Do I not have any alleles from my mom's mom & my dad's dad?

Speaking of your DNA in general, you have alleles from all four of your grandparents.  The 22 pairs of autosomes (non-sex chromosomes) can receive DNA from all four with random mixing.  On a few chromosome pairs you may be missing alleles from one of your grandparents due to the randomness, but on average you will have about a quarter of your autosomes from each of them.
The X (and Y, for males) chromosomes are special, though.  The X you inherit from your mother will have alleles from both your maternal grandparents.  The X that you, as a female, get from your father has no alleles from his father, so that grandfather's X alleles are always missing from your genome.
Because of the random mixing, you will have slightly varying amounts of DNA from each of your grandparents: it won't be exactly 25% for each of them.  Because of the special X inheritance, your paternal grandfather will on average contribute slightly less than the other three grandparents.  (Because of another quirk, mitochondrial inheritance, your maternal grandmother will contribute on average a very small amount more than the other three grandparents.)


What are the implications of tigers being susceptible to SARS-CoV-2?

A partial answer, to the question of how the virus might spread to animals I found several references

The HongKong dogs, the New York tiger, the Netherlands mink farm and the French cat have been sequenced and can be seen on nextstrain. Note the low amount of mutations in each case, which is intriguing because we expect for example that different ACE2 genes will induce some adaptation at in the viral spike. Those animals had an infection and detectable RNA in the nose for several days. For the dogs the viral load was low and in one case the sequence was identical to the owner. The minks and tiger had noticeable symptoms. A Wuhan cat partial sequence has been uploaded too, as well as a full-length French cat sequence.

A lab paper said "SARS-CoV-2 replicates poorly in dogs, pigs, chickens, and ducks, but efficiently in ferrets and cats", in particular dogs can't transmit the disease efficiently. According to them subadult cats are susceptible while adult cats are not, and the disease is upper respiratory tract.
There is a new preprint on a 4 month cat who developed severe disease, dyspnea, and had to be euthanized.

A paper found antibodies in several Hubei cats from animal shettlers and vet clinics, some of the positive cats are "stray cats", others are sick cats, and a few were cats owned by covid positive people, in those the antibodies were found to be neutralizing the virus much better than in others.

Another one found that ferrets are efficiently infected in lab and transmit the disease to each other, even if it is mainly upper respiratory tract (no severe pneumonia).

Rabbits are susceptible though less than ferrets, and asymptomatic.

Mice are not succeptible but human-ACE2 transgenic mice are and develop a mild pneumonia. Note that SARS-CoV and OC43 produced instead a deadly encephalitis.
However, through 6 ($10^{5.8}$PFU) passages into mice lungs the researchers could adapt SARS-CoV-2 through acquisition of a single mutation in the RBD allowing the virus to produce a moderate pneumonia into both young and aged mice.
The same researchers after 30 more passages obtained a super-deadly mouse adapted strain effective even at $10^2$PFU with 3 mutations in the RBD and 9 others mainly in nsp3-4-6 and N. Of note, two of the RBD mutations are in the South African variant N501Y.V2.
Something similar had been done with SARS-CoV.

The Baric lab has compared the RBD from SARS-CoV-2 and previous sarbecoviruses,
the human and mouse ACE2 protein, and through computer simulations they could find two amino acids to change in order to switch the virus from humans to mice. With 10 more passages they obtained a deadly strain in aged mice.

There are several mink farms in Netherlands where the animals got infected, this is possibly the most promising species for inter-species transmission. Edit : as predicted (first reported case) of animal to human transmission is believed to have occurred in such a mink farm. A detailed story including severe pneumonia is described in a paper.

In lab, SARS-CoV-2 is provoking a severe disease in minks as well as in Roborovski dwarf hamsters.

The Pangolin outbreak(s) : not SARS-CoV-2 but the newly discovered Pangolin-CoV in the same lineage, it killed 16 of 21 Malayan pangolins in March 2019. The virus was identified only in February 2020. The Pangolin-CoV whose RBD is very similar to SARS-CoV-2 was in this outbreak.

Cats can transmit the virus to each other. In the nose the peak was $10^{4.5}$ PFU / ml which is a medium viral load.

Similar for hamsters and macaques, the latter are used for vaccine development.
Racoon dogs show high shedding and can transmit the virus through present only minor clinical signs.
This kind of result is not surprising, most human viruses can transmit to some species and not to others, often producing a different and milder disease, which is a problem for vaccines and antibodies development.


It doesn't seem like you need the 31.45 hemoglobin number (which is good because no units are given:

5ml * 34g rbc /dL * 1 dL/ 100 ml = 1.7 g rbc

would fall out from unit analysis


Green Film Build up in Glass Water Bottle

What seems to be forming in reusable water bottles and water coolers is a biofilm. Since it is a complicated system, after maturation biofilm might be very hard to remove without scrubbing. There is a nice article about cleaning water coolers, which might give you some information.

If you look closer on the Google Scholar search results, you'll find that quite a bit of research has been conducted in the area of sanitation of water coolers and study of their flora. For example, consider the following paper from 1996: Analysis of the Virulence Characteristics of Bacteria Isolated from Bottled, Water Cooler, and Tap Water.

There is a very nice list (Table 1) of different bacteria isolated from water. But I would like to point your attention to following table from the paper:

Quote from methods section listing tested antibiotics:

  The
  natural and first generation antibiotics included:
  penicillin, ampicillin, erythromycin, kanamycin,
  streptomycin, tetracycline, chloramphenicol, and
  sulphonamide. The synthetic and later generation
  antibiotics included: gentamicin, cefoxitin,
  cefoperazone, oxacillin, piperacillin, imipenem,
  ciprofloxacin, and sulphonamideftrimethoprim

The green slime you observe, I think, is a combination of all those bacteria, plus some that were brought after the water was poured into the container. And it seems that all commercial sources that you didn't purify yourself, will have a variety of microorganisms growing. And around 5% of the total bacterial cell mass is resistant to common antibiotics.


Why can't cell division happen the other way around?

If you are thinking of a process like meiosis but followed by DNA duplication, the problem is that this would create daughter cells that do not have the same genome as the parent cell.

The diploid genome of a sexually reproducing species' cell has different alleles of the same locus. If the cell replicates itself by passing one chromatid to each daughter cell which then duplicate that to make a diploid genome, the resulting cells will not have the same DNA as the original one since each of the daughter cells will have inherited only one of the available alleles. They will then make an exact copy of the DNA they have inherited and become diploid but with a new genome, one that did not exist in their parent. This is not good since the cells of an organism need to have the same genome in order to function in the same way.


Does GFAJ-1 use Adenosine triarsenate as its energy currency?

I'd have to agree that it's highly improbably that the GFAJ-1 strain used nucleoside triarsenates as an energy source. There are three main lines of evidence pointed out in the Science reviews that were published after the initial publication of the paper.

The incorporation of arsenate ions into NTAs is not a plug-and-play process, per se. Arsenate does not simply replace phosphate ions from molecules. In order for an NTA to form, it must arsenylate (like phosphorylate) a ribose molecule, then have the purine/pyrmidine ring form (and be attached to the ribose), and then two more arsenates have to be linked via ester bond to the other first arsenate. Mind you, this all happens in water. Arsenate esters are notoriously unstable in water, so it's difficult to imagine an NTA forming stably.
The original team in Felisa Wolfe-Simon's lab didn't intentionally add phosphate ions to their growth media; instead, the approximate amount of phosphate impurity was measured and reported. The lab compared this level of phosphate with the minimal levels reported in E. coli from another paper and basically said, "There isn't enough phosphate in our growth media for our GFAJ-1 strain to grow solely on phosphorous." Well, that logic is a little non sequitur  because GFAJ-1 is a halomonad (they said so themselves) and there is literature pointing to a species within Halomonadaceae that can grow on phosphate levels lower than that of the impurities reported.
Although the Wolfe-Simon team added arsenate into their growth media, it's unlikely that any biologically-useful arsenic ended up in the cells at all. Under physiological electrochemical conditions, arsenate gets reduced to arsenite. Phosphate ions, on the other hand, are stable at physiological potentials.

All in all, there's a reason why life chose phosphorous instead of arsenic. Although both elements have ions with a propensity to make ester bonds, maybe arsenic just doesn't fit into our anthropocentric view of what life is.


What is meant by "neurotransmitters flooding the brain"?

It is very likely what they mean by "neurotransmitters flooding the brain" is the phenomenon called Volume Transmission.

I paraphrase from this source:

  When a neurotransmitter is released at a synapse, it reaches its
  highest concentration inside the narrow space of the synaptic cleft,
  but some of it is certain to diffuse away before being reabsorbed or
  broken down. If it diffuses away, it has the potential to activate
  receptors that are located either at other synapses or on the membrane
  away from any synapse. The extrasynaptic activity of a
  neurotransmitter is known as volume transmission. It is well
  established that such effects occur to some degree, but their
  functional importance has long been a matter of controversy.


Wheels are possible on the molecular level — bacterial flagella are rotating cores inside a molecular motor, but wheels larger than the flagellum have not really been found.

A single animal with a wheel is an improbable* development that would require a single animal have two separable parts (axle/wheel and body).

[*read as: pretty much impossible]

It's hard to imagine how such a thing could evolve.  A wheel and axle would need to be made of living tissue, otherwise it would be vulnerable to wear and tear.  Wheels also have problems going over uneven terrain, which is really all terrain animals live in.  It's difficult to imagine what sort of selection conditions would be strong enough to push animals away from legs.

If you include driver-vehicle symbionts where the 'car' and 'wheel' are actually two animals, then they have evolved. Parasites can have all sorts of symbiotic control over their victims including as means of transport. The Jewel Wasp is one which is the most suggestive of what you may be thinking. The wasp stings its victim (a cockroach) in the thorax to immobilize the animal and then again just behind its head.  After this, the wasp can ride the beetle, steering it by holding its antennae back to its nest where the roach is immobilized to feed the wasp larvae there.

(see section "Pet cockaroaches" in this reference.)

As to the three schools of thought you added to the question, I would probably rather say there were two strong arguments against.  The first is whether there is an evolutionary path to wheels (argument 1 in your question), which I doubt.  Given even a large amount of evolutionary time you will not see a naked human being able to fly on their own power.  Too many structural characteristics of the body plan have been made to all be reversed so that wings or other means of aerial conveyance will show up. The same can be said for wheels when the body plans have fins/legs/and wings already.

Argument 3, which I also tend to agree with, is perhaps more convincing.  By the time a pair of animals makes a symbiotic relationship to do this, or a single macroscopic animal evolves wheels, they will literally develop legs and walk away. When life came onto the land this happened, and since then it's happened several times.  It's sort of like saying that the random movement of water molecules might line up to run a stream uphill. There's just such a strong path downwards, that the statistical chances of you seeing it happen are nil.

This is a hypothetical case, but arguing this in a convincing way I think you would need to lay out:  a) an environment whose conditions created enough of a selective advantage for wheels to evolve over legs or other similar adaptations we already see. Perhaps based on the energy efficiency of wheels;   b) some sort of physiological model for the wheels that convey a reasonable lifestyle for the wheel.

There are lots of questions that would need to be satisfied in our thought experiment.  Here are some: "the symbiotic wheel would be spinning constantly; if it died the driver creature would be completely defenseless"; "if the ground were bumpy, all these wheeled animals would get eaten"; "the wheel symbiont — how would it eat while its spinning all the time? Only fed by the driver? Even symbionts such as barnacles or lampreys on the flanks of sharks still have their own ability to feed."

For many similar questions the same sort of discussion ensues where there are many disadvantages which outweigh advantages for animals. e.g.
"why are all the flying animals and fish and plants even more similar to airplanes than helicopters?"

Sorry if I seem negative, but way back in grad school I actually did go over some of these angles.

UPDATE: First Gear found in a Living Creature.
A european plant hopper insect with one of the largest accelerations known in biology has been found to have gears!  (There's a movie on the article page.
)

The little bug has gears in its exoskeleton that synchronize its two jumping legs.  Once again selection suprises.

  The gears themselves are an oddity. With gear teeth shaped like
  cresting waves, they look nothing like what you'd find in your car or
  in a fancy watch.  There could be two
  reasons for this. Through a mathematical oddity, there is a limitless
  number of ways to design intermeshing gears. So, either nature evolved
  one solution at random, or, as Gregory Sutton, coauthor of the paper
  and insect researcher at the University of Bristol, suspects, the
  shape of the issus's gear is particularly apt for the job it does.
  It's built for "high precision and speed in one direction," he says.

The gears do not rotate 360 degrees, but appear on the surface of two joints to synchronize them as they wind up like a circular spring.  The gear itself is not living tissue, so the big solves the problem of regenerating the gear by growing a new set when it molts (i.e. gears that continually regenerate and heal are still unknown).  It also does not keep its gears throughout its lifecycle.  So the arguments here still stand; the exception still supports the rule.


How do I perform recurring pattern mining or regular expressions of nucleotide sequences?

I'm no expert in MATLAB but I know that it is possible to do regular expressions in MATLAB with the general rules explained here. However there are alternative approaches and softwares you could use to achieve this with softwares that are freely available and quite powerful in performing such functions. Although I'm aware that perl and python are the programs of choice for regular expression analysis; however I would urge you to consider the R language. R allows you to construct your mining results in a format of a table, which each column containing the data you are interested! there are many packages in R that allows you to process many data types. I would say R is worth the investment to learn for any future data analysis. I use the RStudio to interact with the R language software.

The best place to get help for MATLAB or R is the http://stackoverflow.com which you can sign on with you current account. In fact I have asked a few questions there on regular expressions and the community is very helpful however ensure that you show your attempt at the problem and where you are stuck in order to get a constructive responses!


Usually this is used in the context of gene analysis and further characterization. What is done, is that a piece of foreign DNA (either generated by digesting genomic DNA (from human or mouse for example) or by PCR amplification) digested at the end of the DNA to have matching open ends with a bacterial vector.

The DNA of interest is then ligated with the vector and can then be replicated in bacteria and isolated easily in great yields. This plasmid can then further analysed (by restriction analysis, sequencing etc.), the gene or its promoter manipulated and mutated, or in case of protein coding genes the gene overexpressed in the cells. All this is useful to analyze the function of unknown genes. See the figure for a schematic overview (from  Campbell AP Biology Book 8th edition, via this website):

Technically making a clone means that you generate multiple genetically identical daughter cells from one precursor.


Inbred mice has no severe phenotype outcome?

Some information on inbred strains of laboratory mice:

https://en.wikipedia.org/wiki/Inbred_strain

http://what-when-how.com/molecular-biology/pure-line-molecular-biology/

A relevant quote on the consequences of inbreeding:

  Inbreeding in allogamic organisms bring the deleterious recessive alleles to homozygosity; the immediate consequence is an increase in the frequency of defective offspring, or, in another words, an increase in the genetic load of the population. This phenomenon is called inbreeding depression or inbreeding degeneration. As inbreeding continues, the deleterious alleles are selected out and eventually disappear. The original heterozygous populations are often more fit than the resulting pure lines because they profit from heterosis and balanced polymorphisms; the main advantage of pure lines is the quick production of many individuals with the same well-adapted genotype, while the allogamy continuously generates new genotypes.

In other words, inbreeding is harmful because it makes it more likely that offspring will have two copies of bad recessive alleles, meaning those alleles get expressed, meaning the organism gets the bad consequences that wouldn't show up if they had only one copy. This is what happens over a single generation however; over many generations the bad alleles are selected against, precisely because they are harmful to the organism so it reproduces less, and after enough generations of inbreeding you hit a point where all individuals are genetically identical and have all the "good" alleles (if they were lucky; otherwise they die out or stay stuck with some bad-but-not-fatal alleles). They still may be worse off than their more diverse ancestors, but they're not completely messed up like their unfortunate great-aunts and uncles who didn't make it either.

The big difference between inbred mice and dogs or tigers is the "for specific phenotype" aspect. Laboratory organisms are inbred so that you get a large pool of genetically-identical individuals, meaning they're much easier to experiment on. The aim is the inbreeding itself, not any particular phenotype. For example if you look at the page for the most popular strain of laboratory mice, C57BL/6, you can see it has many different properties and is used for many different things.

On the other hand, dogs aren't inbred for the purpose of inbreeding or of being genetically identical; the aim is to get desirable phenotypes, and inbreeding is just an efficient way of achieving that aim. It also isn't obvious that many of the problems purebred dogs have is inbreeding (i.e. lack of genetic diversity, high levels of homozygosy) per se, but the fact that the traits being bred for are just plain unhealthy for the dog, or part of a bell curve that include bad outcomes at the edges. For example, Syringomyelia in the Cavalier King Charles Spaniel:

  Some researchers estimate that as many as 95% of CKCSs may have Chiari-like malformation (CM or CLM), the skull bone malformation believed to be a part of the cause of syringomyelia, and that more than 50% of cavaliers may have SM.* It is worldwide in scope and not limited to any country, breeding line, or kennel, and experts report that it is believed to be inherited in the cavalier King Charles spaniel. CM is so widespread in the cavalier that it may be an inherent part of the CKCS's breed standard.

(emphasis mine)

Same thing for that spine malformation that's related to selecting for corkscrew tails. The genes that make the tail corkscrew also mess with the spine.

In other words, the issue isn't inbreeding or not but whether the genes themselves are harmful. When organisms are selected for traits that are directly harmful in their extreme, or are associated with harmful genes that just happen to be next to those that are selected for in the chromosome, then the harmful consequences will spread through the population. Inbreeding is only a problem insofar as it allows the process go faster (more offspring per generation have the desired trait). On the other hand when you're just inbreeding with no specific focus on phenotype, or not phenotypes that have obvious harm associated (i.e. no lab would select for a frivolous trait that also causes harm. They're either selecting for the harmful trait on purpose, or they're selecting against it, because they'll want animals that are as healthy as possible except for the one variable they're interested in), then you'll end up with populations that are fairly normal except for some of the direct consequences of genetic uniformity.

It should be noted that most purebred dogs probably aren't inbred strains the same way many laboratory animals are; those are genetically identical, so the whole point is that their offspring will be like they are. So while they may be less fit than a non-inbred version of them might be, their offspring won't be any less fit than they are. And this is not what's observed with purebred animals like dogs and horses; individuals aren't identical, and looking at the page on Syringomyelia it seems the problems are getting worse.


How a particular composition of molecules result into life in form of cell?

Science does not have an answer to how the first reproducing cell came about.  The actual event has left no traces except life as we see it today. There are theories about parts of how it might have happened, but evidence about it essentially doesn't exist.  If you want to get a flavor of recent ideas of scientists in this area, here is a video of a lecture on "The Origin of Cellular Life on Earth".


First to address some of the comments:

Concentrated UV damage does hurt your skin, it's called sunburn.  Lighter amounts of UV damage can cause cancer over time.  UV damage can be "felt", as can photonic pressure in extreme cases.  The issue at hand is "what is detection."

Back to your eyes:
As addressed in this answer, the human retina is able to detect UV light if it is not blocked by the lens.

I believe your question, restated slightly, is "can we call the pain experienced by UV damage to our eyes human detection of UV light."  Generically I think the answer is no, because we lack the specificity to determine that it is UV light. Many forms of ionizing radiation can lead to pain, and we would be unable to distinguish between them.  We cannot tell the gradation from UV to gamma, despite the damage they might cause.  Contrast this to the visible light spectrum, where we are quite good at determining the wave length.

Further, you could have similar damage caused by infection, where again you couldn't distinguish between the pain and fuzzy sensation caused by the very beginning of infection vs slight UV damage (though blueberry might help).

Does UV light damage your eyes? Absolutely in large enough doses.  Can it be called detection?  Probably not.  We can deduce UV damage from lots of things, including changes in the color of the pigmentation of your eyes (gold flakes = bad).  When we get to the level of deduction, however, we might as well be using machines to detect UV light and save our eyes (and skin) the trouble.


Death because of distilled water consumption

I'm extremely skeptical of @leonardo's answer.  I suspect that what would happen if you drank only distilled water is nothing perceptible.  The only place where concentrations of distilled water would ever be high enough to conceivably matter is in the tissues of the mouth and throat, and even there, the effect would be temporary.

Compare drinking 8 glasses of either distilled or tap water every day.  With tap water, you're looking at less than 200 ppm of Mg, Na, K, and Ca combined.  That's less than 400mg of total mineral content per day.  Given that the combined RDA of all of those minerals is on the order of 7g for an adult male, this is not nothing, but it's certainly small.  Your dietary intake of these minerals probably varies by more than this daily, and your intestines, kidneys, sweat glands and mineral storage organs (like your bones and muscles) are constantly maintaining the mineral blood levels within a very narrow range, despite handling a throughput of several pounds of water and food daily.  They might have to work slightly harder to manage this range if you drank nothing but distilled water, but in a healthy adult, normal intakes already vary by more than this amount without major problems.  For example, the average American consumes more than 3.4 grams of sodium daily, while a low-sodium diet is on the order of 2g.  Low-sodium diets have been widely studied in the medical literature, and are considered safe.

As for pH, the lowered pH is caused by increased carbon-dioxide absorption to form carbonic acid.  Just as carbon dioxide is more soluble in distilled water, it is less soluble in stomach acid, and may be burped out.  Would you die of acidosis from drinking seltzer water all the time?  If that were the case, I'm sure there would be big health warnings about drinking soda, while it seems relatively benign. Furthermore, your body produces and excretes (through the lungs) around 1kg of CO2 daily, dwarfing any extra CO2 you might get by drinking distilled water.  If the small amounts of CO2 found in distilled water were dangerous, jogging would be invariably fatal.

If you were to drink nothing but distilled water, and eat no food, you probably would die of hyponatremia within a few weeks.  But you would also die of hyponatremia if you were to drink nothing but tap water, though perhaps slightly more slowly.


Downloadable worldwide database of disease statistics?

I took a quick peek and HealthMap and their JavaScripts are publicly viewable.  As such, I believe cross site scripting would be quite feasible.  In other words, call their JavaScripts from a page you develop on your server to create a feed of the data you want.

In this way, minimal effort on your part could leverage their data scraping efforts.  If you're adding your own data then you're basically doing a Mashup.

That said, my concern with doing this is potentially violating their copyright.  I would email them saying if their database is not available then you wish to use cross site scripting to access this data for your project, and unless they let you know otherwise by (specific date) you will assume this is acceptable.

I'm not a lawyer, so use this advice at your own risk.  =)


What is this colourful insect with a large thorn?

As @Kiritee mentioned this is actually a treehopper, due to thier unusual shape they are of long interest of naturalists.
This is a female Umbonia crassicornis.
Here's a female with her colourful nymphs captured by
C. D. S. Molinari
.

Facts:

The females have a pointed pronotal horn (spike), the males' are blunt, with a flat top.

The adults display variation in colour and size.

The pointed pronotal horn is an adaptation as the insectivorous birds mistake them as thorns (on stem) and do not consume them.

This is a variable species as to size, color and structure, particularly the pronotal horn of males (which is more angled posteriorly than the females' and often somewhat expanded apically).
This tall, essentially perpendicular thorn-like pronotum discourages birds and other predators from eating it, if only by mistakenly confusing it with a thorn.
Typically, the adult is green or yellow with reddish lines and brownish markings.
The range of this species is from Northern South America all the way to Mexico and Florida. Its preferred hosts are ornamental and fruit trees of subtropical regions.

Parental care: The females on sensing an intruder would rush to her nymphs and would charge the offender by kicking her legs, fanning her wings and sometimes even buzzing. The females communicate with the nymphs to ensure that they are in a group.
References:
Encyclopedia of Land invertebrate behaviour, Encyclopedia of Insects and Libraries of life

Picture References:

A female with eggs.
Two males (blunt top)
Original size

Good reads:

Thornbug to Thornbug-The inside story of insect song

Libraries of life (audio clips)


Clarification on Hatch and slack pathway

I am not sure about the source of ATP but I can tell you something about NADPH.

The conversion of malate to pyruvate and CO₂ by malic enzyme is carried out in the bundle sheath cell. This process produces NADPH.


Does DNA being circular or linear directly affect the speed of DNA replication?

I am not sure if I well understand what you mean by directly affected.
I will list some possibilities below (For reference you can see any genetics textbook, I use, Genetics: A conceptual approach by Pierce, but I guess any textbook would do).

Porkaryotic polymerases (usually processing circular DNA) have a higher nucleotdie per second speed than eukaryotic polymerases (processing linear DNA). Does this mean that shape directly affects speed? In this case I would say no. It's just a difference between prokaryotic and eukariotic polymerases. Some prokaryotes have linear chromosomes and their polymerase will still be faster than eukaryotic polymerases.

One prokaryotic chromosome has only one origin of replication, while one eukaryotic chromosome has several of them, so that eukaryotes parallelize even in a single chromosome. Does this mean that shape directly affects speed? In this case, I would say yes. Due to steric effects, the shape of the chromosome has to do with the ability of having several origins of replications, even if the lengths are the same. Edit: After Ved's comment, I realized that this is also not necessarily true. Not all circular chromosomes have one single origin of replication; archaea have circular chromosomes with more than one origin of replication

Linear chromosomes are easier to unwind. Does this mean that shape directly affects speed? I would say, yes for large chromosome and no for small chromosomes. Edit: After David's comment, I realized that I am not really sure that linear chromosomes are easier to unwind. A Wikipedia entry states this, but I gave a look at the paper they referenced and found no real statement about this.

Importantly, if the DNA molecules you compare are one prokaryotic and one eukaryotic and they are very short, I would bet my 5 bucks on prokaryotic (circular) being faster, because in absence of all the parallelization the eukaryotic DNA polymerases are slower than prokaryotic ones.


In a sense, there's an easy answer to your question.  Humans became bipedal in Africa, since bipedality is well-established for the first species in the human lineage to leave Africa (Homo erectus/Homo ergaster).  This can be verified in many textbooks.  However if you ask the question when, in what species, or why, there's no easy answer to your question. The question comes down to (a) which fossils are specifically ancestral to humans (b) what fossils have evidence for bipedality, and (c) theories as to why those species became bipedal.

The narrow sense of humans, Homo sapiens, has been bipedal ancestrally.  Other closely related species were almost certainly bipedal (Homo neanderthalensis and Homo heidelbergensis for example).  In fact, the species or species complex from which humans likely arose, Homo erectus, was also likely bipedal (discussion below).  If we take the broadest sense of what "human" means, it could mean any species which split from the human lineage after the split with the extant great apes (specifically, post split with chimpanzees).  Here there's reasonable evidence for bipedality exists around the same time as this split, but not in all species.  Specifically, Orrorin tugenensis is a 6 million year old specimen with some (but not conclusive) evidence for bipedalism.

Question b, how do we know a fossil creature is bipedal, is a challenging question.  Homo sapiens, the only completely bipedal primate, have many adaptations which facilitate walking on two legs.  The shape of our pelvis facilitates the muscle attachments necessary for walking by flaring the ilium (the bone which forms the upper part of the pelvis).  This same flaring is found in Australopithecus afarensis (which includes the famous "Lucy" specimen), about 3 million years ago.  Australopithecus also has a fossil of footprints, which seems to indicate bipedal movement.  The human femur is bent inwards and the neck is thickened to support the weight of someone walking upright.  This same thickening is found in Orroin tugenensis and the angle in Homo erectus/Homo ergaster (these are two names which are either closely related species or the same species, depending on who you ask). The human big toe is also in line with the others in the foot, which likely allows us better motion on the ground.  This feature is also true of Ardipithecus ramidus, at about 4.5 million years ago.

The third part of your question, why humans became bipedal, is largely speculative.  Many theories exist for the process which lead to bipedalism.  A popular theory in the 1970s and 1980s was that humans became bipedal to enhance our abilities to see across tall grass, because many people thought Homo erectus/Homo ergaster was the first upright walking species, and grasslands dominated east Africa at the time.  However since earlier evidence for bipedality, many people have abandoned this hypothesis in favor of others.  These other hypotheses include that bipedalism arose after scaffolding on to arboreal (tree-living) adaptations.  If human ancestors lived in trees, they may have moved in a vertical posture, leading to many of the adaptations needed to move vertically on the ground.  Others include an increased reliance on meat, caught through endurance hunting, or even wading into tidal waters being the key feature (notably this is not the aquatic ape hypothesis, which is pseudoscience), and this reliance on key marine resources provided the essential stable food supply for brain enlargement.  The short answer is that there's a tremendous amount of speculation in this area, and few firm facts.

Whichever of these species you choose as the "first bipedal human," and how confident you want to be about that bipedality, they all evolved in Africa.


Deciding a reasonable threshold for copy number variation in a CNV (SNP array) TCGA dataset

Your suggested approach of comparing to the baseline distribution on a point-by-point basis isn't bad, although it's going to be susceptible to small false positives from noise. You'd probably want to only use events that span a certain minimum number of consecutive observations.

You might also want to look into circular binary segmentation, as described here: http://www.ncbi.nlm.nih.gov/pubmed/15475419.


Inexperienced divers damage coral, but parrot fish eating coral doesn't do damage?

You are absolutely correct in regards that marine life does cause damage to corals. In particular, parrotfish have been found to play an important role in regulating the biodiversity of coral reefs through their feeding behavior. Certain species of parrotfish feed on certain species of coral, typically faster growing species that branch out into easier access bits of corals that the fish can consume. This has the effect of allowing slower growing species that may also be harder corals to consume (in terms of hardness, shape accessibility, or other factors) to grow and compete in the coral reef and prevent the reef from being overgrown with the faster species. A similar process is seen on the land with grazing herbivores which help propagate biodiversity by consuming certain plant species thereby giving increased chances for other species to grow. These ecosystems and the relationships between corals and species like parrotfish have had an extremely long time to come to shape through evolutionary pressures on both sides of the organisms, consumer and producer.

The problem with divers who cause damage to corals is that it is an introduction of artificial stress and arbitrary damage to the coral reef in a short time without much time to adapt, placing additional stress on the environment which is already stressed. Unlike the parrotfish, divers may not discriminate on what corals they damage. Additionally, areas where inexperienced divers damage coral generally will see more inexperience divers often at the same diving site, so from the standpoint of protecting the coral reef, minimizing the damage caused by divers becomes an important priority to the stewards of those areas and the diving shops which bring divers to those areas.


Why have plants evolved to photosynthesize glucose instead of another molecular compound?

This is a brief answer (for me) to point out that:

Your question is not really concerned with photosynthesis but is actually about the choice of the carbon constituents of living cells.

First you talk about photosynthesis as if it is a single process, however it is two separable processes:

The Light Reactions convert solar energy into chemical energy (in the form of ATP and NAD(P)H).
The Dark Reactions use the chemical energy to reduce carbon dioxide and elaborate it to more complex molecules.

Photosynthesis is so elaborate chemically that it clearly was not the first process by which living organisms managed to convert environmental energy into a usable form. So the question becomes:

  Q. Why is chemical energy trapped by living organisms used to make
  compounds such as glucose 6-P?

and giving what may at first sight seem to be a frivolous answer

  A. Because glucose 6-P and its precursors and metabolites were suitable molecules for building the structural components of cells, that had arisen early in evolution.

So the question becomes:

  Q. Why did the structural components, energy storage, genetic information
  etc. of cells evolve to employ the particular molecules that we find
  today, most of which can be formed from glucose metabolites?

And that is a very broad question about a very speculative area of chemical evolution, which cannot be summarized here.

In general one would imagine that the answer is related to the carbon components available in the environment and the possibilities of chemical transformations. However the trap is that one ends up arguing that things are the way they are because that was best. Which is all very well until one discovers dirty little secrets such as the fact that archaea evolved different chemical constituents for their cell membranes.

Footnote

My first degree was in chemistry. Since becoming a biochemist/molecular biologist I have almost never talked in terms of overall chemical formulae of molecules in the manner of the question. It has seldom been a useful way to approach biochemical reactions or intermediates. What has been more important is to look at their structures and ask how they lend themselves to their functions or interconversions.


Where does the 'C' in exhaled CO₂ mostly come from?

CO2 is a product of Cellular Respiration, which generally takes Glucose and molecular Oxygen to produce Carbon Dioxide, water, heat, and allows ADP to be regenerated into ATP (or other various oxidation reactions). The Carbon comes from wherever the acetyl-CoA used in the Citric Acid Cycle came from - either carboyhydrates or fatty-acids (saturated carbon chains).

Simplified reaction:   C6H12O6 (s) + 6 O2 (g) → 6 CO2 (g) + 6 H2O (l) + heat

So, you are correct. CO2 transferring out of the lungs is mostly the result of burning sugars (or fats) for energy (the regeneration of ADP/GDP with respect to human biology).

To that end, the tissues that produce the most CO2 will be the cell-types which constantly require energy. Nominally, muscle tissues.

Per your comment, broken down fat, or rather, the process of Fatty-Acid Catabolism, results in the production of acetyl-CoA, which is a primary player in the Citric-Acid Cycle. The Citric Acid Cycle, which you should recognize as the Cycle that Pyruvate - the end result of Glycolysis (the breakdown of Glucose into 2x 3-Carbon Pyruvates) - also goes into after being converted into acetyl-CoA by Pyruvate Dehydrogenase.

The sum of all reactions in the citric acid cycle is:
Acetyl-CoA + 3 NAD+ + Q + GDP + Pi + 2 H2O → CoA-SH + 3 NADH + 3 H+ + QH2 + GTP + 2 CO2

So, for a basic breakdown with respect to CO2:

Carbohydrates (Sugars, Starches) → Glucose → Pyruvate + ATP + NADH
Pyruvate → Acetyl-CoA
Lipids (fats) → Lipolysis → Acetyl-CoA
Acetyl-CoA + ... + H20 → ... + CO2


Nice question! Unfortunately, the complete list of pathways involved in regulation of sebum production and secretion rate by sebaceous glands are not understood yet (Picardo et al, 2009). However, we know that sebum production is continuous and is not regulated by neural mechanisms (Thiboutot et al, 2004). Retinoids, hormones, and growth factors are known to influence sebaceous gland growth and differentiation (Zouboulis et al, 1998). Also, androgens and growth hormones are known to promote sebaceous gland differentiation (Deplewski et al, 1999, Rosenfield et al, 1998) whereas estrogens and retinoids, like 13-cis retinoic acid, inhibit their differentiation (Strauss et al, 1962).

In retinoids, isoretinoin is shown to have greater sebosuppressive action as compared to all-trans or 9-cis retinoic acid (Hommel et al, 1996). In androgens, androgen receptors have been localized to the basal layer of the sebaceous gland and the outer root sheath keratinocytes of the hair follicle, and testosterone and dihydrotestosterone are the major androgens that interact with these receptors (Liang et al, 1993). However, the molecular mechanisms through which androgens interact with these receptors and sebaceous glands are not understood yet (Thiboutot et al, 2004). Apart from this, insulin and Insulin-like Growth Factor 1 (IGF-1) also play a critical role here. Acne is considered as IGF-1 mediated disease, and high levels of sugar (caused due to diet) induce high levels of insulin and IGF-1. Both these hormones amplify the stimulatory effect of GH on sebocytes and augment mitogenic downstream signalling pathways of insulin receptors, IGF-1 receptor and fibroblast growth factor receptor-2b (Melnik et al, 2009).

Other (known) substances which are found to regulate sebum secretion include histamine (due to presence of H-1 receptor on sebocytes, Pelle et al, 2008), LXR ligands (due to presence of Liver X Receptor, Zouboulis et al, 2009), PPAR ligands (due to presence of Peroxisome Proliferator-Activated Receptor, Trivedi et al, 2006), vitamin D deficiency (Yildizgören et al, 2014), neuropeptides (Ganceviciene et al, 2009), etc. See the image below (from Makrantonaki et al, 2011) for visual representation:

In spite of this, elucidating the mechanism of regulation of sebum secretion by sebaceous glands is a difficult task since, although evidence suggests that nonendocrine factors may also be an important part for regulation along with endocrine factors, the nature of this secretion and the regulation of the secretory process seem to differ among the various types of glands which, in spite of being similar in structure, might be different in function and regulation (Thody et al, 1989).

References:

 1. Picardo, Mauro et al. “Sebaceous Gland Lipids.” Dermato-endocrinology 1.2 (2009): 68–71. Print.

 2. Diane Thiboutot, Regulation of Human Sebaceous Glands, Journal of Investigative Dermatology, Volume 123, Issue 1, July 2004, Pages 1-12, ISSN 0022-202X, http://doi.org/10.1111/j.1523-1747.2004.t01-2-.x.

 3. C.C. Zouboulis, L. Xia, H. Akamatsu, H. Seltmann, M. Fritsch, S. Hornemann, R. Ruhl, W. Chen, H. Nau, C.E. Orfanos
The human sebocyte culture model provides new insights into development and management of seborrhoea and acne
Dermatology., Volume 196, Issue 1, 1998, pp. 21–31

 4. D. Deplewski, R.L. Rosenfield
Growth hormone and insulin-like growth factors have different effects on sebaceous cell growth and differentiation
Endocrinology., Volume 140, Issue 9, 1999, pp. 4089–4094

 5. R.L. Rosenfield, D. Deplewski, A. Kentsis, N. Ciletti
Mechanisms of androgen induction of sebocyte differentiation
Dermatology., Volume 196, Issue 1, 1998, pp. 43–46

 6. J.S. Strauss, A.M. Kligman, P.E. Pochi
The Effect of Androgens and Estrogens on Human Sebaceous Glands
J Invest Dermatol., Volume 39, 1962, pp. 139–155

 7. L. Hommel, J.M. Geiger, M. Harms, J.H. Saurat
Sebum excretion rate in subjects treated with oral all-trans-retinoic acid
Dermatology., Volume 193, Issue 2, 1996, pp. 127–130

 8. T. Liang, S. Hoyer, R. Yu
Immunocytochemical localization of androgen receptors in human skin using monoclonal antibodies against the androgen receptor
J Invest Dermatol., Volume 100, 1993, pp. 663–666

 9. Melnik BC, Schmitz G. Role of insulin, insulin-like growth factor-1, hyperglycaemic food and milk consumption in the pathogenesis of acne vulgaris. Exp Dermatol. 2009;18:833–841

 10. Edward Pelle, James McCarthy, Holger Seltmann, Xi Huang, Thomas Mammone, Christos C. Zouboulis, Daniel Maes, Identification of Histamine Receptors and Reduction of Squalene Levels by an Antihistamine in Sebocytes, Journal of Investigative Dermatology, Volume 128, Issue 5, May 2008, Pages 1280-1285, ISSN 0022-202X, http://doi.org/10.1038/sj.jid.5701160

 11. Zouboulis, Christos C. “Sebaceous Gland Receptors.” Dermato-endocrinology 1.2 (2009): 77–80. Print.

 12. Nishit R. Trivedi, Zhaoyuan Cong, Amanda M. Nelson, Adam J. Albert, Lorraine L. Rosamilia, Surendra Sivarajah, Kathryn L. Gilliland, Wenlei Liu, David T. Mauger, Robert A. Gabbay, Diane M. Thiboutot, Peroxisome Proliferator-Activated Receptors Increase Human Sebum Production, Journal of Investigative Dermatology, Volume 126, Issue 9, September 2006, Pages 2002-2009, ISSN 0022-202X, http://doi.org/10.1038/sj.jid.5700336

 13. Yildizgören, Mustafa Turgut, and Arzu Karatas Togral. “Preliminary Evidence for Vitamin D Deficiency in Nodulocystic Acne.” Dermato-endocrinology 6.1 (2014): e983687. PMC. Web. 23 Apr. 2017.

 14. Ganceviciene, Ruta et al. “The Role of Neuropeptides in the Multifactorial Pathogenesis of Acne Vulgaris.” Dermato-endocrinology 1.3 (2009): 170–176. Print.

 15. Makrantonaki, Evgenia, Ruta Ganceviciene, and Christos Zouboulis. “An Update on the Role of the Sebaceous Gland in the Pathogenesis of Acne.” Dermato-endocrinology 3.1 (2011): 41–49. PMC. Web. 23 Apr. 2017.

 16. Thody, A. J. & Shuster, S. Control and function of sebaceous glands. Physiol Rev 69, 383–416 (1989)


Is there a biological basis for different accents?

No. Accent is purely environmental. The ability to pick up the unique sounds of a language or variation of a language ceases around puberty: http://en.wikipedia.org/wiki/Language_acquisition

This is why adults learning a second language have trouble distinguishing the unique sounds of the second language. For learners of English, the "th" sounds and the difference between "l" and "r" can be difficult. For languages based on Sanskrit, there are a variety of aspirated/unaspirated consonants somewhere between "b" and "v" that English-speakers have a hard time distinguishing, much less imitating.


Photosystem 1 and 2; P680/P700; Chlorophyll a/b

Regarding your questions #1 ("Is the primary pigment reaction centre in both photosystems a pair of chlorophyll a molecules?") and #3 ("How can it be that it absorbs at a different wavelength in the two photosystems if it is the same molecule?"):

Both reaction centers in Photosystem I and Photosystem II contain only chlorophyll a. According to Lodish (Molecular Cell Biology):

  As in the bacterial reaction center, at the center of each chloroplast photosystem is a pair of specialized reactioncenter chlorophyll a molecules, which are capable of undergoing light-driven electron transfer. The chlorophylls in the two reaction centers differ in their light-absorption maxima because of differences in their protein environment. For this reason, the reaction-center chlorophylls are often denoted P680 (PSII) and P700 (PSI). (emphases mine)

Regarding your question #2 ("If so, what is chlorophyll b? Is it simply an accessory pigment?"):

Chlorophyll b has a different molecular structure (and, therefore, a different absorption spectrum) and it's less abundant in the chloroplast than chlorophyll a. Here is an image depicting their molecular structures and absorption spectra:

(a) Chlorophyll a, (b) chlorophyll b, and (c) β-carotene are hydrophobic organic pigments found in the thylakoid membrane. Chlorophyll a and b, which are identical except for the part indicated in the red box, are responsible for the green color of leaves. β-carotene is responsible for the orange color in carrots. Each pigment has (d) a unique absorbance spectrum. Source: "OpenStax College, The Light-Dependent Reactions of Photosynthesis. October 16, 2013."

Both chlorophyll a and b are present in the antenna complex. Still according to Lodish:

  As in photosynthetic bacteria, each reaction center has an associated antenna that consists of a group of light-harvesting complexes (LHCs); the LHCs associated with PSII and PSI contain different proteins.

However, most of chlorophyll b is associated to PSII antenna complex, not PSI, which is one of the main differences between PSII and PSI.

Source: Lodish, H. (2000). Molecular cell biology. 4th ed. New York: W.H. Freeman.


Is nucleoside-triphosphate delivery to RNA or DNA polymerase active or passive?

The amount of dNTPs is so important and sensitive the level of dNTPs should be optimum  not lower or higher. Lower amounts lead to insufficiency  and higher amounts lead to increased mutation rates. Also, this optimum amount of dNTPs should last for a couple of minutes to supply dNTPs needed for replication. The delivery of dNTPs is due to molecular signalling & stochastic diffusion.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2847218/

"Eukaryotic cells contain a delicate balance of minute amounts of the four deoxyribonucleoside triphosphates (dNTPs), sufficient only for a few minutes of DNA replication. Both a deficiency and a surplus of a single dNTP may result in increased mutation rates"

http://onlinelibrary.wiley.com/doi/10.1111/j.1349-7006.2010.01719.x/pdf

"Optimization of intracellular concentrations of dNTPs is critical for
the fidelity of DNA synthesis during DNA replication and repair
because levels that are too high or too low can easily lead to
increased rates of mutagenesis"

http://www.nature.com/ncb/journal/v14/n7/full/ncb2540.html

"Production of deoxyribonucleotide triphosphates (dNTPs) is essential for DNA synthesis during replication and repair, and abnormal or imbalanced dNTP levels increases mutation frequency. Pagano and colleagues now demonstrate that the SCF-cyclin F ubiquitin ligase controls dNTP production during the cell cycle and following genotoxic stress"

http://www.ncbi.nlm.nih.gov/pubmed/22234185

"alterations in dNTP pools are associated with increased mutagenesis, genomic instability and tumourigenesis"


Mineral nutrients are conveyed up the tree via the xylem by transpiration. The phytohormone cytokinin that releases buds/shoots is synthesized in the root tips and is also conveyed via the transpiration stream. Transpiration is driven by the water potential of the air --> ln(rH); transpiration stops when the relative humidity is 100%.

Even though some species are able to generate root pressure that will force water plus minerals plus cytokinin up the xylem, growth must, nevertheless, be faster at moderate relative humidity than when rH is near 100% (because of the reduced availability of minerals for tissue synthesis in the lateral and apical shoot meristems).

Fertilizing will make minimal or no difference at 100% rH as there is not transport up the plant by transpiration. However, mineral nutrition could be via 'foliar feeding' wherein a fertilizer solution is applied to the leaves could be partially effective in overcoming the mineral nutrition issue of 100% rH. Minerals are then distributed by being actively loaded into/out of the phloem tubes.

Photosynthesis would be unaffected at 100% rH since all tissues would be hydrated. The consumption of water by PhotoSystem II, however, is the only mechanism that could cause some transport of water and minerals through the xylem when rH = 100% aside from root/stem pressure generated by osmosis.

REFERENCES:

Wikipedia - Mineral
Adsorption
Water ascent in plants: do ongoing controversies have a sound basis?
Chunfang Wei, Ernst Steudle and Melvin T. Tyree, trends in plant
science, September 1999, Vol. 4, No.
9
biology-pages: Transport of Water and Minerals in
Plants


Is Brain Eye connections reversed in all animals or just Humans?

That's not completely true. In mammals, including humans, the left of an image projects to the right of each of your retinae (this is due to the eye working like a camera obscura), and conversely for the right of an image. So you have 2 eyes, each eye receives mostly identical information but one is on the left and one is on the right of your body. You must somehow recombine this information together in the visual cortex. The way this is done is through the optic chiasma, where roughly half the nerves from the nasal parts (the half closer to the center of your body) of each retina cross. Then connect to a relay called Lateral Geniculate Nucleus and then connect to the brain. Below you can see a drawing from Ramón y Cajal, who first proposed this theory, depicting the process.

As you can see the points on each retina that receive information from the same parts of the visual field (here represented by the arrow) project to identical locations in the brain. So there is not a complete decussation (anatomical name for a crossing of nerves) like for muscles, but only a partial decussation of about half in humans.
Although y Cajal was the first to explain exactly why it makes sense to have partial decussation, this phenomenon had been known for a very long time. In facts Newton (hardly an anatomist) discusses that phenomenon in his Optiks and suggested that it might be related to the amount of overlap between the 2 eyes. So the more overlap, the higher the amount of partial decussation. This rule, later called Newton-Muller-Gudden law by Walls, seems to be approximately correct for mammals. However, as noted by Walls, there is no evidence of partial decussation in vertebrates other than mammals. Meaning that the decussation is complete (like muscles). In his Optiks Newton concludes that (I'm paraphrasing) if his theory is right then animals with no binocular overlap should have no decussation, which if he is well-informed is true for chameleons. His theory was indeed right but he was misinformed, chameleons have complete decussation.
Finally non-vertebrates do not have "contra-lateral" brains. They do not have this strange property of having each hemisphere mostly connected to the opposite side of their body. Therefore they have no decussation at all.
So in short: vertebrates-mammals = partial decussation ; vertebrates-non-mammals = total decussation ; non-vertebrates = no decussation.
Although dated, Walls book remain the most complete reference discussing decussation:
Walls, G. L. (1944). The vertebrate eye and its adaptive radiation.


Does increased physical activity increase the rate of cell division?

My understanding is that telomeres are linked to cell senescence, which is not necessarily the same thing as organism senescence. So even if you could track down a method to slow cell division, it would more likely mess with organ function now rather than extend life.

Here's a nice summary of cell senescence: http://www.ncbi.nlm.nih.gov/books/NBK26877/#A3266

I did look into cell division in muscle, and new muscle cells come from satellite cells, rather than from mitotic division of currently active muscle cells.

Caloric restriction was the hot new way to live longer for a while, but studies in primates found that a sensible diet and good genetics have a bigger effect. Which is pretty much the T-shirt in medical science.

This question was asked last spring as well. Coincidence? Homework?


Transcription and translation of prokaryotic operons

As you pointed out, the repressor gene lacI is transcribed as a one mRNA, and three structural genes: lacZ, lacY and lacA are transcribed into a single polycistronic mRNA. The two mRNAs are translated independently of one another.

The polycisronic mRNA is not broken into pieces. Rather, it is translated by ribosomes (at least three, explanation below), giving rise to three individual proteins.

How from one mRNA three protein products are translated? The polycistronic DNA consists of a promotor (Plac), which ensures that transcription will be initiated, and three open reading frames (ORFs) for for lacZ, lacY, and lacA. Upstream of each of the ORFs, ribosome binding sites (RBSs) are located. Translation is initiated by the binding of the ribosome with both the RBS and the start codon. Thus, multiple ribosomes can bind upstream of the three ORFs and thus resulting into three proteins.

There is not very thorough literature on the translation of polycistronic RNA in prokaryotes, mainly because the condition which is necessary for translation is the RBS and there is nothing specific for polycistronic translation. A brief overview on the subject can be found in several places, as I recommend the following:

Ralston, A. (2008) Operons and prokaryotic gene regulation. Nature Education
From Genes to Genomes: Concepts and Applications of DNA Technology
Molecular cell biology
Analysis of Genes and Genomes


Enzyme Inhibition by alpha-2 macroglobulin

Lets first see the proper definition of Suicide Inhibition as given by Wikipedia (emphasis mine):

  In biochemistry, suicide inhibition, also known as suicide inactivation or mechanism-based inhibition, is an irreversible form of enzyme inhibition that occurs when an enzyme binds $\alpha$ substrate analogue and forms an irreversible complex with it through a covalent bond during the "normal" catalysis reaction. The inhibitor binds to the active site where it is modified by the enzyme to produce a reactive group that reacts irreversibly to form a stable inhibitor-enzyme complex. This usually uses a prosthetic group or a coenzyme, forming electrophilic alpha and beta unsaturated carbonyl compounds and imines.

Now, lets see how $\alpha$-2-Macroglobulin works, again by Wikipedia (emphasis mine):

  $\alpha$M protease inhibitors inhibit by steric hindrance. The mechanism involves protease cleavage of the bait region, a segment of the $\alpha$M that is particularly susceptible to proteolytic cleavage, which initiates a conformational change such that the $\alpha$M collapses about the protease. In the resulting $\alpha$M-protease complex, the active site of the protease is sterically shielded, thus substantially decreasing access to protein substrates. Two additional events occur as a consequence of bait region cleavage, namely (i) the h-cysteinyl-g-glutamyl thiol ester becomes highly reactive and (ii) a major conformational change exposes a conserved COOH-terminal receptor binding domain (RBD). RBD exposure allows the $\alpha$M protease complex to bind to clearance receptors and be removed from circulation.

So, clearly, it is not suicide inhibition as:

$\alpha$M protease inhibitor does not form an irreversible complex with the protease, instead it uses steric hindrance to prevent protease from binding any substrate.
this inhibition does not occur during the "normal" catalysis reaction, it is after the protease has catalyzed a reaction that the inhibitor covers it up, more like the consequence of catalysis.
the inhibitor does not bind to protease active site, it covers the active site like a shield.

Putative mechanism of protease entrapment and inhibition by ECAM (Escherichia coli Alpha-2 Macroglobulin)

References:

Suicide Inhibition
$\alpha$-2 Macroglobulin
Structure of protease-cleaved Escherichia coli $\alpha$-2 macroglobulin reveals a putative mechanism of conformational activation for protease entrapment (PDF)


How can I keep HEK cells alive while expressing NMDA receptors?

Try perhaps lowering the level of expression of your construct. HEK cells are notorious for expressing large quantities of your transfected insert. Do you have it under a CMV promoter? Try a milder one, such as an ubiquitin promoter or similar or, even better, a doxycyclin-inducible system (e.g., clontech's tet off) so you can manage the expression levels through the dox concentration/time of induction.


Is the strength of presynaptic stimulus on the postsynaptic neuron affected more by the dendrites, or the cell body?

It depends on the type of axon, of course.
In Axosomatic synapses the properties of dendrite is not important, but for Axodendritic synapses, the properties of post syn. dendrite is more important as the amplification and other processing happen there. However, Soma is much nearer to Axon hillock, so changes by Soma wouldn't be declined as the impulses won't. It may be depended on neuron properties itself and so that's wrong to generalise!


What's the name of this Heteroptera bug from Toronto, Canada?

This is, indeed, a Heteroptera bug.

Luckily, this is not a kissing bug (which could be infected with Trypanosoma), but just an assassin bug, from the Species Reduvius personatus. Its common name is masked hunter.

Here is an image of the same bug, also in Ontario, from the Canada Pest Control website:

Source: http://pestcontrolcanada.com/5723-2/

And in this photo you can see the long rostrum, just like in your second photo:

Source: https://www.youtube.com/watch?v=9fIBT7IJHn8

Finally, to see an assassin bug in action (a different species, though), have a look at this video from the Smithsonian Channel: https://youtu.be/hXFRAmWiaa4


What is the human ear's temporal resolution?

I will provide an answer in 2 parts. The first part is a theoretical approach based on the absolute possible minimum (my original answer). The second part focuses on experiments in the peripheral auditory system (added edited answer).

PART I: Absolute theoretical minimum (original answer)
As you inquire about electrical signals in the auditory human system I have to say that electrophysiological data at such a fundamental level is scarce in humans. That having said, we can start off by looking at auditory clicks, which are generally the shortest possible well-defined auditory stimuli. The shortest auditory click I was able to find, and which was used in a psychophysical context (i.e., audible to a human) was 10 microseconds (Leshowitz, 1971).

Now, (1) assuming 10 microseconds is the lower duration limit of a click (it may well be lower), and (2) assuming this click duration is representative of the lower limit of a tonal burst duration limit (it may well not be), and (3) assuming you indeed wish to know about/use auditory tones and not clicks, and finally (4) assuming we need at least one wavelength of a tone to fit in this window, then we could present a frequency of 100 kHz, or higher. As 20 kHz is the upper frequency limit of the human ear, we would need at least 50 microseconds for one wavelength, i.e., basically what @Dustin concluded, but it does not end here:

Frequency splatter (Fishbach et al., 2001) limits the lower limit of tonal stimuli. To prevent spectral splatter one needs to incorporate rise and fall times (ramps) onto the tonal stimulus. Hence, again assuming you do want tonal stimuli, an onset and offset ramp of one wavelength each would be advisable (at the very least) and hence 3 wavelengths are needed, increasing the duration of a 20 kHz tone to 3 wavelengths, i.e., 150 microseconds (spectral splatter may not be prevented, but at least reduced).

On top of this theoretical approach, it has to be noted that I started off with taking a click as a starting point. A click, being an impulse signal, basically stimulates the entire cochlea (the inner ear), and hence represents the most powerful auditory stimulus. Pure-tone bursts are, as a consequence, weak stimuli as they stimulate a small proportion of the available hair cells. High sound levels may therefore be necessary for short tonal stimuli, in turn degrading the frequency resolution in the cochlea as excitation spreads away from the characteristic frequencies. Mostly, several milliseconds are used as tone bursts.

Moreover, taking 20 khz is kind of an upper limit, and many folks are not even able to hear 16 khz. An upper limit of, say, 12 kHz would be advisable when grownups are used. This means a wavelength of 83 microseconds and for 3 wavelengths (for ramp times) that means 250 microseconds.

If lower frequencies are needed, this number would increase further.

EDIT: PART II. Phsyiological experiments.
As you are also interested in electrical signals, we might take another approach and start looking at experimental (animal) data. The temporal limits of the auditory system are generally assumed to reside in the ribbon synapse that is situated between the inner hair cells and the auditory nerve fiber (Parsons, 2006):

This synapse is considered to be the limiting factor in the temporal characteristics of the auditory system (Khimich, 2005). By analyzing this synapse using very short tone bursts, it was shown that the vesicles of glutamate (the neurotransmitter activating the auditory nerve fibers that lead the signal to the brain) were released as shortly as 2 ms after tone onset. Tone bursts were 8 - 16 kHz, 10 ms plateau, 1 ms
rise/fall (Khimich, 2005). Note the tone burstduration and rise fall times mentioned in answer PART I.

Indeed, when first spike times in auditory nerve fibers were determined, spikes with the shortest latency occurred just under 2 ms (Heil and Irvine, 1997).

SR in the figure means spike rate, showing that higher spike rates are accompanied by shorter latencies. A1 means auditory cortex neurons, which obviously have longer latencies.

Hence, from these experiments I dare say that 2 ms would be sufficient to elicit at least one spike.

Why then leave part I of the answer? The problem is that the experimental data do not show that a spike wouldn't have been generated at shorter stimuli. The data merely show that with an ongoing stimulus the first spike appears at 2 ms. It does not show whether 2 ms of temporal summation is necessary, and that is why I have left part I of my answer in place, as a theoretical lower bound.

As a side note: the spike rates are highly dependent on loudness levels. Lower sound levels result in longer latencies. Specificaly, acceleration of the stereocilia on the inner hair cells in the cochlea is the primary parameter. The faster the cilia move, the faster the spike response.

References
- Heil & Irvine. J Physiol 1997; 78:2438-54
- Fishbach et al. J Neurophysiol 2001; 85:2303-23
- Khimich et al. Nature 2005; 434:889-94
- Leshowitz et al. J Acoust Soc Am 1971; 49, Suppl 2:462-6
- Parsons. Nature 2006; 444:1013-4


Will the increase in atmospheric carbon dioxide lead to larger insects?

There is the supported theory that insects during the Paleozoic period were larger in size because of the increased oxygen content in the air.

The study adds support to the theory that some insects were much larger during the late Paleozoic period because they had a much richer oxygen supply.
The Paleozoic period, about 300 million years ago, was a time of huge and abundant plant life and rather large insects - dragonflies had two-and-a-half-foot wing spans, for example. The air's oxygen content was 35% during this period, compared to the 21% we breathe now, Kaiser said. Researchers have speculated that the higher oxygen concentration allowed insects to grow much bigger.

This article is based on a paper published in the American Physiological Society:

It is because when the oxygen concentration in the atmosphere is high, the insect needs smaller quantities of air to meet its oxygen demands. The tracheal diameter can be narrower and still deliver enough oxygen for a much larger insect, Kaiser concluded.

There are similar papers that investigate the relationship between oxygen and maximum potential size, such as this article published in Nature (1999):

The tendency of some animals to be larger at higher latitudes ('polar gigantism') has not been explained, although it has often been attributed to low temperature and metabolism. [...] We have analysed length data for 1,853 species of benthic amphipod crustaceans from 12 sites worldwide, from polar to tropical and marine (continental shelf) to freshwater environments. We find that maximum potential size (MPS) is limited by oxygen availability.

Another paper published in Proceedings further supports this theory:

[...] A variety of recent empirical findings support a link between oxygen and insect size, including: (i) most insects develop smaller body sizes in hypoxia, and some develop and evolve larger sizes in hyperoxia; (ii) insects developmentally and evolutionarily reduce their proportional investment in the tracheal system when living in higher PO2, suggesting that there are significant costs associated with tracheal system structure and function; and (iii) larger insects invest more of their body in the tracheal system, potentially leading to greater effects of a PO2 on larger insects.

The question you propose is very interesting, although I am sure it would take thousands of years for these insects to adapt to this oxygen level change (which in itself, to reach prehistoric levels, would take a long time) and in turn become larger.
This article, based on the original APS paper, seems to think larger insects could appear in the future if the limiting factor (in this case low oxygen levels) is removed.

Image from Biotic interactions modify the effects of oxygen on insect gigantism (PNAS, Chown 2012).


Gene APOA2 SNP rs5082 alleles are A or G, but papers describe it with CC and TT?

The rsID letters are assigned based on the genome being the default "forward" direction while the researchers on that gene think of the nucleotides of the context of the transcript, (or in this case the promotor sequence) which runs backwards.


Apart from nerve cells and muscle cells, what types of cells do not undergo mitosis in adult man?

To answer the numbered questions:

In general, neurons never divide by mitosis. However, I believe you may have unintentionally misphrased your question; there are functional neural stem cells in the adult human brain as well, and these are believed to give rise to new neurons throughout the lifespan of an individual. They have only been found in specific parts of the brain, though, such as the SVZ and the subgranular zone of the hippocampus (Gonzales-Perez 2012; Behnan et al. 2017). It also bears noting that following an external insult (such as DNA damage, oxidative stress, hypoxia), even terminally differentiated neurons can re-enter the cell cycle and go as far as to replicate their DNA, but this tends to result in apoptosis or arrest at the G2/M phase; such aberrant re-entry into the cell cycle is more frequent in brains afflicted by neurodegenerative diseases (Frade & Ovejero-Benito, 2015). In addition, the possibility to induce neurons to proliferate and form cancers has been demonstrated in retinal cells in mice (Ajioka et al. 2007).
Correct; as with neurons, muscle cells (myocytes) lack the ability to undergo mitosis. But again, I believe what you really want to ask is whether or not muscles maintain a pool of stem cells that can replace lost cells. The answer to this is yes—there are stem cells within skeletal (Wang, Dumont & Rudnicki 2014)  and smooth muscles (Majesky et al. 2011) that proliferate in response to damage. According to some studies there are stem cells in the adult heart as well, although their regenerative capacity appears to be very low (Bergmann et al. 2009).

If your intention was indeed to ask about which cells are unable to undergo mitosis, then the answer will likely be a very long list, as no terminally differentiated cell type undergoes division under normal circumstances. This would, for example, include all different blood cell types (erythrocytes, megakaryocytes, neutrophils, eosinophils, basophils, B-cells, T-cells, natural killer cells, mast cells, macrophages), most skin cells (e.g. keratinocytes, melanocytes), epithelial cells (such as those that form the intestinal lining) and such. This would likely include most if not all of the cell types listed here that do not have the "(stem cell)" note next to the links (although I did not confirm this by checking the literature on them).

References:

Ajioka, Itsuki, et al. "Differentiated horizontal interneurons clonally expand to form metastatic retinoblastoma in mice."
Cell 131.2 (2007): 378-390.
Behnan, Jinan, et al. "Identification and characterization of a new
source of adult human neural progenitors." Cell death & disease 8.8
(2017): e2991.
Bergmann, Olaf, et al. "Evidence for cardiomyocyte renewal in
humans." Science 324.5923 (2009): 98-102.
Frade, José M., and María C. Ovejero-Benito. "Neuronal cell cycle: the neuron itself and its circumstances."
Cell cycle 14.5 (2015): 712-720.
Gonzalez-Perez, Oscar. "Neural stem cells in the adult human brain."
Biological and biomedical reports 2.1 (2012): 59.
Guo, Dayong, and Lynda F. Bonewald. "Advancing our understanding of
osteocyte cell biology." Therapeutic advances in musculoskeletal
disease 1.2 (2009): 87-96.
Majesky, Mark W., et al. "Vascular smooth muscle progenitor cells:
building and repairing blood vessels." Circulation research 108.3
(2011): 365-377.
Wang, Yu Xin, Nicolas A. Dumont, and Michael A. Rudnicki. "Muscle
stem cells at a glance." (2014): 4543-4548.


You cannot change the oxygen concentration of inhaled air in the absence of an external source of oxygen. However, you can use your lungs at their maximum capacity doing this:

breathe deeply: =increase tidal volume. Your muscles will inflate your lungs as much as they are able to, inflating parts of the lungs that were not fully inflated (atelectases) in the process. This also allows you to inhale a volume much greater than your physiologic dead space (volume of inhalation that does not participate in gas exchanges)
breathe to high enough frequency: the faster you will want to expel $CO_2$ and replace it with room air, the higher frequency you will need to adopt.

Frequency and tidal volume are the two components of minute ventilation (= (frequency/minute) X tidal volume), which is the physiologic value you are working to increase.

Position: The upright position is best suited, since the weight of the lung tissue pulling downwards will facilitate inflation

WARNING: using those techniques unsupervised can cause acute respiratory alkalosis, which is unhealthy and puts you in immediate danger.


Which C. elegans would be appropriate for general study?

I suspect that that dpy-11-mutants (that's what you likely meant) are not very representative neither from the morphological nor from the behavioral points of view, because they have anomalies in body shape (dumpy appearance) and male tail morphology (see in WormBase and in Ko and Chow).

For a general purpose the wild-type should be best.


Do foods with preservatives become less toxic in the gut?

Do foods with preservatives take longer to digest?

Food preservatives are either antimicrobials (e.g. sorbate, sulfite) or antioxidants (free radical scavengers such as butylated hydroxyanisole).

Digestion is initiated in the stomach by hydrochloric acid and pepsin. It continues in the small intestine with the action of numerous other enzymes including amylases, lipases and proteases. There is no obvious way that these digestive processes would be inhibited by preservatives.


Why do cells in meristematic tissues lack vacuoles?

Meristematic tissues or meristems contain cells which can rapidly divide or reproduce and is responsible for the overall growth of the plant. Apical meristems and lateral meristems are found in the roots and stems of the plants. Please note that the whole stem or root is not laded with these tissues. Plant cells usually have a large central vacuole which applies turgor pressure to keep the plant upright, as mentioned in one of your sources.
The tips do not require to be very stiff and straight. So, a central vacuole is just not required. Also, meristematic cells grow various organelles as they mature.


What kind of fish is this (Florida, USA)?

So after much more time on this than I should have, I am pretty confident this is a silver jenny (Mojarra).

Silver Jenny, Eucinostomus gula

  "The Silver Jenny, Eucinostomus gula, whose common Spanish name is
  mojarra Española, is a species in the Mojarra or Gerreidae Family,
  known collectively as mojarras in Mexico. Globally, there are eleven
  species in the genus Eucinostomus, all of which are found in Mexican
  waters, seven in the Atlantic and four in the Pacific."

Dorsal fin structure, tail fin split, location of ventral fins and gill fins all match up, as does color.  So does the faint stripe from top of gill to back of fish. The last clue was the protrusible mouth.

I'm surprised you found it in a canal, as it is a saltwater fish. Were you close to the ocean?  From the link above:

  The Silver Jenny are an abundant schooling species that are found
  seasonally in shallow coastal waters over mud bottoms in mangrove
  lined lagoons and creeks in waters that are between 11oC (52oF) and
  28oC (82oF) at depths up to 175 feet. Juveniles are found in seagrass
  beds. They may also enter freshwater. They are known to make seasonal
  migrations to off-shore warmer waters during the cooler months for
  wintering and hibernation returning to coastal waters in the spring
  for breeding. They reach a maximum length of 23 cm (9.1 inches). They
  are benthic feeders that probe the bottom with their protrusible mouth
  consuming bivalves, crustaceans, ostracods and detritus. They are a
  poorly studied species and very limited information is available about
  their behavioral patterns.

Last Link here


Why the scent of mouth gets dirty after not eating for a long time?

This is caused by a build up of ketone bodies in your blood which lowers the pH of your body and can cause bad breath. Ketone bodies are a response of your body breaking down fatty acids for energy instead of glucose when in a low food intake (fasting) state. This is also true for morning breath since your body has been in a fasting state.
The way to prevent this is to eat the proper amount of calories needed for your body to function normally.


It is assumed that in order for a cell to divide it must progress through a series of gradual stages. At each of these phases certain proteins have to be manufactured through mRNA and/or modified post-transcriptionally in order to serve an specific proliferative or anti-proliferative role, which overall eventually orchestrates the transit to the subsequent stage.

Conventionally the cell cycle is comprised of 3 "interphase" stages prior to execution of Mitosis itself: G1 (growth, metabolically active), S (synthesis of DNA to duplicate genetic material in preparation for its splitting into two daughter cells), and G2 (gap phase where a numerous of quality control checks are undertaken in the form of surveillance of the newly produced DNA for example to ensure viability of the progenies).

Under these premises, the protein content of a cell at an specific phase is expected to cycle or oscillate in accordance with its requirements, and this is linked to mRNA cyclicity as the most direct responsible process for modulation of protein abundance. It is then related to the cell cycle in the sense that in order to transit from the G1 phase for instance, proteins involved in DNA synthesis will need to be produced, and thus protein factors released for the transcription of those certain mRNAs to take place.

Experimentally such dissection of cell cycle-regulated genes is tricky. Extracting mRNA from pure sub-populations of cells at specific stages of cell division is challenging as the isolation of such cell sub-populations is normally through chemical enrichments and sub-optimal synchronisation procedures. The signal to noise ratio is not ideal under these circumstances.

In brief, the cell cycles through stages in order to divide and such cycling is in itself due to the cycling of certain proteins, the most renown ones are called precisely "cyclins", which are protein markers of cells division. Cyclin D, E, A, B prevail differently at different stages of the cell cycle as a result of the balanced equation of mRNA transcription and post-transcriptional protein modifications (phosphorylation events mark them for degradation for example).
Overall an intertwined and well-coordinated process.

*** EDIT

For a suitable selection of some basic bibliography on the subject, robust sources covering the subject with rigour (less specific and dense than the journal articles I comment bellow) please refer to the following links:

Molecular Biology of the Cell
Molecular Cell Biology
Cell Cycle Regulation
The Cell Cycle Principles of Control

& even a review of the latter here.

HTH


A good place to begin is with the experiments of Hans Speymann and Hilde Mangold, done in the 1920s. They transplanted a piece of the dorsal lip in a newt gastrual to the ventral side of another newt gastrula with different pigmentation. Because of this transplant, a "secondary" embryo formed, on what would have been the belly, in addition to the standard embryo expected. (Some picture show this to be rather like a second head.) Use of differently pigmented embryos allowed the researchers to note that the transplanted dorsal lip material developed into a second notochord. But the interesting facet is the newly developing notochord induced the development of a new neural tube in the adjacent cells which were otherwise destined to become "belly stuff".

My appologies for not finding a great reference with diagrams, my source is the 7th edition of Biology, Campbell and Reece. Here's a very thorough reference, with diagrams, if you're up for it.
https://app.shoreline.edu/kwennstrom/spemannmangold.pdf
This work contributed to a Noble Prize for Speymann. The bottom line here is that tissues receive information from adjacent tissues that influence their developmental fate.
Later experiments showed that the inducing agent was chemical in nature


Bright green caterpillar with long white stripes, few hairs, no extensions, possibly Noctuidae

This could be one possibility, two others would be:

Scoliopteryx libatrix (The Herald (moth)), see this image (from here, contains additional information in german):

Orthosia cerasi (Common Quaker) would also fit, see here (from here, contains additional information in german):


What kind of insect is this found in North America in April?

It is a ladybug larva.  They eat aphids.  I have handled many and never been bitten.

https://test.whatsthatbug.com/2010/10/25/ladybird-beetle-larva-ladybug/


This is a tortoise beetle, a coleopteran from the Family Cassidinae.

According to the Queensland Museum:

  tortoise beetles are quite distinctive because they’re actually quite flattened and their wing covers are expanded around the edges. So the wing covers are the hard forewings that protect the hind wings in beetles and because they’re spread out at the sides, they look somewhat like a turtle or a tortoise. So that’s how they get their common name.

There are many beautiful specimens, like these:

Your photo is not exactly the best one, but based only on it I'd say that your specimen is a golden tortoise beetle (Aspidimorpha sanctaecrucis):

Here is another image of it, even more similar to your specimen:


Are human males and females more genetically different than members of other species?

I'm not sure I buy your premise: firstly, the degree and form of male-female differentiation in social roles has varied widely across time and culture in human history so I doubt it forms a uniform evolutionary driver such as you describe. Secondly, the degree of male-female differentiation appears to me to be much greater in species such as gorillas, lions and peacocks than it does in humans so I'm not convinced that humans would stand out on this front as a species we'd expect to have greater genetic differences.

Even so, the only genetic difference between male and female humans is the Y-chromosome. The X appears in both males and females and doesn't have exclusively female lineage so it can't acquire separate genes for male and female. The Y chromosome contains very few genes so its not capable of manifesting a major genetic gap and because there is no recombination in the Y chromosome it is not a fertile ground for new genes anyway.

So males and females have essentially the same genes. However, this isn't the whole story because how, when and whether genes are expressed is about as important as what genes are encoded anyway. It is these differences that enable big differences between the sexes not actual coding differences.


What is accumulation and release centre of neurohormones?

The neurohormones in most mammals include oxytocin and vasopressin, both of which are produced in the hypothalamic region of the brain and secreted into the blood by the neurohypophysis (part of the pituitary gland).

A second group of neurohormones, called releasing hormones, also originates in the hypothalamus. The members of this group, however, are transmitted within the neural cells to a second locus in the brain, from which they pass in the bloodstream to the adenohypophysis, which also is a part of the pituitary gland. There they either stimulate or inhibit the release of the various adenohypophysial hormones.

A third group of neurohormones includes the enkephalins and other endorphins. The endorphins are effective in relieving pain, a property apparently related to their function as neurotransmitters, passing nerve impulses from one neuron to another. Their neurohormonal activity is manifested by their stimulation of the secretion of somatotropin and vasopressin by an indirect process involving a site (other than the secretory neuron) in the central nervous system.


The species in the photo is a carpenter ant (Camponotus irritans), possibly C. i. hongkongensis. More info, photos, and video here.


Is there any free software similar to CellDesigner that allows me to represent large networks of biochemical reactions in the human body?

Here is a list of such programs. It is an old post but most of the tools it lists appear to still be functional. I found this by just googling "celldesigner alternatives", which is always a good idea to search first for these things.

I have used cytoscape and it is ok, maybe too general also for your purposes. For very simple purposes I have used KEGG pathway in the past, which is in addition to the others.


What do arranging and assigning mean in sequence annotation?

Word "arranged" means simply alignment of sequence based on overlapping regions in two sequences. For example:

Seq1: AGTGTCCGTCGTAAGTCA

Seq2:GTCGTAAGTCATCGAGATACC

leading to:

Seq12: AGTGTCCGTCGTAAGTCATCGAGATACC

Maybe he used the word "arrange" as overlapping determines the direction of resultant sequence (for which word alignment is sufficient)

Assignment: Is simply dividing the genome's sequence down as per chromosomes of the species. Like for example, if it's human genome sequence and first chromosome is 2,50,000bp long (just assumption - I don't remember exact figure), then first 2,50,000 nucleotides in the sequence will be "assigned" to chromosome 1. From 2,50,001 onwards to chromosome 2 and so on..


Why is active transport needed in repolarization?

...when the movement of ions is not against their concentration gradient...

This assumption is incorrect: Na+ has to be pumped out of the cell against its chemical gradient (table 1) and against its electrical gradient, given that the inside of the cell is negative (Fig. 1).

  ...potassium ions have diffused out in repolarization, only the sodium ions are left in the intracellular space

This is incorrect: There are heaps of K+ ions in the cell, also after repolarization. A tiny fraction exits the cell during repolarization.

  ...moving out of the cell where there are no sodium ions...

This is incorrect; there are Na+ ions out of the cell, heaps in fact. You should be aware that the flux of ions is not an all-or-nothing phenomenon. It is a flux of relatively few ions out of a pool of them. Action potential formation and ion gradients are membrane-bound phenomena. While Na+ may enter the cell during an action potential, there is still a nearly infinite large amount of Na+ left in the intercellular space.

Table 1. approximate ion concentrations in and out of the cell. source: Med Quarterly

Fig. 1. Action potential. source: UC Davis


Why White Blood Cells (WBCs) do not react to foreign bodies like sperm?

Majority of white blood cells in general are present only within blood vessels, lymph vessels and lymph nodes. In addition various organs have locally adapted specialised immune cells. For example brain has microglia, Liver has kupfer cells, etc... Specialised immune cells are present along the mucosal linings which are named differently in different regions - Peyer's patch in the jejunum and ileum, tonsils in oral cavity, adenoids in the nasopharynx, etc...

As sperm do not enter blood vessels, only local mucosal immunity will act on them. There is a local immune response to the sperm in the vaginal mucosa. However, the immune response to the sperm is transient. Several hypotheses have been put forth to explain this:

The seminal plasma suppresses the immune response. This is supported by the fact that sperm, if introduced without seminal plasma, do elicit an immune response--however this suppression seems to be inconsistent
Insemination might activate a sequence that results in active immune tolerance to paternal antigens (antigens present in sperm)

For details see here:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1782486/


Coniferous trees in temperare rain forests

The largest area of temperate rain forest in the world is on the west coast of North America, which has a summer dry season. In other words, at precisely what would be the best time for plants to grow (based on temperature), there's a shortage of water. (Summer vacation visitors to the rain forests on the Olympic Peninsula are often wondering "where's the rain?")

Conifers have small, waxy, and (generally, with a few exceptions) evergreen leaves. All the conifers in the rain forests of western North America are evergreen; that allows them to grow in the cooler months of the year, when there can occasionally be hard frosts (and when deciduous trees are dormant). The waxy, small leaves help them conserve water in the dry summers. A double advantage.

North of about central BC, there's no longer the summer dry season, but by that point the growing season is getting short enough that conifers have an advantage despite the perhumid climate (Prince Rupert, BC is further north than Edmonton, Alberta).

I'll add that this is not the only non-boreal climate where conifers are abundant: consider for example the piñon-juniper woodlands of the American Southwest or the Piney Woods of the Deep South.


Factors That Would Promote Eusocial Development In Mammals?

What?
Eusociality in mammals can be defined by the following criteria:

reproductive altruism (which involves reproductive division of labor and cooperative alloparental brood care);
overlap of adult generations;
and permanent (lifelong) philopatry (stays (or returns) at (to) breeding ground).

Why?
Burdo et al. (2000) state that eusociality in mammals is a special case of monogamy, involving prolonged pair bonding for more than one breeding period. They argue that eusociality in mole-rats evolved from a monogamous mating system where cooperative brood care was already established. A tendency for group living is considered to be an ancestral trait in some genera of mole rats. The solitary lifestyle seen in some other genera is assumed to be a derived trait.

The aridity food-distribution hypothesis (AFDH) suggests a causal relationship between cooperative foraging for patchily distributed resources and the origin of eusociality. This theory states that limited nest sites or patchy resources leads to benefits of staying within the natal group, including reduced dispersal risk, and the possibility of inheriting the natal nest (Plowes, 2010).

How?
In proximate terms, in eusocial mole-rats either puberty is assumed to be developmentally delayed so that under natural conditions most animals die before dispersal is triggered. If genetic relatedness among siblings is high, then philopatry would not invoke an appreciable loss of fitness, especially if the cost of dispersing is higher than staying within the natal group. High genetic relatedness is more likely in a monogamous mating system or a highly inbred population (Burdo et al., 2000).

References
- Burda et al., Behav Ecol Sociobiol (2000); 47(5): 293–303
- Plowes, Nature Education Knowledge (1010); 3(10): 7


I'm not an entomologist, but it seems to me that this bee is a Xylocopa, or a carpenter Bee:

Xylocopa iris

If this is, in fact, a Xylocopa, narrowing it down to the species level will be very difficult, since the Genus has more than 500 species. You could start with one of the most common carpenter bees in Europe, Xylocopa violacea:

Xylocopa violacea

However, I believe that this may be in fact Xylocopa violacea because of the antennae: you can see a little orange stripe next to the tip of the antenna in the bee of your photo, just like in the bee of the photo above.


It is not trivial to define a "colony/society". Sure, you can say "this bacterial blob is a colony", or "this ant nest is a colony", and so on, but these would be your own definitions. These systems you mention don't have definite boundaries (temporal or spatial). Although physicists like to do gross approximations to things in nature (and I'm pretty sure there is already some paper 'answering' your question), I'm not sure anyone can get a "precise relation" for a concept that even biologists struggle with (that of a "colony"). This is because at core, what you are really asking, is what is a biological individual and how can I measure it? (the individual ant, the individual colony, etc); and that's something we have no answer for. For what is worth, I recommend you read about the problem of biological individuality, which will give you no answer to your question but at least can tell you why you can't really answer it: https://link.springer.com/article/10.1162/BIOT_a_00068


Short answer:

Yes the legume seed protein content decrease when it germinates.

but still;

The sprouting seed is healthier.

Long answer:

Yes it is true that after germinating some of the protein decrease. It is mostly due to breakdown, transport and consumption of protein stored in seed. All fabaceae (former Leguminosae-sensu-stricto) members use a large amount of protein storage, such as Vicillins, Legumins, etc in their seed cotyledons . All edible true-pulses , including pea , mung, etc belong to fabaceae.  When the seed germinates, theses proteins breaks down into simple amino acids and small peptides, and get reallocated*.  In addition, a part of this work as food (respiratory substrate) through amino acid oxidation  **.

  Fig-1

  Protein mobilization in seeds... simplified.
  Source... *

  Fig-2
  .
  The cellular process of protein mobilization in Mung bean cotyledon.
  Source ... *

We are commonly advised to eat sprouting seeds not for their protein content (we get the major portion of protein from daily major foods like meat, fish, eggs, leafy vegetables, etc.); but it is for the vitamin content.

This paper says

  " Mung bean sprout produces several kinds of hepatoprotective compounds such as flavonoid and chlorogenic acid."

There are also many papers related to sprouting mung bean; such as this but I do not have full access to them (sorry for that), such as this, this etc.

  Reference

  * Protein Storage and Utilization in Seeds; by Rod Casey, J.Derek Bewly and John S. Greenwood. Published as a chapter in a book, Plant Metabolism, Edited by Dennis, Turpin, Lefbvre, Lyzell. Second Edition.
  ** Amino Acid Catabolism in Plants; Tatjana M. Hildebrandt , Adriano Nunes Nesi, Wagner L. Araújo, Hans-Peter Braun (NCBI-PMC) (Full-text Free Open access link)


When is Water Produced During Photosynthesis?

Some of the water that's split is regenerated when the hydroxyl radicals (reactive oxygen species) are converted to hydrogen peroxide, water, etc. by superoxide dismutases and antioxidative mechanisms in the chloroplast (peroxisomes/catalases, etc. take care of this). There's also some evidence that the presence of mannitol, ascorbate and glutathione protect against ROS produced in chloroplasts as well. So you input water, and in an effort to avoid oxidative damage, you do get some water generated. However, the balanced equation doesn't reflect this because it's not an actual product of photosynthesis.

About ROS and protective elements

Extra Reading on ROS in photosynthetic systems

I think that's a very obscure fact, and despite the reality of things, it's actually difficult to query the literature. Good question.