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Is an Eidetic Memory (or other unusual forms of memory) less susceptible to anterograde amnesia?
I'm a physicist, so as a fellow scientist I want to apologize because this question will be entirely based on anecdotal inferences and I am well aware how irritating that can be.
I have an eidetic memory and I've never experienced any of the common forms of anterograde amnesia. No blackouts from rapid consumption of alcohol (and believe me, I've tried. That was the fun part. But not for kids; then it's not fun), not from extreme fatigue, head trauma, I even went in for surgery once and the anesthetist said at one point "Well since you asked, the amnesiac should be setting in right about now" and I vividly recall another couple minutes of conversation while we waited for the general anesthetic to knock me out.
So, naturally, I just assumed it must have been because of my eidetic memory. But I've always had an interest in neuroscience and now my curiosity has gotten the better of me. Surely the memory systems of all people are similar enough that amnesiacs and the like should work on everyone. So I ask, are eidetic memories (or perfect, or photographic, or other unusual forms) actually less susceptible to anterograde amnesia? Or perhaps have I just been the victim of probability; this is more a matter of luck not neuroscience?
Please don't spare the gory details, neuroscience is cool (Neuroscientists are brainy guys. Sorry, I couldn't resist that pun). That said, I am physics, not biology; I'm probably under-specifying the question. Let me know if it's too broad and I'll try to focus.

If you have red hair you can expect a different reaction to anesthetic

This question is more of a medical question than one of the underlying mechanisms of biological function.
The formation of long term memories is related to long-term potentiation. There are multiple neurotransmitters involved in this process. Ethanol primarily affects NMDA receptors. Drugs used to specifically induce anterograde amnesia, like propofol, primarily affect other others, like GABAA.
The process of memory formation relies on a variety of factors including the orchestration of multiple neurotransmitters. Anterograde amnesia can be induced by many factors and does not have a single known mechanism of action. It is not possible to conclude any single person will react identically to all inducers of anterograde amnesia. It is often the case that people have unique responses to drugs within a distribution of possible reactions.
The individual nature of responding to drugs is why side effect lists are lengthy, and usually only a few out of this list are observed in any individual.
My hypothesis is, as a regular consumer of alcohol, your liver function is elevated and responsible for your high tolerance. The cytochrome p450 family of enzymes are responsible for much of the metabolism of drugs in the body.
Liver function tests are cheap and interesting, I find. You might have some blood work done at a local lab to check out those stats as well as your cholesterol, etc., if you have an interest in such things.

Hang on, that "might" explain amnesiac drugs (although an anesthetist should account for that), but blackouts from alcohol have more to do with the rate alcohol is consumed than the actual amount. So regardless of my tolerance I should still be able to experience it with a moderate amount. Plus that doesn't explain lack of fatigue or trauma related memory loss or that similarly regular consumers do experience this effect. That said, this definitely supports my "I'm probably wrong with my assumption" suspicions

Everyone reacts differently to drugs. There's nothing extraordinary about not suffering a few symptoms. Some people never have hangovers. You should ask a MD. These are all things that physicians specifically train to address. I think there's talk on StackExchange Area 51 on establishing a medical stack.


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Have there been any theories put forward as to the reasons behind Temperature-Dependant Sex Determination in reptiles?
This applies to most if not all reptiles, but I'll write about leopard geckos since that's what I know.
Incubation temperature of the eggs makes a big difference in the development of the gecko. Obviously excessively high or low temperatures will kill the embryo, but inside the safe temperature range there are some interesting effects. The most well-known is Temperature-Dependant Sex Determination (TDSD).
Studies have been done and it is quite well-documented that:

Incubating eggs at the mid-point of the safe range results in predominantly male offspring.
Incubating eggs at the high or low end of the range both result in predominantly female offspring.

According to my gecko book, there are also some interesting effects regarding males that hatch from female-biased temperatures being more sexually active but less aggressive to females than the "macho" males produced at male-biased temperatures, females at female-biased temperatures being the most fertile and high-temperature females being more aggressive than lower-temperature females.
(Incubation temperature also affects colour - specifically melanin production levels. AFAIK it's not known whether this is a direct effect of the temperature or an indirect effect from the changes in sex hormones at the different temperatures. It's probably a different enough issue to warrant a separate question, though.)
Going back to TDSD, my question is: what theories have put forward to explain this sex determination? Evolutionarily speaking, how did this come about? Are males less likely to survive so they are only produced at safe temperatures? Does the optimal male:female ratio for propagating the species change in adverse conditions?
I'm not looking for random guesses. I'm interested in knowing if there have been any theories put forward from knowledgeable and reputable sources.

How is this possible? per Wikipedia Y chromosome defines gender in mammals but it is different in Non-mammals i.e for reptiles.

Not answering, I was only aware of the mammal process and thought it applied to all species.

I had the chance to read part of this book before its releasing. I'm sure you'll like it.

Welcome to Biology StackExchange!
Environmental sex determination is tremendously interesting.
It looks like the most common explanation is that temperature-dependent sex determination (TSD) is the original form of sex determination, and genetic sex determination has evolved multiple times in different animal groups since then. Reptiles are a mish-mash of different mechanisms.
If TSD came first, then the real question is not why did it evolve, but why is it still around. And the answer is likely because it works well enough. I couldn't find a lot of evidence that females make varying choices for next temperature, so in "real life" it might mostly be that plenty of males and females are always born. There is also recent evidence that genes affect when the temperature has an effect, so again, temperature alone is unlikely to drive sex ratios.
As far as possible advantages of TSD there is no definitive explanation that has held up to testing. It is possible that ideal female development has slightly different requirements than male development, so nest location choice by the parent may act to produce more females if the current environment supports them more than males. For instance, it has been shown that having more female offspring when temperatures are higher results in larger females.
Sorry to not have a simple answer for you. The whole idea is fascinating, along with other environmental triggers to development, like worker ant larvae becoming a winged queen if given the right nutrition, or butterflies that add "eyespot" pigmentation to their wings in wet years with increased predators.

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Are more animal species edible than plants?
While grocery shopping I was thinking that we restrict ourselves in regard to which animals we eat. I surely don't want to eat spiders and ants, for example, but I know that this is just because of my upbringing. But a lot of plants are actually inedible. So, is my idea correct that we can eat far more animal species than plant species? And if so, why? The reasons why certain plants are inedible seem to me also as rather diverse, like most plants
developed their own special molecule(s) to avoid being eaten by us. :)
I would be interested in some more educated opinion on this thought than mine. Thx in advance.

It is estimated by some that on earth there are

7.77 million species (of which 953,434 have been described and cataloged) of animals
298,000 species (of which 215,644 have been described and cataloged) of plants
611,000 species (of which 43,271 have been described and cataloged) of fungi
36,400 species (of which 8,118 have been described and cataloged) of protozoa.

with 6.5 million species found on land and 2.2 million (about 25 percent of the total) dwelling in the ocean depths.[1][2]
Despite the existence of toxic plants and animals, from the numbers alone it is clear that there are more animal species we can eat than plant species.
This does not take into account population or individual sizes, just species.
[1] How Many Species Are There on Earth and in the Ocean?
[2] How many species on Earth? About 8.7 million, new estimate says

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How do membrane proteins find their target locations?
The question might be asked for any kind of "bound" proteins, but I'd like to restrict it to membrane proteins.
Assuming membrane proteins (or their main parts) don't (or aren't) build in situ but at some distance of the membrane, I wonder by which mechanisms they travel from their generation site to their final destination inside the membrane (inner or outer).
Proteins that are distributed roughly evenly (or randomly) over the membrane don't pose a big conceptual problem: they could have gone their just by diffusion, possibly from many generation sites, distributed roughly evenly (or randomly) inside the cell.
But what about uneven distributions, where some proteins are more densely and non-randomly packed (significant and functional) at some sites of the membrane than at others, e.g.

receptors at postsynaptic densities
Na+ channels at action potential initiation sites like the axon hillock or the axon initial segment
Na+ channels at nodes of Ranvier?

By which mechanisms (forces, signals or structures) are these proteins led to
 their targets?
Maybe it depends, and there are different mechanisms. These I came up with (by contemplating first principles):

uneven distribution of generation sites inside the cell (due to what?)
uneven distribution of origins of attracting signals inside the membrane (due to what?)
some "self-attracting" forces or signals (leading to accumulation by positive feedback)
microtubules

Which mechanism is — possibly — predominant?

Related questions:

Life cycle of proteins
Pathways of ligand-gated ion channels
Distribution of synapses of CA1 neurons
Distribution of dendritic spike generating ion channels on the dendritic tree
Visual maps of the neuronal membrane
Distribution of sodium–potassium pumps

This is a great question. A comprehensive answer would be beyond the scope of an answer on a forum like this. I will summarize the best I can here, but if you are really interested in this you should look at some of the work by Randy Schekman and Tom Rapoport, who have done a lot of pioneering work in this field and have papers from more than two decades ago on their lab websites. I'll talk about membrane proteins generally, but I'm not sure what the state of the field is for Na+ channels specifically, so I can't comment too much on that particular case. Many of the details of the processes I will mention are still areas of active research, so I will try to stick mainly to what has been well-characterized (to the best of my knowledge).
To restate the problem, proteins are generally synthesized in the lumen of the endoplasmic reticulum, which is an aqueous environment similar to the cytosol in many (but not all) ways. However, membrane proteins, which are not stable in aqueous environments, must:
1) Find a way from the ER lumen into a membrane.
2) Get from the ER into the correct membrane so they may perform their cellular function.
We will start with step 1, but the key to both is a critical but often underappreciated aspect of protein biology called the signal peptide. The signal peptide is simply an N-terminal sequence of amino acids that precedes what we would normally think of as the beginning of a mature protein. It is relatively short, usually only ~30 amino acids in length. It is cleaved off the mature protein by a protease once the protein is folded and in the membrane. Until that time, the signal peptide serves as a molecular marker that indicates where the nascent protein should be heading and how it should be handled. Not surprisingly, there are many different signal peptides that serve multiple functions, and they are not only used for membrane proteins.
So let's say we are in the ER lumen, and have some mRNA coding for a membrane protein that is destined for the plasma membrane. The first amino acids that will emerge from the ribosome is the signal sequence, in this case a specific signal sequence indicating that this is to be a plasma membrane protein. Once the signal sequence emerges from the ribosome, it is recognized by a ribonucleoprotein complex (that is, a complex of RNA and protein) called the signal recognition particle. Once the SRP binds to the signal peptide, translation is halted, and the whole complex moves to the ER membrane, where it forms a complex with another large protein complex called the translocon. I can't go into the intricacies of these complexes and their functions in this answer alone, but the simple description is that the translocon contains an ATPase that can insert the membrane protein into the ER membrane as it is translated, with the correct orientation. The hydrolysis of ATP provides energy to move the emerging polypeptide chain into the hydrophobic membrane, where chaperones help it fold. This process is in part driven by the recognition of hydrophobic transmembrane regions of the proteins by the translocon. It can also move soluble, cytosolic proteins across the membrane through a similar mechanism.
Now that the protein has been translocated, a peptidase will cleave the signal sequence off the protein. From here, sorting signals will take over. Generally, these are simple sequence motifs in the first transmembrane domain that act similarly to a signal sequence, but they are not cleaved. However, sorting signals can be stretches of peptide throughout the protein too, in some cases.
These sequence motifs will be recognized by cell trafficking machinery. Without going into too much detail, the proteins will be gathered into vesicles, and transported to other organelles. Usually, the first stop for proteins is the golgi apparatus, which is typically where many post-translational modifications, such as glycosylation, take place. I am a biochemist and not a cell biologist, so I am not the most qualified to go into the details of subcellular trafficking. Suffice it to say, once the protein is finished being processed in the golgi, it will be trafficked into other organelles, such as the plasma membrane using vesicle transport as before. From my understanding, the protein will be sorted into the proper vesicles based on its sorting signals, as well as other markers (in some cases, certain post-translational modifications on certain proteins can influence its trafficking). The vesicles recognize the proper destination membrane in part by the lipid composition of that membrane. For example, phosphoinositides have extensive influence on membrane trafficking, and many membranes can be differentiated by their phosphoinositide signature.
Anyway, that is a very broad overview of the answer to your question. I'm sorry I can't comment too much on the intricacies of cellular trafficking, I don't quite have the expertise to go through that literature quickly enough to answer your question in a reasonable time frame. I hope this is helpful in pointing you in the right direction, and good luck!

Is active transport an answer?
With special signalling and interaction peptides inside of the protein, proteins can be targeted to different sublocations.If you are interested in how Na+ channels accumulate at the AIS, read for example Gasser et al. 2012, that is a very nice paper that shows the ankyrin binding motif is sufficient to cluster Na+ channels at the AIS.

Might be. But HOW are the proteins targeted to different sublocations (specifically)? I'm probably NOT interested in how Na+ ions do accumulate anywhere.

But I may be misled. Maybe Na+ accumulation is the answer.

Sorry, I meant channels, was missing the word.


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A question concerning the strength of synapses
Synaptic strength can be defined

»as the average amount of current or voltage excursion produced in the postsynaptic neuron by an action potential in the presynaptic neuron«

Synaptic strengths and their changes depend on many factors and mechanisms, from LTP and LTD to STDP and STF and STD. Possibly, also neuromodulators should belong to this list – but maybe they shouldn't.
Assuming that synaptic strength is a well-defined quantity even when the synapse is at rest, the strength of a synapse is a continuous or non-continuous function over time, that ideally can be plotted.
Now I wonder whether there have been recordings and/or simulations of the synaptic strength of a single synapse as such a function over time - and how the plot would look like at different time scales: long term trends superimposed by shorter and shorter fluctuations?

What you are describing is exactly how long-term potentiation/LTP (or depression/LTD, for that matter) is measured electrophysiologically.
Here's an example from a 1988 review by Nicoll et al:

Nicoll, R. A., Kauer, J. A., & Malenka, R. C. (1988). The current excitement in long term potentiation. Neuron, 1(2), 97-103.
The x-axis is time in minutes, the y-axis is a measure of synaptic strength: the slope of the local field potential response to simulation of a particular pathway. You could also measure an EPSP internally, measure voltage with a voltage-sensitive dye, etc.
At the point marked "tetanus", a long train of pulses is delivered that is known to cause LTP. Afterwards, you see an increase in synaptic strength that is maintained for many minutes.
It's also possible to perform these experiments over longer time scales, with different paradigms, in the presence of various drugs that influence LTP, etc. Different protocols will give different durations of LTP.
These sorts of plots are ubiquitous in the LTP/LTD research field, so if you read any papers in that area you are likely to come across many similar presentations.

Thanks a lot, but what about larger time-scales, from days and months to years and decades? And what about smaller time-scales, down to seconds and milliseconds (why not)? Or will the concept of synaptic strength loose sense on the millisecond level?

@Hans-PeterStricker At a millisecond level you would be thinking about short-term plasticity rather than synaptic strength. At very long time scales the answer is far too much "it depends" to be contained in a stack exchange answer.

But what is plasticity the plasticity of if not of synaptic strength? The other way around: What's the difference between plasticity and synaptic strength?

@Hans-PeterStricker I suppose in a sense you could consider it a measure of synaptic strength, but it isn't a mechanism typically employed in artificial networks, where "synaptic strength" is used as a concept. Read up on "short-term plasticity" and contrast it with what you know about long-term plasticity - they are really quite distinct biologically.

May I note that by definition "synaptic strength" is a purely physical concept (it's all about voltages and currents) - the underlying biological mechanism don't really matter (in my understanding and in the context of my question).

@Hans-PeterStricker In a biological system, there is no way to measure synaptic strength by any one number the way you can in an artificial one without adding further information to that definition.

Let us continue this discussion in chat.

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Can you identify the bird in this photo?
I spotted this bird in Bangalore, atop a building on a September morning.

He is Shikra (Accipiter badius) in India worldwide he is goshawk

Looks like Butastur indicus, the grey-faced buzzard. The spotted breast and the greyish chin fit well.
A nice picture can for example be seen here

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What is the specific role of the cerebellum when it comes to 'coordinating movement'?
In elementary biology (high school level in the UK - A levels), we are told that the cerebellum is the part of the brain that 'coordinates movement'. Literally nobody takes the time to explain what the word 'coordinates' encompasses. Hence, I do not know the specific role of the cerebellum in coordinating movement.
For example, one very daunting thing that we are told is that the frontal lobe contains the 'primary motor cortex', which supposedly contains motor neurons that connect to the spinal cord and brain stem and can send nerve impulses that enable movement in the body. Where is the distinction between such a role and the role of the cerebellum in 'coordinating movement'?

The principal function of the cerebellum, which was detected years ago, is to calibrate detailed movements rather than initiating movements or deciding which movements to execute (Ghez et al, 1985). This was concluded by observing the changes which occurred after damaging cerebellum. Animals and humans with cerebellar dysfunction show, above all, problems with motor control, on the same side of the body as the damaged part of the cerebellum. They continue to be able to generate motor activity, but it loses precision, producing erratic, uncoordinated, or incorrectly timed movements. Thus, cerebellum helps in coordinating fine-tuned movements and inhibits involuntary movements. Apart from this, fMRI studies have indicated that more than half of the cerebellum is intertwined with association areas (Buckner et al, 2011). But since it is out-of-scope here, I'll leave it at that much.
See it like this:

For a more detailed mechanism and circuitry of the cerebellum, you can have a look at this interactive page from the University of Texas. @FilipeRocha have also come up with some fine details in their answer.

References:

Ghez C, Fahn S (1985). "The cerebellum". In Kandel ER, Schwartz JH. Principles of Neural Science, 2nd edition. New York: Elsevier. pp. 502–522.

Buckner RL, Krienen FM, Castellanos A, Diaz JC, Yeo BT (2011). "The organization of the human cerebellum estimated by intrinsic functional connectivity". J. Neurophysiol. 106 (5): 2322–2345. doi:10.1152/jn.00339.2011.

When attempting to execute a movement, a signal is not only sent from the motor cortex through the spinal chord and to the muscles, but also one is sent from the same motor cortex to the cerebellum, containing the information of what is the intended movement (this happens via the cortico-pontocerebellar tract, and enters the cerebellum through the middle cerebellar peduncle, in case you are familiar with some neuroanatomy).
At the same time, the cerebellum is receiving information about the current position and forces of the body, called proprioception, through signals that come from proprioceptors located on bones, muscles and joints, which travel up the spinal chord (through the spinocerebellar pathways) and enter the cerebellum (through the inferior cerebellar peduncle). The cerebellum then processes both pieces information - intended movement and current mechanical state of the body - and sends out a signal back to the motor cortex (via the superior cerebellar peduncle) containing information that will improve the overall execution of the movement, by correcting and smoothing out with how much force, how much time and to what extent each component of the movement should be done.
The cerebellum is also implied in the learning process, not only movement-wise (learning to ride a bike or swim), but also cognitively.
To learn more:
http://www.brainfacts.org/brain-basics/neuroanatomy/articles/2012/the-cerebellum/
https://www.youtube.com/watch?v=mpO4lTDr1to&index=21&list=PLp9HSlEm97VXyQ32Uwjfz3dpmQ8nl63zJ


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Are SNPs and alleles the same thing?
It seems to be quite difficult to find an answer to this. Are SNPs the same thing as alleles?

Alleles are variations of a same locus that codes for a protein (gene). These alleles can come in different forms, one of which is SNP. For example, sickle cell anemia arises from an allele of the beta-globin gene which has had a change from A to T.
Meanwhile, for the ABO gene that determines your blood group, the O allele has a missing nucleotide (G) that leads to a frameshift in the gene and a loss of function.
So alleles are caused by SNPs, but can also be due to deletions, additions, insertions and other genetic changes.
Note that SNPs not always lead to new alleles. Sometimes they occur in non-coding areas and nothing happens.
Edit:
SNPs do not need to be gene specific, but this was for simplicty.
@Artem added nicely to the answer, I'm quoting it here:
"Single Nucleotide Polymorphisms (SNPs) are Single Nucleotide Variants (SNVs) at a population allele frequency greater then 1%. Alleles are any variants of the same position of DNA, which includes SNVs, insertion/deletions, or structural variants and at any frequency." - @Artem

Allele doesn't have to be in the coding region

I have two comments:

An SNP is just a substitution, correct?
AN allele can be more generally defined as a variation in a section of a gene, correct? I assume that that's why @student states that alleles can happen in non-coding regions of the DNA, and that makes sense now that we know that these sections are actually useful.

@Mathematician SNP is also known as substation. 2. Yes, but that doesn't have to be in a gene coding area. Anywhere in the genome is okay.

Please add some references to your answer.

What is the basis for  assertion by @Artem that SNPs have to occur at a frequency of greater than 1%? It may be a general agreement in the field — I don't know — but if so a reference is needed to back this up.


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Well Plate Method VS Kirby Bauer Method
Any pros and cons? One puts the test substance in sterile discs, while the other one puts it directly into wholes in the agar. Any thoughts?

I came across a nice Master's thesis that investigated precisely that. The conclusion reads as follows:

Automated microbroth dilution-based testing methods are increasingly used by many
  clinical microbiology laboratories to determinate antimicrobial susceptibility. Thus, it is vital that
  these methods are able to accurately determine the correct antibiotic susceptibility patterns of
  microorganisms being tested. In our laboratory, we use the Trek Sensititre system (Well Plate Method). However, if
  this system cannot accurately detect resistance visualized as inner colonies on the Kirby Bauer
  Assay, then the clinical importance of the Trek Sensititre may be called into question.
Our study showed that the Trek Sensititre was unable to detect the
  additional resistance of inner colonies that are detected using the
  Kirby Bauer Assay. Nevertheless, there are a number of important
  limitations associated with the study: Firstly, the inner colonies
  used in the study were pooled from all inner colonies from the Kirby
  Bauer plate. Because the colonies were pooled, in some cases from
  different antibiotic zones, it is possible that a mixed population of
  resistant organisms that were selected for by the different
  antibiotics were tested. This possible mixture of multiple different
  subpopulations may make the results difficult to interpret. Secondly,
  some inner colonies were selected from antibiotics that do not have
  any CLSI- 47 approved interpretations and would be considered
  inappropriate to report. For example, some Pseudomonas aeruginosa
  isolates displayed inner colonies to ertapenem, an antibiotic that has
  no CLSI interpretations and a drug that would not be used clinically.
  The Trek Sensititre results from those inner colonies showed
  additional issues with multiple different antibiotics. Clinically, the
  patient would not have been treated with that antibiotic, so that this
  resistant set of subpopulations may not have been selected for. Thus
  the results from the study may not be clinically significant but it
  does open up questions to the possibility that the Trek Sensititre may
  not detect clinically significant resistant subpopulations.
Given that
  the Trek Sensititre can miss resistant subpopulations in Gram negative
  bacilli, it is important to establish the clinical relevance of this
  finding. If the inner colonies selected for by each of the antibiotic
  discs was sub-cultured individually instead of pooled together and
  then run on the Trek Sensititre, then the following results may
  possibly differ from the pooled inner colonies. An important future
  direction would be to determine whether the unreported resistance from
  the organisms in the study had an effect on patient care however, this
  was beyond the scope of this thesis study. Thus, the clinical
  significance of this study’s findings require future study.
  Nevertheless, laboratories should be aware of the potential for
  missing sub-populations of antimicrobial resistant organisms using
  broth-based microdilution methods.


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What does it mean when you "extract the filtrate with ethyl acetate three times?"
"The fermentation broth (600 mL) of each endophyte was filtered, and the filtrate was extracted three times with ethyl acetate at room temperature and further concentrated in vacuo to give dried residues prior to antimicrobial assays"

This procedure is referring to chemical extraction, which is a separation process used in chemistry (and biochemistry) to isolate compounds of interest by using two immiscible phases in which the compound of interest has differential solubility.
For example, in a liquid-liquid extraction, often one of the phases contains a polar solvent like water, and the other phase contains a nonpolar solvent like oil. Water and oil won't mix, but after stirring them together and waiting some time, the more polar molecules in solution will tend to concentrate in the water, and the less polar molecules will tend to concentrate in the oil. Because the phases are immiscible, it is relatively straightforward to separate them once equilibrium has been reached.
Ethyl acetate is a fairly non-polar molecule often used in organic extractions. In the process that you described, the result will be that non-polar contents of the fermentation broth will be extracted into the ethyl acetate, and hydrophilic contents will remain in the aqueous phase.
Because this process is never 100% efficient (the efficiency will depend on the concentrations of the solutes and relative affinity for the two phases), it is often repeated several times to improve the extraction.


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Why do we have more sweat glands in our palms?
Why is it that we have more sweat glands in areas such as the palms of our hands and the soles of our feet? I just learned that there are more there but I am curious as to why that is.

That increases sensitivity of receptors

You sweat much stronger in the palms of your hand and the soles of your feet, because they contain a much higher density of eccrine sweat glands. According to Sato et al., (see reference 1) there are something like 64 glands per cm² on your back, 108/cm² on your forearm and 600-700/cm² on the palms of your hands.
This is thought to have different reasons: First, sweating is an important way to control the body temperature.
Sweat works as a defense by anti-microbial peptide dermcidin, it is also seen as am important way to maintain the conditioning of the skin and as well as a lubricant for contact surfaces. (references 2-4)
Sweating is controlled by the sympathetic (autonomic) nervous system, and can be triggered by acetylcholine and adrenaline. This explains why you get wet palms when coming into stress.
References:

Biology of sweat glands and their disorders. I. Normal sweat gland
function
Systematic review focusing on the excretion and protection roles of
sweat in the skin.
Dermcidin: a novel human antibiotic peptide secreted by sweat
glands.
The human eccrine sweat gland: Structure, function and disorders

Good answer, +1! But I just wanna say that you added very little about the exact point the OP asks 'why?'. Please try to elaborate that point :)

@another'Homosapien' No problems, editing is fast, I have not much time not to look up more references. BTW: A number of references also state that sweating on the hands is important for thermal regulation, which is the most important role of the eccrine glands.

@Chris gave a nice answer, but I thought it would be better to include an answer to the 'why' part of the question. To start with, let me first say that the eccrine sweat glands on palms and soles respond to emotional stress, rather than increased body temperature 1. With that being said, the answer to the 'why' part becomes likely to get changed.
As one might know, its pretty difficult to answer the 'why did this happen during evolution?' question; there can be only theories with (usually) no conclusive proof. So, in this case too, the 'why' part remains without conclusive answer, and just theories prevail. According to the most prevailing theory, the emotional sweating causes sweaty palms that can help control the humidity of the outer layer of the skin. This could improve the friction on the skin thereby helping when you begin to sense you will be hunting an animal, fighting enemies, or about to climb a cliff (just to add, ever thought why your fingers get wrinkly after a long bath?). The generalized sweating that results from your hypothalamus then helps cool the body when these intense physical activities are happening. It also produces an odor that sends out pheromone signals to those same enemies/animals. The pheromones also could help signal potential mates that you are natural selection’s answer to their mating needs2. Again, this is just a theory and likely to have flaws, while the definitie answer is still not known. You can also have a look at the answers to this question for some more details.
References:

Sokolov, VE; Shabadash, SA; Zelikina, TI (1980). "Innervation of eccrine sweat glands". Biology Bulletin of the Academy of Sciences of the USSR. 7 (5): 331–46.
Wilke, K., Martin, A., Terstegen, L. and Biel, S. S. (2007), A short history of sweat gland biology. International Journal of Cosmetic Science, 29: 169–179. doi:10.1111/j.1467-2494.2007.00387.x


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Why do bad smells make us vomit?
According to my understanding, vomiting happens when the body wants to get rid of something that we have ingested or put in our mouths to get it out of the body.
So why is it that when something smells really bad our bodies make us vomit even if we have not ingested the food, or not even put it in our mouth yet? Is this something psychological?
Thanks!

The current hypothesis is anytime what your senses are telling you do not match your brain assumes you are hallucinating and thus want to get rid of as much of the toxic substance making you hallucinate as possible before it kills you.

It is not really making you vomit not directly, it is making you nauseous if you become too nauseous you vomit.(nausea has multiple triggers but for this I will stick to smell) Nausea exist to keep you from eating toxic food and to help you get rid of it if you do, the reflex is a balance between the biological cost of a meal(minimal) and the cost of being poisoned(extreme) so you can see why it might favor vomiting and losing a meal vs not vomiting and dying of poisoning than it would the two costs were not so drastically different.
Now your body can't really tell the difference between a smell coming from inside your mouth and one from outside, they both reach the nose by a roundabout course, and your mouth cannot smell. The closest your instincts can come is assuming a stronger scent is coming from the mouth since it is close and enclosed. That's why a stronger disgusting smell results in a stronger feeling of nausea. the stronger the smell the better the chance it is coming from inside your mouth.
Combine these two concepts and you can see how the stronger the smell and the more disgusting it is the more likely it is to make you nauseous it is the best protection our anatomy allows for. Now of course this is only the the current hypothesis, Nausea is not easy to study nor is it a in high demand for research.
Additional sources

wakes you up at night is not being triggered by smell but by something else, like an illness. nausea does have multiple triggers.

@GyroGearloose - Studies have actually shown that very few humans wake up to the smell of smoke, and certainly not milllions. During sleep, the brain mostly turns off processing of smells (unlike sounds, touch, and light, for example. Hence the dire importance of smoke alarms.

@GyroGearloose - I refer to scientific studies, not anecdote. Also, I mentioned the importance of smoke alarms for smoke, not the number of other things which you refer to. Maybe you believe smoke alarms are not so useful, but they, not our noses in sleep, save lives.


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Reusing frozen blood
Considering the short supplies of blood in hospitals, why can't we freeze on our blood from time to time and and have it stocked for reuse in an emergency?
That could make ourselves responsible for own our blood supply in case of an emergency.

where have you looked for answers to this question? can you add some of that detail? it would definitely add quality to your question.

Freezing cells is difficult, almost an art form. It depends largely on the types of cells being frozen, the program to be used in freezing and the program used to thaw. You can end up with a massive loss in viability if a technician doesn't follow a freeze or thaw protocol to a tee, and there are release criteria where products of low viability cannot and should not be infused.
Being said, cryopreservation of blood for transfusion exists, and has since the Vietnam war. We're getting better at the process, but barriers such as cost and training probably still pose a hindrance.
Another barrier is maintenance of stocks, especially if you're considering monitoring your own blood supply. A cryogenic freezer would need to be maintained and monitored for constant -160-170°C. Cells do not undergo multiple freeze-thaws and thus once thawed you have a short shelf life.


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Why do sharks continually regrow their teeth?
Other animals don't do this. What is unique about sharks that requires them to regrow their teeth over and over, or what benefit does it provide them (that wouldn't also be evolutionarily advantageous to other animals)?

They routinely lose them in struggles with prey. I suppose a backup is useful. See this question on why traits with an advantage don't evolve. That should explain why perhaps other species don't have this ability:

Actually, most animals with teeth are polyphyodonts - they regenerate teeth throughout their lifespan. This includes sharks, crocodiles, fish and some mammals (kangaroos, elephants and manatees). Diphyodonty (only replacing teeth once) is the exception. I have a vague memory from undergrad that the evolution of specialised teeth in mammal-like reptiles, and specialised jaw musculature (which happened at the same time) is/was believed to be the reason behind this - for a reason I can sadly no longer remember, tooth specialisation and tooth regeneration are incompatible. When I can find more details and a source for the latter I'll edit them in.


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

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

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

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

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

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

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

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


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Where to find morphometric data for fish?
I need data regarding the aspect ratio for caudal fins of different Elasmobranchii. It should be some easily retrievable information but apparently fishbase doesn't have this type of data for many species.
Do you know any other database maybe that is specific for morphometric measurements?

update: the answer below describes a database for freshwater ray-finned fish (Actineropygii), which does not cover the taxa you want (elasmobranchs are a subclass of the cartilaginous fishes, Chondrichthyes, which is a separate taxon). I'm going to leave the answer up anyway in hopes that it's useful/interesting to someone.
(Searching for elasmobranch morphometric database finds a description of the MEDLEM database (Mediterranean elasmobranchs, Mancusi et al 2020) which (1) doesn't seem to be publicly available and (2) probably has only overall length measurements, not the details you need ...)
Brosse et al. 2021 report on a global fish morphology database. I think you can almost but not quite get aspect ratios of caudal fins from this database. Specifically, they state that they have taken all of the measurements listed in figure 1a:

I'm not sure exactly how you define aspect ratio of the caudal fin, but I'm assuming that it would be something like (tail length/tail depth), or based on the measurements here, ((max body length - body length)/caudal fin depth) = (MBl - Bl)/CFd. However, the authors don't make the raw morphometric measurements available, only derived values that are listed in their figure 1b, which include MBl (in centimeters), "body elongation" = Bl/Bd, and "caudal peduncle throttling" (CFd/CPd).
If you had the raw morphometric values you would almost have what you needed (I'm a little surprised they're not included in the database along with the derived measures), but you'd have one more big problem. To get caudal fin length you would need max body length measured in pixels rather than cm (MBl is taken from Fishbase; the rest of the measurements are taken in pixels, since they're derived from analysis of images with unknown scales). If the authors measured max body length in pixels when they did their image analysis, you could derive what you need from that ...
One could contact the database maintainer / contact (their e-mail is in the README file from the database, which you can get from the link below) and ask for help.

Data availability statement

FISHMORPH is publicly available through figshare (https://doi.org/10.6084/m9.figshare.14891412). We kindly ask users to cite the
present paper in any published material produced using these data.
Users are free to use the FISHMORPH data and to contact the au-
thors for details or collaborations. We also encourage any potential
data contributor to contact S.B. with potential datasets to expand
the database

Brosse, Sébastien, Nicolas Charpin, Guohuan Su, Aurèle Toussaint, Guido A. Herrera-R, Pablo A. Tedesco, and Sébastien Villéger. “FISHMORPH: A Global Database on Morphological Traits of Freshwater Fishes.” Global Ecology and Biogeography 30, no. 12 (2021): 2330–36. https://doi.org/10.1111/geb.13395.
Mancusi, Cecilia, Romano Baino, Caterina Fortuna, Luis Gil De Sola, Gabriel Morey, Mohamed Nejmeddine Bradai, Argyrios Kallianotis, et al. “MEDLEM Database, a Data Collection on Large Elasmobranchs in the Mediterranean and Black Seas.” Mediterranean Marine Science, April 28, 2020. https://doi.org/10.12681/mms.21148.

Thanks for the answer, it's very detailed. Aspect ratio is the ratio between the maximum width of the fin to the power of 2 ($Cfd^2$ in this case) and the actual surface area of the fin. From data you described I don't think it's possible to obtain this metric. Thanks though, its definitely useful in other cases.


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Ecosystem Control Theory
I've used EcoNet online tool to analyze an ecosystem. You can run the default model by pressing "run model" in order to follow my question.
Among the extended results there are 2 'Control Matrix' but unfortunately they don't state the source for the calculations in their documentation. In the documentation, right below Utility Analysis, there's a blank paragraph intended for Control Analysis.
I'm looking for someone that knows some articles explaining the math behind those matrixes and also their interpretation.
I'd be really glad if you could help me.


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How are isopotential maps computed from EEG channel data
I have some EEG recordings of $1$ minutes, with $500$ samples per seconds and $63$ channels. For each recordings, this effectively yields a $30,000\times 63$ matrix $M$.
How do I extract isopotential maps from the data?
My first try was to simply take each row $m_i\in M_{i,j}$ such that $m$ has length $63$ and plot them with respect to the $x,y$ coordinates given by the location of each of the $63$ channels... However, I seem to get bad plots...
I also tried to bandpass the data first. For alpha waves, my Mathematica code looks like this:
BANDPASSALPHA[x_] :=
 BandpassFilter[x, {8 Pi, 13 Pi}, SampleRate -> 500]
bpalpha = Map[BANDPASSALPHA, dataz];

I bandpassed the columns of the matrix $M$. That is the signal $x$ that is used in BANDPASSALPHA[x] is one of the columns of $c_j\in M_{i,j}$ and are of length $30,000$
According to Wikiepdia: http://en.wikipedia.org/wiki/Isopotential_map, the spatial derivative needs to be computed first...
Does anyone know how isopotential maps from EEG recordings?


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Does IQOS/HEETS emits CO?
I am researching the safety of IQOS (THS2.2) for heat-not-burn cigarettes (HEETS).
I am particularly interested in appraising the impact of IQOS/HEETS on CO emission and inhalation.
Is there evidence of this?


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Which are the best apps and websites for insect identification?
My kids keep asking me to identify some insects they found, and I am often caught off guard, as I have very little matter knowledge.
I have found the Insect Orders app quite useful, but still quite challenging.
Is there anything else, in terms of apps or websites, which is better for insect identification?

I think many reliable websites and apps of high quality will have a relatively narrow scope both geographically and taxonomically. The exception might be some keys to the level of orders and maybe some families. I therefore think this question is rather broad and opinion-based. Where do you live and what level of taxonomic determination are you after (species, families, orders etc; what taxonomic groups)?

@fileunderwater, though I 100% agree that targeting resources that focus on specific geographic locations is best, there are a number of general sites (such as bugguide and even this site) which can lead to identification of insects from a broad range of locations. If the OP is looking for more general resources, then I think this question is valid (i.e., not too broad) and should be reopened. IMO.

However, given my last comment, @Joe_74, you could provide a more specific location, and we could try to provide some resources that are more specific to your location.

There are not many beginner-friendly apps that I am aware of. However, there are a few websites you can use.
BugGuide has a relatively nice picture-based search system. You will also gradually learn to easily identify various characteristics of an insect, thus making your search easier.
Insect identification is more beginner-friendly and more suitable to your kids.
You can also ask either here, or perhaps in the reddit community if you have trouble identifying a particular bug.
If they become interested I would recommend searching your local book store or library for a good field guide (depending on your location). Entomology can be a fun excuse to get out of your house and learn something in the process.


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Which are the last cells of the human body to die?
When somebody dies, which are the last surviving cells of his/her body? Those of hair, nails, or some other obscure but resilient cells?
Shedding light on why and how they are so vital might boost our knowledge of survival pathways.

Related question: http://biology.stackexchange.com/questions/7548/in-humans-what-is-the-last-metabolic-process-to-cease-after-death

When you say 'vital' do you mean - 'hard to kill'? The most 'vital' cells in the usual sense of the word - 'important for life' - are probably heart muscle, nerve cells etc, and these are exactly the ones that will die first because they use so much energy.

Neither hair nor nails are made from living cells. Also, which individual cells die last has nothing to do with how 'vital' they are.

@Slawomir Andrzej Dziemborowicz I understand that several factor may play a role in determining how much a cell lasts after being its body dead (eg blood flow, oxygen reserves), but anyway it is conceivable that those cells lasting longer could have more protective mechanisms to overcome lack of oxygen and accumulation of toxic molecules.

They found live skeletal muscle stem cells in human corpses 17 days after death (LiveScience, 2012).
They isolated live stem cells from the bone marrow from human fingers 5 days after death and transformed them into cartilage, bone and fat cells (NewScientist, 2013).
The survived cells were in a dormant state with very little metabolic activity.

From what I have read, it looks like white blood cells have been found to survive the longest (up to 70 hours after death). This being said, I have also seen people who say that red blood cells would survive the longest because they do not need oxygen to survive (they have no mitochondria and thus do not do aerobic respiration). Since you seem to be interested in survival pathways, blood cells are probably not terribly useful. It seems that many transplantable organs like the kidneys can survive for up to an hour (provided that they are chilled to avoid cell death).

Welcome to Biology.SE! Answers are more likely to receive a favorable response if they include supporting references. ——— You may wish to consult the help pages for advice on how to provide effective answers: biology.stackexchange.com/help/how-to-answer. Thanks!


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Can DNA barcoding be employed to determine the order of an unidentified haematophagous parasite?
Given: a specimen of an unidentified, highly adapted, haematophagous parasite, perhaps a species nova, contaminated with mammal blood and tissue.
DNA barcoding is readily used to identify cryptic species complexes and superspecies, in diet analysis and for food safety.
However, can DNA barcoding also be employed in a broader sense, up the taxonomic ladder, simply to identify the insect order of a parasitic specimen contaminated with mammal host material?

Yes--this is possible and has been done, e.g.:

DNA barcoding identifies Eimeria species and contributes to the phylogenetics
of coccidian parasites (Eimeriorina, Apicomplexa, Alveolata) (doi: 10.1016/j.ijpara.2011.03.007)
Developing an Apicomplexan DNA Barcoding System to Detect Blood Parasites of Small Coral Reef Fishes (doi: 10.1645/16-93)
DNA barcoding and molecular identification of field-collected Culicoides larvae in the Niayes area of Senegal (doi: 10.1186/s13071-018-3176-y)

There's also a review on the subject:

DNA barcoding of parasites and invertebrate disease vectors: what you don't know can hurt you (doi: 10.1016/j.pt.2003.09.015)


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Have there been any studies on 'surf balls'? (not related to surfing)
I know the title sounds like something else, but I'm actually wondering about these things, which are also apparently called 'whale burps':

This one was found on a beach on Lake Michigan.
Does anyone know if any scientific studies have been done on these? If so, can you refer me to them?

Are they supposed to come out of the lake? To me it looks like it is made up of land plant material, so possibly a birds nest?

Okay, I have to retract my suspicion. I found this, which states that there seems to be a publication, but I can't find the relevant publication mentioned. Maybe someone else has more luck?  http://blogs.oregonstate.edu/breakingwaves/2011/01/12/osg-beach-publication-solves-a-great-lakes-mystery/

The publication @skymningen mentions is "Flotsam, Jetsam, and Wrack", available here. The explanation for "whale burps" in the publication is the same as given in Bob Specter's answer.

These surf or beach balls are made of plant material throughout the structure. They form by wave action along beaches. As the naturalist at Wilderness State Park, the campers and I discovered over 30 of these balls along the beach the summer of 2017.  In previous summers we had found 0. Lake Michigan and Lake Huron were at record levels during the summer of 2017, the highest since 1998. This may explain the formation of these grass balls in abundance. We found some of the balls still in the water, in a depression, just offshore. Others were rolling in and out with the waves. Some had been deposited on the shore and were filled with large quantities of sand. I shook out nearly a cup of sand from one ball. I dissected one surf ball and found predominantly roots and grasses. I will continue to investigate the species of plants that form these curious creations and try to discover the secret to their formation


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Clarification in the name "white cheeked barbet"
Everyday I was listening sound of the birs "white cheeked barbet". Then I was wondering how this name came to it? It should be by certain properties of them. In wikipedia it says

Barbets are named for the bristles at the bases of their stout, sharp bills.

But this statement I couldn't believe from picture, since I couldn't see bristles. The words "white cheeked" can be understood from photo clearly.  I then thought this may be due to some change during the migration, or anything else.
Can one help how this bird gates named "white cheeked barbet"?

It seems as though it is named for feathers below the beak that have a barblike appearance, rather than actual barbs. It may be clearer from these images:

India Nature Watch
Or in this photo: SivamDesign - Flickr


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How many people in the world have bad eyesight?
I was watching this ted.ed episode and heard it was around 500,000 but that didn't sound right-- does anyone know?

Depends on how you define bad eye sight? Visual function is not either good or bad; it's a range.

I do know that the TED Ed episode linked (at 3:50) actually says that 500 million people have myopia or hyperopia, which is 1000 times what the question says, and which seems more reasonable for a world of 7.4 billion people (skewed towards the young).


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Designing degenerate primers using alignment of protein sequences from other species
I am trying to design a PCR primer for a gene whose sequence is not known. Even the whole transcriptome sequencing done in our lab did not identify that particular gene. Hence, I guess I am left with only one option: to design the degenerate primers for this gene by performing sequence alignment of the given protein from several related species and designing primers based on conserved region. Could you please explain the process of primer design by this method. I know some steps which I have described below stepwise:
step 1: download sequence of protein in question from related species from NCBI in FASTA format
step 2: perform alignment using clustal omega
step 3: identify the conserved domains
I am not sure how to move forward from here. I tried J-codehop for next steps but it is asking many parameters for which I have no clue.
Thanks

Try going through this tutorial: http://www.scs.illinois.edu/schulten/tutorials/ef-tu/eftu_tutorial.pdf
It is a nice introduction on how to use multiseq and identify conserved domains from AA or nt sequences across many taxa.
Also check out http://fungene.cme.msu.edu/
The RDP staff at Michigan State University are the masters of doing exactly what you're trying to do.


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How to convert a test tube assay to microplate assay?
I am trying to measure Ascorbic acid levels in tissue using Omaye et al protocol (Methods in Enzymology, Volume 62, 1979, Pages 3-11). This method is based on reduction of ferric chloride and subsequent detection by 2, 2'-dipyridyl. However, this assay is a test tube based assay. I want to convert this protocol into a plate based assay, however, I could not find any already published protocol for this. Is it possible to do it?


text:
Is there any example of genetic mechanism of delayed onset toxic effects?
We know that exposure to many toxic chemicals during embryonic development may show toxic effects later in life. It is called Developmental Origins of Health and Disease (DOHAD). Most of the mechanisms reported behind these kind of toxic effects are epigenetic. I could not find any genetic mechanism in the literature. Is there any example of genetic mechanisms behind DOHAD?

Are you asking for mutagens that are well known for its long term effects when exposed as a embryo?

I would tend to think that this question is off-topic here as it is a health question more than a biology question. MedicalSciences.SE would be a better fit. See for example their radioactivity tag

Mutagens might work but do you know of any specific mutagen, that can cause onset of toxicity only later in life even when the exposure happened during embryo phase?

Any mutagen would have health consequences later in life. I don't know of study on this question though and I can't really help you any further. You state Mutagens might work which makes me confused as to what other than exposure to mutagens would you be interested in.

@Remi.b this question is asking about a biological mechanism behind a medical condition. It is EXACTLY on topic here per the second of only three bullet points on What topics can I ask about on here.

I posted about this question on meta


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What happens to the human brain when unconscious?
What part of the brain gets affected and does it harm the brain? Thank you I just needed some extra info for a video I'm making.

unconsciousness is a broad term. Consciousness itself is a debated term too. Could you add some framework around it? Are you talking of physiological sleep, drug-induced reduced consciousness, unconsciousness caused by head trauma or otherwise?

Unconsciousness induced by head trauma and drug induced reduced consciousness

Those represent different mechanisms of loss of consciousness. Might be better asked separately. I think this is a bit broad as is. Have you googled this? What did you find?

I didn't find anything worthwhile,just something about weed and alcohol harming the brain

Check out the ascending reticular activation system

I did but it doesn't really answer my question, could you explain your point in reference to my question...Thanks!

We don't know. Disruption of cortex, thalamus, or brainstem structures (someone mentioned ascending reticular activation system) all can cause loss of consciousness. Different drugs have different mechanisms of action and some might cause different "types" of loss of consciousness - for example, ketamine and propofol seem very different, and trauma is a completely different issue.
The reason this is such a hard problem is that these structures are all interconnected, and there are likely proximate and distal causes of loss of consciousness. For an analogy, imagine you starve to death. You could make a convincing case that lack of food did it - so conclude food keeps you alive. But you weren't declared dead when you stopped eating; you were probably declared dead when your heart stopped. So conclude your heart keeps you alive. But in the middle somewhere, you had changes in ion concentrations in your blood, loss of glucose. So salts and sugars keep you alive. I can prove these are all true - take out your heart, you die. Stop feeding you, you die. Fill your arteries with KCl, you die.


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Calculation of Malthusian fertility and mortality from birth and death rates
In a simple Malthusian model, the population $p$ grows according to $p = p_0e^{rt}$, where $r = \beta - \mu$, $\beta$ is the "fertility" parameter and $\mu$ the "mortality" parameter. In the case of $\beta$, the closest thing to this parameter is the Total Fertility Rate. Is there a meaningful way to convert from one to the other? An easy formula might be something along the lines of
$$
\beta \approx \frac{1}{2T}\text{TFR},
$$
where $T$ is the reproductive lifetime, but this doesn't account for gender imbalances or a more nuanced way of treating the instantaneous nature of the parameter.

If every member of the population breeds, the mean number of children born from a single individual during their whole life is $\beta$ times the duration of their life. The mean life duration is $1/\mu$. Hence the total fertility rate in the homogenous model you suggest is $$\frac\beta\mu$$ If only some proportion $p$ of the population can breed, the total fertility rate of each breeding individual is $$\frac\beta{p\mu}$$


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iPSC in drug discovery
Pluripotent stem cells are very popular and lots of research has been conducted to use these cells as a tool for drug discovery. My question is how many years would it theoretically safe is we could use iPS cells during the process of drug discovery?

iPSCs are already a common model in industry, obviously depending on what exactly you're researching. I don't have any citations, because all of the work I'm aware of is proprietary (that comes with working in industry...), but lots of companies and labs are using them right now.

People are doing small molecule screens with stem cells right now (albeit embryonic stem cells). Probably a lot more screens of that kind are in progress behind closed doors in the pharmaceutical industry, and we can expect iPSC culturing to get better and cheaper, so sometime in the next decade we'll see them become a common model.
iPSCs will probably be an improvement on existing cell culture models, and will also allow things like the creation of cell lines for specific genetic diseases, but they wont' be a quantum leap forward for drug discovery in general.


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A 10mm long creature in the California dust

I observed this tiny creature burrowing through the dusty soil of Cachuma Lake Recreation Area in Santa Barbara County, California, on June 8, 2014, about 7 a.m. I have really no clue what it could be, other than an annelid, or newly hatched type of legless lizard or snake. But it seems too tiny for the latter. Yet, I would think an annelid would need more moisture, or different soil. Do worms live in dust? I watched it for about five minutes, maybe more. Burrowing under and re-emerging. So that seemed to be its normal environment.
Here's a closeup, and a link to a Youtube page I put up for it. Video on Youtube of animal's movement

The creatures movement (youtube) is NOT that of an annalid. They contract and expand rather than zigzagging like this creature does. Zigzagging is a snakelike movement. Unfortunately, I am by no means an expert an Californian fauna.

Thank you! I couldn't put my finger on it, but yes, that's it - it doesn't move like a worm, which is why I'm very curious what this is. Thanks for helping clarify that in my mind.

could it be an enchytraeidae?

@Jordi_Zambrino Aren't all enchytraeidae aquatic?

Just found here that the worlds smallest snake is still four inches. That makes a snake very unlikely. Hmm confused now.

http://www.agpix.com/view_caption.php?image_id=590425

@Jordi Sorry, still getting used to how this site works. Spent too long editing ...  What I meant to say was: Thanks for the reference to enchytraeidae. At least per the Wikipedia page, there are some terrestrial species, known as potworms.  And, I have to say, the creature in the image on this page looks pretty similar. But ... they tend to live in much wetter environments. This was dry and dusty, and it looked very much at home. You can also find videos of potworms in compost bins, and they move similarly to this.

Also, I did run this by a curator of reptiles, who also said it was not a snake (I thought it might be a juvenile Brahminy Blind Snake, an invasive species). He thought it might be a beetle larva but, while I'm not a professional entomologist, I've seen and handled a fair number of larvae, and this just doesn't scream "grub" to me.

Well, maybe I stand corrected: BugGuide.net has a similar picture of a Stiletto Fly larva found in Santa Barbara County. And The Clueless Gardener blog has some comments on behavior - says they're very strong, and move very fast.

I'm going to answer this question and close it. Based on the location, the environment, its appearance and behavior, I'm 90% sure that this creature was a Stiletto Fly (Therevid) larva. Most likely an Acrosathe sp., as those tend to be very common in the area. Thanks to all for your help in clarifying and narrowing it down for me.

You are probably right. Unless you can find an expert on Californian flies, it's unlikely you will ever be 100% sure.


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Since RNA viruses and retroviruses all have high mutation rates, why do only a few viruses have the virtue of variability?
We have been taught that it's difficult to make vaccines to influenza, HIV and HCV because they lack the proofreading mechanism, hence have high mutation rates. But most RNA viruses and retroviruses are still antigenically stable, such as measles, rabies, polio, yellow fever, HBV etc. So why do only a few viruses successfully become variable? Is it because their receptors allow flexibility, or their glycoproteins have sophisticated conformations that allow more mutations?

The high mutation rate is only a small part of the reason it's hard to make vaccines against those RNA viruses.  The real problem is not that they mutate rapidly, but that they can tolerate high levels of variation in their antigenic regions without losing fitness.  Viruses like polio and measles, as you say, have mutation rates easily on a par with influenza or HIV, but when they mutate antigenically significant regions, those new viruses are much less capable of infecting and transmitting between hosts.  Vaccines therefore either block the virus replication altogether, or force them into a much weaker form that is much less infectious.
Why do some viruses tolerate antigenic changes better than others? It's not known, but presumably there has been selection for it in those lineages.

I can't give an upvote because I am new to here. Your answer is right.

It seems that influenza and HIV have employed some sophisticated mechanisms of immune evasion(I don't know the case of HCV). For example, they use a pocket like structure to protect their vulnerable parts. But these are just guesses.

Every single modern virus has an array of sophisticated immune evasion mechanisms, being the descendant of a billion years' worth of ancestors that successfully evaded increasingly-sophisticated immune systems.  Influenza and HCV are not particularly noteworthy in this respect.

I see, thanks. BTW, can you give me some "noteworthy" examples of the viruses sophisticated at immune evasion? I shall read about them.

The most sophisticated at immune evasion are probably the herpesviruses and poxviruses, large DNA viruses that encode multiple genes specifically targeting the immune system. Here and here are starting points


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Can we develop a nucleos(t)ide analogue to cure rabies?
Nucleos(t)ide analogues have been successfully used to treat HIV, HBV and HCV. Since rabies virus is also a RNA virus that uses RdRp to replicate. If we develop an nucleos(t)ide against its RdRp, will it be able to save rabies victims? What would be potential obstacles?

Are you referring to RNA interference? Can you link some sources about the one used for HIV, HBV etc. ?

No. I mean this https://en.m.wikipedia.org/wiki/Nucleoside_analogue

Examples include Tenofovir to HIV, Entecavir to HBV and Sofosbuvir to HCV. Nucleos(t)ide analogues can serve as substrates of viral polymerase and incorporate into the newly synthesized nucleic acid chain. But it can prevent further incorporation, thereby terminate viral nucleic acid replication.

In theory that would be possible, as you mentioned the rabies virus does have its particular polymerase, and adequate inhibiting substrates could possibly be found.
On the other hand, the current immunoglobulin and vaccination post-exposure scheme is quite effective, and the incidence of rabies in developped countries is pretty low; so it's unlikely an inhibitor could profitably be developped to the market.  That means rabies-directed nucleoside analogues are not priority target for pharma companies, IMO the biggest obtacle.

Here are some of the technical hurdles a drug candidate would have to overcome, as a nucleoside analogue :

Affinity to the viral polymerase : too low an affinity makes competition with the native substrate difficult
Rate of conversion to triphosphate form : a low affinity of the host nucleoside kinase to the analogue can cause a inadequate concentration of active triphosphated inhibitor. Some virus (HSV) have their own kinase that may be less selective, though that doesn't seem to be the case for the rabies virus.
Selectivity for the viral polymerase (versus the host replication/transcription machinery) : a cause of cytotoxicity and, generally, adverse effects.
Pharmacokinetic problems : the analogue has to be able to be taken in through nucleoside transporters (facilitated transport into the cell), or go through other means of active transport, as that kind of compound is usually quite hydrophilic. One could also use the usual prodrug tricks to pass the membrane (see CP-4055 or sapacitabine). This may be particularly problematic for acute-stage rabies, as there would be the blood-brain barrier to pass.

Some additional perspectives on the development of nucleoside analogues
Advances in the development of nucleoside and nucleotide analogues for cancer and viral diseases -- (http://www.nature.com/nrd/journal/v12/n6/full/nrd4010.html)
Discovery and development of clofarabine: a nucleoside analogue for treating cancer -- (http://www.nature.com/nrd/journal/v5/n10/full/nrd2055.html)


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Is it possible a cancer cell don't express any foreign antigens?
For example, there're tumor suppressor genes. Can we just delete them, without introducing neo-antigens? Would the resultant cells proliferate? If so, how do our immune system identify such cells?

This question is far too broad, as explaining the mechanism of immune surveillance and how it applies to cancer is much too large of a subject to explain here.

Many tumor suppressor genes have that function because they prevent mutations, repair DNA or kill the cell if it is "too far gone." If you knockout these genes, you will inevitably get mutations. As the cancer grows, there is a selective pressure which will favor cells that have beneficial mutations, likely in coding regions. These mutations will lead to the production of neo-antigens, which can be recognized by the immune system.
So, basically, I don't think it's likely that there would be a cancer without any neo-antigens whatsoever. That doesn't mean, however, that the immune system will adequately respond to the neo-antigens.


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Do all +ssRNA viruses have similar structures and life cycles?
Take HCV for example. HCV doesn't package any enzymes in it's virions. When it infects a cell, it first translates its RNA genome. It's RdRp is synthesized with other non-structural proteins. Then its RdRp began replicating the RNA genome. Newly synthesized RNA are served as either translation templates or genomes of new virions. Finally new virions are assembled and released.
So do all +ssRNA viruses have the same pattern? There's no enzyme in the virions, and all the enzymes are synthesized after entry into the cells. They have the same life cycles: entry→translation(non-structural)→replication→translation(structural)→assembly→release.


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Which contributes more to cancer clearance, T cells or NK cells?
Both T cells and NK cells have cytotoxicity. However, most immunotherapy targets T cells rather than NK cells, such as CAR T and PD-1 inhibitor. Is it because T cells kills more cancer cells than NK cells?

Note that clinicaltrials.gov lists 628 trials under "NK cancer", so even though there are more T cell trials, it's not as if NK cells are ignored; and there are more ways to manipulate T cells than NK cells, which probably explains the greater number of trials.

T and NK cells have different functions, and respond to different signals for activation - for example, NKs lack CD3 and the entire TCR complex. They are both vital for anti-tumor immunity. T cells are unable to become activated by cells lacking MHC-1/peptide complexes, which can happen in some tumors, so in that case NKs are indispensable. The Wikipedia article on NK cells is pretty good, I'd suggest reading it if you haven't already.


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How does sGP of Ebola virus help it to evade host humoral immunity?
During Ebola infection, the viruses secret a lot of sGP. What's its function? Since anti GP antibodies are effective at inhibiting Ebola infection, wouldn't sGP stimulate host immune system to produce more anti GP antibodies? Why does Ebola virus expose its weakness deliberately?


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Why is the origin (patient zero) required to cure a virus?
I'm not sure if it's just a movies thing but I always notice that the original strain of a virus is required to cure a virus, why is this? is this even true?

Nope. This is a total movie fallacy/exaggeration.
How worthwhile it would be to isolate the original strain is debatable, but certainly not necessary for vaccinology purposes.
On one hand, the inital strain might be interesting to study if its an aetiological agent which has never caused human disease before. It would be the first 'snapshot' of the genomics/transcriptomics of an organism/agent which has been able to jump a species barrier perhaps, or has evolved to survive at our body temperature, evade our immunity and so on.
However, as the infection progresses through a population, in order for it to stay infectious, it must by definition have maintained the molecular patterns that permitted it in the first place, so isolation of the 'zero-th', 10th or even 10,000th infection shouldn't make any real difference from a therapeutic standpoint. It may even be the case that as subsequent infection has in effect, passaged, the organism, that the later strains may even be more dangerous than the initial one.

Oddly enough, we were discussing this at a tea break the other day (I work in a research institute that does a lot of vaccine development).
Firstly (as the other answer notes) this is a complete fallacy, but useful for dramatic purposes. It's basically a "MacGuffin" or "plot coupon".
Secondly, disease-causing agents evolve as they spread. This actually occurs pretty quickly, both because pathogens generally have short lifespans and because our immune systems are adaptive, and "learn" how to fight pathogens they encounter, so they need to adapt to evade that response (continually). This results in what is often called a coevolutionary "arms race" and is why for instance you need to get a flu shot every year.
Mutations may also affect other traits, such as how a pathogen spreads - a well-known example is the appearance of the E1-A226V mutation in chikungunya virus which allowed it to be spread by a different mosquito species.
Lastly, there can be changes that do not affect the ability of a pathogen to spread or to fight the host immune system; for example every time a population passes through a "bottleneck" (for instance if the agent is introduced to a new continent by a single infected air traveller) the new region is populated exclusively by descendants of that small population, and will reflect its genetic makeup.
Now, going right back up to the top you might have already spotted the problem here. Vaccines expose your immune system to a less dangerous (chemically inactivated, thermally inactivated, or otherwise attenuated) form of a pathogen or parts of the pathogen (such as its outer coat) to allow your immune system to recognise it while not actively being under attack. If the vaccine is made from an old strain of the pathogen - let's say, last year's flu - your immune system might learn how to fight last year's flu but won't be equipped to fight this year's.
As the other answer notes there could be research value in having a sample of the original strain (for instance, it might be easier to prove where it came from), but it's much less useful for vaccine development than the latest version.
(We also discussed the frequent fallacies that vaccines are effective within seconds, or work if you already have a disease, but those are separate questions...)


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How allele is related to trait that is more complex than two cases (ex. height)?
Recently I started to learn about evolution and genetics. Simple stuff at the beginning - some videos, some reading. So far, everything seems to be pretty simple and straightforward. I easily grasp the concept of gene, allele and trait as the basic level. What bothers me is, that all of examples shows allele that has two options, sometimes three - peas yellow or green, blood type IA, IB and i - so on and so on.
But traits usually aren't digital in nature, they are analog. They are gradients. You have no people that are 160cm tall or 180cm tall only - you can have one that is 160 tall and another who's 160.1 and another who's 159.95. Height seems to me as a real number which may provide unlimited results.
Is the Mendelian reasoning about alleles and traits still valid in case of height trait? How does it work in such case?

Welcome to Biology.SE! You are correct in saying that 'traits are not digital in nature' i.e. they present a range instead of yes/no, so the actual biochemical mechanism for their expression is much more complex. I recommend that you keep studying more about genetics because at this stage you might not understand the whole concept properly. Someone here can also recommend some good books for you :)

Thank you. I appreciate any help, good sources included.

You are absolutely correct that many traits are not "digital", but "analog". In genetics, these are usually called quantitative traits. Such traits generally do not follow Mendel's laws of inheritance, but are said to have "complex inheritance". Most traits (phenotypes) in biology at the level of whole organisms probably have complex genetics; height is a classic example.
It is thought that complex traits arise by the combined actions of many genes (via their encoded proteins), while Mendelian inheritance occurs when phenotypes happen to correspond to the activity of a single gene. For very complex traits like height, many functions of the body might be involved, so the number of genes that may have some effect on the trait can be very large, but the effect of any single gene on the trait is likely small. In general, it is not understood exactly how genes contribute to the trait in such complex traits, so a phenomenological/statistical approach is used where the trait is modeled as some simple function of the genotype which is fit to data.  Wikipedia's page on quantitative genetics has more information on this.
In addition, traits may of course be affected by environmental factors as well as genetics. Height for example is strongly affected by having access to good nutrition. See this article for some discussion.
For traits with complex genetics, the underlying genes are generally difficult to identify, and for along time we have known almost nothing about the genetics of traits like height, obesity and diabetes. Since the early 2000's, massive efforts have been put into mapping the genetics of such complex traits by brute force --- measuring the effect of all genes on the trait in a very large number of individuals, in so-called genome-wide association studies. These have revealed a large number of genes over the past decade, but as expected each has only a small effect on the trait.


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Species I.D. hardwood tree
There are two of these trees, growing in old fence rows, along my yard, in central VA, Augusta County, Shenandoah Valley.  They have smooth, leathery leaves, pale wood, quite hard to cut, and tough to break.  The close ups are of some limbs I trimmed, yesterday. The biggest is about 10 inches in diameter, and perhaps 40 feet tall.  Branches tend to grow strangely hooked elbows that send branches off into strange directions, which makes trimmed limbs tangle and hook together.  This is what the foliage looks like in mid September.

Have you tried to split it? If you have, and it mangles instead of splits, it's a kind of a gum tree. Gums are very hard wood, impossible to split, and the branches hang down and seem gnarly. It's the only type of tree I know of that looks like that with those smooth, shiny leaves. (I had black gums in my woods.) Not 100% so no an answer.

It is a Bay Laurel Laurus nobilis
If the leaves are brittle and crack when folded and they smell fragrant then almost certainly.
I would ask this first, but unable to comment until 50 reputation

bay laurel is a bushy tree which doesnt have a pronounced trunk below the leaves. i didnt see a bay laurel taller than 4-5 meters.

I think these leaves are flexible and leathery, rather than brittle, though quite smooth and glossy on the upper surface.


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Which variables are controlled in the mammalian womb to ensure a healthy environment?
Recently, researchers have had some success with artificial wombs. Which aspects of the womb are difficult to replicate through technology?

It seems you are referring to this recent advance:
http://www.sciencemag.org/news/2017/04/fluid-filled-biobag-allows-premature-lambs-develop-outside-womb
https://www.nature.com/articles/ncomms15112
Involving putting premature lambs (delivered via caesarean) in bags of nutritive fluid and connecting the umbilical cord to an apparatus to oxygenate the blood.
Your question asks which variables are controlled in a mammalian womb, which I think is a misleading way to look at what a womb does and thus what the difficulties are with reproducing it. Namely, it makes it sound like the womb is a container whose purpose is to keep environmental variables (temperature, pressure, etc) at a good value for the development of a fetus. The problem is the womb doesn't just contain the fetus, it feeds it via the placenta. And the placenta is a structure built by fetus during embryogenesis, that connects to the lining of the uterus and enmeshes itself with it so that there is a huge surface of contact between the blood vessels of the mother and the blood vessels of the placenta, so oxygen and nutrients can pass through the mother's blood vessels to the placenta's and from there to the fetus via the umbilical cord. This allows the fetus to get all the nutrients and oxygen it needs to develop.
The "Biobag" these researchers created for these lambs is designed for fetuses who are advanced enough in their development that the main problem they have with surviving outside the womb is that their lungs are immature; the main purpose of this contraption is to allow oxygenation via their umbilical cord while keeping their lungs filled with fluid. And it also seems like they're being fed via that fluid, which suggests they're mature enough to get nutrition via their digestive system.
The paper gives quite a few details of the challenges involved in even that comparatively low level of uterine service. Infection, setting up the cannulas and oxygenating system so that the blood flow is just right and doesn't overtax the fetal heart, making sure there is no clotting, haemorrhage or brain damage...
I imagine the main challenge of making an actual artificial womb that's usable from implantation on would be emulating implantation itself, with artificial endometrial lining that a placenta could naturally develop in and intermingle its blood vessels with and somehow accurately reproducing the flow of blood that's necessary to feed the placenta. If we assume an artificial womb for a fetus that already has an umbilical cord, so we basically need to emulate the placenta's job not the uterus', but can be used earlier than Partrige et al's Biobag, then I imagine all the concerns they had about cannula size and getting the blood flow just right would be a million times harder with tinier, less-mature umbilical cords and fetuses. Not to mention if they need to put nutrients in the blood and not just oxygen.


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Trying to determine Heart Condition? ECG show no P Wave
A young woman was at the gym doing great her normal workout. She would spend 45 minutes on the elliptical and then 15 minutes doing weight training. This was the regular routine for her as she did this almost everyday. One day her normal routine turned upside-down. As she finished her elliptical workout and was making her way to the weight machines, she experienced a rapid heart beat. This washould nothing alarming at first because she had experienced this rapid heart beat before. When it happened previously the rapid heartbeat lasted only 10 or 20 seconds. However, this time was different. She experienced the rapid heart beat, but this time the heart beat did not slow down after 20 seconds. The rapid heart beat continued and she began to feel shortness of bread, some pressure I her chest, as well as feeling light-headed. Scared for what might be happening in general she went home called her husband. Frantically she tried to explain how she was feeling and how scared she was. They went to the E.R during her sTay in the ER her heart rate was constantly monitored. For five hours her heart rate remained between 130 and 150 bpm. After 5 hours her heart rate spontaneously returned to a normal rhythm. She was kept overnight In the ER and attending cardiologist prescribed low-dose beta-blockers She was given a number of different test and the results were: -blood pressure normal - hematocrit normal -cholesterol normal She is 34 mother of two. She is of adequate weight and BMI for her age and height. She has regular wellness checkups every year and has never had high cholesterol or hypertension.

Personal medical questions and health advice are off-topic on Biology. We cannot safely answer questions for your specific situation and you should always consult a doctor for medical advice.

This is something that you need to see your doctor for.  Until then, do whatever the ER doctors told you to do.  When you go, take all records from your ER visit with you.  The ER doctors' diagnosis should be on the discharge paperwork they gave you.


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What is the statistical relationship between radioactivity and mutation rate?
This question tries to narrow down the scope of that question.
What is the statistical relationship between radioactivity and mutation rate? By how much would the mutation rate be lowered in a idealized world were radioactivity is absent?

According to this wiki page , the average background radiation is 3.01 milli-Sievert per year (including natural and artificial sources). This equals 0.301 rad.
I found a short letter to nature that says the average forward mutation rate in human is 2.6 * 10^-7 per locus per rad = 2.6 mutations per ten million bases. Also it say that this mutation rate is quite uniform among species. The size of the human genome is approximately 3.2 gigabases.
So doing a quick maths: (2.6*3.2*100)*0.301 = 250.432 mutations per year per human. This is an approximation because I rounded the size of the human genome to 3.2 gigabases. Also this doesn't mean that we actually acquire this amount of mutations because we have repair mechanisms.

Interesting stuff + 1 Do you really mean "250 mutation per year per human" or do you mean "250 mutation per reproduction event"? This estimate is huge! A nucleotide typically has a mutation rate of about [$10−7;10−9$]. So random variation of 1 rad (that doesn't seem that huge given the wiki page that you linked) may easily yield to a 10 or even 100 fold higher mutation rate.

You said "this doesn't mean that we actually acquire this amount of mutations because we have repair mechanisms". So they did not take into account repair mechanisms in their study? The letter is 41 years old. I would intuitively think that today's estimate would be lower.

@Remi.b - If you calculate with the mean mutation rate of the interval that you have given (10^-8), that would still give  approx 32 mutation events for the entire genome. If we take the upper limit that is 10^-7, we get approximately 320. Maybe using the term mutation event would be better in my answer but I think based on the letter and wiki info that my calculations are correct. But as you say the letter is quite old, I'll check if there's anything new. BTW this would still result in approx (250/(3.2*10^9))*100 = 0.000007826% of the whole genome.


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How to interpret McDonald-Kreitman test results?
It is easy to get the numbers right and calculate neutrality index. It is easy to memorize "equals", "greater", "lesser", etc. At least on the exams, when certain level of simplicity is assumed. But instead of memorizing I'd prefer to understand. So far I struggle to get past the numbers. Could anyone, please, explain reasoning behind the them? Why certain values means the trait is advantageous or not? An easy to understand example would be helpful as well. Thank you.

This video by Mohammed Noor will be of interest to you!

@Remi.b I'm coming from his lecture exactly. In general the lecture is great and I can understand everything, but not the M-K test part. I even passed the exam - that's why I said above it's easy to pass, not so easy to understand.

A helpful way to phrase it for me is that "If there's a disproportionate fraction of non-synonymous mutations between species relative to what exists within species, it is because non-synonymous mutations are being selected for in the one species but not in the other, thus there's positive selection."
By the way I'm not an expert in this so take the explanation with a grain of salt.

Welcome to the site!  It would be great if you could dig up some sources to back up this answer.  Thanks!

(intraspecies non-synonymous polymorphisms)/(intraspecies synonymous polymorphisms) should equal the (mutation rate of non-synonymous mutations × number of non-synonymous sites)/(mutation rate of synonymous mutations × number of synonymous sites). Note that the mutation rate of synonymous mutations is just µ. Let F be the proportion of the synonymous mutations that are not deleterious so that the mutation rate of non-synonymous sites is Fµ. Let k be the ratio of synonymous sites over non-synonymous sites. Then the above fraction is equal to F/k. The same logic can be applied to find that the fraction of (interspecies non-syn polymorphisms)/(interspecies syn polymorphisms)=F/k, assuming the probability of fixation is roughly the same for synonymous and non-synonymous sites (neutral theory's assumption).

Welcome. Could you add your sources to allow other users to background read on your answer?


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How do molecules signal pre synaptic neurons to activate?
How do molecules signal pre synaptic neurons to activate? and also is it more the structure or the elements in the molecule that allows it to activate the neuron also how do molecules bind to receptors and same as last time what is more important to do so the elements in the molecule or the actual structure? please answer I cannot find the answer anywhere else expert answers are appreciated!
-Gus

Read about neurotransmitters. This question is too broad and would be put on hold unless it is narrowed down.

Activating a neuron generally means depolarizing the neuron, sometimes depolarizing enough to trigger an action potential. In general, molecules activate neurons by binding to their cognate receptors in the neuron cell membrane. Sometimes the receptor is, itself, an ion channel. Other times the receptor initiates a cascade of events in the neuron's cytosol that end up modifying the cytoplasmic portion of an ion channel and thus opening the channel. In both cases, the channel is usually specific for positively charged ions (cations) (e.g. Na+ or Ca2+) whose concentration is greater outside the neuron than in the neuron's cytosol. Activation results when these cation channels open and allow positively charged ions to flow into the neuron. This entry of positive charge reduces the neuron's cell membrane potential, making the potential less negative. If enough positive charge enters, the neuron may be depolarized enough to trigger an action potential on the neuron's axon. This is what is usually meant by activating a neuron. It depends on the three-dimensional structure of the molecule (often a neurotransmitter) and the structure of the receptor. The binding of a signaling molecule to its receptor is usually non-covalent, often mediated by hydrogen bonds.

You've given a nice answer, but references would be much more appreciated. Please add some citations in your answer to make it more helpful.


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Is there a closed path through the circulatory system that never passes through the liver?
I know the liver is responsible for doing lots of stuff to the blood, including both adding glucose and removing "weird stuff" (stuff destroyed by hepatocytes).  And I know that statistically every volume element of blood will eventually pass through the liver.
However, if you were magically minaturized a la Fantastic Voyage, and traveled with the blood flow, making ideal turning decisions at every arterial branching but never going upstream or out of the blood vessels themselves, could you completely avoid the liver?

The liver gets blood from two sources: the hepatic artery and the portal system of venous drainage from the gastrointestinal tract.
As long as you don't follow one of these paths, you'd avoid the liver. Some examples would be circulating through any of the limbs or head, but any path that avoids those two paths will do. As you point out this is statistically unlikely without your magical navigation abilities.


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What animals have a blood-brain barrier?
I am curious about how old the BBB is, in terms of evolution. Is it present in all vertebrates? or just mammals? or what?

It appears it is all vertebrates.
"All vertebrates started out with a glial blood-brain barrier 4–500 million years ago"

All extant vertebrates have a blood-brain barrier (BBB), a specialized layer of cells that controls molecular traffic between blood and brain, and contributes to the regulation (homeostasis) of the brain microenvironment. ... The barrier is formed by vascular endothelial cells in most groups, but by perivascular glial cells (astrocytes) in elasmobranch fish (sharks, skates, and rays). It has been unclear which is the ancestral form, ... we conclude that the ancestral vertebrate had a glial BBB. This means that an endothelial barrier would have arisen independently several times during evolution, and implies that an endothelial barrier gave strong selective advantage.

So, all vertebrates have one; in some fish, it is composed of glial cells rather than endothelial cells.
However, insects do have something similar:
"Evolutionary conservation of vertebrate blood-brain barrier chemoprotective mechanisms in Drosophila"

Insects also possess protective neural barriers, but they differ anatomically from vertebrates (Figure 1). Drosophila melanogaster (Dm) has an open circulatory system that is separated from the CNS by a thin layer of glially-derived epithelial cells (Treherne JE, 1972; Carlson et al., 2000; Stork et al., 2008), making the Dm humoral/CNS interface topologically much simpler than the vertebrate BBB. However on a cellular level, the vertebrate and insect BBBs share many common features.