text:
Why does the HPV vaccine not work on already infected people?
With my limited knowledge, I understand that the vaccine works by inserting fake HPV-like material in the body, thus inducing the immune system to build up defenses against it, so when the body is exposed to real HPV on the wild the immune system will be able to handle it.
That makes sense, however, why can't the body still build up the defenses when there was already an exposure? Specially when the HPV virus is "dormant" and undetectable.
EDIT: After the discussion with @Bob in the comments section below, the hypothesis is:

In an infected person whose immune system was able to clear the acute
  infection, the virus (single infected cells) is constantly trying to
  enter lytic cycle again, only to be defeated by the immune system
  (because one infected cell leaving dormant state alone might not be
  effective); and then when the immune system is compromised for some
  reason, the virus is successful into entering lytic cycle and then
  there is a new clinical infection.
If this is all truth, then the answer to the question is that the vaccine
  does "work" in the sense that the body still reacts correctly (by responding to the antigen)
  to it, but it is, in practice, useless because: 1) when the virus is
  dormant there isn't anything for the immune system to do; 2) when the
  virus strikes, the immune system was already exposed to it anyway, so
  it is generally able to fight and there is no need for the vaccine; 3)
  the infection will get clinical again only when the immune system is,
  for some reason, defective.
The whole point of the vaccine is to never let the virus infect many (or any?) cell in order to avoid this situation where it is always trying to come back - and will do, when the immune system can't fight it off for some reason.

Please, if some specialist can analyze and comment on that it will be awesome.
More questions around it:

Is there the possibility that, while in this "dormant/attack" cycle, every single infected cell is defeated over the course of time, meaning an actual "cure"?
How does the cell replication process impacts the 1) hypothesis? (Maybe it is not possible for the immune system to achieve a natural cure because the virus keeps constantly replicating.)
How "much virus" would be needed for a successful strike in a compromised immune system (and how much compromised that system would have to be to fail)?
If the virus acts locally, is it possible for the vaccine to help other still-not-infected sites? In other words: is the natural immune response from the first infection in, say, the anus, worth anything for a subsequent infection in, for example, the oropharynx?

My guess: since the vaccine would trigger the production of plasma cells that are able to detect surface antigens on the viral envelope. Once the virus has infected a cell, it has inserted its genes into the host genome, and therefore can not be detected. The other thing HPV does is "kill" the the cells surrounding it (creating a wart), thus hiding any infected cells that would be displaying surface - antigens.

Also, the damage to host's genes has already been done during the acute stage of infection, so vaccination afterwards won't prevent HPV-induced cancer. It may reduce the risk, though, if the next exposure will be to a different strain.

@Bob The immune system does not recognize the vaccine material as an antigen, because the virus has already inserted his genes in the host's genome? So what happens with the vaccine material if it doesn't trigger the immune system, it just lays there?

The immune system could still trigger a response to an HPV - however, the antibodies would only target viruses that are outside of the cells (eg. in the circulatory or lymphatic system.) It could not target it once it's inside the cell, and it can not target infected cells that have been enclosed by dead cell material (the wart).

@IMil Is this gene damage systemically relevant? I understand that HPV has local effect, thus vaccination afterwards could still work on non-infected areas of the body since there wouldn't be any damage?

@Bob I understand now, thanks. So, if the immune system of an infected person still recognizes the vaccine antigen and responds to it accordingly; and there is no wart; and there is no virus outside because the virus is hiding for, say, 10 years... Shouldn't the immune system be now prepared for the moment when the virus try to strike again in the future?

As your cells replicate, they also replicate the dormant viral-genes. So, when the cells finally do enter the lytic cycle, there will probably be a lot more viral components than there are antibodies - thereby allowing the virus to infect more cells. And furthermore, just because one infected cell leaves it's dormant state, does not mean that all infected cells will also leave the dormant state.

And I just want to throw this out there again, as I said in my first comment, I am only guessing. If I knew with 100% certainty, I would have submitted an answer. (I've never studied virology). But I feel like I'm probably somewhat on the right track.

@Bob So it is possible that what really happens is, in an infected person whose immune system was able to clear the acute infection, the virus (single infected cells) is constantly trying to enter lytic cycle again, only to be defeated by the immune system (because one infected cell leaving dormant state alone might not be effective); and then when the immune system is compromised for some reason, the virus is successful into entering lytic cycle and then there is a new clinical infection? This all is pure conjecture of mine.

I believe that you are now thinking about it in the same way that I am. I don't think HPV is particularly dangerous (aside from the increased cancer risk), so in most cases what you said is probably what happens. I wouldn't be surprised if just about everyone has some form of viral-infection. But, until your immune system is comprised, you'll probably never know.

@Bob If this is all truth, then the answer to the original question is that the vaccine does "work" in the sense that the body still reacts correctly to it, but it is, in practice, useless because: 1) when the virus is dormant there isn't anything for the immune system to do; 2) when the virus strikes, the immune system was already exposed to it anyway, so it is generally able to fight and there is no need for the vaccine; 3) the infection will get clinical again only when the immune system is, for some reason, defective.

@Bob This spawns other questions (maybe not answerable without practical research - or at all): 1) Can the vaccine at least strenghten the current immune system response that was naturally trained before? 2) Is there the possibility that, while in this "dormant/attack" cycle, every single infected cell is defeated over the course of time, meaning an actual "cure"? 3) Is there any way to detect dormant virus, even if very expensive? 4) How "much virus" would be needed for a successful strike in a compromised immune system (and how much compromised that system would have to be to fail)?

By the way, if it were possible to detect the infected cells and kill them, would them generally be too numerous for that strategy to be effective without side effects on the body, or the whole problem lies in the detection?

To your first comment: 1) Definitely; 2) Probably. Unless there's a chance that it was able to infect a cell undetected? I just thought of something - the virus infects the basal layer epithelial cells, so i dont think it enters circulatory system. That would mean that antibodies would need to detect the virus in the dermal region (underneath the basal layer). And since the virus would need to infect a cell superficially to the basal layer, I suppose there is a chance it goes undetected. So, once the cell is lysed, the immune system wouldn't be able to make a response. Is that how warts form?

2nd comment: 1) No. Immunity, is an all or nothing attack. When your immune system is activated, your body will produce as much antibodies as it can very quickly. 2) I believe so. I know that some people can have warts that disappear/appear for many many years before they never see them again. But does that mean that their body actually defeated the virus? Or is it going to come back in 15 years? 3) You would need to create a protein or RNA or something that can recognize the viral gene-sequence in the DNA. It would need to be very specific. Then you would need

To have this protein/RNA/whatever trigger destruction of only infected cells. 4) I have no idea lol - but figuring this out would answer #2 from the first comment

I think you should add an edit to your question with some of these things that we have discussed. And maybe someone else would be able to clarify where we might have gone wrong - this quite an interesting topic to think about.

I do wonder, though, why the rabies vaccine can be given after a possible infection.  AFAIK it's the only one that acts like this, and though animals (dogs &c) routinely get rabies vaccine, I've never heard of a human getting it unless bitten by a possibly rabid animal.

@jamesqf I realize this is an old thread, but you brought up a good point about the rabies vaccine. Just to clarify: The treatment is called "rabies postexposure prophylaxis" (PEP). It's a rabies vaccine series plus a dose of rabies immunoglobulin (antibodies targeted against rabies virus). Immunoglobulin is an essential part of the treatment, as it triggers a more rapid immune response than you'd see with vaccine alone. Also - it needs to be given before symptoms develop. Here's a link to more information. It includes a link to CDC guidelines:
https://www.medscape.com/viewarticle/877636

This is an excellent question, and it is actually being studied -- but for a different reason than your question suggests. HPV is a bit unique because there is some data showing that infected individuals can become "reinfected" with the same virus type, causing reactivation of the dormant/latent virus that they are already infected with. So the question in this case is whether administering an HPV vaccine to an already infected individual can help prevent (or minimize) reactivation of the latent virus.
Here's a journal article explaining some of this research. Please note that it is not standard medical practice to give HPV vaccine to already infected individuals. This work is still in the research phase, and is aimed at minimizing viral reinfection and reactivation:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5006803/
Simply put, a vaccine only works to prevent infection with a specific virus. It is rarely effective in treating a virus once a person has become infected. The reason for this has to do with how the immune system responds to its first encounter and subsequent encounters with a particular virus:
When the body encounters a specific virus for the first time, the immune system mounts a "primary" immune response specific to that virus. A primary immune response triggers the body to produce virus-specific immune cells that can generate antibodies against that virus. The body continues to make these immune cells in small quantities even after the virus is eliminated.
If the same virus is encountered again later, these cells will proliferate and immediately start producing antibodies against the virus. Thus, the body can mount a much faster and stronger "secondary" immune response. This prevents the viral load from reaching levels that produce physical symptoms, so the person does not become sick (or at most they may have milder symptoms), and the immune system is to able eliminate the virus more quickly.
The purpose of a vaccine is to trigger a primary immune response. With a vaccine, the body is exposed to a weakened form of the virus, and a primary immune response is triggered without the individual becoming sick. When the individual encounters the real virus, the body immediately mounts a secondary immune response, which fights off the virus much more efficiently and quickly, and the person typically has no physical symptoms.
Here's a more in-depth explanation on the difference between a "primary" and "secondary" immune response. Most cell biology textbooks (and all immunology textbooks) will have an explanation of this as well. This is an important concept in understanding how vaccines work:
http://www.microbiologynotes.com/differences-between-primary-and-secondary-immune-response/
If a non-vaccinated person is infected with a virus, administering a vaccine generally has no effect. At that point the body is already mounting a primary immune response, so a vaccine would serve no purpose. Because a primary immune response is slower than a secondary response, when a non-vaccinated person gets infected the viral load is able to increase more rapidly than it would in a vaccinated individual, resulting in the physical symptoms typical for that particular virus.
What makes "chronic" viruses such as HPV and Herpes virus (including chicken pox) harder to eliminate completely is that these viruses enter a dormant/latent (lysogenic) phase. At that point they become "invisible" to the immune system. Even if the person is not visibly sick, they are still infected with the virus. If/when the active (lytic) phase is triggered, the viral load increases rapidly -- more rapidly than if it were a new viral infection. The body still mounts a secondary immune response, but typically this will not completely eradicate the virus. As long as any amount of the virus is in the lysogenic phase, it remains "invisible" to the immune system.
With some viruses (e.g., chicken pox virus, which causes shingles) if a vaccine is administered during the latent phase, this can help somewhat with making symptoms milder if/when the lytic stage is ever triggered. But this doesn't work for all viruses.
If a targeted antiviral medication is available (e.g., Tamiflu for influenza; Harvoni for Hepatitis C) this can slow down the proliferation of the virus, allowing the immune system to "catch up" and eliminate the virus. Antiviral medications aren't vaccines. They are designed to directly target the virus and interfere with a biochemical activity that the virus needs in order to proliferate.
Currently there is no antiviral medication available for HPV, although a few drugs are being researched. One drug in particular (ranpirnase) looks promising, but it is still in early clinical trials.

I believe the following paper discussing the lifecycle of HPV is of use for understanding at least some of the aspects of your question: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5394500/
Specifically:

Viruses like HPV have the capacity to form virions and become transmissible at some point in their natural lifecycles, but within tumors these infections are generally latent so that productive virus replication (also known as lytic replication) is either diminished or absent. Viral latency serves as an immune evasion strategy allowing the virus to hide from the immune system by turning off unnecessary viral proteins that might be sensed by cell mediated immune recognition. The virus persists as a naked nucleic acid, often as a plasmid or episome, which relies on host cell machinery to replicate whenever the cell divides. Viral latency should not be mistaken with clinical latency, which means asymptomatic infection (14).
The most favorable explanation for the connection between virus latency and tumorigenesis is that productively replicating viruses initiate cell death, the known cytopathic effect (CPE). Virus-induced CPE can be harnessed to kill cancer cells in viral oncolytic therapies, illustrating the anticancer activity of active lytic viral replication. Although CPE is often thought of as a virus-induced event, it is in fact a stereotypical and nonspecific innate immune response of cells to infection by many types of viruses. When latent viruses switch to producing virions, virus replication generates pathogen- associated molecular patterns from partially synthesized viral chromosomes, double-stranded RNAs and empty capsids that trigger cellular DNA damage responses and innate immune signalling. For some viruses, lytic replication generates a linear viral chromosome that can be recognized as a DNA fragment unless either the DNA ends are structurally hidden from DNA damage response sensors by encapsidation or these sensors are inactivated (14).

I think this addresses some relevant aspects of your question, namely:

why can't the body still build up the defenses when there was already an exposure?

It can and already has, see my answers to later questions. But it doesn't work on the already present viral infections because:

Is there the possibility that, while in this "dormant/attack" cycle, every single infected cell is defeated over the course of time, meaning an actual "cure"?

Not really, since the immune system cannot 'reach' or 'see' the HPV infected cells and thus isn't attacking them until they enter the reproductive phase.

How "much virus" would be needed for a successful strike in a compromised immune system (and how much compromised that system would have to be to fail)?

There probably won't ever be an exact number here but the paper I linked above does list some (obviously approximate) numbers regarding HPV activity:

After infection of wound basal cells, it is thought that there is a round of viral DNA replication that appears to be independent of the cell cycle and amplifies the viral copy number to around 50 to 100 copies per cell. The infected cell leaves then this primitive compartment and enters the transit amplifying proliferative compartment of the epithelium, where there is a phase of plasmid or episomal maintenance when the viral copy number remains constant and viral gene expression is minimal. In this phase of the viral life cycle of the high-risk HPVs, the expression of the potent oncogenes E6 and E7 is under strict control, and E6 and E7 transcripts of high-risk HPV types are hardly detectable in the proliferating compartment of the epithelium (10). When the infected keratinocyte enters the differentiating compartment, in the stratum spinosum exiting the cell cycle, then there is an extended upregulation of viral gene expression and viral DNA replication, with amplification of the viral copy number to many thousands of copies per cell, gross expression of the E6 and E7 early genes, and expression of late genes from the late promoter, leading finally to HPV formation

Lastly, you asked:

If the virus acts locally, is it possible for the vaccine to help other still-not-infected sites? In other words: is the natural immune response from the first infection in, say, the anus, worth anything for a subsequent infection in, for example, the oropharynx?

The answer to this, I believe, is that if you are speaking of an HPV vaccine of the same strain then it would likely not be useful, since your body's immune system would already recognize the same strain that it already has been fighting off, also in a different location. However, HPV has a couple of different strains and a vaccine for those might help with infections in different locations by different strains. Considering that vaccinations like Gardasil actually cover a lot more than 1 type of HPV, vaccination might still be relevant.
For a source that HPV vaccines cover more than 1 strain, see: https://www.cancer.gov/types/cervical/research/gardasil9-prevents-more-HPV-types and https://www.ncbi.nlm.nih.gov/pubmed/25693011
For a semi-source that already infected people might benefit from vaccination, see: https://www.cancer.gov/news-events/cancer-currents-blog/2015/hpvvaccine-multisite (note that this is from what I can tell pre-publication research presented at a conference and so it all seems quite preliminary).
I also found this paper to be informative on the topic of HPV and the immune system response to it, but it isn't open access so I cannot guarantee that you'll be able to read it. For the sake of completion, I'll still link it: http://dx.doi.org/10.1016/j.ygyno.2013.08.025


text:
Does it make sense to classify all humans in a single species?
For what biological reasons do we consider that all human beings belong to the same species?

A Thai and a Nigerian share a common ancestor that is 140,000 years old (see Gravel et al. 2010 and this post). Would, for example, a mixed Thai - Nigerian baby suffer from any outbreeding depression?

humans have remarkably low genetic diversity especially given our population sizes. On top of that most ~85-92% of our genetic diversity is within population not across populations. Outbreeding depression is not going to happen. http://jorde-lab.genetics.utah.edu/elibrary/Jorde_2000a.pdf

For info: Motivation for the post
There had been a number of questions on whether it makes sense to classify all humans into a single species. Unfortunately, many of them where poorly phrased and therefore did not get much attention or even got closed. Here is my attempt to open a post that will be referenced to for future questions on the subject.

Are you sure this question is fit for Biology SE? To me it seems like it's more a match for some more "social" SE-e.g. it bear more on anthropology (in all of its dimensions), rather than to biology per se or the tag human-evolution.

The definition of "species" is pretty clear-cut.

@CarlWitthoft I disagree. Please have a look at this answer

Possible duplicate of: Outbreeding depression in humans

@theforestecologist This other post had received very little attention (no upvote, no answer, no comment and only 100 views in 7 months). I marked the other post as a possible duplicate of the current one as the current got a lot more attention in only 16 hours.

@theforestecologist Another candidate: Do humans have enough biological differences to be grouped into races or subspecies?

Neither of those two posts cited make any mention of outbreeding depression. Why then do they support the claim that there could be outbreeding depression between Nigerians and Thais? This seems speculative on the part of the OP.

@Will the reference is here to support the estimate divergence times and the SE post is here to offer a visualization of the tree of human lineages (this SE post is arguably not necessary). Sorry if you misunderstood the purpose of the citations. I reordered the sentence to prevent other misunderstanding. The post does not claim that there is outbreeding depression in humans but ask if there is any.

This question sounds quite racist....

@altroware While the question may bring up emotional reactions, the question is by its nature purely scientific. You will note by the way that the OP is the same as the one who wrote the top voted answer (and the same who wrote this comment :) ). You will also note that below the post I explained my motivations for asking this question.

Actually, we not only consider that all human beings belong to the same species (Homo sapiens) but even that we belong to the same subspecies (Homo sapiens sapiens). So, does it really makes sense?
Concept of species
First, please note that the concept of species is more arbitrary than the most layman would think. I wrote my opinion about the concept of species in this post.
Concept of species in sexually reproducing lineages
In sexual lineages, the existence of different species is generally defined by the existence of a reproductive barrier (see reproductive isolation and see UnderstandingEvolution > biological species concept).
A reproductive barrier can be caused by either pre-zygotic or post-zygotic isolation. I will mainly disregard potential case of pre-zygotic reproductive isolation in this answer because such isolation depends highly on the culture and not only on human genetics. I do not mean that pre-zygotic isolation does not matter or are irrelevant, I just decide to focus on post-zygotic isolation because, as being very independent of the culture, it makes its study much easier.
Reproductive isolation might be partial typically leading to cases of outbreeding depression (when it comes to post/zygotic isolation).
If we had many documented cases of outbreeding depression, it would suggest that we should reconsider the decision of considering all human being. So the question is really: Do we have documented cases of outbreeding depression?
Do we have documented cases of outbreeding depression?
Many cases of inbreeding depression have been documented in humans (McQuillan et al. 2012, Strauss et al. 2013, Lettic et al. 2008, Gellera et al. 1990) but cases of outbreeding depression seem much rarer if any!
I spent some time screening through the literature searching for potential evidence of outbreeding depression. The only paper I found is Udry et al. 2003.
Udry et al. 2003:

First, note that they do not place their results in the context of our present discussion and do not talk about outbreeding depression.
They report that children of "mixed-race" in US colleges report having more behavioral troubles. One would obviously note that there could well be true that "mixed-race" children experience a different environment (incl. social environment) than "non-mixed-race" children. Such results, therefore, does not suggest the existence of any outbreeding depression.
They also report more skin problem in mixed-race children. Unfortunately, 1) their p.value is only slightly significant and 2) they track tens of variables without correcting for multiple comparisons and only one came out significant causing the expected family-wise false positive rate to be higher than the observed family-wise positive rates (see false positive and related concept in statistics).

So, in short: No, there is little to no evidence of outbreeding depression in humans
Potential publication bias and taboo
It is not impossible that there is a publication bias in which researchers looked for inbreeding depression more than for outbreeding depression. One would note also that it would probably be quite taboo to attempt to suggest that there are several species of humans for social reasons and such taboo could cause a publication bias too.
I personally doubt it would be the case that such publication bias exists. Note also that if the evidence of outbreeding depression were obvious and common, then we would not have a problem telling that there are several species of humans. In essence, if there is a publication bias that is causing us to fail to see existing outbreeding depression, it must mean that existing outbreeding depression would be relatively rare and with small effect anyway.
Other definitions of species and taboo
Well, the issue is that there is no other commonly accepted definition of species. Typically, above I only considered outbreeding depression and I did not consider a potential pre-zygotic barrier that would result from geographic isolation or from cultural reasons (e.g. maybe on the ethnic group does not like the appearance of people of another ethnic group and vice versa). I don't doubt that for social reasons, we tend to be quite happy that our only definition of species support the idea that all humans belong to the same species.
It is hard (for me at least) to tell whether we might tend to be more permissive in other lineages and naming two sister lineages as belonging to different species.
Why same subspecies and not only species?
Under the biological species concept, H. sapiens and H. neanderthalis should belong to the same species. This is why we now rather call them H. sapiens sapiens and H. sapien neanderthalis. I suppose it would feel painful to many to not highlight our differences with H. neanderthalis and so, we decided to discriminate.
Again, it is hard (for me at least) to appreciate how this subspecies discrimination in the Homo lineage compares to discrimination among potential subspecies in other lineages.
Related posts

Do humans have enough biological differences to be grouped into races or subspecies?
Is there a consensus on whether or not race exists on a biological level?

I may possibly be prejudiced, but casual observation suggests that humans experience the opposite of outbreeding depression.  Don't have a clue as to where or how you'd find actual evidence, though.

The entire issue of inbreeding vs. outbreeding depression makes no sense in the description of the human population since it lives under very diverse natural conditions so something that can be classified as "fit" for some conditions (for example, better thermoregulation good for hotter climate) may actually be disadvantageous for other conditions. This makes the "fitness" of human rather an arbitrary category too broad to define out of particular social and/or geographic context and with the lack of such definition for fitness how can you say depression means anything,too?

@YordanYordanov Great points.  I was going to say that humans are highly adaptive to their environments, but I don't think that's the best way to describe it.  Humans have gotten very good at adapting our environment to us.  In many places in the world "natural conditions" are just the comfort standard we've adopted for day to day activities.  It's only if you're extremely unfit for conditions that you would really be able to tell.

You'll find in any lineage environmental variance for fitness and even eventually environmental variance for fitness in outbred individuals. It does not prevent the scientific community to come with arguments as to whether or not whether the lineage should be considered as a single species of as several.

Of course, the concept of species is largely undefined (see linked post in my answer), this is why I restricted the question to the existence of outbreeding depression. Any evidence of outbreeding depression (under any environment) would already suggest there are more than one species of humans. Failure to find such evidence would suggest that there is only one species of humans.

I'm a bit annoyed that you place your personal pet-peeve of species definitions/concepts that upfront in an answer that is meant as a 'standard' reference for future use (on mostly another issue). I get that you take issue with the species concept (you have expressed this several times at BioSE), but this is hardly an uncontroversial point of view. For more info, you also link to your own answer on the issue, which is (in my opinion) quite unbalanced and biased. This answer would be better and more to the point without this section.

@fileunderwater Yes, I agree with the feeling it may give. However, in this answer (unlike in the comment response to CarlWitthoft), the link to my other answer is to further ones understanding. The answer does not rely on the other post. To clarify the independence of the current answer to my other answer, I added a link to Understanding Evolution that define the so-called biological concept of species to justify why I am focusing on evidence of outbreeding depression. Does it sound better now?

Also, outbreeding depression does not necessarily imply several species (which you seem to say in the comments and in the answer). If this is indeed what you claim, this is definitely not the standard definition of outbreeding depression, and your use of the term would differ drastically from standard use.

A reference to the Biological species concept is probably useful. What I take issue with is the description (and need for) the "concept of species" section.

I am not sure I fully understand the issue. I added "my opinion" somewhere in the "concept of species" section.

Coming from a layman (sorry), what about species inter-breeding? There's a theory that we may be something like 2% Neanderthal.

@JackR.Woods It is a very good remark. The answer is found in the section Concept of species and especially in the linked post (How could humans have interbred with Neanderthals if we're a different species?).

@Remi.b "I will mainly disregard potential case of pre-zygotic reproductive isolation in this answer because such isolation depends highly on the culture and not only on human genetics." I'm not sure how to interpret this, are you saying that you think that reproductive isolation only should be measured by the resulting general genetical fitness of cross-breeding? Isn't the variance resulting from all kind of barriers, even if they are purely cultural or geographical, highly relevant to be a part of a classification system that describes the artifacts of reproductive isolation?

Like what about the enforced reproductive barriers that are created by conscious selective breeding? Especially with pets like for example dogs, where the concept of outbreeding depression is quite irrelevant. Do the breeds of contemporary dogs have a place on a description of the tree of life? Should we only talk about wolfs, and say that the different "variations" of wolf, like bulldogs or poodles, are of no interest when we classify that branch of life?

@Alex That's a good point you are highlighting in your first comment. I added I do not mean that pre-zygotic isolation do not matter or are irrelevant, I just decide to focus on post-zygotic isolation because, as being very independent of the culture, it makes its study much easier. While I would happily down play the conceptual importance of geographical barrier in defining species, I would clearly not do so for other factors causing pre-zygotic isolation (such as not finding each others sexy)

@Alex I don't understand how dog breeds relate to the first comment. I do consider that domesticated species do belong to the tree of life and semantic difficulties of species definition also apply to them.

@Remi.b The comment about dogs was intended as an example to clarify what I perceived to be a problem with the approach of basing the classification of populations on evolutionary fitness. Dog breeds have clearly been under pre-zygotic reproductive isolation, and it's highly useful to categorize the different isolated populations regardless of the fact that they all could interbreed and it's arguably not relevant to talk about evolutionary fitness. Even when you don't care about statistical phenotypical traits.

I find it meaningful that a classification of populations would include significant historical de facto reproductive isolation, whatever the isolation is caused by, that may or may not have resulted in a divergent statistical genotype that you may or may not know about. I get the feeling that you find it more relevant to base the classification on future potential reproductive isolation based on genetical compatability? Not finding each others sexy could be both cultural and genetical, would you distinguish the hypothetical cases where it's 100% genetical from where it's 100% cultural?

Oh I have to apologize, I read this question when refreshing on the human races issue, and somehow fooled myself into thinking that this question and answer were concerned about the subspecies/race level. Seeing that this is actually about the species-level, I agree with you that is is reasonable to focus on genetic compatibility as you describe.

source: Stack Exchange

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

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

sort: votes


text:
What really causes cancer?
A lot of things are claimed to cause cancer, eating red meat, eggs, smoking, using phones, deodorant, breathing.
Surely these can't all actually significantly contribute to the development of cancer.
I've heard smoking is a big one to lung cancer, with someone--I can't recall--saying that most patients with this cancer are smokers.
What kind of activities/foods are sure to, or have high chances to, lead to the development of cancerous cells and how do they cause them, at a molecular level?

Do you want to know which chemical causes cancer? Or what is the general reason behind cancer?

What really causes cancer: mutations in certain genes.

@chris Chemicals, and thus activities/foods.

"Cancer" is not just a single disease. Cancers would be more accurate, but even that doesn't do justice to the vast array of different kinds of cancers at the genetic or molecular level.

As they say, in California, EVERYTHING causes cancer :p

@kmm brings up a good point. As such, this question is way too broad. Tobi, I recommend that you edit this question to focus on a particular type of cancer (e.g., perhaps lung cancer like you already mention). I also recommend doing a bit more research on your own and updating your question w/ what you find. Doing both of those things should reduce the chance that this question gets closed. For more help writing good questions, see here. Thanks!

I've sufficiently edited the question, I'd really like a proper answer.

The Guardian: The 116 things that can give you cancer – the full list

@Tobi - No, this is way too broad. You may have specified one organ system, but you're still asking for a definitive list. "What kind of activities/foods are sure to, or have high chances to, lead to the development of cancerous cells and how do they cause them, at a molecular level?" Can't be done for a number of reasons. Kind of like asking "What do I have to do to roll a 12 three times in a row with fair dice?" Answer: there is no answer to that question, because the outcome of fair dice cannot be predicted if thrown properly.

Cancer is caused by the mutations in cells.
Cancer exists because of the failure of cell cycle checks which could actually allow cells to survive with erratic genomes. However, that alone does not cause cancer.
Cancer is the uncontrolled proliferation of cells. That only happens when cells have accumulated enough errors during cell division and each cell division goes undetected to the point that cells refuse to commit apoptosis; they are no longer receptive to the body's control mechanisms.
Cancer cells are also malignant. That means that cancer cells cannot be called cancer cells until they are invasive. That means a few cancerous cells cannot be caused cancer because they don't take nutrients from the body . Also, tumour  suppressor  genes can also cause cancer when they turn proto-oncogenes into oncogenes.

"please tell me if what are said here is factually true." While it's great that you're looking for feedback, you shouldn't post an answer you're unsure of. There are, however, a lot of interesting facts here that are sure to be helpful to the OP. Please provide a source for those who want to do further reading.

You have missed the very numerous benign cancers, which, though not invasive, are still cancer.  Also, invasive doesn't quite mean what you think it means.

You are correct in that cancer is a result of escaping cell cycle checks. This is usually a result of mutations. Not always.  See mesothelioma resulting from asbestos exposure. There are some cancers that seem to be a combination of genetic and epigenetic mechanisms. Further, you can have cancer cells that have not become invasive. This is what a tumor is before it acquires the ability to extravasate and set up shop elsewhere. That is metastasis. Further confusing the issue, a benign tumor IS uncontrolled proliferation, but usually considered "non-cancerous" (can't metastasize).

@akaDrHouse - "...benign tumor IS uncontrolled proliferation, but usually considered "non-cancerous" (can't metastasize)" I disagree. The ability to metastasize is not what defines a cancer. It is what defines a metastatic tumor from a benign tumor. I can name dozens of cancers that don't metastasize.

Thanks guys for being so negative. I'm quitting stack exchange. At least I tried to help

Thanks for the correction @anongoodnurse. You are right. I was confusing malignant and metastasis. I will change my comment. Edit: it won't let me.

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


text:
How does DNA damage increase the activity of p53?
I understand the steps leading up to the halting of the S-cdK checkpoint from there, but I can't find the mechanism by which DNA damage actually increases the activity of p53.

p53 is expressed constitutively but, in unstressed cells, it is an inactive conformation and its level is kept low by proteasomal degradation. Proteins which are recruited to double strand breaks can start a signalling cascade of protein kinases which leads to 1) stabilization of p53 and 2) activation by phosphorylation. If I find the time, I'll try and write a proper answer.


text:
How Can Homosexuality be Genetic?
I hold no strong opinions towards homosexuality one way or the other; I'll personally refrain, but don't apply my personal tastes to the rest of the world.
I remember seeing some articles a while back, and in some online debates, that there's been evidence in favour of a genetic component of homosexuality. I ignored it back then (before it became legalised), since it didn't affect me. However, after deep thinking, I started to seriously doubt those stories.
My gripe is this, based on my extremely limited understanding of Evolutionary Biology, organisms with genes which boost survivability, will tend to become more abundant. Genes that made organisms more fertile and reproduce more, will tend to become more abundant.
So, if say a particular gene, reduced effective fertility of organisms, that gene may be expected to be absent after a while. Fewer organisms with that gene would reproduce each successive new filial generation. There will be a diminishing marginal increase in the population of these gene bearers, before there eventually starts to become negative growth. I expect that population, may eventually find themselves in extinction, or on the brink of it.
In the few 100,000 years that Homo Sapiens have walked this planet, I guess there's been sufficient time for a population of genetically predisposed homosexuals to become extinct, or reach its brink. Certainly not the 5% - 10% estimated population we have today.
As such, I am unable to understand how homosexuality might be determined by genes in spite of natural selection.
My understanding of Evolutionary Biology may be severely lacking; especially as my teachers in the subject believed it was blatantly false, and were not really interested in making their students understand it. Some even going to the extent of making it seem as ridiculous as possible (I live in a country, where more than 90% of the population are genuinely religous (as in they truly believe in the existence of God) in one form or the other). I would appreciate answers to my question.
Of course, whether or not treatment of homosexuals should change, is another separate matter. It certainly does not follow from any conclusion of this inquiry; the answer to this question, is irrelevant as far as LGBT rights are concerned.

Note that there is no question in the boy of the pot. Only in the title. That makes the post arguably slightly unclear. The title would let one thing you are interested in the mechanistic mechanism by which genes can affect sexual orientation while the body of the post clearly talk about selection pressure toward those potential genes.

I guess my question would be: How can homosexuality be genetic despite natural selection?

Is this any different from How can homosexuality evolve despite natural selection?? Can you please try to clarify in what way these two questions are different?

It is possible that lack of knowledge in evolutionary biology would prevent you from understanding that these two questions are the same. Understanding Evolution by UC Berkeley is a very introductory course to evolutionary biology if you are interested.

Take the advice of @Remi.b, check out the Berkeley site. It's a mistake to assume evolution can eliminate all traits that do not appear to offer a selective advantage.

Consider that evolution works by populations, not just by individuals.  A human tribe that has a proportion of its people not attached to their own offspring seems likely to be stronger than one made up of competing male-female pairs.  To take this to an extreme, you might ask how eusocial creatures like ants, bees, and naked mole rats can be successful.


text:
What kinds of bacteria live in water bottles?
I've always heard not to re-use disposable plastic water bottles.
According to this Huffington Post article, the reason is because:

everyday wear and tear from repeated washings and reuse can lead to physical breakdown of the plastic, such as visible thinning or cracks. Bacteria can harbor in the cracks, posing a health risk.

Also, a study from the Canadian Journal of Public Health found nearly two-thirds of bottles sampled had bacterial levels that exceeded drinking water guidelines. (See here).
So my question is: What kinds of bacteria (or other microorganisms) live in water bottles? In other words, which species should we worry about in these cases?
This Livestrong Article lists species found in the water itself, but I'm more curious about what organisms get introduced and grow through re-use of the bottle.
This is relevant because bottled water just became the most sold consumer beverage in the US.

I usually follow the rule: reusable until perma-stank condition achieved. The water in your faucet is not sterile. It is host to many bacteria, molds and yeast. This is one contributor to contamination. Plus the air you breath is host to microbes, therefore opening the water bottle contributes to contamination. But, if you rinse and wash with soap between uses, it should be good for a few weeks before it's time to be recycled.

In addition to the cracks providing a better place for bacteria to grow, all plastic bottles, when reused, are subjected to high levels of bacteria due to contact with hands and mouths. So your water bottle can potentially host a range of bacteria.
Your water bottle traps humidity inside and provides a perfect growing medium, especially near the threads of the mouthpiece and along/within cracks in the bottle which provide better bacteria accumulation.
Microorganisms that Grow

Overall, most sources I could find remained very vague (numerous News stories) or mentioned bacteria generally:

Staphylococcus and streptococcus species, [Source].

Norovirus [Source].

The seemingly most detailed studies I could find came from Watanabe et al. 2014 and Ohnishi et al. (2012) who examined microbial growth in numerous beverage types. However, I could only find their their abstracts online, which report:

microbial growth was detected in ~20% of poured samples, and in ~51% of drank samples.

225 bacterial strains, 27 mold strains, and 77 yeast strains were isolated

Bacteria: Streptococcus spp. (e.g., S. salivarius) and Staphylococcus spp. (e.g., S. aureus), made up the majority. Enterotoxin-producing S. aureus and Bacillus cereus were also isolated.

Molds: Cladosporium spp., Tramets spp., Bjerkandera spp., and Penicillium spp.

 [I Will hunt down these articles to get more details and will update accordingly when I find them...]
Microorganisms in the Water

Based on a study found here, brand new bottles of water can have fungus spores (typically harmless), but opened bottles can show signs of greater diversity (e.g., fungi, skin Staphylococcus, and yeast.

Igbeneghu & Lamikanra (2014) found Staphylococcus species (notably S aureus) and strains of Pseudomonas in bottled water available in Africa.

Your Livestrong article lists a number of non-human pathogens such as: Ralstonia Pickettii, Acidovorax Temperans, A. Delafieldii, Agrobacterium Rhizogenes, Burkholderia Glumae, and Bacillus Thermoglucosidasius.

Juvonen et al.'s  (2011) "Microbiological spoilage and safety
risks in non-beer beverages" provides a thorough list of organisms found worldwide in different bottled waters and other beverages.

Other Issues

According to Rose State microbiologist, Dr. Amy Hurst:

The plastic materials degrade into the water, so then you're drinking very small plastic molecules. [Source].

PET plastics tend to leach when exposed to realistic though extreme conditions, such as exposure to sunlight, heat and storage time. [See UF article]

Bisphenol-A (BPA) and phthalates present in the bottles can leach into the water and possibly cause harm to humans.

Rochester (2013) provides a good review of BPA effects in humans and other test organisms.

New research shows that BPA alternatives such as BPS aren't any safer either; in fact, in some cases they are considered more dangerous to humans. All bisphenols are capable of mimicking the body's sex hormones, says Robin Mesnage, research associate with King's College London.

Al-Saleh et al (2011) found that  76% of the bottled waters they tested in Saudi markets contained measurable amounts of phthalates.

So Reusable Plastic Bottles are Better Right?

Well, from a bacteria standpoint, this isn't necessarily true.  According to a small study  of 12 reusable bottles being used for a week:

Avg bacteria load: 300k CFUs (colony forming units). Ranged between 25 - 900k CFU/cm$^2$.

Notable types found: E.coli, salmonella, and various gram-positive cocci and gram negative rod bacteria.

They found that different bottle types harbored different amounts and kinds of bacteria.

True enough the re-usability of plastic bottles is quite a problem even in the area I live. This is due to multiple factors; one of those factors is the symbiotic microorganisms that could be living in your mouth (from my lectures)
as well as any contaminant from anything you've eaten$^1$. That however isn't the only thing that could be contaminating your water bottle. The exposure to the air itself may contaminate. (that's why in microbiology we use a laminar flow cabinet or work close to a flame).
That's also why hospitals have air purification systems to avoid infections$^2$.
As a result, the amount of possible contaminants are too big to list. We could list those that I personally think would be more relevant to list -- these include our mouth natural flora since saliva is the most common contaminant of reusable bottles:

lactobacilli;
Candida albicans;
enterococci;
Streptococcus salivarius;
Fusobacterium nucleatum;

List obtained from Almståhl et al.$^3$
Almost all of these microorganisms are associated with some sort of disease or another.
I didn't actually find any specific study on the reuse of water bottles so i apologize for not being capable of giving a more definitive reply.
Sorry if i have failed to answer your question in any way or have misinterpreted what was required, I hope my research was some help to you.
Citations:

(Mahvash Navazesh, DMD, Satish K.S. Kumar, MDSc1, Measuring salivary flow : Challenges and opportunities)
(W.D. Griffithsa, A. Bennettb, S. Speightb, S. Parksb. Determining the performance of a commercial air purification system for reducing airborne contamination using model micro-organisms: a new test methodology.
Almståhl A, Wikström M, Fagerberg-Mohlin B. Microflora in oral ecosystems and salivary secretion rates--A 3-year follow-up after radiation therapy to the head and neck region.

Thanks so much for the edit! It is indeed much better. I apologize for the noobish mistakes.

This is not a problem, but one of the strength of the stackexchange communities. People correct mistakes that happen. Welcome to biology, btw. :-)

Great answer here, +1 and I edited your other post - don't emphasize being a newbie. This style of answering is awesome and a lot better that the average user accomplishes here.

Really? I'm glad to hear that my way of answering is usefull, I have to admit I got corrected and the credits arn't all mine.

@Kiny - my first posts were not only edited; they were blandly shot to pieces. That's how people learn right :-)

@AliceD xD Had that happened to me i would totally learn to fear the community. I'm glad my teachers teach me properly!!

@Kiny and that is exactly my biggest concern of harsh reactions to new users. People need to be given the freedom and help to find their way.

Kiny - sometimes I still correct @AliceD's posts, 30k rep later (and even though I am relatively quite new) ;)

@BryanKrause - never too old to learn :-) Thanks for your efforts !

@Kiny I'm glad you're taking the edits in stride and learning from them. Just know we're all here to help each other learn :). And I agree with AliceD -- we like details and citations here! Good Answer :).


text:
Purpose of intensive protein synthesis in G1 phase of mitosis
What is the purpose of intensive protein synthesis in G1 phase of mitosis, and what purposes do these synthesized proteins serve? Why are lipids and carbohydrates not synthesized intensively as well?

The G1 phase of eukaryotic cell cycle is part of interphase, which is when the cell is replicating its DNA ready for division. To understand the need for intense protein synthesis, we first need to understand how DNA is organised during mitosis.
Before DNA is condensed into chromosomes ready for nuclear division it is in the form of chromatin, a long fiber-like structure inside the nucleus. In order to condense into chromosomes, this chromatin must undergo a process of coiling and folding in order to create the chromosome 'X' structure we are familiar with.
A major part of this DNA 'miniaturization' is the folding of the double helix around proteins called Histones - this creates new structures called nucleosomes.
In order to fully condense the roughly 3 meters of DNA in the average human cell down to a singular chromosome, millions upon millions of these Histone proteins are required.
And that answers your question; intense protein synthesis during the G1 phase is required in order to produce the extremely large amount of Histone proteins that are needed for packaging DNA into chromosomes ready for cellular division.
As for carbohydrates, these are constantly being processed by the body in order for the production of ATP for use as energy. The use of said energy for mitosis is a just another constantly required use of ATP within the body. Therefore there isn't any noticeable increase in carbohydrate processing/production, as it is happening regardless of the cell's stage in its cycle.
-See the image below (from shmoop.com) that explains the process of getting DNA into a chromosome.


text:
Is it possible to intentionally limit bacteria's lifespan?
Say I have a species of bacteria. I want this species to only persist for a set number of generations, after which it simply stops reproducing. Is it possible to do this at all (with known genetic engineering techniques), and if so, how do you prevent bacteria from evolving against it?


text:
How to contract sternocleidomastoid muscle by thought?
If I do not turn my head, how can I contract ( or tighten) the sternocleidomastoid muscle ( like we can intensely tighten muscle in limbs)?


text:
Why is burn feeling 'slower' than touch?
When you touch a hot object you first feel the touch and only after a second you feel the burn too, and if you detach your skin from the object the burn feeling continues for few seconds. I remember i've read something about why this occurs (something like 'burn neurons are slower than touch ones') but it's just a faded memory.
So i'd really appreciate your answers.
Thanks in advance :).

Well, a burn sensation typically will travel via a withdrawal reflex, which should be very quick since it doesn't need the brain to instruct movement. But I guess you're asking more about the perception/feeling of pain from the burn, which would need to travel o the brain. Is this true?

Also, if something is truly hot enough to burn you, I really don't think there is a whole second delay between feeling it (via mechanoreceptors) and feeling the change in temperature (via thermoreceptors).

Thanks for your comments. I know it's not a whole second delay but anyway the two responses aren't synced. I just remembered something else (maybe): it should be related to Na/K pump and the refractoy period.

I think you might be thinking about the unmyelinated C-fibers which carry pain information and are slower?

Yes, thanks, I was looking for this. Anyway thanks to everyone, i appreciate that.

When you touch an object, a compression wave from the collision travels through your body at the speed of sound.  A sensor at any depth in your skin can pick up that signal at roughly the same time as the collision.
When you touch a hot object, heat from it moves into your body via conduction and to some extent radiation.  That heat flow moves much more slowly than the compression wave.  It will take longer for the heat pulse to reach a sensor that is deep in the skin and raise the temperature by a sufficient amount to cause signalling.
There may be further differences in the sensory neurons or in the reaction to the signals.  But there is a physical reason for the temperature signals to lag touch signals from the same object.
"Thermoception and Temperature Regulation" edited by J. Bligh, K. Voigt has some discussion of a study of thermoreceptors in rabbits.  It suggests both that

signal latency increases with increasing depth in skin
while most receptors has short latency, some receptors had much greater latency, and that this disparity in response may aid in determining temperature gradients within the skin, not simply reading instantaneous skin temperature.


text:
Are there any traces for evolution in modern humans over the last 100 years?
I ask that because I had a biology class and my teacher said something about a bone in the back of the head that apparently every male has, and for some reason, in the last 20-25 years, its started to fade away and so even though my father has the bone I don't. Or when I was still in high school, and I had to do X-rays for braces the doctor told me that I don't even have wisdom teeth? Are those traces of evolution or are they just random mutations?

Re: "Are those traces of evolution or are they just random mutations?" These two options are not mutually exclusive.

Your biology teacher was quite misinformed if that is what they told you.

Spotting evolution over only 4 generations would be very difficult. You certainly wouldn't see an entire bone disappear in that timeframe, though it might be slightly smaller in average people today than it was several generations ago. Over the timescale you're describing, the only real option is epigenetic changes, which might not be permanent enough to "count" as evolution.


text:
How detailed a construction of the family tree of known human fossils do we have?
For the sake of this question, by "human" I mean Hominina. The best I could find is this, which isn't very detailed. Of the dozens of paleospecies we'd seek to link up, do we have a more detailed tree attempt? Of course, it would be provisional and approximate, and the details would be somewhat debated; but I'm trying to gauge how fuzzy it is with our current knowledge.


text:
Is there a method to isolate half of the chromosomes of a cell?
Each cell has 2N number of chromosomes, I wonder if currently there is a technique allows isolation of N number of chromosomes out ?

Hi and welcome to Bio.SE! What problem are you having and what research have you done so far? Have you considered extracting DNA from gamete cells, likely sperm? That may suit your purpose.

does meiosis count?

Thanks for the reply , I am thinking some procedure or tech other than gamete cells, like extracting N number of chromosome from a somatic cells like epithelial cells? :)


text:
How do I solve this problem related to specificity and sensitivity?
Consider an autosomal recessive disease with an incidence of 1/10,000 in
the general population of 100,000. Your best friend comes to you very
upset because he has just taken a screening test for this disease and gotten
a positive result. He is convinced he is a carrier, despite having no family
history of the disease. You try to reassure him, but he says, "Don't bother.
The Clinic said this test has 98% sensitivity and 90% specificity. With that
level of sensitivity, it must be correct!" What is the chance your friend is
NOT a carrier?
I have attempted it in this way:
The reason I used Hardy-Weinberg is because there isn't any other way to determine whether he is a carrier or  not.
Case 1: He is AA (double dominant). This has a 0.99^2 = 0.9801 chance. The chance that his result was positive is 1 - 0.90 = 0.1 since that is the chance that the specificity failed since specificity measures the chance of true negatives. Multiplying this gives us a 0.09801 probability of this case.
Case 2: He is Aa (heterozygous). This has a 2*0.99*0.01 = 0.0198 chance. Again his chance of a positive result should be 1 - 0.9 = 0.1. Multiplying this gives us 0.00198.
Case 3: He is aa (double recessive). This has a 0.01^2 = 0.0001 chance. The chance of getting a positive result is 0.98. Multiplying we get 0.000098.
Adding these up, I have 0.100088. We want the probability he is not a carrier, so 0.000098+0.09801 (cases 1 and 3) divided by 0.100088 (the total). This yields around 0.9802 or 98% chance, which isn't one of the choices. What am I doing wrong?

Welcome To Biology.SE. Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. Hint1: You have to use conditional probabilities. Hint2: The question has nothing to do with Hardy-Weinberg equilibrium (unlike you seem to think given the tags used), it is a pure mathematical probability question.

Hint 3: Seriously and truly, this question has nothing to do with Hardy-Weinberg. Hint 2 is a solid hint. Try rethinking your approach. What if your friend really has the disease? What if your friend doesn't? What is going to happen with the test in each case? What do specificity and sensitivity mean?

Does my logic make sense if I do it this way? 1-0.9 (failing of specificity to catch someone without the disease) = 0.1. 0.1*2 (since AA and Aa are two cases that are both cases without the disease) = 0.2 is the chance that he is either AA or Aa. The third probability is 0.98, the sensitivity to aa having the disease. Adding these we have 1.18, and AA + aa = 1.08. 1.08/1.18 giving 0.915.


text:
More *total* oxygen absorbed by breathing fast or slow?
I have heard that human lungs capture/absorb/process more oxygen by breathing slower.
A) Is the above true?
B) If so, if my primary concern was absorbing the most total oxygen (not most efficient), would it better to breathe deeply and quickly or deeply and slowly?
C) Are there any other considerations (e.g., will fast, inefficient breathing make me feel more tired even if I'm taking in more oxygen)?
D) Is there any "ideal" breathing rate (such as for sports) that is a good balance between volume of air intake and efficiency of absorption?
Thanks.

Can you be more specific in stating the desired goal? Is it for a specific time frame/event? Our rate (and depth) of breathing affects CO2 levels well before O2 levels, and we function best within a certain narrow range. "More oxygen" does not equal "better" except in certain circumstances (e.g. Carbon monoxide poisoning, high altitude climbing, etc.)

Your body naturally optimizes breathing rate/tidal volume to minimize energy spent for what level of exercise imposed on it while also maintaining less than a critical level of $PaCO_2$.


text:
Are there organisms with fewer than 1000 neurons?
I'm developing neural networks comprised of just 3 to 10 layers of virtual neurons and I'm curious to know if there are any insect brains out there with fewer than a thousand neurons?

Are there any tiny creatures with small numbers of neurons?
Do neuronal maps exist for those simple nervous systems?

Rotifers have very simple brains with neuron counts in the low hundreds. unfortunately they are not all that well studied. https://academic.oup.com/icb/article/42/3/660/724027/Rotifers-Exquisite-Metazoans1

@Viziionary As an aside, note that number of neurons is not always synonymous with lack of complexity; "simpler" nervous systems in terms of numbers of cells often have more complex interactions between neurons: more bi-directional communication, multiple neurotransmitters involved, etc. For example, in most vertebrate neurons, there is a pretty clear distinction between axons (output) and dendrites (input), with a few fun exceptions. However, the distinction between axons and dendrites isn't always straightforward in a worm or insect. Good luck!

@BryanKrause The intricacies and differences between neural mechanisms for different purposes are almost infinite. Which is why I use an evolutionary model where a very extensive list of mutations can happen not only to the neural structure but also the composition and mechanisms involved with each neuron and connection individually. Turns out my code handling mutation is almost as complex and extensive as the rest of the code combined. By the way, what did you mean by "bi-directional communication"?

Cells that both receive inputs and release neurotransmitter via the same processes. This happens to some extent in vertebrate nervous systems as well, but not with the major neurotransmitter systems.

@BryanKrausen Is it like this?

@Viziionary No, between neurons; that one is about microglia. This isn't my specific area of expertise (I work with mammalian nervous systems), just some peripheral knowledge so I don't know a great source to cite, or even how well those systems are understood. I think, though I am less certain about this, that some c elegans neurons release different neurotransmitters in different contexts - that might be easier to find information about.

From a computing standpoint, trying to model with few neurons isn't necessarily the best approach. Think how our computers are built from huge amounts of virtually identical transistors to get complex behaviour. Few neurons may very well mean that the interactions between the neurons are much more complex than in a "bigger brained" organism. Think the difference between modelling a thousand identical neurons compared with a hundred neurons that each work differently (as in C. elegans). If you're trying to "evolve" a brain, don't look at "least neurons" - those are heavily optimized.

@Luaan My neural model is able to evolve to beat Super Mario Bros (NES) with only 4 layers, and less than 40 neurons. The neurons each individually mutate to take on different characteristics (action potential thresholds, refactory period thresholds, memory length, default built in memory bias, and of course network structure. Just a hand-full of neurons with relatively simple behavior replication (action potential, memory, polarization, depolarization, refactory period, etc) can accomplish fairly impressive tasks in my experience.

Oh, nevermind; I was really talking about mimicking real life; there's a lot of shortcuts you can take in a game (I've done a few worthwhile experiments), and a lot of things that would be very complex in a real organism can be very easy on a computer (e.g. some memory patterns can be built using the computer's flat memory instead of simulating in a complex network of neurons). I assumed you wanted a virtual organism with as little "cheating" as possible when asking about the "least neuron count organism", which depends a lot on the complexity of its virtual environment.

@Luaan Ah, no I'm not trying to simulate physically accurate neurons in my project, just functionally accurate (which is in itself a significant challenge)

Short answer
As far as I know, a complete neural map (a connectome) is only available for the roundworm C. elegens, a nematode with only 302 neurons (fig. 1).

Fig. 1. C. elegans (left, size: ~1 mm) and connectome of C. elegans (right). sources: Utrecht University & Farber (2012)
Background
Looking at the least complex of animals will be your best bet and nematodes (roundworms) like Caenorhabditis elegans are definitely a good option. C. elegans has some 300 neurons. Below is a schematic of phyla in Fig.2.
You mention insects; these critters are much more complex than roundworms. The total number of neurons varies with each insect, but for comparison: one of the lesser complex insects like the fruit fly Drosophila already has around 100k neurons, while a regular honey bee has about one million (source: Bio Teaching).
Complexity of the organism is indeed an indicator of the number of neurons to be expected. Sponges, for instance (Fig. 1) have no neurons at all, so the least complex of animals won't help you. the next in line are the Cnidaria (Fig. 2). The Cnidaria include the jelly fish, and for example Hydra vulgaris has 5.6k neurons.
So why do jelly fish feature more neurons? Because size also matters. Hydra vulgaris can grow up 15 mm, while C. elegans grows only up to 1 mm. See the wikipedia page for an informative list of #neurons in a host of species.
A decent neuronal connectivity map (a connectome) only exists for C. elegans (Fig. 1) as far as I know, although other maps (Drosophila (Meinertzhagen, 2016) and human) are underway.
References
- Farber, Sci Am February 2012
- Meinertzhagen, J Neurogenet (2016); 30(2): 62-8

Fig. 2. Phyla within the kingdom of animalia. source: Southwest Tennessee University College

FYI a full body simulation of the entire connectome of the c elegans - openworm
https://www.youtube.com/watch?v=SaovWiZJUWY

@StefanSzekeres To be clear, that simulation does not model the connectome or include neural activity, it is only a physics simulation of musculature. Their connectome simulation is not complete yet, as the behavior at the synapses is still not completely understood (although this link is dated it still seems to be the case according to the more up-to-date openworm.org). Not quite there yet, but it's an awesome project worth keeping an eye on. It's only a matter of time.

The organism you are looking for is the nematode C. elegans, which always has the same number of neurons, 302, and has been fully mapped, see WormWeb or you can chase original publications from there. C. elegans is particularly suited for this kind of work because it has a constant number of cells which divide in an entirely predictable order and its neurons forms predictable connections. Larger organisms, such as flies, have a variable number of cells and their neurons do not form precisely predictable connections. The immense amount of knowledge about C. elegans, advanced genetic manipulation techniques, and a transparent body also helps.
I am not aware of any insects with such small brains, even a fruitfly has several orders of magnitude more.

I've asked Is C. elegans always observed with precisely 302 neurons? Are there ever individual viable exceptions?

I believe there are types of water snail with 8 distinct neurons in a ganglia, there's a bit of information here: molluscs.at.
The cell bodies of the neurons are massive, visible under a standard dissecting microscope, so they were popular among early electrophysiologists. I guess there are probably more neurons around the snail, but it's certainly one of the simplest "brains" around...

Re: insect brain size
Following article has a good summary — in short insects' nervous systems range from 7400 to 850000 neurons:
http://blogs.discovermagazine.com/notrocketscience/2011/11/30/how-fairy-wasps-cope-with-being-smaller-than-amoebas/
There may be some hope for parasitic insects, e.g. Dicopomorpha echmepterygis where male has neither wings nor eyes, it is not inconceivable for their brains to be simpler.


text:
In microarray normalization, why is the normalization factor this?
I am working on analysis of a huge number of microarray files. I was trying to understand the need for normalization in microarray data and was going through this paper by John Quackenbush(2002). In the paper, the author mentions that

There are a number of reasons why data must be normalized, including
  unequal quantities of starting RNA, differences in labeling or
  detection efficiencies between the fluorescent dyes used, and
  systematic biases in the measured  expression levels

Then he talks about a simple normalization techniques. Assuming that  the total hybridization intensities summed over all elements in the arrays should be the same for each sample, he defines a normalization factor is calculated by
summing the measured intensities in both channels-

where Gi and Ri are the measured intensities for the 'i'th array element (for example, the green and red (or experimental and control) intensities in a two-color microarray assay) and Narray is the total number of elements represented in the microarray.
Then the author says this -

This is the part I don't understand. What is the need to introduce $G_k^{'}$, $R_k^{'}$ and why are they what they are? Most importantly, why is $T_i$ equal to $R_i/G_i$ first and then ($1/N_{total}$)*($R_i/G_i$)?
Any ideas?

$G_k^{'}$ and $R_k^{'}$ are normalized values of $G_k$ and $R_k$.
Take say G as $[1,2,3,4]$ and R as $[100,150,200,400]$ as your values and you want to normalize them. This is scaling one of them onto the other and bringing them on an equal level to compare. So in your case the factor is $85$ units. So a unit of R amounts to $85$ units in G.
So to scale G to R, multiply G by $85$ or you can scale R to the level of G by dividing R by $85$. So the values are either $[85,170,..]$ and $[100,150,200,400]$ or $[1,2,3,4]$ and $[1.17,1.76,..]$ from our example.
I think it should be mentioned as $T^{'} = R_i/(G_i*N_{total})$ as in log ratio from the statement in your question.

does your final line mean that in the text, it should be $T_i$ = $R_i^{'}$/$G_i^{'}$ = $R_i$/$G_i$*$N_{total}$

I mean $T_i = R_i/G_i$ but $T^{'}i = R_i/(G_i*N{total})$


text:
Can conventional PCR amplify DNA from different organisms from a specimen in a single step?
I've understood so far that in conventional PCR, the most abundant DNA/genotype present in the speciment at the beginning of the reaction is selected and esponentially amplified. So that cPCR are likely to miss mixed infections.
But I had 1 case in which when I sequenced the PCR product I got in BLAST 100% similarity for 3 different species at the same time. Is this suggestive of a mixed infection?

If you had a 100% BLAST hit for 3 species from a single amplicon sequence then it only means that region of DNA is conserved in the three species so you have at least one of those species present not necessarily all three.
If you had three different amplicon sequences and each one matched one species to a total of three, then you have all three species present.

I see. Is it correct to say that: 1) it is possible that one PCR product contains more than 1 organism's DNA, for example if your primers are quite generic and you got several unspecific bands. 2) the readable sequence corresponds to only one organism, even if this sequence is equally conserved in more species ?Thanks

You have have more then one species PCR product in the same band. If you get multiple bands then they by definition have differing sequences. That doesn't mean it's two species, it could be one species with two different amplicons in it's genome. And 2) No, if the sequence is equally conserved in more species you can't say which or how many species are present.


text:
Where do the antibodies that trigger the specific immune response come from?
In A level Biology, we are taught that in order to trigger the specific immune response of the body, antibodies must first attach to the pathogen. The macrophages contain antibody receptors, and this allows them to attach to the antibody carrying pathogen and subsequently engulf them by phagocytosis. This then triggers a certain pathway that involves T helper cells activation, which release cytokines to cause differentiation of B helper cells into plasma cells, and THESE release the antibodies.
The question is: where do the antibodies that start off the whole process even come from?

First: What your teacher says about the free floating antibodies is not correct. The first contact with a new antigen to generate specific immunity is done by naive B cells which have a membrane bound B cell receptor and their effector T cells. This contact can either happen directly or by the presentation of the antigen to the cell by antigen presenting cells (APC).
Short answer:
These naive B cells are present in our body without antigen contact, but are not highly specific.
Long answer:
Our body has the possibility to express a vast variety of different antibodies - estimations go up to 10 billion different antibodies which the human body can produce, each of them capable of binding a different antigen (see reference 1).
To begin with, naive B cells express antibodies as a membrane-bound version, the so called B cell receptor. The antigen specificity of these receptors is random and occurs before the individual had contact with the antigen. These receptors bind a wide variety of different antigens, more or less good. This is the so-called affinity of the receptor (or the antibody) against an antigen.
Upon binding of an antigen, the B cells get activated (if the receive a co-stimulatory signal from a T cell). When activated, the cells starts to proliferate and to differentiate, as shown in the figure below (from here).

Basically, the cells start to re-arrange the genes which are responsible for generation of the variable region of the antibody (the part which does the actual binding of the antigen) to generate highly specific high affinity antibodies to the antigen and then mature into relatively short lived plasma cells, which produce big amounts of antibodies and long lived memory cells. The later are dormant in the body and get reactivated, when the body is challenged by the same antigen, against which it already produced highly specific antibodies.
When re-exposed to an antigen, the antibodies in the blood stream bind to the antigen and mark it for phagocytosis. The phagocytes will then take up the antibody bound antigen, process it and present parts of it on their surface to B/T cells. This either starts the process of selection and clonal expansion as described above or if there are specific memory cells, these cells will proliferate and differentiate into antibody producing plasma cells.
The initial process of adaptive immunity takes about two weeks until highly specific antibodies are available, if you only have to "wake up" the cells from the memory pool, this will take a few days. This is also how vaccinations work.
See also the Wikipedia page on Antibodies for much more details.
References:

Development of the immunoglobulin repertoire.

@iayork I changed my answer to adress this more clear.

To address your question about antibodies, produced by antigen-specific B cells or plasma cells, I'm first going to address how you activate a B cell.
Naive B cells are produced in the bone marrow with antigen specificity encoded in it's B cell receptor (BCR), a product of VDJ recombination. Each B cell has a specificity toward a single antigen through it's BCR, much like T cells have a single-antigen specificity through their T cell receptor (TCR).
The ways that B cells are activated differ and I think you can get an idea here in 9.1 and 9.2. The take home point is there are T cell dependent and T cell independent pathways, but typically multiple cells are involved.
So to be certain, however, antibodies come at the late stage of infection, they do not start the process. As a matter of first response, you typically have the innate immune cells and the complement system responding. B cells have complement binding proteins that can link innate and adaptive immunity, like CD21.
Also, In the case of allergic reaction, it's different because it requires a priming stage by an initial contact with an allergen, and then the IgE antibodies present on mast cells during the second encounter cause the reaction, but here we'll focus on pathogens.
The entire process of antibody production takes place generally at the B cell receptor locus. The B cell receptor is expressed as two insoluble isotypes in a naive, circulating B cell: IgM and sometimes IgD. Keep in mind that secreted IgM and membrane IgM are structurally different. BCR IgM is monomeric, not pentameric like its secreted counterpart. The significance of IgD is also under investigation, but some research shows it's indispensible for responding to large multi-valent antigen when the B cell is already anergic (ref).
Whether the antibody is membrane-bound or secreted depends on post-translational modification, and these are affected by the activation state of the B cell (I like this reference). So when the B cell activates as it does in the above reference, either T-dependent or T-independent, two things are necessary: The antigen stimulation, and specific cytokines. Take a look at the B cell receptor locus:

You get an immunoglobulin by taking the variable region produced by VDJ recombination and attaching it to a constant region. The Ig locus has multiple constant regions: Cµ, Cy, Cα, Cδ, and Cε. When it wants to produces IgM and IgD, it transcribes a long mRNA V-Cµ-Cδ and then the cell edits the mRNA into V-Cδ or V-Cµ. The mu and delta C regions are spatially separated so that they are co-transcribed but the other C regions are not. Then it translates and modifies the protein to get a secreted or membranous Ig. B cells that secrete antibody are activated and a referred to as plasma cells.
But, if you're being stimulated by interferon-y at the same time, B cells can class switch to IgG by editing the gene locus so that the mRNA produced is V-Cy. If the cell is receiving Th2 cytokines like IL-4, it can make IgE by editing the gene so that the mRNA is V-Cε. The B cell actually deletes the other C regions in the DNA so it never reverts back. I go over class switching here.
Does that make sense? The antibody requires a concerted effort of other cells, and intracellular splicing and protein-modification machinery. See my favorite text, cellular and molecular immunology, 8th ed. for a powerful reference.

"In order to trigger the specific immune response of the body, antibodies must first attach to the pathogen" - This is wrong. Either you misunderstood, or the teacher was mistaken.  Specific immunity is triggered with no need for antibodies to bind to the pathogen.  Very simplistically, the earliest stages in specific immune responses require T cells and antigen-presenting cells.  The non-specific immune response is also very important in setting up a milieu in which specific immunity can efficiently start and progress.
From Immunobiology: The Immune System in Health and Disease. 5th edition.:

10-4. An adaptive immune response is initiated when circulating T cells encounter their corresponding antigen in draining lymphoid tissues and become activated
As described in Chapter 8, immature dendritic cells in tissues take up antigens and are stimulated by infection to migrate to draining lymph nodes. Antigens introduced directly into the bloodstream are picked up by antigen-presenting cells in the spleen, and lymphocytes are activated in the splenic white pulp (see Fig. 1.9). The trapping of antigen by antigen-presenting cells that migrate to these lymphoid tissues, and the continuous recirculation of naive T cells through these tissues, ensure that rare antigen-specific T cells will encounter their specific antigen on an antigen-presenting cell surface.


text:
Chlamydomanas are present in Kingdom Protista or Plantae?
Chlamydomonas, Chlorella are present in Kingdom Protista as well as  Plantae under division algae.
In which kingdom they correctly belong to?

It is generally accepted now that Chlorophyta are Plantae (see here). They are more closely related to plants than any other group of organism. Protist is a kind of basket term for any eukaryotic unicellular organism that is not an animal, fungi or a plant which is a rather exclusionary definition.
Personally, I think the kingdoms are pretty 'macro' oriented and do not really capture the diversity well of unicellular organisms. If you want to see a bunch of elderly scientist shout at each other over what appear to be arbitrary distinctions, I highly recommend attending the taxonomy session of any unicellular conference

What about Rhodophyta and Phaeophyta?? BTW Thnx;)

The rhodophyta might be monophyletic with the green lineage (have a common ancestor) but the Phaeophyta are definitely distinct and they likely arose during a seperate endosymbiosis event. They just do not fit in the five kingdoms. http://www.algaebase.org/ is quite respected for questions of algae taxonomy


text:
Can insects metabolize poisons?
I am new to this community, and I was wondering if insects could metabolize poisons. I'm not sure if I use the correct concepts, I simply wonder if insects can get rid of non-lethal doses of insecticides, and live as they have never been exposed at them. I know that human liver does this task for us, but I don't know if insects have this mechanism.

Insects absolutely can metabolize poisons. This is because plants are absolutely chock-full of them, precisely to avoid insect predation, and in return many insects have developed immunities to many of these poisons. Or as this paper "DETOXIFICATION OF PLANT TOXINS BY INSECTS", which looks like it would be the answer to your question if it were free to read says:

It is estimated that all plants
  contain some type of defensive compound (Rhodes
  and Gates, 1976). However, plant defensive compounds
  are not universally toxic to insects (Janzen,
  1979). Since almost all plant species are attacked by
  some insects (Schoonhaven, 1972), it is obvious that
  phytophagous insects have been able to develop
  countermeasures which allow them to feed successfully
  (Jones, 1972).

There are three main ways for an organism to neutralize a toxin: sequestering it where it will not harm the rest of the organism (and conveniently, may make the organism itself toxic to its own predators), excreting it (i.e. getting it out of the body altogether) and metabolizing it, i.e. chemically converting it into safer compounds. Often you will actually get combinations of those.
The first page of the paper sadly does not get into details about the extent to which insects use the third strategy, but it clearly states that they do.
This picture from Wikipedia shows some of the digestive organs that contribute to metabolizing toxins:

Organs that appear to deal with neutralizing toxins include the midgut (13), the fat body (not pictured), the hemolymph (not really an organ, it's the blood-equivalent liquid that all the organs bathe in), and the Malpighian tubes (20), though the latter (the apparent equivalent to our kidneys) probably serve more to physically get rid of the toxins than to metabolize them. From the Wikipedia page :

In insects which feed on plant material containing noxious allelochemicals, Malpighian tubules also serve to rapidly excrete such compounds from the hemolymph.

And from here:

Some small organic molecules are also
  actively transported into the tubule
  lumen by the transcellular pathway,
  including alkaloids (plant compounds
  which may be toxic to the insect).

This PLoS One paper (so, free to read) studies the enzymes that insects use to metabolize some toxins and notes among other things that:

One of the best studied examples is the CYP gene superfamily of Papilio butterflies (Papilionidae), which have adapted to furanocoumarins, the toxic components of their food plants [15], [16]. These toxins are degraded by inducible CYPs that are expressed in the midgut and also in the fat body [17], [18].

and

For Tyria, senecionine N-oxygenase (SNO), a soluble enzyme located in the hemolymph, has been shown to convert the pro-toxic free base efficiently into its non-toxic N-oxide [22] (Figure 1).

(emphases mine)
Another paper, "Chemical detoxification vs mechanical removal of host plant toxins in Eucalyptus feeding sawfly larvae (Hymenoptera: Pergidae)" describes how some sawfly larvae have special mechanisms for getting rid of and sequestering toxic oils, but also says :

The oil sequestration is, however, incomplete and chemical gut content analyses by gas-chromatography (GC) revealed that 1,8-cineole does enter the midgut and is metabolised to hydroxycineole.

Another paper studying a class of enzymes generally associated with detoxification (but note the paper itself is about how those enzymes have other roles as well):

Insect monooxygenases can be detected in a wide range of tissues.
  Highest monooxygenase activities are usually associated with the midgut, fat bodies and Malpighian tubules [9], but again the expression of individual P450s can vary between these tissues [17].

Insofar as insects have an equivalent to our livers it would seem to be the fat body. Like the liver this organ has many functions, including fat storage, energy metabolism and regulation, but also metabolizing toxins. From "INSECT FAT BODY: ENERGY, METABOLISM, AND REGULATION" (free to read):

Whereas many insect tissues have vertebrate analogs, the fat body is an organ unique to insects (77). The fat body is a relatively large organ distributed throughout the insect body, preferentially underneath the integument and surrounding the gut and reproductive organ (36). Unlike the solid structure of the liver, the insect fat body is a loose tissue.

and

Most of the insect’s intermediary metabolism takes place in this organ, including lipid and carbohydrate metabolism, protein synthesis, and amino acid and nitrogen metabolism.

and

In addition to its role related to storage and utilization of nutrients, the fat body is an endocrine organ (65), produces several antimicrobial peptides (44), and participates in detoxification of nitrogen metabolism (74).

And from the other link:

As in vertebrates, the oxidative metabolism is mediated via the tricarboxylic acid (TCA) cycle and the electron transport enzyme systems. The fat body contains enzymes mediating the gluconeogenesis process as well as enzymatic systems with a detoxification role to manage harmful endogenous metabolites and toxic xenobiotic compounds. Detoxifying enzyme systems include microsomal mixed function oxi-dases, in which the cytochrome P450 is predominant, various hydro-lytic enzymes (esterases, phosphoesterases), and conjugating systems.

Maybe it's just a matter of semantics, but if an insect can metabolize a toxin, is it still a toxin to that insect?  There seem to be a good number of instances where species A can happily eat something that is toxic to species B.  E.g. dogs and chocolate, or acorns & avocados reportedly being toxic to horses.

@jamesqf I think it's mostly semantics as you say, but I will note a context in which an organism could be able to metabolize a toxin but it would still make sense to call that compounds a toxin for that organism: consider that the processes that metabolize or otherwise neutralize the compound may be limited. For example humans can metabolize alcohol, but you can still die of alcohol poisoning if you drink more than your liver can handle, and you'd be dying of basically the same thing as you'd have died of if you couldn't metabolize alcohol at all, so that clearly makes alcohol a toxin.

But if you follow that logic, pretty much everything is a toxin in high enough doses, even things like water that are absolutely necessary to life in lesser amounts.

@jamesqf excess water doesn't kill you by overcoming the defense mechanisms you have against water, without which even a little water would kill you. So no, it's not the same logic at all. (Note that I brought up alcohol as an easy go-to poison, and it's a decent example for the point I was making, but "poison" and "toxin" aren't synonymous, and I don't think alcohol is a toxin given the definition of the word).


text:
What is the purpose of the outer mitochondrial membrane?
The purpose of mitochondria is to generate ATP, utilising a chemiosmotic gradient across the inner mitochondrial membrane. Protons are pumped out of the mitochondria into the intermembrane space, but because the outer mitochondrial membrane is highly permeable to ions, the pH of the intermembrane space quickly equilibrates with the rest of the cell. As the outer membrane apparently does not contribute to maintaining this chemiosmotic gradient, what is its purpose? It seems to be doubly redundant in chloroplasts as H+ transport doesn't even occur across the inner membrane.

In mitochondria, the protons pumped by the respiratory complexes do not end up in the intermembrane space --- that would be futile, since, as you say, the outer membrane is permeable and the protons would quickly dissipate. The respiratory complexes are located in the christae, which are closed-off invaginations of the inner membrane, from which the protons cannot easily escape (other than via ATP synthase or uncoupling proteins). See for example  http://onlinelibrary.wiley.com/doi/10.1016/S0014-5793(03)00633-1/pdf

@tomd,  Fair enough.  I just wanted to point out that the respiratory chain generally does not pump protons towards the outer membrane (as it is shown in many textbooks).

Structure origins
Originally the mitochondrial outer membrane (MOM) was likely the result of a bacteria that could survive in a vesicle formed of the plasma membrane.

This explains why the plasma membrane and the MOM are structurally similar, however, the proteins that are present in either mean that their functions are very different.The MOM has a specialised translocation complex for example.
Functional significance.
The MOM is actually much more complex than an evolutionary hangover and is essential to modern cells by regulating what that mitochondrial inner membrane is exposed to. The MOM plays this role using porins. Indeed, if the porins of the MOM are disrupted, the entire cell dies (Chipuk et al, 2006). Additionally, the MOM allows a physical association between the ER and the mitochondria called the mitochondria-associated ER membrane (MAM). The MAM is essential for $ {Ca}^{2+} $ transfer.

The MAM thus integrates signal transduction with metabolic pathways to
  regulate the communication and functional interactions between the ER
  and mitochondrion. (Hayashi et al, 2009)

Answer: The MOM is essential in regulating what the MIM is exposed to, and allows signalling between the ER and mitochondria.

Not sure I can help much, but as far as I know the outer mitochondrial membrane is associated with the endoplasmic reticulum as well. This help lipids (apart from proteins) to enter the mitochondria since these lipids originate from the ER. More importantly, the outer membrane has integral proteins called porins present which help in the movement of molecules into the mitochondria. The outer membrane is also required since it's permeable to nutrient molecules while the inner membrane is not.

Please add some references to your answer.


text:
Why do myelinated axons conduct impulses faster?
How does the myelination help in better conduction? I would prefer answers that are not too technical please.

What research have you done before asking it here?

@Imi, be sure to check out my newly added answer to the linked question. I added it here first, but moved it after this question got close votes as a duplicate.

And where did this comment go 0.o?

Here