text:
How can one accurately diagnose the cause of human hearing loss without surgery?
In a human, if you were to avoid a tympanotomy (surgical examination of the middle ear), how could you distinguish between a blocked Eustachian tube, a ruptured eardrum, or a perilymph fistula?
For instance, take the situation where a young man (suffering from a common cold) blew his nose violently, became dizzy for 1 minute, and then reported loss of hearing in one ear of about 40%.  What would your diagnosis be, possible treatments, and expected outcome?

I am not an ENT doctor, but I think the following diagnoses would suffice to determine each of the conditions:

Blocked Eustachian tube: Complaints would be of sudden onset and likely associated with a common cold, or ear infection. Providing the patient with standard decongestant should provide quick relief.
Ruptured eardrum: Patient should have subtle hearing loss apparent on audiogram and it would be relatively easily identified by routine otoscopic examination.
Perilymph fistula: This condition is hard to diagnose and I quote from Vestibular Disorders Association:

A physician can arrive at a presumptive diagnosis [of a perilymph fistula] through a thorough probing for events close in time to the onset of symptoms, along with a variety of tests. These tests can include hearing tests (audiogram, ECOG), balance tests (VNG, VEMP) and some form of a “fistula test.”

The periplymph fistula is by far the most severe condition and the one with the most prominent effects on the vestibular system (balance). Multiple tests and rigorous medical exam is necessary.
With regard to your presented case study: Again, I am not an ENT doctor but a ruptured ear drum can result in dizziness due to the fact that one inner ear is exposed to cold air due to a rupture and the other ear is not. Unilateral inner ear cooling can result in dizziness. However, blowing your nose is unlikely to cause a ruptured eardrum as it is generally caused by more serious barotrauma (diving accidents and in-air plane cabin pressure malfunctions) (Web MD).
Similarly, the fistula is most often caused by more serious traumatic injuries (Vestibular Disorders Association).
A blocked Eustachian tube sounds the most plausible, as it is associated with the common cold (Web MD). Violently blowing your nose can cause fluid to travel up the middle ear, and possibly cause subsequent infections.


text:
Potential between endolymph/cytoplasm and endolymph/perilymph
I am studying for an exam and there is something I can't seem to understand. My textbook says that the endolymph contains 150mM potassium, 2mM Na+ and 130mM Cl-. The perilymph contains 5mM potassium, 140mM Na+ and 110mM Cl-. "Thus" the electric potential between perilymph and endolymph is +80mV (endolymph being positive).
I can see that there are chemical gradients but why is the endolymph so much more positively charged than the perilymph?

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

Marina - @MattDMO is right that you should provide more information. Most importantly, are you referring referring to 'why' (functional aspect to the workings of the inner ear) or to the 'how' (mathematical underpinnings of membrane potentials). If the latter, you should find your answer in this site - there have been many questions on potential differences and their mathematical grounds (search for Nernst or Goldman equations). If the former, then it would be a more interesting question imo. Either way, try to edit your question to make it specific where the bottleneck is.

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text:
Question about the basilar membrane mechanics (cochlea)
I am reading about the mechanics of the basilar membrane in the inner ear.
In various publications, it is said that, at a specific position on the basilar membrane,
the outer hair cells are activated by the amount of basilar membrane displacement
while the IHC are activated by its velocity.
As far as I know each position on the basilar membrane vibrates at a characteristic
frequency. Given that the to-and-fro movements have the same frequency at all sound intensities, isn't the velocity be directly proportional to the membrane displacement?
If that is the case, does this mean that the activation curve is steeper at higher frequencies?

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text:
spinal cord lesion and result in somatic sensation
Jimbo suffers a lesion to the entire right half of the spinal cord at the T6 level. A few weeks after his injury, his doctor tests his right and left legs for somatic sensation and tone.  fill out her chart concerning the absence or presence of different sensations and muscle tone in the lower limbs.
Mark a for absent, P for present
Right leg: Light touch, Pain, Proprioception, Temperature, Hypertonicity, Hypotonicity
Left Leg: Light touch, Pain, Proprioception, Temperature, Hypertonicity, Hypotonicity
what about if the lesion is in C1 or L5? where would it affect (leg/hand..) and fill out the above chart?

Is this a homework question? If so, please use the tag and show how far you got with an answer so far.

it's a practice question. I have no clue how to proceed...

For the sensation aspect, dermatomes are a big hint.  They will give you a rough idea of some of the motor neuron projections.  I'd recommend trying to fill in all that you can and ask specific questions about the portions you don't understand (in the form of "Okay, I know that X ascending tract has been likely damaged, so there's likely to not be any information about Y propagating above a certain level...so, will this mean...") rather than just dropping off the assignment. This is a very useful exercise :)

This is a classic Brown-Sequard syndrome well- studied in the field of neurology. To answer your question, you would need to know what tracts are being severed and what sensations each tract is responsible for. A clean R hemi-section of the spinal cord at the level of T6 would affect the 1) R lateral corticospinal tract, 2) R spinothalamic tract, and 3) R dorsal columns.

The R lateral corticopsinal tract is an upper motor neuron (UMN) pathway, which relays messages from your brain to the periphery. If severed, it would lead to paralysis of muscles below the lesion on the ipsilateral side. This would result in UMN signs such as increased reflexes, increased spasticity, and muscle weakness.
The spinothalamic tract is a sensory pathway connecting peripheral sensations and bringing them up to the brain. Specifically, it communicates sensations of pain, temperature, and gross touch. If severed on the R side, these sensations would be lost on the contralateral side a few levels below the site of the lesion. The reason for this is due to the decussation, or crossing over, of the tract at or slightly above the level of entry of the nerve fibers into the spinal cord from the periphery.
The dorsal columns are similar to the spinothalamic tract, except the sensations communicated are vibration, fine touch, and proprioception. If severed, this would cause loss of these sensations below the level of the lesion but on the same side. A patient would not be able to balance himself/herself without support.

Regarding what areas of the body would be affected based on a lesion in T6, C1, or L5, just as mentioned by jonsca, one would need a dermatome to understand what areas of skin sensation would be affected, and know the nerve root origins of different nerves of muscles. A great book to read to locate these answers in a table format is Neurology BluePrints.
Otherwise, feel free to open any Neurology textbook for a reference, and look for Brown-Sequard Syndrome to read in more detail.

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How can birds disperse seeds when they are able to digest them?
I've just read in a book that birds' guts can digest almost all the consumed seeds with the exception of mistletoe and loranthus (which stays stuck on the branches). On the other hand, I know that the co-evolution with birds caused the enlarging of the fruits - for the fruit trees as an advantage in fast spreading.
But how do exactly birds spread the seeds they consume if they're digested in their guts?

Birds may indeed digest seeds under conditions of rest. It has been postulated that almost all current knowledge on mechanisms of internal seed dispersal has been obtained from experiments with resting animals.
A study with the mallard Anas platyrhynchos (common wild duck), claimed to be quantitatively one of the most important seed dispersing animals in aquatic habitats in the Northern Hemisphere, has shown that physical activity affects gut passage survival and retention time of ingested plant seeds. The authors fed seeds of nine common wetland plants to mallards trained to subsequently swim for six hours. They compared gut passage survival of seeds against a control treatment with resting mallards.
Intact gut passage of seeds increased significantly with mallard activity (up to 80% in the fastest swimming treatment compared to the control), and hence revealing reduced digestive efficiency due to increased metabolic rates. This enhances the dispersal potential of ingested seeds.
An extensive work-out after a meal generally slows down metabolism, as blood is redistributed to the musculature and away from the digestive tract.
These findings imply that seed dispersal potential by mallards calculated from other experiments with resting birds may be underestimated.
Reference
- Kleyheeg et al., Oikos (2015); 124(7): 899–907

Reduced digestive efficiency due to increased metabolic rates?  That seems a bit counter-intuitive, no?  You would think that higher demands on the system would translate to a higher need for efficient energy and nutrient extraction!

@MasonWheeler - An extensive work-out after a meal slows down metabolism, as blood is funneled to the muscles away from the digestive tract.. Good point, and added to answer.

So, are they saying that motility increases with exercise, leaving the seeds less time to be digested, and "pushed out" more quickly, or that the energy demands of the muscles reduce the amount of energy devoted to digestion, and motility remains constant?

@noncom I'm asking what the study concluded, if anything.

The fact that birds are able to digest seeds doesn't mean all seeds get digested. That may depend on activity as in the article cited by @Christiaan. There will probably be other factors like size and shape of the seed and protective coats around the seed.
Humans, whose digestive system is longer than that of birds can digest seeds as well. However, seeds of stratiotes aloides can pass through a human and germinate afterwards.


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Are ribosomes assembled in rough ER and Golgi body, or in the nucleolus?
I mean all the components, such as ribosomal RNA (rRNA) are synthesized in the nucleolus, but is the whole ribosome structure assembled in the nucleolus or is it also done in the rough endoplasmic reticulum and Golgi apparatus?

See https://en.wikipedia.org/wiki/Ribosome_biogenesis

Ribosome assembly starts in the nucleolus (of eukaryotes) and finishes in the cytoplasm. However, in the cytoplasm the Golgi apparatus is certainly not involved, and, as some cells have little rough endoplasmic reticulum, assembly does not require that. Thus, the abstract of a review by Fromont-Racine et al. in Gene (2003) vol 313  pp. 17–42 starts with the statement:

Ribosome synthesis is a highly complex and coordinated process that occurs not only in the nucleolus but also in the nucleoplasm and the cytoplasm of eukaryotic cells.

In the 26 pages of this review there is not a single mention of the words ‘endoplasmic reticulum’ or ‘Golgi’.
A more recent (and freely available) review by Thomson et al. in Journal of Cell Science (2013) vol 126  pp. 4815-4820 is in accord with this. It has a pretty poster insert which presents the assembly as a succession of events, starting in the nucleolus, proceeding to the nucleoplasm, and with some final polishing in the cytoplasm.


text:
Why can't I read everything in my field of view?
When I look at a piece of text, I can see all the text on the paper, no matter where I look, because my field of view covers it all. However, if I stare at a specific word, I cannot read the text a few lines above the position I am staring at, even though I can clearly see there is text there. I don't think it has anything to do with the text being out of focus, since I observe this phenomenon no matter what distance the paper is from me. What are the specific causes of this?

The field of view is determined by the light-receptive parts of the eye: the retinae (Kolb, 2012). The fovea is the region with the highest resolution. It is located in the central part of the retina and covers only about 2 degrees of the field of view (Lauweryns, 2012). The total field of view is roughly 180o (Fig. 1).

Fig. 1. Schematic of the human field of view showing the foveal region. Source: Medical Dictionary.
The reason for the regional differences in retinal resolution (referred to as visual acuity) is that the cone photoreceptors are densely packed in the foveal region, while rod photoreceptors predominate the retina outside the fovea region (Fig. 2) (Kolb, 2012).

Fig. 2. Distribution of rods and cones. Source: Webvision.
The cones sense color and are specialized to work under well-lighted (photopic) conditions. In contrast, rods are hardwired to converge onto a single optic fiber to collect responses for dim lighting (scotopic, or night vision). Because many rods (tens of rods) connect to a single optic nerve fiber, the spatial acuity is dramatically reduced (Fig. 3). Hence, you can read with only a few degrees of your vision. While reading, your eyes continuously scan the page for the next word to center it onto the foveal region.

Fig. 3. Many rods converge onto a single ganglion cell, while one cone synapses onto a single ganglion cell. Source: Slideshare.
This is the big handicap that people with age-related macular degeneration face. The macula (that includes the foveal region, see Fig. 1) degenerates and the cones are lost. Hence, they loose their high-acuity region and cannot read anymore without using magnifiers or other low vision aids.
References
- Kolb, Webvision - The Organization of the Retina and Visual System (2012)
- Lauweryns, Brain and the Gaze: On the Active Boundaries of Vision (2012)


text:
Can jellyfish sting outside of water?
According to my understanding of the Wikipedia page on the stinging cells of the jellyfish, the mechanism of delivering the toxic missile is largely due to water pressure. Does that mean that a jellyfish on land (or brought out water) is unable to, or perhaps less efficient at, delivering its stings?

The wiki article did state the cnidoblasts uses the chemical gradient and osmosis to sting. So i guess it needs those two factors to work.

Short answer
Jelly fish can sting out of the water and even when they are considered to be dead.
Background
I do not have detailed scientific literature available. However, popular sources generally and equivocally warn against touching jelly fish, even on land and even when they appear to be dead. In fact, dead box jelly fish can be as dangerous as live ones (ABC News).
Credible sources
 - National Poison Control Center
 - UK Telegraph
 - ABC News


text:
Which function do nicotinic receptors have in the periphery?
I came across this question today, it says:

Nicotinic receptors stimulation is directly responsible for …....

I should fill the spaces by one of the following choices:

Increasing the excitability of sympathetic postganglionic neurons.
increasing the the force of stomach contraction.
delaying the emptying of liquids from the stomach.
decreasing the excitability of sympathetic postganglionic neurons.

The only article speaking about the nicotinic receptors in my physiology book says that they are cholinergic receptors found in the autonomic ganglia, i.e., they are found on the postganglionic neurons.
So when I tried to solve the question, I thought the upper three answers are correct. Specifically, because stimulating the receptors on the postganglionic neurons will increase their excitability, option 1 seems to make sense.
But if that postganglionic cell happen to be sympathetic it may provoke the emptying of the liquids from stomach to be delayed (choice 3)?
And, if it was parasympathetic the force of stomach contraction would also increase (choice 2)?
I am confused as all three answers 1) 2) and 3) seem to be correct and the question asks specifically for one correct answer. Could someone help me find the correct answer, but put simply please, as I'm just a first-year dental student.

Short answer
1
Background
Nicotinic recepeptors (nAchRs) are widely distributed in the central and peripheral nervous system. Your question seems to focus on the peripheral nervous system. Taken from (Taylor, 2012):
In the periphery, nAchRs are found in:

Innervated skeletal muscle, especially postsynaptically in the motor end plate;
The presynaptic nerve ending in some motor neurons to control Ach release;
Ganglia at the postsynaptic dendrite and nerve cell bodies, and presynaptically to control Ach release.

Now in your answer the options 2 and 3 are incorrect, as muscarinic Ach receptors regulate gastric fluid secretion (Aihara, 2005) and contraction (Kitazawa et al., 2006). Given that nAchRs are excitatory receptors. In muscle cells, the binding of Ach leads to an opening of the associated ion channel, in turn producing a rapid increase in the cellular permeability of sodium and calcium ions, resulting in the depolarization and excitation of the muscle cell, thereby producing a muscular contraction (source: EMBL-EBI). This leaves only one opion left, namely 1). Since this was basically answering the question by exclusion, below Fig. 1 shows that answer 1) is indeed the correct one through a more positive approach - the top panel clrearly confirms that the sympathetic pathway deploys Acetylcholinergic neurons to stimulate its postganglionic adrenergic neurons.

Fig. 1. Ach in the peripehral nervous system. source: Austin Community College
References
- Ayhara, Gastroint, Liver Physiol (2005); 2886): G1199-207
- Kitazawa et al., Eur J Pharmacol (2007); 554(2-3): 212-22
- Taylor, Primer on the Autonomic Nervous System (3rd Ed. ( 2012}


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How do neurons receive the ions needed for creating electrical pulses?
I really wonder how ions are transported into the brain and the neurons for creating electrical potentials - how do ions get from our digestive system to the neurons? Or are the ions just freely released into the brain like hormones? Or are they transmitted during neural signalling somehow (via neurotransmitters maybe)?

There are voltage-gated ion channels in the cell's plasma membrane that controls the release of ions. https://en.wikipedia.org/wiki/Action_potential

I voted to close because the title asks for a cellular/molecular approached answer pitched to neurons, the body text asks for a tissue-level answer. It's unclear what you are after. Feel free to edit. It can be an interesting question.

Short answer
The sodium-potassium pump in the epithelial cells lining the brain capillaries pumps Na+ and K+ into the brain.
Background
The blood-brain-barrier is formed by the endothelial cells lining the capillaries in the brain. Not many compounds can pass this lining, especially not when they are hydrophilic, such as charged metal ions. However, as you rightfully state, somehow these metal ions, and especially Na+ and K+ need to get access to the brain because they are crucial for membrane potentials and action potentials, and hence for neuronal survival and function. And indeed they can, albeit the exchange between blood plasma and brain is slow compared with other tissues.
Intravenously administered K+, for example, exchanges with muscle K+ in 1 hr, but K+ exchange in brain is only half completed in 24 to 36 hr. Na+ exchange is somewhat faster, with half-exchange into brain occurring in 3 to 8 hr. Despite its relatively slow entry into the brain, Na+ exchange across the blood—brain barrier appears to occur by mediated transport. This occurs, in part, through brain capillary Na+,K+-ATPase (the sodium-potassium pump). The Na+,K+-ATPase in the brain also may mediate removal of interstitial fluid K+ from the brain and thereby aid in brain K+ homeostasis.
Reference
- Laterra et al. In: Siegel et al. eds. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th ed. Philadelphia: Lippincott-Raven; 1999

The cells/neurons themselves have Na+ and K+ channels in their cell membranes that allow for passive movement of these ions between the outside and inside of the cell. If you're wondering how the gradient gets established in the first place, simply put, these channels are built to open/close at the right amounts in their environments. Additionally, the cell uses a Na/K ATP-ase pumps in the cell membrane, which uses the chemical potential energy of ATP, to help regulate and establish that gradient.

So they all are pumped into our brains while we are in the uterus? I meant more like how do the neurons get it (the way of the ions from our digestive system to neurons) than how do they get into the correct place in the neuron.

We absorb ions through our GI tract. Those ions are then in the blood. The blood is separated from the brain by the blood-brain barrier, but the endothelial cells can regulate the flow of the necessary ions into the brain, specifically to the cerebral spinal fluid, which bathes the central nervous system with all its neurons.

@Biomed_guy And how does the ATP pump work?


text:
Why do fetuses have membranes between fingers and toes?
Are the membranes present between the fetal fingers and toes a remainder of the phylogenetic evolution, or just a way organs do grow most easily?

It seems difficult for me to define "easily" in the context of organ development. In any case, the way organs develop is mostly inherited from our ancestors, so "it's easy to do so" and "it's inherited" are not necessarily contradictory statements.

Short answer
The transient membranes between the fingers and toes in embryos are a myth.
Background
The presence of transient membranes in developing embryos supposedly points to our fishy evolutionary origins. However, I couldn't find any credible sources to support this myth. In fact, I couldn't find any source mentioning the presence of webbing between the fingers and toes at any stage during development.
To support this lack of evidence, I have posted several photos of embryos and fetuses in various developmental stages. None show any signs of the "swimming webs". Note that the age mentioned is the developmental age, counted from the moment of conception (add 2 weeks to have gestational age):

Fig. 1. Five-week embryo. source: Palm Reading Perspectives

Fig. 2. Seven-week embryo. source: Wikipedia

Fig. 3. Eight-week embryo. source: WemMD

Fig. 4. Fourteen-week foetus. source: WemMD

Fig. 5. Eighteen-week foetus. source: WemMD
Fig. 2 may seem to show some webbing, but if we look at some close-ups of the hand and feet at week 7 in Fig. 6 below, we can see that there is no real webbing; fingers and toes are simply budding from the primordial hand and foot structures.

Fig. 6. Developmental stages of the hand and feet around week 7. source: I am Pregnant
Note that an embryo is called a fetus only after the first trimester, i.e. after some 12 weeks. There is certainly not any sign of webbings in healthy fetuses.
Also note that webbings may be the result of birth defects, such as syndactyly and pseudosyndactyly (Fig. 7):

Fig. 7. Infants with Syndactyly (left) and Pseudosyndactyly (right). sources: Wikipedia & University of Columbia
Original photographic image source (Figs 1 & 5)*
- Nilsson, Ett Barn Blir Till
* Credits go to rg255

Figs. 1 + 5 at least come from Lennart Nilsson's Ett Barn Blir Till (ISBN: 9789174242751) - just thought that deserves proper credit because it's a beautiful book (and has English versions I think)  :)

@rg255 - thanks! - ref added + acknowledgement :-)

There is some "webbing" in very early stages. These cells between the digits undergo apoptosis. At least that's what I have read in the dev bio textbooks.

@WYSIWYG - yes, that's what I thought too. I just couldn't find it. I'll look into some text books and try to find out. Thanks for this.

Thanks. So (if there's apoptosis of the cells between fingers) the second option (it is the easier way to "grow a hand) is correct, isn't it (but yeah, I understand your point, why no "membranes" exist?

@Probably - thanks for accepting. I'm still working on your answer though. I'll try to get back to you asap. The answer as of now is OK, but I'm going to add another line of reasoning. In due time, promised. I've not forgotten about this!

@Christiaan Yeah I realised that it is pretty clear from your answer, thx.


text:
What are the factors on which protein-protein interaction depend?
Does protein-protein interaction only happens when one of them is basic and the other acidic? Do protein interactions also depend on the protein structure? Are there more factors?

Proteins are not acidic or basic per se. It depends on the environment - if this is acidic, than some aminoacids can be protonated, while others cannot. But in a given environment proteins are either acidic or basic, but not both.

so two acidic proteins can interact in an environment?

Yes. Acidity or basicity of a protein is an overall property. What's important is the charge of residues at the interface where the proteins interact (amongst other things).

what are the other things?

Your question seems too broad and dupllcates these: http://biology.stackexchange.com/questions/2965/what-role-does-a-proteins-size-have-on-protein-protein-interactions?rq=1, http://biology.stackexchange.com/questions/1404/what-are-the-various-types-of-protein-protein-interactions

http://biology.stackexchange.com/questions/2965/what-role-does-a-proteins-size-have-on-protein-protein-interactions

possible duplicate of How does temperature influence the rate of protein degradation?

It depends both on structure and charge. Binding sites of proteins are essentially formed by amino acids placed in a particular conformations such that it will match the binding site of their counterpart protein or substrate. This is commonly referred to as the lock and key model of protein binding. This is similar to how two puzzle pieces fit together, the pieces are exactly the same shape at the point at which the puzzle pieces connect. At a protein binding site amino acids are clustered together to form the matching shape to the appropriate binding partner. This however is not just dictated by 'physical shape' of each amino acid but also their charges. This is important because negatively charged amino acids will repel other negatively charged amino acids, and attract to positive amino acids, thereby modulating the exact 'shape' of the protein binding site.

so negative;y charged amino acid will bind to positively charged amino acid. Similarly cant we say the same for proteins as a whole?

apart from charge and structure, is there any other feature on which the binding depends??

so the charge in the binding site of protein is being considered for binding and not the entire charge of the entire protein. Am I right?

Yes you are correct.


text:
What is the protein sequence taken as input in the Path-A prediction system
Considering the Path-A based metabolic pathway prediction (http://nar.oxfordjournals.org/content/34/suppl_2/W714.short). It uses machine learning for pathway prediction. Suppose that the input was a protein sequence of a query organism. I do not understand what these protein sequences are? Are these the enzymes for the reactions?

The basic algorithm has two inputs: a set of protein sequences from the query organism and a set of model pathways, one for each target pathway.

Not necessarily, they can be enzymes, but they include a lot more (the whole proteome).

It takes a FASTA format file containing a set of query protein sequences from a single organism (a partial or complete proteome) and identifies those sequences that are likely to participate in any of its supported metabolic pathways
Path-A predicts the pathways supported by arbitrary sets of proteins, using validated prediction techniques based on sequence alignment and machine learning.

The whole proteome as in the whole genetic sequence available?

@Rishika No, the proteome.

so basically a proteome is the list of all the available proteins in an organism??


text:
Is there a difference between visual sensation and imagination in the brain?
How substantial is the difference between the neural signal associated with seeing an image and the imagination of that image? Surely, it can not entirely copy the pathway from the sensory organs to the emotional centers, but approximately how large is the common pathway for both processes?
Is there some principal difference in the neural pathway of these two processes, or is the imagined image just more of a slurred version of the visual image?

Interesting question, but typos and grammar mistakes in the text severly hinder comprehension. Could you restate your question more simply?

@Nicolas Thanks for your edit. I included the additional question (second paragraph) just to let the reader know that I'm interested in the topic even if the signal would be exactly the same, but in different centres of the brain. But the simpliest (most measurable) version would be, I think: "If I'm imagining stressful situation, does my Amygdala relies stress (hormones)?

Assuming, like most humans, you have a sense of consciousness, then you should be able to distinguish that there is a difference between sensory perception and imagination. Where you may run into problems, and many people do would be when trying to discern memories of actual events versus imagined circumstances. There has been a good amount of research into how false memories can be implanted into a persons brain and that their brain will then embellish on it and fill in the details. See the work of Dr. Elizabeth Loftus

@AMR I wasn't claiming it's the same, then my question would make no sense. My question is how does this difference look like in brain. I think making up fakememories it's something different. This effect has nothing to do with how the brain recieves (and stores) information which comes, I think, the fake memory is being built up continuously as brain makes connections in order to make it sense as is goodly explained in question: http://biology.stackexchange.com/questions/775/how-and-where-in-the-human-brain-are-memories-stored

In a nutshell: Are you asking on the commonalities between sensation and imaginations of sensation, in terms of neural circuitries?

@Christiaan Yes. But this way interpreted it sounds maybe like something subjective, which is not. By the "commonolaty" I mean the shared neural pathway or shared system in different brain center.

I have re-edited the question in the hopes of getting those downvoters to reconsider. It is a great question, albeit, admittedly, vaguely formulated, especially taking your comments into account. Nonetheless, I hope your bounty and some of my edits draw in your deserved answers. If my edits have defied their purpose, feel free to roll back.

Short answer
Visual perception and visual imagery draw on much of the same neural machinery.
Background
I have interpreted your question as: What are the common neural circuitries between visual sensation and the imagination of sensation?
In neuroimaging, mental imagery of visual images is a big deal. For example, there is a large body of literature on cross-modal activation of visual areas in the brain in blind people. It is known that visual deprivation results in neural plasticity and the recruitment of visual areas in the brain for other sensory systems. For example, blind Braille readers show activation of the primary visual cortex when reading Braille (reviewed in Stronks et al., 2015). However, interpretation of these findings is difficult in late-blind individuals, because they have experienced visual input earlier in life. Hence, while Braille reading they can be mentally reproducing the visual representation of the Braille cells using visual neural circuitry.
Indeed, it has been shown with fMRI that visual imagery and visual perception draw on most of the same neural machinery (Ganis et al., 2004). However, the spatial overlap of the activated regions is neither complete nor uniform. The overlap in this study was more pronounced in frontal and parietal regions than in temporal and occipital regions, indicating that cognitive control processes function comparably in both imagery and perception, but not identically.
Various studies reveal different results, however. In another imaging study, 'just' two-thirds of brain regions overlapped in visual sensation and imagery (Kosslyn et al., 1997). Indeed, the experimental task used may have important effects on study outcomes.
Most notably in this regard is that approximately half of the studies done have found activation of the primary visual cortex during imagery (Kosslyn et al., 1999). This is interesting, because the primary visual cortex is generally thought to be an early, low-level area in the visual system that depends on thalamic input that relays information from the optic nerve to the brain. I.e., it is generally believed to depend on sensory stimulation. Generally, only the higher-level associative visual areas are associated with higher cognitive processes.
References
- Ganis et al., Cognitive Brain Res (2004); 20: 226–41
- Kosslyn et al., Neuriomage (1997); 6; 320–34
- Kosslyn et al., Science (1999); 284; 167–70
- Stronks et al. Brain Res (2015); 1624: 140–52

I read some articles on the thalamus, can't currently remember which ones though, that suggested that there is overlaps, but when you are imagining something the thalamus blocks the signals from entering the perceptual system. This is still speculative though, as current the resolution of current measurement methods leaves a lot to be desired.
In some mental disorders the signal isn't blocked by the thalamus (if this is what happens) and is instead experienced as an hallucination, there is also some evidence that this also happens in a less intrusive way in some people we perhaps wouldn't not call mentally ill.
Nikola Tesla for example suffered from what we would call hallucinations, but was able to learn to control it to some extent so he could use them as a tool for helping him making machines. I think the following section of his biography is quite interesting.

There was another and still more important reason for my late
  awakening. In my boyhood I suffered from a peculiar affliction due to
  the appearance of images, often accompanied by strong flashes of
  light, which marred the sight of real objects and interfered with my
  thought and action. They were pictures of things and scenes which I
  had really seen, never of those I imagined. When a word was spoken to
  me the image of the object it designated would present itself vividly
  to my vision and sometimes I was quite unable to distinguish whether
  what I saw was tangible or not. This caused me great discomfort and
  anxiety. None of the students of psychology or physiology whom I have
  consulted could ever explain satisfactorily these phenomena. They seem
  to have been unique although I was probably predisposed as I know that
  my brother experienced a similar trouble. The theory I have formulated
  is that the images were the result of a reflex action from the brain
  on the retina under great excitation. They certainly were not
  hallucinations such as are produced in diseased and anguished minds,
  for in other respects I was normal and composed. To give an idea of my
  distress, suppose that I had witnessed a funeral or some such
  nerve-racking spectacle. Then, inevitably, in the stillness of night,
  a vivid picture of the scene would thrust itself before my eyes and
  persist despite all my efforts to banish it. Sometimes it would even
  remain fixed in space though I pushed my hand through it. If my
  explanation is correct, it should be able to project on a screen the
  image of any object one conceives and make it visible. Such an advance
  would revolutionize all human relations. I am convinced that this
  wonder can and will be accomplished in time to come; I may add that I
  have devoted much thought to the solution of the problem.

The rest of his autobiography has more details

What did you read? Statements without proper referencing, let alone memory recollections alone, are not advisable.

Some articles on the thalamus. I don't remember which ones though, but from a quick search I found one that at least partly deals with the topic http://www.biomedcentral.com/content/pdf/1742-4682-7-10.pdf

You might want to edit your answer accordingly, as you take a very interesting approach in your answer.


text:
What is a functional screen?
I was going through this paper, but did not understand a term.
What is the meaning of functional screen?
(I am not a biology student, I don't understand much, and a small simple explanation would be enough)

From the abstract of the linked article (Guttman, 2002):

We used an in vivo genetic screen to identify 13 effectors [...]. Although sharing little overall homology, the amino-terminal regions of these effectors had strikingly similar amino acid compositions.

And from the body:

The screen relied on the type III secretion signal and the endogenous promoter of the hop gene and was thus highly specific.

Hence, the authors search and identify proteins with a secretory signal under the regulation of a hop promoter. A functional screen in this paper refers to the analysis of protein samples to detect the presence of proteins with a particular function.


text:
Do hermaphrodites have more nerve fibers in their puendal nerve?
Recently I have been thinking, both the glans penis and the clitoris are the most sensitive parts of the body. They contain a lot of nerve endings. Do hermaphrodites share the nerve fibres between the two organs, or do they have double the regular amount of nerve fibers?
Also, at which point does their nerve branch out? Do they have two sets of dorsal genital nerves coming out of the pudendal nerve or does the same set of dorsal genital nerve go into both organs?

Short answer
The genitals of true intersex individuals are not duplicated. Instead, their external genital features are hybrid structures. In turn, it's not a matter of duplicated neural innervations.
Background
Hermaphroditic phenotypes in humans are nowadays preferably described as  intersex phenotypes. In humans they come in different flavors, dependent on the underlying genetic causes, which are often caused by mosaics of X and Y chromosomes. Dependent on the exact genetic underpinnings, various types of intersex phenotypes occur, with different internal and external phenotypes of the reproductive tracts.
To proceed to the most extreme case, namely the true intersex individuals - these people display both male and female external genital tissues. However, this doesn't mean they have fully developed male as well as female genitals.
Now taking a step back to the normal male/female situation - you have to realize the clitoris and glans penis develop from the same tissue (Fig. 1). In true hermaphrodites, the external genitalia are not duplicated, instead they form a hybrid, where it becomes unclear what exactly is present: a small (glans) penis, or an outsized clitoris (Fig. 2).
So in all it is not a matter of duplication, but a hybridization of similar feats.

Fig. 1. Male and female genital development. source: University of the Cumberlands

Fig. 2. Intersex external reproductive organs. source: ImageSlideShare

Hi, Thx for the answer and the edit. That also explains why a quick google search was unhelpful. Searching for "Intersex" revealed the required info much more quickly.


text:
Do acetyl-CoA, acetyl-CoA carboxylase and acetyl-glutamate carry any charge?
Do the following compounds have any charge? If not, then why? If yes, is there any database that would give me this information if the compound is negatively or positively charged?
The compounds are as follows:
Acetyl-CoA
Acetyl-CoA carboxylase
Acetyl-glutamate
I have searched and somehow I am getting more confused.

chemicalize.org is a good utility for predicting many molecular properties such as pKa, pI and charge. The Human Metabolome Database uses the same underlying software but tabulates some of the data (eg charge is explicitly stated).
Acetyl-CoA, for example, has a pI of 1.32 and charge of -4 at pH=7.4.

Your second link is to a portion of an enzyme (a serine residue that gets phosphorylated). Prediction of protein properties can be done with ProtParam.
Human Acetyl-CoA Carboxylase 1, for example, has a pI of 5.95 and charge of -39.

what is the difference between these compounds and lipids?

The first compound you mention is acetyl-co-enzyme A (acetyl-CoA) (first picture, left panel). The acetyl group is uncharged, but the co-enzyme A (CoA) group (Fig. 1, right panel) does carry charge through its phosphate groups. In normal physiologic environments these phosphate groups will donate one or more protons, leaving the molecule negatively charged, as shown in Fig. 1, right panel below:

Fig. 1 Acetyl-CoA (left) and the co-enzyme A group (right).
The second compound is an enzyme, namely acetyl-CoA carboxylase. Consisting of many, many amino-acids it will carry many, many charges under physiological conditions. Some of these will be negative, some positive.
The third compound you mention is acetyl-glutamate:

Acetyl-Glutamate
This compound carries two carboxyl groups, which makes the compound acidic and negatively charged under physiological conditions, as it will donate one or two protons to the environment, dependent on the pH.
PS: For an in-depth answer on the basic chemistry and pKa values I would ask this at Chemistry.SE :)


text:
How can I label cryotubes in a way that eliminates the problem of legible hand-writing?
My lab stores biological material (tissue, cells, plasma, serum) in a -130 C, liquid nitrogen freezer. The cryotubes that we use to store a samples are labelled by hand which frequently creates legibility problems.
Its my understanding we can't print out stickers to use as labels because they will degrade in the cold. The solution of putting barcodes on the tubes has been suggested but its undesirable because in addition to the cost and logistic complications; we would have to choose between thawing and refreezing all of our samples to transfer them to new tubes OR live with the nightmare of having both labeling systems in use at the same time; one which humans can read and one which humans cannot.
The ideal situation would be a small, portable machine that can physically label the tubes for us. I'm envisioning:
 - an adjustable clamp to hold the tube in place; ideally with sensors that would infer the shape, size, and position of the area that can be labelled.
 - a very-fine tipped pen attached to a motor that would mimic a printer's line-by-line printing action; this would have to take into account the shape and size of the area that can be labelled
- rollers in the clamp to adjust the available space for labeling
 - a screen/keyboard interface that would display how the label will appear
Does anything like this exist?
Do you have any other suggestions about how to deal with the problem of legible hand-writing on cryotubes?
Please advise if there is a more-appropriate SE site to post this question

One way to get around this problem is to keep similar samples in the same box; for e.g One box per cell type and label the box nicely [easier to write legibly on a big box]. Keep the marking requirements minimal on the tube (for e.g. just dates)

It doesn't seem that "legible hand-writing" would be a problem. Rather the problem is illegible handwriting. Could you have some technician with legible hand-writing just prenumber the tubes?

Barcodes would not be a good solution due to the ice crystal formation when the tubes are removed from storage preventing scanners from working.

This is indeed a problematic point. I have been using machine printed labels for a while now (sometimes with some extra scotch tape around it to prevent it from falling) off, which worked pretty nicely.
However, there is a printer available on the market (though I haven't tested it yet) which claims that they can print on any tube. This printer is called Tubewriter, which is probably also worth a look. The backside is the price, Fisher Scientific lists them around 40.000$, which will make them unavailable for most labs, except for cell banks etc.

Reminds me of this thing

@chris This is affordable but I would want to test the ink around solvents.   http://www.usascientific.com/dymo-450-printer.aspx

@rhill45 Interesting. I didn't know this machine - since it is labelled with "lab" it should probably adress some problems with the durability.

What I find works is to scotch tape the labels to the tubes, they hold up fine in our -70C freezer.
What I did was go into excel 2010, go to View tab, click on Page Layout on the left side, not normal view! Then, go to home tab, select all the cells on the page. Go to the right side of the home tab, hit Format, then Row Height. This lets you set height in real units, I typically enter "10mm". Do the same for Column Width, I like 20mm. Now reselect the page of cells because changing the cell size will push some off the page. Right click the cells and format them to center the text horizontally and vertically. Now you can type your label text into the cells. I suggest font size 8 or smaller so you can fit it all in the cell. To make cutting the labels easier, put borders on all sides of all cells. Just print it out, cut them apart and tape them on your tubes. Sorry microsoft makes it so hard to set the size of a cell in real units.
Just to see if I could, I tried to create a QR code and make it small enough to fit on the 10x20mm label. But my phone can't read it once I print it out at that size. With a better camera and a good printer you could probably make it work. I don't know enough about alternative bar code systems to try anything else.

I hate this problem but I hate even more when I pull up a cryo vial that some one wrote on with a dry erase marker.
Get printable tough tags.
Two options after that, print on them with your laser printer. Can do many at a time.

You can take a step further and overlay the tag with some 3m single sided tape (scotch tape is gonna brittle up from the N2.)
Write on it with a fisher brand solvent free marker. This is the only marker alcohol will not take off!!!

I would love to find the ink in this market and be able to put it in my printer for the tough tags.
I like these types of questions on here.
There are elaborate systems out there like Chris's answer and they are of course preferable. But expensive.
I didn't think to use the QR codes for as mentioned by 1st answer, I may try this.

However, it seems that the Tough Tags are only rated for -40°C.

For OP's application, I would recommend Cryo-Babies, which are rated for liquid- and vapor-phase nitrogen storage at -196°C

We have used Brother P-Touch printers in the stock at work, but our lowest temperature is -80C. It's ideal for making sure the labels go all the way around the vials.

Welcome to Biology.SE! Can you please provide a little more detail? For example, model numbers, links to the product, and images of successfully labeled tubes. I also think you will get a better reception for your posts if you make sure the spelling and word use are correct. Also what do you mean by "in the stock" — it feels like maybe you left out at least one word? ——— You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Can a heterozygous allele show non-heterozygous expression in a family?
I'm doing a family study looking for novel cancer-associated variants in germ-line samples; the goal is to find candidate biomarkers which might be used for early detection. At an earlier step our analysis, we eliminated a family that showed a heterozygous mutation known to be associated with our cancer under the premise that this known mutation better explained the presence of the disease than any novel variant we may have found.
I've now found another mutation, strongly associated with out cancer, which we does not appear to be heterozygous. 2 out of 3 family members share this mutation with a within-family allele frequency of 0.5.
Trying to decide whether this means I need to discard this family from further consideration, adjust my thinking, or not worry about it. My current thinking is that it'd be safest to eliminate the family from consideration because the mutation pathogenic and found in the germline but I can't wrap my head around how the lack of a heterozygous pattern affects things. Does it absolutely mean the variant was not inherited? Can anyone help me get my thoughts straight?

I don't really understand your question. Basically at a given bi-alleleic locus, you have one allele that you suspect to cause cancer. In your sample (not only in one family), this locus in never found in the heterozygous state? And you ask "how is this possible"? Did I understand your question? Have you performed a chi-squared test (or test based on a binomial distribution) in order to test whether the lack of heterozygosity is really unlikely to happen by chance?

One of the fundamental premises of this project is that the families we are looking at do not have heritable mutations known to cause cancer (at least not the cancer we're interested in). We eliminated one family from consideration because they showed such a mutation in all members with an allele frequency = 0.5; My question is whether I should eliminate this second family in which 2/3 members have the known, cancer-causing variant for being useless


text:
What equation to compare protein isoforms in a Western Blot?
The protein isoforms I am interested in comparing appear as distinct bands on the gel I have already run. I have an Excel sheet with optical density measurements I obtained using ImageJ; it looks something like this:
Lane    Iso1       Iso2       GAPDH
1       149.06     194.646    893.08
2       832.654    494.473    148.335
3       49.998     490.539    147.361
4       29.347     208.53     120.652

For the other proteins I've analyzed so far, I've been computing fold-change relative to my loading control, GAPDH, with the following equation:
Fold-Change = Log2(Protein/GAPDH)

I'm not sure how best to compare my isoforms to each other and considering the following two equations:
1. Fold-Change = Log2[(Iso2/GAPDH)/(Iso1/GAPDH)]

2. Fold-Change = Log2(Iso2/Iso1)/GAPDH

I've already computed both of these values for all my samples, graphed them and found that the resulting graphs look pretty different. Which of the two equations do you think is a better way to compare the relative quantities of these proteins?
Alternative equations are also welcome.

Are your lanes replicates ?

No: each lane was loaded with a different sample.

Now see, the problem here is that in the first equation your GAPDH normalization factor is lost. So finally there is no normalization.

Could you explain more fully how the normalization factor is lost?

Oh, now I see that dividing the numerator and denominator by the same value cancels that value's impact on the final answer.

In my opinion you should use this formula:
$$ \frac{\text{log}_2(\text{Iso}_1/\text{Iso}_2)}{\text{log}_2(\text{GAPDH})} $$
This will normalize the relative fold differences between the isoforms with the loading control- GAPDH.
Since both numerator and denominator are log transformed they are in comparable domains unlike the formula-2 that you mention in your question. This is just a modified formula-2.


text:
Question related to L-arginine biosynthesis
With respect to the L-arginine Biosynthesis pathway, the very first reaction converts L-glutamate to N-acetyl L-glutamate.
In the linked reaction scheme, why are only L-glutamate and N-acetyl glutamate considered, and not acetyl-CoA or the coenzyme? Is this because L-glutamate and N-acetyl L-glutamate are the main compounds to be considered? Why are they the main compounds being considered? Are these two compounds (L-glutamate and N-acetyle L-glutamate) the ligands?

The synthesis of N-acetylglutamate is mediated by the enzyme N-acetylglutamate synthase. This enzyme has L-glutamate as its substrate and uses acetyl-coenzyme A as a co-enzyme acetyl donor. Acetylcoenzyme A (Acetyl-CoA) is generally abbreviated in structural formulas, because it is a relatively complex molecule. The only thing of relevance is the acetyl group which is transferred from a thiol group to L-glutamate.
Note that ligands is a term reserved for molecules binding to receptors; substrates is the proper term for intermediates in enzymatic reactions.

N-acetylglutamate synthesis. Source: The Medical Biochemistry page


text:
What are these pathways called in Biology?
Considering the pentose phosphate pathway and the sulfate reduction pathway in bacteria;
What are these types of reactions called in biology? Bio degradation reactions or bio transformation reactions or something else? I wish to know whether there is a generalized names for these types of pathways.

They usually have specific names - your example is the pentose-phosphate way (or pathway).

is there no generalized names for such pathways?

If you want it short: Pathway. Otherwise you could think about metabolic pathways or the specific names.

so these types of chained reaction like pathways have no special names...

The special names of these chained reaction like pathways is metabolic pathways. This is it. For the first time in science, something actually has an intuitive name.

Metabolism is the term for all biochemical reactions. Degradative pathways (big to small molecules) are called catabolism and constructive pathways are called anabolism.

Short answer
Assuming you wish to have a common name for both of these (widely differing!) pathways I basically agree with @Chris, and I would go for general terminology, namely metabolic pathways.
Background
The pentose-phosphate pathway is neither anabolic nor catabolic so those terms won't do. The pentose-phosphate pathway is, however, closely linked to general metabolism to supply the body with C5 sugars. So metabolic pathway sounds right to me.
The other pathway is a sulfate reduction pathway, which is an anaerobic respiration pathway that uses sulfate as the terminal electron acceptor instead of oxygen. It is an entirely different pathway. However, it too is neither catabolic or anabolic, but still closely linked to metabolism. Hence, metabolic pathway is applicable here too.


text:
What is the maximum electric potential that can occur in the human body?
Neurons can generate a voltage, if there is an action potential. Also, membranes where an ion concentration gradient is present, generate some membrane potential.
What I wish to know is, which cellular element in the human body creates the greatest potential differences? And how high can they be so high? Are there also biochemical reactions, where significantly high electric/electrostatic voltages are important? How strong are these?

What do you mean by "cellular element"? Do you mean different types of cells, or something else?

I mean any microbiological Entity like membranes, ribosomes, Golgi-apparatus, etc.

To the best of my knowledge, the potential difference across the hair cells in the inner ear (cochlea) (Fig. 1) is the highest in the (human) body. It is about 120 mV, mainly due to the exceptionally high positive potential of the scala media as provided by the stria vascularis, referred to as the endocochlear potential. This potential is mainly built up by the high amount of K+ pumped into the scala media by ion pumps located in the marginal cells and basal cells (Salt et al, 1987) in the stria vascularis. Adding the potential difference of -40 mV of the hair cell it yields a total difference of 120 mV (Fig. 2).
References
- Morrill & He, J Otology (2017); 12: 151-64
- Salt et al., Laryngoscope (1987); 97(8 Pt 1): 984-91

Fig. 1. The cochlea. source: Morrill & He (2017)

Fig. 2. The potential difference across the hair cells is 120 mV, due to the endocochlear potential of +80 mV in the scala media. source: University of Minnesota Dulluth

As excellent as this answer is, if you look at the comments in the OP, the asker wants to know about voltage differences within an individual cell

@Astrolamb the question title tells me differently, but you might be right. W'll see if OP updates the Q. I might have been too fast answering.

The inner membrane of the mitochondria has a huge membrane potential generated by the pumping of protons as part of the respiratory chain.
In rat cortical neurons this value is around -140 mV and can variate between -108 and -158 depending on the metabolic activity of the cell.
Ref: J Physiol. 2012 Jun 15; 590(Pt 12): 2845–2871.


text:
What is the physiological mechanism for getting unconscious after a punch to the head?
It is the everyday life in boxing: One boxer gets a smack in the head, cannot do anything for many seconds and then: Victory of his opponent due to a Knockout!
What is the reason for losing consciousness for a short time by e.g. a strong smack in the head?
Are there any neuronal reactions that cause this?

Does this answer your question?

The answers are differing from each other; is it due to the Neuron compression or because the blood flow is truncated after a punch?

Yes, questions often yield different answers. Both answers may, or may not be correct. If the question is the same as yours, and you wish more answers, you can put a bounty on the previous question. I'm marking this as a dupe.


text:
What does sympathetic and parasympathetic 'tone' mean?
My professor's lecture notes say that " The basal rate of firing is called “sympathetic tone” and 'parasympathetic tone"  , but a table I found on the internet  says that the parasympthetic system has no tonic activity.
Does saying the ANS has tonic activity mean that it sends impulses continuously and at a low rate to effectors? How is the ANS considered rapid then?
On Euroform Healthcare
It is written that without the sympathetic and parasympathetic tones, we would not be able to regulate the activity of organs or bring it up and down, I don't understand why that's the case ?
I'm very new to this whole topic (ANS) so please go lightly on me.

Thanks for the edit!  We do still need more context... are we talking about tonic activity in cardiac muscle?  Peripheral blood vessels?  Urethral sphincters?  Without seeing more context my guess is that your professor and the articles / pictures you're running across are talking about totally different physiological systems which accounts for the difference.

The thing is, I am so naive when it comes to this topic so I can't be sure but, my professor's notes seem to give a general idea on the topic but the topic's name in the book is " The Autonomic Nervous System and the Adrenal Medulla" If that helps. Regarding the table and the website, no specifications are made ,  I just want understand the general concept

Short answer
Parasympathetic tone is not necessarily mediated by tonic firing.
Background
Nice question! I think part of the confusion stems from terminology. Let's start with some definitions first.

'Tone' in sympathetic tone can be translated as mean activity level (Hayano & Yuda, 2019).
'Tonic' firing by neurons may be translated as a sustained response, which activates during the course of the stimulus (Wang et al., 2014), although some neurons have intrinsic tonic activity as well, like thalamocortical neurons. This opposes to phasic firing neurons.
'Phasic firing' refers to a transient response with one or few action potentials at the onset of stimulus followed by accommodation (Wang et al., 2014).

In your post you seem to assume that parasympathetic tone equals tonic firing activity. I'm not so sure about this. For example, I found a catching paper on the parasympathetic regulation of lung function in guinea pigs (which lacks sympathetic innervation altogether). The paper nicely illustrates (Fig. 1) that parasympathetic regulation of the bronchi in guinea pigs is mediated by both tonic and phasic (burst) stimulation (Myers, 2000):

[P]hasic neurons in guinea pig bronchial parasympathetic ganglia
  respond to a prolonged suprathreshold stimulation with a
  high‐frequency burst of action potentials ..., whereas tonic neurons are nonaccommodating and will respond with relatively lower
  frequency action potentials...

Fig. 1. Phasic and tonic neurons in guinea pig bronchial parasympathetic ganglia. source: (Myers, 2000)
References
- Hayano & Yuda, J Physiol Anthropol (2019); 38(3) (2019)
- Myers, JCN (2000); 419(417): 439-50
- Wang et al., Channels (2014); 8(4): 298–307

Missed this Q&A when it was posted. I'm not as familiar with peripheral nervous system stuff so I'm not sure what to answer for OP but definitely agree that "tonic" has separate meanings. The tonic/phasic firing mode of certain CNS neurons is pretty specialized and completely unrelated to, for example, muscle tone. I would assume (para)sympathetic tone is referring to something more akin to muscle tone which I wouldn't necessarily characterize as "mean activity level" but rather "activity level when we (experimenters) don't perturb it".

@BryanKrause Agreed! That's a nice way of putting it. Did you downvote btw? Should I adjust my text anywhere? I though this was a quite OK answer imho.

Nope I added an upvote around the time I commented (and just double checked I didn't misclick :-D ). Not sure where the downvote came from, alas, it seems misplaced.

@BryanKrause - thanks for explaining. That helps!


text:
Transplant rejection through direct allogenic antigen detection: where do the T cells come from?
I just read a chapter in Janeway's Immunology on T cell development and thought about transplant rejection. But I couldn't figure out how the t cells develop which lead to the rejection.
So in direct allogenic antigen detection antigen-presenting cells from the donor present peptides on MHCI. The T cells from the receipient then detect directly that the MHC itself is foreign. The MHC here is not digested first.
Based on what I learned about T cell development I don't understand how these t cells develop which can detect foreign MHC directly. In t cell development there is positive and negative selection. T cells which present antigens on self-MHC are selected positively and t cells which interact too strongly with self-antigen die off.
But this suggests only t cells develop which can only interact with self-MHC but not with foreign MHC. So where do these t cells come from?

Janeway's does not seem to explicitely answer your question:
A. "T cells that cannot recognize the body's own MHC molecules  (...) this process of positive selection  (...)"
B. "Lymphocytes whose receptors bind strongly to self antigens, on the other hand, receive signals that lead to their death; this is termed negative selection."
Your question refers to T cells that recognize foreign MHC.  In fact,  Janeway's does not seem to cover that situation relevant for transplantation of "allografts".
This suggests that general principles do apply:
A. Lymphocytes that do not recognize self MHC may still recognize foreign MHC.
Janeway's quote "T cells that cannot recognize the body's own MHC molecules"  - does not exclude that there are T cells reacting to foreign MHC. They would not enter the process of selection and would not be "sorted out". Your question, literally, "where do they come from" thus seems a rhetoric way to wonder a. how their existence can be taken for granted (in literature) and/or b. how it can possibly be that they have not been sorted out and died of neglect because of non binding to self MHC.
Two quotes to a. above:
From Trends in Immunology, 2016:
"Alloreactive T cells include those that recognize intact donor MHC molecules on the surface of donor cells – referred to in transplantation as the direct pathway of allorecognition – and of peptides derived from polymorphic regions of the allogeneic MHC molecules or of non-MHC proteins presented by self-MHC molecules, which is known as the indirect pathway."
Marino et al., "Allospecific T cells become activated through interaction of their T cell receptors with intact allogeneic major histocompatibility complex (MHC) molecules on donor cells (direct pathway) and/or donor peptides presented by self-MHC molecules on recipient antigen-presenting cells (APCs) (indirect pathway)".
There is no need of "presentation" on APC cell's MHC in "direct pathway". It seems consistent with the definitions quoted above to assume the existence of  allo-aggressive T cells (derived from regular lymphogenic stem cells) not binding to self MHC, thus not entering any process of "death by neglect". Put more bluntly: no fostering needed for those to remain.
Random google found this:
J J Ryan et al.(Recognition and response to alloantigens in vivo. I. Negative and positive selection ...):
"This finding may implicate other sites such as the liver where unprimed host alloreactive clones are trapped."
In that passage, if you read "unprimed" as "never got acquaninted with antigen", that quote will appear supporting the view that allo-MHC-binding T cells exist and have not been sorted out, and needed no fostering.
See also Distler et al.  "Alloreactive and leukemia-reactive T cells are preferentially derived from naïve precursors in healthy donors..." Title of paper  seems to respond to your formulation "...where do they come from?"
See also  "Between 0.1% and 10% of naive T cells within an individual are estimated to be reactive with any unique allogeneic MHC haplotype." with further reference, Brehm et al., Rapid quantification of naive alloreactive T cells...
Emphasis in quote to be set  on "naive", which might misleadingly be understood as:  not having undergone positive or negative selection. I refer on my elaboration on distinguishing "selection" and "presentation"(priming) in the very last part of my answer (more learnt then). In any case, those T cells exist and have not died.
The fact that there is "direct pathway" lays proof that, conversely, any "fostering" (survival signal) is not needed for allo-aggressive lymphocytes becoming "activated through interaction of their T cell receptors with intact allogeneic major histocompatibility complex (MHC) molecules", see quote above.
B. Refering to the "indirect pathway" and  "negative selection" (this is even more intricate, to my mind...), the sorting  out of  T-cells  which react to their specific antigen on self MHC seems to eliminate any cell reacting to that same specific antigen presented on foreign MHC by transplant cells. This is a fallacy.
Indeed, there cannot be any presentation of foreign antigen (of transplant cells)  on self APCs if, by negative selection, those specific T cells  have been sorted out. Those T cells do not exist any more.
However, the specifity of the T cell receptor is defined by a duality of signals, by the combination of MHC and antigen. The term "MHC restriction" might be misleading in that context. "Restriction" means that there need to be two signals, not just one or the other. Then,second,  specifity of the T cell receptor has been found being defined by the duality of those two signals. There is only one T-cell receptor, no two
(There is some related question at stackexchange concering "super antigens": certain antigens on certain MHC alleles - however, question of "super antigens" does not refer to the difference between iso- and allo- (transplant) antigen.)
Thus,  T cells that bind to the combination of self MHC plus antigen (possibility to immunize against transplant by presentation on self APC's MHC) may also, at the same time, react to  foreign MHC presenting that same antigen. "MHC restriction" does not rule out "homology" of T cell receptor specifity (for better understanding: antigen, not iso-/allo-MHC "determines")
To sum up, applying general principles,
a. there may be t cells recognizing foreign, not self MHC, which in lack of any binding have not received any "death signal" (cp. quote Janeway's above) and have not been sorted out by positive selection ("direct pathway").
b. negative selection does not eliminate t cells that bind  antigen presented on foreign MHC, which is consistent with duality of signal specifity of T cell receptor thus defined by a combination of MHC and antigen ("indirect pathway").
By the way, you say: "T cells which present antigens on self-MHC are selected positively..."
That should read: "T cells that react to antigens being presented on self-MHC (by APC, not t cells)..."
There is a some other question on stackexchange very much related to yours:
Understanding transplant rejection - how does the cellular, adaptive, response get underway
This question shows that it is not at all trivial to assume the existence of T cells taking foreign MHC as foreign antigen. See  quote at the very end of my answer.
Your question is a valid, my answer very much a personal one,
compare e.g.:
"Alloreactivity, defined as a strong primary T cell response against allelic variants of major histocompatibility complex (MHC) molecules in the species, has been a long-standing puzzle in immunology with some of its details remaining unclear up to now" (Nagy 2012)
Counterintuitively, "positive" selection, more than negative, might be the big exception to some rule that prohibits autoagressive killing of self MHC cells.  Conversely, to  attack cells carrying foreign MHC might be the "general principle" that needs no explanation (Interestingly, T cells are said to - in some cases - be activated by cytokines alone (interferon); interestingly, to find foreign MHC in the blood is no natural situation for human t cells - in that way, transplantation seems to imitate evolution).
Finally, here is some lengthy quote:
"Paradoxically, while T cells that obtain too strong signals from self-pMHC are removed, those T cells that survive and complete their developmental program require a productive, weaker, signal from interaction with self-pMHC to do so. T cells incapable of such signaling die by ‘neglect’ and this requirement for a survival signal from TCR recognition of self-pMHC is known as positive selection. While the experimental evidence for positive selection is overwhelming, just what this process contributes to a useful T cell repertoire has been hard to establish.", Vrisekoop et al. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4152861/
Your question seems to pertain to "death by neglect" of T cells able to respond to foreign MHC (of transplants). "Neglect" might denote nothing more than lack of survival signals; conversely only those lymphocytes able to become cytotoxic, i.e. autoaggressive,  "contribute to a useful T cell repertoire", as any anergic  T cell is no (self-!)cytotoxic killer cell which is the needed function. On the other hand, quote, "T cells that obtain too strong signals from self-pMHC are removed..." speaks in favour of MHC being recognized by lymphocytes basically as some antigen like any other: as there are T cells that attack foreign MHC there do exist - counterpart - T cells that react to self MHC even when there is no presentation of antigen. These cells, in my understanding,  "obtain too strong signals from self-pMHC" and "are removed". Negative selection discards T cells that react to self MHC if there is antigen presentation. This process does not imply the sorting out of T cells reacting to foreign MHC alone.
Cp. answer to another related question here on Stackexchange: "Why do physicians try to match HLA complexes for organ transplant?" (...)
To quote one answer: "In short, if a T cell does not find its corresponding MHC 1 complex on a particular cell, its default behavior will be to attack it." There is no contradiction to this statement assuming that foreign, non self MHC1 is the antigen the allo-aggressive T cell is "specific"; MHC1 is to be considered "antigen" (it is known that peptide parts of foreign MHC are presented on host MHC - "imagine" MHC presented on MHC...).
See comment to quote  by  User inf3rno:
"Regular T-cells (without NK receptor) seem(...) like having the same ability by not compatible MHC1, but I am not sure yet about the mechanism. I think I'll need a (week)  more to read all articles I opened and come to a conclusion about how the immune response works in this case."
Let me add one last quote I came across doing further research:
"...the closer the foreign MHC molecule is related to the T cell's MHC, the higher is the proportion of peptide-specific, alloreactive (“allorestricted”) T cells versus T cells recognizing the foreign MHC molecule without regard to the peptide in the groove. Thus, the peptide repertoire of alloreactive T cells must be influenced by self-MHC molecules during positive or negative thymic selection or peripheral survival, much like the repertoire of the self-restricted T cells. In consequence, allorestricted, peptide-specific T cells (that are of interest for clinical applications) are easier to obtain if T cells and target cells express related MHC molecules.", Obst et al.,  The Role of Peptides in T Cell Alloreactivity Is Determined by Self–Major Histocompatibility Complex Molecules
First, the formulation "T cells express MHC" bears similarity to the  wording of your question "T cells presenting antigen on their MHC" which I denounced as incorrect up above, "by the way..."
Second, I find this quotation consistent with my summing up my answer as follows:
There are a. naive T cells derived from regular stem cells that are solely allo-MHC-reactive and thus have not entered any selection process (they "just survive", direct pathway), there are b. (more intricate, indirect pathway) T cells prone to self MHC having survived selection/tolerization process that not only bind self, but also bind foreign MHC presenting antigen which there has been no tolerization for.
Let me add one quote that speaks against my answer, point A, concerning the existence of allo-aggressive T cells (for illustration's sake: "in peripheral niches")  that have not bound to self MHC and thus have not been sorted out:
"Crossreactivity seems to be an intrinsic property of the TCR required, because a single TCR must possess the ability to interact with both self-MHC during positive selection and at least one combination of foreign antigenic peptide presented by self-MHC. Recognition of allogeneic MHC molecules is an inadvertent consequence of the need for TCR crossreactivity." quoted from:  The structural basis of T-cell allorecognition, A Whitelegg 1, L D Barber, 2004
This refers to any T cell  in need of "survival signals". My answer, point A., argues that during positive selection non- (to modify my answer: too weakly) binding lymphocytes remain non fostered which does not lead to their vanishing (only non tolerant lymphocytes to  receive "death signals").
On the other hand, this quote speaks in favour of point B ("more intricate", see above): T cells that tolerate self antigen might, by "cross-reactiviy",  become cytotoxic when presented same antigen on foreign, non self MHC of allograft.
Your question - there are related ones on Stackexchange - turnes out to be some exiting one. Point A, above, is basis for debate. Here is some empirical study, corroborating my point of view: it is "not natural" for T cells to attack cells of their "own body" (self MHC). The point of "positive" selection, i.e. "nurtering" is, to find auto-aggressive T cells, or even T cells that bind to self MHC. Thus, it becomes natural that T cells that bind - aggressively - to foreign MHC survive non binding self MHC. Positive selection searches for auto-immunity (self MHC cells infected by virus, cancer cells shall be bound to); there is no natural counterpart in the negative.
Here's the quote:
"These findings suggested that the clones recognized determinants on H-2Kb that were independent of peptide.", P A Smith, Brunmarck, Potter, Peptide-independent recognition by alloreactive cytotoxic T lymphocytes (CTL), 1997
This was from 97. More and more as time goes by, from 2017, encore:
"NKT cells—originally defined as cells that co-express key natural killer (NK) cell surface markers and a conserved αβ TCR repertoire—are thymus-derived, innate-like T lymphocytes. The functions of NKT cells are controlled by self and non-self-lipid agonists presented by CD1d molecules.." from: Natural Killer T Cells: An Ecological Evolutionary Developmental Biology Perspective, Amrendra Kumar et al.
Some  reference that speaks against subsets of T cells acting like NK cells would be  Uzhachenko an Shanker (e.g.) say:
"By contrast, NK cells lack antigen-specific receptors but express (...) inhibitory and activating receptors that bind various ligands including MHC and like molecules. A highly calibrated maturation enables NK cells to eliminate target cells with lowered or absent MHC-I or induced MHC-I-related molecules while maintaining their tolerance toward self-MHC
It seems some open question if there is a full spectrum that fills the gap between T cells that undergo positve, negative selection and Natural Killer cells that just do not (but need maturation). As I  understand quote from 1997 above  those T cells may need  presentation of MHC antigen to become alloaggressive. Now, trying to  explain in a fast,  illustrative way: Corresponding to presentation  of foreign MHC peptide on self MHC there should be foreign MHC peptide presented on foreign MHC of the allograft cells to attract the activated Tc cells.  However, presentation of graft MHC as antigen on foreign graft MHC just does not exist,     does not seem to  make sense. Why should the allograft cell present its own MHC on its own MHC? How do host T cells "come on" then?
So the "priming" in that case of "transplants" very much appears as a process of clone expansion. I think it is very surprising to see the "fostering by non neglect" in "positive selection" as a very early priming (not even sure, it's seldom heard I guess to speak of "priming" when dendrite present antigen as APC in lymph nodes) of sought of "rare" - according to my view - potentially self-aggressive self T cells. It's coherent with literature to assume that there are T cells entering "late positive selection" which is nothing else than being presented with foreign MHC peptides - in that case of transplants - by self APCs (or foreign APCs, by the way, no difference).
One more quote to this, from 1991:
"The high determinant hypothesis emphasized the implication of direct contact between the T cell receptor and the MHC molecule; the multiple binary complex hypothesis envisages that alloreactive T cells are specific for self peptide bound by the foreign MHC molecule." From: The molecular basis of allorecognition of major histocompatibility complex molecules by T lymphocytes, G Lombardi 1, R Lechler
It's a possibility that  - according to a basic underlying principle - there are groups of T cells that react cytotoxically to foreign MHC cells without those presenting any peptide - as they bind to foreign, not self, MHC. No sorting out for  "NK T cells" (as NK cells).
To end up I'd like to illustrate: a memo square in "Immunology for dummies", German version, states: for graft rejection to occur  there must be antigen presenting cells  of the host, and this needed no explanation. How could cells presenting on host MHC even contact graft lymphocytes if graft's presenting cell had eliminated any lymphycyte that "does not recognize graft's MHC" in the sense: hence, recognizes any future host's MHC? This is paraphrasing your question and showing why it is a valid one.
To sum up my answer:
In positve selection, there is presentation of antigen; lymphocytes with low affinity to self MHC ("MHC restriction" must not be taken for "restriction to self MHC, it means combined, dual signal) will not be fostered.
In negative selection, there is presentation of self antigen (paralleled: not only antigen, as in positive selection there is not only MHC); lymphcytes with low affinity to self-antigen - are not killed (reverse parallel: in positive selection lymphocytes with low affinity to self-MHC are not killed; this is difficult to find reference, see above).
My hint from a learner's perspective:
Basis is "cross-reactivity" made possible by "MHC restriction" which does not mean restriction to self MHC, but does mean "homology" of dual signals.
When reading about positive selection try to "catch the eye": is there antigen presentation (or "showing self-MHC" and sorting out only, misleading).
When reading about negative selection have an eye on lymphocytes surviving because of their "low affinity" to: antigen (or is there sorting out only of antigen avid lymphocytes, misleading).


text:
Has DNA communication/interaction at a distance been empirically demonstrated?
I recently had a discussion with a statistician in my school about memory. Among other things, he told me that it has been experimentally demonstrated that when one extracts DNA from any organism and then induces a stressful condition on that organism, the same effects on DNA can be observed both in that organism and the DNA sample that was extracted before the stressful condition. From what I could tell it is as if he was suggesting that DNA has some kind of a telepathic property that enables this phenomenon.
Now, I am not a biologist (and neither was he) but I am heavily suspicious of this idea. Also, when I asked him for a specific paper on that, he simply told me that there are many and that it is fairly easy to find them. However, my efforts to find anything on google scholar were fruitless so far.
So I want to know: Is such a thing possible and have there been any experimental studies on that?

Highly unlikely and I dare to say impossible. Maybe he meant that it can be detected after DNA isolation. One way or another, without a proper reference to back it up and given the statistician's background I would quickly forget about it.

When you say "after DNA isolation" do you mean making the isolation after the stressful condition? Because that was what I asked him and he insisted on the isolation being made before the stressful condition.

I would push the person for 1)what modifications of the DNA are being done, 2) what stress.  The problem I think we're going to run into is that no one recently would have had funding to study this due to the absurdity. I know when we take DNA out of NEB 10 beta's it's not true.

yes correct. That is what I mean. DNA has no telepathic properties - if telepathy exists it is associated with living organisms and not with lifeless material such as DNA.

@ChrisStronks while studying psychology, I encountered many claims on parapsychological phenomena but no evidence in support of any. However, unfortunately, I find it difficult to respond to what I find as absurd ideas when it concerns fields where I have insufficient knowledge (such as biology).

I did a search on "dna communicates distances" and "dna and words' AND FOUND a lot of evidence based reports.

Is it possible that your source simply misunderstood what they read? There has been some work on inheritance of epigenetic changes to DNA due to stress. But there is no mysterious telepathy involved, just the transmission of chemically modified DNA from parent to child. It's still a highly speculative subject at this point.

No — typical DNA extraction will not preserve information about the biochemical state of the cell.
During the process of DNA extraction, proteins are removed and DNA from a population of cells gets precipitated. Then you dissolve the DNA. In this process native conformational state cannot be preserved.
However there are techniques (see this post) that can capture long distance molecular interactions of DNA (which reflects a conformational state). To summarize in a line, these techniques "lock" the DNA in its conformation and downstream steps are carefully done so as prevent loss of information.
Stress is just a kind of biochemical response. This technique can be applied to study long range DNA-DNA interactions for different conditions (for e.g. Developmental stages).
Stress can cause RNA in the cell to aggregate; however once you do the extraction you won't be able to know if it was aggregated in the cell before extraction.
An Analogy: Sugar can be anhydrous powder or can be crystalline. But once you dissolve the sugar in water, there is no way to know in what form it existed before dissolution.
Certain processes (epigentic mechanisms) can lead to methylation (sometimes hydroxymethylation) of DNA (at cytosine; Bacteria also have adenine methylation). These modifications can be detected in the extracted DNA by different methods; one of the common techniques employed for this is bisulphite-sequencing.
Final word: all these claims about molecules having telepathic memory is pseudoscience. There is no evidence whatsoever for such proposed phenomena.

Edited. Clear now? I didn't explain too much about the technique because that is a different question.

Looks good to me.


text:
Why extract DNA from certain white blood cells instead of whole blood?
In my lab, human DNA is extracted from whole-blood samples.
I don't actually do the extractions and I am not familiar with the specific protocol but I understand that platelets and red blood cells do not have nuclei and therefore do not have DNA so I presume that isolating the sample's white blood cells is part of the procedure.
I also understand that different types of white blood cells have multi-lobed nuclei but I do not know how that affects the DNA which can be extracted from them.
I've seen a few papers, such as this one: http://www.ncbi.nlm.nih.gov/pubmed/15113441, state that they extracted DNA from specific types of white blood cells; lymphocytes in this case. These papers to not focus on, or even address, immune function.
Why extract DNA from only one type of white blood cell?
Do lymphocytes contain DNA that is more representative of the patient's genome than other types of white blood cells?
Are certain types of white blood cells easier to isolate than others?
Is this just the standard DNA-from-blood extraction procedure or are there multiple options to choose between depending on your research goals?

perhaps to reduce the underlying SNPs variations as much as possible by just looking at one cell type? but I'm not sure and take this with a big pinch of salt

There are several reasons why a lab might choose to get DNA from lymphocytes instead of whole blood. Generating genomic DNA from whole blood is not necessarily the best idea, as all the excess protein (mainly hemoglobin from RBCs) needs to be gotten rid of at some point. By narrowing down your input to just include cells that have DNA, you lessen the amount of protein you need to extract in comparison to the total amount of DNA present.
Lymphocytes include T cells, B cells, and NK cells, and are relatively easy to quickly purify, especially in a lab with the requisite experience and reagents/equipment. They are by no means the only type of white blood cells from which one could purify DNA - peripheral blood mononuclear cells (PBMCs) can also be used, for example. They contain lymphocytes as well as other cell types like monocytes, macrophages, dendritic cells, etc. (In my experience they are even more straightforward to purify from whole blood than just lymphocytes, as it is essentially a single-step protocol with a few washes afterwards.) The end result is the same, though - DNA from lymphs should be the same as DNA from PBMCs, granulocytes, or neutrophils.
Any somatic nucleated cell in the body contains "representative" DNA, as except for in a few specialized cell types like T and B cells that undergo genomic rearrangement to form the T- and B-cell receptors, respectively, all cells from an individual contain the same genomic DNA sequence. Blood is relatively easy to come by from patients and clinical study participants, which is why it is often the source of DNA for studies instead of, say, skin punches or mouth swabs.


text:
Current along an axon
When an action potential is induced on a neuron, the local transmembrane potential jumps from $E_{\mbox{rest}}$, the resting potential of the neuron, to $E_{\mbox{eq}}$, the equilibrium potential of an ion or group of ions in the vicinty. Current thus travels in and out of a part of the neuron's cell membrane as ions are exchanged during an action potential. This effect repeats itself as the neighboring regions of the membrane are depolarized, causing the action potential to propagate along the neuron's axon.
Take $\Delta Q$ to be the total charge exchanged locally during an action potential, $C$ to be the membrane capacitance, and $\Delta t$ to be the duration of the action potential. While we can approximate the local average current through an neuron's membrane by taking $$I = \frac{\Delta Q}{\Delta t} = C\frac{\Delta V}{\Delta t} = C\frac{E_{\mbox{eq}} - E_{\mbox{rest}}}{\Delta t}$$ Is there a way to approximate current traveling along the axon of the neuron? Is there even such a thing?

I might be wrong here, but do you mean to obtain the current in units of amperes or similar? I presume that's going to be difficult as the capacitance (or inversely resistance) will vary from cell to cell due to different densities and will never be accurate enough for  generalization. Thats why perhaps people measure the voltage rather than current?

@RoverEye, yes, current in amperes. Please feel free to make assumptions about average capacitance or inverse resistance. I'm just looking for a very rough way to model this. Thanks!

Well, the thing is you really cant model a neuron, as there are quite a few types of varying sizes and lengths... there is a ppt online which I found, which my be helpful to you? http://www.columbia.edu/cu/biology/courses/w3004/Lecture5.pdf

Can you clarify what you mean by "current along the axon" by describing a possible measurement that would detect the phenomenon?  There isn't really a current travelling down the axon.  The charges that rush in and out aren't being carried down the axon.  They're part of the mechanical system that makes the wave move, but the speed of the wave is not fundamentally related to the amount of charge apart from how the whole thing works; you could do a similar thing with a pressure wave, etc.

As far as I was able to find there exists two models of the action potential by using RC circuits. Do note that there is no flow of electrons per se across a tube, but rather a migration of potential. See this.
The Hodgkins Huxley model :

The Hodgkin–Huxley model, or conductance-based model, is a mathematical model that describes how action potentials in neurons are initiated and propagated. It is a set of nonlinear differential equations that approximates the electrical characteristics of excitable cells such as neurons and cardiac myocytes, and hence it is a continuous time model

http://en.wikipedia.org/wiki/Hodgkin%E2%80%93Huxley_model
The Fitzhugh-Nagumo model:

The FitzHugh–Nagumo model is a simplified version of the Hodgkin–Huxley model which models in a detailed manner activation and deactivation dynamics of a spiking neuron. In the original papers of FitzHugh, this model was called Bonhoeffer–van der Pol oscillator...

http://en.wikipedia.org/wiki/FitzHugh%E2%80%93Nagumo_model
http://en.wikipedia.org/wiki/Quantitative_models_of_the_action_potential
Hodgkin, Allan L., and Andrew F. Huxley. "Currents carried by sodium and potassium ions through the membrane of the giant axon of Loligo." The Journal of physiology 116.4 (1952): 449-472.
Now, I have not dealt with differential equations in quite a while, and hence may not be the best source for explaining the model itself, but I'll try and update the post with what (if anything) I understand.

It would be very helpful if you could explain the terms in the H-H equation in a more physiological context. I am from a non-math background and find it difficult to understand the equation in a bioological perspective

Although it is not a flow of electrons like in an electronic circuit, it is nonetheless current flow which drives action potential propagation. It could be seen as a positive current flow (outward Na+), followed by a negative one (inward K+) going from dendrite to synapse.
In fact, a neuron can be modeled by a a basic electronic circuit with resistors (representing ion channels), capacitors (representing the membrane capacitance) and batteries (representing the various ion charge/concentration gradients that power the action potential), see Fig. 1.

Fig. 1. Model of a neuron. Source: Yale university

Could you please explain the direction of current flow I(Na) and I(K ) in the figure above ?

Of course - Because it is an electronic-circuit model, both Na and K currents flow from + to -, like electrons from a battery.

Usually in a circuit, current flow is from the positive to negative terminal of battery, right ? But here, you have depicted current flow from negative (small bar) to positive (large bar) end ? I may be wrong since I am from a non-phy/math background .

In reality, electrons go from - to +. Often it is still drawn from + to - because it was decided early on (say, in the 1600's) that current goes from + to 1 (electrons and their charge were unknown). Hence, the convention is persistent and + to - is often still in use. I don't like it :)

to - I meant to say, not + to 1 :)