Energy coupling between two spontaneous reactions? This diagram describes energy coupling between a nonspontaneous reaction (the formation of glutamine from glutamic acid and ammonia) and a spontaneous reaction (the hydrolysis of ATP). I can see that if you add reaction 1 ($\ce{Glu + NH3->Glutamine}$) and reaction 2 (ATP hydrolysis), then the overall ∆G will be negative, and this reaction will be spontaneous.

My question is this: why can’t you add the reverse of reaction 1, which would on its own be spontaneous, to reaction 2? Would that not make an overall ∆G that is even more negative (more spontaneous)? This would be even more favorable than what we got from the energy coupling shown in the diagram. Yet it seems that energy coupling can produce the reaction presented in the diagram. How does the universe know to add the nonspontaneous reaction to the spontaneous reaction rather than the spontaneous reaction to another spontaneous reaction? It seems to me that the latter would be more probable.

Points to bear in mind

That the biological coupling of an energetically favourable and unfavourable reaction (I would avoid using the term spontaneous†) is done through a composite reaction involving all the components of the two separate reactions. The reactants and products are the same as in the sum of the separate reactions — so it is valid to calculate the overall free energy change from the separate reactions — but we are talking about a different reaction or serious of reactions that occur on the enzyme. For example in the glutamate synthetase reaction that you mention there are the two reactions shown below. Gamma-glutamyl phosphate can be considered as an activated intermediate to which the free energy of hydrolysis of ATP has been transferred, rather than dissipated in heat, as would occur in the isolated reaction with inorganic phosphate as the product.

Such coupled reactions are no different from non-coupleld thermodynamically favourable reactions in a cell in that they require an enzyme to catalyse them. They do not proceed spontaneously† because there is an activation energy barrier.  If you regard this as “forcing” a reaction, then the answer to the question you pose in your comment to @VonBeche is ‘yes’. However I would describe it as an enzyme having evolved to ‘permit’ or ‘facilitate’ a reaction. It does this by providing binding sites for the substrates and (often) a different reaction pathway that involves a lower activation energy.

So why no reaction Gln + ATP ➞ Glu + NH3 + ADP + Pi ?

This can be regarded in two ways.
(1) Why hasn’t an enzyme evolved to do this sort of thing?
Either there is no selective pressure on an organism for an unneccesary enzyme to evolve, or (in this case) if the organism needs an enzyme to deaminate glutamine one evolves, but this enzyme (glutaminase) doesn’t need to involve ATP as the reaction is already thermodynamically favourable.

(2) Why doesn’t the glutamate synthetase enzyme catalyse this reaction
From your comment, this seems to be your concern. There are three binding sites on the enzyme, one for glutamate, one for ATP and one for ammonia; and I presume you are thinking why can’t glutamine bind to the glutamate site (after all it leaves from there) and react with ATP to form γ-glutamyl phosphate. The answer to this is the chemistry of the reactions shown above. The mechanism of the glutamate synthetase reaction is complex, but at the simplest level the first stage is the nucleophilic attack of the negative acid oxygen (yellow) of glutamate on the γ-phosphate of ATP:

In glutamine there is an amino group instead of the negative oxygen, so the reaction will not occur.

Furthermore, you should be aware that the enzyme is an active participant in the reaction, and the various substrates and products are oriented specifically in relation to residues at the active site of the enzyme to allow the reaction to proceed. To give a flavour of this I reproduce a portion of the summary of a paper by Liaw and Eisenberg on the mechanism of action of glutamine synthetase. I don’t expect you (or anyone else) to digest this — it merely serves to illustrate that enzymes are highly sophisticated machines in which many components participate in producing a specific product.


Is the glomerular filtration rate, per kidney or for both? We say in a healthy human being the average glomerular filtration rate is about 120 mL/min. Is that for both kidneys together (60+60), or just one kidney?

Pardon me if this makes me sound like an idiot, because I have a feeling I'm thinking about this wrong.

The definition of GFR given in Wikipedia -

  Glomerular filtration rate (GFR) is the volume of fluid filtered from the renal (kidney) glomerular capillaries into the Bowman's capsule per unit time.

Since it is difficult to measure the volume entering into each Bowman's capsule, as a proxy, we measure the clearance of a solute that we know isn't going to be absorbed or secreted. For that particular solute,

GFR = (Urine concentration x Urine flow)/ Plasma concentration

The GFR you obtain here is the sum total of volume of all the fluid filtered from all the renal (kidney) glomerular capillaries into all of the Bowman's capsule per unit time.

Obviously, a single Bowman's capsule can't receive 120ml every minute, it is microscopic!!

So yes, the GFR or eGFR we use in clinical practice is the sum total of the function of both the kidneys. In fact, before transplantation, although the left kidney is preferred from the donor (since it is easier for surgery having a longer renal vein), it is more ethical to estimate individual GFR for each kidney and preserving the better functioning kidney. And yes, the total GFR drops after donating a kidney, but the body has sufficient reserve to manage.

If you still have a tough time figuring that out, think of them as many separate taps opened to fill a bucket. One tap for each glomerulus. The net rate of flow is the sum of flow rate in all the taps. The kidney has million such taps! And the taps are being clogged one at a time in chronic kidney disease - decreasing the GFR. And in a transplant, half the taps are suddenly shut down in the donor! But since this is a healthy kidney, the donor adapts and slowly reaches ~70% of original GFR.


What is the reason behind studying seroprevalence of a disease? Scientific literature on viral disease, specifically ones like Zika and Dengue, contains seroprevalence data. What is the reason behind understanding seroprevalence?

Seroprevalence tests people for the presence of a disease based on serologic methods. Often you do ELISA (or related methods) to test for pathogen specific antibodies.

This gives you information on how common a disease is, especially when it might infect people without them showing symptoms. It also can help detecting cross-protection when the seroprevalence is lower than expected. This is something shown in micronesia, where the seroprevalence was much lower than expected (from: Zika Virus Seroprevalence, French Polynesia, 2014–2015)

  Our findings show that <50% of the population of French Polynesia had
  detectable Zika virus IgG. This seroprevalence rate is much lower than
  the 86% attack rate estimated by Kucharski et al. (14) using a model
  that assumed the French Polynesia population was 100% susceptible to
  Zika virus infection. However, in a setting where DENVs are highly
  prevalent (8), the possibility of cross-protecting immunity preventing
  infection from Zika virus (12,13) cannot be excluded. The attack rate
  and the asymptomatic:symptomatic ratio in French Polynesia were also
  lower than those described for the 2007 outbreak on Yap Island (73%
  and 4:1, respectively) (4); this finding supports the perception that
  the drivers of Zika virus transmission vary depending on geographic
  context. For other flaviviruses, such as DENV, previous model-based
  studies showed that the herd immunity threshold required to block
  viral transmission is ≈50%–85% (15). Thus, if Zika virus has the same
  epidemiologic characteristics as DENV, the seroprevalence rate of 49%
  would not be sufficient to prevent another outbreak.

It can also help to make predictions about the spreading of a disease. With a high seroprevalence epidemic spreading is unlikely, while this is pretty much different with a low prevalence. This is something which was observed in Brazil when Zika occured there first.


Percentage of mutations caused by radiation? Consider a gamete in a typical human being. In the interest of being specific, let us say that we're talking about a typical ovum in a typical middle class woman living in a developed nation. What percentage, on the average, of the mutations in the genome of that ovum will have been caused by electromagnetic radiation?

You might use the frequency of thymine-thymine dimers to extrapolate the rate of UV induced damage. This has been studied but I couldn't find a paper in human cell lines. It appears different cell lines have different susceptibilities to thymine-thymine dimers. The majority of DNA mutation in healthy people comes from endogenous sources, not radiation. Recombination during fertilization may also contribute significantly to changes in DNA sequence. Wikipedia nicely breaks down some of the different sources of mutation.

Manifestations of mutations from endogenous sources is measurable as our bodies become genetically more chimeric with time. Regions of our bodies become deferentially susceptible to disease due in largest part to errors in DNA repair and replication, unrelated to electromagnetic insult.

Damage due to UV radiation, like the creation of a thymine-thymine dimer, can be repaired readily by base excision and replacement. While DNA is dividing, it is cut many times to allow the molecule to unwind. Single strand breaks resulting from DNA damage have robust mechanisms for repair. For example, when a thymine-thymine dimer is excised or single strand break is otherwise introduced, enzymatic recognition makes identification of a template for repair possible. It is also very unlikely in a single strand break that another break will occur in the same location, decreasing the mutation effect of UV.

Double strand breaks and errors in DNA replication are intrinsically more permanent as a substituted base is chemically indistinguishable from any other of the same type. Much of the new genetic information introduced into any mammalian genome comes from endogenous sources, not the environment.

Error rate of human DNA polymerase
Deamination is a major contributor to mutation rate


Is it dangerous to rub closed eyes? Phosphene from rubbing the closed eyes where first described at least since Ancient Greece, but I caught myself thinking that I wouldn't want to try it out. So I wonder, how safe it is to actually rub closed eyes or put pressure on the human eye in general? Can frequent but small, or rare but sharp, application of pressure cause myopia or other eye disorders? What is the maximum pressure before the eye is damaged? What happens with the eye if you accidentally hit it?

I remember several times during my childhood accidentally poking myself in the eye with a finger—the experience was very uncomfortable, I couldn't even open the eye for several minutes, but I don't think anything happened to my eyes since then, and my myopia was probably caused by any other factor than pressure damage.

The answer is both yes and no, depending on how often and how hard one rubs his or her own eyes.

Occasional light rubbing is not a problem-- it stimulates tear production and relieves stress by lowering heart rate via the oculocardiac reflex.

Frequent hard rubbing is a problem-- it can worsen eyesight in people who already have progressive myopia, and worst-case-scenario lead to retinal detachment. For those with glaucoma, can interrupt blood flow and even cause nerve damage. It can (but rarely) scratch, tear, or deform the cornea leading to pain and distorted vision. It can lead to damage of small delicate vessels, causing a subconjunctival hemorrhage, which is benign despite its worrisome appearance.

It is generally recommended to just avoiding rubbing the eyes altogether!

References:

www.abc.net.au/health/talkinghealth/factbuster/stories/2012/09/18/3592456.htm
http://www.visioneyeinstitute.com.au/dangers-rubbing-eyes/


How do proteins perform their function I have asked a question on physics stackexchange, but was redirected here. I copy the entire question word for word. The original is here.

Let's, for example, take a ribosome. It is an enzyme that is in turn just a molecule that must follow the laws of physics.

Correct me if I'm wrong, but it can be looked upon as a molecular machine made up of several pieces. What exactly makes those pieces work together?

Why does the ribosome bind to a strand of RNA? Is it just the shape and electric charge or is it something more? Once the ribosome is bound to a piece of RNA, how does it move?

In a way, I'm looking for the "ghost in the machine". I'm interested in molecules in general, not just ribosomes. What is it that, on a level of single atoms, makes molecules "alive" - move, assemble a protein, etc. ?

PS. I'm having trouble phrasing my question, so if anything is not clear, please leave a comment and I will address it.

Edit 1: This is most definitely a physics question. I'm looking at the scale of several atoms.

Let me give a hypothetical example:

Imagine a strand of carbons. Also imagine that there exists a molecule that can move along this strand. How would it do it? What forces would move it along this strand? Is it electromagnetism? Would gravity be involved to a significant degree? What effect would shape have?

Does this make the question clearer?

This question is waaaay too broad, but I'll give some short and simplified answers to the hypothetical you asked at the end. First, let's reformulate your example a little bit:

How does the ribosome move along a strand of RNA?

How would it do it?

By hydrolyzing GTP and somehow coupling the free energy associated with that reaction to forward motion. Keep in mind that both ribosome and RNA are constantly undergoing random-walk Brownian motion (ie jiggling), so it's more a matter of biasing the ribosome's motion in a particular direction than it is of moving the ribosome in the first place.

What forces would move it along this strand?

The current understanding of molecular biophysics, which is by no means complete, says that the primary driver of this sort of protein activity is electrostatic forces.

Is it electromagnetism?

There are no electric currents, per se, so magnetism does not play a role.

Would gravity be involved to a significant degree?

At these scales gravity does not have a significant effect.

What effect would shape have?

Shape has an enormous effect. One of the fundamental axioms of molecular biophysics is that function follows form. The 3D configuration of those electrostatic forces I mentioned is determined in turn by the 3D configuration of the involved macromolecules.

If you want to know (a lot) more about this specific question, and if you have access to journals, check out this review: How Should We Think About the Ribosome?


Why is it harder to sequence plant genomes than animal genomes? Plants seem to be less complex organisms than animals, but despite that there are less plant genomes sequenced. Is that because plant genomes are more complex, for example in terms of regulatory regions and transposons that make sequencing more difficult, or are there other reasons why the number of sequenced plant genomes is smaller than animals?

The authors of this 2012 review article summarize the problem well in their introduction:

  In contrast to the tremendous advances in throughput, assembling sequencing reads remains a substantial endeavor, much greater than the sequencing efforts alone would suggest [22-24]. Large complex plant genomes remain a particularly difficult challenge for de novo assembly for a variety of biological, computational and biomolecular reasons. Plant genomes can be nearly 100 times larger [25] than the currently sequenced bird [26], fish [27] or mammalian genomes [28]. In addition they can have much higher ploidy, which is estimated to occur in up to 80% of all plant species [29], and higher rates of heterozygosity and repeats [30] than their counterparts in other kingdoms. Furthermore, the gene content in plants can be very complex, as shown by the presence of large gene families and abundant pseudogenes with nearly identical sequences derived from recent whole genome duplication events and transposon activity [13]. Plants tend to have high copy chloroplasts and mitochondria organelles, which complicate assembly of their remnants in the nuclear genome and skew coverage levels [12]. Finally, it is often very difficult to extract large quantities of high-quality DNA from plant material, making it difficult to prepare proper libraries for sequencing.

From: Schatz, Witkowski and McCombie. "Current challenges in de novo plant genome sequencing and assembly". Genome Biology (2012). 13:243

As you can see, all of the key reasons have been touched on by the various people who have commented below your question.


What are the constraints when growing an artificial brain? Are there any experiments on growing artificial brains from brain tissue?

What are the constraints? Will such tissue grown to the mass greater than that of human brain surpass it in intellect or it would need additional conditions?

The comments above are quite relevant -- we are years / decades away from growing functional brains in the lab, so there are probably innumerable constraints that we have likely not even thought of yet.

That being said, you might find this paper interesting: "Adaptive flight control with living neuronal networks on microelectrode arrays" [1]. The authors are able to succesfully culture rat neurons and electrically interface with them in order to control pitch and yaw in the XPlane flight simulation software.  It's a very crude system compared to an actual brain, but it's able to successfully use cells as rudimentary living neural networks. If you consider this to be a successful "artificial brain," then your constraints are all the ones associated with culturing neurons.

[1] DeMarse, et. al 2005


What does "optimal balance of biological control" mean in nematodes? I have been reading several articles on nematode life-history for my insects class. Several articles say that Entomopathogenic nematodes(EPNs) are the only nematodes possessing an "optimal balance of biological control attributes". What does this mean?

It is a long-winded way of saying that these are the only nematode genera that are useful for biological control. In particular the article is referring to Steinernema and Heterorhabditis, both of which genera are used for control of some pest insects.


Can pheromones in perfume be formulated to cause agitation? I generally don't care for female perfume. I have very sensitive olfactory receptors and in general, I just find perfume overwhelming.

A couple weeks ago, my wife of almost 14 years and I were shopping. As has happened many times before, she asked me to smell a perfume (Play it Rock by Playboy) to see if I liked it. Shockingly, on first whiff, though still overwhelming, I quite liked it. So she bought it.

Now, when she wears it, I do find the aroma pleasing, however I find myself getting quite agitated, depressed and even overcome with jealousy and paranoia.

Obviously, there are lots of psychological factors in play :

Perfume's primary purpose is to arouse and attract men
She almost only uses it when there are going to be other men around
It is playboy, subtly indicating the promotion of promiscuity

However my internal reactions are so intense I can't help but conclude there something more physiological triggering/intensifying them.

Could the perfume's pheromones be slightly misformulated to cause
this reaction?
Would the same pheromones that arouse a man also inherently trigger the fear of the arousal of others?
Is it possible that my pheromone "sense" is also heightened like my sense of smell, causing an abnormal reaction specifically in me?

Note : I can't find official documentation that the playboy perfumes apply pheromonology (Yes, I did just make up that word), but I have found them listed by other sources in sections of perfumes that do, but Playboy perfumes seem to be priced drastically less than the rest of the pheromoned perfumes.

Insects generate and respond to pheromones. But despite what sci-fi TV might have told you, there is no evidence that humans make or respond to pheromones like that.  Humans don't have that good sense of smell, for one thing.

The fact that you know it's a Playboy brand of perfume is affecting you?  That's obviously not chemical, is psychological.

Also, historically, perfume was used just as much to mask unpleasant odors as it was to attract anyone.  When men go through puberty, their sweat changes odor.  That's not to attract other men.

If this perfume is affecting you emotionally it's psychological, not chemical.


Can domestic breeding be considered evolution? Domestic breeding of animals (and plants) by humans seems to match some of the definitions of evolution I have been able to find:

"a process that results in heritable changes in a population spread over many generations." (the TalkOrigins website)
"cumulative inherited change in a population of organisms through time leading to the appearance of new forms" (Merriam-Webster)
"Changes in the heritable attributes of populations of organisms over time" (this SE's 'evolution' tag info)

But other definitions seem to be less of a fit:

"the way in which living things change and develop over millions of years" (Cambridge)
(domestic breeding does not take millions of years)
"The process by which different kinds of living organism are believed to have developed from earlier forms during the history of the earth" (Oxford)
(Does breeding lead to different 'kinds' or organisms?)
"The gradual development of more complex organisms from simpler ones" (Chambers)
(Breeding may not result in more complex organisms)

I've seen people argue that domestic breeding can not be considered evolution, because domestic breeding:

does not involve natural selection
doesn't direct towards 'fitness'
does not lead to new species
decreases, rather than increases, the size of the gene pool (is this actually true?)
does not (or may not) lead to more complex organisms

I was not able to find whether or not there is a general consensus among experts from relevant fields on whether domestic breeding can be considered evolution. Is there?

EDIT: I've made the list of arguments I've heard against calling it evolution a bit clearer, and also added an extra one.
EDIT 2: Added why the second set of definitions seem to exclude domestic breeding as evolution

Yes, selective breeding results in evolution.

Definitions of evolution

I don't understand why you say that for 3 of the definitions you found, selective breeding would not be considered as evolution. To me, all of these definitions match with the idea that selective breeding results in evolution. If you think otherwise, can you please explain why?

There are a number of related definition out there, some of them being more clear and straight forward than others. The simplest definition is probably the classical population genetics definition which says

  Evolution is a change in allele frequency over time.

See wikipedia > allele. You might want to have a look at How to define evolution? too.

Under this definition, any event of death or birth in a population is evolution as it affects allele frequency. In the human species for example, that means an evolution happens about 254 times per second (computed from these numbers from ecology.com)!

Specific statements

All these statements are stupid and none-sense! The easiest is probably for you to just have a look at an intro course to evolutionary biology (such as Understanding Evolution by UC Berkeley for example) and you will be able to refute those statements yourself.

Let's go through these statements...

  There is no natural selection

First, evolution is much more than just natural selection. There is genetic drift, mutations, gene flow and plenty of interacting processes.

Second, it is silly to separate natural selection from artificial selection (aka. selective breeding). The only difference between these two is that in artificial selection someone is willingly affecting the environment of the individual to affect selection pressures. This is really it.

Note, btw, you never totally get rid of natural selection. Under selective breeding you may affect the environment but some things will remain the same. For example, a mutation causing the cell membranes to be extremely unstable will not be selected for whether under an artificial setting or a natural one.

  It doesn't direct towards 'fitness'

The claim is unclear. What is "it" and assuming it refers to a population, then what does it mean a population is directing toward "fitness"?

Fitness is a function of survival and fecundity. Each genotype is associated to a particular fitness in a specific environment. Ignoring stochastic processes such as genetic drift, the mean fitness of a population is increasing from one generation to the other by the amount of the additive genetic variance. This is true for (artificial or natural) selection.

The only thing to consider is that the environments under which this happen is different. Under selective breeding, the population evolves to a higher fitness for the specific environmental conditions set by the farmer (or who ever who selectively breed). It is possible (and quite common in fact) that genotypes associated with a high fitness under one environment has a low fitness under another environment.

  It does not lead to new species

In short, 1) it does lead to new species 2) the concept of species is often meaningless as poorly defined 3) evolution > speciation. In more details, below..

It does lead to new species. Different lineages of cabbage are considered different species. Cows and ox are different species. Pigs and boars are often considered different species. While wolves and dogs are considered same species, some lineages within this species (such as a Chihuahua and a Great Dane) are, I think, reproductively isolated. You might also want to have a look at the post Have we ever observed two drosophila lineages that evolved reproductive isolation in labs?
The question of whether selective breeding lead to speciation or not does not matter much on the question of whether it leads to evolution. Speciation is one outcome of evolution but is definitely not the same as evolution. Evolution does not need to lead to speciation. For example, evolution of the lactase gene in humans (see this post) did not lead to any speciation. It is still an evolutionary process.
The concept of species is mainly arbitrary. If you want to understand the concept of species, have a look at the post How could humans have interbred with Neanderthals if we're a different species?.

  It decreases, rather than increases, the size of the gene pool (is this actually true?)

The term "size of the gene pool" is very undefined. I suppose, it just means genetic diversity, aka. expected heterozygosity.

All act of selection, whether artificial or natural, decreases genetic diversity. This is correct. Mutations is the fundamental process increasing this genetic diversity and selection selects the variants associate with the highest fitness.

Because, the selection pressures imposed under selective breeding are often extreme, the decrease of genetic diversity via selection is often faster in selective breeding than in nature.

Note however, that if we split a lineage in two and select the two populations under different optimas, then the total genetic diversity will increased (the within-population genetic diversity will still decrease). As such, via selective breeding we created a gigantic diversity of dogs and a fantastic diversity of cabbage but each cabbage lineage (e.g. brussel sprouts) and each dog lineage (cocker spaniel) have very low genetic diversity.

What the claim is suggesting is that because selection is often stronger (and therefore change in allele frequencies is faster) under selective breeding than in natural environments, we should not consider artificial selection as resulting in evolution? How silly is that!


Why is it difficult for germs to jump species? If you haven't watched CGP Grey's video Americapox: The Missing Plague, I suggest you watch it. It's an excellent video.
One assertion he makes is that "germs jumping species is extraordinarily rare [...] being the patient zero of a new animal-to-human plague is winning a terrible lottery."
Why is this true? Why is it so rare for a germ to move from a cow's body to a human's? Is it because it can't travel that distance while remaining alive? Is it because the human's immune system will kill it? More details will be appreciated.

The main reason is the biochemistry of two unrelated species are different. The more closely related two species the more similar things like the hormones and signaling molecules will be and inversely the more distantly related they are the more different those things will be. Even highly constrained molecules like hemoglobin may still pick of mutation that get carried on, and things like an immune system actually favor variation evolutionary speaking. Even within the same species these things vary, and this is often cited as a possible reason sexual reproduction exists at all, to make each individual slightly different, so there is less chance of catching disease or parasites from others.
Animals have many many barriers to infection, getting pass all of them is hard and tends to only occur with organisms that evolve alongside that animal and thus have been selected to get pass that specific combination of barriers. Getting past them all if you have not been evolving along side it is incredibly unlikely, some diseases manage it be cause there are billions of them, and if you run billion upon billion of random keys through a lock some may fit just due to chance. this is also why disease transfer is more likely the more closely related species are. SIV/HIV easily jumps between great apes because they are very closely related (and the insist on eating each other) the chances of a dog catching it are astronomically unlikely because the chances of the viruses surface proteins matching receptor proteins of a dog is basically only chance as there has been no evolutionary pressure to alter it.


What is holding the immune system back to not attack human body cells? There are plenty of loose proteins or other macromolecules free floating everywhere. Why wouldn't they be seized and presented to T cell to trigger an immune response? Does each of these molecules have a signature portion? Or do the presenter cells have some sort of friendly molecule database? Would a normal person's immune system ever possibly generate something like Tocilizumab, i.e. an antibody targeting a normal receptor in most cells?

The immune system of human body can keep human health from disease, but for many people, the immune system is the cause of disease. When the autoimmune system is in disorder, healthy cells and tissues will be killed as viruses, which will lead to a variety of immune system diseases.

Recently, scientists in the United States have discovered the genome that causes the disorder of the human immune system, which is equivalent to the "middle manager" of the immune system. This discovery is likely to bring new hope to the treatment of human immune system diseases, which has been published in the latest issue of nature.

Self defense system out of control immune cells "killing each other"

In the human immune system, a kind of immune cell named T cell is responsible for directly contacting and resisting the invading pathogen. Whether these cells can function normally is controlled by "regulatory T cells". Simply put, "regulatory T cells" are like a "double-edged sword", which can not only prevent T cells from attacking human body's own healthy cells indiscriminately, but when its regulation fails, it will cause immune cells to "kill each other" to normal cells, and its consequences usually include inducing type I diabetes, multiple sclerosis, lupus erythematosus and other immune system diseases.

Scientists have previously found that whether "regulatory T cells" can work normally is related to a major regulatory gene called Foxp3. If Foxp3 is dysfunctional, the human body will lack the active "regulatory T cells". But scientists don't know how Foxp3 controls "regulatory T cells.".

Richard young, a biologist at Whitehead Biomedical Research Institute of Massachusetts Institute of technology and Alexander Marson, a doctor of medicine, and other researchers recently discovered 30 genes directly regulated by Foxp3. It is by combining with these specific genes and regulating their activities that Foxp3 can complete the control of "regulatory T cells". If Foxp3 is the "boss" of the immune system, the 30 genes found in this study belong to the "middle manager".

Immune system diseases are related to the damage of "regulating T cells"

Researchers point out that ten years ago, it was found that the "regulatory T cells" in the human body are responsible for directing the immune system to resist foreign invasion, and the question is why the immune system that should protect health attacks its own cells. Now it has been found that there are gene defects in "regulating T cells" in the body with autoimmune disorder.

When "regulating T cells" cannot guarantee the normal operation of the immune system, the immune system begins to attack cells that should not be attacked. When the "regulatory T cells" were destroyed, several organs of mice developed serious immune system diseases. In some common human immune system diseases, such as multiple sclerosis, there is not no such "regulatory T cells", but there will be some dysfunction. In other words, "regulating T cells" failed to play its due role.

What is the problem of "regulating T cells"? "Studies have shown that when the immune system is disrupted, the activity of these genes is lower than normal. It is this reason that makes the activity of "regulatory T cells" decline, leading to its failure to work properly. Three years ago, scientists have found the main gene controlling "regulatory T cells", which is called Foxp3.

The researchers used DNA biochip technology to scan the complete genome of T cells and map the genes regulated by Foxp3. In the process, the researchers identified 702 Foxp3 binding sites. Until the discovery, the researchers admitted, they had no idea how Foxp3, the main regulator, dictated "regulating T cells.".

Anti rejection treatment for organ transplantation

The latest research shows that the "middle managers" of these 30 immune systems are not working properly. Because "regulatory T cells" are controlled by these specific genes, it can be said that most of the immune system diseases such as type I diabetes, lupus erythematosus, multiple sclerosis, rheumatoid arthritis and so on are determined by these genes.

The next step, the researchers say, is to determine how the 30 specific genes "dictate.". It has been found that these genes are closely related to each other and usually work together to control T cells, but the specific mechanism is still unknown. On the other hand, we should look for chemicals that can simulate the regulation function of Foxp3, the main regulator gene, in order to achieve effective therapeutic immunity.

In addition to the treatment of autoimmune diseases, this finding can also be used for anti rejection treatment in organ transplantation. When performing organ transplantation, once the patient's body rejects the transplanted organ, the operation will fail. Therefore, doctors usually use anti rejection drugs to temporarily inhibit or shut down the immune system.

At present, cyclosporine is mainly used to inhibit the immune system. It can inhibit a protein called activated T-cell nuclear factor (NFAT), which can also be controlled by Foxp3. If necessary, the researchers said, the 30 genes can also be used to "target the target", and the effect of inhibiting the immune system is more obvious.


Help me identify this... plant? fungus? Today I found several of these in my back garden in Sydney NSW, Australia (specifically the north shore). They seem like flowers, except I don't see any attached plant and they have a weird brown goo around the mouth. I've never seen anything like this. Any ideas?

After some Googling, it seems maybe this is a stinkhorn fungus, specifically Aseroe rubra.


Do all living humans literally descend from one ape? In the opening chapter of Sapiens, Harari writes:

  Just 6 million years ago, a single female ape had two daughters. One became the ancestor of all chimpanzees, the other is our own grandmother.

Is there evidence that this is literally true? There seem to be two ways in which it could fail:

(a) Weak version---there is an individual last universal common ancestor, but it's not an ape: that is, all humans (and chimps) share a single individual creature as an ancestor, but that creature was not an ape. It was some earlier ancestor whose descendants would go on to be apes.

(b) Strong version---there is no individual last universal common ancestor: if tracing the entire history of life on Earth and assuming some "stopping point" where we saw life emerge as (e.g.) from a volcanic vent primordial soup, we would find distinct creatures emerging simultaneously in a population, with similar but distinct genetic code, from one of whom some species (such as humans) evolved, and from another of whom others evolved.

Is there evidence that neither is the case? First, (1) that there is an individual creature, rather than a population of creatures, from whom all life descended. If that is true, then it follows that all humans have an individual as a common ancestor, since you can at worst follow the line of descent back to the primordial individual. And, next, (2) that the last common ancestor of all humans (and chimps) was also an ape, rather than say some other animal.

Just 6 million years ago, a single female ape had two daughters. One became the ancestor of all chimpanzees, the other is our own grandmother.

Short answer
Whether or not the claim is true actually depends upon the specific DNA sequence you are considering. The claim is true for sequences without recombination (such as mtDNA and most of the Y chromosome). The claim does not hold true for most of the genome and it is therefore misleading.
Long answer
Basic knowledge required
First, if you don't know the concepts of

allele
haplotype
ploidy
selection
genetic drift
segregation
recombination and crossover

, then you might want to have a look at a short introduction of evolutionary biology such as Evo101 for example. The below answer will make more sense to you with some a priori knowledge.
Coalescence
Imagine there is today a population of $N$ individuals. We are going to look at this population backward in time (which is a little bit unintuitive). For simplicity, we will assume asexual reproduction, no recombination, absence of selection (only drift) and constant population size of $N$ individuals. The assumption of no recombination is key here. The other assumptions are details just to make my job at explaining coalescent theory easier.
We start at time t=0 and are going backward in time. If two individuals are siblings at $t=0$, then, it means that in the previous generation, they share the same parent. Therefore, if we connect individual from generation $t=0$ to their respective parents at generation $t=-1$, we see that some group of individuals (the siblings) "coalesce" to fewer individuals (their parents). Individuals at generation $t=-1$ that are not connected to individuals at generation $t=0$ are those who did not reproduce (or who did not leave offspring that have survived until adulthood).
You can keep iterating over generation $-2$, $-3$, $-4$, etc... At each generation, the number of individuals that are connected (that our ancestors) to present day individuals is diminishing as more and more coalescence happen. After a sufficient number of generations, eventually, only one parent will remain. This single individual will be the ancestor of all present individuals.
If you enjoy math, then note that such process is actually a simple a branching process for which it is relatively easy to calculate the expected time (and the whole PDF) to the next coalescent event and the expected time (and the whole PDF) until all individuals in the population coalesce.
So, assuming no recombination, if you consider individuals in a modern population, then you can be sure that all individuals share a common ancestor who is a single individual, at some point in the past.
Incomplete lineage sorting
The process of all individuals coalescing into a single ancestor takes a little bit of time. For recently diverged species (say species A and species B), it is possible that this common ancestor is older than the time of divergence between species. If this is the case, it is then incorrect to think of a mother who gave birth to two individuals, one becoming the ancestor of all individuals of species A and one becoming the ancestor of all individuals of species B. In such a case, we talk about incomplete lineage sorting.
Note that when we talk about 'incomplete lineage sorting', we are generally talking about specific genes as not all genes coalesce the same way when there is recombination and segregation (see below)
Recombination
Now the trick is that in the presence of recombination, different sequences coalesce differentially. It also means that when you look at two sister species, some sequences can show incomplete lineage sorting while others don't.
The presence of recombination therefore makes the claim false!
Do we recombine?
Yes, all of our genome recombines to the exception of two sequences

mitochondrial DNA (mtDNA)
Y chromosome not including the Pseudo-Autosomal Region (PAR)

mtDNA is maternally inherited (without crossover) and transmitted to all offsprings, while the Y chromosome is paternally inherited (without crossover) and transmitted to sons only.
So, is the claim true?
mtDNA
It is true that there was an ape who had two daughters. One daughter's mtDNA became the ancestor of all mtDNA we have in humans today, the other daughter's mtDNA became the ancestor of all mtDNA that exist in chimps populations today.
Of course, this daughter is the common ancestor of all modern mtDNA but is not necessarily the Most Recent Common Ancestor (MRCA). In humans, the MRCA to all modern mtDNA is called Mitochondrial Eve (mt-Eve or mt-MRCA).
Y Chromosome
The same claim is true for the Y chromosome (although I am not sure there was really not a single recombination event happening on the Y chromosome since). The MRCA to today's all Y chromosome is sometimes called Y-chromosomal Adam (Y-MRCA).
The names 'mt-Eve' and 'Y-chromosomal Adam' have of course been chosen in reference to the creation myth of Abrahamic religions.
Rest of the genome
The Y chromosome and mtDNA together represent less than 0.2% of our genome. The rest of our genome does recombine.
The claim does not necessarily hold true for 99.8% of the genome. I would therefore tend to think that the claim is misleading at best, wrong at worst.
Adam and Eve
We can call Adam the MRCA of all Y chromosomes today. Only Y chromosomes, not the rest of the genome. We can call Eve the MRCA of all mtDNA today. Only mtDNA, not the rest of the genome.
Of course, Adam and Eve did not live in the same time period and did not live at the same place. Adam and Eve never met. And of course, there were plenty of other humans around. They are in no way the first two humans.
Other popular source of knowledge
PBS Eons - The Two People We're All Related To


Understanding Membrane / Resting Potential from the perspective of ions? From wikipedia article RESTING potential: "there is no actual measurable charge excess in either side. That occurs because the effect of charge on electrochemical potential is hugely greater than the effect of concentration so an undetectable change in concentration creates a great change on electric potential."

the effect of charge on electrochemical potential significantly larger then the effect of charge on concentration - is this a general statement or true in all cases?

And if charge is more significant then concentration in influencing electrochemical potential why does a small change in concentration greatly effect electropotential? Or does it mean electrochemical potential? Either way how does it make any sense, is it correct or nonsense and what is the exact meaning behind the message?

other questions I have:

1) What is the reason Na+ stays at its location right across the barrier on the extracellular side of the membrane? Diffusion? Electrochemical potential? Electric Charge.. if so because of Attraction or Repulsion?

2) If the answer is the electrochemical gradient/potential, because it is trying to move to a "less" positive potential.. if its located extracellularlly isn't that the "great unknown" where any molecules/cells/protein etc. are able to float by and possibly influence it? What happens if one of these has a "LESS" positive potential then the membrane that Na+ is currently attracted?

3) Why can't Na+ be used for the entire process to establish the same voltage interactions leading from resting to action potential (as long as thier was less concentration intracellularly... if it is about LESS positivity ..Or vice versa for K+?)?

I am preparing for ACSM certification exam, so any help is appreciated.

Ah, what a classic biophysics problem.

One first needs to understand how a membrane gets a potential. The lipid bilayer is a large sea of hydrophobic interactions that essentially prevents any ion from crossing. As a result, Na+ and K+ concentrations remain constant and different on the cytoplasmic side and the extracellular side. However, ions can pass through ion channels like the K+ channel. It is important to understand that in K+ channels, only K+ can pass and these channels are actually selective against Na+ (answer to question 1).

There are two potentials at work here. First is a chemical potential created by the flux of K+ from high K+ to low K+. The second is a counteracting membrane potential created by a charge imbalance. Note, that the swapping of a few ions will a) result in a negligible change in the concentration ie. the chemical potential, b) result in a large change in the membrane potential. At some point, the flux out due to the chemical potential and the flux in due to the membrane potential will be equilvant and the cell will reach a resting potential otherwise known at the Nernst potential or equilibrium potential (technically a steady state).

When a cell depolarizes by closing these channels, the local charge will quickly go back to an equilibrium or a non-charged state.

So why K+ rather than Na+? For typical cells, the extracellular concentration of Na+ is 145 mM and cytoplasmic is 12 mM. For K+, it is 4 mM and 155 mM respectively. Doing the appropriate calculations of the Nerst potential, for Na+ it is +67 mV and for K+ it is -98 mV. Qualitatively we can see that this would result in vastly different things.

Most of this information can be found from Pollard and Earnshaw's Cell Biology


difference between neurotransmitters and hormones I have been reading a lot about neurotransmitters and hormones but what's the difference between them both or are they the same? It's been confusing for a while now. Also, why do some neurotransmitters act as hormones?

At heart, the distinction between neurotransmitters and hormones is how they are transmitted - not necessarily a difference in the chemicals themselves.

Neurotransmitters are sent over synapses, between neurons. They may be small molecules (e.g. dopamine) or larger molecules such as proteins (e.g. substance P). Conversely, hormones are sent through the circulatory system but could also be small molecules (e.g. adrenaline) or large molecules (e.g. growth hormone).
Looking at the structures of these chemicals, we can see that both neurotransmitters and hormones have an enormous variability in the chemicals they involve. Furthermore, dopamine looks much closer to adrenaline than it does to substance P. But dopamine is primarily a neurotransmitter and adrenaline is typically thought of as a hormone!
There may also be overlap between roles of chemicals as neurotransmitters or hormones. In fact, adrenaline may act as both a neurotransmitter and a hormone. So, to answer your question of "why do some neurotransmitters act as hormones?" - the distinction is in the context of how the chemical is sent through the body. There's variability in which chemicals are used for either purpose, and no rule saying a chemical can't be sent via multiple mechanisms.

Furthermore, neurotransmission also involves spillover of neurotransmitter, which in theory could find its way into the circulatory system. So there could be overlap between neurotransmission and hormone signaling. And lastly, as @Remi.b points out, the particular mechanisms of neurotransmission and hormone signaling have implications on the dynamics of the signaling.


How does allele dominance work in polyploid organisms? You know how there are tables to demonstrate allele dominance in diploids, such as the table found in this question?

Well, I was wondering how this works with tetraploids, hexaploids, octoploids, etc.

One might assume that you would need a four-dimensional table for tetraploids, a six-dimensional table for hexaploids, and an eight-dimensional table for octoploids.

One might assume that if you have an octoploid with a gene that has one dominant allele and seven recessive ones that the dominant trait would be expressed.

One might conclude that recessive traits would be expressed a lot less often in octoploids than in diploids in a population that commonly has both kinds of alleles.

Are all three of these assumptions correct? If not, what is the truth?

Dominance works in the same way.

However, polyploids have complex inheritance patterns!

1. Punnett square for polyploid inheritance

  One might assume that you would need a four-dimensional table for tetraploids, a six-dimensional table for hexaploids, and an eight-dimensional table for octoploids.

The table you mentioned in this case should be the Punnett square. And its two dimensions correspond to two types of gametes that fuses in sexual reproduction. So even if you want to utilize Punnett square to work with tetraploids, hexaploids, or even octoploids, you still use a two-dimensional table because there are only two types of gametes involved. The fundamental difference is that you have to assign combinations of alleles to the first row and first column of the table instead of a single allele as you would do with a monohybrid cross.

However, deciding what combinations are allowed will be really intricate in this case, depending on two different factors: pairing behavior during meiosis and the resulting chromosome segregation. Variations in those aspects make general rules for polyploid inheritance impossible. In extreme cases, we can consider the organism to be either fully autopolyploid or allopolyploid.

An autopolyploid has more than two complete copies of the genome of a single ancestral species, and in the extreme case we consider the chromosomes have multivalent formation during meiosis and undergo unbiased segregation.

An allopolyploid has more than two complete copies of the genome derived more or less complete from different species, and in the extreme case we consider the allopolyploid has strictly bivalent formation between the chromosomes of a common origin.

This is a monohybrid cross, and it seems familiar and boring, right?

The following pictures depict how to use Punnett square with a tetraploid with two different alleles at a certain locus, and they are really captivating...

In this final picture you may find that the cross has "degenerated" into a monohybrid cross. If we try to depict something more complex, like a tetraploid with four different alleles at a single locus, we will obtain resultsvery different from normal crosses for diploids.

2. Dominance in polyploids

  One might assume that if you have an octoploid with a gene that has one dominant allele and seven recessive ones that the dominant trait would be expressed.

This is true based on the definition of dominance:

  Dominance in genetics is a relationship between alleles of one gene, in which the effect on phenotype of one allele masks the contribution of a second allele at the same locus.

3. Recessive traits in polyploids

  One might conclude that recessive traits would be expressed a lot less often in octoploids than in diploids in a population that commonly has both kinds of alleles.

For this one, you cannot simply assume it because as I've said above, the inheritance patterns for polyploids, including octoploids, can be really complex and dependent on the particular species and the multivalent formation at the particular gene locus you wish to investigate. Thus, it's difficult to predict the the portion of individuals with a recessive phenotype in a population. There are so many intermediate patterns between two extremities of autopolyploidy and allopolyploidy that geneticists have to rely on sophisticated computational models to help them explain the data collected from experiments!

Source:

Rieger, R.; Michaelis, A.; Green, M.M. (1968). A glossary of genetics and cytogenetics: Classical and molecular. New York: Springer-Verlag.
Soltis, Pamela & Soltis, Douglas. (2012). Polyploidy and Genome Evolution. 10.1007/978-3-642-31442-1.


Why does cholesterol need to attach to proteins to travel through the blood? I guess the deeper question is: what makes it possible for proteins like those part of HDL and LDL to move through the bloodstream?

It is not LDL that does the Job. The target cells "know" which lipoproteins (LDL,HDL,VLDL...) they should take up. They express the specific Membrane receptor that binds the Protein part of e.g. LDL and therefore take up specifically LDL rather than e.g. HDL from the blood. Example: cells that express receptors for apolipoprotein B-100 (one of the Protein parts of LDL) specifically "filter" LDL from the blood. The "filtering" occurs via endocytosis. Hope that helps.


A doctor might give bicarbonate (HCO₃¯) to a patient who is breathing very rapidly. What is the doctor assuming about the patient’s blood chemistry? The answer is:

The doctor is assuming that the rapid breathing is the body’s response to low blood pH.
(Source: Campbell Biology)

But this answer doesn't make sense. Why would the doctor give the patient even more CO2 if the patient is already suffering from an excess of CO2 that is causing the low body pH?

if a person is both (1) hyperventilating and (2) has a low blood pH then this is a case of metabolic acidosis... in metabolic acidosis the patient compensates by breathing heavy... why? because hydrogen ions are captured by bicarbonate (the conjugate base of carbonic acid) which is then exhaled as carbon dioxide...

metabolic acidosis is not caused by excess carbon dioxide... this is the case of respiratory acidosis... but under respiratory acidosis the breathing is supressed, however tachypnea with frequent shallow breaths could lead to poor removal of carbon dioxide...

here are some causes of metabolic acidosis:
http://en.wikipedia.org/wiki/Metabolic_acidosis#Causes


Late control mechanisms of blood pressure (arterial) level? I first covered the fast and moderate control mechanisms which I think are

  Fast control: Baroreceptive reflex (tonus), Chemoreceptive reflex
  (CO$_2$).
  Moderate control:  Bicarbonate
  (ECF), Phosphate buffer (ECF), Proteins (ICF).

then late control mechanisms about which I am unsure

Capillary fluid shift mechanisms
Stress-relaxation of the vasculature
RAA

What are the late control mechanisms of blood pressure?

Capillary fluid shift mechanisms

If the pressure of the blood is high, there is high hydrostatic pressure. Simply put, this means fluid exits the capillaries at the arterial side due to this pressure, and less fluid returns at the venous side. With less fluid in the circulation, blood pressure falls.

Stress-relaxation of the vasculature

Imagine the arteries are like springs. The more you pull them the stronger the recoil force. However if you stretch them too much for too long, they stay stretched.

Renin-Angiotensin-Aldosterone system

When the blood pressure is high, there is less release of renin from the kidneys. This means less angiotensin II production. Angiotensin acts to increase blood pressure by increasing vasoconstriction and increasing retention of fluid and salt (via aldosterone). With less RAA system activation, the blood pressure drops.


Can the apparent drop in insect population be explained by local insects evolving to avoid traps? In this widely reported Plos One article, it is stated that, after roughly 3 decades of placing Malaise traps in a set of predetermined locations (counting and replacing them regularly), a sharp decline (roughly 75%) of insect population is observed. The idea is that the amount of insects caught in the traps is a proportionate representation of the insect population.

This seems to be a very important publication. It is getting reported in many popular articles as the most compelling evidence for a massive recent decline in insect biomass.

Maybe I didn't read the article thoroughly enough, but I saw no mention of the possibility that the local population (around where the traps are set) are adapting to avoid the traps. Since getting caught in a Malaise trap is lethal, genes that promote the behavior of avoiding those traps would thrive, in a local population of flies, at a higher proportion than their competitors. And since flies reproduce very quickly, 27 years seems (intuitively, to me) like a lot of time for this new local selection pressure, created by the experimenters, to make notable changes in a local fly population--particularly, their tendency to avoid Malaise traps.

Could the result of the linked article be explained by local flies adapting to the new selection pressure of Malaise traps?

When I first read about the methods with which the insect population drop was measured, this was the first possibility that came to my mind. But I can't find anywhere where this possibility is discussed. Could that be because it's so ridiculous that it's not even worth considering?

From your own PlosOne link comes proof that the selection pressure was very weak:
"Most locations (59%, n = 37) were sampled in only one year, 20 locations in two years, five locations in three years, and one in four years, yielding in total 96 unique location-year combinations of measurements of seasonal total flying insect biomass."

"We collected in total 1503 trap samples, with an average of 16 (4–35) successive catches per location-year combination"

"Between 1989 and 2016, a total of 53.54kg of invertebrates have been collected and stored, over a total trap exposure period of 16908 days, within an average of 176 exposure days per location-year combination."

Wikipedia says about houseflies: "12 generations may occur per year"
https://en.wikipedia.org/wiki/Housefly#Life_cycle
27 years gives 444 generations. That is not a lot of time for evolution, especially with such a weak selection pressure.


What is immunosuppression? Why would one use it? What is immunosuppression? I know it is used in cancer patients, but why would one want to suppress the immune system?

Do homeopathic physicians ever use immunosuppression, or do only allopathic doctors practice this?

Immunosuppression is not used in cancer, in fact it is typically harmful unless of course the cancer is a immune or white blood cell cancer where suppressing their growth may be helpful. What you are perhaps alluding to is that an adverse effect of cytotoxic chemotherapy used in the medical treatment of cancer can cause immunosuppression.

Immunosuppression is helpful when it is causing more harm than good. The immune system is powerful and sometimes when its fighting an infection it can go a little overboard and cause enough damage to harm someone in the long term. In this case immunosuppression is helpful in preventing too high a response. For example in an organ transplant the recipient's immune system may destroy the new organ, but immunosuppression can prevent rejection.

Another case is when there is an autoimmune or inflammatory condition occurring. Rheumatoid arthritis being an example of the former and asthma being an example of the latter. In these diseases inflammation due to the immune system perhaps targeting our own body cells causes damage to our organs or cells and causes the disease. Immunosuppression here can limit or prevent further degradation or sometimes even reverse damage due to inappropriate immune responses.

Interestingly the human body must keep a good balance between being under and overactive. Certain individuals with better ability to control HIV infections or other infections are genetically more likely to also get autoimmune conditions.


Are blood vessels organs? Are blood vessels classified as organs? Organs compose of 2 or more tissues and perform a certain function. Blood vessels have 3 different tissues and perform a function (transport blood), yet I do not see them being identified as an organ. Why is this? Are they organs? Or do they hold their own classification?

I don't know if they are classified as organs, but basically, blood vessels match the criteria for being organs.

Quoting SIU School of Medicine:

  Blood vessels are basically tubular organs found within other organs.

Biology Reference states the same:

  Even the glands within the integument can be considered organs; any gland is primarily secretory epithelium surrounded by connective tissue for support and protection. Likewise, the blood vessels and nerves in these organs are organs unto themselves.


Do I have to use sucrose to induce a lac promoter? I'd like to optimize the expression of a Fab fragment in Escherichia coli.
For induction of the lac promoter on the pAK400 vector I use IPTG and sucrose. Do I optimize the expression in case I would just add IPTG?

You can induce the lac operon by two things: Lactose (or more precisely Allolactose a metabolite of it) and lactose analogons which are not metabolized by the bacteria.

Lactose induces the expression and is metabolized while IPTG is not a target of the $\beta$-Galactosidase and will give you a strong and permanent induction. Sucrose will not have any effect on the promoter.


How long does a mosquito take to land on a host, bite, and fly off? How long does a mosquito take to land on a host, start its bite, end its bite and then fly off?

And what about different species?

I am most interested in human hosts.

References to web sites or books would be appreciated.

I cannot find this even after extensive trawling of Google.

That's an interesting question and not easy to answer. I haven't found data for humans but from experiments with mice. They analysed how the mosquito actually bites, probes for the blood vessels (not all bites are successful) and finally sucks bloods. In their research  they observed feeding times between 150 and 329 seconds, depending on the size of the blood vessel. The mean feeding time was 240 seconds. It also depends on the age of the mosquito, older mosquitos suck longer. To this comes the time for probing (mean time 142 seconds) and the time before the mosquito starts probing after it landed (mean time 6.5 seconds). This totals to about 389 seconds (or roughly 6.5 minutes) total time after landing. This data can be found in table 1 of reference 2.

This is pretty interesting, they also show videos of the mosquito probing the skin for a blood vessel. You can find a pretty nice summary in the first reference and the original paper in the second:

Here’s What Happens Inside You When a Mosquito Bites
Visualizing Non Infectious and Infectious Anopheles gambiae Blood
Feedings in Naive and Saliva-Immunized Mice.


Can any other animal choke on food? I read somewhere (I think it was Bill Bryson's book on the origins of the English language) that of all animals, we are the only ones that can choke on food (having something to do with how our larynx is positioned).  I'm unable to find reference to this fact online, however, and am curious if this is just my having misunderstood something (or Bill having led me astray!).

The veterinarian in our group offers this: For humans, who choke much more frequently than other mammals, it is likely to be a cognitive problem. We talk and eat at the same time and so give ample opportunity to allow food passed the epiglottis and choking. Animals do choke - dogs can, cats can. Not all animals can vomit and this is particularly a problem for horses, whose stomachs will rupture instead of releasing contents through the mouth.


What is meant in biology by the term "evolved"? A student asked me this the other day and I thought that I would ask it again here. If one organism is said to be "more evolved" than another, what exactly does this mean?

"More evolved" is actually meaningless in all contexts. See terdon's answer for a good explanation.

In the strictest sense, an organism can be said to be more divergent than another when comparing both to an outgroup, such that there is an inferred most common ancestor in reference to which to make the comparison. In this case, one organism is more divergent if there are more changes to this organism than the other, relative to the reference point.

However, when speaking, many people get lazy, and use "more evolved" as shorthand, wishing it to mean something like "more divergent". Even "more divergent" is meaningless in the following contexts:

when there is no outgroup understood
when describing increasing complexity (obligate parasites have lost complexity and have had more evolutionary changes than their non-parasitic relatives)
when the outgroup is poorly chosen. Mammal vs reptile comparisons should not, in general, use prokaryotes as the outgroup.

Edited 2013/12/06 to reflect the precision in the answer by terdon.


Is the theory of evolution being disproved by bats? For some species the Darwin's theory evolution makes perfect sense. I can easily imagine how, for example, the giraffe has evolved to its current appearance: the natural selection was favoring individuals that could consume more vegetable food from trees using longer necks, and some individuals were getting at birth necks longer than average by pure genetic randomness and the long neck trait was being propagated to descendant individuals by means of genetic inheritance. I have no problem with understanding this kind of evolution.

Now let's have a look at the bat and its relatives. The bat is one of the few mammals that have something to do with flying and the only one that took flying to the bird level. Paleontologically, first mammals date to the dinosaur era and initially looked similar to the present-day shrew (which looks much like a mouse). The question is: how in the world prehistoric mouse-like creatures could grow wings over time? It impossible to believe that some mouse-like individuals were getting wing-like limbs by mutation and the "wings" were growing out accompanied with the knowledge of how the "wings" can actually be used. Ok, then maybe first wings were tiny moth-size wings and then grew larger? But where natural selection would come into play in this case? Such mouse-like individuals would have no advantage over their wingless relatives and thus would not be able to transfer those wing-growing genes to their descendants, quite the contrary, such individuals with useless mutations that interfere with their ability to walk would be suppressed by natural selection and therefore "weeded out".

So what is the story behind the bat's wings and is the Darwin's theory really able to support it?

Take a look at this little fellow:

It's a flying squirrel — a shy little nocturnal rodent which lives in trees and, despite its name, does not actually fly.  It does, however, have a skin membrane called a patagium between its fore and hind limbs which allows it to glide from tree to tree and thus evade ground predators.

It's not hard to see how the flying squirrel's patagium may have evolved: after all, ordinary squirrels, to which the flying squirrel is indeed related, also spend most of their time in trees and avoid the ground, often performing quite impressive leaps to cross from one tree to another.  With sufficient pressure to minimize time spent on the ground, any little morphological changes that allowed longer leaps would be favored by natural selection.

Indeed, there are plenty of other groups of mammals which have independently evolved very similar adaptations to gliding.  Given how many small arboreal mammals there are, this is perhaps not surprising.  What's special about bats is not the fact that they possess flight membranes — it's that they're the only group of mammals, so far, to have taken the next step to actual powered flight.


Kinesiology Tape Benefits Recently, kinesiology tape has become popular, especially in CrossFit. I have also noted its' use in the NFL, and I want to say Tennis as well.

What beneficial effects does this tape offer our bodies (muscles, joints)?  Is there any definitive proof of its' benefits? Can there be negative effects? I don't foresee any, but if it does something to your body, I could see a possibility of prolonged use causing some kind of alternate effects.

This is in the discussion for quite a while. I have found no scientific studies which back the claims of kinesio tape. A review article (from which the quote below is taken) found no clinically important results which support the claims of the tape. The results about range-of-motion were inconsistant and it is not clear if the changes found were beneficial or not. They state:

  KT had some substantial effects on muscle activity, but it was unclear
  whether these changes were beneficial or harmful. In conclusion, there
  was little quality evidence to support the use of KT over other types
  of elastic taping in the management or prevention of sports injuries.
  KT may have a small beneficial role in improving strength, range of
  motion in certain injured cohorts and force sense error compared with
  other tapes, but further studies are needed to confirm these findings.

The study can be found here (links to the PDF):

Kinesio Taping in Treatment and Prevention of Sports Injuries

Other (also critical) studies are these:

A systematic review of the effectiveness of kinesio taping for
musculoskeletal injury.
The clinical effects of Kinesio® Tex taping: A systematic review.

The problem with these studies is that they are obviously not rigorous enough to make clear statements if KT is beneficial or not. Or (and this is also very possible) that the effect which is claimed to be there does not exist. Besides this, a placebo effect exists very well, since there is an intervention and also something present on the athlete.

There is now a new study avalaible which is blinded and placebo-controlled. This study finds no benefits for Kinesio Tape above a placebo. The study can be found here, there is also a summary available here.


Does DNA react in all of the ways most other acids do? As I understand it from my basic chemistry, there are some fundamental reactions that exist between any acid and other substances for example acid-base reactions that form a salt, and the existence of a state of equilibrium in water.

Do these reactions and equilibria occur to DNA (or, for that matter, RNA), which has only ever been described to me as an 'acid', and does this affect the processes DNA goes through, like replication and transcription?

It may seem counterintuitive that deoxyribonucleic acid has nitrogenous bases. Nonetheless, nucleic acids (thus including RNA) were called that way because the phosphate backbone (linked by phosphodiester groups) is a derivative of phosphoric acid.
Phosphoric acid

Image Source
Phosphodiester group

Image Source
Note that the only difference between these two groups is that in the case of the phosphodiester, two O-H bonds are replaced by O-C bonds. This make the last remaining hydrogen atom quite acidic (can quickly be identified by how the conjugate base exhibits resonance). In fact, it is so acidic that at physiological pH, the phosphodiester group is deprotonated, giving that nucleotide a negative charge. This property does have a profound effect on DNA's structure and "behavior" in a cell, and is often exploited in genetics, such as in gel electrophoresis.
An interesting fact is that this acidity of the phosphodiester group actually competes with the basicity of the nitrogenous bases. However, since most often DNA is double-stranded, individuals bases will hydrogen-bond with its partner to make base pairs, which stabilizes and thus reduces this basicity.
TLDR: Although different acids of different molecular composition can act in very different ways, the overall acid-base chemistry is seen in nucleic acids.


What is the pH of cytosol? And plastids? My teacher ask this question, and I answered 7 to 7.4, but she said it's wrong.
I read a lot and found the same answer (wikipedia)
I'm here asking for confirmation of this and the pH inside & outside of the tilakoidal membrane.

The optimum cytoplasmic pH for performing physiological activities in
plant cells is a neutral pH of around 7.2 to 7.4.
The pH of apoplastic space outside plasma membrane and vacuolar pH is
acidic ranging between 5 to 7.
The thylakoid lumen is more fluctuating which varies during light /
dark cycles and is highly acidic.
The mitochondrial compartment and chloroplast maintains a basic
conditions of about pH 8 for optimization of biochemical reactions
occurring in these two particular compartments.

(Via: https://www.frontiersin.org/articles/10.3389/fpls.2017.02079/full#:~:text=Plastid%20stromal%20pH%20could%20only,cytosolic%20pH%20(around%207.3).


What is inside IDL (intermediate density lipoproteïn)? I am studying about the endogene lipidcycle in the human body and I know that VLDL (very low density lipoproteïn) is made in the liver and that it contains triglycerides and cholesterol from your food but also made in the body.

Next with that, I know that VLDL brings triglycerides to the adipose tissue (or fat tissue) and to the muscles with help of the LPL (lipoproteïnlipase) just as chylomicrons do.

Enclosed; VLDL will go over to IDL (intermediate density lipoproteïn).

But what is the definition then from IDL exactly?
Is IDL just a smaller lipoproteïn then VLDL and does it only contains a sort of 'leftover' of the triglycerides? Or does it also contains cholesterol?

And if VLDL brings the triglycerides to the muscles and fat tissue, does it only contains triglycerides then? Or does it also carry cholesterol with it? If yes, what happens with the cholesterol then?

Because my book is only telling me about the transport of triglycerides to the fat tissue and muscles, but in the beginning it also says that it carry's cholesterol, and a little further in my book it even tells it can also carry cholesterolesters from HDL...
It's getting confusing...

Hope somebody can tell me what is exactly in all the kinds of lipoproteïns, where the lipoproteïns are all made, and where the products they carry come from, and where they go to. Because my book is being very indistinct.

Taken from Fundamentals of Biochemistry (Voet et al. 2013). Note the differences in apolipoproteins between LDL and IDL, as well as the ratio triacylglycerol : cholesteryl esters between VLDL and IDL.


What dragonfly is this? I photographed a dragonfly but can't really identify the species using http://www.libellen.tv/. Are there any other resources I could use?

The pictures were taken in early June, around 11:00 next to a lake at 1700 meters above sea level. The pictures were taken in the Alps in Austria.

This is Libellula quadrimaculata, which is a common and very widespread species (North America, Europe, Asia at least). This is based on the relatively wide and flat abdomen (hard to judge due to the angle though), which suggests Libellula, brown/golden colour and a brownish wingbase. The main problem I have with the pictures (which makes my suggestion more uncertain) is that it is really hard to see the wingspots in your pictures, due to sun glare. Libellula quadrimaculata is one of the few European species that has four wing-spots (hence the english name Four-spotted chaser), which is why the wing-spots are important to see. However, I think I see hints of wing-spots at the middle of the wing (greyish patches on the top picture), which suggests four spots on each wing pair.

Edit
The distinctive four spots vary greatly in size among individuals and though small they are clearly present. The yellowish tint in the wings and the hairy thorax are also distinctive. The shining wings suggest this individual just emerged (from its larval stadium).  Colors may be less distinctive in these young individuals.

There are no similair species.

(picture from wikipedia)

More pictures of the species can be found here


Biological implementation of convolutional neural networks In computer science, 'convolutional neural networks' are used, that are meant to be inspired by biological network structures like found in the human brain visual cortex.

In the computer implementation, the 'convolution' means that any neuron of a certain 'layer' is linked with several spatial adjacent neurons in the previous layer. When those networks are trained, the 'weights', which are analog to synaptic strength, of all neurons of one layer have an equivalent local topology, and thus can be mapped between the neurons, and finally unified. This way, only one 'weight' is trained for all equivalent synapses on all neurons of an layer.

Is there any biological mechanism found that may sport this feature? My guess would be that the vision cortex is partly organised by self structuring not depending on neural activation to achieve low level vision processing. Otherwise, all neurons in one 'layer' would need a way to exchange information to synchronize their synaptic structure.

However, I guess that the human brain would have some mechanism of this kind, as it would provide for example the ability to learn the detection of certain visual patterns or events independent of their retinal position, without learning the detection individually for every image location.

Is any such mechanism known or how could it work?

The eye might provide alone an example of a convolution neural network (as made popular for image classification tasks).

The cell types and synaptic connections in the retina are even organized in layers (laminae) to make the parallel clearer, as seen here:

source: http://webvision.med.utah.edu/book/part-vi-development-of-cell-types-and-synaptic-connections-in-the-retina/development-of-cell-types-and-synaptic-connections-in-the-retina/

The topology of the network is in a sense self-structured but a relatively slow process as the blueprint is a product of Evolution and the practical implementation (actual cells and connections) takes place during the development of the organ. "Weight tying" can then be seen as a result of having different cells types in the network.


Is it painful for the hen to lay eggs? My little son just asked me this question. His mother used to complain about the excruciating pain she suffered when she gave birth to him. He is a compassionate kid and wonders whether the hen goes through this pain everyday. Not being a hen, I am not sure if chickens experience pain that is close to the pain associated with giving birth.

We really don't know - we can't really ask the chicken. At least, it's unlikely it's as painful as it can be with humans.

The reason human birth is (or can be) very painful is that the human baby's head has to fit through the woman's pelvis. Since splitting from chimpanzees, human heads have gotten bigger, while the pelvis has gotten more narrow due to adapting to walking on two legs. While chimpanzees give birth in an average of around 2 hours, humans can take over a day to do so, and the baby being too big can lead to maternal and natal death.

Back to chickens, while there are different sizes of eggs,  the larger eggs come from larger chicken breeds. If it does hurt them, at least it takes a lot less time - only a few minutes. From personal experience, the hens do not appear traumatized even seconds afterwards and just go about their day as soon as the egg is out.


What is a substance that is safe to eat, not absorbed and not metabolized? I would like to know whether there are substances that are safe for humans to consume, are not absorbed and do not interact with any digestive process.

So, food is disqualified because although it may be safe, it is processed by the digestive system and is metabolized. I'm looking for things that go entirely unprocessed (other than passage).

One such material, or a discrete class of materials is sufficient.

Simethicone is one example. It is a mixture of silica gel and dimethicone (polydimethyl siloxane); they are individually inert too.

Simethicone/dimethicone is used as antigas (they help the gas bubbles coalesce). It does have a laxative effect, though.


When is Water Produced During Photosynthesis? The formula for photosynthesis is: $$6CO_2+12H_2O \rightarrow C_6H_{12}O_6+6O_2+6H_2O$$

I can count the carbons, the waters on the reactant side, the oxygens, and the glucose, but I cannot seem to locate where in either light or dark reaction 6 water molecules were produced again. Where and when were they produced?

Some of the water that's split is regenerated when the hydroxyl radicals (reactive oxygen species) are converted to hydrogen peroxide, water, etc. by superoxide dismutases and antioxidative mechanisms in the chloroplast (peroxisomes/catalases, etc. take care of this). There's also some evidence that the presence of mannitol, ascorbate and glutathione protect against ROS produced in chloroplasts as well. So you input water, and in an effort to avoid oxidative damage, you do get some water generated. However, the balanced equation doesn't reflect this because it's not an actual product of photosynthesis.

About ROS and protective elements

Extra Reading on ROS in photosynthetic systems

I think that's a very obscure fact, and despite the reality of things, it's actually difficult to query the literature. Good question.


How do the first and second law of thermodynamics adhere to breakdown of glucose? I know the first law is energy can only be converted from one form to the other, therefore in the breakdown of glucose 40% potential energy is converted to ATP and 60% is converted to thermal and unusable.

Does the second law adhere to the breakdown of glucose? Isn't it just the same as the first?

The Second Law of Thermodynamics is intimately linked to the thermodynamics of the breakdown of glucose. By "the thermodynamics of the breakdown of glucose," I mean: is the breakdown of glucose spontaneous, is it thermodynamically favorable?

You may have seen the criteria for the thermodynamic favorability of a reaction in terms of Gibbs Free Energy:

$$\Delta G = \Delta H - T\Delta S\leq0$$
That is, for a reaction to be favorable, the change in Gibbs free energy from the initial state (glucose) to the final state (carbon dioxide, water, and energy) must be negative. This equation is valid for systems at constant temperature and pressure, which is assumed to be satisfied in biological systems. According to Wikipedia, $\Delta G$ for the breakdown of glucose is negative, $\Delta G = -2880$ kJ/mol.

However, there is a nice derivation on Wikipedia that the above equation is nothing more than a statement of the second law of thermodynamics, applied to the case of constant temperature and pressure. So in sum, the second law of thermodynamics is the reason that glucose can be broken down in such a way that useful energy is released in the form of ATP, i.e. that the reaction is spontaneous or thermodynamically favorable. Saying that the Gibbs Free Energy of the breakdown products is lower than that of glucose itself is the same as saying that the breakdown of glucose does not decrease the total entropy of the reaction and its environment.


How does a Plasmodium move? Plasmodium sp. does not have any locomotory organs. So, how does it move? What biochemical process allows it to move?

Short answer: Only some stages of plasmodium are motile.  These use "gliding motility".

Gliding motility relies on actin filaments, which enable the organism to deform it's shape, facilitating movement.

This video provides a good visual representation of the filament-based motility.

  "Gametocytes develop into gametes in the insect midgut, and then fertilize each other to form motile zygotes, which escape the gut."

The ookinete and sporozoite are motile.  The merozoite is non-motile.

Then of course there is the circulatory system of the host.

Source:

https://en.wikipedia.org/wiki/Plasmodium
http://www.sciencedirect.com/science/article/pii/S0092867400812817


For allele frequency determination, is it good to take samples from a college/school or a hospital or any other technique? I am trying to determine allele frequency of a hla allele. Preliminary analysis shows the prevalence of the allele (homo or heterozygous both) is 3%. The allele is related to a disease (After exposure to risk factor). Taking samples from college or university can help reduce time and money. Taking samples from hospital may take time (the hospital I have contact to, has small sample size?). Though both ways may have ethnic diversity, college students are of a given generation only. What to do. Please suggest with references to read.

I suggest this as a starting point.

Basically, if your aim is to determine the population frequency of the alleles, then you should sample from the population.
A possible problem with the university is the age stratification, but also possible different proportion of ethnic groups compared to general population. Also hospital might be biased, because you will have a higher prevalence of people with health issues.
The best thing is to randomly collect samples from the population (but I know it is very hard, especially because you can sample randomly, but the ratio of people willing to give you their blood will be biased!).

One thing that is commonly accepted is to retrieve data from healthy blood donors (which is not unbiased, but is accepted!).
You can give a look at a paper I published a lot of time ago. In that case, the estimation of haplotype frequency was performed on the bone marrow donors registry, and it was considered perfectly fine.

Good luck!


Finding for evolution, comparing past flower numbers with present In a hypothetical species of butterfly, wing spots are controlled by a single locus where BB individuals have blue spots, YY individuals have yellow spots, and BY individuals have green spots. Ten years ago, a previous collector randomly collected 1000 butterflies and reported finding 90 blues, 420 greens, and 490 yellows. You collect 40 blues, 320 greens, and 640 yellows. Has there been evolution in this population? If yes, is natural selection involved?

I have had many attempts at this question I calculated the p and q frequency for each using HW model.

For 10 years ago: 90+90+420/2000=0.3   BB
490+490+420/2000=0.7 YY

For now : 40+40+320/2000=0.2 BB
640+640+320/2000= 0.8YY

But I dont think I can know if evolution happened and natural selection from this (because Y allele in yellow for instance includes heterozygotes as well).

What do I do? Do I calculate the expected number of each and put it in Chi square test but how would I get natural selection from that? Please help

Has there been evolution in this population?

If $p$ differs in the population, then yes. If you $p_1$ and $p_{10}$ (the two different estimates at generation 1 and generation 10) are equal, then any deviation is caused by sampling error. Hence set $P_1 = P_{10}$ as the null hypothesis and performs a chi-square test.

Is natural selection involved?

For this we have to know the generation time and the population size. We can assume the generation to be of one year (10 generations). The population size $N$ could be estimated from genetic data of the sampled butterflies. The expected loss of genetic diversity per generation is $\frac{1}{2N}$ but you will need to consider any possible path by which one can go from $p_1$ to $P_{10}$ using a series of binomial distribution and sum up their probabilities. That being said, it is a little bit computationally expensive if $N$ is large but some Markov Model theory might give you some simplifications.


What species of Cerapoda lived during the Jurassic? So far, I've found eleven species of Cerapoda that lived during the Jurassic period. Are there any other known species that I've missed?

The eleven that I've found out about are:

Agilisaurus
Albalophosaurus
Camptosaurus
Chaoyangsaurus
Dryosaurus
Heterodontosaurus
Othnielosaurus
Uteodon
Xuanhuaceratops
Yandusaurus
Yinlong

I am a game board designer working on a game related to dinosaurs. The "only" research i did is Wikipedia + the DK book "Prehistoric" + Dino Directory web site + several more lesser sites. I would appreciate any information on other species if my list isn't exhaustive, or literature suggestions that might help me.

Here is a cladogram from "The phylogeny of the ornithischian dinosaurs", Butler, Upchurch, & Norman, Journal of Systematic Palaeontology (2008):

Of these, :

Ferganocephale (Pachycephalosauridae)
Chaoyangsaurus
Camptosaurus (Ankylopollexia)
Uteodon (Ankylopollexia)
Callovosaurus (Dryosauridae)
Dryosaurus (Dryosauridae)
Dysalotosaurus (Dryosauridae)

lived during the Jurassic.

The synopsis explains well why this classification is subject to adjustment, and why you may have seen contradictory models in your research:

  SYNOPSIS Ornithischia is a familiar and diverse clade of dinosaurs whose global phylogeny has
  remained largely unaltered since early cladistic analyses in the mid 1980s. Current understanding of
  ornithischian evolution is hampered by a paucity of explicitly numerical phylogenetic analyses that
  consider the entire clade. As a result, it is difficult to assess the robustness of current phylogenetic
  hypotheses for Ornithischia and the effect that the addition of new taxa or characters is likely to have
  on the overall topology of the clade.

  The new phylogenetic analysis presented here incorporates a range of new basal taxa and characters
  in an attempt to rigorously test global ornithischian phylogeny. Parsimony analysis is carried out
  with 46 taxa and 221 characters. Although the strict component consensus tree shows poor resolution
  in a number of areas, application of reduced consensus methods provides a well-resolved picture
  of ornithischian interrelationships. Surprisingly, Heterodontosauridae is placed as the most basal
  group of all well-known ornithischians, phylogenetically distant from a stem-defined Ornithopoda,
  creating a topology that is more congruent with the known ornithischian stratigraphical record. There
  is no evidence for a monophyletic ‘Fabrosauridae’, and Lesothosaurus (the best-known ‘fabrosaur’)
  occupies an unusual position as the most basal member of Thyreophora. Other relationships within
  Thyreophora remain largely stable. The primitive thyreophoran Scelidosaurus is the sister taxon of
  Eurypoda (stegosaurs and ankylosaurs), rather than a basal ankylosaur as implied by some previous
  studies.

  The taxonomic content of Ornithopoda differs significantly from previous analyses and basal
  relationships within the clade are weakly supported, requiring further investigation. ‘Hypsilophodontidae’
  is paraphyletic, with some taxa (Agilisaurus, Hexinlusaurus, Othnielia) placed outside
  of Ornithopoda as non-cerapodans. Ceratopsia and Pachycephalosauria are monophyletic and are
  united as Marginocephalia; however, the stability of these clades is reduced by a number of poorly
  preserved basal taxa.

  This analysis reaffirms much of the currently accepted ornithischian topology. Nevertheless, instability
  in the position and content of several clades (notably Heterodontosauridae and Ornithopoda)
  indicates that considerable future work on ornithischian phylogeny is required and causes problems
  for several current phylogenetic definitions.


Is there a point in our life when ALL the atoms from our childhood's body get replaced? The evolutionary biologist and Oxford professor Richard Dawkins makes on his TED talk the rather interesting suggestion that we human beings, are in nature more similar to a wave than an object. In the sense that we are a persistent structure travelling trough a constant flow of atoms that only transiently form part of our body.
Citing Steve Grand and his book Creation: Life and How to Make It, he argues that the body of a grown up man doesn't preserve any of the atoms that formed his body by the time of his earliest childhood's memories.
Is that fact widely accepted by the scientific community?

I know that this question is a duplicate of Are all body atoms really recycled several times during a life? (or this one), however I want to put the emphasis on the atom constituents of cells, as the accepted answer there doesn't fully answer that question.
Following those answers and the references within, a consensus seems to exist that most of the body is in constant renovation, with the exception of the cells in the cerebral cortex and the inner lens of the eye, whose cells persist trough life. But to what extent cellular metabolism replaces individual constituent molecules and atoms throughout those cell's life? Is that true also for DNA? What about mitochondrial DNA?

Are the processes that repair DNA damage operating only in damaged areas? Or do they constantly "repair" also healthy areas leading to the constant replacement of the atoms that constitute the DNA?

Others argue that tooth enamel does not regenerate or get replaced, been that what allows carbon dating to be accurate to the year of birth plus or minus a few months. However, as my question begins with a philosophical issue, I'm mostly interested in the atom constituents of the cerebral cortex. I am in particular aiming to figure out if we are more precisely described as a brain travelling through time or just a wave in a sea of atoms.

Is there a point in our life when ALL the atoms from our childhood's body gets replaced?

No. There is no point where ALL atoms have been replaced.

This has been shown by tracing distinct carbon isotopes in DNA [which reflect upon atmospheric 14C at the year of their generation (which reflect the extent of human atom bomb testing)]; Bergmann et al. 2009, Science: Evidence for Cardiomyocyte Renewal in Humans.

for your other questions:

  Is that fact widely accepted by the scientific community?

The phrasing of Richard Dawkins, which you also list, uses "more similar" (rather than the absolute ALL). These words provide quite an accurate approximation to express that  most building blocks of cells undergo a constant renewal. The choice of words of Grand seems a bit unlucky, if read out of context.

  Are the processes that repair DNA damage operating only in damaged areas?

As a first approximation: yes. For instance the image below shows the localized detection of H2A.X histones upon damage at the DNA (red: H2A.X staining -> much stronger in treated cells which have high level of damage; blue: DNA staining)

  Or do they constantly "repair" also healthy areas leading to the constant replacement of the atoms

As one approximation this would be true, e.g.: proteostasis  (a process whose failure contributes to aging).

  that constitute the DNA?

Note that DNA molecules are vastly outnumbered by other molecules in a cell.

DNA is quite static (see above publication), although individual parts could possibly be repaired (see above image on H2A.X);

Also there might be a selective retainment of more "healthy" DNA strands with less mutations (the immortal strand hypothesis).


Is intron removal coordinated? Are the introns present in a nascent rna molecule removed simultaneously or are they removed in some sort of sequential fashion or is removal completely random?

There are two different ways to interpret this question:

Does the spliceosome splice all introns of an mRNA simultaneously or sequentially?

Can a spliced mRNA be re-spliced?

How does a spliceosome proceed along the mRNA?
According to this review:

splicing generally proceeds in a 5′ to 3′ direction, although neighboring introns are not always excised in this order, nor are all introns completely removed during synthesis (36).

Splicing tends to happen immediately following transcription of introns, so it is to some extent necessarily sequential (same review):

Time course measurements by RT-PCR of multiple pre-RNA species synthesized after reversing 3 hours of DRB inhibition have shown that intron excision occurs within 5 – 10 minutes of synthesis of the downstream neighboring exon, irrespective of the length of the intron, the length of the gene or whether the intron is excised by the major or minor spliceosome (42).

Thus, it is not physically possible in many cases to splice all the introns of a RNA simultaneously, because splicing begins before pre-mRNA synthesis is even complete.
Re-splicing mature/spliced mRNA
There are a few different mechanisms by which RNA can be spliced at more than one point. For example, ribozyme splicing occurs in a spliceosome-independent fashion, so an mRNA with a ribozyme in it and also non-ribozyme introns will necessarily have multiple rounds of splicing.
There is additionally so-called recursive splicing of very long genes/introns. This is when a spliced intron must be handled in multiple rounds due to its length/complexity; it's a bit involved so I won't go into it here.