text:
Relation between trigeminal and facial nerve in sympathetic response
In my neuro-anatomy course notes I found that the facial nerve "uses" the trigeminal nerve to reach its targets. However, I have yet to find any diagram or reference that indicates how this is done. How is the trigeminal nerve "used" by the facial nerve?

Certain parts of the facial nerve cooperatively share structure of trigeminal nerve. For example, to reach the sublingual gland, the chorda tympani of the facial nerve joins the mandibular branch of the lingual nerve. Additionally, to reach the lacrimal gland of the eye, the greater petrosal nerve branch of the facial nerve joins the structure of the maximallary branch of the trigeminal nerve.
For a pictorial demonstration of this, please refer to page 1069 of Clinically Oriented Anatomy 7th edition by Moore.


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Do plants have preference for the form of nitrogen as nutrient?
In the nitrogen cycle (ecology), it is usually described that plants can use nitrogen in the form of ammonium (NH4+) and nitrate (NO3-). Do plants prefer one form of nitrogen over the other?

Quoting verbatim from this site. The reference is not really a scientific article but you can check the references it cites. Some were not in English so I did not check. However these points are fairly logical

Nitrates are the preferred nitrogen source:

Non-volatile: unlike ammonium, nitrate is non-volatile, so there is    no need to incorporate it in the soil when applied by top- or side dressing, which makes it a convenient source for application.
Mobile in the soil - direct uptake by the plant, highest efficiency.
Nitrates synergistically promote the uptake of cations, such as K, Ca    and Mg, while ammonium competes for the uptake with these cations.
Nitrates can be readily absorbed by the plant and do not need to    undergo any further conversion, as is the case with urea and ammonium, before plant uptake.
No acidification of the soil if all the nitrogen is applied as    nitrate-nitrogen.
Nitrates limit the uptake of harmful elements, such as chloride, into    large quantities.
The conversion of nitrates to amino acids occurs in the leaf. This    process is fuelled by solar energy, which makes it an energy-efficient process. Ammonium has to be converted into organic N compounds in the roots. This process is fuelled by carbohydrates, which are at the expense of other plant life processes, such as plant
  growth and fruit fill.

Many plants can carry out nitrification but this is not universal. From this article:

Nitrification is sometimes considered so universal and rapid that
  applications of NH4-N are considered equivalent to
  NO3-N. This is not true in many forest, orchard, and
  grassland soils.

However, nitrate being more soluble is susceptible to leaching and wash off, care has to be taken when using nitrate based fertilizers. From the previously mentioned paper:

Unlike the positively charged ammonium ion, which is relatively
  stationary because of its adsorption to organic matter or clay
  particles, the negatively charged nitrate ion is freely mobile in the
  soil solution (166). Thus, leaching and denitrification primarily
  involve a loss of NO3-N (171). Inhibition or retardation of
  nitrification of applied NH4-N can reduce nitrogen losses,
  increase efficiency of applied N, and establish a predominantly
  ammoniacal form of nitrogen available for plant uptake (105, 171,222,
  232).

@quibble Ammonium can at high concentrations even be toxic to plant (roots). This is not uncommon in aquatic peat vegetation.

source: Stack Exchange

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authors: أحمد المرادي

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Can brain cells move?
I was discussing this with my brother. I'm pretty sure I read somewhere that they can move.
Thanks
EDIT: By movement I mean long distance migration (preferably within the brain only).

If I recall correctly, there is neuronal migration during embryonic development? If you have a better wording for this, tell me so I can edit my Q. Thanks.

Do you consider the cells of a malignant brain tumor "brain cells"? Because they do move when invading the tissue.

The question is relatively broad and one should take into account that the brain not only consists of neurons, but also glial cells (supportive cells) and pre-mitotic neuronal stem cells. Furthermore, as critical fellow-scientists have indicated, developmental stage is very important, as the developing embryonic brain is very different from the adult brain.
However, after sifting through various publications, the answer to the question is actually remarkably simple: Yes, brain cells migrate.
In  the adult brain glial cells migrate in the brain (Klämbt, 2009). Glial cells are involved in a myriad of functions, but a notable example of migrating glial cells are the oligodendrocytes that migrate relative long distances to find their target axons onto which they wrap themselves to form the insulating myelin sheath (Tsai and Miller, 2002).
Neuronal stem cells migrate over long distances in response to injury (Imitola et al., 2004) and they migrate from specific stem-cell locations (e.g., hippocampus and subventricular zone) to other regions (Clarke, 2003).
Post-mitotic, but non-differentiated neurons have been shown to migrate in the adult brain in fish (Scott et al., 2012), and in mammals and non-human primates as well (Sawada et al., 2011).
Not surprisingly, glial cells, stem cells and neurons also migrate during embryonic development. Most notably, post-mitotic neurons destined to fulfill peripheral functions have to migrate over relatively long distances from the neural crest to their target locations (Neuroscience, 2nd ed, Neuronal Migration).

Great answer. Glial cells (resident, supporting cells) also include resident immune cells, such as microglia, which are related to the monocyte lineage

"oligodendrocytes ... wrap themselves to form the insulting myelin sheath" - wait, what? TIL.

Not only that, I didn't know the myelin sheath is formed by having some extra cells migrate into place. I thought they were acellular and grew from the axon?

Yep, they are definitely cellular - follow the citing link, grab any neuroscience textbook, or everyone's best pal wikipedia: http://en.wikipedia.org/wiki/Myelin. Thanks for the typo though :)

To add to Christiaan's answer, I'll mention one striking example of long-distance neuronal migration in the adult mammalian brain: the so-called Rostral Migratory Stream found in rodents, in rabbits and both the squirrel and rhesus monkey.
Neuronal precursors originating in the subventricular zone (SVZ) of the brain migrate to reach the main olfactory bulb (OB), and it's quite a distance for the small cells.

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Speciation of humans?
Since we homo sapiens (and all other species) are continuously evolving, are humans undergoing speciation based on our environment? OR has there been any difference across people that could say speciation has already happened?
PS: I am asking this question because I have recently seen a documentary in which some Chinese anthropologists claim that Chinese people are a different species altogether. Ref: Incredible human journey (Section Asia)

We are continuously evolving and a speciation could occur, but, by any definition of species that I am aware of, all populations of humans can be considered one species - generally accepted that for two to be considered different species they should not produce viable offspring (though as you alluded to in your other Q - speciation borders are hazy)

From the wiki entry: "The study initially hypothesised that the modern Chinese population evolved from Homo erectus in China but concluded that the Chinese people did in fact evolve and migrate from Africa like the rest of world's population."

Are you asking if Homo sapiens is undergoing speciation right now?

See also Does it make sense to classify all humans in a single species?

While its possible humans could speciate into two distinct groups at some point in the future, it hasn't happened recently (100 kya) and it doesn't seem to be happening now. If it were happening we would see two or more distinct populations that didn't interbreed and over time accumulated increasing differences.
These skin colors track most of the evolution we've done in the last hundred thousand years or so, and none of the people from different parts of the globe have any difficulty reproducing with any of the others. If speciation is happening it hasn't happened yet. I doubt speciation could happen given how much gene transfer there was between populations just on foot and boat, never mind planes and trains. Although, speciation does not require physical isolation to occur. See Wallace Effect and sympatric speciation. If there's enough pressure agaist hybridization, human speciation could occur. Think blue collar versus white collar worker and the disappearing middle class.
Speciation has certainly happened with humans before. Not with 'evolutionarily modern' humans, but 'evolutionarily modern' is mostly defined as 'humans since the last speciation event', so that's tautological. But Homo erectus, the neanderthals, the denisovans, et cetera(seriously, there's a lot of Homo species) were all descendants from one common ancestor.
As for the idea that Chinese people are a different species, or descended from Homo erectus? See the geneticist from the documentary who mapped out the genetics of the Chinese population. Archeological and skeletal evidence is easily blurred, but the genetics can't be explained without an out of africa theory.


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Circulating factors affecting human health/longevity
Circulating factors present in young mice have been shown to promote rejuvenation of aged mice, suggesting that tissues have inherent capabilities to regenerate, and circulating factors may be promoting/inhibiting this [1].
Specifically; supplementation of GDF11 (growth and differentiation factor 11) can reverse some effects of ageing (muscle tissue rejuvenates, and some degree of cognitive improvements) [2]; conversely circulating CCL11 impairs neurogenesis in aged mice and causes cognitive impairment [3]. GDF11 decreases with age, CCL11 increases with age.

(Image from Bitto et al 2014, [1])
These factors (well, GDF11 at least) are not as highly expressed in humans as in mice [4], so the specific mechanisms may differ.
What other circulating factors been shown to affect health or longevity? Particularly in humans, but other mouse (or 'higher' organisms, e.g. primates) experiments would be interesting too.

Bitto, A., and Kaeberlein, M., “Rejuvenation: it’s in our blood.,” Cell Metab., vol. 20, no. 1, pp. 2–4, Jul. 2014.
Sinha, M., et al, “Restoring systemic GDF11 levels reverses age-related dysfunction in mouse skeletal muscle.,” Science, vol. 344, no. 6184, pp. 649–52, May 2014.
Villeda, S., et al, “The ageing systemic milieu negatively regulates neurogenesis and cognitive function.,” Nature, vol. 477, no. 7362, pp. 90–4, Sep. 2011.
Souza, T., et al, “Proteomic identification and functional validation of activins and bone morphogenetic protein 11 as candidate novel muscle mass regulators.,” Mol. Endocrinol., vol. 22, no. 12, pp. 2689–702, Dec. 2008.

What other circulating factors been shown to affect health or longevity? Particularly in human: The study on mice is published recently. I don't think it would have been studied in humans yet.

Oxytocin
It has been shown that oxytocin signaling helps in muscle regeneration by activating MAP Kinase/ERK pathway in skeletal muscles.[1]
Oxytocin is also known to promote adult neurogenesis.[2]
Myostatin
It is a paralog of GDF and like GDF prevents hypertrophy of cardiac muscles.[3]
Leptin
Though leptin is not really connected to ageing but it regulates appetite and thereby the metabolism [4]. It may contribute indirectly to ageing by reducing food intake and preventing obesity and other metabolic syndromes.
This review summarizes different soluble small (synthetic) molecules that have potential to induce regeneration.

Thanks - did not know about oxytocin! There are other things associated with health (like IL6) but I am not sure this falls into the same category really.

@Luke well ILs indicate inflammation but I am also not sure if they will fit the functional category that you are interested in. They may indirectly affect ageing process. But they don't generally affect all cells so they may be excluded. Thyroxine may also be a possible example.


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Why does anxiety cause diarrhea or constipation?
Anxiety sometimes cause diarrhea, sometimes constipation, and sometimes both. It's interesting because it seems their underlying neurophysiology is somehow different. What are underlying physiological processes that lead to these two symptoms in anxious people? Particularly in terms of the activity of sympathetic and parasympathetic nervous system?

Do you have a citation for this claim?

Hraish is right about the relationship between emotions and gut-brain axis. Stress hormones released by the brain are responsible for the gut-brain reflexes. Anxiety is related to stress and stress hormones are released when anxiety is expressed by the individual.
Irritable bowel syndrome(IBS)  symptom-based diagnosis, which is having symptoms such as chronic abdominal pain, discomfort, bloating, alteration of bowel habits, diarrhea, constipation etc.

Irritable bowel syndrome (IBS) is a functional digestive disorder characterized by abdominal pain, bloating and altered bowel habits without any organic cause.
(Drossman 1999b; Mulak and Bonaz 2004).
In addition, stress is able to increase visceral sensitivity either at the central and/or peripheral level. (Mulak and Bonaz 2004; Larauche, et al. 2011).

Stress is enabled through the  corticotrophin-releasing factor (CRF) system (CRF, urocortins and their receptors CRF1,2), is a key factor involved in the pathophysiology of IBS.

Stress is able to modify visceral sensitivity as well as GI motility, permeability, intestinal microbiota, and immunity of the GI tract, all mechanisms that are involved in the pathophysiology of IBS. In addition, stress is able to modulate the hypothalamic pituitary adrenal (HPA) axis and the autonomic nervous system (ANS) which is the link between the gut and the CNS and an imbalance of the ANS is observed in IBS patients. The main brain areas involved in stress are the prefrontal cortex, the limbic system (e.g. the hippocampus and the amygdala) and the hypothalamus. Relations between the prefrontal cortex and the limbic system are important in the management of stress response.
  (Pellissier, et al. 2010a; Mazurak, et al. 2012)

One of the most common gut related conditions seen
  by GPs and Gastroenterologists is Irritable Bowel Syndrome (IBS), previously known as
  colitis,mucous colitis, spastic colon, and spastic bowel disease.Around 10-20% of adolescents and adults have symptoms consistent with IBS (with females twice as likely as males to report IBS symptoms).
  IBS is associated with 12 months of abdominal pain or discomfort which is (1) relieved with
  defecation; and/or (2) associated with change in stool frequency and/
  or form (i.e., constipation and/or diarrhoea). IBS is also associated with other gut-related symptoms including: bloating,nausea,and excessive gas. Non-gut related symptoms include fatigue, headaches, sleep problems,and pain conditions, such as fibromyalgia.
Individuals who experience IBS also identify that their gut problems increase doing times
  of stress.Itcan become a vicious cycle-IBS is exacerbated by stress and stress is inturn increased by symptoms of IBS.With anxiety comes increased muscle tension around the gut
  (affecting gutmotility) and activation of the flight fight response, reducing blood in the gut (this is what causes butterflies in the tummy!). These physical changes cause the
  gut-brain to send signals to the brain which in turn promote further stress and distress, most commonly in the form of anxiety.For individuals with IBS (or actually most gut conditions), the ongoing worry about their gut and unproductive patterns can be very
  debilitating. It can also be the starting point for their anxiety
  and/or depression.
  Reference

From the above definitions it is clear that anxiety and brain-gut relationships are valid and IBS is an important reason for gut related disorders when stress is been experienced by the person. Over 10-20 % of adults have symptoms related to IBS, which means a common type of disorder in the general public.

References
Stress Affects the Amygdala Activity
Anxiety and the Brain-Gut-Axis


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Native vs Immigrant plants
Is this statement applicable to any known plant/region combinations?

Plant species X, Y, and Z are truly indigenous to region R. Other "immigrant" species can be destroyed by drought or harsh weather, but these species will always be part of the region R.

(all species in question are "benign" - like wheat; please disregard climate change and other global disasters like nuclear wars).
PS. Background: I heard this statement (with specific X,Y,Z,R) attributed to a "leading botanist" (probably 20th century), but I don't really see how this can be true (my biology education ended in high school though; I am a mathematician by training).

What is your exact question?

@Chris: "Is this statement applicable to any known plant/region combinations"?

@sds You should probably edit the question to put that directly in the question itself. Also, this seems to assume the foreign plant comes from a region significantly different from R and can't kill off the native plants before bad weather kills off the foreigner. Also assumes native plants will always be able to survive extreme conditions in the region, but with climate change, the region could change beyond what native plants can handle.

@user137: this phrase is the first line of the question!

@sds Sorry, I must not have seen it, I think I was looking for a question mark.

Yes definitely, within sufficiently loose defintions of "indigenous", "immigrant" and "always", and time frame that is not too long. Isn't you questions basically "Is this statement patently false?" (too which I would respond "No").

@fileunderwater: so, as usual, "if you misspell milk 4 times, you can end up with beer". Right?


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What is Environmental Robustness? Is it different from plasticity?
Hansen (2006) in his review uses the concept of environmental robustness independently of the other concepts of robustness (at pages 139 and 140) without defining it.
How is the term environmental robustness usually defined?
The concept of robustness (aka genetic robustness) can be further decoupled into mutational robustness, developmental robustness and maybe some others. I think envirnmental robustness is one of these sub-categories of (genetic) robustness.
Intuitively, I understand environmental robustness as something that is very close to plasticity in the broad sense. What I call plasticity in the broad sense is any phenotypic response to an environment whether or not the response is adaptive or not. Therefore, plasticity in the broad sense is adaptive plasticity + non-adaptive plasticity. I would intuitively think that a genotype is environmentally robust if the phenotype it produces varies little with environment, that is if this genotype has low plasticity (in the broad sense). Am I using a more or less standard definition of environmental robustness?

I think robustness and plasticity are different concepts, although related to each other.
I would define plasticity as the property of a system to adapt to external changes. As defined in the wikipedia page for phenotypic plasticity:

Phenotypic plasticity is the ability of an organism to change its phenotype in response to changes in the environment.

I think this definition agrees with the one in your question.
Robustness in biological systems, however, is defined as (wikipedia article):

Robustness of a biological system (also called biological or genetic robustness) is the persistence of a certain characteristic or trait in a system under perturbations or conditions of uncertainty.

From this article three references are cited, all of which give some definition of robustness in their introductions/abstracts:
Felix and Wagner (Heredity 2008):

Robustness, the persistence of an organismal trait under perturbations, is a ubiquitous property of complex living systems.

Kitano (Nature Reviews Genetics 2004):

Robustness is a property that allows a system to maintain its functions despite external and internal perturbations.

Stelling et al. (Cell 2004):

Robustness, the ability to maintain performance in the face of perturbations and uncertainty, is a long-recognized key property of living systems.

All these definitions imply that robustness is the ability to remain unperturbed under external or environmental perturbations. In a sense this looks like the opposite to plasticity, which is the ability to change under external perturbations. Personally, I think that robustness is accomplished because biological plasticity allows organisms to compensate (with some limits) the external perturbation in order to maintain their state.

This is sort of how I understand Hansen as well. The problem here is that robust is a rather vague word, similar to the observation by Pimm (1991) that ecologists had been using stability in at least five different ways when discussing population and community stability (he mentions: mathematical stability, resilience, persistence, resistance, variability)

@ddiez Thanks for your answer. The concept of (genetic) robustness is further decoupled into subconcepts that are mutational robustness, developmental robustness and environmental robustness (and maybe some others). My question is about environmental robustness. I don't think Hansen meant genetic robustness when saying environmental robustness, but I think he rather meant some subset of robustness. I might be wrong though. I'll edit my question to clarify my understanding of the subconcepts of robustness.

@fileunderwater completely agree robustness is defined in a vague way. I think we all understand the concept, but how to quantify it? For example, it makes sense to imagine some system to be more robust than another to perturbations, but for me there is no clear way to measure it.

@Remi.b thank you for showing us Hansen's review- looks interesting. I will read it (only skimmed over it a bit) and think a bit more about your comments (and maybe modify my answer accordingly). I think the source of confusion is, as fileunderwater mentioned, that usually the term is just vaguely defined.

I am just summarizing ddiez's answer with a small addition.
Robustness is the ability of the system to maintain its steady state or at the very least qualitative nature of the steady state with minor changes in the parameters of the system.
This is different from stability which actually means the ability of the system to return to its steady state when it is slightly displaced from there. A stable system will reach the steady state irrespective of the initial condition. In multistable systems the state where the system eventually converges, will depend on the initial condition.
So stability is meant in the sense of perturbation in the state and robustness, of perturbation in the system parameters.
So, if you have a model and you do a random sampling of parameters drawn from a uniform distribution of lets say ±2×mean, you will end up with a many sets of parameters with fluctuations from the mean values. Now, if you solve for the steady state at each parameter value you will get a distribution. Less the variance of this distribution, more robust is the system (based on the model).
We had discussed plasticity in this post. Plasticity may be in a way synonymous with adaptive; if a system takes an input and gives an output then how plastic a system is can be defined as how fast or easily does a system reach the new steady state. In this case the input is a parameter of the model and only that is changed.
If I put these concepts in the perspective of an organism's metabolism then:

Robustness would refer to how (in)sensitive the metabolic flux is to the minor changes in rates of different reactions (by changes in the enzyme structures perhaps).
Stability would refer to whether the system gets back (or how fast it gets back) to its original state if you add some extra or remove a metabolite.
Plasticity would refer to how fast would the system adapt or reach the new steady state when there is a change of diet/available nutrients.

Having said that I also feel, as fileunderwater said, that definitions are not universal and different people mean different things. Mathematically speaking environment is  an extrinsic parameter i.e. Input. Environmental robustness should mean the maintenance of the steady state response to changes in the input. This makes sense for example in the case of maintenance of body temperature in homeotherms. Environmental plasticity is also important in certain situations.

thanks for your answer. I copy-paste here the comment I made to ddiez "The concept of (genetic) robustness is further decoupled into subconcepts that are mutational robustness, developmental robustness and environmental robustness (and maybe some others). My question is about environmental robustness. I don't think Hansen meant genetic robustness when saying environmental robustness, but I think he rather meant some subset of robustness. I might be wrong though. I'll edit my question to clarify my understanding of the subconcepts of robustness."

Also, it is a bit counter-intuitive to me to define plasticity as the speed at which phenotypic changes occur, rather than the magnitude of the change or the range of environment toward which phenotypic response occurs.

@Remi.b Not really the speed but response time is one way of quantifying a plastic response. How quickly you adjust is important. The magnitude of the perturbation cannot be controlled by the system and you would want to adjust to the new environment without making a great change in your system composition. So magnitude of change has to be minimized and response time too. I think you can define all subsets of robustness depending on what kinds of parameters you perturb.


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Why not use non-visual self-recognition to test for consciousness in an organism?
Background
A well-known test for consciousness in an organism is to observe its ability to recognise itself in a mirror (see wikipedia article: "Mirror test").
Question
Why haven't I come across a "non-visual" mirror test? I.e. one that involves one of the other senses?
For example, how about testing for consciousness in bats by using an "audio mirror", the premise being that perhaps bats may recognise themselves through echolocation?

(image adapted from here)

There are many ways to test higher brain function in animals. The mirror test is by no means robust. Hopefully some questions will touch on this.

Reading the page you linked, I found this

MSR test may be of limited value when applied to species that
  primarily use senses other than vision. For example, dogs mainly use
  olfaction and audition; vision is used only third. It is suggested
  this is why dogs fail the MSR test. (With this in mind, the biologist
  Marc Bekoff developed a scent-based paradigm using dog urine to test
  self-recognition in canines.[19][41] He tested his own dog, but his
  results were inconclusive.[42])

Emphasis mine.
19 Archer, John (1992). Ethology and Human Development. Rowman & Littlefield. ISBN 0-389-20996-1.
41 Stanley Coren. How Dogs Think. ISBN 0-7432-2232-6.
42 http://www.psychologytoday.com/blog/canine-corner/201107/does-my-dog-recognize-himself-in-mirror

Here are my thoughts.

An animal does not chose to emit some light while they have more control over other signals they emit and may likely just not emit it. So it would not be an easy trait to study.
More importantly, animals (almost) always receive feedback for signals they emit. When a dog barks, it can hear itself! Animals are not used to receive feedback of their appearance through a mirror and therefore they cannot evolve to respond adaptively to the signal they emitted. Any adaptive response to a new signal is either due to luck or to cognitive abilities. The advantage of the (visual) mirror is that it is uncommon and their response therefore necessarily reflects cognitive abilities. Typically, if a bat can response to the sound it produces, it doesn't mean it is able of self consciousness (Theory of Mind), it just mean that bats evolved to recognize the sound they produce.

It's got to be because optical mirrors are relatively easy to produce and field, and it's obvious that it presents a duplicate.
I would be interested in designs for a 'sound mirror' that doesn't just look like a wall under echolocation. Maybe a system to dynamically reproduce a 'sound hologram' of the bat?
A 'scent mirror' would be really difficult to build, not to mention 'ability to recognize your own smell' doesn't really imply higher brain function. Perhaps storing urine from dogs in estrus or stress or something to see if their own scents provoke behavior changes as if it was another dog?
A 'touch mirror'? A 'taste mirror'?
Nearly everything can see, and mirrors are way easier than the alternatives.

I mean a scent 'mirror' using urine from other parts of the female estrus cycle for instance might be interesting, but 'it's really hard and/or redundant' covers your question.

Most animals can see, but not all use sight as the primary way to recognize individuals.  For instance, a person with visual agnosia might conceivably be able to "see" but still fail the mirror test.


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Use cases of RNA secondary structure prediction
I'm an undergraduate currently writing a thesis on RNA secondary structure prediction, specifically building upon analysis done by the RNAStructure and Unafold software packages by modifying certain algorithms here and there. I'm actually not a biologist, however. I've taken all of my classes in physics and computer science, and I sort of stumbled into my current research, and since it seemed to be a good fit for my skill set I stuck with it. However this leaves me curious of a motivation for my current work. Why is RNA secondary structure prediction important and what are some of its applications?

RNA-protein interactions?

Our lab has a very particular goal of increasing the amount of double strandedness in RNA so we can intercalate stuff in it more efficiently. Being able to calculate amount of double strandedness under physiological conditions would be nice.

This question is actually a little broad. There are several interactions that RNA has because of its structure. This is because unlike genomic DNA, RNA is single stranded and can thus form different kinds of secondary structures. Common structural motifs include hairpins, pseudoknots, triplex and quadruplex. One can write a huge review on this.

Anyone who's taken introductory biochem has been beaten to death with this phrase: structure is important for function. Usually they're talking about proteins but it really applies to everything.

@WYSIWYG I don't think broadness is a problem here. A detailed review of structural elements is not required for an answer, just an explanation why RNA secondary structure is important to know (and to some degree why RNA is important).

I tend to agree that it is too broad as defined by the rules of this site but it seems like somewhat of a technicality. I'd hate for it to be closed since it is quite interesting so I've edited it slightly to hopefully keep it open.

Short answer
I can think of at least a dozen applications for which it would be useful to know the secondary structure of a given sequence of RNA off of the top of my head. In no particular order:

Simulation/visualization of RNA
Riboswitches
MicroRNA
RNA interference (RNAi)
RNA-RNA interactions
RNA-DNA interactions
RNA-protein interactions
Ribosomal protein expression
Ribozymes
Forced evolution of RNA aptamers
Synthetic tRNAs with four and five base-pair codons
Termination of transcription (the process that makes mRNA from DNA)

Basically anything to do with RNA, which is one of the fundamental building blocks of all living creatures.
More in-depth
Simulation/visualization of RNA
Secondary structure (2°) forms the second (yep) level in the standard 4 level hierarchy of macromolecular structure, and consists of short-range interactions between and among residues. In RNA, 2° is usually thought of as being loosely identical with base-pairing interactions. In order to do a proper simulation/visualization you'll probably also need at least the 3° information, but 2° is important too.
Riboswitches
As an mRNA gets translated by a ribosome, in many cases it can form into a complex 3D structure that will affect the translation process. For example, some of the mRNAs that encode proteins related to the metabolism of metal ions have a riboswitch that will themselves bind to metal ions and inhibit/upregulate expression of the related protein. For various reasons it's usually extremely difficult to get the full 3D structure of a riboswitch, so getting to know the 2° remains an important source of information about them.

Huh, where did you get the idea that it is impossible to get the full 3D structure of a riboswitch? There are structures published for most of the known classes of riboswitches.

@MadScientist citation, please? (good sir, etc)

http://www.rcsb.org/pdb/101/motm.do?momID=130

Another thing, you mention only mRNA translation. Riboswitches can act at transcription or translation, transcriptional riboswitches typically terminate the transcription early to regulate, translational riboswitches typically sequester the Shine-Dalgarno sequence to regulate expression.

Knowing the secondary structure of nucleic acids is very useful in many cases when working with them. The simplest case, and probably the most often used case is when you order or synthesize a small RNA or DNA and actually don't want this to have any stable secondary structure. There are many methods where you use a small nucleic acid that can bind to a complementary part of another nucleic acid (hybridization).
For example in PCR, which is used to amplify small amounts of DNA, you use small DNAs called primers that bind to specific parts of a larger DNA template. If those primers can form stable secondary structures by themselves, those structures would have to be broken up before the primer can bind to the template. Such competing structures can drastically reduce the efficiency of such experiments and are something that people try to avoid, e.g. by predicting secondary structures before choosing primers.
There are also methods that use short nucleic acids with attached labels such as fluorophores. Those labeled probes bind to specific target sequences, and you can then e.g. determine with a microscope where those probes are bound. In all such techniques you don't really want secondary structures in your probes as they interfere with the binding to the actual target.
When RNA is introduced first, it is often said to be single-stranded and secondary structure is not even mentioned. But even when acting as messenger RNA, secondary structure of RNA does play a role. One mechanism for transcription termination works by forming a stem-loop within a certain range of stability, and predicting those is necessary to predict the site where transcription is terminated.
There are also many types of regulatory RNAs, this is a very active and hot topic at the moment. The most well known are probably RNA interference (siRNA and miRNA), but there are also many ribozymes and especially in bacteria also riboswitches. I won't try to list the different types of regulatory RNAs here, there is a large number of different classes that are known, and new ones are still discovered. To understand those it is often necessary to know the secondary or tertiary structure of the RNAs.
You can often at least create some hypotheses on how an RNA could work by looking at the secondary structure. In riboswitches for example you typically have an on- and an off-conformation, and those can often be explained by secondary structures.
While the secondary structure is often not enough to understand how a specific RNA works, you still start by predicting it in most cases. In many cases you would additionally use experimental data to verify the prediction (e.g. SHAPE or inline probing).
Determining the actual three-dimensional structure of RNA is pretty hard. How hard depends heavily on the exact RNA, but it can easily take years to do this. If you're lucky you can crystallize it easily, but RNAs with flexible parts tend to not crystallize well. In that case you can do NMR to determine the structure, but that has a rather severe size-limitation and can easily take years for larger RNAs.
In case of NMR, knowing the secondary structure is very useful in pretty much every case. You need to assign your signals to specific bases, and this is much easier if you know the secondary structure. You can also use NMR to support or disprove specific secondary structure predictions.
More reliable secondary structure prediction would be pretty nice, the current methods still fail often enough. Though there is probably a limit on how good you can get such methods for RNAs with extensive tertiary structure.


text:
How could be the "Eurasian magpie" bird won the "Mirror Test" where Gorillas failed
EURASIAN MAGPIE VS GORILLA
 VS
How could be the "Eurasian magpie" bird won the "Mirror Test" where Gorillas failed ?

In 1982, mirror tests on two, zoo-reared gorillas failed to demonstrate self-recognition. The authors wrote "[These studies]...suggest that the gorilla may be the only great ape which lacks the conceptual ability necessary for self-recognition." In 1993, a report was published that although six gorillas had previously failed to exhibit self-recognition.
The Eurasian magpie is the only bird to pass the mirror test. Researchers applied a small red, yellow or black sticker to the throat of five Eurasian magpies where they could be seen by the bird only by using a mirror. The birds were then given a mirror. The feel of the sticker on their throats did not seem to alarm the magpies, however, when the birds with colored stickers caught a glimpse of themselves in the mirror, they scratched at their throats - a clear indication that they recognized the image in the mirror as their own. Those that received a black sticker, invisible against the black neck feathers, did not react.
Reference

Birds lacks neocortex, the area where self-recognition was thought to reside. Then which part of the brain do birds like Magpies uses to process these complex cognition ?
Why do Gorillas failed the mirror test ?

Pigeons have also been shown to be self-aware
[1]: http://www.robertlanza.com/files/SCIENCE_Self-Awareness_in_the_Pigeon.pdf

I think the mirror test is not a reflection of overall intelligence. It is one of many ways to reflect cognitive properties what we think makes us human onto animals.

@ChrisStronks Neat!  However, as the authors state, "We have demonstrated that a pigeon can use a mirror to locate an object on its body which it cannot see directly.  We should not attribute this, however, to a pigeon's 'self-awareness' or claim that a pigeon has a 'self-concept.'"

Identifying oneself from a reflection needs relative comparison of particular movements and gestures from the image and thyself. Identifying from the mirror reflection is not always attributed to self awareness or overall intelligence, but there is still a complex mechanism working behind to enable this feature. The question mostly regards why gorilla(being a primate) failed and magpie(being a bird)achieved.

I think this website provides a pretty surprisingly thorough breakdown of avian brain anatomy, including historical contexts and debate around what exactly is homologous and what is not, and whether 'homologous' is a useful bit of information.
In short: It was thought until recently that the bird brain was just the core of the mammal brain with some layers peeled off, but it turns out to be more like a scale model, with many of the same parts. Roughly. Sort of.
So birds do not technically have a neocortex. They have a structure that looks like a neocortex, but it also looks like some other things. Gorillas do have a prefrontal cortex etc (even if they are smaller than in humans). The knowledge that structure X performs function Y in an organism generally implies little about a second organism, with or without structure X. Even features like 'wings are for flying' and 'fins are for swimming' have exceptions.

Nice answer (+1) - could you perhaps summarise the detail on the webpage you linked too?

Uh. Is the second paragraph deficient in some way? I've tried to summarize the salient points to this discussion.

The second paragraph summarises the general message of the site linked, but it would be good to expand on the detail of the first paragraph (partly in case the link ever goes dead, that would make the answer obsolete).


text:
Statistical method for characterizing the relationship between body mass and metabolic rate
There is a dataset that contains body mass ($x$) and metabolic rate ($y$) from many different organisms. It is common to fit the data to the model of the form $y=ax^b$ and estimate the parameters $a$ and $b$ (see Kleiber's law and The Metabolic theory of ecology). In doing so, it is also common to log transform $y$ and $x$ and create the linear relationship log($y$)=log($a$)+$b$log($x$) and perform linear regression analysis based on the log transformed data. Is this approach better than directly estimating $a$ and $b$ based on nonlinear regression for $y=ax^b$ (because results are different)?

This is more a statistics than biology question, but before choosing a statistical test it is essential to visually inspect your raw data. Is your data skewed at all? BMI in the normal population already has a Gaussian distribution, and I expect metabolic rate also would - so unless you have a reason to log-transform I would not do this. For me there is nothing wrong with performing a linear regression to test the linear association between these traits, and then also test for any non-linear effects (perhaps by including an interaction term between them).

Are you saying that you've tried both and that the results are different (more than the margin of error from the different methods would suggest)? There shouldn't be a difference, as long as the relationship is linear on a log-log scale, beside the uncertainly that lies in the different estimation proceedures (traditionally, a linear regression has been easier to perform)

When you have a nonlinear curve then you should do a non-linear regression and correlation analysis. You can interpolate an exponential function. People are often more comfortable with linear analysis and that is the reason the curve is plotted in a log scale.

Yes, estimated parameters are different in important ways (not negligible numerical errors). I think this is a biology question but am not sure. I am asking analyzing the data based on minimizing the sum of squares (regardless of linearized or nonlinear models). I think the question is in what (biological) space we want to minimize the sum of squares, which depends on, perhaps, the biological understanding of the metabolic theory, which I don't have.

One thing I can think of is that between-individual variation in metabolic rate would be larger for large (mass) individuals. Taking log will stabilize the variance. This kind of explanation is more of statistics than biology. However, this does not happen all the time, especially when we are studying a single species.

I would post this question to the statistics group on StackExchange (Cross Validated) under the "regression" tag.  Dr. Frank Harrell, Professor of Biostatistics and Internationally Recognized leader in regression modeling is on that community. He's a phenomenal teacher and would easily be able to compare and contrast the statistical pitfalls of linear vs. nonlinear regression for that type of problem.

Short answer: The results of the two approaches (linear versus non-linear model) do not match because the relationship between body mass and basal metabolic rate does not strictly follow a power law.

It is indeed the case that if the relationship between two variables follows a power law the two approaches should provide comparable results, but important differences could arise due to Jensen's inequality. In order to test whether the reported differences between the two approaches are due to Jensen's inequality or to some biological factor I obtained data from Kolokotrones et al. (2010) who have in turn taken them from McNab (2008). Kolokotrones et al. (2010) investigated the issue of whether a power law is appropriate by performing linear regression on log-transformed data but they did not attempt to fit the data with non-linear regression.
I've fitted a non-linear model of the form:
$$ B = \alpha M^b$$ , where $M$ the body mass (in grams) and $B$ the basal metabolic rate (in Watts),
which gave coefficients $\alpha = 0.005$ and $b = 0.87$.
I also fitted a linear model of the form:
$$ log_{10}(B) = blog_{10}(M) + log_{10}(\alpha) $$
which gave coefficients $ \alpha = -1.7 $ and $ b = 0.72 $.
It appears that the results of the two approaches are indeed different. Below I plot the results of the two fits. On the variables' original scale we see that the linear model fails to predict observations from species with large mass and that the non-linear model does much better in this respect (upper left). However, when we look at the two models after log-transform, it is clear that the non-linear model fails to predict many observations from species with low mass (upper right). Looking at the residuals of the non-linear model we see that the errors are multiplicative as the variance of the residuals is increasing with (log-transformed) fitted values (bottom left). This indicates that fitting with a linear model on log-transformed data is warranted. However, the plot of linear model's residuals over log-transformed fitted values (bottom right) confirms that the linearity assumption is violated. Thus, neither method is appropriate for this dataset and the quadratic term the authors of the cited paper added in the linear model fitted on the log-transformed variables appears to be warranted in order to account for the observed convexity.

We can conclude that for this dataset the results of the linear model approach do not match those of the non-linear model approach because the data do not strictly follow a power law. Rather, the megafauna appears to follow a different trend compared to smaller animals. Kolokotrones et al. (2010) found that adjusting for temperature improved the linear fit, in addition to the inclusion of the quadratic term. The resulting model was:
$$ log_{10}B = \beta_0 + \beta_1log_{10}M + \beta_2(log_{10}M)^2 + \frac{\beta_T}{T} + \epsilon $$

The R code used to generate the results for this answer along with the data used can be found in the following git repository in GitLab:
https://gitlab.com/vkehayas-public/metabolic_scaling
 References
Kolokotrones, T., Van Savage, Deeds, E. J., & Fontana, W. (2010).
Curvature in metabolic scaling. Nature, 464:7289, 753–756. https://doi.org/10.1038/nature08920
McNab, B.K. (2008). An analysis of the factors that influence the level and scaling of mammalian BMR. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 151:1, 5-28. https://doi.org/10.1016/j.cbpa.2008.05.008.

What will happen during log-conversion is that the large scale variation that happens in data points with high value will be compressed. This will actually produce an estimate that should be more robust toward outliers (because their deviation from the mean will be compressed).
If the data was perfectly modeled (i.e. no or few errors) then it should not matter.
With that said, I don't expect major differences between the two approaches.


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Balanced vs Maximized Codon Optimization
I have worked with the optimization of several viral proteins, from different viruses/families, with different results.
When Menzella, 2011 was published I tried that method.  I found quite the contrary result, in that randomization did far poorer than straight maximization of codon usage.  I chucked this up to working within the context of viral infection (though it was also true in transient expression from plasmid transfection under CMV promotion).
I was quite excited by Pechmann and Frydman's Nature article which highlighted the importance of the location of the codon within the protein when regarding optimal vs suboptimal codon selection. Oddly enough we were able to deploy this information most successfully with the purposeful deoptimization of a protein.
Pairing a locational awareness, screening for secondary structure, and then maximizing codon optimization has had the best results for more than a year.  By maximization, I mean choosing the most optimal codon in every instance that doesn't violate:

Needed restriction sites
Predicated Secondary Structure
Location gradient to a lesser extent (ibid.)

This is all well and good, but we've been having problems with my institutions preferred vendor for gene synthesis.  A post-doc that just joined my lab recommended a company I had never heard of before, and they posed an optimization strategy I had never considered before.  Instead of maximizing codon optimization, they propose a "balanced" codon optimization that matches the normal distribution of codons in the target organism.
For example, the codon bias for alanine in humans breaks down (roughly) as follows:

GCC 65%
GCT 20%
GCA 11%
GCG 4%

As opposed to a maximization strategy which would seek to use "GCC" when ever possible and only when there was an issue switch to "GCT," the balanced stratgy would seek to replicate the above distribution as closely as possible.
Has anyone tried a balanced codon approach, especially when compared to a maximization technique?  My overall goal is to maximize expression of naturally poorly expressing protein.  I know that straight maximization can occasionally lead to poor expression for a variety of reasons (often fatal secondary structure), but this seems like it would hardly increase expression at all.
I would be further interested if anyone else had experience within a viral context.
I know that there have been a few related questions, mostly in the context of E. Coli.  I don't think this is a duplicate, but would be willing to remove if it is seen as such.  If I run into some extra funds I may test this empirically, but often when I'm trying such a test it's only in relation to 2-3 proteins, which might not be representative.

Do you want to control the protein synthesis rate? Something like you do not want it to be produced too fast because of folding issues? This article summarizes different mathematical models for translation. You can obtain optimal codon usage by fixing the synthesis rate.

This paper talks about codon usage and virus-host interactions. Is it what you are interested in ?

@WYSIWYG I want to maximize protein expression in a human cell line.  While I appreciate David's work, that's not what really is at play here. The empirical observation from the theories leaves more complex modeling to be done. I am mostly interested in the bold question, perhaps I included too much background.

I suppose I mention Menzella solely as an example of what makes me weary to try something different.  If I can reasonable suspect that it will end in failure, I'd just as soon not waste time or funds on it.

I suspect that this maximization and balanced codon usage will depend on your protein; there would be some optimal rate of synthesis at which it will fold properly. IMHO there cannot be a generalized model unless folding dynamics can be predicted solely based on sequence (which is very difficult).

@WYSIWYG I remain unconvinced that the rate limiting factor in many cases is the protein folding, but rather tRNA availability plays a much bigger role in production. Particularly considering time scales involved in active infection (let's say less than 48h as a high limit).

Well. You would want to use sub-optimal codon usage only if you would have folding issues. Correct me here if I am wrong. Else you should go for the maxima of codon usage (which is basically obtained from tRNA availability).

Codon usage optimization is still pretty much heurestic. The most common factor we think are important in E. Coli are:

optimization to highly expressed genes, i.e. maximization of codon adaptation index http://www.ncbi.nlm.nih.gov/pubmed/19359587/
keeping the optimal GC content http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0107319
not introducing motifs that are somehow detrimental, e.g. restriction enzymes, or some dinucleotides http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0056642
adapting to available tRNA http://www.plosone.org/article/info:doi/10.1371/journal.pone.0007002
minimizing folding energy (in the first ca. 30 codons) and minimizing the amount of hairpins at the 5' end http://www.sciencedirect.com/science/article/pii/S0014579305010719
optimization of 'codon context' e.g. dicodons but also using nonoptimal codons between secondary structure for more accurate folding http://www.ncbi.nlm.nih.gov/pubmed/15772378
optimization of codon balance and also maybe the introduction of a 'ramp of slow codons' in the beginning of a gene to avoid 'traffic jams' of ribosomes later on. http://www.ncbi.nlm.nih.gov/pubmed/20403329

Most probably it's a mixture of all of those.
Disclaimer: We are working on a codon optimization strategy for e.coli/yeast/hela and it works in e. coli but is yet untested in human cells. If you want to take a long shot just shoot me a message and we could try it. Apart from this, I would also offer you to have a look at your sequence and see if there is anything 'strange' from the codon usage point of view and what I think what be the best optimization strategy.

It would be great if you provided some references to support your response!

Thanks for the answer. Small editing note, you included the "]" in several of the links (I could change it for you, but as new user you might want the practice).  Looking at references, none seem to be advocating matching the levels found in the host (even if it's E. Coli).  As far as the sequences, we're making about 14 or so different strains of a poly-protein, so that's probably not practical.

@Atl LED, thanks! Just wanted to get the answers out before christmas since I thought it might be time critical for you. I will change the formatting and will look for the mentioned reference as soon as possbile.

In a side-by-side comparison of 3 viral proteins (2 from paramyxoviridae, 1 from caliciviridae) each with both a "maximizing" and "matched" codon bias, we found the "maximized" version produced more protein the "matched" version in each instance.  Protein levels were quantified via Western and flow, cell lines tested were 293T, HEp2 (HeLa contaminate), and Vero.
This is certainly not wide enough testing for any kind of general statement, it's just what we found.  I think this will take a cell bio or pure micro-bio lab to fully study.  We're in infectious diseases, and this question would be off grant and off topic for the paper.  If we can find a way to squeeze it into a publication we will.
I'm going to accept Jan's answer because it contains more information on optimization, but with this answer in place to:

Address what we observed.
Note that Jan's doesn't offer any information on "matching" the codon bias of the target host (other than perhaps noting optimization is heuristic).


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STRING ID - allelic differences and splice variants
STRING has protein (amino acid sequences) mapped to a single gene ID.
I have these doubts with respect to STRING ID.
I find that

1.All alleles of a single gene share the same STRING ID and
2.Especially in Eukaryotes, splice variants of the single gene(which might translate to different proteins) share the same STRING ID.

Does STRING take into account these two things like UniProt and have different IDs based on allelic differences and splice variants?If so,how?

At this moment the STRING database is not accessible. Can you give an example?

Rvxxxx is a gene id.

STRING uses only gene ID to map protein sequences

STRING is now working.Another example STRING ID:4932.Q0010 (Saccharomyces cerevisiae) AA sequence:MYYIMFLYNMLLIIILIFYSIVGVPIIIFNNNYYWDPDIFLFIIYYFIKFIIIFNLYLYYMINYIVYTPSGSPPGRGTYI LLYNMLYSYNMFIDYVMKFITCVTYMYLMFWLLSPTPSPYYVSEVPVS

please don't use (non-biological) acronyms such as w.r.t - it makes things unnecessarily hard to read (http://meta.biology.stackexchange.com/questions/104/use-of-abbreviations-and-acronyms-in-answers)

okay changed it.

STRING does not distinguish between different products of the same gene. E.g. for human, the protein identifier you see (ENSP...) corresponds to the longest splice form for each gene (ENSG...). Therefore, STRING won't help you if you need to distinguish between splice forms.
Splice forms are merged because for most sources of evidence, there is little data for the interactions of individual splice forms.

What about allelic differences?

we also don't distinguish alleles at all, we don't even retrieve them from Ensembl


text:
What specific sensory nerves act as receptors for "pins and needles" (neuropathy)?
According to this excellent answer, the difference between "pain" and "pins and needles" (neuropathy) is that different receptors (sensory nerves) trigger in reaction to different stimuli.
Different types of pain receptors (hot/cold, pressure, etc.) send pain signals to the brain.
Different receptors are responsible for sending neuropathy signals to the brain. These receptors are usually triggered when the nerve receives a shortage of blood flow.
According to the Wikipedia Article on Sensory Receptors, there don't appear to be any nerves that produce pins-and-needles sensations to the brain...
So I ask: What are the specific types of nerves/receptors that send "pins and needles" signals to the brain? What are they called?
I would imagine that it either has to be a specific, specialized receptor that (perhaps) starts firing if its senses "something is wrong" (such as decreased bloodflow to the area, etc.), or it's that all sensory receptors are capable of firing "pins and needles" signals under special circumstances.

Pain is an active neural response (nociceptive pathways). Neuropathy is a neural dysfunction. Where is the confusion?

Thanks @WYSIWYG (I'd upvote you if I had the rep to do so) - You are correct: neuropathhy is neural dysfunction, however, you cannot deny that pins-and-needles does in fact register with the brain as a sensation, otherwise we would never know about it (that our nerves weren't functioning correctly)! So clearly, neuropathy communicates to the brain via signals. Clearly, so does pain. Pain feels different than pins-and-needles. I want to know why.

Are you specifically asking about neuralgia and general pain. Pins and needles dont feel painful.

Thanks @WYSIWYG - I feel like perhaps you're either not reading my question carefully, or you're reading too much into it. I am asking: why do pins-and-needles feel different than pain? And I'm looking for a biological/physiological explanation, not something high-level and lofty that a monkey would understand.

Well.. okay.. I didnt get why you were comparing the both. You should see this post. This one too.

Thanks again @WYSIWYG - so the first post you referenced has one of those high-level, lofty answers that I don't want ("The feeling you describe is called "paresthesia," and ... it happens "when sustained pressure is placed on a nerve."). The second post you referenced almost hits the nail on the head, but still falls short in the specific thing I'm looking for...(continued in next comment)

In that 2nd post, the accepted answer states that pain receptors send one kind of signal to the brain, which interprets those signals as pain, whereas other sensors send different signals to the brain, which the brain interprets as pins-and-needles. So to me this implies that the difference is the kind of sensory nerves that are firing. I'm asking: what are the sensory nerves that send pain, and what are the sensory nerves that send "pins and needles" signals?

Pins-and-needles (PAN) sensation and pain stem from the same nerves. The pathophysiologic process is different, though. PAN is characteristic of nerve lesion, and is therefore a pathologic reaction. Pain is a physiologic reaction to a stimulus perceived as ominous.
Pathophysiologically speaking, the PAN sensation is a distortion in somatosensory stimulus processing due to injury to peripheral nerves.
Of course, the PAN sensation will stem from somatosensory nerves. Pure motor nerves will not cause such a sensation.


text:
Would humans eventually evolve to fight off fatal diseases if we didn't treat/vaccinate for them?
I am definitely pro vaccination, and the question is a bit morbid because people would die, but assuming that we didn't treat or vaccinate people for fatal diseases such as Ebola or the black death, would the surviving people pass along a trait that eventually would lead to near immunity for that disease?
Are there any examples of diseases that humans "contract" but they are immune to? Or any examples of immunity through human evolution?
What about in animals? Are there diseases that have been naturally eradicated?

Sure.
When the Europeans settled the Americas, 90%+ of the native American inhabitants were wiped out due to diseases like smallpox that the Europeans clearly had developed resistance to. Clearly, the surviving native americans had resistance, and the Europeans had gone through some similar event previously in history.
The bubonic plague that was the cause behind the black death wiped out large percentages of populations, but selected for survivors with resistance:
Black Death Left a Mark on Human Genome
Caveats:

Often evolving to fight off disease involves mass death, like with >90% of the native american population dying.
There is always the chance that a future pandemic can come that human biology fails to simply evolve a resistance for and gets wiped out.
The Earth is changing rather quickly. The past is not a guarantee for the future.

There is no resistance against small pox. The disease disappeared with vaccinations, not before. This is slightly different for the pest of the middle ages, but still there is not widespread resistance against the pest. Can you please add some references for your small pox claim?

Why else did small pox cause such a higher incidence of death among native indians? A quick google doesn't answer that question, but I just presumed it was enhanced resistance, and I can't think of any other reasons. Europeans didn't have complete immunity of course, but simply more resistance.

Do you have a source that it was only small pox? There are a number of other diseases (including flu, measles and so on) which got transferred there.


text:
Do distinctions between dry, tickly and chesty coughs have any medical basis?
Background
At least in Britain you normally come across distinct kinds of cough medicine "chesty", "dry" and "tickly".

Questions

Are "chesty", "dry" and "tickly" coughs always due to microoganisms?
For the types of cough that are infectious, are differences due to different species of micro-organism or the same micro-organism at different stages of its development?
Do the alternative treatments (e.g. levomenthol, squill, liquorice for chesty vs. glycerol for dry/tickly) merely deal with symptoms or do they actually help fight the infection?

Related
A related question is: What is the cause of dry cough?

Cough need not be essentially because of microorganisms. It is basically because of airway irritation.

@WYSIWYG Thank you for pointing out that glaring hole, adjusted

I'm not sure what a tickly cough feels like, so I'll leave the answer to someone else. A dry cough produces no mucus, so the lungs are irritated but there's no extra mucus in the upper branches of the lungs. A chesty or wet cough implies both irritation(you're coughing) and extra mucus production. All three are immune responses. As far as treatment goes, blanket anti-cough medicines don't help fight the infection, but deal with symptoms. Expectorants make coughs wetter which help them clear, others just reduce the cough reflex, etc.

If I may add to what Resonating has said, when it comes to infections, dry cough is usually associated with a viral infection, whereas wet cough is usually caused by bacteria. The two are treated very differently - dry cough is remedied with cough-supressing drugs (antivirals are rarely needed), whereas bacterial infections are medicated with antibiotics (antivirals are NOT antibiotics) and drugs that help clear the mucus from the respiratory pathway. Treating wet cough with dry cough medications is not only ineffective, it can also be dangerous. One more thing - not all bacterial infections necessitate antibiotics which should be used sparingly because the world is running out of antibiotics.


text:
Would blue light be effective to help average people when sunsets come much earlier in the day?
I know people with SAD (Seasonal Affective Disorder) benefit from blue light in the winter as night-time comes much earlier (in the UK, sunset is around 4pm in December, compared to 9pm in June).
However, during winter (say the UK), would the average person also benefit from more blue light in the late afternoon/early-evening than standard light bulbs currently supply?


text:
Do snakes get dizzy?
I've seen snakes get captured in sacks and I've wondered if the snake would get dizzy if the sack were twirled around.  I have not done any tests (and don't plan to) because snakes scare me.

This doesn't seem to be opinion-based to me. Either snakes can get dizzy or they cannot. Am I missing something?

@Resonating - Agreed - this seems an entirely valid question.

This question appears to be off-topic because it This post appears to be off-topic because it does not suit the target audience of this site (biology researchers, academics, and students). While questions are welcome regardless of their difficulty, users should have made some effort to find an answer for themselves by, for example, reading basic biology text books or online material first.

In what context have you seen snakes get "twirled around in bags"?

@augurar I was mistaken.  I haven't seen them twirled around in bags.  I've seen the end of sacks twisted that were used to capture snakes.  I guess I just wondered what would happen if you twirled the bag around.

Probably don't do any experiments that involve shoving reptiles in a sack and swinging them around your head, as someone will surely call the ASPCA on you.
The type of dizziness that is associated with spinning around is called "vertigo". From wikipedia:

Repetitive spinning, as in familiar childhood games, can induce short-lived vertigo by disrupting the inertia of the fluid in the vestibular system

So then from a physiological perspective the question is, do snakes have fluid in their ears like people do? And a quick review of snake physiology seems to suggest that they do.
Thus, I'm going to put forward the tentative hypothesis that yes, snakes can get dizzy, but it's still probably very different from you think of as dizziness.

Dizziness is caused by a continuing rotation of the fluids in the semi-circular canals of the vestibular system that transmit rotation information to the brain. After prolonged rotation of the body, the circular canal fluids are engaged in a rotating motion. This fluid motion continues even when the body has stopped moving. The persistent fluid rotation is detected by the hair cells lining the canals that in turn send this aberrant information to the brain that interprets it as continuous motion of the body. A picture from the wiki page on the vestibular system:

All jawed vertebrates, including snakes, have this basic system of a horizontal, posterior and anterior canal filled with fluid (wiki on the vestibular system). Based on this common anatomy, hence, it is reasonable to assume snakes do get dizzy. However, as @tel rightfully indicates, dizziness is a subjective perceptual phenomenon and the assumption of snakes getting dizzy needs experimental verification. Ethically, however, this would (and should) never get through a review board as it is a curiosity-based question only.

I will try to replace the wiki citation with a more trustworthy journal reference later. The wiki cites a book I don't have access to.

Perhaps you could restrain a snake in a long tube, spin it along the long axis, and then measure its ability to strike at a target? I wonder what snakes use their vestibular system for, they are in contact with solid surfaces nearly all the time...

The vestibular system detects motion in general and sends feedback to many systems, including the oculomotor system that keeps the eyes fixed onto a potential prey. No just-out-of-curiosity-experiments on animals, please :)

There's no danger of me putting snakes in socks, don't worry.

@ChrisStronks You're right, you should submit an application to your Institutional Animal Care and Use Committee for permission to swing snakes around.

In fact all craniates have some kind of vestibular system -- hagfish have one semicircular canal and lampreys have two.

It is impossible to objectively answer this question, as there is no defined method to objectively tell if the animal is dizzy.
All that is known is the existence of vestibular system. Vestibular system helps to define ones orientation with respect to gravity.
The response of a reptile to such a stimuli would most probably be freezing as opposed to a four-footed or two-footed beings. This is due to the stabilty of posture present in reptiles which have either their entire body opposed to the ground (in the which the center of gravity touches the ground) or have their centre of gravity very very close to the ground. As the reptile is already stable there would be no movement in the form of corrective reflexes.
The bipedal or quadipedal beings on the other hand have a high center of gravity and when the vestibular system is stimulated, the dizziness will kick in some corrective reflexes which can be objectively measured.
So the answer can only be derived based on observations on humans or other creatures with quantifiable response to the stimulation of vestibular system.


text:
What does 'pedigree information' mean?
This paper uses Pied Flycatcher as a study species. For the population of Pied Flycatchers they studied, 'pedigree information' was available. What exactly does this 'pedigree information' mean?

It means that they recorded family information for the traits that they were investigating in the paper, i.e., they had plumage characteristics for siblings or parent-offspring pairs. Look for this phrase in the paper: "phenotypic data usually available for one or two generations, mostly from parent-offspring pairs or siblings."


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Why do the major and minor groove exist in DNA?
So I know that the major/minor groove arise from the offset pairing of the two strands in the helix.  All my textbook tells me is that "pitch causes the off-set pairing of DNA and this gives rise to the major and minor grooves."
I'm not too sure what this is saying.  What exactly is pitch and how does it give rise to the grooves?

Have you read the articles on DNA, nucleic acid tertiary structure, and the structure of a nucleic acid double helix? They all talk about DNA structure and should be quite informative.

Possible duplicate of How do the major and minor grooves arise in the DNA helix?

Pitch is not a great word for this, as its meaning is ambiguous. It's hard to find a universal nomenclature for DNA geometry, but see the "Base pair geometry" section of this wikipedia page. The relevant property is what they call "opening".
From the biochemistry textbook by Berg:

To explain in words, if the glycosidic bonds (which attach the nucleic base to the sugar in the backbone) stuck straight out at 90 angles on both sides, then the grooves in double-stranded DNA would be symmetrical. Because the glycosidic bonds are at an angle (relative to the interface between the AT or GC pairs), one of the "faces" of the base pair is larger than the other.
Words and flat pictures, however, will never really give you a good intuitive sense of what's going on with the 3D structure of the grooves. A good modeling kit will be of great help to you.

Would it be correct to claim that this is because the nucleobases they're attached to wouldn't base-pair properly (and would likely experience clashes) if they weren't? For instance, in the image in your answer, if the sugar-phosphate backbones were to be diametrically opposite to one another, then, the atoms on the major groove side would clash (i.e., physically encroach upon one another), while the atoms on the minor groove side would be too far away to establish a hydrogen-bond.


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How and where do nerves share pathways to the brain?
I am interested in understanding how pain receptors send signals to the somatosensory cortex (the part of the brain that registers various nerve signals such as pain, presure, temperatures, etc).
Specifically, I'm interested in whether or not two distinct nerves/receptors share, or don't share, "channels of communication" to the cortex.
For example, say I touch the very tip of my finger to a hot stove, and, say, only 10 "temperature-sensing nerves" are triggered to transmit pain signals to my brain:

Do each of these 10 nerves send 10 distinct signals to my brain, traveling down 10 completely 10 channels?; or
Do each of these 10 nerves send 10 distinct signals to, say, my spinal cord, where they are then combined into 1 large pain signal and forwarded on to the brain?; or
Something else entirely?

Here's an awful illustration of the question I'm asking:

In Scenario #1, both nerves send 2 distinct signals to the brain, and those signals are kept distinct/isolated throughout the course of their entire journey to the brain.
In Scenario #2, both nerves send 2 distinct signals to the spinal cord, but the spine then combines them and only forwards 1 signal on to the brain.
I''m sure in reality it's neither of these scenarios, and is something much more complex. But I'm curious and want to know!

The first layer of sensory integration from neural interconnection lies in the spinal dorsal horns (for somatosensory stimuli), and the spinal anterolateral system (for painful stimuli). It resembles option #2 much more than option #1.
Addenda: Since you are asking a lot about neuroanatomy and neurophysiology, I suggest those 2 beginner books:

Neuroanatomy Text and Atlas, John Martin
Neuroscience, Dale Purves


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Anatomy of nervous system's sensory pathways
When I touch my hand on a hot stove, I feel pain. I'm interested in knowing all the main "endpoints" (components/parts of the body) that are involved in relaying this pain signal. As I understand it so far, they are:

Nerve (thermoreceptor)
Fibers
Spinal cord
Brain stem (medula => pons => midbrain)
???
Somatosensory Cortex

A special sensory nerve in my hand, called a thermoreceptor, receives a thermal input (the hot stove) and fires a pain signal to my spinal cord.
My spinal cord then sends the signal up into the brain stem, where the signal travels through the medula, the pons and the midbrain.
At this point the signal is somehow wired to my somatosensory cortex; the part of the brain that ultimately processes the signal and interprets it as "pain".
Have I identified all the key players here? What connects the midbrain/brainstem to the somatosensory cortex?

The key player you are lacking is the thalamus, which integrates a lot of stimuli, and pre-processes them before sending them to the cortex


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Western blotting with multiple antibodies
Normally I wash/detect with one primary/secondary-HRP antibody pair, strip, then wash/detect with the other primary/secondary-HRP pair which works well. However, I recently started working with a HRP-conjugated primary antibody for my protein of interest and wondered if I might add this together with the secondary antibody for my loading control to save the stripping and second washing.
Are there any general guidelines for Western blotting with multiple antibodies at the same time, i.e. changing antibody dilution?
An obvious first step is to make sure the HRP-conjugated primary isn't from the animal recognized by the secondary. I anticipate blotting with mouse HRP-conjugated anti-GFP and a secondary rabbit anti-mouse would not be a very good decision.

Do you mean HRP conjugated secondary? I have not heard of HRP conjugated primary antibodies in the context of Western blotting.

I have a HRP-conjugated primary, yes.

it is generally recommended not to use multiple antibodies at the same time mainly due to cross-reactivity/interference either from your primary or secondary Ab since the primary conjugated can bind to the first primary already bound. Also are you confident you can recognise which signal is coming from which Ab? this can be tricky if you have degradation products or dimerisation of your proteins! I generally use one membrane for 1 Ab and another membrane for another Ab. Although this is time consuming but its the safest!

@Bez using a different membrane kind of defeats the purpose of a loading control, doesn't it? Also, in my case there are definitely no multimers or degradation products and the proteins are quite different in size so there should be no confusion as to what is what.

What you can do depends on your proteins: If both proteins (your target protein and the loading control) are seperated far enough, you can detect both of them in the same step by adding both primary antibodies and both secondary ABs into the buffer at the same time. They will bind only to their specific epitope and you will get nice signals. This is something I have done several time. This avoids the stripping process (which can be tricky sometimes) and you have both signals on the same film. Additionally you save chemicals, film and time.
There is another way with which you can come around the stripping: Do you first primary/secondary antibody combination and then incubate the blot with a buffer containing sodium azide. This inhibits the enzyme irreversibly, you have to make to wash very carefully afterwards. Then you can proceed with the second antibody combination.
If you want work with a marked primary antibody (which is unusual, but will of course work) and your loading control at the same time, I would definitely make sure that the secondary antibody with the HRP is not binding to your marked primary, otherwise the signal might get very strong (from the primary and also from the bound secondary), but I don't think it would cause other problems.


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What is the evolutionary purpose of white spots in nails and how can they be characterised due to Leukonychia?
Suppose you haven't hit your nails so the white spots are due to Leukonychia.
Are the discoloration i.e. the white spots due to lower porosity (less minerals absorbing) or some other factor? I cannot understand their physiobiological chareterisation and why are they created due to evolutionary terms? To show a person that he is lacking minerals? Or why do some people have them?

Do you have any reason to believe there is an evolutionary purpose? Having nail spots don't seem like a fitness increasing feature.

You just stated the person develops the white spots because he hit his nail. Does he get them because he struck his finger, or because he's missing something? Why do some people have them? Or, does everybody have them but don't injure their nails at the same time? Please think about what you're asking. One of the most important principles in science is to ask, and answer (by collecting evidence) one question at a time.

@MarchHo There are different kinds of white shapes: lines, gathered things, surfaces -- what they tell to each person I have no clue. Absorbing not perfect yes due to multiple reasons: diseases affecting absorption rate directly, allergen reactions in which body does not absorb things -- body is all the time in certain mode. Are they really just stochastic noise or is there some real purpose for them like signalling bad nutrition? Has nature developed some mechanism to nails that we should look at to help us somehow?

This is a common misunderstanding from newcomers in evolutionary biology. Not every trait is the result of an adaptation. Evolution is way more than just natural selection and is not as deterministic as you may think. There is stochasticity inherent to mutational processes and there is stochasticity in reproductive success (called genetic drift). This seemingly totally unrelated post may help you getting a quick grasp of what are the stochastic processes in evolution.
The white spots you observe very likely do not result from an adaptive process but it just happen to be the way it is. For the physiology part (but this would be the subject of another question) I have no idea what drives these white spots.

Good point +1! I totally missed the stochastic nature, it would be super cool to understand this process better.


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Why do some animals try to imitate other animals?
There is a tendency of some animals (including people!) to be "copy-cats" and try to imitate members of their own, and sometimes other, species.
The most obvious example is a parrot copying human speech. Humans also try to copy the speech of their parents when they are little. "ma-ma, da-da"
The less obvious examples, I'm not even really sure are occurring. Like when a gorilla at the zoo assumes the same posture as a person sitting on just the other side of the glass. Like my cat, who tries to chew on bones similar to the two dogs we have.
I'm sure there are more/better examples I'm not aware of.
What is it that creates this behavior? Is it something that was learned, or is it some natural tendency? Is there such a thing as behaviors that are "encoded in the dna"?

Disagree with "too broad" closing but wouldn't this question be better suited for http://cogsci.stackexchange.com? (i.e. off-topic here).

I think this question is perfectly on topic here. Cognitive Sciences focuses much more on the human aspects.

Mimicry, in biology, phenomenon characterized by the superficial resemblance of two or more organisms that are not closely related taxonomically. This resemblance confers an advantage—such as protection from predation—upon one or both organisms through some form of “information flow” that passes between the organisms and the animate agent of selection.
This link describes different types of animal mimicry

The two step mechanism of mimicry evolution states that,
1) Mutations at genes of major effect first allow a phenotypic leap
  achieving an approximate resemblance to a particular model.
2) Once these mutations have increased in the population, resemblance can be enhanced through the gradual selection of epistatic
  modifiers.

Considering the case of butterflies, the working of two step mechanism evolved through different types of natural selection process. Experiments show that birds associate certain patterns in the butterfly wings to identify the specie and generalize those features, but a small deviation from the exact pattern is neglected. The increased resemblance is advantageous to species having imperfect mimics. So the species which displays/perform imperfect mimics can some how fall under the list of rejection and manages to survive, thereby passing genes to next generation.

"Largesse of the Genome", an idea put forward by J.R.G.Turner states that, it is believed that the modification of a trait can be achieved by so many different genes that some of them will inevitably happen to be linked.Amoung the many possible combinations of the loci, selection could simply sieve out the ones that involve linked genes.
Encyclopedia of Insects by Vincent H. Resh, Ring T. Cardé

Although the exact mechanisms of mimicry is still a questionable area, experiments are giving hopes regarding the two step mechanism and more over natural selection is the predominant factor which makes a mimicry successful.
This link describes insect mimicry and two step mechanism in detail.

References
A Dictionary of Birds
Encyclopedia of Evolution
Rapidly Evolving Genes and Genetic Systems

I think the question is about imitation, not mimicry.

I did have imitation more in mind when I wrote the question, I hadn't really thought about mimicry like stated here.

My intuition would be that this has to do with the neuroscience of social behavior.  Many animals, especially those that live and travel in groups (eg. humans), have a great deal of brain "wiring" dedicated to engaging in social behavior with other members of their group.  This is an advantage from an evolutionary perspective, since it helps with cooperation, exchange of information, establishment of social hierarchy, etc., which confers survival advantages.  In the absence of other members of their group (for example, in captivity), there are documented cases of animals imitating human behavior, which is thought to be a carry-over of the social bonding behaviors they typically engage in.
There was a NYTimes article that mentioned this phenomenon in relation to parrots imitating human speech, which came to mind when I saw your question  (http://www.nytimes.com/2016/01/31/magazine/what-does-a-parrot-know-about-ptsd.html )--not a very scientific source, I know!

This is just an opinionated guess not an answer, and makes little effort to directly answer the question.


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Cells scatter light in solution. Do they refract?
For part of an exam question, "why do cells grown in liquid cause turbidity?" I answered that cells refract light. The correct answer was that cells scatter light. Isn't the light scattering ultimately caused by lots of refraction events? Is the grader correct to take off full points?

Cells also reflect and absorb light, but this is really a physics question.

You're both correct. Turbidity is causes by excessive light reflection events from all of the particles, and is actually how it is measured in a sample. As to cells, they both both reflect light that is incident on a membrane, but they will also refract light that does manage to enter the cell because of the difference in refractive indices. A portion of the light will also be absorbed by the cells.

Scattering = refraction + reflection. The third optical event is absorption. Cells also absorb light. Does that contribute to turbidity?

Scattering alone contributes to turbidity. Absorbance just causes attenuation of the amount of light (measured in flux) passing through the sample. The light coming out the other side is dimmer than what went in.


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Persistency of botulinum toxin in environment
There is information about decontamination times here on pages 6 and 7. My specific question is how persistent botulinum toxin is in a natural environment, or alternatively, what is the half life of this toxin?

I think you shoudld narrow down the scope by asking about specific biotoxins or groups of toxins. From what I know, persistency can vary dramatically between groups and types of toxins.


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Hot water and bacteria
I know that it is common to say, "use hot water when washing your hands" or when you've got a cut, "wash your hands with warm water," etc. I was wondering, why is this the case? Since bacteria grow in warm environments, you would think that it might be beneficial for bacteria. Is this just another myth or is this actually true?

The bacteria wouldn't see any benefit from the warm water in the ~30-60 seconds you're washing your hands, neither would hot water "sterilize" your hands at temperatures you could tolerate. The reason you wash your hands with hot water is because the hot water+detergent soap mix is better for removing oil and dirt than cold water+detergent, which is supposedly where bacteria reside.
Interestingly, there was a study published saying that washing with hot water doesn't have much of an effect on bacterial load. Hot water for handwashing--where is the proof? (Laestadius and Dimberg, 2005). I'd be interested to look more into their methods but the paper is behind a paywall and I don't have access at home.
Also, this paper, Water temperature as a factor in handwashing efficacy by Michaels et al. is open and shows no evidence that hot water is any better than cold water for removal of microbes.

[W]ater temperature exhibits no effect on transient or resident bacterial reduction during normal handwashing with bland soap.

Perhaps warm water just feels nicer while washing, thus encouraging longer washing. I'd suspect this should then increase the removal of microbes.

@edA-qamort-ora-y I'm sure you're right and that this is a published result - I'll have a look if my journal access is working.

The goal of hand washing is to remove surface debris, including foreign pathogens. Most things that most people encounter on a daily basis dissolve more easily in hot water than in cold water. Thus, hot water around 100° F is used to facilitate this debris removal process, although the ideal culture temperature for E coli and a raft of related bacteria is around there too.
That being said, from the wikipedia on hand washing:

Contrary to popular belief however, scientific studies have shown that using warm water has no effect on reducing the microbial load on hands

"Everything that can dissolve in water dissolves more easily in hot water than cold water." That's not actually true. Gasses are much more soluble in cold water but even some solids, such as sodium sulphate dissolve better in cold water.  (I concede that the removal of adsorbed gasses and sodium sulphate are not major factors in hand-washing. :-) )

@DavidRicherby I changed the wording a little to reflect your comments, but I am curious about what you said. Do you have a reference?

@DavidRicherby I would also like to see any source for a solid dissolving better in cold water

http://2012books.lardbucket.org/books/principles-of-general-chemistry-v1.0m/s17-04-effects-of-temperature-and-pre.html
The curves with a negative slope are the examples you seek.

@user3790338 Just Google "sodium sulphate solubility". One example is the curve at Wikipedia which shows decreasing solubility from 38C to about 120C (presumably under enough pressure to keep the water liquid at those temperatures).

Another indirect but common example of a solid being more soluble at low temperatures is calcium carbonate, which is only weakly soluble in pure water but with carbon dioxide dissolved in the water the solubility increases.  Remove the CO2 by heating (remember gas solubility decreases with increasing temperature) and the CaCO3 precipitates out.

It makes no difference at all. To sterilize your hands you would need to wash them with water at around 115 degrees C at 1.2 atmospheres of pressure for over 30 minutes – that's obviously not going to happen. The bacteria that normally reside on your skin can easily tolerate tap water, no matter whether the faucet is set to maximum hot or maximum cold, or just average. Even if the temperature of the water could appreciably slow down bacterial growth (which it can't), once you've washed your hands your skin temperature goes back to as it was before the washing in a minute or so.

Besides that: The bacteria living on our skin are usually not threat for us and belong to our normal bacterial environment. We learned to live with it and to control it.

The fact that you can't wash your hands in water hot enough to sterilize them doesn't mean that hot water has no benefits. (Though the other answers suggest that it doesn't.)


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Fab fragments of antibodies to fight viral infections
I was reading about Fab fragment and about using them to fight of viral infections. It seems that the Fab attaches to the viral receptors, which stops the viruses from attacking the cells. It seems that it has been done before. I was wondering, since Fab fragments can't activate immune response, what happens to the Fab-virus complex in the blood?

What virus or virus family? Could you also provide us with a link to the paper you're reading?

@Luigi hopefully as many possible viruses.. but the link I have talks about influenza virus

@Luigi here is the link: http://jvi.asm.org/content/77/15/8322.full.pdf

It won't trigger a full immune response since the Fc part of the antibody is needed for opsonization.

There are three pathways by which soluble antibodies (which is what the Fab fragments arise from) can inactivate viruses (from Janeway's Immunobiology):

What you describe with the Fab binding to the viral receptors is a type of neutralization. Janeway claims that the type of naturally occurring antibody primarily responsibly for neutralization, IgA, is mostly exported to mucous secretions, so presumably it gets digested/excreted along with the rest of the mucous proteins.

I want more info about the section your book doesn't talk about... I want to know what happens to that complex...so unfortunately, you have not answered the question.

For opsonization and complement activation the complete Ab is required (i.e. with the Fc fragment). But for neutralization I imagine the Fab is enough to prevent bacterial adherence. Maybe the poster can focus on this aspect.

yes.. I agree with @ddiez (BTW, which page is this on?)

oh.. I found the page.. (it's page 308)