text:
Are neurons clustered? How do neurons make thousands of connections?
According to this source, a neuron can connect to up to 10,000 other neurons. Does this imply that neurons are clustered, that is, not evenly spaced? Argument:
Say axons are length $L$, and dendrites are length $D$. Say a neuron $N$ has 10,000 outgoing connections. Then there must be 10,000 neurons within distance $D$ of $N$'s axon terminal. Then each of those 10,000 neurons are within distance $2D$ of each other by the triangle inequality. Assuming $2D<L$, then all of those 10,000 neurons are less than an axon's distance from each other. But for this to be true, the 10,000 neurons must be closer to each other than they are to $N$. Since this argument holds for any neuron, we get the result that neurons must form clusters of around $10,000$ neurons, or their dendrites must be longer than half their axon length.
Similar to this question.

Why should spacing and number of connections be inversely proportional? Different regions of brain have different types of organisation. Perhaps you should read about it and narrow down your question. In some lower organisms there is no centralized nervous system but a "neural net". You can read about that too.

Say each neuron had exactly one connection. Then neurons could be evenly spaced. However here I argue that if neurons have many connections, then they must be clustered.

It is not really necessary. Check neural nets in hydra.

Hydras have a decentralized nerve network, true, but here I'm referring to the local neural topology. I argue that if a hydra's neurons had thousands of connections, then they would still be locally clustered, even if there is no "central authority" like a brain.

Your assumptions about the length of axons and dentrites are incorrect. They can vary tremendously from one neuron to another, and in the same neuron. There could be very short connection lengths between two adjacent neurons, and much longer ones between the same neuron and one on the other side of the brain.

@MattDMo Okay, so it's not usually true that $2D<L$?

I think for neurons to be truly evenly spaced, we'd need $D>L$ on average for thousands of connections.

It's possible the info in the link was incorrect. Another source says that neurons have up to 10,000 synapses, so maybe the actual number of unique neurons connected to is far less.

In addition to the comments pointing out other inaccuracies, I think the biggest, most obvious misconception that completely invalidates the whole premise is that axons most certainly do NOT have a single terminal; axons branch and make thousands of individual synapses along their length and at the ends of any branches. For excitatory projection neurons in the cortex, for example, the axons can stretch for many millimeters (or centimeters in larger brains), but also typically branch near their origin to contact the dendrites of neighboring cells.
The number of synapses and number of neurons contacted varies greatly across brain areas, species, cell types, etc.
You might be interested in "small world" organization, such as at link, which I suppose could be considered a form of clustering, but it has absolutely nothing to do with the mathematical distance explanation you are proposing.
The only correct equation you can write here is that the spacing S between neuron A connected to neuron B, must be S<=D+L, where L is the length of A's longest axon, and D is the length of B's longest dendrite; for many pairs, S << D+L. These equations will not lead you directly to any valid conclusions of clustering.


text:
An introduction to nuclei in the pons?
I have a couple of questions regarding the nuclei in the pons, thus I figured it would be best to frame the main question in the way that I did.
My main question, however, is whether the basal pontine nuclei is part of the "cranial nerve nuclei" in the pons or is a separate pontine entity.
Quoting Kandel's Principles of Neural Science (2013),

The ventral portion of the pons contains the pontine nuclei, groups of neurons that relay information about movement and sensation from the cerebral cortex to the cerebellum.

Quoting Carlson's Physiology of Behavior (2013),

The pons contains, in its core, a portion of the reticular formation, including some nuclei that appear to be important in sleep and arousal. It also contains a large nucleus that relays information from the cerebral cortex to the cerebellum.

And while Wikipedia might not be the best source of information all the time, I must quote a few relevant portions which is causing me confusion,

A number of cranial nerve nuclei are present in the pons:
mid-pons: the 'chief' or 'pontine' nucleus of the trigeminal nerve sensory nucleus (V)
mid-pons: the motor nucleus for the trigeminal nerve (V)
lower down in the pons: abducens nucleus (VI)
lower down in the pons: facial nerve nucleus (VII)
lower down in the pons: vestibulocochlear nuclei (vestibular nuclei and cochlear nuclei) (VIII)

I now have broken information about these different kinds of nuclei but I do not know whether the basal pontine nuclei is a part of the cranial nerve nuclei or not.

source: Stack Exchange

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

sort: votes


text:
How much does one stem cell cost?
I am interested in scaled price on 1 stem cell, only for educational purposes. I couldn't find any information about pure price on stem cell, only whole procedure price. So if anyone know, I'll be very appreciated.

I'll hazard a rather educated guess that nobody on the planet sells single stem cells. The problem is that single cells usually do not do well on their own and normally you order them in bulk or isolate a population yourself; there will be loss in each cell recovery step in your procedure, and one is hardly enough for any step, ever. Maybe a (fertilized) zygote... and those rapidly develop out of the one-cell stage and cannot really be easily stored. I'm sure some may exist, but are probably not commercially sold. On this basis I hope you understand that the question should rather be closed.

I'm voting to close this question as off-topic because it is not about Biology in terms of SE Biology.

@David So, where can I ask it?

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


text:
The concept of backpropagation in neural networks actually occurs in the brain?
I am aware the Human brain has many functionally distinct components, but let us specifically consider the Human visual cortex: could Artificial Neural Networks (ANNs) be "trained" (through, e.g. backpropagation) in an analogous way to how the visual cortex "learns"?
Is the concept of backpropagation in ANNs a phenomena actually observed in the Human brain?
Related

Books on machine learning applications in Biology

Is this a homework question? Have you done any research about it before asking it here?

No, its not a homework question, I'm just an amateur in neuroscience and I have this doubt. I thought some here could help me with the answer instead of having to read a book to find out.

I recommend Yoshua Bengio's recent works. E.g.: https://arxiv.org/abs/1502.04156 and his slides from the NIPS 2016 Brains and Bits workshop.
Also, Timothy Lillicrap's work: http://www.nature.com/articles/ncomms13276
This is still a big open question. In short, we (the neuroscience community) have little idea on how the brain learns at a circuit/systems level in general. We know a thing or two about how individual synapse changes under specific experimental protocols, but those are phenomenological models (e.g. STDP; there has been many many normative models of learning that concludes their learning rule is STDP-like). (Some systems such as cerebellum, we know relatively more, but the learning seems to be more specific to motor timing.)
The main technique we use in machine learning and artificial neural network are mostly gradient descent (or some sort of stochastic optimization algorithm), and people have been trying to find if the biological neural network learns in a similar way. There are several issues:

There's no error gradient being propagating according to chain rule. Information gets mushed together within a neuron, so there's no plausible way to trace exactly the forward-path during an backpropagation.
There's a lot of recurrent connections but they are not symmetrical.
Temporally, it is implausible that there's a clocked signal to backpropagate after a each forward path. Neuronal network doesn't seem to operate with clocks (some thing there are precise clocks, but I think there's little evidence).

Recent efforts have made some progress with random backprojection, decoupled updates using synthetic gradients, target prop, autoencoder, weight/signal quantization, deep belief networks, etc. But there seems to be several more jumps needed to make it biologically plausible such that it agrees with the neural architecture and information flow. Even then, there's no guarantee that neocortex is learning with a similar principle.

See also: https://cogsci.stackexchange.com/questions/16269/is-back-prop-biologically-plausible

Not in the same sense as in artificial neural networks. Importantly, there is no biological mechanism for errors to be back-propagated further than a single cell/synapse.
You can look into spike timing dependent plasticity which uses a back-propagating signal within a single neuron, but this is not a back-propagation of an error so it does not accomplish the same thing.
I found this answer on another site had some useful references for further reading, as well.

I don't know much about backpropagation, but I'd have thought the only way to know if "learning" in an ANN is analogous to learning in the visual cortex would be long term comparisons to a developing neural cortex. Possibly having a microelectrode array in the VC of a test-subject throughout development (30 odd days for a mouse) and I'm not sure if they've done this kind of long term study. This paper looks like it might be interesting in terms of changes to the VC after motor task learning, but doesn't seem to have looked at backpropagation.
So I guess my answer is maybe ANN's can learn analogously to brain structures, but we don't know enough about how the brain learns yet to be able to know if the learning observed in an ANN is comparable to a brain.

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


text:
Egg mass on glass
mid-April, East Texas
Can someone ID the egg mass deposited on our window? It's about the size of a fingerprint.

I may have to try again with photo- thanks for forbearance
Eggs are bright green, mass is oval in shape but each is round and linearly arranged. On glass.

Can you get a picture from the other side of the glass?

Mollusc or insect I suspect. Slug or snail  most likely.

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


text:
Can adenosine be cleared?
I've been thinking about this question for awhile, since reading this question: What causes adenosine build up in the brain when awake?
We know that a couple of things will block adenosine receptors: caffeine and hops. If you're overloaded with adenosine and it's early in the day, coffee (or other caffeine sources) make you feel alert by tricking your brain by blocking the adenosine receptors. The dubious downside is that when it finally quits blocking the receptors, you've got a much bigger load of adenosine. Which might not be a downside if it means you fall asleep more easily and deeply.
But what about just clearing the adenosine?

Adenosine breakdown / removal is usually handled by the enzyme Adenosine deaminase.

In order to do this you would need to find a compound that does all of the following:

Crosses the blood-brain barrier. Many pharmaceuticals are not able to do this.
Binds strongly to, or has some metabolic effect on adenosine. The resulting product must also cross the blood-brain barrier, and be excreted.
Not bind or react with other molecules that are similar to adenosine and cause side effects.
Not cause some sort of immune response - along with the blood-brain barrier issue, this rules out any sort of protein, and really limits the potential specificity for items (2) and (3): there simply isn't a lot of chemistry outside of biochemistry that is that specific.
Not cause systemic effects via depletion of adenosine and products of adenosine. There are several problems caused by a failure of the enzyme that metabolizes adenosine but it seems like most of the primary symptoms are due to an accumulation of adenosine rather than an absence of inosine, so I am not certain how much of a problem this would be.

And probably numerous other issues I haven't thought of yet. The point is, adenosine is a useful biological molecule, not just junk to get rid of, and developing something to "clear" just one specific compound is actually really complicated. If the main concern is the sleepiness caused by adenosine build-up, caffeine is widely available and relatively safe compared to some novel way of actually clearing adenosine.
In fact, I can't really think of many pharmaceuticals that work by actually "clearing" something, but feel free to leave any suggestions in the comments. Chelating agents come to mind, but those are only used in some very specific circumstances.

As @Bryan Krause pointed out before me, unless you can regulate adenosine signaling in a selective way any manipulation is probably going to cause important side-effects.
If your goal is to regulate adenosine signaling in a more specific way than caffeine, one way could be to selectively manipulate adenosine receptors of specific pathways. This approach was taken by Blundon et al. (2017) who used a compound that is able to cross the blood-brain barrier (FR194921) to selectively affect cortical map plasticity. It so happens that this compound selectively targets thalamocortical projections, so it could be a promising strategy. But even with such a selective approach side-effects cannot be excluded.

Full disclosure:
I have contributed a preview article for that study (Kehayas and Holtmaat 2017).

References
- Blundon, J. A., Roy, N. C., Teubner, B. J. W., Yu, J., Eom, T.-Y., Sample, K. J., … Zakharenko, S. S. (2017). Restoring auditory cortex plasticity in adult mice by restricting thalamic adenosine signaling. Science, 356(6345), 1352–1356. https://doi.org/10.1126/science.aaf4612
- Feldman, D. E., & Brecht, M. (2005). Map plasticity in somatosensory cortex. Science, 310(5749), 810–815. https://doi.org/10.1126/science.1115807
- Kehayas, V., & Holtmaat, A. (2017). Rejuvenating brain plasticity. Science, 356(6345), 1335–1336. https://doi.org/10.1126/science.aan8374


text:
Help me identify this Bug species
I found this insect in Pune/India. Its body size was less than 1 cm. It was near light source. I suspected it to be Juvenile Thread-legged Bug, but i am not sure. Is my suspicion right or is it some other insect?

Yeah the Emesinae family is a good guess. It will be hard to tell what species, but on this page you may find more information about Reduviidae insects in India (pdf available) : https://www.researchgate.net/publication/237676358_A_checklist_of_Indian_Assassin_Bugs_Insecta_Hemiptera_Reduviidae_with_taxonomic_status_distribution_and_diagnostic_morphological_characteristics

This isn't a juvenile; zooming in shows me wings.  It isn't a member of the Reduviid subfamily Emesinae (the front legs aren't modified for grasping prey); I believe it to be a Stilt Bug (family Berytidae), but not knowing the Indian fauna cannot go any further than that,

It is Pneustocerus gravelyi, a species of stilt bug that lives in India.
In both of these images, you can clearly see the the bright red coloration of the joint on each leg. The pronotum is also the exact same shape and color, and the bright red abdomen extends beyond the closed wings.

original unmodified image source

It certainly seems correct identification. Thank you!


text:
Help me identify Grasshopper
I found this Grasshopper in Goa/India. It was about 2cm long. I suspect it is from Cataloipus genus or Gomphocerinae subfamily. Am i correct or it also seems to be juvenile from some other species?

This does appear to be a juvenile; zooming in shows me wing buds.  Under those circumstances further identification is unlikely.


text:
Help me identifiy this insect
I found this insect in Pune/India. It looked like a fly, and it was running over a leaf.
Size is about 2mm-3mm. Is it juvenile of some fly species or is it not even a fly?

Yes, this looks a lot like a fly (six legs, two wings, shape of the body and head), but I am clueless what kind.

Another possibility is a Hymenopteron of the superfamily Chalcidoidea (parasitoid "wasps"); I base this on the clubbed antennae, small size, and what appears to be very reduced wing venation.  If this guess is close to correct, good luck getting the animal much further (a good stereoscope is practically a requirement just to get to family, and going deeper than that may require a compound microscope -- as for species, what we see here may or may not have a formal name; there are LOTS of Chalcidoids).


text:
Will the N- or the C- terminal soluble domain be on the extracellular side?
Here is a homework question

A single-pass transmembrane protein is destined to be transported to the plasma membrane. In the wild-type protein, a lysine flanks the transmembrane domain on the N- terminal side, and a glutamic acid flanks on the C-terminal side. Both the N- & C-terminal soluble domains carry sequences that can by glycosylated by oligosaccharyltransferase.
After the protein is transported to the plasma membrane, will the N- or the C- terminal soluble domain be on the extracellular side?

My answer is

N-terminal with lysine will be towards the extracellular side and C-terminal will be towards the cytoplasm.

Does this seem right to you?

I made a major edit to your post. Please roll back if you don't like the edit. If you agree with the edit, take advantage of it to learn how to ask a good question on Biology.SE (explicit title, highlight the quotation, clearly specify your question, etc...). You should try to add why you think your answer is right.

Hints: 1. Consider the structures of lysine and glutamate. What's the main difference between the two amino acids? 2. What are the rules governing how proteins are trafficked to the cell membrane? When a protein is synthesized, where is it processed and what does this involve?

Well I know that lysine has a overall positive charge and glutamate has an overal negative charge. So just considering there charge, does the more positive one (lysine) on one side of the transmembrane protein face the extracellylar space?

At the moment this is at risk of closure - I think it can stay open, but only if you add an explanation of why you think that is the answer...

Luminal/cytoplasmic orientation of single-pass transmembrane proteins is mostly dictated by positively charged residues residing on the cytoplasmic side (positive-inside rule) and negatively charged residues being suppressed on the cytoplasmic side/preferred on the luminal side (negative inside depletion/outside enrichment rule).
Since your molecule has a positively charged Lys residue on its N-terminus and a negative negatively charged Glu residue on its C-terminal side your protein would most likely acquire a type II integral membrane protein topology, i.e. the C-terminal part would be directed towards the extracellular space while the N-terminal part is in the cytosol.
Further references can be found here:
Baker JA et al., Charged residues next to transmembrane regions revisited: “Positive-inside rule” is complemented by the “negative inside depletion/outside enrichment rule” BMC Biol. 2017 pubmed
Ott CM and Lingappa VR, Integral membrane protein biosynthesis: why topology is hard to predict. J. Cell. Sci. 2002 pubmed

Hello! This question was deemed worth of an answer, so why not upvote it? Vote early, vote often to encourage new users and keep the community alive!


text:
Is there any difference between strain and mutation/mutant?

Experts are closely monitoring the strain, which has rapidly spread
through the country's south.

Source
Most of the media/newspapers are calling VOC-202012/01 a COVID strain, instead of a COVID mutation/mutant.
Is there any difference between strain and mutation?

You can think of "strain" roughly analogous to how you would think of "breed" in the context of dogs or horses.
There might be some key mutation that identifies members of a strain over non-members, but you would expect to find other genetic differences as well. "Strain" for a virus is not referring to a particular mutation but to the viruses on one side of some fork in their evolutionary history.

As @BryanKrause has correctly pointed out, strains for viruses and bacteria are the same as breeds/races for mammals and birds - the differences between strains are sufficiently small that they cannot be considered different species, yet they may differ by more than one mutation.
Strain is a somewhat generic term, whereas more refined terminology may exist for every particular virus. For example, in case of HIV one distinguishes types of virus (HIV-1, HIV-2, SIV), the groups within each type, and the subgroups. Depending on the context any level of this taxonomic division can be referred to as "strain".
What further makes distinguishing strains difficult is that breeds/races are usually defined by having different phenotypes. The phenotypical differences between different viral strains are more difficult to define, so it is not uncommon to distinguish different strains (or even species, as in the case of flaviviruses) simply by the number of mutations or the fraction of nucleotide differences between sequences.


text:
Could plasmids and conjugation mechanisms be used against antibiotic-resistant bacteria?
I'm surprised no one has mentioned something like this.
Plasmids are often exchanged between bacteria, sometimes through conjugation. In particular, conjugation could be considered an "open-port" vulnerability.
Intuitively, there are several schemes that exploit plasmids and bacterial conjugation that could form alternatives to antibiotics:
1: Pwnage by Conjugation
A specially engineered nanoscale capsule or specially rigged bacterial cell is programmed to call out to target bacteria for conjugation. When the conjugation tunnel is opened, the capsule or rigged bacterial cell floods the target bacterium with toxins or malicious RNA designed to sabotage it.
2: Fake Conjugation
A specially designed novel antibiotic contains a conjugation-signaling structure. When a bacterium docks with the antibiotic molecule, the antibiotic irreversibly latches on and tears a massive hole in the bacterium from the inside.
3: Backdoor Plasmids
Plasmids that confer significant advantages are isolated from naturally-occuring bacteria and a special "crash gene" is added to the plasmids. The modified plasmids are implanted back into bacteria that are known to spread them around.
The crash gene's promoter listens for a small set of chemical cues. If it detects a certain threshold of 1 of these cues, it becomes active and sabotages the bacterium. The gene could code for a toxin that specifically damages bacteria. Alternately the promoter could be specifically designed so it never releases the chemical cue, forcing the bacterium to repeatedly produce a garbage produce and waste its resources.
4: Bad Neighbor Plasmid
This might be more difficult to build. A synthetic plasmid encodes 2 products: The first confers a significant benefit to prevent bacteria from discontinuing it through natural selection. The other product is periodically ("randomly") transcribed and vandalizes other plasmids, causing large numbers of nonsense mutations. A set of special markers on the synthetic plasmid protects it from vandalism by its own product. This could silently remove antibiotic resistance from bacterial populations and the bacteria have no way of "knowing" they've been sabotaged until it's too late.

What is the question?

If we assume all of these things could be practically done at least at some point in the future, here are the problems I see with the suggestions, and why they might not work (others may spot additional ones).
1 Translocation of a sabotaging 'agent' via the conjugation apparatus.
This basically already exists, look up the various secretion systems of bacteria. In particular, the Type 6 Secretion System does exactly this (though with a somewhat limited target range).
The first paragraph on wiki summarises:

The type VI secretion system (T6SS) is molecular machine used by a wide range of Gram-negative bacterial species to transport proteins from the interior (cytoplasm or cytosol) of a bacterial cell across the cellular envelope into an adjacent target cell.

The reason this wouldn't work is that bacteria have already evolved to deal with such mechanisms, and one we engineer is unlikely to fare much differently.
You can take it from me (as my PhD concerns exactly this!) that changing what the secretion systems translocate, while possible, is very difficult.
2 Phony conjugation
Antibiotics tend to be small molecules. They bind and dock with enzymes or substrates in order to inhibit some kind of activity typically, e.g. cell wall synthesis in the case of Beta-lactam antibiotics such as penicillin. I'm not sure how you imagine it would "tear a hole in the bacterium" really?
Related to the T6SS, are R-type Pyocins, which are co-opted bacteriophages that sort of do this. It requires no conjugation, and the currently proposed mechanism is that they either deliver a payload of toxins or molecules in to the cell by puncturing the exterior, or they simple create a pore in the membrane causing cellular depolarisation and death. As with phage and antibiotics however, these mechanisms can have resistance evolved against them.

As an additional point, unless you could somehow guarantee that the conjugations were sabotaged or ineffectual in some way, promoting conjugation artificially is almost certainly going to aid the spread of resistance and virulence determinants, actually worsening the situation.

3 A suicide plasmid
It is not trivial to 'confer significant advantages' on a cell. Most plasmids are maintained by amelorating a significant disadvantage that is often supplied artificially, e.g. auxotrophy or antibiotic selection. Given the 'choice' bacteria tend to kick out the plasmids unless they simply cannot afford to live without it. Maintaining the replicon is an expensive process in terms of cellular metabolism and resource utilisation.
'In the wild' the weaponised plasmid would likely not persist long enough to be translocated in to any target of interest in a significant enough proportion to have a real effect. The key is that and of these ideas mentioned cannot simply kill a single target cell, as they will not have an appreciable effect on the population. The bacteria will recombine or straight up remove the plasmid if it's in any way deleterious or even neutral to them, until they've 'corrected' the problem.
Addiction modules and toxin-antitoxin systems are common to see in natural plasmids, as with the other ideas mentioned. Bacteria can recombine out the 'poison' though, and eventually over time lose the plasmids. If the toxin is encoded on the chromosome, it's a little more robust.
4 Bad plasmids
See addiction modules and toxin-antitoxin systems above.
I'm afraid in general I think you're underestimating evolution!

On #2: If enough phony/dangerous conjugation agents were present (such that conjugation is much more likely to be lethal than helpful), that would promote the growth of bacteria that avoid conjugation and slow the spread of plasmids. Another effective approach might include lysogenic (conditionally nonlethal) bacteriophages that only sabotage their host cell on the presence of any of a small set of synthetic signals.

While you may be right in your first point (I don't have any facts to say the dynamics wouldn't work like that, though I'm dubious), conjugation is not the only way bacteria obtain plasmids, so I'd say it's still very unlikely to be viable. On your second point, about triggering lysogeny of bacteriophages, that is both feasible, and practical - and we are actually doing just that (or a slightly modified but similar idea) in my lab presently.

Could plasmids and conjugation mechanisms be used against antibiotic-resistant bacteria?
Apparently yes. At least, it's plausible. The study is very new and, even though it was conducted in vivo, it was still under artificial conditions. We'll have to see what comes out of it.

Most important modern antibiotic resistance genes spread between such species on self-transmissible (conjugative) plasmids. These plasmids are traditionally grouped on the basis of replicon incompatibility (Inc), which prevents coexistence of related plasmids in the same cell. These plasmids also use post-segregational killing (‘addiction’) systems, which poison any bacterial cells that lose the addictive plasmid, to guarantee their own survival. This study demonstrates that plasmid incompatibilities and addiction systems can be exploited to achieve the safe and complete eradication of antibiotic resistance from bacteria in vitro and in the mouse gut. Conjugative ‘interference plasmids’ were constructed by specifically deleting toxin and antibiotic resistance genes from target plasmids. These interference plasmids efficiently cured the corresponding antibiotic resistant target plasmid from different Enterobacteriaceae in vitro and restored antibiotic susceptibility in vivo to all bacterial populations into which plasmid-mediated resistance had spread. This approach might allow eradication of emergent or established populations of resistance plasmids in individuals at risk of severe sepsis, enabling subsequent use of less toxic and/or more effective antibiotics than would otherwise be possible, if sepsis develops. The generalisability of this approach and its potential applications in bioremediation of animal and environmental microbiomes should now be systematically explored.

The idea is that a natural, addictive plasmid conferring antibiotic resistance is displaced from a bacterial community by an incompatible plasmid expressing the appropriate antitoxin for the addiction system, and tetracycline resistance.

Replicon (solid circle), antitoxin and toxin genes (arrowhead, arrow) and antibiotic resistance genes (CTXR, orange and TETR, black solid blocks). Interference plasmid not excluded by entry exclusion system (EES) is incompatible (INC) with resident CTXR plasmid and is selected by TET.

In the top pathway, conjugation has not occurred and the bacterium retains the original plasmid. Tetracycline kills this population. In the bottom pathway, conjugation has occurred and, because of the incompatibility between the natural plasmid and the interfering plasmid, binary fission results in asymmetric segregation of them. Again, the natural addiction system is bypassed because the interfering plasmid expresses the antitoxin. The population containing the original plasmid is killed by tetracycline but that containing the interfering plasmid is resistant. However, because the this plasmid doesn't have the complete addiction system, it is lost over time in the absence of selection. Thus the resulting bacterial population is antibiotic susceptible.
You may ask why not just use tetracycline to kill all the cells in the first place. That's not the point! This is a proof of concept.

Purifying selection using antibiotics is not ideal, both because of the effects of the drug on other cells and because effective antibiotics for this purpose may be increasingly hard to identify in future. TETR bacteria are not uncommon in the human gut but TETR (or FOSR) populations that arise by plasmid acquisition will not only lose their TETR or FOSR plasmids spontaneously but are made immediately vulnerable to other commonly used antibiotics (e.g. GEN, CTX) in the process. A target plasmid that acquires FOSR by recombination with the interference plasmid will likely acquire the immediately adjacent antitoxin. An important future challenge is to develop interference plasmids with non-antibiotic selection but the inclusion of fosA3 also means that plasmid eradication is compatible with existing use of fosfomycin as a ‘rescue’ therapy of last resort.

This was in 2017, have further developments occurred here? I think de-antibiotic-resisting bacteria would probably be an incredibly useful technology to have

Your ideas are not bad, but in all cases there are a few reasons that make them pretty much unusable in a real world (medical) application. Also none of your approaches solve the problem of resistance: bacteria can just become resistant to this new type of treatment (the bacteria using slightly different conjugation methods are immune and will have an evolutionary advantage).
1) This could work - but not today.
You either need some sort of nanobots or very advanced genetic engineering to pull it off. While the technology to make such advanced 'killer machines' should be available within the next few centuries, the ethical question of 'letting them loose' into a human body or the environment will always remain very tricky.
2) I think this is too complicated.
Antibiotic drugs are very small chemical molecules whereas the bacterial conjugation machinery is very large biological complex. Trying to make something bind the machinery and then make it able to kill the bacteria is superfluous - you could just make antibodies against the bacteria in the first place (they can also be coupled with effectors). Also it does in now solve the problem of evolving resistance
3/4) The added level of complexity does not help.
Trying to trick bacteria with 'trojan horse' plasmids won't work. First of all evolution will work against the whole plasmid and just because it has one favourable gene does not been bacteria can't just get rid of it, if it would kill them otherwise. Secondary, mutations can act on the genes on the plasmid indecently so the bacteria can just shut down the part that's supposed to kill them and keep the rest.


text:
Plant-human hybrid?
I was bored on YouTube so I searched "plant-human hybrid" and this video came up https://www.youtube.com/watch?v=MiZ35pkxG-k. and I want to know if this is actually possible, I checked the comments but they where mostly weed jokes, so is this possible

Welcome to SE Biology. I would ask you to relieve your boredom by reading the guided tour and finding out what constitutes a suitable question. Questions should be comprehensible in themselves and not require one to follow a link to find them. You need to describe what was proposed in the film in your question. Otherwise it is likely to be closed.

This is already a common phenomenon in biotechnology. Perhaps it is exactly not what you think or saw in the video. By the way, in the video the plant was Mimosa pudica and the phenomenon was seismonastic movement...so a very misleading video.
Biotechnology already harnesses plant-non plant hybrids to be specific to produce transgenic plants which uses the useful genes from a different organism to produce a particular vitamin, drug, enzymes, etc in large amount.This phenomenon is called molecular farming and such hybrid plants act as bioreactors.
Similarly mouse genome segments may be used to produce antibody producing plants through their fruits or seeds. Brassica napus uses segments of DNA from Hirudinea organisms like leech to mass produce hirudin used in medicinal product.
It is quite similar to E. coli in which segments of human genes are introduced to mass produce insulin.The E. coli serves as a bioreactor in this case.
I'm mentioning only a few references which explains the detailed processes by which the entire plant cell is endowed with the special traits from other organisms.
FOR REFERENCE:https://www.ncbi.nlm.nih.gov/pubmed/9274048E
https://www.nature.com/nature/journal/v342/n6245/abs/342076a0.html
https://en.m.wikipedia.org/wiki/Genetically_modified_crops


text:
Is there any justification for the claim that blood travels 12,000 miles per day?
An oft-quoted "fact" on the internet1,2,3 (and at least once in print4) is the claim:

Your body has about 5.6 liters (6 quarts) of blood. This 5.6 liters of blood circulates through the body three times every minute. In one day, the blood travels a total of 19,000 km (12,000 miles)—that's four times the distance across the US from coast to coast.
Source: https://www.pbs.org/wgbh/nova/heart/heartfacts.html

None of the instances I've found provide any justification for the 12,000 miles figure; nor do they cite any authoritative source.
Although the 12,000 miles figure occurs often, it is fairly obvious that most (if not all) instances are copied from one of the other instances. Sometimes word-for-word, sometimes paraphrased; sometimes with a mention of the other instance, more often with no mention of the source. It is therefore quite possible that someone "plucked a number out of the air" and the meme-dispersal properties of the internet have done the rest.
In trying to justify this claim (see Background and Further Research below), it becomes clear that an awful lot depends on what precisely is meant by "the blood" and – to a lesser extent – what is meant by "the distance traveled". Some plausible definitions could put this figure at anywhere from around 70-90 miles up to around 90 million miles (and, in extremis, even a couple of thousand trillion miles!). It is entirely possible that there is no meaningful answer to the question of how far blood travels in a day.
Question(s)

Is there any extant, authoritative (ideally peer-reviewed) source for the 12,000 miles claim (i.e. that might have been the original source for the above "fact")?

If the 12,000 miles has simply been plucked from the air, is there any extant, authoritative source for a different figure?

If there is no extant authoritative source for any such figure, can someone provide a justifiable and evidence-backed answer to the question "How far does blood travel in a day"? (But see note below.)

Please note: I am slightly hesitant at including the third option above, and may remove it if felt appropriate. I recognize that the underlying question is likely ambiguous, and that any attempt at an answer might well be "opinion based" (as it will probably need to interpret exactly what is meant by "the blood" and "the distance traveled"). At the risk of being over-demanding, any attempt at answering under this option must include fact-backed justification for any such interpretation(s) and ideally would justify why such interpretation(s) are the only valid ones. I an not
looking for speculation along the lines of "If we define "the blood" this way and follow these calculations, we end up with this figure.".

Background
In the pub a while back, someone had the book 1,342 QI Facts To Leave You Flabbergasted4. This was opened at random to the "fact" that in one day, "blood travels 12,000 miles". I don't have the book in front of me to give its exact wording, but the accompanying Source Finder website5 points to the PBS quote at the top of this question.
Our first thought was "that's Quite Interesting" (which, after all, is the point of the show/book). Our second thought was "that sounds very high"... if "the blood" travels 12,000 miles in a day, it travels 500 miles in an hour, and clearly (at least at a simplistic level), blood isn't coursing through our body at 500 mph!
Some further pondering, and a little web-searching on mobiles didn't clarify things: our conclusion  was (as noted above), that too much hinged on what exactly is meant by "the blood" and how you measure "the distance traveled". Some clearly wrong interpretations:

We found a figure of 3-4 mph for the average speed of blood-flow6 . Treating "the blood" as a homogeneous fluid, this would give a "total distance traveled" of between 72 and 96 miles over a 24-hour period.

Clearly 12,000 miles isn't the distance traveled by an individual blood cell, as that would necessitate it traveling at the aforementioned 500 mph.

It's clearly not based on the total distance traveled by all blood cells. An adult male has around 25 trillion (25,000,000,000,000) red blood cells (RBCs)7.  If each is traveling on average at 3-4 mph, the total distance for all cells would be roughly 2,000 trillion miles in a day (or about 350 light-years – a little more than the distance to Canopus, the second brightest star in the sky). Conversely, if the total distance was 12,000 miles, each RBC would travel less than a thousandth of a millimetre (about the wavelength of red light).

We did have some thoughts about trying to account for the multiple paths that "the blood" flows through. In an extremely simplified example, suppose blood from the heart split into two parallel paths, each of which went around the body before merging just before re-entering the heart. It could be argued that "the total distance" was 2 x 4 mph x 24 hours, since "the blood" was going down two channels. However, it could also be argued that what is going down each channel is not "the blood" but "half the blood".
Things get more complicated when more realistic topologies are considered: if the blood flows through a common vessel (e.g. the aorta) before splitting, if you count each path separately (as above), should the shared path count double or only once? You probably want something in between based on the relative lengths of the single path and the multiple paths.
My view is that while this might be a way of deriving a plausible figure, it is not without problems. One is practical: you'd need to map the entire circulatory system in order to correctly assign weights to each branch and arrive at an overall multiplier. Another is numerical: as we scale up to the full system, there is a danger the multiplier grows too quickly (remember: 80% of the system is formed from capillaries, and the smallest of these are no wider than a blood cell... there will be a lot of paths). Finally, what's being measured feels increasingly arbitrary: the contribution from the aorta is from all the blood at once; but from the capillaries it is almost cell-by-cell.
Between the two extremes above – 70-90 miles when treating blood "as a whole", and 2 thousand trillion by counting each cell – you could probably arrive at almost any number for the total distance traveled. Our problem was that we could not think of a natural way of "dividing the blood" and counting "the distance" that would arrive at 12,000 miles. Further research would be required...

Further Research
Over the next couple of days, I did some dedicated web-trawling... with little success.
The 12,000 miles kept cropping up, but with no justification as to where the number came from, and no references to an authoritative source. I also collected the following, potentially relevant "facts" about the heart and circulatory systems (generally, where it matters, for an adult male):

Blood travels an average of 3-4 mph6. Faster in the aorta; slower in the capillaries (where cells need to pass in single-file, and sometimes have to "push" their way through). Another source10 gives a slightly wider range (2.2 to 4.5 mph).

The total length of all arteries, capillaries and veins is about 60,000 miles8,3,9 (with capillaries making up about 80% of this total).

There is about 5.6 litres (6 quarts) of blood in the body1,6,9.

Blood takes about 20 seconds to circulate throughout the entire vascular system1,9.

The only discussion I could find on the subject was a Reddit thread11, which starts:

Does human blood really travel 12,000 miles every day?
Someone posted that on Facebook and I thought it was total bullshit. So I Googled it and it seems it's not bullshit? I guess my real question then would be: isn't there something more to this? That's 500 miles per hour. I can't understand how that wouldn't rip your body apart.

which neatly mirrors our experience: lots of pages quoting 12,000 miles, no references, and a feeling that 500 mph is clearly wrong. There follows some loose speculation, including that the total distance traveled by all blood cells is clearly massively too high; as is a figure of about 90 million miles calculated by multiplying the number of times the blood circulates in a day (1,440) by the total length of the circulatory system (60,000 miles). To me, the most pertinent comment is the closing one from user rm999:

I searched online, there's nothing reputable backing this. The figures I see are closer to <1 mph, which would be on the order of ~20 miles a day.

although rm999's figure for the overall speed is less than the most common figures I saw (although 3 quotes this speed for the aorta).

References
1 Amazing Heart Facts on the Nova section of the PBS website.
2 The Journey of Blood (PDF). Lesson plan on the American Heart Association website.
3 Slideshow on "Circulation" on slideplayer.com by Dwain Gibbs.
4 1,342 QI Facts To Leave You Flabbergasted: a spin-off book from the British TV comedy panel game-show "QI" (for "Quite Interesting") – see entry on Wikipedia. Despite being primarily an entertainment show, it has a pretty good reputation for research, although it does sometimes make mistakes and issue corrections. I suspect the book is less thoroughly researched than items appearing on the TV show.
5 The book lists its sources on https://qi.com/1342/index.php (this can be seen using the Look Inside! feature on the Amazon page above, under "Read This First"). The "12,000" miles fact is the second entry on page 186, leading to the aforementioned http://www.pbs.org/wgbh/nova/heart/heartfacts.html.
6 Our Bodies' Velocities, By the Numbers on the Discover magazine website. Note, though, that after giving the 3-4 mph figure, it goes on to say "But this blood speed is just an average. It starts out by rushing through the aorta at an impressive 15 inches a second, then slows to different rates in various parts of the body." I suspect the "inches" is a mistake: 15 inches/second equates to less than 1 mph; whereas 15 feet/second equates to about 10 mph, which fits better.
7 How many blood cells are in the human body? from the article "How Many Cells Are in the Human Body?" on the Healthline.com website.
8 11 Surprising Facts About the Circulatory System on the Live Science website.
9 Heart Facts on the Health Essentials website of the Cleveland Clinic. The "20 seconds to circulate" fact was originally taken from Amazing Heart Facts on the Arkansas Heart Hospital website, but that link (https://www.arheart.com/heart-health/amazing-heart-facts/) is no longer valid.
10 What is the speed of blood circulation in human body? on Quora.
11 Does human blood really travel 12,000 miles every day? on Reddit.

Welcome to SE Biology. You are to be commended on the thoroughness of your investigation. This sort of question is not the sort of thing that concerns the majority of professional scientists — I personally term it "freak show science" or "Guinness Book of Nonsense" — but there may be someone here interested enough to check your figures. They seem plausible enough to me.

This might be more on-topic at skeptics.SE ? You're asking to confirm a published statement/claim, that happens to be about biology.

A single erythrocite travelling from the heart via the aorta, a certain artery, capillary and vein back to the heart would make about 1 meter in average, I guess.
If the blood volume of an adult is ~5 liters and if the cardiac output is ~5 liters per minute, then "all the blood" travels 1 meter in a minute, which is 60 meters per hour or 1,440 meters (~0.9 miles) per day.
This seems to roughly agree with:

Average peak and mean blood velocities were 66 and 11 cm/sec in the
  ascending aorta, 57 and 10 cm/sec in the pulmonary artery, 28 and 12
  cm/sec in the superior vena cava, and 26 and 13 cm/sec in the inferior
  vena cava. (The blood velocity...(Circulation))

So, if you say that the average blood velocity in big vessels is 12 cm/sec or 432 m/hour and consider that the velocity in smaller vessels is much lower, then it is possible that the average blood velocity in all the vessels could be ~60 m/hour, as I estimated.

But if you took all the blood vessels out of an average child and laid
  them out in one line, the line would stretch over 60,000 miles. An
  adult’s would be closer to 100,000 miles long. (The Franklin Institute)

You can then say that "all separate blood streams" (5 liters in summary) going through all the vessels would make 100,000 miles in a minute or 144,000,000 miles in a day. But not "all the blood" travels all that distance in a day.
I'm not sure how they came to 12,000 miles per day, but this just shows how different the things can look from different perspectives.
EDIT: I just noticed that my "calculation" 144,000,000 miles is 12,000 miles squared.

Just guessing, but I would suppose that someone saw the figure 1200 m(eters) per day, read it as 1200 m(iles) per day, sayd "Oh, wow!", posted about it somewhere, and the post repeatedly got copied without fact-checking.

@jamesqf, such things can happen...Anyway, blood travelling 12,000 or no matter how many miles or meters per day is not really an useful information. I answered just to show how the confusion can develop.

The radius of Earth is ~25,000 miles, so using the center of the earth as a reference frame someone at a moderate latitude would see their blood (and the rest of them) travel about 12,000 miles in a day. I think the 1200 meter explanation is a likely explanation, but overall I think the point that this answer makes (i.e., it totally depends on how you define the trivia) is important, and is consistent with David's point that this sort of estimation isn't really relevant to a biologist.

@BryanKrause, you probably meant circumference...and the blood would then travel 25,000 miles a day...?

@Jan Er, yes of course circumference. Only at the equator would it be 25000, somewhere in the mid latitudes it would be 12000.

@Bryan Krause: But you're still neglecting the motion of the Earth as it revolves around the Sun (about 67,000 mph/107,000 km/h), the Sun moving around the galactic core, our galaxy's motion WRT the local group...

@Jan: The speed of blood flow would be useful information when designing things like stents & replacement heart valves.  E.g. if blood actually did travel 12,000 miles per day, that would be 500 mph, which would cause some serious turbulence, among other problems.

@jamesqf, knowing the speed is useful, of course - and the actual speeds are not calculated but measured. They are all those miles that I don't find useful.

@jamesqf I know, that's why I referred to the center of the earth as a reference frame (I got that detail right even if I misspoke about the radius/circumference ;) ) And yes, knowing the speed of blood flow itself is useful, but the way you'd figure that out is by measuring the speed of blood flow in a vessel of interest. You don't much care about it's velocity elsewhere, and it would likely mislead you if you calculated an average velocity given the differences between capillaries, veins, and arteries.

I tried to come up with an explanation with approximate values. It looks like 12,000 miles is actually milliliter-miles per day. The way to think about is to consider a drop of blood that is part of a heart pump (1 ML) doing roundtrip though the body (say a string of 3.33 meters). There are 56 drops of blood in a heartbeat. If you are to keep 56 strings end to end then the cumulative distance travelled by 56 drops of blood is 3.33*56=186.48 meters. Then if we multiply this distance by number of heart beats per day then we get the 12000 miles number.

56 : milliliters - amount of blood per pump
72 : pumps per minute
56*72 = 4,032  : milliliters per minute
4032*60 = 241,920  : milliliters per hour
241920*24 = 5,806,080  : milliliters per day
1.67 : meters - height of average adult
1.67*2 = 3.33 : meters - roundtrip travelled by blood
5806080*3.33 = 19,353,600 : milliliter-meters per day
19353600/1000 = 19,353 : milliliter-kilometers per day
19353/1.61 = 12,021 : milliliter-miles per day
Note: I am not the person who came up with 12,000 miles per day claim. Since there is no citable source for the claim, I am only trying to come up with a possible explanation for the circulated number.

References:

The web pages below claim that blood travels approximately 12,000 miles per day.
https://www.pbs.org/wgbh/nova/heart/heartfacts.html
https://www.heart.org/idc/groups/heart-public/@wcm/@fc/documents/downloadable/ucm_454347.pdf
The web page below says heart rate range is 60 to 100 beats per minute. I chose 72 which is within the range.
https://www.mayoclinic.org/healthy-lifestyle/fitness/expert-answers/heart-rate/faq-20057979
The web page below says amount of blood per pump is 55-80 milliliters. I chose 56 which is within the range.
https://www.smm.org/heart/lessons/lesson2.htm
The web page below talked about human height. I chose 167 which is within the range.
https://ourworldindata.org/human-height

I'd understand if it got a quarter of the way there with every pump, but that's not what your calculation shows. Do you have a ref. to show that your assumption is correct? I.e. that a particular set of blood goes out the heart, and back again in one beat-cycle?

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

As blood flows at a rate of 3 to 4 mph or 4.8 to 6.4 kph call it 5kph in 24hours it will have travelled some  120km or 12,000 metres please note METRES not miles.
Too many people misread or misquote things without checking and some actually get printed in quiz books.

Thanks for this, although that should be "120km or 120,000 metres", shouldn't it? However, someone confusing meters and miles and slipping a power of 10 seems a very plausible explanation for where the "12,000 miles" came from (I only ever worked things out in miles, so never spotted the similarity of the "simple" distance in metres).


text:
What is meant by genomic imprinting being reversible?
I'm not trying to understand the underlying molecular processes, rather understand it conceptually.
This is what it says in my coursebook:

"The imprint, obtained during gametogenesis, is reversible: an allele
with paternal imprint will, after transmission through the female
germline, be changed into an allele with maternal imprint.
In other
words:
Paternal imprinting means that some gene obtained from your
father is 'silenced'. These 'silenced tags' remain during your whole
life, but are reset during the formation of egg-cells or sperm-cells.
Some genes are always silenced in egg-cells, others in sperm-cells.
There is a continuous activation and deactivation in function of the
parent who transmits the gene"

I don't understand how the first paragraph and the last paragraph can both be correct.
If the paternal imprint changes into a maternal imprint after passing through the germline, this implies that the gene is just deactivated in the chromosome that is passed on and we call is paternal or maternal depending on who passes it on.
On the other hand, the last paragraph (and the middle one) imply that, if you receive a gene with maternal imprint from your mother as a man, your body resets the 'silencing' during gametogenesis, realizes a sperm cell is being made and decides not to silence it since it will now be passed on from a father. Only this can explain why it would lead to continuous activation/deactivation or reversibility.
Which of the two is correct?


text:
Why is a hippo so big if it has round about the same genes as a mouse
My science teacher told us that all mammals have round about the same number of genes. This confuses me, since there are very big and very small mammals. Where do genes come from and why do animals have such large differences in size between one another even if they have around the same amount of genes?

@stormy The comments are not a place to talk about pet theories, especially those unrelated to the question. Please only use comments to improve questions and answers.

@stormy Science isn't based on what you find fascinating, it is based on empirical observation. Plant DNA does not have 99% of the information that human DNA has, nor 99% of what a bacterium has.

Genes are the "plans" for proteins in an organism; in turn, those proteins do all sorts of things, catalyzing chemical reactions and making up much of the structure of an organism.
A hippo is much bigger than a mouse, but it isn't that much more complex: both are going to have the same sorts of organs like a heart, lungs, kidneys, liver, brain. If you look at an individual cell from each animal from the same tissue, they will probably look almost identical! They are going to have similar metabolic pathways, etc. Their genes will be different, because some differences in proteins are necessary to build organisms of different structure and size, but the number of genes doesn't have to vary much, the hippo just needs to produce a lot more of the gene products, not have more plans.
A hippo will of course have way more genetic material, because it also has more cells and there is a copy of the DNA in every cell, but what your teacher is talking about is the number of genes within each cell.
Ultimately, genes come from evolution. You can read more about the basics of evolution somewhere like Berkeley's Evolution 101.

@stormy Ok first, what does 'asteroid mimi' have to do with this answer? Second, if organisms didn't evolve, why are all organisms different? Third, DNA that'll never be used? Fourth, how can a virus seed life with DNA?


text:
What is trans-complementation?
Is trans-complementation a complementation of transgenes?

The crystal structure reveals a trans-complementation mechanism whereby an incomplete immunoglobulin-like domain assimilates an isoform-specific myomesin interdomain sequence.
https://www.ncbi.nlm.nih.gov/pubmed/27989621

The term complementation refers to the recover of a phenotype or characteristic ("or function of a protein") that was altered due to mutations. The complementation can be a cis, a mutation in the same gene that restores function, or trans mutation on a secondary gene that restore the function.
An example from wikipedia:

For a simple example of a complementation test, suppose a geneticist is interested in studying two strains of white-eyed flies of the species Drosophila melanogaster, more commonly known as the common fruit fly. In this species, wild type flies have red eyes and eye color is known to be related to two genes, A and B. Each one of these genes has two alleles, a dominant one that codes for a working protein (A and B respectively) and a recessive one that codes for a malfunctioning protein (a and b respectively). Since both proteins are necessary for the synthesis of red pigmentation in the eyes, if a given fly is homozygous for either a or b, it will have white eyes.
  Knowing this, the geneticist may perform a complementation test on two separately obtained strains of pure-breeding white-eyed flies. The test is performed by crossing two flies, one from each strain. If the resulting progeny have red eyes, the two strains are said to complement; if the progeny have white eyes, they do not.
  If the strains complement, we imagine that one strain must have a genotype aa BB and the other AA bb, which when crossed yield the genotype AaBb. In other words, each strain is homozygous for a different deficiency that produces the same phenotype. If the strains do not complement, they both must have genotypes aa BB, AA bb, or aa bb. In other words, they are both homozygous for the same deficiency, which obviously will produce the same phenotype.

So, my first guess was wrong and trans-complementation term stands for complementation of genes arranged in trans-configuration?

@user619271 indeed.


text:
glossary of biotechnological engineering
Similar to A good book for history of biology/biotechnology for lay people
but not for lay people.
Can anyone recommend an advanced dictionary of biotechnological engineering concepts in English (contemporary, not historical)?
There doesn't seem to be anything adequate at my research institution nor even country.  I have been looking for PDF's and e-books since they can be previewed more easily than ISBN #'s, but any suggestions are welcome.

I found this glossary of Biotechnology and Genetic Engineering off Wikipedia, what do you think?
Or The Facts On File
DICTIONARY of
BIOTECHNOLOGY
and
GENETIC
ENGINEERING
What concepts are you necessarily hoping to include? I'm hoping someone actually experienced in this field can advise.


text:
Is a "Fact" any theory for which there is overwhelming evidence in any field other than biology?
Evolution is often described as a fact, and a theory. Evolution is a heavily overloaded term, with one definition being the fact that, "changes in the frequency of alleles in populations of organisms from generation to generation." This is a measurable fact, but not the usage of the word evolution that I am in interested in.
Wikipedia has several quotes on the matter, including the Webaters definition used in this questions title, but also includes clearly observational facts like the Earth revolves around the sun.

A fact is a hypothesis that is so firmly supported by evidence that we assume it is true, and act as if it were true. —Douglas Futuyma
There is no sharp line between speculation, hypothesis, theory, principle, and fact, but only a difference along a sliding scale, in the degree of probability of the idea. When we say a thing is a fact, then, we only mean that its probability is an extremely high one: so high that we are not bothered by doubt about it and are ready to act accordingly. Now in this use of the term fact, the only proper one, evolution is a fact. —H. J. Muller
Scientists most often use the word "fact" to describe an observation. But scientists can also use fact to mean something that has been tested or observed so many times that there is no longer a compelling reason to keep testing or looking for examples. The occurrence of evolution in this sense is fact. Scientists no longer question whether descent with modification occurred because the evidence is so strong. —National Academy of Science

Do scientists refer to any theories for which there is overwhelming evidence as a "scientific fact", other than in biological sciences?
Note: Good answers will include quotes from scientific organizations or prominent scientists using the term fact to describe the theory, and will include references to the theory itself.

the definition of observation and fact (which is not often used in scientific discussions in my experience) are messier than you might think.  scientific proof is a messy business and different fields have different levels of evidence for publication, but they also have varying levels of application.  There is in practice no standard definition of these words in 'science' or 'biology' that I have seen, certainly none is taught in graduate school.

@PaulA.Clayton, indeed. "Law" is an appropriate term, and is used often in Physics. I am interested in the supposed misuse of the term "fact" that scientists supposedly use according to the NAoS and others in fields other than biology. (Bonus points for not using climate scientists "fact" of the majority of warming is human caused in reference to the AGW theory.)

user1873-> Isn't the point of @PaulA.Clayton that the use of 'Law' in physics is an example from a field other than biology of a similar expression to denote a theory (in that both 'law' and 'fact' indicate a high degree of 'truth'). If you accept that 'scientific law' == 'scientific fact' then you have at least one example.

@fileunderwater, I don't accept scientific law == sci fact. The whole point of the question is that "fact" is supposedly used to indicate a high decree of certainty, and is used by scientists in this way. I cannot find any examples other than the very popular, "evolution is a fact." (And perhaps the AGW is a fact, but I am not sure if the source was a climate scientist). I doubt the claim that "fact" is used by scientists in this way.

@user1873 Is your disagreement only semantic? Or do you specifically have a problem with labelling 'evolution' or 'AGW' as law/fact? Your question seems to imply that you are asking for examples of other scientific fields where scientists are using a (casual) wording that implies that a theory is 'absolute truth'. If so, I think that the example from physics is valid. If you have a problem specifically with evolution (as a scientific theory or as as a theory deemed as'true' by most working scientists), that is a completely different question.

@fileunderwater, I suppose in a sense it is "only" semantic, since that is the root of the claim. I don't have any issue with the entomology of the word "fact" taking on this new meaning of  "any theory for which there is overwhelming evidence," my issue is with the claim that it has taken on that meaning when it appears that it only has in one specific case.  For example, If I claimed that the most women support abortion outside the womb, but insist that "abortion" meant, "to bottle feed an infant," some would take issue.

AFAIK, there are (1) evolution, (2) the Theory of Evolution and (3) Darwin's Theory of Evolution. (Other 'theories of evolution' could be counted.) The three are not equivalent. It seems that that you are asking about one of the three, but it's not clear which one.

Your question really applies to any scientific theory, not just evolution.
The problem is that, outside of the scientific world, a theory is often thought as something unproven, an unproven guess if you wish. This is not true for scientific theories, which, instead are confirmed by experimental data.
The OED defines theory as:

A scheme or system of ideas or statements held as an explanation or account of a group of facts or phenomena; a hypothesis that has been confirmed or established by observation or experiment, and is propounded or accepted as accounting for the known facts; a statement of what are held to be the general laws, principles, or causes of something known or observed.

and fact as:

Something that has really occurred or is actually the case; something certainly known to be of this character; hence, a particular truth known by actual observation or authentic testimony, as opposed to what is merely inferred, or to a conjecture or fiction; a datum of experience, as distinguished from the conclusions that may be based upon it.

So, essentially we start with an unproven idea, we corroborate it with facts (=experimental data) and we define our theory accordingly to facts.
So, why don't we say that evolution is true or that it is a dogma or that it is a fact?
Well, that is not how science work. Evolution is a scientific theory, and it always will be. Maybe (hopefully, dare I say) in 50 years from now new evidence will have make us change the theory of evolution, at least some bits of it.
Luckily evolutionary biology is not stuck at the time of Darwin and genetics is not stuck at the time of Mendel. Many new pieces of evidence have made us improve the theories that they initially defined.
Does that mean they were bad scientist or that they experiments were faked? Not at all!  Simply as their knowledge was more restricted than ours, they could not formulate a more advanced theory. Mendel's experiments still hold true, but now we know that transmissions of characters is not as simple. He was just looking at a special case. And his experiments still fit in our current theory, and will have to fit in any future one.
A scientific theory is defined by its falsifiability, that is

the trait of a statement, hypothesis, or theory whereby it could be shown to be false if some conceivable observation were true. In this sense, falsify is synonymous with nullify, meaning not "to commit fraud" but "show to be false".

The famous black swan example by Karl Popper (see e.g. Conjectures and refutations, 1963, chapter 11.6), can be exemplified by (source: Wikipedia):

One notices a white swan. From this one can conclude:
      At least one swan is white.
  From this, one may wish to conjecture:
      All swans are white.
  It is impractical to observe all the swans in the world to verify that they are all white.
Even so, the statement all swans are white is testable by being falsifiable. For, if in testing many swans, the researcher finds a single black swan, then the statement all swans are white would be falsified by the counterexample of the single black swan.

So, our theory of the white swan is accepted as "temporary true", as long as a black swan is not found. Obviously the more white swans we count (i.e. the more experimental evidence we have), the stronger our theory will be. But it will never be true.
I would like to finish quoting Richard Feynman:

It is scientific only to say what is more likely and what less likely, and not to be proving all the time the possible and impossible.

and

We never are right, we can only be sure we're wrong

I suggest to watch the full video of his fantastic lecture on scientific method on YouTube.

An biologist, a physicist and a mathematician are on a train in Scotland. The biologist looks out of the window, sees a black sheep standing in a field, and remarks, "all sheep evolved in Scotland to be black because selective forces killed off the white sheep." "No, no, no!" says the physicist. "Only some Scottish sheep are black." The mathematician rolls his eyes at his companions' muddled thinking and says, "In Scotland, there is at least one sheep, at least one side of which appears to be black from here some of the time."

@user1873: you seem to have misread my answer. I never said scientists use fact in reference to theories. I am saying that a scientific theory, or a scientific model, is based on facts, that is experimental proofs. One, however, can never be certain a theory it is true (instead one can be certain a fact is true). So, if a scientist or a journalist or anyone else uses "theory" and "fact" interchangeably... well, they are doing it in an incorrect way as the two terms do not mean the same thing.

@user1873: the example of the sheep you make is a very good example of how a theory is just an interpretation of facts. The experimental evidence (the black sheep in the field) can be interpreted in (at least) three ways. All of those three are equally good scientific theories, as they are all falsifiable. You just need to go and look at the sheep from the other side of the field, or look at sheep in another country etc etc and some (or all) of those theories will be falsified. [cont'd]

[cont'd]You can then formulate a fourth theory, which is still consistent with that data but that takes into account the new data. All of the four theories are based on facts, but they are not facts, they are interpretations of the facts.

I just reread your 2nd comment. It seems you are saying that the NAoS is indeed full of it. It is unfortunate that Wikipedia keeps such misinformation on its pages for so long.

I am indeed disagreeing with what the NAoS says (just my opinion...). I don't doubt that sometimes if a theory is proven over and over again we take the "shortcut" of calling it a fact, but I am saying this is not really correct. I agree much more with the first quote when it says: "we act as if it were true". It is a shortcut, and I understand that sometimes it is handy to say "evolution is a fact" to respond to creationists arguing that "evolution is just a theory". But really, the way one should respond to that is "evolution is a theory, proven over and over again".

A direct quote to Popper on black swans could be: That this minimum requirement cannot be satisfied ... may be shown with the help of Carnap's example, the law 'all swans are white'. This law ought to be considered *falsified* if our evidence consists of a flock of *one* black and, say, 1000 white swans. But upon this evidence, the instance confirmation, instead of being zero, will be very near to 1.. This is from chapter 11.6 in Conjectures and refutations. I have added a reference in our answer to this passage, but as a stand-alone explanation the Wikipedia quote is better.

@nico In your answer and comments you write that a theory is an interpretation of facts, and that one can be certain a fact is true. This is however (as you probably know) a very simplified view. More modern descriptions of the scientific method all highlight how observations cannot be simply decoupled from theory (see e.g. Lakatos in Criticism and the Growth of Knowledge and Kuhn's The Structure of Scientific Revolutions, or, in more extreme form, Feyerabend's Against method). Therefore, you can just as well argue that observations and "facts" are theory dependent.

@fileunderwater: Thanks for the ref. Obviously theory and observation are not independent, but whereas theory can be viewed as an interpretation of observation, the other way around seems less likely. I can have my theory that cells are triangular, and it may be as nice a theory as I wish, but that will not have the effect of making cells triangular... :)

@nico Well, neither observations nor theories will change the physical reality, so no difference there. While I agree in practice that observations and theory have a different standing, with observations being closer to "actual facts", I still think that the point of theory-dependent observations cannot be so easily written off. A classical example would be astronomy, where raw 'observations' can consist of photon recordings from a distant star. For this raw 'observation' to be made into an observation (fact?) that has bearing on a particular hypothesis (e.g. dealing with ...

contd: ... the composition of the star) an entire body of work must be assumed. Auxilary theories and methods that has to be assumed true could include recording equipment, diffraction of light in the atmosphere and in space, how electromagnetic radiation is emitted etc. The point being that these observations don't exist except in relation to a complex network of theories. The astronomy example might be seen as extreme, but I can easily envision many similar situations in biology. But I probably digress from the main topic....

@fileunderwater: surely, I agree with you on that, but that is mostly because, for practical reasons, you cannot expect everyone to repeat every single experiment needed to justify his/her theory. A scientific experiment, however, should be repeatable, so in theory all those auxiliary theories could be reconfirmed (and if they are assumed as correct by the scientific community they probably have been reconfirmed over and over again). Still, that does not make them TRUE, just not false in accordance to what we know.

@user1873 I know this is old, but I had to steal that first comment. :D


text:
Beginning with centrifuge experiment
This is the first time I do a centrifuge experiment with my own centrifuge machine, it's just simple made by a rotor that can rotate the tube at high speed. As I know a centrifuge machine can be using for separate biology samples like bacteria, cells, molecules ... But I need some advice to understanding more how to working with it.
As the suggestion from Alan Boyd, I'm planning to separate Lactobacillus from diluted yogurt. How do I know where the bacteria will be located in the tube after centrifugation (is it usually in bottom ?) and how do I  calculate the RPM that is suitable ? And any other interesting diy experiment to do with it ?

It would be interesting to see a picture of your centrifuge, which you appear to have built in a few days.
Centrifugation simply accentuates the effects of gravity, and since bacteria are denser than aqueous solutions they will move to the bottom of the sample to form a fairly tight pellet.
The conditions for your centrifugation will depend very much on the design of the centrifuge since as well as the rotational velocity, the radius of rotation is also important.
I found a suggestion on the internet to use a relative centrifugal force (RCF) of 12000 g for 2 minutes (I must admit that from memory I always spun slower and for longer than this suggests). Anyway...

using RCF = 1.12 * 10-5 * r *N2
r = radius of rotation
N is revolutions per minute
and plugging 12000 g into that, for a rotational radius of 10 cm, I get 3300 rpm.

Don't know if you can manage that with your machine, but as I say, a lower RCF with a longer spin will probably be ok as long as you can dilute the yoghurt sufficiently to reduce viscous drag. Of course if you have access to any microbiological growth media you could grow a standard liquid culture by inoculating some sort of broth with a small amount of yoghurt.
Try a Google image search for hand powered centrifuge to get an idea of what has been used in the past.
after comment from Mad Scientist
see here for a typical large table top centrifuge maximum RCF is 3120 g at 4600 rpm. You can certainly pellet bacteria in something like this in tens of minutes.

12.000g sounds rather high to me for a tabletop centrifuge. For bacteria I'd use 4000-6000g for 15-30 minutes.

@Mad Scientist - agreed, I have supplemented the answer, which was only intended to get the questioner thinking about his own centrifugal circumstances.

@MadScientist depending on his design, it could be closer to a microfuge, in which 12,000g is quite reasonable. I'm more worried about balance and shielding in case the thing goes off kilter (that's a technical term, by the way :)

Ok, i'm fairly new to the "g" unit because i never using it before and familiar to the "rpm" unit. But i will research more about it now, thank you so much.

@AlanBoyd thank you so much, your information is very detailed.

I certainly don't want to discourage experimentation and self-learning, but please be extremely careful. A centrifuge has to be perfectly balanced at high speed to stay stable. As an example, one of the table-top centrifuges I use has a steel jacket that's perhaps 1 cm thick or more surrounding the rotor, just in case there is a balance issue or the rotor breaks from mechanical stress. A Google image search for centrifuge accident shows what mechanical stress can do when an improper rotor was used on a high-speed centrifuge for just a few hours. Keep in mind that angular momentum increases both with the mass of the object being rotated, and with the moment of inertia, which increases as the radius of the object being rotated increases. In other words, if you tie a ball to a short piece of string (say 0.5m) and swing it around your head, you can feel a certain amount of force. Take that same ball and tie it to a 2m piece of string, and at the same number of rotations per minute the force will increase substantially. All this means is that as the radius of the rotation increases, the amount of g force increases as well, but the stress on the machine also increases, especially if the balance is off.
So, good luck with your experiments, just remember that safety always comes first. You can replace samples, and you can replace equipment, but you can't replace you. Even simple precautions like always wearing goggles or protective safety glasses should always be followed. Don't work alone, or in a situation where there is no one to call for help if you get hurt. If something doesn't feel right, don't do it.

thank you so much for your advice, i deciding to add a chip for detect vibration - automatic stop, and using a secure box to cover the motor.


text:
How many species have existed on earth?
I found a paper estimating the number of species currently living on earth. Now I'm wondering If anybody tried to estimate the number of species that have lived on earth. I'm familiar with problems of "species concepts". But I'm sure, there is at least a number of all known fossils.
EDIT: In contrast to the question How many organisms have ever lived on Earth?
I'm asking for species and not for individuals. The answer to my question can be used to ansewer the queston for the number of organisms. But still, The questions is different.

Did you read the answer to the linked question? I believe it adequately describes the problems with estimating the number of species (along with the number of individuals) that have ever existed on Earth, and gives some links for further reading.

See the answer to the linked question

In my opinion, as it is, it is not fair to mark this question as a duplicate, because it doesn't duplicate any other question (even though there is an answer to this question in another question). My more practical suggestion is to 1) reword the linked question just like this question or 2) transfer shigeta's answer here. I like the wording of this question better, because I don't see how would the number of individuals that have lived on Earth be of any use to someone, it would be impossible to comprehend such a number. Species is a more interesting wording.

It's patently incorrect to mark this as a duplicate. The distinction is huge--species number versus individual number (which is 1 and 8 billion, respectively, for humans). Someone so empowered should remove that designation, because it discourages answers.

A quote from a Discovery movie:

Scientists have estimated that over the course of Earth's history, anywhere between 1 and 4 billion species have existed on this planet.

I know, I know... sorry. I hope someone has the original research, but in case no one does, or if you are just curious, and Discovery is fine for you, I decided to share what I know for the time being.


text:
Why do toenails grow much slower than fingernails?
As the title suggests, I've noticed that my fingernail grow much faster than my toenails. For instance, I usually trim my fingernails every two week or so, but for toenails the number would be about 6 to 8 weeks.
A bit of research revealed this wikipedia article:

In mammals, the length and growth rate of nails is related to the length of the terminal phalanges (outermost finger bones). Thus, in humans, the nail of the index finger grows faster than that of the little finger; and fingernails grow up to four times faster than toenails. [12]
In humans, nails grow at an average rate of 3 mm (0.12 in) a month.[13] Fingernails require three to six months to regrow completely, and toenails require 12 to 18 months. Actual growth rate is dependent upon age, sex, season, exercise level, diet, and hereditary factors. Nails grow faster in the summer than in any other season.[14]

But correlation does not imply causation, so why should the growth rate of nails depend on the  length of the terminal phalanges? Then why do babies grow nail much faster? I wasn't satisfied by its answer, so I looked a bit more where I found this other article. They had two possible candidates:

because hands are physically closer to the heart than are feet, fingers get better blood circulation and consequently better access to oxygen and nutrients.

Fingernails experience almost constant trauma through tapping, typing, bumping, and other seemingly insignificant actions. These persistent minor traumas stimulate fingernail growth. Toes, on the other hand, are not exposed to nearly as much trauma as they are usually bundled up safely inside socks and shoes. Similarly, fingernails on a person's right hand grow faster in right-handed people than on their left hand and vice-versa.

However they don't give actual experimental results. So my question is which of the above is the real cause of this difference in the growth rate of nails; or simply why toenails grow much slower than fingernails?

P.S. The season dependence and the lefthand-righthand asymmetry were news to me; it would be really nice if the answer explains them as well.

Interesting! We could test "These persistent minor traumas stimulate fingernail growth. " by doing a study of people who primarily walk barefoot (beaches, temperate climate, etc).  Mark the toenail, measure actual growth (since they will wear faster, being exposed), and compare it.

One factor that occurs to me but I don't see mentioned in your research, and this is just from my personal experience but it seems to me toenails are significantly thicker than fingernails. I might be mistaken of course. But if that is the case, could this not account for at least some slower growth ? (as in, even if they have equal growth on a mass basis it would translate to faster length growth if the nail is thinner).

Going on the abstract of a study by J.P. Pessan, et al., fluoride intake, as well as "the fact that toenails are less prone to environmental contamination," constitutes a lesser need for growth in toenails than that in fingernails. Also, fluorine being a crucial component in maintaining the solidity of bones, the body may redirect more fluorine that is ingested by various means, to the hands than to the feet, due to the arguably more necessary functions of the hands (in that they are used them for agile and precise motions that tend to influence our survival), meaning less growth in toenails as evidenced in the first citation.

are toenails are less prone to environmental contamination?

Well they are kept in shoes most of the time, whereas we stick our hands in everything.


text:
Proving time travel
Consider this answer to an interesting question. It's not possible to prove completely that someone is the descendant of someone else, there's always a nonzero probability that the results are a coincidence.
How confident can you get that genome T is the descendant of four unrelated grandparents? How would you tell?
Restrictions: You're not allowed to sequence all other humans and rule out other possible parents. Time traveller is has the normal number of chromosomes. You can test people's parents if that would help.
The maternal grandmother would share mitochondrial DNA, and the paternal grandfather would share the Y-chromosome, or the paternal grandparents would have one X chromosome between them. I'm not an expert on SNP accumulation but would there be enough information to conclude this person was from the future? Would there be too much mutation in two generations to pick out the relationships under it?

This should be pretty easy to demonstrate. Over the two generations, there would be 200-300 mutations in the entire genome of 3.3*109 base pairs, i.e. about 1*10-7 of the base pairs should be altered. If Time Traveler is male, for example, imply sequencing the Y chromosome and mitochrondrial DNA and comparing to the paternal grandfather and maternal grandmother should be adequate to decisively validate the claim.
If this isn't sufficiently satisflying could then move on to the autosomes and note that only about 200-300 base pairs max should be different from the union of the four grandparental genomes. The chances of this occurring given random set of four unrelated genomes will be vanishingly small.


text:
Why do sneezes come out the mouth?
As anyone who's ever sneezed can tell you, it's caused by irritation in the nose.  And the answer to a question on this very SE attests that "sneezing is a reflex, partially autonomous, to clear the nasal cavity of particles that don't belong there."
That being true, the sneeze mechanism is a little bit strange: if you hold your hand up in front of your face when you sneeze, you'll feel that all of the rapidly-expelled air that ought to be cleaning out your nasal cavity is coming out your mouth, not your nose.  In fact I don't think I've ever felt air coming out my nose when I sneeze.
So what's going on there?

Your premise is wrong: http://si.wsj.net/public/resources/images/PJ-AT748_respor_F_20100222143757.jpg

@kmm: Is it? I see a huge spray of droplet-stuff coming out of the mouth and a tiny bit of barely anything coming from the nose.

To say that "all of the rapidly-expelled air" comes out of hte mouth is not accurate. Maybe the amount that comes out of the nose is sufficient.

If you keep your mouth closed, the sneeze will come out of your nose.  From an evolutionary perspective, the mouth being open might help to reduce pressure which is good for preventing an aneurysm.

I've pondered this question too.  It's very clear that when we sneeze, the expelled air comes mostly from our mouths.  However, at least as far as my own sneezes are concerned, some of the air comes from my nose as well.  I know that if I pinch my nose closed as I sneeze, my ears hurt and pop.  If my nose is sniffly, I usually notice mucus come out.  Our soft palate partially lowers and our tongue rises as we sneeze, in order to divert a portion of the air up into our noses.  That position of our tongue is why our sneezes make a CHHH sound. If people intentionally keep their mouths wide open as they sneeze, that could explain why nothing comes from their nose, as there's nothing to divert the air.

A good book to learn as background is called 'Why We Get Sick: The New Science of Darwinian Medicine'.
In a sense you can consider us vectors for some microorganisms. When you cough you spread germs to other individuals (other vectors). Thus, it would be evolutionarily advantageous for a microorganism's genes if they were to infect more vectors.
How many germs are spread from the nose rather than the mouth? I don't know. However, expulsion of germs from your mouth will reach further than from your nose. It might be that there is a greater density of germs coming out of your nose, but that they don't travel as far in the air.
The above is slightly speculative, though, and I could speculate more but from what I can tell that is to be kept to the comments. (I can't comment due to <50 rep).
TL;DR More germs being spread from the mouth due to increased capacity for infected droplets and increased potency in terms of expulsion - advantageous evolutionary mechanism for spreading germ's genes.


text:
What happens once a brain is full?
I just read the answer to this question, and it got me thinking...
If the human brain (or any other brain) has a finite amount of storage, what would happen once the brain has taken in its maximum amount of information?
This is, or course, assuming that the individual can live long enough to acquire that much information.
I would take a guess that just like how we forget things all the time, the new memories would "override" some older ones.
Has there been any research or hypotheses on a brain's behavior once the its storage has maxed out?

It's very likely that memory is "lossy" and holographic, such that you can keep adding more information indefinitely, but retain it with less and less accuracy.
Memory isn't a digital storage system with X gigabytes of capacity, and the inputs to memory aren't neat little packets. What we remember are a web of associations and patterns. Vastly oversimplified, we group similar memories together into a baseline, and remember the deviations from that.
If you walk the same route to work every day, you take in a huge amount of information the first few days: stretches of residential buildings, cars parked on the street, portions of curb painted red, trash in the gutters. In successive days different cars will come and go, front yards will get overgrown and trimmed, etc, but these details get mixed in with what you saw the first few days into a blurrier and blurrier sort of average. Trillions of impressions from hundreds of days take up very little more capacity than the first day did, and still tell you what you need to know about the route.
Imagine that there's a particular green car of common make and model, that was parked in front of a certain house about 3/4 of the time for the first hundred days you walked the route. Your memory reduces this to something like "green car usually along here somewhere". If the green car stops parking there, you'll probably notice "green car not there today" because that's a contrast to the common case that you've memorized. But if a week goes by with no sightings of the green car, it's very hard to remember which day you last saw it, because you don't remember individual sightings. (I actually had this happen to me with my own car; I discovered it stolen on a Wednesday and could not for the life of me recall whether I'd seen it on Monday or Tuesday even though I'd walked past the spot it should have been parked both days.)
As you remember more things, you remember them in less and less detail; you can't remember if you've been to New Orleans once or twice; you can't remember which memories were from your first trip to Las Vegas or your second, etc. So the brain never becomes full, it just becomes fuzzy.

Three possible mechanisms are mentioned in the first referenced article [1]:

Attentional blink - the failure to detect a (visual) stimulus [2].
Visual short-term memory - non-permanent storage of visual information over an extended period of time [3].
Psychological refractory period - the period of time during which the response to a second stimulus is significantly slowed because a first stimulus is still being processed [4, 5].

References:

Marois R, Ivanoff J. Capacity limits of information processing in the brain. Trends Cogn. Sci. (Regul. Ed.). 2005 Jun;9(6):296-305. doi: 10.1016/j.tics.2005.04.010. PubMed PMID: 15925809. Full text available on http://www.psy.vanderbilt.edu/faculty/marois/Publications/Marois_Ivanoff-2005.pdf
Wikipedia contributors, "Attentional blink," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Attentional_blink&oldid=615277943 (accessed July 12, 2014).
Wikipedia contributors, "Visual short-term memory," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Visual_short-term_memory&oldid=508372290 (accessed July 12, 2014).
Pashler H. Dual-task interference in simple tasks: data and theory. Psychol Bull. 1994 Sep;116(2):220-44. PubMed PMID: 7972591.
Wikipedia contributors, "Psychological refractory period," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Psychological_refractory_period&oldid=603184270 (accessed July 12, 2014).

I'm not sure this actually answers the question. It was about storage capacity, not processing capacity.

This answer only talks about short-term aspects, while the original question is about long-term perspectives, I think.

I realize that this answer doesn't really answer the question I had. The sources seem to be talking about an overflow of information at a single time rather than taking in over the long run. However, I may just need more explanation.


text:
Why does the sacrum fuse together?
Everywhere I look describes how the 5 sacral vertebrae start fusing together during adolescence and are totally fused by the time you're 30 or so. But nobody seems to explain why this happens.
It seems like it would be disadvantageous for women, since presumably having a fused sacrum makes giving birth more difficult- apparently post-partum fractures are not uncommon (http://rheumatology.oxfordjournals.org/content/42/2/384.long). So why does it happen?
EDIT: Matthew McTernan gave a great answer, but I am greedy and would like to know more: Why does the sacrum only start fusing together in adolescence, and then finish in your late 20s - early 30s? Most major development ends in your early 20s. Does this have something to do with reproductive concerns? If so, why does it happen on the same timescale in men and women?

It isn't just humans that have fused sacral vertebrae. Animals on the phylogenetic tree ranging from Squamata (lizards), to Aves (birds), to even Monotremata (egg-laying mammals) all have fused sacral vertebrae. The fused vertebrae can serve as a stronger, weight-baring structures for animals that do land locomotion, including humans. Any bones that have evolved to withstand extensive force will also be thick or fused together: and example is the fusion of the radius and ulna in frogs. This fusion of bones allows for the forearms to withstand the force of landing after a large leap.
Photo references:
Bird Sacrum: http://www.discussfossils.com/forum/uploads/842/sacrum_2.jpg
Frog Radioulna: http://classconnection.s3.amazonaws.com/573/flashcards/4420573/png/appendicular_skeleton-frog-142D89D722717E64724.png