text:
Can the human chin have developed to protect against combat strangles?
Has the mechanical explanation of headlock defense ever been discussed by scientists to explain the chin(protuberantia mentalis)? A mechanical advantage that prevents death and being beaten up by another male would undergo a type of topological optimization that could be measured.

Positions where an assailant wraps his arm around a defendant's neck constitute 3/4rs of professional wrestling submissions. It's even more prevailant in amator wrestling where the contestants don't learn conplex arm and leg locks, in children, and in young adults.
When the neck is lowered, arm is barred from the neck, and the commentator shouts"will he manage to keep his chin down"
That kind of defense of the neck with the chin lowered can last 2-3 minutes, after which time the assailant's arms tire and the position changes.
The chin can therefore play a major role in human defense, mate selection, dominance tussles, and it's morphology may be designed to be vertically long and lower into the solar plexus.
There is a pit at the top of the sternum into which the chin fits when it is lowered.
Any kind of space under the chin can serve as leverage to push the head upwards and access the neck, so a chin that specificially points downwards flush with the solar chest and which deflects the arm upwards towards the mouth is an advantage to humans.
The chin size is promoted by testosterone which happens to be a hormote that encourages fighting.
The human chin is more powerful than in all other primates and can withstant more PSI force, which suggests that it is made to withstand a lot of clunking damage.
Actually 70 percent of paleolithic mandibular fractures could derive from fighting, that's in line with today's epedimeology figures, minus car accidents.
I believe that the chin comes from a range of selective factors, and i am curious about it's topological optimization, they precise shape and it's mechanical advantage. I believe that the current theories are true, and I wouldn't be surprised if the defense of westling positions can account for a lot of it's precise shape similar to a snow plough and it's alignment with the chest.
If any anthropologists are vaguely entertained by this theory the effectiveness of the chin in wrestling defense can be measured by studying archive of the number of successful defenses against wrestling strangleholds, which outnumber the attempts by 2-5.
Mechanism of injury of mandible fracture patients. MVC Motor vehicle collision, GSW Gunshot wound

To counter Johns odd claim about eye gouging as an alternative human wrestling action, punch damage accounts for 99% more hospital submissions than eye gouging.
Strangulation is unique to our species, so it is fitting to question: which hominids first used them? Was the bite force of a Neanderthal the previous best defense for choke holds? Is the Neanderthal physiology or mind not conducive to that kind of wrestling interaction? When did hominids develop aggression traits and cognitive forethought and a wiry physique that made choke holds possible?
Did the advent of a snowplow chin as a strangulation defense even facilitate the reduction of the jaw size of humans to it's present scale?
Anthropologically, human faces are not level with the genitals, as in dogs and monkeys, who inspect each other's genitals to gather information about their sexual state. Humans communicate with the eyes diverted towards the mouth, and face, they express their sexual state with mouth movements, side motions, and an array of gestures. The Chin also serves a display purpose in that end, so mechanical forces are not the only things that should be considered, but they count alot!! The development of complex facial expressions to describe sexual communication may have also encouraged the formation of a robust chin.
A lower and more forwards pointed chin protects the neck better, other animals develop pronounced features related to their rutting combats, crabs with a large arm, antlers, https://www.sciencedaily.com/releases/2012/07/120726142202.htm
Children learn head locks from an early age, head locks are a combat action singular to humans.
The human jaw is as strong or stronger than that of other primates. The incisors can deliver 70 PSI to the chin, and a human punch can deliver 1700 PSI. 6Mpa is about 800 pounds.
The chin serves as a crash guard to intercept whacks at the apex of the triangle, It is used as a life saving neck guard in the most common wrestling submission by providing no leverage under the jaw, and it is a masculin trait controlled by testosterone, quite contrary to the general neotenic traits of homo sapiens.

Chins developed long before humans (pretty much anything that has a lower jaw has a chin, even if it's hidden under soft flesh), so I doubt your hypothesis is correct.

Are you sure that your vote to close the question is not related to our heated disagreement on the other thread? you were inaccurate about the age of menarche, because you overlooked that urban medieval late development was due to malnutrition compared to paleolithic times. Again you are wrong about chins. The science correspondant from the BBC states: It becomes even stranger when you consider that among the all primates – including our extinct relatives – only we have chins. ... So honestly i believe that your comment is not related to actual knowledge and accuracy, which is quizzical.

it's hard for me to see how this could be tested ... what stops it from being an evolutionary Just-So story?

Thanks for your comment! indeed theories on primate orofacial anatomy are specialist post doctoral research topics, and i should read how their papers and measurements are constructed. From one of the postdoctoral journal articles i have just read:  The chin, however, appears to be a uniquely modern human trait. so, The question is open to scientific discussion, with much precedent, although my reasoning for it is perhaps a new one.

You should add a link in your question to the article you mention in the comment to @John answer, as well as the piece from the Atlantic that it links to, to provide better context and a clearer definition of what aspects of the lower jaw you're talking about. A picture of a human skull would probably also be useful. If those articles are true (which I have no reason to doubt), the human chin does indeed seem quite unique.

The unique features of the jaw evolved at the same time our faces and jaws shrunk. humans cranial structure is unique in many ways.

That's a very good counter theory John. I believe that it probably has a fair statistical contribution to play for the reproduction advantage conveyed by the chin. If the chin plays an important role in human defense and male hyerarchy, and protects the neck from a mortal hold, i believe that it provides a statistical contribution to survival fitness too. The chin is actually a hook shape that hitches a forearm above the neck, and males don't need a larger and more hooked chin by Holton's theory. I added pics

I am curious why you think primitive weapons are unsuitable for combat? we have been hunting large game with spears long before we had chins.

Because combat with weapons is a declaration of intent to kill. humans think twice to compete for a woman with a stick. Combat within a tribe for a woman in heat is safer for all parties if it is a primate show of force. The advantage of against strangling is purveyed in all kinds of fighting. I was an adept fighter john i had some wrestler brothers. a bola or a spear and a rear ambush are dangerous to cavement, but a frontal mohawk attack is a joke. i can fling any mohawk, spear etc and catch it because it's inertial mass manipulated by the thin hand is very predictable. hands are agile.

@comprehensible I had forgotten all about that question. Votes are on the question, not the questioner. I still think this question is opinion-based, as the question "Why did this feature evolve like so?" Is almost impossible to answer.

Stackexchange is not a forum for extended discussions - it is in a question-answer format. This question seems to either look for the confirmation of a posed hypothesis or is discussion,  which to me would both seem off topic.

No
We know why the chin exists, the jaw has to be strong to be stable and not twist during under strain. humans have tiny jaws, large tongues, and sharply angled neck that leaves no room for a large enough interior ridge, so the jaw has to protrude forward or get taller to compensate. Our large facial muscles and tongue encourage the former, as does the overall shrinking of the face and jaw. The development of the chin lines up perfectly with the shrinking of the jaw and face and expansion of the tongue in hominid evolution.
Now the size of the chin may very well be influenced by sexual selection, your hypothesis might even fall into this if you had any evidence. sexual selection could exaggerate it once present, but we know why the chin originates.Like everything in evolution there are multiple factors at play but you have yet to show yur ideas is even a factor much less an important one.
For your idea to hold water you need to show several things.

That headlocks are a significant and persistent problem in human history. Which is unlikely given how many skeletons are known that were killed with weapons.
That the chin actually does protect against it, especially more than say a wider neck or taller jaw, which we lost.
If it does help and headlocks were a significant problem, why does the size of the chin varies so much.
Why the chin develops so much later than the when the neck shrank, which is when humans would have started being vulnerable to headlocks.
That other explanations are not better supported.

Also there are lots of ways to kill someone while "wrestling", statistics from a sport competition with restrictive rules are not helping your case. I can't claw someone's eye out or stab them in the UFC.  And I want you to think of why a human seeking to kill another would forgo the many weapons they would have, to wrestle them instead. especially why this would would happen so often a defense would need to evolve.
All you ever wanted to know about the chin

From a survey of 40 people whose measurements were plotted from toddler to adults, researchers concluded that the mechanical forces needed to chew are incapable of producing the resistance needed for new bone to be created in the jaw area.
"In short, we do not find any evidence that chins are tied to mechanical function, and in some cases we find that chins are worse at resisting mechanical forces as we grow," Dr. Nathan Holton

@comprehensible, Dr Holton shows the chin is not an acquired characteristic which is very different from an evolutionary adaptation.

I would want to see a source for headlocks end a large majority of fights, especially in pre-industrial societies. ditto for the chin playing a part in defense in such cultures.  Statistics from sport fights with rules are pointless, I can't claw your eyes out or stab you in the UFC. And by your statement about men and women I'm guessing you did not read my statement about sexual selection.

Also not all primate males fight, but if you were right why would women have chins? sexual selection could explain the difference in sexes, we both use it after all)but if it was the only cause as you claim women should not develop chins. I also feel I should mention some neanderthal do have chins,

I am adding in some stuff from Holton's actaul published works, http://www.sciencedirect.com/science/article/pii/S0306987706009091 where he shows the tongue is having more effect than bite forces.

You provide good arguements, thanks. There is a major disadvantage to the tonge reinforcement theory: There are zero chances of a human breaking his jaw from using his tongue forcefully and from chewing. In that sense, the reinforcement of the jaw is excessive. The tongue simply has never broken a single jaw in zero recorded humans, nor has chewing. The shape is reinforced for more brutal defense, and a fighting stress on the chin is hundreds of times larger than the pressures exerted by bite force etc. fighting has broken millions of jaws jaws and strangled millions of humans.

actually biting can injure the jaw. It doesn't happen much in developed countries becasue thanks to industrialization we have an abundance of calcium in our diets and eat really really soft foods.. To the point it often creates an overbite becasue the jaw is not stressed enough to induce proper development. But the biggest thing over flexing can cause is tooth loss and fracture.  And of course why would you expect the jaw to be damaged if we evolved improvements, a fractured jaw would be terminal in the wild so it should be overbuilt. So far my five points still stand.

HAHA! your are inventing now, your previous phrases were totally convincing and eloquent but that was not reasonable! the statistical death rate from jaw fracture on food compared to human attack and strangling are statistically microscopic. Find a single written example of a fractured jaw from biting? the break happens in the teeth, and the flexor muscles at the back tear and strain before the jaw fractures, on any food.

So humans need a proportionally larger base to support tiny teeth which work less? Irrational and inconclusive. The human teeth reduced because they didn't need to be as robust. you will find millions of articles concerning injury from strangling, and practically zero on injury from biting. the statistical bias is giant. You should find a single reference to jaw damage from biting, i belive that your comment about overbite stems from an inability to find any references of jaw fracture due to biteing.

Hi, sorry, I found a graph that of mandibular epidemiology (sounds cool?) which illustrates the strength of the chewing fracture argument as 0% of mandibular injuries. also, the fractures happen on the sides, not near the chin. ZERO PERCENT from a 181 patient study! that doesn't strengthen the logic that you defend. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2690628/

@comprehensible if you feel that you have enough sources to convincingly defend your hypothesis, then write an answer and let the voters decide who is correct. At this point, I feel that you are arguing just because you are so wedded to your hypothesis that you don't want to accept any opposing evidence, which is the opposite of how the scientific method is supposed to work. Additionally, your point about a lack of modern jaw fractures related to chewing doesn't make any sense - if we evolved to have a strong jaw/chin to prevent such injuries, then of course we won't suffer from them!

So,  I'm busy with geometry and it was only supposed to be a 46 word post to jot the theory online.. With your refutations to discourage further consideration of such a vast and curious thoery, and your and closure vote as an opening statement, you demonstrated the kind of lack of consideration which stifles science. Top scientists are ecouraged to use words like may, maybe, seems to, in my view, because stentor terminology to kick off a discussion results in a mess. Elder statemen qualify used terms in a way which gives the original speaker wise perspective on his possible misuse of words.

Darwin found 5 odd finches and turned his puzzle around from all angles to measure it's significance, and that's what i was hoping the forum would do. I don't care i have too many thoeries:). measure the idea from all angles and state the pros and cons. There's clearly about 3 factors that shaped the jaw bone, mostly defense related. A professional anthropologist is free to develop a statistically viable carachterization of this documented and life saving function of chin's precise jutting form. I'm fine to wait 20 years or never for a doc to shaft or clarify it. Its unstudied science!!! So

You can call zero percent incidence in an epedemiology a significant proportion, and fail to cite a single case worldwide of some enraged human cracking his jaw on pecan nut (recall that Dr Holton ruled out bite injury as the cause of hte chin, and suggestedthe tongue instead) ... I encourage you the best of luck to defend a zero incidence of records and a zero percent epidemeiology result. a jar reces which guides the arm towards the neck is not significant in a violent species... That's fine, It's not a very valuable technology to divest time on.

I asked them for a statistic to support their claim that chewing fractures are significant, to counter the statistic showing that collision causes 100 percent of the kinetic stress on the jaw... They refused to provide statistics and reference, so the comments dragged on. Do to their lack of statistics about kinetic stress from chewing compared to collusion, i consider that they have valiantly but totally lost the debate for lack of evidence.

Comments are not for extended discussion; this conversation has been moved to chat.

@comprehensible the discussion has been moved to chat. http://chat.stackexchange.com/rooms/50648/discussion-on-answer-by-john-can-the-human-chin-have-developed-to-protect-agains

It's naive and wrong to state that the theories for the chin are agreed upon and and comprehended, else that protection from strangling is an impossibility in selective pressures which contribute to it's current shape:
Protective reinforcement of the hominin face is a 2014 study.
A search of google indicates that:

"punched police report" returns 1mn results on google
"choked police report" returns 7mn results on google
"punching police report" returns 4mn results on google
"choking police report" returns 14mn results on google

The previous answer is based on the impossibility that choking can be of any significance in human interaction. For the idea to have any merit, you would have to demonstrate that:

Chokes contribute a few percent of human tribal fatalities or tribal mate choice.
The downwards inflection of the bone is an arbitrary construction for reinforcement and display, and that it's non-arbitrary for protection of the larynx.

40-90% of street fights caught on camera ended up with wrestling on the floor. https://martialarts.stackexchange.com/questions/1342/is-it-true-that-most-fights-end-on-the-ground-what-is-the-evidence
Neck constrictions end 70-80% of human wrestling fights, and are common in the schools.
John suggests that eye gouging can be a major statistical result in wrestling, however eye pokes only account for 1.7 to 2.1% of all eye traumas, which is of low significance including sport which contributes most of that 1.7%, compared to jaw fractures, 42% of which are caused by assault. 13% of eye traumas are from violence, mostly from punching, but also from sticks bottles knives and weapons, and very few from fingers.
Men don't gouge their wives' eyes out in order to assert dominance in studies of domestic abuse.

"... later than the when the neck shrank ...".

The musculature of the neck changed when humans became more gracile and lithe. Their necks allow them to play the piano and contributes to their intelligence and the development of their brains.
Evolution of speech caused the hyoid bone to drop (which allows primates to breathe and drink at the same time, and prevents choking) and without the change of the larynx and the hyoid bone, we'd still garble and hoot much like our chimpanzee cousins, scientists say.

"...why does the size of the chin varies..."

The growth and forwards slant of the chin ("mental eminence" from Menton, french) vary relative to testosterone, which is a fighting, sexual appetite, and strengthening hormone, though shape of the chin doesn't vary a lot. A large majority / all sapiens have a chin which does not allow leverage under the neck compared to ancestors. Neanderthals had much more of a chin than homo heidelbergensis.
Here is an example of a skull of a man who was exposed to high levels of testosterone (right), compare to a females skull (left):

When the body was less gracile and more muscled, the arms were more articulated, Is when the chin was weaker in PSI resistance, and the superciliary arch and the skull was stronger.
Previous studies have shown that the chin could be due to a range of factors, and it might be wrong to say that defense is the only cause for selection.
It would be wrong to say that the selection pressure on the chin from fighting is known, and to say that we have measured the mechanics entirely, sexual selection is very closely associated with the chin, as women are interested in beard and chin size of males.

This could really use some sources to back up its claims, and meaningful claims made from the sources it does provide. Unfortunately, most of what you've put seems irrelevant, or requires heavy speculation and misunderstanding of context to approximate a valid affirmative answer.

You only have one citation, and that is behind a paywall. Please add support for each of the claims made here. "Scientists say" is not a citation.

Starting with your statement "humans aren't the only animals to have a chin, so i doubt your hypothesis is correct" your contribution to this page has shown a lack of intellectual accuracy which suggests that your access as a moderator on stack exchange is a matter of couchpotato attrition and not of intellectual depth. In biology, specific terms have specific meanings, so bipedal, chin, have established meanings. Elephants are accepted as having a chin. if you blur terminology, semantics degenerate into a dulled confused perception, i just had to embelish/improve that theory while at 41'C.

@comprehensible Your point about including unrelated chin examples has merit, but resist the temptation to lead that into speculative ad hominem attacks. It's a complete waste of time. Focus instead on finding strong evidence for your answer and/or deriving a strong answer from your evidence.

@Harris Weinstein, Sorry the phrases and stats are quoted from an array or results and surveys, i ll add the references, fair comment thanks.


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Staining cells for FACS at 4 degrees or ambient temperature
I'm sorting a 293 derived line. One thing that is worrisome for me is cell viability after the sort. Usually I have been staining and washing at room temperature (on the benchtop) on a nutator. I have been reading that most sorting procedures indicate that you should be doing this at four degrees in the dark. It is my understanding that this helps with clumping, but is this at the expense of viability? Does the cold cause these cells to apoptose?
Currently my procedure is the following -
Using HBSS + 1 mM EDTA + 1% BSA (sort buffer) I suspend approx 10-15 million cells per/mL.

Stain with primary
Spin at 300 x g for 5 minutes
Add 15mL of sort buffer, spin again
Stain with secondary in 1 mL of sort buffer
Wash x2 with 15mL
Strain
Sort

One thing I can do to minimize cell death is do a live/dead stain (we just added that capability). The other thing I read was to use 50% FBS in your collection tube.
The other thing that might be of concern is that if we are doing many sorts, then some of the tubes may be sitting in sorting buffer for a long time in the queue. How long is too long?
Lastly, we use puromycin and blasticidin as selection markers for our libraries and we usually add these right to the sort after we replate. Should we wait a while?
Thanks for the advice

Low temperature will arrest all cellular processes. The cell will not undergo apoptosis or division, or carry out any other metabolic process. What are you staining the cells with?

You have several questions, please try to limit your posts to one question each. That being said, I'll try to address each of your concerns.

Does the cold cause these cells to apoptose?

No. The purpose of staining at 4°C and washing with cold buffer is twofold - to maintain viability (all cellular processes slow down at lower temps) and to prevent receptor internalization. This second point is especially critical as you're using a primary and conjugated secondary, which I really wouldn't recommend for sorting unless absolutely necessary, for example if the antibody you're using isn't available in a directly-conjugated format.

One thing I can do to minimize cell death is do a live/dead stain (we just added that capability).

Live/dead stains are generally a good idea, but make sure the stain you're using isn't cytotoxic. L/D should always be the last staining step before running your samples. A better way (if your sorter supports it) is to use forward scatter (FSC) and side scatter (SSC) height and area measurements to discriminate single, appropriately-sized cells, then gate on them first before gating on your antibody stain (FITC or PE or whatever your secondary is).

The other thing I read was to use 50% FBS in your collection tube.

I'm not sure how much that will help, especially 293s, which are pretty tough. Just make sure you're diluting the collected cells enough in medium to bring the serum percentage back down to 10%.

if we are doing many sorts, then some of the tubes may be sitting in sorting buffer for a long time in the queue. How long is too long?

As long as your samples are kept in the dark on ice or at 4°C, they should be fine for several hours at least (I wouldn't go overnight, though). Also, make sure your collection medium is chilled, as it can shock the cells to go from 4° to 37° too rapidly. Collect your sample, plate it, then put it at room temp or in the incubator (depending on your workflow) and let it warm up that way.

Lastly, we use puromycin and blasticidin as selection markers for our libraries and we usually add these right to the sort after we replate. Should we wait a while?

Nah, don't worry about it. You can wait if you want, or add it right away - I would lean towards adding it more quickly than not, so you don't give unwanted cells any chance of growing out.

source: Stack Exchange

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

sort: votes


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What triggers the release of gonadotrophin-releasing hormone with the onset of puberty?
I am interested to know the process of development of puberty. During puberty, when boys/girls reache 12-14 (puberty) years of their age, their hypothalamus releases gonadotropin releasing hormone (GnRH) and then this hormone in turn affects the pituitary gland which releases FSH and LH. FSH/LH hormones promote male/female features. For e.g. girls start their first menstruation cycle and males start to produce sperm; their voices become smooth and intense respectively. So all these phenomena are dependent on GnRH.My question is that if those hormones are produced due to the effect of GnRH then how is GnRH production itself regulated. In other words how does our body "know" that we are in the age of puberty and it should secrete GnRH?

GnRH-secreting neurons are not fully independent. To date, their most studied regulators are kisspeptin-secreting neurons. During childhood, kisspeptin-secreting neurons are off, due to GABAergic higher level structures and to lack of free leptin. So both brain and body fat have a word on it.
Caveat: most of the evidence is circumstantial (for example, higher circulating kisspeptin in naturally occurring precocious puberty) and I am oversimplifying, so the picture is more complex and will become even more so.

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


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What is the biggest structure in nature for structural coloration?
I'm interested in the actual sizes behind structural coloration: I find it fascinating and I think it may have a couple very nice applications.
The problem is I couldn't find anything but vague references about the actual structures' dimensions. Like, the thickness of the walls, their diameter, the height...
I'm sorry about the tags but I couldn't find anything fitting. Is this, like the wrong stackexchange section?
Edit: For what I mean by structural coloration please refer to https://en.wikipedia.org/wiki/Structural_coloration.

Structural coloration[a] is the production of colour by microscopically structured surfaces fine enough to interfere with visible light, sometimes in combination with pigments. For example, peacock tail feathers are pigmented brown, but their microscopic structure makes them also reflect blue, turquoise, and green light, and they are often iridescent.

You should define what you mean by "structural coloration", because with just the information in the question you could be talking about house paint. .


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What's the max speed that humans could run?
Assuming humans could use all of their muscle strength at once, with no need of cooling or energy, how fast could we theoretically run?

This is without current human limits of how much muscle you can use at once.

Exactly what do you mean with "limits on how much muscle you can use at once"? An organism is an integrated whole with different functions, and single muscles cannot be viewed in isolation. Also, running at top speed is not something that is achieved instantaneously, but is a process and a sequence of events, and is dependent on e.g. ATP and anaerobic glycogen use during start and acceleration.


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Why African species are larger in size compared to other parts of world?
Why are African species larger in size compared to other parts of world?
Best Example: African elephants are very famous for Giant ears.
So many African Animals listed in Guinness World of Records. (Source)

When it comes to mammals this cannot really be evaluated without taking the Megafaunal mass extinction into account. This mainly refers to the extinction of large mammals from the Pleistocene Megafauna, which affected different parts of the world differently. More species were extinct in the Americas, Australia and northern Eurasia, and fewer species in Africa and southern Asia. One of the reasons for the differential extinction is thought to be the shorter evolutionary history together with humans in the areas that were more affected (since over-hunting is though to be one of the main explanations, see e.g Sandom er al. 2014).
If you only look at currently extant animals, you ignore the Wooly mammoth, the Woolly rhinoceros, Ground sloths and many other large species inhabiting higher latitudes, and this will give a very biased picture when searching for evolutionary reasons for the differences in body size between continents.

The organisms listed in the question (elephant and the snail) are found in warm tropical regions (Africa is not completely hot continent 1). The organisms dwelling in tropical region shows adaptation for loosing excess heat by having longer extremities. This is known as Allen's rule 2.
This explains larger ear of African elephants.
In case of snail, probably it has to be vast resources which are available in tropics. The large amount of resources would cause a larger population to exist, resulting into more competition. The larger size of snail must be conferring increased fitness to snail.

But India & adjacent areas that are home to the smaller-eared Indian elephant are also warm tropical areas.

@jamesqf: Well that is true. In fact Asian animals are bigger than African animals. For example one horned rhinoceros is the biggest of all. Small size of Indian elephant could be due to several probable reasons:

Indian forests were quite dense and hence in order to move through the forest, the evolution favoured the small sized elephant

Continued....
2) India was densely civilized with great kingdoms and tribe and they hunted big and fierce animals which led to selection of small sized elephants on Indian subcontinent.

I was really just thinking about the size of the ears :-)  But there are two distinct species of African elephants, the large bush elephant (Loxodonta africana) and the much smaller forest elephant (L. cyclotis), with the Asian elephant (Elephas maximus) being intermediate in size between them, so there must be more at work than just climate.

@jamesqf Well in that case there is this circumstantial evidence (and we know these circumstantial evidence are only sometimes right) that forest species are shorter for easy movement.

But then we might have expected the Asian elephant to have evolved down to about the size of a deer, or the now-extinct dwarf elephant species that lived on Mediterranean islands.

@jamesqf Yes that may happen (can't deny possibilities in evolution). But evolution (which is dependent on fitness) is directed by many forces. In case of Asian elephant, the access to resources were ample and that encouraged increase in body size at the same time a very large size would hamper movement. This resulted into size of present day Asian elephant.


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Could we slow down life?
As far as I know there is no absolute time measurement (one that would measure time in a non-environment-dependent fashion) in any life form. Only such time measurements exist, which are dependent upon cyclic changes like the strength of the sunlight, heat, amount of water, etc. (In case this assumption of mine is false, than please answer it in mind of life forms which in deed have only relative)
Theoretically, if we could change everything a given life form is dependent upon, could we increase it's entire lifespan?
For example if we were to put a plant inside a manually controllable environment and slow down the day/night cycle to it's third, maybe even decrease air pressure and the strength of gravity(thus eliminating any problem that might arise from the actual transport of water and the solution of organic matters produced in photosynthesizing cells), change (even though I'm not sure if this could be physically possible at all, but my whole question is theoretical, thus it should not cause a problem) the adhesion/cohesion as well (so the speed of transports in the cells would change accordingly) and change other, (for me) unthinkable aspects that, for example, regulates the time between cell divisions, would it live for longer?
Even if we could not change every aspect that regulates a given life form's working, changing many could we (although this time not linearly) increase it's actual lifespan?

I find this too broad, speculative and opinion-based to be suitable for the SE format. You mention a huge number of processes, which will also interact with eachother.

I work in a fly lab, flies kept at 18 degress live longer than those at 25 degrees... though I agree with fileunderwater that this is too broad

I voted to close this question. I think it holds great potential, it just needs some tinkering and especially a narrowing down of the variables as well as species. I think many non-complex life forms adapt to environmental factors by going into some kind of low-metabolic state- a bacterial spore for example. This is not what you are after. Perhaps focus on humans and specify some parameters of interest. As of now it only generates answers that are commented upon with "yes, but no... I want to know this..." Such comments on answers identify it as a poorly defined question.

Short answer: Changing something (instead of everything) yes.
There are several studies on the impact of environmental factors on life span.
Of course it depends from organism to organism. Diet restriction for example has been shown to extend life span of worms and mice. Temperature is also working well, at least with microorganisms, the metabolism of E.coli for example (that usually grows at 37 Celsius) can be greatly slowed down at lower temperatures. Also, there are enzymes involved in the "ageing pathway" some of these enzymes can be promoted or repressed by small molecules, like resveratrol does, and as result you get some increment in life span. The opposite is also true, you can accelerate ageing with external factors. For plants works as well, changing the environment you can definitely have an effect on the life span and the overall metabolism rate, indeed tricking the light cycle is a very well known method to induce flowering for example.
Here some interesting links if you wanna dig more into this topic.
http://web.mit.edu/biology/guarente/
http://genetics.med.harvard.edu/sinclair/
http://www.ted.com/talks/cynthia_kenyon_experiments_that_hint_of_longer_lives?language=en
http://jxb.oxfordjournals.org/content/58/12/3099.full

But these are only defensive reactions to the environment. What I would like to know is how would changing many (as everything is impossible) aspects modify the life span of our average life form.

I don't get what do you mean for "defensive reactions"... The point is that organisms respond to external stimuli and that there is data pointing out that also life span can be influenced by such a stimuli. Isn't that you were looking for? I cannot really answer to "how would changing many (as everything is impossible) aspects modify the life span of our average life form" because is too vague, it depends from the organism and many other factors so there is no simple protocol for that. Have you check the links I posted? The last one is about slowing down plants growth with light.

First, I find this too broad, speculative and opinion-based to be suitable for the SE format. You mention a huge number of processes, which will also interact with eachother.
However, taking a general view, life span and generation time can definitely be increased. Changes in temperature and nutrition will often change the metabolic rates and growth rate of organisms, but the actual effect will depend on which organism you are looking at. For instance, the length of the larval stage of many longhorn beetles can increase by several years in colder climates or site conditions, under shorter growing seasons and/or poor wood substrates, compared to ideal conditions or warmer microclimates. The mechanism here is often lower activity levels or lower nutrient contents, leading to lower growth rates, which means that it will take more time before the larvae reaches maturity. This means that individuals of the same species (also the same genotype) may have a life span of 6 years in one location and 2 ys in another location. This is just a single example, and lots of similar processes can also be found in other organism groups, especially considering the large number of factors that you mention in your question.
References:

Bilý, S. & Mehl, O. 1989. Longhorn Beetles (Coleoptera, Cerambycidae) of Fennoscandia and Denmark. Fauna Ent. Scand. Vol. 22: 47–48.

Cherepanov, A.I. 1990. Cerambycidae of Northern Asia. Leiden, The Netherlands: E.J. Brill Publishing Company.

Quite some experiments like this have been done with C.elegans, also.

That's not actually the same thing I'm interested in. In this case, the given specie is genetically coded to work like that. I would like to know whether this thing works on species which are not supposed to live longer than they do now.

@FloriOn And how are you actually going to determine that? You cannot separate the genetical background of a species and its reaction norms from the equation. If you do, this is pure science fiction and answers will only be based on speculations. Also, how do you determine how long a species is "supposed to live", and under what conditions?


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RACE pcr product
I'm a molecular bio novice, and I'm trying to understand the differences between regular PCR and RACE PCR.  If it wanted to sequence my PCR product that might be hundreds, if not thousands of bps long, I should use RACE PCR correct?  My goal is to sequence the active site of some enzymes I'm interested in, but I'm not sure how to go about designing PCR primers for a specific site on my protein.  Additionally, the active site is over 100 amino acids long, which would imply that my PCR product has to be over 300 bps long.  Regular PCR amplicons have trouble amplifying long strands of DNA correct?  I was thnking about using RACE PCR to amplify my entire cDNA strand that is 4000 bps long and then just sequencing the RACE product.  Would RACE work for that many bps in my cDNA?

This is a lot of questions in one very compressed paragraph.  It would probably be best if you asked separate questions.


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Sequencing rtPCR product
So I have a validated set of primers for rtPCR from Biorad that contains SYBR green.  If I do rtPCR, can I use the rtPCR product after purifying it with a Qiagen PCR purification kit?  Also, I'm under the impression that the sequencing company needs primers to do sequencing, do I just use the PCR primer or one of the "universal" primers the company has?

You can use the PCR purification kit for cleaning up the DNA.
You can use the primers that you used for RTPCR for sequencing. The universal primers would work only if the sequence complementary to it is there in the 3' end of your amplicon.


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Electron balance for biomass synthesis: is my professor right?
I'm studying for my exam and I came across these notes written by the professor himself. He's talking about the general reaction of biomass production in a bioreactor:
$$\ce{C6H12O6 + NH4+ + O2 -> $\mathrm{C_wH_xO_yN_z}$ + CO2 + H2O + H+}
\\\text{(not balanced)}$$
At some point he proceeds to do the "reduction balance" for this reaction: he calculates the "reduction degree" of the elements (which he defines the same way I define the oxidation number) and here comes the problem.
He states the "reduction degree" of C in glucose is +4 and the one of O in O2 is -2.
Is "reduction degree" different from oxidation number? Are there any particular ways to calculate oxidation numbers when you talk about biomass?
Thank you for your help.

The terms are different.
Oxidation number is the difference in number of electrons (not pairs) from the elemental form (which for many elements exists only on paper) of an atom.
Degree of reduction is a more uncommon term that is basically the number of electrons that atoms in a molecule are donating per atoms of a given element. It is calculated formally by summing the number of electrons donated to reach a full shell (H=1, C=4, N=-3, O=-2, P=5, S=6 etc.) divided by the number of a given element, but that is more confusing than anything.
Carbon can be oxidised four times, e.g. methane > methanol > formaldehyde > formate > carbon dioxide (not biological route, just an example), while oxygen can be reduced twice: to hydrogen peroxide and then to water. As proof, most O2 dependent enzymes produce hydrogen peroxide (e.g. FADH2 enzymes). That is a cheat way to work out where those numbers come from.
I would recommend forgetting about the formal calculations of oxidation numbers —in biology oxidation numbers of carbon are generally not discussed.
I will open the brief parenthesis of the oxidation states of carbon just to point out they are not those: -1 for a bond with hydrogen, +1 with oxygen and 0 for a C-C bond. Carbon monoxide therefore has an oxidation state of +4, while a C in glucose (on average) has a -1. Molecular oxygen has two identical atoms therefore is 0. Elemental carbon has 6 electrons so hypothetically you cannot strip carbon more than +6.
Here what is important is figuring out how many times a carbon in a molecule can be oxidised, that is how many electron pairs a molecule can give away as every time that happens an NAD+ (catabolism) or NADP+ (anabolism) is reduced, which is key to the cell. A dehydratase removes a hydroxyl group leaving an alkene, but it does not carry out a redox reaction: the geometry is no longer sp3, but sp2, and the oxidation state has decrease by 1 in that carbon, yet carbon kept its electrons —the other carbon increased by 1 as it deprotonated, so no net change and NADH is not generated.
Knowing how many electron pairs are given away going from glucose to carbon dioxide is important because cells cannot make them disappear and a terminal electron acceptor is needed either in the form of respiration or fermentation. There is a further concept, that of reduction potential. Different forms of terminal electron acceptors are employed in Nature: oxygen, Fe(III), sulfate etc. and these have different "energy" levels at which they accept the electrons (reduction potential, measured in volts), which translated to different amounts of energy that can be syphoned off during the reaction.

I don't think you answered the question --- what is "reduction degree", and is it different from oxidation number / oxidation state? You mention "redox potential", by this do you mean "reduction degree"?

Sorry, you are right. I edited my answer.

Thanks, it is improving!  Can you provide some references on "degree of reduction" ?  This seems like a pretty obscure concept --- I teach cell biology / biochemistry but I have never heard about this, and I have a hard time finding anything.

Sorry, after staring at this for some time, I still don't get your definition of "degree of reduction". What do you mean by "divided by the number of a given element" ?  Atom number?  Stoichiometry coefficient?  As I understand it, you should multiply the atom valence by the stoichiometry coefficient ?

I also didn't quite get how you determine the reduction degree..
For example: I can follow you when you talk about different oxidation states of carbon, but still I don't get: what is the reduction degree of carbon in glucose and carbon dioxide?

The crux of what I tried to say is to not concentrate on the maths and to focus on the concept that the more the carbon is bonded with oxygen and less with hydrogen, the more electron pairs the molecule gives away (= oxidised). Hydrogen is happy as a proton, not a hydride. If the latter were true all of this would be meaningless. Instead you have to have NADH carrying the hydride (and the energy with it).


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Butterfly wings with ragged edges - worn out, camouflage, fungus, or something else?
Here are two different butterfly individuals of different species in northern Taiwan whose wings had ragged edges.
The whitish one was pretty lethargic and just wanted to stay in the grass and be left alone. The dark one with four purple spots (two per wing) on the other hand was flying from leaf to leaf, and even tried to land on my green cellphone case. He also seemed to just want to rest, rather than look for flowers.
So my first suspicion is that these (like me) were nearing the end of their life and just wanted to take it easy.
In both cases I noticed that the back edges of their wings were ragged. I'd never seen that before. Do butterfly wings normally wear out like this? Could it be camouflage (straight abrupt edges might be easier to discern when resting) or perhaps a fungal infection of the wings?

Individual #1 April 7, 2024 in northern Taiwan:

Individual #2 April 21, 2024 in northern Taiwan:

In both these cases, the butterflies are old (relatively speaking) and worn. Usually, adult butterflies only live during a specific season (which usually can last weeks to months) or with several generations during a season. It is then common to see this kind of appearance on individuals at the end of the season, when they are close to the end of their normal life span. They are often ragged, have lost most of their wing scales, can have pieces of their wings missing (from e.g. attempted bird attacks), and they often have quite faded colours compared to newly hatched specimens. That the wing veins are sticking out (as in your pictures) is also normal. In general, most butterflies can fly quite well with surprisingly large portions of their wings missing.
A "ragged" appearance can sometimes also be found as part of camouflage or mimicry, but this is not the case here. However, some quite normal examples (i.e. not the most extreme examples) of this can be seen in these pictures. Here you can see relatively jagged edges and wing appendages, but still a somewhat "cleaner" appearance than in your pictures.

Polygonia c-album (pic from wikipedia), showing example of ragged camouflage

Thecla betulae (pic from the Swedish species information centre), with  example of mimicry/diversion (false antenna, indicating location of the head).
As a sidenote, I think the latter of your butterflies is Hypolimnas bolina, which is relatively common in Southeast Asia.

Oh wow, thanks for the beautiful examples of ragged camouflage! Also, thanks for Hypolimnas bolina, yes it certainly looks like a match for the male. So now I need to go back there and start looking for a female - I'd love to have photos of both.

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


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What instances are there in which two species share the same binomial name?
Since binomials are required to be unique only within a kingdom, two species can share the same binomial name if they are in different kingdoms. I know of one instance of this, Orestias elegans: this name denotes a species of fish (kingdom Animalia) as well as a species of orchid (kingdom Plantae).
Are there other instances where one binomial name validly refers to two (or more!) species?

This is a fascinating and surprising tidbit of information that practically begs to be used as the point of a puzzle story.

But why on earth did anyone think it would be a good idea to allow such a thing?

There are four other instances of species-level hemihomonyms I can find:

Agathis montana can be either a critically endangered species of conifer or a parasitic insect.
Centropogon australis can be either a fish or a plant with a long red flower.
Asterina gibbosa can be either a sea star or a type of fungus
Baileya australis can be a moth or a yellow flowering plant

Deep in the Binomial Nomenclature wiki citations!

The "wiki citations!" link in the previous note was a (now broken) indirect reference to https://species.wikimedia.org/wiki/Category:Species-level_hemihomonyms ,

Looking for hemihomonyms here: http://www.irmng.org/homonyms.php

In addition to the five listed above, Wikipedia currently shows two others, for a total of seven:
Ficus variegata can be either a sea snail or a fig
Tritonia pallida can be either a nudibranch or an iris
See "Hemihomonyms" here.

Two others for posterity, since I haven't seen others bring it up. Rhaphidophora is a genus of flowering plants AND of cave crickets, and there are two species-level hemihomonyms. R. beccarii is an uncommon houseplant and its relative R. neglecta is much rarer, but both are still documented. There's hardly any record that the cave crickets with these names exist, but they both seem to be accepted species with type specimens and all. I looked hard for images of either one and came up empty handed.

Very nice first post, welcome to Biology. Please take our [tour] and refer to the [help] for guidance as and when, enjoy the site.

Wikispecies has a Category with 28 hemihomonyms. A homonym is forbidden and only happens inside the same nomenclature code (zoological, botanical or bacterial). These cases are valid homonyms, so they're called hemihomonyms. These are:

Adesmia muricata
Agathis montana
Asterina gibbosa
Baileya australis
Centropogon australis
Cuspidaria cuspidata
Erianthus versicolor
Eulalia aurea
Ficus variegata
Fritillaria gracilis
Fritillaria messanensis
Fritillaria tenella
Gaussia princeps
Graphis albida
Herbertia brasiliensis
Iris orientalis
Myrmecia pyriformis
Orestias elegans
Ormosia formosana
Ormosia nobilis
Pilophorus clavatus
Schaefferia oaxacana
Thysanotus gracilis
Trentepohlia flava
Tritonia pallida
Tritonia striata
Uronema marinum
Viola minor

If you're interested in genera names that occur in two or more codes, there are over 1,400 currently, here: Category:Hemihomonyms

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


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Problem involving selfing (inbreeding it with itself) a plant to generate purebred lines
I am working on a past exam problem where the first bit is as follows

A plant is repeatably selfed to generate inbred lines. Let $\mathbb{P}(He|He)$ denote the probability that a heterozygous parent gives rise to a heterozygous offspring, and let $\mathbb{P}(Ho|He)$ denote the probability that a heterozygous parent gives rise to homozygous offspring.

I am asked to work out the two probabilities as well as an interpretation and state the value of $\mathbb{P}(Ho|Ho)$. The interpretation is obvious and I calculate the conditional probabilities to be
$$\mathbb{P}(He|He)=\frac12, \quad \mathbb{P}(Ho|He)=\frac12, \quad \mathbb{P}(Ho|Ho)=1$$
Next I am given the following

The inbreeding protocol is carried out $i$ times in an effort to obtain representatives of all alleles that can occur at a locus of interest. Suppose that there are 3 alleles, equally prevalent in the population at large and not under selective pressure during the inbreeding experiment. Let $p_j(i)$ denote the probability that, after $i$ repetitions the lines share $j$ distinct alleles between them. Let $p(i) \in [0,1]^3$ be a vector whose $j$th element is $p_j(i)$. Consider the following equation: $$p(i+1) = M p(i)$$

I would like to calculate the transition matrix $M$ and explain the boundary condition $p(1) = [ 1, 0 ,0 ]^T$.
I am lost on how to do this, I'm given the answer for $M$ to be $$\begin{pmatrix} \frac13 & 0 & 0 \\ \frac23 & \frac23 & 0 \\ 0 & \frac13 & 1  \end{pmatrix}$$
But for example looking along the first line I would interpret this as $$\mathbb{P}(\text{There is 1 distinct allele between all lines at time t}) = \frac{1}{3} \mathbb{P}(\text{There is 1 distinct allele between all lines at time t-1})$$
However if there is a single allele between the lines at time $t-1$ then this means every line is homozygous for a single allele so why would that change at the next time step?!
As for the boundary condition, I would of thought it would be $[0, 0, 1]^T$ since is the alleles occur with equal chance and you select a large enough number of lines, you should find all $3$ alleles between them. I was thinking perhaps there is a mistake in the question/solution and the vectors are defined the wrong way round, but even then I would be confused. Surely the number of lines we have makes a large difference, if every line is of genotype $\alpha_1 \alpha_2$ and we would like the probability that there is a single allele between lines at the next selfing step, then every single line would need to become homozygous for the same allele, which seems unlikely if we have a massive number of lines.
Can someone help me work out what is going on here?


text:
Is there a meaningful difference between direct and indirect light
I don't see a basis for a distinction, but I've heard several people distinguish between direct and indirect light for people, claiming that indirect light would be better in many cases. "Direct" means that the light goes from the source to your eye without intermediary, and "indirect" means that the light bounces one or more times off other objects before entering your eye.
An example of indirect light, for the purposes of this discussion, is sunlight or indoor artificial light, reading an old-fashioned print book or a non-backlit Kindle. An example of direct light would be any modern computer screen, or a backlit Kindle. The one context I've heard of direct light being preferred is a light alarm clock, where it was stated to be an advantage that light from the alarm clock goes directly to your eyes and is not exclusively bounced off objects in a room.
Now I can see one or two obvious differences; direct light tends to come from a small source (we don't tend to cover walls with LED's), while indirect light is more likely to bounce off everything or at least much more of what you can see. Furthermore, all other things being equal, direct light should be brighter as I am not aware of anything that reflects fully 100% of the photons that strike it (maybe some odd variant on superconductors)? However, I see only superficial distinctions between the two, and not a reason why, if all other things are forced to be equal (e.g. an indirect source being made brighter to compensate for the photons that physical surroundings absorb instead of being reflected), there should be the fundamental difference between direct and indirect light that I have repeatedly heard from people I trust.
Is there such a basic difference, or not, and if there is a difference, what does that difference consist of?
TIA,

@AlwaysConfused That thought is part of why I asked the question (instead of simply agreeing with my friends). I see possible differences in a (theoretical) blackbody room where everything was covered with low-light LED's so that theoretically there is only ambient light but it is 100% direct and 0% indirect; or light not visible to the viewer could bounce off a single object the light was shining on and that object would seem isomorphic to a direct light source. Part of the assumption that led me to post here rather than physics.SE is I'd expect any valid answer to be biology, not physics.

I'm voting to close this question as off-topic because it is more suitable for Physics-SE

The best difference I can find is not a different in physics. There is a difference (I don't know what significance it does or does not have for biology) between light that comes through a large area of a person's visual surface, and light that comes through a concentrated area. There are occasional differences with that reformulation (a fire in one's surroundings may provide direct light to a large portion of your visual surface), but that may be a more biological question.


text:
Help in identifying an unknown arthropod
I'm not even sure it's an insect:  the best I can do is identify it as an arthropod.  I captured this slow-moving organism and after a period of observation under high magnification, I concluded that it appears to construct a "shell" from miscellaneous particles or debris.  With a scalpel, I carefully cut this outer casing open to observe the organism, and the pictures show what I found.  It seems to have six legs, like an insect, but is oddly worm-like and wingless.  Total length is approximately 1 cm.  I do not believe that this is a juvenile/larval/instar form.  I've seen several of these where I live, and they always look like this (with maybe a +/- 20% size variation).

Edit:  This specimen was found in San Diego County, California, United States.

Closely related question/answer: http://biology.stackexchange.com/questions/15845/what-insect-is-this/15856#15856

We have a lot of these in our house.

We have a ton of these in our garage! (Los Angeles) Thanks so much for asking, I've always been curious about them.

These case building moths have shown up a few times on this site. Hands down, though, these are the best pictures.

It is the larva of household casebearer moth (a Lepidoptera), named after the larval stage. It is scientifically called Phereoeca uterella.
It is found through out South and North America.

The larva constructs a protective case from silk and camouflages it with other materials such as soil, sand and insect droppings.

References:

Wikipedia
bugguide

Further reading: Household Casebearer, Phereoeca uterella by
Juan A. Villanueva-Jimenez and Thomas R. Fasulo

so does cutting off it's shell (like the OP did) harm it? Or can it just grow another shell?

@user17915 There is no scientific work on the impact of removal of the larva from its case but I think it does affect the larva if done so because there must be a real significance behind spending a lot of energy synthesising the threads of the case which begins even before the larva hatches out.


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Why are prions in animal diets not destroyed by the digestive system?
According to CBC:

Mad cow disease is the common name for a condition known technically as bovine spongiform encephalopathy, or BSE. [...] The only known source of mad cow disease is from animal-based feed contaminated with tissue from a diseased animal. The original source of BSE is believed to have been feed containing tainted meat from sheep with a related disease called scrapie.

As prions are proteins, I would expect any that were contaminating food to be broken down to amino acids by the proteases in the digestive system. Why does this not occur?

I have reworded your question which confused me so much originally that I downvoted it (now revoked). There is no question that prions are proteins, so my rewording focuses on the question of proteolysis during digestion.

Proteases are enzymes in your digestive system that help break down food, acting like molecular-sized scissors that cut up proteins.
Proteases have clefts, or subpockets, into which proteins fit, where the substrate (protein) gets cut.
Infectious or pathogenic prions are resistant to proteases, because of their three-dimensional shape, which hides away parts of the prion that would normally fit in proteases and which would cause the prion to be digested.
Prions that do not cause disease — normal prions — have a different three-dimensional shape that allow them to fit into proteases, and so they are not resistant to digestion:

A wealth of evidence contends that the infectious pathogen causing the prion diseases, also referred to as spongiform encephalopathies, is solely comprised of PrPSc, the pathogenic isoform of the prion protein (21-23). Both PrPSc and its normal cellular counterpart, PrPC, are encoded by a cellular gene (2, 19). Physical and molecular characterization of PrPSc and PrPC has failed to reveal any chemical differences between the two isoforms (32). However, PrPSc acquires distinctive conformational characteristics upon its conversion from PrPC. Whereas PrPC is soluble in most detergents and can be easily digested by proteases, PrPScis insoluble in detergents and maintains a protease-resistant core, designated PrP27-30, which polymerizes into amyloid (25).

Dr. Neena Singh also discovered that prions "piggyback" or attach to another protein called ferritin, as they make their way through the digestive system:

Disease-causing prions are thought to have passed into people when they ate beef from infected cattle, triggering the brain wasting condition called new-variant Creutzfeldt-Jakob disease, or vCJD. But researchers have not been sure exactly how prions enter the body.
To find out, Neena Singh and her team at Case Western Reserve University in Cleveland, Ohio, mimicked the process of eating and digesting infected meat.
They mashed up brain tissue that contained prions from patients who had a form of Creutzfeldt-Jakob disease. They then exposed it to a range of harsh digestive enzymes from the mouth, stomach and intestine, which normally break proteins into pieces.
Prions, which are known to be enormously tough, escape this attack almost unscathed, they showed, as does a second type of protein called ferritin, which stores iron and is abundant in meat. The two proteins seem to stick together, they report in the Journal of Neuroscience.
The researchers next added the digested slurry to a lab model of the human gut: a growing sheet of cells from the intestinal lining. By attaching fluorescent tags to the two proteins, they showed that they are transported through the cells hand-in-hand. "Prions probably ride piggyback" through the gut wall into the body, Singh says.

Attaching to ferritin may provide additional protection from digestion, insofar as this removes prions from the digestive system, where proteases are concentrated.

Proteolytic enzymes present in human body mostly catabolize the Alpha helical protein. Prions are Beta sheet proteins hence they survive during digestion.
(We also can't digest silk because it is made up of beta sheet protein)
A protein is very resistant (Biological molecule) towards the environmental conditions. As chances of survival for a protein coat virus is higher then a virus having lipid envelope in the environment.
When we intake a pathogen by food. The food is contaminated with thousands of pathogen. Digestion may destroy most of the pathogens but many get access to infect the person.

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.


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What is the spacing between stop codon and transcription terminator?
When one tries to express a protein from a synthetic plasmid in E. coli, how many base pairs should there be between stop codon and the transcription terminator site?

A related post

In general, there is no need for a spacing between stop codon and terminator. They can be right next to each other.
When transcribed, transcription terminator forms a hairpin-like structure which interacts with the RNA polymerase to stop the transcription. Usually, the upstream sequence will not interact with the terminator and it will be transcribed normally. In a rare case the coding sequence might contain sequences that extend the hairpin and might result in interrupted translation. This can be avoided by doing a thermodynamical inspection of the secondary mRNA structure, but this is usually unnecessary.


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Why does contracting the iris allow less intense light to go in?
The iris contracts automatically in the presence of bright light. This makes a flashlight appear bright in darkness, but outside in daylight you can't even see it's light.
The iris is changing your sensitivity to the intenseness of light. But physically all is happening is the iris is getting smaller or larger. I can see how this allows less light to go in if it gets smaller, because it's less surface area. However, I would imagine this would change the field of view though if I didn't know any better. Why does it change the intenseness of light instead?

Imagine the iris like a shutter in front of a focussing lens (which, in fact, it is; see the diagram).

This means that any light going through the iris will be focussed on a very small point on the retina, and your eye is wonderfully developed in a way that this exact spot is the fovea, the only spot in the retina that allows you to see colour and high-resolution.
The iris does not modify the focussing function, it merely changes the amount of light going through into the lens to then be focussed onto the fovea. Imagine that every single object in your field of view reflects/radiates light in every possible direction - narrowing the shutter won't exclude parts of the field of vision, it will only exclude some of the rays coming in at very flat angles and thereby reduce intensity.
Only if your lens is deformed, focussing (adaptation) will malfunction (directing the gathered light to the wrong spot; or focussing the incoming light in front of or behind the retina) and blur your vision.


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Living organisms with properties similar to both plants and animals?
Is there any example of currently living organisms that shows close resemblance to both being a plant and an animal?
What is the plant with the closest possible resemblance to animals, and
What is the animal with the closest possible resemblance to plants?

I have added important new information in a new answer to the proposed duplicate question.


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Is it possible for bacteria to acquire family-wide antibiotic resistance?
If there is bacteria, lets say Enterococci that is sensitive to:

Amoxycillin-Clavulinic acid
Ampicillin-Sulbactam
Ofloxacin
Ciprofloxacin

Is it possible to become resistance to Ampicillin-Sulbactam by using Amoxycillin-Clavulinic acid ?
Is it possible to become resistance to Ofloxacin by using Ciprofloxacin ?

It depends on the mechanism of resistance..

Yes, via point mutations, which can happen spontaneously and doesn't depend on anything.

The two amoxycillin formulations you mention pair the amoxycillin with a Beta lactamase inhibitor. This is because of the prevalence of resistance to beta lactam drugs including amoxycillin. If we were to invent a brand new never before seen beta lactam drug and started using it irresponsibly, there would probably be resistant bacteria within 5 years. The same beta lactam core structure that makes the drugs work against the peptidoglycan synthesis machinery make it susceptible to attack by beta lactamase. A new beta lactam could avoid the lactamase for a while, but the same evolutionary pressures that selected for resistant mutants against the other beta lactams would select for mutants resistant against the new one.
The same goes for the fluoroquinolines you mention. Their mechanism of action is different, they inhibit DNA synthesis by blocking topoisomerase II activity. But once a bacterial strain is selected for that has resistance against one member of a class of antibiotic it's relatively easy for it to acquire the mutations that confer resistance against other members of the class. Changing the structure of the drug enough so that cannot be defeated by the mechanism of resistance while retaining the drugs mechanism of action is probably impossible, or at least we haven't done it yet. Even vancomycin, one of our most powerful antibiotics, has some bacteria resistant to it.


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Is it theoretically possible to create two humans by splitting one human in two?
There have been cases where a person has had one of their brain hemispheres removed, and they ended up living a fairly normal life. Could it be possible to split a normal person down the middle and create two people, each with a brain hemisphere? Machines could be used to replace organs that can't be split, like the heart.
I'm assuming there would exist some very advanced technology to prevent excessive blood loss and other problems with splitting a person down the middle.

If you split a human early enough (in the first weeks after fertilization), you can get monozygotic twins.
Other than that, you are in the field of science fiction and we cannot safely answer such question on a science website. I am not sure your question will be accepted in its current format but you may try WorldBuilding.SE.
And if you like fantasy novels, I recommend The Cloven Viscount by Italo Calving! You will definitely not learn much about biology in this book though.

Given how some parts of the brain control the opposite hemisphere of the body, and how this is not consistent throughout the entire brain, you would have to do a lot more than split someone in half down the middle.
Importantly, in split-brain patients only the cerebral cortex is hemisected, and only at a particular (though significant) point of connection, called the corpus callosum. It would not be possible to do this through the entire brain.
Especially in adult humans, some functions become lateralized, as well, so each "person" would be capable of different functions.

I see, the hemispheres would need to be swapped after separating them so a hemisphere stays with the side of the body it controls.

@Thomas It's not possible to separate in that way. Things are too intertwined. You can refer to it as a sci-fi possibility, but in the real world it isn't even close, not even with the most expert surgeons or even futuristic robotic abilities.

In split-brain patients, only corpus callosum is hemissected because its the only point where thetwo hemispheres connect. IMO spliiting hindbrain into hemispheres wouldn't be very logical...

@another'Homosapien' That's actually not true - there are the anterior and posterior commissures, and there are some other indirect pathways between cerebral hemispheres. The corpus callosum is just the bulk of the connectivity. But yes, there  is no sense in splitting the hindbrain, nor parts of the midbrain.

Although there have actually been some cases where a human have survived with half-a-brain after one hemisphere was surgically removed - the remaining hemisphere took up the slack.   http://mentalfloss.com/article/70120/how-removing-half-someones-brain-can-improve-their-life

@BaardKopperud The extent of the ability of the brain to compensate depends a lot on age. The most extreme examples in that article are for people who lost a hemisphere at a very young age. Also remember that the cerebral cortex is only a portion of the whole brain. An important one at that, but a lot of function is possible without any cortex at all, so it's important to keep that in mind.


text:
Are genotypes with the same two alleles equivalent even if the alleles come from different parents?
I am looking at the following question

If $m$ alleles may occur at a given locus, how many distinct diploid genotypes are possible at that locus?

The obvious answer is that there their is $m$ possible paternal alleles and $m$ possible maternal alleles so the solution is $m^2$. However this considers inheriting allele $a$ maternally and allele $A$ paternally as the same as inheriting $a$ paternally and $A$ maternally.
If they are considered distinct we have double counted all matchings apart from matchings where the same allele is inherited maternally and paternally so I think the answer to the question if $Aa$ is the same as $aA$ would be $\frac{m(m-1)}{2}+m$
My question is which if any of my interpretations is correct?
Thanks in advance

1 allele (a) means one possible genotype (aa), 2 (a,b) means four possible combinations, but three distinct genotypes (aa, ab, ba, bb... I say three distinct genotypes becuase ab and ba would not be distinct when looking at the offspring unless you can determine parent of origin)... that would be my interpretation at least. What is the source of the question?

Okay @GriffinEvo, so if we have 3 alleles then we have 9 genotypes, 6 of which are distinct? If we had two loci one with 2 alleles and another with 3 alleles would the number of distinct genotypes be $3 \times 6 = 18$ (just to check I understand)

(a,b,c) = (aa, ab, ac, bb, bc, cc) so according to my logic, yes, but I don't know whether the question is looking for my logic.

My instinct is inline with your logic but we'll see what others have to say if you aren't 100%. Thanks

If you have genomic imprinting then $k^n=m^2$ (with k=m and n=2 because of diploidy) is correct as inheriting a from the father and b from the mother (i.e. ab) is not equivalent to inheriting b from the father and a from the mother (i.e. ba). For 3 alleles (a,b,c) you have 9 possible genotypes (aa,ab,ac,ba,bb,bc,ca,cb,cc).
Under no genomic imprinting, ab and ba are equivalent. This is equivalent of calculating the number of elements of a triangular matrix which is $\frac{(m+1)*m}{2}$. So for m=3, you have 6 possible genotypes (aa,ab,ac,bb,bc,cc), for m=4 you have 10 possibilities (aa,ab,ac,ad,bb,bc,bd,cc,cd,dd) etc...
I hope this helps. Your formula is actually equivalent.


text:
Why do we need red blood cells?
From what I know, the main function of red blood cells (RBCs) is hemoglobin transport. So, why do we need cells packed with hemoglobin: why can't it travel freely in the bloodstream?
My own thoughts were:
1) Having hemoglobin packed into cells means it can be released where it's most needed. For example, when we are exercising, our muscles need more oxygen, so more erythrocytes release their oxygen in the muscle tissue.
2) The diameter of a capillary is much bigger than a single protein molecule's diameter, but comparable to a cell's diameter. So, when cells are traveling through a capillary, all of them are close to its walls. However, when free molecules are traveling through it, some of them are close to the walls, while the others are in the "middle". I figured, those in the "middle" can't exchange oxygen with the surrounding tissues. So, red blood cells make gas exchange more effective.
Do you think any of this makes sense? Why in reality do RBCs exist?
Any insight or book recommendations would be very appreciated:)

#1 doesn't make sense. Whether in cells or not in cells, O2 binding to Hg depends on O2 concentration in solution. #2 doesn't make sense, but you are close to the interesting idea "having objects with diameter close to the blood vessel has unique and desirable hydrodynamic properties", but I would suspect it's more that capillaries evolved to track particle size, not the other way around. A useful insight would be to look at closely related animals with and without RBCs. Also, consider nucleated bird RBCs.

If you want a good look at why free hemoglobin is a bad idea, read an article about transfusion reactions (hemolysis) and the organs it damages.

Hemoglobin molecules used to manufacture these products are not
  contained by a red cell membrane, and when released into the
  vasculature, these molecules rapidly scavenge nitric oxide.This can
  result in systemic vasoconstriction, decreased blood flow, increased
  release of proinflammatory mediators and potent vasoconstrictors, and
  a loss of platelet inactivation,17- 20 creating conditions that may
  lead to vascular thrombosis of the heart or other organs. This
  mechanism has recently been shown in preclinical models to be
  responsible for injury during hemolytic states, in which hemoglobin is
  also released into the circulation.21
Unlike naturally occurring hemoglobin, manufactured cell-free
  hemoglobin-based blood substitutes (HBBSs) can be chemically altered
  to theoretically minimize such toxicities. It has been postulated that
  cross-linking, polymerization, or pegylation of hemoglobin will create
  larger, more stable HBBS molecules, preventing extravasation and
  thereby leading to a reduction in toxicities related to nitric oxide
  scavenging. At least 1 manufacturer has also chemically increased the
  affinity of its HBBS for oxygen (lower P50, the partial pressure of
  oxygen required for 50% hemoglobin saturation) to decrease arteriole
  oxygen transfer and thereby potentially eliminate untoward
  cardiovascular effects.

2008 - Cell-Free Hemoglobin-Based Blood Substitutes and Risk of Myocardial Infarction and Death

So cell free hemoglobin is toxic. As you can see this toxicity can be reduced in other ways too, so it seems like there is an evolutionary pressure in the direction of having blood cells, maybe it is simpler this way. To answer the other question, I think there can be free HGB in the blood when blood cells fall apart because of an infection e.g. malaria, etc...

Hemolysis in falciparum malaria results in NO quenching by cell-free
  hemoglobin, and may exacerbate endothelial dysfunction, adhesion
  receptor expression and impaired tissue perfusion. Treatments that
  increase NO bioavailability may have potential as adjunctive therapies
  in SM

2008 - Relationship of Cell-Free Hemoglobin to Impaired Endothelial Nitric Oxide Bioavailability and Perfusion in Severe Falciparum Malaria

Btw. I agree with rhill45, I think too that it is easier to regulate O2 and CO2 exchange if you have a specialized cell type, so it might have regulation purposes. It can have recycling purposes either, because it is hard to distinguish between old (damaged) and new HGB when they are in a cell-free form. This problem probably can be solved by destroying only glycosylated hemoglobin, but I guess it is much easier to filter out the old RBCs in the spleen...

In the process of maturation, a basophilic pronormoblast is converted
  from a cell with a large nucleus and a volume of 900 fL to an
  enucleated disc with a volume of 95 fL. By the reticulocyte stage, the
  cell has extruded its nucleus, but is still capable of producing
  hemoglobin.

according to wikipedia (without citation).

Other sources claim the same, with the extension that this period lasts only for a short time, because the cell soon loses its mRNA and so it stops producing HGB. So according to these articles RBCs create the HGBs in the early stages of their life. (I did not find a real scientific article about this, but I can accept this theory.)
According to Chris this toxicity is just a protection mechanism, so I dug deeper.

Bacterial virulence is greatly enhanced by freely available iron, such
  as that in fully-saturated transferrin or free haemoglobin. Following
  trauma a fall in tissue Eh and pH due to ischaemia, plus the reducing
  powers of bacteria, can make iron in transferrin freely available and
  abolish the bactericidal properties of tissue fluids with disastrous
  results for the host. Hyperbaric oxygen is a possible therapeutic
  measure that could restore normal bactericidal systems in infected
  tissues by raising the Eh and pH.

2006 - Iron and infection: the heart of the matter

Iron lies at the center of a battle for nutritional resource between
  higher organisms and their microbial pathogens. The iron status of the
  human host affects the pathogenicity of numerous infections including
  malaria, HIV-1, and tuberculosis.

2012 - Hepcidin and the Iron-Infection Axis

So RBCs protect the iron against microbial pathogens, that's their key role. I think every other related problem, like O2 release regulation, free HGB toxicity, HGB recycling, etc... can be solved with free HGB as well, so most probably iron protection is the evolutionary pressure to store HGB in blood cells instead of letting it be in the blood in a cell free form. It's funny that every single book gets this wrong, and they claim that carrying oxygen is the most important role of this cell type, while they aren't mention anything about iron protection... :-)

One point of free hemoglobin in the blood being toxic is the fact this happens when red blood cells get damaged, which is obviously not a good thing. So this is a protective mechanism as well.

Hmm interesting theory. RBCs might be protecting the Fe from infectious microbes. I heard a theory that by infections the human body clears up Fe from blood, because microbes need Fe for multiplication, creating metalloproteins etc... I never investigated... :-)

@Chris thanks, this iron theory seems like really true.

Oh wow, thank you for your response. The 'iron protection' reason is a beautiful explanation :) I wonder if there are any other proteins with iron incorporated and whether they are protected as well, I'll try to look into it

@Eva Ofc. there are, e.g. transferrin, but by infection they are cleared from the blood (hepcidin regulates their level), but HGB cannot be removed, because it is the oxygen carrier, so you would drown in the lack of HGB...

This is not a topic I know well, and the answer clearly contains lots of useful information. However, I find this answer really problematic since it is filled with teleological arguments in relation to evolution, e.g. "...why evolution created this cell type..." and "...creating a new cell type was the easiest way to the evolution..."  This is simply not how evolutionary processes work, and even if this is not intentional, it can still cause a lot of confusion.

@fileunderwater Yes you are right, I weren't accurate. I meant that there is an evolutional pressure to store the HGB (and iron) in blood cells instead of let it run in a cell free form in the blood stream. Is this acceptable for you?

@inf3rno Yes that would be better, to remove the appearance of evolutionary purpose and that evolution is actively searching for "easy" solutions.

@Eva http://www.ncbi.nlm.nih.gov/pubmed/15095784
There are RBC derived vesicles. This study estimates that RBCs lose about 20% of HGB during their lifetime (120-150 days) by creating vesicles. These vesicles have a short lifetime, they are degraded by the liver. Another article in the topic: http://journal.frontiersin.org/Journal/10.3389/fphys.2013.00365/full . So there is always HGB in blood, but I don't think it is relevant by respiration, it is just part of the degradation process.

@Eva Note that vesicles have phospholipid membranes just as cells do.

@inf3rno- Do you think Hemophilia is a beneficial mutation?

@TheVoid I don't know of any reason because of hemophilia could be beneficial. By some of the heritable diseases there are hypotheses that the mutations had advantages at some time during our evolution. E.g. the sickle cell anaemia point mutation was beneficial when malaria was more common. https://en.wikipedia.org/wiki/Human_genetic_resistance_to_malaria#Sickle-cell If you find a similar selective pressure by hemophilia, then it can be a possible cause of the mutation.

@inf3rno- I know i'm getting off topic but DVT is one of the highest causes of death, So could a Hemophiliac die of DVT? Im asking because you seem to have a interest in hematology.

@TheVoid They could, but it is very rare. http://www.ncbi.nlm.nih.gov/pubmed/12945884 So yes, this can be a selective pressure, which can make these kind of mutations more widespread/prevalent. I don't know which would the proper word here, since it is still rare. And most probably it is rare, because its costs are higher than its benefits.

This is a well worded question. There are more reasons than the following but the most apparent is hemoglobin production and its transport. The erythrocyte is a cell whose structure is optimal for its function-the production and transport of hemoglobin.
It lacks a nucleus and organelles so that it can devote almost 100% of its energy to hemoglobin production. It has this  bi-concave disk shape to increase its surface area thus increasing the exposure of hemoglobin to oxygen and CO2.
It's a small and flexible cell allowing them to easily maneuver the capillaries (where they work).
Because it's anuclear it has a short lifespan but they are rapidly produced and regulated by erythropoietin.
In order for tissues to receive oxygen and rid themselves of carbon dioxide there needs to be an orderly transfer and movement of hemoglobin from the tissues to the lungs and back-and-forth. Without this cycling of hemoglobin on the erythrocyte the protein would move more in the body through diffusive means. This would not promote the required segregation of oxyhemoglobin in the tissues and carbaminohemaglobin in the lungs.
Check out any edition of Anatomy and Physiology by Marieb. All editions have an entire chapter related to the subject

Thank you for your answer! I didn't know that hemoglobin is synthesized in RBCs, it makes more sense now. However, I still have a question: how do red blood cells help segregation? When gas exchange happens, is hemoglobin free in the tissue or still actually inside a cell?

Cause the hg is on the rbc, wherever the rbc is the hg is. Only the rbc can effectively be circulated, if was just swishing around the body too much hg would diffuse where it not needed  in respect to oxyhemoglobin and carbonMinohemoglobin

Do you have any references for this? It seems unlikely to me that a red blood cell can produce haemoglobin without DNA or RNA (once it's degraded).

It's not an easy concept because you have to think of the requirements of the whole organism additionally the requirements of specific regions of the body tissues versus Lungs.

Your claim about diffusion is interesting but, again, do you have a reference?

Check that text out most of what I learned is from there

It's not degraded it has ribosomes it produces hemoglobin

So, hemoglobin is actually NEVER free in the body? (In normal circs, of course)

Never say never look up what a contusion is and where bilirubin comes from

These are good new questions your asking

Okay, I think I understand it better now, thank you!

This is not an answer to the question, but tangent comments that might be useful for how you look at the problem (and too long for a comment). First, for a question like this it is useful to look at other solutions to the same problem. For instance, the second most common molecule for oxygen transport is Hemocyanin, and this is not bound to cells but is directly suspended in hemolymph (arthropod/mollusc "blood"). So specialized cell types for oxygen transport is not a necessity for effecient oxygen transport in rather advanced organsism. So your question; "why do we need cells packed with hemoglobin: why can't it travel freely in the bloodstream?", while being true for humans and other vertebrates, is not true for oxygen transport in all "complex" animals.
Second, while there seems to be good reasons for why hemoglobin is bound in RBC, you should at least entertain the idea that the cause of RBC-bound hemoglobin in vertebrates is an evolutionary contingency (i.e. a random historical event). Evolution is always constrained by previous evolutionary history, and the reason that all vertebrates (+ a number of other organsisms) share RBC-bound hemoglobin may simply be that they share a common ancestor. This does not mean that it lacks advantages, but it also means that it might be misleading to search for the reason for RBC-bound hemoglobin in a particular species. For some background on evolutionary contingencies and many useful references in the intro, as well as an interesting experiment to test for contingencies, you can have a look at Blount et al. (2008) (part of Lenski's Long-term Experimental Evolution project).

I remember going to a chemistry lecture which mentioned this (the lecture was on blood transfusion in general).
The main reasons are:
1) Hemoglobin is toxic to the human body: Hb in RBCs is a tetramer, but in the plasma it breaks into two dimers --> toxicity in the kidneys. Hb needs modification by cross-linking or recombination. Wikipedia states that this is Acute Tubular Necrosis.
2) Hb in plamsa decreases osmotic pressure
3) Hemoglobin removes the NO from the vessel walls causing vasoconstriction, shrinkage of the vessels.  --> this was the main focus of the chemistry lecture; there was a lot of talk about free radicals and stuff but I've unfortunately forgotten the details
I've also searched a bit on the web and some people (one yahoo answers) confirm rhill45's answer.
I think searching failed blood transfusion products (people have tried transfusing Hb directly) will be of great help.

Could you please add some references to support your response!

for 1) and 2) http://www.chm.bris.ac.uk/motm/mpg/whymod.htm
for 3) I got the info. from a chemistry lecture I attended, so it's just personal notes

See one of my references. It writes the exact same thing that Hg binds to NO. Removing NO from blood is a problem because NO is a gasotransmitter causing vasodilatation. So having less of it causes vasoconstriction. https://en.wikipedia.org/wiki/Gaseous_signaling_molecules#Nitric_oxide


text:
Why do the proportion of predators increase at mass extinction events?

Why does predation surge with mass extinction? It is caused by extreme selective pressures over resource competition that forces certain species to adapt to predatory niches?

Interesting question. Do you know whether this pattern repeat with the 3 other mass extinctions? Can you please link to the article who produced this figure? That will probably help.

@CN7 What book/paper is the graph from, and how to they discuss the dashed ranges?

The data used in the graph you posted seems to be from Bambach. 2002. Supporting predators: changes in the global ecosystem inferred from changes in predator diversity (in Kowalewski & Kelley. The Fossil Record of Predation) - see fig 19b - and, if so, is specifically dealing with marine predators.
I don't have time to look at that paper closely (it is quite long), and paleoecology is not my field, but a couple of relevant sections are:

However, the diversity of predators and the proportion
  of total faunal diversity composed of predators have both increased over time, implying that ecosystems have
  increased their ability to support either more predators or more specialization among predators. Also, turnover
  in diversity dominance among predator groups, with more energetic predator taxa replacing or being added to a
  fauna of less energetic groups, implies that the energy available in marine food webs has increased.

and

If
  the efficiency of energy transfer between levels in
  the food pyramid has stayed nearly constant (and
  there is no evidence that it has not), then a reasonable
  hypothesis for the increased proportional diversity
  of predators is that either the biomass of prey species
  has increased or the populations of prey taxa have
  become more stable (or both), permitting greater
  specialization by predators on more reliable food
  supplies. Thus, predators could increase their
  proportional share of total diversity by specializing
  on fewer prey taxa.

So according to the author, energetics, energy flow and predator specialization seems like likely reasons for the change. However, the paper also discuss factors such as rates of fossilization and also the fact that predators are generally rarer than prey means that there is probably more stochasticity in the fossil occurence process, which could affect estimated turnover rates and maybe also the proportion between predator and prey. You'll have to look at the entire paper for a fuller picture, and maybe somebody more knowledgeable can fill in later. I also think that you need to look at radiation patterns in certain taxa to fully understand these stepwise changes, and also to consider oxygenetion events as possible underlying reasons, but these are just my speculations.
The reasons given above also in one sense echoes the "biotic" explanation for the latitudunal diversity gradient (see e.g. Gaston, 2000 and Mittelbach et al, 2007), where high levels of primary production can support more specialized predators/parasites in more complex food webs, then leading to higher species diversity. So there might be interesting connections to contemporary patterns and processes of biodiversity as well. However, I haven't seen a compilation of %predators over different biomes or latitudes to match the graph in the question. Also, the "biotic" explanation for the latitudunal diversity gradient has been criticized and is not without problems (see papers above for more).


text:
How to translate a blood type used in Eastern Europe?
What are the I-IV blood type descriptions shown below (commonly used in Eastern Europe), and how do you translate them into the ABO-system?

What do you mean by translate?

@WYSIWYG: Convert it to the system used in the West: http://www.redcrossblood.org/learn-about-blood/blood-types

I still don't understand. Isn't it already clear from the image?

@WYSIWYG: What's this (I), (II), (III), etc. stuff? I guess that's what I'm asking.

I think this description is wrong. Blood type used to be described as AB-I, A-II, B-III and O-IV plus Rh Positive or Negative.

You should provide references for your answers. The article linked to in my answer describes two numerical systems: one created by Jansky (which is what is shown in the question and referred to in my answer) and one created by Moss (which is what you are describing).

It is a direct correlation between the ABO blood groups and the Roman numerals.
 O: I

 A: II

 B: III

AB: IV

This numeric system was pioneered by Jan Jansky of Czechoslovakia in the early 20th century. Apparently it is still used in some former Soviet states.
Erb IH. 1940. Blood Group Classification (A Plea for Uniformity). Can Med Assoc J 42(5):418-421.

I can't upvote it (not enough rep.) But thanks for the info!

@MikeF you should be able to accept it by clicking the check mark.

What would O+ in the US be in the UK?


text:
Moth with silver marking on wings
This is a moth that we found on a curtain inside the house a couple of days ago. Unfortunately, these pictures did not come out as well as I thought before I realized it outside. But I was struck my the silver-white eyeglass-shaped spots on the wings. It also had an interestingly shaped head, but that didn't come out well. The closest I have come to identifying it is that it looks similar to a Dot Moth, but those don't seem to be native to Southern California (Los Angeles).
It was about an inch long, maybe less. It vibrated its wings after I disturbed it.

Based on the overall apparence and the distinctive metallic patches on the wings it looks like a moth from the subfamily Plusiinae (Looper moths). I'm not familiar with North American moths, but after a quick check at species found there Megalographa biloba (Bilobed looper moth) seems likely, and this species is also found in California.

(picture from wikipedia)
Also see the pictures at Bugguide.net.

Excellent! I agree with your determination - I think you have it right. The front legs are similar, as are the markings (I hadn't even noticed the smaller silvery one). And the Wikipedia page shows the distinctive shape of the head that I wasn't able to capture in the photo.I would have had a lot of trouble determining that species on my own. Much appreciated!


text:
Which animal that lives in the forest makes this noise?
Which animal makes this noise? Link to audio file
The file was recorded next to a forest in Germany.

You might get lucky, but noise to animal mapping is rare indeed.  Your recording is only picking up the higher frequencies this animal made, and I know a few human animals that can make a variety of non-human animal noises :)  Good luck with it!

It is a bird sound and most probaby a young bird of prey. It might be a young buzzard. Or, if it's in the eveving or night it might be the sound of a young owl.


text:
What is the coefficient of relatedness between a queen bee and her daughter if the male that mated with the queen was the queen’s own son?
What is the coefficient of relatedness between a queen bee and her daughter if the male that mated with the queen was the queen’s own son?
The answer should be 0.75, but I keep getting 1 because 0.5(queen-daughter) + 0.5(queen-male) * 1(male-daughter) = 1.
1 also makes sense because all of the daughter's genes come from the queen. However, I do understand that there is a chance that the genes inherited from the daughter's mother and father may overlap. How is that calculated?

When dealing with haplodiploidy (male are haploids and females are diploid as it is the case in bees), there are several ways at looking coefficient of relationship and the coefficient of relationship between A and B may differ from the coefficient of relationship between B and A. Considering (male-daughter) as being 1 is the source of your issues

I misread it as Rotatedness, and I thought that scientists had figured out that bees signal to each other at N degrees between queen bee and her daughter if the male that mated with the queen was the queen’s own son. that was funny.

Remi, I understand what you’re saying and also that bees are haplodiploids. I thought that when tracing from Queen—>male—>daughter, I’d consider them in the same order that they appear. So regarding queen-male, queen has 1 of male’s genome. Regarding male-daughter, the male has 1/2 of daughter’s genome, on average.

See the answer to this question: How to calculate relatedness in haplodiploid organisms (mainly full sisters and full brothers)?