text:
What dangers would the wireless transmission of power through microwaves pose to living organisms?
If we were one day able to harness the power of "wireless electricity", and INTEGRATE it into society, what disadvantages and/or dangers to living organisms would become relevant at that point? To my understanding, the power would be transmitted through microwaves, which may or may not be correct.
The example I will use in regards to "wireless electricity", would be... The transmission of power from one source to another without the need for power cords, or power lines.
One such instance, according to "http://phys.org/news/2015-03-japan-space-scientists-wireless-energy.html", states "The idea, said the JAXA spokesman, would be for microwave-transmitting solar satellites—which would have sunlight-gathering panels and antennae—to be set up about 36,000 kilometres (22,300 miles) from the earth."

Perhaps my question should be reformulated to, what are the immediate and long term effects, if any, of microwaves on living organisms? Although I'm sure this has already been asked. Even more specifically, If some day in the future, this wireless power transfer was integrated and power lines/ electrical cords became obsolete and these microwaves were abundant, could it cause damage to living things?

Whether wireless power transfer is safe depends on the type of power transfer. Inductive coupling is generally safe, but only works across small distances (i.e., millimeters to centimeters). The other option is far-field or radiative technology, where either visible light (from lasers) or microwaves are used. The latter has not been applied much, some uses have been found in space technology. Their safety in general will depend mainly on the power being transmitted. For example, a laser can be destructive if it is powerful enough.
I will focus on inductive coupling, because it is not only safe, it is commonplace. The prime example being cochlear implants. Cochlear implants are basically electrode arrays implanted in the inner ear to directly electrically stimulate the auditory nerve in deaf people where the hair cells have degenerated (or were never there). The implant is powered by an external battery worn behind the ear. It is coupled to a head-worn external coil that wirelessly transfers the power needed to drive the implant to an internal, surgically implanted coil. I'm not entirely sure about the exact numbers, but more than 100,000 folks around the globe have received one or two cochlear implants.

Cochlear implant showing the external and internal coil to transcranially transmit power to the implant.Source: Extreme Technology
Very similar technology is used in retinal implants. Retinal implants electrically stimulate the degenerate retina to [partly] restore vision in the blind. For example, the Argus II deploys an external coil mounted on a pair of glasses that wirelessly couples to a surgically implanted coil in the eye to power the implant. Being newer technology, there are not more than two hundred or so people implanted worldwide as we speak, but this number will definitely sore in the near future, all, or at least many relying on wireless power transfer.

Schematic of the Argus II retinal prosthesis showing the wireless link. Source: Ars Technica.
These examples may not be exhaustive. For example, transcranial magnetic stimulation of the brain is another example of wireless energy transfer across the skull, making use of magnetic induction to stimulate the cortex. However, these examples do show that medical bionics is already making use of wireless power transmission technology.

Very intriguing perspective! I never would have considered this. Thanks!

@marcbally - Thanks :-) It's not exactly what you're after, but it's just my 2-cents worth. I'm not familiar with microwave technology. Perhaps others are.

Yes, I posted this in physics first. They immediately shot me down saying it was an environmental or politics question. It's very abstract and hypothetical so I'm open to all kinds of input

@marcbally - yes it is certainly a question prone to close votes. I just happen to be in bionics and it's very relevant stuff from an engineering point of view.


text:
Do all different types of neurons serve different roles?
I know from my basic education in neurology that the brain has various sorts of neurons. These are usually bunched into 3 different categories (sensory, moto and interneurons).
I read in a recently published book, and papers on modern neuroscience that there have been thousands of different types of neurons identified in the brain. Does this mean that there are different types neurons each dedicated to a very specific task in the brain? If that is true, then what is each individual neuron's job (a few examples would be sufficient)?

Short answer
Neurons were (and still are) often identified based on their histological features (e.g., by Cajal). In turn, the structural hallmarks of neurons are often related to their specific functions.
Background
The question is broad and difficult to answer without restricting to some example types of neurons. As you say, about 10,000 types of neurons have been identified. Their roles are often obscure. I will restrict the answer below to a few examples of neurons with relatively well characterized histological features and relatively established functionality.

Fig. 1. Examples of neuronal cell types. A. Purkinje cell B. Granule cell C. Motor neuron D. Tripolar neuron E. Pyramidal neuron F. Chandelier cell G. Spindle neuron H. Stellate cell.source: Ferris (2012)
The Purkinje cell (Fig. 1A) receives large amounts of input in the cerebellum, integrates it and sends it away to deeper layers. Hence, as an integrator, it has an elaborate input side (large dendritic tree) and a single output axon. The basic  function is similar to the pyramidal cell in the cerebrum (Fig. 1E) and their appearance is hence similar.
On the other end of the spectrum is the spindle neuron (Von Economo neuron, Fig. 1G), which is believed to receive simple input and generate simple output and is built for speed. Less integration allows for faster responses. Hence, its dendritic tree is much less elaborated than the Purkinje cell (cf. fig. 1A) (Allman et al., 2011).
As a last example: the Chandelier cell (Fig. 1F); these neurons have axons that form elaborate collaterals that are believed to form local inhibitory connections in the cortex to keep (excessive) stimulation in check; hence their output is more elaborate, with relatively simple input. Dysfunction is believed to be associated to epilepsy (excessive stimulation) (Inan & Anderson, 2014).
References
- Allman et al., Ann N Y Acad Sci (2012), 1225: 59–71
- Inan & Anderson, Cur Opinion Neurobiol (2014), 26: 142–48
- Purves D et al. (eds.) Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates (2001)
Source
- Ferris, 2012, Sci Am blog

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text:
How is the flicker fusion rate interpreted as an on-off rate?
In our experiment we use a fly to determine the flicker fusion frequency, i.e., that frequency where the fly starts perceiving a pulsating light as a constant light source. The human eye also has a flicker fusion frequency. For example, most people cannot see the flickering of a fluorescent tube, which equals the main frequency (60 Hz in Europe & USA).
Our experimental light source needs two input durations, namely how long the light is ON and how long it is OFF for. The input is provided in ms. From what I found out so far is that the unit Hz equals the frame rate, namely pictures per second. So a frame rate of 50 Hz is 50 pictures during 1 second.
But in my experiment it is about flashes of light, namely a light phase and a dark phase. Does the dark phase then count as a picture? So what I mean is whether 50 Hz represents 50 times lights ON + 50 lights OFF, or does it mean 25 times lights ON and 25 OFF?
Also, how long is then each light pulse?
My assumption is:
50 Hz are 25 lights on and 25 lights off within 1 second.
50 pictures in 1000 ms
1 picture per 20 ms
20 ms / 2 = 10 ms lights ON, 10 ms lights OFF

Besides the fly, I don't think the main question has anything to do with biology. I'm voting to close as off topic

@theforestecologist - I think questions like this are not Bio per se, but frequencies and cycle times are so fundamentally important in the visual and acoustical sciences that I strongly argue to keep this post alive. Biologists often don't receive training in signal processing, although it's an essential part of some pretty big disciplines. I have attempted to make the question biologically more interesting too, adding the key term 'flicker fusion' in there + a link

@AliceD I agree that they are important, and I can see why the OP asked this question here. However, unless the OP edits in a way to make the question more biologically relevant, I think it's off topic. This is more for their sake b/c they could likely get good answers if asked elsewhere. However, I just saw that you provided a perfectly viable and useful answer (+1), so that seems moot at this point :p. But even your answer does not mention anything biological. This whole Q&A would still probably be more appropriate on Physics.SE in my opinion.

If questions about chromatography get closed, I can't imagine how this one would be on-topic.

@canadianer I think everyone here is biased toward their own interests. The question here is so fundamentally linked to my areas of research I find it on topic. Others outside this field think differently. That's OK.

@AliceD I disagree, it's not okay. If this or any other question is about biology then it shouldn't be closed because some people don't realize the connection. I'm not sure what can be done about this, though.

@canadianer - it's not that black and white I'm afraid. I've added substantial biological context in the question when 2 votes were in, and despite these efforts  it still got closed.

@AliceD That suggests to me that we have a problem with the way we close questions. I would re-iterate my point that if a question is about biology it should be on-topic on this site.

Also, mains frequency in North America is 60 Hz.

Short answer
A light flashing at 50 Hz means there are 50 flashes of light per second. The unit hertz means cycles per second. 1 cycle is the time it takes for the light to be ON and OFF. 50 Hz cycle time means a cycle time of 20 ms. If light ON and OFF times are equal, then the ON and OFF times are both 10 ms each.
Background
The unit hertz (Hz) is a frequency unit in the International System of Units (SI) and is defined as

one cycle per second

A textbook example where the unit Hz finds its use is a sine wave (Fig. 1). 1 cycle per second would be 1 Hz. A cycle, as can be seen in the figure, is a complete wave consisting of a positive phase followed by a negative phase.
In the right panel of figure 1, a square wave is shown. Again, a cycle time is the time it takes for one complete square wave to develop, i.e. a positive phase and a negative one.

Fig. 1. Sine wave (left) and square wave (right) sources: Simon Fraser University, Integrated Publishing
Now, in your example, you can depict the lights ON as the positive block in the square wave in Fig. 1 above, and the lights OFF as the negative phase. Together (light ON + OFF phases) they form one cycle. So a light pulsing at 50 Hz means it flashes ON and OFF 50 times.
The cycle time then is 1 second/50 = 20 ms. If we assume that the ON and OFF times are equal, which they obviously do not have to be, then light ON is 10 ms, lights OFF is 10 ms.
On the wikipedia page on the hertz unit, a flashing light example is actually illustrated and explained.

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What happens when the congenitally blind brain receives visual input?
If a congenital blind person gets eye sight (either hypothetically, or in the near future due to advancements in technology), will their brain be able to handle that information, or will it become overloaded?

Short answer
Congenitally blind people can regain visual function at a later age.  However, the longer they were blind for, the lesser their visual function will be and the longer it takes for them to rehabilitate. Immediately after receiving first eye sight, the visual experience of congenitally blind people is not comparable to that of normally sighted people. They may need months of rehabilitation training to make sense of their newly acquired sight, especially when they were blind for many years.
Background
There are various treatments for blindness to date. Since you mention technology in the question, visual prosthetics come to mind. Visual prosthetics already exist, and there are at the time of this writing two retinal implant systems commercially available; the Argus II and the alpha-IMS (Stronks et al., 2014). Retinal implants are used to provide a crude form of vision to those with severe retinal degenerations, such as end-stage retinitis pigmentosa. However, visual prosthesis technology is still in its infancy and at the time of this writing, only people that lost their vision later in life are implanted. So there is as yet no data available on your question whether congenitally blinded people can benefit from it.
However, from a related technology, cochlear prostheses, we know that the earlier a congenitally deaf person is implanted, the better the result is. Early-implanted folks can learn to understand speech, and develop speech relatively normally. Nowadays infants as young as 3 months receive cochlear implants. Early implantation is critical, because the brain is plastic. When the auditory cortex is not used due to sensory deprivation, it will quickly be taken over by other cortical areas. Once this cortical recruitment progresses for too long, a person can never gain functional hearing at the level reached by early-implanted people (Teoh et al., 2012).
Very likely the same holds for visual prosthetics. A congenitally blind person should be implanted as soon as possible after birth. This, because it is known that cross-modal plasticity results in the visual cortex being recruited for tactile and auditory processing. As with the auditory system, once this restructuring progresses long enough, my educated guess is that a person will never be able to develop functional vision comparable to an early implanted subject. And this is the reason why at present, only the acquired blind receive retinal implants.
For example, a case report of a subject who was blind for over 50 years regained his eye sight after corneal surgery. Although the subject did develop visual function after the surgery, visual performance remained greatly compromised. This was particularly evident when the tasks targeted finer levels of perceptual processing Siki et al., 2013).
Important clues are being obtained in the "Project Prakash", an ambitious project to provide opthalmological support to the people in poor, rural parts of India. Routine cataract surgeries have been performed in people with cataracts, including in people with congenitally present cataracts, where the lenses in the eyes were opaque from birth. Older kids, like teenagers, that were blind from birth typically show non-functional vision after the bandages are removed after surgery. It is thought that these first moments for the newly sighted are blurry, incoherent, and saturated by brightness, akin to swirls of colors that do not make sense as shapes or faces or any kind of object. However, after months of rehabilitation, they do develop functional vision. The lower-level markers of visual function never reach normal values. Specifically, they continue to suffer from poor visual acuity - the gold standard to assess visual function. Nonetheless, some higher-order aspects of vision do seem to be improving. Within a week to a few months after surgery, the children can match felt objects to their visual counterparts (source: The New Yorker, August 28, 2014).
References
- Siki et al., Iperception (2013); 4(8): 498–507.
- Stronks et al., Expert Rev Med Devices (2014); 11(1):23-30
- Teoh et al., Laryngoscope (2004); 114(9): 1536–40


text:
What is the difference between the cellular affix -cyte and -blast?
The affix -blast means an immature cell, and -cyte indicates any cell. So how do we define if a cell is mature (-cyte) or immature (-blast)? How does this apply to odontoblasts and ameloblasts? Why are they not simply called odontocytes and amelocytes, respectively?
What are the criteria for using the affix -cyte versus -blast?

Because they have different meanings? Wikipedia says, -cyte means "vessel, jar" while -blast means "germ, sprout". Those are quite different things. The -blasts usually have some function in being precursors or "generators" of something else, while the -cytes are often the result of such precursors.

@skymningen.   So odontoblasts are precursor for which cells?

@JM97 Odontocytes: http://amigo.geneontology.org/amigo/term/CL:0000140

I'm actually not convinced odontocytes even formally exist. I think this is a great question! +1

Short answer
 - The affix -cyte means cell;
 - The affix -blast means a germ (bud) cell or a cell that produces (building) materials.
Background
Cells are denoted as -cytes. There are many of them, e.g. melanocytes in the skin and chondrocytes in the cartillage.
Germ cells are denoted as -blasts. These cells typically are precursor cells such as the lymphoblasts that are undifferentiated precursor (stem) cells situated in the bone marrow that produce leukocytes.
Blast cells may also be cells that produce materials. Your examples are of that category; odontoblasts generate dentine, the main hard tissue of the tooth; ameloblasts deposit tooth enamel, which is the hard outermost layer of the tooth forming the surface of the crown. in that sense, also progenitor cells produce something, namely new cells. Hence, blast cells are cells with a chief building function, either materials or new cells.
There are also -clast cells - cells that destroy something. Fig. 1 below gives an overview of these cells as present in the bone, namely osteoblasts (bone builders that secrete the matrix), osteocytes (osteocytes are osteoblasts that are embedded in bone; they stop secreting matrix and only maintain it) and osteoclasts (different class of cells that mediate bone resorption).

Different cells in the bone. source: University of British Columbia
Why then do not call odontoblasts odontocytes? - Because it would mean loss of information. It would be the same as calling a car and a bike both transport vehicles. Moreover, the example in Fig.1 is quite convincing, as osteocytes and osteoblasts are considered to be different cells altogether (although the former is derived from the latter).


text:
What is the course of inter auricular line?
BACKGROUND: The interauricular line is the line connecting two auricles.

I wish to know the exact route through which this line passes. I want to be sure whether it passes through the parietal prominences, or in front of them.

Could anyone create a tag for cephalometry?

@JM97 Please do not create new tags for every single possibility. This tag is relatively pointless at the moment and will most likely be orphaned.

Do you mean the interaural line? If so it is ventral, rather than in front, of most of the parietal bones. This seems like a really odd question - you are using fairly outdated/underused terminology, and the answer is pretty clear if you know what landmarks you are talking about it and just have a look at a skull.

No I didn't mean interaural line. The terminology is used in my textbook but it doesn't say anymore about its course, so I wondered what could it be.

Please state the source of your background in the question. That way people trying to answer your question can [possibly] look up your information.

I found very little use of the term interauricular line in a web search (only about 800 results in Google), and those that gave some sort of definition suggest that it is indeed the same thing as the interaural line. The auricles in this case are a sort of outdated term for the external ears. The interaural line isn't a real thing, it is just a reference point that refers to an imaginary line between the openings of the ear canal. The interauricular line is the same thing but is poorly named, because it is still referring to a line between ear canals, not really the auricles themselves.

Up front - I have never heard of this term and I could not find information on the interauricular line. The only thing I was able to dig up was the term auricular line, which is (Fig. 1):

[The] [l]ine pass[ing] perpendicular to the anthropological baseline,
  through the cent[er] of the external auditory meatus.

Fig. 1. Auricular line. source: Radiology Key
The anthropological line being (Fig. 2):

[The] [l]ine join[ing] the infraorbital margin to the superior border
  of the external auditory meatus.

Fig. 2. Anthropological line. source: Radiology Key


text:
Are Protocadherin Gamma Cluster transcripts considered separate genes?
The PDCH@ cluster of genes share exons and are therefore isoforms of each other.  However, they are considered separate genes, by both HUGO and Ensembl.
A "gene" is defined as "a locus of co-transcribed exons" (Venter 2001), and this locus clearly fits that definition with no ambiguity. So why are these transcripts considered separate genes?

What is your question exactly?

The question is, why are these transcripts considered separate genes?

Thanks, I slightly modified the question to improve clarity. Feel free to roll back. You may want to add a link to Venter, 2001 too. And transcripts are not genes.

Related: http://biology.stackexchange.com/questions/31766/can-intron-become-exon-in-alternative-splicing/

I would say they are considered different genes because each isoform is under the control of its own promoter.

Having multiple promoters doesn't mean isoforms are different genes.  E.g., http://www.pnas.org/content/97/5/2291.full


text:
Can stress-induced cortisol reduce diabetes type I?
Let us consider a patient with type 1 diabetes.
I think it would be safe to say that diabetes is an autoimmune disease. Now let us suppose this patient comes under stress. As far as I know, cortisol is a stress hormone and is released when a human is under stress. Now cortisol, as far as I know, increases the amount of blood sugar and at the same time is an immunosuppressant.
I would like to know whether this stress-induced cortisol can suppress the immune system, which has gone haywire, and help against diabetes - thereby rendering a suitable amount of stress useful.

Short answer
Stress is not a good candidate to treat autoimmune disease like diabetes type I.
Background
Stress indeed weakens the immune system, and diabetes type I is indeed caused by an auto-immune response against the insulin-producing beta cells in the islets of Langerhans. However, autoimmune diseases like diabetes type I need chronic treatment (i.e., insulin treatment and dietary changes).
Even if stress would help reduce diabetes type I (admittedly, theoretically it could), chronic stress would also reduce the immune response against viral and bacterial infections, it would reduce wound healing and perhaps even increase the risk of contracting cancer (Glaser & Kiecolt-Glaser (2005), as well as increase the risk of depression and cardiovascular disease (Cohen et al., 2007).
Hence, it is safe to say that deploying chronic stress as a treatment against auto-immune disease effectively means substituting one life-threatening condition with another.
References
- Cohen et al., JAMA (2007); 298(14): 1685-7
- Glaser & Kiecolt-Glaser, Nature Rev Immunol (2005); 5: 243-51

What about deliberately going through a little amount of stress everyday in a manner which is controlled enough to even reach up to the periphery of being chronic.

It is an idea, but I doubt anyone has tested it. Which patient would prefer to be stressed as opposed to regular treatment with insulin? Would you? Further, how to stress someone daily for years in a controlled way? I doubt anyone has tested it for these reasons.


text:
Is RNase AWAY in the lab dangerous?
I use RNase AWAY in the lab. I would like to know how dangerous this chemical is for health. For example, when I remove my gloves my hands smell because of the RNAse AWAY

"Also, when i removed my gloves my hands smell because of the RNase AWAY." - so?

@TanMath. Everyone in a lab is entitled to be provided with the equipment and take the necessary precautions to protect their health or address concerns related to their health. If the OP has concerns about the nature of RNase Away in regards to their health, then the smart thing for them to do is ask the questions and get the information that they need to evaluate the risk that they are putting themselves under. That being said, it would likely be better to raise the concern with her lab head or a university safety officer than on a forum.

Have you read the MSDS (Material Safety Data Sheet) for the product? In general RNAse-Away (or whatever brand specific variant) is just considered an irritant.

RNase AWAY is marked for Category II skin corrosion/irritation and Category II eye irritation/serious eye damage. Recommendations by the MSDS followed by definitions as follows:

Skin contact Wash off immediately with plenty of water for at least 15 minutes. Remove and wash contaminated clothing before re-use. Immediate medical attention is required.
Eye contact Rinse immediately with plenty of water, also under the eyelids, for at least 15
minutes. Immediate medical attention is required.

SOURCE
DEFINITIONS FOR GHS LABELING
More information is included in the MSDS provided.
As for any smell, RNase away is reported to be a proprietary alkali hydroxide solution, so without any additional information it's difficult to tell.

You mean I wasn't supposed to be spraying my hands before I gloved? Oops....

You should, in general read the Material Safety Data Sheet for whatever chemical you are using. This is always provided by the vendor.
For RNAse-AWAY (Sigma-Aldrich):

Gloves should be worn when handling this product. RNase
  Decontamination Reagent is alkaline in nature and will cause
  irritation if prolonged contact with the skin is allowed. In case of
  contact with eyes, immediately flush with water for fifteen minutes
  and contact a physician. If swallowed, do not induce vomiting. Give
  plenty of water and contact a physician immediately.

According to the MSDS:

Not a hazardous substance or mixture according to Regulation (EC) No.
  1272/2008. This substance is not classified as dangerous according to
  Directive 67/548/EEC.

First Aid measures as per the MSDS.

If inhaled If breathed in, move person into fresh air. If not breathing, give artificial respiration.
In case of skin contact Wash off with soap and plenty of water.
In case of eye contact Flush eyes with water as a precaution.
If swallowed Never give anything by mouth to an unconscious person. Rinse mouth with water.

I would however say that even if the MSDS says the chemical is not hazardous, a person should make the risk assessment themselves and decide how comfortable they feel working with the substance under certain conditions. Take Ethidium Bromide. While it is a known mutagen that intercalates DNA, if you read the MSDS, it is only dangerous if inhaled of if it comes in contact on an area of the skin that is broken, (cuts, cracks, etc.). Yet most people treat it like the plaque, and while it is irrational and not supported by the known science, they should have the prerogative to protect their...

... health how they see fit. And I am not saying your answer isn't implying that, I am only adding that even if the MSDS says its probably safe, it is still up to the person to decide what is best for them.

@AMR In reality EtBr is not as hazardous as people panic about it. It was used as an antiparasitic drug in cattle.

I am one of those who is not panicked by EtBr, but in fairness to those who are, we mark out the area where it is used and only use dedicated equipment. I am far more concerned and careful with bleach, having evolved Cl gas after washing a container, that had been washed before with bleach, that was not supposed to contain an acid, but had residue from someone who performed a plasmid prep.

If you are doing RNA preps, there isn't much of a way around it. RNase are everywhere and the only way not the degrade your sample is to use proper technique, barrier protection such as nitrile gloves, certified RNase free containers (macrophage tubes, pipet tips, etc.), and saturate your work surface and instruments with RNAse away.
If you really have a concern and it is available to you, a BSL-2 tissue culture hood with laminar air flow, that you get permission to use for the purpose of an RNA prep, is an option for an added level of safety. You still have to prepare your work surface with it, but the laminar air flow will keep any fumes away from you. A regular fume hood would probably be enough of a precaution, again if you are concerned, and it is less likely that anyone would take issue to you working in it if the BSL-2 hood is set aside for the exclusive use of tissue culture work.

Using something like RNAse Away is not always necessary, we don't use it at all. Working entirely with disposable containers or containers that were treated with DEPC or heated up high enough, as well as starting with RNAse free water and chemicals is generally sufficient.

@MadScientist - Who, we? You talk like Louis the Eleventh. user17471 does use RNAse AWAY.

That is fine if you are working in an area that is set aside specifically for RNA work and is isolated so that contamination is limited, and that area was likely treated in some way to begin with to destroy all biological contaminants. But if you are working on your day-to-day bench, you need to treat the work surfaces with something that will get rid of the enzymes and Ethanol will not cut it. I guess you could bleach everything, but bleach is far more corrosive and toxic that RNase Away.

And it is up to your labs protocol anyway. If your lab has decided that RNase Away is not a part of your protocol and you have engineering controls in place that can mitigate contamination, then that is great. Most labs don't and user17471's lab protocol is to prep with RNAse away, so using a fume hood or BSL-2 cabinet is about the only alternative available to them to protect their health if they are concerned.


text:
What is this structure in human brain?
Scientists made a new image of brain.
I wonder, what is this arc (denoted by blue)?

Is it the caudate nucleus?

That blue outline is huge and honestly I can't see what structure you wish to show us with that?

See at right, it is clean there.

is that blue line outlining something or did you exactly trace the structure? Could you work with a few arrows with their tips just touching the structure of interest? Your blue outline would be a huge structure. It's probably the corpus callosum you are after that lies within the blue outline afaik.

@AliceD see my update please

Short answer
Based on shape and approximate position, I think it is the corpus callosum.
Background
I think it is the corpus callosum (Fig. 1). The corpus callosum is approximately 10 cm in length and is C-shaped. It becomes thicker posteriorly, as is also evident in your image. The corpus callosum is a structure consisting of white-matter, containing about 200 million axons.

Fig. 1. Mid-saggital section of the brain showing the corpus callosum. source: University of Central Florida
I think it is not the caudate nucleus, alhough it has also the curved shape. The caudate is positioned more laterally than the corpus callosum and by the looks of it your picture shows a mid-sagittal section of the brain. The caudate seems to be positioned too far laterally in the brain as far as I can see (Fig. 2).

Fig.2. Nucleus caudatus. source: Brain Notes


text:
Why are eyes more sensitive to flicker in periphery — contradictory answers
In terms of the perception of flickering by CRT monitors, This answer suggests that peripheral vision has faster response and is thus more sensitive to flicker due to being provided by rod cells.
But in another answer it's said that rods are saturated at daylight and even at twilight. These two answers are in contradiction, since the light from CRT mentioned in the question pointed to by the first link above is quite above the photopic threshold.
So, how to reconcile these two answers?

It's not entirely clear what you mean by "why".  Do you mean the mechanism by which the sensitivity is accomplished, or the evolutionary reasons why such sensitivity might increase survival.  (That is, something moving fast at the edge of your visual field might want to eat you :-))

@jamesqf I'm interested in the mechanism.

I think the most likely explanation is that ambient lighting conditions in the room where OP was sitting, as described in the original question, might not have been bright enough to saturate the rods. Under mesopic conditions, both rods and cones are active. Hence your statement that

...since the light from CRT mentioned in the question pointed to by the first link above is quite above the photopic threshold.

may not hold. Since rods indeed have quicker responses, the periphery may be more sensitive to the flickering of a CRT or light bulb.
Note, however, that cones have flicker fusion frequencies of up to 90 Hz (reviewed by Perz, 2010), and CRT screens and light bulbs flicker at frequencies following the mains (50 or 60 Hz). Hence, cones may still be able to pick up the flickering. Since OP reports on an anecdote, experimental conditions may have been suboptimal and their report might have been unreliable. So we cannot exclude OP was using photopic vision, regardless their report.
Reference
- Perz, Master's thesis, Eindhoven University

"Hence your statement <...> may not hold" — how can this happen? Typical monitors have brightness on the order of hundreds of cd/m² (sRGB standard mandates 80 cd/m²). This is far above the photopic threshold of 5 cd/m² given in BIPM Rapport (Principles Governing Photometry. 2nd Edition. 2019, section 4.5).

It depends on the distance you are from it and the angle you are looking at it.

Brightness is distance-invariant. But OK, I don't know what angle of view typical CRTs have...

@AliceD In units of luminance, it shouldn't depend on distance.  FWIW, I much more clearly perceive 120 Hz flickering in LED lamps through my peripheral vision, even for very intense lighting thousands of times more than the photopic threshold, so I suspect that the answer is more complex. Cones in the perhery are sparse and physically larger, so their sensitivity to flicker/saccades may be different.  That would make some sense, since peripheral vision is there to alert you to something you need to look at with foveal vision.

@user1850479, that is interesting. Thanks for that

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text:
Plant tissue culture
Tissue culture means that cells are propagated and multiplied under controlled conditions. Suppose the following situations:

a) A seed being is embedded in an Agar medium and germinated under controlled conditions.
  b) An individual cell is extracted from a parent plant and embedded in a medium, resulting in the formation of a callus (germination).

Are these both examples of tissue culture? Both situations seem to fall under my definition of tissue culture.

quite different.  for one thing the cell will produce a clone of the parent plant.

Why is this question closed as being too broad? Any more specific is hardly possible. It could, arguably, be a bit homework'ish

In situation A) there is no mention of growth, so there is no reason to assume something is cultured. If we assume that in A) a germ plant arises, it is no tissue culture but a regularly bred plant. It is no tissue culture, because a seed is typically formed after pollination, which involves the recombination of parent genes to form reproductive cells (pollen) and the fusion of these reproductive cells after pollination. Because the definition of plant tissue culture is:

"... a form of cloning in which the plants are all genetically the same - similar to taking cuttings." (quoted from: Royal botanical gardens, NSW, australia).

it follows that seedlings are not clones of their parents.
Situation B) therefore meets the criterion of tissue culture, as new tissue grows out of a single progenitor cell.
So the answer is: they are not 2 examples of tissue culture, the difference being that A) is the result of a normal breeding and B) meets the criteria of tissue culture.


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Can people with paralyzed eye muscles see?
As far as I am aware, the saccades of the eye are central to visual perception. If the eye is held still, the human stops seeing, even if light is reaching the retina and the visual pathway is intact.
But we recently had a question on UX.stackexchange about possible improvements to a visual+EEG interface used for communication with locked-in patients. The designer asking it mentioned that eye tracking devices are unlikely to work, because the patients' eyes can't move. This surprised me, as I would have thought that the patients must be able to move their eyes if they are able to read the device's screen. But I have never had contact with a locked-in person, and assume that the asker knew more about them than I do.
So, are there situations in which a human's eye muscles are paralyzed, so the eyeballs cannot be moved in their orbits, but this human still has visual perception and can mentally process information in his/her field of view?

Why will the human stop seeing if eyes are held still?

@CRags - through adaptation (image fading). See my answer below. Good question, though.

@ChrisStronks Sorry Chris, now got it. I didn't read the full answer. It is nicely explained.

Short answer
Visual perception persists in the absence of functional eye movement.
Background
An example case would be retinal implants wearers. Retinal implants like the Argus II consist of a set of electrodes placed onto the degenerate retina of blind folks. Electrical stimulation of the electrode array elicits flashes of light (phosphenes). Visual input is provided via a head-mounted camera, and the device translates the camera images into patterned electrode stimuli. Hence, because the camera is head worn, Argus II wearers cannot use eye movements to scan the world. They have to use head-scanning techniques. Still they are able to perceive flashes of light (phosphenes) and can recognize simple shapes and perceive motion.
In fact, eye movements such as saccades are detrimental in Argus II wearers, because the oculomotor system feedbacks muscle movements to the brain when a saccade is made to stabilize the perceptual field of view. In normally sighted people the oculomotor feedback system is important, as it tells the brain to compensate the retinal image position shift when a saccade is made. Compensation occurs through a shift in the brain representation of the retinal image to the opposite direction, thereby stabilizing the image representation. However, this is detrimental in Argus II wearers, because the position of the electrode array and hence retinal position of the image is unaffected by eye position. Hence, when subjects use their implant, any saccades will disrupt visual processing, because the oculomotor system will abberantly compensate the perceived location of the object being viewed.
More importantly, perhaps, are micro-saccades. Micro- saccades are small, involuntary eye movements. When images are present stably to the retina the images fade very quickly due to adaptive processes in retinal neurons. Micro-saccades are thought to prevent fading, as they constantly produce small, involuntary fluctuations in gaze, thereby shifting the image quickly over the retina, and thereby refreshing the retinal image and preventing adaptation (Stingl, 2013). When Argus II wearers stop scanning the image, images indeed fade within seconds (Stronks, 2013).
To get back to your question and summarize:
Title question: No, eye muscles are not needed for sight, given that Argus II wearers have sight (though artificial, crude vision). However, a functional saccade system in normally sighted folks improves scanning, and anecdotally micro-saccades prevent image fading by constantly refreshing the retinal image.
Body question: Argus II implant wearers are an example of vision without oculomotor control. Although they cannot use their eye muscles for scanning, they still have functional vision.
 However image fading is a problem in Argus II users and folks without functional eye muscles alike, so head scanning techniques will be needed.
PS: Other implant systems, such as the Alpha-IMS use light-capturing methods inside the eye. Hence these subjects can use normal eye scanning and saccades for scanning. Also, albeit anecdotally, fading is reduced in Alpha-IMS wearers, because of the micro-saccades preventing adaptation (Stingl, 2013).
References
- Stingl et al., Proc Royal Soc B (2013); 280(1757)
- Stronks et al., IOVS (2013); 54(6): 3891–901.

Can add refs when needed later, I am mobile now unfortunately.

Good answer, why are saccades essential to see in a normal person?

@CRags - Thanks! Saccades are not essential, just beneficial for scanning and preventing adaptation. Answer adapted :)

Could you add some references on micro-saccades and image fading? You say "anecdotally" in your answer, does that mean no studies have been performed on it?

@MattDMo. I am still mobile. Will work on refs when possible. Anecdotal evidence is published, but as far as I can see not thoroughly investigated.

Finally - references!

Is the author of the second paper same as the Chris Stronks on this site?

@MarchHo - shush, I'm hiding behind my nick name :-)


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How to make GABA pass the blood brain barrier?
I thought of methylating GABA at the gamma amino group in order to make it pass the blood brain barrier, but would it work?
The goal is to make a sedative. Like GHB or benzodiazepines (I know that benzos have a totally different structure)
Any ideas on how to make GABA  pass the blood brain barrier?

Short answer
Chemical reversible shielding of the aminogroup in GABA seems to be sufficient to get it into the brain as a Trojan horse.
Background
Given that you ask

...how to make GABA pass the blood brain barrier?

I assume that

You wish to elevate GABA by exogenously administering a compound;
That compound has to cross the blood-brain barrier (BBB) and physically turn into GABA;
A drug indirectly elevating GABA through unknown (e.g., GHB) or known mechanisms (Gabapentin) does not suffice your needs.
If you are happy with indirect actions, the links above will help you out. Now on to the real stuff :-)

GABA (Fig. 1) has 3 hydrophylic groups that may prevent it to cross the blood-brain barrier (BBB), namely a hydroxyl-, a keto- and an amine-group. The BBB generally only permits passive entry of small hydrophobic molecules. The amino-group in turn is also prone to de-amination by mono-amino oxidase inhibitors.
An often-used method to get drugs into the brain is shielding of pesky hydrophilic and/or fragile chemical groups by certain molecules that are irreversibly bound to them. A well-known example of shielding a fragile amino-group is the B-methylation of phenetylamine compounds into their amphetamine analogues. Alpha-amination to a methamphetamine further stabilizes the essential amino-group. Amphetamines and methamphetamines are way more stable in the brain than their phenetylamine precursors and likely enter the BBB also more swiftly because they are more hydrophobic by shielding the amino group (Shulgin, 1990).
However, those methyl groups are irreversibly bound, so it's not an option here, as apparently you wish to increase GABA, and not an active derivative of it.
Now, another way is using a Trojan horse method (Pardridge, 2006); by reversibly shielding the essential amine group the drug can enter the brain, where it is converted back to its original compound. Picamilon does the job here. Smarter Nootropics say;

First developed in the early 1970s in the Soviet Union, picamilon (alongside phenibut) is an “enhanced” form of GABA that is capable of crossing the blood brain barrier when taken as a supplement.Inside the brain, picamilon is rapidly hydrolyzed into its constituent parts; niacin and GABA. Niacin helps to enhance brain blood flow through its vasodilatory properties [].

Fig. 1. GABA and Picamilon. source: Smarter Nootropics
Reference
- Pardridge, Discov Med (2006); 6(34):139-43
- Shulgin, PIHKAL, Transform Press, U.S. (1990)

By the way, if I methylated GABA just before the amine group (like phenethylamine to amphetamine), would it be a GABA receptor agonist or at least a PAM? (positive allosteric modulator)

@ostal123 I guess yes, but it's an interesting question for sure!


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What determines the shape of the center-surround receptive fields of retinal ganglion cells?
The wikipedia article about receptive fields of visual system tells us the following:

The receptive field is often identified as the region of the retina where the action of light alters the firing of the neuron. In retinal ganglion cells (see below), this area of the retina would encompass all the photoreceptors, i.e., all the rods and cones in the retina.

Then it shows some pictures

I understand the part where it says that the neurons firing increases as we put light on the center of the receptive field (for ON center type) and etc.
What I'm not sure about is the location of this circle; where is this circle that we put light on?
What I think might be the answer is that, as the quote says, the circle is the area of retina where we have the rod/cone shaped photoreceptors.
So this means that, for every ganglion cell, the photoreceptors connected to it are always shaped like a circle?

The center-surround structure is created by the horizontal connectivity of the horizontal cells (Periman et al., 2012)  that receive input from multiple photoreceptors (Fig. 1).

Fig. 1. Retinal patch showing the connectivity between a horizontal cell and photoreceptors. Source: Harvey Mudd College
The horizontal cell passes on the congregate output to the bipolar cell, which in turn drives the retinal ganglion cells (RGCs) that send their axons to the optic nerve and send the signal on its way to the brain.
The photoreceptors are connected in two concentric circles to the horizontal cell. When light stimulation of the inner patch (center) evokes an excitatory response in the RGC, and the outer circle (surround) inhibits this response, the receptive field is said to have an ON-center configuration. In the reverse scenario, it is OFF-center (Fig. 1). This center-surround configuration is one of the first visual processing steps in the visual system and enhances contrast in the perceived image.

Fig. 2. ON and OFF center-surround receptive fields. Source: Brain Connection
Reference
- Periman et al., Webvision. The Organization of the Retina and Visual System. Utah


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Do primate RGCs have overlapping receptive fields?
According to this link,
http://hubel.med.harvard.edu/book/b10.htm
retinal ganglion cells (RGCs) receive input from overlapping receptive fields (RFs). This is also an idea used in convolutional neural networks for deep learning of images.
On the other hand, this one, for the primate retina, states that there is no such overlap:
http://www.sciencedirect.com/science/article/pii/0042698995001670
So do primate RGCs have overlapping RFs? If not, how does the primate visual system deal with this sparse input? How does it fill in the blanks?

Another one that says "no overlap in mammalian retina": http://webvision.med.utah.edu/book/part-ii-anatomy-and-physiology-of-the-retina/morphology-and-circuitry-of-ganglion-cells/
And yet another that says "overlap in cat retina": http://faculty.washington.edu/jpalmer/files/Teller/ByChapter/tellerChapter08.pdf (pg 214, fig 8.14)

A paper with overlap in cat retina: http://www.ncbi.nlm.nih.gov/pubmed/480198

Short answer
Associated ON- and OFF-center retinal ganglion cells can show 100% overlap in their receptive field.
Background
When looking at the elementary neurophysiology of the retina, we can see that a single cone generally synapses onto two bipolars. Because photoreceptor cells hyperpolarize when illuminated, glutamate release from their synapse is inhibited. In turn, OFF-center bipolar cells are hyperpolarized and ON-center bipolars are depolarized. The OFF-center bipolar synapses onto an OFF-center retinal ganglion cell (RGC), while the ON-center synapses onto an ON-center RGC (Fig. 1).

 Retinal circuitry linking cones to bipolar cells (left panel) and bipolar cells to retinal ganglion cells (right panel). source: Washington University.
Then to your question - the basic circuitry shows that the ON- and OFF-center RGCs receive their input from a single cone and hence have 100% overlapping field. In the foveal region, bipolars link 1:1 on cones, as in Fig. 1, so in this example case, they show 100% overlap.
Note that there are an estimated 30 types of retinal ganglion cells, about half of them being not even described yet, as per a 2015 review article (Sanes & Masland, 2015). Hence, this answer is anywhere from exhaustive, but it does show there can be substantial overlap between RGCs.
Reference
- Sanes & Masland, Ann Rev Neurosci (2015); 38: 221-46


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How to improve DNA extraction
I am using the following protocol to extract chromosomal DNA from bananas:

Cut up one banana into small pieces, approximately (1 cm3)
Add ½ a cup of warm salt water and the banana pieces into the blender and set to max for 5-10 seconds
Poor into a beaker and add 1 teaspoon of detergent to the beaker
Stir for 5 mins with a spoon to break down the plasma membrane
Place the mixture into a centrifuge for 30 seconds
Pour the mixture through a gauze with a beaker catching the liquid underneath
Smoothly pour cold ethanol into the mixture at a 1:1 ratio so a clear layer of liquid will form on top of your mixture

Why is the centrifuge step (5) needed? Why would that increase the yield of DNA?

In a protocol like this, a low centrifugation is typically used to separate DNA in solution from larger, heavier components of the mixture. By lightly pelleting the banana slurry at the bottom of the tube, the DNA in solution is less likely to stick to that fraction of the mix when you pour it through the gauze. That's where your increased yield will come from.

Yes. that is correct.

@Rob - do you mean that this answers your question? Don't forget to vote an answer up, if it solves your question. :-)


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What causes spontaneous muscle twitches?
Sometimes a small region of my body starts shaking, without any reason and then stops abruptly. Apparently this is a common phenomenon (source: NIH).  I researched its cause for a bit and came to know that it is because of nerve excitation.
Why do those nerves get spontaneously excited in the first place, without any conscious, voluntary, internal stimulus being presented?

Short answer
Spontaneous muscle twitches are thought to be caused by spontaneous activation of motoneurons controlling the muscles.
Background
Spontaneous muscle activity (twitching) is referred to as muscle fasciculations. Most commonly, they are benign, but they can be associated with certain pathologies too, such as ALS.
Fasciculations are thought to originate due to spontaneous activation of muscle fibers due to processes in the motoneurons. At the axonal endings there are synapses that junction onto the muscle. The axonal tips of motoneurons are thought to be highly sensitive to depolarization (electrical firing), which is what triggers acetylcholine release and muscle contraction.  The complicated process itself takes a small fraction of a second.  If any of this happens involuntarily, then the muscle fiber contracts spontaneously (source: ALS Association).
Specifically, it is thought that spontaneous depolarization of motoneurons are the cause of fasciculations. This decreased firing threshold can be the cause of disease, disrupted ion homeostasis in the body, fatigue, drugs and other causes (Blum & Rutkove, 2007).
Note that spontaneous / random activity in neurons is not only possible, it is quite common. Especially in neurons close to firing threshold, such as the motoneurons responsible for muscle activity, slight perturbations in ion concentrations inside or outside the cell can trigger an action potential. Further, channel opening is a stochastic process, meaning that even voltage-gated Na+ channels can open without a depolarization being present; although the chance is slim that will happen, it can statistically still happen. Stochastic processes like this can cause neurons to fire spontaneously, without a stimulus being present.
Reference
- Blum & Rutkove, The Clinical Neurophysiology Primer, Springer (2007)

So how does it happen involuntarily? Where do they get that stimulus from?

@Polisetty - There is no verifiable stimulus, inherent to spontaneous phenomena in general

@Polisetty - Some neurons happen to cross threshold for non-apparent reasons (local irritation causing surrounding tissue fluid electrolyte imbalance, for example.) Neuronal membranes do not always work predictably (unlike, say, gravity.) It happens all the time, all over the mody, and mostly it goes unnoticed because we become habituated to these minor glitches.

@Polisetty - I totally agree with anongoodnurse and I have added a paragraph to my answer. I hope this helps.


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Interplay of neuritic and synaptic growth
Let me try to give a picture of my understanding of neuritic and synaptic growth and their interplay.
Pick two neurons in corresponding areas of opposite hemispheres which are connected by a synapse (and a rather long axon).
Both neurons were originally born at approximately the same time t during brain development in a given distance d, without already having neurites.
They necessarily have a latest common ancestor (stem cell), which doesn't have to be the same parent cell, but maybe the same grandmother or great-grandmother cell.
Now several processes start with different delays and at different speeds:

the two neurons wander away from each other
they specialize thus expressing specific "markers" on their membranes
their axons grow
their dendritic trees grow

Case 1: If neuritic growth is fast enough, the two neurons can meet and build a synapse early (recognizing each other by markers they have in common due to their common ancestor). While wandering away from each other, the neurites have to grow accordingly.
Case 2: If neuritic growth is too slow, and the neurons wander away from each other too fast, the growth of axons and dendrites at least has to be guided somehow (by glia cells or by molecule gradients?) such that later they have a chance to find each other. Finally they recognize each other by markers expressed eventually during specialization.
I could imagine that both cases do occur purely, but even that they can be somehow intermingled.
Question: Is this picture essentially correct or flawed? (A yes/no answer would suffice!)

Furthermore, I am looking for a concise presentation of (resp. gentle
  introduction to) these processes (and maybe others?) and their
  interplay that lead to specific synaptogenesis.

Not an expert on this but Case 1 is mostly wrong. Have you read this: https://en.wikipedia.org/wiki/Axon_guidance. Also, interhemispheric connections are rather rare, at least in the cortex.

What do the commissural fibers connect? (See https://biology.stackexchange.com/questions/65351/development-of-the-commissural-fibers)

The Wikipedia article describes Case 2. But does it explicitly rule out Case 1?

I cannot believe that all neurons have to be at their final positions before synaptogenesis starts. It  must be (in my humble opinion), that at least some neurons already connect during their travel to their final positions, so there must also be axon growth just by lengthening, not only guided. But of course I may be wrong.

For example, it might be the case that some "pioneer" axons connect rather early to their target neuron, then follow it (during its travel) by lengthening, and thus help somehow to guide the following axons (somehow like the emigrant trails led by pioneers in North America in the 19th century), which connect to their targets only later.

That may happen to some extent (that's why I said mostly), but it's highly unlikely, based on first principles: if it was extensive at all, it would prevent neural migration. Don't confuse "pioneer neurons" and their axons with how you used the term, as they project after they have arrived at their target area.

My comments are here to help you revise your question, so please refrain from starting a conversation in the comments unless something I said is not clear. Your last three comments could be incorporated in the question, IMHO.

Let us continue this discussion in chat.

Short answer
Both short and long-distance synapse formation can occur.
Background
Short-distance connections can be made between adjacent cells (Van den Pol et al, 1988). Your 'common ancestor part' is a bit obscure to me. In the end, every cell is born out of a single one :)
Long-distance connections can also be made. For example after neuroneogenesis either during development or even in the adult brain, whole neurons can migrate from their origin to a new part (Kaneko et al., 2017), or axons can grow to find a new target distally, for example after neural injury (Purves et al., 2001).
References
- Kaneko et al., J Neurochem (2017); 141(6): 835-47
- Purves et al. (eds), Neuroscience (2001), 2nd ed. Sunderland (MA): Sinauer Associates
- Van den Pol et al., J Comp Neurol (1998); 399(4): 541-60

But the OP is asking about connections that are formed when cells are very close to one another with axons that later stretch as the neurons migrate to their target area. Can that happen in vivo in the case of neurons so far as to be in different hemispheres?

@vkehayas - I don't see that particular question framed as such in the question


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coverage calculations approach for clipped reads
Experiment: deep sequencing for mutants in 700nt fragment.
the fragment of dna was preamplified by primers flanking the fragment followed by hiseq.
per base coverage was calculated by coverageBed -d -abam in.bam -b ref.bed > out.cov
Observation: two distinct peaks in coverage at the ends as below plot.. coverage vs positions

the peaks are made from reads having part of primers..thus also show soft clipping at ends..
there is a huge difference in the calculations if i include such reads And if I exclude them.
Question: is there anyone who knows how to handle such a situation?

It's absolutely not clear, how you prepared your library for sequencing, where the boundaries of your primers are and what exactly bothers you in this context.


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Difference between 'fitness' and 'fitness effects'
Term 'fitness' is pretty obvious, but, often 'fitness effects' is commonly used in many research articles in the field of evolutionary biology.
I suspect that 'fitness effects' has a different meaning than just 'fitness'. I found that it's really difficult to find the distinction between the two terms just by googling.
So, if some expert in the subject is reading, please clarify.

Fitness
Fitness is some function of the probability of survival and fecundity for a given genotype. Fitness is therefore a single value per genotype.
Fitness effect
A fitness effect is a component of fitness. For example, for a given bi-allelic locus, the fitness effect of allele A is -0.05 in comparison to the allele B, meaning that the allele A is deleterious and the allele B is beneficial. There is a fitness effect for each allele, for each trait and, if you interested in  genetic interaction (epistasis) and genetic-environment interaction, then there can be a fitness effect for each gene and each trait in each genotype in each environment.
Example
It is typically common to assume a model of $n$ loci, where the fitness effects at each loci are $1$, $1-hs$ and $1-s$ for the three genotypes AA, AB and BB respectively (diploid population). $s$ is the selection coefficients and $h$ is the dominance coefficient. The fitness of the individual is often obtained by multiplying out the fitness effects at each loci. The worst possible fitness is therefore $\left(1-s\right)^n$.

Fitness effect of an allele seems to be an 'effect size' which is calculated relative to fitness of other allele.


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Does increased physical activity increase the rate of cell division?
Ever since learning that the shortening of telomeres is linked to aging I've tried to figure out what causes cells to divide, and if it's possible to slow down the rate of cell division through life style changes.
How would, for example, increased or decreased metabolism affect the cell cycle? If we exercise a lot, would it tear on the cells in any way, forcing faster cell division?

My understanding is that telomeres are linked to cell senescence, which is not necessarily the same thing as organism senescence. So even if you could track down a method to slow cell division, it would more likely mess with organ function now rather than extend life.
Here's a nice summary of cell senescence: http://www.ncbi.nlm.nih.gov/books/NBK26877/#A3266
I did look into cell division in muscle, and new muscle cells come from satellite cells, rather than from mitotic division of currently active muscle cells.
Caloric restriction was the hot new way to live longer for a while, but studies in primates found that a sensible diet and good genetics have a bigger effect. Which is pretty much the T-shirt in medical science.
This question was asked last spring as well. Coincidence? Homework?

Metabolism does affect cell cycle. Stress is known to affect ageing.
Mitchell et al., (2014) report that there is a telomere shortening in kids who grow up in disadvantaged social environments.
Metabolism and stress are known to affect longevity and general health. After much research on genomic associations of diabetes, people have come to the conclusion that physical exercise helps.
Physical exercise is also known to stimulate neurogenesis in the hippocampus; the causes are not well understood (van Praag, 2008).
There are more of such reports. If you search you'll find.

Little occupied now- so couldn't post a more elaborate answer.


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What is the difference between myopia and hyperopia?
In myopia the lens is bending the light too much even in the most relaxed state. Thus the image is produced in front of the retina. If the object comes closer  the lens just adjusts a bit less than a healthy eye and the myopic subject is able to see clearly.
Why is the hyperopic eye not able to do that? If the object is far away, could the lens not just bend a bit more to elicit normal vision? So, why is the Myopic eye able to adjust its focus, but the Hyperopic not?

Short answer
Myopic eyes can still focus on nearby images as the lens needs to relax a bit more than in a normally-sighted person. However, objects far away cannot be focused, because in a complete relaxed state (for distant objects), the lens focuses the image in front of the retina. Hyperopic eyes cannot focus on nearby objects as, at a certain close distance, the lens reaches maximum accomodation (maximum roundness) and objects cannot be focused any longer.
Background
Myopia or near-sightedness is a condition of the eye where the light that comes in does not directly focus on the retina but in front of it, causing the image that one sees when looking at a distant object to be out of focus, but in focus when looking at a close object. Often the eye ball is too long, or the cornea has too much curvature (Web MD).
Hyperopia ("over-measured sight") or farsightedness, is a defect of vision caused typically by the eyeball being too short, or a lens that cannot accomodate/become round enough. It causes difficulty focusing on near objects (wikipedia).

Source:Monroe Publishing


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What will happen if there is high concentration of both calcitonin and PTH in blood?
What will happen if there were a high concentration of both calcitonin and PTH (parathyroid hormone) in the blood? In that case, will calcium resorption from bone occur, or absorption from intestine, or deposition of calcium in bones? Also, will blood calcium level rise or fall?

It depends on duration of PTH , whether its intermittent or chronic hyperparathyroidism, in different cases effects will be different.

Thanks @David for all your effort in improving this post. Your comments were flagged for deletion and the mods did so. However, they were quite helpful and if you feel they should stay in place, let me know. Cheers.

To OP, is this a homework question? You are required to show prior research effort. We're not here to spoonfeed the answers to your assignments.

@AliceD This aint homework. I was reading this in book and question spoofed in my mind. There was no where to research properly. The two hormones works on different osteocytes, I had no such idea,  to search anything relevant.

Short Answer: quite surprisingly, both will occur.
Long Answer: as is quite well known, calcitonin lowers blood Ca2+ levels. It performs this task by two methods:

it inhibits the activity of osteoclasts in the bones (Custoff, 2008)
it inhibits reabsorption of Ca2+ in renal tubular cells, allowing it to be excreted in urine (Potts et al, 2008)

However, the second mechanism is only minor. On the other hand, parathyroid hormone (PTH) performs just its opposite: it increases Ca2+ levels in the blood.
So, lets come to the main point: since calcitonin and PTH have opposing functions, what would happen if both were acting simultaneously?
It seems, funnily though, that both the functions will occur simultaneously. Wong et al, 1975, in their research, showed that the target cells of calcitonin and PTH are different i.e. calcitonin and PTH act on different osteoclasts. So, to put it simply, while activity of some osteoclasts would be decreased, that of some others would be increased. Overall, Ca2+ levels in the blood would remain pretty much constant.

Would be much better if this is also added, PTH is not always reabsorbing the bones, https://www.ncbi.nlm.nih.gov/pubmed/16563840


text:
Why are skin moles (pigmented spots) circular in shape?
I have never seen a rectangular or triangular shaped mole.
Is there any reason for why moles are roughly circular in shape?

Totally unscientific personal remembrance: I knew a guy who had a big mole which did have one nearly rectangular "edge". So it seems they can be "edgy", but just usually aren't?

Dude! Gorbachev is your best shot!

Note: I am not stating that moles are in general circular in shape because there are no statistical studies to conclusively state so. This answer is mostly about default circular shape of cell colonies.

Moles (melanocytic naevi) are not strictly circular but generally have  have a rough circular shape. Moles can have irregular shapes too and you can easily check that by a simple google image search.
The exact causes and mechanisms of mole formation are not known but the somewhat circular shape can be explained by a simple spatiotemporal model of growth.
Moles are formed because of pigmented cells called melanocytes (which contain the dark pigment melanin). A mole would grow when a very small population of these pigmented cells divide and expand. In a 2D surface, cells would continue to divide and expand along both the axis at an equal rate, if there are no specific constraints. Since the expansion is same along both the axes, you get a roughly circular shape. For similar reasons, bacterial colonies (on petri plates) are also more or less circular. Note that there are stochastic factors that would contribute to irregularity.
Triangles and rectangles are very specific geometries. There need to be some constraints that would limit the cell growth to adopt these geometries. So the default shape would be mostly circular.

Short answer
Naevi do not have to be circular in shape. In fact, they come in a wide variety of shapes and colors.
Background
A beauty spot, or mole is called a naevus. Naevi (plural) are formed by the growth of the pigment cells in the skin, the melanocytes .
There are various types of naevi:

Congenital naevi are present from birth and occur in about one in 100 people. They may be more likely to develop into melanoma (cancer) than nevi appearing after birth (WebMD).
Acquired naevi develop later in life (Dermatology Net NZ);
Dysplastic naevi are typically larger than average and more irregular in shape. They tend to have uneven color with dark brown centers and lighter, uneven edges. These nevi are more likely to become melanomas (malignant skin cancer) (WebMD).
Dysplastic naevi may turn into melanomas (NIH), but melanomas are outside the scope of this question.

Now let's turn to your question - not all naevi are circular. Below I have illustrated just a mere tiny handful of the wide gamut of shapes found among different types of naevi. In fact, naevi come in a wide variety of shapes and colors (source: Dermatology Net NZ):

Small congenital naevus ; medium congenital naevus ; and hairy congenital naevus

Café au lait macule ; Speckled lentiginous naevus ; and Naevus of Ota

Reticular naevus ; Junctional naevus ; and Starburst naevus
In fact, naevi occur in more extreme forms too:

source: No Hands but Ours
Reference
- Cichorek, Postepy Dermatol Alergol (2013); 30(1): 30–41


text:
What is the difference between the neural tube and the dorsal ventral cord?
I was wondering what the difference is between the neural tube and the dorsal ventral cord.
I know that the neural tube forms during embryonic development from the ectoderm layer that folds inwards.
I thought that the neural tube gave rise to the central nervous system, however sometimes I see the following:

"the central nervous system develops from the hollow dorsal nerve
  cord"
   for example: https://en.wikipedia.org/wiki/Dorsal_nerve_cord

question
What is the difference between the neural tube and the dorsal ventral cord or are they both the same?
(talking about humans)

The terminology can be confusing, and I suspect the question you meant to ask was: what is the difference between the neural tube and dorsal nerve cord?
In vertebrates, the neural tube and the dorsal nerve cord are two names for the same structure. It develops into the brain and spinal cord.

Neurulation occurs during the early embryogenesis of chordates, and
  it results in the formation of the neural tube, a dorsal hollow nerve
  cord that constitutes the rudiment of the entire adult central nervous
  system.

Source: Colas J-F and Schoenwolf GC. Towards a cellular and molecular understanding of neurulation. Developmental Dynamics. 2001. vol 221(2): 117–145.
This differs from invertebrates, some of which have a ventral nerve cord that does not invaginate and form a neural tube. As the name suggests, in contrast to vertebrates the nerve cord in these species is located ventrally.
In summary:
Dorsal nerve cord = neural tube
Ventral nerve cord ≠ neural tube

The neural tube (Fig. 1) is the embryo's precursor to the central nervous system, which comprises the brain and spinal cord. Its structure can be described in standard anatomical terms of location and their respective axes.
The dorsal - ventral axis (back to abdominal side) can be visualized by dissecting the neural tube transversely (Fig. 2). This axis is important for development. In the spinal cord, for instance, the dorsal region is the place where the spinal neurons receive input from sensory neurons, while the ventral region is where the motor neurons reside. In the middle are numerous interneurons that relay information between them. The polarity of the neural tube is induced by signals coming from its immediate environment. The dorsal pattern is imposed by the epidermis, while the ventral pattern is induced by the notochord (Gilbert, 2000).
Conversely, the anterior - posterior axis (head to tail) can be seen by a longitudinal transection (Fig. 1). Here, the important regions of the brain can be identified; the neural tube balloons into three primary vesicles, namely the forebrain (prosencephalon), midbrain (mesencephalon), and hindbrain (rhombencephalon). The prosencephalon becomes subdivided into the anterior telencephalon and the more caudal diencephalon (Gilbert, 2000).
Hence, regarding your question - there exists no such thing as a dorsal ventral cord.

Fig. 1. Anterior-to-posterior axis of the neural tube. Early primary structures (left) and adult structures (right). source: Gilbert (2000).

Fig. 2. Dorsal-ventral axis of the neural tube. source: Gilbert (2000).
Reference
- Gilbert, Developmental Biology. 6th ed. Sunderland (MA): Sinauer Associates (2000)


text:
Why is the thalamic reticular nucleus called a nucleus?
In the Wikipedia article on nuclei I read:

A nucleus is one of the two most common forms of nerve cell
  organization, the other being layered structures.

Is there a specific and plausible reason, why the  thalamic reticular nucleus is called a nucleus, even though it is - anatomically - a layer?
Has the TRN once been a somehow spherical nucleus and evolved into a two-dimensional layer? Or does the TRN play a functional role that normally nuclei play, but not layers?

The thalamic reticular nucleus (TRN) is a thin layer of GABAergic cells adjacent to the thalamus (Fig. 1).  Because of its strategic location between the thalamus and cortex, the TRN is often suggested to be important to attention and regulation of information flow between the thalamus and cortex (Lam & Sherman, 2011).
A nucleus is defined as a

[p]ortion of tissue that are compact accumulations of neurons having roughly similar connections and functions

Reticular is defined as

A fine network or net-like structure.

So reticular nucleus translates itself as a net-like accumulation of neurons.
In contrast to the wikipedia meaning, therefore, I interpret nucleus as more of a cluster of functional organizational units rather than a morphological characteristic of that cluster per se.

Fig. 1. Thalamic reticular nucleus. source: Dana Foundation
Reference
- Lam & Sherman, J Neurosci (2011); 31(18): 6791-9

Thanks for the clarification. But this makes things terminologically difficult:  applying - maybe unreflectedly - anatomical terms to functional concepts.

@HansStricker happy to help. I have attempted to further clarify the answer (last sentence). Also note these kind of questions are welcome over at CogSci too. Up to you.

My question stated otherwise: In which respect is TRN a "portion of tissue that is a compact accumulation of neurons having roughly similar connections (what to?)"? And don't have the neurons of a layer have roughly similar functions?

@HansStricker This is a good question (I promise I don't hate you, I just don't like some of your questions). The distinction that the Wikipedia article makes is between "layered structures" and "nuclei", not between "layers" and "nuclei". Thalamus is not a layered structure; the cells are clustered into nuclei, not into laminae like cortex or cerebellum. There isn't any structure consisting of just one layer that is thought of as "layered", you really need at least 2 layers to be layered. TRN projects inhibitory connections into the rest of thalamus.

Also you should note that in general, most anatomical terms for the brain far predate knowledge about their functions. If you want to really dissect out (pun intended) the reasons for the names of everything you are risking some level of insanity, unless the curiosity interests you. Some nuclei are named by color, some by what they happen to be under even if they are completely unrelated, some are named from an almost imperceptible similarity to sea creatures.

@Bryan: Thanks for your kind and helpful comments. I do appreciate them.

Obviously, I didn't read the Wikipedia article on nuclei carefully enough. Anyway, it was great to get some learned opinions. In the Wikipedia article on reads:

The term "nucleus" is in some cases used rather loosely, to mean
  simply an identifiably distinct group of neurons, even if they are
  spread over an extended area. The reticular nucleus of the thalamus,
  for example, is a thin layer of inhibitory neurons that surrounds the
  thalamus.


text:
What are Intersensory Associations?
While I was reading about "Neural Control and Coordination" I came across this
"Association areas in the forebrain are responsible for complex functions like intersensory associations, ....."
What are "intersensory associations"? I have searched the net but could not find anything useful.

They mean integration of information from more than one sense. For a human example, think of when you are having a conversation: you are not only listening to what someone is saying but also watching their lips move. Both give you information about what they are saying. Or you see a cat and hear a meow: you have an association between the two that allows you to identify the meow as emanating from the cat you see.

A more common terminology regarding 'intersensory associations' is multisensory or crossmodal integration. Crossmodal integration takes place in the association cortices in the brain (Fig. 1). An example is the coupling of auditory and visual input during lip reading, as mentioned in the comments. Lip reading can aid in acoustic speech understanding, especially so in the hearing impaired.
The association cortices include most of the cerebral surface of the human brain and are responsible for integrating the sensory input that arrives in the primary sensory cortices. The diverse functions of the association cortices are loosely referred to as “cognition,” which literally means the process by which we come to know the world. Cognition enables us to attend to external stimuli, to identify the significance of stimuli and to plan meaningful responses to them. The association cortices receive and integrate information from a variety of sources and in turn influence a range of cortical and subcortical targets (Purves et al., 2001).

Fig. 1. Association cortices. source: Brown, Physiology & Neuroscience websites
Reference
- Purves et al., Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates; 2001


text:
What are garlic's effects on DHT?
Most antiandrogens inhibit DHT. DHT is connected to testosterone. [1] shows a beneficial effect on prostate cancer which can be caused by DHT. However, according to [2] garlic also increases testosterone.
What are the effects of garlic on Dihydrotestosterone (DHT) or 5α-dihydrotestosterone? Can it be used as an antiandrogen?
[1] Hsing AW, Chokkalingam AP, Gao YT, et al. Allium vegetables and risk of prostate cancer: A population-based study. Journal of the National Cancer Institute 2002; 94(21):1648–1651.
[2] Oi, Y; Imafuku, M; Shishido, C; Kominato, Y; Nishimura, S; Iwai, K (Aug 2001). "Garlic supplementation increases testicular testosterone and decreases plasma corticosterone in rats fed a high protein diet". The Journal of nutrition 131 (8): 2150–6.

This should be migrated to Biology.SE

@Oddthinking I think the comment for migration to Biology is accurate and I agree with that. Though, I am not sure how I can migrate it there.

I added a further explanation in order to be a candidate for Biology.SE. Any help on that is welcomed.

Garlic may affect testosterone metabolism. Its beneficial effect on prostate cancer is not attributed to this, but it is attributed to the direct effect on prostate cancer cells.

What is garlic's connection to DHT?

Cytochrome P450 enzymes. Diallylsulfide, a constituent of garlic, suppresses oxidative demethylation by competitively inhibiting cytochrome P450 2E1, an enzyme that activates carcinogens. Since testosterone metabolism occurs through the mixed function oxidase cytochrome P450 system, garlic may affect the rates of metabolism of testosterone and dihydrotestosterone. The metabolism of testosterone is catalized by inducible P450 1A1, 1A2, 3A3, 3A4 and 3A5 enzymes. These mixed function oxidases can be modulated by a wide variety of environmental facts and dietary constituents. Little is known about the potential for modifying testosterone risk or its treatment modality by administration of garlic constituents [1].

S-allylcysteine (SAC), a potent compound derived from garlic, suppressed the proliferation of PC-3 cells and led to cell cycle arrest at the G0/G1 phases, as well as induced cell apoptosis, which was accompanied by the decreased expression of Bcl-2 and increased expression of Bax and caspase 8. This demonstrates the chemopreventive activity of SAC in vitro, and that SAC may be a promising candidate for prostate cancer treatment [2, 4].
Diallyl disulfide (DADS) is another major component of an oil-soluble allyl sulfide garlic (Allium sativum) derivative. Inhibitory effects of DADS on prostate carcinoma LNCaP cells motility and invasiveness were found to be associated with increased tightness of the tight junctions (TJ), which was demonstrated by an increase in transepithelial electrical resistance (TER) [3, 4].

References:

Paul A. LaChance. Nutraceuticals: Designer Foods III: Garlic, Soy and Licorice. John Wiley & Sons, 2008. Pages 177-180.

Liu Z, Li M, Chen K, Yang J, Chen R, Wang T, Liu J, Yang W, Ye Z. S-allylcysteine induces cell cycle arrest and apoptosis in androgen-independent human prostate cancer cells. Mol Med Rep. 2012 Feb;5(2):439-43. doi: 10.3892/mmr.2011.658. PubMed PMID: 22052207.

Shin DY, Kim GY, Kim JI, Yoon MK, Kwon TK, Lee SJ, Choi YW, Kang HS, Yoo YH, Choi YH. Anti-invasive activity of diallyl disulfide through tightening of tight junctions and inhibition of matrix metalloproteinase activities in LNCaP prostate cancer cells. Toxicol In Vitro. 2010 Sep;24(6):1569-76. doi: 10.1016/j.tiv.2010.06.014. PubMed PMID: 20600798.

Bhandari P. Dietary botanicals for chemoprevention of prostate cancer. J Tradit Complement Med. 2014 Apr;4(2):75-6. doi: 10.4103/2225-4110.130371. PubMed PMID: 24860728.


text:
Does DNA replication in 5' to 3' (leading strand) need RNA primase?
https://www.youtube.com/watch?v=27TxKoFU2Nw
In the above video it shows that during DNA replication, the lagging strand require RNA primase to add 3' -OH group for further addition of nucleotides. However, it hasn't been shown that the above strand ( leading strand) require it.
Besides, RNA is needed to initiate the polymerization because it has the 3'-OH.
But when I look at the structure of deoxynucleotide, it also has the 3'-OH but it does not have the 2'-OH. So why DNA cannot initiate the polymerization?
Thanks for your answer!

The DNA polymerase also needs a RNA primer on the leading strand to be able to start polymerization. Afterwards this is not needed anymore, since the replication goes on without a break. On the lagging strand polymerization replication can only work between the replication fork and the next region of double-stranded DNA. See the figure (from here):

The reason for the need for RNA primers is located in the function of the enzymes. While the DNA polymerase can only work on a double stranded template (add nucleotides to the 3'OH-end of the strand) the DNA Primase (actually an RNA polymerase) can work on single stranded targets and thus add the RNA primer there.

I see! DNA primase cannot work in double stranded template. Thanks a lot.


text:
What is the smallest known organism with a skeleton?
See question title. After doing some looking around on my own I haven't found much so I figured I'd ask some experts.

What kind of skeleton?

what he's asking is if you are talking about bones or including chitin (insects and things like crabs and shrimps) or other exoskeletal structures?

Shall we include the cytoskeleton?

further information http://en.wikipedia.org/wiki/Smallest_organisms

The smallest vertebrate is the male Photocorynus spiniceps anglerfish at 6.2-7.3 mm, females are over 50 mm. Schindleria brevipinguis is 6.5-10 mm, and Paedophryne amauensis is 7.7 mm. Paedocypris progenetica is 7.9-10.3 mm.

The smallest vertebrate (if that's what you mean; there are many invertebrates with endoskeletons that are not made of bone) is Paedophryne amanuensis, a Papua New Guinea frog that's about 7 mm long.

do you have a reference for this?

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0029797

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


text:
Why do I still see a bright light after looking directly at it?
When you look directly at a bright light, maybe accidentally when looking at the sun, the shape of the image may persistently be perceived even after you look away.
Does this image persistence have something to do with the light hitting the back of the eye and leaving an imprint, or is something else going on?

What do you know about the retina and sight? If you know, share. If you can, try to find an answer and share that, too. That way, we don't have to explain from the ground up, which would take a very long answer.

@anongoodnurse oh ok

@anongoodnurse - you're totally right but I couldn't help myself answering O.o

@AliceD - I know; this is one of your areas of expertise. ;) And an optical example, too!

@anongoodnurse - biased to the bone

Short answer
The effect you describe is called a negative after image. It can be explained by adaptation effects of the photoreceptors in the eye.
Background

source: Dresden University
Steadily fixate on the black lightbulb for thirty seconds or more and then immediately turn your gaze to the white region on the right. The illusionary glowing white bulb you perceive after fixating on the black picture is called an afterimage.
When the eyes and hence the photosensitive layer therein, the retina, is focused on an image, light-sensitive photoreceptors in the retina respond to the incoming light. In turn, secondary neurons carry the information to the brain via the optic nerve. When photoreceptors are continuously activated, they become desensitized (or fatigued); it is said they adapt to the stimulus (Kalloniatis & Luu, 2012).
Adaptation occurs at multiple stages in the visual system. One of the important processes behind visual adaptation in this example is photopigment "bleaching" due to constant stimulation. The desensitization is strongest  for cells viewing bright stimuli and is caused by the photopigments in the photoreceptors being all used up after continuous activation.
Back to the light bulb illusion above: photobleaching is strongest for cells that were activated by the bright parts of the image, but weaker for cells viewing the darkest part of the figure. Then, when you avert the focus onto the white screen, the least depleted cells (the ones not adapted) will respond strongly, while the adapted cells will be unresponsive. hence, the retina focused on the black light bulb will respond vigurously, while the more peripheral parts of the retina that received the white part of the image surrounding the bulb will be silent. Hence, a glowing light bulb will be perceived in the after image.
This particular phenomenon is called a negative afterimage, in which bright areas of the figure turn dark and vice versa. This will happen when looking for prolonged periods of time to a certain image (this answer), or when looking directly in very bright sources like the sun (as in the question). Positive afterimages also exist, but do not apply to this specific question.
Reference
- Kalloniatis & Luu, Light and Dark Adaptation. In: Webvision (2012). Utah University

It's also worth knowing that photoreceptors are technically activated by darkness, from a physiological point of view. Light hyperpolarises the photoreceptor, which reduces neurotransmitter release.
Fatigue and photobleaching still occur, but it's the time taken to restore neurotransmitter release that leads to the afterimage.

Interesting notes, but could you add sources?

The original article's a bit old: 1979, here's a more up to date review.


text:
What is the name of this series?
My biology teacher used to show us videos (actually animations) on the human immune system. What I remember is that one video was on a virus (represented as a purple colored sphere with spikes) that a woman (who is a part of a music band) inhales in an elevator when a man sneezes.
The documentary shows how the virus travels to her throat and enters one cell, multiplies, and spreads. Then the video shows how white blood cells and T-cells defend the body. In the end, when she drinks coffee, she leaves the virus on a coffee mug and her friend takes on that virus when he drinks from the same mug.
Other videos of the same series include a documentary on fractures, another one on obesity, another one on a disease transmitted when one eats chicken, etc. Can someone tell me what is the name of that series?
I think (not sure) it is a national geographic series?

This question is off-topic as it is not about biology but about a video documentary. This question would be put on hold. In future, if you have such questions please use the chat.

belongs on tv&movies stack exchange

Link to meta; as it serves an educational purpose in Biology I consider it to be on-topic.

The Body Story.
--Have to add some characters for the system to be happy--


text:
Relaxing Eyes when using Virtual-Reality-Glasses?
Accommodation is the process by which the vertebrate eye changes optical power to maintain a clear image or focus on an object as its distance varies (eye focusing). For distant vision, the ciliary muscle must relax and the eye’s crystalline lens is stretched out.
When using a Virtual Reality Device (Occulus Rift, Samsung VR, Sony VR, Google Cardboard etc.) the eye has to focus on the screen that is only a few centimeters away from the eyes. I am aware of the Vergence-Accommodation Conflict. Yet I ask myself,
Is the ciliary muscle relaxed or contracted when looking at a (virtually) far distant object projected on the LCD of the VR-Device?

The eyes cannot focus on something a few centimeters away. The average maximum distance where the eye can still focus is 14 Diopters in young people (Duane, 1922) (approximately 7 cm in 8-year olds). The distance to the eyes of the display in a head-mounted display (HMD) is often less than this and hence the eyes cannot possibly focus on this. Instead, with the use of lenses, a virtual image is created at a virtual distance approximately a meter away (Fig. 1). In the Oculus Rift DK1, for example, the virtual screens were infinitely far away; in the Oculus Rift DK2, they are about 4.5 feet (1.4m) away (source: Immersive Computer Graphics). One meters is a comfortable viewing distance with minimal accommodation needed and hence little eye strain (source: Immersive Computer Graphics). At around 6 meters the eye is unaccommodated.

Fig. 1. Virtual image in a HMD. Left: eye failing to focus on a very close real screen. Right: eye able to focus on the virtual image of the same real screen created by an interposed lens. source: Immersive Computer Graphics
Reference
- Duane, Trans Am Ophthalmol Soc (1922); 20: 132–57

Did you notice that the image you've posted gives an optical illusion when scrolling page up/down?! Or is it just me? ;)

@another'Homosapien' - wow! I hadn't noticed :D


text:
How many mosquitoes would it take to "drain" enough blood to put a person into shock?
I'm just curious, how many mosquito "bites" (mosquitoes which have removed blood from a person) would it take to remove enough blood to put a person into shock? (Putting aside all reasons why it wouldn't happen, how many would it take?)

I don't have any mosquitos on hand to test this, but lets assume an average mosquito has a carrying capacity of 50uL of blood. If the average human has 8L of blood, 8 million uL / 50uL is 160,000 mosquitos. That's probably a decent first order approximation. I don't know how much blood a person has to lose before they go into shock, and that 50uL per mosquito estimate is based only on what I remember a full mosquito looking like, but I've never been good at measuring volumes by eye.

@user137 I don't know about your mosquito numbers, but 8l of blood sounds very unusual. I've always thought that the average is 4-5. Else, good starting point for the calculation.

@rumtscho You're probably right, I just remembered hearing somewhere that a human had 8 quarts of blood and 1 quart is about 1L.

@user137 Chris's approach sounds right - estimating the amount of blood based on body weight. Maybe you encountered the 8 quarts figure in a text on obese patients. I already thought after leaving the comment "wait, there's no way everybody has the same amount of blood".

@user137: maybe you saw "8 pints", a volume I've seen offered before. However, those are Imperial pints, a US pint is sufficiently smaller to matter. Even a "finger in the air" estimate in US pints should be 1 bigger than a UK estimate :-)

This question falls into different subquestions:
1. How much blood does a mosquito take when feeding?
This is not so easy to answer, but there are publications which measure the volume of different mosquito species. Reference 1 lists volumes between 2.85 and 11.99µL per meal and mosquito. Reference 2 lists 3.07 and 5.71µL. To make the approximation a bit easier, let's assume that mosquitoes drink about 5µL per bite (which should be near enough).
2. How much blood does a human have?
According to Wikipedia, humans have around 77mL blood per kilogram of body weight. If we take a 70kg human, we get around 5L of blood.
3. How many mosquitos does it take to get a human into shock, and how many to suck him out completely?
According to the Medline, Hypovolemic shock occurs when a human loses about 1/5 (or more) of his blood volume. 1/5th of 5L is one litre. Since each mosquito sucks 5µL, this would take about 200.000 mosquitoes. To suck out all blood would take 1 million mosquitoes. (This is not possible since mosquitoes depend on an existing blood pressure, as reference 3 shows. If a capillary is empty due to massive blood sucking, they change to another.)
Besides this theoretical (but interesting) calculation, there are some real problems about getting biten by so many mosquitos. First, this is a question of available skin. The human skin is about 2 square meters in size, which would require 100.000 bites per square meter. To break this down further, a square meter has 10.000 square centimeters, so there would be 10 mosquitos which need to bite you per square centimeter. Rather unlikely.
Then each mosquito injects a mix of anti-coagulants, pain killers etc. prior to sucking to keep the blood from clotting and also to make sure you won't notice the bite immediately. As pointed out in the comments, this would already cause a lot of trouble and probably cause massive bleeding, since the effect of the anti-coagulants would sum up when biten by thousands of mosquitos. Additionally the body reacts by releasing histamines and since the amount would also be massive, this would cause real trouble and probably kill you.
References:

Regulation of blood meal size in the mosquito
La Crosse Virus Infection Alters Blood Feeding Behavior in Aedes
triseriatus and Aedes albopictus (Diptera: Culicidae)
Visualizing Non Infectious and Infectious Anopheles gambiae Blood
Feedings in Naive and Saliva-Immunized Mice

Great detective work Chris!

This reads like http://what-if.xkcd.com.

This question would clearly fit there. My drawing skills are less developed, though. :-)

I wonder whether the anticoagulants from 200K mosquito bites would cause more problems than the loss of blood.

@JeremyStein: indeed, it seems likely you'd be poisoned somehow before passing out from blood loss. The histamine system would be berserk, for example. Fortunately that's not the question ;-)

@JeremyStein I have been wondering about this myself, but had no time yet to follow this up.

there would be 10 mosquitos which need to bite you per square centimeter. Rather unlikely. Doesn't seem unlikely at all, assuming that they don't all have to be there at once. If a mosquito drinks for 5 minutes at a time, then one mosquito per hour per cm^2 would do it.  Images like this one from the Alaskan Arctic make that seem quite plausible.

Everyone seems to forget that the human body replaces blood that is lost quite rapidly. When I donate blood to blood bank they take half a liter or something and I was informed my body will replace it within 30 minutes, I just need to drink plenty of fluid after.
I think it would take a fairly concentrated effort by mosquitoes to do any damage from blood loss.

Nope, this is wrong. Otherwise blood transfusions would not be necessary, you would only have to supply enough liquids. It takes several days to weeks to fully replace it, see for example here.

It takes several weeks to replace the red/white/platelets yes, but the blood volume is replaced much faster as it is mostly comprised of water.

Hi welcome to Bio.SE! Please provide reputable sources to back up your claims. Anecdotal evidence should be reserved for comments or as supplement to claims supported by trustworthy citations. We ask that all answers on this site provide support, and failure to do so will result in your answer being downvoted or closed. Thanks!