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What is the convention for log notation in biology?
I'm reading through some oldish (1980s) papers on length-weight relationships in fish and crustaceans. Many report log-log relationships without specifying whether this is natural log, base 10, etc. In mathematics log is typically assumed to mean natural log, but the results reported in these papers make more sense if you assume "log" means "log base 10".
Is there a convention in biology that I should be aware of?

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I typically use log10 for doing things like dose-response curves, but something like fold-induction of genes may be better expressed by log2. It would probably be safe to assume log10 if they don't specify, but for your own work you should definitely specify which base you're using. I can't recall ever seeing the natural log (base e) in biological papers, but that may just be my fields of interest, which aren't terribly mathematically-heavy.

There is a reason for prevalent usage of log2 and log10 compared to loge in biology and other experimental sciences. Usually while doing measurements we are generally interested in fold changes and we generally talk in the sense of two-fold (or multiples of two) or ten-fold.
Doubling is a common phenomenon at least in case of growth and so a two-fold change would represent an event of doubling. log2 gives you the extent of "doubling". Even in computer systems memory is always in the exponents of two (because of binary); so even there log2 would make sense.
In biology you would generally not see a ten-fold change but in physics it is relatively common. Most values are represented in scientific notation which basically uses an exponent of 10. Also the metric units are in multiples of 10. Here log10 would be more suitable.
loge has a special mathematical importance i.e. it can be denoted as a series. The euler's number has other important properties too. Therefore in most theoretical studies, both in biology and physics, loge is preferred because it makes more mathematical sense.
To sum up, experimentalists prefer log2 or log10 because they are better for representing measurements whereas theoreticians prefer loge because of its mathematical importance.
W.r.t the old paper that reports log-log relationships, the base of the logarithm wouldn't make any difference to the slope. But most likely it must be log10 (I think back then log10 was the default log; log2 would be much more suitable for lengths and weights of organisms compared to log10 because these measures would not vary in multiples of 10).

i'd say that there is no special "mathematical importance" in $log_e=ln$, it is just cleaner. If $x=e^t$, then $ln(x)=t$, without any hanging constants of conversion $log_e\rightarrow log_{10}$. In experiment it makes more sense to measure change in 2 or 10 times, than 2.71

@aandreev well it is easy when you are writing functions to describe a system. you can always convert the scales but when you are writing equations then ln is a direct result of some equations such as $\int \frac{dx}{x}$


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NCBI-geo differences between platforms,series and samples
This is the first time that I use NCBI-GEO and I've faced with 3 different categories inside it. They are platform, sample and series.
NCBI-GEO have GEO-Overview section to explain these terms to ones who are new to this website, however; although I read it a couple of times, I could not understand it totally.GEO-Overview page The terms are a bit complex for the ones who are not familiar with the concepts. Therefore, is there anyone who could explain them with simpler words ?
In my situation, I use NCBI-GEO to get RNA-seq data for the C. Elegans organism. I've downloaded the following SRA file : NCBI-geo C. Elegans sample
As far as I understood, a sample contains an individual organism's information.(In my case its a single C.elegans organism)
Series are somehow the collection of multiple samples I guess. I wonder what is the criteria to put different samples into same series?
And lastly, what is the differences between platforms and series ? I thought that each organism have a single platform, in other words, I thought I could find all the things about lets say C.elegans in its platform but I saw that a single organism type may have a lot of different platforms.
So, I'm seeking to learn these concepts and I think this website is the correct place to ask it. If my question is off topic, sorry about that I was not aware of it.

You should have a look at the overview of GEO more carefully or go through NCBI handbook on GEO

Why is this being closed for homework?

@MarchHo that link answers this completely. I VTDed because reading the help would have been sufficient for the basics. I am not too sure if VTC was appropriate in this case or not. And it is not closed yet; it requires 3 more votes.

The platform at NCBI-GEO means the particular microarray that was used (because originally most of GEO was just microarrays), OR, more recently, it could mean the type of NGS machine that was used.  For example, every microarray manufacturer creates an ADF (array data file) that maps the DNA sequence at every position on the Chip to an accession ID. And this ADF mapping file gets registered at GEO as a GPLxxxxxx. This was presumably to facilitate direct comparisons between different experiments from various labs using identical Chips (e.g. Affymetrix, or Nimblegen).
With the advent of NGS the Platform has to be a name from an approved list of companies and devices: ILLUMINA, HiSeq, etc.
A series is constructed by the data providers and allows them to cluster the results from related samples. So, for example, in the modENCODE consortium, I believe all of the C. elegans RNA-Seq from Bob Waterston's lab/Project are clustered together under one overarching GSExxxxxxx. More details at www.modencode.org and links therein.

so, every GPLxxxxx number corresponds to either a single microarray or type of NGS right ? I mean, lets assume I have a microarray. It has a GPLxxxx number and if I searched it on NCBI-GEO, I can find the experiments in which  same microarray chip was used? "Same microarray" means produced by same factory and have identical features.

@stackunderflow Check the link I mentioned. Everything about GEO is nicely explained there.

@WYSIWYG  thanks for your helps, I think I got the main idea behind these terms. Since I'm completely new in this area, some keywords are really hard for me to understand  at the first time, therefore I really appreciate your helps.

source: Stack Exchange

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What is the difference between polar and charged amino acids?
Chemically polar amino acids have an uneven (AKA  polar) distribution of electrons over their surface.
Charged amino acids have a charged ion in their structure. This is probably where my knowledge is a little shaky!
I guess I am confused at this point. Does this just mean that charged amino acids are really polar amino acids? If that is correct that would explain why I have seen histidine categorised as a charged amino acid, but has no clear ions.

You can see this post on why histidine has a low tendency to form ion compared to other positively charged amino acids.

A related question: http://biology.stackexchange.com/questions/23763/is-there-a-difference-between-polarity-and-hydrophobicity/23777

All amino acids with side chains that are charged at physiological pH are, by definition, also amino acids with polar side chains (e.g., lysine or glutamic acid). The converse is not true; in other words not all amino acids with polar side chains are necessarily amino acids with side chains that are charged at physiological pH (e.g., threonine or asparagine). The pKa of the nitrogen in histidine's imidazole ring is quite close to physiological pH, and in some situations would be charged and in other environments would be uncharged. In either case it would be considered polar (or largely hydrophilic in nature).

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Is blood typing still useful for analysis of ancient tissues?
Modern techniques.
In recent years, DNA sequencing has become extremely cheap. This, compounded by the ability to PCR miniscule samples to viable samples for analysis, means that aDNA can be extracted and analysed from ancient tissue samples that 20 years ago would have been impossible to sequence.
Pre-sequencing techniques.
However biochemical analysis of ancient tissues preceded the human genome project, which revolutionised sequencing technology.
Although blood typing was fiddly, grossly time consuming, and expensive, people were able to define historical lineages.
Question
How does the "old-school" approach of blood-typing compare in terms of cost, accuracy, sample required, and speed against the modern aDNA analysis? Do those sort of experiments still have a place in a modern ancient tissue lab?

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How is cancer associated with host pathogen interaction?
Does cancer by any chance fall under host pathogen interaction domain? What I mean to ask is that, is there pathogen interaction involved in cancer? I went through this article:
http://en.wikipedia.org/wiki/List_of_human_diseases_associated_with_infectious_pathogens
In the cancer category they have used the phrase "can be cause" by this and this pathogen.. Isn't cancer a disease that occurs due to abnormal growth of cells due to genetic change?

No not necessarily. Cancer can also be caused by bacteria and viruses in your body

The regulation of cancerous tumor development is converged upon by multiple pathways and factors. Besides environmental factors, gastrointestinal (GI) tract cancer can be caused by chronic inflammation, which is generally induced by bacteria, viruses, and parasites. The role of these inducers in cancer development, cell differentiation and transformation, cell cycle deregulation, and in the expression of tumor-associated genes cannot be ignored.
Although Helicobacter pylori activates many oncogenic pathways, particularly those in gastric and colorectal cancers, the role of viruses in tumor development is also significant. Viruses possess significant oncogenic potential to interfere with normal cell cycle control and genome stability, stimulating the growth of deregulated cells. An increasing amount of recent data also implies the association of GI cancers with bacterial colonization and viruses.

You can read more here: Aituov, Bauyrzhan, et al. "Pathogen-driven gastrointestinal cancers: Time for a change in treatment paradigm." Infectious agents and cancer 7.1 (2012): 18.

can pathogens initiate cancer? or do they just add to the problems in human body when it is affected by cancer??

@user3237995 Did you read the paper I mentioned...the answer is in there.


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Does breath-holding cause permanent brain damage?
My question is: Does voluntarily holding your breath at atmospheric pressure for a few minutes can cause brain damage? I'm talking about periods of time around 3 minutes.
I've read there are some studies showing brain damage in deep-water divers. However, it seems to me as insufficient evidence for breath-holding in general: it could be that frequent changes in pressure are the cause for damage, for example. Or the fact that the person cannot resurface immediately after feeling the need to breathe, which might cause them to hold their breath for a longer period of time than their body allows.
So are there any studies showing results for the effect on the brain in (healthy) humans holding their breath?

It's going to be very variable, some people struggle for 30 seconds, some manage (e.g. freedivers) 10 minutes at a time. Do you have links for these studies?

there is health.SE if you were searching for more medicine-related stuff. However, i think your question will do fine here. +1

@rg255 For example this: http://www.the-aps.org/mm/hp/Audiences/Public-Press/Archive/09/32.html (I'm not a neuroscientist so I don't know how credible this source is, though). I know people can manage to hold their breath (I used to do it for 3 minutes at a time), I'm wondering whether damage can be made even if the person doesn't feel great discomfort.

I'm pretty sure that your brain will force you to take a breath before it takes damage. This is also the reason why you can't commit suicide by holding your breath (http://en.wikipedia.org/wiki/Breathing#Interaction).

Look at this very related question: http://biology.stackexchange.com/questions/31554/if-oxygen-deficiency-is-bad-even-for-a-short-while-why-do-people-swim/31561#31561

In freediving people usually black out if the dive is too challenging. If you are not immediately brought to the surface there is a high chance of brain damage. I would imagine that for untrained individuals it would be almost impossible to ignore the need to breath until blacking out. Also I think it very unlikely that brain damage occurs while you are conscious.

In order to reply to your question I (*) need to dissect it into 3 parts.
1 - Can you voluntarily hold your breath so long that damage actually occurs?
There is evidence that apnoe-divers damage their brains while diving. In the above, the marker protein S100B, representing brain, damage was elevated. This marker had been found previously to be increased in stroke and other forms of brain damage. Therefore, it appears that brain damage occurs when trained freedivers hold their breath on average 335 s (range 281-403 s). I could not find published data on whether this results in cognitive changes. Another really interesting study I found was also on US Navy divers but with oxygen supply. Their cognition was tested and transient alterations in affect, visual focusing, and physical activity were temporarily seen for 10 days after diving. Pressure changes might have an impact on top of the lack of oxygen.
2 - To summarize a study from a good previous post, researchers measured oxygen saturation in the blood while subject were holding their breath. Oxygen saturation dropped as low as 75% (see original paper).
3 - Additional studies. A blood oxygen level dependent functional-MRI study in adults and children showed similar activated regions while holding their breath. Breath holding in childrens’ brains causes stronger alterations. Their brains seem to be more vulnerable than adult brains. The insular cortex was identified as a specific region in the brain, being responsible for breathing again after holding breath. These findings originate from a positron-emission study which was able to localize air hunger to the insular cortex. The insula is part of the limbic system which regulates essential tasks in humans including temperature, nausea, and pain. Feeling shortness of breath is important for survival and therefore as shown with PET also located in the limbic system.
(*Note that I'm submitting this well researched answer for Tim, an MD, who took the time to write the text but doesn't have the time to sign up or reach the required reputation limit to post. I only filtered out some medical lingo and streamlined the text. The kudos are his.)


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Questions regarding a particular paper
With respect to the following paper:
Automated identification of protein-ligand interaction features using Inductive Logic Programming: a hexose binding case study
I have a few questions:

in page 2, in the table, what does 501 mean in GLC-501(I searched for GLC-501 in PDB,couldnt find anything)
in page 3, in the table, the cavity center column has got two entries, what does that mean? does one entry belong to the protein and another entry to the ligand(left for protein and right for ligand)??

related http://biology.stackexchange.com/questions/31918/how-is-protein-cavity-centre-related-to-binding

501 denotes 501st residue in the corresponding PDB entry — 1BDG. See here
A single protein can have multiple cavities (see here) and the multiple entries denote centres of different cavities.

so why exactly two has been given? Has this paper calculated these centers or are these available somewhere?

and why is a number given to a residue? What does that imply?

@user3237995 I am not an expert in this but I think all ligand residues are numbered in the PDB file. Just a way of listing the number of entities I guess. From this page:  The ligand is assigned a unique residue number within chain to which it is bound. The residue that binds the ligand retains its standard name in both coordinate and SEQRES records.

and why only two numbers listed?

@user3237995 Regarding your first comment. Perhaps they are interested in checking all possible binding sites in the protein. And why 2 sites; perhaps there were not more. Note that some have three as well

@user3237995 They have possibly taken this data from Nassif et al. Their negative dataset consists of 80 PDB examples: 22 binding sites that bind hexose-like ligands (e.g. hexose or fructose derivatives, 6-carbon molecules, and molecules similar in shape to hexoses), 27 other-ligand binding sites and 31 non-binding sites. The non-binding sites are sur- face pockets that look like binding sites but are not known to bind any ligand. The negative dataset is presented in Table 2 (non-hexose binding sites) and Table 3 (non- binding sites)

one more question, is L-glutamate a ligand??

@user3237995 In some cases it is; for example, in glutamate receptors.

how is it different in different cases

@user3237995 L-glutamate can be a part of the polypeptide chain also. In some cases it acts as a ligand.


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RF Cautery DNA damage?
I'm concerned about the safety and mechanism of RF cautery. The frequency of the radio waves used is 4Mhz so normally there should not be any DNA damage BUT the thing you read everywhere is that only UV, X-rays and Gamma rays have enough energy to pop an electron from the orbit. Can't the same energy be reached with radio waves (higher amplitude instead of higher frequency). After all the RF cautery evaporates the cells why wouldn't it damage the DNA of the remaining cells?

Please read the basics of electromagnetic radiation.

This might be better suited to physics, but I've answered it anyway from a biological point of view.

The thing about DNA is that it's very durable, compared to the rest of the cell. It's not too difficult to extract DNA from cooked and processed food, even though the definition of "cooked" is "denatured and broken many of the proteins in the cell". The long DNA strands may be broken into long pieces, but overall the DNA holds up very well to heat. There's no risk of DNA damage to neighboring regions with RF radiation because the primary way RF energy destroys DNA is through heating, and at the temperatures where DNA starts to accumulate damage the cell around it is cooked/destroyed.
The quantum explanation for why ionizing radiation can destroy DNA is that high-frequency radiation is powerful enough to zip through the surrounding tissue and break/damage individual DNA molecules. Individual radio photons can't "gang up" on a DNA strand to do the same thing because of how quantum mechanics works, so you won't be able to break the strand or damage the bases without high-energy ionizing radiation.
Metaphorically speaking it's like trying to get at a peach pit. Ionizing radiation is like a knife, it zips through the flesh and can get at a peach pit without damaging the peach much. RF radiation is like a belt sander. You can definitely get at the peach pit, but you'll cause a lot of collateral damage doing it.
Mutations or DNA damage that might cause cancer can only happen to cells that are alive that receive DNA damage. If the DNA is damaged by heat, the cell around it is dead, and that DNA damage doesn't really matter.
I encourage you to read about ionizing radiation and the photoelectric effect.

Excellent answer. What you say does make sense. But the thing is that some (turned into a lot during the years) studies do show DNA damage in the microwave range. Quote: "The early studies showed that DNA tended to absorb microwave radiation “in the kilocycle range” (Takashima 1963, 1966, Grant 1978, Grandolfo 1983), but no biocidal effects in the range of 1 MHz to 60 MHz were observed." (http://www.rfsafe.com/dna-and-the-microwave-effect/).

I don't trust RFsafe (they're trying to sell me something). There have been no conclusive studies linking RF or microwave radiation to nonthermal damage of DNA, and several studies showing no effect. Either the effect is ridiculously hard to find, or it doesn't exist. Long story short: it doesn't exist.

Excellent response. I especially like the knife vs. belt sander example :)

@AlBundy interesting that the page you linked to doesn't indicate where the study was published. Anybody can run a study and publish on the internet, citations and all, but unless it's peer-reviewed and approved by a group of independent scientists in the field, it's meaningless.

The EMF/RF doesn’t directly damage the cell. It just deranges cellular metabolism.
The free radicals that are produced by this change in metabolism are what causes the damage.
OXIDATIVE STRESS AND DAMAGED DNA
In contrast with Xrays and gamma rays, Microwave radiation does not have sufficient power to directly break covalent bonds in DNA molecules. But microwave RF can produce resonance interactions with ions and with charged macromolecules, and such interactions can significantly alter biochemical functions. A large body of research has shown that microwave RF causes an increased production of free radicals and reactive oxidant species in living tissues, and that this increased oxidant stress damages DNA. This damage can and does occur at power levels well below those levels that could produce damage by thermal mechanisms. Any chronic exposure to conditions that damage DNA can lead to an increased risk of cancer.
Evidence of increased risk of certain types of cancer has been demonstrated in groups with occupational exposure to microwave RF, including radio technicians in private industry, military personnel, commercial airline pilots, and ham radio operators. Elevated levels of cancer have been demonstrated in populations with increased residential exposure to radio transmission towers. And in the last ten years, studies fro Israel, Germany, Austria, and Brazil have documented significant increased in breast cancer and other cancers in individuals living less than 500 meters from cell phone towers, with measured exposure levels much lower than those permitted by current FCC guidelines.
Research has also shown that RF exposure levels well within current guidelines can cause DNA damage and reduced fertility in insects, birds, amphibians and mammals, and can lower sperm counts, sperm motility, and sperm motility in human beings
http://apps.fcc.gov/ecfs/document/view?id=7520940898

Thanks for your detailed answer. Though you provided a reference it would be great if it is an actual peer-reviewed article as they are considered more authentic than reports and monologues.


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Oxygenated hemoglobin in MRI
I have read the following sentence:

Because this oxygenated hemoglobin is unaffected by magnetic fields,
  the response RF signal returned to the fMRI scanner is stronger when
  there is more brain activity and therefore more oxygenated hemoglobin
  in that brain tissue.

Oxygenated hemoglobin does not react to magnetic fields, while deoxygenated hemoglobin does. So in my view, if there is more brain activity and therefore more oxygenated hemoglobin, the signal should be weaker because the oxygenated hemoglobin does not react to the magnetic field? Why is it the other way around?

I think that the type of fMRI you are referring to is blood-oxygenation-level-dependent fMRI or  BOLD fMRI.
The principle behind MRI in general is the detection of proton signals from water molecules. The proton signal is generated by magnetizing the protons in tissue, which causes their spin to change. A subsequent powerful radio wave disrupts this spin and the following relaxation phase of the protons to the original state can be detected by MRI. Water, and hence protons are everywhere in the body, including the brain and the blood.
Deoxygenated hemoglobin (hemoglobin without oxygen) in blood changes the proton signal in its immediate surroundings due to the magnetic properties of deoxyhemoglobin. This is caused by the fact that deoxygenated hemoglobin is paramagnetic and decreases the proton signal. In fact, the paramagnetic influence of deoxyhemoglobin has been regarded as noise in structural MRI scans, before its use in BOLD-fMRI became clear. Oxygenated hemoglobin does not have this property.
Radiopaedia has a nice explanation as to exactly how the BOLD signal is used in BOLD fMRI, and I quote:

When a specific region of the cortex increases its activity in response to a task, the extraction fraction of oxygen from the local capillaries leads to an initial drop in oxygenated haemoglobin [...]. Following a lag of 2-6 seconds, cerebral blood flow (CBF) increases, delivering a surplus of oxygenated haemoglobin, washing away deoxyhemoglobin and with it the attenuating effect on the MRI signal. It is this large rebound in local tissue oxygenation which is imaged, as it is accompanied by an increase in the MRI signal. The difference is used to generate the BOLD fMRI response.

So brain activity increases the BOLD signal by picking up oxygen-changes after an increased blood flow to that specific part of the brain.
So your statement [...] If there is more brain activity and therefore more oxygenated hemoglobin the signal should be less strong because the oxygenated hemoglobin does not react to the magnetic field is incorrect, because oxyhemoglobin attenuates the proton signal.


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Analytical Methods for Estimating Probability of Fixation
The probability of fixation $P$ of an allele is an very important measure and there exists several solutions to estimate this probability. Each method has its own assumptions and it is often hard to remember the methods that exists and what are their assumptions.
For example some use $P=2s$, this obviously cannot be right for be values of s, neither for deleterious mutations, and therefore, this approximation seems to make sens only for big population size. Haldane developed a method to calculate the probability of fixation based on the assumption that the fecundity follows a binomial distribution. Kimura used diffusion equation to approximate the probability to fixation. There might exist other solutions. I don't think I ever seen an equation that allows for varying dominance effect $h$.
Can you make a summary of the methods you know for calculating the probability of fixation? Don't forget to highlight the assumptions. A comparison between the accuracy of the different methods would be great as well.


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Insect (I hope) identification
Look, let's get something straight.  I am not the worlds biggest sissy when it comes to bugs, but I'm not David Attenborough either.
Now that that's out of the way, down to business.  Living in Michigan as I do, I was quite surprised to find what looked like the spawn of Predator and a cicada living in my back yard.   Suffice to say it made me nervous.  In one of the pictures below, I have included a cigarette with about 3 drags smoked off of it for sizing.
Please offer insight into the true nature of this animal.

Looks like a crayfish to me. Did it smell bad? It looks pretty dead, was it in fact dead? Do you live near a river?

Yes.  Almost certainly dead.  Or very very chill.  I don't live near anything remotely resembling a river.  Where the picture was taken is in an electronics box just under a panel in my yard.  Not deep (10 inches tops).  Box is covered.  This is what I saw when I lifted it.

How far away is the local water table? if you live in a wettish area it's probably a prairie crayfish. They're local to the region, apparently really common, and will live anywhere the dirt is wet. Or damp. (also, have you ever seen a live lobster?)

I have seen a live lobster.  Not on land though.  I guess I live in a wettish area (it's on a golf course and there is varying terrain), but there is (too my knowledge) no immediate source of water within a couple 100 yards.  In retrospect, it does look like a crayfish; I just was a bit shocked to find one in what I thought of as a relatively dry area.

Now that I think about it, that may be why it's dead. They're great for the soil, at least.

This is not insect at any rate )))

Looks like a scorpion or such, for me.

In the absence of someone more qualified, I believe this to be a prairie crayfish, based on where it was found (land) and what it is (decapod of some kind that looks like a crayfish). Therefore it is unfortunately not an insect.
It's in the right range and roughly the right terrain.
I welcome entomologically qualified advice!

Yes, definitely a crayfish (Crustacea) and not an insect. Both groups belong to Arthropoda though.

Well; I guess it's okay that it's not an insect since it's a crayfish.  I was more concerned about it being one of Satans minions. : [


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Horizontal gene transfer from humans
It is known that some viruses embed themselves in the human genome. Is there a mechanism by which human genes can be transferred to other animals or plants by means of viruses shuttling them from humans to other organisms?

Yes, Horizontal gene transfer (HGT) can happen in both ways, from prokaryotes to eukaryotes and vice versa. So far less attension is given to from eukaryotes to prokaryotes HGT. It has played very important role in eukaryotic evolution also. Following figure from (Patrick and Palmer 2008) shows some potential cases in eukaryotic phylogeny.

You can find many such examples from above reference. Coming to human part, there are few cases like From Humans to Plasmodium vivax and From human to Neisseria gonorrhoeae , where researchers have shown evidence of HGT from humans to prokaryotes. Unfortunately , there is very little on mechanism by which they transfer. It is matter of speculation right now as these studies are controversial.

Is this only about organelle genes?

No, even nuclear genes undergo HGT as mentioned in reference articles. You can check that paper, it has few examples.


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How does CO₂ concentration affect photosynthesis?
I have heard the theory that with the increase of CO2 in the air, the speed of the photosynthesis would increase, thereby limiting the increase of CO2 levels.
What is currently the rate limiting factor of photosynthetic reactions in plants? Is it really CO2, or rather the limited energy that a plant can absorb from sunlight?

Do you have a source for that theory?

@MattDMo Unfortunately, no. I think I've heard it back in highschool in connection with the Gaia theorem, as an example of a homeostatic process of Earth (along with the theory of increased oxygen increasing the chances of forest fires,thereby regulating itself ) I wonder if these have scientific basis.

@WYSIWYG - how on earth did you get the subscript in the title?

@AliceD It is UTF. You can either get it from the character map or enable compose key in your keyboard and then use [hold compose] : _ → [number] for subscripts and [hold compose]:  ^ → [number] for superscripts. It doesn't work with alphabets (no alphabet subscripts/superscripts in UTF yet)

The rate-limiting step of photosynthesis is the CO2 assimilating enzyme Rubisco (short for ribulose-1,5-bisphosphate carboxylase/oxygenase) (Jensen, 2000). It uses ribulose-1,5-bisphosphate and CO2 as substrates to generate glucose.
Given that Rubisco is the rate limiting step in photosynthesis, an increase in its substrate CO2 would expectedly lead to an increase in photosynthesis. However, the regulation of Rubisco is complex and is influenced not only by CO2, but also by O2 (which competes with CO2 for the active site), Mg2+ and a regulating enzyme called Rubisco activase (Jensen, 2000). Hence, the effects of an increase in atmospheric CO2 may be more complex than simply enhancing photosynthesis by increasing Rubisco activity.
Indeed, a review by Poorter (1993) showed that a doubling of CO2 lead to an average increase in photosynthesis of only 37% across more than 150 plant species. He describes various factors that determine photosynthesis rates other than CO2:

One factor that limited photosynthesis under high CO2 was nitrogen (N). Since Rubisco is an enzyme, it has to be synthesized from amino acids. As Rubisco constitutes about 30% of the total protein in a plant leaf, Rubisco is probably the most abundant protein on earth and a major sink for plant nitrogen (Jensen, 2000). For example, C3 species capable of symbiosis with N2-fixing organisms had higher growth increases compared to other C3 species under high CO2;
Certain plants utilize CO2 better than others. CAM species were the least responsive, followed by C4 plants, while C3 plants increased their photosynthesis rates the most under high CO2. Examples of C3 plants are herbaceous crop plants (Poorter, 1993);
Plants with a large intrinsic growth rate may benefit more from high CO2. These plants are said to have a high sink strength, as they rapidly convert additional photosynthesis products into outgrowth.

References
- Jensen, PNAS (2000); 97(24): 12937–38
- Poorter, Veg (1993);104/105: 77-97

Isn't the available sunlight the primary rate limitation?  After all, a plant with access to abundant CO2, water, and other nutrients still can convert only as much as the incoming solar energy allows.

@jamesqf -The question is on the rate limiting step under high CO2. CO2 fixation is part of the Calvin cycle and hence independent of sunlight. However, you are right that, quite obviously, the Calvin cycle cannot run without sufficient sunlight for the Krebs cycle. The studies cited revealed limiting factors other than sunlight or CO2 when sunlight was abundant. In other words, with enough sunlight and increased CO2, other factors become rate limiting preventing the fixation of more CO2.


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determining meaning of basic biological keywords about C. elegans
First of all I have to say that I have no biology background since I'm a undergraduate computer science student. Nowadays, for my research I need to use some of the databases related with bioinformatics (modENCODE and NCBI-GEO). Currently, I'm searching RNA-Seq data and I have found the following one in modENCODE website which is stored in NCBI-GEO database.RNA-Seq data
In the description part of it, it is written that:

Synchronized L1 worms cultured at 25degC for about 91 hrs to a point
  at which ~100% worms are resistant to 1% SDS treatment. Illumina
  sequencing of C. elegans dauer daf-2(el370) sample 2-1 DauerDAF2-2-1
  polyA+ RNAseq random fragment library This sample is available through
  the modENCODE DCC (www.modencode.org) as: DauerDAF2-2-1 Local library
  name: DauerDAF2-2-1 Quality values are ASCII encoded Phred + 33.

Regarding with this paragraph, I want to ask that, what is C. elegans dauer daf-2(el370) . I've searched on the internet and I have found that dauer is kind of development stage of C. elegans. However, I could not find any information about the daf-2(el370) part (Actually all I found was that daf-2 is name of a gene of C. elegans). Actually, my primarily concern is whether this RNA-Seq data contains the C. elegans' whole transcriptome or it contains only mRNAs related with daf-2 gene.

I might be wrong here, but daft-2(el370) looks an awful lot like a nomenclature of a transgenic worm. And RNA Seq doesn't do it on a gene by gene basis if I remember my basics. It does it on the whole transcriptome.

@RoverEye Although I have limited information, I agree that RNA-Seq does it on the whole transcriptome, I just wanted to be approved. Thanks for the information.

I think it is daf-2 mutant which prolongs dauer stage. Did you read the corresponding paper??

@WYSIWYG corresponding paper is not available to publicly access therefore I could not read it.

@stackunderflow Here you go: http://genome.cshlp.org/content/19/4/657.long

Have you discovered wormbase yet? It will become your new best friend. In worms gene names reflect the loss-of-function (lf) phenotype. Daf means "abnormal DAuer Formation," so daf-2 was the second daf gene identified (ref). The mutations are called alleles and each worm lab has their own allele designation. e was for England and in that lab's strain list the daf-2 allele was the 1,370th on their list. So daf-2(e1370) designation means that the strain carries a lf mutation in the daf-2 gene, and the specific allele is one that was isolated in Cambridge, UK. I believe that allele is temperature-sensitive (ts) dauer-constitutive.
So at 25⁰C 100% of the animals were dauers. That is when they harvested RNA. It is the entire transcriptome. It sounds like you may be familiar with modENCODE Data Warehouse. You can still ask questions about modENCODE datasets at help@modencode.org. While the modENCODE Data Coordination Center was mothballed at the end of the NIH funding period, there are a few people who still field queries like yours, to the Helpdesk. Also, moving forward the new ENCODE DCC has taken over curation of archival modENCODE metadata.


text:
Is it safe to look indirectly at the Sun?
I.e., is exposure of sunlight onto the peripheral vision less damaging than exposure onto the fovea?

Behar-Cohen et al. notes the periphery of the cornea has a focusing effect:

UVR incident from the periphery is refracted into the eye, and due to the focusing effect of the cornea, UV radiation is on average 22-fold stronger at the nasal limbus, which is the typical site for pterygium and pinguecula. Moreover, UV radiation is on average eight times stronger at the nasal lens cortex, the typical site for cortical cataract.

Authors note this in further papers as peripheral light focusing. Essentially, the light is refracted from the periphery of the cornea into the anterior segment of the eye. By this notion, I'd say indirectly looking at the sun is no less damaging than directly looking at it (given there are no other restrictions, such as special lenses, etc.).

Interesting that they only say, 'never look directly at the Sun,' then


text:
Wearing sunglasses during a solar eclipse
Note: I had asked this on Physics, but it is off-topic there due to being about safety.
On the BBC's guide to eclipse-watching, Dr Lucie Green says:

Watching an eclipse with normal sunglasses provides virtually no protection. In fact, they trick your eyes to let in more light, so they can cause even more damage.

This doesn't seem right, because proper sunglasses should block UV to a safer level. Surely wearing proper sunglasses at any time is safer than not? Whilst I can understand staring at the sun with sunglasses on still allows too much UV in, why couldn't someone just glance at the eclipse from time to time?

Your eyes can dilate behind sunglasses, especially when the main source of light (the sun) is blocked, and ambient light decreases. Regular sunglasses offer some protection against certain UV wavelengths, but not enough to protect your eyes when looking directly at the sun (or, during an eclipse, the corona). Most sunglasses are mainly designed to, first and foremost, look good. After that, there is some protection against UVA (400-315 nm) and UVB (280-315 nm) light. Some sunglasses also offer "UV400" protection, which is short-wavelength blue light longer than 400 nm. Polarized sunglasses do not protect against UV at all, only reflected light (such as shining off the water or from an automobile's body or glass) and glare. Different sunglasses tints (or colors) also do not protect against UV, but they can affect color perception.

Surely wearing proper sunglasses at any time is safer than not?

That is true, it is safer, the question is to what degree? Sunglasses offer some protection from indirect UV and visible light that has been scattered by the atmosphere and reflected off of things around us. However, the number and energy of photons (the "particles" of light) reaching your eyes when looking directly at the sun is dramatically greater, and so much more dangerous. Eyes can be damaged quite quickly by high-energy light of many wavelengths, including UV and visible, with the magnitude of the damage correlating to the energy of the light. Damage is also cumulative, accruing over a lifetime. Even small peeks directly at the sun will contribute to your overall lifetime risk of eye damage, and may cause permanent, irreversible harm very quickly.
There are a number of much safer alternatives for watching solar eclipses, including pinhole projectors, welding goggles rated higher than 14, various solar filters for cameras, telescopes, and binoculars, and fully exposed and developed black-and-white film (good luck finding that nowadays), among others.
Above all, make sure you're safe, and if you have any doubts consult with an expert, such as a science/natural history museum or local university's astronomy department.

So, if this answer http://biology.stackexchange.com/questions/34286/is-it-safe-to-look-indirectly-at-the-sun is correct, then we should avoid looking in the general direction of the sun at all times?

@BrianFunt yes, that is correct.


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Were we able to create vitamin B12 in past?
All herbivores produce vitamin B12 de novo. Gorillas, for example, are "vegans" so I suppose some human ancestor was also herbivore.
Have we ever been B12 self-producers? If so, why have we lost that ability and do we have to obtain B12 from our diet? Have we just gotten "used to" being omnivores (i.e., we don't need self-production anymore)?

Can you provide a source for your claim that "all herbivores produce vitamin B12 by themselves"? If that was true, humans would be able to as well, since we consume plenty of vegetables, and some of us are on the vegetarian-vegan spectrum.

http://en.wikipedia.org/wiki/Vitamin_B12#Foods If cow eats a fly, the species doesn't get carnivore, doesn't?

from the very first sentence of the section you link to: "Ultimately, animals must obtain vitamin B12 directly or indirectly from bacteria...". Therefore, herbivores don't produce B12 themselves - it comes from bacteria in their gut. I don't understand what your statement about cows and flies means...

It means that "If that was true, humans would be able to as well, since we consume plenty of vegetables, and some of us are on the vegetarian-vegan spectrum" doesn't make any sence. Regarding the difference between self-producing and permanent symbiosis with  bacteria in the digestive system you're definitely right, but I don't think it's so significant difference (and if so it has to have some evolutionary explanation)- there is just some mechanism producing B12.

Bacteria (and archaea) produce B12, not mammals. Full stop. It is absorbed into the host's body, and passed along when those hosts are consumed by other animals, including humans. The difference between self-production and symbiosis is the point. You claim that herbivores produce B12 by themselves, and that is simply not true, any more than saying humans produce iron because it is found in our hemoglobin is true. Animals have never been B12 producers, because we lack the necessary biochemical pathways.

Do you mean Vitamin C instead? The statement is true for Vitamin C.

@MattDMo Ok, but anyway bacteria in animals produce B12, but in humans not. There is no evolutionary process behind it?

Because it would be quite funny if we developed to get B12 only from diary sources and also were able to eat only cooked meat. (you know we would be stuck somewhere between carnivores and herbivores). So no, I didn't mean vitamin C.

There are bacteria in the human gut who produce cobalamins, including vitamin B12. http://www.ncbi.nlm.nih.gov/pubmed/7354869

@skymninge Wow, thank you. I was really confused of this from many sources: https://www.google.cz/webhp?sourceid=chrome-instant&ion=1&espv=2&ie=UTF-8#q=vitamin%20b12%20only%20in%20animal%20products

@skymninge So why humans don't create it enough that vegetarians have to take supplements?

It is still the bacteria creating it. I am not an expert in cobalamin synthesis pathways of bacteria, but I guess they need something which is more prevalent in non-vegetarian food to produce it. After all, the bacteria in you gut mainly eat what you eat.

@skymninge Wait... so where does the herbivores get it from? Or have they got just more bacteria-producers?

Remember that a herbivore still eats a very different diet compared to a vegetarian. (Raw, high in fiber,...) And they do also have different microbiota, yes. But again, as I am not an expert in the cobalamin synthesis, I cannot explain you the mechanism and thus also not decide how it would be different in a herbivore.


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Are flowers / flowering plants vital to all life on Earth?
Not a biology student so forgive me if this is a very basic question. Are flowering plants (angiosperms) vital to all (or most) life on Earth?
In other words, if flowering plants disappeared, would all (or most) life on this planet be gone as a result?
To give a bit more context, I'm arguing with a friend who claims (from a biblical perspective) that without flowering plants life couldn't exist.

I'm curious, what is this biblical argument that life can't exist without flowers? (if you know)

Angiosperms -- that is, flowering plants -- only evolved relatively recently on an evolutionary timescale, about 125 millions years ago. So for most of the history of life on earth there have been no flowering plants. Thus it seems highly likely that if angiosperms were to suddenly disappear, life on earth would continue. There might be a massive disruption of current terrestrial communities, but it's hard to imagine this resulting in total global extinction. In particular it seems unlikely that ocean communities would be undermined by the loss of flowering plants.

To put that in context, the earliest life dates from at least 3 billion years ago (from stromatolite evidence). Of course, some Christians may dispute that the earth was around even 125 million years ago, so this argument probably doesn't hold in the face of such claims.


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Why do cows (and other hooved animals) need a hierarchy?
Clearly numerous animals have a hierarchy - hereditary one.  For example, I understand zebras have a pecking order, and must map this hierarchy from highest to first in line and lowest to last in line when traveling, and they can be brutalized for breaking this hierarchy.  (Interestingly, they allow looser rules for their young.)  (Reference.)
Cows apparently spend inordinate amounts of time with certain other animals, and avoid others still. (Reference.)
My question is: why do animals need the hierarchies and alliances?  Because human adults tend to make friends with people based on the kind of people they are.
I would imagine that they may have signals that indicate competing survival strategies (for example, a man with thick, tattoo covered arms vs a man in a tie) and that these likenesses try to propagate at the expense of others by forming alliances using organisms that possess these attributes (very vaguely akin to "the selfish gene.")
Or does it have something to do with advertised fitness?  I just have to wonder how grazing animals manage to compete over food.  Does it control access to reproduction?

Practically all social groups have hierarchies. Why shouldn't cows?

Why is this closed? The question is super clear and well bound.

@bobthejoe Why is this closed? I explained my reasons in a "comment-answer" below. I still don't think it is clear. But if you understand the question, you can maybe address my misunderstanding below to help others. Or you could eventually directly try to answer the question.

I think this is too broad an unclear. There are many types of herds and social groups in different species, some loose, relatively  unstructured groups used e.g. during migration and others based on territorial males, with intermediate stages in between these extremes. Some might also be based on relatedness between individuals in the group (so aspects of inclusive fitness might apply). I therefore think this currently is too broad to answer in a Q/A format, and it is also unclear exactly why you are asking and what species you are interested in.

@fileunderwater, I frankly disagree. Meaning that a question covers a large amount of space should not rule out its answer-ability. If the question contained multiple questions, then I would agree. However, this is directly asking for the social hierarchies of herd animals which I think is a well bound question.

Could not fit in a comment...
There are several issues with your question.

The correct question is not why such species need something but rather why it occurs in this species. In other words, why did a hierarchy evolved in a given species?
It is unclear to me why your are interest in cows (or other grazing animals) rather than any other species that has some kind of hierarchy and therefore your question is a bit unclear.
There are several questions in your post. A post should always be limited to one question.
I personally have never heard of the concept of "advertised fitness". How do you define it?
I am not sure how much you are interested in the evolution of social traits and especially about reputation and how much you are interested in Machiavellian intelligence. In any case, you may probably want to read about the evolution of social traits (kin selection, it may take you some time) and about the social selection pressures for the evolution of cognition, such as Machiavelian intelligence.

For all those reasons I vote to close. But I hoped that those comments can help you to clarify your post and to seek for more information.


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Are fish roe unicellular?
Are roe (fish eggs, caviar, etc.) single cells?
I have tried looking this up on google (sadly, to no avail), and I am guessing they might be multicellular (like bird eggs) or consist of one cell plus corona cells, or indeed unicellular.

I was under the impression that bird eggs (unfertilized or immediately after fertilization) were unicellular.

I always assumed, that the yolk sack consisted of lots of other cells which are responsible for repositing all the nutrients. Otherwise all of that would just have to be secreted by cells outside of the egg somehow? But now that I actually looked it up, I was unable to find any reliable info on that either :-/

Be careful not to confuse "egg" (the macroscopic structure) with "ovum" (the haploid cell). The vast majority of a bird's egg--even the yolk--is external to the ovum. (The wikipedia entry on yolk gets this wrong, by the way, based on a citation to a 65 year old embryology text).

@Corvus Do you have an actual citation? A similar question on Reddit had the opposite answer, backed by a link to a dev bio textbook. I would not personally upvote the Quora answer were it posted here.

@TheChymera Related question from here at BioSE on egg anatomy: Why are hard boiled eggs so homogeneous?

@Corvus Are you sure? From my understanding, yolk granules are stored in the oocyte cytoplasm, and is therefore part of the actual egg. See also the answer to the question I linked above.

@fileunderwater My comment was based on what we were told in an embryology lecture I had as an undergraduate many decades ago, so I acknowledge that I could easily be wrong. My impression was that the yolk was external to the ovum in the germinal disc.

Yes; the first division starts at around 45min post fertilization in zebrafish. This picture is stuck in every zebrafish lab.

If the fish eggs are unfertilised, then they are single celled (but in the haploid state - a state with half of a full set of DNA for an organism). However, if it is fertilised it will only remain in the single celled stage for approximately 45 minutes (depending on species (in this case I'm using the zebra fish). After that 45 minute period the cell begins to divide.
What actually makes caviar so expensive is that (according to most websites I've found) it actually is an unfertilised egg collected from a Sturgeon. There seem to be a few different ways that caviar is extracted. Extracting the ovaries after stunning the fish (which is explained on Science: How Stuff Works - and gives more information on caviar), more or less giving the fish a Caesarian section, and the final way that I noticed was called "stripping" which is a non-sergical way using an ultrasound.
The News Article on the ultrasound procedure of collecting the roe suggested that it wasn't yielding good results.
So, caviar is actually a single haploid cell.

Do you have a source for your claim? Also, did you mean "Caesarian section"?


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Neuston vs pleuston
I was recently reading about the wonderful chondrophores, and came across the terms "neuston" and "pleuston".  According to Wikipedia, "neuston" are "the organisms that float on the top of water ... or live right under the surface", while "pleuston" are "the organisms that live in the thin surface layer existing at the air-water interface of a body of water".
How are these terms used in the scientific literature?  Are pleuston considered a subset of neuston?  Some examples of organisms in one category but not the other would be helpful.

I think, these terms represent special phase where there is a confrontation of fresh water with air and marine water with air, respectively.


text:
What is this flying insect?
This insect was captured in Australia near Canberra. It has a very hard exoskeleton and is over an inch long. It seems to have 6 wings - 2 large pairs and one very small pair. I did not see a stinger - however I have no idea.

I believe this is the Hairy Flower Wasp, Scolia soror. I don't know what you mean when you refer to six wings, however. Like all other wasps, this species has four wings.

he might be referring to the beetle-like carapace as another set of wings.


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Inoculation vs. vaccination
Is there any actual difference between inoculation and vaccination or are these terms interchangeable?
In case the difference exists, would it be correct to say that inoculation is purposefully infecting a person with a pathogen in a controlled way, even when the person is already infected, to induce immunity while vaccination is administering dead or weakened pathogens to a healthy person as a preventive measure to check future infections?
Also, would it be correct to say that vaccination is an advanced form of inoculation?

Both are forms of immunisation.
Inoculation is exactly that. A live organism is introduced in a controlled way, so as to minimise the risk of infection, and is essentially the same process followed by many people in history.  It is inherently risky.
Vaccination is introducing a weakened version of the pathogen, so that the immune response is triggered and the body is prepared to fight the actual pathogen if necessary. This was pioneered by Edward Jenner, wherein he noticed that cowpox (related to smallpox) immunised the milkmaids against smallpox.

Cowpox (Vaccinia) is not "weakened smallpox" (Variola). They are entirely separate, but related, viruses.

@MattDMo True. It slipped my mind. Corrected the post.

Interestingly, the word vaccination is derived from vacca,  the Latin word for cow.

I'd maybe clarify. A vaccination isn't necessarily the whole pathogen, like the tetanus vaccine is the injection of a tetanus toxoid prepared from the toxin, so you build antibodies toward that (inactive) structure. Likewise, Gardasil is simply inactive viral proteins from HPV. Flu vaccine, however, is indeed attenuated flu strains. I would argue the fundamental difference is inoculation used live organisms where this isnt necessarily true of a vaccine in the modern sense.

@RoverEye That helped. However, I am still not sure if it would be correct to say that vaccination is an advanced form of inoculation.

In a general sense and as per the current scientific parlance, inoculation is used to mean introduction of a microbe to a system. This can refer to immunization procedures as well as for addition of a microbe to a culture medium in microbiological procedures.
Vaccination specifically refers to an immunization procedure which may involve attenuated pathogens, inactivated toxins (tetanus toxoid) or even specific proteins which are expressed in a lab microbe using recombinant DNA technology (as in case of hepatitis-B vaccine).
Etymology of both the terms, however, pertains to smallpox immunization. "Inoculation" is derived from Latin inoculatus, past participle of inoculare "graft in, implant a bud or eye of one plant into another [1]. In this procedure, the immunization was done by infecting an individual with a smallpox pustule from a patient (in a way grafting the pox).
"Vaccination" comes from the latin word vacca which means cow. This refers to the vaccine that Edward Jenner derived from cowpox.

This is much better answer alhough seems to be less liked. When we transfer microbes to a petri dish, it is called innoculation, although it has nothing to do with immunuty.

If you got your flu shots you could say that you got your vaccination, your immunization or your inoculation
and you would be correct with all three words.  However the words do have different yet overlapping meanings.
Vaccination is the act of administering a vaccine. Although the word "vaccine" started with Jenner's cow pox it was expanded by Pasteur to mean all inoculations intended to perform immunity. The vaccine is a pathogen or toxin rendered survivable either by altering it or,  most commonly, by using minimal amounts.
Immunization is any part of the process of becoming immune, but particularly the part taking place within your body as a response to a vaccine. You could gain immunity without a vaccine, and you could get a vaccination without gaining immunity.
Inoculation is a wider term for any transfer of tiny amounts of a material to a living organism, but the word has expanded beyond biology and is used in varied ways. An inoculation does not need to be for the purpose of immunization although immunizing is the most common usage. Intentionally infecting a lab mouse with a disease is inoculation but not intended to immunize. The original use of the word was to graft seeds (also called "eyes" thus the "ocula" etymology) which has nothing to do with immunity.
In some medical circles, inoculation is skin administered,  while vaccine is oral or both oral and skin, but there is no such concise definition by universal agreement.

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


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How does loss of the electrochemical gradient result in heat production?
As far as I understand, uncoupling of the flow of protons and ATP-synthase  provides a bypass for protons between the outer and the inner membrane of mitochondria so that the protons don't have to go through the ATP-synthase on their way to the matrix. I see how it results in loss of electrochemical gradient. But why is heat produced?

The same reason as what happens when you short-circuit a battery :) Same principle, same effect.

ALiceD's comment is perfectly true. (Though in real cases, the short circuiting is seldom absolute as there is usually some finite resistance in the short circuiting wire.)
You can understand this in two ways.
Intuitively, the uncoupling provides a channel for the hydrogen ions to move across the membrane in the direction of their electrochemical gradient without having to do any work. Therefore, the energy it gains by traversing a potential difference, can be thought of as being converted to kinetic energy, i.e. the hydrogen ions are accelerated by the potential difference which causes them to gain speed and hence move at a higher speed than the average in the final compartment. This will cause increased collisions (and more energetic) with the surrounding molecules, slightly increasing their kinetic energy too, which will ultimately increase the average kinetic energy, the measure of which is called temperature. If it was coupled, the hydrogen ions would not have gained the kinetic energy, as the energy they gain by traversing the potential difference would have been used to do work in the ATP synthase machinery.
Rigorously, you can show this using some chemical thermodynamics which includes using $\Delta G$ functions, $\mu$ functions and some related thermodynamic variables. Let me know if you want that explanation.(though I stand the risk of having lost the touch to the mathematical aspect of thermodynamics)
PS:- While the thermodynamic explanation also accounts for the increase in temperature due to obliterated concentration gradient, it is difficult to explain with the former model. You can think of this, as the neutralising of the concentration gradient changes the number of collisions per unit volume (and time), and hence also contributes to the observed temperature change.

The way that you have explained the mechanism is very nice +1

Thank you for your answer. I am quite happy with the intuitive approach for now. I am not sure I would be able to fully understand the strict mathematical explantion at this point, I feel I have to do some reading first.


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Explanation of ECG in MI using an electrostatic model
I found a paper presenting an electrostatic model to explain the ECG recorded in various leads. This model essentially calls for considering the depolarization wavefront to be the major contributing factor to the potential difference measured at the leads, especially the limb leads, by means of an aggregation of momentary dipoles with dipole moments organised according to the direction of propagation. It is also used in this book here, under the ECG section under Measurements of cardiac function.
The paper does not explain the observed ECG deformities in case of MI in detail. ST elevation, is a common finding in most MI cases. How do we explain this in light of the aforementioned model?
My thoughts
In the normal case, ST segment is isoelectric, as there is no depolarisation/repolarisation wavefront propagating. How is this isoelectric nature compromised in MI? Assuming most infarcts include muscle death or damage due to focal insufficiency of coronary circulation, even if a region of heart was dead, during the ST segment, the graph should show an isoelectric line (no deflection) as the living tissue will either be depolarised or polarised, (but not switching states) and the dead tissue will have either a completely obliterated membrane polarity or an altered polarity throughout the cardiac cycle. In any case, no part of the heart will be switching its polarity then. Why is then, some resultant dipole (which indicates a propagating wavefront of altering polarities)obsereved during the ST segment?

alternative model
   To explain the elevation, this book (pg 522) provides a two cell model, and explains that the anoxic damage somehow
  causes the basal depolarised state of the cell to have a lower
  membrane potential difference, which causes all the segments of the
  ECG except the ST segment to be lowered, making the ST segment appear
  raised. I don't understand three things regarding this explanation.
  How will anoxic damage cause such a specific alteration in the polarity and the subsequent action potential? How can this two cell
  model be extrapolated to the whole heart with a focal infarct? How
  does this explanation be reconciled with the model presented at the
  head of the question?

Let me know if the question appears too broad and needs to be split, or if my assumptions are wrong in any way.
MI-Myocardial Infarction
PS:-  I seem to have lost the touch with the formatting on this site, and hence don't know which tags to use. Will take some time to get back :)

formatting and tag edits are fine! :) +1

The concentration of K+ inside the cell is 30 time more than outside. Hypoxia causes loss of this intracellular Kalium and consequent/premature repolarization when measuring the potential of action.
As the all the ECG theory is Vector based, any abnormality in the electric pathways and myocytes will result in changes of ECG.
This picture depicts the ST changes due to different extension of injury. In addition, the explanation on this site will probably resolve the issue of understanding.

ADD
The article explains the ECG phenomena as a result of electric propagation of dipoles. If the dipoles propagate towards the lead we get upward wave etc.
As the electrostatic model takes the whole heart as one dipole (as a sum of multiple dipoles) the minor infarcts can be missed on ECG. It is an actual fact, this is why other tests are important (for example, the troponin test).
The confusion point in your understanding is a "dead" tissue. In a case of infarct there is an hypoxic damage which leads to elevated permeability of the cell membrane with resulting K leak (as I explained above there are 30 times more Kalium inside the cell than outside). This means that "dead" area will have abnormal depolarization/repolarization pattern just because there are multiple "non grouped" dipoles in that area (look at the picts). There are diastolic and systolic theories of ST elevation, but none of them has won the battle yet.
With time the scarring tissue replaces the infarcted myocardium and in that case the ST-segment will not be affected and will look nearly normal. This is the case you meant as "dead" tissue - scar tissue does not leak any electrolytes and consequently the ST segment is not affected in a chronic stage.

Thanks for the answer. But I want to understand the genesis of the resting and the repolarised-state dipole which causes the said changes in the graph, considering the electrostatic model presented.

@SatwikPasani I'll read the article and add the explanation if it could be reliable.


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Pits and Pores in Vascular Tissue
What purpose is served by the pits and pores in xylem and phloem cells? I cant find what purpose that these components serve in the vascular tissues in plants

Welcome to Biology S.E.! If you need additional assistance with the site, please visit The Help Center.

Welcome! Could you provide a reference to where you have encountered these features? A picture might help too. Good luck.

those are on side walls of xylem? they allow side-wise flow of water. In cases a bubble blocks a xylem, through side-pits the water bypass. In many plants there are a sort of torus-margo structure that blocks the water-flow if side-flow crosses a limit.

In case of phloem, if the sieve tubes (which are metabolic-active and full of cytosol) did not contained pores in their tops and bottoms (sieve plates), it would have problem in transport, as-well, through fine pores in sieve plate there are cytoskeletal structures those possibly have some active role in transport. The sieve pores sometimes blocked by callose and P-protein, especially to resist stress like cut and bleed, and also in certain stages of dormancy.

Xylem vessels are wide and 'dead'  (empty, without any cytosol), to avoid the friction to drag water.

The main large holes and cavity (Xylem lumens) that we could see on TS (often on naked eye), exists because without them no flow of water will take place.

I'll write more elaborately in answer. I'll take time for that.


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What portion of the electromagnetic spectrum do cats see?
I have seen numerous articles and various information about how cats and dogs see into the ultraviolet spectrum with interesting artistic renderings such as this:

http://www.livescience.com/40459-what-do-cats-see.html
But I have been unable to find any specific parameters of what wavelength boundaries actually exist for cats.
We know that humans see from around 750 to 400 nm, but what would a cat's range be?

Short answer
Spectral sensitivity of cats indeed ventures into the UV, but not beyond ~320 nm. Their maximum is likely similar to ours, i.e., ~750 nm.
Background
The spectral sensitivity of blue cones (photoreceptors detecting low wavelengths) of many species, including humans and cats, extends into the UV range (Fig. 1).

Fig. 1. Human cone absorption spectra. Source: University of Kentucky
However, the various structures in the eye, most notably the lens, filter out UV in humans (Fig. 2). Indeed, surgical removal of the lens in humans results in enhanced sensitivity to UV light below 420 nm (Griswold & Stark, 1992).

Fig. 2. Human transmission spectra. Source: Columbia University
In the cat, however, the lens transmits a large portion of the UV light in the range of 320 - 400 nm, while primates transmit virtually no light of these wavelengths. Figure 3 shows the lens transmission spectra of various species. At 50% transmission the second (dotted) line from the left is the cat (50% transmission at ~340 nm), while a primate (squirrel monkey, species representative for humans and other primates) in this graph is line number 7 from the left with (50% transmission at ~410 nm). Hence, cat lenses absorb less light in the UV region, but transmission is virtually nil at 320 nm (Fig. 3). Given that their cones, just like humans, are sensitive to UV, we can reasonably expect that cats can see in the UV region including wavelengths of 320 nm and up. Cats also have the 560 nm (red) cones, like we do, so their maximum wavelength is expectedly similar to ours (~750 nm).

Fig. 3. Lens transmission spectra of various species. Source: Douglas & Jeffery, 2014
References
- Douglas & Jeffery, Proc R Soc B (2014); 281: 20132995
- Griswold & Stark, Vis Res (1992); 32(9): 1739-43

So is it theoretically possible that I could surgically adjust my lens somehow to obtain some sort of extra vision?

@leekaiinthesky - Correct - I have added some text + a reference on aphakia (eyes without a lens) and increased UV sensitivity in humans

Here is a real life account of a very interesting fellow who had this experience after cataract surgery: http://www.komar.org/faq/colorado-cataract-surgery-crystalens/ultra-violet-color-glow/ @leekaiinthesky

Aren't cats missing red cones? That might make them less sensitive to long wavelengths than humans. Too bad there is no spectral plot for cats.

Cats also have the 560 nm (red) cones, like we do, so their maximum wavelength is expectedly similar to ours (~750 nm). Cats indeed cannot see red, i don't know what this conclusion is not corrected.


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What does the Gini index mean in a biochemical context?
What is the meaning of the Gini index, as specificed in this link, which describes the Gini index of beta-glucopyranose bound to hexokinase?
Is this true that if Gini index has a very low value that means it doesn't interact much? If Gini index is high for a compound, it will interact?

they had a heature called gini index, wanted to know what that was

+1, thanks for the clarification. Edited answer to make more sense to me, feel free to roll back if that was wrong.

The paper by Graczyk (2007) is probably relevant for you. It says that the Gini index is a measure of reactive selectivity of kinases, with values close to zero indicating no selectivity and values close to one indicating high selectivity, and it is created in direct parallel to the Gini index in economics, which is used to describe economic inequality. In its basic form, the Gini coefficient is a measure of statistical disperson. Also see Anastassiadis et al. (2011) for a more recent example where the index is used.

Abstract
  A novel application of the Gini coefficient for expressing selectivity of kinase inhibitors against a panel of kinases is proposed. This has been illustrated using single-point inhibition data for 40 commercially available kinase inhibitors screened against 85 kinases. Nonselective inhibitors are characterized by Gini values close to zero (Staurosporine, Gini 0.150). Highly selective compounds exhibit Gini values close to 1 (PD184352 Gini 0.905). The relative selectivity of inhibitors does not depend on the ATP concentration.

References:
Graczyk. 2007. Gini coefficient: a new way to express selectivity of kinase inhibitors against a family of kinases. J Med Chem. 50(23)
Anastassiadis et al. 2011. Comprehensive assay of kinase catalytic activity reveals features of kinase inhibitor selectivity. Nature Biotechnology 29: 1039–1045

"expressing selectivity of kinase inhibitors against a panel of kinases is proposed" what does this line mean, please explain

@user3237995 I assume that it means that the gini index is calculated in relation to a specific set of kinases. Biochemistry is not my area though, but I'm interested in the Gini index in general. If you look at the paper they show e.g. that the Gini indices calculated from a set of 20 kinases are very similar to the indices calculated using an expanded set of 85 kinases.


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Question related to L-arginine biosynthesis
With respect to the L-arginine Biosynthesis pathway, the very first reaction converts L-glutamate to N-acetyl L-glutamate.
In the linked reaction scheme, why are only L-glutamate and N-acetyl glutamate considered, and not acetyl-CoA or the coenzyme? Is this because L-glutamate and N-acetyl L-glutamate are the main compounds to be considered? Why are they the main compounds being considered? Are these two compounds (L-glutamate and N-acetyle L-glutamate) the ligands?

The synthesis of N-acetylglutamate is mediated by the enzyme N-acetylglutamate synthase. This enzyme has L-glutamate as its substrate and uses acetyl-coenzyme A as a co-enzyme acetyl donor. Acetylcoenzyme A (Acetyl-CoA) is generally abbreviated in structural formulas, because it is a relatively complex molecule. The only thing of relevance is the acetyl group which is transferred from a thiol group to L-glutamate.
Note that ligands is a term reserved for molecules binding to receptors; substrates is the proper term for intermediates in enzymatic reactions.

N-acetylglutamate synthesis. Source: The Medical Biochemistry page


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Evolution of Wheat
In the evolution of wheat, there are two instances of chromosomal doubling, when Emmer wheat Triticum turgidum was formed from Einkorn wheat, and when Triticum aestivum was formed from Emmer wheat.
When allopolyploids are artificially made, chromosome doubling is done by chemicals. Here, it occurred by natural endoreplication. But for the entire plant to turn out with allotetraploidy and allohexaploidy respectively, wouldn't it be necessary for endoreplication to occur just after zygote formed--quickly, so all, or most, cells of the plant would have this genotype?
Isn't the probability of that happening twice in the process of evolution, both times in those incidences when the wheat crossed with the goatgrass species, very low? Is it just coincidence that it happened this way, at the right time, to allow for the allohexaploid species to develop naturally?

But for the entire plant to turn out with allotetraploidy and
  allohexaploidy respectively, wouldn't it be necessary for
  endoreplication to occur just after zygote formed--quickly, so all, or
  most, cells of the plant would have this genotype?

Yes, it should have happened right after the embryo was formed in nature.  But in artificial settings, this can be done after growing the seed to a small seedling then dipping its roots in colchicine for 12-24 hours.

Isn't the probability of that happening twice in the process of
  evolution, both times in those incidences when the wheat crossed with
  the goatgrass species, very low?

Yes, it is very low, but consider the fact that nature never sleeps.  Einkorn existed for millions of years before the Emmer wheat came into existence.  And hexaploid wheat only came line 8000-10000 year ago (about half a million years later).  You don't see these events in nature that frequently.  So it is slow.

Is it just coincidence that it happened this way, at the right time,
  to allow for the allohexaploid species to develop naturally?

Yes, it was part coincidence that it occurred naturally.  Right conditions at the right time.  But really important was the role of early hunter gatherers turned farmers who identified the potential of the new allohexaploid and selected it to grow grains.


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The Uniqueness of DNA Paradox
How can everyone have unique iris and fingerprints? After a certain amount of human beings have lived on earth, wouldn't it be possible to exhaust all possible combinations?
The same principle applies to DNA. Lets say counting all the nucleotides on a strand of DNA we find that there are a total of $N$. We know there are 4 types of nucleotides, thus the total number of possible DNA sequences equals $4^N$. This is exponential, and since $N$ is immensely huge, $4^N$ will be unthinkably huge as well. However, since $4^N$ is a finite number, how can DNA be guaranteed to be unique? Doesn't that contradict the pigeon hole principle?

There is always a chance of identical DNA sequences, and perhaps even identical biometrics between subjects. However, the chance is simply so small that it is of no problem for forensics and the likes.

I guess the assumption is wrong, that only DNA is responsible for the layout of iris and fingerprints. Even people with identical DNA (like twins) shall have different iris and fingerprints? So comparing the number of resulting combinations to the number of people would probably exhaust the lifetime of our universe.

This really does not relate to DNA, specifically. I say this because there are likely not that many allelic differences that account for pigment in the iris or patterning of fingerprints. This is a developmental question. It is the randomness of how cells migrate and the timing of gene expression that dictates. Each cell will either express from both alleles of a gene or there will be gene choice. The choice however does not need to be the same for each and every cell in a tissue. So where a cell ends up in development and whether it is expressing Maternal, Paternal, or both alleles determines

The uniqueness of irises and fingerprints are, as you said, limited to the number of possible permutations of irises and fingerprints.
A similar problem exists in computer science, and is known as a hash collision. Given sufficient samples, there will always be a collision for a hash of finite size. However, the sample space is sufficiently large for iris and fingerprint analysis for this to not be a problem.
A typical iris analysis system produces 2048 bits of entropy, while a typical fingerprint analysis system produces about 82 bits. Even accounting for the birthday problem, the information space is large enough that the chance of a given false positive is sufficiently low to prevent a random person from passing fingerprint/iris authentication.
For comparison, the current world human population is 7.2 billion, or slightly under 33 bits. The risk of a hash collision occurring is small enough to be negligible.
Of course, side-channel attacks against such biometric systems are relatively simple, but that's another issue altogether.

@Gordon That would be somewhere around 108 billion which has a collision probability of approximately 0.1% assuming a fingerprint is used.

@Gordon you should also consider that the same DNA would not make the exact same individual. There is a lot of randomness involved. Consider, for example, identical twins and their differences in character. You also have random mutations occurring during an individuals lifetime or development. In any case, you should not confuse 2 people with identical DNA with reincarnation which implies some sort of continuity or link between these individuals.

@terdon Unrelated to this question, but this is essentially the main plot point of Jupiter Ascending.

To add to what @terdon said, imagine the probability that two people, with the same DNA and chemical makeup, go through all the exact same experiences in their lifetime. The people they meet would all have to be similar enough to provide the same exact experience. Not to mention language, technology, and other things which are part of society. If the universe is really "infinite", there is an infinite number of positions the objects of the universe could be in. If you argue for a finite universe, then maybe eventually it could happen.

@Gordon My point was that much, much, much longer after that, if the Universe has a finite space and amount of matter/energy, and continues indefinitely without "dying", a person with the exact genetic make up and exact same life could exist on a planet exactly like Earth again. Proof: Pigeon hole principle

@DoubleDouble you are assuming the person is male. X-chromosome inactivation in females is stochastic, and as every woman is a mosaic of expression from either the maternal or paternal X-chromesome for each and every cell, then even a female "clone" would not be identical.

@March Ho's answer is an excellent answer based on the assumption that all of the observed phenotypic variance is due to genetic variance.
Environmental variance
The genetic variance is not the only underlying variance that can explain variance in phenotypic traits. There is probably quite a lot of phenotypic variance that is caused by the underlying environmental variance between individuals. To have a better understanding of what are the different kind of variance you may want to have a look at this post for example. The heritability is typically equal to 0.3 (in fact most studies to report measures of heritability that are not significantly different from 0.3). If this was to be the case for the trait of interest, it would mean that 70% of the observed variance in fingerprints would be due to environmental variance.
Developmental Noise
Also, when talking about minor differences in phenotypes (such as fingerprints), developmental noise (inherent stochasticity of biological processes such as the decay rate of proteins or the production rate of mRNA) might be of real importance. (Raser and O'Shea, 2013) uses fingerprints as example of phenotypic trait which variance is in part determined by developmental noise.
Relevance of an answer that cares only about genetic variance
While @March Ho's answer is pleasant and interesting, I think that it is not of great relevance to the problem given the important amount of non-genetic variance that is underlying the phenotypic variance of interest.

+1, good catch! I didn't think about the correlation of the two variables.


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How to calculate the number of sterile insects that must be released in SIT?
The sterile insect technique (SIT) is used to control insect pests through overwhelming the population in sterile males. The increase in sterile males released into an environment causes the increase in infertile matings. This, in theory, would reduce the population.
However, how would you calculate the number of sterile flies needed to be released in order to be effective? It would be dependent on the reproduction rate of the insect, initial density, and sex ratio in the young, but is there an equation to express this? Or is there simply a generic ratio of the target population that is used?
I'm looking at the example of the New World Screwworm fly, and the eradication in Central America.

You might also want to consider the relative reproductive capacity of a sterilised vs a wild type fly.


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Neuroscience behind the crash
After experiencing things like stress, intense exercise, or using drugs such as caffeine and amphetamine, subjects often assume a depressive and lethargic state afterwards, known as a "crash." What is the neuroscience behind it? Could it have to do with the depletion of neurotransmitters such as the catecholamines, or a downregulation of certain receptors in response to the overproduction of such neurotransmitters?
(This question is a remix of a previous question I posted, which was not focused enough)

In terms of specifically caffeine, caffeine is an inhibitor of cAMP phosphodiesterase. Your glycogen phosphorylase will be active to a higher level (this also means the glycogen synthase is downregulated!) All the glycogen will clear out of your muscle eventually, and when your caffeine levels fall, all the cellular cAMP will begin to degrade. There's suddenly no glycogen, however, and your muscle cells will pull what they can from the blood to replenish it. Especially combined w/ high sugar intake, the pancreas tends to release too much insulin and clear too much blood sugar.

so if your hypothesis accounts for the main symptoms of the crash (that low blood glucose is at fault), adequate nutrition, for example snacking on carbohydrate heavy foods throughout the day but not having large meals, would eliminate the crash? Or, more directly, a glucose clamp would counter the effect completely?

this study indicates that under a hyperinsulinemic-euglycemic clamp, subjects ingesting caffeine has less glucose disposal than subjects ingesting dextrose.

The "crash" effect is typically perceived as a deterioration in affect. With drugs, this deterioration happens as the drug is cleared from blood circulation, particularly cerebral circulation. With the ingestion of amphetamines, there is a brief reuptake of certain neurotransmitters, particularly dopamine and norepinephrine. Amphetamines also temporarily prevent the 'recycling' of said neurotransmitters, so the reuptake effect can last anywhere from 4 to 24 hours. The brain regulates internal homeostasis of mood based on perceived 'high' and 'low' elevations; thus, after an extended elevation in mood, there must be a 'comedown' period, or a deterioration in affect.
Further essential to this idea of homeostasis are the stress hormones, cortisol and adrenaline. Upon release, these hormones may raise blood sugar levels, blood pressure, and/or heart rate. As heart rate increases, the flow of blood goes to the heart, with less going to the brain. This causes the groggy and tired feeling afterwards that might be associated with a 'crash'. Stress hormones also impact the thyroid (which controls how fast the body uses energy, and controls hormonal sensitivity) as well as the central nervous system.
Exercise also leads to increased heart rate, as well as muscle fatigue. However, exercise itself doesn't typically lead to a depressed, lethargic state, as exercise promotes the release of endorphins (which are known to improve general sense of well-being). However, it is not uncommon for some people to experience "endorphin withdrawal" after suddenly stopping excessive exercise, which could mirror the crash that comes from the 'comedown' after drug use.


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How did the endoplasmic reticulum come to be?
Organelles are sub-cellular compartments in cells. However prokaryotes don't use organelles to organise their intracellular space.
Evolutionarily, there is evidence that mitochondria and chloroplasts are ancestors of symbiotic prokaryotes. This theory is called the endosymbiotic theory.
I've tried to find an evolutionary story that explains other organelles, specifically the endoplasmic reticulum. There is plenty of literature about biogenesis of these organelles, but nothing about the history of their evolution. I don't think I have found the right area of literature. What did organelles originate from? I'm happy just to know a few keywords or a citation to look it up myself.

This seems rather broad since there are many organelles and nobody really actually knows how they evolved.

@canadier I wasn't sure how broad this would be. For example is there one core theory or multiple theories for each organelle. I'm only really interested in the ER, so I'll edit that in. The gap in knowledge explains why it seems quite hard to pin down a good source! Thanks.

I'm not sure how broad it is either, it just seems broad. I haven't read this, but the abstract sounds promising: http://link.springer.com/chapter/10.1007%2F978-0-387-74021-8_5

To me, an important observation to make is the resorption of the nuclear envelope into the ER during mitosis, and then it's protein-chromatin-protein interactions that reassemble the nucleus.

Found the following on wikipedia. Seems pretty self explanatory:

The Golgi, ER, and lysosomes are likely to have evolved as a result of
  the plasma membrane going through invagination. An increase in the
  overall volume of a cell would require the plasma membrane to fold in
  order to maintain a constant surface area to volume ratio. These folds
  may have led to the specialization of internal membranes to maintain
  communication with the environment. In the first stages of eukaryotic
  cell life, the membranes may have been interconnected and attached to
  the plasma membrane. Later on, as their functions diverged, the
  membranes may have become separate structures

This is ideal and seems, at least to me, hypothetically plausible. The reference is a bit dated though (1994) and their only evidence is that these organelles use a different membrane transport pathway to the chloroplasts or mitochondria, rather than any sequence analysis. So it is somewhat conjecture... It's a start though! I'll trawl through pubmed to see if anything similar cited this paper.

further support for comes from the fact that the Endoplasmic Reticulum of many living groups are connected directly to the exterior. In red algae for instance the ER is contiguous with the plasmalemma (exterior membrane) .

From (brief) section, Evolution, in Wikipedia's article, Endomembrane system:
The most recent concept suggests that the endomembrane system evolved from outer membrane vesicles the endosymbiotic mitochondrion secreted. This OMV-based model for the origin of the endomembrane system is currently the one that requires the least amount of novel inventions at eukaryote origin and explains the many connections of mitochondria with other compartments of the cell.
The text above includes references to two articles published in journals in 2016.
https://en.wikipedia.org/wiki/Endomembrane_system#Evolution


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How can computer predictions of protein folding be verified computationally?
Currently, there is a lot of research focused on solving the folding patterns of proteins using computers (Folding@Home, https://fold.it/portal/, etc.).
The question that I have is: How do you know when you get it right?  Is there some way of verifying, in silico, that you have found a legitimate/correct structure for a protein?

Normally you have an output in silico you'll have to verify by NMR, xray crystallography, or experimentally in other words. If your protein is particularly disordered, however, you must compile many techniques into a conformational ensemble as outlined here. The computational techniques provide lots of data but there's no 100% without experimental verification.

http://biology.stackexchange.com/questions/30240/proteins-folding

@Kendall Although experimental analysis "trumps" modelling, there are methods to analyse the viability of a model (see my answer for more depth).

the best you can do is, modelling using  I-TASSER server or may also prefer Rosetta package, but the question you asked is still a "million dollar question"...

Overview
Modelling has come on leaps and bounds over the last decade or so and in many cases has acted as a sometimes viable, and inexpensive substitute for experimental structures.

How do you know when you get it right?

Ultimately, one still needs experimental evidence to know when a model generated in silico is right. But there are ways of scoring a model for how likely it is to be right.

Is there some way of verifying, in silico, that you have found a legitimate/correct structure for a protein?

There are lots of ways to score and verify your models. Each method tells you something slightly different about the merits, or lack thereof, of your structural model. Some are designed to weed out the obviously awful models and some allow you to detect exactly where your model looks to be accurate or inaccurate.
MODELLER Homology modelling output verification on the fly.
I am most familiar with modeller for homology modelling. Other softwares are available and they are each evaluated by CASP every two years since 1994.
In homology modelling there are 3 common scoring systems that can be used to assess the biochemical viability of a model. This email covers when to use each one. My answer expands and explains a bit more.
molpdf is the Modeller objective function.
GA341, discussed here is derived from  Z-score (calculated with a statistical potential
function), which is a target-template sequence identity, and a
measure of structural compactness.
DOPE is a more up to date method, first published in 2006, and is more true to "biological viability". From the publication:

DOPE is based on an improved reference
  state that corresponds to noninteracting atoms in a homogeneous sphere with the radius dependent on
  a sample native structure; it thus accounts for the finite and spherical shape of the native structures.

Which to use depends on what you want to do with the model, but of those three scores, DOPE is the most reliable at separating native-like models from "decoys".  DOPE is usually the starting place for figuring out which models might be right and which models are just plain rubbish.
Note:  If you use Rosetta then there will be equivalents to these, or you can run your generated models through these techniques. If you are using SWISS MODEL that comes with it's own somewhat black box verification techniques but you can still export the model for further verification.
General model check against experimental data.
A further validation of homology modelling methods or other structural models is ProSA. ProSA provides a great visual representation of where the z-score lies amongst actual crystal and NMR structures. There are probably others that do similar functions, but this is my personal go-to to get an idea of where my structure lies among experimentally gathered structures.
Sensitive residue by residue verification.
Although the aforementioned methods examine each residue, they usually output an overall score. Residue by residue scores are also available and require a lot of careful interpretation. For example, if you are analysing catalytic activity, a surface looping region that scores poorly might not be an issue, but a core catalytic residue that scores poorly renders the model useless. This means that just because your model has a good (lower) overall DOPE score than another model, doesn't mean it is necessarily a more accurate model for what you are interested in.
There are plenty of sensitive modelling scoring systems. Some of which are XdVal, MTZdump, the famous albeit old-school Ramachandran Plotting method, pdbU, pdbSNAFU, PROCHECK, Verify3D, and ERRAT to name a few. Each has a place when checking how correct your model is.

Thanks, this is very informative.  I was always wondering if there was some kind of "magic formula" which told you that your folding was correct.  I'll take a better look at specifics of those models, but this now leads me to wonder how Folding@Home and others manage to "solve" protein structures.

At this point, it must be verified experimentally.
In this foldit research paper, they use software and user input to design essentially an enhanced version of a naturally occurring protein, but they then physically make their new protein and determine its structure experimentally, using x-ray crystallography. Overall, they use a lot of trial and error
http://homes.cs.washington.edu/~zoran/foldit-nbt-2012.pdf
Projects like this are kind of geared towards towards the goal of being able to determine a protein's structure from its amino acid sequence in silico. Once we achieve this ability, it will be revolutionary. However it is very difficult, because making such predictions accurately would require the use of quantum mechanics in a way that is extremely difficult to computationally model. These projects use shortcuts to get around this problem, so their results aren't very accurate, but they can be accurate enough to be useful, as shown in that paper.

Here you are discussing ab initio modelling which is complex as you state. However, "in silico" modelling also includes homology structural modelling, something you miss out entirely from the answer. Homology modelling is a much more established method and has been shown to be very accurate in many circumstances. The key is that structural information from similar known structures can aid the prediction. ab initio is only used in some rare instances if homology modelling cannot be used and experimental analysis is not available.