text:
Evolution of sexual reproduction from asexual
How exactly did asexually reproducing organisms evolve into sexually reproducing ones? Why was it considered more favourable?

The evolution of sexual reproduction is very much a field in progress. There in any case not a single simple answer to this question. A number of reviews exist on the subject. One of the reason being that the dichotomy sexual vs asexual reproduction is misleading as reproductive methods are immensely diverse. I think the question is therefore too broad.

You could give it a start with the wikipedia article about the evolution of sexual reproduction or maybe you could have a look at the SE posts Why asexual reproduction? and Why are not all species hermaphrodites?.

You will find in any intro textbook on evolution a whole chapter about the evolution of sex. You should have a look at it.

I agree with "JJ": Answer not good enough.

Why not add a definition with references on what sexual reproduction is?

Sexual reproduction is a process where two cells fuse to form a diploid cell. Unicellular organisms (or even multicellular lower organisms like alga, fungi and protists) prefers to reproduce by asexual means under favourable conditions. But when the conditions become unfavourable, they opt to follow sexual reproduction. This suggests, sexual reproduction evolved to increase the chances of survival under unfavourable condition.
So how does sexual reproduction helps in increasing survival rate? By fusion of cells i.e., sexual reproduction a cell now becomes diploid and hence have two copies of its genome. This increased copy of genome is beneficial in repairing any breaks or alteration in genome, as the other copy will act as a template for repair (via homologous recombination).
To get a better hold of this, let us take an example. Let there be a population of haploid cells. This population was exposed to conditions which would cause damage to genome, specifically would cause breaks in DNA. There were two cells "Fella A" and "Fella B". They both knew that their genome has suffered damages, but neither was successful in repairing the DNA as they required an intact DNA template for repair. Suddenly "Fella B" came up with this great idea to fuse with "Fella A". This would work, reasoned "Fella B", as the position of damage in the DNA in his genome is different from the position in "Fella A". Fusion of cells was the first step towards evolution of sexual reproduction.
Later on the biological system realised importance of variation generated by sexual reproduction and hence this mode of reproduction caught on with various lineages.

But I want to know HOW the change occurred from asexual to sexual

@Tushar You are presenting one of the many arguments people put forward. Barton and Otto 2005 is just one example of another explanation.

@Remi.b: Agreed! There are many hypothesis (arguments) and to the extent I was able to understand work of Barton and Otto, it discusses "if cells gained the capability of fusion (probably for DNA repair, my view) then what factors will promote its spread to entire population". While my answer explains why cells would start fusing leading to sexual reproduction.

@user29774: I made an edit. Does this answer your question?

@user29774 While I consider the the current answer gives a poor representation of the diversity of explanations and diversity of mating systems, I think that if you feel like the post has answered your question, then you should accept it (and check the checkmark).

This isn't really an answer to the first part of the question.  I wouldn't expect the anthropomorphic explanation of two single celled organisms 'knowing' they have genetic 'damages' and one coming up with an 'idea' to fuse together being up to snuff.

This is your own private theory? What are your references? I like the simple logic very much. As other answers show "where two cells fuse to form a diploid cell" is no trivial approach. I guess at school you may learn about maiosis and mitosis without even "diploid/haploid" being called up as words. I would like to hear about Soma cells in mitosis not changing anything whereas haploid cells departed from the same zygote have mingled but will stop that. What's more chromosomal exchange is decisive - very different, still the same.

Do you think of a diploid soma as a prerequisit of sexual reproduction? If yes, prokaroytes would be out?

Sexual vs asexual is not a binary condition it is a spectrum. Many organisms do both and/or a wide range of things in between. One of the most basic is plasmid swapping Bacterial conjunction in unicellular organisms.Even asexual selction has multiple forms of reproduction such as budding vs fission.  Exchanging genes can be highly beneficial for multiple reasons including but not limited to; making infection far more difficult for parasites or giving a  favorable gene a better change to spread since they are not stuck in the same genetic line forever.
Many organisms are opportunistically sexual, using sexual reproduction when they can (when they can find a mate or when resources are abundant) and using asexual selection when they cannot. this implies that there is an advantage to sexual selection even if what it is is debated, but it also shows it is an an either/or question the two forms of reproduction coexist quite well.
As for why sexual selection evolved, this is a hotly debated topic with no clear answer, it might be as simple as a way to get the benefits of gene exchange without the virus vulnerability plasmids create.  It also a vague question by its very nature, because many organism engage in many different forms and combinations of forms of reproduction AND becasue many of these appear to have evolved independently the question is horribly muddled.
In short we know sexual reproduction has benefits but we can not say which ones were the deciding factors in its early evolution partially becasue there are  several different instances of it evolving..

No, you've got the wrong end of the stick... asexual reproduction came from sexual reproduction, not the other way around! Asexual reproduction is a degenerate state that has benefits but is an evolutionary dead end because sexual combination is necessary to promote beneficial alleles and build new genes.  See:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4231362/
The answer that says "Sexual vs asexual is not a binary condition" is misleading; yes, that is true.  Sexual species will start to experiment with asexual forms if they can because that confers advantages.  The ability to be parthenogenic is very useful, but since it is a dead end, the ability to reproduce sexually should not be lost.
Although sex was quite tricky to evolve in the first place, it was necessary from the very beginning.  It evolved from simpler systems of gene swapping and building that were needed from the beginning.

This answer is just plain wrong. The article you cite only claims that asexual animals are an evolutionary dead end. Animals are just one branch of the tree of life, not its root.


text:
Correlation between menstrual period and lunar revolution
Is it just a coincidence that the the length of the entire menstrual cycle from one flow to the other lasts almost exactly as one lunar month?

Do you mean if there is any correlation between day and night (specifically light as a zeitgeber) on menstrual cycle? Yes. There is.

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text:
Time for rigor mortis to set in
Rigor mortis sets in due to non-functional "ATP powered calcium pumps" as a result of which the calcium ions stream out & the muscles remain in a suspended animation state.
But, it's a frequent observation (as can be seen from a coroner's report) that the time for rigor mortis to set in depends on external temperature, like it's earlier in summer, but late during winter.
So why this fluctuation?
Wikipedia has got an answer, but it's too brief.

When conditions are warm, the onset and pace of rigor mortis are sped
  up by providing a conducive environment for the metabolic processes
  that cause decay. Low temperatures, however, slow them down.
  Therefore, for a person who dies outside in frozen conditions rigor
  mortis may last several days more than normal.

@ChrisStronks , look up the highlighted text...

ATP is necessary to relax muscles. Perhaps depeletion of ATP is quicker at higher temperatures as any chemical reaction speeds up by about a factor of 2 (Q10). What is an ATP pump by the way? If it exists it is not involved in rigor mortis

I meant ATP-powered calcium pumps or simply calcium ATP-ase...

Small point of clarification, are you asking why most biological process slow down at lower temperatures, including the process of decay?  That is the essential point here.  You're going to get slower onset and longer duration simply because you're going to get a lot less biochemical turnover and vibration (in the muscle as well as everywhere else).  Fun fact: frozen stiff bodies, if done quick enough, might not develop rigor at all until thawed.

what is the question here? you already mentioned in the question the effect of temperature. For a more detailed report see this

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text:
What prevents backflow of blood from right atrium to vena cava during atrial systole
Vena cava is valve less. So,  during atrial systole what prevents backflow of blood to them?

Besides @Bryan Krause answer, there's another very important factor that prevents the blood from flowing back from the right atrium to the vena cava during systole.
Part of the muscle that constitutes the atrial walls also wraps around the site of entrance of the vena cava. Thus, during systole, the muscle contracts, closing (or almost closing) the passage and doing the job of a valve.
Nature!
EDIT: because of the high skepticism over what I have said in this answer, and having no references, I went to search for the class where I studied this, and here's the slide containing the information. Unfortunately, it is in Portuguese, but I will translate what it says, and you can check in any translator.

Venous myocardium: Cava Veins and Lung Veins
The veins that open in the heart don't have functional valves, meaning that the atrial systole could cause blood backflow through these veins.
Venous myocardium: The cardiac muscle tissue is prolonged through the vein walls that bring blood into the atrial cavities to the point of insertion of the fibrous pericardium.
Physiology: The venous myocardium contracts at the same time as the atrial wall, preventing the backflow of blood to the veins during atrial systole.

Do you have a citation? I don't believe that is accurate. If it does close at all, it certainly isn't enough to prevent blood flow in either direction.

@BryanKrause I have studied this in anatomy class, I can search later for a citation in the internet if you wish. It does close, and even if it doesn't close completely the passage, it turns it much thinner, meaning much less blood can pass through it an só the blood will go the other way - to the ventricle. It's both this system and the different pressures that you talked about that contribute to the prevention of backflow to the vena cava

@BryanKrause this is just a drawing but you can see the atrial muscle also wrapping around the entrance of the superior vens cava https://goo.gl/images/io75Jw

@FilipeRocha - I don't think hat shows what you think it shows...

@anongoodnurse what do you mean?

i dont know why the downvote, but I have edited the answer and added my "source"

Ah, thank you I found same in my book as well.

Pressure differences. Atrial contractions are much more gentle than ventricular ones, and in normal circulation the venous pressure in the vena cava often stays higher than the right atrium, even during atrial systole. If the pressure in the atrium does rise above the vena cava pressure at the peak of systole, there can be some backflow, although it is slight and brief in normal physiology.
The major veins are typically somewhat distended so they are constantly pushing blood into the right atrium. Blood continues to flow from the veins into the right atrium and from the right atrium into the right ventricle throughout ventricular diastole, including during most of atrial systole.
References:
Anderson, R. M. (1993). The gross physiology of the cardiovascular system. Robert M. Anderson.
Wexler, L., Bergel, D. H., Gabe, I. T., Makin, G. S., & Mills, C. J. (1968). Velocity of blood flow in normal human venae cavae. Circulation Research, 23(3), 349-359.

Venous pressure increases during atrial systole,  can we say it is due to backflow of blood?

@AnubhavGoel I think it's more accurate to say it's because of briefly reduced blood flow to the heart rather than from blood actually flowing backward. Maybe think about a highway, if something happens that causes some cars to slow down on a congested road, you are going to get more congestion ("pressure") behind them, but no one has gone in reverse, just slowing down is sufficient. That said, I have certainly seen this abbreviated as a "backflow" when describing venous pressure during the cardiac cycle. From a strict sense I would say this is wrong (in normal physiology).

I agree with you but regurgitation of blood do take place.

@AnubhavGoel It shouldn't happen (in the human) outside of pathology, because right atrial pressure doesn't exceed vena cava pressure. In cases of pathology, yes of course reverse flow can occur. Filipe's answer is wrong and based on a single slide with no further reference.

Look at my answer.

@AnubhavGoel Interesting, that conflicts with my source. I did a little more research and found an actual original source that indeed supports that there is backflow, albeit quite minor and brief, see here: http://circres.ahajournals.org/content/circresaha/23/3/349.full.pdf

@AnubhavGoel I updated my answer appropriately.

The atrial pressure  when equal to that in the  incoming vein will contain blood which will be propelled  into the right ventricle without  the need for any increased  pressure [as  does the ''muscular  pump' in the body. In other words  the right  atrium is ' functionally a sophisticated  valve'

Welcome to Biology.SE! Please elaborate on your answer by providing references. For more information on how to provide good answers on this site, please see: https://biology.stackexchange.com/help/how-to-answer. Thanks!

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What is a 5'-cGMP?
I know in cGMP , there is a bond between phosphate, 5' and 3' C of sugar , but what is 5'-cGMP?
[It is involved in cascade of vision.]

As you will see from the Wikipedia article, you can talk about cGMP, Guanosine cyclic monophosphate  or cyclic 3',5'-GMP. The 3' and 5' indicate the positions bridged by the phosphate in the cylization. Thus, ‘5'-cGMP’ is chemical nonsense.


text:
Why are the granules of pancreatic beta cells larger than those of alpha cells?
Why are the granules (insulin) of β cells larger than the granules (glucagon) in α cells in pancreatic islets of Langerhans?
Also is there any size difference between alpha cells and beta cells?
Source: Inderbir Singh , Text book of Human Histology. Ed 8. Ch-16. Pg 202.

This may help: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909340/#!po=55.1282  smaller granules=>more precision. Large granules=> more economy is excreting large quantities.

May be thats the case here as well as..


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Stable isotope sample preparation: Bone Collagen
I am performing research in which I need to extract bone collagen from the foot bones of American Beaver (Castor canadensis).  I have read through the literature fairly thoroughly on both the archaeological/anthropological side and the wild life side and have been finding a many tweaks to a fairly simple extraction process, but I still have a few questions.

When processing bone I split the bone and removed the center, which was red/ light pink, (I thought it was the marrow and wanted to make sure that I was getting collagen from only 1 part of the bone to not confuse my isotope data with varying tissues)
There is also some variability across papers in the time that people allow bone to demineralize in a strong acid  ranging from 20 mins to upwards of 10 hours.  Does anyone have any experience with this and size to which you ground your samples.
The literature has a variety of temps ranging from 58 C to 95C, it proposes to gellatinize the collagen in a weak acid over a variable number of hours (approx pH of 3), does anyone who has experience offer a temp and time that worked for them.

Any help is much appreciated, Thanks


text:
Are there ways to speed up the growth of plants?
I'm interested in what humans can do to speed up the rate of growth in a plant. I'm interested in both the context of home gardening and large-scale, institution-backed projects.
Obviously, optimal growing conditions are one factor that can be modified. I imagine that there are also genetic mutations that can be done (possibly even at home!). Botany is not my field so what I'm looking for here is are the basics and some good resources for further reading.

Yes.

The research team, led by the Durham Centre for Crop Improvement Technology, and including experts at the University of Nottingham, Rothamsted Research and the University of Warwick, have discovered that plants have the natural ability to regulate their growth independently of Gibberellin, particularly during times of environmental stress.
They found that plants produce a modifier protein, called SUMO that interacts with the growth repressing proteins.
The researchers believe that by modifying the interaction between the modifier protein and the repressor proteins they can remove the brakes from plant growth, leading to higher yields, even when plants are experiencing stress.[1]

Bacterization is the process by which bacteria applied to the soil and plant parts. Under certain conditions yields were able to increase 10 to 13 percent. However, not all results were able to be reproduced so this is something you can look into more as well. [2]
Another option is to artificial increase the amount of CO$_2$:

Over the years there have been numerous laboratory experiments which conclude that increases levels of CO2 result in increased plant growth no matter how that plant growth is quantified. Sylvan Wittwer in Food, Climate and Carbon Dioxide tabulates the results. [3]

Lastly, you can look into genetically modified organisms (GMOs) which is a hotly debated topic.
With a Google search, you will see that that there are numerous articles on methods to increase plant growth, to numerous for me to give a blurb about them all. Therefore, I linked a few that seems promising as well as interesting.


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How many metabolites are in the metabolome of (almost) all eucaryotic cells?
Which small biomolecules (up to the size of amino acids) are present in (almost) every eucaryotic cell and thus part of its biochemical network, constantly and inevitably being produced and metabolized?
Is there either a comprehensive list (e.g. being a sublist of this one) or at least a number: How many are there (roughly)?
To ask it differently: How many small molecules are in the metabolome of (almost) all eucaryotic cells?
Side question: Does the famous Metabolic Pathways poster contain all of them, or which percentage (roughly)?


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How sharp are the borders between Brodmann areas?
How does the border between two Brodmann areas look like in Nissl stains? How large is the transition zone where one cannot tell to which of the two areas a neuron belongs to? How many neurons are ambiguous compared to the number of unambiguous ones, roughly? 1%, 5%, 10%?
Is the inner connectivity of a Brodmann area greater than its connectivity with a neighbouring area across the border? Can this be seen in Nissl stains? Or is short-range inner-cortical connectivity somehow homogenuous over adjacent Brodmann areas?

Hi Hans, this might be the sort of question that's best answered yourself by looking at some labeled Nissl sections, or by reading about criteria used to determine areas.

@BryanKrause: I'll try, but I'm afraid my view is too unexperienced. Could you  give me a reference explaining the criteria to determine areas?

I tried searching Google Images for "brodmann nissl" (but no quotes); one example led me to https://webvision.med.utah.edu/book/part-ix-brain-visual-areas/the-primary-visual-cortex/ (figure 9 on that page). Figure 1 here: http://www.nibb.ac.jp/brish/Gallery/cortexE.html also looks like a place to get started in looking at the layers. Note that there is a huge variety in the discriminability of Brodmann areas (and one reason there are so many different parcellations of cortex): some are really easy, others require an anatomist's trained eye and I can't tell them apart myself.

I think you'll get a better picture by going through some examples to get a sense for yourself, rather than trying to quantify it.

@BryanKrause: Figure 9 is great and gives me a better sense: It's about "distinctness of appearance" (in this case of layer 4 which is also present in V2 but not so distinct as in V1). What can be seen also: The border is only sharp in layer 4 (and here, it is astonishingly sharp) but its sharpness does not extend to the other layers: there it becomes diffuse.

@BryanKrause: With "so many different parcellations" you mean "by so many different authors"?

Let us continue this discussion in chat.


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How to fit simulated with measured data having systematic errors?
Consider a given time series of measured data, i.e. the number of persons tested positive for COVID-19. And consider a simulation - consisting of a model, possibly fed with some parameters estimated a priori (not via the measured data) - which gives another time series.
More often than not these two time series won't fit at once. But the goal of a simulation usually is to have a fit with measured data, and finally one wants to show: "See, these two histograms do match essentially."
That they don't match may have two reasons:

the measured data are erroneous (possibly in a systematic way) and/or
the model and/or the estimated parameters are erroneous

Assuming that the model is roughly correct (i.e. an advanced SEIR model) what are acceptable ways to "explain away" the gap between measured and simulated data?
The measured data may have two sources of error that are known in principle but not quantitatively:

a reporting delay (which includes incubation and latency time, time for testing, and time for proper reporting), giving rise to a shift of data.
a dark figure (i.e. cases that were not detected, falsely attributed, or false negative or positive cases), giving rise to typically lower values of the measured data (than in reality).

What is the "right way" to reflect these sources of errors, especially when drawing diagrams?

First correct and adjust the measured histogram, assuming some estimated reporting delays and dark figures, and then compare the corrected histogram with the simulated histogram?
First adjust the simulated data in a reciprocal way (by artificially adding some fictuous estimated reporting delay and dark figures) and then compare adjusted histogram with the non-corrected histogram of measured data?

Is one of these the one and only "good practice" - or are both or none of them scientifically tenable.

This is an interesting question, though I think you're more likely to get a rigorous answer addressing your problems (time series modeling, error correction) on stats.SE, no? The bits of your question concerning COVID could be removed without changing the meaning.

Am I understanding the question correctly: to remove errors, should changes be made to the stimulated model or to the data? Wouldn't it depend on the phenomena you are trying to model, and what the sources of error are? Like here, both the mentioned errors appear to be due to the data, not the epidemic that you're modelling.

@AP2261: You are understanding correctly. And yes, you are right: both errors are due to the data, but they are only examples. Possible sources of errors of the model are countless.


text:
If a particular protein contains 178 amino acids, and there are 367 nucleotides that make up the introns in this gene,
what is the number of nucleotides that make up the coding and noncoding regions of the gene including the start and stop codons

where is this question from? is this for homework? can you give any rationale for what you think the answer is?

178 amino acids => 178 codons =>178 *3 nucleotides => 534 nucleotides for the coding region. Plus 3 nucleotides each for start and stop codon. So the grand total will be (534+367 +6= ) 907 nucleotides


text:
What is the thickness of endothelial lining in blood vessels?
In capillaries, endothelial lining is one cell thick. Is same the case with bigger blood vessels?

Related http://biology.stackexchange.com/q/54562/3340

I believe apart from natural fluctuations of cellular size, the size of squamous epithelial cells (the cells making up the endothelium of blood vessels) remains the same. Therefore, the thickness of the endothelium does not significantly change for any blood vessel.

This is correct. Just to add on, capillaries are walled by essentially only endothelium; larger vessels are thicker because they have other types of tissue: elastic laminae, media and adventitia that contain smooth muscle cells and connective tissue.


text:
Where are action potentials initially created?
Is the axon hillock still the place where one thinks and talks of that action potentials are initially created? (I've heard this place moved into the direction of the axon initial segment.)
If one doesn't want to commit oneself whether it's the axon hillock or the initial segment where action potentials are initially created – because it's somewhere inbetween or at both of them, or it depends on the type of neuron, or we don't know, or we don't care:

How does one talk about that place unequivocally?

Is there an abstract (non-anatomical) terminus technicus for "the place where action potentials are initially created"?

Action potentials are initiated where there is a high density of voltage-gated $Na^+$ channels and that may vary from cell to cell, as you guessed. For an illustrative example see the figure below, reproduced with permission from Kole et al. (2008).

Density of voltage-gated $Na^+$ channels and $Na^+$ influx along the axon of a cortical pyramidal neuron.
Reproduced with permission © Nature Publishing Group
As you can see, in this cell type voltage-gated $Na^+$ channels, labelled in green in the left-most image, are predominantly expressed away from the axon hillock. We can also observe that the expression of voltage-gated $Na^+$ channels correlates with the degree of $Na^+$ influx in a monotonic relationship (right-most panel).
In smaller cells action potential initiation can happen closer to the axon hillock and in cells of some invertebrates even in multiple locations (Kole and Stuart 2012). What may be the advantage of using the axon initial segment (AIS) as the sole site of initiation of action potentials (APs)? Here is a direct quote from Kole and Stuart (2012):

[The AIS] has a small local
  capacitance ($C$) and therefore requires less inward current ($I$),
  that is, a smaller number of $Na^+$ channels per unit area, to
  generate APs compared to larger structures, such as the soma
  or proximal dendrites. Hence, the AIS is also an energetically
  favorable site for AP initiation. Furthermore, the small capacitance
  of the AIS favors rapid changes in membrane potential,
  as occurs during the upstroke of the AP ($dV/dt = I/C$). Finally, it
  is worth noting that having a single site of AP generation provides
  neurons a single locus where inhibition can gate AP initiation. [...] Initiation of APs
  further from the soma, taking advantage of the electrical isolation
  of this region, is a strategy used in some neurons to increase their
  capacity to discriminate the arrival time of different synaptic
  inputs.

References
M. H. P. Kole et al., Action potential generation requires a high sodium channel density in the axon initial segment. Nat. Neurosci. 11, 178–186 (2008). doi: 10.1038/nn2040
M. H. P. Kole, G. J. Stuart, Signal Processing in the Axon Initial Segment. Neuron. 73, 235–247 (2012). doi: 10.1016/j.neuron.2012.01.007

So wouldn't something like "spike-generating density" be a perfect name, analoguous to postsynaptic density

I only addressed what I think is the essence of your question, i.e. where are action potentials generated, and avoided the linguistic aspect. Usually, terms are established by use in the literature when there is a purpose for them and it's not my place to create new terms in this forum. Suffice it to say that the phrase predominantly used is "action potential initiation site" or a variant thereof.

That's what I wanted to know! I didn't want to invent a new term, when there is already an established one.

By help of the term you gave me, I immediately found this article:  https://www.ncbi.nlm.nih.gov/m/pubmed/8786434/

... and this one about multiple AP initiating sites: https://www.ncbi.nlm.nih.gov/m/pubmed/11535672/?i=2&from=/8786434/related

In the meanwhile I also found the phrase "trigger zone".


text:
Parts of the brain pivotal for maintaining consciousness
From an answer to another question (on conscious experiences by coma patients) I have learned that

no conscious experiences, complex thoughts, or complex emotions can
  occur when one is in coma (clinically unresponsive, with absent or
  minimal brainstem reflexes, and with severely abnormal EEG)

This means that proper modes of activity of the cortex and the brainstem are necessary conditions for conscious experiences.
Two questions arise:

Has it been shown that proper activity of the brainstem and the cortex is also a sufficient condition for conscious experiences, i.e. all other parts of the brain might be mute or otherwise improperly active? Or are there other parts of the brain whose proper activity is also necessary for conscious experiences?
Why is it that next to the newest parts of the brain (cortex and neocortex) also its oldest part (the brainstem) is pivotal in maintaining consciousness? What about other parts that evolved later?

Note that with "necessary" I don't mean causally necessary but merely logically or observationally necessary, i.e. "not observed without".

The minimal neural mechanisms that are jointly sufficient for consciousness (conscious percept, thought, memory, etc.) to occur, under constant background conditions, are called the neural correlates of consciousness (NCC) [1]. The background conditions are enabling factors that must be present for the NCC to be able to function (e.g., the heart must beat and the lung must exchange air to supply the brain with oxygenated blood, the blood levels of sugar and other blood constituents must be in normal ranges, the ascending reticular activating system (ARAS) must be functioning, etc.), but they are not the NCC.
The ARAS is the neural network in the core of the brain extending from the rostral pons to both thalami and the basal forebrain, and from there it sends extensive axonal projections to the cerebral cortex, including the consciousness neural network (which is the anatomical part of the NCC). The ARAS is responsible for the alertness of consciousness, but it is not responsible for the content of consciousness. So, it is not part of the NCC proper. However, there can be no consciousness if there is no stimulation from the ARAS, even if the consciousness neural network is intact and able to function, such as in the case of extensive brainstem hemorrhage, infarct, and trauma. And the level of conscious alertness depends on the activation from the ARAS – the more activation, the higher level of alertness. This results in various conscious level’s states, such as (from lower to higher level of alertness) coma, stupor, drowsiness, normal alertness, and heightened alertness [2]. So, the answer to question #2 – why this oldest part (the brainstem) is pivotal in maintaining consciousness – is that it is the way the consciousness neural process has evolved to be dependent on the ARAS for its level of function (i.e. its alertness).
On the contrary, if the ARAS is working normally but the consciousness neural process is not, there can be alertness without, with minimal, or with some awareness. The degree of impairment of awareness depends on how much the consciousness neural process is dysfunctional. For example, in the case of damages to the consciousness neural process from diffuse cerebral hypoxia, extensive bilateral cerebral infarcts, or diffuse cerebral cortical injury, the results can be various abnormal conscious awareness’s states that range in severity of abnormal conscious awareness, depending on how much the consciousness neural process is impaired, such as (from mild to severe) acute confusional state, akinetic mutism, minimally conscious state (MCS), and vegetative state (VS). In the latter two categories, which are severe conditions, the patients can open eyes and have some reflex responses, such as blinking, chewing, and yawning, but show no (in VS) or minimal (in MCS) signs of conscious awareness of self and the environment (by clinical testing or by special investigations such as EEG, evoked potentials, and fMRI) [2].
Regarding the neural circuits of consciousness, as far as one can conclude from the evidence at present, it seems very likely that the Default Mode Network or Resting State Network [3], which includes the medial prefrontal cortex, posterior cingulate cortex, precuneus, hippocampal and parahippocampal cortex, retrosplenial cortex, and some parietal and temporal cortices, is the network of the consciousness neural process when the mind is in the state of passive internal mentation, not performing cognitively demanding tasks, and not attending to outside stimuli. This network overlaps with the network that functions for access consciousness (consciousness of episodic stimuli, not consciousness of continuous stimuli as in the former case). At present, evidence shows that the network of Global Workspace theory proposed by Baars [4] or the network of Global Neuronal Workspace hypothesis of Dehaene [5], which includes the cortico-thalamic (C-T) core and a network of neurons with long-range axons densely distributed in the prefrontal, fronto-parietal, parieto-temporal, and cingulate cortices, is the network of access consciousness. So, the complete neural network of consciousness that functions to be conscious of continuous events and episodic events is likely to be some form of combination of these networks, such as the neural network in the extended theory of global workspace of consciousness proposed by Song [6].
The complete neural circuit of consciousness, whatever it is finally found to be composed of, and the way it functions will constitute the complete NCC. The complete NCC is necessary and sufficient for consciousness to occur. Even if we do not have the complete NCC now, the above current models that we have are fairly well supported by experiments. I hope this answers question #1.
References.

Tononi G, Koch C. Consciousness: Here, there and everywhere? Philos Trans R Soc Lond B Biol Sci. 2015 May 19;370(1668):20140167. DOI: 10.1098/rstb.2014.0167.
Ukachoke C. Chapter 6 – Consciousness. In: The Basic Theory of the Mind. 1st ed. Bangkok, Thailand; Charansanitwong Printing Co. 2018.
Andrews-Hanna JR. [The brain’s default network and its adaptive role in internal mentation.(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3553600/) Neuroscientist. 2012 Jun;18(3):251–270. DOI: 10.1177/1073858411403316.
Baars BJ, Franklin S, Ramsoy TZ. Global workspace dynamics: Cortical “Binding and propagation” enables conscious contents. Front Psychol. 2013;4:200. DOI: 10.3389/fpsyg.2013.00200.
Dehaene S, Charles L, King JR, Marti S. Toward a computational theory of conscious processing. Curr Opin Neurobiol. 2014 Apr;25:76–84. doi: 10.1016/j.conb.2013.12.005.
Song X, Tang X. An extended theory of global workspace of consciousness. Progress in Natural Science. 2008 Jul 10;18(7):789–793. DOI: https://doi.org/10.1016/j.pnsc.2008.02.003.

Thanks for this comprehensive answer!

You don't mention the claustrum which is according to Crick and Koch one of the seats of consciousness in the brain. Would you consider it as part of the NCC or as an enabling factor like the ARAS?

I think the case for claustrum is still controversial. For example, “… another case report describes a patient who was conscious despite the fact that the claustrum and … had been destroyed bilaterally as a consequence of herpes simplex encephalitis” Koch C, 2016 and please search discussion about claustrum in this paper.

However, because claustrum is higher up in anatomical level than the thalamus and basal forebrain, which are the terminal nuclei in the current ARAS network model, it shouldn’t be part of the ARAS. Also, studies have shown that it has extensive connections to cortical and subcortical regions and its functions are complex integration of various cortical inputs (ex. color, sound and touch) into one experience, not just simple stimulation of consciousness. So, if it’s one essential part of consciousness network, I believe it’s part of the NCC, not the ARAS.


text:
Inhibitory functional connectivity
Functional connectivity may be defined as

»the temporal correlation between spatially remote neurophysiological events, expressed as deviation from statistical independence across these events in distributed neuronal groups and areas«

or alternatively as

»the presence of statistical dependencies between two sets of neurophysiological data«.

Images of large-scale brain networks typically show highlighted regions of interest that - in my humble understanding - are supposed to be functionally connected. But being highlighted means being active (at least more active than other regions), and thus functional connectivity seems to be mainly excitatory (even though only virtually).
But what about inhibitory functional connectivity? Can it be found by equal statistical means as excitatory functional connectivity - and how would it be "highlighted" in brain images?

On Neuroimaging Analysis

But being highlighted means being active (at least more active than other regions)

This is not the case in functional connectivity analysis, or indeed not necessarily the case in any sort of functional neuroimaging analysis. The colormap highlighting in such images as you referred to (see the primary reference for that particular image) reflect statistic scores, commonly z- or t-statistics. Correlation simply means that time-courses behave similarly over time, and the color coding tells you how strongly they correlate with the “common profile” of the cluster. This makes no direct statement regarding the total “activation level“ over time, as represented by e.g. the area under the curve of the timecourse. In fact, such a metric would be meaningless, since fMRI signals are de-meaned so that they fluctuate around zero (as seen e.g. in the timecourses depicted here). Functional connectivity networks thus do not imply in whatever fashion a higher level of activity in highlighted networks. For further visual clarification you can consult Figure 1. of this article showing that functional connectivity networks can be and often are active at the same amplitudes and have similar levels of “total activity“ as visually inferred from the integral of the power spectra. This integral analysis is not presented, however, as it is meaningless.
On Inhibitory Functional Networks
Whether functional connectivity networks are implied to be excitatory depends on the exact mode of analysis. If the analysis is truly based only on detecting large correlation scores, identified networks will not resolve inhibitory projections, as such connections would cause anticorrelation rather than correlation. It could still be that a functional connectivity network is based on multiple areas receiving strong inhibitory input from an upstream node, yet that node would not be part of the network. Consequently, proficient functional connectivity analysis will identify networks via methods such as independent component analysis (ICA), which are able to group both strong correlation and anticorrelation together, as seen here.
TL;DR
Yes it can, it often is, and it's generally highlighted in blue.


text:
How superficial an artery has to be for pulse to be measured manually?
Why arteries  pulse? How superficial an artery has to be for pulse to be measured manually?

They pulse because the blood flow follows the heart beat. I do not think there is a specific depth that they need to be to be measured, the ones from the wrist and neck are usually used.

The larger the artery, the deeper it can be and still be palpated, e.g. the descending aorta is palpable in the abdomen of the average person.


text:
Why and when did the misconception about the Panther being a species came to be?
People usually call Panther to any big black cat, I did so until I watched Apocalypto and saw they were calling the black cat Jaguar which confused me. (I have no biology knowledge)
It was kind of a shock to discover that Tigers and Lions, among other species, where Panthers too, and it surprises people when I tell them.
Does anybody know why and when this started to happen?
* I realize this might not be related to biology but actually to popular culture, but I couldn't find a stackexchange site about that.

Tigers, lions, jaguars and leopards are all different species. Panthera is a genus, a broader classification than a species. Tigers are Panthera tigris, lions are Panthera leo, and jaguars are Panthera pardus. In each cases the formal species name is the genus followed by the species identifier. Common usage rarely gives a hoot about the subtleties of biological classification.
Your initial impression was correct: any member of the Panthera genus that has a black coat is called a black panther. In South America they are jaguars, in Africa and Asia they are leopards.

Now I am somehow wondering if there could be black tigers.

@skymningen Yes, (sort of): https://en.wikipedia.org/wiki/Black_tiger_(animal)

@KoenvdH Is it just me, or is there something strange about black tiger and her cub? The face/head seems a bit unusual.

@HarrisWeinstein the small head/big nose might mean they are south chinese tigers from what little looking around I did.

Oh I see, I was using Panther and Panthera interchangeably. Mainly because both sound the same in spanish (Pantera and Panthera) my native tongue.


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Phronima sedentaria anatomy
I would like to know how many appendages the arthropod Phronima sedentaria has, and how they are arranged. It's not hard to find picture references, but Phronima's transparency makes it difficult to tell from live photos, while what drawn diagrams and text descriptions I've been able to find diverge wildly.
From what I've been able to determine, it has a bulbous head which may or may not have antennae, near to which are two to four pairs of limbs. There is a small gap, then a much longer pair of limbs ending in claws, followed potentially by a second longer pair, and then two to four shorter pairs of limbs. The tail is lined by three pairs of swimmerets, possibly tipped with paddles or bristles.
The best possible answer for this would be a picture like this one, with the assurance that it does indeed represent Phronima sedentaria accurately, though I would be happy with a confirmation of appendage count. Additionally, while I would prefer information about Phronima sedentaria specifically, I can make do with such information about any member of the genus so long as it is specific.

After finding some higher-quality images/videos with some views of the creature from the front, I can say that the image I linked is mostly accurate, if lacking in detail. There does appear to be a set of antennae, though they are significantly shorter than the legs, the front two pairs of legs are shorter than the others and end in small claws, and are positioned more 'underneath' than 'to the side of' the body relative to the other legs. The reason for the confusion seems to have been a combination of the different position of the front four legs, some pictures of other Phronima species misnamed as sedentaria, and that the antennae appear to be able to fold in close to the head, making them nearly invisible.


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What happens to lactic acid I eat?
Let's say I drink some Kefir Milk, what happens to the lactic acid in the Kefir Milk that has entered my digestive system?

First, there are two different isomers of the lactic acid, the L(+)- and the D(-)-form. Both differ in the position of the OH-group in the molecule:

Both turn polarized light in different ways, the D(-) to the left and the L(+) to the right. The physiological form of lactic acid for the human body is the L(+) form, which is taken up in the gut and then metabolized by the L-Lactatdehydrogenase to form pyruvate and NADH.
For the D(-)-Lactate is has been thought the the D-Lactatedehydrogenase is only present in some lower animals and bacteria and that this lactate isoform is mostly excreted. This seems not to be true and there is some D-Lactatedehydrogenase in humans (and other mammals) as well.
See these publication for more information:

D-lactate in human and ruminant metabolism.

Lactic acid has been found to act as a fuel for the muscles. Refer to:  http://www.nytimes.com/2006/05/16/health/nutrition/16run.html?_r=0

Most athletes consider lactic acid their enemy, and think that training helps eliminate the metabolic waste product from their muscles so the muscles will function longer and harder. But UC Berkeley physiologist George Brooks has found that training actually teaches muscle cells how to use lactic acid as a fuel to get more bang for the buck. With training, mitochondria grow, take in more lactate via a shuttle and burn it to generate more energy.
"I gave rats radioactive lactic acid, and I found that they burned it faster than anything else I could give them," Dr. Brooks said.

You may also refer to http://www.eatmoveimprove.com/2009/11/the-truth-about-lactic-acid/ for details on lactic acid metabolism.

Hi, thanks. But what happens to it when it's in my stomach? Will it ever get to my muscles or will it simply pass through my digestive system?

where can I buy some of that radioactive lactic acid; is that at GNC or what

lactic acid undergoes radioactive dating in the lab


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Is there a realistic "family tree" model for the human population?
I would like to do some gene inheritance simulations, and I was wondering if there is an accepted model for what mating looks like in the general human population? I am not necessarily looking for the exact graph of any population.
For example, my current model has generations 1, 2, ..., n, n+1, ... where each individual in generation i is the product of a mating between two individuals in generation i-1. This is obviously over simplistic, and I was wondering if there are better models out there?

Well, there are some questions regarding what population. I don't have 50 rep, so I can't really ask for clarifications; populations range a lot, from your typical avoidance of inbreeding (laws against cousin marriage) to Tamils with their high rates of first cousin marriage (so high that they don't have any pedigree inbreeding depression due to selection, so it's not unhealthy).
Mating in humans is often assortative for many traits including education, vocation, etc. When the Americas were settled (after aboriginal Americans were devastated by disease), skin color was a source of assortative mating. Arguably it still is. On the other hand, people tend to mate disassortatively for traits such as Major Histocompatibility Complex.
Furthermore, isolation in human populations tends to be by distance (though this is of course changing, leading to a lot of admixture in recent population history).
As a result, what your population is will have a huge impact on your results; you'll need to calculate f for any particular locus, and take a look at admixture. If f is 0, then you have a random mating scenario (neither preference nor avoidance of inbreeding, and neither assortative nor disassortative mating).
TL;DR if you're doing a very simple analysis on dummy data, you can probably get away with assuming that mating is totally random. But if we're talking about actual populations, you'll need to run the models/calculations of f and other population measures.

My analysis applies first to the United States. Perhaps I can generalize after that. It is okay if subpopulations are neglected as long as I can make get good results for the vast majority.  I might just start with a random mating model as you suggest.

On the one hand, there's papers such as this that discuss assortative mating. On the other hand, you have things like this that indicate some level of disassortative mating as well -- but note that that only applies to some of the populations. If you can't do any analysis of f values, then you could also try doing a statistical test of f; for instance, run a simulation using f=0 and compare to your data.

An unbounded model with no carrying capacity(unregulated reproduction) will be easier to model, but it would have no long term resemblance to actual population change. It is easier to model by virtue of one not being required to know the carrying capacity. That being said, the carrying capacity is important in a realistic model since the population is naturally regulated by external factors. You might do well to look at Discrete time logistical model. The reason I suggest this model is that it is discrete and recursively defined, thereby lending itself to represent each iteration as a likely branch in the graph.


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Why do almost all SNPs have two alleles?
Reading the Wikipedia page for SNPs I find the sentence "Almost all common SNPs have only two alleles." This is consistent with terminology elsewhere, such as the therm "Minor allele frequency", which references the least common allele, which implies there are generally only two alleles for a given SNP.
But there are 4 common nucleotides, A, T, C, and G. Why wouldn't it be common to have 3 or 4 alleles at a certain location? The only way this seems possible to me is if strand is ignored, and so at any given location "A" and "T" are considered the same allele and "C" and "G" are considered the same allele. Is this the case, or am I misunderstanding things.

Well, though it is possible to have SNPs of more than two alleles, and some exist, due to the low probability of having a basepair change twice in the same base-pair (there are aproximately 3.000 Mb in the human genome) and have it in more than 1% of the population (remember we are talking about single nucleotide polymorphism) to classify as a polymorphism is a very rare phenomenon.
I can check the maths for it if you need it, but it's just matter of probability.

To be sure I understand, the idea is that say 100% of a population has an "A" at some loci at some point in time. Then say a mutation causes a member, call her Alice, of the population to have the loci at that base replaced with a "C", and they pass that mutation on to their offspring. After some time, that loci would be considered a SNP if enough of Alice's descendants survived such that they make up 1% of the population. The only way for another allele to exist is is if someone else at some other point in time ALSO has a mutation at that loci that switches away from "A" or "C", which is rare

The percentage varies between definitions of polymorphisms, some say 1%, some say 5%, but you got the idea. You have to think that is not a loci, but rather a single position of a loci. Even if all locis accumulated 1 single base mutation each generation with a 2.5 kb length (that is the average loci if i remember correctly) it would still be 1/2500 probability of affecting the aame letter and times 2/3 (as one of the mutations would be a reversion to the original). So yeah, it is highly improbable.


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How can eyeglasses improve vision beyond 100%?
The result of a vision test by my oculist yielded a result of more than 100% while wearing prescription glasses. I wonder, how can a person see better using eyeglasses?

What do you mean by 100%? Can you give us acuity measures? Like Snellen fractions (20/20 or 6/6 etc)? If you scored above the norm, say 6/20 that means you perform above the normative value. Those normative  values are simply averages and one can surpass that. Also with conventional corrections like glasses.

@ChrisStronks I wasn't told any measures or units. Just the result that was a percentage. Actualy I was too pleased at the moment to ask the doc this question.

maybe they meant you were shortsighted and your glasses made you longsighted (rather than "normal" sighted)?


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Why are there no marine birds?
Walking  by the lake and watching the ducks the other day a thought struck me; there are lots of aquatic birds but all remain at least somewhat terrestrial, nesting on land.
Why is it that no birds have taken the evolutionary route of the dolphins and whales and returned to the sea?
Is there something in avian biology that means this is not possible?

Feathers require a lot of maintenance with fats to be waterproof, which would be quite impractical for a bird which constantly lives in the water.

Penguins are probably one of the farthest along the evolutionary path you describe, as they spend a large amount of time in the water, not just on the water.

egg laying in general makes it harder, placental mammals have a much easier time going back to the ocean since they carry their young internally. cetaceans had a much easier time of it then aquatic birds and reptiles.

Apart from one isolated group of birds in Australia (i.e., mound nesters found in Australia that use external heat for incubation - see link), all birds incubate their eggs (see link). All species that returned from land to sea have retained their reproductive cycle (marine mammals still give live birth and suckle their young) and still rely on air for oxygen intake. Extrapolating this mammalian evolution to birds would result in a creature that returns to sea, with all ties to land cut off, but that still has to incubate their eggs under water. As they would still rely on air, this is not very feasible as they would need to go up often to breath. This would leave the eggs vulnerable to predation. Even worse, it would leave the eggs at the mercy of a relatively cold ocean cooling them down quickly. Incubation means that the eggs are pretty much kept at body temperature which is difficult in the sea regardless of breathing parents. In all, while there may be certain benefits of underwater life for birds, it will require some drastic evolutionary changes in terms of the reproductive cycle. A more parsimonious way of colonizing the sea is to go back to land once and a while to lay eggs, incubate them, and raise the young until they are sea-worthy, like penguins do as @MattDMo mentioned.

All birds incubate their eggs? You forgot the cuckoo!

I think that sea snakes have returned from land to sea and have altered their reproduction to fit that. Sea snakes are truly vivipare, they give birth to live babies. This is an adaptation necessary for them to remain in the water. For laying eggs, the snake would have to go on land.


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Estimating RPM to RCF in Methods from Older Papers
I'm attempting to replicate a cell biology method from a 1958 Laboratory Investigation paper. The protocol is for the isolation of an extracellular matrix protein, and a key step is a centrifugation carried out for 2 hours at 2300 rpm. Apparently it was not common practice to list make, model, and rotor size of centrifuges, so I am a little lost as to what settings to use on my own centrifuge to get the same rcf.
Are there any good starting points for estimating the proper settings? e.g. who the major centrifuge suppliers were at the time or what models would be seen as 'standard' for a cell biology lab?

Do they at least list what kind of tubes the samples were in while spun? Knowing the size of the tube would help narrow down possible rotor sizes.

CAn you provide a link to that article.

@user137 Good point! They use "250 mL centrifuge bottles"

@WYSIWYG here is the pubmed link, but I don't know where to find the article online. http://www.ncbi.nlm.nih.gov/m/pubmed/13540204/

I am not sure about what they used in 1958 (perhaps Sorvall). However you may look at recent papers for ECM protein isolation (if that was your objective).
Have a look at this article.
From materials and methods:

ECM protein isolation.
Fibroblasts or A431 cells were removed from the
surface of the culture plate with 2 mM EDTA in PBS for 3–5 min at
37⁰C. Detached cells were discarded, and remaining ECM proteins
attached to the surface of culture plates were washed with the same
solution. Cell removal was controlled under the microscope. After
cells were completely removed, matrix proteins were covered with 5%
acetic acid and incubated at 4⁰C overnight. Then, acetic acid was
removed and exchanged with a buffer containing 125 mM Tris-HCl, pH
6.8, 0.1% SDS, 10% glycerol, 1% DDT, 0.05 mM PMSF, protease inhibitor cocktail (Roche, Germany), and incubated at 37⁰C for 1 h. Proteins
were removed with a scraper. The procedure was repeated three times.
All protein extracts, including acetic acid, were combined and ECM
proteins were precipitated by five volumes of acetone. After
incubation at –20⁰C overnight and centrifugation at 7000 g for 15 min,
the protein pellets were dissolved in an appropriate buffer for
further analysis by one- or two-dimensional gel electrophoresis.
In addition, we obtained a Triton X-100-soluble fraction of ECM
proteins. Cells were removed as described above; dishes were filled
with 1% Triton X-100 and incubated at 37⁰C for 30 min. The extraction
was repeated three times. The following procedure of ECM extraction
was the same as described above. Samples obtained from both fractions
were dissolved in a buffer for one-dimensional (Laemmli) or
two-dimensional (rehydration buffer containing 8 M urea, 2% CHAPS, 20
mM DDT, 0.1% Triton X-100) electrophoresis. Proteins that remained
after Triton X-100 extraction were dissolved in Laemmli sample buffer.

Thanks! That seems like a really good way to get the ECM into a pellet, but the purpose of the centrifugation in the article is actually to keep the ECM protein in the supernatant while letting the tissue it is digested from pellet.

@Chastain The tissue is removed prior to protein precipitation.


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Why can't people talk while inhaling?
Why do we have to exhale in order to talk? From looking on Wikipedia, it seems like it has something to do with the glottis, but I'm not clear on the mechanism that makes speech sound so different when air is coming in.

As I understand it, speaking requires exhaling because air must pass in a forward motion across the vocal chords.

Via deep scientific analysis (i.e. trying it myself 5 seconds ago), I have determined that you can in fact speak while breathing in, it just sounds funny.
Think of the vocal chords as being like the body of a flute. As air passes by them, they vibrate and make sounds. Through careful modulation of their shape, specific sounds can be reproducibly made (this is equivalent to opening and closing the stops on the metaphorical flute). The way the pressure in your throat changes when you inspire (breathe in) is very different from the way in which the pressure changes when you expire (breathe out). These pressure differences are a large part of the reason why you sound different when you speak during inspiration as opposed to expiration, just like breathing into a flute differently would produce different sounds (although potentially the same notes).
Other physiological, neurological, etc. effects probably also cause differences in the vocal cords during expiration/inspiration and thus also contribute somewhat to the differences in the sound.

I agree. I knew someone who spoke on inhalation most of the time. It was disconcerting.


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How long does it take for a cricket to die at subzero temperatures?
I am on a number of reptile groups and I often hear freezing recommended as a humane way to get rid of surplus feeder insects.
However, they can also revive if you don't leave them in there long enough.
If I had a bag of crickets and put them in the freezer, how long would it take for them to die in this way?

The actual paper that the linked article cites never mentioned about freezing the crickets:

We examined CCR (Chill Coma Recovery) in G. pennsylvanicus exposed to 0 °C. The time
  required for crickets to recover movement of the abdomen and legs
  increased exponentially with the duration of exposure to 0 °C; after
  more than 12 h of cold exposure, recovery time reached a plateau at
  ca. 15 min

And this is how CCR is performed

A total of 60 crickets were placed individually into 14-mL plastic
  tubes and cooled from 25 °C at 0.25 °C⋅min−1 and held at 0 °C for 2–42
  h. At 2-h intervals (first 24 h), and every 6 h thereafter, four
  crickets were placed on their dorsum in a Petri dish at room
  temperature. Times of four indices of chill-coma recovery were
  recorded: (i) first foreleg movement, (ii) first hind leg movement,
  (iii) initiation of abdominal contractions (active ventilation), and
  (iv) righting. Foreleg and hind leg movement were identified as a
  coordinated directional movement of the limbs, distinct from twitches
  of the limbs observed during rewarming. If crickets had not righted
  within 3 h of removal from the cold, they were considered to have
  incurred chilling injury that precluded recovery.

So, the crickets were never actually subjected to subzero temperatures or freezing or even cold shocks.
How long it takes to die depends on the freezer temperature; based on personal experience I can say that they die in ~10min @ -20⁰C.
Didn't find much information on crickets but according to this paper Drosophila will die in less than 2 hours at -5⁰C upon transferring them to the cold temperature directly (cold shock). However, if the larvae are "hardened" by keeping at +5⁰C before cold shock, their survival chance increased — the temperature required for killing them in 2h (Lowest Lethal Temperature) reduced. Now cricket is bigger than Drosophila but the surface area is also higher. I cannot do more than speculate at this moment (you can apply complex heat transfer equations and see how the rate changes with the size).

Thanks, that's useful info. Obviously completely different conditions to simply throwing them in the freezer then.

@starsplusplus yes. That would subject them to cold shock and they would die sooner. Also, during freezing the tissues would be damaged; they won't come back to life (very few organisms can tolerate freezing; they produce cryoprotectants). Please accept the answer if it answers the query (the tick on the left). You can upvote as well if you found it useful.

I found the information you provided helpful because it addressed the fallacies in the article's reporting of the paper. However, my actual question was "How long do crickets take to die?" and you only have a single line addressing that which is based on personal experience. If you could expand on that and preferably include some references I would be happy to upvote. :)

I also prefer to leave it a couple of days before accepting an answer, so as not to discourage further answers. I've seen this encouraged on multiple SEs for that reason; hope you don't mind.

I used your answer in a footnote to my other answer here and credited you.


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Mechanism for earthworms to get into a roof gutter
While cleaning accumulated muck from a roof gutter on my house, I found a few earthworms living in the muck. I am intrigued about what mechanism may have allowed the earthworms to reach that location. Some hypotheses:

Live worm crawls up a downpipe
Live worm dropped by an overflying bird
Cocoon is stuck to the outside of a bird (feet), falls off while the bird is overflying the roof
Cocoon passing through bird digestive system and deposited on the roof

What is the likely mechanism for earthworms to reach that location?

I wanted to use the tag dispersal for this question, but it doesn't exist and I don't have the rep points. But perhaps there is another better term?

Birds dropping their meal :p

I would say that the reason why a given organism reaches a given space relies on four main factors:

Morphology and physiology: can that organism reach that place physically?
Food distribution: is there enough food to reproduce and spread in that specific spot?
Habitat: does that habitat fulfill its environmental/physiological needs? Is it environmentally safe for that species?
Abiotic factors: wind, water, etc...

I know it's a very general answer, but consider that the main goal of every organism seems to be to survive, spread and reproduce as much as we possibly can.
For example, if the gutter accumulates moss, earthworms will most likely crawl up the wall and into the gutter to feed on the precious organic matter. Also, gutters, due to its function, tend to be wet at times, and earthworms need a moist environment, so it seems like an ideal spot for them (earthworm climbing up).

Live worm dropped by an overflying bird

Seems likely too: the term ornithochory defines seed dispersal by birds. I guess it could also be applied to dispersal of other animals (at least anthropochory can be applied to both seeds and reproductively capable animals dispersal by humans, in this case, earthworms being transported by the bird's beak). I think the most likely scenario in this case is food availability and a good environment to proliferate and make more earthworms (mostly because it would take a couple of clumsy birds to drop their prey on top of your gutter to establish an earthworm colony up there although it depends on the specific earthworm species and whether it is parthenogenetic or not, of course, but still within the realms of possibility).
When it comes to species distribution, it normally tends to be a mixing of different mechanisms rather than one single specific mechanism.


text:
What is the function of oxyphilic cells in the parathyroid?
Apart from the chief cells, which produce and secrete parathyroid hormone (PTH), the parathyroid gland has another type of cells, which are large and fewer in number, have small, dark nuclei and an acidophilic cytoplasm with many mitochondria. These cells increase in number with aging. As far as I know, we still have no knowledge of what role they perform, or why they increase with age.
Is this true, or are there already some concrete ideas about this?


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Why do humans require vitamin B12 supplementation while herbivores do not?
This question came about from reading the comments of this (very unclear) question, which the author did not properly clarify.
Vegans are often recommended to take vitamin B12 supplements, as the vitamin is not present in sufficient quantities within vegan food. This implies that plants do not produce (or need) vitamin B12 in their metabolic processes.
However, herbivorous animals do not require any vitamin B12 supplementation, yet contain significant amounts of vitamin B12 in their food products.
What, then, is so different about the digestive tracts of humans and other herbivores that prevent humans from obtaining sufficient vitamin B12 from bacterial sources? Can humans be supplemented with gut bacteria from herbivores, allowing them to obtain sufficient vitamin B12 while on a vegan diet without requiring supplementation?

Could be due to 1. non-human herbivoure animals have large cecums in their digestive tracts, located between the small and large intestine where bacterial fermentation takes place. 2. They are mainly depending on bacteria for B12 synthesis. 3. They eat soil which provides cobalt for synthesis :P 4. Humans are hindgut fermenters. It could also be a good reason to observe the dietary habits of these animals in the wild - which are naturally way different from human vegans. Also the metabolism and related biochemical pathways. I am curious to know the answer myself.

The bacteria in the foregut of cud chewing animals (e.g. cows) provide enough B12 and other B vitamins. Uptake of B12 happens mainly in the small intestine. There are lots of bacteria in the human intestine but most fermentation of plant matter happens in the hindgut.
Hindgut fermentation also produces B12 but since this happens past the small intestine it is not sufficient to provide enough B12. Therefore non foregut fermenting herbivores (e.g. rabbits) get their B12 when they consume their own feces, which they do anyway to obtain higher digestion efficiency of plant matter. I would not recommend this process to any vegan human though.
As mentioned by bonCodigo, these animals need to take up enough cobalt, and their requirements for this element are higher than our own.
Source:
Contributions of Microbes in Vertebrate Gastrointestinal Tract to Production and Conservation of Nutrients
C. EDWARD STEVENS , IAN D. HUME
Physiological Reviews Published 1 April 1998 Vol. 78 no. 2, 393-427

+1, I highly recommend that one read this paper, it includes a large amount of information about other species of animals and their nutrient uptake strategies.

Primates are especially interesting as even the most herbivorous of them eat animal sources high in b12 like insects, eggs, or meat. Even gorilla the most herbivorous primate eats insects, and sometimes even have to reprocess their feces to get b12.


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How does the immune system distinguish between commensal and pathogenic bacteria?
There are billions of bacteria living harmlessly in our gut, and in fact most are helpful to us, aiding digestion, producing vitamins and maintaining gut health. The immune system is able to suppress immune responses against these organisms, avoiding killing such beneficial microorganisms in this way. However, it is still able to detect and mount an immune response against those microorganisms that are or would be pathogenic. How does it distinguish them?

This can be a good reading.


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How do we know with so much detail the molecular structure and composition of some molecules?
I can't understand how can we get to and be so sure about so detailed information about the molecular structure of certain substances. How do we get this information? What tests are used to such?
Let's take for example somatostatin:

you can see it is a big and extremely complex molecule, and my question is, how have we arrived to this structure? How can we know this to such detail? What tests do we use to know this?

Although this does not answer the general question, I should point out that your example is a polypeptide, so the atom connectivity could be determined mostly from its sequence (AGCKNFFWKTFTSC). That, plus the disulphide bond

@gilleain that is one possibility for my example, in fact. But I'm still curious about a general answer

I'd take a look at this wikipedia page on chemical structure. The take home point wont be whats on the page, but the techniques it references. Sometimes it's a combination of 3 or more different techniques that elucidate the final chemical structure, and all of them are somewhat difficult to understand at first.

Usually X-ray crystallography maybe, have a look at PDB for proteins. It (probably) has info on the original observations of discoverers. Also, many such structures are flexible and the accepted structure is chosen by consensus.


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Why human endometrium doesn't stay constant?
Is there any explanation or evolutionary advantage to the endometrium constantly cycling between the proliferative and menstrual cycle? Wouldn't it be more advantageous if it kept always fully thickened? I imagine it is less energetically expensive than to be always producing and losing all those cells, blood vessels, etc.

One hypothesis is to protect the uterus and oviducts from sperm-borne pathogens.
Also Beverly Strassmann has proposed that the energy savings of not having to continuously maintain the uterine lining more than offsets energy cost of having to rebuild the lining in the next fertility cycle, even in species such as humans where much of the lining is lost through bleeding (overt menstruation) rather than reabsorbed (covert menstruation).


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Parents that eat their own children
I am told that there are some species, like fish or rabbits, that if let, will eat their own children. If this is true, how does a species like this exist? Shouldn't the fact that they kill their own lineage make them nonviable?

Just keep the offspring away from the hungry adult.

You assume there are many chances the parents individuals can even meet their offspring. This doesn't hold true in a variable environment like the one most species in Nature normally live in. I will give you one simple example. When I was a child I had an aquarium with little tropical fishes in it. In this closed space (non-natural environment) the very parents ate their own children when they were still very yound and no child fish could get to adulthood. However, if these very same fishes were living in Nature-like in some small river or marsh or any other natural pond,

their youngsters wouldn't even had the chances of meeting their parents (and being eaten by them) because immediately after hatching the small fishes would have gone into hiding among the vegetation in this natural pond and because they re small enough to hide easily they would most likely never have met with their parents (and thus avoid being eaten by them). There are many other similar cases with other animals where the hatchlings are so small they virtually live in other environment then their parents live in.

Rabbits (at least in captivity) will only eat their young if there is a protein shortage. Obvioulsy, any aminal that eats its young doesn't eat all of them.

Yes, it is true.
Prairie dogs
Prairie dogs for example are known for frequent infanticides.

Many other species kill their babies too
But of course, such behaviour also exists in other lineages such as grey langurs, gerbilles, lions, giant water bugs and Bottlenose dolphins (just to cite a few examples).
How does that evolve
It will be impossible to provide a complete universal explanation to this behaviour because the evolutionary processes causing this behaviour varies from lineage to lineage. For examples, in lions, only males kill young of the females that are still nursing and they do so when taking over a new harem only. In prairie dogs, mothers cause infanticide preferentially on others' babies but also on their own babies.
Going into the details of how such behaviour evolves in every specific lineage would probably require writing an intro on kin selection and other fields of evolutionary biology which is way too much for a single post. You may want to have a look at the wikipedia article infanticide for a start.

Shouldn't the fact that they kill their own lineage make them nonviable?

Of course, they don't kill all the babies. Only a fraction of them!

"In prairie dogs, mothers cause infanticide preferentially other babies but only its own babies." - Could you rephrase that? I'm having trouble understanding which infants the prairie dog mothers tend to kill.

@HarrisWeinstein Thanks for noticing the typo. Fixed!


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What is the meaning behind Kcat / Km?
I'm trying to understand enzyme kinetics, the formula for Km and Kcat make sense to me.

Km , the substrate concentration at which the reaction rate is half of Vmax
Kcat, used to describe the limiting rate of any enzyme-catalyzed reaction at saturation. Most of the time
  Kcat just equals K2 (NOT the case when there are
  more reaction steps)

I can find information about the calculation of the specificity constant (Kcat / Km) and what it means:

specificity constant,the rate constant for the conversion of E + S to E + P

However I can't find any detailed explanation WHY you should devide the Kcat by Km. Secondly Km is HALF of Vmax (so actullay at half saturation) but Kcat is at full saturation, deviding these two numbers makes no sense to me. So to summerize I'm asking : What is the "meaning" of the division of these two consants?
definitions are derived/edited from Lehninger principles of biochemistry

Just as $k_{cat}$ represents the rate of reaction at saturating substrate concentration, $k_{cat} / K_m$ represents the rate of the reaction at negligible substrate concentration.
If we take a look at the standard one substrate/one product Michaelis–Menten kinetics rate equation:
$$v = \frac{k_{cat}[E][S]}{K_m + [S]}$$
We can imagine what happens when $[S] \to 0$, we see that when $[S] \ll K_m$, the denomiator can be reduced to $K_m$, and thus the rate equation becomes
$$v = \frac{k_{cat}}{K_m}[E][S]$$
Or in other words, $k_{cat} / K_m$ is the (pseudo-)second order rate constant between the enzyme and the substrate, when $[S] \ll K_m$.
In fact, when you get into more complex rate equations (like inhibitors, pH effects, and kinetic isotope effects) there's a decent argument (one often made by W.W. Cleland) to be made that the two key constants for enzymatic reactions are $k_{cat}$ and $k_{cat} / K_m$, and it's $K_m$ that should be thought of as the "derived" constant. (The fact that we write the rate equation in terms of $k_{cat}$ and $K_m$ is a historical accident - we could have just as easily had $ v = \frac{k_{cat}\Phi [E][S]}{K_m + \Phi [S]}$, where I've arbitrarily chosen $\Phi$ as the symbol for $k_{cat}/K_m$.)
This still leaves the issue of why $k_{cat} / K_m$ is often referred to as the "specificity constant" of the enzyme. The reason for this is that if you have a single enzyme in the presence of two different substrates, you have a competitive inhibition setup. The math is a little dense (see here or here for examples), but the end result is that the ratio of reaction rates for the two substrates is related to the ratio of their respective $k_{cat} / K_m$'s:
$$\frac{v_a}{v_b} = \frac{k_{cat,A} / K_{m,A}}{k_{cat,B} / K_{m,B}}\frac{[A]}{[B]}$$
This actually makes intuitive sense, with the right mindset - the only stage where the two substrates are competing (where you make the decision to do reaction A versus reaction B) is when they're binding to free enzyme. "The rate when you only care about free enzyme" is equivalent to the negligible substrate case. With negligible substrate, all you have is free enzyme - there isn't enough substrate to have appreciable amounts of substrate-bound form, and the rate of enzyme-substrate encounter is much lower than the rate of product formation, meaning that in the steady state you don't have appreciable amounts of product-bound form, either. Thus the $k_{cat} / K_m$ for a particular substrate is representing how good the free enzyme is at performing that reaction.

Thankyou nice explanation! However there is one thing that's not quite clear for me because your example with two substrates for the SAME enzyme makes sense now (negligible [S] --> [S] <-- Km etc.) However Kcat/Km is also used to compare between different enzymes, doing that the argument about low [S] is not valid (unless they are both using the same substrate offcourse) or am I missing something? @R.M.

@RickBeeloo Do you have a particular example of the sort of comparison of $k_{cat}/K_m$ between different enzymes that you're talking about? Because you can certainly compare different enzymes via $k_{cat}/K_m$ -- just like you can compare different enzymes based on $k_{cat}$ or $K_m$. Comparing based on $k_{cat}/K_m$ gives you information about rates in the low (respective) substrate regime, just as comparing $k_{cat}$ gives information about rates in the high (respective) substrate regime. - I'm not sure if you're talking about this sort of comparison, or something else.

This ratio is more often called the "catalytic efficiency" and it's a bad measure. In many cases, enzymes are only better when they have a higher kcat, because the substrate concentration is always way above the Km. Using the ratio when this is obviously the case is just misleading imo, but this happens way too often.
In some cases it could be a useful measure to compare to enzymes. For example if you're unable to measure at higher substrate concentrations. You'd just have the initial slope of the [S] vs vmax graph. At low concentrations this slope approaches kcat/Km.
The kcat/Km ratio doesn't represent something real, it's just a lazy way to compare enzymes, combining two numbers that each represent something different into one number that's only looking good because it's one number.

"There is an upper limit to Kcat / Km, imposed by the rate at which E and S can diffuse together in an aqueous solution. This diffusion controlled limit is 10^8 to 10^9 , enzymes with a Kcat / Km near this range are said to have achieved catalytic perfection"(Lehninger) This would be a strange assumption if the value "doesn't represent something real' ? @VonBeche

I don't think that value is based directly on kcat / Km. It can be described in this way because Km = (k-1 + k2) / k1. But someone else might be able to help you more here, I'm not that at home in the maths behind this.


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Why denatured proteins can't fold back in their native form
I was wondering why a denatured protein isn't able to fold back into it's native form again.
Because a polypeptide before it's folded has a enthalphy and entropy drive to do so. What does the denaturation process do whith this favouring force to fold into the native structure.
In my opinion I can't see the differences between the unfolded protein (direct after translation) and the denaturated protein.

Some denatured proteins can refold into their native state, although at varying rates. The classic (if slightly dubious) Anfinsen experiment demonstrated that. (see e.g. http://sandwalk.blogspot.co.uk/2007/02/anfinsen-experiment-in-protein-folding.html)

In short: the unfolded state is a high-energy state of the protein, which will move towards lower-energy states. Some of these states are the folded protein, while others states are denatured protein (forming "wrong" interactions with itself or other proteins). Energy barriers between these states keep the protein in the denatured state even though the folded state might me more favorable.
Or in other words: it's trapped in the denatured state because of kinetics, even though thermodynamics would favor the folded state.
A nice figure to illustrate this: http://www.ghrnet.org/index.php/jbmbr/article/viewFile/1027/1397/6798
If you go into a little bit more detail, you will find that a lot of proteins (especially larger ones) are usually folded by chaperones. These helper proteins will bind to the emerging protein chain to prevent it from aggregating. In a sense they guide the protein to a folded state. In a similar way, chaperones can help proteins overcome the energy bariers that normally prevent it from going from an aggregated state to a folded state.
This review in Science  is very complete, but also contains some nice figures that give you an idea of what happens:
http://science.sciencemag.org/content/353/6294/aac4354.long /
If you're a pirate: http://science.sciencemag.org.sci-hub.bz/content/353/6294/aac4354.long

You have not explained how the 'energy landscape' differs between the newly synthesized protein (which folds) and the denatured protein (which may or may not fold).

Any discussion about protein folding also needs to include chaperones, without which many newly-synthesized proteins would not be able to fold (or re-fold after some sort of conformational "damage").

There would be only one energy landscape for the protein. Denatured protein in my answer is specifically aggregated denatured protein, as I assume this is what OP is talking about. A perfectly lonely heat-denatured protein would fold just as easily as a freshly synthesized one, but usually this is not the case that's discussed when talking about denatured proteins.

@MattDMo: I think most proteins fold just fine without chaperones. In bacteria chaperones are all called heat-shock proteins, so to me it seems they're only required under stress. Do you have any sources showing that these chaperones are folding a large proportion of all proteins all the time?

@VonBeche I'll find you some references in a minute. Yes, many chaperones are called HSPs because that is the context in which they were discovered, but further research has shown their indispensability in the "normal" cellular context (at least in mammalian cells, which I am most familiar with).

Might explain the difference. I work with bacteria, and I see a lot of heterologous proteins being expressed just fine without their own chaperones. I'll just believe you when you say it's much more common in mammalian cells.

@VonBeche here are some references. Some may be paywalled, I apologize if that's the case and you can't get access. If you really want to read one, just let me know and I'll get a PDF for you on Monday. http://www.ncbi.nlm.nih.gov/pubmed/18432918, http://www.ncbi.nlm.nih.gov/pubmed/27365453, https://en.wikipedia.org/wiki/Chaperone_(protein), http://www.ncbi.nlm.nih.gov/pubmed/27134861, http://www.ncbi.nlm.nih.gov/pubmed/26973652, etc.

@MattDMo: I skimmed the Science review a bit, and it looks really really good. Turns out it's mostly "it depends", and for small (bacterial) proteins chaperones are not required, but I'll add a bit to my answer.

Thanyou for the information! @MattDMo


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Correlation between morphology of neurons and neurotransmitters
Are there known significant (positive or negative) statistical correlations between the morphology type of neurons and the neurotransmitters that they use (presynaptic, i.e. transmitters that are released, and postsynaptic, i.e. transmitters that are received)?
This question assumes, that a definite set of morphology types has been defined. The answer depends on this definition, of course.

Yes, at least for the neurotransmitters that a given cell releases.
As far as the neurotransmitters a cell responds to, you are really better off thinking in terms of receptor expression. Most neurons will express receptors for many different neurotransmitters. It's far too broad to go into them all in an answer here.
As far as the transmitters that cells release, morphological types of neurons are very often associated with release of particular neurotransmitters. In the cortex, for example, pyramidal cells principally release glutamate while there are potentially dozens of morphological types (again, depending on how you define them) that release GABA; in the cerebellum, Purkinje neurons release GABA whereas granule cells release glutamate.
However, be careful: some terms like "granule cell" don't really refer to a special morphological type. They are really just describing "small cells in close proximity": these can be completely different types in different brain regions. It really makes no sense to ask these types of questions for the brain as a whole, you have to study individual brain regions, each of which is organized quite differently from the others.

Thanks a lot for this instructive answer, especially for the remark on granule cells and your last remark.


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How to interpret this statement on missing heritability
I'm currently studying a behavioral genetic course, but still, I feel that I'm lacking many basic concepts.
A particular topic I don't understand is missing heritability.
Here's an example regarding the genetics of schizophrenia, this is what is stated in my course material: "GWAS studies have identified 240 genes associated with this disorder, but these only explain less than 10% of heritability, the missing heritability for schizophrenia is around 90%".
What does it mean that 90% of heritability is missing?
I'd like to understand the math behind this concept but I don't care if this statement is actually true, I don't know where this data came from.
PS
I know how heritability is generally defined in a narrow and broad sense.

Can you please clarify what you are asking: it seems clear from what you wrote that missing = unexplained (by known genetic factors). Does that help or is there some more subtle question that I'm missing?

Still unclear. Let's say you have a $ h^2 = 0.5 $. What exactly does it mean 90% is unexplained? How do you obtain 0.45 as a value for this missing heritability?

@Mirko It means that if we knew the effects of every SNP, we could make a predictor explaining 50% of the variance. But right now, we only can explain 0.10*50% = 5% of the variance with our current predictors.

Missing heritability refers to the fact that while we make heritability estimates using e.g. midparent regression, we can't actually find gene variants whose effects we can add up to the amount of heritability we think we should find.
This is in spite of the fact that we have sufficient statistical power that we should have found such gene variants given how many people we have genotypes and phenotypes for. (Under the normal assumption that they have effects at least somewhat independent of the environment or of other genes, and that we are actually observing the relevant genetic variation.)
As an allegory, let's say we have a bucket of apples. There are 20 apples in the bucket. I know that I picked one apple, and my friend Jane picked one apple, but I don't know where the other 18 apples came from, even though I have been watching the bucket and I should have seen anyone else put apples in there.
People are getting very clever with machine learning models that try to relax various assumptions and incorporate extra data to detect weaker effects.
At an extreme, people have resorted to arguments that literally everything in the genome contributes to every trait, the so-called omnigenic model. In this case they leverage gene expression data as a covariate to add information to models, since you will probably never have enough power to find all of those individual associations/interactions. I am unsure if this has gained much traction in the years since.
Perhaps more promising (IMO, I am not sure that anyone agrees with me) is that people are starting to incorporate more different kinds of variants (not just relatively common single nucleotide variants). There is perhaps some evidence that these sometimes rarer but more dramatic variants might explain more variance.


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Alkaline Phosphatase and Ligase Protocol for Cloning

In the image the circular molecule is a restricted vector and the linear red molecule is a DNA insert.
I found this protocol in my lessons notes, but I don't understand how it is possible that ligase catalyzes a reaction between 5'-OH and 5'-P. This reaction should form as product a 5'-5' bridge between the 2 nucleotides of the insert and the vector.
Usually Ligase repairs nicks between 5'-P and 3'-OH thus creating 5'-3' bonds between nucleotides that are normal in nucleic acids, so my question is how is it possible for the DNA to be functional even though it has a 5'-5' bond?

DNA ligase catalyzes the formation of a bond between 3’-OH and 5’-PO4 of its nucleic acid substrate. (See Lehnman, 1974) The ligation bond will be formed when the proper ends are close together, allowing the ligase to act. Lets redraw your diagram and add the 5’ and 3’ designations to it. I think this may help clear out some points.

Regarding the alkaline phosphatase treatment with ligation, I think Dale and Greenaway said it so much better than I can. Quoting (Dale and Greenaway, 1985):

[The strategy] is to treat the cleaved vector DNA with alkaline phosphatase that removes the 5’-phosphate group from the DNA. Since the presence of a terminal 5’-phosphate is necessary for the action of DNA ligase, a dephosphorylated DNA strand will not be able to participate in a ligation reaction. Since this will apply to both ends of the linearized vector, the ends cannot be joined together again, i e , parental vector regeneration is impossible. This results in a very low frequency of transformation by the vector (since linear DNA transforms very poorly). However, the vector 3’-hydroxyl ends are available for joining (by DNA ligase) to the 5’-phosphate termini of any DNA fragments to be cloned. This will result in a circular recombinant molecules with a single-stranded nick at each end of the vector portion. These molecules usually transform as efficiently as the fully ligated product, and the nicks are repaired in vivo after transformation. Thus the phosphatase treatment of the vector molecules increases the proportion of hybrid DNA molecules in the population of transformed cells, and also prevents the formation of oligomeric forms of the vector.

References
Dale, J.W. and Greenaway, P.J. (1985) “The use of alkaline phosphatase to prevent vector regeneration” Methods Mol. Biol. 2:231-236. Link to paper
Lehnman, I.R. (1974) “DNA Ligase: Structure, Mechanism, and Function” Science 186:790-797. Link to paper


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In the process of oogenesis, when the egg completes meiosis 2, what actually happens?
oogenesis is the process of egg formation in females.
The process of formation of the ovum is as follows

oogonium
primary oocyte
secondary oocyte
ovum


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Colonizing Mars: Is research being done to find the most radiation-tolerant plant species?
Due to Elon Musk's stated objectives to colonize and live on Mars in his lifetime, is there research occurring to determine what plants would be the most hardy to survive in the extreme environmental conditions of the planet?
Direct surface growth appears to be impossible due to strong ultraviolet rays reaching the planet's surface due to the lack of an ozone layer, and also the direct unimpeded cosmic ray bombardment leads to surface radioactivity, due to the lack of geomagnetic field protection.
But are there any research studies being done to try to determine what plants if any would be most tolerant of partial or minimal shielding from these otherwise life-ending and mutation-forming environmental conditions?
It is well known that initially all colonization support materials are going to have to be transported to the red planet from Earth. It will be a long time before the initial colony would be capable of mining, sorting, processing, and producing anything useful from surface materials already on the planet.
If it would be possible to design a reduced-shielding Mars greenhouse roof material that is lighter and thinner than one that provides the full filtering needed to produce safe Earth-like solar irradiance for common food crops, then it would be possible to build larger and more expansive in-ground / underground greenhouses for hardy slow-growing but radiation tolerant plants, to help support slow-but-steady oxygen production for the more fragile parts of the rest of the Mars survival mission.

There is a Space Exploration SE

I was not aware of that. Should I vote to delete and then repost there, or can it be moved by a moderator?

this question have been asked over at https://space.stackexchange.com/ before and you can find some good links there.https://space.stackexchange.com/search?q=plants+on+mars

No need to flag your own post – just click on the 'Delete' button (grey text at the bottom of your question).


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What is the effect of TSH on the calcitonin?
I know that TSH is released from the pituitary gland and it motivates the thyroid gland to release thyroxine, and calcitonin is released when the calcium level is high in the blood, but is calcitonin affected by TSH or not, I didn't find a specific answer on google, could you help me please?

I found a paper, where it is postulated that TSH secretion is inhibited by calcitonin. However, the paper is quite old (1984) and I'm not sure if there are any more actual paper.


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How to interpret weighted Robinson-Foulds distance between phylogenies?
The Robinson-Foulds (RF) metric provides symmetric distance between two phylogenies as a sum of monophyletic groups present in one tree but not in the other. The normalised RF distance is given as $\frac{RF_i}{RF_{max}}$. Let's consider an example:
require(phangorn)
set.seed(123456)
tr = rtree(10, rooted = FALSE)
tr2 = rtree(10, rooted = FALSE)
RF.dist(tr, tr2)
# [1] 12
RF.dist(tr, tr2, normalize = TRUE)
# [1] 0.8571429

The last row would mean that the trees differ by 86 % of their maximum distance. But how does one interpret the RF distance if it is weighted on branch lengths?
wRF.dist(tr, tr2)
# [1] 13.20986
wRF.dist(tr, tr2, normalize = TRUE)
# [1] 0.7600115

Is it 76 % of maximum tree distance given the sum of tree lengths of the compared trees?

You could look at the help from within R (try ?wRF or ?wRF.dist). If this doesn't give you an answer, the best way to be sure would be to look at the source code of this package. There may be ways to do it from within R: https://stackoverflow.com/questions/19226816/how-can-i-view-the-source-code-for-a-function


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MHC-I presentation during infection
Which cell type cannot process and present antigen peptide in association with MHC-I when it is infected?

All nucleated cell (cells with defined nucleus) are able to present MHC-1 on their surface.  Since red blood cells do not have nucleus, they are not able to represent antigins in MHC-1 molecule.
Hope that helps check wikipedia for reference