Are there differing organelle to cytoplasm ratio in animal cells?

Yes.

The structure of a cell is highly related to its function. For example, a plasma B cell (a type of immune cell) contains lots of ER and Golgi because its job is to secrete antibodies, which are proteins, in your body. It has to create a lot of proteins, so a plasma B cell has a lot of organelles that help create, assemble and secrete proteins.

There are so many examples you can use.


Preface:

Any question about adaptation on macro-level has very little meaning and no precise answer.
There are two types of larvae in invertebrates: primary ("original") and secondary (evolved from post-larval stages). Not digging into the details, nauplius (together with metanauplius) is the only type of primary larvae in Crustacea and it never has a carapace.
"Majority" is by far too strong term, even if we are talking about all larval types. If we just take the largest crustacean orders with species numbers > 1000, together comprising 92% of crustacean species (species numbers are from Ahyong et al, 2011, they seem to be largely correct):

Decapoda - 14.7 k species - rarely have nauplius, marine forms do have planktonic carapaced larvae (principally - zoea)
Isopoda - 10.7 k - no carapace
Amphipoda - 9.9 k - no carapace
Podocopida - 6.2 k - no carapace
Harpacticoida - 6.0 k - no carapace
Cyclopoida - 4.2 k - no carapace
Calanoida - 3.1 k - no carapace
Siphonostomatoida - 2.5 k - no carapace
Cumacea - 1.5 k - have carapace, but development is direct
Mysida - 1.2 k - have carapace, but development is direct
Tanaidacea - 1.1 k - have carapace, but development is direct

So, "majority" could be applied to Decapoda only.

Fabula:

If we substitute "adaptation" with "main biological function" (as you have done) or more correctly "main physiological role":

I would prefer the (a), because carapace does function as a protective structure in those decapod larvae which don't rely on behavioral anti-predatory defenses: see Morgan: "Fishes quickly learned to avoid spined prey, which ... may also increase the rate of evolution of the character". Non-carapaced larvae rely principally on behavior only.

The only contribution of carapace to planktonic life-style in zoea is participation of its spines [when they are pronounced] in parachuting (Chia et al).

[The above should be largely true also for the cypris larva of the cirripeadians, which are enclosed in a non-spined bivalve carapace.]

From the morphological point of view, [at least in adult forms of decapods] carapace creates a chamber for gills, so a morphologist would argue that this is the "main function" of carapace.


What does enzymatic equilibrium in % represent?

You are correct in stating the relative rates of the two reactions.  What may have you confused is the percent sign in the statement.  The percent sign is not a unit in the sense that you are taking it.

What you have in a simple reaction like you are examining are two opposing rates of reaction.  The rate of a catalytic reaction, like others, usually depends on the concentrations of at least some of the reactants in the direction under consideration.

At equilibrium, by definition, the concentration of every material involved in the reaction is unvarying.  Otherwise, the reaction would not have reached equilibrium yet.  What that also means is that the rates of the forward & inverse reactions are equal at equilibrium.  So what does the statement signify?   It means that thermodynamically, the synthase reaction is the more unfavorable direction.  That is, at equilibrium, the product concentration of the synthase direction will be in the minority.

The statement involving the percent sign is just giving the ratio between the [arbitrary] forward direction, here stated as the synthase direction, and the inverse reaction.  The percent sign is just a mathematically short way of stating that the number stated is parts per hundred.

The equilibrium constant K is exactly the same ratio, stated as a decimal value rather than a integer per hundred.


What organisms are Chloroperoxidase enzymes found in?

It is only found in an ascomycetes which is named Leptoxyphium fumago, also known as Caldariomyces fumago.

It isn't found in any other specie that we know of yet as searched on the RCSB PDB and Uni-Prot.

In researches that uses it they extract it from the organism, it is also available to buy from companies like Sigma Aldrich who extract it from the ascomycete too.

Sources:

Improvement of activity and stability of chloroperoxidase by chemical modification

Over-expression of chloroperoxidase in Caldariomyces fumago.

RCSB Protein Data Bank

Uni-Prot


Inhibition of beta-oxidation by acetyl- or malonyl-CoA

Mammalian $\beta$-oxidation occurs in the mitochondrion, whereas fatty acid biosynthesis is cytoplasmic.

The rate-limiting in mammalian fatty acid oxidation is considered to be carnitine palmitoyltransferase (CAT), a key enzyme in the transport of acetyl-CoA across the inner mitochondrial membrane.  This enzyme is inhibited by low micromolar concentrations of malonyl-CoA (see Beta oxidation of fatty acids by H. Schulz).

Malonyl-CoA, of course, is a key intermediate in fatty acid biosynthesis.  Salih Wakil showed that CO2  is required for fatty acid biosynthesis, but that carbon atoms from CO2  do not appear in fatty acids, and it is now known that this is due to the formation of .malonyl-CoA by acetyI-CoA carboxylase, the rate-limiting reaction of fatty acid synthesis.

Thus when fatty acid biosynthesis is taking place, the concentration of malonyl-CoA is high and CAT (and therefore $\beta$-oxidation) is inhibited (Schulz, 1991).

However, as the OP points out, micromolar concentrations of acetyl-CoA inhibit 3-ketoacyI-CoA thiolase when the concentration of CoASH is low, and the Acetyl-CoA/CoASH ratio within the mitochondrion may also play a role in the regulation of beta-oxidation (Schulz, 1991).

As the OP says, it is a debatable point, and it seems to me, an example of a badly worded exam question.  I think the 'expected' answer is probably malonyl-CoA, and there is no doubt that this molecule plays a key role in the regulation of both fatty acid oxidation and fatty acid biosynthesis.  Nevertheless, the inhibition of thiolase by Acetyl-CoA may also play a role in the regulation of beta-oxidation.

Perhaps your Professor is an example of the type that Warburg told Hans Krebs to attach himself to? :-)


Ribosomal Turing Machines, DNA/RNA computation

I'm no expert at this but I don't think you need a Turing machine to achieve this, at least for DNA, since in conventional sense (not including carcinogenic factors such as UV) the most probable stage in which a DNA mutation can happen is during DNA replication so DNA polymerase engages in proofread to ensure accurate DNA replication, and then the DNA can get back into being heterochromatic (eventually). This will be more difficult for RNA as they are single stranded although they do fold onto themselves.

Also there many many strands of RNA that are produced through alternative splicing, VDJ recombination and RAG imprecise rearrangements for antibody production, which can give rise to infinite possible RNA productions. So how would you know what is "good" and what is "bad" in terms of RNA and its production. Half the time we don't even know what they do and what their roles are and the only reason we call something as a "bad" or "faulty" RNA is because it is having a negative effect not because we understand the precise role of the sequence, which means a theoretical table would be useless.

So in short, a turing style protein machinery is neither possible (due to almost infinite potential number of RNA produced) nor feasible (since the number of proteins that would have to check each RNA sequence would in turn have to be almost infinite). And none of these takes into account SNPs i.e. individual variations, which can produce proteins with different sequence but identical structure/function, since obviously any lethal variations would be selected against but thats a whole different argument.


Why can human viruses that can't infect chickens be grown in embryonic chicken cells?

The measles vaccine uses an attenuated virus: one that has been  modified to reduce virulence such that it is (hopefully) no longer harmful to the host but still retains the antigenic determinants to induce acquired immunity. Although in modern times rational attenuation by genetic engineering is becoming established [1], the traditional method involves simply growing the virus under conditions abnormal for it such that it must evolve to survive. This often involves culturing the virus in cell types (or possibly organisms) in which it does not typically cause infection. Due to existing variation within the viral population or novel mutations, the virus may, over time, adapt to infect these cells with some degree of efficiency. Importantly in the context of vaccine development, the genetic changes generated during this adaptation may also reduce the pathogens ability to causes disease in the host organism [2].
This effect was originally observed by Louis Pasteur in 19th century who subsequently used it to develop a vaccine against the bacterium Erysipelothrix rhusiopathiae, which infects pigs [3]. Pasteur noticed that propagating this bacterium in rabbits, in which it did not initially cause disease, increased its pathogenicity in rabbits while at the same time reduced its pathogenicity in pigs. The virus had evolved and this attenuated form was used as a vaccine in pigs.
The attenuated virus for measles vaccine was created by the same principle in the 1950s to 1960s. An isolate of the measles virus from an infected patient was successively passaged through human kidney cells, human amnion cells, fertilized hen's eggs [4] and chick embryonic cells [5]. This attenuated virus, which was now replicative in chick embryonic cells, was no longer infective in humans and was used as the basis of the measles vaccine [6].

References
[1] Bull JJ. 2015. Evolutionary reversion of live viral vaccines: Can genetic engineering subdue it? Virus Evol 1(1):vev005
[2] Badget MR, Auer A, Carmichael LE, Parrish CR, Bull JJ. 2002. Evolutionary Dynamics of Viral Attenuation. J Virol 76(20):10524–10529
[3] Bazin H. 2003. A brief history of the prevention of infectious diseases by immunisations. Comp Immunol Microbiol Infect Dis 26(5-6):293-308
[4] Milovanovic MV, Enders JF, Mitus A. 1957. Cultivation of Measles Virus in Human Amnion Cells and in Developing Chick Embryo. Exp Biol Med  95(1):120-127
[5] Katz SL, Milovanovic MV, Enders JF. 1958. Propagation of Measles Virus in Cultures of Chick Embryo Cells. Exp Biol Med 97(1):23-29
[6] Enders JF, Katz SL, Milovanovic MV, Holloway A. 1960. Studies on an Attenuated Measles-Virus Vaccine — Development and Preparation of the Vaccine: Technics for Assay of Effects of Vaccination. N Engl J Med 263:153-159


SRY translocation to the X chromosome clinically exists and characterizes the De La Chapelle Syndrome. The phenotype associated to this syndrome demonstrates the necessity of other components on the Y chromosome to develop full masculine characteristics.


Background (null) distribution for higher observed frequency of an allele

I don't really understand your hypothesis you want to test. Here are two things that may help you.

Test if allele frequency is the one expected from the genetic and demographic properties

The expected allele frequency is not that easy to calculate as you need much information. You need to know the mutation rate, the population size, the migration rate, assume random mating and most importantly know the selection coefficient associated with this allele. Once you've got all that, you'll find the equation in the old paper Wright 1937.

How to test?

Maximum likelihood ratio test is probably the way to go.

Test if heterozygosity is the one expected from the allele frequency

Now if you want to test if heterozygosity is not the one expected, it is much easier. The expected genotype frequencies are given by Hardy-Weinberg rule (see here for explanation on Hardy-Weinberg's rule and see here for the assumptions of this rule).

In short, for a bi-allelic loci with allele frequencies $p$ and $1-p$ the three genotype frequencies are $p^2$, $2p(1-p)$ and $(1-p)^2$, where $2p(1-p)$ is the frequency of heterozygote.

How to test?

You can simply do a chi-square test or a binomial test.

  I ask if being heterozygote increases the odds of carrying a certain allele compared to being homozygote. So can I just compare the allele frequency in two populations (hetero- and homozygotes) using fisher exact t

Oh ok. If I understand you correctly, you have two loci. One for which heterozygosity is the variable of interest, while for the other locus, the variable of interest is the presence / absence of a certain allele is that right?

Sounds like your question is a pure question of statistics, not biology. Stats.SE is the place to go to but I will still try to address your question now that I started.

You can do a simple chi-square test you have the following 2 by 2 chi square table with the count of individuals in each cell

$$\begin{array}{c|c|c|}
 & \text{Homozygote} & \text{Heterozygote} \\ \hline
\text{Allele 1} & w & x \\ \hline
\text{Allele 2} & y & z \\ \hline
\end{array}$$

Now, that works well if you consider only a single, randomly picked allele per individual but that would reduce your sample size. If you pick both haplotype per individual, then I am not sure of whether you might suffer from pseudo-replication. In such case, you could do a logistic regression with a nominal random effect that is the individual ID. They will be better than me at giving you such advice on stats.SE though.


Can immunity to diseases vary by populations?

Is it just a shorthand for "the adult population was not subjected to these patogenes during childhood and is therefore more susceptible to them" or is there maybe a certain genetic component to it?

It's a little of both. You can read some of the math behind this in Infectious Diseases of Humans: Dynamics and Control, by Anderson and May.  Chapter 2 gives an overview. The behavior of an epidemic depends a great deal on the specifics of the host-pathogen interaction, but generally you can say that the epidemic curve in a a naive population will have a larger and sharper upswing than in a previously exposed population. You can attribute some of this different behavior to lack of adaptive immunity in the adult population. Again, depending on the pathogen, you can also attribute some of this different behavior to lack of selective pressure in the naive population on highly variable loci involved in the immune response.
To address more directly what seems to be your primary question: yes, there is a genetic component to the susceptibility of a host (e.g., a human) to a pathogen (e.g., a microbe that can cause disease).
Non-heritable aspects:
There are certain aspects of what we call the adaptive immune system in jawed vertebrates that are not directly heritable. You are a jawed vertebrate, and the DNA in each of your B-cells and T-cells that produces B-cell receptors (BCR) and T-cell receptors (TCR) goes through a number of changes outside of the germ line. You can read about these changes in, for example, How the Immune System Works, Chapter 3, by Lauren Sompayrac. It's an excellent introduction if this is new to you.
In addition to the exact set of BCRs and TCRs in the pre-immune state, your current repertoire of cells and molecules is determined by your history of exposure. While some of this can be vertically transmitted, the majority of it is not. This is one of the reasons why, when you look at this repertoire, much of the variability is attributable to non-heritable factors. A not insignificant proportion is attributable to heritable factors, though. So if TCRs and BCRs are not encoded in your germ-line, and your environment obviously has a strong influence on your current immune state, where does the heritable component come from?
Heritable aspects:
All of the other proteins involved in the immune system response are encoded in the germ line, and are thus heritable. Some of them are highly variable, and since they are very important they are under strong selective pressure. You can see important changes in the population distribution of these loci over a relatively small number of generations. There are many other heritable components of an individual or population's susceptibility to infectious disease. There is a great deal of work on this. Casanova has a great article about this in PNAS, which I've linked to in another answer to a related question. A more traditional review of his is here. Of course, he's not the only one working on this. I just like the way he writes. Here's a good one by Baker and Antonovics.
A simplified and speculative example
Re: your comment about measles in the Polynesian islands, we don't have scientific consensus about the relative importance of non-heritable and heritable factors for this particular case. Instead of getting into the nitty gritty details, I'll walk you through a hypothetical:
Imagine an isolated population with a lot of variability in germline genes that code for a special protein that helps their immune system mount a full response to viruses.
A very nasty, very contagious virus is introduced to this previously isolated population. The characteristics of the population help determine the outcome of their interaction with this new virus. Here are 3 important characteristics:

Because nobody has ever been exposed to this virus, nobody has neutralizing antibodies or the rapid immune response that happens the second time you're exposed to a pathogen.

Some versions of that special protein with all that variability don't do a good job of helping the immune system mount a response to this new virus.

Luckily though, some other versions of that special protein with all that variability do an especially good job of helping the immune system mount a response to this new virus.

Because of (1) the disease spreads broadly throughout the population. Because of (2), a specific group of people get especially sick, die, and (because they are dead) don't reproduce, and don't pass on their version of the gene that codes for special protein. Because of (3) a specific group of people do very well, are only sick for a little while, and do an especially good job at generating long lived immunity, and (because they are alive and well) reproduce a lot, and pass on their version of the gene that codes for that special protein.
The epidemic is eventually controlled. Years go by, and the virus starts circulating again.
Now the characteristics of the population are quite different, so the dynamics of the host-pathogen interaction will be different.
Many of the people that were alive during the first epidemic now have neutralizing antibodies and a memory response, so this second epidemic will not spread as quickly or as broadly. This is a non-heritable factor. Previous exposure to the virus has changed the repertoire of cells and molecules in people's blood.
Among the younger generation, more of them have the helpful version of the special protein that helps the immune system generate a response, so not as many of them will die. This is a heritable factor. Previous exposure of the population to the virus has exerted selective pressure, changing the frequency of the helpful and unhelpful alleles in the population.


Can one type of bacteria cause several diseases?

Yes, one type of bacteria can cause multiple diseases.  For example:

"Rheumatic fever is caused by group A Streptococcus. This bacterium causes strep throat or, in a small percentage of people, scarlet fever. It’s an inflammatory disorder." [https://www.healthline.com/health/rheumatic-fever#causes].

The difference is in how the individual's immune system responds to the infection (and how the infection is treated).  Everyone responds a bit differently to the same infection.


The concept of a human/chimp hybrid is called a humanzee. No humanzees have ever been recorded despite the fact that sexual intercourse between humans and chimps have been recorded on several occasions. This suggests that male-human/female-chimpanzee is not capable of producing viable offspring, at the very least.

As to why, several reasons will contribute: humans and chimps have a different number of chromosomes, making cross-fertility unlikely (although animals with different chromosome numbers can and do breed so this isn't absolute). Humans and chimps are anisomorphically quite different (i.e. the ratios of limbs are different and so on) so it's quite plausible that the growth patterns are not compatible. I'm not aware of any exhaustive studies into reasons why cross-breeding is impossible but it's also quite plausible that there are changes in the chemistry of fertilisation, etc. that will limit cross-breeding.

I'd note, finally, that there's evidence from the X chromosome that the human line continued to have some level of interbreeding with chimps for some million years after the initial split (Patterson et al, 2005†).

†  I see that there are some later publications that have disputed the claims made in that paper. So I'll leave you to judge the merits of the arguments.


Regarding your first question, I don't know of any instance in which irradiation was used to select for a beneficial trait in humans. I italicized 'used' because I think that you could argue that naturally occurring sources of irradiation have led to the selection of traits that protect us from radiation damage.

That might sound like a bit of a circular argument, but keep in mind that in the case of the rice you mention, the discovery of beneficial traits came at the expense of a lot of dead rice that suffered deleterious effects of radiation. Unfortunately, the deleterious effects are a lot more likely to occur than than any really useful ones.

That leads to your second question. Conceivably, radiation could lead to a beneficial mutation. However, there are some pretty big caveats with that. First, in order for it to be beneficial, this hypothetical mutation would have to occur very early on in development, otherwise it would be limited to, at best, a handful of cells, probably in your skin, which would just get sloughed off anyway. So the second caveat is that in order for such a beneficial radiation-induced mutation to occur in the right place at the right developmental time, it would have to penetrate all the layers of your mother's genetic material that separate your fetal cells from the outside world without losing the energy needed to damage your DNA.

I couldn't tell you what sort of radiation might be capable of pulling that off with what probability of success, but my guess is that it's really unlikely.


There's no harm in plucing a hair, but it won't do you much good

Plucking the hair will indeed get rid of the hair - but only temporarily

  "The follicle (the little tube beneath the skin that produces the
  hair) is still alive and will produce another hair to replace the one
  that was pulled out

So actually if you DON'T damage the follicle (which is really rare, this could be the case if you remove skin) the hair will definitly grow back.
To get into more depth here is a figure that shows the root and the follicle so it's clear what the difference is:

I don't know in how much depth you want this question to be answered but if you are interested in the growth stages (which can influence the hair regrowth) you should take a look at this answer, I won't copy someone else effort here..
source: Randy Schueller (link)


External tissues, connected to the body?

I've actually wondered this myself from time to time, without ever bothering to look it up.  Well, it's actually happening.  That WSJ article says the following, which just blows my mind:

Researchers at the Rogosin Institute are taking tumor cells from mice, encapsulating them in beads made from a seaweed-derived sugar called agarose, and implanting them in the abdomen of cancer patients. There, cells in the beads secrete proteins researchers believe could signal a patient's cancer to stop growing, shrink or even die.
So far, at least 30 patients have been treated with the cancer beads in an initial human study, and a phase two or intermediate-stage trial has been launched—with the approval of the U.S. Food and Drug Administration—to test the technique in patients with advanced colon, pancreatic and prostate cancers.

You can find the info on the Phase II trial here; they are currently at the "recruiting participants" point.

[The treatment] consists of small beads that contain mouse cancer cells from a mouse kidney cancer cell line. The cells in the beads produce substances that have been shown to slow or stop the growth of tumors in experimental animals, veterinary patients, and 23 humans with different types of cancers in a Phase 1 safety trial.


Why does evolution only involve heritable traits?

There is a lot to say to address this question fully. I will be brief and a little messy to try to introduce you to some concepts and that will hopefully push you to learn more by yourself.

Heritability in genetics

In genetics, heritability is a statistic that describe the fraction of the phenotypic variation that which is caused by underlying genetic variation. Please have a look at this post to understand the concept of heritability as used in genetics. Note that there are two such statistics, named heritability in the broad sense $h_B^2$ and heritability in the narrow sense $h_N^2$.

Basics of non-genetic inheritance

Here, I will refer to "heritability in the broad" as the passation of trait value (such as behaviour for example) and environment characteristic to another organism. One must not confound what I call here "heritability in the broad" and heritability in the broad sense as defined in genetics ($h_B^2$).

Sure, a lot of things can be inherited from one organism to another. Any such heritable (in the broad sense) trait is susceptible to show interesting variation in the frequency at which trait values are found in a population. If, in addition to that, this trait is susceptible to spontaneous changes (the equivalent of mutations in genetics), then this trait can show interesting evolutionary patterns. If in addition to that, different trait values have different aptitude to replicate (the equivalent of natural selection in genetics), then such trait can evolve in an "even more interesting way".

What can be non-genetically inherited?

Two things can be inherited without the use of any sort of genetic information (I also exclude epigenetic information incl. DNA methylation or protein concentration in the yolk).

Environment (Ecological inheritance)
Meme

See more on Ecological inheritance and memes below.

Ecological inheritance

This is probably the first type of inheritance one would think of when not thinking about biology. In humans, it is not uncommon for offspring to inherit "stuff" from their parents when they die. Similarly, beavers can inherit a dam that has been built by their parents. This type of inheritance in generally called Ecological inheritance.

This type of inheritance might eventually be important to evolutionary processes (see literature on niche construction).

Inheritance of a meme

Definition

A meme has been named by the analogy to a gene. A meme is any idea, behaviour, thought or tradition (piece of culture) that can be inherited. The concept of an internet meme is now quite popular, but a meme is more than just an internet meme. While genetics is the study of genes (and much more actually), memetics is the study of memes. Memetics is a very interdisciplinary field of study that attract biologists, philosophers, mathematicians, linguists and archeologists among others. The hypotheses built in the field of memetics rarely offer predictions that can be easily tested, and therefore a good part of the work in this field remains very uncertain.

Analogy to genes

A meme could be a joke for example. If the joke is funny it will replicate easily and enter in new brains. This meme could be said to have high fitness. The joke may come into spontaneous changes (mutations). Be careful with analogies and they may show nothing but similarity. For example the nature of memetic mutation seem to be quite different than from the nature of genetic mutation.

Example

In humans, the examples are very easy to find. As I am writing this answer, I am currently trying to pass on a meme which has been given to me by some other authors. Hopefully I won't mutate this meme too harshly.

Lots of monkeys and apes are transmitting traditions, foraging methods and other memes to their offspring, sometimes through active teaching but often through imitation (or emulation). A classic example is the one reported in Rhythms of Vision in 1975 (I could not find the original peer-reviewed paper). A female monkey, one day had the good idea of washing a sweet potato. This behaviour has since increased in frequency throughout the population so that most monkeys now wash their sweet potatoes.

Pitman and Durban (2011) (and others before them) report that some population of orcas use cooperative hunting while some other population does not. Variation for this trait seems not to be caused by genetic variation.

How does inheritance work?

Inheritance can be "vertical" (parent to offspring) or "horizontal" (between individuals of the same or different species). This holds true for both genetic (consider transduction) and non-genetic inheritance (teaching to offspring or to the neighbors).

In addition to that the passation of a meme can be active (teaching) or passive.


What is the smallest pressure differential that humans can detect?

Short answer
The sensitivity to pressure differences highly depends on the study setup used. A paper resembling the conditions in your kitchen experiment concludes that the just noticeable difference ranges from 19 to 35 kPa.
Background
The smallest difference that can be perceived between two stimulus levels is called the just noticeable difference, or JND. The issue with determining pressure difference JNDs is that it may be dependent on many things. To name a few important factors are the place on the body and the type of stimulus used. The fingertips and tongue are among the most sensitive parts of the body, while the back is way less sensitive to mechanical stimulation. The type of stimulus may also dramatically affect the findings, because vibratory stimuli are sensed by other types of mechanoreceptors than static pressure stimuli.
Having said that, I found a paper describing an experiment that resembled your kitchen experiment pretty well . The authors used air puffs applied to the fingertips. They used an apparatus where the nozzle could be adjusted to accommodate different aperture sizes. The authors tested 10 normal, right handed controls and used a standard 2 alternative forced choice (2AFC) task applied as a method of constant stimuli. Personally I would have adopted an adaptive 2AFC task, but both methods are valid. The authors conclude that

Subject-averaged pressure JND values ranged from 19.4 – 24.7 kPa, with no statistical differences observed between aperture sizes.

Reference
- 33rd Bianchi et al., Annual International Conference of the IEEE EMBS Boston, Massachusetts USA, August 30 - September 3, 2011


Is there such substances that body can only send to storage (as fat)?

An empty calorie is still a calorie.

"Empty calories" was coined to describe foods that only provide calories without significant amounts of other nutrients. The idea is that if you're eating a lot of empty calorie foods, you're eating less food with proper nutrition. The implication is that you will not be getting the vitamins, amino acids and other essential nutrients required to sustain you in a healthy manner.

If you can store it as fat, your body can use it. Where does the fat go when people lose weight? Those calories get "burned" when there aren't enough calories in your current diet to provide energy for your metabolic needs.


What biological functions does crying serve?

Lets break this question into parts and answer them one by one.

  Do tears really save us from harm?

Well, yes. Tears, mucus and saliva contain an enzyme lysozyme that breaks down the cell wall of many bacteria. Those that are not killed immediately are trapped in mucus and swallowed.1

You can, obviously, search on google for another reference if you do not believe this one.

  Or are they just the reflex shown?

It depends on what type of tears you are talking about. Tears are divided into 3 categories:

Basal tears
Reflex tears
Psychic tears

In "reflex action" part, the cause is reflex tears. Reflex tears result from irritation of the eye by foreign particles, or from the presence of irritant substances in the eye's environment, which trigger TRP (Transient Receptor Potential) channels in the ophthalmic nerve. It can also occur with bright light and hot or peppery stimuli to the tongue and mouth... These reflex tears attempt to wash out irritants that may have come into contact with the eye.

These are, of course, different from those tears which "suddenly start flowing out of our eyes when we find our long lost friend or when someone unexpectedly decides to break up with us". These are psychic tears i.e. increased tearing due to strong emotional stress, pleasure, anger, suffering, mourning, or physical pain. This practice is not restricted to negative emotions; many people cry when extremely happy such as during times of intense humour and laughter.2

But the actual relation of tears with emotions can be summarized as:

There is an area of your brain specifically to deal with your emotions, called the limbic system (specifically the part of it called the hypothalamus), which is hard-wired into your autonomic nervous system (that’s the part you don’t have any control over).
This system, via a neurotransmitter called acetylcholine, has a degree of control over the lacrimal ‘tear’ system; and it is this tiny molecule which then stimulates tear production.
So in short, your emotional reaction to the break-up triggers your nervous system, which in turn, orders your tear-producing system to activate.3

Moving on to next part:

  crying causes endorphin release...Are tears the only way to accomplish this?

Certainly not. Even when you exercise, your body releases endorphins. These endorphins interact with the receptors in your brain that reduce your perception of pain. So, tears are not the only way to accomplish this.4

At last, I would answer this part

  What biological purpose do tears serve for the body?

as tears are necessary for the continued health of the ocular surface. Normal constituents include water, mucin, and lipids, electrolytes, non-electrolytes, and proteins. Retinoids are also important for ocular health and prealbumin may be a carrier for vitamin A in the tears to supply corneal epithelium with its requirements. Changes in tear constituents may cause certain ocular disorders.5

It is important to know here that by the above part, I meant basal tears and not psychic ones. Basal tears lubricate the eye, and help to keep it clear of dust. Tear fluid contains water, mucin, lipids, lysozyme, lactoferrin, lipocalin, lacritin, immunoglobulins, glucose, urea, sodium, and potassium. Some of the substances in lacrimal fluid (such as lysozyme) fight against bacterial infection as a part of the immune system. Lysozyme does this by dissolving a layer in the outer coating, called peptidoglycan, of certain bacteria. It is a typical body fluid with a salt content similar to blood plasma.

EDIT 1: Now, as you asked in the comments

  what if we don't maintain our ocular surface?

I can tell you a very common example of dry eye syndrome. Dry eye syndrome is a common tears and ocular surface multifactorial disease, described by changes in the ocular surface epithelia related to reduced tears quantity and ocular surface sensitivity, leading to inflammatory reaction. It is believed that decrease in the tear volume on the corneal and conjunctival surface caused by either a decreased tear secretion or accelerated evaporation plays the main role. The clinical features of dry eyes include ocular discomfort, feeling of dryness, feeling of eye fatigue, hyperemia, kerato-conjunctival epithelial disorders and abnormalities of vision.6

EDIT 2: When it comes to function of psychic tears, then how could one leave talking about why we feel better after crying (except headache). It is now proven that psychic tears contain a higher amount of hormones than basal or reflex tears. See this article7:

  Emotional tears are composed of more protein-based hormones, such as prolactin, adrenocorticotropic, and leucine enkephalin (a natural pain killer), which is suggested to be the mechanism behind the experience of crying from emotion making an individual feel better.

Though these hormones do not have any direct relation with emotions (excluding prolactin which counteracts the effects of dopamine), they can be related to emotions as long as another biological reason for their secretion through tears is discovered.

Bonus: From the same article 7, here is a very unusual function of tears i.e. controlling arousal! See this paragraph:

  On a study conducted by the Weizmann Institute of Science in Rehovot, Israel, emotional tears from women have been found to reduce sexual arousal in men. Also, emotional tears are made up of a different chemical component than those evoked by eye irritants and can relay chemical messages to others. The change in sex drive could be attributed to a drop in testosterone provoked by the tear chemicals, reducing aggression. In the animal world, it has been found that some blind mole rats rub tears all over their bodies as a strategy to keep aggressive mole rats away.

This way, we can soon have a long list of functions. I hope these many functions are enough to answer your question.

References:

1: The body’s first line of defence

2: Tears - Wikipedia

3: Why do we cry? The science of tears

4: Exercise and Depression

5: Eyelid secretions and the prevention and production of disease

6: Recent developments on dry eye disease treatment compounds

7: Chemicals in tears - Wikipedia


Blebbistatin inhibits myosin II by blocking it's attachment with actin. Myosin II and other actin based motors have shown to be involved in vesicle budding from trans golgi network. Given this information, I think correct answer will be

  The formation of vesicles would cease.

Following cartoon from (Stow et al 1998) shows proposed mechanism,

However looking at this paper, option (2) The movement of vesicles within the cell would cease, also sounds reasonable.


SEREX serological analysis of cDNA expression library

With this method you want to identify proteins on cancer cells which are immunogenic so you can use them to boost an immune response against the cancer cells.

To do so, you extract the complete mRNA from a cancer. These mRNAs represent all the genes which this cancers expresses (which then also contains the immunogenic proteins). These mRNAs are cloned into bacteriophages (viruses that only infect bacteria) and are then used to infect bacteria. During this infection the virus expresses the protein which has been cloned into his sequence and which originates from the cancer cell. The infection of the bacteria leads to the formation of plaques (wholes) in the bacteria which grow on the surface of a culture plate.

You then use the serum of cancer patients on these expressed proteins to see, if there are antibodies which can recognize these cancer antigens (and could be used to detect and mark them). If there are proteins which only react to the sera of cancer patients but not to controls (to exclude) unspecific reactions, then these proteins are identified and can be used to generate antibodies against this specific cancer type. It works like in the figure below (from this paper):


Here's some step-by-step advice on good pipetting technique:

Make sure the pipette is set for the correct volume
Ensure the tip is firmly attached
Keep the pipette vertical when pipetting
Slowly and smoothly depress the plunger to the correct point (the first stop position)
Insert the tip in to the liquid to be pipetted. Ensure the tip is properly immersed in the liquid, but not touching/near any surfaces of the container
Slowly and smoothly release the plunger back, keeping the pipette upright, and tip immersed, and making sure no bubbles form - you can try pre-wetting (see video linked below, around 3:00)
Withdraw the pipette from the liquid
Carefully dispense the liquid in to the desired container by steadily depressing the plunger to the second stop position (fully depressed), making sure all liquid is dispensed without spills or splashes.

  "Put the tip in a 45-degree angle onto the wall of the container; then
  start pushing down up until the first stop; then push through to the
  second stop; keep the plunger depressed and remove pipette and check
  whether the drop is in the container and pipette tip is empty" -
  Christiaan

Discard the tip using the release plunger

Also check you've got the right size/type of tip, and are using a suitable pipette (e.g. don't use a 10-100 µl pipette for 120 µl)

If this still causes incorrect measures then you could need to get your pipette calibrated.

Test a pipette by taking several samples. If the pipetted volume is consistent but incorrect (e.g. always 10% under the target) it suggests the pipette needs calibrating, it's probably not the technique that's wrong. If it is inconsistent (both under and over pipetting) then it's either technique or the pipette (bad/damaged pipettes can be inconsistent, poorly but good calibrated pipettes will more likely be consistent and only need calibrating).

Try using multiple pipettes, if they are each consistent but variance is among them (pipette 1 is always under by ~10%, pipette 2 is always over by 15%, pipette 3 is always over by ~2%...) then your technique is good, and you need better pipettes. Also get an experienced pipetter to check your technique and try the pipettes themselves.

Calibration can be done internally by lab techs or by external specialists, speak to your lab responsible person.

Also see this video which is well explained.


Answer is quite simple as from @Alan Boyd link. They are cold blooded and thus, can go out for hunt in cold, they need to stay put till they get some prey.

So, it mainly depend on the temperature of the outside, I found this interesting paper on relation of body sizes and latitude.

  Body sizes of poikilotherm vertebrates at different latitudes

  Maximum sizes of 12,503 species of poikilotherm vertebrates were
  analyzed for latitudinal trends, using published data from 75 faunal
  studies. A general trend appears which may be summarized by the rule
  "among fish and amphibian faunas the proportion of species with large
  adult size tends to increase from the equator towards the poles". The
  rule holds for freshwater fish, deepsea fish, anurans, urodeles, and
  marine neritic fish arranged roughly in order of decreasing clarity of
  the trend). In general the rule applies not only within these groups
  of families but also within single families. In reptile groups, the
  rule holds weakly among snakes and not at all among lizards or
  non-marine turtles. Possible explanations include an association
  between small size and greater specialization in the tropics; the
  possibility in poikilo-therms of heat conservation or of some other
  physiological process related to surface/volume ratio; selection for
  larger size in regions subject to winter food shortages; and an
  association between large adult size and high reproductive potential
  in cold regions. Other suggestions can be advanced, but all are
  conjectural and few are subject to test. Global size - latitude trends
  should be looked for in other living groups.

  Cite: Lindsey, C. C., 1966: Body sizes of poikilotherm vertebrates at
  different latitudes. Evolution: 456-465

Now lets compare some of the largest cold blooded Animals:

Reptiles
Amphibians
Fishes (Pisces)

Reptiles:

The smaller size of Reptiles give them more agility to hunt andsave them predators but some times when they are top of food chain they can grow as giants.
Anacondas (Eunectes), gigantic snakes from South America, are undoubtedly the largest living snakes.
The largest species, the green anaconda (E. murinus), likely only rarely exceeds 9 metres (30 feet) in length; nonetheless,
persistent but unsubstantiated reports have been made of anacondas that are 12 metres (40 feet) long.
The reticulated python (P. reticulatus) of Southeast Asia and the East Indies has been recorded at 10.1 metres (33.3 feet).

Others:

King Cobra(Ophiophagus hannah) 5.5 meters (18 feet)
Keeled rat snake (Ptyas carinatus), at about 3.7 metres (12 feet).
Nile crocodiles (Crocodylus niloticus) 6 metres (20 feet)
American crocodile (C.acutus) 4–5 metres (12–15 feet).
Marine leatherback sea turtle (D.coriacea) 2.7 metres (9 feet)
Galápagos tortoise (Geochelone nigra) 255 kg (560 pounds).
Komodo dragon (Varanus komodoensis) 3 metres (10 feet)
Green iguana (I. iguana) 2 metres (7 feet)

Green Anaconda http://www.wallshq.com/wp-content/uploads/main/2013_01/green_anaconda-wide.jpg
Green Anaconda

Amphibians:

According to Wikipedia:

  "The Chinese giant salamander (Andrias davidianus) is the largest
  salamander and largest amphibian in the world, reaching a length of
  180 cm (5.9 ft), although it rarely—if ever—reaches that size today"

Others:

West African goliath frog, 30 cm (12 inches) 3.3 kg (7.3 pounds)
Caecilia thompsoni 1.5 metres (5 feet)
Axolotl(Ambystoma mexicanum) 30 cm (12 in)

Chinese giant salamander

African goliath frog

Axolotl (Small 12 inch)

Fish:

West Indian Ocean coelacanth, (Latimeria chalumnae), is 80 kg (176 lb), and they can reach up to 2 m (6.5 ft)
African lungfish (Protopterus aethiopicus), 2 m (6.6 ft) and may weigh as much as 50 kg (110 lb)
Ray-finned bony fish (Actinopterygii)
Ocean sunfish (Mola mola) 4.3 m (14 ft) from fin-to-fin, 3.1 m (10 ft) in length
and weighed about 2,300 kg (5,100 lb)
King of herrings or oarfish (Regalecus glesne) 6 m (20 ft)( The longest
known king of herrings, which was hit by a steamship, was measured as 13.7 m (45 ft) long)
Bowfin (Amia calva)  109 centimetres (43 in) in length, and weigh 9.75 kilograms (21.5 lb).
European conger (Conger conger) 3 m (10 ft) and a mass of 110 kg (240 lb)
Lancetfish (Alepisaurus ferox) 2.1 m (7 ft) long and can weigh up to 11 kg (24 lb)
Houndfish (Tylosurus crocodilus) 1.5 m (5 ft) and a weight of 6.35 kg (14.0 lb)
Giant Tigerfish (Hydrocynus goliath) 1.5 m (5 ft) and 50 kg (110 lb)
Golden Dorado (Salminus brasiliensis) 1 m (3.3 ft) in length and weigh 31.4 kg (69 lb)
Tambaqui (Colossoma macropomum) 1 m (3.3 ft) and 32.4 kg (71 lb)
Giant barb (Catlocarpio siamensis) 3 m (10 ft) and a weight of as much as 300 kg (660 lb)
Muskellunge (Esox masquinongy)  1.8 m (6.0 ft) and 45.4 kg (100 lb)
Atlantic tarpon (Megalops atlanticus) 161 kg (350 lb) and length is up to 2.5 m (8.2 ft).
The Atlantic cod (Gadus morhua) grows to 2 m (6.7 ft) long and 96 kg (212 lb)
milkfish (Chanos chanos) 22.7 kg (50 lb) and 1.84 m (6.1 ft) long
Electric eel (Electrophorus electricus) 2 m (6 ft 7 in) in length, and 20 kg (44 lb)
Opah (Lampris guttatus) 2 m (6.6 ft) in length and weigh up to 270 kg (600 lb)

Source: http://en.wikipedia.org/wiki/List_of_largest_fish
Source: Britannica.com

Mola mola

Oarfish

West Indian Ocean coelacanth

Bowfin


what kind of dinucleotides can be considered important from a mutational point of view other than CpG islands?

In some types of cancers like breast cancer, APOBEC3 cytidine deaminases can become upregulated and enhance mutagenesis. As shown in this mutational signature from cancer tissue data the enzymes prefer TC motifs.

Source: https://cancer.sanger.ac.uk/cosmic/signatures/SBS/index.tt


Why a cell contains all DNA when it only needs a few genes?

Why does a cell contain all DNA when it only needs a few genes ?

I interpret this question to mean "why does every cell contain the whole human genome even though it doesn't use it all, i.e. why does a liver cell contain the genes for eye color?"

If that is what you meant, then we can easily answer the first question in your actual text:

  Is that what they called junk?

No, that is not what is called "junk DNA". "Junk DNA" can refer to many concepts, but generally it refers to parts of DNA that serve no function in the body: they are not transcribed into proteins, they don't serve to regulate other genes, and if you remove them or change their sequence this will have no effect on the overall organism. This means it refers to parts of DNA that are used nowhere in the body, not parts that are used in one place but not in others.

How much DNA is "junk", how useless it actually is, and why we have it are complex questions that don't all have known answers, but it is completely different from your headline question.

I don't have the time to look up a detailed answer to your first question so I will leave that to others, but here are some elements that might help:

1) I think cells use more genes than you realize. I don't know the proportion of genes that are used for the cell to live as a cell vs those that are used for the specific tasks this cell needs to do beyond maintaining itself and reproducing, but I'm pretty certain there is no cell in the body that "only needs a few genes". I would even guess all cells in the body use most of the genes they contain.

2) not all cells contain an unmodified copy of the whole genome. Some cells lose their nucleus, i.e. their DNA entirely (red blood cells); others multiply some genes that they use a lot.

3) having said all that, I would guess that liver cells indeed don't need the genes for eye color, yet they might have them. Consider that cells reproduce by copying themselves, and copying their whole genome. Is it more of a waste to keep the copy as it is, or to go around before or after the copying cutting out all the bits this specific cell won't use? Do I go around editing the code of my text editor and recompiling it to get rid of all the functionalities I don't use? I might save some space on my hard drive but it is very obviously not worth my time to do that either. If the extra DNA doesn't do enough harm, there is no reason it would be taken out; indeed the wasteful thing would be to do so.


I just had my genome sequenced. Can someone tell me what these different file formats are?

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology. I'm glad we encourage such questions from curious people who want to learn more.

Your genome has a sequence that is unique to you, gifted to you by your parents and by small changes from random chance.

Your genome is pretty close to what is called the reference genome, which gets updated — infrequently1 — as sequencing platforms, pipelines, and algorithms change.

The reference genome is the "standard bearer". All other individual genomes are compared against it. This lets everyone compare apples to apples when trying to say something about the genome, in the aggregate or "big picture" view.

The files associated with the VCF format specify places in your genome that differ from the reference genome — and how they differ. These differences include:

Indels — insertions or deletions of DNA, as compared with the reference.
SNPs — single bases that differ from the reference.
CNVs — repeated stretches of DNA that differ from repeats in the reference.

The specifics of each of these classes of variants can be associated with various diseases or other attributes that make you unique and interesting. More on that later.

Each of these VCF files in your dataset has an associated TBI file. This is an index file, which helps you to quickly retrieve elements of interest from these datasets using a command-line tool called tabix.

If you are looking for differences within a specific genomic interval — say, all the differences on chromosome 4, from bases 123456 to 567890 — then you can pass that interval to tabix along with your VCF file of interest, and it will return all the indels, SNPs, or CNVs within that range, if there are any within that interval. This subset is VCF-formatted, so by knowing the format, you can get more detail about those differences.

The BAM-formatted file collects all the individual sequencing reads in a form that is mapped or aligned to the reference genome, along with some summary information to tell you how those reads differ from the reference genome.

As with the VCF files, this BAM file has a BAI index file to go along with it. Like tabix, you can use the samtools command-line tool to extract the set of reads over your genomic region of interest, if you want to examine them further.

Both tabix and samtools are available from the same author. If you have questions about these tools, the Bioinformatics Stack Exchange site is a great place to ask questions3. Lots of bioinformaticists  there have a great deal of experience with those toolkits and can help answer more specific questions.

The two FASTQ files are the raw sequence data coming off the sequencer, along with quality data. The sequence reads in these two files are paired for higher quality and longer reads, which makes the sequencing platform faster, cheaper, and better.

I walked a bit backwards, here, on purpose.

The raw FASTQ files are starting material for making the BAM file. The BAM file is then, in turn, used with variant calling software (example) to generate the variation (VCF) datasets.

Why walk backwards through these datasets?

Most people don't care about the raw FASTQ data, except perhaps to do manual alignment or check data quality. What is often more interesting or useful to most is how one's genome differs from the reference, which is captured in the variation data.

Those differences, in aggregate, are how companies like 23andme sell a product2 that tells you that you are more related to so-and-so population than so-and-so population, or whether you are more or less likely to have some disease or other odd, interesting phenotypic trait.

1. Even when new versions of this reference genome are released every few years or so, if you know what original reference genome was used to generate your BAM and VCF files, you can redo analyses based on that knowledge. There is likely some metadata associated with your sequencing results that you can look up to find this out, or you can ask the sequencing center from where you obtained these results.

2. For a bit more context, in this answer to another SE question, I talk a bit about SNPs and how they are used for testing association with so-called Mendelian disorders, diseases caused by single base changes, which may be of interest to you given what motivated you to get your genome sequenced, in the first place: https://biology.stackexchange.com/a/88839/5075

3. You can ask questions about them here, too, but you'll make certain people grumpy. Better to go to the other SE site for that.


Are there examples of the green beard effect in humans?

Your examples are way too broad. A green-beard effect only applies to the effects of a single gene or group of linked genes, not to just any trait. Racism and your Mongol war example are too complex to be explained by this effect. In reality examples will mostly be found in single-celled organisms where expression of a single protein can have whole-organism effects such as causing aggregation, or in larger organisms where some highly visible effect is possible such as a colour change.

There are very few real known examples of the green-beard effect, but four are listed on the Wikipedia page:

The killing of red ant queens carrying a particular allele by workers with a different allele (Keller & Ross, 1998)
Altruism in social amoeba resulting from homophilic adhesion of a protein (Queller et al., 2003)
A multi-locus example in which similarly-coloured male lizards protect one another (Sinervo et al., 2006)
A neat example in yeast whereby individuals sharing an allele for a particular locus selectively aggregate, preventing those without the allele from benefiting by proxy from their trait (Smukalla et al., 2008)

References

 Keller L, Ross KG. 1998. Selfish genes: a green beard in the red fire ant. Nature 394: 573–575.
 Queller DC, Ponte E, Bozzaro S, Strassmann JE. 2003. Single-Gene Greenbeard Effects in the Social Amoeba Dictyostelium Discoideum. Science 299: 105–106.
 Sinervo B, Chaine A, Clobert J, Calsbeek R, Hazard L, Lancaster L, McAdam AG, Alonzo S, Corrigan G, Hochberg ME. 2006. Self-recognition, color signals, and cycles of greenbeard mutualism and altruism. Proc Natl Acad Sci U S A 103: 7372–7377.
 Smukalla S, Caldara M, Pochet N, Beauvais A, Guadagnini S, Yan C, Vinces MD, Jansen A, Prevost MC, Latgé J-P, et al.. 2008. FLO1 Is a Variable Green Beard Gene that Drives Biofilm-like Cooperation in Budding Yeast. Cell 135: 726–737.


Why differentiated cells can't "undifferentiate" (under normal conditions)?

This "undifferentiation" is actually possible and it is known as induced pluripotent stem cell (iPSC). The first "undifferentiation" cells i.e. iPSCs were mouse fibroblasts created in 2006 by researchers in Shina Yamanaka's lab who got the Nobel prize in 2012 for this work.

You can find further reading on this topic on the according Wikipedia-Page or more scientific details on the according nature.com topic.


Why we need an egg cell donor and a surrogate mother in an organism cloning process?

Could a whole set of artificial organism-cloning process only be
  operated on a somatic nuclear donor?

No, this would not be possible. Single-cell reprogramming would enable you to reset the potency status of that cell up, yielding an embryonic stem cell (ESC). However, ESC do not have the ability to generate extra-embryonic structures (e.g. placenta), which are known to be required for providing oxygen and nutrients to the embryo, amongst other relevant functions.

Theoretically, it could be possible to replicate the embryological environment, and I think this is the second part of your statement. Nevertheless, in practice this is not possible... the amount of signals and parameters that one would need to control simultaneously is far too extensive.

I don't quite see the point of having an enucleated egg and performing somatic cell transfer, when you're not really interested in implantation in utero. Somatic cell reprogramming would be sufficient (see iPSC)


Is it impossible for a retrovirus to be lysogenic?

Both things are not exclusive of each other. Retroviruses are RNA-based viruses which need to reverse transcribe their RNA genome into DNA before they can multiply. This is done by the reverse transcriptase enzyme, which is part of the virus and is incorporated into the cell.

Once the reverse transcriptase has been active and made the DNA, this DNA can also be incorporated into the hosts genome. If you look into the Wikipedia article on Bacteriophages, you will find a list of different bacteriophages, with all kind of genomes, among them as well a number of RNA-based viruses.

RNA-based viruses which enter the lysogenic pathway are obviously either pretty rare or they haven't been discovered yet in bigger numbers. Two examples are the phages F2 and MS2 (which are closely related).


Explanation for hyenas asymmetric legs length

First most animals have limbs of different lengths. consider a house cat at full extension its hind limbs are much longer than the forelimbs.

The relative length of the limbs means almost nothing functionally, it is the relative length of the gait, or the distance the limbs can swing that is important, a longer less flexible limb may swing the same distance as a shorter but more flexible limb. Source

When the limbs have very different gaits you end up with hoppers or so called pendulum runners like rabbits and kangaroo or they do not fully utilize the possible arc of one limb like gorilla this second one pops up when ground travel is not the primary means of locomotion. Hyena do fall in either category their limbs are close enough for a normal gait.

Hyena limbs are not as different in length as many people think, the massive neck and shoulder muscles make the front limbs look taller than they are in many photographs, but yes they are longer. The heavy musculature plus the longer forelimbs are all adaptation to make the animal stronger with more leverage, better able to rip apart a carcass and crush bones. They do not need the massive hind limbs of the large cats becasue they do not "pounce", you see the same adaptation in the so called "Fanged Cats" or saber tooth cats they have massive forelimbs. More importantly the massive muscles on the shoulder and neck make the forelimbs less flexible so to get the same arc swing out of the limb, it has to be longer.


Choosing a book to gain general knowledge about biology

The books you have

The books you cited won't help you to get a solid and general basic knowledge in biology. I haven't read those books but I think that This is Biology is a book of philosophy of biology written by a biologist and philosopher. What is life is a very influential book written by a physicist who more or less predicted the structure of DNA that was later discovered by Watson and Crick. You won't learn much of biology through these books.

Book Suggestions

This post offers book suggestions for general introductory biology. Here is another post that may also interest you

If you are interested in a specific field of biology, then you may want to ask for book suggestions for this particular field. I think that most biologists that come from a background in physics are in the fields of theoretical evolutionary biology, bioinformatics and biophysics (incl. molecular biophysics).

Here are a bunch of other posts asking for book recommendations that I imagine you may like reading about.

What physics knowledge can be applied to biology of organisms and ecosystems?
Book recommendations for algorithms used in evolutionary biology
Book recommendations for evolutionary models
How to learn biomathematics?
Book recommendation on population/evolutionary genetics?
Introductory literature for synthetic / systems biology?

And eventually you may want to read Value of mathematical models in biology although the post has been closed.

Of course, you might want to read a bunch of wikipedia pages such as Biophysics, Molecular Biophysics, Mathematical and Theoretical Biology, Biostatistics, Computational Biology, Bioinformatics.


Are cerebellar basket and stellate neurons actually different cell types?

You are completely right with your guess that is was Ramón y Cajal who first described these cells in his famous monograph "Histologie de systeme nerveux de l'homme et des vertebres." published in Paris Maloine in 1911.

Since the only method he had at his disposal was Golgi's staining which is a pure anatomical staining (there is no living cell left in the tissue after the treatment with  potassium dichromate and silver nitrate) with silver chromate filling completely single cells at random.

Using only this staining and his eyes Cajal did classify the neurons according to their size, location in the brain and their shape. This is why we have such names like basket, stellate, moss, pyramide etc. in neuron description. This classification is purely anatomical and does not reflect any intrinsic properties of these cell, as for example being motor neurons or interneurons.

When I was studying histology at my medical school I was always told that there is new "mollecular biology"-based classification of neurons is about to come and to replace the existing classification by Cajal, many cell types were supposed to be merged there, among others also different anatatomical groups of interneurons. (This was one of the major research topic of the research facility where I studied neurohistology).

As far as I can see, this classification is still not here...


"Immortal Genes" common to all organisms?

Introduction
I believe that Sean B. Caroll is confusing:
• the minimum number of genes required for a viable organism
with
• those genes that are present in all organisms — so called ‘immortal genes’
I will deal with each in turn.
The minimum number of genes required for a viable organism
I have not read the book from which the quotation is taken. From its context and my knowledge I think that the author is mistakenly interpreting ‘the minimum number of genes required for a viable organism’ as ‘the genes present in all organisms’. This is because he seems to be referring to work from the laboratory of Craig Ventner on engineering mycoplasma.
Mycoplasma are among the smallest organisms capable of independent life. They have a genome of about 500 coding sequences, but as parasitic organisms they devotes some of these genes to their parasitic mode of life, while they lack others that the host provides.
The number of 500 may actually be too high: a figure of 300 is quoted in this description, who had plans of Ventner’s plans to build an organism containing a minimal genome containing only such essential genes. There is more on this in a Wikipedia article entitled Mycoplasma laboratorium. It should be noted that the word “immortal” does not appear in either account.
‘Les Immortels’ — genes present in all organisms
The poster would like a list of those genes essential to life, but I know of no such list. How would one go about composing one?
First, one has to set the rules. Do parasites, such as mycoplasma, which are dependent on their host organism, count? Do human beings count? We require amino acids and vitamins, but obtain them from food rather than synthesizing them ourselves. So although it is necessary that a self-sufficient organism have the enzymes for synthesizing the 20 amino acids of the genetic code, these are not all present in humans. I would suggest that we have to restrict ‘les immortels’ to self-sufficient organisms.
Second, one has to decide whether one is talking about a set of genes for accomplishing a function, or individual genes with a structural relationship in all living things that suggests a common identity. For example all cellular organisms (i.e. excluding viruses) must have ribosomes to synthesize proteins, but the protein complement of those ribosomes differs among organisms. Thus, the ribosomal proteins necessary to engineer a minimal mycoplasma may differ from those present in a bacterium such as Escherichia coli, and will certainly not be common to humans. I would suggest we would have to go for the latter.
Having made this decision, one  would get a team of undergraduate students to take all the genes in the genome of E. coli (or even of a mycoplasma) and perform BLAST searches to see whether they are present in representative organisms. Unfortunately I am no longer in a position to torment undergraduate students in this way, so I will have to start a list myself and encourage others to add to (or subtract from) it.
The List — a start
The genes for DNA replication, transcription of RNA and protein synthesis constitute the low hanging fruit here. My area is (used to be) protein synthesis, so I will start there:
Protein Synthesis
Large and small subunit and 5S ribosomal RNAs (3)
Ribosomal proteins (≤32)
Protein synthesis factors — EF1, EF2, IF1 and possibly others
Aminoacyl tRNA synthetases (20?)
tRNAs? — but all that is conserved is probably the anticodon (and sometimes not even that)
Accessory enzymes for protein synthesis:
Pseudouridine synthase
rRNA methylases?
DNA synthesis
B-family DNA polymerases?
RNA synthesis
? Evolutionarily related, but complicated because of multi-subunit nature
But if DNA synthesis is a problem, the reactions leading from RNA to DNA are surely not:
Enzymes of nucleotide metabolism
Ribonucleotide reductase (two subunits)
Thymidylate synthase
Uracil DNA-glycosylase?
Tetrahydrofolate reductase?
Enzymes for interconversion of nucleotides — Adenylate kinase? Nucleoside-diphosphate kinase?
Metabolism
This requires some work. One cannot specify either aerobic or anaerobic metabolsm, but in either case one needs oxido-reducto enzymes. Enzymes of hexose metabolism — hexokinase? Enzymes to metabolize key intermediates like glutamate and glutamine, and enzymes for introducing different groups in synthetic processes. This could make an interesting crowd-sourced project, or, failing that, a game for your next Biochemistry Christmas Party.


How can I make a protein interaction/protein-complex network?

This is not a trivial task depending on how well studied your network is or what information you want to gather. It sounds like an interaction dataset is what you want rather than scouring the PDB for static structures (that would be such a hit and miss process I'm not sure it's worth bothering).

Upload you list of gene codes to string-db.

You'll see the network here, and structures are made clear of known complexes in an expandable thumbnail.
It's a limited web-server tool, and whilst very powerful, isn't very flexible. Cytoscape might be needed for a more novel study because it is scriptable.

You can probably stop here and investigate your network.
From string-db download the .txt file (TXT - simple tab delimited flatfile). I think it's an old-school save icon on the web-server, although if you're uploading multiple identifiers, it is simply the "save" button at the top left.
Download Cytoscape here.
Then use File>Import>Table>From file.
This will build an interaction network and you'll see which genes/proteins interact with one another.

Catch: whilst this provides spacial information, you can't get a picture of temporal information: i.e you know what is interacting, but not when nor for how long.


Is there a photobleaching-resistant, cell-permeant viability stain in the far red part of the spectrum?

You could try SYTO Orange. Unlike SYTOX, which is a fixed-cell marker, SYTO works with both live and fixed cells.


Yes, they do.

Pilots normally say that "birds are day VFR only", you're gonna read this a lot on the internet. VFR means Visual Flight Rules, where the pilot operates the aircraft in weather conditions clear enough to allow the pilot to see where the aircraft is going. Thus, they are implying that birds avoid flying at night and inside clouds.

However, this is wrong. Birds do fly inside clouds (and at night), especially migratory birds that have to fly non-stop for weeks or months. They cannot avoid flying at night (of course) and, in several situations, they cannot avoid flying towards a cloud.

According this paper in Science, from Weimerskirch et al. (2016), frigatebirds can even do this on purpose!

  We studied the three-dimensional movements and energetics of great frigate birds (Fregata minor) and showed that they can stay aloft for months during transoceanic flights. To do this, birds track the edge of the doldrums to take advantage of favorable winds and strong convection. Locally, they use a roller-coaster flight, relying on thermals and wind to soar within a 50- to 600-meter altitude band under cumulus clouds and then glide over kilometers at low energy costs. To deal with the local scarcity of clouds and gain longer gliding distances, birds regularly soar inside cumulus clouds to use their strong updraft, and they can reach altitudes of 4000 meters, where freezing conditions occur. (emphasis mine)

Source: Weimerskirch, H., Bishop, C., Jeanniard-du-Dot, T., Prudor, A. and Sachs, G. (2016). Frigate birds track atmospheric conditions over months-long transoceanic flights. Science, 353(6294), pp.74-78.

PS: You have two questions here, specially after your edit. I suggest that you post another question regarding the spatial orientation, since asking different questions (even if they are related) in the same post is not nice, and it's a reason to close ("Too broad: Avoid asking multiple distinct questions at once"). However, it's worth mentioning that apparently birds do suffer from spatial disorientation when there is no visual cue. According to this relatively old paper, "Spatial Disorientation in Birds":

  The only conclusion is that birds are susceptible and suffer from spatial disorientation, and further that the causes of spatial disorientation in birds are exactly the same as those which affect the human pilot, namely; (a) the loss of true visual cues to the horizontal; (b) inexperience in flying under such conditions where visual cues are lost;


Is there a specific suffix for "within a cell"? i.e. in a similar manner to how -aemia refers to within the blood

"Cyto"/"cytic" and similar are common prefixes/suffixes to refer to things associated with cells; however they don't necessarily specify intracellular space, they are more often referring to specific cell populations, counts, etc.

The word "intracellular" is, however, commonly used terminology for "inside the cell."

For the specific case you mention, I would simply write "high/elevated intracellular glucose" - I am unaware of any reference that uses a individual word for the same meaning. Some others have referred to "intracellular hyperglycemia" which may be a bit odd since the -emia refers to the blood, but they are specifically referring to the case where high intracellular glucose is a direct consequence of overall hyperglycemia.


Why so fewer birds in the yard come late summer and early autumn?

One possible cause is Cooper Hawks. We are in east TX and put out a lot of seed ; we had more birds. Fewer in recent months due to the Cooper Hawk(s). Our yard is a buffet for them ,I hear them often, see them occasionally ;they will perch in the under story.  And we hear birds hit the windows as they panic from the hawk ; it happens 0 to 4 times a day. The hawk has developed a technique of diving and after the small birds when they knock themselves out on the windows , the hawk walks on the patio to pick one up. I have been going out after a bird strike and picking up stunned birds and put them in a shoebox for 30 minutes. They usually recover, had a cardinal yesterday. If you are home during the day , listen for window strikes and watch for sudden flights of all the birds. The Sharpshin Hawk is also here but not a problem.......... And there is a degree of randomness to migrations: Some years we get many Goldfinches, Pine Siskins, Robins, and some years a few or none. And birds like Cedar Waxwings are notorious for their unpredictable movements.


What does it mean: carrying the stably integrated gene

According to Merriam Webster, an exogeneous gene is defined as " introduced from or produced outside the organism or system; specifically :  not synthesized within the organism or system—compare endogenous".

I believe they refer to the tetO::tdTomato transgene as an exogeneous, or not originating from the species of study


GenBank and RefSeq have a huge collection of DNA sequences that can be downloaded in Fasta format. GenBank makes it very easy to search for sequences (for example, using the organism name) but will often have redundant data and varied types (everything from whole chromosome sequences to mRNAs to gene sequences to ESTs). RefSeq has much cleaner, non-redundant data but might take a little more effort for you to find the sequences you want. Depending on whether this has any effect on your project, you might want to consider that. On the RefSeq page, under the FTP menu you can click Genomes to see which genomes have RefSeq data available. The Fasta sequences for a particular genome will be stored in a dedicated directory, possibly subdivided into further directories by chromosome. What you want are the Fasta files (ending in .fa, .fasta, .ffn, or something like that), keeping in mind they may be compressed (.fa.gz, fasta.gz, etc).

Alternatively, if you already have a specific organism in mind, then you could do a Google search to see if the genome for that organism has been sequenced. If so, there is almost always a dedicated website where you can download DNA sequences for that genome.


Why do the fastest runners tend to be black?

It's an interesting question and one that has been asked before. NPR did a story in 2013 on this topic, but their question was a bit more focused than just "why are so many black people good runners?"

The observation that led to their story wasn't just that black people in general were over-represented among long-distance running medalists, but that Kenyans in particular were over-represented. Digging deeper, the story's investigators found that the best runners in Kenya also tended to come from the same tribal group: the Kalenjin.

I'm not going to repeat all the details in that story (which I encourage you to read), but the working answer that the investigators came up with is that there are both genetic traits and certain cultural practices that contribute to this tribe's success on the track. Unfortunately, from the point of view of someone who wants a concise answer, it is very difficult to separate and quantify the exact contributions that each genetic and cultural modification makes to the runners' successes.

Pubmed also has a number of peer-reviewed papers detailing the Kalenjin running phenomenon, but I could only find two with free full-access and neither had the promising title of "Analysis of the Kenyan distance-running phenomenon," for which you have to pay. Insert annoyed frowning face here.

I did a quick search of some Kenyan gold medalist runners in the 2016 Olympics and sure enough, several (though certainly not all) are Kalenjin. I'm less sure about the Ethiopian runners, since most research that I found online seems to focus on the Kenyans, but I'd feel safe hypothesizing that something similar can explain their dominance at the podium.

So, the short answer to your question is that it's not just "black people" who dominate the world of competitive long-distance running, but that very specific subsets of people (who, as it turns out, are black) do display a competitive advantage and that both genetics and culture account for much of this advantage.


How do burrowing animals get enough oxygen?

As the body mass of an organism decreases, their volume decreases with direct proportionality, so their metabolic needs are also reduced. The result is that small organisms like worms and insects have a much larger surface area to body mass ratio, which lets them passively transfer oxygen into their bodies much more easily.

I am by no means an entomologist but most species of insects are able to exchange gases with the environment without any active respiration at all. Due to their small size, gases can passively diffuse through the trachea and spiracles directly to their internal fluids/muscles.

That said, insects simply have much much lower basal metabolic rates compared to even small vertebrates. Lower metabolic rates mean lower oxygen needs, so that's why its not uncommon to see insects surviving in cracks and crevices that don't have a lot of air circulation. The little air circulation that does occur in the temperatures that insects thrive in is more than enough to support their oxygen needs.


Allosteric regulation: why involve extra molecules

It's an interesting question, and there are a lot of potential explanations.

I can at least hypothesize a little bit for the case of 2,3-BPG and 1,3-BPG. I think the key point is that it's not obvious to me why sensing the 1,3-BPG concentration would be useful. This concentration actually has to be maintained in a pretty tight range for glycolysis to function (note that the entire lower portion of glycolysis is very close to thermodynamic equilibrium). The reason that I think 2,3-DPG is a useful regulatory molecule is precisely because its levels can be regulated independently of the function of glycolysis. The activity of the enzymes in the 1,3-BPG -> 2,3-BPG -> 3PG shunt can controlled independently of the control of normal glycolysis and can be regulated by whatever physiological parameter you want 2,3-DPG concentration to represent.

One other thing to note is that typical red blood cell concentrations of 2,3-BPG are actually many orders of magnitude higher than 1,3-BPG. The very low concentrations of 1,3-BPG are a necessary consequence of the thermodynamics of glycolysis as mentnioned above -- if 1,3-BPG concentrations are too high, the GAPDH reaction will become unfavorable. Thus it may be that the typical concentration of 1,3-BPG is too low to be an effective regulator of anything (because it would have to bind very strongly). But I think this is a less important point than asking the question of "what does the concentration of my regulator represent".

There may be biochemical reasons at work in other cases -- for instance, some molecules may just bind better to the protein that you want to regulate, and that's why they're chosen by evolution. I think this is a case when it will be hard to come up with a blanket explanation -- it's better to look at each case, consider what signal biology is trying to measure, and look at the relevant constraints.

I don't know the answer for 1,6-FBP and 2,6-FBP, and note that in other species, 1,6-FBP does appear to be the major regulatory molecule. You could argue that by having 2,6-FBP be the regulator, there are more enzymes whose activity you can control and thus somehow you have more fine-tuned regulation </hand waving>.


Why Insect bites are itchy rather than pain?

You're more likely to have an allergic reaction if you're stung by an insect. The reaction can be classed as:

  Minor localised reaction – this is normal and doesn't require allergy testing, although the affected area will often be painful for
  a few days

  large localised reaction (LLR) – this can cause other symptoms, such as swelling, itching and a rash

  systemic reaction (SR) – this often requires immediate medical attention because it can cause a potentially life-threatening allergic
  reaction (anaphylaxis)

Taken from : http://www.nhs.uk/Conditions/Bites-insect/Pages/Symptoms.aspx

You can read up on this here:

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

http://primer.crohn.ie/the-inflammatory-response

For a more detailed look, I would suggest papers like this:

Loza, Matthew J., et al. "Assembly of inflammation-related genes for pathway-focused genetic analysis." PLoS One 2.10 (2007): e1035.

or a good immunology textbook.


Does protein kinase A accelerate glycolysis or slow it down?

There is a fallacy in your argument, which is the parenthetical statement:

  so that when energy level is low, the increase in cAMP will cause protein kinase A to increase in activity

The activity of adenyl cyclase (the enzyme catalysing the production oc cAMP) is not controlled by energy charge, but by hormones such as glucagon. That is how glucagon has its effect on protein kinase A (better thought of as cyclic AMP-dependent protein kinase to remind you of this fact). That is why cAMP is known as a ‘second messenger’ — the hormone being ‘first messenger’ (and the enzyme that becomes phosphorylated being the recipient of the message). See, for example, Figure 21.14 from Berg et al.

Therefore the explanation in the Wikipedia article on PFK2 is quite self-consistent:

  When glucose level is low, glucagon is released into the bloodstream, triggering a cAMP signal cascade. In the liver Protein kinase A inactivates the PFK-2 domain of the bifunctional enzyme via phosphorylation, however this does not occur in skeletal muscle. The F-2,6-BPase domain is then activated which lowers fructose 2,6-bisphosphate (F-2,6-BP) levels. Because F-2,6-BP normally stimulates phosphofructokinase-1(PFK1), the decrease in its concentration leads to the inhibition of glycolysis and the stimulation of gluconeogenesis.[8]

So the answer to the question posed in your title is: in liver cAMP causes the inhibition of glycolysis.


Stem cell that can pass through blood vessel

Yes, stem cells can pass through blood vessels and capillaries (as @WYSIWYG points, these cells should be small enough to fit inside that capillary). The interesting thing is that they posses multiple mechanisms of transmigration. They are attracted by TNF-alpha activated endothelial cells [1] and can pass through by [1]:

leukocyte-like diapedesis
paracellular migration between endothelial cells
transcellular, directly through individual endothelial cells

  I am thinking of some type of encapsulated stem cells where ultrasound, heat or magnetic fields from the MRI would break up the encapsulation releasing the stem cell at the targeted area.

Note: I don't know if the following is plausible. It is just something I thought of and I consider it to be more effective than what you suggested.

Then what is the purpose of using stem cells that are capable of chemotactic movements and can go by themselves in targeted areas? The encapsulation you propose could be used to fit inside the cell a drug-containing capsule that would break upon external electromagnetic, ultrasonic (etc.) stimulation. This means that the capsule would also contain a substance capable of inducing cytoplasmic membrane lysis, so the drug could reach the interstitial space. Or the cell could be genetically engineered to secrete that drug, when available in cytoplasm, through exocytosis.

But why not get rid of that capsule? A cell could contain (for example) a cytostatic drug in its cytoplasm and also be fitted with membrane receptors for a specific tumoral marker. When it reaches the tumor, receptor stimulation should trigger exocytosis of drug.

References:

Teo GS, Ankrum JA, Martinelli R, Boetto SE, Simms K, Sciuto TE, Dvorak AM, Karp JM, Carman CV. Mesenchymal stem cells transmigrate between and directly through tumor necrosis factor-α-activated endothelial cells via both leukocyte-like and novel mechanisms. Stem Cells. 2012 Nov;30(11):2472-86. doi: 10.1002/stem.1198. PubMed PMID: 22887987.


Can animals make their own unsaturated fatty acids?

Yes, animals can make their own unsaturated fatty acids.

Mammalian fatty acyl desaturases can introduce double bonds at the Δ5, Δ6 and Δ9 positions (i.e. numbering from the functional group). As shown in the diagram below, this means that we cannot introduce double bonds at the ω3 or ω6 positions (i.e. numbering from the methyl end of the molecule) in fatty acids of a reasonable length (see any Biochemistry textbook for confirmation).

I've illustrated the impossibility of us making α-linolenic acid as an example.


Why do some tissues have insulin-dependent glucose transporters and others not?

Summary

The whole point of hormones is that they allow the organism to control the metabolism of tissues in an integrated manner, rather than each tissue acting independently. Insulin, glucagon and epinephrine are classic examples of this in relation to carbohydrate metabolism. In the fed state, the fasted state and in stress situations it is appropriate for different tissues to respond in different ways. The presence or absence of a hormone receptor — together with the enzyme complement of the tissue — achieves this. Allowing all tissues to have only GLUT-3 (or all GLUT-4) would mean they would all respond to changes in glucose availability in the same way — a totally inappropriate situation for the organism, with potentially disastrous consequences.

More Detailed Answer

Insulin is an indicator of the fed state. In such circumstances there will be a surplus of glucose and it is of benefit to the organism for it to be taken up by muscle and adipose tissue for storage as glycogen and fat, respectively. Conversely it is important that in starvation blood glucose is not so utilized, but spared for those tissues for which it is vital in any conditions. (Muscle can utilize other metabolites such as fatty acids.) Hence, for these tissue allowing glucose transport to be controlled only by blood glucose concentration would not produce a sharp cut-off and result in deny this resource to those vital tissues which cannot replace glucose by other energy sources.

The tissues you mention such as brain (and erythrocytes) depend absolutely on glucose, irrespective of whether the organism is in the fed or fasted state. If they had only an insulin-dependent transporter they would be starved of glucose during the fasted state, with lethal consequences. The insulin-independent transporter allows continued transport down the glucose concentration gradient, even as the blood glucose concentration falls.

Note that blood glucose concentration in the fasted state is maintained by the liver, so that this tissue has an insulin-dependent transporter, not to allow glucose uptake, but to allow the glucose produced by gluconeogenesis to be transported out into the blood.

Further Reading

I would hope that the logic of my answer will be sufficient convincing, but it is good practice in Biology-SE to provide references to support one’s arguments. Section 30.22 of the online edition of Berg et al. discusses the metabolic profile of different tissues and includes some discussion of glucose metabolism and glucose transporters. (The liver glucose transporter is actually different from that in nervous tissues, as is that in erythrocytes — see Wikipedia article.)


What equipment is needed to perform simple plant electrophysiology?

Electrophysiology on plant cells means single-cell recordings, as there are no gross compound action potentials.  As you correctly say, this means micro-electrodes; this in turn means computerized manipulation of the pipettes, a decent microscope, signal amplifier, recording software, stimulator slash voltage/current control, Faraday cage, analysis software (Matlab), and not unimportantly a vibration-free workbench (whole departments have moved house due to micrometer vibrations in the building). I guess you should think anywhere between 10k - 100k (dollars, euros whatever) as a reasonable estimate.

A student internship would be advisable finance-wise, but especially because single cell recordings, and electrophysiological skills in general, are relatively difficult to master.


How do developing neurons become tuned to fire only on receiving specific inputs?

The only "good model" I know of is hebbian plasticity* or hebbian theory, here's a link: https://en.wikipedia.org/wiki/Hebbian_theory

Usually what we mean by neurons "listen for" or are "tuned for" or even "like" a particular stimulus is that spiking activity in those neurons is significantly increased (or decreased) in the presence of that stimulus as compared to equal amount of time in the absence of it.

*Plasticity refers to the capacity of the brain to change both the strength of connection as well as number and configuration of connections.


Difference between viral and human genetic material

To sum up: If we are not talking about chromosome organization, nucleotide sequences and overall genome architecture (which are incomparably different in eukaryotes and [even their] viruses) the differences in the genetic material are as follows:

viruses are much more diverse in their choice of genetic material, which is in the cornerstone of viral higher systematics. It can be DNA or RNA, single- or double-stranded, circular or linear. Animals, in turn, possess only double stranded DNA as their genetic material: linear dsDNA for the nuclear genome and [usually] circular dsDNA for the their mitochondrial genomes.
DNA termini pose a special problem for the maintenance of the molecule and show very unusual organization in terms of DNA sequence and structure. Repetitive terminal sequences of eukaryotic chromosomes have 3'-overhangs, which form a special quadruplex form of DNA. Termini of viruses are naturally much more diverse and are (nearly?) never of the same structure as in Eukaryotes. [Circularization/decicrularization is one of the mechanisms recruited by viruses]. (Deng et al 2012)
DNA methylation is normally present in varying degrees in animals and in vertebrates most of the cytosines in CpG dinucleotides are methylated. Viruses differ considerably from one another in this respect, but it seems that smaller viral genomes are generally under-methylated and larger genomes do not show under-methylation, although it depends on the stage. This conclusion is based partly on indirect evidence that CpG motifs are considerably much less frequent in smaller viruses. Integrated "genetic parasites" like retroviruses are normally rich in CpG and are highly methylated. (Hoelzer et al 2008)
although I couldn't find relevant literature, I'd hypothesize that the highly packed genetic material in viral particles may potentially exist in more compact forms of the DNA helix (in dsDNA viruses). Most of the dsDNA in cells is present in a so-called B-form, but there are more compact A-form and less compact left-turned Z-form (there are other forms, most of which are biologically not relevant). (cf. Wikipedia for an introduction)


Are all prokaryotic promotor regions the same, or do they differ depending on the product of the transcript?

Definitely not. There is a ton of variation from gene to gene, otherwise, as you say, regulation wouldn't work.

That said, the word "promoter" sometimes gets used in different ways. Especially in eukaryotic systems, people will sometimes say "promoter" to mean the entire region upstream of the gene where transcription factors can bind (for yeast, typically within a few hundred base pairs, for mammals, could be many kb away). These regions are extremely variable from gene to gene in all organisms. But for bacteria, the word is more commonly used in a much stricter sense, to mean the region where the polymerase and the associated sigma factor binds -- this is typically one or two very short stretches of DNA (maybe 5-10 base pairs) very precisely located at a specific position from the start of the gene. These regions are much more conserved, but there will still be some variation. Check out http://nar.oxfordjournals.org/content/40/7/2907.full for a very detailed characterization of some of these sequences in E. coli.


What makes certain obligate anaerobes viable in fermentation starter cultures?

Here (mic.sgmjournals.org/content/127/1/121.full.pdf) is a link to a paper in which P. shermanii is grown in flask culture. Although the conditions are clearly designed to achieve low oxygen concentrations in the culture (the flask is almost full and is only shaken occasionally), they also indicate that oxygen is not toxic for this organism.

Also, this is from the WP page you linked to:

  Obligate anaerobes are microorganisms that are killed by normal atmospheric concentrations of oxygen (21% O2). Oxygen tolerance varies between species, some capable of surviving in up to 8% oxygen, others losing viability unless the oxygen concentration is less than 0.5%.


How does high-fidelity of DNA replication depend on the formation of hydrogen bonds?

DNA polymerase must catalyse the addition of 4 different nucleotides to the growing strand. This means that it cannot directly determine which base to incorporate at a specific point (how would it 'know' which base to incorporate and how it would it change its specificity for different bases). This means that the specificity for which base pair to incorporate is dependent on the template DNA strand.

Correct Watson-Crick base pairing (that is, hydrogen bonding) between the template strand and the nucleotide to be incorporated triggers the closing of the finger domain of DNAP around the primer-template junction and positions the latter in the optimal position for catalysis (with the $\ce{\alpha-PO_4}$ of the incoming nucleotide near the $\ce{3'-OH}$ of the primer for a nucleophilic attack catalysed by two $\ce{Mg^{2+}}$ ions). This is where the conserved tyrosine residue you mentioned comes into play. An incorrectly paired nucleotide will not trigger this conformational change and will not be positioned optimally, thus catalysis is less likely.

Furthermore, the DNA polymerase makes contacts with the minor groove of the primer-template junction through hydrogen bonds. This interaction is not base-specific (all Watson-Crick base pairs have he same pattern of hydrogen-bond acceptors in the minor groove) but only occurs when the correct nucleotide is incorporated, thus stabilising the complex.

Finally, discrimination between ribonucleotides and deoxyribonucleotides is done by steric exclusion of the $\ce{2'-OH}$ by amino acid residues in the binding pocket.

These factors can be thought of as kinetic proofreading as they simply slow down the reaction rate and provide time for an incorrectly paired nucleotide to dissociate. However, they can still be incorporated and many DNA polymerases have a $\ce{3'->5'}$ proofreading exonuclease that can remove incorrectly paired nucleotides. This proofreading is again mediated by interactions between the DNAP and the primer-template junction (ie hydrogen bonding with the minor groove). A weakened interaction due to an incorrectly paired base reduces the affinity between DNA and the catalytic site and increases the affinity between DNA and the proofreading site (because it has a preference for cleaving ssDNA from the 3' end).


For fluid to flow from a wound there needs to be a significant pressure gradient between where it is now and the outside of the body. Your skin generally does not have a strong compressive effect, which is why a deep cut exposing fat will not lead to the fatty tissue being expulsed from the body any more than the interstitial fluid is.

Blood, however, flows. For it to circulate there needs to be a pressure gradient between where it is now and where it is going. Since veins (including the vena cava, which channels blood back into the heart) do not have vascular walls strong enough to create a suction effect (i.e. lower pressure than the surrounding tissue), you can conclude that the pressure of blood vessels is always higher than that of surrounding tissues, and thus higher than the pressure outside of your body. This is why all blood vessels, including veins, will bleed, whereas less pressurized systems such as interstitial fluid will not.