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Avoid Blood lyse color remain in DNA extraction
I tryed several times to extract DNA from freezed blood sample whit Qiagene kit but it gave very small amount of product due to good purity then I try extract manually by using CTAB PVP method and finaly gain a much more DNA but the lysate color in sample remain in DNA pellet an do not disolve in any solvent to seperation I tried to add small amount of accorbic acid but just the color get reduce to red from gray:'( . If every one have a idea which can help me please gave in a small answer.

Sounds like your DNA isn't pure.

The kit likely has a way of dealing with the RBCs, where as your CTAB PVP may not. Did you centrifuge the sample? If human, RBCs are not going to have genomic DNA, so you can extract the WBC layer and plasma and try purifying that.


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kinetics question
An enzyme has a $V_{max}$ of 50 $\mu$mol product formed $(min * \text{mg protein})^{-1}$  and a $K_m$ of 10 $\mu$M for the substrate. When a reaction mixture contains the enzyme and a 5$\mu$M substrate, which of the following percentages of $V_{max}$ will be closest to the initial reaction rate ($V_o$)
a) 5%
b) 15%
c) 33%
d) 50%
e) 66%
Can someone explain this to me; I know michaelis-menton but I don't understand the solution to this or how to find it.

You literally just have to plug in the numbers in the Michaelis Menten equation.

I don't think you understand MM kinetics.
In your case the $V_{max}$ value depends on the amount of the protein. If we assume 1mg protein, then $V_{max} = 50\frac{\mu{M}}{min}$.
According to MM kinetics:
$V = V_{max}.\frac{S}{K_M+S}$
so
$V_0 = V_{max}.\frac{S_0}{K_M+S_0} = V_{max}.\frac{5\mu{M}}{10\mu{M}+5\mu{M}} = V_{max}.\frac{1}{3}$
or in other terms
$\frac{V_0}{V_{max}} = \frac{1}{3} = 33.3\%$

@ChrisCook If you consider that inf3rno answered your question, then you should check it to indicate future users that you received an answer that helped you. It also reward the one who answered with 15 points of reputation and therefore encourage users to answer your future posts.

sorry, new to the site; I checked the check under his answer, I assume this is what you meant?  thanks

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Why does mud therapy work by some pain related diseases?
Apparently, some users here agree there is no ion exchange through the skin. Mud therapy has some therapeutic effect for pain related diseases. As an anecdotal example, I experienced pain relief by treating my sport injury using mud therapy. If it is not ion exchange, then what is the mechanism behind mud therapy?

Never underestimate the power of the placebo effect, especially in pain related disorders. Treatment can change neuronal signaling, which can in turn influence gene expression. It may be as simple as the increase in buoyancy relieves force on the affected tissue, and this in turn allows a different series of neurotransmitters to be released. The article you linked to makes it sound like there is a significant immunological component, so if you can influence the chemokines in the area of injury, you may be able to reduce inflammation to a certain degree.

@AMR Placebo is about 3%, it is significant, but you cannot explain everything with it. At least show some placebo controlled study in the topic, if you claim, that it is only placebo.

it is my opinion, that is why it is a comment and not an answer. However anything that can change cell signaling has the potential to change gene expression, and the study linked to apparently showed a change in levels of protein products that was statistically significant.

Here is a review article that asks the question "How can placebo effects best be applied in clinical practice?" You will likely have to dig into the references to find quantified studies, however, in the their summary, the authors state "Placebo effects have been demonstrated in a number of experimental trials and clinical studies. These effects cause physiological responses, such as reduced activity in the pain-sensitive areas of the brain."

The answer on the linked question is apt: transdermal administration of medications or other compounds include exclusively lipophylic compounds, i.e. uncharged 'fatty' materials, such as nicotine, opiate-bases and steroids. Minerals, like those found in clay, are highly hydrophylic and are therefore unlikely to be taken up by the skin.
A search through a bunch of articles makes me believe that mud therapy has mainly a thermal effect, i.e. a mud pack heats the underlying tissue and thereby relieves muscle spasms and pain (Espejo-Antúnez et al., 2012; Liu et al., 2013).
References
- Espejo-Antúnez et al., Rheumatology (2012); 258: 1-10
- Liu et al., J Int med Res (2013); 41(5): 1418–25

I heard/read from a non scientific resource that mud with high sulfur content was the only cure of lead poisoning in the old times, because of the Pb2+ + S2- = PbS type of reaction. I have not found any proof of this. It is hard to find old articles in the topic. :S If Chris is true (and I think he is), then this type of reaction does not happen, because there is no ion exchange, so mud therapy did not help by heavy metal poisoning. Unless... I don't know. :D Maybe if the heavy metal is not in an ionic form, e.g. Hg can be absorbed through the skin.

@inf3rno The most toxic forms of mercury are the organomercury compounds, for the exact reason that they are hydrophobic and can thus pass through the skin and into fat stores where they bioaccumulate. I don't know how easily you could draw them back out through the skin, but if possible, then sulfur chelation might work.

@Filipq I'll try to find some evidence about this kind of mud therapy later. Currently I have other things to do, maybe next weekend.

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Summarising ChIP-seq and controls needed
As part of my study I have to present on a method of discerning binding sites of proteins to DNA, for which I have looked at ChIP-seq. This is a brief overview of what I have so far, and was wondering if there are any particularly glaring omissions that I have made so far.

Cells treated with formaldehyde to cross-link proteins such as transcription >factors (i.e. HIF) covalently to DNA and incubated for 2-30 minutes. After >incubation glycine is added to terminate the cross linking and dissipate the >formaldehyde.
Cells are lysed, and sonication (application of sound waves to agitate a >sample) is used to fragment the DNA into sizes between 200-1000 base pairs.
HIF–DNA complexes are selectively immunoprecipitated by using antibodies >specific to the HIF protein of interest, complexed with a matrix of either >agrose or superparamagnetic beads.
HIF-DNA-antibody-matrix complexes are isolated through the use of either a >centrifuge or magnetic field (depending on the matrix employed). Several >washings take place to further purify the sample.
Cross-linking of the protein to the DNA is reversed by way of heating, >separating the DNA and protein-antibody-matrix complex. Proteinase K is used to >digest proteins, leaving only the DNA.
Oligonucleotide adaptors (primers) are then added to the small stretches of DNA >that were bound to the HIF to enable rapid simultaneous sequencing.
DNA sequences are then mapped to the reference genome to determine the binding loci.

I would also like to discuss controls that are used in these procedures. So far I have found limited mention of negative controls, positive and negative control loci, non-template control and positive control antibody, but am having trouble discerning what any of this actually is referring to.
I would seriously appreciate any help available on this topic!

The most stringent antibody control is the pre-immune serum from the same animal that was immunized with the Transcription Factor, but if you are purchasing the antibody from a company that control is almost never available. A non-specific serum from the same species can usually be purchased (e.g. Sigma), and is often used as a negative control. Some people just leave out all antisera and use that (with the beads, etc) to see what is pulled down. If the antibody recognizes an epitope tag then you can use that Ab on a cell that does not contain the epitope.

Full disclosure: I am a co-author on this paper:  ChIP-seq guidelines and practices of the ENCODE and modENCODE consortia http://genome.cshlp.org/content/22/9/1813.full

Good experiment! ChIP-seq is good for a whole genome look at transcription factor binding. KEY POINT:  The data generated are only as good as the antibody. Considerable effort needs to taken to prove antibody is specific for only the protein of interest.  It is for this reason, that some TFs still haven't been characterized by ChIP-seq.
As far as controls for your experiment:
The breaking of DNA from sonication isn't uniform from experiment to experiment, and sonication will preferentially break at some regions of open chromatin more often.
Controls for this:

Isolate DNA from cells that have been x-linked and fragmented under same conditions but don't use antibodies to IP.  This is "Input" DNA.
You can conduct a "mock" ChIP using a control AB that reacts with some non important non-nuclear protein, such as IgG.

Then sequence these samples to same depth as the Immunoprecipitated DNA.
Here is a good paper that is a little dated, but still relevent: Go to Control Sample Section
Here is a link to the guidelines for ChIP-seq for ENCODE PDF
Last but not least, if you are working on a much smaller scale, don't forget about things like DNA footprinting and EMSA to identify the ACTUAL binding site.


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Which Lactobacillales (Lactic acid bacteria — LAB) strains are capable of degrading starch?
I've been researching bacteria strains but am having trouble finding amylolytic LAB strains with amylolytic and lactic acid producing character. The only species I've found, that are capable of amylolysis (correct me if I'm wrong) are Lactobacillus amylovorus, Lactobacillus manihotivorans, Lactobacillus plantarum.
If any, what other LAB strains provide amylolysis? Also, can anyone verify if the above strains also meet the criteria?
Edit
The keyword here is strains. Many species can degrade starch but most strains cannot.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3458588/ L. acidophilus can be another species on the list.

http://www.genome.jp/kegg-bin/show_pathway?lrl00500 Lactobacillus rhamnosus

http://www.tandfonline.com/doi/abs/10.5504/BBEQ.2011.0124 it is not that hard to find articles in the topic. there are many species with this ability

@inf3rno That's only partly true. e.g. Propionibacterium freudenreichii subsp. shermanii CIRM-BIAlT is able to metabolize lactose, although this trait is strain-dependent, since the Lac genes may have been acquired through a horizontal transfer event mediated by phage infection. Many strains can degrade starch but few species cannot.


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Plasmid choosing
To design a experiment in feeding of C. elegans. It has to choose a plasmid vector to insert the gene of interest that can feed to C. elegans. Many paper are using pL4440 for the feeding vector, saying it is the first used in feeding C. elegan and because of the two T7 promotor, so it easy to perform the experiment. There also paper saying T3 promotor is not fit for feeding in C. elegans. I am curious about why T3 is not fit? and because I didn't see many paper using other vector to perform the feeding experiment in C. elegan. So I wonder that is it ok if I choose a plasmid that has two T7 promotor and is used to express in worms like pLT61, will it influence the feeding or the efficiency so that people use pL4440 for feeding in C.elegan? Or is people use pL4440 vector because it is specific designed to the feeding experiment of C. elegan? Thank you!

PREFACE:
There's a text, C. elegans: Methods and Applications, specifically doi: 10.1385/1-59745-151-7:109. They outline this exact experiment in it's essence, and one of the diagrams (page 110) notes that for the purposes of RNAi in C. elegans, the T3 promoter specifically doesn't work for the bacterial feeding method, but works for injection or soaking procedures. I absolutely can't figure out why that is specifically, but i'll keep researching.
UPDATED:
Much thanks to mdperry for clearing things up! As it turns out, this is a matter of experimental design. Using information from Ingestion of bacterially expressed dsRNAs can produce specific and potent genetic interference in Caenorhabditis elegans, and Source Bioscience:
HT115 (DE3) is a feeding strain engineered like so,

The genotype is as follows: F-, mcrA, mcrB, IN(rrnD-rrnE)1, lambda -, rnc14::Tn10(DE3 lysogen: lavUV5 promoter -T7 polymerase) (IPTG-inducible T7 polymerase) (RNase III minus). This strain grows on LB or 2xYT plates (and is resistant to tetracycline, see below), and competent cells can be made using standard techniques.

We can go through these and look at the changes as well:
F- means no F plasmid for conjugation. mcrA/B refers to mutations made which reduce the ability of the E. coli to attack foreign DNA. IN(rrnD-rrnE)1 is an inversion in the region of some rRNA operons that I'm unsure as to the effect. Lambda- removes the lambda lysogen. You can see that they have the lavUV5 promoter for an IPTG-inducible T7 polymerase which is important for getting the E. coli to begin producing T7 polymerase to express the associated cloning vector. You can also see that HT115 (DE3) is deficient for RNase III, however, which normally degrades dsRNA, making it suitable for the feeding experiment.

The L4440 (pPD129.36) cloning vector contains two convergent T7 polymerase promoters in opposite orientation separated by a multicloning site and was made using standard cloning techniques (Timmons and Fire, 1998).
pLT61 contains 0.8 kb of unc-22 inserted into the L4440 vector.

I think the L4440 plasmid is probably easy to optimize for this experiment, and cheap. If you can access the article I linked above, they catalogue some additional plasmids. In conclusion though, it'd seem that if we in fact had a system where the E. coli themselves could produce T3 polymerase, it'd be fine to use those promoters. In the case of this experiment, the genotype of the feeding strain of bacteria nicely complements the vector being used.

One also needs to use the appropriate bacterial host. As I recall HT115 is engineered to carry a copy of the gene for bacteriophage T7 RNA Polymerase, and this polymerase is being driven by the lacUV5 promoter. So in the absence of an inducer for the lac operon the T7 RNAPol is not made, and the dsRNA is not made. When you add IPTG the polymerase is turned on, and the insert in pL4440 is transcribed from both strands. The reason you can use the T3 promoter for injections or soaking is because the T3 RNAPol is added to the test tube.

Is there a molecular explanation for why T3 isn't fit for feeding ,i.e. the same inducible system doesn't work for T3 polymerase? Or is it just a matter of experimental design?

The bacterial cells carry a prophage, lambda DE3 integrated into the bacterial chromosome at the att site. This phage is the source of the T7 RNA Polymerase. If you had some way of producing T3 RNA Polymerase then a plasmid carrying T3 promoters should work fine

The pLT61 contains 0.8kB 0f unc-22, on the internet saying it is a gene influence the muscle in C. elegans. does it mean that it will influence the effeniency of the experiment? Such as if I put the my gene of interest that is relevant to function of pumping, after it either injected or fed into the C. elegans, will it have a conflict or will it interrupt the experiment? to be clear, like will it express both of the genes? Thanks

This article shows the effect of a stem-loop GFP-unc-22 structured dsRNA in RNAi. Basically, it can potentially knock down both GFP and unc-22, and what this does to the worms is induce a twitching phenotype because it alters the contractility of the muscles. It also produces issues with egg laying.

If your endgame is to simply knock down GFP expression and visualize that and be done, there may not be a huge effect, but prolonged exposure to unc-22 knockdown might be deleterious to the numbers of worms in your culture. Let me know if anyone more experienced has input!

In that article, though, they did find that unc-22 dsRNA exposure had to be rather continuous to evoke unc-22 knockdown, so injection with a specific amount of dsRNA didn't work for long.


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Do dingoes show wolf 'characteristics'?
I've read that Russians have been performing selective breeding on Red Foxes for about fifty years, aiming to make them tame. The wikipedia article says

The experiment was initiated by scientists who were interested in the
topic of domestication and the process by which wolves became tame
domesticated dogs. They saw some retention of juvenile traits by adult
dogs, both morphological ones, such as skulls that were unusually
broad for their length, and behavioral ones, such as whining, barking,
and submission.

I wonder, since dingoes are completely wild dogs that have only relatively recently split off from domesticated dogs, do they show more 'wolf-like' characteristics? That is, has their life in the wild selected against domestication genes?
Perhaps the best way to phrase the question is have dingoes gained more of the genes/traits that silver foxes lost in the Russian domestication experiment?

Just to clarify, by "wolf-like characteristic", I suppose you mean "characterstics that are shared with wolves but not with dogs", is that right?

Well, I suppose "not all dogs", since there may be kinds of dogs that have some of those traits. I guess "non-domesticate traits" might be a better phrase, but the whole subject seems tricky.

The question is interesting +1. To my knowledge, the level of domestication of Dingo's ancestors is debated. And when having a quick look at the wiki article it seems to be quite a mess indeed. I think one could draw quite a good answer from wiki>Dingo and its references.

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Is intelligence (or mental ability) genetically transferred (inherited characteristic) from the parent to the offspring or is it an acquired trait?
The question is simple- whether our mental ability i.e. ability to acquire and store knowledge and comprehend and analyse the stored bits, an inherited trait (i.e. genetically transmitted from the parent to the offspring) or is it an acquired trait (depends on environmental, social factors)?
P.S. - Please attach the link of any reference/research (if any) with your answer.

This question is probably more appropriate on the Cognitive Sciences S.E..

Thanks for you suggestion @AMR, posted it on Cognitive Sciences S.E.

What do you mean by intelligence? there are many different forms of intelligence... you have social intelligence for example, which if you're born with or develop autism, like me, you tend to lack here... There is also a difference between knowledge and wisdom. Without having done any research, but using myself and my family as example, I seem to be mathematical or logical, while the rest of my family fails in this area. The difference between me and the rest of my family, is simply that I learned programming as a 9 year old... This has consequences and advantages.

point being, does it really have to be either inherited or acquired? can't it be both? and could there be a connection between what you occupy yourself with as a child and your intelligencies? I haven't answered your question, but I hope I gave you something to reflect over.

Standard IQ test are often considered the best proxy for intelligence. Studies show IQ heritability varying between 0.5 (ref) and 0.8 (ref).
TO make sense of these numbers, you will need to understand the concept of heritability. You can find info on this important concept in the post Why is a heritability coefficient not an index of how “genetic” something is?. Other posts also offer an intro to this concept (see this, this, this or this post). You can also simply have a look at wiki. You might want for example to be able to understand the equation $H_N^2=\frac{V_A}{V_P}$ without further explanations.
The H2DB database may interest you as well and of course the wiki page on heritability of IQ

I think epigenetic factors and training will affects this more than heredity.

I think that this is a good technical starting point but it does not fully address the rather larger controversy. (And it's somewhat old)


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Have there been any macro-evolution experiements?
I'd like to start first by saying that I don't believe in creationism at all, nor any non-Darwinian-evolution explanation of the diversity of life on Earth. The theory, the fossil record, and the genetic, morphologic, and biochemical evidence are more than overwhelming in support of it.
Also, I understand that the term 'macro-evolution' is a "weasel word" invented by creationists to make a bogus distinction of two supposed kinds of evolution.
But for this question, I think the term is useful. I'm happy to take any corrections or qualifications in comments or answers.
I wonder if there has been any long-term experiment performed to attempt to induce 'macro' changes in a species-- something that would make this lab-based population considered to be a subspecies, or even a different species, if it were found in the wild.
I'm aware of the long-term E. Coli experiment that resulted in bacteria that developed mutations that allowed them to completely metabolize citric acid. I understand that's a change of a few genes (amongst other recorded changes).
What I'm looking for is something a little larger, more than a new protein. I was thinking something like 1. a new organelle, 2. a new type of cell or tissue, 3. a new organ, or 4. a new type of limb or radically different limb use (something like reptilian jawbones re-purposed in mammalian ears_.
I understand there are numerous incidents of organisms losing useless features, such as eyeballs in dark caves, flight ability, etc. For this experiment I don't think it's enough to show the loss of something-- genes turning off, but novel characteristics must arise. To rebut creationists, I think it's necessary to show 'new' information, not just loss of information (I'm speaking of the genes responsible for morphology).
With my laypersons' imagination, I was thinking of a species with a relatively fast reproductive cycle, put in an environment that had some selective pressures. Perhaps one without much room to fly, not enough food, but plenty of food in a water area where they couldn't normally get to it. Something that might encourage them to adapt to taking to water to exploit a new food resource.

The timescales over which your suggested changes could happen makes them infeasible to directly observe. Of course, there is plenty of indirect evidence to support the idea that such processes have already occurred. Also, science isn't concerned with rebutting creationists. We make observations and develop theories to explain them; that's it.

@canadianer If you know, what is a rough estimate for the time of any of these features to develop? I know there's not a (meaningful) average, and that no example would be representative, but any that you know of offhand would be informative to me.

@user151841 We could calculate an average (if if it would carry little info) if we could accurately define the evolution of a specific trait. But the question does not so there's really no way to answer it. I just tried to give a few examples that are of eventual interest. For more, we will need a more accurate question.

Would you accept Humanized mice that can be infected with the HIV or with Kuru or Creutzfeldt - Jakob brain homogenates and develop human prion disease? Wild type mice could not be infected with either the HIV virion or the misfolded human prion protein.

@Remi.b That is why I say there's not really a (meaningful) average. To take an example, we could say that, since it took ~ 10 million years from pakicetus to Mysticetes, two clearly different species, macroevolution can take about 10 million years (http://evolution.berkeley.edu/evolibrary/article/evograms_03) . Of course, tough, we want to find a shorter example in the interests of this experiment. But since the distinction between 'species' get fuzzier the more closely related populations are (subspecies, etc), finding the 'shortest' timeframe becomes more difficult.

@AMR Is that the expression of a protein on the surface of a cell that allows humanized mice to become thusly infected? If so, I'm looking for something that would involved the expression of multiple proteins to become a new organelle, cell, etc. as a outlined above. Creationists argue that human genetic experiments are examples of intelligent design, so I'm looking for something that's not consciously planned. While I somewhat agree with canadianer that it's not scientists' job to rebut creationists, somebody needs to fight back, and they are going to need the help of science to do so.

In order to have any chance at seeing what you want to see, you need lots of generations to do it, and about the most complex organism we will see this in, is the fruit fly. And there is no way of winning that argument. Logic cannot compete with magic in the eyes of a believer.

@AMR I'm more interested in convincing the uninitiated or the people who are up for grabs, such as a sixth grader who is in a school where creationism is taught next to evolution in a "science" class.

@ARM this article http://news.bbc.co.uk/2/hi/science/nature/4530959.stm says that the pygmy goby fish has a reproductive cycle of 59 days, which by my reckoning is 3 times as long as the fruit fly reproductive cycle (19 days http://www.orkin.com/flies/fruit-fly/fruit-fly-reproduction-rates-data/). That would turn a 20 year experiment into a 60 year experiment, which is still feasible, if we consider vertebrates more complex than flies.. The pitch drop experiment (https://en.wikipedia.org/wiki/Pitch_drop_experiment), while not as serious and maintenance-intensive, has been going for 98 years.

Issue with the question
The question of what is an evolved phenotype that is "seemingly significant enough to the layman to be called macro-evolution" is very unclear and it makes it hard to answer.
Most experimental evolution are performed on lineages that have very short generation time (for obvious reasons) and on these lineages it is hard to even imagine the evolution of something that a layman would consider to be "significant enough to be called macro-evolution".
The whole issue is that one will probably consider a change in phenotype to be "seemingly significant enough to the layman to be called macro-evolution" if it occurs on lineages that have long generation time and therefore cannot be observed within a lifetime.
The question interesting. However, I think the best one can do is to look at the wiki article for experimental evolution who already offer quite an interesting list of examples. I tried below to highlight a few cases of eventual interest

Long term artificial selection on "large living things"
If one wants to consider artificial on "large living things", then probably artificial selection on crops and cattle will be a good place to look at. I think I don't need to list and make extensive description of how artificial selection has changed their phenotypes (and genotypes). Consider the pigs, banana and corn as examples.
A few evolved features that has evolved in labs in small organisms
We have observed evolution of multicellularity form unicellular organisms, observed new metabolic pathways and change in ploidy level just to cite a few major things that we evolved.
Lenski experiments
The Lenski long term experiments is the longest in lab evolution experiment performed today. They made a lot of different observations and not only the case of citric acid metabolization that you mention. Note that being able to metabolize a new compound is a pretty considerable evolved feature that only those who can't go further than considering evolution of extra legs as something significant would fail to appreciate.
Drosophila and Waddington's experiment
If one must restrict I suppose that looking at experimental evolution on Drosophila would be our best bet.
Change in allele frequency through selection is a relatively fast process. Creation of beneficial variants through mutations is often the limiting process. Cases where very different phenotypes exist in natural population and selection over these phenotypes (change in frequency only) will probably not be considered to be "impressive enough". However, one can consider Waddington's experiments (and further experiments inspired by Waddington's work) as an example of experimental evolution where standing genetic variance existed before the experiment started but was hidden in the environment they experimented (the exact process here might well be too advanced for a layman). Waddington in his experiments showed one can evolve Drosophila to have a double thorax or lose their halteres in only 20 generations.
Other Drosophila experiments
We evolved Drosophila to live in hypoxic conditions. It took about 200 generations that is more than 4 years. We have also selected Drosophila for cognitive abilities and food preference (and many other things).
Note on the term "macro-evolution"
The term "macro-evolution" hasn't been invented by creationists. It has been invented a long time ago, in 1927 by a russian entomologist. T. Dobzhanski and E. Mayr (two famous evolutionary biologist) have used this term without ever quite defining it. Because the term was never correctly defined, the vast majority of evolutionary biologist have either criticized the term.
It is true that the term is now sometimes used by creationist as any poorly defined term is one of the finest solution to build questions that can't be properly addressed due its lack of clarity.


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Is there any possible way to take a DNA test without using blood in humans?
Is there any possible way to take a DNA test without the need to draw blood in humans? Any information will be useful for me.

Hair follicle, Oral mucosa, Semen...? On theory, every cell contain chromosomes could do the DNA test, but it should depend on when and where you wanna to do the test. Some agencies don't have the ability to do small amount od DNA test, and also preservation of DNA sample is another point.

I think a more interesting question would be 'from what cell type can't we extract DNA for testing'

Yes, we don't have to use blood to extract DNA for testing.
There are many resource we can use include: hair, buccal swabs and urine. And it seems hair can provide good quality of genome DNA.
Here is the paper you may interested: A Simple Method of Genomic DNA Extraction from Human Samples for PCR-RFLP Analysis

Also this section of an article https://en.wikipedia.org/wiki/Genetic_testing#Medical_procedure

Thank you for your answer, and is there possible To use finger print for DNA test?

@Rani Yes as epithelial cells are deposited upon contact with objects/surfaces but it is not trivial due to 1) the very low number of cells and 2) cross-contamination as, for standard protocol, dusting is first needed to see fingerprints (and you don't change the brush usually) and 3) the powder used to see fingerprints may interfere with the DNA extraction. See this paper.

So, DNA test through our fingerprint is little bit difficult right sir?.. may i know is possible to take grouping blood via our fingerprint?. I mean, is it possible to find A+, O- ,.... something like this? Thank you...

Can anyone guide me please...

For a cheap and fast test of blood groups, you need blood. Unless your fingerprint has it's owner's blood, this gets more difficult. In principle, you could extract DNA (caligari2005 already explained that is bothersome) and then check the DNA sequence for the blood group alleles. But if you did extract the DNA from a fingerprint, you would have much better individuation chances with standard forensic tests than looking for a blood group allele.

@jkadlubowska: how would you told using blood, its a fast method for blood groups,.. If we use blood, it will take more time to find the blood group than the using fingerprint right? thanks..

https://en.wikipedia.org/wiki/Blood_residue http://www.nejm.org/doi/pdf/10.1056/NEJM194910062411414

@jkadlubowska: actually i m not a medical student, can you please elaborate in the above link? thanks


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Bio-fuel efficiency as aviation gasoline
Can biofuels replace petroleum for aviation fuel?
I've read in the news that Alaska Airlines was flying with 10~20% biofuel and 80~90% petroleum. Is biofuel efficiency comparable to the efficiency of petroleum? I am curious whether or not the maximum speed of the airplane is same when it uses bio-fuel 100%.

The term biofuel refers both to the source of the fuel, as well as (currently, at least) the compounds contained in it. If the production quality is strictly controlled, eventually there should be no detectable difference between a fuel mixture derived directly from biological sources, and one derived from petroleum products (which, technically speaking, are of biological origin themselves, just a few million years removed). However, due to technological limitations, biofuels and petroleum-based fuels do have different chemical components today.
The reason we hear of differences in mileage or "energy density" in biofuels used to power automobiles as compared to gasoline/petrol is because they are not the same mixture of chemicals. This page goes into detail (the whole site is actually quite clear with its explanations), but the basic difference is that petroleum products are essentially 100% hydrocarbons (only containing hydrogen and carbon atoms) while nearly all biofuels contain oxygen as well, which has numerous effects on the fuel's physical and chemical characteristics, altering everything from polarity to reactivity to stability over time to the types of byproducts (and pollutants) produced during combustion.
There is much more to the story, but the basic answer to your question is yes, biofuels could replace petroleum-based products for aviation and many other types of fuels, and not impact the maximum speed of the aircraft. It may require engine modification, and the energy density may not be exactly the same (possibly reducing range), but for the long-term health of our planet we MUST reduce and eventually eliminate our use of petroleum.

By the way, the Aviation or Chemistry StackExchange sites would likely be able to provide you with much more in-depth answers, as ultimately this question is better suited to either or both of those sites than Biology, which would be more concerned with the production of biofuels by living organisms.

Thanks a lot for your great answer and guidance to the aviation stackexchange. I will check it out to find the detail.

@Trailblazer glad I could help. If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered.


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Does the new virus tree of life change their position between living and non-living things?
Viruses still do not fit the criteria of living or it's simplest form (the living cell), why would some say that the new virus tree of life makes it more closer to life? Aren't mitochondria in a point of view closer to life than viruses?

You will probably want to have a look at why-are-viruses-considered-microbes and why-isnt-a-virus-alive.

The definition of life is a question of philosophy
The definition of life is a question of philosophy and not of biology. However, because discussing it often require some knowledge of biology and because it is so common for the general public to misunderstand that the definition of life is not of biological interest, the question has already been addressed on this biology.SE. Please have a look at:
why-are-viruses-considered-microbes and why-isnt-a-virus-alive.
Why would the tree of viruses affect our definition of life?
It is impossible to say much without a link to the original claim. I will need to speculate on what the authors of this claim first meant.
A tree of viruses gives a visual representation of a feature that we tend to associate to living things only, that is they evolve and speciate. Of course, we did not need to build a tree of viruses to understand that they evolve and speciate but a visual representation can sometimes offer an emotional response that will push some to prefer considering viruses as living things. In consequences, it is possible that the vision of this tree affect the emotional aspect of what we define as "living things" and might push the community to expand their standard definition to include viruses. Again, it is important to understand that the definition of life really has absolutely no impact on Biology.


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Mitotic chromosome condensation screen
If I want to screen for mutant yeast (S. cerevisiae) colonies that have defects in mitotic chromosome condensation, can I screen for colonies arrested in Mid-M phase? Would that work?

It is going to need to be a temperature sensitive mutation, so that you can get them to grow at the permissive temperature and arrest during mitosis at the restrictive temperature, because otherwise your cells would not grow.

You probably would also want to do a thorough research review of Leland Hartwell and Paul Nurse's work as they worked out the cell cycle using yeast.

The ts mutation would be like a "primary screen" from there one can do a more sensitive secondary screen? Thank you!

Right. So you find the ts mutant, and then you isolate mRNA from population grown at permissive temp and population grown at restrictive temp. Then you make cDNA and run that out on a microarray (They probably have plenty of whole genome chips available for yeast). You can then see the genes that are down (or up) regulated from a comparison of the two arrays, and that should tell you where gene expression has changed. You will then need to make probes for those genes and do FISH to try and determine where they are localized in the nucleus.


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Transcription when Chromosomes are Condensed
Are genes transcribed just as well when chromosomes are condensed?
I want to design a screen that depends on genes not transcribed when chromosomes are condensed (to identify cells that can't condense).

I think you are going to need to add a little more detail than this. Do you mean condensed like metaphase condensed, or do you just mean genes normally found in heterochromatic regions of the nucleus? If the latter, then you will want specify the cell type you are thinking of using as different cell types will have different genes silenced in heterochromatin and accessible in euchromatin. A lot of it has to do with the transcription factors reaching the nucleus and also chromatin remodeling complexes. some heterochromatin is more accessible than others.

The compaction of DNA into chromatin is a very complex process that involves not only DNA, but on the histone code. Some may say that the histone code plays more of a role in chromatin state To develop a screen you would have understand the act of methylation, acetylation, ubiquitination, and phosphorylation of all modifiable histone residues. The modification of histone residues determine if the chromatin is in a heterochromatin or euchromatin state and even in which sections of DNA are accessible and transcriptionally active.
It is also important to note that the same modification of any of the 8 histone proteins in any nucleosome (the fundamental unit of chromatin) may not produce the same result.
For example: The methylation of H2 histone in the first nucleosome of a chromatin "string" may cause silencing while the methylation of H2 histone further down the chromatin "string" may cause activation.
It's alot of information but maybe one day you will be the one who solves the pattern! It sure is fascinating.

@cagliari2005 I think that you may need to review your histone tail modifications, which can undergo Methylation, Phosphorylation, Acetylation and Ubiquitination and those modifications are on the Proteins, not on the DNA. And the "string" reference is referring to the "Beads on a String" fiber that is the first level (and only confirmed) of DNA compaction. It yields the 100 Angstrom fiber. And while neither question nor answer is worded that well, I think both users know at least the proper use of the vocabulary. The OPs other question is about mitotic arrest in yeast.


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Does exercising increase the rate at which UV rays are absorbed and cause affects?
Does exercising while in sunlight affect the rate at which the human body absorbs and reacts to UV rays? As sunburn is the secretion of fluids, increased dilation of blood vessels and inflammation of skin would exercising (as it also increases blood vessel dilation for heat loss) accelerate the "sun-burn" process in skin?

reacts? probably. absorbs UV? no.

The only pathways in which I would see more sensitivity to UV light would be

If you were drenched in sweat and somehow the sweat focused the light/UV.   This is highly unlikely as I don't believe any studies have been done to show that a water based solution causes a more intense sunburn.

(Here is a further explanation by another poster on wetness and sunburn https://physics.stackexchange.com/questions/71263/why-does-wet-skin-sunburn-faster )

The increased dilation of blood vessels results in a more red thus darker and more absorbent skin tone leading to more of a sunburn

Both of these are highly unlikely of increasing the sunburn, so in my opinion exercising shouldn't increase UV absorption or make a sunburn worse. Hope that helps.


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Description of the paramaters in the packing parameter?
For a phospholipid, the critical packing parameter is given by:
$$P=\frac{v}{a_0l_c}$$
And I know that

$v$ is the volume of the hydrocarbon tail.
$l_c$ is the critical length of the hydrocarbon chains.
$a_0$ is the optimum surface area of the head group.

But what do these actually mean?
For example what is the volume of the hydrocarbon tail, since it can't be simply the volume of all the atoms that make it up else this would be negligible? What is the critical length of the hydrocarbon tail? And What is the optimum surface area of the head group?

Following image from (Salim et al 2014) will makes thing clear to you,

When they say volume, it is volume of shape of lipid. Shape can be determined by many factors as described here. Following is modified images from (Sprong et al 2001) which will tell you how change differ in general. Here are examples of few common lipids.

+1 Wrt the second figure: perhaps you can also say what these phospholipids are (expand the abbreviations). It would be useful.

LPC: lyso-Phosphatidylcholine, PC : Phosphatidylcholine  and  PE: phosphatidylethanolamine


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Neanderthal and modern human population sizes
Are there any estimates of both the modern human and Neanderthal population sizes over the last, say, 100 k years? Since "purebread" Neanderthals are extinct, their population has to hit zero; that happened sometime around 30 k years ago. We have good estimates of both the Neanderthal (zero) and modern human (millions, billions) population sizes in the recent past -- what I'm wondering is what the numbers were (roughly) when modern humans and Neanderthals came into contact. How many people were there in each group? How many interbred? Is there any reliable way to estimate those numbers given what we know today? If not, would it be possible, if we sequenced the genomes of a large number of Neanderthal fossils, to get a sense of how much variation there was in their gene pool, and use that to estimate the size of their population? Could we also look at how much of that variation survives today in the homo sapiens gene pool?
In Why Did 6 Great Ape Species Survive But Only 1 Hominid Species? the poster states that "following the eruption of the Toba volcano 70,000 years ago, there were between 1,000 and 10,000 mating pairs of Homo sapiens left." Was the Neanderthal population of a similar order at that time? Was it ever larger than the modern human population? We'll never know the exact numbers -- and the exact numbers don't really matter. I'm interested in orders of magnitude. When homo sapiens and Neanderthals interbred, did sapiens already outnumber them, or were the populations roughly equal? Were the number of Neanderthal - sapiens crosses tiny relative to both populations, or were they perhaps large relative to the smaller of the two populations?
A related question:  Of the Neanderthals living, say, 100 k years ago, what fraction have descendants who are alive today?  Is that a question we can answer either now or in the near future, after sequencing more Neanderthal genomes? According to http://www.nature.com/scitable/knowledge/library/what-happened-to-the-neanderthals-68245020

recent research on Neanderthal nuclear DNA has found evidence for
  limited admixture: a small portion (up to ~4%) of the genomes of
  non-Africans so far examined may derive from Neanderthals, suggesting
  that interbreeding probably occurred in the Near East during the
  earliest dispersal of modern humans out of Africa, but prior to their
  arrival in Europe (Green et al. 2010). Demographic modeling of
  admixture combined with territorial expansion, however, indicates that
  this level of introgression would be produced under very low (<2%)
  interbreeding rates and strong barriers to reproduction between
  Neanderthals and modern humans, arguing against assimilation (Currat &
  Excoffier 2011). Pending the completion of the Neanderthal genome and
  ancient DNA analyses of early modern Europeans dating to the Upper
  Paleolithic, and following the recent discovery of a third possibly
  coexisting species from Denisova cave (Krause et al. 2010), it is
  premature to conclude that the currently observed level of admixture
  constitutes assimilation.

That would suggest that the fraction of Neanderthals with living descendants is very small -- most Neanderthal lineages died out. What evidence would it take to conclude the reverse -- to conclude that the Neanderthal population was very small, and was largely assimilated?

Just to clarify: in the second part of your question, I think you're asking about neanderthals with living descendants, rather than ancestors. I would make the edit myself, but you've used the term 'ancestors' twice, so I want to make sure I understand correctly.

You're absolutely right, I meant descendants in both cases.

Briggs et al. 2009, using mtDNA report an estimate of 3500 females. They failed to offer any estimate of the male population size. Their estimates is much  lower than previously thought. They report two hypotheses of why their estimate is so low:
Hypothesis 1 - Low population size
H. neanderthalis population size was indeed really low. After all, they mostly had to live in harsh ice age conditions.
Hypothesis 2 - Slow decline in population size
H. neanderthalis population size were quite high at some point and their population size slowly decreased in size up to the point of being completely wiped out. Such low decline in population size may explain the low level of genetic diversity observed (yielding to an estimate of small population size) in their sample. If the decline of H. neanderthalis was sudden, then even the last survivors of the lineage would have shown quite a high level of genetic diversity. Their decline may have started about 40,000 years with the arrival of Homo sapiens in Europe but this is just a speculation. This second hypothesis is congruent with the evidence of a rather rapid rate of evolution observed in H. neanderthalis
In short, we don't really know what the population size of H. neanderthalis was but it might have been as low as 3500 females only


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Is it possible for two people to repopulate earth?
Today I was wondering this question whether it is possible for two people to repopulate Earth.
What if everyone else disappeared, except for two people (man & woman)? Can they repopulate? In that case, what are the odds against and in favour of that ever happening?

Possible?: of course. Probable?: hmm... . Would it generate a healthy human population?: No.

Possible duplicate of How many people are required to maintain genetic diversity?

You cannot predict that. They may or may not lead to an unhealthy population of descendants but surely they'll face the risk of extinction because of lack of diversity. Extinction is dependent on the environment and it may or may not be adverse to this population. Since there are so many unknowns here, the answers would most likely be based on guesses. Hence I am closing this question as opinion-based.

Well, mathematically it might be possible. But, I would rather worry about the low amount of genetic diversity that the growing population would have, which would make it extremely sensitive to external stresses.
To repopulate earth from such a small pool of genetic material, one would need an organism that is much more sturdy as compared to humans in extreme conditions, multiplies fast and is much more prone to mutations that actually convert to a phenotypic significance so as to increase the genetic diversity of the total population.

Update (after receiving many comments)
Before you read answer, note that this is hypothetical question and I am trying to answer it by creating hypothetical situations with some reasonable numbers
Short answer: Yes, hypothetically it is possible for two people to repopulate earth.
Quoting from Popsci website:

Maybe, but they'd be very busy

Hypothetically it is possible but practically it has very less probability. Let us calculate probability of repopulating earth to it's 10% population.

Let us assume one female can give birth to 50 children throughout her reproductive life spam and assume there is no death/disease/natural crises and other factors which might restrict this 'ideal' growth.
To get 'maximum' number of births in next generation, assume she gives birth to 1 male child and 49 female children. Probability of having that is $\left(\frac{1}{2}\right)^{50}$.
Now again assume all 49 females gives birth to again same ratio of children (too much work for male :P). Probability of happening this will be $\left(\frac{1}{2}\right)^{50+49}$.
If you go by same logic, you need at least 5 generations to make 10% of earth's population. That gives probability of $\left(\frac{1}{2}\right)^{50+49+49+49+49+49} = \left(\frac{1}{2}\right)^{295}  = 1.57 \times 10^{-89}$

It is much lower than probability of we finding electron in nucleus :P
Now if you want to consider little bit realistic model where each couple will have two more couples and so on, It will need at least $2^{30}$ generations to repopulate to 10% of today's population. Considering average lifespan of 60 years, it will take $2^{30}\times60 = 6.4 \times 10^{10}$ years to do that. It is higher than entire biological evolution time scale.
Point of these calculations are to show that, hypothetically repopulating earth with one couple is possible but very less probable.

5 generations for all those people seems very reasonable space of time and isn't the real issue of "is it possible". I think the answer here needs to approach genetic bottlenecking, survival scores of individuals over extended periods of time, and optimum conditions required for repopulation.

I doubt in this hypothetical situation genetic bottlenecking will matter and I don't know how will you implement survival score here.

But if we are here in these numbers within some few million years when homo appeared - how would you explain that? And that probability calculation for 1:49 male:female is not to the point here.

Down vote ? It is hypothetical question. I have also mentioned in answer that "Point of these calculations are to show that, hypothetically repopulating earth with one couple is possible but very less probable"

The probability statements in this answer are not very precise. Let X(t) be the population t years after the human population is reduced to two people. What are the probabilities you are interested in? Pr[X(1000) > 0]? Or maybe the limit of that probability as t goes to infinity? Or the probability of reaching some threshold population in a certain amount of time?

When you write "Let us calculate probability of repopulating earth to it's 10% population", for example...  in what time frame?

@Adrain Well, in first calculations I don't consider time period because biologically that kind of dynamics is not possible. In second calculation I have mentioned biologically plausible dynamics with time period.

Correct me if I am wrong: in your first example, haven't you merely calculated the likelihood of 1 male descendent per female (while having 49 female offspring per female) over 5 generations? Yes, this chance is minuscule, but what has this to do with repopulation - apart from that this might be the "ideal" growth curve? Also - from a genetic point of view, a 50:50 male/female ratio would be a lot healthier.


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Depolarization and hyperpolarization in stereocilia of the inner ear
It’s a well mentioned fact that when the stereocilia of the cochlear hair cells bend in one direction, the hair cell depolarizes, and when the stereocilia bend in the other direction, the cell hyperpolarizes. When the basilar membrane vibrates, the stereocilia are bent back and forth, creating depolarizations in the hair cells followed by hyperpolarizations. What I’m having trouble understanding is why this is significant. This does not determine the frequency of the sound wave, as that is determined by the location along the basilar membrane that the wave impinges on. I don’t see how this would determine amplitude either, seeing as a greater amplitude would only create more drastic bending of a greater number of hair cells. Can anyone shed some light on this?

Great question, and such a pity that the highest quality questions tend to receive the lowest number of upvotes - you have mine!

There are roughly two modes of pitch coding in the cochlea: place-coding and temporal coding. The place-theory is the most prevalent accepted model of how the cochlea realizes pitch coding (e.g., Zwislocki, 1991). Basically, it is based on a frequency-to-place Fourier transformation on the incoming sound, where each frequency is coded on a different place on the basilar membrane, as described accurately in the question.
However, there is another, much overlooked way of coding pitch, namely temporal coding. Up until about 1 kHz, spiral ganglion cells in the auditory nerve and acoustical brain stem regions (such as the inferior colliculus) have been found to respond in a phase-locked pattern (Du et al., 2011). Electrophysiology in auditory nerve fibers illustrates the phase-locked activity in response to low-frequency sounds (Fig. 1). This phase-locking behavior of neurons in the auditory system is called the frequency-following response (FFR).

fig. 1. FFR in auditory nerve fibers. Upper trace shows the stimulus, middle trace a single fiber, and the lower trace the compound activity of many fibers. The group-response faithfully codes the stimulus waveform. Source: New York University.
However, as you rightfully state in your question - why would inhibition of auditory nerve fibers (ANFs) be helpful? Figure 1 illustrates nicely that the auditory nerve FFR is rectified, i.e. only the upper half is coded, while negative action potential counts obviously don't exist; ANFs fire, or they don't, they don't fire negative action potentials. However, one has to realize that a relatively large proportion of ANFs in healthy ears spontaneously fire, i.e., in the absence of sound the auditory nerve is still remarkably active. Spontaneous firing rates vary from 0 to more than 100 spikes/s (Jackson & Carney, 2005). Hence, suppression of spontaneous activity codes pitch too.
Moreover, as a theoretical and un-referenced side note - the auditory system processes acoustic information on the sub-millisecond level. Left/right sound localization is performed by the auditory system by resolving inter-aural time differences (ITDs). By analyzing the delay at which sound arrives in one ear with respect to the other, the localization in the horizontal plane can be estimated. ITDs do not exceed 0.8 ms, given the speed of sound and the size of the human head. This is well below the time it takes for any action potential to develop(!). Hence, by deploying both phases of the sound, one phase being excitatory, the other inhibitory at the ANF level, no time is lost when a sound wave happens to enter the cochlea with its inhibitory flanking phase first.
References
- Du et al., Neurosci Biobehav Rev (2011)
- Jackson & Carney, JARO (2005); 6: 148–59
- Zwislocki, Acta Otolaryngol (1991); 111(2): 256-62

The depolarization and hyperpolarization of stereocilia in the ear is significant for its role in transduction. Hair cells are involved in changing mechanical energy into changes in membrane potential, a process called transduction.
When the cells are displaced and move in the direction of the tallest stereocilium, K+ enters the cell and causes depolarization which allows more transduction channels to open. This depolarization opens voltage gated calcium Ca2+ ion channels. The influx of Ca2+ causes neurotransmitter release from the basal end of the hair cell to the auditory nerve endings which sends signals to the brain.
Movement of the hair cells in the opposite direction causes hyperpolarization which prevents influx of K+ and closes the Ca2+ channels at the base resulting in smaller release, or no release of the transmitter. This allows hair cells to generate a sinusoidal receptor potential in response to a sinusoidal stimulus which preserves the temporal information present in the original signal up to frequencies of 3 kHz.
So the depolarization and hyperpolarization of hair cells is significant because the constant release of transmitter drives the spontaneous activity in the auditory and vestibular nerve fibers. The interaction of Ca2+ influx and Ca2+ dependent K+ efflux lead to electrical resonances that enhance the tuning response properties within the inner ear.
For a more detailed response see: http://www.ncbi.nlm.nih.gov/books/NBK10867/ and http://homepage.psy.utexas.edu/homepage/class/psy394U/hayhoe/perception/Chapt.%201%20Hair%20cells%20of%20the%20cochlea%20copy%203.pdf

So this mechanism codes for frequency?

@lightweaver The mechanism is important because it allows for the conversion of a mechanical sound signal into an electrical nerve signal. Plus the leakage of Ca2+ causes release of neurotransmitter to the synapse which allows hair cells to respond quickly to mechanical stimuli.

This does not answer the question. Albeit accurate, it's not more than an overview of how mechanoreceptors work in general.


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Telomeres and daughter strands
How is the primer present in the daughter, leading strand replaced? I've circled the primer in question.

I don't see how this primer can be replaced by DNA polymerase; there is no free 3' end for DNA pol to act on.
My book, however, says there is no telomere problem with the leading strand.
Other sources say there is a telomere problem.
So what is it?

Replication doesn't start at the very end of a chromosome, so there is no problem with leading strand synthesis. It's probably easiest to see if the other half of the image was there:

Forgive the lion; plain white paper seems to be in short supply. Also my writing. Too much tea this morning. Hopefully you can see that leading strand synthesis can continue right to of the end of the chromosome as the fork progresses. The leading primers at the replication origin can be replaced once the first Okazaki fragment from the other replication fork is synthesized.
There is, however, a problem, aptly termed the end replication problem, with lagging stand synthesis:

The dots just mean the chromosome continues in that direction. Important to notice is the lagging strand RNA primer at the end of the chromosome. When this is removed, there is apparently no way to synthesize DNA there. Repeated replication cycles progressively shorten the chromosome and cause the Hayflick limit to cell division (the number of times a cell can divide before dying). To solve this problem, some cell types express an enzyme called telomerase. This is an RNA directed DNA polymerase that adds deoxyribonucleotide repeats to the 3' end of a DNA strand, using its own internal RNA template, to prevent information loss.

Actually, the lion is positioned pretty well to be a topoisomerase. Just about to cut…

thank you so much for this helpful answer. I think I see it now. You are saying that the primers for leading strand synthesis are always sandwiched between DNA segments, while one primer for lagging strand synthesis is unfortunately found alone and un-sandwiched? And that it is these sandwiched primers, that, upon removal, can be replaced by DNA because there is a free -OH end on one side of the sandwich?

@Dissenter You're welcome and yes I think you've got it.

Cells need not die, the will enter into senescence when their telomeres get too short. Also, this may confuse the issue slightly, but the 5' end, though synthesized to the end of the chromosome, is processed to create a 3' overhang. Both ends need a 3'overhang in order to strand invade the telomere to form the T-loops at their respective ends of the chromosome. If the T-loop does not form, this can lead to chromosomal translocations or it can cause the cellular repair mechanisms to recognize the ends as DS breaks and that can trigger the apoptotic pathway.

I think the confusion is coming from the way this picture is drawn. The leading strand does not begin at the end of a chromosome, there is in fact more DNA to the right of your picture that is not shown. This picture is showing the left half of a replication bubble.

I think I understand this. Replication will occur bidirectionally from the the origin inside the replication bubble. If we focus just on 1 parent strand being replicated, on one side of the origin, the daughter stand replication will be continuous. However, on the other side of the same parent strand, the replication will require Okazaki fragments.
So for the same daughter strand, on one side of the replication origin, it will be leading, and on the other side of the origin it will be lagging!
Back to the telomere shortening (end replication problem), this will mean that each daughter strand will end up too short on it's 5' end after the RNA primer (Okazaki fragment) is removed.

Welcome to Bio. We encourage the use of references and sources to allow people to read the backgrounds of your answer.


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What is the global average BMI?
I have been looking for hours trying to find this number, and can't seem to get a straight answer.  I've seen some studies that calculate the change in BMI, but for some reason they don't give you the actual numbers, just the rate of change.  I've also found information for individual countries, but I want the global average, and would prefer not to do a calculation with 196 different sets of data.

The answer might be a little late, but it was published after you asked the question. See the following publication for estimated global BMI averages from 1975 to 2014: http://thelancet.com/journals/lancet/article/PIIS0140-6736(16)30054-X/abstract

World Health Organization data
World Health Organization (WHO) is your friend for this kind of question. You can find loads of data on BMI per country, per region, per sex and even see the individual data points on here on the WHO website. They also have maps and graphs. Have a look!
Graphics from daily.co.uk
Daily.co.ok have an article (there) with some interesting graphics that I am reporting below. Please note that they made a mistake in the header of each graphics, so just look at the bars below the map and not the range indicated above the map.
Here are some countries with...
...the highest BMI:

... average BMI:

... low BMI:

... the lowest BMI:

BBC applet
You might also want to play around with this applet on the BBC website who allows you to compare yourself with the average in your country for your gender  and age and the world wide average for your gender and age. For example, I entered my personal data and it allows me to see that 69% of the world-wide (my age category and gender) population has a lower BMI than me and 64% of the population of the country I am living in (my age category and gender) has a higher BMI than me. This number goes down to 56% when considering the country where I grew up.
Average BMI
I don't think that knowing the world average will tell you much. What is important is to consider variation within countries, comparison between countries and consider age category and gender. The WHO data set indicate the percentage of individuals that is in a given BMI range per country but not the average value from I got so far.

The table is showing population, not BMI.

Oh I just understood how the data works. So apparently, the WHO don't show average per countries but only the fraction of the population in a given BMI range for each country. Thanks for your help

I looked through this data before, but unfortunately it doesn't really give me what I'm looking...I just want a single number on the estimated global average.


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What happens to the food you accidentally aspire?
I'm well aware of the health effects of aspirating solid food and liquids, but I'm interested in the reaction of the body on the biological level to the strange body on our lungs.
After I almost aspirated corn, I started to wander: what does the body do when food got on our lungs?
Will it be eventually absorbed? Destroyed by our white cells? Or just lie there forever until it fully decomposes?
The body has mechanisms to prevent food to get into the lungs, so the body is aware that eventually some food will get into the lungs. As a result, it makes sense to believe that our body would have a mechanism to deal with such issue if all other mechanisms fail ( coughing and etc.,) yet I couldn't find anything on Google.

https://www.youtube.com/watch?v=I40Qr9bOLOY

wow that's terrifying...I want to see a doctor now lol

Don't worry, this outcome is very rare. :D

I still don't like the idea of having corn inside my lungs, and I can get quite paranoid with thinking on that lol

You mean you really inhaled corn?

People can drown because of aspired food. If they don't then it can cause diseases, for example pneumonia. In extreme cases a tree can grow in the lungs. There are other aspiration/inhalation related diseases like silicosis or asbestos lung cancer. So it depends on the composition of the object (or liquid or powder) and other factors whether it causes a disease or not. I did not find anything about what exactly happens with these objects in the lungs. Probably the lung tries to get rid of them mechanically, if there is no success in that, then they cause a local inflammation, which can lead to diseases if it becomes chronic and/or the object contains pathogens.

Common presenting symptoms (information available in 36 cases)
  included dyspnea (14), fever (9), and cough (6). A history of
  recurrent pneumonia was present in 9.

2007 - Pulmonary Disease due to Aspiration of Food and Other Particulate Matter: A Clinicopathologic Study of 59 Cases Diagnosed on Biopsy or Resection Specimens

The annual overall inpatient cost associated with pediatric bronchial
  foreign-body aspiration is approximately $12.8 million. Combined, the
  rate of death or anoxic brain injury associated with pediatric foreign
  body is approximately 4%.

2014 - The national cost burden of bronchial foreign body aspiration in children

Gastric aspiration is a high-risk condition for lung injury.
  Consequences range from subclinical pneumonitis to respiratory
  failure, with fibrosis development in some patients. Little is known
  about how the lung repairs aspiration-induced injury.

2015 -Resolution of Lung Injury after a Single Event of Aspiration : A Model of Bilateral Instillation of Whole Gastric Fluid

Aspiration is a common but underrecognized clinicopathologic entity,
  with varied radiographic manifestations. Aspiration represents a
  spectrum of diseases, including diffuse aspiration bronchiolitis,
  aspiration pneumonitis, airway obstruction by foreign body, exogenous
  lipoid pneumonia, interstitial fibrosis, and aspiration pneumonia with
  or without lung abscess formation. Many patients who aspirate do not
  present with disease, suggesting that pathophysiology is related to a
  variety of factors, including decreased levels of consciousness,
  dysphagia, impaired mucociliary clearance, composition of aspirate,
  and impaired host defenses.

2014 - Aspiration-Related Lung Diseases
2012 - Aspiration and Infection in the Elderly
2015 - Pediatric foreign body aspiration: A nidus for Aspergillus colonization
2012 - All that wheezes is not asthma: a 6-year-old with foreign body aspiration and no suggestive history


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Why do males have more birth defects?
I taught in elementary school for 20 years and noticed that males were far more likely to be classified as handicapped than females.
More males than females die at birth and are more likely to have birth defects. Why?

Do you have a reference that supports these claims?

I guess you mean "taught" elementary school. I am taking the liberty to edit that. However, you have to provide or cite a well documented data for making such a claim.

Welcome to Biology.SE Wendy.
Issue in your post
There are a few issues in your post.

You made a personal observation that males tend to more often be diagnosed with a handicap than females (in frequency). You probably did not keep track of the numbers and you probably did not make any statistical analysis. So there is really no reason to trust this observation. The idea that males are more often classified as handicapped than females is opinion-based for the moment and you will need a reference for this before asking why it is true.
You also claim that most birth defects occur in males and not in females. You should also include a reference.
You are talking about gender difference in "handicap frequency" and "birth defect frequency". It is a little unclear what the question (your last sentence Why) refers to. Maybe both. In such case, why would you expect that a common mechanism explains both observations? You should probably restrict your question to one or the other only.

For these above reasons, the question cannot be correctly answered in its above form. But below is something that may already help you.
Birth defects
It is true that birth defects is more prevalent among males than among females (in humans). According to Lary and Paulozzi 2001:

The overall prevalence of major defects at birth was 3.9% among males and 2.8% among females.

Reading their abstract only, one can see that they go on saying

Defects of the sex organs were eight and one-half times more prevalent among males and accounted for about half of the increased risk of birth defects among males relative to females. Urinary tract defects were 62% more prevalent among males, and gastrointestinal tract defects were 55% more prevalent among males.

In consequence, it seems at first sight that the difference in birth defects frequency is very much related to the development of sex organs. In their abstract they announce that they discuss the mechanisms that account for such difference.
I currently don't have access to the paper (I am not on campus) to report more details of their findings.

Although this isn't the determining factor in why males have more birth defects but it should be noted that the the fact males have only one X chromosome means they are very susceptible to X-linked recessive diseases.
As females receive two X chromosomes the chance of them obtaining an X-linked recessive disease is reduced significantly.
(And not all X-linked diseases produce cognitive impairment in individuals but if you sift through all the X-linked diseases it is easy to see the relationship.)


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Metabolic efficiency for fats and sugars
I am making an exercise for physics students about the first law of thermodynamics, burning heat and evaporation heat. So my idea is to use cycler which runs on fats and sugars where proportion determined by respiration quotient. The amount of evaporated sweats would be determined from inefficiency of using the fuel. Unfortunately I am unable to find efficiency data to form the exercise.
So what are typical efficiencies to run skeletal muscles on either fat or sugar molecules?
EDIT
Assuming respiratory quotient measured at the time of cycling is 0.7 so all energy is obtained from oxidizing fats:
$$ C_{16}H_{32}O_2 + 23 O_2 -> 16CO_2 + 16 H_2O + \Delta G$$
what part of the $\Delta G$ can do mechanical work $A$ or simply what is typical value of efficiency coefficient:
$$\mu = \frac{A}{\Delta G}$$

A quick google on "muscle efficiency" turns up a number of articles.  Wikipedia gives an estimate of 18--26% efficiency, https://en.wikipedia.org/wiki/Muscle

Muscles first transform those compounds to ATP.

This is a very complicated question. You need to rephrase your question to be more specific.
Efficiencies of energy utilization from glucose in the presence of O2 (aerobic respiration) are considered to be in the 40% range. Quite good when you consider that an automobile combustion engine is in the 20-25% range.
There is some evidence that betahydroxybutarate (B-OHB) actually provides more available energy for work than does glucose.  See Paper Here.
However, what is often overlooked is the energy needed to generate B-OHB from fat during ketosis, which results in a net loss in efficiency compared to glucose.
One of my favorite blogs is Peter Attia's "The Eating Academy."  He has a Post that goes into this subject somewhat.
I know this isn't a complete answer to your question, but again, you need to be more specific.
Respiration with or without O2.  Efficiencies in generating ATP from source material or only net efficiencies after the ATP -> ADP.

I made second part more specific. In your language I want efficiency of energy utilization from fats in the presence of O2.

If its needed you can also assume that fats are taken only from tissues

Ok I got right source http://www.ncbi.nlm.nih.gov/pmc/articles/PMC543577/pdf/1743-7075-1-15.pdf the lipids have the same efficiency of generating ATP specificly 40%

Excellent. If my answer was useful, please do indicate so.


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Which is more susceptible to dehydration — extracellular and intracellular fluid?
I want to ask in human body, there is intracellular and extracellular fluid that makes up the total body water of our body, which is drained first when we do activities? extra or intra? if I want to do a bioimpedance measurement, does measuring only the extracellular fluid good? Thankyou

I edited your title such that it summarizes your actual question. Let me know if that is fine.

You should understand that the body is an open system which is held at a steady state. Water can diffuse in and out of the cell such that the osmolarity is balanced on both sides of the membranes. If the water potential changes in either of these compartments (intra- and extra- cellular) because of addition or removal of water molecules, both the compartments would be affected such that finally the osmolarity is same in both the compartments. It may, however, take some time to achieve the steady state.
If you refer to sweating when you say "activity" then you should note that it is a complex process with extensive neurological control. The water that is secreted by the eccrine sweat gland primarily comes from the blood. However, profuse sweating will lead to water loss from both the intra- and extra- cellular compartments.

Prolonged exposure to hyperthermic conditions and/or prolonged
  exercise in the heat can induce water deficits due to profuse
  sweating, resulting in hypohydration. This water deficit lowers both
  intracellular and extracellular volumes and results in plasma
  hyperosmolality and hypovolemia; both of which impair sweating.

Shibasaki, Manabu, and Craig G. Crandall. "Mechanisms and controllers of eccrine sweating in humans." Frontiers in bioscience (Scholar edition) 2 (2010): 685-696.

So, for your experiment it is better to measure the osmolarity of the extracellular fluid or the blood plasma because:

It is easier to measure
It would not be sensitive to local and temporary effects


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How does soap affect membrane permeability? Which component of the membrane does it affect?
In a lab we used distilled water + 3 drops of soap to examine how beetroot would be affected by it. I believe the beetroots membrane denatured and a red pigment leaked from it. However, I cannot explain why this has happened. Can anyone explain the topic question to me?

Detergents like soap solubilize, or dissolve, lipids. The cell, or plasma, membrane is a lipid bilayer. The detergent molecules form water-soluble micelles that contain the membrane lipids, so the membrane is completely ruptured, or gone.

@mdperry answered well. If you need some diagrams to help with understanding, this article Should be helpful.
As you surmised, when you add detergent, it is lysing some cells of the beetroot that contain pigment.  That pigment then gets released into solution.  I've annotated the image below for the micelles that gets formed, except I spelled it wrong :/


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tandem repeat sequence; causes of contraction and/or expansion question
Question:
Which of the following events, occurring within a tandem repeat sequence, will cause an expansion or contraction of the array?
A) Endoduplication    B) homologous recombination    C) Unequal
   crossing-over   D) Error-prone DNA repair    E) Inversion
I know for a fact that upon replication, tandem repeats of DNA (specifically trinucleotide repeats) can form loops which are repaired by mismatch repair enzymes (MSH2-MSH3); and failure to correct this would lead to an expansion of the array post-replication. However, this answer was incorrect.
Could someone assist me with this question? I read up on the topic but its not clear to me why DNA repair defects do not suffice as an answer. I don't also necessarily understand the correct answer (C)
Thanks so much
-Chris

Gene-duplication would not result in contraction (only expansion). Endoduplication would affect all the genes in the chromosome. Error prone repair would cause small-indels but not expansion of the repeats. Inversion will certainly not do anything to the sequence except changing its orientation.
During unequal crossover, the chromosomes can align imperfectly because of multiple alignment sites in the repeat region, thereby leading to unequal crossover products.  Crossing over however essentially happens because of homologous recombination. Crossover is a "phenomenon" and not a "mechanism" in a true sense.

Mechanism of crossover
Reproduced from: Bugreev, Dmitry V., et al. "The resistance of DMC1 D-loops to dissociation may account for the DMC1 requirement in meiosis." Nature structural & molecular biology 18.1 (2011): 56-60.

Another thing to note is that homologous recombination in the absence of crossover can lead to expansion of repeats but not contraction (see below).


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mutations induced by transposons
Question:
In contrast to chemically-induced mutations, mutations induced by transposons are more likely to ...

be lethal
de dominant
be stable
revert to wild types
be a gain of function

The answer is 4; but I have no understanding of why this is the correct answer, or, why the others answers are not correct.  Could someone help to explain why this is the case?

Transposons are mobile genetic elements, or jumping genes. If a Tn can jump into your gene then it can also often jump out again later, so sometimes the mutation reverts. This means the mutation is unstable, so 3. is incorrect. As an RFLP the Tn is dominant in a diploid, but usually a Tn mutation causes a recessive loss-of-function phenotype, so 2. and 5. are incorrect. In a diploid a recessive cannot be lethal on its own, because then it would be dominant, so 1. is incorrect.

@mdperry you can make that an answer. However, transposon can affect the X chromosome of the male and can show dominant effects. But since that is only a specific case we can dispose it.


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Recombination between DNA segments question

In the diagram shown above, segments A and C are copies of a repeated DNA sequence, flanking a unique stretch shown as B. A and C are in an inverted orientation relative to each other, as indicated by the arrows. Intramolecular recombination between segments A and C would most likely lead to ...

duplication of segment B only
duplications of segments A, B, and C
inversion of segment B
deletion of segment B only
deletion of segments A, B, and C

I do not understand this question. Or how the answer was arrived it. Can someone provide some light on the subject? Is this related to transposons?

Redraw the diagram so it looks like a horseshoe on its side, such that the two arrows lie parallel, pointing in the same direction. 2. Now draw the 'X' to show the recombination crossover between the homologous segments. 3. Starting at the leftmost end of the DNA (the end with segment 'A' in your drawing, trace the path of the recombinant DNA product after the crossover has occurred. The segment labelled B will have under gone an inversion.

So, apparently the "trick" to this question is in the wording. "between A and B" appears to mean one crossover somewhere in the B segment, which could destroy (delete) a gene in the B sequence if present at the cut.
The answer involving the horseshoe "trick" implies that the chromosome has looped so that the A and C sequences match up, an extremely unlikely condition. Then a crossover occurs while the loop is in place, also an extremely unlikely event.
Another problem is that the horseshoe solution apparently implies that it is a single chromatid that is looping to itself and forming the crossover. That's weird. I could more easily visualize a different solution: One chromatid is aligned tail-to-head with respect to the other chromatid (head-to-tail). This would allow the corresponding A and B segments on the two chromatids to match up, thus allowing a crossover point anywhere (except inside B) to result in an inversion of B. This is also weird.
These two solutions are much weirder and unlikely than a simple crossover inside B: Picture the two chromatids aligned a little off target so that one is cut at the start of B nearest the A segment, and the other chromatid is cut at the other end of B, nearest the C segment. The result is an uncomplicated deletion of the B segment from one of the chromatids and duplication in the other (no inversion). This scenario seems at least as valid as the "correct" choice given in the practice exam.
While I'm glad to have learned the "trick" in this question for when I take the exam, I consider this question "bad".


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Genotype-Phenotype databases?
Beyond the Stanford HIV database, what other databases out there provide a dataset linking virus/bacterial genotype to quantitative phenotype? I'm looking for high quality datasets to test machine learning pipelines. My own searches usually yield only databases that curate mutations related to drug resistance class ("resistant, possibly resistant, susceptible), but not quantitative information in a standardized form like the Stanford database.

There are thousands of phenotypic variables. The most commonly documented is that of growth rates (or colony size). Also you can have 2^n genotypes for an organism with n genes, assuming there are only two alleles of a gene. Whole genome single and double knockouts experiments have been donee for yeast and E.coli, afaik, but I am not aware of a database. These experiments just measure the growth and fitness.


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How are CheY, CheA, CheW, CheZ pronounced in speech?
This is a quick followup question to this question about proteins that play important roles in chemotaxis:
How does one pronounce the protein names "CheY", "CheW", etc., in English?  My guess would be that they're pronounced like "key why", "key double-u", etc.
(I want to refer to these proteins in a philosophy of science presentation, but don't have much background in molecular biology. I know about chemotaxis only from reading.)

That's certainly how I would pronounce them: you're abbreviating 'chemotaxis', so "key-Y' makes sense. You could probably get away with 'C-H-E-Y' or 'Chemotaxis-Y' but I'd use the first one. When they're unpronounceable spell it, otherwise say it if you can. There aren't official guidelines on gene symbol pronunciation, so you're on your own.

These are not English words that have any defined pronunciation. These are more like code-words. You can pronounce them as you want. For these proteins, I just pronounce them as if they were abbreviations and not acronyms.

@Resonating, WYSYWIG, these are answers, and the best answers possible, I suspect.  Each of your comments helped me.  You should post them as answers, so that I can upvote them.

Resonating, @WYSYWIG, these are answers, and the best answers possible, I suspect. Each of your comments helped me. You should post them as answers, so that I can upvote them.

As was mentioned in the comments, these are not real words and there is no authority on their pronunciation. Given that Che is an abbreviation of chemotaxis, I would pronounce it the same as key.


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How are reflexes suppressed?
What neurophysiological process keeps reflex arcs in check? For example, the withdrawal reflex causes the hand to jerk back when the fingers touch something painfully hot incidentally. However, that reflex can be voluntarily suppressed when one deliberately touches that same hot object on purpose. What neural process is involved in conscious suppression of reflexes?

Short answer
The pain withdrawal reflex can only be suppressed when touching something painful on purpose. Deliberate, conscious contraction of the extensor muscle before reflex initiation can prevent the contraction of the flexor muscles once the reflex is started.
Background
The pain withdrawal reflex arc (Fig. 1) receives input from sensory neurons that enter the dorsal part of the spinal cord via the dorsal root of the spinal nerve and synapse onto interneurons within the spinal gray matter. The interneurons in turn synapse onto motor neurons, which send axons that exit the cord via the ventral root. They conduct information to the muscles. The resulting withdrawal reflex is initiated by activating motor neurons of the flexor muscles (agonist), and simultaneous inhibition of the motor neurons to the extensor muscles (antagonist). This loosening of the antagonist while the agonist is being contracted is referred to as reciprocal inhibition (Crone, 1993). More important to the question is the fact that the motor response is well under way before the signals responsible for the conscious sensation of pain (which exit the reflex pathway in the spinal cord) ever reach the brain (Cornell University).

Fig. 1. Schematic of the pain withdrawal reflex arc. Source: Washington Uni.
Hence, the reflex pathway is initiated even before we are aware of any pain. The only possible way to suppress a reflex that is faster than perception is to start counteracting the agonist (flexor) before the reflex is initiated, i.e., by contracting the antagonist (extensor) before touching the painful object.
Reference
- Crone, Dan Med Bull (1993); 40(5): 571-81


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Why does the direction of endolymph flow oppose direction of body motion?
In the semicircular canals, the endolymph always flows in a direction that is opposite to the motion of the vestibular apparatus itself. I’m having trouble grasping why this is, and I would greatly appreciate it if anyone could give me some physics insight into this.

Perhaps it would help to think of the endolymph as trying to stay in the same place while your ear moves around it?

The endolymph inside the ear, like any kind of matter, has mass and so is subject to inertia.  This means any change in speed and direction will be resisted.  The ear and semicircular canals themselves are fairly solidly connected to the rest of the body and so accelerate smoothly.  But since endolymph is fluid, it cannot be brought up to speed as fast, so it lags behind in moving.  So, as the ear moves forward, the endolymph stays behind and so in relation to the ear, flows backward.
This is like what you experience when a car or airplane accelerates: you "flow" backwards into your seat as the vehicle surges forward.

Does this cause dizziness after twirl? (am I using the right word? :D)


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Entropy and Open Systems - AP Biology
I had the following question on an exam of mine and I got the points for the question, but I am wondering if someone could please explain why it is correct, or rather, if it is correct at all:

As living organisms grow, they increase in complexity and decrease in entropy. How does this relate to the second law of thermodynamics?
(A) Living organisms, like everything else in the universe, spontaneously decrease in entropy over time.
(B) The increase in entropy of the universe exactly balances out the decrease in entropy as the organism grows.
(C) Energy cannot be created or destroyed, so the energy used for growth is later used to increase entropy.
(D) The resulting increase in entropy of the universe is greater than the decrease in entropy associated with the growth.

I answered D, as it seemed like the most likely answer out of all of them, and I got the points.
According to the 2nd Law of Thermodynamics, the entropy of the universe will increase with time.
Please correct me if I am wrong, but from my understanding this only applies to closed systems--so how exactly would it apply to organisms (which are open systems)? Is it because organisms release heat through chemical reactions and thus add to the entropy of the universe while decreasing their own entropy?
Thank you!
-Aleksandr

If you mean "von Neumann entropy", (B) seems correct. However, if "thermodynamics entropy" is meant, the correct answer would be  (D).

You are correct. Anything within the universe is part of the closed system of the universe. Therefore, they must also increase the entropy of the universe. You are correct, they do release a lot of heat. Plus, while making ATP, the major source of cellular energy, they convert a complex molecule, glucose, to simpler molecules, H2O and CO2, increasing entropy as they release these chemicals.
Also, the key fact is that to lower entropy in their body, organisms must use up energy. Energy is required to avoid the entropy from increasing (which actually means they actually expend energy to prevent equilibrium; high entropy means reaching equilibrium). So they would follow the 2nd law of thermodynamics. Which reminds me of a joke!
Old chenists never die, they just reach equilibrium!

I would say D.) too.

The resulting increase in entropy of the universe is greater than the
  decrease in entropy associated with the growth.

We can argue that the cells and the universe together are a closed system and entropy increases in a closed system by time. So the sum of their entropy changes must be always positive.


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Is this a simple Hardy-Weinberg problem?
Phenylketonuria is a severe developmental disability due to a rare autosomal recessive allele. Approximately 1 in every 10,000 newborns suffer from this disease. Calculate the frequency of the allele causing this disease and the frequency of heterozygous "carrier" individuals.
What I've come up with is that this is a Hardy-Weinberg problem. Is this true?
My answers:
frequency of allele causing disease = 0.01
frequency of heterozygous "carrier" individuals = 0.0198

Yeah you are right but what are your reasons for thinking that this is a Hardy weinberg problem ?

I honestly have no idea. I just tried the numbers that semi made sense and it seemed to answer the questions at hand. Is there a method that reveals why this is exactly a Hardy-Weinberg problem?

See my ans. And yeah I also think this is the "bestest" site ever !!

Yes, your answers are correct. Of course, your calculations forced you to make the standard Hardy-Weinberg assumptions such as random mating. Good job!

This should be a comment.

Well... The OP is asking did I get it right? The answer is either no, because... or yes.

Too long for comment :
If you want to solve the question by Hardy Weinberg, there are certain assumptions involved :-
1.There is random mating. People do not choose their mates on the basis of whether they carry PKU gene or not & mating among close relatives is not there.
2.No new PKU mutations happen.
3.There is no difference in the reproductive capacity of people with or without PKU gene.
If your study population fulfills these criterias, you can apply Hardy-Weinberg to calculate frequencies of various genotypes.
Because this question is  homework ,such assumptions are not mentioned. And, at undergrad level,there is no other concept by which you can solve this question except HWE.
PS: Try to think what would happen if these assumptions are not fulfilled.
PSS: Even if you are solving a small homework question, do think about the logic behind every step. Though it may seem like a lot of work initially , it has enormous potential to teach you subtle concepts !

The fact that PKU is a "severe developmental disease" makes me think that assumption #3 is violated. It could be that the students are meant to solve the problem with the HW equation anyway, though

@cactuswoman If PKU is diagnosed early and diet restrictions are followed, it is possible to live "normally".


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Are there any biological obstacles prohibiting lighter-than-air organisms?
Why there are no organisms that use cavities filled with lighter-than air substances (e.g. hydrogen) to fly and remain in air?
Given that there are a lot of fish and algae that use similar cavities to float, it is surprising that no organism utilized the same mechanism to fly.

I don't know of any organism that uses cavities soley to fly; birds have air sacs to help them fly, and very light bones. https://en.wikipedia.org/wiki/Air_sacs

@Ro Siv what's the purpose of air sacs filled with normal air? It only worsens aerodynamics.

This tends to be a question like If a trait would be advantageous to an organism, why hasn't it evolved?

Because organisms would need to develop an electrolysis system or a steam refractory apparatus. Rather energy consuming. Better to flap some wings I reckon.