text:
Why does a light object appear lighter in your peripheral vision when it's dark?
So, I am not sure I can reproduce it via images, but the steps are:
1) At night, open a window and have a look at the surface of the earth
2) Suppose there's an object that reflects a tiny amount of light
3) When you actually try to focus your eyes at this object, you either don't see anything (depends on the amount of light it reflects) or you can hardly see it
4) When you focus your eyes on something that is 3-10 metres away, you can easily see this object with your ambient vision. Not the details, but it seems that it reflects more light.
Why does it happen?

An evolutionary development to 'see' better in the dark, not only light objects but movement!

Short answer
Peripheral vision is more light-sensitive than central vision.
Background
When you look directly at an object the image is projected onto the fovea. The fovea has maximal visual acuity (high resolution) and a high density of cones, which are specialized photoreceptors to sense colors. However, cones are not very sensitive to light.
Here is a picture showing the foveal field of view:

Source: Pinhole Eyeglasses
If you look at the same object using peripheral vision, the image is formed more eccentrically on the retina. Here, cones are sparse, but high densities of rods are present. Rods do not detect color, but are much more sensitive to light than cones. In fact, they can faithfully detect a single photon! (Webvision) Moreover, many rods converge onto a single ganglion cell, and rod responses are therefore summated. This spatial  summation further increases light sensitivity in the periphery, but degrades spatial resolution.
Here is an image on rod and cone distributions on the retina, showing a high cone-density in the fovea and a high rod density more eccentrically:

Source: Webvision
And here is an image showing the higher light sensitivity of rods over cones:

Source: Webvision
Hence, peripheral vision is more light sensitive because: (1) there are more rods in the peripheral retina; (2) rods are more light sensitive; and (3) eccentric retinal rod circuitry further amplifies the rod responses. However, color perception and spatial resolution are better developed in the central field of view.

Further reading (Cognitive Sciences.SE)

Rod and cone distributions: "Why can we not see around our point of focus of our eyes?"
Visual acuity as a function of retinal eccentricity: "Visual acuity and offset stimuli"

One of the absolute best answers ever, Alice!  I just wanted to add that peripheral vision is a critical survival mechanism that humans have forgotten how to access and use.  Like you have explained so perfectly, we are able to see more in the dark using our peripheral eyesight as well as detect movement far better.  People need to learn "owl eyes" versus "eagle eyes".  Focusing on one spot is eagle eye.  When focusing on one spot one loses their peripheral vision to a large extent.  By allowing one's focus to soften changes eye sight into 'owl eyes'...they use their peripheral vision better.

@stormy - thanks a lot for your words and your comment.


text:
How does a fetus retain a blood group different from its mother?
It's a well-established fact that blood group is decided by genotype. But, when a new child starts its journey in the womb, the mother's blood (along with it's agglutinins and agglutinogens) flows into the baby's heart. So, how does a baby (having a blood group different from that of the mother) retains it's own blood group (with it's own agglutinins and agglutinogens) instead of the mother's blood group, which moves in and out of the baby through the umbilical cord.
Do both kinds of blood flow in the baby's body constantly in such a case?
Apart from that, I know of rhesus incompatibility. But there are also incompatible blood group types. How does a baby survive agglutination in those cases?

maternal circulatory system is separated from fetus in the womb

What happens before then? And answer my second question if you can.

I mean, if there's Rh incompatibility, there's gotta be interaction between both types of blood. So how come nothing unusual happens when incompatible blood groups interact with each other, but agglutination occurs due to Rh incompatibility?

Rh incompatibility is due to fetal blood which escapes into the maternal circulation during delivery. It does not occur always and depends on labor conditions. There is absolutely no mixing of fetal and maternal blood otherwise.

I see. Then, when the fetus doesn't have any blood within at first (after fertilization); how does the blood come into it's system for the first time? Is it the bone marrow?

Note also that Rh-incompatibility is most often an issue with second or later pregnancies, after antibodies have been formed during earlier pregnancies, see e.g. http://www.nhlbi.nih.gov/health/health-topics/topics/rh for more. @CRags

Fetal heart starts beating at 4 weeks. The fetal blood cells are formed in liver, spleen, yolk sac. Very little gets formed from bone marrow proper

@CRags I suspected that, and my comment was mostly directed to the OP.

So lemme get things straight, RBCs present in the baby comes from the baby's liver, spleen, yolk sac and it's own system; and not at all from the mother. So, apart from yolk sac, those other two starts functioning even before the heart starts beating and starts pumping blood!!! Unbelievable...

The maternal and fetal blood circulation systems are completely separate. The embryo's blood cells start developing at around week 5 gestational age (3 weeks after conception), the same way any other tissue is developed by the fetus itself. By around week 7 gestational age, a circulatory system has developed and the heart has started beating.
All nutrition goes through the placenta, which keeps the two circulatory systems separate by the so-called placental blood barrier.
Rhesus incompability is only a concern after the first birth (or miscarriage) because then the maternal and fetal blood had the opportunity to mix and lead to the mother developing antibodies.
Also, as AMR pointed out in the comments, blood group incompatibility is mediated through IgG antibodies - those don't start to be produced at all until birth and at higher levels not until six months to a year after birth. See also At what age do babies begin to synthesize their own antibodies?

I wrote the answer before reading that there are already comments answering the question :-/ Still, this shouldn't be in the list of unanswered questions.

You may want to add that the fetus does not develop the ability to produce antibodies until around six-months after birth, so even if the mother's RBC's did circulate in fetus, they wouldn't be producing antibodies against them and by the time they started to, all the maternal RBCs would have degraded. Fetal blood crossing to the mother would be far more relevant as the mother would make antibodies against it which you mention with your last paragraph about first birth or miscarriage.

@AMR good point, thanks! Though, I think six months is too late - isn't it way earlier?

Class switching takes a while. "After birth, the production of IgM starts almost immediately; the production of IgG, however does not begin for about 6 months, during which time the total level of IgG falls as the maternally acquired IgG is catabolized." - Janeway's Immunobiology 8th Edition.

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sort: votes


text:
Do both ends of a muscle contract?
I was under the impression that both ends of a muscle contract. For instance, the fibers of the biceps run parallel to the humerus so I thought they pulled toward the middle.
But now I'm confused because it sounds like the contraction of the fibers doesn't necessarily have to parallel the motion of the muscle itself. In other words, just because the fibers contract doesn't mean that the muscle lengthens or shortens in a particular direction.
Can someone clarify if muscles contract in both directions?
Or perhaps a better question is do muscle contract in a particular direction and is this the same direction that the fibers contract or does the muscle as a whole move in a different direction in comparison to the direction the fibers are contracting?

fibres contract towards their centre thereby generating equal force on both ends.

Thank you! I have been using that assumption for years so I'm glad to know it's correct.

The nerves link to the muscles at the center. So contraction is from center to periphery. So the upper half and lower half contract in opposite directions.

The muscular fibers (or more exactly the actin and myosin filaments) are contracted towards each other. This makes them "move to the middle" and you build up a force on both sides of the muscle. See this image (from the Wikipedia), which illustrates this process:

There is also an animated picture available, which illustrates this process even better (from here):

The process of the contraction applies a equal force to both endpoints of the muscle.

I like the moving GIF! Nice answer overall +1

@ChrisStronks I sometimes regret that we cannot embed videos. Sometimes moving pictures make things easier to understand.

Man, when following Biochemistry and Human Biology classes I struggled for hours at those static pictures of filaments doing wacky stuff. This tells it all in one glance :)

It is difficult to understand what happens at the full muscle level with this description. But the OP is asking about that

@Chris wait for HTML5. It would be much easier to embed videos then.

The above answers are correct, I just want to add a distinction between the different muscle types.
There are 3 types of muscle tissues:

Skeletal muscle (locomotion)

Striated
Voluntary

The skeletal muscle has visible striations under the microscope, because the myofilaments are aligned: they are all parallel. During contraction, the thin filaments slide over the thick filaments - at the end of the contraction the Z lines will be closer together. The filaments stay the same length, they just slide over one another, shortening the muscle. The muscle doesn’t contract by “going” in a particular direction, it shorts everywhere and the alignment of the filaments enables the muscle to shorten in only one dimension. The muscle is connected to the bone by tendons. When it shortens, it pulls on the tendons which pull on the bone, bringing it closer. A skeletal muscle cell can be up to 30cm long (Sartorius muscle).

Cardiac muscle (in the heart)

Striated
Involuntary

Cardiac muscle cells are very similar to skeletal muscle cells, however the fibers are interconnected via intercalated discs, which enables them to work in an even more synchronized way.

Smooth muscle (in the vascular system, the gastrointestinal tract, etc.)

Not striated
Involuntary

Smooth muscle filaments aren’t as organized as the ones in skeletal muscle. Therefore, the shortening can occur in all directions within the cell. It results in the shortening of the cell in more than 1 dimension.

Also, many organs such as the stomach have more than one layer of smooth muscle, providing constriction in many different “directions” (longitudinal layer, circular layer and oblique layer).

Muscles do contract in both directions. To understand this better you need to know few things:

The smallest unit of a muscle is called myofiber or a muscle fiber. It is basically a multinucleated elongated cell. Each muscle fiber is covered by a layer called endomysium
A bunch of myofibers arranged linearly is called a fascicle. The fascicles are covered by a sheath called perimysium.
A muscle as you see in a cadaver or a picture is a group of fascicles surrounded by epimysium.

source: classconnection
A single muscle fiber is made up of numerous myofibrils which are basically the sarcomere arranged side-by-side.
The junction between the neuron and muscle fiber is called motor end plate. A single motor neuron innervates a group of muscle fibers. The whole assembly of muscle fibers innervated by the axon from one neuron is called a motor unit
The Key:
The key to understand muscle contraction on a macro level is in the fact:

Typically, an axon makes a single point of synaptic contact with a skeletal muscle fiber, midway along the length of the muscle fiber.1

So when an action potential arrives at the neuromuscular junction (another name for end plate), the muscle starts depolarising and contracting from the center towards the periphery. In other words both the ends of the muscle contract toward the center.

source:encrypted-tbn1.gstatic.com. Image has been cropped and edited to illustrate the point
tl;dr:
Every skeletal muscle contracts toward its center, such that the proximal and distal ends act in opposite directions causing tension generation. The proximal end pulls the tendon down and the distal end pulls the tendon up thus generating tension.

1: Medical Physiology A Cellular and Molecular Approach, 2nd Edition, Boron and Boulpaep p.217

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text:
Chromosome and chromatid numbers during cell cycle phases
A diploid cell in G1 has 6 chromosomes. How many chromosomes and how many chromatids are present in each of the following stages?
Here is what I am guessing

G1: 6 chromosomes ; 6 chromatids
G2: 6 chromosomes ; 12 chromatids
Prophase: 6 chromosomes; 12 chromatids
Metaphase: 6 chromosomes; 12 chromatids
Anaphase: 12 chromosomes; 12 chromatids
Telophase: 12 chromosomes; 12 chromatids

The chromosomes copy at S phase. So S/G2 checkpoint up to early anaphase has 2n. You are on the right track to understanding the cell cycle, important to note the differences between homologous chromosomes (homologous pair) and sister chromatids, while understanding  ploidy.
During S (synthesis) phase which occurs between G1 and G2 , all the somatic DNA replicates. So every chromosome gets copied and thus  has a sister chromatid.
Animals that undergo sexual reproduction have 2 sets of chromosomes, one from mom the other from dad. The chromosomes of each pair represents homologous chromosomes.
Your answer is almost correct. I believe it could be adjusted to:
G1: 6 chromosomes
G2: 6 chromosomes /12 chromatids Prophase: 12 chromatids
Metaphase:  12 chromatids
Anaphase: 12 separating chromatids
Telophase: 12 chromosomes, 6 one each pole of the cell
These very simple figures explain the principles I mentioned earlier

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text:
What is the expected number of children that need to be born for every possible point mutation to occur once?
I'm reading The Perfect Health Diet, and in it the author says that the probability of a point mutation is (175/3*10^9) per new child. He then goes on to write:

In the Paleolithic, with 100000 children per generation, it would have taken 8000 generations, or 160000 years, for each possible mutation to occur once.
Today, with more than a billion children per generation, every possible point mutation now appears about twenty times per generation, or almost yearly.

Using his probability, I get that you need 1 / (175 / (3 * 10^9)) (which is about 17 million children). But he writes that for the Paleolithic era, you need 10000 * 8000 = 80 million children! Can someone help me reason out how he got that number?
EDIT
My math was wrong :-) leaving up the og calculation. Here's the reference that he cites:
"Estimate of the Mutation Rate per Nucleotide in Humans" by Michael W. Nachman and Susan L. Crowell
In the abstract they write "The average mutation rate was estimated to be 2.5x10^-8 mutations per nucleotide
site or 175 mutations per diploid genome per generation."

Does he give a reference for this mutation probability? I remember smaller numbers.

This is assuming that mutation rates are constant across the genome, which is generally not the case (see e.g. Smith et al. 2002. Deterministic Mutation Rate Variation in the Human Genome). So I think the statement/calculation rests on unfounded assumptions, and therefore vote to close as "primarily opinion-based".

The authenticity of that text seems doubtful.

I added the reference that he cited.

I don't think the book's reasoning is correct.
There are about 3 billion base pairs in the human genome, but only ca 25.000 protein-coding genes. From the top of my head, I recall that each child has about 30 mutations. If that's in the total genome and if they were all point mutations and there's 4 options for the base pair, then we have $30$ mutations out of 12 billion options in each child. So that each possible point mutation has a probability of $30/12 \text{ billion} = 2.5 \times 10^{-9}$ or $1/(2.5 \times 10^{-9})$ if you like. The book's number is 23 times larger but in the same ballpark range. Lets call this probability $p$.
Now the probability of a mutation occuring in n children at least once is equal to one minus the probability of it never occuring in n children. In other words:
$$1 - (1 - p)^n =$$
$$1 - (1 - 2.5 \times 10^{-9})^n =$$
$$1 - (0.9999999975)^n$$
If we want the mutation to occur with probability 95%, we have to solve:
$1 - (0.9999999975)^n = 0.9$
This has the solution $n = 1 \times 10^9$
In other words, with 1 billion children, each point mutation has a 95% probability of having occured at least once. Mathematically this is not the same as saying that every mutation will have occured. In fact, this implies that 5% of the mutations will not have occured. But perhaps surprisingly, we only need 4-5 billion to up the chance to 99.999%. That still leaves out thirty thousand point mutations, but is sufficiently close to "everyone".
Compare this to the numbers you mentioned:
n = 17 million gives each gene a 4% chance of occuring
n = 80 million gives each gene an 18% chance of occurring.
Secondly, a mandatory rant. :-) "The Perfect Health Diet" is written by Paul and Shou-Ching Jaminet, an astrophysicist and molecular biologist respectively. This has the potential to marry the physicist's penchance for oversimplification with the biologist's lack of mathematical prowess. We see both in the passage you ask about. A shoddy calculation about an oversimplification of what mutations and evolution is about.
Both the book's dustcover use of a word like "detoxifying" and mention of how diseases spontaneously resolve if you eat right, are both strong crackpot indicators. It's the kind of thinking that killed Steve Jobs because he didn't seek medical help soon enough but tried to eat his way out of his illness.

There are not 4 chances for each basepair, but only 2. We are diploid, not tetraploid.

@chris: I was thinking of the 4 bases A, T, C, G. But maybe that should be counted as two too..

Thanks for busting my 2AM calculation :) nice explanation


text:
Why can good music raise goosebumps?
Listening to really good music right now, I was wondering why it raises goosebumps.
Is there any physiological reason for this reaction to specific wavelengths or something?
EDIT:
Due sometimes strong vibration, roadwork for example,  raise goosebumps too I reckon it's about the wavelengths but if someone could explain what is happening and why, that would be great.
CROSS-POSTED

I hope this is the correct SE, music.SE is not i guess.

It may be on-topic here, but Cognitive Sciences.SE may also be worth considering - feel free to cross-post.

Chris makes a good point here but I do like this question. Check this information out seems like this is an active field of study (ie how it results in a sympathetic response).  http://www.exploratorium.edu/music/questions/goosebumps.html

Just read this...  http://www.nature.com/neuro/journal/v14/n2/abs/nn.2726.html

It's a phenomenon called Frisson.  From the wikipedia page.

Frisson (French for 'shiver') is a sensation somewhat like shivering, usually caused by stimuli. It is typically expressed as an overwhelming emotional response combined with piloerection (goosebumps). Stimuli that produce a response are specific to the individual.
Frisson is of short duration, usually no more than 4–5 seconds, usually pleasurable.1 Typical stimuli include loud passages of music and passages that violate some level of musical expectation.[2]

There is some interesting research that shows it occurs when a sound contains certain chords or has certain notes because of how our biological setup reacts to those specific notes.  See the "crying chords" that were supposedly present in Adele's song "Someone Like You". npr article about crying chords

This is an emotional response which elicits a physical response. All emotions stimulate the hypothalamus, a part of the brain, which controls responses such as goose bumps, increased heart rate, and sweating. With goose bumps, the hypothalamus is sending messages through the nerves to contract muscles in the skin, in effect creating 'goose bumps'. More chemical research needs to be done to further understand the pathways of emotional responses to music.

can you come up with some analogy, for example, to behavior of other animals? It seems that as is your answer is too non-specific, would be cool to add details


text:
Superhuman eyesight
My ten year old son was reading car number plates that were too fast, too far away and at the wrong angle for any of us to read or even believe that it was possible for him to read. We thought he was lying as he reeled off the whole number plate and not just some. My husband went across the road to prove him wrong and get him to admit he was making it up but he wasn't. We even asked people in the restaurant and waiting staff for their opinion and everyone was blown away. I'm totally astonished and slightly freaked out by his sight and I'm hoping someone can explain for me.
Specifics

I believe it was approx 20-25 metres away and I am under guessing.
He had only 1 or 2 seconds as the cars drove left to right.
Cars would be travelling 30/40 kmph along that road.
We were sitting in the restaurant at night time so not in a car
ourselves

Why is this off-topic or unclear? Please comment and we can work on the question. Aging is a hot topic in Bio.

You should provide additional details about approximate distance and speed of your car relative to other cars and size of the letters. Otherwise it would be difficult of anyone to ascertain if that was really an above-average perception.

He could perhaps be far-sighted.  How does he do with close-vision tasks like reading?

Thank you for all your responses! I believe it was approx 20-25 metres away and I am under guessing. He had only 1 or 2 seconds as the cars drove left to right. Cars would be travelling 30/40 kmph along that road. We were sitting in the restaurant at night time so not in a car ourselves

@Claire the distance may have helped with the speed - something further away has a lower angular speed and so is easier for the eyes to track (think of an airplane in the sky that is moving hundreds of mph but is very far away)

If memory has anything to do with it, I'll call - with high statistical sensitivity over specificity- Aspergers!

@jamesqf he is not as fluent with his reading as his 8 yr old sister although he can read and doesn't have trouble with pronunciation. I put it down to a girl/boy development thing....I have just booked an eye test because everyone's valuable comments are making me think about all possibilities....

@hello_there_andy memory?? Not in the case of the other night as it was there and then however he has an absolutely amazing memory too? He remembers things that he has seen that most people would not even bother to notice, ie that car (recollecting colour, model and plate) is always parked there, or, that lorry was the one that we saw driving down the highway when we were on our way to 'xyz' and it was raining really hard and u had a blue top on mum.....two yrs ago! Are you suggesting that eyesight and memory are an indication of aspergers?? I know little a out aspergers, maybe I should read

@Claire it really is a long-shot and I fear of making a hassle and run into a common cognitive bias related to self-diagnosis (see wiki: labeling theory). I'm a strong believer that society and expectations of people with disorders hinders them (see wiki: Daniel Kish for inspiration on what Humans can do w/o social expectations).

@hello_there_andy just briefly read symptoms for aspergers and there is not one symptom that I could say is possibly apparent. He's advanced beyond his years socially and has been from an early age, motor skills- fine, rides quads and bikes and horses from a young age...above average academically and extension in lots of subjects too. The only thing with social or behavioural interaction is his frustration at others and often not handling situations calmly enough?

I know what you mean, it appears that there are so many labels on lots of people compared to maybe the odd person years ago who was categorised as dyslexic if they couldn't spell and sometimes wonder what new labels will be born over the years ahead. I haven't ever felt alerted by anything enough to look into labelling for him however sometimes amazing traits such as this baffling eyesight and prob memory too, could also fall under such umbrellas as you've suggested. Maybe not aspergers but there may be another label for him!?

@Claire: I didn't mean reading ability, but reading (especially small print) as one example of a task that would require good close-up vision.  Other examples might be threading a needle, or assembling electronic parts on a circuit board.

The "normal" visual acuity in the Anglosphere is the 20/20 vision which means that on a Snellen chart characters with 8,86 mm height can be read conveniently from a distance of approximately 6 m.
Now there are many known people who have very sharp eyes, having the doubled acuity of 20/10. This means they can discern characters of only 4,43 mm height from 6m.
The normal car signs in the EU (and I think it is not very different in size in other countries) is 75 mm. So a very good observer can discern number plates from a distance of
(75 mm / 4.46 mm) * 6 m = 100 meter or 109 yards, a normal observer from half the distance (50 m or 54 yards).
People are mostly not aware how their sight is deteriorating. Chris already said that the acuity goes down with age, but the other problem is that the lens is less flexible with age and therefore not able to focus a fast approaching car. Your son has no problem with that.
Sorry, I don't think your son is superhuman.
FOR THE CURIOUS: A rule of thumb is that normal sight has an acuity of 1 arcminute ('), the 60th part of a degree angle. This is a ratio of 0.000291 or 3 cm per 100 m (1 inch per 1 yard).
A character to read consists of parts, let's look for example at E. E has five vertical
sections and if you think about it, all other characters can be displayed if you have five
sections available. So Snellen set the height of the characters to 5 arcminutes and the stroke width to one arcminute. The patient looks from 20 ft (= 6.096 m) away. So the height
of the characters must be (5*0.000291)*6.096 = 8.866 mm

That's helpful seeing the distances thank you. I believe the distance was approx 20-25 metres away.

Short answer
Visual acuity decreases with age. Your son's age is within the age range that visual acuities are best. Acuity starts to decrease from about age 45.

Background
Visual acuity (visual resolution) first increases from birth up until around 4-6 years. Note that in the following graph better acuities are represented by lower numbers (logMAR scale):

Source: Pan et al, 2009
Visual acuity starts to decrease after 45 years. The acuity of a 6-year old is about 1 on the scale in the next figure, showing the decline in acuity in older folks. Note that the graph starts at 30 years and acuities are already less than that in the former study's end point (look at the lower set of lines, i.e., the uncorrected ones). Also note that better acuities are higher up in the scale as this graph expresses acuities in decimal Snellen equivalents

Source: Gittings & Lozard, 1986
Hence, very likely, your 10-year old's vision is not superhuman (sorry!), it's just a lot better than yours. However, if you are younger than 45, we might conclude your acuity should be comparable and your son may be a visual rock-star - statistical outliers do exist and a simple visit to the optometrist will tell you! However, if you are near-sighted and are not using corrective vision aids (glasses or the likes) then this may be the cause of your lesser visual acuity.

References
Pan et al., Optom Vis Sci 2009;86:607–12
Gittings & Lozard, exp gerontol 1986;21:423-33

Thank you. Yes I am 40 which is why we asked others in the restaurant and one guy was 18 and he laughed but I hadn't thought that he perhaps had terrible vision for his age! My 8 yr old daughter also couldn't decipher even one letter either so may be more important to check hers! It was approx 25 metres away, was dark and there was prob 1 or 2 seconds for him to capture it as it drove left to right and at a speed of 30/40kmph

@AliceD, Why did you protect this thread for? It's only 2700 views.

@Pacerier - not so much because of #views, but it has received multiple good quality answers and it was drawing in low-quality answers (since deleted and hidden from your view).

He may have extreme acuity, or he may even have an extra cone type that allows him to see extra colors (and more color attunement may allow easier reading of those particular plates). But, you won't know anything for sure by asking on here. Take him to an ophthalmologist and let us know what the doc says! If you aren't 40+ and have 20/20 vision and he's seeing things better than you, then yeah, he probably is special!

Thank you for your reply! My daughter is 8 and she could just see a blur and the 18 guy sitting next to us just laughed and said no chance he could see either but yes as per other responses above, I hadn't thought that everyone else compared may have particularly poor eye sight! I think I shall pop to have his eyes tested and will post on here the results

@Claire you should get in the habit of upvoting answers that have helped, some of us crave unicorn points

@hello_there_andy......how do I do that apart from singing praises in comment box!?

@Claire Just click the up arrow at the top left of the answer - but you need to collect some amount of points yourself first - so maybe it does not work yet - there would be a message explaining it when you try. You have 36 points "rep" ("reputation") currently. Three upvotes on your question would get you to 51, for example.

A functional male tetrachromat has yet to be found.  Finding one might count as "superhuman" vision, as much as any trait possessed by a human could be called such.

Hi everyone that kindly commented on my question a month ago. I have been to the optometrist this afternoon as suggested with my son and she has confirmed that he has 20/10 vision.


text:
Can DNA & RNA be considered as nature's programming language?
The final frontier of Biological Sciences could be considered understanding the effects of variation in the DNA (and RNA).
If after fertilization the DNA of the zygote could be genetically engineered to prevent complications occurring later in the life of that human being, it could become the ultimate medicine.
Also, we know that (in humans) only 2% of the genome encodes genes that are translated into proteins; is the rest required for function?
Can DNA & RNA be considered the ultimate blueprint of all living organisms?

Answers to your main question (the bold part at the end) will to a large extent "primarily opinion-based" (and speculative). The relationship between DNA/RNA and the functioning of organism is also a very broad topic. I think you should try to ask several narrowed down questions instead.

Will you answer my title as an yes or a no?

"...all other fields in Biology is just beating around the bush" - tsss...

Was literally just writing an answer :/ in my eyes there is nothing opinion-based about this (although the question could be phrased better): classical molecular biologay says DNA makes RNA makes Protein. Whilst this is true, less than 2% of the genome is protein-coding, with the rest coding for regulatory regions and non-coding RNA molecules (often with important functions of their own). So whilst in some respects DNA could be considered the 'code' for organisms, it is much more complicated than this: each cell of an organisms has the same genetics but different phenotypes, so clearly ...

... there is more at work than simply the DNA. This field of regulation and differentiation concerns epigenetics, which are modifications to the DNA that do not change the genetic sequence, and is to some degree hertiable. Therefore it is incorrect to say that DNA alone makes an organism, and it is incorrect to say that other fields of biology are just beating around the bush - there are many more factors at play than just the genetic code.

Hi @a.aniq I have made some edits to your question, to give you an idea of how a question might be structured (i.e. remove anything subjective - clarified meaning); but there are still massive assumptions that you made that I have left in - if you do a little research to clarify your own understanding and substantiate some of your assumptions with sources this question may qualify for re-opening and one of us can provide you with a much more detailed answer :)

@Luke You wanted to answer this question; would you convert your comments to an answer?

"Can DNA & RNA be considered as nature's programming language?" Yes. It is Turing complete.

This question can't be answered with a simple yes/no, but I would say that the analogy of DNA being the "code" used by cells is a reasonable one, if taken with a number of other considerations.
DNA function
When Watson and Crick first described the structure of DNA (being a double-stranded sequence  of the nucleotides Adenine, Cytosine, Guanine and Thymine) this led to what is known as the Central Dogma of Molecular Biology [1], which posits that DNA makes RNA makes Protein (figure from [2], as originally produced by Watson).

As you correctly point out, less than 2% of the genome is protein-coding, however our understanding of the rest of the genome is increasing manifold due to projects like ENCODE [3], which are discovering not only the "regulatory" regions that control the expression of protein-coding genes, but also the discovery of non-coding RNA's, many of which are totally uncharacterised [4].
The point of this section is to clarify that although only 2% of the genome codes for protein, it is incorrect to say the rest is "junk" or non-functional. The Central Dogma described above is now an outdated model - certainly some DNA makes RNA makes Protein, but not all; many RNA molecules are functional in their own right.
You could argue that proteins and non-coding RNA molecules are the product of "scripts" in the DNA that are run or performed by cells, although you are unlikely to find any genomic scientists talking in these terms.
Epigenetic control
Where the analogy breaks down is that all* the cells in an organism have the same genome, yet they are vastly different to one another. These differences are due to epigenetic processes, which are described as non-coding modifications to the DNA that affect expression of transcripts. A basic overview can be found here [5].
These modifications come in several forms and include:

DNA methylation

the addition of a methyl-group to cytosine nucleotides that can affect binding of transcription factors etc,

Histone modifications

DNA is actually a 3-dimensional structure, and is wrapped around proteins called histones, which wrap together to form chromatin and the characteristic chromosomal structure.

The availability of DNA to transcription factors is completely dependent on these modifications to the DNA, which are specific to individual cell types and prevent retinal cells, for instance, expressing liver enzymes. (Below figure from [6])

Overview
In short, genetics and the DNA sequence can certainly be thought of as the blueprint for an organism - changes to this sequence can profoundly affect phenotype - however it is too simplistic to imagine that the sequence alone provides all the information needed.
Not only are there many non-coding molecules essential for functioning in cells, there is exquisite control over expression by DNA modifications that do not affect the sequence of nucleotides and are essential for cellular differentiation.
The ENCODE (Encyclopedia of DNA elements) project [7] is making headway into the interpretation of the non-protein-coding elements of the DNA, but there is still a long way to go.

* not quite all, for instance B-cells have a hypervariable region to enrich antibodies for variation [8]

http://www.ncbi.nlm.nih.gov/Class/MLACourse/Modules/MolBioReview/central_dogma.html
http://sandwalk.blogspot.co.uk/2007/01/central-dogma-of-molecular-biology.html
ENCODE Project Consortium, “The ENCODE (ENCyclopedia Of DNA Elements) Project.,” Science, vol. 306, pp. 636–640, 2004. PMID: 15499007
http://www.nature.com/encode/threads/non-coding-rna-characterization
http://www.whatisepigenetics.com/fundamentals/
http://www.eusem.com/main/CH/epi
http://www.genome.gov/encode/
http://www.anaptysbio.com/technology/somatic-hypermutation/

Quite a comprehensive answer :)

This is an excellent answer from the biology side (which is appropriate since this is a biology site), but perhaps more could be said from a CS perspective. In particular, I think it's important to distinguish between DNA's self-regulatory mechanisms (e.g. TATA boxes) and fully Turing-complete coding languages. There's a strong distinction, I think, between the epigenetic mechanisms necessary within organisms and the hardware capabilities used to run computer code, and this is probably most clear once it's recognized that DNA is very unlike Turing-complete computer languages.

I was somewhat busy all these days, and I didn't even imagine this question of mine would get such an elaborate answer. Thanks for answering my question.


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Can genetically engineering the DNA of a human zygote, make it a twin of another human in entirety?
My question is simple. If I wanted to make an exact twin of an individual, will genetically engineering the DNA of the zygote to match with the individual suffice?

Can you please expand and better explain your questions? At the moment they are often hard to understand.

Edited. Is there any more doubts?

Is it possible, from any cell of an individual? (speaking theoretically) Then are you saying it won't be an identical twin if just the DNA contained within the cell was identical? If so, which traits would differ specifically?

No, playing with the zygote will not do it. It needs to be the nuclear material of the individual you want to clone inserted into a donor egg after it's nuclear material is removed. When one starts dividing, the embryo can be transplanted into a surrogate mother. Read about Dolly the sheep.

Yeah, are you asking about strange cloning variation?

The answer is no, and it is because sequence of the genome is not all information that is required for gene expression and development, there are also epigenetic factors.
A lot of patterns of epigenetic marks, such as most of DNA methylation and some histone modification patterns, are set during parental germline development, and these marks are transmitted to the zygote by gamets (except paternal histones, those are not transmitted because they are temporarily substituted for protamines in sperm for greater compaction). Therefore, the naked DNA inserted into zygotic nucleus will not have access to the machinery that established epigenome during development of the gametes.
And even though nucleosomes may assemble in the zygote on the naked DNA and histones may acquire post-translational modifications, and cytosines may get methylated, but most definitely the zygote is going to have no means to correctly set distinct patterns of epigenetic marks at alleles that are normally imprinted, i.e. those alleles whose epigenetic state depends on the gender of the organism that produced the gamete.
Therefore, the twin created in this way will have the same DNA sequence, but it will be a  subject to disorders associated with imprinting

If the epigenetic state of the alleles depends only on the gender of the organism producing the gamete, then it won't matter, or rather should it?

Majority of genes in gametes have similar epigenetic marks irrespective of the gender that produced them. However a small number of genes are modified differently in female gametogenesis in comparison to the male gametogenesis (i.e. the sexually imprinted genes). And I don't think that there is a way for such differential pattern to be established correctly in the zygote in your hypothetical experiment.

From your answer and comment, I am assuming that the epigenetic marks are the same for a gender (of a particular species, just for safety an extra assumption). And, for a cell to avoid disorders associated with imprinting it should have the same epigenetic markers, before it can undergo successful cloning process. So, if an in-vitro fertilization is done of two healthy gametes each from a male and a female humans. It should have the same epigenetic markers as any other fertilized human egg. Because here, as you say, in case of epigenetic markers, only the gender matters, not the individual.

DNA duplication (imagine, we PCR it) will net be enough. First of all, you also will have to duplicate and pack mitochondrial DNA into the cell. next, as been mentioned, epigenetic modification (methylation) and histone packing are crucial for proper development.
And these markers should essentially replicate state of the host cell.
My best guess is that all-synthetic replication atomic-resolution of zygote will be enough, but not just bare DNA code (750MB of information)

Mitochondrial DNA is also a DNA. Apart from that, the mother could be kept the same, if that becomes a major hurdle.


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Why are there no artificial wombs yet?
If the conditions within the womb are mimicked, and proper amniotic fluid with constantly recycling nutrients is maintained, is it not possible to obtain an artificial womb? Is there anything missing? I think, artificial womb, if possible, could open new ways to study human anatomy and development and further the research studies. Starting with test tube fertilization, one could observe the entire process of growth of a zygote to a fetus.

It is impossible at present to reproduce all the conditions of a womb.
A womb is more than a warm fluid-filled home for nine months. A few days after fertilization, the trophoblast portion of the conceptus attaches itself to the uterine wall where it develops into a placenta and umbilical cord while the rest (the epiblast) becomes the baby.
Throughout the pregnancy, the mother delivers oxygen, nutrients and hormones through the her blood flow to the placenta, while carrying away waste. The womb also prevents infection of the placenta and amniotic fluid.
In addition, the placenta contributes to amniotic fluid production. Production and reabsorption of amniotic fluid is a very dynamic process; it isn’t just there. It is estimated that more than 95% of amniotic fluid turns over on daily basis, and the fluid composition changes throughout pregnancy.
While cell cultures of the womb's endometrium have been grown, there is nothing artificial which is close to this kind of environment yet, nor is there likely to be in the near future.

I think the trophoblast entirely forms extraembryonic tissue.

Thanks for the insight, I hope it becomes a reality sometime in the future.

@a.aniq I'm afraid your not seeing most of the (generally bad) implications of such invention, I hope it won't be created any time soon. Sometimes it's better to don't create sth.

@Mithoron I understand your concern, but artificial sperm and eggs have already been created, has it changed our culture? It is just for research purposes, nothing else. International Regulatory committees will absolutely put restrictions on it's use. And only a handful of authorised individuals will be allowed access to this technology, if it becomes viable sometime in the future. Who knows? Maybe something good will be discovered which will accelerate our endeavour further. We can use nuclear energy to destroy our world, and also to create a viable energy source. It's up to us to decide.

Artificial amniotic fluid has been used on goats, and for premature human babies.

In the 1996 experiment, Thomas Shaffer, a scientist at Temple University, used an oxygenated liquid in a clinical trial with thirteen infants born at twenty-three to twenty-four weeks who were not expected to survive, and seven babies were discharged healthy. Jonathan Knight, An Out of Body Experience, 419 NATURE 106, 106-07 (2002); Partial Liquid Ventilation with Perflubron in Premature Infants with Severe Respiratory Distress Syndrome, 335 N. ENG. J. MED. 761, 761 (1996)
(documenting scientific results from Shaffer's experiment).

Also in 1996, Japanese professor Dr. Yoshinori Kuwabara of Juntendo University, successfully gestated goat embryos in a machine that holds amniotic fluid in tanks.
Dr. Helen Hung-Ching Liu, Director of the Reproductive Endocrine Laboratory at the Center for Reproductive Medicine and Infertility at Cornell University.  In 2003, her team was able to grow a mouse embryo, almost to full term, by adding engineered endometrium tissue to a bio-engineered, extra-uterine "scaffold." Recently she grew a human embryo, for 10 days in an artificial womb. However, legislation imposes a 14-day limit on any research project of this nature.
Even if we do get a working artificial womb - we don't know how much we might be missing.  Something that appears to work, may not be as good as the natural system.  And we will have some difficulty in testing it in non-animal applications.
I'm trying to find the laws, but I believe we're currently precluded from pursuing artificial wombs mostly because of legal measures, not particularly by engineering problems.  Also, allegedly, the US is one of the most un-regulated first world nations for this type of research (while saying you can only research this for 14 days, smh).

Your first sentence is misleading. You have over-estimated the benefits of the technology you advocate. Note Partial-Liquid ventilation of perflubron a nebulized solution (gas/droplet mixture). Full liquid resulted in improvements on parameters but death of all neonates on removal of fluid, imparting no benefit whatsoever. Of embryos - goat or human - several days survival (not what you infer) was the max. Please link sources to your citations so that your interpretation can be verified. In the case of Hung-Ching Liu, you are totally misrepresenting her work and her findings.

Umm, 7 babies were discharged healthy seems like a benefit.

Partial-Liquid ventilation is not artificial amniotic fluid. It seems like you still don't get the point. The fact is that your answer is essentially incorrect.


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What species is this? Seashell from Indonesia

Anyone know exactly what species this is?  I gather it may be an auger (family) or cerith (family) of some sort.
This particular one is native to Indonesia's black beaches.
I would like to know what is the genus and species of this specimen.

That is a piece broken off of a sea urchin shell.

Without it's spines, it's not possible for me to say which species it is.

Good eye anongoodnurse +1

WOW!  Holy cow anongoodnurse, I am impressed.  You are totally right.


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How does Hemocytoblast constantly get formed into so many blood cells and yet remains there in the bone marrow throughout the lifetime?
I mean, Hemocytoblast is a stem cell which is constantly being differentiated into daughter cells and leads to formation of all the blood cells (having short and limited life spans), so how come those stem cells remain there and continue to function, even when we grow up and finally grow old (i.e for 70 years approx)? The no. of those stem cells gotta be limited.

The trick for the stem cells lies in the way the proliferate and differentiate. See the image (from the reference 1):

Stem cells have the problem that they need to differentiate and maintain their population at the same time (subfigure a). This can either be done by asymmetric cell division which leads to one daughter which is still a stem cell and one which has been differentiated (subfigure b). Then it is possible that the cells divide only symmetrical (as shown in subfigure c) so they will either deliver two stem cells or two differentiated cells. And then it is possible (shown in subfigure d) that both possibilities are mixed and that symmetrical and assymetrical division occurs. Either way you get both: Differentiated cells and you still manage to maintain the stem cell pool.
References:

Asymmetric and symmetric stem-cell divisions in development and
cancer
Asymmetric cell division of stem and progenitor cells during
homeostasis and cancer
Asymmetric cell division

your first link is broken

Can this asymmetric cell division be defined as mitosis?

Is this the only way, how these stem cells remain active for so many years? I don't think, that even with your answer taken into account, that's possible if we consider 70 years of average life span.

@MattDMo Thanks for the notification, I fixed this.

@a.aniq yes, it's mitosis. What else would it be? Also, since these cells do remain active for an entire lifetime, your assumptions need to be re-evaluated.

Yes, this happens via mitosis. The cells most likely get additional signalling when they differentiate in this process which is different from the signals they get when they should maintain their stem cell properties.

From where do they get the signals?

They get them from the environment, see here for some basics.

Data shows lipid metabolism is a big factor in determining how the stem cells differentiate.


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What happens to the umblical cord inside the mother?
After giving birth to a child, the umblical cord is cut (and stored if they want). The end connected to the child's navel will fell off eventually but what happens to the end inside the mother?
Will it be removed right after birth by doctors or what happens?

The umbilical cord is connected to the placenta, which is expelled shortly after birth.

Labor is typically divided into 3 stages:

Stage 1: From the onset of contractions (true labor pains) to full dilatation of the cervix (which is about 10 cm) - this takes about 12 to 18 hours
Stage 2: From full dilatation of cervix to expulsion of fetus - This takes about ~ 30 minutes
Stage 3. From expulsion of fetus to expulsion of placenta - this takes about ~ 15 minutes. During the third stage, the umblical cord which is attached to placenta is expelled along with the placenta. This would be the answer to your question.

Source:Hympath.com


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Why is the upper respiratory tract so vulnerable to infections?
Wikipedia has the following statement on its Upper respiratory tract infection page:

In United States URIs are the most common infectious illness in the
  general population.

What is it about the upper respiratory tract that makes it so vulnerable to infections?

I'd argue it's the exposure to foreign bodies which predisposes the upper respiratory tract to infection. Though, it's not until these invaders begin penetrating the tissue or in some way evading the immune response that we see any sign of infection. All things equal, you could even argue the entirety of the alimentary canal is at risk. However, in most instances, all is not equal, and most foreign bodies are in for some real punishment trying to invade those areas.

That makes sense, but beyond upper respiratory tract and the digestive system, there are many other tissues in constant contact with foreign bodies, like most of our skin, eyes, lips, the ear canal; and even though there is more air flow in our respiratory system, which could help explain its vulnerability, we don't see the same rate of infection along the lower respiratory tract. That's why it seems probable to me that there's something about those tissues that makes them so reliably exploitable by pathogens in well known cyclical patterns.

Well, the lower respiratory areas have whats known as a "ciliary escalator," as well as IgA in the mucus and alveolar macrophages. Which, you find that lower respiratory infections are more relatively severe given the evasion of such a complex of defenses. Other parts of the body, microbes are at competition with your normal flora, immunoglobulins in secretions like saliva and tears, lymphoid tissue, etc.

Mostly because it is in almost constant contact with aerosols from the outside world (with regard, of course, to a thin layer of mucus), therefore any pathogens they might contain.
You also have to remember what separates an airborne pathogen from any other pathogens- infection location. A pathogen is airborne when it infects and irritates the throat or nasal passage enough to make the organism's normal deterrence functions kick in. In most cases this would be coughing or sneezing, which produce contaminated aerosols for other organisms to inhale through their own upper respiratory tract.
I hope this answers your question!

It partly answers the question, but only partly. The external skin is also in almost constant contact with aerosols (and other forms of contamination) from the outside world, but it is not nearly as vulnerable to infectious agents as the upper respiratory tract. A full answer to the question would explain what constraints prevent the upper respiratory tract from being as well defended as the external skin.

The external skin is most definitely not in contact with aerosols (the living part at least). The first layer of skin we have is the epidermis, the first layer of the epidermis is the stratum corneum, which is composed of dead skin cells that form an infection-proof layer over the living skin cells (which is why cuts get infected). I apologize for the confusion, I was under the impression that this was common knowledge.

Sure -- but this just begs the question of why a similar infection-proof layer could not coat the upper respiratory tract as well.

Well, think about it. If there were a layer of dead cells in our lungs, oxygen would not be able to enter the alveoli and diffuse into the blood. However, you must remember that there actually is a layer like this, the mucus layer of course (oxygen can diffuse even while the mucus is present), but it does not protect nearly as well as a layer of skin, as we can see by the infection rates.

This doesn't answer the question either, because the question was asking about the UPPER respiratory tract, not the lower. The upper respiratory plays little if any role in oxygen exchange.

Aha, but that's where you're wrong. The upper respiratory tract plays a vital role with this in that it is designed to purify the air before it even reaches the lungs (lower respiratory tract) by pulling most of the contaminants out using mucus, which, of course, pathogens stick to, thus why it is prone to infection. You see, my comment certainly does answer the question, you just need to think about it a little.

Let us continue this discussion in chat.


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Can the human brain be reduced to a binary system?
Does the brain really function like a computer as in, ultimately every response is related to a binary sequence based on whether particular neurons fire or not?

First of all, I would like to point out that making analogy between digital computers and the brain is often very misleading.
That being said, my answer is, some scientists believe so, some don't.
Several things to consider:

Some neural systems are not spiking. C. elegans for example has a nervous system that is entirely analogue. Human nervous system also contains neurons with graded responses (mostly in the sensory front-end though).
Spiking neurons may be binary at each time point, but time itself is continuous. Firing at 0.003 seconds later can represent something different. (in contrast to the usual synchronous digital architecture of computers)
The neuron doctrine is sometimes challenged. Glial cells that do not fire may have important functions for information processing. See:

Bullock, T. H., Bennett, M. V. L., Johnston, D., Josephson, R., Marder, E., and Fields, R. D. (2005). The neuron doctrine, redux. Science, 310(5749):791-793.

That's exactly what I was wondering; if in fact, some brain signals are propagated on a grade. Thanks!

Plus neurons have modulators that change the way they behave. Some modulators may cause hyperpolarization while others may decrease the threshold for depolarization.

While action potentials are usually binary, you should note that synaptic communication between neurons is generally not binary. Most synapses work by neurotransmittors, and this is a chemically mediated graded response that, for example, act on voltage-gated ion channels. So even though action potentials are often binary, communication between neurons are most often not, and action potential firing can involve the integration of synaptic information from many different neurons. Therefore, the brain as a whole cannot be reduced to a binary system.
See this as a complement to @Memmings answer.

Many neurotransmitters (also) have metabolic G-protein-coupled receptors as their target. E.g. Glu has NMDA-receptors (Na,Ca-channels) and AMPA receptors (Na ion channel), but also a gamut of metabolic GLuRs as target. I slightly adapted your answer by adding 'e.g.' Fine answer. +1, therefore removed the intro line - unnecessary :)

Very interesting. Thanks for the response. I am not familiar with voltage-gated ion channels and will definitely be reading up on them. Thank you!

John vonNeumann, the famous computer scientist, tackled this idea in his last book, 'The Computer and the Brain.'  He personally landed on the side of the brain being a binary system, due to the behavior of neurons which either fire or do not fire.
While that is an important observation, and will have significant consequences to people trying to create artificial brains within computer systems, I think a more important observation has to do with computational complexity.  It is very easy to build systems which, at least theoretically, have the potential to be universal computers.  From that fact, it is fairly trivial to see that whatever definitions you choose to work with in terms of brain input and output (sensory nerve cells feeding electrical impulses from organs of perception being a possible definition of 'input' and propagated impulses to muscles, or changes in the neural structure itself being possible definitions of 'output' for example), yes it is possible to construct a binary system which can perform the same calculations as a human brain.
However, there is a catch.  Because it is impossible to perfectly know the complete state of the brain, and because any degree of inaccuracy in the starting state of the binary system, no matter how small, will cause the behavior of the binary system to diverge completely from the behavior of the specific brain being modelled, it is reasonable to say that no particular individual brain can be reduced to a binary system.

as far as I know the brain processes data in stages the neurons themselves are not purely binary as in a computer in that every action has a predetermined output. the neuron response tends to be goverened by sigmoid function output and hence the use of this function in artificial neural networks. further, the synapses have strengths that is depended on the amount of neurotransmitter in there which obviously varies from cell to cell and even in the same cell and hence one speaks of the probability of a neuron firing given a certain stimulus. additionally the neurons from sensory organs fire pulses at a frequency that increases with the strength of the stimulus. furthermore, the data from sensors is processed in layers of neurons lower layers have rapidly firing neurons whule higher layers fire at much lower rates.
you also have to consider the fact that the brain is actually a complicated network of "recurrent" neurons meaning that the output is fedback as an input and this is different from simple computer gates such as AND gates or XOR gates it is similar to counters may be but obviously on a very bigger scale. one more point is that recurrent neural networks have built in memory that enables the pattern recall and recognition and so the study of the brain as a binary system is very complicated and will fail to explain how the brain works.
on the macro scale the human brain operates as a bayesian inference engine more or less I mean when it comes to thinking and inference i.e. it relies on probabilities and knowledge gained from past experiences to deal with current problems and new data

It's theoretically possible, because all information can be well approximated/copied in binary, and it's
practically impossible because of size, energy, and program size/depth.
A fly brain is <1mm wide and an intel fly brain equivalent is >1000mm wide... much slower than the fruit fly. (Thats why flies see your hand coming in slow-mo).
This intel chip has as many neurons as a slug, far less than a fly:
https://www.cnet.com/google-amp/news/intel-packs-8-million-digital-neurons-onto-brain-like-pohoiki-beach-computer-loihi-chips/
he binary model has to include "chemical modelling" and "physical modelling" like a graphics card which models light and creatures as binary.
Except that there is an added issue: processing speed. The brain can grow direct connections which are very fast. Silicon signals have to travel 1000 times further for every calculation.
2d chips take as much space as a skyscraper and a small nuclear station for energy, and future mythical 3d transistors would take space and would be slower because they require direct chemical processing and flexible internal connection to be as fast.
AI is very performant and is one of the future paradigm changes like "internet/mobile phone / electric car / AI "

human brain is strictly digital device using defined action potentials (0 volt as logical 0 and specified (fixed) voltage potential as logical 1). these two potentials work same way as complex logic gates systems. brain processes all types of analog-like variations (signal amplitude or response strength) as very short time based sums of logic gates operations. there is no other applicable description of brain functionality

Welcome to Biology.SE! This seems to conflict with the accepted answer and could easily be mistaken for an opinion rather than an answer based on facts.  Consequently, I think will find that supplying supporting references (primary literature is best) will help your answer receive a more favorable response. ——— You may also wish to take the [tour] and then consult the help pages on the standards for additional advice on [Answer] effectively. Thanks!

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text:
How does one calculate how to dilute a solution to working strength?
If I'm loading a 3.5ul PCR onto an agarose gel, how do I calculate how much of the 6x loading dye to add?

Since its 6x (6 times concentrated), you have to dilute it 1:6, so you add 1ul of 6x dye for every 5ul of reaction.
5 +1=6ul final volume
6ul final volume / 6x concentrated = 1x working concentration
Now the dye is diluted down to a 1x(working) strength.

You want to dilute concentrations to 1x, therefore a 1:6 ratio for dye:reaction.


text:
Lyonization vs Genetic Imprinting
Lyonization is the process in which there is inactivation of an X chromosome in females. This process is implicated in mosaic forms of turner's syndrome (in this case the altered X chromosome is Lyonised, thus allowing the normal X Chromosome to express itself).

Is Lyonization considered as a form of genetic imprinting? What is the difference between the two (if no)?
Lyonization is a random process (according to the extent of my knowledge which X chromosome is inactivated is not predicatable). Is genetic imprinting also random?
Is there any known aberration of Lyonization in males? (meaning the single X Chromosome or Y Chromosome gets silenced)

A bit related: http://biology.stackexchange.com/questions/27681/what-effect-does-the-barr-body-have-in-relation-to-female-turner-syndrome

I use the term "X-inactivation" instead of "lyonization". Anyway, X-inactivation is a very specific process by which an entire X chromosome (or equivalent sex chromosome) in a female mammal is completely silenced.

"Imprinting" is typically applied to single genes, wherein genes inherited from a specific parent are always epigenetically silenced. The genes are usually autosomal. Thus, we're talking about scales : entire sex chromosome composed of thousands of genes (x-inactivation) vs single genes (imprinting)

The choice for which X-chromosome is inactivated is sporadic and different in different cells within the body. It is controlled by opposing expression of different non-coding RNAs (XIST on the inactive X and TSIX on the active X).

Imprinting is very specific to the allele that is inherited from a specific parent (for example, some genes are paternally imprinted, while others can be maternally imprinted).

Males with aberrant X-inactivation will lack any expression of genes carried on their single X-chromosome, a condition that will not result in a viable fetus. However, whether there are aberrant X-inactivations in single cells or tissues of ageing adult males....perhaps likely yes, given all the other aberrant somatic mutation events that occur over the course of life.

I guess, we are talking about mammals here (because in other organisms leveling up of expression on sex chromosomes happens differently: e.g. in flies females express both X chromosomes, while fly males express their single X at twice as high level).
In embryo proper the decision of whether to inactivate maternal or paternal X seems to be at random. This inactivation adjusts level of expression of genes on X to be in the same ball park as on autosomes and in the same ballpark between males and females. Neither farther nor mother cares about which copy of X gets inactivated in individual cells of an embryo.
When we say that a gene is imprinted, that means only one copy of the gene is expressed  but, to the contrary of what happens with X, maternal or paternal origin of the expressed copy is predetermined (so there is no randomness in which copy is inactive). Imprinting is usually a property of genes expressed during embryonic development and it is related to tug of war between farther and mother's interests: the farther "wants" embryo to take as much resources from the mother as possible (so paternal copies of some genes tend to be highly expressed), while mother wants not to give too much to one embryo, so that she can raise many more progeny (so maternal copies of some other genes tend to be highly expressed). This whole thing is interestingly described Matt Ridley book The Red Queen: Sex and the Evolution of Human Nature.
Note, that to confuse matters a little bit, in placenta of female embryos it is always the paternally inherted X that gets silenced, so the whole X chromosome is imprinted in extra-embryonic tissues of female embryos.
And in males X chromosomes do not get inactivated, since many genes are present solely on X chromosome and not on Y, so inactivating the only copy of X chromosome is lethal.


text:
Authority on Microbiological Definitions
Is there an authority on definitions for molecular microbiology concepts, like an IUPAC book for chemical definitions?
The particular definition I am debating is chromatin. Some say it encompasses DNA, RNA and protein, whilst others say that it contains DNA and only during the mitotic interphase can it transcribe to produce RNA and protein.

What you are asking about is molecular biology, not microbiology.

So in a very broad definition, yes, chromatin encompasses DNA, RNA and protein. The primary function of chromatin is to provide a method to effectively package all the DNA in a cell. This packaging is dynamic, and it's constantly regulated in a cell type-specific manner. We can see the broad interactions of protein and DNA in this cartoon representation from wikipedia:

Combined with histone-modifying complexes, and chromatin remodeling complexes, we obtain the aforementioned mode of regulation. Histone protein can be modified (acetylation, methylation, glycosylation, phosphorylation, etc.), they can also be moved, substituted in their subunits for specific pruposes (think H3.3 or H2A.X). We can also end up with varying regions of dsDNA, 10nm or 30nm fiber.
The RNA comes in as a structural and functional components of the chromatin, participating in many controls as noncoding RNAs.
I believe most of the method in defining chromatin comes in very much as the amassed literature on the subject to-date. You'd even consider it "common knowledge" entering the field (i.e. a quick google search can return you the right definition).

"only during the mitotic interphase can it transcribe to produce RNA and protein."

Transcription halts entering M phase or mitosis, transcription may occur during G1, S, G2, or "interphase."


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Can a portion of human skin cells be modified in some way to generate light?
I have come across some species of living organisms who are able to emit light at whim. Can that ability be incorporated into a portion of human skin (a specialized tissue)?

Genetic modification of any cell to overexpress a fluorescent protein will not 'generate' light, per-say: fluorophores absorb particular wavelengths and re-emit in less energetic wavelengths, dispersing some energy as heat. (Perhaps there is some semantic choice here, but there is no transduction to light from another form of energy.)
Bio-luminescence, on the other hand, can be considered generation of light. There are proteins commonly found in marine animals (which skin cells could be engineered to express) which convert chemical energy to emit light.
With regards to generation of electricity, I think this gets a bit interesting...
The electron transport chain (ETC) in the inner membranes of our mitochondria carry out a series of redox reactions which serve to oxidise food metabolites (thus freeing electrons). In order to maintain the free energy gradient that favours this directional cascade of reactions, electrons and protons are finally accepted by a continual supply of oxygen atoms, producing water. (You may be aware that aerobic respiration consumes oxygen and produces water.) In nature (in aerobes), oxygen acts as the final electron acceptor, or an electron sink.
Bacteria also have electron transport chains for their respiration (mitochondria were once bacteria, after all), and people have wondered whether these redox reactions could be used to produce a current instead of reducing oxygen to water as the final step. We normally use current in the form of electrons moving along a metal wire.
This is the idea of a "microbial fuel cell". Just like a battery produces a current from a chemical redox reaction, the ETC might be recruited in to producing a current from its chemical redox reactions.
I think this is a very difficult piece of bioengineering, since the ETC is integrated in to respiration and needs to be de- & re-coupled to some kind of inorganic mediator and ultimately a circuit; and also because the ETC produces very low voltages, I think.
There is a nice wikipedia page on microbial fuel cells that you might find interesting, if you think this is relevant to your question.

I understand your point from this answer all right.But please add a para explicitly stating "Is it possible for humans to generate electricity and light from skin tissues and natural energy, similar to that of those animals by any means, using current state-of-the-art knowledge about Biology?"

The part about using luciferase to produce light is only a partial answer. Expressing the luciferase is the easy part. Producing enough luciferin to actually make visible light would be very hard, since the luciferin biosynthesis pathway isn't fully understood yet, and is pretty energy intensive. Trying to regulate the lighting would be very hard, so even if you could get sufficient luciferin production, don't plan on turning it off, or flashing it, or anything complex.

a.aniq, your question needs a lot of work, in my opinion; it's not clear what you really want to know. Are you really asking: "Can I have skin like a fire-fly, or an electric-eel?". The answer is no, for the reason Kendall gives - these organisms have quite extensive physiological adaptations in order to luminesce or produce electric shocks, tissues very unlike human skin. My answer was instead about transducing energy and the idea of a microbial fuel cell, as I wasn't sure what you were asking, and since these small steps are more realistic.

Sort of problematic is the "at a whim" part. Just a brief search to wikipedia on electric organs, here, we see that the electrocytes are controlled by a nucleus of pacemaker neurons. This is all unique to electric fish, and you'd have to express that whole system in a human being to elicit the same effect. You'd also have to consider how your organism is engineered to withstand the actual electric shock emitted by the electric organ.
We can already tag molecules with luciferase to emit light as a mode of bio-luminescence. To get an appreciable reaction, or rather an appreciably bright light, I can imagine we'd need a ridiculous amount of luciferin in vivo, though. We also get stuck at the part about it being on a whim. The control mechanisms/structures for the light-emitting reaction simply aren't present.

As noted above, the problem with bioluminescence is not in producing luciferase in vivo - I have a mammalian plasmid in my lab that can do that. The issue is producing and trafficking luciferin (luciferase's substrate).

Yes, the fibroblasts of skin cells can quite easily be Transfected with a fluorescent gene such as GFP. Fluorescence doesn't actually produce light, the fluorescent molecule just changes the wavelength of light shining on it.
Fibroblasts can also be made luminescent (light producing) by acquiring  genes for firefly luciferase or aquoren from jellyfish. This is a little more tricky since luminescent molecules typically require cofactors such as ATP, Calcium or other proteins.
Both methodologies are readily performed in vitro.

And what about electricity?

That's a much more complicated physiology based on  tissue arrangement. Although I'm not 100% on this I think introducing a phenotype like that into a transgenic animals at this point is still science-fiction

I don't know if what you are saying is possible or not. I'll wait for somebody to comment on this answer, before thinking on it.


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Human leukocytes (re)circulation/migration in homeostatic state
One can easily find information on the topic of leukocytes trafficking between vessels and peripheral tissues during inflammation.
But what happens during normal states when there is no pathology? Do all the subtypes of granulocytes, monocytes, and lymphocytes leave the blood vessels and enter healthy tissues in the same way they do under pathological (inflammatory) conditions?
References and thoughts are very welcome.
Thank you.

Which leukocytes do you mean? Peripheral memory b cells?

I have edited your question a bit. Please feel free to roll back if you think it alters your question.


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Is there a graph or ontology that maps diseases to its possible causes or causing diseases?
I am looking for a mapping, list, ontology or graph that shows the connection between a diseases and its (currently known) causes and/or risk factors.
For example a well known risk factor for acute kidney injury is diabetes. There are other diseases whoms risk factor is diabetes. This meanse diabetes is a risk factor for many diseases. Maybe if one traverses trough this dependencies and builds a graph out of it, there will interesting clusters and lineages.
I dont know if this is inherent knowledge or formulated somewhere in a formal and explicit way (e.g. as ontology).
There is http://disease-ontology.org/, but it does not contain any causes, risk factors, etc.
Thanks in advance!

Welcome to Biology.SE! I think it would help if the question is further specified. As of now it is rather broad and at least to me unclear what you are exactly after.

So you are basically looking for an enormous data base that connects diseases with their risk factors and known causes?

@fileunderwater: Yes, could be a database. I think a ontology would model this behaviour very well. In this sense every node would be a disease or a risk factor (because not every risk factor is a disease), between the nodes you have different links of type "has_cause" and "has_risk_factor". Very much in the way http://disease-ontology.org/ is modelled (click on some concept and then "Visualize"). So this is what i had in mind, but if there exists a database or just a massive text-file, it would also help me!


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Core architecture of the body encoding
First of all, I am not a biology guy; I am in Computer Science. But, I have a strong interest in all the mysteries of nature, from universe to human body. So, I want to ask a question related to genetics.
As I have read that all(both male's and female's) the biological traits of a person are passed genetically to the offspring(of course assuming the crossing). So if my mom's eye color is blue and my dad's eye color is also blue, I will get blue color too, but what about the core architecture of the body? I mean I have 2 legs at a certain location from my body(my waist but, not from my head!) and similarly other orientations. Why they are that certain way? If they somehow got changed, would the resultant body be stable?Is the answer different in case change is artificially engineered or natural?
Where is this core architectural information exactly stored(If the answer is DNA then how?) and in what form is it stored?How come that information is not changed in thousands of years or even millions of years? And is that information of such nature that it contains "exact" steps to develop a healthy say, brain structure(which is a really complex)?
My another question is: If there is a community of mutated people, will their offsprings be mutated always with 100% certainty?
I know these are a lot of questions but you can see that, they basically revolve around the information that I am curious about. Can someone address my curiosity?

Welcome to Biology.SE! And thanks for sharing your question. I think it may hold potential, but it needs some work I think. Most importantly it is a stack of broad questions. Some research from your own may help to pin down a good question.

@ChrisStronks: Yeah, sure then you may give me some pointers

It's your question, your call. Just trying to help.

Btw, the Biology community here is so small compared to Computer Science community!

Perhaps you'd like to read a popular science book about genetics and development, as it is really the intersection of these two fields ('developmental genetics') that is concerned with how an ordered body arises from a fertilised egg and its genetic information.
It's a fascinating question, I feel it might be too challenging to cover properly on this website.
Try "Endless Forms Most Beautiful" by Sean B Carroll, to learn a little about embryo patterning and homeobox genes. Historically scientists studied frankenstein-ish developmental mutants with disordered body plans. It's a complex system

For my two cents', as regards body structure development specifically, genes don't code for final shape but for the developmental process; in some ways, it's abstractly similar to the development of a fractal. The sheer number of genes which can come together to create a single particular result further complicates things.

Welcome to Biology.SE!
Your question is very broad. Also, your post has the default of containing severals questions in it. Make sure in the future to restrict your post to only question, it will be much more likely that you receive a good answer then. I hope that I can give some indications about how to get some more knowledge in this answer. In this answer, I do not consider all your questions one by one to answer them (or guide you to the answer) but I think that all your questions will get an answer as you learn more about the subjects I cite. Hope that answer will help you.
Very basics of molecular genetics
You should start to have a few ideas about genetics. Make sure you know what is a chromosome, a gene, an allele, a protein and a phenotype. Wikipedia will help you with that. Come back on Biology.SE if something seems unclear to you.
Basics of genetics and evolution
You are definitely interested in concept of segregation. This is a very fundamental concept in genetics. The basis of the laws governing segregation has been first discovered by Gregor Mendel and we still name these basics laws after Mendel. We talk about Mendelian segregation. You may want to google that.
Then you are interested in the concept of heritability. I have been talking about heritability in different posts. In the third sentence of my answer here, there is a short list of posts that define the concept of heritability.
Eye color you said?
You talked about the genetics of eye color inheritance. Here is a post that will interest you then.
The Genetics of Development
Your question is not only about genetics but is about the genetic of development. You may want to have a look to the basics of developmental biology. The most famous DNA sequence  involved in determining the body plan of many different living things are the so-called homeobox. There is plenty of interested things about this homeobox. This post may interest you btw.
Rough details about the evolution of development along the tree of life

How come that information [architectural information] is not changed in thousands of years or even millions of years?

It really depends on what you call architectural information. But in any case it does evolve. If you think of things such as like size of an animal. Then it may evolve fairly quickly. You may thing of more important change, such as evolving a new pair of legs or evolving wings or a head, then it tends to take more time. Below are just a bunch of examples of how animals differ in terms of body plan along the tree of life.
You might be interested to study a bit the development or early animals. Some have a radial symmetry while other (like us) have bilateral symmetry (see wiki). Some animals have a head, some don't. Some animals have two dermes while others have three dermes. The Deuterostomata (vertebrates, tunicates, echinodermes, ...) have a development where the blastopore of the gastrula becomes the anus while in the protestomata (now thought to not be monophyletic and divided into ecdysozoa and lophotrocozoa (see here)) the blastopore becomes the mouth. Among the arthropoda (insects, spiders, millipedes, ...) the story is very interesting as well. Some have a highly segmented body with a pair of legs at each segment (millipedes) while other groups have fused those segments. Spiders have only two big body parts, while insects have three big body parts. In insects, the thorax (one of the 3 body parts with the head and the abdomen) contain three segments and each segment hold a pair of legs. The first flying insects also had three pairs of wings, now degenerated into two and even into one in Diptera.

Hox genes are found on chromosomes 2, 7, 12 and 17. They are also not the only genes to contain a homeobox.

Oops. That's not what I had in mind but I know little about the subject. I corrected it my answer. Please let me know if my answer there contain mistakes!


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Determination of a chemical compound in a non-homogeneous sample
This is a more generalized question of my other question here.
I want to know if it is possible to determine a chemical compound in a non-homogeneous sample. I am asking this because we are aiming to create a device that will detect histamine level in fish without homogenizing the samples. In all the journals we've read (which are a lot), fish samples are homogenized (blended + chemically-treated) before histamine is determined.
I am a computer engineering student with basic knowledge on biochemistry. I'm researching on this because this is our thesis topic (which our adviser has forced recommended to us).
Any help/recommendation regarding this is appreciated. Thank you!

You should not actually homogenize samples because histamine works locally. If you know which region is releasing histamine then you can just study those regions. You can actually create a transgenic fish with GFP that is a target of histamine receptor signaling.
Using mathematical models or statistical correlations you can obtain the level of histamine based on fluorescence.
Activated histamine receptor H1 causes production of inositol triphosphate (IP3) which in turn causes release of calcium form ER. You can use Cameleon-GFP to sense the change in calcium levels. However, there are many events that may result in calcium release; you should carefully design your experiment.
This is another possibility (just a guess)- a FRET based study using GFP-YFP FRET Pairs (or other variants). Since histamine receptors are G-protein coupled receptors you may fuse the GFP to alpha subunit and YFP to beta subunit. When upon signaling, the subunits dissociate, you would see a decrease in FRET.

It is correct that imaging-based studies are super-awesome, but question seems to be about chemical. I don't know if there are antibodies available for histamine, if yes, then you can fix and label all sites of histamine.
But imaging through fish tissues (say, more than 1 mm) is close to impossible with molecular resolution and sensitivity.
My best guess would be following. If you are OK with blood level measurements, then try spectroscopic approach. That is measure Raman NIR scattering or fluorescence/absorption in UV-visible regions of light spectrum.
Fun option is to develop chemical-reaction based assay. Say, engineer reaction that will modify histamine using radioactive-labeled compound and then measure how fast/slow amount of the compound decreases


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Why doesn't crossing over happen in mitosis?
If there was crossing over in mitosis, then there would various nature of somatic cells. May be that's the logic, but what is the mechanism? Why are there no crossover events during mitosis?

http://en.wikipedia.org/wiki/Mitotic_crossover

During mitosis both sister chromatids are identical si there would be no benefit to crossing over. During mieosis a person receives one chromosome from each parent which will encourage homologous recombination or crossing over to promote gebetic diversity.

during mitosis both sister chromatids are identical so no benifit of crossing over..During meiosis there are paternal and maternal chromosomes so crossing over promote genetid variability.

It can actually on very rare occasions however, it is also highly problematic and generally creates deleterious mutations and can inactivate genes. Depending on the location of the cell and the cross-over within the genome, it can also contribute to the formation of cancer. For instance, in the case of retinoblastoma, if there is one mutated copy of RAS on one chromosome and a normal copy on the other and mitotic crossing over occurs, then you can potentially remove the protective nonmutant copy of RAS from one of the daughter cells. This cell is then one step closer to becoming tumorgenic.
Thus, one reason this may not occur ordinarily is to reduce the chance of causing such a cancer. As for why it does occur on the rare times it does, I am not certain as of the time of writing this.
Reference: The Biology of Cancer, by Robert A. Weinberg

The mechanism is straightforward: in Metaphase I of Meiosis, chromosomes line up in two lines, with homologous across from each other, which allows them to interact by crossing over. In Metaphase of Mitosis, the chromosomes are all lined up single file, so the homologous chromosomes cannot interact.

This seems to contradict the possibility of mitotic crossover.

Yes, but mitotic crossover does not usually happen. It's more of a bug than a feature.


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What is the difference between organelle membranes?
Cells and organelles are contained in lipid bilayers. I'm particularly interested in eukaryotic organelle bilayers and the biophysicochemical differences between them.
Many papers assume a difference in membrane characteristics and some like Anderson et al., 2007 have categorised the relationship between these characteristics and protein function in depth.
Do any reviews or comprehensive studies exist in the field that compare the thickness of the membrane, the rigidity of the surface, any differences in lipid entropy, or the overall charge inside and outside across different types of organelle membranes?

Are you interested in all types of membrane bound organelles? I am sure there are studies on membrane composition individually for different organelles. I guess you have to do the comparison yourself. I remember that there was an article that compared chloroplasts of different origin and one of them still retains the peptidoglycan cell wall; I'll find that and let you know

I am interested in the biophysicochemical differences between membranes themselves of membrane bound organelles. Generally I am more interested in the net biophysical differences, but any references are more than welcome.

Great question. Turns out, there is some information about it.
For example, consider following resource: Membrane Protein Lipid Composition Atlas. Published by University of Michigan, it provides information on, primarily, protein content of different membranes from different species, but also has a list of lipid content.
Just as an example, consider following difference between membranes of mitochondria in yeast:

Now, concerning your interest in biophysics. To my taste, starting with just bulk lipid composition is a good first approximation. Although you also want to know about lipid raft formation and density/distribution of proteins. Next step, probably, will be symmetry considerations, that is, difference between sides of same membrane. You can imagine membranes with same bulk composition, but because of different lipid position (in/out) properties will be different.
It seems you can assess raft composition based on membrane lipid composition. Membrane capacity also is a property of membrane content.
Following quick walk through this Google Scholar search provides even more links between biophysical properties and lipid bilayer composition. However, it might be challenging to find exactly what you are looking for.


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What is an auditory upward sweep?
I was reading an article in nature communications, when I came across this sentence: "The ‘match’ rule was indicated by either a blue circle or a auditory upward sweep".So I tried googling what was an upward sweep, and came across this: "natural and complex vocalizations consist of basic elements such as upward sweeps, downward sweeps, constant frequency components, amplitude modulations..." I don't understand this. Can someone explain what is an upward sweep?
Here is the link to the article: http://www.nature.com/ncomms/2013/131128/ncomms3878/abs/ncomms3878.html,
But I think you have to pay to view the whole article, so here is another link that discusses the findings of the article:
http://www.uni-tuebingen.de/en/landingpage/newsfullview-landingpage/article/von-wegen-spatzenhirn-wie-nervenzellen-schlaues-verhalten-bei-rabenvoegeln-ermoeglichen.html

You should provide a link to the article.

Yes definitely include the article link. It sounds to me that the authors used a sound that started at a low frequency and increased in pitch over time.

It just means a sound that starts at a low frequency and goes up to higher frequency like a whistle sound. Perhaps someone can give you an example sound file and/or a spectrogram representation of it.

Copied from my comment:
It just means a sound that starts at a low frequency and goes up to a higher frequency like a whistle sound. Perhaps someone can give you an example sound file and/or a spectrogram representation of it.

http://jn.physiology.org/content/jn/94/2/1299/F2.large.jpg


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Total dark deprivation at day-neutral plants
First of all, I am not a biologist.

Almost for a week, a question has come to my mind:
"Is it harmful ceaselessly exposing a plant to light?"
(I mean with natural & artificial light with proper spectrum)
I have been searching for a week, and I stumble upon many weird and wonderful things, and by them, I have become able to consider this topic more deeply, and refine my original question. However I have still not found the answer.
I am already familiar with these topics:

Light-dependent reactions
Light-independent reactions
Calvin cycle
Photoperiodism
Phytochrome
Cryptochrome
Long-day, Short-day, Day-neutral plants
Grow light

So my main question:
Does ceaseless light exposure with proper spectrum adversely affect a day-neutral plant?
As a layman I have started to fumble towards light-independent reactions, but I have not found strong claim. I have learnt that there are processes which taking place during dark phase, but are these reactions impossible in presence of light?
But probably there are other factors.

My resources were: Google, Wikipedia, (a tons of) academic paper, many article from Botanical Gazette, many blog & webpages about botany & greenhouses etc.

I cannot say anything about the general case, or specifically for day-neutral plants. However, Sforza et al. (2012) have studied the effects of light conditions on algae (used for biofuel production), and their results indicate several problems with continuous light. In continuous light conditions they find lower chlorophyll contents and higher carotenoid concentrations in cells, which leads to lower photosynthetic efficiency.

This figure shows chlorophyll contents (black) and chlorophyll/carotenoid ratio (red) under different conditions, with the two treatments to the left representing continuous light. (graph from Plos One)

Results show that Nannochloropsis can efficiently exploit even very intense light, provided that dark cycles occur to allow for re-oxidation of the electron transporters of the photosynthetic apparatus. If alternation of light and dark is not optimal, algae undergo radiation damage and photosynthetic productivity is greatly reduced.

However, they also experiment with pulsed light, which in some cases lead to even lower rates of photosynthesis:

However, similar experiments, at different frequencies, also showed that alternating dark and light may be detrimental, as demonstrated by the growth inhibition observed in the 1200-1 and −5 Hz curves. These cells showed a decrease in Fv/Fm values similar to that observed under constant strong light, indicating that the inhibition of growth was due to photoinhibition.

They also find that light pulses can be very short, and still allow for the photosystem to reset:

The optimal duration of light pulses was found to be around 10 ms, which is consistent with the suggested PSII turnover rate in whole cells [4], [46]. Accordingly, after photon absorption by the photosystem, 1–15 ms are needed to reset the system, before it is ready to receive another photon [22]. If the illumination is this short, most photons are exploited for photosynthesis and do not lead to the formation of ROS which then causes photoinhibition. These results indicate that even strong light does not cause damage if it only lasts a short time. Conversely, longer exposure allows the generation of ROS and damage and, in this case, the abrupt changes in illumination undergone by the cells are as harmful to the photosynthetic apparatus as constant high light.

Different species of plants can have mechanisms to handle light stress in different ways, so the effects on different species and types of plants are likely to differ. However, their results should generalize to some extent/for some plant species.
You may also find this paper by Li et al. (2013) interesting.

Astonishing!!!
That is way more what I expected as answer.

@osiixy Glad you found it useful. I also want to compliment you on a nice first question, with a good background.

Your answer was an amazing start point.
One of the most important keywords was light stress, which gave me a huge momentum (as it turned out it is very basic concept - but as not to be biologist I did not even think to seek that way).

About dark processes:
I find a paper which mentioned that spirulina for example needed long dark stages because the protein synthesis taking place in this phase.

@osiixy Goes to show that the proper key words can be a large part of finding useful information, especially if you are new to a field. Also, feel free to post an answer to your question if you find good information during your studies - to post complete or partial answers to your own questions is encouraged at StackExchange sites.