text:
Is the fixation rate always equal to the mutation rate for neutral alleles?
Background
A classical result of population genetic is that the rate of fixation of netreual alleles is the mutation rate $\mu$. The reason is that each generation $PN_e\mu$ mutations enter the population, where $P$ is the ploidy number (e.g. 2 for diploids) and $N_e$ is the effective population size. The probability of each neutral mutation to reach fixation is simply its frequency $p$. When the mutation occur $p=\frac{1}{PN_e}$ and therefore the rate of fixation is:
$$\lambda = PN_e\mu \frac{1}{PN_e} = \mu$$
This result s typically very much used in phylogenetic, as assuming a constant mutation rate only, one can estimate the divergence time between two extant lineages.
The above is also explained on wiki>fixation_rate
Question
How robust is the result $\lambda = \mu$?
I understand that the result $\lambda=\mu$ is independent of the effective population size but is it also independent of..

changes in population size?
background selection?
selective sweep?
population structure?
selfing rate?
etc..

It is special case of Wright-Fisher game right ? In that case how it is independent of population size?

What do you mean by Wright-Fisher game? It is independent of $N_e$ (at least for constant population size) as I showed in the background. It is also explained in this wiki article

See Write-Fisher model of genetic drift. And see introduction of these notes.

I know the Wright-Fisher model of genetic drift. We also talk about Wright-Fisher population but I've never heard of Wright-Fisher game.

The answer to your headline question is that no, fixation rate is not always equal to the mutation rate for neutral alleles. For instance:
Fixation rates for neutral alleles are affected by changes in population size, given a constant mutation rate. In general, fixation rates are lower in growing populations (Waxman 2012).
This makes instinctive sense if you consider the single-generation fixation probability of a neutral allele which only exists at all but one copy in the population, i.e., the common allele (A) exists at 2N(t)-1 copies, whereas the less common allele (a) exists at 1 copy. To simplify, let's assume complete random mating. Under negative population growth (say N(t+1) = 0.9N(t)), there will be 0.9*(2N) places that the rare allele could possibly exist at t+1, and it has a 1/(2*N(t)) chance of filling each of them. Under positive population growth (say, N(t+1) = 1.1*N(t)), the rare allele could potentially occupy 1.1*(2N) places at t+1, but still has 1/(2*N(t)) chance of filling each of them. It is clear in this case that A has a reduced generation-wise likelihood of fixation under positive population growth than under negative population growth, simply because the rare allele has an increased chance of doggedly persisting. The finding applies to any allele near fixation.
If I have understood Kim and Stephan (2000) correctly, then overall fixation rates are also reduced by background selection. The main mechanism for this is that background selection purges linked neutral alleles, decreasing overall heterozygosity and thereby reducing the chance that a new, rare allele will become established. The same surely applies to selective sweeps, given linked neutral alleles.

Thank you for your answer +1. I suppose that your answer also suggest that population structure and selfing aren't modifying the result $\lambda=\mu$, right? Is there anything else that you can think about that might affect this result? Thank you!

I didn't mean to imply that population structure and selfing wouldn't modify the λ=μ relationship - I didn't find literature that tested those hypotheses. My instinct is that both structuring and selfing would reduce the fixation rate by reducing population-wide heterozygosity, but I would want to do some more reading (or run some simulations) before I included that in an answer.


text:
What happens after the purification step in Hi-C sequencing?
I am a statistician reading an article on Hi-C, and I am trying to better understand one of the steps in the DNA isolation and sequencing process.
Since I'm a statistician, please try to avoid too much jargon in your answers, and if you must use jargon, please define/explain it.

Specifically, I am confused about the isolation and shearing step.  To explain myself, I will make reference to the following images, labeled 1 through 4.
Image 1)

Image 2)

(source: nature.com)

Image 3)

(source: babraham.ac.uk)

Image 4)

(source: nature.com)

I understand that the DNA is cut up with restriction enzymes, producing a cloud of DNA fragments, some crosslinked and other not. When these pieces are attached with biotin and ligated in a dilute mixture, it is highly likely that these pieces will ligate with themselves, resulting in either; 1) a ring from strands that were NOT crosslinked (as in the third drawing in Image 3 marked "self-ligation"), or 2) figure-eights from strands that ARE crosslinked (as in the fourth drawing in Image 1).
Now, the following is what I find confusing:

The pull-down step draws down the rings containing biotin, but Image 1 and Image 4 make it seem as though only the crosslinked bits are pulled down, and not the solo rings. Don't both have biotin?  And thus would both be drawn into the pulled-down sample?  Or does the pull-down process rely on a molecule having 2 biotins?  If not, can one discern whether a pulled-down piece of DNA is the result of a cross-linked or solo piece of DNA?
Why aren't all of the loose ends of the DNA ligated in Image 2?  Incomplete digestion?  Does this affect the biotin linkage?
My next question.  Assuming that the pull-down process only selects the figure-eights that are crosslinked, then purified (i.e. the cross-linking protein or formaldehyde is removed) forming a ring that is composed of two strands of ligated DNA (as in the upper-right corner of Image 4).  The process then records a genome-wide contact matrix $m_{ij}$, the number of "ligation products" between locus $i$ and locus $j$.  What is a "ligation product"?

Sorry, I know the above is a lot, but I want to understand the nature of the data before I analyze it.  Thank you for your help.

So, after the restriction digestion, the sample consists of DNA fragments with 5' overhangs. These are filled in by Klenow DNA polymerase, adding biotin-dCTP to both ends of each fragment. Then the fragments are ligated under conditions (ie low DNA concentration) such that ligation between non-crosslinked DNA is less likely. This reduced ligation efficiency (which is already lessened by the use of blunt end fragments) means that all crosslinked fragments may not be ligated, which I imagine is what they are showing in Image 2. Any two molecules which become joined by this reaction are called ligation products (ie they are the products of the ligation reaction).
After this step, the sample is treated with T4 DNA polymerase which, as well as having polymerase activity (obviously), also has 3'->5' exonuclease activity. Thus, any free DNA ends which have not been ligated will be trimmed, removing the biotin. After this step, biotin will mostly be present at ligation junctions, and these molecules can be selectively pulled down by the beads. I say mostly because some of these so-called dangling ends will still retain biotin, but these can be distinguished during mapping (see image below).
As for self circles: because they have been ligated, they will contain biotin and be pulled down with the crosslinked DNA. However, since this DNA is from the same genomic locus, they can also be distinguished from valid interacting pairs during mapping:

[source]
Finally, a quick note on the pull-down mechanism. The beads are coated with a protein called streptavidin (or avidin), which just binds to biotin very tightly. Only one biotin need be attached to any molecule (such as DNA) for it to be captured.

Does that answer your questions? Let me know if I can explain something better.

Very helpful, but can tell me what a "ligation product" is?

@Lewkrr, just dissect the word: a ligation product is the product you get after the ligation step in the hic protocol. So basically ligated (glued) pieces of DNA.

@Lewkrr It's in the answer.

@canadianer  I don't understand how glued molecules translates to something informative in the genome-wide contact matrix, with $m_{ij}$ being the number of "ligation products" between locus i and locus j.  If I have two loci, how does the number of glued-DNA-molecules provide me with any information?  I mean, why bother counting them??

@Lewkrr The point of this experiment is to find distant genetic loci that are interacting and have come in close contact. Loci that are close are cross linked and then ligated together. Loci that are distant and are less likely to be ligated (and any ligation will be random). Thus the extent of interaction between two loci is directly proportional to the amount of ligation products formed between them. Does that make sense?

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text:
Is there a known or quantifiable correlation between capsaicin and its effect on the body's metabolism?
I've often heard that spicy foods can speed up your metabolism, I presume, due to the capsaicin.  Though I'm sure this is a minor effect - I doubt eating a pound of jalapenos a day will help me lose weight - has the medical/nutrition community quantified how various levels of capcaicin affect the body's metabolism?

Capsaicin do affect your metabolism. It affects your Capsacin receptors ( scientifically TRPV1 receptors). These receptor starts calcium influx into various types of tissues. In endothelial cells because of this it mimics stress response (McCarty et al 2015). Quoting from McCarty et al,

Clinically, ingestion of capsaicin-or its less stable non-pungent analogue capsiate-has been shown to boost metabolic rate modestly. opical application of capsaicin via patch was found to increase exercise time to ischaemic threshold in patients with angina

Coming to your question, there are scientific studies which suggest that capsaicin helps in maintaining weight by limiting weight regain after weight loss. Not just this, capsaicin has also shown potential in treatment of obesity. However you should remember that it will required specific amount of dose (you can check details in papers I cited ) to help maintaining your weight. Do not eat pound of jalapenos a day :P

Scoville scale is used by legislators to specify the allowed concentrations on pepper spray used by the police.
Although that is most important for excessive concentrations, you'll find more studies using this scale in relation to the effects you look for (for instance: https://scholar.google.com.br/scholar?q=Scoville+scale+metabolism).
The Wikipedia article cited talks about "sensation of heat", and indeed we sweat a lot when we eat strong peppers. But I think that eat the maximum diversity of food is healthier than seek the "best foods" according to the "public opinion" of the season. You should be worried about living healthier, not just losing weight. Seek the former and you'll reach the latter.

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text:
What will happen if the biceps stop contracting and instead triceps contract?
For example if i bend my arm the biceps contract and triceps relax but if I bend my arm and the triceps contract instead of biceps what effect would it have?

your arm wouldn't bend...

I'm voting to close this question as off-topic because this question is too trivial

When your triceps contract your arm straightens out.

This can be termed co-contraction of antagonist muscles, and it can occur in several pathologic processes. It essentially results in a spastic state.
Yelnik et al. describe the state as:

Spastic co-contraction is defined as an "unwanted, excessive, level of
  antagonistic muscle activity during voluntary command on an agonist
  muscle, which is aggravated by tonic stretch in the co-contracting
  muscle" (2, 8). Spastic co-contraction in patients with spastic
  paresis is a descending phenomenon, most probably due to misdirection
  of the supraspinal drive. It may be facilitated by increased recurrent
  inhibition, causing loss of reciprocal inhibition during voluntary
  command (2, 9).

For example, this can occur with perinatal brain damage. See a study by O'Sullivan et al. titled "Abnormal development of biceps brachii phasic stretch reflex and persistence of short latency heteronymous reflexes from biceps to triceps brachii in spastic cerebral palsy."
The state of co-contraction can be produced in healthy individuals as well, and studies on joint biomechanics under these conditions have been done. See Wise et al.


text:
Why did life on Earth develop with two sexes?
If evolution gives us the best adapted organisms for survival of the fittest, why does so many of Earth's organisms require two sexes for reproduction?  Shouldn't this have been bred out of our populations millennia ago?

BTW - I (naively) suggest the tags [tag:evolution], [tag:gender] & [tag:sex], but don't have the rep. to suggest tag edits.

Welcome to Biology.SE. I agree the question is a duplicate and I closed to vote. Note also that your first sentence If evolution gives us the best adapted organisms for survival of the fittest is both wrong and misleading. You might want to have a look at an introductory class to evolutionry biology such as Understanding Evolution.

I don't think this is a duplicate. As I understand it, this Q is asking about why we have sexes and why all organisms dont reproduce asexually (so the costs and benefits of sex), while the other Q is asking why we only have two sexes and not more. This Q has a very weak background though.

If it is not a duplicate then it is unclear for 3 reasons: 1) because we don't if it ha to do with sexual reproduction or the number of genders. 2) because it is unclear why it is especially talking about the earth. 3) Because it is unclear why the OP would expect the two sexes to be bred out of our populations millennia ago. It is also primarily-opinion based because the first sentence is wrong. Finally, the answer (to whatever question the OP is asking) may well ask for writing A LOT given the current OP's knowledge (that we can guess from the post) in evolutionary biology.

I agree with @fileunderwater, it's an entirely different question. And even when we have lots of similar questions, they usually put together so many different interesting answers (because of the scoring logic), that some SHORT AND GOOD answers end up arising. And since SHORT AND GOOD answers are quite rare, I think we should go in the direction of having more repeated questions, instead of less.

Richard Dawkins describes an elegant solution to the puzzle in his memorable Selfish Gene: in the beginning, all gametes were similar, and many sexes could coexist (like in fungus). But when some lineages began to specialize in different strategies (ESSs, Evolutionarily Stable Strategies), with some increasing and other decreasing the size of the gametes, then there was room for two sexes. Probably a third sex would only compete with one of the others, without space for niche drift, and thus one of them would usually become extinct, driving it back to two sexes again.


text:
Does melanin protect humans from gamma radiation?
It is known that radiotrophic fungi use melanin to make use of gamma radiation. It is also known that melanin protects human skin from UV radiation.
Thus I wonder whether melanin protects humans from gamma radiation as well?
Are the black people and tanned white people less vulnerable to gamma radiation?
http://web.archive.org/web/20080424001002/http://www.sciencenews.org/articles/20070526/fob5.asp

Please provide  a reference for the claim in the first sentence. Also just because a simple organism may have developed a novel use for a compound doesn't mean that can be extended to humans. And as gamma radiation penetrates deeper than UV, its effects go beyond the layer of skin that melatonin serves to protect.

http://gtcceis.anl.gov/guide/rad/index.cfm

@AMR the fungi use gamma-ray energy as energy source for growth. The growth in fungi is not because of mutations but because it is such a biological mechanism to utilize energy from environment.

You do not want human cells to get a growth advantage, and no it is not even remotely protective against gamma rays to have extra melanin. You cannot compare the adaptations of a single celled organism to the processes of a complex multicellular organism in that respect.

@AMR it protects from UV, any hint that it would not work against gamma?

Because when you get an X-Ray they cover the unimagined areas with lead shields. Because the firemen of Chernobyl died quick and horrific deaths due to Gamma radiation exposure from Gamma radiation from Cesium-137. Because we use gamma rays to kill cancer cells.

@AMR the Chernobyl radiation during the fire was orders of magnitude greater than what the fungi can utilize (which is some 500 times the norm).

Organisms on Earth DID NOT evolve with a higher than background level of gamma radiation. UV is a far more prevalent form of radiation which life on Earth evolved and adapted to. That it can still cause damage over prolonged exposure just means that modern advances in medicine, sanitation, and nutrition are keeping us around long enough to see the effects of its damage. We have no such evolutionary experience with Gamma radiation. You have a novel, single celled organism that has adapted, that happens all the time, just look at antibiotic resistance. As I said before you cannot draw a parallel

Since it is clear from the source in your question that melanin can absorb energy from gamma rays, yes higher concentrations of it would reduce the energy of gamma rays getting through the skin.  However this would not provide any real relative protection, the gamma rays are still going to go right through your skin and start damaging DNA.
Gamma rays are three orders of magnitude higher frequency and therefore carry much more energy than UV.  Of course there are energy transfer inefficiencies but since the fungus are not growing at even an order of magnitude faster, it's fair to say that melanin is not absorbing all of the energy in a gamma ray.
Since the gamma rays are not fully absorbed by melanin, they will still go through the skin and will still be able to do significant DNA damage.
So yes, but not enough to really matter.
Frequency Differences
http://www.davidterr.com/science-articles/electromagnetic_spectrum.html

Not so fast with this answer! When gamma radiation is absorbed by melanin, the energy is converted into an electrical response via the photoelectric effect. At this stage, the gamma radiation is no more. Provided that the intensity (number of) photons is not sufficient to destroy the melanin molecule, and also assuming a one-to-one mapping between photon interaxction and melanin molecule, for every absorbed photon there will be one or more electrons liberated. In theory, a melanin endowed human being exposed to gamma radiation could use it as an additional source of energy.


text:
Evolution home experiment?
If I were to take bakers yeast and put it in medium of minimal sugar(whatever quantity that would be) and rice(for a source of starch), could the yeast have a "evolutionary leap" and adapt to use the starch in its environment? I remember reading something similar in a report of E.coli bacteria and citrate adaption, under the heading:
 Catching evolution red-handed.
The passages in question are so:

"Every night, the bacteria run out of the sugar glucose and go
  dormant. The following day around noon, a researcher plunges a pipette
  in and sucks up 1% of the culture to inoculate a fresh flask. Those
  faster at gobbling up glucose will send more of their descendants to
  the following day's pipette and, after a few weeks, descendants of the
  fastest one will be the only ones transferred as the mutation 'sweeps'
  to fixation."

Under the heading: The rise of Escherichia erlenmeyeri, (bold emphasis mine).

"One morning, at the turn of generation 33,127 according to the lab's
  log book, a massive increase in turbidity was recorded on the vial
  labelled Ara-3. The sugar-starved bacteria had suddenly 'discovered' a
  vast new source of carbon by importing citrate, a pH buffer that had
  been in the growth media all along, and it sent the population size
  through the roof. "

So if I understand this correctly, there is evolution going on through the differential reproductive success of the bacteria, via their fitness which is affected by the glucose levels?
This "pressure" caused a type of "hopeful monster" in the form of Escherichia erlenmeyeri, the bacteria that could metabolize citrate, in which it didnt have the means to do so before.
So then could I replicate this concept with baker's yeast and starch metabolism and hope for similar results hypothetically? Or am I misunderstanding this?

You might also want to consider going with a molecular biology supplier... I wouldn't think that quality control on baker's yeast would be sufficient to be starting with a single strain, or have a sequenced genome.

Keep in mind that the citrate utilizing strain appeared after over a decade. Also, Escherichia coli could always metabolize citrate, but the citrate transporter that brings it into the cell is only expressed under anaerobic conditions [1]. The strain that evolved to import citrate under aerobic conditions had a duplication of the transporter gene which put it under the control of a different promoter that drives expression under aerobic conditions [2]. Baker's yeast doesn't have amylase or debranching enzyme genes [3], so a similar evolutionary mechanism cannot occur. Developing such enzymes de novo doesn't seem trivial, but perhaps the enzymes involved in glycogen metabolism can be repurposed. The only way to know is to try.

References:

Blount et al., 2008
Blount et al., 2012
Ostergaard et al., 2000


text:
Can anyone please help me identify this plant?
Please help me identify this plant. My aunt had one but it died due to the drought in California. She wants to get a new one but she doesn't know what it's called. The leaves are around two inches and it is seedless, though I'm not sure if it's native in California. Suggestions are welcomed!

Welcome to Biology. Species identification questions are warmly welcomed, but without knowing more details it is impossible to identify this plant. Important things to mention are: 1) Was this an indoor or outdoor plant 2) Was it a native or not 3) Where do you live 4) Did it flower, and if yes, what did the flowers look like 4) How big was it 5) How old was it 6) What was the size of the leaves? ...etc.

Thanks for the edit, but please answer all 5 questions that AliceD asked.

Not sure but looks like Acacia auriculiformis (Mimosaceae) and Eucalyptus sp (Myrtaceae) , both big trees. Provide image of  fresh/ pressed leaves, and a much better description.


text:
Was this snake behaving abnormally?
This morning, I walked out front of my house to find a medium-sized snake balled up on my driveway beneath my motorcycle. I spotted it from my porch so I didn't walk any closer. I believe it was a Texas rat snake.
I've seen a few snakes in my area but none really up close, so I watched it curiously for a few minutes. It seemed to be acting oddly - its head was tightly bent sideways at its "neck," and it was slowly coiling and writhing while opening and closing its mouth. It didn't seem very alert.
Then, a friendly neighborhood cat began batting at the snake's head, and while the snake was not acting aggressively, it did haphazardly snap back in self-defense a couple of times.
I (subjectively) assumed that the snake was injured or otherwise "done for," so I ended up moving it into the street with a long pole and crushing its head with a large rock. I had taken its lack of objection to agitation with the pole as another sign of distress.
I really don't like killing other creatures. In retrospect, maybe I could have handled the situation differently, maybe by capturing the snake and releasing it somewhere else. At the time, for whatever reason it seemed like it was suffering and I felt like I was doing it a favor, as well as potentially saving some local pets from injury.
Moral questions aside, does it sound like this snake was in fact behaving abnormally? Are the actions I described typical of a distressed snake (at least of this species), are there other plausible explanations, or is it unclear? I can elaborate if there are any specific questions.

You shouldn't have killed it. From my point of view, never kill a critter unless it is 100% obvious it is going to die. I killed a pigeon once after it crash-landed into our window. It was crippled and didn't move for a day. We had a cat too and I decided to kill it. In your case it wasn't obvious why the snake behaved the way it did and I would have let it live and relocate it. Others may disagree with me. I vote to close because it is opinion based and an ethical question. +1 because I admire your thoughtfulness.

Thanks @AliceD - I appreciate your point of view. I was hoping to frame the question in a more objective way, so maybe I should downplay the moral uncertainty and update it to something more answerable like "what kind of behavior was this snake exhibiting?"

That sounds like a great edit. if you do so, please ping me @AliceD and I'll remove the vote. Thanks and good luck! Would've loved to see that snake :)

Thanks @AliceD - question updated. Yeah, I really feel bad about it now. It was a beautiful snake. That may be the only non-insect creature I've ever killed, at least intentionally. At least I know to stop and think harder about alternatives next time.

No worries, I slightly edited and formatted the question to make it more information dense.

Not an answer because I can't be sure, but I've seen this behaviour in snakes that have taken a hit from a car etc. It usually means the backbone is injured/broken. I suspect you did the snake a favour.


text:
Can females be recreated from male DNA?
A chromosomal male is XY and a chromosomal female is XX. Now imagine if, one day, this world has only males - is it possible to "recreate" a female by using two X chromosomes from two different males?

Do you want to clone yourself with certain benefits?

Short answer
Technologically yes, but practically no, because there would be no surrogate mother available to bring the artificial XX zygote to term.
Background
Theoretically a cell with two male Xs can be generated, given that it is technically possible to shuttle single chromosomes between cells (Paulis, 2011).
However, assuming that in your future world oocytes are available from oocyte banks and sperm from sperm banks just like they are today, then the artificial combination of two Xs from male cells wouldn't be necessary in the first place, as regular IVF could be used.
Note that in both the chromosome transfer and IVF scenario, a female would still be necessary to implant the zygote. Until artificial wombs become available (they are not), it is impossible to generate females without females.
Reference
- Paulis, Methods Mol Biol (2011); 738: 57-67

So, with artificial womb, we can do that? We can recreate female using two X's from men?

@JesusChrist - Given that we can transfer chromosomes between cells, I can see no reason why not.

so there's even possibility to create a female version of me using only my genetic material?

@JesusChrist - theoretically, yes. However, as far as I know it hasn't been done.

@JesusChrist, and it's probably unwise to do so. Any recessive traits on your X chromosome are, by default, winners - you're just shortening up the generational problems experienced by inbreeding. Caveat: I'm not a biologist, but that's the way I understand it to work.

@JesusChrist Your name is just godly for this question.

I would have used induced pluripotent stem cells to generate sperm and eggs. Since these eggs would likely be either X or Y, 25% of all embryos would be YY and probably nonviable. The remaining 75% would probably be ok. Similar research has already been done in mice.

Note that in birds and some other species with the https://en.wikipedia.org/wiki/ZW_sex-determination_system the reverse is the case--males are ZZ and females are ZW.

@Jason I'm not sure how accurate that actually is.  With the other chromosomes, that would be spot on, but with the X/Y ones, you have all sorts of traits (such as male pattern baldness) that are expressed in men more often than women simply because a man only needs the one chromosome bearing the gene for the trait, which means anything that would be fatal would probably have killed the man in the first place. Caveat: I don't know of any disorders on the X that aren't expressed depending on the Y, but that doesn't mean there aren't any, and if there are, you'd be right.

@soong I think jason was trying to say that if male chromosomes were used to make a female, then both X chromosomes would be identical. If the male donor had x-linked recessive diseases, the resulting female would have those too, because both her X chromosomes would carry the defective gene.

Yes I understand that. However, x-linked recessive diseases are, too the best of my knowledge, always expressed when a man's only x chromosome has it. An example of that is male pattern baldness. Women can have it if both x chromosomes have it. So, any disease on x that is recessive, the man would already have because he has only one x.

Note that not only mammals have XY sexual chromosomes and your answer assumes we are talking about mammals. I assume the OP was thinking of mammals as well so it is fine but it might be worth to add a note


text:
How quantitative is the theory of evolution right now?
We developed complex structures like eyes and brain, whose mechanisms rely on specific species of molecules and relevant chemical reactions. But we did not develop an enhanced night vision, the ability to fly, or a built-in silicon-based integrated circuit.
As I understand, we did not develop the latter set of abilities because they are either not so much needed, cost too much energy to be beneficial, or that they required so many information to be coded into our genome that it would take forever for the mankind to produce sufficient mutations. But could this be quantified? Can we tell if a species will develop a specific character, based on the environment they're in?

By "we", do you mean humans or animals in general?

I don't think so.  You can say, if I throw this fresh water fish into salt water it will have to evolve or die.  You could even say that a population living in a delta where they are exposed to fresh or salt water could possibly develop mechanisms for both.  But you couldn't say with any certainty that they will.  Maybe the species moves further inland as they get better characteristics for fresh water.  I doubt that antibiotic resistance was predicted to occur before we started seeing it in labs.

"But could this be quantified" -- what is "this" in this sentence? What is it that you wonder whether it is quantified or quantifiable? You have to be looking for numbers somewhere, so could you state which numbers you are after? Your last sentence seems less directly related to quantification.

There are some suggestions that evolution is quite predictable, more predictable than many of us think. Richard Dawkins is one proponent. If this is true, there is indeed some elements of predictability in the higher-level results of evolution.

Can we tell if a species will develop a specific character, based on the environment they're in?

This is a major part of what quantitative genetics does. Or more detailedly, quantitative genetics can predict, for a population, changes in a trait given a selection pressure. First of all, for evolution to occur there must be variation in the trait you are making predictions about. Secondly the accuracy of the scale of the predictions matter greatly for the evolutionary model to be tested (eg, "Will body size increase?" vs "Will incisors increase 3mm in 300 generations?").
Several things have to be known to predict the evolution of a given trait:

The number of genetic sites controlling this trait (QTL, or quantitative trait loci). If the all the loci for a trait are known, the nucleotide heterogeneity within the population of those sites can be quantified. The number of genetic loci are important for estimating how often they will change from new mutations.
The effect of each genetic locus on contributing to variation to the trait (additive genetic effects).
The heritability of the genetics controlling this trait, (does the environment contribute to variation in the trait (low heritability) or do genetic differences cause more variation in the trait).
The strength and consistency of selection  (how fit are individuals in that environment along to phenotypic distribution compared to previous generations). Is this trait being selected in isolation, or are other traits which share the same QTL also under selection.
The effective population size.
The rate of migration between this and other populations.

So yes, given the our knowledge of quantitative and population genetic theory, predicting evolution of a given trait is possible. Just as predicting the future is possible with the laws of physics if you know the position of every atom in the universe. It's important to remember that organisms are constellations of 'traits', so predicting the evolution of all traits which make up the individuals within a species could be similar to predicting the futures of several multiverses.

Clarification on the question
The question is a little unclear and I will try to interpret it and answer it. I hope I won't fail to see your goal.
Quantitative vs predictive
There is a big difference between quantitative and predictive. To understand the difference you might want to ask the question on Philosophy.SE.
Quantified vs quantifiable
As @chelonian said in the comments, if you are asking Is evolution quantitative, then you would need to say whether you meant quantified or quantifiable. Almost everything in evolutionary biology (just like in other sciences) is quantifiable but most of it is not quantified as it takes a lot of money and time to do so.
What I think you are trying to ask
Paying attention to the question in your post Can we tell if a species will develop a specific character [..] and assuming that by develop, you meant evolve, then what you meant is Is evolution predictive rather than quantitative.
What I am answering
I will try to answer to the question How good are we to predict future evolution? and just say a few words about how quantitative a science is evolutionary biology.
Evolutionary Biology is a quantitative science
Evolutionary Biology is definitely a quantitative science. It relies a lot on mathematical modelling (incl. statistics and probability theory) and numerical modelling. You might for example want to have a look at Population Genetics and Quantitative Genetics which are at the core of evolutionary Biology.
What are we good at predicting?
Here are a few examples of things we can predict. We can predict how many pairwise differences (or other measures of molecular differentiation) do we expect between two lineages that recently split in a given number of years. We can predict how many mutations of a given fitness effects (whether beneficial or deleterious) do we expect to accumulate over a given period of time in a population. We can make also some predictions about the evolution of multicellularity, sociality, etc. in lineages that are limit-cases (relating again to our ability at a short time only). We can make predictions about the speed of evolution measured in Haldanes or in Darwins (these are units) if we know the genes involved and the heritability of the trait of interest. We can predict the heterozygosity of a structured population. I could cite many other examples. Generally speaking, we have good predictive abilities at short time scale OR for neutral sequences OR for conserved (DNA) regions (strong purifying selection).
In short, we can predict a lot of things but by far not everything yet.
What are we bad at predicting?
I would suggest to decompose the reasons for why predictions can be hard into the following categories. However, I might well forget something and one could argue that my semantic is less helpful some other semantic.

Environment

One issue related to make predictions at long time scale is that the environment changes through time in a way that we are not able to predict accurately enough yet.

Noise

I am not here talking about measurement error or sampling error (these are concept of statistics you may want to check if you don't know them), I am talking about the stochastic process that are inherent to biological systems such as the randomness of mutation processes and genetic drift.

Genotype-phenotype map

We have too little understanding of molecular genetics in order to be able to predict how different specific mutation would affect the phenotype. As a consequence, we today still have very little predictive power about the evolution of a phenotypic trait that is currently totally inexistent.

Complex systems

For example: demography affects evolution which affects the social environments, which affects demography which affects pattern of species competitions which affects the evolution of another species which affects its demography which affects the evolution of a third species which affects the demography of our first species, etc... These kind of complex systems are often mathematically not tractable.

Parameters

We often don't know the exact parameters of the lineage we are interested in. There is a lot of measures to take to be able to make predictions and we often don't have the money (or the time) to make all these measurements (assuming we are able to accurately measure them). For this reason, we are often relatively good to make predictions for a few model organisms but pretty bad for the vast majority of species.

I apologize for my total lack of reference but it would take hours to search references for every claim
Applications of evolutionary biology
There are not a lot of applications of evolutionary biology for the moment but still there are some proving its predictive power. These applications include

medicine and epidemiology (incl. evolution of resistance)
artificial selection and other technics mainly to improve crops nut not only
Various search algorithm such as genetic algorithm

General Advice
The best way to learn about evolution and to answer your own questions (or help you to ask more accurate questions) is to actually take a short course. Understanding Evolution by UC Berkeley is probably a good place to start.


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Do drugs' levo isomers have a better interaction with the receptors in our body than dextro isomers?
Examples of levo drugs include levothyroxine, levocitrizine, and levodopa. Is there any specific reason why the receptors in our body exhibit this stereoisomerism and hold a high preference for the levo isomer form of any drugs?

I can't answer this definitively, but I believe it's because the amino acids that make up the normal binding partner for the receptors are levo.  So the parts fit together better and easier than trying to me dextro versions.  It would be interesting to know if the HTS and Fragment libraries used in modern drug discovery even include D- rotated molecules for this reason.

This is purely coincidental. The term levo simply means the direction that the pure enantiomer of the compound rotates plane polarized light at a specific wavelength and has no direct bearing on the interactions with biological systems. A quick search of the Dictionary of Drugs database gave 6845 compounds with optical rotation >0 (dextro-compounds) and 8406 compounds with optical rotation <0 (levo-compounds). So there are plenty of chiral drugs that rotate plane polarized light each direction.
The inclusion of 'levo' (or 'dextro' for that matter) into the name of the compound was done to distinguish enantiomers of chiral compounds. This naming convention as fallen out of favor due to the improved ability of chemists to know the absolute stereochemistry (e.g., R/S) and distinguish enantiomers based on their structure.
Dextroamphetamine (Adderall) and dextromethorphan (Robitussin) are a couple of examples of drugs with 'dextro' in their names.
With respect to the stereochemical nature of HTS and fragment libraries, most compounds are achiral (do not rotate plane polarized light). I'm not aware of any library biased toward optical rotation, and I'm not aware of any chemist making any selection of compound based solely on an optical rotation measurement. In fact, chiral compounds are often studied first as the racemate. If there is activity, the individual enantiomers are tested.


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Did we evolve from monkeys?
Since I was young, I always understood that evolution taught that we descended from monkeys (or apes, not too sure a distinction was ever made). However, someone recently told me that this isn't correct, and that we actually share a common ancestor, but not a direct line of evolution.
Can anyone clarify which approach (if either) is correct?
Assuming the latter is correct, doesn't it raise problems of missing fossils? If we descended from monkeys, there is less of a gap to fill, but if we share a common ancestor, we would need to fill a much bigger gap, right the way back to the point where our family trees diverged.
As I said, I don't know much about this, and find most of the online material too technical to understand. If anyone could explain this in simple terms, I would be very grateful.

The essence of what you say is all true, but some very important details are missing.  Generally the comparison is to chimpanzees, which, as Remi.b points out, we did not descend from.  We do share a common ancestor with chimpanzees which you can call a monkey.  The concept of "missing fossils" or "gaps" is and has always been a red strawman herring.

Well, first of all scientists are not sure that we eloved from monkeys. They arent 100% sure! None knows that.

Nor do we know 100% whether or not we are in The Matrix.

Welcome to Biology.SE.
About your post
It is a very standard question and a common source of misunderstanding from the general public. If you just google do we descend from monkeys you will get tons of hits that will answer your question.
Because this question is introductory and has already received a lot of answers online, there is therefore no point for me to make a long and extensive answer here. I will just state the essentials and let you investigate it further through the multiple online sources that exists.
Note by the way, that if you want to get some introductory knowledge in evolutionary biology, you might want to have a look at a few course on Understanding Evolution by UC Berkley
The actual answer
In short, It makes no sense to say of any species that it descends from any other extant species. Two extant species share a common ancestor though. The Most Recent Common Ancestor (MRCA) is of particular interest. Following this logic, humans do NOT descend from modern days chimpanzee, but humans and chimpanzee have a common ancestor. Their MRCA was another ape, but not an ape that exists today (even though it may look like one).

I believe chimps and our MRCA were apes, not monkeys. Big difference.

That was a language issue. I meant that their MRCA was a primate. Thanks for the comment. I edited my answer.

"It makes no sense to say of any species that it descends from any other extant species."  It does if both are still extant.

@endolith while your claim may hold playing out with the definition of species (see here), it is never considered as such. At a speciation event, the ancestral species stop existing under its name as it evolves into the two descendant lineages. Have a look to any introductory course to evolutionary biology for more information.

@endolith You may also want to have a look at this answer for an intro to phylogenetics

Remi provides a great answer here. One thing I would like to add is an analogy: Humans and Chimps are both modern species (i.e. existing today).  Compare this to you, your brother, and your cousin all of whom are in the same generation.
To ask whether Humans evolved from Chimps is comparable to asking if you are a descendant of your cousin. Neither of you descended from the other, instead, all three people have a common ancestor - in this case, your grandparents (which, in very real terms, are your MRCAs).

Assuming the latter is correct, doesn't it raise problems of missing fossils? If we descended from monkeys, there is less of a gap to fill, but if we share a common ancestor, we would need to fill a much bigger gap, right the way back to the point where our family trees diverged.

The missing fossil thing isn't really much of a problem. Fossils are hard to find - they're often burried and poorly preserved.
And we have found plenty of fossils of early homo and pre-homo hominids.
Have a look at these for example.
Examples of early homo fossils include: Neanderthals, Denisovans, Floresiensis, Heidelbergensis, Erectus, Antecessor, Naledi
Examples of pre-homo fossils include: the various australopithecines (afarensis, africanus, anamensis, bahrelghazali, garhi, sediba), the various paranthropus (robustus, boisei, aethiopicus), the various ardipithecines (ramidus, kadabba)
Not only that, but we have sequenced Neanderthal and Denosovan genomes and found instances where they are more similar to chimps than we are as well as instances where we are more similar to chimps than they are.
It simply isn't true that missing fossils present a problem.


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Why are bovines different genera if they can interbreed?
Why are bovinae a "subfamily", above Genus, when members can interbreed?  Some like the beefalo are fertile, which is the normal defining characteristic of a species. And Genus are groups more distantly related, so by definition they should not be closely related species.

Species are not defined by whether they can interbreed, not even close.
In fact, there is no objective, scientific standard for what defines species, or genera, at all. What is a species is determined by little more than the "feels" of the individual naming it, or the committee approving it.
And the same is true of the entire rest of taxonomic structure. It's not really science, it's just a way of organizing ideas that got popular, and in fact is under constant assault now by somewhat more scientific things like genetic testing. The hierarchy of the taxonomic system changes pretty much daily, and has no official structure or definition at all. Even the number of kingdoms is entirely up in the air.
Getting back to the specifics here, since there is no objective, scientific standard for what is a species or genus, it's no surprise that separate ones can interbreed.
And it's not like bovines are the only ones. There are many other intergeneric hybrids possible, like sheep and goats, wheat and rye, camels and llama, house cats and servals, marine and land iguanas, et cetera.
Perhaps someday there will be objective definitions to establish a truly scientific taxonomy. But for the moment, it's just whatever people in positions of power feel makes sense, at any given moment.
List of Intergeneric hybrids

Although binning organisms into "species" is an artificial construct to allow conceptualization and organization of life's diversity, your post is misleading and seemingly misinformed. There are dozens of ways to "define " a species, which we term species concepts -- many of which do not rely on the ability for interbreeding as part of the "definition". These concepts are not defined by "people in positions of power", but rather used to varying degrees in the scientific literature as support for certain taxonomies.

...In other words, it's the peer review process that ultimately decides the value for binning species according to the concepts defined in various papers; not "people of power". Perhaps becomign more common are concepts based on genetics/phylogenetics as they seem to be somewhat more objective than more historically utilized concepts (e.g., morphology).

You say that as if peer review were in any way a valid part of the actual scientific method, instead of being an impediment to it that cultivates conventional wisdom and censors ideas that sometimes turn out to be correct.

Different genus doesn't mean that they are very far away genetically, it means that they can be classified at a clear level above species.
Genus are not strict and codified, they give order in the animal world for groups of the nearest affiliation after species... based on: common ancestry, reasonably compact groupings, distinctness (of ecology morphology etc).
There are 143 bovidae in 50 genera, sheep to gazelle to wildebeest. cows are in the subfamily bovinae, made of 9 or 12 genera and three tribes.
They have decided that cows are of three types, buffalo's, bison's and bos/ox, in the tribe bovini, and that there oryx, kudu and bongo antelope are cousins of cows from a different bovinae tribe.
Scientists have agreed that bison can be grouped in a different group, genus, that zebu and cattle. It's logical.

vs

vs

They have agreed that indian cows, zebu, from indian aurochs, is in nearly the same as a cow derived from eastern aurochs, compared to the 5 species of buffalo.
For example with pigeons, they have decided to group all the species related to the wood pigeon into one group, and the columbidae family actually has 42 genera of pigeons, mostly exotic and tropical ones, and even stuff like dodo's.
https://simple.wikipedia.org/wiki/Bovinae
They make mistakes regarding genus as often as for species, and may have to swap around a species from one genus to another based on genetic evidence, even if two genus have members with parallel ecologies and appearances.
Taxonomists will say "Tragelaphus and Taurotragus genera are sometimes included with bovinae", the groups can be blurred and flexible.
It's a messy job for taxonomists.
http://bioweb.uwlax.edu/bio203/s2007/hayes_katy/images/ruminants.bmp
https://encrypted-tbn0.gstatic.com/images?q=tbn:ANd9GcSWBirAqviIKqUNdGHbxfhZJ9JcK57jU8mYD5iydpV5wFIARCQJ
https://www.researchgate.net/publication/225666813_DNA_barcoding_of_18_species_of_Bovidae
https://ai2-s2-public.s3.amazonaws.com/figures/2017-08-08/9b140afd9d0d3eaf61ac9bde4560f8c9c207e380/9-Figure4-1.png

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


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How do muscles help erect the spine?
Muscles of the spine help to support it against gravity. For example, the multifidi interweave throughout the vertebrae and, as I understand, sort of reinforce the spine. So let's suppose muscles help to make the spine more stiff and rigid and this somehow helps it fight gravity.
What portion of support comes from the muscles? Would a spine by itself be able to support itself? In other words, to what extent is our ability to support our spine to remain upright due to muscles and how exactly do they help keep the spine erect in this capacity?

A biomechanical analysis can be done to determine how much support comes from the muscles vs other (skeletal) support structures. Assume the body is standing upright, in static equilibrium. Consider this (over simplified) free body diagram of the upper torso where the sum of the forces equals zero in static equilibrium.

Here the diagram over simplifies the analysis with one general equation: Fsupport = sum of all the weights. Since we are considering only how much weight muscle supports, we deduct Wbones from Fsupport.
A spine by itself would not be able to support itself because the sum of the forces do not equal zero in static equilibrium. (Wgravity + Wspine) > Fsupport.
In reality, each muscle, bone, and organ has many more forces with specific magnitudes in different directions that altogether equal the weight of the specific region of mass it supports. I imagine these forces as many vectors over an area/field. A more detailed analysis would require a program like MATLAB that uses triple integrals in calculus to visualize these forces in 3D. This kind of visualization can help us color code only the muscle vectors which answers your question, "to what extent is our ability to support our spine to remain upright due to muscles," as a percentage of the sum of all the forces input into the program. How the muscles keep the spine erect can be determined from such visualizations as descriptions of directional forces.
For an example of how this kind of analysis is done, see this paper on lumbar spinal support. http://www.uvm.edu/~istokes/pdfs/stab-model.pdf

I disagree on the interpretation, see my answer.

Spine is the only element between thorax and pelvis that can support compressive stress, and thus the weight of the upper body. So the spine needs to support all that.
However, the spine is not rigit enough, and would buckle without muscles. Muscles stabilize it by pulling in a coordinated manner, just as ropes can help stabilize an erected mast. The paper cited by Anna Lu, http://www.uvm.edu/~istokes/pdfs/stab-model.pdf, illustrates this, and states that muscles have both an active role (their relative tension can be tuned) and a passive role (they behave as elastic ropes).
Note however, that this is done at the price of exerting even more compressive stress on the spine!


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Do the bacterial species X, Y, Z code for proteins A, B, C?
My PI has assigned me a task to gather evidence to determine whether or not a list of particular species of
Campylobacter and Helicobacter code for a list of several proteins.  To put it simply I’ve been asked, “Do species X, Y, Z code for proteins A, B, C?”  The genomes of these bacterial species have been fully sequenced and I am able to retrieve the FASTA files for each of them.  I am having trouble deciding on the proper method to screen these genomes for the genes.  I have been given the names of the proteins, i.e. VgrG and HCP, but the amino acids sequences listed on databases are annotated to different species of the bacteria.  I seem to be stuck in a grey area and am having trouble connecting the overwhelming amount of resources available on the NCBI website.  I have not found a specific guide to perform this task - Could you please provide me with a solution to my problems?

First of all, don't reinvent the wheel, search for annotated homologs first. Assuming you don't find them, the next step is:

Collect the sequences of your query proteins (not genes) from one species in a multifasta file.
Run a tBLASTn with those sequences against the genomes of all the other species of interest.
Analyze. Look for HSPs with a certain level of sequence identity. The details of what threshold you choose will depend on your data, I can't help you  there.

While the tBLASTn approach is going to be more sensitive, an easier method that can find gene structures and not just HSPs is to use exonerate:
exonerate -m p2g proteins.fa genome.fa

Finally, for a more sensitive search than either of the above, useful for finding more distant homologs, run a Psi-tBLASTn of your proteins against the genomes of interest.
In all of these approaches, the tricky bit is to choose the right threshold. Unfortunately, there is no golden rule here. It all depends on how closely related your species are and how similar the homologs. You will have to try a few different ones before you can choose the right one.

I am unclear as to how I could go about obtaining these query proteins.  They are not listed in any databases yet. I think my PI wants me to predict whether or not a protein exists in these organisms.

@codax that's a completely different question! What are you trying to do? WHat do you have and what are you looking for? Don't you have a list of proteins in species X and want to find them in species Y?

I'm really sorry if I was unclear, but your advice is invaluable to me and I'm learning so much. I have a list of species and I need to find if they contain genes that code for specific proteins.  Ex. Campylobacter Jejuni and VgrG.

@codax OK, if you have a list of proteins you want, get their sequences from a related species of bacterium, the closer the better, and use those sequences to query your target genomes. The methods I describe are sensitive enough to deal with small differences in sequence.

I've tried your approach to this problem.  The HSP's indicate an overall similarity to all of the sequences entered into the query.  From what I understand, there is a near 100% identity ranging from 97-100%. Now I know that there is a high similarity between the list of proteins entered and the species I've entered. Would I have to put one query at a time and blast it against one species to confirm if the sequences code for the individual proteins?

@codax no, each query protein should have its own set of HSPs. You are looking for HSPs that have i) high sequence identity and ii) cover the entire length of the query sequence (or nearly). Now that you know they are there and have high similarity, you  can also use exonerate to match the genes more precisely.

Do multiple sequence alignment of your protein sequences. This will give you evolutionary relationship between your sequences.

I think the OP needs to identify genes in the genomic sequence and only has proteins from one species. Multiple alignment won't help.

I have to identify if these genes exist in a list of species.  I have the names of a few proteins.  MSA would not apply in this situation.  I can retrieve the FASTA containing the entire genomes of these species.  Is there a way that I could retrieve the protein sequences and compare them with the nucleotide sequence somehow?


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How many diseases can be linked to disruption in the microbiome of a human?
I was listing to the radio and heard recent research found a link between children and higher cases of asthma when certain bacteria are missing from the microbiome. How many other diseases can be linked to a disrupted microbiome and are there ways in repopulating missing bacteria?

It is an open question and an active area of research. You will not be able to get a definitive answer to your question of number, as each new discovery will add to the total.
As for repopulating, we have not even determined all of the strains of microbes that populate us, many are very difficult to culture in vitro, and we do not know of all the functions for each species, so we do not have a clear picture of which need to be there, which don't, and whether or not some species work together to provide us with a benefit. For certain conditions such as Irritable Bowel Syndrome, one of the treatments that has been tried is fecal transplant.
Do a literature search for recent reviews. Nature Reviews tend to do detailed reviews, especially on topics as in the news as the Human Microbiome. That is probably the best first place to start. Then you can start to drill down into the reference papers that are cited in the review. That will generally give you a good state of play in the field.

Thanks for the reply I will definitely take a look at some of the literature out there, I was very surprised to find out how many bacteria live on and inside of us. And I was told all this time growing up that "germs" are the enemy!

@DanTerry They are actually a very important part of the innate immune system. One aspect of immunity is keeping pathogens out. One way we do that is mucus. Another way is to provide a favorable living environment for microorganisms that don't harm us. The term for these is Commensals. Basically commensals, yeast, bacteria, etc, that are non-pathogenic to us, grow on our exposed surfaces, i.e. skin, respiratory tract and our gastric tract. The are there to basically just take up space that would otherwise be populated by pathogens. There are 10x more microbes than human cells making up a human


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Does exercise really reduce stress in the biological meaning?
It is a very widespread claim, that movement in general helps body to get out stress hormones. It is used as a warning for long sitting at the computer and I also heard it as a pro-vegan argument (We receive stress hormones by eating cows which have no option to release it in the closed areas).
How literal this rumour is?

With "... helps body to get out stress hormones ..." you mean to reduce the amount of stress hormones? Could you reference this "widespread" claim? In fact, strenuous exercise induces release of stress hormones. Without some sources to back this "claim" up this question may be opinion based. A more likely cause for stress hormones in meat may be the unpleasant last hours of these animal's lives spent in crowded cattle trucks and waiting for their deaths in the slaughter house.

@AliceD Yeah, the claim is just that they can not reliese it this way, unlike freely captive cattle.

I'd like to see sources as well.  I rarely see cows running in open areas like a field.

@Nathan I gave there a source for the stress release claim for human during exercise. I'm looking for the issue with captive cattle without movement now (but I just heard it  so it can take a while).

http://animalstudiesrepository.org/cgi/viewcontent.cgi?article=1019&context=acwp_faafp Page 316

That link says exercise reduced stress, not that it reduces stress hormones.

@Nathan - I've lived in three countries across three continents and I have seen many, many cows in open fields O_o I don't know where you're at but, no, at Times Square you won't see any cattle grazing

@AliceD You can't say anything about the percent of cattle reared on huge open air areas because the closed ones aren't just avaiable for your sight. I'll try to find better links (unfortunately I won't have internet for next few days)

have a look at: http://www.ncbi.nlm.nih.gov/pubmed/18787373

Neurologically speaking, β-endorphin molecules (amongst other opioids) function to relieve pain or produce pleasurable feelings, thereby facilitating an individual to continue functioning in spite of injury or stress.[1]
β-Endorphin release in response to exercise has been known and studied since the 1980s.[2] Studies have demonstrated that serum concentrations of endogenous opioids, in particular β-endorphin, increased in response to both acute exercise and training.[2] The notion of β-endorphin release during exercise is colloquially known in popular culture as a runner's high.[3]
tl;dr: Yes, it has been shown that exercise can really reduce stress in the biological meaning.
[1] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3104618/
[2] http://www.ncbi.nlm.nih.gov/pubmed/6091217
[3] www.webmd.com/depression/guide/exercise-depression

Hm, that sounds trustful. But where do the stress hormones come to? Are they only beated by the amount of endorphin?

The question is not why exercise reduces stress, but reduces stress hormones.


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Does loud music affect hearing and balance?
From many sources I understand that strong disturbances can destroy hair cells in the cochlea.

Does the sound damage always counts simply as the number of decibels recieved by the ear? E.g., if you listen to music in the train and you have to play it louder to hear it clearly?
Is therefore a one-shot of noise less damaging? I.e., hair cells are not as disturbed?
How long would you have to listen to the 120 dB music to lose your hearing? What is the healthy limit per day (how fast do the hair cells recover)?
Could it also affect your balance (since it is managed by the same organ)?

Nice question +1. However, I do not understand two aspects: Which sources say that earbuds cause more damage? And more importantly, what is "disponsable" noise?

@AliceD From English sources I found arguments talking about dangerous bacteria, so I asked different way.

First off, there are many flavors of decibels, as it is a relative measure. For the sake of clarity I assume you are talking dB sound pressure level, or dB SPL, which is a unit of sound pressure relative to a standard sound pressure of 20 µPa and widely used.

The damaging effects depend on the sound pressure received by the ear. Whether this is a compound signal or a single source doesn't matter. Like whether you crash your car against a wall at 80 mph, or head's on against a truck both travelling at 40 mph - it doesn't really matter. It's the mechanical energy transferred to the hair cells that counts.
A one-shot noise... I don't really understand what you're aiming at, but as said above, it's the raw sound pressure that counts. Further, prolonged exposure is definitely more damaging than a short exposure. However, when the sound pressure is strong enough, e.g. a bomb blast which lasts just a fraction of a second, hearing can still be permanently lost provided the sound level is high enough.
According to the Ear Center of Greensboro, a rule of thumb is that the maximal safe exposure to sound of 100 dB is half an hour, and for every added 5 dB that time is cut in half. Thus, for 120 db that would add up to 7.5 minutes before permanent damage occurs. The safe loudness limit per day has primarily been established in terms of maximum sound levels for occupational exposures (i.e., sound exposure for 5 days per week, 8 hours per day). Likely it is dependent on where you live, but here in Australia, the Government has set the safe occupational limit to 85 dBA. The dB(A) is a weighted unit of loudness that is corrected for the hearing sensitivity of the human ear.
The labyrinth of the inner ear is a system of interconnected chambers and canals. The fluids in the cochlea (responsible for hearing) and vestibular system (responsible for balance) are indeed interconnected (fig. 1).

Fig. 1. The ear (upper panel) and structures of the inner ear (lower panel). Source: Washington University.
However, sounds enter the inner ear via the tympanic membrane that connects with low impedance to the cochlea, but there is no direct connection to the vestibular system. Hence, only very loud sounds may affect balance, but that are likely accompanied by mechanical blasts that will physically damage the delicate inner ear structures. Loud music of 120 dB will not damage the vestibulum.

Sorry, I just got unsettled one more time: Is there a difference in music damage between listening music on 120db and in a calm room?

@Probably - I don't understand the question. If you mean whether background noise adds to the damage, then yes.

@Christaan sorry, I meant: Is there a difference in music damage between listening music on 120db in a loud place and in a calm room? Pretty much the opposite, if the music damage adds to the background.

@Probably - You have to measure the sound level. In principle, sound adds. So music+background > music. Higher level means more damage. But depending on the levels


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How to identify a pseudogene to a specific protein coding genes?
Pseudogenes are those sequences in the genome that bear similarity to specific protein coding genes, but nevertheless are unable to produce functional proteins due to existence of frameshifts, prema- ture stop codons or other deleterious mutations (Mighell et al., 2000). While I doing some research on protein PLEKHA7, I use the PseudoPipe(an automated pseudogene identification pipeline)(Zhang et al.,2006) to find out the pseudogenes of PLEKHA7. But I am confused that the DNA sequence is 226929bps in length, its pseudogene is only about 100bps long but with a much higher identification like 41.1% and 71%. (chr = chromosomes,start = start position,end = end position,query =  parent protein,frac = fraction of the parent protein that is overlapping with the pseudogene,ins = number of insertions in the pseudogene sequence,del = number of deletions in the pseudogene sequence,shift = number of frame shifts in the pseudogene sequence compared to parent,stop = number of stop codons in the pseudogene sequence,expect = e-value for the sequence identity between parent and pseudogene,ident = sequence identity  between parent and pseudogene,polyA= presence of polyA signal,type = pseudogene biotype : PSSD =  processed, DUP =  duplicated, FRAG = ambiguous )
So how does these pseudogenes have such high identification to the parent gene as they are only very short sequences?

It would probably much easier for us if you could paste the relevant lines in plaintext and also add a link to the specifications of the output file.


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How can I interface cAMP signal or membrane potential from slime mold to an electrode?
I am very much interested in measuring cAMP (cyclic adenosine mono phosphate) signal and membrane potential from amoeba. Since I want to try this as a hobby, what are the basic steps I must do to view these signals on a CRO (cathode ray oscilloscope). Cyclic-AMP being a biochemical, how can I view it as a corresponding electric signal?

For cAMP there is only one electrophysiological technique I've found.  You can use cyclic nucleotide-gated channels in the cell as a secondary indicator of cAMP activity.  When cAMP increases in the cell, these channel will fast gate which you should be able to pick up.
The issue is standard CNGC's are not overly sensitive to cAMP and are typically more sensitive to cGMP.  But there have been mutants created that have a high affinity for cAMP.  You can transplant these in and have an easier time with the detection.
This paper goes into a a lot more detail on it.

What do "fast gate" mean here ? Also how can I convert this biochemical signal to electrical so that I can see in a CRO?


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Why can't we use plasmids to add genes to ourselves?
Reading these answers I wonder, why doesn't "gene therapy" use self-contained plasmids instead of trying to splice a length into a chromosome?

IIRC humans have several mechanisms that digest extra-nuclear DNA. Unfortunately I don't have a reference handy, but I'm 95% sure any plasmid would just be destroyed.

That makes sense.  So "some yeasts" is the exception, having first evolved a mechanism to allow importing of survival traits, possibly trading off resistance to viruses.

In mammalian cells, Plasmids are not replicated, which is why in cell culture, you need the extra step of recombining the vector into the genome via homologous recombination. The issue is that this can be done in vitro to cells, but once you try doing it on an organism level there are many problems. One is that Adenovirus usually needs to be used to insert the vector. But adenovirus' capsid can only accommodate about 10kb of DNA. As most homology arms are at least 10kb, each, you cannot do targeted integration. You would need to rely on random integration, and you couldn't predict the effects.

First, plasmids do not usually integrate into the chromosomes of human cells. In the laboratory, plasmids can be introduced into the cytosol of cells, and plasmid DNA will then be "read" by the host cell and used to make new proteins, for example. But plasmids usually remain separate from the cell's own DNA, and in that sense they are not effective for gene therapy.
Second, our cells are quite good at detecting and destroying plasmids, as well as other foreign DNA. This is a self-defense mechanism, evolved to get rid of viruses and other nasty parasites that might be trying to hijack the cell. In the lab, where we are working with isolated cells in a culture dish, with no immune system, plasmids are typically tolerated. But in a human being, immune cells that have specialized in detecting intruders are very competent at detecting such manipulations, and they will quickly sound the alarm and wreak havoc ... So if injected into the body, plasmids are quickly detected and destroyed.
Research in gene therapy aims to find more efficient ways of "editing" the DNA of human cells, ultimately in a way that can be safely applied in the body. Such a technique does not exist yet. The latest CRISPR-Cas9 gene editing system is a phenomenal tool, and is very efficient at getting into the DNA of human cells; but the CRISPR-Cas9 proteins must themselves be delivered into the cell, for which a virus is typically needed, and this would again cause immune reactions if attempted in a human body.

I believe we could use plasmid insertion to assist with gene therapy. EBV can maintain a plasmid in the cells it infects and the plasmids can effectively replicate. With a greater understanding of the latency and the implications of inserting genes using EBV, it may be possible for gene therapy to occur via genes on a plasmid.
references: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2562867/
http://jvi.asm.org/content/65/1/483.full.pdf

Can you elaborate on «EBV can maintain a plasmid in the cells it infects» in light of Roland’s answer that they are seen as invadors?

This is a very interesting answer. Whether or not it has any relevence to gene therapy, it  is valuable as background information that most people will not be aware of. It could be improved further by better layout and some elaboration. I would split it into three paragraphs: 1. Explain what EBV plasmids are, stressing the eukaryotic replication origin as opposed to the bacterial one the poster may have been thinking of,  2. Suggest how they might be used for gene therapy, 3. list the references.


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Can ampicillin resistant bacteria survive penicillin plate?
in my molecular bio class we were asked a trick question:
If the bacteria has a plasmid with that grants it ampicillin ressistance, can the bacteria survive if placed in penicillin?
I gave it  a thought and said that it cant, since amp differs from pen by an extra amino acid that could harm the bacteria, the answer corresponds with the class material but amp is known as the broad spectrum antibiotic.... so should i go with the  class flow  lured by the experimental assumption and assume it dies  or persist on whether it will survive? i'm really confused at this point, any input is appreciated

Neither of the two answers provided give the full answer, both touch on it, from different perspectives, but neither address it completely.
Given your description, it sounds as though the question is being asked in the context of a lab strain.
Plasmids for ampicillin resistance carry the AmpR gene on them which encodes for the enzyme beta-lactamase.
Beta-lactamase hydrolyses the beta-lactam ring, which is the 4-membered ring that has the carbonyl group and the nitrogen in the ring.
It then decarboxylates the carboxy group that results from the hydrolysis, removing the threat to the bacteria's ability to make cell walls, as Chris explains.
As both ampicillin and penicillin are closely related beta-lactam antibiotics, and have the same beta-lactam ring moiety which is the substrate of beta-lactamase, both molecules are neutralized by the enzyme and the bacterial cells will divide and not be inhibited from forming a cell wall.

The down votes without explanation make no sense at all. Both the answer that @Chris gave and the answer that I gave are factually correct. Ampicillin and Penicillin are Beta-lactam antibiotics and resistance to them is provided by the beta-lactamase enzyme. As the question said plasmid and not F-factor, we talking about transformation and not conjugation. In the lab, you use a Plasmid with AmpR to confer resistance, and pretty much any of the common beta-lactam antibiotics will be resisted by transformants.

Out of interest: Why the downvote? What is wrong with this answer, what needs to be changed?

Short answer: Your assumption is wrong and bacteria, which are resistant to penicillin are are also resistant to ampicillin.
Long answer: There are different classes of antibiotics, which have different mechanisms of action. Penicillin (and also ampicillin) belong to the class of beta-lactam antibiotics which are an irreversible inhibitor of the bacterial transpeptidase, which is needed for the proper formation of the bacterial cell wall.
There is a number of different natural occuring penicillins as well as some which have been generated by modifications of the general structure. The general chemical formula for these is shown below (from the Wikipedia article), the different penicillins differ only in the "-R"-group shown in the molecule (in the upper left):

If you now compare Penicillin G (which occurs naturally and is still used) and ampicillin side-by-side, you will see the the difference is not very big, basically only one amino group:

Penicillin G on the left, Ampicillin on the right.
The difference of this one amino group makes ampicillin more polar and allows it to penetrate the cell wall of some gram negative bacteria (the main action goes against gram positive bacteria).

The down votes without explanation make no sense at all. Both the answer that @Chris gave and the answer that I gave are factually correct. Ampicillin and Penicillin are Beta-lactam antibiotics and resistance to them is provided by the beta-lactamase enzyme. As the question said plasmid and not F-factor, we talking about transformation and not conjugation. In the lab, you use a Plasmid with AmpR to confer resistance, and pretty much any of the common beta-lactam antibiotics will be resisted by transformants.

Out of interest: Why the downvote? What is wrong with this answer, what needs to be changed?

My first reaction to your question was that it would depend on the mechanism of resistance. As Chris pointed out, ampicillin differs from penicillin only by the addition of an amino group on the amide alpha carbon. While the similarity may suggest that resistance to one confers resistance to the other, the amino group does provide a means to distinguish between the two and, through the happenstances of evolution, I could imagine cases where bacteria evolved resistance to one antibiotic while remaining susceptible to the other. This paper describes penicillin resistant but ampicillin susceptible Enterococcus faecalis strains isolated from clinical samples. While this describes somewhat of the opposite scenario as your question, I don't see any reason to say unequivocally that ampicillin resistance implies penicillin resistance.

For lab strains, with the AmpR gene encoding beta-lactamase on a plasmid it does, and based on the wording of the question I am going to say that it is referring to lab strains on to Amp or Pen plates.. The article you linked to does not give an explanation of the method of resistance. It could very well be that these bacteria have a different form of resistance than beta-lactamase, and it could be that ampicillin greater polarity, as Chris pointed out, makes it more effective against these bacteria.


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Why do adult insects have 6 legs?
Apparently, there is an advantage to having 6 legs in the insect world. What is that advantage, if anything? Why would such an advantage exist for insects, but not for other, larger land animals?
What do those middle legs do that the front and hind legs cannot, if anything? Are they really essential, or do they just generate more muscle power?

It seems like this question presupposes perfect adaptation. Many features of modern life-forms aren't necessarily 'better' than other possible features, but are the way they are as a result of historical chance and the constraints imposed by development. Would you be satisfied with the answer "the last common ancestor of all insects had six legs, and that worked well enough that it has been kept by most of its descendant lineages"?

Insects are not the ancestors of higher organisms. And BTW octopus is one organism which will be a counter-example.

@WYSIWYG hmm great point. Nevertheless, there is an apparent advantage to having 6 legs as an insect that does not seem to exist for us larger land creatures. I want to know what that is. What are those middle legs used for?

@bshane No I'm not satisfied with that answer, but I edited the 1st paragraph to make it clear there is an apparent advantage. At the very least, I want to know what the middle legs of insects do...and if it's something that 4-legged critters cannot.

This is a little semantically tricky, because not all insects use all of their 'legs' as 'legs', in the sense of 'a thing to walk with'. Consider the raptorial forelegs of mantises - the animal uses them to catch prey, not to walk. They are called 'legs' because of homology, not function. So if your question is 'why do insects have six things that they walk on?' then the answer is that often, they don't. In that case, there is no apparent advantage to explain. If your question is 'why six "legs"?', then the answer is 'by definition, from common descent'.

As it stands I agree with @fileunderwater -- this is a question about evolutionary advantages. However, if you were to make this question about the various functions that insects put their "legs" to then it is no longer a "duplicate" of that question. Even if this question is closed as a duplicate, you can edit it and it can be reopened :)

The question is actually very related to Why don't mammals have more than 4 limbs?

@bshane I disagree that this pre-supposes perfect adaptation. Rather I think we should focus on highly-preservedness. Very few members of Insecta have lost a set of legs. Why would such a body plan be highly preserved, when it has such obvious costs? It must offer broad-ranging adaptiveness. What would that be, exactly?

Short answer
Six legs allow for locomotion, while maintaining a supportive tripod at all times.
Background
There are several million species of insects, all on 6 legs. This implies that any change in this number is promptly selected against. It is generally agreed that insects were derived from many-legged ancestors, e.g. centipedes.
One explanation is the tripod gait that results from having six appendages. This hypothesis, formulated more than 6 decades ago (Lanham, 1951), reasons that a reduction of the number of legs during evolution did not go further than 6, because locomotion of a small animal encased in a rigid exoskeleton is not effective with less than 3 pairs of legs. Insects generally walk by lifting the two outer legs on one side and the middle on the other side, sweeping them forward and placing them down together. Hence, insects support their rigid structures with a tripod at all times. Tripods are among the most stable configurations, and they never wobble (why on earth do tables have 4 legs?). Figure 1 shows an illustration of insect locomotion (Lanham, 1951).

Fig. 1. Insects' locomotion resembles a double tripod. Insects have a cyclic gait which consists of two phases, the stance phase and the swing phase. The stance phase is the power stroke, it pushes the body forwards in the direction of travel while the leg remains on the ground. Three legs are used is this phase by forming a tripod with the front leg and the hind leg on one side of the body and the middle leg on the other side. This formation is why this gait is known as the tripod gait. Source: Insect robotics.
Larger animals can afford to have less legs, because their vestibular systems have more time to maintain balance and adjust gait during locomotion. Because insects are so small, their strides are so quick that the nervous system may not be fast enough to deal with gait control. Instead, insects rely on the tripod gait to prevent any imbalance, rather than adjusting it. In addition, the exoskeleton effectively restricts small bodily movements to control balance. Larger animals such as mammals make small adjustments in their gait constantly to maintain balance. An insect has less opportunities to do so, because of their rigid exoskeleton (Lanham, 1951).
Reference
- Lanham, Science (1951); 113(2946): 663

Great answer! I'm going to go saw a leg off of all of my tables now, that sweet sweet tripod stability!

This answer is interesting and informative but also has many problems. First, "This implies that any change in this number is promptly selected against..." is completely unreferenced and could just as well (probably?) be due to developmental constrains. Overall, developmental constrains is completely overlooked in both the question and the answer, and is me the main reason why this question should be closed as duplicate. [cnd...]

[...cnd] I can also think of several alternative explanations for why 6 legs is useful for insects, which are not mentioned in this answer. To me, this answer is an interesting hypothesis, but it currently reads as an evolutionary just-so story. "*[R]eduction of the number of legs during evolution did not go further than 6, because locomotion...'" is another really strong statement that is not supported at all.

@fileunderwater all the info is obtained from the Science paper, and the figure legend is from the linked robotics web page. There is nothing that I made up and nothing is unsupported. If anything is lacking from my answer, feel free to write a better one. No need to close a question, and especially not due to it being a duplicate of an abstract, general philosophical community question. If you don't like the answer, -1 will do, throw these questions open to allow others to share their views!

So you are saying that the two quotes I highlighted are supported by the Science paper (ignoring for a moment that the paper is from 1951, when quite a lot has happened in evolutionary biology since that time)? Is so, that should be made more clear (direct quote?). And about the reference - is this what you are referring to? If so, it is a book published in 1950 from Cambridge Univ. Press, and not a science paper (it might have been reviewed in Science though).

@fileunderwater - Thanks for the downvote, but I asked for it didn't I :) Somehow I linked the wrong page to the reference - nice catch. I inserted the correct one (Science paper) and placed some direct references in-text. It's not open source, got it through uni library. Thanks. I'm not an evolutionary biologist, just very interested in it. Downvote away, shoot at interesting questions, close the best ones, whatever - I'll stand my ground 8)

And about writing a "better answer": 1) the problem here is that the Q is speculative and extremely broad, which is why it should be closed. It is nearly impossible to write a short consise answer that actually tries to "answer" the question. This is exactly why short, punchy, plausible-sounding, just-so stories (that are not clearly presented as a hypothesis) are problematic. They can be extremely misleading, and might be taken as "truth". 2) I have other things to do, but that doesn't make this answer "better".

Let us continue this discussion in chat.

This article says that cockroaches use the tripod movement at low velocities (upto 1m/s)  but adopt bipedal/quadripedal movement at higher velocities.

@WYSIWYG - There are probably many examples of adaptations in appendage use. Familiar examples being the praying mantis that uses the front two appendages for hunting purposes and the dung beetle walking on fours while rolling a ball with the front two. I have never suggested my answer is all-inclusive, nor that it is the answer to the question. It is an answer. No more, no less.

@AliceD I didn't deny. Was just adding a point :)

Apparently, there is an advantage to having 6 legs in the insect world. What is that advantage, if anything? Why would such an advantage exist for insects, but not for other, larger land animals?

"Legs" is a tricky term, with insects. Colloquially, in the terrestrial world, they are things that an organism walks on. But the scientific definition of 'legs', for insects, relies on homology: many insects have six 'legs' because they all descend from a common ancestor, which had six legs. The anatomical structures derived from those legs, regardless of whether they are functionally used as paddles, or as claws, or as feeding appendages or elaborate mate-signalling devices, all get called 'legs'. Referring to all of these as 'legs' makes as much sense, from a functional perspective, as referring to our arms as 'legs'. We only do it to keep the homology clear when talking about evolutionary relationships between species.
The diversity of uses to which insects put their legs makes it clear that there is no single universal advantage of having six - it is just that completely losing (or gaining) appendages is a difficult evolutionary process, so it seldom happens over evolutionary time. Regardless, some groups of insects (members of the Coccidae and Diaspididae, for instance) have lost their legs completely - an apparent adaptation to their obligate parasitic lifestyle.

What do those middle legs do that the front and hind legs cannot, if anything? Are they really essential, or do they just generate more muscle power? If it's an advantage either way, why don't bigger life forms like mammals have 6 limbs?

In the insect groups which use six legs for locomotion, AliceD's answer provides an excellent description of how all six legs are used. However, there really is nothing special which can be achieved with six legs, which could not be achieved with some other number of legs: mantises handle their locomotion perfectly fine on just four of their six legs, and arachnids (not insects, I know - but with many of the same design challenges such as a rigid exoskeleton) manage equally fine on eight.


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Reasons for strange heart rate graph following exercise (line going up and down)?
Following a 2 minute general jumping and movement exercise designed to involve the entire body, the pulse was taken every minute for ten seconds. Strangely, the graph appears to jump up and down, for which I have little understanding why.
The pulse was measured simply and crudely with the traditional "fingers on the wrist" method.
If it is not clear, time is on the x axis and no. of heartbeats per minute on the y.

Thanks in advance

If the graph were what I would consider to be "normal", the general motion of the line should be downwards, settling to the normal heart rate. Instead, the graph has decided to jump up and down yet there should be no or little error.

A possible answer to this question could be user AliceD's suggestion in the chat room that "If sampling rate is low, you get this jumpy behavior because variations result in these 'binary' jumps."

Given the manual way the heart rate was determined I question the accuracy of the data. I would suggest to repeat the experiment and check repeatability of the data. Accuracy can be increased by determining the pulse heart rate over a longer interval than 10 seconds.


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Blood testing for chlamydia
I am working with the bacterium Chlamydia trachomatis.
The main test for this species is the naat test, which is based on amplification. But I would like to know how the bacteria affects the blood composition, and if there is a method of diagnosing it from the blood.

Blood antibody tests for Chlamydia trachomatis can be done, but they are far less reliable than amplification:

According to our results, serologic testing for Chlamydia can exclude active infection of the lower genital tract with a high reliability (> or = 95%). However, detection of C. trachomatis can only be reliably achieved by nucleic acid amplification assays.

Low correlation of serology with detection of Chlamydia trachomatis by ligase chain reaction and antigen EIA

Well, I checked your question about chlamydia and there is a way to check if someone has chlamydia from his blood. They take some blood and after they check if there is the Chlamydia bacteria. If they are not sure they simple do a NAAT test. The NAAT test will sure sow if there is chlamydia or something else.


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Energy produced from respiration
Why is the amount of ATP Produced from anaerobic respiration is less than the amount produced from aerobic respiration?

Anaerobic respiration does not completely oxidize the glucose, and as a result, pyruvate is not completely broken down, yielding fewer ATP molecules, and there are leftover molecules: lactic acid in animals and ethanol in yeast. This is because anaerobic respiration does not utilize oxygen, which is required for the electron transport chain, where most of the ATP comes from in aerobic respiration. In aerobic respiration, the glucose molecule is completely oxidized, and so (through the Krebs cycle and the electron transport chain, which requires oxygen and which produces the majority of the ATP) is completely broken down into carbon dioxide and water.


text:
Are oxygen and carbon dioxide simultaneously present in red blood cells during gas exchange?
From my understanding, the process that displaces the carbon dioxide and oxygen in our erythrocytes and lungs is diffusion. I've been taught that diffusion is the net movement of particles from a region of higher concentration to a region of lower concentration, until an equillibrium is reached.
For there to be an equillibrium in carbon dioxide and oxygen, doesn't that mean that there should be equal portions of those elements present at all times? So therefore, erythrocytes should contain both of those chemicals simultaneously. Am I correct in assuming this? If I am, then I have a follow-up question: wouldn't carbon dioxide floating about in our blood indefinitely cause some unhealthy side effects, and is there something that prevents it from doing so?
I'm currently only in GCSEs, so apologies if this question might actually have a very simple answer.
Thanks

For diffusion to occur there must be a "concentration gradient", that is one area where the substance that is diffusing from, to where it is diffusing to. Where the substance is diffusing from, the concentration is high and where it is going to, the concentration is low. Our bodies continually use up oxygen and produces carbon dioxide. Carbon dioxide is generally carried in the blood plasma, and oxygen is generally carried by the red blood cell (erythrocytes).
Whereas, it is true that in diffusion an equilibrium is usually achieved, in this case you mention there is no equilibrium. Our physiological processes (respiration) continually maintains that concentration gradient and so carbon dioxide always flows out and oxygen always comes in. Too much carbon dioxide in the blood will raise the pH and cause serious metabolic problems with enzymes and their efficient function.

Diffusion can (and in this case, typically does) lead to local equilibrium in lung gas exchange. This was determined by extensive work during the first 3/4 of the 20th century. Also, increasing carbon dioxide lowers rather than raises blood pH; acidification is a lowering of pH.

There in fact typically is an equilibrium of diffusion for both oxygen and for carbon dioxide by the time the blood finishes gas exchange in the alveoli of the lung. One confusion in the OP is that there is no real meaning for a chemical equilibrium between carbon dioxide and oxygen, as they are separate chemical entities. Carbon dioxide in the lung capillary blood equilibrates with carbon dioxide in the lung alveolar gas; oxygen similarly equilibrates between blood and gas. Each effectively on its own.
Yes, oxygen is continually being consumed and carbon dioxide being produced by the body, so from that perspective we have a whole body steady state. At overall equilibrium we are dead. But at the site of gas exchange in the lung, there is generally no difference in the chemical activity of either gas between the alveolar air and the capillary blood leaving the alveolus. So from a chemical perspective there is generally local equilibrium of both gases at that point.
In some circumstances this local equilibrium is not reached. The transport of carbon dioxide is very complicated, as it exists in several inter-convertible forms: dissolved carbon dioxide gas, a form called carbonic acid where it has chemically reacted with water, the bicarbonate and carbonate ions that come from dissociation of carbonic acid, and a carbamate form that is a reversible chemical bond with amino groups on proteins. The reaction with water is slow on its own; it is catalyzed by the enzyme carbonic anhydrase in red cells. If that enzyme is inhibited (for example, by the drug acetazolamide) then there might not be chemical equilibrium of total carbon dioxide between alveolar air and capillary blood as there might not be enough time, as blood flows through the alveolus, for all the other forms to convert to the dissolved gas that can diffuse from blood into alveolar air.
Another complication is that transport of oxygen and carbon dioxide in the blood are somewhat interdependent. Acidification by carbon dioxide (lower pH is more acid) affects the ability of hemoglobin to bind oxygen, tending to release more oxygen. Nevertheless, in most circumstances in humans, both gases are individually at equilibrium between alveolar air and the blood that leaves the alveolus.
Finally, the continued presence of carbon dioxide in the body is a normal, healthy part of physiologic functioning. It does have to be kept in balance, but it does have to be there.


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Does anybody know what this shark is eating?
Looking for a species identification on the orange fish that the shark is eating. The shark is a goblin shark filmed as part of the BBC's 'Legends of the Deep: Deep Sea Sharks'.

It might be Helicolenus dactylopterus, but it is difficult to say for sure without being able to see the dorsal fin.

That's great, thank you. Just had a quick Google image search and I think you're right. Answer the question rather than a comment and I shall accept it!

The fish in this image is Helicolenus dactylopterus. Shown below;

This fish, is more formally known as a Blackbelly Rose-Fish. This fish, is one of the Goblin Sharks' many prey in the deep sea.
In the photo you posted it looks as if the Goblin shark effortlessly and oddly so caught the fish - it did. This is due to how it consumes most of its prey:

When they approach it their jaw goes out similar to how a human can stick out its tongue. Then with a sucking motion they draw they prey into their mouth where very powerful teeth are waiting to consume it.

Goblin sharks are quite terrifying...