall call 'completely average looks' (a hypothetical state of
  the average of everyone in the world, which is acceptable as we're
  looking at a process of millions of years) becomes less and less the
  further into the future we go. Eventually, there is almost no range
  between people and 'completely average looks'.

In summary: take the hypothetical average of everyone in the world, and because the offspring of two people is a slight mixture of those two people, they are a tiny bit closer to the hypothetical average of everyone in the world, which means that eventually people will be getting closer and closer to this average, so will one day look the same.
So he's suggesting that slowly people will become more and more similar.
My argument is that, although this baby may be that tiny bit closer to the overall average, they're new look has effectively altered the average, meaning that they aren't actually getting closer to the average.
I'd like an opinion and flaw from some experts, such as yourselves, so please...

What he's getting at is called homogeneity, for future reference. At least, I think so. 'Completely average looks' means very little in a biological context since evolution works on a genetic scale.

It sounds like they are saying all brothers would look alike, but that isn't true either.

Edited for what he actually meant, cos i misinterpreted it

Quantitative genetics is one reason why this doesn't happen. For example height is affected by many genetic loci, not just 1 gene, and we can for the sake of the following illustration call them Locus A through Locus J - 10 Loci.
Now this is purely illustrative and hypothetical - in actuality there are some differences between this example and the real world, but nevertheless I shall plough on. Imagine everyone carries a basic set of genes which makes them 150cm tall. Loci A-J each have two alleles, either T or t, with one inherited from each parent. Each T allele adds 2.5cm to the basic height per copy (each parent has two copies, one goes to the offspring) and t has no effect. The parents are both heterozygous at each loci, that is they have one T and one t at each pair of loci. Therefore both parents are 175cm tall.
When these parents mate the offspring inherit one copy of each parent at random. As such the most likely single outcome is that the offspring will inherit 10 T's and 10 t's - roughly five of each from each parent. However, purely by chance they could receive 10 T alleles from each parent, giving them a height of 150+(20*2.5) = 200cm. Likewise, a sibling could also inherit only t alleles thus giving them a height of 150+(0*2.5)= 150cm. Thus variation can actually increase from one generation to the next.
There are other reasons why we do not regress to the mean as well, but I am writing a quick answer over breakfast, but I will be in the office soon where I can get some more thorough explanations from text books. E.g. (Dis)assortative mating, Mutation, Recombination, Environmental variance, Selection. However, with the increase in global movement it has become easier for dominant alleles to spread which is why the number of blue eyed people in the US is decreasing.
Here is an interesting article which backs up what I said about quantitative genetics, called "Will humans eventually all look like brazilians?" Also for good quantitative genetics texts take this as a basic intro and this for further reading.

Also, I think we many of the answers to this question are the same as would answer the question "why don't siblings look identical?" - simplified to "polymorphism exists."

Please look at my edit, which is in bold, as well as the new paragraph below it. Do you have anything more to say?

well for everyone to look the same it would require that they are a) genetically identical, this would require ubiquitous inbreeding (everyone homozygous for the same allele at all loci) and b) everyone experiences the same environment all the way from development Hutterites but you will still see "considerable" variation within those - basically it is impossible for us all humans to be identical because we have so many people so inbreeding is low, mutation occurs in the DNA regularly, and complete inbreeding would likely cause the species to collapse at the hands of disease.

@ollyprice and, if you read my original answer you will see that even if both parents are average (175cm) it does not necessarily mean that their offspring will be average (anywhere from 150-200cm, and possibly further with mutations and environmental variance).

The basic point your friend is missing is that offspring appearance is not simply a mixture of their parents'. Each child also has individual characteristics which were not present in the parents. This is due to a variety of processes, the most important of which is chromosomal cross over.
Each offspring will be a mixture of its parents and its own individual characteristics. Therefore, your friend's argument does not stand because each generation causes novel characteristics to appear so each successive generation changes in unpredictable ways.

Please look at my edit, which is in bold, as well as the new paragraph below it. Do you have anything more to say?

@OllyPrice your friend's entire argument is based on a wrong assumption. Offspring are not simply the average of their parents. Consider siblings, you can have a couple with 18 children, each of these will be different not simply the average of their parents. Mutation and cross over and simple errors in DNA replication ensure this.

Here's another take on it:
Suppose, for starters that you have only one gene that is responsible for your trait. Say, having version 1 (denoted T) gives you +1 to height, and having version 2 (denoted t) gives you -1. Suppose further that each version occurs in half the population.  Now every individual has 2 copies of each gene, so that 1/4 of people has TT for +2, 1/4 has tt for -2 and 1/2 has Tt or tT for 0 change in height.
Now suppose two people with Tt or tT mate. If traits followed simple averaging pattern your friend suggested we would get the average of 0 and 0, that is 0 - all the time. But in genetic model (which is what really happens)  1/4 of the ofspring will get TT for +2, 1/4 will get tt for -2 and only 1/2 will actually get tT ot Tt for 0. Note that the variance - amount of variation - increases (everyone was 0 before mating, but some of the offspring has +2 or -2), whereas with the "mixing" model this does not happen.
For another mating paring - TT with tT - 1/2 of offspring will have TT for +2 and 1/2 will have tT for 0, effectively replacing the parents, so that the amount of variation stays the same (since the mean of the population is 0 variance contribution of these two individuals is 2^2+0^2=4 in both parental and offspring populations). Note that the mixing model would have all offspring at +1, which decreases the amount of variation  (variance contribution going from 4 to 1^2+1^2=2).
In general, the mixing model of mating always decreases variance - leading to the "everyone looks average" result in the long run, but the actual genetic mating keeps variance constant (unless another factor - like preferential mating, mutation, or environmental factors intervenes; this was pointed out in other answers).
The same thing happens if the proportion of T and t are not 50-50. This is called the Hardy-Weinberg principle.
Finally, if there are many genes that contribute to height, the variance in a trait (like height) can be modeled as the sum of variances from each gene. Now if each one of the genes is inherited through the same genetic mechanism that preserves variance, the total variance will also be preserved. So we will not actually all become "average".

You should add to that the fact that height does not only come from genetic traits, the environment (nutrition, pollutants, stress, etc) plays an enormous role there.

That is most certainly true. I suppose the point of the above is that the part of the variance that comes from genetic factors does not decrease. What happens to the variance due to environmental factors is a completely separate matter, of course.


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Why can we breathe only oxygen?
Plants has the capacity to take in both CO2 and oxygen, that's during day CO2 and at night oxygen. Why don't humans have such a capability?

Remember that O2 is also taken by the plants during the day !

You should have a look biological processes which are:

cellular respiration
photosynthesis

Loosly speaking, these two processes are just the opposite but deal with the same chemical compunds.
$C_6H_{12}O_6 + 6O_2 \xrightleftharpoons\  6CO_2 + 6H_2O (+ Energy)$
or in words...
glucose + Oxygen $\xrightleftharpoons\ $ Carbon Dioxide + Water (+ Energy)
From left to right is the process of respiration and from right to left is the process of photosynthesis.

Respiration releases energy from glucose (sugar). Therefore, animals, plants, fungi respire in order to get their energy from their food. More information on the chemical pathways on  Krebs cycle (or citric acid cycle). The main organelle involved in celullar respiration is the mitochondrion. Note: (Loosely speaking) the glucose is the end product of the digestion
photosynthesis allows organisms to create its own tissues from water and $CO_2$. But this cost energy. This is why plants use capture the energy form the sun with their leaves. More information on the chemical pathways on Calvin Cycle. The main organelle involved in photosynthesis is the chloroplast.

Note: In our lungs comes air which is a mixture of different gases (just like coke (Coca-Cola) is a mixture of different compounds). The two main compounds of air are Nitrogen (~78%) and Oxygen (~21%). We use only Oxygen. More info on the air composition here

Humans breathe in air, which contains both oxygen and carbon dioxide. But we do not photosynthesise and so we do not take in CO2. The CO2 produced from respiration in our body builds up in the blood and through diffusion escapes into the lungs and out when we exhale.


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How does entry of Ca²⁺ to the myocardiocyte make it more contractible?
I'm trying to understand why an increase of Ca2+ entering into the cell, increases the force of the heart contractions. Based on what I have watched in many lectures videos on Youtube (this one- "interactive biology" for example on 4:45), Ca2+ basically slows the repolarization in phase II of the action-potential membrane, and I don't understand how it does the cardiac cells more contractible. Or maybe the answer is pinned in the words "typical cardiomyocytes" and then I didn't get it.

The answer is a bit more complex. Calcium ions have a lot of effects in the cardiac myocyte. Apart from the increased contractility (positive inotropy), extracellular calcium concentration also alters chronicity as you mention by altering the rate of repolarisation. An attempt at a simplified picture of the inotropic effects follows:

First is to increase the contractility via directly sensitizing the tropomyosin system. Have a look here. Quoting the paper, "...In both cardiac and skeletal muscle, the force-generating molecular motors (crossbridges) are turned on by increasing the intracellular free calcium level that regulates the troponin-tropomyosin system. However, calcium activation is a two-way process in the sense that activated crossbridges also affect the troponin-tropomyosin system...An increase in Ca2+ activity causes an azimuthal shift of tropomyosin around the filament (by about 30 degrees), thereby increasing the probability of low-force crossbridge interaction, a process which by cooperative effects induces further tropomyosin movement (by an additional 10 degrees) which results in the open state of the filament characterized by forceful cross-bridge interaction...". Hence, higher the intracellular concentration of Calcium, greater is the maximum force.
Sarcomere length also affects the sensitivity to calcium. This increase in contractility is not because of calcium but is mediated by calcium. The reason has something to do with lateral filament lattice spacing decreasing, increasing the probability of cross-bridge formation, increased strain on titin alters lattice spacing and myosin packing.

As I said, this is a bit too oversimplified. There a lot of inter-regulations taking place. Have a look at these papers here.

Myofilament Calcium Sensitivity: Role in Regulation of In vivo Cardiac Contraction and Relaxation (A good review plus a bit of quantification on the topic being discussed)
The negative inotropic effect of calcium overload in cardiac Purkinje fibers (To present the complexity)

Two different but related processes i.e excitation- contraction coupling could possibly answer your question. Please see the simple diagram:
https://image.slidesharecdn.com/heartcirculation-120511091224-phpapp01/95/heart-circulation-47-728.jpg?cb=1336727680
 "Ca2+ basically slows the repolarization in phase II of the action-potential membrane" what you said is one of the excitation phase during which Ca2+ influx cause more Ca2+ release from endoplasmic reticulum, increasing Ca2+ concentration in the cytoplasm leading to more binding of Ca2+ to troponin C and subsequently increase force of contraction.


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Immunity during pregnancy
I have learnt that our immune system distinguishes self from non-self by using MHC. So a mother during pregnancy should also develop antibodies against the fetus as it is also a genetically different individual. Answering by saying that antibodies won't cross the placental barrier seems wrong as there is so much research going on this thing that such a simple explanation wouldn't suffice.
Why doesn't the mother reject the baby?

Perhaps an equally interesting question is why the immune system doesn't attack sperm. I've seen the answer before (but don't have a reference handy) and if I remember correctly, there's some special hard-coded marker, which is actually pretty scary. In any case, I think the mechanism is quite different from the one involved in your question.

In fact antibodies do cross the placental barrier:  there is active transplacental transport of maternal IgG into the foetal circulation.

Actually her body can reject the embryo. That can be one cause of infertility, and a mild immunosuppressant can help...

Awesome question! The immune system detects the presence of non-self using MHC and T cells and the lack of self using NK cells. The placenta first of all doesn't display MHC so T cells can't detect it, and expresses NK inhibitory receptors which stop NK cells killing it. Furthermore, the immune system isn't able to get to the foetus so it isn't able to activate against these antigens nor produce the antibodies which require T cells to be activated first, which then activate B cells. This is because the placenta is a syncitium, thus no spaces between cells for immune cells to slip through (a mechanism used by viruses). The placenta also secretes Neurokinin B, this makes it hard for the immune system to see the baby, and is a mechanism used by parasites. There are T reg cells which act to supress an immune response.

thank u so much for answering . Your explanation seems quite plausible but I read in a book (Campbell Biology 9th edition) that still research is going on for finding explanation. So why is your answer not actual "answer" ?

I would imagine because it isn't the complete picture. I would imagine (but am not sure) that investigating the above features doesn't sufficiently depress the immune system preventing rejection of the foetus.

I think the research is far from complete in this topic. Afaik. there can be cells from the children in the mother and these cells are tolerated by the immune system.

http://www.ncbi.nlm.nih.gov/pubmed/23049819

@inf3rno yeah... microchimerism..


text:
A question about the intersection of evolution and thermodynamics
From this 2014 article in Quanta magazine by Natalie Wolchover there is a quote from a physicist with an intriguing idea about evolution:
“You start with a random clump of atoms, and if you shine light on it for long enough, it should not be so surprising that you get a plant.”
Jeremy England's idea is that the attributes associated with life have a lot to do with absorbing and dissipating energy. He insists he is not saying Darwin is wrong, and that his thermodynamics-based idea in some sense subsumes Darwinian evolution.
(The Quanta article links to a recent paper of England's which is somewhat technical, but deals with bacterial replication and thermodynamics. I include the link to give a sense of his ideas in his own words.)
My question is  whether his idea, taking it at face value, might furnish a better explanation of something already explained in Darwinian terms or fail to account for some detail of current evolutionary theory?
So if someone had a lot of examples of different aspects of evolution s/he might be able to say, "Here is a situation in which the thermodynamics do not work out as England suggests but which is explained in evolutionary terms," or conversely, "Here is something contrary to evolutionists' expectations that seems to be pretty well explained by the thermodynamics." I suspect that there are several candidates and England's paper gives a hint in one direction.
Thanks for any insights.
Some helpful reading:

Thermodynamics, Enrico Fermi (1936) [Dover reprint].
Understanding Thermodynamics, Ness (1969) [Dover reprint].
What is Life?, Schrodinger (1944).
Entropy Production..., Crooks (2008).
Schneider and Kay, Life as a manifestation of the Second Law of Thermodynamics, Math. and Computer Modeling 19 (6-8): 25-48 (1995).

The last paper is a very readable and non-technical introduction to this topic. If one works through the equations in Chapter 7 of Ness and ref. 4 the idea should be quite clear. Basically, systems (both nonliving and living) which are at some remove from equilibrium devise ways to dissipate energy that involve a decrease in entropy, increasing the entropy of the surrounding system.

The paper seems interesting. Thanks for sharing. I'll read it and get back :)

that article is has quite many technical details that i am not aware of.. it would take me an entire day to read through it :P

it is taking a lot of time for me too.. it is fully in thermodynamics jargons... but one of the references is good and I am reading it. It is called Handbook of Stochastic Methods

Getting long for a comment
I can only comment that evolution does not proceed towards thermodynamic optimum. Adaptation is thermodynamic optimization but evolution is directionless. Otherwise the extant species would not suffer from tradeoffs (which they have even in their usual habitat). Establishment of a self replicating cell may be thermodynamically driven and given the conditions, irreversible; macroscopic evolution is like die roll where some states are randomly⁺ selected and eliminated.
⁺Not really random but a complex non-linear function which seems unpredictable
You can imagine a chamber with particles exhibiting brownian motion. Assume that particles have a random size distribution (lets say they are crystals of different topologies). Now if you keep a separator with few holes wide enough for a just one particle of a given size to pass. Then you'll end up getting only few particles of a narrower size distribution on the other side. This no way ensures that these were the most thermodynamically stable particles.

I added a ref. to the question which I think is very helpful. The thermodynamic idea is almost certainly correct. The only question is, how does this idea relate to the idea of evolution when both are addressing the same local situation. Taking the physics idea as stated it can't be completely inconsistent with evolution. The two will point in the same direction most of the time. The question is, when might one do better than the other and why? Your example appears designed to show the two ideas are incompatible but if you read ref. 4 this seems... Quixotic.

I am sorry.. I was a little occupied with other things.. give me some time to think over it.. this is an interesting concept and I have also myself thought occasionally about thermodynamic explanation of evolution. I just echoed in the example what some "experienced" people told me. I'll get back on this.

authors: Виктор шевченка


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Should heart-to-body energy consumption ratio equal oxygen consumption ratio?
The human heart pumps oxygen to the body, and the heart itself requires oxygen.
Both the body and the heart use energy, usually expressed in calories or ergs.
If we look at the energy consumption (in Watts) of the heart as a fraction $F$ of the energy consumption of the body as a whole it is about
$F \approx \frac{1.3}{91.3}=0.014.$
Humans consume about 550L of oxygen per day per this website and the heart itself consumes about 8 ml of $O_2$ per 100g per minute at rest according to this site. Assuming an average global human heart mass of about 310g (Google) the daily total heart oxygen consumption is about  (8ml x 3.1 x 1440 min) = 35712 ml or 35.7L of oxygen. The ratio $R$ of heart to body oxygen consumption is thus about
$R \approx \frac{36}{550-36} = \frac{36}{514} =0.07$
These figures are rough at best but not rough enough to account for a discrepancy of a factor of 5 in the ratios. Can someone suggest what might account for the difference?
The calculation seems to show that the heart's proportional consumption of oxygen is a lot higher than its proportional consumption of energy. My understanding is that the respective oxygen consumption of the heart and body are a good reflections of their respective energy consumption. Is that a sound assumption?
Thanks for any insights.

This is a really stupid question from me to you. Do you mean to say 7% percent when you say factor? But then you say factor in the ratios. Do you mean the consumption of heart versus body ratio amounts to 7? If so, I am not sure the word ratio is mathematically applied, but I might just be confused.

Also, I think oxygen consumption most likely varies by cell/tissue type. Cardiac muscles may consume more per sq.m or cu.m compared to skeletal tissue and smooth tissue. You are also probably right in that resting heart rate might lead to a more steady, lower consumption rate. Other tissue, might consume even lesser than muscle tissue, etc. So maybe heart to body rate consumption is not all too meaningful. You could look at cardiac to overall muscle energy consumption, etc.

@SrihariYamanoor: I may have worded it badly. What I mean is that 0.07 is very roughly 7 times 0.014. It should be 5 and I will edit. Yes, I mean that the heart's proportional consumption of oxygen seems to be a lot bigger than its proportional consumption of energy. Does this help?

@SrihariYamanoor: Yes, yours is a possible explanation. My assumption has always been that oxygen consumption mirrors energy needs. Maybe that is wrong?

In the case of the heart, aerobic metabolism is necessary for it to work. But that's not the case for all tissues (some have significant anaerobic metabolism). The difference being only 6% that would not strike me as too much of a stretch to explain it this way, but I have nothing reliable on the subject so that's just speculation.

@ElianeB.: How do you reckon 6%? (Not saying you are wrong...)

0.07-0.014, considering the total energy expenditure/total oxygen consumption. That's ~7 times but also absolute value 6% of total expenditure.

At first glance there are a few major issues with your calculation and assumptions.

You're comparing the energy output in work (pumping action) with the energy consumption of the rest of the body in input (oxygen consumption). I don't know how efficient the heart is, but I'd guess only somewhere from 20-40% of input energy is actually converted to pumping action.
Oxygen consumption is correlated with energy consumption, and would be a good way to measure energy consumption if you know exactly what the subject is burning. However, if you have a big difference between the preferred fuels between the heart and the rest of the body, this doesn't really apply  anymore. A quick google leads me here: https://www.ncbi.nlm.nih.gov/pubmed/17081788, showing that the heart prefers to burn fat over glucose, and this creates a significant difference:

Carbohydrate oxidation typically generates approximately 120 kcal per mole of respired oxygen, whereas fatty acid
  oxidation typically generates only approximately 100 kcal per mole of oxygen.

This means that the heart needs more oxygen than the rest of the body to generate the same amount of energy.
I think combined this could explain the 5-fold difference.

You say you compare consumption, but the link you use actually has a list of outputs, based on the mechanical work of the heart. One of the lines actually reads: "The mechanical power of the human heart is ~1.3 watts. It takes a much higher rate of energy turnover (~13 watts) to provide this mechanical power, since the mechanical efficiency of the heart is very low (less than 10%)"

And the 6% of Eliane B is relating to something completely different. The difference between one calculation and the other is 5x, that this number is also only 6% of some larger number doesn't really change that.

The only thing is that 1.3 watt is not the input, it's the estimated output. You can infer this by looking at the numbers they use for their estimates: all numbers related to the output power, not input.

Come on! In the second line you cite they even write Pmech = 1.71 (Nm)/s and Pchem = 8.6 (Nm)/s. There's your 5-fold difference.

Let us continue this discussion in chat.

There is a figure from an article in Cont. Rev. in Card. Medicine that suggests your figure of 20% efficiency is quite good. I don't really trust the figure 1.3W but if we use it there is no explaining to do and it seems that the heart's proportional energy consumption is pretty much the same as its proportional oxygen consumption. Here is the link for 20% (Appendix A): http://mathscinotes.com/2014/11/heart-energy-per-day-versus-truck-energy-consumed-over-20-miles/. If you edit your first paragraph to show your comment calculation I will accept. You were right. +1

Oh--and the second paragraph is not really necessary. Since your first point seems to eliminate the discrepancy there is nothing left to explain.

Since you took the trouble to debate this I am giving the 50 pts and will also accept if you edit your answer just a bit. Don't want it to lapse before you return to the site.

You are comparing the theoretical mechanical work performed by the heart (your 1.33 W number) with the chemical energy consumed in accomplishing that in a biological system. One is theoretical and one is empirical. The heart in fact consumes about 10% of the energy of the body even though it’s only 1% of the weight, owing to the special nature of cardiac muscle tissue (which is unique to the heart organ). It’s a “design” that can go nonstop for one billion contractions or more, and which would have been ludicrously inefficient to use for skeletal musculature. Your 5x factor is in line with typical efficiency measurements of muscle work, around 20-25%.

Cites would help. Your 10% is not in line with the sources I checked (doesn't mean it's wrong).

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


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What are the molecular mechanisms that make the turtle brain more resistant to hypoxia?
I know that turtle brains, particularly those of individual species that hibernate and burrow are particularly resilient to hypoxia and any tissue damage secondary to a hypoxic event.
What are the known molecular mechanisms behind this resiliency?  Does it have to do with the ability of their blood to store/release oxygen over extended periods, or is it molecular factors in the neural tissue that protect it from insult?

There is a bunch of literature on the topic. A good starting point is probably a short description with lots of references in this thesis (page 8), not to talk about other articles, which pop up in google scholar: 1, 2.
The mechanisms are multifaceted and involve principally decrease in oxygen and ATP demands: reduced neuronal activity, lower density of ion channels (but hyper-polarization of the membranes) and so on. Concerning blood flow: "Brain blood flow was continued or increased, and oxygen and creatine phosphate (PCr) stores offered some immediate protection. As PCr declined, turtle brain became increasingly reliant upon anaerobic glycolysis."


text:
Are there any situations in which phenylephrine is preferred to pseudoephedrine?
In the mid 2000s in the US, due to issues of drug enforcement, pseudoephedrine containing medications were brought behind the pharmacy counter and in most cases require ID, and phenylephrine was substituted in most over-the-counter products.
Pseudoephedrine increases the amount of endogenous norepinephrine, whereas phenylephrine works on α1-adrenergic receptors directly.
There are numerous cases where experts have spoken out about the effectiveness of phenylephrine, so it likely is a less effective substitute for pseudoephedrine in its main role as a decongestant.
What I'm curious about is whether there are clinical indications for which the phenylephrine is actually preferred (so situations where the α1-agonist nature without the increase of endogenous NE is sought after)?

I suppose phenylephrine might be indicated in cases where there is an interest in maintaining levels of neurepinephrine, such as when antidepressants or other medications are being administered.

Yes, in all clinical situations where you need pure vasoconstriction without heart rate acceleration (mostly valid for iv administration route).
The classical example would be in the operative setting. If the patient is in a hypotensive state due to hypnotic drugs, opiates, etc. and has atherosclerosis, you will prefer a drug that will reverse the hypotension without an increase in heart rate, i.e phenylephrine. The reason is that an increase in heart rate will shorten the duration of diastole, which will therefore shorten the time interval where the coronary arteries are perfused. Moreover, an increase in heart rate also means an increase in heart oxygen consumption. The end result will be an imbalance between oxygen input and requirement, i.e ischemia and potential heart infarction.
Conversely, if you have a patient with aortic valve insufficiency (regurgitation), you will prefer ephedrine (or any drug with beta 1 activity), because you will be aiming at shortening the available time for regurgitation to occur.

Would phenylephrine be called "non-inotropic" or something of that nature, or is that an abuse of terminology?

@jonsca it is true that (to my knownledge) phenylephrine has no inotropic effect, and can be called as such. But since it is the only pure alpha agonist commonly used for blood pressure control, it isn't really defined as part of a "non-inotropic" class in usual medical jargon.


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Is the poly(A) tail added while transcription is still underway?
I read in Campbell that

....splicing and poly A tail addition may also occur while transcription is still under way.

How can the poly(A) tail be added while transcription is still going on?

splicing is co-transcriptional not polyadenylation. You might have missed a clause in the statement :P

@WYSIWYG The whole statement says " In the cell, the 5 cap is added soon after transcription is initiated, splicing and poly A tail addition may also occur while transcription is still under way."

polyadenylation signals are present at the end of the gene. so it is not possible.. that means this textbook is wrong

@WYSIWYG Yup that is what I think too, but it would be better if we wait for some other people to answer as this textbook is a reputable source.

the textbook will have a reference for this statement. check that.

@WYSIWYG The textbook contains no references at all...

then it's a bad textbook :P

@WYSIWYG Wohoo !!

@WYSIWYG Wikipedia says " Polyadenylation occurs during and immediately after transcription of DNA into RNA."

let us continue this discussion in chat

It's slightly more complicated than the comments above indicate.

Glover-Cutter, K et al. (2007) RNA polymerase II pauses and associates with pre-mRNA processing factors at both ends of genes. Nature Structural & Molecular Biology 15: 71-78

The authors present evidence that RNA polII pauses 0.5 - 1.5 kb downstream of the poly(A) site where processing factors are recruited (cleavage stimulation factor, or CstF, and cleavage polyadenylation specificity factor, CPSF). So the polymerase is still engaged with the template and the premRNA when processing is initiated, although it may not be actively elongating the transcript.

"Localisation of the active polII-3' end processing complex well downstream of the poly(A) consensus sequence agrees well with the cleavage of Chironomus BR1 transcripts after 600 bases of downstream sequence has been transcribed. This model is also supported by the fact that efficient poly(A) site cleavage requires an intact RNA tether linking the poly(A) site with the downstream polymerase." (references are cited in the original).

It is a semantic question as to whether you call this cotranscriptional processing.
[Incidentally this is yet another example which contradicts the commonly-stated idea that evolution acts to optimise everything to conserve ATP - here we have the transcription process discarding the energy from approximately 1000 phosphodiester bonds per transcript.]
UPDATE
@WYSIWYG The polymerase goes past the site where the poly(A) will eventually be added, and makes another 1000 bases of RNA before pausing to recruit factors that are needed for the subsequent cleavage at the pol(A) site which now lies "behind it". After that the poly (A) tail is added at the newly created 3' end. So the initiation of poly(A) addition (in the sense that the cleavage is an obligatory first step in the process) is accomplished while the polymerase is still engaged. I agree that the actual addition of the poly(A) cannot in any way be considered to be cotranscriptional.
I was trying to make the point out that it isn't simply a case of the polymerase encountering the cleavage site and dropping off to allow a second unlinked process to take place.

But recruitment of CstF or CPSF can't be considered as an event of polyadenylation. Splicing does indeed happen co-transcriptionally but it is theoretically impossible to have a co-translational polyadenylation for the accepted unidirectional transcription model. Besides, how would the polymerase sense the polyA signal 1.5 kb upstream without actually sensing it (or else it needs an accomplice); perhaps the assembly just happens as a result of processes initiated during transcription start.

IMHO it is still incorrect to say that polyadenylation happens during transcription. It is equivalent to saying that ovulation happens since the infancy of a female.

As others have stated, splicing does happen cotranscriptionally but you cannot be actively transcribing the RNA while it is being transcribed. However, it is generally accepted that a transcript can be polyadenylated while the RNA polymerase is still transcribing - this is called the torpedo model. The distinction is that the transcript has been cleaved between the polymerase and the polyA, but they were still part fo the same transcriptional event.  See the figure here...
http://www.nature.com/nsmb/journal/v11/n12/fig_tab/nsmb1204-1156_F1.html


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Quorum Sensing in Vibrio cholerae

This is a figure summarising the quorum sensing mechanism in Vibrio cholerae.
In this video by Bonnie Bassler, she explains how quorum sensing can be targeted to control infections.
At 15:09 she explains why cqsA- mutants show more dramatic effect when external CAI1 is added - because we are not fighting against the endogenously produced autoinducer1.
My question : But won't endogenously produced autoinducer help in controlling virulence, as the more the auto inducer lesser the virulence ? Why should we be fighting against endogenously produced autoinducer 1 ?

I haven't watched the video and I don't know the details, but doesn't induction of virulence depend upon auto-inducer in these systems?

its true the compound (homoserine lactone?) is produced by the individual cells already.  but yes we can engineer the bacteria to be non virulent, but in general the problem is not the stuff coming out of the labs, but the stuff that's out there already.

@AlanBoyd Yes it is usually that, but Vibrio Cholerae has exactly the opposite mechanism - it switches off virulence when in large numbers and activates genes that help it go out of the body via diarrhea.

@biogirl but isn't diarrhea = virulence in this case since it is the main pathological effect?

@Alan yeah you are right but when it is in large number it activates a gene for chopping off the protein by which it was attached.

@Alan i feel i havent answered your question and to be honest i really dont know. Does it cause diarrhea and then suddenly switch off its vir genes and on the prot cutting genes ? Is there some way of continuing diarhhea while it is detaching ? I couldnt get the exact mechanism from the video. So i am not sure.

First of all I find quorum sensing to be generally facinating, so I'm happy to see the topic brought up here.
Dr. Bassler has many papers on the subject, but I think one of the most relevant ones to this question is here.
Regarding your question, you have the right idea, but you're missing the point of her comment.  The Western shows a more dramatic difference in cqsA- bacteria because they are not inhibiting themseleves (as you suggested).  Thus the lower concentrations have much higher levels of the toxin produced because the only CAI-1 being provided is the synthetic one.  This makes the ramp up in administered CAI-1 seem more drastic because you start at a higher level.
I hope that makes since, if I can find an open writes version of the Western, I'll come back and give further analysis on it.
Regarding @AlanBoyd 's comments, V. cholerae is different because it seeks to create an acute infection, not a persistent one.  Cholera toxin is what causes the majority of diarrhea and virulence from cholera.  V. cholera produces the toxin until it's inhibited by ether auto-inducer (which should be after the pt already has massive diarrhea), then it switches to produce enzymes which detach it from the gut.  The pt still has diarrhea at this point, cholera just doesn't need to make any more toxin for it to continue.  To do so would probably waste energy, and not help the bacteria make it back to a water supply.

Thanks u ! And to add to your last point , if it secrets excessive toxin it might also kill the host before it has chance to escape.

i would want to add a point that V. cholerae  is not an obligate pathogen.. Being a mild alkalophile, it cannot tolerate the stomach acidity. Infection happens only if there are too many bacteria.


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Are there any alternatives to the Epicentre product Plasmid Safe?
I need to remove any traces of linear DNA (both single and double stranded) from a ligation reaction while keeping circular DNA intact. Up to now, I have used Epicentre's Plasmid Safe to do the job. I would like to try another solution (mostly because of the unreliability of our supplier: it takes weeks to get a batch!).
Has anyone replaced Plasmid Safe with other nucleases? Which one?
I have been looking at the NEB nucleases and I was thinking to use ExoV and T together to get rid of any linear DNA (both ssDNA and dsDNA). Does anyone have any other solution to propose?

"any other solution" How about separating them on a gel?

I would like to avoid gel-purification, the input DNA is already low, plus, some linear DNA is running at the same height of the circular one. I really need to digest specifically the linear ss and ds DNA.

alec_djinn, did combining ExoV and T work for you? I am also looking for methods alternative to Plasmid Safe. Thank you!

Yes, it worked. All the linear DNA is digested. But be careful to do not let the reaction go too long. In my case, 15 min was enough to digest 500 ng with 5 units of both enzymes. Try it out.


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Is there any biological reason that professional swimming is dominated by white people?
I suppose that the question should be turned around to "Why is it extremely rare to see black people competing in professional swimming?" because it is the absence of this phenotype while watching the Olympics that caused me to ask this question.
So,

why are there very few black people competing at world class level swimming?

While I'm here I may as well ask the question:

Why are black people faster sprinters than white people when it comes to world class level?

And of course I want biological reasons.

Why would you downvote this?

It will get downvoted because it's perceived as racist to highlight or suggest biological differences between races (I'm not saying I agree with the downvotes). The answer to your question is no, there's no biological basis, the explanation is most likely cultural.

+1 agree with @Richard Smith, strongly disagree with the downvoters. There is nothing racist in this question, although it has to do more with anthropology than with biology. It would be like downvoting a question asking why Asian people get drunk easily because it is racist. In any case, when you downvote a question you should leave an explanation so that the question can be improved. 6 downvotes and no explanation so far.

Hmm, I was sure that we had the question on Skeptics but I can’t find it now. Since the black/white divide isn’t a meaningful biological distinction (i.e. it is not correlated with genetic background – which, incidentally, is also why I cringe whenever I hear “race” applied to this, because it’s just wrong) the real reason is almost certainly cultural, not biological.

+1 the question is not racist, but I suggest to edit the question and replace 'race' with 'phenotype'. I'm sure there is a good cultural explanation, but this does not rule out genetic basis: Asian people get drunk easily because of the DNA. Looking forward for a GWAS study of olympic players: it will be very interesting!

Well, a friend of mine, an annoying one mind you, keeps telling me that he saw a SCIENTIFIC program on tv which explained that there aren't many black swimmers because they don't float as well, I remember it had something to do with bone density or lung capacity, I forgot..

Yeah I've been told about the bone density one, sounds like a load of rubbish.

It's not biological, it's simply an education issue, and googling would give you:
Just under 70% of African-American children surveyed said they had no or low ability to swim. Low ability merely meant they were able to splash around in the shallow end. A further 12% said they could swim but had "taught themselves".
http://www.bbc.co.uk/news/world-us-canada-11172054
Unlike the UK, where learning to swim is enshrined in the national curriculum except in Scotland, the ultimate responsibility in the US often lies with parents.

if you look at kenyan runners they have a similar acculturation to running - nearly every child there tries. on the upper end of the sport, there are genetic advantages i'm sure, but the more kids who try the sport, the more exceptional athletes will be found.

@shigeta: +1 for acculturation

@rwst Good evidence is seen for this in the pool also - Chinese athletes are now starting to be more competitive in swimming than they used to be thanks to more training. Also it would be great to see some of the endurance athletes from developing countries, like the superb Kenyan distance runners, try cycling from a young age but the cost of the sport is generally prohibitive to those in developing countries, hence it is dominated by Europeans (and increasingly North Americans -excl. Lance now.) whereas running is free!

Really interesting Radiolab podcast episode about Kenyan runners here: http://www.radiolab.org/story/runners High probability of trying the sport + cultural pain tolerance + high altitude + genetics (e.g. thin ankles)

While its true that training is important, black people do have a higher body density compared to caucasians. It is of course possible to train any type of human to swim at world-class level, but people saying that "floating just a little less well doesn't change anything" have a very dim idea of swimming technique. It's just the same as saying "being 1.5m tall will absolutely not decrease your chance to enter the NBA".

I've recently seen this video: Juan Enriquez: Will our kids be a different species?, in which the speaker discusses differences between humans currently inhabiting the planet. At one point in the video,he does touch on the olympics and mention that a lot of the Olympic powerlifters have a certain gene expression.
Power lifting is quite different from swimming, but from the top of my head, I can recall that people from east Africa excel at running. So the difference may be genetic, at least on some level.
The idea of differences between races is very "not politically correct", and as the speaker suggests, we still live int he world that remembers the Holocaust.

The presence of absence of any genetic effect would be completely overwhelmed by the disproportionate makeup of the pool(haha) of young swimmers. It's not impossible, but it's definitely negligible in the present day.


text:
How to store vegetables in the refrigerator: In plastic bags or not?
My wife and I are having a debate similar to this one:
I claim that it's better to take the fresh veggies out of the bags and put them in the crisper with humidity control because:

That's what the crisper with humidity control is for.
If they are in the (plastic) bag, the humidity control is pointless.
It's easier to notice vegetables in their early stage of rotting (it doesn't feel right to throw out an entire bag of rotten cucumbers or zucchinis before we got a chance to enjoy them).
It's more pleasing to the eye. It's more convenient.

She claims that it's better to leave the fresh veggies in their supermarket bags when putting them in the fridge because she could swear she noticed that they rot more slowly when left in their bags.
As you can see from the few links in this question, I tried to conduct my own search on the subject, but all answers seem to be opinions or "experiences", not an authoritative answer based on scientific research or knowledge.
So I am hoping that with the help of biology professionals (or students) I can finally find an authoritative answer to the question: Do vegetables really last longer if they are kept in their (supermarket) plastic bags when put in the crisper?
Update: I found this formal excerpt from the refrigerator's manual:

Low (open) lets moist air out of the crisper for best storage of fruits and vegetables with skins.

Fruit: Wash, let dry and store in refrigerator in plastic bag or    crisper. Do not wash or hull berries until they are ready to
  use.    Sort and keep berries in original container in crisper, or
  store in a    loosely closed paper bag on a refrigerator shelf.
Vegetables with skins: Place in plastic bag or plastic container and store in crisper.

High (closed) keeps moist air in the crisper for best storage of fresh, leafy vegetables.

Leafy vegetables: Wash in cold water, drain and trim or tear off bruised and discolored areas. Place in plastic bag or plastic container and store in crisper.

While this seems a bit more authoritative (because it comes from the manufacturer of the refrigerator), it still leaves quite a few questions open:
If leafy vegetables should be "placed in plastic bag or plastic container and stored in crisper", why set the humidity on "High"? How does humidity get the lettuce inside the plastic bag or plastic container? (is it sealed?)
Assuming that some humidity does get into the bag, why is the bag needed? Why not let humidity flow freely?

Apples and other kinds of fruit use ethene as a hormone which promotes ripening. They give it off themselves and they also utilise it themselves - but it can affect fruit around them once it's in the air. I don't know whether vegetables use the same mechanism but maybe that will lead you to find some things.

@Armatus That's a great tip. I wish I had enough points to vote your comment up. To simplify my question I am trying to stay focused on vegetables only, but the truth is that we use the refrigerator's crisper for both fruits and vegetables. Your answer may hint that if we keep each fruit/vegetable in its own bag, perhaps that will slow down ripening/rotting? If so, by how long? This is truly intriguing.

If you only store one kind of fruit, it wouldn't do much - they wouldn't "pool" their ethene anymore but they would still accumulate their own in their bag. But if you separate different kinds of fruits with bags, it can keep apples from making bananas go bad quickly. I haven't actually read this in a scientific context though, I'm not sure where I got it from :)

You may want to make a scientific experiment with your own fridge. That would be the most authoritative source for your own conditions. Just split the same veggies in two groups (with or without bag) and consume them after few days. Replicate the experiment at least three times. If you find differences, you have the evidence. If you don't find differences, forget the conundrum and make peace with your wife.

If you put ripen fruits together with fruits that use the same hormones for maturation in the same bag, they will all mature quicker than they would if you keep the unripe ones in a separate bag. There are roughly 4-5 classes fruits by their hormones, although new subclasses and mechanisms are still being discovered.

Related on Seasoned Advice: http://cooking.stackexchange.com/questions/23691/how-can-i-let-fruit-ripen-faster/ and http://cooking.stackexchange.com/questions/12014/is-it-scientifically-verified-that-bananas-will-ripen-faster-when-kept-in-a-bowl and http://cooking.stackexchange.com/questions/23237/what-to-do-with-under-ripe-figs and possibly others

One more important thing would be rotting. If one veg or fruit rots, all other vegetables are liable to rot as well

Based on what I've been able to locate on the USDA website:
Refrigeration & Food Safety
It would be better to take the foods out of the bags and put them in the crisper if you're using the crisper solely for vegetables:

Some refrigerators have special features such as adjustable shelves, door bins, crispers, and meat/cheese drawers. These features are designed to make storage of foods more convenient and to provide an optimal storage environment for fruits, vegetables, meats, poultry, and cheese.

And:

Sealed crisper drawers provide an optimal storage environment for fruits and vegetables. Vegetables require higher humidity conditions while fruits require lower humidity conditions. Some crispers are equipped with controls to allow the consumer to customize each drawer’s humidity level.

Therefore, keeping your stuff in the bag would negate the purpose of these specialized compartments. Too bad the USDA doesn't specifically address the issue of bags...


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Is every cell competent?
I would like to know if every cell is competent or if there are any cells that are not competent.

Assuming that you are asking about E.coli cells being made competent for transformation using plasmid DNA, an answer is cached here from this source:

Hanahan, D. & Bloom, F.R. (1996). Mechanisms of DNA transformation. In F.C. Neidhardt (ed.). Escherichia coli and Salmonella : Cellular and Molecular Biology. (pp. 2449-2459). Washington D.C., United States: ASM Press.

The source (and it is perhaps worth emphasising that Hanahan is/was a transformation guru) states that treatment with divalent cations can achieve 10% of cells rendered competent, whereas treatment for electroporation can achieve transfer into 95% of cells.
This information was, of course, published in 1996 so it is conceivable that advances have been made in the case of the former method.


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Why are enzyme-catalysed reactions slower at lower substrate concentration?
Suppose I'm using 200 nmoles of enzyme and 2 mmoles of substrate. The enzyme should be saturated but if I use 50 mmoles of substrate, the reaction will be faster. Why?
I just can't get it! Even at lower concentration of substrate the enzyme is saturated (all enzyme molecules are engaged in the reaction) but still the reaction rate is lower.

Alan Boyd's answer covers the mechanistic aspects quite well, but there is another aspect he didn't quite touch on - what's going on at the molecular level. To understand this, you need to think about the actual conditions of the reaction: unless it's taking place inside a cell, which straight biochemical reactions of the kind you're talking about almost never are, then the enzyme, substrate, and product are all floating around at a certain concentration. The enzymatic reaction is proceeding nicely, and as the substrate binding pocket is freed as product dissociates from the enzyme and diffuses away, allowing another substrate molecule to take its place and the next reaction to occur. This is the situation at your 2 mmol [substrate] level. At 50 mmol, the concentration of substrate is much higher, and so even though the actual catalytic portion of the enzymatic reaction is taking place at essentially the same speed, the rate of substrate diffusing into the active pocket is somewhat higher because the local concentration of substrate is higher, allowing for an apparently slightly faster reaction rate.

I think I get what you are saying, but I don't understand your concept of "fairly low local concentration". Concentration is an intensive property of a system, it is what it is.

@AlanBoyd - I reworded it a bit and took out the somewhat confusing reference to local at the beginning. As I was beginning to write it I was going to try to explain a certain phenomenon of some reactions (very high substrate concentrations can actually lead to a slowdown of the reaction as substrate is produced faster than it can diffuse away, inhibiting the enzyme), then I realized the question wasn't really about that and changed the direction I was going, but not all of the wording. Thanks for catching that!

that's it! I think this is the answer I was looking for. Thanks.

In terms of Michaelis-Menten kinetics, the rate never reaches the maximum rate:
$v = V_{max} \times \frac{S}{K_m + S}$
where $S$ is substrate concentration. Notice that however large $S$ is, the term on the bottom line ($K_m + S$) will be larger than $S$, so $v$ will be less than $V_{max}$.
You can think about this in terms of the binding equilibrium between the enzyme and the substrate:
$E + S \leftrightarrow ES$
Since it is an equilibrium, it can never lie completely over to the right hand side.
This is why $V_{max}$ is always determined by extrapolation. In practice of course, at very high substrate:enzyme concentrations your measurements would have to be very accurate to see the difference: if $S$ is $100 \times K_m$ you are looking at a 1% difference. In your hypothetical example you don't mention what the value of $K_m$ is.

Didn't get the last part, 'In practice of course, at very high substrate:enzyme concentrations your measurements would have to be very accurate to see the difference: if S is 100×Km you are looking at a 1% difference. In your hypothetical example you don't mention what the value of Km is.'

@Tytoalba the absolute value of Km doesn't matter because I am simply replacing S with (100*Km) in the 1st equation. My last sentence is just to say that the OP gives values of S but not Km so we can't judge where we are on the curve.


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Why are mammals unable to produce Essential Fatty Acids?
Why do we have to get them from our diet, and if they aren't taken in our diet we will face disease? Then why we don't have the enzymes which are require for EFA synthesis?

It's not really like your body can decide like 'hey, lets synthesize the enzyme required to catalyze the reaction for the creation of this EFA'. Apparently, we're just fine without them due to ample EFAs in our diet.

Have a look at this topic: http://biology.stackexchange.com/questions/16962/can-animals-make-their-own-unsaturated-fatty-acids

i don't understand will u plzz elaborate it more

I would speculate that since essential fatty acids are so abundant in our diet, there was no selective pressure for the maintenance in our genome of the enzymes that produce them.

@canadianer can you add more details if you can and post your comment as answer

@WYSIWYG I would if I could find any literature about it.

I agree with @canadianer - from an evolutionary standpoint it takes a lot of energy to maintain genes required for enzymatic synthesis of essential nutrients. If there's no selective pressure then the body has no reason to "waste energy and resources" on unnecessary enzymes.

Well, the essential fatty acids that humans fail to produce are not the same ones that other species fail to produce. For example, while cats produce their own Vitamin C and will therefore never develop scurvy, they can't produce their own taurine and will become sick if they don't consume enough of it.
To answer why a species might lose the ability to produce an essential amino acid, you have to consider what that species is eating most of the time. If its diet is rich in the amino acid anyway, individuals who lose the ability to synthesize it either feel no cost or--possibly more likely--even benefit by not wasting resources synthesizing compounds that may be abundant already in the diet and must be excreted if unused.
Turns out that this loss of ability to synthesize your own fatty acids is a particularly common consequence of evolving parasitic lifestyles, which makes sense: if you're just stealing someone else's acids, why bother to produce your own? Even outside of parasites, there's some interesting discussion on why the nine amino acids essential to all animals might have evolved from a genomics paper here, discussing which amino acids you really do have to make on your own and which you can get away with consuming depending on your species' lifestyle and dietary habits.

Are you confusing essential fatty acids with essential amino acids? I'm sure the general principles apply, but still…


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What is the functional significance of the difference in cardiolipin/cholesterol ratio in different membranes?
I have read somewhere that the plasma membrane has little cardiolipin but excess cholesterol whereas the inner mitochondrial membrane is rich in cardiolipin and has little cholesterol.I just wanted to know why there is this difference.

I don't know the answer for sure but the thing with cholesterol is that it makes the membranes rigid. So, it might not be very suitable for mitochondria. Cardiolipin could also be just an evolutionary remnant

According to wikipedia, cardiolipin is found in two places, the inner mitochondrial membrane, and bacterial membranes. Given the endosymbiotic origin of mitochondria, it makes sense that they would retain some remnant of their bacterial ancestry. But more importantly, cardiolipin plays a role in the enzymatic functions of mitchondrial membranes. Cardiolipin forms a bicyclic resonance structure that allows it to trap a proton, which helps oxidative phosphorylation.

Because this structure also responds to pH and divalent cations, it can change it's conformation and aggregation behavior as cellular conditions change.
Cardiolipin also plays a role in holding enzyme complex quaternary structures together. Mitochondrial Complex III requires 1 cardiolipin, Complex IV requires 2 cardiolipin, and Complex V binds 4 cardiolipins.
Cardiolipin also plays a role in apoptosis, where it is oxidized and undergoes conformational changes that cause it to move from inner to outer mitochondrial membranes and generate pores that cytochrome C can escape through and trigger apoptosis.
Cholesterol can be easily oxidized into oxysterols, which are thought to perform a variety of functions, but are not fully understood. If cholesterol levels in the mitochondria were high, I think it would be oxidized and cause trouble.
http://en.wikipedia.org/wiki/Oxysterol


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How was the Huntington's disease gene's location found?
I read in the book "Why we get sick." by Nesse and Williams that:

Steady detective work and fabulous luck have enabled geneticists to
  pinpoint the Huntington's gene on the short arm of chromosome 4.

I want to know what was the "detective" work and the fabulous luck - the whole story of the discovery of the location of the gene.

A Google search for "Huntingtons disease gene discovery" yielded this page at the Nature Education Scitable website. The following citations are provided regarding the molecular basis of HD:

Huntingtin (HTT) was the first disease-associated gene to be
  molecularly mapped to a human chromosome (Gusella et al., 1983)2. Ten
  years later, scientists identified the DNA sequence and determined the
  precise nature of the HD-associated mutation in HTT (MacDonald et al.,
  1993).

Gusella et al. used restriction fragment length polymorphism (RFLP) analysis to locate a RFLP marker linked to Huntington's disease on chromosome 4. From the introduction of their paper:

We have now identified an anonymous DNA fragment from human chromosome
  4 that detects two different RFLPs in a HindIII digest of human
  genomic DNA. This polymorphic DNA marker shows close genetic linkage
  to the Huntington's disease gene in two separate families, although a
  different haplotype of the marker segregates with the Huntington's
  disease gene in each family. We infer that the Huntington's disease
  locus resides on human chromosome 4.

Further details given in the paper might justify the description given in the question. "Fabolous luck" could refer to the discovery or availability of suitable families and pedigrees for the genetic studies. The "steady detective work" would be the genetic mapping and fieldwork required to establish the link. The following quotes describe some of the efforts spent on the project:

The success of any genetic linkage project depends in large part on
  the quality of family material available for study. We initially
  invested considerable effort in identifying a useful family from the
  National Research Roster for Huntington's Disease Patients and
  Families at Indiana University. An American family of reasonable size
  was selected and blood samples were obtained (...). Subsequently, a
  substantially larger Huntington's disease family was located. This
  pedigree stem from a unique community of interrelated Huntington's
  disease gene carriers living along the shores of Lake Maracaibo,
  Venezuela. (...)For the past three years an expedition has spent one
  month annually in Venezuela collecting pedigree information, tissue
  samples, and clinical data. (...) In Venezuela, many family members
  were examined for three consectuvie years. Permanent lymphoblastoid cell lines were
  again established for each individual to act as a permanent source of
  genomic DNA. In both families each individual was examined by at least
  one neurologist experienced and knowledgable about Huntington's
  disease.

The Scitable page also summarizes the approach and results described in the paper. For the RFLP analysis, several DNA probes were tried, of which one, "G8", resulted in a HD-linked pattern:

James F. Gusella and colleagues carried out a study to determine
  whether they could identify a DNA probe that would show an
  HD-associated restriction fragment length polymorphism (RFLP) when
  used in Southern blot analyses of chromosomal DNA digested with the
  restriction enzyme HindIII (palindromic recognition sequence
  5'-AAGCTT-3'). The team identified one probe out of 12 tested, called
  G8, that showed a specific RFLP pattern associated with HD in two
  large families with a history of the disease (Gusella et al., 1983).
  Using the G8 probe, they next identified two HindIII sites (called H1
  and H2) that were palindromic within this chromosomal region. DNA
  fragments at these sites vary in length among different HD lineages.
  Because researchers used two large pedigrees in these experiments,
  they were able to obtain statistical support for their discovery
  (Figure 3).

However, at the time the origin of the G8 probe DNA in the human genome was not known, so human-mouse somatic cell hybrids were made to identify where the G8 probe DNA belonged. This showed that the G8 probe corresponded to chromosome 4, and indicated that the HD gene would be found there:

Researchers found that the G8 DNA probe hybridized only to Southern
  blots using chromosomal DNA from human-mouse somatic cell hybrid lines
  that contained human chromosome 4. Therefore, researchers determined
  that the G8 DNA probe is located on human chromosome 4, and they
  concluded that the HD gene is located on chromosome 4 near the region
  corresponding to the G8 DNA probe (Figure 5; Gusella et al., 1983).

It was fascinating because Huntington himself described what we now call genetics before the field existed. Then to locate the gene scientists used essentially trial and error. They took enzymes that cut different parts of the DNA and looked at which of these were inherited. If it were inherited then there would be cuts made, otherwise not. Then they matched it up to who had the disease. Of course with 46 chromosomes there were thousands and thousands of places to check but they somehow luckily managed to find it on their twelfth try!
The full story can be found here: http://www.dana.org/Cerebrum/Default.aspx?id=39308


text:
Correlating beta-lactamase expression to absorbance

When penicillin-resistant bacteria are grown in liquid culture media,
  β-lactamase is secreted into the medium. The supernatant of such a medium can be assayed for β-lactamase activity. Culture supernatants
  different organisms , which are suspected to be penicillin-resistant,
  were obtained and were assayed for β-lactamase activity. The corresponding absorbance value were measured at a certain wavelength.

Let us assume that supernatant from organism 1's culture had absorbance value X and 2 had absorbance value Y.
My question : If X>Y, does that mean that more β-lactamase was being produced by organism 1 ?

How does this beta-lactamase assay work? If it works in a way that more secreted enzyme metabolizes more substrate resulting in more absorbance, than yes.

@chris It's been treated with an inhibitor of B-lactamase.

The supernatant is treated with a b-lactamase inhibitor? And what happens then? Or does the inhibitor change its color due to the inhibition?

@chris Yes the color becomes yellow. What would happen to the absorbance then ?

Ok, then more b-lactamase means more inhibitor binding and this results in more color development leading to a higher absorption. So higher absorption means more b-lactamase in the supernatant.

Hi @Chris You have answered my question in the comments. Do you want to write an answer ?

I can do that later today.

In the β-lactamase test, an inhibitor of β-lactamase is added to a sample of the culture medium. The inhibitor binds to the enzyme and changes its color, which is in direct correlation to the concentration of the β-lactamase. More β-lactamase means more inhibitor binding and this results in more color development leading to a higher absorption. So higher absorption means more β-lactamase in the supernatant.


text:
Why use DNA polymerase in making cDNA?
RT is capable of synthesizing a complementary dna strand ( as in HIV life cycle.) Then why is
DNA pol used when cDNA (synthesizing the second strand of it ) has to be synthesized from mRNA ( For eg.to construct a cDNA library) ?

where did you read that DNA pol is used ?

@WYSIWYG I read that in Campbell.


text:
How is the effective dose calculated when only part of the body is irradiated?
For calculating the effective radiation dose in Sv, the equivalent dose absorbed by each body part is averaged according to tissue-specific weighting factors, which sum up to 1.
If not the whole body is irradiated, how are these factors used?

Not sure that I understood your question correctly.
The concept of "effective dose" was specially introduced to provide a mechanism for assessing the radiation detriment from partial body irradiations in terms of data derived from whole body irradiations. The effective dose is the mean absorbed dose from a uniform whole-body irradiation that results in the same total radiation detriment as from the nonuniform, partial-body irradiation in question.
What is probably misleading you is the sum of the weighting factors to be 1. This is because we try to liken the partial body irradiation and the whole-body irradiation and the weighting factors represent the relative tissue sensitivity and susceptibility to the radiation. Your radiation should not go over all possible tissues and organs, you just assume the irradiation to be zero at them that cancels their summands so that they can be ignored in the final calculation. In other words, it is absolutely fine (and it is even so "by design") to have only some of the WT*HT factors in your formula.

I don't quite follow. What would x and y be in the following sentence? "A whole-body irradiation of x would be equivalent to irradiation of y of the thumb (weighting factor 0.01)". I suppose x and y could be chosen such that y=100x for some unit (Gy?), and this would mean that those two irradiations would have the same effective dose measured in Sievert? That doesn't completely make sense for me, since Gray already compensates for tissue mass.

@Poshpaws: Sorry, I can't upvote because I'm not registered :( Also, I still don't know what "effective dose" means. hopefully, someone can answer my questions in the comment above!


text:
Do orcas react differently to swimmers in orca-like dresses?
Question on animal behaviour. This video shows the trainers of the orcas in swimming pool with them. Why do they use orca-like dresses? Is it just for the show, or do orcas then treat them more peacefully? :)

there is an "ethology" tag already :)

To close-voter(s): this question can definitely be answered without the use of opinion, so I disagree regarding the VTCs. I vote to keep open.

This is hard to answer and doesn't seem to have been directly studied anywhere. However, my guess is that it's just for the show. Orcas readily eat penguins and Commerson's dolphins, which are both at least as 'dressed like' them as the humans are in this picture.

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


text:
Is the "Great Pacific Garbage Patch" beneficial for marine wildlife?
A study was just released by researchers at Scripps Institute of Oceanography revealing a drastic increase in the amount of plastic adrift in the Pacific Ocean. According to the paper, the amount of plastic in the North Pacific Subtropical Convergence Zone has increased 100-fold over the last 40 years.
But most of the news stories coming out about this discovery are thin on facts about the dangers of plastic. And the research even suggests marine wildlife may be benefiting from the artificial flotsam.
Clearly this increase in trash can't be good. Can it?

There are very few things in the world that aren't beneficial to some lifeform.  Even if you were to, say, spill a mixture of persistent broad-spectrum poisons on an area that killed off 99.9% of all species there, the remaining 0.1% that did survive would benefit from the lack of competition.
The "great garbage patch" is hardly so extreme a phenomenon, but similar effects can be seen there: some species suffer, others benefit.  In that sense, it's no different from any other changing habitat.
From a conservation viewpoint, there are two issues here that one might find worrying:

First, novel, extreme or rapidly changing habitats tend to have lower than average biodiversity, at least initially: the few species that thrive in the new environment tend to proliferate at the expense of others, forming a relatively simple (and often not very stable) food web.  Of course, over evolutionary timescales we'd expect the surviving species to adapt and diversify and the ecosystem to settle into a more stable state, but that tends to take a long time compared to the human timescale on which such novel habitats are created.
Also, the effects of the "garbage patch", or ecological changes in general, are not limited to the directly changed area.  Creating a new habitat in one part of the ocean is one thing; disrupting the ecosystem of the entire ocean is something else, as doing so leaves no unaffected refuge for the species that are harmed.
For example, fish, birds and marine mammals passing even just occasionally through the patch might end up swallowing plastic and accumulating it in their gut; meanwhile, even for less motile organisms, the patch might act as a population sink, depleting their population density in nearby areas.  And if some organisms, such as the sea skaters mentioned in the article you cite, thrive in the patch, the increased population will likely spill into other areas, potentially harming their competitors or prey species.

As for why the news are focusing on the beneficial effects of the garbage to the sea skaters, well, that's what the study that prompted this current batch of news stories was about.  It's also seen as newsworthy precisely because it seems so unexpected: we've all heard stories of plastic flotsam harming wildlife, so finding out that some species are actually benefiting from it has some "man bites dog" style news value.
Also, it's a lot easier and more convincing to observe something that is there than something that isn't: we can directly see these insects laying their eggs on the bits of plastic, giving direct and incontrovertible proof of a causal connection.  Meanwhile, simply observing that some species used to be more common in the area of the patch than it is now is a lot less direct and informative: we might never be sure just how the patch is harming that species, and it always leaves skeptics an opening to claim that the decline might be caused by other factors.  With the sea skates, on the other hand, we're not just observing the effect, but the direct mechanism as well.

References? especially for the effects of habitat on biodiversity?

@David: I'll see if I can dig up some.