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Can 'hardware' thermalization explain memory decay?
Often we are able to memorize very precise bits of information (exact addresses, birthdays of inlaws, number of dirty socks under the bed), but over time our recollection tends to become fuzzy. We no longer recall the day and month a certain president was killed, only the year, or maybe the decade (despite being straight A students in junior high). Like the smoothing out of a delta function under the heat equation, instead of a pin-sharp value we're left with a range of values where the correct one is likely situated. However, most of the time we are perfectly satisfied with such approximate information and can work with them just fine (except in some extreme cases of function impairment, such as Alzheimer's or the aftermath of binge drinking).
Discrete data must be stored in low entropy structures in the brain that over time spontaneously shift to a higher entropy state. Meanwhile, our biology tries incessantly to slow down the decay by expending energy (with the frequently utilized neural pathways being better maintained than the abandoned ones). Even processes analogous to error correction take place, e.g. when we arrive at a certain lost piece of information by lateral thinking and piecing together available data.
My question is whether the fading of memory exactitude can be explained in terms of the thermalization of the digital-like structures where discrete information is stored, and if anyone can point me to studies in this direction.

Discrete data must be stored in low entropy structures in the brain that over time spontaneously shift to a higher entropy state

How on Earth could you possibly know that? You are overextending physics to the workings of the brain and there is nothing that says this is necessarily so. Memory decay is not fully understood but it is known that the more features(i.e sound ,taste) are used when forming the memory and the more it is associated within an existing knowledge framework, the higher the chance that the memory will persist.

What exactly are you disputing exactly? Information is pretty much synonymous with low entropy (i.e. ordered) structure. E.g. a magnetic tape whose domains are collinear is seen as holding information, whereas a random distribution of the domains corresponds to no information. It takes a lot of data (i.e. high entropy) to describe a randomly ordered structure. Roughly, total degrees of freedom = useful information + entropy. Finally, the second law of thermodynamics states that entropy spontaneously increases.

Interesting point, but I think there is a simpler and possibly more widespread reason for the decay of memories. Namely, as new memories need to be stored in the same neural networks, the weights, timings and other properties of the network links are constantly changed. In other words, there is competition for the limited amount of memory. This re-use of the same networks for multiple functions and memories is the same reason we have redundancy in our brain - it's also largely why they are as fuzzy in remembering as they are. And since memories are recalled associatively, the more connected two networks that encode different memories, the more likely it is that activations of one will activate the other. But that also blurs the boundaries between specific bits of information stored. It's a trade-off between fidelity of the memory stored and recalled and generality of the recall and associations possible.

Good point. There are various theories on memory loss but I wanted to address the problem of organic decay specifically, which seems prevalent in some situations. In particular, older people suffer from memory decay more than young people, even though they're arguably faced with less new information and the corresponding need to free up space is also smaller, so your argument doesn't provide a full explanation.

No, you are right, it doesn't. But we could extend the point I'm making to older people as well: they have a significantly smaller number of neurons so that while there may be less new information to deal with, there is also more competition from the memories previously stored.
Also, on a different note, it could be that there is memory decay due to a greater inability to sustain the current memories - for example, because of lower production of certain crucial cell-adhesion and receptor proteins.

Great, I'm not debating all these phenomena you mention, in fact they're all organic ways of decay, but let's look at how they are essentially able to turn digital values into fuzzy feelings of what the value should approximately be. I'm convinced that only a small, high-level, conscious part of the human mind deals works digitally as an emergent feature of a larger, fuzzy mechanism (without breaking it all the way down to quantum mechanics).

My understanding is that there are two major reasons for not being able to recall where your socks are or when your anniversary is:

The information was not committed to short term memory in the first place when you initially encountered it, so there was never anything to remember.
The information is intact, but you are not able to effectively retrieve it, because other memories compete and act as noise when you try to remember a certain specific one.

Neither of these scenarios involves actual loss of long term memory, which is more commonly a result of concussions, or other sorts of serious brain damage.


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Is end-systolic volume (ESV) the same as residual volume?
I am reading this site and my study materials.
The end-systolic volume (ESV), 50-60 ml, is the volume of blood found in ventricles after systole and contraction of ventricles.
I think ESV is the same as residual volume because residual volume is always the volume found in ventricles.
Is ESV the same as residual volume in normal physiological situations?

I am not completely sure that ESV can correspond residual volume in all cases.

The ESV is the residual volume of blood remaining in the ventricle after ejection.
It is the minimum volume of blood in the ventricles (residual volume).
Note that you can also have residual volume of air in the lungs after exhalation.

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How do duplicate brain regions (ex: left/right amygdaloid body) operate together?
I frequently hear talk about parts of the brain like "Amygdala" or "Hypothalamus", so I looked them up in an app called "essential anatomy". What I see is that there's mirror symmetry, and most of these glands/nuclei are actually mirrored in two halves of the brain.
I'm trying to understand how two halves of nuclei like amygdala work together. For example, it is frequently said that Amygdala processes fear response. If it was a single nucleus, it is conceptually easy to comprehend, but what about a "multi core" nuclei with two halves? Which half would process the fear response?
Additional questions to help clarify this question:

Are duplicate nuclei connected through some nerves, making up a single organ?
Is there a dominant/non-dominant relationship between halves (like dominant hand)?
Or do nuclei fulfill identical role within different brain halves (right half gets scared, then left half gets scared)?

Here's an image that prompted my curiocity - it is a 3D model of nuclei that sit on top of brain stem and under white matter.

Regarding to amygdala, I have read somewhere that they have slightly different functions like processing negative and/or positive emotions. So maybe they are not have to be in communication? I am not sure tho. I hope somebody explain and we can learn it.

The two symmetrical counterparts of a brain compartment can interact with each other through connections in the corpus callosum. The purpose behind two regions of the same kind differs. For example, often it is to handle inputs from the two sides of the body respectively. Check out http://en.wikipedia.org/wiki/Lateralization_of_brain_function to get started.

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Calculating photosynthetic efficiency
While calculating photosynthetic efficiency, do we take into account the Gross Primary Production or the Net Primary Production ?

We can actually use either depending on the specified convention, but a more convenient way to characterise the photosynthetic efficiency is:-

Considering the total incident solar radiation instead of that part which is absorbed (so that the calculated efficiency takes into account the total available solar energy on earth)
Using Net Primary Productivity instead of Gross PP.(so that the efficiency is characterised by the useful output (product) of photosynthesis by removing the non-useful respiratory losses of plant.)

I should also mention that using GPP instead of NPP was the practice followed in a large number of texts I read. But I think using NPP is not only the modern view, but also scientifically more convenient.
Here is the wikipedia page on photosynthetic efficiency and here is the book which houses the technicalities of these definitions along with several values of the various efficiencies.


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Why do hummingbirds build nests with live ferns instead of dead materials?
Hummingbirds prefer to build their nests with spore-bearing ferns, and mosses. This is helpful for the reproduction of the ferns, which are then better able to spread their seeds. But how is this beneficial for hummingbirds? Building in this manner is more difficult and energy-consuming.
Do live ferns make for better building materials? Is there a scent that these ferns are giving off to attract the hummingbirds? What kinds of research exist on this question?
References:
Carl Zimmer's National Geographic article, "A Living Nest?" (Feb 4, 2014) http://phenomena.nationalgeographic.com/2014/02/04/a-living-nest/
Question by Twitter-user Jessica: @LadyJaya

A wild guess: Where living ferns and mosses thrive it is a damp environment. In a damp environment, dead plant material would start rotting fast. Thus, using living plants guarantees a more durable nest.

From the article titled "Evidence of mutualistic synzoochory between cryptogams and hummingbirds", the specific advantage for the hummingbird is that it gets good nest building material through the selection of cryptograms. The cryptograms though have its seeds dispersed over large distances by birds which is a process called synzoochory.

Great answer / citation! I might rephrase as "the specific advantage given for the hummingbird is good nest building material" - it seems unlikely the authors would call it a mutualism unless they believed that there was a real benefit to both.

@Oreotrephes You are right.. I'll edit it.


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In vitro transcription, contamination problem
I am using a RNA which is in vitro transcripted before I started my project. It turned out it is not prepared properly and has DNA contamination.
Instead of perform the in vitro transcription again, I want to try to clean it with DNase treatment and LiCl precipitation afterwards. Do you think would that work?
And second thing, in vitro transcipted RNA is in different dilutions, so I have a little bit of stock (maybe 5 uL) which is around 200 ng/uL and I have other dilutions 1 and 0.1 ng/uL. I would like to clean all of them. Do you think if I just mix all of the dilutions with the stock and determine the concentration and do the rest? Is it appropriate?
Thanks!

DNase treatment is actually one of the optional steps if you want to get rid of the original DNA template: https://www.neb.com/protocols/2013/04/02/standard-rna-synthesis-e2050
If you know, your the contamination happened after the transcription, DNase treatment should obviously help.
Concerning the aliquots: your stock is 200 times more concentrated than the aliquots (so to get equal amounts of RNA as in 1 µl of the stock, you'd need to take 200 µl of the 1 ng/µl aliquot). I don't think it's worth mixing them (and the efficiency of RNA precipitation will likely be decreased), otherwise just make another transcription.

Thanks @har-wradim. You are right about the aliquots, I will just try to clean the stock even though it is not that much.
I think the contamination is due to original DNA template. Do you think it would still help?

It should, that's precisely the purpose of the optional DNase treatment step. For many tasks the presence of the DNA template is not a problem though.

I am mixing it with another RNA and performing qPCR. So for me, I need to see if I get the exact amount of RNA that I put after certain steps. And with -RT reaction of this RNA (without RT enzyme) it gives signal. That's why I am not sure if the signal that I get from my experiment belongs to my RNA input or DNA template contamination.


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Gene distance and Recombination Frequency: Mechanism
Why is the recombination frequency higher if the genes are farther apart?

Alan, thanks for your excellent analogy. We're talking about the probability of a random event happening at some place on the string.To me the key in the analogy is the probability of this random event happening. Whether that's "cutting", or "tied-up", or even "melted together", the random event, in my mind, is affected by how many marks there are on the string, and how far apart they are relative to each other. This probability calculation is the recombination frequency.

The genetic phenomenon referred to as recombination reflects the process of crossing over which occurs during meiosis. Crossing over creates an exchange of genetic information between homologous chromosomes. To a first approximation cossing over events take place at random positions along the aligned chromosomes. Consequently the further two loci are apart, the more likely that there will be a crossing over event between them. Thus the recombination frequency can be used to measure the distance between two genetic loci (or genes).
Supplement added in response to comment from OP

An analogy
Imagine a piece of string. It has 6 marks on it (1-6 on the diagram) which divide it into 7 intervals (A-G). We are going to cut the string at one of the marks. We throw a die to decide which position to cut.
What is the probability that our cut will separate A and G? It's 100% since all single cuts will do this.
What is the probability that our cut will separate A and D? It's 50% since single cuts at 1,2 or 3 will do this.
What is the probability that our cut will separate A and B? It's 16.7% (1/6) since only a cut at position 1 will do this and the probability of throwing a 1 on our die is 1/6.
Think of the intervals (A-G) as genes and the cut sites (1-6) as possible crossing over events. If two homologous chromosomes are going to undergo a single crossover somewhere at random, then the closer together are the genes (intervals), the less likely is it that the crossover (cut) will take place between them. This assumes of course that the site of crossing over is chosen at random.
In the model presented here, if the order of the letters was scrambled and didn't know what it was but we were told the frequencies of occurrence of the separation of the intervals with random cutting we could deduce the order of the letters.

To me the statement "Consequently the further two loci are apart, the more likely that there will be a crossing over event between them" is still not obvious. It is the core of my question. Please elaborate further.

Thank you very much for the effort. However, I am not yet clear, sorry for this. Crossing-over involves genes physically being 'tied up' temporarily. I fail to see how is cutting analogous to it? Why should chances of such 'tying up' increased if the genes are farther apart?

I don't know what you mean by being 'tied up'. Crossing over involves a physical interaction between two aligned chromosomes at a randomly chosen point. The further that two genetic loci are apart then the more likely it is that the randomly chosen point of crossing over will lie between those loci. I really can't think of any other way to explain this, so I hope someone else comes along and gives you the explanation you are looking for.

@DurgaDatta, i absolutely got it why you're not understanding. You simply don't understand how the crossing over happens on a visual level. https://www.youtube.com/watch?v=jd3H0pgVCr8. Minute 1:06 . If you pay atention to this frame, you'll see that, had the cut been a little over the loci on the top, the meiosis would yield the "same" old gametes - at least in terms of these loci. But, since the cut was between the two loci, we're having recombined gametes, like Ab and aB. Thats why one would say that if two loci are very further apart, crossing over between them is very likely.


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How to design an experiment with scent triggered memory recall in humans?
I've recently learned that scents can trigger memory recall in humans, and am thinking about setting up an experiment where I would attempt to induce memory recall through exposure to scents.
In order to help reduce the amount of experimentation required to actually trigger recall, I'm interested in - What kinds or qualities of scents have been demonstrated to trigger memory recall in humans? Are they pleasant smells/unpleasant,  sharp or subtle?
Is there any information about how long of an exposure is needed to trigger such recall? Is it 2 seconds, 15 seconds, an hour?

From personal experience and also being curious about this phenomenon I can add: Sometimes normally unpleasant smells get "pleasant" by triggering a pleasant experience. And it does work the other way round as well: specific situations can trigger "smell hallucinations" of former similar situations. All in all, this is a very tricky thing to study, so you best start by asking around how it works for different people. For me, it is instant, it does not matter if the smell is pleasant/subtle/..., the memory is more important than the type of smell and a situation also triggers a smell.

Originally I wanted to try this experiment during sleep, however, the K&R "Principles and practice of sleep medicine" 4th edition, on page 16, under "Olfactory system" mentions that both pleasant (peppermint) and unpleasant (pyridine) smells were poorly recognized during sleep:

Both well recognized during stage 1 sleep
Peppermint not consciously smelled in stage 2, stage 4 and REM sleep.
Pyridine not smelled in Stage 2 sleep
Pyridine occasionally smelled in Stage 2 and 4 sleep

It suggests that one conclusion would be that olfactory system of humans is not a good sentinel during sleep.

Scents can make memory recalls. We experience this very often, like when we repeatedly smell a good perfume in ,say a shopping mall , and when some person uses it too, we recall the memory of the shopping mall. This hqppens especially when the smell is associated with a very good or very bad incident.
For an experiment, you can expose yourself or someone to a particular smell ,either very good or very bad at any one time, like during examination or holidays for a couple of times. Next when the person again smells the scent he/she will be reminded of the previous exposure.
As regards to how long the exposure is required to trigger recall,it depends upon how strong the smell is (subtle smell takes ponger time) , how good/bad the memory is (very good or very bad memories will be recalled faster) and ofcourse on the memory associativity power of the person.


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Can you approximate Cardiac Output by Ohm's law?
I found this sentence from my notes which I cannot understand
PR < CO, CO $\uparrow$, PR > CO $\downarrow$

where
\item CO = AP / PR, Cardiac Output = Arterial P / Peripheral Resistance

I cannot understand the first sentence.
I cannot understand how you can deduce by Ohm's law the relationship.
What is the point of the first sentence?

I don't get the first sentence either, since PR and CO in your notation are in fundamentally different units. It's like saying '4 Celsius < 5 meters.' You will have to think about what you are implicitly holding constant and ignoring in that relationship to make it meaningful. I suspect the first sentence is just emphasizing the inverse relationship between CO and PR (PR goes up, CO goes down, etc).
As for Ohm's law, absolutely! You have it written right there. I assume Cardiac output is the flow rate of fluid in a blood vessel, and AP is arterial pressure, and PR is peripheral resistance. Stated another way,
$\textrm{Flow} = \frac{\textrm{Pressure}}{\textrm{Resistance}}$,
which is exactly Ohm's law. Frequently electrical current is described with a Hydraulic analogy, with pressure$\rightarrow$voltage, fluid flow$\rightarrow$current, and flow resistance$\rightarrow$electrical resistance. It makes a lot of sense, since electric current is literally flow of electrons. Poiseuille's Law that makes this analogy rigorous, deriving an Ohmic relationship between those variables. Interestingly enough, Poiseuille derived the law in the context of blood flow, making it particularly applicable.


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Correlation between muscle size and absolute strength
Is there a linear connection between muscle size and the power it can produce?
If not, why? And what is the true correlation if any, can it be described with an appropriate function? What other factors modify it? (Red/white fiber for instance?)

The short answer to your question is that the work output from a muscle is a combination of physiological cross-sectional area, length, fiber type, and recruitment (how many motor units are activated).
Read on for more details.
Force output (tension) of a muscle is proportional to its physiological cross sectional area (Fundamental of Medical Physiology), and shortening is proportional to the length of the muscle. Work output (force X length) is a function of both. Power (work / time) involves both force, length change, and the shortening velocity. Shortening velocity is related to muscle fiber types.
There is a complex relationship between force output and length. In the graph below, the x-axis is relative length (1.0 being resting). When muscles operate outside a relatively narrow range (gray box), the cross-bridges are either too close together or too far apart to optimally generate force. When the muscle gets really stretched, force goes up, but only because passive tension (the intramuscular connective tissue is getting stretched) increases.

The force-velocity curve below relates relative force output to how fast the muscle is shortening (which can be negative; i.e., lengthening contraction). The green part of the curve is muscle shortening. As velocity approaches 0, the muscle produces maximal shortening force. When the muscle goes into the red part of the curve, force is even higher. In order for a muscle to shorten very quickly, it can't produce a lot of force (far right).

Muscle fiber type generally relates to both the force output of a muscle fiber and it's shortening velocity. There are different ways to classify muscle fibers (enzyme activity, myosin isoform, or the "classical" method):

SO ("slow oxidative"; the dark meat of a chicken) fibers contract slowly, produce lower force but are fuelled by oxidative reactions and thus have good endurance. At the other end of the spectrum, FG ("fast glycolytic"; the white meat of a chicken) fibers contract quickly with high force, but fatigue easily because they get energy from glucose, which is rapidly depleted. FOG fibers are intermediate between the two.

The muscular fiber cross section and length would be proportional to its strength, but there are also many different kinds of cellular types and structures which can result in muscles which are quicker or stronger, have better endurance etc.
This post from 2009 ago puts forward the hypothesis that chimpanzees, who weigh 70 to 130 lbs (32 to 60 kg) are typically capable of lifting 3-4 times more weight than a human being can. They also put forward that the coordination of the muscle with other muscle fibers makes up the gross difference in strength. Human beings have much better fine motor control for delicate operations than chimps, which might cause the muscles to be less in synch resulting in lower strength despite the fact that we have about the same amount (or less) of muscle tissues in say our arms or legs.

Muscle length doesn't have any effect on force output, only the range of useful shortening distances.

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How many blood types are there?
In total how many blood types are there?
And why do people normally know only 8 of them? (A+, B+ , AB+ and O+ and Rh- counterparts)

As I remember from my physiology studies that there are more systems. So you're interested in the ABO system only or the other ones as well? check this: http://en.wikipedia.org/wiki/Human_blood_group_systems#Blood_group_systems

@zeller Thank you, anyway I cannot understand why normally we know only ABO system and I cannot understand if each system is only a different "convention" of if it denotes a somewhat different blood system.

Unfortunately I can't answer that, as I haven't studied immunology, but based on my recent readings (on wikipedia...), most of them check different antigenes/ligands/whatevers.

Adding insults to the question will not help to reopen it. Working on the content will. Comments should be added into the comment field.

@Chris insults? What's not clear in "This question has been asked before and already has an answer."? I repeat: the time line goes from left to right, from lower numbers to higher numbers. It's pretty easy.

@HAL9000 The question is not whether ur query was answered first or not.. In general it has been answered. Shouldn't you just be glad that you have been pointed to the answer. Just ask a new question for any further clarifications


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To understand Second messenger signalling in I/c and E/c
I found this picture in my study materials.
I think it is too schematic and ignores the big pictures.

I think the thing connected to the hormone is receptor.
The second messanger is then connected to the receptor which stimulates the effector cell in the cytosol.
The cell then response both to cytosol and to extracellular space.
How do you understand this picture?
Do you know any similar pictures which present the same thing but clearer and more exactly?

I think the schematic you have there and the one that @Masi posted are pretty good.  A better way of getting a grasp of intercellular signaling would be to study a specific hormone and understand how each of the elements in the block diagrams here could vary.
For instance take a look at this diagram from a journal article where they are tinkering with yeast mating factor, one of the first discovered extracellular signaling pathways.

alpha factor and 'ligand' (I assume its not known at this point) bind to their receptors Ste2 and hGPCR respectively.  They then activate G protein complexes and both activate the same kinase cascade Ste4/18 -> Cdc42 -> Ste20 -> MEKK/MEK/MAPK/Ste5 which then may activate Far1 (or not) and Ste12.  Far1 and Ste12 are migrated into the nucleus to activate genes for cell reproduction.
By actually filling out the boxes in your diagram you can see dozens of different paradigms for how cell signaling may work, and why the diagram you have needs to be so simple.  Hope this helps.

Glad it makes sense!

I found this picture from my old study materials which I edited little to show the I/e and E/c spaces.

I think some arrows are missing. Probably, some arrows should go from specific modifications of enzymes or proteins to I/c and E/c. What do you think?


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What percentage of the fitness variance is explained by the 'n'- most important loci?
Introduction
Standard models in population genetics look up at the evolution of few loci which impact fitness. The variance in fitness is determined by the genetic variance and the environmental variance (and the co-variance between environment and genetics). In this question I am interested only about genetic variance and about what percentage of the total (additive or not) genetic variance in fitness do 'n' loci explain.
Question
In general, in natural populations, what percentage of the total genetic variance is explained by the 'n'- most important loci?
Here, by "most important loci" I mean loci which variance explain much of the total genetic variance.
In other words, the subquestions are of the kind:

how much of the fitness variance does the most important locus explain?
How much of the fitness variance do the 3 most important loci explain?
How much of the fitness variance do the 100 most important loci explain?

Of course, the answer depends on the population under consideration. Factors that might influence the answers are for example

species
population size
environment stability
…

Beside this question, I also welcome some insights concerning how different factors are likely to influence the answer.

Do you have at least one example of an empirical study of the type you are looking for ? It may be a helpful starting point for us in finding other ones.

No, unfortunately I don't know any empirical study that investigates my question.

And do you have any study, which measures percentual increase in fitness, regardless of the cause ?

Could you phrase this in terms of just one question?

@Atticus29 Thanks for your comment. I updated my post in order to have one clearly stated question. Does my question makes sense to you?

I think its exceptionally rare for the most important loci to collectively explain more than a small percentage of the total genetic variance, it's a fundamental problem with QTL - looking for something of large effect when by definition we expect most or all effects to be tiny. I'm looking forward to seeing an answer to this one! It's going on my favorites

I don't think there's a great answer to this one, partly because fitness is a tough trait to measure. I think more is known for other traits like height, but even there, if we want accurate estimates of the variance associated with 100 alleles, we're limited to humans at best.

I agree with Daniel. Maybe you should open your question to other polygenic trait. A lot of money is being invested in genomic selection and most of the time the target is yield. here we have hundred of markers with effect lower than 1%.  Fitness seems to be quite integrative and therefore very polygenic and environment dependent. Do you have study showing heritability of this trait? Another factor that could influence your variance is allele frequency. See GWAS model. Are you interested in study doing that on other trait? I may answer in that case!

This should be taken less as a holistic answer than as a case study describing an extreme example of very strong selection in a particular environmental context, yielding a particular natural experiment. I suspect that this question may be very difficult to answer in a general case without more work!!
This answer should not be taken to show any general case or reflect anything about the distribution of variant fitness effects of a relatively stable population.
I hope that posting this very partial and contextual answer might inspire other answers to this very interesting question.
In sticklebacks, armor morphology is mostly controlled by a single large-effect variant locus at the Ectodysplasin (Eda) gene, ~85% of phenotypic variance is associated with this locus. It is known that there is a strong fitness relevance of armoring according to environment, wherein freshwater fish are under selection for low armor (due to metabolic cost), and saltwater fish are under selection for high armor (due to predation pressure).
This pattern is highly repeatable across events of colonization by saltwater fish of new freshwater habitats, wherein populations are swept by the low-armored allele of Eda as soon as they become resident freshwater populations.
Recently, Dolph Schluter and colleagues set out to directly quantify the fitness effects of this variant in a newly colonized population of sticklebacks that was undergoing the microevolutionary shift from high to low armor. In this population, the selection coefficient for the lower-armor allele was extremely large ($s = 0.5$).
Schluter and colleagues mapped QTLs for female reproductive fitness in an F2 cross, unsurprisingly yielding the Eda locus. They detected no other loci, though this should not be taken to mean that there are no other loci, due to power issues. They found that Eda explained 8% of the variation in fitness across their F2 panel.
In summary, in this particular case of very strong selection and quite high fitness variation of the population, one locus explains 8% of the fitness variation in an F2 cross (which is likely not completely representative of the population). No other loci have any detectable fitness effects compared to this.
It would be very interesting to see how this is repeated in other case studies, more stable populations, more polygenic cases, or measured at the whole-population (GWAS) level rather than the F2 intercross case.

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To understand synthesis of e-NOS and n-NOS with respect to Ca and calmodulin
I found this sentence in my notes interesting

E-NOS and n-NOS are Ca-calmodulin dependent ferments.
  They are synthesized in small concentration as a response to physiological signals which increases the level of Ca2+ in cell.

Does it mean that e-NOS and n-NOS are synthesized by mediation of Ca and calmodulin?
I remember how RNS can be derived from nitric oxide and superoxide.
Are e-NOS and n-NOS expressed on macrophages after induction by cytokines and microbial products, notably interferon-gamma and lipopolysaccharide?

What is the reference for your notes? Can you cite a valid reference?

Sorry, I cannot. This is a classroom discussion, mostly based on current textbooks in Physiology and Pathophysiology. Good bet would be in Robbins.

Does it mean that e-NOS and n-NOS are synthesized by mediation of Ca
  and calmodulin?

Calmodulin is activated by binding to calcium and NOS is activated by binding to Ca2+-calmodulin. The binding changes the structural conformation which renders the enzyme active. See this.

Are e-NOS and n-NOS expressed on macrophages after induction [...]

Macrophages generally express iNOS upon induction by cytokines. The activity of iNOS is shown to be different in humans compared to mice; humans have low activity [ref]. However mouse macrophages have been shown to express eNOS constitutively and eNOS-knockout mice show reduced NFkB production and iNOS induction.


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Death by exsanguination not painful?
Several places on the internet seem to purport that animal sacrifice is painless because exsanguination causes no pain. That sounds unscientific to me and an attempt to appease culture than than using science. For instance this question on the se and others like it on the internet. Is there a difference between pig and cow anatomy that makes religious slaughter of the latter less painful?
Could someone comment on the validity of this research?
Schulze W, Schultze-Petzold H, Hazem AS, Gross R. Experiments for the objectification of pain and consciousness during conventional (captive bolt stunning) and religiously mandated (“ritual cutting”) slaughter procedures for sheep and calves. Deutsche Tierärztliche Wochenschrift 1978 Feb 5;85(2):62-6.

I just mention this as a tangental point because taking a step back and looking at the bigger picture may be helpful in some way when thinking about animal slaughter methods: human-devised methods are typically a lot less painful than being run to exhaustion, then torn to pieces and eaten alive by a pack of wild hyenas. I imagine being old and decrepit then starving to death is not much fun either. :)

This is of course a controversial topic with there being supporters for both methods of slaughter. First of all, The research paper that you have mentioned is a highly cited one and it is the foremost study that supporters of exanguination use to support their method of slaughter. However, the author himself (Wilhelm Schulze) has stated and I quote

"objective results presented for the captive bolt application in sheep
  indicates that the captive bolt device used is suspect" and that these
  initial "scientific findings and the results presented are only a very
  first contribution" and that they "need to be followed as a high
  priority by further investigations in the continuation of the
  scientific clarification of the issues of loss of pain and
  consciousness during slaughter of this kind with and without stunning
  using the same experimental approach with a representative number of
  grown cows of various breeds." (reference)

Since stunning methods have advanced (reference) from the time this paper was published (1978), it would probably be a bit unfair to hold onto this paper as proof for supporting exsanguination. Moreover, in another study, in which measurements were done with an electro-corticogram it was found that

Captive bolt stunning followed by sticking one minute later resulted
  in immediate and irreversible loss of evoked responses after the stun.
  Spontaneous cortical activity was lost before sticking in three
  animals, and in an average of 10 seconds after sticking in the
  remaining five animals. The duration of brain function after shechita
  was very variable, and particularly contrasted with captive bolt
  stunning with respect to the effects on evoked responses. These were
  lost between 20 and 126 seconds (means of 77 seconds for somatosensory
  and 55 seconds for visual evoked responses) and spontaneous activity
  was lost between 19 and 113 seconds (mean 75 seconds) after slaughter (reference).

The two questions that have to be answered in exsanguination are
-- Does the neck cut cause pain?
-- How long does it take for the animal to lose enough blood for insensibility to occur and for any perception of pain or suffering associated with slaughter to disappear?
With regard to pain, in the process of cutting the major blood vessels leading to and from the brain a number of other tissues are also severed by the extensive neck cut including muscle, skin, sensory and motor nerves etc. There is a chance that this might cause significant shock and fear to the animal. The time to lose consciousness is highly variable in  exsanguination. (reference)
Very good arguments are presented in this article and I highly recommend that you go through it.


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Elution of biotinylated RNA
I am using Neutravidin Agarose beads to isolate biotinylated RNA. The thing is, in the manual it says to use 8M Guanidine-HCl, pH 1.5 for elution biotinylated molecules. As far as I know it is a very harsh elution buffer. Do you think it would effect my RNA? I have isolated my RNA with TRIzol which also contains Guanidine salt but the concentration is not that high.
As a second question, do you know other ways to elute my biotinylated RNA from beads?
Thanks!

The biotin-streptavidin interaction is extremely strong, one of the strongest (if not the strongest) non-covalent interaction between biomolecules. So you'll need pretty harsh conditions in any case.
Extreme pH values are generally a very bad idea for RNA. I'm pretty sure that the conditions you mentioned are not meant for elution of nucleic acids. Such low pH values (and high pH values as well) lead to a quick hydrolysis of the phosphoester bond of RNA, you can read more about the mechanism of that in this review.
A quick Google search lead me to the following protocol:

To dissociate biotinylated nucleic acids from Streptavidin-Coupled
  Dynabeads®, incubate the beads in 95% formamide + 10mM EDTA, pH 8.2
  for 5 minutes at 65°C or for 2 minutes at 90°C.

This sounds reasonable to me, as formamide is also commonly used in sample buffer for denaturing gel electrophoresis of RNA. I haven't done anything like that myself, so I can't guarantee that this would work in your case.

Hey,
thanks a lot for your answer.
I found an other solution. Instead of destroy the bond between biotin and Neutravidin which is obviously so strong, I am going to cleave the bond between biotin and RNA which seems more logical for downstream experiments. The biotin that I am using is binding to RNA with disulfide bonds. So, I am going to use 100 mM 2-mercaptoethanol to achieve it. What do you think about it?

@golgicik Cleaving at a different point is the easiest way if you don't need the biotin later and only use it for purification. I can't comment on the practical aspect as I haven't done something like that myself.

I will use RNA in RT-qPCR so I do not need biotin. Thanks a lot for your input!

i guess pH 8 won't be good for RNA. Mercaptoethanol or DTT would be a decent option.. I am not sure about this but you may use proteinase-K as well.. It would destroy streptavidin and other protein contaminants.

I'm way late to comment, but thought I should add that I was able to displace biotinylated protein from avidin with a large excess of free biotin. I can't remember the exact concentration, but it was pretty high, and I had to let it sit overnight.


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Characteristics of radius of blood vessel
Which properties do determine the radius of blood vessel?
I have these thoughts

distension,
elasticity,
contractility and
cross-sectional area of the walls.

Is there any other properties?

The radius of a blood vessel is entirely defined by only two parameters:
1.blood pressure
2.compliance of the vessel walls
Of course, active contraction can decrease the vessel radius. Physically, this is a decrease in compliance, so the above relation always remains true.


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Birds and Dinosaurs
This came up in an argument with some friends. I know that birds are direct descendants of dinosaurs, shown pretty clearly through the fossil record. However, is it proper to say that birds are dinosaurs, or is there an actual distinction?

Do you know the concept of monophyly?

To comment on common scientific usage, I definitely hear paleontologists refer to "non-avian dinosaurs" when they want to exclude birds. Which implies that they would refer to birds as dinosaurs.

I bet you'll be interested about the concept monophyly. Any human-made group of species (or taxon) like birds dinosaurs, primate, bacteria, angiosperm, reptiles, … are either monophyletic, polyphyletic or paraphyletic. This picture explain the concept When the taxon is monophyletic it is called a clade.

Monophyletic taxon are those groups of species that can be considered to be objective in the sense that it represents a group of species where each species in the taxon is more related (in terms of time to common ancestor, not according to their genetic similarity) to any other species within the same taxon than to any other species outside this taxon. This is obviously not the case for paraphyletic or polyphyletic taxon.
Typically, we do not consider a parrot or a deer to be reptiles. Therefore, the ususal understanding of "reptiles" makes this taxon paraphyletic. Now, one should not confound the common understanding (what is a reptile in our everyday life) with the strict definition of the taxon Reptilia, which is a monophyletic taxon (or a clade in other words). Probably the best source for exploring the tree of life is tolweb.org. Here, you will find the clade Reptilia (who include birds, snakes, turtles and lizards). Note: Mammals are within the Reptiliomorpha, not the Reptilia.
It is exactly the same issue with the dinosaurs. When we talk about dinosaurs in our everyday life we do not mean birds. But there is a clade called Dinosauria, which include both dinosaurs and birds.
In short, I would say that a bird is a Dinosauria (monophyletic taxon) but is not a dinosaur (paraphyletic taxon). But this little play on word is not a scientific issue but an issue of english usage.
You will also find in this post an introduction to phylogeny

Some comments: 1) "paraphyletic clade" is an oxymoron; 2) "Monophyletic clades are those clades": again, clades can be only monophyletic by definition; 3) "clades ... can be considered to be objective": clades exist or do not exist irrespective of our considerations; 4) "more related" is very dubious term in this context, which could be here incorrectly understood as "more (genetically) similar"; 5) Reptilia doesn't include mammals on tolweb.

@har-wradim Indeed there were many corrections to do. I hope I fixed the problems. I confused the words taxon and clade. Thank you for your comments. Please feel free to edit the answer yourself in order to improve it.

English usage is definitely evolving on this one. I'd say "Birds are dinosaurs" is the new "spiders aren't insects" - it's getting into the repertoire of the annoying know-it-all who has learned cool scientific facts and insists on sharing them with the world. Some references : https://xkcd.com/1211/, https://en.wikipedia.org/wiki/Origin_of_birds (notice "birds are a group of theropod dinosaurs"...)

@RozennKeribin Except that insects (not counting spiders) are a monophyletic group. Dinosaurs (not counting birds) are not monophyletic (as your xkcd comic indicates).

@RozennKeribin I strongly disagree - the distinction between birds and dinosaurs is much muddier (@Remi.b's mono/paraphyletic distinction is excellently described) than the distinction between spiders and insects.

@Remi.b but dinosaurs (counting birds, and excluding pterosaurs and other dinosaur-like reptiles, which many paleontologists and nerds who employ this usage do) are monophyletic.

@BryanKrause I wasn't comparing birds/dinosaurs to spiders/insects from a biological standpoint, but from a meme/English usage standpoint. My point being that while the vernacular "dinosaur" usually represents a different group from the clade "Dinosauria", the usage is evolving in certain circles at least to make them coincide (and that group are those that will tell you that birds are dinosaurs and pterodactyls aren't).

Spider + insects (+ crustaceans and other things): monophyletic. spider: monophyletic. insects: monophyletic. birds+dinosaurs: monophyletic. brids: monophyletic. dinosaurs: not monophyletic. Dinosaurs is not a stand-alone mnonophyletic group unlike spider and insects are. In other words, spiders and insects are sister(-ish) taxa while dinosaurs contain birds. This is why I think your comment is misleading.

You are begging the question. Dinosaurs: not monophyletic if "Dinosaurs" is defined so as to exclude birds. And what I am saying is that in modern English usage, that definition is no longer so clear-cut as to exclude birds; there is an increasing number of people who use the vernacular "dinosaur" to mean "belongs to the clade Dinosauria", and to explicitly include birds. I'm not talking biology here, I'm talking an evolution in the English language.


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Identification of a mysterious lifeform, what is this?
For the third time in a row, I found a mysterious life-form inside my house. I live in the Netherlands in the Eindhoven region, in a city called Oss near a forest area. Before I set it free outside, I put it in a jar to make a few pictures for identification purposes. What is this creature?

How big is this bug? Do you have a photo where the markings on the back can be seen better?

Wow, the site is getting bigger, we actually already have a question about this insect (or a very close cousin), voting to close as a duplicate.

@Chris The creature is about 3~4 centimeters long, including the legs. If I'd have to estimate the body, I'd say roughly ~2 centimeters. terdon; It does not seem to be the same one?

@terdon I think so, too. Its hard to say which one exactly from the images since the back is not clearly visible.


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Staphylococcus AG structure?
I found this statement in my study materials in the section of Staphylococcus

The AG structure:

protein AG (species specific);
polysaccharide AG (serotype specific).

I know what is Protein A/G, a recombinant fusion protein that combines IgG binding domains of both Protein A and Protein G.
What is the point of this AG structure thing in the contex of Staphylococcus?
Can we say that staphylococcus have AG structure?
I think it has properties related to protein A\G and also to polysaccharide A\G.
I know very little about polysaccharide A\G and not sure how it is related to serotype specificity in the context of staphylococcus.
Extension to the question
Antigenic structure of Steptococcus pyogenes:
the group AG is unique, placing streptococcus in group A.

What is the AG here?

After puzzling over this for a while I think I have the answer . It's nothing to do with protein A or protein G. I think that whoever wrote your study materials meant Ag which is a common abbreviation for 'antigen'. I guess this was in the context of immune responses, or strain typing.
Looking back over your last few questions, it seems that you are at the mercy of a teacher who specialises in ambiguity.

I added one more confusing statement which I do not understand about S.pyogenes. Do you understand AG there?

http://en.wikipedia.org/wiki/Lancefield_grouping
"a method of grouping beta haemolytic bacteria based on the carbohydrate composition of bacterial antigens found on their cell walls."


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How does Mupirocin affect in staphylococcal infection?
I found this sentence confusing
Transitor carriers of staphylococcal infections 70% because of mupirocin i/n.

Mupirocin is drug which affects some way.
I am not sure if the statement means inner neuronal.
I am little confused by the abbreviation i/n.
What is the point of the sentence?

This comes from the usage of the Mupirocin: Its an antibiotic, which is used topically (on the skin, its not taken in form of pills). It binds specifically to the isoleucyl t-RNA synthetase in gram positive bacteria and Streptoccus and Staphylococcus and is used to fight intranasally (that what i/n stands for) infections with these bacteria. It inhibts the introduction of isoleucine into proteins. More informations can be found here.


text:
How many (taxonomic) families are there?
Approximately, how many families have been identified?
I've often often come across figures for the total number of species on Earth. Recently, I found myself wondering about the encompassing ranks above them, specifically family, but I can't recall any figures on family and it's a little difficult finding what I want by typing "family" into a Google search. ;)

Families (and really, any taxa except species, to some extent) are artificial, fluid and ever-changing. That's not to say they aren't useful, but the number of families is likely to be changing quite a lot on a nearly daily basis, as more and more families are converted into monophyletic groups based on DNA evidence.

... but just as a round estimate its thousands at least.  browsing encyclopedia of life I see scores just in the flowering plants...

This was asked three years ago. I am curious what the numbers look like today.

Not so many they couldn't fit on a very big boat.

The 2011 paper How Many Species Are There on Earth and in the Ocean? indirectly answers this question as well as any other source you'll find I imagine. It estimates how many species there are total based on the rate of discovery of higher taxa; it includes plots of number of taxa over time for the major groups of life in Figure S1. Which gives:
Animalia - 5300 families in 2011 (the plots are given with only one significant figure, the second one's my estimate) (estimated total: 5800)
Chromista - 270 families (estimated total: 360)
Fungi - 550 families (estimated total: 620)
Plantae - 750 families (estimated total: 800)
Protozoa - 280 families (estimated total: 310)
Archaea - 27 families (no estimated total; the number has been increasing exponentially so far)
Bacteria - 300 families (same as for Archaea)
Which gives us a total of 7477 families in 2011, with an estimated total of (ignoring Archaea and Bacteria, who don't really fall in the same kind of classification anyway) 7890 families. (make that 7500 families discovered by 2011 and 8000 estimated in total given the imprecision involved in my reading the plots).

The NCBI Taxonomy statistics page displays the following information:
There are currently 73540 genera, 331418 species, and 23127 taxa of higher order. Since the number of taxa decreases with the genericity of the taxon, there are probably around 20000 families, give or take a few thousand.

The Plant List has 642 families listed: http://www.theplantlist.org/1.1/about/#changes.
For a quick comparison, Wikipedia lists

522 fish families:
en.wikipedia.org/wiki/List_of_fish_families
136 mammal families:
en.wikipedia.org/wiki/Mammal_classification
61 amphibian
families: en.wikipedia.org/wiki/List_of_amphibians
57 reptile families: en.wikipedia.org/wiki/List_of_reptiles.

This only covers a subset of the total, however (see here for other animal classes). It is relatively difficult to find a good, and relatively complete answer to this, though.

I don't know about other groups, but about plants, number of families depends on the system you follow. Recent version of The Plant List (1.1) estimates about 352 000 species of Angiosperms and lists over 400 families. See http://www.theplantlist.org/1.1/browse/A/ It is very good and reliable source of information. Second very good source about plant systematics is database Tropicos provided by Missouri Botanical Garden and Angiosperm Phylogeny Group. See list of families according to APG3 http://www.mobot.org/MOBOT/research/APweb/ and click to "Families" on the top of the page. Just note, that there are also synonyms, so that You can't just count the rows. ;-)

I'm adding this as another answer since it's a different source, but Gaurav gave this excellent resource as an answer to this related question:

The Integrated Taxonomic Information System (ITIS) is maintained regularly by a consortium of North American governmental agencies, and will give you a list of all the classes, orders, families or genera in any of seven kingdoms they recognize. It might be biased towards North American taxa, but it might be quicker to get a list from then rather than extracting them from Wikipedia.


text:
Regional circulation and Cardiac output?
I am reading my study materials and think what is the systemic POV here

Regional circulation Blood flow within the tissue/organs based on the functional demands of the tissue.
      E.g. The blood flow to the brain should remain relatively constant from a systemic POV (13% of CO at rest).

What is the POV here?
Extension to the question and explanation.
The last part is just 13% of maximal cardiac output.

I'd guess venous P[O_2], maybe. Who gives abbreviations without a key? Although the suggestion of "point of view" make sense in context.

Use the homework tag?

Given the answer this is more of an English Language question than Biology so I'll close it.

This question appears to be off-topic because it is about an abbreviation commonly used outside of the field of biology.

It might be as simple as 'point of view'.

Thank you very much! I really sometimes get confused by the abbreviations used in my study materials.


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What do you see if you look at your own retina with the same eye? (optical feedback)
When you record a video while pointing the viewfinder towards the screen showing a live preview you create optical feedback: video example. An anoalogous effect occurs when you turn your microphone towards the speaker.
Once you look at your own retina with the same eye, does our brain create a similar effect as recorded in the video? Or could it be something different all together?
Obviously the best way to find out is to 'just go ahead' and see for myself, but it seems as if I don't have the proper conditions to test this at home: The pupil gets too small in the mirror and thus the retina is plain dark. Such an experiment would require eye drops to force widen the pupil and allow for more light onto the retina.

Dear mods, I'm not confident if this question is fully appropriate for your site or if it's better to post at http://cogsci.stackexchange.com/. Please decide if you need to migrate this question.

There wouldn't be any feedback loop, because retina is not an "output device". You'll need to wire the eye to the visual cortex or something to have a feedback loop you want.

@Memming Indeed, thanks! This is what I have been trying to say in my answer as well.

@gentmatt - why do you link to a youtube video which is private/unaccessible ?

There was an answer posted here and deleted again - which I think has found the error my question. Please undelete it :)
What the eye observes once it glances at the retina is a physically constant image of the retina.
In order for the optical feedback loop to work however, the retina image 'in' the mirror would need to be affected by what is projected onto the retina of the observing eye. Since the retina image in the mirror is constant (there is no link of any kind between whe mirrored retina an the observing retina) the projected image onto the retina of the observing eye is constant as well.
The loop is broken and there is no optical feedback.

I deleted my question just after posting it because I had some doubts and wanted to improve my answer (which I didn't finally :)). But re-reading it, I bet you were right I shouldn't have deleted it.

You would see your retina and that's all. There would have no "mise-en-abyme".
In order to experience this feedback loop you describe, you need to see something which includes the total picture of what you see. For example: You might see a woman holding a frame of the totality of what you see.

When you look at your retina, you can't see something which includes the total picture of what you see, you just see your retina! It would probably work if the retina was a mirror (or any output device)
This question might not really a good fit for Biology.SE. You might have a chance to make a good fit by asking a question on the mechanistic nature of the process called mise-en-abyme on Phylosophy.SE. And ask wether one can live this same process with any of their sense (perception). You can ask whether the Larsen effect (audio feedback) is a similar process to the one we experience when looking at this picture and in what terms they are similar and in what terms they differ. If you ask such question, I welcome you to add the link on this post (except if the post get closed)!

Feedback means that the output from a device is fed back to it as new input. You can feed input to a retina, but cannot take its output.
You will get no feedback if the microphone is not linked to a speaker, or cannot hear the speaker.
You will get no feedback if the video camera is not pointing to the display.
Your eye consumes input, but this input is only used to change the state of your brain in mysterious ways. No output is produced. There is no "Kodak" organ in the human body which reproduces with fidelity the image seen by the retina*. Without output, there is nothing to feed back - same as how you can't get feedback when a camera is not linked to a display. A display, with human beings, would be analogous to a magic machine that reads your mind.
If you looked at your retina, you'd see your retina. Just like a camera pointed at a mirror would see a camera.
The closest thing you can do is imagine yourself, imagining yourself, imagining yourself... Although you would probably need to take mind-altering substances to experience this fully.

*: I say no organ exists, but it is possible for humans to reproduce an image they've seen. It's called "painting". Some famous painters apparently have included an image of themselves in their picture, depicted while painting the picture.
This isn't really a classical painting, but to give an example:

The trouble is that actually painting a picture takes a long time, so the feedback is very slow - each iteration may take days.


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Which of the cell types commonly found in mammals has the greatest number of mitochondria?
This is basically a fun question, inspired by this answer on scifi.se. So, which cell type will have the greatest number of mitochondria? Obviously, I am talking about wild type, healthy individuals and am looking for a rule of thumb. I realize that the number can change under different conditions/ between different individuals.
Off the top of my head, I would say that it's sperm cells given the strenuous exercise they need to perform and their MT-packed axonemes but perhaps there are better contenders?
I am primarily interested in human cell types but answers dealing with other mammals are welcome.

I'd expect a correlation between cell size and number of mitochondria. Therefore, my guess is that the ovule has the greatest number of mitochondria. On this wiki article it is said: "the number of mitochondria in a cell varies widely by organism and tissue type. Many cells have only a single mitochondrion, whereas others can contain several thousand mitochondria." and give two book references: Alberts and Voet.

Assuming @Remi.b 's correlation between cell size and number of mitochondria, then muscle fibers should win hands down. They are IIRC the largest cells in the body, and they have a need for significant amounts of energy.

oocyte, cardiomyocytes, skeletal muscle.. check this: esp page 11.. Oocyte has to provide miotochondria for the embryo.. so i guess it has the most

To study mitochondria, mitochondria are often isolated from brain, liver and muscles. Mitochondria are abundant in those tissues.

In terms of number, it could be tricky because sizes of mitochondria vary a lot.

try to get this article - http://www.unboundmedicine.com/medline/citation/2318903/Distinct_genomic_copy_number_in_mitochondria_of_different_mammalian_organs_

It's commonly believed that it's muscle cells that have the largest amount of mitochondria, and for good reason.  Muscle cells are continually used to move the body, so they have the most mitochondria because of the large energy requirement.  If you want to be more specific, the muscle cells of a marathon runner have even more since the muscle cells involved in running need to be able to do a lot of aerobic respiration.  Another example is the cells in the heart; the amount of mitochondria makes up 40% of the cell.
The truth is, retinal cells with photoreceptors most likely have the most (80% of the cell volume) since they need to reset the potassium/sodium pump to keep the action potential in the nerves the same.
If you're curious, the cells with the least amount of mitochondria are skin cells and erythrocytes (red blood cells) since skin is just a protective barrier and red blood cells don't need to exert any effort or energy to move.
Sources:

http://hyperphysics.phy-astr.gsu.edu/hbase/biology/mitochondria.html
http://www.ncbi.nlm.nih.gov/pubmed/12511073

Welcome to Biology. It would be great if you could add some references to your answer.

Sorry about that.

That explains what mitochondria do, but gives no reference for the claims you make.

I'm not able to add any more links because I have limited privileges.

That's fine, just paste the URL as is and someone can edit it for you. Your answer makes a lot of sense, and I agree that it is very likely going to be muscle cells, but neither of your references support it. They just explain what mitochondria are. I would particularly like to see a reference supporting your claim about photoreceptor cells, that's an interesting point. I can't accept this since you're just giving numbers with no references.

You can also edit your answer and remove the irrelevant links and replace them. If you have more links, post them in the comments and someone will edit your post accordingly.

I was under the impression that hepatocytes had the highest concentration of mitochondria, as so much of a muscle cell's cytoplasm is taken up by the contractile apparatus.


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Do humans have a "dominant" neurotransmitter system/sensitivity within their brain?
I've recently heard a podcast, in which Dr. Helen Fisher suggests that there are "4 broad personality types", and each one is associated with a particular neurotransmitter:

The corresponding Platonic thinking style, Keirsey temperament type (according to some readers, not Fisher herself), and color can be seen in parenthesis.

Explorer (creative; Artisan temperament, yellow) = dopamine
Builder (sensible; Guardian temperament, blue) = serotonin
Director (reasoning; Rational temperament; red) = testosterone
Negotiator (intuitive; Idealist temperament; green) = estrogen/oxytocin

I'm interested if there's indeed scientific evidence to support that for different people their affinity for a certain neurotransmitter is increased to such degree that it manifests in a noticeable difference in personality?

Dr. Helen Fisher's conclusions are plain bunkum. What does it even mean when she says associated with a particular neurotransmitter? The sheer work required to even get at this question is vast and difficult so it is unsurprising that she is venturing as much as a guess.There is scientific evidence to support different neurotransmitters systems can go awry in diseases but Fisher is overinterpreting the literature. Take a look at the neurotrasmiter table and you can see what each does and how malfunctions can result in certain diseases.
http://en.wikipedia.org/wiki/Neurotransmitter
Also testosterone and estrogen are thought of primarily as hormones not neurotrasmiters.So Fisher is saying women(who have more estrogen) are better negotiatiors whereas men(more testosterone) are directors. Even these banal conclusions are contentious and debatable.

I know that the Keirsey model itself is rather unsubstantiated. It's a sort of simplified version of MBTI. So I am not sure if relating the neurotransmitters to Keirsey temperament would work due to the fallibility of temperaments.
However, different neurotransmitter levels certainly contribute to different moods. That has been proved. Does that translate to personality? Don't know.

This just equivocates. Not a helpful answer.


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Why is Aorta sometimes called Compression chamber?
I find this statement that Aorta is called Compression Chamber in my study materials.
Aorta can

it keeps blood flowing
it can accumulate potential energy for bumping and compression

However, why aorta is called chamber and particularly compression chamber?
I heard this term today first time.

The aorta is a compression chamber because it is an important drive for diastolic perfusion. To keep the blood flowing constantly, and not only during systole (as would be the case with a rigid aorta), the high elasticity of the aortic walls allows it to dilate as a consequence of the high systolic pressure. This allows the aorta to accumulate blood in its proximal part, which is then propelled by the passive elastic contraction of the aorta during diastole.


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Voltage-gated Potassium channels in the action potential of cardiomyocyte?
There is one type of potassium voltage-gated channels open in Phase 1 too.
Some call them early repolarization channels.
I am not convinced that the channels are different in different phases: 0, 2, 3 and 4.
I think all these potassium channels are voltage-gated.
However, they probably differ in some places.
I am not sure if one type of channel can be open in all these five phases.
Which types of potassium channels are open during the action potential of cardiomyocyte?

Two main types of action potentials occur in the heart . One type, the fast response, occurs in normal atrial and ventricular myocytes and in the specialized conducting fibers (Purkinje fibers of the heart)and is divided into five phases. The rapid upstroke of the action potential is designated phase 0.The upstroke is followed by a brief period of partial, early repolarization (phase 1) and then by a plateau (phase 2) that persists for about 0.1 to 0.2 second. The membrane then repolarizes(phase 3) until the resting state of polarization (phase 4) is again attained (at point e). Final repolarization (phase 3) develops more slowly than depolarization (phase 0).
Genesis of the Upstroke (Phase 0)
The action potential amplitude (the potential change during phase 0) is dependent on [Na+ ]o.
The Na+ channels open very rapidly or activate (in about 0.1 msec), thereby resulting in an abrupt increase in gNa . However, once open, the Na+ channels inactivate (time course ˜1 to 2 msec), and gNa rapidly decreases.
Genesis of Early Repolarization (Phase 1)
In many cardiac cells that have a prominent plateau, phase 1 is an early, brief period of limited repolarization. This brief repolarization results in the notch between the end of the upstroke and the beginning of the plateau . Repolarization is brief because of activation of a transient outward current (ito ) carried mainly by K+ . Activation of K+ channels during phase 1 causes a brief efflux of K+ from the cell because the cell interior is positively charged and [K+ ]i greatly exceeds [K+ ]o . The cell is briefly and partially repolarized as a result of this transient efflux of K+ .The size of the phase 1 notch varies among cardiac cells.
Genesis of the Plateau (Phase 2)
During the action potential plateau, Ca++ enters myocardial cells through calcium channels During the flat portion of phase 2 , this influx of Ca++ is counterbalanced by the efflux of K+ . K+ exits through channels that conduct mainly the ito , iK , and iK1 currents. The ito current is responsible for phase 1, as described previously, but it is not completely inactivated until after phase 2 has expired.
During the plateau (phase 2) of the action potential, the concentration gradient for K+ across the cell membrane is virtually the same as it is during phase 4. However, Vm is now positive. Therefore, there is a large gradient that favors efflux of K+ from the cell. If gK were the same during the plateau as it is during phase 4, efflux of K+ during phase2 would greatly exceed the influx of Ca++ , and a sustained plateau could not be achieved. However, as Vm approaches and then attains positive values near the peak of the action potential upstroke, gK suddenly decreases . The diminished K+ current associated with the reduction in gK
prevents excessive loss of K+ from the cell during the plateau. This reduction in gK at both positive and low negative values of Vm is called inward rectification. Inward rectification is a characteristic of several K+ currents, including the iK1 current For these channels, large K+ currents flow at negative values of Vm (i.e., gK is large). However, when Vm is near 0 mV, or positive, as occurs during the plateau (phase 2), little or no K+ current flows (i.e., gK is low). Thus, the substantial gK that prevails during phase 4 of the cardiac action potential is largely due to the iK1 channels, but current through these channels is greatly diminished during the plateau.

Other K+ channels play a role in phase 2 of the action potential. These are characterized as delayed rectifier (iK ) channels. These K+ channels are closed during phase 4 and are activated very slowly by the potentials that prevail toward the end of phase 0. Hence, activation of these channels tends to increase gK very gradually during phase 2. These channels play only a minor role during phase 2, but they contribute to the process of final repolarization (phase 3), as described later. Two types of iK channels exist, depending on their rates of activation. The more slowly activating channel is designated the iKs channel, whereas the more rapidly activating channel is designated the iKr channel . The duration of the action potential in myocytes in various regions of the ventricular myocardium is determined in part by the relative distributions of these iKr and iKs channels.
Genesis of Final Repolarization (Phase 3)
The process of final repolarization (phase 3) starts at the end of phase 2, when efflux of K+ from the cardiac cell begins to exceed influx of Ca++ . As noted, at least three outward K+ currents (ito , iK , and iK1 ) contribute to the final repolarization (phase 3) of the cardiac cell.
Restoration of Ionic Concentrations (Phase 4)
The steady inward leak of Na+ that enters the cell rapidly during phase 0 and more slowly throughout the cardiac cycle would gradually depolarize the resting membrane voltage were it not for Na+ ,K+ -ATPase, which is located in the cell membrane. Similarly, most of the excess Ca++ ions that had entered the cell mainly during phase 2 are eliminated principally by a 3Na+ -1Ca++ antiporter, which exchanges 3 Na+ ions for 1 Ca++ ion. However, some of the Ca++ ions are eliminated by an ATP-driven Ca++ pump.


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is it possible to completely reconstruct a family tree by DNA comparison alone?
Having DNA samples of all or almost all members of a population of, say, a few hundred or thousand individuals, is it possible to draw the entire family tree of those individuals? (Let's not assume monogamy or any other facilitation).
This may be a sum of two different questions:

does comparison of two DNA samples give any information other than topographical distance between individuals? In other words, is it possible to tell two sisters from a mother and a daughter by DNA alone?
(more a mathematical question than a biological one, maybe) having the relative topographical distance of all members of a group, can their full graph be drawn?

Not confident enough to post an answer but I very much doubt it. There is a large element of randomness involved, I am not simply a mixture of my parent's DNA. Processes like chromosomal crossover ensure that a significant part of my genome is original so to speak. Therefore I doubt you can reconstruct a genealogy from this information.

@terdon: recombination is easily modellable. I'm pretty much sure it is possible even with relatively sparse genotypic data, not to talk about whole genomes.

@har-wradim how can it be modeled? It is a largely stochastic process so I don't see how you could infer my parent's genomes from mine.

@terdon: it's not completely stochastic on the one hand and many stochastic processes are modelled on the other. You are still nearly 50% identical to each one of your parents and this identity covers long stretches of DNA.

@terdon: The task is not to infer your parents' genomes - the task is to find them in a set of genomes known beforehand.

@terdon: but, could you tell someone's parents from someone's two children?

@har-wradim re not completely stochastic: no it's not, that's why I said largely. As for choosing the right genome from a set, absolutely, that's a completely different proposition. However, in the OP we have to choose between siblings or mother/daughter so we don't have a set to choose from, we need to decide which hypothesis fits the data. That's what I don't think is possible but this is way out of my field so I don't pretend to know.

No, it is not possible to determine ancestry with just two DNA samples, but it is possible with three: http://www.nature.com/nature/journal/v487/n7407/full/nature11251.html.
Essentially, each sequence region in the progeny can be traced to either the mother or the father, but you really need both sequences to have any confidence.  That would get you one node on your tree.  You would need additional samples from higher generations to rebuild an entire ancestry.
However, it might be possible with hundreds of samples from laterally related individuals.  In fact, I think this is the fundamental hypothesis of the 1000 genome project, http://en.wikipedia.org/wiki/1000_Genomes_Project, and it pretty much worked.  Isolated populations can be discriminated by broad DNA sequence analysis.
To reconstruct your tree for a single ancestry, you would just want to use more closely related individuals (many, many of them), and then generate a phylogenetic tree, which should roughly correspond to the family tree you are investigating.


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Amber eye color in Neolithic Africa
Given what we know of the genetics of eye color and their historical distribution, is it possible or at least plausible for a person born in the Horn of Africa during the early Neolithic (ca. 9000 BCE), assuming no recent ancestors from outside this area, to have had amber eyes (or in general anything other than brown?) If so, would one or both parents need to have that color as well, and what of siblings?
I know that today there is much less isolation and much more crossing of genetic lines, so that pretty much any combination of skin and eye color is likely possible, but no doubt it was different back then.

I think my personal experience might be interesting even if this is an old post. I'm Italian, both my parents have green eyes and come from families of light eyed people (blue, green or gray eyes are the norm). My mom's eyes also change with the weather and can become gray when it's cloudy/ raining. I was born with amber eyes. Most people think they're light brown but when I'm in direct light they're bright amber/yellow. I definitely think it's some sort of green eyes mutation where the lipochrome is in excess and prevales on the melanine (if it makes any sense). Genetically, there's no way I

There are two possibilities: First, that an individual develops a mutation de novo and is the first to carry it.
When we talk about recessive expressed allels, than both parents need to have a copy of the allel, otherwise it will not show up in the kids. In this case a mixed population of siblings is to be expected (some carrying both recessive allels, some only one).
However, its most likely, that the eye color at this time was brown. As far as I know, there has been no evidence so far from ancient DNA that this has been different.
The oldest DNAfrom Europe, which has been analyzed and which showed a difference for the eye color comes from Spain (La Brana-Arintero site in Valdelugueros) and is about 7.000 years old. See this report about it. This individual is thought to have an "african" type of pigmentation but blue eyes. The original publication is called "Derived immune and ancestral pigmentation alleles in a 7,000-year-old Mesolithic European."
Another paper claims that the blue eye color comes from a mutation which occured in a gene called "OCA2" in the black sea region some 6-10.000 years ago. See here: "Blue eye color in humans may be caused by a perfectly associated founder mutation in a regulatory element located within the HERC2 gene inhibiting OCA2 expression"
.

Thanks. My searches turned up nothing on genetics of amber eyes, except we apparently don't know which genes control it. It may be caused by a pigment (lipochrome) which is also present in green eyes, but I can't tell if the genes involved in brown and blue eyes have any effect on the gene(s) for amber eyes. If amber/green is caused by an entirely different pigment, shouldn't the other genes (which regulate melanin) only affect how light or dark the amber is? Or whether the result is green or amber? I assume green may be "blue+lipochrome" and amber is "brown+lipochrome", but do we know?

@adcoon The eye color is build by both: Melanin and Lipochrome. Amber comes up when you have very little melanin and a lot of Lipochrome. The deposition of Lipochrome into the eye is controlled by EYCL1 and EYCL2. Have a look on this Webpage which has a ton of references at the bottom.

Given that chimps can also have amber eyes (along with brown) it may well be an allele the predates the human species.


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Is a neurostimulation implant for the soft-palate component of obstructive sleep apnea plausible?
There are currently ongoing clinical trials for neurostimulation implants designed to keep the tongue from blocking the airway in obstructive sleep apnea.  The nerves for this are in the neck and surgically accessible.
Where are the nerves that control the soft-palate, and would it be plausible to implant a similar device for them (given years of development obviously)?


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RNA secondary structure comparison
Do you know any program which can compare two and more different RNA secondary structures? I need find some (dis)similarities between lots of predicted secondary structures. And create maybe common sec. structure/shape.

You can use R-coffee of the T-coffee suite of tools. In general, the *coffee tools are excellent and work very well if you can get over their author's self obsession1. R-coffee can align RNA sequences taking into account structural information:

1 The guy actually adds his name to the output of all his programs! Seriously, he does. Apart from being simply ridiculous, this also affects other programs you might want to pipe your data to. For example, I wanted to pipe t-coffee alignments to an alignment viewer and I had to parse out his effing name in order to be able to do it.

I was amused by your remark - but from what I can see, you'd only have to delete the second line of text.

@Superbest yes, isn't that enough? The default output of t-coffee is in clustal format, a standard and widely used format for alignments. Because of the author's self importance, I had to edit the output to remove his name before being able to view the alignment in another program. Just cause the guy likes to see his name written everywhere.

there a number of tools in the Vienna package (RNAalifold, RNALalifold):
http://www.tbi.univie.ac.at/~ronny/RNA/index.html
some other tools are available from Freiburg Univ. such as:
LocARNA or CARNA (http://rna.informatik.uni-freiburg.de/CARNA/Input.jsp)


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Why does the arch of aorta coils?
My study materials use the word vesselcompression chamber of aorta to emphasize aorta's elastic property.
The arch of the aorta only coils, not its straight part.
I think the reason why the arch coils is the elasticity of aorta (artery) is high.
If the elasticity is too low, then the aorta is more stiff.
This means that heart has to work harder so higher systolic pressure and lower diastolic pressure.
Why does the arch of the aorta coils?

It's not clear to me what you mean by "coils". The aorta itself does not coil. Except for the arch, it's rather straight. Are you asking about the orientation of collagen and elastic fibers in the wall of the aorta?

@kmm This was the question which I got. It probably refers to the fact that it coils very little, exactly in the arch. Yes, I think the coiling of aorta can refer to the orientatino of collagen and elastic fibers in the wall of the aorta.

So if that is the case, then can you rephrase or narrow down your question?

@kmm I narrowed to question to the arch.

@Masi - I'm still confused by "coils." The aorta, as you said, is an elastic artery, and has many layers of smooth muscle and elastic fibers in the tunica media. Don't you mean: "if elasticity is low, then the aorta is stiff"? It requires high elasticity to help maintain a higher diastolic pressure.

@jello The topic is related to Pressure in Aorta and its characteristics. I do not understand why arch of aorta coils yet.

The main question can be answered in a very dumb way: because the lower part of the body also needs blood... and this configuration is the surest way of doing that because of reasons given below (among many others, I am sure).

If you want an anatomical reason, well the most pertinent one would be that embryologically, the heart and vascular system are derived from a single straight tube, that then begins contracting and folding over itself to form the heart chambers, the aorta, and the pulmonary trunk.
If you want a physiological explanation, the aorta curves slowly because it is a point of the circulatory system where pressure is high. Apart from the fact that sharp kinks would cause a massive and useless loss of kinetic energy on blood flow from shear stress over the aortic walls (and therefore more heart workload), the induced shear stress would also damage the aortic walls much more quickly than in the actual configuration.

The third reason is just theory on my part, but it seems the vascular system is designed by priorities: you could imagine a system with two aortas. One for the upper body going up, and a second going down. However, such a configuration makes it mechanically impossible to balance perfusion to the organs, and especially ensure brain perfusion. For example, how would the body compensate if the upper aorta got clogged while the other stayed wide open? The single aorta configuration allows the heart to adapt to such mechanical perturbation scenarii using, for example, left ventricular hypertrophy.
However to add to some elements of your question:

the reason of the aortic coiling has certainly very little to do with elasticity and the vessel compression chamber principle.
Higher elasticity means the aorta is less stiff, not more.
When the aorta gets stiff (elasticity decreases) as it is often the case with age and calcification of the aortic walls, it is correct that the heart will need to work more, that systolic pressure will get higher, and diastolic pressure lower. This gives the classical clinical symptom of "cannonball" or "gunshot" pulse

Excellent answer! Thank you! Can you provide me more information about the gunshot pulse. It reminds me about one case where the insulin secretion is like cannonball, here described: http://biology.stackexchange.com/q/17466/86

The other way of rejecting the two-aortic system away is the impossibility of having atrophy in the heart, I think. The cell size of the heart cannot decrease. I have listed some factors here what it would require http://biology.stackexchange.com/a/16928/86


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Sitting much, thrombosis and hypoxia
I am thinking the more reasons why sitting much lead to thrombosis i.e. clotting of blood in blood vessels and then hypoxia in the deep tissues eventually.
What are the physiological mechanisms for this to happen?
One student said hormones.
It can be right, but I am thinking how.

Venous return from the limbs is largely facilitated by the action of neighbouring skeletal muscles compressing the veins and forcing the blood proximally past the valves which prevent back flow.  If you are inactive for a long time by sitting, or are sitting in such a way as to impede blood returning from your calves (i.e. with the back of your knees pressing into the edge of the chair) blood movement in this manner is greatly slowed.
Blood that is moving more slowly or turbulently has a greater propensity to coagulate and form a thrombus.  This is similar to the rationale for prescribing anti coagulants to patients with atrial fibrillation - the turbulent and slow movement of blood through their atria leaves them at greater risk of throwing a clot to the brain causing a cerebrovascular accident.
Hypoxia isn't really that relevant in the case you describe as arterial supply is unaffected (much higher pressure) meaning tissues do not become ischaemic. There is also collateral venous drainage from the limb although this can subsequently cause problems in the form of post thrombotic syndrome.  The most significant risk would be that of the thrombus breaking off and lodging in the lungs - a pulmonary embolism.

I think the oxygen supply is deprived in some tissues too. So therefore I think some local hypoxia can occur.

@Masi one hypothesis for the original formation of the VTE is that venous stasis causes the haemoglobin in the static blood to desaturate resulting in hypoxic insult to the vein endothelium that then triggers the coagulation cascade. However, there isn't much of an evidence base behind this and it would be a cause of VTE rather than a consequence.


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To define the total Resistance of Systemic Blood Circulation
Some systems are in parallel.
For instance, the resistance of lungs $R_{\text{lungs}}$.
Assume here for simplicity that these parallel systems can be handled linearly.
We also consider only Total Vascular Resistance for simplification.
So we have now only systems in series under consideration.
Linear system  for Systemic Vascular Resistance
Formula for the total resistance as mechanical definition as assuming linear connections between those systems:
$$R_{\text{total}}=R_A+R_a+R_c+R_V+R_v$$
where appropriate resistances are

$R_c$ capillaries,
$R_a$ arterioles,
$R_A$ Small artery,
$R_v$ venules and
$R_V$ vein.

Nonlinear system for Systemic Vascular Resistance
There are many factors involved in these locations:

permeability
vasoconstriction
...
growth factors (FGF) for renewal of the vessel wall
different channels (activated, deactivated - mostly potassium channels)

where I skip the consideration of vasoconstriction, growth factors and different channels.
Permeability is one which applies to all types of vessels.
Change in permeability of one location does not mean a linear change in permeability in another.
A change in the permeability of small arterioles does not lead to a similar change in the arteries or venules.
The vessel is permeable to gas and liquid.
Let's consider only these components.
I want to include these facts into the definition because, in the pathological situations, different state of inflammation for instance can apply to a vessel.
Let's call total permeability $S$ which is dependent on gas and liquid components, first on liquid component (so inner integral).
I could give you the nonlinear formula of the total resistance but I think it goes over the skills most here.
Let's call the nonlinear resistance dependent on permeability of the vessel, $W(x,y)(t,f)$ in time and space.
So consider only the nonlinear component of the permeability formula after parametrisation i.e. permeability, let's call it $T$, which is dependent on changes in water (w) and gas (g) components over a path integral.
The path covers all components in the vascular system that are in series.
So total resistance defined nonlinearly
$$W(x,y)(t,f) = \int_{\gamma} T(u) \frac{1}{u} \int_{t-u/2}^{t+u/2} T(w) \, S(x,y)(t,f) dw \, du$$
where the inner integral corresponds to the water component while the outer integral to the gaseous component.
There is only an averaging in the inner integral when the width of the window is $u$.
However, we do not any windowing here actually, just because of this averaging, so we lose no data and can handle the total resistance as a single process.
Notice that change in $T(u)$ leads to a change in $T(w)$ nonlinearly.
I skip the nonlinear definition of $S(x,y)(t,f)$ which stands for the energy in time in each instance - you can think it as the amount of permeability in each position of the vessel.
Actually, I also skipped the explicit definitions of the water and gaseous components too.
I have not found any work done on the nonlinear development of the resistance.
I think this is necessary for defining inflammation explicitly.
How can you describe the total resistance as an nonlinear operation better?

Most people talk about SVR/TPR (systemic vascular resistance/total peripheral resistance) and PVR (pulmonary vascular resistance). You're welcome to re-name the variables, but how this culminates in the question about a "way to define system circulation" I don't know. (Maybe you just forgot the word "resistance" there?) This wikipedia article gives a good overview of the formulas that can be brought to bear.

@Susan I really had a completely different target here for getting some nonlinear definition of the systemic vascular resistance. You will not find pieces of information about this in literature.

Can you shorten the question with just the essential elements. Also please add a reference for the equation. I did not understand your final question — How can you describe the total resistance as an nonlinear operation better?... Are you asking why nonlinear model is better than linear model or how to make the nonlinear model better?

We do not need to compare apples and cars. Linear case is straightforward. Thinking now the presented question. This applies necessary dependences and connections, mostly in electrophysiological level now.

I see no reason to model the components of the vascular system as a series circuit. Also, I see no reason to model the system's components as "gas" and "liquid" because the gases are all dissolved (until they're outside the system). I think the systemic blood circulation is analogous to the movement of air through the pulmonary tree. You should locate those references, which definitely treat the flow as turbulent. Also, defining "inflammation" in terms of this quantity "resistance" is confusing.

@Ryan Good comment! I cannot agree with the analogy to pulmonary tree and blood circulation because of inflammation and other processes in vessels. The turbulence absolutely should be taken into account in the definition. It actually inside the energy term S(x,y)(t,f) which I have not explicitly defined here but where the separation of different flows is done. Actually, I do not define inflammation into resistance; I used inflammation's effect on permeability (T) for water and gas in the definition.


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Which processes are during the latent period of ventricular contraction?
The latent period is the time between the start of depolarisation and the start of contraction.
I know that the contraction of ventricles starts after sufficient influx of Ca2+ and threshold potential is met.
The influx of Ca2+ is at start of Phase 2, so Phase 0 and 1 are included in the latent period.
Comparing to electrocardiogram is not simple, since there is always at least some time lag between the event and the recording.
I think there not much sense to compare cellular model events to ECG recordings here.
Which cellular processes does the latent period include?

During the latent period of ventricular contraction, excitation-contraction coupling takes place.
There may be other processes, but I think most are these from Wikipedia:

An action potential is initiated by pacemaker cells in the Sinoatrial node or Atrioventricular node and conducted to all cells in the heart via gap junctions.
The action potential travels along the surface membrane into T-tubules (the latter are not seen in all cardiac cell types) and the depolarisation causes Ca2+
to enter the cell via L-type calcium channels (also known as Dihydropyridine receptors) and possibly sodium-calcium exchanger during the early part of the plateau phase. This Ca2+
influx causes a small local increase in intracellular Ca2+
.
The increase in Ca2+
is detected by ryanodine receptors in the membrane of the sarcoplasmic reticulum which releases Ca2+
in a positive feedback physiological response. This positive feedback is known as calcium-induced calcium release and gives rise to Calcium sparks.
The spatial and temporal summation of ~30,000 Ca2+
sparks gives a cell-wide increase in cytoplasmic calcium concentration.
Contractile mechanism similar as in skeletal muscle about cytoplasmic calcium binding to troponin C and so on.

Note that to fully answer this question you should include figures about mechanisms of excitation-contraction coupling, cardiac action potential -figure and permeabilities of different ions.

The phases from the stimulus to the force contain latent period, contraction phase and relaxation phase. This applies to all muscles, not just muscles associated with ventricular contraction.
So the Latent period, about 5-7ms, contains the following:

skeletal muscle prepares for contraction

phase between stimulus and beginning of contraction (response)

the muscle doesn’t change length or tension

influx of Ca2+

inhibitory proteins of contraction:

binding to Troponin and removing Tropomyosin
Troponin: T binds with tropomyosin, I binds with actin, inhibits ATPase, C has high affinity to calcium ions.

ATPase activity increases

where some parts such as biomechanics is mostly ignored.