text:
Why are turtles classified as reptiles and not amphibians?
I understand that turtles are reptiles because like all reptiles, they have scales on their body. But turtles (specifically sea turtles) live on both land and water, very much like amphibians. Also, don't sea turtles have more of a moist skin unlike reptiles? So is there any anatomical difference which makes turtles different from amphibians?

Once upon a time, taxonomists argued endlessly about things like this. These days, classification is done by sequence, which takes precedence over anatomy or behavior.

1 sea turtles have scaly skin 2 amphibians were defined by having to lay eggs in water, which sea turtles most definitely do not. Classifications have changed since then but even using early definitions it doesn't work.

Amphibians are not defined for having a moist skin, neither are reptiles defined for having scales on their body.
In biology, organisms (elements) are grouped according to their evolutive history in monophyletic groups, also known as clades. Basicaly, a monophyletic group is

A group consisting of an ancestral and all its descendants.

"Tetrapoda" is a monophyletic group, formed by vertebrates with four limbs. Inside Tetrapoda, there are two groups: "Amphibia" and "Amniota". Amphibians are non-amniotes tetrapods, and we have some doubt if they are a monophyletic group. Amniotes, on the other hand, are tetrapods having an amniotic egg, including you and me, and they form a monophyletic group.
The amniotes are divided in two monophyletic group: "Mammals", which are amniotes with a synapsid skull, and "Reptiles", which are amniotes with diapsid skulls (I'm using "reptiles" as synonym of Sauropsida).
Reptiles include turtles, lizards, snakes, alligators and dinosaurs (which include the birds: all birds are dinosaurs). It doesn't matter if a animal has or has not scales, or if it lays eggs or if it is viviparous, or if it has 5 fingers or 3 fingers: All the descendants of a given ancestor are included in the monophyletic group that contains that ancestor.
Turtles, despite being strange or somehow different, are descendants from the same most recent commom ancestor of Reptilia... that's why turtles are reptiles (and that's why birds are reptiles as well).
To make this more clear, have a look at this cladogram (from Hickman, Integrated Principles of Zoology):

The apomorphy that defines the tetrapods is "paired limbs". You have Amphibia to the left and Amniota to the right, whose apomorphy is " egg with extraembrionic membranes". Inside them, you have Reptilia, whose apomorphies are "skull with upper and lower fenestra and beta-keratin in epidermis". Turtles came from an ancestor with these characteristics. So, turtles belong to the monophyletic group of "Reptiles".
Post scriptum: You wrote that "turtles (specifically sea turtles) live on both land and water, very much like amphibians". Just a curiosity: the reason why sea turtles leave the water (sea) from time to time shows exactly that they are not amphibians! Amphibians, being non-amniotes, have eggs that survive under water (actually, with few exceptions, they need to be under water). Turtles, on the other hand, are amniotes, and the amniotic egg cannot be laid under water. That's why the turtles have to leave the water to lay eggs: because, contrary to the amphibians, they cannot lay eggs under water.

Wait, mammals are classified by their skulls?  I had always heard that they were classified by mammary glands, the anatomical feature that is the root of the word mammal...

@MasonWheeler The diagram mentions both, which is still unclear.

@MasonWheeler Although compare "vertebrata" - where "having a spine" isn't actually sufficient (assuming "axial skeleton" means "some kind of spine")

The reptiles, as usually defined, are not a monophyletic group and the distinction between amphibians and reptiles pre-dates modern cladistic forms of classification.

What I wrote is that "Mammals are amniotes with a synapsid skull", which is correct. They are not the only amniotes with synapsid skull, but the only extant group with that characteristic. Regarding the apomorphies that define "Mammalia", the presence of mammary glands are not the only one, but simply the one that gives the name of the clade. There are a lot: 1. One single dentary, 2. three bones in middle ear, 3. diphyodontism, 4. sweat glands, 5. mammary glands, 6. rbc without nucleous, 7. hair, among others. Btw, mammals that have lost any of these characteristics are still mammals.

Given the level at which this question is asked, I think this answer would be much more helpful if you defined the technical terms. At the very least, "amniotic", "synapsid", "diapsid" and "apomorphy" are unlikely to be familiar to somebody at the level of the asker, and there are lots of terms in the quote marks in the last paragraph that are also highly specialized.

@DavidRicherby given that 1) the terms are correct  - - 2) there's google - - 3) this is a technical site. - - - - - -  I think OP and the casual biology enthusiast can overcome this little jargon hurdle.

@Mindwin Fine. There is, after all, nothing quite so welcoming as "Go get a dictionary if you want to talk to me."

Assuming that the diagram is not your original creation, please cite a source and note its usage terms.

Wait just a minute. You say "Turtles came from an ancestor with these characteristics" but present no proof for this. Isn't it really the case that a turtle's apomorphy is "skull with upper and lower fenestra and beta-keratin in epidermis", and this is why it is considered a reptile? The belief that turtles came from ancestors with this trait is because turtles have this trait, right? Why state a derivational statement for which you provide no proof, instead of stating an objective statement for which you do?

@DavidRicherby I'm not telling OP to get a dictionary. I am telling that in a technical circle it is fine to use technical terms. It is assumed that the enthusiast will not be bothered to learn the jargon.

Perhaps you would want to clarify that both "reptiles" and "amphibians" are kind of an obsolete classification. These classifications were done when there was not much data. Moreover, reptilia is paraphyletic because it does not include birds.

The currently accepted answer contains an error. Reptiles are not a monophyletic group. Of the related species from which one evolved into all the mammals we know today, several others evolved into still extant reptile lineages.

@Mindwin The jargon doesn't bother me. And the answer's pretty clear, but of course I had to make a bit of an effort to understand specific terms.

@Imi was it worth? that "bit of effort"? Did your horizons expanded? I also had first contact with some terms in this Q&A.

I'm going to answer this (hoping  it's not a rhetorical question) -- I've got a reply up here which emphasises on the phylogenetic and ancestral relationship, and this is exactly what I did not know and wanted to. So everything right from that effort to googling the professional jargon becomes worth the time.

Wait.. Birds are reptiles?

@GerardoFurtado So, hypothetically: Say there were another species identical to humans in every way; except they just happened to only ever develop 2 bones in the middle ear, as opposed to 3.. Would they be considered something other than mammals?

@tjt263 it depends on the ancestor. If that specie's ancestor is a mammal, it doesn't matter if it has two or twenty bones, they are mammals. In that case, its particular feature (2 bones instead of 3 in the middle ear) is an apomorphy, or an autapomorphy.

then what about Gymnophiona or Apoda like caecilians?! "they live underground in burrows in damp soil, in rotten wood and under plant debris" and "most species lay their eggs underground and when the larvae hatch, they make their way to adjacent bodies of water" and yet they are amphibians. and you said: "contrary to the amphibians, they cannot lay eggs under water" and neither can caecilians. but yet they are amphibians.

In addition to @Gerardo's answer:
Reptiles
The term Reptiles as used in popular language does not represent a monophyletic group. When using the term Reptiles, one is typically thinking of turtles, snakes and lizards but excluding birds and mammals (and a few other things not worth mentioning). There are two clades (monophyletic groups) whose name sounds like Reptiles and whose meanings are related; Reptilia and Reptiliomorpha.
Reptilia
Reptilia is the clade that @Gerardo discusses in his answer. Reptilia includes turtles, crocodilians, snakes, amphisbaenians, lizards, tuatara and birds.
Reptiliomorpha
Reptiliomorpha is a clade that includes Reptilia, Synapsida (mammals and close relatives) and a few extinct lineages.
Visualizing the tree of life by yourself
There are two good online resources: tolweb.org and onezoom.org.
Onezoom.org is better updated and has a nice pleasant look. However, I often find tolweb.org more convenient for investigating the true meaning of a specific clade.
Further reading
You might want to have a look at Understanding Evolution by UC Berkeley. It is a very introductory course on evolutionary biology and it includes a part on the phylogenetic tree.
I also strongly recommend having a look at the related question If dinosaurs could have feathers, would they still be reptiles?

Thank you. These sites you mentioned are very helpful and informative.

Turtles are not amphibians because they have (largely) non-permeable skin whereas amphibians can absorb oxygen through their skin. There are also differences in their reproductive cycle: turtles are amniotes, so they produce eggs that must be laid on land, whereas amphibians - like fish - are not and must lay their eggs in water.
Since the categorisation pre-dates the development of cladistics, and the group normally called reptiles are not monophyletic, I don't think cladistic based answers are a good answer to this question. It is the morphology and physiology that matters.


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What types of species can produce genetically identical offspring?
Talking about identical twins, triplets, etc.  I'm curious which types of species are able produce genetically identical offspring.  Let's limit the scope to species that reproduce sexually and instances where the offspring differ genetically from the parents but are identical to that of at least one of their siblings. Are there phyla, classes, et cetera that do not ever produce identical twins?  Kingdoms?  Are there cases of plants producing genetically identical offspring?

you ought to clarify as well whether or not you mean fraternal versus identical twins (or higher level pregnancies) - - - many animals (e.g. cats, dogs, rodents) have "litters" of offspring, but whether or not any of those might represent 'twins' is probably difficult to tell (or not easily detectable)

Are you looking for a list of all known species that have been documented to produce twins etc? If so that is too broad a question. If not, it remains unclear what you're asking.

@James It sounds like they're asking which taxonomic groups are capable of genetically-identical multiple births, rather than a list of species. Which sounds to me like it could be an interesting question, except that I strongly suspect there will be some species in almost any higher level group for which they haven't been documented, so I'm not sure it's answerable in its current form. Maybe it could be edited to "what biological processes facilitate or prevent viable genetically-identical multiple births" or something - OP, would you be happy with that?

@arboviral That would be a more satisfying question.

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Optical Density conversion to cfu / ml
I am having troubles understanding the correlation between OD measurements and CFU/ml. What is the conversion factor between the two units, and does this conversion factor somehow compensate for dead cells OD might be reading? (Also lets say the OD is set at the standard 600nm).

The optical density measurement is the quantity of living and non-living cells in a sample. The colony forming unit measures only the viable cells in a sample. An OD 600nm is equivalent to approximately 8 x 10^8 CFU/ml. However, this is only an approximation and cannot fully take into account the dead cells the OD may be reading, it also depends on the microorganism that is being researched. A standard curve can be calculated from data, but it is quite difficult to attain an exact result.
A very useful article on the correlation between the two measurements can be found here (from the Brazilian Journal of Microbiology).

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What's the mechanism for being mentally tired?
I notice that after long tests, or long periods of critical thinking, my body and mind feel noticeably tired. Why does this happen? Are the neurons in my head not firing as quickly, or is there just a perceived lack of mental concentration?
What exactly is the mechanism that makes my brain feel worn out, or at least gives me the perception of my brain being worn out?

There is ongoing research on this topic, but there is a theory known as inhibition theory. It has been defined as:

Inhibition theory is based on the basic assumption that during the performance of any mental task requiring a minimum of mental effort, the subject actually goes through a series of alternating latent states of distraction (non-work 0) and attention (work 1) which cannot be observed and are completely imperceptible to the subject.

For a more in-depth explanation, see this paragraph from Wikipedia:

Directed attention fatigue occurs when a particular part of the brain’s global inhibitory system is overworked due to the suppression of increasing numbers of stimuli. This temporary condition is not a clinical illness or a personality disorder. It is rather a temporary fatigue of the inhibitory mechanisms in the brain. According to inhibition theory, it is natural for one to alternate between periods of attention and distraction. Although one’s efforts may involve very different tasks, each incoming stimulus calls upon the same directed attention mechanism.

or this paragraph from NCBI:

Recently, it has been shown that the neural mechanisms of mental fatigue related to cognitive task performance are more complex than previously thought and that mental fatigue is not caused only by impaired activity in task-related brain regions. There is accumulating evidence supporting the existence of mental facilitation and inhibition systems. These systems are involved in the neural mechanisms of mental fatigue, modulating the activity of task-related brain regions to regulate cognitive task performance.

In short, it is now believed that the brain contains mental facilitation and inhibition systems, which control mental freshness and fatigue. Basically, when you concentrate, you actually stop all distractions from taking over (and not give more focus to the main point). This mechanism is governed by the inhibitory system of the brain. After some time, this system stops working ('it gets tired') and you become unable to pay attention towards anything. That's  why it is advised that after some time of concentration, you need to distract yourself (to refresh your inhibitory system); like, say, while preparing for exams, you should have a break of 5-10 minutes after studying for about 45 minutes.
Now, why mental tiredness causes physical fatigue can be (I think) summarized by the diagram below from here:

The exact process at this part is rather very interesting. Here, the neurons are not firing as quickly as they do normally. See this Wikipedia page:

Physical fatigue can be caused by a lack of energy in the muscle, by a decrease of the efficiency of the neuro-muscular junction or by a reduction of the drive originating from the central nervous system. The central component of fatigue is triggered by an increase of the level of serotonin in the central nervous system. During motor activity, serotonin released in synapses that contact motor neurons promotes muscle contraction. During high level of motor activity, the amount of serotonin released increases and a spillover occurs. Serotonin binds to extrasynaptic receptors located on the axon initial segment of motor neurons with the result that nerve impulse initiation and thereby muscle contraction are inhibited.

The same might happen in the case of mental fatigue i.e. the excess serotonin released from frontal or parietal lobes, or even the inhibition system itself, can cause the same effect i.e. inhibition of muscle contraction.
References:

Inhibition theory
Directed Attention Fatigue
Neural mechanisms of mental tiredness
Mechanism of physical fatigue from mental tiredness
Fatigue

this is awesome. Can you please add some references for us who would like to read more? Thanks!

I've already done, I'll add 'em separately too. Sorry BTW :)

Well, there's a proximal answer and a distal answer. The distal one:
When we study zoology (and one must study zoology in order to understand the human being), we see the evolution of cells taking us back to the first animals, like Porifera, where important functions such as communication, movement and digestion - were all performed by the same type of cells.
Even in the more complex triploblastics, like Gymnotiformes and others, we still see muscle cells emiting electric discharges, like neurons do.
So, the brain is not totally dissimilar to the muscle, and just like fermentation in the muscle produces Lactic Acid, some similar system might cause us the need for rest and sleep (a need universal in the animal kingdom, by the way - the "laborious" individual ant spend more time sleeping than working, it seems).
When we do the same sort of tiresome mental work (processed in the same nerves and brain areas), the fuel - oxygen - must get scarce in that region, just like in the muscles, where the lack of oxygen activates the alternative fermentation, leading to painful skeletal muscle cramps.
So I take a guess: can it be the Lactic Acid that causes us to be "mentally tired", in a process similar to a cramp? (Though certainly different - the pain looks different - and probably more complex, enriched by layers of signals and alternative resources, increasing the versatility and effectiveness of the brain in a species where mental skills are the only weapon left.)

I could have have given an upvote if you had references. "a need universal in the animal kingdom" you know that some (though less) animals don't need sleep at all?

It was a lecture I attended many years ago, about sleep and dreams in the animal kingdom. The need for sleep is widespread in the animal kingdom. If I'm not wrong, Edward Wilson wrote about how ants spend more time sleeping than working (in Sociobiology or The Insect Societies? Not sure.) Some migratory animals "don't sleep", but actually each half of their brains sleep separately.

I think even that much of a reference would work, if you're sure about it. I think you should have a look at this.

@another'Homosapien' Nice link. That's what I meant: "Sleep is pretty much universal. Practically every animal sleeps in one way or another."


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Does the formation of water inside the mitochondrial matrix help contribute to the proton gradient during the electron transport chain?

Does the synthesis of water in the final step of the electron transport chain significantly increase the electrochemical gradient across the matrix? I understand that pumping protons out of the matrix clearly increases the positive charge in the intermembrane space, but the chemical reaction in Complex IV O2 + 4H+ + 4e− → 2H2O also reduces the protons in the matrix by binding them in water.
Since ATP synthase relies entirely on the electrochemical proton gradient, it seems like this might be worth mentioning, yet I haven't seen this explicitly explored in any textbooks. If there is any literature about this topic, I would love to see it.

Your description of it is largely correct, but the electron transport chain does not simply "dump" charged oxygen ions in the mitochondrial matrix. Instead, cytochrome C oxidase (complex IV) binds the O$_2$ molecule to one of its heme groups, and the reduction O$_2$ + 4 H$^+$ + 4 e$^-$ $\rightarrow$ 2 H$_2$O occurs at the heme group before water is released. Some more details on the enzyme is found here and here (or in any biochemistry book).
In theory you're right that producing water in the mitochondrial matrix would dilute the H$^+$ concentration there a little (along with the concentration of everything else). But this dilution is negligible: the mitochondrial matrix has pH $\approx$ 7.8, which is the same as a H$^+$ concentration of about 15 x 10$^{-9}$M, while the concentration of water (yes, there is such a thing ;) is 55 M. So adding a water molecule has virtually no effect compared to removing a proton.

Thanks for the explanation. Although I still have the same question - does the removal of the protons (H+) inside the matrix in the the final reduction step (O2 + 4 H + 4 e− → 2 H2O) increase the electrochemical gradient? Protons are not only being pumped out of the matrix, but they are being bound up - 2 per water molecule. Then in addition to being bound up, they're also diluted. I could've been a little more eloquent before.

Ah, I see. Yes, in this sense respiration does affect pH I think, although it is counterbalanced by H+ production in metabolic pathways. But I think the H+ concentration in the intermembrane space (cristae) is much more important for the concentration gradient, since this space is much smaller, adding a protein there has a larger effect than removing a proton in the mitochondrial matrix.

The missing science to the question is the failure to realize that water inside a cell is bound to hydrophilic proteins which form an exclusion zone.  This EZ is well described in the literature by Pollack.  The EZ carries a strong net negative charge and it excludes protons.  This has also been confirmed by numerous researchers across the world.  The exclusion zone has specific physical properties that make it a different form of matter from bulk water that biologist normally are familiar with.  This is why Cayetano's question is excellent and why the answer he has been given is incomplete.  Any addition to the charge dramatically affects the charge across the membranes in mitochondria because they are only 4-6 microns thick.  The biophysics and mathematics of cell membrane electrochemistry prove that small charge differences are magnified on membranes of this thickness. The charge across this inner mitochondrial membrane is massive. It has been shown that this change across this membrane causes a pH gradient as well as an electrical charge of about 150 millivolts across the inner mitochondrial membrane. This may sound like a small amount of charge, but consider how charge is calculated and then scaled by math: the inner membrane is only 4-5 nanometers thick, so the voltage across this membrane is about 30 million volts per meter! Dr. Nick Lane from the UK has done this work and it is published in his book called "The Vital Question"  You can google his name for all the cites you want.  For comparison, that is equivalent to the energy in a bolt of lightening.  It is an electrical gradient that drives electrons from food to reduce oxygen from our lungs.I would also direct the readers to Dr. Martin Chaplin's work on water which takes Pollack's work to the quantum level.  EZ water is a capacitor for light energies from the sun.  All redox reactions in the body are tied at some level to the photoelectric effect, water chemistry, and the electromagnetic force. I will remind everyone reading this that the EMF only deals with charge particles.  Electrons and protons are those particles and both are found in mitochondria in massive quantities.  All foods are broken down into electrons to enter ECT.
Glutathione production in cells links the photoelectric effect in foods.   When we are oxidized,  we use up our stores of cysteine and glutathione.   Excessive inflammation (High proton content), from any cause, does not allows cells to replenish its levels and it does not allow us to separate water into its positive and negative charges and create large exclusion zones in mitochondria.  This limits energy production in a cell while slowly degrading cell signaling.  We see this in % heteroplasmy increases as laid out by Dr. Doug Wallace's seminal work on mitochondria.
References:

Gerald Pollack "The Fourth Phase of Water." 2013
Dr. Jodi Nunnari, Professor and Chair of Molecular and Cellular
Biology at the University of California, Davis was one of Wallace's
post doc's: Her work in size and shape links water thermodynamics to
mitochondrial energy production, see this article.
Dr. Doug Wallace: Head of mitochondrial medicine at the Children
    Hospital of Philadelphia.
     - youtube.com/watch?v=KwbIR2yUziw
     - youtube.com/watch?v=ahlDLjf8c90
Dr. Nick Lane You can google his publications which are large or
just read his books "Oxygen", "Power Sex and Suicide", "The Vital
Question".
ER-mitochondria contacts couple mtDNA synthesis with mitochondrial
division in human cells
Genetics: Mitochondrial DNA in evolution and disease
Scientists Learn How Mitochondrial DNA Replication is
Controlled
Here is Martin Chaplin website: He is a PHD researcher from the
UK.

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What is the relationship between independent assortment and cross over?
During meiosis, the independent assortment will be made first and then cross over will be made. I am so confused, what is the difference between this two process? I looked at the diagram on internet.It is said that law of independent assortment is alleles of genes on non homologous chromosomes assort independently during gametes formation, but I don't quite understand that.
So, another way for understanding this topic, independent assortment is tetrads can line up four different ways between homologous separate. Is that right.
Appreciate your help.

During meiosis, the independent assortment will be made first and then cross over will be made.

No, independent assortment occurs after crossing over. Crossing over occurs in prophase I while independent assortment occurs in metaphase I and anaphase I.

I am so confused, what is the difference between this two process?

During prophase I, a process called synapsis occurs. That is, homologous chromosomes (one from your mother and one from your father) come together and bind together, forming a tetrad. This binding is due to crossing over, which is when the genetic material on the maternal chromosome and the paternal chromosome exchange places. The maternal chromosome gives some of its genes to the paternal chromosome, and the paternal chromosome gives some of its genes to the maternal chromosome. Crossing over increases genetic variety by creating a new chromosome with a new combination of genes.
During metaphase I, the tetrads line up at the equator of the cell. During anaphase one, the tetrads are broken apart and each homologous chromosome that made each tetrad up is pulled toward one end of the cell. Look at the image below, where the blue represents paternal chromosomes and the red represents maternal chromosomes.

Independent assortment describes the phenomenon where the paternal and maternal chromosomes can be lined up randomly at the equator. There are many combinations. For example,

Both red chromosomes could face the top pole and both blue
chromosomes could face the bottom pole.
Both blue chromosomes could face the top pole and both red could face the bottom.
One red on the left and one blue on the right could face the top, as shown in the picture.
One blue on the left and one red on the right could face the top.

This random alignment at the equator makes it so that during anaphase, random proportions of maternal and paternal chromosomes get assorted into each of the resulting daughter cells. Some cells could get more maternal chromosomes and the other would get more paternal chromosomes, and vice versa. On the other hand, they could get similar amounts. Independent assortment increases genetic variation by allowing daughter cells to each randomly receive a different proportion of paternal and maternal chromosomes.
In conclusion, crossing over and independent assortment (sometimes called random assortment) are different independent processes that both lead to an increase in genetic diversity.

References

Reece, Jane A., Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, and Robert B. Jackson. “Meiosis and Sexual Life Cycles." Campbell Biology. 10th ed. Glenview: Pearson, 2014. 252-266. Print.
https://www.quia.com/files/quia/users/dschnepp/Meiosis/Metaphase-I

I'm interested in the randomness of the "Independent assortment" of the genetic material. How specifically is randomness achieved, to create the specific unique variation out of the 2^23=8388608 possibilities. Are certain combinations naturally more likely than others, and how does the cell make the components line up randomly at the equator?


text:
Trying to identify an insect
Toady a friend saw an insect in his garden, in the UK (England).
It looks like a combination of a hover wasp, a wasp and a dragonfly. Whist flying, I'd describe it more similar to a dragonfly.
I've used Google images to try and identify it, and come close, but the creature was about 3 inches long and up to 1 inch wide. I thought it was a broad-bodied chaser but he assures me (possibly incorrectly) it wasn't big enough

I would agree with you on this one - looks like a female or young male Libellula depressa (the 'broad bodied chaser') to me. It has the characteristic broad, flattened abdomen and the distinctive brown-yellow abdomen with bright yellow patches and the dark wing bases are both visible (the latter only just, to be fair). The broad abdomen differentiates it from the other Chaser and Skimmer dragonflies while the colour is quite distinctive (the species is sexually dimorphic; mature males have a blue abdomen while females and young males have a yellow abdomen). Not sure what you friend is talking about regarding the size; 3in long is about right for L. depressa. It's in the right geographical region too.
(thanks to @RHA for pointing out to me that young males also have yellow abdomens!)

Citation from Wikimedia Commons: By No machine-readable author provided. Bogdan assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=754252

You are correct, this is undoubtely libellula depressa. However, immature males lack the characteristic blue color and look the same as females. So it can be a young male as well.


text:
I found this insect in Utah, USA. What is it?
I keep seeing this insect around my house. What is it?

Here is another image:

A better pic would help. Keep this one for reference to the size, but could you post another?

sure. I may need to look for one again. let me see if I took a regular one.

ok The image is too high quality for me to load it here so I put a link to it right under the other image which is on this page.

This might not directly related to your question but as you found the animal inside your house you should REALLY make an effort to get rid of it. It can be a real plague and infest all your dry foodstuffs like cereals, pasta, nuts, ... !

It looks very much like the Indian meal moth, Plodia interpunctella, to me. The size, morphology of the antenna and wing tips, and the pale band of scales are all fairly distinctive. (The proboscis isn't very clear in the photo below but it is in most other images you could find via Google; I just couldn't find a better one with a license allowing me to post it here.)

(Image by Kaldari (Own work) [Public domain], via Wikimedia Commons; URL https://upload.wikimedia.org/wikipedia/commons/5/50/Indianmeal_moth_2009.jpg)


text:
Humans genetic/phylogenetic "next relative" in central Europe?
What species in central Europe in the phylogenetic tree shows the closest difference in time to the most recent common ancestor with Homo sapiens?

Could you define central Europe?

What do you mean by "next relative"?

I am not sure I understood the question. Is the following your question?

Among all species living in central Europe, which one is the most closely related to homo sapiens?

Source of information
opentreeoflife.org (nice vizualisation on OneZoom.org) is one of the most update synthesis of existing research inn phylogenetic reconstruction. I base my answer in consideration of the tree on OneZoom.org.
Answer
Outside Homo sapiens, there is no living primates (or any other Euarchonta) in Central Europe. The sister branch of primates include Lagomorpha (Hares and Rabbits) and Rodents (mice, rats, squirrels, prairie dogs, porcupines, beavers, guinea pigs, hamsters, and capybaras). In other words, any Lagomorpha and any Rodents are all equally related to any Primate (incl. Homo sapiens). Their Most Recent Common Ancestor (MRCA) lived about 75 millions years ago.
Examples of species of lagormorpha and rodents that live in Europe include Mus musculus, Rattus norvegicus, Lepus europeanus and Sciurus vulgaris.
How about Hedgehogs?
Hedghogs are Insectivora and they are a sister group to all primates, lagomorpha and rodents. Their MRCA lived about 80 million years ago. So, no there are species currently living in Europe that are more closely related to us than hedgehogs.
Note
The term "next relative" does not mean anything! You might want to understand your understanding of phylogeny with an introductory course.

Yes this was my question. Would it "theoretically" be possible to measure the individual distances of each Lagomorph or Rodent species to the MRCA? I mean it is for instance known that some are more "archaic" then others. So that the question would be what is the most archaic of all Lagomorpha and Rodents? I see that the answer ideally would theoretically require a complete knowledge of the MRCA, nut maybe some guess is possible?

For example Aplodontia rufa
(if it only lived in Centraleurope) would be a candidate in the sense of my question.

Aplodontia rufa lives in north America (California, Oregon, Washington and British Columbia). I added examples of species in my answer.

Nice answer. I would just note that OneZoom.org doesn't assemble the data themselves; they get it from http://www.opentreeoflife.org/ (as acknowledged in http://www.onezoom.org/about.html). They do a nice job of presenting it though, which is also important!

I have updated the question and choose one possible specification of the heuristic term "next relative".

Shortest distance is still very unclear. Do you mean minimum number of average genetic pairwise differences on putatively neutral sequences (which result will slightly depends on the alignment methods and consideration of gene/chromosome duplication/deletion)? Maybe you are referring to some other measure such as chosing a number of quantative traits and compute the average (over all traits) difference between species average trait value.

As you used the term "phylogenetic" in your question, it totally makes sense to consider the time to the MRCA as a measure of distance. It is what we mean when we talk about how closely related are two different lineages/species anyway. It will be a very very good proxy for the number of pairwise differences at neutral sequences also.

Is it better now?

by "time of branching", I suppose the oly thing you can mean is "time to the most recent common ancestor", which is exactly what I answered. Do you feel like my answer does not answer your question?

It doesn't answer, because it implies that all recent rodents and lagomorphs  "to a very good approximation" show the same number of pairwise differences at neutral sequences. Since this is counterintuitive (see my example of an "archaic" rodent (it does not live in Central Europe but just for the sake of this argument)). So the intermediate question would be: What kind of measure would allow us to make a distinction is distance between the relation between an "archaic" rodent and a more evolved one? Is the simplest answer already "number of pairwise differences at neutral sequences"?

The terms "archaic" and "more evolved" make little sense. You seem to assume there is a thing such as "distance between species" and then we try to estimate it with different statistics. The reality is that the term "distance between species" is undefined and you have to chose a statistics and make sense for your particular interest. The very standard is to consider the time to MRCA which is a very proxy anyway to many other statistics of species divergence such as typically the number of pairwise differences at neutral sequences. By the term "relatedness", we also refer to time to MRCA only.

If things are still unclear, I invite you to (1) follow an introductory course to phylogenetics and (2) ask your question regarding your misunderstanding about phylogenetics in a separate post as such discussion would be off-topic here. I you clarify your post by rewriting the question I suggested at the top of my answer (and remove the unclear concept of "next relative"), then you will be able to consider your question has been answered (and your post could well be re-opened).


text:
Difference between water and tea
My friend heard that tea is worse for drinking than water because "cells have a special membrane and tea has special supplements and membrane doesn't let tea pass and this is why skin is dry even when you hydrate with tea a lot", something about "lipid bilayer".
Is there is some nice scientific article on water andd tea difference to human organism?

Your question is very awkward.
Let's define Tea as boiling leaves in water. At the end, you remove the leaves and drink the flavoured water.
At this point, the "tea" is still very much water - as in tea is water with dissolved chemicals from the leaves. Note, the word chemicals is not to be interpreted in a negative way because everything (including water) is a chemical.
So, the difference between tea and water are the chemicals that dissolve. What are these chemicals? The answer to that depends very much on the tea. Another difference is the temperature - tea is typically hot.
You can look at this article about chemicals in green tea and their associated health benefits. You can do further searches for other tea types and for each of those chemicals.
In short, no you do not get dehydrated because of tea vs. water. Dry skin can be caused by a lot of different reasons. Oh and no, caffeine doesn't cause any significant amount of dehydration as far as I know.

Depends on the tea, but most tea (unless herbal) contains caffeine, which is a diuretic. This means it dehydrates, and why one might experience drier skin. However, this is not a direct relationship and the actual reason why one's skin might be dry is a lot more complex. However, for a basic answer, caffeine is your culprit.

Please add citations to relevant scientific literature supporting your claim. The old wives tale about caffeine dehydrating you is completely false. Yes, it may increase your urine flow, but not enough to counteract the actual fluid intake from the tea (or whatever beverage) itself. Plenty of construction workers in the US rely solely on tea or soda beverages for their hydration during the day, and they have no symptoms of long-term dehydration. These actions are unhealthy because of the massive sugar intake, but they don't dehydrate.

@MattDMo Caffeine can be diuretic - but only in high concentrations (much higher than found in a cup of coffee).

@Chris yes, I know. My point was that the amount of water you are consuming outweighs any minor diuretic effect of the caffeine.

@MattDMo For normal beverages, there is no effect.


text:
Is there more diversity in marine species?
I was reading about how life emerged from oceans, and the following question occured to me. Do land species suffer from the founder effect and is there more (genetic) diversity in marine species? A quick google search pointed to the fact that a majority of species live on land. Is that a paradox?

I know that marine habitats have a higher phylogenetic diversity (see also Faith 2006) than terrestial habitats, even though they host far fewer species, which is a result of their deeper evolutionary history. Unfortunately, I cannot find a good reference to this claim right now (see http://biodiversity.europa.eu/topics/ecosystems-and-habitats/marine for some support though).
I wouldn't really call the difference in species numbers a paradox though, since speciation rates depend on habitat complexity and dispersal rates (which are generally higher in marine habitats). In either case, the knowledge of marine habitats and species living there are much poorer than for terrestial habitats, so differences in species numbers are highly tentative.

The estimated diversity, in this case species richness, is higher on land than in the ocean. To resume the state of knowledge of biodiversity, here's an excerpt from an open-access paper by Mora et al. (2011) How Many Species Are There on Earth and in the Ocean?
"...(our analysis) predicts ∼8.7 million (±1.3 million SE) eukaryotic species globally, of which ∼2.2 million (±0.18 million SE) are marine. In spite of 250 years of taxonomic classification and over 1.2 million species already catalogued in a central database, our results suggest that some 86% of existing species on Earth and 91% of species in the ocean still await description."


text:
Why do the hormones FSH and LH decrease when the follicle is maturing and does size of follicle change during menstruation phase
There are three phases in menstrual cycle. In follicular phase of menstrual cycle, the level of FSH and LH would rise because they would stimulate ovarian follicle to mature. However, when I check with diagram of menstrual cycle, I find FSH and LH hormones do actually decrease during day 4-14. Is that because of increase of oestrogen? However, by the time when FSH decreases, the follicle hasn't fully matured. Also, will follicle grow during menstruation, because in diagram, the size of follicle actually changes during Day 0-4, and FSH and LH hormones increases.

I find FSH and LH hormones do actually
  decrease during day 4-14. Is that because of increase of
  oestrogen？

You first need to note that during one ovarian cycle, multiple follicles are stimulated to grow at the same time by FSH. However, one follicle ends up being the dominant follicle, and it is the oocyte housed within this follicle that is released on day 14. The dominant follicle is the one whose cells express gonadotropin receptors the earliest and so have the greatest sensitivity to FSH. Its growth would outcompete the other developing follicles. During days 4–14, FSH begins to decline because the granulosa cells of the follicles secrete inhibin, which—just like in males—causes the release of FSH and LH from the pituitary to drop. Only the dominant follicle is capable of withstanding this FSH drop; the other developing follicles are thus eliminated.

Also, another question is will follicle
  grow during menstruation, because on diagram,the size of follicle
  actually changes during Day 0-4, and FSH and LH hormones increases.

As user19099 explains, yes, follicles grow during menstruation. With the degeneration of the corpus luteum, the negative feedback effect of estrogen and progesterone (in combination) on the hypothalamus is relieved. Thus, GnRH levels increase, causing FSH and LH levels to increase (as reflected on the graph you included), and FSH will stimulate follicular development.

References

Marieb, Elaine Nicpon, and Katja Hoehn. Anatomy & Physiology. San Francisco, CA: Pearson/Benjamin Cummings, 2008. Print.

Another question is how can the level of FSH and LH decrease once they start in follicular phase. It's said the level of FSH and LH would increase to mature follicle. Is there a clash between knowledge and fact? As you mention, the drop is because of inhibin. So, body would release inhibin once going into follicular phase?

@Q.MEO FSH and LH increase during the early follicular phase. As ovulation approaches (i.e. late follicular phase), inhibin is released by the granulosa cells, so then FSH and LH decrease. There is a rise in FSH/LH levels, and then a fall, as you can perceive from the graph. I think your graph is unclear, as it makes it seem as though follicular phase lasts from day 4–14. That is untrue. Follicular phase starts from day 0 to day 14. Note that just because FSH falls does not mean there is no FSH to stimulate the dominant follicle; there’s still FSH—just a lower level than before.

Does it mean follicular phase include menstruation???

@Q.MEO Menstrual cycle has 3 phases: menstrual, follicular and luteal phase. Menses occur in menstrual phase i.e. day 0-4.

@Q.MEO Yes, it does. You should differentiate between the ovarian and the uterine cycles. The ovarian cycle includes the follicular phase and the luteal phase, while the uterine cycle includes the menstrual flow phase (menstruation), proliferative phase, and secretory phase. The two occur simultaneously and relate to each other hormonally but occur in different locations—one concerns the ovary and one concerns the uterine lining. The follicular phase overlaps with the menstrual flow phase and the proliferative phase.

My (honest) opinion, don't pay too much attention on the graph. While looking at other graphs on the internet, I found that many graphs show different levels of hormones on the same day. See these two images (upper one from here and lower one from here) for example:

See the level of FSH and LH on same day in both graphs, you'll find difference. In short, the graphs are just to show approximate value, don't try to derive answers from them.
For your next question will follicle grow during menstruation, yes the follicle grows continuously through the menstrual and follicular phase. A primordial follicle (dormant one, which was arrested in diplotene stage) has a diameter of about 25 μm1, which grows upto 16-20 mm2 before ovulation, as a Graafian follicle.

Source
References:
1.http://www.glowm.com/section_view/heading/Follicle%20Growth%20and%20Development/item/288
 2.http://www.fertilitytoday.org/frequent_questions.html

But I am still confused about why there is no increase in follicular phase. According to knowledge, it's said there is a increase of level of FSH and LH. Is there a clash between knowledge and fact. Or it is just about accidents?

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text:
A New Antiviral Drug Strategy?
I am studying viruses and I have a question about antiviral drug strategies. Why haven't researchers tried finding small molecule drugs that will bind to receptors on the host cell, thereby preventing viral attachment to the host cell? I feel as though with this strategy, virus resistance and mutation wouldn't be an issue. Thoughts?

According to wikipedia, there have been drugs targeting CCR5 coreceptor approved for treating HIV. These drugs work by binding to CCR5, thereby prevent binding of HIV and CCR5.
However, drug resistance can still develop. Some HIV can bypass it by shifting tropism to CXCR4. While others can increase its affinity to CCR5.
And some receptors are vital for the functions of cells. If we design drugs to these targets, we should make sure that the drugs only prevent binding of viruses specifically without disrupting their normal functions.

Maraviroc was approved for use by the FDA in August 2007.It is the
  only one thus far approved by the FDA for clinical use, thus becoming
  the first CCR5 inhibitor. A problem of this approach is that, while
  CCR5 is the major co-receptor by which HIV infects cells, it is not
  the only such co-receptor. It is possible that under selective
  pressure HIV will evolve to use another co-receptor. However,
  examination of viral resistance to AD101, molecular antagonist of
  CCR5, indicated that resistant viruses did not switch to another
  coreceptor (CXCR4) but persisted in using CCR5, either through binding
  to alternative domains of CCR5, or by binding to the receptor at a
  higher affinity.
  https://en.m.wikipedia.org/wiki/CCR5

http://www.ncbi.nlm.nih.gov/pubmed/11782552
http://www.sciencedirect.com/science/article/pii/S0042682206008245

Please add relevant citations to your answer.

I learnt it from wikipedia, it didn't show any external links about drug resistance. If you want more credible sources, I'll try to find them.

I posted two additional paper. I haven't finished reading them. I hope these can help.


text:
Why does liver wrap around inferior vena cava?

As shown in the image, the liver wraps around inferior vena cava, which takes blood from liver via hepatic veins. Is there an advantage of having the inferior vena cava closer to the liver rather than abdominal aorta? I am guessing it has to do with lower blood pressure in the veins, but I want to check.
It could also be evolutionary thing that has no reason for such structure, but that wrapping around structure seems to have a purpose.

Nice image, where'd you get that from? ;) I don't know much about this, so my guess would be that hepatic portal vein joins in to vena cava after leaving the liver, so the liver forms such structure around inferior vena cava instead of abdominal aorta.

I got took a screenshot from this website: http://www.healthline.com/human-body-maps/hepatic-veins.
Also about your point, there are also arteries flowing to the liver from abdominal aorta, so I can imagine liver wrapping around the abdominal artery as well.

I get your point. I think it could be that keeping vena cava nearer would be better (maybe to easily transport blood from hepatic portal vein due to its low pressure or some other reason I can't think of) or keeping abdominal aorta at an inch distance wouldn't be any bad or probably it was just a matter of chance ;)

It is really only a matter of two vessels passing "through" an organ; where they are situated depends entirely on their function. The IVC delivers it's supply to the right side of the heart "through" a right sided organ; the aorta leaves the left side of the heart and so is situated to the left of the IVC. Just makes the most sense anatomically in this case.

Possibly related to the absence of valves in the hepatic veins


text:
4DGenome or another comprehensive database of chromatin interactions
I'm searching for the most comprehensive source of chromatin interactions to support enhancer targets (data such like Hi-C, ChIA-PET, IM-PET, 5C, 4C, 3C, etc.) and my question according that could be split into two following parts:

On page http://epigenie.com/epigenetic-tools-and-databases/ I've found out links to two databases, but the reference to 4D Genome doesn't work. Does anybody know whether this database
http://4dgenome.int-med.uiowa.edu was moved somewhere else or maybe its only internally available for U Iowa community? (I'm asking about probably exclusive access, because on Tan's lab page http://www.healthcare.uiowa.edu/labs/tan/software.html only the 4DGenome has the trailing part of the link int-med.uiowa.edu (presumably this int-med strands for internal/general medicine or maybe in the sense of internal/intranet access), whereas all other services like IM-PET has its link starting with http://www.healthcare.uiowa.edu/labs/tan/.
Maybe you know even better database for chromatin interactions covering as much as possible cell lines/tissue types for GRCh38 assembly or any other whose coordinates could be easily converted, e.g. by liftOver? I need data only for human and mouse, but I would be grateful also for solely human data.

Thank you in advance for your answer.

All the sequencing data can be found in SRA. You just have to use the keyword to get the data. However, these would be raw data. This seems to be another database on long range chromatin interactions.

This problem has been finally solved with help from prof. Kai Tan.
It occurred that his lab has been moved from University of Iowa to Children's Hopspital of Philadelphia, so has been this service.
Now, the working link is:
http://4dgenome.research.chop.edu


text:
Would a transparent iris serve its purpose?
The function of the iris is to regulate the aperture of the pupil. How does the iris obstruct light? Is it due to the pigment present in it? Or is it just due to the sheer presence of it?
I am doing a project where I need to maintain a constant light intensity for albino rats. I was suggested to administer a mydriatic topically but when their iris is transparent, does dilating their pupil make sense?
How is it in human albinos? Does pupil dilation and constriction make a difference in them?

Human albino Iris is not transparent. Translucent maybe. Administering mydriatics might be at least slightly better than relying on their transparency.

What did you do in the end? Feel free to self-answer, if you have one?


text:
Do flowers transpire?
I have googled this out but no where found a satisfactory answer. The definition of transpiration states that it is the evaporative loss of water from the aerial surfaces of the plant but I am really unsure as to whether flowers transpire or not.

Short answer: yes.
Floral parts, as petals and sepals, have stomata, and transpire just like a normal leaf or a primary stem (that is, a stem covered by epidermis, not periderm). And, besides stomatal transpiration, flowers have cuticular transpiration, like most of structures covered by epidermis.
This is a SE micrography of a petal's stoma:

(source: http://www.sciencephoto.com/media/32403/view)
There is a very famous experiment that we make with the kids in primary school: take a white flower and put it in a vase with coloured water. The petals will become coloured. This experiment shows that there is an ascendent flux of water, and this flux depends on transpiration. You can see it here: https://youtu.be/y9hprlmck44


text:
After a bacterial infection is dealt with, do any of that colony of bacteria remain?
Suppose that I get a bacterial infection, which my immune system deals with. Are there any remnant bacteria, or are they all gone? Now consider the same scenario, but having been treated with a full course of antibiotics - are there any bacteria left alive? Now suppose I take a partial course of the antibiotics - enough to reduce the bacterial population to a level that my own immune system can deal with by itself. In this last case, if I beat the infection, is there any chance of bacteria having evolved resistance to those antibiotics, or are they all dead?
I ask having recently read an article claiming that conventional wisdom on antibiotics might not be as useful as once thought.

Have you read anything on resistant bacteria?

@rg255 yes; what are you getting at?

I think @rg255 is on the generation of resistance by not finishing antibiotical treatments...

Which is exactly what I'm interested in, but am questioning the 'accepted' wisdom of the matter.

Can you point out exactly where the article states "a full dose of antibiotics is somewhat arbitrarily determined and based on a single case study"? (It did state recommended "antibiotic courses are often arbitrary; they may reflect long-standing convention or be based on a manufacturer’s decision during an initial drug trial." Note that an initial drug trial is light years from a single case study. (cont.)

Furthermore, the paper states that "Recent clinical trials show that even for some serious infections, shorter antibiotic courses can be as effective as conventional, longer ones," which directly contradicts your assertion that duration of antibiotic treatment is arbitrarily determined. The article has a lot of correct information, but can be easily misinterpreted, which I believe you have done.

@anongoodnurse fair call; which is why I'm asking the question here.


text:
Can a color-blind person see color with filter glasses?
Why does color vision improve in color-blind persons using these filter glasses from Enchroma? Will a color blind person be able to see the same colors on a television? I'm asking, because the colors for every point on a TV screen are combinations of red, blue and green.

Short answer
Optical filters can optimize color contrast, but never restore color blindness. Filters remove colors, they can never add something. However, glasses like this can prove helpful for certain sub-populations of people that are partially color blind.
Background
First, the term color blindness is deceptive. It is better to talk about colour vision deficiency (CVD). This, because many people labeled as color blind in fact have all the red, green and blue cones like the normally-sighted. These people have protanomaly (abnormal, but still functional red cone photopigment), or deuteranomaly (abnormal green cone photopigment). These two conditions are mild and don't affect daily life too much (source: NEI / NIH).
The other two most common forms of CVD are protanopia and deuteranopia. Protanopes have no working red cone cells and deuteranopes have no green cones. These conditions are more severe and do affect daily life as color perception is compromised. These conditions can be coined color-blindness, as these folks miss one type of cone altogether (source: NEI / NIH).
The glasses of Enchroma target the first two conditions, namely the anomalies and not protanopia or deuteronopia. The Technology page of Enchroma explains why. Basically, protanomaly and deuteranomaly are characterized by the red and green pigments having a shifted spectral maxima. The end result is the same, namely more overlap between the spectral absorbance curves (shown for deuteranopia in Fig. 1). In normal vision, the overlap is already pretty extensive, meaning that green light activates a large portion of red cones and vice versa. In protanopia or deuteronopia this effect is further increased, resulting in a degraded capability to separate reds and grees. For example, protanopes perceive reds, oranges, and yellows as greener, and colors are not as bright. Deuteranopes perceive yellows and greens as more red and they have difficulty telling violet from blue (source: NEI / NIH).

Fig. 1. Left: normal cone spectral distribution vision, right: cone distribution in Deuteranopes. source: Enchroma
What Enchroma has come up with is actually really clever (!) - they've put a spectral notch filter in place and wedge it in-between the red and green spectral optima, thereby removing the large area of overlap. This reduces brightness, but it will enhance contrast when the glasses are worn (Fig. 2).

Fig. 2. Spectral notch filter to enhance green-red color contrast. source: Enchroma
And yes, above considerations hold for any colored object, including monitor pixels.

I am colourblind and own a pair of the enchroma glasses. For me (experiances seem to vary) the glasses certainly make colours look different however there is only limited improvement between difficult red-green differentiation. I've yet to try a colourblindness test wearing them!

I've been reading around a lot and I still don't understand how this is meant to work. Surely it just makes the wearer blind to wavelengths of light filtered out by the glasses? The wavelengths on either side of the notch (not being blocked) are going to excite the red and green cones about the same amount, just as they were before, and so will still be difficult to distinguish. I haven't found an explanation that feels sufficient yet.

The wavelengths on the side will excite as they did before, but the regions of high overlap are excluded by the notch. Imagine that the area on the left excites G 1 unit and R 0.2 units, while the are covered by the notch is 5 units G and 5 units R. With the notch, you have 1:0.2 or a contrast of 5. Without the notch you have (1+5):(5.2) or a contrast of 1.15. Contrast would be enhanced almost 5-fold.

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text:
Is there an evolutionary advantage associated with migraine?
I have read Wikipedia article on Genetics of migraine headaches and I don't buy it

Because genetics influence susceptibility to migraine, it can be
  shaped by evolution. Fitness-impairing disorders, including severe
  headache, tend to disappear as a result of natural selection, and
  their frequency decreases to near the rate of spontaneous
  mutation. However, migraine has not
  diminished over millions of years of evolution. Its prevalence has at
  least been maintained at a high level, and has even been shown to be
  increasing.
  This phenomenon suggests that a central nervous system (CNS)
  susceptible to severe, intermittent headache has been linked to an
  important survival or reproductive advantage.

the argument in wiki is equivalent to since we know that evolution is correct - it means that headaches must benefit us somehow otherwise we wouldn't have it so let's think of some reasons - which is in my opinion is a fallacy.
I could believe that this is a bad side effect of some more efficient to survival trait like being smart, (which is partially covered in same article)

Finally, migraine may be a component of imperfect central nervous
  system design. Evidence has suggested a dysfunction of pain-inhibitory
  pathways in migraine and discordant interaction between the ancient
  brain stem design and the more evolved neocortex.

EDIT:
I have read the meta post and answer from WYSIWYG, and I agree that they do partially answer my question in regard that a mild 'badness' can get past. I would argue that my question is different in a way that I am referring to specific point The trait might have a tradeoff which essentially makes no change to the overall fitness
The way I understand it is that one gets some 'perk' that is beneficial in some situations and disadvantageous in others and they cancel each-other out. (I just don't see how without some huge benefit migraines would get past). What I am asking is what so advantageous we must have gotten - that such horrible thing like migraines got through.
Are there any studies done - that incapacitating migraines are coupled with an evolutionary trait?

There is no need for a benefit from a trait to stay - it is necessary that it is not selected against this trait.

@Chris Hi Chris, I see what you are saying, don't you find it hard to believe that incapacitating migraines would not get selected against? I can't think where whey would not reduce performance be it mental or physical.

We don't know the exact genetic basis for migraine as far as I know (might be wrong). Unless we do, we cannot decide, if migraine is the backside for some other, much more beneficial trait also connected with these genes or gene variants. The classic example for this is sickle cell anemia - not beneficial unless you live in an area where malaria is endemic.

@Chris Thanks Chris, there is this article on twins with migranes, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2779399/pdf/10194_2007_Article_427.pdf  At present, several loci 4q21-q24, 5q21, 6p12.2-p21.1, 11q24, 14q21.2-q22.3 and 15q11-q13 linked to common forms of migraine with evidence of linkage have been reported.

See this.

@WYSIWYG Hi WYSIWYG, I have read the meta post and answer you have linked, and I agree that they do partially answer my question in regart that a mild 'badness' can get past. I would argue that my question is different as it is referring to specific point in your answer, The trait might have a tradeoff which essentially makes no change to the overall fitness.. What I am asking is with which trait did we get migraines (that was so great that even such incapacitating thing like migrenes got past). If you think I should change the wording, please just say so. Thanks.

@WYSIWYG edited the question.

I've updated my answer here - it should answer your question -  see the last bullet point in particular

I have altered your title, correcting the grammar and phrasing it in a scientific manner.

smart apes stayed on the cave with his migraine, while the dumb ones were killed hunting, and that's why we have migraine today.

@montelof and he died from starvation....

no, in that case migraine would not exists, he probably discovered agriculture.


text:
How valid is the theory of human's chimp-pig origin?
Edit: I have also asked the question on skeptics.stackexchange.com and it has been answered there. Here is the link.
There is a person called Dr. Eugene McCarthy who has a theory that the origin of humans come from pig-chimp hybridization (online article about his theory). How acceptable is his theory in comparison to the other common theories?

Welcome to Biology.SE. This question would be better on-topic on skeptics.SE.

As an evolutionary geneticist, I have never heard of such hypothesis and it sounds like a non-sense, silly joke! Note that the article you link is NOT a peer-reviewed paper and therefore does not make any contribution to our knowledge (but it is good that you linked it). If you ask your question on skeptics, they will likely trace back the origin of this (a priori) myth and debunk fake evidence (if any).

The word "theory" here hurts my eyes... please change it for "hypothesis" or, even better, "baloney".

To further @GerardoFurtado, theory in science means a hypothesis (or a set of hypotheses) that is very highly supported by tons of evidence. In popular language however, theory is often used as a synonyme of hypothesis.

Note that this so-called  Dr. Eugene McCarthy does not seem to have ever published anything on the subject and is not associated to any university or other recognized institution. It is possible that this person does not even exist!

I have read part of the linked article. It really makes no sense whatsoever and as @iayork said, it is unclear what must be debunk as there is so little that make any sense in any way! But again, on Skeptics.SE they will probably do a better job than we want to here on Biology.SE

This guy is so unsure of himself that he feels the need to spread random tweets and quotes from supporters throughout his work, as if science was some sort of popularity contest where the most Facebook "likes" wins.

While the article referenced in this question is patently ridiculous, I don't see how this question is off topic here, even if it is in fact on topic on Skeptics SE. This seems like a perfectly reasonable question here.

The post has been opened (and answered) on here on Skeptics.SE.

@Remi.b Should I remove the question here or it's OK?

It is now on hold anyway. I think the best would be to add the skeptics.se link at the top of the post (saying the question has been answered there) and leave the post as it is. Thanks

Briefly, the "theory" makes no genetic sense. Pig and human genomes have both been sequenced, and their sequences are completely incompatible with this model.
The "theory" is completely idiotic in many other ways -- debunking it almost becomes difficult because there are so many ways it fails to make sense -- but the genetics alone make it impossible.

It is not always easy to say this with full force in natural sciences, but: NO, this theory is NOT true, probably not even by any means. Extraordinary claim require extraordinary evidence. But wow, there is NO evidence AT ALL for this claim.
Before tackling the main point, I give a side note that would actually be sufficient to not be concerned with the argument itself: Extraordinary evidence is rarely (if ever) presented (i) by single people's research (rather then by a really large body of evidence provided by several independet reseearch groups, different lines of arguments, ...) and (ii) outside of peer-review high-quality journals. For example, you do not report major findings on your dubious website relating to a reference like this:

To cite this publication
  McCarthy, E. M. 2013. Mammalian Hybrids. www.macroevolution.net/mammalian-hybrids.html (Add access date).

However, I would also adress one actual issue. For the sake of argument, I consider the claims to be just as valid as any other claim I ever heard based on morphological features (and with that I do not say that anatomical comparsions in general are nonsense. Au contraire, I believe that these comparisons are important to reconstruct evolutionary histories, especially but not only in extinct organisms where DNA comparison is not an option).
In extant animals (like humans), however, anatomical and genetic comparisons tend to converge and/or the anatomical evidence is adjusted to insights gained from genetic comparisons (meaning that anatomical similarities supporting the findings of genetic comparisons are found really often. Do I provide a citation for this? No, there are thousands or even millions. This is SO well-known that any journal probably accepts this as common textbook knowledge and does not even ask for one).
Long story short: There is NO genetic evidence AT ALL that indicates a mixed descendence of humans from chimpanzees and pigs (wow, I would never had thought, I would write a sentence like this, ever in my life). Additionally, there is NO anatomical evidence for that mixed descendence AT ALL apart from McCarthy (2013) - haha.
PS: I posted a corresponding answer to the skeptics.SE question as well.

both Suidae and Primates  like every creature on earth have a common ancestor in history , but they are simply too different to breed together .
Therefore the theory makes no sense , unless it uses pig and chimp in a metaphoric sense .


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Phase Transitions of Purified Proteins
Why do solutions of purified protein condense into droplet phases?
I'm trying to understand the protein phase transitions.
Here is the article http://www.cell.com/cell/fulltext/S0092-8674(12)00634-4#
It's on Intracellular Granules as Liquid Droplets

Welcome to BiologySE! Thanks for your question... it always helps if you can give some additional information so others can understand what you're asking. Also, links embedded in the question that re-direct to other sources may be helpful as well.


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Do Tumor-Infiltrating T Cells Experience Any Prolonged Effects Due To Hypoxia After They Return To Normoxia?
Adoptive cell transfer (ACT) therapy using tumor-inflitrating lymphocytes (TIL) is at the cutting edge of immuno-oncology treatments involving metastatic melanoma and other indications (1). The idea is that at some point during the growth of a tumor, some T cells attempted to mount an immune response, extravasated and got into the tumor, but they became overwhelmed and exhausted. The therapy itself involves taking these cells out from some excised tumor, reversing their condition and since they're already neo-antigen specific from having attempted an attack on that cancer: Expand them, put them back in the patient, let them hit the tumor much harder than before.
Not only do you need to reverse exhaustion in the TIL, but you also need to have the right population of T cells to get the best response. The factors involved are beyond this question, and so I'll get to the point.
In the tumor environment, the T cells become exhausted and their expression profile changes (2). It makes them more prone to apoptosis and they lose effector functions like GranzymeB production. You can tell how this is problematic. My suspicion is that in the tumor the T cells may become hypoxic, and what we know is that in the oxygen-sensing pathway, hypoxia inducible factors exert their effect. Normally, these should be kept in check by inhibiting proteins if they get produced under normoxia:

And so to my question:
After prolonged exposure to hypoxia, are there any regulatory or transcriptional changes that after prolonged return to normoxia render either of HIF1α or HIF2α active where they would normally be repressed?
Whether I just need a fresh set of eyes or the data just doesn't exist, I haven't necessarily found it obviously. I'd like to know if there's a remnant hypoxia-like regulation framework that remains after O2 gets back to normal that affect pathways like mTORC1/2. Thanks if advance for any insights!

It seems like you've made up a hypothesis with no evidence, and rather than actually look for evidence for the hypothesis you're charging down the pathway and asking about hypothetical recovery from hypothetical effects of hypothetical problems.  Why not actually try to validate your model before asking about far-downstream effects?

@iayork It seems that way when I type things up (I miss a lot), but it's established that the T cells we're getting out of these tumors are in bad shape due to many factors including hypoxia, and that HIF very much modulates T cell responses (1) (2). If there's even a mundane tidbit I'm missing while I trudge through tons of papers, however, it will be great to find out.

Have you actually looked at HIF1α/HIF1α-Pro-OH levels in your TILs compared to circulating T cells with the same or similar surface markers, then made the same comparison after culturing TILs under normoxia for some period of time?

Alternatively, you could label the cells, then do an adoptive transfer of extracted TILs into non-tumor-bearing mice and follow them that way, if you're afraid that ex vivo culture might muddle the picture too much.

@MattDMo Just because it's not on our project list, I haven't run any such tests. We also don't work with mice (that's a collaborators' job). I'd like to do something similar, however, at some point in the future. I'm just looking for data that exists so i can come at the issue from the correct angles.


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Age-Dependent STD Infection
It seems that young females (comparing age 15 vs age 24) are 20x more likely to get chlamydia
from a single unprotected sexual encounter with an infected male.  What are the reasons for
this?  Are there other diseases with such extreme age-dependence?
Reference:

Estimating age-dependent per-encounter chlamydia trachomatis acquisition
risk via a Markov-based state-transition model.

The "Description of the analyzed data set" section seems suspicious to me:

In a nutshell, young women between the ages of 14 and 17 years old
were identified and recruited by the project.
...
At each follow-up visit during the study period, enrolled participants
underwent STI testing and treatment. Also at each follow-up visit, the
participants received follow-up interviews, in which they were queried
about the number of unprotected coital events since previous visit.
Most of the participations did not visit the clinic every quarter and left the project before its completion.
For our analysis, we collected 1173 quarterly test results from the
first 200 participants who were never infected and have completed at
least two follow-up visits. Their average enrollment age was 15 years
with standard deviation of 1.1 years.

It means that data is biased as for some reason most of girls were not able to participate in the study.
And I'm not sure about the correctness of your interpretation. I'd interpret it as "females are 20x less likely get chlamydia infection after being treated and warned about STD" as there were relatively continuous followed-up 15-17 y/o females and no older females. And I guess it was one of the goals of this "Young Women’s Project".

I'd like to simply ignore this paper too, but I'd also like to believe that the authors would have enough integrity to recognize and stop the error first!  I had thought there were other sources showing age-dependence, but now can't find them...

In this case the authors appear to imply that the mechanism is primarily the accumulation of partially protective immunity resulting from earlier infection.

From Table 1, we observed that 1) [p-bar] monotonically decreases as age
  increases; 2) [p-bar] decreases as q increases. [...]
The first observation support the concept that some degree of
  protective immunity against reinfection develops after first-time
  infection, although it appears to be partial at best [53, 54]. The
  second observation supports the concept that acquired protective
  immunity may restrict chlamydia replication in older persons [55].

There are quite a lot of diseases (infectious and non-infectious) with strong age-dependence - sometimes positively correlated, sometime negatively. For example, most severe disease associated with Plasmodium infection (such as cerebral malaria and severe malarial anaemia) occurs in infants and young children (source), while with chicken pox (varicella zoster virus) infection, adults and teenagers (or very young children) are more likely to develop severe disease and complications (source).


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What is the effective population size of a simple two deme metapopulation?
I am confused as to how to compute the effective population size $N_e$ of a theoretical structured population. Let's consider here a simple case study.
Imagine a 2-deme metapopulation. Each deme is of constant size $N$ with a (forward and backward) migration rate $m$. Mating is random within each deme.
What is the effective population size of such population? In other words, how fast does the population loses heterozygosity through time?

this book looks useful - see page 109 (there is restricted access) https://books.google.se/books?hl=en&lr=&id=pjo5FP5gpFIC&oi=fnd&pg=PA87&dq=effective+population+size+metapopulation&ots=J_z6Ygwl_X&sig=O0Op0mXXYKHdW2OweT8CJKew79Y&redir_esc=y#v=onepage&q=migration&f=false

There is no single effective population size when there is population structure. Suppose structure is strong, $Nm \ll 1$. If you start with very high heterozygosity, it will first decay at a rate close to $1/N$, then more slowly at a rate close to $m$ after the diversity within each deme has been lost.


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Can the respiratory quotient be calculated from a formula or must it be measured directly?
I found the following question on the Respiratory quotient:

A normal human diet has a  Respiratory quotient (RQ) of approximately 0.85. Given that pure oxidation of fatty acids has a Respiratory quotient (RQ) of 0.7 and pure oxidation of carbohydrates has Respiratory quotient (RQ) of 1, can one determine the fraction between the amount of oxygen used for aerobic respiration of the fat and the amount used for aerobic respiration of the carbohydrates?

My solution:
$$\text{glucose} + \ce{O_2} + \text{fat} + x \, \ce{O_2 \rightarrow} \ce{CO_2} + 0.7x \, \ce{CO_2} \, + \ce{H2O}$$
Note that I haven't balanced the equation excepted for $\ce{O_2}$ and $\ce{CO_2}$ where I added coefficients based on the given RQ. This equation gives $$\text{RC}_{total}=\frac{1+0.7x}{1+x} = 0.85$$
Hence $1+0.7x=0.85(1+x)$, which gives $x=1$, so the amount of oxygen used for Aerobic respiration of the fat and the amount used for Aerobic respiration of the carbohydrates is equal.
Is this correct?

Note: This is not really homework, but a question that can be seen as a more challenging problem. There are unfortunately no solutions for the challenge problems.

I'm not sure I follow the point of your question? are you just trying to be able to calculate a theoretical RQ based on the theoretical values for oxidizing 100% fat versus 100% glucose? - - - if that is the case, I don't think that's possible - (also, you have ketogenic and glycogenic amino acids that also can be oxidized that will also alter the RQ)


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Can a small polypeptide fold over itself and have a tertiary structure?
What I want to know is if polypeptides (those which are not considered as proteins) can also "exhibit" a tertiary structure.

Welcome to BiologySE! I don't think I'm following your question... can you be more specific? Polypeptides are proteins... what polypeptides "are not considered as proteins"?

@VanceLAlbaugh I think my problem comes from that direction. I understand that proteins are a specific case of polypeptides. Is this wrong?

a chain of amino acids connected through peptide bonds is a polypeptide - that chain is primary structure of a protein... there are some semantic differences... there is a nice overview of the basics of protein structure on wikipedia - basically what is covered in a basic biochemistry text...https://en.wikipedia.org/wiki/Protein_structure#Tertiary_structure

I believe the OP is referring to an old and outdated system of classification, in which all proteins are polypeptides but not all polypeptides are proteins: some books put a lower limit of 50 AA residues, others talked about 60 or 70 AA for a polypeptide being considered a protein. Once again, this system is no longer used (just check Lehninger, "Principles of Biochemistry").
But let's pretend that this system is valid and use it just to answer this question: can a small polypeptide that is not a protein, ranging from 2 to 50 AA lenght,  have a tertiary structure?
To answer that, we have to remember that the tertiary structure is not (as some defines) simply the "3D structure of a polypeptide". After all, a single amino acid has a 3D structure, as any molecule indeed. The tertiary structure is the specific 3D format of the polypeptide, but due to interactions of its amino acid side chains.
So, the question is: can a small polypeptide fold over itself and have a tertiary structure? The answer is yes. Apparently, peptides with more than 10 AA can fold: http://www.ncbi.nlm.nih.gov/pubmed/12729764

Just one more thing. Does the current system of classification have a name? Or can you summarize the idea? Thank you in advance.

I don't think so. I know the "old system" because I started giving classes in the early 90s, and some books used it. But today we don't set a limit of AA to define a protein.

Your instinct is valid, there are other molecules which can be defined as having tertiary structure.
The most common example is RNA, which can fold into a vast array of conformations. These can be part of ribonucleoprotein complexes like telomerases, spliceosomes, or ribosomes or they can function on their own like tRNAs and many ribozymes such as RNase P. An example of a common tertiary structural motif in RNA is the pseudoknot; a haripin loop in which some of the bases in the loop have base paired to another portion of the RNA molecule.

It is also possible for DNA to possess tertiary structure, though the term is used less often when referring to DNA. Usually DNA tertiary structure describes topological structures formed by supercoiling, protein scaffolding, etc. However, DNA can also form cruciform motifs similar to RNA hairpin loops (though it is less common). If multiple cruciform motifs and other structures were to interact in three dimensions, this could be another form of DNA tertiary structure.

You may also be interested in DNA origami, in which 3D building blocks made from DNA are assembled in desired ways by using sequence complementarity (generally).
I think that polysaccharides and oligosaccharides are also sometimes referred to as having tertiary structures, but I don't know as much about those. I encourage you to look into pectin, amylopectin, branched oligosaccharides, etc in the context of tertiary structures.

All this information is very useful. Thank you.


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Why does crippling pain exist?
Some kinds of trauma can cause pain so severe that it makes you unable to move or do anything at all.
It may put you out of action and unable to help yourself because of how excruciating it is.
Although I understand that pain is necessary to alert the brain that something is wrong and need to be fixed, I imagine it like an alarm going off alerting about trauma. But a crippling pain would be like a deafening siren hooked up to your ear making you unable to do anything to correct the problem, instead it might send you into a shock. It would be total disaster which could prevent you from taking any step about it. So, why does excruciating pain exist? Or in other words, why has this feature not gone extinct during the course of evolution in spite of its harmful effects?

Pain tells your body that something is wrong and needs to be fixed. Crippling pain is telling you that the "something" is an immediate danger to life or limb, and needs to be paid attention to NOW. Continuing on with your normal activities will be severely detrimental to your health.

@MattDMo but what good is it if you can't do anything more than moaning, rolling and eventually dying from shock while if it wasnt crippling you could have done something to save yourselves like moving to safety or applying pressure to bleeding wound etc that would have avoided death

To this point, I would like to tell you an incident which I saw once on TV (so I don't have reference for it). Once a mountain climber fell from height ~300m straight on a rock. Her hip joint, both knee joints, and some bones broke & she fainted. When she was unconscious, her brain decided that the pain is too excruciating to do anything and should be switched off (by endorphins). When she woke, she didn't feel any pain and somehow reached paramedic camp. When she reached, then she started feeling pain again.


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Insect species identification

I think it's a moth and need further identification like scientific name, order and family.
The picture was taken on May 30/2016 in my university laboratory window in South Korea. At that time there were so many moths on this building. The temperature was also high and it was also daytime around lunch time. What I want to ask related to flying time is do moths fly at daytime? as far as I know moths are nocturnal. Please clarify this too if this insect species is moth.

Hi, maybe you'll find these hints helpful in improving your question: http://biology.stackexchange.com/help/how-to-ask. Temperature was high... high for where? Also do moths fly in the daytime is a seperate question, as is are all moths nocturnal.

@ Troyseph what is wrong with my question,Sir?

It was poorly formatted such that the picture wasn't visible and you had a block of text with random '[' characters in it. You ask multiple questions. You show no attempt at your own research into its type. You gave details which are completely useless to us, i.e. the temperature was high... did your building have the heating on? Do you live in Florida or Iceland? is high 24 degrees C or 34 degrees c? Please put some effort into your question so that someone might put effort into an answer for you =]

@ Troyseph I think it's better to focus on answering the question rather than editing the grammar since there is n o misunderstanding. lol If it's useless and do not know the answer just stop criticizing period

I wasn't criticising your grammar, spelling or punctuation. Please read the guidelines and take my advice, then your question will be clearer and easier to answer.

@Meti please [edit] your question and post where exactly the picture was taken. in my university laboratory window is not helpful at all. I would also strongly suggest you take the [tour] and read carefully through the [help] to learn more about the site. Editing of questions (and answers) is encouraged, subject to some guidelines. You should also read this Meta.SE question, especially the section Editing and Formatting.

Am very sorry @ Troyseph I didn't know that. @MattDMo I will take all your suggestions and advice into consideration.

It is a moth and all moths and butterflies belong to the order of Lepidoptera. Based on the shape of the forewing and the orange color of the hindwings I think this moth belongs to the genus Catocala https://en.m.wikipedia.org/wiki/Catocala, see also here for some pictures.
EDIT:
theforestecologist did a excellent suggestion that this might be Catocala streckeri based on the wing pattern. This species does occur in Korea, see this website for a distribution map. So it may indeed be Catocala streckeri. However, Asia is very rich in Catacola species, and I know that this family often has species looking very alike, so I can't say with 100% certainty.
Most, but not all, moths are nocturnal. Some Catocala species are known to fly on sunny afternoons (Waring&Townsend 2006).

thank you for your response. The picture was taken in South Korea.

Catocala streckeri seems like a pretty good guess given the wing pattern. I'd add it as my own answer, but obviously cannot because the question is closed.

@theforestecologist: excellent find. I'll add it to my answer.


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What made this black cluster on a leaf?
I found this black slug-shaped thing on a leaf by my pond in western Sweden. It's about 15 mm long, positioned on a vertical leaf (I bent it to take the picture).

And I don't even know where to start looking. I was thinking it might be an egg cluster, but can't find anything useful without knowing at least what kind of organism made it.

@Canheguess I can't see any parts that I recognize as a larva (head, legs) and it's been completely still for at least 24 hours. Possibly a pupa I guess?

If you see them hatching can you take a photo of that too? I've wanted to see one of these for a long time but never found one.

Nice picture and good question!

After a lot of scrolling through image searches I stumbled upon the answer: this is the egg mass of some sort of horse-fly (Tabanidae). Almost identical egg mass here: http://bugguide.net/node/view/21171

I'm assuming I won't get a more specific answer than this.

Thanks for giving an answer yourself. I was really curious. :)

@AlexDeLarge Yes, me too! (Obviously enough to keep searching, compensating my lacking biology skills with patience.)

I am impressed! +1

Try to hatch them! Another nice picture is found here, which includes recently laid and mature eggs: http://www.pbase.com/image/132217026

@fileunderwater Good idea! But I'm not sure I want to handle a bunch of horse-fly larvae, I would really prefer it if I could watch it happen out where I found it. It's just 50 m from my front door so I could go check it out quite often. Today is the third day that I've seen it in this black "mature" state, so it should happen within a couple of days (6 days seems to be a normal time until hatching) This page http://animaldiversity.org/accounts/Tabanus_similis/ says that they all hatch at once, so it's probably easy to miss!

@picapica You can put the leaf section in a jar (with very small holes for air). When little horseflies hatch out, you can choose their fate :P

picapica , if these are horsefly eggs (which I'm pretty sure looking at BugGuide), do you have many in your area? And do they bite you? I've been bitten by deerflies and they hurt! But never horseflies as they're slow and noisy. Easier to avoid

@Jude Yes, we have quite a few of them around. Mostly to slow to be a problem, but sometimes they manage to bite. The bite is a little bit painful, and then the swelling and itching is worse (but the reaction is very different from person to person).

Thank you! Any deer flies? I'd assume so if horseflies are around.

@Jude Those too! In Swedish (at least in my usual vocabulary) we don't have separate words for the different kinds of Tabanidae, so I can't really tell if some are worse than others.


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Binding kinetics of 6xHis-Tag
For the planning of an experiment I would like to know the binding kinetics (kon and koff) of a 6x-His-tag to a Ni-NTA surface.
I know they should differ due to surface quality and position of the His-tag in the protein. But maybe there is some literature out there (that someone of you knows) from which one could get at least a rough estimate of the kinetics.

What sort of research have you done so far? Both Entrez PubMed and Google Scholar have very good search functions.

It seems I didn't look thoroughly enough at the results PubMed and Scholar returned yesterday. Hope it helps someone in the future…

Some more hours of literature research finally produced a result:
As published by Khan et al. 2006 6x-His-tag has two distinct dissociation constants of koff1 = 6.3 10-3 and koff2 = 1.8 10-3.


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Has research indicated how much koinophillia preferences are learned vs insinctual
I'm curious about rather the definition of 'normal', as it affects  koinophillia & mate choice, is something instinctual or learned.  To clarify I'm not asking if koinophillia itself is instinctual (I take that for granted), but instead the definition of what constitutes 'normal' vs 'abnormal' for a species which drives instinctual attraction via koinophillia.
Basically, does the definition of normal get affected by those around an individual as they grow and/or select a mate?  Can a trait that would be considered abnormal for a species be considered accepted or attractive if it is common amongst a small subset that the individual spent time in?  For instance, has any study be done in which an animal grew up among a large number of 'abnormal' phenotype animals to see rather the would later be drawn to mates that look like the peers they were raised around or the more normal appearance for their species?
In fact I'm particularly interested in the case of humans.  Does anyone know if koinophillia and attraction is affected by the environment one is raised in?  For example if someone was born in an isolated island where their populations physical features were rather unique and there was limited genetic variation/gene flow from outsiders but was raised in a family/community of people on the other side of the world with very different physical traits has a study been done to indicate rather they are more likely to be attracted to individuals from their home island, individuals that look like the community the were raised in, or no strong indication either way?