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Why pouring salt in the wounds is painful?
Pouring salt in the wounds is so painful. I am sure you all experienced this. whats happend there?

De salt particles are alien bodies and can damage the tissue by mechanical means (This would also happen if you pour sand into an open wound). Also, the exposed tissue is vulnerable to dehydration, wich happens faster if the osmotic pressure is higher. Finally, nerve tissue is particulary sensible to changes in the ion composition of its sorroundings, so the added sodium may affect the action potential of the nociceptors.


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Are there any studies on the fertility levels of humans/mammals as a function of their stay at Antarctica?
Wikipedia, and Space.SE seem to indicate humans become infertile in space due to the increased exposure to cosmic rays. Knowing as we do that Antarctica is holey, and subject to increased radiation (atleast UV if not broad-spectrum), I find myself wondering whether any studies on fertility were ever conducted on that continent.
So ... Are there any studies on the fertility levels of humans/mammals as a function of their stay at Antarctica?

I haven't been able to find a study on fertility, but it would be important to note the difference between radiation considered.  The dangerous radiation discussed in both of your links are cosmic rays as you noted.  Our main defense against this sort of radiation is the earth's magnetic field.  The hole you are talking about is in the ozone layer, which is much more important in UV protection than cosmic ray protection.  The amount of incident cosmic rays is slightly more at latitudinal extremes due to the deflection away from the equator by the magnetic field, but this is only 1.5 to 2 times greater, see fig. 8.
Unless we figure out how to punch a hole in the magnetic field as well, the main threat in the arctic is skin cancer from UV, not infertility from cosmic rays.

Agreed on your final remark. A study would still be atleast partially relevant with the ATS coming up for renewal in a decade or so ...

I've found a number of health-related reports but none of them have mentioned radiation in that way.  Only radiation-related health issues I could find is this, which is fascinating.. apparently the US ran a nuclear reactor in Antarctica for a decade from the early 60ss to early 70s.  It was complete with 438 malfunctions and a rather sizable spill.  http://www.vbdr.org/meetings/2012/Presentations/McMurdo_Station_Nuc_Reactor_Final_Report-Sec6-OCRed.pdf

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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What is the best color for a PPG signal (photoplethysmography)?
What is the best color for a PPG signal?
Red, green, blue or infra-red?
I'm asking because commercial oximeter sensors usually use a pair of red and infra-red LEDs. But recently, I've seen a lot of sensors using green LEDs.
Thanks.

The reason red and infra-red are used is the difference in absorbance at those two frequencies between oxygenated and unoxygenated hemoglobin. Using the difference in these two frequencies allows the concentration of oxyhemoglobin to be calculated. (The red LED is at the frequency where oxyhemoglobin and hemoglobin have identical absorbance).
As far as I know, there's no reason why a green LED wouldn't work. You would only be able to measure the PPG signal and not the oximetry data (unless you used two different LEDs and did some math).
Absorption curves.

Found the difference in colors :
Longer wavelenght penetrate deeper.
because main artifacts are caused by changes in the blood volume at the measurement site. During movement, the changes in venous blood volume are larger than those in arterial one. While the penetration depth of light is dependent on its wavelength, and green
light do not penetrate as deeply as infrared light. Therefore, the green PPG would include less information from various non-pulsatile sources than the infrared PPG.

I also looked up multi-spectral ppg and from what I read they all give you an exploitable PPG signal, it really depends from what you want to do.
For oximeter you need red and ifr light source. but if ou just want a pulse meter shorter wavelenght are better.
Sources :
http://embc.embs.org/files/2013/3170_FI.pdf
http://www.biofotonika.lu.lv/fileadmin/user_upload/lu_portal/projekti/biofotonika/Publikacijas/A3/Asare_8073_76_Praga.PDF

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Visualizing secondary RNA structure binding to target
I am designing synthetic ribozymes, and need to see the secondary structure that arises from its flanking arms binding to a target mRNA. I've used Mfold as well as IDT's OligoAnalyzer (Hairpin), but these only allow from prediction of secondary structure of the ribozyme folding on itself (which is thermodynamically less stable that 20-40 perfectly complementary nucleotides along the arms).
Is there any software that will allow for simultaneous prediction of secondary structure of two RNA molecules?

there is a software called UNAfold (same website as mFold) which allows nucleic acid hybridization.


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If a dead snake reflexively attacks itself, why does it not always attack itself?
Recently there has been this video going around of a snake that had been decapitated.  Its body swung around to the decapitated head and the head attacked the body on "reflex".  Now we know that most reflex arcs bypass the brain.  So if it is the case that this strike attack is reflex then how is that suppressed when the snake is alive? Why aren't snakes always reflexively attacking themselves?
Here is the video.
Is this some other phenomenon than reflexive attack?

It seems that National Geographic were just as curious, in their interview in this article with James Murphy, he states the answer to your final question - that even though the snake is dead, it can still reflexively 'attack' the nearest object - in this case, the remains of its own body - as it is not attached, it is a 'foreign object' and the reflexes result in an 'attack'.

I guess one can presume that from reading that article but it is not clear.  "That’s what is available, that’s what is next to him. Even when you take the head off, a snake can continue to bite and open its mouth. "  Yes that is understandable but then suppose its tail slithered by the snake's head when it was attached and the snake was alive... What would prevent that same reflex to not strike?  Or is it only a reflex for dead snakes?

I think it is reflexive for a dead snake, as any higher order processes (higher than reflexes) have ended on death.

+1 to Damien, just a few more thoughts.
If you notice it took several whacks of the head to get the bite reflex to trigger. I know that many animals have reflexes that will suppress other reflexes so that fluid motions can be achieved (righting reflexes are examples).
I don't know if anyone has studied the species enough to know this definitely, but I bet that snakes behaviorally/reflexively doge their own tail so that they don't keep hitting themselves in the head.  After the head is severed, higher level restrictions are lost, fight paths are probably lose inhibition, and the reflex to bite anything hitting you in the mouth takes over.  That said it probably had to hit the mouth just right to get this to trigger.
I'm looking for some definitive information on bite reflexes in snakes, and will edit if I find anything relative.  I have experience from studying amphibian reflexes years ago, and I have feeling this general trend will hold true for snakes (but I'm looking for someone who has actually studied it).

Interesting. Yes perhaps there is inhibitory behaviors or reflexes to avoid the snake's tail bumping into its face, thus avoiding the strike.  I am interested if anyone ever studied this, but you are probably right.


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How do plasmids protect themselves against restriction enzymes?
How do plasmids protect themselves from restriction enzymes released by bacteria (i.e., against bacteriophages)?

The strains that we use in the lab have defective restriction machinery.
In the case of DH5α it is mostly because of the endA1 and hsdR17 mutation. The former mutation eliminates an endonuclease that can degrade plasmids and the latter one eliminates the restriction system.
Check this.

What about the plasmids naturally present in bacteria ?

usually they are compatible and have undergone methylation at these restriction sites. since you compared it with immune response i'll give you an analogy. The proteins that are already present in the system are not considered antigens because the immune system actively tries to not launch a response against them. Similarly the natural plasmids are marked to be treated as endogenous. You may ask how they acquired the plasmids in the first place which is something like a chicken-egg question; the likely explanation is that they acquired it during the time of stress (nutrient deprivation etc)


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What is the advantage of restriction enzymes cutting only at specific sites?
Bacteriophages have sequences which often do not have specific sites for restriction enzymes of bacteria to cut at and so can attack the bacteria.
Wouldn't it be better if bacteria had something "universal" like an enzyme that simply cuts the nucleotide sequence "randomly"? Is there any particular advantage of cutting at only a few restriction sites?

Such universal restriction enzymes would be very dangerous to leave lying around even if contained within a vacuole. Remember that bacteria are prokaryotes and have no nuclear membrane to protect their DNA.
The analogy would be having a burglar alarm capable of burning down the house in order to protect it against thieves.

But bacteria can definitely protect against it by methylating their own DNA or by any other mechanism.

You mean methylate the entirety of their genome?

You are right , it would be really difficult . Thanks !

Methyltransferase is just an enzyme.  The cost of failure seems high if a reversible reaction must protect each and every codon.

Yes ..In case of restriction sites , they would have to methylate just those areas.

So can I say this is a compromise between protecting the bacteria from any bacteriophage and the cost of continuously maintaining a methylated genome ?

Sometimes the best defense is a good offense.

Notice that viral DNA is not the only foreign DNA that a bacterial can meet during its bacterial adventures. Plasmids, conjugated DNA and DNA inserted by transformation exist, and it may confer ecological advantages. Because of that, even if the enzymes would recognize only non genomic DNA and destroy it effectively, it's still more useful to have some criteria and allow to stay some alien DNA, while destroying some other.
Restriction sites are pretty small, so the chances of getting one target in a viral genome is quite big. Bacterial DNA is protected by methylation, which is recognized by this enzymes and prevents them to break the DNA.
Restriction enzymes are not the only means bacteria have in order to defend from foreign DNA. Bacteria usually carry exonucleases that recognize single stranded DNA and linear DNA, which is common in viral genomes, but not in non-infected bacterial cells. This enzyme lacks the specificity that restriction systems possess, and can work combined (for instance, a restriction cleavage may form linear DNA, which will be detected by exonucleases as potentially harmful DNA).
In addition to this, bacteria and archaeons have a special antiviral defense, named CRISPR-CAS system, that acts like an immune system. CRISPR-CAS inserts in a special region of the bacterial genome viral DNA fragments from previous infection. When a new virus infects the cell, those viral fragments are expressed as a special kind of RNA (CRISPR-RNA) which, if the virus has already infected this cell, will attach to viral DNA and will serve as a marker. Then, the RNA-marked DNA is recognized by special nucleases. This defense system allows to obtain acquired resistance that (unlike vertebrate immune system) is also inheritable.
Concluding, not all foreign DNA is harmful, since plasmids and other could provide some advantage to the cell. Restriction-modification systems aren't the only defense system that the bacteria has against foreign DNA, but all of them must be able to differentiate between desirable and harmful DNA. The combination of many different defense systems allow to patch the limitations of them individually, and so different species will invest differently in one or other, depending of the ecological pressures they have to face.

Restriction enzymes are only half of the system. The other half is the methylation system. The majority of restriction enzymes won't cut at their target site if it is methylated in the correct way. The system works to identify foreign DNA because the foreign DNA is not methylated in the correct way so it will be cut but the bacteria's own DNA is methylated so it will not be cut. Think of it as a lock and key mechanism.
A generic DNAase wouldn't be able to function in this fashion.

There are generic DNA cutting enzymes! E.g. DNase A  (journal), DNase I  (wikipedia), and NucA (Bacillus subtilis annotation). The outer layers of human skin contain active dnase, with just such a protective role as one apparent reason. This is one of the (many) sources of contamination that can mess up dna experiments.


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Statistics on energy consumption breakdown per biological functions across organisms?
Are there any statistics available on how much energy organisms use for each biological functions (i.e. something similar to the line of "Bacteria spend X% of energy on information processing, Y% for tissue maintenance and Z% for locomotion. Mammals spend..."). I'm particularly interested on how much energy is spent on information processing.
I vaguely remember seeing such stats somewhere, but for the love of god I can't remember where...

Out of curiosity, what do you mean by information processing? I can see this being used in several ways in biology: transcription/translation, signal transduction, you might even make an argument that some forms of enzyme binding kinetics are information processing (identifying the correct input from a sea of possible inputs). Of course also these numbers would only be meaningful in very specified and constrained environments.

In bacteria this has been studied in great detail for cells growing in steady balanced exponential growth. The classic reference work for this is Physiology of the Bacterial Cell by Neidhardt, Ingraham, and Schaechter: http://www.amazon.com/Physiology-Bacterial-Cell-Molecular-Approach/dp/0878936084 . Over the course of a few chapters they painstakingly identify how many ATP molecules are consumed for each process, from replication, transcription, translation, cell wall synthesis, etc, over the course of a single cell cycle. Not sure if this has been done in eukaryotes.

@A.Kennard: I mean the energy spent on sensing external stimuli (light, sound, pressure, smell...) and making decisions based on it. I realize making such categorization would be very hard and error prone (just like in real economies, I guess), but I imagine it could still yield interesting insight, like parasitic insects can get away with only x% while mammals typically have to spend y% etc.

Awesome. You're right that the categorization may be difficult, but I absolutely see the potential interest. Narrowing down the question like this to the fraction of energy consumption in signal transduction already makes it more tractable.
Complementary to your question about energy consumption, are you aware of the bioinformatic research on genome reduction in parasites? I think interesting trends can be observed comparing the loss of signal transduction proteins compared to other protein groups. An example of this type of analysis: http://ijsb.sgmjournals.org/content/54/6/1937.full

This is not a proper answer. Bear with me. I'm in a hurry; will edit the answer to a decent form when I find time.
From the abstract of this paper:

Of the 80% of oxygen consumption coupled to ATP synthesis,
  approximately 25-30% is used by protein synthesis, 19-28% by the
  Na+-K+-ATPase, 4-8% by the Ca2+-ATPase, 2-8% by the actinomyosin
  ATPase, 7-10% by gluconeogenesis, and 3% by ureagenesis, with mRNA
  synthesis and substrate cycling also making significant contributions.

Also check this out.


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Genetics - Is this hybridization possible?
Suppose you hybridize two plants - One has a red flower and a long stalk, the other has a pink flower and a short stalk. This resulted in these 4 type of plants, with ratio 1:1:1:1

Long stalk red flower
Long stalk pink flower
Medium stalk red flower
Medium stalk pink flower

What possible genotype could the parents have that would result this way?

Do you mean "genotype"? Unless I'm missing something, it seems like you've already described the phenotype (red/long and pink/short) of the parents in your first sentence.

Flower Color
A Heterozygous (Rp) x Homozygous recessive (pp) cross can produce the distribution:
         p      p

   R    Rp     Rp  = Red, Red

   p    pp     pp  = pink, pink

Stalk Length
To me, there appears to be another allele involved or a lack of allele, and definitely Co-Dominance. The only way I could think of a way to get the ratio of stalk lengths in the question after a few minutes thought is if one of the plants are missing a gene before the cross (akin to Turner Syndrome) - the example that follows puts the missing gene on the Short-stalked parents:
SS = Short
TT = Tall
ST = Medium
SX = Short
TX = Tall
X = Missing Gene / Nothing
         S      X

   T    ST      TX = Medium, Tall

   T    ST      TX = Medium, Tall

So ultimately the cross would look like this:
        Sp     Xp

   TR   STRp   TXRp = (#3), (#1)

   Tp   STpp   TXpp = (#4), (#2)


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Are there more/less favourable phases of menstrual cycle to donate blood?
I was wondering whether it makes a difference when during the menstrual cycle a female is donating blood in terms of:

Blood quality (iron or hormones levels)
Her health/safety

I am aware that females can donate blood during menstruation as the blood they lose does not directly come from circulatory system and the amount is not that big after all. As for the hormones - their levels do change considerably during the cycle and can affect a whole range of things. Can they also affect the blood quality or are such fluctuations rather negligible?

1)
Hormones involved with Menstruation (FSH, LH, Estrogen, Progesterone, etc.) will vary depending in concentration depending on the time-frame:

You are correct in saying that not much blood is actually lost in the menstrual fluid: Less than 80mL (80cc), although the blood's origin is ultimately the circulatory system. Does it affect the quality of the blood? No. Usually not enough iron is lost during menstruation to make a difference between being able to donate blood and not donate. However, women who bleed heavier than the average can experience anemia (iron deficiency) - although anemia attributed to menstruation is often misdiagnosed gastrointestinal issues (up to 86% error rate).
One thing to consider is that common pain medications can affect blood content, and thus a woman taking aspirin cannot donate platelets for 5 days after she stops, and a woman taking NSAIDs (like Ibuprofen) cannot donate for 2 days after she stops.
2)

...the combination of blood loss from periods and donation will make iron deficiency anaemia more likely, particularly if the periods are heavy or prolonged. This effect can be minimised by taking supplemental iron.

In general, as long as the woman feels well or the pain is controlled, she is perfectly capable of donating as long as her iron levels reach the minimums. The blood makeup is not significantly different, although hormone and iron levels will minimally fluctuate.

As always, this response is based upon information during some light research. I am not a doctor, and the information presented in this response may be modified later to increase accuracy or remove errors upon the discovery of new information.


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What is a DNA-binding domain?
I am confused about the term DNA-binding domain. Does it mean that there are some parts of the DNA that tend to coil up? Does it happen because some proteins tend to stick around that area? Also it is my understanding that with some proteins DNA (say for bacteria like E. coli) tends to coil up. Do we know what is the approximately the size of these coils? What is a ‘motif’ in this context.

Welcome to Biology.SE!
The term "domain" in biochemistry and molecular biology is usually used to refer to a part of a protein that has a conserved structure and function, is similar between related proteins, and can generally exist or function on its own if it was separated from the rest of the protein. A DNA-binding domain is a protein structure that has a high affinity for DNA, and so binds to it when the two molecules are in the same vicinity. An example is a type of protein called a transcription factor, which binds to DNA in the nucleus of the cell (in Eukaryotes, bacteria and Archaea don't have nuclei - the DNA just floats free) and causes changes in the transcription of genes. The following image from WikiMedia shows how transcription factors work in general.

"DNA coiling" is a very generic term that describes many different things. The basic structure of DNA itself is a coil, with two sugar chains (the deoxyribose in DeoxyriboNucleic Acid or DNA) coiling around each other, and attached by nucleic acid bases. In the eukaryotic cell, individual strands of DNA are associated with structural proteins to create chromatin, which is what makes up chromosomes in the nucleus of each cell. In the first stage, naked DNA is wrapped or coiled around structural proteins called histones into a structure called a nucleosome. These then stack into a "solenoid" or fiber structure, which makes up so-called "relaxed" chromatin - regions of the genome where active transcription is taking place. If a part of a chromosome has been marked as inactive, or during certain steps in the cell cycle when one cell splits into two (mitosis), the fibers further coil into condensed chromatin, forming the typical structure many people associate with chromosomes. This image, from Wikipedia, visualizes each step in the process.

The word "motif" can sometimes mean the same thing as domain - for example, someone might refer to a "DNA-binding motif" in a protein. However, a motif is typically smaller than a domain, can occur in DNA, RNA, and proteins, and has to do with the specific sequence. A "structural motif" in a protein is something like a helix-loop-helix or a beta-hairpin turn that can appear in multiple different kinds of protein domains, and doesn't necessarily have the same exact function in those different domains, but typically has a fairly conserved sequence that is very similar. As an example, the zinc finger motif is found in protein domains that bind DNA, RNA, and other proteins.
All of this terminology can be very confusing at first, but if you stick with it it'll get easier over time. Biochemistry and molecular biology are fascinating fields, so keep up your studies!

Does "binding" mean the protein attaches to the DNA? In the figure the pink protein seems to attach to the DNA.

@anvSnMusater yes, binding means that the protein and the DNA are attached to each other, but they can separate later.

Thanks, finally, I want to ask you, does the binded protein fold the DNA?

It can, especially if it is part of a large complex of proteins, like those involved in replication or DNA damage repair.

This answer is vastly overweight. You should use your discretion in choosing illustrations. The first is especially incomprehensible. Do you really expect the poster to be able to follow it?

@David who cares? The question and answer are 3 1/2 years old, and my answer has apparently been found useful by at least 6 people, so it's not all bad. Remember, the point of Stack Exchange is not to just help the OP - in fact, that's only a side effect. The point is to assemble a compendium of knowledge in Q&A format. I link to all my sources in case the reader is in need of more details or explanation. Additionally, the meat of the answer is really contained in only three paragraphs, which I wouldn't characterize as "vastly overweight."

@MattDMo — didn't notice it was you, but there it is. That's how I see it.

Domain and motif are indeed related, but I would think that domain indicates the region in a protein (or DNA) involved in the function (be it DNA binding, catalytic etc for protein / transcription factor binding etc for nucleic acids), while motif is used to describe the particular sequence of building blocks in that domain / region. Motif is used to indicate the particular amino acids that one typically finds in the protein domain, but also to indicate the particular nucleotides in a DNA/RNA strand.

can you add some references to back up your answer? it would definitely add strength and credibility.


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Is this case Histoplasma capsulatum?
A 62 year-old male was admitted to the hospital complaining of shortness of breath. His chest X-ray showed a rightsided cavitary lesions. His medical history indicated he had smoked one pack of cigarettes per day for past 40 years and has had cavitary tuberculosis in about 20 years ago. Recently he is receiving cytostatic therapy for his acute myeloblastic leukaemia. A biopsy specimen of the lung was obtained. Biopsy from lesion shows tubular eukaryotic septated hyphae with diameter of 510 μm that are infiltrating the lung tissue. Culture on Saboraud’ media shows conidia with spores in radiating columns. Which is the most like cause of the findings?
The disease is systemic - affecting lungs.
Organism has septated hyphae with conidia.
Is there any other possibilities for the disease?

Any more information about the pathology?  IPA? Sloughing, consolidation?  IF we had a little more info we might be able to shed more light.

Is the hyphae diameter really 510µm? That seems exceptionally large.  Could this be the length instead?

Is there any other possibilities for the disease?
Yes.  At 37°C, Histoplasma capsulatum usually doesn't form hyphae.

Were the hyphae branching, like this?
If "conidia with spores in radiating columns" means the pictures below,
We have enough to say that this is not a case of Histoplasma capsulatum and there is definitely another possibility for this disease.
Conidia with radiating chains of spores is pathognomonic for aspergillosis.

I do not know if hyphae was branching like that. I have only the text. It is at least septated hyphea like in your picture. No information about temperature where the sample is cultured. Histoplasma capsulatum is a possibility here.

Not the temperature of the culture, the temperature of the biopsy—because the patient is still alive, you have reason to believe that the biopsy was warmer than 30°C. As explained at the previously linked site, H. capsulatum is dimorphic, growing as a mold at room temperature and as a yeast at body temperature.

Tissue morphology
Histoplasmosis: Small narrow base budding yeast cells (1-5um; 5-2um in var. duboisii)


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Bee (?) identification
I live in Michigan.  I just saw a bee that I think I've seen before, but only this time was I so struck by its uniqueness and - for lack of a better word - scariness.
I'll describe it.  It was maybe an inch and a half long.  Maybe bigger, maybe smaller (I'll admit that I was hurrying to get away from it).  It looked like a queen bee, but longer and slightly thinner.  However it had wings that were very profoundly orangish-red.  Like burnt orange maybe.
I haven't been able to find any matching pictures online.  It is theoretically possible that it was covered in pollen, and I am incorrect about what I think I saw, but assuming it wasn't (as I do believe this isn't the first time I've seen this guy or one of his friends), does anyone have any clues as to what this could be?
EDIT:  PHOTOS
After considerable patience. I was able to capture some photos of this guy.  One of these photos is post-processed a little to emphasize the color.
A couple things about these photos.

They were extremely difficult to take because the bee never stops moving.  I don't know if this behavior is useful for identification, but he is always in the same place (in front of one house), and he flys back and forth between a small crack in the sidewalk (a nest?), and between 5 and 10 feet away.  He moves like a dragonfly (that's the best way I can think to describe it), and he doesn't stop - he'll seem like he is going to land, and then flies off.  This morning was an exception.
These photos do not fully capture the depth and vividness of the redness of his wings, nor do they adequately convey just how large he is.

"Thin" and the red color of the wings makes it sound like a bit like a hornet, as Damien says. Here in Asia, I'd guess the Japanese Giant Hornet, but it doesn't range to the US, so maybe a similar species? Although if you do think it's a bee, often the scarily large bees you see in the US are carpenter bees. They're on the rounder side though, so perhaps not.

Well - I've seen pictures of the scary Asian hornets, and the body type isn't all that far off.  I only say thinner because it was longer, but the overall body shape came closer to a large furry bumblebee than to a yellow jacket.   It resembles a big Queen bee in shape and overall appearance more than anything else.  Definitely did not look like what I commonly associate with a hornet or wasp.  Do carpenter bees match that description (with the red wings as well)?

Nice pictures! From the back pattern, size, and antennae shape, I'd say this is very likely a Cicada Killer wasp (Sphecius speciosus), cf., for instance, this picture taken at a similar angle to yours.
There are many good resources online about Cicada Killers, including this page from the MSU Extension Office, and the Wikipedia entry Sphecius speciosus.
It would be interesting to see if you could find the distinctive burrow (photo / video) of your resident wasp!

Interesting observation about the flight patterns seeming similar to a dragonfly. It's possible you're seeing flight strategies that are good for aerial predators, like dragonflies and Sphecius. I imagine a pollen-gathering insect's flight might look very different.

Wow!  That is almost certainly what it is.  The links were great.  I especially like how the first one mentions people having reactions just like my own.  Thanks!

And reactions like my own, in guessing that it was a Japanese Hornet!

Regarding the flight patterns - that's an interesting correlation.  It sounds logical.

@Oreotrephes, is there any particular reason you didn't embed the image you linked? From a UX viewpoint, it's surely better to embed? Are SE services really so hammered by doing so? If the answers to those are "embed", I'll take that as "go ahead" and do it myself as an edit... the only explanation for "no way", is perhaps users would be "too scared" to see such a "graphic image"?

@hello_there_andy for SE I tried to avoid embedding pictures that were not creative commons shareable, see for example my answer to http://biology.stackexchange.com/questions/9576/goats-are-so-fearless-but-sheep-are-not-is-there-any-genetic-difference-respons/9577#9577. However, I don't know whether there's now a meta consensus for this. I'd say best way forward if you want to embed is to ask for permission from GCMGA.

Handy info @Oreotrephes, thanks. Also nice goat pictures in that answer :)


text:
What animal's lower eye lid moves to upper one when closing eyes?
I know cock's lower eye lids moves to meet the upper one when it closes its eye.  What other animals does this?  BTW, "cock-eyed" can mean upside down, I think.

Actaully there are quite a few animals which actually moves there lower eyelids:

Most of the birds
Reptiles(Except Snake)
Amphibians

Are you sure? https://www.youtube.com/watch?v=dgh6ABfdlAU shows a hawk's nictitating membrane moving from sidewise.

Nictitating membrane (inner eyelid) of sharks can cover sharks eye as it moves from the upper to the lower eye lid (http://en.wikipedia.org/wiki/Nictitating_membrane).


text:
How can fruit flies and mice share the same gene that says to build an eye if they evolved separately?
I saw a documentary where they inserted the gene of a mouse that basically is the starting "build an eye" command into a fruit fly, and a fruit fly eye grew. My question is, if eyes of different types of animal had different evolutionary beginnings (I don't know much about arthropod eye evolution, but for a different example, as I understand it, cephalopod eyes evolved from skin cells while vertebrate eyes evolved from brain cells), then how is it that the same gene controls the growth of two such evolutionary different eyes?

Both fruit flies (Drosophila) and mice (Mus) are classified  under Bilateria.
The presence of such a highly conserved sequence in both species suggests that they share a urbilaterian ancestor who also used a similar gene to turn on eye formation (not create the whole eye, just start the process).
Even though the structure of insect and mammalian eyes diverged evolutionarily after the common ancestor, the switch that starts eye development worked so well there was little need to change it.  I suppose one could say that it remains backwards compatible.

Okay so to clarify one point, going back to the example of cephalopods, which are also Bilateria, if one eye evolved from skin and one eye evolved from brain tissue, how can they have the same origin of the eye? Was the brain and skin part of the same thing in the common ancestor?

Yes, in a way.  The outermost layer of a gastrula, the ectoderm, gives rise to both skin and neural tissues.

So the first bilateral animals had a mush of quasi-skin neurons for an eye or what?

Perhaps something like we see in the chiton, not quite an eye but definitely light-sensitive.  But as a soft-bodied animal without the mollusc's shell, there was usually very little left of early bilaterians for fossil records. Another intriguing example of the skin--brain conection is the parietal eye still seen in some ampibians, fish, and reptiles.

The documentary was probably talking about Halder's paper in Science (Science, Halder et al., v.267). If you'll read the abstract (especially the bottom part) You'll notice that the gene is a control gene that is responsible for starting a chain of interactions at the end of which the real fly-specific 'eye-building' process begins. Basically this is like using the same kind of electrical switch to turn on the light in your room (mouse) or an air conditioner (fly).

I understand that part. My question is how is it that they both use the same genetic switch if arthropod and vertebrate eyes had completely different origins? Wouldn't they each have their own unique switch?

To extend the metaphor, in evolutionary history it wasn't a light or an air conditioner, but something much simpler, like a bare light bulb or something. The light bulb needed to be upgraded, but the switch was fine.

So the gene that was implanted from the mouse to the fly is called a homologue/homeotic/hox gene which doesn't actually build the eye it just switches on the genes that build the eye. The reason that this worked is because hox genes are found in most or all multicellular organisms. In terms of evolution this is most likely evidence for a common ancestor.

thanks for your effort... can you add some references with hyperlinks so that others can follow you answer?


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How come that we "feel" it when someone's watching us
The question is relatively easy (the answer however..). We all know this feeling "being watched" and more often than not this is a real thing. If someone is staring at us from the side or from the back we sort-of "feel" it and we evenf eel the direction where it's coming from.
I can't seem to find a plausible answer for this though:

We actually see the people staring from the corner of our eyes - false, I tested this thoroughly and it also happens when your eyes are closed or someone's behind you.
Eyes don't send out energy (or "beams") as far as I know. They "receive" light but don't send any out, except for reflection.

So, what causes this strange phenomenon?

I'm wondering if carbon dioxide, body odour, infrared radiation could have an effect. I wouldn't be too surprised if the spiritual realm was at play somehow either.

Unless you describe your testing protocol, so that it can be verified by us, you shouldn't use it as evidence.

I think that this question would be a better fit at the Cognitive Sciences StackExchange.

This may be a better fit on the Cognitive Sciences SE [cogsci.stackexchange.com]

You do not have evidence of this "phenomenon" happening. What you do have is the impression of it happening.
So a better question is: what are the biological correlates of the "being watched" feeling. Or better yet: when you feel being watched, on average, is someone actually watching you?

possible duplicate of What portions of the brain have drastic changes in activation when we "sense" someone is there?

(answer to both questions is the same, I think)

To quote the University of Sidney site:

People often think that other people are staring at them even when
  they aren't research led by the University of Sydney has found.
When in doubt, the human brain is more likely to tell its owner that
  they're under the gaze of another person, researchers from the
  University of Sydney and The Vision Centre reveal in a recent article
  in Current Biology.

Also, from the scientific paper:

We presented participants with synthetic faces viewed under high and
  low levels of uncertainty and manipulated the faces by adding noise to
  the eyes. Then, we asked the participants to judge relative gaze
  directions. We found that all participants systematically perceived
  the noisy gaze as being directed more toward them. This suggests that
  the adult nervous system internally represents a prior for gaze and
  highlights the importance of experience in developing our
  interpretation of another’s gaze.

So you, and I, overestimate how often people is staring at us.
For details, see: http://sydney.edu.au/news/84.html?newsstoryid=11335 and https://www.cell.com/current-biology/retrieve/pii/S0960982213003321

I would guess hearing plays a part, as a powerful human sense  that works in 360 degrees.
Just as a hypothesis, I'd imagine that small sounds help you sense people behind you, and that this, plus chance, plus the very human capacity to see meaning in random events, gives the impression that there's a way to sense that someone not just behind you but actively looking at you.
In our every-day experience (that is, not in an artificial experimental setting), there are a lot of ways to bias our observations / data collection. For instance,

a half-conscious glance behind you is quickly forgotten (data discarded) if you realize it was just somebody strolling past, but remembered (data retained) if you see someone staring fixedly at you. This will spuriously increase your positive results (that is, the impression that "every time I look behind me, my sense that someone is looking is confirmed")
on the other hand, if someone is staring at you from behind, but you don't notice, you also do not retain that negative data, because, by definition, you didn't notice. So there is a strong effect that is spuriously decreasing your negative results.

So, as Brandon Invergo mentioned, we'd like to see a testing protocol along the lines of a blindfold and earphones playing white noise on the "senser", and the "watcher" behind the senser staring or looking away at random intervals, and a large number of trials.
This is not to diminish the fact that some people have much better situational/interpersonal awareness than others (say, a ninja vs. me), but I really imagine that this is more an effect of cognition (putting together small cues from hearing/peripheral vision/smell etc.) than of any difference in sensation.

I think the phenomenon should be studied separately in two conditions it happens (though in one of them it only happens subjectively):

When it happens outside of the peripheral vision, e.g. when your eyes closed, or  someone's behind you
When it happens within the peripheral vision (approximately 180), i.e. corners

For the first part, I agree with Sherin quoted the scientific paper "People often think that other people are staring at them even when they aren't".
But for the second part, we often experience that when we stare at people from the corners, they turn their heads and say "What ?". Perhaps recognition of this corner staring has something to do with extra foveal perception and of course the emotional part of it would be the emotional salience of being stared at. And because this extra foveal perception is less accurate than the perception in eyes' focus, it may result in false perception of "being watched" too. It's worth to mention that, because "eyes", "faces", and "staring" really have a high emotional valence for us,maybe we became very adept in recognition of them in our peripheral vision through many years of accumulative experience (I'm a fan of information processing approach to cognitive development). For more information about extra foveal perception, you may take a look at the seminal research carried out by Henderson (2003), "Human gaze control during real-world scene perception".


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Do voltage-gated calcium channels affect neuronal conduction speeds?
We have a hypothesis that a drug may block the voltage-gated calcium channels (VGCC) in annelid worms. We are wondering whether there are any correlations between VGCCs and neuron conduction velocities.  If there are fluctuations in calcium ion contents, would there be any changes in conduction velocities? Or if the channel is blocked, would it block the entire action potential along the worm's giant axon?

Most of the time, calcium is not the most important ion in terms of active propagation of an action potential along an axon. It is usually sodium and potassium which play the key roles here. In most living things the concentrations of ions for the intracellular and extracellular solutions are similar. For an action potential, you usually have an influx of sodium followed by an efflux of potassium. The sodium influx depolarizes the membrane and the potassium efflux re-polarizes it. The speed of conduction is determined by the membrane resistance and its "leakage". That is to say, how easily can a single travel along an axon? This is determined by the diameter of the axon, the greater the diameter, the faster the conduction. The leakage refers to ease with which ions leak out of the axon as the signal is propagating. Insulation via myelin sheaths help in preventing this, and, less leakage, the greater the signal at the next propagation site.
Calcium is the most important ion for the transmission of a signal from a pre to post synaptic cell. Without calcium, you have no neurotransmitter release. This is because the influx of calcium triggers a series of events involving the snare complex which eventually leads to vesicular release of neurotransmitter in quantal units. If you remove calcium from the extracellular solution, you will have no neurotransmitter release. If you block the calcium channels, you will have no neurotransmitter release.


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Does pain scale with mammal mass?
Some biological features scale with the animal mass (see previous Q&A).
Assuming the same concentration of nociceptors on the skin surface, I'm wondering how painful a 1 cm wound will be perceived in mouse, human or elephant. Despite the same firing number of nociceptors, will the mouse feel more pain as a bigger percentage of the body has been injured? Is it known whether pain sensing follows allometric rules?

As you cannot really ask a mouse to rank her sense of pain on a scale of 1 to 10, it will not be possible to find a definitive answer for your question.

@skymninge there are at least 40 [animal models of neuropathic] (http://www.ncbi.nlm.nih.gov/pubmed/20030738), but I'm not inside the field and cannot judge if some of them can be used for allometric studies.

The question if the mouse will FEEL bigger pain is still debatable. As pain is a feeling, not even by questioning different humans you could measure how much pain is felt. You can measure reactions, but pain is a subjective feeling. If I have an especially bad day, cutting my finger might (feel to) hurt more, than on a day I feel very euphoric.


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Method to inject genes into cells
The famous Hershey and Chase Experiment uses phages to inject genes into cells.
In the beginning, Professor Yamanaka injected 24 types of genes into cells to figure out which genes turn a cell into ES cells.
Did he also use phages?

Remember, phages infect bacteria. It looks like he used something called pMXs-based retroviral vectors instead, which is based on the Moloney murine leukemia virus (MMLV).
I have never heard of that virus before, but I do know of others used in vivo to deliver genes, including Lentivirus, Adenovirus, and Adeno-associated virus. All have their strengths and weaknesses. Adenovirus is large so you can fit a big gene inside it, but it tends to illicit a high immune response. AAV, on the other hand, is very small but has a much more mild immune response. It can fit a gene about 4kb long inside or half that if you use a fast expressing form called self-complementary AAV. What is nice about AAV is one of the subtypes (technically callled serotype) can cross the blood brain barrier, so it has already been used in clinical trials to try and treat neurological diseases, including Parkinson’s.

+1. You will want to note the methods section the linked paper entitled "Retroviral Infection." The pMX vectors were used to make the retrovirus, which was used to deliver genes to the cells, which were selected for using G418 (an antibiotic). You may want look into transfection and transduction.


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How do small animals make loud sounds?
Walking past the park today, I heard a cicada so loud I thought at first it must be some sort of large power tool. How is it that that very small animals like cicadas (crickets, etc.) can make such loud sounds? It seems intuitive that larger animals should be able to make louder sounds, but perhaps:
a) I just fundamentally misunderstand the physics involved
b) A theoretical larger animal should be able to make louder sounds, but cicadas are just extremely efficient, making up for their small size
c) ?

c) might be 'they can make louder sounds, but usually choose not to'. Blue(?) whales can be heard for thousands of miles underwater. I imagine alerting every lion for thousands of miles isn't a great thing to do if you're an elephant.

It is true that the total energy budget for smaller animals should be smaller. Perhaps it's because cicada sounds are spectrally narrow? The total power of the sound might be small, but it's concentrated around a specific pitch. Just a hunch.

Also note that size isn't everything here. Cicadas broadcast at a high frequency because they are moving so fast (which does take up a relatively large amount of energy).  If you could get an elephant to move as fast you could probably make some defining sounds, but the energy requirement would probably be to large.

I know that "high frequency" affects pitch - does it affect loudness too?

Yes, since high frequencies have higher energies. Low frequencies can travel further, though.

Large animals (which tend to be mammals), have vocal chords rather than some insects vibrating/rubbing membranes, and possibly vocal chords are less efficient.

The Cicada
A careful study of the noise-making apparatus of the cicada can be found in a 1994 paper by Young and Bennet-Clark.$^1$ The authors generated sounds at about 0-16 kHz at peaks on the order of 100 dB using cicadas in various stages of deconstruction.  The cicada uses a resonant organ-system called the tymbal which buckles and unbuckles rapidly to produce sound. The buckling-in is caused by muscle contraction and is louder than the buckling-out (relaxation) phase. Air sacs (a feature of many other small noisemakers) serve to amplify the sound.  The tymbal itself, for the species in this paper, has a resonant frequency of about 4kHz (Young, page 1017). The song of the cicada as modified/amplified by air sacs and other structures, is often around 10kHz.$^{2}$
Pure Tone vs. Diffuse Tone?
The vocalizations of large vertebrates are a complex superposition of waves that in the frequency spectrum are somewhat spread out. To the extent that a frog or a bird emits a pure tone, the energy will be confined to a narrow frequency range and this may be a strategy for achieving greater amplitude. Given comparable audio sensitivity, however, the intensity of pure tones will depend on amplitude (intensity), regardless of frequency.$^{3,4}$
Other Small Loud Animals
While the songs of cicadas are intense, especially in concert, on an individual level there is competition from other species. According to a Gizmodo article quoting assorted scientists, the snapping shrimp produces a transient snap that is around 200 decibels, a level that one site describes as "deafening." For perspective, dolphins can emit short chirps of 220 dB but these are outside the range of human hearing. The lion emits a roar of 115 dB which is sustained and audible 5 miles away, according to the article. Elephants also are capable of 117 dB cries, as are howler monkeys.
Both the shrimp and the cicada use non-vocal vibration to create their sounds. The shrimp uses a "spring-loaded claw" (the spring is muscle). The localized force of one part of the claw hitting the other generates a bubble (this is known as inertial cavitation). When the bubble collapses it generates a shock wave (noise) that stuns fish (prey).$^5$ The noise of frogs is produced as air passes from the lungs through the larynx, amplified by distended air sacs which resonate. Birds can produce up to 135dB (the Mollucan Cockatoo). They generally force air past (membranes and) a specialized organ called the syrinx located at the bottom of the trachea (see the Wikipedia note on bird vocalization).
Micronecta scholtzi, a 2mm-long aquatic insect, is for its size the loudest known animal. It creates a sound of 99.2 dB intensity which (despite being largely lost in transition from water to air) is audible to humans ashore. According to the Wikipedia note it creates this sound by "stridulating a ridge on its penis across corrugations on its abdomen." The area involved is about 50$\mu m$ across. Details of the mechanism are poorly understood. The article's comparison of the sperm whale's 236 (underwater) dB song gives perspective, as a sperm whale can weigh 14 metric tons.
A Common Aspect of Sound Intensity: Cavity Resonance
Descriptive studies of sound-creation by small animals (with the possible exception of the snapping shrimp) do not fully explain why a one-gram bug can make a bigger noise than a lion. Purely vocal methods of larger vertebrates produce sustained noise on the order of 100 dB but the non-vocal instruments of smaller creatures are capable of short bursts of amazing intensity.
It is difficult to generalize but because air sacs are part of many sound-making schemes, cavity resonance probably plays an important role. Like spring-mass systems or RLC circuits, cavities have resonant frequencies at which amplitude of a signal may be increased (the policeman's whistle is a familiar example). Another paper by Bennet-Clark and Young gives a sketch of a theory along these lines. At resonant frequencies the impedance of the instrument falls sharply and instead of being dissipated (generally as heat) the energy emerges as sound.$^6$

$^1$ Bennet-Clark and Young, The Role of the Tymbal in Cicada Sound Production, J. of Experimental Biol. (1995) 198, 1001-1019.
$^{2}$ The frequency of cicadas is variable, mostly on the order of 10kHz but occasionally very low (< 1kHz), mostly due to body size. See this article.
$^3$ Sound--essentially a compression wave--diminishes with distance. So when the Wiki article on noise levels compares noise levels it includes the distance from the object. For example, 100 db (comparable to the cicada) is the level of noise associated with a jack-hammer at 1 meter away.
$^4$ Audible range for humans is roughly 15 Hz-16000 Hz. As mentioned below, the dolphin can emit very intense high-pitched sounds that we don't hear at all, so the analogy to EM waves (higher frequency = higher energy) doesn't help predict perception. See Pfaff and Stecker, Loudness and Frequency Content of Noise in the Animal House, Lab. Animals (1976) 10, 111-117.
$^5$ M. Versluis, B. Schmitz, A von der Heydt & D. Lohse (2000). "How snapping shrimp snap: through cavitating bubbles". Science 289 (5487): 2114–2117.
$^6$ Bennet-Clark and Young, Short Communication, The Scaling of Song Frequency in Cicadas, J. Exp. Biol. 191, 291-294 (1994).

intuitively, I would say that small creatures are not seen easily. therefore they need audible lighthouses to signal to others their location
big creatures don't usually have this need, though some do such as whales which can emit sounds heard hundreds of kilometers away

This is an interesting point, but note that I'm specifically interested in how small animals make loud sounds, not why.


text:
Confusion regarding the ventricle system in the brain
I have a hard time finding out a small detail about the ventricle system.
As the CSF flows into the 4th ventricle, there's a small foramen in the lateral aspect, as well as an open space bounded by the medulla and cerebellum.
Do both these lead the same place? Is the space under the arachnoid matter only accessed through the small foramen, whereas the space between the medulla and cerebellum leads into the spinal column?

Not sure if it is of any help, but have you tried googling 'ventricles of the brain 3D'?

I've found the answer. The entire brain and spinal cord is bounded by the arachnoid mater, thus both channels would lead into the subarachnoid space, which also circulates the fluid into the spinal cord region. The CSF exits through the arachnoid granulations, which are like valves, found on the dorsal midline, into the superior sagital sinus, where it returns to the blood stream.


text:
Does sleep duration vary for animals based on time of the year?
I'm interested in the sleep patterns of wild animals, that still use sun for controlling their biological clock.
Animals entrain their biological clock to the day/night cycle using light as the entrainment signal. The biological clock follows the day/night cycle: dim light initiates melatonin secretion, while bright morning light stops melatonin production. Melatonin is involved in sleep regulation
Here, I have plotted the day duration over the course of the year for Northeast US, around Washington DC.
My question is given the day duration plot below, would the total sleep duration for wild animals vary over the course of the year?
In other words, would animals sleep longer in the winter time and shorter in the summer time?

Yes, people, as well as animals regulate their drowsiness by light. There's a well known experiment conducted by Michel Suffre on himself in 1972. When he spent a month with no light and no information about the time, his sleeping cycles prolonged up to 48 hours.


text:
What is the genetic basis of blood type (ABO) system?
What is the genetic basis of the A/B/B+/O/etc. blood type system? Are there definitive loci that correspond to each or can multiple different genotypes produce the same antigen profile? Also, is the blood type of a child necessarily one of the blood types of the parents, or can an A/B female cross to A/B male produce a child with blood type O?

I can answer only half your question.
It is not necessary that the child has to have the blood group of parents.
The inheritance is like this :
1.There are 3 alleles Ia , Ib and Io.
2.Ia and Ib are codominant i.e. they will both be expressed if present together.
3.Ia and Ib are dominant over Io. So, blood group O can only be expressed if the genotype is IoIo. IaIa or IaIo is blood group A and IbIb or IbIo is blood group B.
5.IaIb is blood group AB
So in the case of both the parents being AB blood group,the child can not have O group.S/he can have any other blood group.
The inheritance of negative and positive blood group follows simple mendelian inheritance.
Please feel free to correct me!

There is only one locus involved in ABO blood type, the ABO gene on chromosome 9. It has three alleles: A, B, and O.
We have two copies of every gene, one from each parent. Because the O allele is recessive to A and B, there are blood types with multiple genotypes. AO and AA will both produce blood type A, and BO and BB will both produce blood type B. Only OO will produce blood type O, and AB will get you blood type AB. The specific cross you mentioned (AB x AB) will never produce a child with blood type O, because neither of the parents had any O alleles for the child to inherit. However, any other blood type is possible with this particular cross.
The + or - you sometimes see is a separate system called the rhesus blood type system. The genetics involved in that are actually a bit complicated, but they don't involve the ABO gene at all.


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Is reproduction intrinsically part of life?
If all of the characteristics of life are required for something to be defined as living, how can we account people or other life that can not reproduce?

Every species has the ability to reproduce.  Of course, individuals within a species can be born with a mutation that keeps them from reproducing, or lose the ability to reproduce at some point in life.  However, to say that once these individuals fail to meet that criteria they are no longer forms of life would be a fairly absurd semantics argument.  It might be useful to note in an evolutionary sense that those individuals can no longer pass on their genes, which is could select against whatever it was the resulted in that individual being sterile.
You could probably reword the characteristics of life to stress species instead of individuals, but then theres a problem with microbes which have very poorly, or non-existent species.  But in general, this is not something a biologist is going to lose sleep over.


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Can someone provide resources on human electromagnetic frequencies?
Pardon all of my questions below.  I'm basically looking to find online resources regarding my inquiry.  If you can answer any of them off the bat, that would be awesome!!
It seems that humans and mammals give off certain frequencies from our nervous systems.  For example, dogs are able to sense when their master is coming home, even when their distance is close to a mile away.  Also, cats are able to sense when a human is about to die.  They can feel the frequency the person is giving off, and react differently.

Where can I learn more about this frequency that humans give off?
Has anyone ever done research on this subject?
Is this electromagnetic frequency or something else?
Are there devices that can measure this frequency that the human nervous system gives off?
Are there devices that can generate this frequency that the human nervous system gives off?

are there any references at all about the frequencies?  or is it a case of other senses at play?

http://www.ncbi.nlm.nih.gov/pubmed/15197761

" For example, dogs are able to sense when their master is coming home, even when their distance is close to a mile away."  Do you have a citation for that?

I saw it on a documentary, but I cannot recall which one it was.  It might not have been one mile, but it was a long distance.

I'm sorry, but much of this is pseudoscience. While animals do release electromagnetic radiation, mammals are not capable of detecting it. For example, cats may be able to sense that someone is about to die because they have an excellent sense of smell.

For a start, you could learn about Bioelectromagnetics which is the study of the interaction between electromagnetic fields and biological entities (reference). Electro-magnetic fields are generated by the heart, brain, tissues and cells. These fields are in-turn affected by temperature and the overall mood of a person (reference).
There is a lot of research that is being conducted in the field. You can find a lot of papers relating to the field with a simple search on Google Scholar.
Well technically electromagnetic fields.
There are instruments to measure EMF which are detailed in the Wikipedia page. Here is an article on an instrument made to measure the electromagnetic field of the heart (reference).
Generally, if you have measured the electromagnetic fields in different parts of the body (eg: this article states that the electric field of the heart is up to 50 mV/m, and that of the brain and other vital organs up to 5 mV/m) then it shouldn't be too hard to generate them seeing that EMF generated is a low value (reference).


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How to deduce if RNA virus infection or DNA virus infection
Is there any general rule to say this must be RNA virus infection and the other one DNA virus infection?
Example of a case: 5 children develop a bright red rash on the face and turns violet after a few days and then disappears. Then maculopapular rash appears on the trunk, buttocks and extremities. It soon fades from the trunk but persists on the thights and forearms. Two children have also had a slight fever and a sore throat, but all were not terribly sick. What is the genetic material of the most likely causative agent?
Right answer is: Single-stranded DNA, since most probably causative agent is erythema infectiosum caused by parvovirus B19.
I do not want to remember all microbes by heart.
How can you deduce that this must be a DNA infection and probably single-stranded?

Regarding 1st q) I will wait in hopes that I'm wrong, but I think the answer is you can't. There is still a lot of work being done just show bacterial vs viral using host markers, let alone breaking down viral.  There would also be little clinical significance to knowing, other than epi.  I think this is why the red book is now in App form: you ID the pathogen, and then you can know more specifics about it. 2nd question is a totally different question that I would be happy to answer separately (unless someone who can answer 1 in the affirmative can tie them).

Just as an example of where you can't.  Let's say you have a PT with an URI. Most likely cause is viral. Could easily be RSV (-ssRNA), Adeno (dsDNA), HRV(+ssRNA), or any number of others (these were listed for types).  Just on the numbers your best guess is HRV, but that could easily be wrong.

@AtlLED The second question moved here: http://biology.stackexchange.com/questions/9934/how-can-a-respiratory-infection-lead-to-a-skin-infection You are welcome to answer. I want to know.

@AtlLED You're right, there's no way to tell. It's a false dichotomy based on the wording of this exam question.  This exam is actually asking us to consider a chain of three questions: What is the disease described; What causes this disease; and How does this causative agent store genetic information.  The instructor in this case assumes that if one can answer correctly the last question in this chain then one understands the first two as well.  In short, this more a matter of pedagogy than pediatrics.

@Gossar Off idle curiosity, what is the class you two are taking?  Seems like ID, but it's an interesting approach given the questions.

@AtlLED I'll have to let Masi answer that question; I'm not in a class with him.
Perhaps I should have phrased that previous comment differently.  The us there was an editorial we.

@AtlLED Microbiology course, 2nd year, in Medicine.

If you mean simply by looking at symptoms, then there is no way, especially if in the context of a medical visit.  You're better off learning the usual suspects and figuring out the patients risk and likelihood for a given infection.  A good example is Hepatitis.  Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) have similar (enough) outward symptoms, but the former is a DNA virus and the latter an RNA virus.  In fact, looking at enWikipedia's list of acute causes, it's all over the place!
If you can actually assay for it in the lab, then of course.  Although...


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Why doesn't human consumption of plants cause infectious diseases the way consumption of animals can?
At first I want to clarify that I do know that there are naturally poisonous plants and plants that can hold radioactive stuff or toxic material from the environment.
What I mean by "diseases" (I guess there is a special term for that in English) is Bovine Spongiform Encephalopathy and similar serious issues caused by eating animals, by that you cannot develop when consuming plants.
As far as I know there are no diseases causes by eating fruit and vegetables (of course, except parasites if you don't wash it properly and an infected cow or bunny pooped on it ;D)
Is it because the parasites and diseases infecting plants are so specialised for their "body-type and genetics" that they cannot operate inside an animal body?
Could somebody explain that to me in more depth why by eating plants you cannot get a disease (except allergic reaction/intolerance or toxicities as mentioned earlier)?

It is because every pathogen has a specific host range(organisms which it can  infect).

Food poisoning is caused by organisms which are symbiotic and adjusted to plants, that might be an exception.  the illness is not from animal contamination.

I think you can get salmonella from both animal products like eggs and plant products like flour.

There is an entire journal dedicated to harmful algae. Many land plants also produce potent toxins. (Diseases such as botulism, tetanus, cholera are effected mainly because of the toxin, rather than the bacterial growth).

If you mean if there are viruses, pathogenic bacteria or fungi that may cause diseases both in plants and in animals, the response would be that this is very unlikely (But even so, some fungi and bacteria could do it if some circumstances are given). This is due to some key factors:
First of all, the philogenetic distance between plants and animals is huge. Diseases transmitted by the consumption of animals are called zoonosis, and obviously it is more likely to catch a zoonosis by eating pork than eating shrimps or clams. While it's true that certain parasites have different hosts and use them to transmit themselves (for instance, many platyhelmintha uses mollusks or insects to spread themselves towards mammalian or avian hosts) parasites than have only one kind of host usually are adapted to live inside them, and they usually are unable to infect different organisms. Very few parasites can infect a human and a starfish, and even fewer can infect at the same time a human and a tomato plant.
Second, and related to the first, plant physiology differs completely from animal physiology. Plants usually defend themselves by their natural barriers (cuticles, cell walls), hypersensitive response (programmed cell death in order to limit the spread of a pathogen), isolation and/or outgrowing of the pathogen and accumulation of chemicals. Animals main mechanism is immune system. There are very different strategies and very few organisms can effectively avoid all of them at the same time. In the case of viruses, they would even have to face the fact that animals and plants have huge genetic differences.
Third even if they could, the pathogen will face competition against other pathogens that would be more specialized. Bacteria and fungi can be really hostile towards their microfoes, using a wide array of strategies. This hypothetical pathogen would be very unspecific, so they would have a hard time against more focused microbes. It should be noted, however, that unspecialized organisms usually have a great advantage if the environment have some perturbation, and they also are more resilient toward stress. Many plant pathogens are generalistic organisms that attacks when the plant is harmed or stressed. The same applies to many opportunistic infections in animals.
Despite all of this, there are some diseases that should be mentioned. Some fungi of the Clavyceps genera are plan pathogens, but they produce toxins than can affect the nervous system of animals, causing an intoxication called ergotism (the most famous of this chemicals is the lisergic acid, also known as LSD). Other fungi can produce toxins while they grow in plant tissue. Moreover, there are many fungi that can grow both in plant tissue and as animal parasites (mainly arthropods and nematodes), but in this case the plant pathogenesis usually occurs only when high fungal concentration is achieved or the plant is already damaged. While it's not a real infection, plant pathogens can cause allergic reactions. Finally, phytopathogenic fungi and some bacteria can cause infections in wounds or mucoses in individuals with a compromised immune system, but in this case the source seems to be the spores in the air.

The classical example of fungal toxins are aflatoxins, which are very nasty.

I think a main problem here is limiting logic.
By eliminating both toxic/poisonous plants, plants that have evolved to discourage you from eating them, and improperly "washed" plants, things which contain non-plant mater that can make you sick, you are not left with the possibility of diseases.
BSE is caused by prions, which are mater of serious debate and research in academics at the moment.  The leading cause of transmission is likely ingestion (1, 2), but it is quite possible that it arises as a mutation sporadically in certain mammals (3).
Coming back to your question, let's suppose two scenarios:
First let's suppose that a prion, or really any other pathogen, were to fall onto a piece a fruit from another mammal.  If you, or a cow, were to eat it in this unclean state you have the chance to develop disease.  But we would not eat the plant in this unclean state because we are to have it properly washed.  The same is true for pathogenic microorganisms that are naturally occurring on plants.  I think you addressed this well in the question.
But let us propose another situation where a plant evolves a new protein, or a new form of a protein as is the case in the prion.  For simplicity let's call this protein "X."  X may or may not be toxic to the plant, and cause disease in the plant.  If it does, it would likely have selective pressure against the population it was in (even if it was infectious to plants like a prion).  But we may not, at least in the beginning be able to tell if the plant has the protein in it, so we go ahead and eat it (and for the sake of argument, we won't cook it, which is bad news for all kinds of pathogens).
If that protein causes sickness in an animal (like humans) we would say that it is toxic, and we would exclude it per your preamble.  If it is stable enough, it would remain toxic in our bodies, and should anyone be unfortunate enough to eat us or roll around in are carcass, there would be a small but theoretical chance they could get sick as well.  Again it would likely be excluded from this question as a toxin.
I think these get at what you are asking, but I think there is a spirit of what you are asking which goes further:
Why aren't contagious agents produced by plants?
Miguel addresses the problem quite nicely.  First, the genetic distance between humans and plants is so vast that a prion-like protein developing is highly unlikely.  Second, plants themselves are unlikely to make good pathogens.  Finally, natural selection has favored the production of toxins and irritants when plants have sought chemical means to deter animals (as opposed to a physical deterrent like a thorn).
Prions work because of shared/similar proteins existing within species.  A similarly shared protein that we would had with plants would probably be so basic that it was shared by the vast majority of eukaryotes, and if it existed, would likely be capable of destroying a good deal of life, including the plant itself.  Thankfully most of the very basic proteins we make a well regulated, and have mechanisms in place to “throw away” miss folded questions.
If we move past the genetic distance, and ignore the conditions that would be needed to select for plant being pathogens, let’s look at other obstacles plants would face.  Plants aren’t very good at locomotion, so it would need to get on us by direct contact, carried to us from the elements, or by some other animal.
A good case example would be C. immitis, a fungus.  It needs the spores to be kicked up and inhaled by an individual who is in some way compromised (normally).  Once this happens, it can begin the next hard step which is to grow.
The immune system of a healthy individual would definitely recognize any fungal or plant matter as foreign object and try to get rid of it.  Also note that a pathogenic plant would be limited in size by our behavior.  I think even a sloth would not allow a flower or tree to grow out of its back or arm.  Anything big enough would cause itching and/or illicit a behavioral effort to physically remove it.  Many microbial infections do cause itching, which if you are larger than a microbe, is a good way to have your whole body scratched off your host.
But let’s assume that our pathogen has made it on a human, found a place where it can grow, found enough food to live there (presumably us), has matched our immune system, is small enough that we haven’t been able to physically remove it (think algae), and/or made it to an internal part of body like our lungs where we have a harder time getting rid of it.  After doing all that, it has to grow to the point where it can get back out of bodies, and then back into another human and start over.  A prion-like pathogen would also have to replicate to significant enough numbers to be transmitted host to host.  Transmission is a very difficult process, and as Miguel points out, normally requires a good deal of species dependent specialization and adaption
In summary:
I have hard time imaging how a plant, even a small one like alga, could undergo enough selective pressure to become an infectious agent.  It would be further complicated by that fact that you were eating it in your question, which means it would have to contend with the GI track.  The genetic distance makes a prion like pathogen highly improbable if not outright impossible.  Toxins, however, are in great abundance in the plant world, and seem to be a good way to get animals to leave you alone.
When I think about plant toxins, I always like to think of the Sumac family.  Cashews evolved to be delicious and were cultivated for it, poison ivy evolved to be painful and is destroyed for it, and when we think of the family, we always think of the pain first. [Sorry I know that’s entirely off topic, feel free to delete via edit.]
(1) Johnson CJ, Pedersen JA, Chappell RJ, McKenzie D, Aiken JM (2007) Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles. PLoS Pathog 3(7): e93. doi:10.1371/journal.ppat.0030093
(2) Bartelt-Hunt SL, Bartz JC (2013) Behavior of Prions in the Environment: Implications for Prion Biology. PLoS Pathog 9(2): e1003113. doi:10.1371/journal.ppat.1003113
(3) Liberski PP. (2012) Historical overview of prion diseases: a view from afar. Folia Neuropathol. 50(1):1-12.


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Difference between 'Orbit' and 'Globe' in eye anatomy?
What's the difference between 'Orbit' and 'Globe' in eye's anatomy. Do they refer to the same ? I encountered this in this text:

... ciliary ganglion, which is approximately 3 mm in size, and located
  2-3 mm posterior to the globe and lateral to the optic nerve,...

I've found a rough answer myself:

The globe of the eye, or bulbus oculi, is the eyeball apart from its
  appendages

http://en.wikipedia.org/wiki/Globe_%28human_eye%29

... the orbit is the cavity or socket of the skull in which the eye and
  its appendages are situated. "Orbit" can refer to the bony socket, or it can also be used to imply the contents.

http://en.wikipedia.org/wiki/Orbit_%28anatomy%29

Hi, please don't offer bounties on questions that are 1) Off topic and 2) bad questions. This site is not for medical advice and the question does not give the information needed to make it answerable.

@terdon I understand that the question might not be on-topic or a good question, but offering a bounty could even help this improved. When a question didn't receive any attention, it can neither be improved nor the asker can be trained. There are many options in this website to train people to ask good questions. You even changed the title of two links you provided to sound 'pessimistic'. Instead of comparative commands, I think it would be better if you just train people with optimism and provide the links accordingly.

Well yes, if you think you can improve it edit it. However, personal medicine is very correctly off topic here, we are not MDs and do not have access to the patient. If people base their treatment on our answers, they can cause themselves serious harm. A mod has asked for more information on that question and none has been offered. If this is someone you know tell them how to improve the question. Adding a bounty is not helpful in this situation.


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Missing cells from immunopanning
Why do I not have any cells left in my positive panning plate after transferring from the negative panning plate during immunopanning? I am trying to purify retinal ganglion cells from postnatal rats and use a Thy1.1 antibody harvested from a hybridoma cell line supernatant in the positive panning plate.
Following transfer of the cell suspension from the negative to the positive panning plate there are no cells in the pre-trypsinization supernatant, nothing stuck to the panning plate, and no cells in the post-trypsinization supernatant so I have no idea where they could have gone. Checking the negative panning plates however shows that there are many cells stuck to those plates, so could my RGCs have been lost at some point during the transfer and when?
Thanks v much in advance for your help.

Did you check the actual transfer material for cells before you added it to the positive plate? It may be they all stuck to the negative plate...

Is immunopanning better than labelling with an antibody and sorting by FACS?

Or using MACS for sorting?

Immunopanning in my experience takes an awful lot of optimization, but is worth it when it works.  I would plan, if you have the resources, to sac rats just for assay optimization before you even begin to try to get real data out (assuming your planning for a steady stream of primary cells).
That said, there are some real easy checks you can try do first.  Try to get a rough cell count on what you put on your negative plate (depending on your prep steps, that can actually be a bit tricky), and then count the cells again as you transfer the cell suspension to the positive plates.  If you don’t have any cells left, or you have very little cells left, then you might be losing all your population on your negative plate.
If you do have cells in suspension, I would start to question your positive plate.  Are you making them yourself or are you buying them coated? Which rat strain are you using?  Perhaps you need to titer your antibody concentration on the plate.  There are really a whole lot of steps in immunopanning that can be optimized.


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Why does it hurt when you take sweets, if you have cavities in your teeth?
When you have cavities in your teeth taking any sweetend drinks or food causes sensitivity or pain. What could be the reason?

I think bacterial metabolites cause the pain. At least my experience that salt water kills bacteria (except halophiles) with it's high osmotic pressure and so the pain goes away almost immediately. Hyper pure chlorine-dioxide (as an oxidizing agent) has the same effect, but it is a bit expensive compared to salt.

The outer shell of a tooth is enamel, which is hard and dense so that not much can penetrate it.  Under that is dentin (or dentine), which is bony but has microscopic channels running through it to the center of the tooth where the pulp and nerve reside.  If the enamel is breached, as with a cavity, crack, or wear, the dentin is exposed to the environment of the mouth.  When sugar comes against the dentin, it draws fluid out of the microscopic channels (because sugar attracts water strongly).  The fluid flow causes pressure changes around the nerve of the tooth, which reports the change to the brain where it registers as pain.  Dentin is highly sensitive not just to sugar, but also to hot, cold, pressure, and other stimuli.  (This sugar response is a short term one; the influence of sugar on bacteria is a longer-term effect in which the acid generated by the bacteria eats away the enamel layer.)

Well if it was the osmotic effect of sugar then salt should also elicit pain which is not the case. Can it be the acid produced by the acidogenic microorganisms? but then there would be a time lag or unless the acid production is very rapid.

This is a bit of a basic answer.
According to the website article "Dental cavities" (Medline Plus), the bacteria normally in your mouth converts many foods, particularly starch and sugar into acid that forms a part of plaque.  These in turn cause dental caries or decay, according to this Wikipedia article:

Dental caries, also known as tooth decay or a cavity, is an infection, bacterial in origin, that causes demineralization and destruction of the hard tissues (enamel, dentin and cementum), usually by production of acid by bacterial fermentation of the food debris accumulated on the tooth surface

A possible reason you would feel pain from a cavity in contact with sweet foods and drinks, or anything really, is due to the cavity being large enough that nerves are exposed.

You are right when the cavity is large enough to expose the pulp and the nerves within. I am refering to pain when only the dentin is just exposed as seen in xrays.


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Can Naegleria fowleri enter through your ear?
Is it possible to get infected with the amoeba, Naegleria fowleri, through your ears, or is the nose the only way it can enter to cause infection? How commonly is it found in your stool as well?

what if a kid has tubes? or a hole in the eardrum?

@KyleCares - Naegleria fowleri eat myelin and neurons. The closest nerve bundle in the ears is in the Inner Ear (Vestibular Nerve) behind the Oval Window, Semicircular Ducts, and wedged between the Ducts and the Cochlea. Even if the Eardrum is compromised, it would still be almost impossible.

Ears? No. The tympanic membrane (eardrum) is a watertight barrier between the outer ear and middle ear.

Exposure to the organism is extremely common due to its wide distribution in nature, but thus far lacks the ability to infect the body through any method other than direct contact with the olfactory nerve, which is exposed only at the extreme vertical terminus of the paranasal sinuses; the contaminated water must be deeply insufflated into the sinus cavities for transmission to occur.

In short: Don't huff warm lake water too deeply through your nose, and you'll probably never get it.
You shouldn't find it in your stool. Other amoebic infections can be found in your stool, as they can attack the lining of your intestines, but Naegleria, specifically, will reside in your sinuses and brain until you die or receive treatment.


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Suggestions for an experiment?

I would appreciate suggestions for my year-long AP Biology project. Such a project would consists of a standard experiment, to be done over the period of a year, so it would have >to be fairly substantial.
I'm interested in anything cell/DNA/molebio related with a mathematical connection. I >would prefer something other than mere statistical analysis, maybe something like >differential equations.
I have access to standard undergraduate lab equipment; assume that I'm able to procure all necessary materials and that I'm capable of performing the experiment. Thank you for the help.

As per the suggestion of shigeta below, I leafed through the links, and found gene circuits interesting. So, what exactly is a gene circuit, how are they modeled, and what are they used for?

systems biology.. do a cell bio experiment and develop a mathematical model for the system. you can validate the model using the experiments..

You really need to narrow this down. We don't know your competences, the materials you have available, the fields of the various labs you may have access to, there is no way of answering this question without a much more specific scope.

Yes, I probably should have been more specific about that; it'll be edited. I'll look into systems biology.

Still going to need a little more on the equipment side.  I consider tissue culture standard undergrad work because that's what I did a lot of the time in undergrad.  I also have been doing Westerns since high school.  You mention cells, do you have a way to culture them, you mention DNA, do you have gel rigs and the means to isolate DNA, and molebio is so broad it's not really limiting.

Yes, I will have access to everything you mentioned.

I'm still not certain that this is a good question for SE, because I'm not sure it can be answered, but I would look into a forward genetics experiment.  You can do predictive and analytical modeling, and push the forward genetics over a whole year easily.

I suggest you ask the gene circuit question as a separate question. And you can get specific with it, too – as in "how would I construct an experiment with such and so requirements/resources to do such and so regarding gene circuits"

This is a bit hard - most possible answers you still aren't going to like, but I'll give you three suggestions.
It sounds like you want to take something with a mathematical model and try to modulate it with molecular biology.
It seems unlikely that I can really give you a specific project, but there are four sources  I will recommend you look at.
I think I'd suggest the further limiting assumptions:

you want to work with E coli - its the easiest and most readily available organism to work with.
you want to work with a system that is self contained within a single plasmid - so it relies only upon 2 genes to act, 3 at the outside or you will have issues getting it all to work.
you want a mathematical system that already has a well fit model that  you will peturb.  building a new model might be a bit of a big first off project.  (but who am I to tell you what to do - these are just suggestions).

The First suggestion I have is Jeff Hasty at UCSD.  He has focused a lot on oscillating gene circuits.  He has simple systems that might be reproducible with a small lab, most recent work that combines a GFP oscillator with LUX is pretty cool. Both oscillators and LUX are independently good systems to work with. .  I've been a science fair judge and I can tell you, just reproducing one of his systems would be an impressive lot of work
Another body of work to look at is Adam Arkin. He has looked at lots of circuitry component candidates.  Articles such as "The hunt for the biological transistor" might get you thinking.  This is a broader body of work, and so it might take a while to get an idea from it.
Third, if this is boring to you and you want to look more broadly, you can look through the iGEM competitions.  These are projects with oscillators and bio synthesis systems which sometimes have mathematical models associated with them.  The big advantage here is that you might be able to start or join an iGEM team and then some or all the plasmids will be made already - mol bio gets very expensive if someone doesn't gift you some materials.


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Why do mosquitoes not collect blood after platelets activate?
This may be anecdotal...
The Indian sub-continent is in the rainy part of summer. It follows the mosquito population goes up.
So when I sliced my palm, I expected the mosquitoes to collect there in force. Yet whilst they continued to go about their business on the forearms, face and elsewhere - the blood flowing out of my palm held no attraction for them. This even after I deliberately stood still for nearly a minute! Perhaps the clotting process/platelets/etc were a repellent.
Why do mosquitoes not collect blood after platelets activate?

I guess mosquitoes rarely have the opportunity to have available fresh blood. Therefore they did not evolve to recognize blood smell but only sweat smell (skin colors and animal shape). In other words, even if they had the physiology to take advantage of your injury, they are just not adapted to recognize it as an opportunity because they did not evolve for this purpose.

I do not know why they wouldn't try, but there may also be a physical reason why they would not: once platelets are activated, a clot might form and block their alimentary tract.

I just went to an interesting talk about malaria and asked the speaker about this. I will try to source and write an answer, but it would seem that mosquitoes can't detect the flowing blood vs the host (as @Rami.b pointed out).  The cut was probably small enough that there was low chance of the mosquitoes landing there vs the rest of your body.  They seem to be attracted to other excretions we produce constantly.

Here's an interesting publication: http://dx.doi.org/10.1016/j.cell.2013.12.044


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Why does freshly cut grass smell like a watermelon?
I found that, when I smell watermelon aroma outdoors, someone nearby has mowed  the grass. Is there an underlying basis?

I can't say I've ever experienced that, but a cursory Google search indicates this is not unheard of.  Also, a weird Harry Potter fanfic.

Are you saying that when grass is mowed, you smell watermelons, or that when you smell watermelons, someone has cut grass near you?

I meant that the aroma of the freshly cut grass is like a watermelon smell.

cis-3-hexenal is probably the main reason.  It is one of the main chemicals in fresh-cut grass smell (lots of references besides wiki if you google it).  This fairly comprehensive paper on watermelon odorants also says that they find a lot of cis-3-hexenal in fresh cut watermelon.  See tables 3.1, 3.2 and 3.3.

Is this chemical a GLV (Green Leaf Volatiles)

i think so, you can see cis-3-hexenal in this reference on the GLV wiki page: http://www.olfacts.nl/index_bestanden/Page7.htm


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Why do bats huddle during late fall?
In the late fall, bats hibernate in clusters with many bats pressed together and holding on to one another. Which of the following supposed advantages of huddling behavior is, in reality, not true?

Any heat generated by any bat is shared by other bats.
Less surface area is exposed to the environment.
Huddling behavior decreases the amount of food needed for bats to stay warm.
In this configuration, less heat is needed for each bat and, therefore, each bat requires less food.
Huddling behavior helps bats stay warm while they feed.

this looks like a homework question!  we don't play that here.

@shigeta she did actually tag it as homework.

Think about where/when bats huddle, where/how/when they feed.

@biogirl What do you think? What's your reasoning so far?

ok fair enough.  still this seems like a hard one to help with.  'one of these things is not like the other' is about all i would say.

@kmm I think huddling helps them stay warm but the answer given in book is 5th. I think 3rd and 4th say the same thing and 1st and 2nd are definitely true.So only 5th can be the answer but I think huddling behavior does help in staying warm .

Huddling behaviour can help in staying warm, but think about @terdons comment some more.

This is basically a trick question and a bit of a cheap shot. All of the reasons cited boil down to "bats huddle to conserve heat", they are basically the same, single, reason.
In order for bats to feed, they need to move, fly out of their cave or wherever they happen to sleep and go forth and look for food. Therefore, they will not be able to huddle while feeding because they will be flying around trying to find fruit or donkeys or whatever each species feeds on. Unless they can figure out a way to huddle while flying, they will not be able to huddle while feeding and so number 5 is wrong.


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What happens during metamorphosis?
We were studying butterflies in class and I asked my 7th grade teacher, but she deemed the concept "too complicated." I'm really curious now, not only about butterflies but insects in general...
Thank you!

Could you add some detail to your question? To start, what species(s) are you interested in?

It depends of what order and even what family of insects we are talking about. Insects may have complete or incomplete metamorphosis, being the complete more complicated. Even inside the first group (wich in fact contains most of the insects since coleoptera, diptera, lepidoptera and himenoptera have complete metamorphosis) there are important differences. However, I'll try to explain some basics.
First of all, metamorphosis is a molting-related process. It's regulated by the same hormones and they share many characteristics. In insects with uncomplete metamorphosis, this is very visible, since the "metamorphosis" is the last molt, wich usually involves growth, sexual maturity and the development of functional wings.
The choice between a regular larval molt is determined primarily by the levels of juvenil hormone, wich decays during the last larval instar (pupae and adult are instars, too). The molting is triggered by a peak of ecdysone, an steroid.
Once the insect has entered into the state of pupae, the organs start to suffer diverse changes. The formation of adult organs de novo arise from some special structures called imaginal discs, wich are clusters of stem cells that are more or less isolated in the larvae.

Position of the imaginal discs in Drosophila. Source.
Note that diptera larvae lack legs, mandibles and even head, while coleptera larvae usually have true legs, a set of mandibles and many other adult features.

A typical larva of a coleoptera of the genus Lucanus. Note the mandibles and the legs. Source.
Some other organs remain more or less the same, such as the hearts or many parts of the nervous system. On the other side, some larval organs needs to dissapear and suffer programmed cell death. The gut, many parts of the nervous system, between others, suffer modifications that may be more or less drastic. In many cases this happen by simple growth and differenciation of the tissue or degeneration by apoptosis, but in some others the whole organs suffers apoptosis and regenerates itself with adult characteristics.  For example, the innervation of the abdominal parapods (false legs) in caterpillars suffer a progressive degeneration, while the opposite happens in toracic nerves, wich will have to control legs and wings. This whole process is pretty similar to embrionic development and it shares many traits with it.
Finally, metamorphosis in other animals, such as crustaceans, vertabrates (fishes and amphibians), echinodermae, annelidae, cnidaria and many others will probably vary widely. I know for sure that amphibians metamorphosis is regulated by tiroid hormones, but I'm not even sure that many of the other examples have even been studied at a phisiological level.


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copper vs aluminum, what's the safest for health?
I'm working on a mini project for a milk dispenser machine, using a peltier device to cool the milk down, I have to choose between a copper or aluminum cooling block (see pictures bellow).
But I'm worried about health issues in the long run, (oxidation and stuff), I have no idea what to choose.
What would you guys recommend me ?

What are the temperature and pressure conditions of the milk coming in and out?  With Cu oxidation could occur, and I would be less inclined go with it.  Al is already going to be oxidized, but Al2O3 is harder and on the outside of almost any Al product.  The only downside with Al are possible correlates with neurological disorders, and that would be over lots of exposure (probably not nearly the dose from deodorant).

Household water is typically run in copper pipes.

@AtlLED Pressure would be gravity based, not really high, and temperature around 0°C (~32°F). The neurological thing you mentioned is scary stuff, looks like maybe copper is safer based on kmm's comment ?

@kmm I think that copper piping is only a good solution so long as you have very clean and controlled water running through it (as is common in the US).  Just searching about copper pipe corrosion show examples of where that can go bad with just water, let alone milk (see my answer).

Assuming the answer can't be C) Stainless Steel I would go with Aluminum.
The USDA specifically mandates (1) stainless steel 300:

"Milk contact surfaces shall be made of stainless steel of the 300
  series, equally corrosion-resistant non-toxic metals or heat-resistant
  glass."

Is the copper tinned?  From what I can tell after reading some old sources (2) un-tinned copper will be corroded by milk.  You have the advantage of a cool temperature lowering contamination risk (3), but many states following the FDA specifically removed the allowance of tinned copper (Sec. 22-201).
While the effects of life long dosing of Al are becoming more and more clearly tied to Alzheimer's (4), the effects build up over time.  Copper has a tendency to be more acute (5) and pronounced (6, 7), and further it can tasted in low amounts  and discolor the food (8).  It can be said that water flows through Cu pipes, but soda is put in Al cans.
The research for this has been quite enjoyable, and led to things I didn't even think of.  A alternative cleaning site has even recommended using milk to clean Cu pans.
Again so my final recommendation is to follow USDA guidelines and use stainless steel, but my second choice would be Aluminum.
Citations:
(1) USDA. 2011, July. Milk for Manufacturing Purposes and its Production and Processing.
(2) US DOC. 1917, April. STRUCTURE OF THE COATING ON TINNED SHEET COPPER IN RELATION TO A SPECIFIC CASE OF CORROSION. Technologic Papers OF THE Bureau of Standards.
(3) COMMITTEE ON COPPER IN DRINKING WATER, NATIONAL RESEARCH COUNCIL. Copper in Drinking Water. NATIONAL ACADEMY PRESS. 2000.
(4) Walton, J.R. Aluminum Involvement in the Progression of Alzheimer's Disease. Journal of Alzheimer’s Disease 35 (2013) 7–43. DOI 10.3233/JAD-121909
(5) Reilly C. The dietary significance of adventitious iron, zinc, copper and lead in domestically prepared food. Food Addit Contam. 1985 Jul-Sep;2(3):209-15.
(6) Conor Reilly. Metal Contamination of Food:
Its Significance for Food Quality and Human Health. Pg 50. John Wiley & Sons, Apr 15, 2008
(8) ibid pg. 16
(7) Lee A. Price, et al. Chronic copper toxicosis presenting as liver failure in an Australian child. Pathology. 1996, Vol. 28, No. 4 , Pages 316-320 (doi:10.1080/00313029600169264)