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What was the reason for some plant and animals to become giant in course of evolution?
The dinosaurs, mammoths, giant plants etc are known to be bigger than modern animals. I wonder why they had been lived and why they are not living now? I really don't know much but is it something about oxygen balance or something similar?

The wording of your question is somewhat obscure. Do you mean "what was the reason for some plant and animals to become giant in course of evolution?" or probably "What are the advances and drawbacks of being a giant plant or animal organism?"

Sorry for my bad English. I mean "what was the reason for some plant and animals to become giant in course of evolution?"

Your English is not at all bad, I just wasn't sure what you mean and wanted to ask before I correct the title of your question. My native language is Russian, by the way, so don't take my English for "granted"  :-)

You might find the following question helpful, but (replying to the duplicate flag) I don't think that these questions are exact duplicates...

But note that the largest animal ever to have lived (blue whale) is alive right now!

consider the current era is also a time of giants, the largest whales, the largest cephalopods, and the largest trees all all alive right now. Basically you can find something giant in every era.

Thanks for asking an interesting question which made me think.
The short answer is that something evolves if there is an advantage to the genes involved, and, by 'advantage' I mean it produces more copies of the genes in the next generation so more individuals with that characteristic will be present in the population.
As to what particular advantage increased body mass had to any particular species that would depend on the particular species and its environment at the time.  There is almost certainly not a 'one-fits-all' answer.
Most very big land mammals are herbivores and there is an advantage in having a large digestive tract when you eat a lot of plant material with a fairly low nutrient level.  However, when there are also predators around, getting big and slow might be more of a disadvantage than staying small and fast. With evolution there is often a balance of competing forces which are traded of against one another.
Where large mammals have become isolated on islands with no predators, such as a species of now-extinct elephant on the Flores Island, they tend to become smaller so this suggests avoiding predators by simply being too big for them to kill might be an important factor.
And of course with many species we have the effect of sex-selection. If females select for the biggest males, there will be a selection pressure towards greater size.
With plants it could be something else entirely. Trees, for example, have long trunks basically for one of two reasons.
Firstly to put their leaves and seeds out of the reach of herbivores, so we have a kind of arms race like that between giraffes and acacia trees in Africa.
Secondly, when they grow in close clumps like woods and forests, there will be competition for sunlight and soil resources like water. A species which can reach higher and put it's leaves above those of it's neighbours will win the competition and there will also then be pressure on it's neighbours to evolve longer trunks.  Long trunks mean that water must be pumped a long way to the leaves so the tree with the longest trunks will also need bigger root systems.  Again a trade off between making a long trunk and dominating the water supply underground.
Many trees are also believed to have formed symbiotic associations with fungi in their root systems which help them take in the nutrients and water required to 'service' a long trunk and high-up leaf crown so they may be the only types of plants capable of doing this anyway.
One thing you might like to think about is why some whales are very big and some are relatively small (dolphins, porpoises, killer whales). What is the difference in their life-style, food, habitat, and so on, which could drive these evolutionary differences.

Getting big is not necessarily disavantageous when there are carnivours arounds. If you are big enough there needs to be a big number of predators to bother you, especially if you travel in big groups (think about elephants, for instance).

another big advantage is resource and environmental fluctuation , a big animal can survive sudden changes in the environment or resource availability better than small ones, https://pubmed.ncbi.nlm.nih.gov/16701331/

to expand on Rose's answer, certain environmental factors are what people cite with unusual size changes in an animal over time as it diversifies into new species.
Gigantism (and dwarfism) on islands are a particular example.  In this case an animal may arrive on an island and some of the predators or competitors that it is used to will not be there.  Then a single species will spin off many species, each one will fill one of the niches that are unfilled on the island - eating bugs from bark, breaking open nuts.  The lack of large carnivores will allow a nice juicy herbivore to get larger without fear of being eaten.  Similarly the Moa was a bird that became an aggressive carnivore in its island habitat, where it's very rare to see an aggressive land bird when a big cat or other carnivore is already present.  Such large changes in environment can also result in dwarfism - smaller species as smaller animals like squirrels or mice might not be present to consume all the food that are available.  The Hobbits recently discovered in Indonesia are an example of island dwarfism.
That being said, selective pressure can probably make many animals larger or smaller - lots of the dog breeds are smaller than wolves that they descended from.  I think steers are as large as we can make them and are larger than native cattle stock.
As far as the environment that caused dinosaurs to be so large, the higher levels of oxygen on the planet at the time is a common theory for why they were so large.  I also think that at least early on, the selection conditions that favored larger animals were probably put in place as animals evolved without any competitors whatsoever (first animals on land or sea).  If this were to happen again, its not clear whether dinosaurs would have been so large - perhaps we could have had gigantic mammals or descendants of trilobites.

It needs to be recognized that this is an outstanding question in biology, i.e., there is no certain answer.
This review considers the various theoretical and empirical evidence for phenotypic selection on body size:

Blanckenhorn WU (2000) The Evolution of Body Size: What Keeps
Organisms Small? Quarterly Review of Biology 75: 385-407.

Some have hypothesized a connection between body size and the evolution of endothermy:

Clarke A, Portner HO (2010) Temperature, metabolic power and the
evolution of endothermy. Biological Reviews 85: 703-727.

And others have suggested a link to oxygen in the atmosphere:

Harrison JF, Kaiser A, VandenBrooks JM (2010) Atmospheric oxygen
level and the evolution of insect body size. Proceedings of the Royal
Society B: Biological Sciences 277: 1937.

And I'll throw this hypothesis into the ring.  The large dinosaurs only went extinct 65 million years ago.  That's basically yesterday in terms of the geological time scales across which body size may evolve - they (dinosaurs) originally evolved 230 million years ago.  That means we've got at least 165 million years to go before you can see if our current diversity of life on earth can evolve similarly large organisms!

One significant point not considered in previous answers is the reproductive rate and environmental variability.  Larger animals have longer times between generations and generally reproduce less rapidly.  In a less stable environment, more rapid reproduction allows more rapidly adapting population to the availability of resources, providing a larger population so that random events are less likely to eliminate the entire species (genetic variation can be a factor here), and minimizes the absolute amount of resources needed for a stable population.
There are significant benefits to being larger.  In addition to interactions with other animals, a larger animal has lower surface area to mass ratio and so will lose less heat per unit mass (which might have been significant for ice-age mammals?).  A larger animal can also support larger organs (not just digestive tract as mentioned by Rosa Rubicondior, large brains would not be possible in small animals) or substantial-sized specialized features (where utility is not a linear function of size).


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Why is rabies incurable?
I'm still not sure about the mechanics that lead to rabies being incurable. I know that it can be treated before any symptoms show up, but why is it that once symptoms show the person is a dead man walking?

I understand what you are asking, but I think the wording is a bit odd. There is not a mechanism that renders rabies uncurable. We simply have not managed to create a cure yet.

This is because rabies is a viral infection of nervous tissue that propagates through peripheral nerves into the brain and causes brain tissue inflammation (encephalitis).
As long as the virus is in the brain there is no way to get rid of it. The main trade-off here is that everything that would kill the virus will be as (or even more) aggressive against the brain tissue, and impairment of the latter will lead to really heavy deficits in vital functions like breathing and thermoregulation.
The first manifestations of rabies are those due to brain damage. This means, the virus is already there and the brain is already fatally damaged.

Ok, so the virus is already in the brain tissue if treatment isn't started. Thank you.

@Robinabo - Well not exactly. The virus starts out infecting peripheral nerves, and takes advantage of the transport mechanisms to be transported up the PNS toward the CNS until it gets to the brain. You have a very limited window to receive treatment (anti-rabies vaccine). Once a human is symptomatic, odds of survival drop precipitously toward 0% (there are only one or two cases of humans that have survived a symptomatic infection).

It may actually be curable, as shown by success stories involving the Milwaukee protocol in which the brain is effectively shut down to allow for the immune system to eradicate the virus.  In most cases, however, it is fatal once symptomatic.  Note that the Milwaukee protocol boasts an imporessive (sarcastic) survival rate of under 15%

Interesting! But I can't see it being adopted with <15% survival (although this is better than 0% if no treatment is administered)! But work will undoubtedly continue.

Also, even if you survive, you'll likely still have suffered permanent brain damage.

It's a small price to pay, in most cases.

The consensus among doctors and researchers is now that the Milwaukee Protocol not only only useless, it's worse than useless. E.g (one example of many)  "The recommendations made by the Milwaukee protocol warrant serious reconsideration before any future use of this failed protocol." --Critical Appraisal of the Milwaukee Protocol for Rabies: This Failed Approach Should Be Abandoned

I couldn't get that article through the paywall, so I wanted to add this non-academic article which explains some of the problems with the Milwaukee Protocol.

source: Stack Exchange

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Altering the human genome
I recently had a conversation with a rather unusual gentleman who was, let's say, more than a little partial to conspiracy theories. He has this idea that governments are lowering "nanowires" from drones, to inject people with chemicals that modify their genetics in order to reduce their lifespan dramatically, or change their opinions and thoughts.
Clearly this man was a fruitcake, and the complexities of his psychology probably warrant a whole separate debate, but he did get me thinking about the theoretical side of how such a thing might be done.
So, as such, I have a few questions on the matter:

Is it even theoretically possible to alter human genetics using only an injected substance? I'd imagine trying to get a single DNA change to propogate through the entire body without being killed off by the immune system would be near impossible.
Since we are aware of genetic markers that are related to predispositions to certain medical conditions (e.g. heart problems, cancers, high blood pressure, strokes, etc), is it possible to modify human DNA to create these issues in a living person?
Has much research gone into how genetics affects thought and opinion, or the way we perceive and react to situations at an emotional level? If so, is it theoretically possible to alter this at a biological level?

I'm certainly not advocating any of this, and I apologise for the unusual nature of the question, but it's something I certainly find interesting to think about!

It's not adviseable as a resource, but I suggest you look into Ender's Shadow (specificly pages 131-138) that has some information on the possibilities of the human genome. Again, not advisable as a source of knowledge, but the points made in those pages are worth looking into. Sorry if its not useful.

First of all it is important to note that, within certain limits, human DNA is not much different than, say, a mouse DNA: it has the same structure, it is constituted by the same bases etc etc. Therefore it is teorethically possible (leaving aside ethical issues, of course) to selectively modify it as you would do for a mouse. There are, however, some technical issues and obviously many ethical ones.
To answer specifically to your questions

Is it even theoretically possible to alter human genetics using only an injected substance?

Yes it is. Aside from the good example of radioactive substances given by Alexander, another good one (and probably one that is more common) is that of chemical mutagens.
It is important to understand that the mutation caused by these substances are random, or only partially selective.
For instance, certain substances, called intercalating agents can interpose themselves in between the bases of the DNA, interfering and possibly giving rise to mutations during DNA replication.
Other substances such as alkilating agents are a bit more specific, although still not gene- or locus- specific.
For instance ethylnitrosourea (ENU) favours A->T base transversions and AT->GC transitions.

I'd imagine trying to get a single DNA change to propogate through the entire body without being killed off by the immune system would be near impossible.

The immune system would not necessarily kill cells with mutations. Think of what happens during cancer developement.
Also, an extremely important point: mutating a somatic cell (i.e. not a sperm or an egg) can induce a mutant phenotype in the individual but it will not be transmitted to his/her progeny.

Since we are aware of genetic markers that are related to predispositions to certain medical conditions (e.g. heart problems, cancers, high blood pressure, strokes, etc), is it possible to modify human DNA to create these issues in a living person?

As Alexander says, there is much research in this field.
Some attempts of gene therapy have indeed been made, and some have a big potential. We are, however, still far away for gene therapy to become a routine treatment.
Also, remember that:

not all diseases are genetic diseases
not all genetic diseases are monogenic: some derive from a complex interplay of different factors and hence curing them is not as simple as providing the correct version of the mutated gene.

Has much research gone into how genetics affects thought and opinion, or the way we perceive and react to situations at an emotional level? If so, is it theoretically possible to alter this at a biological level?

Yes, but I would say that we are very very far away from a complete understanding of how thought and emotions are coded in our brain. The very difficult point is that one needs to study these events at multiple scales. We can study a big region of the brain and say that it is involved in fear coding, for instance. But then if you want to go deeper and study what happens at the single cell level you need to look at a lot of different cells to see how they interact between each other.
From the other side of the "size scale", it is possible to study biochemical processes in the single neuron, but then again it is difficult to study how these processes are integrated in big networks of cells, especially in vivo.

Thank you very much for the detailed answer. I'll certainly have to read into behavioral genetics!

Concerning the first question, it is very well possible to alter human genetics by injecting a highly radio-active substance that will eventually cause mutations almost all cells. The lifespan will be dramatically reduced, however and the condition is known as "radiation sickness"(link to Wikipedia).
But the person probably means so-called "directed mutations" (link to Wikipedia), when the changes of genetic information is not random, but rather at a certain place and towards a certain function.
Second point, this is the area of extensive research: if we could specifically cure a gene than many diseases that are incurable now (like cystic fibrosis) could be effectively treated.  The complete nanotechnology (link to Wikipedia) is all about it.
As to the third point, this is also a very old discussion about the role of nature (=genetics) and nurture (environment). Answering this question in the scope of other questions I can suggest that (genetic) knocking-out some inhibiting receptor systems in brain can lead to certain malfunctions and deceases, including the lymbic system that is responsible for emotions and perception.

Thanks for the answer. I hadn't considered nanotechnology as a possible injection payload - certainly very interesting stuff! I'll read through those wiki articles for more information.

Small point; if you're thinking about genome-altering nanotech, perhaps you're thinking of one of many viruses.

Is it even theoretically possible to alter human genetics using only
  an injected substance? I'd imagine trying to get a single DNA change
  to propogate through the entire body without being killed off by the
  immune system would be near impossible.

Yes, it is possible to alter human genetics through injectable carrier. You are also correct that it is currently impossible to make a DNA change to the entire body. It is possible to transform a a few percent of cells in a single tissue.

Since we are aware of genetic markers that are related to predispositions to certain medical conditions (e.g. heart problems,

cancers, high blood pressure, strokes, etc), is it possible to modify
  human DNA to create these issues in a living person?
  Yes, in theory. You genetically alter a human embryo... let said embryo grow up to a person. Then harvest that tissue from said living person. Similar to what is done in mice... just on humans. As you can imagine nobody is doing this right now. Breeding human for scientific experiments is very unethical (can slow... who want to wait 9months) and will unlikely to get public funding.

And also no, as in not in the way you are thinking The tech is no there yet.

Has much research gone into how genetics affects thought and
  opinion, or the way we perceive and react to situations at an
  emotional level? If so, is it theoretically possible to alter this at
  a biological level?

Yes there is. https://en.wikipedia.org/wiki/Human_behaviour_genetics
But as you can imagine, genetics affect behavior in broad strokes. Genetics does not affect if you are prefer to buy Airbus stock vs Boeing stock. It does affect board things like how much anxiety you can tolerate. How short a temper you have. How much preference do you have to novel experiences.
And upon this broad stock that genetics gives you, you as a person will write if you like challenging jobs, going places, new places, etc.

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How do I prepare a PDB for submission to the Protein Data Bank?
I have a couple structures that are nearly ready to be deposited in the PDB.  Out of curiosity, I ran them through the ADIT's precheck tool and they failed with one error after another, as I lacked all sorts of additional records (TER, SEQRES, HETNAM, etc.) that my refinement and modelling tools don't seem to care about.
From what I understand/guess, the online submission tool will help fill in all the metadata (REMARKs, etc.), but how do I turn my coordinates into something acceptable?

Question has been reasked at http://www.biostars.org/post/show/42502/how-do-i-prepare-a-pdb-for-submission-to-the-protein-data-bank/

If you don't mind I'll borrow this question to add it to the crystallography.se proposal as an example

These two links go through the specifications required for the PDB format:
Link1: http://deposit.rcsb.org/adit/docs/pdb_atom_format.html
Link1 primarily goes through the specs. required if you say have a NMR file you would therefore require the MODEL statement. It also goes through other statements such as when to use TER and how each ATOM line should look etc...
Link2: http://www.wwpdb.org/documentation/format33/v3.3.html
Link2 goes through the other statements such as HEADER, REMARKS and TITLE


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What actually happens when my leg 'falls asleep'?
Most people have experienced the temporary loss of feeling and tingling in their leg resulting from sitting in an abnormal position for a short while. Usually you get a loss of feeling in your leg while it is being compressed/constricted at some point and then the tingling sensation as the pressure is removed. But what is actually happening? I understand the the blood vessels are probably constricted from the pressure, but how does this lead to loss of feeling and later the strange tingling sensation? Are there any other things that extended compression on the leg does to cause this? What exactly are the requirements to get the sensation of a one's leg or other limb falling tingling in that manner?

Whilst it's not particularly academic or explanatory, this article does give you a basic explanation in layman's terms: http://health.howstuffworks.com/human-body/parts/question552.htm  -  I too would be interested to know the details, though.

This happens to arms, too. It hapens to my arms a lot during a sleep. I have feeling nerves are involved here not blood vessels.

Your circulation is being cut off when this occurs.

related: http://biology.stackexchange.com/q/16032/10198

The feeling you describe is called "paresthesia," and according to the NINDS info page, it happens "when sustained pressure is placed on a nerve."

Yes, a phenomenon also dubbed "saturday night palsy" when you nursed the bottle a little too closely ;-)

Does a choked blood supply play a part?

@atichnyu Blood flow can cause similar tingling sensations but I don't think they're otherwise related.

updated NINDS link

The explanation in the link Polynomial posted is essentially correct.
Whenever there is a reduced or blocked blood supply (ischaemia) to your extremities, the 'five P's' can occur: pulselessness, pain, pallor (colour), paresthesia (numbness) and paralysis (or weakness).(1).
The numbness and weakness happen after the blood flow have been reduced for a particularly prolonged period.
Cells in our body require a blood supply to stay alive (think about a stroke or heart attack for example). So a reduced supply can cause them to function abnormally or after a time (depending on the cell or tissue type) die.
So with a 'sleeping leg', staying in an awkward or particular position where arterial blood supply is blocked or reduced to the leg, the muscle, nerve tissue etc all lack supply hence causing sensory disturbance and weakness.
The possible buildup of metabolites could also contribute to the symptoms (pain).
Hope that helps!

Miller's Anaesthesia - Miller.

The linked explanation talks about squeezed nerves, and not about blocked blood supply. So I'm afraid your answer is actually incorrect: the arterial blood supply isn't blocked!

Check out the 3rd paragraph in that article Biocs - "This pressure can also squeeze arteries, stopping them from carrying nutrients to body cells."

The article states: "The pressure squeezes nerve pathways" and "This pressure can also squeeze arteries". Your answer does not mention nerves at all, whereas the article gives most weight to nerves.

Cheers Biocs. Good point. I haven't found an academic source in any of the textbooks or material I have access to regarding the nerve nerve compression mentioned in the article. I'll check it out and edit it accordingly.

I wouldn't recommend deletion of an answer just because it is not exactly what the OP is looking for. The information might be of use to others.


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Mechanics of going from DNA sequence to metabolic network
My apologies for possibly a naive question. I'm a statistics type and have been asked to assist with analysis of metabolic pathways (and networks). However, I would like to have at least a layman's understanding of how metabolic pathways/networks relate to DNA sequences. Been doing the Google for a few days and, given the results, it's clear I am not formulating the query correctly since nothing seems to be clicking.
Something that helps me understand the mechanics behind going from a string of T,A,G, and C's to a network of substrates,enzymes, and products.
Thanks in advance for your patience.

Welcome to Biology.SE, I fear this question might be too broad to be reasonably answered here. You might want to just start by reading an entry-level molecular genetics textbook. Any chance you can make your question about specific things you have a problem understanding?

Yeah, I was afraid of that. I was looking for a very introductory level bit of material(s) and was hoping that someone had put something together.  I'll understand if you close the question.

Do you mean the connection as it occurs in the cell, or how to model it (like, how to predict a function for a particular gene)?

The long Question is how to predict a function. To try to be more specific, I've tracked down the paper by A. M. Feist, M. J. Herrgård, I. Thiele, J. L. Reed, and B. Ø. Palsson, “Reconstruction of biochemical networks in microorganisms,” Nat Rev Micro, Feb. 2009. I'm trying to dig into Figure 1.

The question is not too broad, just involves a fair bit of work to both do the research and compose a response. I'll do the latter, but in brief.
The strings of the four nucleotides encode genes. Sometimes these genes are broken into protein-coding portions (exons) and sometimes intervening, non-coding regions (introns). Bacteria, for example do not have introns within genes while most human genes do. The nucleotides in the protein-coding portion of the gene do just that - give instructions on how to synthesize the protein by directing which tRNAs the ribosome uses to translate the genetic code into a protein chain.
A useful phrase is protein sequence dictates protein structure and that structure dictates function. So, the proteins do things and many act as enzymes or modulators of enzyme activity. An enzyme catalyzes a biochemical reaction, lowering the activation energy to go from reactant(s) to product(s). One enzyme can be thought of as one unit within a metabolic network. A modulator might activate or deactivate an existing enzyme. A protein kinase is a good example of a modulator.
Next, string some of those enzymes together to build a pathway. A common example is glycolysis. Think of this as a chain where the output or product of enzyme A serves as input to enzyme B, whose product is the input to enzyme C, and so on. These pathways are two-way, but it is exceedingly difficult to travel from the final product all the way up such a pathway to the initial input within the confines of a biological system. Thus, the pathways in practical terms are thought of as one-way.
However, the pathways do not function in isolation. The final product may serve as input to one, two or more other pathways. Your pathway of choice may begin with the output of another process. Furthermore, pathways can branch: Glycolysis can proceed to glyceraldehyde 3-phosphate and pyruvate, or directly after glucose 6-phosphate formation can be shunted to the pentose phosphate pathway to yield reducing power and 5-carbon sugars (to be used in ATP, CoA, FAD, NAD+, DNA and RNA). Now, pathways leading to other pathways and branches and such make a network.
You and your colleagues might want to know if genes within a metabolic network are over- or under-represented in a test compared to control. Or, genes for a given network are not present in one species compared to several others. Or, one could estimate the flux through such a network given a set of measures.
Peruse examples at both KEGG and Reactome, expecially at KEGG where you can view pathways pertinent to your organism(s) of choice.

Many thanks for getting this started. I understand (or least have an intuition about) everything after "... and that structure dictates function"; and I've wandered through the KEGG database.  So maybe the question is better phrased: How is the protein structure determined/predicted from the protein-coding portion?  (I think this is the 'reconstruction' part?)
Thanks again for you patience.  (I should add that I'm not immune to doing my own digging; a few pointers in the right direction would be appreciated.)

In general, assignments of function are based on sequence similarity (tools like BLAST) - comparing protein sequences to those with known or demonstrated function - or identification of functional motifs as in the Pfam, SMART, INTERPRO and others (http://ca.expasy.org/tools/).

Still a few open questions, but I think that gives me enough to start doing more focused background work.  Thanks!


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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.

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'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.

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...


text:
Descendants of dinosaurs
It is commonly accepted that birds are descendants of dinosaurs. It is nice that not all dinosaurs died out.
Are there other animals, descendants of dinosaurs,
 that survived ? (Maybe not till our time, but survived the time when most dinosaurs died).
By the way, what made flying dinosaurs survive and not die like other dinosaurs?

The fact that you do not limit answers to extant decendents makes this very hard to answer.  The taxonomic group "dinosaur" was on the earth for millions of years, so the answer will depend on where you start counting decendents.

Looks like Aves are the only ones that survived to the modern day. https://en.wikipedia.org/wiki/Dinosaur_classification

It is very hard to answer your second question since we still don't know for certain what made most of the dinosaurs/reptiles disappear.

Are you trying to understand if reptiles like lizards are descended from dinosaurs?

No. No other group found in the fossil record after the K-T boundary (the extinction "event") descends from dinosaurs.
It is likely that the extinction event was not itself instantaneous so if you wanted to be extremely picky you could argue that small numbers of individuals survived the K-T boundary but, apart from birds, none of these survivors went on to form long lasting lineages.
Non-avian dinosaurs that survived the extinction event are referred to as "palaeocene dinosaurs", there are some links on Wikipedia that might interest you.
You can see a diagram linking vertebrate groups here, similar diagrams can be found in most evolution texts.

Do you have good standard reference on dinosaur extinction at hand to back this up, e.g. a review paper (I'm not doubting it, just curious to read myself)?


text:
First pass protein structure prediction
I'm working with a protein that doesn't have any homology to other proteins so it will likely require ab initio structure prediction. However, since I don't work for a structure prediction lab and I don't have a stringent requirement to have a high resolution structure, I'm fine with a 6-10 angstrom resolution prediction to help me visualize the protein.
I'm imagining I-TASSER to get an initial idea of the topology. SWISS-MODEL doesn't find any homologs to template against. I'm trying to avoid using Robetta since it will probably take a month. What other low-resolution webservers should I test?
Alternatively, you could just tell me to suck it up and submit it to a month-long prediction.

Have you used hhpred to search for homologues? What was your criteria for defining there was no homologues? You could potentially go down to around 30% sequence identity to model.
I would submit the the query sequence to both I-Tasser and Rosetta and see if both of the servers agree on the topology. I-Tasser will always provide 5 models of your query sequence (even if they are rubbish) ranked by a confidence score.
While you wait for the above servers to finish, I would submit the sequence to a number of secondary structure prediction servers to come to a general consensus for the secondary structure of your protein. Some servers you could use are:

Predict Protein
Phyre2
Raptor X
Jpred
Psi-Pred

If the servers come to a consensus, compare the secondary structure prediction with that of the secondary strucutre of the models, to see if the ab initio modelling concurs with that of the secondary strucutre prediction. This will give you more reason to be confident in your model.
I would then validate your models using:

Prosa - This calculates a Z-score, and plots where it fits with structures with a similar amino acid length, from the PDB.
DOPE Score - This is employed in Modeller and measures the "nativeness" of your model, the lower the score the better. But you will need to install Python and have some knowledge of how to use the command line. I can provide the code to Run Dope with modeller.

Finally, are there any constraints you could introduce such a oligomerisation site or a protein-protein interaction site, to help with the modelling?

Robetta's the best service I've found for a protein I'm working on that doesn't have a solved structure. It's down right now for the CASP10 competition, but I would submit it and wait. The wait time lately has been ~2 months.

CASP10 would certainly explain the wait time. Guess I'll just add it in and download Rosetta@Home to make it go faster (slightly).


text:
Do probiotics survive digestion?
Pretty much this. I've been wondering if any of the yogourt and other "health" foods containing living probiotic cultures survive digestion to populate our intestines? If so, is there peer-reviewed evidence you could point me to?

Related: http://skeptics.stackexchange.com/questions/6180/do-probiotics-have-health-benefits

Closely related, I'm wondering if pills containing bacterial cultures would keep the bacteria alive through the stomach - it seems like the coating would, but has it ever been tested?

@JohnC: there is a big difference if we are speaking of pills. Gastro-resistant capsules are made expecially to resist the acid in the stomach and only dissolve at the high pH of the intestine. I do not know any specific study on coatings of probiotics pills, but I think it is safe to assume that they would use the same coating as many drugs.

Apparently, some do and some don't.
I just tried searching for yogurt lactobacillus survival on Google, and the first hit I got was an article titled "Survival of yogurt-containing organisms and Lactobacillus gasseri (ADH) and their effect on bacterial enzyme activity in the gastrointestinal tract of healthy and hypochlorhydric elderly subjects" by Pedrosa et al. (1995), published in the American Journal of Clinical Nutrition, vol. 61, pp. 353–359.  The abstract reads:

"The effect of the live bacterial yogurt cultures, namely Streptococcus thermophilus and Lactobacillus bulgaricus, and a mucosal adhering strain of Lactobacillus gasseri (ADH) on small intestinal and fecal bacterial characteristics was examined in 10 elderly subjects with atrophic gastritis and 23 elderly normal volunteers (11 received yogurt and 12 received ADH). Neither S thermophilus nor L bulgaricus was recovered from the stomach or small intestine of subjects fed yogurt or pasteurized yogurt. ADH was recovered from gastric or small intestinal aspirates in three of four subjects and in the stools of four of five subjects diagnosed with atrophic gastritis. In 11 of 12 normal subjects, ADH was isolated from stools. There was a significant reduction in fecal bacterial enzyme activity in both normal volunteers and subjects with atrophic gastritis after being fed with viable ADH. Adherent strains of bacteria such as ADH are likely to survive passage through the gastrointestinal tract and thus have greater metabolic effects."

Here's another result from the same search, "Survival and therapeutic potential of probiotic organisms with
reference to Lactobacillus acidophilus and Bifidobacterium spp." (PDF) by Kailasapathy & Chin, Immunology and Cell Biology (2000) 78, 80–88, which says:

"Lactobacillus delbrueckii ssp. bulgaricus and S. thermophilus (yoghurt starter cultures) are not bile resistant and do not survive the passage through the intestinal tract [Gilliland, 1978]. However, L. acidophilus and B. bifidum incorporated into the yoghurt starter culture have the ability to establish themselves among the gut flora [Tamime & Robinson, 1985]."

but also points out that, for survival in the gastrointestinal tract to matter, the bacteria must first survive long enough to get there:

"Strains of bifidobacteria used in some commercial products neither survive gastric transit nor product acidity during storage [Varnam & Sutherland, 1994]. [...] Eight commercial yoghurt samples claiming to contain viable bifidobacteria, sold in London, were enumerated for the presence of this organism. Only five of the eight yoghurts tested contained viable bifidobacteria at > 106 per mL, while the remaining three did not contain any bifidobacteria [Masuda et al., 1993]. Modler and Villa-Garcia [1993] reported that bifidobacteria do not survive in several yoghurt products in North America, due to highly acidic conditions. [...] It is considered misleading to describe probiotic yoghurt as having health promoting properties unless the minimum level of viable cells is present at the expiry date."

This is interesting that some species are viable and others are not. Thank you for the quote.

When I took Microbio we had a entire lecture on this. My professor's view was that they do not survive due to the pH of the stomach.  He told us that there are microbiologist on both sides as to whether they do make it to the intestine (or enough of them to make much difference) or that they do survive and help. I have added a link below to a article by the American Society of Microbiology. Here it is saying that it may be helpful, but that more studies are being conducted.
http://cmr.asm.org/content/16/4/658.short

You may also want to cite the EFSA report on this matter.

@Danielle - I gave Ilmari the accepted answer since it was better researched.

Thanks for the searching and quoting Ilmari. According to some theories, and perhaps there is some research on stool to support these, we can aid our intestines for producing beneficial bacteria by eating PREbiotic foods which supposedly help create a good environment in the intestines for producing healthy bacteria on its own.  Some foods that are supposed to be prebiotic are onions, garlic, and fermented foods such as sauerkraut, kimchi, cortido, miso, kombacha, and sour cream, and also saturated fats such as butter and animal lard. Non-pasteurized full-fat yogurt is not only supposed to be PRObiotic but also PREbiotic as well.  That many priobiotic cultures do not appear to survive digestion perhaps our focus should be more on eating PREbiotic and not so much on consuming PRObiotic cultures.
There are also foods that are could be harmful to the environment in the intestines.  These, according to theories, include refined sugar, soy, processed foods, and seed oils (the process of extracting oil from seeds and dry plant components is highly refined).  For some people, again according to theories, the harmful foods also include gluten and lactose from Holstein Friesian cattle (the most common dairy cow in the USA and I think Europe).


text:
Small worm living in some kind of cocoon, what are these animals?
I am curious what animal is this. It is/lives inside some kind of cocoon, about 1 cm in length. They are attached to walls and to the ceiling, but sometimes they fall off. Inside the structure there is a small worm that can come out at both ends alternatingly. It can then hold on to the ground to move the cocoon around. They are said to feed on paper.

I just found these in Miami,fl where I just moved to and they freaked me out! They are EXACTLY as the original poster has shown us, same wiggly head, striped hair,and locomotion with cocoon...did anyone find an exact name for this little guy?
Liz

Related: Can you Identify this Creature?

This little dude is not a Caddisfly, but a true moth,  Tinea pellionella, a case making clothing moth.  Confusing because they do resemble caddisfly larvae cocoons more so than those of their own family (Tineidae).  Sort blurb Here:

"The brown-headed larva spins a silken case that is open at both ends. The case in the above image is covered with fine sand and debris, and superficially resembles a caddisfly case. The flattened case is about 10-11 mm long (3/8 to 1/2 inch). When crawling, the larva's head, thorax, and three pairs of legs protrude out of the case, and drag it along. According to Internet sources, the larva feeds on a variety of material, including hair, fur, silk, felt, feathers, woolen clothing, upholstered furniture and carpets. It apparently prefers darkness and soiled clothing, and is not fond of synthetic fabrics, such as nylon and polyesters."

This is probably caterpillar of one of the moth species from family Psychidae. They larvae looks like Trichoptera larvae and builds similar cases out of silk and material found in nearby surroundings. In contrast to Trichoptera, Psychidae caterpillars don't live in water, and some of them inhabit stones and walls, where they feed on lichens.

This is a wild stab in the dark, so downvote me as you see fit: Caddis fly larvae (Insect Order Trichoptera). I thought caddis larvae were aquatic though.

You are correct that caddis larvae are aquatic - thus these are not caddis larvae.


text:
Protein Biology Cheat Sheet
I'm looking find a cheat sheet for protein biology to stick on my desk to remind of some of the key principles of protein biology. I seem to remember the specific and complex principles in protein biology but at the expense of the basics.
Can anyone point me to a protein biology cheat sheet or formulate some suggestions to go on one?

EDIT
What I am looking for:

Amount of amino acids in a helix turn
Amino acids typically found in Beta sheets and Helices
The types of protein interactions (i.e. ionic, hydrophobic) and the  amino acids usually involved.
Definition of Globular and fibrous form
Types of post-translational modifications
Any other useful characteristics

Welcome to Biology.SE. This question may be too vague to be reasonably answered here. I would suggest by starting to read an entry-level molecular or cell biology textbook. Perhaps you could more specifically narrow down which subset of protein chemistry you are looking for a cheat sheet on. For example, amino acid properties, classes of protein structures and functions, post-translational modification.

Related: a friend of mine created this periodic table of aminoacids. The original is in Italian, but an English translation is attached at the end of that forum post. Also, svg sources are available and it is under a BY-NC-SA CC license so you can modify/expand it to your liking.

For 95% of the work I do with protein, I find this chart very helpful, showing common post-translational modifications, for each amino acid, with molecular weights, associated codons, pKa values, 1- and 3-letter amino acid codes, chemical structure and chemical properties (polar, non-polar, aromatic, acidic, basic).

I think this is a question about what else should be on a protein cheat sheet.
If you are clever you can format this to have a very high density of information. A good project.
Here's my list - I never made a sheet though.  Also I tend to be interested in protein structure, so there's a bias here.

The frequency of the amino acids in say e coli or the PDB
The average molecular weight of an amino acid (~110 daltons)
avg backbone width of a sheet (5 x 6 Ang) and helix (12 Ang.) DNAMajor groove is also 12 Ang btw.
common non standard amino acids (ornithine, seleneomet, etc).
common post translational modifications (e.g. T/Y phosphorylation)
common non standard secondary structure (3-10 helix etc) or a small ramachandran diagram
pKas of amino acids - remember that charge is defined at pH 7
the genetic code

For alpha/beta propensities, I would use chou-fasman's numbers.  Its annoying because there are some amino acids in both lists.
I will try to think of more and add later...

You can find the answer in any university-level biochemistry textbook.
I would recommend you Lehninger Principles of Biochemistry, if you could find it in your university library.
Skim the list of content, find corresponding chapters and write it down. It won't take you several hours.


text:
Weighing 2 vertical halves of the human body
I had this thought while bathing:
Assume a perfectly developed physical human body and anatomy in terms of size, dimensions and proportions. In theory, if I cut the body vertically into two exact halves from the center of the head downwards, would the two halves weigh the same?
I tend to think that the 2 halves would weigh differently, and if so, I find this quite interesting because it is strange to me that our body would - perhaps unecessarily - evolve in such a manner that requires it to balance itself on a symmetrical skeleton.
Are there any topics that touches on this... phenomenon?

My gut reaction is no as the body isn't symmetrical.  In most individuals the heart will be on the left, just as an obvious example.

I think it would also be quite impressive that given the asymmetry, the 2 halves weighs almost the same for balance.

The two halves likely do weigh approximately the same. Since the density of most tissues that are not filled with air is basically equal, it doesn't matter that, e.g., heart, spleen, and stomach are on the left and liver is (mostly) on the right. In the left/right axis, it evens out.
As for the location of the center of mass of a human: it's located about 10 cm below the navel, at the level of the S2 vertebra approximately midway between dorsal and ventral surfaces of the body (assuming that the person in question is neither pregnant nor obese).

Afterthought: CG of human body is well known, could have inferred that both halves weigh the same. Still interesting that this could happen.

Humans, like all vertebrates, belong in subregnum bilateria, a broad class of animals whose characteristic trait is having a bilaterally symmetric body plan at least in some of their life stages.
The common ancestor of all bilaterians was presumably something like a small marine worm.  For a primitive animal living in water, an obvious advantage of bilateral symmetry is that it makes directed swimming easier.  If the animal were completely asymmetric, it would have to continually exert active control over its heading to be able to swim straight.   On the other hand, an even more symmetrical animal (such as one with 90° rotational symmetry) might have trouble controlling its vertical and lateral heading separately, which could be a problem in aquatic habitats where staying at a certain depth is often useful.
(Indeed, in many ways these reasons are the same as why pretty much all aircraft are bilaterally symmetric: in the absence of active steering, we want them to fly straight and level.  That requires at least rough left–right symmetry and generally also some degree of top–down symmetry, although some breaking of the latter is usually needed both for landing and to account for the effects of gravity on flight dynamics.  We could build completely asymmetric aircraft if we wanted, they just would be harder to fly.)
As for why this ancestral bilateral symmetry has survived so well throughout the course of evolution, that's presumably both because it's so deeply embedded in the genes that control our ontogeny, but also because the basic reasons why such symmetry is useful still remain, even though our size, shape, habitat and locomotion are very different from those of the first "urbilaterian".  Even though we mostly move by walking instead of swimming, it's still useful for us to be able to walk straight without having to pay constant attention to it.  Furthermore, once we've first learned to walk (or crawl) straight, it's useful that we can also learn to run, swim and jump (and ride a bike or drive a car) straight without having to always re-learn the exact amount of control needed to maintain a given heading with each of these modes of locomotion.

Ps. To answer your actual question, I'd guess, like Rory M, that the two halves of a human body probably won't weigh exactly the same, both due to the asymmetrical distribution of the internal organs and also due to uneven muscle development.
However, the difference is quite small compared to the total mass of the human body, so that the center of mass is presumably still quite close to the body's centerline.  As I noted above, any significant deviation from that would cause issues with gait and balance.  Although such issues can certainly be adapted to and overcome with active control — after all, even people who've lost a whole leg manage to get around one way or another — they're presumably still significant enough to be selected against over evolutionary timescales, which is why our body shape remains so nearly symmetrical.

I also had this thought about the bilateral symmetry of the body and the weight distribution. I'm sure if we were to Q & A a kinesiologist about this particular query we would find that the arrangement of the organs left and right and the difference in weight muscular development left to right is off set by our arms which move in and out from our body to maintain balance. When we eat, we gain weight in the form of fat. A full belly makes us front heavy, but by leaning back we maintain the balance. I would wager that the two halves of our body are no more than ten pounds off from each other and the arms used as ballast keep us upright. Hope this helps.


text:
PCR primer in highly repetitive region
Is there any way to design a PCR primer if region of interest is highly repetitive (tens of kilobases only SINE's & LINE's)?

This paper describes some PCR strategies with LINE and SINE PCR identification (Shedlock and Okada. SINE Insertions: powerful tools for molecular systematics. BioEssays (2000) 22:148-160.).
I have no experience with PCR amplification of SINEs or LINEs, however I can think of two strategies right now.
1) You may be able to find a unique 18-20 nt region flanking those regions. If you can, great. If not, perhaps there is a unique site somewhere in the middle of these regions, then you can amplify from the middle outward to both upstream and downstream regions.
2) If there are no unique sites that you can exploit, that would imply a highly regular (ie, repetitive) pattern, but you can take advantage of this too. You can pick primers such that they are on the extremes of the repetitive subunit within these structures. For example, if your sequence looks like this:
A------>BA------>BA------>BA------>BA------>B

Then you can pick primers A and B for PCR use. You will have non-specific primers, and therefore when you amplify the DNA, you will get all possible permutations of DNA that these primers will produce. Specifically, you will get:
A------>B

A------>BA------>B

A------>BA------>BA------>B

A------>BA------>BA------>BA------>B

A------>BA------>BA------>BA------>BA------>B

         A------>BA------>BA------>BA------>B

                  A------>BA------>BA------>B

         A------>BA------>BA------>B

and so forth.
This last approach is obviously inefficient, because your possible products scale exponentially, and will be produced with equal likelihood, minimizing the DNA yield of any particular segment.


text:
How does a tree trunk sprout and grow after being cut?
After I cut trees into logs and remove the branches in winter, they start growing. They sprout out and grow completely normal looking stems and leaves and maintain them all summer. The sprouts mostly appear around the cut branches.  Sometimes they last all winter and grow for another year. How does it find the energy and water necessary to maintain and grow these stems without ground connection and a water source?

I guess it is similar to what happens with onions, garlic, potatoes etc, that will sprout even outside of the ground.

Does this happen to other people? I've cut trees before, and never seen that happen... Exactly what trees are you talking about? From what part of the tree were cut the sprouting logs, top or bottom? Be more specific please!

From my experience this does NOT happen to people.

I encountered this in the context of a type of evergreen referred to in the vernacular as 'subabul'.

This is basically the same that happens after pruning and involves a basic hormonal regulation mechanism in the plants.
What happens is that the cut piece of the wood forms a new meristem which allows the growth of new organs. What’s important is that there is no other growth happening nearby, since that would hormonally inhibit any further growth. This is why such growths happen once you’ve cut the wood, not before (on the healthy stem). This inhibitory effect is known as apical dominance, which has now been disabled.
As to where the energy and water comes from, to some extent it is stored within the branches themselves. That’s why you need to dry them before being able to use them in a fire. However, this growth is pretty limited. Further water is probably collected by condensation of water vapour in the air.

Very interesting!

I would guess that the nutrients and water they need to survive are still in the logs.  This is Common with willow trees, and mulberry trees.  I’ve cut many of these species, and it always happens.  they are two very hardy trees.  Do you know what kind of tree you cut? It appears it is a willow.

Welcome to Biology.SE. While anecdotes are potentially interesting, speculation is not welcome on this site, particularly on subjects for which research is available — consequently your answer is much more likely to receive a favorable response if you [edit] it to include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and thus is inappropriate for this site. ——— Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then edit your answer accordingly.

Also note that, it is generally best to avoid adding additional answers to questions unless you have something new and well-supported to add. As a new user you can find many unanswered questions, which I suggest could be a better use of your time.

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text:
Can all mammals swim?
When I checked it seemed trivial to answer: yes, all mammals can swim. But research on the internet provided different information. I found:

people and primates cannot swim, but can be taught how to swim
giraffes can't swim
someone claimed elephants can't swim, but this video ad shows the reverse
porcupines nor rhinos can't swim
at least some bats can swim, but according to this source there's insufficient data.

Of each hit, I found other hits that claimed the reverse, sometimes with proof. Common sense tells me all mammals can swim, but is this true?

There are over 5,000 species of named, extant mammals. So to show that all can (or cannot) swim would be a monumental task.

@Kevin: fair enough. Yet, to prove that all mammals can swim may require research on each of the species, but to prove the opposite only requires proof that one species really can't swim.

Well, what is your definition of swimming? That needs to be cleared before getting any further.

@CHM: the way I see it, moving through the water without drowning and without walking on the bottom of the river/lake.

possible duplicate of Why can all animals swim in water without learning to swim but humans cannot?

@dustin I am in a dilemma about which one to close. I VTCed the other one.

I'm votin this to be left open as the other one has already been flagged as duplicate and voted for closing on that one.

@WYSIWYG this is is more general where the other is more specific which is why I think this one should be closed as opposed to the other one.

@poka.nandor close votes can be retracted. Click close again and you will see the option. Also, just because one has been voted on doesn't mean we have to leave it if it doesn't make sense.

@dustin - I know clos votes can be retracted, I just try keep my voting consequent. As WYSIWYG, I too have dillema. I'll read both questions for a few more times and revise my decision if needed.

Plenty of primates swim, the Japanese macaque is famous for it.

With respect to the giraffe claim, this article seems relevant:
D. M. Henderson, D. Naish, Predicting the buoyancy, equilibrium and potential swimming ability of giraffes by computational analysis, J Theoretical Biology 265 (2010) 151-159.
It cites several non-"random person on the internet" claims that giraffes cannot swim:

It is generally thought that giraffes cannot swim, but relevant
  observations are few. Shortridge (1934) and Goodwin (1954) state that
  giraffes were poor waders and unable to swim. Crandall (1964)
  discussed a case where a captive giraffe escaped from a carrying
  crate, ran to the end of a jetty, and fell into the water. The animal
  reportedly sank without making any attempt to swim. MacClintock (1973,
  p. 54) stated ‘Giraffes cannot swim. Rivers are barriers they do not
  cross’. Wood (1982, p. 20) noted that ‘Because of its extraordinarily
  anatomical shape the giraffe is one of the very few mammals that
  cannot swim – even in an emergency! Deep rivers are an impassable
  barrier to them, and they will avoid large expanses of water like the
  plague’.

They then go on to show that a model giraffe could plausibly swim, writing: "For practical and ethical reasons we are unable to use live giraffes..."
They conclude:

In summary, the results and speculations of this study show that it is
  not impossible that a giraffe could propel itself in water, but in
  terms of energy efficiency relative to that of the horse, it would
  appear that the costs of aquatic locomotion might be too high. It is
  reasonable to expect that giraffes would be hesitant to enter water
  knowing that they would be at a decided disadvantage compared to being
  on solid ground.

+1 Interesting, nice find! I just found out that hippos can't swim either, because they're too dense and would sink. They "walk" across the bottom.

I feel like the answer by Kin invalidates the part of the quoted claim that says "Rivers are barriers they do not cross", perhaps deep rivers yes but there is video showing them at least attempting to cross a river.  Not that this is evidence of them swimming, because it looks like they're just walking.

I have found videos of porcupines, armadillos, anteaters.. all swimming.
The porcupine seemed to have no trouble at all.
As for apes - quite well it seems. http://newswatch.nationalgeographic.com/2013/08/20/new-surprising-video-shows-apes-swimming/
Rhinos:
www.youtube.com/watch?v=DbqF4AA0Z8U
The water looks deeper than it's head at times, for sure. But whether it is actually swimming or can just/almost reach the bottom is unclear.
Giraffes:  http://www.arkive.org/giraffe/giraffa-camelopardalis/video-ti06.html
It seems to me that if these animals couldn't manage at all in the water, that they wouldn't likely do so, from an evolutionary standpoint.
I'm sure not all manage terribly well, but the videos seem to show that they managed at least.
Pretty cool.  :)

The video of the giraffes shows that they don't swim, as the moment that they consider it too deep, they instantly return to shore. And indeed, the rhino walks across the bottom of the riverbed.


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How To Avoid Macro-Evolution Confusion?
I regularly encounter students who believe humans came from amoebas and when asked why they often say Macro-Evolution has been scientifically proven.
Macro-evolution is defined as evolution at or above the species level, which leads to the problem: Scientific evidence does exist for speciation at the Biological Species Concept (BSC) level, but not for all species concepts and only if a helpful definition is employed. Lions and tigers are considered different species and have been know to reproduce--sometimes with fertile offspring. Therefore, what benefits are there to such a broad category as macro-evolution?
The distinction between lions and tigers is so much smaller than feathered vs. scaled creatures! Surely the current definition of macro-evolution is overly broad and confusing to newcomers. Only the fuzzy edge of the macro-evolution definition has been proven. Proving that 1 inch of a yardstick exists does not prove that the rest does. There is a distinct lack of rigor to the statement that "macro-evolution has been scientifically proven."
Surely the definition of macro-evolution could be chopped in half with the goal of distinguishing between relatively trivial changes (Lion vs. Tiger, but beyond micro-evolution) and relatively non-trivial distinctions (either at and above the genus or the family level). The "trivial" changes could be termed "Middle Evolution" and work something like this:
1.) Middle evolution: evolution at or above the species level, but below the family level.
2.) Macro evolution: evolution at or above the family level.
Substitute the word genus for family in the above definitions if that seems better. I admit that line would be somewhat arbitrary, but would not the term "Middle Evolution" be informative?

Two observations: 1. Species speciate. Genera don't generate. 2. Any taxonomic distinction above the level of species is meaningless.

Macro-evolution is a nonsense terms as far as biologists are concerned.  All it really means is evolution over a long time-period.  All the macro/micro/middle is dishonest manufactuvorsey foisted off by liars and deluded individuals.

Would not a better term be Mesoevolution?

This is really more of a discussion than a question and not a good fit for this site.

The only place that the terms "macro-evolution" or "micro-evolution" are generally used, are in creationist rhetoric. They are not terms used by biologists. This is because there is no need to create distinct categories. In reality there is only "microevolution". Macro-evolution is not a different thing, merely an accumulation of many micro-evolutions.

what benefits are there to such a broad category as macro-evolution?

None. Which is why such a term has been abandoned.

“They are not terms used by biologists” – that’s not true. They do have a biological meaning … which is of course distinct (but sufficiently similar to cause confusion) from what creationists mean, and has been around long before they started using the term. I try not to use the terms myself due to the confusion that has been engineered by creationists but some biologists do use them.

@KonradRudolph I know they have meaning, but that doesn't mean they're used still. Our advancing understanding of evolution has made them irrelevant.

No, they still have meaning and are still used by evolutionary biologists. They have been made irrelevant only insofar as there are other terms that can be used instead, but not because “macroevolution” is an inadequate term (it isn’t, it’s a well-defined, actively studied concept), rather in order to avoid confusion because it’s being misused.

There were 1920 scientific works in Google Scholar with the keyword or title "macroevolution" in 2018. https://scholar.google.com/scholar?q=macroevolution&hl=en&as_sdt=0%2C14&as_ylo=2018&as_yhi=2018


text:
Why are there N's after Sanger sequencing?
After sending a DNA sample for sequencing, the resulting sequence had N's in the beginning and end of the sequence.  I know the N's mean that the computer can't tell what the base pair is, but why is this?

Typically Sanger sequencing will run into a few errors. Sometimes the traces will overlap as below in red and the computer will call N. If you truly wanted to figure out the correct basepair, you can look at the trace.

I'll add on to this answer. A Sanger sequence is really only good for (at best) 800-900 bp. After this time, there is simply too little DNA left to have a reliable signal that you can confidently say is a specific nucleotide. A good habit to get into is always examine your chromatograms and trace, and reject everything after you start getting your first run of N's. I don't usually worry about my first N at the end of the read however because it can be attributed just to error, and the following bases are still confidently called.

This is not really an answer. In effect it just says “it happens” but not why. The wisdom of crowds seems an oxymoron in this context.

As you accurately stated, N bases in sequence data generally means the software is unable to identify the base. N bases may appear at the beginning of the sequence result for a number of reasons. One reason would be purification of the amplified product before electrophoresis. Salts in the sample or a poor purification could leave excess dyes in the sample and appear as "dye blobs." Another reason is the software may have started analysis too soon before accurate sequence begins. Typically, quality sequence data begins 30 bases from the primer. N bases at end of the sequence simply could be the end of sequence data as stated earlier. Other reasons include hairpin loops and poly base regions that cause early termination. The best way to determine the cause is to look at the trace data.


text:
Does a theory exist for the formation of thylakoid structure?
I'm interested in how the structure of the thylakoid forms into its characteristic highly rugose stacks of grana. What causes the thylakoid to invaginate and self-associate, albeit with what appear to be fairly large gaps in between folds?

I think I found a reference.  Most of these papers are behind paywalls - its a pretty obscure topic in biology, though not because it isn't interesting...
For those not familiar with the question, the thylakoid membranes are an organelle structure in the chloroplast, which contains all the photosynthetic machinery in the plant cell.  The chloroplast is though to be a symbiotic cyanobacterium captured to make eukaryotic plants.  Like mitochondria, the chloroplast maintains its own chromosome and some ribosomal machinery.
The stack (grana) and extended (stromal lamallae) structures of the thylakoid no doubt help optimize light/energy capture by distributing the light gathering proteins in an advantageous way.  It was previously believed that the electrostatic charge of the thylakoid membrane helped make the stacks, but this Trends in Plant Science review article (Allen and Forsberg, 2001) discusses how the distribution of photosystem (PS) I and II are more concentrated in the stroma and grana respectively.
They put forth that Light Harvesting complex II (LHC II), which gathers photons for PSII tends to cluster in a trans fashion - forming contacts with LHCII in membranes above it, specifically forming the grana stacks enriched in PSII.


text:
Dimensionless number for blood volume
Comments from the question How is the blood volume of a living organism measured without killing it? by @Nico discussed that the time of blood recirculation scales with the size of the organism. I was curious if there were a series of dimensionless numbers that characterize blood flow, blood volume, and time of blood recirculation?
Such dimensionless numbers exists for stride length and drug penetration.
Edit
I like @Nico's comment so much it's going to part of the question. Any description of the circulatory system doesn't necessarily have to be dimensionless. However, I would imagine that one could develop a characteristic time (lets call it Tau) based on blood flow (L/t), cross-sectional area (L^2), and circulation time (t). From that characteristic time Tau, interesting observations and appropriate comparisons about the various ratios and how they vary amongst species.

Why would it need to be dimensionless? Blood flow is a speed (mm/s), blood volume is a volume (ml) time of blood recirculation is a time (s).

By the way, to further expand my comment, I was considering that the ratio between cardiac output and the volume of the circulatory system would vary between species. I wasn't necessarily implying that it would be higher in smaller animals, although re-reading my comment it looks like I was saying exaclty that!! :)

It is perfectly valid to make normalized comparisons that have dimensions. I think the stride length being dimensionless was coincidental (body length/stride length). An example measurement that normalizes body parameters is the Body Mass Index (BMI) which scales mass:height^2, or the fuel economy of cars express as miles per gallon.

The trouble with miles/gallon is that it has square-cube problems. Motorcycles get far more miles/gallon despite being less aerodynamic, because they are smaller. So if you wanted a measure of how efficient motorcycles as a design independent of their size were, a dimensionless measure would resist scaling problems. It's especially important in biology because nothing is the same size as anything else.

What blood volume can be normalized to is body volume. Since body volumes is slightly difficult to measure you can assume the density to be equal to that of water and calculate volume from body mass (bad approximation when comparing species with different bone and muscle densities).

Blood volume is not a dimensionless number - it's a volume. Historically we used to measure this in patients or volunteers by giving a large carbohydrate molecule like a starch that is not digestible or harmful to the body. Just like every other body fluid compartment volume (i.e. plasma, interstitial fluid, intracellular and extracellular) that we have, blood volume is estimated by intravenously injecting a known concentration of a particular compound. Once that compound equilibrates you take a blood sample and measure the compound's concentration again.
Initial Concentration * Initial Volume = Final Concentration * Final Volume
When you inject a known volume of a known concentration that only fills the "blood" component, and then you measure a final concentration - you can then solve for the "Final Volume" for "blood volume".

Great that you dug up this old question and answered it. +1

This does not really answer the question. The OP wishes to know if blood volume can be non-dimensionalized. My opinion is that it can be normalized to body size (which seems quite reasonable; larger people would perhaps have higher volume of blood) but I haven't seen any literature on that.

I see what you are saying - larger individuals would have larger volumes of blood. Similar to energy expenditure, though, that's a nonlinear relationship that you would need a large, diverse sample size to measure empirically (not sure if that's been done yet). The numbers we use clinically, like blood volume being 7% of total body weight, only holds in a 'normal size' or near normal weight individual around 70-80kg. Even though the numbers don't hold at the extremes of weight they remain "close enough" for clinical estimation when needed.

@VanceAlbaugh So like there is BMI, is there not a blood volume to body weight ratio such that a range of that factor may be considered healthy?

There is no unit that I am aware of for an index of blood volume for research purposes.  Clinically we use the historical values of 7% of total body weight - but realize that is based on 70kg males from 50+ years ago. Obese and morbidly obese individuals have different values because the relationship is nonlinear.  Check out this for one model (but definitely not the only one) that has been 'attempted' to model blood volume.  http://www.ncbi.nlm.nih.gov/pubmed/16756741

Thanks for answering but at @WYSIWYG mentioned, it doesn't really answer.

@bobthejoe that's because volume is not dimensionless

@vancealbaugh, neither is time and length yet we frequently find ways to nondimensionlize those properties.

Like? @bobthejoe

@VanceAlbaugh, Tau, Damkholer, f-number, Knudsen number, Radians, etc. Nondimensionalization is pretty standard in a lot of engineering fields. I would guess that BV is a good factor to normalize against. That way you can say that a "heart contains 0.05 BV" or "there is a flux of 0.01 BV/minute through this artery".

@bobthejoe - cool... we don't use any of those types of numbers clinically when treating patients. On the research side the bioengineers might use numbers like those you mention for modeling purposes. Clinically we have estimates of blood volume that are "close enough" for treatment purposes. 50+ years ago when you wanted to experimentally measure a volume of any fluid within the body, you used the dilution technique that is shown in my answer above.


text:
How do we know that dinosaurs were related to lizards and/or birds?
Do we clearly know what the living closest relative of the dinosaurs are? And connected to the first question, in scientific manner how do we know these relationship between extinct species and living ones?

In general the answer is always the same: you construct a phylogenetic tree. In order to locate different species on this tree in relation to each other, you use various features to compare which species are more similar to each other than others.
The best way of doing this is by comparing their DNA sequence, especially orthologous genes (i.e. genes common to the species compared).
Unfortunately, genetic sequences usually aren’t available for extinct species. You can still compare homologous features though. For instance, the class of mammals are all characterised by the possession of mammary glands. Similarly, all vertebrates have a vertebral column and all aves are feathered, warm-blooded, egg-laying vertebrates.
The collection of many such features from fossile records allows the creation of more or less detailed phylogenies. The Wikipedia explanation mentions several transitional fossil forms which trace the evolution from dinosaurs to modern birds via several intermediates. All of the inferences are based on anatomical resemblance.
This may sound weak evidence but in fact anatomical homology has proved to be sufficiently accurate in constructing other phylogenies, where we have been able to verify the correctness using genome comparison data. So while there is much uncertainty about the precise branching point of birds from dinosaurs (or maybe archosaurs), there is near-certainty that the common ancestor of birds and dinosaurs was, in fact, an archosaur.

Tolweb.org is a website that offers a good summary of our current knowledge of the phylogenetic tree. You (The OP) might want to have a look to it.

Extending Konrad Rudolph's answer, research has been conducted into reconstructing the phylogenetic tree via protein sequence data of the T. rex (one of the latest living dinosaurs):

C. L. Organ et al, Molecular Phylogenetics of Mastodon and Tyrannosaurus rex, Science 320 (2008), p. 499.

They use a variety of standard methods for the phylogenetic analysis.  The real challenge was collecting protein sequence data for the T. rex (which has been extinct for ~65 million years).  They succeeded in collecting and sequencing collagen α1(I) from Mastodon and T. rex, and compared it to the same protein in extant species.
They write:

Despite missing sequence data, the mastodon groups with elephant and the T. rex groups with birds, consistent with predictions based on genetic and morphological data for mastodon and on morphological data for T. rex.

This is an old question, with two highly-upvoted answers (one of which was accepted), but still there is an issue in both answers: both of them fail to explain that birds are not related to dinosaurs. Instead, birds are dinosaurs.
In this cladogram, all organisms from the dinosaurs node up are dinosaurs. Look at the birds in the top right corner.

That's quite well known for anybody familiar with phylogenetic systematics: "Dinosauria" is a monophyletic group that include birds (the purple clade in the image below).

According to University of California (Understanding Evolution):

Another cool thing about phylogenetic classification is that it means that dinosaurs are not entirely extinct. Birds are, in fact, dinosaurs (part of the clade Dinosauria). It's pretty neat to think that you could learn something about T. rex by studying birds!

Thus, technically speaking, the living close relatives to dinosaurs are crocodilians. Birds are not the living close relatives to dinosaurs because birds are dinosaurs.

It is also interesting that some archaeologists now believe that the ancient dinosaurs (that we see in movies) actually had feathers and communicated by chirping (not roaring)...just think of a T. rex now :P

Yes, there are a lot of good materials on the feathers of Tyrannosaurus and other Genera.


text:
What's the aim of genetically modifying of foods/organisms?
On news, articles etc. experts talking about Genetically Modified Foods and Organisms often mentions about their disadvantages like,

their potential to harm human health
allergies may become more intense, new allergy types may develop
possible damages to the environment

So I wonder, what's the aim of genetically modifying of foods/organisms? In other words, what are advantages of that?

GMO foods have a huge potential to make food cheaper to produce and more nutritious.
The most common GMO foods have at least one gene added to them - an enzyme that makes the plant resistant to RoundUp - an herbicide made by the same company (Monsanto).  this makes the farmers able to grow their crops with much less intensive labor to keep the plants healthy. It does cost some money and people wonder whether using so much roundUp is good.  I won't come down on the benefits of this, but you can see how it might be more economical way to grow crops.  roundUp is biodegradable and does break down in about 3 weeks, just FYI.
Other GMO foods can make the crops more resistant to drought, disease or insects. This might enable crops to be grown in areas and or with longer growing seasons - a big advantage for thirsy crops like tomatos or rice. Other GMO project may allow us to make the crops more nutritious.  A famous example of this is golden rice, which has been enhanced to produce pro-vitaminA, which will help malnutrition in millions of children who can die annually because of a lack of vitamins in their diet.
There is also an effort in nutriceuticals, where vaccines and common drugs maybe produced by edible plants for easily processing or even direct distribution of pharmaceuticals.
For people who can afford organic food and free range beef, I think its great that its available, but at for a hungry world, GMO foods can help solve some vital problems.

There's also a similarly modified cotton plant. While not nutritious, this cotton can be cheaper to produce. A GMO cotton could be engineered to require less treatment to make cloth, with lower environmental impact. I don't think the golden rice actually had very much bioactive vitamin A per serving.

On the example of "golden rice" already raised here I took the liberty of looking up some literature about this GMO varietal. This article by Beyer et al. describes the introduction of the beta-carotene biosynthetic pathway into the strain of rice. About a decade later, Tang et al. followed this up with a clinical trial to measure how much beta-carotene a population defined to be clinically low in vitamin A are able to obtain. They found that there is efficient and significant conversion of beta-carotene into vitamin A within this population, providing evidence that the theoretical goal to reduce the vitamin deficiency is actually achievable.
As Larry pointed out, lab modified GMO plants allow a very specific gene or set of genes to be targeted, rather than crossing two plants together and screening the offspring for more desirable than undesirable characteristics. It is important to know that ever since homo sapiens created the primitive form of agriculture called farming, we have been engaged in producing GMO plants. Every time a farmer select seeds form the plants that grew a little heartier in cold weather, or produced fruit just a little more juicy, it was a deliberate act to produce a higher quality crop (for some trait) the next season. The only difference between what we called and still call farming and GMO agricultural practices, is how finely controlled the individual genes are manipulated. The obvious by product from being able to sequence and manipulate a genome is that we can much more rapidly and broadly create and test new varietals at a pace that could have taken decades or generations earlier. This represents a very important opportunity to improve our quality of food and robustness of crops, and is just as "natural" as what has happened for 10,000 or so years.

In terms of crops, plants that are grown for food, one advantage is the targeted modification of a single gene. Classical plant breeding is slow, imprecise and carries many traits of negative benefit. For example, if you cross plant variety A with variety B for the purpose of obtaining one of B's traits (say oil content of the seed), the resulting progeny will have half of the B genome (which half? each offspring a different half of all possible alleles, and many of the hybrids may carry less desirable traits of B like altered germination and maturation times, which would be quite problematic for a farmer). Back-crosses to variety A are then necessary in order to make, in successive generations, offspring that are 75% A, then 87% A, then 93% A and so on. This takes time - to do those back-crosses and to test that the trait of interest remains. Knowing the gene for oil content, or a set of genes, can speed this process by modifying that gene alone while maintaining all the other advantageous traits of variety A.
This is but one example. If I think of others and find the time to describe those, I'll add such information here.

I'd like to add that most of the GMOs that might most dramatically improve human condition (ie via drought/salt resistance, greatly increased yield or nutritional value) are all unfortunately still under development (or not even that), partially because of the general public resistance to GMO in some regions of the world (like Europe; anyone remembers the tomatoes?) and organized campaigns against GMO (not really fact-based; ie Greenpeace & Co).
So yes, GMO can lead to development of crops with increased nutritional value, better resistance to environmental conditions or changes and/or increased yield, but we're not there (yet).
The above should not mean that what we have so far (insect resistant crops, disease-reducing GM insects or the golden rice) is not important, because it is, and it should not mean that the current legal/political context of GMO is fine, because it isn't.

I believe that there is a GMO potato now grown in Europe for paper production.

Imagine an apple which won't get brownish (oxidised) after being cut..

Imagine a tomato which will not get wrinkles and will not perish for a long time
Imagine a chicken and fish which gives more flesh in short incubation time

In endocrinology to get one unit of growth hormone one have to get 1000 pituitaries from cadavers.
Imagine a bacteria which produces growth hormone and other hormones like insulin for therapeutic and research purposes
Imagine a vaccine against flu in cow's milk and hepatitis in Banana. Eat it earn the protection
Imagine a iron rich rice ( fortified ) maize with complete nutrition without any amino-acid lag
Imagine glowing trees by the road side in night which prevent accidents
And there are much more and most advantages are coming out from GMO's.
The only problem is ethics i.e if we change our ecosystem to our wish it may collapse and either we may become extinct or else we may lead other species to it's extinction. But it's only a chance and it's a pointless fear. In the view of science logic is the prime and we can even bring the extinct alive. So we have got the power and we gotta use it and not waste it