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What is a 5'-cGMP?
I know in cGMP , there is a bond between phosphate, 5' and 3' C of sugar , but what is 5'-cGMP?
[It is involved in cascade of vision.]

There is no 5'-cGMP. That's probably a typo.
In the phototransduction process, there is the breakdown of cGMP to 5'-GMP, catalysed by a Phosphodiesterase:

PDEs hydrolyze the cyclic phosphate ring that's unique to cAMP and/or cGMP by insertion of a solvent derived hydroxyl at the phosphorous atom in the 6-member cyclic phosphate ring. The product of this reaction is either 5'-AMP or 5'-GMP.

Thus, 5'-GMP is the same of GMP, that is, Guanosine Monophosphate.
(source: cGMP: Generators, Effectors and Therapeutic Implications)

As you will see from the Wikipedia article, you can talk about cGMP, Guanosine cyclic monophosphate  or cyclic 3',5'-GMP. The 3' and 5' indicate the positions bridged by the phosphate in the cylization. Thus, ‘5'-cGMP’ is chemical nonsense.


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Identity and similarity for Multiple Sequence Alignment (MSA) of proteins
I have to do homology modeling for a transmembrane protein (sodium channel) and right now I am in the process of aligning the sequences of the template with the homologous proteins I have found. I am using T-Coffee to do the alignment. I would like to have some numerical descriptors of the different sequences and I have been told to include the percentage of similarity and identity. How can I compute them? Is there an on-line tools to do this? Thank you.

I've never used T-Coffee but it looks like the web-server version gives you a total score as well as a score for each individual sequence; do you know if those numbers are related to the numerical descriptors you need?
A good place to start would be to read the documentation. Another good place to look would be the Google Groups page for T-Coffee.

Thanks you for the reply. I just finished reading the documentation. I found out that I can use Chimera to see the percentage of identity, so one problem is solved. The main problem is of a different nature: let's say that I have the MSA from residue 1 to 100 of the query. I would like to have a tool that automatically computes the number of insertions, deletions etc... Some numerical quantities that I can use to see if the alignment is good and how much. Thank you.

It would appear that this answer solved the user's question. His comment includes an additional question which is not relevant. I have therefore upvoted it in response to the Cummunity homepage bump.

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Enzyme kinetics types?
In lectures, we have discussed Michaelis Menten enzyme kinetics, but from lectures it was clear that this was not the only type of kinetics.
After looking into this, I have found enzymes that give a sigmoid curve relating initial rate of reaction to substrate concentration.
So so far I have:

Michaelis Menten Kinetics

For which I think the only conditions are that the enzyme reaction follows

and the enzyme does not bind more than one substrate molecule (isn't allosterically binding)

'sigmoidal' kinetics

Where the enzyme is an allosteric enzyme and binding of more substrate to the enzyme increases the enzyme's affinity for the substrate.

Are these the only two main types of enzyme kinetics?

As the figure you reproduce appears to be from the article on "Enzyme kinetics" on Wikipedia, didn't you see the section on multi-substrate kinetics there?

The issue with Michaelis menten curves, is that they presume only one pathway the enzyme can act by. Therefore if an enzyme has multiple pathways the presumptions fail. An example of this is monoamine oxidase, (Ramsay, R. R., Olivieri, A. & Holt, A. An improved approach to steady-state analysis of monoamine oxidases. J. Neural Transm. 118, 1003–1019 (2011).) This paper has the enzyme specific kinetics for monoamine oxidase - the development of the models is incredibly complicated but if you look at the equations you can see how there are multiple pathways.
They also presume only one substrate, so multi-susbtrate reactions need to have the kinetics modified as such. For that the mechanism are: Ping-pong, ternary- ordered and random, all of which impact on the kinetics.If the concentration of the intermediate complex is presumed not to change with time, then another model is the Briggs-Haldane model, known as quasi-steady state kinetics.
Then there are the kinetic models for inhibition. Of which the michaelis menten, where the kinetics vary according to how the inhibitors binds. But as is seen with the above MAO paper, can vary depending on the pathways and binding affinities.  If an enzyme is irreversible then the kinetics also differ (Mcdonald, A. G. & Dublin, T. C. Enzymes : Irreversible Inhibition. 1–17 (2012). doi:10.1002/9780470015902.a0000601.pub2).
It is also worth noting, it is better to use non-linear regression to analyze kinetics as linearizing the data can lead to calculation errors (despite admittedly being the easier and clearer option).

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Is it feasible to eradicate a virus without vaccines?
Although a vaccine for hepatitis C virus (HCV) remains elusive, new direct-acting antiviral (DAA) drugs can cure HCV effectively and conveniently. The latest DAA, Epclusa, can cure 95-99% of chronic hepatitis C regardless of genotype (e.g. see here). So if DAA drugs become universally available, will HCV be the first virus eradicated solely by drugs?

It is not the answer you are looking for, but for the fun of it: Yes, simplest situation being to eradicate all the vectors of the virus = eradication of the virus itself. :)

Is it feasible to eradicate a virus without vaccines?

It is possible? I would say yes. But feasible... I think not. Consider this, once vaccinated, a person is usually immune to the virus. And you only need the vaccine to take hold, for an individual to acquire life time immunity. However with drug treatment... even once the treatment succeeds, the person can be reinfected. And you will have come back with drug treatment again.
Given the difficult in vaccination campaigns (ie polio) to eradicate the last reserved of a virus... I think a similar drug based campaign would a lot more difficult. There is no herd immunity to prevent the virus from reinfecting the wider population when it leaves its strong holds.

You're right. Chronic hepatitis C doesn't confer any protective immunity, and those cured are still susceptible to reinfection.

Herd immunity is a good point. I haven't thought of it.

I would also add that outbreaks of measles when herd immunity breaks down show how easy it is for a virus to breakout.

To the question I would say certainly yes, since the only viruses that have been eradicated (to my knowledge) are smallpox and rinderpest, both via vaccine campaigns (as well as the usual tools of quarantine/isolation).
Note: I did not mean to suggest that "if drugs are widely available they will definitely eradicate HCV".  I interpreted the question as "if HCV is eradicated by DAA, will this be the first disease eradicated by drugs?"
Vaccines are typically used as prophylactic treatments, i.e. they are applied before an individual gets infected. Drugs can also be applied prophylactically (e.g. antiretroviral drugs against HIV), and vaccines can also be used post-infection, e.g. for rabies. In order for a cure (i.e., a treatment that is applied after an individual becomes infected) to eradicate disease, it must be applied soon after enough infection that it cuts down the infection period sufficiently to reduce the average number of secondary infections per infected person below 1. Analogously, when prophylactic treatments are given by age, as in the case of vaccines for childhood diseases, they must be administered to children young enough that most of them will not already have been naturally infected [and passed the virus on to others].

I think it is interesting to see how it goes. For HBV, we have vaccine but not cure, while for HCV we have cure but not vaccine. We can compare which is more efficient at shrinking the reservoir.

My guess is that vaccines are more efficient at eradicating acute diseases(smallpox, polio, measles) because you can hardly have those infected get treated before they can transmit the disease. While for persistent infections(HIV, HCV, HBV) a cure may be more efficient. Because it takes long time for infected people to die out.

Due to the long time people can be infected with no or almost no symptoms, I doubt that. A vaccination is much more reliable here.

One could certainly evaluate all of this using a simple model. To know the cure rate, you'd need to know (1) the untreated R0 of the disease; (2) how much of the force of infection is mitigated by the cure [i.e., we need to know the infectious period, how much of it is asymptomatic, and the rate of cure administration - expected time from appearance of symptoms to cure]


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Vaccination and Immunisation
Why are oral polio vaccines advantageous over the killed ones?  I was told that the orally given polio vaccine prevents infection by causing intestinal immunity. How does it do that? Also, how does this make it superior over the intravenously injected polio vaccine?

What research have you done on your own to answer these questions yourself? For example, Google searches or even simply reading the Wikipedia pages for polio vaccine and intestinal immunity would give you a lot of information. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions.

There is a killed oral polio vaccine?

Just look up the 'cutter incident'. Use of OPV is more of a historical and silly reason than the IPV. For example, India after recent eradication of polio has started to switch from OPV to IPV. There are serious plausible risks of using OPV but was still used due to one cutter incident that tainted IPV

@polisetty thanks. For your reference. It did help. PS: irrelevant though I wanna say this :/ (don't blame me) I guess I know you! Vashishta polisetty?

@user129402 yup :) Hope I'd known you too.. only if you could give yourself a name :P

@user129402 because it's the virus's natural route to infection, hope you now understand.

Oral polio vaccines are delivered in the site of the potential infection. You may think about them as about a realistic simulation of the infection. As it is not scientifically sound explanation, please see the answer about whether intramuscular vaccination leads to intestinal IgA secretion which protects against intestinal route of infection.
Oral polio vaccine (Sabina) contains attenuated (alive but weakened) polio virus, which can proliferate and compete in the environment with the really dangerous wild polio virus. That way also people which has not been  directly vaccinated may be protected - both by development of immunity after less severe infection, and by reduction of exposure to the wild virus.
The route of delivery is much more acceptable by children.


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Pigment returning to my grey
In the past I dyed my hair to cover the grey, but it became a more frequent event so I decided to just go grey.  My hair has been almost entirely white for nearly 20 years.  The pigment has been returning to my hair gradually for the last 18 months.  Do you have any explanation for this?  I have tried to research this, but have not found any answers.  There is information for reasons why hair looses pigmentation, but not for its return.  Any ideas?

Hello, and welcome to the site! Personal health questions aren't allowed here, but your question might be adaptable into a more general question about pigmentation that could be answered. Check out the Help.

I can't explain the phenomenon, but have experienced it to a lesser extent as well. And I studied dermatology. I thought it was impossible. Clearly it's not.

Do you get any new medications in that time?

There have been more questions on exactly this phenomenon on this site. Unfortunately it's off topic as said by others.


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Why hand washing causes skin to dry?
This seems counter intuitive: dry hands mean low humidity, so why when humidity is increased, by washing hands, they become even more dry, eventually?
In particular, why such hand dryness is usually observed in a dry climate?

What did you find when you googled the question? What is it about the answer (which you should summarize in your post) that confuses you? Do you understand the role of oils in skin health and hydration?

I washed my clothes in India using clothes powder. my hands were peeling after 2-3 months. i used moisturising lotion. they were fixed.

@Christiaan. I disagree and think the question is relevant here.I  think a biological  answer about membranes, body oils, skin characteristics etc.  would be a  useful response

I will assume the hand washing you speak of involves soap.
The human skin (which also covers hands) is a complex organ with an underlying system of glands.
One of these is the exocrine sebaceous gland which is responsible for the production of a substance known as sebum. This substance is primarily composed of triglycerides, wax esters and other fatty acids. Sebum makes human skin waterproof as it's constituents are not water soluble (oily).

The action of soap on oily substances typically involves increasing their solubility in water so that they can be easily rinsed upon being dissolved. So when one washes their hands with soap they remove the oil layer secreted by the glands under their skin.
Removing the oil layer makes the skin susceptible to drying up as oil reduces the rate of evaporation of water on the skin to maintain a moisture balance. This is the reason why most brands of lotion have a moisturizing effect (or marketing statement).

Good that you mentioned lack of oil,  but to really answer the OP's  question, I think you need to extend your answer to discuss WHY lack of sebaceous oils leads to skin drying out

The temperature of the water can also affect skin dryness. Hotter water increases solubility of oils, and in turn contributes to dryness.


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Does anybody know which plant (or tree) is this?

Thus one has teased me a lot. This is just a small plantlet, the actual one went about 5 feet in height before we had to cut it. Whenever we cut it, it grew back within weeks. And soon small plantlets grew near it in a radius of about 3 meters. Today, we called 2 men to take off its root. They dug a hole about a foot deep and discovered that its roots had spread all across our garden. All the people we asked gave us different speculations of what plant it could be, but nobody was sure. Does anyone here know about it?
Data:

It has lots of thorns, even in its roots!
This plant is about 25 cm in length.
Its leaves are about 4 mm long and 1 mm wide.
A compound leaf is about 1.5 cm long.

Location: Northern plains region, India

Does it have branched thorns?

It seems to me a Fabales from the Genus Mimosa (https://en.m.wikipedia.org/wiki/Mimosa), maybe Mimosa hostilis

@Chris doesn't look like it. Though it has some thorn-like structure around the thorn, which is probably its covering.

Yes, you're right, Mimosa is from South America...

I just saw the correct answer, it's a Mimoseae... At the end, I was not that wrong.

It looks like albizia julibrissin

The plant scientific name is Prosopis juliflora. It is widely found in our country (India) which is a major problem because of its impact in agricultural land. It can withstand any harsh climate also.
Initially it was introduced to our country around 1950s to be used as firewood under drought situations. But later it became a major threat, since it absorbs as much as water (approx 4 litres of water to produce 1 kg of biomass) from the soil which spoils the cultivable land and also this plant grows very fast and spreads easily as weed which also causes a major problem to the underground water table.
The government also realised its mistake later, but still this is found in most of the places in our country, particularly in the southern part of India.
You can find further details from the below links:

https://www.hort.purdue.edu/newcrop/duke_energy/Prosopis_juliflora.html
http://www.cabi.org/isc/datasheet/43942

Nice answer +1 can you add some more details along with a picture so that I can select it as both correct and complete?

Is it the common thorn tree that plagues our cricket playgrounds? The bane and final purgatory of cricket balls.

it looks similar to an acacia.

@sundar Yes it is.

This plant, Mesquite, is a major invasive species in several regions in South America, here in Brazil it's widespread and competes with native plants, often causing the local exctiction of some native plants due to this competition. That's an attestation on how dangerous it is to introduce alien species in ecosystems. In Rio there's a natural reserve, the biggest in the city, it's called White rock state park (The Pedra Branca State Park), that has been basically destroyed by anthropic interference and introduction of foreign species in the environment, the park has a myriad of non-native species of plants, including Bananas and Coconut/Palm trees, all native from Asia, and animals such as dogs and squirrels. And of course Human. The Ecosystem has been heavily affected and unbalanced, many native species of plants and animals have disappeared from the region due to the competition with the foreign species, this particular plant is widespread. The water fountains that provide the main water body of the region, a huge river that supplies fresh water for the human populations of the city, have decreased significantly due to the human interferece in the environment, and deviation of the water springs' natural course. This ecosystem is a heavily damaged secondary succession case.
Most part of the atlantic coast of South America is comprised of the biome called [Atlantic forest][1], which is very rich in wildlife, the city of Rio is almost entirely comprised of the Atlantic forest biome, however a huge part of it has been destroyed by either deforestation for human occupation, or indirectly through the introduction of foreign species in the environment, that has created a huge instability in the ecosystem, many native species, such as the Jaguar, have gone extinct locally in Rio already. (See: WWF's report of endagered biome)
This map shows the location of the park, it's the biggest in the city and as can be seen it's near the rivers that supply water to the population.

can you add some references to your answer and potentially another picture for comparison? thanks for your efforts.

The answer does not contain any scientific name, so it is not clear to me that you are telling about same plant of previous answer (Prosopis juliflora) or some-other different plant?

Vance L Albaugh Of course I can! I have edited the post providing some resources, but it says I need more reputation to post more than one link in this post so I can't put more for now.

Always Confused I'm indeed talking about this plant, it's widespread in this protected natural reserve, however I'm simply offering my personal experiece with the topic of this plant and other invasive species since I'm living in this city, I'm just adding something to the topic of this question that I though could be a good contribution to this topic, ecological succession caused by the introduction of foreign species to a biome


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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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Phenol Red Broth question; what is point of broth without carbohydrate?
Without carbohydrate in the broth (some) bacteria would then degrade the peptone, which from its end products would increase pH and then turn zhe phenol red pink. So I think this is some type of control just to make sure the test parameters can produce a pink broth. Is there something more here that I'm missing though? The question is asking what function phenol red broth without carbs serves, and that's only thing I can think of. Is this correct or is there something else that is more relevant?

Indicators in media are usually used to monitor the degradation of the media due to growth. If the pH falls too much, living conditions are much worse to the point that the cells will die. So this is more a quick check.


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What is the energy consumption of an insect quantified?
Allegedly humans have an average power consumption of 97.2 watts, but what about something smaller like a housefly or an ant? What is their energy consumption measured in watt?


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Basic question about symbiosis( or about kinds of symbiosis)
Is there a type of symbiosis where an organism is harmed and the other is neither harmed nor helped?
If not, do you think there's a term for this sort of relation between two organisms?

Related: http://biology.stackexchange.com/questions/53975/is-apparent-competition-a-suitable-term-in-situations-where-one-species-is-not-n

Related: answer to "how to determine the relationship of competition or cooperation"

I see that there exists some confusion over the meaning of Symbiosis itself [in reference to the comments and answer(s)].
Your question/ query seeking information about "some type of Symbiosis" that harms one organism without affecting the other in any form is very much legitimate.
Amensalism (as responded by Sanjukta) is indeed the answer, but saying that "No. There seems to be no intimate association (symbiosis) that does not benefit any partner" is suggesting that Amensalism is not Symbiosis (which is not true).
Amensalism is one of the types of symbiotic associations only (Symbiosis is nothing but 'Living Together' of two / more organisms - which may or may not benefit/ harm either or both or none of the parties involved in the association).
Point to be taken is that, Symbiotic relation refers to the members of two different species (i.e., two populations) engaging in interaction and the interaction can be of any type (Amensalism is just another Symbiotic association).
Edit:
If one looks into the Etymology of the word, Symbiosis, he/she should be able to decipher the meaning of Symbiosis:

One may support the argument using latest updation of Encyclopedia of Evolutionary Biology (Amensalism=Symbiosis) and the classical example of Walnut tree (which tends to kill or inhibit the growth of shrubs that grow around its roots) may be cited. Their growth is inhibited,  but their niche still remains the same. More importantly, the Honeybee - wasp relationship (a long term one) is best fit for Symbiotic Ammensalism.
So, Mutualism, Commensalism, Amensalism, are all Symbiotic Relations.
References:
Miami College of Arts and Sciences, Department of Biotechnology Lecture Notes
Wiki Link about Biological Interactions

The books I've been referring to do not include Amensalism as a symbiosis. Symbiosis is not a synonym of biological interaction. It is an association,often phrased 'intimate association' between two species(something that doesn't exist between amensals). Book.

Hi Sanjukta,
I just added the Etymology of Symbiosis, hope that helps in clearing the doubt...

Yes it is so. But amensals do not live together.

This reference is from the latest updation of Encyclopedia of Evolutionary Biology (http://www.sciencedirect.com/science/article/pii/B978012800049600189X) and the classical example of Walnut tree (which tends to kill or inhibit the growth of shrubs that grow around its roots) may be cited. Their growth is inhibited,  but their niche still remains the same. More importantly, the Honeybee - wasp relationship (a long term one) is best fit for Symbiotic Ammensalism.
But I very well acknowledge the point you are trying to put forth. I guess, it's a clash of two different schools of thoughts..

Is there a type of symbiosis where an organism is harmed and the other is neither harmed nor helped?

No. There seems to be no intimate association (symbiosis) that does not benefit any partner.

If not, do you think there's a term for this sort of relation between two organisms?

Yes, Amensalism is the  biological interaction you are talking about in which one organism inflicts harm to another organism without any loss or benefit to itself.

A clear case of amensalism is where sheep or cattle trample grass. The presence of the grass causes negligible detrimental effects to the animal's hoof but the grass suffers from being crushed.

For more read wikiedia.

And good to add that strictly speaking, it's not exactly a symbiosis

@BioGeo Yeah. It'll add it to the answer.

@BioGeo It seems there is huge etymological mess up with the terms Symbiosis and Mutualism.  My textbook, Concepts of Ecology/ EJ Kormody / 4th edn; uses the term Symbiosis to include all-sorts interspecific biological interaction. That even includes predation! (Chapter 11, page No. 233).

@AlwaysConfused Yes, indeed. But when I was taught ecology, things were simpler... :)

@AlwaysConfused To be honest, symbiosis etymology means living together. Depending on the perspective, we could take it as mutualism or as all kinds of interactions... But maybe if one dies in that interaction, there is not really "living" together... hehe

@BioGeo Exactly. And What we've taught as "mutualism" or "mutualistic-symbiosis"  at my college and university classes; the same thing was taught in the name "symbiosis" at school level and old-books. It seems to me the original meaning of "symbiosis" is what is now  called mutualism; but later-on the usage got changed.


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Normal TSH Levels in Hyperthyroxinemia
When it comes to hyperthyroxinemia, how is it possible for TSH to be normal when there is an elevated thyroxine concentration? What I know so far is that it is caused by a mutation in the Human serum albumin (P02768)that carries normally around 10% of the thyroxine.The mutation apparently makes it have a higher affinity for thyroxine, but how does it allow the TSH levels to remain normal?

bound thyroxine in the plasma is different from the "free" thyroxine in the plasma - it is for the most part the free T3/T4 that is able to feedback to regulate TSH secretion

Since you're asking about hyperthyroxinemia with normal TSH serum levels, I suppose you're talking about euthyroid hyperthyroxinemia.
In euthyroid hyperthyroxinemia, the serum T4 and T3 concentrations are increased, but the TSH concentration remains normal. Besides that, there are normally no clinical signs.
The cause of that increase, as you explain in your own question, is a mutation in a transporter protein (like TBG), or an increase in their concentrations (which can happen in patients with hepatocarcinoma, for instance).
However, the free T4 concentration remains the same, and that is the important value for the negative feedback mechanism that regulates the concentration of TSH:

The euthyroid status of subjects with FDH has been
  confirmed by normal TSH response to TRH, normal free T4 concentration
  measured by equilibrium dialysis using appropriate buffer systems, normal T4
  production rate and normal serum sex hormone-binding globulin concentration.

Thus, without an increase in free T4 levels, there will be no drop in the TSH concentration.
Source: Impaired Sensitivity to Thyroid Hormone: Defects of Transport, Metabolism and Action.

Differential diagnoses of hyperthyroxinaemia with non-suppressed TSH levels include secondary or tertiary hyperthyroidism (e.g. due to TSH-secreting pituitary adenoma, resistance to thyroid hormone or paraneoplastic TRH production, respectively, all of them being very rare) and transient activation of the feedback loop in situations of type 2 thyroid allostasis1. In the context mentioned by you, elevated concentrations of T4 are most likely caused by increased plasma protein binding (which leaves free T4 normal)2.

Chatzitomaris A, Hoermann R, Midgley JE, Hering S, Urban A, Dietrich B, Abood A, Klein HH and Dietrich JW (2017) Thyroid Allostasis–Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming. Front. Endocrinol. 8:163. PMID 28775711 doi 10.3389/fendo.2017.00163
Bianchi R, Iervasi G, Pilo A, Vitek F, Ferdeghini M, Cazzuola F, Giraudi G. Role of serum carrier proteins in the peripheral metabolism and tissue distribution of thyroid hormones in familial dysalbuminemic hyperthyroxinemia and congenital elevation of thyroxine-binding globulin. J Clin Invest. 1987 Aug;80(2):522-34. PMID 3112186.


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How often does pre-mRNA processing lead to midstream off-frame errors in eukaryotic mRNAs?
As I understand it, the splicing of introns from pre-mRNAs is not incredibly precise. I've only ever seen nucleotide position ranges given in any description of the involved processes. Since there is quite a bit of looping of pre-mRNAs during processing and given that involved proteins often have effects well downstream from where they bind, this intuitively makes sense.
However, this would be incredibly problematic if true. Most pre-mRNAs are more intron than they are exon. While the precise base offset for the bases padding the start and end of an mRNA are irrelevant due to the start and stop codons, the precise offset for cut locations is very important for any splicing between the start and stop codons. If the splicing of introns regularly lead to cuts that are 1 or 2 bases off (in addition to 0 or more whole codons that have been accidentally removed), then all eukaryotic cells should have lots of (junk) mature mRNAs that have the proper reading frame at their 5' ends but off frame codons at the 3' end or just for stretches in the middle.
Specifically, if pre-mRNA processing has mostly random cut locations in its splicing, I would expect only ${^1/_3}^{rd}$ of mRNAs to retain the reading frame of their parent genes from from start to poly-A. In turn, that would mean only about ${^1/_3}^{rd}$ of synthesized proteins have the proper primary structure. There's no way eukaryotes function with that much kludge running through them.

"the splicing of introns from pre-mRNAs is not incredibly precise.".. Why would you suppose so? Do you have any reference to support this? AFAIK, splicing is decently precise in cases where precision is needed (when there is no alternate splicing involved). However, there can be such frameshifts but since they are not detected with decent coverage in RNAseq experiments, we can assume that such missplicing events are not significantly frequent.

As noted in the comment above, our understanding is that splicing is generally quite precise. Keep in mind also that if you do get a splice error, you have a very high probability of introducing a premature stop codon, which, among other things, will mean that the rest of the mRNA is not translated and is likely to be degraded.


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Are Sloth tongues soft or rough?
Are Sloth tongues soft or rough?
Dogs have soft tongues, while cats have rough tongues, so the feeling when they lick e.g. a human hand is quite different. So what about sloths?
This question came up in a recent discussion but I was unable to find any materials as google queries for sloth tongues leads to tons of cute pictures.

Cats have hairs like structures called papillae on the upper surface of tongue that's why they are rough. The same could be for sloths if they have any.

Sloths have long, thick, sticky tongues covered in a carpet of tiny, rear-ward pointing spikes that they can pull leaves in with.
So the tongues are quite different from human tongues and likely much less "soft" to touch and more "rough".
According to scanning electron microscopy studies on the topography of a sloth's tongue, the following results were found:

The results revealed that the rostral part of the tongue presents a
  round apex and covered by filiform and fungiform lingual papillae and
  a ventral smooth surface.


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Is it fair to say that the majority of alleles of a typical diploid organism are homologous at each locus?
I'm trying to get an overview of when zygosity actually comes to bear in regard to the entire genome, the following statement represents my understanding so far...

In a typical diploid organism, most of the genes/alleles on each locus are identical/homologous (say in the order of 95-99%) with the corresponding gene/allele on the other chromosome.
  When compared to the overall genome, it is only on a relatively small number of genes/alleles where the degree of similarity of the alleles for a trait becomes an issue.

So in other words would it be fair to say that, for a typical diploid organism, most of the genes on each chromosome are identical to their counterpart, it is only on a relatively small number where differences occur. e.g. most of the genes/alleles in a pea plant are the same and the resulting traits can be easily predicted. It is only a relatively small number of genes e.g. the genes responsible for flower color in a pea plant, or eye color in humans that the issue of zygosity, and using statistical techniques like Punnet squares etc comes play?

Please cite some evidence that supports your assertion. SNPs are incredibly common and widespread, so that would seem to rule out your hypothesis right away, as any two alleles would not have 100% nucleotide identity.

@MattDMo thanks, its of course possible my statement was wrong, it was not something I had derived from a credible source I could site it was my intuitive "guess" at the role zygosity played in the larger overall context of the genome. Something that has been omitted from any biology lessons I have studied. It wouldn't surprise me that the answer to my question is there is alot more going on and its more complicated than can be explained in a single statement


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why a testosterone pill can't be effective?
Why estrogen, progesterone etc. in the contraceptive pills survive the acid environment of the stomach and all the digestive enzymes, while testosterone needs to be injected or spread with a gel on skin?
I have no idea of why this difference in assumption, because I know testosterone and "feminine" hormones have the same steroid based structure...so I can't pick up why testosterone differently from "feminine" hormones can't resist the digestion.

Testosterone can be administered orally as undecanoate ester (brand name Andriol). The big challenge of oral steroid hormones is not the acid degradation, but liver first pass metabolism. (Which is mitigated by adding alkyl group at the alpha-17 position, or use of fatty acid ester; see for instance ethinylestradiol, levonorgestrel, or estradiol valerate)

so why the testosterone pill is very rarely prescribed? It is proved that the female pill with the chemically modified hormones is effective. So why the testosterone pill is not considered enough effective in the oral form so that It is rarely prescribed.

Probably depends on where you live, it isn't rarely described here in the Netherlands, although transdermal gels are winning terrain. I think an argument from a pharmacological point of view would be the varying bioavailability of oral testosterone undecanoate.

As stated in the comments by Eliane B., testosterone can actually be administered orally when an undecanoate ester is attached. The reason regular testosterone cannot be adminstered orally is because it undergoes extensive first pass metabolism (oxidation of the 17b-hydroxyl group to a 17-keto group, catalyzed by 17b-hydroxysteroid dehydrogenase enzymes, which are active in the liver). The undecanoate ester makes the substance lipophilic enough to be transported by the lymphatic system to the circulation after absorption by the intestines. Without the ester it will first reach the liver via the portal vein, thus exposing it to first pass metabolism. Nevertheless, bioavailability of oral testosterone undecanoate is estimated to be less than 10% [1].
Besides that, there are also derivates of testosterone which have a high oral bioavailability. These derivates have an alpha-oriented alkyl group, usually methyl, at position C-17, which retards hepatic metabolism. However, this can lead to hepatotoxicity [2].

https://www.ncbi.nlm.nih.gov/pubmed/3770015 (note, the subjects were women, but in the literature it is assumed that similiar bioavailability is obtained in men)
https://www.ncbi.nlm.nih.gov/pubmed/27372877


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Which contributes more to cancer clearance, T cells or NK cells?
Both T cells and NK cells have cytotoxicity. However, most immunotherapy targets T cells rather than NK cells, such as CAR T and PD-1 inhibitor. Is it because T cells kills more cancer cells than NK cells?

Note that clinicaltrials.gov lists 628 trials under "NK cancer", so even though there are more T cell trials, it's not as if NK cells are ignored; and there are more ways to manipulate T cells than NK cells, which probably explains the greater number of trials.

T and NK cells have different functions, and respond to different signals for activation - for example, NKs lack CD3 and the entire TCR complex. They are both vital for anti-tumor immunity. T cells are unable to become activated by cells lacking MHC-1/peptide complexes, which can happen in some tumors, so in that case NKs are indispensable. The Wikipedia article on NK cells is pretty good, I'd suggest reading it if you haven't already.


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Why must bacteria outrun diffusion?
In 'E.coil in Motion' Howard Berg says that

'If it [a cell] is to go far enough to find out whether life is
  getting better or worse, it must outrun diffusion.'

I am confused about the exact meaning of this expression and can't seem to find an explanation. What is meant by 'life is getting better or worse' and why can't a cell just wait for things to come to it by diffusion?

Because then it wouldn't be going anywhere, and the first part of the sentence is specifically about traveling.
Without more context that might make me wrong, I think the statement is intentionally tautological and is just meant to set up a problem to solve.
By "better or worse" I think the author means to generalize about conditions that an organism may prefer: nutrient concentrations, temperatures, etc.
Restated, I think the author is roughly saying "For cells to spend more time where conditions are best for them, they have to move on their own power."


text:
Do blood vessel walls have blood vessels in them?
If so, do those blood vessels have no walls because they don't need them because they're in the same tissue as that of a blood vessel wall? Are the cells alligned diffently at the edge of the blood vessel than in the rest of the blood vessel wall? Do blood vessels in blood vessels have an outer wall defined a sudden change in orientation of the cells?

This question is not very clear. The oxygen just diffuses into the cells of the blood vessels. What is confusing?

I just answered your title's question and the first question in your post. I confess that I didn't get your second and third questions.

Do blood vessel walls have blood vessels in them?

Yes, they do: the vasa vasorum.
When a blood vessel is too large, like the aorta or the cava, it has vessels to supply blood to their outer layers (where the cells are too far away from the lumen), not only to the Tunica adventitia (if by wall in your question you mean only that most external layer), as you can see in this image:

(note: this image is from a quiz in McGraw-Hill site, and the legend is not correct, "intima" and "media" are swapped)
Those vessels inside vessels are thus called vasa vasorum, which in Latin means exactly this: a vessel ("vasa") of a vessel ("vasorum"). You can read more about them in this Wikipedia page.

If so, do those blood vessels have no walls because they don't need them because they're in the same tissue as that of a blood vessel wall?

No, they do have their own walls. Despite being inside another vessel, the vasa vasorum have the same basic structure of any other vessel with their same width.
Therefore, vasa vasorum vary in size, from vessels with single or multiple smooth muscle layer(s) to simple endothelial channels.
Interestingly, vasa vasorum are normally found next to nerves and lymphatics (see the image above). This close structural relationships "provide evidence that adventitial vasa, nerves, and lymphatics provide arteries and veins with nutrition, neurohumoral input, and an effective pathway to remove waste products from the parent vessel" (Williams and Heistad, 1996).
(source: Williams, J.K. and Heistad, D.D. (1996) "Structure and function of vasa vasorum", Trends in Cardiovascular Medicine, 6(2), pp. 53–57).


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Is it possible a cancer cell don't express any foreign antigens?
For example, there're tumor suppressor genes. Can we just delete them, without introducing neo-antigens? Would the resultant cells proliferate? If so, how do our immune system identify such cells?

This question is far too broad, as explaining the mechanism of immune surveillance and how it applies to cancer is much too large of a subject to explain here.

Many tumor suppressor genes have that function because they prevent mutations, repair DNA or kill the cell if it is "too far gone." If you knockout these genes, you will inevitably get mutations. As the cancer grows, there is a selective pressure which will favor cells that have beneficial mutations, likely in coding regions. These mutations will lead to the production of neo-antigens, which can be recognized by the immune system.
So, basically, I don't think it's likely that there would be a cancer without any neo-antigens whatsoever. That doesn't mean, however, that the immune system will adequately respond to the neo-antigens.


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On which DNA strand is TATA box present?
My book (Snustard and Simmons) mentions that TATA box is present on the non-coding DNA strand but that was for the promoter of mouse thymidine kinase gene.
I have tried to find out more information and stumbled upon these in wikipedia articles which actually said something else:

The TATA box can be an AT-rich sequence "located at a fixed distance upstream of the transcription start site. (from a paper "The RNA Polymerase II Core Promoter'')

Then (from a book: Understanding bioinformatics),

The Transcription start site is the location where transcription starts at the 5'-end of a gene sequence.

So my question is, on which strand is TATA box actually (or generally) present?

TATA box is a feature of organisms that have dsDNA as a genetic material. Like most dsDNA promoter elements, TATA box is basically a section of dsDNA.
However a question like "On which DNA strand is TATA box present?" depends on what you define TATA-box as.
If you go by this definition:

In molecular biology, the TATA box (also called the Goldberg-Hogness
  box)[2] is a DNA sequence (cis-regulatory element) found in the
  promoter region of genes in archaea and eukaryotes

then TATA-box is merely a DNA sequence and is just a representation of a ssDNA region. However, TATA-box is also the binding site for TBP (TATA-binding protein; part of the TFIID complex). While the recognition of DNA elements by the TFs is effectuated by the interaction of amino acid residues with DNA bases and backbone on  one or both the strands, the TF binding and its activity has a stereochemistry.
Likewise, TBP also interacts with bases as well as the sugar-phosphate backbone on both the strands (Juo et al., 1996; PDB:1TGH).

Figure 2. Stereo pair drawings of the human TBP/DNA complex, with TBP at right and the sharply bent C-G-T-A-T-A-T-A-T-A-C-G duplex at left. (a) Molscript skeletal drawing (Kraulis, 1991). TBP residues that interact with the floor of the minor groove are shown in red with one-letter amino acid codes, and residues that interact with the sugar/phosphate backbone are shown in green. The coding strand of DNA is dark blue, and the non-coding strand is light blue. The two yellow-green base-pairs at bottom are the T1-A2 step that is kinked by interstitial phenylalanine residues, while the equivalent kinked step at T7-A8 is marked in orange. (b) Secondary structure diagram, with a-helices as coils and b-sheet strands as flat ribbon arrows pointing along N-to-C chain direction. Color coding as in (a).

Considering this, you can say that TATA-box is essentially a dsDNA region.
However, another twist in the story is that TBP can also activate genes with TATA-less promoters (Kamenova et al., 2014) and this is possibly facilitated by other protein partners of TBP in TFIID complex.

Our results are consistent with the model that sequence-specific
  TBP-DNA contacts are not important at yeast TATA-less genes and
  suggest that other general transcription factors or coactivator
  subunits are responsible for recognition of TATA-less promoters. Our
  results also explain why yeast TBP derivatives defective for TATA
  binding appear defective in activated transcription.

This, still does not contradict with the fact that TATA-promoters need TBP and the binding is on both the strands.
So, my conclusion is that TATA-box is a dsDNA element but has a polarity in its mode of action.

It's probably too late, but that's what I found in a book:
''Also, by convention, the DNA regulatory sequence elements (TATA box, etc) are described in the 5′ to 3′ direction and as being on the coding strand.''
Reference: Harper’s Illustrated Biochemistry, twenty-sixth edition,  Chapter 37 RNA SYNTHESIS, PROCESSING, & MODIFICATION, page 345, Figure 37–5.

Its never too late to answer a question ;)


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Do all polygenic traits involve epistasis?
Consider the following statement

All polygenic traits involve epistasis.

I think its true because polygenic traits involve several genes interacting together to result in a certain phenotype and if one of these genes is altered, the resulting phenotype is different.

Eh, I guess you could talk like that? But I think it'd be unusual and confusing. One thing is that in quantitative genetics, you don't usually talk about eg. a "gene for being x feet tall"; you only talk about a "gene for being x feet tallER" (than you would be otherwise, with the competing allele). If you talk like that, then only if the latter acted non-additively with other loci would you say there was epistasis.

eg. Suppose that in your population A's are always a foot taller than a's; and that there are also other genes affecting height. In this case, for the trait of being "1 foot taller" there isn't epistasis; for the trait of being "5 feet tall" there is. Quantitative geneticists generally talk in terms of the former.

This is a sort of weird question, because it is so vague, but it is still important because quantitative genetics seems incapable of giving a coherent answer even for people with PhDs.
The idea of "additivity", for instance, is a statistical rather than biological concept. It was first applied to quantitative genetics by Fisher in his 1918 paper, and it comes down to a neat trick developed for predicting the phenotypic correlations between relatives (what we would now call "heritability"). Fisher showed that if you assume that genes are roughly additive/independent in their contributions to traits, that makes the math much simpler for calculating heritabilities. He goes on to argue that the approximation works ok as long as you let the number of genes tend to infinity.
More recent research, notably by Peter Visscher and co, suggests that the additive approximation is in fact pretty good for all measured human traits for which there is data. So, this would argue against a big role of epistasis.
The problem with all this is that there is no reference to biology whatsoever. Anything that happens in a cell is governed by interactions, e.g. epistasis. When two proteins work in the same pathway, their genes have an epistatic relationship. So, anything that happens in a cell is entirely dependent on epistasis. In fact, in highly controlled experiments where you can directly measure the epistatic component by measuring all possible genotypes, you generally find that epistasis is a really important component of variation, because additivity is just a best guess at the sum of all epistasis effects in a sample population.
Visscher and co have argued back that while all this epistasis stuff could be interesting, Occam's razor means that additivity is probably good enough for the purposes of quantitative genetics. Yet more recent work has suggested that you in fact improve predictions a bit if you consider pairwise epistasis, so it's very much an active field of research.
In summary: this is a question that sort of depends on where you fall on the experimentalist-to-statistician continuum, with the experimentalists saying it's all epistasis because look at their data showing epistasis, and the statisticians saying that additivity is probably ok on its own because look at the quality of the predictions. Epistasis is important if you care about things that happen inside of cells and organisms but not so much if you just care about easy phenotypic predictions.

A polygenic trait is a phenotypic trait for which the variance in the population is explained by two or more loci. Epistasis is a case there is a statistical interaction between several loci on the value of a phenotypic trait.
The several loci underlying a polygenic trait might be purely additive (no interaction) and therefore a polygenic trait does not necessarily involve epistasis.


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Usage of the terms: Enhancer, Upstream activating sequence and Downstream activating sequence
From wikipedia

An upstream activating sequence or upstream activation sequence (UAS) is a cis-acting regulatory sequence. It is distinct from the promoter and increases the expression of a neighbouring gene.

Again,

In genetics, an enhancer is a short (50-1500 bp) region of DNA that can be bound by proteins (activators) to increase the likelihood that transcription of a particular gene will occur.

I find no difference between them, are they synonymous ?

Due to its essential role in activating transcription, the upstream activating sequence is often considered to be analogous to the function of the enhancer in multicellular eukaryotes.

There appears to exist another kind of regulatory sequence, downstream activating element.I think it's another synonym for enhancer located downstream the transcription start site.


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Is brain plasticity such that we can train ourself to see with our ears?
I am finishing writing some code which will parse a photo (eventually video) and use all the RGB information to synthesize an audio representation. I am wondering whether a typical person has sufficient neural plasticity to learn how to listen to this audio to understand an image in a general sense? I am not looking for perfection.  If the person has good vision they would do well to spend time listening to such synthesized audio while simultaneously viewing reality to give some training to enhance their interpretative abilities.  Once trained they could augment or supplant vision with its sonic equivalent.

How plastic is our audio-visual brain? Is there hope this will work ?

PS.  Once working I will update this Q

For those wondering about the details :  I am traversing the image using a Hilbert Curve which tends to preserve spacial relations amongst pixels to minimize re-training upon change to pixel resolution.  This flattens the 2D photo into a 1D line sprinkled across from left to right with points storing respective pixel values (at a 1st approximation I collapse RGB into grayscale 0.21 R + 0.72 G + 0.07 B)
... to create the audio representation I visit each pixel position on this line and introduce an audio frequency oscillator per pixel at a unique frequency such that the beginning pixel at far left is given the lowest frequency in our range (say 200 hertz) on upward until the oscillator frequency at the far right pixel renders the highest frequency (say 10 khz) ... the grayscale value drives the volume of that pixel's oscillator
... further details at:  isomorphism between video and audio
                https://www.youtube.com/watch?v=DuiryHHTrjU
Beauty of this approach is it lends itself to performing this transformation in reverse (a bijection) - from audio to video we can use a Fourier analysis ( FFT ) of audio mapped into pixels - then back again to audio, rinse and repeat ...

Please send in some sounds for the mapped images!!!

Short answer
Yes, we can see with our ears.
Background
Bach-y-Rita famously stated "We see with our brains, not our eyes". Bach-y-Rita worked for decades on sensory substitution. Sensory substitution approaches in general aim to replace for a lost sense by redirecting information normally captured by that sense to another still functional one.
Bach-y-Rita focused on substituting vision by tactile information. His Tactile Vision Substitution System (TVSS) captured camera images and translated them to tactile images projected onto the back of blind subjects. His decades of research eventually culminated in the commercially available BrainPort device (Stronks, 2016).
Vision-to-auditory substitution devices have also been developed, most notably the vOICe by Peter Meijer and the prosthesis-substituting-vision-by-audition (PSVA) device, among others. The vOICe translates images into sounds by re-mapping their x-axis into the time domain, and their y-axis into the frequency domain (Meijer, 1992). This “image-sweepline” technique has subsequently been deployed in the EyeMusic device for use in sensory substitution (Abboud et al., 2014). The PSVA makes use of a pixel-by-pixel acoustic frequency transformation,where vertical position is coded as pitch and horizontal position as binaural intensity and phase differences, and brightness into loudness (Capelle et al., 1998).
Peter Meijer refers to the vOICe as generating 'soundscapes', much like the approach you are describing. I seriously encourage you to contact him, he is a very nice guy and open to exchange.
Anyway, to come to your question - can we see with our ears? Yes we can. Several studies have indicated that sounds can successfully be used to perform visual tasks, including localization (De Volder et al., 1999), pattern recognition (Arno et al.,2001a, 2001b) and depth-perception (Renier and DeVolder, 2010).
Several studies have shown that the visually deprived brain is capable of re-routing auditory sensations into visual equivalents by re-routing this information to the de-afferented visual cortex in the blind (reviewed in, e.g., Poirier et al., 2007). This is referred to as cross-modal plasticity of the brain.
However, the learning curve is quite steep, in that a lot of practice is needed to obtain useful information from visual information coded through sound (Stronks et al, 2015). Further, what is probably the biggest issue in analyzing soundscapes is visual clutter. While the visual system is very well capable of filtering out image clutter and extract the useful information, soundscapes will inevitably turn every irrelevant object in the scene into a corresponding sound. Front-end visual processing techniques are likely to be key to turning an auditory visual substitution device into a practically feasible device for the blind, or the sighted for that matter.
The visual cortex is recruited for auditory tasks in the blind, but not in the sighted. However, I am inclined to believe it is practice, and not visual deprivation per se, that determines the performance with sensory substitution approaches in general (Stronks et al, 2015).
References
- Abboud et al., Rest Neurol Neurosci (2014); 32: 247–57
- Arno et al., Neuroimage (2001a); 13(4): 632–45
- Arno et al., App Cog Psych (2001b); 15(5): 509–19
- Capelle et al., IEEE Trans Biomed Eng (1998); 45(10): 1279 - 93
- De Volder et al., Brain Res (1999); 826(1): 128–34
- Meijer, IEEE Trans Biomed Eng (1992); 39: 112–21
- Poirier et al., Neurosci Biobehav Rev (2007); 31(7): 1064–70
- Renier and De Volder, J Integr Neurosci (2010); 4(4): 489
- Stronks et al., Brain Res (2015); 1624: 140–52
- Stronks et al., Expert Rev Med Dev (2016); 13(10): 919-31

If a lot of practice is needed to obtain useful information, than the learning curve is quite shallow, rather than steep (that increase in learning doesn't happen until you've moved a long ways along the x axis and put a great deal of practice in). But this is a wonderful answer on a very interesting subject all the same :)

@DeNovo yes the meaning of a steep learning curve is often used as it is used here, but honestly I've always wondered why it is used often in the sense that 'much learning is needed'. I'll think of improving my answer. Thanks

I would like to add to the great answer by AliceD with my own experiment.  I wish to add this because the results, while intellectually natural, were intuitively fascinating, and because my sample size is tiny (read: N=1), and I'd love to have others go out and repeat the experiment.
I don't quite show that you can see with your ears, but I do think it shows that you can hear with your eyes.  (Or, more formally, we fuse our senses in a remarkable way)
The bill of materials is daunting:

Two spoons
Willing test subject

In my case, the subject was my girlfriend at the time.
It is known that we use spectral effects to determine the elevation angle of a sound.  Our ears and our shoulders are known to shape the sound, emphasizing some frequencies and muting others.  Of course, this process is impossible to do if you don't know what the sound was "originally."  If you don't know what the sound was as it reached you, you can't figure out how much the ears have colored it.
For this experiment I picked two spoons, and verbally described what I was going to do.  I was going to click the spoons in various places and have her reach for them.  I intentionally did not click the spoons together in this demonstration because I did not want her to get to hear the spoons until the experiment started.
I first asked her to close her eyes.  I clicked the spoons in various places, and she identified which direction she thought it came from.  She was reliably accurate in left/right direction, because she could hear the time delays between the sound hitting her left and right ear.  However, her elevation angle was rather random.  There did not appear to be any pattern at all to it.
Then I asked her to open her eyes, and do a very boring version of this experiment.  With her eyes open, she of course was able to point to the clicking spoons 100% of the time.  (This was actually the hardest part, because it seems absurd to the test subject.  They start to think it's a trick).
Then, I had her close her eyes again, and repeat the experiment.  The results?  She was dead on every time.  Didn't miss a single one, both azimuth and elevation.
So what do I claim happened?  When we started the experiment, she did not know the frequency spectra of the spoons clicking.  As such, she could not effectively back out what transform her ears and shoulders were applying, and could not figure out elevation angles.  She could make some guesses, as a human that has heard things clacking together, but that was insufficient to accomplish the task.
In the boring second phase, she could now fuse the information she got from her eyes in with that from her ears.  Now she could determine what angle the sound was coming from with her eyes, figure out what the transform of her ears/shoulders should be, and back out what the "true" sound of the spoons was.
In the third phase, she now knew the "true" sound of the spoons, so whenever soundwaves hit her ears, she could use that knowledge to figure out what transform her ears/shoulders must have been applying, and figure out angles.
I used this to argue that we can hear with our eyes, but it might be more effective to say that the brain doesn't pay as much attention to the division between the 5 senses as we do when we talk about our sensory experience.  As far as it is concerned, it's all simply neural stimuli.  It will fuse these into one coherent image, and that is what really matters.

+1, but the anecdotal report, while making an interesting read, is not too convincing as no one can verify your findings and their validity. Could you add sources of any kind?


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What is regulatory promoter?
I came across this term in University question paper.

What is the difference between core promoter and regulatory promoter?

I have googled (Web, Scholar and Books) it but couldn't find any information from any authentic source.

I don't understand this. Promoters are regulatory per se, so this doesn't male sense to me.

@Chris I don't know, may be it has something to do with Proximal and Distal promoters.I've edited the post with the question I found.


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Do squids or octopus suffer from myopia(hyperopia)? Do other vertebrates get myopia(hyperopia)?
Both vertebrates and cephalopods evolved very sophisticated camera-type eyes, and both are capable of focus. But it also pose a risk of inability of focusing, such as myopia in human. So is myopia a common problem of vertebrate eyes or just occurred in a few vertebrate species?
Cephalopods also have the ability of focusing, but they focus in a different way. They focus by changing the distance between lens and retina, instead of contracting the lens like human. So are cephalopod eyes more flexible and less prone to get myopia?


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How the size of ribosomes are calculated?
When I was studying microbiology, something didn't make sense to me. We all know ribosomes have two subunits; the large subunit and the small subunit. Such as for eukaryotic cells, the large subunit has 60 S (svedberg) and  small subunit has 40 S. When they combine with each other they are considered as 80 S. Why it is 80 S instead 100 S?

Because Svedberg is not a measure of weight, but it is a measure of a relative sedimentation after centrifugation.
"It is defined as the ratio of a particle's sedimentation velocity to the acceleration that is applied to it (causing the sedimentation)."
The high number of S are correlated to the shape of the particles as well.
https://en.wikipedia.org/wiki/Sedimentation_coefficient

@AhmetÖz If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered. If you have >= 15 reputation points, you may also upvote the answer if you wish. There is no obligation to do either.


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Why is reducing the amount of detail required to remember the location of an object in one's environment adaptively significant?
In Campbell's Biology Chapter 51, question 36 reads:

Which of the following shows the adaptive significance of cognitive mapping to animals that employ this type of learning?
A) It increases the ability to visually recognize landmarks.
B) Cognitive maps reduce the amount of detail required to remember the location of an object in the animal's environment.
C) Animals can locate essential locations in their environment, such as nests, hazards, and feeding areas.
D) Animals can outmaneuver predators by planning and memorizing getaway routes.
E) Animals can determine their position relative to landmarks by a triangulation process.
Answer: B

I answered by saying that Cognitive Mapping is especially important because animals can locate locations essential to its survival (e.g. nests, hazards, and feeding areas), but the answer was B. Why is that more important?

Hi and welcome. The question you ask here should be self contained. I edited the question; if you don't think it's helpful, please feel free to roll back.


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How does hydration affect digestion?
My textbook( biochemistry by Satyanarayana, 4th edition pg.no:166) says:

The polysaccharides get hydrated during heating which is essential for their efficient digestion.

(I think there is a typo , heating should be replaced with eating)
How does water add into polysaccharides? Am I right if I say it is by hydrogen bonding? It also says  that efficiency increases, is it so because the substance is now more diffused so that enzymes act on an effectively larger surface area(making colloidal solution)? Or if the added(hydrated) water plays some role in interaction between enzyme and polysaccharide?

That's not a typo. The author is talking about cooking polysaccharides (gelatinisation), which in fact increases the digestibility:

Gelatinization refers to the irreversible loss of the crystalline regions in starch granules that occur upon heating in the presence of water. The temperature range during which the crystalline structure of the starch granule is lost is dependent on the water content, and on the type of starch. The gelatinization dramatically increases the availability of starch for digestion by amylolytic enzymes. (emphases mine)

Source: FAO: Effects of Food Processing on Dietary Carbohydrates.
You can read more about it in this Wikipedia page.


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Correlation between genetic distance and birth defects
It is folk knowledge that in-breeding causes birth defects due to similarity of genetics between parents. Consequently, is there a similar correlation between genetic distance of parents and probability of birth defects?
The best reference I can find of this is this handout by the Australian Centre for Genetics Education which says:

If parents are unrelated, their chance of having a child with a birth
  defect or disability is between 2% and 3%.
If parents are first cousins, the chance is a little higher at 5% to
  6%. This is due to the increased chance that they will both carry the
  same autosomal recessive mutation, passed down through the family.

However this doesn't talk about genetic distance in particular.
This question is really just a more specific version focused on a single metric (genetic distance) and outcome (birth defects) of two previously answered questions:

Genetic pros or consequences of children born to parents of mixed nationalities?
Does it make sense to classify all humans in a single species?

Are you looking for any evidence of the effect of inbreeding on fitness? Are you specifically interested in humans? What is your goal? Are you trying to estimate something specific such as the number of lethal equivalents of inbreeding for example, or are you just looking for any reference showing evidence of inbreeding depression to cite?

@Remi.b yes, I am specifically interested in humans, as per the tag. I'm looking for any evidence that can show a correlation between genetic distance and "inbreeding depression". Although, I must admit I had not heard of the term "inbreeding depression" until now and am embarrassed by this.

It depends how much the source populations share the same defects. If chinese and euro villages parents both had high prevalence of clubfoot, they would have worse outcome than close source parents. ... besides, an Italian village of 400 people genetics was studied because they have the lowest heart problem percentage in europe. They found that nearly all the village was inbred from 2 ancestors. they were all similar and healthy. Secondly, another study found that cousins breeding is about as troubled as late motherhood at the age of 38 onwards, i.e. having one after 38 is as good as a cuzin.

For humans the closest argument may come from observational studies (since experiments aren't possible due to ethical reasons).
One example for the correlation of genetic distance and "defects" comes from a recent study of Chagnon et al. PNAS, 2017 http://www.pnas.org/content/114/13/E2590.full . Rather than asking for birth defects directly they however survey the number of children, and survival of children to age 15 (which would be one example of the term "inbreeding depression" that is more general than "birth defects")
Note that their study also sheds some light on the underlying big question, why certain types of kin relationships can be common despite their effect on the creation of healthy offspring - and why certain types of cousin relations are different from others.

I was hoping to extend the level of observation to an even larger dataset/population. Is there reasons why this dataset wouldn't exist?

Suggestions, if want to look for large dataset: check Danish statistics, as Denmark has good records for several generations and is thus a model system for population-wide studies of health (note: kin relations will be unusual - nowadays). Since question relates to a phenomenon that isn't that exciting to contemporary research, but would seem to fit the 20ies-60ies, and large scale studies tend to get many citations: Look for old reference in the paper mentioned above. Search for reference in google scholar, select citing paper with most citations -> look at oldest reference --> iterate

Legit. Currently don't have the motivation to make the time to do that, but that's my problem.

ad larger dataset/population: Being able to observe something within a small population makes an even stronger argument than something that is only seen in large populations (since it effect size must be relatively large)


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Why is mutation rate high in introns?
Principle of genetics mentions

The fact that introns accumulate new mutations much more rapidly than exons indicates that many of the specific nucleotide-pair sequences of introns,excluding the ends, are not very important.

Though 'are not very important' is not true as introns do have a number of functions (both discovered and undiscovered).
But why is DNA polymerase less efficient at replicating introns? Is it known?

Note it doesn't say polymerase is less efficient; rather that mutations accumulate. This could be because of things other than different rates of new mutation creation.

Some introns might contain functional parts is very different from all introns are functional. The web site you linked is no proof. Indeed, it seems to be written by someone supporting the intelligent design hypothesis for the human genome (which of course, IMO, is wrong). So it is an opinion-based site containing also some information about biological facts. I would stick to more neutral references including standard Biology books.

"Accumulates" is the key term, the mutation rate is not higher, mutations are just less likely to be removed, which makes sense if the area is non-functional, most of the mutation will have no effect thus are unaffected by selection.

Is there any evidence that the mutation rate is higher in introns than exons? Isn't it the fixation rate that is higher in introns than in exons?

Not less efficient, but introns are under less selective pressure than exons. Exons actually encode the protein. A single bp insertion will ruin a mRNA encoding a protein by causing a frame shift in how the sequence is read.
However the same is not true for introns. 1bp insertion even if the intron has function such as transcription or translation factor regulation has a higher chance of not damaging anything important. Simply because such factors are spaced apart and the space is not really important.
http://www.nature.com/scitable/topicpage/rna-splicing-introns-exons-and-spliceosome-12375
https://www.ncbi.nlm.nih.gov/pubmed/17570818

This is not completely true. Insertions in introns also cause frame shifts which may render splice acceptor sites non-functional. This also affects the protein coding sequence.

Only the very terminal ends of an intron are involve in splicing and the branch point can tolerate fair amount of change as long as the 'A' branching point is unchanged. So only a few bp of an intron in constrain by splicing requirements. And given that mammalian intron are large, most of the intron is just space.

@JayCkat It would be great if you can add some references.

@JayCkat It is OP's job to clarify the question but is there any evidence that the mutation rate is higher in introns than exons? Your answer seem to rather tackle the question "why is fixation rate higher in introns than in exons?" and not "why is mutation rate higher in introns than in exons?"

If you ask the question "Do intron have a higher replication error than exons during DNA replication", the answer is maybe. Longer answer is DNA polymerase have difficulty accurately replicating nucleotide repeats (mono, di, tri). Such repeats are more likely to appear in Introns compared to exons. These repeats do expend and shrink during DNA replication, independent of homologous recombination. However accurate sequencing of such repeats is difficult, so in vivo occurrence is next to impossible to verify. Only real solution is to wait for minion seq tech to mature.

One paper after this question was asked indicates that it might be both stronger purifying selection in exons and a higher basal mutation rate in introns, likely due to the different accessibility of the DNA.
You are correct that introns play an important role in regulation (perhaps both timing and overall expression, in addition to the presence of enhancers and the potential for alternative splicing that affect the actual protein produced).

It is OP's job to clarify the question but is there any evidence that the mutation rate is higher in introns than exons? Your answer seem to rather tackle the question "why is fixation rate higher in introns than in exons?" and not "why is mutation rate higher in introns than in exons?"

Please see the first linked paper (someone else chose the link location, and maybe I should change this). The other answer addresses fixation rate and it's well established so I didn't link anything about that. Perhaps you meant to add this comment to that thread?


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Does protein consist of repeating units of amino acids?
I am currently studying the chapter called macromolecule. I get that a nucleic acid consists of repeating units of nucleotides, and I personally think "the repeating units" does not mean the nucleotdes are all the same, as nitrogen bases have four types either in DNA or RNA. How about the protein molecule. A protein molecule is made up of amino acids. However, I am sure about whether a protein molecule are made up of same and repeating units of amino acids. Theoretically, the R group in each protein is differed from one another. Therefore, does that mean we cannot state that a protein molecule is made up of repeating units of amino acids?

They are repeating units in the sense that all of the units are amino acids. The R group is different in different amino acids (it is not just different theoretically). The different R groups contribute to the different shape, structure, function of proteins, and if all were the same, then we would have a very limited range of proteins.You will still say it is composed of repeating units, since all units are amino acids, and there are no foreign groups between them.
Similarly, all repeating units of DNA/RNA are nucleotides, even if they aren't the same nucleotides.

Proteins are composed of repeated units of aminoacids with different R groups.
CO-CH(R1)-NH - CO-CH(R2)-NH - CO-CH(R3)-NH -
See how the aminoacid backbone is repeated again and again even if the R groups attached to that backbone is different.

Proteins are heteropolymers of amino acids. Many Amino acids are joined together by peptide bond. During peptide bond formation C terminal of former amino acid & N terminal of successive amino acid join  , that's why proteins always start with the N terminal and end with C terminal.
4 Amino acids are shown in the section. This order repeats itself many times.
The image shown above is only a primary structure. Functional  and structural proteins can never exist in this form.In reality a protein coils around itself or attains a fixed shape due to intermolecular and intermolecular  interactions ; like the Beta pleated sheath in fibroin(silk protein) is due to hydrogen bonding.