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Does the number of nodes determines the rate at which a neural signal is transmitted?
I know that the the bigger the neuron's diameter is, the faster the neuron signal is transmitted. This makes sense according to the proportionality of resistance to the inverse of area and thus, in physics, there is lower resistance in wires that have bigger diameters (cross-sectional areas). I can imagine that this is the same logic for our neurons as well because they are like wires. I also know that the more myelinated a neuron is, the faster the neuron signal travels too because myelination acts as an insulation that reduces resistance in signal transmission.
But then, my question is: does the number of nodes matter and affect the rate at which a neural signal is transmitted? Can you please help explain why or why not? Let's say for example, that two neurons have same amount of diameter and myelinated sheaths hypothetically, but one of them has more nodes. Does that number of nodes of ranvier make the saltatory conduction faster?

The number of nodes is a trade-off between speed of conduction and reliability. The fastest transmission would be where nodes are spaced at roughly the maximum distance to trigger sufficient depolarization at the next node - however, small changes in ionic concentrations or channel densities could lead to failures, so in practice the nodes are typically a bit closer.
The slowest transmission would be to have no saltatory conduction at all.
(I mean these to be general principles; one could probably design a hypothetical system with very close nodes that is actually worse than having no saltatory conduction, and there is probably a perfect edge case where nodes that are spaced at the maximum distance are slower because of membrane time constants)
The reasons for this are: that travel between nodes is very fast, regeneration at nodes is comparatively slow. However, there is a maximum distance for reliable transmission, so we can't simply have one long stretch containing no nodes in between.
edit: references were requested. This was off the top of my head so I would suggest any introductory neuroscience textbook, Purves is a preferred one of mine, but this will run you significant $ if you are not/have not been a student in a neuroscience course. The Wikipedia articles for https://en.wikipedia.org/wiki/Node_of_Ranvier and also for Saltatory Conduction both look good to me, though they do not address the specific issue in detail. This brief Neuron review is more appropriate to the specific question asked, though I am not sure people without an academic library subscription will have free access: http://www.sciencedirect.com/science/article/pii/S0896627300803232

can you provide some references to your answer? we always appreciate outside literature/references

Saltatory conduction is faster, because between nodes, the action potential skips the intervening distance. There, passive spread of charge takes over, which is much faster than channel-mediated conductance which is restricted by protein gating mechanics as passive currents can travel with speeds approaching the speed of light (through metal wires that is).
The optimal internode distance for speed of action potential transmission is that distance where the depolarization currents just do not die out before reaching the next node through passive charge conduction. A bit further, and the depolarization current of one node doesn't reach the next due to current leakage. A bit shorter and more nodes are necessary per unit of axon length, slowing down saltatory conduction as more (slow) ionic channel conductance will replace passive current spread.
In other words, your notion that more nodes speed up transmission is incorrect. On the contrary, less nodes speed up transmission. The extreme case is no nodes at all, where a continuous channel density lines the axon (an approximately infinite number of nodes). This would boil down to to normal, slow action potential transmission.
Further reading
- Saltatory conduction of nerve impulses
- Why is saltatory conduction faster than continuous conduction?

Your answer is the same as the question you cited http://biology.stackexchange.com/questions/8282/why-is-saltatory-conduction-faster-than-continuous-conduction which has been negated by the answer to it.

@Hans - what do you mean? My answer is redundant; my answer is inferior; the question is a dupe? Answer above does contain additional info.

I am saying your statement is confusing and possibly self-contradictory.You say "on the contrary, less nodes speed up transmission." That is incorrect as is answered by the cited answer. There is an optimal positive, non-unit density of nodes, less or more of it slows the transmission speed. The statement "the extreme case is no nodes at all, where a continuous channel density lines the axon (an approximately infinite number of nodes)" contradicts itself: no nodes at all vs continuous, infinite number (imprecise, do you take the size of a channel into account?).

I say that a continuous array of channels is slower

You are not responding to all my points which point out all the confusion/contradictions in your answer. Are you going to respond to those point by point? As for your last comment "I say that a continuous array of channels is slower", it is again unclear: slower than what?

@Hans - updated


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Why do so many people have group O blood?
Please forgive me in case my question wouldn't make much sense. I was reading about ABO blood groups on Wikipedia, where I learnt that O is a recessive allele, and that it seems the A allele predates the O allele. My question is, therefore, how is it possible that almost half of the human population is group O?
For instance, I would expect (quite naively I reckon), if only alleles A and O existed, that around 75% of the population should be A, and 25% should be O.

You are wondering because O is recessive and A is older?

Exactly. Unless there were an evolutionary advantage to having group O (which I could find no evidence of by searching the web), it would appear logical to me that there should be more people with group A, for both of these reasons.

There are many different variants of O (all loss-of-function) indicating that this mutation has arisen many times in the human population. The prevalence of O is indeed taken as evidence of balancing selection. Various pathogens use the A or B antigens as receptors. The cited paper presents evidence about the phylogeny of the ABO gene in human populations and reports that there is clear evidence of balancing selection.

We propose several hypotheses for the cause of [balancing selection], which most likely involved interactions with multiple pathogens at different geographic regions and timescales.
Calafell et al (2008) Evolutionary dynamics of the human ABO gene. Human Genetics 124: 123-135

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Function of NaCl in yeast shuttle prep of plasmids
What is the role of NaCl in plasmid isolation from yeast cells using plasmid rescue solution? If the basic theory behind the method is alkaline lysis, then we is NaCl used and not NaOH?

High salt concentrations will cause the proteins and lipids to precipitate out, as in salting out. Free Na+ ions may also bind the negatively charged DNA backbone and give the molecules a neutral net charge, allowing them to concentrate as well.

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Did we evolve from monkeys?
Since I was young, I always understood that evolution taught that we descended from monkeys (or apes, not too sure a distinction was ever made). However, someone recently told me that this isn't correct, and that we actually share a common ancestor, but not a direct line of evolution.
Can anyone clarify which approach (if either) is correct?
Assuming the latter is correct, doesn't it raise problems of missing fossils? If we descended from monkeys, there is less of a gap to fill, but if we share a common ancestor, we would need to fill a much bigger gap, right the way back to the point where our family trees diverged.
As I said, I don't know much about this, and find most of the online material too technical to understand. If anyone could explain this in simple terms, I would be very grateful.

The essence of what you say is all true, but some very important details are missing.  Generally the comparison is to chimpanzees, which, as Remi.b points out, we did not descend from.  We do share a common ancestor with chimpanzees which you can call a monkey.  The concept of "missing fossils" or "gaps" is and has always been a red strawman herring.

Well, first of all scientists are not sure that we eloved from monkeys. They arent 100% sure! None knows that.

Nor do we know 100% whether or not we are in The Matrix.

Welcome to Biology.SE.
About your post
It is a very standard question and a common source of misunderstanding from the general public. If you just google do we descend from monkeys you will get tons of hits that will answer your question.
Because this question is introductory and has already received a lot of answers online, there is therefore no point for me to make a long and extensive answer here. I will just state the essentials and let you investigate it further through the multiple online sources that exists.
Note by the way, that if you want to get some introductory knowledge in evolutionary biology, you might want to have a look at a few course on Understanding Evolution by UC Berkley
The actual answer
In short, It makes no sense to say of any species that it descends from any other extant species. Two extant species share a common ancestor though. The Most Recent Common Ancestor (MRCA) is of particular interest. Following this logic, humans do NOT descend from modern days chimpanzee, but humans and chimpanzee have a common ancestor. Their MRCA was another ape, but not an ape that exists today (even though it may look like one).

I believe chimps and our MRCA were apes, not monkeys. Big difference.

That was a language issue. I meant that their MRCA was a primate. Thanks for the comment. I edited my answer.

"It makes no sense to say of any species that it descends from any other extant species."  It does if both are still extant.

@endolith while your claim may hold playing out with the definition of species (see here), it is never considered as such. At a speciation event, the ancestral species stop existing under its name as it evolves into the two descendant lineages. Have a look to any introductory course to evolutionary biology for more information.

@endolith You may also want to have a look at this answer for an intro to phylogenetics

Remi provides a great answer here. One thing I would like to add is an analogy: Humans and Chimps are both modern species (i.e. existing today).  Compare this to you, your brother, and your cousin all of whom are in the same generation.
To ask whether Humans evolved from Chimps is comparable to asking if you are a descendant of your cousin. Neither of you descended from the other, instead, all three people have a common ancestor - in this case, your grandparents (which, in very real terms, are your MRCAs).

Assuming the latter is correct, doesn't it raise problems of missing fossils? If we descended from monkeys, there is less of a gap to fill, but if we share a common ancestor, we would need to fill a much bigger gap, right the way back to the point where our family trees diverged.

The missing fossil thing isn't really much of a problem. Fossils are hard to find - they're often burried and poorly preserved.
And we have found plenty of fossils of early homo and pre-homo hominids.
Have a look at these for example.
Examples of early homo fossils include: Neanderthals, Denisovans, Floresiensis, Heidelbergensis, Erectus, Antecessor, Naledi
Examples of pre-homo fossils include: the various australopithecines (afarensis, africanus, anamensis, bahrelghazali, garhi, sediba), the various paranthropus (robustus, boisei, aethiopicus), the various ardipithecines (ramidus, kadabba)
Not only that, but we have sequenced Neanderthal and Denosovan genomes and found instances where they are more similar to chimps than we are as well as instances where we are more similar to chimps than they are.
It simply isn't true that missing fossils present a problem.


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Help me understand voltage patch clamping
Before I type my question it is important to know that I already tried looking this up on my own and could not find an answer because the answers are all in complicated physics terms and this topic is only half a page in a chapter on Action potential in my 1st year physiology textbook.
My textbook says:

This apparatus is used in the following way: The investigator decides
which voltage to establish inside the nerve fiber. The electronic
portion of the apparatus is then adjusted to the desired voltage,
automatically injecting either positive or negative electricity
through the current electrode at whatever rate is required to hold the
voltage, as measured by the voltage electrode, at the level set by the
operator. When the membrane potential is suddenly increased by this
voltage clamp from −90 millivolts to zero, the voltage-gated sodium
and potassium channels open and sodium and potassium ions begin to
pour through the channels.

1: Does that mean that the change in membrane potential that I did resulted in changes in the conformational states of ion channels which in turn changed the membrane potential that I need to control ?

To counterbalance the effect of these ion movements on the desired
setting of the intracellular voltage, electrical current is injected
automatically through the current electrode of the voltage clamp to
maintain the intracellular voltage at the required steady zero level.

2:Is this all still the step of setting the membrane potential to a certain specific value ?

To achieve this level, the current injected must be equal to but of
opposite polarity to the net current flow through the membrane
channels.

3: I'm not sure I understand this.

Finally, the investigator adjusts the concentrations of the ions to
other than normal levels both inside and outside the nerve fiber and
repeats the study.   When sodium is the only permeant ion in the
solutions inside and outside the squid axon, the voltage clamp
measures current flow only through the sodium channels. When potassium
is the only permeant ion, current flow only through the potassium
channels is measured.

4: do they make sure that the flow is only from sodium channels by setting the membrane potential to the equilibrium potential of other ions or a potential between the equilibrium potential of the other ions (so greater than it) and the equilibrium potential of Na (and also less than it )?

I'll try to answer the sub questions 1-by-1

Does that mean that the change in membrane potential that I did resulted in changes in the conformational states of ion channels which in turn changed the membrane potential that I need to control ?

It's the other way around; your book is right - "When the membrane potential is suddenly increased by this voltage clamp from −90 millivolts to zero, the voltage-gated sodium and potassium channels open and sodium and potassium ions begin to pour through the channels". So the voltage step (depolarization) induced by the apparatus triggers voltage-operated channels to undergo conformational changes, this in turn results in additional current flowing through them. On the other hand, hyperpolarization of the potential from say -40 to -90 causes the neuron to close these channels, blocking current to flow. In other words; the patch clamp apparatus controls the membrane potential, the state of the ion channels has little to do with that, as the apparatus will automatically adjust the current injection.

Is this all still the step of setting the membrane potential to a certain specific value?

Yes.

"To achieve this level, the current injected must be equal to but of opposite polarity to the net current flow through the membrane channels."
I'm not sure I understand this.

To set a certain stable potential across the membrane, the flow of current needs to be stable, otherwise it will fluctuate; Ohm's law tells us U = IxR. The resistance R is set by the channels. Let's consider that R is stable for the moment. In that case, you will set the membrane potential U by tightly controlling the current I. If I fluctuates, i.e., when the apparatus doesn't balance the flow of current through the membrane channels exactly and oppositely, a net current will start flowing and u will change. You don't want that to happen.

do they make sure that the flow is only from sodium channels by setting the membrane potential to the equilibrium potential of other ions or a potential between the equilibrium potential of the other ions (so greater than it) and the equilibrium potential of Na (and also less than it )?

This part has nothing to do with equilibrium potentials. They substitute negative ions simply by ions that are not membrane permeable, and the only positive ion available in the test tube is Na+. In that case, only Na+ can flow and you are sure that it is Na+ that is flowing. At least, this is what I make up of this text.

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Can skin become denser?
I heard that after injury or repeated damage bone becomes denser, can skin become denser as well?

refer this question http://biology.stackexchange.com/questions/8687/is-it-possible-to-condition-the-body-to-reduce-bruising/17904#17904

a large part goes to the type of injury inflicted, eg: sun damage makes it wrinkly and weak while repeated injury could cause the accumulation of dead cells reducing sensitivity.

look up somthing called a callus.

The structure of skin (epidermis) can change with damage, when the skin is broken the body repairs this partly by recruiting cells called fibroblasts. These fibroblasts lay down collagen fibres to repair the skin. These fibres a normal component of skin are not as neatly arranged as the original fibres and may also higher in number leading to 'denser' skin. This is essentially what a scar is. In some cases the above process can go awry forming what is known as keloid scars.
The other thing that can happen with repeated pressure exposure the skin can become callous, this is when there is thickening of the outer layer formed of cells called keratinocytes increase in number due to recurrent damage. These form typically on pressure points such as balls of feet.

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What will happen to a neuron if I suddenly remove the pump but not the leaky Na+ and K+ channels?
K+ is more abundant inside the cell and thus has a propensity to move outwards. It has an equilibrium potential of -80 mV. Na+ is more abundant extracellularly and thus has a propensity to move inwards. It has an equilibrium potential of 58 mV. The resting membrane potential of a cell is about -70 mV. So, K+ moves out (more towards its equilibrium potential) and Na+ moves in (more towards its equilibrium potential). The pumps throw out the Na+ and bring back in K+ thus maintaining their concentration and hence the membrane potential.
Now if I suddenly remove the pump from the cell, what would happen? Will the cell moves towards K+'s equilibrium potential or towards Na+'s equilibrium potential? I know that the answer is that the cell will discharge and have a membrane potential of 0 mv, but I don't understand why.

Both Na+ and K+ will move according to the electrochemical gradient. Given that K+ leaky channels are ever present, the cell is already around its K+ equilibrium. If you introduce leaky Na+ channel and remove the pumps, eventually the cell will be nothing more than a passive membrane and it will adopt the same concentrations of ions as the extracellular space, i.e., Na+ will pour in along its electrochemical gradient, after which K+ (formerly already at equilibrium) will start pouring out alongside its chemical gradient, due to the reduced electrical gradient because of Na+ coming in.

Why will K+'s electrical gradient reduce due to Na+ coming in? And say, if I remove the pump but do not introduce Na+ leaky channels, then what will happen? Will the K+ still pour out?

@BlackDagger -  1) inside less negative 2) more slowly - eventually every battery discharges

Why will it discharge eventually --- I'm asking from a theoretical point of view.

@BlackDagger stochastics; channels are never fully closed. A cell is not a sealed container. Even batteries discharge spontaneously.

No I mean, why will the cell discharge? The K+ will pour out but as soon as it reaches the equilibrium potential of K+, it should stop pouring out and reach a steady state. Why will it further discharge and go to 0 mv.

cause Na+ goes in


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Why do we feel numbness and an electric sensation in our legs after standing for too long?
We have all felt that numbness while standing immobile for a while.It gets difficult to walk.It can also happen if we are just putting some pressure on our legs
Why does this happen?
I'd like to know what specifically happens in the muscular tissue(if that's the origin of this sensation) for us to feel like this

Not all of us have felt that.  Is it in your calves or thighs or both?  Is it any different from the numbness and tingling when a leg or arm "falls asleep" from sitting or lying on it too long?

Its in my calf. Apparently it occurs due to pressing of sciatic nerve but still I'd like to know a tad bit more if you know

This relates more to nerves than muscles. Each nerve has a small artery supplying it with nutrients and oxygen. A good example is the sciatic nerve, which is the largest nerve in the human body and requires a relatively large artery to supply it with blood:
http://article.sciencepublishinggroup.com/html/10.11648.j.ijcda.20150103.14.html
When we sit in a particular way that causes pressure over that nerve, or stand for a long while in a way that stretches the nerve, we effectively reduce or block its blood supply. This may result in temporary loss of signal leading to numbness, weakness or even temporary paralysis. If the pressure on the nerve is prolonged beyond a certain point, there will be irreversible necrosis of the nerve causing permanent nerve damage. An example of this is when a drunk person sleeps on the floor with pressure on the outside of the knee over the "Peroneal Nerve", causing "Peroneal Nerve Palsy" or "Zenker Paralysis".
https://en.wikipedia.org/wiki/Zenker%27s_paralysis
As for the electric sensation we might feel as a result of nerve damage, the answer is more interesting:
The transmission of signal in the nerves requires variable amounts of energy depending on the type of nerve fibre. Nerve fibres are mainly divided into "Myelinated" and "Demyelinated" ones, with further subdivisions. To put it simply, myelinated nerves have a coating of myeline formed by specialist cells called Schwann cells. Myeline allows the nerve fibre to act as a super conductor to transmit signal faster, but needs more energy to do so compared with demyelinated fibres, which are thiner, slower and more energy efficient.
One of the functions of the super-conducting large fibres is to modulate the pain signal. The damage or loss of these fibres results in "neuropathic pain", which is felt as sharp electric shocks or pins and needles along with many other reported descriptions. This is thought to be the result of the small pain fibres working uncontrolled, leading to the perception of pain without an actual painful stimulus. The super conductors "Myelinated Fibres" are much more vulnerable to injury due to reduced oxygen, while the smaller fibres, some of which conduct pain, are more resilient. This is why we might feel neuropathic pain as a result of reduction in signal rather than due to a painful stimulation. A good example is what happens in an auto-immune disease called Guillain-Barre Syndrome, where the immune cells attack and destroy Schwann cells, leading to significant neuropathic pains as a result of the loss of signal in the corresponding nerve:
https://en.wikipedia.org/wiki/Guillain–Barré_syndrome
Another common example is first degree burns, where the pain continues for a few days following a minor burn due to selective damage of the highly sensitive myelinated fibres leaving the non-myelinated ones intact. Pain improves gradually as the Schwann cells regenerate, improving the signal speed.

Next to the fine answer from MattDee, I just wish to add that the 'pins and needles feeling' is called paresthesia.
Paresthesia can be caused by a variety of mechanisms and can be reversible or permanent, the latter usually due to nerve, spinal cord, or brain damage.
While the nerve is squeezed as in your prolonged standing example, so are the arteries that feed blood to the nerve. The nerve can't work for long without a steady supply of oxygen and glucose. This causes a limb to “fall asleep.” When the pressure is relieved is removed, the nerve cells start to be active again, and this is the uncomfortable pins-and-needles sensation, as the nervous system tends to become hyperactive as nerves regain normal function. This irritability is caused by spontaneous neural firing in the affected area (source: University of Rochester Medical Center).


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What is the signal conversion from hair cells to cochlear nerve cells?
If I understood correctly, inner hair cells generates a graded potential (receptor potential), this potential maps the stereocilia deflection. On the other hand, the cochlear nerve cells transmit action potentials to the brain.
The question is how and where the graded potential is converted to action potentials. In particular, as action potential signals are characterized by the interval between triggers, how are the sound properties (power and frequency) mapped into this interval?

Short answer
Sound level is coded in spike rate, frequency is coded by a place-frequency map.
Background
Spiral ganglion cells (SGCs, the secondary sensory neurons making up the auditory nerve) are continuously firing cells in a healthy ear (they fall silent when the hair cells degenerate, leading to deafness). In fact, their base frequency in silence is pretty high. The only thing the hair cell input does is lowering, or elevating the threshold and hence affecting firing rate. During a sine wave stimulus (a pure tone), the stereocilia of the hair cells deflect in one phase, and inflect on the other. One phase hence depolarizes the SGC, the other hyperpolarizes it. This generates a near-perfect representation of the sine wave input at low frequencies. At high frequencies the SGCs may skip a phase or two, but because multiple SGCs are involved, the population code is still stochastically spot on.
Sound level is coded in spike rate, frequency is coded by a place-frequency map (Müller, 1996). The base of the cochlea codes high frequencies, the apex low frequencies. Hence, loudness is coded by every SGC, while frequency determines which SGC is activated. An informative overview of hair cell signalling is provided in Fig. 1.

Fig. 1. Hair cell transduction. source: Pasadena City College
References
- Kandel et al., Principles of Neural Science, 4th ed.
- Müller, Hear Res (1996), 94(1-2): 148-56


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Paper shows 2 hours of high humidity and hot temperatures kills corona virus, does this stop the spread of the virus?
I found this paper (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2863430/) which says these corona virus strains live for months at 4 degrees C, 20% relative humidity. But at 40 degrees C and 80% relative humidity, 90% of it dies in 2 hours.
For example, if people set the furnace to 40 degrees and humidifier to 80% relative humidity for a couple hours each day, does this stop the spread of the virus?

There's a lot of outdoors, in which many people spend a good deal of their time.  2) The virus exists inside people, where the temperature is fairly well regulated.  As soon as the external temperature is decreased, the virus they shed will survive.  3) If 90% is killed, 10% will survive.  The 10% will presumably reproduce, passing along whatever characteristic made them more tolerent of higher temperatures.

Hi Mark, and welcome to Biology SE. Your question is very similar, but not syntactically a duplicate of this question/answer.

Your proposal is still interesting, because based on that, one may speculate if it would be possible to artificially induce a fever to 40°C in a controlled manner such that it would weaken the virus in most of the body.

SE Biology is concerned with the mechanisms of biological processes, and questions are generally answered by people with biological rather than medical or epidemiological expertise. It is possible, therefore, that some questions about coronaviruses relating to the recent 2019-nCoV outbreak may not receive a satisfactory answer. You may therefore wish to consult this list of reputable external sources of such information.

It's probably easier/more efficient to use standard cleaning/disinfection practices on surfaces ... COVID-19 (as far as we know) isn't hanging around in airborne particles.


text:
Sensing weather conditions through bodily reactions (e.g. dry hands, arthritic pains)
Two fairly known examples of the effect of certain weather conditions on the body are dry hands due to decreased air humidity around us (more commonly in the winter, as described here), and flaring of arthritis immediately before or after it rains (as described here and here).
I was wondering if there are more examples of this kind, when what I am specifically looking for are bodily reactions through which one might be able to forecast or know something about the weather (i.e. if you have arthritis, you might be able to know it is going to rain sometime soon according to what you feel in your legs; if your hands are dry and chapped, you know that the air is drier than usual).

There is no scientific evidence for weather pains.

@JM97 Actually there is some scientific evidence, and in fact the OP linked to some studies showing that evidence. However, it is certainly true that there is not scientific consensus and studies I am familiar with show peoples' perceptions to be very exaggerated vs the actual evidence.

It's sad to see these close votes. Arguably this could be a Skeptics. SE question, but it is very interesting as weather related pains are a widely known phenomenon in rheumatic patients.

Thank you all for your interest. I saw people voted to close the question because it is "too broad". Since I didn't emphasize it, some people may have overlooked the fact that I was asking for more examples, i.e. if anyone knows of such examples they could post them as an answer or a comment. Is it really "too broad"? Perhaps this question doesn't have a single definite answer (or an answer at all), but I don't think it is too broad as phrased. As for skepticism, it COULD be an interesting subject for discussion, but that wasn't my original intention.


text:
How to use DRAQ5 and MitoTracker CMXros dyes to stain turtle erythrocytes?
I am working on turtle species and want to use DRAQ5 and MitoTracker CMXRos to stain turtle nucleated erythrocytes. Can anyone suggest me a protocol to carry this stain out? Would the two stains complement each other?

Welcome to Biology. Why use two stains and not one? Could you provide additional info and a link to these staining methods?

Have you tried just using the manufacturer's recommended protocols? The structures bound by DRAQ5 and MitoTracker are pretty conserved across eukaryotes, so these reagents should work in just about any cell type.

I havent tried this yet, I got to know that DRAQ5, a far red fluorescent  stain is most used for flow cytometry analysis. Can any tell me whether it can be used for fluorescent microscopy observation along with Mitotracker red?

If yes suggest me the protocol to start.


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Why can humans feel electricity?
What evolutionary process has provided humans with the ability of feeling electric current? Besides lightning and electric eel, what natural hazards include electricity that poses a threat to humans?

Electrical currents stimulate neurons aspecifically. For example, the BrainPort artificial vision device conveys visual information through electrical stimulation of mechanoreceptors in the tongue. Similarly, cochlear implants and retinal implants convey acoustic and visual information through electrical stimulation of the inner ear and retina, respectively. The list goes on. Bottom line is, none of these organs (tongue, ear or eye) evolved to process electrical stimuli. And in fact, there are no specific current or voltage sensors in man. Electric currents aspecifically stimulate neurons, causing them to fire. When sensory afferents are activated in this way, sensory perceptions are generated.
In case of lightning (electrical shock to the skin) it is mainly pain and heat receptors that mediate the sensation. In the case of the BrainPort, it is the tactile receptors on the tongue that are mainly stimulated (taste perceptions are rare). In case of cochlear implants it is auditory nerve fibers and in retinal implants it is optic nerve fibers that are stimulated. Hence, various, and in fact all, neurons can be stimulated by electric current.
Note that sharks feature Ampullae of Lorenzini. These sensory organs are electroreceptors, which allow sharks to sense the bio-electrical fields of prey under water.

Electricity directly stimulate neurons. You have to understand that neurons basically work via electric currents , which occur due to a difference in membrane charge. So when you give electricity to a neuron, you basically give electrons to the extracellular membrane, which makes it much more negative compared to the intracellular or the stuff that is inside the membrane. This offsets the concentration gradient that kept the careful balance until now, and then neuron fires. Anyway, i hope you got that. Note that you can't directly "feel" electricity, or electrostatic force. That is impossible, nature has not given us the mechanism to do so. What you feel is a direct consequence of electricity interfering with the functioning of your muscles and nerves.

Electricity is essential in order to control and coordinate neurons and skeletal muscles activities. You should imagine a neuron as a very complicated logic port of an electronic circuit, that receives information through its dendrits from other neuronal cells and then integrate this information in its body. If the spatial and temporal summation of inhibiting and stimulating signals is overthreshold, then at level of the first part of the axon, there is the creation of the all-or-null response of the neuronal cell: the action potential. In general, there is the simultaneous activation of the voltage-gated sodium channels that elicit spikes spreading them along the whole axon that is connected to other neuronal dendrits or skeletal muscle cells. These ones, receive and integrate in the same manner the stimuli sent to them. As you can easily imagine, external electric stimuli, like electrostimulators or instrument used by neurologist to analyze neuronal and muscle activities in diagnostic tasks are able to alterate the natural electric potential present across the cell membranes of these excitable cell types and response to this  electric field. Indeed, cells possess and actively keep an electric potential among the two sides of the phospholipidic bilayer of the cell membrane of about -70mV. This one is due to the asimmetric distribution of ionic species (sodium, potassium and chloride mainly) sustained using chemical energy obtained from exogenous sources. Thus, in general, our cells are not able to feel electricity directly but every phenomena, either phisical or chemical, able to alterate the electrical equilibium (homeostasis) of the cell membranes induce a response at inner cellular level leading, for example, to neuronal cell response or skeletal muscle contraction. You can think to the use of defibrilator to treat cardiac arithmias that send to the hearth strong current pulse-wave, that in case of fibrillation or ventricular tachycardia is frequently capable to restore normal cardiac activity and save life. Also pacemaker acts in a similar manner. Some pathologies like ALS, Alzheimer's, Parkinson, Myotonia involve also alteration of this electric mechanism leading to modified capacity of the cells to handle and interpret these electric message. In electrophysiology research, external stimulation of cells by electrodes (see patch clamp technique) is used to test the effect of drugs to treat these pathologic conditions.
Finally, I can say that evolution didn't give us the ability to feel electricity, instead it has been adapted as a cellular-level instrument handled by cells to communicate and integrate (or store in brain) stimuli and information.


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Can females be recreated from male DNA?
A chromosomal male is XY and a chromosomal female is XX. Now imagine if, one day, this world has only males - is it possible to "recreate" a female by using two X chromosomes from two different males?

Do you want to clone yourself with certain benefits?

Short answer
Technologically yes, but practically no, because there would be no surrogate mother available to bring the artificial XX zygote to term.
Background
Theoretically a cell with two male Xs can be generated, given that it is technically possible to shuttle single chromosomes between cells (Paulis, 2011).
However, assuming that in your future world oocytes are available from oocyte banks and sperm from sperm banks just like they are today, then the artificial combination of two Xs from male cells wouldn't be necessary in the first place, as regular IVF could be used.
Note that in both the chromosome transfer and IVF scenario, a female would still be necessary to implant the zygote. Until artificial wombs become available (they are not), it is impossible to generate females without females.
Reference
- Paulis, Methods Mol Biol (2011); 738: 57-67

So, with artificial womb, we can do that? We can recreate female using two X's from men?

@JesusChrist - Given that we can transfer chromosomes between cells, I can see no reason why not.

so there's even possibility to create a female version of me using only my genetic material?

@JesusChrist - theoretically, yes. However, as far as I know it hasn't been done.

@JesusChrist, and it's probably unwise to do so. Any recessive traits on your X chromosome are, by default, winners - you're just shortening up the generational problems experienced by inbreeding. Caveat: I'm not a biologist, but that's the way I understand it to work.

@JesusChrist Your name is just godly for this question.

I would have used induced pluripotent stem cells to generate sperm and eggs. Since these eggs would likely be either X or Y, 25% of all embryos would be YY and probably nonviable. The remaining 75% would probably be ok. Similar research has already been done in mice.

Note that in birds and some other species with the https://en.wikipedia.org/wiki/ZW_sex-determination_system the reverse is the case--males are ZZ and females are ZW.

@Jason I'm not sure how accurate that actually is.  With the other chromosomes, that would be spot on, but with the X/Y ones, you have all sorts of traits (such as male pattern baldness) that are expressed in men more often than women simply because a man only needs the one chromosome bearing the gene for the trait, which means anything that would be fatal would probably have killed the man in the first place. Caveat: I don't know of any disorders on the X that aren't expressed depending on the Y, but that doesn't mean there aren't any, and if there are, you'd be right.

@soong I think jason was trying to say that if male chromosomes were used to make a female, then both X chromosomes would be identical. If the male donor had x-linked recessive diseases, the resulting female would have those too, because both her X chromosomes would carry the defective gene.

Yes I understand that. However, x-linked recessive diseases are, too the best of my knowledge, always expressed when a man's only x chromosome has it. An example of that is male pattern baldness. Women can have it if both x chromosomes have it. So, any disease on x that is recessive, the man would already have because he has only one x.

Note that not only mammals have XY sexual chromosomes and your answer assumes we are talking about mammals. I assume the OP was thinking of mammals as well so it is fine but it might be worth to add a note


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What is the best argument for maximum parsimony method in phylogenetic tree construction?
Beside the fact that maximum parsimony is computationally cheap, what other good arguments are there for it? Is there any model behind this principle? Why would one expect this principle to provide right phylogeny in any situation at all ?

I've programmed a phylogeny tree data parsing program which uses standard tree of life OTT files. I had never heard of maximum parsimony and the topic on Wiki exceedingly complex. They just say it's popular because it's simple. computationally speaking the data in pylogeny tree file can't actually be wrong if the tree does not contain errors unless you skip some nodes, a tree can easily be checked by counting the branches up and down from a species and into their shared nodes, and a check can't present an error. that said I don't know if the OTT even has taxon and information of that kind.

The idea of parsimony is that when constructing phylogenetic trees a simple hypothesis (e.g., four evolutionary changes are necessary to connect two taxa) is more likely to be true than a more complex hypothesis (e.g., 15 evolutionary changes) (source: Berkeley University).
The reason is that for a certain taxon to evolve, there must be a certain number of evolutionary changes. In the end, this happens by more or less stochastic processes (Dingli & Pacheco, 2011) that randomly generate genetic changes (mutations). The characteristics of better fit individuals survive, while those of the least fit are terminated from the gene pool. Hence, every additional change that must be adopted to create a new taxon from another means that the chance that that happens decreases exponentially; it's all a matter of statistics. The less the number of changes needed, the higher the chance that that might have actually happened.
Reference
- Dingli & Pacheco, BMC Biology (2011);9:41

Generally speaking, parsimony consists in not making unnecessary ad hoc hypotheses.
In the case of phylogeny, parsimony can be used at two stages: when inferring the number of character changes for a given topology and then when choosing among topologies.
One does not expect parsimony to provide the right phylogeny in any situation. It is just the most sensible we can do when no further information about evolutionary processes is available. This is why parsimony is a popular choice when it comes to deal with morphological data: models of character evolution are not as easy to devise for morphological data as for molecular data.
In the case of phylogeny based on molecular data such as protein or DNA sequences, models of evolutionary changes exist, which are not based on ad hoc hypotheses, but on reasonably good knowledge gathered from disciplines such as molecular biology, biochemistry, etc.
Under these models, "hidden" multiple character changes are expected along long enough branches. This may lead to differences with respect to the most simple parsimony criterion, when inferring the number of character changes in a topology.
In such a case, simple parsimony may not be the most sensible approach to phylogeny resconstruction.


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Cardiac vs. skeletal muscle contraction
For the heart muscles, it is the extracellular Ca2+ that is necessary for the contraction, but for the skeletal muscles, it is intracellular Ca2+.
One of my answers on a test was the following: "In cardiac muscles, an augmentation of the intracellular Ca2+ concentration is necessary for muscle contraction".
Therefore, I'm confused. For the heart, is it extracellular or intracellular Ca2+ that determines contraction?

Perhaps your confusion will be helped by separating for you 2 processes that occur in both skeletal and cardiac muscle contraction.  The first process is the electrical change (action potential) in the muscle cells membrane that triggers the contraction and the second is the contraction of the muscle cell itself.
The latter process, contraction of the muscle cell, is basically the same for both muscle types.  Simplistically this requires high intracellular Ca in both skeletal and cardiac muscle.  In short, when the intracellular Ca in the cell is high all muscle cells will contract and when it decreases they will relax.
The difference between the cell types is what triggers this increase in intracellular Ca when the cells are stimulated I.e. what causes the increase in intracellular Ca.  In skeletal muscles the action potential moving through structures called t tubules directly causes release of Ca from the sarcoplasmic reticulum.  In cardiac muscle this is different as the action potential here causes Ca to enter the cell from outside and it is this small amount of Ca coming from the extracellular space that triggers release of the far larger amounts of Ca in the cell that are needed for contraction.  This is called Ca Induced Ca Release or CICR.
Schematic pictures are the best way to understand the differences in the processes in the 2 muscle types so try these 2 links (Cardiac (https://courses.lumenlearning.com/boundless-ap/chapter/cardiac-muscle-tissue/) & Skeletal (https://opentextbc.ca/anatomyandphysiology/chapter/10-3-muscle-fiber-contraction-and-relaxation/)
You can also access the Textbook of Medical Physiology by Guyton and Hall online or at a school/university library which will give you more detail.


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Is there a lower temperature limit, below which we cannot sense a difference in temperature?
At work I have to handle samples stored at -20 and -70 degrees Celsius, and they don't feel that different to me.

So you're handling things nearly as cold as dry ice without protection? Sounds like a bad idea.

I touched -70 accidentally, it didn't felt as cold as I had expected.

Are you referring to the difference limens in the -20oC range at normal hand temperature, or when the hand is cooled to such temperatures? One way or another, scientific studies addressing either question have probably not been carried out due to ethical considerations. Very brief touching of cold objects may be ethically OK since the skin is not under-cooled, but such experiments are for the same reason futile because they don't tell you anything.

@AliceD Normal hand temperature.

This article goes into detail about what affects thermal thresholds in human skin.  http://www.scholarpedia.org/article/Thermal_touch

I always hated opening the -80 freezer, because it felt... just incredibly cold! (With protection, but obviously not to my face over the freezer.) You just touched something shortly, probably with a short area of skin contact. With larger area of contact and longer exposure you will feel the difference. Like it is the case for hot things. But as far as reflexes go, you're supposedly already letting go/getting away before you really feel the full cold/heat.


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What makes learning more difficult as we age?
Why is it harder to adapt yourself to different cultures, places, and languages as you age? What makes breaking up with emotional patterns or ideas after years of habit more difficult?
Is there a natural process in which the neuron's synapses are set, while later in life the plasticity of the brain is nearly lost?

I think you need to first provide some evidence that is actually is more difficult.  (Leaving out degenerative disease &c, of course.)  You're perhaps confusing a lack of desire with a lack of ability.  After all, most of us spend much of our lives arranging our circumstances in ways that we enjoy.  Without some strong motivation, why should we want to change?

I don't think age is the major factor.  There is plenty of evidence that physical and mental exercise are both important.  Most people stop being forced to learn after school, and most people don't take the initiative to continue to do so on their own.  Procedural thinking gives way to repetition and reliance on declarative memory; people fall into patterns in their lives that do not require them to continue learning but simply re-inforce what they already know once it is sufficient to get through life with.  Without regular practice, the skill atrophies.

By contrast, plenty of people are engaged in work that does require them to continue learning - sometimes intensely so - for the duration of their careers.  Among those people, my experience is that learning gets easier and faster with age since it builds upon mental tools, information, and experiences that have already been internalized.  In the same way that it's harder to lift weights when you haven't exercised in 20 years, so too is it difficult to suddenly put demands on the brain after leaving it idle for a similar period.

The answer(s) to this question can fill libraries. But I can give a few pointers here, as the question is relevant and timely, giving the tendency to an ever increasing life expectancy of the general populace in developed countries (notable exception: US).
I think your question can broadly be answered by the fact that degenerative processes in the brain slowly, but steadily, impairs all of its functions. Possible reasons for the specific decreased capability of the brain to adapt itself to new situations are:

The hippocampus plays a critical role in forming memory representations that are important for flexible cognition and social behavior (Rubin et al., 2014). Decreasing hippocampal neurogenesis during aging may impair the functioning of the hippocampus (Couillard-Despres et al., 2011)
Degenerative processes in the striatum impairs implicit learning that is necessary for mastering new tasks (Rieckmann & Bäckman, 2009);
Deficits in serotonin and dopamine neuromodulation in various brain structures due to degenerative processes during aging results in decreased learning and decision making (Eppinger et al., 2013);
Age-related altered neurosteroid levels may impair cognitive abilities (Vallée et al., 2011).

And the list goes on.
References
- Couillard-Despres et al., Gerontol (2011); 57: 559–64
- Eppinger et al., Ann N Y Acad Sci (2011); 1235: 1–17
- Rieckmann & Bäckman, Neuropsychol Rev (2009); 19(4): 490–503
- Rubin et al., Front Hum Neurosci (2014); 8: 742
- Vallée et al., Brain Res Rev (2001); 37(1–3): 301-312

There is growing evidence that loss of learning capacity is not primarily age related
Below are just a few articles on this topic... I know there's more.
The short answer is, there is growing evidence that the loss of memory and learning capabilities is NOT a foregone conclusion of aging by itself, but is, in fact, a byproduct of other health issues, specifically not controlling blood pressure and not being "heart healthy".  From a layman's view, this is because damage to the small blood vessels in the brain will slowly damage the surrounding nerve tissue.  If this occurs, you end up with all the affects that AliceD points out.
The point is:  Do not assume that loss of learning is "just a fact of aging".
References:

Protect your heart, preserve your mind?
Intensive treatment of blood pressure helps prevent memory decline in older adults
Can blood pressure drugs help reduce dementia risk?

I felt the need to downvote because the cited references do not support the title conclusion of the answer.


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Schematic of neural lineage tree and position of Choroid Plexus cells
I am trying to understand which are the different type of progenitors in the human brain and I am currently following this schematic.
My question is, are Choroid Plexus cells progenitors to Radial Glia (is this paper basically stating that they might work as progenitors)? Otherwise, do they reside out of the provided neural lineage tree? I am aware of their functions related to CSF.
Otherwise, do you have reference papers on neural lineage tree that you can share?


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What does units/mg mean for Streptavidin
I got streptavidin for surface reaction. The label says "biotin binding: 16 units/mg". What does units/mg mean?
Does it mean "1 mg biotin can bind to 16 units SA"?
How much is the unit here?

From which company do you have this product?

@Chris from invitrogen

16 units/mg means 16 units per milligram of protein.
Many companies, including Invitrogen, define 1 unit streptavidin as the amount of streptavidin necessary to bind 1 microgram of biotin.

Thank you for your answer. Then 16 units/mg actually means 1 gram of SA could bind to 16 gram of biotin? How come this happen? The molecular weight of SA is hundred times larger than of biotin, is it possible to have thousands of binding position?

"Milli" means one-thousandth, "micro" one-millionth :)

@leetom The units are not same. The label says 16 units/mg. You must find out how much 1 unit of biotin weigh to make a comparison. For example if one unit of biotin weighs 1/16 milligram then 1 mg SA will bind to 1 mg biotin.

@CRags ChrisStronks,  Ah sorry, I made the mistake ;)

Just to add to Chris Stronk's answer:
1 U SAV can bind 1 ug biotin
This tells you that in a 16 U/mg SAV sample, every mg of SAV will bind 16 ug of biotin. You can figure out the molar ratio from this:
$16\mu g\ BIO\cdot\frac{1mol\ BIO}{244310000ug\ BIO}\cdot\frac{52800000mg\ SAV}{mol\ SAV}$
Which equals:
$\frac{3.46mol\ BIO}{mol\ SAV}$
Theoretically, each SAV tetramer can bind 4 biotins. This tells you that there is some heterogeneity in the sample and that, on average, each SAV tetramer can bind 3.46 biotins.

it does not reflect protein heterogeneity, but sample impurity (some 14%). Probably mostly water or salts. +1 for the clear calculation.

@ChrisStronks Yes it may be true that some amount of the sample is be salt, depending on if a buffer was used prior to lyophilisation. However, reduced binding capacity may certainly be due to protein heterogeneity. One, biotin is essential to all organisms and, during production of SAV, it is expected that some amount will bind to endogenous biotin, using up a binding pocket. This cannot be accounted for in the common binding assays. Two, depending on the method, purification of SAV can require harsh elution conditions which can deform some of the binding pockets.

that's interesting. Thanks for the explanation.

@canadianer Thank you for the explanation! :)


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Cannot conjugate Biotin-labeled DNA to Streptavidin-labeled solid surface
I have been trying to immobilize DNA by the bioconjugation of biotin and streptavidin, but I cannot get this work.
I added EDC and streptavidin to COOH functionalized resin, reacted for 3 hours in room temperature, and then washed with PBS.
Then I tried to anneal biotin-labeled primer and FAM-labeled complementary sequence. (Heated it up to 95 degree then let it cool down to room temperature.
After I added SA-functionalized resin and FAM-Biotin strands together, the conjugation wouldn't work. The resins are not fluorescent after wash.
I also tried to use PCR products which are labeled on both side.
Is there any problem with my assay? How long it takes for the conjugation of biotin and SA at very low concentration?
Thank you for any information.

Are you certain the resin has streptavidin? Can you get some biotinylated fluorescein or other dye just to check the streptavidin? HABA dye might also be helpful to determine if streptavidin is bound.

@user137 Thank you for your advice! I am not sure if resin is successfully functionalized, as I don't have any dye to check for now. Maybe I should purchase one for this. I don't see any reason that SA is not bond, I saw a lot of paper use this method.


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What's it called when a male seahorse gets "inseminated"?
I am looking for the scientific term for the process where a male seahorse receives eggs from the female. For example, we usually say, "the male inseminates the female with sperm." What is the correct term to use for seahorses? Would you say "the female inseminates the male with eggs", or is another term more appropriate?

Short answer
I think that "egg deposition" by means of the female "ovipositor" seems the most commonly used terminology.
Background
A cursory Google search yielded quite a few alternatives, ordered here from the most fancy to the least:

...that are deposited directly into the brood pouch ... (Look et al., 2007)
...transferring their eggs directly into the male brood pouch... (Masonjones & Lewis, 1997)
...the female injects her eggs into the male’s pouch using her penis-like ovipositor
...once all the eggs are inserted

References
- Look et al., J Exp Biol (2007); 210: 432-7
- Masonjones & Lewis, Copeia 1996; (3): 634-40


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Is there any possible way to take a DNA test without using blood in humans?
Is there any possible way to take a DNA test without the need to draw blood in humans? Any information will be useful for me.

Hair follicle, Oral mucosa, Semen...? On theory, every cell contain chromosomes could do the DNA test, but it should depend on when and where you wanna to do the test. Some agencies don't have the ability to do small amount od DNA test, and also preservation of DNA sample is another point.

I think a more interesting question would be 'from what cell type can't we extract DNA for testing'

Yes, we don't have to use blood to extract DNA for testing.
There are many resource we can use include: hair, buccal swabs and urine. And it seems hair can provide good quality of genome DNA.
Here is the paper you may interested: A Simple Method of Genomic DNA Extraction from Human Samples for PCR-RFLP Analysis

Also this section of an article https://en.wikipedia.org/wiki/Genetic_testing#Medical_procedure

Thank you for your answer, and is there possible To use finger print for DNA test?

@Rani Yes as epithelial cells are deposited upon contact with objects/surfaces but it is not trivial due to 1) the very low number of cells and 2) cross-contamination as, for standard protocol, dusting is first needed to see fingerprints (and you don't change the brush usually) and 3) the powder used to see fingerprints may interfere with the DNA extraction. See this paper.

So, DNA test through our fingerprint is little bit difficult right sir?.. may i know is possible to take grouping blood via our fingerprint?. I mean, is it possible to find A+, O- ,.... something like this? Thank you...

Can anyone guide me please...

For a cheap and fast test of blood groups, you need blood. Unless your fingerprint has it's owner's blood, this gets more difficult. In principle, you could extract DNA (caligari2005 already explained that is bothersome) and then check the DNA sequence for the blood group alleles. But if you did extract the DNA from a fingerprint, you would have much better individuation chances with standard forensic tests than looking for a blood group allele.

@jkadlubowska: how would you told using blood, its a fast method for blood groups,.. If we use blood, it will take more time to find the blood group than the using fingerprint right? thanks..

https://en.wikipedia.org/wiki/Blood_residue http://www.nejm.org/doi/pdf/10.1056/NEJM194910062411414

@jkadlubowska: actually i m not a medical student, can you please elaborate in the above link? thanks


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Why is one testicle larger than the other?
Why is one testicle generally larger in humans? Just due to asymmetric development, or is there a hypothesis as to some utility it serves? I read that the different heights may be attributed to attempting to keep them from hitting against one another. Is there a similar guess to the purpose for the difference in sizes?

Welcome to Biology. Could you tell us where you got this information from? It's interesting, though, given that one lung is larger than the other.

@AliceD And if I am not wrong, its true for our feet as well?

I would strongly question whether the underlying claim that testicular asymmetry is generally true. While there is no known clinical significance of testicular asymmetry, most men probably have no noticable difference in testicular size. There have been a number of studies over several decades, and findings have been inconsistent.
Braus (1956) stated that the left testis was heavier and lower; Chang et al. (1960) determined on study of cadavers that the right testis was generally larger than the left.
A 2008 study in 0 to 6-year-old boys found no difference in testicular volume measured ultrasonographically.
Age or level of sexual activity may also play a role; it is known that testes get larger during sexual activity.
The reason for testicular asymmetry is unknown. It has been reported in many different species (see Yu, 1998). The most common explanation provided in humans is that the right testis is more commonly larger than the left due to a difference in vascular anatomy: the left testicular vein empties into the renal vein while the right testicular vein empties into the inferior vena cava. However, anatomy alone would not explain testicular asymmetry in other species as well, so there is no doubt more to this than presently understood.


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What are the key differences in giant and large unilamellar vesicle preparation processes?
I have to study my peptide's folding on membrane mimetic (model membrane) by circular dichroism spectra. Now I'm looking for suitable methods for preparation of vesicles: LUV, SUV, GUV- large, small and giant unilamellar vesicles.
I have studied several methods but I am having a hard time grasping the key factors that affect the resulting vesicle size (LUV, SUV, GUV, etc.)
Any pointers are greatly appreciated.

Giant unilamellar vesicles (GUVs) are made by methods like hydration of phospholipid membrane generally by use of some solvent , use of electric current, combining small vesicles etc.
large unilamellar vesicles (LUVs) are made by methods like evaporation with low concentration of phospholipid, dialysis etc.
Small unilamellar vesicles (SUVs) are made by methods Injecting solution spontaneously, microfludic methods etc. There are many methods reviewed extensively (just search in pubmed you will get lot of them)
Now coming to your question, factor which affect sizes are depends on method you are using. I will list out few, rest you can check in references of each method I gave above. Most of times these methods will have all kinds of vesicles. Success of these methods relies on which method gives you highest proportion of vesicle size you desired.

Microfludic method - total flow rate, ratio of solvent to aqueous phase (Kastner et al 2014)
Electric method - rate of application of electric field (Angelova and Dimitrove 1986)
Hydration method - amount of phospholipid, evaporation rate (Lasic 1988)

Besides all of this, basic physics behind this explained here like energy difference shown below
(Image taken from (Lasic 1988))


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Polymerase Chain Reaction Questions
First question is about why we use primers in PCR. It requires two reasons. I know only one reason though. It is so that DNA polymerase can attach to primer and make a copy of nucleotide from there. But i don't know what is the other reason.
Another question is about why the primer bonds to 3' end of the DNA you want to copy. and explained why. I really have no clue for this one. Plzz help.

"why the primer bonds to 3' end of the DNA you want to copy. and explained why. I really have no clue for this one." How did you get to learning about PCR and not learn that DNA is antiparallel? DNA always has a polarity. Single stranded DNA has a 5' to 3' polarity. So do primers, which are just short ssDNAs.

We use primers in PCR because we are mimicing natural processes. DNA polymerase cannot act without primers. It needs primers to start it's work. Binding of molecules happen by chance, so the more there are of your primer, the more likely it is that it would bind to any given string of complementary DNA. DNA replication occurs in the five prime to three prime direction because phosphate doesn't allow the reverse reaction.

When a new nucleotide is added on to a growing DNA molecule, the reaction takes place on the hydroxyl group at the 3' end. The 5' end is a phosphate group, so it can't add there. It always has to add to the OH at the 3' end, so we say DNA always grows from 5' to 3'. Alcohols are fairly reactive and are intermediates in a number of reactions, if that helps you to remember.

Beside helping Taq to add dntps to the growing strand
Primers minimize the risk of mishybirdization as they are designed specifically for a specific region of DNA


text:
Which of the two chromosomes in a pair is expressed?
I have completely dummy question.
I have 23 pairs of chromosomes in the cells 23 single coming from my mother and 23 single from my father. So how my cell choose which chromosome, mother's or father's to use to synthesize peptides?

Actually, both sets of chromosomes are used to synthesize proteins. This is true for most proteins, ignoring things like imprinting and X-inactivation, which is a bit more advanced to grasp.

I dont find it a dummy question. Article "gene expression" on wikipedia does not provide a solution to this question.

The majority of normal autosomal genes have biallelic expression, i.e. the alleles on both chromosomes are used to make protein. This is why mutations in a gene which cause non-function of the product can be silent if the mutation is heterozygous (only found on one of the alleles), because the effect is masked by the second, fully-functional, copy of the gene. In other cases heterozygous mutations may cause slight phenotypes, because half of the protein produced is non-functional.
A small minority of autosomal genes have monoallelic expression, through a process called imprinting. This is where one of the alleles of the gene is modified by methylation of the DNA, or of histones (the proteins which are used to package and condense DNA). This imprinting switches off the expression of that allele, so that protein is only made from the other allele of the gene. Usually in this case, which allele is switched off depends on which parent it came from.
Things are slightly more complicated in the case of genes on X or Y chromosomes. Men have only a single X chromosome, and a single Y chromosome. This means that any mutation on X or Y which causes a phenotype will always present itself, because there is no second copy to mask it.
In the case of women, who have two X chromosomes and no Y, something similar to imprinting happens, where one of the X chromosomes is chosen to be inactivated. This X-inactivation process occurs very early in development, and the inactive X chromosome is kept that way for the rest of that person's life. In this case, however, the choice of which chromosome is inactivated is not dependent on which parent the chromosome came from, and is entirely random.
Some further reading:
http://www.nature.com/scitable/topicpage/monoallelic-expression-8813275
http://www.nature.com/scitable/topicpage/genetic-imprinting-and-x-inactivation-1066

According to some moderators you need to go into the intricacies of monoallelic expression in detail or else this is an incomplete answer.

@OmarMourad how is it now? thanks for the feedback, this is the first question I've answered on SE

I considered this to be an extremely clear and thorough answer.


text:
How does the flow of ions along voltage-gated channels lead to nerve conduction along axons?
Let's say the axon lies along the x axis, and voltage-gated sodium channels lie parallel to the y axis. When a channel is opened, sodium ions will flow along the y direction into the cellular fluid. My question is, how does this flow of ions in the y direction cause a flow of electric current in an entirely different direction (i.e., the x direction along the axon)?
Both layman and technical explanation would be appreciated.

The flow of current during action potential generation is perpendicular to the axon length. The channels that transmit ions in neurons are often voltage-gated. Voltage-gated Na+ channels (VGSCs) open when the membrane depolarizes. So when excitatory neurotranmitters (e.g., glutamate) open up channels (e.g., AMPA receptors) in the dendritic region, anions (e.g., Na+) flow in. The ensuing membrane depolarization opens up VGSCs in the axon hillock, that subsequently opens VGSCs adjacently in the axon, that opens up VGSCs a little further up in the axon etc etc. Hence, while the flow of Na+ is perpendicular to the axonal membrane, the net effect is a wave of VGSCs opening up along the axon length. With some delay, voltage-gated K+ channels open that allow K+ to flow in, repolarizing the membrane, preparing the neuron for another action potential (fig. 1).

Fig. 1. Action potential mediated by step wise activation of voltage-gated ion channels. Source: Human Medical Physiology
Hence, although neuronal ion fluxes and networks can be modeled by electric currents flowing in electronic circuitry (Fig. 2), nerve conduction is not anything like it. Current flow in electronic circuits is a flow of electrons. In action potentials in neurons it is ions that carry the transported charge.
.
Fig. 2. Hodgkin & Huxley's axon model. The power sources are the electric gradients of Na+, K+ and a leak current source. The conductances are represented by those same ions. The cell membrane is modeled by a capacitor. Source: Bonabi et al. (2014)
Reference
- Bonabi et al., Front Neurosci (2014)

@Christiaan I have got a question with respect to this topic- What causes the adjacent VGSC to open? Is it the flow of Na+ along the x axis that cause conformational change in the adjacent VGSCs and thus they open ? Could we call this motion of Na+ ion, electric current?

@Tytoalba - yes, pretty much


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Are there electron or proton receptors in our nose?
We can easily smell chlorine gas and its irritating odour, but we cannot smell oxygen gas. Do few protons and electrons make such difference to our olfactory receptors?

Chloride (Cl2) carries 34 protons and electrons.
A common example of a relatively heavy odorless gas is CO2, carrying 22 protons and electrons.
All noble gases are odorless. The heaviest, naturally occurring noble gas is Radon, which has a proton count of 86. Ununoctium, an exotic artificial element with atomic number 118, is a noble gas too. However, with a half life of approximately 0.9 ms it's difficult to sniff out whether it's really oderless.
Sulfur hexafluoride is odorless too, with a proton count of 72.
Hence, the atomic number per se is not the determining factor reason for generating the sensation of odor.
What determines whether a compound generates the sensation of odor I am unsure of, but the above compounds mentioned are all chemically inert. Note that Ununoctium decays rapidly, it doesn't react with anything. I have not been able to verify whether inertness always means odorless, but with the above examples I am inclined to believe it holds true. However, the reverse is definitely not true, as carbon monoxide is odorless, but reactive.

Your point is well noted @AliceD .. i am curious about how is the nose able to discriminate these gases... i mean there will be a well marked difference between odorless gases and gases with odor which the nose recognises. Thanks!

Actually this idea that chemically inert substances should not produce odour may seem correct but is not in a strict sense correct. Odour perception as you know happens when the odorant molecule binds to and activates a receptor. Xenon is known to bind to NMDA receptors and cause anaesthesia. It is not strictly an odorant but inert gases my point is that inert gases can initiate/block neural response.

I think we have evolved to develop perception of odours that are indicate  harmful or beneficial substances (wrt CO, I think it is one of the case of why a trait has not evolved). This is my guess that the ubiquitousness of oxygen made its perception unnecessary. Bacteria can, however, sense oxygen and swim towards it (aerotaxis).


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What is the role of gills in terrestrial Crustaceans?
Why do Crustaceans that live on land have maintained their gills? In aquatic species, the gills play a pivotal role in respiration, but terrestrial crustaceans have tracheal lungs. So why do they have gills?

Short answer
Gills in terrestrial crabs serve a role in water storage and ion homeostasis.
Background
Crustaceans are a huge group of species within the phylum of arthropods, including crabs, lobsters, crayfish, shrimp, krill and barnacles. Because of the huge variety of species within the crustaceans, I'll focus this answer on terrestrial crabs.
Air-breathing crabs have universally retained gills, but have also developed accessory breathing organs, usually lungs formed from the inner lining of the gill chamber. Aquatic crabs generally have large gills with very thin closely packed lamellae. Land crabs feature lungs that are well vascularized, have short blood-gas diffusion distances and often have adaptations to increase surface area, all of which greatly increase the diffusing capacity of the respiratory
system (Farreley & Greenaway, 1994).
In contrast, the gills in land crabs  are reduced in size and in surface area. The epithelium is usually modified for ion transport as indicated by the presence of densely packed mitochondria and relatively long blood/gas diffusion distances. Hence, the gills in land crabs are thought to primarily serve an osmoregulatory role, rather than a gas-exchange function (Farreley & Greenaway, 1994). The gills are thought to be involved in salt and water uptake. Their spongy structure is thought to aid in their function as water storage areas in periods of molting (Edney, 1977).  However, the gills in many species are still capable of gas exchange, although less efficiently than the lungs (Farreley & Greenaway, 1994).
References
- Edney, Water Balance in Land Arthropods, Zoophys & Ecology, Springer, New York (1977); 9
- Farreley & Greenaway, J Exp Biol (1994); 187: 113–30


text:
Caterpillar on milkweed not monarch
Southern California, US and less than 1cm
Please help identify this caterpillar.

Are you sure the plant is milkweed?  The flowers do not look correct.

Welcome to Biology.SE! For identification questions please edit your post to: 1) include the location (e.g. country and region — the more specific the better), and 2) an estimate of the size of the creature. The location and size can be essential clues for identification. ——— If possible clear, closeup photos of the open flowers on the host plant would also be helpful. ——— Please also take the time to go through the [tour] and then the help pages starting with [Ask] questions effectively on this site. Thanks!

I have the same caterpillar on yellow milkweed in San Jose CA and can't figure out what it is either! It doesn't look like traditional photos of tussock moth....

The milkweed looks like Asclepias curassavica, or tropical milkweed. In southern California, it won't die back in the winter, which can throw off the Monarch's normal migration and can cause a harmful parasite to build up. Please be sure to cut it back in the fall and throughout the winter, and consider replacing with a native species.

Ok, firstly:
That plant is not any type of milkweed i know, the flowers are too different.
And secondly:
That's not a caterpillar. It's a hoverfly maggot.
Rather than grubbing about inside decaying roadkill or rotten fruit, hoverfly maggots are predators, actively roaming and searching for prey insects, which in this case would be those little yellow aphids on your plant. After a few weeks of devouring aphids, your little friends will turn into small, skinny flies that greatly resemble wasps(This is so predators leave them alone) and feed on nectar and pollen.

Well done, so +1! There’s even its food source on those leaves. However swamp milkweed and some others have narrow leaves and there appears to be a milky sap on a spot in the first picture right atop a vein. Since the flowers aren’t open yet (the sepals are right), it’s still possiblet that it’s a kind of milkweed.

Hover Fly or Flower Fly larvae.  Feeds on aphids which are most prolific on milkweed plants. They can eat small caterpillars, but aphids are primary. Flower flies feed on nectar and are pollinators. Not annoying house fly category.
Yes, that IS milkweed.  Tropical milkweed brought from Mexico originally and therefore not native to the US.  Considered bad for Monarch butterflies.  Now banned from sale in California in 2022.

Welcome to Biology.SE. You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images (make sure these are public domain). Without this your answer is indistinguishable from opinion. ——— Please also take the [tour] and then consult the [help] pages for additional advice on [answer] and [ask] effectively on this site.


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What is the effect of reduced gravity on human height?
There has been talk recently of building a base on either the Moon or Mars. What I'm wondering is, if you are born and grow to adulthood on the Moon, where the gravity is a tenth of the Earth's, would you be taller than if you had been born and grown up on Earth?

This sounds like a question about biology rather than physics.

As far as I am aware, no one has ever been born in space, so your answer cannot be answered directly. However, it is known that the absence of gravity results in an increase in body height by a few centimeters. This is due to stretching of the vertebral column, which is no longer being pressed together by the downward pull of gravity1. For example, the astronaut Richard Hieb, who spent 2 weeks in space, found that his height had increased by 1 inch (~2.5 centimeters)2. Loss of gravity also causes the blood and other fluids to migrate from the legs to the upper part of the body, resulting in swelling of the face and protrusion of the veins of the neck1. I assume that these effects reported at zero gravity at least partially apply to 10% gravity.
Sources
- Airbus Defence & Space
- NASA


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Why are nerves blocked even though potassium channels are not blocked?
One could read "Local anesthetics produce a very slight, virtually insignificant,
decrease in potassium (K+) conductance through
the nerve membrane." At Handbook of Local Anesthesia 7th edition by Stanley Malamed.
If potassium ion diffusion is not blocked, that means that there is still an ionic current which means electricity production and most important, the production of a magnetic field, which I assume is what depolarizes adjacent parts of the membrane, why this potassium ion current is not enough to start an action potential? Do the voltage generated by sodium and potassium ions must be add up in order to trigger an action potential?

In general, action potentials are initiated by an inflow of Na+ that depolarizes the neuron. Only after that, K+ channels open up that re-polarize the membrane potential to get the neuron back in business for a next action potential. In a way, the K+ channels open only at the tail end of the action potential, Na+ leads the potential change (Fig. 1). Here is a link to a credible chapter on the action potential that describes it all in more detail.
Note that K+ channels mediating action potentials are mainly voltage gated, meaning they start opening only when the membrane potential depolarizes. The same goes for the Na+ channels; they need an initial depolarization of the cell membrane due to neurotransmitter release to start opening. It has nothing to do with electromagnetic fields.
Anesthetics work in a variety of ways, so to answer any question on the relation between anesthetics and K+ channel kinetics, more information is necessary, but I think the matter is already cleared up by this answer.

Fig. 1. Channel dynamics during action potential generation. source: Idaho University

Thank you very much! I really appreciate it!

@Quique - no worries. If this is the answer you are looking for, please accept to let others know you found your answer

I don't know much about the effects of anesthetics, but I have taught basic nerve function at university level, so I hope I can help a little with that part.
Potassium flow does not start an action potential - on the contrary, increased potassium flow makes it harder to depolarize the membrane and initiate an action potential.
A brief explanation on membrane potentials and action potentials:
During rest the flow of potassium is much higher than the flow of sodium (and also chloride) and hence the membrane potential is driven towards the Nernst potential for potassium. The resting potential is often somewhere between - 40 to - 80 mV depending on cell type. To initiate an action potential the membrane potential needs to depolarize enough to exceed the threshold for opening voltage-gated sodium channels. The ion flow across the membrane will then be dominated by sodium and the membrane potential then moves towards the Nernst potential for sodium (which is positive, maybe 40-50 mV). These voltage-gated sodium channels will then close shortly after and then stay closed for some refractory period where they can't open, which brings the membrane potential back to the resting potential, because the flow will then again become dominated by potassium flow. There are also voltage-gated potassium channels in the membrane that open with a slight delay compared to the voltage-gated sodium channels. The opening of these potassium channels result in a faster return to the resting potential after the peak of each action potential.
Regarding your question on a small (but insignificant) decrease in potassium conductance:
Decreased potassium flow will bring the membrane potential further away from the Nernst potential for potassium and closer to the Nernst potential for sodium, i.e. causes a slight depolarization, which makes it slightly easier for the membrane potential to exceed the threshold for opening voltage-gated sodium channels and initiate an action potential. If the flow of potassium is completely blocked, the membrane potential would be determined by the relative permeability of chloride and sodium.
The Goldman equation is the key to understanding membrane potentials, and relative permeability changes between the potassium, chloride and sodium ions (and in some cases calcium ions) is what drives an action potential.
Neuroscience by Purves et al is a good resource on all of this.


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Why do blobfish become bloated when they are brought to the surface?
There are several things that can happen to deep sea creatures that are brought up to the surface, but none of them explain why the blobfish becomes deformed. Blobfish don't have swim bladders, so that can't explain it. I'm pretty sure water isn't compressible enough to noticeably expand from the decompression. Wikipedia wasn't able to answer my question.

"Yes they do" referred to the article and the wiki answering the question. The linked post indicated "the bends". The Wikipedia page specifically states: "The popular impression of the blobfish as bulbous and gelatinous is partially an artifact of the decompression damage done to specimens when they are brought to the surface from the extreme depths" - i.e. it's in all the tissues that dissolved gas comes out within the cells and between them (as in the bends).

Blobfish don't have swim bladders, they also don't have a lot of other things we associate with surface animals, like much of a skeleton or many muscles. This is fine under the extreme pressure they live in, the pressure alone provides much of the bodies support, but on the surface tissues that are nice and rigid at depth become soft and droopy.
Also water may not be very compressible but that does not mean they do not subject the tissues containing them to pressure, especially when there a drastic difference in pressure, especially when you consider that that water at depth is almost 20 degrees colder than surface temperatures. Then you also have osmotic effects since the osmotic balance at 1000m down will be different than the surface, their tissue may well take on water as they are raised to the surface.
Finally and most importantly, it is not just water that is compressed, gasses like oxygen and CO2 are also present in their tissues (and in sea water), which can most definitely expand, this is why rapid decompression kills humans so often, dissolved gasses within tissues outgas. The bends are not your lungs over inflating, it is dissolved gasses in your tissue suddenly not being dissolved.
Sources:
Cossins, A. R., & Macdonald, A. G. (1989). The adaptation of biological membranes to temperature and pressure: fish from the deep and cold. Journal of bioenergetics and biomembranes, 21(1), 115-135.

Tokranov, A. M., & Orlov, A. M. (2007). Some biological features of rare and poorly-studied sculpins (Cottidae, Hemitripteridae, Psychrolutidae) in the Pacific waters off the Northern Kuril Islands and Southeastern Kamchatka, Russian Federation. Raffles Bull Zool, 2007, 187-98.

Pflugrath, B. D., Boys, C. A., & Cathers, B. (2018). Predicting hydraulic structure-induced barotrauma in Australian fish species. Marine and Freshwater Research, 69(12), 1954-1961.
Brown, R. S., Walker, R. W., & Stephenson, J. R. (2015). A preliminary assessment of barotrauma injuries and acclimation studies for three fish species (No. PNNL-24720). Pacific Northwest National Lab.(PNNL), Richland, WA (United States).


text:
Animal models to study depression
Is there a non-invasive animal model to study the pathogenesis (i.e., the development of) depression?

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

You might be interested  in Scientists investigating the DNA outside our genes - the ‘dark genome’ - have discovered recently evolved regions that code for proteins associated with schizophrenia and bipolar disorder. (from the University of Cambridge web site)

TL:DR: A simple question doesn't usually have a simple answer in science.
To a great extent, the answer to your question depends on what, exactly, you mean by non-invasive. Please know that it is exceedingly difficult to study the pathogenesis of depression by non-invasive methods.
If by non-invasive, you mean the animal is not killed and the brain examined, then yes, there is a great deal of literature studying depression without sacrificing the animal. Blood tests can examine the presence of specific hormones, etc. and imaging studies can see brain changes associated with depression to localize which areas are affected, etc.
But if you consider blood tests to be invasive (which, technically, they are), that narrows it down greatly.
In studying animals and depression, the researcher must treat the animal in a way which is highly likely to result in depression, or the study will be fruitless. If you define treating the animal with means that would be considered unethical in humans (or outright cruelty) as invasive, that puts most serious research into the illness outside of the scope of reliability. In designing a study, the researcher must ask themselves, "What events might make an animal become depressed?" It can be as minimally cruel as prolonged social isolation, or can be stepped up to discomfort  (e.g. a repeated shock) when performing pleasant tasks (e.g. eating something tasty), or repeated restraint of an animal significant enough to cause distress, or stepped up to discomfort when performing life-necessitating tasks (getting to food), etc.
If you accept certain stress-inducing events as non-invasive, the researcher can certainly wait until the animal dies of natural causes to do a post-mortem exam, but that becomes problematic in that the more time passes from the event, the more questionable the findings are as related to the event.
If you allow a non-life threatening but technically invasive procedure as acceptable, e.g. a fecal transplant from depressed humans to gut-microbiota-depleted rats to see if depressed behavior occurs due to the gut microbiome, it is still invasive, depending on the definition.
Depression is defined by a number of parameters. Most animal studies will not meet all the criteria to begin with, but a non-invasive one will most likely be severely deficient in meeting any of the criteria for pathogenesis of depression.
PET scans are non-invasive and can be/are used to study depression, but the pathogenesis may remain unclear. For example, a dog's beloved caretaker dies, and the dog exhibits clear signs of depression (lack of appetite, energy, anhedonia, etc.) A PET scan will correlate with that seen in humans who suffer deep losses. But, short of waiting for a lot of people beloved by their pets to die and seizing their dogs to do PET scans, it doesn't give us much information that we don't already have in humans or can intuit.
The link below is a fairly recent (2021) overview of animal models for studying depression and their limitations (including animal-sized imaging machines). Still, the animal must be stressed into depression, which can be considered invasive/inhumane.
All this to say that a simple question doesn't usually have a simple answer in science.
Benefits of animal models to understand the pathophysiology of depressive disorders


text:
Width of vein in finger
I am working on my bachelors thesis, where one part of it is to find width of vein in fingertip. I use database images and extract vein patterns from it, but i have to calculate the width of vein and I have no comparison of how many pixels in pic refers to how many milimeters in real.
I would like to ask how wide is the vein approximately in fingertip or in finger.
Thanks a lot, it would be really helpful.

Here is an image. My best guess is its in the order of 1-3mm.  The challenge you face is, absent any other features that provide scale, you don't know the  size of each hand in those stock images.  So you have two (too many) variables..(i) hand/finger size and (ii) vein width as a proportion of finger size.  I don't see how it can be done.  Imho, safest would be to image your classmates hands, beside a scale, and choose illumination that shows veins.

"Database images".  Provided these were acquired systematically in a lab using fixed imaging conditions (eg camera distance) then you can stick with pixels as your size unit for computation.  If you have access to the imaging setup, go ahead and image a scale.  I'd also just make a plot of your complete dataset for finger length and width and look for a 'biological' -type distribution without skew or  bumps. And the image files themselves may have camera meta-data such as aperture and exposure, also useful for quality assurance.  But images without scale, not ideal, for sure...

Thank you for your answer @PlaysDice.Unfortunately, I dont have access to image setup or the sensor, I used the database I found on the internet.Neither I have device capable of providing images link.I tried to build one, but didnt have proper LEDs(couldnt shine through the finger with my LEDs).
My results are between 1.2mm to 1.8mm and i used my finger as ethalon taken as normal image from approx. same heigh as in databse. Its not as good as it could be, but didnt come up with anything better.
Thx for post

Venous anatomy is highly variable from the start, there will also be changes with age and activity - I think this will b to calculate


text:
is there a way to do batch download for all gene pathways?
I would like to download all the gene pathways and genes of each pathway. Preferably, gene length of each gene as well. It would be a lot more convenient if there is an R package.

in what format do you want the pathways? You can bulk download the SBML files. Also, please clarify what you mean by "download the genes of each pathway".

What pathways? From which database? What species?

Try using KEGG REST.
http://rest.kegg.jp/link/pathway/hsa ## list of all genes and pathways in Humans

Do you mind showing me how you got this file?

You can find it in the rest page.

If you're working with BioCyc pathways you can use their REST-API for batch-downloading all genes for their pathways. You can run a wide range of queries including BioVelo-queries for all genes/compounds in a specified pathway, all pathways in organism etc. A query for all the pathways in B. subtilis would look like:
http://biocyc.org/xmlquery?[x:x%3C-bsub^^pathways]
Where you get an XML with the Cyc-IDs for the pathways which can be used to search for the genes. A query for all genes in the Arginine synthesis pathway in B. subtilis would then look like:
http://biocyc.org/xmlquery?[x:y:=bsub~argsyn-pwy,x%3C-%28genes-of-pathway%20y%29]&detail=full
Which returns an XML with information regarding the genes, start and end positions including (i.e. gene length). Since I don't work very much in R I don't know if there exists an R-package. But it is very straightforward to write Python scripts for downloading and XML-parsing.