text:
What features cause mechano sensory adaptation?
In relation to mechanoreceptors (e.g. pacinian corpuscles), what stops a constant stimulus from producing action potentials?
I understand that adaption is used to filter out stimuli that aren't changing, but what are the cellular mechanisms going on within the neurone that drive this process?

At the molecular level this is called receptor desensitization. This is the reason why for example spices (like red hot chili paper) taste more pungent the first time you put them in your mouth and less and less subsequent times (in this case the receptor is called TRPV1).
Mechanosensory perception is mediated, at least in part, by similar transient receptor potential (TRP) channels therefore mechanosensory perception is also subjected to desensitization at the molecular level. In this particular case it is specifically called homologous desensitization.
This is, in my opinion, the primarily reason why a constant stimulus will stop producing action potentials, in essence the receptor will be desensitized and does not provoke a membrane-potential change that mediates the transmission of a neuronal signal.

Footnote
Desensitization in TRP channels happens because those channels open to let $Ca^{2+}$ ions to enter the cell and after prolongated stimulation the intracellular $Ca^{2+}$ concentration will reach the same $Ca^{2+}$ level of the extracellular medium preventing more $Ca^{2+}$ ions to enter the cell.
$Ca^{2+}$ influx into the cell is what provokes a difference in membrane-potential (i.e. the cell is now electrically charged) which mediates a signal that is then transmitted to the neuronal circuitry.

@AliceD Never said TRP are the only mechano receptors, yet some TRP channels respond to mechanical stimuli as well. As an illustration Chapter 3.9 here.

@AliceD Are we talking about molecular receptors? Because it seems you understood some of my "receptor" terms as neurons which is definitely not what I meant. I did not search for the main mechano receptor on the skin but I strongly guess my answer hold true for those as well.

@AliceD Not that far actually as at the molecular level receptors (such as GPCR and TRP channels) work the same. Again I am talking only about what happens at the molecular level and in this specific case it doesn't really matter if the receptor is in a taste cell or a nerve ending on the skin.

Short answer
In case of Pacinian corpusles, the adaptation is generally ascribed to the mechanical characteristics of the outer capsule of the receptor. The capsule's onion-like structure quickly molds itself to pressure stimuli, thereby rapidly desensitizing the receptor.
Background
There are two classes of mechanoreceptors in the skin based on their rates of adaptation, namely rapidly adapting and slowly adapting receptors. The Pacinian corpuscles (and hair follicle receptors) are of the rapidly adapting type. These receptors swiftly become unresponsive (they adapt) when a pressure stimulus is applied, but faithfully transmit rapidly changing stimuli (such as vibrations).
Pacinian corpuscles are specialized vibration receptors. Their dendritic region is shaped as an onion-like structure with layers of stacked lamellae:

Specialized dendritic capsule of the Pacinian corpuscle. Source: Biologymad
These lamellae act as high-pass filters that result in a sharp drop in sensitivity below 150 Hz (Johnson, 2001). If this capsule is dissected from the receptor and a pressure stimulus is directly applied to the sensor element underneat the capsule, the receptor response to a sustained stimulus substantially increases (Mendelson & Loewenstein, 1964). Basically, these elastic lamellae mold their shape to the stimulus and pressure stimuli are only transmitted for a few milliseconds, after which the lamellae absorb the pressure. So only a one or a few spikes are generated at the start of a pressure stimulus. Upon release of the pressure stimulus another spike or two are generated. Hence, a continued pressure stimulus is not faithfully reproduced. However, vibratory stimuli generate spikes on the pressure onset as well as offset as well, and this happens on every phase of the vibration. Hence, vibratory stimuli are faithfully transmitted.

Response of Pacinian corpuscle to a sustained pressure stimulus (indentation of the skin) and superimposed vibratory stimuli. Note the vigorous response to vibrations, but the rapid adaptation to the static pressure stimulus. Source: Zavantag
Although the adaptation of the Pacinian corpuscle is generally ascribed to the mechanical properties of its capsule, further high-pass filtering may be accommodated by neurophysiological properties that limit spike initiation, as described by Cagliari2005.
References
- Johnson, Curr Opin Neuobiol 2001;11:455–461
- Mendelson & Loewenstein, Science 1964;3618:554-5
Further reading
Why are skin tactile receptors considered to be phasic receptors?


text:
What would happen if brain neurons did not reduce their sensitivity to neurotransmitters after prolonged exposure?
From my understanding, neurons decrease their sensitivity to neurotransmitters by reducing the amount of receptors on the cell membrane in response to sustained neurotransmitter activity. One explanation I heard is that cells do that to protect themselves from damage.
This makes me ask - what kind of damage could be caused by sustained neurotransmitter activity in the brain, if cells did not reduce their sensitivity? Can a brain survive/thrive if neurons always had the same number of neurotransmitter receptors?

I never heard about damage. However, decreasing number of channels/receptors in synapse leads to lower noise among other things. for example, you need to support number of channels metabolically.

Short answer
As far as I am aware, neurotoxic effects of chronic excitatory stimulation are not prevented by receptor trafficking.
Background
I think the question assumes that 1) neural damage related to continuous activation (excitotoxicity) is preventable by 2) the dynamic regulation of receptor numbers on the neuronal membrane. As far as I can see, these two processes are unrelated.

Excitotoxicity is

...the ability of glutamate or related excitatory amino acids to mediate the death of central neurons [...] for example, after intense exposure. [...] Excitotoxicity has substantial cellular specificity and, in most cases, is mediated by glutamate receptors. On average, NMDA receptors activation may be able to trigger lethal injury more rapidly than AMPA or kainate receptor activation, perhaps reflecting a greater ability to induce calcium influx and subsequent cellular calcium overload (Choi, 1992).

Hence, it is the influx of toxic amounts of Ca2+ that induce cell death. Not much Ca2+ is needed to accomplish this. For example, a status epilepticus (a sustained epileptic seizure) can lead to hippocampal damage, due to persistent excitation and glutamate release (Meldrum, 1991). Epileptic seizures lasting longer than 5 minutes are regarded as dangerous in this sense and after 30 minutes they are potentially fatal (often not directly related to excitotoxicity though) (Cherian & Thomas, 2009). In this short time span regulation of cell-surface receptor densities are unlikely to play a substantial role. For example, serotonin-specific reuptake inhibitors need 2 weeks to lower the amount of 5HT1A receptors (Tylee & Wolters, 2009).

Dynamic regulation of receptors. The regulation of the number of receptors is linked via feedback loops. A great example is the way glutamatergic AMPA receptors are regulated through endocytosis (Fig. 1).

Fig. 1. AMPA receptor trafficking. Source: Anggono Lab.
AMPA receptors are the principal receptors that mediate most of the fast excitatory synaptic transmission in the mammalian brain (Purves et al., 2001). The dynamic trafficking and proper synaptic targeting of AMPA receptors are crucial in determining the strength and plasticity of excitatory synaptic transmission. This dynamic regulation may also impact learning and memory processes. The process of receptor trafficking is, as far as I know, typically not associated with emergency rescue operations to prevent excitotoxicity. Nonetheless, these mechanisms, are essential to sustain an adaptable brain capable of learning, forgetting and restructuring itself.
References
- Cherian & Thomas, Ann Indian Acad Neurol (2009); 12(3): 140–53
- Choi, J Neurobiol (1992); 23(9):1261-76
- Meldrum, Epilepsy Res (1991); 10(1): 55-61
- Purves et al., Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates; 2001
- Tyllee & Wolters, BMJ (2007); 334(7600): 911–2

In principle, many neurotransmitter receptors work as ion channels and the actual mechanism of signalling involves allowing the influx/efflux of calcium, potassium, magnesium, etc. A good example of this is the acetylcholine receptor. Presumably, if the cell retained the same number of receptors even in the presence of abundant ligands, the cell would flood with ions. Not only would this render the signalling pathway insensitive it may lead to survival issues for the cell/inappropriate cross-talk with other pathways.
That is at least how it should work in the models of neurotransmitter signalling I'm familiar with, it seems quite likely that a neuro lab somewhere has a cell, or animal model that can provide a real world answer.

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text:
Which enzymes degrade dynorphins and what drugs inhibit these enzymes?
Which enzymes degrade dynorphins and what drugs are there available to inhibit said enzymes?

This paper was looking at inhibition of dynorphin converting enzymes and their importance. Although they don't seem to know if it is a single enzyme, or if it is multiple enzymes.
This paper looked at bikunin as an endogenous inhibitor of dynorphin convertase in human cerebrospinal fluid.
This paper looked at several inhibitors (some of which are known to irreversibly inhibit other enzymes), like N-peptidyl-O-acyl hydroxylamines and their effects on hCSF-DCE, the enzyme that cleaves dynorphin A, dynorphin B and alpha-neoendorphin to release Leu-enkephalin-Arg6. However, it is known to inhibit serine and cysteine proteinases.
However, I don't see any actual medications that are meant to inhibit Dynorphin enzymes. Instead I found Al-Fayoumi et. al were actually looking to identify stabilized dynorphin A derivatives instead of just inhibition of enzymes.

Although nicely referenced, a list of articles touching on OP's question is not a suitable answer. The answer should be supported by references, a reference list in itself is not an answer.

I did say at the end of my answer that I hadn't come across any medications that specifically inhibited Dynorphin enzymes @AliceD and pulled from those articles what they had used to inhibit the enzymes. I also noted that hCSF-DCE is the enzyme responsible for cleaving dynorphins.

Yes I agree that your answer is quite complete and I removed my downvote. I do still believe it is not a well-formulated answer, so I will not upvote.

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text:
Do taller people have larger somatosensory cortices than short people?
When we assume that peripheral touch receptor densities are equal in tall and short people, then tall people should have more touch receptors than short people, given the larger amount of skin surface in the former. Hence my question:
Do taller people have larger somatosensory cortices than short people? And analogues to that, what about larger motor cortices in tall people? If tall people need larger somatosensory and motor areas, could this imply that they have less space devoted to other functions, like functions devoted to the prefrontal cortex?

Do you mean mass-corrected size or absolute size? If the latter, then I would say probably due to the laws of scaling.

Absolute size. Mass-corrected size would be interesting too though

If you are interested in the anatomical differences between small and large people, then I'd think you want mass corrected. My brain is larger than my 2-year-old nephew in absolute size, but his is probably larger than mine in relative size.

I would say no.
Your question somehow implies that somatosensory cortex is equally distributed among the different sensory areas of the body, whereas in the reality this is the known "cortical homunculus" concept of how this distribution looks:

If you look at this representation you'll see that chest and legs take only about one third to one fourth of the cortex, thus the changes between short and tall people don't seem to have noticeable contribution to the overall cortex size.
If we just walk away from cortex size and discuss the amount of nerve cells in these areas I would say that these numbers should correlate with the number of peripherial receptor cells that provide input for them, and since there is no known changes in receptor density among different body sizes, even the amount of nerve cells seems to be more or less same.

If there is no change in receptor density, but an increase in body surface area (from being bigger and all) then wouldn't one expect an increase in the number of nerve cells? Basically, I don't understand your last sentence.

I agree with @ArtemKaznatcheev - The core of the question is whether the density of peripheral mechanoreceptors is identical across people of different posture. If yes, a large person (in length, or otherwise) would have more skin receptors and hence a larger afferent input to the cortex, and hence a larger cortical surface needed, as evident in the homunculus.


text:
What is the meaning of this poor sequencing result?
What is the meaning of this poor sequencing result? What is the problem?
Can anyone guide me, please. Thank you.

It means that your srquencing failed. In my sequencing experience there is nothing so to save here, you simply have to repeat the reaction. What have you exactly done? Are you sure that your primer works on your template?

Was your template a PCR product or a plasmid ? Have you seen your template DNA on electrophoresis before sequencing ? If yes, was it just one band, or many ?


text:
Do humans have skin cells that trigger oxytocin release in the brain?
I was reading an article by Montgomery on the therapeutic effect of pets (Boston Globe, January 12, 2015), and I found this quote:

All animals appear to have cells directly under the skin that activate oxytocin in the brain. So gentle touch — from grooming your
  horse’s coat to making love with your spouse — is a powerful trigger.
  But so is simply thinking about someone you love, whether it’s a
  person or a pet. And in fact, a small study published this fall at
  Massachusetts General Hospital found that MRI scans of women’s brains
  lit up in the same areas when shown pictures of their pets as when
  shown pictures of their children.

Do humans have oxytocin triggering skin cells or formations under the skin? If so, are there higher concentrations of these cells in certain areas of the body? In the human erogenous zones, like neck, lips, etc?

Short answer
Oxytocin release has been associated with the cutaneous low-threshold (CT) afferent fibers in hairy skin.
Background
Oxytocin is released from the paraventricular nucleus in the brain in response to low intensity stimulation of the skin, such as touch, stroking and warm temperatures.
In a recent review Uvnäs-Moberg et al. (2015) report that the specific sensory nerve type mediating oxytocin release in the brain is unknown. Although myelinated somatosensory fibers mediating the discriminative sense of touch may be involved, a more likely candidate mediating affective touch are the unmyelinated low-threshold mechanosensory nerves, called C low-threshold mechanoreceptors (CLTMs) in animals or C-tactile afferents (CTs) in humans. Their terminal morphology (i.e., the skin receptor they connect to) is currently unknown. The fibers have been characterized mainly through  electrophysiological and electron microscopy research (McGlone at al., 2014).
The association of CT fibers with affective touch stems mainly from the finding that their activation patterns with various stroking velocities correlates with subjective pleasantness ratings. Specifically, the relationship between brush-stroking velocity and firing rate was distinctly different between CT and myelinated afferents. CTs showed an inverted U-shaped relationship,
whereas mean firing rates increased monotonically with brushing velocity in all myelinated afferents (McGlone at al., 2014).
However, CT fibers have only been identified in hairy skin in mammals, and the fibers mediating affective touch through glabrous skin (including the fingertips, palms and lips) are unknown (McGlone at al., 2014).
References
- McGlone et al., Neuron (2014); 82: 737-55
- Uvnäs-Moberg et al., Front Neurosci (2015); 5(1529): 1-16

to clarify - are hairs involved in triggering those fibers? For example, would a person who undergone laser hair removal feel the same as a hairy person?

@AlexStone:  Their terminal morphology (i.e., the skin receptor they connect to) is currently unknown This includes the hair follicle receptors.


text:
Does RNA polymerase move around DNA or does DNA rotate beneath the polymerase?
I'm thinking of the human genome specifically, but more general answers are welcome.
As RNA polymerase moves along the DNA helix it follows a single strand.  The two DNA strands are unwound locally by a helicase enzyme. However, after some distance, I imagine that either the polymerase must move around the axis of the DNA OR the DNA must somehow be rotated along it's length to relieve the twisting by the polymerase.
I can't quite understand how the DNA is free to rotate, being part of a very long molecule. However the other option is also causing me a problem: the growing (nascent) mRNA can be tens of thousands of bases long while still attached to the RNA polymerase and the DNA template.  If the RNA polymerase follows the helix of the DNA, does it also drag the full transcript around with it?

My bounty is prompted by watching this WEHI animation, where the first sequence ignores the need for rotation and shows both the RNA polymerase and the DNA as lacking any rotation. The second sequence shows the DNA as spinning and the RNA polymerase as static. Is the second sequence accurate or also an approximation of reality? How does the DNA accommodate tens of thousands of revolutions required for long sequences?

I'm not sure the question makes much sense. Whether an object is 'rotating' or not, needs to be discussed in relation to a common frame of reference or to another object. An enzyme (like a polymerase) is much smaller than a chromosome, by many orders of magnitude. The DNA is flexible, of course, and requires bending, twisting, and other local configuration changes to function. But, again, a chromosome is a huge molecule! Is like asking if a passenger (polymerase) is moving, or if it's the train (chromosome) what is moving. Clearly both are moving, but at different temporal and spatial scales.

@TumbiSapichu the bottom line is that the RNA polymerase must rotate with respect to the DNA. The obvious frame of reference is the solvent they are both suspended in. If the polymerase rotates w.r.t. the solvent then the RNA that it outputs will end up wound around the DNA - is it? If not, then the polymerase must have been stationary and the DNA was the one rotating w.r.t. the solvent. The question is which is it, and if it's the latter, how does the DNA accommodate such twisting, being a very long molecule.

Both the DNA and the RNA polymerase complexes moves along the DNA molecule like it was a track. While the new mRNA is big, it would never be as big as the whole genome, so the reference point is the DNA molecule. Plus, the functioning of the movement of this enzymes is quite similar to other proteins that move "climbing" long polymers, such as actin polymers or microtubules.
One of the theoretical models that describes the movement of this kind of proteins is the model of rectified thermal diffusion, based on Richard Feynman's idea of the Brownian ratchet. A Brownian ratchet is a device that allows the conversion of Brownian random movements into a directional force.
http://en.wikipedia.org/wiki/Brownian_ratchet
The polymerases consume ATP, which enable them to suffer cyclic conformational changes (one change per ATP consumed), which allows the complex to attach to the molecule and detach. Once the complex has detached, by simple diffusion it moves in a random direction. Then, it attaches again. If the movement has occurred in the right sense, it will stay where it ended, while if it has gone in the wrong sense it will return to its previous position. As only a few movements are allowed, the complex will only move in that sense, even if the motor force is random.
I don't know exactly what conformational changes occurs in the RNA polymerase, but this general process seems to apply to almost any motile protein, including those enzymes that travel across polymers. Since the motor force is simple diffusion, and since the mRNA molecule doesn't need to "travel" with the polymerase (it just floats joined to it, but doesn't "pull"), I think there isn't any trouble with this.

I'm thinking more of the topology of strands of RNA and DNA. What happens to the mRNA/DNA as the polymerase moves around the spiral of the DNA?

mRNA are single-stranded, so they don't have problems with supercoiling. RNA polymerase complex carry helicase and topoisomerase activity in order to relax the DNA, because it needs to separate both strands of the DNA and because the movement changes the coiling in the DNA, as they cause positive supercoiling in front of the enzime and negative supercoiling behind. The wikipedia article is pretty good: http://en.wikipedia.org/wiki/RNA_polymerase

I think he is asking a different question. At some point the RNA should be wound around the DNA if the RNAP is spinning around the DNA.

The partial answer by Miguel helped a lot but I needed to go and read about the extra part that I was missing: Topoisomerases.
The DNA is unwound beneath the RNA polymerase, which causes supercoiling in front and behind.  For long transcripts to proceed, the current theory is that the DNA template has to be cut, unwound and re-ligated and that this is performed by Topoisomerases.
This raises the questions as to how often the DNA gets cut and re-ligated during active transcription and does this produce a noticeable effect (i.e. mutation)?

There is an alternative view that polymerases are sort of DNA motors that move DNA while they themselves remain static. I cannot find that reference now but I read this ~5 years back in a Nature Reviews article. The notion of transcription and replication factories also fits this model.
Highly transcribed regions do have a higher propensity to acquire mutations [1].
Although I am not sure about it but sequence composition of genes might also have a role. The pitch of the helix along with other physical parameters are dependent on sequence composition. It has been shown that geneic regions have different composition compared to non-transcribed regions (geneic regions have higher GC content [2].

I would have to agree that the "transcription factories" (several RNA Polymerases and some other proteins combined) attract DNA and transcription factors, and then start transcription while they remain static.  One such factory can actually transcribe many genes at once.
Most books and online sources still describe the Polymerase as moving along the DNA and carrying out transcription, but this has been proven wrong.
source:
http://www.ncbi.nlm.nih.gov/pubmed/8799830
can't find the article on Nature either, but I heard about it too.

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text:
Why did the sensitive plant (Mimosa pudica) evolve its leaf-closing mechanism?
Why did the sensitive plant, Mimosa pudica, evolve its leaf closing mechanism? Does it help in a heavy storm? Does it scare off whatever animals might think it a good meal?

By the way, I am not an evolutionist.

Are you sure you mean evolutionist? An evolutionist is someone who thinks the theory of evolution by natural selection is largely accurate. Are you saying you don't think evolution by natural selection is likely?

There are many reasons why Mimosa pudica (More commonly now referred to as the TickleMe Plant) may have evolved it's leave- closing mechanism. I have observed the movement when insects have landed on my plants. The insects apprear to be frightened by the movement as they do move on rather quickly when the plant collapses. The movement of the TickleMe Plant also occurs when the sun sets or if I place the plant in a dark room. This may be a way to reduce water loss by transpiration as the leaves fold down upon each other. Another reason for the leave movement may be to expose the few thorns found on adult plants. This could be another warning for herbivores to stay away. In cold weather TickleMe Plants will close their leaves as well, could this be a way to maintain its body temperature. All in all, this is the most amazing house plant and I am always learning new things about this plant and its beautiful cotton candy like TickleMe Plant pink flowers.


text:
Can the human eye distinguish colors in the periphery?
In the back of my mind I have the idea that human eyes can't notice the color of objects in the far periphery, and that any subjective perception of colors is done by the brain that tries to fill in the color percept.
Is that true?

It depends to some degree on what you define as peripheral vision. Until relatively recently, color vision in the peripheral field has been thought to be substantially less developed than color vision in the central field.
Most estimates of peripheral color perception place the limit of trichromatic (RBG) vision at no more than 30 degrees from fixation; the visual field was thought to be completely color blind at about 50 degrees of eccentricity.
Within the last 30 years, an increased understanding of the changing spatial scale in the peripheral field has led researchers to reevaluate what is believed about peripheral function. Virtually every measure of peripheral color perception can be improved by using a suitably large stimulus in the peripheral field.1
Here is a schematic of distribution of cones in the retina. While cones are decreased in number at 60°, they do exist.2

Here is a schematic of angles on peripheral vision.2

Previous measured sensitivity curves farther into the periphery than thought. In one paper, detection thresholds for colored disks showed that color vision, in particular color vision mediated by the L – M cone-opponent channel (luminance or blue–yellow colors), persists up to at least 50 deg. The larger the color disc, the better the peripheral color vision.[3]

The range of eccentricities over which red–green color vision is still possible is larger than previously thought. Color stimuli can be reliably detected and identified by chromatically opponent mechanisms even at 50 deg eccentricity. Earlier studies most probably underestimated this range. Differences could be caused by technical limitations and the use of stimuli of non-optimal size. (Emphasis mine) In agreement with previous studies we found that the decline in reddish-greenish L − M color sensitivity was greater than for luminance and bluish-yellowish S − (L + M) signals. We interpret our findings as being consistent with a functional bias in the wiring of cone inputs to ganglion cells (Buzás et al., 2006) that predicts a decrease but not a lack of cone-opponent responses in the retinal periphery.

1 Color vision in the peripheral retina
2 The Retina: Rods and Cones
3 Color perception in the intermediate periphery of the visual field

There are two types of photoreceptor in the eye, known as rods and cones. Rods are spread equally throughout the whole retina, whereas cones are focussed in one spot known as the fovea:

Cones are the only type of photoreceptor that can sense colour, so rods can only sense black and white. However, rods can work in much lower light and will also work when not being focussed on. Due to what is known as 'summation of action potentials', through which nerve impulses from multiple rods add together to cause a signal to be sent to the brain, rods are much more effective than cones at sending impulses. If you've ever seen something flickering in the corner of your eye and not been able to see what it is when you've looked properly, this is probably why (Wikipedia: Peripheral vision characteristics).
Edit: Further information on how vision is perceived can be found in this answer.
As for the question of whether or not the brain tries to guess the colour I don't know. I would suggest yes, the brain compensates as much as possible for a lack of information. It's known that the brain can compensate for the blind spot where the optic nerve passes out of the eye and compensates for it using the other eye and other information (Why every human has a blind spot, and how to find yours). However that is just my opinion, I haven't been able to find any research relating to the idea.


text:
How well does it actually work to surgically reroute the optical nerve?
Two publications, Roe et al, 1992[1] and Metin & Frost, 1989[2], describe results pertaining to the ability of a region of cortex to process information from a different sensory mode than the one that it normally does.
Specifically, they describe studies in which:

input from the retinas of newborn rodents was rerouted, by
surgical methods, to parts of the cortex other than the visual;
the rodents were allowed to mature;
the responses of cortical cells in the new target region to visual stimuli were assess.

Now it's 20 years later, so I'm sure there have been many others.
Something of which these publications seem to make no mention is the behavior that developed in the test subjects. For example, did they appear to be completely blind from a behavioral standpoint?
Is anyone aware of any publication, relating to these studies or other, similar experiments, which addresses this question?

Roe AW, Pallas SL, Kwon YH, Sur M. 1992. Visual projections routed to the auditory pathway in ferrets: receptive fields of visual neurons in primary auditory cortex. Journal of Neuroscience, 12(9): 3651-64.
Métin C, Frost DO. 1989. Visual responses of neurons in somatosensory cortex of hamsters with experimentally induced retinal projections to somatosensory thalamus. Proceedings of the National Academy of Sciences USA, 86(1): 357-361.

Have you looked at the forward citations of the articles: RPKS92 and MF89?

I had read through most of the first, but only glanced at the second, one of which turns out to be what I was looking for.

@mac01021 - Thanks for accepting my answer, despite the fact you more or less answered your own question earlier. I did find an additional publication though :) Very nice question. I +1'd it earlier.

This seems more of an engineering-limitation than a biological-plasticity limitation: to sever a nerve and reconnect it with reasonable fidelity sounds VERY hard.

At least two follow-up studies have investigated the behavioral consequences of the re-routing of the optic nerve to the auditory cortex. In these animals the visual cortices were ablated, and the optic nerve re-routed by combined lesions of the superior colliculus and ascending auditory pathways to the thalamus. These lesions induce retinal axons to form permanent ectopic (i.e., re-routed) projections to the auditory thalamus and cortex. These ectopic visual projections result in the formation of retinotopic maps in the auditory cortex and in visually responsive neurons with receptive field properties reminiscent of cells in the visual cortex.
These re-wired ferrets and hamsters were shown to have functional vision, as shown by their ability to tell light from dark and to recognize simple visual patterns. Visual pattern recognition was absent in control animals that were blinded, but not re-wired. Visual function, as measured by grating visual acuity in re-wired hamsters and rats, was however not as good as in control animals with normal vision (Frost et al., 2000; Melchner et al., 2000).
References
- Frost et al., PNAS (2000); 97(20): 11068–73
- Melchner et al., Nature (2000); 404: 971-6


text:
Parents are Rh +ve and child Rh -ve
Suppose the two parents of a child have blood groups A+ve and O+ve, and the child has O-ve type. For blood group, there are two alleles. Since the child has O, the father must have one 'A' allele and one 'O' allele.
Does such a reasoning hold for the Rhesus factor too? Should I interpret that both the parents have one + allele and one - allele?

Since the Rhesus antigen is inherited in a dominant negative way, both of your parents need to be heterozygote for it, so you can carry -/- for your alleles.

I edited the question to remove reference to self. Good question.

Rhesus antigen (Rh-D) is inherited in an autosomal dominant pattern.  Therefore you are correct in your reasoning.
Simple problems like this are often best worked out using Punnet Squares, shown below for the scenarios you have considered.

Because the inheritance pattern is dominant, if either parent was homozygous (DD) for Rh-D then 100% of their offspring will be Rh+ve.

In order to have a rhesus negative child, neither parent must be homozygous for the D allele.  You are correct that one possible scenario is a matching pair of heterozygotes:

In this situation 3/4 of the children are rhesus positive and 1/4 rhesus negative.
There is an alternative where one parent is Rhesus negative and the other positive.  In this case there is one heterozygous parent and one homozygous negative parent:

In this scenario, half of the children are rhesus positive and half rhesus negative.

Thanks. The second case does not arise because the mother is Rh- positive, in my question.

@Bravo ah of course, I missed that element!


text:
What is the healing process of mouth wounds?
When we have an external wound, blood generally tends to clot there, forming a layer of solid scab.
Yesterday, while brushing my teeth, I somehow hurt my gums and it got all bloody. However, it did not clot, neither did it hurt just after the incident.
After maybe like 12 or 15 hrs I had trouble opening my lips and when I looked at the spot in the mirror the gum tissue around and on the wound had colored white/yellowish.
Our mouths are supposed to be the among the most contaminated parts of the human body, so why do mouth wounds heal in just about a week and don't get infected?
What is the healing mechanism found in the mouth tissue, because I figure it is completely different from the processes in wounds occurring in the external skin.

To build on the answers from @Armatus and @S-Sunil
The healing mechanism involves the inflammatory process, which is the same in almost the entire body. In particular in both skin and mucosa (both referred to as "epithelial" tissues), when there is a break, platelets and clotting factors clot off any bleeding vessels, white blood cells (neutrophils and macrophages in particular) collect and destroy any bacteria, dead cells and muck, and then the process of regeneration occurs (with ongoing inflammation), where stem cells in the surrounding tissue regrow cells, new blood vessels may be formed and scar tissue is laid down to give extra strength. Eventually after these stages of healing, there is "remodelling" where the structure basically gets better.

As to why oral wounds heal quickly and don't get infected that much? There are a bunch of reasons. One is that the head and neck has an excellent blood supply- just think of scalp wounds where you bleed like crazy but then they heal very well. Another is that mucous membranes have immune functions that stop invading microbes. Generally speaking we divide this into "innate" immunity which is a general response, and "adaptive" immunity which is tailored towards specific bugs. The mucosa has both. There are neutrophils and macrophages (innate) which live in that area, there are lymphoid patches (like lymph nodes, and adaptive), there are immunoglobulins specific to mucosa (IgA) which is adaptive in nature, and the epithelial lining cells themselves will signal to the rest of the immune system if there is damage or an infection. Plus, saliva itself has chemicals and enzymes which break down oral bugs.

Most of the oral bacteria themselves are not particularly invasive. Just think, every time you brush your teeth, you cause multiple abrasions in your mouth. In fact, measurable amounts of bacteria from the mouth end up in your bloodstream every time  you brush your teeth! And yet, we don't end up with bloodstream infections as a result. This is partially because the rest of our immune system (and the structure of our heart and vessels) is intact, and partially because oral bacteria are not very invasive or pathogenic. They kind of have a sweet deal living in your mouth minding their own business and not killing their host, and even causing infection in an oral wound would make their continued survival less likely.
In addition I should probably point out that skin has a great deal of bacteria on it as well, and yet we rarely get infections from them (unless colonised by an invasive species), for the same reasons.

@UV-D Cheers! NP!

The mucosa ("slimey" skin) of course has different properties from your epidermis (outer skin) but the wound healing process is pretty much the same; the blood clotting process might be different though. About this I'm not entirely sure, but my best guess is that the "scab" is washed away by mucus and only the clots inside vessels remain, making them invisible from outside.
The white/yellowish colour is the underlying layer of fatty tissue. Chances are your wound does get infected but your immune system is able to clear it away easily. If infection is a bit heavier, it can strain the immune cells a bit more and some of them may die - you can then see them as pus (which is mostly white blood cells).

The mechanism of oral wound healing is similar to that elsewhere in the body. Depending on the type/ extend of wound, it may be primary or secondary.The clot and the encrustations are the part of the healing process.


text:
What determines the perceived pitch (frequency) of tinnitus?
I noticed that every time I suffer temporary tinnitus after going to a very loud concert, the frequency I perceive is identical. I'd put it somewhere around 17 kHz, but it's difficult to pin down with any real accuracy due to the dulling effect it has on external sound sources.
Is this frequency constant across all humans? If not, what determines the frequency? Note that I'm only interested in tinnitus caused by exposure to loud sounds, not other types of tinnitus such as idiopathic tinnitus or tinnitus caused as a side-effect of medication.

This question has been asked (and answered) on CogSci.SE as well: What's the Frequency of the ringing in my ear?

@Jeff Interesting, but rather indigestible and verbose. Would be nice to get an answer that explains things in simpler terms.

Is this frequency constant across all humans? No. If not what determines the frequency? In part, experience. You may consider leafing through some of the references if you find the answer insufficient.

Short answer
Perceived tinnitus pitch tends to resemble the frequency content of the loud sound that induced the tinnitus.
Background
Solid, laboratory-controlled studies to the perceived pitch of temporary, noise-induced tinnitus ("ringing in the ears") are ethically questionable, because researchers have to deliberately expose study subjects to potentially damaging loud sounds. Therefore, data on temporary noise-induced tinnitus are scarce and confined to a small handful of studies done in the 1960's (Henry & Meikle, 2000).
In one of these studies (Atherly et al., 1968) the authors exposed the study subjects to loud acoustic stimuli of various pure tones. The subjects reported to experience tinnitus pitched within a certain frequency band around the tonal stimuli received. The stimulus frequency and perceived pitch approached a 1:1 relationship, such that the tinnitus pitch was e.g. 4 kHz when the noise frequency was 4 kHz. Between-subject variability was, however, considerable. For example, at a stimulus of 6 kHz, the range of perceived pitch was 4-9 kHz.
The other study I found based on the review by Henry & Meikle (2000) showed that the perceived tinnitus pitch increased when the frequency of the loud tonal stimulus or frequency content of broadband noise increased (Loeb & Smith, 1967). Basically this confirms the data from Atherly et al. (1968). However, the perceived pitch did not coincide with the stimulus frequencies, and there was considerable variability between subjects. For example, some subjects reported multiple frequencies in their tinnitus, some reported a hissing tinnitus, while others did not develop any tinnitus at all (Loeb & Smith, 1967).
In all, your suggested perceived tinnitus pitch of 17 kHz is unexpected, given that noise-induced hearing loss (by loud music exposure etc.) typically results in a 4-kHz notch in the audiogram where hearing loss is greatest. Hence, tinnitus would be expected to occur around this frequency as well. But again, variability is very high and it may well be possible it is higher pitched in your case. Also note that 17 kHz is very high and near the upper audible frequency limit for humans (e.g., the sound an old CRT screen makes, i.e., hardly perceivable for many adults).
Most research on tinnitus has been done regarding patients with chronic tinnitus complaints that suffer from sensorineural hearing loss (i.e., damage to the hair cells in the cochlea). Typically, the perceived tinnitus pitch in this group is associated with their hearing loss. In other words, the pitch of the tinnitus generally matches a frequency range within the region of frequency loss (Eggermont & Roberts, 2004).
References
- Atherly et al., JASA 1968;44:1503-6
- Eggermont & Roberts, Trends Neurosci 2004;27:676-82
- Henry & Meikle, J Am Acad Audiol 2000;11:138-55
- Loeb & Smith, JASA 1967;42:453-5
Further reading
- What's the Frequency of the ringing in my ear?
- Can humans perceive sounds above 20 kHz?

Fantastic answer. Well sourced, too. I had all but forgotten about this question, so I'm glad you happened upon it. Regarding the 17kHz figure, I just ran a few pure tones (sine, saw) through my headphones and would say 14-15kHz is a more accurate ballpark.

@Polynomial - I never expected this late answer to be accepted :D Thanks :) 14-15 kHz sounds more plausible, but still very high. But possible, given the variability. It is a high pitched peep?

Given your comment as to why you asked this question - I am a bit afraid it is even more verbose than the related one at CogSci :) But I hope the 'Short answer' solved this somewhat

It's much more readable as prose, in my opinion. The other answer just seemed to be some snippets without context. And yes, the sound is very high, like a high-pitch squeal. I'm lucky enough to have retained my auditory sensitivity up to about 18kHz, despite the damage I've no doubt done at concerts, which may explain why I experience a higher pitch squeak.

Sounds all very reasonable, although noise-induced hearing loss typically results in a 4-kHz notch, well below the high frequencies. http://www.aafp.org/afp/2000/0501/p2749.html

I added these considerations in the answer - thanks for the addition :)

Good point. I hadn't considered that the hearing loss range was independent of the perceived frequency of the tinnitus squeal.


text:
Do fish increase or decrease pH of aquarium water?
If I understand it correctly, aquarium fish produce NH3 as their waste product and CO2 due to respiration. Producing NH3 increases water pH due to its equilibrium with NH4+. Producing CO2 decreases pH due to its equilibrium with H2CO3 and its equilibrium with HCO3-. My question is: Which of these effects is more important in most common aquarium fish? Do fish increase or decrease water pH?

Like a glass of beer going flat, any excess CO2 that your fish produce will quickly and irreversibly escape into the atmosphere. Thus, at least in terms of the pH battle between NH3 and CO2 that you describe, NH3 would win.
boilerplate "science is complicated" disclaimer
That said, it's likely that the total environmental effect that fish have on a tiny non-circulating volume of water will be much more complicated than the interaction between two basic chemicals. For example, say one of your fish sheds some scales and they start to rot. All sorts of things would be happening at that point which could affect the pH.


text:
Kinases that are ATP-sensitive at physiological conditions?
Phosphorylation is an ATP-dependent process performed by kinases. At physiological conditions it is generally assumed that ATP concentration is high enough so that ATP is not a limiting factor. Therefore the phosphorylation rate is independent of ATP concentration variations. At least this is the case in the examples I came across.
Are there known counterexample? A kinase that is sensitive to ATP concentration at physiological conditions?

Yes - AMP-activated protein kinase - or better known as AMPK. This kinase is sensitive to the ATP to AMP ratio with himself – search pubmed for any review on ANP kinase and you'll find more information.

Great, thanks! I would like to get other examples, I searched the literature with the keywords "ATP-sensitive kinase", or "ATP-regulated kinase" but couldn't find any. Maybe there are better keywords?


text:
If oxygen is such a good energy source, why do plants release it?
Why do plants release excess oxygen, rather than consuming it entirely given it is an excellent energy source?

I guess because plants don't walk around collecting food and it doesn't rain carbohydrates to burn oxygen with. But this gives me ideas for a sci-fi story involving farting trees.

One thing worth noting is that, at night, most plants 'breathe' oxygen and use it to metabolize stored sugars, just like animals.  However, they don't want to keep extra oxygen around during the day, when they're photosynthesizing, as oxygen actually competes with carbon dioxide during the photosynthetic process, slowing it down.

oxygen is not energy, its needed for energy, like when you want fire, you need oxygen.

As wonderful and abundant oxygen is, it is also highly reactive (consider rusted metal), and can contain ozone and oxygen singlets (a free radical). Free radicals are highly mutagenic and lead to double-stranded breaks in DNA. When cells die by programmed cell death they lyse their mitochondria, possibly to hasten the process. Finally, the enzyme super oxide dismutase exists to safely remove these free radicals from cells.

Short answer
Plants release O2, because it is not an energy source. Instead, it is used to free energy from energy-rich organic compounds.
Background
Plants are solar powered. They release oxygen as a waste product during carbon fixation. Carbon fixation is basically the storage of solar power into carbon-bonds in glucose, a process referred to as photosynthesis or the Calvin Cycle.
To release the solar energy from glucose it has to be burned (oxidized). Oxidation of glucose can be realized via the the citric acid cycle (or Krebs cycle) and electron transport chain to generate ATP. O2 only comes in in the very last step by acting as the final electron acceptor to produce H2O (Fig. 1.)

Fig. 1. Electron transport chain in mitochondria. Electrons are sent through a chain of proteins that drive hydrogen transport out of the mitochondrial space. ATP-synthase uses the proton gradient to generate ATP. Source: Davis University College
Hence, O2 is not the source of energy, it is merely used to free it from energy rich compounds such as glucose. Because it is so abundant in the atmosphere, it doesn't make sense to store it.
Reference
- Berg et al., Biochemistry. 5th edition. New York: W H Freeman (2002)

"Because it is so abundant in the atmosphere, it doesn't make sense to store it." this makes only sense today, it made no sense when the first photosynthesis was done.

@plasma perhaps early plants (/weed/phytoplankton/...) did retain oxygen and released it when out of storage space. You could also drop evolution for intelligent design and be done with it.

@PlasmaHH - defintely true. But the fact that oxygen levels only increased when plant life became abundant still supports it being a waste product.

@AliceD: of course it is a waste product, but I do also throw away my waste because it is waste, not because it is abundant on the streets...

@PlasmaHH - the argument is that you don't have to store it because it is abundant. Not that you have to throw it away because it is abundant.

@AliceD: So why would I keep my waste products with me when they are not abundant in the environment? And why did the first organisms did not keep it, although it was not abundant?

@PlasmaHH - let's go to chat.

Another reason that oxygen is not stored could be that it would result in Warburg effect i.e, reduction in photosynthesis due to decreased functioning of RUBisCO due to increased O2 conc. and also due to photooxidation of chlorophyll due to same reasons.


text:
How is color information transmitted from the eye to the brain?
Is color information sent from the eye to the brain frequency-modulated, or are different colors transmitted by different axons?
I know that each ganglion cell is connected to multiple photoreceptors. How do ganglion cells tell the brain which photoreceptors were exactly activated and by what color?
Do ganglion cells correspond to particular colors?
Can one ganglion cell transmit different signals to the brain?
How does the brain know which color the light has, if signals of different receptors are mixed in the ganglion?

I believe that some preprocessing takes place in the retinal ganglion cells (see also http://en.wikipedia.org/wiki/Color_vision#Color_in_the_human_brain), so the brain does (probably) not have any information on which types of cones that are activated. I dont know how the colour information is transmitted from ganglion cells to brain though.

possible duplicate of What gives things their colour?

@The Last Word no, that answer deals with the eye.

@fileunderwater I heard somewhere that without preprocessing the optical nerve would have a diameter of several centimeters. :-)

Short answer
Color vision is mediated by spike rate modulation (frequency modulation if you like), as well as ganglion-cell specific stimulation.
Background
Ganglion cells exist that transmit opponent colors. The color opponency model predicts that we cannot perceive a greenish-red or yellowish blue, which is quite right. We can, however, see mixtures of the two channels, such as red and yellow (orange), and red and blue (purple).
Then opponent model predicts the existence of ganglion cells that are sensitive to red/green opponency and blue/yellow opponency (in trichromats like humans):

Indeed, it has been shown that these ganglion cells exist, i.e. cells that increase their firing in response to short-wavelength-sensitive (S+) and decrease their firing to middle-wavelength-sensitive (M-) and vice versa (Yin et al., 2009). Hence, it is not so that the frequency of light is represented in firing rate per se, but the frequencies of light are translated in spike rates, because spike rate is the only means in which neurons can transmit graded responses. In other words, every type of graded information is translated into spike rate eventually, including pressure differences, acoustic loudness etc.
Hence, as ganglion cells are sensitive to opponent pairs of colors, they do respond to particular colors. However, a "purple ganglion cell" does not exist, it is the combination of red and blue activations that lets us see colors due to synthetic processes in higher neural centers.
One ganglion cell can send different signals to the brain as it is basically an analogue converter of the red/green and yellow/blue opponent colors.
These inputs are sent to the thalamus (lateral geniculate nucleus) and higher visual cortices, where color-selective cells pick up the signals and integrate them for further processing. Here color mixtures are made to present the full gamut of colors as we know it:

Source: Dot-Color
Reference
- Yin et al. J Neurosci 2009;29:2706-24
Further reading
- Advantage of opponent color?


text:
Are there terrestrial plants that thrive on sea water?
Given the existence of coastal deserts such as in the picture below, I was wondering whether terrestrial plants can survive on sea water alone? If yes, why then do coastal deserts exist, instead of being grown over with belts of such plants along the shores?
If terrestrial plants thriving on sea water do not exist, then why? Especially given that there are marine plants like kelp and sea grass?

There are mangroves that live their lives immersed in salt water. Does that count as a terrestrial plant?

@Resonating Mangroves are considered terrestrial and they are not fully submerged. But I have seen mangroves only in backwaters and estuaries/deltas.

The University of California, LA mentions some genera and species of salt-loving plants (halophytes):
The genus Atriplex (Family Chenopodiaceae), saltbush, is found worldwide along saline shorelines. On the surfaces of the leaf are vesiculated trichomes (hairs). Each trichome has a stalk and a balloon-like tip, the bladder cell. The leaves use the bladder cells to excrete salt.

Coastal saltbush. Source: Enviro Active Australia.
Excreting salt glands occur in numerous unrelated plant groups, including grasses that live in alkali sink and salt pans and in warm temperate to tropical salt marshes (Sporoboleae, Chlorideae, and Aeluroideae (Family Poaceae)). These include such well-known tidal saltmarsh plants as the cordgrasses (Spartina alterniflora, S. patens), alkali grass (Puccinellia phryganodes), saltgrass (Distichlis spicata), and shoregrass (Monanthochloe littoralis). Short, two-celled trichomes have evolved as collecting chambers for salts, from which salts are excreted through tiny pores.

Cordgrass in the Chesapeake Bay. Source: Chesapeake Bay Program
Frankenia (Family Frankeniaceae) is a genus found both in coastal salt marsh and inland saline habitats. Saltcedar (Tamarix, Family Tamaricaceae) grows around the world in arid and semiarid regions. All of these taxa have salt glands, i.e., trichomes, in which salts are accumulated and excreted.
Several common mangroves secrete salts from leaves. So much crystalline salt can occur on the leaf of black mangrove, Avicennia germinans, that it appears whitish. Aegialitis annulata is a salt-excreting mangrove of Family Plumbaginaceae, a group in which other species are salt excreters in salt marsh and oceanside (Limonium and Armeria) or have chalk glands and live in dry, alkaline habitats.

Black Mangrove. Source: PlantDex.
Halophytic succulence is demonstrated in many genera of plants that inhabit saline environments, such as the mud flats of coastal salt marsh, but also is commonly observed on the leading edge of vegetation on coastal beaches, i.e., in strand vegetation. Common examples of succulence can be found in Family Chenopodiaceae: Allenrolfea, Arthrocnemum, Halimione, Nitrophila, Salicornia
Suaeda.
Succulence (fleshiness) also occurs in other famous and widespread species, such as Batis maritima, Sesuvium portulacastrum, Trianthema portulacastrum, and many Old World species of Zygophyllum. True succulents in the ice plant family, Aizoaceae, are also commonly found in saline habitats: Aizoon and Mesembryanthemum. By depositing salts in vacuoles, the toxicity is partitioned from the cytoplasm and organelles of the cells. As in Atriplex, salts are removed from the plant when the leaf of stem segment is shed.

Halophytic succulent Trianthema portulacastrum. Source: Altervista.
Among the halophytes, the seagrasses, which are submerged plants of shallow marine meadow, have salt tolerance, because the osmolality of cytoplasm is adjusted to match the osmolality of the seawater, so that desiccation of the plant does not occur. This contrasts the strategies of excluders and succulents, which are primarily salt avoiding mechanisms, attempts to reduce salt concentrations within the cytoplasm of photosynthetic cells.
As to why some shores may be devoid of plants, it may have to do with extreme temperatures, lack of nutrients, phytotoxic material etc.


text:
What are the major steps of follicular B cell development
This is a learning objective in my curriculum, and after having spent two hours trying to answer it for myself using official course resources (many of which are online, but some of which are behind paywalls and so may be inaccessible to other community members), it's clear to me that I need some assistance.
So I would just like to know what is the latest understanding of the major steps of follicular B cell development in mouse and human.

According to Basic Immunology - Functions and Disorders of the Immune System (3rd Ed.) by Abbas and Lichtman (Copyright © 2011 by Saunders), p.133:

A majority of B cells are called follicular B cells because they
  reside in the follicles of lymphoid organs. These follicular B cells
  make the bulk of T-dependent, class-switched, and high-affinity
  antibody responses to protein antigens and give rise to long-lived
  plasma cells.

and in the caption for FIGURE 7-2:

Subsets of B cells. Follicular B cells make T-dependent responses to protein antigens, and marginal zone and B-1 B cells account for
  most of the T-independent antibody responses. In mice it has been
  shown that B-1 B cells arise earlier in development, from progenitors
  in the fetal liver, and follicular and marginal zone B cells arise
  later, from bone marrow precursors. Comparable differences in the
  origins of these subsets have not been defined in humans. Note also
  that the distinctions in the type of response are not
  absolute—follicular B cells can make T-independent responses and
  marginal zone B cells can make some T-dependent responses. Ig,
  immunoglobulin.

(emphasis not in original)
From the sentence I emphasized, it seems to me that as of 02011, there is still a great deal that is not well-understood about the origins (and perhaps also development?) of human follicular B cells.
Interestingly, in the 4th edition of this textbook (Copyright © 2015 by Saunders), the details have changed slightly (as below):

Subsets of B cells. Follicular B cells make T-dependent responses to protein antigens, and marginal-zone and B-1 cells account for most
  of the T-independent antibody responses. In mice, B-1 cells arise
  earlier in development, from progenitors in the fetal liver, and
  follicular and marginal-zone B cells arise later, from bone marrow
  precursors. Note also that the distinctions in the type of response
  are not absolute; follicular B cells can make T-independent responses,
  and marginal-zone B cells can make some T-dependent responses. Ig,
  Immunoglobulin.

Most interesting to me is the removal of the 3ed sentence: "Comparable differences in the origins of these subsets have not been defined in humans." Which leads me to believe that comparable differences in the origins of these subsets have now been defined in humans (in the past 4 years).
So I have a definition and description of follicular B cells, but I am unable to find anything else in either edition of this book on the development of follicular B cells (in either mouse or human).
Another reference in my course resources is Cellular and Molecular Immunology, 8th ed., 2014, by Abbas, Lichtman, and Pillai.
In it (Chapter 12: B cell activation and Antibody Production), I find the following about follicular B cells:

Distinct subsets of B cells respond preferentially to different types of antigens ( Fig. 12-3 ). Follicular B cells in peripheral
  lymphoid organs primarily make antibody responses to protein antigens
  that require collaboration with helper T cells.

Which strikes me as yet another description of follicular B cells, but not a list of steps in their development (which is my learning objective).
The same textbook makes several other mentions of follicular B cells, but does not address their development. Although I should probably already know this (and this may be in some of my lectures but these are not universally searchable and I have precious little time to read), I do not know about either their progenitors or their progeny, and I think this is what is meant by this learning objective: the major steps in their development.
In the same chapter of the same textbook, I also see:

Most mature naive B lymphocytes are follicular B cells (sometimes also
  called recirculating B cells) that constantly recirculate in the blood
  and migrate from one secondary lymphoid organ to the next in search of
  antigen. Follicular B cells enter secondary lymphoid tissues (spleen,
  lymph nodes, mucosal lymphoid tissues) through blood vessels located
  in the T cell zones, and then they migrate into the follicles, the B
  cell zones of these tissues. The movement into lymphoid follicles is
  guided by the chemokine CXCL13 secreted by follicular dendritic cells,
  the major stromal cell type in the follicle, as well as by other
  stromal cells. CXCL13 binds to the CXCR5 chemokine receptor on the
  recirculating naive B cells and attracts these cells into the
  follicles. As we will discuss later, the same chemokine-receptor pair
  is also important during immune responses because it can attract a
  subset of activated T cells to the follicle.

This seems like a great description of the follicular B cell that also delves into its function, but seems to include nothing about its development.
The same chapter of the same textbook also includes:

Naive follicular B cells survive for limited periods until they
  encounter antigen (see Chapter 2 ). Follicular B cell survival depends
  on signals from the BCR as well as on inputs received from a tumor
  necrosis factor (TNF) superfamily cytokine called BAFF (B
  cell–activating factor of the TNF family, also known as BLyS, for B
  lymphocyte stimulator), which provides maturation and survival signals
  through the BAFF receptor. BAFF and a related ligand, APRIL, can
  activate two other receptors, TACI and BCMA, which participate in
  later stages of B cell activation and differentiation (and will be
  discussed later). These cytokines are produced mainly by myeloid cells
  in lymphoid follicles and in the bone marrow.

This paragraph briefly address a little bit of what seems like the development of the follicular B cell ("Follicular B cell survival depends on..."). And in chapter 2 I see that follicular B cells are a class of B lymphocytes (along with Marginal zone B cells), but I interpret this learning objective as about the development of follicular B cells after they become follicular B cells, not before this point in their development.
So this is the best answer I can find on my own after many hours of searching and reading relevant passages in recent textbooks on the subject. Yet this answer also seems incomplete to me. After all this reading, I still have no "steps (per se) of follicular B cell development."
So I could really use a more complete answer.

Try Janeway's Immunobiology 8th edition, Chapter 10 The Humoral Immune Response. It is a bit too long to summarize in an answer here, but it should give you everything that you want to know about B-Cell development, maturation, and differentiation.

Very basically it is, migrate to secondary lymphoid organs, have antigen presented by follicular dendritic cells, migrate to boundary with T-cell area, (for simplicity) get activated by Helper T-cell, proliferate, migrate to red pulp (if the secondary lymphoid organ they were activated in was the spleen) and differentiate (or while differentiating) into a plasmablast, then terminally differentiate into antibody-secreting plasma cells, start pumping out Immunoglobulins and let the opsonization begin.

Thanks @AMR for this very helpful comment. I actually do have Janeway's so I'm looking at Chapter 10 now. But I'm not seeing what you described in your second comment. Do you have a page number or a section number? The caption for Fig. 10-7 talks some about this, but I don't see in Janeway that very comprehensive list of steps in the development of a follicular B cell that you listed. I'm in chat right now if you can spare the time to continue the conversation there. What are all the synonyms for "follicular B cell"? Not obvious to me.

Section 10.5 beginning on 392. It is summarized in Figure 10.7 on page 394. I think that they are called follicular B cells for the simple reason that the area where they migrate to and are activated in secondary lymphoid organs is known as the B-cell Follicle. Biologist are nothing if not unoriginal... Except for fly geneticists...


text:
What will happen if we expose the brain to intermittent light?
If a brain is exposed to an intermittent light source, are specific areas going to fire? If yes, which of them? Is there a experimental data about this effect?

What do you mean? Cutting open a skull and shining light into it? Why would the brain's cells be able to sense light? Even if they did, how could we possibly answer your question without knowing which areas of the brain you were illuminating?

as @terdon said, just shining light on the brain wont make it sense it (unless of course it is a laser of sorts which causes a lesion :P) . You need photoreceptors for sensing light.
In fact I have heard that brain doesnt have mechanoreceptors and nociceptors so someone wont feel that their brain is being cut <read and seen it in the Hannibal (by Thomas Harris): Not a very reliable source, though :P >.

It is thought that there are no active optical receptors in the brain normally, its possible some effect might show up in the future, it would be minor at best.
Shining light into the brain is standard procedure in optogenetics experiments. A subpopulation of neurons is transformed to express an optical receptor to modulate genetic or signalling properties of the cell.
So the reason I say it would be small effect on a native brain is that these experiments do give good results and are run with controls which do not have the optical receptors added, which typically show no change in brain activity.

Channelrhodopsin-2 (ChR2) induces temporally precise blue light-driven activity in rat prelimbic prefrontal cortical neurons. a) In vitro schematic (left) showing blue light delivery and whole-cell patch-clamp recording of light-evoked activity from a fluorescent CaMKllα::ChR2-EYFP expressing pyramidal neuron (right) in an acute brain slice. b) In vivo schematic (left) showing blue light (473 nm) delivery and single-unit recording. (bottom left) Coronal brain slice showing expression of CaMKllα::ChR2-EYFP in the prelimbic region. Light blue arrow shows tip of the optical fiber; black arrow shows tip of the recording electrode (left). White bar, 100 µm. (bottom right) In vivo light recording of prefrontal cortical neuron in a transduced CaMKllα::ChR2-EYFP rat showing light-evoked spiking to 20 Hz delivery of blue light pulses (right). Inset, representative light-evoked single-unit response.

Image taken from the linked Wikipedia page and originally from Baratta et al..

Short answer
Illumination of neurons with light of varying wavelengths can activate them, causing them to fire action potentials. It may, however, not be the photons that activate the neurons per se, but the resulting temperature changes.
Background
In contrast to the comments and original answer, it is possible to activate neurons, other than photoreceptors, with light.
Infrared laser light (~2000 nm) has been demonstrated to activate neurons in the periphery, including neurons in the sciatic and facial nerves and the spiral ganglion cells in the cochlea (Thompson et al., 2014). Interestingly, green laser light in the visible spectrum (532 nm) has also been shown to activate neurons (Wenzel et al., 2009). In the brain, laser light has been shown to activate neurons, including the primary visual cortex and somatosensory cortex. Typically, short (intermittent) bursts of stimulation are used, with exposure times in the millisecond range (Thompson et al., 2014).
The underlying mechanism of laser-activation of neurons is debated. The current evidence points to the possibility that focal illumination of neurons with light may increase the temperature of the cell, which may result in changes in membrane capacitance. Changes in membrane capacitance can cause voltage differences. Hence, lasers may induce action potentials by causing heat-induced depolarizations. Further, it is thought that temperature changes affects transmembrane ion channels and TRPV channels that in turn play a modulatory role in the laser-induced activation of neurons. TRPV channels, for example, include the heat-sensing TRPV1 receptor, that is thought to be activated by laser light-induced temperature changes (Thompson et al., 2014).
Why the fuzz about laser-induced neuron activation? Cochlear and retinal implants restore limited auditory and visual function in the deaf and blind, respectively. In both techniques, electrodes are used to activate spiral ganglion cells (in the inner ear) retinal ganglion cells (in the eye). Electric currents have the tendency to spread laterally through the tissue, preventing focused activation of specific localized regions of the cochlea and retina, respectively. Hence, both approaches suffer from channel-channel interactions, leading to crude stimulation profiles and reduced frequency resolution (cochlear implants) and low spatial-resolution (in case of retinal implants). Lasers, on the other hand, can be made into nearly infinitesimally small rays that have minimal scatter compared to electric current spread. Hence, laser-induced activation may be useful for specifically stimulating small populations of neurons in a certain tissue, opening up great possibilities in neural-prosthetics, such as auditory and visual prosthetics (Rettenmeijer, 2014).
References
- Thompson et al., Curr Mol Imaging (2014); 3(2): 162–77
- Rettenmeijer, Biomed Opt Express (2014) 5(4): 1014–25
- Wenzel et al., J Biomed Opt (2009); 14(4): 044007


text:
Could being exposed to excess UV in the arctic lead to a human eye color change? If so, what is the mechanism?
The CBS News article Expedition Antarctica: A father and son's journey to save the planet says (in part):

Thirty-two years ago, Robert Swan made history as the first person to walk to both poles. Even as a young man, these grueling expeditions took a harsh toll on his body. Passing directly beneath the hole in the ozone layer, Swan's face became badly burned and his eyes even changed color. But the Arctic explorer now says that all of that physical duress pales in comparison to the agony of watching his son go through the same experience 32 years later. (emphasis added)

Skin color change can happen after exposure to UV light. From Wikipedia:

Melanin is a natural pigment produced by cells called melanocytes in a process called melanogenesis.

Question: Can the human eye really change color due to excess UV light from the Sun, in this case through a polar "hole" in the ozone layer? If so, what is the mechanism?

above: "This winter, Barney and Robert Swan became the first explorers to ever trek to the South Pole surviving exclusively off of renewable energy." Robert (the elder) is on the right. From here. Credit: SHELL-Technical Partners

I find this a pretty bold statement from this article. The second this, I would like to see at least before and after pictures. Additionally, the color of the sons eye doesn't seem to bright to me.

@Chris pigments can degrade and change color from exposure to UV or even blue light, so it's certainly plausible, but I would think that eye protection usually used in sunlit, reflective, snowy conditions would have prevented this. I'm going to ask for a better source for this in The Great Outdoors SE right now, and I'll keep an eye on answers and comments there and here. I understand it's important to avoid the false premise in a question so if I can't get this resolved shortly I'll delete the question until I can. Thanks!

"Credit: SHELL-Technical Partners " is it real?  Because that it is not so trust worthy but still i look forward to some answer here.

I've just asked Has extended exposure to sunlight and UV in the arctic or antarctic ever caused someone's eyes to change color?

@uhoh I will look into this later. Exposure to UV also promotes pigmentation, which puzzles me a bit here. Yes, the eyes are pretty sensitive to UV radiation and sunburn there is pretty painful.

@Chris possibly related: https://www.independent.co.uk/news/science/british-scientists-discover-reindeer-eyes-change-colour-from-gold-to-blue-over-course-of-the-seasons-8916008.html

@L.Diago As far as the SHELL-Technical Partners goes, check out the Shell Corporation video The South Pole Energy Challenge which is also found here which comes from this answer to my question looking for additional information on this.

@Chris some results! outdoors.stackexchange.com/a/20291/12619 Still no hard data yet, but "bleached his eyes and burned his face" does seem to have some plausibility, as mentioned here update: Ah, I've just found this: https://edition.cnn.com/2015/03/04/tech/mci-brown-eyes-blue/ and also https://www.techly.com.au/2014/12/03/want-change-eye-colour-brown-blue-possible-via-laser/

@uhoh Interesting. I actually looking through the journal databases now, lets see, if there is something.

It's a four year old question and so far nothing definitive, but the September 30, 2022 BBC Future article How our eyes can change colour throughout our lives includes the following quotes from David Mackey, professor of ophthalmology in the Lions Eye Institute at the University of Western Australia.
Unfortunately there is no smoking gun here, yet.

Through apparently spontaneous change or through mishap or illness, our eyes can change colour in surprising ways.

But, surprisingly, our eye colour doesn't always remain constant throughout our lives – in fact, a wide range of external influences can change it, from injury to infection and sun damage. And sometimes the change appears to happen spontaneously.

It may be a similar story for eye colour, he suggests, with greater quantities of pigment building up in the months or years after birth. "The main pigment in the eyes is melanin and it's the way that melanin is distributed that gives you the different eye colours," he1 says. "Simply classifying them: you've got blue eyes, some people also talk about grey but really it's a variant of the blue, then you've got the hazel and green combinations, and then you've got the brown, and that can be slightly brown or extremely brown. All of that's related to how much melanin is there."

Higher levels of melanin can have a beneficial function in intense sunlight – as in the skin, the pigment offers protection from sun damage.

In irises with little melanin, the blue colour comes from the way the fibres of collagen at the back of the iris scatter light, in the same way that the sky appears blue because of way light is scattered in the atmosphere.

As to why some children's eyes express more melanin over time, this remains mystery, says Mackey.

"We actually don't know what influences those colour changes," says Mackey, but there could well be an environmental factor at play. "You can almost say that for everything there's an interaction of genetics and environment, even for things we think of as totally genetic or as totally environmental," says Mackey. "But what environmental factors could influence it? We don't really have that data for the general population."

1David Mackey, professor of ophthalmology in the Lions Eye Institute at the University of Western Australia.


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Is this a moth? How do these wings unfold?
I'm having trouble understanding how these wings might work. Are they somehow folded or bent by 90 degrees so that part of the wing is vertical and part is horizontal to be more compact?
If so, how mechanically are they then made quickly more rigid and straight each time it enters flight, which should be fast to avoid being eaten?
Also, I'm guessing this is some kind of moth, but I have no idea. I don't really need an exact species ID, but some classification guidance would be appreciated!
This individual is about 2 cm long, and was seen recently (late July) in Taipei, on a hot, sunny day.

moths don't have 2 wings they have 4 wings, the forewings and hindwings are just being held apart in this image. https://en.wikipedia.org/wiki/External_morphology_of_Lepidoptera

@John oh, that makes quite a bit of sense. Do you think this is in fact a moth? I've just guessed at that.

Yes definitely a moth, although I have no idea what the species is. You could ask for identification as a separate question. just be sure to include the last sentence of the post, where it is found is very helpful.

Okay thanks. I'm still interested in how these wings would OPEN (be deployed) without bumping into each other. There must be some kind of rotation involved; perhaps the ones that are vertical in the photo would rotate forward first?

Not a moth. It is a skipper. Family Hesperiidae. https://davesgarden.com/guides/articles/view/5254

I'd be prepared to guess genus Telicota also known as the Palm Darts.

@bob1 https://www.flickr.com/photos/77600294@N07/17632334189 :-) you're on to something http://dearlep.tw/species.html?namecode=345508, http://butterfliesvietnam.blogspot.com/2015/08/118-telicota-hoara-narrow-branded-palm.html

Uhoh, thanks to @KarlKjer for pointing in the right direction. I just put Hesperiidae into google and found the wikimedia page and browsed through for something similar to your photo, then did a bit more searching based on that.  I think the vietnam link you provided looks like a dead-ringer for your photo. Seems the ID is all around the wing patterns, so very hard to do to species from a couple of photos.

@bob1 well we don't have separate family- or genus-identification tags, so please feel to just write up something; I'm particularly interested in how the wings unfold and I think that part should be similar for many of them.

@uhoh - I'm no entomologist so I don't actually know, but it looks like the vertical wings are the fore-wings and as there are 4 wings (2 fore, 2 hind) each of the 4 is on its own joint (i.e. controlled at least semi-independently). The position is just fore folded up like a moth, hind folded flat

@bob1 I think it's maybe this one? http://dearlep.tw/species.html?namecode=345510 I see what you mean, I was so interested in photographing it that I didn't want to disturb it and make it fly :-)


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Is this a type of fruit fly?
I live in Taipei, and these flying insects are about 2-4 millimeters long (body length). They are very active when it's over roughly 24C indoors, and will fly, land and run around randomly on interesting surfaces then fly again, all in one continuous motion.
Some have moved into my apartment again.
They are attracted to food, especially coffee grounds!, vinegar, bread, and dark, moist areas. I can use these attractants to catch them inside bottles or plastic bags, but can't ever seem to get the last one.
I see them fly around while mating end-to-end (twice as long as a single fly) and they often go right past my face while doing so as if to say "ha! there's more of us on the way!"
The heads seem smaller than in images of common fruit flies that I've seen.
Are these likely to be fruit flies, or something else? I don't need an exact species identification, I'd just like have some kind of classification to describe them with besides "little flies".
In this answer to a related but different question, it was proposed that they were something very different, but I don't think that's the case.

Photos: the best I cold do with my cell phone plus a magnifying lens.

Didn't the last answer say it was a baby cockroach

@SonicSplasher That was an answer to a question about pesticides, not a species identification question, so even though it was suggested, I'm pretty sure these are not baby cockroaches. See my comment there. I can't help it that that answer's formatting makes it look like it's answering a species id question.

Search for drosophila buzzati and drosophila buskcii and drosophila simulans

This has been recently bumped by community; I add this comment for closure. This is a six-legged (hexapod) two winged (dipteran) fly. It is a female drosophilid, and identifying the species and subspecies from such a photo is impossible; typically, correct identification requires careful morphological assessment using a microscope, by a specialist/insect taxonomist. I don't think this fly is shaped like a Drosophilia melanogaster member. It seems a bit too long. Source: personal daily experience with manipulating fruit flies on a CO2 pad.

@SPr Thanks for your comment! The "ultimate closure" in Stack Exchange is of course acceptance. If you'd consider writing up something along the lines of "...without the possibility of genetic analysis... correct identification requires careful morphological assessment using a microscope, by a specialist/insect taxonomist." I could probably accept it.

I can't pinpoint on the species name but a quick common fruit fly should give you a image which look very similar to the one in your photos.

these Bois are around 1/8 in inches long
-striated abdomen

Hope this is the one

I mentioned that, but: "The heads seem smaller than in images of common fruit flies that I've seen." Your guys have a big head with a tiny neck, my guys seem to have a "unibody"

The thing is baby roaches cannot fly and the ones you mentioned are flying so this is the most similar one I can come up with or maybe some sort of Taipei variant

Thanks, I didn't think they did, I'm glad to know for sure now. I really appreciate the confirmation on the "no fly" baby roaches.

What kind of insect is a Bois?

"bois" here was another word for boys and i used boys informally to you know call them that without addressing them with their scientific name


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Does a mydriatic drug neutralize the action of a miotic?
If a person were administered a mydriatic, would the subsequent application of a miotic neutralize the action of the former? If the sequence were reversed would a mydriatic neutralize the effect of a miotic?

The iris has 2 sets of muscles:

The circular muscle (Sphincter iris) - This causes iris constriction and is supplied by the parasympathetic system - Acetyl Choline muscarinic receptors
The radial dilator muscle - This causes dilation of the iris and is supplied by the sympathetic system - The Adrenergic receptors (Alpha 1)

Theoretically speaking, there can be four sets of drugs:

Alpha 1 adrenergic stimulators - will cause midriasis
Alpha 1 adrenergic blockers/antagonists - will cause miosis
Muscarinic blockers - will cause midriasis
Muscarinic agonists/stimulators - will cause miosis

In practice,

Midriatics:

Alpha 1 agonists: Phenylephrine
Muscarinic antagonists: Atropine, Homatropine, cyclopentolate, tropicamide

Miotics (mainly used for Glaucoma):

Muscarinic agonists: Pilocarpine, carbachol, etc...
In practice alpha 1 antagonists are not usually used to effect miosis

There are two ways to achieve either midriasis:

Stimulate the Adrenergic receptors
Inhibit the Muscarinic receptors

Similarly miosis can also be achieved vice-versa.
The answer to your question is yes, when given the proper counter-acting agent, depending on the concentration of the agents and the mechanism of actions opposite effects are achieved. This is primarily because the drugs act on different sets of muscles. If a adrenergic stimulator - phenylephrine is instilled with a muscarinic stimulator - cyclopentolate, both sets of muscles will be acted upon and based on the concentration of the drugs, the decay rate and the efficacy, the iris diameter will either increase or decrease to variable degree. The point is that both the drugs will affect the final diameter of the iris (which is based on the autonomic state of the patient and the strength of drugs administered)
Now the special cases will be to administer a inhibitor of a receptor followed by an stimulator of the same receptor or vice-versa - In this scenario, the duration of action and the affinity of the given drugs to the receptor in question will play a decided role in determining the final action as both drugs act on the same muscle. If the inhibition is permanent or long-acting then inhibition of the muscle action is predominant. This may change if the stimulator has a very high affinity to the receptor - Higher affinity will result in tighter binding of stimulator and remove the chance for the inhibitor to work - i.e. increase the probability of the clearance of inhibitor. As you can see from above statement, if the clearance rate of inhibitor is slow (takes too long to metabolize), then the effect will ultimately be inhibitory effect. Similarly in case of poisonings where the stimulating effect is permanently achieved (Organo Phosphorous poisoning will cause permanent damage to acetylcholinestrase the enzyme responsible to remove acetyl choline) the reversal will depend on the affinity of the inhibitors (in this case, of acetyl choline) to the receptors (muscarinic).
Thus the question must be more specific to get a proper answer, as the effect is totally dependent on the drugs administered.

very comprehensive answer +1

yes, very nice one indeed


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How does one maintain balance sleepwalking?
Anectodal. Feel free to shoot it down.
Walking is an acquired skill; As far as I'm concerned exhaustion causes disorientation. Even after waking up it sometimes takes a second or so to get balanced.
How is it sleepwalkers don't stumble around when walking?

Balance is maintained by the cerebellum, not by any of the cortical areas that are less active during sleep. Thus, there's no reason sleep should affect your ability to balance.
Being asleep doesn't mean that you're fatigued. I wouldn't be surprised if a highly fatigued person who was sleepwalking did have poor balance.

In fact, repetitive actions like riding a bike or playing the piano (when experienced) are also stored in the cerebellum so should in theory be possible for sleepwalkers to do :D

An interesting question. When a person is asleep and dreaming, the person's brain is fairly active, similar to the waking state levels. The person is not exhausted, and sleepwalking is when muscle atonia is lost, and the dreamer is acting out actions in the dream. Maintaining balance in a dream might translate to maintaining it in a waking world (we all walk on floors after all, not mountain slopes :) )

@AlexStone: Agreed. But the floor is not a plain surface. There're various pieces of furniture on it. Perhaps even a step between one room, and another

Balance is mediated by 3 things: the cerebellum, vision and the ear via the semicircular canal + vestibular nerve (i.e. the ear).
Sleepwalkers lack the visual feedback, but they have a functional cerebellum and semicircular system which is sufficient.
As for waking up and feeling disorientated, if that's when you get up fast that's because your semicircular system hasn't yet reset (as well as your blood pressure has just dipped).

Mind all of you, even the cerebellum sleeps. The waves that are generated in the neocortex predict the same waves in the cerebellum. There probably is no active vision, but the activation patterns of the dreaming visual cortex may give the sleep walking person an idea of the world around him/her. This might, however imply that a great deal of luck is involved in getting somewhere in one piece (given that the patient even moves outside...). During normal REM sleep we speak of complete muscle atonia, the eyes not included. However, this does not work that well in all patients, meaning that they start living their dream. Mind you as well that keeping balance is partially programmed in the muscular innervation (connection patterns in the spinal cord that registers and partially controls muscle tone of agonists and antagonists), and in part by the cerebellum indeed. The cerebellum, however can be devided in a cortex and in cerebellar nuclei. The cortex is not involved in keeping balance as such, much of this is programmed by the cerebellar and pontine nuclei.

The part of the brain that maintains balance acts subconsciously, and so while you are sleeping in the behavioral sense, you part of your brain (the cerebellum) do not necessarily have to be asleep. And so it can still maintain balance.


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Can white eggs be considered as non-vegetarian?
I am basically a vegetarian and I find it very difficult to get an actual biological answer for this question on search engine.
There are couple of links which discuss these argument but can not be acclaimed as a proof as being Egg either a veg or non-veg food item. Below are couple of links which I found depicted this in authors perception:

Egg Non-Veg (a proof)
Egg is veg
Types of vegetarian
If it is veg why products are marked with red dots

Is there any biological proof to consider White Eggs either as vegetarian or non-vegetarian?

Is there a reason you're asking about white eggs, vs., say, brown eggs? Does color make a difference?

@MattDMo Yeah ! I heard that brown eggs can be fertilized to get a chicken but white can or can not be (which sounds confusing to me).

That is untrue. The color of the egg is simply a function of the genetics of the chicken - different strains of chickens lay different-colored eggs - google "chicken egg colors" for some interesting pictures and articles

@MattDMo one of the links the OP posted mentions that the shell changes color when the egg has been fertilized and claims that unfertilized eggs are vegeterian (!).

@terdon That is headshaking stuff.

Of course eggs are not vegetarian. Eggs are, well, the eggs of chickens (usually). Chickens are animals so their eggs are animal matter as well. Whether or not the egg has been fertilized is completely irrelevant, eggs are chicken just as much as drumsticks are.
The color of the egg has nothing at all to do with it. All eggs are, by definition, animal cells. Basically, the chicken's egg is the equivalent to the human ovum. In both humans and chickens, the female will regularly produce eggs and discard them. In the case of a human woman this is the monthly period. When an egg is not fertilized, it is discarded along with some cells of the wall of the uterus. Similarly, in chickens, the female produces and lays eggs. If an egg has been fertilized, it can grow into a new chicken. If it has not been fertilized, it cannot become a new chicken but is most certainly still an animal cell.
So yes, eggs are most certainly animal, not plant or any other kind of matter. Whether or not you should eat them is up to your own moral guidelines to decide. While they are animal tissue, no animal has been killed to obtain them and no harm comes to the chicken if we harvest them.

Great answer @terdon, but I'd suggest changing the first sentence. I think the whole premise of OPs question is that "vegetarian" is a loose cultural concept and doesn't necessarily mean "eating no animal matter". As you suggest at the end it might mean "causing no harm", or not eating animals of certain types (the "vegetables and fish" vegetarians).

@Oreotrephes the OP is free to use the word as he or she desires but asked specifically for a biological answer. From a biological point of view, eggs are categorically animals and not plants or fungi and as far as this biologist is concerned, anything that consists of animal cells is an animal and can therefore not be vegetarian in the strictest sense.

Point taken, and I suppose OP specifically asks: "vegetarian or non-vegetarian"

@terdon +1 Thanks for the nice explanation. May be that's why even being a animal product milk doesn't comes under non-veg food items because it does not contains animal cells. Am I correct ?

@Zerotoinfinite that depends on your definition of vegetarian. Vegans, for example, do not eat milk or dairy products. Milk is bound to contain at least some animal cells. It is not made of them but it will contain some. In any case, there is very little (basically none) scientific basis to any of these categories, its a personal choice, do whatever feels right to you.

"While they are animal tissue, no animal has been killed to obtain them and no harm comes to the chicken if we harvest them." - There are still a lot of chickens hurt or killed in the process: Roosters go straight into the chicken nuggets and when hens stop laying enough eggs after 70 weeks of age they will also be "disposed". Also caged eggs and free-range eggs come from chickens in cages or sheds (they will never come outside). Chickenfoods can come from animal parts (even chicken itself). Your best bet on animal wellfare is biological eggs or no eggs at all (like vegans do).

Most of the egg's matter does not consist of cells. It is just a big bag of proteins.

I think eggs are OK for most vegetarians, but definitely a nogo  for vegans. Often, it is specifically meat that is avoided by vegetarians, and many allow themselves to consume fish. "Vegetarian" is a loosely defined term and I'm afraid I have to disagree with your claim that eggs are not part of a vegetarian diet.

@Anixx actually, none of the egg's matter consists of cells. The egg itself is a single, huge cell.

@ChrisStronks I never made any such claim. The OP asked for a biological answer, not a cultural one. Eggs are animal cells and, therefore,  animals. Whether you should eat them or not is up to your own sense of morality and I wouldn't presume to offer an opinion. That they are an animal cell is not debatable however, that is a simple fact.l

@terdon no, it has a cell+a lot of protein. Fertilized egg does NOT divide into two halves as a whole, only the cell divides in a tiny piece of the egg.


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Is the motor cortex identical to the sensorimotor cortex?
As far as I understand, the primary motor cortex (M1) and primary sensorimotor (SM1) are notations for the same cortical area in the brain. Am I right that there is no dedicated motor cortex, and that M1 actually processes both sensation and movement functions?

I edited the question wording to improve clarity. Feel free to roll back.

@AliceD tnx for the edit

The primary somatosensory and primary motor cortices are distinct cortical areas. According to the structural classification of Brodmann, the primary somatosensory cortex is referred to as Brodmann's areas 1,2 and 3 (BA1, BA2 and BA3). The primary motor cortex is referred to as Brodmann's area 4 (BA4). The primary sensory cortex is sometimes denoted by S1, and primary motor cortex by M1.

Source: My Brain Notes
The primary somatosensory cortex is concerned with the processing of somatosensory input, such as tactile stimuli coming from the skin. The motor cortex is concerned with executing movements and hence with motor output. As such, there is a functional as well as structural distinction between the two areas.
Within the primary somatosensory cortex, basic processing of somatosensory information takes place in BA3, while more advanced processing takes place in BA1 and 2. Neurons in the somatosensory cortex project to adjacent regions, including the motor cortex (Kendal et al., 2000).
Because the primary sensory and motor cortices are four strips of cortex closely situated together, and because they are functionally coupled at the physiological level, they are sometimes collectively referred to as the sensorimotor cortex.
Reference
Kendal et al. 2000. Principles of Neural Science