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What plastic eating organisms are there to help with plastic in landfills problem?
I see some popular science articles on the plastic eating bacteria and fungi appearing on the web since 2009. Most of the articles praise discoveries, because such organisms promise to break down plastics which were previously thought to be indestructible. However, from the articles it is hard to understand the total number/names of promising organisms that can biodegrade plastic.
Additionally, it's hard to gather from the dated articles if these plastic eating organisms have passed safety testing - for example that they don't break down plastic into something volatile and toxic.
My question is - which organisms as of 2013 are seriously considered for solving the plastic in landfills problem?

Do you have URLs to the articles you found? Adding these to your question would improve its specificity and allow others to answer your question more easily. Your comment that you find it, "...hard to understand the total number/names of promising organisms..." might be a non-issue for another user who might be able to just look at the words and answer your question "off the top of the head" without additional research.

I remember this link - about a high school student who's science fair project was a basic but effective selection experiment.  He cut up plastic and put it in a yeast medium (growth medium for microorganisms) for a few weeks.  It says he tweaked the temperature and other incubation conditions for a few weeks and got a significant degradation of the plastic in the media.  The microorganisms in the media were not characterized.
That article is great because the bloggers compiled a list of similar work.
There are a couple of links that point to styrene degradation by Pseudomonas putida variants.  Pseudomonas putida is a likely candidate from bacteriology - it was first isolated near chemical and petroleum spills - they can degrade petrochemicals and organotoxics, so researchers might tend to start with this bacteria or an isolate of it.
This paper identifies Phanerochaete chrysosporium, a white rot fungus as an organism that can degrade phenolic resins.  White rot fungi are found in wood rot and can degrade lignin which is derived from a poly-phenolic like biosynthesis pathway.  So this is also an interesting lead.  It doesn't always grow to industrial scale - I've known people working on this even in the early 80s.
So it seems despite the fact that plastic never seems to go away, there are organisms in the wild that will chew away at the plastic, and with a little bit of selection work you can pick them out pretty easily.  This survey of the plastic dump in the Pacific gyre found that there were marine microorgs that might be eating plastic there too.  They had a preliminary report:

So far, the DNA sequences obtained by her lab show that almost 25% of the bacteria on one polyethylene surface were vibrios

A survey of the tropical rainforest also found a collection of fungi that can subsist on polyurethane. These included Pestalotiopsis microspora which seems to be have the so far unique property of anaerobic degradation of polyurethane.
Overall it seems that finding organisms in the wild is of ongoing interest.  This may be because biodegradation of plastic tends to be slow, which makes sense because if it were quick there would be no problem with dumping it into the dirt of into the ocean, but it would also rot over time in the back yard or in your boat.  While its possible that more fishing trips may find the perfect plastic eater, its also possible that industrial processes for the bioremediation of plastics may have to wait for some engineered organisms.

I know this is an old question however when it was posted there was not as much information as there is today. I have heard about two insects that have bacteria in their gut that degrade polimers. One of them is Tenebrio molitor which was reported to degrade polyatyrene. The other one is the waxworm, it was reported that waxworm larvae degrade poliethylene. This is really exciting news, currently we are working in Guatemala with a couple of insects that also degrade polymers, but we still have work to do before publishing.


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How does natural selection favour large body mass and size (or so it seems)
I was walking through a park this afternoon and observed a few birds having fun flying around and it got me thinking why would natural selection favour birds with flesh at all if it hinders their flight.
We started first with single-cell and micro-organisms flourishing the ponds and then they evolved into massive dinosaurs. It therefore seems, there are some unique reasons for growing to such a large size.
However, I thought it's counter intuitive because the large body slows down locomotion, requires lots of food and energy upkeep, is a big flesh target for predators, makes hiding ineffective.
Although it is obvious that the flesh protects the internal organs, but it seems like a chicken and egg problem because without a massive body, perhaps then there is no need for the internal organs.
On a different perspective, perhaps those animals that evolved without flesh are called plants.
That sums up my naive train of thoughts.
So, any expert can shed some light?

Situations where large body could help (some are estimations, some are known): birds in winter - large birds can go without food for longer, larger shelled turtles are harder for sharks to attack - they don't fit in to the sharks mouth so easily so less likely to be crushed, blue whales are large - the sea is cold and large animals radiate heat less rapidly.

Similar to http://biology.stackexchange.com/questions/111/do-large-animals-often-evolve-into-smaller-animals/114

Also similar to http://biology.stackexchange.com/questions/1767/what-was-the-reason-for-some-plant-and-animals-to-become-giant-in-course-of-evol

Well first of all I don't know if natural selection favors larger animals - most of the living things in the world are single celled.
Still there are advantages to being larger.  I don't know if I can list them all!  In no particular order:
1) Living things that are large are more metabolically efficient. The amount of food required goes as a 3/4 power of the size of the animal.  Thus a cat 100 times the mass of a mouse requires only 31 times more food.  I don't believe that it is not known how this works.
2) r vs K selection: larger animals have greater individual "value".  Smaller animals tend to live by r-selection - they are cheap and reproduce in large amounts, then lead short and highly competitive lives where most offspring die without reproducing.  Larger animal tend to live longer and reproduce offspring with a greater chance of life. In the extreme case you can compare a cockaroach to an elephant here.  This is not a hard and fas rule, but cheap offspring do tend to be small.
I seem to remember that there are lots of other surveys done and body size correlates to life span and any number of other attributes, which I will try to add after I get some sleep unless someone slips in and lists them all.
3) Cope's rule - an observation as much as a rule that size must convey some advantge because most animals become larger the longer they are around.  Not always true, but there is a trend that the longer evolution works, the more likely a large animal will show up.  This might be because as niches for smaller animals are filled, niches for larger animals become more accessible?

also a lot of direct benefits to survival and mating https://pubmed.ncbi.nlm.nih.gov/16701331/

i'm a personal fan of both of those things @John :)

Another reason could be that bigger animals can better fight for resources like food or sex. Ususally it's the stronger (and often bigger) male that gets a chance to mate or defend their prey.
Bigger animals are also harder to kill and therefore have to fear less predators.

Unless you're living on an island! If you're reasonably large but got stuck on an island for a long time, you will get smaller. This phenomenon (which also goes the other way - if you're small you tend to get bigger if stuck on an island) is called insular dwarfism: http://en.wikipedia.org/wiki/Island_dwarfism

yes - lots of reasons to be small too.  insects rarely get large (or smart) for instance.

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What's the Efficacy of Ampakines in the Treatment for ADHD?
What's the Efficacy of Ampakines in the Treatment for ADHD? Ampakines are a class of drugs that serve as potentiators of the AMPA glutamate receptor. By so doing they serve as nootropic, anxiolytics and antidepressants.

Health stackexchange?

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


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Are there grass or fiber eating birds?
My understanding, that may be wrong, is that cellulose/fibre has little nutritional value to many animals because it's hard to break down thus making consumption inefficient. However, Ruminating mammals, other mammals such as black bears, and many insects such as grasshoppers digest grasses.
Are there any birds with the gut flora to break down fibre? Or even some that eat grass but digest it in another way?

The hoatzin has a digestive system that makes use of bacterial fermentation. Many other birds also consume grass, e.g. ostriches, ducks and geese.
There's also a large body of literature on how birds can digest cellulose.

+1 It could also be noted that the fact that Canada Geese eat grass is one of the reasons that they are thriving (i.e., a nuisance) in the human constructed suburban environment of lawns and ponds.

My society finch love to eat moist grass particularly orchard grass. Nibbling the whole strand they have chosen back and forth until they are satisfied with the texture and then proceeds to swallow it. They brake most grass into no bigger than an inch in length. I buy the orchard grass from most pet stores. problem with that is the grass has been dried. not very suitable for eating but Fantastic Four nesting. I grab a handful of dry grass and mist it with water then place it in a plastic sandwich bag, put it in the microwave for 30 seconds.
Do not completely seal the bag.
When i place it in the enclosure its like bird ice cream. fantastic treat!

Welcome to Biology SE and thanks for your interesting comment on your finches. However, while this answer would be more than suitable at Pets.SE, here at Bio.SE we expect a little bit more science behind answers. I have flagged it to be converted into a comment instead. Once you gain enough reputation you can place comments anywhere.

If possible can you add a picture or something.


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How long does it take for the Opioids listed in the Description to induce Analgesia when Administered via IV?
How long does it take for the Opioids listed in the Description to induce Analgesia when Administered via IV? Now I don't mean how long it takes for euphoria to come on but analgesia.
The opioids I would like to know this information to include:

Buprenorphine
Butorphanol
Fentanyl
Hydromorphone
Methadone
Morphine
Oxycodone
Pentazocine
Pethidine (meperidine)
Sufentanil
Tramadol

These are 'peak' values when administered via IV, with the exception of oxycodone. There will be some variation person to person depending on their opioid tolerance and any concomitantly administered medications.
Buprenorphine: 60m
Butorphanol: 5m
Fentanyl: 5m
Hydromorphone: 30-90m
Methadone: 1-2h
Morphine: 20m
Oxycodone: Not administered intravenously
Pentazocine: 15m
Sufentanil: 3m
Tramadol: 2h


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Primary cilia: what cell types have non-motile cilia that migrate?
My understanding is that there are two broad categories of cilia: motile and non-motile (also called primary.
Examples of the former include sperm flagella and the cilia of epithelial cells that line the airways.
Examples of the latter are mostly single cilia that protrude from the cell and act as an antenna, usually packed with certain receptors (HH pathway, Notch pathway etc.)
In the inner ear, a primary cilium called the kinocilium extends out of the center of the apical side of hair cells and migrates to the lateral side over the course of a few days. This cilium is non-motile, it is simply anchored to a basal body which is pulled to one side of the cell.
Does anyone know of another such example in any other tissue? A single non-motile primary cilium whose basal body migrates along the apical plane of the cell after docking with the cell cortex.
Thanks.

It's hypothesized that planar cell polarity is many cases functionally associated with asymmetry of (primary) cilia (Axelrod (2008)). So, the phenomenon of primary cilium migration could be not that infrequent. One example is the development of ependymal cells in brain ventricules: They are multiciliated and the cilia are motile, but ciliogenesis starts from a single cilium, which is not motile and which migrates from the apex to the rostral end of the cell:

Mirzadeh et al (2010)
Bayly & Axelrod (2011)

Seemingly less clear (for me, at least) cases are non-motile single cilia on the lens fiber cells and may be, embryal node cilia (which are motile in the mature state):

Wallingford (2010)
Sugiyama et al (2010)


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I'm 20. Can I still grow taller?
I'm 20, in about 6 months I turn 21. For some time I've been wondering whether there are natural, non-surgical and non-pharmaceutical ways that humans can continue to grow after reaching adulthood.
Please answer only if you are certain about this or you can reference any
trustworthy source.
Thank you a lot friends.

This is probably not an on topic question as it is more of a personal medical question rather than broad biological question- read the posting guidelines and try a more broad rewording of the question (about variation in growth rates with age - i.e. "when do we stop growing and how much variation is there?") other wise someone will come along and close it. But to answer your question, yes you can still grow, I'm 23 and have only recently (seemingly) stopped.

There's no normal way of getting 5cm at the age of 20. I'd say that you're more than fine, with 1.75 cm. The best thing to do is work on your posture.

Edited question to better fit Bio.SE guidelines.

Also, exercise promotes testosterone production and increased testosterone levels promotes growth - that probably partly explains my own late growth spurt (loss of asthma at 18, started sports, then grew 30cm in a year - most of which was in the first 3 months, if you want to know what growing pains feel like I am the one to ask!).

The answer is probably No.
"Long" bones - like the tibia, fibula, femur, humerus, etc. grow at the ends during childhood via a special formation called the Epiphyseal plate (also known as "growth plates"). The plates are composed of a special cartilage that grows, and slowly calcifies as a person reaches adulthood.
When the growth plates completely stop expanding is left to genetics, but generally happens 2 years after puberty finishes - about 16 for women and 18 for men. So after those ages there's little, if any, significant growth - though it can happen in very rare cases.
To date there aren't any exercises you can perform that will elongate bones. It doesn't make physiological sense; stretching puts stress on muscles and tendons - not bones. Weight lifting will compress bones, making them more dense and will make you shorter in the long run.
While there's been some success in getting chondrocytes to grow cartilage in vitro, there has yet to be significant gains in vivo, thus there aren't any medications available that would cause growth.
The only widely practiced way of gaining height after adulthood is with very painful surgery that involves a lot of braces. The bones are systematically broken, held in place, and allowed to heal. The setup looks like this:

While we get closer and closer to being able to control such things every day, for the time being (and I wouldn't count on this changing anytime soon) everybody is stuck with the height they were genetically programmed with.
As an aside: Being tall isn't all it's cracked up to be. At ~197cm I can tell you it is hell finding pants that fit.

I'd say the answer is Yes (but unlikely to be significant growth) given my own personal experience, the average may be 18 for men but there will be variance around that. A school friend stopped growing at 14, I stopped at 22.

@rg255 - Sure, there's going to be variance in everything. However, I don't want to mislead, so I use the averages. Answering 'Yes' when you're talking about 10% of the population is misleading to me.

this (http://www.cdc.gov/growthcharts/data/set1clinical/cj41c021.pdf) would certainly suggest I'm way outside of the averages - up until the age of 18 I was below the 5th percentile, now I'm above the 90th! Imagine what my growth line would look like on there. I hadn't realised there was so little variance so perhaps "no" is broadly the right answer, but there are some cases of growth right up to the age of 25 - it seems most stop about 2 years after the end of puberty which in men is marked by this event (http://en.wikipedia.org/wiki/Spermarche).


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Is 1 g/l living biomass for a Biogas fermenter plausible?
A usual number for a healthy biogas fermenter is $10^9 - 10^{10}/mL$ Bacteria, 10-15% of which would be methanogenic archae. Exceptionally healthy fermenters have more total bacteria and up 25% archae.
The mass of E. coli is given with 670 femtograms. If E. coli is representative for fermenting bacteria that would put us on the order of magnitude of 1 g/L living biomass.
This seems like much to me, though this is just a gut feeling.
As additional information, such a fermenter will have a total solids content of about 10%. A typical loading rate will be 4-5 g VS/d l *, two thirds of which get metabolized to gas. To put it another way: The amount of digested biomass per day would be the same order of magnitude as the living biomass. However, as anaerobic digestion is a multistage process, with at least three steps, each population will have a higher rate of digestion to mass.
Are the numbers basically sound? Is E. coli an exceptional bacterium in terms of mass? Are archae generally as massive as bacteria? What are bacteria counts for other fermentation processes?
(*) g volatile solid per day and liter: for each liter fermenter volume, this many g potentially degradable matter are added per day

Not sure if the tag 'digestive system' is really appropriate.

could you write out some of your abbreviations?  a bioengineer might not be here to answer your question, but someone will probably find it for you if someone not from the field could read it.  Also I expect that there is a huge variation in this behavior for archaea.  you want to make a methanogenic fermentor and are looking for an upper limit, yes? this might help...http://www.sciencedirect.com/science/article/pii/S0723202008000222

I think the only possivle abbreviation was VS, did I miss any other?

VS yes; VS/d volatile solids is days- ok. TS, AD?

Fecal matter can contain up to 10^12 microbial cells/gram. The colon is essentially an incredibly efficient biogas fermenter. So your numbers seem plausible to me.

I've done experiments with yeast, and they can easily ferment glucose at the rate of 4g/L/d.  Probably faster, if one were to optimize it.  So your numbers don't seem crazy.

Can you provide a source for that?


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Melting point of a fatty acid?
What factors determine the melting point of a fatty acid?

Chain length
The number of methylene group
The ionized state of the fatty acid
Its degree of saponification
Its ability to alter the entropy of water

Are you looking for one answer of the 5, or are multiple answers possible? If it's the latter, then it's 1, 4, 5 from a quick recollection.

You'll want to wait for a full answer. All of the answers will affect the melting point to some degree, but whether it's a significant amount is another thing.

You might look at this question and answer which was posted to SE.Biology but moved to SE.Chemistry. Logically I would expect that your question will also be moved.

melting point of fatty acid increases with increasing chain lenth

(1) Chain Length

Will definitely affect melting point, as this website explains pretty well:
"Melting point principle: as the molecular weight increases, the melting point increases."

(2) Number of Methylene groups.

This is another way of describing unsaturated from saturated fats. The more saturated a fat is, the straighter it is. Methylene groups cause kinks, which disrupts the Van der Waals forces along the rest of the carbon chain.
As such, from the link above again:
"On the other hand, the introduction of one or more double bonds in the hydrocarbon chain in unsaturated fatty acids results in one or more "bends" in the molecule. The geometry of the double bond is almost always a cis configuration in natural fatty acids. These molecules do not "stack" very well. The intermolecular interactions are much weaker than saturated molecules. As a result, the melting points are much lower for unsaturated fatty acids."

(3) Ionized state of the fatty acid.

This will have a very minor affect. The fatty acid generally has an unpaired ester (-ate at the end) which can have a negative charge. However, from the link above again:
"However, in fatty acids, the non-polar hydrocarbon chain gives the molecule a non- polar character."
So even if the ester had a charge, the negative character is miniscule compared to the intermolecular forces exerted by the non-polar tail. Particularly since the charge can distribute amongst the two oxygen molecules which are conjugated, reducing the reactivity further.

(4) Degree of saponification.

I'm not super-familiar with the degree of saponification, but from a quick overview of the process I'd say this wouldn't affect melting point - counter to my comment. The process of making soap involves only the acidic portion of the fatty-acid triglycerides. That portion of the macromolecule is going to be pretty much the same regardless of the fatty acid, so it will have nearly the same reactivity regardless of its chain length and conjugation.
What will not saponify are usually waxes - which are pretty much fully-saturated hydrocarbon chains with very few (if any) acidic sites. Parafin Wax, for instance, does not saponify, and has the formula ${C_{31}H_{64}}$.

(5) Ability to alter entropy of water.

Like the degree of saponification option above, the ability of a fatty acid to alter the entropy of water correlates to the number of reactive sites throughout the molecule. As-such, unsaturated fats (those with methylene groups) are going to be slightly more reactive as pi-bonds are more reactive than sigma bonds.
So, given that this answer relies on a previous option, it's probably better to go with the previous option.
Ultimately, if I were answering the question I'd choose 1, 2 since the rest either depend on those two or are miniscule. However, beware that it's your question to answer and not mine.


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When can I assume individuals marrying into a pedigree are non-carriers?
If I'm not told that they're non carriers, and if I don't have proof of their geneotype based off of progeny, when can I assume they're non carriers for a trait?

All the time.
Unless you are specifically told/shown they are carriers, they are assumed to be Wild Type and do not carry the mutation.

You can only rely on statistics in this case. Check the population the person is coming from for statistical probability to be carriers.

Usually you assume neither situation. You are given some probability that they carry the trait based on measured allele frequency in the population. Then you use that probability in any downstream application, such as calculating the probability the children are carriers or affected with the genetic condition.


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How can the child and the mother have different blood types?
As far as I know the fetus is fed by the umbilical cord which basically connects his/her circulatory system with the mother's in order to supply oxygen and nutrients. But how is this possible if they (the mother and the fetus) have different incompatible blood types?
It is possible that the father has A blood type, the mother B and the child A and thus incompatible with the mother's.

The fetus makes its own erythrocytes from a combination of the father's and mother's genome. If the mother is B and the father is A, the child will be AB as they are co-dominant. Only 'O' is recessive. This may be a too-basic question for this site...

If the mother is BB and the father is AA. In practice, the kid could be AB, B, A, or even O, if the mother and father are both heterozygous. BO/AO.

The blood of the fetus does not mix with the blood of the mother.  Instead, the placenta provides a system where the two separate blood streams flow past each other with thin separation allowing nutrients to flow between the two streams but the not the blood cells and other large components.

what's more, fetuses use a different set of hemoglobin genes, designed to take oxygen from the hemoglobin in mother's blood stream by diffusion through the placenta.


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Can a person really die quickly from biting their tongue?
A common trope in certain circles (like Eastern martial fiction), is someone committing quick suicide by biting his or her tongue.  But is this really possible?
The internet turns up millions of pages of speculation, but no Straight Dope.  People have been removing the tongues from mammals, and each other, throughout human history.  There has to be some scientific data on this somewhere.
Will an untreated, severe, lingual laceration, really result in bleed-out of an otherwise healthy human?
Or will lingual trauma facilitate swallowing the tongue sufficiently to cause asphyxiation?
What does the science say?
Thanks!

generally untreated and severe laceration of any body part can is at risk of causing death. But according to this book the tongue tends to stop bleeding quickly  (http://books.google.co.uk/books?id=a7CqcE1ZrFkC&pg=RA1-PA1014&lpg=RA1-PA1014&dq=lingual+laceration&source=bl&ots=lgjuQlh93C&sig=th6-PfF54HbnpzkFyHotBqF1Z1U&hl=en&sa=X&ei=EUYjUcmECYXVtAb9w4DYCg&ved=0CEAQ6AEwAg#v=onepage&q=lingual%20laceration&f=false)

@rg255: Excellent. This article says that Lingual artery hemorrhage is "life-threatening".  Although it's reporting an injury caused by a botched biopsy.  It's not at all clear (to me) that a sufficiently similar wound could be caused by a person's own teeth.

I guess there is an element of "luck" if suicide is the intended outcome - it will likely depend on how hard one bites, how sharp the teeth are, and how many blood vessels one punctures severely (do not try this at home)

@rg255, If it depends on hitting the artery with your teeth, it might not be anatomically possible. Hoping for some experts or citations to chime in.

Looking at the diagrams of tongue blood vessels it looks like the ranine artery runs a long way along the tongue, and if you hit enough other veins and arteries there's no reason to not expect a high enough bleeding rate

The following letter and references therein may perhaps shed some light on the matter: http://pmj.bmj.com/content/77/913/743.1.full

Thanks @jarlemag.  The references seem to pertain to five-ish cases of tongues that were amputated to some degree.  Best I can tell -- this side of the pay-walls -- is that no immediate fatalities occurred in those cases.

One of the comments expressed surprise that the patient didn't die, though, so it seems possible. I'd read the articles and post an answer, if not for the paywall!

How about biting it off and choking on it?

I've seen it done in anime before. Not sure about real life though.The proof is in Death Note and the original Naruto anime

No, unless you like bite your hole tongue off that's not really a thing it would be like saying (with no hate of thinking your stupid), you got a cut on your leg when your messing around out side and died. and i bite my tongue allot when i am eating.

I know of an ER doctor who had a patient who removed (by biting and pulling) every last part of her tongue, she survived that (although, her ability to speak was probably shot). The stump of her tongue clotted before she could even go into shock (at least where it was really serious).
Here is a quote from the book Angels in the ER  (this is a paramedic speaking with the doc):

"Every bit of it. Gone. And the funny thing, Doc, is it didn't even
  bleed very much."
  The doctor then asked his patient to open her
  mouth... "it was gone!"

It would certainly be possible to commit suicide doing this if one was a hemophiliac or continued to remove the clot from the hole(s) in their tongue (although the latter could be a potentially painful and I have a feeling that it would take a very, very long time!).

@BrockAdams I will get you a direct quote ASAP, right now I'm not at my house and don't have the book at my disposal. There are plenty of places you can get a PDF download, and it would be chapter 11. However, if you are willing to wait a day or two I can probably get you a quote.

@BrockAdams I edited my answer.

Thanks!  Looks like a reputable counter-example.  This answer will do unless an authoritative analysis or statistical result is posted. (Previous comments are now obsolete.)


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Does every human eye see the same visible spectrum?
It is said that human eye can see light with wavelength approximately between 400nm and 700nm.
Are these upper and lower bounds same for every human? If not, what are the means and standard deviations of these upper and lower wavelength values for human eyes?

just the fact that people can be color blind should answer that for you. I think this question is more appropriate to a biology site, because color percetion depends on the biological receptors of the eye  not in one to one correspondence with wavelength.

Basically every human sees the same spectrum as we all have the same four types of photoreceptors: rods and a cone for green, red, and one for blue light.
In very rare cases there are women who have a duplication of one of their cone genes (usually the red one). If one of those duplicates mutates slightly, this results in a kind of fourth type of cone (see it mentioned here at Wikipedia), so they see a different spectrum.

This is not entirely correct, there are multiple variants of each of the three colour photoreceptors that have slightly different response curves. I do not know whether these variants result in different minimum and maximum sensitivities.

Also, you've somewhat confused the women having a fourth type of cone too. What happens in some women is that they have two variants of the same colour photoreceptor (red, almost aways).

I've also read studies on intraocular lenses that suggested that the humans eye sensitivity to light changes with age.

The variants would produce different maximum and minimum sensitivities. The bounds aren't sharp, they are soft. As light moves out of the visible spectrum the response gets weaker and weaker, but it's not just a sharp drop. So different variants of photoopsins would change those "boundaries".

Human eyes all use the same optical pigment photopsin, so they all have the same basic frequency response.
There are differences. For example cataracts will change the sensitivity of the eye to colour, and people with colour blindness have various defect to cone cells that affect colour response. However these are secondary effects.


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Why doesn't recombination occur in male Drosophila?

"Males do not show meiotic recombination, facilitating genetic studies."

For a while I have known that this phenomenon occurs, this quote comes from the Wikipedia page on Drosophila melanogaster, and I frequently use this feature of Drosophila in constructing hemiclones for my own research in quantitative genetics.
But, until now, I have never asked why doesn't recombination happen? Why would this feature evolve?
Further, why is the absence of recombination sex-limited to males, why do females have recombination?

This is a venerable fact.  Exceptions in D. melanogaster strain Y-007 have been observed and D. ananassae has consistent male cross-overs, but this work dates back to the 1970s.
This Current Biology 2002 paper is not exactly new, but sheds some light on the issue in question.

In male Drosophila melanogaster, meiosis occurs in the absence of recombination or a recognizable synaptonemal complex (SC).

The authors used a GFP-lac fusion to observe a series of sections of the male fly in meiosis with integrated lac - specific binding regions.  They see for the most part that the GFP bound segments of the DNA are not associated in cell division.  That is, homologous chromosomes physically associate during meiosis (via the SC) and in male drosophila, they do not.
It seems from more recent work, that the details of how this work is still being worked out but several gene regions and factors have been identified.  Suspected factors that help conspire to align the various homologous chromosomes are being looked into.  Take a look at the P.I.s biblio for more.
This isn't my main field, but as I understand it, many aspects of meiosis are still being mapped out.
As to the question of how this evolved and why; its definitely strange.
 It looks like there is a gender selected trait where the SC doesn't form in males.  Its easy to imagine a mutation that caused males only to lose recombination - the process is so complex its hard to imagine such a trait not showing up.
Still it's surprising to think that the trait has not only survived but become dominant in Drosophila all over the world.  To be a common traits to so many Drosophila species, it must have happened more than 10 million years ago.  Explanations of the advantages of sexual reproduction often include recombination.  Even the human Y chromosome has a self-recombination mechanism that reduces error in the coding regions.  As such, its hard to believe that this is not a huge disadvantage for the flies.  Still, if if it were such a big deal, you'd imagine Y-007 would have dominated and re-introduced the trait.
The only theory I can think of might be called 'lazy males'; that the males got the females to do one more thing for the offspring and it somehow outcompetes the sperm of the recombining males.  Lots of sperm are non-motile; that's a fact for humans, I have no idea what its like for flies that recombine.  Take a look at the variance in morphology as well - sperm are really crazy ugly sometimes and a good deal of the mating process is to help weed out the defective ones.  Without recombination, might it be that males produce viable sperm at a greater rate, helping them in sperm competition, which I'm sure is the case for fly mating - Drosophila are not monogamous too I'd guess?  Anyway that's not a researched idea, just a guess on my part.

thanks, this is a good answer so far, could you shed any light as to why that might evolve?

thanks for asking this question! the answer is I don't know and it seems like a lot of the speculation behind this would be buried into the fly literature pretty deeply.  I put a guess into the entry.  I'm actually going to write one of the authors and ask them what they think though.  It's the sort of question some of us scratch our heads about while a dozen or so talk about the fine points over coffee every day.

@shigeta The link to the "Current Biology 2002 paper" is broken. Do you remember the reference? Thanks

To the best of my knowledge there is no strong evidence as to the reason why. The most reasonable explanation seems to be that it evolved as a crude mechanism for preventing recombination of the male sex-chromosome.
You might then ask why a mechanism targeted to the sex-chromosome specifically (as in humans) did not evolve to which I'd suggest that evolution frequently continues with "good enough" solutions where the benefits of apparently better solutions are small or don't involve incremental benefits and note that there is some evidence that lower rates of recombination are beneficial in Drosophila (ref]).

This phenomena is known as achiasmy, where recombination is absent in one sex in a species. The Haldane Huxley rule states that in achiasmic species, the sex without recombination will always be the heterogametic sex (XY or ZW). This is basically the only consistent rule relating to recombination. There seem to be exceptions to every other theory and pattern observed.
The Haldane Huxley rule supports the theory that achiasmy evolved to prevent non-homologous recombination between X and Y. However there are species (most mammals) where the X and Y do experience recombination, but recombination is limited to a small part of the chromosomes called the psudo-autosomal region.


text:
Solvent Accessibility, the 20% cut-off method
I'm reading the papers linked below and all three of them mention a 20% cut-off for buried/exposed residues, by calculating a relative solvent accessibility (RSA) value.
I understand how the RSA is calculated, by dividing the calculated solvent accessibility against its total solvent accessibility values from paper 4 table 2.
RSA = calculated/total
e.g. if arginine is calculated to have a solvent accessibility of 55.43 and its total solvent accessibility is 241 then the RSA = 55.43/241 = 23%, so this arginine is considered exposed (see statement 1 below).
What leaves me confused is the definition or lack of the 20% method for defining an exposed or buried residue.
I am assuming it means one of the following:

If an amino acids RSA is below 20% it is buried and above 20% it is exposed. So for an amino acid with an RSA of 21% is considered exposed, this value seems a little low for me. I think statement 2 would make for sense.
If an amino acids RSA is below 20% it is buried and above 80% it is exposed.

Which statement if any is correct?
Paper 1 - see methods section first paragraph
Paper 2 - see figure 5 and table 3
Paper 3 - see abstract and dataset
Paper 4 - see table 2 for total values

Its 1.  Below cutoff, buried, above cutoff accessible.
Paper 1: "A cutoff of 20% was used to define the two states, buried or exposed. With this definition, the dataset was, roughly, evenly split between the two states."
Only two states are possible: solvent accessible and buried.
Paper 2: "A given residue is defined as exposed (e) if its RSA is larger than the cutoff
value, and otherwise it is defined as buried (b)."
Abstract for Paper 3: a cutoff of 20% for two-state definition of solvent accessibility.
If it were def #2 it would be a three state definition.
Paper 4: "On average, 15% of residues in small proteins and 32% in larger ones may be classed as “buried residues”, having less than 5% of their surface accessible to the solvent..."
This paper, by the dean of structural analysis Cyrus Chothia, uses a 5% cutoff, not 20%...
The abstract goes on to say... "The accessibilities of most other residues are evenly distributed in the range 5 to 50%."
This passage hints that SA doesn't even go up to 80%.  Just considering that you often won't get more than say 60% with this calculation.  I'm just guessing; but the thought being that unless you are at a terminus of the protein, which is often disordered and doesn't show up in a crystal structure, you will have two adjoining amino acids for each residue - just the solvent accesible area taken up by the contact with neighbors could easily be 20% of total.

y welcome!  papers are like a wall of words.  This belies the fact that the methods are often the simplest method you can think of.

Are you sure that the RSA formula is right?
I have found a different description：Relative solvent accessibility classes are usually derived from the DSSP program by normalizing it at the maximum value of exposed surface area obtainable for each residue.Different arbitrary threshold values of solvent accessibility are chosen to define binary categories (buried and exposed) or ternary categories (buried, partially exposed, or exposed).
Pollastri, G., Baldi, P., Fariselli, P., & Casadio, R. (2002). Prediction of coordination number and relative solvent accessibility in proteins. Proteins: Structure, Function, and Bioinformatics, 47(2), 142-153.


text:
Very high 260/230 absorbance ratio of an RNA sample
After my most recent RNA extraction, the RNA samples had very high 260/230 absorbance ratios, (ranging from 5 to 25).
I've never gotten numbers like this and I know the ratio is supposed to be ~2 in general.
What could be the reason for such a high 260/230 absorbance?

http://www.scientistsolutions.com/t11627-high+260_230+ratio+for+dna.html suggests that high ratios are caused by high salt concentrations in your sample?

Thanks for the link, but in my experience salt contamination would cause a low 260/230 ratio, as salts absorb at 230 nm.

Gergana is right about the effects of the Guanidine isothiocyanate, but not the details there of.  Guanidine isothiocyanate absorbs strongly at 260 and NOT 230 (guanidine hcl is the one that absorbs strongly at 230).  As such if your RNA is highly contaminated with guanidine isothiocyanate, which is used in at least one buffer in just about every RNA prep kit, your 260/230 is going to be much larger then 2 (also the "concentration" will be artificially high.  So if you are getting a 260/230 of 25 and have a "concentration" of "1000 ng/µL" you may actually have less then 200 ng/µL of RNA and a ton of Guanidine isothiocyanate throwing everything off.)

The 260/230 ratio gives you idea about the contaminants in your sample. Guanidine isothiocyanate, which is usually used for RNA isolation, absorbs at 230nm, so that might be what you see. But another explanation might be that your sample is very dilute (how much RNA did you get?), so that your A260 is also very low. Then it would be difficult to accurately measure A230, which will result in overestimated 260/230 ratios.

The RNA concentration was not lower than usual (1000 ng/µL), but in the future I'll keep this possibility in mind.


text:
Are there examples of encryption in nature?
There are examples of mathematics in nature such as Fibonacci number, fractals, etc.  Are there examples of encrypted information?
What I am looking for is a pattern that seems random on the surface, but once you put it through a "decryption" process, it is actually something else.  Not patterns that seem random because they are complex.
One example that comes close is DNA.  But I see DNA as a form of encoding, not encryption.

You may want to define what you're looking for a bit better. Isn't something that appears random, but is actually a complex formation practically the same as encryption? I don't see the difference between your first and second sentences in your second paragraph.

I see encrypted information as needing to be decrypted before it can make any sense.  Whereas given enough resources, complex patterns can be understood without modifying the data itself.
For example trying to read an encrypted text vs trying to read Chinese (if you don't know Chinese).

@KarnRatana: encryption implies the concept of "secrecy". You encrypt data so that only a certain individual or group of individuals can access it using a certain key. See also http://stackoverflow.com/questions/4657416/difference-between-encoding-and-encryption . It is difficult to imagine a biological situation where secrecy would be an issue.

@nico Thank you.  I am not looking for encoding but encryption.  Which, as you mentioned, does imply secrecy.  I'm not well versed in biology and couldn't think of any example, hence the question =)

I can think of microbiological examples of stealth technology, where viruses, such as HIV can down regulate the production of MHC I molecules in an infected cell to avoid Cytotoxic T-Cell detection or bacteria like S. pneumoniae using the virulence factor of a smooth sugar coat to avoid immune system detection.

pollen-flower interaction probably.

@KarnRatana The question is very interesting but I think it is currently unclear. Would you consider machiavelan intelligence in primates (I groom an individual but I hiding form another individuals when doing so) and camouflage or mimicry as examples of encryption when only individuals of the same species are able to see/disantangle? Can you please try to accurately define encryption for its application to biology?

One example is in the development of the immune system. V(D)J recombination, antibody production, and T-cell receptor production generates a specific "key" that, in most cases, can only be bypassed by that individual's molecular inventory.
In that sense, parasites, mutualists, and commensalists could be viewed as black, white, and grey hat hackers, respectively.
Another example is the organism-specific tRNA synthase inventory and the matching tRNAs.

This sounds similar to what @Nick mentioned (in concept not biology). Which deals more with authentication than protecting a "message".

One example is sperm-egg attraction. Many species release their egg and sperm to be joined in water. The egg must try to avoid being fertilized by the sperm of a different species. So an egg secretes a special peptide which attracts the sperm to its location. The amino acid sequence of that peptide is unique for each species and sperm can only recognize the peptide secreted by the egg of their own species. To any other sperm, the peptide is just another molecule present in the water. http://www.ncbi.nlm.nih.gov/books/NBK10010/

Isn't this just signalling?

Yes, but isn't encryption a form of signaling? If signaling is communicating biologically, it follows encryption will involve some signaling, but the message will be masked, so that not everyone will understand it.

I don't see there's anything masked here; it's just a matter of using different signals.

Perhaps protein folding is an example of decryption? From a single primary sequence (i.e. the string of amino acids), it is impossible to guess the function of a protein. The folded protein is the functional unit (of course it might be further modified).

Encryption is not about the impossibility of deciphering, that would rather be hashing. Also note that knowing folding does not immediately give you the function, just the structure.

I would think that the Bacteria - Phage restriction enzyme and methylation enzyme race could be thought of as a form of encryption. If your DNA isn't "signed" with the appropriate methylation patterns then it gets chopped into pieces and destroyed. This is the signing/verifying side of encryption rather then the encrypt/decrypt side, however.
http://en.wikipedia.org/wiki/Restriction_modification_system

This sounds similar to what @nbogard mentioned (in concept not biology).  Which deals more with authentication than protecting a "message".

R-M systems are fascinating, but it seems to me that there is no message that is encrypted.

@JackAidley modern encryption is used for signing/verifying messages as much as encrypting/decrypting them. The RM system is a form of signing/verifying.

@Nick: I disagree, my view is closer to that in Wikipedia - "[E]ncryption is the process of encoding messages (or information) in such a way that eavesdroppers or hackers cannot read it, but that authorized parties can".

@JackAidley Well if you want to be pedantic they can be examples of Cryptography rather than Encryption, but its the closest example in Biology I can think of.

I actually think I may have come up with a biological analogy to encryption.
If you define encryption as taking information, breaking it up into random pieces or just small packets of data, that are sent on their way and when they reach a source are put back together based on a key, so that unintended recipients cannot interpret the information, then I would say that how the senses process the information that we experience, process it, send it along its way and then it is recompiled to form our experience of reality, is something akin to encryption/decryption.
Take vision. Our eye receives and focuses photons of light into electrochemical signals that get relayed to the visual cortex. In the visual cortex, that data is reassembled into our experience of reality of the world around us.
If, experimentally, we were able to tap into that signal running along the optic nerve and tried to interpret it just from the data flow, then it is unlikely that we would be able to reproduce the image being collected the way we could read the electrical impulse being transmitted from a CMOS or CCD sensor chip. I say this because our visual system is predictive. There is actually more information generated by the visual cortex than is being received and transmitted from the eyes.
We develop these keys in early child development and lay down these neural networks so that we are able to build and interpret an image without all of the data. This is how we can navigate through the world, drive a car, fly a jet fighter and cope with the signal delay that is inherent in the system. This may be more an example of compression of signal, but a compressed signal without the correct decompression algorithm would be a rudimentary form of encryption.
We can also see, with synesthesia, that when there is crosstalk between the regions of the brain that are are different from the norm, messages will be perceived in possibly unintended ways. Letters and numbers have colors, sounds produce visual imagery, etc.

I think breaking information up into pieces as part of a transfer is not really encryption.
If a data is encoded, then with enough samples, we should be able to learn how to decode it.  But if a data is encrypted, then even with all the samples we want, we might not be able to decrypt it without first figuring out the key.
So if there's any data in nature that seems random and we cannot understand it even with a lot of samples, then maybe it is encrypted.  If so, then we might need to try a different approach in trying to decipher it.

Not sure we can name it encryption, but

a pattern that seems random in surface but once you put it through a
  decryption process, it is actually something else

reminds me about some forms of predatory camouflage. I'm talking from the perspective of the prey: the predator blends with the environment and what the prey perceives is just 'random' environment. When the prey 'decrypts' that there is actually something else, it is generally too late.

Predator prey situations are assumed to have a reason for encryption, as they have signaling.  Thus could be the change in appearance of a coiling snake, not only preparing to strike, but sending fake codes to prey at the same time, or coiling differently for mating.
On the recieving side, the timing of the length of gaze and head movements of deer in the midst of observing a scene might be considered cryptoanalysis, as they absorb and process data and carefully select responses and countermeasures.

Please add some references to support your answer.


text:
Difference between "transcriptional activity" and "RNA expression"
I am working with a network object where the nodes are different events in molecular biology.
Specifically;
Catalytic activity of X,
RNA expression of X,
GTP-bound activity of X,
Kinase activity of X,
Oxidoreductase activity of X,
Phosphatase axtivity of X,
Transcriptional activity of X,
Phosphorylation at residue Y.
What is the difference between RNA expression and Transcriptional activity? And which is the one that an Affymetrix microarray is measuring?
eg.;
transcriptional activity of KLF2, transcriptional activity of ATF2 RNA expression of HSPA1A RNA, and expression of CYP1B1

I'm not familiar with what you're doing, but off the top of my head I'd say that the RNA Expression might be referring to everything post-nucleus in that the Introns are missing. The Transcriptase would show more activity because it would still Transcribe both Introns and Exons.

In your case, RNA expression and transcriptional activity probably differ in the stage of processing. Transcriptional activity refers to the binding and processive activity of RNA polymerase. There are different ways to measure this experimentally, but with a microarray you are measuring the amount of actual transcripts relative to the control array.
RNA expression usually refers to the amount of mature transcripts but is often used interchangeably with transcriptional activity. The distinction is made at the sample extraction stage and whether or not the RNA was selectively recovered using poly-A selection or other methods that isolate mature transcripts.
What your microarray will measure depends on the probe library constructed on the array and whether you are applying total RNA or selective RNA. Probes matching mature transcripts report for RNA expression. Probes matching immature or nascent transcripts can be used to measure transcriptional activity.
Careful probe design is required to distinguish between the different levels of processing.


text:
Can the Human body Synthesise Vitamin D from Phytosterols?
I know that the human body can synthesise vitamin D from cholesterol, but can it do so from phytosterols?

Is this article helpful? http://journal.frontiersin.org/Journal/10.3389/fpls.2013.00136/full Can you also give me a link to an article which states that Vitamin D is synthesized from Phytosterols in the first place.


text:
What are the limitations of commercial-grade DNA genotyping compared to full sequencing?
I've heard about services like 23andme, which offer genetic testing to the general public. As a person who knows very little about genetics, I'm interested in the subject and would like to know what the modern "commercial grade" genotyping really does.  What are the limitations of commercial-grade "genotyping"?  From what I've been reading, they test DNA against ~100 different markers, but do not really sequence it.
If I understand correctly, if DNA is sequenced, genetic markers and genes can be identified in it, including the newly discovered ones. However, (if I understand correctly) if DNA is genotyped, the genotyping is a one shot operation which states if some genetics markers are present in the DNA. To test against newly discovered markers, it would have to be genotyped again, right?
Thank you for any clarifications!

23andme briefly describes the technology they use here. They are testing the genotype of your DNA at roughly 1 million locations. The technology they use to do this is known as a microarray.
The limitations of using a microarray, as compared to sequencing, is that you will only find what you are looking for -- people often describe the disadvantages of microarrays as compared to sequencing with the streetlight effect/metaphor.
Arrays can only measure regions of the genome that they were designed to probe. Technically, if they probe 1,000,000 million locations, and the human genome is roughly 3.4 billion bases ... you can do the math.
In practice, SNPs tell you a bit more about just the nucleotide being interrogated, due to linkage disequilibrium (cf. tag/proxy SNPs), so the array might tell you more than you expect.
Of course, modulo sequencing errors, whole genome sequencing will tell you "everything" as far as recovering the NTs that make up your genome, but how much information that will provide you is another thing altogether (for now, that is).

+1: on the other hand, 23andme proposes a certain type of analysis to their clients that does not require whole genome sequencing. They say "We will test such and such SNP and tell you that you have x% probability of having an heart attack in your 60s"...

@nico: Yeah, very true. You can also get a copy of the data, though, which is cool. Also, they're also currently offering exome capture for some already existing members ... a look towards what the future may hold, perhaps.

Just to be transparent, I work at a microarray company, but I've also attended high throughput sequencing workshops.  I think this is a pretty fair assessment, but leave me a comment if you see anything out of line...
As pointed out by @SteveLianoglou, Genotyping microarrays are best for revealing whether a particular variant (not only SNPs but short insertions and deletions, copy number variations (CNVs) reliably and cheaply.
High Throughput DNA Sequencing has made great strides and the latest cost estimates are in the few thousands of dollars for a full human genome.  This is better for discovering new variants but currently its not a great way to do do say a medical test to see if you have a particular mutation.  The problem with sequencing right now is that sequencers have systematic biases - the local sequence can give the same error over and over again.  It takes some significant effort to differentiate the error from the real variant data.  In the workshop I attended, the data consisted of 38 full human genomes at 30-40x coverage. Despite this deep level of sequencing, systematic errors were still obvious (the proceedings are in press now - reference should show up at the link provided soon).  So it can be fairly expensive when you have done all your data analysis and validation data to get the variants via sequencing.  All this could change very quickly, but I think this is accurate in the current state of things.

I want to give the OP a slight variation on Steve's answer.
It is important to note that most of the genome is the same between different people. That isn't surprising, since we belong to the same species.
For example, it is estimated that there are about 10,000,000 SNPs (single basepair positions that may vary) in the human genome. So if you check 1,000,000 SNPs with a microarray (genotyping), you are covering ~10% of the possible differences. In addition, variation in some of the SNPs is very common while others are very rare, so if you check the most common 1,000,000 SNPs with a microarray, you might actually cover a very large portion of the differences. It is also possible that if you know in advance some general information about the person you are testing, such as ethnicity, you might be able to eliminate many uninformative SNPs.
This of course only refers to variation in SNPs (but these are the most common variations).

This is a good point - to test only what varies the most


text:
What species of bird is on this coin?
What species of bird is depicted on this coin?

http://www.artic.edu/aic/collections/citi/images/standard/WebLarge/WebImg_000100/139651_846511.jpg
Thanks in advance for your help!

well I don't think this is really a biology question given that it is probably quite an "artistic" impression of the bird, but some clues as to the coins origin would help people hazard a best guess at most.

The coin shows Ptolomey I Soter I, a ruler of ancient Egypt c. 367 BC – c. 283 BC. This Source suggests that it is an eagle standing on a thunderbolt.  This is corroborated here and again here so this seems most likely.  This question isn't really answerable from within our site scope, however, see the species identification tag wiki.  Hope the above helps though!

It said to be an eagle.
It looks like a Ptolemy V (204–181 BC):
http://www.bonanza.com/listings/-DD-G-068-Ptolomy-V-Octadrachm-COPY/16293418?gpid=21297750541&gpkwd=&goog_pla=1&gclid=CMWBpbOaxrUCFYx_Qgod6TsA9w
it looks to be a pretty standard motif of that era:

From: http://www.worthpoint.com/worthopedia/alexander-iii-great-336bc-greek-coin-150614256
I agree that this is not really a biology question.. but what the hey.

this is why we need new answer notifications when writing comments!

I know a professional ichthyologist who once had to propose an identification for a fish painted on a cave wall. Surely it is more difficult than identifying from a real specimen, a photo or a scientific drawing, but in some case, artistic representations have a precise biological source of inspiration, and it is meaningful to try identifying it.
If we didn't already knew what species of bird is represented here:
http://en.wikipedia.org/wiki/File:Seal_Of_The_President_Of_The_United_States_Of_America.svg
I think it would make sense trying a identification.

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


text:
Do women have greater reproductive success than men?
What proportion of men who go through their whole lives and never find a mate at all, and what proportion of women do? And is the proportion of men greater than the proportion of women?

Related

I think the answer runs along the same logic as this question: Which sex has higher variance of reproductive rate in modern societies - male or females?
Because its easier for a male to have offspring with multiple partners, more women would typically produce offspring than men.  In polygamous cultures, it can lead to significant differences of reproductive success between the genders.


text:
Confusion related to the DAVID tool
I am trying to use the DAVID tool to do some gene analysis. I have some probe set intensities for some cancer cell lines. I found this link in the DAVID tool http://david.abcc.ncifcrf.gov/tools.jsp. I am a bit confused with the terminology introduced here. It says gene list for the probe sets why is it so? I mean in the example you can see the probe sets like
1007_s_at
1053_at
117_at
121_at
1255_g_at
1294_at
1316_at
1320_at
1405_i_at
1431_at
1438_at
1487_at
1494_f_at
1598_g_at
Buy why are they called gene list not probe sets. Why?

Its a bit confusing, but DAVID uses the term Gene List as a generic term.
Looking at Step 2, you can submit many kinds of lists to DAVID, including actual gene symbols, Ensembl or RefSeq Accessions, etc... actually nearly 30 kinds of terms including 'not sure' which probably looks at your list and tries to guess.
Affymetrix or Illumina probe set IDs are each designed to measure a gene, ideally, though its not precisely a one Probe Set to one Gene relationship.  This is because when the array is designed there may be a partial transcript RNA records which turn out later to be parts of a single gene.  There are also probe sets which may turn out to hybridize to similar sequences in more than one gene.
Its messy, but its also true that often more than one gene symbol will appear for the same gene because of historical naming conventions...


text:
Can any animals photosynthesize?
Plants and animals have the following distinct properties:

Plants live from solar energy by photosynthesis, they use solar energy to make sugar and oxygen out of carbon dioxide, which gives them energy. Animals live from the sugar and oxygen plants created and produce carbon dioxide for their energy.
Animals can move across the planet while plants are tied to the ground.

Clearly, animals have a harder time to survive with no plants within their reach than plants have without animals coming close. This is logical because solar energy is always there while plants are not.
So my question is: Are there animals that can do photosynthesis? It's obvious that an animal with plant-like stateliness would be non-beneficial since it relies on eating other plants for it's energy and there may not always be plants within reach from it's spot.
But animals using the sun and carbon dioxide for energy production does not sound so stupid.

Night animals could also gather energy in their sleep.
Much easier than plants, animals could make sure nothing blocks their sunlight.
Many animals go through periods of hunger because food is scarce, for some of them this period is paired with high sunlight levels. (the dry season f.e.) (EDIT: This is just an idea, of course photosynthesis requires water, which is absent in the dry season. But still, in warm period with enough water, there's sometimes too much animals to feed from the available vegeation.)

Some things I already took into consideration:

I know that plants, because they are small in mass (compared to the area with which they can collect sunlight) and static, don't need nearly as much energy as animals do. Is this the main reason?
I know that f.e. reptiles, but in fact all cold-blooded animals, already use the sun's energy. But they only use the heat from the sun to warm their bodies, they don't photosynthesize.

Does symbiotic photosynthesis count?

@DVK What's that? I can't seem to find a good information source on that.

That's when an animal hosts some photosynthetic symbiote, like algae.

You might want to change your question title to : Are there animals that can do photosynthesis? The term "race"  doesn't have much meaning in biology.

More a comment rather than an answer, but there is some evidence of both natural and artificial transfer of genetic material between plants and animals - if you google "plant genes in humans" you will come up with some fascinating results. I don't have authority to make comments yet.

It's better if you give some examples of "fascinating results" I suppose.

@RobertJones I converted it for you :)

It actually has many example, there are already accepted answer. But I want to point out one thing. Solar energy per area on earth is not enough to be used as main source of energy for movement. Movement and thinking, in fact a whole animal lifestyle, consume too much energy to live with photosynthesis. It is far more easier to consume other organism for energy. That's why almost all autotrophes are stay still like plant or being a plankton like bacteria

first search for "list of photosynthetic animals" ...Sea Slug - Elysia chlorotica. ...
Spotted Salamander - Ambystoma maculatum....
Oriental Hornet - Vespa orientalis....
Pea Aphid - Acyrthosiphon pisum.... and corals also

There are 5 answers, all "yes" (though the first one is disputable).

First: there exists at least one animal which can produce its own chlorophyll:

A green sea slug appears to be part animal, part plant. It's the first critter discovered to produce the plant pigment chlorophyll.
The sea slugs live in salt marshes in New England and Canada. In addition to burglarizing the genes needed to make the green pigment chlorophyll, the slugs also steal tiny cell parts called chloroplasts, which they use to conduct photosynthesis. The chloroplasts use the chlorophyl to convert sunlight into energy, just as plants do, eliminating the need to eat food to gain energy.

The slug in the article appears to be Elysia chlorotica.

Elysia chlorotica is one of the "solar-powered sea slugs", utilizing solar energy via chloroplasts from its algal food. It lives in a subcellular endosymbiotic relationship with chloroplasts of the marine heterokont alga Vaucheria litorea.

UPDATE: As per @Teige's comment, this finding is somewhat disputable.

Second, animals need not produce their own Chlorophyll, and instead symbiotically host organisms that use Photosynthetis - e.g.  algae and cyanobacteria. This approach is called Photosynthetic symbioses.

Overall, 27 (49%) of the 55 eukaryotic groups identified by Baldauf (2003) have representatives which possess photosynthetic symbionts or their derivatives, the plastids. These include the three major groups of multicellular eukaryotes: the plants, which are derivatives of the most ancient symbiosis between eukaryotes and cyanobacteria; the fungi, many of which are lichenized with algae or cyanobacteria; and the animals. We, the authors, and probably many readers were taught that animals do not photosynthesize. This statement is true in the sense that the lineage giving rise to animals did not possess plastids, but false in the wider sense: many animals photosynthesize through symbiosis with algae or cyanobacteria.

Please note that while most organisms known for this are fungi, and some rare invertebrates (corals, clams, jellyfish, sponges, sea anemones), there is at least one example of vertebrate like this - spotted salamander (Ambystoma maculatum)

Non-chlorophyll synthesis

A 2010 study by researchers at Tel Aviv University discovered that the Oriental hornet (Vespa orientalis) converts sunlight into electric power using a pigment called xanthopterin. This is the first scientific evidence of a member of the animal kingdom engaging in photosynthesis, according to Wikipedia.

Another discovery from 2010 is possibly a second piece of evidence:

University of Arizona biologists researcher Nancy Moran and Tyler Jarvik discovered that pea aphids can make their own carotenoids, like a plant. “What happened is a fungal gene got into an aphid and was copied,” said Moran in a press release.

Their research article is http://www.sciencemag.org/content/328/5978/624, and they did not consider it conclusive:

The team warns that more research will be needed before we can be sure that aphids truly have photosynthesis-like abilities.

Third, depending on how you understand Photosynthesis, you can include other chemical reactions converting sunlight energy.
If the answer is "usual 6H2O + 6CO2 ----------> C6H12O6+ 6O2 reaction done via chlorophyll", then see answers #1,#2.
But if you simply literally translate the term (synthesizing new molecules using light), then you can ALSO include the process of generating Vitamin D from exposure to sunlight that
humans do thanks to cholesterol (link)

Non-biological answer.

As a side bonus, Ophiocordyceps sinensis is referred to as half-animal half-plant (not very scientifically IMHO). But it doesn't do photosynthesis.

I don't think it is really clear that sea slugs actually incorporate algal genes in to their own genome for the purpose of photosynthesis. Your link is based on this paper: http://mbe.oxfordjournals.org/content/29/6/1545.long
The possibility that the low number of reads is due to the presence of algae in the powdered sea slug is high and is the most parsimonious explanation of the results.
The paper is super interesting & provocative - how would this gene transfer occur? Also, it takes complete thylakoid membrane for photosynthesis, not a few components - possibly there's complx host intercton

I was all set to answer anothervquestion which has now been marked as a duplicate of this one. My answer adds new information relevant to the accepted answer here, so I have decided to post it here..
One longstanding candidate for something approaching this idea is the green sea slug Elysia chlorotica which uses chloroplasts derived from the alga Vaucheria litorea. Various pieces of evidence have indicated that the longevity of these chloroplasts in cells of the sea slug's digestive tract is explained by the presence of algal genes that have been transferred to the mollusc genome. However the most recent analysis of germline DNA  in the sea slug has revealed no evidence for such horizontal gene transfer. It seems that all of the evidence for algal genes and algal gene expression in the sea slug must now be explained in terms of somatically-acquired algal DNA.

Bhattacharya et al. (2013) Genome Analysis of Elysia chlorotica Egg DNA Provides No Evidence for Horizontal Gene Transfer into the Germ Line of This Kleptoplastic Mollusc.
  Mol. Biol. Evol. epub ahead of print

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


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How does inorganic phosphate inhibit alkaline phosphatase?
I want to know how is inorganic phosphate able to inhibit alkaline phosphatase.

When alkaline phosphatase dephosphorylates a substrate one of the intermediates in the reaction pathway is a phosphorylated form of the enzyme in which the phosphate from the substrate has been transferred to the enzyme. This phosphate is subsequently lost by hydrolysis. Under certain conditions alkaline phosphatase will actually catalyse a reverse reaction - the addition of inorganic phosphate on to alcohol substrates, and this also proceeds via the phospho-enzyme intermediate, but proceeds in the opposite direction.
This means that phosphate will inhibit the enzyme as a phosphatase via the formation of the phospho-enzyme, thus blocking the active site to substrates for dephosphorylation.

Reaction mechanism of alkaline phosphatase based on crystal structures: Two-metal ion catalysis
  Kim, EE &  Harold W. Wyckoff, HW 1991 Reaction mechanism of alkaline phosphatase based on crystal structures: Two-metal ion catalysis. J Mol Biol. 218: 449-464

So does that mean that inorganic phosphate actually can act as a competitive inhibitor and bind to the active site of the enzyme and interfere with its activity? Can it also act as a mixed inhibitor and bind to the Enzyme-Substrate complex as well or just the enzyme?

Yes it can bind to the active site. According to this abstract the kinetics are consistent with primarily competitive inhibition.


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How does plant grafting work?
Plant grafting is a process whereby a piece of one plant is inserted into another and results in a change of the original plant. For example, grafting a piece of a lemon tree into a bitter orange tree will cause that tree to produce lemons instead of oranges for the rest of its life.
How does this work? I mean, at the genetic level. I guess the grafted plant is now a chimera of some sort but if so

How does the grafted DNA affect the host cells?
Are all of the host's cells affected?
If we were to sequence the grafted tree which genome would we find?
Is it perhaps that the host DNA is not affected at all and the effects come via a change in expression levels? If that is the case I would assume grafting will only work between very closely related species. Is that so?

Basically I know very little about plant genetics and physiology. I remember from my undergraduate days that plant genetics are just plain weird. Most, if not all, have various levels of polyploidy. Is that relevant?

Surely the grafted part retains its genetic identity and grows normally (as "lemon" in your example) while the rest of the tree retains its "orange" identity. It is a chimaeric plant. You could think of it like an organ transplant in a mammal.

@AlanBoyd, yes I imagine it is chimerism of some sort. Yet you can take a normal bitter orange tree, cut off most of its branches (not even sure that is necessary) and graft a piece of lemon tree bark onto it. From that day on, the entire tree produces lemons, not oranges. So, somehow the grafted tissue is suppressing the original plant. Not what happens in an organ transplant.

This article analyses the exchange of DNA during the process of grafting
Exchange of Genetic Material Between Cells in Plant Tissue Grafts - Stegemann and Bock, Science 2009
Quoting from the article:

Although the grafted tissues fuse and establish vascular connections,
  the stock (the lower part of the graft) and scion (the upper part,
  usually supplying solely aerial parts to the graft) are thought not to
  exchange their genetic materials. But grafting (whether natural or
  assisted) provides a path for horizontal gene transfer. Gene transfer
  is confined to the graft site and no long-distance transfer may occur.
  Analyzes indicating that large DNA pieces or even entire plastid
  genomes are transferred. Only plastid genes may be transferred, no
  transfer of nuclear genes occur. Plant cells are connected via
  plasmatic bridges called plasmodesmata, but the passage of large
  macromolecules requires the action of specific plasmodesmata-widening
  proteins. Whether large DNA pieces or even entire organelles can
  travel through plasmodesmata requires further investigation.
Finally, although our data demonstrate the exchange of genetic
  material between grafted plants, they do not lend support to the tenet
  of Lysenkoism that “graft hybridization” would be analogous to sexual
  hybridization. Instead, our finding that gene transfer is restricted
  to the contact zone between scion and stock indicates that the changes
  can become heritable only via lateral shoot formation from the graft
  site. However, there is some reported evidence for heritable
  alterations induced by grafting and, in light of our findings,
  these cases certainly warrant detailed molecular investigation.

Wow, so you're teling me that the genes controlling fruiting are in the plastid genome?

NO. The stock and scion are not to exchange their genetic materials. Only in graft site and only in the plastid genome exchange are possible.

I'll read the article and get back to you, thanks.

This is fascinating, what the article suggests is hybridization does occur at the graft location. So traditional grafts of fruit trees won't completely hybridize, however different methods could. In theory, you could take two suckers from different tomatoes and split them lengthwise and graft, the new plant material would be a collage of genetic traits.


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What is the difference between abiogenesis and spontaneous generation?
As we all should know, abiogenesis and spontaneous generation are far from identical. For one, spontaneous generation was disproven with Pasteur, and abiogenesis seems to be a solid scientific theory. However, one can loosely summarize both as "the emergence of life from non-living materials" which, at the very least, is confusing for the layman.
My question is: What truly differentiates abiogenesis from spontaneous generation? For example, if abiogenesis were to happen again, how would we differentiate the two terms?
Is time the most contributing factor (abiogenesis happened over hundreds of millions of years)? Or the fact that abiogenesis generates "primitive organisms", while spontaneous generation assumes the generation of evolved, complex organisms?

I’m not sure why this question resurfaced after seven years, but is a good example of a bad question. It gets off to a bad start with “As we all should know”. This really antagonizes me. I don’t know, I feel there is no reason why I should know, and I resent being told I should by someone who doesn’t seem to know himself. If you talk about scientific terms on a science site you should define them, or if you don’t know the difference cite the definitions you have read that are causing you confusion. You are supposed to do some research yourself before posting here.

One important difference is that spontaneous generation is a form of "mechanism" by which a certain species is "born", so it is repeated many times. For such complex organisms this would be part of their "life cycle". It would also need to be a regulated, robust process.
Abiogenesis, on the other hand, would create an organism which from that point on does not rely on abiogenesis in any way, so it would be a unique event. Abiogenesis is highly probabilistic which is why it would result in very simple organisms.

What truly differentiates abiogenesis from spontaneous generation?

There are three differences.

Frequency

Abiogenesis occurs very infrequently. Perhaps only once in all of earth's 4.5 billion year history.
Spontaneous generation happens very frequently, in fact every new species could be a product of spontaneous generation. It occurs so frequently you just need to wait a week (given the Spontaneous generation example of fly generation from rotting meat)

Complexity.

Abiogenesis only make very primitive organism... there are even thoughts that the abiogenesis event on Earth produced something that was only half alive, the ability to multiple and maintain a separate internal environment with a very basic and simple metabolism.
Spontanous generation on the other hand can produce both simple and complex organism. Bacteria, worms, cows, flies, humans. Anything.

Reproducibility

Abiogenesis if it were done again... we might get very different biology. There are more than the 20 types of amino acid.  There are actually a few more bases than the 4 we have in our DNA. And the codon usage...  ie which 3bp of DNA encode for which amino acid could also be very different.
In spontanous generation events, you can get it to produce the same organism multiple times, right down to ability to mate with each other. Flies were the example.

The only reason abiogenesis is not disproved is because it can't be tested like evolution it is supposed to have happened in the past and won't happen again  (at least not in the same way) abiogenesis is a theory proposed only because the origin of life is unexplainable by normal natural means.
Spontaneous generation was an earlier attempt at answering the origin of life that could more easily be proven or disproven.

Please add some references :)


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Are animals that live in areas where avalanches happen equipped to deal with that?
Humans take courses to learn how to assess the risk of avalanches and how to deal with it. Additionally, they often use special gear to survive avalanches if they got caught in the middle of one.
What about animals that live in these areas like mountains with snow where avalanches occur (maybe wolves, deer, etc.)? Are they somehow aware of the risk? Do they handle it in any way (e.g. avoid especially steep regions) or able to manage getting out of it?

It seems this is harder that what I thought...

I don't have a definitive answer for you so this is a comment but my gut feeling is that most animals would not encounter avalanches often enough for them to act as a selective force.  I can't think of any animal that lives on steep snow covered slopes.  There are mountain dwelling animals (mountain goats) but I don't think they spend a lot of time in snowy slopes, but not bc of the avalanche risk but bc it is hard to walk in deep snow.  Note that humans encounter avalanches mostly when skiing, which is a pretty odd behavior as behaviors go.

Most animals are not well adapted to deal with avalanches. For example, more mountain goats are killed by rock slides than by predators. http://www.nationalgeographic.com/lewisandclark/record_species_150_11_2.html
Meanwhile, a mountain at risk of snow avalanche must be deep in snow, right? At that point, there is very little food to be found; it's all buried. So there won't be many animals on the surface. Most of them would leave for more hospitable locations, or hibernate.


text:
Can this theory on the evolution of human appearance be flawed?
This is what a friend of mine said:

When there's human offspring, it will look a rough 'medium' between
  the two parents, with it sharing features from the two. well if the
  offspring of one set of parents has sex with the offspring of another
  set, the outcome becomes a 'medium' of those two. So the range from
  what we shall call 'completely average looks' (a hypothetical state of
  the average of everyone in the world, which is acceptable as we're
  looking at a process of millions of years) becomes less and less the
  further into the future we go. Eventually, there is almost no range
  between people and 'completely average looks'.

In summary: take the hypothetical average of everyone in the world, and because the offspring of two people is a slight mixture of those two people, they are a tiny bit closer to the hypothetical average of everyone in the world, which means that eventually people will be getting closer and closer to this average, so will one day look the same.
So he's suggesting that slowly people will become more and more similar.
My argument is that, although this baby may be that tiny bit closer to the overall average, they're new look has effectively altered the average, meaning that they aren't actually getting closer to the average.
I'd like an opinion and flaw from some experts, such as yourselves, so please...

What he's getting at is called homogeneity, for future reference. At least, I think so. 'Completely average looks' means very little in a biological context since evolution works on a genetic scale.

It sounds like they are saying all brothers would look alike, but that isn't true either.

Edited for what he actually meant, cos i misinterpreted it

Quantitative genetics is one reason why this doesn't happen. For example height is affected by many genetic loci, not just 1 gene, and we can for the sake of the following illustration call them Locus A through Locus J - 10 Loci.
Now this is purely illustrative and hypothetical - in actuality there are some differences between this example and the real world, but nevertheless I shall plough on. Imagine everyone carries a basic set of genes which makes them 150cm tall. Loci A-J each have two alleles, either T or t, with one inherited from each parent. Each T allele adds 2.5cm to the basic height per copy (each parent has two copies, one goes to the offspring) and t has no effect. The parents are both heterozygous at each loci, that is they have one T and one t at each pair of loci. Therefore both parents are 175cm tall.
When these parents mate the offspring inherit one copy of each parent at random. As such the most likely single outcome is that the offspring will inherit 10 T's and 10 t's - roughly five of each from each parent. However, purely by chance they could receive 10 T alleles from each parent, giving them a height of 150+(20*2.5) = 200cm. Likewise, a sibling could also inherit only t alleles thus giving them a height of 150+(0*2.5)= 150cm. Thus variation can actually increase from one generation to the next.
There are other reasons why we do not regress to the mean as well, but I am writing a quick answer over breakfast, but I will be in the office soon where I can get some more thorough explanations from text books. E.g. (Dis)assortative mating, Mutation, Recombination, Environmental variance, Selection. However, with the increase in global movement it has become easier for dominant alleles to spread which is why the number of blue eyed people in the US is decreasing.
Here is an interesting article which backs up what I said about quantitative genetics, called "Will humans eventually all look like brazilians?" Also for good quantitative genetics texts take this as a basic intro and this for further reading.

Also, I think we many of the answers to this question are the same as would answer the question "why don't siblings look identical?" - simplified to "polymorphism exists."

Please look at my edit, which is in bold, as well as the new paragraph below it. Do you have anything more to say?

well for everyone to look the same it would require that they are a) genetically identical, this would require ubiquitous inbreeding (everyone homozygous for the same allele at all loci) and b) everyone experiences the same environment all the way from development Hutterites but you will still see "considerable" variation within those - basically it is impossible for us all humans to be identical because we have so many people so inbreeding is low, mutation occurs in the DNA regularly, and complete inbreeding would likely cause the species to collapse at the hands of disease.

@ollyprice and, if you read my original answer you will see that even if both parents are average (175cm) it does not necessarily mean that their offspring will be average (anywhere from 150-200cm, and possibly further with mutations and environmental variance).

The basic point your friend is missing is that offspring appearance is not simply a mixture of their parents'. Each child also has individual characteristics which were not present in the parents. This is due to a variety of processes, the most important of which is chromosomal cross over.
Each offspring will be a mixture of its parents and its own individual characteristics. Therefore, your friend's argument does not stand because each generation causes novel characteristics to appear so each successive generation changes in unpredictable ways.

Please look at my edit, which is in bold, as well as the new paragraph below it. Do you have anything more to say?

@OllyPrice your friend's entire argument is based on a wrong assumption. Offspring are not simply the average of their parents. Consider siblings, you can have a couple with 18 children, each of these will be different not simply the average of their parents. Mutation and cross over and simple errors in DNA replication ensure this.

Here's another take on it:
Suppose, for starters that you have only one gene that is responsible for your trait. Say, having version 1 (denoted T) gives you +1 to height, and having version 2 (denoted t) gives you -1. Suppose further that each version occurs in half the population.  Now every individual has 2 copies of each gene, so that 1/4 of people has TT for +2, 1/4 has tt for -2 and 1/2 has Tt or tT for 0 change in height.
Now suppose two people with Tt or tT mate. If traits followed simple averaging pattern your friend suggested we would get the average of 0 and 0, that is 0 - all the time. But in genetic model (which is what really happens)  1/4 of the ofspring will get TT for +2, 1/4 will get tt for -2 and only 1/2 will actually get tT ot Tt for 0. Note that the variance - amount of variation - increases (everyone was 0 before mating, but some of the offspring has +2 or -2), whereas with the "mixing" model this does not happen.
For another mating paring - TT with tT - 1/2 of offspring will have TT for +2 and 1/2 will have tT for 0, effectively replacing the parents, so that the amount of variation stays the same (since the mean of the population is 0 variance contribution of these two individuals is 2^2+0^2=4 in both parental and offspring populations). Note that the mixing model would have all offspring at +1, which decreases the amount of variation  (variance contribution going from 4 to 1^2+1^2=2).
In general, the mixing model of mating always decreases variance - leading to the "everyone looks average" result in the long run, but the actual genetic mating keeps variance constant (unless another factor - like preferential mating, mutation, or environmental factors intervenes; this was pointed out in other answers).
The same thing happens if the proportion of T and t are not 50-50. This is called the Hardy-Weinberg principle.
Finally, if there are many genes that contribute to height, the variance in a trait (like height) can be modeled as the sum of variances from each gene. Now if each one of the genes is inherited through the same genetic mechanism that preserves variance, the total variance will also be preserved. So we will not actually all become "average".

You should add to that the fact that height does not only come from genetic traits, the environment (nutrition, pollutants, stress, etc) plays an enormous role there.

That is most certainly true. I suppose the point of the above is that the part of the variance that comes from genetic factors does not decrease. What happens to the variance due to environmental factors is a completely separate matter, of course.


text:
Do ant pheromones indicate the direction to go?
I know that ants communicate with pheromones but I am wondering if these pheromones can indicate in which direction to go. For example the ants leave pheromones to indicate a food source and when they find food they eventually create a "highway" of ants running to the food.
If I disturb the ants while they're going to the food source in such way that they don't know anymore in which direction is the food will they choose a direction randomly (nest or food) or will the pheromones also indicate in which way to go to get the food?

I think the ants usually start at the nest and they know which way is away from the nest.

I guess they know where they're going depending if they have collected food or not, that's why I specified "If I disturb the ants...". For example if I blow air on them so that they fly away 15-20cm so that they are close enough to the pheromone trail to get back on it right way but since they flew in the air they have no idea about the orientation they're looking compared to before I blew on them.

@shigeta is correct.  Trail disruption is actually a method of controlling ant populations.
For an example, see http://www.ncbi.nlm.nih.gov/pubmed/20077128

I have ants in my kitchen and this is a reproducible result :)

Great ! Now I have to apply this in my house...

Pheromone sensing in ants is pretty cool.  The results from this paper indicate another way of potentially controlling ant populations on a larger scale (similar to introducing sterile insects): http://www.cell.com/abstract/S0092-8674(12)00523-5?switch=standard

Of course, that sort of control is far off, and what the paper really shows are the channels mediating pheromone detection and somehow, courtship behavior, in fruit flies.  Also, look up "male-male chaining in Drosophila" on YouTube.


text:
Does frequency of eye blinking reveal anything about human biology/nervous system?
I'm looking at an output of a single dry sensor EEG headband with the sensor positioned above left eye. As a side effect of it's placement, the device picks up eye blinks, and some eye motion as changes in the amplitude of the raw output waveform. It is clearly visible, and I can probably detect it algorithmically.
My question is - does frequency of eye blinking (not controlled) reveal anything about the state of (autonomous?) nervous system, or processes that take place within the brain? For example, what is the difference between blinking involuntary X times per minute versus Y times per minute for the same individual? Does blinking get suppressed in response to some stimuli, like loud noises, speech, etc?
I appreciate your input!

People avoid looking at what they don't like thinking about.
A feared enemy, an individual whom you have something to hide from..
Avoidance of looking/excessive blinking is a sign of fear.
It's basically a sign that the individual is not having a good time looking at what he is looking.
Sometimes people are lying and then they don't like looking at whom they are lying to... for them it would be nicer to look out the window or something that takes them away from their subject for a bit of time.
I would expect blinking to increase when lying.
Personally I have noticed excessive durational closing of eyes (a second or so), exactly at the moment of stating their lie.
Those are off course people who are honest to themselves but are trying to be dishonest to you. But some people lie to themselves as well and they may be more difficult to detect.

I have read that blinking is associated with the brain performing "default processing", which is needed to maintain attention properly. Here is the first thing that came up in a google search for "blink default processing":
Blink-related momentary activation of the default mode network while viewing videos
I think that it is also related to the Alpha State, in that people blink much less while "entralled" in that state of awareness. Sometimes when I am driving and listening to music, I feel like I go in to that state, and not blink for a long time, so I remind myself to. Otherwise, all conscious-verbal thinking just runs down and stops, leaving me aware, but as if I was deeply meditating. It is fun.


text:
Which enzymes degrade dynorphins and what drugs inhibit these enzymes?
Which enzymes degrade dynorphins and what drugs are there available to inhibit said enzymes?

This paper was looking at inhibition of dynorphin converting enzymes and their importance. Although they don't seem to know if it is a single enzyme, or if it is multiple enzymes.
This paper looked at bikunin as an endogenous inhibitor of dynorphin convertase in human cerebrospinal fluid.
This paper looked at several inhibitors (some of which are known to irreversibly inhibit other enzymes), like N-peptidyl-O-acyl hydroxylamines and their effects on hCSF-DCE, the enzyme that cleaves dynorphin A, dynorphin B and alpha-neoendorphin to release Leu-enkephalin-Arg6. However, it is known to inhibit serine and cysteine proteinases.
However, I don't see any actual medications that are meant to inhibit Dynorphin enzymes. Instead I found Al-Fayoumi et. al were actually looking to identify stabilized dynorphin A derivatives instead of just inhibition of enzymes.

Although nicely referenced, a list of articles touching on OP's question is not a suitable answer. The answer should be supported by references, a reference list in itself is not an answer.

I did say at the end of my answer that I hadn't come across any medications that specifically inhibited Dynorphin enzymes @AliceD and pulled from those articles what they had used to inhibit the enzymes. I also noted that hCSF-DCE is the enzyme responsible for cleaving dynorphins.

Yes I agree that your answer is quite complete and I removed my downvote. I do still believe it is not a well-formulated answer, so I will not upvote.