text:
Can signals travel "backwards" in the sensory pathway?
My understanding of the "sensory pathway" is that its a linear, directional pipeline as follows:

Nerves (fire various signals depending on the type of sensors they are)
Fibers (transmit signals from nerves to spinal cord)
Spinal cord (transmits signals from fibers to brainstem)
Brainstem (transmits signals from spinal cord to brain)
Brain (the somatosensory cortex register signals as pain/pressure/temperature/etc.)

So again, my understanding is that sensory nerves are 1-way sensors, and that once they fire a signal, its 1 and only ultimate destination is the brain.
So, as a precursor to my question, if anything I have stated is incorrect, please begin by correcting me!

I read that pinched nerves in the back and neck can cause neuropathy ("pins and needles") all over the body: hands, feet, face, etc.
But how can this be? If my understanding of the sensory pathway is correct, then a pinched nerve in one's neck should only send "pins and needles" signals directly to the brain; it should not at any point forward/relay signals on to any other areas of the body.
To state that a pinched nerve in one's neck could possibly cause neuropathy in their arm, then that insinuates there is some connection between the pinched "neck nerve" and the nerve(s) in the arm that are experiencing the pins and needles sensation.
In fact, unless I completely misunderstand the entire sensory pathway and how pain signals transmit, this implies that a pinched nerve sends signals out to the spinal cord, down the spinal cord and into, say, an arm, and that the sensory receptors in the arm subsequently react to these signals.
How is this possible?!? Is there some kind of feedback mechanism at play where nerves in the neck and back can relay signals on to other areas of the body, instead of just feeding directly into the "spinal cord => brainstem => cortex" pipeline?

Individual nerves are one-way, but there are plenty of nerves running both ways along the "pipeline"

Thanks @Luigi (+1) - however I'm not following you. First you say that individual nerves are 1-way, but then you say nerves run both ways...which is it?!? Are there certain types of nerves that are bidirectional? If so, what are they called? How would they fit in to my scenario of pinched neck nerves causing neuropathy in an arm or other area? Physiologically, how does all this map out? Thanks again!

By "plenty" I mean that there are more than one. Think of a four-lane highway. Four run north, four south. Each individual lane goes in only one direction, but the highway carries cars in both directions.

Thanks again @Luigi (+1 again) - I feel like you're holding back! Don't be afraid to hit me with some science here! I get your highway anology...but does that mean that the 4 lanes going back are for motor nerves? Or can a sensory nerve handle "traffic" going both ways?

So, continuing my metaphor, pinched nerves would be an earthquake destroying a few lanes of the highway. You can see ill effects in either or both directions.

Motor nerves control your movement (brain->muscle) and sensory nerves send info to the brain (extremities->brain). No single nerve handles two-way "traffic"

Right @Luigi (+1) - that's what I figured. So you see, your analogy and reasoning isn't quite adding up (respectfully, of course). You say that sensory nerves can only handle "extremity -> brain" traffic. So if I have a pinched nerve (of any kind; motor or sensory) in my neck, how can that possibly send out signals that sensory nerves in my arm respond to? Thats the root of my question: How do sensory nerves in my arm "read" signals sent to them from my neck?!? It just doesn't make sense!

Let us continue this discussion in chat.

Reverse signals (dendrite -> axon) do occur in neurons, and are called back propagating action potentials (bAPs). However, whatever role bAPs play in the nervous system at large is subtle/small enough that we don't really understand them at all.
In any case, as @luigi points out, pinched nerves don't have anything to do with bAPs. The reason why a pinch in one place (the neck) feels like it has an effect in another place (the arm) is because some neurons trace long (on the order of several feet) pathways through the body. Ultimately, the sensory input of everything below your head passes through neurons in your neck at some point. If there is a pinch in the neuron in your neck that relays sense information from your arm, that neuron in your neck can activate spuriously, even in the absence of any stimulus acting on your arm. In that case your brain will interpret the spurious activation of that neck neuron as being the result of some kind of strange arm stimulus, and so you feel pins and needles.
See here for more information on the sensory cortex in your brain and the "sense image" it maintains of your body.
Edit
To clarify what I mean by a "pathway",

The part marked "proprioceptors or mechanoreceptors" is what's buried in your skin. If you poke a mechanoreceptor, it evokes a signal in the neuron marked "first-order". In some cases, that first-order neuron will reach all the way to brainstem (as in the picture above), and in some cases that first-order neuron will interface with an intermediate neuron in the spine, but the effect is the same in any case. A first-order neuron stimulates a second-order neuron, which in turn stimulates a third-order neuron, etc., all the way until the original signal arising from the mechanoreceptor reaches the somatosensory cortex. A pinch in any of those first, second, etc. order neurons will potentially send spurious signals to the somatosensory cortex.
Second edit:
Rereading your question, I think a lot of the trouble that you're having has to do with your understanding of how the brain assembles sense information. In order to feel pain in your arm, it is not necessary for anything to be happening to the arm itself. Your arm could be perfectly healthy and normal, but as long as your brain is receiving a signal equivalent to the one produced by a damaged arm you will still feel the same sensation of pain.

Thanks @tel (+1) - however your answer completely pummels my understanding of this "sensory pathway"! My understanding is that nerves connect to fibers, which connect to the spinal cord. The spinal cord connects to the brainstem and then the brain. When you say "Ultimately, the sensory input of everything below your head passes through neurons in your neck at some point.", this seems to imply that the spinal cord connects back to fibers/nerves and then the brainstem after that... Can you confirm all the major elements of this pipeline/pathway?

...And perhaps elaborate on how a signal sent from a neuron in my hand passes through a neuron in my neck? Again, as I understand the pathway, any neurons in my neck would connect to the spinal cord, then the brainstem, then the brain; and a nerve in my arm would never send signals that pass through a neuron in my neck. Thanks again!

@smeeb tel means that your spinal cord passes through your neck, so you can pinch a nerve in your spinal cord (which happens to be in the part of your spinal cord that passes through your neck) and it could affect the sensation your brain feels in your arm. Please look at this discussion for more

Pinching a nerve in a different part of your neck, i.e. trachea or throat, will not and can not have any effect in an unrelated area (arm)


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Satisfication with irrelevant things
I am not sure if this question is better suited CogSci.SE so please tell me.
My question is why are we satisfied when we get things that aren't useful in any important way? For example, relating to Stack exchange, why are we satisfied and happy when we get badges because badges don't increase reputation or help you get privileges in Stack Exchange. Similar with Winter Bash. Why are we happy when we get hats? They are just for decorations. Is there a biological explanation for this?
What chemical leads to us getting that feeling of satisfaction?

In the grand scheme of things, stack exchange reputation seems about as irrelevant as stack exchange badges…

@canadianer well not for me bcos for some of these questions, the topics are based of projects I am doing so I need reputation to do more with my question so I can get answers so I can finish my projects...

If the question is re-stated as "what is the neurotransmitter mediating the sense of reward" this question is acceptable (DA, as answered). As the question stands now it reads "what is the neurotransmitter mediating the sense of irrelevant rewards?". That doesn't make sense to me, as relevant and irrelevant rewards are highly subjective and opinion based.

Dopamine is one of many neurotransmitters which modulate information passage between one brain area to another. Dopamine is thought to play important role in  pleasure, addiction,
and learning.Massive increase in the
amount of dopamine released in the brain during video game play, the releasing of dopamine
are in areas thought to control reward and learning.

Reference

Certain neural structures, called the reward system, are critically involved in mediating the effects of reinforcement. A reward is an appetitive stimulus given to a human or some other animal to alter its behavior. Rewards typically serve as reinforcers. A reinforcer is something that, when presented after a behavior, causes the probability of that behavior's occurrence to increase. Note that, just because something is labelled as a reward, it does not necessarily imply that it is a reinforcer. A reward can be defined as reinforcer only if its delivery increases the probability of a behavior.

The reason why we are happy when we get these decorative items is because they are things which we can possess. Reward system is responsible for this kind of behavior, when we gain or achieve something in life its usually gets rewarded in the form of a pleasure. Foraging ants and bees are provided with these reward systems and which in turn makes these animals to derive a pleasure out of their daily achievements. Whether in life, video game or stack exchange or anything, an achievement is something brain thinks relevant and rewards it with a pleasure in mind.
Considering badges in stack exchange, really badges are an analogy to reputation. When we have more badges usually our charisma increases like in the case of reputation. Also levels and scores in games,achievements in office, stack exchange badges and hats all fall under the same analogy. So when we have more badges we are meant to be more successful and brain will reward us to attain more badges and also people like hats too.

References
Digital Media: Transformations in Human Communication - Paul Messaris, Lee Humphreys
Cyber Junkie: Escape the Gaming and Internet Trap - Kevin Roberts

source: Stack Exchange

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

sort: votes


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Is it possible to dock multiple ligands with the target?
Is it possible to dock multiple ligands with a target? If so, what is the suitable software used for? -- Is it possible to fix specific docking region for the target (or) automatic?

Huameng Li and Chenglong Li have done multiple ligand docking in two (AFAIK) of their works:

Multiple ligand simultaneous docking: Orchestrated dancing of ligands in binding sites of protein
Drug Design Targeting Protein–Protein Interactions (PPIs) Using Multiple Ligand Simultaneous Docking (MLSD).....

The method is called Multiple Ligand Simultaneous Docking (MLSD). I am not at all an expert in this field and you should read the first paper for details on how they implemented this. This algorithm was implemented on AutoDock.

I thank and appreciate [WYSIWYG] for your wonderful answer. I have referred the both articles before, but there is no proper protocol for applying the problem in the AutoDock.

Perhaps you can see this paper. They talk about implementing automated docking and this is referred by Li and Li.

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


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Physiologically, how can stress/anxiety cause neuropathy?
According to the Mayo Clinic, stress/anxiety can cause "pins and needles" (neuropathy) sensations all over the body.
But how can this be? My understanding of the sensory pathway is that sensory receptors (nerves) fire "pins and needles" signals to the brain whenever there is a lack of blood flow to them.
So does stress reduce blood flow to nerves? Is it a chemical reaction, perhaps where stress releases hormones that prevent the nerves from functioning correctly? Something else?
I'm looking for a biological/physiological/scientific explanation of what stress does to make nerves misbehave.

Something related http://biology.stackexchange.com/questions/24492/how-does-anger-relate-to-blood-pressure/24498#24498

Thanks @Jvrek (+1) - thats a pretty darned good answer to that question! So, can you (please) confirm my newfound understanding here: that stress produces various hormones that in turn regulate blood flow/pressure, which can then (under the right circumstances) reduce bloodflow to individual nerves? Am I on track or way off? Thanks again!

pins and needle sensations are not always pointed to lack of blood in nerves. http://biology.stackexchange.com/questions/24555/what-causes-feeling-of-feet-falling-asleep-to-be-delayed/25807#25807

Thanks again @Jvrek (+1) - I understand; however can you at least confirm that stress-induced neuropathy is chiefly a result of hormones which interact with neurons and cause them to malfunction? Thanks again!

There is a big difference between a pins-and-needles sensation and *neuropathy. Are you sure stress can cause neuropathies?

I wouldn't make drastic assumptions about cause-effect relationships or whether it is even neuropathy.  Anxiety may cause neuropathy-like symptoms or the symptoms may be a side effect of another biological process that is causing the anxiety. My personal theory is that there is something electrical going on, because magnesium is known to help mitigate anxiety symptoms.


text:
How can I purify RNA after gel electrophoresis to remove residual acrylamide?
I sometimes use denaturing gel electrophoresis on a preparative scale to purify RNA produced by in vitro transcription. The major issue with this is that the sample after extraction from the gel still contains significant amounts of acrylamide, or acrylamide oligomers/polymers.
Exchanging the buffer using Vivaspins doesn't reliably remove it, precipitating the RNA also only reduces the amount, but can't remove the acrylamide entirely.
In some cases the acrylamide doesn't interfere much with the later experiments, but there are some experiments that won't work with acrylamide in the sample.
What are the options to purify the RNA after gel electrophoresis that would reliable eliminate acrylamide from the sample? Preferably they should be simple and fast, not something like a full FPLC/HPLC run.

May I ask why you need to purify your in vitro transcribed RNA? I've been making mRNA by IVT and have gotten good results without any purification beyond phenol:chloroform extraction and isopropanol precipitation.

@user137 I use the RNA itself for NMR experiments, I need it in a different buffer and without the DNA and protein to get good quality spectra. And anything else that is still in there will likely overlap some of the signals of the RNA.

How much RNA do you need for NMR? I've always heard that NMR needs a lot of material for good signal.

@user137 Depending on what exactly you want to do you need about 0.2-1.0 mM protein or RNA in your sample in a volume of 300-500 microliters. And for many experiments you also need it 13C and/or 15N-labeled.

@MadScientist Maybe I did my math wrong, but 500uL of 1mM of my mRNA (1860 bases) would be 300mg of RNA. Even if 300uL of 0.2mM would be about 36mg RNA. With a good in vitro transcription reaction I can get 200ug of RNA. Obviously a short RNA would need a lot less mass for the same molarity.

@user137 The RNA you would investigate with NMR is usually around 15-150 nt long, you don't see much with NMR for anything larger. And we simply do the in vitro transcriptions on a larger scale, typically around 10-30 ml. RNA is also almost always measured in Shigemi tubes, so the volume is 300 ul, and while 1 mM concentration is ideal, but you can't always get that much.

If you don't want acrylamide in your preparation, don't use it, as you will always have some carry-over in the solution. And you will not get rid of it completely, as it at least partly co-precipitated with the nucleic acids (it's used as a co-precipitation agent for this purpose).
I think the best solution is to use chromatography, either size-exclusion or charged resins. See these two papers for more information:

Large-scale preparation and purification of polyacrylamide-free RNA
oligonucleotides
Rapid, non-denaturing RNA purification using weak anion-exchange fast
performance liquid chromatography

We also use chromatographic methods, but gel purification has certain advantages like better resolution. I don't need to get rid of acrylamide completely, reducing it significantly below the RNA concentration would be sufficient.

Gel is easier and faster, chromatography has a better resolution and takes longer. Now you have to choose what is more important...

I suspect if there would be any residual unpolymerized acrylamide after the run. Heating should decompose acrylamide to gaseous products (ammonia, hydrogen and carbon monoxide). Seehere. I am not sure about thermal decomposition though (no solid reference).

authors: Аня Пахомова


text:
Nerves, Neurons, Axons and Dendrites by Example
Here is a simple diagram of a neuron:

A few (very closely related) questions:

Where are receptors located (for pain, pressure, temperature, etc.): in the axon terminals or the dendrite tree?
Please confirm: for sensory nerves, signals travel from axon terminal to dendrite tree, yes?
According to Wikipedia, axons communicate with each other across synapses, and nerves are chained bundles of axons (basically forming a cable with each other). However, if sensory signals travel from axon to dendrite, then how can axons be chained together? In other words, if axons are a "male" recepticle, and dendrites are a "female" recepticle, then how can you have a chain of all-male recepticles?
Please confirm: a nerve is just the cabling that houses bundles of long, individual strands of neurons, yes?

many questions in one is generally considered sub-standard here - could you edit in to individual questions please.

Receptors are typically not located in a neuron. Instead, receptors generally synapse onto a primary neuron, and specifically on the primary neuron's dendrite;
Within the neuron physiological signals are received in the dendrite and are transmitted uni-directionally via the axon to the axon terminal. Between neurons the signal is transmitted from axon to dendrite via the synapse (see figure).
Although axo-axonal communication exists, it is not the typical way of neural communication (they are regulatory in nature and do not convey information as such). Typically, axons synapse onto another neuron via the dendrite of that second neuron.

The typical connection is the following:

Nerves typically do not contain cell bodies, only the elongated parts of neurons, i.e. the axons. A nerve is a bundle of axons that contain closely related signals from closely related structures in the body.


text:
How do PER/CRY complexes accumulate in the cytoplasm?
The Period/Cryptochrome (PER/CRY) complex is a heterodimer that transcriptionally regulates circadian rhythm. When it is phosphorylated, it is transported to the nucleus and it inhibits a transcription factor that regulates the synthesis of its own subunits (negative feedback).
Research on the circadian molecular clock speaks of an accumulation of PER/CRY complex in the cytoplasm during the day phase (see review The circadian clock: pacemaker and tumour suppressor, Fu and Lee, 2003). Why does this complex not move to nucleus during the day? In other words how is the phosphorylation-dephosphorylation switch controlled?

Welcome to Biology SE! In order for people to grasp your question, please clarify the question by explaining the acronyms (i.e., get rid of them :) and work a bit on the grammar as it is very hard to read. a citation may help a big deal as well.

With the edit, the answer is there in the question itself.

@WYSIWYG Maybe my edit wasn't clear--PER/CRY builds up in the cytoplasm during the day because it is not phosphorylated (and therefore not transported to the nucleus). At night, it is phosphorylated and negatively regulates itself. I know the answer has something to do with blue light and Cryptochrome but I don't actually know the reason

@Luigi added an edit to mention the phosphorylation


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How do I get recombinant proteins into the nucleus of mammal cells?
I know that there are Nuclear Localisation Sequencenes (NLS). They can be taken from endogenous or viral proteins and fused to the N or C terminus of my recombinant protein.
Which is the best one? Which the best short one (so that it can be more easily added with a Primer)? Should it be attached to the N or the C terminus?
Do they influence expression?
I have heard that size does matter (Too large wont fit through the nuclear pore, too smalll will diffuse out again). What is the range of protein sizes that can be targeted efficiently?

To use a N-terminal or a C-terminal tag depends on your protein. I can only say that you can try both and see which one does better.

It also depends if your protein has important domains on one of the sides. If so, I would start by using the other end to avoid interference.

Thanks for the general tip. In my case I have seen people putting stuff (including NLS) to both ends of the protein. Here I am really more concerned about transport efficiency.

I've seen people use 3 NLS sequences in a row, I assume this improves transport efficiency, but they never explained their reasoning.


text:
Single long axon vs serial neurons
Based on the comments in this post and also this chat. For discussions and speculations please comment in the chat.
The basic question is what is the advantage of having a single long axon such as that of sciatic nerve (~1m) compared to a series of neurons?
The primary advantage is surely the conduction speed which will get affected because of chemical synapses. However, gap junction synapses can reduce that delay. The larger volume of the soma of the post synaptic neuron may also reduce the conduction speed, but signal strengthening can also happen. Cell architecture can be adjusted to minimize the loss of speed.
The obvious disadvantage of having a single large cell is that there would be tremendous burden on the nucleus for the cellular maintenance. There would be delays in transfer of non-electrical signals such as biomolecules from axon termini to soma and vice versa. Long axons also means continuous transport along them which in turn demands large number of molecular motors and therefore ATP. Moreover, a small injury can disable the entire conduction channel. It can be imagined that this trait (long axons) can also be selected against; injury leading to inability to move and thereby causing perishment.
EDIT (Based on comments to Anne's answer)
Time is of course a valid advantage for having a single axon as an information conduction channel. However, the energy or the maintenance cost is the factor that I am actually interested in. Maintenance cost would increase with cell volume (in fact surface area) and having serial neurons would demand more energy (cumulative) than a single axon (including costs of maintaining a nucleus). However a long cell would need much higher number of molecular motors to maintain the traffic flow rate. All responses that require transcriptional control would be slow (such as response to injury). Moreover a single soma also imposes a limit on the number of mitochondria. There should be a limit on how long an axon can be. I am especially interested in case of big animals (with long hindlimbs) that also have a good reflex (perhaps camels, even horses).
Has someone tried to analyse the tradeoffs of having a long axon vs series of neurons connected by gap junctions? If not is this problem worth modeling or quite trivial?

Saw this in Quora:

My first thought mostly agreed with the question details, except I'm
  pretty sure that the dorsal root ganglion (DRG) has a longer axon than
  the motor information carried in the sciatic nerve (which is the
  longest nerve in the body, but not axon).

Does this mean that sciatic nerve has serial neurons?

Forget conduction speed. What about signal fidelity? How much noise does each extra gap junction add to a signal?

@tel I am not sure about the noise at the gap junction (GJ). Can you tell me how is noise generated at the GJ?

I'm not a neruo guy, so I can't give you any specifics, but in terms of general information theory/2nd law considerations, every time you convert a signal from one form to another (axonal current to neurotransmitter gradient, say) your signal/noise ratio gets a little worse. You can recover the original signal somewhat, but it always involves an expense of free energy.

@tel Oh well.. but in the gap junctions the wave can move to another cell. There are no neurotransmitters involved.

If you want to reduce the variance in signal transmission with n serial steps, then you need to add more steps. Therefore to achieve signal transmission with really low variance, you either want a single axon (case A) or really lot of them connected in series (case B). May be overall, case A is not so bad compared to case B not to be selected for.

First, I must clarify that a nerve is not the same as a neuron. A nerve is a collection of axons (with each axon a part of an individual neuron) in the peripheral nervous system. Thus, when you mention “single long axon such as the sciatic nerve”, this is technically an incorrect phrase as the sciatic nerve is a collection of many long axons. If one of these axons is nonfunctional, this would not severely affect the function of the entire sciatic nerve. However, you are right that if the entire sciatic nerve is severed, then there would be serious consequences downstream.
Second, the primary advantage of conduction velocity is less dependent on length and more dependent on presence and degree of myelination (directly proportional to fiber diameter) and presence of nodes of Ranvier.
With regards to the content of your question, the advantage of length is exactly what one might think--- greater distance. The sciatic nerve is the longest nerve in the body in order for our nervous system to innervate as far as the tip of our toes. Having hundreds of side-by-side series of neurons compared to hundreds of side-by-side axons seems like a far less efficient system in a couple of ways in exactly the two ways you mention: energy and time.
Energy: Having serial neurons would require an increase the number of neurons needed to transmit a message. Having more neurons requires more Na+, K+ and Na/K pumps and individual channels, requiring more energy.
Time: Having serial neurons would also require an increase in the number of synapses between neurons— either electrical or chemical. If the synapses are chemical, then time is increased many-many fold. If the synapses are electrical, then time is slightly increased by 10-fold per synapse compared to chemical synapses, but this would still take more time compared to having a single axon with myelination and nodes of Ranvier which by about 100-fold faster than a single electrical synapse.
In summary, having longer nerves made up of axons rather than serial neurons is beneficial by improving energy and time efficiency, which allows our bodies to effectively innervate structures farther away.
Ref:

Regarding delay of conduction: Chemical v. Electrical/Gap  Ch 10 of Principles of Neuroscience- "Synaptic Integration in the Central Nervous System" (Siegelbaum,
Kandel, Yuste) 5th ed. McGraw-Hill Medical, c2013.
Regarding conduction velocity of myelinated versus nonmyelinated
cells

Regarding the ATPase absolute number increase in serial vs one long axon, I assume this will depend on the number of neurons in series. However, I read this paper, which says that increased length between each node of Ranvier has been physiologically associated with increased conduction velocity. This suggests fewer needed nodes, despite concentrated ATPases at these locations, and thus fewer ATPases. I haven't been able to find studies which compare ATPase concentration in the soma compared to nodes of Ranvier within axons.
Regarding energy use in soma vs axon, mitochondria are not only made in the soma but are concentrated in pre- and post-synaptic membranes (and growth cones). The more of these structures there are (as in serial neurons), the more presumed mitochondria. See mitochondria and neuronal activity.
Finally, my literature search could not find studies which showed longest possible energetically feasible length for myelinated or unmyelinated neurons.

Why would multiple neurons need more ATPases? The only difference is more cell bodies? Could you provide a citation for the gap junction transduction velocity? I would think it would be about as fast as myelinated conduction. If I am wrong than this is a likely answer!

@ChrisStronks I will add references tomorrow, I used quite a few so it will take time.

@ChrisStronks Multiple neruons need more ATPs as they will have other soma related function to which they have to cater to. More soma=more protoplasm=More volume of space where electrolyte balance need to be maintained=More channels active=More ATP

@Anne "primary advantage of conduction velocity is not dependent on length".. yes I meant in the context of uninterrupted myelinated axon. And length does have a role in velocity (see cable equation). Your point on time is correct but I am slightly skeptical about the energy part. What about larger animals; would there be an optimal length of a single axon?

@ChrisStronks Besides, energy is expended for other cell functions - facultative and constitutive cell functions which would not be expended otherwise

@CRags Requirement of ATP is more or less related to total volume of the cell which would be slightly more in case of serial neurons but not overwhelmingly high. Also a long cell would need much higher number of molecular motors to maintain the traffic flow rate. All responses that require transcriptional control would be slow (such as response to injury).

We are not talking about responses though. Purely from a energy point of view, more cells=more energy expenditure. The longer length of the axon does not mean more molecular motor. As the organ/part which is ennervated is at a fixed distance, one neuron or multiple neuron would have the same number of molecular motors. Infact in this scenario, multiple neurons would require more energy than a single neuron due to the above mentioned reasons.

What I would grant you is the time taken to resolve any disruptions. This would be undisputably longer for longer neurons

@WYSIWYG With neurons, diameter plays a much larger role than length. Nernst Potential and Nerve Conduction Speed

@Anne Did not discredit that. Was just saying that length does have a role :) And yes with the introduction of another soma the diameter will change; however increase in diameter is favorable for longitudinal current (as resistivity is constant; conductance ∝ Area); the problem is the case of less insulation i.e low transverse resistance leading to leaks. In any case I accept that time is an obvious advantage. My question is would energy be a tradeoff at some point: single soma also imposes a limit on number of mitochondria.

@Anne I am also confused here: myelination directly proportional to diameter. Can you provide a link for this; Do schwann cells have a limit on how much can they extend (the coiling during myelination). Of course they cannot myelinate the soma but this is still an interesting point. However I guess there can be ways to reduce membrane resistance without myelination- perhaps by having anchored cytoplasmic domains to confine the leak channels (this can be regulated at the soma). This is just my guess. I think I am raising too many arguments; forgive me I don't have much knowledge of this area.

@WYSIWYG Myelination + axon cross section = fiber diameter.  This applies only of course if we are talking about myelinated neurons. If you have a non-myelinated neuron, axon = fiber diameter. See yellow and green picture on the bottom the page.

@WYSIWYG Mitochondria and neuronal activity. You make a good point about limitation of mitochondria based on capacity of a neuron, and it is unknown whether more neurons in series would require overall less mitochondria than a long axon of a single neuron. However, the references states that mitochondria are not only made in the soma but are concentrated in pre- and post-synaptic membranes (and growth cones). The more of these structures there are (as in serial neurons), the more presumed mitochondria.

@Anne I understand the point about the fiber diameter and myelination. I thought you meant (in the answer) that extent of myelination is dependent on diameter of the axon. Yes mitochondria are localized in axon termini and are transported there via axons. I meant that neuron in series can accommodate more mitochondria to cope up with energy demands. Single soma would be overburdened. Sorry for asking another question: what is the longest axon known. I want to know till point having a single axon would be be an optimal solution (beyond which it is infeasible).

@WYSIWYG Longest axon in humans belongs to the neurons of the sciatic nerve, though some debate it's the DRG. In the world, probably the same structures in a blue whale or other creature we may not have discovered. How long can it get before it is not energetically feasible? That's an experiment yet to be done. Diameter was meant in context of fiber, not axon.

@Anne Can you add these points in the answer. I can accept it then. So I guess the question "How long can it get before it is not energetically feasible" is worth pursuing, at least theoretically. You sure there are no theoretical studies on this?

@WYSIWYG I edited my answer, hopefully that helps. As far as I have searched in pubmed, google scholar, etc haven't been able to find studies regarding energetic feasibility, unfortunately. Please let me know if you have any other questions.


text:
Can I drink warm/hot tap water?
I live in Canada and tap water is drinkable, as a matter of fact, the government puts a little bit of flouride in the tap water so it cleans your teeth.
My wife and mom always tells me not to drink the tap water when it's warm/hot.
Is there something in the water that's bad for the body or is this a myth? (bacterias in warm/hot water vs cold)
Added info: The water is heated in the water heater which is in the basement of my house. It is a new water heater, only a year old. My house is built 7 years ago, which for a house it's not old. I don't know about the pipes though

No, there is no reason to not do this. Lead pipes are a danger with cold water as well, and lead will only be found in old houses.

This is off topic - we can not possibly know about the quality of water coming out of your tap and its not really a biology problem

@GriffinEvo isn't it? I was thinking more towards bacterias in the water against the human body

@Huangism judging by the answers it has so far it seems more chemistry (though I can understand you posting it here) - it would be interesting to post a follow up question on the Chemistry stack exchange to see why more contaminants are released in to hot water than cold

This actually depends on how your tap water is warmed.
If you have a personal water heater, which is connected to your tap with non-corrodable pipes, then there is essentially no difference.
However, if the heating comes from a common source, then it would be very difficult to verify that the heater-tap connection does not contain any corrodable pipes. In this case, it might be better to not use the warm water for direct drinking, especially if the building is old.
A 7-year old house should not have lead pipes installed, since the Canadian Plumbing Code has banned lead pipes since 1975. As such, I believe that your warm water is safe to drink.

The National Plumbing Code allowed lead as an acceptable material for pipes until 1975 and in solder until 1986. All provinces and territories use the National Plumbing Code as a basis for their own regulations.

The water is heated in the water heater which is in the basement of my house. It is a new water heater, only a year old. My house is built 7 years ago, which for a house it's not old. I don't know about the pipes though

Edited to fit the new information

Added to the question

The reason for this worry is chemical--as water warms up, more contaminants can dissolve in the water. With water pipes specifically, people worry about lead contamination. Modern pipes are not as likely to corrode (or even be made of lead) as old pipes, so this is more of a concern in older buildings.
See this NYT article for more information.


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Regarding tumors and their developement
If certain cells or tissue in a specific part of the body are for some reason overworked; like the cases of severe acid reflux damaging the throat repeatedly and the cells in the throat having to do growth and repair a lot more than they would with a healthy person -- or problems in the stomach attacking the stomach lining a lot, causing 'extra' growth and repair; could these situations of 'extra' growth and repair cause various cells used in these processes to mutate with all the cellular division and replication required? And maybe some of these extra-growth-and-repair induced mutations might cause the apoptosis mechanisms to malfunction?

If a cancerous cell has a horrendous amount of mutations and yet it still functions ( if abnormally) it must be able to keep existing without 'alerting' the immune system or interfering 'too much' with other subsystems. How is this possible? Wouldn't all the mutations if 'expressed' cause all sorts of 'activity' the cell or other neighboring systems might not be able to cope with?

There is indeed a positive correlation between gastric reflux disease and esophageal cancer, and also between stomach ulcerations and stomach cancer. There are more than one possible mechanisms for these correlations to arise, but what you are proposing is definitely a prime suspect.
http://www.webmd.com/heartburn-gerd/news/20130523/chronic-heartburn-may-raise-odds-for-throat-cancer-study
http://www.ncbi.nlm.nih.gov/pubmed/10658066


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Binding of Multivalent Antibody to mutiple epitopes?

A multivalent antibody molecule such as Immunoglobulin M Immunoglobulin A etc bind to more than one antigens or epitopes but I am confused about that wheather these multivalent antibodies bind to identical epitopes or can bind to different epitopes? means if one molecule of Immunoglobulin M being pentameric can bind to 10 epitopes at a time the 10 epitopes that it binds Will be identical or can be different..? Confused about that..       2. And also another Question I want to ask that as Immunoglobulin G,Immunoglobulin D and Immunoglobulin E are monomers but all of them have 2 antigen binding sites so we consider them as Mutivalent antibodies or not and if we cnsider them as multivalent antibodies then what are the Examples of monovalent antibody that Specifically only bind to One antigen molecule or epitope? Because as far as i Have studied Antibody or Immunoglobulin molecule hae specific "Y" structure that contains 2 binding sites. Similarly in this case also want answer that these momomeric ImmunoglobulinsG,D,E each binds to 2 identical antigens or epitopes or can bind to two different epitopes. Means that if Immunoglobulin G is binding to two epitopes these epitopes will be identical or can be different...??? :/

Please separate this into two questions.

Any one Plasma Cell that is producing antibody is making one kind of Heavy Chain and one Light Chain. In an IgG, there are two heavy chains each associated with a light chain. Together, a heavy and light chain have one epitope binding region - so in toto, an IgG is multivalent because each heavy chain : light pair can bind a single epitope for a total of two.
If a Plasma Cell is making IgM, it still is making only one kind of heavy chain and one light chain. Because they are pentameric, that does add up to 10 binding locations, but as Matt says above, sterically, all of these sites are unlikely to bind at the same time.
This multivalency is important in crosslinking antigens. Crosslinking is required for the original B Cell Recpetors to activate the B Cell, and it is also useful in clumping antigen in a way that it can be eaten by macrophages or otherwise interfering with the function of the antigen.

Non-engineered IgM (such as is produced in vivo) has the same binding domain on all "arms" of the pentamer. They don't bind to more than one antigen, instead they can bind to multiple copies of the same epitope. Due to steric hindrance, a single IgM molecule generally will not bind at all 10 binding sites.


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Why are irises unique?
I heard that irises are different and unique for every person. According this link, probability of two irises having identical pattern is 1 in 10 to the 78th power. That's how iris scanners identify the identity of people. This technology is becoming very evident. So I ask, why are irises for each person different and unique?

What research have you done before asking this (interesting) question? Do you have evidence for, or have you "heard" that irises are unique (the latter, and lack of support for this statement can render this question off-topic). Can you support this statement? Do you think the same factors that control fingerprints can actually control the formation of the iris?

@anongoodnurse I edited it.. I added evidence and links... and you're right, the same factors that control fingerprints probably don't control the formation of the iris...Thanks 4 the help!

Iris is a thin, circular structure in the eye, responsible for
controlling the diameter and size of the pupil and thus the amount of
light reaching the retina. The color of the iris gives the eye its
color. In optical terms, the pupil is the eye's aperture and the iris
is the diaphragm that serves as the aperture stop.

Color and structure of iris is greatly depended upon genetic links, but the patterns are not. Iris is developed by the prenatal(before birth) growth through a process of tight forming and folding of the tissue membrane.

The human iris begins to form during the third month of gestation. The structures creating its distinctive pattern are complete by the eighth month of gestation, but pigmentation continues into the first years after birth. The layers of the iris have both ectodermal and mesodermal embryological origin, consisting of (from back to front): a darkly pigmented epithelium; pupillary dilator and sphincter muscles; heavily vascularized stroma (connective tissue of interlacing ligaments containing melanocytes); and an anterior layer of chromataphores and melanocytes with a genetically determined density of melanin pigment granules. The combined effect is a visible pattern displaying various distinctive features such as arching ligaments, crypts, furrows, ridges, and a zigzag collarette. Iris colour is determined mainly by the density of the stroma and its melanin content, with blue irises resulting from an absence of pigment: longer wavelengths differentially penetrate while shorter wavelengths are reflected and scattered, a phenomenon resembling that which makes the sky blue. The heritability and ethnographic diversity of iris colour have long been studied, but until the present research, little attention had been paid to the achromatic pattern complexity and textural variability of the iris among individuals.
Reference

Iris Recognition vs. Retina Scanning
Iris and retinal scanning are ocular based biometric identifiers. Iris recognition uses a camera to capture image of the iris. Iris is the only internal organ visible from outside the body. Iris scanners can acquire an image of the eye from a distance of 3 to 10 inches.
In retinal scanning, the device send a beam of light deep inside the eye to capture the image of retina, which is located on the back of the eye. retinal scanning is not widely used due to the intrusive methods used to capture the image.
Factors which enhance the iris scanning system,

reference

In the list titled "The Advantage of Iris Recognition", only the first two items are really biologically relevant.  The other points are just advertising the technical features of some particular iris recognition system.

@augurar:Uniqueness of iris is described above the title you mentioned. Your point is right but I deliberately put it there for sharing some knowledge about background working of an iris scanner


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What does pain look like in wave form?
I am interested in understanding what "pain" and "hot/cold" look like, as far as waves signatures (signal processing) go.
My general understanding of how pain (nociceptive pathways) and hot/cold (thermoreceptive pathways) works are as follows:

A sensory receptor (nociceptor for pain and thermoreceptor for temperature) responds to analog stimuli, and synapses an appropriate signal onto a first-order neuron (the neuron it directly connects to); then
The signal travels up the nerve, neuron to neuron, through the spinal cord, up into the brainstem, and finally into the somatosensory cortex; then
That cortex decodes the signal and interprets it as "pain" or "hot/cold"

Further, my understanding is that these signals are electrochemical in nature:

While passing through a neuron (dendrite -> axon) the signal is of a purely electrical form, no different than the electricity racing around the motherboard of my laptop right now; but...
To synapse from the axon of one neuron to the dendrite of the next sequential neuron, the electrical signal is transformed (somehow, this is where I'm fuzzy) into a chemical signal, and essentially hormones/messenger chemicals ferry the preserved signal to the next neuron's dendrite. At that point, the dendrite converts the chemical signal back into electricity, and on and on this goes until we reach the cortex.

So, only because I am a total neophyte here, I have to preface my actual question by asking the greater community at large: is my general understanding here correct? If not, please begin by correcting me!
The question at hand
If everything I've currently stated is more or less correct, then this implies that, while traveling inside a neuron (dendrite -> axon), neurological signals such as pain or temperature exist as waves of electricity.
I'm wondering:

What do these waves look like? Do they have special names? Are they sinusoidal in nature? Do they travel with known periods/frequencies/amplitudes? Can I represent these waves as trigonometric functions?
I'm sure this differs based on genetics and all sorts of other factors, but what are the general power ratings for the central nervous system? How much Watts/Volts/Amps travel with these signals? Are there standard ranges?

Please note: This is not homework! I am a grown man who works as a software engineer by day and I migrated here from the Stack Overflow community. I am asking this question because I have absolutely zero background in biology, and after scouring the internet for an answer to this, I could find nothing.
Please don't hold back with lofty, low-level explanations. Give me science here! Though I am not a biologist, I'm certainly no dummy either.

"Can I represent these waves as trigonometric functions?" Not really.. You can have a look at Hodgkin-Huxley model or the FitzHugh-Nagumo model.. These are frequently used to model neural impulses.. These are not actually sinusoidal. You can also have a look at what is known as relaxation oscillator

Welcome to Biology.SE! You may want to have a look at action potential.

Thanks for the welcome Remi.b, and thanks for the links @WYSIWYG (+1 to both)!

RE "This is not homework!..." if this is reference to a question which garnered close votes as "homework" you should note that the homework close vote is often used as closure on "poorly researched questions" not just homework (just in case you were a bit confused by this happening when it is not homework)

Thanks @GriffinEvo (+1) - I don't have enough rep to see if my questions are even garnering closevotes or not :-) I put that disclaimer in there because I asked a previous question yesterday and I quickly received comments from other users who obviously assumed I was a student looking for a "quick answer". We get this all the time on Stack Overflow, and so I wanted to combat any potential nay-sayers right up front; hence the disclaimer.

I wouldn't say that the signal in a neuron is the same as in your motherboard. Electrical current is the flow of charges (electrons) parallel to the wire. A nerve impulse is the flow of charges (cations) perpendicular to the nerve (which propagates a signal parallel).

I don't want to comment about the nature of electric signals in neurons (as I know only little about physiology and neurophysiology). But here is a short answer that may already help you.
Neuronal electric signals are called action potential. If you register the voltage at a given location on the axon of a neuron through time you will see something like this:

This picture shows one action potential. Of course when you feel pain it lasts for more than 5 milliseconds. In such case, if you record the voltage for a longer period of time you will just see a series of action potentials. You should have a look to the wiki page for more information.

Awesome answer, thanks @Remi.b (+1)! Quick followup question: say this graph above is what pain "looks" like as a wave. What about "pins and needles" (neuropathy) signals? Again, if my naive understanding of biology is correct, neuropathy occurs when a neuron ceases to function properly and sends junk/garbage signals on to the brain. The brain, in turn, can't make heads or tails as to what the signal is trying to convey, and so we experience the pins and needles sensation.

So: (1) is the pins-and-needles "wave" a specific type of wave (distinct from the "normal" one above) that the brain knows to interpret as pins and needles, or (2) does the brain just interpret anything it doesn't understand as neuropathy? Thanks again so much!

@smeeb there is no general difference in the waveform between types of perception. pain perceiving neurons are non-myelinated and are therefore slower in their conduction.

Hmm interesting @WYSIWYG (+1 and thanks) - but obviously the brain knows to interpret pain and pins/needles differently. So if these sensations don't differ by wave form, then how are the different (in other words, what is electrically-different about them that allows us to distinguish the sensations)?

They come from different neurons. Analogy in that your two USB cables both conduct electricity, but the one connected to your hard disk has different information than your charging phone.

Sorry, it is not my field of expertise, I am not able to tell much more. But the picture shows what basically any neuronal message looks like in term of voltage through time along the axon. Different tactile perception may use different neurons I think (pain, touch, warm/cold) but all of these neurons, always send message through the same kind of electric waves.

Thanks @MarchHo (+1) - what neurons do pins-and-needles come from?

http://biology.stackexchange.com/questions/24555/what-causes-feeling-of-feet-falling-asleep-to-be-delayed/25856#25856 is an answer I recently put up on the origin of pins and needles. Consider reading the question and other answers too for a general overview.

Thanks again @MarchHo (+1) - I'll dig in more tonight, and I appreciate your USB analogy. But to summarize: are you saying: (1) that "pins and needles" (parasthesia/neuropathy) travels to the brain with the same waveform as any other signal but simply carries different encoded "data" on it; or are you saying that (2) there are special neurons that specifically transmit parasthesia signals to the brain? And if, #2, then I'm curious: what are the names of these specialized neurons? Thanks again!

What is important is the sequence of action potentials. I would suggest reading about temporal coding and rate coding as a start. For instance a (very lightweight) introduction can be found on Wikipedia: http://en.wikipedia.org/wiki/Neural_coding Also, note that much of it is how we INTERPRET a certain neuronal signal; our brain is easily fooled! For instance, when eating spicy food we perceive it as "hot", even if it is not at high temperature. This is because the receptors mediating the "hot" sensation are the same for spice and temperature.

Since the action potential question has already been answered, I will attempt to answer

I'm sure this differs based on genetics and all sorts of other factors, but what are the general power ratings for the central nervous system? How much Watts/Volts/Amps travel with these signals? Are there standard ranges?

You are right in that there is a large amount of variation in the electrical variables, however neurons generally have an action potential voltage of ~70mV, give and take 30. I could not find any papers in a cursory search on the power of neurons.
To answer your "comment question" due to lack of space, (1) neurons encode data in a binary fashion due to their on or off mechanism of impulse transmission, and there have been studies done in deciphering what these pulses mean. However, it is still an active field of research with many questions. (2) However, pain signals are only transmitted on sensory neurons containing nociceptors.
You should also read up on how an action potential is generated, as that would help you understand the concept better.

Thank you so much @March Ho (+1) - last followup question (I promise), and it should get to the root of my question here: if pain signals are only transmitted on sensory neurons containing nociceptors, then what is the equivalent for "pins and needles" signals? What exact receptors are required to exist on a sensory neuron in order for that neuron to transmit pins and needles/parasthesia signals? Thanks again!

This is still an active field of research, and not being a specialist in the field I cannot say what this specific signal is. It is possible that this signal has not yet been discovered by science.

That makes sense and +1 @March Ho for the excellent help thus far. Just out of curosity, what field or specialty would be actively researching this topic? Biomedicine? Bioelectricity?


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Spironolactone's role with adrenergic agents in heart failure?
I am studying the treatment plan of adrenergic agents for heart failure.
Then, in the group discussion, spironolactone was included.
But I cannot understand how it is relevant when considering adrenergic agents for treatment of heart failure.
It is probably that it was only mentioned because adrenergic agents are usually used in combination with ABC therapy (antiplatelet, beta blockers, ...).
This includes also diuretics.
Spironolactone is diuretic and antihypertensive.
But I cannot understand how one can classify it adrenergic.
What is the role of spironolactone with adrenergic agents in heart failure?

Please could you add a definition of adrenergic and explain why you are asking - ie where is it defined as adrenergic?

@GriffinEvo: adrenergic refers to stuff acting on adrenaline recpetors.

Do you mean SPIRONOLACTONE?

Spironolactone works through a mechanism different than the adrenergics.
You said of the ABC approach, "This includes also diuretics." That's why Spironolactone was included.
Spironolactone is a specific pharmacologic antagonist of aldosterone, acting primarily through competitive binding of receptors at the aldosterone-dependent sodium-potassium exchange site in the distal convoluted renal tubule. Spironolactone causes increased amounts of sodium and water to be excreted, while potassium is retained. Spironolactone acts both as a diuretic and as an antihypertensive drug by this mechanism. It may be given alone or with other diuretic agents which act more proximally in the renal tubule. Aldosterone interacts with a cytoplasmic mineralocorticoid receptor to enhance the expression of the Na+, K+-ATPase and the Na+ channel involved in a Na+ K+ transport in the distal tubule . Spironolactone bind to this mineralcorticoid receptor, blocking the actions of aldosterone on gene expression. Aldosterone is a hormone; its primary function is to retain sodium and excrete potassium in the kidneys.

The lack of a decrease in the neuroendocrine prognostic markers, norepinephrine and endothelin-1, suggests that the beneficial effects of spironolactone are mainly related to mechanisms independent of the adrenergic and endothelin systems. The escape of AII and aldosterone, probably reflecting activated feedback mechanisms, confirms the specific activity of spironolactone on the renin-angiotensin-aldosterone system and supports the hypothesis that the beneficial effects of spironolactone on the progression of heart failure are mediated by the blockade of aldosterone receptors.

PubChem
Beneficial neurohormonal profile of spironolactone in severe congestive heart failure: Results from the RALES neurohormonal substudy


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Names of nerves in hands, shins and face
I am looking for the names of the nerves in 3 specific locations of the human body:

The nerve running along the "top" (opposite side of the palm) portion of the thumb, from knuckle to fingernail (see 1st picture below); and
The nerve running along the anterior tibia (also see 1st picture below); and
The nerve(s) of the face running along the eyebrows and outer edges of the eye sockets (see 2nd picture below)

After looking here, here and here, the best I could muster was:

The median nerve is the nerve that carries sensory signals from the top of my thumb; and
The superficial peroneal nerve is the nerve that carries sensory signals from my anterior tibia

But in every diagram of the face's nerves, there are simply too many for the article/blog/diagram to enumerate, and I can't discern which specific nerve or nerves runs outside of the eyes and across the brows.
Any ideas? Here are the pics to solidify the specific areas I'm looking for:

Please note: this is not homework! And although it may be considered by some to be a rudimentary question, I have actively tried to research this myself and have come up short. Below, I explain all the failed methods I attempted to figure this out on my own. So all this to say: if you do down/closevote this, please don't do it because you think it's homework or because you think it shows a lack of research!

I have made some structural edits by placing the this-is-not-homework comment below the question. Hope that's fine. You can roll back easily if you don't like it. I edited the tags. This is definitely unrelated to the central nervous system.

http://classes.kumc.edu/sah/resources/handkines/nerves/nerve.htm

https://home.comcast.net/~wnor/antlegdorsalfoot.htm

You are looking for the Trigeminal nerve, the largest nerve in the face. Here it is with its branches.

It is both afferent and efferent.

Afferent and efferent components of the facial nerve in the bullfrog (Rana catesbeiana)
Cranial Nerves Illustrated: Figure V-4 General sensory component of the trigeminal nerve, ophthalmic (V1) division.
General sensory afferent (blue-green)


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Are transgender people born physically different from others?
Are all children born with only either male or female body parts (other than exceptions), or is there actually a natural third gender with the physical characteristics of both genders, e.g. the child has the genitalia, or reproductive organs, of both sexes?
According to Wikipedia they are only either male or female when born. They only feel different later on in life.

@MattDMo I edited out the reference to breasts and made it more comparable (i.e. male and female genitalia)

Why all these down votes? I was being told this from a long time that they are physically born different. It is obviously noob's question.

I don't know why you've tagged me in that comment (I haven't downvoted) but it's probably because you are incorrectly trying to label Transgender and Hermaphroditism as the same thing.

@GriffinEvo I didn't tag you in that comment. You can see that. Anyway I didn't knew the correct word.

Seems you did because it flagged my inbox, it only does that if you use "@username" (it also does notifies the author of the original post when you comment)... maybe something glitched. Regardless, I'd guess that's the reason - I can imagine some might find it offensive that your question makes them out to be the same thing.

@GriffinEvo FYI, if the author of a post writes a comment but does not tag anyone and there is only one other user that has commented (note MattDMo's comment has been deleted), the system assumes it was intended to be in response to the other user, and notifies them automatically. See How do comment @replies work?

@p.s.w.g - Thanks, I'd never noticed it happening before!

The concept of transgenders has nothing to do with sexual organs at birth. Transgenders is a concept that has to do with sociology, not biology. See the wiki link.
intersex (previously called Hermaphroditism) has to do with biology. The wiki link makes a great job at defining intersex.
In short: A transgender person is born anatomically either male or female (with eventually exception of intersex who go on to become transgender) and they then identify themselves to the opposite sex (or a third sex) rather than identifying themselves to their actual anatomic sex.
Note that this post is closely related.


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What is the biggest facultative anaerobic metazoan known to science?
Related: What's the biggest obligate anaerobic organism discovered till now?
I had always assumed that the Riftia tube worms were obligately anaerobic since they lived next to anoxic volcanic vents, but a quick literature search showed it to be a facultative anaerobe, being able to survive at least 60 hours without oxygen.
If "facultative anaerobe" is defined as being able to survive at least 24 hours in the absence of molecular oxygen in an otherwise normal environment, are there any metazoal organisms larger than Riftia (which are up to 1.5m long)?

The answer to your question is going to be some plant or fungus. You might want to stick the word "metazoan" somewhere in your question.

Tapeworms? They can grow much longer. Are you specifically interested in free living metazoans?

I didn't specifically ask for free-living metazoans, so tapeworms would be a good answer.

@MarchHo am not able to find a reliable evidence for the anaerobic metabolism in large cestodes.

I think a tapeworm is your best bet. For tapeworms specifically, I found this textbook, Animal Physiology: From Genes to Organisms, which claims:

Active facultative anaerobes include some parasitic worms such as tapeworms that can survive without oxygen indefinitely...

I was not able to find any primary research on the subject either @WYSIWYG (other than a paper from 1951 that doesn't seem to be available anywhere), but if the textbook's claim holds, I can't think of anything larger than a tapeworm.


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Are the Chromosomes organized in any meaningful way?
So my major is in pharmacy but both my master and my (currently in progress) doctoral degree are both in theoretical chemistry. My thesis is about quantum chemistry and proteins, but it has a certain amount of phylogeny and evolutionary biology such that I've had to learn some phylogenic analysis methodology and have had my share of experience using sequence databases and analysis tools around the web. Although I do not focus particularly in the human genome, or even human proteins for that matter, I got myself thinking about a rather curious question.
I am by no means a specialist in molecular and evolutionary biology, but I do understand that chromosomes and genes come up in the population by several mechanisms. Now, it is interesting to me that all the information regarding biological sex in humans is contained within a single chromosomal switch, the Y chromosome. Given that fact, I asked myself
"Do we have some order in the arrangement of our genes in their chromosomes?"
So now I turn that question to you people, who seem to be more well-equipped to tackle theses questions than I certainly am. Forgive my ignorance and indulge my curiosity!
[EDIT FOR CLARIFICATION]
Okay, clarifying some points that were raised in the comments:
The question is about whether there is a pattern in the organization of genes into chromosomes. For example, the Y chromosome clearly contains a lot of genes associated with sexual dimorphism in humans. I was wondering if chromosomes in general follow that general pattern. If, for example, Chromosome 1 contains such and such kinds of genes, as if it had hints of an overarching "theme" to it.
Is that clearer?

Welcome to Biology.SE! From wiki: "In classical genetics, synteny describes the physical co-localization of genetic loci on the same chromosome within an individual or species"

Welcome! What exactly is your question? The title indicates that your question concerns (1) the organization in the ordering of the various chromosomes, the question in the body hints that (2) you are interested in the Y chromosome, while the quoted question asks about (3) gene placement/localization on chromosomes in general. It is unclear as of know what exactly you need to know.

You should narrow down your question a bit..

I don't think this is too broad or unclear. It's a simple yes or no question: are genes arranged in a specific way? The answer happens to be yes for some and no for others.

This can be narrowed down. The point that is a bit unclear is this: are you interested to know if the order is conserved — homologous syntenic blocks or if the order itself has a significance. If you clarify this then at least the first question is answerable. The second question can be answered at least with respect to E.Coli with some precision. For eukaryotes there are many factors to be considered. I haven't voted for closure yet because the question is interesting.

@WYSIWYG Ah, I see your point now.

@OP.. this is still not clear.


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Specific location where nerves converge
I'm looking for the "earliest" specific site where the 3 following nerves' sensory signals "converge":

Trigeminal nerve
Median nerve
Superficial peroneal nerve

By "earliest", I really mean the first location in the sensory pathway (to the brain) at which these 3 nerves' sensory signals converge.  And by "converge", I mean "feed into each other". My understanding is that, with sensory nerves, all tactile reception roads lead to the somatosensory cortex, and so, I would imagine all the nerve signals converge/merge into one another at some point.
I would imagine the location I'm looking for is the brainstem, probably the pons, but I'm not a biologist and am looking for either correction or confirmation here. This uneducated guesstimate comes from two sources:

Wikipedia - which states that the cranial nerves feed into the pons; and
The fact that the median and peroneal nerves are spinal nerves, which ultimately feed into the medula, which then turns into the pons.

Am I right or way off track?

Please note: this is not homework!

Not all roads lead to the somatosensory cortex. E.g., visual input is funneled to the visual cortex.

Do you mean where the signals from these nerves integrate? Because the "nerves" can anatomically terminate without converging; the first is a cranial nerve whereas the others are spinal nerves. Moreover a "nerve" has both sensory and motor fibres. This question is a little broad.

Thanks @WYSIWYG (+1) - yes, I do mean nerve signals and have updated my question to reflect that. Thanks again!

@smeeb You really don't have to disclaim all of your questions with "This is not homework!" That close reason is mainly to prevent questions with no research effort that are just copy-pastes from assignments (i.e. "List the organelles found in human mast cells.") Your questions are good and show research effort, so even if they were homework, they would still probably not be closed.

By reasoning, we can make the following distinction:

the trigeminal nerve is a cranial nerve.
the 2 others are peripheral
nerves.

Cranial nerves take their origin into their respective nuclei, and bypass the dorsal columns (main spinal tract for sensory information). Peripheral sensory nerves stem from the spinal roots, and from there go up through the dorsal columns. This would bring you to the thalamus, where all sensory information is regrouped. However, somatosensory information from the face and the rest of the body happen to travel through different thalamic nuclei (ventroposterolateral for the body, ventroposteromedian for the face, If my neuroanatomy is not too far behind me...). This leaves us with the internal capsula (fibers that link the thalamus to the cortex), but I do not think much signal integration occurs there.
In conclusion, the first anatomical level of convergence between the 3 above-cited nerves would indeed be the somatosensory cortex.


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Is there any evolutionary advantage of selection of L-amino acid over D-amino acid?
After listening to a scientific talk, I had this question that why in the natural selection process, are the L-amino acids selected over the D- form. However, we still we produce D-amino acids; specifically in the brain there is a higher concentration of D- amino acids. One possible reason is that they act as neurotransmitters.

It would be nice if you can add a reference for brain having D- amino acids.

http://www.ncbi.nlm.nih.gov/m/pubmed/18564180/

Just in case the situation changes.

As you say yourself, biological molecules are usually available in both chiralic possibilities, yet nature uses only one of the two possibilities. At some point in our molecular evolution (and at a very early one) L-amino acids were stochastically "chosen" over their D-equivalents (I think that the choices would have been equiprobable). There is no reason why D-amino acids shouldn't work here as well.
There is some discussion on why L-amino acids are used, see the references for some ideas. It might be that the proteins made from it where slightly more stable or because they were more abundant. D-amino acids are in use today as a protective step - most proteases for example cannot hydrolyse the D-amino acids in the peptidoglycan wall of bacteria. Using this "unusual" amino acids gives some protection here.
References:

Mirror symmetry breaking in biochemical evolution
Mirror symmetry breaking at the molecular level
Origin of homochirality in biological systems

I added a small comment in the bracket if you don't mind.

You mean that organisms use the D-variant in their cell wall? Interesting.

@ChrisStronks yes.. the peptidoglycan of gram positives have D-amino acids

The current thinking amongst biophysicists is that if we all woke up tomorrow to find that someone had edited the book of life so as to exchange all of the L-'s and D-'s (and made similar mirroring changes to all of the molecules that any protein interacts with), everything would be exactly the same.
Milton, et al. (Science, 1992) lent supporting empirical evidence to this view by carrying out the total chemical synthesis of a D-enzyme, D-HIV-1 protease. They showed that the L- and D- versions of the enzyme had identical and reciprocal activity, meaning that L-enzyme cut the L-substrate well and the D-substrate poorly, and vice-versa for the D-enzyme:

They also showed that the structures the L-enzyme and D-enzyme were mirror images of one another:

The preference for L- forms over D- emerged sometime early in evolutionary history, and there's a lot of speculation as to how the preference arose (it could have been cosmic rays!), but the evidence is thin.

Interesting! But do you think their results (mirror structure and swapped substrate preference) extrapolates to all enzymatic reactions or is this a lucky shot?

@ChrisStronks At least for enzyme activity, I think that the invariance of L- and D- follows from the fact that electromagnetic interactions don't change for a parity transformation (reflection is a type of parity transformation). So it would probably be the same for any enzyme.

@ChrisStronks And the mirror structure result would almost certainly be the same for any protein. A protein is the same as any other molecule in that if you flip all of the chiral centers you end up with its mirror image.

This question is a matter of discussions, but I'd like to mention that there's basically two viewpoints. The first viewpoint is that the symmetry breaking is global (in other words, there's a reason why exactly L-amino acids; if there are other planets with Life, L-amino acids should be "used" on all of them or at least on the major number of them). The second viewpoint is that the symmetry breaking is local (or spontaneous; and hence Life outside Earth can "use" aminoacids of arbitrary sign).
The only global reason for global symmetry breaking known in physics is weak interaction. There were some efforts to connect weak interaction and symmetry breaking in biomolecules, starting from Vester-Ulbricht hypothesis, but it seems that there's no confirmed mechanism of this connection. You may read this review which may be outdated (2000) but at least it can give you an idea about what kinds of mechanisms were tested.
The science around the local symmetry breaking is much more rich but works like Sutherland's (Powner, Gerland, Sutherland, «Nature», 2009, 459, 239—242, doi:10.1038/nature08013) are about the mechanism of possible local symmetry breaking, and the question "why L?" is meaningless in frames of this view (or in other words answer is "it was just a random choise"; in fact, it is not even concluded if this "choise" was made on a chemical level or during biological evolution).
PS By the way, more recent papers (1, 2) suggest there's some progress in the field.

There were some efforts to connect weak interaction and symmetry breaking in biomolecules. That is the most crazy-yet-still-vaguely-plausible thing I have ever heard. Well done

@tel yeap, that's because it's a very attractive approach for physicists. Actually it's not that vague if you read that review, but the point is -- there's no reasonable success in proving that point..


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What is the science behind the inaccurate perception of colors?
If I go into a green room (all walls are semitransparent and green) and spend some time - around 10+ min - in there, when I come out all my eyes see is white as pink. I see no (or very few other) colors due to this for a while - around 2 minutes. What is the science behind this? Why do eyes lose color perception in this case?

To explain the neurophysiological background to the existing answers I would like to add the following:
The effect you are describing (pinkish appearance of white) is generally referred to as a negative after image and it is a direct reflection of the color opponency in the retina. The effect is caused by adaptation of the (in this case green) cones in the retina. This adaptation occurs through photobleaching, which means that the chromophore (cis-retinal) in the visual pigment in the cones is converted to the inactive state (trans-retinal). The conversion of retinal forms the basis of the detection of photons by the cones. When you look at a green stimulus for a long time, the photopigment in the green cones is progressively converted to the inactive trans-retinal state and the green cones will stop responding to the green light stimulus. Why then does this lead to a pink'ish (magenta) perception of white? This is because color vision is based on color opponency.
The visual system in the retina is based on three cones: red, green and blue cones.
These cones feed into three channels: a red-green, a yellow-blue and an achromatic (luminance) channel. Note that yellow is formed by adding the red-green color signal, while the achromatic channel is formed by adding the red and green cones as well, where only light intensity information is extracted.
The red-green and yellow-blue channels are opponent channels. For your specific example, the latter is important. Red-green opponency means that at the neural level, red responses cancel green responses and vice versa. Therefore, we are not able to perceive a "reddish green". White is perceived when light activates all cones, such that red cancels green, green cancels red and yellow cancels blue.
However, if the green cone system is adapted due to the green pigment being bleached, the opponency of green is diminished and the red response will dominate. In addition, as the yellow channel will be reduced as well, there will be a bit of blue added as well due to reduced blue suppression, explaining the pink'ish (i.e., magenta) appearance you describe. A nice example of the negative after-effect is the following:
Stare at the colored dots on the girl's nose in the negative photo image below for 30 seconds. Then look at a white surface and start blinking. You should see a non-negative image of the girl (see here for image source).

Reference on the opponency model:
Mather, Foundations of Perception, chapter 12 Colour Vision.

First recall that pink is white minus green, more or less.
Now, your perception can be explained by adaptation: Neurons try to control their gain (amplification factor) to have roughly the same range of output. So if there's a lot of stimuli they like, they will reduce their gain, and vice versa. It can be thought of as a form of fast time-scale homeostasis in this case.
While you were in the green room, your neurons that represent 'green' gets less sensitive to green stimuli due to strong green input (adaptation). Additionally, the 'non-green' representing neurons become more sensitive, since there's less visual stimuli that they like. When you suddenly come out of that room, now the green neurons do not respond as strongly as the non-green neurons in response to white, hence your perception of pink.

I don't think the process is primarily mediated through gain control. Rather, it is disrupted color opponency through pigment depletion.

I like this answer because I always like analogies between electronics concepts (or terms) with human/natural systems and it is easiest graspable answer. Still the depth seekers might not satisfied ;)

@ChrisStronks pigment depletion can be thought of as a form of adaptation. I guess 'gain control' would be a wrong analogy though. Thanks for your comment and answer.

The shift in color is caused by the proteins in your photoreceptors being used up and thus no longer being able to absorb the light.
If you stare at a green wall, you're using up green sensing proteins. When you switch to a white wall you're now seeing more red and blue compared to green, and thus it appears pinkish.
Your brain somewhat tricks you into thinking that the green you're seeing is the same was it was when you first looked at it, but you're actually sensing less of it the longer you look.

Perhaps "temporarily deactivated" or "in a refractory period" is a better term than "used up", as the latter term implies the protein was destroyed by the process.

The cones are definitely not in a refractory state (they don't spike) and, technically, not deactivated either. "used up" is actually pretty apt.

@ChrisStronks Can you explain why they are not, though? https://books.google.co.uk/books?id=ask7iOrvjJIC&pg=PA481&lpg=PA481&dq=color+cone+refractory+period&source=bl&ots=3fU0u3trDO&sig=QaP522JuocfShsu7squ1LIY4h-A&hl=en&sa=X&ei=28uTVPK0PNCv7Aat-ID4Dg&ved=0CDMQ6AEwAw#v=onepage&q=color%20cone%20refractory%20period&f=false is an example of scientific literature using the term.

Refractory periods refer to action potentials causing sodium channels to enter an inactivated state. Deactivated implies regulatory action of some kind. That is not the case. The active cone rhodopsin is simply depleted.


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G>T transversion VS. T>G transversion?
So I'm reading about how mutations in DNA can be caused by oxidative damage. An example of a product of oxidative damage is given: 8-oxo-7-hydrodeoxyguanosine
My textbook says that this product frequently mispairs with A, resulting in a high level of G-->T transversions.
What I'm not understanding is why it's a G-->T transversion. If the 8-oxo-G is pairing with A, resulting an an A-G pair, isn't this a T-->G transversion? Or does the order not matter?

Originally the position had a G:C pair. After the mutation, there is an oxoG:C pair. Upon replication, the strand with C will pair to G and the original pair will be created as expected. However, since oxoG can also pair with A, the strand with oxoG may form an oxoG:A pair. Another round of replication gives the products T:A and oxoG:A. Thus the G in the original strand is replaced by T (ie it is a G$\ce{->}$T transversion).


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Evolution: One big population vs. many small populations
Let's say I want to evolve a bacterium that is resistant to an antibiotic. I want to do this by growing initially clonal populations of bacteria in presence of this antibiotic for a long time.
I have two options:

Make one 50 ml flask culture
Make ten 5 ml tube cultures

What are the comparative advantages and disadvantages of these two? Clearly, the ten culture version is better at probing the space of all possible resistance mechanisms. However, what about the rate of evolution? If I just want to get a resistant strain as fast as possible, which one should I use?
Note that "antibiotic" is just a proxy for any selective pressure, and "bacteria" is proxy for any organism. If possible, I think it will be interesting to address the effects of sexual vs. asexual reproduction in the organism that is being evolved.
There is already a question, How does rate of evolution/innovation scale with population size? that is very similar. I think mine is different, because it is not one small population vs. one big population, but one big population vs. many small populations. In other words, I am attempting to control for number of selection/mutation events, and focus only on the stratification of the total population.

Here are my thoughts. I might be wrong. Such process are mainly limited by the availability of mutations. In consequence, as long as the product of the selection differential and the population size is high enough, it does not really matter whether you split your populations or not.

If it's the same number of individuals in either set up then the rate of mutation will be the same, smaller populations are prone to drift so this could reduce the speed/quality of response in the smaller populations, but replicate populations will be requisite if you want to publish something, and interesting comparisons could be made between replicates (e.g. do they evolve different solutions to the same problem?) - my preference would therefore fall to many replicates

Note: This is not an area where I know the litterature well

Where are many counteracting processes to consider for this question. For instance, the rate of evolution will be affected by the rate of mutation, the distribution of positive and deleterious mutations, strength of selection, whether the fitness effects are small or large, if fitness effects depend on interactions between multiple mutations or single mutations with large effect, asexual vs. sexual populations, and processes such as genetic drift.
A recent review that is useful for your question is Lanfear et al (2014). They focus on how substitution rate is affected by effective population size, and go through both theoretical and empirical evidence. They conclude that in most cases, most mutations are deleterious, and that drift and selection are the most important effects in determining rates of evolution. They also state the effect of effective population size (Ne) is likely to depend if mutations are dominated by deleterious or advantagious mutations, and they expect the rate of evolution to be negatively correlated with Ne when deletious mutations dominate evolution and a positive correlation to Ne when advantagious mutations dominate.
A paper by Rozen et al (2008) indicates that while large populations are more effective in fixing mutations with large positive effects, small populations can be more effective in complex "rugged" adaptive landscapes.

While such determinism speeds adaptation on the smooth adaptive landscape represented by the simple environment, it can limit the ability of large populations from effectively exploring the underlying topography of rugged adaptive landscapes characterized by complex environments.

However, this does not deal directly with the rate of evolution, but mostly about attaining the highest possible fitness in a particular fitness landscape. Another interesting paper is Desai et al. (2007), but I haven't looked through this yet.  However, they find (for asexual bacteria) that the speed of adaptation scales less than linearly with population size, and similar results have also been found in studies from Lenski's group. Their interpretation is that evolution is driven by multiple concurrent mutations of small effect and not one-by-one fixation of single mutations (which would favour large populations more).
For your case of evolution of resistance, I think one crucial thing is if you expect resistance to be driven by a few single mutations or combinations of many mutations that interact (related to whether resistance is "easy" or "hard" to evolve). From what I understand, the first case should favour a single large population (since they will fix mutations for resistance more quickly), while the second case might favour many smaller populations (since you might get more effective exploration of combinations of mutations)
These are just a few starting points in a very large field, and I hope that you find them useful.

Very helpful! I especially appreciate the links to literature, thanks.

Nice answer (+1). As I said in my comment (and I might be wrong) I would tend to think that the difference between several small or one big population is totally negligible in this case because 1) $2\cdot N\cdot s$ will much large than $1$ anyway and 2) adaptation is mutations limited

With very large population sizes like this the effect of genetic drift goes to zero, which is greatly simplifying. I'm also assuming selection is very strong, so that fixation times are small, and that mutation rates and population size more or less cancels out, so there are a finite number of mutations and the selection space is relatively unexplored. If selection is weak everything takes longer, but I'm pretty sure the results are the same. There's greater exploration of alternatives, but that doesn't affect our thought experiment comparing population size.
In asexual populations: 10 cultures will give you ten answers to your selection criteria, one of which will be 'best'. One culture will give you the best solution a little bit later (larger populations take longer to reach fixation).
In sexual populations: One culture is better. The space of alleles is larger, and positive or conditionally positive mutations will be tested against more possible synergistic partners.
Consider that there are ten positive mutations split across your population. A sexual population in ten sub-populations has a tiny chance of getting all ten mutations into the same gene pool, but all ten sub-populations combined make it near-certainty that all ten mutations will make it into the same organism.
There's a limit to sexual population size above which evolution doesn't accelerate with additional individuals, because any additional mutations they bring to the table are eventually guaranteed to already exist in the gene pool. That limit is related to the genome size and mutation rate and probably other things, but for biological species it is enormous.

Both have its benefits and drawbacks.
The single big culture would have a bigger risk of contamination, but a bigger chance that the resistant mutated individuals are present, so in this case you would have a lower risk of complete extermination of your culture.
The smaller several cultures on the other hand will let you try several dosages of the antibiotic without fearing exterminating your culture. On the other hand each individual culture probably will have lower diversification, so lowers the chance of new strains.

RE the first segment of your answer, @superbest is using clonal populations as a base so this is not true in this case. There would be no standing genetic variance in the population(s) regardless of the population size, all resistance would have to come via new mutation. If the meta populations are of equal size (e.g. one population of $N$ individuals or 10 populations of $1/10N$) then there is no difference between the expected number of mutations between the two alternatives.

While you are correct and make valid points, in retrospect I realize that I failed to adequately specify that I am interested in the biology, not the methodology. As such I neglect contamination risk, and apply the same conditions to all cultures. (this is more realistic, if you think of natural populations)


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What is the purpose of segments in citrus fruit?
What is the purpose of segments in citrus fruit? In my experience, each segment usually contains from zero to two seeds. I may have seen more but only rarely, if I remember correctly. What is the significance of having more than one seed in a section (twinning, perhaps)?

The citrus fruits belongs to the type hesperidium, which is a highly specialised form of berry specific to citrus fruit.The hesperidium is derived entirely from the ovary, other features of hesperidium includes leathery exocarp, spongy mesocarp and juice filled endocarp.

A hesperidium has an aromatic, leathery exocarp (the "rind") and mesocarp and endocarp compartmentalized into sections (each representing a carpel), each of which contains one to several seeds. This type of berry is unique to the genus Citrus, which produces fruits such as oranges, grapefruit, lemons, limes and tangerines.
Reference

The edible flesh of a mature citrus fruit is divided into segments, each derived from an ovary locule.The number of segments varies widely but is typically between 10-15.Each segment is surrounded by tough endocarp membrane and filled with tightly packed juice sacks or vesticles.
Reference

There are several major ways that plants have evolved for constructing
fleshy fruits.  Oranges etc. belong to the family Rutaceae, which is
unique in filling its "locules" (the spaces in which seeds are produced)
with "juice sacs" that are attached to the outer walls.  Each of the
locules probably represents a structure, known as a "carpel" that was
at one time distinct, but now has fused together with its neighbors.
The outer skin of most citrus fruits shows no sign that the interior
is sectioned, but this is a result of the fusion occurring early in
the development of each individual fruit (rather than early in the
evolution of the Rutaceae).
Reference

Segmentation inside the citric fruits are due to its development from the ovary, as each of the segment is evolved from the ovary locule, the number of segments varies according to species(also there are variations in single species). The evolutionary advantage of segmentation inside the fruit is a debated topic.A digestible theory is that, each segment of the fruit contains 1-3(in the case of orange) seeds, due to the evolution by mammalian resources, keeping segments inside the fruits helps in the dispersal of seeds by different agents. When a ripe fruit falls down, its individual segments are broken apart and eaten by different animals/birds, this in turn helps in dispersal of seeds to geographically distinct(distant) locations. With each segments featuring seeds inside them, its a good adaptation to produce a single fruit which can be distributed by different agents.

My issue with segmentation as a distribution strategy is that the segments are often stuck to each other. However, I've never observed citrus in the wild so I have no idea what goes on there. Thanks for the very well done answer.

The selectionist part of the answer lacks refs. I personally doubt, it has any scientific basis.

@har-wradim: Is it so much difficult to believe "With each segments featuring seeds inside them, its a good adaptation to produce a single fruit which can be distributed by different agents."

@Jay That's exactly my point: science is not about believing.

@har-wradim: Some times we have to believe something in order to get a conclusion !