text:
Clarification on the "orientation" of chromosomal rearrangements
I need some clarifications on the concept of "orientation" in case of chromosomal rearrangements.
Given a deletion event on a chromosome for example, is the resulting DNA at the breakpoint always in TH (Tail to Head) orientation? Do all duplications lead to HT orientation? And in case of translocations, inversions, etc..?
Can someone give a clear definition of "orientation", and make some examples?
Here some specific examples found in the Cosmic database:
CRC-3  large_intestine  NS  carcinoma  adenocarcinoma  intrachromosomal inversion  28066  0  2  53774826  53774826  +  2  53775947  53775947  +    21892161

CRC-3  large_intestine  NS  carcinoma  adenocarcinoma  intrachromosomal inversion  28072  0  2  60783417  60783417  -  2  60786447  60786447  -    21892161

0006_CRUK_PC_0006_T1_DNA  prostate  NS  carcinoma  adenocarcinoma  intrachromosomal inversion  113193  0  18  60375963  60375963  +  18  77010169  77010169  -      538

0006_CRUK_PC_0006_T1_DNA  prostate  NS  carcinoma  adenocarcinoma  intrachromosomal inversion  113314  0  7  153608258  153608258  -  7  153610727  153610727  +      538

As you can see, they have inversions having all of the possible strand orientations, '++','--','+-','-+'.
How is this even possible?! How to convert to H/T orientation in this case?
P.S. This is the description of the header of the data:
               HEADER[IDX] : IDX : DATA[IDX]
               Sample name :   0 : 0006_CRUK_PC_0006_T1_DNA
              Primary site :   1 : prostate
              Site subtype :   2 : NS
         Primary histology :   3 : carcinoma
         Histology subtype :   4 : adenocarcinoma
             Mutation Type :   5 : Interchromosomal unknown type
               Mutation ID :   6 : 113196
          Breakpoint Order :   7 : 0
         GRCh37 Chrom From :   8 : 6
  GRCh37 Location From min :   9 : 129148581
  GRCh37 Location From max :  10 : 129148581
        GRCh37 Strand From :  11 : -
           GRCh37 Chrom To :  12 : 7
    GRCh37 Location To min :  13 : 153610712
    GRCh37 Location To max :  14 : 153610712
          GRCh37 Strand To :  15 : -
     Non-templated ins seq :  16 :
                 Pubmed ID :  17 :
                  ID_STUDY :  18 : 538

Adding a NCBI bookshelf link.

I think the picture will help you. In fact, to determine which kind of rearrangement for the chromosomal, we need to define an "orientation". However, this orientation is not fixed. It is a definition compared with the two chromosomes before and after the rearrangement. As the picture shows, the duplicated sequence after rearrangement should be in the same orientation, if one of them not, it should be described as "inversion after duplication". For deletion, there is no difference in the orientation if the remain parts still in their previous pattern. The key point to understand,  is to check the sequence before and after the rearrangement and find difference(s) between them, then compare to this picture(which is the definition of rearrangement) to find if the chromosome has one or multiple rearrangements.
Hope this could help you.

Translocations are often between two different chromosomes (that situation is not depicted here).


text:
What are the requirements for a stable carbon cycle in sealed "bottle gardens"`?
The most famous example of a sealed bottle garden is David Latimer's bottle with a Spiderworth plant, pictured below, which has been sealed for 40 years. My own attempt at a bottle garden is failing and I'm looking to "debug" what's going on.
My garden is a 2 litre glass jar filled with gravel, sand and soil, filling about a quarter of the jar. The soil is rather damp. I'm observing the following: When the bottle is sealed, plants such as moss, strawberry shoots and seeds thrive for a couple of weeks. They will then wilt and worms that had hitched a ride in the soil try to escape. When opening the bottle, there is a strong smell exactly like manure. The brief exchange of air when opening the bottle is enough to allow the plants to properly rot over the coming days, with mold only now spreading. (This proves that oxygen was depleted before I opened the jar) I removed the dead plants, sprinkled seeds on the soil and closed the jar. The seeds germinated and thrived for a couple of weeks until the process repeated.
At first look, it appears that when oxygen has been depleted, anaerobic bacteria take over, producing H2S, which I assume kill the plants. Or are they killed by changes in pH under high CO2 concentrations? Why does this not occur for all bottle gardens? Is the problem that there's too few plants to keep up the oxygen level which keeps the anaerobic bacteria at bay, is it the waterlogged soil or some other factor I'm unaware of?

Latimer did something right with his bottle garden, which started with a seedling and some compost.

@j.musser may be the one to say something intelligent about this, but did mr. Latimer on the photo perhaps use sterilized materials (flask, soil, water etc.,)? Even seeds can be treated to kill most germs. It seems that bacteria/fungi seem to thwart your goals.

@ChrisStronks: There appears to be a healthy bacterial culture in Latimer's flask. The bacteria decompose dead leaves from the spiderworth, turning these into soil and releasing CO2 for consumption by the plant, completing the carbon cycle.

Have you ever played the Conway's Game of Life? From random beginnings you can have a fast-dying "life", or you can have an almost eternal "life". It probably has a big amount of chance going on. I heard that the project Biosfere II has had no luck at all, even with thousands of bottles...

The problem lies in soil bacteria.
There has been a project on a larger scale: Biosphere 2. After their initial trial they realised $O_2$ levels are getting much lower from what was predicted. The scientists team investigated the problem deeper and came to the conclusion that there was a lot of dead organic matter in the soil, which got consumed by aerobic bacteria. There were also other hypotheses: not enough sunlight and $O_2$ sequestration by concrete.
A solution for you would be to make sure there is little organic matter in your soil. Perhaps use inorganic "soil" like sand + some nutrients. And also make sure there is enough sunlight.
Start also with small plants - too large plants in the beginning might change $O_2/CO_2$ ratio to abruptly during day and night cycle. (remember that plants are also consuming oxygen at night).

That would make sense, the H2S (if that's what it is) occurs because the bacteria are gobbling up oxygen faster than the plants can produce it. I'll reduce the soil content and make it less waterlogged

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text:
Where can I find mutation datasets for cancer?
My lab has been using TCGA data (somatic mutations and clinical data) to develop panels of genes and of mutations we expect to see in certain cancer populations. We'd like to validate our panels by checking how they hold up against other cancer datasets.
I know that one resource we can use is the International Cancer Genome Consortium but I'm wondering if members of this forum can suggest a few other places we can get both clinical and somatic mutations data for cohorts of cancer patients.

As I'm sure you're aware, there is no complete centralised database for cancer gene mutations. The most comprehensive database is the TGCA as you've already mentioned. That doesn't mean that other data isn't out there.
A broad option that might fit your needs is to query OMIM hosted by NCBI. You can search "cancer" or something more specific and then select the dbSNP tab and it will return a list of gene locations of mutations that match the query.

For a more specific search, COSMIC hosted by SANGER allows downloads of the "cancer genes" in fasta format, and various other downloads with other information are available. It's manually curated which is always a bonus, however this does mean that it's limited to just a few genes. There is also BIC. This is specifically focussed on genes related to breast cancer and is hosted by NHGRI. Again, an account is required for the download and it is limited to genes affecting breast cancers.

The cBioPortal is an extraordinarily useful centralized source of cancer datasets. As of this date, it contains data from 105 cancer genomics studies. Many of these are TCGA studies, but the list includes many others as well. Furthermore, the human interface to the data is among the best I've seen.

That's a really neat portal I was unaware of, and I'll certainly have to edit my answer now! But since the question needs a comparison dataset against TGCA, what is the use of more TGCA data?

@James : many of the studies listed there are not TCGA. In my field of head and neck cancer, there are 2 (partially overlapping) TCGA data sets and 4 other data sets. The balance differs among cancer types. The TCGA data sets, of course, are typically the largest.

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text:
Why is pericardium muscle repolarizated earlier than endocardium?
I was reading about heat muscle contraction and I read:

The endocardium depolarization happens earlier than pericardium , but
  pericarduim repolarization happens earlier, therefore the T wave in
  healthy people is always positive.

I have two questions:

What's the reason?
Why doesn't it happen in atrium and atrial repolarization(T wave)?

Can you please add information to your question? In particular, please define "pericardium", which is commonly defined as the fibrous sac around the heart and should have no effect on the EKG except in illness. Please include the difference between endocardium, myocardium and epicardium if pertinent.

Ah.. I attempted an answer, but until we clarify some of the language I'm unsure my response will be correct. Waiting on these corrections.

I think Majid means to ask why the repolarisation occurs from outside to inside when the depolarisation occurs from inside to outside

I'm just going to link you to another post here, which I believe answers the same question. It's because the facilitation of the transient outward current if much more prominent in epicardial regions than in endocardial regions.
And the following citation, "Transient outward potassium current, ‘Ito’, phenotypes in the mammalian left ventricle: underlying molecular, cellular and biophysical mechanisms," provides some mechanistic insight.
To answer the rest of the question:
So in an ECG you have leads that record whether a charge is moving toward, or away from the lead. These net charges are reflected on the ECG as either positive or negative deflections. You have a signal from the sinoatrial node that causes a depolarization in the right atrium, then the left atrium (biphasic p wave). In each case, however, we see the positive p wave because in this depolarization the net charge is moving toward the electrodes. Studies on atrial repolarization note that yes, the atrial repolarization is generally obscured by the QRS complex but occurs with polarity opposite that of the p wave.
With the ventricles, and the T wave you end up with a special case. The endocardial regions and the interventricular septum are the first to depolarize, and you get the QRS complex. These regions have a longer period of contraction than the epicardial regions, however. The outside of the ventricles begin to repolarize quickly (transient outward current, surface becomes more positive), and this repolarization begins at the apex and propagates toward the base of the heart. Where you'd get a negative T wave with the change in charge, the direction that the repolarization travels causes you to get a positive reading.


text:
Clumping factor test
I'm come across this question and I'm somewhat confused:
In the test for staphylococci, the clumping factor detects:

staphylothrombin
DNase
mannitol fermentation
Fimbriae
fibrinogen-binding protein

I know that bound coagulase can convert prothrombin into staphylothrombin and eventually fibrinogen into fibrin.
I'm thinking it's staphylothrombin, but when it says ''detects'' does it mean that the test concludes whether staphylothrombin is produced or does it mean that the clumping factor actually ''detects'' a substance?

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text:
What is the most condensed form of (stored) energy used in biology?
When considering how organisms store energy for later use, I was wondering what substance known in Biology is best for compacting the most energy in the smallest space(volume-wise).
With my (limited) knowledge, I would guess that it would be what we would normally call "body fat". However, I know I am probably not aware of most forms of stored energy, and I considered that perhaps substances like egg-whites may potentially contain more energy in the same amount of volume.
So, the question as in the title: What is the most condensed form of (stored) energy used in biology?
Alternatively, if there is no known "best": What would the leading competitors be?

The best ratio between weight and energy content (and of course also stability) has indeed fat. It's energy content is more than twice as high as for carbohydrates (sugars).
See this table from here on the energy contents:

This is the reason why animals which hibernate or migrate fed up to build up fat resources before the winter or their journey. With carbohydrates they would need more than the double amount of stored carbohydrates to get the same energy. Proteins are approximately on the same level as carbohydrates.
If you look on this problem not by energy per mass but volume per mass, fat still wins. For this we need the density of protein (muscles in this case) and fat. Paper 1 (see reference below) say that the human muscles have an average density of 1.06g/cm³. Paper 2 lists a density of 0.92g/cm³ for fat. So fats (this is practically only valid for the human body, but should be in the same range for other animals) are about 15% less dense than muscles. As the energy density per weight is about double as high for fat, this compensates for the lower density.
Carbohydrates are better, but are still not as good as fat. It's a bit hard to find specific densities for carbohydrates in the human body, so let's use Glycogen (which is a widely found carbohydrate used for mid-term storage of energy) for this purpose. Paper 3 lists a density for Glycogen between 1.40–1.62 g/cm³, so fat has only 55-65% of it's density. Since the energy density of fat is about 2.25x that of carbohydrates, fat is still better.
If you look at ATP in comparison, it has relatively little energy to provide. ATP delivers about 32.3 kJ/mole (with 507.18 g/mole this make around 64 J/gram) per phosphate released from the molecule, which is 128 J/gram if both phosphates are released. This is approximately 300x less energy per gram than fat. This makes sense, since fats are completely oxidized (down to water and carbon dioxide), while in ATP only the phosphate bonds are broken. ATP acts as an energy carrier in the body and not as an energy storage molecule.
References:

Specific Force Deficit in Skeletal Muscles of Old Rats Is Partially
Explained by the Existence of Denervated Muscle Fibers
Association of adiponectin and resistin with adipose tissue
compartments, insulin resistance and dyslipidaemia
Shifts in the Distribution of Mass Densities Is a Signature of
Caloric Restriction in Caenorhabditis elegans

Do you have any information on more exotic chemical stores, such as the bombardier beetle's hydroquinone and hydrogen peroxide?  The peroxide alone is a mere 2.9 KJ/kg, but I could not find a figure for the reaction of the two.

What about "pure" energy (in terms of biology) like ATP? I guess this is probably not what the question means though.

@Sparhawk I added a paragraph on ATP.

Huh, interesting! Thanks for doing the maths.

@Sparhawk: It's interesting. I didn't expect the difference to be so big.

Yes, absolutely! I always imagined that that ATP was utilised not only for ease in energy exchange, but also some measure of efficiency. I guess not!

The question says "volume-wise", not "mass-wise", so a comparison of the density of fat to the others seems in order. Just to establish whether it wins both ways despite being less dense than protein. (Or at any rate, fatty tissue is less dense than muscle tissue).

@SteveJessop Interesting point. But even if you put this into account, fat still wins. I updated the answer.

Shouldn't "volume per mass" be "energy per volume"?

What about PHB? IIRC, PHB has similar energy per mass as fat, but a higher density, so the same amount of energy would take up less space. Can't find references at the moment though.

What do you mean with PHB?

Polyhydroxybutyrate

http://en.wikipedia.org/wiki/Energy_content_of_biofuel has a table of biofuels by density, it seems that oils and biodiesel beat fat slightly in both density and weight.


text:
Can we artificially increase human growth using HGH?
Robert Pershing Wadlow was a man who lived in the first half of the twentieth century. He had hyperplasia of his pituitary gland, which caused him over-produce human growth hormone (HGH), and as a result, he grew to nearly 9 feet (2.75m). He had difficulty managing his body size and died at age 22, with no sign that this growth was slowing down.
HGH can be used for medicinal purposes, and it seems that doctors prescribe it for conditions like chronic underdevelopment and HGH deficiencies.
Putting aside ethical or government regulation issues, is it theoretically possible for someone (like a "fully grown" adult) to artificially grow beyond their genetic potential by providing them with regular doses of HGH? If not, what was different about Wadlow's case?

Do you mean grow someone from scratch ( :-) ) or just substantially increase their growth?

@HDE226868 lol... Increase their growth (or generally prevent them from ceasing to grow).

You have to note that Robert died at a young age. Usually when the puberty hits and androgens are being produced at appropriate levels the growth plates of the bones would fuse and the person would cease growing.

@CRags That's true, but he was well past puberty, and bone plates usually fuse around 20 (if I'm not mistaken). It could be that if Robert had lived a few years more, he would have slowed down, but unfortunately there's nothing to suggest either way.

It varies but growing at 22 years is not unheard of.

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It's very slippery question. Because some doctors give a prescription for HGH when you genetically have not enough of this hormone. So Wadlow's case was something unique. Otherwise, it's always better to go for diagnoses it in clinic and read an article like thisabout HGH deficiency testing.

You asked

... is it theoretically possible for someone (like a "fully grown" adult) to artificially grow beyond their genetic potential by providing them with regular doses of HGH?

For an adult, the answer is no. Human growth means skeletal lateral growth, which is indeed mediated by human growth hormone. But during normal human development bones ossify in the process, and in human adults the bones are completely ossified and can't grow in length anymore.
From the cancer.gov site on Bone development and growth:

When cartilage growth ceases, usually in the early twenties, the epiphyseal plate completely ossifies so that only a thin epiphyseal line remains and the bones can no longer grow in length

Further reading: NEJM Osteogenesis: The Development of Bones
This point is usually reached around the early twenties in humans. The case mentioned in your question is different because in this case, the human growth hormone was "given" before this process had finished and thus the bones grew longer. He was 22 when he died, so we will never know if he would have finished growing in his mid- to late twenties.
Giving adults (that don't suffer from an HGH deficit) more human growth hormone has been done and does not result in lateral growth, but it does result in increase in lean body mass in both young adults and the elderly


text:
Why oxLDL accumulate to form foam cells?
In atherosclerosis, why macrophage store all the cholesterol from oxLDL inside, and turns to foam cell, and not just degrade it and going back to blood? (there are some amount that leave the plaque, but much more stay (J Clin Invest. 2011 May;121(5):2025-36. doi: 10.1172/JCI43802. Epub 2011 Apr 18.))
Reading a lot about atherosclerosis, but no explanation about why macrophages stay there and form a plaque, instead leave or at least break the cholesterol.

If you need more information about oxLDL provide more details about what you need out of your question so answers would be more direct and problem solver and if one answer is not what you are seeking for just comment on the answer

In short, rate of expression of intracellular cholesterol removal proteins like ABCA1 in macrophages and cytokine waterfall molecules in T-lymphocytes beside other anti-inflammatory cytokines has an important role in AS and why oxLDLs accumulate in intima.
When there is high level of oxLDL, rate of removal mechanism must increase to take extra cholesterol out of macrophage and after that to the liver.
And it(increasing the rate of reverse mechanism) could be done by inhibitors or regulators(when natural way could not effort enough excretion). => drugs like TONSHINONE
There is huge amount of information about how regulation of adhesion molecules, costimulatory molecules, antigen presenting molecules and anti-inflammatory or inflammatory molecules could have effect on oxLDL accumulation in macrophages and T-lymphocytes which cause damage induced by hydrogen proxide.
So accumulation of oxLDL molecules in Macrophages has genetic reason and why human being evolved in this way is a question for geneticists but how this happens could be explained by tracing adhesion and signaling molecules.
This is one of the texts about oxLDL accumulation and AS.
Macrophages take in, a large number of oxidized low density lipoproteins (oxLDL) under the intima and then become foam cells, which is one of the early signs of atherosclerotic lesions.
ATP-binding cassette transporter A1 (ABCA1) is an integral membrane protein that transports lipid from the cells to the liver with subsequent lipid excretion by bile at last. This reversal transport inhibits the formation of lipid.
This text shows how regulating cytokine waterfall and pro-inflammatory cytokines could have impact on creation or removal of foam cells.
They experimented that Tanshinone IIA (a molecule extracted from root of Salvia miltiorrhiza) significantly increased expression of ABCA1 in macrophage-derived foam cells, raised the outflow of intracellular cholesterol, and inhibited the formation of oxLDL induced foam cells.

Furthermore, the liver X receptor (LXR) and peroxisome proliferator activated receptor (PPAR) which are members of nuclear receptor superfamily can increase expression of ABCA1 through coupling path. Tan IIA inhibited the formation of foam cells. The mechanism might be that Tan IIA increased expression of PPARa, LXRa, and ABCA1, facilitated reversal cholesterol transport, and ultimately promoted cholesterol efflux.
T-lymphocytes in plaques are mostly CD4+ T-lymphocytes which belong to Th1 subtype. Most of CD4+ T-lymphocytes are active and can induce “cytokine waterfall” as well as secrete proinflammatory cytokines interferon-gamma (IFN-y), IL-12, and other cytokines, eventually leading to inflammation. Experiments showed that Tanshinone significantly inhibited production of Th1-derived IL-12 and IFN-y in a dose-dependent manner. T-lymphocytes play a role in the formation of AS, mainly because of proinflammatory cytokines secreted by T helper type (Th) 1 or Th2. Therefore, Tanshinone can inhibit the formation of AS and stabilize plaques via reducing the secretion of Th1 or Th2. Moreover, T-lymphocytes are activated to express CD40L, and the expression of tissue factor and matrix metalloproteinases (MMPs) is then promoted by interaction between CD40L and CD40.
TanIIA could improve the activity of superoxide dismutase (SOD), decrease the level of malondialdehyde (MDA), and reduce both the expression of CD40 and the activity of MMP-2.
So normally macrophages could excrete cholesterols but problem occurs when your diet contains high level of cholesterol and oxLDL goes high in your blood.
Evidence-Based Complementary and Alternative Medicine
Volume 2014 (2014), Article ID 267976, 6 pages
http://dx.doi.org/10.1155/2014/267976


text:
Do humans perceive temperature or heat-flux? (or both?)
The general understanding is that when I touch an object, I perceive its (relative) temperature.
A metal object at room temperature, however, will often feel cool to the touch.
This leads me to believe that the skin senses heat flux in addition to, or instead of temperature.
(The metal conducts heat well, and therefore creates a greater flux when touched than a more insulative material.)
I am unfamiliar with the chemical process by which temperature or flux is converted into meaningful signals.
Do humans perceive temperature or heat-flux? (or both?)

related to: http://biology.stackexchange.com/questions/27535/why-do-we-experience-temperatures-below-37-degrees-celsius-as-hot/27541#27541

check my answer now - I have written in greater detail

I am not really convinced by the arguments in support of flux perception; I'll also think about it but here is a point that you (and @CRags) can also think about: If our body could really perceive flux then it can anticipate the final temperature before it actually reaches. In differential control mechanisms, this is used to regulate the levels of any feature in advance (See PID controllers). I haven't heard of differential control of thermoregulation or any biological process, yet. Though I agree that one can perceive flux with conscious effort.

@WYSIWYG But the final temperature is already fixed (the set point) which the body is trying to maintain?

@CRags It is better if we discuss this on chat

It is really easy to show we sense heat flux, just hand someone two materials that are drastically different thermal conductors but are the exact same temprature (room temprature) and the person will tell you the better conductor feels colder.

Short answer
Humans sense temperature differences.
Background
(Including edits based upon comments)
Because the question is "Do humans perceive temperature or heat-flux?", I will answer the answer from a psychophysical perspective, i.e., by dealing with sensory awareness.
Just as with many other sensory systems, temperature sensors in the human body adapt to ambient stimuli (i.e., constant absolute stimulus levels). In other words, after being exposed for a while to a certain temperature, one looses the perception of temperature per se (assuming temperatures are within comfortable limits of course, otherwise general discomfort will arise such as shivering or sweating etc.).
Therefore, temperature sensing in humans is not absolute, but differential, and occurs when differences occur relative to the baseline.
Holmes and Wood (1968) mention in their Introduction the following, and I quote:

...three variables of thermal stimulation [...] affect the sensitivity of human subjects to warm and cool stimuli. These are (1) the temperature to which the skin has been adapted, (2) the area of skin over which the thermal energy is applied, and (3) the rate at which the temperature of the skin is changed.

Variables (1) and (3) clearly emphasize the differential nature of temperature perception in humans. Variable (2) is a general psychophysical phenomenon, and basically shows that when a stimulus is sufficiently large, temperature differences will be more easily felt, while when the skin surface being stimulated is excessively small (say a needle with a small temperature difference is pressed against the skin) certain temperature differences may not be felt any longer.
With regard to your question on metal and whether heat-flux can be sensed: a metal surface will feel cool only when it is lower in temperature than your body. Suppose now you touch a metal object at room temperature, i.e. lower than your body temperature. In that case, as you already indicate, it will draw away heat quickly from your skin by conduction, creating a 'heat-flux' if you like. The extraction of heat thereby elicits a powerful stimulus, because a large temperature difference creeps into your skin as heat is drawn away from your skin and underlying tissues. As such, and contrary to other answers given elsewhere, I explicitly say yes, 'heat-flux' can be sensed as it per definition generates a temperature difference. This in contrast to touching insulators like wood or plastic, which will quickly adopt the temperature of the skin very locally where you touch it. However, as has been pointed out by others - this does not mean that temperature is measured by heat-flux sensors per se. In contrast, temperature is measured by temperature sensors that detect temperature differences (differential stimuli) between skin and external media. Because a temperature change is also a differential stimulus, it will also be detected, and hence 'heat-flux' will therefore be detected as well.
Reference
Holmes & Wood, Perception & Psychophysics 1968; 3:81-4

"I say yes, heat-flux is definitely sensed as it per definition generates a temperature difference." I disagree with this statement. The temperature difference causes heat flux and not vice versa. Heat flux is dependent on the nature of the material and this may differ for skin types. But ultimately thermal equilibrium is reached.

I can understand the point on adaptation that you raise but temperature ultimately affects metabolism. Adaptation has a limit. For pain sensations the responses can be heightened if the tissue is already sensitized. Temperature difference is sensed but this doesnt mean that the response will be the same as long as the difference is the same. The operations of temperature sensor is non-linear. Nothing in biology is linear.

Your first comment: (1) no, nothing needs to be fixed - when equilibrium is reached, you don't feel temperature differences, that's the whole point. (2) Heat flux is definitely dependent on the material, see my answer last paragraph. With regard to your second comment: (3) Adaptation has of course limits. Everything has. I am talking physiological conditions. (4) Of course pain increases on top of an already existing pain. It is a difference! (5) Many sensory systems are non linear! I have never mentioned linearity. Don't put words in my mouth. I don't see any points in your two comments.

when you say that absolute temperature doesn't matter as long as the temperature difference is the same means: f(T₁-T₂)=f(T₁)-f(T₂) which denotes linearity. I am saying that this is not true. The function does not behave the same at all points as long as temperature difference is the same

I have never mentioned linearity. Adaptation is what I explained and I support that to the fullest. I have never said sensations are identical across the dynamic range. Again, don't put words in my mouth.

I believe this answer is most correct of the three submitted.
The disagreement over the phrase, "heat-flux is definitely sensed as it per definition generates a temperature difference" seems to be largely a case of semantics.
Temperature difference will cause heat flux, but flux will always be accompanied by a temperature difference. The key is that the temperature of the skin will decrease over time, not that the skin and surface were different temperatures to start with.

SYSIWYG's answer added valuable information on the chemical sensing, which seems to be absolute in some regards, but this is mitigated perceptually by the effects of habituation. (C Rags makes good points about the body's drive to achieve homeostasis, but I feel this only impacts conscious perception minimally in normal operating conditions.) Thanks everyone!

@ChrisStronks Check my answer below

@th3ophilos - This is most definitely a heated and fluxed discussion here :) The best questions generate discussions. Hence - my compliments to your excellent question! Thanks for your careful analysis of the answers. Most definitely WYSIWYG has added important points about the definition of heat flux (which was indeed a source of confusion). He excels in bringing terminology down to its core. However, his answer was at the physics and protein level (bottom-up), while I have chosen a top-down answer, which is a choice one has to make given the question and/or based on ones expertise.

This is the modified answer in response to the discussion:
Facts:

There are warmth and cold receptors in the body at two places: The Peripheral receptors and the Central Receptors
The peripheral receptors are present in skin and the central receptors in the body core at multiple sites the notable site being the hypothalamus
The Temperature receptors have two patterns of firing - The tonic response (sustained firing rate due to steady rise and maintainance in temperature over long time) and the phasic response (also called dynamic response - response to short changes in the temperature)
The Warmth receptors fire maximally at 44 - 46 degrees celcius. The firing stops almost completely at about 48-49 degrees celcius beyond which there is no effective thermoregulation
The Cold receptors fire maximally ar 20 - 35 degrees celcius.

What is measured?

The peripheral receptors sense the temperature of skin.
The central receptors measure the core body temperature.

Only the temperature is measured as WYSIWYG mentions.
However the frequency of stimulus (How frequently the nerves fire - this depends on the temperature range in which the respective receptors fire) and the two types of receptors present on the skin allows the brain to interpret the flux. So Chris Stronks is correct in telling the heat flux is perceived.
Mechanism of feeling cold:
When you touch a cold object the heat is lost through conduction and radiation through the portion of skin that is in contact with the object. The cold will cause vasoconstriction of that part of skin - This means that the temperature of that part of skin rapidly equilibriates with that of the object. As there is rapid cooling (assuming that the object is cold) the rate of firing of the warmth receptors decrease and the rate of firing of the cold receptors increase. This allows the brain to interpret that the skin is losing heat (the flux).
The radiation part of heat loss is more appreciated when you pass a uncurtained window during the winter - the temperature difference is so great that very high loss of heat occurs through radiation that you shiver. You have to note that during these instances there is no decrease in the core body temperature. The actual decrease in core body heat needs a long exposure to such conditions. In the scenarios detailed above the heat loss is primarily from skin which reflects the ambient conditions (very quickly). Thus the peripheral receptors effect Anticipatory Control which is effectively measuring the flux of heat through skin.
The opposite occurs when you suddenly stand beneath the sun coming from a cold room - the radiant temperature of the sun being so great will cause the skin temperature to rapidly rise causing the body to feel very hot (though the core body temperature has not changed much).
Interesting details that may increase your understanding (though not directly related to the question):
The heat control effected through sensing the change in the skin temperature is called Anticipatory Control. In this the brain "anticipates" what is going to happen - for example a sudden cold draught - and will respond to it - reponds by increasing the heat production (shivering).
The heat control effected through sensing the core body temperature is Negative Feedback Control. In this the brain responds to increase in the core body temperature and takes steps to remedy this (the response will bring the temperature back to the set point).

For more see:Boron & Boulpaep Textbook of Medical Physiology, 2nd Edition, Chapter 59.

I disagree. There is no way to perceive heat flux.

@WYSIWYG I did not say our body measures heat flux. I said our body is concerned about heat flux (loss or gain).

I think this is the correct answer, but you should point out that receptors measure temperature rather than heat flux. However, the main process that causes body temperature to increase/decrease is heat flux.

@CRags I would say that the body is finally only concerned about its temperature because the metabolism will get affected. The flux is an effect of how effectively the environment transfers heat to the body. The body just responds to the heat and not explicitly to its rate - Mathematically it is $f(T)$ and not $f(\frac{dT}{dt})$.

@WYSIWYG: I agree with your last comment which is basically what I was trying to say.

@ChrisStronks The beneficial point was raised by CRags. Not me.

@WYSIWYG Check out my answer

@CRags I totally agree that firing rates are affected by temperature difference and ranges. I also agree that flux can be deduced with conscious effort but is not measured which I mentioned in the comments. What we basically have is like a water level sensor- we can deduce the flow rate but all the control systems (except differential control, the example of which I have not seen in biological systems) are regulated by one parameter i.e the level. Same is with temperature. I still don't buy the "flux" argument.

@WYSIWYG I am saying that the flux is deduced by the brain. I clearly pointed out that flux is not measured and only temperature is measured. But coupling the fact  that the skin temperature rapidly equilibrates with the ambient temperature and the rate of firing of the temperature receptors, the flux is perceived and the response is effected

@CRags - Nice answer !! I +1d already :)

I still feel that this statement, "However the frequency of stimulus ... and the two types of receptors present on the skin allows the brain to interpret the flux" is incorrect.
These stimuli allow us to perceive a delta in temperature. Given that we do not have any perceived area metric, we cannot (it seems to me) call it flux.

It seems to me that Anticipatory Control attempts to guess at a flux value over the surface of the body, and uses the internal temperature changes to confirm its modifications. (If the core is slowly dropping, the guessed flux must be low.)

So I'd say Humans sense changes in temperature (which would be absolute, but are modified by our body's adaptation to a specific environment), while our subconscious uses the same information to guess at flux and compensate.
(Sorry for the multiple comments, I keep accidentally posting them with the return key and then timing out the editing period.)

Yes thats basically it. You can also view the chat room conversation between Chris, WYSIWYG and me which is linked in the comments for more details. @th3ophilos

Flux is defined as amount of heat transferred per unit area per unit time.
Our body does not perceive heat flux. It perceives temperature and tries to adjust heat exchange mechanisms until thermal homeostasis is achieved (in all warm blooded animals). This is a feedback controlled process.
If it were to measure heat flux then the body cannot sense if it is at 47⁰C and the environment is at 60⁰C or if it is at 37⁰C and the environment is at 50⁰C. The heat sensors in our body have evolved to function at 37⁰C. Their conformation changes with increase/decrease in temperature thereby opening or closing the ion channels. The conformation is a function of temperature. If you put that channel in 45⁰C and try to measure a temperature higher that that then it wont work in the same way.
Body function and metabolism are sensitive to absolute temperature. Also see this post.
So while temperature sensing is absolutely necessary even for cold-blooded animals, plants and other organisms, there is no mechanism to measure heat flux. You can just measure the effect of heat not the flow of heat. For e.g. you cannot say if a body is cooling more rapidly than the other just by perceiving it for a short duration. It is possible to consciously calculate heat flux but it is neither measured nor (afaik) is fed in as a parameter to any control systems that regulate body temperature.

I've got two examples that I can't really bring in line with that: First, why then do we feel such a difference between, for example, 10°C cold water and air? Second, what about the density of the surrounding medium? I was once told that you would still freeze in the thermosphere (up to 2000°C) because of its low density.

@Hav0k heat perception is different from the density problem that you are talking about. It is because of the relationship between boiling/melting points and pressure. State transition is dependent on not just temperature but pressure too. Now heat essentially needs molecules for its effect. There cannot be a hot vacuum. Temperature is a measure of the heat (so it is not possible that something is 2000⁰C and not hot)

@Hav0k Regarding your first question. It is like asking why does polyester feel different from wool. The perception of a material is not solely because of its temperature. For perceiving temperature the heat signal has to be relayed to the thermoreceptor neurons. This will depend only on the thermal conductance of your skin; not of the material that you are touching. Moreover this just affects sensitivity.

@ChrisStronks Can you explain how. I cannot see the reason. Imagine two bodies are cooling by dissipating heat with different rates. You get to touch both of them at a point when they have the same temperature. How will you tell which one is cooling faster unless you make another measurement.

I disagree strongly with some of your statements. Most of all your last sentence "...you cannot say if a body is cooling more rapidly than the other just by perceiving it for a short duration" is nothing less than exactly the opposite of how sensing in general works. Moreover, your answer has a tendency to explain things teleologically, like 'why would the body need data on temperature differences?'. This may often work in evolution, but in physiogical mechanisms it can easily put you on an incorrect mindset

i added another critique in my comment. To your question - Yes, indeed, when you touch something an infinitesimally short of time, then yes, of course no temperature difference is felt. Likewise, if a digital sensor has a sample rate of 1 kHz and you sense 1 ms, then of course, no difference can be registered regardless of how sensitive it is to temperature differences as there is just one sample to be analyzed... This then should be added very explicitly to your answer and not in a generalized way as it is an exception to the rule

@ChrisStronks A thermometer measures temperature. But it can be used to measure heat transfer rates. This is not the equivalent to thermometer measures heat transfer rate.

@ChrisStronks Shall we debate about this in the chat


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What happens to our umbilical cord internally as we age?
I was always curious as to if or how much of the internal structure or workings of the umbilical cord are still in existence as we age.  What happens to it over time?
The wikipedia article naval almost exclusively describes physical appearance and only touches on some disorders that affect physical appearance.
Then the wikipedia article on umbilical cord explains what happens briefly after birth, and only touches on it becoming part of the circulatory system.  What does it actually do in later life, as part of that system?

It's considered appropriate on biology.se that you present some of your reading/research with your question. What have you read about the human umbilicus? The site tour and the help center  provide guidance on how to use this site. Please take a few minutes to read about the kind of questions which are on topic here.

@anongoodnurse added research that was useless

The research wasn't useless. It actually had links to every last bit of what happens to the remains of the umbilical structures in the adult. Had you clicked through, you would have found them.

The umbilical cord, which contains the umbilical arteries and vein so important for nutrient, oxygen and waste transport before birth, becomes useless pretty much the moment the lungs start working (the kidneys already started before birth). As the baby breathes, the two arteries constrict to stop flow from the newborn to the placenta. The Wharton's Jelly, a structural element in the cord, causes collapse of the vein on cooling to outside temperature. Within a matter of a few minutes, the whole system is shut down.
Within the infant, the umbilical vein and ductus venosus (which carried blood to the liver and the inferior vena cava) close up and degenerate into fibrous remnants known as the round ligament of the liver and the ligamentum venosum respectively. The round ligament basically just divides the left part of the liver into medial and lateral sections. The ligamentum venosum does basically the same thing on the posterior surface of the liver. Both ligaments maintain their attachment to the umbilicus. (The small paraumbilical veins are unimportant except in the case of severe portal hypertension, where they act as a portacaval anastomosis.)
The parts of the arteries closest to the navel degenerate into what are known as the medial umbilical ligaments (which basically serve no purpose whatsoever and are buried in the abdominal wall), while the more internal remaining sections are retained as part of the circulatory system as the umbilical artery.
The umbilical artery in adults is a branch of the anterior division of the internal iliac artery. The umbilical artery is found in the pelvis, and gives rise to the superior vesical arteries (supplying the superior part of the bladder, and parts of the ureters. In males, it also gives rise to the the deferential artery which supplies the ductus deferens.

Don't forget the urachus.

I didn't. I didn't think it would missed. :-/

Just a wow answer. What is the urachus?! +1

Is this one of your my-duty-is-fair-thus-I-close-vote-but-answer-for-the-sake-of-cool-answers projects?

@ChrisStronks - yep! :-) To be fair, the OP did, at least, indicate that he tried to find out. The urachus is a channel between the bladder and the allantois in the embryology. If it remains patent, urine can drain from the umbilicus, or a cyst can form. Normally it forms the median umbilical ligament, which is just a shriveled piece of tissue.


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What actually are thoughts?
The human brain consists of neurons that transmit impulses like wires that conduct electricity.I am confused about where are our thoughts stored and what really are thoughts? For example if I think about space, what is actually happening in my brain, and in what form is my memory that there are black holes in space, stored?
After doing a little bit of research I somehow came to the conclusion that thoughts are nothing but the electro-chemical reactions that are triggered by external stimuli and Hippocampus is responsible for storing long term memory. But I was unable to understand what the following paragraph means:

"The hippocampus helps to solidify the pattern of connections that form a memory but the memory itself depends on the solidification of connections between the individual brain cells".

Please explain it. Am I correct so far? Please help.

In short -  it's more complicated than that ;)

@Mithoron, am I correct when I say that thoughts are nothing but the electro-chemical reactions that are triggered by external stimuli, ?

I think we don't know how thoughts arise from incredible amount of chemical reactions in brain. And of course internal stimuli are important.

@Mithoron, Can you please frame an answer explaining the above paragraph, :)?

I know nothing about neuroscience! Your question is on-topic here but I thought I would let you know that your question would also be a very good fit for CognitiveScience.SE

Not just hippocampus, but even cortex is involved.

But what are thoughts? :) I don't think the question is well defined yet. If you indicate a specific "thought" or "thought process" in mind, you may get a better answer.

I have edited the question. Please have a look.

The question is still ambiguous. Memory can be explained as done below in terms of short-term memory by @WYSIWYG. Long-term memory, and 'thoughts' are a whole other matter and involve large areas of the cortex, as mentioned by WYSIWG. This question needs work.

What does the "black holes" part mean?

@HDE226868 OP's reference to black holes isn't important. I think it should be read as "How is my knowledge of some arbitrary fact, X, stored?"

The hippocampus helps to solidify the pattern of connections that form a memory but the memory itself depends on the solidification of connections between the individual brain cells".

This refers to the phenomenon called Long Term Potentiation which regulates synaptic strength between neurons. Certain patterns of firing (high frequency) causes the post synaptic neuron to strengthen the synapses. One way of doing that is by increasing the number of receptors (Usually NMDA receptors). Due to this, the response would be stronger in the next firing event. You can imagine its effects- more number of times you read a passage better will you remember it.
Hippocampus is involved in this process (it is one region where a lot of synaptic dynamics happens) but consolidation and long term storage of memories is handled by the cortex. Essentially what happens when a memory is formed is strengthening of synapses.

Thanks @WYSIWYG, but I could not understand what "...patterns of firing.." means.

@Abdullah Pattern means the how the frequently and at what intensity is the synaptic signal given. I said patterns because in certain cases continuous firing can also cause weakening of synapses. This is called Long Term Depression.

+1.Moving on to my original question,is it yet to be discovered what thoughts are and in which form are they stored?

@Abdullah To an extent. The term "thought", itself is quite broad.


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Biphasic T wave caused by digitalis toxicity

Digitalis is a drug that can be used during coronary insufficiency to
  increase the strength of cardiac muscle contraction. But when
  overdosages of digitalis are given, depolarization duration in one
  part of the ventricles may be increased out of proportion to that of
  other parts. As a result, nonspecific changes, such as T wave
  inversion or biphasic T waves, may occur in one or more of the
  electrocardiographic leads. A biphasic T wave caused by excessive
  administration of digitalis is shown in Figure.

Therefore, changes in the T wave during digitalis administration are often the earliest signs of digitalis toxicity.
I was reading about it in Guyton and Hall Physiology (volume 1, heart , chapter 12) and there was nothing about this that answers my questions.
And my questions are:

Why is T wave more affected by digitalis toxicity?
Why does it cause Biphasic T wave?

Can you reference the reading you did on why this might be? Or perhaps write what you think? It's considered a requisite on biology.se that at least some research into the question you ask is carried out and presented with your question.

@anonoodnurse I wrote the reference in my post. and I don't have no idea about it, but I'm really enthusiastic to know and think about answer of question.

Digitalis (which was by the way originally synthesized from Digitalis Purpurea) has two mechanisms of action:

The action by which digoxin improves contractility appears to be inhibition of the sarcolemmal Na$^+$K$^+$-ATPase "pump", normally responsible for maintaining transmembrane Na$^+$ and K$^+$ gradients
The major therapeutic electrical effect of digoxin occurs at the AV node, where it slows conduction velocity and increases refractoriness.

So it has a mechanical and an electrical mechanism. About the toxicity:

For example, in atrial and ventricular Purkinje fibers, a high dixogin concentration has three important actions that may lead to dangerous arrhythmias:

less negative resting potential

decreased action potential duration

enhanced automaticity

All quotes are from the book Pathophysiology of Heart Disease by Leonard S. Lilly, 5th edition.
So, I would assume one of the three (or a combination of them) is the reason for the biphasic T-wave. I hope someone more experienced can improve upon this answer.
This maybe has something to do with the relative refractory period ending during the T-wave.
Also, since the figure is from lead I, you can use that information for looking at where the net electrical axis is pointing at during the T-wave. Refer to the hexaxial system.

It is not written but it should relate to lead I .


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DNA barcoding and real-time PCR
I recently read an article on how DNA barcoding was used to identify species present in health products.
I also read an article about how Real-Time PCR was used to identify meat species in meat products.
I'm curious as to why one method is used over another. I know that DNA barcoding uses mitochondrial DNA to detect species, and Real-Time PCR uses species-specific primers to detect species.
Am I correct in thinking that real-time PCR cannot identify unknown species, but can tell you if the DNA matches a specific species you're looking for? For example, if I test for E. zebra but find something else, I cannot identify that unknown species and more testing is required?
Whereas in DNA barcoding, all I do is match the results against a huge list of known species in a database, which means I can identify unknown species without providing any prior knowledge?

PCR cannot identify species - this is usually done by sequencing. The only way to do so (for known species only) is to use species specific primers which either give you amplification of DNA or not. So can make a relatively simple yes or no decision on the presence of the species, but you cannot go further beyond this.

You've done a pretty decent job of answering your own question, but there are a few things that can be elaborated on.
The general convention is to use the mitochondrial Cytochrome C Oxidase 1 (COI) gene for barcoding animals and chloroplast genes (rbcL, matK, and trnH-psbA) for plants. The three biggest reasons for selecting these genes are 1) their ubiquity; 2) the presence of many copies per cell, so it's easier to PCR amplify the sequences; and 3) mitochondrial and plastid DNA has a much higher mutation rate than nuclear DNA, making it possible to uniquely barcode very closely related organisms. This method is incredibly sensitive, reliable, and easy. The original DNA barcoding publication can be found at doi: 10.1098/rspb.2002.2218
Thanks to the efforts of consortia like CBOL, BOLD and iBOL, there are now many millions of reference sequences databased, covering pretty much any multicellular organism you are ever likely to encounter (assuming you don't work on a deep-seq sub or something).
As you say in your post, there are significant limitations to using qPCR to identify species. You have to know beforehand what it is you are looking for, and you are left with a simple yes-no. This is not to say there is no place at all for qPCR in the species identification game, however. The method is very fast, and in cases where you are only interested in detecting a single species or small number of species, it's much more convenient than getting the DNA sequenced (for example, during quality control in a meat processing plant, doi: 10.1080/02652030701584041).

DNA Barcoding is a method or a protocol which, as you have already mentioned, uses genetic markers to identify species. The barcodes can be "scanned" using PCR.
Now Real-Time PCR is just a quantitative version of PCR. You don't need that to look for qualitative aspects. However in a mixed sample you may be able to calculate percentage constitution of the sample by each species, using Real-Time PCR.


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Protein Design - Target Structure Specification
I'm curious about how protein structures are defined in general, but in particular, I'm wondering how a target structure can be specified without knowing the amino acid sequence.
For example, in protein design (or from what I gather on the wikipedia page http://en.wikipedia.org/wiki/Protein_designs), scientists design a 3D structure that will perform a particular function.  They then try to come up with an amino acid sequence that will fold properly into that structure.
How can a 3D structure be defined if no amino acid sequence (and hence no molecular geometry) has been determined?

You don't create some structure and then try to find the amino acids that will create it; the residues themselves are important. Generally modelling is based on known motifs. The basic steps are: model in silico, test in vitro, fail, repeat.

Hmm, how is de novo protein design done?  From the article: "In de novo design the entire sequence is designed anew, based on no previous sequence"

Right, the sequence is designed anew. I also said generally.

I think that's what I was going for in my question - how can a sequence be designed anew?  I understand the idea of protein prediction - design an amino acid sequence, try to predict how it folds. But protein design is the reverse. Am I misunderstanding the meaning of "target structure"?

Afaik. they use quantum-mechanical models to calculate the active site and probably the whole enzyme structure. Enzyme designing is a very new topic and you'll need a lot of math to understand it.


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What mechanism is responsible for germinating in the right direction (root towards gravity)?
Regardless of the initial seed orientation, the root always grows/sprouts/germinates "towards gravity" (see picture), sometimes curving around in sharp 180°. What is the mechanism responsible for the gravity sensing and for the growth adjustment?

@WYSIWYG -the answer of the linked question indeed covers this question. The questions are however different. What to do?


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How well does the radius of a tree correlate with its age?
I'm looking for a cheap non-invasive ways to approximate the age of a tree (a birch). Measuring the radius pops up in the mind as the first alternative. How would one do that? Measure at multiple defined heights?
I'm hoping that I could get some kind of confidence interval for the approximation, so that the data could be used in a scientific publication.
Or is there any reliable DIY radiocarbon dating technique?

I'd take a look here: http://www.arborilogical.com/tree-articles/how-to-age-a-tree/

It's going to depend very strongly on species.  I have some cottonwoods which I know were planted in the mid-60s, and which are about 4 feet thick at the base.  (Some of the annual growth rings are almost an inch wide.)  OTOH, some of the mountain mahogany I have for firewood is much older, yet only around 6 inches thick.

Radiocarbon dating won't work. For a start the tree needs to be dead, which since you're not using the rings I'm assuming it isn't. Also the atomic testing in the 20th century completely messed up the level of C14 in the atmosphere, so radiocarbon dating can't be used for anything that didn't die 70 years ago or more.

@RobMackinnon But it looks like the C-14 from bombs has been utilized in other tests. And as far as OP's original question goes, C-14 dating would not be a cheap way to do it, and you couldn't do it yourself. The uncertainty in the measurements also means that C-14 is only good for approximate age, and may be off by around 100 years, which is a lot compared to the lifespan of most trees. Dating based on bomb carbon might actually be better for recent objects.

The radius of tree is not a good measure of the tree age, the most efficient technique to know the age of a tree is with dendrochronological methods, this is the less invasive technique. However, knowing very well the dynamics of growth of each species you can infer the age, check out this study:
Jan Lukaszkiewicz and Marek Kosmala. 2008. Determining the Age of Streetside Trees with Diameter at Breast Height-based Multifactorial Model (note this is a direct link to a pdf)

A tried and true method is to measure the diameter of the tree (which plays into your radius idea). Measurements are taken at "breast height" (~4.3ft, 1.3m from the ground). You can purchase a 'diameter tape' or 'girth tape' which consists of pre-calculated measurements, this way you will not have to measure circumference and derive diameter from this measurement. Breast height has been a consistent standard measurement over time, despite where a tree may begin to buttress, or flare out at the base. Below is an image detailing atypical tree measurements.

This does not deal with age correlations at all, and does not answer the question.

Can you add references to your answer and change it in a way it actually answers the question?


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Maximum RPM in zero-g before losing consciousness, spinning head-over-heels
There are more than a few scenes in Gravity that I find dubious. Specifically the ones where people are revolving very quickly, either about their own center of gravity or at the end of a rather long pole. I'd guess we'd need to know how long the pole was, but I'm more concerned with a person themselves, just flipping around out there (and I suppose we'd need their height, or does that cancel out?). How fast can they spin until it's night-night? Is it reasonable to assume they should've passed-out in at least one of those scenes?

I think people can easily endure head-over-heel revolutions in space such as seen in Gravity. I am no mathematician (let alone physicist, both of whom could answer this more accurately) but here is my reasoning (faulty though it may be).
You are assuming that someone would pass out from lack of blood supply to the brain.  Given we have absolutely no problems normally at 1 g (the force of gravity on earth), the average non-couch-potato person can tolerate forces of up to 20 G for less than 10 seconds, to 10 G for 1 minute, and 6 G for 10 minutes before passing out.
But g is very dependent on (as you stated) distance from center. It's also very dependent on revolutions per minute.
$$g=\frac{R\left(\frac{\pi\times rpm}{30}\right)^2}{9.81}$$
or
$$R=\frac{9.81 g}{\left(\pi\times rpm\over30 \right)^2}$$
g = Decimal fraction of Earth gravity
R = Radius from center of rotation in meters
π = 3.14159
rpm = revolutions per minute
The average North American male is 1.75m tall. That means the distance of the top of the head and bottom of the feet (if stretched out at full length) from center is under a meter (.875m). At 60 rpm's (that's pretty fast), solving for the above, g = 3.52.
g = [.875({3.14159x60}/30)^2]/9.81 = 3.521 (so just over 3.5G)
Gravity at the top of the head and the bottom of the feet would be 3.5G, while the gravity at the center would be zero G. The heart can easily compensate for that for a while. An astronaut, trained for increased Gs, can do well for longer.
Much worse than too little blood to the head is too much, which is what I would be worried about. Eventually, slightly less than half the blood volume would end up below the waist with the feet feeling the most pressure, and the rest above, with the brain being engorged with blood, which can cause hemorrhage (not taking into account here precise fluid physics). I'm not sure how this would play out in space over longer periods of time, but survival would be the norm for the scenes we see in Gravity.
An Air Force physician named John Stapp was the first to determine just what humans could take in the way of G forces. On his final run, firing nine solid-fuel rockets, his "sled" accelerated to 632 miles per hour in five seconds, slamming him into two tons of wind pressure, then came to a stop in just over one second. A witness said it was "absolutely inconceivable anybody could go that fast, then just stop, and survive." But Stapp did—in fact, he went on to live another 45 years, dying quietly at home in 1999 at the age of 89—and he experienced a record-breaking 46.2 G's. For an instant, his 168-pound body had weighed over 7,700 pounds.  Stapp's efforts put him on the cover of Time, and he was called "The Fastest Man on Earth." More importantly, his work led to greatly improved safety in both planes and cars, and he gave us a much-improved understanding of human tolerance to G forces.
All About G Forces

Very interesting that you would have to flip three times a second to put you into the one minute danger zone; not as dubious as I thought.

Nice fact too :)

I think "too much blood to the head" is in fact the problem that would be experienced, since centrifugal force would force the blood away from the axis of rotation and thus towards the top and bottom of the body. Per this, the tolerance limit for that would be only ~2G, making 60rpm readily fatal. That tolerance is less time-dependent than most. Of course, the rush of blood to the legs as well may play with that result, as may the high centre-of-mass of a human; I'd also be interested to see the effect of the spinning on venous return, cardiac preload etc.

@Watercleave - According to xkcd, Dr. Stapp would not have survived (even though he references Stapp's work. His stick figure model doesn't mention time.

@Watercleave - I alluded to this in my answer; I also mentioned that more like half the blood would go to the head; that factors in as well. xkcd is incorrect. Refute me with NASA's numbers (which xkcd references but doesn't use) which states that -4 - -6Gz (that's 6G blood to head position) would be uncomfortable but tolerable for 6 seconds. -3Gz doesn't mention blackout at all. Also, it doesn't change my conclusion: that for what we see in Gravity, the spins would be survivable.


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Neural correlates of the function of the cardiovascular system?
Are there any known neural correlates of the function of the cardiovascular system? I'm looking for research results that use standard brain imaging techniques (e.g. electroencephalography, magnetoencephalography, or functional magnetic resonance imaging), and compare the brain signals to respiratory and/or electrocardiographic signals.
Actually, ECG is frequently seen in EEG and MEG recordings. It is considered as an artefact, and typically removed in an early phase. Only the QRS complex is usually visible (or the R wave). If the ECG was recorded from the chest/limbs, proper signals would be gained. It would be interesting to compare the heart rate variability etc. to brain signals but has this for example been already done?
I don't have much background to respiratory signals, so I'm particularly interested about that.

Welcome to Stack Exchange. Here at Biology.SE we tend to like specific, solid questions. I would recommend you to do a first search on e.g. Google Scholar with the keywords "electrocardyogram electroencephaolgram" or "ECG EEG", or "ECG fMRI" etc etc. Try to pin down your question and specify it. As of now, it is too broad. If the question is put on hold it is likely for this or a related reason. You can always edit it and try to re-open it after that. Some cool questions have gone through this cycle. Interesting question though! Good luck.

I added some more text to the post.

Great addition. +1 and I retracted my close vote.


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How do scientists decide which version of a polymorphism is the main one?
This in fact has bugged me for years, but now I finally remembered to ask.
I suppose that if one variation is more frequent, it can be labeled as the default, but what about variations that are equally as common?
The example that I just saw, it seems that the frequency of both variants is the same, and yet somebody claims that G is the default and C is the polymorphism:
Polymorphism with genotypes CC, CG and GG occuring in 30, 40 and 30% of the control group, respectively http://hell.org.pl/~kamyk/stackexchange/Zorena1.jpg
Maybe it is possible to determine which one was first, but how? Is there ancient data about polymorphism frequencies?

A DNA locus may have two (or more) variants (alleles), but there isn't one termed a main or default variant.  In the example you cite, Myśliwska 2009, the only asymmetric distinction between the G and C alleles that I could see was in this passage:

The polymorphic region −174G>C of IL-6 encoding gene is implicated in
  transcription of this cytokine. The G>C nucleotide substitution
  creates...

This passage uses "substitution" (and "G>C" in −174G>C), which suggests that "G" is what is termed the ancestral variant, and "C" a later variant. The ancestral variant was the form that is believed to have been essentially the only form in some ancestral population; the later variant is a mutation (substitution in this example) which became established in part of a later occurring population.
Not all polymorphisms have their variants characterized in this way.  Those that do usually have DNA sequence evidence showing that species other than humans have a homologous gene, and those genes appear to have only the "ancestral" variant.  For the locus in the example you cite, the human IL6 -174 locus, a early paper by Fishman et al. (1998) says this:

Considerable interethnic variation in the frequencies of these
  polymorphisms has been demonstrated (39), which is consistent with our
  data for the -174C allele, which is considerably rarer in Gujarati
  Indians and Afro-Caribbeans, compared with UK Caucasians. As all of
  the primates examined were GG homozygotes, it is likely that this
  allele is ancestral and that the C allele represents a relatively
  recent change in the IL-6 5' flanking sequence.

This assessment seems to have become generally accepted.  The rather even distribution of G and C variants in the table you show is likely due to the subjects being of European ancestry, as suggested by this from SNPedia:

It [IL6 -174] tends to be quite polymorphic in Caucasians, but Asian
  and African populations are almost monomorphic (for the (G) allele).

[..] G is the default and C is the polymorphism

An allele (or just a nucleotide variant) cannot be "the polymorphism". There is polymorphism, if a given locus (or just a given nucleotide position) is polymorphic, that is, if as this position, there are different variants existing in the population. Therefore, an allele cannot be called polymorphism, only a locus can be called to be polymorphic and if a locus is polymorphic, then there is some polymorphism in the population.
I have never of people talking about the main or default variant. Do they use this word in the article you link? If yes, can you please indicate where?
Commonly, people talk about the wildtype versus the mutant variants. In this case, the wildtype variant is just the most common variant. Rarely I have seen people referring to wildtype variant when talking about variants that are at low frequency because the mutant is increasing in frequency and slowly reaching fixation. In such case, the wildtype mutant would correspond to the original variant at an arbitrary time point in the past but would not depend on the frequencies observed today.

I am not sure whether I answered your question or whether I missed the point you were trying to make. Let me know!

In this case, G is the genotype used for comparison because that's what's in the reference sequence for humans. Of course, this raises the question of why that's the reference. The answer is that it's because that's the sequence from the sample used to create the BAC that was sequenced and used to create that portion of the reference sequence.
Of course, it's not always like that. For example, when we discovered KCNJ18 and I submitted it for inclusion in the genome, I specifically submitted a sequence that represented the most likely haplotype given all of the samples we had sequenced. Of course, "most likely" may be population dependent.
As an aside, this is actually a bigger issue with some regions of the genome, where polymorphisms describe whole regions rather than just single bases. In the reference genome, these are the _hap_ chromosomes, which will often contain things like common structural rearrangements. These present a problem currently because they lead to biased mapping and variant calling. The first program known to make proper use of these was only released within the last month, in fact. One of the goals for the next human reference genome is to come up with a convenient graph representation of the genome that can include common polymorphic regions. This should lead to better quality genotyping of patients and study subjects.


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Do variant callers miss rare variants in reference?
Generally variant calling programs (such as GATK-UnifiedGenotyper) look for differences between reference genome and submitted sequence. However, we all know that reference genome consist rare variants in various positions. If submitted sequence has this rare form of that variant, variant call doesn't see it and doesn't report at all. However, that variant could be very precious for analysis.
So, how can I solve this problem? What should I do to not miss that rare variants even they are in reference genome?

Please don't cross-post, as you did here: http://seqanswers.com/forums/showthread.php?t=50289

Thanks for the answer. But Why shouldn't I? I want to reach people as many as possible. Actually I asked the same question on Quora. I don't think that it wrong. Seqanswers and Stackexchange are different platforms and may have different users. So, a user that is member of only single platform may miss my question. Cross-posting increase the possibility to get answer.

Cross-posting is convenient for you, but doubles/triples/etc. the work expended by the community to help you. Why should people in a community B expend time helping you when those in community A have already provided you with the answer to your question?

Actually, I'll share the answer that I found in every platform that I asked question. So, everyone in both platform will learn the answer. More people will benefit. It's better right?

If the reference sequence is associated with a disease or increased susceptibility to some phenotype, the the population you're using to compare against (with a variant) will show protection to it. So either way you're going to find an association, this will just change the sign of the coefficient.

Well, you'd hope that the "reference" sequence is of a healthy individual, and won't be carrying a highly detrimental allele that you care about.
Or get a bunch of control data from the 1K genome project, and compare them to the reference as well; they won't carry the rare alleles that your reference does.

The reference genome is a composite sequence from multiple individuals therefore scenario A should hardly occur, if at all. The unsatistying answer is that it is very unlikely that the rare variants of interest to you will be in the reference.


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Metabolism of different saccharides
Learning about carbohydrates, I wonder what the differences there are in terms of metabolism, and overall health between the different types of saccharides. In other words, does the body use polysaccharides, such as starches the same, or similar to how it would use a disaccharide like table sugar, sucrose?
It piqued my interest because people seem to put sugars and other types of carbohydrates into totally different categories, and one is seen as "healthy", the other "unhealthy".

Sucrose is made of glucose and fructose, both of which can enter glycolysis. Starch is made form glucose; if it can be digested, it can thus also enter glycolysis. Is that what you're getting at?

If you can digest (break down) the polysaccharides to useable monosaccharides, then they can be incorporated into glycolysis (or some other metabolic pathway!). The metabolic pathways around glycolysis are complex, but here is a representation of some of them:
As you can see in, in the top right corner, sucrose/starch, but also other sugars like nucleosides, can enter the overall simple sugar metabolic pathways. How and what exactly happens to the complex sugars will depend on how they are broken down (if they can be broken down at all) and they will have their own more or less complex metabolic pathways associated with that.


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Is brain transplantation possible?
Many organs can be transplanted nowadays, including the liver, lungs and kidneys.
Can the brain be transplanted?

@ChrisStronks Now I think it's too broad, unfortunately. There's a laundry list of assumptions that have to be built into any answer, and so narrowing it down to whether one would want the CNS to be functional, be able to vascularize itself, or to maintain histocompatibility would be helpful, but even bearing that narrowing of the question, this is still really a fanciful idea.

@jonsca - I disagree - it is not too broad as it is a specific, quite technical question now. It is fanciful, yes, but it has been tried in the past. A quick search on the web brought me to some interesting stuff going on recently as well. I'd like to answer this question by giving a short review on what has been done and these few studies obviously ran into all the issues you are describing. Nothing fancy, not too broad at all.

@ChrisStronks go for it, it's been reopened.

Short answer
Yes, brain transplantation is technically possible, but only for short periods of time, and only in experimental settings.

Background
In terms of a full-brain transplant there has been only one group that have made serious attempts in doing this (according to wikipedia and a literature search on my end). In the 1960's White and colleagues transplanted canine brains from one animal to another (White et al., 1965). In total 6 brains were transplanted. However, the recipients' brains were not removed and the brains were merely surgically transplanted into the neck region of the recipient animal, and connected to the recipient's cervical vasculature (carotide arteries and jugular vein). Hence, the recipient canines ended up with two brains. The authors, however showed with these experiments that the transplantation of brains was feasible, and that the transplants survived and remained functional, which was evidenced by EEG activity. The brains survived from 6 hours up to two days.
Later, White and colleagues worked out a way to keep an isolated (but blood-perfused) monkey brain alive outside the skull, potentially allowing for a primate brain to be transplanted (White et al, 1975). The procedure could include longer-term 'storage' of the brain by cooling it, making the possibility of transplantation more feasible. However, White realized the difficulties with this approach, since, and I quote:

[...] by definition the brain must be isolated before the transplantation, and thus requiring all nervous tissue connections to be severed (e.g. cranial nerves and spinal cord), the isolated transplanted monkey brain is without a mechanism to receive or transmit information.

To address this issue White et al. set out to transfer  the entire cephalon (head) of a monkey to the body of a recipient whose own cephalon had been removed at a mid-cervical
level. Under these circumstances the brain, being within its own cephalon, still connects to the cranial nerves:

source: University of washington
White et al. succeeded in transplanting a head, but the preparation rarely survived longer than three days due to haemorrhagic shock (White et al, 1975). Basically the recipient was quadriplegic, as the face was fully functional and White comments, and I quote:

Observe the wakeful appearance of the cephalon and the obvious movement of the facial musculature with open mouth and eyes. This preparation gives every evidence of being in intelligent contact with its environment. [...] Cortical [EEG] activity in this preparation demonstrates awake recordings.

Hence, with the current available technology it does not make much sense to perform a brain transplant, as the transplanted brain cannot be functionally (neurally) connected to recipient body. However, strides are being made in re-connecting a severed spinal cord (Canavero, 2013), endeavors that could bring head transplants a little closer.
Quadriplegic people obviously face extreme psychological challenges (Sane Australia). However, even when they have become quadriplegic due to an event later in life, they are not mentally changed, in that they are still 'themselves'. Therefore, although human transplants never have been done, I dare to say that the transplanted head will determine the psychological 'self' of the recipient body, which includes memory and personal traits. At least, assuming the brain can be transplanted without inflicting neuronal damage.

References
- White et al. Science 1965;150:779-81
- White et al. Resuscitation 1975;4,197-210
- Canavero et al. Surg Neurol Int 2013;4:S335–S42

Further reading
- CBS News

Wow! This is amazing. Though I feel sad for the animals used in experiments.

@CRags - when I first read about these (horrific) experiments, I couldn't help myself and felt a certain thrill. Obviously, and luckily, these kinds of experiments would never pass any ethical committee as of now.  At least not until functional re-connection with the peripheral nervous system can be potentially made.

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


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Why are fingerprints different even in identical twins?
Why are fingerprints different from person to person? It can't be genetics. Even identical twins has different sets of fingerprints. What is the deciding factor that form and shape our fingerprints?


text:
How does aging affect fingerprint?
Do fingerprints change as we grow from child to adult? Most notably, what is the effect of the increase in surface area of palms and fingers on the finger print? Does the finger print simply increases in size, and/or does the pattern change?
And what about old age? As the connective tissue in dermis get lax, how is the fingerprint affected?

All the evidence I found says that fingerprints do not change over time. However, I also found a paper from the National Academy of Science of America, which concluded that there is not peer-reviewed scientific report on fingerprints and if and how they possibly change over time. I think this question cannot be answered right now.

Fingerprints form in the womb at 22 weeks and after that, all they will do is expand as you grow. Therefore, it is possible that a fingerprint 22 weeks after conception could be used to identify a 50-year-old criminal.

can you please add a source?

Can you add some references to your answer?


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Time lapse between fresh blood's exposure to air and that same blood turning darker red-brown
For investigative purposes, I'm searching for a tool that can be used as a quick visual assessment of the the length of time that blood has been exposed to air after the blood flow has stopped.. Let's say that you walk into a room and see someone unconscious. Where blood appears, it had already stopped any fresh flow & has already dried to a dark brown similar to mahogany wood.  That person has been there longer than how many minutes? Please understand that I'm not asking how long the person has been lying there but for at least how long?
You come upon a dazed person unsteady on their feet with an injury to the face. The blood flow has stopped: the person may have smeared the blood when touching their face but you  see that the blood has not changed to a deep brown and still retains a bright red color..approximately how much time has likely elapsed between the injury occurring and your encounter with the injured person?
I know there's no exact time estimate possible without testing but simply for quick field assessments, is anyone willing to hazard an opinion?
In summary: How can I tell the age of a blood stain?

It appears you are asking about blood clotting time. You should clarify your question to prevent misunderstandings on what the question is about.

I don't think it's unclear at all what's be asked; it's not about clotting necessarily.

If the coloring process is gradual, then the question needs specification as to what the PO regards as the end point

Is this what you are wanting to know about?

Good Gravy - thanks so much ...while not the answer I seek, very interesting none-the -less

I edited this... Y'all see what he wants now?

In comments it been discussed that clotting is partial answer to OP. I would say, that is is somewhat tangential to the original question.
If I may re-phrase, OP asks: how one can estimate age of blood that has been exposed to air? Problem is that you will have to have a starting point to solve that backwards, like having an initial condition for solving differential equation.
One example that can be used is measurement of $pCO_2$ content in blood serum. If it is available, someone already collected this data. In 2 hours $pCO_2$drops 30% and total $CO_2$ drops about 6%.
Moreover, it seems that during hemorrhagic shock RBC shape changes, which means that sampling patient you will be able to approximate time since bleeding started. However, you will need an electron microscope at your disposal...
Finally, and I'll leave it like that, cellular death is a powerful process that leaves a lot of traces. Apoptotic cells have mitochondria bursting (except in RBC there are no mitochondria) and releasing, for example, cytochrome C. In case of bleeding probable cause of cellular death is necrosis, so different biochemical changes will occur. Point is that you can measure time since necrosis/apoptosis started by careful measurement.


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Which method would more accurately help to identify the unknown concentration of a protein sample between the A280 and the Bradford methods?
I quantified my protein using the standard Bradford method and the A280 methods and obtained values that were far off from the theoretical value of the protein of interest, and therefore was wondering if one method is better to use than the other.

Did both assays agree though?

Hi Sara I Have a nice guide method for you. In this time I cant send it to you because...' I will send it to you soon

Is the Bradford result much higher than the one for the A280?

Bradford is better and better than that is BCA. A280 relies on the presence of tryptophan which is not necessarily present in all proteins in same numbers.

@WYSIWYG For A280, shouldn't the tryptophan (and tyrosine and cystine) be accounted for in the extinction coefficient? Bradford/BCA is also dependent on amino acid content and is relative to a standard. If the unknown and standard proteins have a wildly different Arg/hydrophobic content, the results won't be very accurate.

I suppose the AA content will be important for A280 if it's being done relative to a standard as opposed to using the extinction coefficient.

Make sure the buffer your sample is in is compatible with the assay you're using, and that is is free of detergents, etc., as they can skew both assays. There are detergent-compatible assays available, check Pierce. I agree with @WYSIWYG that BCA is superior to the two you're currently using, just make sure you're using an appropriate standard. For example, if you're measuring IgG, don't use BSA as the standard.

I suppose SDS-PAGE could be another approach to estimate a concentration, but mostly to make sure you protein solution has protein.

Chris- Both methods were equally far apart from the literature value. And thank you everyone else for your input.

@canadianer tryptophan quenches the fluorescence of tyrosine and phenylalanine afaik. Moreover 280 is the absorption maxima for trp; others absorb shorter wavelengths.


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Stem cells and if they can correct a lack of apoptosis
If a cell ,call it C1 has no functioning apoptosis mechanism could a stem cell somehow be 'induced' to be like C1 , at least have the same genome as C1. Then use this stem cell 'duplicate' to 'restart' the apoptosis mechanisms in C1 or even replace C1? ( forgive any broadness or vagueness, I'm trying to be specific)

If I understand what you're asking (which I'm not sure I do...), no, it's not possible. Cells don't transfer their genomes between each other, so any defects or advantages in one cell won't transfer to a neighboring cell. The only way genes are transferred is down a lineage, with the genome of a parent cell being replicated and passed on to daughter cells.

But can a stem cell be made to 'copy' the genome of a cell with no apoptosis mechanism. Or at least be almost identical to the damaged cell?

Once you copy the genome of a cell into another cell (something that has to happen in the lab, a cell just can't "pick up" a neighboring cell's genes), it becomes a clone of that cell, and loses whatever properties it had before. So, if you have a cancer cell with no functioning apoptosis mechanisms, and copy its genome into a stem cell, the stem cell becomes a cancer cell, and no longer has the properties of "stem-ness".

I think you might have a fundamental misunderstanding of what stem cells are, and what they can do. Given the proper chemical pushes, a stem cell can differentiate into nearly any cell type in the body. However, its DNA remains the same - it's just gene expression that changes. Like I said earlier, genomic changes (mutations) cannot be transfered from one cell to the one next to it.

Can a stem cell's gene expression be made to be like some damaged cell's gene expression that has no apoptosis mechanism.

No, unless you make the exact same genetic changes in the stem cell as occurred in the damaged cell. Once you do that, it's no longer a stem cell. In fact, there's no point in starting with a stem cell, because you're not taking advantage of any of its unique properties.

Maybe you should step back and explain the bigger picture - what exactly are you trying to do? I think you're focusing too narrowly on one particular thing which doesn't do what you think it does.

I'm trying to research or figure out if there are useful ways to reactivate an apoptosis mechanism in a damaged cell. If a cell's gene expression has been damaged or distorted by many aquired mutations and it's apoptosis processes aren't functioning maybe if the cell's gene expression can be somehow 'reset' to when it didn't have mutations it's apoptosis mechanism would 'work' again.

That would be nice, but unfortunately it's impossible, at least with today's knowledge and methods. It takes a lot of mutations to completely knock out all mechanisms of apoptosis, and along with that a ton of other mutations occur, as well. The genome of a cancer cell is pretty screwed up. There's just no way to repair it, you've just got to kill the cell and start over. Incidentally, this is one reason why cells have so many different ways to commit suicide - as they start accumulating all these mutations, if they can detect them, they take themselves out of circulation.

And these aren't just nice little point mutations, either - entire chromosomes get duplicated, chopped up, rearranged, amplified, etc. There's no template present to "start from scratch."

If it takes a lot of mutations to shut down all mechanisms of apoptosis does that mean apoptosis 'shut-down' doesn't occur that much? If a cancerous cell is extremely 'screwed up' why can't the immune system detect it? Do cancer cells emit some chemicals that can mask it?

The answer is no.  There is no method currently known whereby we could get a stem cell to transfer its genome to a cancerous cell and thus get its apoptosis mechanism functioning again.  It's just not that easy to get a genome transfered - destroying the defective copy of the genome which is stored in the nucleus and getting a new copy of the entire genome into the same.
Remember that to transfer almost anything (except small non-polar molecules) in and out of the cell, you need highly specialized transporters (ie., ion channels, Na+/glucose pumps).  This is particularly true of large molecules like glucose and sucrose (plants). But even those molecules are extremely small compared to an entire chromosome, for which there is nothing even close to a transporter.  It would therefore be impossible to get the chromosome into the cell.
But even if you could, you have yet another hurdle: you have to get the new chromosomes into the nucleus... and that only after having destroyed the original genome in Cell 1, without making the environment in the nucleus toxic for the new genome (ie., CAD activity...)  This represents innumerable challenges, including the fact that you're going to need to alter the nuclear membrane to allow the entry of a massive macromolecule, without impeding the function of the cell...  The problems, unfortunately, go on and on.
TL;DR:  Nice idea, and would be really cool if it worked, but it has way, way, way too may complexities and insurmountable hurdles to be even remotely workable.

Sources:

Lemoine R. 2000. Sucrose transporters in plants: update on function and structure. Biomembranes 1465 (1–2): 246-262.


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Which will produce more oxygen? A few large trees or a greater number of smaller plants?
In a given area A, we have two choices -
(i) we can plant maximum number of trees (which are larger in size) possible in A, say m
OR
(ii) we can plant maximum number of plants (which are smaller in size) possible in A, say n
(evidently m will be smaller than n)
Which choice will yield more amount of oxygen?
It can be assumed that the total number of leaves capable of Photosynthesis is N and is same for both the cases.

The largest amount of Carbon-di-Oxide to Oxygen conversion in the world is done by single celled ocean phytoplankton (I think I saw in some documentary)

Hard to plant them on land, though :-)

I once read a study (but I don't remember the reference) that shows that you need a diversity of plants of different size to maximize the rate of oxygen production. I think, the rational behind this observation is that having a diversity of plant size increases the surface contact between leaves and air.

Welcome to Biology S.E! If you need additional assistance, please visit The Help Center. This looks like it maybe a homework question; if it is then please show any work you have already done or what you think the answer may be.

@Remi.b It could also reduce intraspecific competition.

@L.B. I don't see from which angle it appears as a H.W. problem to you. I thought of this question long back, as an optimization problem. But I could not think of a solution, since I thought I lacked some specifics which might be important inputs from biological view-point.

@DevashishSingh Okie, my apologies! I was concerned that it was due to the wording.

one word, algae.

I think it should depend on the number of autotrophs and kind of plants you are asking about?

It's hard to generalize, you need to experimentally determine it.

Ignoring parameters such as:

Leaf shapes
Difference in photosynthetic efficiency due to other metabolic factors
Unequal illumination of leaves
Nutrient content of the soil

Photosynthesis rate of a plant1 depends on the [total number of leaves] × [surface area of a leaf].
Assuming that a tree occupies same ground area as a shrub, there will be same number of trees as shrubs.
A tree is taller and can bear more number of leaves and if we assume that the surface area of the leaves are similar between trees and shrubs then the tree would carry out more photosynthesis.
However you say that the number of leaves is the same; in this case both will carry out same amount of photosynthesis (the shrub may outlive the tree though, as the latter won't be able to support its huge size with same level of photosynthesis as the shrub).
A note on phtoplanktons and algae: One reason amongst a few for why they are efficient at photosynthesis is because the number of photosynthetic cells per volume is higher in them.

1 I am using the term plant to denote all plants. Big trees are called trees and small plants are called shrubs, for convenience.