text:
Largest direct ancestor of humans
Going back the genealogical lineage from present humans to the beginning of life, what was the biggest - in terms of body size or mass - animal in this sequence?
More generally, what would a time vs. size graph look like? Obviously the first ones were tiny microbes, but do we have "deep valleys" and high peaks one after the other? I know that our ancestors at the time of the dinosaurs were very small rodents. Were there some even smaller ones earlier (not referring to the microbes)?

I would tend to think that the tallest individual of a given human lineage is just a Homo sapiens, but I am really not sure. Is there a reason why you are specifically interested in human lineage?

In the absence of fossile records, the standard method for estimating te phenotype of a given ancestor species is to take the average phenotype of the descendent. Such methods is unlikely to give a result indicating a very tall ancestor. Primates tend to be smaller than humans, first mammals were very small, amphibians (sister group) are small, fishes are smaller than humans as well. You can go over the phylogeny here

@Remi.b Because it's my lineage. Just recreationally wondering about it and connecting science to everyday life in my head. I'd like to have a better mental picture of my ancestors.
I was specifically thinking about something like the Dimetrodon. While I know it's not a direct ancestor, it's often included in illustrations because it's a mammal-like reptile. Was maybe the common ancestor of us and the Dimetrodon also quite large?

Oh well. I didn't know about the Dimetrodon. I had in mine that when the first mammals came to existence, they were quite small but that sounds totally wrong when considering the Dimetrodon and the size of the basal mammals (monotremata and marsupials).

Except among the very recent ancestors of modern humans (and there is debate even there), generally we do not consider fossil species as direct ancestors. All fossil species are endpoints, tips of the phylogenetic tree.

@Remi.b the Dimetrodon is not a mammal. I can't find it on NCBI Taxonomy oddly enough, but according to the Wikipedia link you posted: "Dimetrodon is nevertheless more closely related to mammals than it is to any living reptilian group, though it is not a direct ancestor of any mammals."

@terdon Indeed, Dimetrodon (sphenacontidae) is a Synapsida(position on tolweb). the fact that sister species of mammals are quite big suggested that the direct ancestor of mammals might have been big. Looking at the tolweb tree, again, it would be interested to know what cutleria, panetelosaurus, paleohatteria and other closely related groups look like.

We can't really say for sure, because we have insufficient information about this. We can't trace every step of evolution through fossils. We can make educated guesses for most stages of evolutionary history, but they remain guesses.
Please note: Most of what we find in the fossil record are species that are not directly our ancestors, but rather branched off our evolutionary line and then went extinct. Those fossils can still give a good indication as to what the morphological features of our common ancestor were. And a lot of this is guesswork with some evidence behind it.
Going "down" the timeline of humans, we roughly encounter these steps:
Homo
The genus Homo: appeared roughly three million years ago, includes species such as Homo erectus and Homo habilis. Fossils of Homo habilis point to a height of around 100 to 135 centimeters, fossils of Homo erectus are closer in size to modern humans with 145 to 185 centimeters. The rest of the Homo genus was smaller than modern humans (Homo heidelbergensis/rudolfensis/neanderthalis)
Australopithecus
The fossils from Australopithecus are around 3 to 4 million years old, the most famous is probably "Lucy", a member of Australopithecus afarensis. Since members of all Australopithecus species appear to be smaller than humans (afarensis: 100-150 centimeters, africanus: 115 to 140 centimeters, etc.), it is likely that our common ancestor was smaller than modern humans. (Our ancestors likely were Australopithecus, we just don't know which species)
Apes
The split between the line leading to modern humans and the line leading to modern chimpanzees occured somewhere around 4 to 7 million years ago. The clade is called Hominini. The split between those and the line leading to modern gorillas occured around 8 to 19 million years ago (yes, the dates are getting fuzzier). A fossil coming close to this ancestor may be Nakalipithecus nakayamai, however, we only have a fossil jaw from that species.
Going back, we get to the split between modern-day humans/chimpanzees/gorillas and modern-day orang-utans. This is the "ape" family, Hominidae. The largest ape that we know of, Gigantopithecus, that grew to about 3 meters, is classified as an orang-utan. Note that this is not a direct ancestor of humans. Even if our ancestors were larger than modern humans at this point it's unlikely that we are talking about anything larger than a big gorilla.
Primates
Going a bit in the reverse order here: The first true primates evolved around 55 million years ago. Fossils from that time are about the size of squirrels. Humans are "old world monkeys" who first appeared around 40 million years ago - the fossils from that clade we know, for example Apidium or Aegyptopithecus are a bit larger, some as large as a dog.
Primate-like mammals
The first primate-like mammals, called Plesiadapiformes appeared around 60 million years ago. We don't know all that much about them, but the most famous Purgatorius was the size of a rat or mouse.
Mammals / placenta mammals
Going back even further, things become even murkier, but early mammals were small. Placentalia, placental mammals appeared around 90 million years ago. They were small, arboreal (tree-dwelling) animals. Early mammals appeared around 160 million years ago and fossils we have from that time place them around the size of a shrew.
Now, is it possible that there were larger mammals in there somewhere, that then "shrunk" again? Sure. Just unlikely.
Therapsid
Therapsis are mammals and their ancestors, evolved around 275 million years ago. The most well-known fossils from around then are Tetraceratops insignis. All we have from it is a skull of about 9 centimeters size.
Synapsid
Synapsis are making things complicated. As you mentioned in a comment, there were some really big synapsids. According to the Tree of Life project:

Early synapsids were moderately large (body length between 50 cm and 3 m)

Tetrapods
Tetrapods is the name for the clade that encompasses what we now call amphibians, reptiles and mammals - those animals appeared around 380 million years ago. An example of an early fossil from that time is Dendrerpeton, which was up to 1 meter in length.
Vertebrata
Synapsids are vertebrates. Vertebrates first appeared more than 450 million years ago. The time period following that, the Silurian, is called the "age of fishes".  Those fish could get really large, some of their jaws being over one meter wide. That's really all the information I could find.
Chordates
Taking another big step back, vertebrates are chordates, a group that first appeared in the Cambrian, somewhere around 550 million years ago. Early fossils are mostly small, for example Pikaia is about 5 centimeters large. Yannanozoon lividum is around 3 centimeters.
Before chordates
Before chordates, we really don't know all that much, the fossil record is poor because the structures that usually fossilize hadn't even evolved yet. For example, Hiemalora is around 3 centimeters in diameter. Whether it is our ancestor, we have no idea.
And before that come the first multicellular animals, the first animals, the first eukyrotes, and the archae,...
In summary
In summary, while we can only make guesses, the history of animal size from unicellular organisms to us probably wasn't spectacular. We go from very small (pre-Cambrian), to small (Cambrian), large or small (fish and synapsids), around 1 meter-ish (tetrapods), smaller again (early mammals, mammals), a bit larger (primates), again a bit larger (apes), and then to "human-sized".

This is a well thought out answer +1

I believe, you wanted to put Synapsids above Tetrapods.

@EliKorvigo I believe so, too! Thanks for pointing it out.

Therapsids were the largest of the direct ancestors of humanity. Even we can't reach their sizes yet. (Yes our line was probably 6-7 feet in that stage but the largest therapsid which was not in our line, Lisowicia, was a staggering 15 feet long — higher than the tallest human (which was about 9-10 ft)!)
Extra: The time of the therapsids, which was before any dinosaur or crocodilian, was arid and savanna-like — similar to how the place where Homo had evolved. The therapsids also had larger brains, compared to all other organisms at that time, or maybe even the largest (evidence in endocast).

Welcome  Illil. Please take our [tour] and refer to the [help] as and when  for guidance as to our ways. The Therapsids are mentioned in the other answer, but do you have any reference to support your assertion that their size is that great?


text:
How does the body survive Ebola?
Because Ebola takes over the immune system and uses it to replicate more and more of the virus, how does the body survive?
Is it a case of the virus being self-limiting and eventually just getting 'too big for its britches' so to speak? Or does the body somehow eventually start producing antibodies to fight it off?

From your text and the tag "retrovirus", I am wondering whether you are confusing ebola and HIV?

Nope I wasn't mixing up the two, I know that Ebola attacks the dendritic cells, monocytes, and macrophages. But I forgot about the T-cells and how it doesn't do much with them, HIV attacks those.

While the ebola virus infects a lot of human cells, immune system cells it infects are mainly monocytes and macrophages. The cells in our body mainly responsible for adaptive immunity, T cells, are at least not completely infected:

Our data indicate that 20–30% of CD4 and CD8 T cells died during the course of infection1

That's a lot, but the ones that survive get activated and it's apparantly enough that between 80 and 10% of the infected (depending on the strain) can survive the infection. Little is known about the details of the immune reaction to ebola, but the immune system does get activated. The immune system even remains on "high alert" for quite some time after infection and recovery.
And the antibodies do stick around, at least for 10 years. Whether they confer immunity against all strains of ebola, we don't seem to know - ebola isn't very well-researched yet.

So, basically, if you can outlive the initial damage, you'll recover, no? That seems to be the gist of the treatment: keep them alive with fluids and, if necessary, blood. I remember a student nurse saved almost her entire family at home (not hospital) that way.

@anongoodnurse possibly? I think the morbid guideline I heard was that whoever isn't dead 7 days after onset of symptoms will probably make it. CDC says it's a mean of 7 days: http://www.cdc.gov/vhf/ebola/healthcare-us/preparing/clinicians.html with the dehydration being really horrible in the end

source: Stack Exchange

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

sort: votes


text:
Why do humans have 46 chromosomes?
Humans have approximately 25000 genes. Why are these genes on 46 chromosomes? Why not 40 or 50?

In general, the chromosome number has to be even because each set of chromosomes comes from 1 parent, so 2 x N is always even. But different species have different chromosome numbers. No real reason why humans have to be at 46. There are plenty of people who survive with 47.

Chromosome rearrangements are just a type of mutations, hence the process is stochastic. Some chromosomes split, some merge, some duplicate etc. These events are very rare, though. Like all mutations these influence fit to some extent, since karyotype structure is known to play important role in epigenetic regulation.

user137 and @EliKorvigo I think one of you can extend your comment into an answer.

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


text:
Is DNA replaced after organ donation?
If an organ from person A is transplanted to a new human body B, is it possible that we can detect A's DNA in B?
How long until the organ's DNA is replaced by B's DNA so that we are no longer able to detect any signature of A?

The organ from person A will never have it's DNA replaced to match that of its new host B. This is actually a good thing, because many organ transplants are done to treat genetic diseases. If the new organ had its DNA replaced with the host's faulty DNA, the transplant would be ruined. As far as detecting the organ's foreign DNA in its new host, that depends on how the sample was collected. If you look really hard at DNA in blood samples, you might find some evidence of the donor's DNA in the host's blood, but how much probably depends on what organ was transplanted and other factors.

@user137 But cells of the new organ may die and be replaced at least. The new cells have the host's DNA or the new organ's DNA?

If the transplanted organ's cells die, they probably have to be replaced by other cells in the transplanted organ. These would carry the foreign DNA from the donor. The only way for new cells in the organ to carry the host's DNA would be if host cells colonized the new organ from the outside, which doesn't seem significant. There are cells that can colonize tissues, such as Kupffer cells in the Liver, but these don't make up the bulk of the liver, those are hepatocytes.

DNA will be never replaced (unless you are speaking about something, where DNA might be only trash, like in the case of blood transplantation or in the case when "organ" would be slowly replaced itself by host regenerative power and "organ" transplantation would be only something temporary, but then we are probably speaking about wider definition of organs).
For further evidence, you may look at cases of chimerism. That is, when young embryos fuse together and create single one with two different cell-lines, which later differentiate to create different organs.
https://en.wikipedia.org/wiki/Chimera_%28genetics%29
Furthermore, rather more common but with less drastic effect can be somatic chimeras, that is when (usually) early, when embryo is formed only by small amount of cells, one of cell has a mutation, then later in life, this cell again can give rise to organ or several of them. In that case, those organs will carry this mutation while rest of the body will not. This can be potentially more common as this can happen in any single time during development and even after it (in fact, cancer cells are sort of product of that).
More interesting cases here:
https://en.wikipedia.org/wiki/Mosaic_%28genetics%29
So, from simple fact that these cases exists and are well-spread, and basically means that several different cell-lines can live in the same body, the answer on your question, if organ DNA will be replaced after transplantation is no.
edit: In the case of whole cell replacement, they can be from both donor and host. However, there are a few problems:
Most of cells that we have are not totipotent, not even pluripotent or multipotent (see: https://en.wikipedia.org/wiki/Cell_potency), most of our cells are plain and stupid. This means that highly specialized cells of some organ would probably be replaced only by other highly-specialized cells of that organ (or their precursor cells that are kept for this solo reason, keep regenerativ ability of particular organ, as quite a lot of highly-specialized cells can't divide any more). However, there are a few documented cases with regnancy, where a few cells (embryogenic, thus with bigger "healing" power) migrated through placenta to mother's body and healed her diabetes. So theoretically this is possible, as well as host getting cancer from donor's organ. But again, reason why we are transplanting organs is because human body is not particularly great in regenerating itself and those organs won't grow. So theoretically possible, but not great concern (except for cancer).

DNA will be replaced as long as cells die. But new cells carry whose DNA?  It is possible an organ carry A's and B's DNA simutaneously?

@questionhang It's not just the DNA that's replaced, it's the cells that are replaced. And they are replaced by cell division. So they get the same DNA as the other cells of that organ have.

@yvide I know. The cells of the donor's organ die too. The new cells carry the host's DNA or the donor's DNA?

@questionhang: Did edit. Does that answer your further question?

@Colombo So it is possible the organ can have host's cells and donor's cells simulatenously? Many years later, the donor's cells will not be purged?

Yes, they can have donor cells and host cells simultaneously. Donor cells would not be purged. Unless host stop taking medicine to slow down immunity response, because donor cells are still alien and would be destroyed. And with them, whole organ.


text:
Does the second law of thermodynamics cause aging?
What is the current understanding as to why organisms age and die? In the following explanation on Ask an Engineer, entropy is not even considered (despite it being answered by an engineer). Unless you consider

accumulation of damage to an organism over time

as a result of entropy ?
In the end, is the eventual death of any organism a result of how the laws of universe? In the paper Aging of the brain, entropy, and Alzheimer disease, the author states that

Increasing entropy, manifest through a complex network of interacting ARCs, is seen as the fundamental driving cause of neural and cognitive decline in the elderly

where the abbreviation ARC stands for age-related changes.

Living organisms are not closed systems, and as far as I am aware, the laws of thermodynamics only apply to closed systems.

Second law of thermodynamic and ageing
The second law of thermodynamic applies to closed system. Organisms are not closed system. The second law of thermodynamic is a fundamental principle of our universe and any biological processes do follow the principles of physics. However, stating that biological ageing is (partially) caused by the second law of thermodynamic suggests a big misunderstanding of what the second law of thermodynamic is.
To have a better understanding of the second law of thermodynamic, check up the wikipedia article or one of the many other sources of information on the subject and ask questions on Physics.SE if needed.
Ageing and its evolution
The evolution of ageing (or senescence) is a big subject and has already been subject of a large number of questions on Biology.SE. Have a look at the questions tagged . Below are two examples of post that will interest you:

Why do we age? or Do we have a theory of senescence?
Why does evolution not make our life longer?

There is also a wikipedia page on the evolution of ageing.
Note btw that biological immortality and negligible senescence do exist.


text:
Why is the penicillin/ceftriaxone hypersensitivity test only done once?
I have had a severe bacterial infection. I was prescribed ceftriaxone, and when the time came for injecting it the nurse asked me whether I have an allergy to ceftriaxone. I answered that it's my first time, so she did the test and it was negative.
I was expecting a second test because as far as I know from type 1 hypersensitivity the body -  even if it is sensitive to an allergen - won't show a reaction the first time. The body makes the particular IgE and in the next exposure of same allergen it will have an allergic reaction.
So why is only one test done, considering the first two columns of the following picture?

From: Harsh Mohan's Pathology textbook 7E

When were you expecting a second test? Directly afterwards? After taking the antibiotic?

If you are not allergic, you are not allergic, and it's unnecessary to do the test more than once. If, on subsequent treatment with the same (or similar) antibiotic,you do develop an allergy, you'll know from then on, and they'll know not to give it to you. Finally, it's not necessary to test for every allergy that might possibly be present. Most allergies are not life threatening, and if you don't have a history of allergy, that's a good enough reason to believe it won't be a problem.

Can you please specify the time frame you were expecting the second test to occur? Were you treated at a later date with ceftriaxone, or were you expecting the nurse to give you a second test after she had just performed the first test? It is unclear from your question what the timeline was and what your expectations was.

You are misinterpreting that table. Peak action time refers the time after exposure if you have already been exposed to the antigen. Raising the adaptive response to the first exposure to that antigen will then take 8 to 14 days. Even if you are genetically predisposed, you need to activate that B-Cell to make IgE which acts as the Mast Cell receptor and triggers the degranulation that triggers anaphylaxis.

Please somebody read the first column (features) and it's first row (definitation). it says crystal clear what i want to know

I did read it and you are misinterpreting it. "...previously sensitized person" does not mean sensitized 5 minutes ago or an hour ago. It means weeks, months, or years prior. Reaction to humoral antibodies, means that you would have had to make the antibodies first from a prior exposure. That would be at the minimum 8 days to two weeks after exposure.

ok then why the nurse or doctor didn't recommend me to take a second test 2weeks or one month later if not directly (based on your explaination which is right )? because you too said that in your comment that the body first should be sensitized (making IgE's) in order to create allergy!

Was it a single bolus? You said it was by injection, so were they treating you over a period of more than two weeks? Or was it one and done? They aren't going to tell you to come in for a second test if you aren't receiving the drug, because you might develop a sensitivity to it. They would cross that bridge if and when they ever got to it. For the most part, you do not test healthy people for anything more than vital signs unless they are at risk or they have a complaint. Do you have other allergies, to other drugs or are you healthy? If you are healthy, then there is no point to test you.

The caveat to that is if that healthy person will be going someplace where they will not have ready access to medical care, such as an Antarctic research station or the International Space Station. Then you would give then a complete battery of tests, because there is no way to get to them with trained staff if something happens. The only other reason would be if there is something that suggest that their might be some problem. Like they warn you about the flu shot if you have allergies to eggs. Etc.

Because developing a hypersensitivity takes time. If you get exposed to an allergen, the body first has to produce those antibodies that then get used in the hypersensitivity response at the second, or subsequent, exposure.
If you are talking about taking a second test just minutes after the first one, how would your body even "know" that this is a second exposure? Two exposures within minutes are not distinguishable from one exposure for the body.
Usually, an allergic reaction shows the second time a patient takes a full course of antibiotics. It does not show at the second oral dose or injection, which are way too close to the first dose to have already lead to the developing of a hypersensitivity.
So, why test you in the first place? Because you might have been exposed previously without remembering it - people misremember what medication they got during their childhood all the time, I imagine, and your doctor/nurse seem to just routinely do the test before giving these antibiotics.
Sources/Reading
Drug allergies
Update on the Management of Antibiotic Allergy

Personally, my amoxicillin allergy decided to show itself on day 8 of a 10 day treatment, the first time taking it.

I'm not sure of something you assume in your answer  (because the question is unclear): I don't think the OP is talking about the second dose (though he might be), but rather the second course of antibiotics (at least, I hope that's what was meant.) Also, you might want to read about amoxicillin-associated rashes.

@anongoodnurse I thought he was talking about the course of antibiotics being the second exposure, the first being the skin test. But it's unclear. What do you mean with those rashes? Or rather, what do you mean with them in relation to this question/answer?

There already has been an answer but I'd still like to clarify further. I'm assuming the OP was expecting a second skin test because type 1 hypersensitivity requires a repeat exposure. Getting exposed to the antigen will just get you sensitized but will not precipitate the reaction.
What I want to clarify is that the skin test doesn't test whether you are allergic to a medication but if you are already sensitized to it. It is important to get the difference.
If you have. never been exposed (hence sensitized) to ceftriaxone before, the test would be negative even if you are actually allergic. And as sensitization needs time, you wouldn't be getting tested right afterwards (as mentioned in the comments). Instead, you'll be given the dose.
So why skin tests? That's because the dose is low and intradermal - chances of a full blown anaphylaxis are lower (not zero) even if the pt. is previously sensitized.
So, to conclude, as mentioned in the previous answer, the skin test is done just once to check if you've already sensitized, since rarely do people precisely remember the medications they have been previously exposed to.


text:
How does waking up from an alarm clock work?
During sleep, one's brain is shut down. All it can do is to see some dreams from the semi-conscious mind.
Then how does it hear when the alarm clock rings?

The brain does not "shut down" during sleep. While not everything about sleeping is understood, we do know that certain areas in the brain remain active during sleep. There is a good overview on sleep on the website of the National Institute of Neurological Disorders and Stroke.

Until the 1950s, most people thought of sleep as a passive, dormant part of our daily lives. We now know that our brains are very active during sleep. Moreover, sleep affects our daily functioning and our physical and mental health in many ways that we are just beginning to understand

As for hearing, that part of the brain doesn't shut down during sleep - and for good reasons. Sudden, loud noises for example may be a sign of immediate danger. Any animal that just stops hearing a third of the day would be at a huge disadvantage.
The brain even processes the sounds we receive during sleep and doesn't wake on every loud noise. You might find the following article interesting: How do we hear while we sleep?

Using electrodes implanted directly on the human cortex, a Johns Hopkins University undergraduate has located the part of the brain that appears to process sounds while people sleep. This site, in the frontal lobe, may be part of a vigilance system that, for instance, rouses a mother when her baby cries but lets the woman sleep when a truck rumbles by.

Alarm clocks are usually designed to just get louder and louder until we do wake up. Even despite that, some people actually do manage to sleep "through" the sounds, for example of they were very tired and haven't yet had enough sleep. This is speculation, but maybe in that instance the brain prioritizes sleep.
Other articles on the subject are for example Odd Sound Processing in the Sleeping Brain and Auditory information processing during human sleep as revealed by event-related brain potentials, but the main point is that we don't stop processing what happens around us just because we are asleep.


text:
How does a fetus retain a blood group different from its mother?
It's a well-established fact that blood group is decided by genotype. But, when a new child starts its journey in the womb, the mother's blood (along with it's agglutinins and agglutinogens) flows into the baby's heart. So, how does a baby (having a blood group different from that of the mother) retains it's own blood group (with it's own agglutinins and agglutinogens) instead of the mother's blood group, which moves in and out of the baby through the umbilical cord.
Do both kinds of blood flow in the baby's body constantly in such a case?
Apart from that, I know of rhesus incompatibility. But there are also incompatible blood group types. How does a baby survive agglutination in those cases?

maternal circulatory system is separated from fetus in the womb

What happens before then? And answer my second question if you can.

I mean, if there's Rh incompatibility, there's gotta be interaction between both types of blood. So how come nothing unusual happens when incompatible blood groups interact with each other, but agglutination occurs due to Rh incompatibility?

Rh incompatibility is due to fetal blood which escapes into the maternal circulation during delivery. It does not occur always and depends on labor conditions. There is absolutely no mixing of fetal and maternal blood otherwise.

I see. Then, when the fetus doesn't have any blood within at first (after fertilization); how does the blood come into it's system for the first time? Is it the bone marrow?

Note also that Rh-incompatibility is most often an issue with second or later pregnancies, after antibodies have been formed during earlier pregnancies, see e.g. http://www.nhlbi.nih.gov/health/health-topics/topics/rh for more. @CRags

Fetal heart starts beating at 4 weeks. The fetal blood cells are formed in liver, spleen, yolk sac. Very little gets formed from bone marrow proper

@CRags I suspected that, and my comment was mostly directed to the OP.

So lemme get things straight, RBCs present in the baby comes from the baby's liver, spleen, yolk sac and it's own system; and not at all from the mother. So, apart from yolk sac, those other two starts functioning even before the heart starts beating and starts pumping blood!!! Unbelievable...

The maternal and fetal blood circulation systems are completely separate. The embryo's blood cells start developing at around week 5 gestational age (3 weeks after conception), the same way any other tissue is developed by the fetus itself. By around week 7 gestational age, a circulatory system has developed and the heart has started beating.
All nutrition goes through the placenta, which keeps the two circulatory systems separate by the so-called placental blood barrier.
Rhesus incompability is only a concern after the first birth (or miscarriage) because then the maternal and fetal blood had the opportunity to mix and lead to the mother developing antibodies.
Also, as AMR pointed out in the comments, blood group incompatibility is mediated through IgG antibodies - those don't start to be produced at all until birth and at higher levels not until six months to a year after birth. See also At what age do babies begin to synthesize their own antibodies?

I wrote the answer before reading that there are already comments answering the question :-/ Still, this shouldn't be in the list of unanswered questions.

You may want to add that the fetus does not develop the ability to produce antibodies until around six-months after birth, so even if the mother's RBC's did circulate in fetus, they wouldn't be producing antibodies against them and by the time they started to, all the maternal RBCs would have degraded. Fetal blood crossing to the mother would be far more relevant as the mother would make antibodies against it which you mention with your last paragraph about first birth or miscarriage.

@AMR good point, thanks! Though, I think six months is too late - isn't it way earlier?

Class switching takes a while. "After birth, the production of IgM starts almost immediately; the production of IgG, however does not begin for about 6 months, during which time the total level of IgG falls as the maternally acquired IgG is catabolized." - Janeway's Immunobiology 8th Edition.


text:
What happens to dextrorotatory amino acids in humans?
As indicated by this question, most of the amino acids in the human body have the L-chirality. As enzymes also have handedness, what happens to the D-amino acids that end up within the human body? Are they simply excreted? Are there enzymes (perhaps not in humans) that convert a D-amino acid to a L- one?

For the most part they are not used.  there are amino acid racemases, which interconvert L- and D- forms of some specific amino acids, which may be used in some particular biosynthetic or metabolic pathways.
In particular I'm thinking of firefly luciferase which uses D-Cysteine as a re-dox reagent to regenerate the luciferin substrate that the light - generating enzyme consumes.  see slide 4 here.
Nonribosomal peptide synthases often use D amino acids too.
I don't believe that d- amino acids are really incorporated into proteins though.

Don't most viruses rely on the availability of some amino acids that humans don't need or use? For example it is to my belief that the herpes virus relies on the availability of a amino acid that is not used by humans and is commonly found in chocolate?

Its pretty rare to require a nonstandard aa at all and a fast growing virus would be strongly inhibited by such a requirement.  The viral proteins I know of don't require a special amino acid.  I'm sure there are exceptions, but they are rare I believe.

You may also be interested in D-amino-acid oxidase (EC 1.4.3.3), a flavoprotein  (FAD) highly specific for the D-form of amino acids, which was discovered by Hans Krebs in 1935 (see here), and which has a wide distribution (including in humans).
The enzyme has been very thoroughly investigated, in particular by Massey & co-workers (see here for example)
D-amino-acid oxidase (EC 1.4.3.3) catalyzes the reaction which results in the following transformation

D-amino acid + H2O + O2 = 2-oxo carboxylate + NH3 + H2O2

2-Oxo-carboxylates are what used to be called α-keto acids.  For example, pyruvate is produced from D-Ala.
The product of the enzymatic reaction is the imino-acid which is nonenzymatically
hydrolyzed to a-keto acid (see Pollegioni et al., 1994, and references therein)
An excellent review

D-Amino Acid Oxidase: Physiological Role and Applications
by S. V. Khoronenkova & V. I. Tishkov,
Biochemistry (Moscow) is freely available from here

These authors have some intersting things to say about D-Serine, D-Proline and D-Alanine, and much more.
Additional Reference

Pollegioni L, Fukui K, Massey V. (1994) Studies on the kinetic mechanism of pig kidney D-amino acid oxidase by site-directed mutagenesis of  tyrosine 224 and tyrosine 228.  J. Biol. Chem. 269, 31666-31673. [pdf]

many D-amino acids are not used at all, although some have rather elaborate metabolism, both synthesis and utilization: D-alanine for example.

This sounds interesting. Is there any chance you could add some details (and/or links) to your answer?


text:
How is the appropriately-stratified gut microbiome acquired in organisms performing horizontal transmission?
I am studying horizontal transmission of primary symbionts in insect reproduction. This reminded me of an earlier question I had asked, in which I learned that humans analogously acquired their particular microbiomes. It is also known how the human gut can be stratified in microbial content along the digestive tract. My question is what mechanisms are employed in ensuring that organisms acquiring their microbiomes from outside sources via horizontal transmission acquire the correct microorganisms in the correct parts of the gut? As the human gut metagenome does show "homology" between individuals, it can be safely assumed that the process can't be due to random chance.

Relevent: http://www.ncbi.nlm.nih.gov/pubmed/15831718 and http://www.sciencemag.org/content/312/5778/1355.short

Initial gut microbiota development is influenced to an unknown degree by the fact that human milk contains oligosaccharides that promote the growth of certain strains of Bifidobacteria (see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2596198/).

tl;dr it really might be due mostly to random chance, in terms of intentional mechanisms at least.
One thing that is important to remember about the gut tube is that conditions of life for microflora vary dramatically from one end to the other. This is true of nutrient availability, pH, and antimicrobial load. For example, the bacterial load of the lower intestinal tract is approximately seven orders of magnitude higher than the upper GI tract (stomach). They're just completely different places.
In some cases you can try to impute the bacterial assemblage in some part of the gut to a specific biological cause furnished by the host, for example the role of bile salts in controlling which organisms are able to colonize certain locations.
But a more parsimonious explanation is that the bacteria are growing in the places where they are good at growing. This brings up the old ecological saying: "Everything is everywhere, but the environment selects." We aren't necessarily trying explicitly to reinforce a certain assemblage, that's just the assemblage that works in niches with very low pH, very high nutrient load, bile salts, etc. And most of those features are unavoidable consequences of the gut's main function, digestion/excretion.
It certainly doesn't seem that e.g. behavioral strategies for exposing yourself to the "right" microbes gets you the right microbes in the right places. Recall that fecal microbiome transplant is one of the most successful strategies- just take some healthy poop and put it into a sick person's GI tract, they get better! That's not a very controlled horizontal transmission strategy.
You could propose that there is some second-order selection going on in which we have constructed GI niches in such a way that they encourage certain assemblages. Certainly, dysbiosis occurs and is bad in such cases as e.g. C. difficile infection, we would like to avoid those. Probably some coevolution has occurred between host and microbe, for example immune responses and butyrate production. That Foster paper has some more examples of possible mechanisms for a couple of specific cases, for example mucus. But they are probably not sufficient to explain the full compartmentalization of the microbiome in the way that you seem to be asking.

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


text:
On the definition of gDCW (gram dry cell weight)
I need some clarification on the concept of gram dry cell weight.
The unit acronym gDCW stands for gram dry cell weight. My interpretation is that 1 gDCW is equivalent to 1 gram of dry cells, but I am not sure. Is this accurate?
For example, the dry cell weight of mouse cells is roughly 300 pico grams. Therefore, in this case, one gram of dry mouse cells contains $10^{12}/300$ mouse cells (1 picogram $=10^{-12}$ grams). And if one says that there are 0.6 mmol of alanine per gDCW of mouse cells, this means that the total alanine content of $10^{12}/300$ mouse cells is 0.6 mmol. Is this accurate?


text:
Modern immunology textbooks
I am looking for recommendations to good textbooks introducing modern immunology. Review articles, preferably modern (post 2000) would also be useful.
Please, include a brief comment with each book recommendation.
About book listing questions on SE: I understand that SE sites in general have adopted in the last year a policy against book listing questions. Instead, book lists should be moved to tag wikis. However, since BiologySE is still beta and young and the tag-wiki for immunology is mostly empty, I believe we would benefit from a question listing good introductory books to modern immunology, at least temporarily. Eventually, when Biology.SE matures, this question should be closed or locked, and the book recommendations herein moved to the tag-wiki for immunology. Moreover, for most other SE sites I have seen, the tag-wikis usually gather information that first appeared in questions like this, even if the question is eventually closed or locked. That's why I think this question will be useful to the community, at least temporarily.

I am surprised Janeway's Immunobiology is not listed here:
Murphy K. Janeway's Immunobiology. 8th ed. New York: Garland Science; 2011.
It is very comprehensive, accessible and goes beyond any graduate course I know. Most immunology researchers I know have a copy of this handy somewhere in their office. A particular highlight are the very clear illustration.
I would suspect that a new edition is currently in the works, so I recommend checking if a new edition is due to come out before you buy.

The MCM's book is good one.
I recommend the book BRS Microbiology and Immunology, because then you can see the thing in the real context and have good exercises too.
First Aid for the USMLES Step 1 then explains you how to read for immunology and gives you rather good summary about the topic and some mnemonics.

Cellular and Molecular Immunology
 Abul K. Abbas MBBS (Author), Andrew H. H. Lichtman MD PhD (Author), Shiv Pillai MD (Author)
This was my Fall 2011 Basic Immunology text for a hybrid med-school/undergrad class at my University.
I have not read others, but every time the topic of Immune responses comes up in other Undergrad courses, I have been well or exceedingly informed because of it.

Given @becko's note on putting references in tag-wikis, maybe we should put this listing in the tag wiki for immunology

@A.Kennard But, as I said in the note, the question should remain open until it accumulates more answers.

I took an undergraduate immunology class for fun a few years ago while I was working at a university (taught by a Ph.D. from MIT).
"The Immune System" by Peter Parham (3rd ed. 2009) was really enjoyable and seems to have taught me well. So well that although I had very little background in biology, after taking that class I was able to discuss and sometimes even help my (then)girlfriend in her graduate level immunology class. I praise the book highly.
https://www.amazon.com/Immune-System-4th-Peter-Parham/dp/081534466X
edit: Apparently there is a 4th edition now, 2014.

If you actually read the link you provided, you'll see that there's a new edition of that book, from 2014. Answering a request for "modern" immunology texts with a book from 2009 is not helpful at all - a lot has changed and been discovered since then.

Then take the time you spent writing that comment and edit the answer with the new link. Yes, immunology is changing wonderfully fast. However, the asker qualified post-2000, so 4th ed. is even better.
Instead, @MCM and Rob Hall both suggested books two years older, which apparently is your threshold (perhaps more likely, reputation bias is acting). Content-wise, they provided similar information.
But not to worry for you, it is very likely I will not attempt further contributions to stack biology. The integrity of your stack is safe another day.


text:
Genotype of children conceived after stem cell transplant?
If you have sickle cell disease and have a succesful stem cell or bone marrow transplant, your blood type changes to AA. But what about your future children? Do your sperm or egg cells continue to express the SS genotype or do they become AA as well?

Bone Marrow Transplants should not make any changes to the germline. I say should not, because killing the bone marrow prior to transplant usually involves full body irradiation and or chemotherapy, and there is the possibility that you could accumulate mutations in the germ cells, however that genome will still be that person's and not the donor's genome.

Infertility is common after chemotherapy or irradiation done for transplants, so the question in that case would be moot.

Spermatozoa are produced in a process called spermatogenesis. They come from germ cells, which in the human males are located in the testes. These are not affected by stem cell transplants.
In females, the equivalent oocytes are already present at birth. They undergo meiosis later, but since their genetic composition is already set at birth, they, too, are not affected by stem cell transplants.
This might make the process clearer: Primordial Germ Cells and Sex Determination in Mammals

In all vertebrate embryos, certain cells are singled out early in development as progenitors of the gametes. These primordial germ cells migrate to the developing gonads, which will form the ovaries in females and the testes in males. After a period of mitotic proliferation, the primordial germ cells undergo meiosis and differentiate into mature gametes—either eggs or sperm

A stem cell / bone marrow transplant only affects the bone marrow, where the blood cells are produced.


text:
Can Biologists identify all viruses?
I went to the doctor today with my girlfriend, and the doctor said that she had a virus but doesn't know which one and she should let the infection heal with some rest.
The fact that the doctor didn't know what type of virus she has bothers me.
Do physicians/biologists not know all the different types of viruses out there? Is it not possible to identify all of them?

Identification of the virus will generally not help the doctor or the patient, just wasting time and money - I'm not sure there's many countries where there is an abundance of doctors and funding for healthcare that this wouldn't be a problem! :) If your Dr had suspected it to be a dangerous virus I'm sure they would have investigated further.

I, for one, certainly cannot. And since viruses recombine and produce new and new variants on a much faster scale than humans do, there is no chance that we can identify all existing viruses in the near future (or ever). Practically speaking, there is an infinite amount of different possible combinations of viral components.

Immunity to many pathogens manifests similarly; there's enough evidence to discern viral vs. bacterial most of the time, though. Viruses are often self-limiting at that, and end up clearing after a few days, making it relatively pointless to prescribe an antiviral. Flu is tricky, to make things more complicated, since going with an antiviral is really only helpful soon after onset of symptoms.

To give you a picture of how little we actually know about microorganisms, if you take a soil sample from your back yard you are guaranteed to discover new species of microbes. Someone did this several years back simply to gauge how many more species there are to discover and to his surprise every time he did this experiment he always discover new species. Think about that: always. He could not find any soil sample that only contained known species of microbes.

Do physicians/biologists not know all the different types of viruses out there?

No, Biologists don't know all the viruses that exist out there. There's a lot! We do know many of the ones infecting humans, though, especially the ones leading to the most common diseases.

The fact that the doctor didn't know what type of virus she has bothers me.

Without knowing any symptoms, your girlfriend likely had was some kind of influenza (flu), rhinovirus (cold), norovirus (diarrhea, etc) or respiratory syncytial virus (strong). That's just the most common virus infections. Identifying those is possible (see lab tests for norovirus or influenza), but it's unnecessary in most cases.
The thing is, no matter which of these she has, the medical advice will stay the same - rest and fluids. So identifying them is just going to add time and money.
There are some cases where viral identification is done even for these diseases. For example, before giving an antiviral like Tamiflu, which is for example given to pregnant women with the flu. Before giving an antiviral, it should be established that she is indeed infected with the influenza virus. These tests are also done in patients who are hospitalized. In some countries and years, all influenza cases are screened to later know what strains of the virus infected how many people and how it spread.
As an example, if the result of the test doesn't change the treatment, the influenza test is recommended against by the CDC. With a gastrointestinal issue where norovirus is suspected, nobody is going to make an identification for a straightforward case.

+1 for "There is a lot". It seems that the virus diversity of the oceans is more or less known now, at around ~5500 species: Scientists Map 5,000 New Ocean Viruses. (Most?) of these are not infectious for humans though.

It's a cost/benefit situation.  Yes they could have taken samples, processed them,  teased out the virus, and eventually identified exactly what virus (sort of*) that your girlfriend had by its gene sequence.  But do you want to pay 10k-100k per virus to find that out, or just pay $20-100 and take some fluids and be fine.
I say sort of because viruses tend to mutate quite a bit.  A great example is the influenza virus.  There are many strains, with genotyping you can say this is H5N1 vs H1N1.  But typically the result for a person is going to be "You have the flu. <Insert generic flu advice here.>"
There are some tests specific to families, again flu is a great example.  Because the flu virus can be deadly to certain groups of people, and because it affects a lot of people, it's important to have a rapid test for it.  I just got the test today, only took about 15 minutes, thankfully I do not have the flu.
But for what I will call everyday cold viruses, there's no need for advanced or rapid detection.  And that's where you get the answer you got today.


text:
How do neurons inverse an action potential?
See the following figure (source):

The pathway on the right (SN $\rightarrow$ interneuron $\rightarrow$ F Neuron $ \rightarrow $ flexor muscle), is explained as follows:

The action potential in the sensory neuron invades the synaptic terminal of the sensory neuron causing the release of transmitter, and subsequent excitation of the postsynaptic interneuron colored black.  This neuron is called an interneuron because it is interposed between one neuron (here the SN) and another neuron (here the MN).  The excitation of the interneuron leads to the initiation of an action potential and the subsequent release of transmitter from the presynaptic terminal of the interneuron (black triangle), but for this branch of the circuit, the transmitter leads to an IPSP in the postsynaptic flexor (F) motor neuron (colored red).  The functional consequences of this feedforward inhibition it is to decrease the probability of the flexor motor neuron becoming active and producing an inappropriate flexion of the leg.

Specifically, it states that but for this branch of the circuit, the transmitter leads to an IPSP in the postsynaptic flexor (F) motor neuron. But it doesn't give an explanation of how this works.
How can a neuron generate an inhibitory postsynaptic potential when it is given an action potential? Can this specific neuron inverse the signal? How does that work?

The University of Texas site where you obtained this picture states in section 6.7:

What about the transmitter substance that is released by the inhibitory interneuron in the spinal cord? The transmitter substance is glycine, an amino acid which is used frequently in the central nervous system as a transmitter that produces inhibitory actions. It is not the most common, however. The most common transmitter with inhibitory actions is gamma amino butyric acid (GABA).

Glycine receptors activate a chloride-selective transmembrane channel, which is predominantly expressed in the spinal cord and brain stem (Rajendra et al, 1997). Chloride hyperpolarizes the neuron, thereby inhibiting the motorneuron controlling the flexor muscle, and thereby facilitating the extensor muscle to contract. If the opposing flexor muscle would not be inhibited, the extensor muscle would be counteracted and the knee jerk reflex would be less efficient, if present at all.
Typically, an inhibitory interneuron will only release inhibitory neurotransmitter. In the example here, the opposite circuit to bend the knee would activate the flexor muscle. This would be accompanied by opposite events. However, the inhibitory F neuron above in your figure would not reverse its action though, it will simply be silent, thereby allowing the acetylcholine from the E neuron do its job. In more general terms, neurons cannot reverse their action from inhibitory to excitatory. Their outputs are typically simply the release of a pre-defined vesicle pool, which is a yes/no event without further qualities. In other words, an inhibitory neuron will be inhibitory and it cannot change the nature of the neurotransmitters released (excitatory versus inhibitory) based on different inputs.
Reference
- Rajendra et al, Pharmacology & Therapeutics (1997), 73(2): 121–46

Thank you! That explains a lot. Just one more thing so I fully grasp the concept: some neurons will only release inhibitory neurotransmitters when receiving an action potential. These neurons cannot release excitatory neurotransmitters. Am I correct?

@Jean-Paul Yes, a neuron will release the same set of transmitters at all of its synapses--often it will release just one neurotransmitter, but sometimes two or more at the same time. An inhibitory interneuron will not, for instance, release an inhibitory transmitter onto one cell and an excitatory transmitter onto a different cell. This is known as Dale's principle (https://en.wikipedia.org/wiki/Dale%27s_principle).

@yamad To be very precise, the effect upon the postsynaptic neurone is determined by the type of receptor that is activated. With regard to the figure, is it true that the sensory neurons in the knee transmit neurotransmitters that generate an excitatory effect in combination with the receptors of the motor neuron that flexes the extensor muscle, and an excitatory effect within the inhibitory interneuron too? Then, does the inhibitory interneuron release neurotransmitters that in combination with the receptors of the motor neuron that flexes the flexor muscle yield an inhibitory effect?

@Jean-Paul Close, but with one major misunderstanding. In this reflex, the flexor muscle is not flexed (contracted). It is being relaxed by the reflex. How does this work? In the diagram, activating the E neuron contracts the extensor muscle, activating the F neuron contracts the flexor muscle. No activity in these neurons means the corresponding muscle is relaxed.  By inhibiting activity in the F neuron, the interneuron indirectly causes the flexor to relax. All the connections in the diagram are excitatory, except for the interneuron to F neuron connection which is inhibitory.

@yamad That is exactly what I meant: I referred to the motor neurons as "flexing the ... muscle" to indicate which motor neuron I was referring to (I should have used their names, E and F, to avoid confusion). But your comment nevertheless completely answered my final question. I fully understand the concept now. Thank you :)


text:
Dendrodendritic synapse through axodendritic synapse at same dendrite?
Reading Wikipedia's article of dendrodendritic synapse, I find that:

Dendrodendritic synapses are activated in a similar fashion to axodendritic synapses in respects to using a chemical synapse. These chemical synapses receive a depolarizing signal from an incoming action potential which results in an influx of calcium ions that permit release of Neurotransmitters to propagate the signal the post synaptic cell. There is also evidence of bi-directionality in signaling at dendrodendritic synapses. Ordinarily, one of the dendrites will display inhibitory effects while the other will display excitatory effects.

Now I was wondering, does dendrodendritic synapse occur only when the neuron reaches the threshold action potential and "fires" or is it possible that dendrodendritic synapse occurs as a result of, for example, an axodendritic synapse at the same dendrite? (even though the neuron doesn't fire)
Edit

Clearly, we can see that the dendrite has multiple 'endings'. I was under the impression that a synapse can happen at any such 'ending'. Assuming that a synapse happens at one ending of the dendrite, is it viable that anything happens to a neighbouring neuron that is connected with a dendrodendritic synaptic connection to the other ending of the dendrite?

I'm not sure if you are asking if an axon that sends a signal to a dendrite would then be released from that dendrite to another dendrite?
I don't see how this is possible seeing as the dendrite is already paired with the axon and downstream of said dendrite there would be a neuron.
A dendrodenritic synapse is two dendrites of two different neurons in contact with each other. For there to be a signal an action potential must have been reached.
Synapse is a junction between two neurons where chemical signaling occurs, but it is not the definition of a signal occurring. If that makes sense.
It seems like you are confused on the location and anatomy of a synapse.
There wouldn't be an axodendritic synapse followed by a dendrodendritic synapse then the neuron. It would either be axodendritic or dendrodendritic. Now there can be multitudes of connections between neurons but I don't think that is what you were asking.
Edit: Seeing your edit makes your question much clearer.
If the signal from the axodendritic synapse excites the neuron enough to reach action potential then that signal would be sent out through its synapses, including the dendrodendritic ones. So I guess in this way it was a "consequence" of the axodendritic synapse.
Though I would rather you think about it in that the action potential of one neuron sent a signal through it's connections to the neighborhing neuron, thus causing that neuron to reach action potential and further send out the signal. It's not really a "consequence" of the synapse, the synapse is more a pathway for the signal to travel.
The stimulus for the action potential is what causes a signal to fire and travel through a synapse.
Hopefully that answers your question.

Yes, I might be confused. Thank you for your answer, I think you are right. See my edit for further explanation.

It does indeed answer my question. I already understood your answer, but I wanted to make absolutely sure that a dendrite cannot cause a synapse to another neuron if the initial neuron didn't fire.


text:
Do individual neurons communicate with the origin of thoughts?
When mapping the different neural pathways in the brain, often pictures such as these are drawn:

Or similar versions. Clearly these sketches draw the neural pathways as being a two-sided connection, as can be judged from the double arrows. I was wondering, how such bidirectional pathways work. Specifically, I am interested to know whether individual neurons constitute such a bidirectional pathway between different parts of the brain, or if the bidirectional pathway can be thought of as a 'circuit': a pathway of neurons that eventually comes back to a certain part of the brain.
This question is especially interesting in light of abstract thoughts. Let's make some extremely generalising (and ludicrous) assumptions and assume that our conscious thoughts are governed by our hippocampus only. That is, we assume that thinking about a matter without input from sensory neurons causes the hippocampus to fire an action potential into some specific cluster of neurons (somewhere in the brain). E.g. we assume that thinking about the letter 'A' causes the hippocampus to fire an action potential into the cluster of neurons that represents the letter 'A'. Let's also assume that the memory we have regarding the letter 'A' must be returned to the hippocampus, in order to continue our thought process. For example, I might want to recite the alphabet in my head. Starting with the letter 'A', I then continue to the letter 'B', which arises in my conscious thoughts as a result of the firing of the cluster of neurons that contain information regarding the letter 'B'.
So if we assume the circuit, conscious thoughts $\rightarrow$ cluster of information fires $\rightarrow$ conscious thoughts to exist, then how would its feedback most likely work?
Let's take the example where we think of the letter 'A' and want to think of the letter 'B'. I have sketched two different theories about how the communication between these two clusters of information and the 'governing body of thoughts' (which I assumed to be the hippocampus), might be:

The difference is the following: in the second theory, all individual neurons are expected to be able to communicate directly to the hippocampus. Whereas in the first theory, the feedback to the hippocampus arises only when we have reached our destination: the letter 'B'. Clearly, if we assume that a specific thought process is able to self-induce action potentials (of course, this is highly debatable), at least one of the two theories must be partially true. For which one exists evidence?
My first intuition would be to say that the first theory is more likely, but this is ambiguous under Dale's principle: why would only some cells be connected to the hippocampus? On the other hand, I found it hard to believe that every individual neuron is directly connected to the hippocampus.
So now that I have explained my thought process, my question can be formulated as follows:

How are clusters of neurons that are involved in abstract thoughts bidirectionally connected to the thought-governing-body (whichever actual part(s) of the brain this is)? Can we say that just a single neuron in the cluster provides the feedback to the thought-governing-body, or is every individual neuron that is involved in conscious thought potentially capable of a feedback loop?

Disclaimer: Yes, I'm not up-to-date to all the latest advances in neuroscience. Yes, I'm aware that my question might be ambiguous with respect to all the different types of neurons, connections and theory about neuronal networks and micronetworks. My question, however, is concerning the likelihood of the theories I presented. For which one do we have evidence. Are both wrong? If so, in what way? Are both right? If so, when does their difference play a role? etc.

To give a simple answer to the first part, the feedback generally happens in circuits of at least two neurons. A synapse is generally one way, transmitting information from the presynaptic neuron's axon to the postsynaptic neuron's dendrite. I'm sure there's caveats and exceptions because biology always has that, but that's the norm. A simple feedback loop might look like this: A excites B which excites C. C inhibits A as negative feedback.
The second question relies pretty heavily on the assumption that conscious thought originates from a particular part of the brain, or that one neuron is dedicated to one concept. This doesn't seem to be true. Things like memory and thought appear to be distributed, emergent properties of several circuits and areas. They might be organized or integrated by a particular part of the brain but it's not the same as having one central executive looking at all the inputs deciding what you think.
Think of it like a person working on an Excel spreadsheet. There's all the code for the OS, the software, the formulas in the spreadsheet. Those are all important parts of the process but the user doesn't need to see any of that. All they need to see is the end products of each process, and then they can figure out what to do with those products. So circuits and neurons can be involved in lower processing without connecting directly to the area that organizes and integrates information. Also, because higher level processes like thought are so distributed, there's likely to be multiple centers organizing/integrating information and all giving feedback to each other. Does that make sense?
Side note: I think you might be misunderstanding Dale's principle. When it says that neurons have the same chemical action at every synapse, that means they release the same neurotransmitter(s) but that doesn't mean they have to be connected the same way or that the neurotransmitter release has the same results. For example, say a neuron releases the excitatory neurotransmitter glutamate. If it synapses on another neuron that releases glutamate, that will promote excitation. But if it synapses on an inhibitory neuron that releases GABA, then exciting that neuron will actually result in inhibition.

Thank you for your answer. I understand that the brain processes information in different clusters but I can't grasp the theory that conscious thoughts are distributed over clusters of neurons. Taking the Excel spreadsheet example: even though we don't see the lower-level tasks, we are still presented with the lower-level's output. This is what my question is about: assuming that A and B are such lower-level processing clusters, they must report to some central place in order for the information to enter our conscious thought. Much like when I use an Excel formula, I am given the result.

It makes sense to me that such clusters can intercommunicate, but one of the clusters has to report back to some centralised 'conscious thought'. How else can I think of an abstract principle? Surely, when thinking of this principle a cluster of neurons fires. But is this firing all there is? Is my conscious thought within this cluster of firing neurons or does the cluster communicate to a centralised area (like the hippocampus), where connections to my short- and long-term memory are also present (this seems more likely to me than to say that conscious thought is the firing of neurons alone)?

@Jean-Paul Thanks for the clarification on the question! Unfortunately I'm not sure there's a real satisfactory answer out there, but let me try...
First, it might help if you try to think of higher-level brain activity less like a modular machine and more like an overall  pattern of firing. We talk about areas of the brain being involved in one thing and it's easy to get caught up in that, especially when you're looking at imagine studies where it looks like one area lights up neat and tidy.

The truth is that most of your brain is active most of the time. In order to get that clean picture that you see in the paper, they had to do a lot of statistics and filter out a lot of noise and hope that their baseline was decent. This is a big issue in functional brain imaging, especially fMRI, and it's pretty interesting so I'm going to paste some references at the bottom in case you want to check it out. That's not to say that localization isn't useful! But it has to be taken as one data point, not the whole picture.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC60127/ An article on issues with fMRI baselines http://journal.frontiersin.org/article/10.3389/fnins.2012.00149/full Another on problems with reliability and data interpretation in fMRI https://mitpress.mit.edu/books/new-phrenology Great book about the limits of localization

Anyway, try to imagine things mapped as patterns of firing. For an oversimplified example, maybe the concept 'dog' isn't stored by cluster A, it's what you get when cluster A is firing at a low rate, cluster B is firing at a higher rate, and cluster C isn't firing beyond random baseline noise. If all 3 clusters fire at a high rate, you might get 'cat.' 'Dog' and 'cat' don't belong to any one of the clusters; they're stored by the pattern of firing from all 3. This is more complex, but it lets you store more concepts. That's why there's such an emphasis on the whole connectome thing right now.

As for where conscious thought comes from, that's kind of out of the scope of neurosceince right now. It's a fascinating question but it's difficult to impossible to study it. How do you define conscious thought? How do you measure it? We can pick at parts of it. The insula, for example, seems involved in self-awareness, and thought can light up areas involved with speech and language. But the overall concept of conscious thought is too abstract for us to handle right now. We need more information and more tools before we even know how to study the origins of conscious thought.

Thank you for your extension! I am starting to grasp the difficulties of investigating the brain. Apparently we still know too little about the problem to make any conclusive statements about such concepts. The information you have presented, however, is extremely educational about our current knowledge of the matter. I am definitely going to read those papers to get a better insight. Thank you!


text:
yeast protein secondary structure
i have a fasta file of yeast orfs (from the SGD database) and i need to find out(predicted) secondary structure/classification for all of them (so ~6K queries and doing this by hand on numerous available websites is not an option). is CATH database a place that can give me this info? (so far i struggle to recover anything that can help me from the website but perhaps i am missing something), if not what's the best way/software to go about it? surely, these predictions have been done before and there is a databse somewhere -- yeast is too much of an important organism, with a lot of information about its genome.

Lot of resources are available online, choose depending on your requirement and protein of interest.

@Dexter, thank you. i am well aware of this site and others but i need the procedure automated: i have ~6k ORFs and i need to run all of them through the algorithm to obtain secondary structure.

Then you need little bit programming with server queries. Alternately, search for server which accept batch sequences.

@Dexter unfortunately this is not something i am able to do, so i was more after either a piece of code (R/python) or a relatively easy to use software. i am struggling with installing and running s2D (whose server version i've tried and approved) at the moment and it's a nightmare.

From comments I understood that you need to predictions in bulk. You can use API based system of JPred. They allow you to submit more than 1000 jobs per user per day. You can go through instructions step by step from their documentation. It looks simple !
Another hit I got while searching is Phyre2. I am sure there are many such servers.

Phyre2 took a non-trivial amount of time for me to get a model back. I don't know if their batch processing is any quicker, though.

@canadianer I haven't checked any of these sites. API integration sounds interesting. My personal choice will be submit to ExPASY server through python queries but OP is not (or don't want to be) a programmer I guess.

@Dexter like you said JPred was very easy to set up and use, thank you again. and i am programming myself, however i am not very experienced in python and i don't have much time to learn how to submit queries etc in python at the moment

No problem. Go with whatever you find easier. At the end only thing matter is to get your job done.

in addition to Dexter's answer i found that the s2D does exactly what i need. setting up might be a bit tricky and is certainly more involved than setting JPred up but using it is easy and the output is in a nicer format.


text:
identifying which SNPs sit in TFBS (Yeast)
i have a set of ~11k SNPs for Saccharomyces cerevisiae, baker's yeast and i would like to identify which ones of these sit in transcription factor binding sites and if they do information on the relevant TFBS.
i've scoured this site and the internet and i couldn't find a downloadable database that would give me locations of all known/verified TFBS for yeast. i've studied the YEASTRACT website thoroughly but didn't find such database to download information about TFBS for all the ORFs/genes in one go.
moreover, when i tried getting the information manually through YEASTRACT search on-line i found results confusing. for example: searching for TF for ORF "YOL166W-A" returns a list of 4 TFs. clicking on one of them, say Sok2p, takes you to another page which says, amongst other things, that the corresponding TFBS is "acMTGCAKg"... what does it mean? (i know the ACTG alphabet but what are the 'a', 'c', 'K' and 'g' symbols?) and what does this tell me about the actual location of the binding site? do i have to BLAST the whole genome to identify it? (shouldn't there be a database with this info for yeast already?) if so, how do i BLAST for symbols like 'K' and 'g'?
i have background in stats but currently work in genetics applications, hence extracting relevant bioinformatics data is very confusing for me on occasions. any help will be appreciated.

In addition to the 4 nucleotide letters, there are letters that mean "the letter is one of these two or three:
M = aMine = A or C
R = puRine = A or G
W = Weak (two hydrogen bonds) = A or T
S = Strong (three hydrogen bonds) C or G
Y = pYrimadine = C or T
K = Ketone = G or T
B = not A
D = not C
H = not G
U = not T
I would guess the the lowercase means that those letters are not as important as the uppercase ones in terms of determining binding.

I agree it can be extremely confusing sometimes to find the right data.
Do you know RSAT (Regulatory Sequences Analysis Toolkit) ?
If you go in "help & contact", and "motif databases", you'll find the Yeastract database: http://rsat-tagc.univ-mrs.fr/rsat/motif_databases/Yeastract/
I thought it would also be on JASPAR, but couldn't find it.
Then for your analysis where you look for SNPs in the motifs, there is a tool on RSAT, that unfortunately works only with the Metazoa database right now, but you might be interested to check it out, and the corresponding paper: http://rsat-tagc.univ-mrs.fr/rsat/variation-scan_form.cgi


text:
Fine permanent fluorescent marker for blue light
I am looking for a fine- (or small-)tipped permanent marker to write on Petri dishes that is visible under a blue light or a transilluminator. It would seem obvious, but it is a nuisance.

The Sharpie Neon series are too thick.
Highlighters and all the arts pens I have tried rub off the polycarbonate.
The red colour from Staedtler lumocolor (black body) shows up faintly —none of the other do— but too faintly.
The Neon series from Staedtler triplus fineliner (gray body, triangular) rub off

So I would like to find what solutions other have come up with or if there is a brand that works well.
EDIT. This is how the Sharpie series look:

I have had this problem before... this is what I ended up using:
https://www.amazon.com/Invisible-Blacklight-Marker-Blue-Yellow/dp/B004C89M9Q
You may have to write on a tape or something so that the ink doesn't come off. (Ink may come off if you incubate plates)


text:
Energy of flight styles (birds)
What does take more energy (for a bird): to dive or gliding? My teacher thinks that gliding takes more energy, but I'm not sure about this: when a bird glides, it doesn't do anything (pretty much). But diving is stress, which takes much energy. Or am I wrong?
(edit: I don't mean the "going under the water" diving, but "nose dives")

How is diving stressful? The bird is just letting gravity do its thing.

Imagine: you're a bird flying towards the ground, getting faster and faster... not stressful? @MattDMo

No, not at all. Birds are not people. They have wings and are perfectly capable of controlling their descent.

But gliding souds much more like chilling, doesn't it?

For people like me ^^ ;-)

And you (as a bird) have to stop after that and fly up again... If you glide, you don't have to.

Google: (bird flight energy expenditure gliding) gives e.g. The Energetic cost of short flights in birds, Heart rate and estimated energy expenditure of flapping and gliding in black-browed albatrosses, Efficiency of Lift Production in Flapping and Gliding Flight of Swifts and ... [cnd->]

[...cnd:] Energy Expenditure and Metabolic Changes of Free-Flying Migrating Northern Bald Ibis. This might be a start.

@fileunderwater this articles are very detailed. But Strg+F gives no results for "dive", only for "glide", means that the article has nothing about diving. But it's a good beginning, thx.


text:
How "old" is a specific snake venom?
This is a World Building question, but it's biology specific (I think).
I'm looking for an approximate answer on how long, evolutionary, a specific venom has been roughly the same.  Is it pretty much species based (although I know that's a problematic term), so it would be the same as the "age" of the snake's evolutionary tree since it last branched?  Or is it based on something else?
Specifically looking for information on the Eastern Diamondback.  I am ok with extremely approximate/vague answers, or even just a hypothesis/educated guess.
If it helps, a possible rephrase of this question would be:
How far back in time could you time travel before a modern anti-venom starts to lose effectiveness?

definitely on topic!

This is a really interesting question. The best statement I could quickly find was in this paper. Snake venom glands evolved a single time, at the base of the colubroid radiation, 60-80 million years ago, with extensive subsequent “evolutionary tinkering”. ... I work some with peptide venoms from Naja cobras, so there's some personal interest. It should be simply a matter of sequence divergence. I'll keep looking :)

This article is interesting and contains some sources.

https://www.oist.jp/news-center/news/2013/12/9/biting-snake-venom-mysteries This story may be of help?

According to the following sources, venom resistance has evolved in both snake prey and predators. Also, resistance can be just regional/confined to a certain population. That suggests that arms races occur, where the composition of the venom of a certain species is constantly changing, and so are the defenses of the prey and/or predators who get bitten. In that case, a snake venom is not the same in chemical composition for very long, and might not be the same across populations of the same species of snake. But those differences might be on a smaller scale than you are looking for. I don't know anything about how this affects effectiveness of antivenom. However long it is until the antivenom loses effectiveness, it might be much shorter than the divergence time since that snake species branched off from the evolutionary tree.
Ground squirrels and rattlesnakes:
"Snakes win: Coevolution of venom function and prey resistance in a rattlesnake-squirrel arms race;
"Coevolution of venom function and
venom resistance in a rattlesnake predator
and its squirrel prey"
"How is rattlesnake venom like fine wine? Both have regional varieties"
(I wanted to make this a comment but don't have the rep for that).


text:
Why does the proportion of transposable elements vary so much across species?
Intuitively, transposable elements (TEs) are harmful as they may cause genome instability. However, some people argue that TEs are also sources of variations, especially regulatory sequences[1].
If TEs are harmful, then their proportions may be low in most species. And if they are beneficial, then their proportions should be high. Either case leads to the conclusion that their proportions should stay close to each other. However, the fact is that the proportion varies greatly across different species:

Maize: 85% [2]
Human: 45% [3]
Arabidopsis: 10% [4]
Plasmodium: absent [5]

Why is that? Is there other factors that influences the proportion of TE, such as evolutionary pressure?

Reference
[1] Rita R, et al. 2012. Transposable elements: an abundunt and natural source of regulatory sequences for host genes. Annu. Rev. Genet 46:21-42
[2] Schnable PS, et al. 2009. The B73 maize genome: complexity, diversity, and dynamics. Science 326:1112-15
[3] International Human Genome Sequencing Consortium. 2001. Initial sequencing and analysis of the human genome. Nature 409:860-921
[4] Arabidopsis Genome Initiative. 2000. Analysis of the genome sequence of the flowering plant Arabidopsis thaliana. Nature 408:796-815
[5] Biemont C, Vieira C. 2006. Genetics: junk DNA as an evolutionary force. Nature 443:521-24

I can think of two factors that would influence this, but there are probably more.
1) How do transposable elements (TE) get into the genome in the first place?  The answer is both vertically and horizontally.  Vertical transmission needs no explanation.  Horizontal transmission of TE has been documented in several cases.  In some cases, infectious agents can transfer them between species individuals, for instance, viruses can package transposable elements in addition to their own DNA.
http://www.cell.com/trends/ecology-evolution/abstract/S0169-5347(10)00123-0
2) How efficient can the TE replicate?  For example, in the human genome there are a variety of different types of retrotransposons, but only the L1 element can replicate.  Others like Alu and SINEs parasitize their replication machinery and therefore replicate also but at much lower frequencies.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884099/
So, the difference between species has to do with both of these and probably other factors.  I would imagine in the 2nd case, the selective pressures put upon a given species at any point in time, due to infections or inter-species competition, would surely impact the efficiency of TE replication because they are so important to genomic evolution and adaptation.


text:
Which of the cell types commonly found in mammals has the greatest number of mitochondria?
This is basically a fun question, inspired by this answer on scifi.se. So, which cell type will have the greatest number of mitochondria? Obviously, I am talking about wild type, healthy individuals and am looking for a rule of thumb. I realize that the number can change under different conditions/ between different individuals.
Off the top of my head, I would say that it's sperm cells given the strenuous exercise they need to perform and their MT-packed axonemes but perhaps there are better contenders?
I am primarily interested in human cell types but answers dealing with other mammals are welcome.

I'd expect a correlation between cell size and number of mitochondria. Therefore, my guess is that the ovule has the greatest number of mitochondria. On this wiki article it is said: "the number of mitochondria in a cell varies widely by organism and tissue type. Many cells have only a single mitochondrion, whereas others can contain several thousand mitochondria." and give two book references: Alberts and Voet.

Assuming @Remi.b 's correlation between cell size and number of mitochondria, then muscle fibers should win hands down. They are IIRC the largest cells in the body, and they have a need for significant amounts of energy.

oocyte, cardiomyocytes, skeletal muscle.. check this: esp page 11.. Oocyte has to provide miotochondria for the embryo.. so i guess it has the most

To study mitochondria, mitochondria are often isolated from brain, liver and muscles. Mitochondria are abundant in those tissues.

In terms of number, it could be tricky because sizes of mitochondria vary a lot.

try to get this article - http://www.unboundmedicine.com/medline/citation/2318903/Distinct_genomic_copy_number_in_mitochondria_of_different_mammalian_organs_

It's commonly believed that it's muscle cells that have the largest amount of mitochondria, and for good reason.  Muscle cells are continually used to move the body, so they have the most mitochondria because of the large energy requirement.  If you want to be more specific, the muscle cells of a marathon runner have even more since the muscle cells involved in running need to be able to do a lot of aerobic respiration.  Another example is the cells in the heart; the amount of mitochondria makes up 40% of the cell.
The truth is, retinal cells with photoreceptors most likely have the most (80% of the cell volume) since they need to reset the potassium/sodium pump to keep the action potential in the nerves the same.
If you're curious, the cells with the least amount of mitochondria are skin cells and erythrocytes (red blood cells) since skin is just a protective barrier and red blood cells don't need to exert any effort or energy to move.
Sources:

http://hyperphysics.phy-astr.gsu.edu/hbase/biology/mitochondria.html
http://www.ncbi.nlm.nih.gov/pubmed/12511073

Welcome to Biology. It would be great if you could add some references to your answer.

Sorry about that.

That explains what mitochondria do, but gives no reference for the claims you make.

I'm not able to add any more links because I have limited privileges.

That's fine, just paste the URL as is and someone can edit it for you. Your answer makes a lot of sense, and I agree that it is very likely going to be muscle cells, but neither of your references support it. They just explain what mitochondria are. I would particularly like to see a reference supporting your claim about photoreceptor cells, that's an interesting point. I can't accept this since you're just giving numbers with no references.

You can also edit your answer and remove the irrelevant links and replace them. If you have more links, post them in the comments and someone will edit your post accordingly.

I was under the impression that hepatocytes had the highest concentration of mitochondria, as so much of a muscle cell's cytoplasm is taken up by the contractile apparatus.


text:
Two-fold cost of sex and r/K selection theory
This article cites a bunch of articles (I haven't been through them) that the effect of the two-fold cost of sex is "reduced" in stable environment or in K-selected environment. It says:

[..] the infamous ‘two-fold’ cost may be reduced or, perhaps more accurately, more easily balanced in K-selected species. The ‘cost of males’ is with respect to reproduction. Abugov (1985) argued from life history theory principles that the two-fold cost of sex might be easier to pay with K-selection. The two-fold fecundity advantage of asexual reproduction is always a two-fold fitness advantage, regardless of whether it is in a K- or r-selected environment. However, a survival advantage is worth more under K-selection than under r-selection. Consequently, it is easier to balance the two-fold cost under K-selection if sexually derived genotypes have a survival advantage.

I think that k-selection, k-selected environment and stable environment describe (more or less) the same kind of environment. Let me know if this sounds wrong to you. Here is wiki for r/K selection theory
From the same article K-selection is defined as:

K-selection might favour slower development, greater competitive ability, delayed reproduction, higher survival rates, lower resource thresholds, leading to ‘efficiency’ (rather than productivity) and constant population sizes at or near carrying capacity of the environment.

It sounds really strange to me. Can you please help me to understand why the two-fold cost of sex is lower in stable environment than in unstable environment?.

r/K selection has become more of an heuristic for characterizing a species' strategy of reproduction and less a matter of predicting what sort of species will emerge from a given environment as it had originally been proposed by MacArthur and Wilson in 1967. The paper you cite tries to determine whether rotifers become more r or more K selective in different environments.
The thought here on k-selection is not almost from the definitions of the term, which is why it isn't explained in the paper.
In R-selected strategies, many more offspring are produced, but less investment is made in each one.  Think about a cockaroach laying thousands of tiny eggs.  The hatchlings might be eaten by their own mother; they are so 'cheap' the insect who layed the eggs doesn't have any anxiety about their survival.  In extreme cases, most of these hatchlings will not reproduce, they may even be a bit of food for the ones which do reach maturity.
In k-selected strategies, very few offspring are produced.  In addition to the 'cost of sex' limitation, they are invested in so heavily that the female may stop being fertile for a while.  An example would be how female mammals which are lactating are not fertile or seasonal mating like many birds do; the females turn off reproduction so that they can focus on the success of one or two produced offspring.
k-selection is advantageous over R-selection when more of their investment pays off.  If one out of ten R-offspring survive and one out of four k-selected offspring survive, then for these competing rotifers, the k-selected strategy is advantageous.
The cost of sex is that its half as efficient as asexual reproduction because males don't really reproduce - they only provide genetic material for females.  You can argue r/K selection independently of this factor, but the article is suggesting that k-selection can be so advantageous as to also give sexual selection an advantage over asexual selection.  I think asexual reproduction could be k-selected as well, but that seems to be the point being made here.
The reason that k/R has toned down in importance in the past couple of decades is that it has been found that individual species can adapt to shift their k/R strategems.

Can you elaborate upon what you mean by "individual species can adapt to shift their k/R strategems"?

There are definitely limits but if a bird or insect starts laying larger eggs or if elephants start to become smaller, then their offspring become more or less expensive to produce respectively.  this means that their k/R strategy (cheap or expensive offspring) is changing.  Humans are an extreme case.  children take 8 or 20 years to become independent depending on parental life styles...big difference!


text:
Empirical evidence for species selection
Do we have any empirical evidence in favor of species (or lineage) selection? Do we know some cases that can only be explained (or seem to be only explained) by lineage selection? What are today the best study cases in favor of lineage selection?
If not, how could we find any evidence for lineage selection?
Note: I call lineage selection a differential in speciation and/or extinction rate that drive the proportion of lineage (species for example) displaying a given trait (emergent traits or not) to increase or decrease over time.

A commonly used empirical example of species selection (a.k.a clade selection, lineage selection) is pelagic larvae in sessile ocean species. See Maliska et al (2013) for a recent paper discussing this in Tunicata and Jablonski & Hunt (2006) for larval modes in gastropods. The idea is to some extent really intuitive - pelagic larvae means higher dispersal rates, so the species will be exposted to and can colonize new environments. This can lead to speciation through adaptive radiation. Larger ranges also means lower extinction rates (e.g. through less population synchrony). If the trait is fixed within a lineage, this lineage as a whole will, as compared to an sister lineage lacking the trait, contain more species (i.e. species selection).
However, you can also argue that pelagic larvae will lead to higher gene flow between populations, which could inhibit speciation. Therefore, the effect of pelagic larvae, and how these mechanisms are weighted in practice, is really an empirical question (see Duda & Palumbi, 1999 and Jablonski & Hunt, 2006 for discussions on this issue).
Jablonski (2008) provides a nice general review of species selection (concept, mechanisms, theoretical models and data), and Okasha (2006) (chap. 7) is good for a theoretical/philosophical treatment of levels of selection. Also remember that traits are selected for at the individual level, but can (especially if fixed) still act on a lineage level.


text:
Do animals commit suicide?
Do we have documented cases of animals purposely and consciously trying to end their own life? What leads to animal suicide, and is it preventable?
I've heard mixed answers from various biologists. Is anyone here capable of providing an answer?

how much googling have you done on your own so far? that might be useful to know

@kmm, arguably the current question is different because of the vertebrate restriction and "purposely, consciously"

@ConnorSmith, they could get killed in the food chain, but I highly doubt they are as mentally messed up as humans though.


text:
Could viruses be used as antibiotics?
Could we use viruses that only affect bacteria to act as antibiotics?
The more bacteria, the more times the virus divides, so the stronger it gets. Is this practical?

Look up Phage Therapy, that's basically what they're doing. In fact, it's used in many cases where antibiotic resistance is high. My  college lab was actually researching the use of Phage Therapy with E. coli infections.

Yes, it is practical. Assuming you have or create a virus that attacks the bacteria you want to destroy, the nature of the virus should wipe out the bacteria. The problems that could arise, as with any genetic manipulation, are the potential for an out of control mutant.

You may already be eating cold cuts that are treated using this method.

Could we use viruses that only affect bacteria to act as antibiotics?

Yes. The specific class you're referring to is called a "bacteriophage".
There's quite a bit of research going on surrounding phage therapy as a stand-in or replacement for traditional antibiotics. Here's a Nature Biotechnology article from 2004 that discusses your very topic.
It is practical, carries some risks (mutations being a known and accepted risk), and I wouldn't be surprised to see phages in practice now or sometime soon.

Yes you could.
It used to be a big deal before antibiotics were discovered, and continued for a bit in the Soviet Union.
However, due to the success of antibiotics, it fell out of grace. Due to the lower level of applied research in the Soviet Union (not research itself, although equipment might have been often outdated a bit and the Soviets did isolate themselves quite a bit, but a great deal of research originally discovered behind the Iron Curtain was actually commercialized in the US, such as contact lenses; many Soviet research projects are actually getting rediscovered, such as the great experiment about the domestication of foxes), it never became the thing, and after the fall of the SU, it was nearly forgotten.
However, now it is becoming trendy again. There are several reasons:

resistance against antibiotics have grown out of proportions
it is quite trendy to use "natural predators" against pests

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

In fact, you could say that_ there's a phage for that_. They take water from a river, for example and see which phages feed and reproduce on the germs you are targeting, and cultivate them, benefitting from artificially induced natural selection.


text:
Why are certain cells more likely to be attacked in autoimmune conditions?
For example, type 1 diabetes occurs when the immune system attacks and kills beta cells in the pancreas. This is relatively common.
What makes beta cells more likely to be targeted than, say, alpha cells in the pancreas?

Autoimmune reactions each have their target antigens. They'll "attack" wherever those antigens are expressed. In the case of Type 1 diabetes, many specific antigens have been identified, and they all correspond to regions on the surface of pancreatic islet β cells. Ultimately, however, the immune reaction is targeting proinsulin and its processed product insulin, which are produced by solely by β cells. This is an interesting review covering the topic.

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


text:
Would a human survive eating only living ants?
After reading an admittedly foolish question about 1 googol ants vs. 1000 humans, I had a question. Could a human survive solely on eating ants (common ants, not the stinging kind, or leafcutters etc.)

This study in 1984 suggests it's a bad idea and other sites have said eating ants is for weight loss.
The abstract says that it goes into detail about the problems associated with eating ants as well as their low nutritional value.
So I believe the answer is no. You could not survive long term on a diet of only ants.


text:
E value cutoff for RNASeq search
I am trying to narrow down the possible search criteria from an RNASeq experiment. I already have the cds sequences so I took these and used Blast+ program to blast the data against itself to find sequences that were the same.
From what I have read the E Value is based on the database size. My database only has ~27,000 sequences in it, does this mean that only exceptionally low E values will be relevant to me? Are there any other criteria I should search for before writing the program to eliminate similar sequences?

What are you mapping to the database- RNAseq reads? How long is the query?

Going by an e-value or bitscore cutoff will give you possible homologs, but it sound like you want to remove redundant sequences. If you want to cluster and combine similar sequences to make a smaller database, you could just go via sequence identity using something like CD-HIT. This, for example, is what's done to produce the UniRef set from the UniProt database.