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What is the minimum air pressure the human body can tolerate if oxygen supply is not an issue?
Disregarding hypoxia, what is the minimum air pressure that the human body can tolerate?
(i.e. at what air pressure would the blood start to boil, or skin start to burst, or whatever else might happen that would kill you but isn't related to oxygen?)

Can you separate lack of oxygen from low pressure?

@kmm: I don't see why not. Just because there's not enough oxygen reaching the brain doesn't mean your blood would start boiling or your skin would start bursting...

I think one cannot really separate the lack of oxygen from air pressure. Because the inside pressure balance the outside pressure, if the pressure is low outside, one cannot inhale lots of air without lung injury. Similarly, a scuba diver always inhale air at the pressure associated with its depth. (In consequence divers absorb much more oxygen (and consume more air) in deep water than in shallow water). You may eventually separate air pressure from oxygen if you consider someone who put a single arm or leg in a artificially very low pressure environment.

@Remi.b: I don't see what's so hard about separating the two. Let me reword the question for you. Let's pretend the human body did not need oxygen/respiration at all, i.e. whatever you breathed in was exactly equal to whatever was breathed out (with no O2 or CO2 or anything else added or removed). What would be the minimum pressure it could survive in in that case? (If you're saying this has never been measured because, perhaps, it is impossible to measure, then please post that as an answer.)

You might be interested to know what happen to our body in a vacuum. It does not tell you "the minimum pressure under which we can survive if we were to assume we don't need oxygen" but it might give you some sense of what you're looking for.

@Remi.b: Thanks for the link, that's very enlightening -- definitely not what I expected! I guess for the purposes of my question, we can consider the minimum air pressure for a longer term (say, a few hours), not just for a few seconds. (Still reading the link.)

Last link seems to have broken; new link is this.

The lowest pressure a human can survive is time dependant. https://www.scientificamerican.com/article/survival-in-space-unprotected-possible
Up to 15 seconds before loss of consciousness and a minute or more before death. Can’t post an answer here as I don’t have enough reputation

@Slarty: I think for this question I was looking for pressures that allow survival indefinitely, not merely for a few seconds or minutes. Still, good to know, thanks!

@user541686 I suspect that you may be right, but indefinitely is a long time and I doubt very much that anyone could survive at the Armstrong limit for a very long period.

@Slarty: Yeah, quite possible. I just don't have better information unfortunately.

Disregarding hypoxia, the lowest atmospheric pressure the human body can withstand is around 6 percent sea level pressure, or 61.8 millibars, below that pressure the water and blood in your body starts to boil. Harry George Armstrong, a physician, and an airman, was the first to recognise this limit, which on Earth occurs at an altitude of roughly 63,000 feet, beyond which humans absolutely cannot survive in an unpressurised environment. The limit was named in his honour and so is called the Armstrong Limit. The lowest atmospheric pressure humans can breathe in, with a pure oxygen supply on hand, is roughly around 12.2 percent sea level air pressure or 121.7 millibars, the pressure found at 49,000 feet. Or, as a slightly madder alternative example, in a terraforming Mars situation, which might arise one day; a fit person could in theory walk around outside without a spacesuit on, but breathing from an oxygen tank, only when the atmospheric pressure got above about 120 millibars, and hope to survive for long.

For reference the natural atmospheric pressure on Mars is around 6 millibars.

At sea level, where atmospheric pressure is 1 atm and oxygen is about 21% the partial pressure of oxygen is enough to saturate hemoglobin.
The lowest tolerable pressure of air is about 0.47 atm (475 millibars of atmospheric pressure) - recorded at 5950m altitude.
At about 0.35 atm (less than 356 millibars at around 8000m) life is impossible. Pulmonary and cerebral edema lead to death.
Source: Wikipedia, Effects of high altitude on humans

You've got at least one number wrong. The "Death zone" at Mt Everest is considered to start at about 8000 meters, and the pressure there is about 0.75 atm. See http://www.engineeringtoolbox.com/air-altitude-pressure-d_462.html

Just to clarify, I didn't mean that the "Death zone" altitude is the answer to the question, just that your altitude and pressure numbers don't match. Also, I couldn't find those numbers in the linked article.

@jarlemag In the article Death zone pressure was in milibars. I converted it to atm.

Sorry, my mistake. I mistook feet and meters in the table. There's still one mistake though: The lowest tolerable pressure (inhabited for two years) and 475 millibar figure is at the height of 5950 m. 5100 m is the height of the highest permanent settlement.

Humans can tolerate huge pressure changes with only a little oxygen  in their lungs and blood system . IE: deep sea divers that dive down hundreds of feet into a huge pressure zone with out air tanks  but just one big breath. Therefore,  we should  be able to live for a short while as well in the very low pressure area that is in the vacum of space. If placed in space suddenly, we would surely get the bends if we lived long enough. If still inside our damaged space craft the heated air would surely be sucked  out,  but the radiant heat of the mass of the whole area should still keep us warm enough for a short while. Outside the capsule in the direct radiation of the sun should not kill us suddenly either. Earth bond fire victims can tolerate over 70% damage and still live a short while. If forced outside into the shade of the damaged space craft, I believe it would be very cold but still very livable until we ran out of oxygen in our blood.  Therefore I think we should have time left to think and  do something physical to save ourselves from the very quick on set of asphyxiation before anything else takes it turn.  IE: like do something like reach for the pressurized oxygen mask hanging on the wall like they have in airliners. If possible then we should freeze to death suffering from the bends.

Add some references to your claim.


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What is the film that covers the tongue?
What is the film that covers the tongue in the mornings, even after brushing the teeth and tongue the night before and why does it have color variations?  Do the different colors mean anything?

You should see a dr. You could have thrush or something

It isn't really a film. The tiny bumps that cover your tongue are called papillae, and are normally pink in color. However, they can become inflamed and white when irritated. The appearance of the white "coating" is caused by debris, bacteria and dead cells getting lodged between the papillae.
You may be breathing through your mouth when you sleep, which is drying it out. Bacteria may also still be the cause; you may not be brushing well enough or your toothpaste may not be correctly doing its job.
The color variations may be due to different types or amounts of debris, or the color may vary with different conditions listed here. Tongue color changes also often occur with glossitis (inflammation of the tongue itself).

Great answer.  To follow up and highlight one thing in the list given, another possible cause is a yeast fungus called Candida albicans.  It's called "thrush" as buzrw mentioned. It's not very common in healthy people.  It's a normal yeast in the human body that can overgrow if the immune system is suppressed (systemically like AIDS or locally by improperly administered long-term steroid inhalers), sometimes with overuse of antibiotics, and in some other conditions.  It differs from other films by being unable to scrape off.  And it's usually painful.

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Why does rabies cause hydrophobia?
What feature of rabies pathophysiology causes hydrophobia? Why is hydrophobia unique to this one particular type of viral infection?

Related question

Hydrophobia and aerophobia occur as a consequence of involuntary, painful contraction of the diaphram and the accessory respiratory, laryngeal and pharyngeal muscles in response to swallowing liqiud or air.

Rabies causes hydrophobia in the encephalitic stage which means when it affects the brain and causes swelling and inflammation of multiple areas of the brain. Hence, it affects the complex areas in the brain needed for swallowing. Initially into the course of the disease, the patient has involuntary contractions of neck muscles when he drinks water.  At later stages of disease, the patient starts contracting his muscles even at the thought of water. Rabies virus is a neurotropic virus which means that it travels through nerves because of its preference to attach to acetylcholine receptors in the neurons.  That is how the virus spreads from the bite site to the brain(via the nerves).

Why hydrophobia specifically and consistently? Most diseases causing encephalitis or other pathology to the brain has very varied clinical spectra.

Yes why specifically

This is a good answer above but would like to let this question sit a little longer. What are the swallowing areas of the brain etc...

The swallowing areas of the brain are located in temporal cortex, pons and medulla oblongata

Explains problem swallowing, but hydrophobia?

It starts off with difficulty swallowing water, progressing on to fear of water just on mentioning it.  I guess it affects the center of the brain subserving fear.  Why fear to water specifically, I do not know the answer.  As a clinician, it doesn't bother me much because it has no therapeutic implications. It only serves to me as a marker to suspect rabies.  There are many things in medicine which haven't or cannot be explained by reasoning but have shown to be significantly(statistically) associated. But I appreciate your inquisitiveness.

The evolutionary "why" is that the virus spreads through bites, and drinking water or swallowing would decrease transmission. As for "how" the virus affects the brain so specifically, I have no idea and would like to know also.

No doubt, the selected answer is sufficient for the question. But for the ones more interested in citations, here is a more credible answer.
When the rabies virus attacks someone, it begins with muscle cells, so that it is not detected by the host's immune system. There, it binds to neurons at neuromuscular junction1. Rabies virus, being neurotropic, binds preferentially to neurons, specifically the acetylcholine receptors on neurons. After binding to neuromuscular junction, it uses retrograde transport to travel to the axon, as its P protein interacts with dynein in neurons. As soon as it reaches in neuron cell body, it rapidly reaches the central nervous system, where it replicates in motor neurons and quickly reaches the brain2. From here, it travels to peripheral and autonomic nervous system and then reaches the salivary glands3.
Now, lets come from the how part to the why part. Rabies virus gets accumulated in salivary glands of the host so that it can get transmitted further on to the next host. And, as one might expect, drinking water or other fluids can decrease the virus's ability to get transmitted4. To prevent this, the virus causes painful spasms in throat and larynx so that not only saliva production in host is greatly increased, but also drinking, or even thinking about drinking, causes excruciatingly painful spasms in throat. Since the muscular movements during drinking (or eating) are involuntary, and the virus has already infected autonomic nervous system and motor neurons, it is thus able to control involuntary muscle movements of throat and larynx in the host5.
References:

Gluska, Shani & Zahavi, Eitan Erez & Chein, Michael & Gradus, Tal & Bauer, Anja & Finke, Stefan & Perlson, Eran (August 28, 2014). "Rabies Virus Hijacks and Accelerates the p75NTR Retrograde Axonal Transport Machinery". PLOS Pathogens. doi:10.1371/journal.ppat.1004348.
Cotran RS, Kumar V, Fausto N (2005). Robbins and Cotran Pathologic Basis of Disease (7th ed.). Elsevier/Saunders. p. 1375
Baer, George (1991). The Natural History of Rabies. CRC Press. ISBN 9780849367601. Retrieved 31 October 2011.
"Symptoms of rabies". NHS.uk. June 12, 2012. Retrieved 3 September 2014.
"Rabies". AnimalsWeCare.com.

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Why is it that drinking caffeinated tea does not help one to stay awake?
I have never felt after drinking tea that I can have the power of being able to work late at night. Neither have I felt that it helps me to be awake while working or keeping eyes opened while I am not in mood for sleeping.
Drinking tea, then, does not helps me to stay awake.
Is it the nature of the tea itself, or does it have to do with how the body processes caffeine?

@jonsca, I would like if you edit it to make it more meaningful or more powerful.

I have given it a try, you can always modify it again if necessary.

Another idea I have come across is that caffeine absorption is much slower with tea, though my source is a Good Eats Episode.  The relevant information can be found at approximately 19 min.  Maybe it's true, maybe it's not, but regardless, it's a great episode to watch if you are into tea.

It could be tolerance if other caffeinated beverages are usually consumed, however it also depends on the type of tea itself, and other properties, such as how long the tea has steeped for.
For example, brewed black tea can have anywhere from 14-61 mg of caffeine, which is a large range and depends on which tea you are drinking specifically.  Whereas if you were drinking green tea that has not been steeped for long, it can have 24-40 mg of caffeine, which at the lower range will probably not help you stay awake.
From MayoClinic.Org:

The actual caffeine content of the same coffee drink can vary from day to day — even at the same coffee shop — because of various factors, such as roasting and grinding, as well as brewing time. The caffeine content of tea also is affected by how long it's brewed.

Caffeine beverage levels can be found here:
http://www.mayoclinic.org/healthy-living/nutrition-and-healthy-eating/in-depth/caffeine/art-20049372

What is happening to you is 'tolerance'. It is a term used in pharmacology. It is a phenomenon by which a drug/medicine becomes less effective the body gets used to it. One explanation is less receptors for that drug are manufactured because of negative feedback.  You may have developed tolerance to tea.

He said that he has never felt that tea has been helpful. Couldn't another explanation simply be that there's less caffeine in tea than coffee?

@jarlemag, thanks but even coffee is not helpful to stay awake. So can I say that my body is not consuming Tea or Coffee as they should affect to my body? I am not saying I am unnatural but many people complains if they drink Tea or Coffee they could not sleep easily but for me drinking them never helps.


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Why do oranges in the US have a small separate part?
Why do oranges in the US have a small separate detachable part at the tip which is separate from the other pods? It looks like a tiny orange itself and has a long fiber attached to it.

This is specific to navel oranges, which have a conjoined twin fruit.
This blog gives an account of this.


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How are oranges in the US or anywhere made seedless?
How are oranges in the US or anywhere made seedless? Please explain the broad principles and not the technicalities.

Neat question! No time to write up an answer now, but I'm sure someone will. In the meantime, see: http://www.scientificamerican.com/article/how-do-seedless-fruits-ar/

Related question: http://biology.stackexchange.com/questions/2124/why-cant-we-breed-watermelons-without-any-remaining-seeds-in-the-flesh

Oranges and other fruits are generally not actively made seedless. Rather, seeds may fail to develop due to either lack of fertilization (pollination) or a natural tendency. The natural production of unfertilized and thus seedless fruit is called Parthenocarpy.
To quote the Scientific American article (3) mentioned by Oreotrephes:

Fruit development normally begins when one or more egg cells in the
  ovular compartment of the flower are fertilized by sperm nuclei from
  pollen. In some plants, however, fruit develops without fertilization,
  a phenomenon known as parthenocarpy. Parthenocarpic fruit has
  advantages over seeded fruit: longer shelf life and greater consumer
  appeal.
The most frequent reasons for lack of seed development are pollination
  failure, or nonfunctional eggs or sperm. In many plants,
  self-incompatibility genes limit successful fertilization to
  cross-pollination between genetically different male and female
  parents. This property is exploited by citrus farmers who grow
  seedless fruits, such as navel oranges and clementines. Because these
  cultivars are self-incompatible, they fail to set seed when they are
  planted in orchards of identical plants (clones). These plants have a
  high frequency of parthenocarpy, however, so they still produce fruit.

Parthenocarpic varieties may arise from a lack of pollinators. From the Wikipedia page on Parthenocarpy:

Plants moved from one area of the world to another may not always be
  accompanied by their pollinating partner and the lack of pollinators
  has spurred human cultivation of parthenocarpic varieties. Some
  parthenocarpic varieties have been developed as genetically modified
  organisms.

To preserve the seedless trait, parthenocarpic trees can be propagated by grafting. It is possible that more kinds of seedless fruits will be engineered in the future (3):

Plant biologists have learned that if the plant hormone auxin is
  produced early in ovule development, parthenocarpic fruit can grow on
  plants that do not usually exhibit this property. Thus, genetic
  engineering will most likely give consumers parthenocarpic fruit in
  many other species in the near future.


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How does cold water help to overcome high fever?
Why cold water helps to overcome from high fever in body? As fever is inside the body and we're applying cold water over the body!

cold water helps lower body temperature

Fever is triggered when pyrogens cause release of prostaglandin that acts on hypothalamus (which is the center of thermoregulation).
Fever assists in the healing process by:

enhancing phagocytosis
decreasing negative effects of endotoxins
stimulates proliferation of lymphocytes

Although is a good reaction, when the temperature gets too high it could determine negative effects, like convulsions at children. Brain damage appears when the temperature rises as much as 42 degrees Celsius, and most febrile conditions go up to 40.6 degrees Celsius.
So fever must be kept under control, and cold water helps lowering body temperature. Lowering the temperature will prevent negative effects of fever. Cold water is a symptomatic treatment for fever. Most important is to determine cause of fever and do an ethiological treatment.
Source: Wikipedia contributors, "Fever," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Fever&oldid=614212619 (accessed June 27, 2014).

You missed the question a bit. The question not about why water is used; it is about how the water that is applied externally can regulate the internal temperature.

     As far as how the water cools the body it's simply a matter of physics. Water has a higher specific heat also called heat capacity than the air, clothes, or other matter that normally surrounds the body.       Specific heat refers to the amount of heat (keep in mind that heat is essentially the measure of the average movements of the molecules in a substance) per unit of mass it would take to raise it's temperature by 1 degree Celsius. Water is useful for temperature regulation because it takes so much energy for it to change temperatures. Metals tend to have low specific heats which is why we make frying pans out of metals like iron. They take less energy to become hot.      As systems naturally fall back to equilibrium, if the body is hotter than the water heat will be transferred from the body into the water until they are the same temperature which will be a lot closer to the temperature of the water (compared to the initial temp of the body) because changing the temperature of water 1 degree takes more heat energy than changing the same mass of human to change 1 degree in temperature.      While this primarily acts on the outer portions of the body, the process continues into the core of the body as now instead of having hot skin and cold water, you have hot muscles and cold skin, from there you have hot organs and cold muscles, and so on and so on.      I hope this is helpful! For more information on specific heat you can check out: http://hyperphysics.phy-astr.gsu.edu/hbase/thermo/spht.html


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Can human survive falling from 30,000 ft without a chute?
If someone falls 30,000 feet without a parachute; what are the chances of survival if they landed in the water?

There are alternatives to parachutes which would slow ones descent.

I don't think it matters that 5000 or 30000 feet... As you descend the air will become more and more dense which will slow you down... Afaik. it is survivable, with severe injuries.

Summary: A fall from "any height" may be survivable, depending on what you hit, but with an expectation of severe injuries. A water impact at terminal velocity will in all likelyhood result in immediate death.
The Serbian Flight attendant Vesna Vulović holds the Guiness World Record for surviving a fall without a parchute with an estimated fall height 10,160 metres. However, some doubts have been cast on the accuracy of the record, with claims that the fall was actually only several hundred meters. Vulovic was found partly in the wreckage of the plane, so it can be discussed whether she had a truly "free fall" for the purposes of this question. However, several other persons have been known to survive completely "free" falls from great heights. Although it is hard to verify the exact altitudes, the WW2 aviators Alan Magee, Nicholas Alkemade and Ivan Chisov are reported to have survived falls of about 6700 m, 5500 m and 7000 m, respectively.
The exact altitudes are in any case not necessarily of interest, as it can be assumed that all persons falling from a height of more than about 500 meters will reach terminal velocity, the velocity where air resistance prevents the fall speed from increasing, before hitting the ground. As such, above a certain height, other factors become determining for the survivability of a fall. As has been demonstrated by the listed examples, it is clearly possible to survive a fall at terminal velocity. However, this requires favorable conditions at the site of impact, and will likely result in severe injuries.
Due to the flat surface and the surface tension of water, it is hard to imagine an unprotected impact with water being survivable at terminal velocity. The best chances for survival will likely be in areas with foliage, snow and/or a hilly landscape allowing the kinetic energy to be dissipated through rolling downhill. Of the listed aviators above, Nicholas Alkemade appears to have been the least injured. About him, it is reported that

His fall was broken by pine trees and a soft snow cover on the ground.
  He was able to move his arms and legs and suffered only a sprained leg

To put it simply... NOT GOOD!!!

US Coast Guard rescue swimmers will not do a free fall deployment from above 200 ft (actually, I think it is less, I cannot remember right now) into water, this is too dangerous.

I personally think you'd be better off trying to find about fifteen feet of soft snow to land in! In reading trying to find additional information with which to answer this question, I stumbled upon someone who said they knew of a pilot in Vietnam who's 'chute didn't open when he ejected. He survived with "only" broken bones and a ruptured spleen. I have included a link that I hope is helpful!

https://physics.stackexchange.com/questions/9059/jumping-into-water

isnt falling into water safer compared to concrete-pavement ?

@BeyondProgrammer Sure, it is safer, but, it is still going to feel about like hitting a concrete block if you're coming from 30,000 feet!

@BeyondProgrammer It's surprisingly little difference.


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Why basement membrane thickens in diabetes mellitus?
Untreated diabetes mellitus may lead to blindness and kidney failure because the basement membrane of small blood vessels in these organs thickens due to increased production of collagen and laminin.
My questions : why are these organs most susceptible ? Why will collagen and laminin production increase in diabetes mellitus ?

The endothelial cells in small blood vessels take in more glucose (as glucose levels in blood are high due to diabetes.) Thus they form surface glycoproteins which causes the basement membrane to become thicker yet less strong. This leads to blood and protein leakage from the blood stream in other tissues in the space between cells. Blood leakage alters cellular blood supply for all cells.
Less blood means less oxygen and less nutrients. As you probably know nervous tissue gets damaged fastest without oxygen thus explaining diabetic neuropathy. Also retina and kidney contain cells that get easily damaged when there is not enough blood.
Probably the worst complication is neuropathy, because the person suffering from it may suffer a heart attack (caused by the accelerated process of atherosclerosis in diabetes) and feel less pain (http://medlineplus.gov).
Collagen and laminin poduction increases as a result of the fibrosis process that takes place when a tissue gets less nutrients than it needs.
Diabetes affects all blood vessels, even the larger ones. See macroangiopaty.
From http://en.wikipedia.org/wiki/Microangiopathy

Plasma glucose can react (non-enzymatically) with the side chains of some amino acids to form Advanced Glycation Endproducts (AGEs).  AGEs are pro-inflammtory and can cause signalling via specific receptors for AGE - the RAGE family.  This, in large part can drive OP's thickening. Do you have a reference for reduced pain in heart attacks ?

@playsdice Could you please elaborate it in the form of an answer ?

@biogirl - comments were to suggest tweaks to this answer.  You should also search 'complications of diabetes'.  Its a fascinating field.

@cornelius could u explain ur first statement ? increase insulin level leads to increase in uptake of glucose in cells. Instead of saying that cells take inglucose EVEN THOUGH insulin level is high u should say that because insulin level is high.

@biogirl insulin has nothing to do with the amount of glucose that endothelial cells take in. They simply take in glucose based on its concentration in blood.


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Degenerate primer design for DIG in situ hybridization
New to molecular and have learned to design primers from google/youtube so any info would help
Would someone be willing to share their protocol for degenerate primer design?
Breakdown:
Trying to design degenerate primers to amplify/clone specific GPCR genes from an unsequenced genome of a particular fish.
I'm using Ensembl and Genbank for sequences of closely related fish but the complete gene has only been sequenced in 2 other fish species.
I use ClustalOmega for alignment. Is it okay to just use 2 other species for generating degenerates?
1) are there any other good databases for gene sequences?

If the gene is supposed to be well conserved then you can use the sequence from the related species.
For protein coding genes target the ISH probe to the coding region which is more likely to be conserved.
What you can also do subsequently is to:

amplify the CDS
do 3' and 5' RACE
Clone in a plasmid (do a blunt end or TA cloning)
Sequence the insert
Design exact primers

are there any other good databases for gene sequences?

EMBL and DDBJ


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How is the transcription direction of RNA polymerase determined?
When transcription factors attach to the DNA strand - How do they know in which direction they have to initialize the transcription by rna polymerase? Is it always read in the same direction anyway? What about those 'promoters'? Do they influence the transcription direction?

Do you mean by direction which of the two DNA strands is transcribed? Or do you mean whether the polymerase goes from 5' to 3', or from 3' to 5' on a single strand?

@MadScientist Although the first question is also interesting, the second one is the one which I am interested in at the moment.

Transcription always proceeds in the direction 5' (5-prime) to 3' (3-prime) on the coding strand of DNA. Binding of both transcription factors and RNA polymerase to DNA depends on sequence motifs in the DNA. Transcription always happens in the same direction with respect to the chemical structure of the coding DNA strand, while the transcription direction with respect to the structure of the chromosome depends on which strand the coding sequence is found on (and thus which strand is defined as the coding strand for that gene).

Just to clarify, RNAP moves relative to the template strand from 3' to 5'. The transcript is polymerized from 5' to 3' and has the same sequence as the coding strand (except U instead of T).

Thanks, good point. The whole process is described, with figures, in an NCBI online book here: http://www.ncbi.nlm.nih.gov/books/NBK22085/

Glad to hear that. You can also communicate that an answer is useful by clicking the checkmark next to the answer, "accepting" it.

I don't think transcription always goes $5' \rightarrow 3'$ wrt to coding strand. See https://en.wikipedia.org/wiki/Promoter_%28genetics%29#Bidirectional_promoters_.28mammalian.29

In that instance there are two coding strands, so the transcription still goes the same way with respect to each coding strand.

What about in negative-sense ssRNA in viruses?

I think that during replication there was a subunit that ensured directionality, but I don't remember which. Maybe a similar situation occurs in transcription?

I think the more important thing to understand here is how these enzymes "know" what to do. I find it fascinating that the polymerase can actually move backward to perform error corrections. How do they know do do that? Is there some kind of biological software in an enzyme that tells them how to do these things?

user38945 "is right". Seriously: Any "promoter" is just a grain of sand in the strand, it's true that there are - right or left, from "that" promoter  - some nucleotides that define "its" direction, i.e. its directing.  (With my maths, two of them would suffice (as Polymerase is one trick pony, does from '3 to '5, always does it.))


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What nutrients do I lose in the water when I boil vegetables?
What nutrients do I lose in the water when I boil vegetables. Has to be some water-soluble and heat labile ones right? Which ones?

Vitamin C and the B complex vitamins are water soluble.   Thiamine and folate are also heat labile.
Overall there are hundreds or often thousands of kinds of small molecules (not protein or DNA) in the cell and many of them are water soluble or heat labile.  Plants especially have many unusual small molecules.  Its not known how many of them affect human health, but may affect factors like the gut microbiome quite a bit and have an effect on well being if not mortality.
Some people think that live uncooked vegetables have enzymes and other proteins which are good for you since cooked proteins are denatured and may be taken in differently.  At the very least they are probably easier to digest when they are not heat denatured.

Why would non-denatured proteins be easier to digest? Got any links on that?

I could site a couple of papers, but it would still need some explaining because its common sense.  thoroughly cooked protein is a lot like a fried egg - its a solid.  The same can be said for cooking a prep of tissue or bacteria - the protein tends to aggregate.  As such, proteases or even acid can't diffuse as readily into the matrix of glop as well as through a solution of soluable protein.

Interesting. But then, why do we prefer to eat protein-rich food, such as meat and eggs, cooked? Any idea?

Jarlemag Why do you want to eat Salmonella and E coli from uncooked meat and eggs

what @speedohack is saying is that meat rots quickly and cooking is more necessary when eating meat.  that's more a preference of appetite.  We eat protein when we can get it but our dietary requirements as adults are not as much as many people in industrialized nations eat.


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Which types of hydrogen bonds are known to exist in RNA secondary structures?
I'm programming an implementation of an algorithm for pattern matching in RNA structures.
The algorithm assumes the following types of base pairs:

Plain: No base pairs (just the primary structure of the RNA)
Single: Each base can be connected to at most one other base
Multiple: Each base can be maximally connected to a number of other bases (where 'number' can be constant or infinite)

Although there is no problem with the implementation of the above types of base pairs (apart from the probable high computation complexity), I wonder if all of them were observed in real RNAs?
In particular, I'm interested in the following cases:

A base pair between two adjacent bases i,j.
One base (i) which connected to two different bases (j,k) (i is not adjacent to j or/and k).
One base (i) which connected to more than two different bases, all of them not adjacent to i.

Can these exist? Some of them?
If they can, how common is their existence?

A base pair between two adjacent bases i,j.

It is not possible. To form an intramolecular hydrogen bond, the RNA has to bend. The persistence length i.e. the minimum length of the chain required for bending, is around 4 bases for ssRNA (I am not very sure about this number. At this moment I am not able to locate the exact reference. I remember this number from the back of my head which I heard somewhere).

One base (i) which connected to two different bases (j,k) (i is not adjacent to j or/and k).

It is definitely possible for one pair after considering the persistence length. If a single base is bound to more than two bases then atleast one interaction should have to form a non Watson-Crick type bonding, as indicated by Mad Scientist.

One base (i) which connected to more than two different bases, all of
  them not adjacent to i

Very less likely. There are no known reports. Even if it happens, the bond will be weak because of limitation in the number of H-bond donor/acceptor sites in the bases.

By far the most common type of base pair is the Watson-Crick base pair in an RNA helix. Those are comparably easy to predict, e.g. Mfold and the Vienna RNA package can do this.
Base triples, three nucleobases that form hydrogen bonds to each other are not uncommon in RNAs with a complex tertiary structure. There is even a database of RNA triples, though this one also contains triples where not all three bases make contact with each other.
There are also quadruplexes, but there each base only makes contact with two other bases. I don't know if there are any structures where one base makes contact with more than two other ones.


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Specifics of decussation
Beginner question here:
The definition of decussation I see is the crossing through the midline of a bunch of neurons.  But I was wondering if there was a little more to it than this, because I'm given the impression in readings that this is a somewhat difficult task to perform developmentally, like the body might have to take extra effort to regulate the crossing so that the neurons do not interfere.  So when nerves from both eyes cross, for example, do they pass AROUND each other or do the bundles of nerves all weave through each other?
Thanks in advance.

The optic nerve fibers cross inside the optic chiasm sharing the same shell:

The crossing fibers go ones between others, like on this classical picture -


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How to determine whether the energy of a stem-loop fold is significant or not?
If I have a predicted RNA stem-loop of energy -0.30 kcal/mol, and another of -4.9 kcal/mol, how do I tell whether such a structure is a significantly stable structure or not? Our two competing hypotheses are that there is some structure with sufficient energetic stability to fold inside a cell, versus the one that there is not.

A predicted stem loop of what? A nucleotide chain presumably, and most likely RNA but you need to tell us.

Yes, it is an RNA. Allow me to update the original question. Many apologies for being unclear.

probably the best way is to make it and see if the sequence forms a stem loop. there are lots of energy calculations based on 3d models and sequences if you'd like to know, but i'm not clear on what is best myself.

I don't know what you mean by significant. More negative the value of folding energy more is the stability. For better predictions you can use the salt correction formulae.

are you working on miRNA or tRNA or just other rnas?

@caseyr547: I am working on a substring of mRNA that is thought to fold independently of the other substring, because it is not complexed with other proteins.

@ericmjl ok my answer will work for you then and it will work well. I'm a published author on this topic.

You can convert the $\Delta G$ values into equilibrium constants $K$ using the formula
$$ \Delta G = R T \ln K $$
This might help you understand what those energies roughly mean.
But the more important and also more difficult part is judging how good your predicted free energies actually are. I assume you used a secondary structure prediction program like Mfold to calculate this. They typically have a several parameters you can adjust like ion concentrations and temperature, you should make sure that you have some appropriate values here.
Without knowing anything more about your system or data I'd ignore the -0.3 kcal/mole result, the -4.9 kcal/mole structure could be formed, but I wouldn't regard this as certain.
Now, in the in vivo situation the whole thing gets far more complicated. The presence of RNA binding proteins, helicases and the generally rather complex environment in the cell makes it much harder to predict which secondary structures will actually form.
If you wanted to know for sure you could e.g. do SHAPE experiments on your RNA. This is a technique that also works in vivo.

no thats too much work

RNA folding is definitely a lot of work if you are not an RNA molecule :)


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What is the nature of action potentials in autonomic nervous system?
My conjecture is that the natures of sympathetic and parasympathetic action potentials are different.
My findings propose me that

sympathetic action potential is little longer lasting than parasympathetic

there may be another mechanism in sympathetic action potential - some sort of plateau phase which does not exist in parasympathetic action potential
however, I have not managed to gather any convincing evidence on this claim

parasympathetic action potential has greater energy per one time instance, while the energy of sympathetic AP is distributed along wider time space

My hypothesis is that the energy of parasympathetic and sympathetic action potentials is equal.
This would suggest me that the action potentials of the autonomic nervous system are coming from the same source.
Their nature is just different.
What can this source be exactly?
I have read the recent Physiology and Pathophysiology books where this topic was not covered rigorously.
I did not manage to find any good publication about the topic, probably, I missed something.
What is the nature of autonomic nervous system action potentials?
You can select what ever condition you want and see if you can get some findings as I have got.

What makes you say the action potentials are different? From my knowledge APs are uniform across all nerves

See the energy spectrum of APs. You have to define uniform. They seem to have the same energy (uniform; thing which has confused people to think that they are uniform also in nature), but different energy spectrums.


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Do cell walls prevent cancer?
To my knowledge plants do not have an uncontrolled growth disease similar to cancer. Is the function by which they avoid uncontrolled growth related to their cell wall and preventing damage to DNA/RNA? Is their telomerase special in some way in that it does not indefinitely replicate?

Plants do have uncontrolled tumorous growth. Though in almost all known cases, it is pathogen induced; such as in the case of the bacterium- Agrobacterium tumefaciens. Viruses can also induce plant tumors. Theoretically, the cell wall will pose a mechanical barrier to cell division. Also, cell wall synthesis is an extra biochemical step during cell division. Surely, the presence of a cell wall will disallow any metastasis if it might occur. There is an old article which says that cell wall structure differs between the normal plant tissue and the crown galls (tumor). However, this is with respect to Agrobacterium adsorption sites.
I am not aware of any natural plant tumor or the role of telomerase in plant tumorigenesis. However, there is one paper that says that telomerase dysfunction leads to disorganized growth.


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Could humans theoretically see infrared better than regular light?
I have noticed that in infrared film, people's eyes reflect that light within their eyes much like nocturnal animals (and many other animals for that matter) do with regular light. I know that this is in order to maximize their night vision capabilities by reflecting more light onto the retina.
My question is this: If a human had the nerves in our eyes to process infrared light, would someone with these 'special' eyes be able to see better than someone with 'regular' eyes? What would they see? What about in low-light conditions?

...Infra-red illumination of the eye produces the 'bright pupil' effect

Source: http://www.museumsandtheweb.com/mw2003/papers/milekic/milekic.html
(most of the way down the page)

Although interesting, this question is quite philosophical. It is like asking what if we had an extra pair of hands- would it help us to work better and faster.
Infrared detection goggles are there and are used for seeing in dark. But as we have evolved we cannot differentiate objects just based on their heat signatures. So just infrared vision wont be good.

I was in the military for a bit. There was a guy I met who when the lights were turned off had eyes that glowed in the dark. It was like an animal at night. He showed this to me in confidence, we were alone, but didn’t say it was a secret or anything. He said he had a retinal or cornea transplant. I can’t remember what he said but I’m not sure if that was even the real story. I’m still not sure if a transplant would have that effect without the lining animals have called the tape firm lucid something.....

There are animals that can sense into the infrared spectrum and this seems to help them detect prey.

No, retina doesn't have or has too few infrared receptors.
Practical example: most remote controls use IR LEDs (infra red light emitting diodes) to send commands to a receiver device. So take a remote control, keep pressing a button and look at its front. Do you see any flashing light? Now take a camera (phone camera, photo camera or video camcorder) and look with it at the remote while pressing a button. Now you see it producing white light. The camera sensor detects IR. That is how night vision in cameras work.
What you read in that article is about how light is reflected by the eye (the pupil). There is nothing to do with the retina which is on the 'back wall' of the eye ball.

This just states that humans can't see IR, which we already know. I think the question was more along "If we could choose to see IR, would that be better than seeing regular light?"

Infrared light is emitted by warm things, like our head.  We'd be detecting it ambiantly all the time.  That's why animals that can detect infrared are not warm-blooded.

My eyes are not warm. Air does not reflect infrared light (you don't see an infrared aura around warm objects in infrared captures). Therefore, I could implant infrared sensors into my eyes without seeing myself all the time. And even if, the self-ambiance could still be subtracted out. And cold-blooded animals are not cold all the time, especially not after a sun bath.

Infrared is a very wide spectrum.  The long-wave infrared produced by animal body temperatures is a much different "color" than the near infrared which is part of normal sunlight - and which can be photographed with ordinary digital cameras by removing the IR blocking filter: https://en.wikipedia.org/wiki/Infrared_photography


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identification of species of tree
I just want to confirm the species of the tree in the middle of the picture. Is it the "Flame of the Forest"? This is taken in my school campus. Thanks in advance!

I would be good to be able to see the leaves in detail. This makes an identification easier.

This question appears to be off-topic because it is about plant identification. These questions are usually asked on Gardening and Landscaping Stack Exchange.  This topic is not found in the following appropriate topics listing in the Help center:                          1) General questions about biological concepts
2) Questions about the biological mechanisms behind medical conditions
3) Questions about techniques in a biological or biochemical laboratory

It looks like a Royal Poinciana tree with the scientific name Delonix regia..

Please refer to this link for more info

I actually should write it in comment, but I did to upload a few photos.
From the distant-photo of the tree, I couldn't understand clearly; however from a trace of vertical long patches (long hanging fruits?) it seems to be Delonix regia, but I'm not sure.
If you could upload some more close-up photos, focusing more features, it will help. In-fact Delonix is easily identifiable.
In-advanced I posted some photo, it will help to think-out how-to capture the  possible important features in photograph.

Flowers:

http://chalk.richmond.edu/flora-kaxil-kiuic/d/delonix_regia_MERIDA_06s.JPG
Flower is approx 8 to 10 cm wide. 1 petal (out-of 5) is different- colored from other, yellowish.  If the Tree is delonix, you'll obtain flower and petals scattered  beneath the tree.

http://www.kew.org/files/styles/content_featured/public/Delonix_regia_02_Fl_main_web_2015.jpg
The flowering season is normally late-spring to late-summer.
If it is Delonix regia, it would yield fruits like this:

https://txtriffidranch.files.wordpress.com/2014/06/orangebloom_62714_4.jpg
The fruits are pods (legume-fruits) , flat, big, could be 1 foot to more than a meter; 4 to 6 cm wide. Green and tough when young , but when ripen, become brown, very hard , woody and lose flexibility.
You'll find fallen fruits below the tree, entire fruit and splitted fruit both find. Splitted fruits look like this,
http://www.backyardnature.net/q/delonix.jpg
(and this is a good plaything for school-going kids and village kids)
Leaves:

http://static.memrise.com/uploads/things/images/18258191_130813_1724_38.jpg
The small leaf-like objects are leaflets of delonix. The single big thing is 1 leaf. The leaf is pinnately compound twice... i.e. bipinnate. with each step of fractal is paripinnate (even-pinnate). Look the pulvinus.

http://static.memrise.com/uploads/things/images/18258191_130813_1724_38.jpg
This is what several leaves look like.
phyllotaxy is alternate and spiral-type.

https://en.wikipedia.org/wiki/Delonix_regia

Are these match to your tree? If not, then bring me back to reality.


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identification of species of this bird
Hi I saw this bird near my school canteen in Singapore in Spring. Can anyone identify the species of this bird? Thanks in advance!

Can you add the geographic location where it was found and the time of year?

@kmm: Singapore, and recently, a few days ago.

I would say that it would be a subspecies of a raven or a crow but it is hard to identify seeing that the bird has been through a disease or met with an accident..

This question may be difficult, but it isn't too broad. In fact, I can't imagine a narrower question than "Which species is this animal?". I think that the question should be reopened.


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identification of this flower
I saw this flower in Pulau Ubin in Singapore. Can anyone identify the species of this flower?

Looks like some type of oleander.

It is indeed the Nerium oleander.. For more info refer to this link and also this


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How to maximize lung oxygen intake?
What method of breathing provides a sudden surge of oxygen into the lungs filling it as full as possible in volume and density. Deep breaths? Shallow breaths? Breaths taken while bent over? Deep inhales followed by further inhales. Breaths held? Movement while breaths are held?

@WYSIWYG can't we just talk about it from a scientific perspective in abstract? assuming ease and procedure are a non-issues. of all the variant methods which is the most optimal and what makes it so.

@WYSIWYG what about this question will it work?

Don't quite understand why this is an off-topic. Anyway, the deep inhales with full exhales are the most effective when it comes to lung ventilation. This is because you have a so called 'dead space' - about 150 ml of air in your pathways (mouth, trachea, etc). So if you inhale 200 ml, only 50 ml will get its way to alveoli which is 25%. If you breath in 600 ml, 600-150=450 of air will get to the lungs which is 75%.

@ctapobep. The question was explicitly about usage of inhalers, which as per the site's policy is off topic (medical advice). This edit seems to be fine and can be reopened.

I don't see any question seeking medical advice here

The safest way to maximize oxygen intake is to do it slowly over a period of weeks to months using breathing exercises and aerobic anaerobic exercise combination. This will increase the hemoglobin concentration of blood leading to increased oxygen carrying capacity as well as capillary density of the muscles ensuring good oxygen supply

You cannot change the oxygen concentration of inhaled air in the absence of an external source of oxygen. However, you can use your lungs at their maximum capacity doing this:

breathe deeply: =increase tidal volume. Your muscles will inflate your lungs as much as they are able to, inflating parts of the lungs that were not fully inflated (atelectases) in the process. This also allows you to inhale a volume much greater than your physiologic dead space (volume of inhalation that does not participate in gas exchanges)
breathe to high enough frequency: the faster you will want to expel $CO_2$ and replace it with room air, the higher frequency you will need to adopt.

Frequency and tidal volume are the two components of minute ventilation (= (frequency/minute) X tidal volume), which is the physiologic value you are working to increase.
Position: The upright position is best suited, since the weight of the lung tissue pulling downwards will facilitate inflation
WARNING: using those techniques unsupervised can cause acute respiratory alkalosis, which is unhealthy and puts you in immediate danger.

Actually, you are working to increase alveolar ventilation...


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identification of species of snake
Can anyone identify this colorful snake found at Pulau Ubin in Singapore?

It is the paradise tree snake (Chrysopelea paradisi). It is a colubrid snake and is common in south-east asia. See this site for a better image.

And great flying snake movies at http://www.flyingsnake.org/


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Why is post-vaccination fever for 4CMenB so frequent?
When considering the introduction of 4CMenB vaccine, the Joint Committee on Vaccination and Immunisation said:

The sub-committee noted that the clinical trials data suggest that
  when  4CMenB vaccine is given concomitantly with other routine
  childhood  immunisations a substantially increased frequency of
  vaccine-induced  fevers should be expected. Vaccine-induced fever
  rates may be similar to  those associated with whole cell pertussis
  vaccine used in the past.

What is the likely explanation for the higher rate of fever for 4CMenB in comparison with other vaccines?


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fibrinogens and fibrins - are they the same molecule?
Some proteins are "activated", like fibrinogens; they are turned into fibrins by thrombins, and then the fibrins can aid in blood clotting.
Are fibrinogens and fibrins the same molecule, just in different states? If so, are all "-ogen" ending proteins and their activated forms the same as well?
If they are different molecules, why do us even bother to convert a protein into anotherto work, instead of simply activating a protein?

You could say they are the same molecule, but a molecule whose function is to change its state and properties very quickly when activated by thrombin.
Fibrinogen is a soluble protein - a complex of six protein chains.
Thrombin is an enzyme called a protease which very specifically cuts the ends off of two of those protein chains.
Once those bits are removed from Fibrinogen, the resulting molecule creates fibers very quickly to form clots.
You could also say that fibrin is a different molecule than fibrin because it really consists of many fibrinogen fragments.


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How to increase the rate of absorption and assimilation of food?
i was reading this
and want to know
excerpt from the above linkThus, the time for food to travel from one end to the other probably ranges from about 20 to 30 hours
I believe it's 24 hours for a normal person going for poop every morning, But I was curoius if anybody could increase the rate of absorption making my digestive and defacaeting system better performing.

The rate of absorption is controlled by two essential physical factors:

Contact surface between intestinal content and intestinal mucosa.
Time of contact.

There are many other factors including intestinal peristalsis, gastric, pancreatic and bile secretions that stimulate/help absorption.
So increasing or accelerating intestinal passage of food won't do any good (see diarrhea). Water will not be absorbed into the blood flow thus leading to dehydration and hypovolemia. Also the alimentary principles, vitamins, essential aminoacids won't be absorbed.
On the other hand, slowing down the passage has negative effects. It allows bacterial saprophytic flora to multiply so much that those microorganisms become pathogenic by producing toxins. And increased contact time equals increased absorption both of toxins and food principles.

OOps! i was totally wrong


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How to interpret the breeders equation?
The univariate breeders equation is defined as,
$\ R = h^2 s$
where $\ R $ is the response, $\ h^2 $ is the heritability (additive genetic variation), $\ s $ is the selection differential. The multivariate equation is similar to this in principle but includes a multiple trait variance-covariance matrix and multiple selection differentials.
Essentially the breeders equation tells us how strong the response to selection will be as a result of the additive genetic variance within a trait (and between traits in the multivariate) and the selection applied to that variation ($\ s = cov (w,x) $ = the covariance between fitness ($w$) and the trait $x$).
For example, in trait $x$, $s$ = 0.8 and $h^2$ = 0.5 the value of the response for $x$ is $R$ = 0.4. Compared to another trait, $y$, where $s$ = 0.8 and $h^2$ = 0.1 and thus $R$ = 0.08.
My question is, if we look at a trait in a population, measure it's population mean and define $h^2$ and $s$ values, can we then predict the change in the population? IE. can we predict (with the values of $s,  h^2$  and the population mean) what the mean population mean trait will be in the next generation directly from the result of the breeders equation? Does the value of $R$ give us anything of use?
Following from the example above, I examine a trait (wing length in chickens) and find the mean to be 24 cm. I select birds to start my next generation in a way that causes $s$ = 0.8. The additive genetic variance for the wing length is quite high, $h^2$ = 0.5. The predicted response is $R$ = 0.8 x 0.5 = 0.4. What does this tell me about the next generation?

The breeder's equation as you wrote it:
$$R = h^2S$$
The heritability that is the ratio of additive genetic variance over the total phenotypic variance is called the heritability in the narrow sense and is noted $h_N^2 = \frac{V_a}{V_P}$, where $V_A$ and $V_P$ are the additive genetic and phenotypic variance respectively. In contrast the heritability that consider the total genetic variance is called the heritability in the broad sense and is noted $h_B^2 = \frac{V_G}{V_P} = \frac{V_A + V_D}{V_P}$, where $V_G$ is the total genetic variance and is equal the sum of the additive genetic variance $V_A$ and the genetic dominance variance $V_D$. We can rewrite the breeder's equation using the standard notation for the heritability in the narrow sense:
$$R = h_N^2S$$
The so-called response to selection $R$ is the mean deviation of the trait in the next generation. In other words, $R$ is the difference between the mean trait of the parents and the mean trait of the offspring, So to answer your question, yes, the breeder's equation gives the value of the mean trait in the following generation. It does not give any information about the frequency and number of alleles though.
$S$ is the the mean trait of the individuals which reproduce weighted by their reproductive success minus the mean trait of the parents. In other words, it is
$$S=\frac{1}{\bar w}\sum_{i=1}^{\text{nb inds}}m_iw_i - \bar m$$
, where $m_i$ is the trait measurement and $w_i$ is the fitness of this individual, $\bar m$ is the mean trait of the parents and $\bar w$ is the mean fitness.
The mean trait of the parent generation does not appear in the breeder's equation but only their mean trait weighted by their reproductive success. In the standard case of truncated selection (common in artificial selection programs) all $w_i$ are equal and $S$ becomes the mean trait of the individuals that we allow to reproduce in the parent population. And it is exactly the same thing for the multivariate case except that the variance-covariance matrix should be taken into account.

@GriffinEvo Let me know if I answered your question or if I missed your point.

Following on from @Remi.b and @Ell :
z score = (x - μ)/ σ from https://ncalculators.com/statistics/z-score-calculator.htm
Z score (predicted response in standard deviations) = X - adult population mean / standard deviation of normal distribution
0.4 = (X) - 24 cm/ (1)  solve for X
X= 24.4 cm, which would be the expected value of the mean trait in the following generation.

See this example as well: https://math.stackexchange.com/questions/1318981/z-score-and-stats


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Source of information on the evolution of aging/senescence
Do you know a good review (published peer-reviewed or an online course or whatever) that offers a good overview of all hypothesis explaining the various patterns linked with aging?
I'd like this review to make the following things clear; antagonist pleiotropy, Gompertz and Weibull models and what theoretical explanations are underlying these models, mutation accumulation, reliability theory, eventually group selection, age-specific efficiency of natural selection, telomere length, the definition of senescence, and all not-cited hypothesis to explain the patterns of aging/senescence.

this is one paper which covers some of that - http://www.cosmoid.de/zajitschek/papers/Bonduriansky2008FunctionalEcology.pdf - you've asked for quite a lot of coverage there so I'll throw together a few papers tomorrow.

@Remi.b: Have you found the book?

I don't know about just one source that fits everything you've asked, so here's a custom bibliography to get you started instead.
General Sources
I first learned about biogerontology from the excellent series of introductory essays at João Pedro de Magalhães' website, senescence.info; I definitely recommend starting here.
A short book written by two experts, for Scientific American Publishers, is Finch and Ricklefs' Aging: A Natural History. "The" book on the Evolutionary Theory of Aging is Michael Rose's Evolutionary Biology of Aging. "The" book on comparative biogerontology is Finch's Longevity, Senescence, and the Genome. A "pop" account of recent research (esp. to do with caloric restriction and long-lived mutants, which have people excited right now, and the search for longevity drugs) is David Stipp's The Youth Pill. A constantly-updated-with-new-editions-reference is The Handbook of the Biology of Aging. In 2008 (just missing the 2009 rapamycin excitement), Cold Spring Harbor Press published a collection on Molecular Biology of Aging. The Gerontological Society of America has an e-textbook out, that I think is going to be updated on the regular, called Molecular and Cellular Biology of Aging.
The Definition and Measurement of Aging
Usually, people define senescence as an increase in "mortality" with age. Mortality roughly means vulnerability; the older you are, the easier it is to die. Mortality is measured/estimated demographically, in terms of (hypothetical or actual) cohort survivorship. There are two quantities usually used: one for discrete-time, and one for continuous-time. Where $N_x$ the number of survivors still alive in a cohort at age $x$,
$q_x = \frac{{N_x}-{N_{x+1}}}{N_x}$ discrete-time; The Age-Specific Probability of Death.
$\mu_x = -\frac{N^{'}_{x}}{N_x}$ instantaneous; The Force of Mortality.
The first one is the fraction, of those alive at age $x$, who will die before age $x+1$. This estimates the probability that an individual aged $x$ will die before age $x+1$. This is intuitive: to age means that an 80-year-old is less likely to make it to 81, than a 20-year-old is to make it to 21. Notice that $q_x$ is bounded between 0 and 1.
The second one is the instantaneous rate of death, normalized against cohort size at that instant (whereas the first was the number of deaths in an interval, normalized against cohort size at the beginning of the interval). It is the instantaneous, age-specific, per-capita death rate. It can be visualized as the slope of the survivorship curve, divided by its height, times -1 to make it positive. It is not a probability. It has a dimension of rate ("per-second", "per-hour", etc) and it has no upper bound.
This way of defining senescence is described in Nature Scitable's Aging and its Demographic Measurement (although the authors give an erroneous definition of the force of mortality). It is discussed and justified intuitively, and at length, in Peter Medawar's The Definition and Measurement of Senescence.
Sometimes, you might want to count a decline in fecundity as aging, too, even if mortality wasn't changing. Or, you might want to define senescence in terms of various kinds of physiological performance. This is really a matter of taste, I suppose, or of what kinds of question you're trying to answer. Ageing or Senescence is just the part of getting older which, on top of having more birthdays, is somehow or other "bad" for you.
But the most common criterion is that $q_x$ or $\mu_x$ grows with age.
Mainstream Evolutionary Theory of Aging:
The mainstream idea is that aging evolves because of the declining force of natural selection with age. Natural selection "cares less" about things that happen late in life, than about things that happen early in life.

Mutation Accumulation (MA): the theory proposed in Peter Medawar's An Unsolved Problem of Biology. (Theory that aging is due to genes that are silent or neutral in early life, and deleterious in late life.)
Antagonistic Pleiotropy (AP): the theory proposed in George C. Williams' Pleiotropy, Natural Selection, and the Evolution of Senescence. (Theory that aging is due to genes that are beneficial in early life, and deleterious late in life.)
Disposable Soma: Proposed by Thomas Kirkwood and Robin Holliday; sometimes considered a version of AP. (Theory that aging is due to a tradeoff, in turn possibly due to allocation of limited resources, between reproduction and maintenance; selection favours less than perfect maintenance. Can be considered a version of AP where the "early beneficial effect" is increased maintenance, and the "late deleterious effect" is decreased survival.)

Summarized in Nature Scitable's The Evolution of Aging. Note that both MA and AP could be partly true; both kinds of genes could exist.
Both MA and AP are commonly cited as predicting that higher extrinsic mortality should lead to the evolution of earlier / faster senescence; but things may be more complicated than this.
The Declining Force of Natural Selection: Hamilton's Formalization
Medawar's and Williams' insights were verbal. William Hamilton did the math, and showed that certain formal indicators of the strength of selection on a genetic effect, necessarily declined with the age at which that effect occurs. These indicators were I think: 1) the partial derivative of $r$ (the intrinsic rate of increase / malthusian parameter, which he took to be fitness) with respect to the force of mortality at age $x$; and 2) the partial derivative of $r$ with respect to fecundity at age $x$. (The first starts declining at the age of first reproduction; the second starts declining immediately.)
In passing, this also demonstrated that a remark R. A. Fisher had previously made, and which Medawar had accepted, was fallacious. Fisher and Medawar had assumed that the strength of natural selection was proportional to age-specific reproductive value; but since reproductive value can increase with age, and Hamilton's indicators can't, reproductive value can't be measuring the sensitivity of $r$.

Hamilton's paper: The Moulding of Senescence by Natural Selection.
Charlesworth summarizes Hamilton's results and puts them in context in Fisher, Medawar, Hamilton and the Evolution of Aging.
Charlesworth's book Evolution in Age-Structured Populations is supposed to be quite important and to have furthered and refined stuff in this area.
Apparently things might be a bit more complicated than this? Baudisch has claimed that although Hamilton's indicators must decrease with age, other indicators, which aren't obviously unreasonable, can increase.

Gompertz, Weibull, and Gompertz-Makeham
The Gompertz equation is intended to describe how the Force of Mortality $\mu_x$ grows with age. The Gompertz equation was come up with empirically, not for any theoretical reason; it just seemed to Benjamin Gompertz to fit the data quite well, for a good stretch of adult lifespan. The same goes for the Weibull equation, as far as I know, and for the Gompertz-Makeham equation.

Gompertz is an exponential growth equation: $\mu_x = \mu_0 \cdot e^{Gx}$ (where $G$ is a parameter). It looks like a straight line when graphed on a semilog plot.
Weibull is a power growth equation: $\mu_x = A \cdot x^B$ (where $A$ and $B$ are parameters). It looks like a straight line when graphed on a log-log plot.
Gompertz-Makeham adds a constant to the Gompertz equation: $\mu_x = \mu_0 \cdot e^{Gx}+C$. This ruins the elegance of the semilog-graphing, alas; it doesn't look like a straight line.

Apparently some people have tried to show how eg. Gompertz can evolve in MA models, but the generality of this is questionable (see Box 2 in this Trends in Ecology and Evolution paper). Gavrilov and Gavrilova (proponents of the "reliability theory of aging", have said something about Gompertz and Weibull being special: ("Both the Gompertz and the Weibull failure laws have their fundamental explanation rooted in reliability theory... and are the only two theoretically possible limiting extreme value distributions for systems whose life spans are determined by the first failed component... In other words, as the system becomes more and more complex (contains more vital components, each being critical for survival), its life span distribution may asymptotically approach one of the only two theoretically possible limiting distributions—either Gompertz or Weibull (depending on the early kinetics of failure of system components).") I don't know what that means.
Gompertz is the most commonly cited / used equation, I think. It's supposed to be more accurate than Weibull. Gompertz-Makeham I guess is more accurate, but of course it would be - it has an extra adjustible parameter, which, if it isn't helping, you can just set to zero!
Sometimes these equations are erroneously presented in terms of $q_x$ instead of $\mu_x$. This is erroneous historically, but also because $q_x$ has an upper bound of 1 and couldn't possibly obey any of the equations, at least not indefinitely.
Sometimes people find it more intuitive to describe Gompertz' exponential growth in terms of how long it takes $\mu_x$ to double; in humans, this "Mortality Rate Doubling Time" is about eight years.
Note that the equation does not accurately describe early life; mortality often starts high in infants, before falling to its minimum, and then starting to grow again. Thus $\mu_0$ isn't the actual mortality rate at age 0, but the backwards-extrapolated mortality rate you would have had at age 0, if you were perfectly Gompertzian (or whatever).
It also may not describe very late life. A hot topic right now is "late-life mortality deceleration", where the exponential growth seems to slow down such that Gompertz overpredicts mortality in the very old; whether this is so, and why, is debated.
Reliability Theory and the Reliability Theory of Aging
"Reliability Theory" itself is just a mathematical framework for describing survival / failure rates and stuff. (Engineers use it to quantify stuff like, the rate at which parts have their first breakage, or whatever.) Some of the quantities it describes are basically the same as some analogous quantities in demography / life histories, if "first failure" is taken to mean death. For example, the "Survival Function" $S(t)$ is the probability, at time $0$, that failure will not yet have occurred by time $t$; this is obviously analogous to the probability $l_x$ that a newborn will still be alive at age $x$.
Systems can be made of parts; if you know the survival/reliability patterns of the parts, and how they go together, you can tell something about the survival/reliability of the whole system. To illustrate, compare two kinds of reliability structure:

A "series reliability structure" is one where, if any part fails, the system fails. An example would be a block held up by a chain; if any link breaks the block falls.
A "parallel reliability structure" is one where, if all parts fail, the system fails. An example would be a block held up by a number of individual rings, attached separately; only when the last ring breaks, does the block fall.

"The Reliability Theory of Aging and Longevity" is a specific theory proposed by Leonid Gavrilov and Natalia Gavrilova, intended to explain patterns of organismal failure ("death") in terms of component failure, and how the components are put together. If I recall, they propose that aging organisms are made up of redundant blocks of non-aging components; supposedly, this can explain near-Gompertzian aging over most of adult life, as well as apparent late-life mortality deceleration.
Group Selection
Heresy! Most evolutionary biologists / gerontologists, I assume, are happy with the mainstream theory and don't take the group selection theory seriously. Iunno, try Mitteldorf? Here's a paper and he also wrote a pop book with Dorion Sagan. On group selection in general as an explanation for altruism, I think David Sloan Wilson's the guy trying the hardest to defend it (or "a new version of it").
Molecular Mechanisms
Iunno, try The Hallmarks of Aging? The trouble is we really don't know what mechanisms cause aging. There's some good ideas, but finding evidence is haaaaard. One problem is that, if you want to know why some species live longer than others, and you're looking for physiological correlations, body size is a huge confound (elephants and whales live longer than mice and dogs), and so might be phylogeny.


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Measurement of glucose concentration in the human brain
If I want to measure the exact glucose concentration in a human brain then how can I proceed to do that? Is there any technique or assay to do that?

It is possible by using 13C NMR Spectroscopy.
It has been done after infusing enriched D-[1-13C]glucose in six healthy children. The results showed that at euglycemia glucose concentration is about 1 micromol/ml.

Source: Gruetter R, Novotny EJ, Boulware SD, Rothman DL, Mason GF, Shulman GI, Shulman RG, Tamborlane WV. Direct measurement of brain glucose concentrations in humans by 13C NMR spectroscopy. Proc. Natl. Acad. Sci. U.S.A. 1992 Feb 1;89(3):1109-12. PubMed PMID: 1736294.


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How and when did sex evolve?
As I know evolution comes bit by bit mutation by mutation
How sex evolved which requires a major change in at least two individuals one to become male and one to become female ?
When that happened as we can see sex in all animals and most plants?

possibly of interest: http://biology.stackexchange.com/questions/15990/how-did-the-first-sexual-animal-come-to-exist/16014#16014

If you're interested in a deep exploration of the subject at a more readable level than articles in PubMed, I strongly recommend this book:
http://www.amazon.com/Power-Sex-Suicide-Mitochondria-Meaning/dp/0199205647

Sex (depending on how you define it), evolved very early (more than a billion years ago). Even species like yeast have a type of "sex" (see below).
Also, this doesn't mean there is necessarily a big difference between the two sexes.
The yeast Saccharomyces cerevisiae, for example, also has two "sexes", called mating types. One is called alpha and the other is called a. They can only mate if they have different mating types, so it is analogous in a way to mammalian sex. However, the genetic difference between these two types is tiny. There's a specific location in the genome that's called the MAT locus. This location can have either an alpha sequence or an a sequence, an that will determine the sex. The rest of the genome will be the same between sexes.
So it really doesn't seem like it is a huge evolutionary step to go from no sex to some simple version of sex.
See more details about yeast mating here.
Also see this wikipedia article on the evolution of sexual reproduction.

@TheLastWord yes, the name is the letter a.

The oldest evidence we have of sex comes from the fossil record which shows it was present more than one billion years ago - it could be even longer (it would be naive to think we have found all fossils or that all organisms that ever existed became fossilized). Sexual reproduction introduces potential benefits because it allows recombination meaning useful gene combinations are created more regularly and deleterious mutations are lost more efficiently (see Muller's Ratchet).
It is thought that sexual reproduction first occurred in single celled eukaryotes. In bacteria it has been shown that stress can induce the process of transformation. Transformation is a sex-like process in bacteria where one bacterial cell takes DNA from a donor bacterial cell and incorporates it in to it's own cell, it could help to repair DNA damage caused by stress. Transformation could represent one early form of sex.
It is difficult to put a timeline on it because it can only be seen from fossil data. But from early primitive haploid organisms we would need the evolution of diploidy, some sex-determining mechanisms, anisogamy, and reproductive physiology for basic recognisable sexes. From transformation you could get early eukaryotes that take up extra copies of genes from donors, leading to primitive diploidy.
To put down some unsupported thoughts (because this question is very hard to answer - there is no really firm consensus)... Once diploidy (having more than one copy of a section of DNA) is established it may be possible to form some gamete type functions, and anisogamy, where donors can more actively package, send, and receive large sections of DNA. From there anisogamy could encourage the specialization of gamete cells more similar to what we are familiar with (eggs and sperm). One likely next step would be through hermaphroditism - the ability to be produce both gamete types simultaneously or sequentially. Then some individuals would specialize in being one or the other (sex-determination). Continued evolution would lead to more distinct male and female phenotypes.


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Can paralogous genes be under negative selection?
I have just aligned 9 paralogous genes from human, uploaded them into MEGA and calculated  negative selection. Can there be negative selection acting in between paralogous genes? Or how should I interpret this result?


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Relationship between small and large fast-twitch motor units
When large fast-twitch motor units are temporarily fatigued, non-fatigue small motor units in the same muscle are impaired for small delicate tasks. Why?
When impulses from the brain comes down, the impulses from interneuron goes to small diameter motor neuron, which are associated with non-fatigue motor units, and large diameter motor neurons, which are associated with fast-twitch motor units. More impulse is necessary to activate the fast twitch-muscles because the larger neurons have higher leak current and capacitance. Thus, we have an ascending activation of muscle units, from least forceful units to most forceful. Now my question is, if the fast-twitch muscle units are fatigued, why cant we perform delicate movement/ task?
Fatigue is mainly caused when the motor unit runs out of ATP. So, is that the bridge between these to things, or is it something else?
Or, is it related to how motor units are used is a fixed ascending order for completing tasks? If so, how?
Thanks for all the help!

I am finding it difficult to understand what exactly you are trying to ask here.

When impulses from the brain comes down, the impulses from interneuron goes to small diameter motor neuron, which are associated with non-fatigue motor units, and large diameter motor neurons, which are associated with fast-twitch motor units. More impulse is necessary to activate the fast twitch-muscles because the larger neurons have higher leak current and capacitance. Thus, we have an ascending activation of muscle units, from least forceful units to most forceful. Now my question is, if the fast-twitch muscle units are fatigued, why cant we perform delicate movement/ task?


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Neurology: spinal tract
I have had a few difficulties finding answers for the questions below. I have tried answering the first two myself; but, I am not sure they are correct or not. And I am not too sure about the third one.

In which structure of the brain does the axon from the spinocerebellum tract synapese? Is it the cerebellum?
Are the cell bodies of axon in the gracile tract located at the dorsal root, tectospinal tract located in cerebral cortex?
Which region  of spinal cord carries feed-forward information to help accommodate for upcoming motor movement?

Yes, the spinocerebellar tract ends in the ipsilateral cerebellum.
The gracile tract is a bundle of axon fibers in the dorsal root. The neural cell bodies are in the dorsal root ganglions. The tectospinal tract is part of extrapyramidal tract that connects midbrain (mesencephalon) with the spinal cord.
Didin't get exactly what you meant but: the lateral corticospinal tract (part of pyramidal tracts) controls fine movement of ipsilateral limbs, while the anterior corticospinal tract (part of the pyramidal tracts) conducts voluntary motor impulses from the precentral gyrus.

Source: Wikipedia: Tectospinal tract, Spinocerebellar tract, Dorsal root ganglion, Pyramidal tracts, Anterior corticospinal tract, Lateral corticospinal tract.


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Name of scientist who discovered lifesaving drug and chose not to patent it?
I recall reading about a 20th century scientist who made a life-saving drug that could have patented it and made millions. He chose not to and saved the lives of millions around the globe.
I thought it was Frederick Banting - but it doesn't sound quite right.
None of the others in this list seem quite right.
My question is: What is the name of scientist who discovered lifesaving drug and chose not to patent it?

It's just possible that you are thinking of the failure to patent hybridoma technology. Georges Kohler and Cesar Milstein developed this at the MRC lab in Cambridge, and won a Nobel prize. Milstein was probably philosophically opposed to patenting, but the failure to do so was essentially a bureaucratic decision. It's an interesting story.

Patenting may not always be for earning profits. Patent also protects an invention form others who intend to make a profit out of it. I don't think any researcher became rich by selling drugs- it is the pharma companies that set high margins between the production and market price and make millions of dollars from other's illnesses (and in most cases the product is not developed by their R&D)

Dr Jonas Salk or Dr Albert Sabin who did not patent their respective polio vaccines. There are some more such researchers so I am not sure who exactly you are looking for but this would be a start.

You could've been thinking correctly. Banting did patent insulin but felt it was unethical to profit from such a critical drug. He sold the patent for a dollar to a (now nonexistent) pharmaceutical company.


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To have TBE vaccine during allergic times with mild asthmatic symptoms?
My assistant says that if you have asthmatic symptoms you cannot have TBE (Tick Born Encephalitis) vaccine, although you are living in the active zone of TBE.
Cases

mild allergic symptoms
allergic symptoms under control of Montelukast (asthma in control)
asthmatic symptoms (bronchitis, rhinosinutis, repeated cough)

What are the risks of having this vaccine during allergic symptoms when you have mild asthma medication (Montelukast)?
I still think the risk of encephalitis is higher if you get TBE from nature than from vaccine.
Are there really some cases where encephalitis is caused by the TBE vaccine?

Can you define the acronym TBE in the question?

Interesting question!
The Tick Borne encephalitis vaccine is an inactivated vaccine. It is therefore impossible to get the infection from the vaccine. Reports of fever have been noted but that is due to the body mounting an immune response not due to infection. There are therefore no reports of encephalitis or other markers of infection following the vaccine.
Not only may you have the TBE vaccine if you are asthmatic, but if you are at risk due to your lifestyle and location then, particularly if you have chronic asthma, the TBE vaccine might be a good idea.
Asthma is usually treated by inhalers and montelukast is reserved for uncontrolled/severe asthma. However in the rarer case of aspirin induced asthma, it is much more first line and used for mild asthma. Montelukast is not considered a mild medication.
I hope this answers your question :) if not, comment below!


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Why rectus abdominis is not proximal muscle?
I am thinking this picture which shows proximal muscles.

Why for instance pectoralis major, subclavius and rectus abdominalis are not included in proximal muscles?

It's not clear what "proximal" means in this context. It's not a standard use of that anatomical term in English. I'd also say that the figure on the left actually does show the pectoralis major.
The author of this figure might be trying to show the muscles that cross the proximal joints in the upper and lower limbs. For example:
Upper limb

Pectoralis major
Biceps brachii
Triceps brachii
Latissimus dorsi

Lower limb

Adductors (brevis, longus, magnus)
Rectus femoris
Semimembranosus, semitendinosus, biceps femoris (long head)
Gluteals (maximus, medius, minimus)

Muscles that do not cross the shoulder or hip are not included. This explains the lack of rectus abdominis or subclavius. Though it is not clear to me which the paired muscles in the posterior view are running craniocaudally from the thorax to the gluteal region.


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Are bronchioles and alveoli covered by respiratory epithelium?
Which parts of respiratory apparatus are covered by respiratory epithelium and which are covered by other kinds of epithelium?

What do you mean by respiratory epithelium ? Do you mean squamous epithelium ?

From the nose to the pharynx and larynx: stratified squamous epithelium
From the end of larynx to the bronchi: pseudostratified columnar ciliated epithelial cells.
From the small bronchi cartilage is being replaced by elastic tissue.
Bronchioles: ciliated simple epithelium with club cells (known as Clara cells). Also they lack cartilage and glands.
Alveoli are covered with squamous alveolar cells which form the wall (also known as type I pneumocytes). They also contain great alveolar cells (which produce surfactant) or type II pneumocytes and macrophages.
From http://en.wikipedia.org/wiki/Respiratory_tract , http://en.wikipedia.org/wiki/Pulmonary_alveolus and http://en.wikipedia.org/wiki/Pharynx

The major parts of respiratory apparatus are covered by ciliated respiratory epithelium with goblet cells.
The trachea and bronchi are covered by pseudostratified columnar ciliated epithelium with goblet cells. Terminal bronchioles are covered by ciliated cuboidal epithelium. The alveolar duct, alveolar SAC, alveolae are covered by squamous epithelium and no goblet cells.

*The cartilage is present only untill the initial bronchioles.
image source: Laniece, Alexandra. (2018). Alveoli-on-a-chip : A close-contact dynamic model of the alveolar capillary barrier: micro-engineering, microfluidics and induced pluripotent stem cells.


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How does tree resin capture arthropods?
In regards to a published paper of a spider about to make a meal out of a parasitic wasp (http://www.tandfonline.com/doi/abs/10.1080/08912963.2011.640399#.U1kSV14gVBU), it reminded me of a issue I've often contemplating for some time:
Isn't tree resin very slow moving, for instance maple sap has an extremely high viscosity and therefore how does the resin engulf both an arthropod, such as a spider, quick enough for it to not move away from the slowly moving amber?

I believe it is more of the fact that the organism gets stuck to the residual resin on the plant itself, and becomes encased and later fossilised in the amber.
From LiveScience.Com:

A host of bugs, fungus and other life forms have been found trapped in amber from the time of the dinosaurs.  Bugs can become encased in amber if, while alive, they get stuck in the resin.

Although plant resin is slow-moving, the bug stands to be encased in it if it is already stuck to the tree itself, as there is a large amount of resin on the surface of the plant.  If they are crawling over the plant, or land on the surface, they would become stuck and later encased. It would be similar with other organisms as well, as plants and other organisms have been discovered preserved in this way.

These fossils represent some of the earliest African fossil records for a variety of arthropods, including wasps, barklice, moths, beetles, a primitive ant, a rare insect called a zorapteran, and a sheet-web weaving spider. Parasitic fungi that lived on the resin-bearing trees were also found, as well as filaments of bacteria and the remains of flowering plants and ferns.


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Definition of Linkage Desiquilibrium (LD)
According to wiki, linkage disequilibrium $D$ equals
$$D = x_{11} - p_1\cdot q_1$$
where:
$$
        \begin{matrix}
        \text{Haplotype} & \text{Frequency}\\
        A_1B_1 & x_{11}\\
        A_{1}B_{2} & x_{12} \\
        A_{2}B_{1} & x_{21} \\
        A_{2}B_{2} & x_{22} \\
        \end{matrix}
$$
and
$$
        \begin{matrix}
        \text{Allele} & \text{Frequency}\\
    A_{1} & p_{1}=x_{11}+x_{12} \\
    A_{2} & p_{2}=x_{21}+x_{22} \\
    B_{1} & q_{1}=x_{11}+x_{21} \\
    B_{2} & q_{2}=x_{12}+x_{22} \\
        \end{matrix}
$$
According to Hartl and Clark, linkage disequilibrium $D$ equals:
$$D = x_{11}x_{22}-x_{12}x_{21}$$
Question
Can you please prove that these two formulations of linkage disequilibrium are equivalent (assuming that they are equivalent)? If they're not… Do we use different definitions? What are their respective meanings?

none of your references seem to have links?

Yeah, where are the links?

Thanks for noticing. don't know what happened to them. I added the links.

Just need to solve the equation. p1 = X11 + X12; q1 = X11 + X21; 1 = X11 + X12 + X21 + X22.
D = X11 - (X11 + X12) * (X11 + X21)
D = X11 - (X11X11 + X11X21 + X11X12 + X12X21)
D = X11 - X11X11 - X11X21 - X11X12 - X12X21
D = X11 * (1 - X11) - X11X21 - X11X12 - X12X21
D = X11 * (X11 + X12 + X21 + X22 - X11) - X11X21 - X11X12 - X12X21
D = X11 * (X12 + X21 + X22) - X11X21 - X11X12 - X12X21
D = X11X12 + X11X21 + X11X22 - X11X21 - X11X12 - X12X21
D = X11X22 - X12X21
Sorry for the very long answer, but I thought it would be more clear if I wrote everything out.


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definition of tempo and mode in evolution
I am reading Punctuated Equilibria: The Tempo and Mode of Evolution Reconsidered, which mentions the "tempo" and "mode" of evolution. I'm not familiar with the related literature and when I google the concept, what I got is something like:

One general topic, suggested by the word "tempo," has to do with "evolutionary rates..., their acceleration and deceleration, the conditions of exceptionally slow or rapid evolutions, and phenomena suggestive of inertia and momentum." A group of related problems, implied by the word "mode," involves "the study of the way, manner, or pattern of evolution, a study in which tempo is a basic factor, but which embraces considerably more than tempo''

This is as elusive as a definition can be. A clear definition should be something like "tempo is ...."
So what are the definitions of mode and tempo in evolution?

Actually, we can go right to the source on this: George Gaylord Simpson's Tempo and Mode in Evolution (1944).
Tempo is the rate of evolution. Simpson was a paleontologist, so he was trying to answer questions like "what is the percent change in the size of this tooth per million years?" He has a chapter estimating these rates for various characters in horses, which have a very good North American fossil record.
Mode encompasses the mechanisms responsible for evolution and their patterns. Simpson was working at the time of the Modern Synthesis (the wikipedia page is decent and brief enough on the topic, about which books are written), coming from the perspective of a paleontologist trying to reconcile genetic evolution with the macroevolutionary patterns he was seeing in the fossil record.
Simpson was really the first paleontologist to look at fossils in a quantitative way, trying to understand of connections between microevolutionary processes and macroevolutionary patterns. He even co-authored one of the first quantitative and statistical methods books for "organismal" biologists: Quantitative Zoology.
Specifically, of tempo, he says (p. xvii):

"...evolutionary rates under natural conditions, their acceleration and deceration, the conditions of exceptionally slow or rapid evolutions, and phenomena suggestive of inertia and momentum."

Of mode, he says (p. xviii)

"...the study of the way, manner, or pattern of evolution, a study in which tempo is a basic factor, but which embraces considerably more than tempo. The purpose is to determine how populations became genetically and morphologically differentiated, to see how they passed from one way of living to another or failed to do so, to examine the figurative outline of the stream of life and the circumstances surrounding each characteristic element in that pattern."

Mode basically encompasses all the processes of evolution. Tempo is the subset of mode that concerns how fast evolution is (or is not) happening.
The great thing is that 70 years after Simpson's book, biologists are still trying to understand tempo and mode of evolution.

It's great that you clarify tempo IS the rate of evolution. However, I'm still not clear about the relation between mode and tempo. Since tempo is a "rate" of evolution, in the context of dynamics, it is a rate of the underlying process, or generally speaking, a property of the process. How should I understand "mode ... encompasses all ... processes .... Tempo is the subset of mode..."? The sentence seems to suggest tempo is also a process.

Does it help to think of mode as all the processes involved in evolution? The rate of evolution is one of those processes, but there are additional processes (e.g., classical modes of speciation: allopatric, parapratric, etc.). So an "evolution" textbook probably has a chapter on rates. The rest of the book would be classified as "mode".

the textbook metaphor is a nice one.


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How does a TOPflash/FOPflash assay work to detect beta-catenin protein expression?
I am reading an article (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3596711/) wherein a TOPflash/FOPflash assay is used to detect beta-catenin protein levels in a COS-7 cell line. I can't find a good explanation in the article, or in any other article, as to how this assay works. I understand the cells are transfected with TOPflash/FOPflash reporter plasmids, but that's about it. Any insight or redirection would be much appreciated.

From what I can understand, TOPflash is a luciferase reporter plasmid that contains two sets of 3 copies of the wild-type TCF binding regions. If the canonical Wnt signaling is activated, beta-catenin will translocate to the nucleus to associate with TCF/LEF transcription factors to activate transcription of Wnt target genes. Since this is a luciferase plasmid, you should see an increase in relative luciferase activity when substrate is added. If Wnt signaling is inhibited, you will see loss of luciferase expression. The FOPflash is used as a negative control because the TCF binding regions upstream of the luciferase gene is mutated so even if beta-catenin translocates to the nucleus to activate TCF-mediated transcription, you should not see any luciferase activity.
Hope this helps.

Would you please provide a reference or two that supports your otherwise good answer. Good references helps to improve the overall quality of Biology.SE. :)


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In which direction plants' root grow in weightlessness?
As far as I know, roots of plants grow to the direction of Earth's gravity - this is called gravitropism.
But what happens if plants are in space? Are they able to perceive gravity in state of weightlessness? Either way, where do they grow their roots in those circumstances?
Note: this question may fit better either to Space.SE or to Astronomy.SE, but I was not sure about it.

@TheLastWord I couldn't use Stack Exchange for a very long time because of various reasons.

Astronomers on the International space station have done exactly that and grown Arabidopsis Thaliana in space. You can read the whole article here.
Plant roots apparently grow away from the seed exactly like on earth seeking out nutrients.

either you or me should remove the answer because both are exactly the same.. I am removing mine but take care not to post an answer that is exactly same as a previous one.

but wasn't mine listed before yours..

well.. the listing it seems is not chronological. When I posted there was no answer. Nevermind. The objective is achieved. Mission accomplished :)

It is actually. When I started typing, there was no answer listed.. You started answering after me but submitted before me.. But yes Mission accomplished.. :)

Roots are negatively phototropic in addition to being positively gravitropic. Both growth patterns are mediated by the same hormone, auxin. Removing one factor or the other will not prevent roots from growing "down."


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Preventing paracetamol overdose
Paracetamol overdose is one of the most common drug toxicities. It may be treated by intravenous N-acetylcysteine which replaces the glutathione that is used up in paracetamol metabolism to prevent the harmful effects of NAQBI.
Why can glutathione, NAC nor an inhibitor of the alternate cytochrome metabolism be added to paracetamol to prevent the possibility of acute liver failure? I imagine there is a reason as this is too obvious a solution.

I cannot recall the sources, but I remember that a) glutathione is not well absorbed as a supplement and b) N-acetycystein has some possible side-effects that are too harmful to give it regularly together with paracetamol. Maybe checking the wikipedia article of glutathione might give some of the sources for this, but I think parts of it I got from the german version.

As skymninge correctly states N-acetycysteine has some side effects. Most serious of which is anaphylaxis. I should think giving a medication to huge amounts of people that can cause anaphylaxis would cause more deaths than it would help prevent due to paracetomol overdose.

I assume you mean "why can't glutathione, NAC .. be added"
From lef.org

There is one problem. The FDA prohibits combining existing drugs and
  dietary supplements unless a New Drug Application is filed, tens of
  millions of dollars of clinical studies are performed, and the FDA
  agrees to allow the combination to be sold. The whole process can cost
  upwards of $100 million and take a decade to complete.

It's sad that would would be very likely an effective solution for the deaths and liver damage is not available or made more widely known.
Only about 10% of acetaminophen is metabolised through the glutathione conjugation pathway via NAQBI (the other 90% is direct sulfation and glucuronidation of acetaminophen). Many people take NAC supplements regularly (I used to).  While high does can have some side effects, a typical supplement level dose of a few hundred milligrams daily are well tolerated.