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Which viruses still present today caused a deadly pandemic/epidemic in the past?
The current Covid-19 pandemic and its virus Sars-Cov-2 can be dangerous, especially for vulnerable groups like the elders. But however, I have seen studies that this virus become less dangerous in the future, when human population has built some immunity against it.
There are many other viruses still present and most of them produce only harmless diseases like the cold. But were some of such viruses really dangerous in the past and cause only mild symptoms on infected persons in present day (due to immunity)? Perhaps thousands of years they caused a bad epidemic?

The variant which caused the Spanish flu is still circulating today.

There are a few viruses which are around for a long time and have caused recurring episodes of disease. Most of these where not pandemic, which is probably more of a problem for modern times due to fast travel/exchange of people and are also a problem of "modern" cities where many people come together in a limited space.
Among theses viruses are:

Measles: This virus is around since at least 400 BC, profiting from the first big cities. (see reference 1 and 2 for more details)

Polio: This virus has been described already in ancient Egypt, although major outbreaks didn't happen before the early 20th century. There is a nice article in Wikipedia about it, see reference 3.

Smallpox: These are only not threat anymore because mankind successfully eradicated them. They have been described first around 1500BC in India, later also in China and Egypt. See reference 4 and 5.

Not viruses but also pathogens which caused historic epidemics: Typhoid fever, Cholera and the Yersinia Pestis (also known as The Plague or the Black Death).
References:

The history of measles: from a 1912 genome to an antique origin
Measles may have emerged when large cities rose, 1500 years earlier
than thought
History of Polio
Emergence and reemergence of smallpox: the need for development of a
new generation smallpox vaccine
History of Smallpox

Lovely answer, but what is the "Pest"? Did you possibly mean Yersinia pestis (the Black Death aka. the Plague and apparently also as the Pestilence)?

@tyersome Yes, you are right. I edited my answer.

Great answer. I'd add that we can't definitively identify many historical illnesses, even those in well recorded history because medicine, diagnostics and even language has changed, so things that were recorded as an illness a few hundred years ago might have been ascribed to "humors", but we now know as a virus. There's also different diseases being lumped together into one name or vice versa. Also, there are lots of unknowns - what caused "dancing mania"? Could it have been an illness?

The 1890 "Russian Flu" pandemic is now believed to have been caused by one of the common cold Coronaviruses, HCoV-OC43. At the time of historical pandemics, there was no way to identify the infectious agent, though. So connecting the pandemic to the virus is based on descriptions of symptoms, and patterns of which demographic groups were most affected; as well as genetic analysis to estimate when the virus jumped from animals to humans.

Accounting for expected mutation rates and working backwards, they calculated that the jump into humans occurred around 1890.

That date isn't the only thing linking OC43 with Russian flu. Many patients of that pandemic had pronounced symptoms affecting their central nervous system. Today, although mostly associated with mild colds, OC43 is also known to infect nervous tissue.

It's likely that all of the common cold Coronaviruses caused pandemics when they first started infecting humans. For the others, that happened much longer ago than OC43, so the historical record is less detailed, and there is more uncertainty in the genetic analysis.
In fact, it's possible that many or even all of the viruses that currently circulate among humans without problems were much less benign when they first emerged.
Another example is the outbreak of severe symptoms from Zika infections in the Americas when the virus arrived there, after circulating in humans for (at least) decades in Africa with only mild symptoms:

In the outbreaks reported up to 2013, most of the infected patients were asymptomatic and only 20% of them had mild symptoms such as fever, arthralgia, maculopapular rash, and conjunctivitis.

So it's suspected that many "harmless" viruses were worse when they first emerged into humans, but with the tools that are currently available, there is no way to establish definitively whether any particular virus caused major pathogenic outbreaks in the past.


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How does natural selection explain sexual display?
As I understand it, animals sometimes grow more vibrant colors, bigger feathers, elaborate dances, build shiny nests, all to impress the other sex. However, these are all superfluous to survival -- any nutrition or energy spent developing these attributes or conducting these rituals are no longer usable for hunting or child rearing, for example. Given the same animal who does one of these wasteful practices versus the same animal who doesn't, in theory the latter should have the advantage in its chances of passing its genes down.
Why is it then, that sexual preference grows towards these wasteful growths and habits, rather than ignoring these sexual displays for sheer survival efficiency?

Does this answer your question? Why does sexual selection evolve beautiful features?

@kmm No, because the answer doesn't explain why those sexual traits are interpreted as beneficial

Short answer
Survival does not get your genes into the gene pool, reproduction does.
thus reproduction based selective pressures can be stronger than survival based ones. there are plenty of organisms that die during or right after mating because of this.
Consider an example In species A finding a mate is fairly rare, it may only happen a few times in an organisms life. if individual X is guaranteed to mate and reproduce when they find a mate but will die after mating, and individual Y will not die after mating but only has a low chance to mate then the genes from X will spread much faster than the genes for Y, because mating is already a rare event, but X genes spread every time while Y genes will also only spread once or often not at all, and will also take much longer.
Or to put it another way, a chicken is just an eggs way of making another egg, the survival of the chicken is only useful as much as it facilitates reproduction.
Any mutation  that happens to make you better at attracting a mate will spread, how it does so is basically irrelevant as long as it works, loud noises, bright colors, eye spots anything that draws the females attention works. studies on several bird species have shown even the colored bands used to identify birds for study effect their mating chance is they are right colors. Animals often already have a variety of biases for their attention hijacking them is an easy way to improve your chances of mating.  Of course once a way evolves that reliably improves mating chances preference for that becomes favorable as well which can lead to a run away selection feedback loops AKA Fisherian runaway
https://link.springer.com/article/10.1007/BF00172135

I don't understand, how does this explain the development of sexual display traits and the attraction to them?

@personjerry What part don't you understand.

You've explained why a male would develop such features if the female finds it attractive, but why would the female evolve to find these features attractive in the first place?

@personjerry they don't have to anything that grabs the females attention works, there are plenty of existing attention managing processes tp exploit survival has already shaped brains to notice things that stand out with bright colors, to notice eyes, and react to loud noises. to use a human example we evolved to notice red colored fruit and plenty of males and advertisers exploit this with red coloration. there was a study on crows that showed putting any brightly colored tag on a bird made it more likely to mate.

So it's not so much that we evolved a taste for sexual display specifically, rather sexual display traits hijacked existing systems to become relevant? Do you have any citation for that? And if you edit this part into your answer Ill accept it

The point is that it's not only wasteful, but counter-productive to survival.
If you're a red bug in the lush green of the amazon you are painting a target on yourself. This has the effect of increasing your selective pressure. If you survive with a target on your back, and wasting energy on pigments, then you must be very good all of the other things necessary for survival.
So, with natural selection, the higher selective pressure on an organism with a target on its back will be a more selective filter, only allowing the most performant little red bugs to survive and mate with each other, "quickly" giving them an edge over their less colorful brethren, and resulting in a biodiversity that flaunts its ability to survive today with extravagant colors and nests.
The mating dances might be a different story, I'll let someone else tackle that.

Don't many of these displays also function as health indicators, as unhealthy individuals are likely to have less vibrant colors/feathers?

How could natural selection come up with the logic to figure out that surviving with a target on your back suggests a more fit individual?

Natural selection doesn't come up with anything. You have 100 bugs, 10 of them are bright red and die at a faster rate than the other 90. So of these 10 bugs at a disadvantage, 9 die before reproducing. The last one, with the highest fitness, is the only one to reproduce, so its offspring inherit its fitness. For the other 90 non-bright red bugs, that process is less selective, because they have an easier time surviving with their natural camouflage. So fitness enhancing changes take longer to set in the population.

source: Stack Exchange

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What are these bugs wiggling white fluffy hats?
Seen yesterday (October 10) in Southern Ontario (near Muskoka), near a lake. Maybe 0.5cm in size or so, during the afternoon.
Hundreds of these little bugs seem to be holding or attached to a curly white piece of fluff each and swinging them back and forth wildly.
What are these? And what are they doing?
Video: https://i.imgur.com/t7kWyKr.mp4
Image (image sucks, please see video):

My research suggests the Woolly Aphid or the Beech Blight Aphid

I am not very particular but I think they are Beech blight aphid(Grylloprociphilus imbricator)
Beech blight aphid is a small insect in the order Hemiptera.The aphids form dense colonies on small branches and underside of leaves.
You can get more info https://en.wikipedia.org/wiki/Beech_blight_aphid

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Can mushrooms spontaneously die?
These are called mushrooms I believe, had been growing on my door for a few weeks. It's monsoon here. Last night I took a picture of it and it looked like this . Today when I woke up it became like this: . All this within 12 hours. I'm pretty sure nobody touched the fungus so I'm inclined to believe this was spontaneous.

nice door! if you want to prevent mould on a door, the least you can do is infuse it with bleach. I imagine the TV has moss on it and the bath has ducks in it.

Of the thousands of shaggy manes I have seen ( and eaten most) , I never saw one growing directly on wood , nearly always they grow in grass .

Those shaggy manes are very fast rotting mushrooms

There are several fungi that autodigest  their lamellae  to release spores. Yours seems to be one of them. Due to the black liquid they release during autodigestion, they have the common name inkcap.
As an example, read this Wikipedia article about Coprinus for more details.

It is said the mushrooms deliquesce when they liquify fairly suddenly. Note that the edible version of that mushroom is always nice until the first gray tones appear in the gills, at which stage they are past their prime and way less palatable... they are only worth picking when completely white and when the mushroom is completely closed, otherwise you have to cut the dark bits off. And there are unpleasant copy cats of the same mushroom so you must ID them well. take the spores of shaggy ink caps, mix them with flour and water in a blender, and throw them around some overturned decayed ground

Actually the coprinus comatus ( pictured) , gets pinkish before grey. I have eaten them with traces of pink, no problem.

Actually "shaggy mane" is the common name in US ; inkys and micas are other closely related species.


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How do point mutations arise from mistakes in DNA replication?

Hi! I'm trying to make sense of this illustration (from the textbook Biological Science by Scott Freeman).
The general question is: How do point mutations arise from mistakes in DNA replication?
If you don't mind, however, I'd like to explain how I interpret the illustration so you can see the confusion. As the original molecule of DNA is replicated (in gray), a mistake occurs in the synthesis of the bottom strand in the new molecule (the noncomplimentary bases G and T have been paired together). Now, it seems like a second replication is required for the mutation to arise: the defective molecule is replicated resulting in two new molecules, one free of mistakes (because it takes as its template the top strand) and one "wrong" where the mutation is present.
But my doubt is, wouldn't the middle molecule already constitute a mutation? If a mRNA were to transcribe that sequence, the codon is already different from the original molecule. Must a DNA molecule be replicated two times for a mutation to arise (where the first time a mistake is made and a second where such mistake is, let's say, "consolidated")?
Thank you very much in advance.

Welcome to Biology.SE and congratulations for asking a question that explains so well the origin of your misunderstanding (+1).

Source of your misunderstanding
Your misunderstanding is very comprehensible as the figure is misleading.
The figure only shows a single event of replication. What you see as a second replication resulting into two double stranded molecules is NOT an event of replication. It actually represents the two possible outcomes from a 'mismatch repair mechanism'. The term DNA replication written on the figure should be replaced by Possible outcomes of DNA repair. The molecule that contains the G-T mismatch is therefore just a temporary state that will very quickly be changed to either the T-A state (bottom right of your figure) or to the G-C state (upper right of your figure). More information below.
DNA repair

DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome.

The type of DNA repair that is of interest on the figure is called "DNA mismatch repair"
DNA mismatch repair

DNA mismatch repair is a system for recognizing and repairing erroneous insertion, deletion, and mis-incorporation of bases that can arise during DNA replication and recombination, as well as repairing some forms of DNA damage.

There are specific enzymes to repair a mismatch such as the G-T mismatch represented on your figure. These enzymes can either repair G-T into G-C or into A-T. If the repair is A-T (lower outcome in the figure) then a mutation would have occurred. If the repair is G-C (upper outcome in the figure) then we are back to the original sequence and no mutation would have occurred.
Note that the probability of the two possible outcomes is different from 0.5 as these enzymes have ways to try to figure out which was the original strand and which was the newly replicated strand. You can learn much more about the mechanism of DNA mismatch repair on the wikipedia > DNA mismatch repair.

Thank you very much for this excellent explanation. I have corrected the figure in my textbook and I've certainly solved my confusion thanks to your answer.

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Insect identification (Brazil, orthoptera?)
This insect appeared in my indoor yard, in southeastern Brazil. The body is roughly 2cm in length and it makes very distinct beeping sounds, in a pattern that sounds almost like morse code, unlike the crickets I've seen around here. Any ideas?

According to the author of this blog, this appears to be an Endecous Phalangopsinae/Luzarinae, but they don't rest with the wings like that. I'll try to capture it the next time. http://www.ib.usp.br/~silvionihei/2014%20Souza-Dias%20Endecous%20apterus.pdf https://www.researchgate.net/publication/230188107_New_Brazilian_species_of_Endecous_Saussure_1878_Phallic_sclerites_calling_song_and_tegmen_morphometry_Orthoptera_Grylloidea_Phalangopsinae

The species in the question's picture could very well be related, but the papers you reference describe different colored/sized species that, more importantly, live in different habitats (i.e., caves). Unless your yard is near a cave or major source of bat guano, I'd say you'll have to keep hoping someone finds a more accurate answer.

@theforestecologist The identification seems to be fair, see my answer appended. Disclaimer: I am no specialist myself but I really trust the web of contacts at the blog

By far the best online forum and resource for the identification of Brazilian arthropods is the website below (in Portuguese): http://www.insetologia.com.br It adds to the discussion offered by @theforestecologist in this thread, given the identification of similar specimens at: http://www.insetologia.com.br/2017/12/provavel-grilo-endecous-em-sao-paulo.html http://www.insetologia.com.br/2017/01/possivel-grilo-endecous-em-minas-gerais.html
[This one looks like the OP here?] This is one interesting occurrence.

Its a cricket with bad moulted wings. (Probably)

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Potential immunization against airborn viruses
I have had an idea based on the principals of a virus and their properties and how they enter the cell by tricking it into believing it is a protein etc.
If we coated a copper particle (or another type of metal which should neutralize the atomic structure) and utilize the process they use to induct themself into our cells by mimicing the methods they connect by, would ejecting it in an aerosol steralize the earth from that specific airborn virus?
My ideology seems to fit that if we don't immunize the atmosphere against viruses that they will always naturally occur due to the Entropic nature of the universe. Does this fit into current medical science?

A lot of airborne viruses enter through sialic acid receptors. If someone can make a spray that blocks those, viruses will have no receptors available to bind. It's similar to closing unused ports or banning incoming connections on a computer network interface to prevent hack attacks and block self-replicating malware. I'm surprised there aren't known examples of cells that retract or alter/randomize the shape of commonly infected receptors when they aren't in use.

Could you clarify what precisely do you want to coat the particles with. Ligand molecules to block the cell receptors or receptor molecules to "mop up" the viruses?


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What effect is seen when the extracellular concentration of sodium is increased?
I can't seem to figure out how this would effect the cell since sodium is not very permeable.

Welcome to Bio. What cell? A human neuron behaves very differently than a bacterium at the bottom of the sea.

Don't expect tags to provide question background; they are basically not more than search terms. The answer below is likely not what you are after, but it answers your question perfectly. Vote to close.

The membrane isn't sodium permeable but it is water permeable.  Water will move from areas of high concentrations to low.  So when you increase the extracellular concentration of sodium, water will move out of the cell and into the extracellular matrix.  This causes the cell to shrink.

The question is closed, so answers can't be added, and existing answers generally should not be edited to add material.  Welcome to Biology stackexchange Patricia; try adding an answer to an open question instead of this closed question.


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What is the relationship between stroke volume of blood and ventricular end-diastolic volume?
I do know what each term means. That is, i know that stroke volume is: the volume of blood pumped by each contraction of a ventricle, while ventricular end-diastolic volume is: the volume of blood in the ventricle just before systole. However I can't relate the two in terms of, say, graphs or in the mode of action of the heart between this period(s).

I'm not sure what you're asking. Both are simply volumes of blood. They are different because not all of the blood in the ventricle is ejected. It sounds like you're asking about the cardiac cycle, not volumes, but I'm not sure. (The red line is the graphic "relationship" between the two.)

Thanks! I did see this diagram before on Wikipedia but i might have overlooked the label of ventricular volume. Thanks again!

The simplest relationship is "EDV=SV+ESV", "EF=SV/EDV" (EDV: end-diastolic volume, SV: stroke volume, ESV: end-systolic volume, EF: ejection fraction)


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Do cortical cells in root have higher water potential than endodermal cell solution?Or is it the other way round?
Well, water normally passes from root hair cells to cortex to endodermis, and from there to the xylem vessels. All of this occurs down the water potential gradient by apoplastic or symplastic pathway through these cells. I was wondering how water potential differs in each of these cells for water to be transported. BTW I'm confused why my teacher said that the water potential in xylem vessels(the tracheids) is highest among all the cells I mentioned. Then how come water can move down the water potential gradient?

So the water is moving from less to more negative water potential, but at the end of the day it will be the tracheids which will have most of the water, right?

Thank you so much for explaining. It's all clear to me now.


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A question regarding trichomes in plants
Trichomes in general are features of xerophytic leaves, which reduce water loss by evaporation by trapping water vapor and increasing humidity (as a result lowering the water potential gradient).
BUT I wanted to know whether trichomes also reduce water loss by decreasing "surface area" of the leaf, so that less water loss occurs (considering they occur as finger-like projected structures that occur in large numbers)?

Trichomes can serve the purpose you ask about, but certainly not only that. They also appear on a great many other, some very delicate, plants from many different habitats. Decreasing water loss is only one of a number of different functions they might serve.
But with respect to xerophytic plants, trichomes are still a projection from the leaf surface and so, by definition, increase the surface area of a leaf by a significant amount.  However, it's not the surface area per sé that leads to water loss, it's increased evapotranspiration which can be caused by and mitigated by many different factors, one of which is, indeed, trichomes.
Some trichomes, such as those on Tillandsia species, occlude or reflect light.  This reduction in incident light is primarily what protects the leaf tissue from damage and helps reduce water loss due to heat. Such trichomes may also function, as you mention in your question, by creating a insulating layer of still air around the leaf, thereby reducing diffusion of water vapor away from the leaf and creating a smaller gradient, though this is usually not their primary function.


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In terms of ecology what is optimality?
I am studying animal science and I have been learning about reproductive theories however i cant seem to understand the theory of optimality

Can you give more context to your question?  In biology, most references to optimality mean passing on your genes more successfully than others.  However many proxies for this exist, such as gaining food, or investing energy in offspring.  Usually these proxies are optimal in the context of a model which assumes some connection to the general problem of passing on your genes.

What type of optimality are you referring to, i.e. what is optimalized? Fitness, energy use, foraging, life-history trade-offs etc?

Optimality theory
Optimality theory is a concept of linguistic. See wiki > Optimality theory. This is probably not what you were referring to.
What is optimality
Optimality is the condition under which something is maximized! In behavioural ecology, this something is often fitness and the condition is often measured in terms of magnitude/intensity of a behaviour.
Optimality models
In ecology, we call optimality model any model that separate the benefits and costs (in terms of some measurement, often fitness) of a given phenotype (often behaviour). By weighing benefits and costs one can figure out what is the optimal phenotype. The principle is extremely simple. Such graphs are quite standard:

In the graph, the X-axis represents the magnitude of a phenotype (often a behaviour) and the Y-axis represents the benefit and cost of this behaviour (with the same scale) often in terms of fitness.
By definition, the fitness is maximized when $B-C$ is maximized. In other words, compute B-C and look for the maximum (through derivation) and you found the optimal phenotype (often behaviour). In the above graph, the optimal phenotype is a little bit left to the position of the B label.
Optimal foraging theory
Foraging behaviour has been subject to much investigations using optimality models. We refer to this body of knowledge as Optimal foraging theory.


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Botulinum Toxin
I asked on the cooking site, but was directed here.  This is my original question https://cooking.stackexchange.com/questions/35726/botulinum-toxin-in-home-canned-green-beans
The reading is quite long, however I merely want to know the minimum temperature and minimum time at which that temperature must be maintained in order to destroy botulinum toxin.  I want to review a study where the determination was made.  Can anyone assist?

The short answer is: unless you burn the sample completely to ashes, you cannot be sure you destroyed all BT particles.
Denaturation is a naturally occuring process and it works pretty much like radioactive decay. It happens over time, so if you had a solution of BT without any bacteria or spores and left it at room temperature, after some (very long) time the toxin would be destroyed. By adding heat (or acid) you accelerate the denaturation, but it still is a statistical phenomenon. If at a certain temperature half of toxin particles are destroyed within a second, it means that within a minute one in $2^{60}$ will be left. But 1 in $2^{60}$ is not zero. If you keep the temperature for two minutes, one toxin particle in $2^{120}$ will be left. You can never be 100% sure all toxin was destroyed.
This also means, that there is no one set "minimum time and minimum temperature". The higher the temperature, the lower the time needed. You can keep food at room temperature for a very long time and the toxin will be destroyed (though I doubt that the food itself will survive that kind of time).
On the other hand, one molecule of toxin will not kill you. Think about BT injections as anti-wrinkle therapy. A small amount of toxin in injected, it paralyses small facial muscles and the face looks smoother, younger. The effect wears off, so you have to repeat the injection every now and then. In order to make food safe to eat, you don't have to destroy all BT molecules. From a booklet Food Safety Hazards and Controls for the Home Food Preparer (2006 edition, available at http://www.hi-tm.com): a healthy adult can eat up to 1000 spores with no ill effects, Clostridium botulinum bacteria and spores are considered destroyed after 2.4 minutes at $250^\circ \mathrm{F}$ ($121^\circ \mathrm{C})$ - this in fact reduces the number of spores $10^{12}$ times and is called commercial food sterilization, the toxin is considered destroyed after boiling for 10 minutes but the temperature of $165^\circ \mathrm{F}$ ($74^\circ \mathrm{C})$ will not destroy it. This booklet also advises to boil for 10 minutes any homemade canned food if you are not perfectly sure the original procedure was appropriate.

what a great answer!

That's interesting.  I never considered a half-life decay, but merely once the food reached a certain temp throughout, they would all be destroyed. So for reasons of statistical decay, do you doubt there are published studies of experimentation?

Yes, I doubt that. I think there might be very old studies showing the principle - how it was discovered, or studies pinpointing the exact curve in order to formulate those recommendations that I quoted.

Denaturation is a naturally occuring process and it works pretty much like radioactive decay.... hmmmm.... no it is not. Radioactive decay is irreversible, denaturation is not, as renaturation can occurr.


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What is the best way to calculate the biological diversity of samples from bacterial/viral OTU tables?
I have a few large OTU tables of bacterial and viral datasets. The samples are across different sites and times.
I would like to visualise the community 'diversity' across the times for which I have data. For example it would be interesting to see if community diversity peaks in the summer months and falls in the winter months- in a repeating pattern.
I have not come across much advice or literature which looks at looking at diversity for large OTU datasets. Considering the OTUs are essentially arbitrary and that there are thousands of them, what is the best way to calculate and visualise the each samples diversity?
With the vegan package on R it is quite easy to calculate the Shannon/Simpsons diversity index for an OTU table. Can you simply use this on a 'raw' table of OTUs?

There are no best way I think. Those indices are different definitions of diversity. I don't think there has been much argument of whether one is of greater of interest for, say conservation purposes or whatever. I think you'll just have to pick one you like! The fact that OTU is a rather arbitrary grouping concept won't change much to the discussion. Note that there are many other indices of diversity (have a look at this answer for a list of measures of diversity)

I don't know much though on this topic and it might be worth having a look at the book Measuring Biological Diversity from Magurran

I mostly concur with @Nathan's answer, and in particular with the references he provided.
As Shannon & Simpson indices can be hard to interpret and can be non-intuitive, I prefer using Hill diversities as suggested by Nathan (the Jost 2006 and 2007 refs are great to read up on this). The main argument is that Hill diversities give effective number of species that are comparable between samples and follow the duplication principle.
Hill diversities rely on a unified formula (see this wikipedia article) with one parameter, q. Increasing values for q correspond to increasing weighting of taxa abundances in the diversity calculation:

D with q=0 does not account for taxon abundance, so is just the number of taxa, or richness
D with q=1 is not defined, but asymptotically approximated by e^H where H is the Shannon entropy. D_q1 is the effective number of species with abundance weights.
D with q=2 corresponds to the Inverse Simpson index (1/D_Simpson). D_q2 weighs more abundant taxa even more strongly.

One can choose any value for q (with q=1 with the limit e^H), and comparing diversity estimates for varying q can give you an idea of sample evenness. Setting q=∞ gives the Berger-Parker index (the fraction of individuals in the sample belonging to the most abundant species).
Importantly, for alpha div analyses on (16S/18S-based) OTUs, I would always generate rarefaction curves first, and then generate diversity estimates at a common, rarefied number of reads per sample.
You can do most of this using the R package vegan. The phyloseq package provides various alpha div estimates in one command, but no Hill diversities. I've written a few simple functions to perform rarefaction and calculate (rarefied or non-rarefied) Hill diversities from an OTU count table matrix:
function.rarefaction.R
function.alpha_diversity.R

The vegan package is suitable for your needs, but you may find you need to use others or code your own functions.
Due to sequencing biases, you shouldn't trust the 'raw' counts of your OTUs (unless you have a good reason to do so—I'm not sure how your OTUs were obtained). Rather, you may consider relativizing your site-by-species matrix. You can do so using the decostand() function.
Then, you can use the diversity() functions to analyze diversity; but you may also consider looking into other approaches to assess local diversity, such as rarefaction and sampling-based approaches, species equivalents and Hill numbers (Hill 1973, Gotelli and Colwell 2001, Jost 2006, 2007). The books by Magurran and McGill (2011) and Legendre and Legendre (2012) are extremely helpful.


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Should you perform an ordination (such as PCA) of abiotic variables before a Redundancy analysis (RDA)?
I have a dataset of viral 'OTUs' across various sample points from different sites/times.
I also have meta-data collected at these same sample points, for things like temperature and the concentration of key chemical compounds.
My goal is to identify if these (or some of these) abiotic variables correlate with the variation in the OTU community diversity- for now I am planning to do an RDA.
What I am wondering is whether or not it makes sense to conduct ordination on the abiotic variables before doing the RDA? I have done a PCA on these abiotic variables and it is clear that these variables alone clearly do not cluster in any sort of recognisable pattern (for example if you colour them by 'season' there is no clear clustering at all).
So I was thinking that perhaps doing an RDA would not be valid, because if the abiotic variables don't cluster logically in an ordination of them alone then surely it doesn't make sense to plug this data into an RDA?

I really don't know much about RDA (so correct me if I am wrong), but to me RDA is a method of ordination as well, so the sentence makes sense to conduct ordination on the abiotic variables before doing the RDA makes little sense. When you state your goal, it seems like you would like to perform some hypothesis testing which is, I think not what an RDA does. Am I wrong? Why don't you just have OTU community diversity as response and your abiotic variables as explanatory variables in a simple GLM? You don't even seem to need a MANOVA (which would require ordination + regression).


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How should you choose from the various methods of constrained ordination?
I have a bacterial OTU matrix from various sample points and times. So for each sample I have the sequence counts across the various OTUs that they were assigned to.
I also have a corresponding matrix of abiotic variables including temperature, pH and the concentrations of a range of nutrient compounds. This data was collected at the same time as the bacterial OTUs.
This is a tutorial written by the people behind the R package 'vegan', it offers three separate types of constrained ordination. I just don't understand what the differences are between these and what would suit my data-set best. There is not much advice out there at all for this sort of thing so any help would be appreciated.

You might want to check out Mike Palmer's webpage on ordination, specifically the constrained ordination section: http://ordination.okstate.edu/
The main difference between constrained ordination techniques is the distances that are preserved. Redundancy analysis (RDA) preserves Euclidean distances, so in order to use it, you need to transform your OTU table with an appropriate transformation (e.g., Hellinger), after which a Euclidean distance calculation is appropriate. It also works best identifying linear relationships between environmental variables and species responses. Canonical correspondence analysis (CCA) preserves the chi-squared distance, which tends to emphasize common taxa, and looks for unimodal responses to environmental gradients. Distance-based redundancy analysis (dbRDA) accepts any distance matrix, allowing you to use non-metric distances, and then looks for linear relationships with distances and environmental variables.
Before applying these metrics, you'll need to understand their advantages and limitations, and then you'll need to make a decision about which combination of constrained ordination techniques and distance metrics are best for answering your questions. This is something you'll need to justify yourself, based on your own question, because different approaches are better at emphasizing different aspects of your data. I strongly suggest you study a copy of Legendre and Legendre (2012) for more information about these methods.

There is also a good chapter about ordination in this book


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Terrestrial Vertebrate Limbs
This question is regarding the conversation that took place here: Why don't mammals have more than 4 limbs?. I'm not sure if someone mentioned this and I just missed it, but everyone is talking about two pairs of limbs for all terrestrial vertebrates; what about the case of kangaroos? If we are analyzing this from a locomotion point of view, and tails are being considered limbs, then wouldn't the kangaroo be considered to have five? They use their tail for balance and to push forward in "walking" (not exactly a walk, but I am lacking the proper term at the moment), resting only on the tail and forelimbs as the hind limbs swing forward. Does anyone have thoughts on this?

This has recieved a fair amount of attention recently, as it made it into the lay press, Unique Among Animals, Kangaroos Use Tail as Fifth Leg, Scientists Find

I did not realize that was out there. Thank you for sharing that article!


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Derivation of discrete replicator dynamics
Related: Discrete vs Continuous Replicator Dynamics
I am trying to perform a derivation of the discrete time replicator dynamics, but I am unable to get through Cressman's derivation in "Evolutionary Dynamics and Extensive form games" on page 21

Basic notations:

$S = \{e_1, \ldots, e_n\}$ are pure strategies
$\pi(e_i, e_j)$ payoff of player using strategy $e_i$ versus strategy $e_j$
$p \in \Delta^n = \{(p_1, \ldots, p_n) | p_i \geq 0, \sum_i p_i = 1\}$ mixed strategy
$\pi(p, \hat p) = p \cdot A\hat p = \sum\limits_{i,j = 1}^n p_i a_{ij} \hat p_j$ is the payoff of strategy $p$ versus $\hat p$

Derivation of the discrete replicator dynamic:

Let $n_i$ be the number of individuals using $e_i$ at generation $t$.
Then $n_i' = n_i (e_i \cdot Ap)$ be the expected number of individuals at generation $t+1$
Let $p_i = \dfrac{n_i}{\sum_j n_j}$ and $p'_i = n_ie_i \cdot \dfrac{Ap}{\sum\limits_j n_j e_j} \cdot Ap = (\sum_j n_j)p_ie_i \cdot \dfrac{Ap}{\sum\limits_j n_j}\sum_j p_je_j \cdot Ap = p_i(e_i \cdot \dfrac{Ap}{p}\cdot Ap)$
Then the standard discrete time replicator dynamic is
$p'_i = p_i \dfrac{e_i \cdot Ap}{p\cdot Ap}$

Questions: There are numerous moving parts in this derivation and little explanation as to where each item came about

Just to make sure, $n_i' = n_i(t+1)$ right?
Why is that $n_i' = n_i (e_i \cdot Ap)$ is the expected number of individuals at the next generation? This is just the number of individuals at the current generation times the payoff to pure strategy $e_i$, is there a derivation for $n_i'$?
I understand $p_i$ is the fraction of players using $i$ versus all the other strategies. But can someone explain how $p_i'$ came about, where are all its pieces? I am especially confused about the part where it says $Ap/p$, because $p$ is a vector and you can't divide it...
Is there another derivation of the discrete time replicator dynamic?

Any help is appreciated.

I think you misunderstood some of the nominators/denominators in the text you cited. In the cited text, the whole stuff after the / sign is the denominator of the fraction. So there is no division by p, but division by (p \cdot Ap), which is a scalar.


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XXY (Klinefelter's) & Trisomy 21 & X-inactivation
I read that X-inactivation doesn't tend to happen in males, but then when someone is XXY, they are a male because of the Y. However these individuals tend to live. So does that mean that X-inactivation happens in males or else these individuals would die?

Trisomy 21 (of the 21st chromosome) and being an XXY individual are two quite different things. Isn't your question about the XXY sexual chromosome pattern (which is BTW not trisomy, but Klinefelter's syndrome)? Or is it about a special case of Klinefelter AND trisomic 21 individual (I don't even know if that exists...)?

Do you confound the Down syndrome (Trisomy 21) and the Klinefelter Syndrome (XXY)?

So basically, the question is: "Do XXY (Klinefelter Syndrome) individuals inactivate (dosage compensation) one of their X-chromsome?". Why is it written Trisomy 21 in the title?

X-inactivation does occur in XXY individuals.
In phenotypically normal XX females, one X chromosome is inactivated.  Which one of the two X chromosomes is inactivated in any given cell is random. Therefore, about one half of the cells should have the maternal X active and the other half should have the paternal X active.
XXY individuals show a wide range of clinical symptoms and intellectual ability.  Iitsuka et al. (2000) suggested that this variation may be explained by a bias in X-inactivation.   They found that about 31% (5 of 16) individuals (either XXY or XXYY) shows a very strong bias of X inactivation, which they defined as at least 80% of the cells inactivating one particular X chromosome. Two individuals has biased inactivation of the paternal X and the other three had biased inactivation of one of the maternal X chromosomes. The sample size is rather small (not surprising) but X inactivation is occuring.  Samango-Sprouse (2001) argues that incomplete inactivation of one X chromosome may also explain some of the more severe clinical mental disorders.
For Trisomy 21 (Down's Syndrome), the individual as three copies of chromosome 21, so X inactivation is not an issue. However, scientists are studying whether Xist can shut down the third copy of chromosome 21.  The Xist gene is transcribed to produce a large molecule of RNA. That RNA is what usually causes X inactivation.  Jiang et al. (2013) were able to show that Xist can coat one of the chromosome 21 copies, performing essentially the same inactivation function that it does for the X chromosome. So far, though, this work has been entirely in the lab (in vitro).


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Regarding kidney transplant
One of the options is correct

Kidney can be taken from a dying person who has the
a) cessation of neurological function only
b) cessation of cardiac function only
c) cessation of respiratory function only
d) cessation of kidney function only

I think that answer should be b. as if heart stops working then the person is definitely dead. but m not sure if on the cessation of neurological/respiratory function, one still has chance of revivial. Moreover answer is given as A. I don't know how. Could it be that on cessation of cardiac/respiratory function, kidney gets damaged while not so in case of neurological dysfunction?

This link describes the different ways of diagnosing/confirming death prior to organ donation. It might help answering your question.

I amn't really sure - but the answer given is A may be because there are many cases where cardiac function has been restored after hours of its cessation

There are actually very few situations where organs can be harvested from donors. For all deceased donor transplants, the donor must be confirmed as being brain dead (both brain stem and higher cortical functions).  However, in order for the organs to remain viable they must not become ischaemic - which is obviously a huge problem when the patients heart has stopped beating.  For this reason most patients who die and go on to become organ donors were already on a ventilator in intensive care in order to keep their blood oxygenated and circulating to perfuse their organs.
Kidneys are listed by NHSBT as a special case where a ventillator may not be required in advance to maintain viability - offhand I'm not sure why this would be - however to answer your question:
A. Neurological death - correct answer - the patient must be deceased without chance of recovery (hence brainstem and cortical death)
B. Cardiac function - were this to stop unilaterally then the patient may still be recoverable whilst the organs may be damaged due to lack of perfusion and thus not be viable for transplant
C. Respiratory function - almost identical to the cessation of cardiac function (and indeed will lead onto it very quickly)
D. Renal function - there's no point transplanting useless kidneys!
Have a look through the NHS Blood and Transplant Organ Donation site linked above, it's a great and trustworthy resource.

There's dead, and there's mostly dead.  Let's not give up on the "dying" pt who may only be in renal failure. :)

@AtlLED I'm not following you?


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How to distinguish between a genetic bottleneck and directional selection?
Genetic bottlenecks and directional selection should have relatively similar genetic signals: reduced heterozygosity and greater genetic divergence (Fst?) in contemporary populations compared to the past
How would one be able to distinguish between these two evolutionary forces if their signals are so similar?

Distinguishing between selection and specific demographic events can be quite complex and there exist a large set of tools to investigate such things. You might want to have a look at How to determine whether changes of an allele's frequency are due to genetic drift or selection?

I'm asking how one would be able to distinguish whether a population had undergone a bottleneck OR if directional selection had occurred given the high frequency/fixation of a specific allele(s) and reduction in expected heterozygotes in a population

I read "local selection" instead of "directional selection" for my first comment. Sorry! I removed my comment and my close vote and answered the question!

Population bottleneck will have genome-wide effect while directional selection will affect only the locus (and closely linked loci via a selective sweep).
You can typically screen through the genome and calculate Tajima's D. Under a bottleneck scenario, Tajima's D will be expected to be negative everywhere. Under a directional selection scenario, Tajima's D would be negative only at the locus (and closely linked loci) to the one that is under selection.
There are of course a whole lot series of technics but the above is probably the simplest and most straight-forward (it probably lacks in power though).

Makes sense: a population bottle neck will affect all loci the same way, while directional selection will only affect the loci under positive selection (and other linked loci due to selective sweep)

Some species are regarded as having a very wide genetic base and some less so, which commensurately signals that a bottleneck has taken place, and that diversity takes a while to be amended. You can make some measurements on when the species population may have been small in the past, although some of those kinds of study have been found to be very misleading, because populations can interbreed cross species, like neanderthal, which brings up a much more complicated picture to the genetic bottleneck model, and makes some research results seem over stated. In otherwords, recent studies in that field by trained scientists have found errors.
here are some measures of recent or distant small populations: http://www.tiem.utk.edu/~gross/bioed/bealsmodules/bottlenecks.html
Directional selection generally is related to a considerable force on the population which changes is population dynamics and can therefore amount to a bottleneck, or which selects only one type of adaptations from a population in a region, which is then transferred to the rest of the population by a less sudden kind of evolution, which amounts to a semi bottleneck with a wider base. different branches can converge from 40,000 generations distance in speciation, or in 50, which means that it's difficult to gauge a bottleneck without very complete studies.
Take for example moths at the beginning of industrialization when coal was used in large amounts. They noted that the same species of moth could change from light to dark to blend in with the background, and that the white moths dissapeared.
That illustrates a kind of bottleneck as a result of directional pressure, although the species may have been far from failing, it just underwent a bottleneck to some degree.
Bottleneck genetics is very complicated and difficult to understand, because they have quite a strong effect on the genetic base of the animal and it variability. and because low genetic variation implies a range of mutations which can be fitness or protein malfunctions or dynamic changes depending on the kind of bottleneck.


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Do non-migratory canada geese still exhibit migration behaviors?
I have noticed that many of the geese in my region (NE US) remain overwinter. I also see many of what I guess (but am not sure) may be the same geese flying in migration patterns. One thing that makes me think that non migrating geese do this, is that I observe group formations flying in all directions, not just southwards in the fall.
Does anyone know whether the resident geese still like to fly in migration patterns, or is it always the migrating geese that you see doing this?

The answer is yes, also sedentary geese do use migration patterns (V-formations). When they move from roosting place to feeding areas (or vice versa) geese always tend to fly in formations. I speak for personal experience of resident and wintering birds in Europe and America.
They do so because they save energy as explained here: http://jeb.biologists.org/content/128/1/445.short and here: http://www.nature.com/nature/journal/v413/n6857/full/413697a0.html
The second study also show how not all the positions in the formation are the same regarding energy expenditure. The one closer to the front of the V shape need to flap the wing more often.
Have fun


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Why is Mus Musculus a good model organism?
I'm reading through a number of articles that use partial hepatectomy in Mus Musculus to study the mechanisms for liver regeneration (1, 2, 3). I have no doubt that a better understanding of hepatocyte regeneration mechanisms will allow scientists to discover/create new theurapetic targets that would improve liver regeneration in mice. However, these articles seem to imply that the results of the research will be applicable to liver regeneration in humans as well.
What makes Mus Musculus a good model organism? I'm inclined to think that some mouse genes might have homological human genes; is there more to that? Bonus points for answers that would show how research on non-coding RNAs, as compared to protein-coding genes, in mice would apply to humans.

"I'm inclined to think" that you should do a little research before posting if you don't know the extent of the genetic similarity among mammals. And what species would you expect experiments on liver regeneration to be performed? Homo Sapiens? Finally this is not a quiz show and you can only award points by accepting or up voting an answer. We don't do bonus points here.

@David "bonus points" was a figure of speech. I would gladly rephrase the question as a resource recommendation one. Go-to sources such as Model organism didn't help much, and, as an outsider to biology, I know no better sources. Finally, thanks for taking your time to explain the downvote.

Your question certainly needs revising because (1) it is unclear what you are asking (2) part is based on a false premise. First, you do not define model organism. Do you mean "why do scientists work on mice?" or "why is mouse a model organism for liver regeneration in humans?". Second your "thought inclinations" do not take into account that scientists have been studying liver regeneration in rodents since the middle of the last century, at which time nothing was known about non-coding (or coding) RNAs, and little about protein sequences. You should find out for yourself what is known now.

Mice are mammals, like humans, so their proteins tend to show more homology with human proteins than non-mammalian options. They are also actually more closely related to humans than cats or dogs due to the relatively recent (~80 million year) separation of lineages that led to modern rodents and primates.
Mice breed fairly quickly year-round and have relatively large litters. Laboratory strains are also quite tolerant of research lab conditions.
Mice are inexpensive to keep: they are small, require little food and care, etc.
People tend to have less opposition to research in mice due to their status as pest species.
Many genetic tools are available for mice, which makes them better models for the next generation of science, which means there are more genetic tools available for the generation that follows, etc. There are now many specialized mouse lines, some for particular diseases, some for particular techniques, etc.
Mice are well-studied, so experiments in mice can be easily compared to other experiments, and there are a lot of standards for protocols. Most experiments are done on inbred mice, which have the advantage of being nearly genetically identical to each other, so experiments done in different labs are done in (nearly) genetically identical subjects which can help with reproducibility and comparisons across studies (though there are also downsides to inbred animals; see below).
None of these factors make mice perfect model organisms. Many successful experiments and treatments in mice have not translated to human outcomes. Laboratory mice are typically highly inbred and may display characteristics thought to be "normal" that are actually the result of genetic drift, founder effects, etc. These can include preferences for alcohol, tendencies toward obesity, poor immune systems compared to wild mice, etc. Some get particular tumors early. Some have seizures. Some lab mice are blind at birth or shortly after. Others have hearing problems.
References

Abolins, S. R., Pocock, M. J., Hafalla, J. C., Riley, E. M., & Viney, M. E. (2011). Measures of immune function of wild mice, Mus musculus. Molecular Ecology, 20(5), 881-892.
Beck, J. A., Lloyd, S., Hafezparast, M., Lennon-Pierce, M., Eppig, J. T., Festing, M. F., & Fisher, E. M. (2000). Genealogies of mouse inbred strains. Nature genetics, 24(1), 23.
Battey, J., Jordan, E., Cox, D., & Dove, W. (1999). An action plan for mouse genomics. Nature genetics, 21(1), 73-75.
Gordon, J. W., Scangos, G. A., Plotkin, D. J., Barbosa, J. A., & Ruddle, F. H. (1980). Genetic transformation of mouse embryos by microinjection of purified DNA. Proceedings of the National Academy of Sciences, 77(12), 7380-7384.
Justice, M. J., & Dhillon, P. (2016). Using the mouse to model human disease: increasing validity and reproducibility.
Kurien, B. T., Gross, T., & Scofield, R. H. (2005). Barbering in mice: a model for trichotillomania. Bmj, 331(7531), 1503-1505.
Lynch, V. J. (2009). Use with caution: Developmental systems divergence and potential pitfalls of animal models. The Yale journal of biology and medicine, 82(2), 53.
Martin, B., Ji, S., Maudsley, S., & Mattson, M. P. (2010). “Control” laboratory rodents are metabolically morbid: why it matters. Proceedings of the National Academy of Sciences, 107(14), 6127-6133.

You could also add that it is relatively easy to produce inbred strains that will be more likely to show consistent experimental results.

@David I don't know if mice are particularly easy to produce inbred strains compared to others species, though I'd happily add a reference if that's the case for some reason. I did add a section on the advantages of standardized inbred strains since I spent a paragraph describing the disadvantages.

I don't have a reference. It must be easier than in rats (or mice are easier to breed) because there are so many more cited in the literature. Perhaps I should have said more are available. The other mundane factor is how much tissue you need and can obtain from the organism. Don't try isolating erythropoietin from fruit flies (even assuming they have it).

Understood. My experience in using both mice and rats is that there just as many "wild type" inbred strains of rats as of mice, at least as would be expected by each of their prevalence as research animals. The huge numbers of available mouse strains are mostly on the same several inbred backgrounds, and that's just because of all the available genetic tools for mice to generate mutants and transgenic animals.


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When salivary amylase breaks down starch, are those substances tagged or destined for a particular use in the body
When salivary amylase breaks down starch, are those substances identified for a particular use in the body?

Salivary amylase breaks starches brown into shorter chain of sugars. In the beginning of the small intestine, this process is continued by pancreatic amylase. Other enzymes at the surface of the intestine's lining complete the process resulting in simple sugars which absorbed into the circulatory system. Some of these sugars, if there is an excess in your diet, will be converted to fat and stored.
The rest of the sugars will ultimately be taken into cells and undergo a process termed cellular respiration. The bulk of these sugars will be broken down and used to create (recharge actually) ATP, a substance that just about any process in the cell requiring energy can use for energy. The atoms in the sugars used in this process end up as carbon dioxide, which you breath out, and water. But a certain percentage of the sugars only get partially broken down. These fragments can be used to synthesize many different substances depending on what's needed in the cell at that time.


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The pectoral fins of a whale and a shark. Are they analogous organs?
Analogous organs: Different origin, same functions,
Homologous organs: Same origin, different functions but same main structure//  right?
So, what is the case for the pectoral fins of a shark and a whale?
Are they analogous organs, because the two animals have different ancestors(shark-Some Chondrichthyes fish, Whale-some mammal) but have organs that do the same thing?
Or are they homologous organs, because the two animals have the same ancestor(A vertebrate animal) and have organs that have a similar structure?(I learned that it is alright for homologous organs to do the same function, for example the wings of a bat and a bird are homologous organs, although they do the same thing)

The ancestors of all jawed animals probably had pectoral fins [Ref]. This primitive feature is homologous to shark pectoral fins (fig. 1). The forelimbs of quadrupeds are evolved from the pectoral fins of lobe-finned fish (fig. 2), and the pectoral fins of whales evolved from the forelimbs of their mammal ancestors. Thus, these organs are homologous as one can follow the gradual changes in morphology and find continuity between the fin to leg to fin transitions.
However, the internal structure of the fins themselves are quite different between whales and sharks as they evolved from a leg structure with fingers (fig. 3 & fig. 1). The external similarity of the fins is an example of convergent evolution, not directly the result of their shared origin. Some of the internal features of the fins may be homologous (I haven't checked), but you should not assume that a shared origin for the fins means they are the same.
Fig 1. Shark anatomy

Fig 2. Lobefinned fish and amphibian homologous limbs.

(source: ftexploring.com)

Fig 3. Whale fin
Reference:
1. New study showing pelvic girdles arose before the origin of movable jaws, : Institute of Vertebrae Paleontology and Paleoanthropology, 2012

They are analogous at to function. Whales derive from terresterial animals that "returned" to the sea. Evolution adapted the forearms to fins. Here's a great diagram: http://evolution.berkeley.edu/evolibrary/article/evograms_03
The bat wing and the bird wing are also analogous as to function. Their functional aspects evolved independently. But as forelimbs they are homologous sharing a common ancestor with forelimbs.http://evolution.berkeley.edu/evolibrary/article/evo_09
We haven't yet answered the question of whether the whale fin and shark fin are homologous in origin: http://evolution.berkeley.edu/evolibrary/article/similarity_hs_09

There is more recent evidence they are homologous as limbs, shark pectoral fins and bony fish fins (and thus tetrapod limbs) share the same hox genes. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1937022/


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In the transition to multicellularity what function becomes specialized first?
It's my understanding that in the transition from single celled to multi-celled organism a lineage will transition between stages where existing in a colony of cells is optional to one where it is obligate. Integral to this process is the parts of the colony taking on specialized roles in the colony's survival. First is tissues, and eventually full blown organs.
With that as background (please correct any misconceptions), which job tends to be taken over by specialized cells first in the transition? The three main ones in every multicellular organism I can think of are: digestion, structure (including skin and any rigidity), and reproduction (please suggest roles if I missed any, or over-included). Is there a single answer to this, or does it vary between lineages?


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How is epinephrine and norepinephrine different?
Is there any difference between epinephrine and norepinephrine?
https://www.quora.com/What-is-the-difference-between-epinephrine-and-norepinephrine
This site says that norepinephrine is also a neurotransmitter.
Is there any major difference between them?

Epinephrine: https://en.wikipedia.org/wiki/Epinephrine
Norepinephrine: https://en.wikipedia.org/wiki/Norepinephrine

Please can you list the major differences.

But little amount of epinephrine also serve as a neurotransmitter.
Iam mentioning here some of the differences I found out myself when I had the same question.
If you need further reading you can visit the site  as mentioned by @Spartacus9
https://en.wikipedia.org/wiki/Epinephrine
https://en.wikipedia.org/wiki/Norepinephrine
1)Norepinephrine is mostly made inside nerve axons and released when an action potential travels down the nerve.
Epinephrine is made from norepinephrine inside the adrenal medulla.
2)Norepinephrine acts mostly on alpha receptors.
Epinephrine is relatively non specific,stimulating both alpha,beta1,beta2,beta3 receptors more or less equally.
3)In medicine, norepinephrine is used to increase and maintain blood pressure related to cardiac arrest,spinal anaesthesia,septicaemia,etc.
Epinephrine is used in medicine to treat low blood pressure associated with septic shock and also for the emergency treatment of allergic reactions.


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Origin of logarithmic sense responses?
It's my understanding that most human sensory systems obey an approximately logarithmic stimulus/response curve. This includes the visual system, auditory system, and the smallest perceptible difference on things like weight. Do we know the origin of this pattern? Is it something inherent in how neurons encode information and fire (for example, maybe the refractory period reduces neuron responsiveness to stimulus in just the right way relative to how information is encoded)? Or is it something that specifically evolved to give us the ability to handle a wide range of stimulus amplitudes? If it's the latter, how is the transformation from linear stimulus/response to logarithmic response achieved?

First, the curves are not really logarithmic.
Instead, according to the Stevens' power law, the curves are of the form:
Perceived = k (actual)a
where "a" could be greater, less than, or equal to 1.
When "a" is 1, the curve is linear.
Examples of a=1 (linear), are:
brightness of a "point source briefly flashed"
length perception
cold perception of skin
radiant heat perception
If "a" = 0.5, the curve is a square root curve.  Brightness perception follows the square root (or de Vries-Rose) curve in some intensity regions, and a nearly-linear response in other (Weber's law) regions.
Examples of "a" being positive are perception of electric shock and perception of heaviness of lifted weights.
So, since the perception curves can be linear (a=1), more sensitive than linear (a>1), or less sensitive than linear (a<1), there is no general logarithmic property of neutrons that is responsible for the curves.


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Do the neurogenic chemicals in mushrooms get transmitted to milk?
In a recent video by SciShow they discussed several studies showing that several compounds in lion's mane mushrooms encourage neuron growth. Do we know if these chemicals get passed into milk if a lactating female consumes them? I'm curious about both human breast milk for supplementation purposes (and possible safety concerns about whether this could cause overgrowth in an already rapidly developing infant brain) and ruminant milk (cows, goats, and sheep for possible commercial applications).
List of sources SciShow used:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3924982/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3449638/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4583117/
https://hrcak.srce.hr/file/52615
https://www.mdpi.com/1422-0067/20/4/859/htm
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5237458/
https://www.jstage.jst.go.jp/article/biomedres/40/4/40_125/_pdf/-char/en
https://www.jstage.jst.go.jp/article/bpb/31/9/31_9_1727/_pdf/-char/en


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Is arachnophobia connected to lower immunity against spider toxins?
Are arachnophobics more subceptible to toxical effects coming from spider toxins?

You would have to test a pair of identical twins to see.

@Charlie ?? What is wrong about classical treatment groups?

How common are toxic - that is, with sufficient venom to pose a threat to humans - spiders? Especially ones that will bite humans?  AFAIK they're common only in Australia & Latin America, extremely rare elsewhere.

This is an interesting question and may stem from the fact that spider phobias tend to run in families and thus have a genetic link - assuming susceptibility to toxin levels can be passed from parent to offspring.  However, instead a study found that the fear of spiders was caused by social learning of disgust reactions.
Source: https://www.psychologytoday.com/blog/why-we-worry/201407/why-are-we-afraid-spiders
Directly from source:

In relation to the first question, it has been known for many years
  that spider phobia tends to run in families. It has often been assumed
  that this may represent a biological predisposition caused by the
  transmission of genes between parents and offspring. However, we found
  that this relationship was considerably more complex and indirect. We
  found that the only significant predictor of a child’s spider fear was
  not the level of spider fear in the parents, but their levels of
  disgust sensitivity. One interpretation of this finding is that spider
  fear may be transmitted within families as the result of social
  learning of the nature and intensity of disgust reactions–including
  disgust reactions to spiders.

Link to study abstract: http://www.sciencedirect.com/science/article/pii/000579679390041R

@Charles- Is the toxin immunity element not addressed by the author when he mentions that it was long assumed that there was a 'biological predisposition' which caused spider phobia to run in families before going on to conclude that fear of spiders is a result of social learning (behavior)?  Unfortunately, the author does not go into detail of what he means by biological predisposition but wouldn't at least a portion of that include some type of increased susceptibility?  I appreciate your response and would like to see a more definitive study directly relating immunity and behavior myself.


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How to evolutionary explain menstrural cycles synchronization?
Sorry, I can not indicate the source, but I read that menstrual cycles of women who live in the same house over time sync. Is it true? How does it work?

It is a myth which most likely came from methological flaws in the original study. It could never be reproduced. Read here for details.

@Chris that's really interesting, I am aware of much anectodal evidence that suggests this is true. The wikipedia link you gave cites PMID:23480070 but I don't have access to it. Do you? Does it indeed confirm that it is a myth (the abstract suggests so but I don't know for sure)?

@terdon You can find the paper here, the part regarding the mentrual synchronisation starts on page 30 in the document. If you want to summarize the criticism in an answer, go for it.

This question appears to be off-topic because the claimed fact is not supported by any reference. Suitable for Skeptics SE.

@ChrisStronks I guess you meant to ask Chris not me. There is nothing in my comment

Ok, made the comment into an answer.

This is a myth which most likely came from methological flaws in the original study. It could never be reproduced. This paper ("Darwin’s Legacy: An Evolutionary View of Women’s Reproductive and Sexual Functioning") deals with it. The interesting part starts from page 30 and says (the references can be ressolved in the article):

Critiques of MSH Studies
Wilson (1992) and Yang and Schank (2006),
  among others, have criticized the study design, methods, and
  statistics used by McClintock (1971) and others who have claimed
  evidence of MS. For example, McClintock
  incorrectly used the Page test for ordered hypotheses with multiple
  treatments (she used the same groups of women repeatedly instead of
  independent treatments), making it impossible to evaluate the true
  level of significance of her reported findings. Likewise, reports of
  greater estrous synchrony in chimpanzees caged together than in those
  caged apart (Wallis, 1985) and synchronization of estrogen peaks in a
  sample of five golden lion tamarins (French & Stribley, 1987) are
  rendered moot by the use of unsuitable statistical tests (Schank,
  2001). Furthermore, computer simulations suggested that the null
  hypothesis of no synchronization could not be rejected in either the
  chimpanzee or tamarin samples (Schank, 2001).

Thanks for this enlightening answer Chris. It has been a long-standing myth that I believed for true.


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Will the climate change help the trees to grow?
I've heard several contradictory views and I'm not sure which factor do climatologists count with. Counting with all the effects of the current climate change (including changes of biotopes on places such as Siberia, as well as the higher percent of CO2 in the atmosphere), will the conditions help make better conditions for growing trees (I know the effect on biosphere is usually claimed to be synergic, e.i. for example coral reefs will have less CaCO3 to work with so they will make the global warming appear faster. So please consider just the average effect on trees)

I think it's safe to say that a changing climate will be a selective force, making many species extinct. The cream will rise and the the diversity will decline. Diversity takes many years... diversity is a sign of a (previously) stable climate. The ability to adapt is/was the selective advantage for humans. The earth is experiencing a dramatic extinction event, and we are a major part of it.

@BenWelborn — Please do like it says when you click in the box and do not use comments for answering questions.

@david It's hardly an answer.... at least not one about various factors or biotypes of siberia, and certainly not containing references. So for these reasons, such an answer is liable to be voted down, despite being a relavant truth. What the comment does do (appropriately), is help clarify that a comment such as the one above would not be an answer to the question despite the relevance. So it really is a clarification and/or embellishment of the existing question.

I don't think anyone knows for sure. It will certainly depend on which spatial location, and which tree species, you're thinking of: while "global average effect on growth (e.g. measured by change in net ecosystem exchange of forested ecosystems) of all tree species" is at least well-defined, it will be an average across an enormously variable set of communities, and species within communities. Some of the relevant factors:

if you count the direct effects of increased CO$_2$, this will generally increase growth rates, although it will be highly variable across ontogeny (life stage, i.e. seedling vs sapling vs adult) and species. In general changes in growth rate will be higher for seedlings and for early-successional/fast-growing species, which may in turn change community structure: see Bolker et al. 1995 for one synthetic study of this.
increased temperature would be expected on average to increase growth rates
decreased moisture availability (potential evapotranspiration) would be expected on average to decrease growth rates
increased microbial activity (e.g., due to increased temperature and/or moisture availability) would be expected to lead on average to increased nutrient availability, increasing growth rates
if you're just measuring "net biomass accrual to trees", then changes in large-scale disturbance (wildfire, windstorms, pest and pathogen outbreaks ...) will tend to decrease standing biomass (although it may also lead to temporary pulses of increased carbon accrual as forests re-grow after disturbance)
note that almost all of these driving factors (temperature, precipitation, water availability, frequency of disturbance) will themselves vary a lot in space.

For a summary, you could start by looking at Purves and Pacala 2008 for some of the ways in which people are trying to put these pieces together.


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SEREX serological analysis of cDNA expression library
What is Serological Analysis of cDNA expression library? I went through this article:http://cancerimmunity.org/serex/introduction/ but could not really make out. Can someone please explain this to me in a simpler manner?(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

With this method you want to identify proteins on cancer cells which are immunogenic so you can use them to boost an immune response against the cancer cells.
To do so, you extract the complete mRNA from a cancer. These mRNAs represent all the genes which this cancers expresses (which then also contains the immunogenic proteins). These mRNAs are cloned into bacteriophages (viruses that only infect bacteria) and are then used to infect bacteria. During this infection the virus expresses the protein which has been cloned into his sequence and which originates from the cancer cell. The infection of the bacteria leads to the formation of plaques (wholes) in the bacteria which grow on the surface of a culture plate.
You then use the serum of cancer patients on these expressed proteins to see, if there are antibodies which can recognize these cancer antigens (and could be used to detect and mark them). If there are proteins which only react to the sera of cancer patients but not to controls (to exclude) unspecific reactions, then these proteins are identified and can be used to generate antibodies against this specific cancer type. It works like in the figure below (from this paper):

I hope this is understandable. If there are any questions, let me know.

" mRNAs are cloned into bacteriophages (viruses that only infect bacteria) and are then used to infect bacteria." so basically the bacteria now has the characteristics of the cancer cell? Meaning it becomes a substitute for cancer cell right??

@user3237995 No, the virus expresses (as a part of the genome of the virus) one of the proteins from the cancer cell. The virus causes then the bacteria to lyse (destroys them) which releases this protein.

The bacteria is destroyed?? or is it that the bacteria destroys the virus?

If you look on the image above, then you see these plaques in the bacteria. This is caused by the infection of the bacteria with a virus. The bacteria are used to produce the cancer protein and get subsequently destroyed. This is useful as it releases the protein for further testing.

"If there are proteins which only react to the sera of cancer patients but not to controls (to exclude) unspecific reactions, then these proteins are identified and can be used to generate antibodies against this specific cancer type."
Can you please explain what this line means?

It means that these proteins from the cancer cell cause an immune response. The hope is to mount this immune response against the cancer cell. To be able to do so, you have to be sure, that you are not targeting other cells of the body as well, which would obviously have bad effects.


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Localization of B and T cell
What does localization of B-Cell mean?? "Localization of B and T cell in allergens may not coincide". What does this statement mean? (I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

Can you tell us, where this statement originates?

What is the source of the statement? Is this really an exact quotation?

http://www.springer.com/biomed/immunology/book/978-1-4939-1114-1  this book

I think the reason you are having trouble discerning the statement is because it doesn't really make much sense, nor is it in my opinion sufficiently explained in the paper. The sentences preceding the it give a little explanation as to what the author may be getting at:

So far, 1500 allergenic structures have been identified. Online allergen databases and allergy prediction tools are being used to find cross-reactivity between known allergens. Localization of B and T cells in the allergen may not coincide.

During an exaggerated immune response (allergy) the lymphocytes (B and T) will localize (travel or accumulate at) to the site of the antigen (allergen).
If I could guess I would say the author is stating that data has shown that no immune response is taking place (data generated by assessing the accumulation of lymphocytes near the allergen), despite the fact that these online allergen predictors say that an immune response should be generated.
The statement in my opinion moves to discredit these online allergen predictors.
I did look over some of the rest of the manuscript, and found two other ambiguities within.
The author does cite another paper in your sentence that may shed more light on this:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2686541/?report=reader
An overview of it provided little clarity however.
I fear that only  a crystal ball or this question addressed to the senior author may answer your question with complete certainty:
Dr. Rajat Kumar De
Professor
Machine Intelligence Unit
Indian Statistical Institute
203 Barrackpore Trunk Road, Kolkata 700108, India.

"Localization of B and T cell in allergens may not coincide".
That sentence is written poorly, it confuses more than inform.
What the author means is: The epitopes that B cells and T cells can recognize are not the same in one particular allergen.
We have to remember that almost all allergens are proteins and proteins are made up of aminoacids, and that's what make up epitopes.
For one same particular structure or say, an allergen, the T cell can only recognize LINEAR epitopes whereas the B cell can recognize LINEAR or CONFORMATIONAL epitopes (that is, they recognize a 3d-like structure and not just a sequence of aminoacids).
What I always tell my students so they can grasp the concept is that the T cells are able to "see" a photograph of a chair to recognize it. While a B cell can do that and even more it can actually "see" a chair for what it is.

Welcome. Please add resources to your material so that others can background read on your material.


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What is hTAP?? Please help
Could not find a single article regarding this. What is hTAP? Tap is Transfer associated protein, that I know, but what is hTAP??(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

From which context do you have this?

I recommend that you put some more effort into your questions, they're mostly lacking context and are often rather easy to google.

I did search for hTAP, did not find any useful information

You definitely need to add some context - what sentence(s) did you see it in, and where? A Web Of Science search for hTAP in the TITLE field points to "Human thyrotropin-releasing hormone-associated peptide" but that doesn't appear to be relevant. It isn't unusual for acronyms like this to have several meanings.

I'm voting to close this question as off-topic because the question lacks any effort whatsoever.

hTAP refers to human TAP protein (reference). And how do you know that TAP refers to Transfer Associated Protein? I believe it stands for Transporter Associated with Antigen Processing (reference). Your facts are wrong which is why your question couldn't be answered.

http://www.springer.com/biomed/immunology/book/978-1-4939-1114-1
this book has TAp written as transfer associated protein

@user3237995 I don't know about the book because I don't have it but that article definitely mentions TAP as Transporter Associated with Antigen Processing in the abbreviation section. So why did you link me to it?


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How is cancer associated with host pathogen interaction?
Does cancer by any chance fall under host pathogen interaction domain? What I mean to ask is that, is there pathogen interaction involved in cancer? I went through this article:
http://en.wikipedia.org/wiki/List_of_human_diseases_associated_with_infectious_pathogens
In the cancer category they have used the phrase "can be cause" by this and this pathogen.. Isn't cancer a disease that occurs due to abnormal growth of cells due to genetic change?

No not necessarily. Cancer can also be caused by bacteria and viruses in your body

The regulation of cancerous tumor development is converged upon by multiple pathways and factors. Besides environmental factors, gastrointestinal (GI) tract cancer can be caused by chronic inflammation, which is generally induced by bacteria, viruses, and parasites. The role of these inducers in cancer development, cell differentiation and transformation, cell cycle deregulation, and in the expression of tumor-associated genes cannot be ignored.
Although Helicobacter pylori activates many oncogenic pathways, particularly those in gastric and colorectal cancers, the role of viruses in tumor development is also significant. Viruses possess significant oncogenic potential to interfere with normal cell cycle control and genome stability, stimulating the growth of deregulated cells. An increasing amount of recent data also implies the association of GI cancers with bacterial colonization and viruses.

You can read more here: Aituov, Bauyrzhan, et al. "Pathogen-driven gastrointestinal cancers: Time for a change in treatment paradigm." Infectious agents and cancer 7.1 (2012): 18.

can pathogens initiate cancer? or do they just add to the problems in human body when it is affected by cancer??

@user3237995 Did you read the paper I mentioned...the answer is in there.


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Properties that can be derived from amino acid sequences
What are the properties that can be derived from an amino acid sequence apart from those mentioned in the website? In the mentioned website, the properties that can be calculated from amino acid sequence are:
 1. Molecular weight of protein
 2. Number of amino acids in the protein sequnece
 3. Composition of charged residues (DEKHR)
 4. Composition of aliphatic residues (ILV)
 5. Composition of Aromatic residues (FHWY)
 6. Composition of Polar residues (DERKQN)
 7. Composition of Neutral residues (AGHPSTY)
 8. Composition of Hydrophobic residues (CVLIMFW)
 9. Composition of Positive charged residues (HKR)
10. Composition of Negative charged residues (DE)
11. Composition of tiny residues (ACDGST)
12. Composition of Small residues (EHILKMNPQV)
13. Composition of Large residues (FRWY)

Other than the first two, the rest of the groups seems like a list of binary sets based on specific chemical properties of the amino acids. Without any additional information, this question is too broad.

what additional information do you want. please tell me. Dont just close it. I need this question open.

What exactly do you define as a "property"? The current list is not well defined, and arguably silly examples like "Composition of residues with "E" in their name" are also "properties".

This approach (that you linked to), wherein one takes a purified protein and subjects it to amino acid analysis (or amino acid composition), dates back to a period in time from ~ 1960-1980.  Once molecular cloning was developed it became much faster to clone the gene for a protein to determine its identify rather than sequence the polypeptide itself. Around the same time a gas-phase chromatography device was coupled to a mass spectrometer and marketed commercially by Applied Biosystems, permitting so-called microsequencing of peptide fragments. BLAST is going to be way more sensitive.

Sensitive as in?

Just look at NCBI , EMBL and DDJB tools. These three are premier and global database centres. Their tools are self explanatory. You can calculate lot of things from these sequences. Besides these there are many in house tools for calculating specific information from sequences from many bioinformatics research labs across the world.

Using a helical wheel projection you can make predictions of regions that are likely to form, or adopt, amphipathic helices. These are alpha-helices where one face, or side, of the helix  is largely polar while the opposite, side, or face, of the helix is largely non-polar.
Also, based on known X-Ray crystal structures, there are some residues that are known as helix breakers, like Pro and Gly, and there are other residues that are often found in beta sheets, so you can make secondary structure predictions, based on the primary amino acid sequence.
However, in the absence of extended regions of amino acid sequence identity, these predictions are just hypotheses.

No, i don't want to predict anything, i want confirmed properties, not predictions

Good luck with that.


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Changing genetic code of E. coli to accept synthetic amino acids?
I read in my Biology textbook that an experiment has been done in which one of   E. coli's stop codon has been altered to accept a synthetic amino acid. I do not get how it can be done. Taking the fact into account that every permutation of the 4 natural nitrogenous bases codes for a particular amino acid means that if the stop codon, let's say UGA, is altered to UUA it will code for Leucine. How does this leave a possibility for the production of a codon which codes for a synthetic amino acid? I will appreciate your kind explanation. Thank you a lot.

They would use the codon UGA to code for a synthetic amino acid.

This has been done by engineering a synthetic tRNA that can recognize the stop codon. The synthetic tRNA possesses a non-natural amino acid that is processed normally by the Ribosome and incorporated into the growing polypeptide chain.

This answer was accepted; however, it is still advisable that you add references :)


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Tissue identification in vascular bundle sections
I always have trouble differentiating the tissues in a vascular bundle. I specially cannot properly identify the vascular cambium and phloem. I know xylem vessel elements are large cells with thicker cell walls, that makes them clearly different from other cells in the vascular bundle. However, the difference between vascular cambium cells and phloem cells is unclear. I would like to know how I can identify these tissues accurately. A photomicrograph with marked borders would be appreciated along with explanation of cell appearance in these tissues. Thank you a lot.

Here is a single Helianthus (sunflower) vascular bundle, complements "The" Ohio State University. The xylem in a vascular bundle is generally the easiest to discern. The phloem tissues is always exterior to the xylem and the cells are generally more uniform and smaller than most of the xylem. Picking out the phloem is also more complicated by other cell types exterior to the xylem such as the "fibers" shown here. The phloem will always be interior to the sclerenchyma or collenchyma "fibers" when they are present. That is, the phloem is always adjoining, and exterior to, the cambium.
The most difficult to precisly locate is the vascular cambium since it is very thin. Notice in the diagram below, the relatively continuous line that is being pointed to by the dashed line from the label. As you go inward toward xylem and outward toward phloem, the smoothness of trying to trace a line parallel to the vascular cambium becomes much more "bumpy" as the cells are already beginning to differentiate.

To find many more images on the web, search "vascular bundle labeled photo". You should investigate further, appearance of these bundles varies between dicots, monocots, roots, shoots and species.


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How does Vibrio cholerae benefit from infecting its host?
As far as I know, V. cholerae secretes a toxin called choleragen into the intestinal lumen which affects the intestinal epithelial cells causing release of Na+ and Cl- ions into the lumen and reducing the lumen's water potential which causes water to flow into the intestinal lumen resulting in diarrhea. How does this benefit V. cholera in any way?

Related http://biology.stackexchange.com/q/45099/3340

After V.cholerae gets into the human intestine it starts to multiply its numbers, and then becomes virulent after sufficiently expanding its numbers. This virulence drives the diarrhea which in part causes the bacteria to slough off into the intestinal lumen, and then into the external environment again.
So in short it uses the human intestine to increase cell numbers.
See work by Bonnie Bassler for a really fascinating understanding of the complexity of this infection.

How does the human intestine help V. cholera multiply? I mean, why cannot it multiply in the external environment?

@Taimur Perhaps it is better to look at this as an empty niche. If the bacteria can expand both in the intestines and in the ocean than it would be advantageous to do both. I don't believe that there is any requirement that that bacteria must infect a host in order to expand.

Okay, wait, I actually did some research and found that only humans get cholera. This means that V. cholerae secrete choleragen only to grow and escape human intestines and not of other mammals. Why so? Also, if they can grow in water bodies, why have they developed a specific human-affecting toxin and not a general mammal-affecting toxin?


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What is the name of a gene whose effect comes from the dominant and recessive alleles
The p53 gene has a mutation which results in the cell having a cancerous phenotype.  This effect is dominant as one allele being mutated is enough to result in this effect.  However when both alleles are mutated then the phenotype changes / become more pronounced so it's not a simple dominant mutation.  What is this kind of mutation called?  Is it hemi-dominant or something?

Allelic effects

What is the name of a gene whose effect [..]

The concept of dominance make sense for alleles. The gene has no name to refer to the allelic interaction.
Patterns of dominance
Patterns of dominance and recessivity are typically used for quantitative traits. Can you somehow put a a number into the phenotypes of all three genotypes? Making some kind of association table would help even if the phenotypes are not quantitative. See below.
Attempt to answer the question
It looks like you are considering a case where the phenotypes
aa -> healthy
Aa -> sick
AA -> very sick

Under this model, it is hard to tell whether you would consider sick half way through healthy and very sick or not. It feels like you want to consider sick as being closer to very sick than to healthy so if we put numbers we could get something like
aa -> 1 (healthy)
Aa -> 2 (sick)
AA -> 2.5 (very sick)

As such, A shows partial dominance (aka incomplete dominance or semi-dominance).


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What happens if nerve impulses go the wrong way?
So in nerve impulses, I get that the refractory period is important because it stops the action potentials going the wrong way along the axon. I have two questions:

What would the impact be of the action potential going the wrong way along the axon?
Are there any diseases that maybe cause the refractory period to be shortened so that the action potential goes the wrong way?

Thanks for any help!

I'll try to write up a full answer unless someone beats me to it... in the meantime, no it isn't really possible for the refractory period to be short enough for the action potential to travel in both directions. You can sort of think about it like the refractory "zone" is "chasing" the action potential down the axon. Making the refractory period shorter in time just shortens in space this refractory "zone".

(of course, if you induce an action potential artificially by using an electrical shock midway down the axon, it will travel in both directions; this has some important experimental implications but wouldn't occur otherwise in most neurons of a vertebrate nervous system)

There are some exceptions in insects and some special neurons elsewhere that have a looser definition of axons and dendrites, where signals can propagate in more than one direction, but this is part of the normal function of those circuits.

The propagation of the action potential is MUCH slower than the refractory period. The propagation speed is determined by the cable equation http://www.cnbc.cmu.edu/~bard/passive2/node9.html which is a formalism developed by Hodgkin & Huxley in the 1930s to measure signal transmission through a biological cable (e.g. an axon). The speed of the propagation is measured by a constant. The voltage does decay and thus spread in all directions, but the propagation only matters towards the direction of signal transmission. Ionic action in the soma would destroy the usefulness of transmission not down the axon. With that being said, neurites in arthropod nervous systems for instance http://stg.rutgers.edu/ can receive input and deliver output leading to very complicated patterns of waves inwards and outwards. Despite this, the stomatogastric ganglion can produce very robust and stable rhythmic neural patterns.

"The propagation of the action potential is MUCH slower than the refractory period" - is this a typo? It is very much not correct.


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X-recessive disorder pedigree confusing me

This is a pedigree of a family in which bleeder disease, an x-recessive disease, is present. I am asked which marker, A or B, the disease is linked to.
I've asked about this type of problem before: X-recessive disorders and genetic markers
The solution there was the fact that the families were unrelated so the disease being linked with a marker in one family did not correspond to the disease being linked to the same marker in another family.
The answer to this problem is "A". However this is ONE family and there are males in this family with the A marker on their only X-chromosomes who are unaffected and women with two A markers who are also unaffected. How would you explain that? They have the marker for the disease on both alleles but not the disease?

Look at my answer in this post http://biology.stackexchange.com/questions/30885/understanding-recombination-scoring-in-family-pedigrees/30887#30887. That should answer why some males can carry the A marker and not get the disease.

So I:1 is a recombinant and the sick allele is the A allele from the mom?

Your account should be closed for asking several homework questions every single day.

Remember: A and B are genetic markers that might be linked to the disease gene. Neither A nor B are actually the hemophilia disease mutation (or gene), A or B are proxies, or substitutes for the mutation in the disease gene.
Since it is an X-linked recessive, it is only the Mother's two X chromosomes that are candidates.  You can completely ignore the Father's copy of X that also happens to carry the A marker.
In the F1 generation every male who received the copy of the Mother's X marked with A died, and every male who received her X marked with B survived. Therefore her X marked with A is linked to the mutation.
Those other AA females are either heterozygotes, or outsiders who married into the family. The outsiders do not carry the mutation.
Perhaps your confusion is due in part to the fact that some key facts are not explicit in the pedigree diagram from your instructor's course materials? Try drawing the various genotypes out like this: