What is the standard deviation of adult human heights for males and females?

It's probably around 7 cm for men and 6 cm for women.

The Evolution of Adult Height in Europe, which is a source for some of the statistics reported on that Wikipedia page, gives averages, standard deviations, and sample sizes for both sexes across 10 european countries (and across a number of different age cohorts).

Taking their numbers for men and women born between 1966 and 1978, the average male standard deviation of height across all ten countries is 7 cm (range 6.7-7.3) and female 6.1 (range 5.6-6.4).

For a more global context, Subramanian et al. give heights with standard deviations for a much wider selection of countries, mostly "developing countries". Unfortunately for your question, they only report numbers for women. However, these  look pretty similar to the Europe numbers: the across-country average SD for women is 6.3. (with all these countries, the range is greater at 5.4-8.1, but 32 out of the 54 countries have SDs within the Europe range for women, i.e. 5.6-6.4)

Note: for this estimate I just ran averages across years/countries, I didn't weight the averages by sample size.

 Subramanian SVS, Özaltin EE, Finlay JEJ. 2010. Height of nations: a socioeconomic analysis of cohort differences and patterns among women in 54 low- to middle-income countries. PLoS ONE 6: e18962–e18962.


It is  the skeleton of Sea Urchin or sea hedgehog.

There are a lot of species (nearly 1000), so it is very difficult to identify just in five minutes, but in general you can start from knowing the Subclass Perischoechinoidea.


human body in an environment where temperature is above body temperature

There are many ways by which a healthy human body deliberately dissipates heat. First, it is important to note bodily temperature is not uniform. Our skin is generally colder or warmer than the rest of the body, which is the reason why we place the thermometer between our armpit or inside our mouth, instead of just placing it in our say, fingernails.
Vessel dilation
Arterioles can tighten or relax, increasing or reducing blood flow. High CO2 concentrations and heat cause the arteriolar diameter to increase, allowing larger blood flow. High oxygen concentration and cold cause the opposite effect. At normal conditions, about 0.2 to 0.5 liters of blood pass through the skin. But under stress, this can rise up to 8 liters per minute. What this response entails is an increase in cardiac load.
Sweating
We have up to 4 million eccrine sweat glands. Normally, they secrete an extremely filtered version of blood plasma, which is odorless. Exercising or heat changes this. As it is mostly water, which has a specific heat of 4.2 joule per gram, its evaporation releases quite a bit of heat. So what this mechanism requires is greater hydration, or else there is risk of hyperthermia (increase in core body temperature unrelated to fever).
References
This text is a very resumed version of this article:
Physiological Responses to the Thermal Environment


The protostome/deuterostome distinction and why it is important

The terminology is really just describing the process in embryonic development that you describe: deuterostome means "second mouth"; protostome means "first mouth."

The significance of these groups is in evolutionary history and cladistics. All of the deuterostomes have a shared common ancestor that is not shared with any protostomes, and vice versa. Regardless of developmental pattern or number of openings during development, no other organism should be given these names (and if it is, and the correct ancestry is determined later, they would be moved out of those categories accordingly).

This is actually really important in biological classification of organisms, and before modern genetic techniques these types of shared characteristics were the best way to determine shared ancestry. Think a bit about what it means for an organism with two openings to differentiate one as mouth and the other as anus: once they are strongly differentiated, there is a huge barrier towards going "backward" and "switching" openings because mouth and anus have very different functions. However, if you go from having one or no openings to having two, before there is specialization, the distinction of which one develops first isn't likely to be that advantageous one way or the other.

Nephrozoa contains the deuterostomes and protostomes, consisting of almost all extant animals. However there are also other animals that are neither. For example, Xenacoelomorpha might be the closest thing to a bilateral animal with only one orifice, though they don't really have a true gut at all.


What is the difference between second and third generation sequencing

I'm assuming you mean DNA sequencing (excluding things like RNA-seq).

Is Sanger sequencing the first generation?

From Metzker 2010:

  The automated Sanger method is considered as a "first-generation" technology

Some of the technology that was in development when this review was written is no longer in development, but this is still an excellent review and a great place to start.

Is second generation sequencing the same as next generation sequencing?

Also from Metzker 2010:

  and newer methods are referred to as next-generation sequencing (NGS).

The "newer methods" in the review are:

Emulsion PCR based like Roche/454
Solid phase amplification like Illumina/Solexa
Single molecule like Helicos BioSciences and Pacific Biosciences

As of today, is there any commercial 3rd generation sequencing technology in use (or is it still in development)?

The development of single molecule methods (third item in the above list) has historically taken longer than the other two, so sometimes they are referred to as third generation. However, note how Metzker above considers them all "next-gen".

A recent paper from PacBio itself makes the distinction of halting:

  Second-generation sequencing (SGS): Sequencing of an ensemble of DNA molecules with wash-and-scan techniques.

  Third-generation sequencing (TGS): Sequencing single DNA molecules without the need to halt between read steps (whether enzymatic or otherwise).

Ultimately, I think the "generations" are more useful to make the "Sanger vs. Not Sanger" distinction. Sanger sequencing is very different than next-gen in terms of what kind of experiment you can do and what sort of data you obtain.

Past that, the number of a generation is more of a marketing term. For instance, at the bottom of the PacBio paper:

  Conflict of Interest statement. All authors are employees of Pacific Biosciences and own stock in the company.

In practice, PacBio competes with second generation platforms. It is in their interest to say their technology is on "another level" compared to what's available on the market, but in practice, this is debatable.

Anyhow, to answer your question:

There is a technology in use and commercially available which has been referred to as third gen (PacBio)
There was a technology in development that falls under most definitions of third gen (Helicos), which went bankrupt in 2012
There is a technology in development (ON MinION) that is single-molecule based and was introduced after PacBio, so if PacBio is third generations, so is MinION (although the MinION is apparently very different from PacBio)


Short answer is that higher temperature favors annealing of longer sequences. There are number of ways to calculate melting temperature, but all of them produce similar results: longer polymers require more thermal energy to melt. Hence, quick cooling from higher (say, from 95C thermocycler can cool in 10-12 sec) to RT/4C will favor re-annealing of circular strands. Slower cooling should allow more ssDNAs to bind.

But again, if end goal is to select for circular dsDNA, simple transformation should take care of that.


Why is it always Sodium that we talk of in blood pressure?

The key is in fluid compartments and osmotic activity. For the purposes of this discussion, let us say that there are two fluid compartments the ExtraCellular Fluid (ECF) and IntraCellular Fluid (ICF). Only the ECF contributes to blood volume and blood pressure.

Na is not only the major ECF ion, but it is also confined there. The ICF concentration of Na is much lower than in the ECF, and it is continuously, invariably and actively kept out of the ICF. In other words, the vast majority of ingested Na ends up in the ECF, and drag the associated amount of water (ie volume, thereby increasing blood pressure). It is the opposite for K, which is mainly in the ICF. As for Cl, it is more or less equal in the ICF and ECF, and is allowed to move freely between them, meaning that you need to ingest twice as much as a given amount of Na for a similar effect on volume distribution. Bicarb is a minor ion, and moves freely between compartments. These are the reasons why, clinically, if someone is hypovolemic (ie dehydrated, losing blood) they are given a sodium based fluid or a protein based fluid (colloid), because both will drag volume and stay in the ECF.

As for the other part of your question, isn't it tightly regulated? Yes, but extra sodium takes some time to get excreted (much less than 1% of sodium that goes through the kidneys is excreted). In other words, any extra sodium (i.e. extra volume as we have established) will stay there for some time, and if you are continually having high sodium meals, every day, you will walk around with extra sodium most of the time. Therefore, your blood pressure will be higher than it would be, if your diet was lower in sodium.

So, no, sodium is not stealing the spotlight from anyone when it comes to ECF. But the other ions have their glory under other spotlights.


Heteromaternal Superfecundation - Any known cases?

This would be termed superfetation rather than superfecundation. While this extremely rarely happens in humans, superfetation does occur naturally in some mammalian species. These pregnancies occur when the mother ovulates after she is pregnant.

Superfetation consisting of a natural pregnancy and implanted embryo has been done in cattle. In this case, 7-day embryos were successfully transferred to 14-day pregnant cows to produce superfetation. See Joel Carter's dissertation Superfetation in Beef Cattle (2002).

There have also been successful cases of superfetation in cows that were first implanted with a 7-day embryo, and then followed by natural service. See WH Hall, Bovine superfetation by natural conception secondary to an embryo transfer pregnancy, Cornell Vet. 1987 Jul;77(3):282-3.

An excellent summary of the existing literature on superfetation in many species is K Roellig et al., The concept of superfetation: a critical review on a ‘myth’ in mammalian reproduction, Biol Rev Camb Philos Soc. 2011 Feb;86(1):77-95.


What is this 5"-across spider found in my bedroom in France?

It looks like a type of Wolf spider https://en.wikipedia.org/wiki/Wolf_spider


Will a nucleic acid sequence deduced from a protein sequence be expressed from a plasmid?

I lack the knowledge to fully answer your question but I can give some potentially useful pieces of information:

In theory you can easily in-silico reverse translate a peptide
sequence to an unambiguous nucleotide sequence using the GMOs
optimized codon usage. I can share a Python script for that.

Also you could easily search for the 'real' nucleotide sequence in
databases. For example use 'Blast' to find the gene of your peptide
sequence.

But attention! There are known cases of codon-optimized sequences
causing bad protein folding or even (paradoxically) worse expression
levels than the native sequence.

There is software that helps with the design of plasmids, also in
light of use of unique restriction sights, helping to decide which of
your restriction enzymes are applicable.


What physiological processes give rise to a linear cell survival curve?

Progressive cell death along a spatial dimension would be consistent with this. For example, imagine a cylinder of tissue in which cells at one face die, inducing adjacent cells to die. This would yield linear decay in viability to 0.


At what temperature do human bones disintegrate?

Boiling point of hydroxyapatite is around 1500°C so you will need this temperature to make bone literally evaporate.
Prolonged exposure to lower temperature (like reference in other answer 220°C) will break collagen and make bones weak and extremely fragile.


The terms intron and exon were coined by Walter Gilbert in a renowned 'News and Views' article, Why Genes in Pieces, published in the journal Nature in 1978.

Introns are the intragenic regions and exons are the regions which are expressed.

This is the relevant passage in full:

  The notion of the cistron, the genetic unit of function that one thought corresponded to a polypeptide chain, now must be replaced by that of a transcription unit containing regions which will be lost from the mature messenger - which I suggest we call introns (for intragenic regions) - alternating with regions which will be expressed - exons. The gene is a mosaic: expressed sequences held in a matrix of silent DNA, an intronic matrix.


Probability of all alleles represented in a sample

I'm going to strictly answer the questions, rather than step through the proof, because it involves a lot of formatting that I'm not familiar with.  Other folks are welcome to edit this!
Equation 13
This equation assumes a diploid genotype, given by the $2n$ power with $n$ individuals.  For anything with greater ploidy than mono-, it's mathematically simpler to determine the probability that an allele is not present.  As an example, see this calculation of a triploid Hardy-Weinburg equilibrium equation.  Using this simplification,
$P(single$ $allele$ $not$ $present)$ $= (1$ $- P(allele$ $present))$ ^ $(ploidy)$ ^ $(n)$
$= (1$ $- P(allele$ $present))$ ^ $(ploidy$ * $n)$
With $k$ segregating alleles, each allele has its own non-presence probability.  The probability of total non-presence is $1 - (sum$ $of$ $P(each$ $non$-$presence))$
Equation 16
In this equation, the author describes the probability that all alleles are present at a given frequency.  These allele presences are independent of each other and therefore multiplicative.  Since $P(allele$ $present)$ is vectorized, this product can be simplified to $^r$


Does a critical mass of infected individuals exist after which mutations will overtake vaccination attempts?

Epidemiological modeling
If a virus is able to change so that it renders previous vaccination inefficient, reinfecting those who were previously vaccinated, one could describe this process using epidemiological SIS model (Susceptible-Infected-Susceptible) or its modification that includes a vaccinated group (like SISV model), and indeed estimate how quick should be vaccination in order to eradicate dthe virus before everyone gets infected. One could even add a D (deaths) compartement and study whether the virus may lead to extinction of the huiman species (unlikely, since the survival rate is very high).
Real viruses
In reality we are not dealing with such a situation, since there is no reason to think that mutations make SARS-CoV-2 able to overcome the immune defenses (although they do make it more contagious and more dangerous to non-vaccinated individuals).
To clarify the issue let me outline the scenarios where viruses do escape vaccine resistance.
Influenza
Flu is known to be susceptible to vaccination, and this is a lasting vaccination. What makes this virus to come back every year is gene reshuffling, where it exchanges some of its several genes with similar viruses living in animals (the roles of some of these animals in flu outbreaks gave rise to such names as swine flu, * birs flu*, etc.). This means that every few years we are dealing with an essentially new virus (rather than a virus that has accumulated many mutations), which is not visible to the antibodies created by previously administered vaccines. In this sense, one cannot exclude a possibility of a new coronavirus causing a pandemic in a decade or so, just like the current outbreak follows similar ones due to SARS in 2002 and MERS in 2012.
HIV
HIV is know to adapt very quickly to the new antibodies, evading the immune defenses. This makes it impossible (or at least very difficult) to develop a vaccine against this virus. However, HIV is much less contagious than flu or coronavirus, since it needs to infect specific cells/tissues. In orther words, it is stopped by the barriers of the immune system other than those boosted by vaccination. Coronavirus is a much simpler virus than HIV and will never reach the same degree of sophistication via mutations.
Bacterial pathogens
Bacteria are known for routinely developing resistance to antibiotics, which has been somewhat of a hot issue in terms of antibiotic development. They however share the same weakness as HIV - being less contagious (and far more complex).
To summarize, the devil is in the details: the scenario outlined in the question is good for science fiction, but it has very low probability to be realized in real life.


Yes, the bark scorpion can still sting after death. I learned this myself after stepping on one. As I make a nightly habit of patrolling inside my home for their presence, I can conclude the offender had died within 12 hours of my stepping on it. When they die their tails stretch straight behind their bodies, this was the position I found it in.


If human eyes watch an area, what's the shape of its capturing shape? Rectangular? Half spherical?

The capture area of the eye is a bit fuzzier and harder to define than that of a camera.

A camera captures consistent, fully detailed data right up to the edge of its sensor, and no data at all beyond it. Captured data is clipped by an ideally uniform sensor, augmented a bit by the lens, and is well-defined during design and manufacturing.

The eye can capture higher "resolution" near the center of its capture area and also has very little information about color near the edges (see also Peripheral Vision); so it's not quite as clean cut depending on your goal of "capture area". The eye also has a bit of a "blind spot" near the middle, which our brains basically Photoshop out. Additionally, it varies from person to person.

The effective capture area would really depend on your application (e.g. the "capture area" for, say, reading text, would be narrower than the area for, say, detecting motion).

Here is a typical diagram for a single eye, showing just the ability to see something in that area (does not show details related to peripheral vision quality):

Here is a typical diagram for both eyes combined, the solid white area is the overlap:

Both of those images are from a 1964 NASA report detailing aspects of the human visual field. If you want the detailed answer to your question and more, you probably want to take a look at that.

Note that our field of vision is very wide, those diagrams may not do it justice. As an experiment, close one eye, stare straight ahead and hold your arms straight out to the sides. Wiggle your fingers and slowly bring your arms forward until you can just see your wiggling fingers in your peripheral vision, and you will get an idea. As an added experiment, hold a piece of paper with text on it, and repeat the same experiment until you can read the text - this region will be extremely narrow and will give you an idea of how the quality of vision changes across the field. Also try with a colored object and bring it in until you can clearly identify the color.

There are also some simplified mentions of it in wikipedia:

http://en.wikipedia.org/wiki/Field_of_view#Humans_and_animals
http://en.wikipedia.org/wiki/Human_eye#Field_of_view
http://en.wikipedia.org/wiki/Visual_field#Normal_limits

A good set of search keywords is "human field of vision". There is also a nice related article entitled The Camera Versus the Human Eye.


What exactly are computers used for in DNA sequencing?

Computers are used in several steps of sequencing, from the raw data to finished sequence:
Image processing
Modern sequencers usually use fluorescent labelling of DNA fragments in solution. The fluorescence encodes the different nucleobase (= “base”) types (generally called A, C, G and T). To achieve high throughput, millions of sequencing reactions are performed in parallel in microscopic quantities on a glass chip, and for each micro-reaction, the label needs to be recorded at each step in the reaction.
This means: the sequencer takes progressive digital photographs of the chip containing the sequencing reagent. These photos have differently coloured pixels which need to be told apart and assigned a specific colour value.

As can be seen, this (strongly magnified; the image is < 100 µm across!) image fragment is fuzzy and many of the dots overlap. This makes it hard to determine which colour to assign to which pixel (though more recent versions of the sequencing machine have improved focussing systems, and the image is consequently crisper).
Base calling
One such image is registered for each step of the sequencing process, yielding one image for each base of the fragments. For a fragment of length 75, that’d be 75 images.
Once you have analysed the images, you get colour spectra for each pixel across the images. The spectra for each pixel correspond to one sequence fragment (often called a “read”) and are considered separately. So for each fragment you get such a spectrum:

(This image is generated by an alternative sequencing process called Sanger sequencing but the principle is the same.)
Now you need to decide which base to assign for each position based on the signal (“base calling”). For most positions this is fairly easy but sometimes the signal overlaps or decays significantly. This has to be considered when deciding the base calling quality (i.e. which confidence you assign to your decision for a given base).
Doing this for each read yields up to billions of reads, each representing a short fragment of the original DNA that you sequenced.
Most bioinformatics analysis starts here; that is, the machines emit files containing the short sequence fragments. Now we need to make a sequence from them.
Read mapping and assembly
The key point that allows retrieving the original sequence from these small fragments is the fact that these fragments are (non-uniformly) randomly distributed over the genome, and they are overlapping.
The next step depends on whether you have a similar, already sequenced genome at hand. Often, this is the case. For instance, there is a high-quality “reference sequence” of the human genome and since all the genomic sequences of all humans are ~99.9% identical (depending on how you count), you can simply look where your reads align to the reference.
Read mapping
This is done to search for single changes between the reference and your currently studied genome, for example to detect mutations that lead to diseases.
So all you have to do is to map the reads back to their original location in the reference genome (in blue) and look for differences (such as base pair differences, insertions, deletions, inversions …).

Two points make this hard:

You have got billions (!) of reads, and the reference genome is often several gigabytes large. Even with the fastest thinkable implementation of string search, this would take prohibitively long.

The strings don’t match precisely. First of all, there are of course differences between the genomes – otherwise, you wouldn’t sequence the data at all, you’d already have it! Most of these differences are single base pair differences – SNPs (= single nucleotide polymorphisms) – but there are also larger variations that are much harder to deal with (and they are often ignored in this step).
Furthermore, the sequencing machines aren’t perfect. A lot of things influence the quality, first and foremost the quality of the sample preparation, and minute differences in the chemistry. All this leads to errors in the reads.

In summary, you need to find the position of billions of small strings in a larger string which is several gigabytes in size. All this data doesn’t even fit into a normal computer’s memory. And you need to account for mismatches between the reads and the genome.
Unfortunately, this still doesn’t yield the complete genome. The main reason is that some regions of the genome are highly repetitive and badly conserved, so that it’s impossible to map reads uniquely to such regions.
As a consequence, you instead end up with distinct, contiguous blocks (“contigs”) of mapped reads. Each contig is a sequence fragment, like reads, but much larger (and hopefully with less errors).
Assembly
Sometimes you want to sequence a new organism so you don’t have a reference sequence to map to. Instead, you need to do a de novo assembly. An assembly can also be used to piece contigs from a mapped reads together (but different algorithms are used).
Again we use the property of the reads that they overlap. If you find two fragments which look like this:
ACGTCGATCGCTAGCCGCATCAGCAAACAACACGCTACAGCCT
ATCCCCAAACAACACGCTACAGCCTGGCGGGGCATAGCACTGG

You can be quite certain that they overlap like this in the genome:
ACGTCGATCGCTAGCCGCATCAGCAAACAACACGCTACAGCCT
                  ATCCCCATTCAACACGCTA-AGCTTGGCGGGGCATACGCACTG

(Notice again that this isn’t a perfect match.)
So now, instead of searching for all the reads in a reference sequencing, you search for head-to-tail correspondences between reads in your collection of billions of reads.
If you compare the mapping of a read to searching a needle in a haystack (an often used analogy), then assembling reads is akin to comparing all the straws in the haystack to each other straw, and putting them in order of similarity.


What is the length of tunnels puffins dig in the Farne Islands?

If that's the current number of tunnels at any one time, it can be right, it depends if they dig a new nest every year.

Farne islands has mostly horned puffins with rainbow beaks as opposed to tufted puffins which have an different beak, the former makes nest around 1 meter and the latter up to 2.75 meters,

Puffins lay one egg per year, there are 30-50,000 pairs of them on Farne islands, that's about 40km of new tunnels every year.

Every five years the trust carries out a larger audit, the last being in 2013, when puffin numbers on the islands were strong, at just under 40,000 pairs.

That was an increase on the 2008 figure when a stormy summer hit numbers hard from a high of more than 50,000 down to 36,000 breeding pairs.


Here are some figures from Cellular and Molecular Immunology, 8th Edition:

Hopefully they're helpful in some way.


Why does cell waste energy in meiosis, between meiosis 1&2

There is a phase between meiosis 1 and meiosis 2 called Interkinesis.
During this phase centrosomes or centriole pairs undergo replication in animal cells, which is important for bringing true haploidy.

Refer - meiosis-ii


What causes a selective shift of colour perception after removing wavelength filtered glasses?

The short answer is you don't see light you see a reconstruction of your environment made by a learning organ, your brain adapts to changes in stimuli. Color in particular is tricky because there is no objective way for your brain to determine somethings color, it can only see the wavelength that reaches the eye which are affected by everything along the way including the color of your eye's tissues.  Your brain adjusts to the filter, until it sees the colors it expects to see again. It does this by becoming less responsive to some signals, in the case of the glasses the colors in between certain ranges. when the glasses are removed the brain is still largely ignoring those signals and has to learn to accept them again in exactly the same way it learned to ignore them.

You can do something similar with glasses that flip the visual field, (turn everything upside down). The work was done by This is a good article. Follow the link for more information. George M. Stratton, and after wearing the glasses eventually you start seeing things right side up again, then when you remove the glasses everything is upside down again, the brain has to again relearn to see right side up.


What reasons allow for women to outlive men?

In a study on longevity in 121 countries, women tended to outlive men by about 5 years [1]. The suggested causes for this are numerous, some of which are temporally, geographically, or culturally specific.

On the terminology, sex tends to refer to the absolute biological differences, whereas gender relates more to differences in perception/lifestyle (for instance, socio-economic differences).

Evidence

In a study on Greek centenarians the authors found that women outnumbered men (1.68:1), with men having a higher likelihood of smoking, and thus are more at risk of smoking-related illness and mortality (historically this was more true than today) [2]. This is also true for alcohol consumption. The authors also report that having a first degree relative who was also a centenarian is associated with longevity (highlighting the importance of genetic factors in lifespan determination).

There is also evidence that the rate of telomere shortening (number of cell-divisions until cell-cycle arrest) is sex-specific [3].

rwst cites an interesting paper, that presents evidence that suggests male hormones may decrease lifespan [4]. This may be due to differential onset of atherosclerosis and cardiovascular disease, caused by exposure to different sex hormones [5].

In a review on the brain/behaviour specific aspects of differential ageing between the sexes, the authors discuss differences in brain anatomy and cognitive (and emotional) functionality between the sexes [6].

Remarks

This is by no means an exhaustive list of the reasons for differences in lifespan between the sexes in humans. There are likely to be many other causes, such as men tending to have more 'risky' behaviours, and possibly other unknown genetic effects, such as having 2 X chromosomes, vs. XY.

References

Møller, A. P., et al (2009). Why men have shorter lives than women: effects of resource availability, infectious disease, and senescence. American journal of human biology : the official journal of the Human Biology Council, 21(3), 357-64. doi:10.1002/ajhb.20879
Tigani, X., et al (2011). Gender differences in Greek centenarians. A cross-sectional nation-wide study, examining multiple socio-demographic and personality factors and health locus of control. BMC geriatrics, 11, 87. doi:10.1186/1471-2318-11-87
Barrett, E. L. B., & Richardson, D. S. (2011). Sex differences in telomeres and lifespan. Aging cell, 10(6), 913-21. doi:10.1111/j.1474-9726.2011.00741.x
Min, K.-J., et al (2012). The lifespan of Korean eunuchs. Current Biology, *22(18), R792-R793. doi:10.1016/j.cub.2012.06.036
Pérez-López, F. R., et al (2010). Gender differences in cardiovascular disease: hormonal and biochemical influences. Reproductive sciences (Thousand Oaks, Calif.), 17(6), 511-31. doi:10.1177/1933719110367829
Kryspin-Exner, I., et al (2011). Geropsychology: the gender gap in human aging--a mini-review. Gerontology, 57(6), 539-48. doi:10.1159/000323154

Update

Just been reading this interesting paper by Maklakov, et al (2013, BioEssays) titled "Evolution of sex differences in lifespan and aging: Causes and constraints", which presents a more evolutionary/genetic argument for the differences.

Abstract

Why do the two sexes have different lifespans and rates of aging? Two hypotheses based on asymmetric inheritance of sex chromosomes (“unguarded X”) or mitochondrial genomes (“mother's curse”) explain sex differences in lifespan as sex-specific maladaptation leading to increased mortality in the shorter-lived sex. While asymmetric inheritance hypotheses equate long life with high fitness, considerable empirical evidence suggests that sexes resolve the fundamental tradeoff between reproduction and survival differently resulting in sex-specific optima for lifespan. However, selection for sex-specific values in life-history traits is constrained by intersexual genetic correlations resulting in intra-locus sexual conflict over optimal lifespan. The available data suggest that the evolution of sexual dimorphism only partially resolves these conflicts. Sexual conflict over optimal trait values, which has been demonstrated in model organisms and in humans, is likely to play a key role in shaping the evolution of lifespan, as well as in maintaining genetic variation for sex-specific diseases.


I think you mean mitochondria and chloroplasts and are referring to the endosymbiont theory (Reference to the unedited question as it was originally asked).

The definition of symbiosis for the most part tells you how coevolution can be accounted for by this theory.

The larger Eukaryotes provided the protomitochondria with a protected environment for growth and the protomitochondria produced usable nutrients for their hosts from molecules that the eukaryotes were unable to process on their own.

The two organisms struck up a balance and the mutually beneficial relationship allowed both to prosper. As the Eukaryotes with protomitochondria were better able to utilize more of the chemicals from their environment than those that did not play host to the protomitochondria, they had a survival advantage that other early Eukaryotes did not.

As plant cells have both mitochondria and chloroplasts, it is believed that one of the eukaryotes with a mitochondria endocytosed a photosynthetic prokaryote. This event wasn't as much of an advantage as the first symbiotic relationship. Since all eukaryotes have mitochondria or evidence of ancestors that had mitochondria, but not all have chloroplasts, then it was beneficial enough that the photosynthetic organisms were also able to coevolve within the eukaryotes and alongside the mitochondria, but they were not beneficial enough so as to give those cells that hosted chloroplasts enough of an advantage that they took over all life on Earth.

Mitochondria also have their own DNA, so their complete genome is not found in the eukaryotic genome. Over evolutionary time, mitochondria have lost the genes that allowed them to live freely, so you could not extract them from eukaryotic cells today and expect them to grow external to the eukaryotic cell. They require substances that the eukaryotic cell makes. Whether there was recombination between the two genomes or just that both had the same function at one point and then through genetic drift caused the mitochondria to lose the homologous gene, I could not say.


Are any arthropods poisonous to the touch?

The blister beetle genus Meloe, also known as oil beetles, secrete an oily substance containing a poison called cantharadin which causes blistering and swelling of the skin.

Source: http://statebystategardening.com/state.php/articles/do_not_touch_these_backyard_bugs


Why does getting soap in your eyes cause redness and irritation?

This is because of the soaps chemical nature. They are alkaline agents and human eyes have a very low tolerance for alkalinity. Human eyes are roughly neutral with a pH of around 7, and soaps are around 7.5 to 9.

The eye can't handle the alkaline object as it is potentially harmful to the eye so it will start watering to get rid of the alien substance. Blood vessels then enlarge, coming closer to the surface of the eye, making them appear red.

Most soaps are tested before released to make sure if they come into contact with eyes they are non-toxic. Baby soaps have a lower pH as well to make sure that the baby doesn't come to harm.

Either way, its probably best not to put it in your eyes.

See here for more information.


Does cooking ginger reduce its anti-nausea effect?

Good news! Some Australians have published on the stability of aqueous gingerol at elevated temperatures: http://onlinelibrary.wiley.com/doi/10.1002/jps.1116/full

Gingerol turns out to be stable enough to make a cup of tea with at neutral pH. They also note that gingerol and its primary decomposition product form a 50-50 mixture that doesn't degrade further over shortish time periods, and that the decomposition product is probably restored to gingerol in the stomach's acidic pH -- so you're good to make your tea, and probably to hold on to it for at least a few days.


Is egg white lysozyme different from bacterial lysozyme?

PubMed query: "lysozyme"[Title] returns 8673 papers (many of which contain useful data about the activities of bacterial- and chicken-type lysozyme/muramidase against Gram-positive and Gram-negative bacteria).

For example, Gajda & Bugla-Płoskońska (2014, Postepy Hig Med Dosw 21, 1501-1515) write:

  Lysozyme (LZ, muramidase, N-acetylmuramylhydrolase) is a protein occuring in animals, plants, bacteria and viruses.

  Lysozyme hydrolyzes the β-1,4 glycosidic bonds between N-acetylmuramic acid (NAM) and N-acetylglucosamine (NAG) of cell
  wall peptidoglycan (PG) in Gram-positive and Gram-negative
  bacteria.

  In the animal kingdom, three muramidase types have been
  identified: the c-type (chicken type), the g-type (goose-type) and the
  i-type (invertebrates).

  Muramidase shows bactericidal activity mainly against Gram-positive bacteria. Cytolytic activity against cells of Gram-negative bacteria
  has not been proved.

Lysozyme hydrolyzes bacterial cell walls, which is why its muramidase activity is more effective against Gram-positive than Gram-negative bacteria, for the former have thicker cell walls. Whether or not there is any difference in the effectiveness between the bacterial- and chicken-type lysozyme can be found in the papers; i have not read them.

But one of the 8673 papers is titled Hen egg white lysozyme permeabilizes Escherichia coli outer and inner membranes (Derde et al., 2013, J Agric Food Chem. 16: 9922-9929).

The quick-and-dirty answer to the question, is it true that bacterial lysozyme affects Gram-negative bacteria but hen-egg (chicken-type) lysozyme only affects Gram-positive bacteria? is: No.

The 'slow-and-clean' answer can be found in those 8673 papers.


When in Ampicillin degraded (gone) in liquid TB-media? Concerns about selectivity

rather interesting question. Selection pressure is very important for any type of work. And it is true, amplicilin will degrade in media due to the secretion of beta-lactumase. This is a limitation that we must face, though there are ways of getting around this.

For example, when cloning, on a plate sometime you will notice "smaller" colonies growing around a central large one. This is due to beta-lactumases. They are not a problem if you are going to take the central colony and place it into fresh media with new amplicilin. They will simply die out. No harm done.

In liquid culture it is good to not "oversaturate the culture". Usually, do not let it get over OD600 = 1. In addition, do not use old stocks, as this causes problems with selection and use higher concentrations of ampicillin if you are still having troubles selecting!

Generally speaking, 100ug/ml is standard for most selection with cloning, and should be sufficient for what you are doing. It seems that your protocol should work fine for protein isolation.

Last remarks -- it is a problem that most microbiologist do not think of. Ampicillin has its limits!

https://www.addgene.org/mol-bio-reference/antibiotics/

https://bitesizebio.com/10188/whats-the-problem-with-ampicillin-selection/


I'm not sure if they will be useful for your application, but you should look into software used to visualize ecological networks (and maybe also software used for drawing electrical charts). The type of data used there is very similar to what you want to plot, with nodes and links along with metadata for links on e.g. rates or connection strenghts.

I can point you to mangal by ecologist Tim Poisot (blogpost on mangal here), SBGN (Systems Biology Graphical Notation), and there is also the R-package diagram. However, I haven't used them much so I cannot say how useful they will be.


First question:

B. The net gain of ATP in Photosynthesis is 0, so it cannot be A. C & D are obviously not true.

Second question:
B. D is not true, C is not true (it is actually the opposite- Chloroplasts absorb all BUT green, so only green would be bad). Like another commentator said, the level of CO2 only aids the rate to a point, at which the rise is not great.
http://www.rsc.org/learn-chemistry/content/filerepository/CMP/00/001/068/Rate%20of%20photosynthesis%20limiting%20factors.pdf


How does the value of K determine number of local optima in NK model?

Let's take the opposite extreme, $K=0$, so that each site has an independent effect on fitness. Without loss of generality, we can say that at each locus $n$, the $1$ allele confers an advantage $s_n$ over the $0$ allele. Then there is just one local optimum, the global optimum, at $\vec{1}$, so $M_1=1$ (and $P_m=2^{-N}$).

The key difference is that in the $K=0$ case each fitness comparison of a focal genotype with a neighbor is independent of the rest: the fact that mutating the first gene decreases fitness, for instance, doesn't make it any more likely that mutating the second gene will decrease fitness. For any $K$, it is necessarily true that the focal genotype has a probability $1/(N+1)$ of being fitter than all of a set of $N$ other randomly chosen genotypes, but we're interested in comparing it to its neighbors, which are not a random selection, and are only equivalent to a random selection when $K=N-1$.


Difference between autonomic and paratonic movements in plants

its about the gene that is involved in autonomic movements. while, there is no gene involved in plants for paratonic movements.furthermore, autonomic movements are presents in plants by birth, and paratonic movements are induced in plants by an external stimuli only and not present in plants by birth.


When does the first "random mutation" of DNA (have to) occur?

Random mutations happen everywhere in the body all the time. Most are harmless, some cause problems, some cause cancer. Some are beneficial. If a beneficial mutation occurs in the germ cell line, it will be passed on to the offspring. Depending on how beneficial it is, it can spread like wildfire (the mutation allowing lactase to continue to be expressed after infancy is a good example of this, as is sickle cell trait); if it is harmful, the carrier may die before birth, in infancy, etc. If it causes a later onset disease (e.g. early Parkinson's)1, the carrier has time to mate, reproduce and pass the disease on to their offspring. More and more diseases are being found to be genetic in nature now that genetic studies are so much easier to perform.

Again, for a mutation to be passed on, it must occur anywhere in the germ cell line of a parent, right up to the last stage before being released as an ova or a sperm cell, during fertilization, or during the very early stages of embryonic development in cells genetically programmed to become germ cells. If it occurs after fertilization, it will not affect that person, but its offspring. Depending on how early the mutation occurs, it may affect other parts of the reproductive system as well.

If a mutation happens in an embryo in a non-germ cell line, it may affect that person mildly, profoundly, not at all, or the embryo may die if it is a deleterious mutation in a critical organ system, say the heart.

But you need not put random mutations in scare quotes. I'm pretty sure you don't trust me, but they happen all the time, in every tissue, in you yourself as well as in everyone you know and everyone you don't know. And, by the grace of God, many of them can be repaired, and we don't ever have any ill effects from them. Alas, not all are repaired, and some lead to cancer.

Hereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1


Ethidium bromide and mutagenesis on cloning

Purified DNA contains negligible amounts of ethidium bromide. PCR and gel clean-up kits remove it quite well. There is, though, a risk of mutation from the fact that you're visualizing the gel in UV light with ethidium bromide. The risk of mutation from UV is minimized by exposing the gel as little as possible, and by using "preparative" transilluminators that come with a low-light setting for cloning purposes. If you work well and quickly, the chance of mutagenesis isn't higher than the chance of a polymerase incorporating the wrong nucleotide.


Do all microRNA isoforms need to be known and sequenced to obtain microRNA expression?

I had worked on a similar problem and I am telling my experience.

First, you have to consider the fact that a mature miRNA can arise from multiple genomic locations i.e. many pre-miRNAs can give rise to same mature miRNA.

As you said there are products of pre-miRNA cleavage with heterogeneity at their ends i.e. there are sequences that do not exactly match the annotated mature region. While products with 3' heterogeneity can be called isoforms, products with 5' heterogeneity are likely to have different targets as the seed sequence is disrupted and hence they are technically different miRNAs (by definition).

Now, the best technique to analyse isoforms is small RNA sequencing (NGS). qPCR would not be a good technique as primers cannot always differentiate highly similar sequences (worsened by the fact that miRNAs are too small). A NGS library is a set of DNA sequences that you obtain from shearing the RNA/DNA followed by adapter ligation (reverse transcription for RNA). Since the adapter sequence is known, the sequencing reaction does not require you to know the sequence of the products. However, you would need to know the reference genome for finding novel miRNAs. This is primarily due to the fact that it is very difficult to sequence pre-miRNAs (low abundance and hairpin structure). You can identify new small RNAs very easily but cannot say that they are miRNAs unless you can map them to a stem-loop precursor (pre-miRNA).

You can very well discover new reads and people have discovered a lot of new miRNAs using NGS. I can tell you the methodology I followed to find atypical products of the same pre-miRNA. I for simplicity I call the 5' heterogeneous products as badseeds (because they have disrupted seed sequence) and 3' heterogeneous products as isomiRs. I used a methodology that is similar to that of a well known program – miRdeep.

Get the pre-miRNA sequences from miRbase
Get mature miRNA sequences from miRbase
Use bowtie-1 to build an index from the pre-miRNA sequences
Remove adapter from your fastq reads and remove low quality reads. There are many tools to do that. You can try Trimmomatic.
Map mature miRNA sequences to pre-miRNA index using bowtie to find the exact location of mature miRNA in pre-miRNA
Map reads to pre-miRNA region. Filter reads that do not map in a pre-defined window around mature region.
Classify the reads as badseed or isomiR

Now, isomiRs and reads that perfectly map to mature miRNA region can be considered as contributors to total miRNA expression. However, badseeds should not be considered as an isoform. You can likewise allow a certain level of mismatch and count these reads. Sequences with mismatch in seed region would again be badseeds. You can additionally have scoring schemes for your reads.

There are not many studies on such analysis. I did not get any publishable result with our data but the methodology is reasonably correct. You can go ahead an apply it for your study.


Blood circulation - How to expand blood capillaries?

Capillaries are the smallest blood vessels. They are unique in that:

They don't have any muscular component like arterioles or venules do.
They are lined by a single layer of endothelium  (cells lining blood vessels are called endothelial cells) overlying the basement membrane.

Due to these reasons the capillaries are very permeable facilitating nutrient and gas exchange.

The capillaries don't expand as they do not have muscular or elastic components. However exposure to heat do increase the circulation. This is due to the following facts:

Exposure to heat dilates the pre-capillary arterioles - this would inevitably cause improved capillary circulation in capillaries that are already open.
Increase in pre-capillary flow opens up collapsed capillaries. In the human body roughly only one-fourth of the capillaries are open during rest1. As the pre-capillary arterioles dilate, the collapsed capillaries open up thus further improving circulation.

To improve capillary perfusion:

Temporary improvement can be achieved by activity (exercise), exposure to warmth, emotions (flushing is due to vasodilation), even exposure to cold causes vasodilation after the initial vasoconstriction
Permanent improvement of capillary circulation can be achieved by increasing capillary density. Capillary density refers to the number of capillaries present in 1 cm2 area. Capillary density can be increased by consistent anaerobic (isometric and to some extent isotonic) exercise.

References:

1: Boron and Boupaep text book of medical physiology, 2nd Edition, p.467

For more:

http://corporate.dukemedicine.org/news_and_publications/news_office/news/6597
http://www.ncbi.nlm.nih.gov/pubmed/8852622


What is holding the immune system back to not attack human body cells?

The immune system of human body can keep human health from disease, but for many people, the immune system is the cause of disease. When the autoimmune system is in disorder, healthy cells and tissues will be killed as viruses, which will lead to a variety of immune system diseases.

Recently, scientists in the United States have discovered the genome that causes the disorder of the human immune system, which is equivalent to the "middle manager" of the immune system. This discovery is likely to bring new hope to the treatment of human immune system diseases, which has been published in the latest issue of nature.

Self defense system out of control immune cells "killing each other"

In the human immune system, a kind of immune cell named T cell is responsible for directly contacting and resisting the invading pathogen. Whether these cells can function normally is controlled by "regulatory T cells". Simply put, "regulatory T cells" are like a "double-edged sword", which can not only prevent T cells from attacking human body's own healthy cells indiscriminately, but when its regulation fails, it will cause immune cells to "kill each other" to normal cells, and its consequences usually include inducing type I diabetes, multiple sclerosis, lupus erythematosus and other immune system diseases.

Scientists have previously found that whether "regulatory T cells" can work normally is related to a major regulatory gene called Foxp3. If Foxp3 is dysfunctional, the human body will lack the active "regulatory T cells". But scientists don't know how Foxp3 controls "regulatory T cells.".

Richard young, a biologist at Whitehead Biomedical Research Institute of Massachusetts Institute of technology and Alexander Marson, a doctor of medicine, and other researchers recently discovered 30 genes directly regulated by Foxp3. It is by combining with these specific genes and regulating their activities that Foxp3 can complete the control of "regulatory T cells". If Foxp3 is the "boss" of the immune system, the 30 genes found in this study belong to the "middle manager".

Immune system diseases are related to the damage of "regulating T cells"

Researchers point out that ten years ago, it was found that the "regulatory T cells" in the human body are responsible for directing the immune system to resist foreign invasion, and the question is why the immune system that should protect health attacks its own cells. Now it has been found that there are gene defects in "regulating T cells" in the body with autoimmune disorder.

When "regulating T cells" cannot guarantee the normal operation of the immune system, the immune system begins to attack cells that should not be attacked. When the "regulatory T cells" were destroyed, several organs of mice developed serious immune system diseases. In some common human immune system diseases, such as multiple sclerosis, there is not no such "regulatory T cells", but there will be some dysfunction. In other words, "regulating T cells" failed to play its due role.

What is the problem of "regulating T cells"? "Studies have shown that when the immune system is disrupted, the activity of these genes is lower than normal. It is this reason that makes the activity of "regulatory T cells" decline, leading to its failure to work properly. Three years ago, scientists have found the main gene controlling "regulatory T cells", which is called Foxp3.

The researchers used DNA biochip technology to scan the complete genome of T cells and map the genes regulated by Foxp3. In the process, the researchers identified 702 Foxp3 binding sites. Until the discovery, the researchers admitted, they had no idea how Foxp3, the main regulator, dictated "regulating T cells.".

Anti rejection treatment for organ transplantation

The latest research shows that the "middle managers" of these 30 immune systems are not working properly. Because "regulatory T cells" are controlled by these specific genes, it can be said that most of the immune system diseases such as type I diabetes, lupus erythematosus, multiple sclerosis, rheumatoid arthritis and so on are determined by these genes.

The next step, the researchers say, is to determine how the 30 specific genes "dictate.". It has been found that these genes are closely related to each other and usually work together to control T cells, but the specific mechanism is still unknown. On the other hand, we should look for chemicals that can simulate the regulation function of Foxp3, the main regulator gene, in order to achieve effective therapeutic immunity.

In addition to the treatment of autoimmune diseases, this finding can also be used for anti rejection treatment in organ transplantation. When performing organ transplantation, once the patient's body rejects the transplanted organ, the operation will fail. Therefore, doctors usually use anti rejection drugs to temporarily inhibit or shut down the immune system.

At present, cyclosporine is mainly used to inhibit the immune system. It can inhibit a protein called activated T-cell nuclear factor (NFAT), which can also be controlled by Foxp3. If necessary, the researchers said, the 30 genes can also be used to "target the target", and the effect of inhibiting the immune system is more obvious.


To have TBE vaccine during allergic times with mild asthmatic symptoms?

Interesting question!

The Tick Borne encephalitis vaccine is an inactivated vaccine. It is therefore impossible to get the infection from the vaccine. Reports of fever have been noted but that is due to the body mounting an immune response not due to infection. There are therefore no reports of encephalitis or other markers of infection following the vaccine.

Not only may you have the TBE vaccine if you are asthmatic, but if you are at risk due to your lifestyle and location then, particularly if you have chronic asthma, the TBE vaccine might be a good idea.

Asthma is usually treated by inhalers and montelukast is reserved for uncontrolled/severe asthma. However in the rarer case of aspirin induced asthma, it is much more first line and used for mild asthma. Montelukast is not considered a mild medication.

I hope this answers your question :) if not, comment below!


What happen if we inject restriction enzyme into the blood

The appearance of any foreign antigens (e.g., proteins like restriction enzymes fall n this category) in the circulatory system should trigger an immune response.

There are actually two membrane barriers that the enzymes have to traverse to gain access to the nuclear genome: the cell membrane, and the nuclear membrane.  Proteins are typically too large and too charged to cross a lipid bilayer membrane--unless there is a pore (like on the nuclear membrane) or receptor for the protein on the cell surface.

When cells are engineered to express foreign restriction enzymes using transgenes, then yes, if the protein can enter the nucleus then the enzyme will start to digest all of its recognition sites.

Jasper Rine demonstrated this for the Baker's Yeast S. cerevisiae in 1986.


How to protect my mounted insect specimens from ... insects?

I ran into the same issue when collecting bees in a hot, humid environment.  As arboviralstated, freezing is a great way to help with the infection but keep in mind:

It may not kill all of your pests
It will not keep your specimen from future pests
It may damage your samples

From the USDA website, you could pretty cheaply use paradichlorobenzene or naphthalene:

  Two of the most widely used fumigants are paradichlorobenzene (PDB)
  and naphthalene, both of which are obtainable in balls or flakes.
  Never mix PDB with naphthalene as they react chemically and produce a
  liquid that may damage the collection. It should be noted, that most
  major collections are now moving away from the use of solid fumigants
  because of health concerns and in some jurisdictions, it is now
  against regulations to use some fumigants.

That being said, I used a combination of freezing and then naphthalene (moth balls).  It's cheap and anecdotally pretty effective for my purposes.  I also didn't access my collection frequently once established, so the health concerns were less of a worry for me.

Definitely worth mentioning that there has been talk that using naphthalene  or PDB may damage DNA and hurt DNA extractions on down the road, but this is demonstrably false.  That being said, keep in mind these chemicals still pose some heath effects - especially with prolonged or occupational exposure - such as poisoning and carcinogenic risk.


What is the purpose of an siRNA screen in drug discovery?

According to the Labome article "siRNAs and shRNAs: Tools for Protein Knockdown by Gene Silencing" siRNA does stand for small interfering RNA.
siRNA is used to silence genes via mRNA degredation:

NA interference (RNAi) is the process by which the expression of a target gene is effectively silenced or knocked down by the selective inactivation of its corresponding mRNA
[...]
The silencing mechanisms can either lead to the degradation of a target mRNA, as induced by small interfering RNAs (siRNAs) or short hairpin RNAs (shRNAs), or the suppression of translation of specific mRNAs, as induced by microRNA (miRNA).

There are also Wikipedia articles discussing these concepts that didn't come up in my search somehow, but a colleague linked me to:

Gene knockdown
Small interfering RNAs


What type of cell do you start with in Meiosis?

Meiosis starts with a diploid cell and produces four haploid cells.  In animals, the starting diploid cell is usually called a germ cell and the surviving haploid cells become gametes (sperm and ova).  (In animals, the female mitotic sequence produces only one ovum; the other three haploid cells become "polar bodies".)

In other organisms such as plants, the starting diploid cell is typically not called a "germ cell" as it is not distinguished early in the organism's life.  Instead the starting cell can be any undifferentiated diploid cell that finds itself in the appropriate location (e.g. in a flower) at the appropriate time.


What are treatable foetal conditions during pregnancy?

Your question probably expresses a subtle confusion about the prenatal diagnostics and genetic testing.

So, genetic testing is one of the diagnostic methods in prenatal diagnostics (among with the other methods, see the list) which is used to diagnose genetic disorders of the foetus, whereas the disorders that are diagnosed on this stage are mostly genetic anomalies with dramatic impact on the feotus development, for example chromosome aberrations (like Down or Turner Syndromes). Should these conditions be diagnosed, the woman is given a choice to interrupt the pregnancy prematurely.

Less dramatic conditions (like sickle-cell disease) can be diagnosed at this time too, but are not treated before the birth.

The genetic disorders that are amenable to the dietary or medical treatment (like phenylketonuria or congenital hypothyroidism) are usually diagnosed in the newborn screening tests (newborn heel prickle test), because these screening is more precise and less dangerous compared to the pre-born diagnostics.


What is this feather like bug with no legs?

It is a specialized feather called "down" (like in down pillows, etc.)

  Down feathers have a rachis that is shorter than their longest barb. They are completely plumulaceous and have a fluffy appearance, which results from filamentous, noninterlocking barbules.

Anatomy, Clinical Presentation, and Diagnostic Approach to Feather-Picking Pet Birds


How to transform snail shells into a fertilizer?

Snail shells are composed largely of calcium, which is often used as fertilizer. As for wastewater treatment, I've heard about shells in general being used, mostly for their absorbent properties. I found this paper, which isn't long & might provide a bit more detail.

Hope that helps!


What are the differences in the two possible methods to calculate the Hardy-Weinberg Equation?

Okay, so the Hardy-Weinberg Equilibrium is just that: an equilbrium.

In physics, a system (some object) is at equilibrium when no net energy crosses its boundary with the surroundings.

no energy change means no change in motion (the state of the object) due to outside influence on the system.

In chemistry, a system (the beaker/reaction container/cytosol) is at equilibrium when no change in the concentration of the chemical species inside of it occurs over time

no chemical makeup change means the (molecular) state of the atoms in the system is free of energetic influence from the outside world.

In the H-W Equilibrium, a system (the gene pool) is at rest when no change in the frequency(concentration) of its alleles occurs over time.

no change in the frequency of alleles means that there is no outside influence on the state of the gene pool.

Just like in basic physics, we have to define our system. If our system is the gene pool, then even the behaviors of the organisms in whose cells those alleles are found are outside of the system. The system is only the alleles aka gene pool.

The most important part about understanding the H-W Equilibrium is that it only applies when those conditions of the gene pool being free from outside influence hold. In fact, in the link you gave, the introduction has it in the second sentence (don't feel bad, I missed it the first few times, too—too focused on applying the algebra to understand what it was really saying):

  The model has five basic assumptions:

  1) the population is large (i.e., there is no genetic drift)

  2) there is no gene flow between populations, from migration or transfer of gametes

  3) mutations are negligible

  4) individuals are mating randomly

  5) natural selection is not operating on the population.

Let's break them down/group them:

2: Obvious in terms of equilibrium == system is in isolation from surroundings
4 & 5: Selection pressure (4: sexual selection, or 5: natural selection) is not pushing on the system.
1 & 3: Random effects are not pushing on the system (1 = statistical sampling error that can push small populations, and 3 = mutation that pushes the system like adding a new chemical species to a system at rest.)

With that solid grounding in the theory, let's move on to your questions about the algebra. Remember, the equilibrium only applies when the gene pool is not being pushed around by external factors. Which means that the physical copies of alleles (gametes) should pair randomly with the possible gametes at every mating. If those assumptions didn't hold true, then the math of the equilibrium wouldn't hold up. If you run the numbers on a system at equilbrium, barring small amounts of sampling error (reducible with a bigger n), the H-W Model's predictions will be accurate. All the methods will yield similar results.

However, if the predicted values don't match the actual with one method, you can assume that other methods will also yield inaccurate predictions, and that the two different calculation methods' predictions will vary widely from each other, largely because of the assumptions you are making (Method 2: 1 = p+q), or aren't making (Method 2).


What is the probablity that SARS-CoV-2 will mutate?

I don't see how you want to prevent mutations - and these don't have to be a bad thing as the mutation of SARS (the original one from 2003) shows, here the mutation (or better the deletion of a part of the viral genome) led to an antenuated pathogenic virus. Since this mutation happened in the early phase of the spreading, it became the major virus. See reference 1.

Mutations are a statistical process which happens all the time, especially for RNA viruse due to errors in the polymerases (see reference 2). So the answer to your first question would be: 100%. It is mutating, which can also be seen in the sequences which have been published so far. The differences are only minimal with a sequence homology between 99.91 and 100% (see reference 3), but this can already lead to changes in the amino acid sequence. You can see this in the screenshot from phylogenetic tree of all sequenced SARS-CoV-2 viruses on [Nextstrain] (see the site for the actual development):

To your question 2: You cannot really predict where mutations happen and which will come through in the long time, as this is a statistical process and the sheer number of viruses around in each infected patient. But there are positions which are more prone to mutations, while mutations at other parts of the sequence will lead to much less fit virus. There is not so much data available yet (remember that this virus is only around since the end of last year), but reference 3 has some data on it (figure 3):

Question 3: I don't see how this should happen, as this involves the polymerases which are involved in replication.

References:

Attenuation of replication by a 29 nucleotide deletion in
SARS-coronavirus acquired during the early stages of human-to-human
transmission
Why are RNA virus mutation rates so damn high?
The establishment of reference sequence for SARS‐CoV‐2 and variation
analysis
On the origin and continuing evolution of SARS-CoV-2


How does herpes (HSV) infection suppress HIV?

Alright, having read the citation linked, and doing a little poking of my own, here's my approach at an answer:

Some human herpes virus infections may compete with HIV infection. Essentially, some strains (not the ones you normally think of) infect CD4 cells - the same cells targeted by HIV. These strains down regulate transcription in CD4 cells, which in turn interferes with the HIV infection process. This pertains, it appears most notably, to HHV-7.

However the actual impact on HIV disease isn't clear. Strain competition triggers some fascinating evolutionary pressures, but HIV is notoriously prone to mutation, and competition for CD4 cells might not impact HIV infection on a clinical - rather than microbiological - scale.

Additionally, the two most commonly thought of forms of herpesvirus infection, HSV-1 and HSV-2 are associated with increased acquisition of HIV infection. The clearest reasons for this are genital lesions and inflammation at the site of HIV infection. There's also some interesting dynamics in play for active coinfection, such as the impact of acyclovir treatment for HSV impacting HIV, or HAART treatment for HIV impacting HSV.


Do we know how animals refer to us, humans?

The question seem to assume that animals (as a weirdly inclusive group) have a "word" to refer to humans. The vast majority of animals species do not use any specific signal to refer to humans. Very few species has the social intelligence needed to communicate about the the presence of individuals of a difference species and among them few have important enough direct relationship with humans to have do so.

Consider vervet monkeys as an example. Vervet monkeys make sounds to indicate the presence of a flying vs terrestrial predators. If a human shows up, then the sound should be the one associated to terrestrial predator but that would not qualify as a sound to refer to humans. See Seyfarth, R.M.; D.L Cheney; Peter Marler (1980). "Vervet Monkey Alarm Calls: Semantic communication in a Free-Ranging Primate". Animal Behaviour. 28 (4): 1070–1094. doi:10.1016/S0003-3472(80)80097-2

Outside of a very small zoo population of some vertebrate species, I doubt (but might be proven wrong, who knows?!) there is any species that would have a term for "human". If you have any reason to think the opposite, can you please try to focus on this specific species for which you think individuals might vocalize (or signal in any way) to convey the concept of "human" to its congeners. Likely the only species that has a "word" for "humans" are humans!

  Do scientists know of a particular sound (or maybe a sign, a movement, or related form of communication) used by any animal which signifies "human"?

It is not a matter of knowing what sound they use. Excluding humans, animals likely don't use any sound to refer to the concept of "human".

  In case the current answer is no, is this ever possible to know?

The answer is not "no, we don't know" but rather "there is nothing to be known here as animals just don't do that."


GWAS terminology "Tag" vs "Lead" vs "Index" SNP

I found a review paper that addresses your questions, see

Schaid, Chen, Larson (2018): From genome-wide associations to candidate causal variants by statistical fine-mapping

Tag SNP. You correctly identified tag SNPs. From the paper:

  [T]he SNPs on microarrays, called tag SNPs...

Lead and index SNP. These are apparantly synonyms. From the paper:

  This allows one to focus on the SNPs with the smallest
  (that is, most significant) P values in distinct regions,
  sometimes called the lead or index SNPs.


The term pan, in my opinion, is perhaps one of the most vague that exists in science! I can partley answer this question (ironically as vague as the term pan) by referring you to the term pan-neuronal. A pan neuronally expressed genes has features, which include the expression of many "generic" genes required non-specifically for neuronal function, such as components of the synaptic vesicle machinery, so pan-neuronal genes are not neurone class specific (http://www.wormbook.org/chapters/www_specnervsys/specnervsys.html). So with that token pan-caspases are a term referring to a general caspase activity/function/structure and not a specific caspase type activity but I would welcome any corrections or edits to this response.


what is the difference between pituitary dwarfism and thyroid dwarfism?

Pituitary Dwarfism is a condition where less amount of growth hormone results in abnormally slow growth and short stature. Growth hormone is released under the influence of hypothalamic growth hormone-releasing hormone(GHRH), and is inhibited by hypothalamic somatostatin. Growth hormone deficiency has different negative effects if happens according to age it manifests;  in newborn, the primary manifestations may be hypoglycemia, while in later infancy and childhood, growth failure is more likely. Growth hormone deficiency can be congenital or acquired. It is usually permanent, sometimes transient.

Thyroid dwarfism is a condition arising from the deficiency of a thyroid hormone. It happens when there is lesser thyroid hormone secretion (defect of manufacturing or lesser supply of Iodine) before attaining the full development congenitally. It causes retarded growth and development of bones with disproportionate body proportions (that's dwarfism ).


What were the symptoms of Phineas Gage after suffering his brain injury?

Gage suffered a massive injury to the frontal cortex due to his accident in 1848 (Fig.1). Recent work using computer assisted tomography (CAT) has shown that contrary to popular belief, the injury was probably not bilateral, but confined to the left-lateral frontal lobe (Ratiu et al, 2004).

Fig.1. Original drawing of the wound sustained by Gage (left). Source: Harlow (1869) and the reconstructed injury using modern CAT scanning techniques on the original tamper and Gage's skull (right). Source: Ratiu et al., (2004).

The question of OP is not very particulate about the nature of symptoms (physical or psychological symptoms), or about the time window of interest after the accident (acute or chronic symptoms). I assume that OP is asking about the behavioral changes of the subject after he was physically fully recovered. The following is a formatted quote from the original publication written by his treating physician (Harlow, 1869) describing the subject's behavior approximately 6 months after the incident:

  His physical health is good [...], but says [he] has a queer feeling [in the head] which he is not able to describe. [...] His contractors, who regarded
  him as the most efficient and capable foreman in their employ previous
  to his injury, considered the change in his mind so marked that they
  could not give him his place again. The [...] balance [...] between his intellectual faculties and animal propensities, seems to have been destroyed. He is fitful, irreverent, indulging at times in the grossest profanity (which was not previously his custom), manifesting but little deference for his fellows, impatient of restraint or advice when it conflicts with his desires, at times pertinaciously obstinate, yet capricious and vacillating, devising many plans of future operation, which are no sooner arranged than they are abandoned in turn for others appearing more feasible. A child in his intellectual capacity and manifestations, he has the animal passions of a strong man. Previous to his injury, though untrained in the schools, he possessed a well-balanced mind, and was looked upon by those who knew him as a shrewd, smart business man, very energetic and persistent in executing all his plans of operation. In this regard his mind was radically changed, so decidedly that his friends and
  acquaintances said he was "no longer Gage."

The symptoms of Gage indeed match the current understanding of the functions of the frontal lobes. The frontal lobes are thought to be involved in a multitude of cognitive processes, such as executive function, attention, memory, and language, affect, mood, personality, self-awareness, as well as social and moral reasoning (Chayer & Freedman, 2001).

References
- Chayer & Freedman, Curr Neurol Neurosci Reports (2001); 1(6): 547-52
- Harlow, Bulletin of the Massachusetts Medical Society (1869) and see wiki page
- Ratiu et al., J Neurotrauma (2004); 21(5): 637-43


.. according to a taxonomical key that I found, I think it may belong to the genus 'Hestiasula'.

You're absolutely correct! This is of the species Hestiasula brunneriana, and is belongs to a group of praying mantis that are referred to as "Boxer mantises", due to their enlarged raptorial forelegs, of which are used for communication.

And though I can't quite tell, but at first glance this appears to be a female, due to what seems to be a longer than not abdomen; a female will only have 6 segments, whereas a male will have 8, however, the segments belonging to the female will be longer than that of the males. If you can somehow get an underbelly image, a much more definitive statement can be made.

The following image accurately matches your aerial image:

And then here's an image that demonstrates those distinct black markings on the raptorial forelegs:


You can definitely make such gRNA, but chances of off-targeting increases as you decrease the size of gRNA. It is always better to have 17-20 bp gRNA. However, you can check off-targets of a gRNA through several online tools.


Why do spiders make their web near the ceiling and near a light source?

Because many insects (their food) are attracted to light. This attraction is called phototaxis.

Hypotheses for why insects are attracted to light

The leading hypothesis for why so many insects are attracted to light is that before artificial existed, insects were using the light from the moon in order to navigate. They would keep themselves at a given angle relative to the light source in order to navigate straight.
Another hypothesis is the presence of light indicates that the pathway is clear.
A third hypothesis is that some insects may confuse artificial light source with the other sex. This appeared to be true for moths for example

These three hypotheses are not mutually exclusive.

How do spiders chose their habitats

For more information about the abilities of spiders to find a good habitat, have a look at this very interesting answer.


How does the enzyme Dicer function in the RISC complex?

Dicer is an endo-ribonuclease belonging to the RNAse-III class. Dicer is not a part of the RISC. It however helps in the formation of RISC by cleaving dsRNA or the stem of hairpin RNA on two ends which liberates a small dsRNA product. Then one of the strands is loaded into the RISC.

There are several reviews on this topic and there is a video as well which you can find on youtube.


Can you accelerate the growth of a plant by accelerating its surroundings?

This is not the best answer, but see that as a starter! Feel free to use my answer to build yours!

I have found a so-called professor speaking of advantages to go on a 24h light/12h dark cycle (36h cycle) to accelerate the growth of cannabis. I'm not sure of the reliability of this source.

I think the main problem we will encounter with that reduction of cycle would be the trouble with the circadian clock inside the plant. This clock is quite stable and I suspect some deregulation would happen if you desynchronize your day-night cycle with that clock.

See the effects we show on humans in the section Enforced longer cycles of
 Wikipedia or this stack question

  Researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions - both physiological, behavioral, and cognitive.


Help identifying an insect by its remains

It is probably a beetle.
The shape of legs and the two big eyes are an insect thing.
Lyme desease is transmitted by ticks, so i would not worry.


Is it possible to train allergic resistance by exposing yourself to allergens?

The phenomenon called oral tolerance is quite a common way to reduce allergic reactions. Basically patients have to eat a lot of the antigen with their daily diet under the supervision of doctors, so in time allergic reactions can be alleviated. The idea behind this is that our immune system is much more tolerant to things that get in our digestive system (in most cases). Here is a good article on oral tolerance from Nature.

Citation: Pabst, O; Mowat, A M - Oral tolerance to food protein Mucosal Immunology 2012 https://doi.org/10.1038/mi.2012.4


What impacts penetrance of Huntington's disease?

Penetrance describes the frequency of a gene's expression:

  Penetrance refers to the proportion of people with a particular genetic change (such as a mutation in a specific gene) who exhibit signs and symptoms of a genetic disorder. (Genetics Home Reference nih.gov)

More specifically:

  [P]enetrance is defined as the percentage of individuals with a given genotype who exhibit the phenotype associated with that genotype. For example, an organism may have a particular genotype but may not express the corresponding phenotype, because of modifiers, epistatic genes, or suppressors in the rest of the genome or because of a modifying effect of the environment.

Note that the environment is only one factor affecting the expression of an allele.

Retinoblastoma and achondroplasia are often referred to in discussions about penetrance.

Retinoblastoma is caused by mutations in the Rb gene. Not all people who carry this mutation suffer from retinoblastoma (about 90% do). There are numerous inherited diseases (including cancers) in which the same mutation is not expressed in all the individuals who carry it. Achondroplasia, on the other hand, has 100% penetrance: every person with the specific point mutation in the fibroblast growth factor receptor 3 gene always has abnormal bone growth and dwarfism.

Huntingtons is a little different in that patients with 36 to 41 HD CAG repeats exhibit reduced penetrance; that is, some may not develop HD in their lifetime; however 100% of those with the mutation produce the abnormal/polyQ/polyglutamine-enlarged huntingtin. The age of onset is dependent on number of repeats but is affected by other modifiers (both genetic and environmental); this becomes less obvious in individuals with higher repeats sizes (e.g. greater than 44).

Huntington's is not a genotype affected only by environment.

 Genetics in Medicine
 A new model for prediction of the age of onset and penetrance for Huntington’s disease based on CAG length


Why do I want to urinate when I touch water?

FIRST PART:
I am writing this answer with an analogy.I have analogised your question to a childhood habit developed by our mothers-when she would want us to urinate all she had to do was to take us to the toilet and make a "siiii" "siii" sound to mimic the sound of running water(more or less)
Since I have analogised in that way I think the third hypothesis (referred in your question)is more apt.
SECOND PART:
What fascinated me more about your  question was your comment-"I'll also be interested to see why the people will learn to have desire to urinate at the sound of tap water. Is there any reason that for that? – Hosea Jul 14 "
Indeed there is because we still have our mirror neurons
[SOURCE]
What I wanted to understand is if mirror neurons contributed to Pavlovian reflexes.The answer was yes
Furthur I could find out from sources that the micturition process has centres in the brain stem which are controlled by higher centres in the brain.One of them was the "medial frontal cortex".
Read the following article:

The Pontine micturition center (PMC, also known as Barrington's nucleus) is a collection of neuronal cell bodies located in the rostral pons in the brainstem involved in the supraspinal regulation of micturition. When activated, the PMC relaxes the urethral sphincter allowing for micturition to occur. The PMC coordinates with other brain centers, including the medialfrontal cortex, insular cortex,hypothalamus and periaqueductal gray(PAG). The PAG acts as a relay station for ascending bladder information from the spinal cord and incoming signals from higher brain areas.[source]

From the outline in the following lines I could conclude that there are mirror neurons in this region which 'may' be involved in the micturition control:

Yoshida et al. [26] recently recorded from neurons in the medial frontal cortex, some of which selectively responded to self or observed actions within a social context
[source]

Although research has confirmed that mirror neurons contribute to Pavlovian reflexes no such pathway has yet been discovered which can directly help us to confirm  and understand its relation to urination urge in contact with water.


Why the genome is divided into several chromosomes and not just a single big chromosome?

The leading contender of "why" in my former lab, is that if a chromosome becomes too long, a cell cannot fully isolate the chromatid to a daughter cell. Ie in a giant chromosome, the chromosome arms trail so far behind centromere, that the arms are of two sister chromosome are still touching each other even through the centromere have reached the opposite poles of a dividing cell. This prevents nuclear reformation. It would also mean, that the size of the cell will determine the chromosome maximum size.

At present this is a hypothesis. We have only just created the method to make ultra large synthetic chromosomes. I expected an answer is 3-5 years (2021-2023). However we say there is nothing special to a chromosome number.


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.


According to Sigma-Aldrich,

  1 USP Unit = 3.0 BAEE Units
  1 NF Unit = 1.1 USP Units

So 1 NF unit is roughly equal to 3.3 BAEE units. You can then directly compare the two trypsin powders, since they are preparations of the same enzyme.


Is there a non-bacterial source of lipopolysacchrides

Yes, there is.

Lipopolysacchrides have been found in eukaryotes. The most famous example is green algae from Genus Chlorella.

According to Armstrong et al., (2002):

  The lipopolysaccharides (LPS) are ubiquitous components of the outer leaflet of the outer membrane of all gram-negative bacteria and are the principal toxic products of these organisms (1). The membrane anchor of LPS is lipid A, a central phosphodisaccharide unit that is attached to multiple -hydroxy fatty acid chains. LPS also contains the novel sugar, 3-deoxy-D-mannooctulosonic acid (KDO). Although generally believed to be restricted to prokaryotes, specifically the gram-negative eubacteria and the cyanobacteria (2), an LPS-like molecule has recently been reported from a eukaryote, the green alga Chlorella sp., strain NC64A. (emphases mine)

Also, for further discussion on LPS in eukaryotes, please see Histochemical Evidence for Lipopolysaccharide (Endotoxin) in Eukaryotes.

Source:

Armstrong, P., Armstrong, M., Pardy, R., Child, A. and Wainwright, N. (2002). Immunohistochemical Demonstration of a Lipopolysaccharide in the Cell Wall of a Eukaryote, the Green Alga, Chlorella. The Biological Bulletin, 203(2), pp.203-204.


In an open circulatory system, how is blood moved?

In a closed circulatory system, all of the blood stays within blood vessels or the heart itself.

Organisms that have open circulatory systems, such as arthropods, have hemolymph (a fluid that is essentially a mixture of blood and interstitial fluid). The hemolymph actually does travel in vessels for a very short amount of time, as it is leaving the heart. After this, it goes to the body cavities of the animal and directly bathes the tissues in the fluid in order to deliver oxygen, nutrients, etc.

Hemolymph moves throughout the body when the animal moves. Also, when the heart relaxes, hemolymph is drawn back toward the heart through ostia, or open-ended pores.

So to answer your question, yes, these animals can survive just by pumping hemolymph straight into the body. This is only effective because their body cavities are very small. In humans, an open circulatory system would never work because it would require an enormous amount of work to pump and circulate blood throughout our entire body cavity.


What is the quality rate of intrinsic autoregulation in the heart?

My conjecture: Intrinsic regulation is done in the heart the second best, after the brain.
This idea is based on the fact that the brain controls heart's some autonomic functions.

It is an open research question how the autonomic nervous system affects the intrinsic functions of the heart - and the reverse is true too.

To answer this question, we need to understand the autonomic regulation of the heart better i.e. the inner-physiology of the heart's electrical activity.


Why do fishes have both a gustatory and an olfactory system?

In addition to olfactory and gustatory, fishes have two more chemoreceptor systems, solitary chemoreceptor cells and free nerve endings (Finger TE 1997). Asking why do they have all these chemorecepor systems is 'little bit' difficult in the light of evolution. But we can definitely look at this question by using some comparative studies. Hence, this answer will not give you answer to 'why' but will give you enough information to understand roles of these systems.

Reference provided by you explains much of the mechanism of olfactory and gustatory system. I will highlight the important difference between these mechanisms.

In olfactory system, signal is directly detected and transmitted to Central Nervous System (CNS) by neurons of cranial nerve I (Liu and Zhang 2019)
In gustatory system, signal is first detected by specialized gustatory cells and then transmitted to CNS via cranial nerve VII (Purves D et al 2001)

As both of them have similar function, it has been difficult to assign specific function to specific system due to lack of robust behavioral assays (Hara TJ 1994)*

Nonetheless, there are following functions in different kinds of fishes are preferred by one system over another,

Hara TJ 1994 comment that spatial feeding behavior is supported by olfactory system in contrast to gustatory system which helps in consummatory feeding like turning, biting, snapping and mastication**
Morais s 2016 suggests, olfactory system is involved in kin-nonkin recognition, prey–predator interactions, and territory or homing recognition because it is less plastic while gustatory system only plays a role in feeding behavior.
Discrimination of Pheromones is done by olfactory system (Lastein et al 2014)

From reading all these papers, I can 'guess' answer lies in the physiology of these sensory systems. Following conclusion is mine and I am no expert to tell whether this is correct. So just take it with pinch of salt :)

Fish has to survive in the water which is filled with tons of different chemical signals. So it has to distinguish these signals from each other. Many functions might not need very careful separation of signal (e.g. searching for resources) while other might need (e.g. which resources to eat). Some functions might need quick response (e.g. presence of predator) while other can be delayed for short time (e.g. migration). If you give responsibility to one system to perform all these functions simultaneously, it might get confused when multiple important signals arrive. From this I can speculate that this would have put some selection pressure during evolution so that there are multiple chemosensory systems.

From the literature cited above it looks like, Olfactory is less plastic and less sensitive than gustatory and hence involved in functions where you need little sensitivity to distinguish between multiple signal. While gustatory is involved where you need more specific selection of chemical signal.

*I could not get any recent paper directly comparing these two systems in fish. My hope is now we will be in more favorable place to perform some complex behavior experiments. **I did not understand difference between these behaviors conceptually, but you can look it up if you are interested.


Health benefits & enzymes different between Thermophilic and Mesophilic Probiotic cultures?

Thermophilic and mesophilic enzymes differ in the optimal working temperature, due to a structural adaptation: thermophilic enzymes have more stiff surface-exposed loops than their mesophilic orthologs. Human is mesophile, which means that mesophilic enzymes, no matter whether human or bacterial, will work in human more efficiently.

Bjelic, Brandsdal, and Aqvist (2008) Cold adaptation of enzyme reaction rates. Biochemistry 47: 10049-10057; emphasis mine:

  [P]sychrophilic, mesophilic, and hyperthermophilic citrate synthases
  ... have increasingly stronger electrostatic stabilization of the
  transition state, while the energetic penalty in terms of internal
  protein interactions follows the reverse order with the cold-adapted
  enzyme having the most favorable energy term. The lower activation
  enthalpy and more negative activation entropy observed for
  cold-adapted enzymes are found to be associated with a decreased
  protein stiffness. The origin of this effect is, however, not
  localized to the active site but to other regions of the protein
  structure.

https://www.ncbi.nlm.nih.gov/pubmed/18759500

Aqvist (2017) Cold adaptation of triosephosphate isomerase. Biochemistry 56: 4169-4176; emphasis mine:

  The results show that the enzyme from the psychrophilic bacterium
  Vibrio marinus indeed displays the characteristic shift in
  enthalpy-entropy balance, compared to that of the yeast ortholog. The
  origin of this effect is found to be located in a few surface-exposed
  protein loops that show differential mobilities in the two enzymes.
  Key mutations render these loops more mobile in the cold-adapted
  triosephosphate isomerase, which explains both the reduced activation
  enthalpy contribution from the protein surface and the lower
  thermostability.

https://www.ncbi.nlm.nih.gov/pubmed/28731682


The fundamental principle behind this is a "sensor" or the excitation-contraction coupling, regardless where you are.
Let's consider the striated muscle and the cardiac muscle.

The function of excitation-contraction coupling in skeletal muscle is as voltage sensor to tell the SR, "We have got an action potential; release Ca2+ for contraction".
This is a contrast to a heart muscle which works like a Ca2+ channel (i.e. Ca2+ is flowing in cardiac muscle continuously).
Similarly, xcitation-contraction coupling in cardiac muscle translates the action potential into the production of tension.
There are individual steps in this process of cardiac muscle:

The cardiac action potential is initiated in the myocardial cell membrane, and the depolarization spreads to the interior of the cell via the T tubules.
Recall that a unique feature of the cardiac action potential is its plateau (phase 2), which results from an increase in Ca and an inward Ca2+ current in which Ca2+ flows through L-type Ca2+ channels (dihydropyridine receptors) from extracellular fluid (ECF) to intracellular fluid (ICF).

Entry of Ca2+ into the myocardial cell produces an increase in intracellular Ca2+ concentration.
This increase in intracellular Ca2+ concentration is not sufficient alone to initiate contraction, but it triggers the release of more Ca2+ from stores in the sarcoplasmic reticulum through Ca2+ release channels (ryanodine receptors).
This process is called Ca2+- induced Ca2+ release, and the Ca2+ that enters during the plateau of the action potential is called the trigger Ca2+.
Two factors determine how much Ca2+ is released from the sarcoplasmic reticulum in this step: the amount of Ca2+ previously stored and the size of the inward Ca2+ current during the plateau of the action potential.

and 4. Ca2+ release from the sarcoplasmic reticulum causes the intracellular Ca2+ concentration to increase even further.
Ca2+ now binds to troponin C, tropomyosin is moved out of the way, and the interaction of actin and myosin can occur.
Actin and myosin bind, cross-bridges form and then break, the thin and thick filaments move past each other, and tension is produced.
Cross-bridge cycling continues as long as intracellular Ca2+ concentration is high enough to occupy the Ca2+-binding sites on troponin C.

A critically important concept is that the magnitude of the tension developed by myocardial cells is proportional to the intracellular Ca2+ concentration.
Therefore, it is reasonable that hormones, neurotransmitters, and drugs that alter the inward Ca2+ current during the action potential plateau or that alter sarcoplasmic reticulum Ca2+ stores would be expected to change the amount of tension produced by myocardial cells.

I like this figure about the topic in summarising stimuli in the smooth muscle:

In heart

In the gastrointestinal tract, we have then again special cells, Cajal cells, that work as "pacemakers" of the GI tract.
Myenteric Interstitial cells of Cajal [ICC-MY] serve as a pacemaker which creates the bioelectrical slow wave potential that leads to contraction of the smooth muscle.
This activity differs along the length of the system

3 per minute in the stomach
11-12 per minute in the duodenum
9-10 per minute in the ileum
3-4 per minute in the colon

You can see them as to work analogously through the "all-or-none" principle.

Sources

Costanzo, Physiology
Pocock, Physiology
My notes during during years 2011-2014 (in three Physiology courses and research)


What is an on-line measurement? What is an off-line measurement?

On-line means that's it's generally continuous, or constantly taking the measure, through a tube connecting the batch.

Offline is used for things that are taken out of the reactor, or removed from the process.

Thus it's "on" or "off" the system depending on whether it's contained within the normal piping/fludics of the system: "On" is in the system, "Off" is out of the system.