If $W$ is a parameter, I'd expect (in the simplest case) that $W$ itself is a constant (i.e. it doesn't have a distribution). (By the way, I would normally use $T_{1/2}$ to denote the doubling time, $\ln 2/\ln W$, and would use $\lambda = \ln W$ for the exponential rate, i.e. $W^t= \exp(\ln W)^t = \exp(t \ln W) = \exp(\lambda t)$. I don't normally see people express rates scaled by $\ln 2$.)

In the case of a continuous-time birth-death process (the technical jargon for your model), I believe the analytical answer will be that the standard deviation of the population size at time $t$ will grow at the same exponential rate as the mean population size, and that the variance will grow twice as fast (because it has units of $\textrm{population size}^2$), i.e. $\propto \exp(2 \lambda t)$)

I don't have a derivation/reference handy, will dig around for one. This is fairly basic stochastic-process math, but stochastic-process math also gets pretty hairy-looking (to a biologist) quickly. Bartlett 1960 (Stochastic population models in ecology and epidemiology) is one place to look for basic results, although I'm sure there are many others. This recent PhD thesis gives a thorough introduction to the math of birth-death processes ... although, not to my disappointment, a canned derivation of the variance result I'm too lazy to derive for you.


Do pharmacodynamics and pharmacokinetics of the drug in animals are the same as in human?

Drug metabolism in humans is different than animal models.

Here is one example: http://www.ncbi.nlm.nih.gov/pubmed/17125407

The link is a review where they compare different animal models to humans with a focus on CYP enzymes commonly involved in drug metabolism.  While they describe similarities, they note:

  CYP2C, -2D and -3A show appreciable interspecies differences in terms of catalytic activity and some caution should be applied when extrapolating metabolism data from animal models to humans

Essentially your instincts that different species have different pharmacology is accurate and based on the many genetically-based differences in the drug processing machinery.

Similarly, there are differences in drug metabolism between humans with different genetic backgrounds, which is the basis for pharmacogenetics (https://en.wikipedia.org/wiki/Pharmacogenetics).

More recently, differences in gut microbes have also been raised as contributory factors (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3529681/).  In this case, identical twins with different diets could conceivably have different pharmacokinetics.

  Tying this all back, the reason human drug trials are needed is because animal and tissue culture models are necessary, but insufficient to predict drug efficacy or safety.


Are there neuronal firing artifacts produced by head movement?

There are certainly head-orientation cells (e.g. in the hippocampus).  But neurons are reasonably immune to the kind of mild physical stresses that come from turning the head around; computing head orientation requires complex analysis of input from e.g. the visual system (optic flow) and vestibular system.

However, the electrical activity of muscles tends to swamp that of (nearby) neurons, so various muscle-related artifacts are often visible in an EEG if not carefully filtered out.  And, of course, if the contact is poor you'll get artifacts from that: you're just measuring the variability in resistance between the sensor and your skin, not anything interesting about what faint potential changes are visible at your skin as a result of neuronal activity.


How do mushrooms react to being grown in a microgravity environment?

There were some experiments done in microgravity in longer space shuttle missions. The reports show that the fungi develop relatively normal but grow in random orientations instead of orientating upwards. See this images:

The upper image shows fungi grown on earth which are subjected to normal gravity. The lower image shows fungi (actually only the fruiting bodies) which are grown during 7 day on the Spacelab D2 mission. The fungi obviously have a way of detecting gravity to let their fruiting body grow upwards. The image is from here, the article contains more information about this.
There is also a publication in this topic:

Mushrooms in microgravity - Mycology at the final frontier


Is a wild-type strain more "fit" than its mutant strains?

I will assume the mutation is not under some kind of balancing selection such as negative frequency dependent selection. As fitness is conditional upon the environment, I will assume a constant environment (heterogeneous environment can also lead to balancing selection).

  Is WT expected to be the ONLY strain to persist in the long run?

Yes. In fact, even if the mutation was beneficial, as it starts out at low frequency it still has a low probability to actually fix (fixation = reaching a frequency of one).

  How common is this scenario?

Mutations happen constantly. For example, every new human baby carry something like 10-100 new mutations that were not present in any parent. Most mutations are neutral or deleterious, only very few are beneficial. New mutations have a low probability to reach fixation even if the mutation is beneficial. The exact probability depends upon the selection coefficient $s$, the dominance coefficient $h$ and the effective population size $N_e$.

  What about co-existence?

In absence of balancing selection (or frequent recurrent mutations) and assuming that ressources are limited, then one strain will necessarily end up fixing. Note that this is also true under genetic drift only and does not even require any selection.

  Examples and references for beginners will be very appreciated.

Evo101 is a very short, very easy introduction to evolutionary biology. You should probably have a look at it.

Then, for something a bit more advanced, and because your background in mathematical modelling, I recommend having a look at the book Population Genetics: A Concise Guide by Gillespie

For more book recommendations, please have a look at the posts

Books on population or evolutionary genetics?
Text Book Recommendation: Organic Evolution


What is the "leaky valve" between the esophagus and stomach?

The structure is called the lower esophageal sphincter:

Basically, its function is to prevent the contents of the stomach, including stomach acid, from "backwashing" into the esophagus. The stomach is protected from acid by a protective layer of mucus, while the esophagus is not, so any number of medical issues which cause problems with this sphincter may lead to erosion in the esophagus, which is quite painful and can lead to serious long-term consequences if not addressed.


Can viruses survive Super saturated salt solution?

This issue was studied in Virus inactivation by salt (NaCl) and phosphate supplemented salt in a 3D collagen matrix model for natural sausage casings International Journal of Food Microbiology Volume 148, Pages 128–134.

Saturated NaCl was tested on 4 types of virus, foot-and-mouth-disease virus (FMDV), classical swine fever virus (CSFV), swine vesicular disease virus (SVDV) and African swine fever virus (ASFV) at four different temperatures:4, 12, 20 and 25 °C for a period of 30 days.

For ASFV, but not the other 3 viruses, saturated NaCl had a significant effect of inactivating the virus, on a days timescale.


How does drug-induced photosensitivity work?

Drug induced photosensitivity (DIP) refers to the development of a cutaneous disease in response to the drug chemical in combination with light. Only the drug or light alone cannot cause the reaction and both are required to be present together. The underlying pathophysiology is important clinically to identify the type of cutaneous manifestation the drug-light combo has caused. There are majorly two types of reactions, phototoxic and photoallergic reactions.

Also, the kind of light required depends on the kind of drug and the the wavelength at which it gets photoexcited. Although UV-B is a mojor cause of sunburn, the wavelength required for DIP for most drugs falls in the UV-A part of the spectrum.

Phototoxic reaction

Phototoxic damage refers to the direct damage the photoactivated drug can cause to the tissue. Light leads to excitation of electrons and as they return, they can lead to formation of reactive oxygen species which damage the cell membranes and DNA. This tissue damage leads to activation of proinflammatory cell signal transduction pathways and leads to inflammation in the area. Clinically, it looks like an exaggerated sun burn.

Photoallergic reaction

This is similar to the same old hapten story. A drug which is otherwise non-antigenic turns antigenic after a photoreaction. Most probably, the reaction should have caused the modified drug to bind to cutaneous proteins leading to cell mediated immune reaction. This T-cell mediated inflammatory response usually has an eczematous morphology if the photoallergen is applied topically or the characteristics of a drug eruption if the photoallergen is administered systemically

It is important to differentiate the kind of reaction, a drug would cause.For example, the tetracyclines that you mention are phototoxic but not photoallergic. Photoallergic reactions have far lesser incidence than phototoxic ones.

Coming to the other part of your question, on the treatment, most important is to educate your patient for appropriate photoprotection. If severe, the drug could be withdrawn and switched to a safer one. Treatment includes topical corticosteroids to bring down the inflammation in either reactions. Oral antihistaminics are reported to have limited advantage. Why this is so,I'm afraid, I do not know. Hence your question remains partly answered.

Reference: http://emedicine.medscape.com/article/1049648-treatment


How does vasoconstriction increase the pressure of blood?

Because pressure is inversely proportional to area. If you consider a pipe, if you squeeze it's tip to decrease it's area you'll observe that the velocity of water flow becomes high due to high pressure. Same is with blood in veins.


Immunological factors for the cause of headaches following SAR-CoV-2/COVID vaccination

Headache is one of the various side-effects of vaccination. Typically, a person will have pain in the site of injection, muscles throughout your body and head.
The immunological reason is the network of our immune system. Whenever a foreign antigen (vaccine) is detected by our immune system, antigen-presenting-cells (macrophages, dendritic cells) takes the antigen to nearest lymph nodes where it is presented to the adaptive immune system. Due to this invasion, strong immune response starts which leads to the pain.

Image Source: wikipedia.org/wiki/Lymphatic_system


Understanding F-statistics in population genetics

I am a bit wobbly on the subject, but I think the most important bit of information is that they are re-parametrising Wright's (1951) hierarchical analysis of variation, "F-statistics," "hierarchical partitioning of variation," or "population parameters," depending on whom you ask. The parameters correspond as follows (on the bottom of p.1358): Fit=F, Fis=f, Fst=θ.

The relationship arises given some assumptions. Crucially here, if Fis (or f) is a measure of departure from Hardy-Weinberg Principle, and all populations identically depart from HWP, then Fit = 1 - Hi/Ht. It follows that, 1 - Fit = Hi/Ht. As well, we can rewrite this, so that, Hi/Ht = (Hi/Hs)(Hs/Ht).

Together, you can (maybe) see that, 1-Fit = (1−Fis)(1−Fst). Substituting, 1-F = (1-f)(1-θ).

(I realise that this is not a complete answer, but you can rearrange it with some algebra to get the Weir&Cockerham equation, I think).

[Update Oct 25, 2016]: it eventually yields f = (F-θ)/(1-θ). I think the posted question (above) contains a typo--specifically a missing division operator. Perhaps someone missed the stroke on a typewriter in the original paper?


Coincidence that navel is near the womb?

I would say it is a coincidence because:

the navel is in the same place in males, so if it was there for some evolutionary advantage the charachter would be sexually dymorphic, which clearly is not the case.
I cannot think of any specific function of the navel that is related to pregnancy or delivery (or of a specific function of the navel at all for that matters)


Why does a housecat (or other predator) play with it's food before killing and eating it? Does it make the food taste better?

Animal Planet is quoting researcher Dennis C. Turner who claims this is an instinct which is supposed to tire the prey:

  Cats, rather, wear down prey to avoid sustaining injuries. They're motivated by self-preservation, just like most other animals, and they know what could happen if they aren't careful. Mice and rats, for example, can deliver nasty bites that can cause injury or spread disease. Birds, for their part, are able to scratch and peck. So, what's a cat to do? Rather than playing with their prey for amusement, cats tire out their victims to the point where they're too worn down to fight back. And after that, the cats will feel better, and safer, about finishing them off, according to researcher Dennis C. Turner. So while it might look like a display of cruelty, a cat playing with its prey is just an (admittedly harsh) example of animal instinct in action [1].

Karen B. London (animal behaviorist) agrees:

  Actually, the way that cats let go of and then recapture their prey is not a way for them to have fun, but rather a way for the cats to protect themselves from serious injury. Cats kill their prey by breaking the spinal cord with a strong bite to the neck. If a cat must let go of the animal in order to grab it on the neck, that cat is risking escape or retaliation by their prey [2].

Playing (not only with prey) also gives cats experience and improves their ability to make judgments [3].

References:

Animal Planet. Why do cats play with their prey? Available from http://curiosity.discovery.com/question/why-cats-play-with-prey (accessed 27.07.2014)
Karen B. London, Ph.D.. London Zoo: Why do cats play with their food? Available from http://azdailysun.com/lifestyles/pets/london-zoo-why-do-cats-play-with-their-food/article_46a97775-232d-5e56-b0ea-dd1c8782b062.html (acessed 27.07.2014)
Perfect Paws. Predatory Behavior of Cats. Available from http://www.perfectpaws.com/help3.html#.U9TLpON_tJk (accessed 27.07.2014)


Cholesterol and fatty acids role in bile?

The main function of bile is to emulsify large fat molecules into small fat droplets. You must have heard about micelle formation by soaps. Well, bile acids perform quite similar function. Bile acids, having both hydrophobic and hydrophilic parts, form micelles and trap fat molecules and form emulsion, hence naming the process emulsification. Similar function might be performed by fatty acids. See this article:

  Bile acts to some extent as a surfactant, helping to emulsify the lipids in food. Bile salt anions are hydrophilic on one side and hydrophobic on the other side; consequently, they tend to aggregate around droplets of lipids (triglycerides and phospholipids) to form micelles, with the hydrophobic sides towards the fat and hydrophilic sides facing outwards. The hydrophilic sides are negatively charged, and this charge prevents fat droplets coated with bile from re-aggregating into larger fat particles.

Now lets have a look on bile acids. The principal bile acids are cholic acid, chenodeoxycholic acid, glycocholic acid, taurocholic acid, deoxycholic acid and lithocholic acid, all of which are synthesized from cholesterol (see this). Now this partly explains why a small amount of cholesterol is released along with its derivatives; it might be the 'unprocessed' cholesterol which 'leaked out' from liver. But, in fact, it seems to do a bit more. Actually, cholesterol secretion into bile needs to be carefully controlled; too less secretion may lead to accumulation of cholesterol in blood vessels, leading to cardiovascular diseases (this is why cholesterol secretion is the final stage of elimination of cholesterol from reverse cholesterol transport), while too much secretion into bile may cause gallstones (see this). Hence, cholesterol secretion into bile also serves as a way to maintain cholesterol homeostasis (see this). In fact, bile acids serve as hormones in cholesterol homeostasis in the body. Similar reason may cause fatty acid elimination through bile.

Cholesterol and fats are hydrophobic, so they cannot be released as it is into GI tract. This is why they are released with bile. Bile acids are amphiphatic i.e. have both hydrophilic and hydrophobic parts. Hydrophilic part helps it in dissolving in chyme (containing HCl) while hyrdrophobic part helps it in dissolving fats and cholesterol (and lipids of course) into itself.

source


Well, to rationalize everyone's comments, I think @leonardo is right.

This is a denaturing SDA PAGE gel.  The migration of the SDS Micelles which are negatively charged, depends upon the shielding of the solution around it.  The difference in mobility is because the SDS micelles will experience a slightly different field at pH ~6.2 (MES) vs 7.2 (MOPS).

The thought that these have the same charge would be right at exactly the pH corresponding to the pKa.  For these two ions the proportions will not be the same when running 0.8 pH units from their respective pKas. the ion concentration goes as +/- log ([BH]/[B-]) and the charge environment of the buffer should not be the same.  I think that the higher pH for MOPS running will tend to create more negative charge in the solution from MOPS- but also OH- in solution, slowing the mobility of the micelles and favoring the resolution of the larger proteins with MOPS.

This is all given even if the buffering ion concentration is the same.

I'm sure the gory details are buried in the musty tomes of some physical biochemistry journals deep in the library, but this is how it sounds to me.


Which Enzymes Catalyse the Deacetylation of Drugs in the Human Body?

Acetyl esters can be deacetylated by carboxylesterases.

In case of an acyl/aryl group attached to acetate group (e.g., benzoate), I guess it will first undergo ring opening and then beta oxidation (as in case of tyrosine).

Paracetamol -> p-aminophenol is a deamidation (I am not sure, but enzymes like ornithine decarboxylase can do that job... just a guess).


What is the difference between influenza A and B viruses that causes their distinct seasonal patterns?

Regrettably, I don't believe we know - we don't actually know why influenza is a seasonal disease in the first place. There are a number of possible theories, discussed in this review, but none of them are compelling enough to be a definitive causal explanation

In terms of the difference between Influenza A and B, B mutates at a much lower rate, which may explain the slower rate of dramatic antigenic shifts, but that isn't enough to disrupt the seasonal cycle by a few months at most.


Does your iris color have an effect on your vision?

Firstly, note that "eye color" is actually iris color.

The person with a lighter iris will have more straylight compared to person with brown iris:

The graph represents Intraocular straylight of the age-matched groups. Participants with light-blue-colored iris showed significantly higher values for intraocular straylight than those of the other groups.

  Persons with light-blue-colored eyes have significant higher IOSL
  (intraocular straylight)
  values than persons with darker-colored irises (blue-grey,
  green-hazel, and brown). Light-blue-colored eyes had 0.07 to 0.08 log
  units higher IOSL values, which is an increase by a factor of 1.2. In
  regard to CS (contrast sensitivity), subjects with light-blue iris color showed also lower CS
  values than subjects with other iris color.

Edit: The study concluded that in people with blue irises, IOSL was significantly higher. Although IOSL did not affect best-corrected visual acuity (e.g. visual function based on a standard letter chart test at the optometrist), it did affect contrast acuity, meaning that folks with blue eyes had more difficulty assessing contrast differences (e.g., telling apart two grays with a slightly different brightness).

Christian Nischler & al. Iris color and visual functions. Graefes Arch Clin Exp Ophthalmol (2013) 251:195–202.


Is there a purpose for nucleated red blood cells in reptile, avian and fish blood?

It's difficult for vertebrates to aquire/evolve enucleated cells, that's why they are very rare previous to the mammalian adaptation. Salamanders have evolved enucleated cells. Research suggests that it may be due to a salamanders big genome and big cell nucleus, compared to the salamanders small body size.

Mammals may have acquired the trait because they evolved from small animals with miniaturized capillaries and blood cells and large genomes, and the advantage was kept afterwards. Large genomes inhibit flow and flex of nucleated blood cells.

The smallest bird genomes are found in the most miniturized clades of birds at 1 Gb. Mammals of a similar size can have carry 2-3 Gb of chromosomes.

Lizards have lower energy than mammals.

Fish are most active in highly oxygenated water, i.e. salmon, which allows them to be very energetic, water is a more efficient breathing medium than air, hence the small size of gills. fish and humans both contain 6-7 percent blood by volume.

Birds have smaller haemoglobin including the nucleus, and have a different kind of capillary size and structure with advantages and disadvantages, and lighter hollow bones with less marrow. Birds didn't radiate to new shapes as well as mammals did.

Enucleate cells are fairly rare in the plant and animal world, so they perhaps have a hidden expense. Maybe it's not just a factor of shedding the nucleus, and in fact there is a cost of adapting the primary circulation system's immunity against paramecia and pathogens without a nucleus. various viruses can take advantage of enucleate cells.

Perhaps that is the reason why birds did not evolve backwards into dinosaurs. some factor made their genome comparatively small. It could be the lack of enucleated bloodcells that forced them to shed genes as an alternative. Perhaps that's why they lost the dinosaur genes which held code for quadrupeds, arms, jaws, horns and teeth and the things that birds don't have.


You have some misconceptions about visual acuity. You need to understand how lenses work to understand why objects up close are blurry in myopia.

Sure, if one elongates the orbit, blurring will occur, but that's not usually the cause unless it's in childhood. As we age, the elasticity of the lens has more to do with it.

Light comes in through the pupil. The amount of light is what determines brightness; too little, and we can't see, too much and we look away. In between we "see". Being able to focus doesn't have any effect on brightness; the size of the aperture does, however (the aperture in this case being the pupil.)

Blurriness is caused by where the light rays striking the object we're looking at come into sharp focus in out eye. Sharpness falls within a very small range, then once the range is exceeded, the image becomes progressively blurrier because the rays scatter again. This is why looking through a pinhole improves our vision: less scatter. If your pupil could constrict down to a pinhole, that would be pretty amazing, but it can't.

The purpose of the lens is to focus the image. It can do so (with the help of ciliary muscles) by changing shape. But it can only change shape within a range. If it cannot change shape enough to focus the image where it needs to be - on the retina itself - you have blurry vision.

That's why additional lenses (or changing the contour of the cornea) help.


Do any predatorial animals attempt to appear smaller?

In order to answer your question, two things must be demonstrated: First, we must demonstrate that the prey animal has perceived the predator. Second, we must demonstrate that the prey animal believes that it has perceived a small animal (which poses no threat).

There are several ways that a predator might achieve these outcomes. The first way is to present a small part of its' body as an independent animal, and the rest of its body as something innocuous, like a rock. There are many examples of this type of deception: you've already identified anglerfish lures. My personal favourites are frogfishes. Several other examples are discussed in the Wiki on Aggressive Mimicry.

Another way is to present the whole body in a way that makes it appear small, for instance by presenting a silhouette with a small apparent area to the prey. This has long been thought to be part of the foraging strategy of some ambush predators which have bodies with a small cross-section, such as pike and dories.

In addition to visual deceptions, some predators may use other signals to be perceived as animals that are smaller than themselves. Atkinson (1997) suggests that predatory Northern Shrikes impersonate the songs of smaller Passerine birds in order to lure them into striking range. This behaviour would also qualify as a predator attempting to be perceived as something smaller than it really is in order to gain prey.


The temporal lobe is in the temporal region of the head, near the temples of the skull, hence the name. It's name does not relate to it's biological function, it is mainly involved in processing language, visual memories, and emotions. The medulla oblongata is one region of the brain that deals with a lot of the "tempo" type functions (tempo as in keeping rhythm) such as controlling the heart beat and breathing rate.

  Temple indicates the side of the head behind the eyes.


How can GMO contaminate biologic plants?

First let me say this: I am no gardener. Every plant that enters my home or yard dies a slow death of neglect. I do have some experience trying to remove weeds from other non-weeds, and there is a practical aspect of "uproot every GMO plant" that I think may be impossible, but this is speculation. Let's get into a literature review.

A frequently cited paper is Dröge, M., Pühler, A. & Selbitschka, W. Horizontal gene transfer as a biosafety issue: A natural phenomenon of public concern. Journal of Biotechnology 64, 75–90 (1998). Table 3 contains the most relevant information about horizontal gene transfer between plants.

In situation number 1, consider that the rhizosphere (the area of soil around the root of a plant) is constantly populated with bacteria. These bacteria are shown to sometimes transfer genetic material to and from the plant, through the roots. Unless you somehow sterilize the soil after uprooting your previous crop, consider everything you plant in that field possibly contaminated.

Situation 2 is less clear, but Monsanto does sue farmers found to be using their seeds without a contract, and many farmers say this is because of cross-pollination. I think you should assume that your field will soon be contaminated.


In flowering plants food is transported in which form?

This is a homework question but I will answer it (forgive me moderators ;).

You will get your answer from this answer:

  Sucrose and starch are more efficient in energy storage when compared to glucose and fructose, but starch is insoluble in water. So it can't be transported via phloem and the next choice is sucrose, being water soluble and energy efficient sucrose is chosen to be the carrier of energy from leaves to different part of the tree. Another problem exists, glucose is highly reactive and this may result in some intermediate reactions while transporting glucose. Being a complex structure, sucrose is not as much reactive as glucose. So plants uses the sucrose as a medium to transfer energy. Inside the cells, sucrose is converted back to glucose and fructose.

Once again:

Glucose- too reactive: CANCEL
Fructose- too reactive, again: CANCEL
Starch- insoluble in water: CANCEL
Sucrose- no problem: ACCEPT


How is it possible to breathe perflurocarbon?

In liquid breathing systems the perfluorocarbons are simply an inert carrier for dissolved oxygen. It turns out that oxygen and other atmospheric gasses readily dissolve in perfluorocarbons without chemically reacting with them. Some perfluorocarbons can carry over 300 times as much oxygen as the equivalent amount of water. Perfluorocarbons are incredibly stable under conditions compatible with life, they aren't being broken down into free fluorine in you lungs or blood, or reacting with your tissues much at all. The perfluorocarbons don't cross the lung-blood interface in significant amounts.


Preamble

From the point of view of understanding I think it is better to talk about the constant and variable regions of antibodies, rather than Fab and Fc, as these are historical designations for fragments of the molecules that were useful in research, but do not exist as separate entities.

Cartoon representation

It is possible to represent the immunoglobulin molecule diagrammatically as shown below. In the left-hand diagram V = variable and C = constant, and the suffixes H and L refer to the heavy and light chains. The right-hand diagram, which purports to be more three-dimensional, shows how the variable regions are responsible for binding the antigen — different manifestations of the variable region have different antigen-specificity.

The different iotypes for an immunoglobulin with a particular antigen-specificity are shown next, with a pre-colour scheme that focuses on the difference between the constant regions of each isotype.

Functions of the constant region of different isotypes

The variable region of an immunoglobulin does the exciting stuff — it binds an antigen, but that is not sufficient for its action. As well as the specific discriminatory action of the variable region, there are roles in presentation and disposal that are the same for all antibodies of a class, but may differ between classes. That is what the constant regions do.

I am not an immunologist (although had to teach the biochemistry at one time in my life — hence the diagrams) so the examples I present are simplistic and incomplete. However here are a few:

IgM is made early in the immune response and hence is not very abundant. In order to enhance its response it forms pentamers in which the constant region of the heavy chain interacts with an additional J chain.
IgA is involved in immune protection in mucous regions of the body exposed to the exterior. It is directed there by interaction with a receptor on the appropriate epithelial cells, which binds the constant regions of an IgA dimer attached to a J chain.
IgE stimulates mast cells to produce histamine. These mast cells have receptors for the constant region of the heavy chains of IgE.

There are many sources on line dealing with this topic, including a section in Berg et al. that has a similar structural approach to that presented here.


Which types of hydrogen bonds are known to exist in RNA secondary structures?

By far the most common type of base pair is the Watson-Crick base pair in an RNA helix. Those are comparably easy to predict, e.g. Mfold and the Vienna RNA package can do this.

Base triples, three nucleobases that form hydrogen bonds to each other are not uncommon in RNAs with a complex tertiary structure. There is even a database of RNA triples, though this one also contains triples where not all three bases make contact with each other.

There are also quadruplexes, but there each base only makes contact with two other bases. I don't know if there are any structures where one base makes contact with more than two other ones.


You're right, A and B both are normal thermoregulatory responses, so those can't be the right answer.

I'm guessing the rationale for C is that, if the dog's body temperature is increasing to match that of the hot environment, it must mean the dog has an impaired thermoregulatory response. It's kind of tautological.

But D also seems correct to me. If a dog is in a hot environment, and its blood vessels near the skin are constricting (say, because it's sick), that's counterproductive to the normal thermoregulatory response. If the dog isn't dilating its blood vessels near the skin, that's an impairment to the normal thermoregulatory response.

Perhaps the question is written wrong? Maybe D was supposed to say "vasodilation" instead of "vasoconstriction"? If this is a question written by a teacher I'd say you have a case for arguing it.


Turning publicly available genome data into proteins

No, your approach will not work, you are taking a very simplistic view of an extremely complex system. Some of the problems you are ignoring are:

Genes (eukaryotic genes anyway) are spliced to produce mRNA, a process that removes introns and leaves only the exons. If you just translate the entire chromosome file you will get noise.
Splicing also changes the frame a gene is read in, you don't mention frames at all in your question but you can't work with sequences unless you deal with them.
Many genes (most even, in some species) are alternatively spliced. One gene can give rise to multiple protein sequences. Which one is produced at any one time can depend on a multitude of factors ranging from pure chance, through environmental conditions to the cell type where the gene is expressed.
Genes can be present on both strands of DNA and a gene on the + strand can overlap with a gene on the - strand. In some cases they can even overlap on the same strand (nested genes). You need to check both strands for coding sequences.
You're assuming that all coding sequences start with ATG (most do, not all) and you seem to be assuming that an ATG always starts a coding sequence. A given gene can have dozens or hundreds of ATG codons, how can you know which one is used as a START codon?

The process of identifying the parts of the genome that get translated into protein is not trivial. It is the subject of countless PhD theses, mine for example. There are many programs (gene predictors) that are designed specifically to detect genes in genomic sequences. Having spent many years working with them I can assure you that they're not something you can just whip up one afternoon. They tend to involve very complex models of coding vs. non-coding sequences and are way more sophisticated than simply looking for START and STOP codons. Trying to write one without knowing a lot more about biology than you seem to is just a waste of time.

Your specific questions are basically irrelevant because of the points mentioned above. Nevertheless, the answers are:

They vary but not much. For well annotated genomes like the human one, the differences will be negligible. That is not why you have strange results though as I explained above.
All public FTP sites tend to have a README file that explains what the files provided are. You should read the relevant README from ftp://ftp-trace.ncbi.nih.gov/1000genomes/ftp/
Answering that question will get you a Nobel prize. There simply is no way of predicting what genes will be activated in a particular cell. We're not even close to that level of understanding of how a cell works but I can tell you that it will not depend on the sequence, you will never be able to predict whether a gene is active in a particular cell based on its DNA sequence. It will depend on various things including the gene's methylation state and is largely an emergent quality of the cell's complexity (think of various proteins interacting with one another, leading to the activation of a gene).  The best you can do is get a list of genes that are known to be active from the literature.

In summary, if you want to do something as complex as modelling a cell I suggest you first take the time and study some basic biology so you can understand the system you are trying to model a bit better. The cell is not only an extremely complex system that we don't fully understand yet, it is also not wholly deterministic and contains a lot of stochasticity that you seem to be ignoring completely.


Why are nausea and dizziness such common side effects from medication?

Some medications because they are taken orally do cause nausea. Many medications, because they have an effect on blood pressure, or are central acting in some way, do cause dizziness. However, nausea and dizziness in particular are two highly subjective symptoms which are difficult to quantitate or verify, and which can occur with simple anxiety or stress. Several more such highly subjective and difficult-to-verify symptoms are numbness, tingling, headache, insomnia, fatigue and difficulty concentrating, all of which can be brought on by stress.

Switching for a moment to a drug with a measurable side effect of beta-blockers: erectile dysfunction (ED). In a study of men treated with beta blockers, the patients were separated into three groups with the following results:
a) the group who were not told the name of the medicine nor informed of the ED side effect had the lowest incidence of ED (3.1%)
b) the group who were told the name of the medicine but not informed about the ED side effect had a 15.6% incidence of ED
c) the group who were told the name of the medicine and informed of the ED side effect had the highest incidence of ED (31.2%)

Hypervigilance is an increase in attention to bodily cues or symptoms for any reason. It has been well documented in many studies that if you give one group of people a list of possible negative side effects, and another group a list of possible beneficial effects, then give both groups placebos (usually a small coated sugar or cornstarch tablet), the first group will experience negative effects while the second will feel better. The negative expectation producing a negative side effect is called the nocebo effect (the opposite of the placebo effect).

Interestingly, recent studies where anti-anxiety medications were administered before the nocebo dramatically decreased the nocebo effect.

For ethical reasons, in all clinical trials of drugs, patients in the treatment group and the placebo group must be given an extensive list (standardized) of possible negative side effects, introducing a negative expectation into both populations.

Two of the most common negative side effects in both groups are dizziness and nausea. Therefore, they must be reported as possibly occurring side effects with the medication.

This is not to say we're all imagining things. Nocebo effects have been correllated with reproducible effects on functional MRIs. They have a basis in reality, even if it's caused by negative expectations.

It's a problem being discussed a lot now by medical ethicists.

The influence of the nocebo effect in clinical trials
Avoiding Nocebo Effects to Optimize Treatment Outcome


Do all species have asymmetric female meiosis?

Plant meiosis gives rise to four megaspores but usually upto three of them die by apoptosis leaving only one megaspore. But they are symmetric and three of them need not die all the time as it seems [REF].

Plasmodium being a haploid organism undergoes meiosis after fusion of gametocytes. Sexual differentiation is initiated at some point during the merozoite stage (See here and also the cross references).

Chlamydomonas is also haploid during its vegetative phase, and produces four flagellated haploid gametocytes. Sexual differentiation is apparently stochastic.

Perhaps there are more examples of organisms that do not undergo asymmetric division as seen in metazoa. There may be some stochastic asymmetry which leads to differentiation of sexes in the haploid unicellular eukaryotes and apoptosis in plant megaspores; these stochastic events may happen later as well. For plasmodium this is not really known; others I am not sure of.


How is the timing of gene expression controlled in developing embryo?

How can gene expression timing affect the formation of a developing embryo?

We should know that genetic imprinting is passed down. The formation of an embryo is not. Some takes on form when provoked, it is much like when oocytes are stimulated with a prod duplication
Happens automatically. The embryo is affected by the proximity of cells. Clusters, spread out, far apart. All make the cells behave automatically. But it's the first ignition of development that sets off growth. The cells have been through many phases and timing is not controlled by either proteins or genes.


How do mosquitoes maintain telomere length?

It seems that the current model is that recombination is the mechanism by which telomere length is maintained in the malaria vector Anopheles gambiae. Here is an exerpt of Roth et al paper that proposed the recombination mechanism:

  The insertion of a transgenic pUChsneo plasmid at the left end of chromosome 2 provided a unique marker for measuring the dynamics of the 2L telomere over a period of about 3 years. The terminal length was relatively uniform in the 1993 population with the chromosomes ending within the white gene sequence of the inserted transgene. Cloned terminal chromosome fragments did not end in short repeat sequences that could have been synthesized by telomerase. By late 1995, the chromosome ends had become heterogeneous: some had further shortened while other chromosomes had been elongated by regenerating part of the integrated pUChsneo plasmid. A model is presented for extension of the 2L chromosome by recombination between homologous 2L chromosome ends by using the partial plasmid duplication generated during its original integration.

You might also be interested in this paper: Genes required to maintain telomeres in the absence of telomerase in Saccharomyces cerevisiae and then look at whether there are mosquito homologs of the identified yeast genes that might be involved in telomere maintance.


Can there be only one allele at a given locus?

An allele is a variant of a gene. If there is only one allele at a given gene, it means that there is no genetic variance at this specific locus (a locus is a position in the genome. It can typically correspond to a gene). It is not rare at all that the whole population is fixed for the same allele at a given locus.

Number of alleles

In courses, it is common to consider only the case of 2 alleles. In reality, there might be any number of strictly positive allele. At a given locus, you might have 1, 2, 3 or 11 alleles for examples. The reason why we typically teach about the 2 allele case is that 1 allele is not of much interest as there is not genetic variance at this specific locus and 3 or more alleles makes everything a little more complicated.

Dominance relationship

In courses, it is also common to consider diploid individuals, 2 alleles and the phenotypes of the three possible genotypes assuming $h_N = 1$ (see here to understand $h_N=1$). In reality, the relationship between two alleles may be vastly more complicated. There is a gradient from complete recessivity to complete dominance (passing through perfect additivity). It is also possible that the heterozygote is more extreme than any of the two homozygotes.

Dominance relationship - Number of alleles

As the number of alleles varies, any pair of alleles have a specific relationship of dominance. While empirical studies suggest that if allele A is dominant over B and B is dominant over C, then A is likely dominant over C, it is not impossible that C could be dominant over A. And again here, I am considering only cases of complete dominance but any scenario is possible.

Dominance relationship - Ploidy

The ploidy also varies from one species to the other (and also from one moment in the life cycle to the other for sexually reproducing organisms). If you have  a polyploid, then the number of possible genotypes is higher than 3 (even for a 2 allele case) and therefore the concepts of recessivity and dominance don't necessarily apply that easily.

Dominance relationship - Epistasis

Finally, there might have interaction between loci making that the relationship of dominance at one locus may depend upon the genetic background (that is the other variants present at other loci). Of course, it may as well depends upon the environment but let's not talk about that for the moment.


The textbook descriptions of fatty acid synthesis can be confusing because although the underlying chemistry of the process is universal, the way that it is organised is different in the systems that have been characterised, which include E. coli, yeast and vertebrates.
In vertebrates:
The fatty acid synthase is a dimer of identical multifunctional single polypeptides. The synthesis process involves two -SH groups: one is the terminal group of the pantothenate of the acyl carrier protein domain (Pan-SH) and the other is an -SH group of the condensing enzyme (CE-SH).
For the first condensation step the initiating acetyl group is attached to the CE-SH of one monomer and the incoming unit (malonyl CoA) is attached to the Pan-SH of the other monomer.
The condensation reaction between these two results in the new elongated unit being attached to the Pan-SH. This unit then goes through the reductase/dehydratase/reductase steps to form the new acyl CoA which is finally transferred to an CE-SH group, opening up the Pan-SH for the next incoming malonyl CoA.
This will happen repeatedly in each cycle of the process. Obviously since each monomer has both -SH groups a single fatty acid synthase dimer can be engaged in two elongations at the same time, but these will always include a transfer. It is thought that the initiating acetyl group comes in via the Pan-SH group.
You say:

And after that the acetoacetylACP will be swept back to the other monomere (to the reduction part), is this also right?
Then the reduction-dehydration-reduction steps are happening and at the end of the road you will get butyrylACP which will cut off from the ACP and migrate on the same monomere to the cysteïnresidu at the condensing enzyme (CE) (= translocation).

The diagram that you included clearly shows that the acetoacetyl group is formed via the reduction-dehydration-reduction steps on the same Pan-SH where its precursor was formed by condensation. Only then is it transferred to the CE-SH group. The diagram also indicates that the acetoacetyl group is transferred to the CE-SH of the same monomer. This implies that a growing chain never transfers from one monomer to the other. I have seen other sources which seem to suggest that this step does involve a transfer between monomers.
In fact it would appear from the discussion on the WP page for fatty acid synthase that this is an unresolved issue - see for example:
Joshi et al. (2003) Engineering of an Active Animal Fatty Acid Synthase Dimer with Only One Competent Subunit Chemistry & Biology 10:169 - 173

Abstract
Animal fatty acid synthases are large polypeptides containing seven functional domains that are active only in the dimeric form. Inactivity of the monomeric form has long been attributed to the obligatory participation of domains from both subunits in catalysis of substrate loading and condensation reactions. However, we have engineered a fatty acid synthase containing one wild-type subunit and one subunit compromised by mutations in all seven functional domains that is active in fatty acid synthesis. This finding indicates that a single subunit, in the context of a dimer, is able to catalyze the entire biosynthetic pathway and suggests that, in the natural complex, each of the two subunits forms a scaffold that optimizes the conformation of the companion subunit.


What sequences are between adjacent genes?

No. The intergenic regions are not necessarily heterochromatin. Chromatin conformations are usually very long range and are not usually confined to a single gene. The spread of chromatin state can be prevented by insulators/boundary elements, which again are not a part of the transcribed region. The intergenic regions can also harbour distal regulatory elements such as enhancers and silencers; they can have microsatellites, transposons etc too. To know what all are there in a specific region, you can look at the different tracks in the UCSC genome browser.

In short, there can be functional and/or non-functional DNA in-between the transcribed regions.

Repeat regions need not be heterochromatinized and conversely not all heterochromatic regions consist of repeats.


Is there any scientific evidence that a human has ever grown a third set of teeth?

There are legitimate case reports in credited journals of hyperdontia, or the condition of having supernumerary teeth. Such cases are often associated with congenital syndromes-- cleft lip and palate, trichorhinophalangeal syndrome, cleidocranial dysplasia, and Gardner's syndrome. I included a case report and a comprehensive review for you below.

Case Report from American Journal of Orthodontic Dentofacial Orthopedics, 2011.

Comprehensive Review from Journal of Oral Science, 2014.


Can you build muscles from watching point of view videos of people weightlifting?

That is highly unlikely.

The article to which you linked specifically states:

  While watching other people exercise may increase your heart rate and have other physiological effects, nothing can replace the health benefits of getting off the couch.

With proper nutrition, muscle is built through exercise by

  adding sarcomeres [to muscle cells which is] physiologically determined by the degree of force a muscle can generate that is in turn dependent on the degree of overlap of the thick and thin filaments. Thus, the amount of tension would control the number of in-series sarcomeres in a single muscle fiber.[1]

Watching a show about cooking might stimulate hunger, but it won't put food into your stomach. Watching something that evokes a sympathetic response (fear, fighting, an attractive person exercising vigorously, an athlete in a competitive event, etc.) will elevate heart rate, sweat production, and resting muscle tension, but there is not enough tension to produce muscle growth.

In addition, there might be small deleterious effects to watching emotionally charged movies which elicit a sympathetic response: they cause stress. An effective horror film will elicit tension and maybe even a startle response - making you jump in your seat - but it will also elevate your blood pressure, etc.

Exercise is good for you physiologically. Simple stress without exercise is much less so.[2]

[1] Muscle growth and exercise
[2] The Physiology of Stress: Cortisol and the Hypothalamic-Pituitary-Adrenal Axis (simplified but relevant)


Confusion over equations for population's heterozygosity vs. heterozygous individuals

One is a recurrence equation and the other is a general solution. These are basic concepts of mathematical modelling.

Reccurence equation

A recurrent equation describes the state of a system (here, heterozygosity $H$) at the next time step given the state in the previous time step. The recurrence relation is $H' = (1-1/2N)\times H$. Given the state $H$, at a given generation, one can know the state $H'$ at the following generation (given the population size $N$).

General solution

A general solution describes the state of a system at any time step given an initial state. Not all recurrence relation have a general solution. Here there is a general solution and it is $H_t = H_0 \times (1-\frac{1}{2N})^t$. Given the initial state $H_0$, one can know the state $H_t$ after $t$ generations (given the population size $N$).

Two equations for the same model

The two equations both refer to the same model and therefore the same statistic of expected heterozygosity which, as you said, is $H = 2 p (1-p)$ (for a bi-allelic locus) by definition.

Understanding the basics of mathematical modeling in ecology and evolution

Have a look at A Biologist's Guide to Mathematical Modeling in Ecology and Evolution by S. Otto for an introduction into mathematical modeling in the field of interest.


How correlated are the lengths of tendons in different part of a human body?

I couldn't find studies analysing clearly enough tendons size, but a couple of sources show that they are probably correlated:

One study found correlation between dimensions of Achilles'tendon and other ankle tendons (see table 2).
Another study found correlation between height and dimensions of some tendons (see table 2).

Anyway, since correlation is not very strong, I doubt if the effect found is just the obvious correlation of dimension of all body parts to the general dimension of body - that is, bigger people tend to have bigger tendons, bigger bones, bigger livers, and so. It would be interesting to do a regression analysis of tendons dimensions taking in account body dimensions and other tendons dimensions. This way we could be able to see if people with some bigger tendon (compared with people of the same body size) tend to have other bigger tendons.


Cats, Dogs and Bears - how are they related?

Cats, dogs and bears all belong to the Carnivora clade of mammals, but they are not the only ones belonging to this clade.
For instance, cats are more closely related to mongoose and hyenas than to dogs or bears, who in turn are more closely related to raccoons, weasels, and walruses.

Their common ancestors likely displayed various adaptations to a carnivorous diet, as the name of the clade suggests, and which are still present in many extant Carnivora (the panda being a well-known exception).

Together with many other groups of mammals, Carnivora are part of a clade named Laurasiatheria thus named because they may have originated in the Laurasia supercontinent, which comprises nowadays north America and Eurasia.


Why would mutation rates increase in a tumour?

Cancer cells generally lack the "safety mechanisms" or "check points" that prevent normal cells from replicating, and some of these mechanisms are also involved in ensuring that DNA replication proceeds without serious errors. Inactivating these safety mechanisms lets cancer to cells divide rapidly, but at the same time also causes their genome replication to be "sloppy", introducing various errors.

The P53 protein is probably the most well-known example of such a "safety mechanism". In normal cells, P53 arrests the cell cycle if breakage occurs in the DNA strands; but cancer cells often inactivate P53, and consequently they tend to proceed with DNA replication even if DNA is damaged. A consequence is that DNA is often in a state of disrepair in cancer cells. (A review of P53 here.)

This lack of proper "quality control" can lead to loss of large pieces of the genome, even entire chromosome arms. While it may seem strange that the cells can survive this, keep in mind that the genome encodes information to support the complex working of an entire organism. Loss of a chromosome arm would indeed be lethal to the organism as a whole --- perhaps it would disrupt brain development, or the immune system. But for single cell to survive and develop, most genes are actually not essential, likely because there are so many redundancies. This is frequenly seen in genome-wide RNA interference screens, for example this paper. Remarkably, cells can even lose the entire mitochondrial DNA (which means they cannot even respire anymore!) and still survive.

It is not clear that "non-cancerous cells would perish" if they would similarly lose DNA. They would likely arrest and turn senescent because they detect DNA damage, precisely because of these safety mechanisms --- but that is different. The loss of genes in itself may not be lethal to a normal cell, it's rather that normal cells "choose" not to continue when this happens. But this distinction is probably difficult to test experimentally.


How do I know which alleles the parents have?

Let's go step my step here.

Going by your notation I'll call the square as Male and Circle as female.
So from this information I can confidently say that you disease is not X linked dominant.

Why?

Because Females carry XX, that would mean to be X linked dominant she had to be X'X' for the disease allele to manifest it's phenotype. But if it were X'X, it would lead to a loss in fitness. And since the Male is normal and XY he does not carry the disease which tells us that the disease is definitely not X linked dominant.

Therefore in a cross of X'X' and XY you get individuals X'X and X'Y in the ratio 1:1

Coming to AD Autosomal Dominant may mean A'A' as the disease allele is present in homozygous condition. A heterozygous condition would lead to loss in fitness, not necessarily a disease.

A Father may be AA or AA'

so this cross would give you individuals

AA' for A'A' x AA
A'A A'A' for AA' x A'A'

so in this case you always get the disease in autosomal dominant, what remains is recessive.

AA or AA' Father x A'A' Mother

Products AA' for AA x A'A'
or AA' and A'A' for AA' x A'A'

which tells us that the disease is actually Autosomal recessive on the mother.

The father's genotype for the allele is AA or homozygous dominant

and the disease is autosomal recessive for the disease in the mother.


According to the following sources, venom resistance has evolved in both snake prey and predators. Also, resistance can be just regional/confined to a certain population. That suggests that arms races occur, where the composition of the venom of a certain species is constantly changing, and so are the defenses of the prey and/or predators who get bitten. In that case, a snake venom is not the same in chemical composition for very long, and might not be the same across populations of the same species of snake. But those differences might be on a smaller scale than you are looking for. I don't know anything about how this affects effectiveness of antivenom. However long it is until the antivenom loses effectiveness, it might be much shorter than the divergence time since that snake species branched off from the evolutionary tree.

Ground squirrels and rattlesnakes:

"Snakes win: Coevolution of venom function and prey resistance in a rattlesnake-squirrel arms race;

"Coevolution of venom function and
venom resistance in a rattlesnake predator
and its squirrel prey"

"How is rattlesnake venom like fine wine? Both have regional varieties"

(I wanted to make this a comment but don't have the rep for that).


Pathophysiology of pink frothy sputum in pulmonary edema

Even though the fluid in pulmonary edema is a transudate, there is blood in it. This is substantiated by the fact that there are microhemorrhages in acute lung congestion and hemosiderin laden macrophages or 'heart failure cells' in long standing pulmonary congestion on histology. These signify that RBCs have escaped the vasculature to enter the tissue (and failed to get back to the blood), while the macrophages have consumed them later on.

Since the blood loss isn't very high, the color is pink rather than red as seen in hemoptysis.

The reason for this is likely due to the significant differences in hydrostatic and oncotic pressures when compared with the rest of the body. In the Lung, one edge of the capillary is up against a single, extremely thin alveolar cell that provides very little pressure to counterbalance the increased forces present in pulmonary edema. Without this inward pressure to stabilize the capillary wall, you end up with a situation in which small ruptures occur at weak points in the AC membrane, unlike elsewhere in the body where pressures are more equalized and change is an osmotic process rather than one of cellular disruption.

Although hemosiderin laden macrophages can be a proof that RBCs leave the vasculature, it is important to note that they can be found in other organs too. One example is the chronic venous congestion of the liver, where the hypoxia (due to congestion) can lead to endothelial damage letting out the RBC, which later get engulfed by macrophages.


Yes, it can, but it is extremely rare.

  ... nosebleeds are rarely fatal, accounting for only 4 of the 2.4 million deaths in the U.S. in 1999 [1].

The main issue is that epistaxis can be a sign of potentially fatal diseases:

  The instances in which nosebleed is potentially fatal are those in which there is a history of recent head injury, severe arteriosclerotic cardiovascular disease or an underlying vascular tumor in the nasal chambers. Fatal nasal bleeding has not been reported in children [2].

Here are some causes which can lead to fatal complications if left untreated [3]:

  Leukaemia
  Hypertension
  Coagulation disorders
  Hepatitis
  Head injury
  Myelodysplastic syndromes - Epistaxis

Death by massive hemorrhage can occur when epistaxis is the result of a ruptured aneurysm [4, 5, 6]:

  An instance of fatal epistaxis is reported in a patient with an unsuspected aneurysm of the infraclinoid portion of the internal carotid artery. There was no known history of trauma. The aneurysm was subsequently detected on an old X-ray film. Epistaxis from an aneurysm at this site is nearly always preceded by significant head trauma and is associated with cranial nerve palsies, a syndrome with a high mortality. Epistaxis from rupture of a non-traumatic aneurysm is very rare [4].

References:

Work Table I. Deaths from each cause by 5-year age groups, race and sex: US, 1999 Page 1922. U.S. Centers for Disease Control Published 2001-05-11. Via Wikipedia contributors, "Nosebleed," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Nosebleed&oldid=617613780 (accessed July 21, 2014).
QUINN FB. Fatal epistaxis. Calif Med. 1961 Feb;94:88-92. PubMed PMID: 13738727.
Right Diagnosis (tm). Epistaxis Deaths. Available from http://www.rightdiagnosis.com/symptoms/epistaxis/deaths.htm (accessed 21.07.2014)
HORNIBROOK, J. and RHODE, J. C. (1981), FATAL EPISTAXIS FROM AN ANEURYSM OF THE INTRACRANIAL INTERNAL CAROTID ARTERY. Aust. N.Z. J. Surg., 51: 206–208. doi: 10.1111/j.1445-2197.1981.tb05942.x
P. N. Pathak (1972). Epistaxis - due to ruptured aneurysm of the internal carotid artery. The Journal of Laryngology & Otology, 86, pp 395-397. doi:10.1017/S0022215100075423.
Urso-Baiarda F, Saravanappa N, Courteney-Harris R. An unusual cause of massive fatal epistaxis. Emerg Med J. 2004 Mar;21(2):266. PubMed PMID: 14988378.


So if you're reading the flowchart, understanding the notation of the arrows is important:

We have rectangles around the gene products
There's a circle, denoted by DNA, noting that the proteins are expressing the product that follows through interaction with DNA
The solid line with an arrowhead means there's some sort of interaction
The solid line with the blunted or T head means this pathway or interaction has been abrogated somehow
The solid line with the slash through it means there's some missing interaction that we don't see
The +p means phosphorylation
The double solid line to the left is the plasma membrane, whereas the dotted line central to the figure is the nuclear envelope
The dotted line means an indirect effect

Source: http://www.genome.jp/kegg/document/help_pathway.html

The pathway is kind of broad but it provides some mechanisms for tumorigenesis from two standpoints: chromosomal instability, and microsatellite instability. The pathways we're seeing promotes the tumor development by upregulating proliferation signals, and downregulating apoptosis pathways. There's bound to be more to it, especially since we see other players involved when we get into cases like metastasis like snail1/2, Met, Src, etc. Below is a survey of apoptotic pathways from Nature, with pro-apoptotic in red, and pro-survival in green:

Source: http://www.nature.com/reviews/poster/apoptosis/index.html

Ignoring the therapeutic targeting jargon, you can see that when growth factors bind, the cell generally pushes towards a survival state. When death factors bind or something goes wrong, the cell pushes toward an apoptotic state. Cancers, however, are intrinsically disregulated:

They have methods of overstepping their boundaries as cells, which is what makes them problematic. The general conclusion I'd draw from that KEGG pathway, though, is that many pathways need to be disregulated to end up with colorectal tumors, and the method of disregulation is (a) downmodulated mismatch repair, and (b) chromosomal aberrations due to duplication, etc. Andkeeping in mind the box of oncogenes vs tumor suppressors in the corner: "An important difference between oncogenes and tumor suppressor genes is that oncogenes result
from the activation (turning on) of proto-oncogenes, but tumor suppressor genes cause cancer when they are inactivated (turned off)"


Improving transformation efficiencies- induce supercoiling?

Here is a report that shows significant increase in transformation efficiency for large plasmids (transformation was by electroporation. However the paper has been cited fewer than ten times so clearly the technique did not catch on.

  Zhixing, Y and Nahon, J-L (1995) DNA gyrase improves DNA transformation of E.coli cells with large recombinant plasmids. Nucleic Acids Res. 23:3353-3354


Cancer is commonly defined as uninhibited cellular replication caused by mutations to the genome.

Genes where cancer-causing mutations have been identified are known as oncogenes; the COSMIC (Catalogue Of Somatic Mutations In Cancer) database lists all of the known oncogenes (547 to date - 23rd Jan 2015 - 1% of all human genes!) [1].

The effect of a particular mutation would be to alter in some way the expression of a gene or genes. This may be directly, for instance rendering a tumour-suppressing gene unable to fulfil its role [2], or indirectly, for instance by affecting epigenetic mechanisms that in turn affect expression of genes involved in cell cycle regulation [3].

To my knowledge cancer is not 'caused' by just a change in expression of a gene, although it may be mediated by it. The change in expression or effectiveness of a gene (such as tumour suppressor p53) resulting in uncontrolled cell division is caused by mutations at the genomic level.

What causes the mutations?

Lots of factors can cause mutations, from chemicals (e.g. from cigarette smoke, not just restricted to the lungs either [4]) to mistakes in the DNA replication machinery as somatic cells undergo normal cell division [5].

The last reference there provides very compelling evidence for the reason that some tissues are more predisposed to cancer than others; tissues with higher cell turnover (and thus require more cell division) have higher incidences of cancer - see the below figure from [5]! This figure separates "lung cancer" into two groups to show that even non-smokers have risk of developing lung cancer, but not as high a risk as those who smoke.

http://cancer.sanger.ac.uk/cancergenome/projects/census/
Muller, P.A.J.; Vousden, K.H. (2013) p53 mutations in cancer. Nat Cell Biol. 15:2-8
Hamamoto, R.; Saloura, V.; Nakamura, Y. (2015) Critical roles of non-histone protein lysine methylation in human tumorigenesis. Nat Rev Cancer. 15:110-124
Cancer research UK report on smoking and cancer
Tomasetti, C. & Vogelstein, B. (2015) Variation in cancer risk among tissues can be explained by the number of stem cell divisions. Science 347, 78-81


Why Egg shell is not called a cell wall?

Egg shells are actually porous so that the organism inside can aquire oxygen and get rid of carbon dioxide as it develops (http://www.scientificamerican.com/article/bring-science-home-chick-breathe-inside-shell/).

Although gametes (eggs and sperm) are single cells, an egg shell (or "wall" if you like) is created by the mother (therefore external to the egg cell) and contains many compartments separated by protein membranes:

https://www.exploratorium.edu/cooking/eggs/eggcomposition.html

The initial egg cell is a tiny fraction of a size of the egg visualised here, so it would therefore be incorrect to call the egg shell a "cell wall" as it is a structure independent of the egg cell itself.


This is a diagram of a cross-section of the cornea:

It is an amazing but relatively simple structure, the shape of which is responsible for about 60% of our focusing power, and the clarity of which allows light to enter. It is avascular (no blood vessels), and the non-mylenated nerve endings are very tiny and present in the epithelium.
Transplanting this relatively simple tissue is easy (well, not do-it-at-home easy, but easy.) The only problem with cutting all those nerve endings is that the new cornea will feel nothing if there's dust in the eye, etc. This is a problem, but nothing compared to blindness.
This is a diagram of a cross section of the retina:

As you can see, it is not nearly as simple as the cornea. The nerves (to the left: yellow, light blue, medium blue and darker blue), which collect information from the rods and cones (pink and purple) are very numerous, and absolutely vital to the ability of the brain to interpreting information from these photoreceptors. Therefore, a cut piece of retina immediately loses the ability to send any information to the brain. To transplant it into an eye with a damaged retina would do nothing to improve vision. Also, it is not easy surgery. It's very difficult.
What has been called "retinal transplants" in the recent past have been tiny pieces of embryonic retina, about...

4 millimetre square of retinal tissue, complete with retinal progenitor cells and the retinal pigment epithelium that nourishes them. The tissues were placed in the sub-retinal space beneath the fovea, the area of the retina responsible for sharp central vision.

Note, they didn't try to connect nerves or blood vessels. And, it came from an embyro (so the supply is a problem.) The improvement in vision - which was significant in 7 out of 8 recipients (one patient going from 20/800 to 20/160) - is not long lasting, and believed to have been not from the transplanted retina connecting to the existing retina, but from the release of growth factors from the embryonic tissue improving the health of the degenerating retina.
The newest in "retinal transplants" (which might be better called stem-cell-supplied growth factors implanted in the retina) actually derives from the patient's own stem cells:

A Japanese woman in her 70s is the first person to receive tissue derived from induced pluripotent stem cells, a technology that has created great expectations since it could offer the same regenerative potential as embryo-derived cells but without some of the ethical and safety concerns. [No news yet on whether it worked.]
In a two-hour procedure... a team of three eye specialists lead by Yasuo Kurimoto of the Kobe City Medical Center General Hospital implanted a 1.3 by 3.0 millimetre sheet of retinal pigment epithelium cells into an eye of the Hyogo prefecture resident, who suffers from age-related macular degeneration, a common eye condition that can lead to blindness.

TL;DR: It's not as easy as taking cadaver retina and replacing a patients retina (that would result in immediate and permanent blindness). Whereas corneal transplantation is very easy.
Corneal Innervation and Cellular Changes after Corneal Transplantation: An In Vivo Confocal Microscopy Study
Retinal transplants see fleeting success
Japanese woman is first recipient of next-generation stem cells


There are two different ways to interpret this question:

Does the spliceosome splice all introns of an mRNA simultaneously or sequentially?

Can a spliced mRNA be re-spliced?

How does a spliceosome proceed along the mRNA?
According to this review:

splicing generally proceeds in a 5′ to 3′ direction, although neighboring introns are not always excised in this order, nor are all introns completely removed during synthesis (36).

Splicing tends to happen immediately following transcription of introns, so it is to some extent necessarily sequential (same review):

Time course measurements by RT-PCR of multiple pre-RNA species synthesized after reversing 3 hours of DRB inhibition have shown that intron excision occurs within 5 – 10 minutes of synthesis of the downstream neighboring exon, irrespective of the length of the intron, the length of the gene or whether the intron is excised by the major or minor spliceosome (42).

Thus, it is not physically possible in many cases to splice all the introns of a RNA simultaneously, because splicing begins before pre-mRNA synthesis is even complete.
Re-splicing mature/spliced mRNA
There are a few different mechanisms by which RNA can be spliced at more than one point. For example, ribozyme splicing occurs in a spliceosome-independent fashion, so an mRNA with a ribozyme in it and also non-ribozyme introns will necessarily have multiple rounds of splicing.
There is additionally so-called recursive splicing of very long genes/introns. This is when a spliced intron must be handled in multiple rounds due to its length/complexity; it's a bit involved so I won't go into it here.


No, this will not happen. mRNAs are inspected in the nucleus before they are exported into the cytoplasm (at least in eukaryotes), where transcription and translation don't happen at the same place. This ensures that no mRNAs without stop codons or premature stop codons are exported. This phenomenon is called
"mRNA surveillance". mRNAs that do not pass this quality check, are degraded. See the Wiki reference for some basic information and the references below for more.

References:

Process or perish: quality control in mRNA biogenesis.
The exosome and RNA quality control in the nucleus
A faux 3′-UTR promotes aberrant termination and triggers
nonsense-mediated mRNA decay


What will happen if mitochondria had a structure like lysosomes?

Mitochondria are double membraned organelles with an outer membrane which is a rod-like shape, and a convoluted inner membrane (Figure 1).

Figure 1

On the other hand, a lysosome is a single-membraned vesicle containing digestive enzymes, with no internal structure. Its function is to keep these dangerous enzymes in a compartment.

The "purpose" or "role" of the mitochondria is to do cellular respiration to provide energy (as ATP) to the cell. To do this, the mitochondria have many respiratory complexes (groups of proteins which make respiration happen) embedded in their internal membrane (Figure 2). As you can see in Figure 1, this membrane is convoluted with many folds; this is to increase the surface area of the membrane to have more space for respiratory complexes.

Figure 2

Moreover, these complexes pump out H+ ions into the intermembrane space. The fact that there is this thin intermembrane space allows for a buildup of H+ concentration which is crucial for ATP production (through the action of ATPase). This process is called chemiosmosis and you can learn more about it here as a starting point. A lysosome with only one membrane does not have an "intermembrane space", so this buildup in concentration cannot happen.

If you would like to learn more about mitochondria, I would recommend reading Power, Sex, Suicide: Mitochondria and the Meaning of Life by Nick Lane.


Fst genetic distance: Autosomal vs. mtDNA

Yes, you are correct.

$F_{ST}$ can vary among specific genetic regions considered. If for example there is a strong influx of females from population A to population B, then the mtDNA and the X chromosome (excluding the pseudo-autosomal region) would show much smaller $F_{ST}$ between the two populations than the Y-chromosome would.

Many other non-demographic processes can affect $F_{ST}$. Background selection (Charlesworth et al., 1993; Matthey-Doret and Whitlock, BioRKiv, 2018), selective sweep (e.g. Chen et al., 2010), heterozygote disadvantage (Ingvarsson and Whitlock, 2000), negative epistasis and other processes can affect $F_{ST}$ as well and cause $F_{ST}$ to differ among genetic regions. Even mutation rate variation (Whitlock and McCauley, 2001) can affect $F_{ST}$ (if the mutation rate for the loci considered is not ridiculously small compared to the migration rate).

For an introduction into the common misunderstandings of how $F_{ST}$ works, Whitlock and McCauley (2001) is a must read!

  Just to complete this answer, would Fst computed from autosomal SNPs be fully representative of the genetic distance between two populations? Say for the influx of females from A to B, will the autosomal Fst correctly show that the admixed population is between A and B (depends on mixture proportion)?

The difficulty here is in the phrasings fully representative of the genetic distance and correctly show. There is no correct (true) genetic distance among populations, there is only the statistics of genetic distance that one wants to define and those statistics are affected by various processes.

Would an influx of female among populations affect $F_{ST}$ at autosomal loci? Yes. Would this effect be the same than at mtDNA? Not exactly, no. Is the entire parsing of genetic variation among population represented by $F_{ST}$? No, $F_{ST}$ is just a summary statistic (just like a mean or a variance is).

If there is a specific statistic (such as the effective migration rate, the effective population size or the location of loci involved in local adaptation for examples) that you are trying to infer from these $F_{ST}$ calculations, then maybe you should ask whether computing $F_{ST}$ by a specific method would allow you to make good inference of a specific statistic of interest.


Looks like a house spider (Tegenaria domestica)


According to wikipedia and MedlinePlus muscle cramps can be caused by muscle overuse or injury or dehydration and lack of minerals (eg. potassium or calcium). In this wikipedia page you can read about the mechanism of muscle contraction. I'd emphasize and quote the most important parts here:

  ATP binds to myosin, allowing it to release actin and be in the weak binding state (a lack of ATP makes this step impossible, resulting in the rigor state characteristic of rigor mortis). The myosin then hydrolyzes the ATP and uses the energy to move into the "cocked back" conformation. In general, evidence (predicted and in vivo) indicates that each skeletal muscle myosin head moves 10–12 nm each power stroke, however there is also evidence (in vitro) of variations (smaller and larger) that appear specific to the myosin isoform.
  Steps 9 and 10 repeat as long as ATP is available and calcium is freely bound within the thin filaments.

As you can see ATP is essential in the release of myosin from actin. In case of muscle overuse and dehydration ATP is depleted from the muscle cells and may cause the muscle to cramp.

Also according to this site it is said that repetitive firing of motor units with high frequency is associated with muscle cramps, although tehe origin of this is yet not clear. It can be either from the central nervous system or the peripherial.


Is saturation of olfactory cells able to create a feeling of another odour when it stops?

Yes, there is something like an "odor afterimage", at least in rodents. This is the paper:

http://www.pnas.org/content/110/35/E3340.abstract

But have in mind that this phenomenon is quite different from visual afterimages. First, it doesn't depend strictly on "adaptation", because adaptation is a property of the sensory organ, not of the brain. Second, besides all the qualia questions, it doesn't seems to create different olfactory sensations, or a "complementary odour" as you said. One of the reasons for this lack of "complementary odour" is that the complexity of olfactory receptors (simply put, the number of different receptors and their activity) is way higher than that of visual receptors, so, it's not a simply matter of receiving more impulses from the non-adapting receptors than from the adapting ones, as in vision.


So most cells require growth factors and survival factors to stay alive in an organism. Cells which stop receiving survival factors, such as sperm, undergo a process of programmed cell death (PCD) called apoptosis. Some cells will also undergo necrosis, or autophagy, among other types of PCD. Lachaud et al. performed a study in 2004 on the contribution of apoptosis and necrosis in ejaculated sperm. They make note in the intro that from other literature that we see some hallmarks of apoptosis like externalized phosphatidylserine, fragmented DNA, etc. despite inactivated nuclei and a small cytoplasm. Their data notes that ejaculate sperm cell death mainly occurs from necrosis, however, because sperm themselves lack the ability to initiate apoptosis. However, in the testes, there's data to note that apoptosis plays a role, and the presence of apoptotic spermatozoa in the ejactulate may be result of the inititation of apoptosis by factors which still inside the body. Apoptosis of spermatozoa in the testes is currently under investigation in male infertility, and damage in cryopreservation.

Just to give you an idea of the difference, necrosis is a much messier outcome derived from physical factors, or those factors external to the cell. Apoptosis is organized, controlled, and modulated by cellular signals.


When running gels what is the difference between constant volts or constant amps?

I'll answer only for SDS-Page, which is the system I am most familiar with.

With a discontinuous buffer system, such as the well-known Laemmli system, resistance increases during electrophoresis, as (very mobile) chloride ions are replaced by glycinate (glycine ions).

From Ohms law:

  Voltage (V) = Current (I)  x Resistance (R)

and the definition of power (Watts):

  Watts (W) = Current (I) x Voltage (V) = I2 x R

At constant current electrophoresis will proceed at a uniform rate, however, as the resistance increases, so too will the voltage and the amount of heat generated.

In some discontinuous buffer systems, such as the Tricine/SDS system due to Schägger & von Jagow, this may be enough to crack the gel plates!

At constant voltage, the current will decrease during electrophoresis; as a result less heat will be generated than constant current electrophoresis, but the rate of migration of the sample will decrease with the decrease in current.

References

Laemmli, U.K. (1970) Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature 227, 680-685. [PubMed]

Schägger, H. & von Jagow, G (1987).
Tricine-sodium dodecyl sulfate-polyacrylamide gel electrophoresis for the separation of proteins in the range from 1 to 100 kDa. Anal Biochem 166, 368-379.[PubMed]


I know it is some sort of clown but I cannot find the specific type after that.

This is a juvenile Plectorhinchus chaetodonoides, which carries the nickname of "Harliquin sweetlips". With respect to the clownfish, they are similar up to the order Perciformes.

  Juveniles are brown with large white blotches and mimic the movement of a poisonous flatworm for defence against predators. They gain more spots and the spots reverse from white to black as they age.


Why do three nucleotides code for one amino acid? Why not 5 nucleotides?

The more bases there are per codon the more information you can code for. There are only 22 different amino acids, in consequence we need minimum 3 bases per codon.

1 base-codon --> 4^1 = 4 possible codes which are:

A / T / C / G

2 base-codon --> 4^2 = 16 possible codes which are:

AA / AT / AC / AG / TT / TA / TC / TG / CC / CA / CG / CT / GG / GC / GT / GA

3 base-codon --> 4^3 = 64 possible codes which are:

AAA / AAT / AAC / AAG / ACA / ACT / ACG / ACC / AGA / AGT / etc...

4 base-codon --> 4^4 = 256 possible codes which are:

AAAA / AAAT / AAAC / AAAG / AATA / AATC / AATG / etc..

5 base codon --> 4^5 = 1024 possible codes

If we had only 2 bases per codon we couldn't code for all of the possible different amino-acids.

On the other hand there are several costs associated with carrying lots of DNA. It takes space, it takes energy and matter to get copied, it takes time to copy it (generation time might be limited by copying time), … I have just asked this question hoping to make things clear about the possible costs. If there is a cost associated with having a 4-base codon system compare to a 3-base codon system but there is no associated benefit. Such trait (that has a cost with no benefit) are not expected to evolve (counter-selected).

You'll notice that there are 64-22=42 extra possibilities. In consequence the genetic code is redundant. Meaning that several codon codes for the exact same amino-acid. And interestingly, it is often a the last of the three bases of the codon the does no yield to any change in the coding sequence as you can see here.

This post about the evolution of genetic code might interest you.


How is protein cavity centre related to binding?

As you can find under the table with cavity centers in pdf version of this article:

  The table lists the protein’s PDB ID, the ligand considered and the specified cavity center. 22 ligands are similar to hexoses in shape and/or size. The cavity center is the centroid of the reported PDB atom numbers.

And a little later:

  The binding-site center is computed as the
  hexose pyranose ring centroid for the positive examples,
  and as the ligand or empty pocket centroid for the negative
  ones. The hexose pyranose-ring atoms are located up to
  2.9
   ̊
  A away from the ring’s centroid. Since some atomic
  interactions can be important up to 7
   ̊
  A [22], we consider
  the binding-site as all protein atoms present within a 10
   ̊
  A radius sphere around the binding center. All other atoms
  are discarded.

So basically @aandreev is right. You can read about centroids here


Plants that are siblings: How does this impact pollination?

In your case, your two bushes might well be half sib (the pollen might come from different donor) and one (or maybe even both) bush might result from selfing event. In any case, if the species is able to self, I don't see why full sib mating would cause any trouble.

Many species protect themselves from selfing. These plants are said to be self-incompatible. The evolution of the genetic mechanism underlying such self-incompatibility has been highly studied and is fascinating. The wikipedia article offers a good overview.


Online multiple sequence alignment with constraints

Answer

You can't. Clustal doesn't provide the options of setting the sort of restraints you would like. Multiple Sequence Alignment (MSA) is difficult to program and the authors of Clustal have been refining their algorithm for years. If it were perfect and completely robust they might be in a position to add more user tweaking, but at the moment you're stuck with those provided.

Comparison matrices and forcing alignments

It may be worth while to mention how one can force particular correspondences in simpler pairwise alignments. This involves manipulation of the comparison matrix used to score the comparison. DNA comparison matrices may be very simple, scoring, say, 1 for a perfect AA, TT, GG, CC match and 0 for any mismatch. Protein comparison matrices are more complex, with the values for perfect matches dependent on rarity and unique function (e.g. In the PAM250 substitution matrix WW scores 17, whereas GG scores only 5) and the values for mismatches also varying markedly (e.g. ED scores 4, compared with 5 for EE; but EW scores –7). There are various matrices available, so implementations of the Smith Waterman and Needleman and Wunsch pairwise comparison algorithms generally allow you to specify your own.

Suppose you have biological information (not intrinsic in the algorithm) that makes you wish to force an alignment. For example, AAATAA sequences near the polyA tail of two mRNA 3'UTRs should align, but sometimes do not because other stretches of As give better scores. What you can do is replace the AAATAA by AAAZAA in each case, and then modify the scoring matrix so that ZZ scores very highly (e.g. 20) compared with AA. This will force the alignment, after which you can change the Zs back to Ts.

Multiple Sequence Alignments tend to to use position-specific dynamic scoring matrices. As the overall sequences align, the original scoring system is adjusted to reflect the frequency found at a particular position. (For example if a position is skewed to E in 90% if cases, EE will score more than at a position in which E is found only in 20% of cases).

I'm not saying it would not be possible to change the initial Clustal matrix with Zs at a particular position, but I don't think this possibility is provided. (Anyway your situation is more complex.) Glancing at the Clustal Omega paper, I see that they allow, indeed encourage, you to build up alignments from previous profiles. If you managed to force the alignments of a few sequences and input the profile derived from that, you might get what you want. But I imagine that requires the command-line program from Dublin, rather than the EBI online version.


How are at home fermentations without starter cultures controlled?

A "starter culture" is just a culture of preferred organisms. They probably differ little from local wild organisms. For example, a mixture of flour and water left to stand will (with luck) be colonized by yeast in the air that result in a serviceable yeast culture. Control of this process entails nothing more than observation over time. The environment and nature of the medium suffice to control the bugs that colonize it.

Both the Korean and Chinese versions of kimchee depend on moisture and acidity (and perhaps salinity) to inhibit unwanted molds/bacteria. The process is evidently self-controlled, but I recall seeing a film in which it was said that failure to add salt to the mixture could result in spoilage. Note that in the linked article, the author says cavalierly that one can scrape any mold that forms off the cabbage and continue with the fermentation because mold will not grow in liquid--patently false but probably "true enough" not to affect results.

Aspergillus oryzae colonizes rice, and rice with Aspergillus growth can be subjected to a secondary yeast fermentation that yields sake. The commercial production uses highly-prized starter cultures for both the mold and yeast, but it is possible to substitute other varieties of Aspergillus. For example, one can induce A. niger to grow on a citrus peel, and transfer the colony to rice. The sake that results is fine. But in this case one would want to rule out species of Aspergillus that are associated with toxins. For similar reasons some care is taken in sterilizing containers used to make wine.

In any of these processes there is a possibility of colonization by the wrong flora. The cultures are controlled by the content of the nutrients and climate and observed carefully. Over centuries there have probably been many unfortunate accidents involving unwanted organisms. There is nothing like violent illness to bring the integrity of a process into focus.

In short, the control of home fermentations lies in (1) statistical likelihood that the right organism is present in the environment; (2) the nature of the nutrient and climate; (3) the experience of the person(s) monitoring the process; and (4) luck.


How do animals learns seductional behaviour?

Some behavior can be traced to the genome. In Drosophila there are many interesting studies that show how genes and courtship behavior are related Example.

In mammals, the environmental component in determining courtship behavior is for sure, much more relevant than in Drosophila.


How does natural selection process escape from local optima?

From your profile, I see that you have some knowledge in computer science so I will try to use some terms from the field of machine learning!

Natural Selection

Natural Selection (NS) can only lead a population toward local optimum. In other words, NS is like a greedy algorithm. Mutations and genetic drift do not behave like a greedy algorithm.

Genetic drift

Genetic drift may allow to go toward the other direction than the heuristic of NS allowing eventually to reach another attractor. This concept is called shifting balance theory.

Mutations

Mutations can allow all sorts of jump! Mutations Causing large jumps are generally called large-effect mutations (see this section of the wikipedia article for more information).

Fitness landscape changes through time

Also note that the fitness landscape is not stable over time. The fitness landscape depends upon the environment the individuals experience. It would therefore be naive to assume that a specific population had to go through a specific fitness valley in the past just because the valley exists today.

Sexual reproduction and recombination

The fitness landscape analogy depicts the genotype - fitness relationship (some fitness landscape depict the phenotype - fitness relationship but I will ignore them here) for a given individual. One can place all individuals of a population over this landscape and may have some feeling of where the population position over the landscape is. However, this may be misleading.

The fitness landscape is highly multidimensional (one dimension for each amino acid and there are billions of them) and therefore through sexual reproduction and recombination, it is possible that an offspring finds itself in a totally different attractor than the rest of the population. As such, in presence of sexual reproduction and recombination, NS only could lead a jump from one attractor to another one (see Bergman and Feldman 1992). This effect is even more considerable in presence of epistasis.


Is it "easier" for researchers to detect evolutionary ancestry than distance in the evolutionary tree?

If you take two modern species (let's denote them with A and B) you can't really say that A is an ancestor of B or vice-versa, but you can say that they are related to some extent, that is they have a common ancestor that lived X years ago. But then all eukaryotes are believed to have a common ancestor that lived an eon ago. Hence the notion of phylogenetic relatedness  is relative by definition. That means that all species are related, but when you take a bunch of them you can try to reconstruct the order of speciation. This can be achieved by calculating distances (e.g. genetic sequence distances, morphological distances) and applying an evolutionary model. A brief summary is that you NEED to have a sort of distance to investigate ancestry in the first place and then you clearly NEED more than 2 species for your phylogenetic constructs to make any sense.

Since I find that your statement makes little sense, obviously I can't find a reference to bake your words. But I can give you an exhaustive list of good phylogenetics textbooks for your erudition.

EDIT

I believe that one thing is worth a remark. In fact it is easier to correctly reconstruct the order of speciation events than it is to precisely estimate any sort of evolutionary distance, because the distances we have are models. Simply put they approximate the number of evolutionary events that have happened since the last common ancestor of some species (or better to say the last common set of genomic and/or phenotypic traits, because speciation is a lot more than simple trait-wise divergence). From this point of view you might say that it's easier to estimate ancestry than it is to estimate distance, but then you will be over-simplifying things to such an extent, that you will drop the fact that there is no way you can speak about ancestry without having some distance estimations in the first place. The precision of distance estimations is a separate topic. So your statement will make a lot more sense if you modify it accordingly.


How many paraphyletic groups can be formed from a phylogeny?

If we define a paraphyletic group as any group on a phylogeny that is not monophyletic, I count there to be 2^n - 2*n paraphyletic groups for a fully ladderized tree with n tips.

There are 2^n possible groups of n species. Of these groups, 2*n of them are monophyletic: n groups containing a single species, and n groups containing multiple species.


What are the criteria for determining the origin and end of muscle anatomically?

This is more of a convention.

The start point or origin is considered to be:

bone which is proximal
bone with higher mass
bone with higher stability during muscle contraction

The end point or insertion is:

the structure that tends to be moved by contraction
tendon
distal end of a bone

Reference: Wikipedia - Anatomical terms of muscle


Is the frequency at which a species mutate affected by natural selection?

Drake's rule

Let $L$ be the size of the genome. Let $\mu$ be the average per nucleotide mutation rate, then the genome-wide mutation rate $U$ is $U=L \mu$. There is a general relationship between the genome size of an organism and the nucleotide mutation rate that makes that the genome-wide mutation rate is often approximatively 1. There is of course several orders of magnitude of variation around this value of 1 among organisms.

This rule is called Drake's rule after the name of the author who first discovered it (Drake, 1991).

To my knowledge, this relationship is not fully well understood. Because you are looking for an adapted mutation rate in your question, I would like to highlight that I would not go about assuming this is adaptive. I could imagine that some molecular genetic constraint of the replication process could be causing this type of relationship between $L$ and $\mu$.

You will probably want to read this post about Drake's rule.

Mutation rate in humans

In humans, the average mutation rate is estimated to be around $\mu=2.5 \cdot 10^{-8}$ (Nachman and Crowell, 2000; see also this post), with a genome size of about $L=3 \cdot 10^9$, leading to an estimate of the genome-wide mutation rate of 80.

Interestingly, the mutation rate is in fathers is age-dependent. See the post Gender and age-specific mutation rate in plants.


Would muscle fatigue still occur if aerobic conditions for a working muscle is maintained?

It seems that you are asking about activity significantly above basal metabolic rate. If aerobic conditions are maintained (and with appropriate training), muscles can operate more or less continuously for very long durations, days to weeks. In non-humans:

Godwits have been recorded flying over 7000 miles (>11000 km) without stopping for 9 days
Arctic terms migrate 44000 miles (>70000 km), albeit with stopovers
Humpback whales migrate 5000 miles (8000 km). Their muscles are probably operating close to continuously.
Many (most?) species of sharks swim continuously.

There are probably other examples as well (feel free to add). For humans, usually the limit to endurance is sleep. Two forms of racing push human endurance, but the longer races almost always require at least minimal sleep:

Ultramarathons, foot races of 50 mi (80 km), 100 mi (160 km) or more (e.g., 24 hours, multi-day).
Race Across America, Paris-Brest-Paris, and similar endurance bicycle races. The RAAM has a record time of 3107 mi (4971 km) in 8 days, 9 hours for a mean velocity of 15.4 mi/hr (24.6 km/hr).


What are senescent cells doing in our bodies?

Senescent cells are cells that go into permanent cell cycle arrest. Although they may be metabolically active, they are not actively dividing. This may occur when cells in our bodies undergo damage from an extraneous or endogenous source. I understand that its role in cancer and aging is a great topic of study.