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probability of having normal daughter

If  father has hemophilia, mother is a carrier of the disease, then
  what is the probability of having a normal daughter ?

My question: Should the probability of having a daughter be also multiplied ? Should the answer be 0.5 or should it be 0.25 ?

Unfortunately, the question is ambiguous.

@ChinmayKanchi umm..I am not able to understand how this is ambiguous.Could you please elaborate ?

I can't understand what you mean by "Should the probability of having a daughter be multiplied?" But yes, the probability of having a normal daughter is 0.25, but she will be a carrier like her mother.
Let H represent normal allele for blood clotting (dominant); h represent allele for hemophilia, XY represent the male chromosomes and XX represent the female chromosomes.
Parental Phenotypes :
   Normal female(carrier) x Hemophiliac male

Parental Genotypes (2n) :
   X(H)X(h)         x     X(h)Y

Gametes (n) :
   X(H)     X(h)    x   X(h)     Y

Possible Outcomes :
X(H)X(h) - A normal female, carrier.
X(H)Y    - A normal male.
X(h)X(h) - A hemophiliac female.
X(h)Y    - A hemophiliac male.
So probability of having a normal daughter, that is X(H)X(h) is 0.25.

I couldn't find a way to write superscripts, so I put the alleles in parenthesis. Its usually written in superscript. Hope this helps. :)


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Hibernation in ectotherm and endotherm

Both snake and weasel hibernate. Which of the following is correct?
A. They will die when temperature decreases below the critical
  temperature.
B. Weasel will die when temperature decreases below the critical
  temperature.
C. Snake will die and weasel will wake up when the temperature
  decreases below the critical temperature.
D. Weasel keeps low body temperature and slow heart rate during the
  entire period of hibernation.

I don't think any of them should die, they would have some adaptation to prevent that. So,is the answer (D) ?
What is the snake's adaptation in this situation ?

A relevant article

Weasels don't hibernate.  See http://icwdm.org/handbook/carnivor/Weasels.asp
Both will die when the temperature falls below a certain level.  The difference between snakes (ectotherms) and weasels (endotherms) is that the snake's body temperature will fluctuate more, depending on the surrounding temperature.

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Molting in arthropods
Do all the arthropods molt ? Which ones do not molt ? Why don't they need to molt ?
I tried googling this - but did not get satisfactory answers.

in my opinion all arthropods molt. In fact arthropods are a part of clade called ecdysozoa, the members of which undergo ecdysis (molting).
Molting is necessary because arthropods have an exoskeleton which has to be removed if the organism has to grow.

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Refractory period in action potential

I know that the part E in this graph is definitely the part of refractory period.
My question : Will there be any effect on B,C or D if a stimulus is given at  time B,CorD respectively ?

If there is a stimulus at E, there will be depolarization (membrane becomes relatively more positive). It is just that no action potential is fired. Therefore, if a strong stimulus does arrive, it will depolarise the membrane to an extent depending on its strength. It will increase the height of the succeeding B phase or decrease the dip of E phase. If it is strong enough, it might persist above the threshold till the refractory period is over, and then an action potential can be fired.

@SatwikPasani I'd say that's a great answer, would you like to add it as one?

If there is a stimulus at E, there will be depolarization (membrane becomes relatively more positive). It is just that no action potentials are fired. Therefore, if a strong stimulus does arrive, it will depolarize the membrane to an extent depending on its strength. It will increase the height of the succeeding B phase or reduce the dip of the succeeding E phase. If it is strong enough, it might persist above the threshold till the refractory period is over, and then an action potential can be fired.


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Determining whether X chromosome from sperm or egg
Is there any way of determining which X chromosome a female inherited from her father and which from her mom ?

You could try to follow this up by sequencing the X chromosome from the father and try to find unique polymorphisms which are not present in the X chromosome of the mother. You can than try to find them in the childs "X". This makes not much sense though, since one of the X chromosomes is ramdomly inactivated.

@Chris So, we could use RFLP for this ? Could we also use FISH ?

RFLP could work, I am not sure if the resolution of fish is good enough.

@Chris Thanks! I don't know much about FISH, so what exactly do you mean when you say that resolution won't be good ?

For FISH you need a probe that binds to the chromosome. If the difference you want to see is so small (a SNP for example), that the probe will bind anyway, than the resolution of the method is too small to detect the difference. Insertions or deletions are bigger an can be detected.

yes it is possible... in placenta (trophectoderm) the paternal X is epigenetically silenced [ref].
That is if you do the test in the pre/neo-natal stage. Otherwise, at later stages, you have to check by DNA fingerprinting + karyotyping/FISH as Chris suggested.


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Why is Turner syndrome rarer than Klinefelter syndrome?
Turner syndrome occurs in 1-1000 to 1-5000 females, and Klinefelter syndrome occurs in 1-500 to 1-1000 males.
Why is Turner so rare even though they both are caused basically by the same mechanism?

First of all, they are not caused by the same mechanism. They are both aneuploidies, but the mechanism is different.
Turner syndrome happens when one of the gametes (most commonly father's) lacks a copy of X chromosome, or the X chromosome is heavily damaged. This means that while normal women have two X chromosomes, Turner women have only one, and nothing else.
Klinefelter syndrome happens when one of the gametes retains an extra copy of the X chromosome. This way a Klinefelter man has two X chromosomes and Y chromosome instead of one X and one Y.
As you can see - the Turner woman is lacking some genetic information, while the Klinefelter man has too much of it. Generally, having too much genetic information is much easier to survive than not having enough of it, so this explains the relative difference on the most basic level.
But, you might say, what about Barr's bodies? Don't the women use only one X chromosome in each cell? And wasn't Y chromosome almost empty?
Yes, these are an important consideration for these two syndromes. In each cell of a women's body one of the X chromosomes is inactivated and folded into a Barr's body. This inactivation is random, so part of the cells keep mother's and part of the cells keep father's X chromosome active. The trick is that the Barr body is not entirely inactive (Genes That Escape From X Inactivation). Only about 15% of the genes are active, but just the lack of them is mostly lethal (Turner fetuses are usually aborted, Wikipedia quotes olny 1% surviving until birth), and accounts for the health problems and deformations in Turner women.
A Klinefelter man has two X chromosomes in addition to his Y chromosome, so one of the chromosomes inactivates into a Barr body. The presence of Y chromosome directs his body to develop into a male pattern, but at the same time, the existence of Barr's body with those still active genes, causes his body to develop also feminine features. There is little to cause spontaneous abortion.


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What is this image?

What I understand is- I think this is picture of DNA. But why is it in this conformation ? What types of cells have this type of DNA ?

It is called a Holliday junction. It forms during recombination.

Well, I am curoius - how did you find this out ?!

Just guessed it.. It resembled the textbook diagram of Holliday junction. :)

This is a pretty well known image and you definitely come across it, when you study in this direction.


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Why bacteria produce light?
After seeing this video I am curious to know why the free living bacteria produce light. What advantage will they have ? Or is it just an "unintentional" result of one of their pathways ?

Go for the  link below, you will find an article on "How do marine bacteria produce light, why are they luminescent, and can we employ bacterial bioluminescence in aquatic biotechnology?"
www.biology-online.org/articles/marine_bacteria_produce_light/abstract.html
From this article :

The question remains whether quorum sensing regulation of bacterial
  luminescence is a kind of a ‘social behaviour’ in which cells
  ‘predict’ the possibility of increased mutagenesis where conditions
  allow for efficient metabolism leading to extensive bacterial growth.
  Such conditions may cause the appearance of large quantities of
  metabolites, including mutagenic agents. Thus, one could speculate
  that enhanced light emission at a high cell density may ensure more
  efficient DNA repair in response to potentially increased
  concentrations of mutagens. Alternatively, quorum sensing may be
  needed for another role of bacterial bioluminescence, besides
  stimulation of photoreactivation.


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Are human infants inherently frightened by anything?
Naïve question - feel free to shoot it down.
To the best of my knowledge an infant doesn't really 'shrink' from something without first trying it. Even the action of looking at the fierce expression is undertaken without qualm - squalling comes later (if at all!)
Are human infants inherently frightened by anything?

this is more a developmental psychology question.  I have kids and they are quite easily feeling afraid and threatened.  Being left alone without their parents or other close family is very common.

Loud noises are something that infants of any age certainly are not fond of?


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Genetic Epistasis Question
I need help with this practice question.

I'm assuming that would a epsitatic recessive question since the parents are true breeding and then the ratio would be 9.3.4. But I am not so sure.
Any help would be greatly appreciated thanks!

The answer to the third question should be recessive epistasis.

The Magenta variety is pure breeding, and hence must be homozygous at both loci, (Dominant at Gene A and recessive at Gene B), otherwise, in some of the generation along the family line, there would have been a non-magenta flower, which contradicts the pure breeding nature. But the same cannot be said for the pure breeding white variety, as it can still be homozygous recessive at Gene A and heterozygous at Gene B, it would still exhibit white flowers in all of its progeny after any number of generations.
But the fact that all the progeny of the cross between white and the magenta variety turns out to be red, removes the possibility of the white variety being heterozygous, as that would have produced atleast some magenta plants. Since all were red, we can be certain of the genotype of both the parents, and consequently of the F1 progeny.
This solves your first question. The second question needs the extrapolation of the information gathered while solving the first question into a Punnett square and a simple probability calculation. The third question is a factual question, but it must be mentioned, that this particular type of interaction can be classified under more than one type, and hence a single answer would not be possible for your third question.
ADDENDUM
The third question is actually a bit difficult to answer. The phenotypes will be $\text{A*B*}$=Red, $\text{A*bb}$=Magenta, $\text{aa**}$=white. This gives us $9:3:4$ for Red:Magenta:white. Now the fact that recessive at one locus , Gene A, suppresses the phenotype altogether no matter what the genotype at the other locus, means that one of the phenomenon exhibited is recessive epistasis, where Gene A is the epistatic loci and Gene B is the Hypostatic loci. But, the fact that there are two distinct phenotypes with the epistatic gene dominant, means the interaction is not complementary ($9:7$) but is supplementary ($9:3:4$). This distinction is necessary, and it essentially means that the "intermediate" of the elucidated pathway is also coloured. Otherwise, like in Flower colour in Lathyrus Odoratus, the phenotypes of $\text{aa**}$ and $\text{A*bb}$ are same, and hence the phenotypic ration remains $9:7$. For a ratio of $13:3$ you need domianant epistasis and the phenotypes of double recessive and the epistatic recessive must match. Here, it is recessive epistasis, as the recessive condition at one locus suppresses the expression a other, and not dominant. Feel free to seek further clarifications or simplification.

Thanks for the answer Satwik. Really appreciate it but stil for question 3b, i understand that if the F1 are self-crossed then that would yield a 9:3:3:1 ratio I also understand that there are a number of deviations from that ratio depending on the interaction. I'm assuming it might be a 9:3:4 ratio but I'm not sure since others are also reasnable. What deviation do you think is the correct one?

Also, just to confirm for question d, if we cross BbDd and BbDd and end up with BD, Bdd, bbD, bbdd, then those carrying a dd would not be expressed and only those with with Bdd can produce the phenotype concerned, then that would be dominant suppression interaction? is that true and the ratio then would be a 13:3?? Thanks in advance

@ApothemCyte See the addendum in my answer

The way I understood the problem is like this.
a) The parents are said to be pure bred so we can assume that both parents posses homozygous for each of the traits. Hence, the genotype for both are:
P1: Magenta AAbb x aaBB White
So this will result to all F1 consisting of Red flowered phenotypes (AaBb)
-since the absence of gene A will not code for the magenta intermediate, it's fine to activate gene B because this will not work without gene A.
b) the ratio that will be observed on the F2 generation are:
9 red: 3 magenta: 4 white
c) the interaction of the genes pertains to recessive epistasis. The following ratios are constant for each of the epistatic interaction:

Dominant epistasis: 12:3:1
Recessive epistasis: 9:3:4
Double Dominant epistasis: 15:1
Double recessive epistasis: 9:7
Dominant-recessive epistasis: 13:3


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What happens if someone with mutations to alcohol dehydrogenase (ADH) drinks alcohol?
ethanol then doesn't get converted to acetaldehyde.
in fact, could someone KO'ed for ADH be resistant to methanol poisoning?

In theory I believe that's true, but they'd also be much more susceptible to the normal intoxicating properties of ethanol / methanol, which might be just as harmful.

uh there are not individuals so ADH definition that survive. when the mother drank fruit juice or cough syrup they would be poisoned and brain dead.

People, which have no ADH wouldn't be able to process methanol. Since the specificity of the ADH is higher for ethanol you get quite large amounts of ethanol for days (until the methanol level is under a specific level). Another possibility is to treat patient with the ADH inhibitor Fomepizole.
This also makes problems for the ethanol metabolization, but according to this paper ("The biochemistry of alcohol metabolism - a brief review") there are two other pathways of breakdown. One takes place in the peroxisomes and utilizes catalase and hydrogen peroxide (but is limited by the availability of peroxide), the other take place in the smooth endoplasmatic reticulum and uses the Cytochrome P450 enzyme.
I am not sure, if complete losses of ADH really happen (haven't found any reference) but mutations in this enzyme are quite common leading to a lower enzyme activity.

The flush reaction is caused by reduced activity of ALDEHYDE dehyrdogenase. The question is about alcohol dehydrogenase, which is necessary for alcohol to be converted into acetaldehyde in the first place.

You are absolutely right. I changed my answer and will look up some other reference.


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Why do all particles have the same influence on osmosis?
When people talk about osmosis, they say that when we add a mole of NaCl, then each its molecule gets dissolved into 2 separate particles and therefore we have 2osM/L solution.
But both Na & Cl are attached to molecules of water which means that those water molecules are not water anymore and they can't penetrate the membrane. Thus not only the presence of Na & Cl itself changes the concentration of water in solution, but also the number of water molecules taken by those particles.
Therefore if we put 1 particle that binds to 1 water molecule and 1 particle that binds to 5 water molecules - they change the water concentration differently.
Please somebody tell me where I'm wrong.

Just wanted to add that the kind of salt or solvent in the water does matter. The Chemical Activity of the ions or other soluates matter quite a bit.  For example osmosis can be caused by sugar, organic molecules fats as well as salts. Here, Chemical Activity is a general idea of the relative effect of different molecules on osmosis.
Different soluates can cause drastically different effects on osmosis.  e.g. see Table 1 in this reference.

You can see the importance of the number of molecules if you imagine a semipermeable membrane, on one side there is water, and on the other there is the salty water solution. Water molecules can pass the membrane but ions cannot. On the side of the solution, because Na and Cl are taking space and covering some parts of the membrane, the water molecules are "touching" the membrane less, so the flow of water molecules out from solution side is slower than the pure water side. This means that more water is flowing into the solution than out of it, slowly decreasing the concentration of the solution, until they reach an equilibrium when the flow of water to both sides is equal.
You are incorrect to say that the "water molecules are no longer water", because their interactions with the ions are intermolecular (ion-dipole), not intramolecular. Intermolecular interactions may slow down molecules, but since they do not lock the water molecules in place, they could still pass the membrane. Although, the concentration of solute is important in calculating osmotic pressure. The formula used when the contentration is low is different than if the concentration was high. For the formuals see Osmotic Pressure on Wikipedia.
The visualization with the membrane is my interpretation of Silberberg's explanation of osmotic pressure in Principles of Chemistry, page 412.

When you dissolve something in water, you build a solvation shell around this - so each ion (in the case of salts) gets surrounded by a number of water molecules. For more details read this Wikipedia article.
The concentration change in free water molecules is usually not taken into account since it can be neglected due to the vast number of "unbound" molecules. So if you have one litre of water, it contains approximately 56 moles of water molecules. If you dissolve 1 mole of sodium chloride in this water, and take in account that this takes quite some water to get solvated, there is ways more water available. So the water concentration is almost constant (especially when you work at physiological osmosis condition).

Okay, let's calculate this scenario: we add 1 mole of NaCl (~60g) into 56 moles of water. Each Cl atom binds to 6 atoms of water at average (according to wiki: http://en.wikipedia.org/wiki/Sodium_chloride). Let's suppose that Na takes up the same number of water molecules. Then 1 mole of salt takes 12 moles of water which doesn't look negligible to me. On practice the number will probably be lower because a single water molecule can be bound to both Na & Cl atoms which means that in highly concentrated solution 1 mole of NaCl will bind to 6 moles of water which is still not negligible.

It indeed sounds that its not neglectable. But you still have 80% of the water present. And: Water is a neutral molecule that can pass through the cell membrane, other dissolved substances cannot do this.

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Mites on ginger root
I was just looking at some mouldy ginger found in the fridge under the microscope and was horrified/delighted to find (what looked to be) mites growing in it. I have searched the web and can only find references to red spider mites which these are certainly not. They were clear white and under 40x zoom about less than a mm across - does anyone know what they could be? Furthermore, what are they feeding on (ginger root is only ~15% carbohydrates - is that enough?) and has a minimal (~1%) amount of protein.
Here is a picture (sorry for the quality but the white thing looks to be a mite).

LOL "horrified/delighted to find..."

Pictures? Or, lacking that, can you tell how many body segments they have?

@Oreotrephes Have fished piece of ginger out of bin and added pic

Saw a bbc program the other day which talked about mites on cheese, they are (deliberately) all over the rind of some cheeses! I'll try to find it, might (or mite) inspire you to look at other things in your fridge too!

Does this look like the same bug to you ?
.
This one is a bulb mite, Rhizoglyphus robini, see here.

Yes - I think that's it! I'ts amazing how you can be both fascinated and disgusted at once ;) (It does seem to be harmless though nonetheless)

I share your feelings :-)

This is very interesting. We think about microbes (micrometer) and insects (centimeter) as main plant pathogens, but know very few about what fills the gap between these 2 different sizes. At least I learned a lot about medical microbiology, and I know a few plant pathogens as well, but I know nothing about mites. :-)

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Need help distinguishing between a primary and secondary source
I am trying to figure out if the following article is a primary or secondary source.
I'm leaning towards secondary but here are my cases for both.

Primary: Published in a peer-reviewed journal.
Secondary: It seems to be mostly a summary of other works so it might
  not be original research.

Can anyone confirm this for me? Thank you!

probably better on Academia?

This would be a better fit on academia.stackexchange.com

Too long for a comment: Although this is a review article which summarizes the findings of other researchers, considers this as a primary article. The author gives you all the resources he used in the reference section of this article and summarises their finding. Additionally, review articles in renowned journals (and Genome Research is definitely such a journal) are peer-reviewed. Primary vs. secondary sources would be more the comparision of research articles and news articles. In my observation, news articles hardly ever name the sources or the original articles about which they report. Plus they sometimes have problems of getting the message wrong.


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How does human body deal with inert solid material in the bloodstream?
How does human body deal with inert solid material in the bloodstream? For example, if there is a powder of glass injected into our bloodstream, will the white blood cells do anything or will kidney excrete these materials? Thanks.

I once read a crime story (fictional), where injecting solid material like glass powder into the bloodstream was used as a means of deliberately murdering the patient :-). That would imply, that the body would not deal with such a condition very well. My mother is a medical doctor, read the same story, and did not say it was nonsense, recommended the book.

in some cases it will form scar tissue around it and even try to expel it by moving through the tissue.  in many cases it won't actually go anywhere, but form lump in the tissue.

As @shigeta points out, it would matter where the insult occurs and also what "inert" real means.  Glass could easily not be inert, and even if it were, you could easily kill someone with fine glass in a central line, just from the damage that would produce.  You want to look into inert foreign bodies.

Non-opsonized particles (Particles that can't be coated with opsonins like antibodies or complement proteins) can be engulfed by macrophages which could end up, for example, in the lung secretions and be coughed up one day. Note that a cell can only engulf a particle so large, so you'll not feel yourself coughing up anything out of the ordinary. Only tiny particles can be dealt with like this. Bigger particles can become trapped in fine vasculature (small veins; venules, and small arteries;arterioles). This can lead to abscess formation necessitating amputation of the affected limb.

It will not lead to abscess formation (that's a bacterial problem), but will lead to ischemia. Remember, most likely it will be injected into the venous side, which gets progressively larger until the pulmonary system is reached, so obstruction can occur in arterioles and capillaries of the lung.


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What is meant by "neurotransmitters flooding the brain"?
I frequently hear expressions like "Dopamine flooding the brain" or "X neurotransmitter flooding the brain" used to communicate with general audiences. For example: "Following [orgasm]? oxytocin floods the brain, causing feeling of deep connectedness between people"
What exactly do they mean by "Oxytocin flooding the brain"? I'm interested in where and how it happens. Do they mean that excess neurotransmitters are released in the synaptic cleft? Is it localized to some brain areas, or is it indeed throughout the brain?
If they are indeed talking about the synaptic cleft, then I'm interested in how such "flood" triggers the change in state - the answer to this question suggests that the half life of dopamine is only about 2 seconds in prefrontal cortex. Assuming that the half life of oxytocin is similar, in the "oxytocin floods the brain and produces feeling of connectedness" example, does it mean that a single burst of oxytocin(x seconds in synaptic cleft) is enough to produce such feeling, or are they talking about sustained release or some kind of release loop mechanism?

WOW! Whenever I have read about drug addiction, I have come across"flooding" but never wondered what actually it meant ! +100000000000

I'm pretty sure the answer is that it's a sensationalistic media term with no specific meaning. It probably covers a variety of different underlying biological mechanisms.

@octern I disagree, my answer elaborates...

It is very likely what they mean by "neurotransmitters flooding the brain" is the phenomenon called Volume Transmission.
I paraphrase from this source:

When a neurotransmitter is released at a synapse, it reaches its
  highest concentration inside the narrow space of the synaptic cleft,
  but some of it is certain to diffuse away before being reabsorbed or
  broken down. If it diffuses away, it has the potential to activate
  receptors that are located either at other synapses or on the membrane
  away from any synapse. The extrasynaptic activity of a
  neurotransmitter is known as volume transmission. It is well
  established that such effects occur to some degree, but their
  functional importance has long been a matter of controversy.


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PedigreeAnalysis Genetics

Hello! I need help with this exercise question. I am not really sure which pedigree diagram is autosomal and which is not. But, is question b 1/2. Can someone give an explanation? Thanks very much in advance? Appreciate any help!!

According to the key given, the one shaded black on the right is autosomal and one on the left is sex linked.
Yes, the answer to b is half because Maria is XhX ans Peter is XY and so the probability of the child having this disease is 1/2.

@ApothemCyte Does this make sense ? Ask, if u need help !

Thanks for the reply! But if the the diagram on the right is concerned with an autosomal disease, shouldn't we use Gg/gg/GG notation in place of XhX (for Maria).

Also, I'm a little bit unsure as to whether the genotypes I have for the diagram are actually correct. So, a brief explanation would help. Thanks in advance!

ApothemCyte, the diagrams are concerned with both the autosomal disease and the X-linked disease; look at whether the person symbol is shaded on the left side or the right side.

@mgkrebbs I filled them up that way but pretty sure it's completely messed up. Can you please check to see if they are right? Thank you in advance! link: http://s837.photobucket.com/user/apothemnew/media/1557562_10152265905761177_608325393_n_zps950a5df1.jpg.html?filters[user]=138960233&filters[recent]=1&sort=1&o=0

The G's seem mostly ok, but you don't know that Maria's grandmother is "GG".  The A/a's are messed up; you're treating the disease allele as recessive, but it's dominant (XA). [but then I have no formal training; I've never had a genetics course or even college biology.]

@mgkrebbs So here is my 2nd attempt. Do they look right now? (even to a person with no formal training) link: http://s837.photobucket.com/user/apothemnew/media/attempt2_zps419409e5.jpg.html

@ApothemCyte U have written Gg for peter's father but he could also be GG !


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Why do peas change colour?
I am doing an experiment on preservation of peas.
The first notable change to the peas over a period of one week is that they have changed colour from bright green to a dull colour... Why is this so?
The only test tube which did not have peas which changed colour was the one which was kept at 4 degrees Celcius in a fridge, so it probably has some relation to temperature...
Many thanks
N.B.: I know that the bacteria reproduce and could use the pea as their source of food, but how do they have any relation to the colour of the pea? I also put the tag "bacteria" and "thermodynamics" as I couldn't find any other related tags.

Have you preserved them in a refrigerator ?

Might be interested in reading this

@biogirllajja Interesting, but I'll still have a look at the answers to this question...

I am tempted to post an answer, but I am not sure if it is ethical to do your homework for you completely. Do you have access to the full text of article biogirl lajja linked ? The introduction section, page 2, contains your answer.

One more keyword - chlorophyll.

its okay to post an answer Barbara.  homework questions are allowed

@Barbara I've done my homework, by using information on this site: http://faculty.weber.edu/coberg/class/3853/3853%20MOs%20and%20Food%20Spoilage%20notes.htm (though I can't write the answer myself as I'm not a proper biologist) Don't worry, if you answer this question, you will help the community and others who wish to know the answer to this question (and you'll get more rep). Thanks ;)

Chlorophyll is a dye that makes leaves green, it plays a key role in photosynthesis. It is present also in unripe fruits, young peas etc. Maybe I should say chlorophylls, because it is a group of similar chemicals. They get degraded by heat.
(No assistence of microbes needed).
Bonus: Chlorophyll contains magnesium at the molecule core, which facilitates the green color. There were some creative people, who were upset, that the canned cucumbers are not green enough, so they added some copper-containing molecule during canning. It replaced magnesium and was more stable, so beautiful bright green cucumbers were on the market for a while. However, they turned out to be slightly poisonous and are not sold anymore.
Bonus 2: Most varieties of peas change color also naturally as they rippen. The seeds become yellow. The chlorophyll gets degraded in plant metabolism. The chloroplasts, i.e. the cell organelles responsible for photosynthesis change function to become storage organelles called leucoplasts.
(Edit: Ooops, I first wrote that chlorophyll supposedly contains iron. That was wrong, it is magnesium. Iron is present in a similar die called heme, which makes blood red. Probably I am getting too old :-) )


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Pedigree Diagram help

I am asked to fill the genotypes in the spaces provided but looks like I am aving a little bit of trouble. can anyone help? thanks in advance!

Here are a few hints that might help:
Talking about Maria's pedigree:
Firstly, it seems as if you have mixed up with $X^a$ and $X^A$, see that the disorder is X-linked DOMINANT. Anyone with either heterozygous or homozygous dominant expression would have the disease expressed. So the first generation male should have a genotype: $X^aY$, because if it were $X^AY$ then Amelogenesis imperfecta would be expressed as his phenotype and the first generation female should have a homozygous recessive genotype. Also no child in the second generation would suffer from the same.
(NOTE: The one suffering from Amelogenesis in the second generation would have genotype $X^AY$)
As for Gunther disease, both the parent in the first generation should have a heterozygous dominant expression and the offspring suffering must have a homozygous recessive expression. And you can apply the same basics in Peter's pedigree.
I think this much should be enough to complete the task, but if you still have some doubt you can put it forward in the comments.

Thank you very much Shefali for the explanation. I truly appreciate it. Here is my second attempt: http://s837.photobucket.com/user/apothemnew/media/attempt2_zps419409e5.jpg.html?filters[user]=138960233&filters[recent]=1&filters[publicOnly]=1&sort=1&o=0 does it look ok now? Thanks in advance. Sorry for the inconvenience :)

Well, in the first place I did not understand what does H or h and - indicate?

@ApothemCyte U have written Gg for peter's father but he could also be GG !

@Shefali Hello Shefali. Would you please if at all possible be able to help with my new question: http://biology.stackexchange.com/questions/15142/genetic-linkage-mapping-question-help Thank you so much in advance!!


text:
Why do we assume that the first humans were dark-skinned?
According to the article Dark skin and blue eyes: How Europeans once looked:

It is widely accepted that Man's oldest common forefather was dark
  skinned, and that people became more pale as they moved further north
  out of Africa into colder climates with less sunlight.

I thought that humans' oldest common ancestor was light-skinned, because

Dark-skinned people have white palms and soles, but light-skinned people have more consistent skin tones. This suggests that light skin is more ancestral and dark skin evolved to protect skin from the sun.
Bonobo chimpanzees, our closest primate cousins, look like they have light skin under black hair.

I understand we all originate in Africa, but I thought that the environmental conditions in Africa were different from today. How do we know that the first humans were dark-skinned?

The first men were not only blacks, they were also homos (If I may)

According to wikipedia, "comparisons between known skin pigmentation genes in chimpanzees and modern Africans show that dark skin evolved along with the loss of body hair about 1.2 million years ago and is the ancestral state of all humans." This is several million years after after the time estimated for the last common human-chimpanzee ancestor, but at least 1 million years before the emergence of Homo Sapiens. This suggests that the earliest species in Homo may have had lighter skin, but that the advantageous genes for dark skin were universal by the time of the first true humans.

The first modern humans evolved about 200.000 years ago in Africa. When they lost their body hair (or at least most of it), they needed some other protection of their skin from the sun - otherwise they are prone to develop melanoma. Melanin is such a protection, and the rate of melanoma is much lower in dark skinned people.
There is also a nice correlation between latitude and skin color - the more to the north (and to some degree to the south as well) you get, the lighter the skin color of the population gets. The reason for this is likely the better ability to synthesize Vitamin D (for which you need sunlight on the skin):

The evolution of human skin coloration.
The evolution of human skin ans skin color.
Development of different human skin colors: a review highlighting
photobiological and photobiophysical aspects.
North-South gradients of melanomas and non-melanomas: A role of
vitamin D?

The lightening of the skin occurred after humans moved to Europe:

The Timing of Pigmentation Lightening in Europeans

And we even know, that this occured more than once, since the genetic reasons for lighter skins are different between europeans and light skinned asians.
A lot of this we know via sequence comparisions of genes involved in pigmentation, there you can trace mutations and see, where they show up first and how they migrate over time. One very good example is the melanocortin-1-receptor (MC1R), which is mutated pretty often in europeans (mutations in this gene are generally associated with lighter skin and hair color; people with red hair carry certain mutations in this gene) but its under selection pressure to not mutate in africa (there are almost no known mutations in MC1R for africans). Another example would be a mutation in the SLC24A5 gene, which is exclusively found in europeans, but not in asians and which accounts also for lighter skin. I stop here for the moment, if there are more specific question, go ahead.

The genetic architecture of normal variation in human pigmentation:
an evolutionary perspective and model
Genetic Variation at the MC1R Locus and the Time since Loss of Human
Body Hair
SLC24A5, a putative cation exchanger, affects pigmentation in
zebrafish and humans.

Nicely referenced answer.

As per the linked article, new research suggests that Europeans evolved light skin because of diet, not latitude.

+1 for mention of the european 'innovation' of being pale!

@anomal This is discussed, yes.


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Phylogentic Footprinting Project
I'm working on performing phylogentic footprinting to figure out how many TRE sequences there are in the TWIST1 gene. (Sequence motifs). I'm trying to use ENSEMBL to gather orthologues of species in which the gene twist1 is present, compile it into a FASTA file and upload it to MEME SUITE. However, I'm having trouble understanding how to compile the file. I also don't know how to read SEQUENCE LOGOS. If anyone can help me, I would appreciate it SOOOOO much.

Can you post an image of your logos? Its easier to explain then.


text:
Evolutionary conservativeness

List the following proteins in the order of decreasing evolutionary
  conservativeness of their primary structure:

Somatotropin.
Catalytic subunit of a DNA – polymerase.
Histone H1.
Prolamines (storage proteins of cereals).

What I think : I am sure that 4th one should be last. I believe that H1 sequence is not that important as I had read somewhere that a cell can survive even without H1 histone. I also think that catalytic subunit is most important. So, according to me the order should be : 2,1,3,4.
Am I right ?

I believe it should be 2,3,1,4, since the histones are involved in several epigenetic regulations, lyonisation and transcriptional regulations, and since these regulations greatly change the phenotype under consideration, I think conserving the histones' primary structure should be more favourable as compared to Somatotropin, since slight modifications in hormones might not affect much due to absence of perfect specificity, presence of hormones with supplementary action, and so on.

@chris Thanks! yes, it was in yeast. I remember reading it in Bruce Alberts.

One of you should attempt an answer !

Do you think so? It would still be something like a comment.

@Chris I guess Unless there are any publications to provide data on the conservativeness of these proteins' primary structure, your comment is the best answer that can be given, as far as logical reasoning is considered.

Ok, if you say so...I can have a look if there is some data available later.

This is such a crappy question (not yours @biogirl, your teacher's). You cannot answer this question without actually checking the sequences. For example, the cell can survive without H1, OK, but H1 cannot function without it's structure since it's function is very dependent upon the structure. Therefore, it would not surprise me if it were exceedingly conserved. The question is an example of a lazy teacher, all you can offer is conjecture.

Even when you can live without Histone H1, its a widely distributed protein which you find in basically all living cells (except for some yeasts if I remember correct). This points to the fact that it must be available for quite a while. The same is true for the catalytic subunit of the DNA polymerase. Somatropin is still pretty important (and can be found in a lot of organisms), prolamines are quite specific to certain cereals. I would group it 2-3-1-4.

bacterial requirements for histones is not as great as euks I would say - what cell can reproduce without DNA polymerase?

@chris Does conservnativeness mean that it is present in most organisms or does it mean that the sequence/structure is not changed?

@shigeta hats why I think that the DNA polymerase is higher conserved. But the histone comes next.

@biogirllajja It can mean both :-) And its connected - proteins which are old in an evolutionary sense (like a DNA polymerase or something like cytochrome P450) are also highly conserved (for structural and functional motifs) on the sequence level.


text:
Insect identification
It is found in my apartment in Finland. I had to kill it to stop it from getting away before looking for the camera, but it looked pretty much the same alive and intact. It's length is about half a centimeter, and the younger ones look darker. It is often found in dark. Since their appearance, I often notice red and slightly itchy bug bite in the morning. The question is what is this insect?

Where in your apartment did you find them (what environment)?

@fileunderwater I don't know where did they come from, but they are just found on the wood and ceramic floors. The environment is warm and reasonably dry.

It reminds me of silverfish, a common wingless house insect.

yeah, my first idea as well, and the environment fits. I first thought that the legs looked a bit long though. However, environment + movement patterns is a good way to identify them by.


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DNA content in plant seeds vs. fruit flesh
Is there a publication comparing DNA yield and/or PCR-amplifiability after extraction from fruit flesh (like apples, oranges, cherries etc) in comparison to seeds of the same fruits?
I would prefer a reference, but your unpublished experience is also interesting to me.

A quick guess is that it will be easier to extract DNA (without inhibitors) from fresh material, since the seeds are made to survive. This can cause problems in the preparation.

Cell walls are a major problem for (sequencing length) DNA extraction. You will normally have more usable yield from the fruit flesh than from hard seeds. Another problem might be essential oil in the fruit flesh, though.

It depends on the seed and fruit you're talking about.
The amount of DNA in your crushed up sample of plant matter depends on only one thing--how many cells are in your sample. Look at this diagram of a kernel of corn (U of Indiana):

There are different cell densities in each area--in the endosperm, the cells can be huge (and therefore have a lower density of DNA when compared with the embryo).
Let's look at a stained mustard seed (U of London):

As you can see, the cells here are very dense. More dense means more DNA per unit sample.
As far as fruit is concerned, the same rule of thumb applies. Verner, 1938 shows some cool apple tissue histology that might give you an idea of cell density in fruit tissue (again, it will be different in different fruits--search for "fruitname histology" if you're interested).
However, now that we've talked about density, we need to actually think about getting the DNA out. The extraction process is actually much more important in terms of your final yield.
Many plant seeds contain polyphenolics, which can cause DNA degradation. This protocol (Cornell U) details many of the possible shortcomings:

These compounds have also been reported to cause difficulty in DNA purification in other plant species; polysaccharides (Murray and Thompson, 1980; Fang et al., 1992); polyphenolic compounds (Katterman and Shattuck, 1983; Couch and Fritz, 1990; Howland et al. 1991; Collins and Symons, 1992); and sticky and resinous materials (Webb and Knapp, 1990).

These contaminants can degrade DNA, but also render it unusable in PCR amplification and endonuclease digestion (Kim et al. 1997, Cornell U, EPICENTRE Biotechnologies).
Overall, there are definitely species-specific differences in fruit/seed plant DNA content. Practically, however, the most important factor in DNA yield and viability for future experimentation is sample purity and contamination. Specific fruits and seeds may contain one or more of the above contaminants, so the answer to "Seeds or fruits?" definitely depends on the species of plant you're working with.


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For people who work in microbiology labs, what software do you use to manage your strains?
It's just a small microbiology lab that currently records everything on paper, and there's quite few mutants as well. Is Excel commonly used for this sort of thing? Or is there a better software to manage a lab?
Thanks for any help

check out benchling for constructs... is that the sort of software you mean?

@shigeta not exactly, although this is pretty cool. But we're just looking for something offline, to keep track of all the different strains in a fridge, and when they mutate to somehow show that the mutants are related

What I think you're looking for is normally called an LIMS (Laboratory Inventory Management System), and I've never used a good one.  Seriously, decided to spend the effort to build one in house because everything else we tried was horrible.

That's why most people who can afford it write their own LIMS systems - few labs ever do things the same to use a 'generic' LIMS.

@AtlLED Thanks, and yeah I've been looking around for the past couple days and it seems like most free LIMS are pretty terrible. And when you say you built one, did you end up designing it with SQL? Or did you use an Access database (or something like that)?

In my old lab we started with a .Net solution and then moved to an SQL/web based one. Now my lab uses a very similar modification of the SQL one. I want to add that my experience with LIMS that you pay for "semi-out-of-the-box", ie Nautilus, are also crap.

I would go for StrainControl Laboratory Manager. Works perfect and covers all needs of a lab. Do not go for all the "free" stuff since they rely on a active sponsor and your data is never safe.
StrainControl is free for 3 months and if you want to continue use it you simply purchase the Admin password and all your data is saved.


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Why don't surfactants destroy or incorporate into cell membranes?
How do surfactants remain on the surface of pneumocytes without  (1) acting as a detergent or (2) the phospholipids getting incorporated into the membranes of pneumocytes...
I'm guessing the answer has something to with the secretions of clara cells, but I'm curious for a more biophysics-y answer... for example how do the phospholipids that compose surfactant not form miceles or are the miceles simply larger that the individual component phospholipids (I'm basing this off the answer to "how do detergents get in hydrophobic membrane interior"), but even so why wouldn't the micelle simply fuse into the membrane

Found this so far, it's from "Topology and lipid selectivity of pulmonary surfactant protein SP-B in membranes:
Answers from fluorescence"--
"The presence of the hydrophobic surfactant proteins SP-B and SP-C is strictly required to facilitate an efficient transfer of phospholipids from surfactant stores (in the form of bilayers) at the aqueous hypo-phase into the interfacial film, and to maintain the film operative along the compression–expansion breathing cycles"


text:
Constitutive mutation in operator gene
If a constitutive mutation happens in the operator of an inducible operon, does that mean that repressors won't be able to bind them ? Or does it mean that even if repressors are bound, they will not have any effect on the gene ?
I am specifically talking about lac operon.

For the lac operon there are two possibilities for constitutive expression mutations:

The operator is never closed.

Reason: Mutation of the repressor, so its not present, doesn't bind or binds only with very low affinity for the operon.

The repressor can not bind.

Reason: The binding site for the repressor is mutated.
See this Website or this Website for more information.

What is the meaning of "the operator is never closed" ?

I have expanded my answer.


text:
maximum # of generations possible in a population of cannibalistic rats
Assume a sufficiently large population of rats (to allow genetic variation and facilitate inbreeding) in a place with abundant water, sunlight, shelter but no food. For how many generations can this population persist solely by cannibalizing?

Here's a back of the envelope answer: one generation if you have a LOT of rats.
Numbers according to the Great State if Indiana.
Assuming also that we start with adult breeding rats.  50% females / 50% males.
The gestation period is 21 days.
The adult rat can eat 1/3 of its body weight each day. Assuming that the rat is eating about 80% of the 'victim' rat body weight, the colony reduces in size about 40% each day.
Lets say the rats are going to be a bit hungry and the colony loses 30% of its size each day. And they don't eat their own feces, which I think they can do, but also assuming that the malnutrition from eating only rat for food will not cause problems.
Over the period of gestation, 21 days the colony will have a final size of 0.3^21 = 0.000559 times its original size.  So in order to have a surviving gestating female you'd have to start with 1791 rats.  Also assuming that the last rat is a very pregnant female who can compete with the male cannibals who are not pregnant.
Then the average litter is not 1790. So you'd need something like 1790^N rats for N generations.  and they'd have to be pretty lucky rats to boot.
BTW similar numbers would be true for any animal including human beings. This is one reason that cannibalism is usually only a social ritual, not a means of acquiring nutrition except in extreme cases.

It may be possible that only a few male survive (having cannibalized all the others) and persist by eating females, and impregnating all of them at the same time. Also they CAN eat 1/3 of their body weight each day but maybe can survive on significantly less than that, and as they grow weaker and lose body tissue they become even less active and less cannibalistic, requiring fewer calories to survive. Ultimately I guess it's a question of how efficiently the rat transforms solar energy and water into body tissue. Perhaps a mammal with lower metabolic rate can achieve cannibalistic equilibrium.

Animals are way to dependent upon plants overall and photo synthesis - the poo just keeps piling up until its all you have.  This question might demonstrate why you need some photosynthesis to maintain a stable ecosystem. http://biology.stackexchange.com/questions/7400/plants-without-bacteria-is-it-theoretically-possible/7409#7409


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How good is information transfer between the hemispheres of the brain?
I sometimes listen to lectures on my phone using ear buds, but occasionally with only one ear bud in. Is the other half of my brain losing out on any aspect of the lecture? Just how good is the corpus callosum at sharing information between the hemispheres?

Have you read experiments in which patients with corpus callosum  severed were asked to do various things ? You will then appreciate the functioning of it .

Auditory information is routed to cerebral hemispheres via the brainstem and midbrain.  Structures in the midbrain receive information from both ears and combine it (including differencing it for spatial location) before sending the combined information on to both cerebral hemispheres.  Usually only the left hemisphere interprets the sound for language content, but it is doing so based on the sounds perceived from both ears.  The corpus callosum would not be involved in the hearing pathways.  So sound coming from the left ear should work as well as sound from the other if the perception level is adequate and not interfered with by sounds from the other ear.  It is likely the sound perception is somewhat better if both ears are receiving input from the source.


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What is the name of the smallest self-replicating thing?
Some time last year, I found an article on Wikipedia about the smallest something to be able to reproduce.
I don't remember exactly what it was, but I am fairly certain that after the initial discovery another of the previous organism (this one slightly smaller) was discovered.
I think that the smallest something might have been the smallest self-replicating protein, or smallest self-replicating molecule, or something like that.
It was not mentioned in this thread: Which organism has the smallest genome length?
It had a strange, stand-out name and I believe it was discovered in the 90s.

Also see http://en.wikipedia.org/wiki/Smallest_organisms

You're probably thinking of the Spiegelman Monster. It was actually discovered in 1965, but it was discovered that it became shorter over time in 1997.
It also wasn't included in that thread, and it has a strange name.
http://en.wikipedia.org/wiki/Spiegelman_Monster

I don't understand how this fits the criterion of 'self-replicating' since it seems to require the addition of a replicase enzyme to the in vitro system.

@AlanBoyd Neither do I, but it seemed to fit (some of) the criteria, and I thought it was worth a shot. Apparently it was correct!

A research team (Lee et al.) has discovered what maybe the smallest known self replicating RNA molecule - actually a 32-unit-long "a-helical peptide" whatever that is. It is based on the yeast transcription factor GCN4. The 32 peptide sequence is so small, that one could describe it in text form simply as:
ArCONH--RMKQLEEKVYELLSKVA-CLEYEVARLKKLVGE--CONH2
ArCONH--RMKQLEEKVYELLSKVA-COSBn
H2N--CLEYEVARLKKLVGE--CONH2

Two of those lines are likely to be pre-cursor molecules required (the food), and one is likely to be the RNA sequence, I think the final line.
This is a lot smaller than the smallest known or simplest genome, which could be Carsonella ruddii, which lives off sap-feeding insects, has taken the record for smallest genome with just 159,662 'letters' (or base pairs) of DNA and 182 protein-coding genes.
Source: https://www.nature.com/news/2006/061009/full/news061009-10.html
Also, it's likely you should checkout this study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4187685/ "Systems Biology Perspectives on Minimal and Simpler Cells
"

The first part of this answer is complete nonsense. It talks about RNA and shows a peptide sequence, refers to a precursor as food, and quotes something called the journal of creation.

Although this answer cites "creation.com" as the source and (as David says) includes some obvious gibberish, the actual source is a 1996 Nature paper A self-replicating peptide. It is, obviously, about a peptide rather than RNA. It is not particularly responsive to the question, but may still have some relevance.

Fair call, I was too excited to quote that sequence, which I like a lot. It was good to learn about Spiegelman Monster, I should have taken a squiz at that: I'd agree the dwarf genome with only 218 bases AFAIK would be likely correct, because it is a organism whereas mine is just..... a "thing". Half correct. The question is wrong! :)


text:
Does a phenotype include the presence of a recessive gene
I am trying to understand what exactly a phenotype is to try and understand a genetics database. (Ie I don't really know very much about genetics at all)
I've been reading through wikipedia on what a phenotype is and from what I can gather it is an observable trait which may be impacted by a specific gene.
What I would like to know is if you were looking for the presence of a phenotype such as red hair, would characteristics like not red hair and carrier of red hair also be phenotypes?
For example the following table is named Phenotype,
+------+------------------+
| Code |   Description    |
+------+------------------+
| RR   | Red Hair         | this makes sense with my understanding of phenotype
| RN   | Red Hair Carrier | this doesnt
| NR   | Red Hair Carrier | this doesnt
| NN   | No Red Hair      | this doesnt
+------+------------------+

The whole code column looks like it represents a gene not a phenotype

I agree with one of Alan's comments when he says:
"I think this comes down to whether you include being a carrier of a genetic "condition" a part of your phenotype. It's almost a question of semantics"
To expand on this, I would say there are two major definitions of phenotype, and both are employed by geneticists depending on the context.  Definition one is a bit more naive, and I tend to use it when teaching or trying to explain phenotype to a layman: anything you can observe is a phenotype.  Under this definition, having red hair is a phenotype, not having red hair (or, more directly, having black, brown, blonde, etc. hair) is a phenotype, but carrying the recessive gene for red hair is not a phenotype.  I can observe without checking your genome that you do or don't have red hair, I cannot tell without checking your genome that you have one copy of the recessive gene for red hair.
Definition two is more complete, and I tend to use it more in a lab research setting: anything that is the OUTCOME of a genotype can be defined as a phenotype.  Again, red hair and not red hair (meaning brown, black, blonde, etc) are outcomes defined by the genotype.  However, depending on the context (let's say I'm interested in understanding heritable potential and not the color of hair) I'd say that the phenotypes would be 1) the ability to pass on red hair to progeny (outcomes of genotypes RR, RN, RN in your example), and 2) lack of ability to pass on red hair to progeny (outcome of genotype NN in your example).  In both cases, the phenotype is the outcome of the underlying genes, I just have to make sure I frame my scientific context appropriately.

I think you are correct, "phenotype" really should be what you observe, or measure in the organism, and genotype is what the underlying genetics is, either inferred, or experimentally determined.
Keep in mind, Mendelian genetics makes for great homework exercises, but there are a million more phenotypes that don't fit the Mendelian paradigm than there are ones that do.  Hair color is a phenotype, but it has a lot more genetic components than the simple "one gene, two alleles, one completely dominant over the other" model that Mendel found applied to his 7 phenotypes.

Thanks that's what I though, obviously the data is a little different to what's above but it demonstrates the point.

You say it yourself: The phenotype is the observable trait. So this means if you have red hairs, your hair phenotype is red. The most likely reason for it, the mutation of the melanocortin-1-receptor, is the underlying genotype.
Or: The phenotype of mouse coat color is black, white, brown, speckled, whatever. That what you see, the reasons for that can be (and are) completely different between different mouse strains.
The first column of the table is the genotype and showing that red hair is a recessive trait (without naming a gene, but this doesn't matter), the second only is a representation of the first and makes actually no statement about the actual phenotype.

Thanks that half answers what i was after, im really interested in the counter case, what shouldn't be a phenotype. I have a table in a database called phenotype which has things like carrier of red hair and no red hair these dont really match what i have read and understand a phenotype to be but its really hard to tell as ive only just read some wikipedia articles. are these phenotypes?

I am not sure, if I understand your problem: You are thinking about comparing red hair carrier to not red hair? Simply speaking: Hair color is a phenotype, as is skin color (or the color of your eyes). The reason for it (the genes underlying and causing your hair, eyes, skin to have the color it has) is the genotype. Can you show this table?

i added the table into the question, does this make a bit more sense?

I think this comes down to whether you include being a carrier of a genetic "condition" a part of your phenotype. It's almost a question of semantics.

I depends on the definition. I learned a quite strict one (actually what you see), so this doesn't fall under phenotype.

The table in your question is a derivative of a punnett square, which shows how different dominant Vs recessive alleles go on to inform phenotype in a logical way; In this case R is dominant red and r is recessive red.
RR = red : rr = not red :  rR / Rr = carrier of red. Red is the phenotype expression (for red hair).
A carrier can pass on either the (R)ed or the (r)ed during meiosis, whereas a totally dominant (R) or totally recessive (r) will pass on just one type, to be combined with the other contributing parent chromosomes during meiosis 1.
I hope this helps.

Hmmmm... no, that is not what a Punnet square does. A Punnet square gives you the expected outcome of a specific crossing. In any case the table in the question has nothing to do with it, aside from having some genotypes written in it...


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Are there baby drinks closer to breast-milk?
Many women cannot or will not feed their children with breast-milk. It is my understanding breast-milk has many advantages over formula. Some psychological like oxytocin and some physiological like advanced antibodies. Have there been any attempts to create a formula with better psychological and physiological properties? Is it even possible to include antibodies in formula or milk?

How can artificial milk induce psychological response ?

@biogirllajja adding oxytocin or something simular

The psychological effect is two-way - Both Mother and Child are involved. Any formula would affect only child.

It is definitely possible to include antibodies and other biological molecules in formula to better approximate that of its mother's milk.  However, there's no way you could mass-produce this. Every mother has unique antibodies, even horomones that are the same in different people are present at different concentrations. The current "formula" on the market is good for as many people as possible.
Isolating antibodies from a mother to include in formula milk would be insanely, insanely expensive. Think thousands of dollars for a carton of formula. Not to mention the hassle of frequent blood and serum draws from the mother for antibody isolation.
So, yes, this is possible (and I wouldn't be surprised if someone with a lot of money to burn has tried it). It's not remotely cost-effective or feasible, though.


text:
Is it possible to create an experiment in house conditions to prove the existence of germs?
I realise that the best way to prove the existence of germs or single-celled organisms is by looking at them through a microscope.
But I don't have a microscope at my home, how can I design an experiment in a normal house environment to show the existence of germs (or other single-celled organisms) without spending too much money?
By "house environment" I mean that I have access to normal stores and the internet. If it's something that can be bought in a "normal" store or on-line without getting me into trouble, and doesn't cost a lot then I can have access to it. I don't have access to lab grade equipment or conditions, so no sterile rooms or special growth environment.

I thought about the following experiment, inspired by the mythbusters pyramid power episode. In the episode they cut an apple in half and put one half under a pyramid and the other not under a pyramid. In the first attempt one of the halfs rotted quicker than the other, they concluded that it happened because the saw they used to cut the apples wasn't sterile.
So I thought about taking 3 apples, contaminating a knife (by rubbing human saliva on it). Cutting one apple with the contaminated knife, one apple with a sterile knife (using rubbing alcohol to sterilize it) and one apple by a knife that has 1 contaminated side and one sterile, which is a contaminated knife, that had only 1 side sterilized with rubbing alcohol. Then leaving the 6 halves in separated sealed containers (some tupperware) for a few days and then looking examining the rott. The expected result is that the "contaminated apple" will have a lot of rot on both halves, the "sterile" apple will have no (or close to no) rot, and the half and half apple will have one rotten side and one not rotten side, and the sides will coincide to the contaminated/sterile sides of the knife touching them.
Will this experiment work?

Do you have access to growth media (agar plates)?

I have access to normal stores and the internet. If it's something that can be bought in a "normal" store or on-line without getting me to trouble, then I have access to it.

Is proving existence of fungi relevant ? If so, you could wet a bread with water and keep it in a hot and humid place. You will see moulds growing after 2-3 days.

@biogirllajja, what is the control group? how do I prove that those are microorganism and not just a property of the bread?

@IlyaMelamed You could keep the bread in a refrigerator where the fungi will not grow.

We can see the moulds growing with naked eyes but you could see them better with a good magnifying glass.

@biogirllajja, what you describe is an experiment on best environment for fungi growth, what I'm looking for is to take 2 (or more) exact environments and show that by introducing bacteria to one of them I create a difference. A wet and hot bread is not the same environment as a refrigerated bread.

@IlyaMelamed I think keeping a bread dry and another wet but keeping them in the same environment should also work. (Not sure though)

You might be interested in the BBC documentary "Afterlife: The Strange Science of Decay", which can be found on youtube. In the experiment, a full apartment + garden enclosed in glass was left to decay. Very interesting to watch, and might give you some ideas for possible home experiments.

You could use Jell-O for growing bacteria if you don't have access to agar ! (I have never tried this but I think it should be possible because the gelatin in Jell-O is like agar.)
You should first sterilize a small knife on a gas stove or with alcohol and then gently rub it on any surface (where you think bacteria are likely to be found ) and then rub it on Jell-O taken in a dish. You should then place it in an environment similar to the one from where you isolated the bacteria. After one or 2 days the bacteria should grow.
For control : You could simply put a plate of Jell-O in the same place but without inoculation of bacteria.
Disclaimer : I am not a microbiologist and I am not sure this would work but you could give it a try as it will not be really expensive :)

Agar is easily available online (~5 euros for 100 g on eBay). For how to make the plates, and a sample experiment see here

I see no reason to restrict yourself to jello or buy agar (its not expensive tho).
Every piece of rotting leftover in the fridge pretty much proves that bacteria and fungi exist....
You can always sterilize any food by boiling it (like jello).   A pressure cooker is better than just boiling it. You will have to boil the dishes you are using too.
Then expose one dish  to something that contains germs and compare it to a sealed sterile container of the food.   Breathe on it or put your finger in it - that should be enough.
Seal the exposed container up good after exposure tho - it can get messy!
Fruit and even coffee will grow the junk you want pretty quick.  Leave it at room temperature for faster results.

Good point. We always tend to think to complicated. The above example with the bread works as well....


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Removing a restriction site and introducing other at its place

What would you do if you want to remove an EcoRI restriction site
  and introduce BamHI restriction site at apprx. the same location ?

One of the answers in my textbook was : To construct a DNA fragment with the structure:
5'AATTGGATCC3'
    3'CCTAGGTTAA5'

I understand that this would ligate efficiently to the sticky ends generated by EcoRI cleavage and would introduce a BamHI site but I don't understand how this will remove/not regenerate the EcoRI site.

The recognition site for EcoRI is GAATTC, and the enzyme cuts after the first base. See this picture from NEB:

The overhang is: AATT, which is supplied by your oligo and fits into the overhang. If the next nucleotide whould be a C than the site would be recreated, since its a G its not. The new sequence of the old EcoRI site is GGATTG which is not recognized by EcoRI.
One technical note: To avoid religation of the digested DNA which carries this site, I would treat it with alkaline phosphatase to remove the phosphate end at the 5' end of the DNA.

I am still not able to understand how it destroys the EcoRI site. Sorry for being so slow !

Look at the sequences: EcoRI needs GAATTC to recognize and cut DNA. After the ligation with your BamHI oligo the sequence of the site is GAATTG so it cannot recognize the site anymore.

I get it now. I also understood why I couldn't figure it out at first - because I thought the RE just cares about G and A not any further sequence but now I understand that the whole sequence is important. THANKS A TON !

Just in case you are having difficulty visualising what happens in the answer from @Chris, here are the steps with the linker shown in lower case
...NNNNNGAATTCNNNNN...           ds DNA
...NNNNNCTTAAGNNNNN...

          |
          V

...NNNNG          AATTCNNNNN...  after EcoRI digestion
...NNNNCTTAA          GNNNNN...

          |
          V

...NNNNG      aattggatcc        AATTCNNNNN...   incoming linker
...NNNNCTTAA      cctaggttaa        GNNNNN...

          |
          V

...NNNNGaattggatccAATTCNNNNN...    after ligation
...NNNNCTTAAcctaggttaaGNNNNN...

The left hand "EcoRI" is now GAATTG and the right hand "EcoRI" is CAATTC.

I was wrong reading the sequence. Removed that part.


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Can pheromones in perfume be formulated to cause agitation?
I generally don't care for female perfume. I have very sensitive olfactory receptors and in general, I just find perfume overwhelming.
A couple weeks ago, my wife of almost 14 years and I were shopping. As has happened many times before, she asked me to smell a perfume (Play it Rock by Playboy) to see if I liked it. Shockingly, on first whiff, though still overwhelming, I quite liked it. So she bought it.
Now, when she wears it, I do find the aroma pleasing, however I find myself getting quite agitated, depressed and even overcome with jealousy and paranoia.
Obviously, there are lots of psychological factors in play :

Perfume's primary purpose is to arouse and attract men
She almost only uses it when there are going to be other men around
It is playboy, subtly indicating the promotion of promiscuity

However my internal reactions are so intense I can't help but conclude there something more physiological triggering/intensifying them.

Could the perfume's pheromones be slightly misformulated to cause
this reaction?
Would the same pheromones that arouse a man also inherently trigger the fear of the arousal of others?
Is it possible that my pheromone "sense" is also heightened like my sense of smell, causing an abnormal reaction specifically in me?

Note : I can't find official documentation that the playboy perfumes apply pheromonology (Yes, I did just make up that word), but I have found them listed by other sources in sections of perfumes that do, but Playboy perfumes seem to be priced drastically less than the rest of the pheromoned perfumes.

You are really getting at psychology here as opposed to the biological question(s). As written, it's really too general. There is no way to answer a question about your specifically or anyone else.

@kmm - This question presents a scenario in which the sample group (me) is far too specialized to draw a conclusion. Thus, presenting some, specifically physiological (biological), hypotheses is seeking response from the biology community. You state that this is getting at psychology, which is true, however it's specifically the biological causes of psychological response.  I'd also like to note that ALL psychology boils down to biology.

The point is that your question is too broad as written, about your specific experiences rather than general phenomena. If you have a specific biological question about pheromones and behavior, then feel free to edit your question.

Insects generate and respond to pheromones. But despite what sci-fi TV might have told you, there is no evidence that humans make or respond to pheromones like that.  Humans don't have that good sense of smell, for one thing.
The fact that you know it's a Playboy brand of perfume is affecting you?  That's obviously not chemical, is psychological.
Also, historically, perfume was used just as much to mask unpleasant odors as it was to attract anyone.  When men go through puberty, their sweat changes odor.  That's not to attract other men.
If this perfume is affecting you emotionally it's psychological, not chemical.

Thank you! Your response shows notable intellect though you may have skimmed through my question a bit too hastily.
First, I was specifically highlighting the purely psychological components to consider. However, the experienced result seemed to outweigh the sum of their potential.
Second, perfume's primary purpose WAS for masking odor. I'd submit that WAS to prevent repulsion, thus attract. It's current iteration is simply more direct.
Finally, by simplest definition pheromones are chemicals released that affect an animal's own species. This definition leaves little room for human exemption.


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Could a normative population ever be non-heterosexual?
In the modern documentary called "Bi the way", one American geneticist said that if modern American youngsters may as well be functionally bisexual, then some generations ahead Americans could be possibly born with a strong inclination towards the bisexual lifestyle. If we let aside the futuristic theory according which bisexuality should become an evolutionary norm concerning the human species in the long run, then is there a strong bio-sociological possibility that modern societies could transform normally to sexually fluid homogeneous spaces?
So the problem is if humans will naturally evolve to a species which is homogeneous in terms of dynamic bisexual differentiation, while in the meantime producing stable behavioral norms.
Then it has to be decided if society will integrate this procedure naturally or through competition.

I doubt it's a biological question in this formulation. And I personally have no idea, what "normative population", "functionally bisexual", "evolutionary norm by necessity", "bio-sociological possibility" or "sexually fluid homogeneous spaces" mean.

@mad-scientist - I accept that Valintine Wiggin's wording was a bit incoherent, particularly the infusion of terms which I'm pretty sure were coined on the fly. However, I think the academic scenario and theoretical implications were quite clear.  Hence why I took the time to reply!

Evolution does not think. It does not have a goal or aim in that sense. It just is, because some individuals within a population manage to reproduce. What it comes to bisexualism, who says that it is a new phenomena among American teenagers? An American geneticist. There are indications of bisexualism in the history from the Ancient Greek and beyond. Maybe bisexual individuals have a higher fitness? Men/women are attracted to individuals who show an interest to their own sex and these individuals get to reproduce. In that case bisexual life-style would likely remain in the population.

First, your question makes a few assumptions. We can totally run with those assumptions, but I thought two needed to be noted:

There is a genetic predisposition to bisexuality.
This genetic predisposition does not already dominate the population. (Perhaps suppressed by social pressure)

A genetic predisposition in a small minority, in order to infiltrate and achieve dominance, would need to either:

Directly possess advantages over the absence of said predisposition
Be "luckily" carried by hosts which maintain some other advantage in order to infiltrate the population.

Off the top of my head, some direct advantages of bisexuality could be:

Arousal of opposite gender with homo/bisexual acts or displays
Maintenance of psychological and physical fitness during short term gender imbalance
Self advancement socially regardless of audience's gender
Frequent physical activity (exercise) in a sedentary culture.

I'm sure the list could go on. Specifically with this sample of potential advantages, a cultural stigma would likely both :

Suppress the fulfillment of this predisposition, thus leaving it unhindered in their offspring
Produce reproductive hostility toward those who exhibit signs of this predisposition

Lifting such stigma, and assuming the advantages somehow outweighed the innumerable disadvantages, I would conclude "yes", it is possible for a society to be birthed where sexual exclusion by gender was not even considered.  That is, there would be no such thing as "sexual orientation" in the populace's mind share.

"one American geneticist"?  You realize that that's how you would describe a crackpot, right?  It's not clear to me at all the American youth are "functionally" bisexual.  For one thing, I don't think American high school culture is all that encouraging of boys experimenting with each other, though I can easily imagine straight girls being under pressure to titillate the boys in their group with lesbian displays.


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Determining a patients biological age?
I am looking for an algorithm that shows the exact coefficients some variables that have on a hospital patient's chronological age versus their biological age.
I understand a lot of the variables that go into determining ones biological age (i.e. Blood pressure, diet, family history of disease, obesity etc.) but not the amount of impact that it has on the actual scoring of their age.
I have found many sites that will calculate it, however I need the actual variable coefficients and influence in order to produce a proper score for thousands of patient records.
Thanks in advance for your input!

How is a "biological age" defined? It doesn't sound like it would have a precise definition, but maybe I am ignorant.

Biological age is considered one's "real" age based on how their body is behaving versus someones actual age.

So for example. A 65 year old who still works out, and eats healthy and is of normal weight has a biological age of 55.

There is no rigorous standard for "biological age".  It makes no sense.  A fit 65 year old might have a heart that, in some tests, performs as well as the "average" 55 year old, but that's just one organ, and one set of tests.

As the definition of biological age is very ambiguous, I propose that to generate an algorithm, you first need to create a quantifiable definition. I submit:

Biological age is a measure indicating what portion of one's calculated life expectancy is already expended, adjusted proportionately for the average life expectancy of their major demographic.

Wow, that's a mouthful! So, let's break it down.
Life expectancy is calculated :

Ascertain a person's major demographic (Geographic residence, Race, Gender and Generation).
Find the average life span of that demographic.

This is negligibly speculative as a living person's Generation has not yet fully perished
Statistical outliers, such as infant mortality, are generally excluded from this calculation

Adjust for known major factors that have accepted statistical impact.eg:

Lifestyle
Current medical conditions
medical history

Average Life expectancy of subject's demographic was calculated in #2 above.

So, now let's throw in some sample numbers.
Statistical Facts: (totally made up)

Caucasian males living in the France, born in the 1970s have an average life span of 72 years.
Exercising 30 minutes or more daily increases life expectancy 6 years
Smoking decreases life expectancy 7 years
Not smoking increases life expectancy 2 yearsHold on a second?! Wouldn't not smoking already be accounted for in the "Smoking..." section? Well, no, because our demographic sample are all "unknown" so having specific knowledge would statistically change the results in either direction
Heart Disease decreases life expectancy 8 years
Devout religious affiliation increases life expectancy 6 years.
Family history of diabetes decreases life expectancy 2 years.

Two subjects both Caucasian, french males born in 1974 (40 years old chronologically):Their mom's actually shared a labor and delivery room!

Beavis - known: Smoker with heart disease.
Butthead - known: Devout Buddhist, very athletic, non smoker with a family history of diabetes
Beavis' life expectancy is 57 (72-7-8)Butthead's life expectancy is 84 (72+6+2+6-2)
Beavis has expended 70.2% (40/57) of his life expectancyButthead has expended 47.6% (40/84) of his life expectancy
Despite sharing a birthday:Bevis' biological age is 50.5 years (.702*72)Butthead's biological age is 34.3 years (.476*72)

Note: It's almost 6 hours past my bedtime, so please excuse any stupid mistakes or miscalculations.  The general concepts are what is important

From the way you phrased your question, it sounds like you are doing this programmatically.  As that was not explicitly stated I reserved this suggestion for the comments:  I would recommend storing the statistical factors with both true and false adjustment values (like we did smoking above) as, inherently, any factor's inverse will also have an impact. Then when a factor is unknown you just don't apply any adjustment. Also, in the unlikely event where a factor's inverse is negligible or unknown you can just store an adjustment value of zero.

The problem with calculations like this is that the time-spans (smoking lets you die 7 years earlier) are based on population wide statistics. They include healthy, 95 year old smokers, which smoke 2 packs a day as well as 35 year old smoking lung cancer patients. What you can derive from this are general recommendations, but hardly specific calculations, as they have to include a lot of personal factors which are unknown.

@Chris Agreed wholeheartedly. This flaw is inherent in statistics universally and is why we use non-precise titles like "life expectation". Additionally, using the following statement highlights the accepted variability:
"Adjust for known, major factors that have accepted statistical impact."  There are literally infinite variables in play, some may have nanoseconds in actual lifespan impact some could eliminate a teenage athlete mid stride. An infinitesimal fraction of these variables are known, a smaller fraction are studied and the minority of those have an accepted statistical impact.

Thank you for your input @trex005, I have taken your factors and took a adapted approach with my data variables and took some additional factors from the cdc life tables as well as Moran E. Levine from his article: Modeling the Rate of Senescence: "Can Estimated Biological Age Predict Mortality More Accurately Than Chronological Age?" and from L. Galzigna and M. Cecchettin their article "a simple procedure for calculating biological age."


text:
Botany related question: liverwort sporophyte
Is perianth part of the sporophyte or gametophyte in liverworts (Marchantiophyta)?

I think it should be a part of the gametophyte because it is formed from the fusion of leaves (which are haploid) and protects the archegonium and the developing capsule.
It also can be logically thought out. Since it develops before the sporophyte forms , it should be part of the gametophyte.

Here it is stated explicitly.


text:
Classification of glycosidic anomeric bonds (alpha vs. beta)
In the process of studying for my upcoming biochemistry exam, I have stumbled over the classification of glycosidic bonds. I want to be able to distinguish $\alpha$- from $\beta$-glycosidic bonds. Unfortunately, even after reading through this page, I don't really understand how to go about classifying the bonds in e.g. an oligosaccharide.

(Source)
Now, I am inclined to say that both of these anomeric linkages are of type $\alpha$, because the O-glycosidic bond is axial to the respective sugar rings. Is that a correct way of reasoning?

Here's my interpretation, as far as I can get, which agrees with your deduction that both of the O-glycosidic bonds involve α epimers. (If the epimeric carbon has an -OH in the axial direction then this is the α anomer.)
Do you have the name of this compound?
Let's hope that a real glycobiologist comes along.
Supplementary
I'm now not sure that it is even possible to assign an anomeric state to the sugar marked as ?. There is no indication in the diagram of the presence of a -CH2OH substituent on the ring - it appears to have a methyl group instead. If that group was a -CH2OH then the putative anomeric C would indeed be in the α form since it is pointing in the opposite direction from the "-CH2OH" (c.f. the two galactose residues). If ? is a deoxy- derivative of a sugar then it may be that the convention still holds.

Unfortunately, I don't have a name for the compound, I just grabbed an image from the internet that looked roughly like the exam problem I was trying to solve.


text:
Pharmacodynamics of Ethinyl estradiol + Drospirenone and interactions with istotertinoin
Does pharmacodynamics of Ethinyl estradiol + Drospirenone in OCP pills like (Yaz, Yasminelle etc.) while using isotretinoin (Axotret, Roaccutane etc.) is changed? Does isotretinoin weakens the OCP pill by any means in any situation?
I know about interaction towards incrase of lipids. The only info I have found is this: https://www.ncbi.nlm.nih.gov/pubmed/15116059 and results could be translated: we discovered nothing.

I'll give it another look tonight, thanks for editing the advice portion out of the picture

@jonsca Thank you very much. I will be waiting for your reply.


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What's the recommended maximum passage number for mammalian cells (NCI-H441)?
Is there a generally accepted maximum number of times you should split and reseed mammalian culture cells before restarting cultures from new stock?

I only know the maxime to keep the passage number as low as possible. Especially in immortalized cell lines funny things can happen, we once found a cell line in the lab (I think it was 293T) that was hexaploid for some chromosomes...So split cell lines in early passage numbers and make stocks. The problem you have with cells from other labs is that you often don't know how long the line has been in culture...

Yeah, unfortunately this was the first time I had done any mammalian tissue culturing, by the time I had grown enough to make a sufficiently large stock of frozen cells, I had already hit passage number 6. I was thinking I would draw from frozen stock each time my current line hits passage number 10. Does that seem reasonable or should I buy new cells? We sourced our current cells directly from the American Type Culture Collection.

How long does it take to do six passages?

About 9 weeks. :/ I made a lot of dumb errors at the start.

If your cells come from ATCC they shouldn't be in culture for ages, since they are one of the good cell banks. I would still use this cell stocks and I would also test, how long you can keep them in culture without noticing changes in behavious and/or shape. What does ATCC recommend here?

This is a very good question and it highlights a very frequent misconception about cell culture and it is using the passage numbers as an indication of how well a cell is behaving. Although this can be a good barometer but it is misleading. Passaging can stress the cells if performed very frequently, although again that depends on how fast the cells are dividing.
You should not think of passage (and cell culture in general) in terms of the procedure itself but in terms of population doubling (PD) which can be calculated using the formula provided here (http://www.sciencellonline.com/site/techsupport.php). I personally use [Log10(harvesting cell No/seeding cell No)/Log10(2)]. This should allow you to characterise your cellular behaviour between every passage and allows you to draw a cumulative PD graph. Once the cumulative PD versus time becomes non-linear, then you would know that the cells have changed behaviour and it might be best to use a fresh stock.
The main advantage of this method is that you are not relying on guess work and deal with solid numbers and allows you to predict when you should expect to start a fresh batch for passage. Although passage numbers can do the same job if you assume per passage, the cells have done a certain PD but this is more of a guess work and you can not track how well your cells are doing at a given time point. For example one of the main problems with using a passage as a measure is that you can passage the cells at 98% confluence to a fresh flask and although that counts as a passage but it is pretty uninformative in terms of cell behaviour and gives you no solid numbers and you can do this many many times and although you would have done high number of passages but your cells would appear ok. Although such an exercise is pointless and will probably stress the cells but it is just to make the point that passage numbers are not necessarily a very informative and quantifiable measure of how well the cells are doing or behaving hence PD and cumulative PD should be used. Another advantage is that since you are dealing with actual cell numbers, if you changed your cell culture flask size from lets say T-75 to T-25, you don't have to be worried about changes to your frequency of passage or having to make further guess work on how that has effected your cell behaviour.
My main advice is that you should keep you frequency of passage the same at least in the beginning (although keep an eye on the cell density as you don't perhaps want to let cells to be too over-confluent or unconfluent when passaging, depending on your specific methodology and what has been established in your lab), but count your seeding and harvesting density (cell No) and calculate the PD and cumulative PD and draw a cumulative PD vs time graph and monitor the behaviour of cells. This should give you a good indication of you cellular behaviour under the conditions you are working with them since guidelines are just that, guides and they can never substitute experimental characterisation of your cells under your conditions and handling method!


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Why are dolphins so smart?
It seems that dolphins have (among?) the highest encephalization quotients found outside of humans, higher even than chimpanzees. By the "use it or lose it" principle this indicates that intelligence must be particularly valuable in their niche. Why is that? They are predatory and social, and both of those are associated with intelligence, but why are dolphins smarter than other predatory pack animals? For example, is there something about being an air-breathing organism living in water that makes having a high EQ particularly adaptive?

I would also like to point out that they are intelligent in the way we perceive "intelligent". It would be interesting to know what help, if any, they get by having " human type - intelligency"

Aren't bacteria and viruses just as intelligent as any master criminal ? Changing their appearance so often that they do not get caught !

It's less about the brain size, I think, more about the metabolic cost of brains. Brains are among the most costly organs to keep what it comes to oxygen demand. Air-breathing increases available oxygen for the body, hence mammals have larger brains that for example fish.
In diving animals the metabolic cost of brains is connected to the diving time (can't find the reference at the moment). Sperm whales shut down parts of their brains on long dives and do not have particularly active brains in general. Dolphins are mostly shallow diving animals. Maybe the selection favors higher brain metabolism potentially increasing the ability to catch prey and avoid predators? Pure speculation, though.

It might not fully answer your question…
Cost of having a heavy brain
Generally speaking, having a heavy organ is an important cost for flying animals, a medium cost for terrestrial animals and a low cost for marine animals. Loosely speaking, the principle "use it or lose it" does not apply with the same strength in all animals in regards to brain weight. If you create a regression between "intelligence" and "need of being intelligent"(supposing it means something!) in terrestrial mammals and add the dolphin on your graph, you might be surprised that the dolphin does not fit on the regression but it might only be due to the fact that they live in water which is much more dense than air so that it is less costly to carry a big brain. So, yes there might have something to do with "living in the water".
Indexes of intelligence
EQ does not mean intelligence! It is just an index. And we have to understand that people first were happy to think that humans are very smart because they have a big brain but they were terribly confused when they've learned that sperm whales brain weight 8kg! So they tried finding other indexes. EQ is one of them and we're quite happy to use it because it places humans at the first position. But it does not mean that this index is a good representation of intelligence. Some small birds with their tiny brain were shown to be have a spatial memory that is much more efficient that the one of humans for example.
Something else. When looking at these indexes one should not forget that size (or weight) does not equals efficiency. Let's make an analogy with computers. You can have a good software or a good hardware. Big brains are not necessarily very efficient!

Now, it is still true that dolphins are good at performing many tasks that we link to the concept of intelligence. Dolphins have complex social organization that is probably link with their intelligence. I would tend to think (just a guess) that there are many social factors involved into the evolution of their cognitive abilities. Because the social structure changes as cognitive abilities evolves, it seems to me quite hard to know what factors made that clever individuals were more fit than stupid ones at every moment during the evolution of dolphins. But I might overlook the complexity of the problem. And I honestly never learned any article concerning the role or the evolution of cognitive abilities in dolphins.