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Can we determine a person's age by dating methods or other means?
There are many sports restricted to players of a certain age (e.g. 16 and under, 18 and under, etc.) What if a person is older and fakes his birth certificate to say that he is younger? Is there any way to expose this person?
Can we determine such a person's age by radiocarbon dating methods or other means?

Have you read the Wikipedia article? In the very first paragraph it states that the object to be tested must be dead, as it stops exchanging carbon with the environment. So, no.

You'd have to kill them first…

Even if possible C14 dating would not be sensitive enough as the resolution (see wiki: http://en.wikipedia.org/wiki/Radiocarbon_dating#Errors_and_reliability) is about 80 years :)

If you dated a person for long enough, I hope they'd tell you their real age eventually. Sometimes I think biologists should get out more.

No, one can't confirm age by carbon dating. That doesn't mean we can't make a decent guess by other methods.
There is an interesting case of a 33 year old Texas woman who enrolled in 10th grade in Texas. She said she had no transcripts because she had been homeschooled. She looked like a teenager and acted like a one too. She even fooled her new 23 year old boyfriend. So it happens. It also happened in the Little Leagues World Series, if I remember correctly. A twenty-something guy passed himself off as a 14 year old. He was a star (for a while).
In children and adolescents, the combination of a dental exam, dental films and bone X-rays can narrow a one's biological age well. Once the bones are done growing in length, that avenue is closed.
After that, someone might have to provide a tooth. Chemical analysis of tooth dentin, such as aspartic acid racemization, has shown reproducible and fairly precise results.
Global levels of carbon-14 (14C) have been carefully recorded over time. In one 2010 study, forty-four teeth from 41 individuals (one per individual) were analyzed
using aspartic acid racemization analysis of tooth crown dentin or radiocarbon analysis of enamel. Teeth from individuals with dates of birth ranging from 1936 through 1994 (aged 13–70 years) were analyzed, and where the date of birth was known, yielded a 14C-based date of birth estimation accuracy of 1.3 years (S.D. = 0.9 years). In one case, a date of birth was determined to be 1948.4. In another, it was determined to be 1988.

[T]en of these were split and subjected to both radiocarbon and racemization analysis. Combined analysis showed that the two methods correlated well (R2 = 0.66, p < 0.05). Radiocarbon analysis showed an excellent precision with an overall absolute error of 1.0 ± 0.6 years. Aspartic acid racemization also showed a good precision with an overall absolute error of 5.4 ± 4.2 years. Whereas radiocarbon analysis gives an estimated year of birth, racemization analysis indicates the chronological age of the individual at the time of (tooth extraction).

During the course of aging, l-forms of amino acids are transformed by racemization to the d-forms.

[T]he extent of racemization of amino acids may be used to estimate the age of various tissues. Of all stable amino acids, aspartic acid has one of the fastest racemization rates and is therefore the amino acid most commonly used for age estimation....[T]eeth are the tissue of choice for age estimation analysis.

Both methods have strengths and limitations.

The radiocarbon birth dating method can tell the birth date of the person regardless of the time of (extraction). However, the time window for this analysis is limited to subjects born after the early 1940s because the calculations are based on the measurement of bomb pulse-derived 14C.

Clearly this wouldn't be of too much use in people trying to pass themselves off as teens.
Some studies of aspartic acid racemization report accuracies of age ±3 years. The radiocarbon and racemization can further narrow it down.
Why did Charity Johnson pretend to be a teenager for 20 years?
Age Estimation in Forensic Sciences APPLICATION OF COMBINED ASPARTIC ACID RACEMIZATION AND RADIOCARBON ANALYSIS
Strategy for the estimation of chronological age using the aspartic acid racemization method with special reference to coefficient of correlation between D/L ratios and ages

To grab this opportunity to sum up the comments for the C-14 dating method, including those of of @MattDMo and @canadier: Theoretically spoken - Yes we can! But only after (1) killing the person and (2) waiting a few hundred years. As carbon keeps on being recycled in a living carbon-based organism, it has to be dead first. Secondly, because the margin or error is about 80 years, mainly due to the relatively long half-life of C14 (5730 years) and the variability in the C14 dating method (see wiki on C14 dating) one should wait, ideally between 1k and 1000k years. But given the error margin a few hundred years may suffice to get a rough idea. So to sum up - practically this test, although it is objective and free of subjectivity and robust to false pretenses, makes no sense as (a) a human life is about the same a the error margin of the test and (b) the competitor cannot participate in the contest after his or her life has being taken.
I am not aware of any biologoical methods to objectively measure age.


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Predictive Single Nucleotide Polymorphisms (SNPs) for Bipolar Disorder
Are there any validated SNPs that are either predictive of developing bipolar spectrum disorder or are associated with its pathophysiology?

What do you mean by validated SNP? An association that has been further confirmed?

Yes, that's what I mean.

Yes, there have been a variety of studies that do association analysis of variants with bipolar disorder. Here is a recent one that validated 11-30 variants depending on how you count.
However, in these kinds of analyses you should be somewhat cautious as the associations are extremely weak (as they generally are for complex traits in humans):

Eight of the 19 variants that were genome-wide significant (P < 5 × 10−8) in the discovery GWAS were not genome-wide significant in the combined analysis, consistent with small effect sizes and limited power but also with genetic heterogeneity.

The statistics of how you interpret such variants are rather dodgy/uncertain, so I would put very little stock in any particular variant. Maybe if you take the genome-wide significant variants only and added them all up you might start to get a little predictive power.
In terms of other more speculative observations (again from the abstract of that study):

The significant loci contain genes encoding ion channels, neurotransmitter transporters and synaptic components. Pathway analysis revealed nine significantly enriched gene sets, including regulation of insulin secretion and endocannabinoid signaling. Bipolar I disorder is strongly genetically correlated with schizophrenia, driven by psychosis, whereas bipolar II disorder is more strongly correlated with major depressive disorder.

I would suggest reading that paper and finding some further citations from it if you are interested in more detail.

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small RNA bioanalyzer traces showing miRNA enrichment for sRNA-seq
I am bioinformatician trying to support some small RNA-seq experiments. All bioanalyzer traces that I have seen for RNA at the small RNA range show at peak at 22. But probably it depends on the protocol for the RNA purification (in this case only experience with RNeasy Qiagen).
I would like to know if some of you have some examples/experience of good bioanalyzer results after RNA purification that have been sequenced and got a big percentage of miRNA detected.
Currently I have a example where there is a broad peak at 25 and in some cases a small peak at 22. After sequencing there is almost not data. So at some point we lost the data. Trying to figure out if the bioanalyzer was good at that point, or already was something wrong.
thanks.

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What is the use of eye banks, if eyeball transplants do not exist at present?
Corneas are donated and transplanted, but not the eyeball.
I don't understand. What is the purpose of donating a cornea without an eyeball to a blind person?

Some types of eye illness just affect the cornea and can be treated by replacing the cornea, hence a value in storing them.

So why their name as eye bank instead of cornea bank?

I'm guessing it's called an eye bank because it stores eyes! The parts useful with present day medical techniques, such as the cornea and sclera, are extremely thin and delicate, and are presumably removed from the donor eyeball just before use.

No-one can re-implant an entire eye, because the optic nerve has been severed in one who has lost an eye. A cornea can't be grafted to a glass eye. But blindness isn't only caused by loss of the entire orbit. It's also caused by cloudy corneas, which is the purpose of eye-banks.
The optic nerve is a cable of nerve fibers that carry  visual information from the eye to the brain. In adult mammals, any damage to the optic nerve caused by injury or disease tends to be permanent, because the cells that form the optic nerve cannot regenerate. Any injury or disease that involves optic nerve damage can lead to permanent loss of vision. Obviously the loss of an eye would sever the optic nerve.
However, if the future holds success for optic nerve regeneration, it would also open the door for entire-eye transplantation. In which case, a new cornea might come in handy.

You are asking two questions that you think are connected but are actually not.

Question 1 - What is the use of eye banks?

Answer: It's to store corneas for transplant for people with cornea damage.

Question 2 - What use is cornea transplant to a completely blind person?

Answer: It depends. If the blindness is due to clouded cornea (several diseases cause this) then replacing the cornea will reverse the blindness. If the blindness has other causes then cornea transplant is of no use to the person.

If patient's eye ball get damage, then eye banks will help him?

No. Eye banks will only help if his eyeballs are not damaged. Eye banks are useful if your cornea are damaged but your eyeballs are healthy.

Of course, since the cornea is part of the structure of the eyeball it depends on how you define "eyeball damage". If the eyeball damage is cornea damage then yes you can get healed by a cornea implant. If the eyeball damage is other causes then no, it won't help. Of course, I've already said this above in my answer to Question 2 but using slightly different words.

To imply that the cornea is the only part of the eye that is useful for eye repair is misleading.  There are sometimes reasons that the sclera (white part) is used to repair parts of the eye, though generally this is not because of unexpected trauma, but because of reconstruction from other surgeries, such as glaucoma valve implantation or complete enucleation prosthetic covering.

@Beska: It's less misleading than the belief that the eye cannot be repaired at all. Which is what all the answers here have been trying to get through to the OP. I was just trying to do the same with simpler language. Though I do admit that I oversimplified a lot.

@slebetman Yep, true.  It's a difficult situation...presenting the entire picture may be more "accurate", but may not be as helpful to someone who just wants/needs a simple answer.

I used to work at an eye bank so I have a bit of knowledge about this, though some of it may be out of date.
There are several aspects to an eye bank.  The corneas are one of the primary things that are kept for transplantation.  Of course, this will not repair blindness in someone that has problems in other areas of the eye, but corneal transplants are helpful for people who have corneal damage for one reason or another (such as a foreign object, age, or disease damaging the cornea.)
Beyond this, small parts of the sclera (the white part of the eye) are also sometimes used to patch damage (though generally this is not because of unexpected trauma, but because of reconstruction from other surgeries, such as valve implantation because of glaucoma.)
Finally, of course, many people would not understand what the purpose of the organization was if it was called a "Cornea Bank".  "Eye Bank" is more descriptive.

The eyeball is basically the sclera that surrounds the delicate inner structures of the eye (see wiki on the eye). The cornea is the transparent window in front of the pupil that transmits light to the retina. It needs replacement when it turns opaque, often due to damage or infections. The cornea can be replaced on its own, without the need for transplanting other tissues of the eye, as an opaque or otherwise damaged cornea does not necessarily mean that other structures of the eye are damaged. If the light-sensitive parts are damaged, including the exceptionally rare case that the entire eye ball is missing, corneal transplants have obviously no use.
Eye banks are necessary to properly retrieve and store eyes. They extract, preserve, and dispatch corneas when necessary (eye bank wiki).

sorry, my exact question is: if patient don't have eye ball, then what is the use of cornea transplant to him?

you provided information of eye ball in your answer, but i am asking, What is the use of eye banks? which is completely inappropriate asnwer. i didn't ask what is eye ball, how it works? sorry!

@johnson316, most blind people do have eyeballs.

In addition to providing tissue for transplant, eye banks also provide tissue from all parts of the eye to medical schools and universities for teaching and research purposes. There are many medically relevant questions that can only be answered by examining human tissue, and eye banks facilitate this research.

It seems to me that really your whole question seems to be much simpler than it seems and it is just
"why are eye banks called eye banks when they can't transplant eyes, just bits of them like corneas"
The answer is:
In the english language and in various cultures, the names of things often have a loose and not entirely accurate relationship to the product at question.  For example a person might be a screw loose mentally but that doesn't mean a physical screw, etc, etc.
English is not a consistent scientific logical language for describing the world.

Although I agree with you it is more a comment than an answer.

Perhaps this is true but it would be great if you can add some notes about the origin of the term.


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How did birds survive the KT impact?
As I understand it, the ejecta resulting from the K-T impact (also known as the end-Cretaceous or Cretaceous-Tertiary extinction event) re-entered the atmosphere all over the world; the heat from friction with the atmosphere raised the air temperature to a few hundred degrees C. All organisms all around the World were incinerated, except those that could bury underground or move into water.Now birds don't bury underground, nor do they   bury their eggs. So, how come birds didn't go extinct?
To clarify, I'm not considering the longer term cooling effect (which was in turn followed by a longer term warming effect due the CO2 dumped in the atmosphere). What happened just after the impact was that a sizable fraction of the entire volume involved on the collision would be on ballistic trajectories. Most of these would fall back to Earth, while a small fraction would escape Earth's gravity. Now, these ejecta actually contain a significant fraction of the total energy of the impact and almost all of that in then dissipated as heat when they re-enter the atmosphere. This leads to shock heating of the atmosphere to at least a few hundred degrees celcius, but much higher temperatures are also possible, see also this article.

what is the KT impact? a meteorite?

Are you sure about this: "raised the air temperature to a few hundred degrees C"? I'm not too into paleontology, but I admit I never heard that before. Could you please add a link to support that?

Unfortunately the premise underpinning this question is false. The Cretaceous–Paleogene extinction event did not raise temperatures (other than shortly and locally at the impact site) but rather lowered temperatures and light levels through additional particulate matter in the air. Birds survived due to being small (like mammals of the time) and thus requiring less food. Birds could also travel to where food was, as applicable.

+1 @LateralFractal I heard from non-scientific resource too, that the survival was dependent on the weight.

@inf3rno A faster reproduction rate would have also allowed bird species to adapt faster. Whilst non-avian dinosaurs as egg layers offloaded some of their reproductive burden, each large dinosaur still had to grow (slowly) to maturation for their next generation of reproduction.

My answer to a related question about aquatic dinosaurs may help, I at least point to a Radio Lab episode where they discuss the KT impact with geologists. Basically, anything that was on the surface of the Earth got cooked, but anything under a few inches of soil would be ok. This favored small mammals, birds, and reptiles that nested underground. While modern birds don't typically bury eggs, ancient birds may have, to hide them from predators.

@LateralFractal I think you're confusing short and long term effects on temperature. While the dust kicked up by the impact would have blocked sunlight and cooled the Earth, that took much longer than the initial firestorm immediately after the impact. Further complicating the issue would be the fires themselves, which would have released smoke that blocked additional sunlight, but also released CO2, which would have caused a longer term greenhouse effect.

@user137 I'm afraid you are going to need to provide a source for the claim that an asteroid impact globally roasted the fauna.

I've added a source in the question.

@CountIblis I can't find the originating peer-review journal article for the claim described on livescience.com. My initial scepticism is driven by 1) Air isn't a good conducter of heat and 2) Oxygen rich wild fires would have been common on that basis anyway.

@LateralFractal While Radio Lab is not a peer reviewed scientific article, they do name all the geologists they interviewed. A quick search on their names gives more information about Kirk Johnson, Peter Schultz, Jay Melosh, and Douglas Robertson who made the claim about temperatures.

Looking at some of the abstracts to the newer journal articles on the subject, there may be some question as the impact in the Gulf of Mexico may predate the KT boundary by a few hundred thousand years. Though if you base the extinction on the asteroid strike, then as described on the NASA JPL http://www2.jpl.nasa.gov/sl9/back3.html The heat and fires would have been local, and the cooling global. The asteroid could have caused immense tidal waves.

The premise 'birds do not bury themselves underground, nor do they bury their eggs' is also false. Burrow-nesting is not uncommon among modern birds, and incubating burrow-nesting birds will often spend extended periods (multiple days, sometimes weeks) attending the nest. Example: https://en.wikipedia.org/wiki/Wedge-tailed_shearwater

Detailed answer given in this article

This article hypothesizes that the surviving avians had large and quite complex brains, giving them an advantage in finding food in the aftermath.


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Human longevity interventions ranked by effectiveness
Generally living longer and with a better quality of life is considered a good thing, if not for ourselves then for our family and friends who care about us. Some factors that influence human longevity are outside our control or only currently exist in a research laboratory; others factors we can control but vary in their impact and effectiveness.
What interventions (preventative or curative) applied by individuals have been proven to increase human longevity, ranked by their effectiveness?
The interventions can be ranked by the ratio of Time Spent vs. Time Gained or Money Spent vs Time Gained. A centuries' worth of data driven medicine and longitudinal studies should provide some answer as to what works and what doesn't.
For purposes of this question, please exclude future interventions that have not yet or never been tested on a sizable portion of population.
Some of the biggest improvements in collective aggregate life expectancy in a society have been communal solutions such as elimination of pathogens. As these either exist or don't exist for a given community - I'd like to narrow the scope to interventions applied or chosen by individuals (such what they personally do or don't do). That is, interventions that supplement communal improvements.

Time Spent vs. Time Gained is not a concept I'm familiar with, because much of the time, the gain was an entire lifetime. I don't know that any studies have averaged it out for entire populations.
Four generations ago, the average Swede had the same probability of dying as a hunter-gatherer, but improvements in our living conditions through medicine, better sanitation and clean drinking water (considered "environmental" changes) decreased mortality rates to modern levels in just 100 years, researchers found.
The most significant advances which promoted health and longevity include (as mentioned above):

improved sanitation.
improved water quality.
vaccines.
antibiotics.
improved living conditions.
improved nutrition.

Since you posted a comment indicating a change in your question, I'll stop here.

My bad. I'll need to narrow the question to mean individual interventions that supplement overarching communal interventions.

Time Spent vs Time Gained is a way to attempt to remove nation-specific costing from an assessment of effectiveness. For instance, 1 hour of Intervention X every day adds 10 years if applied from Age Y. But then it removes a whole class of interventions that are not time based (excluding a Labor Theory of Value). In practice, studies that separate out communal interventions from individual interventions may or may not be common, depending on who's driving the report or research grant. Typically government studies aim for bang-for-buck on interventions they can directly apply (i.e. communal).

Woah! That is totally out of my league! Thanks for clearing that up before I got too deeply into my answer.

+1. Your answer was very useful in helping me clarify what I meant by longevity interventions.


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Publicly available resources for learning metagenomics
We are starting a metagenomics project in our research group to study microbiota in the respiratory tract. Since the are no books yet about metagenomics, seems reading some reviews and online tutorials is the only alternative.
Could you suggest me essential papers, websites or other resources useful for my purpose.
Thanks

You can have a look at some of the lecture slides of previous years' EBI-Metagenomics course.

The Coursera Bioinformatic Methods courses include classes on metagenomics and, more importantly, tools to use when applying these methods. I have not taken this particular course, but Coursera is generally very good with getting hands-on experience using computational tools. A course-like setting may also be conducive to group learning.

In the paper here compared lots of different tools for the different parts of the anlysis in metagenomics. It is a comprehensive study in which several labs participated.
You need to take into account that not necessarily the most popular tools are the best. And in the end it will depend on what you want to and how you do it.


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Effect of recombination on the rate of loss of genetic variation
Following up from this question: Does recombination increase the additive genetic variance for fitness?
(I'm thinking about the evolution of additive genetic variance and differences between the sex chromosomes and autosomes. Assume males are heterogametic (XY) and females XX, recombination occurs on the X in females, but not between X and Y in males. This means X chromosomes recombine at 2/3rds the rate of autosomes. Answers need not necessarily relate to sex chromosomes as many other factors should be affecting their evolution and additive genetic variance)
As far as I can tell, recombination should improve the efficiency of selection as variance in fitness of the population of chromosomes increases (because favourable mutations can combine more easily and deleterious ones do too) which should in turn reduce additive genetic variance (right?). But then recombination means many more combinations occurs which means additive genetic variance might be higher.
So, if I sample the additive genetic variance in a trait in a population where chromosomes that do recombine and a population where chromosomes do not recombine, where should we see the most variance (the recombiners or non-recombiners)?

(answers should point to theoretical papers please)

I found a key paper for myself from an issue of Nature Reviews Genetics last year. It discusses and reviews how recombination affects the rate of genetic variation at the sequence level.
A key concept is that of selective interference, which is what I had stumbled across in the question, this is when the efficacy of selection is reduced because "recombination fails to break down linkage disequilibrium at selected loci." Simply, a beneficial mutation in a system of no recombination is only as fit as the background it is in, if recombination is extremely high (no LD whatsover) then the fitness is defined only by it's own effects. This means that recombination can reduce polymorphism because selective interference will reduce the speed at which non-neutral alleles are fixed or lost.
However, recombination maintains polymorphism, because without it there is a greater potential for hard sweeps, soft sweeps, partial sweeps, and background selection to all remove genetic variance. For sweeps a beneficial mutation will drag any mutations it is linked with to fixation, the further from the allele the weaker that effect is.
It seems that over riding effect of recombination is to maintain genetic variance despite the increased rate at which an mutation can fix when there is no selective interference because it reduces the polymorphism reducing effects of sweeps and background selection.

"It is expected that neutral genetic variation will be systematically
  depleted in genomic regions with little recombination."


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Calculating number of amino acids in mRNA
Assuming there were 20 different amino acids and less than 40 types of different tRNAs found in this alien organism. How many amino acids would be found in the translational product of a 600-nucleotide mRNA?

I am very confused over how I should solve this question.
If we assume 1 codon = 1 nucleotide,
20 amino acids require 20 different codons = 20 different nucleotides < 40 different tRNAs.
If we assume 1 codon = 2 nucleotides,
20 amino acids require 20 different codons = 5 x 5 combination of nucleotides? (considering A, T, C, G, U)?
5 x 5 = 25 < 40 different tRNAs.
The correct answer is to consider 1 codon = 2 nucleotides.
My question,
Since both 1 codon = 1 nucleotide and 1 codon = 2 nucleotides fit the requirement of this question, why is 1 codon = 2 nucleotides the correct answer?

You could have more than 1 tRNA for each amino acid, as well as stop codons. Both of these features are found in Earth's genetic code.

Wait, are we supposed to assume that this alien uses both T and U in it's RNA? To solve this we need to know how many types of nucleotide it uses.

@user137 thanks for your reply, that is the exact question, no additional information  given. I am assuming the organism uses all 5 different nucleotides.

The problem is I don't know how you could use both U and T and tell them apart because they both bind to A. Furthermore we can't assume an alien biochemistry would be at all similar to Earth biochemistry and their "RNA" could use entirely different bases.

If this is the original question accurately and in full it is meaningless and unanswerable. If, as your answer about codon length implies, it is a garbled version of the question, please present it carefully and word for word. As it stands, If the question means how many amino acids in the peptide produced you can't tell because it doesn't tell you where the start and stop codons are. If it means how many different amino acids there are, you cannot tell because you do not know what the sequence is. In either case the number of tRNAs can have no bearing on the answer.

I think I have this figured out. Had to do some math. With our 4 nucleotide system, the number of possible codons is 43 = 64. That is number of nucleotides to the codon length power. The question asks us to determine codon length while giving us the number of amino acids and an upper limit on tRNAs. Using the same formula,  #Nucleotides(Codon-Length) = #Codons, we must find a combination of nucleotide number and codon length that gives between 20 and 40 codons.
                               Codon Length
Nucleotides    1         2        3        4        5
     2         2         4        8        16       32
     3         3         9        27       81       243
     4         4         16       64       256      1024
     5         5         25       125      625      3125
     6         6         36       216      1296     7776
     7         7         49       343      2401     16807

So using this table we see that a few different combinations of Nucleotide number and codon length will fit in that range. A 2-nucleotide system could work if each codon was 5 bases long. A 3-nucleotide system could work with 3 base long codons. A 4-base system cannot work, it goes from less than 20 to more than 40. A 5-base system can work with 2 base codons. A 6-base system can also work with 2-base codons. 7 or more bases fails because even a 2-base codon will make more than 40 codons.
A codon length of 1 nucleotide would require at least 20 nucleotides, so it would not be a good answer.
5 is probably the correct answer because it works with the shortest codon length, though I don't know how you'd get base pairing with an odd number of bases. Perhaps the 5th base pairs with itself. A 6 base system can also work with the same codon length and wouldn't need a self pairing base. However that table shows several combinations could work, so this question might have been to see how you defend your answer.


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Does the Peptide bond produce water in our organism?
According to Wikipedia http://en.wikipedia.org/wiki/Peptide_bond , when a peptide bond is made a water molecule is released as a secondary product.
So, my question is simple (perhaps silly). Considering that proteins are being made every time in our organisms and this water molecule is being released in every peptide bond, why our bodies are not flooded of water?
Thanks!

The simple answer is that there are literally thousands of chemical reactions (mediated by enzymes) going on in the cell. Some produce H2O, others consume it. For example, when proteins are broken down into their individual amino acids as part of normal turnover in the cell, a water molecule is necessary to break the peptide bond. Therefore, the overall balance of water produced vs. water consumed is fairly equal, especially when you take into consideration the consumption of water and its excretion via urine and sweat.

I was thinking about this recently and I'd be curious if there was ever any study into the net water usage or production in a cell.

@canadianer I suppose it would depend on the cell type and what it's doing. An active muscle cell hydrolyzing ATP at a rapid clip would probably be different than an inactive neuron, for example.


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During bridge amplification of DNA sequences, why aren't sequences amplified in both orientations?
During bridge amplification, when sequences attached to adapters on the surface form "bridges" and are replicated, it seems like sequences with either end attached to the surface will be created.
For instance, in this link in figure 7, there are sequences facing both ways on the plate. In step 8, all the sequences are oriented in the same direction (pink end attached to the surface)
How are does this occur? How are the other sequences removed?

See this document on how Illumina sequencing works.
When you are doing a single end sequencing, the reverse strands produced after the bridge amplification + denaturation (step-7) are specifically removed (clipped at the junction of primer and the "insert" region). Furthermore, the free 3' ends are blocked (by chemical modification) to ensure that there is no unwanted priming.
For paired end sequencing, both strands are sequenced; so in one flow cell the forward strand is cleaved while in the other the reverse strand is cleaved.

Presumably they removed one set of fragments from their figures for clarity of demonstration. In reality, both fragments remain immobilized on the chip. The sequencing primer only anneals to one adapter which allows selective extension of one of the sets in each run. For fragments of sufficient length, this provides an easy mechanism for creating paired end sequence reads as you can use one primer to read one strand and, subsequently, another primer to read the other strand.


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Does prolonged exposure to low pitch but low volume noise affect hearing or stress?
This is similar to another post but not quite the same... At work, our ventilation system produces a constant low pitched sound - like a rumble - as well as the sound of air blowing through the vents. It's not very loud, we can certainly talk, even whisper to each other, but when it shuts off, it's like a huge weight off my shoulders. My ears don't really pop but there's sort of a slight "tingling" sensation - like when the blood starts flowing to a hand or foot that fell asleep. You can usually hear several people in the same room say "Ahhh" as in we are all glad the noise has stopped. I have worked in this location for over 10 years and in that time I have developed tinnitus which is probably attributed to a number of bad behaviors as a youth. But I was wondering if this constant noise could contribute to the decline in hearing? Also, that sense of relief when the noise stops makes me wonder if the constant noise adds to our stress levels?

All unnecessary noise (noise pollution) causes some degree of stress; often one accommodated to it well. Clearly the noise in your office is loud enough that you find it stressful, as do others. Most times, the cause of tinnitus is unknown; noise can make it worse, however. You might want to try to protect your hearing at work?

Basically you are asking: (1) does the low-pitch noise affect my hearing sensitivity; (2) has the noise aggravated hearing loss acquired earlier in life; (3) if the noise can induce stress and (4) if the noise may cause tinnitus (kind of a hidden question).
(1) Is the ventilator noise damaging?: Noise-induced hearing loss typically occurs at high sound levels. Occupational safe noise levels are set at around 85 dB SPL (Nat. Stand. Occupational Noise). This is comparable to listening to traffic on a busy road from 10 meters away for 8 hours/day for 5 days/week (see wiki on sound levels), or a diesel truck at 15 meters going 64 km/h. If you can still talk normally, the noise cannot be much more than 60 dB SPL, which is normal conversational level (see sound chart). So the ventilation noise is not bad for your ears as it is well below 85 dB SPL.
(2) Does the noise aggravates present damage?: Similarly to the answer under (1), the noise is not loud enough to be regarded damaging even with existing hearing loss.
(3) Does it cause stress? As @anongoodnurse suggested: yes it causes stress, apparently. Every unpleasant sensation will do so to a certain level.
(4) Effects of the noise on tinnitus: Typically, tinnitus is caused by hearing loss (see cause of tinnitus) and the pitch of tinnitus often coincides with the lost frequencies (see cause and effect of tinnitus). So if your "bad behaviors" at youth refer to loud music, then it is probably noise-induced hearing loss that has resulted in a dip at your hearing acuity at 4 kHz (the 4-kHz notch). In effect, the tinnitus you are experiencing will be around this frequency and therefore high-pitched. As the loudness of the ventilator is too low to cause damage, it is probably unrelated to your tinnitus.

Noises over 75dB can cause temporary damage (temporary threshold shift), noises over 85dB can cause both temporary and permanent damage (permanent threshold shift). The size of the permanent damage depends on the intensity of the noise, the duration, and many other parameters e.g. genetics, antioxidants, time between two exposures, etc... For example daily 8h of 80dB is considered safe, while daily 8h of 85dB or 20mins of 100dB is considered unsafe. Tinnitus is a sign of hearing loss, so it can be both temporary and permanent.
You should measure the noise levels. For example install Sound Meter to your mobile phone. (The results can depend on the microphone. Most of the mobile phones cannot measure 100dB+ sounds, but I think this is not your case.) For example the ventilator of my computer is 35dB. I agree with Chris Stronks, that it is unlikely that your noisy ventilator caused your tinnitus or has any effects on it.

A TERM PAPER ON NOISE - INDUCED HEARING DAMAGE
2013 - Noise induced hearing loss: Research in central, eastern and south-eastern Europe and newly independent states
Noise-Induced Hearing Loss

Sound is measured in units called decibels. Sounds of less than 75
  decibels, even after long exposure, are unlikely to cause hearing
  loss. However, long or repeated exposure to sounds at or above 85
  decibels can cause hearing loss. The louder the sound, the shorter the
  amount of time it takes for NIHL to happen.

1953 - TINNITUS AURIUM IN NORMALLY HEARING PERSONS
1974 - Hearing loss due to continuous exposure to steady‐state broad‐band noise

The limit of permissible noise exposure, defined as the maximal level
  which did not cause measurable noise‐induced shift in hearing levels
  of workers exposed to it irrespective of exposure years, was shown to
  be NR 75 or 80 dBA.

2012 - 10-Year prospective study of noise exposure and hearing damage among construction workers
2013 - Noise-induced hearing loss in the 21st century: A research and translational update
2014 - Early prognosis of noise-induced hearing loss

At this occasion, a standardised noise exposure was applied (20 min,
  200–500 Hz, 100 dBA) and the TTS at 4 kHz was determined during at
  least 10 min after exposure.

1989 - Noise level, inner hair cell damage, audiometric features, and equal‐energy hypothesis

According to new studies continuous exposure to low dB (65-70) sound (which don't damage inner hair cells) can cause neural changes in sound processing. Constant noise can cause annoyance, concentration disturbance, etc... as well.

2013 - Effects of passive, moderate-level sound exposure on the mature auditory cortex: spectral edges, spectrotemporal density, and real-world noise.
2014 - Is the din really harmless? Long-term effects of non-traumatic noise on the adult auditory system

People are increasingly being exposed to environmental noise from
  traffic, media and other sources that falls within and outside legal
  limits. Although such environmental noise is known to cause stress in
  the auditory system, it is still generally considered to be harmless.
  This complacency may be misplaced: even in the absence of cochlear
  damage, new findings suggest that environmental noise may
  progressively degrade hearing through alterations in the way sound is
  represented in the adult auditory cortex.

2012 - Effects of repeated "benign" noise exposures in young CBA mice: shedding light on age-related hearing loss.
2012 - Environmental noise exposure degrades normal listening processes.

Here we show that exposing adult rats to structured noise at a sound
  pressure level of 65 dB, which is markedly below the broadly accepted
  safety level standard, results in behavioural impairments and
  substantially impairs the function of the auditory cortex. The strong
  deterioration in cortical processing of acoustic inputs is independent
  of the modulation rates of structured noises. Almost equally strong
  effects result from 10-h daily versus 24-h daily exposure regimens.
  These results indicate that there can be substantial negative
  consequences for the auditory system documented at the cortical level,
  attributable to environmental exposure to structured noises delivered
  under conditions that do not directly impact hearing sensitivity.
  These noises are deemed to be 'safe' and are often present in modern
  human environments.

2013 - Noise and health in vulnerable groups: A review

A cross-sectional study in Nigeria [36] among children frequenting a
  school near a major road (noise range: 68-85 dBA) found at least some
  annoyance and concentration disturbance in 70% of the children.
  Fatigue and lack of concentration came forward as the most prevalent
  noise-related health problems.

I am a Noise Engineer and an Air-conditioning (Mechanical) Engineer, and it is my job to understand the effects of noise to our hearing capability.  To start with an analogy, can you smell yourself on your pillow that you used for a long time (say 3 months)?  You cannot, but a visitor who just borrowed your pillow for a night can smell it.
Now to answer the question directly, a "prolonged and constant" exposure to a low level noise, even less than 30 dBA (whisper), can cause hearing loss.  Specific study showed that exposure to 40 dBA on specific frequency for 3 months will cause a hearing loss on that frequency.  Notorious about this common occupational risk are those working in an improperly designed air handling system, those living/working a 2 km radius from a Wind Turbine, those living within a 1.5 km from a sub-station transformer, and many more.
What causes hearing loss is not the sound(pressure/level) itself, but the SOUND POWER.  Power is a product of sound level/pressure/energy and TIME!  A Firecracker is an explosion that has very high sound energy but short duration.  A wind turbine sound has very low  sound energy but very long duration.  In effect, the product or result is the same.
I hope this has answered directly the question and put the issue to rest.

Can you please provide some references to support your answer (preferably research articles)? It could be your own research too but should be published in a peer-reviewed journal.


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Why did many odd-toed ungulates become extinct?
There were a lot of odd-toed ungulate animals in the ancient times but now just few of them survived. What is the reason for that?

I edited the question somewhat. You need to provide some more details such as how many/what fraction of odd-toed ungulates got extinct. Compare it with other group such as even-toes ungulates. Because a lot of species perish during selection event. When saying a lot of group-A organisms perished you should mention with respect to what?

there are two suborder under perissodactyla that are still suvival, Hippomorpha and Ceratomorpha. many perissodactyla species become extinct may bacause the member of perissodactyla animals have sample stomach, compared with artiodactyla, so after the plant change on the earth, they cannot adapt it. and also hinting was one part of reason.
http://en.wikipedia.org/wiki/Odd-toed_ungulate

If you downvote an answer (or question for that matter) please leave a comment with an explanation. Users cannot improve their posts without some feedback.

@user137 I am not downvoting but I have to admit that the answer is grammatically wrong, badly linked and hard to understand


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Do human cells contain only one copy of the genome?
Does each cell contain only a single copy of its genome? Or are there ever 'extra' copies present.
Reason behind question: Wondering whether gene mutations could be corrected by referencing a 'backup copy'.. If such a thing exists..

As a quick answer, yes, most human cells carry 2 copies of the genome and are known as diploid cells. One copy comes from each of your parents, so they aren't identical, but usually pretty close. Sperm and egg cells only carry one copy of the genome and are known as haploid. During fertilization the 2 cells merge their copies and make a diploid zygote. At the chromosomal level, humans have 23 chromosomes, so a diploid cell has 2 copies of each so a total of 46.
As far as repairing damaged DNA, using one chromosome to repair its damaged counterpart is known as Homologous Recombination.

except the sex chromosomes in males of course

Fascinating related video: Why Women Are Stripey

And individual's genome includes both sets of chromosomes and mitochondrial DNA. So while most human cells have two full sets of 23 chromosomes and they are diploid, that is just a single copy of the genome.

Diploid cells contain two copies of the genome. Additionally, each copy of the genome can have multiple copies of certain genes. Which can provide a level of protective redundancy.
However, there are a number of potential problems with having multiple copies of portions of the genome such as trisomy disorders (e.g. Down Syndrome). Which is why therapy like you describe is still highly experimental.

An aside that doesn't warrant its own answer: chromosomes not splitting up correctly on division (hence one daughter cell having an extra chromosome the other lacks) doesn't only happen in germ cells but can happen on any cell dvision. While incorrect division of germ cells is usually deadly (except e.g. the already mentioned Down Syndrome), this is not always the case with [somatic cells] (http://en.wikipedia.org/wiki/Mosaic_%28genetics%29).

Addition to other answers.
Usually a human cell is diploid. Sometimes there might be extra copies of a chromosome and this phenomenon is called aneuploidy (Downs Syndrome, Klinefelter's syndrome etc). This always has deleterious effects because of changes in stoichiometries of different gene products (dosage effect).
Some other organisms also tolerate polyploidy (more than two copies of the entire genome) — salamanders and a lizard whose name I can't remember right now.
Would an extra copy help in providing a functional gene when the other copy is mutated?
Yes and it is the case with all recessive mutations. The effect of loss of function is not seen because the other allele is providing a functional copy (sometimes the dosage is reduced and it affects the system in subtle ways).
However, it the mutation is dominant then extra copies won't help much. For example, a mutation that leads to the formation of a toxic or hyperactive protein (gain of function), then extra copies may at best reduce the overall relative concentration of the bad allele but cannot eliminate its ill effects.

Some of the organisms on this list have really high chromosome numbers. I can't find a reference right now, but I've heard of plants with something like 8 copies of each chromosome, must make recessive alleles really hard to express.

Yes.. many plants including wheat and maize\

To address the "reason behind the question" - no, this doesn't work as you seem to assume it does. It is the whole point of sexual reproduction to have two slightly different copies of the genome. Mutations are not "corrected" within an organism, because they are not considered a bad thing per se. Mutations are "corrected" across generations, in the sense that maladaptive mutations are selected out of the gene pool, because their carriers don't manage to reproduce well.
If there were a mechanism in the cell which would decide that "this copy of the genome is 'correct', this is 'incorrect', I will replace all differing places in the 'incorrect' copy with the information from the 'correct' copy", evolution would never have happened.
An individual has two genome copies, and each of them gets transcribed from. If one of them contains a mutation with negative effects, then it's bad luck for the individual. The purpose of the two genome copies is to increase genetic variability, not to reduce it.

Most of the above answers are incorrect.
The definition of the genome is all of the encoding genetic material. An individual human genome includes two full sets of 23 chromosomes as well as mitochondrial DNA. There is one copy of this genome in most human cells. A few exceptions:

Red blood cells don't have nucleuses and have no chromosomes. They don't have a copy of the genome.
Human sperm cells have only one set of 23 chromosomes. This is not the complete genome of the individual.
Despite comments above, human egg cells have a full two sets of chromosomes until ovulation. The fertilized zygote gets one set of chromosomes from an egg cell and one set from a sperm cell. However, the actual egg cell in the ovaries has a full two sets of chromosomes which don't all get transferred to the zygote.
There is genetic variation between cells due to damage and copying mistakes.
Some living humans are chimeric and are often unaware of this. They are individuals formed from distinct egg/sperm combinations. That adds extra complexity to this answer.

Thank you! This has been driving me nuts! The amount of imprecision in a science that requires precision is astonishing. I see books say that we have 'two copies' of our genome in most cells. No we don't. We have one copy of our genome, consisting of two sets of chromosomes. And the two sets of chromosomes that we do have are different not copies!


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Which virus capsids consist of only one type of capsid protein?
The Tobacco Mosaic Virus (TMV) capsid consists of many copies of one protein (http://www.rcsb.org/pdb/101/motm.do?momID=109).
Which other viral capsids consist of only one kind of coat protein?
Does each copy of the protein in these also have the same tertiary structure?

Interestingly, the fact that viruses might be made up of repeating subunits was a hypothesis by the famous Watson and Crick in 1956.
A useful resource for this is the Viral Zone website maintained at by the ExPASy bioinformatics system. It contains an easily browsable and human interpretable list of viral families and their characteristics. In particular, you can "browse by virion" which will show you different structural classifications of viruses; make sure to look at all the different genetic classes of viruses (single-strand RNA, double-strand RNA, DNA, etc).
From my preliminary investigation, it appears that many capsids are composed of only a single subunit; in addition to TMV, some other examples I found are the totiviridae family of viruses which infect single-celled eukaryotes such as Giardia lamblia, the human-infecting astroviridae and calciviridae families, and (as far as I can tell) the Heptatitis B virus. It also appears that Dengue virus has a single capsid protein.
As for the tertiary structure of capsid subunits, you might find this review of interest. Basically, due to symmetries in the shape of icosahedra (or helices or other geometric shapes adopted by capsids), you can argue that the structure of subunits in certain symmetrical parts of the capsid has to be the same (because they are copies of the same protein and, by positional symmetry, they have to be experiencing the same forces). When there are asymmetries in the structure of the icosahedron, then it is often hypothesized that there exists a state of "quasi-equivalence;" that is, the deviation from symmetry is small enough that the tertiary structure of each subunit is not affected very much. The review goes into these points in much greater detail.


text:
The suspended cat clavicle
I know the clavicle of the cat floats freely as opposed to be attached as in humans. This is supposed to allow them to be able to squeeze through spaces, according to a quick google search. But how does that allow them to move through tight spaces in comparison with humans?

Based on what I learned from my comp vert anatomy class, the clavicle does not articulate with other skeletal elements, thus allowing the scapulae to retract further along with the forelimbs

Can you add a reference to your answer?


text:
Incestual Reproduction in Animals
I'm quite curious on how animals view incestual pairings. Given there are enough mates around, i have quite observed that most females (subjects are dogs, cats, pigeons and chickens) would go choose another mate that is not a direct family member (parent, sibling, offspring). How does this work? Is it instinct to not favor family members or does it still revolve around who's the fittest mate?

Is your observation borne out in any studies? It's hard to explain how something works when one is unsure if that is true to begin with. For example, if I said, "I've observed that when I mix yellow and blue, I get orange. How does that work?" I had a farm, with lots of different animals and dogs and cats. If there was an animal in heat, the males of the species didn't seem to be hesitant in my experience. There is evidence that males like to cat around, but I don't know that this prevents him from going after a relative as well.

No it's not. Just a random observation on our domestic animals. True. Males would not mind relatives but most females choose those who are not directly related. Came here to read about specific studies about this and get enlightened.

Since inbreeding can lead to greater chances of genetic abnormalities, it seems reasonable that individuals who avoid it would be selected for in the long run but I don't know of any studies on this.

Interesting. Thought there would be tons about it. Found this one reference saying they actually rely on to avoid similar scent. But then read on few other sites saying this behavior greatly depends on the animal's social structure. http://www.thenakedscientists.com/HTML/questions/question/2908/

@anongoodnurse It's standard practice on farms to have a small number of bulls or boars or whatever breeding with all the females for several years, inbreeding is inevitable in this situation. Our own farm had 1 bull for about 10 years before we bought a second bull, but kept the first bull for another 5 years, so there was a lot of opportunity for inbreeding.

Anecdotally I have never observed a preference in lab mice, but we have never made a detailed study of it. Males do not seem to favor non-incestuous over incestuous breeding. Though inbreeding does tend to produce smaller litter sizes over generations and inbred strains of lab mice do tend to be less hearty. Though lab mice are a bit removed from the situation in the wild.

edited my question to be female focused. right, males would not hinder kin-breeding but observation seems that the females avoid it as much as possible.


text:
Safe level of chlorine in water
Chlorine is usually mixed in water to make it safe for consumption. What is a safe quantity of chlorine that can be consumed? What are the side effects of chlorine and does this include hair loss? What are some common chemicals utilized for water purification? Thank you.

What has this got to do with governments?

You are asking many questions here. Q1 is in any case off-topic. Question 5 is too broad.

Chlorine is a reactive substance and an oxidizing agent. It can cause damage to surfaces exposed to it such as eyes, skin etc but it cannot penetrate deeper. Chlorine can damage your hair by oxidation — hair becomes rough and brittle. This is not same as hair loss — chlorine doesn't cause hair to fall out because it cannot penetrate to the follicles. See here
EPA has set maximum residual disinfectant level for chlorine (as Cl2 and other chlorinating agents such as chloramine [NH2Cl] and chlorine dioxide [Cl2O]) beyond which it is considered unsafe.
Chloramine       :  4.0 mg/L or 4 ppm
Chlorine         :  4.0 mg/L or 4 ppm
Chlorine Dioxide :  0.8 mg/L or 800 ppb

thanks for the answer, I mentioned "govt", as different countries have different standards.


text:
What are some difficulties animals had to overcome to reproduce on land?
This is for AP Biology, but the assigned textbook chapter doesn't contain any information about the question.

What are some difficulties animals had to overcome to reproduce on land?

Some disadvantages I brainstormed are

the formation of bones—need for vertical structure and support against gravity (?)
development of lungs

Are there any more?
Thanks,

Are you asking about specifically reproduction or land-survival in general?

Are you thinking of vertebrates specifically? Or animals more generally (including insects, mollusks, etc.)?

Just reproduction. Hm, no really specifics—any animals.

I would have thought finding a way to get away from spraying a bunch of eggs on the water bottom, and then spraying them with a bunch of sperm and hoping for the best would have been the initial problem. Sea creatures that carry the developed eggs around would have been one approach (sea horse does that?)  Impregnating females to carry around eggs would have another approach (reptiles, then snakes on land for example). Eventually leading to live birth, and the mammals that returned to the sea? (dolphins, whales).

The disadvantages you mention have not much to do with reproduction, but with locomotion and oxygen absorption.
Difficulties to reproduce on land are the fact that aquatic egg-producing creatures typically lay soft eggs with porous shells to promote exchange of water and waste products with the surrounding water. Water is essential for growth as a typical creature consists for some 70% of water. Soft-shelled porous eggs when laid on on land dry out very quickly and are prone to predation.
The main adaptation to reproduce on land instead of water has been the development of the amnion. The amnion is basically a membrane filled with water (the amniotic sac) in which the embryo is immersed during development. Hence, you could argue that the transition to land in terms of embryonic development has never taken place, as the embryos develop in a protected aqueous environment contained within the amnion! The early amniotes laid eggs on land where the embryos develop, while the later ones such as humans carry their embryos/fetuses around. But early as well as late amniotes are characterized by a developing embryo immersed in a watery environment contained in the amnion. Other structures that aided the transition to land were eggs with hard shells, and the allantois. A hard outer shell in amniotes that lay their eggs on land  helps to protect them against drying out, the harsh terrestrial environment and predators. The allantois helps to exchange and store waste products produced by the embryo, a structure not needed when eggs are immersed in water and waste products can diffuse freely through a weak and porous shell.


text:
What is possibly wrong in my gel electrophoresis when I didn't see bands of DNA ladder on gel?
What was possibly wrong in my gel electrophoresis when I didn't see bands of DNA ladder, and genomic DNA sample on gel ? I could see bands of genomic PCR and RNA solution.
Edit
Thank you all of guys for sharing your opinions. From some opinions, I found out the possible error that my genomic DNA didn't show up because it was not pure (I forgot the detail that our group used a sample of DNA which was extracted from a previous lab and we didn't obtain an expected ratio for the purity of DNA. Then, we also used the impure DNA sample to do PCR, and finally used the amplified DNA for gel electrophoresis lab). However, the reason for DNA ladder didn't show up I'm not sure. I just can suppose that my groupmate who handled with DNA ladder solution possibly contaminated it.

Can you tell us how you are visualizing the gel? The answer probably revolves around the way the gel and samples are prepped and imaged.

Perhaps your ladder has gone off!

Can you show an image?

I observed it under a UV-spectrophotometer. Actually, the bands which I observed was RNA/cDNA RT-PCR product, genomic PCR product, and RNA solution, but the bands of genomic DNA sample and DNA ladder didn't show up. I set the voltage to 120 and allow to run for 30 mins which worked for my classmate.

This picture is still not very clear. Don't you have a gel-doc in your lab?

I know the image is not good. My groupmate took it.

So that isn't your ladder on the far left side of the gel?  How about some lane labels.

No, it's just a ruler on the frame of the mold. Acctually, I don't have any bands of DNA ladder and my teacher also suppose so.

This question appears to be off-topic because it does not provide sufficient details required for a precise answer. Questions related to experiment troubleshooting should provide all necessary details about the experiment.

I'm not talking about the ruler.  I'm talking about what's fluorescing pink down on lane 1, starting from the left.  That looks like poorly resolved and partially degraded ladder to me.  What was your gel composition?

Just to help you with future gels, take the gel out of the plastic and put it right on the glass. The plastic can absorb some of the UV and reduce the intensity in your dye, which I'm assuming is ethidium because it's pink. Also, are you using lithium borate buffer with orange G loading buffer? The voltage and time you mention are consistent with that, and your dye front is yellow, but you have a second dark blue dye front near the top. But we shouldn't have to guess at your experimental details.

Possibly You don't mix ladder containing microtube by Sampler. You should slowly Fill and emptying Sampler for several times when pick it for use, mix it well, but do it without creating a bubble.one more thing, check your ladder by "NanoDrop"

Do you think a sample of DNA which was not pure can influence to my result? Could you explain more why creating a bubble can cause a bad result, please?

@Kim well, there are number of reason in each part of protocols lead to make bad results so each idea that friends have mentioned are also considerable and having Inappropriate sample is one of them. creating a bubble can cause a bad result because When you use small amount of Ladder so if bubble will be taken as samples, your measurements will be very low and inefficient. I propose check process of preparation of Ladder work.

@Kim can you please check your ladder by nanodrup?and compare result for each of DNA and RNA and proteins?

I'm afraid I can't. You know, we just could follow a protocol which was given to us. I was doing the experiment for a class at college level. What is nanodrup?

@Kim For more information about nanodrup please visit this and this links


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Alternatives to commercially available flow cytometric analysis software for use in cell cycle analysis?
I know that many labs use either FlowJo or FCS Express to plot and analyze their flow data. These seem like the two standards for most labs (and I have used FlowJo before). However, my current funding does not cover software licenses and I'm not keen to pay $500-2000 out-of-pocket for a license.
Are there alternatives that approach the quality of FlowJo/FCS Express but are open-source/free with an academic license? I'm looking for an approach which will allow me to fit G1/S/G2-M curves to my data.

Meta-question on Meta: http://meta.biology.stackexchange.com/questions/743/is-my-flow-cytometry-software-question-on-topic

Excel would do perfectly fine :)
there are several plotting tools- R and Matlab have good plot tools. Get the text file out and plot anywhere you like. $500 is too much for that; just ridiculous. What you must know is how to analyze and what different parameters are— that you in any case must; you cant depend on a black box.

Sounds like you should look into Bioconductor's flow suite.  I actually really like doing flow analysis in R, but it takes some practice and getting used to.
The biggest problem you will run into (in my opinion) is gating.  It's not easy to setup a GUI point and click gate.  Rather, you'll be more forced and inclined to set limits with algorithms or hard value limits.
I found .Net Bio to be fun, but not nearly as powerful as Bioconductor.
Meta note, couldn't think of a less opinion oriented way to answer other than just to say "It can be done in R utilizing Bioconductor."  If this is still off, I'm fine with deletion.

I created a free flow cytometry tool that works on any device https://www.redmatterapp.com/
The benefits of this tool is that it works on any device and analysis can be shared via a URL.

Hi Mark. Instead of simply posting a link to your tool, please provide some context and perhaps screen shots. Your answer should be able to stand on its own as being useful/informative without the need to visit other sites. A short one sentence answer with a link is likely to be deleted. Thanks.


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Is excessive hydration a risk factor for cancer in humans?
I was reading a book on radiation biology, and the book describes the process of "indirect action", where radiation can first ionize a water molecule forming a free radical, which then may interact with important cellular molecules, such as DNA.  This contrasts with "direct action" which involves direct ionization of a key cellular molecule.
The book states that as hydration increases, the probability of indirect action occurring increases.  Given that indirect action normally predominates over direct action in cells, could this mean that over-hydration could be a risk factor for developing cancer in humans? Has there been any research into this?
In addition, would larger humans, who obviously have a larger bodily water content, have an increased risk of developing cancer compared with smaller humans?

What do you mean by over-hydration? Humans consist to a high percentage of water - it is present in every cell and necessary for out biochemical reaction, so there is already plenty of water present.

@Chris, I don't mean any strict definition of "over-hydration".  If a human is dehydrated, the intracellar water volume will decrease, and if a human has renal impairment leading to anuria, it is likely intracellular water volume will increase.  So by overhydration I simply mean more intracellular water than otherwise, that may result from increased water intake, or decreased water excretion.

In the most technical sense, yes. In a practical sense, no. Average background radiation dose from food and water sources is ~.3 mSv according to the UN. Given that it takes 1 full Sv to increase cancer risk by ~5-6%, it seems unlikely that, under normal conditions, variability in consumption of water will change risk in a significant fashion.
Now, when dealing with highly contaminated water, there may be a more exaggerated effects, scaling with an increased concentration of radioactive particles per unit of water. Of course, in highly radioactive situations the risk of radiation poisoning may be a more immediate worry.


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Time for rigor mortis to set in
Rigor mortis sets in due to non-functional "ATP powered calcium pumps" as a result of which the calcium ions stream out & the muscles remain in a suspended animation state.
But, it's a frequent observation (as can be seen from a coroner's report) that the time for rigor mortis to set in depends on external temperature, like it's earlier in summer, but late during winter.
So why this fluctuation?
Wikipedia has got an answer, but it's too brief.

When conditions are warm, the onset and pace of rigor mortis are sped
  up by providing a conducive environment for the metabolic processes
  that cause decay. Low temperatures, however, slow them down.
  Therefore, for a person who dies outside in frozen conditions rigor
  mortis may last several days more than normal.

@ChrisStronks , look up the highlighted text...

ATP is necessary to relax muscles. Perhaps depeletion of ATP is quicker at higher temperatures as any chemical reaction speeds up by about a factor of 2 (Q10). What is an ATP pump by the way? If it exists it is not involved in rigor mortis

I meant ATP-powered calcium pumps or simply calcium ATP-ase...

Small point of clarification, are you asking why most biological process slow down at lower temperatures, including the process of decay?  That is the essential point here.  You're going to get slower onset and longer duration simply because you're going to get a lot less biochemical turnover and vibration (in the muscle as well as everywhere else).  Fun fact: frozen stiff bodies, if done quick enough, might not develop rigor at all until thawed.

what is the question here? you already mentioned in the question the effect of temperature. For a more detailed report see this


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Why do humans have irregular teeth and impacting wisdom teeth?
Imagine that horses, dogs, bears, and gorillas had teeth as unreliable as humans do, The interruption in behaviour and stress brought by teeth would cause them to be more prone to sinus infections, jaw abscesses, and general poor performance.
The stress from cavities and wisdom teeth growing sideways would affect their survival rates.
Humans have evolved slow maturation times, including teeth, have shortened jaws with compressed teeth, and errored, unvariable, DNA from inbreeding after near extinction 100k years ago (lake toba caldera) which makes us biologically quirky and unreliable.
Why does our jaw have to be so short that we could live with impacting wisdom teeth? because it places strain on the neck to have a long jaw?
Why didnt face infections and tooth misalignment cause humans to select each other strongly with straight teeth?
Are wonky teeth a feature of cold climates, where people dont have so much fruit, and in hot countries, ethnicities have straigher teeth?

Teeth first:
The vast majority of people have no problems with their wisdom teeth, whether they emerge or not. Impacted wisdom teeth are very common and are usually painless. They do, however, sometimes mess around with other teeth and throw off our bites (which will always readjust, not necessarily in a cosmetically pleasing manner, but the bite will adjust). Today, because we value straight teeth, impacted wisdom teeth are often removed prophyllactically, even if we have no proof that it/they will cause any problems.
Since impacted wisdom teeth are not evident until well after reproductive ability is attained, there is no reason to believe that malocclusion from wisdom teeth should be evolutionarily selected against. If problem teeth are so bad as to cause disability for an individual, that individual is removed from the gene pool.
Given two equivalent males, there's no reason not to entertain the notion that a female did not choose the one with better occlusion. So, it is theoretically possible that what we have now is an improvement over what was the state of our occlusions long ago. But there is rarely only one reason for two individuals to choose each other as partners, so... the teeth are relatively unimportant evolutionarily.
Or, if impacted wisdom teeth hurt enough to interfere with reproduction ("Not tonight, Og, I have a killer toothache.") the individuals who don't reproduce because of it will be dropped from the gene pool.
There may have been selection against wisdom teeth, because there are populations who have a lower incidence of third molars.
80% of all people will have problems with their backs at some point in their lifetime, which is a direct result of bipedalism in humans. You might ask why we became bipedal with that painful trade off. But bipedalism gave us some distinct advantages in survival. So did the expansion of our brains. The greater advantage has precedence in evolution.
Impacted tooth
Ancient Mutation Explains Missing Wisdom Teeth


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What are parental antagonism & parental conflict?
I've been reading the chapter by Haig et al in The Genetics and Biology of Sexual Conflict. I think this chapter has them quite unclearly defined. Could anyone describe these two phenomenon more clearly than the chapter does? Real or hypothetical examples would be good to give clarification, and clarification of how they are distinct from sexual conflict and antagonism.

"Parental Conflict will refer to phenotypic interactions in which
  matrigenes and patrigenes prefer different outcomes"
"Parental Antagonism occurs when an allele has a relative advantage
  when inherited from one sex but a relative disadvantage when inherited
  from the other."

Do you know about genomic imprinting? This seems very linked to your question.

You may inherit a gene, which is actually detrimental to your (most efficient) functioning and hence has a cost (eg. gene for being small when food is available from tall trees). On the other hand, you may inherit a gene which has a benefit for you (gene for being tall with food available from tall trees).
Sexual Antagonism:

What’s good for the goose may not be good for the gander. Thistwist on
  an old proverb captures the notion of sexual antagonism.Traits that
  confer high fitness on geese (females) may confer lowfitness on
  ganders (males), and vice versa.

In sexually dimorphic species (like all common complex life), the evolution of males is usually decoupled from females. This is not as bad as it seems, as females and males may have different patterns of selection, different phenotypes of mutations all at the same time dodging pleiotropic effects. Hence mutations benefiting one sex will sometimes be deleterious to the other (i.e. their fitness effects are ‘sexually antagonistic’)
Sexual Conflict:
Males and females have divergent interests in reproduction that are rooted in anisogamy and lead to distinct roles, due to sexual antagonism. Sexual conflict occurs between the same or different genes,  when there are different optima for a trait expressed in both sexes (intralocus conflict) or when there is conflict over the outcome of a male–female interaction (interlocus conflict).
Intralocus sexual conflicts are potentially very common. Researchers have found a strong positive genetic correlation between male and female fitness at the larval stage in the fruit fly (when interests of the males and females are essentially the same -> survive and grow), but a strong negative genetic correlation between adult male and female reproductive success (when the sexes are expected to have different genetic interests). This is possibly due to sexual antagonism.
Interlocus conflicts occur when there is conflict over the outcome of male–female interactions, so that the optimal outcome is different for the two sexes,as occurs in yellow dung fly mating behaviour. In a rare instance, wikipedia does a good job of explaining the example:

In the yellow dung fly Scathophaga stercoraria, females can be injured
  in the battles between males suitors. Males are selected to evolve
  traits for competitive ability that would increase their reproductive
  success, but females would evolve a set of antagonistic adaptations to
  reduce their chances of being injured in battles between the males.
  Therefore, there is an interlocus sexual conflict in males and females
  that could possibly lead to an "unresolvable evolutionary chase" when
  a novel trait in males increases their competitive ability while
  harming the females

[5,6]
.
Parental Antagonism:
An allele in a gene is said to be parentally antagonistic if it has an inclusive fitness benefit when derived from one parent (say the mother), but an fitness cost when derived from the other parent (in this case the father)
There are many different theories out there, but the gist of it is essentially some process creating an asymmetry between the genes that you inherit from your father and mother (patriGENIC and matriGENIC), that causes differential expression of alleles (silencing the other copy) [2]
Parental Conflict:

When parent-offspring relations in sexually reproducing species are
  viewed from the standpoint of the offspring as well as the parent,
  conflict is seen to be an expected feature of such relations. In
  particular, parent and offspring are expected to disagree over how
  long the period of parental investment should last, over the amount of
  parental investment that should be given, and over the altruistic and
  egoistic tendencies of the offspring as these tendencies affect other
  relatives. In addition, under certain conditions parents and offspring
  are expected to disagree over the preferred sex of the potential
  offspring. In general, parent-offspring conflict is expected to
  increase during the period of parental care, and offspring are
  expected to employ psychological weapons in order to compete with
  their parents. [7]

Reading:
[1] Haig, David. "Parental antagonism, relatedness asymmetries, and genomic imprinting." Proceedings of the Royal Society of London. Series B: Biological Sciences 264.1388 (1997): 1657-1662.
[2] Patten, M. M., et al. "The evolution of genomic imprinting: theories, predictions and empirical tests." Heredity 113.2 (2014): 119-128.
[3] Patten, Manus M., and David Haig. "Maintenance or loss of genetic variation under sexual and parental antagonism at a sex‐linked locus." Evolution 63.11 (2009): 2888-2895.
[4] Normark, Benjamin B. "Perspective: maternal kin groups and the origins of asymmetric genetic systems—genomic imprinting, haplodiploidy, and parthenogenesis." Evolution 60.4 (2006): 631-642.
[5] Connallon, Tim, and Andrew G. Clark. "Evolutionary inevitability of sexual antagonism." Proceedings of the Royal Society of London B: Biological Sciences 281.1776 (2014): 20132123.
[6] Chapman, Tracey, et al. "Sexual conflict." Trends in Ecology & Evolution 18.1 (2003): 41-47.
[7] Trivers, Robert L. "Parent-offspring conflict." American zoologist 14.1 (1974): 249-264.

This reply may be overly scientific and jargon riddled. If so give me a shout, and I'll try and make it more easier to understand. And also note that I have lifted out paragraphs from papers and stitched them together, and have duly supplied the references for further reading.I did this, because the seminal papers which these ideas have been published in are the best way to learn the same.

No worries on that front - about defend a phd about intralocus sexual conflict! Thanks for the excellent looking answer, I'll give it a proper read tomorrow to see if I get it clear! (Expect either 15 points or a comment looking for clarification tomorrow!)

Just noticed did I just necro this thread from last year...?


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Does methanol fixation deform cultured cells?
I use methanol fixation (@ -20⁰C for 10 minutes) when performing immunofluorescence assays on cultured cells. Generally speaking, this results in very good antibody staining. However, the cells tend to look markedly different than they did under phase contrast microscopy prior to fixation. This has my PI worried about how these images will be received by reviewers.
How does a methanol fixative work, and why does it cause a change in cell morphology? Are there parameters that can be adjusted to mitigate this effect?

Give me one last bit of information, and I will throw up a re-write of why MtOH causes changes in cell morphology, why I really think you should be using acetone, and the unmasking information I already put up.  What are you culturing the cells on, and what are you fixing them on?  Is it a PP chamber slide, trans-well, what?  Direct trouble shooting a specific problem is a cornerstone of SE sites, check out stack overflow if you haven't looked at it already.  If you want a more general answer, be prepared to show what research you have already done to answer the question yourself.

Yes, fixation of almost any kind can have effects on morphology.  When you take a free flowing, protein spiked fat-blob (ie cell membrane), and make it rigid, you are going to get some differences.
A fun visualization of this can be done by wrapping cellophane/shrink wrap around a serological pipette and dipping it in a dry ice and methanol bath.  It's something I show students all the time before getting into histology work.
Back to what you need.  What cells are you using and what are you growing them on?  Have you tried acetone fixation and you know it destroyed your plastic?  The amount of time and concentration needed for acetone fixation is low enough that most modern chamber slides can handle it.  Do you need the membrane to be permeabilized in fixation?
I don't know the main effect you are measuring, but assuming you have good controls, you should be able to see it past the fixation.  The effect in your controls should be similar to your treated groups, unless the treatment is specifically effected by your fixative.
Moving to some more general recommendations.  I think you should reconsider the fixative’s you’ve ruled out, because I am unconfident about their application.  The base source I always recommend students to turn to is the Wiley "Current Protocols in X" book that is relevant to the task at hand.  In this case, I think the most relevant text is Current Protocols in Immunology, and the appropriate unit is 21.4 "Immunohistochemistry."
I think a particularly useful, and relevant to this question if you are concerned with formalin masking, is Table 21.4.3.

That is for human antigens, but the “antigen retrieval” process works for murine cells in most cases.  You are right that you antigen could be blocked by formalin, but the solution is often unmasking as MtOH are often more harsh to morphology.  To support protocol 1:

Formalin or paraformaldehyde fixation cross-links protein, often
  making antigens inaccessible to specific antibodies. The antigen
  retrieval protocol, which combines high temperature with buffers at
  different pH, has been very effective in unmasking antigenic
  determinants which may be masked in fixed tissue or fixed cell
  preparations, particularly determinants within the nucleus or
  cytoplasm (Taylor and Shi, 2013).

My modification of the protocol is:
Sodium citrate buffer: 0.1 M citric acid/0.1 M sodium citrate, pH 6.0

Wash sample on a liner rocker for 5 min w/2x culture volume of d.i. H2O
Place your slides in 1mM citrate buffer in Coplin jars with the lid slightly off
Weigh the jar in final state so you know how much water to add back
Microwave 4-7 min.  You don’t want it to go to a boil, and you need to remember to allow for venting
Weigh the jar again and add back water
Microwave another 4-7 min, again you don’t want a boil
Take out of the oven and allow it to come to room temp by sitting it on the bench.  If you do it too fast you’re going to disrupt the membrane.
After it’s back to room temp, wash 2x PBS+0.05% Tween20 for 10 min each
Try your IHC again, it will probably work now.

It's a surface antigen on endothelium, so I'm trying to leave the membrane as intact and possible. Acetone ruins our culture vessels pretty quickly. How long do you fix for? I am generally against the use of kits. They're too much of a black box (one of the many reasons I dislike the growing role and dubious business practices of some vendors). If you check the MSDS on that life technologies kit, you'll see that the fixation medium is just formaldehyde. Which I have already tried once, but am going to give another go tomorrow.

@Chastain First, you should almost never be using straight formaldehyde on an endothelium. You should be using a buffered formalin, about 10% in concentration. Second what's the tissue source? (Animal/organ)

I will also note that side by side with a buffered formalin and tissues from BALB/c mice, we saw much better preservation with the kit.  Could just be how they are buffering things.  I will post up the MtOH and Acetone protocols I use after my morning meetings.

Thank you. It's murine and isolated from several different organ systems. To be clear, the question is not about tissue section morphology. Morphology of sectioned and stained tissue is fine. This question is specific to cultured cells. Which is one of the reasons that it is so frustrating.

This perhaps could be settled out better over chat.  Histology, fixation, and IHC are things that have to be highly optimized. My staining of primary human lung epithelium was tweaked over several years and labs. I understand you are trying to fix cultured cells. Is it a monolayer or transwell system? From the sound of your last comment, you are co-culturing multiple types of cells (as they are from different tissues). Are they primary or imortalized? I'm trying to get you a solution rather than a general answer on fixation. If you don't want 1, I can write up an in-depth answer on fixation.

I'm new to stack exchange, so I'll have to figure out how to use the chat. To be clear though, and maybe I should edit my original question to reflect this, I am looking for the general principle. I love to chat about my work, but that seems outside the scope of the q & a format here. I want to know 1) if methanol fixation deforms a cell (I think that's been answered as a resounding yes!), 2) how methanol fixation works and why it deforms a cell, and 3) variables, if any, that enhance or mitigate this effect. It's important to me to understand the principle at work here.


text:
Why do people and animals stretch out their bodies and what is causing this behaviour?
I noticed that my cat which is only 6 months old has started stretching its body from time to time. Then I thought that this motion doesn't seem very natural from another cat's viewpoint, so my cat probably didn't try to imitate some other cat all of a sudden and learned it like that. This action must have been caused by something else then. Or at least that's what I think.
Both animals and people stretch their muscles from time to time, but it doesn't seem to be caused by memory of others doing it. So how does this action originate in them?

stretching also occurs in animals that wake up and when yawning.

Stretching is usually accommodated with a yawn in humans & animals. This is because when we are tired & sleepy, our breathing patterns slow down, letting half of the oxygen we normally breath in slow down to a minimum rate. When we wake, our body's suddenly needs to pull in a high amount of oxygen so we can function at full energy levels/ being alert. When we yawn, we pull high volumes of oxygen into the lungs which distribute it throughout our blood stream. When we stretch, this allows the oxygen breath in while yawning to flow throughout the body faster.

Humans and other animals have lots of innate behaviors that are not learned from observation, i.e. behaviors that are hard-wired into our nervous system, and this is one of them. Suckling reflexes in mammals and the Moro reflex is human babies (which we grow out of) are other simple examples.
The stretching behaviours you are referring to are usually labelled pandiculation in humans (defined as involuntary stretching of the soft tissues), and yawning is often considered a special case of this. These kinds of behaviours are also normally related to transition periods between high-low activity in animals (Walusinskie, 2006). In practice, stretching functions as a way to reverse the muscular atonia during REM sleep, and is in this sense a way to restore homeostatic functions (Fraser, 1989; Walusinskie, 2006).
A paper by Rial et al (2010) deals with the evolution of sleep and wakefulness in mammals from our reptile predecessors, and indicates that stretching behaviours might have originated/evolved from post-basking activities, more specifically risk-assessment behaviours, such as:

...risk assessment behaviour (RAB) and consists of the suspension of current behaviour, to be replaced by head dipping movements, eye scanning, rearing and
  adopting stretch attending postures...

There is most likely much more to be said about this, and the paper cited above contains many references that can provide further clarification and evidence. A short comparative discussion of pandiculation is found in Frasier (1989).


text:
Testing monophyly from per site log-likelihoods without optimising branch lengths
How can I obtain per site log-likelihoods for a topology against an alignment without optimising branch lengths? (which software can I use to do this)
Per site log-likelihoods can be used for various tests of whether a topology fits the data in a multiple sequence alignment well using e.g. the Shimodaira-Hasagawa test, the AU test etc.
RAxML, Garli and FastTree and other software packages can calculate per site log-likelihoods given a tree, alignment and substitution model but all will automatically optimise branch lengths first.
I would like to test a tree in which a pair of sequences (A and B) are monophyletic, where in the maximum likelihood topology they are not. My problem is that when I infer a tree with a constraint requiring A and B to be monophyletic, the edge length is set to the minimum within the allowed precision. But having an edge length so close to zero does not make biological sense if the tree is describing a monophyletic clade for A and B: the minimum length of the edge must be equivalent to one substitution or character change, else A and B are in a polytomy containing clade with other sequences which is not the biological scenario I'd like to test (in that case there would be ambiguity regarding the relationship of A and B to other groups emerging from that polytomy).
So . . . I'd like to edit my constrained tree and increase the edge length to the A and B clade to the minimum one substitution length, then perform the AU test against the per site log likelihoods for that topology. But the above software optimises the edge lengths, resetting the edge length to A and B to effectively 0!
thanks

If you have the budget for it, I highly recommend Geneious for topology work.  It was a real saver for me on an epi paper last year.
Anyway, they allow for testing per-log likelihood without adjusting edge length.  If you want to throw up some dummy data somewhere I can throw up an example.
I have no connection or stake with the company, just happy with it.

It turns out the tests I mentioned (SH, AU) are strictly tests of topology, not branch length. So choosing arbitrary branch lengths as I proposed would bias the test (according to Prof Alexandros Stamatakis; I'm assuming choosing an arbitrary topology does not cause a similar bias, because that is what the test is designed to assess). Thanks for answering the question though.

Yep, that's why I mentioned without "adjusting" or scaling edge length.  I don't think you would ever want assign an arbitrary branch length, or at least I can't think of a reason to.

Because a bunch of adjacent internal edges of length zero makes a polytomy but a bunch of adjacent internal edges of non-zero length does not make a polytomy - it makes a series clades with events between them that may be inferred from the sequence data in the same way a particular topology can be. These are different biological hypotheses that you might want to test, in the same way assigning arbitrary topologies are different biological hypotheses.


text:
Why we do not use RNAi to control ebola?
As you know using RNAi we are able to prevent gene expression. so why we do not use it to stop viral genes expression?

Because siRNA is very hard to deliver to tissues in an animal. That said, Tekmira is working on an siRNA based ebola therapy called TKM-Ebola. I've seen the preclinical data on monkeys at a conference last May, and it looked pretty good. Will take some time before we know if it works in humans.

Question: How do you deliver ths siRNA into the body without having it degraded? Free nucleic acids outside of cells are an alarm signal for the body.

siRNA can be chemically synthesized, allowing for modifications with 2'F or phosphorothioate backbones that resist RNase activity. I've been trying to deliver mRNA, which is too large to chemically synthesize so we're still trying to figure out how to avoid degradation.

Delivering siRNA in vivo is a difficult prospect, but has been overcome in research environments and several commercial in vivo solutions are on the market see examples from Life Technologies here.
The bigger problems come from potential off-target effects. siRNA tend to be double stranded and both the 'guide' and 'passenger' strand can occasionally target multiple sequences that you did not intend. Additionally, siRNA tend to activate the body's immune system in ways that would inhibit therapy or cause excess inflammation and cell death. See the detailed review here.
In short, it is a good idea, and the current research in the field is working to overcome technical challenges, but we are not there yet.

The siRNAs offered by life technologies look like the siRNA itself. How are the RNAs targeted to specific tissues and passed through cellular membranes?

RNAi therapies can be targeted by nanoparticle encapsulatin. Generally, a nanoparticle containing the siRNA can be conjugated to an antibody for the (cell surface) disease marker. Antibody brings nanoparticle to the diseased cell, cell endocytoses nanoparticle, siRNA is delivered. Alternately, I have delivered RNAi therapy by local injection in in vivo models. However, the Ebola case is much simpler. Ebola infects the endothelial cells and liver. siRNA packaged in lipid nanoparticles will accumulate in the endothelium and liver cells when intravenously injected.


text:
What's the max speed that humans could run?
Assuming humans could use all of their muscle strength at once, with no need of cooling or energy, how fast could we theoretically run?

This is without current human limits of how much muscle you can use at once.

Exactly what do you mean with "limits on how much muscle you can use at once"? An organism is an integrated whole with different functions, and single muscles cannot be viewed in isolation. Also, running at top speed is not something that is achieved instantaneously, but is a process and a sequence of events, and is dependent on e.g. ATP and anaerobic glycogen use during start and acceleration.


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Counting the number of hydrogen bonds of multiple PDB files
I've been trying to figure out a systematic way to count the number of hydrogen bonds for multiple PDB files.
DSSP shows me the total number of hydrogen bonds when I make dssp.exe 1A11.pdb, giving me the total number of 24 (am I correct, ok?)
24 96.0   TOTAL NUMBER OF HYDROGEN BONDS OF TYPE O(I)-->H-N(J)  , SAME NUMBER PER 100 RESIDUES

But when I run this command in R:
> require(biod3d)
> x=dssp(read.pdb("1A11"), full=T)

it doesn't look to have the number of hydrogen bonds. It shows this:
> x$hbonds
     BP1 BP2 NH-O.1   E1 O-HN.1   E2 NH-O.2   E3 O-HN.2   E4 ChainBP1 ChainBP2 Chain1 Chain2 Chain3 Chain4
1-A   NA  NA     NA  0.0      5 -2.1     NA  0.0      4 -0.3     <NA>     <NA>   <NA>      A   <NA>      A
2-A   NA  NA      3 -0.2      6 -1.5      4 -0.2      7 -0.2     <NA>     <NA>      A      A      A      A
3-A   NA  NA      4 -0.2      7 -1.8      5 -0.2      2 -0.2     <NA>     <NA>      A      A      A      A
4-A   NA  NA      1 -0.3      8 -1.5      6 -0.2      7 -0.6     <NA>     <NA>      A      A      A      A
5-A   NA  NA      1 -2.1      9 -1.9      6 -0.2     10 -0.2     <NA>     <NA>      A      A      A      A
6-A   NA  NA      2 -1.5     10 -1.3      1 -0.3      5 -0.2     <NA>     <NA>      A      A      A      A
7-A   NA  NA      3 -1.8     11 -1.3      4 -0.6      5 -0.2     <NA>     <NA>      A      A      A      A
8-A   NA  NA      4 -1.5     12 -1.2      3 -0.2      6 -0.2     <NA>     <NA>      A      A      A      A
9-A   NA  NA      5 -1.9     13 -1.1      4 -0.2      7 -0.2     <NA>     <NA>      A      A      A      A
10-A  NA  NA      6 -1.3     14 -2.3      5 -0.2     13 -0.4     <NA>     <NA>      A      A      A      A
11-A  NA  NA      7 -1.3     15 -1.8     12 -0.2     16 -0.3     <NA>     <NA>      A      A      A      A
12-A  NA  NA      8 -1.2     16 -1.8     13 -0.2     11 -0.2     <NA>     <NA>      A      A      A      A
13-A  NA  NA      9 -1.1     17 -2.4     10 -0.4     18 -0.5     <NA>     <NA>      A      A      A      A
14-A  NA  NA     10 -2.3     18 -1.6     15 -0.2     13 -0.2     <NA>     <NA>      A      A      A      A
15-A  NA  NA     11 -1.8     19 -1.8     17 -0.2     20 -0.5     <NA>     <NA>      A      A      A      A
16-A  NA  NA     12 -1.8     20 -0.8     17 -0.3     14 -0.2     <NA>     <NA>      A      A      A      A
17-A  NA  NA     13 -2.4     21 -1.9     19 -0.2     16 -0.3     <NA>     <NA>      A      A      A      A
18-A  NA  NA     14 -1.6     22 -2.0     13 -0.5     21 -1.0     <NA>     <NA>      A      A      A      A
19-A  NA  NA     15 -1.8     23 -2.0     20 -0.3     24 -0.3     <NA>     <NA>      A      A      A      A
20-A  NA  NA     16 -0.8     24 -1.5     15 -0.5     19 -0.3     <NA>     <NA>      A      A      A      A
21-A  NA  NA     17 -1.9     25 -1.0     18 -1.0     19 -0.2     <NA>     <NA>      A      A      A      A
22-A  NA  NA     18 -2.0     25 -0.3     23 -0.2     20 -0.2     <NA>     <NA>      A      A      A      A
23-A  NA  NA     19 -2.0     22 -0.2     18 -0.3     21 -0.2     <NA>     <NA>      A      A      A      A
24-A  NA  NA     20 -1.5     23 -0.2     19 -0.3     22 -0.2     <NA>     <NA>      A      A      A      A
25-A  NA  NA     21 -1.0     23 -0.2     22 -0.3     24 -0.2     <NA>     <NA>      A      A      A      A

So, my question: Is the total number of hydrogen bonds hidden somewhere in this output or somewhere else (or doesn't exist)?
If I manage to count the number of hydrogen bonds in a single PDB using Bio3D and R, then I can create a loop and iterate over all remainder PDB files.
Thanks for all!

This an initial solution, but can be improved:
out = system2("f:/stride/stride.exe", "f:/stride/1a11.pdb -h", stdout=T)
nh  = strsplit(out[grepl("HBT", out)], "  ")[[1]][2]
print(nh) # Output: 26 (hydrogen bonds)

I compiled an Windows version of Stride and uploaded here:
http://lcrserver.icmc.usp.br/~daniel/bin/stride.exe

I am also interested in this approach. @daniel-bonetti could you make a Linux binary for STRIDE? Thanks.

Apologies, no need, I managed to download and compile it.

The number of hydrogen bonds cannot actually be said from software only inferred. But you could try using STRIDE (http://structure.usc.edu/stride/) which takes the file name with a -h flag to output the number of hydrogen bonds. You could then write a small shell script which would pass in each file and store the data you wanted in whatever format you liked.

It's true! I thought it could exist a direct way to do that :)