Pedigree analysis : autosomal or mitochondrial

Mitochondrial because all the offsprings have the same trait as that of the female parent. Lets go through the possibilities one at a time. Assuming you have no carriers (you do not have any carrier symbols) we can work out the following.

Autosomal Recessive?

This might be the case if we assume the male in the first generation is a carrier.

Autosomal Dominant?

This might be the case but it is unlikely. Looking at the first generation possibly yes, as 50% of offspring have the trait. Looking at the second generation however only 3 out of 9 offspring have the trait. Making autosomal dominant unlikely (but it is still a possibility.)

In the test, if you have to go with one option, mitochondrial inheritance is the best because there are no assumptions at all but if multiple options may be correct, you can have any of them.


A trivial question on the meaning of "relatives" in an article on horizontal gene transfer

You are correct.

From the author's point of view there is not much difference, however. Phylogenetically speaking 'species' are kind of artificial distinctions that exist only as sets of individuals and don't usually convey information, so it makes sense to forget that species exist when talking about HGT. Hopefully that helps provide context for why such imprecise wording is so common.


TL;DR: It's highly variable. Don't go whacking people over the head.

All of those things are factors, yes; the two most important ones being force and location. There are subsidiary factors, but most of the time, insofar as there is and identifiable proximate cause of death, it boils down to force and location.

There are two primary paths to death when whacking someone over the head: trauma to the brain, and trauma to the spine. Trauma to the brain is caused by significant force applied to the cerebellum; either in one-off high-impact events, or repeated blows; and trauma to the spine is much the same, injuries caused by shear force to (in particular) the cervical spine; again either in one-off high-impact events or repeated blows.

(There are also secondary paths to death, such as blood loss or infections associated with lacerations of the scalp, face or neck.)

Blows to the top of the head, or blows delivered when prone tend to introduce direct damage to the brain, whereas blows to the side and back of the head tend to introduce damage to the spine. Either is fatal, but for different reasons: Cervical spine injuries hamper communication between the central nervous system and vital organs such as the heart and lungs, leading to hypoxia and suffocation, as well as cascade effects with lesser injuries, whereas brain injuries are more directly deleterious and fatal.

All of that being said, however: While cervical spine injuries can be debilitating, they can be ameliorated by muscles associated with the damaged structures. Direct brain injuries aren't nearly as forgiving, but some people do have Simpson Syndrome to varying degrees.

In addition, there are various somewhat common congenital defects that due to the relatively peaceful nature of our day-to-day are never discovered, but can have a significant effect on response to blows to the head. (This is part of why, if you're ever in a car accident, paramedics will be very keen to evaluate you, even if you have no outwards signs of injury.)

Long story short: Punching someone in the head is a bad idea, unless they pose a very direct threat to you; and you mean to incapacitate them; and you don't mind said incapacitation being potentially permanent (to the point of death).


What is this insect? (Location: Hong Kong; size: 8 mm long, 4 mm wide, 2 mm thick; color: black with some brown at center on the top)

This is a cockroach.

Although about 30 species typically associate with humans and human habitats [source], the only ones that I know that have strong parallel dark lines running in the rostral/caudal direction are the Asian cockroach (Blattella asahinai) and the German cockroach (Blattella germanica).

According to Wikipedia, these 2 species appear very similar. At the adult level, it's actually more behavior (B. asahinai is a better flyer and tends to fly toward light) and habitat (B. asahinai prefers living outdoors while B. germanica prefers living indoors) that "best" differentiates these two species.

Your specimen is not an adult, however, as is made very clear by the extension of the dorsal parallel stripes extending beyond the pronotom, by the relatively small size of your specimen (<10 mm long), and by the absence of clearly-developed wings [see here for descriptions].

This wingless and long-striped specimen is an immature nymph. Although UFL indicates that late instar roaches of these two species can be identified by the presence of white spots on the dorsal abdomen of the Asian roach, your specimen appears to be an earlier instar and does not yet have this spotted pattern.

As in the adult stage, the early instars of B. asahinai and B. germanica also appear quite similar:

 German (left) and Asian (right) early instar nymphs. Photograph by Dina L. Richman (University of Florida); [source].

German nymphs are slightly smaller than Asian roach nymphs, but again they are quite hard to tell apart (often times being less distinct that the above picture).

I've been told that the most useful way for differentiating is simply by location: if found indoors it's more likely German and if found outdoors it's more likely Asian.

Regardless, if it was found inside, you need to act quickly to prevent an infestation...


Can someone tell me the species of this lizard?

I know nothing about lizards, but this looks like a Carolina anole (Anolis carolinensis), also known as a green anole. Apparently they can change colour:


Why is the resting potential of a neuron so close to the equilibrium potential of K⁺?

Lets just go with the basic Hodgkin-Huxley equation:

$$C_M \frac{\text{d}V}{\text{d}t}=-g_{Na}(V-E_{Na}) -g_K(V-E_K) -g_L(V-E_L)$$

At rest ${\large\frac{\text{d}V}{\text{d}t}}=0$ and therefore $V$ is dependent on the conductances ($g_X$) of different ions. Since $g_K \sim 30\times g_{Na}$, the resting potential is closer to $E_K$ (Nernst equilibrium potential of K+).

What it basically means is that since potassium has higher membrane conductance, it diffuses faster thereby attaining equilibrium faster than sodium (in isolated cases assuming only one ion at a time). When both ions are present the resting potential is because of both the ions but since K+ diffuses faster, it has a major contribution to the resting potential compared to Na+. Leak current that is described in the above equation is a general leak (non-specific). Other channels like rectifiers and voltage gated channels are important when talking about action potential and all these channels contribute to the conductance; however you can group all that into a single metric called membrane conductance. Voltage gated channels can be considered separately when studying the dynamics (in this case the conductances themselves become a function of voltage).


Why WHO has not eliminated chicken pox like smallpox?

Eliminating a virus from the world is an immensely costly undertaking. As with most things in real life, cost vs. benefit (and feasibility) need to be taken into account. Unfortunately, there is a limited amount of money available to fight disease.

The overall mortality rate of smallpox is about 30%. That's a very high mortality rate, one that shaped history significantly.

By contrast, of a yearly 4 million people who contracted chicken pox (in the US, before the vaccine), only 100 to 150 died each year.

The death rate of smallpox: 30%. The death rate of chicken pox: .00375%

Maybe someday chicken pox will go the way of small pox. But our limited monies need to be devoted to eliminating viruses that cause greater harm, e.g. polio and others.

Also, not all viruses are equally "eliminatable", e.g. H1N1, HIV, etc.

Smallpox Vaccine: The Good, the Bad, and the Ugly
Monitoring the Impact of Varicella Vaccination


I think the protocols to clean glassware take no chances and just care about RNA degradation rather than targeting one class of enzymes.

EtOH is supposed to denature RNAse and any other proteins on the surface.

Other chemicals such as Diethylpyrocarbonate  (DEPC) used to wash glassware kill all biochemical activity by reacting with nucleophilic moieties in the protein (-OH, -SH -NH(2/3) ).   (See comments below for more.)

These treatments are followed by heating at 300-450 F for 2-4 hours.  This is not a specific RNAse decontamination - all biological activity is killed.

RNAse activity is not assessed by specific detection of a particular enzyme, but rather judged by the degradation of an RNA sample in the lab environment.  So specific inhibition isn't worthwhile - any protein that might interact with and degrade RNA is called an RNAse in these protocols.


In plasmids with high number of copies, the plasmid needs a certain density to be able to supply its function. If a given cell contains a few dozens of plasmid mollecules, and this is its optimal density, the easiest way to achieve this is to downregulate the replication by its own presence or the presence of one of its components. This also allows a random segregation during cell division, due basically by simple diffusion. It's also easier for the plasmid to achieve its optimal density once it has enter in a new cell by conjugation or transformation.

Plasmids are also subject to selection, so it is reasonable to assume that the more independent and more contagious a plasmid is, the bigger its presence in the population. In fact, it is a reasonable hypothesis to assume that many viruses are parasitic plasmids (many viruses in fact have a similar genomic structure and share many traits with them).

However, in plasmids with low number of copies the replication events can be dependent of the genome replication as you describe (despite the fact that many plasmids of this kind still regulate its own replication by itself). In this case, though, the line between plasmid and chromosome is less clear. In some organisms some big plasmids seems to form part of the genomic organization in the whole strain, and they usually contain important genes. This plasmids behave just like regular chromosomes, and they segregate by the same mechanisms the rest of the genome use. For those plasmids the terms minichromosome and megaplasmid are used, and the choice usually depends of the kind of genes it contains.


First question: No, all Down Syndrome patients have a inappropriate duplication of part or all of chromosome 21.
Second Question: More complicated.  The phenotype can vary in severity depending how much much of chromosome is duplicated, whether it is duplicated and stuck onto the end of chromosome 14 (translocation vs. non-disjunction).  Lastly, a rare form of this event is defined by incomplete penetrance or mosaicism of cells that contain duplication.  Short Answer: No, In rare cases, a carrier can pass on trisomy 21 without being affected themselves but they themselves are a "balanced carrier" and don't have extra chromosome 21 material. See last paragraph below from the NIH and this quote from the Mayo Clinic:

When translocations are inherited, the mother or father has some rearranged genetic material, but no extra genetic material — this means he or she is a balanced carrier. A balanced carrier has no signs or symptoms of Down syndrome, but he or she can pass the translocation on to children, causing extra genetic material from chromosome 21

Types of Down Syndrome details from: NIH Down Syndrome Information Page

Research shows that three types of chromosomal changes can lead to Down syndrome.
Complete trisomy 21. In this case, an error during the formation of the egg or the sperm results in either one having an extra chromosome. So after the egg and sperm unite, the resulting cells will also have three copies of chromosome 21. The complete extra copy of chromosome 21 is in all of the person's cells—or a complete trisomy. Complete trisomy 21 is the cause of about 95% of Down syndrome cases.1,2,3
Mosaic trisomy 21. Not every cell in the body is exactly the same. In about 1% of Down syndrome cases, most of the cells in the body have the extra chromosome, but some of them don't. This is called "mosaicism." Mosaic trisomy 21 can occur when the error in cell division takes place early in development but after a normal egg and sperm unite. It can also occur early in development when some cells lose an extra chromosome 21 that was present at conception. The symptoms of someone with mosaic trisomy 21 may vary from those of someone with complete trisomy 21 or translocation trisomy 21, depending on how many cells have the extra chromosome.1,2
Translocation trisomy 21. In this type of chromosomal change, only part of an extra copy of chromosome 21 is in the cells. The extra part of the chromosome gets "stuck" to another chromosome and gets transmitted into other cells as the cells divide. This type of change causes about 4% of Down syndrome cases. There are no distinct cognitive or medical differences between people with translocation trisomy 21 and those with complete trisomy 21.
Sometimes, a parent who does not have Down syndrome may carry a translocation in chromosome 21 that can be passed on to children and cause Down syndrome. Studying the parents’ chromosomes can reveal whether this is the cause of the syndrome. A genetic counsellor can assist families affected by translocation trisomy 21 in understanding the risk of Down syndrome in future pregnancies.1,2,3

Added EDIT:

Also important to note that people can have trisomy 21 develop in somatic cells spontaneously, later in life without having most of the effects of DS. But this can significantly predispose to leukemias shown here, which is an interesting area of study.  Thanks to @The Nightman.


Allamanda blanchetti fertilization mechanism

As far as the ID goes, this looks like Allamanda blanchetti.  See this question.


OK, so the first thing you always do when recreating a cell microscope slide (like drawing or modelling the cell) is that you only draw or model what you see. In your case, this would just be the nucleus, the cell membrane and the cell wall.

To answer your question, onion cells (you usually use epithelial cells for this experiment) are ‘normal’ cells with all of the ‘normal’ organelles: nucleus, cytoplasm, cell wall and membrane, mitochondria, ribosomes, rough and smooth endoplasmic reticulum, centrioles, Golgi body and vacuoles. You cannot see most of these as they appear translucent as well as being too small to see under the light microscope. You need an electron microscope to view these. Note: chloroplasts are not present in an onion cell as it is not a photosynthesising cell.

This is a typical onion cell slide with labels:


First life forms to evolve controlled flight

It was probably an early Pterygota (winged insect).

To my knowledge, the phylogeny of Pterygota is not completely resolved.

Hennig (1981) describes the following phylogeny

Boudreaux (1987) describes the following phylogeny

Wheeler et al. (2001) offers good evidence for this phylogeny

Odonata encompasses dragonflies and damselflies. Ephemeroptera are commonly called mayflies. The origin of pterygotes was about 300 million years ago.

The very first flying(ish) insect had three pairs of wings (Kukalova-Peck, 2005). The pair present on the first segment of the thorax (counting from the head) was then lost in all extant species. Note however than membracidae are using the developmental pathway for this third pair to make elaborate display (mainly for defence; see below).

Some clades further lost both pairs of wings and one clade, the Diptera (flies) lost only the last pair of wings. This last pair is replaced by halteres that are particularly visible in crane flies (see below)


What's the difference between a simple and 1-foliolate (unifoliolate) leaf?

Short answer:

Look for a pulvinus at the leaf-stalk/leaf-lamina junction.

Long Answer:

So from a strictly anatomical identification standpoint, this can be a bit confusing.

According to "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001):

  Simple: Undivided, as a leaf blade which is not separated into leaflets.

Where:

  Leaflet: A division of a compound leaf

and

  Compound Leaf: A leaf separated  into two or more distinct leaflets.

So the definition of a compound leaf is to have "two or more distinct" leaflets.

But wait...

From plantnet:

  one-foliolate (1-foliolate, unifoliolate): a compound leaf reduced to a single leaflet, usually recognized by the articulated or jointed ‘petiole’, which is in fact a petiole plus a petiolule.

So what gives?

Perhaps this is due to a deficiency in terminology, as discussed (and corrected) by Jiménez-Saa 2011.

But, again Harris & Harris (2001) hint toward how this might arise [emphasis mine]:

  Unifoliolate: a leaf theoretically compound, though only expressing as a single leaflet and appearing simple.

So there is still a fundamental difference between the two.

Structurally, we can see the difference at the basal joint of the foliar structure:

  Simple or unifoliolate: The leaf is undivided...with (unifoliolate) or without (simple) an articulation between the leaf lamina and leaf stalk. [source]

Put differently:

  Unifoliolate leaf is usually recognized from a simple leaf by the presence of a distinct joint or a pulvinus at the lamina-petiole junction, which is in fact a petiole plus a petiolule.

Note: Pulvinus = a distinct enlargement/swelling at the base of (sometimes at the apex of) a petiole or of a petiolule.

Note: a discussion about the developmental evolution of unifoliolate characteristics in Cercis canadensis is discussed here.


Why do some organelle (like ER and Golgi complex) cannot be seen under microscope during cell division?

A cell when undergoes the process of cell division there are structures known as spindle fibres that are required to pull the chromosomes off to the poles of the cell so that it can be segregated into the cells properly while division. These spindle fibres are made of microtubules that are protein molecules constituting the cytoskeleton of a cell. Endoplasmic reticulum and Golgi apparatus are also providing a lot of support to the cells.
Also endoplasmic reticulum and Golgi apparatus are the sites where most of protein forms. While cell division these two organelles disintegrate so as to provide protein for microtubules formation, and so as to reduce support of the cell so the division of the cell is comparatively easier.
Also, during the cell division everything divides equally between the two daughter cells, so ER and Golgi bodies disintegrate so they can be equally divided into the two daughter cells.
Also, nuclear envelope is the continuation of the endoplasmic reticulum. Hence endoplasmic reticulum disintegrates with the nuclear envelope.

Here I have provided a set of possible reasons for your question.

You can refer Raven's biology for further information.


How to parse SCOP parseable files PDB residue identifiers?

PDB residues are described by the residue number and an insertion code. Residue numbers can be any number, including negative values. In 3CKR the first residue has nr. -6, followed by -5, etc. This might indicate that there are additional residues at the beginning of the sequence, relative to other PDB entries. In 2P83, the first residue has the number 61P. Take a look at https://lists.sdsc.edu/pipermail/pdb-l/2004-March/001513.html for an explanation why PDB residue numbers have insertion codes.


You're looking for the extracellular matrix:

  In biology, the extracellular matrix (ECM) is a collection of extracellular molecules secreted by cells that provides structural and biochemical support to the surrounding cells.

Its main component are fibers, that can be strongly interlaced as in the case of the dense connective tissue or more loosely distributed as in the loose one.


Is there more diversity in marine species?

I know that marine habitats have a higher phylogenetic diversity (see also Faith 2006) than terrestial habitats, even though they host far fewer species, which is a result of their deeper evolutionary history. Unfortunately, I cannot find a good reference to this claim right now (see http://biodiversity.europa.eu/topics/ecosystems-and-habitats/marine for some support though).

I wouldn't really call the difference in species numbers a paradox though, since speciation rates depend on habitat complexity and dispersal rates (which are generally higher in marine habitats). In either case, the knowledge of marine habitats and species living there are much poorer than for terrestial habitats, so differences in species numbers are highly tentative.


Why is insulin given in type 2 diabetes?

Isn't it illogical to give more of insulin for a deficit amount of receptors?

Seems like there is some confusion in the definition of type-2 DM itself. According to the American Diabetes Association:

  If you have type 2 diabetes your body does not use insulin properly. This is called insulin resistance. At first, your pancreas makes extra insulin to make up for it. But, over time it isn't able to keep up and can't make enough insulin to keep your blood glucose at normal levels.

So the problem in type-1 DM and type-2 DM is quite same; both because of less insulin present than required, the difference being that in type-2 DM the cells need more insulin than normal. And that apparent deficiency of insulin is overcome by insulin injections. Also, the definition you cite doesn't say receptor deficiency anywhere, it just says decrease in receptor's response to insulin.

So why don't we give people a medicine which just increases the number of receptors or increases the sensitivity of receptors?

This is not quite possible yet. Increasing the number of receptors means increasing the gene expression for that receptor, something that is called 'upregulation'. Now, just to add, the cause of type-2 DM has been regarded to be downregulation of insulin receptors on cell surface by high concentration of insulin. See this article:

  The process of downregulation occurs when there are elevated levels of the hormone insulin in the blood. When insulin binds to its receptors on the surface of a cell, the hormone receptor complex undergoes endocytosis and is subsequently attacked by intracellular lysosomal enzymes. The internalization of the insulin molecules provides a pathway for degradation of the hormone as well as for regulation of the number of sites that are available for binding on the cell surface. At high plasma concentrations, the number of surface receptors for insulin is gradually reduced by the accelerated rate of receptor internalization and degradation brought about by increased hormonal binding. The rate of synthesis of new receptors within the endoplasmic reticulum and their insertion in the plasma membrane do not keep pace with their rate of destruction. Over time, this self-induced loss of target cell receptors for insulin reduces the target cell's sensitivity to the elevated hormone concentration.

Now, coming back to the main point, it is not yet possible to inject transcription factors in every cell of body so that more and more receptors can be produced. It is possible in vitro, but not in vivo yet. However, it is possible to inject something else instead of insulin which might have similar effects on the body, something known as insulin agonist. Researchers are already trying to create insulin agonists, but haven't achieved much success. See this paper for example, in which they talk about a peptide S961. The problem here is that most of the molecules synthesized act as both agonist and antagonist based on different concentrations. That is why this field has not seen much success.

EDIT: As mentioned by @Don_S in comments, some drugs reportedly do increase insulin sensitivity and number of receptors in cells. Though they have indirect mechanisms for this, unlike insulin itself, but this works too (at least in vitro). One of them, thiazolidinediones, activates a nuclear receptor PPAR $\gamma$, which in turn increases transcription of proteins involved in glucose and lipid metabolism and energy balance. Another drug, pioglitazone, works even in vivo and has been suggested to work by activating receptor kinases and thus increase insulin sensitivity.

Thus, in future, it is very likely that type-2 DM patients would get prescriptions of such drugs instead of insulin injections, but not until there are more such drugs available and at an affordable cost.

References:

Type 2 — American Diabetes Association
Downregulation and upregulation — Wikipedia
Knudsen L, Hansen BF, Jensen P, Pedersen TÅ, Vestergaard K, Schäffer L, et al. (2012) Agonism and Antagonism at the Insulin Receptor. PLoS ONE 7(12): e51972. doi:10.1371/journal.pone.0051972
Hauner H. The mode of action of thiazolidinediones. Diabetes Metab. Res. Rev. 2002;18(Suppl. 2):S10–S15. doi: 10.1002/dmrr.249.
Kobayashi, M, Iwanishi, M, Egawa, K et al, Pioglitazone increases insulin sensitivity by activating kinase of insulin receptors. Diabetes. 1992;41:476–483.


What leads to the different types of navels?

After childbirth, the umbilical cord is either tied (similar to a tourniquet - the cord itself is not tied into a knot) or clamped to cut off the blood supply. It is then cut distal to the clamp/tie, separating the child from the rest of the cord and the attached placenta. The remaining cells die and dessicate, and the stump eventually falls off, forming the umbilicus or belly button. The default result, barring any issues, is an "innie". However, an "outie" may form if the child was born with a tiny umbilical hernia, or there was a small unnoticed infection at the base of the umbilical cord. Either of these could lead to the formation granulation tissue, described colloquially as an "outie". People can also have combination navels, with the indentation of an "innie" but a small amount of protruding granulation tissue inside.


Which class of animals constitute the largest biomass?

Following from MarchHo's comment, I have not been able to find class-specific (in the formal sense) estimates, but if you meant 'class' in an informal sense, the following may be useful.

A nice infographic covering the relative biomass of all land mammals is here, and a full table for species groups (at the level of domesticated vertebrates, invertebrates, etc) is here (reproduced below).

Short answer: amongst animals, invertebrates are where the mass is.


Is it possible to create an experiment in house conditions to prove the existence of germs?

You could use Jell-O for growing bacteria if you don't have access to agar ! (I have never tried this but I think it should be possible because the gelatin in Jell-O is like agar.)

You should first sterilize a small knife on a gas stove or with alcohol and then gently rub it on any surface (where you think bacteria are likely to be found ) and then rub it on Jell-O taken in a dish. You should then place it in an environment similar to the one from where you isolated the bacteria. After one or 2 days the bacteria should grow.

For control : You could simply put a plate of Jell-O in the same place but without inoculation of bacteria.

Disclaimer : I am not a microbiologist and I am not sure this would work but you could give it a try as it will not be really expensive :)


It looks like this could be Lotebush, Ziziphus obtusifolia. The thorny branchlets and blue-green color (at least, as it appears in the photos) suggest Ziziphus to me, although you could compare it with the photos or description here. If it is in the buckthorn family, it does seem to key out to Ziziphus using the Christie et al. key.

If you wanted to be sure, you could follow up with the ASU herbarium (see citation).

Christie, K., M. Currie, L.S. Davis, M.-E. Hill, S. Neal and T. Ayers (2006). Vascular Plants of Arizona: Rhamnaceae. Canotia 2(1): 23-46. Open access


Transverse diffusion of lipids in red blood cells

There are two reasons for the asymmetry for the lipid composition of membranes in cells usually.

The first which was mentioned by @Superbest is proteins which are called 'flippases' which describes three broad categories of proteins which facilitate the translocation of the lipids through the membrane, despite the fact that they all have polar or even charged head groups.

This is not really an answer to your question here though - they will have little to do with asymmetry of lipids in erythrocytes I think because the these proteins will only allow lipid diffusion to equilibrium on either side of the membrane.  To force an energetically unfavorable mixture of lipids they would require the use of energy.  While some lipid translocases can force the composition to change against the equilibrium, these seem to require ATP and human erythrocytes do not have mitochondria.

The second, probably better answer is that the lipid composition of a membrane at equilibrium is dictated by of the curvature of the membrane.  The outside of a membrane takes lipids with larger head groups and shorter or fewer chains, the interior will compose more of lipids with smaller head groups and longer and more aliphatic chains.
This capacity of a lipid to take up a greater volume in its head group vs its non-polar end is called its 'intrinsic curvature'.

Erythrocytes have some cytoskeletal structures such as ankyrins which give the cell its characteristic curvy 'dented lozenge' shape, which must also drive some of the lipid composition in some parts of the cell.


Do non-functional (‘junk’) protein sequences exist?

This question is unanswerable as, if a protein exists as a physical entity in a cell it is possible to demonstrate it has a functional or structural role, but it is logically impossible to demonstrate it has no such role. The best one can say is that “it has no known function (role)”.

That said, in the course of evolution following gene duplication and divergence it is theoretically possible that on the way to acquiring a new functional role there is a stage at which a protein has no such role. One might be able to identify such proteins in a gene family like the globins by examining a range of species, as has been done for the globin genes. I am not aware of any such studies.


Why and how is DNA synthesis so much faster then RNA synthesis in bacteria?

I wouldn't call them hypotheses, but the question is intriguing, and, as it seems to be ignored in the literature, I'll make a couple of suggestions.

Perhaps it has something to do with recognition of termination signals in relation to selective pressure for speed in the two processes.

Perhaps if elongation of the RNA chain were any faster it wouldn't be able to respond to the rho-independent termination signals which are thought to be specific stem–loops in the DNA that cause the RNA polymerase to pause and fall off the DNA. The speeding RNA polymerase might disrupt the loops instead. The termination system for DNA replication may have evolved to be much more robust so as to be able to bring faster elongation to a stop. (Note: my suggestion of different ‘robustness’ in termination is not based on any data, it's pure speculation.)

If this were true, it would beg the question of why transcription hasn't evolved a more efficient termination system in concert with the a evolution of a smarter RNA polymerase. Perhaps the answer here is that there is no selective pressure for faster transcription — the rate is clearly sufficient to supply the needs of the cell — whereas the rate of DNA replication determines the time between cell divisions and thus the rate of growth, which is subject to selective pressure.

Perhaps it has something to do with error frequency in relation to selective pressure for speed in the two processes.

First I'll make it clear that I think the proofreading argument in the question is a bit of a red herring. If the rate replication is 20x as fast as transcription, the occasional backtracking will not have much effect on the overall difference. However errors and proofreading could be involved in a different explanation.

RNA transcription does not have proof-reading. The length of RNA transcripts is such that the cell can tolerate the errors that occur. However if the speed transcription were increased it is reasonable to expect an increase in error frequency, which might be detrimental. The current rate of transcription may be a trade-off between efficiency and accuracy. Of course one can imagine a proof-reading system for transcription evolving if it were necessary, but, as discussed above, if the rate of transcription is adequate there would seem to be no selective pressure to produce.


How much of my ancestry will match with my brother?

As both you and your full sibling are males, it means that you share the exact same Y chromosome. You also share the same mtDNA as you have the same mother. All the rest is just a bit of segregation and recombination that will lead to minor differences but generally speaking, your ancestry data should be very similar. Specific disease related data might vary though.


In what stage of bacterial growth can penicillin inhibit the growth of the cellular wall?

This is a really good question that requires you to appreciate a few different details and to overcome a few implicit assumptions that you might perhaps have.

The bacterial growth stages you refer to only apply to a population of bacteria. Individual cells do not undergo these stages.
Relatedly, bacterial population growth stages are independent of the stage of bacterial cell wall growth.

You can have mature or immature bacteria at any stage of "bacterial growth", with either fully formed walls, or with none. This understanding should answer your question partially.
Here are a few more things to consider, for a more complete understanding:

Penicillins are a class of molecules, of varying efficacy and bioavailability across the body and across different kinds of walls and membranes.
Inhibiting the spread of bacteria can be achieved using two types of antibiotics... bactericidal or bacteriostatic ones. Bactericidal means the bacteria die, while bacteriostatic means their growth is slowed or stopped.
Penicillins are bactericidal agents that exert their mechanism of action by inhibition of bacterial cell wall synthesis and by inducing a bacterial autolytic effect. So even mature bacteria will die off in the later stages of outgrowth. In principle, it does not matter what growth stage the bacteria are at, the bactericidal mechanism will take place regardless.
Pencillins are more effective against Gram-positive bacteria. Gram-negative bacteria have a lipopolysaccharide and protein layer that surrounds the peptidoglygan layer of the cell wall, which acts as a barrier for the penicillin from reach its target (which is responsible for completing the synthesis of peptidoglycans, the structural component of bacterial cell wall). However, penicillin can get into Gram-negative cells, for example through channels called porins.

This is more or less very standard knowledge that is easy to look up. Wikipedia's entry on penicillin is a good place to orient yourself if you already haven't.


What are the biological processes of ingesting radioactive particles?

Your question has a rather glaring assumption which is that the amount of radiation emitted by food sources is equivalent to the amount of radiation received while sitting on top of the Fukushima plant. Even if a fish was as radioactive as an equal mass of concrete at the site, the dose you are getting at the site is because of all of the other things surrounding you.

The answer is simply that the food sources near the plant have been deemed (by the officials you mention) to emit a dose of radiation that is less than the level deemed harmful (again, by the officials you mention). It is of course possible that either the estimate of the radiation dose from the food is low, or the level deemed harmful is too high; that discussion is too broad for an answer here.


The imnstrument is shown here upside down. If it is turned around, it looks like this:

The glass disc are placed around the middle tube. The operation principle can be seen in this image:

The specimen is placed in the tube in the middle and pushed out by turning the knob at the bottom. The minimal increment for this kind of microtome is 10 micrometers. The razor knife is used to cut the slices of the specimen.
An operation manual can be found here.


Which organisms have the neuroanatomy Roger Penrose supposes play a role in consciousness?

Microtubules are a structure in the cytoskeleton, they are rope like polymers that grow to a length of about 25 micrometers (25000 nm), and have an outer-diameter of around 25 nm. For comparison, the mean spacing between atoms is on the order of 0.1  to 0.2 nm; so the micro tubule really is micro: about 200 atoms across. In terms of quantum effects though, this is pretty big but not unreasonable. Researchers commonly use quantum dots to play with quantum effects, and these are typically spheres on the order of 10 to 50 atoms in diameter. Note, that we don't know how to couple 5000 quantum dots in one coherent chain (how many you would need to get the length of a microtubule).

So microtubules are small, but they are common! Microtubules are found in all dividing eukaryotic cells and in most differentiated cell types. In other words, that mosquito you just smacked and that philosophers always give as an example of something non-conscious is full of microtubules. This should raise some red flags, but we don't need to go into more detail of microtubules to discredit Penrose and Hammeroff. However, if you love cell biology, take a look at Desai & Mitchison (1997).

So microtubules are probably a bad basis, but why did Penrose want quantum effects in the brain? In The Emperor's New Mind, Penrose suggests consciousness is non-algorithmic and suggests that a magical quantum computer could do these non-algorithmic tasks. The reason I use 'magical' is because a real quantum computer is Turing-complete, if a classical computer cannon solve a problem then neither can a quantum one (of course, if a classical computer can solve a problem, then quantum one can as well and might be able to do it qualitatively faster). For a nice computer science debunking of this part of Penrose's argument take a look a Scott Aaronson's lecture notes.

Why did Hammeroff want quantum-ness? To avoid dualism in explaining consciousness. However, he has gone so far down the reductionist rabbit-hole that he popped out on the other side. He arrived at the same 'magic' we feared in dualism except now he called it 'quantum mechanics'.

The biggest irony of this approach is that Penrose was inspired in many ways by Schrodinger's beautiful take on life. Although Schrödinger does bring in quantum mechanics (both as a useful reduction and as an analogy) he uses completely different parts of it (he uses the discritization of energy levels, and specially avoids issues of the uncertainty principle and superposition of states that made him famous).  Schrödinger would completely disagree with Penrose and Hameroff::

  [I]f we were organisms so sensitive that a single atom, or even a few atoms, could make a perceptible impression on our senses -- Heaves, what would life be like! To stress one point: an organism of that kind would most certainly not be capable of developing the kind of orderly thought which, after passing through a long sequence of earlier stages, ultimately results in forming, among many other ideas, the idea of an atom.

This response can be made precise through quantum decoherence (Tegmark, 2000) and there is little regard for the physical importance of quantum mechanics in the brain (Litt et al., 2006) although Hammeroff (2007) still defends it.


Why do only two sexes exist for animals?

To get a non-circular answer to why humans and other mammals have only two sexes, it's helpful to take a look at our evolutionary history.  While mammals possess several adaptations to a terrestrial life cycle, including internal fertilization and gestation, which require substantial anatomic specialization between males and females, these are all secondary features that evolved long after our aquatic ancestors had acquired two distinct sexes.

Indeed, if we look at animals like fish, which reproduce via external fertilization, it's not at all obvious why they might not have more than two sexes.  After all, for many aquatic animals, mating involves little more than the female and the male releasing their respective gametes into the water, where they meet and fuse to a form new zygote, which can then divide and grow into a new adult.  Seen that way, there seems to be no reason why there could not be more than two "mating types", as in many fungi, such that gametes of any two distinct types could fuse into zygote.

The answer lies in the fact that the male and female gametes aren't actually that similar: the female gametes, or eggs, are typically large cells that contain all the nutrients necessary for the new zygote to develop into a viable individual, whereas the male gametes, or sperm, are tiny and produced in huge numbers.  This asymmetry is known as anisogamy, and modeling its origin has been an important topic in the theoretical study of evolution.

Without going into details on the evolution of anisogamy, once it exists, it clearly forces the mating types to also split into two groups: there's no advantage in two microgametes (sperm) fusing, since the resulting zygote would lack the nutrients it needs to be viable, whereas the fusion of two macrogametes (eggs) would simply be inefficient — eggs, being large, are comparatively rare and expensive, and wasting two of them to produce only one offspring would be suboptimal even if the resulting zygote was viable.  Nor is there really room in such a scheme for gametes of intermediate size: they'd be too small to fuse into a viable zygote with sperm, but too large to be produced in sufficient amounts to be effective in fertilizing eggs.

Of course, there's nothing that would stop a single adult from producing both micro- and macrogametes, but such an adult would not really be a third sex — it would just be male and female at the same time, a mating strategy known as (simultaneous) hermaphroditism, which indeed occurs relatively often in nature.

So, if pretty much all animals are anisogamous, why do fungi remain isogamous (and often have multiple mating types), then?  Well, one explanation is that the main drivers for the evolution of anisogamy — sperm competition and transportation risk — don't really apply to fungi, which mate when two sessile haploid mycelia grow and come into contact with each other.  Since the gametes are not motile, there's no advantage for either/any sex to produce more of them (at the cost of smaller size) in order to increase the chance of successful mating.  Thus, isogamous mating works fine for the lifestyle of fungi, and having multiple mating types is then a useful adaptation to make successful mating between neighboring mycelia more likely.


Do species which have a closer common ancestor to humans tend to be more intelligent?

Several issues here that make your question unanswerable:

Intelligence is not defined. How would you define it?
What kind of relationship are you exactly looking for? Comparing average intelligence between groups or trying to fit a regression with intelligence on the Y-axis and relatedness to human on the X-axis?
The general issue hidden behind methods of species comparison is "How do you define a species?"

If you want to compare average intelligence between groups, meaning that you want to compare average intelligence of a group of closely related species of human to the average intelligence of all animals? Then the answer to your question will probably be "Yes" as primates seem in average to be more intelligent than the average animal and mammals tend to be in average more intelligent than the average animal. I'd expect too that vertebrates are probably on average more intelligent than the average animal. Let's not forget that some animals have no brain (e.g. Sponge).

But now if you want to fit a regression between intelligence and relatedness to human for all animals, you will probably have some trend (a regression with a significant slope (positive correlation)), but you will have many group of points that will not fit on your line. Many birds for example may be considered as much more intelligent than humans depending on your definition. Many invertebrates such as octopuses are very intelligent, too. If you allow for a broad definition of intelligence, then you may also consider the intelligence of social insects which may be surprising. Some aquatic mammals are very intelligent although other, more seemingly stupid mammals, are closer to humans than aquatic mammals.

In short, keep in mind that intelligence is not easy to define, and depending on the definition, the answer will be different. Typically, if you use a very human-like definition of intelligence, you will probably find that intelligent species are more closely related to human. There is a correlation between intelligence and phylogeny (=tree of life), therefore yes, closely related species to humans may have some tendency to be fairly intelligent, but there are many other clades (groups of species on a phylogeny) that show some impressive intelligence, especially in insects, in mollusca, in  birds, the carnivora and the cetacea.


layman inquiry into mechanics of evolution

The question is a very deep one, and the answer is 'it depends'. Organisms can in general only evolve by taking rather short steps through genome space, where each step is better than the last. This could mean one or two nearby basepairs change, or one or two segments of DNA get duplicated, inverted, deleted, etc. It's the DNA that evolution acts on, not the organism's 'qualities', or as we call them, it's phenotype.

In your example, there might be a single piece of DNA which when duplicated, causes the organism's number of legs to go from 4 to 6. In this case the mutation can happen and be selected for and extra legs can evolve. If however the evolution of new legs requires a lot of mutations, non of which are individually useful, then the trait won't arise before the intermediate mutations are selected away.

What may happen instead is something more complicated. E.g. the many mutations for the new legs could initially arise because they are doing something different, and then gradually get selected for other purposes.

In general though the problem of how organisms' move from one peak in the 'fitness landscape' to another is an ongoing topic of research.


Does artificial heat (shower/tea) affect diurnal rhythms in humans?

Yes, the human body has thermoreceptors that "sense" the current temperature, but these merely help with regulation--you know, shivering to raise internal body temperature and sweating to cool via evaporation. The hypothalamus is primarily responsible for making sure that the circadian rhythm itinerary is adhered to reasonably well. So no, if the thermoreceptors detect that the body temperature is 97 deg F but it's 5 pm, the body will not "get confused" and decide that it is actually 4 am because a human body is about 97 deg F at 4 am.


Why don't rats have a gallbladder, unlike other rodents?

There are many different theories on this aspect of evolution, some of them are proved and others are just conjectures. Materials and research in this particular aspect is very few. Here I tried to provide an answer in reference to the particular animal you mentioned, i.e. rat.

Rats don't have a gallbladder possibly due to the following reasons -

The concentrating power of bile in rat's liver is high, so the main function of bile concentration by gallbladder is unnecessay in them. This is probably the most supported theory regarding this.
Rats frequently take their food so they require a continuous supply of bile. This eliminates the necessity of bile storage.
Harbivore animals relatively lack fat in their food. This reduces the need of large amount of bile salts in the intestine.

References -

https://theparadigmshiftgroup.com/animals-no-gallbladder/
Zoology textbooks
http://www.sciencedirect.com/science/article/pii/S0375090613000323?np=y


What is the difference between a signal peptide and a transit peptide?

Signal peptides are typically located at the N terminus of a protein. The signal peptides are processed by the translocon machinery and are cleaved off after sorting through the membranes of organelles in the secretory system:

  endoplasmic reticulum
  Golgi apparatus
  ER-Golgi transition vesicles
  plasma membrane
  lysosomes

Transit peptides target the protein to other subcellular organelles such as (from UniProt):

  Mitochondrion
  Apicoplast
  Chromoplast
  Chloroplast
  Cyanelle
  Thylakoid
  Amyloplast
  Peroxisome
  Glyoxysome
  Hydrogenosome

N-terminal transit peptides are quite rare. C-terminal transit peptide motifs are much more common. UniProt holds transit peptides as a discrete controlled vocabulary, separate from signal peptides.


That is an Isopod crustacean, in the suborder Oniscidea https://en.wikipedia.org/wiki/Woodlouse. These are harmless, so I would not worry about contacting pest control. They are also known as "pillbugs".


1 and 2) You need to build/use a calorimeter : http://en.wikipedia.org/wiki/Calorimeter
Different types exist, depending on your constraints.

3 and 4) It will depend on the size of your system.

If you decide to use an adiabatic calorimeter: First have an estimate of their metabolism (see e.g. [1]), then divide the energy spent over the duration you think you'll use by the heat capacity of the water volume you have, you get the temperature elevation.

If you use a flux calorimeter, then you don't multiply by the duration but check that the calorimeter will be sensitive enough.


Why is the current flow shown to be flowing from the negative area towards the positive area?

By convention, positive current is assumed to be the direction of flow of positive charges. The trouble is that in many common situations (like this one), the current is actually carried by electrons which are negatively charged.
It can be confusing. Blame it on Benjamin Franklin. The convention for current flow was based on his work, before anyone knew about electrons, protons, and ions.


What is the effect of self envenomation on reptiles?

TL;DR
No, it won't die. Lizards/snakes are usually immune to their own venom.

Since I couldn't find a good answer to this recurring question on this site, I will try to summarize it here. I found more research on snakes than on lizards, but for now we will just assume that similar mechanisms can be found in lizards.

First, the question is how the venom kills the prey. What does it do in the body?

A common mechanism is a block of acetylcholine receptors at the neuromuscular junction. Simplified, these receptors activate muscle contraction upon a neuronal signal. When the receptor is blocked by the toxin, the neuronal signal cannot be transmitted to the muscle, which paralyzes the animal. Research has shown, that some snakes and lizards have evolved different acetylcholine receptors, that can still bind acetylcholine (and activate muscles), but not the toxins (source1, source2). This makes them immune to the most common neurotoxins found in reptile venom.

Another mechanism is hemorrhagic activity of the toxin, which is a disruption of blood vessel integrity resulting in bleeding and death. This was linked to a proteolytic ("destroying proteins") function of venom compounds (source3, source4, source5). The blood serum of snakes can contain factors that block the hemorrhagic function of toxins, possibly by neutralizing the mode of action (inhibiting proteases). This could be specific antibodies/inhibitors or an adaptation of serum proteins (source6, source7, source8).

Further research has implicated phospholipidases (destroying phospholipids like used in cellular membranes) as the mode of action for snake venoms. Again, phospholipidase inhibitors can be found in the blood serum of the snakes themselves. There were also reports, that the expression of these inhibitors changes from younger to older snakes (source9, source10) and can be induced by venom injection (source11). It is therefore hypothesized that venomous snakes or lizards are repeatedly exposed to small amounts of their own venom, building up immunity over their life span.

Other modes of action include myotoxicity (destroying muscles), edema-formation or blood thinning. Again, it depends on the specific mechanism and how snakes and lizards have adapted to be immune to these.

Since similar toxins are found in several species, snakes and lizards are often not only immune to their own venom, but also to bites of other members of the same species or other related species.


Are platyhellmintes and annelids segmented?

Here are the first sentences from the wikipedia articles for platyheminthes and annelids:

  The flatworms, or Platyhelminthes, Plathelminthes, or platyhelminths (from the Greek πλατύ, platy, meaning "flat" and ἕλμινς (root: ἑλμινθ-), helminth-, meaning "worm")2 are a phylum of relatively simple bilaterian, unsegmented, soft-bodied invertebrates.

  The annelids (Annelida, from Latin anellus, "little ring"),2[n 1] also known as the ringed worms or segmented worms, are a large phylum, with over 17,000 extant species including ragworms, earthworms, and leeches.


The short answer, which has already been pointed out by user137, is that females are diploid while males are haploid. Bees do not have sex chromosomes per se; rather sex is determined by the csd gene on chromosome III (csd stands for complementary sex determination). Diploid bees that are heterozygous at the csd locus (i.e. contain two different alleles (versions of a gene) for csd) are female (workers).

Bees that are haploid at the csd are males. Interestingly, diploid bees that are homozygous at the csd (i.e. contain two copies of the same csd allele) are also males. But in the honey bee, these bees do not survive as they are killed by workers before they mature. In some other haplodiploid species, however, both haploid and diploid males are viable (the bumble bee Bombus terrestris for example). Also note that diploid honey bee drones can be viable if they (somehow) make it to maturity without being killed by workers (e.g. see here).


Will the interaction of two proteins vary across different tissues?

Your example of an interaction mediated by a scaffold protein is certainly one way of controlling protein interactions. This doesn't just happen in different tissues either, it is also used to fine-control the interaction of certain proteins within one cell, the most notable example for this are the kinases in the MAP pathway (see for example this paper).

Another possibility I can see is that A and B can interact, but only if (at least) one of them is modified, e.g. by phosphorylation - so the actual interaction happens with A-p and B. In a case like this it's not unlikely that the protein that modifies A is only expressed (or active) in certain tissues, which then mean A(-p) and B can only interact in these tissues.


Withdrawal reflex

You asked specifically about the withdrawal reflex and the receptors that trigger this. The initiation of the reflex arc is determined at the level of the nociceptors (pain-transducing receptors) in the epidermis. For the most part, these are part of “free” (not encapsulated) nerve endings of sensory fibers. These fibers course within spinal nerves whose cell bodies are located in the dorsal root ganglia adjacent to the spinal cord. There are two types of nociceptive endings:

mechanical: with parent fibers Aδ

transduce severe mechanical deformation

polymodal: with parent C-fiber units

transduce heat, cold, irritant signals

This picture shows free nerve endings in the epidermis. The boxed portion of the big picture is expanded in the bottom right.

The withdrawal reflex initiated by these receptors is mediated by a polysnaptic (multiple neurons) arc. The sensory neuron synapses with interneurons in the spinal cord.1 Some of these use glutamatergic connections to activate appropriate muscle groups mediating withdrawal. Others inhibit the reciprocal muscle groups (reciprocal inhibition) to allow this movement to be unimpeded.

Here is a cartoon diagram showing the spinal components of the reflex arc in a cross-sectional level of the spinal cord. Notice the interneuron between the sensory and motor neurons (although it's not labeled as such here):

Stretch reflex

In order to provide a broader picture of the basic principles involved in spinal reflexes, it's helpful to also mention the stretch reflex. This is perhaps the quintessential reflex arc because it is monosynaptic, exemplified by the patellar tendon reflex. The stretch reflex is fast, with a latency (stimulus–response interval) of about 15–25 ms (contrast the polysynaptic withdrawal reflex with latency ~70-100 ms.)

The stretch is initiated at the Golgi tendon organs. These are found at the junction between muscle and tendon. The (Ib) nerve fiber splays out and intertwines with tendon fiber bundles. The  nerve endings are activated by the tension of muscle contraction (either passive (as when the patellar tendon is tapped), or active (as during voluntary movement). The afferent sensory neurons directly excite homonymous motor neurons  (i.e. motor neurons supplying the same muscles), and inhibit (via interposed “Ia internuncials”) the antagonist muscles.

I have limited the discussion here to the withdrawal reflex you asked about and another basic spinal reflex arc as an illustration of principle. There are many other, mostly more complex reflex arcs that are beyond the scope of this answer, but I highly recommend checking out a neuroanatomy or neurophysiology textbook such as the one I've listed below if you'd like more information.

Note

1. Although the discussion here is limited to the anatomy of the reflex arc, there are additional synapses within the spinal cord that connect with ascending circuits, as described in the section about afferent neurons of spinal nerves in another answer. Some of these tracts end up at the cortex and are the basis for conscious perception. However, note that this process is multisynaptic and takes longer. The beauty of the spinal reflex arc is that it does not require information to travel all the way up to the brain and back down, which would slow down the response considerably. Practically, this means that you will pull your hand away from a hot stove before you have conscious sensory awareness of the burn.

Reference

Apart from linked article and images with sources below, all information is summarized from:

MJ Turlough FitzGerald,  Gregory Gruener, Estomih Mtui. Clinical Neuroanatomy & Neuroscience © 2012, Elsevier Limited.

Image 1 from: http://en.wikipedia.org/wiki/Free_nerve_ending

Image 2 from: http://www.tutorvista.com/content/biology/biology-iv/nervous-coordination/natural-reflex.php


Carrying out a BlastP on ORF and achieving hits but 2 have the exact same score, evalue and query cover?

If I understand it correctly, you have two subject protein sequences that are exactly the same as your query. You say they are different species, so I guess you made sure they are not the same species and different strains, or subspecies.

I would suggest to now query your nucleotide sequence using blastn against both results (since a priori it could be either species, or neither), and focus on the one that gets a higher score using blastn in your phylogenetic analysis. Due to codon degeneracy, it could be that your blastn results differ between the two.


De-husking and industrial storage reduces the germ's longevity quite a lot, although quite a lot of germs will still be viable if the humidity and microbial conditions are very stable, perhaps even a year.
De-husking will accelerate this graph:

The husk is designed to keep the germule in peak condition in the wild until whichever season it is supposed to germ, through droughts, rains, cold weather, changes in humidity, predation, infection.
If the germ is de-husked and left in natural conditions, it rapidly loses vitality and deteriorates. In storage it's kept in conditions made to discourage microbes, so it will last longer, but it will absorb ambient humidity changes and deteriorate much faster than with a husk.


Welcome to Biology.SE

Assumption

I will assume it is true that the allele causing a ash-red plumage is dominant over all other alleles. Note however that you should cite your reference when making such claim in your post.

Dominance and allele frequency

Phenotypes associated to a dominant allele A aren't necessarily more common than the phenotype of the recessive allele a. It all depends on the allele frequency. If the dominant allele is at low frequency then both AA and Aa (both displaying the dominant phenotype) are at low frequency (esp. AA individuals) and most individuals are aa and show the recessive phenotype.

Learn more

You might want to read about Hardy-Weinberg rule with this post for example.


501 denotes 501st residue in the corresponding PDB entry — 1BDG. See here
A single protein can have multiple cavities (see here) and the multiple entries denote centres of different cavities.


Why does eating saturated fat increase blood cholesterol?

In short: It may not be saturated fat by itself but high saturated/unsaturated fat ratio and high animal/plant fat ratio in the diet that increases the risk of heart disease.

A systematic review of the effect of dietary saturated and polyunsaturated fat on heart disease (NMCD Journal, 2017)

  Reducing saturated fat and replacing it with carbohydrate will not
  lower cardiovascular events or CVD mortality although it will reduce
  total mortality. Replacing saturated fat with mono- or
  poly-unsaturated fats or high-quality carbohydrate [from whole-grain
  food] will lower cardiovascular events.

Saturated Fatty Acids and Cardiovascular Disease: Replacements for Saturated Fat to Reduce Cardiovascular Risk (PubMed, 2017)

  Replacing dairy fat with carbohydrates from refined starches and added
  sugar was not associated with increased or decreased risk of coronary
  heart disease (CHD), stroke or total cardiovascular disease (CVD).
  However, replacing dairy fat with carbohydrate from whole grains
  reduced the risk of CVD, CHD and stroke. Relative to other animal
  fats, dairy was found to have less impact on CVD. When 5% of energy
  from dairy fat was replaced with animal fat from non-dairy sources,
  risk of CHD increased by 6%. However, when 5% of energy from dairy fat
  was replaced with an isocaloric amount of polyunsaturated fats, risk
  of CHD was reduced by 26% and CVD risk was reduced by 24% [41].

A basic explanation of the underlying mechanisms:

The liver produces low-density lipoproteins (LDL) and high-density lipoproteins (HDL). Lipoproteins are composed of triglycerids, phospholipids, cholesterol and proteins.

LDL caries cholesterol from the liver to the peripherial tissue, including arterial walls, where it can accumulate and cause atherosclerosis. This is why LDL is called "bad cholesterol" (even if LDL is only a carrier for cholesterol). HDL clears excessive cholesterol from the blood and carries it to the liver for disposal, so it is called "good cholesterol. (Heart.org.uk)"

High LDL levels are associated with an increased risk of coronary heart disease (Bentham Open).

One possible mechanism by which saturated fats increase (LDL) cholesterol (PLOS):

  Saturated fat is thought to increase LDL-C primarily through
  down-regulation of hepatic LDL receptor activity, leading to reduced
  clearance of LDL particles [from the blood].


How to interpret McDonald-Kreitman test results?

A helpful way to phrase it for me is that "If there's a disproportionate fraction of non-synonymous mutations between species relative to what exists within species, it is because non-synonymous mutations are being selected for in the one species but not in the other, thus there's positive selection."

By the way I'm not an expert in this so take the explanation with a grain of salt.


Why biologic systems tends to become more complex?

This is an old and interesting question: how do we explain apparent trends in evolution without falling into the trap of teleology or goal-directed evolution, the idea that evolution is working toward a particular end point?

I don't know the answer, and I don't know if anyone knows the answer, but at least two books have tackled the question in a serious way.

John Tyler Bonner argued in a 1988 book that complexity tends to increase because of the correlations between organismal size and complexity. Cosma Shalizi's summmary of his idea is that:

  ... [f]illing a previously empty niche does wonders for the reproductive success of an organism; variations which increase size make new niches available, and so are favorably selected. But, owing to constraints imposed by basic physics and chemistry, larger organisms must be more specialized internally, i.e. more complex, to be as efficient as smaller ones, or even just to survive, so the selection is especially favorable for larger and more complex organisms. Because of the way developmental processes work, this complexity will probably be retained even by later, smaller organisms in other niches. Voila: the evolution of complexity, by means of natural selection.

Bonner's argument might or might not work at the level of cultural evolution.

In contrast, McShea and Brandon argued in a 2010 book that random variation by itself should tend to increase complexity. McShea's summary:

  even when forces and constraints are present, a tendency for complexity to increase is always present. The rationale is simply that when selection is absent, the parts of an organism should tend spontaneously to accumulate variation, and therefore to become more different from each other ... A consequence of the [Zero-Force Evolutionary Law ] is that we do not need natural selection to explain complex tissues and organ in organisms.


Covid-19: Is it possible to get to r0 < 1 through social distancing measures?

I believe r0 is an exponent...

It is the average number of individuals who become infected by each infected individual.

If one infected individual infects exactly one other individual (r0 = 1), the progress will be straight line; the rate will be a flat line based on "mean time between infections"; total number of infections over time will be linear sloping upwards.

If r0 > 1, then it will be an exponential increase; how rapidly/steeply it curves up depends again on the mean time over which that propagation of infection occurs.

If r0 < 1, then it will be an exponential decay. New infections continue to occur, but the overall rate of infection decreases toward but never quite reaching zero.


A cladogram does not indicate time. That would be a calibrated phylogram. We can tell from the above cladogram that the two synapomorphies "Hair" and "Eggs" with shells are the two most recent, and happened after all the other ones because cladograms do indicate the relative timing of events. However, knowing a bit about mammals, "Hair" is the more recent than eggs with shells. Actually, eggs with shells should be on the same internode as "Amniotic eggs" in this cladogram, because Montreme mammals had eggs with shells, which were lost in the most recent common ancestor of Marsupials and Eutherians (Primates and Rodents/Rabbits are both Eutherians). So "eggs with shells" came first.


SHORT ANSWER

From the air

LONG ANSWER

Trees are autotrophs, which means that they create their own compounds from inorganic carbon. So, carbon comes from inorganic carbon. This carbon comes from $CO_2$ (carbon dioxide) that is present in the air. The process by which this carbon is transformed into organic matter is called photosynthesis. More specifically, the carbon get fixed through a chain of reaction called the Calvin cycle that are part of the photosynthetic process.

The great cycle of life

You'll note that while plants (and some other things) uses $CO_2$ to build their mass, animals (and some other things) exhale $CO_2$ when they breathe. In other words, respiration frees up carbon dioxide while photosynthesis fixes carbon dioxide into organic matter.

Then you may want to ask where does the carbon we exhale come from. From our food. If you eat a beef burger for example, you'll the carbon that was present in the cow. The beef got its carbon from the grass that she grazed on. The grass got its carbon from the air and there is carbon in the air because animals (and some other things) exhale carbon when we breathe. respiration and photosynthesis are two essential series of chemical reactions that explain the existence of this cycle.

The (very simplified) chemical equation for those two processes are

Introductory sources of information

Here is a video by Veritasium that answers your specific question

Here are a series of videos of Khan Academy to increase your knowledge about photosynthesis


How does the social structure of lion prides prevent incest?

It is true that African lions have recently become more prone to inbreeding, largely due to human actions (reasons include limited dispersal and at least temporarily reduced pride sizes). see here
Generally though, lions likely avoid mating with close relatives innately as most animal species do. see e.g. here
A few things about the social structures of lions (ref.):

First, many prides are not controlled by a single male. Although the males might often be related to one another.

A single male might often not be in control for long enough to mate with his grown daughters.

Females do not only mate with the leader of their pride, but mate sometimes with males from outside of the pride.


How do cats survive falling from great heights?

The reason why cats are superb jumpers has not received much attention, but one article in Nature was entirely devoted to just this (Diamond, 1988). Here follows a partly quoted and partly adapted text from this article:

First , because mass increases as the cube, but surface area as the square of linear dimensions, falling large animals are in general more injury-prone than small ones, as they suffer greater impact stress, their bones experience greater stress, and they reach higher terminal velocities in free-fall because of a less favorable area/mass ratio. While a small drop breaks an elephant's leg, a falling mouse reaches terminal velocity in the atmosphere much sooner and at a much lower value than do falling elephants.

Second, falling cats have a superb vestibular system and make gyroscopic turns
such that all four feet are soon pointing downwards, regardless of the cat's
orientation at the start of the fall. Hence cats dissipate the impact force over all four limbs. Falling human adults  tend to tumble uncontrollably but land most often
on two feet, next most often on their heads. These facts contribute to the low mortality of falling cats and to their low chance of breaking limbs after the fall.

Third, a cat falling in the atmosphere reaches a terminal  velocity  of  about  60 m.p.h. (compared with 120 m.p.h. for adult humans) after only  about  100 feet. As long as it experiences acceleration, the cat probably extends its limbs reflexively , but on reaching terminal velocity it may relax and extend the limbs more horizontally in flying-squirrel fashion, thus not only reducing the velocity of fall but also absorbing the  impact  over  a greater  area of its body. This may explain the paradoxical decrease of mortality and injury in cats that fall more than 100 feet.

Finally, cats that land with their limbs flexed dissipate much of the impact force through soft tissue. Parachutists are trained to dissipate impact forces by landing with knees and hips flexed, then rolling.

Reference
Diamond. Nature 1988; 332:586-7

Further reading
BBC news


Between 1956 and 1977, 4 human cases of rabies virus infection were
  attributed to aerosolized rabies virus;

Possible but very rare.

https://academic.oup.com/jid/article/195/8/1144/816583


Is the problem of cryonics only the pressure?

The major problem in cryonics is that when an organism is frozen, all of the organism starts freezing. The cell start expanding since ice expands too. The sharp edges of the ice crystals can destroy a lot. Also, your blood would freeze. Again, the sharp edges of the ice crystals would destroy major blood vessels. That is why currently, they have to insert antifreeze into the blood, but it still might not be effective.

Now, to answer your question, many cold-blooded organisms can survive freezing cold temperatures. Some frogs (like the wood frog), for example, have anti-freeze in their blood vessels! So some actually have special adaptations to survive freezing cold temperatures.

I hope this answered your question. Please ask in the comments if you want more information on this. I will gladly research up for you.


Where does the mass come from when you grow plants in water?

Short answer
Plants with storage compartments can grow for extended periods on water alone.

Background
It indeed seems the question is indeed different from the suspected dupe after all.

According to Turesson (2014)

  Seeds, tubers and roots are the most common sites for [...] energy storage and the forms in which energy is stored are predominantly oil, starch and sugars. Underground storage organs mainly store starch and sugars, while seeds from different plant varieties accumulate high levels of starch and also oils and proteins.

So storage compounds like "seeds, tubers and roots" can sustain prolonged growth in the absence of pretty much anything, except water; just consider the familiar seedlings of cress on cotton wool (Fig. 1). There's basically nothing there, just water.

Fig. 1. Cress grown on cotton wool and water. source:Dreamstime

Reference
 - Turesson,  Carbon Allocation in Underground Storage Organs, Doctoral Doctoral Thesis (2014), Swedish University of Agricultural Sciences
Alnarp


Consumer water is not flavorless. Sources of flavor include (1) the chemical and microbial content, which is most influenced by geology and ecology; (2) chemicals added or removed during water treatment, and (3) inputs and reactions that occur during distribution and storage (Dietrich, 2006).

Two examples of ecology-related flavors are geosmin and 2-methylisoborneol, which are respectively responsible for earthy and musty odors, produced by cyanobacteria and actinomycetes (Izaguirre et al, 1982). Humans detect these earthy and musty odors at concentrations of only a few ng/l. The ability to smell geosmin and 2-methylisoborneol is affected by other factors, such as the presence of chlorine, which masks odors (Dietrich, 2006).

The capability of organisms to detect microorganisms like cyanobacteria is not trivial, as cyanobacteria produce toxic microcystins with hepatotoxic and neurotoxic properties that can cause illness and even death (Blaha et al, 2009).

In my opinion, from an evolutionary perspective, it would be more important for survival to taste pollutants in the water than to mask these components by generating a taste to water that could potentially make the detection of toxins less effective.

References
- Blaha et al., Interdiscip Toxicol (2009); 2(2): 36–41
- Dietrich, J Water and Health (2006); 4(Suppl 1): 11-6
- Izaguirre et al., Appl Environ Microbiol (1982); 43(3): 708–14


Has a new functional structure ever been observed arising spontaneously?

It seems like you are attempting to frame this as a question about current evolutionary theory. However, current evolutionary theory doesn't expect anything as complex as an organ to arise spontaneously without any precursors. You suggest a new claw in an insect would be something "spontaneous" enough for you. This again shows that your question and the answer you are looking for are not related to evolutionary theory. The insect organs you are talking about are all modified appendages. This includes claws, mandibles, antennae, legs, fangs. These appendages all share a common genetic and developmental framework that has been slightly modified over long periods of time to give raise to the variety of insect appendages that we see today.

The idea that evolutionary theory supports the spontaneous creation of organs is a willful ignorance of evolutionary theory. The molecular mechanisms that generate novelty (e.g. genome duplication, gene duplication, de novo genes, mutation, gene regulation) for natural selection to work on are relatively well understood. Since we have an understanding of how novelty is created it is known that spontaneous organ generation has never happened or is expected to happen under evolutionary theory.

Here is link to the University of California, Berkeley's webpage designed to teach the public about evolution.


The Jaccard index is a measure of similarity between two sets. Take a look at the Wikipedia article here. It is very easy to compute:

The Jaccard similarity coefficient for sets X and Y is defined as:

J(X,Y) = |intersection(X,Y)| / |union(X,Y)|

Where | | indicates the size (number of elements) of the set. Imagine you have two sets X and Y defined as follows:

X = {A, B, C, D}
Y = {C, D, E, F, G}

Then:

intersection(X,Y) = {C, D} => |intersection(X,Y)| = 2
union(X,Y) = {A,B,C,D,E,F} => |union(X,Y)| = 5

Therefore: J(X,Y) = 2/5

Alternatively, the Jaccard distance would be D(X,Y) = 1 - J(X,Y) = 1 - 2/5 = 3/5

In Biology the Jaccard index has been used to compute the similarity between networks, by comparing the number of edges in common (e.g. Bass, Nature methods 2013)

Regarding applying it to compounds, if you have two sets with different compounds, you can find how similar the two sets are using this index. The elements on the sets, in this case the compounds, correspond to A, B, C, etc. in my example.


How does gene expression work in an adult organism? Is everything encoded everywhere?

With some exceptions (one being red blood cells), all cells in the body contain the complete genome of the individual. The expression of the genes however is, as mentioned in the comments, heavily regulated and different in various tissues. Early efforts at gene therapy have had mixed results, including some fatalities, and the field is still highly experimental.

Depending on the trait you want to change, you might have to manipulate the genes and/or gene expression in just a particular tissue, or in several. The rates of cell death and replenismhent varies between tissues, and will affect the stability of any introduced mutation. Some traits may depend on too many genes to effectively manipulate with current technology, and eye color does depend on several genes. From the Wikipedia page on Eye color:

  Eye color is an inherited trait influenced by more than one gene.
  These genes are sought using associations to small changes in the
  genes themselves and in neighboring genes. These changes are known as
  single-nucleotide polymorphisms or SNPs. (...) There is evidence that
  as many as 16 different genes could be responsible for eye color in
  humans; however, the main two genes associated with eye color
  variation are OCA2 and HERC2, and both are localized in Chromosome 15.

So depending on the original and desired color, you may or may not get away with changing a single gene. However, the pigments that determine eye color are produced in two separate tissues in the eye, making matters a bit more complicated:

  In humans, the pigmentation of the iris varies from light brown to
  black, depending on the concentration of melanin in the iris pigment
  epithelium (located on the back of the iris), the melanin content
  within the iris stroma (located at the front of the iris), and the
  cellular density of the stroma

Note that cellular density also plays a role, and this presents a much harder property to change with gene therapy, if it is at all possible.

Eye diseases have been a popular field for gene therapy research and trials lately, and there seems too have been quite some progress. However, the possiblity of using gene therapy for changing eye color has understandably not received much attention, and so there are few if any papers to consult. What can be said though, is that eye color is a complex trait, with a partially known genetic basis. It is plausible that gene therapy can be used to change pigment production and thus eye color, but even so there would likely to be many limitations. on the changes that can be made.


What does irregular heartbeat mean in simple language?

The normal cardiac cycle is comprised of two distinct phases: the systolic phase in which the heart contracts, ejecting the blood, followed by the the diastolic phase when the cardiac muscle relaxes, refilling the heart with blood.

This cycle is assured by specialised cardiomyocytes (Cardiac muscle cells) that conduct electrical impulses through the heart. When there's interference in this electric activity, the cycle becomes irregular or arrhythmic.

Arrhythmias can be divided by their place of origin:

Atrial (atria are the upper chambers of the heart)
Ventricular (ventricles are lower chambers of the heart)
Junctional (the junction between the two)
Heart blocks (caused by a blockade in the conductivity of the electrical specialised cardiomyocytes)

Some arrhythmias are physiological, such as the Respiratory sinus arrhythmia, a naturally occurring variation in heart rate that occurs during a breathing cycle. Also, in healthy individuals, some extra sistoles might occur without being the translation of a subjacent heart condition and have benign prognosis in individuals without other conditions.

However, some arrhythmias can have a wide range of health implications, from asymptomatic, to a mild intolerance to exercise, to Cerebrovascular Accident (CVA or stroke) or even sudden death due to cardiac arrest.

Therapeutic varies with the underlying cause but can be medical (with drugs such as Na+, K+ and Ca+ channel blockers, beta-blockers and Digoxin) or surgical (ie: Artificial pacemaker).


Is there a short-term, very strong anesthetic, which can be blocked/delayed by other substances?

Xenon. It is like an ideal anaesthetic. See here.

  Xenon is an interesting anesthetic as it appears to lack negative
  inotropicy and vasodilatation, giving great advantages to both
  patients with limited cardiovascular reserve or those who require
  hemodynamic stability. It has low toxicity and is not teratogenic.
  Xenon gives rapid induction and recovery, due to its low blood/gas
  partition coefficient (0.15), and has a MAC of 63%. Several vitro
  studies showed that Xenon may protect neural cells against ischaemic
  injury. Its low blood solubility can take to diffusion hypoxia if
  Xenon is not substituted by 100% oxygen at the end of anesthesia. It
  has been shown that, compared to other anesthetic regimens, Xenon
  anesthesia produces the highest regional blood flow in the brain,
  liver, kidney and intestine. In conclusion, the most important
  positive effects of Xenon are cardiovascular stability, cerebral
  protection and favourable pharmacokinetics. Negative points are high
  cost and the limited number of ventilators supplying Xenon.


Devices that bypass the hair cells in the inner ear and directly stimulate the auditory nerve are called cochlear implants. Cochlear implants are used to treat deafness caused by the loss of hair cells in the cochlea. The hair cells are the sensory cells that convert sound vibrations into electric neural signals (Purves et al., 2001). With state-of-the-art devices, the better performing implant wearers are able to talk over the phone(!) An exclamation mark is in place, because it means they can understand the spoken word without the need for lip reading or sign language. Hence, cochlear implants are the answer to your question, but they definitely are not designed to generate fake signals. Instead, they are used as an effective treatment for deafness and are capable of transmitting meaningful speech information.

Cochlear prosthetics consist of an array of typically 20-24 electrodes that are inserted in the scala tympani of the cochlea. The inner ear is tonotopically organized, which means that high frequencies are coded in the base of the cochlea, while low frequencies are encoded in the tip. Hence, each electrode stimulates a separate frequency band (Fig. 1). By using a microphone and sending the acoustic signal through a filter bank, a number of auditory frequency bands can be obtained equal to the number of electrodes in the implant. After this speech processing step, the acoustic frequency bands are converted into trains of biphasic pulses. These pulse trains are sent to the electrodes in the cochlea, which then activate the auditory nerve directly, effectively replacing the degenerated hair cells in the inner ear (Stronks, 2010).

Fig. 1. Cochlear implant. Source: Mayo Clinic.

References
- Purves et al., Neuroscience (2001) 2nd ed.
- Stronks (2010). PhD thesis, Utrecht University


Mechanism of Myosin Head Bending in Cross Bridge Cycle Power Stroke Phase

Introduction:
This is going to be quite a long answer. To have an introduction to the topic, you can have a look at articles from Wikipedia and RCSB Protein Data Bank.
The exact mechanism of physical interactions in myosin head during powerstroke cycle are not yet known. The only thing we definitely know about how release of Pi from myosin causes conformational changes (and hence, force) in it, as given at MJC website is:

This is a very basic description of the powerstroke cycle, so we'll move ahead for more detailed explanation of physical interactions during the cycle.
Details:
I have found three theories regarding physical interactions during the powerstroke cycle. Let's discuss them one by one.
THEORY 1: I could not find much explanation about physics of the cycle, the only thing I could find was at the JBC website (emphasis mine):

Mutation R759E in the myosin converter domain results in biochemical and biophysical defects as well as aberrant muscle structural and physiological properties. The central portion of the converter domain is encoded by exon 11e in indirect flight muscle (Fig., green), and the converter interfaces with the exon 9a-encoded relay domain (Fig., blue). Molecular modeling indicated that residues 508–511 in the relay loop are located near the converter residue 759 and defined weak and strong interactions of residues 509 and 511 during the rearrangements of the relay loop that are affiliated with the mechanochemical cycle. Furthermore, Ile508 can be cross-linked to Arg759 in Dictyostelium non-muscle myosin II when they are each substituted by cysteine. Therefore, we hypothesized that specific amino acids in the relay domain interact with converter residue 759 and that second site mutations in the relay residues may suppress the defects associated with converter mutation R759E.

They couldn't give much explanation of the physics involved in it. Maybe this is because I missed it or because there hasn't been much research on this because Dissecting the molecular mechanism of muscle myosin function in vivo has proved difficult. as said at JBC website.
THEORY 2: This theory, given at PNAS, provides a more detailed view of the physics, so we'll have a more thorough explanation of it:

Molecular motors produce force when they interact with their cellular tracks. For myosin motors, the primary force-generating state has MgADP tightly bound, whereas myosin is strongly bound to actin. We have generated an 8-Å cryoEM reconstruction of this state for myosin V and used molecular dynamics flexed fitting for model building. We compare this state to the subsequent state on actin (Rigor). The ADP-bound structure reveals that the actin-binding cleft is closed, even though MgADP is tightly bound. This state is accomplished by a previously unseen conformation of the $\beta$-sheet underlying the nucleotide pocket. The transition from the force-generating ADP state to Rigor requires a 9.5° rotation of the myosin lever arm, coupled to a $\beta$-sheet rearrangement. Thus, the structure reveals the detailed rearrangements underlying myosin force generation as well as the basis of strain-dependent ADP release that is essential for processive myosins, such as myosin V.

Just so that you know what it is, let me add a few points about Molecular Dynamics Flexible Fitting:

The molecular dynamics flexible fitting (MDFF) method can be used to flexibly fit atomic structures into density maps. The method consists of adding external forces proportional to the gradient of the density map into a molecular dynamics (MD) simulation of the atomic structure. For examples of MDFF applications, visit the websites on Mechanisms of Protein Synthesis by the Ribosome, Dynamics of Protein Translocation, Molecular Dynamics of Viruses, and Intrinsic Curvature Properties of Photosynthetic Proteins in Chromatophore.

Now, returning to the main point (results & discussion sections):

The equilibrium and rates of transition between the Strong-ADP and the Rigor states vary greatly among different myosin isoforms and predominantly determine how long a myosin motor can remain bound to actin in the absence of load. This kinetic tuning must be achieved by structural differences in the regions that we have seen to change in our Strong-ADP structure as well as regions involved in stabilizing the lever arm position...Our structures show that the Loop 1 conformation alters in the transition from Strong-ADP to Rigor. Thus, different sequences likely favor one conformation over the other, or promote the transition from the ADP-bound conformation to the Rigor conformation, providing a structural basis for this kinetic tuning.
For myosins, such as myosin V, that function in a cell as two-headed, processive motors, the length of processive runs and the initiation of processive runs are both enhanced by “gating” of the heads. For a two-headed molecule with both heads simultaneously attached to actin, gating refers to the fact that a lead head is essentially stalled in an ADP state strongly bound to actin, until the rear head is detached from actin by binding MgATP. This gating is attributable to the strain dependence of MgADP release. Although we do not know whether some of the subdomains of myosin may be deformed by strain, our Strong-MgADP actomyosin structure clearly reveals that strain must prevent the rearrangement of the $\beta$-sheet from the Strong-MgADP conformation to the Rigor conformation, based on the data presented in Results. Preventing this rearrangement is thus the basis of gating.

For better understanding, you should also see this video (same website) which shows animation of different conformations of myosin in different stages of the cycle:

The transitions are animated by direct morphing between the three structures Pre-Power Stroke (PPS), ADP state, and Rigor. Starting with the PPS conformation, myosin first rearranges to allow phosphate release without much change in its lever arm. Then, the first step of the powerstroke consists of a large swing of ∼58° of the lever arm toward the ADP state. The actin-binding cleft [between the U50 (blue) and L50 (white) subdomains] is closing for this transition, leading to the only state of the actomyosin cycle, which exhibits high affinity for both actin and the nucleotide. The second step of the powerstroke occurs upon ADP release and ends in the Rigor state after an additional lever arm swing of 9.5°.
THEORY 3: This theory gives even more detailed, but a bit different from the previous one, view about how the energy, released by ATP hydrolysis, is stored in myosin head. It is called Rotation-Twist-Tilt (RTT) energy storage mechanism. See this:

According to the mechanism, ATP hydrolysis in the catalytic site rotates the top of the regulatory domain, which, being connected to the coiled coils of the S-2 region, causes twist between them to increase, and leads to the twist in the myosin head. Since, at the time of hydrolysis, the myosin molecule is not bound to the actin filament, the head is free to rotate and tilt. The increase in twist is instrumental in storing the energy of ATP hydrolysis, while the rotation and tilt of the myosin head brings it sufficiently close to the actin so as to form the actomyosin complex. Untwisting of the coiled coils and the subsequent untilting and constrained reversal of rotation of the head cause the power stroke. This strain decreases the energy of interaction between actin and myosin and thus enables ATP to dissociate myosin from actin. The system is now in such a state that after the next ATP hydrolysis event, the myosin head can bind to actin, and thus, a new contractile cycle can be initiated.

The original paper of RTT mechanism (by Nath and Khurana, 2001) is available here. Since the detailed mechanism is too long, I am not posting it here. You can read the full process, just remember to have a pen and paper with you!

Conclusion:
All of the above theories provide an in-depth view of the powerstroke cycle. However, I'd still conclude that the exact physics behind the powerstroke cycle is not yet fully known, only the transitions in conformation of myosin head have been observed and interpreted to some extent.
References:

Myosin head: Wikipedia
Myosin: RCSB Protein Data Bank
Journal of Biological Chemistry: Mapping Interactions between Myosin Relay and Converter Domains That Power Muscle Function
Proceedings of the National Academy of Sciences of the United States of America: Force-producing ADP state of myosin bound to actin
Theoretical and Computational Biophysics Group: Molecular Dynamics Flexible Fitting
Cell Movements: From Molecules to Motility
Molecular mechanisms of energy transduction in cells: Biotechnology in India II
Molecular mechanism of the contractile cycle of muscle; Sunil Nath and Divya Khurana, March 2001


Why digest proteins into peptides for Liquid Chromatography - Mass Spectrometry?

This is going to be a very long answer but to give a short response.

You have to consider that MS for peptide detection works on the bases/principle of mass to charge (m/z) to detect an AA molecule, which is then normalised and analysed etc etc (http://en.wikipedia.org/wiki/Mass_spectrometry). Once you have the amino acids, then you just look at the order in which they get through and then you have your peptide sequence. Please read about the B, A and Y-type ions although this page is slightly technical (http://www.matrixscience.com/help/fragmentation_help.html). If the proteins was not digested then it would be far too big to be analysed since it would be read as one massive blob of m/z, which could be anything! So once you have your spectra from a peptide, you need to compare it to a model spectra, and based on that you predict what the sequence is as fragmentations peaks can be anything. Look at SEQUEST (http://en.wikipedia.org/wiki/List_of_mass_spectrometry_software). Now there are tons of correction algorithms that are applied, which you can look up.

Now RP-LC is carried out before MS to prevent all the sample rushing into the MS machine all at once as the machine can not cope if too much sample is inserted hence the flow rate is controlled. What I think you are thinking in terms of the set machine limit, is the (digested) peptide fragment that enters the machine, before undergoing electrospray. Now the experts that run the MS machines do set a peptide mass upper and lower limit, for what size/mass of fragment to accept and what size/mass to ignore. Look at this theoretical digest example (http://prospector.ucsf.edu/prospector/cgi-bin/msform.cgi?form=msdigest). This happens frequently with trypsin digest as it recognises specific AA before cleavage (http://en.wikipedia.org/wiki/Trypsin). Now a days, MS has advanced so much that we have machines such as Orbitrap (http://en.wikipedia.org/wiki/Orbitrap), which can cope with peptides, digested with elastase, which cleaves non specifically, which means you are less likely to get peptides that are far too big for analysis, hence increasing the protein coverage.

Hope this helps!


Can our body adapt to periodic fluctuations in sleep?

In the same way that it takes time to fully adjust to jet lag (~ 1 timezone/day), it is unlikely that the body can adjust to alternating patterns of 3hr gaps on wake time on a daily basis [Ref. 1].  We simply have not evolved to jump timezones.  The most healthy thing to do is to have one time to get up each day (5am) so that your body is in sync.

[Ref. 1]: Review about circadian rhythms