Here's a hint: you're right about 0.01 being the recombinant (crossed-over) double homozygous recessive offspring. I think you're forgetting that each offspring contains 2 gamete haplotypes, and so predicting the percent of offspring with a given genotype involves multiplying the frequencies of the individual gametes that produce that offspring. To calculate the gamete frequencies (and thus the recombination frequency) you need to reverse that multiplication process.
Full answer:
I find it easiest to deal with uniform genotypes first. Of the 4 offspring phenotype categories, only the double homozygous recessive category (short/green) has uniform genotype - llss. If l and s were unlinked, 1/16 of the total offspring would be short/green=llss.
However, many fewer than 1/16 are short/green=llss, so linkage is confirmed and (as you note), ls must represent one of the crossed-over haplotypes. The other crossed-over haplotype is then LS. Thus, the parental (non-crossed-over) haplotypes must be lS and Ls.
Let's call r the recombination distance (in map units) between l and s. Each recombination between l and s produces 2 recombinant gametes: 1 ls and 1 LS.  Thus the fraction of ls gametes - f(ls) - will be (r/2)/100 and the fraction of LS gametes - f(LS) - will also be (r/2)/100.  Since each F1 offspring consists of 2 gametes, the fraction of offspring with an ls/ls genotype will be f(ls) x f(ls) = (r/2)/100 x (r/2)/100 = r^2/40000 = 0.01 (from F1 data).
Solving for r, r^2 = 0.01 x 40000 = 400, so sqrt(r^2) = r = sqrt(400) = 20.
r = 20 map units


Is it better to take a half dose of paracetamol and a half dose of ibuprofen together rather than a full dose of either?

There are many different reasons for an acute pain and inflammation (both directly via pain receptors, and indirectly via swelling etc.) plays not the least role in this phenomenon. Therefore the combination of a classic analgesic without anti-inflammatory activity (as paracetamol) with a strong anti-inflammatory agent (as ibuprofen) is a reasonable one and potentially alleviates the pain manifestations in more cases than a single administration of every agent.

You are right with you suggestion that the doubled dose could be dangerous: even though the complications of Paracetamol administrations are not often, they are very dramatic (acute liver failure) with rather pessimistic prognosis. This is why one generally tries to half the doses if combined with other similar-acting agents (historically paracetamol was for the long time a member of the non-steroid anti-inflammatory agents).

Caffeine is generally believed to be a pain reliever, especially as concerns the pains with migraine background (source). One review, however, points out that there are still not enough data to support this belief (source).


Amount of variation between a canonical gene sequence in various samples

Your question is quite vague so I can only give you a vague answer saying what I would expect given only the information of your question.

The vagueness mainly comes from the huge amount of functional sequences in the genome, particularly also in enzyme-coding genes, each being more or less conserved. You say

  I am surprised that there is no information of how much of a within species variation there is in enzyme sequence. I am having a hard time getting this info. too.

I would say that there is no feasible way of studying this question. You will find different selective constraints on every single enzyme and breaking this down to DNA this means that every single locus can be target of different selective pressures. And even if you figured out how to answer that question comprehensively for a given species (which probably will not happen), generalising it to every single species in every ecological niche, with every possible population history and so on is close to impossible. That is why one studies sequence diversity/conservation in model organisms and mostly on a per-gene basis.

In general, without knowing any background of a species and enzyme, I would however expect two things when looking at molecular variation between individuals of that species. These are merely based on general evolutionary principles and the nature of the genetic code. Keep in mind that these are trends, meaning that many genes will match these expectations but some definitely will not due to lineage-specific evolution.

First, I would expect generally high levels of amino acid conservation (but not always identity) especially in functional enzymes of core pathways. However, this depends on the function of the gene product. If the gene is a target of balancing selection, which maintains genetic variation within a population, there can also be considerable amino acid variation.

Second, there will generally be higher levels of DNA variation because of mutations with little or no fitness effect (synonymous variation or intronic variation which tends to have lower selective pressure).

To relate this to your last question: even though I would always expect a general amount of variation, even in the amino acid sequence of core enzymes, this variation will probably not be the main reason why you see different phenotypes. Phenotypic plasticity - the differential response of a given genotype to a given environment - is often stronger in plants than in animals as plants are stationary organisms. This plasticity will probably be the main cause of striking phenotypic differences between individuals.


Why extract DNA from certain white blood cells instead of whole blood?

There are several reasons why a lab might choose to get DNA from lymphocytes instead of whole blood. Generating genomic DNA from whole blood is not necessarily the best idea, as all the excess protein (mainly hemoglobin from RBCs) needs to be gotten rid of at some point. By narrowing down your input to just include cells that have DNA, you lessen the amount of protein you need to extract in comparison to the total amount of DNA present.

Lymphocytes include T cells, B cells, and NK cells, and are relatively easy to quickly purify, especially in a lab with the requisite experience and reagents/equipment. They are by no means the only type of white blood cells from which one could purify DNA - peripheral blood mononuclear cells (PBMCs) can also be used, for example. They contain lymphocytes as well as other cell types like monocytes, macrophages, dendritic cells, etc. (In my experience they are even more straightforward to purify from whole blood than just lymphocytes, as it is essentially a single-step protocol with a few washes afterwards.) The end result is the same, though - DNA from lymphs should be the same as DNA from PBMCs, granulocytes, or neutrophils.

Any somatic nucleated cell in the body contains "representative" DNA, as except for in a few specialized cell types like T and B cells that undergo genomic rearrangement to form the T- and B-cell receptors, respectively, all cells from an individual contain the same genomic DNA sequence. Blood is relatively easy to come by from patients and clinical study participants, which is why it is often the source of DNA for studies instead of, say, skin punches or mouth swabs.


It's essentially genetic. The mule is a hybrid of a male donkey and female horse. A donkey has 62 chromosomes, a horse has 64 chromosomes, and a mule has 63 (mix of 62 and 64). There is a mismatch between both number and structure of the chromosomes and as a result, most mules are infertile.


What does pan-specific antibody mean?

The combining prefix pan- means "all" or "every".

Antibodies are specific because they bind specifically to an epitope ('target') on a molecule. A pan-specific antibody is one that binds specifically to all desired targets, within a defined range.

Here are three correct examples of how the word could be used, to help you understand. Only the first two are relevant for your particular case:

In your case, there is an antibody for the phosphoprotein, the unphosphorylated protein, and both. The antibody that targets both is pan-specific because it binds both ("all", or "every") forms of the protein.
Another possible use for pan-specific is that some antibodies bind to some members of a protein family, but not all, so they are not comprehensive enough. Other time, antibodies bind to all members of a protein family, but bind additional targets, so they are not specific enough. Pan-specific is a great way to describe an antibody (monoclonal) or set of antibodies (polyclonal) that are both specific and comprehensive enough to adsorb an antigen of choice.
An antibody that binds specifically to a protein called pan.


As you can see from the bottom of the gel, the brightness of the bands have reduced even for the DNA ladder/marker. The main reason for this is that when you are running an agarose gel containing EtBr, due to the positive charge of the EtBr, the stain runs to the negative chamber, against the direction of the DNA migration as @Chris has pointed out! Although some of the DNA will stain but the rest of the EtBr will migrate towards the top of the gel (where the DNA is loaded).

A quick remedy for this is once you ran your gel is to soak your gel in a separate container containing your stain and running buffer such as TAE. I do this for one hour and that makes a huge difference!! Also make sure you regularly change the buffer in your agarose gel running apparatus and don't use the same buffer for a long time since again as @Chris has correctly pointed out there is a reduced conductivity in the older buffers when they heat up so migration does not work as well! Obviously this response assumes that you have a good degree (amount) of DNA in your gel bands, which can be calculated by nanodrop once you extracted the DNA using an extraction kit, or whatever method you normally use. I hope this helps!

This answer is more suited to the title of the question since after reading the main question a bit more carefully I'm slightly confused! So do you see anything at all or your product is far too faint? could you tell us where on the gel, relative to the ladder you expect to see this band? are they the ones at the button of the gel, below the loading buffer?


Do neurons secrete multiple neurotransmitters, or just one type?

I've googled this for a biology class I taught, and the quick answer is that both possibilities happen in different instances.  Some specialized neurons secrete more than one type, even though the ruling concept used to be one neurotransmitter for one neuron.


Can tubular secretion regarded as local hormone?

First of all, I can't understand how can you regard an electrochemical process (tubular secretion) as chemical substance (hormone).

Tubular secretion is the transfer of materials from peritubular capillaries to renal tubular lumen. Tubular secretion is caused mainly by active transport.
Usually only a few substances are secreted. These substances are present in great excess, or are natural poisons. Many drugs are eliminated by tubular secretion [1].

The substances that are secreted into the tubular fluid (for removal from the body) include [2]:

Potassium ions (K+),
Hydrogen ions (H+),
Ammonium ions (NH4+),
creatinine,
urea,
some hormones, and
some drugs (e.g. penicillin).

Tubular secretion occurs from the epithelial cells that line the renal tubules and collecting ducts [2].

Uptake transporters in the basolateral membrane and export transporters in the luminal membrane of renal tubule cells are involved in tubular secretion of their substrates (organic anion transporters and organic cation transporters - these are transmembrane proteins) [3].

Despite considerable advances in the understanding of basic transport pathways and mechanisms involved in the tubular secretion of organic compounds, there is still relatively little information on the regulation of this transport [4].

References:

Wikipedia contributors, "Renal physiology," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Renal_physiology&oldid=608689347 (accessed June 26, 2014).
http://www.ivy-rose.co.uk/HumanBody/Urinary/Urinary_System_Kidneys_Actions_3.php
Müller F, Fromm MF. Transporter-mediated drug-drug interactions. Pharmacogenomics. 2011 Jul;12(7):1017-37. doi: 10.2217/pgs.11.44. PubMed PMID: 21787191.
Berkhin EB, Humphreys MH. Regulation of renal tubular secretion of organic compounds. Kidney Int. 2001 Jan;59(1):17-30. doi: 10.1046/j.1523-1755.2001.00461.x. PubMed PMID: 11135053.


How could a species be engineered to go extinct?

Short answer

The article in particular that you reference is discussing the possibility of using a mechanism called gene drive. The concept of gene drive breaks the normal "rules" of inheritance and allows a gene to spread much more rapidly than normal in a population.

Longer answer

Gene drive depends on the idea of a selfish gene. There are naturally occurring genes that make copies of themselves to other parts of the genome. Selection pressures can operate at the level of these genes: a gene that can copy itself is going to end up in more offspring than would be expected due to random assortment.

For example, imagine a gene present in one chromosome of one parent. Typically, only half of that parent's offspring will have that gene. However, if the gene is able to copy itself to the parent's other chromosome, now all offspring of that parent will have that gene. The prevalence of the gene just doubled. It's possible that the gene will also confer some negative traits, but as long as those negative traits aren't sufficient to cause a >50% reduction in later reproduction of the offspring, they are going to do just fine and go on and mate, spreading the gene further, potentially to an entire population fairly rapidly.

The new technology CRISPR makes it easier to create synthetic genes that selfishly copy themselves within the genome (note: this is definitely not the only application of CRISPR) and could confer positive traits that are helpful to humans, like mosquitoes resistant to being carriers of malaria, or to introduce deleterious mutations into a population.

As you point out, introducing a mutation that causes sterility and having it spread is still not easy. There are a few clever approaches, though, that can make it possible. Note that the strategy does not to have 100% effectiveness to wipe out a population: once below a certain level, members of the population may have trouble finding mates and face greater predation pressures and the population can collapse.

One technique is to boost the proportion of males. If you can force all the offspring of one male to be male, the proportion of males in the next generation will be higher. Those males-that-only-produce-males don't have any immediate reproductive disadvantage versus normal males. If they survive and mate normally, they will continue to compete with normal males (they may also compete with females for food resources during their lifetimes). Any time a normal male mates, sure, it will create a new generation of some females, but every time a transfected male mates it will effectively double the number of transfected males. Even as the total number of individuals in the species drops, the proportion of transfected males remains high. Eventually there are too few normal males to mate, the number of females drop to unsustainable levels, and the population crashes.

This approach is similar to the technique of releasing sterile males which has been used successfully for population control. The difference is that the gene drive technique raises future generations of the (sort-of) sterile males by itself, which might mean it can be used in population control when it is not possible to lab-raise large numbers of sterile males.

Note that use of these technologies is very controversial. There are concerns that such a gene could accidentally move from one species to another, for example. Future use of the technique will require combined research into safety and efficacy.

References

Burt, A. (2003). Site-specific selfish genes as tools for the control and genetic engineering of natural populations. Proceedings of the Royal Society of London B: Biological Sciences, 270(1518), 921-928.


Help me identify these creatures found in sink

I think this will be a larva. Check this video. If it was in a sink, is very probably than will be a fly. But the specie only will be identified with a genome assay, or taxonomically once they out the pupa.


Pangenesis and Lamarck's theory of inheritance of acquired characteristics

Pangenesis and Darwin's Gemmules theory suggests a mechanism so that the body's information can travel to and be transmitted by the gametes. Today we know that the information is present in every cell.

Stephen Gould estimates that Lamarck was the first to develop a truly coherent evolutionary theory.

Lamarck's biological and metaphysical theories comprised entirely correct premonitions, 70 years before Darwin. His book was "Philosophie Zoologique" and Lamarck was not illustrious in his lifetime. His lack of evidence made him an impious, profane author, of the pre-enlightenment style of Voltaire, Rousseau, and prior to Emile Zola and Jules Verne.

Scientists have recently attacked Lamarck with great energy, in favor of Darwin:
http://www.textbookleague.org/54marck.htm

Basically Darwin emulated Lamarck's skeletal theory, perhaps independently, and fleshed it out in a modern writing style. He also discovered the foundations of an entire scientific field of his own which tied into Lamarck's, and he fought the church and the science institutions with it.

The evidence of Darwin was copious and meticulous, completing the work of Lamarck (with lesser or greater brilliance, for you to judge).

Lamarck's speciation theories were correct, and his trait-inheritance theory was metaphysical.

First law
Life by it's own force, tends to increase the volume of all organs which possess the force of life, and the force of life extends the dimensions of those parts up to a extent that those parts bring to themselves;

Second law
The production of a new organ in an animal body, results from a new requirement arising. and which continutes to make itself felt, and a new movement which that requirement gives birth to, and it's upkeep/maintenance;

Third Law
The development of the organs, and their ability, are constantly a result of the use of those organs.

Fourth Law
All that has been acquired, traced, or changed, in the physiology of individuals, during their life, is conserved through the genesis, reproduction, and transmitted to new individuals who are related to those who have undergone those changes.

Darwin convinced many scientists and wrote about it continuously from his 30's till his 70's non-stop, sent letters to everyone, and used evidence to define a scientific and mechanical reality to the theory of adaptive radiation. Darwin also coined catchy phrases:

The English and French view of Lamarckism differ.

The English view slights his status, due to lack of evidence and some alchemical bases for the selection process, even though Lamarck is the father of adaptive radiation theory, in the age of the printed book.

The French view gives him more influence, firstly because he may have inspired Darwin as an eloquent writer on the topic of adaptive radiation, the father of the adaptive radiation theory, and secondly because a glimmer of Lamarckism can be found in the new discoveries of Epigenetics, non genetic inheritence.


It is important visualize more faces to design primer or oligo and PCR experiments:

- calculate thermodynamic parameters of DNA Hybridization (Oligo/Template)

compute hairpin-loop, dimer, bases penality and melting temperature about primer or pair primer
calculate statistics about melting temperature with the change in composition and mix PCR concentration

with google you could find more tools but you must choose a tool of a sequencing team.
almost all tools use mfold algorithm, it's simple and effective:

M. Zuker, D. H. Mathews & D. H. Turner. Algorithms and Thermodynamics for RNA Secondary Structure Prediction: A Practical Guide In A Biochemistry and Biotechnology, 11-43, J. Barciszewski and B. F. C. Clark, eds. , NATO ASI Series, Kluwer Academic Publishers, Dordrecht, NL, 1999.

I worked in a sequencing team and there was a programmer. he developed a fantastic tools. he is a little english, but he could support you: http://promix.cribi.unipd.it/cgi-bin/promix/melting/melting_main.exe


What is the main challenge in creating a chemical male contraceptive?

I am going to summarize a few reasons for both why contraception is "easier" for women, and for why it is "harder" for men. They are both biological and sociological.

Easier for women

The female cycle is more complicated

The female cycle leading to ovulation is regulated by several hormones that interact. As such, it is easier to disturb.

  The system is so sensitive that even the slightest alteration in any of these factors can disrupt its fluidity and lead to anovulation

(Anovulation = a cycle where no ovulation occurs) Source: Anovulation: Background, Pathophysiology, Epidemiology

Even in young women, this occurs naturally.

  Estimates of chronic anovulation rates range from 6-15% of women during the reproductive years

Female bodies l already have a "built-in mechanism for contraception

As ovulation needs to be suppressed during pregnancy, there is already a mechanism in place by which this can happen.

Women are more affected by pregnancy

Since women are more affected by pregnancy and childbirth, the risk they feel they have when they don't use contraception or use it incorrectly is larger.

Contraceptives for women have more than one use

  More than half of pill users, 58%, rely on the method at least in part for purposes other than pregnancy prevention. Thirty-one percent use it for cramps or menstrual pain, 28% for menstrual regulation, 14% for acne, 4% for endometriosis, and 11% for other unspecified reasons.

Beyond Birth Control: The Overlooked Benefits of Oral Contraceptive Pills

Harder in men

It only takes one

While the saying "it only takes one sperm"  is probably an exaggeration, it carries a certain truth - you really need to shut down the production of sperm or the risk of a pregnancy is too high. Both the pill and the various IUD options have set a high bar for what's considered an acceptable risk.

Side effects and effectiveness

While hormonal contraception for women already has a multitude of side effects, often unrelated to the reproductive system, this is certainly not easier in men. The most prohibiting side effect encountered so far is impotence - not much use in taking birth control to have sex without risk of pregnancy when doing so leads to no sex at all.

  Progestins have been used in multiple small studies of men for suppression of spermatogenesis and testosterone production. Progestins used alone result in significant side effects such as loss of libido and erectile dysfunction.

Update on Male Hormonal Contraception: Is the Vasectomy in Jeopardy?

(Decreased libido is also a side effect in female hormonal contraception, though. The reasons why it's seen as more acceptable there are probably sociological)

That review is a good overview on what has been tried until 2010. Many solutions failed because of side effects or because they didn't work well enough.

On testosterone:

  Of note, this international study revealed that 91% of Asian and 60% of Caucasian patients became azoospermic, suggesting an ethnic difference in endocrine response

Testosterone proved to be rather good in other doses and combinations, but is not that easy to handle because it requires injections and can't be taken orally.

  Testosterone alone has side effects, including acne and oily skin, mood changes, increased hemoglobin and hematocrit, weight gain, decrease in testicular volume, sleep apnea, gynecomastia and possible effects on cholesterol. There are no long-term data with testosterone use and normal men regarding prostate symptoms, growth or cancer. In an era of fear of using medications on relatively healthy individuals, acceptability of routine use may be a major concern, given recent data on medical treatment of menopause with estrogen/progestin therapy. In addition, anabolic steroids are a controlled substance and regulation of this industry is very strict at this time. Abuse of these drugs could easily become prevalent with its widespread use and availability for contraception.

On cryproterone acetate:

  Doses ranging from 25 to 100 mg per day have suppressed spermatogenesis, but side effects have precluded subsequent studies.

And so on...

The market factor

A side effect of the contraceptive options for women being so well-accepted, women often feeling responsible for contraception and also using hormonal contraception anyway, for reasons unrelated to pregnancy, is that the market for male contraception is not that easy and pharmaceutical companies have been pulling away from it. Especially in light of the research difficulties.

  Although Bayer, Wyeth and Organon were once active in research and development of a male method, all three discontinued their programs between 2005 and 2008 although the industry continues to actively pursue programs for hormonal contraception and hormonal-replacement therapy for women. In withdrawing support, company representatives cited corporate changes in direction and the perception that safety standards demanded by regulatory bodies would require such extensive evidence as to make further research financially infeasible

Current challenges in male contraceptive research

This is not to say that there really is no market. As you mentioned in the comments, at least in questionnaires, many men say they would use male hormonal contraception and many women say they would like their partners to use it. See, for example, Market size for male contraception (plus the following pages of that paper)

But you asked about the challenges ;-)

I think it's also interesting to note that the search for hormonal contraception started for both men and women. It's just that the "solution" was found for women first and then got popular really fast.


That's an apple snail egg cluster. They're freshwater snails, and by placing their egg clutches above the water line they protect them from predation.

We actually have an issue with apple snails in Florida, because while the Florida applesnail Pomacea paludosa is native, three different invasive species have been introduced that are eating through native vegetation without many predators (1).

Different species produce different colors of egg mass, and a good example of the green egg masses includes Pomacea haustrum, the titan applesnail, which is present in the continental US, but actually native to Bolivia, Brazil and Peru (2, 3). Since other species also produce green eggs, it's difficult to tell exactly what snail produced those, however.


Are all healthy animals more likely to defecate near the end of a rest-cycle?

I think we can actually go farther than mere behavioral argumentation. The separation of the autonomous nervous system into parasympathetic and sympathetic is, one the one hand, associated with the sleep/wake cycle, on the other with parasympathetic/sympathetic activity (low/high epinephrine secretion). This duality certainly applies to all vertebrata (i.e. big animals), as fight & flight is associated with all vertebrata, see e.g.

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

In other words: from the existence of fight or flight in all vertebrata I infer the existence of a dual autonomous nervous system (parasympathetic and sympathetic) in all vertebrata, although there may be other proof. Since in sleep the parasym. NS is active, the bowel moves. Conclusion: the bowel moves in the sleep of all vertebrata.


There are a couple of caveats that need to be addressed before answering this question:

We don't know all of the regions in the human genome that can be heterochromatic. In some cases large chunks of heterochromatin are simply missing from the genome assembly. For a somewhat outdated but still informative review of the topic see here.
Which regions are heterochromatic differs from cell to cell. For example, I would recommend reading about the differences between constitutive and facultative heterochromatin at wikipedia.
Heterochromatic regions of the genome are very important biologically and not taking them into account could be a mistake, though it depends on your motivations.

The human genome project initially estimated that 92% of their original genome build is euchromatic, 2.85 Gbp total. However that original genome build has been substantially updated. That estimate is close enough for many purposes, probably. But we've learned a lot about genome structure and biology since that time.

We do have a lot of data that is highly correlated with what we think of as heterochromatin. The UCSC human genome browser has a lot of information about chromatin modifications (I would look at the ENCODE analysis section here). In principle you can make educated guesses about regions of heterochromatin based on chromatin modifications. This will be somewhat noisy, and you will have to make decisions about which cell types are relevant, as they will have somewhat different regions.

For more information about which chromatin modifications might be relevant, you might start looking here. You will likely need to analyze some data yourself to find a more precise answer.


Basically, they don't. Ecosystems are pretty much either de facto, delimited by geographical boundaries, or defined by us. For example, an underground lake would be an ecosystem and it is organized in such a way for the simple reason that there is no communication between it and any other system.

Most ecosystems however, do communicate. For example, we call a desert an ecosystem but what of creatures living in the borders? That can survive both the harsh desert and the milder outskirts. Do they belong to the desert ecosystem? To the surrounding one? To both?

Basically, we divide nature into ecosystems because we can study them better that way. Species that form part of the same ecosystem tend to interact in one way or another and species from completely separate ecosystems tend not to. This is not some kind of rule however, it is simply the way we categorize things.

To take a different example, how would you define a city? Where does a city end and the countryside begin? Ecosystems are similar, there are seldom very clear cut lines separating them, they sort of bleed into one another.

In other words, your question is moot, ecosystems don't really self organize as such. The organization that does exist is between the different species and is an emergent quality of the complex system that is the ecosystem. Thinking of ecosystems, however, as distinct and well defined entities is generally wrong.


How does (action potential) hyper-polarisation work?

I'll borrow a diagram from another answer to a similar question, but not quite a duplicate (I hope @AliceD won't mind my laziness):

Fig. 1. Refractoriness. source: University of British Columbia

One important concept to understand about the refractory period is that it has two components. One is the hyperpolarizing part, which is due to open voltage-gated potassium channels. Because there is more potassium conductance than at rest, the membrane voltage gets closer to the reversal potential for potassium.

If you were to open a sodium conductance during this period, you would indeed get a larger sodium current than you would get at rest (because you are further from the sodium reversal potential), however it will also be accompanied by potassium leaving the cell (because there is more potassium conductance), such that the net current and net change in voltage may not be much larger than at rest. Voltage-gated sodium channels that open to cause an action potential are gated by voltage, not by sodium. However, this type of refractory period is referred to as a relative refractory period because you can overcome it if you open a large enough sodium conductance (or inject a bunch of current with a patch clamp amplifier).

However, there is also a second part to the refractory period, the "absolute" part, which is shown in the diagram above. The voltage gated sodium channels themselves are not only closed but they are also inactivated. While inactivated, those channels will not open even in response to depolarizing voltage. It takes some time for the channels to return to the 'closed' state where they can be opened by voltage.

Summary

To speak to your question more directly, nothing prevents sodium from diffusing 'backwards', but action potentials travel quickly, sodium channel inactivation prevents them from traveling into axon segments where the sodium channels were just recently open, and the open potassium channels that cause hyperpolarization will 'shunt' current out of the cell while they remain open. Lastly, voltage-gated sodium channels are gated by voltage, not sodium.


What are these caterpillars eating a potato plant?

I believe this is the middle instar of a Southern Armyworm (Spodoptera eridania) larvae. Or some closely related species in the Spodoptera genus (family Noctuidae).

 © 2016 Wings, Worms, & Wonder

The larvae undergo six instars as they grow to attain a length of about 35 mm.

You can see a series of life stage pictures from Mississippi State.

Armyworms are so called because you typically find 100s at a time on a single leaf or plant. According to here:

  Armyworms strike in the blink of an eye, and there are so many in their army that you will be finding them for weeks after the primary attack.

Behavior: larvae are mostly active at night and hide on leaf undersides, in curled leaves, or in leaf litter during the day.

This University of Florida site claims

  Young larvae feed on under surface of leaflets leaving upper epidermis intact ("windowpaned"). Older larvae consume foliage and eat large holes in fruit.

Range: native to the American tropics (occurs widely in Central and South America and the Caribbean). Also found in US (principally in the Southeast but extends West to Kansas and New Mexico). It also is reported from California.

Here's a map showing some confirmed sightings [source]:

Host Plants:
This species has a very broad host range including important crops (including potatoes).

I would be concerned for your nearby tomatoes, because thy too are a favorite food of these insects.

See here for more information including management suggestions.

Defecation vs. Eggs??

The picture in the question shows S. eridania's feces.

This Mississippi State site includes a great zoomed-in picture of S. eridania's feces:

 © Lee Ruth
Note: caterpillars don't lay eggs. Only adult moths/butterflies lay eggs.

Eggs: large masses of 100-200 eggs covered with moth body scales, found on underside of leaves, hatch in 3 days.

 © 2016 Wings, Worms, & Wonder

Here's a picture of inside the seed casing of closely related S. exigua [source]:

 © 2016 Wings, Worms, & Wonder

Finally, here's a picture of the nocturnal adult:


It is the caterpillar of Papilio polyxenes.

  The pupae may be green or brown, but not depending on surroundings or the background on which they have pupated. The color of the chrysalis is determined by a local genetic balance that ensures the majority of pupae will blend in.[10] A section of the green pupae will turn a much darker green at the very end of the pupae stage. This color change occurs a few hours to a full day before hatching.[10] Unusually, this butterfly's chrysalis is girdled with a loop, with its feet attached to the silk pad, which helps the butterfly to unfold its very large wings when crawling out.[11]

Here is a photo of black swallowtail caterpillars at different life stages:

Here is a link to a post, which describes all the stages your caterpillar will eventualy go through.


Splicing and “the dominance of RNA-world”

This is a badly-worded phrase that means nothing in the context of the paragraph in which it occurs. There is no way the reader could be expected to understand it from this awful book on its own. Normally I would not think it the role of this site to remedy deficiencies in text books. However, as this involves some interesting questions I will try to read the author’s mind.

The author probably means something like:

  “splicing is a relic of the RNA world”

…although a more measured statement would be:

  “the existence of self-splicing supports the idea that the current DNA/protein world was preceded by an RNA world”

The author’s use of the word “predominance” is just incorrect English. (Sloppiness or deficient vocabulary.)

An RNA world?

So what is all this about an ‘RNA world’? The author refers to this on p. 104. He states as a categorical fact what it is important to realize is only a theory:

  RNA was the first genetic material…RNA used to act as a genetic material as well as a catalyst…

Why is splicing relevant to this? Some types of splicing are catalysed by the RNA itself — self-splicing — an example of an RNA enzyme (ribozyme). From the existence of these and other ribozymes it is argued that originally all enzymes may have been ribozymes, and protein enzymes only developed later, taking over most, but not all enzyme functions.

It is important to realize that RNA preceding DNA, and the first enzymes being RNA rather than protein, are two independent ideas. Although both these ideas are widely held, and I personally tend to favour them, certain scientists have argued strongly against them, as discussed by Harold S Bernhardt.


Can insects or mosquitoes be astonished(shocked)?

I originally thought there was no way anyone had studied this - it felt like one of those questions we get here a lot where people seem to assume "scientists know (almost) everything" - but I decided to give a check anyways.

Short answer

There is in fact evidence that some insects could be scared to death. However, the process is a bit less dramatic than the one you suggest.

I didn't see much on mosquitoes specifically, but your question seems to allow extrapolation from other insects.

Longer answer

I found at least one paper, McCauley, et al. 2011, that studied whether the mere presence of a predator could cause fatal reactions, in this case in dragonflies. There are several others that show more generic stress-induced responses.

McCauley, et al. exposed dragonfly larvae to predators (either fish or a larger dragonfly) who were unable to actually eat the larvae because the larvae were contained within a 'cage' within a larger aquarium.

The larvae exposed to either predator type had substantially more mortality, and only about 30% as many survived to adulthood. This is not precisely insects being startled to death, but rather they propose that the chronic stress of predator exposure caused their growth to be impaired. An alternative explanation is that the larvae exposed to predators simply spent too little time eating to obtain enough nutrition, but they argue in their discussion that this is not likely to be the only cause in the case of the dragonfly predators, because unlike the fish those predators did not reduce their foraging behavior.

There are many other papers that talk about "non-consumptive mortality" more generally but these often include causes of death such as succumbing to injury from failed/incomplete predation, energetic expenditures, etc (Siepielski et al., 2014; Veselý et al., 2017) - few others actually use a highly controlled environment to prevent physical contact between predator and prey like in McCauley. Other studies do show that exposure to increased stress levels causes changes in gene expression and impacts on the immune system in insects (De Block & Stoks, 2008; Slos & Stoks, 2008).

On the point of mosquitoes, I did find one paper that showed reduced lifespan duration in adult mosquitoes exposed to increased predation as larvae (Bellamy & Alto, 2018) - again not exactly what you were looking for in terms of an acute event, but still somewhat related.

In summary

I think an important takeaway is that insects, like vertebrates, can be susceptible to stress.

References

Bellamy, S. K., & Alto, B. W. (2018). Mosquito responses to trait-and density-mediated interactions of predation. Oecologia, 1-11.

De Block, M., & Stoks, R. (2008). Compensatory growth and oxidative stress in a damselfly. Proceedings of the Royal Society of London B: Biological Sciences, 275(1636), 781-785.

McCauley, S. J., Rowe, L., & Fortin, M. J. (2011). The deadly effects of “nonlethal” predators. Ecology, 92(11), 2043-2048.

Siepielski, A. M., Wang, J., & Prince, G. (2014). NONCONSUMPTIVE PREDATOR‐DRIVEN MORTALITY CAUSES NATURAL SELECTION ON PREY. Evolution, 68(3), 696-704.

Slos, S., & Stoks, R. (2008). Predation risk induces stress proteins and reduces antioxidant defense. Functional Ecology, 22(4), 637-642.

Veselý, L., Boukal, D. S., Buřič, M., Kozák, P., Kouba, A., & Sentis, A. (2017). Effects of prey density, temperature and predator diversity on nonconsumptive predator-driven mortality in a freshwater food web. Scientific reports, 7(1), 18075.


Do the eyes play any role in producing the visual experiences you have during dreaming?

Your eye doesn't play a part in your dream aside from giving you the basic images which your brain later used to form the dream. The visual image in your dream comes from your brain itself.


Making an antibody-enzyme conjugate isn't trivial. By using a primary/secondary set-up you can use the same well-characterised conjugate in combination with many different primary antibodies (as long as these primaries are all raised in the same species). There is also the possibility of some amplification: for example, if the secondary is an anti-Fab then two secondary Igs will bind to each primary.

Response to OP comment

Most primary antibodies in common use are derived from rabbit or mouse, and most are IgG. So, for example, the secondary antibodies goat anti-rabbit IgG and goat anti-mouse IgG will cover most experiments.


What is Chronic immobilization stress (CIS)?

There are >1200 articles tagged "chronic immobilization stress" on pubmed.

From Hennebelle et al. (2012):

  Half of the 6-month old male rats from each dietary group were subjected to a validated chronic stress procedure (Buyntsky and Mostosky, 2009) based on a restraint stress procedure adapted from Veena et al, [32]. Rats were placed in wire mesh restrainers for 6 h a day (fom 10 am to 16 pm) for 21 days (5 days a week) over a period of 4 weeks. Unstressed rats were handled weekly. The unstressed and stressed animals were housed in different rooms.

Hennebelle, H., et al. 2012. Influence of Omega-3 Fatty Acid Status on the Way Rats Adapt to Chronic Restraint Stress. PLoSOne 7: e42142.


Is sexual desire stronger in men than women?

Some of the work of Bob Trivers makes some sense to me. He talks about parental investment https://en.wikipedia.org/wiki/Parental_investment.
The "investment" of a man could be as little as paying for dinner, followed by a few minutes of sexual pleasure, and then he is free to go. The woman's investment for the same thing is the risk of pregnancy (or cryptic STD). Pregnancy is difficult, and before modern medicine, was one of the most common ways to die for women. Then she must feed a helpless infant with her own body, and tend to its needs for the next 15 years. We have social structures for the man to stick around and contribute. But these are not biological differences. The man can leave. The woman cannot. She bears virtually all the risks of sexual behavior. Of course, sexual desires vary by individuals, likely in a bell-curve that overlaps (I anticipate some PC doofus pointing out that some women have strong desires, and some men don't). But I would not be surprised at all, given the biological differences in risks and investments between men and women, that the peak of these overlapping distributions is higher for men than women. Also, evolutionary fitness is defined by the number of offspring an individual can produce. A man's strategy is fundamentally different than a woman's. A man who has 1000 sexual partners is likely to leave more surviving offspring than a man who marries the woman he loves, and stays faithful. A woman with 1000 sexual partners would not be able to have hundreds of children, and would likely put her health at risk.


Is there any organism that is born with all the nutrients and resources needed for their entire lifetime?

You may need to clarify your question: As written, this would be the biological equivalent of a perpetual motion machine. No such organism could reproduce without either violating the first and second laws of thermodynamics, or ultimately evaporating into nothingness as it divides.


What does saying a phylogenetic tree is 'well resolved' mean?

It means incomplete separation or a failure to split into two groups unambiguously.

There are multiple ways to estimate the resolution of a phylogenetic tree; involving an index to measure the likelihood of observing the phylogenetic tree that you derive relative to those produced by drawing species at random, for instance, or permuting species to produce a null distribution.

A badly resolved tree should show up in sets of randomly generated trees far more often than well resolved ones.

See http://onlinelibrary.wiley.com/doi/10.1111/j.2041-210X.2012.00196.x/abstract


Is there a hypernym for enzymes that "cut" other molecules?

Hydrolases can "cut" other molecules using hydrolysis (see proteases), and Lyases can catalyze "cutting" with other reactions (see aldolases). These are umbrella terms for families of enzymes classified by function.

I think this is a fair open-access review of enzyme classification.


No, not all enzymes (or other proteins for that matter) can be obtained in functional form by recombinant expression with today's methods. As you suspect, problems arise when complex post-translational modifications are necessary to obtain the correct function.

Direct modifications to peptide is one potential problem. Some of these can be resolved by expression the recombinant protein in the right cell type: for example, expression in a bacteria may not provide the right modification, but expression in yeast or a mammalian cell might. CHO cells are a common mammalian cell type used in such cases; antibody production in hybridomas is another well-known example. But there are plenty of posttranslational modifications that are poorly understood, and most likely there are still many completely unknown types; new ones are still being discovered.

Another posttranslational event is association with cell membranes. Membrane proteins (including membrane-embedded enzymes, for example in lipid metabolism) can be very difficult to express properly, as not only the peptide but some surround membrane structure must be reproduced in the expression system to obtain correct function. This is also a major hurdle in obtaining structures for membrane proteins, notably many cell surface receptors. This article is a summary of the current challenges and unsolved problems in this area. And you can imagine the problems with proteins that need to form large superstructures to be functional --- large protein polymers, respiratory chain complexes, ribosomes, DNA replication forks ...

So there is no universal method; all proteins are different, some are easy to express, some are extremely hard.


Sparking during electroporation of plasmid DNA into bacterial cells

In my experience the elution buffer does not matter (both for E.coli and Mycobacteria). I have heard this before from co-workers, but it usually is based on superstition or anecdotal evidence. I have compared water/EB elution and never saw a difference in sparking (in fact, I usually get slightly more colonies with EB).

When I get arcing (sparks), it's usually because I did not wash enough, have bubbles or have to many bacteria. Arcing is a collapse of resistance.


How can I change the payload of a bacteriophage used to transform E. coli?

I am currently using a 'phage integrase' system to insert my gene of interest into P. putida and it is definitely a seamless process with high efficiency so I highly recommend it!
As for your question, the method through which we integrate the gene of interest using the phage integrase system is simpler than you think. We do not change the payload of a bacteriophage. We simply electroporate with two plasmids, one that expresses the BxB1 integrase and another plasmid that has our gene of interest that we want to integrate into the genome of P. putida. This integration is highly efficient, and it operates through a serine recombinase that recognizes specific attP and attB sequences in the plasmid that contains my gene of interest and native genome of my engineered strain. This method is significantly more efficient for engineering certain strains (typically non-model organisms) for genome integration purposes.
References for additional information on the system for your review:
Here is a paper that describes how we use the phage integrase system to effectively edit the genome.
https://www.sciencedirect.com/science/article/pii/S2214030116300438
Here is the paper that discovered and characterized the mechanism this system operates through.
https://www.sciencedirect.com/science/article/pii/S1046202310003142?via%3Dihub


Comparative effectiveness of antibiotics against colonies and growing bacteria

It depends on the kind of antibiotic. Some antibiotic are bacteriostatic  i.e. they primarily stop the growth while some are bactericidal i.e. they kill the living bacterial cells. Some antibiotics can have mixed effects. Bacteriostatic antibiotics would not be very efficient in eliminating a colony.

Apart from the mechanism of action, there can be other factors that would dictate the efficacy of the antibiotic; these can all be considered under pharmacokinetics/pharmacodynamics:

Degradation/clearance rate of antibiotic
Rate of diffusion of antibiotic inside the bacterial colony (this rate would be less when the cells are inside a big colony compared to when they are disperse).
Community organization and dynamics inside the colony (like user137 said in their comment, certain biofilms can be more resistant to antibiotics)


This is just a reference to the feeding groove - a morphological feature that groups these organisms. The presence of the term in quotes as "excavated" is an indication that the word is not meant to be taken literally. Quotation marks used like this are referred to as scare quotes - they are meant to alert the reader that the phrase in quotes is not to be interpreted by its standard meaning.

Instead, you could read the sentence as meaning:

  Some members of this diverse group also have a feeding groove on one side of the cell body, as if part of the cell was excavated.

One should not take the etymology of species names too literally - they are really just names. This is also true of common names of organisms.


Could someone please identify this species?

Looks very similar to Eupeodes corollae (Syrphidae). But only a specialist in the group will tell you if its the same species, genus or family. And not with that low-resolution photograph (sometimes they need to take the genitals off for proper identification).


Do nerves work as I think they work and what does that mean for our senses?

I'll attempt an answer, but please know you don't have a clear nor defining question to address. This is more suited for conversation or open discussion, and I recommend starting a chat on the topic. Please be wary the question may be put on hold. I'll give it a go and respond from the top down. I absolutely don't think this is going to be fruitful for other people. Here goes:

  Our ears have sensors designed to respond to sound. Each and every one
  has a direct connection to the brain via a chain of nerve cells. When
  one of the sensors is sufficiently stimulated, it zaps the neuron it's
  connected to, this in turn causes the neuron to zap the next one and
  so on all the way up to the brain.

Take the example of the eye; the retina is composed of photosensitive neurons, a type of sensory neuron. The inner nose is innervated with olfactory sensory neurons. The cochlea is similarly innervated by neurons. Firstly, you haven't made it clear that the neurons are the sensors. But indeed, the sensory neuron is the first order neuron. The processing of sensory information proceeds through first, second, third and higher order neurons until the information is integrated functionally somewhere in the brain. There exist neurons that modulate the signal along the way (e.g. lateral inhibitory interneurons) that are not on the information highway but rather beside it, regulating the input and output of neurons. It's quite complex, but you have the general gist of the hierarchy of neurons from sensory input (e.g. odor) to output (behavior, response, perception).

  The impulses/spikes themselves contain no actual information [...]
  Nerve cells work something like binary, they are either on or off with
  nothing in between.

The exact temporal dynamics of this communication highway between neurons is very important. At some level, auditory volume may be coded by frequency, but this is restricted only to some level. Information is very quickly encoded and the 'raw' information sensory neurons provides becomes processed and transformed quite early in the chain. For instance, you may trigger circuits responsible for reflexes, which are (so-to-speak) dormant until a kind of neural activity activates them. Vision is well described in terms of encoding; at the first processing area of the brain for vision, things are simple, and are progressively more high-levels of encoding as the information is processed; there are regions responsible for motion, color, object recognition, even specialized regions for the recognition of faces, for instance.

  If the brain didn't know where that chain was connected to then the
  signal could mean absolutely anything.

Correct. Remember though that the brain is very plastic, and can learn. There are many curious cases in neuroscience where this is apparent. One well-known widely described example: you can wear glasses that invert the world, and this would feel strange. After some time though, your perception would switch the world the "right way up". The retina has been largely unaffected, but the perception and the integration of the information can drastically vary quite independently.

  Is there something within the impulses that contains additional
  information?

Remember that there are two kinds of connections between two neurons. Electrical and chemical synapses. A wave of depolarization does indeed travel through a neuronal axis, but in most cases, this does not occur across neurons. Instead, neurons (and related cells such as glia) release chemical messengers (neurotransmitters and neuromodulators) that act as inter-cell signals. These can inhibit or excite the post-synaptic neuron. Simply put, it's not a string of wires; it's a line of wires that interface with each other chemically; at each interface, chemicals must diffuse across the gaps and interact with the membrane-bound sensors found on the receiving neuron. This is not at all binary. And please know we are simplifying the system in order to describe it.

  Is this exactly how nerves and perception work?

This is a simplification of how neural circuits work. How perception works is a completely different thing you have not even begun to address. This is a completely different topic of discussion. Bonus link!

  But most of all, does this mean there are things our senses cannot detect?

A sensory system can only detect what it can detect. Your skin cannot detect radio waves. Your eyes cannot detect infra-red light. Your mobile phone, similarly equipped with sensors, cannot detect neutrinos.

  I don't know the unit of measurement for sound

Decibel (volume) or hertz (pitch or frequency).

  What happens if we try to hear a 1.5 sound? Is it not detected by the
  ear because we don't have sensors in that range?

You are describing the spectrum of volume as a graded, discontinuous thing. It's not! And more generally, yes. If your sensors cannot detect something, the organism is oblivious to it. Obvious.

  Can we only sense something if we have a sensor for it [...]?

Yes. But you underestimate the power of a sensor such as a photosensitive cell. It can transmit information about the amplitude of the light, and responds to a range of light. Moreover, each photosensor has a response spectrum and does not respond equally to different (although similar) wavelengths of light. More so, if you have a patch of photosensitive cells, you can infer motion, direction, speed, size, distance, and all the merry things we associate with vision. The wealth of information is easy to underestimate.

  ... are those sensors only built to sense one ultra specific thing?

It depends on how you define specific. The equipment of a neuron in the retina is usually specific (e.g. expression of proteins responsible for light sensitivity) but it's possible to have a neuron that is responsive to several things. Have you ever tried to rub your eyes, and you see phosphenes? Your retina is responding to the increased pressure. You could say these cells are sensitive to light and pressure. That's not ultra specific. You can similarly activate these neurons at short range electrically, or magnetically. That's starting to sound like a pretty unspecific sensor, depending on how you define it for yourself.

I absolutely don't mean to aggravate, I very much suggest you do some readings on the topic. It's one thing to have a pub-level confidence in vaguely worded funfacts about sensory circuits, and another to understand and appreciate the nuances and complexity and the many knowns and unknowns of neuroscience. It's not too difficult to grasp. I would instead ask you to ask about fundamentals before you ask to correct your outlook on biological sensory systems. Books are cheap and the internet comes in handy sometimes, and you may even spare someone else's time!


It's camel spider, they have large pedipalps, big chelicerae, and their body is covered by little "hairs". As far as I know, there are only 2 families of that order in North America


Any nerves/fibers in foot similar to ulnar nerve in elbow?

Why would peripheral anatomy determine subjective sensation? In the end, the cerebral cortex determines the sensation associated with peripheral input. Rewired hamsters can have visual sensations in their auditory cortex (Frost et al., 2000) and visual sensations through tactile stimulation have been reported in man (Ortiz et al., 2011).

The sensations you describe are related to tactile stimulation of peripheral nerves. Peripheral nerves are pretty homogenous, and typically carry a bunch of afferent nerve fibers up to the somatosensory cortex.

References
- Frost et al., PNAS (2000); 97(20): 11068–73
- Ortiz et al., PLOSone (2011)


What is the advantage of the way eukaryotes initiate translation?

As far as I understand it (and I'll preface this by saying that initiation is not my strongest point), but prokaryotes utilize the beautiful AGGAGG Shine-Dalgarno sequence.  Usually around 8bp upstream of the start codon, it is this sequence that the prokaryotic ribosome seeks out to initiate translation.  It does this through a complementary region in the 3' sequence of the ribosomal RNA.  Upon complementary binding, the ribosome and mRNA are correctly bound.  Convenient!

In eukaryotes, however, there is no consensus SD sequence, so a different mechanism must be used; the complex of 40S and Methionine tRNA serves this purpose.  The two together scan the mRNA, looking for an AUG start codon which the tRNA is complementary to.  This eventually brings the full ribosome (40S + 60S) together to start translation.


Why are $\beta_2$ receptors present on bronchial smooth muscles , considering that they have only parasympathetic innervation?

Good question, but first I'll address a note in the comments.

In bronchial smooth muscle, do β2 receptors receive sympathetic innervation?

Canning and Fischer (2001) claim that bronchial smooth muscle do receive sympathetic innervation. But it would still be correct to say that β2 expression plays little role in regulating smooth muscle tone in the human airway under normal conditions.

How do β2 receptors cause bronchial smooth muscle relaxation?

You already know that this receptor is associated with bronchial relaxation. An article by Billington and Penn (2003) claims it works through Gs coupling. This binds adenylyl cyclase causing it to form cyclic AMP which activates protein kinase A (PKA) which carries out many more functions.

WHY are β2 receptors present on bronchial smooth muscles considering [minimal sympathetic] innervation?

Circulating chatecholamines released due to emotion, exercise and the like. Billington and Penn (2003) note "prophylactic bronchoprotection" as the central role for Gs-coupled receptors in airway smooth muscle.

Why ELSE are β2 receptors present on bronchial smooth muscle?

β2 receptors are important in regulation of airway smooth muscle cytokine/chemokine synthesis, and inhibition of airway smooth muscle growth (DNA synthesis/cell proliferation) i.a. (Billington and Penn 2003).


Are synaptic boutons always located on axons?

Axonal boutons are named as such due to their shape. Dendro-dendritic synapses do not resemble this shape and are never referred to as boutons. It does not appear that synaptophysin is expressed on dendrites (Fletcher et al. 1991), but I am unaware of a study that targeted dendro-dendritic synapses specifically.

References
Fletcher, TL, P Cameron, P De Camilli, and G Banker. ‘The Distribution of Synapsin I and Synaptophysin in Hippocampal Neurons Developing in Culture’. The Journal of Neuroscience 11, no. 6 (1 June 1991): 1617. https://doi.org/10.1523/JNEUROSCI.11-06-01617.1991.


Why would the Camargue horses have a white coat while the foal have a dark coat?

Our own hair will also turn gray (indeed, yours seems to be on its way, if you don't mind me saying so) but there need not be an advantage to that; if it doesn't affect our ability to have successful children it probably doesn't matter much to evolution or selection.  When it comes to animals that interact with humans, though, many traits are selected for, even those without an advantage, in fact often we select for disadvantageous traits (if they were advantageous, we might not need to select for them in the first place).

As this 2008 paper from Nature Genetics goes into, the "graying with age [phenotype] is an autosomal dominant trait" overwhelmingly caused by "a 4.6-kb duplication in intron 6 of STX17 (syntaxin-17) that constitutes a cis-acting regulatory mutation".  To answer your question, though:

  The Gray horse provides a notable example of how humans have cherry-picked mutations with favorable phenotypic effects in domestic animals... The prestige of riding a white horse has thus led to selection of the Gray-causing mutation by humans; this mutation is by far the most common cause of white color in horse.

This phenotype is actually often detrimental, as white/gray horses can have eye problems and higher rates of skin cancer; Camargue's are particularly susceptible to melanomas, present in around 70% of horses by age 15.  There does seem to be some benefit, though, as the second paper I linked suggests these horses are subject to fewer fly attacks.

EDIT: I seem to have been unclear and you seem to have misunderstood my answer.  Let me break it down:

Camargue horses are gray.
Gray color is a simple mendelian autosomal dominant phenotype caused by a loss of pigment in adulthood.
Gray color is generally bad but sometimes good; either way, it's probably not a huge detriment.
Camargue horses are homozygous for gray color.
Humans have in the past selected for gray color in horses in general.

That is an example of why something negative or pointless might persist, as would a dominant inheritance pattern that is fixed in a population: negative traits that are only weakly deleterious have a non-negligible chance of fixation.  Asking what the advantage is is somewhat of a moot question because every single Camargue horse has the trait; asking what caused a seemingly-negative phenotype to become fixed is a good question, but likely an unanswerable one as it occurred long ago.

As a side note, how long a breed has been in an area does not simply imply breed purity.  Here's a quote from the International Museum of the Horse:

  Through the centuries many armies have passed by the Camargue, including the Greeks, Romans and Arabs. The horses brought with these armies influenced the Camargue over time. It has even been suggested that the Camargue has had some influence on the early breeds in Spain as armies took them back home.


Why do our eyes "wrap" hue from UV to IR?

Basically.  You are most likely looking at the electromagnetic spectrum, which is linear and conveniently makes sense... except for magenta.

Colors as we perceive them are additive and made up of Red, Green, and Blue; this is opposed to subtractive color we learned about while finger-painting in kindergarten (Red, Yellow, Blue).  The three types of cones in our eyes each are sensitive to one of these colors, and it is from the combinations of Red, Green, and Blue that we see all the colors we see.  Yellow, for example, is when the red and green cones are both stimulated.  Purple/violet is from red and blue stimulated together.  This is the single special case, as you point out, because red and blue are at opposite sides of the spectrum from each other.  Our brain has two options:

Use the color smack-dab in the middle aka Green
Make a new one as if they wrapped around

Green is far away and already taken, so our brain intelligently invents Magenta.  This produces, instead of a linear EM spectra, a circular color wheel that looks very intuitive.


What you do not want to do is prep all your control samples on one day, and all your treated samples on another day, because you will not be able to separate differences caused by treatment from differences caused by batch effect.  I'd worry more about that than from cross contamination.  Since you probably aren't comparing the different tissues to each other, batch effect between tissues won't be much of a problem.  So do all your spleen samples, treated and untreated, on one day, all your kidney samples the next, etc.


Snail species identification from the United Kingdom

This snail is Cornu aspersum its common name is garden snail, it belongs to Helicidae family click here for more information


What is the largest species of polychaete?

According to the Smithsonian:

The longest of all known polychaetes was found in Port Jackson, Australia. It was a member of the family Eunicidae, consisted of approximately 1,500 segments and was nearly 6 meters long when alive.

The Eunicidae consist of numerous species (including the super cool bobbit worm), many of which get fairly large.

Though, typically 3 m in considered quite large for worms in this group (e.g., see Uchida et al. 2009 for a description of a 3 m long Eunice aphroditois).
Polychaetes & Allies: The Southern Synthesis also suggests that members of Eucinidae can reach 6 m in length. From p. 94 of this report from the Australian Biological Resources Study:

Eunicids have many segments and may attain a length of up to 6m...
...Eunicids range from less than 10cm to 6m in length, and consists of up to 1500 segments (Fauchald 1992a).

Supposedly, according to Schulze 2011:

The Australian museum even holds a specimen that reportedly was nearly 6 m long when
collected (Fauchald 1992 and pers. comm.)

Salazar-Vallejo et al. (2011) also cite evidence of 3+ m long polychaetes in the genus Eunice as evidence that the genus is "the largest polychaete species and placing them among the longest benthic invertebrates."

None of these worms compare to a species of ribbon worm (phylum Nemertea) called Lineus longissimus that can reach 55 m in length! [Sources: 1, 2].


About validation process of phenological study

idea 1) It's possible that some subset of your area has higher-scale / better resolution aerial photographs available. Could you find these and use them to test your model?

idea 2) What geographical area / timescale are you looking at? For certain areas/times, you can get a bit of data on phenology from dated herbarium specimens (ie pressed plant collections). So, for instance, you might select a few plant species that you think are good indicators of whatever phenology you're modelling, search for them on GBIF, consider only those specimens that match your geographical area, and look at what time of year the collections have been made. Then you could look at the first, or last, or various quantiles of phenology. It's not ideal data, but each specimen represents a very direct data point (that is, you know there was at least one individual that had flowered / leafed / whatever at that exact date and georeference), and it's available without getting your feet dirty.

idea 3) Again depending on your geographical area and what measure of phenology you're interested in, you might even be able to use non-aerial photographs, if they're dated.


Is there a record of species kept in zoos worldwide and number of individuals? If yes, can one have access to it?

A potential data source could the data base that stores zoo animal data, where the most comprehensive (to my knowledge) is Species360 ZIMS (Zoological Information Management System). It contains animal records and current breeding programmes, but also information on how to care for animals (best-practices and studbooks).

In your case, the ZIMS for Studbooks module should be relevant, which contains:

  ZIMS for Studbooks improves Studbook Keeper efficiency and record accuracy with suggested animals, notification of records updates, and extensive data quality tools. [...] enabling users to conduct intensive population analysis, improving species and conservation management

However, I do not have access to the data base myself, so I cannot say how accessible the data is. If you are connected to a zoo, teaching institution or research facility you can however apply for access and a membership, but I don't know the specifics of this process (or possible costs). It might be worth checking out either way.


What is the "male gender rudiment" that women allegedly have?

First, let's briefly discuss the development of the the male and female internal genitalia and sex glands:

These include the ejaculatory duct, prostate and seminal vesicles for males, and uterus, uterine tubes and the proximal part of the vagina for females.

They all develop from two tube-like structures called mesonephric and paramsonephric ducts.

These ducts initially exist in both males and females, but normally, only one develops while the other degenerates, depending on the presence of sex-determining factors and hormonal activity.

The mesonephric ducts will develop to the male internal genitalia (the organs are mentioned above), while the paramesonephric duct will develop to the female internal genitalia (also mentioned above).

Now, to your question:

A male rudiment that exists in females is the non-fully degenerated mesonephric duct, named the Epoophoron and Paroophoron in adults, which later in life may form the Gartner’s cyst.


The notation at this site resembles that in your question but preserves the $\frac{x_t}{2N}$ notation for probability of selecting an allele.

$$E[\frac{x_{t+1}}{2N})(1 - \frac{x_{t+1}}{2N} )|x_t] = (\frac{x_{t}}{2N})(1 - \frac{x_{t}}{2N}) (1 - \frac{1}{2N})  $$

The expression $(\frac{x_{t}}{2N})(1 - \frac{x_{t}}{2N}) $ is the probability of heterozygosity at step $t.$

Your expression says that the expected heterozygosity at step $(t+1)$ is equal to the heterozygosity at step at $t$ multiplied by $(1-\frac{1}{2N}).$

For a population of size $2N,~(1-\frac{1}{2N})^{2N}\approx 1/e,$ so large populations are insulated from this effect and small ones may lose genetic diversity rapidly.

A typical explanation can be found here. The notation at this site condenses the expression $(\frac{x_{t}}{2N})(1 - \frac{x_{t}}{2N}) $ to $H_n$ and explicitly says it is $1 - F_n, $ in which $F_n$ is the probability of homozygous at step $n.$


Genes, conventionally, are always written in italic (e.g. SHH) which is not the case for proteins (in the former example SHH). That should allow you to tell apart gene and protein symbols (SHH vs SHH).

The capitalization of gene/protein names is a bit more in the grey area. Usually one will use capitalized gene and protein symbols for human and primates (e.g. SHH and SHH) and use non-capitalized symbols for mice and rat genes (e.g. Shh but still SHH for the protein). This is dependent on the organism and journals usually have specific guidelines on how to exactly write gene and protein symbols.

In your case the article refers to Rab6, Vps53 (not 35) and TNPO3 as proteins, if not clearly stated differently, such as the Rab6 siRNA, not only in the abstract alone but over the entire article. They use italic names for genes as shown in one of the sentence:

  ... and 48 hours later staining for p24, produced from the HIV gag gene...

Just as a footnote, full gene names (e.g. the sonic hedgehog gene) are not italicized.


Why human body cannot defend against HIV?

There are two main components of the immune system that are involved: Antibodies and T-cells.

T-cells are responsible for activating white blood cells to help fight off infection. These are the cells the HIV infects. Antibodies bond to the HIV virus and try to neutralize them before they can infect more cells. Unfortunately as the HIV virus replicates, there is too much virus and not enough antibodies to neutralize.

When a T-cell becomes infected with HIV, the virus takes over and causes it to start replicating more HIV. This eventually causes the T-cell to die. So T-cells keep dying while HIV loads keep increasing. When enough T-cells die, the infected person is considered to have AIDS.

It is particularly difficult for the immune system to fight off HIV infection for a number of reasons, including the following:

HIV attacks the immune system itself, weakening its ability to fight back.
HIV replicates in large quantities that are more than the compromised immune system can handle.
HIV has the ability to mutate (change itself) very quickly, making it more difficult for the body to fight the infection.

So conclusion, our bodies can fight HIV for awhile. It's just a matter of time before the viral load outweighs the capabilities of our immune system.


Why doesn't telomerase activity cause DNA to get longer each time a cell undergoes DNA replication?

I will assume that you are referring to humans, though much of the research to elucidate telomerase function was performed in yeast.

The first reason is that only a small subset of somatic cells express telomerase. Most somatic cells are terminally differentiated and mitotically inactive, so they are not called upon to replicate their DNA and divide. And when they do, their telomeres get shorter due to the 3' end replication problem.

The end replication problem arises due to the biochemical limitations of DNA Polymerase. Pol requires a primer, 5' to 3', in order to bind to the template strand and begin to catalyze the elongation reaction. So when DNA Polymerase gets to the 3' end of the template strand, it is unable to catalyze the reaction because it doesn't have a free 3' hydroxyl. When the end RNA primer that was used to catalyze the Okazaki fragment just before the 3' end is removed, there is no place left on the template strand to prime, so there is no 3' hydroxyl to begin the elongation reaction and you are left with a 3' overhang of single-stranded DNA.

On the 5' end of the Template Strand, even though the polymerase is able to catalyze the reaction all the way to the end, the end of the chromosome is processed and nucleotides are removed to make a single-stranded 3' overhang on this end. The overhangs are necessary to do strand invasion to form the T-Loops of the telomeres. So every time a chromosome in a cell that has inactive telomerase replicates, it gets shorter.

For the cell types that have telomerase actively express, such as lymphocytes, partially-differentiated stem cells, and the precursor cells to sperm, there is a negative feedback loop based on the length of the telomeres, which in turn regulates the activity of telomerase. Telomerase maintains the ends of the chromosomes, especially in these mitotically active cells, but it will only elongate them to a certain point.

  It has long been known that telomere length is regulated by a negative feedback loop (reviewed in Smogorzewska and de Lange, 2004). Long telomeres contain more negative regulators that limit further telomere elongation by telomerase. Because of this, the enzyme preferentially acts on the shortest telomeres in the cell (Hemann et al., 2001; Zhu et al., 1998).
  - Loayza, et. al.; Cell; Volume 117, Issue 3 30 April 2004


Are flowers / flowering plants vital to all life on Earth?

Angiosperms -- that is, flowering plants -- only evolved relatively recently on an evolutionary timescale, about 125 millions years ago. So for most of the history of life on earth there have been no flowering plants. Thus it seems highly likely that if angiosperms were to suddenly disappear, life on earth would continue. There might be a massive disruption of current terrestrial communities, but it's hard to imagine this resulting in total global extinction. In particular it seems unlikely that ocean communities would be undermined by the loss of flowering plants.


Do spinal cord reflexes (such as the knee-jerk reflex) continue to function under general anaesthesia?

The issue is complicated. In general it depends on the specific spinal reflex and on the specific anaesthetic. But it seems that the modern general anaesthetics usually do NOT block monosynaptic spinal reflexes (such as knee-jerk).
Here are two figures from Baars et al. 2009  that show that propofol and sevoflurane strongly inhibit withdrawal reflex (spinal two-synaptic reflex) but have almost no effect on the H-reflex (spinal monosynaptic reflex closely connected to the stretch reflex):

See below for many more details. Disclaimer: I know very little about anaesthesia and am simply writing down what I found after a couple of days searching and reading.

Withdrawal reflex
As @AliceD wrote, withdrawal reflex (a two-synaptic spinal cord reflex) usually disappears under any anaesthesia and this disappearance is used as a clinical sign of anaesthesia being deep enough for the surgery. As an example, this handout on monitoring anaesthetic depth in rodents has the following entry on the list of criteria for surgical anesthesia:

Withdrawal    reflexes    are absent! Try at  least   2   toes    and the ears    so  that    you are  sure   that    this    reflex  is  absent.

Knee-jerk reflex: early history
On the other hand, it is known from the XIX century that stretch reflexes such as knee-jerk (note that they are monosynaptic) are very persistent. They can be abolished under some drugs (such as e.g. chloroform and ether) that act directly on the spine, but keep working under others. I am quoting from three old papers on the topic (here and below emphasis is mine).
Horsley, 1883, Note on the patellar knee-jerk:

In 1881, while experimenting (on myself) with this gas [nitrous oxide] for
a different purpose, it occurred to me to contrast the conditions of the superficial and deep "reflexes," taking the
plantar reflex as an example of the former, and the patellar
phenomenon to illustrate the latter. Being aware of the fact
that deep chloroform-narcosis abolishes all the "reflexes,"
superficial and deep, and yet that with ether-narcosis, however deep, ankle-clonus frequently, appears, I was scarcely
surprised to find that the knee-jerk persisted in the deepest
anaesthesia from nitrous oxide, while the superficial reflexes
all disappeared.

Sherrington, 1892, Notes on the arrangement of some motor fibres in the lumbo-sacral plexus (p 671):

With regard to the effect of anaesthetics on the "jerk," a better proof of
the action of chloroform being rapid and direct on the nervous mechanisms of
the cord itself could hardly be found than in the speedy abolition of the
"jerk" by chloroform inhalation when the cord has been previously divided
in the thoracic region.

Simpson & Herring, 1905, The effect of cold narcosis on reflex action in warm-blooded animals:

The knee-jerk is a very persistent phenomenon. It is known to disappear in deep anesthesia produced by ether or chloroform [Sherrington 1892]. [...] The knee-jerk is as a rule easily elicited, and we find it present when
all the reflexes have disappeared. [...] The lower the
temperature the smaller the jerk. [...] In several animals that died at a low temperature the disappearance of the knee-jerk was simultaneous with death [...] The lowest temperature at which we found the knee-jerk present was 15° C., and this
was also the lowest temperature at which any of our animals were
still alive. [...] Pinching the skin does not provoke any response till the temperature is 25° C. [...] We have compared these results with similar ones obtained from
cats in recovery from deep ether anesthesia and find that the order of
reappearance agrees very closely.

Modern studies in animals
Hara & Harris, 2002, The Anesthetic Mechanism of Urethane: The Effects on
Neurotransmitter-Gated Ion Channels mention in the abstract that

Urethane is widely used as an anesthetic for animal studies because of its minimal effects on cardiovascular and respiratory systems and maintenance of spinal reflexes.

(they don't specify which reflexes specifically).
Ho & Waite, 2002, Effects of Different Anesthetics on the Paired-Pulse Depression of the H Reflex in Adult Rat study the effect of five different anaesthetics (ketamine, halothane, etomidate, saffan, and nembutal) on the Hoffman reflex (H-reflex), a monosynaptic reflex similar to the stretch reflex. They report that it keeps working under all five drugs, but the drugs modulate the decrease of the reflex under repeated stimulation (this decrease depends on the descending controls and is affected differently by different drugs):

The  results  suggest  a  preferential
action  of  some  anesthetics  on  descending  pathways
involved in reflex modulation [...]

Strangely, Ho & Waite do not describe how anaesthesia affects the reflex strength following an unrepeated stimulation, but in any case it is clear the the reflex keeps functioning.
Propofol etc.
What about the anaesthetics widely used in humans, such as e.g. propofol? Matute et al., 2004, Effects of propofol and sevoflurane on the excitability of rat spinal motoneurones and nociceptive reflexes in vitro:

We used an isolated spinal cord in vitro preparation from rat pups and superfused the anaesthetics at known concentrations. [...] Applied at anaesthetic concentrations, [...] sevoflurane produced a large depressant effect on the monosynaptic reflex whereas propofol was ineffective. [...] Sevoflurane produces large inhibitory effects on nociceptive and non-nociceptive reflexes which are likely to contribute to immobility during surgery. Compared with sevoflurane, propofol appears to have much weaker effects on spinal reflexes such as those recorded in an isolated preparation.

Kerz et al., 2001, Effects of Propofol on H-reflex in Humans:

Previous studies of motoneuron excitability using H-reflexes or F-waves during general anesthesia found significant depression after administration of halothane,  enflurane, isoflurane, desflurane, or nitrous oxide. [...]
Recommended propofol doses for induction and maintenance only had a transient effect on the H-reflex and were no longer demonstrable after 10 min of propofol anesthesia. [...] Immobility during propofol anesthesia [...] does not seem to be caused by a depression of spinal motoneuron circuit excitability.

So why is then the withdrawal reflex so easily abolished and the stretch reflex is so persistent (e.g. under propofol)? This does not seem to be well understood. Baars et al., 2009, Effects of Sevoflurane and Propofol on the Nociceptive Withdrawal Reflex and on the H Reflex write

Both H reflex and nociceptive withdrawal reflexes are reduced dose-dependently by propofol and sevoflurane in humans. [...] We have shown a striking difference of the degree to which both reflexes are reduced by the two anesthetics. The relative reduction of the polysynaptic RIII reflex amplitude was more than four times higher than that of the H reflex. This difference can probably be attributed to the higher number of neurons interposed in the RIII reflex pathway in comparison to the H reflex.

Note that the last sentence is very vague; it says that the difference is "probably" due to monosynaptic vs. polysynaptic mechanisms of these two reflexes but does not offer any explanation. Withdrawal reflex is mediated by an excitatory interneuron and propofol acts on GABA (which is inhibitory transmitter), so it remains unclear. This study is from 2009 and I did not find anything relevant in the papers that cite it.


What is the physiological difference between cortisone and cortisol?

Cortisol is directly given to the patient - it is then called Hydrocortisone. I don't know why this is done but probably to avoid confusion because both names are too similar.

The difference between both forms is one hydrogen atom at the C11 position of the molecule in Cortisol (or Hydrocortison) (image from here):

Otherwise is Cortisol (or Hydrocortisone) the active version, while Cortisone isn't very active in the human body.
Both forms can enzymatically turned into the other form (from active to inactive and vice versa). Since Cortisone needs to be activated in the liver, it can only be used for oral uptake. Most of the uses which are colloquially called Cortisone in fact contain Hydrocortisone.


Yes, neurons can be modeled as magnetic dipoles.  In fact, that is the basis of MEG.  Here is an example of a paper that instantiates a computational model of magnetic dipoles in order to explain MEG data Neural mechanisms of transient neocortical beta rhythms: Converging evidence from humans, computational modeling, monkeys, and mice.


Rephrasing your question
Allow me to start by saying that I barely know the term Hadeeth / Hadith mean. Of course I have checked on wikipedia but its definition is vastly unrelated to any concept in science. I think it won't be necessary for me to use this term, I will use a more classical, scientific terminology. As I barely understand the term, I do not really understand your question phrased as

Do you believe this hadeeth based on the experiment?

I can however answer to the questions

Is this document a fair description of a natural phenomenon?
Is this document contribute to our understanding of a scientific phenomenon?

The answer to both of these questions are "absolutely not"!
Lack of methodology and definition of the expectation
The document is extremely unclear, provides a very poor description of the methods and does not provide any suggested interpretation of the results. After reading it several times, I have little idea what the treatments are.
Note that this document is not peer reviewed and does not follow an appropriate format (no introduction, no method section, just a religious quotes, a citation from the Quran and images with a vague legend). It is just a document that someone wrote and uploaded online.
As @BryanKrause perfeclty said in the comment below

[I]n science the burden is on the person making a claim to defend it and provide appropriate support - there is no point in proving a claim true or false if it lacks documentation of the methodology. Being poorly written in terms of lacking adequate description is hardly better than lacking any experiment at all

In short, this document does not make any contribution to our understanding of a natural phenomenon.
The claim is very unlikely to be true
The expectation implicitly suggested to be tested is something like (my own phrasing)

If a fly barely touch (with one wing only) the media, then the media will be full bacteria but if the whole fly (with both wings) touch the media then the media will remain clean.

This expectation is highly unlikely to be true. If it were to be true, it would probably lead to a major revision of our understanding of microbiology or of the biology of flies (whichever species is considered)! Also, there is no reason to expect that in some petri dish only one bacterial species would have invaded, while in another only another bacterial species. Also, the pictures don't really match what the species described IMO. Hence, if the authors claim that this document report the results of a scientific experiment (I am not saying they make this claim), then I very much think this is a case of scientific dishonesty or at least a case of very poor understanding of how to perform a scientific experiment.


Why does not the host produce any immune response to antiserum antibodies?

That's a good question - because its certainly possible to get antisera against antibodies.

Sometimes antisera is actually human antisera, so there would be no rejection at all.  But that is for extreme cases, e.g. serum transfusions from convalescent Ebola survivors to current Ebola patients.

One would expect that you could only give an antiserum once and then it would be less effective each time you get it.  Since antisera to snakebites is the most common application, where its quite possible to be exposed to multiple bites over one's lifetime.

I found one reference to a horse antiserum treatment that's being used. It makes reference to a source of antiserum which sounds like its been designed to reduce the antibody antibody immune reaction:

  Horse-serum antivenin has been available since 1956; a purer antivenin with improved properties was released in 2000 (see Medication). With the reduced side-effect profile of antigen-binding fragment antivenom (FabAV) and the improvement in tissue injury with antivenin administration, the threshold for dosing is lower.

Even before the availability of these new treatments, its probable that most patients can endure multiple anti serum treatments from the same source animal.  Even goat, horse and rabbit antibodies are pretty similar to ours and the reaction will not be as strong, in addition to which, the immune system will tend to clear out the antigen-xenoantibody complexes from the blood.

I can't find references, but my guess is there must have been some cases of rejection and reaction otherwise they would not have bothered to improve the serum treatment.

Update: just read this little blurb in scientific american, that describes how venom antisera will occasionally cause deadly reactions, while most of the time simply disarming the venom.  The new generations of antivenoms described have the Fc portion of the antibodies removed.  This eliminates the adverse immune reaction but I also think also eliminates any immune resistance the patient might get out of the antisera.  The Fc portion of the antibody is the part which our immune cells bind to.  In this case the new antivenoms aren't anti sera exactly, but they do use the antibodies to deactivate the venom toxins and crosslink them to make them less effective.


Part of this depends on the exact nature of "salt depletion" you're referring to. I have never actually heard of a case of hyponatremia being caused by low consumption of salt. We don't need to consume NaCl. It's present in the foods we eat in adequate amounts. We may want to salt our food, but it's not necessary for life.
Hyponatremia is an electrolyte imbalance, be it due to excess intake of H2O, inappropriate H2O retention, excess Na+ loss, hyperglygemia or other osmotic force, or other cause. For ease of explanation, I'll address acute hyponatremia, as it leads to death more rapidly. Hyponatremia kills because of the difference in the concentration of sodium across cell membranes.
Normal serum Sodium (Na+) is ~140mEq/L. Acute severe hyponatremia occurs when serum Na+ falls rapidly below 120 mEq/l (some authors use 125mEq/L) in less than 48 hours.
Water accounts for 60% of total body weight, with approximately two-thirds being intracellular and one-third extracellular; of that extracellular water, ~75% is in the fluid between/surrounding cells, and 25% is in blood vessels. Distribution of water/Na+ throughout the body is very tightly regulated.
When serum sodium falls too low, free water moves from areas of lower concentration to higher (into the cells). Tissue becomes edematous.  While this isn't a great problem for some tissues, it is for the brain.
The brain is enclosed in a rigid compartment (the skull) with a small amount of fluid (cerebrospinal fluid, or CSF) surrounding it. Inferiorly, there is an small opening called the foramen magmun, where the brainstem leads to the spinal cord.

When water moves from the blood into the cells of the brain attempting to establish osmotic equilibrium, the brain compensates for the increase in volume by forcing CSF out. This buys some time, but not enough; there is headache and nausea. As the brain continues to expand, intercellular fluid is forced out into CSF (which is being displaced by the brain.) This causes hyperexcitability which leads to seizures. In the meantime, astrocytes swell. Blood flow to the brain is reduced because of increased intracranial pressure, which further damages the cells, increases cellular edema and coma ensues.
If this isn't bad enough (it is; it's an almost irreparable  cascade of events), the edema can actually "push" the lower part of the brain down through the foramen magnum resulting in brain stem compression and respiratory arrest. At this point, few people make it back intact with even the best help.
You say,

Basically with too little sodium, it goes from bad to worse until the heart and lungs are affected and the person dies.

Not really. In acute hyponatremia, the brain goes before the rest. Once the brain goes, so follows the body.
in layman's terms
not layman's terms but still easily understandable


Which cells release inflammatory mediators?

There are several kinds of inflammatory mediators. You can broadly classify them as cytokines (including interferons) and chemokines.

Cells which sense antigens (or pathogen associated molecular patterns) do secrete cytokines, as you said but infected cells also secrete some cytokines like interferons- α and β. Infected/injured cells also secrete chemokines that attract leukocytes to the site of infection/injury (Saiman and Freidman, 2012).


Correct migration rate expression in infinite island model

Definition of $m$

There is no correct or wrong expression. It all depends what exactly you are interested in and what is the definition of m in a specific paper.

Def. 1

Some models assume that $m$ is the migration rate from a given population to another given population.

Def. 2

Some models assume that $m$ is the probability of migrating to any other population. In a two population case, this definition and the above are the same. In other case, the probability of migration to a given population is $\frac{m}{d-1}$

Def. 3

Some models assume a migration pool. With probability $m$ an individual is a migrant, goes to the migrant-pool and is then redistributed among all other populations (only works for island models). In such model, a migrant could be an individual that actually come back to the same population. So, the probability of really migrating is $\frac{m (d-1)}{d}$ and assuming equal migration rate among all populations, the probability to migrate to a given population is $\frac{m}{d-1}$.

Fst

If you're dealing with $F_{ST}$ in a finite island model, then you will have some $\frac{m d}{d-1}$ terms. I talk about it in this post but it is not complete, so you might want to read Slatkin (1991) and Charlesworth (1998)


Is happiness or pleasure an evolutionary programming for survival?

Our current understanding is that pleasure is one of the major ways your brain gets "you" to do things, it is the basis of positive reinforcement of behavior and associative learning. It can almost be thought of a a tag for an individual behavior that says "do this again/more". That pleasure alone can motivate animals to do things has been understood since way back in the Skinner box experiments where a wire to the pleasure center was inserted in rats and said rats would keep doing whatever behavior they associated with stimulation via the wire foten to the exclusion of all else. The basis of our learning could be summed up as do things that elicit pleasure, don't do things that elicit pain. tying many complex behavior to a single signal seems to make it easier to control and even prioritize very complex behavior, just do whatever yields the most pleasure, of course humans and many other animals have many more competing emotions and other factors, like metacognition. But for simpler animals it is easy to see how this system is efficient, it is easy to tag new behaviors or experiences into this system, at its simplest form just connect (possibly inhibitory)a few neurons triggered by the behavior or memory of the behavior to the pleasure center.

Of course it is not perfect, few things that evolved are, behaviors that are not beneficial can trigger the system, especially novel or extremely rare behavioral options, especially ones created by technological advancement, drug addiction being a great example. Evolution is very poor at preparing organisms for novel conditions like the modern technological world. And the our brain did not evolve under conditions where cocaine (as an example) existed. Just because something is pleasurable does not mean it is beneficial.  The full range of behaviors that can elicit pleasure would be well beyond the scope of a single question but it is quite clear pleasure itself is an evolutionary advantage, it is one of the major reasons we learn to eat, drink, reproduce, and make social connections.

Happiness, is more difficult, mostly because it is a poorly defined term in biology, it is unclear if it is distinct from simple pleasure.