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Hypotonic or Hypertonic solution and why?

A doctor needed to administer 5% albumin to a patient. Albumin is normally administered dissolved in 0.9% saline solution. Since the physician did not have any 5% albumin solution, he diluted 25% albumin with water and administered this to the patient. Describe what you think happened to the blood cells of the patient as a result?

So this is what I think:
If the doctor dilutes the 25% albumin, that will make the solution have a lower concentration of solute, creating a hypotonic solution. Therefore the water will move into the cells, causing them to swell, lyse or burst.
Is this correct?

Sure sounds correct to me.   p.s. Stupid doc's solution will be (0.9/5)% saline = 0.18% saline.  Way too low.

Albumin wont form a true solution and wont affect the osmolarity greatly (colloid forming molecules like proteins can affect osmotic pressure to an extent. See oncotic pressure).. and since there is no solute the solution would be hypotonic..
But what effect it will have on the blood cells depends on how much solution was injected.


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Extremely rare occurence of Heart cancer?
The occurrence of Heart cancer (similar, but not the same as Rhabdomyosarcoma) is extremely rare, about 1 per year according to MayoClinic. The reason for this rarity is explained to be the post-mitotic nature of cardiac muscles. Since they stop dividing early in the life cycle of humans and grow only by increasing in volume, they are very less prone to oncogenic activation events caused due to mutation as a result of an error in DNA replication (since they do not replicate their DNA as they do not divide).
Although I am not an expert in tumours and cancers, I think that malignant tumours in nervous tissue, i.e. brain tumours are fairly common, at least more common than heart cancer by several orders of magnitude. But neurons constituting these tissues are also permanently in interphase and hence do not divide.
 Moreover, secondary malignancies in Brain and nervous tissue is also much more common than secondaries in heart (rare) though metastatic secondary tumours, I believe, do not require oncogenic transformations in the host tissue. A metastatic fragment of a primary malignancy transported by blood is enough to cause secondary tumours.
How then these tumours (primary and metastatic-secondary) are more common in nervous tissue than heart, though both are post mitotic, i.e. permanently in interphase?
Here and here are a few links which give some basics of cardiac malignancies, though they don't address the question quite directly. The study here provides possible explanation of lack of cancer due to high oxygen content.

THe tumors in brain are mostly glioblastoma. Neuroblastoma is rare.

@WYSIWYG That is true, but, if I am not mistaken, the rarity of Neuroblastomas is lesser than the rarity of heart malignancies.

neuroblastoma is more common in infancy and early childhood when there are a lot of neural progenitors. I guess it is not an oncogenic transformation of a mature neuron. Glioblastoma is also not so common; the therapy is more difficult.

@WYSIWYG Whatever may be the rarity of neuroblastomas or glioblastomas, what about secondary tumours?

Well.. i dont know the answer myself; thats why I commented. I am looking up. It is an interesting question.

In case of secondaries, one reason could be that the brain is static (immobile) while heart is dynamic (mobile). It's very difficult for a embolus of tumor cells to adhere to a constantly shrinking and expanding structure viz. heart as compared to a very immobile organ - brain.

This is a specific version of the great cancer question: "Why are some cancers more common than others?" The answer is either "Some have more common causes", and (or) "Some are cured spontaneously more often". So now all you are asking is "What causes cancer?" and "How do we cure it?"
Given that, I don't expect a general definitive answer will be forthcoming. A specific answer might be possible, but I doubt there will be any existing experiments that address this. With the obvious caveat that only experimental or statistical results can really answer your question, here are a couple of off-the-cuff hypothesis for consideration:
1 - Differences in stem cell populations.
Apparently, differentiation can actually be targeted as part of a treatment in some neuroblastoma cases - see the section on "Differentiation therapy" in this page from Sloan-Kettering. Cardiac stem cells seem to exist, but a difference in relative population and turnover rates between brain and heart might be related to the relative frequencies of these types of cancers. @WYSYWIG referred to neural progenitors in his comment above.
2 - A filtering effect due to a more extreme selection pressure in the uniformly stressful environment of the a beating heart.
Although there is a relation between elevated levels of oxidative stress and cancer causing mutations, it could be that this only matters in a punctuated stress environment, where cells have down time to recover. A sustained stress environment might actually helps prevent cancer. The path from normal to cancer cell requires multiple mutations, and I would not expect most pre-cancerous cells to be more fit than correctly wired ones. The extra stress of the cardiac environment might produce an elevated mutation rate, but also produce an even higher rate of apoptosis in early "sick" cells before they accumulate enough mistakes to become become cancerous, resulting in a net decrease in the rate of cancer.
Both of these ideas fit with heart cancer being less common and with metastasis from elsewhere being more common in heart than primary cancer, but unfortunately, a higher rate of clearing of sick cells would necessitate a higher rate of replacement from stem cells, so these two hypotheses partially cancel each other. Again, hypotheses without experiments are not really answers.

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Is love biologically useful?
I thought about this statement a while ago:

Natural selection sucks, it says those who love too much (or too many) will die the easiest and fastest. Sad but true.

Only family (biologically of course) should be loved. This isn't rather an ethics question but whether those who love too many or too much die easiest. true?
NEW QUESTION: What about if you love your subject, mathematics, to death? You'll give up meditating, personality, gym, friends, goldfish, everything just to find out new theorems. What is the take on this?
Surely you'll take a bird's eye view right after the accomplishment (or perhaps failure sometimes) and see what you've accumulated in losses (or in earnings). But Is it in the right path of the true purpose?
Given the person is highly into itself, such that it operates on an ideology instead of what the current trends are (in this case, stay healthy^^), it would be great to love. Nothing else would matter.
Biologically, it wouldn't make sense. If I loved something like mathematics, how in the world could I produce babies? Geniuses like Erdos never had children but, my god take a look at his work.
^^I'm not sure if my claim is correct, which is the matter of this question:
Should we stay healthy or go beyond our health (as the Curie's did) to discover science?

Completely false.  Natural selection is a process by which traits that hurt reproductive success can become less common while traits that improve reproductive success can become more common.  In complex organisms, altruistic behavior and society can be a huge fitness benefit for all creatures in the population.  The ability to love is probably one of the best traits a species can possess.

Also, depending on what exactly you mean by love, the exact opposite may be true. Those who reproduce promiscuously, for example, will be the most selected.

Sometimes fitness may be improved by short lifespan, I'm thinking trade offs between reproductive success and somatic maintenance

@Amory that is very irrelevant. Does it inspire reproduction of genes familiar to the individual?

some animals find that monogamy and small groups and tending to their offspring works for them, others find that having lots of offspring and eating the ones that can't get away fast enough works best.  Biology has a tremendous number of solutions to the one problem.  love is just one of them.

Natural selection deals more with populations and not so much individuals. Its not really accurate to say natural selection says this person will die young if they do X. Its more looking at which traits will proliferate in a population. Obviously since love exists, the quote is not true.

the behavior of individuals are often observed in ethology and the effects of selection/evolution still discussed.  i think the question, to be fair doesn't focus specifically on individuals

@DonLarynx I'm feeling somewhat indebted since I wrote most of the answer before the bounty was put up.  If there's anything I can add or clarify for you, please let me know.

The idea that we only love our family according to biology is not true, but its also not clear what people mean by the word 'love'.  There are many ways to interpret that word!
Hope this doesn't totally suck any romantic ideas out of you, but metaphysical concepts of love and romantic ideas of love are not always relevant when you talk about biology.  A case for the universal human family and world peace can be made.
In evolutionary biology love usually has a different meaning than most people mean, but maybe one similar to what you refer to here; Love is often considered to be the bond with one's offspring to help ensure that they succeed and reproduce.
This idea is most often expressed in terms of "kin selection".  A theory that an individual is helpful to your reproductive success if they carry genes similar to you.  In particular ant colonies may be entirely built around the solidarity of the family unit: all the workers are birthed from the queen and they themselves do not reproduce, but they do work together because, to put it plainly, helping the hive is helping themselves reproduce.
The biologist Sarah Hrdy has written an excellent book that looks at the biological origins and variety of ways that motherhood creates social and emotional relationships, which is not entirely a human idea of motherhood, but biological and mind expanding for the evolutionary take.
However, the idea that only close relatives should be loved is not quite right. Even intuitively we see adults adopting children distinctly unlike them in appearance, people devoting their lives to the general good, etc etc. Biology cannot pretend that this sort of behavior doesn't exist - it can only try to explain it within the framework of what we understand.
Its well understood that cooperation and social cohesion are also the result of evolutionary forces.  The primary reference for this is the iterated Prisoner's Dilemma experiment; in systems where individuals are interacting over and over again, helping others creates a system of cooperation where reciprocity where everyone benefits because the payoffs are stability, security, safety etc.
Again this might not sound like 'love', but in human social, cooperative situations it can be professed as love. Love of country, profession, causes etc if you will.
There is a big debate about whether altruism exists: many biologists believe that an extended from of kin selection is in play - that we're all one sort of human family.  This is essentially an argument that all our energies are self interested on some level - we're just trying to further the interests of the human race because it will help our own offspring do well.
I think it might go further than that - we also care for non human and even ugly very distant forms of life if you look at some people's lives.  One can argue that the realization that caring about the ecosystem is self-interest and not altruistic.  The distance at which this extends kin selection is pretty far, but anyway the argument goes on.
Additional Points: Lots of human interests like science, are a sort of love? They don't seem to help reproduction.
This is a pretty deep point, really.  I'd say it can help to understand question to start with uncles and grandmothers.  Lots of animals do not reproduce, and this is considered okay by kin selection.  Take a look at wolf packs.  The alpha male is the only animal to mate, the other males seem to be hanging out.  First of all the wolves may be closely related, so the avuncular role of taking care of cousins and nephew/nieces is one kin selection argument.  But even if they weren't, there is the fact that pack structure is not biologically altruistic; the other males and females who do not mate may still do so in the future.  In the meantime, the pack cooperation creates a more secure condition where offspring can have a better chance of success.  Lots of creative, cultural, scientific work is similar as far as I can see.  We can adopt non-reproductive pursuits and still feel that we are doing something worthwhile.  I guess the same can be said for adoption, social causes, religion and just about anything else people do which is not having children.
How can this be a selective advantage - included by evolution into the human instinct?  I'd cite the grandmother effect here.  There is some evidence to support the idea that women live longer after menopause because it creates more successful grandchildren.  While this is not a direct effect, any mutation that extends the caregiving instinct would be sustained in the gene pool.  Its possible that if such a caregiving instinct of uncles and grandmothers were to extend to other people, even beyond the family, that it would be sustained in the gene pool.
Indeed being smart and or rich usually doesn't increase the number of children humans have.  In fact the opposite is the case for both statistical and anecdotal evidence.  Few would say that this is a bad thing.  Human being are getting a better deal when they spend energy on better quality offspring, not quantity.  You can look at the r/K selection theory for a better understanding of this argument, but some animals have chosen cheap offspring and many of them - think cockroach or guppy.  These animals would rather eat their offspring than try to feed it.  Humans, more than nearly any other animal i believe, spend their lives caring for helpless offspring until they are ready for life.  Modern life has only extended this from a few years to nearly 20 years.  But it certainly works - the only animal that can compete with human beings is other human beings.
Hope that makes sense.  There's some speculating here, but its hard to dispute that people devote their time and energy to all sorts of things besides mating.  In the end biology has to accommodate such behavior.  Biological theories we call laws don't change the behavior of living things;  its always the other way around.

Shigeta brings up the question of altruism which Richard Dawkins famously explains in the context of evolution in The Selfish Gene. This is probably the easiest way to translate feelings of love into biology.
EO Wilson has also addressed the idea of kinship and  altruism, providing arguments on both sides of the issue at this point. He was an early champion of kinship as a basis for altruism, but has more recently suggested that it requires too much mathematics for the individual to decipher without any real data (I mean you would need a lot of data and some time to figure out whether to save your cousin or your niece and have to make assumptions about your own risk). I think Dawkins ideas make a lot of sense even if they do assume some unconscious math, after all, we can catch baseballs - something that requires a lot of math to solve on paper, but we do it in an instant in our head.
It may be helpful to consider the tribal nature of humans throughout much of our evolution. Who needs math when the real question is merely,'Is this person a member of my tribe or not?'
If we need to consider romantic love, consider couching it in similar language. 'Can I form a strong bond with this person so that we can successfully raise children?'

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Would it be correct to state that any biological difference between the sexes has to be found in the Y chromosome?
If the reason Why Men Don't Listen and Women Can't Read Maps is genetic, then one of the genes in the Y chromosome is to blame and in theory could be identified.
Correct or incorrect?

If it was genetic then the answer is almost certainly yes, but I would think it is more likely due to hormone differences.  Ultimately hormone's are regulated by genetics, but other things can influence them as well, for example tumours, or drugs and many other environmental and epigenetic influences.

check this post. It covers some aspects of what you are asking.

There are two main flaws in your reasoning: 1) you are assuming that male autosomes are equal to female autosomes, which is not necessarily true and 2) you are assuming that such complex traits are monogenic which is definitely false

@Chris why would the answer be yes? See Amroty's answer below and also consider that very few traits are monogenic. I see no reason to expect such differences between the sexes to be confined to the sex chromosomes.

@terdon, I agree with Amory's answer.  I meant if we assume that genetics is the only reason for the difference between males and females (which is the silly assumption made in the question), and considering the somatic chromosomes are selected randomly independent of gender, only the sex chromosomes can account for the difference.  However, that is not to say that the sex chromosomes don't regulate the expression of other genes on other chromosomes, giving rise to gender differences.  So I agree other chromosomes can contribute to gender differences.

...(continuing) other genes can contribute, but they can be present in both males and females, but are just expressed differently.  The reason for their difference in expression is because of the differences in the sex chromosomes that ultimately regulate the other chromosomes.

Here is a book that will probably interest you (it is not published yet)

"Blame" is a strong word.  The human Y chromosome has only a few dozen protein-coding genes.  One of the most important, for males anyway, is SRY, the sex-determining region.  This is a transcription factor that is responsible for modulating the expression of other genes; those genes need not be on the Y chromosome.  SOX9 for example is itself a transcription factor, is upregulated by SRY, and is found on chromosome 11.  Most of the genes associated with maleness are found elsewhere.  Moreover, once the testes form, they can be potent secretors of hormones that cause a number of physical changes.  So is SRY to blame, or SOX9, or the testes?  It depends on how direct you want your genes to be.  If you're blaming SRY you're not wrong, but at that point you might as well blame fate.
Oh, and there are epigenetic differences between the sexes.  You could also make some arguments about the Xist gene responsible for X-inactivation in females.

Imagine a culture where girls are chastised for taking risks, and heavily punished when they take risks and fail, but where boys are encouraged to take risks, and praised highly when things work out their way.
Wouldn't you expect that when put in a situation where such individuals are supposed to make a high stakes action based on risk assessment, that those girls would show much higher stress levels than the boys would?
Big biological difference, having nothing at all to do with the Y chromosome,or genetics at all.  Just the environment.

Good point! It is good to add on Armory's great answer that part of the differences between sexes are due to the fact that both sexes do not live in the same environment (social environment) and this is especially noticeable in humans that have a great culture and (unfortunately) big social considerations of what is a female and what is a male and how they should differ.


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Why don't amino acids get linked in the functional groups of acidic and basic amino acids?
There are 'acidic' and 'basic' amino acids like aspartate and histidine.
When protein is synthesized with those amino acids, what ensures that the to-be-assembled amino acids will not bond to the amine groups or acidic groups in the functional groups of the amino acids in the polypeptide?

When the amino acid comes to the ribosome it is in the form of an aminoacyl tRNA in which the carboxyl group of the amino acid is esterified with the 3' OH group of the ribose moiety at the 3' end of the tRNA.
There is already a growing peptide bound in the P site of the ribosome with a free -COOH group which will react with the -NH2 group of the incoming amino acid in the A site to form the next peptide bond. This reaction takes place in the context of what is essentially an enzymic active site. The reactants will be held in the correct positions for catalysis to take place (in this case the catalysis is carried out by the ribozyme activity of the small ribosomal RNA).
So the answer is that the selectivity of this reaction is just another example of the way in which enzymes are able to carry out highly-specific reactions. So, for example, the enzyme hexokinase, which phosphorylates glucose at the 6 position has, potentially, four other -OH groups that, chemically speaking, could be phosphorylated.

I think it does happen that peptide linkages can happen to side chains.  For the reasons that @AlanBoyd lays out, this won't happen in conventional peptide synthesis and is in principle the answer to the question here.
To add a note though:
Non ribosomal peptide synthases can produce peptides with many subsequent unorthodox modifications.   If you look at the structure of bacitracin, I believe the large ring is closed by condensation between a lysine amine and the carboxylate of the amino acid on the other end of the ring.   There should be plenty of other examples.

So called secondary metabolism pathways create many diverse compounds - nearly anything seems to be possible.

Yes, agreed. A classic example of this is the tripeptide glutathione, a key molecule in controlling redox potential in cells. Glutathione is gamma-glutamyl-cysteinyl-methionine. The bond between the Cys and the Met is a classical peptide bond, but the one between the Glu and the Cys involves the side chain (gamma) carboxyl group of the Glu. This is referred to as an isopeptide bond. But glutathione isn't made by ribosomes, it's made by specific enzymes, so it's the exception that proves the rule.

thanks @AlanBoyd secondary metabolites are a corner case for sure but hopefully useful.

@TomD thanks - was doing the answer from memory. Can't edit the original comment however.


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Does the body lose energy or gain energy relatively when drinking or eating hot things?
Does the body lose or gain energy when drinking or eating hot things compared to more neutral temperature things?
On the one hand,
The body could somehow convert the heat energy into human usable energy,
And on the other hand,
The body heats up and needs to be cooled down, and this way it loses energy.

Depends on the definition of "energy". Energy in physics does not correspond to colloquial word "energy"...

Gains heat; humans are not particularly well-adapted to make use of heat as an energy source.  In a simple matter, if something you eat is hot when it goes in then the average temperature of the body has increased.  More relevantly (and to get this more on-topic for biology), eating anything will generally increase your body temperature, as in order to digest the food your rate of metabolism will rise.  Metabolism produces a lot of heat, and that's what you feel after eating, especially a big meal.
Something like cold water, however, that doesn't require a whole lot of metabolism, will cool you down.  In fact, even drinking hot water might cool you down.  The paper cited there claims that drinking a hot drink on a hot day will disproportionally increase your sweat response such that you actually cool down.


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Why do ladybugs have a different number of points on their backs
Everytime I see a ladybug I ask myself this question.
Why does every ladybug have a different amount of points on its back? Is it because of its age? Or because of its genes? Is it inheritable?

It is unclear if you are asking about variation in the number of spots within or between ladybug species (so intra- or interspecific variation).

I am working on a children's book with a group of friends about a bug named Willow. For this book, we have needed to do research on ladybugs and how they get their spots. Ladybug spots do not tell you the age of a ladybug, but they can tell you the species. Some ladybugs don't even have spots. The most common ladybug is the Coccinella septempunctata or seven-spotted ladybug.

The spots on the back of Ladybugs over the surface is defense mechanism to avoid predators. The spots come in different shapes and different numbers. Some say that those dots tell us their age. Since some ladybugs have 24 spots which means its age would be 24 years and that is not at all possible. So this is a popular misconception running around us.
But the real truth about the number of spots on the ladybugs' back is:

The number of spots on a ladybug does have significance. The spots and other markings do help you identify the species of ladybug. Some species have no spots at all. The record-holder for most spots is the 24-spot ladybug ( Subcoccinella 24-punctata), which has 24 spots, of course. Ladybugs aren't always red with black spots, either. The twice-stabbed ladybug ( Chilocorus stigma) is black with two red spots.

So now we know that the number of spots on the back of Ladybugs will help us to identify what species it belongs to. To give an insight into different species of them you can refer to this Identifying Ladybugs.

The above image shows different species of Ladybugs where you can see the varying number of spots in each bugs' back. More information can be found here Stripes on Ladybugs.

If I am not mistaken there is also intra-species variation in the number and mainly shape of the points.

Though this is a good answer describing how we can use spots for ladybug ID, it doesn't actually answer the OP's question: "WHY do they have multiple spots?" I'm surprised the OP accepted this answer...

Yes, some species like the harlequin ladybeetle (Harmonia axyridis) can have dozens of different morphs, with different number of points.

It is because of genes, and is completely inheritable!   First I want point out that there spots, or points, do not change over time.  Rather the spot number and location is fixed when Coccinellidae are pupa (tween aged insects).
You will notice I said Coccinellidae instead of ladybug.  That is because "ladybugs" are actually several different species of insect.  Thus we refer to the whole family of ladybugs, Coccinellidae.  The spot number, shape, and color is different for different species, which gives you the variation in the number of points.


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Creative ways to deactivate alpha-amylase taken from fungi
I can deactivate $\alpha$-amylase in ways such as extreme temperature controls, pH controls of the solution it stays in, or adding salt to the solution.
However, are there any other unique or elaborate ways to deactivate the enzyme? (maybe the lock-and-key hypothesis also works for enzymes AND enzymes?)

Amylase inhibitors have attracted much attention because of their potential in treating type 2 diabetes.
You can inactivate most enzymes by using a specific inhibitor. One class of inhibitors consists of molecules that resemble the substrate molecules but are not acted upon in the same way. These will bind to the active site and will prevent the substrate from binding. An inhibitor of many amylases is acarbose. This is a competitive inhibitor which means that inhibition is overcome by high concentrations of substrate.
And if that isn't enough to get you started here is an entire thesis on the topic of amylase inhibitors.
If you want to permanently block activity the ideal compound would be one which binds to and covalently modifies the active site, destroying enzyme activity. This would be an irreversible inhibitor. I haven't been able to find a reference to such a compound however.

So, to conclude, does 'enzyme deactivation' simply means 'deforming its active site'? Since both denaturation and using inhibitors basically mean destroying the enzyme active sites.

@Greek Fellows - in fact I almost commented upon your choice of "deactivate". In the context of your question I think that "inactivate" is what you mean. To me the word "deactivate" implies that there is a corresponding activation process - so for example an enzyme might be activated by phosphorylation then deactivated by a phosphatase. Also most enzyme inhibitors don't destroy the active site - they block it by competing for binding.

yeah, I should have been careful about the wording...


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Cytoplasmic determinants - protostomes and deuterostomes
Cytoplasmic determinants are spread unevenly in the egg, and so when embryo starts forming (cells start dividing), the determinants are also unequally divided between cell. This unequal distribution later plays a major role in differentiation and gene regulation.
Protostomes undergo determinate cleavage. Their cells' fates are determined very early in development, whereas deuterostomes undergo indeterminate cleavage. So, if you take away a cell at early stage of development, it can be replaced.
Now if we compare the division of cytoplasmic determinants in protostomes and deuterostomes, what I said in the first paragraph seems true (to some extent) for only protostomes.
My questions:

Do deuterostome oocytes have even distribution of cytoplasmic determinants initially and  divide unequally only after certain number of divisions?
Are there any studies showing correlation between the stage at which determination happens in deuterostome and beginning of unequal division of determinants?

I dont have a definitive answer but the axis of cleavage can determine the nature of the daughter cells. Imagine an antero-posterior (AP) gradient of some determinant X. If the cell undergoes a division along AP axis the resultant daughter cells are identical. However, if the division is perpendicular to the AP axis then two different types of cells are produced (whose fate is in a way sealed).

The two distinct types you have mentioned in your question (determinate/indeterminate cleavage) are actually called autonomous specification and conditional specification, respectively.
In the case of the former one, if we were to remove a blastomere, it would still produce the previously determined type of cells, while in the case of conditional specification the cells, which are going to be produced, depend entirely on the neighbouring ones. The latter's ability to alter their fate is called regulation.
As for answering your questions, cytoplasmic determinants are spread unevenly in deuterostomes as well, as otherwise no axis could be developed.
You might be interested about this answer as well.
I've used the following book as source: Gilbert, S. (2000). Developmental Biology [ online version ]


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What to do with a DNA sequencer?
My school is very fortunate to have a DNA sequencer, and I want to find an opportunity to learn how to use it. I'm currently taking AP Biology this year, and I hope to do an independent study in biology next year, concerning DNA. I'm sure there's plenty I can do with the sequencer, but do you have any cool project ideas?

You might want to narrow that down a little. What kind of equipment do you have access to (apart from the sequencer)? How much time would you have for this project? Do you plan to do this alone or will there be a teacher to help?

Agree with @terdon, but you'll have to do a bit of scouting out of possible options (based on time limitations and supplies), and then maybe this will have a concrete answer based on those.  This is not to discourage you, just to get you a better answer.  IOW, Way to take the initiative so early in your education!

Also, will there be some money available for the project, and if so how much? That may be a limiting factor for certain experiments.

You can [edit] this post to respond to the feedback in the above commments

@Jack What we once did with a sequencer was to isolate bacteria from our rooms and take their dna out and sequence it and then compare the sequences using BLAST and RDP and construct a phylogenetic tree using that. But I think this is a really basic project with no importance except to learn the basic techniques which you can apply elsewhere.

@Jack I had also read an experiment where they isolated microbes from different soils and identified different microbes using PCR and sequencing and then tried to identify which are the most necessary.

Then there was one more experiment in which gut microbes from different people were isolated and it was found that different types of bacteria were present based on whether people were primarily veg. or non veg.

Deciding on your project will also depend on whether you want to use your sequencing machine as a main tool or as a supplement to your project and one more thing - all examples I gave u r regarding microbes but there are gazillion other organisms on which you could try sequencing....This was just to give u a start.


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What is a "pure odorant"?
This article about testing for Alzheimer's, via changes in the ability to smell, said:

She thought of peanut butter because, she said, it is a “pure odorant”
  that is only detected by the olfactory nerve and is easy to access.

I'm not clear on what that means. Assuming a person had their mouth closed, then wouldn't any odor be detected only by the olfactory nerve? Wouldn't a lemon, say, work exactly the same?

good question. you might have to ask the original researcher. This might be her? http://oge.med.ufl.edu/Students/Current/Stamps-Jennifer.htm

To answer this question, you need some background info first.
There are three "systems" used for the sense of smell. The first is the olfactory system. This system allows us to recognize what a smell is. You can tell the difference between gardenias and grass because of your olfactory system. The second system is the trigeminal system. This system tells you whether an odor is irritating or pleasing. It gets its name from the trigeminal nerve--the nerve that gives feeling to your entire face. Your sense of smell is all tangled up with the trigeminal nerve, meaning that some odors are painful to smell and some are not. When you smell ammonia and it stings your nose, that is the trigeminal system at work. The third is the vomeronasal system. It's thought to be use for detecting pheromones. However, it isn't important to this explanation.
So. What is meant by a "pure" odorant? It means that it only smells. It doesn't create a reaction in the trigeminal system. It only activates the olfactory system. Those who have lost their sense of smell are still able to distinguish many smells because of the reaction by the trigeminal system. One study I've read tested 47 different smells for people who have lost function in their olfactory system. Out of those 47, 45 of them were identified by the people with no sense of smell. The two that were not identified (decanoic acid and vanillin) didn't stimulate the trigeminal system and are thus considered to be "pure" odorants. In other words, pure odorants are odors that only smell and don't feel like anything. There are very few "pure" odorants, and peanut butter is one of them.
So, when someone says Alzheimer's changes the ability to smell, they have to make sure they're only testing smell and not touch too. That's why they need to use a "pure" odorant. Otherwise, the Alzheimer's patient might still be able to identify the scent and the test would be useless.

Can you add a reference/review to the description of the three "smell systems", and the reference to the "One study I've read..." section?

One of the downsides to asking questions on this site, (unlike tech-sites), I'm not really qualified to decide if an answer is correct. :) But looking at it, it does answer the issue of "pure-ness" in an odorant, so giving a checkmark.

I could not find a concrete definition after searching several sources, but after reading a few papers I think the term Pure Odorant refers to its Olfactory Bulb profile. Peanut Butter will stimulate specific Olfactory nerves, and only that set of nerves, whereas impure Odorants may stimulate part of the profile and also other parts of the Bulb depending upon the impurity.
Basically, Peanut Butter has a unique smell that you can't replicate, and thus cannot mistake in either flavor or scent when compared to similar compounds. You may  not even be able to tell it was Peanut Butter at all if not for the scent.
A Lemon would not work the same way, as the major Odorant in a Lemon is Limonene - which is present in all citrus fruits. You would activate the same neuronal pathways for Lemons that you would with Oranges, Limes, and Grapefruits.
That's my best assessment.

So you're saying that peanut butter stimulates only a small section (of the Bulb, whatever that is), whereas other scents will trigger multiple nerve sections, and so can be faked with a different set of odorants?

@JohnC - More or less. Peanut Butter has a unique scent and is readily available. Using purified Limonene would work, as I'm sure there's a nerve profile for Limonene - but the purified product isn't readily available. The benefit of Peanut Butter is specificity. It's a known scent (to people in countries that like peanut butter), and a unique scent that's instantly identifiable. You could confuse oranges with limes or lemons by scent, but a healthy person will always recognize peanut butter as peanut butter. It tests sense of smell and cognitive function simultaneously.

Not sure I really understand why a "pure odorant" was needed for the test, then. All they were doing, was measuring the distance at which the odor could be detected, not what it was. While I can see that peanut butter is useful, for non-odor reasons (sticks to a spoon, etc), I still don't see why a lemon (or lemon juice on a Q-tip) wouldn't have worked just as well. Possibly that line was just intended to sound more scientific than, "it sticks to the spoon." :)

@JohnC - There may not have been a very good reason. They wanted something with a unique smell that was cheap, and Peanut Butter was probably a convenient option. More important than the smell is the caveat that the lack of smelling abilities found in the study can be attributed to more than just Alzheimer's. It's a quick and dirty early signal, but it also has a pretty high false-positive rate.


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

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


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When designing primers how important is the GC clamp?
I'm designing a set of primers and reading about the principles of primer design one of which is:

GC Clamp: The presence of G or C bases within the last five bases from
  the 3' end of primers (GC clamp) helps promote specific binding at the
  3' end due to the stronger bonding of G and C bases. More than 3 G's
  or C's should be avoided in the last 5 bases at the 3' end of the
  primer.

From here.
My question is how essential is it to have a GC clamp?

If it is important to have G or C why more than 3 G or C should be avoided ?

@biogirl more G/C should be avoided because in an event of pairing between the primers you don't want the pairing to be too strong. Otherwise you'll get a lot of primer dimers.
Ben, GC clamping is important as it will allow strong bonding at the 3' which is good for elongation but this is not the primary parameter to be tweaked. There are other important parameters to handle (for e.g self complementarity, low-complexity etc).

It's hard to provide an objective answer. If you have a decent length and good complexity, even a single terminal 3' G or C would do. Of course, one has to take into account the primer's overall GC:AT ratio and things like annealing temperature.
Here's a link to diverse opinions on the topic and it has this nugget (which I subscribe to when possible):

FWIW, my preferred offerings to the PCR gods are primers with a single
  G or C 3', FWIW. Seems to keep 'em happy most phases of the moon.

I will offer my own (empirical) account of primer design. A GC-clamp aids in specificity of the priming and therefore contributes to the overall efficiency of the PCR reaction. In the past, I have (out of necessity) designed primers that had both too much GC-clamping on the 3' end, and used primers without any GC-clamping. These PCR reactions were performed successfully, with differing levels of primer-dimer formation and overall efficiency.
In my experience, GC-clamping is nice, but not strictly required for good PCR. My general rule-of-thumb is to terminate my primers with 2 G/C wherever possible. If something is going to fail, it is not usually the PCR.

GC clamping at 3', that is having a single G or C at the 3' end or a couple of G/C within the last 6bp at 3' end of primer, can help retain the primer on the template during elongation, because of stronger bonding compared to A=T. This is not mandatory; it's one of the characters of the primer which might improve your PCR reaction.
At the same time, avoid a sequential combination of GC in the last 6bp which might lead to self-dimers.
Example: 5'-.....GCGC-3' has higher chance of dimer formation than 5'-.........GCCG-3'; in such cases you can still use the latter primer sequence.

Unless you are PCRing something you know to be challenging, just use primer3 and don't worry about it.
http://bioinfo.ut.ee/primer3-0.4.0/

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


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Alternating Ovulation
I have often heard that right and left ovaries alternate in releasing ovum.
Is it always true? What controls this rhythm? Is it simply because the other ovary is unresponsive to LH or FSH? If so, why?

I am not sure if this alternation occurs. Can you post the reference ?

Nope, not true.  It's a pretty common myth; that paper cites a  reference from 1932 in primates claiming to show that the ovaries alternate.  A few papers before this, in particular this one from 1991 showed that ovulation was not alternating, but this was the first to do so in actually fertile woman.  In particular,

Alternate ovulation occurred in 61 of the 119 succeeding ovulations (51.3%, not significant) which means that there was no consistent tendency to alternation.

Alternation only occurred half the time.  Neither did they find a difference between side preference; right-side ovulation occurred in just over 50% of the cases, not significantly different.
FSH, follicle-stimulating hormone, and LH, luteinizing hormone, stimulate each ovary equally, but one ovary will get slightly ahead.  Ovulation (and indeed pregnancy at times) is a positive-feedback loop, meaning the response will be exponential; if one ovary is even just slightly ahead it will rapidly dominate the other.  The less-developed one quickly senses the other is ahead of the game and ceases to respond.

Can you provide details of the positive feedback loop and the sensing the "lost race" by the less developed ovary as mentioned in your answer?


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Presence of MHC on red blood cells
Do red blood cells have no MHC? (I have often heard that they do not.)
If so why are they not destroyed by immune cells?

Actually, effete red blood cells are eventually removed from circulation by immune system phagocytes. While this would not involve an MHC-mediated mechanism, the means the immune system recognizes dying RBC's is an interesting field of current research.

They do not, at least not normally or noticeably.  MHC I occurs on all nucleated cells, and red blood cells do not have nuclei.  If they did indeed have MHC on them, blood transfusions would be as successful and as tricky as organ donation.  There are reports of MHC detection on red blood cells, but the amount is orders of magnitude smaller than elsewhere, only present for certain MHC alleles, and often transient.

So why are they not rejected by immunity cells ?

@biogirl I'm not sure what you're asking.

@Biogirl - They can be if they have the wrong blood-type or Rh factor.

@Amory I think immune system kills those cells who do not have MHC molecules on them. So why shouldn't RBC be killed?

@biogirl Ah, I see.  It's not particularly well known, but the two main theories are that either RBCs lack additional markers needed for natural killer cells to engage, or that RBCs express additional proteins that inhibit destruction, such as CD47 in the case of macrophages.  I'm actually doing research on a very related topic so I'll just say that I think it's closer to the latter.

@Amory Ok, I get it now. Thanks !Hope you find something really exciting with your research !

There are other histocompatibility antigens on the surface of blood cells, e.g. A, B, Rh, etc... (There are probably a lot more which change less by person to person, so they have lower effect on the outcome of blood transfusion.) These antigens can be recognized by immune cells as self, that's why they don't destroy them. Before complete differentiation RBCs have nuclei, so they can have MHC1 remnants on their surface from that period of their development. RBCs are relatively well tolerated by the immune system especially with coverage.

wikipedia - Blood type
2012 - Transfusion in the absence of inflammation induces antigen-specific tolerance to murine RBCs
2014 - Simultaneous Camouflage of Major and Minor Antigens on Red Blood Cell
Surface With Activated mPEGs

you are right.red blood cells do not have noticeable MHC 1 molecules.But rather the have high levels of CD47 markers which are recognized by the immune system as self.On the other hand red blood cells during development are nucleated they may contain small traces of MHC 1 molecules.I hope this answers your question.

Welcome to Bio. Can you add sources to your answer?


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Number of genes required to sustain life
Are there estimates of the minimum number of genes required to sustain life?
In what I mean by life here, I don't include viruses.

Interesting question, but you'll need to define needed as well. There are lists of essential genes, those whose loss is deleterious (at least in yeast). If you are looking for the theoretical minimum possible in an imaginary organism, that is a different matter.

Since RNA is the presumed precursor to DNA and might have sustained life before DNA evolved, do RNA counterparts count?

well.. i think if you exclude viruses then you should also exclude mycoplasma because both are obligate parasites.
So when you say minimal genome it is essential to define the conditions under which a genome has to function. The retroviral genome is sufficient to sustain life given a host. For free-living organisms the number of genes is obviously higher.

Related wikipedia articles: Constitutive gene, Housekeeping gene , Minimal Genome and repressible system. Though they are not same thing, but they are related concepts.

Depends on what kind of life you want!  The Database of Essential Genes lists genes essential for life for a number of species, although I would be wary of some of the numbers; bacterial results are probably more reliable but it lists 118 for humans and 2114 for mice.  There are a bunch of different numbers for different E. coli strains, with larger numbers being published earlier, go figure.
It of course varies by species.  In mid-August of this year, scientists reported the smallest genome yet: 112kb with only 137 protein-coding genes (predicted).  Crazy!  That doesn't mean it's the smallest number of genes though, just what we've found.  Some folks in 2006 predicted the smallest would be 113kb and 151 genes - pretty close close to the above, all in all.
For something a little more familiar and studied, though, Craig Venter has made synthetic biology his goal.  Part of trying to create life is knowing what the bare minimum is.  Working with Mycoplasma genitalium, he and his crew knocked out each gene and found that 381 were indeed essential.


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Blood Pressure: Significance of difference between systolic and diastolic
I wanted to understand what is the difference between systolic and diastolic readings of blood pressure. I understand 120-80 to about 100-60 is considered normal but does the difference in the two values in the reading hold any significance?
I have read some text here and here.

The difference between systolic (the upper number) and diastolic (the lower number) pressures is known as the pulse pressure:

Systemic pulse pressure = Psystolic - Pdiastolic

For a typical blood pressure reading of 120/80 mmHg the pulse pressure is therefore 40 mmHg.
It is proportional to stroke volume, the amount of blood pumped from the heart in one beat, and inversely proportional to the compliance or flexibility of the blood vessels, mainly the aorta.
A low (also called narrow) pulse pressure means that not much blood is being expelled from the heart, and can be caused by a number of factors, including severe blood loss due to trauma, congestive heart failure, shock, a narrowing of the valve leading from the heart to the aorta (stenosis), and fluid accumulating around the heart (tamponade).
High (or wide) pulse pressures occur during exercise, as stroke volume increases and the overall resistance to blood flow decreases. It can also occur for many reasons, such as hardening of the arteries (which can have numerous causes), various deficiencies in the aorta (mainly) or other arteries, including leaks, fistulas, and a usually-congenital condition known as AVM, pain/anxiety, fever, anemia, pregnancy, and more. Certain medications for high blood pressure can widen pulse pressure, while others narrow it. A chronic increase in pulse pressure is a risk factor for heart disease, and can lead to the type of arrhythmia called atrial fibrillation or A-Fib.


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Why are humans and almost every species on earth symmetrical?
I admit I'm not very learned on the subject of evolution, I just started researching it for myself about a week ago. One of the things that I don't understand is why humans and almost every other animal/bug/fish etc. on earth has a symmetrical body. What advantage does this have for the survival of the fittest? It must be quite important, since it re-occurs so frequently and early in the evolutionary family tree.

Related Question: http://biology.stackexchange.com/questions/5588/why-is-most-life-symmetrical-externally-but-not-internally/

Only Bilateria (http://tolweb.org/Bilateria/2459) are bilaterally symmetric like humans. Millions (billions?) of other eukaryotes and  prokaryotes (by whatever names they are going these days) are not symmetric.

still a fair question - perhaps change to: "why are humans and most animalia phyla symmetric - bilateal?"

This is not a duplicate, the other question is about lack of internal symmetry, not the evolution of symmetry in general.

@kmm.. there are others that are radially symmetric too.. some unicellular organisms also have an axis of symmetry..

@WYSIWYG Good point. I assumed bilateral symmetry because the OP asked about humans.

Come to think about it: Almost every vehicle that human beings have designed is bilaterally symmetrical, exlternally at least. Symmetry makes coordinated movements simpler. This is just a thought.

[If we are talking about animals, there is a number of types of body symmetry: asymmetry, radial, bilateral, spiral, rotational, glide and metameric symmetries. Bilateral and radial are the two basic types, which served as main classificatory character for animal mega-systematics in the past.]
It's assumed that body symmetry is associated with general environmental gradients.
Animals with (elements of) radial symmetry have one dorso-ventral axis which echos only one environmental gradient: substrate/water column, depth etc. Besides this polarity, resources/signals/danger may come from any direction. Imagine a Hydra polyp with its foot attached to a waterweed and its tentacles surrounding the mouth on the opposite end and expecting the victim to come from any side.
Body of bilateral animals possesses the same dorso-ventral axis and yet another polarity, orthogonal to it: the anterior-posterior axis. This axis is conjugated with the gradient created by locomotion: the anterior margin of the body is likely to encounter something new first. This principle lies in the basis of cephalization: most bilaterial animals have more or less shaped "head".
Evolutionary changes in body symmetry are thus thought to be associated with changes in life-style, e.g.:

there is a hypothesis that cnidarians were originally bilateral (and many of them still show some degree bilaterality), but lost it after becoming sedentary.
non-walkers echinoderms originated from fully bilateral animals and later acquired their famed pentameric radial symmetry (were they originally fully sedentary like modern stalked sea lilies?). This symmetry, however was again distorted towards secondary bilaterality (not matching the original plane of symmetry) in endobenthic forms: sand dollars and some holothurians.
worms like nematodes or priapulids are dwellers of viscous media, similar in all directions: dorso-ventral gradient of environment in this case is absent or weak. Though the original bilateral symmetry is very clear in their body plans, signs of radial symmetry prevail in some organ systems, including the general vermiform appearance. Thus, nematodes combine triradial (head sensilla, pharynx), biradial (musculature) and bilateral (nervous system, genitalia, tail) symmetries.


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Antibody production in secondary immune response
Can IgG antibodies be produced in the secondary immune response without the help of T cells?
Is the affinity of antibody for antigens higher during secondary immune response?

1)  The secondary response requires CD4+ T cells to activate memory B cells.  That first paper actually gives some evidence that some of the rapidity could arise because T cells and memory B cells are in very close proximity to each other in germinal centers.
2) Yes.  The affinity of antibodies increases during the initial infection, both through isotype switching and affinity maturation, producing far superior antibodies.  Upon reactivation, memory B cells can undergo further somatic hupermutation.


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Shade-loving Plants
In shade-loving plants, the light compensation point is reached at low irradiance because:
A. Leaves have more chlorophyll per reaction center
B. These plants have greatly reduced respiration rates
C. Shade-loving plants synthesize anthocyanins
I am mainly confused between A and C. I am sure that A is factually correct but I don't know whether it is correct in this context.

I think the answer is A. As for C, Anthocyanins are located in the vacuole and their light absorption does not affect the process of photosynthesis which occurs in the chloroplast. Anthocyanins do participate in prevention of High-Light Stress (or Photoinhibition) but they have no role to play in gathering light energy for photosynthesis. Therefore, to improve the quantum efficiency (quanta of light per CO₂ molecule fixed or O₂ evolved, or any other quantifiable photochemical event) of the light reaction, anthocyanins play no role.
But, if there are more chlorophyll molecules per reaction centre, i.e. there is a greater number of chlorophylls in the LHC (Light Harvesting Complex), or the Antennae system, then the quantum efficiency can be improved, the absorption band widened and thus the light compensation point is reached earlier. The extra molecules of chlorophyll  absorb energy at their specific wavelengths of light and transmit this energy to the main reaction centre by FRET(Fluorescence resonance energy transfer). Therefore, greater the number of chlorophylls per reaction centre, greater is the light energy absorbed and transmitted to the reaction centre and hence, better is the quantum efficiency.
More technically, having more chlorophylls open up more pathways for photochemical energy quenching, and thus improves the efficiency by minimizing fluorescent losses.


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What are uses of fossils?
What are the geological uses of fossils and how could it be utilised?
From The Institute for Creation Science:

Fossils are typically found in sedimentary rock, almost all of which were originally deposited as sediments by moving water. Subsequent processes hardened them into sedimentary rock, as overlying pressure squeezed the water out and the grains were cemented together. Often plants and animals were trapped, being buried in the sediments. As the sediments hardened into sedimentary rock, the dead things hardened into fossils.

This question appears to be off-topic because it is about geology.

What exactly to you mean by uses?

Utilized by whom? I use one as a paperweight.

That is a direct quote from a creation science website, a rather disreputable source.

@Amory did you read that article? It contains this wonderful gem of logic: "One more thing. These catastrophically deposited marine fossils, entombed as they are in regionally extensive sedimentary rock, are all found on the continents! There are hardly any marine fossils found in the deep ocean basins." So, fossils are found more often on the continents than in the deep ocean, and this has nothing to do with the fact that it's a wee bit more difficult to search the bottom of the ocean than to search my back yard! Ain't the bible grand?

Beautiful!  I think my favorite was "...these fossils were found as creationists did their research from a creationist/flood perspective. They found what evolutionist/uniformitarian seekers missed."  As if.

I want o lmfao because ...

Since you're talking about Geo, then the short answer to that would be:
To check how long such specie (animals or plants) existed on the planet (earth obviously)!
For example: You came to know about Dinosaurs using the Fossils and you made up their whole skeleton and then using your imagination you created the body.
Usage:
Keeping the above example in mind, fossils are used to know the period of extinction of the living being or the existance or both.
Fossils are sometimes used as Fossil fuel too, but that's in liquid form when they are decomposed anaerobically by the bacteria and all that info, please check the reference for this.
And what is the last paragraph about? Some information eh? I was not able to understand its usage and utility to the question! Sorry :)
Reference
https://en.wikipedia.org/wiki/Fossil_fuel (Fossil Fuel)


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Why do I have a lot in common with my mother?
I have not spoken to my mother in 15 years but recently connected with her and her side of the family. I was primarily raised in a different sub-culture after the age of 4. As it turns out I "accidentally" have a lot in common with my maternal relatives. We like and dislike many of the same things. Is there some dominate trait in our nature which affects our psychology to cause us to agree on everything from TV, food and lifestyle?

Certainly genetic and epigenetic effects could be underlying a tendency to have similar likes and dislikes. Essentially you are asking if behaviour and personality traits are heritable right??

@GriffinEvo yes and if those traits can be dominant and recessive.

@caseyr547 Behaviour, though partly genetic, is highly influenced by epigenetic, environmental effects and hence cannot be attributed to genetic or environmental determinism perfectly. It has some genetic determinism, but it is much complicated by non-allelic interactions, polygenic effects, and also "non-mendelian" allelic interactions, hence is usually not simply dominant or recessive.

@SatwikPasani makes a good summarization, and the same could be said of most traits,  phenotype = genotype + environment

It's also surprising how much your tastes and personality can be set by the time you're four.  We may not remember much from the time before then but those years are hugely formative.

Time in the womb is a major consideration too

All of the other comments are sure true, but you should also consider confirmation bias. You have been reunited with someone after a long time and probably the things you have in common surprise you more than those that you have not in common (which you tend to forget). You should ask someone else (best would be a stranger) to take, say, 50 different "characteristics" (e.g. "like cinnamon in cake", "like skying" etc.), then count how many you have in common with your mother. Then repeat the same exact count with someone who is unrelated to you.

@nico i actually did a comparison with another relative. I didnt keep tabs but the other relative had little in common comparatively.

In this answer I mainly repeat the comments!
There are several reasons why you might share some traits with your mother.

genetic (see below)
epigenetic
environmental influence while being in the womb
environmental influence up to the time you were 4 years old
the two environment were not so different (maybe because your adoptive parents wanted to follow the will of your mother or just because by chance your adoptive parents have similar behaviour that your mother)
multiple testing issue (see below)

These reasons can be classified into three categories:

environmental variance
genetic variance
poor observation (statistic mistake)

The phenotypic variance in a population is influenced by the environmental variance + the genetic variance + the variance due to the interactions between the environmental and genetic variances. The heritability can be calculated as the part of the phenotypic variance which are genetically determined. Such calculations make sense only for populations not for a given parent-offpsring pair.
genetic: It does not make sense to ask whether the variance of a trait is dominant or recessive. It makes sense to say that "liking pink" is dominant over "liking blue". Therefore, you should tell us what is the variant of a given trait that you share with your mother. In such case we might tell you if this variant is dominant or not over the other variants. But of course, this works only for traits that are at least slightly genetically determined. liking a color will certainly not have a strong genetic variance for example. And even if a trait is 100% genetically determined, complex genetic architecture might make it hard to answer. For example a given variant might be dominant in a given genetic background but recessive in another. Finally, I should say that it costs to perform the necessary study (Genome Wide Association Studies) to know exactly the part of the variance of a given trait that is genetically determined. And of course, such studies depend on the population we look at.
Multiple testing issue: Without realizing, you actually looked at many different traits. You might have looked at your favorite color, your favorite beer, the way you wash your teeth, the sport you practice, the color of room, whether you are calm or impulsive, etc... You might not have paid attention only to things that match but you would have found as many similarities (not the same ones though) with any other human on earth.


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Won't natural selection miss the overall minimum of a function?
Suppose we have a population of about 1000 with an environment that does not change a lot (e.g. the atmosphere is more or less the same) and we leave this population to evolve. From what I understand some genes will be lost because they won't be suited enough to continue in the next generation. Also the generations can only reproduce within their generation (e.g. a male can only have reproduce with people from his generation).
My question is: won't some genes, combined with others have a better chance to make the individual "better" but they for example make it less fit right now. Or will the mutation of the genes actually promise that eventually we will hit that minimum of the function.
I want to point out that I'm a computer scientist and my biology is awful. I'm looking at this from evolutionary algorithms point of view in particular genetic algorithms.

Can you clarify what you are asking?  That second paragraph is very confusing.

As in evolutionary algorithms (you might know from computer science), real evolution is random. It might hit a local minimum, but miss the global one. Different to evolutionary algorithms, evolution can even make things worse for a while, so there is a chance to have a "bad" mutation "surviving" long enough to be paired with another mutation that actually makes it "good". But it is random.

Indeed your second paragraph is confusing. What function are you talking about. It seems that in you example, two individuals with the same genotype in the exact same environment have different fitness. It is theoretically not possible. Does your question has to do with genetic interactions [http://en.wikipedia.org/wiki/Epistasis] or gene-environment interactions [http://en.wikipedia.org/wiki/Gene–environment_interaction]. What does your question has to do with game theory? Are you talking about newly arising mutations or only about alleles (gene variants)?

Your second paragraph starts with "My question is..." but does not actually contain a question. What are you asking? There is a well known mutation that  makes individuals susceptible to sickle-cell anaemia but the same mutation also protects from malaria. Is that the kind of thing you're thinking about?

It sounds like you're asking about local minima that is, "dips" you can get stuck in though there might be a "valley" next to you?

If this is what you're asking about, I think is referred it as a "stable state". In ecology, we think about "alternative stable states" all the time, and certainly some might be "lower" than others on whatever metric you're measuring. I think the real question from a modeling perspective is is the population stochasticity/"jiggle" large enough to get over small humps?

You're absolutely right. Evolution is path-dependent. It can't progress toward features that would ultimately enhance fitness unless each step enhances fitness by itself.

@octern This depends on population size. Founder effects or stochasticity in small populations can cause traits to go against fitness gradients, which could potentially bridge local fitness valleys.

Perhaps it would have been more accurate for me to say that selection can't progress in that way. You're right that the overall process of evolution includes random events that prevent it from being a pure fitness maximization function.

very tempted to downvote this, please elaborate on what you mean by overall minimum

What I think the question is "Why wouldn't an organism be more efficient from selection than the environment demands?"  Please let me know if I'm hitting the mark here.
A scenario suggested by the question is this: If there is selection pressure on say an animal to resist a disease, and then it evolves two resistance systems to the disease.  This could be an immune response and a taste for a certain plant containing compounds with remedial properties.  If either system is adequate to resist the disease, hasn't selection gone above and beyond what is needed?
If so, the answer is either not recently, or all the time.
First, for 'not really' you have to consider the importance of competition.  Reading about the Red Queen's Hypothesis is helpful here.. First there is a natural random mutation rate, which can cause one of the system to become less effective.  Or if the disease is also changing to increase its efficiency, then either one or both of the defense mechanisms in this case would fail from time to time.  Then having two systems would not be too much. There is a clear benefit to having redundant systems of resistance here. For both these broad categories of reasons, you have much redundancy and interdependence among the genes which create traits in living things (phenotypes).  Because of the background mutation rate, traits which are not needed disappear relatively quickly; because of competition, those which convey an advantage, even if a small one, have a strong likelihood to stay in the gene pool.
now: "all the time" There are cases where traits are exhibited that are not efficient though. Evolution works over generations, typically selection influences traits on the order of 10s of generations and the population can show traits which are not helpful if the environment or the competition has changed drastically.
An example of this is the current obesity epidemic in the developing world. The sudden availability of cheap food has caused those people who have access to become obese.  This is because they have a heavily reinforced trait to save up fat because humans experience famines regularly.  Its going to take a long time before efficient energy storage in human beings is lost.  In the meantime, people are not living to reproducing age at the same level of fitness they might have.
I want to add a note on genetic algorithms.  The difference between genetic algorithms to achieve the same efficiencies as biological systems are worth thinking about:

As far as failing to find a global minimum, natural selection usually has many more samples.  A typical selection experiment with flies or worms often have thousands or tens of thousands of individuals screened.  GA models of reasonable complexity have usually a few score at most - am I right?  A bacterial or yeast experiment can have 10^9 individuals.

The genetic system of the chromosome itself is tremendously complex.  We can't even model itself and so the product of millions of generations of selection already will has a heretofore unmodelable response to selection.
The typical selection environment is equally undefinable, so a survey of living things in a complex environment has unpredictable effects.  While most of us think as laboratory experiments as being less complex, its not completely true.  I was at a talk recently that mentioned how E coli K12 seems to have diverged in various laboratory environments despite the fact that its mostly been in frozen stocks since being isolated in the mid 20th century.

Re: Red Queen's, van Valen's original paper has perhaps the best acknowledgement ever: "I thank the National Science Foundation for regularly rejecting my (honest) grant applications for work on real organisms...thus forcing me into theoretical work."

@Oreotrephes That's amazing.

@Oreotrephes Van Valen's paper is wonderful in all its weirdness, and provides useful perspectives on scholarly communication.

I'd not read this either - thanks @Oreotrephes!

Im going to take a stab at this. I think he is saying that sometimes there will be mutations that will occur in a population that are beneficial, but only in certain environments. But he is asking, wont these mutations be eliminated often, since they may not be in an environment where their advantage is obvious?
First, there is something incorrect in your original post. You said "From what I understand some genes will be lost because they won't be suited enough to continue in the next generation". It is kind of unusual for a whole gene to be lost. Especially from a whole population! I think what you mean is 'allele'. And yes some alleles will be lost. But fitness is a gradient. Just because a mutation does not have an obvious advantage does not mean it will be lost. Most mutations are not really noticeable. In a recent post here, I think I quoted a website that says there are 70 or so de novo mutations every generation in humans. This means that both you and I have 70 new mutations that our parents did not. But we are both functioning just fine (I hope!).
And some of these mutations may be beneficial in certain environments, but dont do anything in others. Lets say that one of my de novo mutations was to make me sweat less. Not really noticeable, right? And it really wont give me fitness advantage or disadvantage, so natural selection wont really act on it. It's frequency should remain at about a constant level in the population . But now lets say something happens to the world climate and there is a drought that lasts for centuries over N. America. My mutation would now give me a fitness advantage since my body would lose less water.
So, to answer what I think your question was, natural selection will not always act on every mutation. It has to clearly give a fitness disadvantage to select against it, or an advantage to select for it. So if it gives no immediate advantage, it may not spread through the gene pool very quickly, if at all, but it will still be there. So when it is in an environment where it is advantageous, it will still be around, and then it will begin to spread through the population.


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Calling for Free Online Data for Paediatric ECG?
I need free online data about heart murmurs to study these:

heart murmur frequency , S2 heart sound frequency and its split,
  murmur timing, and duration, murmur intensity, S3 sound presence and
  intensity, S1 presence and intensity, presence of ejection sounds and
  arrhythmias

I will cite your source then if I can use your data freely.
I would really have the same data as used in this paper:

Heart energy signature spectrogram for cardiovascular diagnosis
  Vladimir Kudriavtsev, Vladimir Polyshchuk and Douglas L Roy

No pediatric ECG data here

beecardio (aggregation of many ECG databases)

Does anyone have simple data for my task?
I remember that some CD of some book has some standardised nicely organised sounds that you can use freely.

Where does ECG come into this?  It seems like a question about auscultation.  What sort of data are you actually looking for?

Normalised and well measured. This type of data: https://dl.dropboxusercontent.com/u/62073194/bmt-2012-4075.pdf They do not share their data publicly. I have asked for the data, but they have ignored my request and do not want to share it.

I recognize this was asked like 7 months ago, but in case you're still looking for a good resource:
I used a CD of heart sounds that is called something like "Harvey Heart Sounds," which I got with the purchase of my stethoscope.  If you can find a copy of this, I found it an excellent tool when training to recognize the differences.
These are good heart sounds: http://depts.washington.edu/physdx/heart/demo.html
If you were looking for something other than the sounds themselves, then I'm not sure if you're asking about.  There are all sorts of good ECG references, especially Dale Dubin's EKG Interpretation book.  And Kablunde was the cardio textbook I used, which I liked.

Thank you for your good answer! It is never too late. This is a research topic. I need so clean sounds as possible and preferably many so I can then compare and contrast and decide which one is the most cleanest.

Hmm. I am not sure if these sounds are pediatric. Do you know who has recorded them? Any confirmation about how old the patient has been? I am thinking about the normal heart sound.


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cellular respiration
What are the effects of addition of these chemicals to actively respiring cells ?
Which of them would lead to INHIBITION of aerobic respiration ? Would cytochromes be actually taken up by cells ?
a.addition of CO
b.addition of CO2
c.addition of cytochromes and flavoprotein

Come on. I know that you know the answers to almost all of them :)

I hope I'm not wrong here: More CO in the cells cause numbness over that region by temporarily inhibiting the functions performed by the cell. (I guess my Biology teacher once told us how some body parts go numb after sitting for hours. Wherein the respiration process is slow with less intake of O2 which causes accumulation of CO in the cells of the parts which is cut out of blood supply).

@WYSIWYG I actually wanted answers to mainly these 3 and I have edited the question. The question given in my homework is  a bit twisted(not exactly the question I am asking) so I think I just got crazy and asked some silly things :)

If you're loving Biology, then you can either try using some sort of Library or Wikipedia, and I am really amazed with that lot much of Questions :) I don't even have answers that much! :P Good girl..

Carbon Monoxide "CO" would definitely inhibit aerobic respiration. This is in fact the mechanism of the toxicity of compounds such as carbon monoxide and cyanide, namely, carbon monoxide binds (coordinates) with an affinity several orders of magnitude greater than oxygen to the heme group of mitochrondrial cytochrome oxidase, thus inhibiting the enzyme. When the respiratory electron chain is no longer drawn by the reduction of molecular oxygen, the hydrogen ion gradient across the mitochrondrial inner membrane is depleted, and ATP production halts.
Carbon dioxide would not effect the electron transport chain directly, but is rather involved in the reactions of the citric acid cycle, although, in all likelihood, the cell would die of acidosis before CO₂ concentrations became great enough to reverse the citric acid cycle. Cytochromes and flavoproteins are complex molecules that if the cell were to endocytize them, it would simply digest them.
I do not know your degree of experience in biochemistry, but if you wish, search on the internet for protein structural images of cytochrome oxidase or hemoglobin bound to oxygen and carbon monoxide. Oxygen binds the iron of the heme group at an angle, while carbon monoxide binds directly perpendicular to the heme ring. This difference in geometry is partially responsible for the differential affinity of the two species for heme.


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Termination of translation
What dissociates first - the last tRNA, mRNA and release factors or the subunits of ribosomes?
I tried searching this from Lehninger but couldn't get a clean answer.

Shigeta's got a point: the ribosome is latched onto the mRNA so those two are intrinsically linked.  You're really asking whether the ribosome comes off first or whether the tRNA does, but it's actually the new polypeptide, which makes sense:

The stop codon is recognized by a protein, the polypeptide chain release factor (RF), which triggers the hydrolytic release of the nascent polypeptide chain from the P-site-bound peptidyl-tRNA.

This minireview puts forth a model (see below) where, in E. coli at least, the 50S ribosome subunit is then dissociated from the mRNA/30S subunit/tRNA complex, following which the final tRNA is removed.  An in-depth review from a few years later gives more context.

just off the top of my head... since the ribosome is made of 2 large complexes which assemble and clamp onto the mRNA, I'd say it was the tRNA first, then the ribosome and mRNA would detach simultaneously.


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What is the strength of human cornea?
What is the difference of pressure a human eyeball cornea (cornea, lens and other elements separating vitreous body from air) can handle? Or asking differently: what the outside pressure should be to "blow up" a healthy man's eyeball?

Normal pressure in the eye1,2 is between 10 and 21 mmHg (somewhere around 1.3-2.8 kPa or 0.01-0.03 atm) with pathology occurring at around 30 mmHg.3  Clearly the cornea can handle that, but how much more?  There's a lot more evidence as far as I could see for how well surgeries hold up, with 150-300+ mmHg (20-40 kPa, 0.2-0.4 atm).4  One source5 from 1998 cites work supposedly showing that the stroma:

gives the cornea 100 times more strength than is necessary to withstand the maximum intraocular pressure under physiological conditions.

So maybe around 200 kPa, for just the stroma?  Interestingly, a new eye layer was discovered earlier this year; this Dua's Layer is incredibly thin - 15 microns - but can withstand pressures of around 100-200 kPa (750-1500 mmHg, 1-2 atm).6,7  The large range there is due to some conflicting numbers in those links; the 200 kPa is the more widely reported one, but again, that's just for one layer.
Then, of course, there is this: a beautiful 2009 thesis by Jill Aliza Bisplinghoff from Virginia Tech which thoroughly examines the issue.  As an answer to your question, it includes the following such gems:

The high rate pressurization of 20 human eyes resulted in a mean rupture pressure of 0.97 ± 0.29 MPa (7275.60 ± 2175.18 mm Hg)... A student T-test revealed that the difference in the rupture pressure between the equatorial mean of 0.93 ± 0.30 MPa (6975.57 ± 2250.19 mm Hg) and the meridional mean of 1.13 ± 0.21 MPa (8475.70 ± 1575.13 mm Hg) was not significant (p=0.16)

and

A pneumatic cannon was used to impact eyes with a variety of projectiles at multiple velocities... The projectiles selected for the test series included a 6.35 mm diameter metal ball, a 9.25 mm diameter aluminum rod, and an 11.16 mm diameter aluminum rod... A range of internal eye pressures were produced that varied from 1256 mmHg (24.3 psi) to 22843 mmHg (442 psi)... [and] resulted in zero globe rupture.

Every time you mean the relative pressure, not the absolute right? Anyway, thanks for the answer! :-)

@Jantomedes Most of these are absolute pressures, internal where appropriate.


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Difference between mutation and DNA damage
What is the strict difference between mutation and DNA damage?  As far as I understand it, a mutation is an alteration in the genetic sequence, having "tricked" the repairing machinery and thus getting replicated in the future.  DNA damage, on the other hand, is any alteration of the DNA molecule including breaks, chemical alterations of the molecule, etc.
Then, are mutations considered a type of DNA damage?  I would thank the strict definition of both concepts.

Have you read the DNA repair article on Wikipedia?  The DNA damage and mutation section answers exactly what you're asking:

DNA damages and mutation are fundamentally different. Damages are physical abnormalities in the DNA... [and] can be recognized by enzymes, and, thus, they can be correctly repaired if redundant information, such as the undamaged sequence in the complementary DNA strand or in a homologous chromosome, is available for copying.... In contrast to DNA damage, a mutation is a change in the base sequence of the DNA. A mutation cannot be recognized by enzymes once the base change is present in both DNA strands, and, thus, a mutation cannot be repaired.

Here's the entry from the NCBI MeSH Glossary saying the same thing:

Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION... They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR).

And for mutation:

Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.

Usually a mutation occur when one strand got a modified base and the enzyme correct it by choosing the "wrong" strand as a template, therefore both strands are modified and there is nothing to repair anymore. Is it correct?

Basically, yeah.  Errors in the DNA repair enzymes themselves will allow a whole mess of trouble.

i did read the article, but i wanted a more reliable answer as sometimes wikipedia might lack precission

@JunkDNA I won't argue with you there, but for definitions it's usually spot on.  Still, I added the appropriate definitions from NCBI.


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What is needed for a G-matrix?
I have been doing a lot of reading on quantitative genetics and the G- (and B-) matrix lately. I get the principle behind performing the analysis now but I am still not sure how to do it. I'd like to be able to try it out with some dummy/old data in R to see how it is done.
Let's pretend I have measured 5 traits of Drosophila (Wing length, lifespan, eye pigmentation, bristle number, and fitness). Could I construct a G-matrix for the population from this data and also get a B-matrix to measure the selection on the traits?
Aims of the post:
1) What information (trait measurements, fitness scores etc.) is needed to construct G- and B- matrices?
2) I would like to find print or online material that would guide me in actually implementing this method. It seems like there is an awful lot of papers saying that G-matrices are great, but no one actually says how to do them in real life...

Your link talk about G-matrix only. I don't know what a B-matrix is. Do you have a link that explain what is a B-matrix? Thks

@Remi.b The b-matrix is a sub matrix within the g-matrix (the g matrix is constructed of four sub matrices, Gm [male genetic variance and covariance] Gf for female too, B (and B transposed) with the cross sex genetic covariance

A short description of what is a G-matrix can be found in this question

To construct the G-matrix you need additive genetic variances and covariances for all traits, so you normally need results from breeding experiments (e.g. phenotypic midparent-offspring data), that you can do parent-offspring regressions on. Don't know any good online sources but see Balding et al. 2007 p. 534ff for some info. I've seen methods that claim that the G-matrix can be estimated directly from phenotypic data from unrelated individuals (e.g. Zintzaras 2011) or from genomic info e.g. SNPs (Vattikuti et al. 2013), but are not familiar with these and do not know how reliable they are.
A clear background on using mixed models to estimate the G-matrix, including examples/tutorials, can be found in Wilson et al (2009).
Or did you have something else/something more specific in mind?

There is really two aspects to this for me I guess. Firstly, I'd like to know how they can be done. Secondly I am trying to figure if I could do them using trait values from hemiclonal lines of drosophila such that I get sex specific trait values for each haplotype and can therefore make a B matrix.

Well, you should be able to get genetic variances from hemiclonal lines - you need to carefully consider exactly how to calculate them and the amount of heritability captured though. What do you mean with: "Firstly, I'd like to know how they can be done". What the matrices contain, how to technically peform the regressions or something else? I suspected that you were after something more specific, but you should update the question to make it less unclear.

Also, have you looked at Animal models (statistical mixed models), where the entire pedigree can be used to estimate components of the G-matrix?

what I mean by "how they can be done" is what sort of data do I need, what needs to be measured, as it already says in the question

@GriffinEvo I guess this is what is unclear to me; in the simple case, what you need for a G-matrix is phenotypic data on the traits of interest and a known relationship between individuals (e.g. parent-offspring). I also wrote this in my answer, but apparently you are looking for something else. To account for e.g. environmental factors, sex or a known pedigree you need a more complex statistical model, e.g. Animal models. I have updated my answer with a paper that might be of use.


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Cellular components of blood cells
There are different types of blood cells in the human body i.e. red blood cells, neutrophils, basophils, eosinophils, monocytes, T-cells, B-cells.
What are the cellular components of these cells? What are the organelles that are found in these cells? I can't find this information anywhere.

It's pretty straightforward.  White blood cells have all the usual organelles while mature red blood cells are missing most of them.  WBC can have specialized lysosomes depending on their function, as well as granules if they are granulocytes.

I edited to remove a sentence with a dead link that had no attached information to find out what is was.


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Can genes that activate transcription factors also called be called transcription factors?
If the sole known function of a gene is to activate a transcription factor, would that gene also be considered a transcription factor, or is there a word for such genes that are further upstream on the transcription activation cascade?

Yes.  For an example, see this list of targets of NF-kB (a transcription factor).  Many other transcription factors are included there.  As for a TF that does nothing except activate another, single TF?  I don't know that those exist - TFs tend to modulate multiple genes.

From the wikipedia article on TFs:

In molecular biology and genetics, a transcription factor (sometimes called a sequence-specific DNA-binding factor) is a protein that binds to specific DNA sequences, thereby controlling the flow (or transcription) of genetic information from DNA to messenger RNA.

The nature of the gene affected is irrelevant, a protein is a transcription factor if it binds to a gene's promoter and regulates that gene's transcription. Whether the regulated gene also codes for a TF does not enter into it.

You need to re-write your question, it is ambiguous and your use of terms is incorrect... Assumption: by "activation" you mean "activation of transcription resulting in the expression of the transcription factor"
1) Transcription factors are proteins
2) Genes are comprised of DNA elements
A transcription factor can be involved in initiating the EXPRESSION of a transcription factor, whereafter that second distinct transcription factor initiates the EXPRESSION of another gene that encodes another transcription factor.
Answer: No, genes do not "activate" transcription factors*
*Unless you are proposing the philosophical question of whether the DNA binding domain itself, which endows the transcription factor with a state of being active duty (i.e. fulfilling its purpose as a transcription factor), and thus that purpose is fulfilled only when the DNA binds the the TF, then a DNA binding domain can indeed "activate" the TF... but I'm pretty sure this isn't what you're asking.

I simply meant to ask whether there was another term for a transcription factor upstream on the activation pathway of another transcription factor. Does that make more sense?


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.Net DNA/Codon Parser
Does anyone know of an .NET (C#,VB.NET, maybe F#) DNA parser?  If not I will probably make one, it doesn't seem like it would be hard.  My general idea was to generate something that would report the codon biases and go back and adjust the bias for engineering.
I realize the later part is a bit specific, but if anyone knew about an open .NET program that annualized/parsed the codon bias, I'd be interested.
Thanks.

Something like this?  I know nothing about .NET.

Maybe, I'm going to check it out.  I solid library would do the trick.

@amory Looks like it might.  I don't know how I missed that in my searching

Cool.  Posted an answer for the sake of statistics.

If you're thinking of entering bioinformatics, I strongly urge you to use a Unix/Linux platform and not .NET or other MS tools. It will make your life much much easier.

What's cool about bioinformatics is that it has both a father and a mother !

@terdon oh I agree. My real entry into programming was with R on Debian, and I am a fan of BioPup, but I don't think that's being developed anymore.  The only reason I'm interested now, is to throw something into an already existing WPF.

I don't know much (read: anything) about the .NET framework but a little search turned up Microsoft's .NET Bio:

.NET Bio (formerly Microsoft Biology Foundation [MBF]) is a language-neutral bioinformatics toolkit built as an extension to the Microsoft .NET Framework—initially aimed at the area of Genomics research. Currently, it implements a range of parsers for common bioinformatics file formats; a range of algorithms for manipulating DNA, RNA, and protein sequences; and a set of connectors to biological web services such as NCBI BLAST.

Free (as in beer) and open source!  And from this it looks pretty cool.


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Detecting UV by humans
From my experience humans can detect UV - not by seeing it but by pain in their eyes. Many people (me too) feel pain when looking at UV lamps. When looking at sun through clouds I still can feel pain very often even if the after -all-image is not very bright (because of the clouds) but when I look at a light bulb or when I look at sun through sun-watching lenses (which cut all UV) I don't feel that pain despite of them being much brighter than the cloudy sun. I also have read about it once or two.
So, can this be true (I mean humans can detect UV with their eyes) or that's just a coincidence? And if it's true, how it happens?

Related question: Are there specific conditions that allow humans to see ultraviolet wavelengths

I've read that before but this is about seeing UV in specific conditions. I ask about feeling UV with normal conditions.

Well, UV damages your eyes and damage is often expressed as pain. I'm not sure what else you are looking for.

Surely, but is only about damaging eyes and if so, which parts? But this sounds a bit weird for me... UV doesn't hurt (I mean just pain) our skin and eyes of course something different but they... well doesn't see UV.

I am not sure which parts of the eye are being damaged, but I would imagine that skin is much more durable than your lens, retina, etc, which can cause it to be less sensitive to UV. Your skin was meant to take abuse, your eye not so much

Anecdotal comment: Similar to your experience, I also feel pain in my eyes on certain cloudy days, if I stare at things outside. I always suspected it was due to UV, but never measured anything.

First to address some of the comments:
Concentrated UV damage does hurt your skin, it's called sunburn.  Lighter amounts of UV damage can cause cancer over time.  UV damage can be "felt", as can photonic pressure in extreme cases.  The issue at hand is "what is detection."
Back to your eyes:
As addressed in this answer, the human retina is able to detect UV light if it is not blocked by the lens.
I believe your question, restated slightly, is "can we call the pain experienced by UV damage to our eyes human detection of UV light."  Generically I think the answer is no, because we lack the specificity to determine that it is UV light. Many forms of ionizing radiation can lead to pain, and we would be unable to distinguish between them.  We cannot tell the gradation from UV to gamma, despite the damage they might cause.  Contrast this to the visible light spectrum, where we are quite good at determining the wave length.
Further, you could have similar damage caused by infection, where again you couldn't distinguish between the pain and fuzzy sensation caused by the very beginning of infection vs slight UV damage (though blueberry might help).
Does UV light damage your eyes? Absolutely in large enough doses.  Can it be called detection?  Probably not.  We can deduce UV damage from lots of things, including changes in the color of the pigmentation of your eyes (gold flakes = bad).  When we get to the level of deduction, however, we might as well be using machines to detect UV light and save our eyes (and skin) the trouble.